9 


A    MANUAL   OF    TROPICAL    MEDICINE 


31  A  N  U  A  L 

OF 

TROPICAL  MEDICINE 


ALDO  CASTELLAN  I 

C.M.G.,    M.D.,  M.R.C.P. 

LECTURER   AT  THE  LONDON  SCHOOL  OF  T.  OPICAL  MEDICINE;    EM.    PROFESSOR,   CEYLON  MEDICAL 
SCHOOL;   LIEUT.-COLONEL   R.I.N. M.S.,    I916-I918  (BALKAN  ZONE);   DIRECTOR  OF  CLINIQUI 
FOR     TROPICAL      DISEASES     AND      PHYSICIAN     TO     COLOMBO     GENERAL 
HOSPITAL    [903-1915;   MEMBER   OF   ROYAL  SOCIETY'S  COM- 
MISSION  IN   UGANDA   1902-1903 


ALBERT  J.  CHALMERS 

M.D.,  F.R.C.S.,  D.P.H. 


DIRECTOR,   WELLCOME  TROPICAL  RESEARCI 
MEDICAL  SERVICF,    19OI-I911  :   HOOT   FBLLOl 
MEWCAL  OFFICER,   COl 


(ORATORIES  (SOUDAN  GOVERNMENT)  CEYLON 
'UNIVERSITY  COLLEGE,   LIVERPOOL,    1  89C  ; 
ST  COLONY,    1897.1901. 


THIRD  EDITION 


yCcA 


/ 

NEW  YORK 
WOOD     AND 

MDCCCCXIX 


COMPANY 


Printed  in   Great  Britain 


PREFACE  TO  THE  THIRD  EDITION 

The  second  edition  of  this  manual  went  out  of  print  some  years  ago. 
The  war,  however,  prevented  us  from  preparing  a  revise  at  an  earlier 
date,  and  the  same  cause  has  introduced  many  difficulties  in  the 
preparation  of  this  edition. 

We  have  been  compelled  to  rewrite  large  portions  of  the  book,  and 
have  taken  the  opportunity  to  introduce  certain  subjects  hitherto 
omitted,  and  also  greatly  to  increase  the  number  of  illustrations. 

In  order  to  keep  down  the  size,  we  have  omitted  the  list  of  figures 
and  the  index  of  authors'  names.  Notwithstanding  this,  the  manual 
has  become  somewhat  unwieldy,  but  we  retain  it  in  the  form  of  one 
volume  because  our  experience  in  the  tropics  makes  us  believe  that 
this  is  the  most  convenient  form  for  the  tropical  practitioner  and 
student  alike. 

As  regards  nomenclature  of  parasites,  we  have  followed,  as  in 
previous  editions,  the  rules  of  the  International  Committee;  but 
as  regards  the  names  of  the  diseases,  we  are  using,  in  most  instances, 
the  commonly  known  names. 

Much  of  the  work  detailed  therein  is  original  and  based  upon 
our  life  and  experience  in  the  tropics,  in  which  we  have  resided 
upwards  of  or  exceeding  two  decades.  We  know  how  soon  a  work 
on  tropical  medicine  becomes  antiquated,  and  we  have  ventured  to 
look  ahead,  as  subjects  which  to-day  are  nebulous  and  attract  little 
attention  may  become  of  general  interest  and  importance  in  a  few 
years. 

When  we  consider  the  mass  of  material  which  we  have  been 
compelled  to  handle  in  the  preparation  of  this  edition,  it  is  impossible 
for  us  to  hope  that  we  have  not  omitted  reference  to  important  facts; 


vi  PREFACE 

have  not  done  injustice,  however  unintentionally,  to  some  authors; 
have  not  made  errors  of  transliteration  or  otherwise;  and  for  all 
these  we  ask  the  reader's  indulgence,  and  beg  him  to  remember 
that  during  the  war  it  has  been  most  difficult  for  us  to  obtain  the 
time  necessary  for  the  preparation  of  this  work. 

We  desire  to  record  our  grateful  appreciation  of  the  kind  help 
received  from  Colonel  Leiper,  Major  Low,  and  Professor  Simpson. 

We  gratefully  acknowledge  the  kindness  of  the  following  authors 
or  their  proxies,  as  war  conditions  have  prevented  our  direct 
communication,  in  giving  us  permission  to  copy  illustrations: — 
General  Sir  Havelock  Charles,  Colonel  Sir  James  Can  the,  Colonel 
Balfour,  Colonel  Wenyon,  Colonel  Stephens,  Colonel  Richard  P. 
Strong,  Major  Broughton  Alcock,  Captain  O'Connor,  Dr.  Chris- 
topherson,  Princess  de  Poix,  Mr.  Wellcome,  Professor  Pinoy, 
Professor  Legroux,  Professor  Hewlett,  Dr.  Sambon,  Dr.  James, 
Mr.  Hirst,  Miss  Carter,  Dr.  G.  C.  Shattock,  Dr.  Jackson,  Dr.  Lurie, 
and  Dr.  Guilliermond. 

We  more  especially  desire  to  thankfully  acknowledge  the 
generosity  with  which  Dr.  J.  J.  Bell  has  placed  so  many  of  his 
valuable  photo-micrographs  at  our  disposal. 

We  have  much  pleasure  in  acknowledging  our  indebtedness  to 
the  Tropical  Diseases  Bulletin,  which  has  been  invaluable  to  us. 

The  index  has  been  prepared  by  Miss  James,  to  whom  we  tender 
our  best  thanks. 

Finally,  we  wish  to  acknowledge  the  constant  kindness  and 
courtesy  which  we  have  received  from  our  publishers,  Messrs. 
Bailliere,  Tindall  and  Cox. 

ALDO  CASTELLANI. 
ALBERT  J.  CH ALMERS. 

London, 

August,  1919. 


CONTENTS 


PART  I. 
INTRODUCTORY. 

CHAITEK  PAG   E 

I.    HISTORY  OF  TROPICAL  MEDICINE  ...                                 3 

II.    TROPICAL    RACES                       -                    -  -  -  -  "39 

III.  TROPICAL    CLIMATOLOGY  -                   -  -  -  -  -62 

IV.  TROPICAL    FOODS                       -                    -  -  -  -                               94 
V.    TROPICAL    DISEASES              -                  -  -  -  -  -112 

VI.    FITNESS    FOR    TROPICAL    LIFE         -  -  -  -  -        1 27 


PART  II. 
THE  CAUSATION  OF  DISEASE  IN  THE  TROPICS. 


SECTION  A:  PHYSICAL  CAUSES. 


VII.    TEMPERATURE    AND    HUMIDITY      - 
VIII.    PRESSURE    AND    RADIATION 

IX.    TRAUMATISM  -  -  . 


SECTION  B:  CHEMICAL  CAUSES. 


137 
142 

M7 


193 
203 


X.  POISONS  ------_      I6I 

XI.  ARROW    POISONS   -------       !8o 

XII.  POISONS    USED    IN    FISHING,    HUNTING,    AND    TRADE  -  -       187 

XIII.  POISONOUS    FOOD  ----- 

XIV.  VENOMOUS    animals:    PROTOZOA   TO   ARTHROPODA 

xv.  venomous  animals  (continued) :  pisces  and  amphibia  - 

XVI.    VliXOMOUS  ANIMALS  (COM.'/M.W)  I    REPTILIA  AND  MAMMALIA  -       242 

SECTION  C:  PARASITES. 

Division   I  :  Animal  Parasites. 
Subdivision  i  :   Protozoa. 

XVII.  PLASMODROMATA    AND    SARCODINA  ....       2g^ 

XVIII.  MASTIGOPHORA    AND    PROTOMONADINA       -  -  -  330 
XIX.    TRYPANOSOMID.^E                     -                                                                             -  358 

vii 


riii  CONTENTS 

CHAPTER  PAGE 

XX.    DIPLOZOA    AND    OCTOMITIDE      -----  464 

XXI.    TELOSPORIDIA  -------  469 

XXII.    NEOSPORIDIA      -------  528 

XXIII.  HETEROKARYOTA  AND  CILIATA                     -  544 

Subdivision  2 :   Worms. 

XXIV.  TREMATODA        -------  552 

XXV.    CESTOIDEA            -------  596 

XXVI.    NEMATHELMINTHES         -  -  -  -  -  -621 

Subdivision  3:  Leeches. 

XXVII.    ANNULATA    AND    HIRUDINEA       -----  683 

Subdivision  4:  Ticks  and  Mites. 

XXVIII.    ARTHROPODA     -------  689 

Subdivision  5:  Insects. 

XXIX.    HEXAPODA           -------  743 

XXX.    MALLOPHAGA    AND    ANOPLEURA                   -  749 

XXXI.    HEMIPTERA          -------  761 

XXXII.    DIPTERA:   CULICIDiE  AND  ALLIED  FAMILIES         -                    -                    -  77I 

xxxiii.  diptera  (concluded)  :  muscide  and  allied  families  -              -  814 

xxxiv.  siphonaptera  and  coleopiera         -  857 

Subdivision  6:  Addendum. 

XXXV.    ANIMAL    CARRIERS    OF    DISEASE                   ...                  -  872 

Division  II  :   Vegetal  Parasites. 

XXXVI.    SCHIZOMYCETES                  ------  g22 

XXXVII.    FUNGACE^:    PHYCOMYCETES      -----  967 

xxxviii.  fungace^e  (continued) :  ascomycetes              -  978 

xxxix.  fungaces  (concluded) :  fungi  imperfecti     -             -             -  1035 


PART  III. 
THE  DISEASES  OF  THE  TROPICS. 

SECTION  A:  FEVERS. 
Division    I  :    Causation    Protozoal    or    Probably    Protozoal. 
Subdivision  A:  Carried  by  Mosquitoes. 

XL.    THE    MALARIAL    FEVERS  -  -  -  -  -II  2g 

XLI.    THE    TROPICAL    HEMOGLOBINURIAS  -  -  -  -    1213 

XLII.    YELLOW    FEVER  ------    1229 

XLIII.    DENGUE    AND    ALLIED    FEVERS  ...  -    1 244 

Subdivision  B  :  Carried  by  Sand  Flies. 

XLIV.  PAPPATACI  FEVER     ------  1254 


CONTENTS  ix 

Subdivision  C :  Carried  by  Tsetse  Flies,   Cone-nosed  Bugs,  and 
Unknown  Insects. 

CHAPTER  IAGE 

XLV.    THE    AFRICAN    TRYPANOSOMIASES  ....    1259 

XLVI.    THE    SOUTH    AMERICAN    TRYPANOSOMIASIS  ...    I283 

XLVII.    THE    KALA-AZARS  ------    1289 

Subdivision  D  :  Carried  by  Lice,   Ticks,  and  Mites. 

XLVIII.  THE    RELAPSING    FEVERS  -----  1 308 

XLIX.  TYPHUS    FEVER  _----.  1 326 

L.  THE  SPOTTED  FEVER   OF  THE   ROCKY   MOUNTAINS  -  -  I34I 

LI.  TSUTSUGAMUSHI    FEVER  -  -  -  -  -  I35O 

Subdivision  E  :  Carried  by  Mammals. 

HI.    RAT-BITE    AND    CAT-BITE    FEVERS  -  -  -  -    1356 

Division  II  :  Causation  Bacterial  or  Probably  Bacterial. 

Lni.    THE  ENTEROIDEA   GROUP   OF  FEVERS      -  1 362 

LIV.    PLAGUE  -------    iq1£, 

LV.    UNDULANT    FEVER  -  -  -  -  -  "1437 

Division  III  :  Causation  Physical  or  Probably  Physical. 

LVI.    HEAT    STROKE    AND    HEAT    SYNCOPE        -  -  -  -    I44Q 

Division  IV  :  Unclassified,  Cosmopolitan,  and  War-Zone 
Fevers, 
lvii.  unclassified  fevers  -----  t461 

lviii.  cosmopolitan  fevers  -----  1474 

lix.  war  zone  fevers       -  -  -  -  -  -1 50 1 

Division  V  :  Differential  Diagnosis. 

LX.    THE    DIAGNOSIS    OF    A    TROPICAL    FEVER  -  -  -    15H 

SECTION  B:  GENERAL  DISEASES. 
Division  I  :  Causation  Animal. 

LXI.    FRAMBCESIA    TROPICA    -  -----  1535 

LXII.    VERRUGA    PERUVIANA  ------  1 566 

LXIII.    RHINOSPORIDIOSIS    AND    SARCOSPORIDIOSIS         -  -  -  1578 

LXIV.    PARAGONIMIASIS  ------  1 584 

LXV.    KATAYAMA    DISEASE        ------  1589 

LXVI.    THE    FILARIASES  ------  1595 

LXVII.    THE    MYIASES    AND    ALLIED    CONDITIONS  -  -  -  1619 

LXVIII.    POROCEPHALOSIS  ------  1642 

Division  II  :  Causation  Vegetal. 

LXIX.    LEPROSY  -------    1644 

LXX.    HISTOPLASMOSIS  ------    1669 


x  CONTENTS 

Division  III:  Causation  Chemical  or  Probably  Chemical. 
r-u»u^„  Subdivision  i:   Chemical  Deficiency.  „.__ 

CHAPTER  J  ^  1'AGE 

LXXI.    BERI-BERI    AND    EPIDEMIC    DROPSY         -  -  -  -    1 67 1 

Subdivision  2 :  Poisons. 

LXXII.    TROPICAL    POISONINGS  -  -  -  -  -    1695 

Division  IV:  Causation  Unknown. 

LXXIII.    PELLAGRA  -  -  -  -  -  -  -    I7OO 

SECTION  C:  SYSTEMIC  DISEASES. 
Division  I:  Diseases  of  the  Alimentary  Canal. 

LXXIV.  DISEASES    OF    THE    MOUTH    AND    STOMACH  -                   -  -  1 73  9 

LXXV.  HELMINTH    INFECTIONS  -  1752 

LXXVI.  SPRUE    AND    OTHER    DIARRHOEAS  -                                      -  1780 

LXXVII.  THE    CHOLERAS                    -  -  -  1801 

LXXVIII.  THE    DYSENTERIES           -                  -  -                                      -  -  1 82 4 

LXXIX.  INTESTINAL    SCHISTOSOMIASIS-  ....  ^64 

LXXX.  EPIDEMIC    GANGRENOUS    RECTITIS  ...  -  187I 

Division  II:  Diseases  of  the  Systems. 

LXXXI.    DISEASES    OF    THE    RESPIRATORY    SYSTEM  -  -    1875 

LXXXII.    DISEASES    OF    THE    CIRCULATORY    SYSTEM  -  -    1 895 

LXXXIII.    DISEASES    OF    THE    LIVER   AND    PANCREAS  -  -    1 906 

LXXXIV.    DISEASES    OF    DUCTLESS    GLANDS    AND    METABOLISM       -  -    I9I9 

LXXXV.    DISEASES    OF    THE    URINARY    SYSTEM  -  -    1 926 

LXXXVI.    DISEASES    OF    THE    GENERATIVE    SYSTEM  -    1 938 

LXXXVII.    DISEASES    OF    THE    LYMPHATIC    SYSTEM  -  -    I961 

LXXXVIII.    DISEASES   OF  THE   CONNECTIVE   TISSUES,  MUSCLES,  BONES,  AND 

JOINTS         .------    1967 

LXXXIX.    DISEASES    OF    THE    NERVOUS    SYSTEM    -  I981 

XC.    DISEASES    OF    THE    ORGANS    OF    SPECIAL    SENSE  -  -    1993 

Division  III  :  Skin  Diseases. 

XCI.  PYOGENIC    DERMAL    INFECTIONS  ....  2OI7 

XCII.  DERMATOMYCOSES  .-----  2O4O 

XCIII.  MYCETOMA    AND    PARAMYCETOMA  -                                         -                    -  21  IO 

XCIV.  DERMATITIS    VENENATA                   -  -                                         -                    -  2I5I 

XCV.  ULCERATIONS  -                    -                  -  -                                      -                  -  2165 

X(  VI.  DERMATOZOIASES                -  -  2200 

XCVII.  DYSIDROSES    AND    DYSTROPHIES  -                    -  2222 

XCVIII.  MISCELLANEOUS    DERMAL    DISEASES  -  2247 

XCIX.  COSMOPOLITAN    DERMAL    DISEASES  -  2264 

[NDEX  ...-.--  2285 


PART  I 

INTRODUCTORY 

HISTORY  OF  TROPICAL  MEDICINE 
TROPICAL  RACES 
TROPICAL  CLIMATOLOGY 
TROPICAL  FOODS 
TROPICAL  DISEASES 
FITNESS  FOR  TROPICAL  LIFE 


CHAPTER  I 
THE  HISTORY  OF  TROPICAL  MEDICINE 

Primitive  medicine:  Accadia — China — Japan — America— Foundations  of 
medicine :  Indian — Egyptian — Jewish— Grecian — Alexandrian — Graeco- 
Roman — Byzantine — Arabian — Medieval — Foundations  of  modern  medi- 
cine: The  discovery  of  the  tropics — Early  tropical  medicine — Founda- 
tions of  modern  tropical  medicine:  Causation  of  disease — Helminthology 
— -Protozoology  —  Mycology — Bacteriology  —  Serums  and  vaccines — 
Entomology — Toxicology — Climatology — Dietetics — Clinical  medicine — 
Treatment — Prophylaxis — Research — The  State  and  tropical  medicine 
— The  war  and  tropical  medicine — Modern  journals — Special  works  on 
tropical  medicine — References. 

Primitive  Medicine. 

Primitive  peoples  from  the  earliest  times  had  some  knowledge  of 
medicine,  but  they  did  not  understand  the  phenomena  of  disease, 
which  they  attributed  to  supernatural  causes,  generally  to  evil  or 
offended  spirits.  Hence,  in  order  to  cure  their  ailments,  it  was 
natural  that  they  should  seek  to  propitiate  these  spirits;  and  accord- 
ingly we  find  that  the  medicine  of  primitive  peoples  was  part  of  their 
religion,  and  was  administered  by  their  witch-doctors,  fetishmen, 
and  priests. 

This  primitive  condition  is  still  met  with  in  many  parts  of  the 
tropical  world.  Thus,  on  approaching  a  West  African  village,  little 
images  will  be  found  on  the  roadside  with  offerings,  which  are  often 
to  make  'ju-ju  '  against  some  disease — e.g.,  smallpox — which,  in  the 
guise  of  a  malignant  spirit,  might  otherwise  enter  the  village. 

Among  native  peoples  will  be  found  many  curious  medical,  sur- 
gical, and  obstetrical  practices  which  are  very  interesting. 

In  Ceylon  the  superstitions  are  quite  as  elaborate  as  in  West  Africa,  if  not 
more  so.  Pestilences  are  considered  to  be  punishments  on  the  people  for 
wickedness,  and  to  be  brought  about  by  the  conjunction  of  Saturn  and 
Jupiter,  or  Saturn  and  Mars  in  Sagittarius. 

Every  illness  is  supposed  to  be  due  to  a  demon  or  to  the  '  evil  eye,'  and  it  is 
dangerous  for  a  sick  person  to  come  in  contact  with  an  unclean  person — the 
word  '  unclean  '  being  used  in  the  Biblical  sense — who  is  supposed  to  convey 
to  the  sick  man  a  '  killa  ' — that  is  to  say,  a  something  which  increases  the 
severity  of  the  illness.  When  a  person  is  ill,  every  trivial  incident  becomes 
of  importance,  and  is  discussed  seriously  to  discover  whether  it  is  a  good  or 
bad  omen. 

Another  means  of  prognosis  of  great  importance  is  the  horoscope,  which 
is  generally  made  for  the  child  soon  after  birth,  and  is  written  on  a  palm-leaf. 
From  it  the  influence  of  the  planets  with  regard  to  good  or  evil  on  the  individual 
can  be  calculated.  If  the  influences  of  the  planets  are  unfavourable,  some- 
thing can  be  done  by  propitiatory  means.  In  times  of  pestilences,  when  the 
planets  are  contrary,  the  goddess  Pattini  can  still  intervene  and  avert  the 
epidemic  if  proper  devotion  is  paid  to  her. 


4  THE  HISTORY  OF  TROPICAL  MEDICINE 

Charms  are  used  to  drive  out  the  evil  spirit,  or  devil-dancing  to  shame  or 
terrify  him  so  that  he  may  leave  the  body.  Once  out,  amulets  are  used  to 
prevent  his  re-entry,  and  '  pirit,'  or  the  repetition  of  meritorious  verses  by 
priests,  is  also  adopted. 

Before  any  medicine  can  be  administered,  the  position  of  the  '  kalawa,'  or 
vital  spot,  must  be  ascertained.  This  spot  moves  all  over  the  body  in  regular 
succession,  occurring  in  different  parts  in  different  phases  of  the  moon.  Its 
position  must  be  correctly  calculated,  and  it  will  then  be  seen  whether  it  is 
safe  or  otherwise  to  administer  certain  drugs.  Another  important  matter  is 
the  constitution  of  the  individual,  whether  it  is  inclined  to  be  inflammatory  or 
not,  and  the  person  must  be  dieted  so  as  to  counteract  the  baneful  effects  of 
the  constitution. 

During  pregnancy  care  is  taken  with  the  diet  and  to  avoid  unpleasant 
maternal  impressions,  and  many  curious  superstitions  are  connected  with 
child-birth,  such  as  passing  the  woman's  body  through  a  hoop  in  order  to 
bring  about  an  easy  labour.  Great  fear  is  felt  lest  the  severed  cord  should 
be  drawn  up  into  the  uterus,  and  much  good  luck  is  associated  with  birth  in 
a  caul,  or  even  with  its  possession. 

Native  peoples  have  generally  a  good  knowledge  of  medical  and 
poisonous  plants  growing  in  their  vicinity,  and  it  is  well  for  the 
medical  man  living  in  the  tropics  to  remember  that  cinchona-bark 
was  originally  simply  a  native  Ecuador  remedy,  and  that,  therefore, 
it  is  not  advisable  to  entirely  despise  popular  drugs. 

The  earliest  medicine,  like  that  of  certain  races  at  the  present 
time,  was  largely  religious  or  theurgic,  and  this  is  well  exemplified 
by  the  medicine  in  Akkad  (Accadia). 

Accadia. — Excluding  Egypt,  the  earliest  civilizations  with  which 
we  are  acquainted  are  in  the  neighbourhood  of  Mesopotamia, 
where  the  Sumerians,  or  peoples  of  the  plain,  lived  on  the  banks 
of  the  great  rivers,  and  the  Accadians,  or  peoples  of  the  hills,  on 
the  mountains  to  the  east  of  that  region. 

The  latter  evolved  some  knowledge  of  the  arts  and  sciences, 
including  astronomy,  but  their  medicine  was  of  a  very  primitive 
order,  being  a  mixture  of  demonology,  magic,  and  astrology.     Their   c 
priests  were  the  physicians,  who  attempted  to  cure  disease  by  m, 
exorcisms,  and  philtres  or  drinks,  into  which,  it  is  believed,  they    & 
placed  the  few  medicines  with  which  they  were  acquainted.     Their  A 
religion  was  very  similar  to  the  Shamanism  (vide  Chapter  LXXXIX. )  * 
of  the  Siberian  and  Samoyed  tribes  of  to-day,  and  their  language  for 
long  remained  the  secret  language  of  the  exorcisms  and  charms  of 
Babylonia,  Chaldea,  and  Assyria,  while  many  of  the  practices  of 
the  Ancient  Jews  may  be  traced  to  the  same  source.     The  Chaldeans 
had  two  dread  diseases — Nantar,  the  plague,  and  Idpa,  the  fever — 
and  three  kinds  of  doctors — Khartumin,  or  conjurers;  Chakamin, 
or  physicians;  and  Asaphin,  or  theosophists. 

China. — Accadian  demonology,  magic,  and  astrology  are  probably 
the  foundations  of  Chinese  medicine,  as  the  Chinese  are  believed 
to  be  of  Accadian  origin,  and  their  religion  is  as  full  of  magic  as 
that  of  the  ancient  Chaldeans,  while  their  Buddhism  has,  in  certain 
instances,  degenerated  into  Shamanism,  which  is  simply  magic  and 
sorcery.  Nor  is  their  medicine  much  better,  as  diseases  are  held  to 
be  caused  by  demons,  and  to  be  sent  as  punishments  for  the  sins 


PRIMITIVE  MEDICINE  5 

p.  a  previous  existence,  while  the  evil  eye  here,  as  everywhere,  is 
considered  a  fertile  source  of  harm.  Under  these  circumstances  it 
is  not  surprising  that  the  principal  featuie  of  the  treatment  of 
disease  is  by  magic  and  invocation  of  special  gods — e.g.,  of  that 
of  smallpox.  And  the  best  preventive  measure  is  the  charm  or 
amulet,  which  may  be  supposed  to  work  in  one  of  the  following 
ways:  either  to  give  the  person  confidence,  or  to  act  as  a  double, 
so  that  the  demon,  seeing  the  amulet,  may  mistake  it  for  the  part 
of  the  body  which  he  intended  to  attack,  and  thus  waste  his  spleen 
on  an  inanimate  object;  or  as  similars. 

Associated  with  these  primitive  ideas  there  are  signs  that  attempts 
to  advance  the  knowledge  of  medicine  have  been  made  from  time 
to  time.  For  example,  there  is  a  catalogue  of  herbs  said  to  date 
as  far  back  as  about  3000  B.C.  (variously  stated  3216-2699  B.C.), 
and  attributed  to  the  Emperor  Chin-nong,  and  a  work  on  medicine 
called  '  Nuy-kin,'  or  '  Nuei-King,'  is  said  to  have  been  written  by 
Huang-ti  in  2637  B.C.,  while  the  god  of  medicine,  J  oh  Uong  Chu  Su, 
is  believed  to  have  been  a  celebrated  physician.  With  regard  to 
surgery,  there  is  the  god  I-Kuang-Tai-U6ng,  who  is  said  to  have 
been  a  distinguished  surgeon,  and  to  have  come  from  the  Loochoo 
Islands.  The  important  works  on  Ancient  Chinese  medicine  are  : — 
E-tsung-king-kass  or  Imperial  Book;  Chag-Sang,  '  On  Long  Life  '; 
Pim-tsaon,  '  On  Botany  ';  and  Ching-che-chum-ching,  '  On  Medical 
Practice,'  in  forty  volumes  dealing  with  nosology,  pharmacology, 
pathology,  surgery,  and  diseases  of  women  and  children.  A  Chinese 
herbal  was  produced  under  the  Mings  during  the  period  a.d.  1370- 
1650,  but  the  materia  medica  of  the  Chinese  is  a  mixture  of  useful 
drugs  and  gruesome  matters.  Among  the  latter  may  be  mentioned 
the  broth  made  from  flesh  taken  from  living  people,  and  the  use  of 
eyes  and  vital  parts  taken  from  corpses.  These  last  appear  to  play 
an  important  part  in  the  false  accusations  often  made  against 
foreigners  who,  the  Chinese  believe  or  believed,  enticed  people  into 
secret  places  in  order  to  kill  them  for  the  sake  of  these  valuable 
medicines.  Dissection  has  been  much  neglected  by  the  Chinese, 
with  the  result  that  their  knowledge  of  the  human  body  is  extremely 
erroneous. 

A  serious  attempt  was  made  by  some  Jesuits  during  the  reign 
of  Kang-hy,  who  died  in  1722,  to  improve  the  condition  of  medicine, 
but  unfortunately  it  was  not  successful,  and  these  daring  men  were 
banished  during  the  next  reign.  Too  high  praise  cannot  be  given 
to  the  medical  missionaries  of  various  countries,  who,  in  the  face 
of  much  danger,  have  introduced  modern  medicine  and  surgery  into 
China,  nor  to  the  medical  men,  merchants,  and  authorities  who 
founded  the  Hong-Kong  Medical  School,  now  the  Hong-Kong 
University,  which  should  bring  forth  a  changed  condition  of  medicine 
in  China  in  the  near  future. 

Japan. — Chinese  medicine  was  introduced  into  Japan  about  218 
B.C.,  and  remained  paramount  until  the  introduction  of  modern 
medicine  and  surgery,  which  quickly  attained  a  high  degree  of 


6  THE  HISTORY  OF  TROPICAL  MEDICINE 

perfection.  It  is  beyond  our  space  to  enter  into  this  interesting 
history,  and  we  invite  the  reader's  attention  to  the  work  of  Chemin 
and  of  Whitney  mentioned  in  the  references. 

America. — Medicine  was  found  to  be  in  a  veiy  primitive  con- 
dition among  the  North  American  Indians,  but  appears  to  have 
advanced  considerably  among  the  Aztecs  of  Mexico  and  the  Incas 
of  Peru,  although  very  little  is  now  known  of  the  condition  of 
knowledge  among  these  peoples,  because  the  Spaniards  destroyed 
all  the  records  they  could  obtain.  It  appears  that  there  were  public 
hospitals  in  Mexico,  surgeons  for  the  armies,  and  a  knowledge  of 
circumcision,  venesection,  medicines,  and  chemistry.  The  advent 
of  the  Spaniards,  while  destroying  our  sources  of  history,  brought 
America  once  for  all  under  European  influence,  and  the  history  of 
medicine  therein  forms  part  of  the  general  advance  of  medical 
knowledge. 

Foundations  of  Medicine. 

Two  races,  however,  appear  to  have  advanced  far  beyond  this 
elementary  stage,  and  to  have  laid  the  foundation  upon  which 
modern  medicine  has  been  built.  These  two  races  are  the  peoples 
of  India  and  Egypt. 

Indian  Medicine.— In  India  there  are  signs  of  the  existence  of 
peoples  among  whom  at  a  very  early  period  a  better  race  from 
the  north-west  forced  its  way.  This  race  is  often  spoken  of  as  the 
Aryan  stock.  Its  earliest  literature  appears  to  have  been  in  the 
form  of  songs  or  hymns,  and  these  were  collected  into  what  is  called 
the  Rig- Veda. 

Later,  three  more  books,  called  Samaveda,  Ayurveda,  and  Athar- 
vaveda,  were  added,  forming  the  Four  Vedas.  The  word  '  Veda  '  is 
said  to  be  derived  from  the  same  root  as  the  Latin  videre,  to  see. 
The  Vedas  were  said  to  be  divinely  inspired,  and  therefore  to  repre- 
sent the  wisdom  of  God. 

The  Ayurveda,  or  medical  works,  were  believed  to  have  originated 
directly  from  Brahma,  who  communicated  them  to  Dacsha,  the 
Prajapati,  his  son,  by  whom  they  were  passed  to  the  Acwins,  or 
sons  of  the  sun,  Surya,  who  in  their  turn  gave  them  to  Indra. 
Indra  taught  Bharadwaja,  a  learned  sage,  who  is  said  to  be  the 
author  of  the  twelfth  hymn  of  the  tenth  book  of  the  Atharvaveda 
which  belongs  to  the  primitive  age  of  the  priest-physician. 

Bharadwaja  taught  Atreya,  who  may,  perhaps,  be  called  the 
first  physician  of  India,  as  he  taught  medicine  in  Taxila  somewhere 
about  the  sixth  century  B.C.  Six  of  Atreya's  pupils  wrote  com- 
pendia of  his  teachings,  of  which  only  a  single  manuscript  by  Bhela 
(or  Bheda)  and  a  work  by  Agnivesa  exist.  This  latter  has,  how- 
ever, been  edited  by  Charaka  of  Kashmir,  who  left  it  unfinished 
when  he  died,  possibly  in  the  second  century  a.d.  This  unfinished 
work  was  revised  and  completed  by  another  Kashmir  physician 
(Dridhabala),  who  used  also  the  works  of  Vagbhata  and  Madhava. 
The    book    so    compounded    is    the    celebrated    Charaka-Sarhhita 


FOUNDATIONS  OF  MEDICINE  7 

(compendium),  so  well  known  in  India  to-day,  and  refers  principally 
to  medical  matters. 

Surgeiy,  according  to  Indian  mythology,  descended  from  Indra 
to  Dhanvantari,  a  teacher  in  the  legendary  school  of  Benares.  His 
pupil,  Susruta,  who  appears  to  have  been  a  contemporary  with 
Agnivesa,  wrote  a  compendium  dealing  mainly  with  surgical 
matters.  The  medical  chapters  were  added  about  the  second 
century  a.d.  by  an  unknown  writer,  the  result  being  the  Susruta- 
Samhita  as  known  to-day.  Susruta  ascribes  fevers  to  bites  by 
mosquitoes,  and  his  remarks  on  the  physician  and  his  patient 
may  be  quoted :  '  A  physician  experienced  in  his  art,  but  deficient 
in  the  knowledge  of  the  science  of  medicine,  is  condemned  by  all 
good  men  as  a  quack,  and  deserves  capital  punishment  at  the  hands 
of  the  King.'  Again:  'The  patient  who  may  mistrust  his  own 
parents,  sons,  and  relatives  should  repose  an  implicit  faith  in  his 
own  physician,  and  put  his  own  life  into  his  hands  without  the 
least  apprehension  of  danger;  hence  a  physician  should  protect  his 
patient  as  his  own  begotten  child.' 

A  third  system  of  medicine  was  evolved  by  Vagbhata  the  Elder, 
who  probably  lived  in  the  seventh  century  a.d.,  and  who  was 
acquainted  with  the  Charaka-Samhita  and  the  Susruta -Sarhhita. 
His  work  is  called  '  Astanga  Sarhgraha,'  or  the  summary  of  the 
eight-branched  science,  because  Indian  medicine  was  divided  into 
eight  parts — internal  medicine,  major  surgery,  minor  surgery, 
demonology,  toxicology,  tonics,  aphrodisiacs,  and  paedotrophy. 

Madhava  wrote  a  work  on  pathology  (Nidana)  somewhere  about 
the  seventh  century  a.d.,  and  Vagbhata  the  Younger,  in  the  seventh 
or  eighth  century,  a  compendium,  Astanga  Hrdaya  Sarhhita,  based 
upon  the  Astanga  Sarhgraha  of  the  Elder  Vagbhata. 

The  great  works  are  therefore  those  of  Charaka  (really  of  Agnivesa, 
Charaka,  Dridhabala,  Vagbhata  and  Madhava),  Susruta,  Vagbhata, 
and  Madhava. 

After  this  comes  the  period  of  the  commentators: — Bhaskara 
Bhatta,  in  the  early  eleventh  century,  on  Susruta;  Charakapandatta, 
in  the  late  eleventh  century,  on  Charaka;  Dallana,  in  the  twelfth 
century,  on  Susruta;  Arunadatta,  about  a.d.  1220,  on  the  Younger 
Vagbhata;  Vijaya  Rakshita  and  Srlkanthadatta,  about  a.d.  1240, 
on  the  Nidana  of  Madhava;  and  Vachaspati,  about  a.d.  1260,  also 
on  Madhava.  In  the  sixteenth  century  Bhava  Misra  published  a 
compilation  from  the  older  writers,  which  he  called  '  Bhava  Prakasa ; 
or,  The  Manifestation  of  the  Truth.' 

There  is  no  doubt  that  the  Indian  doctors  were  well  versed  not 
merely  in  medicine  and  surgery,  but  in  the  prevention  of  disease 
and  in  operative  midwifery.  They  apparently  knew  diabetes 
mellitus,  dysentery,  phthisis,  syphilis,  and  diseases  due  to  worms, 
etc.  In  diagnosis  they  paid  great  attention  to  the  examination  of 
the  pulse,  the  temperature  of  the  body,  the  colour  of  the  skin,  the 
urine,  fasces,  eye,  voice,  and  the  respiratory  sounds.  They  possessed 
a  remarkable  symptomatology,  and  as  regards  treatment  divided 


8  THE  HISTORY  OF  TROPICAL  MEDICINE 

diseases  into  incurable,  which  they  refused  to  treat,  and  curable, 
which  they  treated  according  to  a  copious  materia  medica.  Among 
the  various  remedies  must  be  mentioned  the  fact  that  inoculation 
against  smallpox  was  practised  at  the  beginning  of  the  warm  season. 
Dietetics  and  toxicology  were  also  well  known. 

Hospitals  were  founded  by  Buddhist  Princes  in  India  and  Ceylon. 
In  fact,  there  is  an  account  of  a  hospital  being  founded  in  Anuradha- 
pura,  the  ancient  capital  of  Ceylon,  as  early  as  the  fifth  century  B.C., 
and  later  many  more  were  established,  as  well  as  a  sort  of  medical 
or  sanitary  department,  having  one  medical  officer  to  every  ten 
villages,  together  with  a  definite  sanitary  organization,  and  with 
institutions  for  the  reception  of  cripples,  deformed,  and  poor  persons. 
One  of  the  Sinhalese  Kings  appears  to  have  known  and  practised 
medicine  himself. 

Under  the  influence  of  war  and  invasion,  together  with  the 
introduction  of  new  religions,  caste  distinctions  became  more  rigid, 
and  the  Brahmans,  fearing  to  touch  blood  or  diseased  matter,  left 
the  study  of  medicine  to  lower  castes,  and  later,  when  the  hospitals 
were  closed,  Indian  medicine  sank  to  a  very  low  position,  and  did 
not  again  revive  till  the  British  Government  founded  its  medical 
schools  and  research  institutions.  Moreover,  the  invasions  of  India 
by  Mohammedans,  and  of  Ceylon  by  Tamils,  seem  to  have 
thoroughly  upset  all  these  excellent  medical  arrangements.  The 
practitioner  who  works  in  India  or  Ceylon  must  not  be  surprised 
to  find  that  the  people  strongfy  believe  in  their  own  system  of 
medicine  and  medical  men.  At  the  same  time,  it  must  be  remem- 
bered that  their  science  and  art  is  a  great  degeneration  from  the 
ancient  Indian  medicine. 

Modern  medicine  has  now  reached  India  and  Ceylon  from  the 
West,  and  native  medical  men  in  increasing  numbers  are  to  be 
found  trained  in  modern  medicine  and  surgery.  In  other  words, 
in  these  regions  there  have  been  three  medical  epochs — the  first,  in 
which  there  was  great  enlightenment  and  study;  the  second,  in 
which  the  knowledge  so  acquired  was  largely  lost;  and  the  third, 
in  which  a  revival  of  medical  knowledge  has  come  about  by  impor- 
tation from  the  West. 

Before  leaving  the  subject  of  Indian  medicine,  it  is  perhaps 
advisable  to  note  the  visits  of  the  Greek  physicians  Ktesias  (about 
400  B.C.)  and  Megasthenes  (about  300  B.C.)  to  Northern  India,  as 
they  are  of  importance  in  proving  the  possibility  of  the  exchange 
of  knowledge  between  India  and  Greece,  and  vice  versa. 

Egyptian  Medicine. — In  the  meanwhile,  and  probably  quite  in- 
dependently, medicine  had  begun  to  be  studied  in  Egypt ;  for  several 
papyri  have  been  found,  one  called  the  Ebers,  or  Leipzig  Papyrus, 
of  the  sixteenth  century  B.C. — i.e.,  about  1550  B.C.;  a  second,  the 
Berlin  Papyrus,  of  the  fourteenth  century  B.C. ;  a  third,  also  in 
Berlin;  a  fourth,  the  Hearst  Papyrus;  a  fifth,  of  little  importance, 
in  the  British  Museum;  and  a  sixth,  in  Paris. 

It  seems  probable  that  the  Ebers  Papyrus  represents  in  writing 


FOUNDATIONS  OF  MEDICINE  9 

the  oldest  Egyptian  medicine,  which  previously  had  existed  engraved 
on  pillars  of  stone,  ascribed  to  the  god  Thot,  who  is  regarded  by 
many  experts  as  the  Egyptian  ^Esculapius,  though  other  authorities 
assign  this  to  Imhotep  (meaning  physician),  whose  temple  was  at 
Memphis.  This  Ebers  Papyrus  is  a  compilation  written  by  several 
people,  one  of  whom  appears  to  have  been  an  oculist  living  in  Byblos, 
in  Phoenicia.  It  is  thought  that  it  was  written  at  On  (Heliopolis), 
where  medicine  was  taught  by  a  kind  of  polyclinic.  This  papyrus 
contains  a  great  deal  of  medical  knowledge,  including  remedies  for 
diseases  of  the  stomach,  abdomen,  and  urinary  bladder. 

Directions  for  the  removal  of  buboes  and  concerning  diseases  of 
the  eyes  and  other  sense-organs,  nerves,  heart,  etc.,  are  given. 
Further,  it  gives  directions  for  getting  rid  of  fleas  and  lice.  It  also 
contains  an  account  of  a  disease  called  'AAA'  and  '  U  H  A,'  caused 
by  a  worm  Heltu.  The  symptoms  of  the  disease  are  described, 
and  a  remedy  is  prescribed  for  the  patient  who  has  the  worms 
in  his  abdomen.  There  is  a  difference  of  opinion  as  to  what  disease 
is  referred  to,  and  what  kind  or  kinds  of  worms  are  meant.  It  is 
quite  possible  that  it  was  not  such  a  small  worm  as  an  ancylo- 
stome,  but  rather  some  other  larger  species — e.g.,  an  ascaris,  or 
a  tape-worm,  or  even  an  oxyuris,  especially  as  these  would  be  passed 
per  anum,  and  would  be  easily  seen.  The  ancient  Egyptians  are 
said  not  to  have  opened  the  bowels  in  embalming  the  body,  though 
they  may  have  washed  out  the  contents  of  the  bowels,  and  thus 
have  found  the  ancylostome.  The  word  '  A  A  T  '  in  inscriptions 
on  the  temple  of  Denderah  is  said  to  refer  to  malaria. 

The  Ebers  Papyrus  is  considered  by  some  authorities  to  belong 
to  the  works  of  Hermes  Trismegistus,  which  numbered  forty,  and 
of  which  six  treat  of  medicine,  surgical  instruments,  anatomy,  and 
therapeutics.  The  Hearst  Papyrus  resembles  the  Ebers  Papyrus 
in  being  a  collection  of  prescriptions  and  invocations. 

The  principal  Berlin  Papyrus  contains  magical  invocations  and 
prescriptions  for  medicaments;  the  other  Berlin  Papyrus  contains 
recipes  for  treatment  of  various  diseases,  including  leprosy,  to- 
gether with  some  anatomical  and  physiological  information  of  a 
very  elementary  nature. 

The  history  of  Egyptian  medicine  becomes  merged  into  that  of 
Alexandrian,  Arabian,  and  modern  medicine;  but  before  con- 
sidering these,  a  few  remarks  will  be  made  upon  Jewish  and 
Grecian  medicines,  both  of  which  owe  much  to  Ancient  Egyptian 
medicine. 

Jewish  Medicine.— The  books  which  refer  to  Jewish  medicine 
are  the  Bible  and  the  Talmud.  In  the  former  there  are  several 
references  of  interest  in  tropical  medicine — e.g.,  in  the  Book  of 
Numbers  there  is  a  description  of  a  plague  of  fiery  serpents,  which 
quite  possibly  refers  to  the  guinea-worm  {Dracunaihis  medinensis). 
Moreover,  it  appears  as  though  Moses  had  taught  the  Israelites 
how  to  extract  the  worm  by  winding  it  round  a  piece  of  stick,  as 
is  done  to-day  in  many  parts  of  Africa.     Further,  he  appears  to 


io  THE  HISTORY  OF  TROPICAL  MEDICINE 

have  made  a  model  in  brass  of  the  method  to  be  adopted — or,  at 
all  events,  of  the  worm — in  imitation  of  Egyptian  customs. 

Again,  in  the  First  Book  of  Samuel,  chapters  v.  and  vi.,  there  is 
an  account  of  a  disease  spreading  among  the  inhabitants  of  the 
cities  of  Ashdod,  Gath,  Ekron,  and  Beth-shemesh,  in  which  places 
no  fewer  than  50,070  men  are  said  to  have  died.  This  disease  was, 
without  doubt,  Oriental  plague.  The  only  point  necessary  in  order 
to  understand  the  reference  is  to  remember  that  '  emerods  '  are 
buboes.  It  is,  further,  interesting  to  observe  that  these  ancient 
people  noted  that  the  '  mice '  died  and  marred  the  land,  showing 
that  the  plague  affected  both  man  and  rat. 

No  one  can  fail  to  be  impressed  by  the  careful  hygienic  precau- 
tions of  the  Mosaic  period.  For  example,  consider  how  animals 
were  divided  into  the  clean  and  unclean,  the  reason  for  this  being 
that  the  priests,  in  preparing  them  for  sacrifice,  noted  the  presence 
of  parasites  in  the  flesh  or  the  viscera  of  certain  animals,  which  were 
therefore  to  be  avoided.  It  is  true  that  the  classification  of  dis- 
ease was  very  simple — viz.,  into  acute  disorders,  called  '  plague  '; 
and  chronic  disorders,  with  some  sort  of  eruption,  called  '  leprosy  ' 
— but  the  extremely  stringent  quarantine  rules  very  likely  did  a 
great  deal  of  good,  though  doubtless  unkind  to  the  unfortunate 
sufferer. 

During  their  captivity  in  Babylon  the  Jews  were  brought  into 
contact  with  Babylonian,  Assyrian,  and  Grecian  influences,  and  it  is 
possible  with  Indian  influences  also.  After  this  period — i.e.,  about 
150  B.C.- — there  existed  in  Palestine  a  curious  sect  called  the  Essenes, 
who  were  also  known  as  the  Healers,  or  Therapeutists.  Still  later 
appeared  the  Talmud,  which  contains  surgical,  medical,  pathological, 
and  anatomical  information,  much  of  which  was  doubtless  from 
Grecian  sources.  Afterwards  Jewish  doctors  are  to  be  found 
associated  with  the  Alexandrian  School  and  the  Arabs. 

Grecian  Medicine. — As  in  India,  so  in  Greece,  medicine  began  with 
a  Divine  origin,  in  the  latter  from  Apollo,  who  taught  Cheiron  the 
Centaur,  who,  in  his  turn,  instructed  iEsculapius,  whose  sons  are 
mentioned  as  surgeons  by  Homer.  Then  comes  the  period  of  the 
Philosophers,  among  whom  Pythagoras  may  be  mentioned,  and 
the  establishment  of  the  schools  of  the  Asclepiades,  of  which  the 
most  celebrated  is  Cos,  because  there  lived  Hippocrates,  who  was 
supposed  to  be  descended  from  iEsculapius,  and  is  said  to  have 
been  born  about  460  B.C.  His  forefathers  appear  to  have  been 
attached  to  this  ancient  temple  of  health,  and  there  is  no  doubt 
that  he  himself  practised  in  the  Asclepion  of  Cos,  of  which  an 
excellent  account  has  recently  been  given  by  Caton. 

The  writings  of  Hippocrates,  the  most  eminent  of  the  eight 
physicians  called  by  that  name,  are  most  interesting;  for  he  clearly 
distinguished  intermittent  fevers  from  continuous  fevers.  Further, 
he  recognized  quotidian,  tertian,  and  quartan  fevers,  and  noted 
their  frequency  in  summer  and  autumn,  and  their  occurrence  near 
stagnant  water  and  after  rains.     He  also  mentions  relapsing  fever, 


FOUNDATIONS  OF  MEDICINE  n 

which,  after  his  period,  was  forgotten  till  the  eighteenth  century, 
but  he  seems  to  have  failed  to  recognize  infection. 

The  works  of  Hippocrates,  who  is  justly  considered  to  be  the 
Father  of  medicine,  are  of  a  very  high  standard,  but  it  is  probable 
that  directly  or  indirectly  he  owed  much  to  Indian  and  Egyptian 
influences. 

Alexandrian  Medicine. — War  produces  great  changes  in  the  social 
life  of  nations,  and  no  exception  is  made  for  that  portion  which 
deals  with  disease.  The  wars  of  Alexander  the  Great  led  to  the 
foundation  of  the  city  of  Alexandria  in  the  year  331  B.C.,  and  this 
was  followed  by  the  transference  of  the  headquarters  of  medical 
knowledge  from  Greece  to  Egypt,  where  this  knowledge  was 
advanced  along  the  systematic  lines  laid  down  by  Aristotle. 

The  result  of  this  was  that  anatomy,  pathological  anatomy,  and 
clinical  medicine,  progressed  hand  in  hand  with  zoology  and  botany, 
and  here  in  170  B.C.  Agatharchides  described  Dracunculus. 

Under  the  Ptolemies  medicine  flourished,  but  with  the  fall  of 
Cleopatra  came  the  end  of  the  first  and  by  far  the  greater  period 
of  Alexandrian  medicine,  but  its  subsequent  history  is  curious  and 
interesting.  Before  the  end  of  the  great  period,  Alexandrian 
medicine  had  found  its  way  into  Mesopotamia,  and  thence  into 
Syria,  which  previously  had  been  under  the  influence  of  Accadian 
medicine  as  handed  down  by  Babylonia  and  Assyria.  Centuries 
later,  when  Alexandrian  medicine  had  fallen  to  a  very  low  level, 
it  was  given  a  flickering  spirit  by  Syrians  driven  to  Alexandria  by 
the  Persian  invasion  of  their  country  in  the  days  of  Heraclius. 
The  result  was  that  Syriac  medicine  took  hold  of  the  city,  and 
works  appeared  in  the  Syrian  language.  Thus,  in  the  seventh 
century  of  the  present  era  a  priest  called  Aaron  translated  into 
Syriac  thirty  treatises  by  Abu  Faraj ,  while  later  Sergius  added  two 
further  treatises  to  this  number.  This  is  the  heyday  of  Syriac 
medicine  and  the  much  lesser  period  of  Alexandrian  medicine, 
which  had  long  ago  given  place  to  Grseco-Roman  medicine. 

Grseco-Roraan  Medicine. — After  Alexandrian  medicine  came 
Grseco-Roman  medicine,  largely  derived  directly  from  the  Greek, 
for  Roman  medicine,  until  this  influence  came  to  be  felt,  was  very 
primitive.  Among  the  physicians  of  this  period  may  be  mentioned 
Themison  of  Laodicea  (50  B.C.),  who  was  the  first  to  describe 
elephantiasis  graecorum,  or  leprosy. 

After  him  comes  the  great  master  of  Roman  medicine,  Aulus' 
Cornelius  Celsus  (25  B.C.  to  a.d.  45).  It  is  quite  possible  that 
Celsus  was  not  a  medical  man,  but,  whether  or  not,  he  has  left 
behind  him  in  his  eight  books  of  medicine  a  most  valuable  treatise. 
To  him  belongs  the  credit  of  clearly  distinguishing  two  types  of 
tertian  malarial  fever — viz.,  a  simple  and  a  much  graver  form. 
Hundreds  of  years  later  this  was  put  upon  a  scientific  basis  by  the 
researches  of  Marchiafava,  Celli,  and  Bignami,  in  the  same  city 
(Rome).  He  also  recognized  the  double  quartan  fever,  and  gave 
a  description  of  elephantiasis,  by  which  he  meant  leprosy. 


12  THE  HISTORY  OF  TROPICAL  MEDICINE 

After  Celsus,  medicine  flourished  in  both  the  Eastern  and  the 
Western  Empires.  Among  the  many  writers  of  this  period,  atten- 
tion may  be  drawn  to  Aretaeus  of  Cappadocia  (a.d.  30-90),  who 
describes  dysentery,  and  gives  a  long  account  of  elephantiasis, 
which  he  considered  to  be  contagious  by  the  inspired  air. 

Graeco-Roman  medicine  reaches  its  zenith  in  Galen,  who  was  born 
at  Pergamos  a.d.  131,  and  died  a.d.  210.  He  studied  especially  in 
Alexandria,  and  carefully  described  tertian  and  quartan  malaria. 

Byzantine  Medicine. — After  the  fall  of  Rome  Byzantium  became 
the  principal  city  of  the  world,  but  as  Garrison  so  ably  puts  it — 

'  the  degeneration  of  the  mind  and  body  with  consequent  relaxations  of  morals 
led  to  mysticism,  to  the  respect  for  the  authority  of  magic  and  of  the  super- 
natural which  was  to  pave  the  way  to  the  bigotry,  dogmatism,  and  mental 
inertia  of  the  Middle  Ages.' 

There  is,  therefore,  no  surprise  in  finding  that  in  one  thousand 
years  of  Imperial  rule  Byzantium  produced  only  four  compilations 
— viz.,  those  by  Oribasius  of  Sardianus,  by  jEtius  of  Amida  (a  town 
in  Mesopotamia),  by  Alexander  of  Tralles,  and  by  Paul  of  JEgina., 
and  some  lesser  works,  among  which  may  be  mentioned  that  by 
Actuarius  on  the  urine. 

All  these  works  are  of  interest,  but  perhaps  that  by  Paul  of 
Mg'ma..  which  appeared  at  the  end  of  the  seventh  century,  deserves 
a  little  further  attention.  It  gives  a  synopsis  of  medicine  from  the 
time  of  Galen  up  to  nearly  the  end  of  the  seventh  century.  In  the 
second  book  considerable  space  is  devoted  to  the  malarial  fevers, 
and  there  is  also  a  section  on  '  Plague,'  but  what  is  meant  by  this 
is  not  certain,  though  Procopius,  of  the  sixth  century,  is  said  to  have 
written  an  account  of  glandular  plague.  There  is  also  an  article  on 
siriasis,  by  which  was  meant  an  inflammation  of  the  brain  in  young 
children.  In  the  third  book  information  -is  given  concerning 
cholera,  tenesmus,  and  dysentery.  His  fourth  book  is  particularly 
interesting,  beginning  with  a  description  of  elephantiasis  graecorum, 
or  leprosy.  It  contains  an  account  of  broad  and  round  worms, 
especially  ascarides  and  dracunculus,  and  further  describes  the 
bites  of  snakes,  dogs,  spiders,  scorpions,  centipedes,  lizards,  croco- 
diles, and  other  animals.  There  is  also  a  description  of  the  stings 
of  wasps  and  bees,  and  an  account  of  poisons. 

Byzantine  medicine  was  superseded  by  Arabian  medicine,  and 
finally  ended  with  the  fall  of  Constantinople. 

Arabian  Medicine. — According  to  Garrison,  Arabian  medicine 
takes  its  origin  from  Nestor,  a  Christian  heretic  priest,  driven  by 
religious  persecution  from  Byzantium  to  Edessa,  in  Mesopotamia, 
where  he  began  the  study  of  medicine.  Pursued  even  here  by 
religious  hate,  he  fled  into  Persia,  where  he  established  the  Gunde- 
sh&pfir  Medical  College,  wherein  were  trained  the  original  founders 
of  Arabian  medicine. 

Under  the  Bagdad  Caliphs  many  Greek  medical  works  were 
translated  into  Arabic  by  Mesue  and  Johannitius,  while  under  the 


FOUNDATIONS  OF  MEDICINE  13 

same  beneficent  rule  appeared  the  great  Arabian  physicians  Rhazes, 
Haly  Abbas,  and  Avicenna. 

Arabian  medicine  was  carried  into  Spain  by  the  Moors,  and 
flourished  exceedingly  under  the  generous  sympathy  of  the  Cordova 
Caliphs,  producing  workers  like  Albucasis  and  Avenzour. 

Even  Egypt  had  its  '  Hall  of  Wisdom  '  erected  by  Hakim 
Biamrillah  in  1005,  under  the  protection  of  the  Cairene  Caliphs. 

During  this  period  medical  instruction  was  given  to  scholars  in 
the  large  hospitals  and  in  the  dispensaries,  which  were  numerous. 

The  features  of  Arabic  medicine  which  are  especially  interesting 
to  us  are  the  references  to  tropical  diseases,  and  these  are  sufficiently 
numerous  because  the  Arabic  physicians  were  brought  into  contact 
with  strangers  from  various  parts  of  the  world  who  had  been 
attracted  to  Arabic  countries  by  the  wisdom  of  the  Caliphs  with 
regard  to  learning  and  liberty.  As  these  strangers  often  brought 
with  them  strange  herbs  and  drugs,  so  Arabic  medicine  abounds 
with  references  to  new  remedies  for  disease. 

Associated  with  Arabic  medicine  is  the  appearance  of  many 
Jewish  medical  works,  and  so  much  so  that  it  appears  to  us  that 
this  should  be  held  to  be  the  second  period  of  Jewish  medicine.  The 
reason  for  this  development  is  because  the  Caliphs  allowed  the  Jews 
to  live  and  work  in  freedom  at  a  time  when  Christianity  as  a  whole 
was  persecuting  them. 

The  decline  of  Arabian  medicine  came  in  the  thirteenth  century, 
with  the  fall  of  Cordova  in  a.d.  1236  and  with  the  Mongol  invasion 
of  Bagdad  in  a.d.  1258,  and  though  it  lived  for  long  in  Spain,  still, 
its  day  was  over  and  its  scholars  were  passing  to  the  School  of 
Salerno,  from  which  were  to  come  those  piercing  rays  of  medical 
knowledge  which  were  to  illuminate  the  closing  years  of  the  Middle 
Ages. 

Before,  however,  passing  on  to  the  consideration  of  medieval  medicine  we 
will  make  brief  reference  to  a  few  of  the  Arabic  works  on  medicine,  which 
included  not  merely  dictionaries  and  translations,  but  original  works  on 
general  medicine,  pharmacopoeias,  works  dealing  with  natural  history,  and 
veterinary  matters. 

Abil  Zakariyd  YHhannd  ben  Mdsawayh,  or  Mesua,  was  the  son  of  a  Christian 
apothecary  in  the  hospital  of  Gundeshapur.  He  was  appointed  by  the  Caliph 
Harunu-'r-Rashid  to  translate  Greek  works,  of  which  he  did  many,  but  he 
also  wrote  original  treatises — e.g.,  one  upon  '  the  Curiosities  of  Medicine.' 
He  died  in  a.d.  857,  and  some  of  his  books,  as  far  as  we  know,  were  the  first 
medical  works  to  be  printed  in  movable  type  in  1471.  He  seems  to  have 
been  the  first  to  write  a  medical  treatise  in  tabular  form  in  his  '  Kitabu-'l- 
Mushajjar,'  which  comprised  treatises  on  the  general  rules  of  medical  art  and 
on  the  diseases  of  regions  and  organs,  including  four  books  on  the  diseases 
of  the  skin. 

Abii  Bakr  Muhammad  ben  Zakavlya-'r-Rdzi,  or  Rhazes,  was  born  at  Ray 
in  'Iraq-i-'Ajam,  but  did  not  commence  the  study  of  medicine  until  he  was 
thirty-two  years  of  age,  when  he  was  taught  at  Bagdad  by  'Ali  ben  Rabban 
at-fabari.  He  was  first  Director  of  the  Ray  Hospital  and  later  of  that  at 
Bagdad.     He  died  about  a.d.  923. 

His  works  are  numerous,  and  we  may  mention  '  Kitabu-'l  Mansiiri,'  or 
System  of  Medicine,  which  is  divided  into  ten  chapters.  It  includes  anatomy, 
diagnosis,  ailments  and  drugs,  preservation  of  health,  cosmetics  and  the  cure 


14  THE  HISTORY  OF  TROPICAL  MEDICINE 

of  pityriasis,  advice  to  travellers,  surgery,  poisons,  regional  diseases,  fevers, 
and  also  the  qualities  necessary  for  a  physician,  and  remarks  on  quacks  and 
impostors.  He  gave  the  earliest  accounts  of  smallpox  and  measles,  which 
earned  for  him  lasting  fame . 

A  System  of  Midwifery — '  Kitab-u-Tadbir-el-Habala  '■ — was  written  in  the 
fourth  century  by  a  physician  Abu-'l-  Abbas  Ahmad  ben  Muhammad  ben 
Yahya-'l-Baladi.  This  book  included  the  management  of  pregnancy  and  the 
diseases  of  the  foetus  and  the  infant,  as  well  as  the  rearing  of  the  child. 

Khalaf  ben  '  Abbds-az-Zahrdwi,  or  Albucasis,  was  born  at  Az-zahra,  near 
Cordova,  and  died  probably  about  a.d.  1013.  His  great  work  is  '  Kitabu- 
'T-Tasrif,'  which  is  an  encyclopaedia  chiefly  valued  for  its  surgical  portion, 
which  was  translated  into  Latin  in  the  twelfth  century,  and  for  long  remained 
the  standard  surgery  of  Europe. 

Ophthalmic  surgery  was  considered  by  'All  ben  'Isd  al-Kuhhdl,  or  Jesu 
Haly. 

Abu  'Ali  al-Husayn  ben  'Abdullah  ben  Sind,  or  Avicenna,  often  called  Ash- 
Shaykh  (the  Reverend)  or  A  ^"'is  (the  Chief),  was  born  at  Ashainah,  in 
Bukhara,  in  a.d.  980.  He  was  -sician  to  the  Sultan  of  Bukhara,  but  later 
he  retired  to  Jurjan,  where  he  v/rote  his  celebrated  '  Kitabu  'L-Qanun,'  or 
Book  of  the  Canon.  He  died  in  a.d.  1037.  His  great  work  is  essentially 
medical,  as  the  surgical  portion  is  poorer  than  that  of  Albucasis,  and  is  in 
many  places  a  treatise  on  tropical  medicine. 

Hibatulldh  ben  Zayd  ben  Hasan  ben  Ya'  qub  ben  Ismd  'il  ben  Jami'al  Isrd'itf, 
or  Ibn  Jami  Isra'ili,  was  brought  up  in  Old  Cairo,  and  was  considered  to 
be  the  greatest  of  the  Egyptian  physicians.  He  was  physician  to  the  cele- 
brated Al-Malik-u'n-Nasir  Salah  u'd-DIn  (Saladin),  for  whom  he  made  his 
Theriac.     He  died  in  a.d.  1198. 

The  last  of  the  great  Arabian  physicians,  Dd'iidben  'Umaral-Antdhi,  wrote 
an  encyclopaedia  of  medicine,  and  after  living  for  a  long  time  in  Cairo  went  to 
reside  in  Mecca,  where  he  died  in  a.d.  1599. 

Medieval  Medicine. — Following  Garrison,  we  may  date  medieval 
medicine  from  the  time  that  the  School  of  Salerno  established  its 
influence  in  Europe.  As  to  the  origin  of  this  epoch-making  school, 
we  know  nothing,  but  we  do  know  that  it  was  here  that  Arabic 
translations  of  Greek  medical  works  were  turned  into  the  Latin 
language  by  scholars  from  Spain,  and  we  also  know  that  the  know- 
ledge so  obtained  led  to  great  practical  results,  in  that  universities 
were  founded,  the  great  movement  of  building  hospitals  was  begun, 
both  of  which  were  founded  and  aided  by  Church  and  State  alike. 
Salerno  laid  the  foundations  of  these  advances  in  medical  teaching 
and  care  of  the  sick,  and  thus  prepared  the  way  for  modern  medicine, 
especially  as  it  encouraged  individual  medical  talent. 

Foundations  of  Modern  Medicine. 

The  revival  of  learning  was  only  made  possible  by  the  destruction 
of  feudalism,  and  this  was  brought  about,  as  Garrison  and  others 
have  pointed  out,  by  the  discovery  of  gunpowder.  To  this  great 
act  of  freedom  must  be  linked  the  discovery  of  printing  by  means 
of  movable  type,  and  the  sack  of  Mainz  in  1462,  which  disseminated 
the  art  of  printing  all  over  Europe  and  thus  enabled  knowledge  to  be 
easily  preserved  and  widely  distributed. 

While  these  events  were  stirring  the  general  public,  medical  men 
were  confronted  with  new  diseases  from  the  East,  which  came  in 
epidemic  form,  and  these  terrible  outbreaks  compelled  them  to 


FOUNDATIONS  OF  MODERN  MEDICINE  15 

observe  and  to  record  their  observations;  and,  indeed,  it  is  during 
this  period  that  Girolamo  Fracastoro,  studying  syphilis  and 
typhus,  started  modern  epidemiology  by  formulating  the  theory 
of  contagion. 

The  subject  of  infection  has  been  recently  studied  in  a  most  able  manner 
by  C.  and  D.  Singer,  who  have  shown  that  to  primitive  peoples  infection  and 
contagion  are  in  the  general  order  of  things,  and  not  to  be  questioned,  but 
that  Hippocrates  had  no  idea  as  to  the  spread  of  epidemic  disease  by  infection. 
They  point  out  that  it  was  Thucydides  (471-391  B.C.),  while  studying  the 
'  plague  of  Athens,'  who  first  established  spread  of  disease  by  contact,  and 
Aretaus  the  Cappadocian  who  added  conveyance  of  infection  from  a  dis- 
tance, facts  recognized  by  some  of  the  Arabians  like  Haly  Abbas,  while  the 
School  of  Salerno  clearly  stated  that  disease  could  be  spread  by  contact,  air, 
and  fomites;  and  Remacle  Fuchs  (1510-1587)  was  not  merely  clear  on  these 
points,  but  wrote  about  the  '  seminaria,'  or  seeds  of  disease.  All  these  were, 
however,  merely  the  precursors  of  Fracast  ;(i478-i553),  whose  doctrine 
of  disease  seeds  or  germs,  foreshadowed  in  spy  Syphilis  '  in  1530,  is  clearly 
stated  in  his  '  De  contagionibus  et  contagiosis  morbis  et  eorum  curatione  '  in 
1546,  in  which  he  details  different  types  of  infection,  by  contact  alone,  by 
contact  and  fomites,  by  contact,  fomites,  and  from  a  distance.  He  considers 
infection  to  be  nothing  else  than  the  passage  of  a  putrefaction  from  one  body 
to  another.  He  distinguishes  infections  from  poisons  because  the  former 
possess  seeds  which  can  reproduce  their  like  in  a  second  body.  In  addition. 
he  was  the  first  to  recognize  typhus  fever  and  the  specific  characters  of  fevers. 

These  factors — viz.,  new  methods  of  warfare  changing  society, 
new  methods  of  spreading  knowledge  and  apparently  new  epidemics 
— were  the  forces  which  in  our  opinion  laid  the  foundations  of 
modern  medicine. 

The  Discovery  of  the  Tropics. — It  will  be  noted  that  in  early  times 
medicine  was  relatively  highly  developed  in  Egypt  and  India,  while 
it  was  very  primitive  in  the  Temperate  Zone,  but  the  question  as  to 
the  supremacy  of  East  over  West  was  settled  by  the  Battle  of 
Salamis,  and  thenceforth  the  general  tendency  was  that  learning 
advanced  in  the  West  and  languished  in  the  East.  But  the  West  knew 
that  there  was  an  East :  the  question  was  how  to  get  there.  A  few 
travellers  lived  to  return  and  tell  the  tale  of  the  overland  journeys 
to  the  East,  and  these  were  sufficient  to  indicate  that  the  overland 
route  was  unsuited  for  traffic  on  a  large  scale,  though  trade  came 
through  gradually. 

The  problem  of  finding  a  way  to  the  East  was  solved  by  the 
Portuguese,  who  in  1415  established  contact  with  the  Atlantic 
Islands,  in  1444  with  the  West  Coast  of  Africa,  and  later  with  the 
Congo  and  Angola.  In  i486  they  reached  the  Great  Fish  River, 
and  in  the  last  decade  of  the  fifteenth  century  the  route  to  India 
via  the  Cape  was  made  known. 

While  this  was  going  on  in  the  East,  Colombus  was  tracing  a 
route  to  America  across  the  Atlantic  in  1492,  and  in  1519  Magellan 
passed  through  the  Straits  to  which  his  name  has  been  given,  and 
showed  the  route  to  the  East,  while  still  later  the  complete  voyage 
round  the  world  was  carried  out  successfully. 

China  and  Tibet,  however,  remained  unknown  until  the  seven- 
teenth century  and  Central  Africa  until  the  nineteenth  century. 


1 6  THE  HISTORY  OF  TROPICAL  MEDICINE 

Early  Tropical  Medicine. — The  work  of  the  last  section  being 
carried  out  in  ships  with  more  or  less  numerous  crews,  it  was 
customary  for  these  vessels  to  be  provided  with  a  surgeon,  or,  at  all 
events,  with  a  person  with  some  knowledge  of  medicine  and  some 
powers  of  observation.  Later,  when  intelligent  people  settled  in 
tropical  regions  they  made  records  of  their  experiences,  and  in  this 
way  a  curious  literature  sprang  up,  partly  geographical,  partly 
zoological,  partly  botanical,  partly  medical,  and  partly  ethnographi- 
cal. It  is  in  this  literature  that  we  find  some  of  the  earliest  references 
to  disease  in  the  tropics.  The  literature  itself  is  sufficiently  indi- 
cated in  the  list  of  works  given  at  the  end  of  this  chapter;  but  being 
so  mixed  in  its  nature,  it  produced  but  little  effect,  and  was  left 
almost  unnoticed  until  after  the  rise  of  modern  tropical  medicine. 

Foundations  of  Modern  Tropical  Medicine. 

The  discoveries  of  new  lands  made  as  indicated  above  by  voyages, 
were  in  due  course  extended  by  land  exploration,  and  later  by 
settlements  founded  by  Europeans  and  their  families,  and  as  these 
grew  in  number  and  in  size,  so  the  number  of  medical  practitioners 
also  increased. 

These  medical  men  studied  the  diseases  of  the  European  settlers 
and  of  the  natives  of  the  regions  in  which  they  resided,  and  recorded 
their  results  in  numerous  publications,  as  is  indicated  in  the  list  of 
works  given  at  the  end  of  this  chapter. 

These  works  naturally  reflected  the  teaching  which  the  author 
had  received  in  Europe  prior  to  his  tropical  career,  and,  therefore, 
as  knowledge  in  Europe  progressed,  so  information  with  regard  to 
tropical  diseases  was  amplified. 

The  factor  which  was  most  potent  in  the  foundation  of  modern 
tropical  medicine  was  the  steady  evolution  and  perfection  of  the 
compound  microscope.  It  was  this  instrument  which  enabled 
Laveran  to  discover  the  malarial  parasite,  and  Manson  to  find  the 
periodicity  of  the  Microfilaria  nocturna. 

These  investigators  may  well  be  called  the  pioneer  founders  of 
modern  tropical  medicine,  and  that  foundation  was  secured  by  the 
world-wide  interest  in  tropical  disease  aroused  by  Ross's  discovery 
of  the  spread  of  malaria  by  the  mosquito.  From  the  date  of  these 
discoveries  modern  tropical  medicine,  in  our  opinion,  begins,  because 
they  opened  up  the  possibility  of  finding  the  cause,  the  treatment, 
the  method  of  spread,  and  the  prevention  of  a  tropical  disease,  and, 
moreover,  for  some  reason  or  another,  subsequent  work  on  these 
lines  has  apparently  been  much  more  successful  in  the  tropics  than 
elsewhere. 

Thus  modern  tropical  medicine  was  essentially  based  upon  the 
microscopical  diagnosis  of  the  disease,  and  differed  thereby  from 
earlier  tropical  medicine,  which  was  entirely  clinical;  yet,  in  our 
opinion,  clinical  and  microscopical  diagnosis  should  go  hand  in 
hand,  and  the  practitioner  should  never  so  depart  from  the  essential 
of  all  medical  knowledge,  the  thorough  bedside  examination  of  the 


FOUNDATIONS  OF  MODERN  TROPICAL  MEDICINE  17 

patient  by  clinical  methods,  as  to  commit  the  error  of  entirely 
trusting  to  the  microscopical  diagnosis.  If  he  trusts  entirely  to 
the  clinical  diagnosis  errors  must  occur ;  if  he  leans  absolutely  upon 
laboratory  examinations,  which  are  often  negative,  he  will  again 
find  himself  in  difficulties.  The  real  foundation  of  modern  tropical 
medicine  is  the  blending  together  of  clinical  work  with  scientific 
research,  thus  making  a  living  progressive  science  of  medicine,  in 
which  causation,  treatment,  and  prophylaxis  of  known  diseases  are 
associated  with  State-aided  research  into  the  unknown.  We  will 
now  briefly  look  at  the  history  of  these  various  points. 

Causation  of  Diseases. — One  of  the  most  marked  features  of 
modern  tropical  medicine  is  the  success  which  has  attended  attempts 
to  find  the  causal  agent  of  the  various  diseases;  and  to  trace  the 
rather  romantic  history  of  these  discoveries,  it  is  necessary  to  sub- 
divide the  subject  into  Helminthology,  Protozoology,  Mycology, 
Bacteriology,  Serums  and  Vaccines,  Entomology,  Toxicology, 
Climatology,  and  Dietetics. 

Helminthology. — We  have  already  noted  that  the  Ebers  Papyrus 
mentioned  the  presence  of  worms  in  the  intestines;  that  Moses  not 
merely  knew  the  guinea-worm,  but  how  to  extract  it  by  winding  it 
round  a  stick;  and  we  have  further  drawn  attention  to  Agath- 
archides'  description  of  this  worm  in  170  B.C.,  and  to  the  reference 
to  broad  and  round  worms  by  Paul  of  ^Egina ;  and  may,  therefore, 
pass  on  to  more  recent  work. 

Trematodes  were  first  recognized  by  Jehan  de  Brie  in  the  form  of  the  liver 
fluke  of  sheep,  which  was  afterwards  described  in  1547  by  Gabucinez.  This 
initial  work  was  extended  later  by  Leeuwenhoek  (1675),  Swammerdam  (1752), 
Rosenhof  (175S),  Muller  (1777),  Zeder  (1800) ,  who^called  them  '  sucking  worms,' 
and  Rudolphi  (1808),  who  gave  the  name  Trematode,  from  Tp-q/xaTud^s, 
meaning  pierced  by  holes.  Quite  recently  these  worms  have  been  the  subject 
of  two  great  discoveries,  which  may  be  briefly  summarized. 

In  1874  the  trematode  Clonorchis  sinensis  (-C.  endemicus)  was  discovered 
by  .McConnell  in  the  liver  of  a  Chinaman,  but  the  method  of  infection  was  not 
known  until  Kobayashi  worked  this  out  in  191 2,  191 5,  and  191 7,  showing 
that  the  encysted  stage  could  be  found  in  twelve  varieties  of  fish,  and  that 
kittens  produced  the  adult  trematode  when  fed  upon  infected  fish,  and  finally 
that  the  first  intermediate  host  is  a  mollusc — i.e.,  a  species  of  Melania. 

In  1 85 1  Bilharz  discovered  the  trematode  Schistosoma  htzmatobium  in  the 
portal  vein  of  an  Egyptian.  Since  1907  Sambon  has  shown  that  under  this 
name  was  concealed,  as  suggested  by  Manson,  a  second  parasite,  which  he 
called  Schistosoma  mansoni.  In  1915  Leiper  not  merely  confirmed  the 
existence  of  these  two  distinct  parasites,  but  traced  their  life-histories  through 
the  molluscs  to  the  adult  form  in  mammals.  This  is  indeed  a  great  and 
valuable  discovery,  and  by  no  means  the  first  by  which  this  distinguished 
helminthologist  has  benefited  mankind. 

With  regard  to  the  Cestoda  and  Nemathelminthes  space  does  not  permit  of 
a  history  at  this  point,  as  this  will  be  given  later;  but  with  regard  to  the  latter 
group  Sir  Patrick  Manson's  researches  into  filariasis  were  epoch-making. 

The  detailed  history  of  Filaria  bancrofti  will  be  given  later,  and  it  will 
suffice  to  state  here  that  the  microfilaria  was  discovered  by  Demarquay  in 
1863,  and  that  Manson  discovered  its  development  in  the  mosquito  in  the 
years  1877-1879,  while  in  1882  he  laid  stress  upon  the  nocturnal  periodicity 
of  the  microfilaria,  a  fact  entirely  disbelieved  when  first  reported. 

The  great  importance  of  the  discovery  of  the  development  of  this  worm  in  a 


1 8  THE  HISTORY  OF  TROPICAL  MEDICINE 

mosquito  is  that  it  paved  the  way  for  Ross's  discovery  of  the  spread  of  malaria 
by  a  similar  agency. 

It  is  quite  impossible  here  to  give  even  a  reasonable  list  of  the  workers  on 
this  important  branch  of  causation,  but  references  to  their  discoveries  will  be 
found  later  in  this  book. 

Protozoology. — Protozoa  were  recognized  by  Leeuwenhoek  in 
1675,  and  the  first  life-history  of  a  protozoon  (a  vorticella)  was 
worked  out  by  Trembley  in  1744-1747. 

Among  the  protozoa  parasitic  in  human  beings,  one  of  the  first 
to  be  discovered  was  Balantidium  coli,  found  by  Malmsten  of  Stock- 
holm in  the  year  1856,  and  now  known  to  be  often  associated  with 
a  chronic  catarrh  and  ulceration  of  the  large  bowel.  Lamblia 
intestinalis,  discovered  by  Lambl  in  1859,  and  Trichomonas  hominis, 
found  by  Davaine  in  1864,  are  considered  by  many  authors  (Ebstein, 
etc.)  to  be  the  cause  of  certain  cases  of  diarrhoea. 

In  1875  an  amoeba  was  found  by  Losch  in  St.  Petersburg,  in  a 
peasant  who  suffered  from  an  ulcerative  inflammation  of  the  large 
intestine,  and  Sonsino  in  Cairo  also  described  the  finding  of  large 
numbers  of  amoebae  in  the  intestinal  mucus  of  a  child  who  had  died 
of  dysentery.  Other  observers,  however — e.g.,  Grassi,  Celli,  and 
Cunningham — found  amoebae  in  persons  whose  health  had  under- 
gone no  change.  Kru.se  and  Pasquale  first  suggested  that  there 
might  be  two  species  of  amoebae,  one  pathogenic,  the  other  harm- 
less. Later  Schaudinn  showed  that  there  were  two  kinds  of  amoebae 
affecting  man — viz.,  Entamceba  coli,  which  was  non-pathogenic; 
and  Entamoeba  histolytica,  described  by  himself,  which  was  the  cause 
of  a  certain  kind  of  dysentery  (amoebic  dysentery)  and  of  the  abscess 
of  the  liver  which  at  times  followed  it. 

The  discovery  which  has  had  the  greatest  influence  on  tropical 
medicine  was  that  of  the  parasite  of  malarial  fever  by  Laveran  on 
November  6,  1880.  True,  this  had  to  some  extent  been  fore- 
shadowed by  Merkel  in  1847,  and  Virchow  in  1848,  both  of  whom 
saw,  and  the  latter  figured,  protoplasmic  masses  and  pigment. 
Still,  the  entire  credit  for  this  great  discovery  is  due  to  Laveran, 
for  the  others  failed  to  recognize  the  parasitic  nature  of  the  forms 
they  saw.  The  development  of  our  knowledge  concerning  this 
parasite  is  due  to  the  valuable  researches  of  Golgi,  Marchiafava, 
Celli,  Bignami,  and  many  others.  Of  great  importance  was  Golgi's 
discovery  of  the  plurality  of  species  of  the  malarial  parasite. 
Laveran's  discovery  and  the  work  of  his  successors  left,  however,  a 
great  gap  in  the  history  of  the  parasite.  They  described  lucidly 
its  life-history  in  the  human  being,  but  could  not  explain  how  man 
became  infected. 

Sir  Patrick  Manson,  reasoning  on  his  work  on  the  mosquito  and 
filaria,  suggested  that  there  might  be  a  stage  of  the  development  of 
the  parasite  in  the  mosquito.  Working  on  Hanson's  theory,  Ross, 
at  that  time  in  the  Indian  Medical  Service,  after  years  of  patient 
hard  work,  was  able  to  trace  the  full  development  of  a  bird's  para- 
site in  Culex,  and  partially  that  of  the  human  parasite  in  the  Ano- 


FOUNDATIONS  OF  MODERN  TROPICAL  MEDICINE  19 

pheles,  and  thus  made  not  merely  a  great  discovery,  but  one  which 
ought  to  be  in  time  of  lasting  benefit  to  mankind.  The  full  develop- 
ment of  the  human  parasite  was  found  out  by  Grassi,  who  also 
showed  that  only  Anopheles  are  capable  of  transmitting  the  para- 
site. Ross  and  Grassi's  most  important  discoveries  have  been 
verified  and  extended  by  many  people — e.g.,  Marchiafava,  Celli, 
Bignami,  Dionisi,  Daniels,  Stephens,  and  Christophers,  etc. — but 
the  account  of  their  work  will  be  given  later.  Thus,  out  of  the  fevers 
all  classed  as  malaria  there  issued  a  type  clearly  defined,  to  which 
the  term  '  malaria  '  must  be  restricted. 

In  1 90 1  Forde  and  Dutton  discovered  a  trypanosome,  called  by 
Dutton  Trypanosoma  gambiense,  in  a  case  of  a  peculiar  irregular 
fever  in  the  Gambia.  In  1902  Dutton  and  Todd  observed  this 
organism  in  several  other  cases  presenting  the  same  type  of  fever, 
which  became  known  at  the  time  as  trypanosome  fever,  Gambia 
fever,  or  Dutton's  disease  (Laveran  and  Mesnil).  In  1902  and  1903 
Castellani  found  a  trypanosome  in  the  cerebro-spinal  fluid  of  cases 
of  sleeping  sickness,  and  first  associated  it  with  the  aetiology. 
Further  investigation  by  Bruce,  Nabarro,  and  numerous  observers 
in  various  regions  of  Africa  confirmed  and  greatly  extended  this 
work.  In  1903  Sambon  and  Brumpt  independently  promulgated 
the  hypothesis  that  the  human  trypanosome  was  carried  by  a 
tsetse-fly,  in  all  probability  the  Glossina  palpalis  ;  and  Bruce  and 
Nabarro  experimentally  proved  that  the  Trypanosoma  czstellanii 
is  in  reality  introduced  into  human  beings  by  the  bite  of  Glossina 
palpalis.  Bruce  and  others  considered  the  transmission  as  purely 
mechanical,  but  the  researches  of  Kleine  show  that  the  parasite 
undergoes  true  development  in  the  body  of  the  tsetse-fly.  In  1903 
Castellani  stated  that  man  in  analogy  with  the  lower  animals 
might  be  infected  by  several  species  of  trypanosomes.  In  1909 
Chagas  discovered  a  form  of  human  trypanosomiasis  in  South 
America,  and  showed  that  the  trypanosome  causing  it  (S.  cruzi 
Chagas,  1909)  was  carried  by  a  Conorhinus.  In  1910  Stephens  and 
Fantham  created  a  new  species  (T.  rhodesiense),  which  Kinghorn  and 
Yorke  in  1912  showed  to  be  transmitted  by  Glossina  morsitans 
(Westwood). 

Trypanosomes  were  found  in  the  lower  animals  long  before  they  were 
discovered  in  man.  Gruby  first  used  (1844)  the  term  '  trypano-oma  '  for  a 
flagellate  he  had  found  in  the  blood  of  frogs  in  1842.  A  similar  parasite  had 
been  found  by  Valentin  in  1841  in  the  common  trout  (Salmo  fario).  Very 
little  progress  was  made  in  the  investigations  of  these  organisms  until  1878, 
when  Lewis,  in  India,  described  a  trypanosome  in  the  blood  of  rats,  which  was 
named  by  S.  Kent  Trypanosoma  lewisi.  In  1880  Evans  discovered  a  trypano- 
some in  animals  affected  with  surra — Trypanosoma  evansi  (Steel,  1885). 
This  was  a  most  important  discovery,  as  it  showed  t  at  trypanosomes  were 
capable  of  producing  disease,  while  previously  it  had  been  believed  that  these 
parasites  were  harmless.  In  1894  Bruce  discovered  the  Nagana  trypano- 
some, Trypanosoma  brucei  (Plimmer  and  Bradford,  1899),  and  experimentally 
proved  that  the  organism  was  conveyed  by  a  species  of  tsetse-fly  (Glossina 
morsitans).  Rouget  in  the  same  year  observed  a  trypanosome  in  the  blood 
of  horses  affected  with  dourine — Trypanosoma  equiperdum  (Dofiein,   1901). 


20  THE  HISTORY  OF  TROPICAL  MEDICINE 

Elmassian  in  1901  described  a  trypanosome  observed  by  him  in  mal  de  caderas 
—  Trypanosoma  equinum  (Voges,  1901).  Theiler,  in  1902,  in  South  Africa 
found  a  trypanosome  in  the  blood  of  cattle  affected  with  a  peculiar  disease 
known  locally  as  '  galziecte.'  The  parasite  was  named  by  Bruce  Trypano- 
soma theileri.  Recently  several  other  forms  of  trypanosomiasis  have  been 
described  in  the  lower  animals  by  Dutton  and  Todd,  Cazalbou,  Lingard,  Ed. 
and  Et.  Sergent,  Shillong,  Martini,  Ziemann,  and  others. 

In  the  meanwhile,  Colonel  Sir  W.  B.  Leishman,  in  the  year  1900, 
discovered  some  peculiar  bodies  in  the  spleen  of  a  soldier  who  had 
died  of  what  was  called  '  dum-dum  fever,'  but  did  not  publish  an 
account  of  his  discovery  till  1903,  in  which  year  Donovan  also 
found  the  same  parasitic  bodies  in  Madras.  This  parasite  was 
first  considered  to  be  a  piroplasma  by  Laveran  and  Mesnil,  and 
called  Piroplasma  donovani  ;  but  Ross  created  a  new  genus  for  it, 
using  the  term  Leishmanial.  Wright  of  Boston  found  similar 
bodies  in  Oriental  sore,  which  he  called  Helcosoma  tropicum.  The 
knowledge  of  these  bodies  and  the  diseases  they  cause  has  been 
considerably  extended  by  Christophers  and  by  Martzinowsky  and 
Bogroff,  while  a  great  advance  was  made  by  Rogers,  who  in  1904 
showed  that  by  artificial  cultivation  Leishmania  donovani  developed 
into  flagellate  organisms.  The  life-history  of  L.  donovani  outside 
the  human  body  has  partially  been  traced  by  Patton,  of  the 
Indian  Medical  Service,  in  the  bed-bug.  In  1904  Laveran  and 
Cathoire  discovered  a  Leishmania  in  films  from  the  spleen  of  a  child 
in  Tunisia.  In  1905,  Pianese,  in  Italy,  found  a  Leishmania  in  the 
spleen  of  children  suffering  from  febrile  splenic  anaemia.  Nicolle  com- 
pleted the  study  of  the  parasite,  and  called  it  Leishmania  infantum. 
Gabbi,  and  later  Cardamatis,  Feletti,  and  others,  have  emphasized 
the  frequency  of  this  disease  in  the  Mediterranean  littoral  and 
islands.  Gabbi  considers  the  disease  to  be  identical  with  Indian 
kala-azar. 

In  1903  peculiar  parasitic  bodies,  certainly  protozoa,  were  dis- 
covered in  rabies  by  Negri  of  Pavia.  Negri's  important  discovery 
has  been  confirmed  by  many  authors,  and  in  the  tropics  by  Cornwall. 

In  this  section  may  be  described  the  discovery  of  the  causes  of 
disease  due  to  spirochetes,  the  nature  and  relationship  of  which 
are  not  yet  clearly  known.  Obermeyer,  as  far  back  as  1873, 
described  the  spirochete  of  relapsing  fever,  which  was  thought  to 
be  spread  by  the  bed-bug.  In  1904  Nabarro,  Ross,  and  Milne,  in 
Uganda,  discovered  a  spirochaete  in  the  blood  of  persons  suffering 
from  tick  fever — i.e.,  a  fever  supposed  to  be  due  to  the  bite  of 
Omithodoros  moubata — and  independently  in  the  same  year  Dutton 
and  Todd,  working  in  the  Congo,  described  a  spirochaete  causing 
tick  fever.  This  spirochaete  has  been  proved  by  Breinl  and  King- 
horn  to  be  distinct  from  the  Spiroschaudinnia  recurrentis,  and  in 
1906  they  gave  it  the  name  of  S.  duttoni,  in  honour  of  the  late  Dr. 
Dutton,  of  the  Liverpool  School,  who  had  done  so  much  for  Tropical 
Medicine,  and  who  himself  had  fallen  a  victim  to  this  disease. 
Novy  and  Knapp  had  a  little  time  previously  assigned  the  name 
Spirillum  duttoni  to  the  same  parasite.     In  1914  Inada  and  Ido  dis- 


FOUNDATIONS  OF  MODERN  TROPICAL  MEDICINE  21 

covered  a  spirochete  in  Weil's  disease,  which  they  called  S.  ictero- 
hcemorragice.  In  1918  Noguchi  cultivated  from  cases  of  yellow- 
fever  a  spirochete  which  he  has  named  Leptospira  icteroides.  Other 
spirochete  have  recently  been  described,  as  will  be  mentioned  later. 

In  1905  Schaudinn  discovered  the  presence  of  a  spirochete- 
like  organism  in  syphilis,  which  he  called  Spirochceta  pallida.  Later 
he  created  for  the  organism  a  new  genus — Treponema.  In  the 
same  year  Castellani  demonstrated  the  presence  of  a  spirochete  or 
treponema  in  yaws,  and  named  it  Spirochceta  pertennis  {Treponema 
pertenue),  and  in  1906  described  Bronchospirochetosis. 

Reference  must  here  be  made  to  the  discovery  of  a  small  pro- 
tozoan parasite  in  sheep  suffering  from  a  disease  called  '  carceag  ' 
by  Babes  in  Roumania  in  1888.  The  name  applied  to  this  parasite 
— viz.,  hematococcus — could  not  be  maintained,  as  it  was  ahead}' 
used  in  botany,  hence  the  generic  name  of  Babesia  was  given  to  the 
group  by  Starcovici  in  1893.  The  term  '  piroplasma,'  which  should 
be  used,  was  introduced  by  Patton  in  1895.  It  is,  however,  mostly 
due  to  the  work  of  Smith  and  Kilborne  on  red-water  in  cattle  that 
Piroplasma  has  become  well  known,  together  with  the  fact  that  it  is 
spread  by  a  tick.  The  parasite  Piroplasma  canis,  discovered  by  Piana 
and  Galli-Valerio  in  1895,  has  been  thoroughly  described  by  Celli 
in  1900  and  Nuttall  in  1904,  and  the  life-history  in  the  tick  has 
been  worked  out  by  Christophers.  At  the  present  time,  thanks 
to  the  researches  of  Koch,  Theiler,  Franca,  and  others,  several 
species  of  Piroplasma  especially  affecting  cattle  are  known. 

As  to  whether  a  Piroplasma  is  the  cause  of  the  tick  or  spotted  fever 
of  the  Rocky  Mountains  appears  open  to  grave  doubt,  although  it 
has  been  described  by  Wilson  and  Chowning  in  1902,  and  supported 
by  Westbrook  and  Cobb  in  the  same  year,  and  Anderson  in  1903, 
because  other  observers  have  failed  to  find  any  such  organism. 
There  is,  however,  strong  evidence  in  favour  of  a  tick  being  the 
spreader  of  the  disease. 

Mycology. — Pathogenic  mycology  takes  its  origin  in  1677  with 
Hooke's  description  and  illustration  of  fungi  causing  the  blighted 
or  yellow  specks  on  the  leaves  of  the  damask  rose,  and  by  his 
illustration  of  the  blue  moulds.  This  pioneer  work  is  continued  by 
Malpighi  (1686),  Ray  (1706),  Plukenet  (1720),  Micheli  (1729),  and 
their  discoveries  were  systematized  and  extended  by  Linneus  (i753)> 
Persoon  (1801),  Fries  (1821),  Link  (1824),  and  so  on  to  the  days  of 
Saccardo,  Vuillemin,  and  last,  and  by  no  means  least,  Pinoy ;  but  more 
detailed  information  with  regard  to  this  history  will  be  given  later. 

Special  attention  must  be  drawn  to  the  discovery  by  Gruby, 
in  1844,  that  ringworm  was  due  to  a  parasitic  fungus,  and  to  the 
extension  of  that  discovery  by  Malmsten  in  1845,  and  to  the  great 
list  of  investigators  of  this  particular  feature  down  to  the  classical 
work  of  Sabouraud. 

This  work  by  Gruby  produced  world-wide  interest  in  parasitic 
mycology,  and  for  a  time  it  made  great  progress,  but  fell  back  into 
a  second-rate  place  when  bacteriology  came  forward,  and  is  only 


22  THE  HISTORY  OF  TROPICAL  MEDICINE 

now  being  rescued  from  this  position  thanks  to  the  labours  of 
Manson,  Blanchard,  Bollinger,  Eyre,  Carter,  Vincent,  Nocard,  Pinoy, 
and  Brumpt. 

Bacteriology. — From  the  most  remote  times  the  suspicion  that 
the  mysterious  cause  of  contagious  and  epidemic  diseases  must  be 
sought  in  living  entities  has  flashed  through  the  minds  of  many 
observers.  Columella,  a  contemporary  of  Seneca,  records  the  belief, 
apparently  popular  in  his  time,  of  the  living  nature  of  miasmata 
and  contagion.  The  idea  of  a  contagium  vivum  was  not  extinguished 
even  in  the  darkness  of  the  Middle  Ages.  Thus,  for  instance,  in  a 
book  written  in  the  twelfth  century,  and  wrongly  stated  to  be  by 
St.  Hildegard,  the  abbess  of  a  convent,  we  find  notices  of  minute 
animals  which  produce  disease. 

Fracastoro's  sixteenth-century  work  is  considered  above,  while 
in  1 641  Athanasius  Kircher,  a  friar,  stated  that  he  had  observed 
minute  living  organisms  in  the  blood  of  a  patient  during  an  epidemic 
of  plague.  Linnaeus  supported  the  theory  that  disease  was  due  to 
minute  forms  of  life  by  inserting  papers  on  the  subject  in  his 
'  Amcenitates  Academicae.'  But  the  first  to  promulgate  scientifi- 
cally a  bacterial  theory  was  Agostino  Bassi,  a  country  practitioner 
of  the  north  of  Italy  in  the  early  nineteenth  century.  At  that  time 
a  peculiar  disease  was  destroying  the  silkworms,  bringing  ruin  to 
the  country  in  which  the  silk  industry  was  paramount.  Bassi,  by 
means  of  the  microscope,  discovered  the  germ  which  is  the  cause 
of  the  disease.  The  organism  received  later  the  name  of  Botrytis 
bassiana.  From  analogy,  Bassi  believed  and  stated  that  human 
diseases  were  also  due  to  micro-organisms.  Bassi's  work  was  not 
appreciated  by  his  contemporaries. 

In  1849  Pollender,  and  in  1850  Davaine,  noted  the  Bacillus 
anthracis  in  the  blood  of  sheep  suffering  from  anthrax,  but  it  was 
not  until  Pasteur,  in  1857,  had  shown  that  fermentation  was  due  to 
a  yeast  and  that  butyric  acid  fermentation  was  due  to  a  bacillus, 
that  Davaine,  in  1863,  considered  that  the  rodlets  which  he  had 
seen  in  the  sheep's  blood  were  the  cause  of  the  disease. 

In  1882  Koch  discovered  the  tubercle  bacillus,  and  from  1877 
to  1 91 1  he  introduced  and  improved  methods  for  the  separation 
and  pure  culture  of  bacteria,  and  laid  down  the  proofs  required  to 
demonstrate  that  a  given  bacterium  is  the  cause  of  a  disease;  and 
acting  on  these  lines,  Hansen  in  1879  discovered  the  so-called 
bacillus  of  leprosy,  Eberth  in  1880  that  of  typhoid  fever,  Nicolaire 
in  1884  that  of  tetanus,  Koch  in  1884  that  of  cholera,  Bruce  in  1886 
that  of  Malta  fever,  Yersin  and  Kitasato  in  1894  that  of  plague, 
Shiga  in  1898  and  Kruse  in  1900  that  of  bacillary  dysentery. 

The  discovery  of  the  typhoid,  paratyphoid,  and  allied  organisms 
has  been  of  importance  in  enabling  the  differentiation  of  fevers 
previously  massed  together  into  a  chaotic  group  labelled  'malaria.' 
Serums  and  Vaccines. — The  discovery  of  the  immune  serums,  and 
their  application  to  the  treatment  of  disease,  marked  a  great  step 
forward  in  the  history  of  medical  science. 


FOUNDATIONS  OF  MODERN  TROPICAL  MEDICINE  23 

Still  more  important  are  the  labours  of  Roux,  Haffkine,  Wright, 
Strong,  Lustig,  Galeotti,  and  others,  in  perfecting  and  applying 
vaccines  to  the  prevention  as  well  as  to  the  treatment  of  disease. 

Those  of  greatest  tropical  importance  are  Haffkine's  plague 
vaccine,  the  same  worker's  cholera  vaccine,  and  Wright's  mono- 
valent typhoid  vaccine  and  his  pyogenic  vaccines. 

A  further  advance  was  the  introduction  of  Castellani's  multiple 
vaccines  for  the  prevention  and  treatment  of  disease.  For  long 
it  was  thought  that  a  vaccine  must  be  monovalent,  but  Castellani's 
triple  vaccine  for  typhoid  and  the  paratyphoid  fevers  has  now  been 
used  on  a  very  large  scale  for  the  British  and  other  armies  with 
success,  and  the  tetravaccine  typhoid,  para  A,  para  B,  cholera  has 
been  adopted  by  the  Serbian  Army  since  1916.  He  has  also  pre- 
pared tetravaccines,  which  include  undulant  or  Malta  fever,  and 
has  prepared  and  advocated  the  use  of  penta-  and  hexa-valent 
vaccines. 

Entomology. — It  is  obvious  from  the  preceding  sections  that 
insects  play  a  great  part  in  the  spread  of  protozoal  diseases,  and  the 
same  holds  good  for  worms  and  bacteria. 

Filaria  can  be  spread  by  Culex,  Stegomyia,  or  Anopheles;  malaria 
by  several  species  of  the  Anophelinas ;  Piroplasma  and  spirochetes  by 
ticks;  Leishmania  donovani  perhaps  by  bugs;  Leishmania  infantum 
probably  by  fleas;  trypanosomes  by  tsetse-flies,  and  possibly  by 
some  kind  of  flies. 

But  apart  from  these  diseases,  of  which  we  know  the  cause, 
there  are  two  infections  the  unknown  agent  of  which  is  carried 
by  mosquitoes.  Thus  Finlay,  in  1881,  formulated  definitely  the 
hypothesis  that  yellow  fever  was  spread  by  a  mosquito,  which 
in  1900  was  proved  by  Reed,  Carroll,  Agramonte,  and  Lazear  to 
be  a  fact,  the  mosquito  being  Stegomyia  fasciata,  now  Stegomyia 
calopus. 

With  regard  to  dengue  fever,  Graham  of  Beirut,  in  1903,  thought 
that  he  had  discovered  a  protozoon  in  the  red  corpuscles  of  persons 
suffering  from  this  disease,  and  that  this  parasite  underwent  develop- 
ment in  Culex  fatigans  (Wied).  Doubt  has  been  thrown  upon 
Graham's  parasite,  but  the  idea  that  Culex  fatigans  (Wied)  is  respon- 
sible for  the  spread  of  dengue  fever  has  been  strongly  supported  by 
Ashburn  and  Craig  in  1907. 

Turning  now  to  bacterial  diseases,  the  work  of  the  Indian  Plague 
Committee,  published  in  1906-1908,  proves  that  the  rat-flea  (Xenop- 
sylla  cheopis)  is  the  main  means  of  the  spread  of  plague.  With 
regard  to  typhoid,  it  was  conclusively  proved  in  the  army  concen- 
tration camps  of  the  United  States  in  the  Spanish-American  War 
of  1898  that  flies  were  great  spreaders  of  the  disease,  a  fact  already 
emphasized  by  Celli  and  others;  and  this  has  been  further  supported 
by  the  work  of  Firth  and  Horrocks  (1902),  Chantemesse,  and  numer- 
ous other  observers.     Dysentery  may  also  be  spread  by  flies. 

A  knowledge,  therefore,  of  ticks,  biting  flies,  and  other  insects  is 
of  the  greatest  importance  to  the  doctor  who  is  to  practise  in  the 


24  THE  HISTORY  OF  TROPICAL  MEDICINE 

tropics.  We  refer  the  reader  interested  in  this  subject  to  the  classical 
work  of  Nuttall  on  insects  as  carriers  of  disease  in  the  Johns 
Hopkins  Hospital  Reports,  1899. 

The  idea  that  the  house-fly  and  its  allies  are  capable  of  spreading  disease 
originates  from  the  time  of  Mercurialis,  who  in  1577  suggested  that  the  virus 
of  plague  might  be  disseminated  by  this  means.  In  1666  Sydenham  remarked 
that  the  presence  of  numerous  flies  in  the  summer  indicated  that  there  would 
be  much  sickness  in  the  autumn,  while  in  1808  Crawford  stated  that  he 
believed  insects  to  be  the  carriers  of  infection.  In  1853  Moore  referred  to 
flies  as  the  possible  carriers  of  cholera,  typhoid,  tuberculosis,  anthrax,  and 
leprosy.  In  1869  Raimbert  performed  the  first  experiments,  showing  that 
anthrax  could  be  disseminated  by  flies.  Tizzoni  and  Cattani  made  observa- 
tions on  the  spread  of  cholera  by  the  same  means,  Grassi  and  later  Stiles 
demonstrated  the  possibility  of  the  carriage  of  parasitic  worms,  and  one  of 
us  the  transference  of  the  Treponema  pertenue  by  the  same  means.  Gayon 
in  1903  indicated  the  possibility  of  the  dissemination  of  fungi  by  flies. 

Toxicology. — Micro-organisms  are  not  the  only  causes  of  disease 
to  be  found  in  the  tropics,  for  poisons  from  plants  and  animals 
are  also  of  the  greatest  importance. 

It  has  been  shown  that  the  most  primitive  peoples  have  definite 
knowledge  of  poisons,  and  it  has  already  been  mentioned  how  early 
the  study  of  snake  and  other  animal  venoms  began. 

It  will  suffice  here  to  indicate  that  the  scientific  study  of  snake- 
venom,  begun  by  Prince  Lucien  Bonaparte  in  1843,  has  been  ex- 
tended by  Fayrer,  Martin,  Lamb,  Calmette,  Noguchi,  and  many 
others,  and  leave  a  fuller  description  of  this  and  the  history  of  other 
poisons  to  a  later  chapter. 

Climatology. — Tropical  medicine  does  not  confine  itself  to  diseases 
caused  only  by  parasites  and  poisons,  for  there  are  such  conditions 
as  heat-stroke,  which  are  entirely  due  to  physical  causes,  and  also 
there  is  the  important  question  of  the  influence  of  tropical  climates 
on  man,  which  must  be  dealt  with  in  a  later  chapter. 

Dietetics. — But  little  work  has  so  far  been  done  with  regard  to 
this  important  subject  in  the  tropics,  though  pioneer  struggles  have 
been  undertaken  most  successfully  by  McCay  in  India,  and  his 
example  deserves  to  be  followed. 

Clinical  Medicine.- — Clinical  researches  into  the  diseases  affecting 
Europeans  and  natives  in  the  tropics  began  with  the  earliest  modern 
travellers,  non-medical  as  well  as  medical,  and  the  earliest  references 
to  tropical  diseases  are  to  be  found  in  these  early  works  on  travel. 
Thus,  as  Singer  has  pointed  out,  De  Oviedo  in  1526  gives  a  reference 
to  a  disease  bubas,  which  we  now  know  to  include  Frambcesia 
tropica,  a  form  of  Leishmaniasis,  and  probably  a  form  of  Blasto- 
mycosis. In  1558  Thevet  described  the  jigger  as  a  little  worm  called 
'  Tom,'  which  entered  into  the  feet,  and  wrote  descriptions  of 
Frambcesia  tropica  under  the  term  '  Pians.'  In  1598  G.  W.  wrote  an 
account  of  Calenture  (heat-stroke),  and  Tabardillo,  which  is  derived 
from  the  Spanish  word  Tabardo,  a  cloak,  and  was  applied  to  the 
typhus  fever  epidemic  in  Spain  in  1557;  anc^  therefore  G.  W.  may 
have  meant  typhus  by  this  term,  though  it  is  possible  that  he  also 
included  yellow  fever  under  the  same  name.     He  also  describes 


FOUNDATIONS  OF  MODERN  TROPICAL  MEDICINE  23 

Espinlas,  possibly  due  to  the  bite  or  sting  of  some  venomous 
animal ;  Cameras  de  Sangre,  or  dysentery ;  erysipelas,  which  probably 
included  filariasis;  and  Tinoso,  or  scurvy.  In  1642  Bontius  wrote 
his  work,  '  De  Medicina  Indorum.'  Chalmers  and  Archibald  have 
drawn  attention  to  the  description  of  dracontiasis,  dermatophiliasis, 
epidemic  gangrenous  rectitis  in  South  America;  simple  continued 
fever,  malarial  fevers,  dysenteries,  smallpox,  climatic  bubo  in 
India;  malaria,  endemic  yellow  fever,  dengue,  smallpox,  filariasis, 
diarrhoeas,  dysentery,  and  yaws  in  West  Africa,  as  indicated  by 
D.  L.  F.  in  1726  and  by  Aubrey  in  1729;  but  these  and  many 
others  are  briefly  mentioned  at  the  end  of  this  chapter  under  the 
heading  '  Special  Works  on  Tropical  Medicine,'  and  need  not  be 
further  described  here. 

It  is  not  possible  for  us  to  trace  out  in  detail  the  history  of  treat- 
ment, but  we  may  .briefly  mention  a  few  points  with  regard  to 
quinine,  arsenic,  antimony,  thymol,  and  emetine. 

Treatment — Quinine. — In  the  seventeenth  century  the  epoch- 
making  discovery  of  the  value  of  cinchona-bark  in  the  treatment  of 
malarial  fevers  took  place. 

In  1638  the  Countess  of  Chinchon,  wife  of  the  fourth  Count, 
Viceroy  of  Peru,  after  nine  years'  residence  in  that  country,  was 
seized  with  tertian  malarial  fever.  Don  Lopez  de  Canizaries,  the 
Corregidor  of  Loxa,  hearing  of  this,  sent  her  a  parcel  of  the  bark 
of  a  tree  called  by  the  Indians  of  Loxa  '  quina-quina.'  The  dupli- 
cation of  the  name  of  the  tree  is  said  to  indicate  that  it  has  medical 
properties. 

The  value  of  this  bark  in  the  treatment  of  fever  appears  to  have 
been  only  known  locally,  but  was  understood  by  the  Spaniards  in 
Loxa  as  far  back  as  1600.  How  the  Indians  became  acquainted 
with  the  bark  is  not  known,  and  the  tales  of  the  curing  of  their 
fevers  by  drinking  the  water  of  a  lake  into  which  a  cinchona-tree 
had  fallen,  or  of  a  sick  puma  chewing  the  bark,  are  considered  to  be 
myths  invented  later  in  Europe. 

Dr.  Don  Juan  de  Vega  administered  the  bark  to  the  Countess, 
who  quickly  recovered,  and  four  years  later  returned  to  Europe 
with  a  large  supply  of  it,  which  she  distributed  to  persons  suffering 
from  fever  on  her  estates  near  Madrid.  Hence  the  bark  was  often 
known  a.s  Pulvis  comitisscs.  In  1670  Jesuit  missionaries  sent  some 
of  the  bark  to  Rome,  whence  it  was  distributed  throughout  Europe 
by  Cardinal  de  Lugo.  Hence  the  names  '  Jesuit's '  or  '  Cardinal's  ' 
bark. 

Linnaeus  named  the  tree  after  the  Countess,  but  spelt  her  name 
wrongly,  calling  it  Cinchona  officinalis.  A  curious  strife  now  rose 
in  Europe  as  to  whether  fever  should  be  treated  by  bark  or  not, 
but  the  labours  of  Morton  and  Sydenham,  together  with  the  dramatic 
cure  of  the  Grand  Dauphin,  enabled  its  true  value  to  be  known. 
The  tree  has  since  that  time  been  introduced  into  several  parts  of 
the  world,  and  grows  well  in  India,  Ceylon,  and  Java. 

Finally  in  1820  Pelletier  and  Caventou  prepared  the  alkaloid 


26  THE  HISTORY  OF  TROPICAL  MEDICINE 

quinine  from  cinchona-bark.     For  further  particulars  see  Chapter 
XL.  on  Malaria. 

Arsenic  and  Antimony.- — -Thanks  to  Morgan's  work  it  is  possible 
to  give  a  brief  history  of  these  two  metalloids,  which  belong  to  the 
nitrogen  group  of  the  fifth  vertical  series  of  the  periodic  classifica- 
tion, and  are  related  to  the  non-metals  phosphorus  and  nitrogen 
and  to  the  metal  bismuth. 

Arsenic  occurs  in  nature  in  combination  with  cobalt,  as  smaltite  and 
cobaltite,  both  of  which  are  included  under  the  term  cobolt,  which  was  found 
by  a  German  artist  to  be  capable  of  making  sympathetic  ink  when  acted  upon 
by  aqua  fbrtis,  the  action  of  which  was  studied  in  1737  by  Hellot  and  in  1760 
by  Cadet  de  Gassicourt,  who  produced  a  highly  inflammable  stinking  fluid 
therefrom,  and  this  Then6rd  concluded  was  a  complex  acetate  containing 
arsenic. 

During  the  years  1837-1843  Bunsen  isolated  this  complex,  to  which  Berze- 
lius  gave  the  name  cacodyl,  and  in  1858  Baeyer,  having  first  made  primary 
methyl  arsenicals,  produced  methylarsenic  acid,  the  soluble  salts  of  which  are 
employed  medicinally  as  new  cacodyl  and  arrpenal.  In  1860-1863  Bechamp 
made  the  first  aromatic  arsenical,  and  in  the  seventies  Michaelis,  in  collabora- 
tion with  other  workers,  not  merely  extended  this  knowledge,  but  prepared 
the  first  aromatic  antimony  compounds.  In  1902  Bechamp's  compound  was 
first  tried  in  medicine  by  Thomas  and  Breinlfor  sleeping  sickness,  being  called 
aioxyl  because  of  its  comparatively  non-toxic  action,  and  it  is  the  drug  which 
has  been  used  with  such  success  in  sleeping  sickness  in  the  Sudan.  Atoxyl 
was  shown  in  1907  by  Ehrlich  and  Bertheim  to  be  the  sodium  salt  of  ^-arsenitic 
acid,  being  a  derivative  of  quinquevalent  arsenic. 

/ONa, 
Atoxyl,   NFX6H4AsG\  contains  from   25-95   to    20-78   per   cent,  of 

\OH 
arsenic,  according  to  the  amount  of  water  of  crystallization.     Mono-acetylated 

/ONa. 
atoxyl  is  CH,CONHCfiH-AsO< 

3  6  \oH 

According  to  Mesnil  and  Nicolle's  experiments,  and  the  observations  of 
Nierenstein,  it  is  not  the  arsenic  in  these  compounds  which  is  to  be  looked  upon 
as  the  effective  agent,  but  the  amido-group,  which  may  possibly  be  the  effec- 
tive agent  in  trypan  red,  afridol  blue,  afridol  violet,  and  parafuchsin,  which 
do  not  contain  arsenic,  but  possess  amido-groups,  and  affect  trypanosomes  in 
a  similar  manner  to  atoxyl.  According  to  Ehrlich,  Levaditi,  and  Yama- 
nouchi,  atoxyl  undergoes  a  reduction  in  the  animal  tissues.  Ehrlich  has 
prepared  two  derivatives  of  atoxyl,  one  of  which,  already  mentioned  (arseno- 
phenylglycin),  is  very  effective  in  mice  on  atoxyl-resistant  trypanosomes. 
Levaditi  and  Yamanouchi  have  also  prepared  an  active  derivative  of  atoxyl, 
which  they  call  trypanotoxjd.  Nierenstein  thinks  that  atoxyl  is  oxydized 
in  the  tissues,  and  it  is  only  in  the  nascent  state  that  it  becomes  efficacious. 

Owing  to  the  fact  that  large  doses  of  atoxyl  lead  to  such  unpleasant  results 
as  optic  atrophy,  gastro-intestinal  inflammation,  and  peripheral  neuritis, 
other  arsenical  preparations  have  been  recommended;  and  the  firm  Burroughs 
and  Wellcome  has  introduced,  under  the  trade  name  of  soamin,  a  prepara- 
tion somewhat  similar  to  atoxyl,  but  said  to  be  less  poisonous.  It  is  given 
in  the  same  doses  as  atoxyl,  but  the  therapeutic  results  do  not  appear  to 
have  been  very  successful.  Soamin',  according  to  the  published  formula,  is 
C2H4NH2AsO(OH)(ONa)5H20. 

Atoxylate  of  mercury  was  introduced  by  Uhlenluth,  but  is  less  satisfactory 
than  atoxyl. 

Combinations  of  Mesnil's  afridol  and  atoxyl,  Ehrlich's  parafuchsin  and 
atoxyl,  picric  acid,  safranin,  trypaflavin,  and  other  dyes  and  atoxyl,  have  been 


FOUNDATIONS  OF  MODERN  TROPICAL  MEDICINE 


27 


suggested  in  the  treatment  of  trypanosomiasis,  but  in  man  the  results  have 
not  been  so  successful  as  in  the  lower  animals. 

Mercury  was  first  introduced  in  1902  for  the  treatment  of  sleeping  sickness 
by  Low  and  Castellani,  using  intravenous  injection  of  Baccelli's  sublimate 
solution  (hydrargyri  perchloridi,  o*io  gramme;  sodii  chloridi,  0-50  gramme; 
aquae  destillatae,  ioo-oo  c.c;  1  to  4  c.c.  per  intravenous  injection),  in  associa- 
tion with  arsenic  and  quinine  by  the  mouth.  A  fall  of  the  temperature  was 
observed  in  some  cases,  but  the  fatal  course  of  the  disease  was  not  influenced. 
Moore,  Nierenstein,  and  Todd  have  used  mercury  and  atoxyl  in  combination 
or  alternation,  with  the  idea  that  mercury  might  act  upon  the  latent  form 
of  the  trypanosome,  while  atoxyl  would  influence  the  active  form.  In  man 
this  combined  treatment  has  apparently  not  given  any  better  results  than 
atoxyl  alone.  This  combined  treatment,  consisting  of  atoxyl  and  an 
inorganic  salt  of  arsenic  such  as  orpiment,  has  been  recommended  by 
Laveran  and  Thiroux,  and  has  already  been  used  in  man  with  good  results. 
The  orpiment  should  be  given  in  pills,  in  the  dose  of  2  grains  of  orpiment  two 
or  three  times  daily.  The  administration  of  orpiment  frequently  causes 
diarrhoea.     Thiroux  therefore  incorporates  in  the  orpiment  pills  some  opium. 

Ehrlich  observed  that  the  aromatic  compounds  of  tervalent  arsenic  were 
more  efficacious  in  attempts  to  kill  protozoan  parasites,  and  after  605  attempts 
in  1909  he  evolved  Salvarsan,  or  606,  also  known  as  Kharsivan  and  Arsenobillon, 
which  is  a  pale  yellow  powder  soluble  in  dilute  hydrochloric  acid  or  aqueous 
sodium  hydroxide  or  carbonate.  Its  formula  is  the  hydrochloride  of  3  :  3'- 
diamino  -4  :  4'-di-hydroxy  arseno-benzene — i.e.  : — 


As 


As 


HC1,  NH„ 


OH 


\J  NH2,  HC1,  2H20 
OH 


On  account  of  its  phenolic  and  feebly  basic  properties,  Salvarsan  fails  to 
give  neutral  salts,  and  the  free  base  is  very  insoluble  in  water  or  in  normal 
saline  solution  ;  therefore  an  approximately  neutral  solution  has  to  be  prepared 
immediately  before  use,  which  is  inconvenient,  and  led  to  the  search  for  a 
compound  with  soluble  salts  giving  a  neutral  reaction  in  solution.  Such  a 
preparation  had  been  foreshadowed  by  Ehrlich's  418  Spirarsyl,  or  the  sodium 
salt  of  arsenophenylglycine,  which  was  the  most  successful  of  the  arsenic 
compounds  prior  to  Salvarsan. 

It  was  found  that  Salvarsan  dihydrochloride  could  be  made  to  produce  a 
compound  called  Ehrlich's  914,  or  Neosalvarsan,  also  called  Neokharsivan, 
Novarsenobillon,  Novarsenobenzol,  or  Sodium  3  :  3*-diamino-4  :  4*-dihydroxy- 
arsenobenzene-N-methylene  sulphurate : — 


As 


As 


NH„ 


V 


NH  CH2,  O,  SONa 


OH 


This  is  a  pale  yellow  powder,  with  (commercially)  generally  small  proportions 
of  inorganic  salts.  It  is  soluble  in  water  and  the  solution  is  quite  neutral, 
but  its  arsenical  content  is  lower  than  that  of  Salvarsan,  and  hence  its  average 
dose  is  larger,  and  the  efficacy  of  the  preparation  should  be  tested  by  intra- 
venous injections  into  rabbits. 

Galyl,  discovered  by  Mouneyrat,  is  4  :  4*-dihydroxyarsenobenzene-3  :  y- 
phosphamic  acid,  and  forms  a  neutral  solution  when  added  to  aqueous  sodium 
carbonate,  and  is  useful  in  syphilis  and  also  kills  spirochaetesand  trypanosomes. 
It  is  very  slightly  toxic.     Ludyl  is  a  complex  disulphonamide  discovered  as 


28  THE  HISTORY  OF  TROPICAL  MEDICINE 

1,151  of  Mouneyrat's  series,  and  like  galyl  is  given  intravenously  and  for  the 
same  conditions. 

We  have  already  referred  to  Spirarsyl,  and  we  may  mention  that  Arseno- 
phenylmethylglycine  has  been  used  experimentally  by  Oechslin  to  kill  Trypano- 
soma evansi  and  T.  rhodesiense  in  experimental  animals. 

In  1913  Ehrlich  found  that  Salvarsan  and  other  derivatives  of  arseno- 
benzene  could  join  with  salts  of  copper,  silver,  gold,  and  platinum,  forming 
combinations  which  could  be  administered  intravenously  and  in  which  the 
heavy  metal  appeared  to  aid  the  arsenic  in  its  germicidal  action.  Luargol 
is  an  example  of  this  type  of  chemical  body. 

Further  new  types  of  compounds  of  organic  arsenicals  with  anti- 
mony, selenium,  etc.,  are  being  tried.  Especial  attention  is  said 
by  Morgan  to  be  directed  at  the  moment  to  certain  partly  methy- 
lated hexaminoarsenobenzenes,  which  give  stable  solutions  with 
soluble  bicarbonates,  and  so  the  final  word  has  yet  to  be  said  with 
regard  to  these  compounds,  which  the  chemist  is  preparing  for  trial 
by  the  physician. 

With  regard  to  the  organic  antimony  derivatives,  the  salts  of  anti- 
monyl  tartaric  acid,  in  the  form  of  lithium  antimonyl  tartrate, 
were  first  used  in  the  experimental  trypanosomiasis  of  mice  by 
Plimmer  and  Thomson  in  June,  1907.  Their  results  were  confirmed 
by  Mesnil  and  Brimont  in  January,  1908,  while  in  March,  1908, 
Manson  used  it  on  man,  giving  it  by  the  mouth.  Also  in  1908 
Boosten  and  Rodhain  used  tartar  emetic  in  human  trypanosomiasis. 

In  1913,  Tsuzuki  introduced  potassium  ammonium  antimonyl 
tartrate,  as  antiluetin,  and  in  the  same  year  Vianna  and  Machado 
gave  tartar  emetic  intravenously  in  cases  of  espundia,  with  good 
results,  which  have  been  confirmed  by  Terra  da  Silva,  Carini  Car- 
walho  and  Christopherson,  and  by  Low.  For  the  same  complaint 
Ludeberg  tried  trioxide  of  antimony  intramuscularly,  and  Martin- 
dale  prepared  an  injectio  antimonii  oxidi,  which  Morgan  considers 
to  contain,  probably,  a  glyceryl  antimonite,  and  this  has  been 
reported  in  191 7  as  curative  of  American  Leishmaniasis  when  used 
subcutaneously,  intramuscularly,  and  intravenously. 

Also  in  1913  Vianna  and  Aragao  reported  that  tartar  emetic  was 
useful  in  the  treatment  of  ulcerating  granuloma. 

In  1914  Castellani  used  tartar  emetic,  together  with  other  drugs, 
in  a  case  of  Indian  kala-azar,  with  satisfactory  results,  and  came 
to  the  conclusion  that  the  drug  was  the  cause  of  the  striking 
result,  and  therefore  he  recommended  it  for  routine  treatment. 
In  the  previous  year  he  had  originated  his  yaws  mixture  (now 
generally  called  Castellani's  mixture),  which  contains  tartar  emetic, 
potassium  iodide,  and  both  carbonate  and  salicylate  of  soda. 

In  1915  Di  Cristina  and  Caronia  reported  the  cure  of  eight  cases 
of  infantile  Leishmaniasis  by  antimony  therapy,  and  later  Rogers 
confirmed  and  extended  this  use  of  tartrate  of  antimony  in  kala- 
azar,  a  line  of  treatment  well  accepted  at  the  present  time. 

Emetine. — For  many  years  it  was  known  that  ipecacuanha  and 
emetine  were  valuable  in  the  treatment  of  certain  cases  of  dysentery, 
and  this  was  crystallized  down  to  the  treatment  of  amoebic  dysen- 


FOUNDATIONS  OF  MODERN  TROPICAL  MEDICINE  29 

tery,  and  more  especially  to  the  presuppurative  stage  of  amoebic 
hepatitis  by  Rogers  from  1909  onwards.  Later  Vedder  in  the 
Philippine  Islands  studied  its  action  on  entamoeba?,  and  Rogers 
devised  the  clinical  application  of  the  drug  by  subcutaneous  injec- 
tion, which  to-day  is  used  as  the  correct  treatment  of  that  form  of 
dysentery  and  its  complications. 

Thymol. — Bozzolo,  in  1880,  was  the  first  to  introduce  this  drug 
for  the  treatment  of  ankylostomiasis.  He  obtained  satisfactory 
results  which  have  been  confirmed  all  over  the  world. 

Prophylaxis.— The  knowledge  of  the  causal  agent  and  its  method 
of  dissemination  have  enabled  reasoned  and  scientific  methods  of 
prophylaxis  to  be  devised  and  carried  out,  of  which  perhaps  the 
most  striking  is  that  performed  in  Panama  by  Gorgas. 

It  is  to  be  hoped  that  in  years  to  come  these  methods  will  be 
extended,  and  that  many  diseases  at  present  hampering  civilization 
will  cease  to  be  terrors;  indeed,  the  present  war  has  amply  proved 
the  wisdom  of  prophylactic  and  sanitary  measures,  especially  the 
polyvalent  prophylactic  treatment  against  the  enteric  fevers, 
cholera,  and  other  diseases,  and  it  is  to  be  hoped  that  now  the 
war  is  over  international  action  will  be  taken  all  over  the  world 
to  combat  disease. 

Research. — Notwithstanding  the  fact  that  so  much  has  been  done 
to  elucidate  disease,  still  there  is  a  great  field  for  research,  and  one 
of  the  direct  blessings  of  the  recent  war  will  be  the  stirring  up  of 
Governments  to  provide  funds  for  this  work,  which  should  never 
be  left,  as  it  used  to  be,  entirely,  or  almost  entirely,  to  individual 
generosity. 

The  State  and  Tropical  Medicine. — Tropical  medicine  has  been 
fortunate  in  that  at  the  commencement  of  modern  tropical  medicine 
there  was  at  the  head  of  the  British  Colonial  Office  a  far-seeing  and 
exceedingly  wise  statesman — Mr.  Joseph  Chamberlain — who  clearly 
realized  the  duties  of  the  State  in  regard  to  the  formation  of  Schools 
of  Tropical  Medicine  in  London  and  Liverpool,  and  of  the  founda- 
tion of  laboratories  in  British  Colonies.  This  policy,  continued  and 
extended  under  the  auspices  of  the  Advisory  Committee  of  the 
Tropical  Diseases  Research  Fund,  has  produced  the  Tropical 
Diseases  Bulletin  and  other  publications  of  great  value. 

The  example  set  by  the  British  Government  has  been  followed  by 
those  of  other  countries,  and  to-day  all  over  the  world  the  State 
supports  tropical  medicine. 

In  many  tropical  countries,  however,  it  appears  to  us  that  the 
State  should  exercise  more  authority  over  the  medical  practitioner, 
native  or  modern  trained ;  that  registers  of  such  practitioners  should 
be  kept,  and  that  this  should  not  be  confined  to  medical  practice 
only,  but  also  to  dental  and  veterinary  work. 

The  War  and  Tropical  Medicine. — The  recent  war  has  dis- 
seminated tropical  diseases  in  such  a  manner  that  many  of 
them  may  become  cosmopolitan.  The  Anophelines  of  England 
have   now    a   chance    to    become    infected    with    malaria,    and, 


30  THE  HISTORY  OF  TROPICAL  MEDICINE 

in  fact,  cases  of  endemic  malaria  have  already  occurred,  but  we 
doubt  whether  there  is  any  real  danger  of  an  epidemic.  Bilharziosis 
has  the  opportunity  to  spread  from  Egypt  to  other  countries.  Are 
sufficiently  strong  measures  being  taken  to  combat  the  spread  of 
these  diseases  and  many  others  like  them — e.g.,  amoebic  dysentery  ? 

Another  point  which  the  war  has  brought  into  prominent  notice 
is  that  so-called  tropical  diseases  exist  in  abundance  in  Europe — 
e.g.,  in  the  Balkans — and  that  agents  like  lice  are  as  prone  to  spread 
disease  in  the  Temperate  as  in  the  Tropical  Zone. 

Certainly  the  massed  formations  of  medical  knowledge  at  work 
in  the  recent  war  at  the  study,  treatment,  and  prevention  of  disease 
will  produce  results  which  would  have  been  but  slowly  evolved  in 
years  of  peace. 

It  is  not  possible  to  close  this  history  without  acknowledging  the 
debt  which  tropical  medicine  owes  to  the  officers  of  the  Royal 
Army  Medical  Corps,  of  the  Royal  Navy,  the  Indian  Medical  Service, 
the  Colonial  Service,  and  to  their  training  schools,  as  well  as  to  the 
officers  of  the  Medical  Services  of  the  armies  and  navies  of  France, 
Italy,  and  the  United  States  of  America. 

MODERN  JOURNALS. 

The  very  excellent  Tropical  Diseases  Bulletin  enables  the  tropical  practi- 
tioner to  keep  himself  abreast  of  the  day  as  regards  current  events  in  tropical 
medicine,  while  the  Tropical  Veterinary  Bulletin  permits  him,  if  he  so  desires, 
to  obtain  the  same  up-to-date  information  with  regard  to  the  diseases  of 
animals.  Both  these  publications  are  issued  by  the  Tropical  Diseases  Bureau, 
the  Imperial  Institute,  London,  S.W.  7. 

If  he  desires  more  information  with  regard  to  bacteriological  work,  he  may 
find  this  and  much  more  in  the  Bulletin  de  I'Institut  Pasteur,  which  is  issued 
by  that  Institute  in  Paris. 

If  he  wishes  more  detail  with  regard  to  Japanese  medical  work,  he  will  find 
a  review  in  English,  written  by  the  Research  Staff  of  the  Severance  Union 
Medical  College,  Seoul,  Korea,  published  in  The  China  Medical  Journal. 
The  names  of  some  of  the  Japanese  medical  journals  are  as  follows: — 

Chugai  Iji  Shimpo,  or  Home  and  Foreign  Medical  News;  Juzenkai  Zas  hi, 
or  Journal  of  the  Perfection  Medical  Society  Alumni  of  Kanazawa  Medical 
School;  Nisshin  Chiryo,  or  Modern  Therapeutics;  Taiwan  Igakukai  Zasshi. 
or  Journal  of  the  Formosa  Medical  Society;  Tokyo  Iji  Shinshi,  or  Tokyo 
Medical  News;  Tokyo  Igakukai  Zasshi,  or  the  Proceedings  of  the  Medical 
Society  of  Tokyo;  also  Acta  Scholcs  Medicinalis  Universitatis  Imperialis  in 
Kioto,  Japanische  Zeitschrift  fur  Dermatologie  und  Urologie,  Kyoto  Igakukai 
Zasshi,  Mitteilungen  aus  der  Medizinischen  Fakutaf  der  Kaiserlichen  Uni- 
versi'a!  zu  Tokyo,  Sei-i-kwai  (Medical  Journal)  of  Tokio,  Tokyoer  Medizinische 
W  ochenschrift ,  Mitteilungen  aus  der  Medizinischen  Fachschule  zu  Keijo. 

If  resumes  of  German  literature  are  desired,  they  can  be  found  in  the 
Archiv  juy  Schiffs-  und  Tropenhygiene  and  in  the  Archiv  fit/  Bakteriologie. 

Apart  from  these  the  following  journals  usually  contain  original  papers 
dealing  with  tropical  medicine: — 

1.  Annali  di  Medicina  Navale  e  Coloniale  (Rome). 

2.  Annales  d'Hygidie  et  de  Medecine  Coloniales  (Paris). 

3.  Annales  de  I'Institut  Pasteur  (Paris). 

4.  Annali  dTgiene  (Turin). 

5.  Anales  del  Instituto  Medico  Nacional  (Mexico). 

6.  Annales  Paulistas  de  Medicina  e  Cirurgi  (San  Paulo). 

7.  Annals  of  Tropical  Medicine  and  Parasitology  (Liverpool). 


MODERN  JOURNALS  31 

8.  Annual   Reports  of  the   Principal  Medical  Officers   of   British,    French , 

Italian,  and  Dutch  Colonies. 

9.  Archives  de  Medecine  et  Pharmacie  Navales  (Paris). 

10.  Archives  de  Parasitologie  (Paris). 

11.  Archiv  fur  Protistenkunde  (Jena). 

12.  Archiv  fur  Schiffs-  und  Tropen-Hygiene,  and  separately  '  die  Beihefte' 

(Leipzig) . 

13.  Arquivos  de  Hygiene  e  Pathologia  Exoticas  (Lisbon). 

14.  Archivos  do  Instituto  Bacteriologica  Camara  Pestana  (Lisbon). 

15.  Archives  de  Medecine  (Athens). 

16.  Archivos  Brasileiros  de  Medicina  (Rio  di  Janeiro). 

17.  Archives  de  1'Institut  Pasteur  de  Tunis  (Tunis). 

18.  Atti  della  Societa  per  gli  Studi  della  Malaria  (Rome). 

19.  Australian  Institute  of  Tropical  Medicine,  Collected  Papers  (Townsville). 

20.  Boletin  del  Instituto  Nacional  de  Higiene  de  Alfonso  XIII.  (Madrid). 

21.  Boletin  de  la  Associacion  Medica  de  Puerto  Rico  (San  Juan). 

22.  Brazil  Medico  (Rio  di  Janeiro). 

23.  British  Guiana  Medical  Annual  (Damerara). 

24.  Bulletin  de  l'Office  International  d'Hygiene  (Paris). 

25.  Bulletin  de  la  Societe  de  Pathologie  Exotique  (Paris). 

2(>.   Bulletin  de  l'Academie  Royale  de  Medecine  de  Belgique  (Brussels). 

27.  Bulletin  de  la  Societe  Portugaise  des  Sciences  Naturelles  (Lisbon). 

28.  Bulletin  de  la  Societe  Medico-Chirurgicale  de  lTndochine   (Hanoi  and 

Haiphong) . 

29.  Bulletin  de  la  Societe  Medicale  de  l'lle  Maurice  (Mauritius). 

30.  Bulletin  of  Entomological  Research  (London). 

31.  Bulletin  de  lTnstitut  Pasteur  d'Alg6~ie  (Algiers). 

32.  China  Medical  Journal  (Shanghai). 
^3.  Cronica  Medica  (Lima). 

34.  Cronica  Medica  Mexicana  (Mexico). 

35.  Commonwealth    of    Australia,    Quarantine    Service    Publications    (Mel- 

bourne). 

36.  Folia  Microbiologica  (Delft). 

37.  Gaceta  Medica  de  Caracas  (Caracas). 

38.  Geneeskundig  Tijdschrift  voor  Nederlandsch  Indie,  Rijswijk  (Batavia). 

39.  Grece  M6iicale  (Athens). 

40.  Illinois  Biological  Monographs  (Urbana). 

41.  Index  Medicus  (Washington). 

42.  Indian  Journal  of  Medical  Research  (Calcutta). 

43.  Indian  Medical  Gazette  (Calcutta). 

44.  Interstate  Medical  Journal  (St.  Louis). 

45.  Journal  of  the  Ceylon  Branch  of  the  British  Medical  Association  (Colombo). 

46.  Journal  of  Comparative  Pathology  and  Therapeutics  (Edinburgh). 

47.  Journal  of  Hygiene  (Cambridge). 

48.  Journal  of  Pathology  and  Bacteriology  (Cambridge). 

49.  Journal  of  the  Royal  Army  Medical  Corps  (London). 

50.  Journal  of  Tropical  Medicine  and  Hygiene  (London). 

51.  Journal  of  Parasitology  (Urbana). 

52.  Kitasato  Archives  of  Experimental  Medicine  (Tokio). 

53.  Lister  Institute,  Collected  Papers  (London). 

54.  Malaria  e  Malattie  dei  Paesi  Caldi  (Rome). 

55.  Malay  Medical  Journal. 

56.  Malariologia  (Naples). 

57.  Medicina  Contemporanea  (Lisbon). 

58.  Medellelingen  van  den   Burgerlijken   Geneeskundigen  Dienst  in  Neder- 

landsch-Indie  (Batavia). 

59.  Medical  Journal  of  South  Africa  (Johannesburg). 

60.  Memorias  do  Instituto  Oswaldo  Cruz  (Rio  di  Janeiro). 

61.  Monthly  Health  Reports  of  the  Department  of  Health  of  the  Panama 

Canal  (Washington). 

62.  Pacific  Medical  Journal. 


32  THE  HISTORY  OF  TROPICAL  MEDICINE 

63.  Panama  Canal  Record  (Balbao  Heights  Canal  Zone). 

64.  Parasitology  (Cambridge). 

65.  Philippine  Journal  of  Science,  Section  B.     Philippine  Journal  of  Tropical 

Medicine  (Manila). 

66.  Proceedings  of  the  Canal  Zone  Medical  Association  (Mount  Hope,  Canal 

Zone) . 

67.  Proceedings  of  the  Society  for  Experimental  Biology  and  Medicine  (New 

York). 

68.  Records  of  the  Egyptian  Government  School  of  Medicine  (Cairo). 

69.  Review  of  Applied  Entomology,  Series  B,  Medical  and  Veterinary  (London) . 

70.  Revue  de  Medecine  et  d'Hygiene  Tropicales  (Paris). 

71.  Revista  Medica  de  Yucatan  (Yucatan). 

72.  Repertorio  de  Medicina  y  Cirugia  (Bogota). 

73.  Revista  Clinica  (Colombia). 

74.  Revista  Medica  de  San  Paulo  (San  Paulo). 

75.  Revue  Medicale  d' Alger. 

76.  Riforma  Medica  (Naples). 

77.  Sanidad  y  Benehciencia,  Bolito  de  l'Secretaria  (Havana). 

78.  Southern  Medical  Journal  (Nashville,  Tennessee). 

79.  South-Western  Medicine,  El  Paso  (Texas). 

80.  Sperimentale  (Florence). 

81.  Studies  from  the  Institute  for  Medical  Research  (Federated  Malay  States). 

82.  Transactions  of  the  Society  of  Tropical  Medicine  and  Hygiene  (London). 

83.  Texas  State  Journal  of  Medicine  (Fort  Worth). 

84.  Veeartsenijkundige  Bladen  voor  Nederlandsch-Indie  (Batavia). 

85.  Zeitschrift  fur  Chemothei apie  (Leipzig). 

86.  Zeitschrift  fur  Hygiene  und  Infektionskrankheiten  (Leipzig). 

87.  Zeitschrift  fur  Immunitatsforschung  und  Experimentell  Therapie  (Jena). 

The  following  journals  have,  from  time  to  time,  valuable  papers  on  Tropical 
Medicine  and  Parasitology: — 

1.  Arbeiten  aus  dem  Kaiserlichen  Gesundheitsamte  (Berlin). 

2.  Archives  of  International  Medicine  (Chicago). 

3.  British  Medical  Journal. 

4.  Boston  Medical  and  Surgical  Journal  (Boston). 

5 .  Bulletins  and  Reports  of  the  United  States  Departments  concerned  with : — 

(a)  Animal  Industry;  (b)  Hygienic  Laboratory;  (c)  Public  Health 
(Bulletins  and  Reports  separately);  {d)  Naval  Medical;  (e)  War 
Department  (Washington). 

6.  Canadian  Medical  Association  Journal  (Toronto). 

7.  Collected  Studies  from  the  Research  Laboratory,  Department  of  Health 

(City  of  New  York) . 

8.  Comptes  Rendus  de  la  Societe  de  Biologie  (Paris). 

9.  Deutsche  Medizinische  Wochenschrift  (Berlin). 

10.  Johns  Hopkins  Bulletin. 

11.  Journal  of  the  American  Medical  Association  (Chicago). 

12.  Journal  of  Experimental  Medicine  (New  York). 

13.  Journal  of  Infectious  Diseases  (Chicago). 

14.  Journal  of  Laboratory  and  Clinical  Medicine  (St.  Louis). 

15.  Journal  of  Immunology. 

16.  Journal  of  Medical  Research  (Boston). 

17.  Journal  of  the  Royal  Naval  Medical  Service  (London). 

18.  Lancet  (London). 

19.  Medical  Journal  of  Australia  (Sydney). 

20.  Munchener  Medizinische  Wochenschrift  (Munich). 

21.  New  Zealand  Medical  Journal  (Wellington). 

22.  Policlinico  (Rome). 

23.  Presse  Medicale  (Paris). 

24.  Proceedings,  Series  B,  and  Transactions  of  the  Royal  Society  of  London. 

25.  Quarterly  Journal  of  Microscopical  Science  (London). 

26.  South  African  Medical  Record  (Cape  Town) . 


JOURNALS  WHICH  HAVE  CEASED  PUBLICATION  33 


JOURNALS  WHICH  HAVE  CEASED  PUBLICATION. 

Since  the  appearance  of  the  second  edition  of  this  book  the  following 
j  ournals  have  either  ceased  to  be  published  as  separate  entities  or  have  stopped 
publication  altogether: — 

1.  American  Journal  oj  Tropical  Diseases  and  Preventive  Medicine.     This  is 

now  included  in  the  New  Orleans  Medical  and  Surgical  Journal. 
Three  volumes  were  issued  191 3-1 916. 

2.  Journal  of  the  London  School  of  Tropical  Medicine.     Two  volumes  were 

issued  1911-1913. 

3.  Journal  of  Tropical  Veterinary  Science,  Calcutta.     Seven  volumes  appeared 

1906-1912. 

4.  Palndism,  Simla.     There  are  five  numbers  only,  1910-1912. 

5.  Scientific  Memoirs  by  Officers  of  the  Medical  and  Sanitary  Departments  of 

the  Government  of  India.  New  Series,  Calcutta.  These  are  exceedingly 
valuable  publications,  and  numbered  some  sixty  volumes  from  1902- 
191 3.  Their  place  and  that  of  Palndism  is  taken  by  the  Indian 
Journal  of  Medical  Research. 

6.  Yellow   Fever  Bureau   Bulletin,    Liverpool.     There   are   three   interesting 

volumes  in  existence  which  appeared  from  1911  to  1915.  Its  work  is 
carried  on  by  the  Annals  of  Tropical  Medicine  and  Parasitology. 

No  Reports  of  the  Wellcome  Tropical  Research  Laboratories,  Khartoum,  have 
appeared  since  191 1.  In  the  meanwhile  much  of  the  original  work  performed 
during  the  last  five  years  has  been  published  in  medical,  chemical,  and 
entomological  journals.  Up  to  date  four  reports  and  two  reviews  of  tropical 
literature  have  appeared  between  1904  and  1911. 

SPECIAL  WORKS  ON  TROPICAL  MEDICINE, 

{In  Chronological  Sequence.)] 

De  Oviedo,  F.  (1526).  Hystoria  Natural  de  las  Indias  (Toledo).  (1547). 
Coronica  de  las  Indias  (Madrid).     (Accounts  of  Yaws  and  Jiggers.) 

Thevet,  F.  A.  (1558).  Les  Singularitiez  de  la  France  Antartique  autrement 
nominee  Amerique.     (Jiggers,  Yaws,  and  Native  Practice.) 

Da  Orta,  G.  (1563).  Coloquious  dos  Simples  e  Drogas  da  India.  (This 
book  is  the  first  European  work  published  in  India,  and  contains  descrip- 
tions of  many  Indian  plants  and  their  application  to  the  treatment  of 
Cholera,  Dysentery,  etc.)  Garcia  da  Orta  was  physician  to  Dom  Marten 
da  Sousa,  Governor  of  Goa,  with  whom  he  travelled  in  India  and  Ceylon 
in  1534.  Antwerp,  1567,  translation  by  Cluscus  into  Latin.  The 
English  translation  (191 3). 

W,  G.  (1598).  The  Cures  of  the  Diseased  in  Remote  Regions  (London). 
Heatstroke,  Typhus,  Yellow  Fever  (?),  Erysipelas  (Filariasis?), 
Espindas.  Dysentery,  and  Scurvy.     (1916)  Reprinted  at  Oxford. 

Bontius,  J.  (1642).  De  Medicina  Indorum  (Lugduni,  Batavia).  (Remarks 
on  drugs,  preservation  of  health,  treatment,  and  morbid  anatomy.) 

Ai.i'iNUS,  P.  (1645).     De  Medicina  .ZEgyptorum   (Parisiis).     (The  first  book 

contains  articles  on  the  state  of  Egyptian  medicine,  on  diseases  endemic 

and  epidemic,  including  plague;  the  second  on  blood-letting;  the  third 

•     on  scarification,  extraction  of  stone  from  the  bladder,  baths,  and  friction; 

the  fourth  on  medicines.) 

Pison,  G.  (1648).  Historia  Medica  Brasilia^  (Lugduni,  Batavia).  (This  work 
is  divided  into  two  parts,  of  which  the  first  treats  of  Brazilian  climato- 
logy; the  second,  of  Brazilian  diseases — e.g.,  catarrhs,  diseases  of  the  eyes, 
spasm,  stupor  of  the  members,  obstructions  of  the  viscera,  hydropsy, 
fluxes,  tenesmus,  colic,  dysentery,  liver  troubles,  worms,  syphilis,  ulcers, 
etc.) 

3 


34  THE  HISTORY  OF  TROPICAL  MEDICINE 

Pison  (Gulielmus)  et  Georgio  Maregravo  de  Liebstat  (1648).     Historia 

Naturalis  Brasilia?. 
Pison,  G.  (1658).     Die  India?  Utriusque  de  Natura  et  Medica  (Amsterdam). 
Clever,  A.  H.  C.  (1682).     Opuscula  Medica  ad  Mentem  Sinensium  (Franc- 

forti) . 
Sloane    (i 707-1 725).     A  Voyage  to  the  Islands  of  Madeira,  Barbadoes,  and 

Jamaica,  to  which  is  prefixed  an  Introduction  wherein  is  an  Account  of 

the  Inhabitants,  Air,  Water,  Diseases,  Trade,  etc.,  of  that  place. 
Kaempfer,    E.    (171 2).     Amcenitatum    Exoticorum.     Politico-Physico-Medi- 

corum  Lengovia.     (This  well-illustrated  book,  dealing  with  Persia,  India, 

and  Japan,  is  composed  of  five  fascicles,  of  which  the  first  is  political; 

the  second  antiquarian ;  the  third  physico-medico,  containing  descriptions 

of  the  Torpedo,  Draciinciilus  persarum,  Asafcetida,  Hydrocele,  Hyper- 

sarcosis  ulcerosa  pedum  malabarica?  genti  vernacula — i.e.,  Madura-loot, 

acupuncture,  cauterization;  the  fourth  and  iifth  are  botanical.) 
F,    D.    L.   (1726).      Traite   des   Maladies    Particuliers   aux    Pays    Orientaux 

(Paris).       (Bound   with   Luillier's    Voyages;    contains    descriptions    of 

Sea-Sickness,    Scurvy,  Colic,  Venereal    Disease,  Fever,    Guinea-Worms, 

Jiggers,  Serpent  Bite,  Smallpox,  etc.) 
Aubrey,   T.   (1729).    The  Sea-Surgeon,  or  the  Guinea  Man's  Vade-Mecum 

(London) .     (Contains  accounts  of  Fevers,  Erysipelas,  Diarrhoea,  Cholicks, 

Yaws,  Negroes  and  their  Food,  etc.,  as  seen  on  the  Coast  of  Guinea.) 
Atkins,  J.  (1734).     The  Navy  Surgeon  (London).     (Contains  an  appendix  on 

'  The  Sleepy  Distemper  in  the  Negro.') 
Atkins,  J.  (1737).    A  Voyage  to  Guinea,  Brazil,  West  Indies.   2nd  edition,  1810. 
Perry,  C.  (1743).     View  of  the  Levant,  particularly  Constantinople,  Syria, 

Egypt,  and  Greece  (in  four  parts,  containing  information  with  regard  to 

Medicine  and  Surgery  in  the  East) . 
Brocklesby,  R.  (1764).     Observations  on  Camp  Diseases,  with  an  Appendix 

on  the  Climate  and  Diseases  in  Africa  (London). 
Lixd,   James  (1768).     Essays  on  Diseases  incidental  to  Europeans  in  Hot 

Climates    (London).     (Other    editions    1771,     1777,    178S,     1808,    1811. 

Translated  into  German  1773.     Also  edition  1792.) 
Hillary  (1772).     Observations  on  the  Changes  of  Air,  etc.,  in  the  Island  of 

Barbadoes  (London).     1766. 
(j.\kk,  John  (1773).     Observations  on  the  Diseases  in  Long  Voyages  to  Hot 

Countries,  and  particularly  those  of  the  East  Indies  (London).     (Other 

editions  1792,  1809.     Translated  into  German  1778.) 
Robertson,  R.  (1779).     A  Physical  Journal  kept  during  Three  Voyages  on 

the  Coast  of  Africa  and  the  West  Indies  in  the  Years  1772-1  774  (London). 
Rollo,  J.  (1781).     Diseases  in  the  Army  on  St.  Lucia  (Barbadoes). 
Fontana,    N.   (1781).  Osservazioni  intorno  alle  malattie   che   attaccano   gli 

Europei  nei  Climi  Caldi  (Livorno).      (Translated  into  French  in  181 8.) 
Sloane  (1784).     Diseases  of  Jamaica,  Geneva,  and  Augsburg. 
D'Azille    (1785).     Observations  generates    sur    les    Maladies    des    Climats 

chauds  (Paris).     (1782)  Observations  sur  les  Maladies  des  Plaies  (Paris.) 
Campbell,  D.  (1785).     Observations  on  the  Typhus  or  Low  Contagious  Fever 

(Lancaster).     (Partly  relates   to    Yellow    Fever   in    Jamaica   and    West 

Indies.) 
MOSELEY,    B.    (1787).     Treatise   on   Tropical  Diseases    (London).     (Another 

edition  1806.     Translated  into  German  1790.) 
Hunter  (1788).     Diseases  of  the  Body  in  Jamaica. 

Balfour,  F.  (1790).     Treatise  on  Putrid  Intestinal  Fevers  (Edinburgh). 
Thomas,    R.  (1790).     Medical  Advice  to  the  Inhabitants  of  Warm  Climates 

(London). 
|\(  kson,  K.  (i  791).     The  Fevers  of  Jamaica. 
Wade,   P.   (1793).     Prevention  and  Treatment  of  the  Disorders  of  Seamen 

and  Soldiers  in  Bengal  (London). 
Hunter,  John  (1796).     Observations  on  the  Diseases  of  the  Army  in  Jamaica 

and  on   the    Besl    Way  of  preserving  the  Health  of  Europeans  in  that 

Climate  (London). 


SPECIAL   WORKS  ON  TROPICAL  MEDICINE  35 

Thomas  (1801).     Modern  Practice  of  Physic  of  all  Climates. 

Clark  (1S01).     Fevers  and  Diseases  of  the  West  East  Indies  and  America. 

Campet,   P.  (1S02).     Traite  pratique  des  Maladies  graves  qui  regnent  dans 
les   Contrecs   shinies   sous   la  Zone  torride  et  dans   le  Midi  le  l'Europe 
Paris). 

Blane,  G.  (1S03).     Observations  on  the  Diseases  of  Seamen  (London). 

WlNTERBOTTOM,  T.  (1803).  An  Account  of  the  Native  Africans  in  the  Neigh- 
bourhood of  Sierra  Leone,  to  which  is  added  an  Account  of  the  Present 
State  of  Medicine  among  them.  2  vols.  (London).  (The  second  volume 
contains  the  medical  informal 

Hunier,  \V.  (1804).  An  Essay  incident  to  Seamen  or  Lascars  in  Long 
Voyages  (Calcutta). 

M'Gregor  (1804).     Medical  Sketches  Expedition  to  Egypt  from  India. 

OiKiis.  C.  (1807).     Diseases  of  India.  (Edinburgh). 

fbHNSON,  [.  (1811).  Influence  of  Tropical  Climates  on  European  Constitu- 
tions (London).  Other  editions  1818,  1821,  1824,  1826,  and  1827,  and  a 
sixth  edition. 

; xi    (1811).     Observations   on   the   Disease   called  the   Plague   or  the 
Dysentery,  the  Ophthoty  of  Egypt  and  New  York. 

Frank    [812        Collection  d'Opuscules  de  Medecine  Pratique  (Paris). 

Johnson,  |.  (1813).  Influence  of  Tropical  Climates  on  European  Constitu- 
tions (London). 

Reece   (181  p.     Medi<  a]  Guide  for  Tropical  Climates  (London). 

SlMPSOM  (1820).  Exposition  of  Elementary  Principles  specially  concerned 
in  the  Preservation  of  Healthiness  and  Production  of  Distempers  amongst 
Mariners,  Travellers,  etc.,  in  Tropical  Climates  (London). 

Chisholm,  C.  (1822).  A  Manual  of  the  Climate  and  Diseases  of  Tropical 
Countries  (London). 

BALLINGALL,  G.  (1823).  Observations  on  Fever,  Dysentery,  and  Liver 
Complaints  in  European  Troops  in  India  (Edinburgh). 

Boyle,  J.  (1823).  Letters  on  the  Prevention  and  Cure  of  Diseases  peculiar 
to  Hot  Climates  (London). 

M'Cave,    J.   (1825).     Military  Medical  Reports  containing  Pathological  and 
Practical    Observations    illustrating   the    Diseases    of    Warm    Climates 
Itenham). 

Johnson,  J.  (1827).  An  Essay  on  Morbid  Sensibility  of  the  Stomach,  etc., 
to  which  are  added  Observations  on  the  Diseases  and  Regiments  of 
Invalids  on  their  return  from  Hot  and  Unhealthy  Climates  (London). 

Hasper,  M.  (1831).  Die  Xatur  und  Behandlung  der  Krankheiten  der 
Tropenlander  (Leipzig). 

Rovle,  J.  (1831).  Medico-Historical  Account  of  the  Western  Coast  of  Africa 
(London). 

KoSER  (1837).     Ueber  Einigen  Krankheiten  des  Orients  (Augsburg). 

Thevenot  (1840).  Traite  des  Maladies  des  Europeans  dans  les  Pays  Chauds 
(Paris). 

McW'n.i  iam  (.  O.  (1843).  The  Medical  History  of  the  Expedition  to  the 
Niger,  1841-42  (London). 

SlGAUD,  J.  F.  (1844).     Maladies  du  Bresil  (Paris). 

Fergusson,  W.  (1846).  Notes  and  Recollections  of  a  Professional  Life 
(London).  (Deals  with  Military  Hygiene,  Ophthalmia,  Plague,  Yellow 
Fever,  Typhus,  Marsh  Miasmata,  and  Cholera.) 

Reed,  McC.  (1846).     Fever,  Contagi  antine,  and  Cholera  (London). 

(Deals  with  Yellow  Fever,  Typhus,  Plague,  and  Scurvy.) 

Wilson,  J.  (1846).     Medical  Notes  on  China  (London). 

Bkyson,  A.  (1847).  Climate  and  Principal  Diseases  of  the  African  Station 
(London).  (This  is  a  book  on  the  diseases  in  the  vessels  of  the  West 
African  Squadron  from  1820  till  1845,  giving  graphic  descriptions  of  the 
ravages  of  Yellow  Fever,  and,  in  addition,  chapters  on  the  Topography 
of  the  Station,  the  Causation,  Treatment,  and  Prevention  of  Disease  in 
the  Station,  and  the  Diseasi  s  most  prevalent  among  captured  slaves.) 

Pruner  (1847).    Die  Krankheiti  n  des  Orients  (Erlangen). 


36  THE  HISTORY  OF  TROPICAL  MEDICINE 

Bryson  (1849).     Account  of  the  Origin,  Spread,  and  Decline  of  the  Epidemic 

Fever  of  Sierra  Leone. 
Heymann,  S.  L.  (1855).     Pathologische  Therapeutics  Darstellung  der  Krank- 

heiten  in  der  Tropenlandern  (Wern). 
Morehead,  Charles  (1856).     Researches  on  Disease  in  India  (London). 
Johnston,  C.  (i860.)     Health  and  Disease  in  Natal  (Natal). 
Martin,    Ronald    (1861).     Influence   of    Tropical    Climates   in    producing 

Disease. 
Moore,  W.  J.  (1861  ?).     Manual  of  the  Diseases  of  India  (London).     Second 

edition,  18S6. 
Dutroulau,  A.  F.  (1861).     Traite  des  Maladies  des  Europeens  dans  les  Pays 

Chauds  (Paris.)     Second  edition,  1868. 
Gordon  (1863).     China  from  a  Medical  Point  of  View  (London). 
Clark,  S.  (1864).     Hyg    ne  of  the  Army  in  India  (London). 
Sabatier    (1864).     Maladies  Observees    dans    les    Mers    de    Chine.     Th£se 

(Montpellier) . 
Mare,  J.  (1865).     Etude  sur  les  Maladies  endemiques  au  Senegal  et  a  la  cote 

occidentale  d'Afrique.     These  (Montpellier). 
Gauthier  (1865).     Des  Endemies  au  Senegal.     These  (Paris). 
Waring,  E.  J.  (1866).     The  Tropical  Resident  at  Home  (London). 
Godard,  E.  (1867).     Observations  Medicale  et  Scientifique  (Paris).     (Relates 

to  Egypt  and  Palestine.) 
Girard,    La    Barcerie    (1868).     Considerations   Medicales   sur   la    Cochin- 
chine.     These  (Montpellier). 
Saint  Vel  (1868).     Maladies  des  Regions  intertropicales  (Paris). 
Gordon,  C.  A.  (1872).     Experiences  of  an  Army  Surgeon  in  India. 
Horton,  J.  A.  (1 874) .     Diseases  of  Tropical  Climates  and  their  Treatment 

(London).     Second  edition,  1879. 
Schlimmer  (1874).   Terminologie  Medico-Pharmaceutique  Francaise-^ersane 

Teheran. 
Laveran,  A.  (1875).     Maladies  et  Epidemies  des  Armees  (Paris). 
Bachoue  (1876).     Etude  sur  la   Constitution  Phys.  et   Med.    de   Zanzibar 

(Paris). 
Roy,  G.  C.  (1876).     Burdwan  Fever  (London). 
Fossageries,  J.  B.  (1877).     Traite  d'Hygiene  Navale  (Paris). 
Sullivan,    John    (1877).       The    Endemic    Diseases    of    Tropical    Climates 

(London). 
Berenger-Feraud  (1878).     Traite  Clinique  des  Maladies  des  Europeens  au 

Senegal  (Paris). 
Horton,  J.  A.  B.  (1879).     Diseases  of  Tropical  Climates  (London). 
Fayrer,  Joseph  (1881).     Tropical  Diseases  (London). 
Berenger-Feraud    (1881).     Traite   Clinique   des   Maladies   des   Europeens 

aux  Antilles  (Paris). 
Nielly,  Maurice  (1881).     Elements  de  Pathologie  Exotique  (Paris). 
Fayrer,  Joseph  (1882).     Climate  and  Fevers  of  India  (London). 
Gordon,  C.  A.  (1884).     Medical  Reports — Chinese  Customs  Service  (London). 

(Almost  a  textbook  of  tropical  medicine,  with  valuable  reports  by  Manson 

on  Filariasis,  Paragonimiasis,  etc.) 
Maclean,  W.  C.  (1886).     Diseases  of  Tropical  Climates  (London). 
Burot    (1886).       De    la    Fievre    dite    bilieuse    inflammation    a    la    Guva.ne 

(Paris). 
Le  Roy  de  M£ricourt  et  Corre.     Du  Traitement  des  Maladies  Tropicales 

dans  les  climats  temperes  (Paris). 
Corre,  A.  (1887).     Traite  Clinique  des  Maladies  des  Pays  Chauds  (Paris). 
Duncan,    A.    (1888).     Prevention   of    Disease   in   Tropical   and   Subtropical 

Campaigns  (London). 
Kelsch    and    Kiener   (1889).     Traite   des  Maladies  des   Pays  Chauds.      (A 

justly  celebrated  book.) 
Davidson,  Andrew  (1893).     Hygiene  and  Diseases  of  Warm  Climates. 
1'i'i.KiM,    K.    VY.  (1895).     Geo  raphical  Distribution  of  Tropical  Diseases  in 

Africa. 


SPECIAL   WORKS  ON  TROPICAL  MEDICINE  37 

Desaint,  Constant  (1895).    Manuel  de  Medicine,  fifth  edition  (Hong-Kong). 

(A  work  on  the  diseases  of  China,  with  an  extensive  catalogue  of  drugs, 

intended  for  missionaries.) 
Scheube,  B.  (1896).     Die  Krankheiten  der  Warmen  Lander  (Jena).     Second 

edition,  1900;  translated  into  English,  1903;  third  edition,  1903;  fourth 

edition,  1910. 
Rho,  F.  (1897).     Malattie  Predominant!  nei  Paesi  Caldi  e  Temperati  (Torino). 
Manson,  Patrick  (1898).     Tropical  Diseases  (London).     (A  very  celebrated 

work).     Second  edition,  1900;  third  edition,  1903;  fourth  edition,  1907; 

translated  into  French;  fifth  edition,  1914;  sixth  edition,  1918. 
Brault,    J.    (1900).      Traite    Pratique    des   Maladies    des   Pays  Chauds   et 

Tropicaux  (Paris), 
l.i:    Dantec,    A.    (iyoo).     Precis    de    Pathologie    Exotique    (Paris).     Third 

edition,  iyn. 
Keynaud,  G.  (1903).     Hygiene  des  Etablissements  Coloniaux  (Paris). 
Audain    (1904).     Pathologie   Intertropicale   (Paris).    (1910).     Fievres  inter- 

txopicales  (Paris). 
Jeanselme  (1904).     Cours  de  Dermatologie  Exotique  (Paris). 
Muzio,  C.  (1904).     La  Malattie  dei  Paesi  Caldi  (Milano). 
Brault,    J.    (1905).        Pathologie    et    Hygiene    des    Indigenes   Musulmans 

d'Algerie  (Algiers). 
Me.nse,  C.  (1905).     Handbuch  der  Tropenkrankheiten,    3  vols.     (Translated 

into  Italian.)     Second  edition,    1913,   Leipzig,  in  5  vols.,  of  which  the 

fourth  and  fifth  are  subdivided  into  two  parts. 
Finlay  (1905).     Manuel  de  Pratique  Sanitare  La  Havane. 
Manson,  P.  (1905).     Lectures  on  Tropical  Diseases  (London). 
Allbutt  and  Rolleston  (1906).     System  of  Medicine.     Vol.  II.,  Part  II.: 

Tropical  Diseases  (London). 
Jackson,  T.  W.  (1907).     Tropical  Diseases. 
Simpson  (1908).     Principles  of  Tropical  Hygiene  (London). 
Gilbert  (1908).     Tropical  Diseases. 
Daniels,    0.   W.    (1909-1912).     Tropical    Medicine    and    Hygiene.     3    vols. 

(London).     Second  edition  1914-1916, 
Jeanselme  and  Rist  (1909).     Precis  de  Pathologie  Exotique  (Paris). 
Guillon  (1909).     Manuel  de  Therapeutique  Clinique  des  Maladies  Tropicales 

(Paris). 
Schilling,  0.  (1909).     Tropenhygiene  (Leipzig). 
Jeffry  and  Maxwell  (1910).     The  Diseases  of  China  (London). 
Grall  et  Clarac  (1910).     Traite  de  Pathologie  Exotique  (Paris).     (Several 

volumes:  not  yet  fully  published). 
Rogers  (1910).     Fevers  in  Tropics  (London). 

Salanque-Ipin,  H.  (1910).     Precis  de  Pathologie  Tropicale  (Paris). 
Ruge  und  Verth  (1912).     Tropenkrankheiten  und  Tropenhygiene  (Leipzig). 
Gabbi  (191 2).     Malattie  Tropicali  dell'  Italia  Meridionale  (Roma). 
Gabbi  (ioii).     Malattie  Pcstilenziali  Esotiche  (Roma). 
Stitt  (1915).    Diagnostics  and  Treatment  of  Tropical  Diseases.     H.  K.  Lewis 

(London). 
Anderson  (191 8).     The  Epidemics  of  Mauritius  (London). 

HISTORY  OF  TROPICAL  MEDICINE. 

The  most  excellent  book  is  Garrison  (1918),  '  History  of  Medicine.' 
2nd  edition,  Philadelphia,  and  the  important  periodicals  are  '  Annals  of 
Medical  History,'  commenced  in  191 7,  and  published  in  New  York;  and  the 
'  Archiv  fur  Geschichte  der  Medizin,'  started  in  Leipzig  in  1908,  and  Janus, 
as  well  as  the  Transactions  of  the  '  Medical  Historical  Section  '  of  the  Royal 
Society  of  Medicine. 

Neuberger  (1910),  '  History  of  Medicine,'  vol.  i.,  English  translation  by 
Playfair,  gives  good  accounts  of  Byzantine  and  Arabic  medicine;  and  Elliott 
(1914),  '  Outlines  of  Greek  and  Roman  Medicine,'  London,  is  most  interesting. 


3>S  THE  HISTORY  OF  TROPICAL  MEDICINE 

Anderson    (1908).     Third   Report.    Wellcome   Tropical   Research   Labora- 
tories,   310;    (191 1)    Fourth   Report  same   Laboratories,   248    (London). 

These  are  most  valuable  observations  upon  Primitive  Medicine  in  the 

Anglo-Egyptian  Sudan. 
Berdoe    (1913).     The   Origin   and   Growth   of  the   Healing   Art    (London). 

(Contains  articles  on  the  Medicine  of  Primitive  Man  of  Egypt,  Judea, 

Chaldea,  India,  Persia,  Mexico,  and  Peru.) 
Castellani     (1916).      British    Medical    Journal,  ii.,    October  21   (London). 

(Tartar  Emetic  and  Protozoal  Diseases.) 
Chalmers  and  Archibald  (1914).    Two  early  eighteenth-century  treatises 

on  Tropical  Medicine,  Royal  Society  of  Medicine.      (Contains  Dracontiasis, 

Dermatophiliasis,     Epidemic     Gangrenous     Rectitis,     Malarial    Fevers, 

Cholera,    Dysenteries,    Smallpox,  Climatic    Bubo(?),    Endemic    Yellow 

Fever  in  West  Africa,  Filariasis,  Diarrhoea,  Yaws.) 
Chalmers  and  Maloof   (1918).     A   Sudanese   Arabic  Medical   Manuscript, 

Royal  Society  of  Medicine.     (Gives  an  account  of  the  method  of  treat- 
ment of  disease  in  the  Anglo-Egyptian  Sudan  some  200  years  ago.) 
Charaka.     English  translation  (Calcutta). 
Chemin    (1914).     Archives    de    Medecine    et    Pharmacie    Navale,     January 

February,     etc.     (Paris).      (Remarks    upon    the    History    of    Japanese 

Medicine.) 
Dabrv  (1863).     La  Medecine  chez  les  Chinois  (Paris). 
Dorothea  Singer  (1916).    Transactions  Royal  Society  of  Medicine  (London). 

(Plague  Tracts.) 
Gimlette  (1915)-     Malay  Poisons  and  Charms  (London). 
Hensinger  (1839).     Geschicte  der  Indische  Medicin,  Sach's  Medicin. 
Jee  (1896).     A  Short  History  of  Aryan  Medical  Science  (London). 
Keegel  (1887).     Superstition  in  Native  Medicine  (Ceylon  Medical  journal). 
Lepage,  F.  A.  (181 3).     Recherches  historiques  sur  la  Medecine  des  Chinois. 

These  (Paris). 
Low  (1916).    Transactions  of  the  Society  of  Tropical  Medicine  and  Hygiene, 

vol.  x.,  pp.  37-42  (London).     (History  of  Tartar  Emetic.) 
Macdonald  (1879).     Historical  Sketch  of  Medicine  (Edinburgh).     (Contains 

a  translation  of  some  palm-leaf  manuscripts,  without  date,  by  Burmese 

physicians.) 
Morgan  (191 8).     Organic  Compounds  of  Arsenic  and  Antimony  (London). 
Oribasius  (1557).     Opera  Basilese. 

Rho,  F.  (1904).     Dal  Vecchio  al  Nuovoin  Patologia  Esotica  (Roma). 
Roth,  W.  E.  (1897).     Ethnological  Studies  among  the  North-West  Central 

Aborigines   (Brisbane).      (Contains  a  chapter  on  Disease.   Accident,   and 

Death.) 
Ross  (1910).     Catalogue  of  the  Arabic  and  Per;  ian  Manuscripts  in  the  Oriental 

Public  Library  at   Bankipore.     (Vol.  iv.   contains  the   Arabic   medical 

works,  and  is  very  interesting  and  useful  to  us.*      (Calcutta.) 
Ki'sii     (1818).     Medical     Inquiries    and    Observations.      (The    first    volume 

contains  an  account  of  medicine  amongst  the  North  American  Indians.) 
Seligmann,  C.  G.  (1902).     Journal  of  the  Anthropological  [nstitute  (London). 

(The  Medicine,  Surgery,  and  Midwifery  of  the  Sinangolo,  an  inland  tribe 

inhabiting  the  Rigo  District  of  British  New  Guinea.) 
Singer  (1912).     Annals  of  Tropical  Medicine  and  Parasitology,  vi.  87,  370 

(Liverpool).     With   D.    Singer   (191 7).     Annals  of  Medical   History,   I., 

i.  1,  New  York.      (Facastoro  and  Infection.) 
Su^ruta.     English    translation    (Calcutta),   also  a   Latin   translation   about 

1837  in  Berlin. 
WlJESINGHE  (1889).      Mahawansa,  pp.  44,  125,  156  (notes),  158. 
WISE,   T.  S.   (1867).      Review  of  the  History  of  Medicine   (London).      (Deals 

with  medicine  among  the  Hindus  and  Chinese.) 
Whitney  (1885).     History  of  Medical  Progress  in  Japan.     Transactions  of  the 

Asiatic  Society  of  Japan  (Yokohama) . 


CHAPTER  II 
TROPICAL  RACES 

The  Tropic-' — Tropical  Races — Primitive  man- — Classification — Caucasic 
division — Ethiopic  division — Mongolic  division — Amerind  division — 
References. 

THE  TROPICS. 

Supan  suggested  that  climates  should  be  classified  as  follows: — 

i.  Tropical  or  warm  climates,  extending  from  the  Equator  to  the 
mean  annual  isotherm  of  20°  C.  or  68°  F. 

2.  Temperate  climates,  extending  from  lands  possessing  a  mean 
annual  isotherm  of  20°  C.  or  68°  F.  to  those  which  have  a  tern 
perature  of  500  F.  for  the  warmest  months  of  the  year. 

3.  Cold  clima'es,  lying  polewards  of  the  isotherm  of  500  F.  for  the 
warmest  months  of  the  year. 

In  Fig.  1  we  have  depicted  the  tropical  or  warm  climates  as 
delineated  by  Supan's  lines  marked  B.B.,  indicating  the  mean 
annual  isotherm  of  200  C.  or  68°  F.  in  north  and  south  latitudes. 
Both  lines  are  very  wavy,  the  northern  being  situate  about  35 
degrees  north  latitude,  and  the  southern  at  rather  less  than  30 
degrees  south  latitude.  This  region  Supan  has  divided  into  two 
zones,  the  Tropical  Zone  and  the  Subtropical  Zone,  by  lines  indicated 
on  Fig.  1  as  A. A.,  which  represent  isotherms  of  200  C.  or  68°  F. 
for  the  coldest  months  of  the  year  in  both  northern  and  southern 
latitudes. 

These  lines  A. A.  correspond  more  or  less  to  23^  degrees  north 
and  south  latitude — i.e.,  more  or  less  to  the  Tropics  of  Cancer  and 
Capricorn. 

1.  The  Tropical  Zone. — Examining  the  map  a  little  more  in 
detail,  it  will  be  noticed  that,  starting  in  the  extreme  west  and 
travelling  eastwards,  the  isotherm  both  north  and  south  of  the 
Equator  is  nearly  the  same  as  the  latitude  23^  degrees  north  or 
south,  but  as  the  coast  of  America  is  reached  it  dips  a  little  to 
the  south  in  the  Northern  Hemisphere,  and  considerably  to  the 
north  in  the  Southern  Hemisphere.  This  variation  is  caused  by 
cold  currents  in  the  sea  running  along  the  west  coast  of  America, 
the  more  important  of  which  (marked  I.  on  the  map)  is  the  cold 
current  from  the  Antarctic. 

Tracing  the  line  farther  eastward,  it  will  be  noticed  that  it  nse> 
towards  the  north  in  the  Northern  Hemisphere,  and  falls  towards 
the  south  in  the  Southern  Hemisphere.     In  the  Northern  Hemi- 

39 


40 


TROPICAL  RACES 


THE  TROPICS  41 

sphere  this  is  due  to  the  warm  Equatorial  Current  (II.),  and  in  the 
Southern  Hemisphere  to  the  warming  effects  of  the  land  and  to  the 
warm  Brazilian  Current  (IV.). 

With  reference  to  the  different  effect  of  land  and  sea,  it  is  neces- 
sary to  remember  that  though  25  per  cent,  of  the  heat  of  the  sun's 
rays  which  fall  on  the  outer  limit  of  our  atmosphere  are  absorbed, 
still  these  rays  do  not  really  warm  the  air  to  any  appreciable  extent. 
The  real  warmth  of  the  air  is  obtained  from  the  dark  heat  radiated 
from  land  and  sea. 

Land  not  only  absorbs  the  radiant  heat  from  the  sun  more  quickly 
than  water,  but  also  more  readily  gives  off  the  dark  heat  to  the  air ; 
therefore  the  presence  of  a  large  area  of  land  upon  which  the  sun's 
rays  fall  more  or  less  vertically  at  noon  all  the  year  round  will  raise 
the  temperature  of  the  air,  and  will  tend  to  extend  the  area  of  the 
warm  climates.  Hence  the  land  may  become  extremely  hot — in- 
credibly high  temperatures  have  been  mentioned  by  authors — 
while  water  never  becomes  very  warm.  The  reason  of  this  is  that 
water,  being  a  liquid,  by  convection  and  by  currents  tends  to  keep 
at  a  more  even  temperature  than  land,  though,  as  already  noted, 
the  currents,  cold  and  warm,  have  a  marked  influence  on  the  climate. 

Turning  again  to  the  map,  and  tracing  the  isotherm  eastwards 
towards  the  west  coast  of  Africa,  it  will  be  noticed  that  again  both 
the  northern  and  the  southern  isotherms  approach  the  Equator, 
and  again  this  is  due  to  cold  currents — in  the  north  to  the  North 
Equatorial  Current  (V.),  and  in  the  south  to  the  cold  Antarctic 
Current  (I.).  Crossing  the  continent  of  Africa,  the  effect  of  land 
is  seen,  and  on  passing  into  the  Indian  Ocean  the  effect  of  the 
Mozambique  and  the  South  Equatorial  Currents  may  be  noted, 
and  finally,  to  the  west  and  east  of  Australia  the  cold  Antarctic 
Currents  produce  effects. 

Thus  the  Tropical  Zone  is  alternately  decreased  and  increased  in 
area,  the  most  marked  diminutions  being  on  the  west  coast  of 
America  and  the  west  coast  of  Africa. 

It  will  be  observed  that  this  zone  includes  Central  America,  a 
large  portion  of  South  America,  the  West  Indies,  a  large  portion  of 
Africa,  Madagascar,  a  portion  of  Arabia,  India,  Ceylon,  Indo-China, 
Sumatra,  Java,  Borneo,  the  Philippine  Islands,  New  Guinea,  and  a 
portion  of  Australia,  and  many  other  smaller  islands. 

2.  The  Subtropical  Zone. — The  Subtropical  Zone  lies  between  the 
isotherms  of  68°  F.  (200  C.)  for  the  temperature  of  the  coldest  month, 
and  the  same  isotherms  for  the  mean  temperature  of  the  year. 

It  is  depicted  in  Fig.  1,  and  will  be  noticed  to  include  a  portion  of 
North  America  and  considerable  portions  of  South  America,  Africa, 
Asia  Minor,  Arabia,  Persia,  North  India,  China,  and  Australia. 

Another  method  of  subdividing  warm  climates,  based  upon  the 
winds,  rainfall,  and  altitude,  will  be  given  in  the  next  chapter. 


4^  TROPICAL  RACES 

TROPICAL|RACES. 

It  is  now  desirable  to  inquire  very  briefly  into  the  races  of  man- 
kind inhabiting  these  tropical  or  warm  climates  as  defined  above, 
in  order  that  the  tropical  practitioner  may  understand  the  racial 
relationship  of  the  peoples  amongst  whom  he  is  working;  and  for 
this  purpose  we  give  the  following  very  condensed  account,  starting 
with  primitive  man. 

PRIMITIVE  MAN. 

From  geological,  zoological,  and  botanical  considerations  there 
can  be  little  doubt  that  in  early  tertiary  times  there  existed  an 
Indo-African  continent  where,  at  present,  the  Indian  Ocean  lies. 
This  continent,  embracing  the  Deccan,  Madagascar,  and  South 
Africa,  is  more  extensive  than  Sclater's  Lemuria,  and  is  now  known 
as  Gondwanaland. 

This  Indo-African  continent  may,  for  many  reasons,  have  been 
the  site  of  the  primitive  home  of  the  human  race,  and  indeed  it 
was  in  Java  that  Dubois  found  those  remarkable  teeth,  calvarium 
and  femur,  which  to-day  are  recognized  as  belonging  to  Pithecan- 
thropus erectus  Dubois  1891,  which,  geologically,  belongs  more 
probably  to  the  early  Pleistocene  rather  than  to  the  Tertiary 
Pliocene,  as  was  at  one  time  considered  possible.  These  remains 
belong  either  to  a  very  early  form  of  man  or  to  an  immediate  precursor. 

Once  evolved,  there  can  be  no  doubt  that  the  main  factor  in 
man's  further  evolution  has  been  the  development  of  the  brain, 
and  this  may  have  been  stimulated  by  his  remarkable  migrations, 
for,  driven  by  food  requirements,  geological  or  meteorological 
disturbances,  man  migrated  from  his  primeval  home  and  spread, 
westwards  into  Africa,  where,  in  the  then  fertile  and  well-watered 
northern  regions  of  the  Sahara,  Caucasic  man  probably  evolved. 
He  also  migrated  northwards  into  Asia,  evolving  there  the  common 
ancestor  of  Mongolic-Amerind  man,  which  eventually  formed  Mon- 
golic  man  in  Asia,  while  the  further  migration  into  America  gave 
rise  to  Amerind  man.  Migrations  from  the  south  were  easier  in  those 
days,  because  the  Himalayas  were  much  lower  than  they  are  to-day. 

In  the  meanwhile  the  non-migrating  common  ancestor  may  have 
evolved  into  Ethiopic  man,  who  was  eventually  compelled  by  the 
subsidence  of  the  land  to  migrate  westwards  into  Africa  and  east- 
wards into  Oceania. 

With  regard  to  these  early  migrations,  it  must  not  be  forgotten 
that  the  climatic  conditions  were  probably  very  different  from 
those  of  to-day,  and,  as  it  was  a  warm  interglacial  period,  were  dis- 
tinctly favourable  to  these  movements;  while  the  abundant  land 
connections  of  Africa  to  Europe,  Asia  to  America,  and  America  to 
Europe,  of  those  days  materially  facilitated  them.  Neither  must 
it  be  forgotten  that  these  migrations,  as  well  as  subsequent  migra- 
tions, were  not  single,  but  multiple,  taking  place  in  successive  waves, 
and  spread  over  a  long  space  of  time. 


PRIMITIVE  MAN  43 

When  considering  the  different  divisions  of  mankind  in  greater 
detail,  it  will  be  noted  that  they  spread  from  their  original  homes 
in  various  directions  and  at  various  times,  until  the  whole  world 
was  populated. 

The  first  dispersal  of  man  over  the  globe  must  have  resembled 
the  migrations  of  animals  in  that  it  must  have  been  performed 
unconsciously  under  the  influence  of  the  factors  just  mentioned, 
though  it  is  possible  that  the  food  factor  was  the  most  potent, 
because,  as  Seligmann  has  pointed  out,  the  hunting  man  of  to-day 
requires  a  relatively  large  area  in  which  to  obtain  his  food,  and  it 
is  equally  possible  thai  primeval  man  soon  found  that  a  given 
district  was  unable  to  feed  his  rapidly  increasing  family  or  tribe. 
Under  these  circumstances  the  family  or  tribe  in  question  would 
move  into  a  more  suitable  region.  When  man  became  more  evolved 
migrations  would  still  take  place  under  compulsion  as  described 
above,  but  might  also  have  taken  place  under  the  influences  of 
attraction  or  expulsion,  by  which  one  means  that  a  powerful  tribe 
might  be  attracted  to  an  area  held  by  a  weaker  tribe,  which  latter 
would  be  compelled  to  submit  to  the  conquerors  or  to  migrate  to 
some  other  area.  If  the  weaker  tribe  remained  with  the  stronger, 
there  would  possibly  be  a  race  fusion,  as  has  so  often  taken  place 
all  over  the  world,  and  a  new  mixed  race  would  appear,  or  the  two 
races  might  live  together  with  little  fusion.  During  these  early 
times  must  have  appeared  many  of  the  diseases,  especially  the  in- 
fectious diseases,  which  to-day  afflict  mankind,  but  what  part  the 
disease  factor  played  in  these  migrations  we  do  not  know.  What 
part  epidemic  parasitic  diseases  have  played  in  evolution  cannot 
be  stated,  but  that  they  must  have  played  some  part  in  the  ex- 
tinction of  animals  seems  possible;  and  it  appears  also  possible 
that  parasites  transferred  from  animals  to  man  at  this  period  by 
the  agency  of  blood-sucking  insects,  etc.,  may  have  formed  the 
basis  of  certain  of  the  diseases  of  man  to-day. 

These  migrations  must  have  been  delayed  or  stopped  by  meeting 
with  natural  barriers,  such  as  deserts,  dense  forests,  Or  broad 
expanses  of  water;  and  probably  at  these  places  settlements  would 
be  made,  from  which  reflux  migrations  into  parts  originally  occupied, 
or  passed  through,  might  arise,  due  again  to  the  influence  of  the 
factors  above  mentioned. 

In  this  way  tribes,  now  modified  by  selection,  environment,  etc., 
re-entered  the  districts  through  which  they  had  originally  passed, 
and,  finding  them  more  or  less  occupied  by  differently  evolved 
peoples,  brought  about  fusion  of  the  early  divisions  and  subdivisions 
of  mankind.  And  thus  at  an  early  period  arose  the  first  of  these 
race  fusions  which  are  ethnologically  so  confusing  to-day.  One 
factor  in  these  early  refluxes  must  be  mentioned,  and  this  is  the 
changed  meteorological  conditions  brought  about  at  the  Glacial 
period  or  periods,  for  during  these  man  must  have  been  driven 
towards  the  Equator,  while  in  the  intervals  he  could  wander  polewards. 
These  early  migrations  and  refluxes  must  have  acted  as  potent 


44  TROPICAL  RACES 

stimuli  to  the  already  rapidly  evolving  brain  of  man,  but  this 
evolution  does  not  appear  to  have  gone  on  equally  all  over  the  world  ; 
in  fact,  it  is  in  the  so-called  Culture  Zone,  situate  between  250  and 
500  north  latitude,  that  brain  development  began  to  be  highly 
specialized.  In  the  eastern  part  of  this  region  arose  the  Accadians, 
the  Egyptians,  and  the  early  Cretans,  from  whom  all  the  culture 
of  Europe,  Asia,  and  Africa  evolved;  and  separately  in  the  west 
the  Mexicans,  Peruvians,  Columbians,  and  inhabitants  of  Yucatan, 
whose  advance  was  ended  once  for  all  by  the  Spanish  conquests, 
leaving  only  the  culture  of  Accadian,  Egyptian,  and  Cretan  origin  to 
supply  the  world  with  knowledge. 

In  other  regions  man  has  lagged  far  behind;  indeed,  in  New 
Guinea  and  in  other  places  we  have  the  native  peoples  just  emerging 
from  a  contemporary  Stone  Age  side  by  side  with  the  newly  migrated 
and  highly  cultured  Caucasic. 

The  tropical  regions  of  to-day  have  therefore  a  most  curious  and 
most  complex  congeries  of  mankind.  First,  the  indigenous  in- 
habitants or  natives  of  the  land  in  question,  together  with  the 
descendants  of  peoples  arising  from  the  intermingling  of  the  original 
native  race  with  other  races  brought  thither  by  migrations  of  long 
ago;  secondly,  peoples  whose  native  habitat  is  a  temperate  or  cold 
climate,  and  who  are  derived  from  the  quite  recent  and  still  con- 
tinuing Caucasic  migration;  and,  thirdly,  the  half-castes,  derived 
from  the  intermingling  of  these  Caucasic  races  and  the  native  races 

From  the  above  it  will  be  comprehended  that  the  study  of  the 
ethnology  of  man  in  the  tropics  is  indeed  complex,  but  some  ele- 
mentary knowledge  of  the  origin  and  relationships  of  the  people 
among  whom  he  is  to  work  may  be  of  use  to  the  practitioner  in 
the  tropics,  and  therefore  we  give  the  following  brief  classification, 
leaving  anyone  interested  in  this  subject  an  opportunity  of  further 
study  by  means  of  the  works  mentioned  in  the  references  at  the 
end  of  the  chapter. 

Classification. — All  classifications  are  more  or  less  artificial,  and 
based  upon  the  generally  accepted  knowledge  of  the  day,  and  are 
therefore  ephemeral,  and  the  various  classifications,  suggested  by 
Bernier  in  1684,  Linnaeus  in  1735,  1740,  and  1758,  Blumenbach 
in  1775,  Virey  in  1801,  Des  Moulins  in  1825-26,  Bory  de  Saint- 
Vincent  in  1827,  Agassiz  in  1850  and  1853,  Isidore  Geoffroy  Saint- 
Hilaire  in  1858,  Pruner  Bey  in  1863,  Haeckel  in  1873,  Broca  and 
Topinard  in  1885,  Flower  in  1885,  Deniker  in  1889,  and,  finally, 
Keane  in  1895,  form  no  exception  to  this  rule. 

The  most  useful  classification  is  that  of  Keane,  in  which  the 
human  species  is  divided  into  four  divisions — viz. :- — 

The  Caucasic  Division. 

The  Ethiopic  or  Negroid  Division. 

The  Mongolic  Division. 

The  Amerind  Division. 

We  will  now  briefly  consider  these  divisions. 


CAUCASIC  DIVISION  45 


Caucasic  Division. 

This  division  of  man  is  thought  to  have  evolved  in  Northern 
Africa  at  a  time  when  the  Sahara  was  a  well-watered  and  inhabitable 
region. 

Characters. — The  characters  of  Caucasic  man  are : — Height,  average  or  above 
the  average;  colour,  florid  or  pale;  hair,  long,  wavy,  soft,  and  flaxen,  or  long, 
straight,  wiry,  and  black,  in  either  case  oval  on  transverse  section;  skull, 
dolichocephalic  or  brachycephalic ;  eyes,  moderately  large,  straight,  blue  or 
black;  nose,  straight  or  arched  leptorrhine;  cheek-bones,  small;  jaws,  orthog- 
nathous;  teeth,  small;  beards,  full.  Three  types  are  recognized  of  these 
physical  characters:  the  Nordic,  with  cephalic  index  74-99,  and  blue  or  grey 
eyes,  fair  hair,  and  height  5  feet  8  inches  to  6  feet;  the  Alpine,  with  cephalic 
index  80-90,  brown  or  black  eyes,  dark  hair,  and  height  5  feet  5  inches  to 
5  feet  6  inches;  the  Mediterranean,  with  cephalic  index  72-78,  black  eyes, 
black  hair,  and  height  5  feet  4  inches  to  5  feet  6  inches.  Speech,  inflecting — 
e.g.,  the  Hamitic,  Semitic,  and  Aryan  languages — except  in  some  instances, 
when  it  is  agglutinating — e.g.,  Basque;  temperament,  active,  enterprising,  and 
imaginative.  Medicine  varies  from  the  highly  evolved  European  medicine  to 
the  primitive  Oceanic  medicine. 

Migrations. — From  his  Saharic  home  the  primitive  Caucasic  man  wandered 
in  Palaeolithic  and  Neolithic  times  eastwards  into  the  Valley  of  the  Nile  and 
on  into  Asia,  where  he  met  Mongolic  man,  and  later  into  Southern  Asia,  and 
so  into  Oceania,  reaching,  as  we  shall  presently  see,  its  farthest  islands.  He 
also  wandered  northwards  in  successive  migrations  across  the  bridges  between 
Africa  anel  Europe,  where  he  was  succeeded  by  the  early  race  to  which  belong 
the  Cannstadt  cranium  found  in  1700,  the  Neanderthal  cranium  found  in 
1856,  the  Spy  cranium  found  in  1886,  the  skeleton  of  Homo  primigenius  found 
in  1908  in  the  Valley  of  Yezere,  and  the  various  skeletons  and  skulls  found 
in  1909.  All  these  skulls  belong  to  the  type  calleel  '  Neanderthaloid,'  after 
their  best-known  member,  and  are  considered  by  some  authorities  as  not 
belonging  to  Homo  sapiens,  but  to  a  separate  species — H.  primigenius  (H . 
neaitderthalensis) — which  is  approached  to-day  most  closely  by  the  Australian 
type.  This  earlier  type  was  followed  by  more  highly  evolved  Caucasic  types, 
as,  for  example,  the  Cro-Magnon  race  of  the  French  anthropologists  founel  at 
Les  Eyzies  in  Perigord.  It  is  almost  certain  that  these  early  peoples  diel  not 
speak  an  Aryan  language,  but  more  probably  a  language  allied  to  that  of  the 
Berbers,  and  therefore  to  the  present  Basque  language.  In  Asia  a  fusion 
took  place  of  certain  Caucasic  races  with  Mongols,  forming  the  Turkoman  and 
many  Tatar  peoples,  such  as  the  Uzbeg  Tatars. 

In  both  prehistoric  anel  historic  times  there  have  been  migrations  of  Semitic 
Caucasians  from  Asia  into  Africa,  of  which  the  most  important  were  the 
Arabic  migrations,  which  have  produced  a  great  impression  on  the  peoples 
of  Northern  and  Eastern  Africa. 

In  recent  times  migrations  of  the  highly  evolved  types  of  Caucasians  have 
taken  place  from  Europe  into  America,  Oceania,  Asia,  and  Africa,  and  to-day 
new  races  are  arising  from  the  fusion  of  native  races  with  Spaniarels  and 
Portuguese  in  Americn  vrith  Dutch  in  South  Africa,  and  with  French  in  Indo- 
China.  It  is,  however,  a  curious  sociological  trait  of  the  Anglo-Saxon  not  to 
amalgamate-  with  the  aborigines  of  the  land  into  which  he  has  migrated. 

Population. — At  the  present  time  the  Caucasic  division  is  estimated  to 
number  770,000,000  of  the  1,570,000,000  of  peoples  which  arc  supposed  to 
inhabit  the  world,  but  there  can  be  no  doubt  that  this  division  is  rapidly 
increasing  in  numbers.     These  770,000,000  are  distributeel  as  follows: 

Europe,  355,000,000;  Asia,  280,000,000;  America,  115,000,000;  Africa, 
f5,000,000;  Oceania,  5,000,000. 

Classification.- — Ethnologically,  Caucasic  man  may  be  classified 
into  the  Xanthochroi  anel  the  Melanochroi,  while-  an  early  wave 


46  TROPICAL  RACES 

passing  across  Asia  gave  rise  to  the  Indonesians,  which  type  is 
difficult  to  define,  though  Haddon  considers  that  its  least  modified 
representatives  are  to  be  found  among  the  dolichocephalids  of  the 
forests  of  Borneo. 

The  Xanthocroi,  or  fair  subdivision,  is  characterized  by  possess- 
ing light  hair  and  light-coloured  eyes.  It  contains  the  modern 
Europeans,  who  can  be  subdivided  into  the  Teutonic  branch, 
consisting  of  Germans,  Dutch,  Anglo-Saxons,  and  Norse  races,  and 
the  Slavic  branch,  consisting  of  Russians,  Poles,  Serbs,  Bulgars  (in 
part),  and  Croats.  It  is  the  Teutonic  branch  which  has  supplied 
many  of  the  peoples  of  the  recent  Caucasic  invasion  of  the  tropics. 

The  Melanochroi,  or  dark  subdivision,  has  long,  straight,  wiry 
black  hair,  black  eyes,  and  only  average  height,  while  their  char- 
acters are  fiery,  impulsive,  and  fickle.  For  the  present  purposes 
the  Melanochroi  may  be  subdivided  into  Hamites,  Semites,  Hindus, 
and  Dra vidians. 

The  Hamites  may  be  further  divided  into  a  western  division  and 
an  eastern  division.  The  Western  Hamites  are  the  Berbers,  some- 
times referred  to  as  Libyans^  who  are  spread  from  the  Canary  Isles 
in  the  west  to  the  Oasis  of  Siva  in  the  east,  and  from  the  Mediter- 
ranean in  the  north  to  the  Senegal  River  and  southern  boundaries 
of  the  Sahara  in  the  south. 

The  original  strain  of  the  Berbers  has  become  altered  by  admix- 
ture with  Arab  blood  in  the  north  and  negro  blood  in  the  south. 
In  the  north  they  have  suffered  much  from  the  irruptions  of  Phoeni- 
cians, Romans,  Greeks,  Vandals,  Arabs,  and  the  European  nations  of 
to-day. 

Two  important  sections  of  the  Berbers  must  be  recognized- — the 
Agriculturists,  as,  for  example,  the  Kabyles  of  Mauretania,  who  live 
settled  lives,  and  the  Nomads,  represented  by  the  Tuaregs  of  the 
Sahara.  Tracing  the  various  groups  of  true  and  mixed  Berbers 
from  west  to  east,  there  are  first  of  all  the  Guanches,  or  original 
inhabitants  of  the  Canary  Isles,  who  show  an  affinity  to  these 
peoples;  then  the  Trarza  and  Brakna  of  the  Coast  Sahara  just 
north  of  the  Senegal  River,  who  have  a  negro  strain.  The  Moors  of 
Morocco  must  be  considered  to  be  Berbers  with  a  strong  Arabic 
strain.  The  principal  groups  of  these  are  the  Riffians  of  the  north 
of  Morocco,  the  Bribers  of  the  Atlas,  the  Shluh  of  Western  Morocco, 
the  Sus  between  the  great  and  small  Atlas,  and  the  Tafilat  to  the 
south  of  the  Atlas;  but  the  last  two  have  a  negroid  strain,  as  have 
the  Wargla.  East  of  these  come  the  Kabyles  of  Jurjura  and  the 
Shauia  of  Aures,  who  are  interesting  because,  according  to  authors, 
some  of  them  have  chestnut  hair  and  grey  eyes.  The  Uled-Nails 
of  the  Biskra  district  arc  mixed  Berbers  and  Semites. 

South  of  the  territories  of  these  peoples  are  the  interesting  veiled 
Tuaregs,  with  their  centre  in  the  Haggar  Mountains,  and  their 
division  into  Asgers  (Asjars)  in  the  east,  Haggars  (Ahaggars)  in  the 
west,  and  Kelowis  in  the  south;  and  Awehmmiden  on  the  Central 
Niger.     The  veil,  or  Wham,  is  used  to  protect  them  from  the  wind- 


CAUCASIC  DIVISION  47 

blown  sand  of  the  desert.  In  the  south  of  Algeria  there  are  mixed 
Berbers,  Arabs,  and  negroes,  such  as  the  Beni-Mzab,  the  Wargla, 
and  other  inhabitants  of  the  oases.  The  Shaamba  are  Berbers 
between  the  south  of  Tunis  and  the  west  of  Tripoli.  In  Tripoli 
itself  there  are  Berbers  mixed  with  Semites.  South  of  these  and 
east  of  the  Tuaregs  lies  Tibesti,  the  headquarters  of  the  Tibus,  who 
are  now  Mohammedans  with  a  slight  mixture  of  Paganism.  Far 
south  there  are  the  Fulahs,  who  are  Berbers  with  a  great  admixture 
of  negro  blood,  who  are  dispersed  among  the  Sudanese  negroes. 
They  took  their  origin  on  the  Senegal,  but  later  invaded  the  Hausa 
States  and  formed  the  Empire  of  Sokoto. 

The  eastern  division  of  the  Hamites  includes  the  Egyptians,  the 
Abyssinians,  and  the  so-called  Ethiopians  or  Nubians.  The 
Egyptians  of  to-day  exist  as  the  Christian  Kopts  and  the  Moham- 
medan Fellahin.  The  Ethiopians  include  the  Bejas  or  Bisharu,  of 
the  land  between  the  Red  Sea  and  the  Nile;  the  Afar  or  Danakil, 
between  Abyssinia  and  the  Gulf  of  Aden;  the  Somals  of  Somaliland, 
who  are  much  intermingled  with  negroes,  Arabs,  Afars,  and  Abys- 
sinians; the  Gallas  or  Ilru'Orma,  in  Southern  Ethiopia  or  Gala- 
land  proper;  and  the  Masai  of  Masailand,  intermediate  between  the 
Galla  and  the  Wahuma  or  Wahima,  who  are  dispersed  among  the 
Bantu  peoples  of  the  great  lakes,  and  are  believed  by  some  to  be  the 
originators  of  the  Bantu  dialects. 

The  Semites  have  their  primeval  home  in  Arabia,  from  which 
they  wandered  in  various  directions — e.g.,  the  Himyarites  or 
Southern  Arabs  to  Abyssinia,  the  Arabs  proper  to  North  Africa 
and  to  the  east  coast  of  Africa,  producing  profound  effects.  They 
may  be  classified  into  South  Arabians,  including  Himyarites  and 
their  derivatives,  certain  tribes  of  the  Abyssinians,  and  the  Northern 
or  true  Arabs,  the  Assyrians,  Amorites,  and  Canaanites,  which 
included  the  Hebrews  and  Phoenicians,  both  of  which  have  pro- 
duced effects  upon  man  in  Africa,  where  to-day  the  Jew  is  found  in 
numbers  in  Tripoli  and  Algeria. 

The  Hindus. — The  Aryans  are  thought  by  Keane  to  have  arisen 
as  a  fusion  of  many  Caucasic  and  some  Mongolic  elements  with  an 
original  xanthochroid  basis,  and  to  have  lived  in  a  Eurasian  home, 
probably  in  the  steppes  between  the  Ural  and  Caucasian  Mountains 
and  in  the  Aral-Caspian  depression  and  the  regions  of  Turkestan; 
for,  as  he  points  out,  in  Neolithic  times  this  region  was  very  suitable 
for  human  life,  being  then  well  watered,  but  the  gradual  drying  of 
Asia  would  compel  these  primitive  Aryans  to  wander  westwards 
ini (i  Europe,  and  south-eastwards  into  the  Iranian  plateau  and 
India,  and  it  is  with  this  last  migration  that  we  are  at  present  con- 
cerned. In  this  extent  there  is  only  one  non-Aryan  survival — viz., 
tin  Brahuiof  Eastern  Baluchistan.  The  important  groups  arc  the 
Hindus,  Bengalis,  Punjabis,  Kashmiris,  Gujaratis,  and  Sinhalese. 

The  Dravidians  include  a  vast  congeries  of  tribes,  which,  if  the 
so-called  Pre-Dravidian  jungle  peoples  be  excepted,  form  every- 
where in  India  the  basis  of  the  population.     The  pure  Dravidian 


4§ 


TROPICAL  RACES 


CAUCASIC  DIVISION  49 

stock  is  represented  by  the  short,  dark,  broad-nosed,  dolichocephalic 
peoples  (recalling  the  noseless  Daezu  of  the  invading  Aryans),  but 
they  have  everywhere  been  modified  by  fusion  with  immigrant 
peoples,  giving  rise  to  the  Aryo-Dravidian,  Scytho-Dravidian,  and 
the  Mongolo-Dravidian  types.  The  Aryo-Dravidian  type  is  princi- 
pally found  in  Northern  India  and  Ceylon,  its  upper  strata  being 
exemplified  by  the  Hindustani-speaking  Brahman  of  Northern 
India  and  the  Tamil-speaking  gentleman  of  Northern  Ceylon,  while 
its  lower  strata  are  exemplified  by  the  Chamar.  The  complexion 
of  these  people  varies  from  medium  brown  to  very  dark,  and  their 
hoses  from  medium  to  broad.  The  Scytho-Dravidian  type  of 
Western  India  is  characterized  by  a  fair  complexion,  with  little  or 
no  hair  on  the  face,  with  broad  heads  and  moderately  fine  noses. 
Riseley  considers  that  this  type  is  a  fusion  between  Dravidians  and 
immigrant  Scythians,  and  Haddon  suggests  that  it  is  a  fusion  with 
the  Alpine  race  from  the  hills  of  South-West  Asia  in  prehistoric 
times.  The  Mongolo-Dravidians  are  best  represented  by  the  inhabi- 
tants of  Lower  Bengal  and  Orissa.  They  are  of  medium  stature, 
and  usually  of  dark  complexion  with  abundant  hair  on  the  face, 
with  broad  heads  and  broad  or  medium  noses. 

Indonesians. — The  greatest  divergence  of  opinion  is  found  with 
regard  to  the  inhabitants  of  Malaysia  and  Oceania.  It  would  appear 
probable  that  the  earliest  inhabitants  belonged  to  the  undiffer- 
entiated negroid  type,  of  which  the  negritoes  gave  rise  to  the 
Andamanese,  the  Semangs  of  Malaysia,  the  Aeta  of  the  Philippines, 
and  the  pygmies  of  New  Guinea,  while  the  negroes  formed  the 
Tasmanians,  the  Papuans,  and  the  majority  of  the  Melanesians. 
In  among  these  peoples  came  the  brachycephalic  Mongols,  called  by 
Haddon  the  Proto-Malays,  who  were  to  be  found  first  in  the  Penin- 
sula, and  later,  driven  south  by  the  Caucasic  migrations  to  be 
presently  described,  in  the  islands. 

Earlier  migrations  still,  perhaps  of  lowly  developed  Caucasian 
stocks,  may  have  given  rise  to  the  Pre-Dra vidian  jungle  tribes  of 
India  and  Ceylon,  and  perhaps  to  the  Kakhyers  of  Northern  Borneo 
and  the  Sakai  of  Malaysia,  and  to  one  element  in  the  Australian 
race. 

An  early  migration  fused  with  the  Proto-Malays,  forming  the 
Proto-Polynesians  of  Haddon,  who  migrated  into  the  Western 
Pacific,  and,  fusing  with  the  early  black  peoples,  gave  rise  to  the 
Melanesians;  while  others,  passing  through  or  round  Melanesia, 
went  on  to  Tonga  and  Samoa,  and  later  to  Tahiti  and  Raratonga 
of  the  Cook  Islands,  spreading  later  to  Hawaii  and  the  Marquesas, 
and  still  later  to  New  Zealand.  These  migrations  or  voyages  are 
supposed  to  have  begun  by  a  migration  to  Java  as  late  as  65  B.C.. 
and  did  not  cease  till  a.d.  1350.  In  this  way  themixed  populations 
of  many  of  the  islands  of  the  Pacific  arose. 


5° 


TROPICAL  RACES 


ETHIOPIC  DIVISION  51 

Ethiopic  Division. 

It  is  possible  that  this  division  took  its  origin  in  the  Indo-African 
continent. 

Characters. — The  characters  of  Ethiopic  man  are: — Height,  either  above  the 
average  (negro)  or  dwarfish  (negrito) ;  colour,  blackish  or  yellowish  brown ;  hair, 
short,  frizzy,  flat  in  section,  or  reddish-brown  and  woolly;  skull,  dolicho- 
cephalic (negro)  or  brachycephalic  (negrito);  eyes,  large,  round,  prominent, 
black,  with  yellowish  cornea;  nose,  flat  and  broad,  platyrrhine;  cheek-bones, 
small;  jaws,  prognathous;  teeth,  large;  beards,  absent  or  small;  speech, 
agglutinating,  with  prefix  and  postfix  types,  or  inflectional.  In  negroid 
Africa  there  are  numerous  languages  in  the  Sudan  and  West  Africa,  but  in 
the  east,  centre,  and  south  there  are  only  variants  of  the  Bantu  stock  language ; 
in  the  far  south  there  are  the  Hottentot  and  Bushmen  languages.  In  Mada- 
gascar and  Oceania  the  Malayo-Polynesian  stock  langiiage  is  prevalent.  In 
America  the  speech  of  the  negroes  has  approached  that  of  the  European 
languages.  Temperament,  indolent,  sensuous,  passionate,  and  cruel.  In 
Africa  there  is  a  lack  of  self-respect,  thus  readily  permitting  slavery.  The 
development  of  the  mind  is  believed  to  be  arrested  at  puberty  by  the  closure 
of  the  cranial  sutures,  and  there  is  also  a  belief  that  the  negro,  left  to  himself, 
without  Caucasic  migrations,  would  have  retrograded  enormously,  some 
stating  that  he  would  have  retrograded  to  the  condition  of  an  animal  (these 
statements  may  be  received  with  caution).  Religion,  fetishism,  nature  and 
ancestral  worship;  medicine,  primitive,  being  closely  associated  with  religion, 
and  therefore  with  the  fetish  priest,  and  therefore  with  magic,  charms,  invoca- 
tions, and  sacrifices;  but  there  is  a  knowledge  of  poisonous  plants,  which  are 
used  in  trials  by  ordeal,  in  hunting,  fishing,  and  war. 

Population. — Ethiopic  man  is  guessed  to  number  some  175,000,000  of 
persons,  of  whom  perhaps  155,000,000  are  in  Africa,  3,000,000  in  Madagascar, 
20,000,000  in  America,  and  2,000,000  in  Oceania. 

Migrations. — -From  his  Indo-African  home  Ethiopic  man  wandered  west- 
wards into  Africa  and  eastwards  into  Oceania. 

Africa. — One  of  the  first  of  the  westward  waves  must  have  been  that  caused 
by  Palaeolithic  man  migrating  into  Africa,  wherein  he  spread  north  and  south. 
Another  very  early  wave  was  that  of  the  pygmies,  who  gave  rise  to  the 
Bushmen  and  negritoes  or  negrillos,  and  spread  along  the  whole  east  side  of 
Africa  from  the  Mediterranean  to  the  extreme  south.  With,  or  perhaps  not 
long  after,  the  pygmy  migration  came  the  taller  negro,  who  possibly  wandered 
into  East  Africa  and  through  the  forests,  together  with  the  pygmies,  to  the 
west  coast,  and  possibly  northwards  as  far  as  the  northern  shores  of  the 
Mediterranean;  but  these  migrations  of  Ethiopic  man  in  Northern  Africa  were 
stopped  by  the  evolution  of  Caucasic  man,  who  not  merely  drove  the  negro 
southwards,  but  made  some  remarkable  race  fusions  with  him.  Thus,  for 
example,  the  Hottentots  are  believed  by  some  to  be  of  Hamitic-Bushmen 
origin,  although  others  consider  it  safer  to  place  them  as  intermediates  between 
the  Bantu  peoples  and  the  Bushmen.  These  Hottentots  were  stronger  than 
the  Bushmen  peoples,  but  not  so  strong  as  the  Bantu  peoples,  by  whom  they 
were  eventually  driven  into  Southern  Africa. 

Another  remarkable  race  fusion  is  that  which  produced  the  Fulani,  who 
are  believed  to  have  been  originally  Berbers  (Caucasics),  but  who  have  inter- 
mingled with  the  negro  races  among  whom  they  have  migrated.  Thus  their 
residence  on  the  Senegal  River  is  traced  by  the  Wolofs  of  the  Senegambia, 
who  are  a  negroid  Fulani  race;  and  along  the  Niger  by  the  Mandingoes,  who 
possibly  have  also  Tuareg  and  Arab  infusions.  These  Mandingoes,  driven  by 
Fulani  migrations,  have  to-day  approached  the  coast  south  of  the  Senegal 
River,  displacing  the  Krus  and  Kpwesi,  who  now  live  in  Liberia.  Migrat- 
ing farther  inland,  these  Fulanis  compelled  the  Ashantis  and  Fantis  to  travel 
coastwards,  and  then  settling  in  the  Hausa  States,  and  forming  the  Sokoto 
Empire,  they  compelled  the  Hausas  to  move  southwards  and  to  force  the 
Yorubas  to  approach  the  coast,  who  in  their  turn  drove  the  weaker  indigenous 


TROPICAL  RACES 


Fig.  4. —  The  Races  of  Africa. 
(From  Hutchinson's  '  Living  Races  of  Man.') 


ETHIOPIC  DIVISION  53 

tribes  into  the  unhealthy  delta  of  the  Niger.     The  Fulani  can  also  be  traced 
by  their  language  right  across  Africa  to  Dar-Fur. 

All  these  negroes,  pure  and  mixed,  living  in  that  region  of  Africa  which  is 
called  the  Sudan,  from  the  Arabic  Bel ed-es- Sudan  (Land  of  the  Blacks), 
speak  languages  of  various  stocks;  but  very  different  is  the  language  of  the 
Bantu-speaking  peoples  of  the  portion  of  Africa  south  of  a  line  approximately 
drawn  eastwards  from  the  Rio  del  Rey  River,  near  the  northern  boundary  of 
the  Kamerun,  which  separates  the  Bantu  peoples  from  the  Sudan  peoples. 

It  is  quite  impossible  here  to  mention  the  many  changes  which  have  been 
brought  about  in  the  position  of  the  various  Bantu  tribes  by  the  slave-trade, 
migrations  of  local  tribes,  as  well  as  those  of  Caucasians;  but  these  influences 
have  produced  many  changes  even  during  the  nineteenth  century,  of  which 
some  are  known,  particularly  in  South  Africa. 

The  slave  raids  began  with  the  expeditions  of  the  ancient  Egyptians,  and 
continued  until  quite  recently,  when  the  last  Arabic  raiders  were  checked  by 
the  Caucasic  migration. 

Locally,  movements  of  Congo  tribes  southwards,  and  southern  tribes  north- 
wards and  interior  tribes  coastwards,  have  caused  much  confusion;  but 
perhaps,  ol  all  the  movements,  those  of  the  Ama-Zulu  and  their  descendants, 
tin'  Zulu,  especially  under  Chaka,  together  with  those  of  the  Barotse  and  the 
Mantati,  and  the  Ova-Herero,  are  the  most  remarkable  or  best  known. 
Curious  causes  have  called  forth  these  migrations.  First  of  all,  the  physical 
features  of  Africa  have  had  a  great  effect  upon  the  occupations,  and  hence 
upon  the  migrations  of  its  people;  secondly,  the  urgent  need  for  salt  in 
vegetal-feeding  peoples,  driving  them  coastwards;  and,  lastly,  the  endemic 
and  epidemic  disease  factor,  which  is  demonstrated  by  the  weaker  tribes 
being  driven  into  the  most  unhealthy  regions.  The  Caucasic  migrations  of 
the  Dutch  and  English  in  South  Africa  have  also  had  great  effect  in  driving 
the  native  tribes  northwards  and  in  exterminating  them. 

Oceania. — The  eastward  or  Oceanic  migration  of  Ethiopic  man  is  extremely 
difficult  to  follow,  and  may  have  taken  place  largely  on  foot  over  land  bridges, 
which  at  that  time  existed,  and  later  in  canoes  by  water. 

The  negritoes,  or  pygmies,  are  represented  to-day  by  the  Andamanese,  the 
Semangs  of  Malaysia"  the  Acta  of  the  Philippines,  and  the  pygmies  of  New 
Guinea;  while  the  Oceanic  negroes  gave  rise  to  the  extinct  Tasmanians  and 
the  Papuans  proper,  the  latter  forming  the  ground  stock  of  Melanesia. 

Classification, — Ethnologically,  the  Ethiopic  millions  are  classified 
into  two  principal  sections — the  Western  or  African,  and  the 
Eastern  or  Oceanic,  section. 

The  stature  of  the  Ethiopics  of  the  Oceanic  section  is  less  than 
that  of  the  Africans,  the  hair  is  more  wiry,  the  nose  is  large  and 
straight,  the  lips  are  not  so  thick,  and  are  not  everted  as  they  are 
in  the  Africans.  The  Oceanics  are  more  savage,  but  they  show- 
artistic  taste  and  execute  wood-carving. 

The  Western  or  African  Section  contains  negritoes  and  negroes. 
The  negrito  is  dwarfish,  with  yellowish-brown  colour,  reddish-brown 
woolly  hair,  and  brachycephalic  skull;  while  the  negro  is  tall,  of 
blackish  colour,  with  jet-black  frizzy  hair  and  dolichocephalic  skull. 

The  African  negro  may  be  subdivided  into  negroes  living  north 
of  the  Equator  and  not  speaking  the  Bantu  dialects,  which  include 
the  West  and  Central  Sudanese,  the  Welle  River  groups,  the  Nilotic 
groups,  and  the  Nubas  of  Kordofan,  and  into  groups  living  south  of 
the  Equator  and  speaking  the  Bantu  dialects;  while  in  the  extreme 
south  are  found  the  Hottentots  and  Bushmen. 

The  Eastern  or  Oceanic  Section  contains  also  negritoes  and  negroes, 
distinguished  as  above  mentioned. 


5^  TROPICAL  RACES 

Mongolic  Division. 

Mongolic  man  probably  evolved  in  the  Tibetan  Plateau  of  long 
ago. 

Characters. — The  characters  of  Mongolic  man  are:  Height,  rather  under  the 
average;  hair,  black,  lank,  coarse,  round  on  transverse  section;  skull,  brachy- 
cephalic;  eyes,  small,  black,  oblique,  with  outer  canthus  slightly  higher  than 
the  inner,  and  with  a  vertical  fold  of  skin  over  the  inner  canthus;  nose,  very 
small,  mesorrhine;  cheek-bones,  prominent  laterally;  yaws,  mesognathous ;  teeth, 
medium ;  beard,  slight  or  absent,  but  moustache  present ;  speech,  agglutinating, 
with  postfixes,  the  families  being  Ural-Altaic,  Tibeto-Indo-Chinese,  and 
Malayo-Polynesian ;  temperament,  reserved,  sullen,  and  apathetic  in  the 
Mongols,  industrious  in  the  Chinese,  and  indolent  in  the  Malays;  they  are  all 
gamblers;  religion,  animism,  Shamanism,  Lamaism,  Buddhism,  Moham- 
medanism, Confucianism,  Taoism,  etc.;  medicine,  mostly  theurgic,  associated 
with  invocations,  but  in  China  there  has  been  an  attempt  to  evolve  a  higher 
state  of  efficiency.  The  Hungarians  have  the  usual  highly  evolved  modern 
medicine. 

Population. — -The  total  number  of  Mongols  is  estimated  to  be  540,000,000 
persons,  of  whom  380,000,000  are  believed  to  reside  in  China,  55,000,000  in 
Japan  and  Korea,  35,000,000  in  Indo-China,  30,000,000  in  Malaysia, 
10,000,000  in  Mongolia  and  Manchuria,  6,000,000  in  Tibet,  7,000,000  in 
Turkestan  and  Siberia,  13,000,000  in  West  Asia,  and  4,000,000  elsewhere, 
but  estimates  vary  very  much. 

Migrations. — The  common  stock  of  Mongol-Amerind  man,  migrating  from 
the  primeval  home  in  the  Indo-African  continent,  passed  into  Asia,  and  while 
the  Amerind  division  travelled  through  that  continent  into  America,  it  is 
probable  that  the  Mongolic  division  made  its  home  in  Tibet.  This  would  be 
in  later  Pliocene  times,  when  the  Tibetan  Plateau  would  not  be  the  elevated 
region  which  it  is  to-day. 

In  Tibet  to-day  the  original  type  is  best  preserved  among  the  Drupa,  who 
are  about  5  feet  4  inches  in  height,  with  light  brown  skin,  somewhat  resembling 
that  of  the  Armerindians,  with  brachycephalic  skulls,  long  black  hair,  brown 
eyes,  slightly  prominent  cheek-bones,  depressed  nose,  wide  nostrils,  and  large 
ears.  They  are  semi-nomadic  pastoral  peoples,  living  at  a  height  of  about 
14,000  feet  above  the  sea-level.  The  other  groups  in  Tibet  are  the  Bodpa, 
the  dominant  peoples,  who  are  of  mixed  descent,  and  the  Tanguts,  predatory 
peoples  along  the  north-east  boundary. 

From  this  Tibetan  home  Mongolic  man  wandered  westwards,  giving  rise  to 
the  celebrated  Akkads  and  Sumerians  of  Babylonia,  and  much  earlier  entered 
Europe,  giving  rise  to  the  many  Asiatic  invasions  of  that  continent.  With 
regard  to  the  Akkads  and  Sumerians,  it  may  be  stated  that  they  early  evolved 
a  form  of  culture  which  grew  and  nourished  after  their  fusion  with  their  early 
Semitic  conquerors,  thus  laying  the  foundations  of  one  of  the  most  ancient 
forms  of  human  civilization.  According  to  some  authorities  (though  by  no 
means  proved),  the  Chinese  took  their  origin  from  early  Akkadian  emigrants. 

Another  migration  from  Tibet  was  southwards  along  the  valleys  of  the 
Irawadi,  Salwin,  and  Mekhong  Rivers  into  Indo-China,  giving  rise  to  the 
Mishmi,  the  Abors  (with  whom  there  has  been  trouble  recently),  the  Kuki, 
the  Luohai,  the  Chins,  the  Nagas,  the  Karens,  the  Khas,  and  the  Moi,  who, 
though  perhaps  not  the  makers  of  the  stone  implements  recently  discovered 
in  the  Irawadi  Basin,  may  be  looked  upon  as  the  aborigines  of  these  regions, 
because  there  is  at  present  no  evidence  as  to  who  these  earlier  peoples  were. 
The  above-mentioned  tribes  have  remained  in  a  primitive  condition,  but 
others  have  developed,  under  Hindu  influences,  a  high  degree  of  civilization — 
as,  for  example,  the  Burmese.  An  immigration  from  the  north  brought  the 
Malayans  and  the  Tai  race,  which,  coming  from  Central  China  about  the 
Yang-tse-Kiang,  gave  rise  to  the  Shans,  the  Laos,  and  the  Siamese;  while 
yet  another  migration,  this  time  from  the  valley  of  the  Si-Kiang  and  South- 
Eastern  China,  gave  rise  to  the  Annamese,  Tongkinese,  and  Cochin  Chinese. 


MONGOLIC  DIVISION  55 

In  Oceania,  taken  in  its  widest  sense  to  include  all  the  islands  of  the  Indian 
Ocean,  as  well  as  what  is  generally  known  as  Oceania,  the  Mongol  peoples 
are  often  known  under  the  term  '  Malays,'  which  is,  properly,  only  applied 
to  the  Mohammedan  tribes  of  Malay  Peninsula,  who  are  the  Malays  proper. 
These  Malayans  are  found  in  Sumatra,  Java,  Borneo,  Celebes,  Bali,  Lombok, 
Billeton,  Bangka,  the  Spice  Islands,  and  the  Philippines,  but  are  much 
mingled  with  other  races — e.g.,  with  the  negroes  of  Bantu  origin  in  Mada- 
gascar, and  the  Caucasic  Indonesians  in  Malaysia  generally. 

Keane  says  that  the  term  '  Malay  '  was  originally  applied  to  the  Orang- 
Malayu,  a  small  tribe  of  the  Menangkabau  district  of  Sumatra,  who  rose  into 
prominence  about  a  thousand  years  ago  and  spread  over  the  archipelago, 
and  whose  language  is  the  chief  medium  of  intercourse  throughout  Malaysia. 

Reverting  to  the  primeval  home  of  the  Mongols,  there  are  still  further  off- 
shoots to  mention — viz.,  the  Hyperboreans  of  Northern  Siberia  and  the 
Mongol-Turki.  These  latter,  who  are  often  called  Mongol-Tatars,  from  two 
words — '  Mongol,'  meaning  '  brave,'  and  '  Tatar,'  the  plural  of  '  Tata,' 
'an  archer'  (while  'Turk'  is  an  Aryan  word  meaning  'swift'),  which, 
again,  is  often  spelt  '  Tartar  ' — spread  in  two  directions — eastwards  and 
westwards.  The  eastward-migrating  Mongol-Turki  gave  rise  to  the  Mongols 
proper,  who  include  the  Kalmuks,  Sharras,  Buryats,  Tunguses,  and  Manchus, 
and  the  Mongoloid  Koreans  and  Japanese.  The  Tunguses  of  the  Amur  Basin 
and  East  Siberia  are  interesting  because  the  great  bulk  of  them  are  Shamanists, 
their  Shamans  being  medicine  men,  often  called  '  priests,'  who  heal  by  magic, 
uttering  oracles  by  which  they  establish  communication  with  the  invisible 
world,  and  thus  are  able  to  coerce  good  spirits  and  evil  spirits  to  work  for  the 
good  of  the  patient,  and  even  to  expel  devils.  The  Manchus  are  the  cele- 
brated imperial  caste  of  the  Chinese  Empire.  The  Koreans,  so  called  after 
the  powerful  Koryo  dynasty  of  a.d.  918-1392,  are  of  mixed  Caucasic  and 
Mongolic  origin,  and  are  the  precursors  of  the  Japanese,  who  are  of  mixed 
Caucasic  origin  from  the  A'inus,  Mongolic  origin  from  the  Manchus  and 
Koreans,  and  Malayan  from  the  Malays  coming  through  the  Philippine  Islands 
and  Formosa. 

The  westward-migrating  Mongol-Turki  need  not  detain  us,  except  to  state 
that  they  gave  rise  to  the  Turki  proper,  the  Samoyedes,  the  Lapps,  the 
Magyars  and  Finns,  and  the  Bulgars,  probably  only  in  part. 

Classification. — The  Mongolic  division  (vide  Figs.  2  and  3)  may 
be  classified  into : —    ■ 

1.  Mongols,  who  include  the  Mongols  proper,  the  Tunguses,  the 
Manchus,  the  Koreans,  and  Japanese. 

2.  Turki  Peoples,  who  are  the  Yakuts,  Kirghizes,  Turkomans, 
Anatolian  Turks,  and  Osmanli  Turks. 

3.  Ugro-Finns,  comprising  the  Finns,  Lapps,  Samoyedes,  Mord- 
vins,  and  Magyars. 

4.  Tibeto-Chinese,  with  the  Tibetans,  Burmese,  Nagas,  Shans, 
Siamese,  Annamese,  and  Chinese. 

5.  Malayans,  who  are  classed  into  the  Malays  proper,  the  Javan- 
ese, including  the  Sundanese,  Madurese,  and  Javanese  proper; 
the  Achinese,  Rejangs,  and  Passumahs  of  Sumatra;  the  Bugis, 
Mangkassaras,  and  Minahasans  of  Celebes;  the  Tagalas,  Bisayas, 
etc.,  of  the  Philippines,  the  Dyaks  of  Borneo,  the  Formosans,  and 
the  Hovas  of  Madagascar. 

Amerind  Division. 
The  Amerind  or  American-Indian  division   of  mankind  has  a 
twofold  origin — irom  Europe  and  from  Asia.     From  Europe  dolicho- 


56  TROPICAL  RACES 

cephalic  Caucasic  peoples  made  their  way  in  Pleistocene  times  along 
land  bridges  connecting  Britain  with  the  Orkneys,  the  Shetlands, 
the  Faroe  Islands,  Iceland,  Greenland,  and  Labrador.  These 
peoples,  making  their  way  across  the  continent,  met  with  later  and 
more  numerous  arrivals,  the  brachycephalic  peoples  of  Mongol- 
Amerind  stock,  arriving  from  Asia  by  the  land  connections  about 
the  Behring  Straits  and  the  Aleutian  Islands.  These  two  races 
fused  and  formed  the  Amerind  division  of  man.  These  Palaeo- 
lithic races  were  apparently  uninterrupted  by  any  Caucasic, 
Mongolic,  or  Ethiopic  migrations  until  the  discovery  of  America  by 
Columbus,  after  which  all  three  divisions  made  their  migrations 
thereunto.  Therefore  all  the  culture  of  the  Mayas,  Aztecs,  and 
Incas,  etc.,  was  an  inbred  culture,  not  dependable  for  its  origin  on 
outside  sources.  Hence  the  absence  of  the  ordinary  animals  and 
plants  of  Asia,  Africa,  and  Europe,  and  the  presence  of  peculiar 
animals  and  plants.  Hence,  also,  the  presence  of  only  stone  and 
copper  ages  until  the  introduction  of  iron  by  the  Caucasians,  and 
also  the  possible  source  of  certain  peculiar  diseases,  such  as  yellow 
fever,  and  perhaps  Frambcesia  tropica,  and,  according  to  some 
authors,  syphilis,  which,  when  introduced  into  Europe,  Asia,  and 
Africa,  produced  such  ravages. 

Characters. — The  characters  of  Amerind  man  are:- — Height,  above  the 
average;  colour,  coppery  or  yellowish;  hair,  long,  coarse,  and  black,  on 
section  round;  skull,  mesaticephalic ;  eyes,  small,  round,  black,  sunken,  and 
straight;  nose,  large,  bridged,  or  aquiline  mesorrhine;  cheek-bones,  moderately 
prominent;  jaws,  mesognathous;  teeth,  medium;  beard,  absent;  speech, 
divided  into  a  very  large  number  of  linguistic  families,  said  to  number  more 
than  those  of  the  rest  of  the  world,  but  peculiar  to  America  by  being  poly- 
synthetic  or  holophrastic — i.e.,  sentences  made  from  single  long  words.  The 
most  important  of  these  linguistic  families  from  a  tropical  point  of  view  are 
the  Ut-Aztecan,  the  Mayan,  Carib,  Arawak,  Quichuan,  and  Guaranian.  The 
Ut-Aztecan  speech  is  used  by  the  Shoshoneans,  or  Snakes,  who  include  the 
Utahs  and  the  Nahuas,  who  also  include  the  Aztecs,  while  the  Quichuan  com- 
prises the  Incas.  Religion,  Shamanism  in  the  north,  Nature-worship,  and 
polytheism;  medicine,  very  primitive,  especially  when  associated  with 
Shamanism,  but  was  somewhat  more  advanced  among  the  Aztecs  and  Incas. 
Cinchona  bark  was  a  native  Ecuador  remedy. 

Population. — There  are  believed  to  be  some  10,000,000  Amerinds  and 
1-5,000,000  to  40,000,000  half-breeds,  but  the  numbers  are  by  no  means  easy 
to  estimate  even  approximately.  It  is  clear,  however,  that  the  Amerinds  are 
rapidly  dying  out  in  Canada  and  the  United  States. 

Migrations. — The  brachycephalic  peoples  whom  we  have  already  noticed 
proved  superior  to  the  dolichocephalic  people  from  Europe,  and  drove  them 
northwards,  where  they  became  Eskimo,  and  southwards,  when  they  became 
the  Tehuelche  or  Patagonians  and  the  Fuegians.  The  brachycephalic  peoples 
then  evolved  the  North  American  Indians,  of  whom  we  arc  only  concerned 
with  the  members  of  the  Ut-Aztecan  Linguistic  family,  because  the  Aztecs 
are  members  of  this  family  in  common  with  the  Shoshoneans,  and  it  is  prob- 
able thai  tin-  Nahuan  family  to  which  the  Aztecs  belong  migrated  south- 
1       from  the  district  of  British  Columbia. 

Coming  to  Mexico  proper,  it  is  found  that  the  archaic  peoples — the  Popol- 
cans,  Mixe,  Chinantecs,  Zoque,  Mazatec,  Cuicatecs,  Chocho,  and  Magahua — 
all  been  pressed  by  the  migrations  presently  to  be  mentioned  into 
secluded  valleys,  where  alone  traces  of  them  can  be  found  at  the  present  time. 
The  Mexicans  proper  are  the  Otomi,  who  arc  related  to  the  Magahua,  and  are 
still  to  be  found  in  the  valley  of  the  Upper  Moctezuma  and  in  Guanjuato. 


AMERIND  DIVISION  57 

A  northern  immigration  may  have  brought  the  Tarascos  of  Michoacan  into 
Mexico,  or  they  may  belong  to  the  primitive  Mexicans.  In  either  case,  they 
are  to  be  found  to-day  in  Guanjuato;  with  these  may  be  joined  the  Ulmecs, 
Xicalancas,  Mestecs,  and  Zapotecs  among  the  early  tribes  of  Mexico.  Of  all 
these,  the  most  important  would  appear  to  be  the  Misteca-Zapoteca  family, 
because  they  are  known  to  have  evolved  a  degree  of  civilization  before  the 
days  of  the  Mayas.  This  culture  is  exemplified  by  the  monuments  of  Mitla 
and  of  Monte  Alban  in  Oajaca. 

The  Maya  people  are  variously  believed  to  have  been  immigrants  into 
Yucatan,  from  which  they  spread  into  Guatemala,  Salvador,  and  Honduras, 
or  to  have  been  original  settlers  therein.  Be  that  as  it  may,  there  is  no  doubt 
that  they  extended  into  Mexico,  both  along  the  coast,  where  one  of  their 
fcribes,  the  1  luantecs,  were  found  about  Tampico,  and  into  the  plateau.  They 
very  early  produced  some  degree  of  civilization,  and  constructed  the  cele- 
brated  monuments  of  Guatemala  and  the  pyramid  of  Cholula  in  Mexico,  on 
the  top  of  which  was  the  temple  of  Quetzatcoatl.  They  invented  picture- 
writing  and  an  almanac.  They  were  divided  into  the  Mayas  proper  of 
Yucatan,  the  Choulats  of  Mexico,  the  Quiches,  the  Pocomans  of  Guatemala, 
the  Chortes,  and  the  Huantecs  of  Tampico. 

Such  must  have  been  the  constitution  of  the  tribes  of  Mexico  when  the 
Nahuans  broke  their  way  in.  This  tribe  is  allied  to  the  Shoshonies,  who 
occupy  the  wide  tract  from  Oregon  to  California  and  New  Mexico,  and  are 
believed  to  have  come  from  the  region  of  British  Columbia.  They  moved 
down  to  the  west  of  the  Rocky  Mountains,  and  spread  as  far  south  as  Oajaca 
and  eastwards  to  the  Atlantic  between  Yera  Cruz  and  Coatzacoalcos.  The 
first  waves  may  have  been  the  Toltecs,  but  there  is  great  doubt  as  to  who 
these  people  were.  The  Alculhuaques  and  the  Tecpanecs  followed,  while  the 
last  immigration  was  that  of  the  powerful  Aztecs,  who,  though  probably  but 
little  civilized  when  they  entered  Mexico,  soon  became  so,  and  remained  the 
masters  of  that  part  of  America  until  subdued  by  the  Caucasic  migration. 

Enumerating,  therefore,  the  tribes  from  the  north  to  the  south,  there  would 
be  first  the  Shoshonies  in  the  west  and  south-west  of  the  United  States, 
extending  into  Mexico;  the  Yumas  of  Arizona  and  the  Pueblo-Indians,  char- 
acterized by  their  curious  rock  structures;  then  would  come  the  Otomi, 
Totonacs,  and  Zapotecu,  with  their  Nahuan  conquerors,  especially  the  Azteca, 
all  in  Mexico.  In  Central  America  the  Maya  people  would  be  found  in 
Yucatan,  Guatemala,  and  Honduras,  along  with  the  Xicaks  of  Northern 
Honduras,  the  Leukas  and  Guatusos  of  Central  Honduras.  Farther  south 
would  be  the  Choulats  of  Nicaragua,  the  Soumoo,  the  Micos  of  the  Mosquito 
Reservation,  the  Moscos  of  the  Blewfields  Lagoon,  and  the  Rinos  of  an  island 
therein. 

Passing  into  South  America,  there  is  the  great  linguistic  family  of  the 
Chibcha  of  Colombia,  whose  empire  extended  southwards  until  it  met  that 
of  the  Incas.  These  peoples,  as  well  as  the  Incas,  are  Andeans — that  is  to 
sav,  arc  peoples  belonging  to  the  highlands  of  the  Ancles.  It  is  curious  that 
all  the  South  Amerind  civilizations  should  have  developed  in  these  highlands, 
but  it  is  probable  that  the  lakes  and  rapid  streams  were  suitable  lor  the 
extension  of  agriculture,  and  thus  led  to  the  settlement  of  peoples,  for  with- 
out a  permanent  abode  any  great  degree  of  civilization  is  impossible.  The 
Chibchas,  also  called  '  Muyscans,'  influenced  the  whole  Panama  region  as 
far  north  as  the  northern  boundary  of  Costa  Ri<  .1 , 

South  of  the  Chibchas  comes  the  ancient  empire  of  the  Incas,  extending 
from  Quito  as  far  south  as  the  Rio  Maule  in  Chili.  It  would  appear  from  the 
megalithic  remains  and  the  ruins  of  Tiahuanacu  that  there  was  an  early 
civilization  in  this  region,  especially  about  Lake  Titicaca.  Who  these  people 
were  we  do  not  know,  bu1  they  must  have  been  conquered  by  the  Quichuas 
or  Avmaras,  who  are  allied  to  them,  as  both  speak  derivatives  of  the  Quii  huan 
language. 

At  the  same  time  there  existed  near  Truxillo  the  Chimu  people,  speaking 
Mochica,  a  language  quite  different  from  Quichuan.  They  reached  to  a 
degree  of  civilization,  but  both  they  and  the  Quichuans  were  conquered  by 


TROPICAL  RACES 


District   v/Jierc     Tupi  prevail 

.1  .,  Qes  ,, 


Fig.  5. —  The  Races  of  South  America. 
(From  Hutchinson's  '  Living  Races  of  Man.') 


AMERIND  DIVISION  59 

the  Incas.  To-day  the  descendants  of  the  Chimu  are  called  the  '  Yum  as,' 
and  live  along  the  coast  from  5  degrees  to  10  degrees  south  latitude.  In  the 
provinces  of  Catamarca,  Tucuman,  and  Salta  of  the  Argentine  lived  a  civilized 
race,  now  extinct,  called  the  '  Calchaqui,'  who  were  also  subdued  by  the  Incas. 

The  Incas  are  possibly  the  descendants  of  the  unknown  peoples  of  the  early 
civilizations  who,  defeated  by  the  Quichuan  peoples,  fled  into  the  Apurimae 
region,  whence  they  subsequently  issued  forth  to  subdue  their  ancient  con- 
querors. Their  rule  was  very  despotic,  and  their  subject  peoples  were  very 
carefully  divided  into  tens,  fifties,  five  hundreds,  and  ten  thousands,  the 
last  being  under  a  chief  talcing  orders  direct  from  the  Inca.  Their  system 
was  very  artificial,  and  absolutely  without  any  freedom  for  the  individual, 
and  hence  the  easy  Spanish  conquest.  They  possessed  no  written  language, 
everything  being  preserved  by  oral  information  handed  down  from  genera- 
tion to  generation. 

Except  in  the  Andes,  there  are  no  civilizations  in  South  America,  and  the 
peoples  whom  we  now  come  to  consider  were  all  backward  in  their  culture 
evolution  at  the  time  of  the  advent  of  the  Spaniards.  They  are  the  members 
of  the  linguistic  families  called  *  Arawak,'  '  Tapuya,'  '  Tupi,'  and  'Carib,' 
in  the  regions  lying  east  of  the  Cordilleras  as  far  south  as  the  Rio  de  la  Plata, 
while  farther  south  lived  the  Pampeans  and  Fuegians,  with  whom  we  are  not 
concerned. 

The  Arawak  would  appear  to  be  the  original  inhabitants  of  the  low-Wing 
lands  to  the  east  of  the  Cordilleras,  and  it  is  possible  that  they  originally 
spread  -to  the  north-east,  the  east,  and  the  south-east  from  a  primeval  home 
on  the  eastern  slopes  of  the  Bolivian  Cordilleras;  but  their  most  important 
migration  appears  to  have  been  that  to  the  north-east,  where  they  populated 
the,  until  then,  vacant  valleys  of  the  Orinoco  and  Amazon,  especially  along 
the  north  bank  and  up  the  Xingu  River.  In  the  east  of  Brazil,  from  the 
Xingu  River  to  the  coast,  lived  the  Tapuya,  who  were  probably  the  aborigines 
of  these  regions.  They  include  the  Ges  and  Botocudos  of  to-day,  of  which 
the  latter  are  degraded  savages. 

The  Caribs,  according  to  Van  der  Stein,  took  their  origin  about  the  sources 
of  the  Xingu  and  Paranatiga  Rivers,  where  the  Caribbean  tribes  called 
'  Bakairi  '  and  '  Nahuqua  '  live.  From  this  source  they  travelled,  probably 
by  water,  along  the  Amazon,  meeting  with  the  Arawak,  till  they  reached  its 
mouth,  when  they  turned  northwards,  probably  because  they  met  the  Tupi 
people  coming  from  the  south,  and  spread  through  Guiana  to  Venezuela, 
where  their  progress  was  checked  by  the  civilized  Chibchas,  though  some  of 
them  entered  the  valley  of  the  Magdalena  River.  From  the  north  of  South 
America  they  proceeded  to  the  Antilles,  into  which  they  were  still  migrating 
when  stopped  by  the  arrival  of  the  Spaniards. 

The  Tupi  people  had  their  primitive  home,  according  to  Haddon,  in  the 
northern  portion  of  the  basin  of  the  Rio  de  la  Plata,  down  which  they  spread 
to  the  mouth,  and  then,  migrating  northwards  along  the  coast,  reached  the 
mouth  of  the  Amazon,  meeting  there  the  Arawak  and  possibly  the  Carib 
peoples,  and,  travelling  westwards  along  the  southern  bank  of  the  Amazon, 
reached  the  Xingu  River,  up  which  they  went,  founding  the  Kamayura  and 
Ancta  tribes  in  its  upper  basin.  Thev  went  still  farther  westwards,  forming 
the  more  civilized  Omagua  between  the  Putumayo  and  Caqueta  Rivers,  and 
the  Cocama  peoples  at  the  junction  of  the  Amazon  with  the  Ucayali  River. 

In  Uruguay  and  Paraguay  the  Tupi  peoples  are  called  •  Guarani,'  or 
'  Warriors,'  and  hence  the  whole  family  is  called  the  '  Tupi-Guaranian 
family.' 

Into  the  races  mentioned  above  penetrated  the  great  Caucasic  migration, 
headed  by  Columbus,  in  the  fifteenth  century  of  our  era,  which,  though 
stopping  the  autochthonous  evolution  of  civilization  in  America,  introduced 
the  more  highly  evolved  culture  of  the  Old  World  at  the  cost  of  millions  of 
lives  of  the  Amerindians. 

The  Latin  races  of  this  migration  have  fused  with  the  aborigines  to  a  great 
extent,  and  thus  have  laid  the  foundations  of  the  new  Latin-Amerindian  races 
which  are  arising  to-dav. 


60  TROPICAL  RACES 

The  Anglo-Saxon  in  North  America  did  not  fuse  with  the  Amerind,  who 
to-day  is  rapidly  approaching  extinction. 

The  negro  migration  was  compulsory,  as  the  negroes  were  introduced  as 
slaves,  but  it  suited  the  race,  which  is  rapidly  increasing  in  numbers.  The 
Mongolic  migration  is  at  present  very  small,  and  of  quite  recent  date. 

Classification. — The  Amerinds  may  be  classified  for  our  purposes 
into  those  belonging  to  the  Northern  Section,  to  the  Central  Section, 
and  to  the  Southern  Section  of  America,  but  only  the  two  last  need 
concern  us  here. 

The  Central  Section  is  formed  from  Mexico  and  Central  America 
as  far  south  as  the  northern  boundary  of  Costa  Rica.  It  contains 
the  Opata-Pima  linguistic  family,  composed  of  the  Pimas  and 
Papajos  of  the  Gila  Valley,  where  the  Gila  Monster  (Heloderma 
suspectum  Cope  1869)  lives,  the  Capitas,  Coras,  Yumas,  and  Tora- 
humeras,  though  these  last  are  mixed  with  Caucasic  blood.  The 
Nahua  or  Aztecs  come  next,  and  include  the  Aztecs  proper,  the 
Pipils  of  Guatemala,  the  Niquirans,  and  the  Chichimccs. 

The  Huaxtecan  group,  often  called  the  Maya-Quiche  group,  in- 
cludes the  Huaxtecs  of  Tamaulifas  and  Vera  Cruz,  the  Mayas  of 
Yucatan,  the  Choulats  of  Mexico,  the  Mopans  of  Northern  Guate- 
mala, the  Quiche  farther  south  in  Guatemala,  the  Pocomans  around 
the  city  of  Guatemala.  The  Mayas  proper  are  divided  into  the 
Itzas  and  the  Lacandons.  The  Chortegans  include  the  Chorti 
living  around  the  ruined  city  of  Copan  as  well  as  the  Bribri  and 
others. 

In  the  Southern  Section  are  the  nations  which  we  have  suffi- 
ciently described  above — viz.,  the  Chibchas,  Ouichuas,  Chimus, 
Calchecaquis,  and  Incas,  all  of  whom  were  civilized,  and  the 
Arawak,  Tapuya,  Carib,  and  Tupi  peoples,  who  were  far  more 
primitive  and  savage,  as  well  as  the  Pampeans  and  Fuegians,  which 
are  not  tropical  races. 

REFERENCES. 

Journals.  Journal  of  the  Royal  Anthropological  Institute  of  Great  Britain 
and  Ireland;  the  journal  Man,  published  in  London;  Annual  Reports  of  the 
fVmeiican  Bureau  of  Ethnology,  Smithsonian  Institute,  Washington;  Zeit- 
schrift  fur  Ethnologie;  Revui  d 'Anthropologic 

Berenger-Fekai'ii  (1879).     Peuples  de  la  Senegainbia.     Paris. 

I ! R ixniN  ( 1  So  1 ) .     The  American  Races . 

Carr,  E.  M.  (1886).     The  Australian  Races. 

1  LAN]  and  Mocm  (1904).     Contributo  all'  Antropologia  dell'  Uganda. 
Roma . 

Codrington  (1891).     The  Melanesians.     Oxford. 

Deniker,  J.  (1900).     Races  of  Man.     London. 

Dowd,  J.  {1907).     The  Negro  Races.     NewYork. 

L>U(  KWORTH,  W.  L,  If.  (1904)       Morphology  and  Anthropology.     Cambridge. 

Ellis    (1887).   Tshi-Speaking    Peoples.     (1890).   The   Ewe-speaking   Peoples. 
(1894).  The  Yoruba-Speaking  Peoples.     London.     Guide    to  the    Speci- 
us  illustrating  the  Races  of  Mankind  (British  Museum,  Department 
of  Zoology). 

Haddon,   A.   C.   (1898).     The   Study  of  Man.     (1910).   History  of  Anthro- 
pology.    (191 1).  The  Wanderings  of  Peoples. 


AMERIND  DIVISION  61 

Hodge  (1907-11).  Handbook  of  American  Indians  North  of  Mexico. 
Washington. 

Johnstox  (1913).  Journal  Royal  Anthropological  Institute,  July  to  Decem- 
ber, p.  375.     Ethnography  of  Africa. 

Keane,  A.  H.  (1901).  Ethnology.  (1905).  Man,  Past  and  Present.  (1908). 
The  World's  Peoples. 

LlNG  Roth  (1896).     The  Natives  of  Sarawak.     London. 

Mayxard  and  Turner  (1914).  South  African  Institute  Medical  Research. 
(Anthropological  Notes  on  Bantu  Natives.) 

Ratzel,  F.  (1896-98).     The  History  of  Mankind. 

Ripley,  W.  Z.  (1900).     The  Races  of  Europe.     London. 

Seligmann,  C.  G.  (1906).  Lancet  articles  on  Natives  of  British  New  Guinea. 
(1910).  Mclaik-sians  of  British  New  Guinea.  (1913).  Journal  Royal 
\nthropological  Institute.     Hamitic  Problem. 

Seligmann,  C.  G.  and  B.  Z.  (1911).     Veddahs. 

Spencer  and  Gillen  (1899).  The  Native  Tribes  of  Central  Australia. 
London. 

Woodrufe  (undated).     Medical  Ethnology.     London. 

Worcester  (1898).     The  Philippine  Islands  and  their  People. 


CHAPTER  III 
TROPICAL   CLIMATOLOGY 

Preliminary  remarks  —  Climate  —  Tropical  climates  —  Temperature  and 
humidity  — ■  Pressure  —  Winds  —  Electrical  conditions  —  Sun's  rays- — 
Moon's  rays — Acclimatization — References. 

PRELIMINARY  REMARKS. 

We  have  delineated  the  tropics  by  Supan's  lines,  as  this  appears 
to  us  to  be  the  most  suitable  method  of  bounding  warm  climates, 
and  we  have  noted  the  characters  of  the  races  of  mankind  which 
occupy  the  lands  so  defined.  These,  we  may  incidentally  mention, 
amount  to  a  little  less  than  one-half  of  the  surface  of  the  earth, 
and  now  we  must  consider  what  is  meant  by  the  terms  '  climate  ' 
and  '  tropical  climates,'  and  then  turn  our  attention  to  the  effects 
of  these  climates  on  mankind. 

CLIMATE. 

Climate  may  be  defined  as  the  combined  effects  of  the  sun,  the 
atmosphere,  and  the  earth  upon  living  objects  at  any  one  place 
on  the  earth's  surface.  The  factors  which  produce  a  climate  are 
therefore  threefold— viz.,  the  sun,  the  atmosphere,  and  the  earth; 
and  the  living  object  with  which  we  are  concerned  being  man,  we 
must  study  the  effects  of  these  factors  upon  him,  but  we  restrict  our 
attention  to  mankind  as  seen  on  that  portion  of  the  earth's  surface 
called  the  tropics. 

TROPICAL  CLIMATES. 

In  the  previous  chapter  we  have  noted  Supan's  simple  division 
of  warm  climates  by  isotherms,  but  there  is  a  better  subdivision 
given  by  Ward,  and  based  upon  wind  systems  and  their  control 
over  rainfall  (vide  Fig.  7). 

Around  the  Equator  lies  the  region  of  equatorial  calms,  called 
the  doldrums  (Fig.  7),  while  north  and  south  of  this  region  are  the 
trade  winds  (Fig.  6).  These  zones  of  calms  and  winds  are  not 
stationary;  on  the  contrary,  they  move  so  as  to  reach  a  maximum 
extension  northwards  of  some  five  to  eight  degrees  of  latitude  in 
July  and  a  maximum  extension  southwards  of  some  three  to  four 
degrees  in  January. 

These  movements  are  dependent  upon  the  changes  in  the  inclina- 
tion of  the  axis  of  the  earth  towards  the  sun,  but  are  not  coincident 
with  these  changes. 

62 


TROPICAL  CLIMATES  63 

A  locality  may  therefore  lie  entirely  in  the  equatorial  belt,  or  it 
may  lie  entirely  in  the  trade-wind  belts,  or  it  may  be  polewards  of 
these  belts;  but  with  the  movement  of  the  system  polewards,  as 
indicated  above,  some  of  the  places  in  a  trade-wind  belt  must  come 
into  the  equatorial  belt,  while  others  usually  situate  polewards 
to  the  trades  must  be  included  in  these  belts. 

Were  the  tropics  flat"  this  classification  would  suffice,  but  there 
are  high  mountain  ranges  in  tropical  lands,  and  therefore  it  is  neces- 
sary to  make  a  division  to  include  these,  because  it  is  possible  in 
the  high  lands  of  the  tropics  to  pass  through  every  degree  of  tem- 
perature, if  you  ascend  high  enough,  as  if  you  proceeded  from  the 
Equator  to  the  Poles. 

There  are  therefore  four  divisions  of  warm  climates — viz. : 

I.  The  Equatorial  Belt. 
II.  The  Trade-Wind  Belts. 

III.  The  Monsoon  Belts. 

IV.  Mountain  Climates. 

I.  The  Equatorial  Belt. — Localities  situate  within  a  few  degrees 
of  the  Equator  are  always  more  or  less  subject  to  rain  and  cloud, 
because  the  heated  air  is  full  of  aqueous  vapour  brought  by  the. 
trade  winds  from  the  sea;  and  as  aqueous  vapour  is  lighter  than 
air  in  the  ratio  of  0623  to  i-o,  it  can  rise  to  high  and  cold  altitudes, 
and  there  be  condensed  into  small  droplets  of  water  forming  cloud 
or  larger  droplets  forming  rain. 

As  the  capacity  of  air  to  hold  water  is  doubled  for  every  270  F. 
increase  in  temperature,  and  as  in  air  saturated  at  850  F.  and  then 
cooled  to  6o°  F.  every  cubic  foot  yields  7  grains  of  water,  the  exces- 
sive violence  of  these  equatorial  and  tropical  rains  is  easily  under- 
stood. 

This  belt  is  subject  to  alternate  seasons  of  wind  and  calm — e.g., 
in  January  it  will  be  subject  to  the  north-east  trades,  followed  by  a 
period  of  calm;  and  in  July  to  the  south-east  trades,  succeeded  by 
another  period  of  calm.  There  are,  therefore,  two  maximal  and 
two  minimal  temperatures  after  the  two  zenithal  and  solstitial 
positions  of  the  sun,  and  two  short  wet  seasons  and  two  short  dry 
seasons. 

Such  places  are  Southern  India,  Ceylon  and  Java  in  Asia,  Columbia 
in  South  America,  and  in  Africa  parts  of  the  Valley  of  the  Nile, 
and  the  Gold  Coast. 

With  the  inclination  of  the  North  Pole  towards  the  sun,  which 
begins  on  March  21  and  ceases  on  September  22,  the  shifting  of 
calms  and  trades  northwards  begins  some  time  after  the  first  date 
and  lags  behind  the  last  date,  and  during  this  period  a  locality  may 
be  in  the  equatorial  belt  for  six  months  in  the  year  and  have  six 
months'  drought  and  six  months'  rain.  Such  places  are  Bengal, 
portions  of  the  Nile  Valley,  Northern  Australia,  and  Central  America. 
The  Sudan  receives  its  rains  when  the  equatorial  belt  is  passing 
northwards — i.e.,  from  May  to  August — and  its  vegetation  grows 


64  TROPICAL  CLIMATOLOGY 

rapidly,  but  when  it  is  in  the  trade-wind  belt,  from  November  or 
December  to  March  or  later,  the  climate  is  dry. 

It  is  the  northern  migration  of  the  Equatorial  Belt  which  brings 
the  heavy  rains  to  the  Uplands  of  Abyssinia,  and  causes  the  rise 
of  the  Blue  Nile  and  the  Atbara,  which  produce  the  rise  of  the  Nile. 

The  same  features  are  to  be  noted  in  the  movement  southwards; 
thus  rain  comes  on  the  pampas  of  Brazil  in  the  months  from  October 
to  April,  while  the  dry  season  lasts  for  the  rest  of  the  year. 

Some  few  places- — e.g.,  Wady  Haifa- — show  only  one  maximum 
and  one  minimum  temperature — i.e.,  the  so-called  tropical  type 
of  temperature  variation. 

II.  Trade- wind  Belts. — The  lands  which  lie  just  outside  the  polar 
boundaries  of  the  equatorial  or  rain  belt  are  situate  some  20°  to 
35°  north  or  south  latitude,  and  are  among  the  driest  in  the  world, 
except  in  India,  where  the  south-west  monsoon  brings  a  little  rain 
into  the  dry  regions  of  the  Punjab  and  Sind. 

The  worst  places  are  the  dry  zones  of  California  and  other  parts 
of  North  America,  the  Sahara  and  Nubian  Deserts,  parts  of  Arabia 
and  Persia,  Argentina,  Eastern  Patagonia,  South-West  Africa,  and 
the  interior  of  Australia.  The  only  rain  these  regions  are  likely  to 
get  will  come  from  the  extension  equatorially  of  the  polar  winds. 

We  may,  therefore,  summarize  the  character  of  the  trade-wind 
belts  as  very  regular  annual  and  diurnal  ranges  of  temperature, 
with  a  complete  absence  of  rain  or  with  slight  showers  at  infrequent 
intervals.  The  range  of  temperature  in  the  desert  is  often  very 
great ;  thus  during  the  day  the  temperature  may  be  very  high,  with 
dry  winds  carrying  dust  and  sand,  and  the  nights,  with  the  clear 
sky  free  from  cloud  allowing  active  radiation,  may  be  cool  if  not 
cold,  or  even  at  times  very  cold. 

III.  Monsoon  Belts. — The  word  '  monsoon  '  is  believed  to  be 
derived  from  the  Arabic  word  Mans  in,  meaning  '  a  season.' 

The  monsoons  (Fig.  6)  are  classifiable  into  three  groups: — 

i.  North-East  and  South-West  Monsoons. 

2.  North- West  and  South-East  Monsoons. 

3.  West  Monsoon. 

1.  North-East  and  South-West  Monsoons. — These  are  typically  met  with 
in  tin.'  Indian  Ocean  and  its  coasts. 

Dove's  explanation  of  these  monsoons  is  generally  accepted— viz.,  that, 
owing  to  heating  of  the  great  plains  of  Asia,  where  the  air  ascends  in  the 
months  of  May,  June,  July,  and  August,  the  south-east  trade-wind,  which  is 
blowing  south  of  the  Equator,  is  drawn  northwards,  at  the  same  time  being 
deflected  to  the  west,  thus  forming  the  south-west  monsoon.  Conversely, 
when  the  plains  cool  in  November,  December,  January,  February,  and  March, 
t  In  1  e  is  a  breeze  from  the  north-east  towards  the  Equator,  which,  though  called 
1  li     north-east  monsoon,  is  really  a  trade-wind. 

The  interval  between  the  two  monsoons  is  characterized  by  changeable 
winds,  which  blow  alternately  in  opposite  directions — north-east  and  south- 
west. 

The  south-west  monsoon  is  laden  with  moisture,  and  on  it  Southern  India 
largely  depends  for  rain,  and  a  failure  will  mean  a  famine,  because  a  large 
portion  of  the  population  is  agricultural,  for  the  natives  depend  for  food  upon 


TROPICAL  CLIMATES 


65 


66  TROPICAL  CLIMATOLOGY 

their  own  cultivation;  and  so  densely  are  they  placed  that  a  failure  to  produce 
their  own  crops  results  in  a  most  severe  famine,  which  can  only  be  coped  with 
by  the  most  energetic  action  of  the  Government. 

2.  North- West  and  South-East  Monsoons. — These  are  to  be  found  in  the 
Southern  Hemisphere,  and  are  depicted  in  Fig.  6  in  the  region  of  Australia. 

3.  West  Monsoon. — Dove  described  as  the  west  monsoon  of  the  line  a 
wind  which  blows  in  a  south-westerly  direction  along  the  coast  of  Africa 
from  Cape  Verde  down  to  Walfisch  Bay.  These  winds,  however,  are  variable, 
and  in  the  Gulf  of  Guinea  are  interrupted  very  often  by  calms. 

Some  people  describe  the  winds  along  the  eastern  and  western  coasts  of 
South  America  as  monsoons,  but  they  hardly  come  under  this  term. 

In  typical  monsoon  regions  the  rains  follow  the  vertical  sun,  and  the  type 
of  temperature  is  the  so-called  tropical  type,  with  one  maximum  and  one 
minimum. 

It  must  be  admitted  that  this  simple  classification,  like  all  classifications, 
fails  to  explain  everything,  and  there  are  numerous  exceptions  showing  com- 
binations of  equatorial,  trade-wind,  and  monsoon  types. 

IV.  Mountain  Climates.— We  have  already  pointed  out  the  effect 
of  altitude  in  lowering  the  temperature,  and,  indeed,  Herschel, 
many  years  ago,  showed  that  for  every  300  feet  of  increase  in 
altitude  there  was  a  decrease  of  i°  F.  in  temperature,  and  for  every 
180  metres  a  decrease  of  i°  C.  These  statements  are  only  partially 
correct,  for  the  temperature  at  a  given  altitude  depends  upon  the 
expansion  and  humidity  of  the  air,  the  clearness  of  the  atmosphere, 
together  with  the  quantity  of  earth  at  the  given  locality,  and  the 
nature  of  the  wind  blowing  at  the  time  of  the  observations.  Perhaps 
of  all  these  the  most  important  is  the  expansion  of  the  air,  for,  as  is 
well  known,  it  expands  when  heated — i.e.,  the  energ}7  represented 
by  heat  is  converted  into  motion,  and  hence  the  temperature  falls. 
This  will  in  part  be  counteracted  by  the  heat  produced  by  the 
condensation  of  aqueous  vapour,  even  at  high  altitudes,  and  upon 
this  condensation  and  cloud-formation  will  depend  how  much 
of  the  heat,  radiating  from  the  earth  into  the  air,  is  retained.  The 
lessened  amount  of  earth  in  high  altitudes  is  also  a  factor,  as  there 
is  less  earth  to  retain  heat,  and  hence  less  heat  is  given  off  into  the 
air.  It  is  obvious  that  movements  of  the  air — the  winds — must 
have  a  great  effect,  depending  upon  their  origin  from  warm  or  cold 
sources.  Hence,  though  in  general  the  rule  mentioned  above  as  to 
a  relationship  between  temperature  and  altitude  holds  good,  it  is 
only  approximate,  as  the  connection  between  the  two  is  complex, 
».ot  simple. 

In  the  tropics,  therefore,  the  low  country  possesses  the  true 
tropical  climate,  while  the  climatological  conditions  of  the  hills  are 
quite  different.  Indeed,  as  Ward  has  said,  the  climates  of  many 
tropical  plateaus  and  mountains  have  the  reputation  of  having  a 
perpetual  spring,  but  though  that  may  be  so  at  certain  latitudes, 
if  considerable  elevations  are  reached  a  peipetual  winter  exists, 
with  snow  all  the  year  round,  even  on  the  Ecmator. 

The  great  blessing  of  these  elevations  in  the  tropics  is  that  they 
provide  cool  hill  stations  to  which  the  resident  of  the  plains  may 
resort  during  the  hottest  months,  and  in  which  sanatoria  may  be  built 
for  the  treatment  of  persons  convalescent  from  lowland  complaints. 


TEMPERATURE  AND  HUMIDITY  67 

This  brief  sketch  of  tropical  climates  must  suffice  for  our  present 
purpose,  and  we  now  turn  to  consider  the  various  climatic  factors 
and  their  effects  upon  man;  but  the  reader  interested  in  this  subject 
may  find  it  useful  to  consult  Chapter  II.,  pp.  28  to  58,  in  our 
second  edition,  in  which  more  details  will  be  found. 


TEMPERATURE  AND  HUMIDITY. 

Heat  derived  from  the  sun  is  capable  of  traversing  the  atmosphere 
surrounding  the  world,  and  thus  reaching  the  earth,  because  this 
atmosphere  is  diathermanous  to  rays  with  short  wave-lengths  coming 
from  so  hot  a  body  as  the  sun.  Dry  air  is  diathermanous  for  all 
rays,  but  aqueous  vapour  is  almost  athermanous  for  infra-red  rays, 
though  largely  diathermanous  for  other  rays. 

In  passing  through  the  atmosphere,  about  25  per  cent,  of  the 
licit  which  has  entered  it  is  absorbed  before  it  reaches  sea-level. 

Tlie  position  of  the  sun  is,  however,  of  the  utmost  importance 
with  regard  to  the  quantity  of  heat  reaching  the  earth.  If  the  sun 
is  quite  vertical,  probably  only  20  per  cent,  is  lost;  whereas,  if 
the  beam  is  nearly  horizontal,  probably  none  reaches  the  earth. 

The  heat  rays  falling  upon  the  earth  are  absorbed  and  converted 
into  dark  heat — that  is  to  say,  into  frequencies  with  longer  wave- 
lengths— and  these  are  radiated  back  into  the  atmosphere  (terrestrial 
radiation).  This  dark  heat  is  absorbed  by  the  atmosphere,  which 
is,  as  already  stated,  almost  athermanous  to  this  kind  of  energy. 
This  atmospheric  heat  is  one  of  the  most  important  factors  in 
determining  the  nature  of  a  climate,  and  shows  daily  and  annual 
periodic  variations,  of  which  the  first  is  due  to  the  sun's  rays  heating 
the  earth,  and  therefore  this  disappears  at  sea  or  during  an  arctic 
winter,  while  the  second  depends  largely  upon  the  inclination  of  the 
world's  axis  as  it  passes  round  the  sun  in  its  yearly  orbit.  As  the 
sun  is  vertical  in  the  sky  at  noon  twice  a  year  in  the  tropics,  there 
is  or  ought  to  be  a  wet  season  at  these  times,  and  in  their  intervals 
a  dry  hot  season. 

It  is  impossible,  however,  to  consider  the  effects  of  temperature 
upon  man  without  at  the  same  time  taking  into  account  the  humidity 
of  the  atmosphere. 

Man  can  bear  very  high  temperatures  easily,  provided  the  air  is 
dry,  but  not  if  there  is  much  moisture  or  humidity  in  it.  The 
humidity  of  the  atmosphere  is,  in  fact,  of  the  utmost  importance 
in  the  study  of  climatic  effects  upon  man.  This  humidity  is  due 
to  aqueous  vapour,  caused  by  the  constant  evaporation  which 
takes  place  from  the  surface  of  all  collections  of  water. 

The  humidity  of  the  atmosphere  presents  three  problems: 
atmometry,  or  the  measurement  of  the  quantity  of  water  being 
taken  into  the  air;  hygrometry,  or  the  determination  of  the  quantity 
of  aqueous  vapour  present  in  the  air  at  any  given  time;  and  hyeto- 
metry,  or  the  quantity  of  water  being  condensed  from  the 
atmosphere. 


68  TROPICAL  CLIMATOLOGY 

Evaporation  takes  place  most  quickly  in  hot  dry  air,  and  causes 
a  considerable  amount  of  heat  to  be  rendered  latent.  This  fact 
can  be  made  use  of  in  hot  climates,  where  it  is  a  common  practice 
to  wrap  flannel  or  felt  round  a  bottle  of  water,  and  after  damping 
the  flannel,  to  hang  the  bottle  in  the  breeze,  so  that  the  contents 
may  become  cooled  by  the  evaporation  of  the  water  from  the  flannel. 
The  same  principle  applies  to  the  porous  stone  or  earthenware 
basins  which  are  commonly  used  in  Ceylon,  Uganda,  Egypt,  and 
other  parts  of  the  tropics  to  filter  and  cool  water.  Hence,  also, 
the  value  of  collections  of  water  in  keeping  the  temperature  of 
places  equable. 

The  amount  of  aqueous  vapour  in  the  atmosphere  is  generally 
spoken  of  as  the  humidity.  Two  kinds  of  humidity  are  recognized : 
absolute  humidity,  which  is  the  weight  of  aqueous  vapour  actually 
present  in  a  definite  volume  of  air  at  a  given  temperature;  and 
relative  humidity,  which  is  the  ratio  of  the  weight  of  water  actually 
present  in  a  known  volume  of  air  to  the  weight  of  water  which  is 
required  to  saturate  the  same  volume  of  air  at  the  given  tempera- 
ture, and  is  generally  expressed  as  a  percentage. 

We  have  already  stated  that  the  humidity  of  the  air  is  of  the 
greatest  importance  in  considering  the  effects  of  a  tropical  climate 
on  man.  The  most  trying  climate  would  be  one  with  a  high  air 
temperature  and  a  high  relative  humidity,  for  it  is  obvious  that  when 
the  air  is  full  of  aqueous  vapour,  evaporation  from  the  surface  of  the 
human  body  must  be  considerably  diminished;  and  as  this  is  one 
of  the  methods  of  regulating  the  bodily  temperature,  it  is  apt  to 
rise  and  cause  great  discomfort,  as  will  be  described  later. 

A  warm  place  with  a  high  humidity  is  less  bearable  than  a  much 
hotter  but  drier  place.  A  fairly  high  relative  humidity  can,  how- 
ever, be  borne  if  there  is  a  breeze,  without  which  a  much  lower 
humidity  is  most  unbearable.  In  fact,  Giles  points  out  that 
Abusher,  in  the  Persian  Gulf,  in  August,  with  a  mean  maximum 
temperature  of  96-5°  F.  (35 70  C),  and  a  relative  humidity  of  05 
per  cent.,  with  no  rainfall  during  the  month,  and  little  or  no  breeze, 
consti  utes  one  of  the  most  unbearable  climates  in  the  world, 
though  neither  the  temperature  nor  the  humidity  by  themselves 
are  high. 

When  the  aqueous  vapour  in  the  atmosphere  condenses,  the  result 
may  be  dew,  fog,  mist,  cloud,  rain,  hail,  or  snow,  of  which  the  two 
last  are  rare  in  the  tropics.  Clouds  in  the  sky  prevent  to  a  great 
extent  the  heating  of  the  earth  during  the  day,  and  at  the  same 
time  they  prevent  radiation  of  heat  from  the  earth  during  the  night, 
and  even  reflect  this  back  to  it.  Hence  cloudy  nights  may  be  very 
hot  in  the  tropics. 

Effects. 

We  must  now  consider  briefly  the  effects  of  high  air  temperatures 
with  and  without  high  atmospheric  humidity  upon  man,  and  we 
will  commence  with  a  consideration  of  its  effects  upon  the  bodily 
temperature. 


TEMPERATURE  AND  HUMIDITY  69 

Normal  Temperature.— The  normal  temperature  of  man  is  the 
resultant  between  the  heat  produced  by  the  oxidation  of  foodstuffs 
in  the  muscles,  glands,  and  other  organs  and  tissues  of  the  body, 
and  the  heat  lost  by  warming  the  urine,  faeces,  and  expired  air,  by 
evaporation  from  the  lungs  and  skin,  and  by  radiation  and  con- 
duction from  the  skin.  In  other  words,  the  temperature  of 
the  body  is  controlled  both  by  chemical  and  by  physical  heat 
regulation. 

1 .  Chemical  Heat  Regulation. — By  this  is  meant  regulation  of  the  bodily 
temperature  by  increased  or  diminished  production  of  heat,  \yhich  can  be 
brought  about  by  alterations  in  metabolism.  Diminished  heat  production 
is,  however,  rare,  being  usually  pathological,  though  it  is  possible  that  it 
occurs  more  frequently  in  the  Tropics  than  in  flu-  Temperate  Zone,  owing  to 
the  lessened  disposition  for  muscular  or  mental  work. 

.:.  Physical  Heat  Regulation.  —The  body  temperature  is  usually  regulated 
by  increasing  or  diminishing  the  loss  caused  by  radiation,  convection,  and 
evaporation.  According  to  Hill,  a  man  weighing  70  kilogrammes  loses  77*1 
per  cent,  of  his  heat  by  radiation  and  convection  and  22-9  per  cent,  by  evapora- 
tion. This  regulation  is  brought  about  by  the  dilatation  of  the  cutaneous 
vessels  bringing  more  blood  to  the  skin  and  by  the  increased  perspiration. 
The  loss  of  heat  caused  by  radiation  and  convection  depends  upon — 

1.  Temperature  and  conductivity  of  the  skin. 

2.  Temperature  and  radiation  from  the  skin. 

3.  Temperature  of  the  air. 

4.  Rate  of  motion  of  the  air. 

Clothing  may,  however,  affect  the  loss  of  heat  from  the  skin,  for,  as  a  rule, 
it  is  composed  of  substances  which  are  bad  conductors  of  heat,  and  hence 
the  loss  may,  according  to  Rubner,  be  diminished  no  less  than  47  per  cent. 
Wet  clothing,  on  the  other  hand,  is  a  good  conductor,  because  of  the  water 
in  its  interstices,  and  hence  the  danger  of  chills  while  wearing  damp  clothes. 
This  latter  fact  is  well  known  to  the  old  resident  of  the  tropics,  who  has 
generally  learnt  its  danger  by  personal  experience. 

Radiation  takes  place  best  when  the  air  is  still,  dry,  and  cold,  conduction 
when  it  is  damp.  Convection  is  only  of  importance  when  the  air  is  in  motion. 
m  which  case  the  loss  of  heat  is  proportionate  to  the  square  root  of  the  velocity, 
and  is  more  marked  when  atmospheric  humidity  is  high. 

With  regard  to  evaporation,  Rubner  has  shown  that  it  is  best  at  medium, 
greater  at  low,  and  still  greater  at  high  temperatures,  as  is  shown  by  the 
following  table  taken  from  his  book  of  an  observation  on  a  man  of  58  kilo- 
grammes weight  lightly  clad:  — 


Air  Temperature. 


2°C. 

io°  to  150  C. 
1 50  to  200  C. 

20°  tO  25°  C. 

250  to  300  C. 
500  to  350  C. 
\^°  to  400  C. 


Grammes  of 

0H2 

Grammes  of  CO.,  lost 

per  Hour 

per  How  . 

37 

29-8 

28 

25-1 

19 

24-1 

23 

25-0 

43 

25*3 

84 

2  3-7 

112 

1 1  •  2 

7°  TROPICAL  CLIMATOLOGY 

This  evaporation  is  very  markedly  diminished  by  humidity,  as  is  shown 
in  the  following  table: — 

Temperature  in  5  to  8  per  Cent.  81  to  89  per  Cent. 

Centigrade.  Humidity.  Humidity. 


15-0  36-3  9-0 

20-4°  54-1  15.3 

25-3°  75'5  23-9 

28-9° 

It  is  also  diminished  by  a  moderately  strong  wind,  but  is  increased  by  the 
sun's  rays  and  by  work  in  a  hot  climate. 

To  determine  accurately  the  temperature  of  a  man  in  the  tropics  is  not  the 
easy  matter  which  most  people  consider  it  to  be,  and  the  principles  applying 
thereto  should  be  understood  even  by  those  not  likely  to  be  deceived  by  an  air 
temperature  so  high  that  a  maximum  thermometer  rises  and,  keeps  above  normal 
without  any  reference  to  the  patient,  a  fact  which  we  have  seen  lead  to  curious 
mistakes.  Under  such  conditions,  the  thermometer  must  be  kept  and 
examined  in  cold  water. 

The  temperature  of  man,  being  the  resultant  between  the  heat  produced 
and  the  heat  lost,  must  vary  considerably  under  many  circumstances,  and 
there  is  no  doubt  that  it  varies  in  different  individuals. 

In  investigating  the  temperature  of  the  body,  one  ought  to  seek  that  which 
most  nearly  represents  the  temperature  of  the  blood,  for  though  the  different 
organs  of  the  body  manufacture  or  lose  heat  in  different  proportions,  the  circu- 
lation of  the  blood  tends  to  bring  about  a  mean  internal  temperature  for  the 
whole  body. 

The  possible  methods  of  investigating  the  temperature  of  the  body  are  by 
placing  the  thermometer — 

1 .  In  the  axilla, 

2.  In  the  mouth, 

3.  In  the  rectum, 

to  which  might  be  added  placing  the  thermometer  in  the  stream  of  issuing 
urine;  but  this  method  is  only  open  to  limited  application,  and  there  may  be 
considerable  loss  from  evaporation  and  radiation,  and,  therefore,  though  it  is 
an  excellent  method  when  used  with  care,  will  not  be  further  considered. 

If  the  thermometer  is  placed  in  a  dry,  well-closed  axilla,  and  kept  there 
long  enough,  the  result  will  be  not  unlike  that  in  the  mouth;  but  if  it  is  thought 
that  any  resemblance  to  the  internal  temperature  of  the  body  is  to  be  obtained 
by  placing  a  thermometer  in  a  perspiring  axilla  for  half  to  one  minute,  then 
the  greatest  mistakes  as  to  the  real  temperature  of  the  patient  are  possible. 
In  our  experience  it  has  not  been  unusual  in  the  tropics  to  find  several  degrees 
of  difference  between  the  axilla  and  the  mouth. 

As  a  rule,  it  may  be  stated  that  the  axilla  is  not  a  good  place  in  which  to 
take  thermometric  observations  which  are  meant  to  indicate  the  true  tempera- 
ture of  the  body. 

With  regard  to  the  mouth  temperature  there  has  been  a  great  deal  of  dis- 
cussion, but  the  most  careful  observations  are  those  of  Pembrey  and  Nicol, 
who  have  shown  that  the  mouth  temperature  is  apt  to  vary  considerably, 
and  that  it  is  not  a  reliable  indicator  of  the  internal  temperature  of  the  body 
in  cold  weather  or  after  exercise.  Haldanc,  in  his  valuable  experiments  to  be 
quoted  presently,  finds  that  it  varies  greatly  with  the  individual. 

In  warm  and  moist  air,  however,  the  mouth  temperature  approaches  the 
rectal  temperature. 

The  reason  why  the  mouth  temperature  is  apt  to  be  lower  than  the  rectal 
and  the  real  temperature  of  the  body  is  apparently  the  cooling  owing  to  the 


TEMPERATURE  AND  HUMIDITY  71 

proximity  oi  the  skin,  and  possibly  of  the  nasal  cavity,  and  therefore  in  warm 

air  this  difference  frequently  does  not  exist.  In  India  Crombie  found  in 
fifteen  carefully  taken  observations  that  the  mouth  temperature  was  0-22°  F. 
below  that  of  the  rectum,  whereas  Pembrey  found  it  as  much  as  4-5°  F. — 
i.e.,  2-5°  C. — below  that  of  the  rectum  in  cold  weather  in  England.  It  is 
possible,  therefore,  that  it  is  a  better  site  for  thermometric  observations  in  the 
tropics  than  in  Europe. 

Rectal  temperatures  under  ordinary  conditions  give  the  highest  readings 
and  are  the  truest  indicators  of  the  internal  temperature  of  the  body;  but  this 
is  not  a  method  open  to  clinical  use,  except  in  children  and  instates  of  coma. 

The  conclusion  is  that  if  care  be  taken  that  neither  hot  nor  cold  articles 
have  been  recently  placed  in  the  mouth,  and  particularly  if  the  mouth  has  been 
kept  closed  for  a  short  time,  the  temperature  from  the  thermometer  placed 
under  the  tongue  is,  without  doubt,  the  most  accurate  for  ordinary  clinical 
work  in  the  tropics,  for  in  that  position  the  thermometer  is  as  completely 
as  possible  protected  from  the  influence  of  the  nose  and  the  skin. 

A  thermometer,  however  quickly  it  reacts  to  its  surroundings,  must  be  left 
a  reasonable  time  in  the  mouth,  by  which  is  meant  two  or  three  minutes,  so 
that  the  temperature  of  the  closed  mouth  may  approach  that  of  the  rest  of 
the  body.  Crombie  gives  the  time  Eor  the  accurate  recording  of  the  tempera- 
ture in  India  as: — 

Ten  minutes  in  the  well-closed  and  dry  axilla. 

Eight  minutes  in  the  mouth. 

Three  to  four  minutes  in  the  rectum. 

The  mean  daily  temperature  of  man  for  the  hours  8  a.m.  to  12  midnight  in 
the  Temperate  Zone  is  as  follows : — ■ 

98-45°  F.  (36-90°  C.)  in  the  axilla. 
98-36°  F.  (36-87°  C.)  in  the  mouth. 
98-96°  F.  (37-20°  C.)  in  the  rectum. 

The  so-called  normal  temperature  of  man  in  the  mouth  mav  be  placed  at 
98-40°  F.  (36-90°  C.)  or  98-6°  F.  (37°  C),  and  was  determined  as  the  mean 
temperature  from  8  a.m.  to  12  midnight  by  John  Davy  in  1S37,  and  by  some 
mistake  it  has  been  interpreted  into  the  mean  temperature  for  the  twenty- 
four  hours,  which  is  different,  being  probably  lower. 

Crombie  gives  the  following  as  the  means  of  the  observations  of  Ogle, 
Allbutt,  Casey,  and  Rattray : — 

.  .      .  ___ 

Mean  Morning      Mean  Afternoon       Mean  Twenty-four       Maximum  Daily 
Temperature.  Temperature.        Hours'  Temperature.  Range. 


97-763°  F.  98-341°  F.  98-084°  F.  1-41°  F. 

But  at  present  there  are  insufficient  data  upon  which  to  base  a  definite 
conclusion  as  to  the  mean  temperature  of  human  beings  for  the  whole  twenty- 
four  hours. 

The  average  temperature  in  the  mouth  varies  from  between  96°  F.  and  97°  F. 
to  a  little  under  99°  F.,  and  the  rectal  temperature  from  97-2°  F.  (36-28°  C.) 
between  2  to  5  a.m.  to  99-4°  F.  (37-45°  C.)  between  4  to  7  p.m. 

Pembrey  gives  the  mean  daily  temperature  as  being  98-0°  F.  (37°  C),  the 
maximum  99-5°  F.  (37*5°  C),  and  the  minimum  96-8    F.  (36°  C.) 

Effect  on  Temperature. — Having  now  defined  what  we  mean  by  a 
normal  temperature  in  man,  it  is  necessary  to  inquire  into  the  effects 
of  high  atmospheric  temperatures  and  varying  humidity  upon  man. 

The  experiments  o l  Lining  (1738),  Ellis  n  and  Pordyce  (1775), 

established  the  fact  that  a  normal  man,  suitably  clothed,  can  regute+e  his 


72  TROPICAL  CLIMATOLOGY 

temperature  so  that  with  high  air  temperatures  it  still  remains  within  the 
normal  limits,  if  the  atmospheric  humidity  is  low,  and  these  experiments  have 
been  well  borne  out  by  life  in  the  tropics. 

It  is,  however,  quite  otherwise  when  the  atmospheric  humidity  is  high: 
as  far  back  as  i  775  Blagden  and  Fordyce  noted  that  in  a  damp  room  with  a 
temperature  of  i23'Q°  F.  (54*4°  C.)  their  bodily  temperature  rose  to  ioo°  F. 
(37*8°  C).  Haldane  observed  that  there  was  no  abnormal  rise  of  the  bodily 
temperature  until  the  wet  bulb  thermometer  indicated  88°  F.  (310  C),  pro- 
vided that  the  experimenters  were  stripped  to  the  waist  or  clad  in  light  flannel. 
If,  however,  the  wet  bulb  exceeded  this  temperature  by  even  one  degree,  then 
the  bodily  temperature  rose  hour  by  hour  in  proportion  to  the  rise  of  the  wet 
bulb  thermometer  above  88°  F.,  but  the  bodily  temperature  increased  more 
rapidly  when  high  wet  bulb  temperatures  were  reached  than  when  they  were 
relatively  low.  With  the  abnormal  rise  of  bodily  temperature  was  associated 
increase  of  the  pulse-rate  by  about  twenty  beats  per  minute  for  each  degree 
Fahrenheit  and  thirty-six  for  each  degree  Centigrade.  All  these  bodily 
temperatures  were  taken  in  the  rectum  and  with  the  patient  standing.  When 
this  rectal  temperature  reached  1020  F.  hyperpncea  was  observed,  while  other 
symptoms  associated  with  the  rise  of  the  bodily  temperature  were  profuse 
sweating  and  a  general  feeling  of  exhaustion  and  discomfort. 

It  was  observations  like  these  that  caused  Tyler  to  attempt  to 
correlate  personal  sensations  with  meteorological  data,  and  to 
formulate  his  '  hyther  '  degrees,  by  which  he  meant  the  degree 
of  discomfort  caused  by  high  air  temperatures  associated  with  high 
relative  humidity. 

Haldane's  experiments  have  often  been  repeated  by  ourselves 
on  normal  people  by  placing  them  alongside  the  condensers  in  the 
engine-room  of  steamers  in  the  Red  Sea  during  very  hot  months. 
Near  the  condensers  one  can  usually  find  a  corner  where  there  is  no 
obvious  movement  of  the  air,  which  is  nearly  saturated  with  aqueous 
vapour,  and  where  there  is  a  high  atmospheric  temperature.  Placed 
in  such  a  corner  and  clad  only  in  loose  pyjamas,  the  skin  of  the  body 
flushes  and  burns,  the  perspiration  rolls  downwards  in  streams, 
and  the  temperature  after  a  short  pause  commences  to  rise  and  goes 
on  rising  until  the  experiment  is  broken  off,  usually  about  1030  F. 

This  is  not  a  pathological  rise,  though  associated  with  throbbing 
vessels,  etc.,  but  is  simply  due  to  atmospheric  conditions  acting 
upon  a  normal  man,  and  all  symptoms  disappear  rapidly  after 
removal  to  cooler  air. 

If  such  a  climate  existed  no  human  being  could  live  therein, 
but  no  such  place  is  known,  and  although  conditions  of  high  atmo- 
spheric temperatures  may  produce  fever,  yet  these  are  pathological 
and  not  physiological,  and  depend  upon  factors  which  will  be  dis- 
cussed later. 

From  the  time  of  Davy  in  1839,  observations  have  been  made 
into  the  temperature  of  healthy  men  during  the  passage  from  the 
temperate  to  the  tropical  zone,  during  their  residence  in  the  tropics, 
and  during  the  passage  from  the  warm  to  temperate  climates. 
In  previous  editions  of  this  work  we  gave  the  known  data,  and  any- 
one who  cares  to  look  at  the  pages  from  91  to  97  in  the  second 
edition  of  this  book  will  observe  how  confusing  and  contradictory 
are  the  results,  while  they  will  be  struck  with  the  relative  paucity 
of  these  results.     The  truth  is  that  the  earlier  observers  omitted 


TEMPERATURE  AND  HUMIDITY 


73 


to  take  into  consideration  the  atmospheric  humidity,  and  this  alone 
vitiated  their  conclusions. 

Our  own  observations  agree  with  those  who  have  failed  to  show 
any  change  in  the  bodily  temperature  in  passages  to  and  from 
the  tropics  and  in  residence  therein,  provided  that  the  individuals 
observed  were  normal. 

Further,  we  have  failed  to  observe  any  difference  in  the  tempera- 
ture between  well-nourished  healthy  natives  and  Europeans,  and 
with  due  allowance  for  individual  and  seasonal  differences  and  the 
effects  of  exercise  and  clothing. 

In  previous  editions  we  have  consumed  much  space  with  discus- 
sions as  to  the  pulse-rate,  and  so  as  not  to  weary  the  reader,  we 
may  say  that  we  do  not  believe  that  there  is  any  change  in  the  pulse- 
rate  of  normal  Europeans  on  entering  or  residing  in  the  tropics,  nor 
is  there  any  appreciable  difference  between  them  and  natives. 

Bussiere  recently  has  invited  attention  to  the  action  of  cold  on 
tropical  natives  brought  straight  to  temperate  climates,  which 
tends  to  produce  attacks  of  malaria,  liver  troubles,  and  inflammation 
of  the  bronchi  and  lungs.  He  especially  lays  stress  on  temporary 
albuminuria  yielding  to  treatment  in  some  one  to  three  weeks. 

Effect  on  Respiration. — As  we  have  no  personal  experiments  to 
record  with  regard  to  respiration,  we  give  the  work  of  other 
observers. 

Rattray  studied  very  fully  the  influence  of  tropical  climates  on  respiratiorj, 
and  gives  a  table  showing  their  effect  on  the  capacity  of  the  chest,  as  indicated 
by  the  spirometer,  on  a  voyage  from  England  to  Bahia  and  back.  The 
average  of  twelve  observations  is  as  follows  (hygrometer  indicates  the  differ- 
ence between  the  wet  and  dry  bulb  ol  a  Mason's  hygrometer): — 


Number  of  Persons, 

12 

Temperature 
65°  F., 

Hygrometer 
2-5°  F. 

Temperature 

780  F., 

Hygrometer 

4°F. 

Temperature 
S30  F., 

Hygrometer 
4°F. 

Temperature 
65°  F.. 

Hygrometer 
i-5°  F. 

Capacity      of      the 
chest  as  shown  by 
spirometer 

Gain  or  loss 

256-083 

280-75 
+  24-833 

287-416 
+  6-5833 

200-25 

-26-333 

Percentage  gain 

12-24 

— ■ 

The  increased  capacity,  according  to  Rattray,  is  not  due  to  any  actual 
increase  in  the  capacity  of  the  size  of  the  chest,  but  to  a  diminished  quantity 
of  blood  in  the  lungs, "which  he  considers  has  been  diverted  to  the  excited 
and  congested  skin  and  liver. 

His  results  may  be  summarized  by  saying  that  the  vascularity  of  the  lungs 
is  reduced  by  23  fluid  ounces,  and  owing  to  diminished  number  of  respirations 
7-5  per  cent,  less  air  is  used  daily,  and  1  •  1  ounces  less  carbon,  and  4-5  per  cent, 
less  aqueous  vapour  excreted. 

With  regard  to  these  observations  of  Rattray,  he  is  apparently  supported 
by  all  observers  as  to  the  increase  in  caparitv  when  Europeans  enter  the 


74 


TROPICA  L  CUM  A  TOI.OG  Y 


tropics.     Jousset,  however,  stales  that  this  is  only  temporary,  and  disappears 
after  acclimatization. 

Rattray  maintained  that  there  was  a  diminution  of  capacity  when  a  native 
of  the  tropics  went  to  the  Temperate  Zone,  ar.d  gave  the  following  table:— 


Temperature     Temperature     Temperature 
79°  F.  78°  F.  320  F. 


Condition. 

Race. 

B.  C,  aged  twenty- 
one;     height,      5 

Native  of 
Sierra 

feet  5J  inches 

Leone 

J.  C,  aged  twenty; 
height,    5   feet    4 
inches 

Native  of 
Sierra 
Leone 

J.  W.,  aged  thirty- 
one  ;     height,      5 

Half-cast, 

feet  4  inches 

210  207  185 

174  166  I5<> 


He  found  that  the  frequency  of  respiration  was  slower  in  the  tropics,  as  is 
shown  in  the  following  table  : — 


Climate. 


,r         e;     ;,         Highest  Lowest  Average 

T  ea+,   ■  lf  &      Number  of       Number  of         Number  of 
empera  urt     Respirafions .   Respirations.   Respirations. 


t,      ,       ,      ( Summer 
England        ,,-     . 
&               \  \\ inter 

62°  F. 
42-25°  F. 

18 
17-5 

13-5 
15 

15-68 
16-50 

rO  u  t- 

Equatorial  |    wart! .  . 

78-74°  F. 

14-5 

11 

12-74 

y  doldruirr  1  1  ■!>  me 

1    ward.. 

78-60°  F. 

15 

12 

1.V74 

Jousset,  Plehn,  and  others  controvert  Rattray's  statement  that  the  respira- 
tions are  slower,  believing,  on  the  contrary,  that  they  are  augmented  before 
acclimatization. 

This  shows  clearly  that  the  question  is  far  from  settled,  and,  in  fact,  requires 
reinvestigation . 

Effect  on  Circulation. — Rattray  investigated  the  pulse-rate  carefully,  and 
gives  the  following  table: — 


Time. 


9  a.m. 
3  P-m. 
9  p.m. 


X umber  of 
I   Observa- 
tions. 


Tropics. 


Temperate 
Zone. 


Averages 


I 


Highest.       Range.     ,  Average.     Average. 


53 

66 

112 

40 

53 

08 

10S 

42 

1  •• 

73 

no 

37 

— 

— 

— 

— 

86-4 

88-8 

_S7'l 
87-5 


91-7 

88-1 
90-5 

90-1 


TEMPERATURE  AND  HUMIDITY  75 

He  gives  the  following  conclusions: — 

1.  The  average  pulse  is  lower  by  2-5  beats  in  the  Tropics  than  in  the  Tem- 
perate Zone. 

2.  This  change  holds  good  for  the  average  morninar  and  evening  pulse. 

3.  The  average  afternoon  pulse  is  higher  in  the  Tropics  than  in  the  Tem- 
perate Zone,  probably  because  the  solar  heat  is  greatest  then. 

4.  The  morning  pulse  has  the  greatest  and  the  evening  the  lowest  range. 
He  considers  that  this  reduction  in  the  pulse-rate  is  related  to  the  diminished 

respiratory  function.  Parkes,  Jousset,  Crevaux,  Feris,  and  Plehn,  according 
to  Huggard,  maintain,  on  the  contrary,  that  the  pulse  is  increased  by  ten  beats 
per  minute.  Plehn  says,  however,  that  on  acclimatization  the  pulse-rate 
sinks  to  normal. 

There  is  said  to  be  a  lowering  of  tension  (associated,  according  to  Huggard, 
with  the  dilatation  of  the  peripheral  vessels),  as  well  as  increased  elasticity 
and  dicrotism,  all  of  which  probably  pass  away  on  acclimatization. 

Chamberlain  in  the  Philippine  Islands  concludes  that  the  average  blood - 
pressure,  measured  by  a  Cook's  modification  of  a  Riva-Rocci's  apparatus 
and  a  1 2-5  centimetre  armlet,  in  Filipinos  and  Americans  of  the  same  age  dwell- 
ing in  those  islands,  does  not  appreciably  differ  from  one  another,  nor  from 
that  of  similar  Americans  in  the  Temperate  Zone,  but  that  the  pulse-rate  of 
active  Filipinos  and  Americans  is  a  few  beats  above  the  usual  standard  of 
72  per  minute. 

In  our  experience,  in  Europeans  coming  to  the  Tropics,  the  pulse-rate  is 
occasionally  slightly  increased.  This  disappears  after  acclimatization,  and 
the  pulse-rate  becomes  the  same  as  in  Temperate  Zones.  We  have  never 
noticed  dicrotism  of  the  pulse  in  normal  individuals. 

As  regards  natives  of  the  Tropics,  it  is  stated  by  some  authorities  that  their 
pulse  is  quicker  than  in  the  inhabitants  of  Temperate  Zones,  but  we  are  unable 
to  confirm  this,  and  find  it  to  be  the  same  as  in  Europeans. 

Effect  on  the  Blood. — Mitchell,  as  the  result  of  his  work  in  the 
Persian  Gulf,  considers  that  damp  heat  of  itself  frequently  produces 
anaemia,  but  gives  no  details  of  the  blood  examinations.  In  1916 
W.  M.  Strong,  noting  that  persons  who  had  lived  for  long  in  the 
Tropics  became  anaemic-looking,  investigated  this  point,  and  con- 
cluded that  the  pallor  was  not  due  to  deficiency  in  haemoglobin  nor  to 
ischaemia  of  the  cutaneous  capillaries,  but  to  pigment  deposited  in  the 
epidermis,  which  becomes  partially  opaque  to  red  light,  which  is 
important  because  the  colour  of  the  skin  depends  upon  the  relative 
amount  of  each  spectral  tint  which  is  reflected  back  to  the  eye. 
Further,  he  considers  that  when  more  pigment  is  deposited  the  skin 
becomes  yellow-brown. 

The  '  Arncth  count  '  (see  p.  1898)  in  healthy  native  children  has  been 
investigated  by  Breinl  and  Priestley ;  taking  the  figure  for  normal  Europeans 
as  40,  native  children  varied  from  71-6  to  83-86,  while  in  adult  natives  it 
stood  at  74*04.  They  are  of  the  opinion  that  the  alteration  of  the  blood 
picture  is  the  outcome  of  climatic  influences,  and  not,  as  suggested  by  Scott 
Macfie,  as  the  outcome  of  abortive  inoculation  with  malarial  parasites, 
though  they  think  that  the  higher  figure — viz.,  83-86 — may  be  accounted  for 
by  infection. 

Sweet  agrees  that  high  '  Arneth  index  '  is  very  regularly  present  in  healthy 
children  over  the  whole  coastal  area  of  Eastern  Australia;  he  maintains  that 
no  factor  apart  from  disease  is  found  definitely  to  influence  this  index,  but 
he  says  that  external  temperatures  do  apparently  influence  the  index  in 
animals,  and  that  further  research  is  required  with  reference  to  this  in  man. 

We  are  disinclined  to  believe  in  a  marked  anaemia  purely  and  solely  due  to 
climatic  influences  without  any  other  causal  factor,  but  diminished  resistance 
against  disease  is  certainly  produced  by  long  residence  in  the  tropics,  and  is 


76  TROPICAL  CLIMATOLOGY 

probably  largely  climatic  in  its  cause,  though  food  may  also  be  a  causal  factor 
therein;  but  the  chemical  factors  of  resistance  to  disease  still  require  investiga- 
tion. 

With  regard  to  the  sugar  content  in  the  blood,  McCay  finds  that  for  Euro- 
peans it  is  o*o8  per  cent.,  while  for  Bengalis  it  is  0*13  percent.,  and  the  increase 
appears  to  be  entirely  due  to  the  excessive  amount  of  the  carbohydrate  in 
their  diet.  In  the  fat  indolent  classes  it  is  0-150  per  cent.,  while  in  the  poorest 
classes  it  is  only  0-125  Per  cent.,  and  he  points  out  that  there  is  a  very  close 
relationship,  other  things  being  equal,  between  the  sugar  content  in  the  blood 
and  the  amount  of  fat  deposited  in  the  tissues,  which  again  is  a  dietetic  and 
not  a  climatic  effect. 

Effect  on  Digestion. — With  regard  to  the  alimentary  canal  there 
is  often  less  appetite  and  less  desire  for  animal  food,  and  greater 
demand  for  spiced  articles  of  diet,  all  of  which  show  a  tendency  to 
lower  power  of  digestion;  but  we  are  convinced  that  the  tropical 
hyperemia,  other  than  alcoholic,  is  a  myth,  and  we  base  this  state- 
ment on  a  large  number  of  clinical  and  pathological  observations 
spread  over  a  period  of  some  twenty-one  years. 

There  is,  however,  one  point  to  which  special  attention  should  be 
drawn,  and  this  is  to  the  danger  of  constipation  in  tropical  climates 
with  low  humidity,  and  to  the  necessity  of  imbibing  daily  a  suffi- 
ciency of  water  to  combat  the  loss  of  moisture  from  the  skin.  This 
tendency  to  constipation  in  healthy  people  in  very  hot  dry  climates 
is  usually  aggravated  by  the  difficulty  in  obtaining  fresh  vegetables 
and  fruits  in  those  regions  during  the  driest  times  of  the  year. 
Constipation,  if  allowed  to  become  chronic,  may  cause  passive 
hyperaemia,  but  this  is  pathological,  and  due  to  the  lack  of  free 
evacuation  of  the  bowels  and  not  due  directly  to  the  climate. 

Effect  on  the  Nervous  System. — It  appears  that  the  cells  of  the 
nervous  system  obey  the  general  law  that  vital  activity  is  increased 
with  a  higher  temperature,  but  only  up  to  a  certain  point,  after 
which  their  functional  activity  becomes  markedly  depressed.  This 
is  the  case  in  most  Europeans,  though  a  great  deal  of  mental  and 
physical  work  can  be  done  in  the  tropics  if  the  bodily  health  is 
maintained.  Natives  naturally  are  less  prone  to  feel  the  depressing 
effects  of  continuous  high  temperature. 

It  is  possible  that  this  condition,  together  with  the  effect  of  the 
actinic  rays  of  the  sun,  may  result  in  weakening  the  control  of  the 
higher  centres  over  the  lower,  and  thus  inducing  outbursts  of  what 
Plehn  calls  '  tropical  fury  '  (Tropenkohler),  by  which  he  means  fits 
of  passion  caused  by  trivial  incidents.  This  is  seen  not  only  in 
Europeans,  but  in  natives,  who  are  apt  to  do  violent  deeds  under 
the  impulse  of  unreasoning  anger.  It  appears  to  be  one  of  the 
causes  <>f  assaults  and  violent  crime  in  certain  parts  of  the  Tropics. 

Effect  upon  the  Urinary  System.-  -Urine  is  diminished  in  quantity 
in  the  tropics,  and  this  is  said  to  be  due  not  merely  to  diminution 
<>f  water,  but  also  of  solids,  among  which  urea  and  chlorides  may 
be  noticeably  mentioned.  Lawson  says  that  the  pigments  are 
increased. 

The  diminution  of  the  urine  is  very  markedly  noticed  in  hot  dry 


TEMPERATURE  AND  HUMIDITY  77 

climates  and  should  be  carefully  combated  by  drinking  a  sufficiency 
of  watery  fluids  because  of  the  danger  of  lithiasis. 

Effect  on  the  Generative  Organs. — The  generative  organs  act  more 
vigorously  in  the  tropics,  but  venereal  excess  is  distinctly  more 
deleterious  than  in  the  Temperate  Zone. 

Menstruation  begins  about  one  year  earlier  in  European  girls  living 
in  the  tropics  than  in  those  living  in  the  Temperate  Zone.  For 
instance,  it  begins  in  48-4  per  cent,  at  thirteen  to  fourteen  years  of 
age,  and  in  50-07  per  cent,  at  fifteen  to  sixteen  years  of  age. 
Eurasian  and  East  Indian  girls,  according  to  Das,  mostly  begin  to 
menstruate  at  thirteen  years  (54-8  per  cent.),  though  a  considerable 
number  do  so  at  twelve  years  (18 -6  per  cent.).  Natives  of  India 
mostly  begin  about  eleven  to  twelve  years  of  age  (63-51  per  cent.), 
and  high-caste  Indian  girls  begin  in  their  eleventh  year  (50  per  cent.) 
or  twelfth  year  (48  per  cent.);  but  this  early  menstruation  may  be 
associated  with  child-marriage  rather  than  climate.  Puberty  in 
boys  appears  at  an  earlier  age  than  in  temperate  climates. 

There  appears  no  reason  to  doubt  that  the  climacteric  is  a  more 
trying  time  for  the  European  woman  in  the  tropics,  and  tends  to 
produce  neurasthenia.  If  possible,  therefore,  such  a  woman  should 
be  sent  to  the  Temperate  Zone  during  this  period. 

It  is  possible  that  fertility  is  not  affected  in  Europeans,  though 
there  is  some  doubt  on  this  subject,  and  evidence  is  increasing  that 
it  greatly  decreases  after  the  second  or  third  generation.  Abortions 
are  said  to  be  more  common  in  the  European  in  the  tropics  than  in 
the  Temperate  Zone,  and  post-partum  haemorrhage  is  also  said  to 
be  more  common,  but  these  statements  require  careful  investiga- 
tion before  being  accepted. 

Effect  on  Growth. — Rattray  made  observations  on  the  weight 
and  growth  of  forty-eight  naval  cadets,  aged  from  fourteen  and  a 
half  to  seventeen  years,  during  four  successive  changes  of  climate 
during  a  voyage.  He  considered  that  they  grew  too  rapidly  and 
lost  weight  considerably  in  the  tropics,  and  that  their  strength  and 
health  was  impaired  by  the  heat. 

These  conclusions  of  Rattray's  are  of  the  greatest  importance, 
showing  clearly  the  necessity  (well  known)  of  sending  European 
children  as  soon  as  possible  to  live  in  the  Temperate  Zone,  not 
merely,  as  some  writers  assert,  for  education,  but,  much  more 
importantly,  for  their  health. 

Effect  on  the  Skin. — The  cutaneous  system  in  all  tropical  regions 
is  flushed  with  blood,  and  in  the  damper  parts  is  more  or  less  covered 
with  visible  sweat,  which  is  apparently  suitable  for  the  growth  of 
fungi. 

In  the  dry  hot  climates  the  skin  is  dry,  and  in  persons  who  possess 
few  layers  of  horny  cells  it  is  liable  to  become  inflamed  and  cracked. 
The  hair,  particularly  on  ladies  who  have  resided  some  time  in  the 
dry  tropics  without  a  change,  is  apt  to  fall  out. 


78  TROPICAL  CLIMATOLOGY 


PRESSURE. 


The  atmospheric  pressure  at  different  localities  scattered  all 
over  the  world  may  be  measured  by  the  barometer,  due  care  being 
taken  to  correct  the  reading  for  index  error,  capacity,  capillarity, 
temperature,  and  altitude;  and  the  data  so  obtained  may  be  entered 
on  a  map  of  Mercator's  projection  of  the  world,  and  hnally  points 
of  similar  pressure,  as  indicated  in  this  map,  may  be  joined  together 
by  curves,  thus  producing  an  isobaric  chart. 

The  result  of  this  investigation  shows  that,  generally  speaking, 
at  sea-level  there  is  high  pressure  at  about  30  degrees  north  or  south 
of  the  Equator,  and  that  from  this  the  pressure  decreases  towards 
the  Equator. 

The  reason  why  the  pressure  is  low  at  the  Equator  is  partially 
due  to  the  heating  of  the  air  by  the  sun's  rays,  but  more  especially  to 
the  considerable  addition  of  aqueous  vapour  to  the  air  in  these 
regions,  with  the  result  that  it  ascends  with  considerable  force, 
and  goes  on  ascending  to  very  high  altitudes,  owing  to  repeated 
warming  from  the  condensation  of  aqueous  vapour  and  the  liberation 
of  latent  heat. 

Though  the  pressure  at  30  degrees  is  higher  than  that  at 
the  Equator  at  sea-level,  it  is  considerably  less  than  at  higher 
altitudes.  Consequently  air  passing  upwards  from  sea-level  at 
the  Equator  into  higher  strata  will  then  flow  either  north  or  south 
towards  30  degrees;  but  as  it  flows  it  is  compressed  as  the  latitude 
increases,  and  hence  the  current  of  air  flowing  polewards  becomes 
narrower  and  narrower,  and  finally,  owing  to  this,  is  forced  down 
by  the  increasing  pressure,  until  it  reaches  sea-level  at  30  degrees 
north  or  south,  causing  the  high  pressure  about  this  latitude. 
This  compression  is  helped  by  the  cooling  of  the  air  as  it  proceeds 
polewards,  and  by  the  centrifugal  force  of  the  earth's  rotation. 

Apart  from  this  general  distribution,  there  are  diurnal  and  annual 
variations  in  the  pressure.  The  diurnal  variation  of  pressure  is 
best  marked  in  the  tropics,  diminishing  as  the  Poles  are  approached 
— e.g.,  at  Calcutta  it  is  0-12  inch,  whereas  at  Greenwich  it  is  only 
0-02  inch.  The  cause  of  this  diurnal  variation  is  the  heating  of  the 
air  by  the  sun,  but  there  is  also  another  cause,  producing,  according 
to  Blandford,  a  variation  of  o-i  inch  in  India,  and  acting  twice 
daily,  the  nature  of  which  is  not  known. 

The  cause  of  these  seasonal  variations  in  the  pressure  is  the 
heating  or  cooling  of  the  land,  which,  in  the  case  of  Colombo,  is 
associated  with  the  monsoons.  Thus,  the  low  pressures  occur  in 
the  season  of  the  south-west  monsoon,  May,  June,  and  July, 
when  air  is  travelling  from  high  pressure  at  the  Equator  to  low 
pressure  in  the  warm  plains  of  Asia;  and  the  high  pressures  are 
associated  with  the  north-east  monsoon,  when  air  is  travelling 
from  the  cold  plains  of  Asia,  where  it  is  at  considerable  pressure, 
towards  the  Equator,  where  the  pressure  is  less. 


PRESSURE  79 

Effects. 

The  effects  on  mankind  of  the  slighter  variations  of  atmospheric 
pressure  are  quite  unknown  and  unstudied,  scientifically,  as  far  as 
we  know,  though  the  subject  merits  careful  research.  It  is  possible 
that  they  are  without  effect,  because  they  decrease  with  altitude  in 
the  same  ratio  in  which  the  pressure  diminishes,  but  without  produc- 
ing any  obvious  effect  from  a  climatic  point  of  view.  When  atmo- 
spheric pressure  is  increased  considerably,  as  in  the  use  of  special 
apparatus  for  deep  diving  and  in  the  caissons  filled  with  compressed 
air  which  engineers  use  to  lay  the  underwater  foundations  of 
bridges,  then  a  series  of  symptoms  are  produced  which  are  called 
caisson  disease,  and  to  this  we  shall  refer  in  a  later  chapter,  as  the 
conditions  are  pathological  and  not  physiological. 

I'here  is  a!=>o  the  condition  of  diminished  atmospheric  pressure  which  is 
found  in  mountain  climates.  Thus,  if  the  pressure  at  sea-level  is  762  milli- 
metres of  mercury  at  250  C,  then  at  an  altitude  of  500  metres,  and  at  the  same 
temperature,  this  becomes  720;  at  1,000  metres  679;  at  2,000  metres  604; 
at  3,000  metres  536;  at  4,000  metres  475;  at  5,000  metres  420;  and  at  6,000 
metres  370.  But  if  the  temperature  at  5,000  metres  were  o°  C,  instead  of 
250  C,  then  the  pressure  would  be  394  millimetres,  and  at  6,000  metres  343 
millimetres ;  while  at  3,000  metres  it  is  517  at  o°  C,  and  536  at  250  C. 

It  must  therefore  be  noted  that  the  mean  pressure  is  not  the  same  at  similar 
altitudes  in  the  tropics  and  in  temperate  climates,  but  somewhat  higher. 

.Mankind  can  live  and  has  formed  permanent  habitations  in  Tibet  at  places 
over  4,900  metres  above  sea-level,  and  Hahn  states  that  in  the  Bolivian 
province  of  Chichas  people  live  at  an  altitude  of  5,000  metres. 

Hahn,  quoting  Poppig  and  Reck,  states  that  natives  living  on  the  high 
Andean  plateaus  suffer  from  certain  disagreeable  effects,  but  we  have  been 
unable  to  find  what  they  mean  exactly  by  this  expression. 

Mountain  sickness  belongs  to  the  pathological  portion,  and  will  therefore 

be  considered  later;  and  all  we  can  write  with  regard  to  the  physiological 

of  pressure  is  to  invite  the  attention  of  observers,  who  live  at  or  visit 

high  altitudes,  to  the  great  lack  of  accurate  information  with  regard  to  these 

matters. 

WINDS. 

I  tie  motion  of  the  air  in  passing  from  regions  of  high  to  those  of 
low  pressure  constitute  the  winds,  which  may  be  classified  into  per- 
manent, periodical,  variable,  and  local. 

Permanent  winds  are  caused  by  the  expansion  of  the  hot  equa- 
torial air  which  rises  to  high  altitudes  and  passes  polewards. 

If  Fig.  7,  which  demonstrated  Ferrell's  latest  ideas  as  to  the 
circulation  of  the  air,  be  studied,  in  general  it  will  be  noticed  that 
the  zones  of  equatorial  calms  and  rains  are  indicated,  as  well  as 
the  zones  of  subtropical  calms  and  drought. 

The  unbroken  arrows  indicate  the  surface  winds,  and  the  broken 
arrows  the  upper  currents.  The  margin  of  the  circle  shows  a  vertical 
section  of  the  atmosphere  in  which  the  arrows  indicate  the  move- 
ments.    The  equatorial  area  is  marked  in  the  centre. 

If  this  figure  be  carefully  examined,  it  will  be  seen  rom  the  section 
of  the  atmosphere  on  the  sides  of  the  figure  that  the  heated  aii 
rises  over  the  Equator  to  high  altitudes,  and  flows  to  the  poles; 


8o 


TROPICAL  CLIMATOLOGY 


but  at  lesser  altitudes  it  descends  in  the  region  of  subtropical  calms, 
and  either  passes  polewards  or  to  the  Equator.  Within  the  area 
from  o  to  30  degrees  there  are  winds  called  the  '  trades,'  which 
blow  from  30  degrees  towards  the  Equator,  and  which  on  reference 
to  Fig.  6,  can  be  noted  as  north-east  trades  and  south-east  trades, 
and  it  will  also  be  observed  that  the  only  portion  of  the  ocean 
free  from  them  is  the  North  Indian  Ocean,  where  the  south- 
west monsoons  occur.  The  north-east  monsoon  is  really  a  trade- 
wind. 

Further,  it  will  be  noted  that  as  the  air  moves  in  opposite  direc- 
tions along  the  surface  in  the  region  of  latitude  35  degrees,  there  is 
an  absence  of  prevailing  winds.     These  belts  of  calms  are  called  '  the 


orial  Cairo?  undRains 


Fig.  7. —  Diagram  of  the  Circulation  of  the  Atmosphere. 
(After   Ferrell.) 

subtropical  belts,'  or  the  calms  of  Cancer  and  Capricorn.  Again,  at 
the  Equator  there  are  calms  for  the  same  reason,  and  these  are  often 
called  '  the  doldrums.' 

The  trade-winds  are  only  to  be  seen  typically  in  oceanic  n  gions, 
where  the  temperature  is  equable,  and  there  are  no  local  conditions 
to  cause  them  to  deviate  from  their  course.  But  they,  together 
with  their  intermediate  zones  of  calms,  shift  their  positions  according 
to  the  temperature,  having,  therefore,  different  areas  in  such  months 
as  March  and  September.  On  an  average  the  north-east  trades 
extend  from  7  degrees  to  29  degrees  north  in  the  Atlantic,  and  the 
south-east  to  20  degrees  south.  During  the  summer  they  advance 
a  few  degrees  north,  and  in  the  winter  recede  to  the  south.  In 
spring  the  centre  of  the  doldrums  is  only  1  to  2  degrees  north  of 


WINDS  81 

the  Equator,  while  in  summer  it  is  about  c,  or  10  degrees  north 
latitude,  and,  as  will  be  explained  later,  the  tropical  rains  of  certain 
regions  depend  upon  this  movement.  Their  easterly  direction  is 
due  to  the  rotation  of  the  world. 

Periodical  winds  arc  the  movements  of  the  air  produced  by  the  alternate 
heating  (by  the  sun)  and  cooling  of  large  tracts  of  lands,  and  the  most  important 
of  these  are  the  monsoons,  to  which  reference  has  already  been  made. 

Variable  winds  are  found  in  the  regions  of  calms  interposed  between  the 
trades  in  the  Atlantic  and  Pacific  Oceans. 

Local  winds  are  of  great  importance  in  the  tropics,  constituting  the  so- 
called  land  wind,  sea  breeze,  mountain  wind,  etc.,  and  several  others  to  be 
red  to  later,  to  which  special  local  names  have  been  given. 

The  wind  about  which  a  great  deal  is  spoken  in  every  tropical  country  is 
'  the  land  wind.'  During  the  day  the  land  becomes  heated  by  the  sun,  and 
causes  the  air  to  rise,  thus  lessening  the  pressure,  and  drawing  the  air  from  the 
sea,  causing  a  sea  breeze,  which  is,  of  course,  very  humid.  During  the  night, 
however,  by  terrestrial  radiation,  the  land  becomes  cooler  than  the  sea,  and 
the  air  travels  from  the  land  to  the  sea,  and  constitutes  the  land  wind.  This 
wind,  as  a  rule,  is  dry,  and  has  a  very  deleterious  effect  on  men  and  animals 
bv  extracting  moisture  and  abruptly  cooling  the  body,  and  thereby  lowering 
the  resisting-power  to  disease.  Hence  the  complaints  made  by  old  residents 
about  the  land  breezes.  On  the  other  hand,  new-comers  delight  in  them, 
because  they  are  so  cool. 

This  land  wind  is  more  marked  at  certain  seasons  of  the  year  than  at  others, 
being  particularly  felt  in  Colombo  in  those  months  when  there  is  less  cloud, 
because  the  terrestrial  radiation  is  then  more  marked.  There  is,  however, 
nothing  like  a  definite  season  for  a  pronounced  land  wind,  for  it  can  take  place 
at  any  time,  only  depending  upon  terrestrial  radiation. 

A  few  remarks  may  be  useful  with  regard  to  some  local  winds: — 

The  Sirocco  (Italian,  scirocco). — The  sirocco  is  a  south-east  wind  with  a 
high  temperature,  which,  coming  from  the  high  land  of  North  Africa,  descends 
to  the  Mediterranean,  and  may  reach  Malta  and  some  parts  of  Italy.  It  is 
considered  to  be  very  enervating. 

The  Solano. — The  solano  is  a  south-easterly  wind,  blowing  from  the  Sahara 
into  Spain. 

The  Harmattan. — The  harmattan  is  a  hot  easterly  wind,  coming  from  the 
Sahara  Desert,  and  carrying  dust  far  out  into  the  Atlantic 

In  the  months  of  November  to  March  this  wind  meets  with  the  north- 
east trade  in  its  most  southerly  position,  with  the  result  that  it  is  deflected 
southwards  down  the  west  coast  of  Africa.  It  is  a  very  dry  wind,  and  there- 
fore extracts  moisture  from  everything  it  comes  across.  Hence  human  beings 
feel  their  skin  dry  and  hard,  and  may  suffer  from  bleeding  from  the  nose 
and  lips,  while  furniture  creaks  and  groans  in  a  most  supernatural  manner. 

The  Khamsin. — The  khamsin,  or  khamseen,  is  the  dust-laden  wind  which 
blows  from  the  Sahara  into  Egypt  at  intervals  during  fifty  days  about  Easter- 
time,  and  is  very  disagreeable,  especially  when  associated,  as  it  often  is,  with 
high  air  temperatures,  when  it  may  produce  pathological  changes  in  persons 
in  poor  health  situate  in  places  unsuitable  for  bearing  heat,  such  as  railway 
trains. 

Pamperos. — These  are  the  south-westerly  winds  of  Brazil.  Europeans  have 
altered  the  significance  of  the  name  to  squally  cyclonic  winds  in  the  same 
vicinity. 

Ghibli. — The  ghibli  is  a  violent  south  or  south-east  wind  blowing  into 
Tripoli  from  the  desert,  and  carrying  with  it  a  quantity  of  sand,  which  causes 
irritation  to  the  conjunctivae  and  which  may  induce  nervous  symptoms. 

The  Foehn. — Though  essentially  a  temperate  or  cool  climate  wind,  still  the 
foehn  exists  in  the  tropics.  The  foehn  is  to  be  seen  in  its  home,  Switzerland, 
as  a  warm  dry  wind  which  blows  with  great  violence  downwards  from  the  crest 
of  the  Alps,  and  has  marked  effects  upon  man  and  animals,  as  it  has  a  depress- 
ing effect  upon  the  mind  and  the  nervous  system.     It  was    thought  at  one 

6 


82 


TROPICAL  CLIMATOLOGY 


time  that  this  wind  came  from  the  Sahara,  but  all  evidence  is  against  this, 
and  the  present  idea  is  that  it  is  a  local  wind  which  is  produced  by  a  high 
south-east  and  a  low  north-west  pressure,  and  attains  its  high  temperature 
as  well  as  its  dryness  in  its  descent  from  the  summits  of  the  Alps  on  their 
northern  side,  and  less  typical  on  the  southern  aspect  when  the  pressure  is 
high  in  the  north-west  and  is  low  in  the  south-east. 

Foehn-like  winds  occur  in  Trebizond,  and  on  Lake  Urmia,  in  Persia,  where 
it  is  called  samitm,  and  blows  down  the  eastern  side  of  the  New  Zealand  Alps 
on  to  the  Canterbury  Plains. 

It  also  occurs  at  Resht,  on  the  southern  shores  of  the  Caspian  Sea;  also  in 
South  Georgia,  as  well  as  in  the  Andes  and  at  Kanazawa  in  Japan. 

We  have,  above,  given  the  usual  explanation  of  the  sirocco,  but  it  must 
be  noted  that  it  is  probably  a  '  foehn  '  wind,  for  Bridone,  many  years  ago, 
noted  that  in  Sicily  it  could  not  possibly  come  from  the  Sahara,  because  it 
would  have  been  most  violent  on  the  south  coast,  whereas  it  is  actually  at  its 
greatest  violence  on  the  north  coast,  especially  at  Palermo. 

The  '  sirocco  di  Levante,'  between  Pylos  and  Kyporissia,  is  also  a  '  foehn  ' 
wind,  as  is  the  sirocco  of  Algiers,  and  probably  the  solano  of  Spain  and  the 
vent  d'Espagne  on  the  northern  aspect  of  the  Pyrenees. 

Cyclonic  Storms. — Besides  ordinary  winds,  cyclonic  disturbances  called 
storms  occur.  Cyclonic  storms  receive  different  names  in  various  parts  of 
the  world,  being  called  cyclones  in  India,  Ceylon,  and  Mauritius,  hurricanes 
in  the  West  Indies,  typhoons  in  the  China  Seas.  Mild  cyclonic  storms  met 
with  on  the  West  Coast  of  Africa  and  elsewhere  are  called  tornadoes. 


Electrical  Conditions. 

Silent  electrical  discharges  are  frequent  in  the  tropics,  and  the 
acidity  which  they  produce  is  supposed  to  be  the  cause  of  devitrifica- 
tion, which  is  so  trying  to  persons  working  with  all  except  the  best 
microscopical  and  other  lenses. 

Thunderstorms  of  astonishing  violence  are  frequent  in  many 
parts  of  the  tropics,  and  generally  cool  the  atmosphere  for  the  time. 

It  is  a  popular  belief  that  the  electrical  condition  of  the  atmosphere 
has  some  influence  upon  life,  but  if  this  is  so  then  it  is  an  untrodden 
field,  as  far  as  we  know,  for  we  have  been  unable  to  find  any  definite 
scientific  observations  which  can  confirm  or  refute  the  popular 
belief.  Hahn  considers  that  there  is  no  indication  that  atmospheric 
electricity  plays  a  notable  part  in  climatology. 

Sun's  Rays. 

Sunlight  contains  heat  rays  (red),  light  rays  (yellow),  and  chemical 
rays  (blue,  violet,  and  ultra-violet);  that  is  to  say,  rays  extending 
from  the  infra-red  to  as  far  as  291  jujll  in  the  ultra-violet  (Gibbs), 
but  is  much  influenced  by  latitude,  longitude,  altitude,  and  the  daily 
and  hourly  varying  local  meteorological  conditions. 

These  rays  reach  the  earth,  according  to  Langley,  in  the  following 
percentages : — 


Ultra-violet 

Violet 

Blue 

Greenish-blue 

Yellow 

Red 

Infra-red 


Per  Cent . 

39 
42 
48 
54 
03 
70 
76 


SUN'S  RAYS  83 

Freer,  Gibbs,  and  Bacon  have  shown  that,  though  the  tropical 
light  of  Manila  contains  few,  if  any,  more  ultra-violet  rays  than  the 
Temperate  Zone,  still  the  chemical  rays  have  more  effect  there 
than  in  a  temperate  climate,  and  these  effects  vary  on  different 
days.  Freer  distinguishes  '  actinic  '  and  '  non-actinic  '  days,  on 
both  of  which  the  sky  may  be  equally  clear.  The  cause  of  the 
difference  between  an  actinic  and  non-actinic  day  is  not  under- 
stood. Gibbs  does  not  believe  that  the  normal  intensities  of  the 
light  in  the  tropics  is  different  from  that  of  any  other  region,  the 
influence  of  local  meteorological  conditions  being  excluded,  the 
most  important  of  these  being  the  humidity.  Aron  suspects  that 
the  deleterious  influence  of  tropical  sunlight  is  due  to  the  long 
heat  waves  rather  than  to  the  short  chemical  waves,  which  we  will 
now  consider. 

The  chemical  rays  appear  to  have,  first,  a  stimulative  and 
beneficial  influence,  and,  secondly,  a  harmful  influence. 

Stimulative  Influence. — Finsen,  by  experiments  upon  tadpoles, 
earthworms,  beetles,  flies,  etc.,  came  to  the  conclusion  that  the 
action  of  the  chemical  or  blue-violet  rays  was  very  considerable  as 
compared  with  light  (yellow)  or  heat  (red)  rays,  and  that,  though 
their  action  was  probably  very  complex,  still,  it  could  be  best 
considered  as  an  excitation  of  the  nervous  system. 

This  excitation  was  so  powerful  as  to  produce  reflex  actions  in 
tadpoles  and  movements  in  other  animals,  while  in  man  he  con- 
siders them  to  be  the  cause  of  the  feeling  of  bien-etre  experienced  on 
a  bright,  sunny  day,  which  he  compares  with  the  depression  felt 
on  a  dark,  cloudy  day. 

Bactericidal  Properties. — Downes  and  Blunt  in  1877  showed  that 
the  chemical  rays  could  kill  bacteria,  while  D'Arsonval  and  Charrain 
showed  that  they  could  kill  the  Bacillus  pyocyaneus.  In  1903 
Bernard  and  Morgan  demonstrated  that  it  was  the  middle  third  of 
the  ultra-violet  portion  of  the  spectrum  which  caused  these  bac- 
tericidal effects. 

Harmful  Influences — Acute  Skin  Irritation.— Charcot  in  1859 
first  expressed  the  opinion  that  it  was  the  chemical  and  not  the 
heat  rays  which  produced  sunburn,  and  showed  that  the  dermatitis 
caused  by  strong  electric  light  was  identical  with  that  caused  by  the 
sun. 

In  1889  Widmark  proved  this  definitely  by  using  an  electric  arc 
of  1,200  candle-power,  the  light  of  which  was  first  passed  through 
water  to  absorb  the  heat  rays,  and  then  allowed  to  fall  upon  the 
Shaven  skin  of  a  white  rabbit,  when  the  characteristic  inflammation 
resulted.  He  then  interposed  a  plate  of  ordinary  glass  to  exclude 
the  ultra-violet  rays,  when  the  skin  remained  unaffected. 

In  1901  Finsen  placed  on  the  flexor  surface  of  his  forearm  a  plate 
of  rock-crystal  and  pieces  of  different-coloured  glass,  and  also  wrote 
his  initials  in  Indian  ink.  He  then  exposed  the  arm  to  the  rays 
from  an  80-ampere  arc  for  twenty  minutes,  ten  minutes  at  a  distance 
of  50  metres  and  ten  minutes  at  75  metres.     The  result  was  that 


84  TROPICAL  CLIMATOLOGY 

first  all  parts  were  slightly  influenced  by  the  heat,  and  then  those 
parts  which  were  unprotected  or  covered  with  rock-crystal  became 
red  and  inflamed,  and  later  desquamated  and  became  pigmented, 
while  the  parts  covered  by  glass  and  Indian  ink,  after  the  slight 
initial  inflammation  due  to  the  heat,  did  not  further  react.  This 
experiment  is  interesting  as  showing  that  the  effects  due  to  heat 
appear  at  once  and  pass  off  quickly,  while  those  due  to  the  chemical 
rays  do  not  begin  until  after  a  lapse  of  three  hours,  which  agrees 
with  the  well-known  fact  that  a  sunburn  takes  some  time  to  develop. 

Freund,  as  the  result  of  his  experiments,  concluded  that  the 
chemical  rays  penetrated  into  the  skin.  Bernard  and  Morgan  found 
that  the  ultra-violet  rays  were  the  active  agent  in  producing  sun- 
burn. 

The  histology  of  solar  erythema  is  not  well  known.  Leredde  and 
Pantrie  made  a  biopsy  on  the  skin  of  the  shoulder  of  one  of  their 
friends  who  was  suffering  from  sunburn  of  three  days'  duration. 
The  skin  was  in  a  condition  of  acute  erythema,  without  oedema  or 
effusion.  Under  a  low  power  of  the  microscope  the  epidermis 
appeared  normal  in  thickness  and  disposition,  but  the  horny  layer 
was  exfoliated  in  places.  The  dermis  was  richer  than  normal  in 
cellular  elements,  and  the  connective-tissue  bundles  were  swollen. 
Under  a  higher  power  the  intercellular  spaces  appeared  larger  than 
normal.  The  vessels  of  the  dermis  were  dilated,  and  there  was 
a  slight  leucocytic  infiltration,  while  the  connective-tissue  cells  were 
swollen.  These  appearances  are  exactly  like  those  produced  by  the 
rays  of  an  electric  light. 

If  the  sun's  action  stops  at  this,  the  only  change  will  be  the 
deposit  of  the  yellowish-brown  pigment  in  the  skin  so  well  known 
in  the  tropics.  If,  however,  the  action  is  more  intense,  an  exuda- 
tion appears,  which  may  be  sero-fibrinous,  cellular,  or  bloody,  while 
the  depth  to  which  these  changes  may  extend  depends  upon  the 
intensity  of  the  light.  The  epithelium  becomes  swollen,  and  bullae 
may  form,  and  the  connective  tissue  of  the  dermis  be  swollen. 

The  pigmentation  of  the  epidermis  is  important,  and  will  be 
referred  to  at  greater  length  in  the  next  section. 

Chronic  Skin  Irritation.— The  chronic  effects  produced  on  the 
skin  by  the  chemical  energy  of  light  are  :— 

(i)  Pigmentation. 

(2)  Vascular  modification. 

(3)  Disease. 

(r)  Pigmentation. — It  is  well  known  that  pigmentation  follows 
sunburn,  but  until  recently  it  was  not  evident  that  it  was  of  a 
protective  nature. 

In  1888  Wedding,  confirmed  by  Charcot,  first  made  this  point 
clear,  though  Unna  in  1885  was  the  first  to  say  that  it  was  to  be 
regarded  as  useful,  inasmuch  as  it  prevented  the  rays  penetrating 
too  deeply,  thus  preventing  inflammation. 

In  1896  Finsen  painted  a  black  ring  2  inches  wide  round  his  arm 


SUN'S  RA  YS  85 

with  Indian  ink  to  imitate  the  colour  of  a  negro's  skin,  and  then 
exposed  it  for  three  hours  to  a  very  hot  sun.  For  a  time  the  skin 
remained  normal,  showing  only  a  little  redness  at  the  edge  of  the 
black  paint,  but  in  due  course  it  became  red  and  inflamed,  except 
where  it  had  been  painted  black.  After  several  days  the  erythema 
disappeared,  and  the  area  which  had  been  red  was  noticed  to  have 
become  distinctly  pigmented,  or,  in  plain  language,  was  sunburnt. 

He  then  exposed  it  again  to  the  sun,  but  this  time  the  area  which 
had  originally  been  covered  with  Indian  ink  was  unprotected. 
The  result  was  that  this  part  became  red  and  inflamed,  while  the 
pigmented  area  was  unaffected,  except  that  it  became  a  little  more 
pigmented. 

This  experiment  of  Finsen's  shows  that  the  colour  of  native  races 
living  in  the  tropics  is  protective,  and  was  possibly  originally  induced 
by  the  sun.  Sambon  and  Baly  found  that  the  ultra-violet  rays  were 
entirely  absorbed  by  a  pigmented  piece  of  skin,  and  therefore  support 
the  theory  that  pigmentation  affords  an  efficient  natural  protection 
against  ultra-violet  rays. 

Dyson  studied  cutaneous  pigmentation  in  1911,  and  concluded  that  the 
formation  of  melanotic  pigment  was  a  normal  function  of  the  nuclei  of  the 
epidermal  cell,  metabolism  being  due  to  a  lipochrome,  in  which  melanin  is 
the  chromatic  protein  portion.  This  pigment  passes  to  the  cutis  by  way  of 
the  lymph  stream.  The  formation  of  the  pigment  can  be  increased  by  agents 
such  as  light,  heat,  and  toxins,  but  the  increase  is  usually  transitory  and  tends 
to  disappear;  but  if  there  is  deficient  drainage  of  the  lymph  from  the  cutis 
the  pigment  accumulates,  and  unless  the  drainage  is  improved  tends, to  become 
progressively  worse.  Decreased  vitality  of  the  cells  may  possibly  cause  the 
overproduction  of  pigment  due  to  diminution  in  nutrition,  but  if  the  cells 
become  functionally  inactive  then  pigment  production  ceases,  and  the  existing 
pigment  being  carried  away  by  the  blood-stream,  the  part  becomes  depig- 
mented, which  is  probably  the  case  in  vitiligo,  in  which,  after  hyperpigmenta- 
tion,  the  skin  becomes  depigmented. 

That  the  dark  pigmentation  is  useful  is  shown  also  by  the  observa- 
tion made  by  us  on  various  occasions  that  natives  suffering  from 
leucoderma  avoid  going  into  the  sun,  as  they  state  that  the  unpig- 
mented  portions  of  the  skin  become  inflamed  and  painful.  In  this 
connection,  an  interesting  case  showing  the  importance  of  these  rays 
came  under  our  notice.  A  native,  who  had  developed  large  leuco- 
dermic  patches  involving  the  whole  of  the  face,  noticed  that 
he  could  no  longer  work  in  the  sun,  as  each  time  he  tried  to  do  so  the 
patches  became  painful  and  he  felt  sick,  very  weak,  and  giddy,  and 
therefore  asked  to  be  relieved  of  his  outdoor  duties;  but  it  was  held 
that  he  was  still  fit  to  discharge  his  ordinary  duties,  with  the  result 
that  the  unfortunate  man  was  compelled  to  resign  his  appointment 
a  few  months  later.  It  is  therefore  well  that  the  importance  of 
skin  pigmentation  should  be  more  widely  known. 

Generally  speaking,  in  regions  where  the  sunlight  is  very  intense  the  race 
is  densely  pigmented.  As  a  rule,  the  people  who  live  nearer  the  Equator 
are  more  pigmented  than  those  farther  away — e.g.,  the  black  colour  of  the 
West  African  can  be  compared  with  the  red  of  the  American  Indian  or  the 
yellow  of  the  Chinese.     But  this  rule  is  not  without  exceptions,   for   the 


86  TROPICAL  CLIMATOLOGY 

Sinhalese,  living  nearer  the  Equator,  are  distinctly  less  pigmented  than  the 
Tamils  of  the  warmer  regions  of  Jaffna  and  South  India. 

There  is  also  not  the  slightest  doubt  that  the  European  living  in  tropical 
countries  becomes  darker,  a  fact  which  specially  applies  to  the  descendants 
of  the  settlers.  On  the  other  hand,  according  to  Finsen,  the  dark  colour  of 
the  negro  diminishes  to  a  sensible  degree  in  Europe. 

It  must  be  noted,  however,  that  a  certain  number  of  Europeans  do  not 
become  sunburnt  in  the  tropics.  On  the  contrary,  their  skin,  especially  in 
localities  where  the  climate  is  damp  and  hot,  may  take  a  peculiar  whitish 
colour,  even  in  cases  in  which  the  blood  examination  does  not  reveal  any 
sensible  decrease  in  the  amount  of  haemoglobin.  As  a  result  of  an  extended 
series  of  observations  made  by  medical  officers  in  the  Philippine  Islands, 
Chamberlain  reports  that  the  red  cell  counts  averaged  5,200,000  per  cubic 
millimetre  in  healthy  American  soldiers,  averaging  twenty-six  years  of  age, 
after  twenty  months'  service  near  sea-level,  which  count  does  not  differ  from 
the  normal  as  at  present  recognized  for  healthy  young  men  in  the  Temperate 
Zone.  The  haemoglobin  averaged  89-6  per  cent.,  and  the  colour  index  o*86 
to  0-87,  both  of  which  were  a  little  low,  but  not  sufficiently  so  to  indicate  a 
definite  anaemia.  He  believes  that  the  pallor  mentioned  above  is  as  a  rule 
due  to  a  superficial  ischaemia. 

The  effect  of  tropical  light  on  man  has  been  made  the  subject  of  a  special 
memoir  by  Woodruff,  who  points  out  that  all  over  the  globe  the  people  who 
live  nearer  the  poles  are  blonder  than  those  residing  near  the  Equator.  He 
thinks  that  insufficient  pigmentation,  by  permitting  the  penetration  of  the 
chemical  rays,  conduces  to  the  increased  activity  of  the  mind  and  vigour 
in  the  muscles  which  is  found  in  new-comers  in  the  tropics.  This  condition 
of  excitation  causes  them  to  overdo  themselves  sooner  or  later,  and  so  to 
produce  a  feeling  of  exhaustion  which  he  describes  as  tropical  exhaustion. 

He  further  considers  that  white  men  cannot  become  acclimatized  in  the 
tropics,  and  also  that  they  should  be  protected  by  clothing  opaque  to  the  blue 
and  ultra-violet  rays.  For  this  purpose  he  savs  that  the  outer  clothing  should 
be  white,  grey,  or  yellow,  because  heat  will  be  least  absorbed  by  these  colours, 
while  the  underclothing  should  be  black  or  yellow,  to  stop  the  ultra-violet 
rays.  For  office-workers  and  others  not  exposed  to  the  direct  sun-rays  he 
advises  black  or  dark  blue,  but  he  states  that  it  is  not  known  whether  blue 
or  black  excludes  the  ultra-violet  rays. 

He  also  strongly  advises  opaque  head-gear,  as  he  says  it  is  surprising  how 
transparent  the  scalp  and  skull  are  to  light  rays,  and  that  it  is  certain  that  the 
ultra-violet  rays  pass  through  them. 

He  points  out  the  nuisance  of  the  glare  from  houses  painted  white  in  the 
tropics,  and  mentions  the  better  colours  of  green,  dark  yellow,  and  brown. 
The  gradual  disappearance  of  the  white  buildings  in  the  business  pari  of 
Colombo,  and  the  appearance  of  new  buildings  coloured  brown,  indicates  the 
correctness  of  his  views. 

While  it  is  not  possible  to  agree  with  all  or  even  with  many  of  Woodruff's 
statements,  there  is  no  doubt  whatever  that  there  is  a  great  general  truth  in 
what  he  says,  though  many  of  the  matters  upon  which  he  touches  arc  purely 
speculative. 

On  the  other  hand,  there  is  most  urgent  need  for  protection  from 
sunlight  both  as  regards  the  eyes  and  the  whole  body.  With  regard 
to  the  effect  of  the  tropical  sun  on  man  and  animals,  some  most 
interesting  experiments  have  been  performed  in  the  Philippine 
Islands  by  Aron  and  Gibbs  separately.  Rabbits  and  monkeys— 
i.e.,  animals  with  limited  power  of  physical  heat  regulation — die  if 
exposed  to  the  sun's  rays.  The  body  temperature  of  these  animals 
rises  to  febrile  heights,  while  the  post-mortem  reveals  haemorrhages 
into  the  meninges,  and  in  the  case  of  monkeys  into  the  heart.  If, 
however,  the  increase  of  heat  absorbed  from  the  sun's  radiation  is 


SUN'S  RAYS  87 

compensated  by  increased  loss  from  the  animal  by  such  means  as  a 
strong  wind,  the  animal  suffers  no  discomfort.  Insolation  of  the 
skull  alone  is  without  effect  if  the  body  temperature  is  kept  within 
normal  limits.  Our  own  experiments  showed  that  rabbits  died 
in  about  an  hour  if  exposed  to  the  sun  with  their  head  shaven, 
and  lived  if  protected  from  these  rays  by  means  of  red  glass.  Aron 
and  Gibbs  have  also  shown  that  if  the  human  skin  is  exposed  to  the 
sun's  rays  the  temperature  of  the  area  so  exposed  rises  as  a  rule  more 
rapidly  and  reaches  a  higher  maximum  in  a  dark  skin  than  in  a 
light,  until  the  nerve  endingls  of  the  latter  are  irritated  by  the  pro- 
longed exposure.  The  black  skin  is  protective  because  it  guards 
the  nerve  endings  from  irritation,  and  because  of  the  more  rapid 
radiation  by  means  of  which  heat  is  quickly  lost,  especially  from  the 
area  in  the  shade,  which  is  usually  greater  in  extent  than  the  part 
in  the  sunlight.  Further,  it  is  probable  that  the  relatively  greater 
number  of  sweat  glands  in  the  dark  skin  is  also  protective.  The  air 
in  the  human  hair,  especially  in  black  hair,  under  the  influence  of 
the  tropical  sun  acquires  exceedingly  high  temperatures.  There  is 
not  the  slightest  doubt  that  the  pigmentation  of  native  races  is 
protective,  and  that  the  older  theories  of  Waltz  that  carbon  was 
deposited  in  the  tissues  owing  to  imperfect  oxidation  due  to  heat, 
and  that  of  Darwin  that  it  was  due  to  a  survival  of  those  best  fitted 
to  withstand  tropical  disease — for  he  believed  that  pigmentation 
prevented  the  native  from  being  attacked  by  the  fatal  miasmata  of 
the  country — -cannot  now  be  seriously  considered. 

As  to  the  origin  of  the  pigment,  this  question  must  be  considered 
as  far  from  settled.  There  are  two  possible  sources  for  the  melanin, 
viz. : — 

(a)  The  haemoglobin  of  the  blood. 

(b)  The  cells  of  the  epidermis. 

(a)  The  Hcemoglobin. — This  theory  suggests  that  haemoglobin  is 
altered  into  melanin  either  in  the  blood-stream,  in  the  connective- 
tissue  cells,  or  in  special  melanoblasts,  which  by  amoeboid  movement 
take  the  pigment  to  the  epidermis. 

(b)  The  Cells  of  the  Epidermis. — -This  theory  states  that  melanin 
is  manufactured  in  situ  by  the  epithelial  cells,  and  is  not  derived 
from  haemoglobin,  and  in  view  of  the  histology  given  above  this 
appears  to  be  probably  the  correct  solution  of  the  problem. 

Melanosis,  which  varies  from  mere  freckles  through  the  diffuse 
yellow  and  brown  pigmentation  to  the  jet-black  of  the  African 
negro's  skin,  is  caused  by  melanin  granules  lying  in  and  between 
the  cells  of  the  epidermis. 

With  regard  to  the  pigmentation  of  different  races,  it  must  be 
remembered  that  it  is  only  absent  in  albinos,  and  that  it  occurs  in 
the  epidermis  of  the  areolae  and  mammillae  of  the  breast,  the  scrotum, 
labia  majora,  and  around  the  anus  in  white  races,  being  contained 
chiefly  in  the  large  basal  cells  of  the  Malpighian  layer,  and  to  much 
less  extent  in  the  more  superficial  layers,  and  the  connective-tissue 


88  TROPICAL  CLIMATOLOGY 

cells  of  the  papillary  layer  of  the  corium.     In  negroes  the  pigmenta- 
tion is  deeper  and  more  diffusely  spread  in  the  epidermis. 

(2)  Vascular  Modification. — Associated  with  pigmentation  there 
is  said  to  be  a  persistent  dilatation  of  the  vessels  and  capillaries  of 
the  skin,  and  it  is  stated  that  hair  and  nails  grow  more  rapidly  in 
the  tropics  than  in  the  Temperate  Zone. 

Light  in  general  is  believed  to  have  an  effect  upon  the  blood, 
which  absorbs  the  violet  and  ultra-violet  rays,  and  the  red 
corpuscles  under  these  influences  probably  absorb  more 
oxygen. 

(3)  Disease. — With  regard  to  disease,  there  appears  to  be  no 
reason  to  doubt  that  the  irritating  effect  of  light  has  at  least  a  part 
in  the  aetiology  of  Kaposi's  disease  {Xeroderma  pigmentosum), 
which  we  have  met  with  in  the  tropics,  where  it  would  naturally 
develop  rapidly  in  children  prone  to  the  disease. 

There  is  also  no  doubt  that  these  rays  play  a  part  in  the  pro- 
duction of  the  erythema  of  pellagra,  as  will  be  described  later  on, 
and  they  may  have  some  effect  in  producing  sunstroke. 

Woodruff  draws  attention  to  the  almost  universal  neurasthenia 
of  white  men  in  the  tropics,  among  whom  he  says  insanity  is  more 
common  than  in  Temperate  Zones.  In  support  of  the  latter  state- 
ment, he  asserts  that  the  insanity  rate  in  the  Philippine  Army  in 
1901  was  2-02  per  mille,  while  in  the  United  States  from  1889-1898  it 
was  1-13;  but  he  remarks  that  the  diagnosis  was  not  confirmed  on 
the  arrival  of  several  of  the  Philippine  soldiers  in  the  United  States, 
as  they  recovered  en  route.  He  draws  attention  to  the  loss  of 
memory  in  the  tropics  {tropical  amnesia),  a  condition  which  is  very 
prevalent  on  the  West  Coast  of  Africa,  being  often  called  '  coast 
memory.'  He  also  mentions  the  midday  siesta  as  useful  in  pre- 
venting this  neurasthenia,  and  in  this  he  is  also  probably  correct, 
especially  for  ladies.  Ordinary  officials  and  business  men,  however, 
cannot  afford  to  rest  in  the  middle  of  the  day. 

Moon's  Rays. — The  extravagant  stories  by  old  writers,  and 
especially  the  tales  given  by  sailors  with  regard  to  the  influence  of 
the  rays  from  the  full  moon,  have  thrown  such  discredit  upon  this 
subject  that  we  have  been  unable  to  find  any  literature  seriously 
considering  the  effects  of  its  rays  upon  man. 

Nevertheless,  in  our  own  experience,  the  rays  of  the  full  moon 
do  produce  headache  and  a  certain  amount  of  nervous  irritability  in 
persons  who  sleep  in  the  open.  The  subject  requires  and  deserves 
scientific  study. 

ACCLIMATIZATION. 

Plehn  seems  to  have  been  the  first  careful  observer  clearly  to  prove 
that  the  changes  induced  in  the  new-comer  as  he  enters  the  tropics 
in  due  course  disappear,  and  his  organs  becoming  accustomed  to  the 
new  work  demanded  from  them,  he  virtually  returns  to  the  same 
condition  of  temperature,  respiration,  etc.,  as  in  the  Temperate 
Zone — in  other  words,  becomes  acclimatized.     Further,  if  constantly 


A  CCLIMA  TIZA  TION  89 

exposed  to  the  sun's  rays,  his  skin  is  apt  to  become  more  pigmented 
than  normal,  and  to  afford  a  certain  degree  of  protection  against 
its  rays. 

Sambon  pointed  out  long  ago  that  if  proper  sanitary  and  other  measures 
against  disease  were  introduced  into  the  tropics,  and  if  care  were  taken  with 
regard  to  food,  drink,  excessive  heat,  and  the  rays  of  the  sun,  there  is  no  reason 
why  the  European  should  not  live  healthily  in  these  regions;  and  this  is  true 
to  a  certain  extent,  but  in  our  experience  the  length  of  residence  must  be 
considered,  as  even  with  every  care  he  may  become  debilitated  by  the  direct 
climatic  influences  and  require  a  change  to  a  temperate  climate,  otherwise 
after  a  time,  the  length  of  which  varies  much  in  individuals,  his  health  will 
be  undermined  and  break  down  in  some  way. 

The  extraordinary  success  of  the  American  sanitarians  in  the  canal  zone 
of  Central  America,  once  one  of  the  most  unhealthy  regions  of  the  world,  but 
where  now  the  sickness-rate  has  been  diminished  to  less  than  half  that  of  the 
death-rate  of  many  a  tropical  town  is  often  quoted.  We  feel  that  the  basis 
of  the  largest  proportion  of  illness  and  death  in  the  tropics  is  bad  sanitation 
and  not  climatic  influences.  Notwithstanding  these  facts,  a  permanent 
colonization  of  the  low-lying  regions  of  the  tropics  by  a  white  race  is,  in  our 
opinion,  not  possible,  as  a  uniformly  damp,  hot  climate  endured  for  years 
diminishes  the  resistance  against  disease,  and  has  a  markedly  deleterious  effect 
on  the  nervous  system.  Fertility  probably  also  decreases  after  the  second 
or  third  generation.  The  climate  greatly  deteriorates  the  physique  of  the 
children,  as  can  easily  be  observed  in  any  district  of  the  tropics  at  sea-level. 
In  the  highlands,  such  as  some  parts  of  British  East  Africa,  colonization  by  a 
white  race  may  be  possible,  though  Van  Standel  has  pointed  out  that  pro- 
longed residence  in  tropical  highlands  produces  changes  in  the  nervous  systems 
of  the  second  and  subsequent  generations,  even  if  it  does  not  do  so  in  the  first. 

These  remarks  in  general  agree  with  Caddy's  work,  as  he  considers  that  the 

European  is  unable  to  rear  strong  healthy  children  in  India,  and  that  even 

those  which  are  sent  home,  when  four  or  five  years  old,  owing  to  the  debili- 

lnfluences  of  the  tropical  climate  at  an  important  growing  period,  are 

not  so  fine  physically  as  their  parents. 

If,  however,  the  new-comer  into  the  tropics  desires  to  become 
acclimatized  he  must  use  some  protection  for  his  head,  and  in  many 
cases  for  his  spine  and  eyes ;  he  must  wear  suitable  clothing,  live  in 
suitable  houses,  work  in  suitable  offices,  dwell  in  sanitary  surround- 
ings, avoid  alcohol  and  exposure  to  the  midday  sun,  while  roads 
in  common  use  should  be  suitably  constructed  and  well  shaded. 

It  is  not  within  the  province  of  this  work  to  go  into  detail  with 
regard  to  these  matters,  but  a  few  brief  remarks  may  be  made. 

Suitable  Head-gear.— All  Europeans  should  wear  a  light  helmet 
or  topee  covered  with  white  or  khaki-coloured  cloth  externally 
and  ventilated.  This  helmet  should  have  a  broad  brim  lined  with 
green  and  prolonged  down  the  back  of  the  neck,  should  be  lined 
internally  with  red,  or  red  and  yellow,  or  black,  and  should  possess 
an  internal  band  attached  in  such  a  manner  that  the  head  does  not 
touch  the  frame  of  the  hat,  while  it  allows  free  circulation  of  the  air. 

When  persons  are  compelled  to  work  under  the  tropical  sun  and 
to  expose  their  backs  to  its  rays,  a  thin  strip  of  yellow  and  red 
coloured  silk  should  be  sewn  into  the  shirt  along  the  spine,  or 
attached  to  the  inner  aspect  of  the  coat  by  means  of  hooks  and 
eyelets.  Eyes  should  be  protected  with  dark  glasses,  or  with 
Sir  William  Crookes'  non-actinic  glass  with  side-pieces. 


go  TROPICAL  CLIMATOLOGY 

Ladies  who  are  particular  about  the  skin  of  the  face  should  wear 
veils,  though  these  are  very  warm. 

The  reasons  of  these  requirements  are,  while  white  reflects  heat 
very  well,  and  absorbs  very  little,  and  is  therefore  excellent  ex- 
ternally, yet  it  transmits  the  chemical  rays,  while  red  and  yellow 
absorb  them. 

Clothing. — Clothing  should  be  loose  and  as  light  as  possible  in 
weight,  and  of  a  white  or  khaki  colour  externally.  Sambon  some 
years  ago  devised  a  cloth,  called  '  Solaro,'  khaki-coloured  externally 
and  red  internally,  with  the  object  of  preventing  the  action  of  the 
sun's  rays  on  the  body.  It  is  made  by  using  threads  of  yellow  and 
blue  twisted  separately  and  together  for  the  warp,  while  red  threads 
are  used  for  the  weft,  but  these  latter  are  brought  back  in  the  pro- 
portion of  three  to  one,  so  that  the  front  has  three  yellow  and  three 
blue  threads  to  one  red  thread,  thus  producing  the  khaki  colour.  It 
should  only  be  used  as  a  coat,  and  should  be  obtained  as  thin  as 
possible,  and  made  up  as  lightly  as  possible  without  linings  or 
doublings.  The  general  opinion  at  the  present  is,  however,  that 
white  is  by  far  the  best  colour. 

As  regards  underclothing,  we  are  of  the  opinion  that  thin  woollen 
materials  are  the  best,  but  we  are  not  in  favour  of  openwork  under- 
clothes. At  the  present  time  the  use  of  abdominal  woollen  or 
flannel  belts  (so-called  'cholera  belts')  is  much  abused;  they  are 
useful,  however,  to  people  with  a  tendency  to  intestinal  disorders. 

It  should  be  remembered  that  when  clothing  is  wet  it  is  a  good 
conductor  of  heat,  and  hence  the  risk  of  sitting  down  in  damp 
clothes.  Clothing  should  not  be  too  heavy,  nor  too  tight-fitting. 
Ladies  should  not  wear  too  heavy  skirts,  which  congest  the  pelvic 
viscera. 

A  silk  hat  and  frock-coat  have  still  to  be  worn  by  men  at  official 
functions  at  midday,  but  the  custom  is  unfortunate,  and  may 
perhaps  in  time  disappear. 

Houses,  Offices,  etc. — Buildings  should  never  be  painted  white 
or  blue,  but  should  be  of  a  dark  red  colour.  The  amount  of  light 
admitted  to  a  room  should  be  restricted,  and  care  should  be  taken 
that  reflection  from  the  ground  into  the  room  does  not  take  place. 
Deep  verandas,  without  which  no  building  in  the  tropics  is  com- 
fortable, are  of  the  greatest  value  in  controlling  the  light,  as  are 
tatties  or  tats  made  of  grasses  and  wood,  and  jalousies. 

Rooms  should  be  capable  of  being  cooled  by  punkahs  or  fans,  and 
should  be  lit  with  electric  light  whenever  possible.  Ice-blocks  are 
very  useful  in  very  warm  weather  or  at  meetings,  or  in  sick-rooms. 
The  walls  of  rooms  should  be  painted  rose-colour,  not  white. 

Damp  courses  are  required  in  the  tropics,  as  walls  are  apt  to 
absorb  moisture  and  become  very  damp.  Round  roof-tiles  and 
ventilated  double  ceilings  are  necessary  to  keep  off  the  sun's  rays. 

Roads. — Roads  should  be  protected  from  the  glare  of  the  sun 
by  shade-trees — that  is  to  say,  trees  with  spreading  branches — 
while  plots  of  green  grass  are  most  valuable  in  towns.     There  is  not 


REFERENCES  91 

the  slightest  doubt  that  red  roads  are  the  most  comfortable  for  the 
eye  and  soothing  to  the  nervous  system,  and  that  white  roads  are 
exceedingly  trying  to  both. 

Avoidance  of  the  Midday  Heat. — If  possible,  travelling  and 
muscular  exertion  should  be  done  in  the  early  morning  or  late 
afternoon,  and  avoided  in  the  middle  of  the  day,  when  a  siesta  is 
most  beneficial.  The  absurd  custom  of  making  social  calls  at 
12  noon  in  certain  parts  of  the  tropics  should  be  discouraged,  and  a 
more  reasonable  hour  substituted. 

Avoidance  of  Alcohol. — Alcohol  should  never  be  taken  before 
the  sun  goes  down,  for  it  unfits  the  individual  for  work,  and  is  the 
most  important  predisposing  cause  of  sunstroke. 


REFERENCES. 

The  most  suitable  work  for  the  tropical  practitioner  is  Harm's  'Handbuch 
der  Klimatologie,'  of  which  there  exists  an  English  translation  of  Part  I. 
'General  Climatology,'  by  Ward;  but  unfortunately  there  is  no  such  transla- 
tion of  Band  II.,  '  Klimatographie,'  Teil  I.,  '  Klima  der  Tropenzone,'  of  which 
the  third  edition  appeared  in  Stuttgart  in  1910,  which  is  the  only  work,  with 
which  we  are  acquainted,  which  deals  with  the  climatology  of  the  various 
tropical  countries  in  at  all  a  full  manner. 

A  much  smaller  but  very  excellent  work  is  Ward's  '  Climate, 'in  the  Progres- 
sive Science  Series,  published  in  1908,  and  also  Giles'  work  mentioned  below. 
Chamberlain  (1913),  Annual  Meeting  of  the  American  Society  of  Tropical 
Medicine,  May  6,  7,  and  8,  Washington,  is  an  excellent  paper  with  full  refer- 
ences. 

Meteorology. 

Abbe     (1888).       Treatise     on     Meteorological     Apparatus     and     Methods. 
Washington. 

Archibald  (1901).     The  Story  of  Atmosphere.     (A  clear,  simple  account  of 
the  atmosphere.) 

Bartholomew  (1899).     Atlas  of  Meteorology.     Edinburgh. 

Bini  (1914).     Studi  di  Medicina  Tropicale.     Contains  Medical  Climatology  of 
Erythra^a  (Eritrea). 

Blandford  (1899).     Climates  and  Weather  of  India  and  Ceylon. 

Dainelli  (1910).     Climatologia  dell'  Eritrea. 

Elliott  (1906).     Climatological  Atlas  of  India. 

Eredia  (191  2).     Climatologia  di  Tripoli  e  Bengasi. 

Ferrel  (1889).     Winds.     New  York. 

Giles.     Climate  and  Health  in  Hot  Countries.     (An  excellent  account  of  the 
climate,  with  data  of  many  tropical  places.)     London. 

Knox,  A.  (191 1).     The  Climate  of  the  Continent  of  Africa.     (A  most  useful 
book.)      Cambridge. 

M.\rriott   (1903I.     Hints  to   Meteorological  Observers.     (A    very    valuable 
little  book.) 

Mohn  (1879).     Grundziige  der  Meteorologie.     Berlin. 

Plehn  (1906).     Tropenhygiene.     (Climates  in  late  German  colonies.) 

Sandwith  (1907).     Journal  of  Tropical  Medicine  and  Hygiene,  x.  361.     (Hill- 
Stations  and  Health  Resorts  in  the  British  Tropics.) 

Supan  (1903).     Grundziige  der  physichen  Erdkunde.     Leipzig. 

Tyler  (1907).     Journal  of  Tropical  Medicine  and  Hygiene,  x.  130.     (Psycho- 
physical Aspects.) 

Waldo  (1893).     Modern  Meteorology.     (A  good  account  of  instruments  and 

winds.) 
Ward  (1908).     Climate.     London. 


92  TROPICAL  CLIMATOLOGY 


Bibliography  of  Meteorology. 

A  Classed  Catalogue  of  the  Printed  Literature  of  Meteorology  from  the  Origin 
of  Printing  to  the  Close  of  1881,  and  a  Supplement  to  the  End  of  1887. 
Washiagton.     18S9-91. 

Current  Meteorological  Literature. 

Meteorologische  Zeitschrift,  Vieweg,  Braunschweig. 

Reports  of  Tropical  Meteorology. 

Algeria.     Observations  Meteorologiques.     Paris. 

Barbadoes.     Practitioner,  1S78.     Climate  of  Barbadoes. 

Brazil.     Annuario  publicado  pelo  Observatorio  do  Rio  de  Janeiro  Imprensa 

Nacional  Rio  de  Janeiro. 
British   Colonies.     Symon's    Meteorological    Magazine    (monthly).     (Data 

concerning  a  number  of  colonies.) 
Ceylon.     Administration  Reports:  Meteorology.     Yearly.     The  Climate  of 

Ceylon,  by  Dr.  W.  H.  de  Silva.     British  Medical  Journal,  1907. 
Egypt  and  the  Soudan.     Climate.     H.  G.  Lyons,  British  Medical  Journal, 

1910. 
Fiji.     Meteorological  Observations  taken  at  Suva.     (Yearly.) 
German  Colonies.     Medizinal  Berichte  uber  die  deutschen  Schutzgcbiete 

Deutsch  Ost  Africa,   Kamerun,   Toga,   Deutsch  Sud-West  Africa,  New 

Guinea,  Karolinem,  Marshall  Inselm  und  Samoa. 
Hong-Kong.     Climate   of    Hong-Kong.     Journal    of   Royal    Army  Medical 

Corps.     Vol.  I.,  No.  1. 
Indes  Neerlandaises.     Observations  Meteorologiques  de  lTnstitute  Botani- 

que  de  l'Etat  de  Buitenzorg.     (Yearly.) 
India.—  {a)  Calcutta.     Annual  Meteorological  Report  of  Government  of  India. 

(There  are  numerous  reports  issued  in  Calcutta  on  Rainfall,  the  Monsoon, 

Weather,   etc.)     (b)  Madras.     Annual   Report   of  the   Kodaikanal   and 

Madras  Observatories. 
Indo-China.     Twenty-one  stations.      Hanoi   Bulletin1^ Economique,    publie 

par  la  Direction  de  l'Agriculture  et  du  Commerce.     Cape  St.   Jaques, 

Pnom-feuk,  Saigon,  Pould-Condorc,  Ong-Yem,  Soetrang,  Pursat,  Kam- 

pob,  Ballambang,  Padaran,  Nhatrang,  Quinlion,  Qwangngai. 
Manila.     Observatorio  Mensual.     (Spanish.) 

Mauritius.     Annual  Report  of  the  Director  of  the  Royal  Alfred  Observatory. 
Mexico.     Mensual  del  Observatorio  Meteorologico  de  Mexico. 
Philippine   Islands.     The   Climate   of  the   Philippine   Islands  in   Bulletin 

No.  2,  Census  of  the  Philippine  Islands. 
Oueensland.     Queensland  Gazette. 
Seychelles.     Annual  Report  of  the  Medical  Department.     Chapter  11.  and 

Annexnrc  II.,  Meteorology. 
Tripoli.     Rapporti  Coloniali.     Ministcro  Colonie  Eoma. 
Uruguay.     Boletin  Mensual  del  Collegio  Pio  de  Villa  Colon.     Montevideo. 
Western  Australia.     The  Climate  of  Western  Australia  from  1876  to  1899, 

by  Cooke.     Perth,  1901.  ^ 

Effects  on  Man. 

Brown-Sequard  (1859).  Journal  de  la  Physiologie  de  l'Homme,  ii.  551. 
(Quoted  in  Wunderlich,  114.)     Paris. 

Caddy  (1914).  Transactions  of  the  Life  Assurance  Medical  Officers' Associa- 
tion 33-70  (Life  Insurance  in  India).     London. 

Crombie  (1873).     Indian  Annals  Medical  Science,  xvi.     Calcutta. 

Davy  (1839).  Researches,  i.  London.  (1850).  Philosophical  Transactions 
of  the  Royal  Society.     (On  the  Temperature  of  Man  in  the  Tropics.) 

Dyson  (191  i).  British  Journal  of  Dermatology,  vol.  xxiii.,  p.  205.  (Cutane- 
ous Pigmentation.)     London. 


REFERENCES  93 

Freer  (1910).  Philippine  Journal  of  Science,  B.,  v.  i.  (The  Tropical  Sun- 
light.) (1912).  Ibid..  B..  vii.  i.  (Two  Years'  Work  in  the  Study  of 
Tropical  Sunlight.)     Manila. 

Gresswall  (1S84).     British  Medical  Journal,  ii.  164. 

Haldane  (1905).     Journal  of  Hygiene,  v.  494. 

Jousset  (1883).     Archives  de  Medecine  Navale,  xi.     Paris. 

Jousset  (1884).  Traite  de  rAcclimatement  et  de  1'Acclimatation.  (Full 
description  of  the  subject  up  to  1884.)     Paris. 

Livingstone  (1857).     Travels  and  Researches  in  South  Africa,  509. 

Maurel  (1884).     Bulletin  Soc.  d'Anthrop.  de  Paris,  vii.  371. 

Mitchell  (1915).  Journal  of  State  Medicine,  xxiii.  272-282.  (Damp  Heat  of 
the  Persian  Gulf.)     London. 

Montegezza  (1863).     Presse  Medicale  Beige,  Bruxelles,  xv.  3. 

Neuhaus  (1893).     Virchow's  Archiv,  Bd.  134,  xix.  365. 

Pembrey  and  Nicol  (1898).     Journal  of  Physiology,  xxiii.  3S6. 

Pin'kerton  (1SS1).     Journal  of  Anatomy  and  Physiology,  xv.  118.     London. 

Rattray  (1870).     Proceedings  of  the  Royal  Society  of  London,  ii.  513-528. 

Reynaud  and  Blosville  (1836-39).  Animal  Heat.  Todd's  Encyclopaedia, 
ii.  658-659. 

Ringer  and  Stuart  (1877).  Proceedings  of  the  Royal  Society  of  London, 
xxvi.  1S7. 

Sambon  (1897).  British  Medical  Journal,  i.,  January  9  (Acclimatization). 
(1907).     Journal  Tropical  Medicine,  67  (Tropical  Clothing). 

Schafer  (189S).  Textbook  of  Physiology.  Pembrey 's  articles  on  Respira- 
tion and  Animal  Heat.  (These  are  most  valuable  to  the  student  of  tropical 
medicine,  with  full  literature  up  to  1897.) 

Sellards,  Bovie  and  Brooks  (191 8).  Biological  Investigations  of  Tropical 
Sunlight.     Journal  of  Medical  Research,  vol.  xxxiii.,  No.  3. 

Woodruff  (1907).  Tropical  Light.  Isew  York.  (1909).  Expansion  of 
Races.     New  York. 


CHAPTER  IV 
TROPICAL   FOODS 

Preliminary  Remarks  —  Evolution  —  Chemical  composition  —  Quantity  — 
Quality — Tropical  food  materials — Calculation  of  diets — Low  protein 
dietaries — Vitamincs- — Lipoids — Little-known  matters — References. 

PRELIMINARY  REMARKS. 

It  is  not  our  purpose  to  attempt  to  give  an  account  of  the  foods 
found  in  various  tropical  regions,  but  merely  to  give  a  brief  summary 
of  some  of  the  more  important  facts  known  to  us  with  regard  to 
tropical  foods  and  their  effects  upon  man. 

The  subject  owes  much  to  the  labours  of  McCay  in  India,  while 
Wilson  in  Egypt  has  shown  how  this  work  can  be  extended  to  other 
parts  of  the  tropics. 

We  will  begin  by  tracing  briefly  the  origins  of  foods  as  far  as  we 
know  them. 

EVOLUTION. 

At  the  present  time  human  food  is  everywhere  more  or  less  cooked,  and  it  is 
rare  for  mankind  anywhere  to  eat,  even  for  a  limited  period,  absolutely  raw 
materials.  Dr.  Campbell,  in  a  most  interesting  manner,  has  traced  the  evolu- 
tion of  man's  diet.  He  distinguishes  first  of  all  the  pre-cookery  epoch,  during 
which  evolving  and  primeval  man  lived  upon  raw  materials,  unaltered  by  any 
of  the  chemical  and  physical  processes  involved  in  cooking;  secondly,  the 
cookery  epoch,  which  may  be  subdivided  into  the  pre-cibicultural  and  the 
cibicultural  eras.  In  the  former,  although  he  cooked  his  food,  man  did  not 
cultivate  vegetal  foods,  nor  did  he  rear  animals  for  purposes  of  food.  During 
this  period  vegetal  foods  would  probably  be  used  in  greater  quantities  than 
before,  as  they  are  easier  to  obtain  than  hunted  animals;  and,  also,  because 
the  processes  of  cookery,  by  breaking  up  the  cellulose,  rendered  them  more 
easily  digestible  and  absorbable,  and  therefore  more  nutritious,  as  well  as 
more  palatable.  Just  as  we  have  already  pointed  out  that  certain  tribes  have 
remained  in  the  status  of  the  Stone  Age  almost  to  the  present  day,  so  certain 
tribes — e.g.,  the  Bushmen  of  Africa,  the  true  Veddahs  of  Ceylon,  the  Anda- 
manese  of  the  Bay  of  Bengal,  and  the  aborigines  of  Australia — have  remained 
in  bbis  pre-cibicultural  era.  These  peoples  obtain  their  foods  from  all  sorts  of 
animals — -e.g.,  worms,  centipedes,  flies,  caterpillars  ants,  etc. — as  well  as  from 
game,  while  their  vegetal  foods  are  collected  and  stored,  but  they  have  never 
Learned  to  <  tra<  I  any  chemical  substance — e.g.,  sugar — from  their  vegetal 
foods.  Probably  this  is  one  of  the  reasons  why  they  prize  honey  so  highly. 
In  the  cibicultural  era  man  cultivated  his  vegetal  foods,  and  reared  domestic 
animals  for  the  purposes  of  animal  food,  and  here  again  his  vegetal  feeding 
increased  in  amount,  as  this  Eood  was  the  cheapest  and  easiest  to  produce. 
Here  again  rose  the  urgent  need  for  salt,  to  which  we  have  already  drawn 
attention  in  the  account  of  the  migrations  of  negro  tribes. 

The  arts  of  cultivation  and  domestication  became  gradually  dispersed  over 

94 


EVOLUTION  95 

the  world,  but  to-day  it  is  exceedingly  difficult  to  trace  the  means  by  which 
this  diffusion  took  place,  though  it  is  probable  that  much  of  it  was  due  to 
Aryan  invasions. 

Primitive  wheats  can  be  found  growing  wild  in  Palestine  to-day,  and  it  is 
probable  that  the  home  of  this  cultivation  was  Mesopotamia.  It  also  seems 
likely  that  the  art  of  bread-making  was  known  to  the  Chaldeans  and  to  the 
Egyptians  some  three  thousand  and  more  years  before  the  commencement 
of  the  present  era. 

According  to  Tibbies,  rice  cultivation  was  in  existence  in  China  some  three 
thousand  years  before  Christ,  and  was  introduced  into  India  by  the  Aryan 
invasion.  From  India  it  passed  into  Europe  with  Alexander  the  Great's- 
army  in  334  B.C.,  and  from  Europe  it  was  introduced  into  America  in  the 
fifteenth  and  sixteenth  centuries. 

Maize,  on  the  other  hand,  was  first  cultivated  in  America  by  the  ancient 
inhabitants  of  Mexico  and  Peru,  and  was  brought  by  the  Spaniards  to  Europe, 
and  has  gradually  found  its  way  all  over  the  world. 

Millet  appears  to  have  been  cultivated  from  very  ancient  days  in  Africa 
ami  Asia,  and  even  in  the  Stone  Age  it  had  extended  into  Middle  and  Southern 
Europe. 

Beans  were  first  cultivated  by  the  Aryans,  but  the  haricot  bean  comes  from 
South  America,  while  lentils  are  of  prehistoric  origin,  and  spinach  was  appar- 
ently cultivated  by  the  Medes  and  Persians.  Onions  possibly  originated  in 
India,  wlule  the  potato  came  from  Chile. 

Fruit-growing  is  not  as  ancient  as  cereal  cultivation. 

The  domestication  of  animals  enabled  man  to  obtain  meat  without  being 
compelled  to  roam  over  large  areas  in  search  of  wild  game.  Man  is  omnivorous 
and  desires  greatly  to  eat  meat,  but  when  this  is  unobtainable  or  in  too  small 
a  quantity  to  supply  the  needs  of  the  population,  as  in  the  present  war,  he 
eats  the  foods  which  are  available,  and  is  thankful,  even  though  they  are  not 
those  after  which  his  stomach  hankers. 

The  reason  why  man  in  Eastern  countries  eats  so  much  rice  must  be  sought 
for  in  the  overpopulation  of  the  Eastern  Asia  of  long  ago,  when  the  great 
food  difficulties  began  those  large  movements  of  peoples  which  we  have  noted 
in  Chapter  II. 

To-day  Governments  place  peoples  on  meatless  days  and  give  them  food 
tickets,  and  the  peoples  obey  willingly  because  they  understand  the  reason, 
but  it  might  have  been  extremely  dangerous  for  a  despotic  monarch  of 
E  tstern  Asia  to  have  issued  orders  of  this  nature  long  ago.  The  ruling  powers 
of  those  days  must  have  invoked  the  aid  of  the  religious  sects,  who,  being 
feared  and  respected  by  the  people,  were  obeyed;  and  to-day  these  religious 
maxims  are  still  in  force,  and  the  people  avoid  animal  food,  although  the  over- 
population on  account  of  which  the  rulers  probably  originated  this  custom 
has  ceased  to  exist. 

During  historic  days  man  has  attempted  to  improve  the  appearance,  the 
smell,  and  the  taste  of  his  food  by  all  sorts  of  devices,  which  vary  in  different 
countries.  These  refinements  include  condiments  and  colouring  matters, 
and  form  part  of  the  basis  of  the  science  and  art  of  modern  cookery. 

But  man  desires  not  food  alone,  but  something  to  cheer  and  exhilarate  him 
when  he  feels  ill  or  depressed,  and  when  he  wishes  to  celebrate  some  occasion; 
and  hence  in  all  countries  some  form  of  stimulating  liquid  is  to  be  found, 
be  it  111  the  form  of  tea,  coffee,  or  cocoa,  of  malt  liquors,  wines  or  distilled 
spirits,  and  all  these  arc  of  great  antiquity. 

Early  dealers  in  Ei  iod  materials  soon  Learned  that  it  was  profitable  to  adulter- 
ate their  merchandise,  as  this  could  be  done  with  impunity.  Of  late,  legisla- 
tion, aided  by  chemical,  physical,  and  physiological  research,  is  endeavouring 
to  insure  that  foodstuffs  shall  be  pure,  though  with  regard  to  some  foods,  such 
as  milk,  the  standard  is  far  from  perfection,  and  certainly  in  the  tropics  mixed 
milk  can  rival  sewage  in  the  numbers  of  its  organisms. 

With  regard  to  quantity  and  composition  of  primitive  foods,  naturally  but 
little  is  known,  and  this  little  is  entirely  due  to  McCay,  who  has  investigated 
the  dietary  of  the  primitive  peoples  of  Chota  Nagpur  in  Bengal.     Among 


96  TROPICAL  FOODS 

these  there  are  peoples  who  have  begun  to  cultivate  the  ground,  while  others 
still  live  upon  the  food  which  they  can  gather.  Thus  the  Dravidian  Mundas 
and  Uraons  eat  insects,  lizards,  snakes,  rats,  jackals,  and  pigs — or,  in  other 
words,  anything  which  they  can  catch.  Their  daily  dietary  is  composed  of 
protein  So  grammes,  carbohydrates  500  grammes,  and  fats  50  grammes,  which 
provides  calories  2,800. 

The  Todas  of  the  Nilghiri  Hills  live  upon  milk,  the  meat  of  buffaloes  and  of 
such  animals  as  they  can  kill  or  capture.  They  take  no  vegetal  food,  and 
hence,  like  the  carnivora,  require  no  salt,  which  is  an  essential  to  vegetal 
feeders  in  order  to  prevent  acidosis. 

The  Bushmen  of  South  Africa  and  the  Bedouin  of  Arabia  are  meat  eaters. 

The  necessity  for  food  is  to  provide  heat  and  energy,  and  to  form 
new  bodily  tissues,  as  well  as  to  make  good  the  wear  and  tear  of 
existing  tissues;  and  to  do  this  a  community  requires  pure  water 
and  plenty  of  it,  and  good  and  varied  foodstuffs  in  quantity  pro- 
portional to  the  numbers  of  the  population,  a  fact  which  the  present 
war  has  made  clear  to  nearly  every  family  in  the  civilized  regions 
of  the  earth. 

Dietetics  are  based  upon  chemical  and  physiological  considera- 
tions, into  which  we  will  now  inquire  very  briefly. 

CHEMICAL  COMPOSITION. 

In  order  to  meet  the  requirements  of  the  body,  foods  must  be 
composed  of  the  same  essential  chemical  substances  as  that  body. 
They  are  therefore  made  up  of  proteins,  carbohydrates,  fats,  mineral 
substances,  and  water,  but  these  alone  are  insufficient  to  keep  the 
body  in  health,  and  they  must  be  associated  with  vitamines  and 
lipoids  or  nitrogenous  fats. 

Proteins  may  be  obtained  from  the  muscles,  bones,  and  organs  of 
animals  used  as  food,  also  from  animal  products  such  as  milk  and 
eggs,  while  the  many  vegetal  substances,  but  particularly  legumes, 
nuts,  and  cereals,  also  provide  this  valuable  food  constituent.  Their 
primary  value  is  as  tissue  formers,  and  their  secondary  value  as 
heat-energy  producers,  but  all  proteins  are  not  of  equal  value,  as  we 
shall  see  later. 

Carbohydrates  are  chiefly  of  vegetal  origin,  and  are  principally 
of  value  as  heat-energy  producers. 

Fats  are  widely  distributed  both  in  the  animal  and  in  the  vegetal 
kingdoms,  and  are  essentially  heat-energy  producers,  while  the 
Lipoids  or  nitrogenous  fats  are  indispensable  to  man,  though  their 
exact  use  is  not  known. 

Mineral  Substances  are  compounds  of  sodium,  potassium,  calcium, 
magnesium,  manganese,  and  iron,  cither  with  carbonic,  sulphuric, 
phosphoric,  and  silicic  acids,  or  with  acetic,  citric,  malic,  oxalic,  and 
tartaric  acids,  or  with  chlorine  or  fluorine.  They  produce  no  heat 
or  energy,  but  are  essentials  for  building  up  the  fluids  and  tissues 
of  the  body,  in  which  they  represent  some  5  or  6  per  rent,  of  the  total 
weight. 

Water,  forming  some  58*5  per  cent,  by  weight  of  the  human  body, 
is  an  indispensable. 


CHEMICAL  COMPOSITION  97 

Vitamines  are  nitrogenous  complexes,  which  are  essential  for  the 
growth  or  the  well-being  of  the  organism. 

The  food  materials  may  therefore  be  classified  into  the  great 
tissue-forming  protein,  aided  by  salts  and  water,  and  the  great  heat- 
energy  producing  carbohydrate  and  fats,  aided  by  protein,  and 
essentials,  the  work  of  which  is  not  understood — viz.,  vitamines 
and  lipoids. 

As  the  heat  and  energy  can  be  expressed  in  terms  of  the  calorie 
(or  large  calorie  written  with  a  capital  C),  which  is  the  amount  of  heat 
necessary  to  raise  the  temperature  of  i  kilogramme  of  water  one 
degree  centigrade,  and  as  protein  is  the  essential  tissue -former,  it 
follows  that  in  calculations  as  to  a  diet  two  matters  stand  out — viz., 
the  quantity  of  protein  in  that  diet,  and  the  number  of  calories 
which  can  be  obtained  therefrom. 

Water  has  a  food  value  of  I  in  1,000,  and  should  be  freely  avail- 
able, and  salt  is  usually  easily  procurable,  though  we  have  lived  in 
parts  of  the  tropics  in  which  neither  were  easily  obtained. 

Vitamines  and  lipoids  we  cannot  measure,  and  at  present  we  are 
merely  concerned  with  their  presence. 

Therefore,  from  a  practical  point  of  view,  the  quantities  which 
require  calculation  are  the  amount  of  protein  in  a  diet  and  the 
number  of  Calories,  and  this  brings  us  to  the  subject  of  quantity. 

QUANTITY. 

The  only  accurate  method  of  determining  the  quantity  of  the 
various  food  factors  of  any  given  diet  is  by  means  of  the  respiration 
calorimeter,  in  which  the  work  done,  the  heat  generated,  and  the 
waste  products  eliminated,  are  expressed  in  terms  of  the  Calorie, 
which,  in  energy,  is  the  equivalent  of  1-54  foot  tons,  or,  in  other 
words,  represents  that  amount  of  mechanical  energy  which  is  required 
to  raise  1  ton  in  weight  1-54  feet  in  height. 

When  the  respiration  calorimeter  is  not  available,  the  quantity 
of  the  total  food  consumed  by  the  person  or  persons  under  observa- 
tion should  be  carefully  weighed  and  records  made.  Then  samples 
of  the  various  constituents  of  this  diet  should  be  analyzed,  with  the 
view  of  determining  the  quantity  of  protein,  carbohydrate,  and  fat 
contained  therein. 

With  regard  to  the  Calories  produced  by  these  various  factors, 
Rubner's  experiments  upon  animals  1  nabled  him  to  enunciate  the 
so-called  isodynamic  law,  which  states  that  227  grammes  of  protein, 
or  of  carbohydrate,  yield  930  Calories  on  consumption  in  the  body, 
and  that  this  is  the  same  as  the  heat  so  produced  by  100  grammes  of 
fat,  and  therefore  227  grammes  of  protein,  or  of  carbohydrate,  are 
isodynamic  with  100  gramme s  of  fat.  In  other  words,  1  gramme  of 
protein  produces  the  same  amount  of  heat  as  1  gramme  of  carbo- 
hydrate— viz.,  4-1  Calories,  while  I  gramme  of  fat  gives  9-3  Calorics. 

It  may,  perhaps,  be  incidentally  noted  that  1  gramme  of  alcohol 
produces  7-0  Calories. 

7 


98 


TROPICAL  FOODS 


Standard  diets  expressed  in  grammes  have  been  determined  for 
an  average  strong  healthy  man  weighing  some  n  stone  (68-70  kilo- 
grammes) and  living  under  average  conditions  of  work  in  the  Tem- 
perate Zone.  The  following  table  gives  some  examples  of  these 
standards: — 


Observer. 

Protein. 

Carbohydrate. 

Fat. 

Calories. 

Ranke 

100 

240 

100 

2,324 

Voit 

118 

500 

56 

3.°55 

Rubner 

127 

509 

52 

3.°92 

Moleschott 

130 

55o 

40 

3.160 

Atwater 

125 

400 

125 

3.315 

As  these  diets  are  on  the  man  value,  it  is  necessary  to  have  a  table 
showing  the  values  of  children  and  women  in  t^rms  of  this  man 
value.  Such  a  table  as  made  by  Greenwood  and  Thompson  is  given 
below : — 


Atwater' s 

Coefficients 

Inter- A  Hied  Food  Commission. 

Ages. 

Man 
Value. 

Ages. 
0  to  5 

Man 
Value. 

0  to  5   . . 

04 

o-5 

6  to  9    . . 

o-5 

6  to  10 

0-7 

10  to  13 

o-6 

1 1  and  over : 

14  to  15: 

Males 

I'O 

Males 

o-8 

Females 

0-83 

Females 

o«7 

16  and  over: 

1 

Males 

.  . 

i-o 

Females 

o-8 

All   children,   combined 

0-51 

All      children ,      co  - 

o-68 

ages 

1 

bined  ages. 

These  figures  may  be  compared  with  some  Indian  dietaries  given 
by  McCay : — 


Class  of  Person.  Protein.       Carbohydrates.         Fats.  Calories. 


Cultivators    .  . 

Poor  middle 

Middle 

Better 

Bengali  prison  diet 


52 

50 

70 

85-100 

93 


475 
400 
300 
300-400 
t>93 


2,390 
2,310 
2,350 
2,950-3,450 
3,5°o 


In  Egypt,  Wilson  has  inquired  into  the  food  of  a  Bedouin,  and 
found  that  large  quantities  of  rice  and  milk  were  used,  while  meat 


QUANTITY 


09 


was  eaten  once  a  week  in  the  winter  and  only  once  a  fortnight  in 
the  summer,  and  lentils  eaten  in  the  winter  were  rarely  used  in  the 
hot  weather,  being  replaced  by  extra  rice.  About  h  pound  of  butter 
was  taken  in  the  winter,  but  less  in  the  summer.  Bread  consisted 
of  a  mixture  of  two  parts  of  dura  and  one  part  of  wheaten  flour, 
but  on  desert  journeys  was  made  entirely  from  wheat.  Onions  and 
cheese  were  also  used. 

He  investigated  the  diets  of  two  Egyptian  men,  with  the  following 
results,  which,  however,  are  complicated  by  the  fact  that  they  are 
calculated  from  the  amount  used  by  the  family : — 


Egyptian  Men. 

Protein. 

Carbohydrate.           Fat.             Calories. 

Strong  and  healthy 
Mot  very  robust     .  . 

89-1 
82-0 

628-0                   47-5 
520*0                   49-0 

3.328 

2,870 

Perhaps  the  best  practical  test  is  the  British  war  ration,  which, 
according  to  Lelean,  was  inadequate  in  the  South  African  War, 
producing  loss  of  efficiency  from  neurasthenia  and  debility,  as  was 
afterwards  proved  by  experimental  marches  performed  upon  it, 
but  which,  in  1913,  was  altered  to  one  containing  a  high  amount  of 
protein,  which,  indeed,  is  required  to  meet  the  needs  of  tissue  repair. 
It  is  as  follows :— 


Protein. 

Carbohydrate. 

Fat. 

Calories. 

175 

218 

515 

4.855 

We  have  already  invited  attention  to  the  possible  simplification  of 
these  tables,  and  have  shown  that  the  essentials  are  the  protein  and 
the  Calories,  and  now  we  will  see  how  Atwater  applies  this  method 
for  determining  the  diet  of  a  man  doing  various  kinds  of  mechanical 
work : — 


Nature  of  Work. 

Protein. 

Calories. 

Rest 

Light  work 
Moderate  work 
Hard  work 

100 
112 
125 
150 

2,700 
3,000 
3.5oo 
4.500 

In  Japan,  Oshima  found  that  a  jinricksha-man  doing  hard  work 
consumes  different  foods  during  his  periods  of  work  and  rest. 
During  work  he  eats  large  quantities  of  rice,  and  during  rest  quanti- 


loo  TROPICAL  FOODS 

ties  of  fish,  eggs,  beef,  and  pork.  He  consumes  about  20  to  30 
ounces  of  beef  or  mutton  per  diem,  which  works  out  at  158 
grammes  of  protein  and  5,050  Calories. 

Light-worked  Japanese  require  100  grammes  of  protein  and  about 
3,000  Calories  per  diem. 

In  India,  McCay  determined  the  amount  of  nitrogen  excreted 
daily  in  the  urine,  and  adding  to  this  the  other  metabolized  nitrogen 
mentioned  above,  and  converting  this  into  terms  of  protein,  obtained 
the  absorbed  protein,  which,  he  calculated,  was  75  per  cent,  of  the 
dietary  protein. 

For  example,  the  urinary  nitrogen  being  6  grammes,  which  is  the 
equivalent  of  35-5  grammes  of  absorbed  protein,  adding  to  this 
the  other  metabolized  nitrogen  and  25  per  cent,  for  that  lacking, 
he  concludes  that  the  average  rice-eating  Bengali  of  50  kilogrammes 
weight  only  uses  55  grammes  of  protein  per  diem— or,  in  other 
words,  lives  on  a  poorer  protein  supply  than  any  other  race  investi- 
gated. 

Further,  this  rice-eating  Bengali  exemplifies  on  a  large  scale  the 
results  of  Chittenden's  experiments,  and  as  claimed  by  this  experi- 
menter, should  exhibit  good  bodily  health,  great  working  power,  and 
freedom  from  disease,  whereas  he  shows  none  of  these  traits,  and,  as  a 
matter  of  fact,  the  reverse  is  true. 

Our  own  experiences  of  Chittenden's  dietary  in  the  tropics  is  that 
the  experiment,  if  continued  sufficiently  long,  lowers  the  resistance 
of  the  body  against  disease ;  and  this  can  scarcely  be  surprising,  as  he 
maintains  that  0-12  gramme  of  nitrogen  per  diem  per  kilogramme 
of  body  weight  is  sufficient  to  keep  a  man  in  health.  This  is  certainly 
not  so  in  the  tropics.  And  we  doubt  its  general  application  to 
temperate  and  cold  climates,  where  one  would  expect  more  food  to  be 
required. 

Chittenden's  figures  of  the  nitrogen  metabolized  per  kilogramme 
of  body  weight  may  be  compared  with  Voit,  McCay's,  and  Oshima's 
figures  as  follows : — 


Bengalis  and  Ooriyas  (rice  diet  largely) 

0,Il6-0,I20 

Chittenden 

0  120-0*130 

Beharis  and  Eastern  Bengalis 

o- 1 40-0*1 60 

Japanese  poorer  classes 

.  .     0-177 

Nepalese 

o*  1 80-0*250 

Sikkim  Bhutias 

.  .      0-250 

Average  European     .  . 

0-270 

Thibetan  and  Bholan  Bhutias 

•  •      0*350 

Nepalese  Bhutias 

0-420 

Indeed,  McCay  found  that  Indian  dandy  carriers,  Indian 
rickshaw-nun,  and  Indian  coolies  performing  exceedingly  hard 
work,  did  so  on  a  diet  containing  175-200  grammes  of  protein 
and  6,300-6,500  Calorics  per  diem,  wheivas  the  British  Army 
ration  mentioned  above  only  allows  175  grammes  of  protein  and 
4,855  Calories. 


QUALITY  ioi 

It  will  be  noted  that  nothing  is  said  in  these  diets  as  to  the  quan- 
tity of  the  food  digested  and  absorbed  into  the  body,  as  it  is  from 
this  alone  that  tissue -formation  and  heat-energy  production  can 
take  place- — -or,  in  other  words,  we  require  to  know  something  as 
to  the  quality  as  well  as  the  quantity  of  the  food  supplied  in 
a  diet. 


QUALITY. 

In  this  section  we  desire  to  know  the  amount  of  any  given  food 
which  is  absorbed,  and  is  therefore  available  for  use  in  producing 
heat,  energy,  and  repair. 

The  amount  which  is  capable  of  being  digested  may  be  determined 
by  artificial  digestion  of  a  sample,  but  though  said  to  give  good 
results,  it  is  hardly  reliable  as  to  absorption. 

A  better  method  is  to  begin  by  giving  the  person  to  be  experi- 
mented upon  a  dose  of  charcoal,  and  after  a  few  hours  to  administer 
a  given  quantity  of  the  food  to  be  tested  of  which  the  protein, 
carbohydrate,  and  fat  factors  are  known.  The  faeces  are  in  due 
course  carefully  collected  and  weighed,  and  the  total  amount  of 
nitrogen  and  of  fat  determined.  From  the  nitrogen,  after  deducting 
0-5  gramme  to  allow  for  the  daily  amount  of  excreted  metabolized 
nitrogen,  can  be  calculated  the  amount  of  protein  in  the  fseces,  and 
this  deducted  from  the  amount  of  protein  in  the  food  gives  the  quan- 
tity absorbed. 

The  fat  is  determined  in  the  same  way  by  ether  extraction,  while 
tin:  carbohydrate  is  obtained  by  calculation. 


Nature  of  Food. 

Protein. 

Carbohydrate. 

Fat. 

Mixed  diet  : 

Total  foods 

92 

97 

95 

Animal  foods 

97 

98 

95 

Vegetal  foods 

• 

97 

90 

Meat  and  fish 

97 

98 

95 

Eggs 

97 

98 

95 

Milk,  cheese,  etc. 

• 

97 

98 

95 

Cereals 

85 

98 

90 

.Starches  and  sugars  . 

— 

98 

— 

Legumes  (dried) 

78 

97 

90 

Vegetables 

. 

83 

95 

90 

Fruits  . . 

•          "•     1 

85 

90 

90 

Langworthy  gives  the  table  above  showing  the  coefficients  of 
digestibility  or  the  amounts  per  cent,  of  the  foods  which  were 
digested.  It  must  be  remembered  that  by  the  word  '  digestibility  ' 
as  used  in  dietetics  is  meant  not '  apparent  digestibility,'  or  the  time 
a  food  requires  to  pass  through  the  stomach,  but  '  actual  digesti- 


102 


TROPICAL  FOODS 


bility , '  which  is  the  quantity  of  a  given  food  which  is  absorbed, 
from  which  alone  tissue  formation  and  heat  energy  can  take  place. 
Benedict,  taking  into  account  this  factor,  together  with  the  work 
done,  gives  the  following  table:— 


Nature  ofWor*.                       ™±       ,       ^gg* 

Calories. 

Light    . .           .  .           .  .           .  .                 ioo                          92 

Moderate         ..           ..           ..                 115                       105 

Hard     .  .           .  .           .  .           .  .                 175                        160 

2,700 

3.30° 
5.500 

It  will  be  noted  that  the  British  Army  ration  is  below  Benedict's 
hard- work  calories  by  745. 

So  far  we  have  been  writing  as  though  all  proteins  were  of  equal 
value,  but  they  are  not,  as  the  researches  of  Rubner  and  Thomas 
have  shown. 

The  minimum  quantity  of  protein  required  daily,  so  that  a  man 
of  average  weight  may  live  without  drawing  upon  the  proteins  in 
his  tissues,  is  30  grammes  of  animal  protein — that  is  to  say,  protein 
derived  from  meat  and  eggs. 

To  reproduce  this  value,  34  grammes  of  rice  protein  and  102 
grammes  of  maize  protein  are  required. 

This  factor  is  called  the  biological  value  of  protein,  and  so  far  as 
we  know  has  only  been  studied  by  its  authors  and  by  Wilson  in 
Egypt,  as  set  forth  below  : 


Absorption  Co- 

100 Grammes  of  Food    1 

A  vailable 

Biological  Value 

efficient  calcu- 

Material. 

Protein. 

of  Protein . 

lated  on  Avail- 
able Protein. 

Meat 

19-00 

19-00 

95 

Wheaten  bread 

5-00 

2-00 

75 

Millet  bread 

3'4° 

1-36 

55 

Rice 

6-50 

6-00 

80 

Lentils 

19-30 

10-70 

70 

Beans 

18-60 

10-30 

7° 

Fresh  vegetables 

I'OO 

0-50 

Dura 

7-80 

2-30 

75 

Millet 

4*45 

1-78 

55 

Milk  (buffalo)    .  . 

5'9o 

5*90 

— 

Dried  dates 

1-90 

0-90 

— 

Ful  Sudani  (shell  d 

19-00 

10-50 

70 

Wilson  gives  the  following  table  of  the  diets  in  use  at  Egyptian 
prisons,  with  suggested  modifications: — 


QUALITY 


Available 

A  vail- 

able 
Protein . 

Biologi- 

Protein 

Carbo- 

Energy 

Details. 

cal  Value 

of 
Protein . 

from 
Animal 
Sources. 

Fat. 

hydrate 

Gross, 

less  Five 

Value  in 

Kilo- 
Calories. 

per  Cent. 

Hard  labour  diet: 

Before  1898 

72-9 

37'0 

8-28 

29*7 

524-0 

2,786-0 

1898-1899 

77-o 

39'5 

6-89 

86-o 

569-0 

3.436-o 

1 900-1 905  .  . 

74-0 

37-5 

6-o 

56-0 

546-0 

3.056-0 

1905  (wheat  bread) 

96-0 

57-8 

22-5 

46-0 

547'° 

3-058-0 

191 1  (millet  bread) 

83-0 

53'34 

22-5 

46-0 

521-0 

2,987-0 

Suggested 

89-2 

45-28 

7.O 

48-9 

588-3 

3,218-0 

Ordinary  labour  diet  : 

1 898-1 899 

68-5 

34*5 

6-o 

56-5 

529-5 

2,978-5 

1900-1905 

57-i 

25-4 

2-5 

48-o 

460-0 

2,561-0 

1905  (wheat  bread) 

82-7 

44-2 

6-o 

43*° 

553-o 

3,010-0 

191 1  (millet  bread) 

69-7 

38-7 

6-o 

4,3-0 

526-0 

2,844-0 

Suggested 

78-I75 

4°'95 

3*9 

17*8 

522-7 

2,861-0 

Non-labour  diet  : 

1898-1899  .. 

49-0 

21-5 

— 

38-5 

404-0 

2,216-5 

1899-1905 

42-8 

20-0 

— 

28-5 

345-Q 

1,890-0 

1905  (wheat  bread) 

70*2 

35*4 

— 

37'° 

499-o 

2,680-0 

191 1  (millet  bread) 

59*2 

31-2 

— ■ 

37'° 

480-0 

2,556-0 

Suggested 

65-29 

32-9 

— 

36-0 

450-5 

2,442  0 

Bread  diet,  1898-1914 

38-0 

16-0 

— 

I2*0 

375-o 

1,803-0 

Millet  bread  diet,  1 9 1 1 

28*0 

II'O 

—  . 

12-0 

354'° 

1,679-0 

Starling  has  recently  drawn  attention  to  the  fat  factor  in  the  diet, 
and  concludes  that  if  the  Calorie  value  of  the  total  diet  is  sufficient 
there  is  no  evidence  of  a  physiological  minimum,  but  the  human 
alimentary  canal  has  become  so  accustomed  to  fat  that  it  requires 
this  factor  in  the  following  ratio : — 


Age  in  Years. 

Total  Calories 
per  Day. 

Fat  in 
Grammes. 

Fat  Calories 
per  Cent, 
of  Total. 

Gross.           Net. 

0  to  6 

1,650           1,500 

62 

35 

6  to  10   . . 

2,310           2,100 

62 

25 

10  to  13   .  . 

2,750           2,500 

74 

25 

13  to  20: 

Males 

3,300           3,000 

88 

25 

Females 

2,750           2,500 

74 

25 

Adult      average      bodily- 

workers  : 

Males 

3,300           3,000 

70-88 

20-25 

Females 

2,750           2,500 

60-74 

20-25 

Adult  sedentary  workers : 

Males 

2.750           2,500 

60-74 

20-25 

Females 

2,200           2,000 

47-60 

20-25 

Adult  very  heavy  bodily 

workers 

3,900  to  5,000 

12-160 

30 

104  TROPICAL  FOODS 

Chalmers  Watson  found  by  actual  analysis  that  the  daily  dietaries 
of  eight  healthy  English  children  between  four  and  six  years  of  age 
contained  protein  71  grammes,  fat  67  grammes,  carbohydrates 
198  grammes,  and  yielded  a  total  of  1,725  Calories. 

A  most  important  matter  is  that  food  must  be  made  tasty,  and 
should  be  well  cooked  and  look  nice — matters  of  great  importance 
in  armies. 

As  emphasized  by  Rho,  in  making  a  dietary  the  racial  food  peculi- 
arities, which  are,  after  all,  adaptations  to  climate,  should  always  be 
taken  into  consideration— e.g.,  the  beef -eating  British  soldier  requires 
a  different  dietary  from  that  of  the  soldiers  of  Southern  countries. 

TROPICAL  FOOD  MATERIALS. 

Excluding  the  work  of  McCay  and  of  Wilson,  there  is  very  little 
information  available  as  to  the  chemical  composition,  the  biological 
value,  or  the  absorptions  of  tropical  food  materials. 

Wheat. — This  is  a  very  important  cereal  in  many  tropical  places.  The  grain 
is  ground  between  small  hand-moved  stones  and  the  bran  removed  by  sifting, 
while  the  meal  contains  the  germ  and  the  endosperm.  Wheat  and  barley 
are  often  mixed,  while  poor  samples  may  contain  gram,  maize,  linseed,  etc. 
McCay  finds  that  the  absorption  of  wheat  in  India  amounts  to  about  80*5  per 
cent,  of  the  protein  contained  in  all  the  elements  of  the  wheat  grain,  including 
the  germs- — everything,  in  fact,  except  the  coarser  parts  of  the  bran. 

In  the  modern  steel-roller  milling  both  bran  and  germ  are  removed  and  the 
flour  is  composed  solely  of  endosperm,  of  which  the  central  portion,  poor  in 
protein  and  rich  in  starch,  forms  the  patents,  and  the  remaining  part  household 
or  bakers'  flour,  while  the  flour  from  the  whole  wheat  is  called  Graham,  and 
from  the  entire  grain — i.e.,  with  germ  and  semolina — is  standard. 

Rice. — Turning  now  to  the  consideration  of  certain  articles  of  food  in 
common  use  in  the  tropics,  one  of  the  most  important  is  rice,  because  it  is 
widely  used  throughout  the  East,  where  it  is  believed  to  be  consumed  by 
over  400,000,000  Indians,  Chinese,  Japanese,  and  Malays,  and  because  it  is 
very  deficient  in  protein  material,  and  for  this  reason  has  to  be  consumed  in 
large  quantities  in  order  that  a  sufficiency  of  this  important  factor  may  be 
obtained.  Unfortunately  dry  rice  absorbs  water  very  greedily,  and  is  increased 
by  boiling  in  water  to  five  times  its  original  bulk.  Further,  its  progress 
through  the  stomach  is  slow,  and  therefore  it  not  merely  distends,  but  keeps 
this  organ  distended  for  some  hours. 

Rice  is,  however,  well  digested  in  the  intestines,  nearly  all  the  starch  being 
absorbed,  while  the  protein  absorbed  varies  from  45*76  to  84  per  cent.  This 
lack  of  absorption  of  protein  leads,  therefore,  to  a  loss  in  the  nitrogenous 
value  of  the  rice,  and,  indeed,  is  the  chief  method  of  loss  of  its  nitrogenous 
value,  as  but  little  disappears  during  cooking.  The  percentage  of  nitrogen, 
absorbed  from  a  rice  diet  has  been  shown  by  McCay  to  vary  directly  with 
the  quantity  of  the  rice.  Thus,  in  a  mixed  diet  containing  32  ounces  of  rice 
6*55  grammes  of  nitrogen,  or  45*76  per  cent.,  were  absorbed;  while  the  same 
diet,  with  only  20  ounces  of  rice,  showed  8*40  grammes  of  nitrogen,  or  68*33 
per  cent.,  to  be  absorbed.  From  this  it  will  be  evident  that  mixed  diets 
containing  large  quantities  of  rice  tend  to  a  low  standard  of  protein  absorption. 

There  are  two  kinds  of  rice  commonly  met  with,  viz. :  — 

(a)  The  Indian,  country  rice,  or  paddy,  variously  described  in  medical 
papers  as  '  cured,'  '  stale,'  '  unpolished,'  or  "  parboiled  '  rice,  which  is  prepared 
by  soaking  in  water  for  twenty-four  to  forty-eight  hours,  and  then  steaming 
in  cylinders,  and  finally  drying  by  exposure  to  the  sun.  This  rice  is  yellowish- 
brown  in  colour,  and  carries  attached  to  it  the  outer  layers  of  the  grain, 
while  it  has  not  lost  much  of  its  protein  in  the  process  of  preparation. 


TROPICAL  FOOD  MATERIALS  105 

(b)  The  Burma,  Rangoon,  or  white  rice,  also  variously  described  as 
'  uncured,'  '  milled,'  or  '  polished  '  rice,  which  is  prepared  by  milling  the  1111- 
husked  paddy  until  the  husk,  the  pericarp,  and  the  surface  layers  of  the 
seed  are  removed,  which  results  in  the  production  of  a  nice  clean  white  grain, 
partially  denuded  of  its  outer  layers  and  to  some  extent  of  its  protein. 

At  the  present  time  many  authorities  believe  that  the  differences  between 
these  two  methods  of  preparation  of  rice  are  the  explanation  of  the  etiology 
of  beri-beri,  as  they  believe  that  the  latter  method,  by  separating  the  sub- 
pericarpal  layers  from  the  rice,  deprives  it  of  a  substance  which  is  absolutely 
necessary  for  the  health  of  the  human  body. 

Maize. — With  reference  to  this  much-abused  and  excellent  food,  which  has, 
in  our  opinion,  been  wrongfully  accused  of  causing  pellagra,  we  may  briefly 
state  that  it  is  prepared  for  food  by  cru slung  between  millstones  or  milling  by 
machinery  to  produce  maize-meal,  which  can  be  made  into  unleavened 
bread  (porous  bread  cannot  be  made,  because  of  the  absence  of  the  gluten 
found  in  wheat-meal),  into  porridge  or  polenta.  Often,  however,  it  is  roasted, 
and  eaten  with  butler  and  salt. 

In  general,  about  74  to  88  per  cent,  of  its  protein  is  absorbed,  and,  as  regards 
India,  McCay  says  that  it  is  decidedly  superior  to  all  the  cereals  experimented 
upon,  with  the  exception  of  wheat.  Woods  says  that  it  is  wholesome,  cheap, 
and  well  suited  to  its  numerous  uses  as  a  food  material,  and  provides  a  greater 
return  in  protein,  carbohydrates,  and  energy  for  the  same  outlay  than  any 
other  cereal. 

Millet.— The  sorghums,  or  millets,  according  to  McCay,  show  a  very  defec- 
tive protein  absorption — e.g.,  Sorghum  vulgare  53  per  cent.,  and  Pennisetum 
typhoideum  only  49*4  per  cent. 

Legumes. — The  legumes  are  extensively  used  in  the  tropics,  and  among 
them  come  the  dais,  or  dhals,  of  India  (Cajanus  indicus,  Ervum  lens  Linn., 
Cicer  arietinum  Linn.,  Pisum  sativum  Linn.,  Phaseolus  radiatus,  Ph.  mungo,  all 
belonging  to  the  Leguminosae),  which  are  allied  to  the  European  pea,  and  all 
contain  a  high  percentage  of  protein,  whereby  they  occupy  an  important 
position  in  the  food  of  tropical  peoples.  They  are  utilized  by  being  ground 
into  meal,  from  which  unleavened  bread,  porridge,  or  sauce  is  prepared,  or 
they  are  simply  dried  (parched)  and  eaten  in  this  condition. 

They  resemble  rice  in  absorbing  a  large  quantity  of  water  when  cooked,  and 
so  becoming  bulky,  but  they  differ  from  this  and  other  food  materials  in  that 
they  are  less  thoroughly  digested.  Moreover,  their  addition  to  diet  lowers 
the  percentage  absorption  of  all  the  food  factors,  but  especially  that  of  the 
protein  factor. 

McCay  considers  that  these  dhals  produce  a  great  waste  of  nutriment,  in  that 
25*42  per  cent,  of  the  nitrogen  of  the  food  appears  in  the  fasces  of  Bengalis, 
while  only  15  per  cent,  appears  in  that  of  Europeans  on  a  vegetable  diet. 
Moreover,  he  considers  that  they  are  a  factor  in  the  production  of  the  bowel 
disorders  so  common  among  the  Bengalis. 

Wilson  has  recently  performed  much  excellent  work  in  investigating  diets 
in  Egypt.  He  gives  a  table  of  food  values,  of  which  the  following  is  an 
extract:  — 


100  Grammes  of- 


Millet  bread 
Dura 

Soya  bean  meal  .  . 
Dried  dates 
Ful  Sudani 
(shelled) 


1  v  iii  Iii  hit- 
Protein. 

1 

I  vailahle 
( 'arbohy- 

ilrate. 

Fat. 

Calorics. 

Cost  in 
Milliemes 

3*4 

7-8 

32-0 

45'0 

65-5 

28-5 

1*5 
54'<> 

2-1 

212-5 

344*3 
269-0 

0-6577 

0-82 

o-8o 

1-9 

47-0 

,,■(< 

253-c 

2-44 

19*0 

16-8 

45'0 

562-0 

1-787 

io6  TROPICAL  FOODS 


CALCULATION  OF  DIETS. 

In  the  calculation  of  diets  it  appears  to  us  that  two  important 
matters  must  be  considered — viz.,  the  quantity  of  protein  and  the 
number  of  Calories. 

With  regard  to  protein,  having  obtained  from  the  tables  of  analy- 
sis the  available  protein  in  the  food,  it  is  necessary  to  determine  its 
biological  value  and  the  quantity  of  the  absorbed  protein,  and  from 
this  the  Calories  can  be  calculated.  The  fat  and  carbohydrate 
present  no  difficulties,  except  that  it  is  necessary  to  know  the  quan- 
tity of  the  available  matter  which  is  absorbed.  Having  obtained 
the  quantities  absorbed,  the  matter  is  simple  arithmetic. 

Protein  :  fat  :  carbohydrate  ::  5  :  3  :  1. 

Having  done  thi?,  certain  facts  must  be  considered.  It  is  neces- 
sary to  remember  that  the  figures  given  for  Europe  will  not  apply 
to  the  tropics,  and  that  as  a  rule  they  do  not  represent  a  minimum, 
and  that  no  diet  should  be  based  upon  a  minimum. 

Wilson  has  invited  especial  attention  to  the  quantity  of  protein, 
which  is  not  a  producer  of  energy  until  the  carbohydrate  and  fats 
are  used  up,  but  repairs  wear  and  tear  or  is  stored  up  as  fat  or  carbo- 
hydrate. 

The  nearer  the  quantity  of  protein  is  to  the  minimum,  the  longer 
will  the  organism  require  to  rebuild  damaged  tissue  and  the  less 
will  its  powers  of  resistance  be  against  disease.  He  states  that 
excess  of  protein  will  mean  increased  heat  production,  and  therefore 
in  the  tropics,  where  there  is  a  cold  season,  two  diets  should  be  in 
existence — viz.,  one  with  less  protein  for  the  hot  weather,  and  one 
with  more  protein  for  the  cool  weather  or  cool  regions. 

If  this  is  not  done,  then  the  increased  heat  must  be  got  rid  of  by 
radiation  and  conduction,  and  this  can  be  obtained  by  natural  or 
artificial  breezes  or  by  exercise,  when  the  extra  heat  of  muscular 
exertion  will  be  dissipated  by  sweating. 

He  also  draws  attention  to  the  low  biological  values  of  the  vegetal 
proteins,  which  are  less  well  absorbed  than  are  the  animal  proteins, 
a  fact  which  he  thinks  is  due  to  the  structure  of  the  food  materials 
rather  than  to  the  nature  of  the  proteins. 

His  conclusion  with  regard  to  protein  appears  to  us  to  be  worth 
quoting. 

'  A  minimum  amount  of  protein  is  required  daily,  over  and  above 
which  a  certain  excess  is  desirable;  this  minimum  is  different  for 
different  proteins,  and  is  measured  by  the  biological  value  of  the 
protein.  In  determining,  therefore,  the  requisite  amount  of  protein 
it  is  essential  to  take  into  consideration  the  biological  value  of  the 
protein  components  of  the  diet,  and  fix  the  daily  quantities  on  this 
basis  rather  than  on  the  nitrogen  content.  In  determining  the 
amount  of  protein  the  defective  absorption  of  vegetable  proteins 
must  be  allowed  for.' 


LOW  PROTEIN  DIETARIES 


107 


We  would  add  that  care  should  be  taken  that  vitamines  and  lipoids 
are  present  in  the  dietary,  and  that  the  former  are  not  destroyed 
entirely  by  cooking. 

Water  should  be  freely  supplied  in  tropical  towns — e.g.,  Calcutta 
and  Peshawar  allow  4-15  gallons  per  head  per  diem  of  filtered  water, 
but  many  tropical  towns  are  not  so  well  provided,  and  the  minimum 
in  the  tropics  for  drinking  purposes  should  be  3  to  4  pints  per  head 
per  diem. 

Salts  are  also  of  great  importance,  and  usually  present  in  the 
food,  but  with  much  vegetal  food  addition  of  ordinary  table  salt 
is  necessary. 

LOW  PROTEIN  DIETARIES. 

In  tropical  lands  there  are  many  peoples  who  live  mainly  upon 
cooked  cultivated  vegetal  foods,  with  but  little  admixture  of  animal 
foods,  and  this  is  due  to  force  of  circumstances  rather  than  to  any 
desire  of  the  peoples,  who  would  be  glad  enough  to  eat  animal  food 
if  it  could  be  obtained.  Among  these  peoples  the  protein  in  the  food 
sinks  to  a  very7  low  amount,  with,  as  we  shall  presently  see,  a 
markedly  deteriorating  influence  on  the  race. 

The  effects  produced  by  this  low  protein  standard  may  be  illus- 
trated by  the  following  table,  which  is  given  by  McCay  to  exemplify 
the  differences  in  the  diets  of  Bengalis  as  compared  with  those  of 
Anglo-Indians  and  Eurasians  :— 


Food. 


alis  I.  Bengalis  II. 


A  nglo-Indians 

and 

Eurasians. 


Proteids  in  grammes 
Carbohydrates 

grammes 
Fats  in  grammes 

in 

67-11 

548-73 
71-55 

43-6i 

200*31 

33-92 

I 

86-56 

376-53 
54-75 

McCay,  in  his  excellent  works  quoted  at  the  end  of  this  chapter, 
has  shown  that  when  the  protein  standard  of  a  tropical  dietary  is 
very  low,  then  the  physique,  the  capacity  for  work,  the  health,  and 
the  resistance  against  disease  are  also  lowered,  and  he  has  illustrated 
these  facts  by  reference  to  the  rice-eating  Bengali.  Moreover,  he 
has  answered  his  critics  in  a  most  able  manner,  and  has  demonstrated 
by  comparing  closely-allied  tribes  living  under  identical  conditions 
of  climate,  solar  irradiation,  sexual  excesses,  early  marriage,  etc., 
that  it  is  the  influence  exerted  by  the  food,  and  particularly  by  the 
proteins  of  the  food,  that  is  all-important  in  determining  the  degree 
of  muscular  power,  the  general  physical  endowment,  the  powers  of 
endurance,  the  resistance  to  disease,  and,  most  important  of  all, 
the  place  which  a  tribe  or  race  has  won  for  itself  in  manliness, 
courage,  and  soldierly  instincts.  It  is  impossible  to  discuss  at  length 
in  this  place  the  facts  which  he  has  adduced,  but  certain  important 
results  may  be  briefly  mentioned. 


loR 


TROPICAL  FOODS 


Thus,  he  has  drawn  attention  to  the  great  difference  in  the  analysis  of  the 
blood  of  male  Bengalis  in  India,  as  compared  with  that  of  the  blood  of  Euro- 
peans in  Europe,  as  set  forth  in  the  following  table: — 


Nature  of  Observation. 

Male  Bengalis  in 
India. 

Europeans  in 
Europe. 

Erythrocytes 

5,300,000 

5,193,000 

Leucocytes 

g, 000 

7,500 

Haemoglobin    (Haldane's 

Si 

100 

method) 
Colour  index 

0*74  to  0-85 

0-95  to  i-i 

Water             

Total  solids 

78-S8 

2I-I2 

78-87 
21-13 

Proteids 

18-26 

19-17 

Salts 

1-06 

0-78 

Blood-pressure    in    brachial 

100  millimetres 

no  to  130  milli- 

by   Riva-Rocci's     sphyg- 
momanometer 

Hyg. 

metres  Hyg. 

Ratio  of  salts  in  the  urine  to 

1-2 

2-0 

those  in  the  blood 

His  observations  show  that  too  little  protein  in  the  food  affects  the  growth 
of  the  Bengali  boy,  who  grows  up  slender,  and  is  defective  in  vigour  and 
vitality;  and  in  conjunction  with  Bannarji,  Dutton,  and  Ghosal,  he  has  demon- 
strated the  differences  in  the  constitutents  of  the  urine  in  male  Bengalis  in 
India,  as  compared  with  male  Europeans  in  Europe,  as  is  shown  in  this  table : — 


Constituent  in  the  Urine. 

Male  Bengalis  in 
India. 

Male  Europeans  in 
Europe. 

Quantity 

1,177  cc- 

1,200  to  1,500  ex. 

Specific  gravity 

1,006  to  1,024 

1,015  to  1,025 

Urea 

5-56  to  19-68  grammes 

30  to  35  grammes 

per  diem 

per  diem 

Total  nitrogen 

5-9  grammes  per  diem 

14  to  1 8  grammes 

Chlorides 

9*43  grammes  per 

15  grammes  per 

diem 

diem 

Phosphates    .  . 

0-95  to  1-4  grammes 

2  to  3-5  grammes 

per  diem 

per  diem 

N :  P205  ratio 

5  or  6  :  1 

Practically  the  same 

Uric  acid 

0-48  gramme  per 

0-3  to  7  grammes  per 

diem 

diem 

Total  sulphates 

1-75  to  2-2  grammes   , 

2'5  t°  3  grammes 

El  in-real  sulphates 

0-15  to  0*22  gramme  ! 

— 

These  are  most  important  conclusions,  and  we  must  state  that 
our  own  observations  in  tropical  practice  support  McCay,  and  are 
directly  in  opposition  to  Chittenden's  observations.  We  have 
observed  that  when  persons  in  good  health  have  for  some  time  carried 
out  Chittenden's  dietary,  the  result  has  often  been  sharp  attacks 
of  illness,  indicating  a  lowered  resistance  to  disease. 


V  IT  AMINES  109 

VITAMINES. 

Eijkmann,  Gryns,  Takaki,  Fraser,  and  Stanton,  have  shown  that 
the  uncured,  milled,  polished,  or  white  rice  is  deprived  of  its  subperi- 
carpal  layers  by  the  processes  of  milling  or  polishing,  and  that  these 
layers  contain  some  substance  of  importance  in  the  prevention  of 
beri-beri.  This  substance  is  present  in  the  proportion  of  o-i  gramme 
to  the  kilogramme  of  rice.  Funk  has  isolated  this  substance, 
called  beri-beri  vita  mine,  from  the  polishings  of  the  rice  mentioned 
above,  and  has  determined  its  chemical  composition — i.e.,  55-63 
per  cent.  C,  5-29  per  cent.  H,  and  7-68  per  cent.  N,  which  corre- 
spond best  to  the  formula  C17Hls04N(HN03) — and  has  demonstrated 
its  power  of  curing  the  polyneuritis  induced  in  fowls  by  a  rice  diet, 
4  milligrammes  being  sufficient  to  cure  pigeons.  In  further  re- 
searches he  came  to  the  conclusion  that  the  beri-beri  vitamine  was 
a  base  belonging  to  the  pyramidine  group,  and  that  its  formula 
was: — 

NH<v 

CO— ^C„;H]S0,:. 

NH/ 

It  was  described  as  being  soluble  in  water,  alcohol,  and  acidulated 
alcohol,  as  being  dialyzable  and  capable  of  being  destroyed  by  heat 
at  1300  C,  while  the  amount  present  in  1  kilogramme  of  rice  is 
o-oi  gramme. 

According  to  Funk,  this  substance  is  essential  for  the  metabolism 
oi  the  nervous  system,  and  if  it  is  lacking  in  a  diet  it  must  be  supplied 
from  the  body,  and  when  this  fails  then  symptoms  of  beri-beri 
appear. 

Beri-beri  is,  therefore,  according  to  general  opinion,  a  deficiency 
disease,  and  is  grouped  with  epidemic  dropsy,  scurvy,  experimental 
scurvy,  infantile  scurvy,  ship  beri-beri,  pellagra,  and  polyneuritis 
of  birds. 

All  vitamines  are  not  the  same,  and  the  scurvy  vitamine  appears 
to  be  different  from  that  of  beri-beri,  being  a  crystalline  substance 
destroyablc  at  1200  C.  or  less,  and  constant  in  fresh  potatoes,  onions, 
cabbages,  apples,  lemons,  limes,  and  lime-juice;  and  being  less  stable 
than  that  of  beri-beri,  is  only  found  in  the  fresh  condition  of  vege- 
tables and  fruits. 

There  appears  also  to  be  a  specific  growth  vitamine,  the  composition 
of  which  is  unknown.  It  is  contained  in  milk,  and  is  necessary  for 
the  growth  and  development  of  the  child.  If  the  mother  suffers  from 
beri-beri,  as  Andrews  has  shown,  there  will  be  great  risk  of  the  child 
dying  either  of  beri-beri  or  some  other  complaint,  owing  to  defective 
growth  and  development. 

There  is  also  a  suggestion  that  pellagra  may  be  a  deficiency 
disease. 

With  regard  to  the  distribution  of  vitamines,  they  are  present  in 


no  TROPICAL  FOODS 

yeast,  milk,  cereals,  and  probably  in  muscle  juice,  brain,  fish, 
legumes,  and  fresh  vegetables.  With  regard  to  cereals,  they  are 
present  in  the  germ  and  subpericarpal  layers  of  the  bran  of  wheat, 
in  rice  bran,  and  in  the  pericarp  and  outer  layers  of  maize. 

Their  action  upon  metabolism  is  unknown,  and  it  is  still  doubtful 
whether  they  assist  anabolism  as  hormones. 

The  processes  associated  with  the  sterilization  and  canning  of 
foods  destroy  vitamines. 

Lipoids. — The  best  known  of  the  lipoids  is  lecithin,  and  it  is  sug- 
gested that  they  are  required  to  enable  amino-acids,  fats,  and  salts 
to  enter  the  cells  of  the  body,  and  so  to  form  the  colloidal  substances 
thereof.  It  is  further  suggested  that  mice  cannot  live  on  lipoid- 
free  food,  and  that  perhaps  vitamines  are  unable  to  enter  the  cells 
except  as  lipoidal  compounds,  but  the  whole  subject  is  very  nebulous. 


LITTLE-KNOWN  MATTERS. 

All  proteins  contain  amino-acids,  but  these  are  not  combined 
in  the  same  proportions,  and  it  appears  possible  that  a  minimum 
thereof  is  necessary  for  the  growth,  if  not  for  the  maintenance  in 
health,  of  the  organism;  but  the  whole  subject  is  in  its  infancy, 
and  the  same  holds  good  with  regard  to  the  salts,  some  of  which 
may  be  necessary  for  proteins  and  others  for  the  lipoids. 


REFERENCES. 

The  most  valuable  works  are  McCay  (1912),  '  Protein  Element  in  Nutrition, ' 
London,  and  Wilson  (1917),  Report  of  the  Prison  Diets  Committee,  Cairo. 
We  feel  that  anyone  interested  in  tropical  diets  ought  to  be  conversant  with 
these  works.  In  addition  Tibbies  (1912),  'Foods,'  and  (1914)  'Dietetics,' 
appear  to  be  those  most  useful  to  the  tropical  practitioner. 

Armand  Hoyson  (191  i).     Philippine  Journal  of  Science.     (Rice  as  a  Food.) 

Atwater  (1902).     Bull.  177,  U.S.  Dept.  Agriculture. 

Belli  (191 8).     Annali  Medicina  Navale. 

Belli  (1919).     Annali  Medicina  Navale,  Vol.  II.,  Fasc.  v.-vi. 

Benedict  (1906J.  American  Journal  of  Physiology.  With  Carpenter  (1910). 
Metabolism  and  Energy  Transformation. 

Campbell.     Evolution  of  Man's  Diet. 

Chittenden  (1907).     The  Nutrition  of  Man,  vol.  xvi.     London. 

Church.     Food  Grains  of  India. 

Fraser  and  Stanton  (1911).  Studies  from  the  Institute  for  Medical  Re- 
search, Malay  States,   No.  12  (Etiology  of  Beri-beri). 

Friedenthal  (1914).  Allgemeine  und  Spezielle  Physiologie  des  Menschen- 
wachstums.     (Good  bibliography.)     Berlin. 

Funk  (1911).     Journal  of  Physiology,  xliii.  395. 

Hindhede  (1913).     Protein  and  Nutrition.     London. 

Hutchinson  (191 1).     Food  and  the  Principles  of  Dietetics. 

Langworthy  (1897).     United  States  Department  of  Agriculture,  No.  46. 

Macknight  (1904).     Food  for  the  Tropics.     London. 

McCay  (1907).  Indian  Medical  Gazette,  xlii.  370;  and  Scientific  Memoirs 
Government  of  India,  Nos.  34,  37,  and  48. 

McKillop  (1916).     Food  Values.     London. 


REFERENCES  in 

Medical  Research  Committee  (1918).     Composition  of  Dietaries,  No.  13. 

Moore  (191  i).     British  Medical  Journal,  ii.  11 37. 

Osborne  (1911).     Science,  725.     (1911).     Carnegie  Institute  of  Washington, 

No.  157,  Parts  1  and  2. 
Oshtma.     United  States  Department  of  Agriculture. 
Peckolt.     Historia  das  Plantas  Alimentares  do  Brasil.     Rio  de  Janeiro. 
Kanke    (1900).       Einwirkung    des    Tropenklimas    auf    die    Ernahrung    des 

Menschen.     (Copious  literature.)     Berlin. 
Rho  (1918).     Annali  Medicina  Navale. 
Rubner   (1902).     Die  Gesetze   des   Energieverbrauchs   bei   der   Ernahrung. 

Leipzig.     With  Gruber   and  Fischer  (191 1).     Handbuch  der    Hygiene. 

(191 3).     Wandlungen  in  der  Volksernahrung. 
Russell  (1906).     Strength  and  Diet.     London. 
Simmonds  (1888).     Popular  Beverages.     London. 
Starling  (1918).     British  Medical  Journal,  ii.  107,  August  3. 
Tigerstedt   (1906).     Nagel's  Handbuch  der   Physiologie  des   Menschen,   i. 

544,  etc. 
Wolpf.rt  (1896).     Archiv  fiir  Hygiene,  xxvi.  107. 


CHAPTER  V 
TROPICAL  DISEASES 

Preliminary  remarks — Evolu  tion — G  eographical  discovery — Endemicity — 
Epidemicity — Eugenics- —  Incidence — Distribution — Prevention — Refer- 
ences. 

PRELIMINARY  RF  MARKS. 

Before  entering  upon  the  systematic  study  of  tropical  diseases  a 
few  remarks  may  be  made  upon  their  evolution,  the  influences  of 
geographical  discovery  upon  their  dissemination,  their  endemicity 
and  epidemicity,  tropical  eugenics,  the  geography  of  tropical  disease 
with  special  reference  to  countries  and  not  to  given  diseases,  and 
finally  the  prevention  of  these  diseases. 

It  will  be  obvious  that,  if  these  subjects  were  to  be  treated  at  all 
fully,  they  would  require  several  volumes,  each  of  which  would  be 
larger  than  the  present  little  book;  but  this  is  not  our  object,  which 
is  to  bring  subjects  to  the  notice  of  the  tropical  practitioner  with  the 
view  that  he  may  apply  them  to  the  diseases  and  peoples  by  whom 
he  is  surrounded,  and  references  are  given  whereby  he  may  extend 
his  reading  and  knowledge  far  beyond  the  confined  limits  of  our 
manual. 

All  tropical  countries  are  inhabited  by  three  different  sets  of 
inhabitants.  Firstly,  there  are  the  true  indigenous  natives ;  secondly, 
there  are  immigrants  from  other  countries;  and,  thirdly,  there  are 
the  descendants  of  an  admixture  of  the  first  two,  and  generally  of  a 
European  with  a  native.  Such  are  the  Mulattoes  of  Central  and 
Southern  America,  the  Eurasians  or  Anglo-Indians  of  India,  and  the 
Burghers  of  Ceylon,  and  it  is  our  duty  to  1  ry  to  trace  out  the  cause 
of  disease  and  death  among  these  peoples. 

EVOLUTION. 

Auckland  Geddes  and  Adami  consider  that  the  Piltdown  skull  is 
pathological,  and  that  its  remarkable  thickness  and  the  bold  out- 
line of  the  temporal  ridges  are  to  be  explained  by  the  assumption 
that  its  original  owner  suffered  from  acromegaly. 

I  he  researches  oi  the  late  highly  talented  Sir  Armand  Rufier  into  palao- 
pathology  have  demonstrated  the  existence  of  bilharziosis,  tuberculosis,  rheu- 
matoid artliritis,  and  pyorrhoea  alveolaris  in  Egyptian  mummies  dating  some 
I ,'  m  ii  i-6,(  x  to  B.C.,  while  certainly  some  of  the  organisms  of  disease  were  present 
then,  as  he  was  able  to  demonstrate  the  tubercle  bacillus  in  mummies  of  the 
Twelfth  Dynasty. 


EVOLUTION  it  3 

But  disease  is  much  older  than  man,  for  Moodie  has  noted  the  presence  of 
arthritis  and  osteomyelitis  in  cave  bears,  of  pyorrhoea  in  early  tertiary  three- 
toed  horses,  and  caries  in  Permian  fish. 

There  can  be  no  doubt  as  to  the  great  antiquity  of  bacteria,  and  it  seems 
possible  that  they  performed  great  geological  works  in  the  early  history  of  the 
world,  and  may  be  largely  responsible  for  the  formation  of  some  of  the  oldest 
sedimentary  rocks,  in  much  the  same  way  as  Drew's  Bacillus  calcis  does  its 
work  to-day  in  the  lagoons  of  Florida  and  on  the  Great  Bahama  Reef. 

When  higher  plants  and  animals  evolved,  the  struggle  for  exist- 
ence must  have  compelled  minute  animal  and  vegetal  organisms  to 
seek  protection  for  themselves  therein,  and  at  first  this  protection 
would  be  used  temporarily  to  tide  over  some  difficulty. 

This  being  admitted,  the  parasite  would  desire  an  easy  method 
of  entrance  into  and  escape  from  the  body  of  the  temporary  host, 
and  hence  the  common  infection  of  the  alimentary  canal  with 
organisms. 

So  long  as  the  chemical  substances  produced  by  the  metabolism 
of  the  parasite  were  innocuous  or  helpful  to  the  host,  there  would 
be  no  reaction  on  its  part  against  the  intruder,  and  the  two  would 
live  together  in  peace,  as  many  bacteria  do  at  the  present  day  in  the 
human  alimentary  canal,  and  a  condition  of  commensalism  may  be 
arrived  at. 

Other  intruders,  on  the  other  hand,  might  give  rise  to  irritating 
chemical  substances  which  would  provoke  a  reaction  on  the  part  of 
the  host.  And  thus  begins  the  long  struggle  between  the  invading 
organism  and  cells  of  the  host  which  has  produced  all  those  compli- 
cated mechanisms  which  are  gathered  together  under  the  term 
'  immunity.'  The  reader  will  notice  that  the  whole  of  this  struggle 
is  adaptation  to  environment— -viz.,  to  that  portion  of  the  host's 
environment  in  which  is  centred  the  invading  organism. 

The  parasite  would  naturally  attempt  to  escape  from  the  defensive 
chemical  substances  poured  on  to  it  by  the  host,  and  in  so  doing 
pierced  more  deeply  into  the  tissues  of  that  host ;  but  now  its  escape 
would  not  be  so  easy  as  when  living  in  some  cavity  freely  communi- 
cating with  the  exterior,  and  hence  it  would  be  to  its  advantage  to 
either  kill  that  host,  or,  if  it  failed  to  do  that,  to  enter  some  cavity 
communicating  with  the  exterior  and  suitable  for  the  parasite's 
existence — e.g.,  the  enteric  bacilli  in  the  gall-bladder  and  the  pelvis 
of  the  kidney. 

All  these  changes  of  environment  would  cause  variation  in  the 
protists  (protozoan  and  bacterial),  and,  if  the  same  environmental 
conditions  acted  long  enough,  then  these  changes  would  become 
inherited  (vide  Adami);  hence  the  origin  of  the  numerous  parasitic 
protists,  animal  and  vegetal,  and  hence  also  the  preservation  of 
characters,  including  those  complicated  phenomena  associated  with 
the  reaction  of  the  host  which  we  call  the  signs  and  symptoms  of 
disease  and  the  natural  recovery  therefrom  It  appears  to  us  that 
ust  as  disease  arose  de  novo  in  the  long  ago,  so  it  has  probably  been 
arising  century  after  century,  and  we  see  no  reason  why  new  diseases 
should  not  appear  in  the  twentieth  century  of  the  present  era  in 

8 


H4  TROPICAL  DISEASES 

man  and  animals,  as  they  did  when  hosts  were  first  evolved,  only 
the  matter  is  more  complicated  owing  to  the  evolution  of  methods 
of  defence  upon  the  part  of  the  host. 

In  his  most  interesting  and  masterly  book  Adami  has  shown  that 
a  non-pathogenic  organism  can  be  made  pathogenic  by  injecting 
into  an  animal  killed  non-pathogenic  bacilli,  and  then  ten  or  fifteen 
days  later  the  live  bacilli.  These,  when  recovered  from  the  tissues 
of  the  experimental  animals,  were  found  to  have  undergone*  consider- 
able variation  due  to  their  altered  environment,  and  had  so  changed 
their  characters  as  to  be  very  virulent  to  guinea-pigs.  In  other 
words,  by  means  of  a  preliminary  anaphylactic  phenomenon  a  non- 
pathogenic microbe  may  become  pathogenic  and  a  new  disease  be 
evolved. 

Similarly,  according  to  some  of  our  observations,  when  man  is 
immunized  artificially  against  typhoid  and  the  paratyphoids,  he 
becomes  more  susceptible  to  infections  by  chance  intestinal  organ- 
isms, which  in  this  way  give  rise  to  new  diseases. 

Finally  a  germ  accustomed  to  a  human  race  which  has  developed 
a  certain  amount  of  immunity  may  meet  with  another  race  which 
lacks  this  immunity,  and  immediately  a  disease  which  is  mild  may 
develop  rapidly  fatal  attacks  and  spread  widely — e.g.,  measles  in 
the  Sandwich  Islanders  in  London  long  ago. 

Enough  has  been  said  to  show  the  line  of  thought — viz.,  the 
importance  of  environment,  the  difficulty  of  impressing  characters, 
but  the  hereditary  transmission  of  these  characters  when  once 
evolved  producing  variation  in  the  parasites,  while  the  reaction  on 
the  part  of  the  host  tending  to  produce  an  immunity  against  older 
forms,  and  yet  leaving,  in  the  phenomenon  of  anaphylaxis,  a  gate 
open  for  further  variation  on  the  part  of  non-pathogenic  organisms 
and  the  possibility  of  the  origin  of  new  diseases. 

GEOGRAPHICAL  DISCOVERY. 

Just  above  we  have  mentioned  the  introduction  of  pathogenic 
organisms  to  races  to  which  they  were  previously  unknown,  and  as 
this  is  primarily  due  to  geographical  discovery,  we  desire  to  invite 
the  reader's  attention  to  this  factor  in  the  dissemination  of  tropical 
disease,  as  the  discovery  of  new  lands  has  eventual^  led  to  the 
betterment  of  means  of  communication,  and  hence  to  the  easier 
and  quicker  transference  of  the  microbes  of  disease. 

Diseases  which  may  have  been  endemic  in  one  region  for  centuries 
may,  by  means  of  geographical  discovery  and  by  means  of  the  present 
and  past  wars,  spread  to  other  regions  where  they  were  previously 
unknown;  and  this  brings  us  to  the  consideration  of  endemicity  and 
epidemicity. 

ENDEMICITY. 

As  so  much  epidemiological  investigation  of  disease  has  of  late 
been  undertaken,  mainly  due  to  the  initiative  of  Manson  and  Sambon, 


ENDEMICITY  115 

we  feel  that  a  few  general  remarks  on  endemicity  and  epidemicity 
as  applied  to  disease  in  general  may  not  be  amiss. 

The  presence  of  a  given  disease  in  a  locality  depends  primarily 
upon  the  presence  of  conditions  favourable  for  the  action  of  the 
causal  agent,  and  upon  the  presence  of  suitable  vehicles  for  its  convey- 
ance into  the  human  body,  which  must  be  non-immune  to  its  attack. 
The  causal  agents  of  disease  may  be  physical,  chemical,  or  parasitic. 

Physical  causes  of  disease  are  often  cosmopolitan  in  their  distribu- 
tion—as, for  example,  the  action  of  gravity  in  producing  the  trau- 
matisms brought  about  by  falls;  but  though  some  causes,  such  as 
the  rays  from  the  sun,  are  also  cosmopolitan,  still  they  are  unable  to 
produce  deleterious  effects  upon  human  beings  unless  assisted  by 
secondary  influences,  such  as  latitude,  altitude,  the  rotation  and 
inclination  of  the  world,  etc.,  while  some  are  restricted — as,  for 
example,  the  traumatisms  due  to  ferocious  animals,  which,  though 
occasionally  taking  place  in  other  parts,  whither  the  animals  have 
been  artificially  conveyed,  generally  only  occur  in  the  natural 
habitats  of  these  creatuivs. 

Chemical  causes  of  disease  have  become  largely  cosmopolitan  in 
distribution  owing  to  improved  methods  of  intercommunication 
,in<l  the  manufacture  of  chemical  principles;  still,  certain  chemical 
causes  have  very  restricted  localities  even  to-day,  because  they  are 
little  known,  and  only  affect  primitive  peoples  living  in  these  regions 
— e.g.,  Glariosa  superba,  etc. 

The  parasitic  causes  of  disease  may  be  animal  or  vegetal.  The 
endemicity  of  a  given  parasite  depends  upon  (a)  the  presence  of  non- 
immune human  beings,  in  which  part  of  the  life-cycle  can  be  gone 
through,  and  which  for  convenience  we  will  term  the  human  hosts  ; 

(b)  easy  modes  of  escape  from  the  human  host  into  the  exterior; 

(c)  suitable  means  of  continuing  the  life-cycle  in  the  exterior- — i.e., 
in  earth,  water,  air,  on  or  in  other  animals  or  plants,  intermediary 
hosts  we  will  call  them;  (d)  ready  means  of  re-entry  into  the  human 
host  or  into  some  other  animal  host  in  which  the  life-cycle  is  com- 
pleted; {e)  partially  immune  animal  hosts  or  partially  immune 
human  hosts  to  act  as  reservoirs  or  carriers,  to  enable  the  parasite 
to  complete  its  life-cycle  without  producing  marked  pathological 
changes  in  the  host.  Examples  of  these  may  be  found  in  the 
malarial  parasite  attacking  (a)  the  white  man  and  the  native  child 
in  West  Africa  and  elsewhere,  and  passing  by  the  agency  of  (b)  blood- 
sucking  into  (c)  Anopheles   costalis,  which,  by  the  act  of  biting, 

(d)  conveys  the  parasite  to  another  non-immune  host  or  to  the 
partially  immune  adult  native,  who  acts  as  a  reservoir  or  carrier. 

Another  example  is  the  passage  of  the  plague  bacillus  from  the 
rat  via  the  flea  back  to  the  rat  or  man. 

Other  examples  are  the  amoebae  of  dysentery,  which  pass  from 
man  by  the  evacuations  on  to  vegetal  substances  or  into  water,  by 
which  they  may  be  reintroduced  into  man  direct  or  by  the  agency 
of  flies. 

By  a  suitable  non-immune  host  is  meant  a  host  which,  while 


n6  TROPICAL  DISEASES 

providing  abundant  suitable  food  material  for  the  parasite,  does  not 
produce  such  a  quantity  of  chemical  substances  antagonistic  to  the 
parasite  as  to  seriously  hamper  or  prevent  its  growth  and  development. 

Given  such  conditions  as  those  just  described,  a  parasite  should 
be  capable  of  developing  enormously  in  a  given  district;  but  there 
are  still  other  factors  to  be  considered,  and  the  first  of  these  is  the 
fact  that  the  intermediary  host,  if  an  animal,  depends  for  its  exist- 
ence upon  the  presence  of  a  suitable  food-supply,  as  well  as  suitable 
means  for  propagating  its  species. 

If  anything  untoward  happens  to  these,  the  intermediary  host 
may  die  out,  but  the  problem  is  not  quite  so  simple  as  this,  because 
the  intermediary  host  itself  may  be  preyed  upon  by  some  other 
animal,  or  may  be  affected  by  disease,  and  so  reduced  in  numbers. 

If  the  intermediary  host  is  reduced  in  numbers,  even  without 
being  exterminated,  the  parasite  will  have  difficulty  in  completing 
its  life-cycle,  and  is  therefore  faced  with  the  problem  of  seeking 
another  intermediary  host,  or  another  entirely  different  method  of 
leaving  the  human  host,  or  of  being  exterminated. 

The  reduction  in  numbers  of  the  intermediary  host  in  a  given  area 
is  one  of  the  bases  of  prophylaxis  in  malarial  fever,  yellow  fever, 
dengue  fever,  and  sleeping  sickness.  Faced  with  these  difficulties, 
it  would  appear  possible  that  the  parasite  can  change  its  inter- 
mediary, probably  undergoing  certain  changes  itself  in  so  doing, 
and  this  would  appear  to  be  a  possible  explanation  of  the  slight 
modifications  of  the  various  forms  of  spirochetes  causing  the  re- 
lapsing fevers. 

On  the  other  hand,  the  malarial  parasite  would  seem  to  be  less 
capable  of  accommodating  itself  to  a  change  of  hosts,  for  it  would 
appear  to  be  only  capable  of  completing  its  life-cycle  in  the  less 
common  anophelinae,  and  not  in  the  more  common  culicinae — a  most 
important  fact  in  malarial  prophylaxis. 

Another  factor  to  be  considered  is  the  effect  of  atmospheric 
temperature  upon  the  parasite,  for  the  study  of  the  life-cycle  of  the 
malarial  parasite  has  clearly  shown  that  this  has  a  marked  effect 
upon  the  development  of  the  oocyst  in  the  anopheles.  It  is  also 
quite  possible  that  other  physical  and  chemical  factors,  concerning 
which  we  are  at  present  ignorant,  may  play  important  parts  in 
controlling  the  life  of  parasites. 

Finally,  the  parasite  itself  may  suffer  from  the  attacks  of  another 
parasite,  a  condition  of  affairs  called  '  hyperparasitism,'  and,  thus 
becoming  diseased,  may  be  unable  to  complete  its  life-cycle,  and  so 
become  extinct. 

It  will  thus  be  seen  that  the  problems  connected  with  the  appear- 
ance and  the  disappearance  of  a  disease  in  a  locality  are  extremely 
complex,  and  that  next  to  the  parasite  itself  the  most  important 
factor  is  the  intermediary  host,  its  food,  its  life-cycle,  and  its  habits 
— in  one  word,  its  cacology. 

Hence,  in  studying  an  endemic  parasitic  disease,  or  a  disease 
thought  to  be  possibly  parasitic,  it  is  not  advisable  to  restrict  one's 


EPIDEMICITY  117 

researches  solely  to  work  in  the  hospital  or  the  laboratory — for  it 
must  be  remembered  that  the  parasitic  causes  of  some  diseases  are 
most  probably  ultramicroscopical — but  to  associate  with  the  clinical 
and  experimental  methods  of  research  epidemiological  researches 
conducted  by  visiting  several  widely  separated  and,  if  possible, 
completely  detached  endemic  areas,  in  order  by  carefully  studying 
therein  all  the  conditions  of  life  and  the  habits  of  the  human  hosts  to 
endeavour  to  find  factors  common  to  the  different  localities.  A 
further  study  of  these  common  factors  from  the  point  of  view  of 
possible  modes  of  infection  may  indicate  one  or  more  possibilities, 
and  then  these  must  be  put  to  the  crucial  test  of  experiment  with  a 
view  of  ascertaining  definitely  the  accuracy  of  the  epidemiological 
obseivations. 

EPIDEMICITY. 

From  an  endemic  area  diseases  due  to  physical  causes  may  spread 
by  the  alteration,  naturally  or  artificially,  of  the  physical  conditions 
in  the  surrounding  regions,  and  would  draw  back  to  the  original 
region  upon  the  return  to  normal  of  these  conditions.  Similarly, 
chemical  causes  of  disease  may  be  spread  from  their  original  re- 
stricted area  by  modern  methods  of  intercommunication — e.g., 
poisonous  plants  or  their  products  may  be  brought  from  the  tropics 
to  the  Temperate  Zone,  and  vice  versa. 

In  order  that  a  parasitic  disease  may  spread  from  its  endemic 
focus  several  factors  are  necessary : — 

(a)  Carriers  to  convey  it  from  one  place  to  another.  These  may 
be  either  the  human  host,  an  animal  host,  or  the  intermediary  host 
— e.g.,  fleas  infected  with  plague. 

(b)  In  order  that  the  disease  may  spread  in  the  new  area  there 
must  be  the  suitable  conditions  already  mentioned. 

(c)  There  must  also  be  suitable  climatic  conditions. 

If  these,  and  perhaps  other  still  unknown  factors,  are  present, 
the  disease  will  be  able  to  spread  with  perhaps  increased  virulence, 
first  within  the  new  area  and  then  from  one  area  to  another,  until 
an  epidemic  or  pandemic  is  produced.  With  the  appearance  of 
partial  immunity  in  the  human  and  animal  hosts,  altered  climatic 
and  other  conditions,  as  well  as  the  aestivation  or  hibernation  of 
one  of  the  hosts,  the  epidemic  will  die  down,  perhaps  only  to  re- 
awaken after  the  hibernation  of  the  host  is  over  or  with  a  change  of 
climatic  conditions;  and  this  may  be  repeated  for  years,  until 
conditions  become  too  adverse  for  the  life  of  the  parasite  or  its  host, 
when  the  epidemic  dies  away,  and  the  disease  again  becomes  re- 
stricted to  its  endemic  areas. 

The  possibilities  of  epidemics  and  the  presence  of  endemic  diseases 
raises  the  question  of  the  possibility  of  giving  man  such  a  start  in 
life  that  he  may  be  advantageously  placed  in  the  combat  before  him. 
The  questions  involved  in  such  a  possibility  constitute  the  large 
and  ever- increasing  subject  of  Eugenics,  to  which  we  will  now  turn 
our  attention. 


n8  TROPICAL  DISEASES 

EUGENICS. 

Any  attempt  to  improve  the  racial  qualities,  mental  and  physical, 
of  the  future  generations  will,  without  doubt,  equip  them  better 
for  the  struggle  for  existence,  including  therein  the  tight  against 
disease.  In  order  to  bring  about  an  improvement  two  factors  are 
open  for  consideration — viz.,  the  parents  and  the  child. 

With  regard  to  the  parents,  eugenics  attempts  to  combat  such 
racial  poisons  as  are  represented  by  alcohol  and  such  social  diseases 
as  are  indicated  by  syphilis,  gonorrhoea,  and  tuberculosis. 

In  regard  to  alcohol,  when  taken  in  large  quantities  and  for  long 
periods  it  is  said  to  act  upon  the  germ  cells,  leading  to  the  produc- 
tion of  children  possessing  a  lower  resistance  against  disease.  Un- 
fortunately, as  we  shall  see  later,  alcoholism  is  common  among  the 
natives  of  many  tropical  regions,  and  has  already  produced  marked 
racial  effects. 

Alcoholism  in  the  mother  is  a  more  serious  matter  than  alcoholism 
in  the  father,  because  in  the  former  the  embryo  is  produced  by 
alcohol-poisoned  germ  cells,  while  during  intra-uterine  life  its  grow- 
ing cells  are  being  constantly  alcoholized,  and  finally  the  child,  after 
birth,  is  either  fed  upon  an  alcoholic  mother's  milk  or,  as  is  more 
frequently  the  case,  is  reared  by  such  hand-feeding  as  an  alcoholic 
mother  may  give  it. 

As  hand-feeding  in  the  tropics  requires  the  greatest  care,  it  is  not 
surprising  that  when  reared  by  an  alcoholic  mother  the  child  usually 
acquires  disease  at  an  early  stage  of  its  life-history,  and  often  helps 
to  swell  the  infant  mortality  rate. 

Alcoholism  is  a  great  social  question,  and  can  only  be  combated 
by  a  sociological  movement  such  as  to-day  is  taking  place  in  England 
and  other  Temperate  Zone  countries. 

With  regard  to  the  so-called  social  diseases,  every  medical  practi- 
tioner is  conversant  with  syphilis  and  gonorrhoea,  and  all  that  is 
necessary  is  to  invite  attention  to  Sir  Malcolm  Morris's  summary  of 
the  Recommendations  of  the  Royal  Commission  on  Venereal 
Disease,  which  include  facilities  for  diagnosis  and  treatment,  diffu- 
sion of  knowledge  with  regard  to  the  diseases,  and  the  collection  of 
statistics.  It  is  particularly  to  be  noted  that  they  conclude  that 
at  the  present  time  any  system  of  compulsory  personal  notification 
would  fail  to  secure  the  advantages  claimed.  The  Commission 
considered  that  undeclared  venereal  disease  should  be  a  ground  for 
the  annulment  of  a  marriage.  They  further  considered  that 
advertisements  of  patent  medicines  should  be  prohibited,  and 
apparently  they  were  in  favour  of  making  it  penal  for  unqualified 
persons  to  treat  venereal  diseases.  Venereal  disease  is  at  the  present 
time  exceedingly  common  in  all  parts  of  the  tropics,  and  undoubtedly 
is  leading  to  racial  degeneration,  and  we  strongly  advocate  that 
some  preventive  scheme  should  be  inaugurated  in  all  tropical 
countries.  At  the. same  time,  we  desire  to  record  our  disapproval 
of  attempts  to  combat  these  evils  by  the  registration  and  general 


EUGENICS  H9 

police  supervision  of  prostitutes  as  we  believe  such  a  system  is 
bound  to  increase  rather  than  diminish  the  disease,  as  it  leads  to 
secrecy ;  and,  indeed,  it  has  so  far  been  a  failure  wherever  it  has  been 
put  to  the  test  seriously. 

With  regard  to  venereal  disease,  there  is  no  doubt  that,  although 
the  war  has  increased  the  numbers  of  infections,  it  has  nevertheless 
acted  beneficially  in  bringing  the  seriousness  of  the  subject  home 
to  the  authorities;  and,  even  in  England,  preventive  measures,  for 
male  and  female  alike,  are  being  widely  distributed  free  of  charge, 
and  institutes  are  in  existence  for  the  diagnosis  and  treatment  of 
these  diseases.  It  is  impossible  to  close  the  section  without  acknow- 
ledging, with  honour,  the  great  work  which  New  Zealand  has  done 
in  Europe  with  regard  to  this  matter.  When  a  country  with  tradi- 
tions like  England  has  awakened  from  its  sleep  of  ages,  a  sleep 
largely  due  to  its  religious  tendencies,  it  is  possible  for  tropical 
countries,  unhampered  by  these  religious  bands,  to  do  even  more 
than  what  we  see  going  on  around  us  as  we  write  these  lines  in 
London. 

Turning  now  to  tuberculosis,  it  seems  probable  that  the  tubercle 
bacillus  has  had  an  opportunity  of  infecting  every  child  living  in  the 
slums  of  the  large  European  cities  before  it  has  attained  the  age  of 
twelve  years.  It  would  further  appear  as  though  tuberculosis  was 
either  being  better  diagnosed  or  was  increasing  in  many  tropical 
lands. 

There  ought  to  be  no  slums  in  tropical  countries,  and  where  they 
exist  it  is  the  duty  of  the  Government,  forthwith,  to  formulate  a 
scheme  of  betterment  whereby  in  the  course  of  years  they  shall  be 
removed,  and  State-built,  State-owned,  and  State-regulated  build- 
ings should  be  provided,  where  ihe  poor  may  live  in  a  reasonable 
condition  of  sanitation.  Further,  it  should  be  the  duty  of  the  State 
to  take  over  and  to  bring  up  such  illegitimate  children  as  cannot  be 
properly  provided  for,  thereby  not  merely  helping  in  the  popu- 
lation and  work  questions,  but  also  in  the  diminution  of  tuberculosis. 

In  the  tropics  there  are  two  other  eugenic  problems  to  which  we 
may  invite  attention,  and  these  are  food  and  half-castes. 

With  regard  to  food,  the  low  protein  dietary  of  the  poorer  native 
population  of  such  regions  as  India  is  a  great  sociological  problem, 
being  connected  with  n."  ^ious  sentiment.  It  leads  to  racial 
degeneration,  as  we  have  already  seen,  but  its  remedy  is  very  diffi- 
cult, and  must  be  done  by  a  social  movement  on  the  part  of  the 
natives  themselves. 

In  regard  to  half-castes,  the  number  of  poor  Eurasians  or  Anglo- 
Indians  in  India  is  increasing,  and  as  their  children  live  in  the  slums 
of  great  cities  they  tend  to  degenerate. 

After  fourteen  years  of  strenuous  work  Graham  has  shown  that 
if  these  children  are  taken  to  sanatoria  in  the  Himalaya  Mountains, 
and  placed  in  a  new  physical,  mental,  and  moral  environment,  they 
do  not  show  this  degeneration. 

This  is  a  great  discovery,  and  if  confirmed  and  acted  upon  may 


120  TROPICAL  DISEASES 

produce  lasting  results,  because,  as  we  have  already  hinted,  there 
is  a  belief  that  the  third  generation  of  children,  with  European 
parents,  born  and  living  entirely  in  the  tropics,  tend  to  degeneration 
in  every  way,  and  yet  it  is  desirable  that  portions  of  the  tropics 
should  be  permanently  colonized  from  temperate  climates  if  possible. 

Lastly,  the  infantile  mortality  of  most  tropical  countries  is  appal- 
lingly high,  and  this  passes  unheeded,  even  in  places  where  a  local 
dearth  of  labour  indicates  to  those  in  authority  the  necessity  for  a 
steady  and  rapid  increase  in  the  population.  This  is  not  a  book  on 
hygiene,  but  perhaps  as  practitioners  for  many  years  in  various 
tropical  countries  we  may  be  permitted  to  recommend  anyone 
anxious  to  reduce  the  death-rate  of  a  district  to  study  the  factors 
which  contribute  to  the  local  infantile  mortality,  and  to  combat 
those  of  greatest  importance,  which  will  often  be  found  to  be  tetanus 
and  diarrhoea,  the  latter  being  associated  with  the  question  of  a  pure 
milk  supply. 

Enough,  perhaps  too  much,  has  now  been  written  as  regards 
lines  of  thought  associated  with  the  word  eugenics  as  applied  to  the 
tropics,  and  we  will  now  pass  on  to  consider  the  incidence  of  disease 
in  tropical  countries. 

INCIDENCE  OF  DISEASE. 

In  previous  editions  we  gave  in  considerable  detail  the  analysis 
of  the  causes  of  death  in  Ceylon,  and  their  incidence  in  the  various 
peoples  inhabiting  that  island.  Several  years  have  passed  since  these 
figures  were  compiled,  and  as  they  are  old  we  omit  them,  and  take 
a  general  view  of  the  distribution  of  disease  in  tropical  countries. 

DISTRIBUTION  OF  DISEASE. 

Asia. 

Asia  Minor  is  not  a  tropical  country,  as  it  possesses  cold  and  prolonged 
winters,  but  it  also  has  very  hot  summers,  during  which  it  resembles  the 
tropics,  and  becomes  the  home  of  many  diseases,  such  as  malaria,  enteric 
fevers,  dysentery,  and  often  cholera,  while  diphtheria  is  usually  present,  and 
cerebro-spinal  meningitis  is  by  no  means  unknown.  Goitre  and  cretinism 
exist  in  the  Valley  of  the  Upper  Euphrates. 

In  Mesopotamia  the  winters  are  temperate,  but  the  summers  are  very  hot, 
and  heat-stroke  is  well  known,  while  malaria,  the  enteric  fevers,  dysentery, 
and  cholera  are  present.  Plague  is  said  to  have  been  endemic  in  this  region 
for  years.  Typhus,  smallpox,  measles,  whooping-cough,  and,  it  is  said, 
scarlet  fever,  occur  there.  Bagdad  sore  is  almost  too  well  known  to  be 
mentioned,  while  beri-beri  occurred  in  the  siege  of  Kut,  and  also  among  other 
troops. 

In  Arabia,  in  addition  to  the  fevers  mentioned  above,  ophthalmia  is  to  be 
noted. 

Very  little  is  accurately  known  as  to  the  diseases  of  Persia,  though  we 
possess  a  large  manuscript  written  thereon  many  years  ago.  Cutaneous 
Leishmaniasis,  leprosy,  and  some  form  of  relapsing  lever  may  be  noted. 

As  regards  India,  in  the  Bombay  Presidency  the  infantile  mortality  in 
native  races  is  220*08  in  males  and  219-07  in  females  per  1,000  births.  In 
Bombay  City  the  ratios  were  557*24  and  569*66,  but  it  is  stated  that  these 
ratios  are  very  fallacious. 


DISTRIBUTION  OF  DISEASE 


The  racial  death-rates  are: — 

Europeans 
Eurasians 
Natives 


1905. 

14-36 
20*89 
31-84 


1906. 
14-41 
26-99 
41-39 


natives 


The  year  1905  seems  to  have  been  unusually  healthy;  only  588,394 
died,  as  compared  with  1,318,783  in  1900. 

The  principal  cause  of  death  was  plague,  which  accounted  for  71,363,  or 
12-13  Per  cent.,  in  1905,  as  compared  with  223,957,  or  29-28  per  cent.,  in  1904. 

The  plague  deaths  in  Bombay  for  the  ten  years  1896-1905  are  as  follows: — 

2,086 
46,944 


1897 
1898 
1899 
1900 
1 90 1 
1902 
1903 
1904 
1905 


Total. 


The  population  in  1901  was: — 

European  (exclusive  of  cantonments) 

Eurasian 

Native 


86,191 

96,596 

33.196 

128,259 

184,752 

281,269 

223,957 

71.363 

1,154.613 


6,557 
18,481,362 


The  above  figures  will  thus  give  the  reader  some  idea  of  the  mortality 
caused  by  the  plague  in  India. 

The  next  important  cause  of  death  is  cholera : — 


1896 

35,404 

1897 

57,109 

1898 

4,368 

1899 

8,579 

1900 

163,889 

1 90 1 

13,600 

1902 

3.229 

1903 

1,825 

1904 

13.156 

1905 

5.396 

The  general  term  '  fever  '  causes  a  mean  of  310,420  deaths  in  the  six  years 
1900-1905;  most  of  this  is  supposed  to  be  malaria. 

The  simplest  way  to  show  the  Bombay  death-rate  is  in  the  ratio  per  1,000 
inhabtiants: — 


Cholera 

2-1  I 

Smallpox 

0-26 

Plague 

9'i8 

Fevers 

17*43 

Dysentery  and  diarrhoea 

4-90 

Injuries 

0-39 

Other  causes 

12-12 

Total 


46-39 


Respiratory  disease  in  1904  caused  3-22,  and  in  1905  2-95,  deaths  per  1,000 
of  the  populatoin. 

The  Bombay  death-rate  indicates  clearly  the  incidence  of  cholera,  plague, 
and  fevers.     In  many  parts  of  India — e.g.,  Madras — kala-azar  is  an  important 


122  TROPICAL  DISEASES 

death-producing  factor.  In  Calcutta,  phthisis  is  causing  some  apprehension 
by  its  increase.  The  importance  of  snake-bite  as  a  cause  of  death  is  marked 
in  India.     Relapsing  fever  is  also  known. 

Ceylon  possesses  a  high  infantile  mortality,  of  which  the  principal  factors 
are  infantile  diarrhoea  and  convulsions,  and  often  the  bad  condition  of  the 
mother  before  the  birth  of  the  child,  associated  with  improper  and  bad  food, 
and  lack  of  proper  care  of  the  child.  Eugenics  requires  more  study  in  that 
island  than,  so  far  as  we  know,  it  has  received. 

The  deaths  of  women  in  child-birth  are  high,  and  the  principal  cause  is 
puerperal  fever. 

Among  adults  diarrhoea,  dysentery,  and  the  various  forms  of  enteric  fever 
are  important  factors  of  the  death-rate.  Plague  has  recently  visited  the 
island,  but  has  been  well  controlled;  cholera  is  present  from  time  to  time; 
while  systematic  steps  have  been  taken  to  deal  with  the  prevalent  malaria 
and  ankylostomiasis.  Cancer  exists  in  all  races,  and  diabetes  is  a  prevalent 
disease  among  better-class  natives,  such  as  lawyers,  doctors,  and  merchants. 
Syphilis  is  common,  though  the  parasyphilitic  diseases  are  very  rare,  while 
insanity  is  also  relatively  less  than  in  Europe.  Leprosy  is  endemic,  and  eye 
diseases  frequent;  though,  thanks  to  the  Victoria  Eye  Memorial  Hospital, 
where  they  are  skilfully  treated,  blindness  is  less  frequently  met  with. 

With  reference  to  the  Straits  Settlements,  the  infantile  mortality,  after 
deducting  immigrant  deaths,  is  256*29  per  1,000  births  in  1905,  and  is  raci- 
ally classified  as  follows : — 


Europeans 


Other  nationalities 

Malays 

Indians 

Chinese 

Eurasians    .  . 


57-32 


224-07 
229-78 
278-72 
302-03 
307-69 

The  general  death-rate  was  40-51  per  1,000  inhabitants,  and  its  factors  were 
phthisis,  beri-beri,  unclassed  fevers,  dysentery,  cholera,  malaria,  cancer, 
anaemia,  sprue,  dropsy,  and  parasites. 

In  Indo-China  the  enteric  fevers,  the  diarrhoeas  and  dysenteries,  liver 
abscesses,  intestinal  parasites,  cholera,  diphtheria,  spreading  ulcer,  which  used 
to  be  called  Cochin  China  ulcer,  scurvy,  purpura  haemorrhagica,  beri-beri, 
dengue  fever,  and  parasites,  are  to  be  mentioned. 

Much  has  been  written  on  the  diseases  of  China,  where  Manson  and  Cantlie 
did  their  work,  and  its  diseases  are  beginning  to  be  known;  but  of  special 
interest  are  its  trematode  infections,  its  beri-beri,  its  plague,  and  its  skin 
diseases. 

Japan  is  now  the  centre  of  much  scientific  work,  and  no  passing  reference 
would  do  justice  to  the  valuable  work  being  performed  therein;  but  it  may  be 
noted  that  it  is  interesting  in  its  parasitic  diseases,  its  tsutsu-gamushi  disease, 
its  trematode  infections,  its  fuguismus,  its  rat-bile  and  cat-bite  diseases,  and 
its  beri-beri. 

The  Philippine  Islands  are  monuments  of  American  carefulness,  forethought, 
and  hard  work,  and  their  diseases  are  well  set  forth  in  the  valuable  Philippine 
Journal  of  Tropical  Medicine.  Especially  to  be  noted  are  their  parasitic  affec- 
tions, their  beri-beri,  and  though  much  remains  to  be  done,  yet  much  has  been 
done  with  regard  to  malaria  ;md  smallpox,  which  has  been  reduced  to  insignifi- 
cant proportions,  while  tuberculosis,  cholera  and  plague,  and  the  enteric 
,  are  present,  and  the  whole  problem  of  eugenics  is  still  in  its  infancy. 

Australasia. 

'1  he  diseases  of  tropical  Australia,  which  includes  Queensland,  Papua,  Torres 
Straits,  Thursday  Island,  etc.,  arc: — Sprue,  amoebic  dysentery,  filariasis, 
malaria,  beri-beri,  ulcerative  granuloma,  frambcesia  tropica,  dengue  fever, 
leprosy.  The  intestinal  parasites  are: — Ancylostoma  duodenale,  Trichuris 
trichiura,  Oxyuris  vevmiatlaris,  Strovgyloides  stercoralis,  and  Tama  saginata. 

Under  the  term  '  sandworm  disease,'  Brcinl  describes  an  inflammation  of 


DISTRIBUTION  OF  DISEASE  123 

the  inner  side  of  the  sole  of  the  foot  in  the  Innisfail  and  Cairns  districts,  which, 
beginning  as  a  small  erythematous  area,  spreads  in  the  form  of  spirals,  and 
after  a  time  disappears.  No  animal  parasite  could  be  found.  It  appears  to  us 
that  this  is  a  form  of  '  creeping  eruption.'     He  also  describes '  barcoo  rot.' 

Seligmann,  during  the  eighteen  months  which  he  spent  in  British  New 
Guinea  and  the  islands  of  the  Torres  Straits  in  the  years  1898  and  1904, 
gathered  much  information  as  to  the  incidence  of  disease  among  the  Papuo- 
Melanesians  of  Papua,  who  are  really  only  just  emerging  from  the  Stone  Age. 

He  found  talipes  equino-A'arus  to  be  common,  while  hare-lip,  meningocele, 
dwarfism,  albinism,  and  erythrism  (i.e.,  aborigines  with  auburn  or  reddish- 
brown  hair,  pinkish-brown  skin,  and  brown  eyes)  occur.  Albinism  and 
erythrism  showed  a  family  distribution. 

Malaria  was  common,  and  children  with  greatly  enlarged  malarial  spleens 
were  easily  found.  Adults  with  large  spleens  could  also  be  seen,  but  this 
enlargement  might  not  be  malarial.  Leprosy  was  endemic  in  the  valley  of 
the  St.  Joseph  River — i.e.,  in  the  Roro-Mekeo  district — and  could  not  be 
attributed  to  foreign  influences.  Yaws  was  common,  but  syphilis  was  con- 
sidered to  have  been  introduced  in  comparatively  recent  times;  in  fact,  he  is 
of  the  opinion  that  in  Oceania  the  introduction  of  syphilis  is  possibly  not 
antecedent  to  Captain  Cook's  voyages.  Respiratory  diseases  and  dysentery 
are  very  common,  as  are  skin  diseases — e.g.,  eczema,  tinea  imbricata,  tinea 
flava,  keratosis  pilaris,  and  leucoderma.  With  regard  to  new  growths,  he 
records  cutaneous  papillomata,  fibromata,  lipomata,  osteomata  (?),  and 
angiomata.  Malignant  tumours  were  rare,  but  sarcomata  were  found.  He 
describes  and  illustrates  subcutaneous  nodules  freely  movable  over  the  deep 
fascia,  over  or  near  bony  prominences,  and  especially  about  the  elbow,  which 
are  probably  juxta-articular  nodules.  He  describes  and  illustrates  a  nasal 
ulceration  somewhat  similar  to  gangosa,  variously  referred  to  as  lupus  by 
Sir  William  MacGregor  and  cancer  by  the  white  residents  of  British  New 
Guinea.  He  also  describes  a  peculiar  ulcerative  process  of  the  legs  and  other 
parts  of  the  body.  He  draws  attention  to  the  impulsive  character  of  the  people 
as  a  crime-producing  factor.  Paralysis  and  psychoses  are  not  common.  The 
presence  of  cretinism  was  noted.  He  did  not  meet  with  tuberculosis  except 
in  natives  in  intimate  contact  with  Europeans,  nor  with  arterio-sclerosis, 
valvular  heart  disease,  rickets,  or  gout,  locomotor  ataxy,  or  general  paralysis, 
while  anaemia  was  rare. 

Oceania. 

This  is  interesting  for  its  diarrhoeas,  dysenteries,  and  elephantiasis,  which 
have  been  studied  in  detail  by  Baker;  for  its  yaws,  leprosy,  and  skin  diseases, 
which  latter  are  common,  and  of  which  tokelau  and  ringworm  may  be 
especially  noted. 

Syphilis  is  believed  to  have  been  unknown  in  the  Sandwich  Islands  before 
the  visit  of  Cook  in  1779,  while  leprosy  is  believed  to  have  been  introduced 
therein  in  18  jo  by  Chinese  emigrants. 

Epidemic  gangrenous  rectitis  and  a  similar  form  of  stomatitis  occurs  accord- 
ing to  Corny  in  Fiji.  Cerebrospinal  meningitis  was  introduced  probably  about 
1S76. 

Tropical  America. 

The  tropical  medical  schools  situate  in  Harvard  University  and  in  other 
parts  of  the  United  States,  the  work  of  the  American  Society  of  Tropical 
Medicine  and  of  the  Canal  Zone  Medical  Association,  added  to  the  researches 
of  the  Institute  Oswaldo  Cruz  of  Brazil,  are  steadily  increasing  our  knowledge 
of  the  diseases  of  Iropical  America,  among  which  malaria,  yellow  fever,  the 
enteric  fevers,  the  dysenteries,  elephantiasis,  Chagas'  disease,  Leishmaniasis, 
verruga  peruviana,  parasites,  yaws,  and  certain  skin  diseases,  stand  out  as 
pathological  features,  among  which  must  be  given  prominence  to  those  caused 
by  the  jigger. 

Moreover,  it  is  in  tropical  America  that  the  most  brilliant  prophylaxis  with 
regard  to  malaria  and  yellow  fever  has  been  conducted. 


i24  TROPICAL  DISEASES 

With  regard  to  Northern  Mexico,  Ales  Hrdlieka  made  six  expeditions  in 
the  years  1 898-1905  to  study  the  physiological  and  medical  conditions  of  the 
Amerinds  residing  in  Northern  Mexico  and  in  the  south-western  portions  of 
the  United  States. 

He  concludes  that  on  the  whole  the  health  of  these  people  is  superior  to 
that  of  whites  living  in  larger  communities,  as  they  do  not  suffer  so  much  from 
inherited  morbid  conditions,  or  from  those  connected  with  teething,  puberty, 
menstruation,  gestation,  puerperium,  menopause,  and  senility,  nor  do  they 
suffer  so  much  from  malignant  growths,  but  they  have  a  weak  resistance  to  a 
few  contagions — e.g.,  smallpox. 

Their  most  common  ailments  are  diseases  of  the  gastro-intestinal  tract , 
especially  dysentery;  of  the  respiratory  organs,  especially  pneumonia,  while 
consumption  is  very  rare;  of  the  eyes,  especially  ophthalmia  due  to  dust, 
which,  being  neglected,  leads  to  blindness,  as  does  smallpox;  of  muscular 
rheumatism  and  arthritis.  Malaria,  smallpox,  and  pemphigus  contagiosus 
in  children  are  very  common.  Typhoid  fever  appears  to  be  rare;  leprosy  and 
elephantiasis  are  known,  as  is  goitre. 

He  very  much  doubts  the  presence  of  syphilis  prior  to  Columbus,  and  points 
out  that  the  bones  in  the  ancient  graves  in  California,  on  the  north-west  coast, 
in  Peru,  and  other  localities  in  South  America,  do  not  show  any  signs  of  the 
disease,  even  when  thorough  examinations  of  extensive  osteological  collections 
have  been  made. 

In  children  the  common  cause  of  death  is  diarrhoea.  He  makes  most 
interesting  observations  on  the  mites  which  burrow  under  the  skin  of  the  toes 
in  the  Huastec,  who  live  to  the  east  of  the  Otomi  (Hidalgo  region),  and  which 
may  cause  suppuration  and  even  loss  of  a  toe.  Injuries  due  to  spiders,  centi- 
pedes, scorpions,  rattlesnakes,  and  the  gila  monster  are  mentioned,  as  well  as 
poisoning  from  aconite,  datura,  and  fungi.  The  narcotic  effects  of  Peyote  are 
noted,  while  two  plants,  cul-ick-um-ek  (Donedia  sufirutescens)  and  ha-van 
tatat  (Phacelia  infundibuliformis),  cause  dangerous  wounds  when  journeying 
through  forests,  leading  to  some  form  of  poisoning,  and  in  the  case  of  the 
former  even  to  death.  He  met  with  albinism  and  leucoderma,  but  pinta  was 
unknown,  though  stated  to  occur  farther  south.  The  diseases  which  were 
rare  were:  anaemia,  diseases  of  breast,  circulatory  organs,  liver,  female  genera- 
tive organs,  and  skin;  while  asthma,  dental  caries,  cancer,  rickets,  hernia, 
idiocy,  insanity,  nervous  diseases  except  epilepsy,  scarlet  fever,  and  fracture 
of  bones  were  also  rare. 

With  regard  to  the  Virgin  Islands,  Butler  and  Hakansson  have  pointed 
out  that  malignant  tertian  and  quartan  malarias  are  present,  but  that  the 
carrier  anopheline  has  not  been  identified,  while  pellagra  is  quite  common  and 
ankylostomiasis  is  present.  The  lack  of  sanitation  causes  considerable 
morbidity  and  mortality,  and  there  is  a  high  illegitimacy  rate,  venereal  disease 
rate,  and  infantile  mortality,  while  the  poor  food  conditions  are  held  to  be  the 
cause  of  pellagra,  and  the  poor  sewage  disposal  and  defective  water-supplies 
to  encourage  diarrhoea,  dysentery,  enteric  fevers,  and  the  encouragement  of 
mosquitoes  to  breed  in  houses  causes  the  high  filarial  infection  and  its  associate 
morbidity. 

Ecuador  has  been  studied  by  Espinosa-Tamayo,  who  finds  Ancylostoma 
duodenale  and  Kecator  americanus  present,  as  well  as  Oxyuris,  Tcenia  solium, 
and  Hymenolepis  nana.  The  jigger  is  noted  and  so  is  Xenopsylla  cheopis  and 
Clinocoris  rotundalus.  Yellow  fever  has  almost  disappeared,  but  malaria, 
amoebic  dysentery,  enteric  fevers,  and  tuberculosis,  are  rife.  Chichismos 
caused  by  drinking'  chicha '  made  from  fermenting  maize  is  said  to  be  like 
pellagra. 

Tropical  Africa. 
The  outstanding  features  of  tropical  Africa  are  its  trypanosomiases,  its 
malarias,  and  its  relapsing  fevers;  while  enteric  fevers  and  typhus  are  more 
prevalent  in  the  north,  where  the  schistosomiasis  and  pellagra  also  abound. 
Porocephalosis  is  likewise  a  feature  of  this  country,  which  is  the  home  of 
numerous  local  diseases,  such  as  guondou,  while  skin  complaints  are  extremely 
common. 


PREVENTION  125 

Whether  or  no  cerebro-spinal  meningitis  originated  in  Central  Africa  is  an 
interesting  speculation. 

The  primitive  forms  of  medicine,  the  venomous  animals,  and  the  poisons 
are  all  of  great  interest  and  require  much  further  research. 


PREVENTION. 

It  is  not  our  intention  to  write  upon  prophylaxis  in  this  portion 
of  the  book,  but  merely  to  indicate  that  many  diseases  exist  in  the 
tropics  which  medical  research  has  shown  to  be  due  to  definite 
parasitic  organisms  spread  in  a  very  definite  manner,  and  therefore 
more  or  less  preventable. 

We  would  venture  respectfully  to  quote  His  Most  Gracious 
Majesty  King  George  V.,  who  long  ago  said: — "  If  preventable,  why 
not  prevented  ?"  We  would  further  venture  to  ask  that  more  regard 
should  be  paid  to  this  memorable  utterance,  which  we  believe  will 
echo  down  the  rolling  centuries  and  will  be  more  and  more  appreci- 
ated as  they  pass. 

We  would,  however,  ask  the  reader  to  remember  that  to  prevent 
disease  <  ntails  hard  unappreciated  work,  usually  in  the  face  of  much 
opposition  and  in  direct  contrast  to  the  comfortable  life  of  letting 
things  drift;  but  in  the  light  of  His  Majesty's  words  this  work  should 
be  taken  up  by  his  subjects. 

Moreover,  the  present  war  has  shown  what  can  be  done  when 
military  authorities  work  hand  in  hand  with  medical  research,  and 
we  are  of  the  opinion  that  civilian  Governments  should  learn  this 
lesson  also. 

It  is,  indeed,  a  satisfactory  sign  that  the  Secretary  of  State  for 
India  is  reported  as  stating,  in  a  remarkable  speech  made  to  a  British 
Medical  Association  deputation,  that  a  modern  Government  required 
and  should  take  all  suitable  means  to  obtain  the  best  and  most 
accessible  advice  on  various  medical  and  sanitary  problems  with 
which  every  such  Government  is  called  upon  to  deal.  If  this  dictum 
is  acted  upon — i.e.,  if  it  passes  the  realm  of  advice — a  new  era  will 
dawn  in  the  tropics. 

REFERENCES. 

If  the  reader  desires  further  literature  with  regard  to  evolution,  we  invite 
his  attention  to  Adami  (1918), '  Medical  Contributions  to  the  Study  of  Evolu- 
tion.' If  he  wishes  to  dive  into  geographical  discoveries,  he  may  well  begin 
with  Keltic  and  Howarth  (1913),  '  History  of  Geography.' 

Balkans.  Castellani  (1917).  The  Diseases  of  the  Balkans,  Royal  Society  of 
Medicine,  and  the  Journal  of  Tropical  Medicine  and  Hygiene. 

Bombay.     Report  of  the  Sanitary  Commissioner. 

British  Guiana.     Reports  of  Registrar-General. 

British  Honduras.  Tobey  Corny  and  Schwitala  in  vol.  xi.,  No.  6,  of  the 
Bulletin  of  the  St.  Louis  University  for  January,  1916. 

British  New  Guinea.  Seligmann,  C.  G.  (1906).  On  the  Morbid  Conditions 
met  with  among  Natives  of  British  New  Guinea.  (191 3).  Vol.  i.,  Reports 
of  the  Cambridge  Anthropological  Expedition  to  the  Torres  Straits. 
(1908).  Third  Report  of  the  Imperial  Cancer  Research  Fund. 


126  TROPICAL  DISEASES 

Ceylon.      Castellani    (1904).     Ceylon   Medical    Reports.      Chalmers    (1907). 

Some  Remarks  on  the  Vital  Statistics  of  Ceylon  (Journal  Ceylon  Branch 

British  Medical  Association^.     Denham,   E.   B.    (1911).      Ceylon  at  the 

Census  of  191 1.     Colombo. 
Egypt  (1901-1906).     Vital  Statistics. 
Ecuador.     See  Espinosa-Tamayo  (1917).     Archiv  fur  Schiffs-  und  Tropen- 

hygiene,  xxi.,  No.  17,  285-291.     Hamburg. 
Jamaica.    Report  of  Registrar-General. 
Mexico.      Ales     Hrdlicka     (190S).       Bulletin     34,     Smithsonian     Institute, 

Washington. 
Oasis  of  Siva  (191  i).     Stanley.     Egyptian  Government  Report. 
Tropical  Australia  (1910).     Report  of  the  Australian  Institute  of  Tropical 

Medicine. 
Virgin  Islands.     Butler  and  Hakansson  in  the  United  States  Naval  Medical 

Bulletin  for  October,  1917,  465-475.     Washington. 
Walsh  (1918).     The  Geographical  Distribution  of  Human  Diseases  and  their 

Control.     Trans.  Soc.  of  Trop.  Med.,  vol.  xi.,  No.  3. 

Eugenics. 

Ashby  (1915).     Infant  Mortality.     Cambridge. 


CHAPTER  VI 
FITNESS  FOR  TROPICAL  LIFE 

Preliminary — Examination — Women — Invaliding — -Natives — Life    assurance 
— Expectation  of  life  in  tropical  natives—  References. 

PRELIMINARY. 

The  selection  of  European  and  American  men  for  service  in  the 
tropics,  the  fitness  of  European  and  American  women  for  tropical 
life,  the  question  as  to  how  long  white  children  should  remain  in 
warm  climates  (Chapter  LXXXVL),  the  invaliding  of  sick  persons 
of  all  races,  the  selection  of  natives  for  employment  under  Govern- 
ments or  in  mercantile  houses,  and  the  problems  of  tropical  life  assur- 
ance, are  all  matters  of  great  importance  to  the  tropical  practitioner. 

He  may  have  nothing  to  say  in  regard  to  the  selection  of  persons 
for  tropical  service,  but  he  has  very  considerable  knowledge  of  their 
after  medical  history. 

We  are  unable  to  allow  much  space  in  the  present  book  for  the 
consideration  of  these  questions,  but  we  will  endeavour  to  touch 
upon  such  points  as  appear  to  us  to  be  of  importance,  and  to  leave 
the  elaboration  of  the  same  to  the  reader,  and  for  this  purpose  we 
give  references  at  the  end  of  the  chapter. 

EXAMINATION. 

We  presume  that  every  medical  practitioner  appointed  for  the 
purpose  of  selecting  men  for  service  in  the  tropics  will  go  faithfully 
through  a  routine  examination  more  or  less  based  upon  that  adopted 
by  the  best  type  of  assurance  companies,  and  therefore  we  need  not 
lay  stress  upon  such  an  examination;  but  there  are  certain  points 
to  which  we  desire  to  invite  especial  attention. 

First-Class  Lives. — Every  selected  candidate  must  be  a  first-class 
life  and  free  from  any  trace  of  albumen  in  the  urine. 

Venereal  Disease. — The  examining  physician  should  make  it  his 
duty  to  exclude  gonorrhoea,  not  by  mere  question,  but  by  actual 
examination,  and  the  same  is  true  for  syphilis.  No  one  should  be 
allowed  to  proceed  for  the  first  time  to  the  tropics  with  an  uncured 
gonorrhoea  or  with  an  imperfectly  treated  syphilitic  infection. 

Further,  we  are  of  the  opinion  that  it  is  the  duty  of  the  examiner 
to  warn  all  selected  candidates  as  to  the  dangers  of  infection  with 
venereal  disease  in  the  tropics,  and  at  the  same  time  to  give  and  to 
read  to  him  printed  instructions,  similar  to  those  provided  to-day 
for  soldiers,  detailing  methods  for  prevention  of  infection. 

127 


128  FITNESS  FOR  TROPICAL  LIFE 

Every  tropical  practitioner  knows  how  much  sickness  and  loss  of 
work  is  due,  directly  or  indirectly,  to  venereal  disease;  and  we  feel 
that  it  is  not  too  much,  in  the  interests  of  the  employer  and  the 
employee  alike,  1  o  ask  that  the  above  should  form  part  of  the  duties 
of  every  medical  examiner  of  candidates  destined  for  the  tropics. 
We  further  submit  that  each  health  report  should  state  clearly  that 
these  duties  have  been  carefully  carried  out  by  the  examiner. 

Vaccination. — It  is  necessary  that  every  selected  candidate,  before 
final  appointment,  should  produce  a  certificate  that  he  has  received 
two  injections  of  a  vaccine  prophylactic  against  typhoid  and  the 
paratyphoid  fevers,  or  of  a  so-called  tetra-  or  penta-vaccine  containing 
in  addition  to  the  already  mentioned  three  diseases,  cholera  or  cholera 
and  plague.  Evidence  of  Jennerian  vaccination  forms  part  of  the 
routine  medical  examination,  and  must  not  be  older  than  seven  years. 

Quinine. — Every  selected  candidate,  before  final  appointment, 
should  produce  a  medical  certificate  that  he  is  able  to  take  a  dose 
of  10  grains  of  quinine  without  developing  serious  symptoms. 

Teeth. — No  candidate  should  be  finally  selected  for  the  tropics 
until  his  teeth  are  in  such  a  condition  as  to  satisfy  the  examiner,  or 
until  he  produces  a  dentist's  certificate  to  the  effect  that  they  are 
in  good  order. 

Alcohol. — The  objections  to  alcoholic  candidates  are  so  well 
understood  that  the  mere  mention  of  this  point  is  sufficient  (see 
Chapters  III.,  V.,  and  LVL). 

Age. — We  are  convinced  that  no  one  under  twenty-one  years  of 
age  or  over  fifty  years  should  be  allowed  to  proceed  for  service  for 
the  first  time  in  the  tropics.  We  are  also  of  the  opinion  that  the 
nearer  the  minimal  age  is  to  twenty-five  years  the  better  for 
employer  and  employee  alike. 

Heat  and  Sun. — Whatever  personal  views  the  examiner  may  have 
as  to  the  effects  of  heat  and  sun,  he  should  nevertheless,  as  part  of 
his  duties,  warn  the  selected  candidate  as  to  the  possible  dangers  of 
careless  exposure  to  the  tropical  sun  and  as  to  the  effects  of  tropical 
heat,  and  should  acquaint  him  with  methods  of  prophylaxis.  He 
should  also  give  advice  on  clothing,  as  we  have  seen  distinguished 
visitors  arrive  in  the  tropics  in  clothing  suitable  for  an  English 
winter.  Then.  -  ~\  of  course,  cold  regions  and  cool  seasons  in  the 
tropics,  but  the  ^  s  not  generally  felt  by  the  new  arrival  from  the 
Temperate  Zone. 

Energy. — The  selected  candidate  should  be  warned  that,  on  first 
arrival,  he  may  not  feel  the  heat  of  the  tropics  to  be  excessive.  On 
the  other  hand,  he  may  feel  that  the  climate  suits  him  admirably, 
and  that  he  is  full  of  energy  for  work  and  play,  and  should  be  told 
that  this  state  of  affairs  will  not  last  for  ever,  and  that,  if  he  allows 
his  energy  to  outrun  his  common  sense,  there  will  be  trouble. 

Moderation  in  all  things  should  be  indicated  as  the  motto  for  a 
tropical  life. 

Duties  of  the  Examiner. — We  have  insisted  upon  the  medical 
examiner  giving  advice  upon  various  points  to  the  selected  candi- 


WOMEN  129 

date.  Our  reasons  for  so  doing  are  because  he  may  be  the  only 
medical  practitioner  to  examine  the  candidate  before  the  tropics 
are  reached. 

We  feel  that  it  is  in  the  interests  of  employer  and  employee  that 
every  opportunity  should  be  given  for  the  selected  candidate  to 
keep  fit  until  he  reaches  the  local  medical  officers. 

Check  Examination. — We  are  of  the  opinion  that  a  check 
medical  examination  by  the  local  medical  officers  immediately  upon 
the  arrival  of  the  new  official  is  advisable,  in  order  to  see  whether 
entry  into  the  tropics  has  induced  any  changes  in  his  health,  and 
also  for  the  purpose  of  giving  him  local  medical  advice. 

This  check  examination  is  very  necessary,  as  we  know  that  persons 
have  arrived  slightly  indisposed,  and  have  allowed  these  slight 
symptoms  to  become  serious  owing  to  lack  of  knowledge. 

WOMEN. 

European  and  American  women  proceeding  to  the  tropics  are 
usually  either  married  or  about  to  be  married,  or,  because  of  the 
scarcity  of  white  women  therein,  are  very  likely  to  be  married  fairly 
soon,  although  they  may  start  as  nurses,  missionaries,  etc. 

We  therefore  consider  that  all  women  proposing  to  live  in  the 
tropics  should  be  medically  examined  in  the  same  way  as  men,  and 
should  be  specially  tested  as  to  their  ability  to  stand  quinine 
therapy;  and  if  this  is  found  wanting,  should  be  educated  up  to  a 
necessary  quinine  standard,  by  regulated  small  doses,  before 
being  allowed  to  begin  their  new  life. 

Our  experience  makes  us  agree  with  Mrs.  Scharlieb  that  the 
medical  examination  of  women  should  include  the  bony  pelvis  and 
the  organs  contained  therein  when  practical. 

Often  women  have  to  live  in  out-stations  far  from  medical  aid, 
and  it  is  little  short  of  criminality  not  to  take  the  external  measure- 
ments of  the  pelvis,  and  if  necessary  to  investigate  the  condition 
of  the  internal  pelvic  organs  by  means  of  a  rectal  examination.  If 
abnormalities  are  discovered  the  woman  or  her  husband,  or  both, 
should  be  warned  as  to  the  possibilities  of  such  abnormalities. 

At  such  an  examination  care  should  be  taken  to  see  that  there  is 
no  obvious  cause  for  dyspareunia,  as  it  may  cause  trouble  to  the 
examinee  and  her  husband.  This  has  been  brought  home  to  us  in 
our  long  experience  of  tropical  practice. 

Moreover,  the  woman  should  be  warned  as  to  the  possibility  of 
menorrhagia  (or  the  much  less  common  amenorrhcea),  which  may 
begin  after  arrival  in  warm  climates,  and  should  be  given  advice  as 
to  clothing. 

The  necessity  of  having  the  urine  examined  on  the  occurrence  of 
pregnancy  should  be  impressed  upon  the  wife  and  her  husband,  as 
well  as  the  requirements  of  diet,  exercise,  rest  in  the  warmer  hours 
of  the  day,  etc. 

White  men,  as  a  rule,  require  at  regular  intervals  visits  to  temperate 
climates  if   their  health,  strength,  and   mental  vigour   arc  to  be 

9 


i.^o  FITNESS  FOR  TROPICAL  LIFE 

maintained  unimpaired;  and  the  same  holds  good,  but  perhaps  with 
more  force,  for  women,  who  should  be  allowed  leave  to  cooler  tropical 
regions  and  to  the  Temperate  Zone  as  often  as  circumstances  permit. 
When  a  woman  returns  to  a  temperate  climate  she  should  be 
advised  as  to  the  necessity  of  an  immediate  medical  examination, 
as  well  as  of  the  dangers  of  the  change  into  cooler  weather. 

INVALIDING. 

Two  classes  of  cases  require  to  be  considered  under  this  heading 
— viz. ,  the  tropical  resident  about  to  be  invalided  to  cooler  climates, 
and  the  cool-climate  resident  about  to  be  sent  to  the  tropics  for  the 
benefit  of  his  health. 

With  regard  to  the  first,  there  are  two  quite  different  aspects  of 
the  case,  viz.  :■ — 

(a)  Invaliding  for  the  Good  of  the  Employer  and  Employee  Alike. 
■ — This  is  a  matter  of  common  sense,  and  is  the  kindest  method  of 
dealing  with  many  cases. 

(b)  Invaliding  because  of  Health. — Temporary  invaliding  or  sick 
leave  should  always  be  advised  if  the  patient's  health  requires  it, 
but  his  financial  status  should  also  be  taken  into  consideration  before 
too  drastic  recommendations  are  made. 

More  difficult  by  far  is  the  question  of  permanent  invaliding  from 
service,  and  in  coming  to  a  decision  the  medical  practitioner  has 
many  points  for  consideration  with  reference  to  the  present  condition 
of  the  patient  and  his  future  prospects. 

The  nature  of  the  illness,  the  physical  and  mental  condition  of  the 
patient,  his  age,  his  pension  or  gratuity,  his  possibilities  of  future 
employment  in  cooler  regions,  his  family,  etc.,  have  all  to  be  con- 
sidered. 

Among  the  many  difficulties  which  present  themselves  under  this 
heading  we  venture  to  express  the  opinion  that  one  attack  of  black- 
water  fever  should  not  constitute  per  se  a  reason  for  permanent 
invaliding. 

On  the  other  hand,  we  are  of  the  opinion  that  mental  symptoms 
should  constitute  a  reason  for  permanent  invaliding,  as  the  tropics 
are  climatologically  unsuited  for  an  unstable  nervous  system. 

As  a  general  rule,  if  an  endemic  infection- — e.g.,  bilharziosis — is 
playing  havoc  with  a  patient,  he  should  be  permanently  invalided 
from  that  particular  area  or  areas,  which  may  not  mean  that  he 
should  be  invalided  from  the  tropics  or  from  the  service. 

NATIVES. 

Natives  should  never  be  accepted  for  employment  unless  they  are 
first-class  lives.  The  eyes  require  careful  attention,  and  colour- 
blindness should  be  looked  for,  especially  in  certain  employments 
such  as  railways,  steamers,  ports,  etc. 

Particular  attention  should  be  paid  to  the  urine,  and  natives 
know  many  tricks  with  regard  to  this  part  of  a  medical  examination. 

Schistosomiasis  of  any  part  of  the  body  should  cause  rejection, 


LIFE  ASSURANCE  131 

and  diffuse  leucoderma  if  the  candidate  is  to  work  in  the  sun,  but 
it  is  not  possible  to  give  further  details,  which  must  be  left  to  the 
common  sense  of  the  examining  officer. 

The  invaliding,  temporary  or  permanent,  of  natives  from  a  service, 
particularly  if  a  pension  or  a  gratuity  is  available,  requires  great 
care,  and  the  possibilities  of  malingering  must  be  remembered.  On 
the  other  hand,  the  effects  of  such  apparently  harmless  diseases  as 
diffuse  leucoderma  should  be  borne  in  mind,  and  injustice  should, 
if  possible,  be  avoided. 

LIFE  ASSURANCE. 

Tropical  life  assurance  is  in  its  infancy,  and  so  far  has  been  mostly 
studied  in  regard  to  India. 

Insurance  offices  usually  regard  330  north  to  30°  south  latitude 
as  including  the  dangerous  climates  of  the  world.  They  usually 
consider  those  lands  which  lie  nearest  to  the  Equator  as  the  most 
dangerous,  because  of  the  heat,  the  endemic  diseases,  the  lack  of 
sanitation,  and  the  imperfect  food-supplies. 

But  the  advance  of  knowledge  with  regard  to  the  prevention  and 
treatment  of  tropical  diseases,  and  the  dawn  of  tropical  sanitation, 
has  reduced,  and  is  reducing,  the  baneful  effects  of  many  of  these 
factors.  For  example,  the  West  Coast  of  Africa  used  to  have  an 
official  mortality  rate  of  80  per  thousand,  and  an  official  invaliding 
rate  of  95  per  thousand,  but  these  had  been  reduced  to  21*7  and 
76*3  per  thousand  as  long  ago  as  1903,  and  to-day  are  probably 
much  less. 

It  is  true  that  the  older  type  of  official,  medical  and  non-medical 
alike,  disliked  spending  money  upon  improved  sanitation  and  upon 
the  prevention  of  disease;  but  this  type  of  official  is  slowly  but  surely 
disappearing,  and  the  danger  to-day  is  that  official  inertia  may 
undo  years  of  official  toil. 

It  is  therefore  necessary  that  a  high  standard  of  sanitation  and 
disease  prevention  should  be  set  for  the  tropics,  and  that  this  should 
be  maintained ;  and  if  this  is  done,  then  many  of  the  serious  objections 
to  tropical  life  assurance  may  be  removed  or  abated  in  the  future, 
and  as  this  is  done  better  assurance  terms  should  be  forthcoming. 

Very  many  tropical  practitioners  have  had  experience  in  the 
selection  and  rejection  of  tropical  candidates  for  life  insurance,  but, 
unfortunately,  there  are  but  few  records  to  be  found  based  upon  this 
work. 

In  1897  and  later,  Cantlie,  writing  with  regard  to  this  matter, 
stated  that  although  the  person  in  the  tropics  was  exposed  to  many- 
deadly  diseases,  he  was  not  very  liable  to  scarlet  fever,  rheumatism, 
and  pneumonia,  and  that,  excluding  malaria,  his  chief  dangers  were 
diseases  affecting  his  alimentary  canal  and  abdominal  organs,  and 
that  alcohol  was  an  even  greater  curse  in  the  tropics  than  in  tem- 
perate climates. 

He  states  that  the  insurance  companies  deal  with  each  case 
individually,  and  he  suggests  that  during  the  first  seven  years  of 


132  FITNESS  FOR  TROPICAL  LIFE 

residence  in  a  proscribed  area  an  extra  premium  should  be  paid, 
but  that  after  that  period  it  should  be  reduced  to  one-half  upon  a 
certificate  from  the  company's  medical  officer  that  no  permanent 
injury  to  health  has  been  incurred,  and  that  the  cost  of  this  examina- 
tion should  be  paid  by  the  insurer.  Further,  after  ten  years' 
residence  the  extra  premium  should  be  reduced  to  one-third  of  the 
original  sum,  and  after  thirteen  years  no  extra  premium  should 
be  charged,  provided  always  that  the  necessary  certificate  was 
forthcoming. 

He  points  out  that  a  period  of  danger  is  the  first  year  or  two  after 
the  old  tropical  resident  takes  up  his  permanent  abode  in  the 
Temperate  Zone,  and  he  recommends  that  an  extra  premium  be 
charged  for  these  two  years. 

The  next  paper,  published  by  Winter  in  1909,  we  have  been 
unable  to  peruse  in  the  original,  but  he  apparently  lays  stress  on 
the  first  few  years  of  residence  in  India,  on  the  ground  that  Euro- 
peans are  very  likely  to  become  victims  to  enteric  and  similar  fevers. 

Caddy  in  1912  came  to  the  conclusion  that  the  European  does  not 
acclimatize  well  in  the  tropics,  meaning  by  this  statement  that  he  is 
unable  to  rear  healthy  strong  children  in  India,  and  that  he  becomes 
debilitated  by  residence  there,  requiring  a  change  to  a  temperate 
climate  every  four  or  five  years,  and  that  after  years  of  residence 
he  is  even  more  liable  to  sunstroke  than  on  arrival. 

Out  of  1,799  cases  ne  rejected  6  per  cent,  and  loaded  8  per  cent., 
making  together  14  per  cent.,  which  was  caused  by  inferior  physique, 
obesity,  glycosuria,  albuminuria,  consumption,  consumptive  family 
history,  bad  family  history,  syphilis,  heart  disease,  sundry  diseases 
(3'39  Per  cent.),  alcoholism. 

With  regard  to  natives  desiring  insurance,  it  is  true  that  years 
ago  it  was  only  the  Europeanized  native  who  sought  after  this ;  but 
to-day  it  is  different,  and  even  native  women  of  due  social  standing 
are  allowed  assurance,  provided  that  careful  inquiries  have  been 
made,  though  years  ago  such  an  assurance  was  never  considered. 

Caddy  adds  to  the  list  of  causes  of  rejection  '  elephantiasis,'  and 
he  is  of  the  opinion  that  opium  and  hemp  are  very  harmful,  but  that 
they  are  not  commonly  consumed  by  the  insuring  classes  of  India. 

He  considers  that  Rajahs,  wealthy  landowner  Marwaris,  or  bankers 
and  money-lenders,  and  petty  merchants,  are  bad  lives,  while  the 
best  native  risks  are  Government  servants  and  native  clerks  in 
European  offices. 

As  a  rule  the  native  does  not  consume  alcohol,  but  if  he  does  he 
should  be  regarded  an  indifferent  risk. 

He  also  states  that  the  native  of  India  is  a  shorter  man  than  the 
European,  and  that  height  for  height  he  is  about  the  same  weight, 
but  he  is  very  subject  to  glycosuria  and  to  hydrocele. 

The  discussion  on  this  paper  was  interesting,  and  in  our  opinion 
some  of  his  views  are  open  to  criticism. 

With  regard  to  life  assurance  in  Egypt,  the  only  publication  with 
which  we  are  acquainted  is  by  Day,  who  distinguishes  four  groups  of 


EXPECTATION  OF  LIFE  IN  TROPICAL  NATIVES  133 

proposers — viz.,  the  Western  European,  the  Southern  European 
the  Eastern,  and  the  Egyptian. 

In  general,  he  considers  the  first  class  to  be  a  good  risk  on  the  same 
terms  as  in  Europe,  but  with  regard  to  the  second  he  considers  that 
they  should  be  examined  in  their  own  homes,  and  each  case  should 
be  judged  on  its  own  merits,  and  the  third  class  is  intermediate  in 
risk  between  the  second  and  fourth. 

The  native  Egyptian  appears  to  be  a  great  difficulty,  owing  to 
the  paucity  and  unreliability  of  the  family  history,  while  sexual 
excess  and  cigarette-smoking  are  considered  to  balance  the  lack 
of  alcoholic  excess.  Rheumatic  fever,  tuberculosis,  and  syphilis 
are  rife,  and  he  is  liable  to  many  tropical  diseases,  including  ankylo- 
stomiasis, pellagra,  splenomegaly,  relapsing  fever,  typhus  fever, 
and  the  schistosomiases,  so  that  he  is  not  a  good  risk  until  education 
and  sanitation  improve  matters ;  but  Day  says  a  proposer  then  in 
good  health,  and  whose  children  are  successfully  reared  and  whose 
education  has  been  sound,  may  be  accepted  for  a  whole  life  on 
European  terms,  but  this  was  contested  during  the  discussion  on 
his  paper. 

The  common  sense  of  the  whole  matter  is  that  there  is  an  increased 
risk  on  the  life  of  the  European  living  in  the  tropics,  and  that  it  is 
most  marked  during  the  earlier  years  of  his  residence ;  there  is  a 
considerable  risk  in  insuring  native  men,  and  that  this  is  greatly 
increased  when  considering  native  women. 

EXPECTATION  OF  LIFE  IN  TROPICAL  NATIVES. 

The  expectation  of  life  in  India  compared  with  the  same  for 
England  may  be  gathered  from  the  following  table  obtained  from 
Hardv  via  McCav's  book:— 


India. 

England. 

Age. 

Males. 

Females. 

Males. 

Females. 

0 

24*6 

25-5 

43-7 

47-2 

5 

37*1 

36-1 

52-7 

54*9 

10 

35'5 

34H 

49-0 

5i-i 

15 

32'3 

3i'7 

44*5 

46-5 

20 

29-2 

29*3 

4C-3 

42-4 

25 

26-3 

27*0 

36-3 

38-5 

35 

2I'I 

22*4 

28-9 

31*2 

45 

16-5 

17-9 

22'I 

24*0 

55 

I2'2 

13-2 

15-7 

17*2 

65 

8-2 

8-7 

io>3 

1 1*3 

The  figures  speak  for  themselves,  but  they  were  compiled  years 
ago,  and  it  is  possible  that  more  modern  tables  might  show  a  better 
expectation  of  life. 


134  FITNESS  FOR  TROPICAL  LIFE 


REFERENCES. 

The  most  valuable  general  work  dealing  with  life  assurance  is  Brockbank 
1908),  'Life  Insurance  and  General  Practice.'     London. 

Caddy  (1912).     Transactions  of  the  Life  Assurance  Medical  Officers'  Associ- 
ation (Life  Insurance  in  India),  33-80.      (1913).  Indian  Medical  Gazette, 
xlviii.  172.     Calcutta. 
Cantlie  (1897).     British  Medical  Journal,  June  30.     (1898).  Journal  Tropical 
Medicine  and  Hygiene,  November  and  December.     (1899).  Ibid.,  January. 
(1903).  Tropical  Life  and  its  Effect  on  Life  Assurance:  Transactions  of 
the  Life  Assurance  Medical  Officers'  Association,  107.     (1904).  Discussion 
on  Tropical  Life  Assurance,  Royal  Institute  of  Public  Health.      (191 1). 
Journal  of  Tropical  Medicine  and  Hygiene,  February.     London. 
Chart.es    (1910).       Journal    of    Tropical    Medicine    and    Hygiene,    xiii.    242 
(Special  Factors  influencing  the  Suitability  of  Europeans  for  Life  in  the 
Tropics).     London. 
Day  (191 3).     Transactions  of  the  Life  Assurance  Medical  Officers'  Associa- 
tion, 219-245   (Life  Assurance  in  Egypt).     London. 
Francis    (1878).      British    Medical    Journal,     i.    785    (Life    Assurance   and 

Residence  in  the  Tropics) .     London. 
Garry    (191  i).     Some  Factors  concerning  Health  in  the  Tropics. 
Giles  (1904).     Climate  and  Health  in  Hot  Countries.     London. 
Green  (1905).     Medical  Examination  for  Life  Assurance   (Residence  in  the 

Tropics),  381.     London. 
Hall  (1903).     Medical  Examination  for  Life  Assurance  (Tropical  Residence), 

p.  80.     London. 
Hardy  (1889).     Imperial    Gazetteer  of    India,    i.    515   (Expectation  of   Life 

in  India  in  Natives,  1881-1891). 
Johnson    (ic  08-09).     Transactions   of   the   Life   Assurance  Medical   Officers' 
Association    (Longevity,   Race,    and    Environment    with    Reference    to 
Foreign  Residence).     London. 
Layet  (1906).     La  Sante  des  Europeans  entre  les  Tropiques.     Paris. 
Owen     (1905).       South     African     Medical    Association      (Some     Effects    of 

Tropical  Life  on  Europeans),  iii.,  in. 
Paulin    (191  i).     Journal    of   Tropical    Medicine    and    Hygiene,    January    2. 

London. 
Scharlieb  (1915).     British    Medical    Journal,  i.,  917-919  (Married    Medical 

Missionaries).     London. 
Sieveking   (1882).     Medical  Adviser    in  Life  Assurance   (Influence    of    the 

Tropics),  pp.  25  and  66.     Special  rates.     London. 
Staley  (1916).     Wives  and  Mothers  in  India.     London. 
Williams   (1900-01).     Transactions  of  the  Life  Assurance  Medical  Officers' 

Association  (Race  in  Relation  to  Life  Assurance).     London. 
Woodruff  (1905).     The  Effect  of  Tropical  Light  on  the  White  Man.     (191 1). 
The  Expansion  of  Races.     (Undated).  Medical  Ethnology.     London. 


PART  II 

THE  CAUSATION  OF  DISEASE  IN 
THE  TROPICS 

PHYSICAL  CAUSES 
CHEMICAL  CAUSES 
PARASITES 


*35 


SECTION  A 
PHYSICAL  CAUSES 

TEMPERATURE  AND  HUMIDITY 
PRESSURE  AND  RADIATION 
TRAUMATISM 


136 


CHAPTER  VII 
TEMPERATURE  AND  HUMIDITY 

Preliminary — High  atmospheric  temperatures — Conclusions — References. 

PRELIMINARY. 

Having  finished  with  the  introductory  portion  of  our  task,  we 
enter  upon  the  second  part  of  this  book,  which  is  devoted  to  the 
causation  of  disease,  and  is  therefore  essentially  pathological.  This 
subject  is  divided  into  three  sections,  embracing  the  physical, 
chemical,  and  parasitic  causes  of  tropical  diseases. 

HIGH  ATMOSPHERIC  TEMPERATURES. 

The  present  short  chapter  is  confined  to  a  brief  consideration  of 
the  pathological  effects  of  high  atmospheric  temperatures,  which 
are  the  most  important  physical  causes  of  disease  in  the  tropics, 
and  are  only  markedly  evident  when  there  is  a  definite  amount  of 
atmospheric  humidity ;  and  therefore  we  have  entitled  this  chapter 
Temperature  and  Humidity. 

To  exemplify  what  we  mean  we  will  quote  a  concrete  example. 
In  a  certain  tropical  locality  there  were  the  usual  high  air  tempera- 
tures with  relatively  low  humidity  and  cool  nights  until  about  the 
middle  of  a  month,  when  the  temperature  rose  to  1160  F.,  the  humi- 
dity increased,  the  sky  became  cloudy,  and  for  twenty-four  hours 
there  was  little  breeze.  During  this  period  about  fifty  laboratory 
animals  died,  though  well  protected  from  the  sun  by  living  in  large 
brick  houses.  They  showed  post-mortem  the  typical  signs  of  heat- 
stroke — viz.,  the  congestion  of  the  meninges  and  brain,  and  the 
marked  congestion  of  the  lungs,  which  were  almost  black  with 
stagnated  blood.  During  this  period  there  were  a  few  deaths  in 
the  population  of  the  place  from  the  same  cause. 

Clinical  experience  has  shown  that  there  are  two  different  pictures 
associated  with  the  pathological  effects  of  high  air  temperatures. 
The  first  picture  is  that  of  extremely  high  fever,  and  is  called  heat- 
stroke ;  while  the  second  is  depicted  by  collapse  and  low  bodily 
temperatures,  and  is  named  heat- syncope. 

We  have  investigated  these  two  conditions  experimentally.  It 
was  our  practice  in  our  journeys  from  Ceylon  to  Europe  to  test  the 
effects  of  high   air  temperatures  upon  ourselves,  and  such  of  our 

i37 


138  TEMPERATURE  AND  HUMIDITY 

fellow-passengers  as  took  an  interest  therein,  when  passing  through 
the  Red  Sea  in  the  hot  months  thereof. 

The  air  of  the  engine-room  in  steamers  is  laden  with  aqueous 
vapour,  and  certain  corners  can  be  found  near  the  condensers  with 
high  air  temperatures  and  practically  no  draught — -or,  in  other 
words,  with  conditions  analogous  to  those  under  which  Haldane 
performed  his  experiments  which  we  have  mentioned  in  Chapter  III. 

When  the  steamer  is  in  the  hottest  part  of  the  Red  Sea  in  a  warm 
month,  if  a  person,  lightly  clad  and  in  good  health,  places  himself 
in  such  a  corner,  with  a  clinical  thermometer  in  his  mouth,  it  will  be 
found  that  at  first  he  begins  to  sweat  violently,  and  for  a  time  remains 
at  a  normal  temperature.  But  in  due  course  his  temperature  will 
gradually  rise  and  his  pulse-rate  increase,  until  temperatures  of 
over  102°  F.  are  reached,  and  the  person  breaks  off  the  experiment 
because  he  feels  uncomfortable,  after  which  his  temperature  slowly 
returns  to  normal. 

We  have  performed  this  simple  experiment  several  times,  but  on 
one  occasion,  in  a  person  who  was  not  in  very  good  health,  the 
temperature,  after  reaching  ioi°  F.,  ceased  to  rise;  the  skin  became 
cooler,  the  tension  of  the  pulse  altered  remarkably,  and  he  began 
to  look  ill.  The  experiment  was  quickly  stopped  and  stimulants 
administered,  so  that  he  did  not  suffer  any  serious  effects,  though 
it  was  some  hours  before  he  felt  quite  right. 

These  two  experiments  show  that  a  high  atmospheric  tempera- 
ture can  act  in  two  ways.  In  the  first  there  was  a  gradual  rise  of  the 
body  temperature,  which,  if  continued  long  enough,  would  probably 
have  resulted  in  hyperpyrexia.  In  the  second,  after  an  initial  rise, 
the  heart  became  embarrassed,  and  if  the  heat  had  been  continued, 
there  appeal's  no  reason  to  doubt  that  this  person  would  have 
passed  into  a  condition  of  syncope. 

There  are,  therefore,  two  distinct  clinical  entities  to  be  considered 
— viz.,  heat-stroke,  characterized  by  high  bodily  temperature; 
and  heat-syncope,  in  which  there  are  symptoms  due  to  cardiac 
failure  but  no  fever,  both  of  which  are  brought  about  by  the  same 
cause — viz.,  high  atmospheric  temperatures  associated  with 
moderate  or  high  humidity. 

Such  are  our  views ;  but  it  is  as  well  for  the  reader  to  be  acquainted 
with  those  of  other  authors,  which  may  be  briefly  stated  in  an 
historical  account  as  follows : — 

High  air  temperatures,  whether  in  the  day  time  or  at  night,  have  been 
known  since  ancient  times  to  have  an  effect  upon  human  beings.  The  case  of 
the  child  of  the  Shunamite  woman  described  in  the  English  Bible  in  2  Kings  iv., 
from  verse  18  onwards,  is  probably  the  earliest  on  record.  The  child  com- 
plained to  his  father  of  his  head  when  out  with  the  reapers,  and  was  carried 
to  his  mother,  and  is  reported  to  have  died  at  twelve  noon — became  insensible 
— but  recovered  under  Elisha's  treatment,  which  appears  to  have  been  of  the 
nature  of  massage.  This  treatment  reminds  one  strongly  of  the  active 
friction  by  which  the  miners  of  the  Comstock  Silver  Mines  of  Nevada  are  said 
to  treat  successfully  those  of  their  fellows  who  faint  when  coming  out  of  the 
warm  mine  in  which  the  hot,  steamy  air  has  a  temperature  of  1280  F. 

It  has  been  said  that  though  old  writers  such  as  Dio  Cassius  described  these 


HIGH  ATMOSPHERIC  TEMPERATURES  139 

conditions,  the  medical  writers  of  ancient  times  were  silent  about  them. 
This  does  not  seem  to  be  quite  just,  for  Paulus  ^Egineta,  Oribasius,  and  the 
Arabians  certainly  understood  that  there  were  head  symptoms  which  they 
called  '  siriasis  '  (after  Sirius,  the  dog-star),  due  to  excessive  heat.  Certainly 
this  knowledge  was  lost,  and  Cardanus,  in  the  sixteenth  century,  describes 
symptoms  due  to  morbus  attonitus  (apoplexy)  brought  about  by  the  heat  and 
drought  of  the  summer  of  1543  in  Florence.  After  this  for  a  long  time  the 
disease  was  considered  to  be  an  apoplexy  till  Boerhaave,  early  in  the 
eighteenth  century,  introduced  the  name'  insolatio.'  and  considered  it  to  be 
a  phrenitis — i.e.,  meningitis. 

Steinkiihl  (1819)  thought  that  the  congestion  of  the  lungs  caused  death  by 
asphyxia;  Swift  (1854)  that  it  was  due  to  exhaustion  produced  by  fatigue; 
Hill  (1857)  evidently  confounded  pernicious  malaria  and  heat  stroke.  Levick 
(1859)  suggested  that  it  was  an  acute  specific  fever;  H.  C.  Wood  (1863)  con- 
sidered that  it  was  due  to  a  poison  developed  in  the  blood,  and  called  it 
thermic  fever;  while  Stiles  (1864)  performed  experiments  on  animals,  and 
concluded  that  the  disease  was  due  to  the  direct  effect  of  heat  on  the  muscular 
system. 

In  1869  Eulenberg  and  Vohl  stated  that  the  disease  was  due  to  sudden 
liberation  of  the  gases  in  the  blood;  and  Weikard  and  Richardson  attributed 
it  to  clotting  of  blood  in  the  vessels. 

In  1870  Yallin  performed  several  experiments  by  locally  heating  parts  of 
the  body,  and  concluded  that  there  were  two  conditions :  (1)  sthenic  insolation, 
due  to  coagulation  of  the  muscle  fibres  of  the  left  ventricle;  (2)  asthenic 
insolation,  due  to  the  action  of  heat  on  the  nerve  centres  of  the  brain,  thus 
disturbing  the  innervation  of  the  heart. 

In  1 871  and  1S72  Claude  Bernard  performed  some  experiments  which 
tended  to  show  that  when  a  warm-blooded  animal  died  as  the  result  of  heat, 
it  was  due  to  rigor  in  the  musculature  of  the  heart. 

In  1872  H.  C.  Wood  performed  experiments  which  showed  that  sunstroke 
could  be  produced  in  animals  as  readily  as  in  man  by  artificial  or  natural 
heat. 

He  came  to  the  conclusion  that  death  took  place  from  asphyxia,  and  that 
after  death  the  rigidity  of  heart  and  muscles  was  due  to  the  coagulation  of 
the  myosin,  and  he  further  pointed  out  that  this  will  take  place  at  once  in  the 
heart  if  the  temperature  of  the  body  reaches  1150  F.,  and  said  that  he  con- 
sidered it  to  be  the  cause  of  sudden  deaths  in  soldiers  in  battle.  Further,  he 
pointed  out  that  the  heating  of  the  brain  of  a  mammal  to  1080  F.  produces 
insensibility,  with  or  without  convulsions,  and  that  when  1 130  F.  was  reached 
the  animal  died,  and  that,  though  the  general  symptoms  of  sunstroke  were 
absent,  the  nervous  symptoms  were  present.  He  came  to  the  conclusion  that 
no  capillary  thrombi  were  formed,  that  no  poisons  were  generated  in  the 
bloodf  and  that  the  real  condition  was  the  heat  acting  upon  the  nervous 
system,  as  a  result  of  which  there  was  rapid  metabolism,  which  used  up 
oxygen  and  at  the  same  time  induced  brain  changes,  causing  asphyxia.  But 
he  distinguished  from  the  true  heat-stroke: — 

1.  Acute  meningitis  or  phrenitis,  due  to  exposure  to  the  sun,  in  which  lie 
disbelieved. 

2.  Heat  exhaustion,  due  to  working  in  a  heated  atmosphere,  which  he  said 
did  not  differ  from  acute  exhaustion  due  to  other  causes,  and  therefore  was 
not  true  sunstroke. 

In  1S79  Jacubash  classified  heat  accidents  into:  (1)  sunstroke  due  to  the 
action  of  the  sun  on  the  body,  when  the  temperature  may  reach  1130  to 
1150  F.  (450  to  460  C);  (2)  heat-stroke,  due  to  exertion,  and  often  seen  in 
marching  troops  in  the  Temperate  Zone;  (3)  thermic  fever,  which  he  considered 
to  be  the  true  heat-stroke  of  the  tropics,  due  to  accumulation  of  heat  in  the 
human  body  in  consequence  of  high  atmospheric  temperatures  without 
exposure  to  the  sun  or  muscular  exercise. 

Dony  (1884)  considered  that  there  were  two  main  conditions:  (1)  sunstroke, 
due  to* the  sun's  rays  acting  upon  the  cranium  and  brain,  only  without  very 
great  rise  of  temperature;  and  (2)  heat-stroke,  due  to  intense  heat  acting  on 


140  TEMPERATURE  AND  HUMIDITY 

the  whole  body  and  after  certain  prodromes,  resulting  in  a  rapid  rise  of  tem- 
perature to  a  great  height. 

In  1893  Saquel  classified  the  diseases  into  (1)  sunstroke,  meaning  the 
erythema  due  to  the  sun's  rays;  and  (2)  insolation,  meaning  the  action  of  the 
sun  on  the  nervous  system,  producing  either  congestion  (mild  form  in  the  Tem- 
perate Zone)  or  meningitis  and  encephalitis  (severe  form  in  the  tropics) ; 
(3)  heat-stroke;  and  (4)  thermopeliosis,  a  combination  of  insolation  andk heat- 
stroke. 

In  1898  Sambon  defined  heat  exhaustion  as  an  ordinary  syncope,  while  he 
considers  that  under  the  term  '  sunstroke  '  there  is  confounded  an  infectious 
fever  which  he  calls '  siriasis,'  due  to  some  micro-organism  as  yet  not  defined. 

In  the  period  1898- 1907  Sir  Patrick  Manson,  in  his  book  on  tropical  diseases, 
recognized  three  conditions:  (1)  heat  exhaustion — sudden  cardiac  failure  or 
fainting,  brought  about  by  exposure  to  high  atmospheric  temperature; 
(2)  siriasis,  an  acute  disease  developing  in  the  presence  of  high  atmospheric 
temperature,  and  characterized  by  sudden  incidence  of  hyperpyrexia,  coma; 
and  (3)  sun  traumatism,  or  direct  action  of  the  sun's  rays  on  the  tissue,  causing 
either  sudden  death  or  a  febrile  condition. 

In  1905  Van  Brero,  in  Mense's '  Handbuch  der  Tropenkrankheiten,'  recog- 
nizes (1)  heat  exhaustion,  due  to  excessive  heat  from  the  sun  or  other  source; 
and  (2)  sun  traumatism,  caused  by  the  direct  action  of  the  sun's  rays. 

In  1907  Sir  Joseph  Fayrer,  in  Allbutt  and  Rolleston's '  System,'  recognizes 
(1)  a  state  of  exhaustion  leading  to  syncope,  and  (2)  an  overheating  of  the 
nervous  centres,  blood,  and  tissues,  leading  to  thermic  fever. 

In  1908  Brook  defines  diathermasia  as  the  effect  of  heat  on  the  thermotaxic 
mechanism,  and  phcebism,  a  kind  of  shock  due  to  the  actinic  rays  from  the  sun. 

(For  the  continuation  of  this  history  see  Chapter  LVI.) 

It  will  thus  be  seen  that  authorities  in  general  recognize  the  action 
of  heat  and  the  action  of  sun's  rays  as  being  separate,  and,  further, 
that  heat  may  produce  a  syncopal  condition  of  fever,  while  the  sun's 
rays  may  also  cause  syncope  and  fever.  Some  few,  including 
especially  Sambon,  suspect  the  presence  of  an  acute  specific  fever 
as  being  concealed  in  the  diseases  above  mentioned.  Others,  again, 
consider  the  symptoms  to  be  toxic  in  origin,  so  that  there  are  four 
theories:  (1)  caloric;  (2)  actinic;  (3)  microbic;  (4)  toxic. 

CONCLUSIONS. 

Personally,  we  believe  that  high  atmospheric  temperatures  with  a 
sufficiently  high  atmospheric  humidity  and  more  or  less  stagnation 
of  the  air  can  produce  the  clinical  pictures  called  heat-stroke  and 
heat-syncope,  especially  in  people  working  hard  at  manual  labour  and 
clad  in  unsuitable  clothing. 

As  to  the  reason  why  some  persons  should  develop  these 
symptoms,  while  others  living  under  exactly  similar  conditions 
escape,  we  believe  it  to  be  a  matter  of  general  health  and  personal 
habits,  which  in  the  one  case  disturb  the  metabolism  of  the  body, 
causing  a  derangement  of  physical  or  chemical  heat  regulation,  while 
in  the  other  case  this  mechanism  is  working  normally. 

The  regulation  of  bodily  heat  can  be  disturbed  by  anything  which 
tends  to  derange  metabolism  or  heat  regulation,  such  as  overwork, 
lack  of  care  in  protecting  the  body  as  much  as  possible  from  heat 
by  the  means  indicated  in  Chapter  III.,  p.  89,  alcoholism,  and  the 
effects  of  bodily  disease. 


REFERENCES  i  4 1 

Muscular  work  is  especially  dangerous,  as  under  certain  conditions 
even  a  couple  of  sets  of  tennis  may  produce  a  temporary  increase 
of  the  bodily  temperature,  which  may  rise  as  high  as  ioi°-i02°  F. 

If  in  addition  to  the  deranged  heat  regulation  there  is  added 
cardiac  weakness  or  lack  of  vaso-motor  control,  then  heat-syncope 
and  not  heat-stroke  appears. 

The  essential  pathological  change  producing  death  from  heat- 
stroke is  the  partial  coagulation  of  the  globulin  found  in  the  cells 
of  the  body.  It  is  possible  that  this  coagulation  takes  place  first 
in  voluntary  and  cardiac  muscles,  thus  leading  to  respiratory  and 
cardiac  failure,  while  later  marked  changes  are  to  be  found  in  the 
nerve  cells,  especially  in  the  medulla,  leading  to  chromatolysis. 

The  clinical  description  of  these  diseases  will  be  found  in  the 
third  part  of  this  book,  in  Chapter  LVI. 


REFERENCES. 

Pembrey  and  Ritchie  (1913),  'General  Pathology,'  London,  contains  a  most 
excellent  article  dealing  with  the  above  subjects  under  the  heading  Tempera- 
ture. 

Duncan  (1904).    Journal  of  Tropical  Medicine.     (1908).  Journal  Royal  Army 

Medical  Corps,  xi.  71. 
Fayrer  (1893).    Davidson's  Hygiene  and  Diseases  of  Warm  Climates,  p.  691. 

(1907).  Allbutt  and  Rolleston's  System  of  Medicine,  II.,  ii.  771-782. 
Gihon   (1893).     Twentieth-Century  Practice  of  Medicine,  iii.  253-285.     (A 

good  description  of  typical  cases  and  a  considerable  literature.) 
Giles  (1906).     British  Medical  Journal,  ii.  596. 
Haldane  (1905).     Journal  of  Hygiene,  v.  494-513. 

Halliburton  (1904).     Bio-chemistry  of  Muscle  and  Nerve,  pp.  107-115. 
Hill  (1906).     Recent  Advances  in  Physiology  and  Bio-chemistry,  pp.  271- 

274. 
Hirsch.     Handbook  of  Geographical  and  Historical  Pathology,  iii.  626-651. 

(A  very  full  literature  till  about  1883.) 
Manso.v  (1904).     Tropical  Diseases,  pp.  282-296. 
Rho    (1907).     Mense's   Tropenkrankheiten    (Italian   translation).     Also   the 

new  German  edition,  beginning  in  191 3  and  still  coming  out. 
Sambon  (1898).     British  Medical  Journal,  i.  744-748.     (This  account  should 

be  read,  if  possible.) 
Sellards,    Bovie    and    Brooks    (1918).      Journal    of    Medical    Research, 

vol.  xxx.,  No.  3. 
Simpson  (1908).     Journal  Royal  Army  Medical  Corps,  xi.  441. 
Sutton  (1009).     Journal  of  Pathology,  vol.  xiii.,  pp.  62-73.     Cambridge. 
Wood  (1887).     Pepper's  System  of  Medicine,  v.  387-400.     (A  most  excellent 

account,  with  many  quotations.) 


CHAPTER  VIII 
PRESSURE  AND  RADIATION 

Preliminary — Increased  pressure — Diminished  pressure — Radiation — 
Electricity — References. 

PRELIMINARY. 

The  present  chapter  is  devoted  to  the  study  of  the  'pathological 
effects  of  atmospheric  pressure  when  considerably  increased  or 
diminished,  and  of  the  rays  from  the  sun  under  conditions  which 
produce  disease. 

If  there  are  pathological  effects,  other  than  those  already 
mentioned  (p.  88),  as  the  result  of  rays  from  the  moon,  they  are 
unknown.  Probably  they  do  not  exist,  and  possibly  the  effects 
already  described  may  be  due  to  the  fact  that  the  moon's  rays  when 
reflected  become  polarized. 

A  passing  reference  will  be  made  to  the  effects  of  lightning,  as 
death  from  this  cause  is  not  infrequent  in  the  tropics. 

INCREASED  PRESSURE. 

The  work  of  facilitating  trade  by  means  of  roads  and  railways 
throughout  the  tropics  necessitates  the  construction  of  bridges 
across  deep  rivers,  and  therefore  for  many  years  to  come  the  effects 
of  artificially  increased  atmospheric  pressure  will  be  more  obvious 
in  these  regions  than  elsewhere. 

Moreover,  for  centuries  tropical  natives  have  been  exposed  to 
increased  pressure  when  diving  for  commercial  purposes,  and  though 
generally  they  do  not  remain  down  long  enough  to  suffer  any  bad 
effects,  still  at  times  these  are  noted. 

The  effects  of  greatly  increased  atmospheric  pressure  are  usually 
termed  '  caisson  disease,'  because  it  was  observed  first  in  connection 
with  the  special  compressed  air  apparatus  used  by  engineers  for 
work  under  water. 

In  1878  Paul  Bert,  as  the  results  of  his  experiments  upon  animals, 
showed  that  the  extraordinary  symptoms  of  this  disease  could  all 
be  explained  by  increased  atmospheric  pressure,  but  it  is  mainly 
by  the  labours  of  Leonard  Hill  that  Paul  Bert's  work  has  been 
confirmed  and  made  known. 

Symptoms  of  the  disease  are  rarely  observed  until  a  pressure  of 
one  atmosphere  (15  pounds  to  the  square  inch)  has  been  reached, 

142 


INCREASED  PRESSURE  143 

but  above  that  point  the  danger  rapidly  increases,  and  at  two 
atmospheres  the  risk  is  very  considerable. 

The  causation  is  due  to  the  fact  that  the  blood  absorbs  nitrogen 
from  the  compressed  air,  and  this  gas  is  retained  in  simple  solution 
in  the  blood-plasma  solely  by  the  increased  pressure.  If,  now,  this 
pressure  be  rapidly  diminished,  the  nitrogen  is  liberated  in  the  form 
of  bubbles  in  the  plasma,  and  these  in  their  turn  block  the  capillaries 
and  also  tend  to  accumulate  in  the  heart.  The  other  gases,  oxygen 
and  carbon  dioxide,  have  nothing  to  do  with  the  causation,  for 
obvious  reasons,  because  oxygen  would  be  rapidly  absorbed  by  the 
tissues,  and  the  other  gas  cannot  be  increased  in  the  blood  affected 
by  compressed  air. 

Nitrogen  is  also  held  in  solution  in  the  tissues,  especially  in  fat, 
and  hence  fat  people  are  more  susceptible  to  the  disease. 

Time  is  required  to  saturate  the  blood  and  tissues  with  nitrogen, 
and  therefore  the  danger  increases  with  the  length  of  exposure. 

The  actual  liberation  of  the  bubbles  of  nitrogen  will  not  take 
place  until  decompression  is  begun.  If  this  is  rapid,  then  the 
symptoms  will  be  severe;  if  slow,  they  may  be  few  or  absent;  but  it 
has  been  found  that  danger  depends  upon  relative  and  not  absolute 
reduction.  Thus,  two  atmospheres  may  safely  be  reduced  to  one, 
four  to  two,  six  to  three,  but  three  atmospheres  cannot  be  reduced 
to  one  without  danger. 

Decompression  should  therefore  be  based  upon  reduction  to  one- 
half  of  that  at  which  work  has  been  done,  and  after  that  there  is  a 
considerable  pause,  during  which  muscular  exercises  are  performed 
to  rid  the  body  of  the  nitrogen;  and,  again,  a  half-decompression, 
and  so  on,  but  each  interval  must  be  considerable. 

As  the  symptoms  are  due  to  bubbles  of  gas,  they  are  extremely 
varied,  but  pain  and  paralysis  are  the  most  marked,  and  should  be 
treated  by  immediate  recompression,  followed  by  slow  decompression. 

The  medical  examination  of  persons  about  to  work  on  these  lines 
is  most  necessary,  and  all  fat  persons  and  those  with  any  organic 
lesion  should  be  rejected. 

DIMINISHED  PRESSURE. 

The  attention  of  tropical  workers  has  been  drawn  of  late  to  the 
effects  of  diminished  atmospheric  pressure  as  exemplified  by  able 
accounts  of  the  mountain  sickness  of  the  Andes. 

Normal  atmospheric  pressure  in  alveolar  air,  which  is  saturated  with  aqueous 
vapour,  is  760  millimetres  of  mercury,  of  which  47  are  due  to  the  pressure 
of  the  aqueous  vapour,  and  therefore  the  rest  is  due  to  air  gases,  of  which 
oxygen,  which  is  present  in  a  proportion  of  14*2  per  cent.,  is  responsible  for 
10 1  and  carbon  dioxide  for  40  millimetres. 

If  the  oxygen  percentage  in  inspired  air  falls  from  20*9  to  12  per  cent., 
hyperpncea  takes  place;  if  to  10  per  cent.,  cyanosis  appears  and  increased 
frequency  of  the  heart;  and  at  5  per  cent,  there  is  loss  of  consciousness. 

If  the  atmospheric  pressure  is  reduced  to  580  millimetres,  the  want  of  oxygen 
begins  to  tell  upon  the  breathing,  and  the  carbon  dioxide  pressure  in  alveolar 
air  is  also  diminished. 


144  PRESSURE  AND  RADIATION 

Mosso  and  Aggazotti,  noting  the  favourable  effects  of  adding  COo  to  inspired 
air  and  reduced  oxygen  pressure,  came  to  the  conclusion  that  mountain  sick- 
ness was  '  acapnia  ' — i.e.,  primarily  due  to  deficiency  in  carbon  dioxide — 
but  the  real  facts  are  that  Paul  Bert  was  right  in  tracing  it  primarily  to  lack 
of  oxygen,  produced  gradually.  Mountain  sickness  usually  begins  about 
6,000  to  7,000  feet,  and  is  more  marked  at  heights  of  over  io,ooo,  but  after  a 
sojourn  of  one  or  two  weeks  the  effects  pass  away.  The  physiological  effects 
of  high  altitudes  have  been  studied  by  Haldane,  Douglas,  and  others,  at  a 
height  of  14,000  feet  and  a  barometric  pressure  of  457,  when  it  was  found  that 
though  persons  became  ill  within  half  an  hour  of  arrival,  their  symptoms  were 
relieved  immediately  by  inhalation  of  oxygen,  and  acclimatization  took  place 
within  eight  to  ten  days. 

The  partial  pressure  of  C02  in  alveolar  air  had  fallen  to  27  millimetres, 
and  the  carbon  dioxide  ventilation  had  increased  considerably,  and  therefore 
the  alveolar  oxygen  pressure  was  raised  above  what  it  otherwise  would  have 
been — i.e.,  52  millimetres. 

The  arterial  oxygen  pressure  was  35  millimetres  above  oxygen  pressure  in 
alveolar  air,  and  accounted  for  the  disappearance  of  mountain  sickness  and 
for  the  bright  red  colour  of  the  lips.  On  arrival  it  is  little  above  that  of  alveolar 
air,  therefore  acclimatization  depends  upon  the  development  of  the  powers  of 
the  epithelium  of  the  lung  alveoli  to  actively  secrete  oxygen  inwards,  a  power 
which  does  not  exist  during  rest  at  sea-level. 

The  haemoglobin  is  increased  in  a  few  weeks' residence  to  115  to  154  per  ce  t., 
as  indicated  by  the  Gowers-Haldane  scale ;  and  this  slow  increase  is  associated 
with  a  slow  increase  in  the  total  haemoglobin  of  the  body  and  a  slight  increase 
in  the  blood  volume. 

The  red  bone  marrow  is  increased  in  amount  (as  shown  by  experiments  on 
dogs  by  Zantz),  and  there  is  new  formation  of  red  corpuscles  and  a  diminished 
alkalinity  of  the  plasma  for  unknown  reasons. 

RADIATION. 

Radiation  from  the  sun,  of  heat  and  chemical  rays,  is  potentially 
an  important  factor  in  producing  pathological  conditions  in  man 
residing  in  all  climates,  but  more  particularly  in  the  tropics. 

In  temperate  climates  its  heat  effects  have  been  especially  studied 
by  Rubner,  Cramer,  and  Wolpert,  who  state  that,  adding  half  the 
number  of  degress  of  difference  between  the  register  of  the  black 
bulb  thermometer  and  that  of  the  shade  thermometer  to  the  shade 
temperature,  one  obtains  a  figure  which  corresponds  to  the  thermic 
effects  of  the  sun.  This  calculation  in  the  tropics  gives  a  tempera- 
ture considerably  above  that  of  the  body,  but  the  only  exact  method 
of  measuring  the  caloric  value  of  radiation  from  the  sun  is  the 
pyrheliometer  of  Angstrom,  as  used  in  Manila  by  Aron.  Schmidt 
estimates  the  heat  effect  of  the  tropical  sun  as  being  equal  to  2  small 
calories  per  square  centimetre  per  minute. 

Now,  the  animal  body  having  a  much  higher  coefficient  of  absorp- 
tion of  heat  than  has  the  air,  is  capable  of  absorbing  these  rays, 
and  hence  of  becoming  hotter;  therefore  in  this  way  exposure  to 
the  sun  tends  to  make  the  body  hotter  and  helps  in  the  production 
of  the  heat-stroke  already  considered  in  the  last  chapter. 

It  is,  however,  with  the  chemical  rays  that  we  are  more  concerned 
in  the  present  section,  and  as  yet  there  are  but  few  observations  on 
this  subject  in  the  tropics. 

The  earliest  experiments,  with  a  view  to  ascertaining  definitely 


RADIATION  145 

whether  there  is  such  a  condition,  were  those  by  Scaghosi  on  rabbits 
exposed  to  the  Sicilian  sun.  Their  temperature  rose  cons'derably, 
and  if  the  experiment  was  continued  long  enough  they  died,  but 
if  it  was  stopped  they  recovered.  The  post-mortem  changes  were 
hyperaemia  of  the  meninges,  heart,  lungs,  liver,  and  spleen.  The 
nerve  cells  of  the  brain  and  spinal  cord  showed  coagulative  necrosis 
and  chromatolysis. 

The  next  experiments  of  importance  on  the  aetiology  of  this 
condition  are  those  of  Moller  on  rabbits,  who  showed  that  thermal 
rays,  with  or  without  chemical  rays,  if  directed  on  to  the  skin  cover- 
ing the  skull,  produced  more  or  less  intense  cerebral  disturbance, 
and  sometimes  even  sudden  death.  The  autopsy  after  intense 
irradiation  showed  the  skin  of  the  head  much  swollen  and  bloody, 
with  gelatinous  exudation  in  the  subcutaneous  tissue.  The  peri- 
osteum, cranial  bones,  and  dura  were  discoloured,  and  covered  with 
ecchymoses.  The  vessels  of  the  brain  surface  were  much  dilated, 
and  showed  numerous,  and  in  part  confluent,  ecchymoses. 

Our  own  experiments  on  rabbits,  performed  yearly  for  several 
years,  during  the  particularly  hot  weather  in  Colombo,  show  that 
if  such  animals  are  exposed  to  the  sun  at  about  twelve  noon  they 
die  with  all  the  symptoms,  post-mortem  appearances,  macroscopical 
and  microscopical,  of  sunstroke,  in  about  sixty-seven  minutes, 
whereas  other  rabbits  similarly  treated  and  exposed  at  the  same 
time  and  in  the  same  place,  but  protected  by  red  glass,  live. 
Although  it  is  true  that  the  red  glass  did  absorb  a  proportion  of  the 
heat  rays,  still  the  rabbit  was  intensely  hot  to  the  touch  at  the  end 
of  the  experiment,  being  kept  in  position  under  the  red  glass  by 
being  placed  in  a  box  painted  black  externally  and  so  narrow  that 
the  sun's  rays  fell  directly  upon  its  shaven  head  and  unshaven  back. 
Nevertheless,  the  protected  rabbits,  though  kept  under  observation 
for  months,  never  seemed  to  be  any  the  worse  for  their  treatment. 

We  came  to  the  conclusion  that  the  ultra-violet  rays  were  not 
the  pathogenic  agent  in  these  experiments,  but  that  the  active  rays 
were  in  the  visible  blue  and  violet ;  and  in  this  we  were  much  aided 
by  Professor  Browning,  who  supplied  us  with  glasses  spectroscopi- 
cally  adjusted. 

Aron  studied  the  action  of  the  tropical  sun  in  the  Philippine  Islands,  and 
concluded — 

1.  Under  climatic  conditions  rabbits  and  monkeys,  having  by  nature  only 
a  limited  power  of  physical  heat  regulation,  die  if  exposed  to  sun,  the  body 
temperature  rising  to  febrile  heights. 

2.  The  post-mortem  findings  are  hemorrhagic  lesions  of  the  meninges  and 
(in  monkeys)  of  the  heart. 

3.  In  animals  with  a  poorly  developed  sweat-gland  system  the  subcutaneous 
tissues  are  heated  by  radiation  from  the  sun  to  temperatures  above  that  com- 
patible with  life. 

4.  The  human  skin  is  warmed  to  about  30  to  40  above  normal  skin  tempera- 
ture, but  an  increase  in  bodily  temperature  is  prevented  by  evaporation  of 
sweat,  which  causes  a  fall  of  skin  temperature. 

5.  Brown  skin  shows  a  smaller  rise  in  temperature  than  white  skin,  due  pos- 
sibly to  an  earlier  and  better  water  evaporation  by  sweat  secretion.  Hence  a 
coloured  skin  is  a  better  heat  regulator  than  a  white  skin. 

10 


14&  PRESSURE  AND  RADIATION 

6.  The  air  in  human  hair,  especially  black  hair,  under  the  influence  of  the 
tropical  sun,  acquires  temperatures  far  above  those  compatible  with  life. 

He  also  states  that  increased  body  temperature  probably  accounts  for  many 
of  the  accidents  called  sunstroke  or  heat-stroke,  and  he  thinks  that  an  excessive 
and  continued  watery  evaporation  from  the  skin,  while  avoiding  a  rise  of  body 
temperature,  may  lead  to  collapse,  unless  the  lost  water  is  replaced. 

We  believe  that  it  is  possible  that  direct  radiation  from  the  sun 
can  bring  about  sudden  death  and  congestion  of  the  meninges  of 
the  brain.  The  connection  between  sunstroke  and  the  chemical 
rays  requires  more  investigation;  but,  whatever  this  may  produce, 
there  is  no  doubt  that  if  the  improperly  protected  head  is  exposed 
to  radiation  from  the  sun,  headache  and  a  feeling  of  illness  is  often 
produced,  and  that  therefore  adequate  protection  is  required. 

As  is  well  known,  monkeys  prefer  the  shade  to  the  sun's  rays,  and 
seem  to  understand  the  danger  therefrom;  and  yet  no  one  is  afraid 
of  monkeys  dying  from  the  heat  in  laboratory  outhouses,  though  its 
effect  on  other  kinds  of  tropical  animals,  such  as  gerbils,  is  a  matter 
of  bitter  experience,  leading  to  the  loss  of  strains  of  trypanosomes. 

We  hold,  however,  that  there  is  no  clinical  difference  between 
heat-stroke  and  sunstroke,  and  therefore  these  will  be  considered 
as  one  and  the  same  disease  in  the  clinical  section  of  this  work 
(see  Chapter  LVL,  p.  1449). 

ELECTRICITY. 

Thunderstorms  are  often  of  extreme  violence  in  the  tropics,  and  death  from 
lightning-stroke  is  much  commoner  than  in  the  Temperate  Zone;  but  the  signs 
of  lightning-stroke  are  exactly  the  same  as  those  usually  recorded  in  books 
on  general  surgery,  and  need  not  be  repeated  here. 


REFERENCES. 

The  most  valuable  work  for  general  knowledge  is  Peinbrey  and  Ritchie 
(1913),  'Textbook  of  General  Pathology,'  where  Haldane's  articles  on  respira- 
tion will  be  found  most  useful. 

Pressure. 

Hill.     Caisson  Disease.     London.     (A  very  important  publication.) 

Radiation. 

Brown,   Carnegie   (1906).     British  Medical  Journal   (Degeneration  of  the 

Myocardium  in  Hot  Climates),  i.  1462- 1463. 
Cleaves  (1904).     Light  Energy,  pp.  253,  254,  and  pp.  798-801. 
Duncan    (1904)-     Journal    of    Tropical    Medicine.     (1908).    Journal    Royal 

Army  Medical  Corps,  xi.,  71. 
Fayrer  (1893).     Davidson's  Hygiene  and  Diseases  of  Warm  Climates,  p.  691. 

(1907).  Allbutt  and  Rolleston's  System  of  Medicine,  II.,  ii.  771-782. 
Freund  (1904)-     Radiotherapy.     London. 

Electricity. 

Adamson  (1900).     Journal  of  Tropical  Medicine  and  Hygiene  (Interesting 
account  of  lightning  stroke),  January,  147. 


CHAPTER  IX 
SOME  TROPICAL  TRAUMATISMS 

Remarks — Traumatisms  brought  about  by  animal  agencies:  the  larger 
Cirnivora;  the  smaller  Carnivora;  the  Ungulata;  the  Proboscidae;  the 
ReptiUa;  the  Selachii;  Man — Traumatisms  due  to  physical  agencies: 
Foot-binding — Heavy  fruits — Electric  fans — Powdered  glass — Bamboo 
hairs — References. 

REMARKS. 

In  the  tropics  many  accidents  and  injuries  occur  whichj  are 
but  rarely  met  with  in  temperate  climates.  These  accidents 
and  injuries  may  be  divided  into  two  categories — traumatisms 
brought  about  by  animal  agencies,  and  those  due  to  physical 
agencies.  Under  the  first  heading  come  those  caused  by  the  bites 
or  maulings  of  wild  and  domestic  animals,  as  well  as  the  injuries 
caused  by  man's  bite.  In  the  second  division  are  grouped  various 
accidents  caused  by  electric  fans,  by  the  fall  of  heavy  fruits  from 
trees,  and,  lastly,  the  peculiar  deformity  of  the  foot  in  high-class 
Chinese  women  brought  about  by  bandaging  the  feet  of  young 
female  children. 

There  are,  of  course,  many  other  traumatisms  which  might  be 
worthy  of  note,  as,  for  example,  penetrating  wounds  of  the  abdomen 
by  sword  fish,  as  described  l^y  Renner,  or  bites  by  Congo  fish,  as 
privately  mentioned  to  us  by  Christy ;  but  they  are  either  too  rarely 
met  with,  or  else  they  are  too  well  known  in  the  Temperate  Zone  to 
require  notice  here. 

It  will  be  observed  that  we  make  a  distinction  between  the 
physical  injury  caused  by  the  bite  of  one  of  the  larger  animals  and 
the  chemical  injury  caused  by  a  venomous  animal,  and  we  do  this 
advisedly,  while  fully  recognizing  that  the  former  may  introduce 
septic  toxins,  sometimes  in  large  amount,  as  well  as  germs  into  the 
wounds  so  produced. 

TRAUMATISMS  BROUGHT  ABOUT  BY  ANIMAL  AGENCIES. 

Traumatisms  caused  by  the  Larger  Carnivora.— The  word  '  trau- 
matism '  is  peculiarly  suitable  for  this  nomenclature,  as  it  is  derived 
from  the  Greek  words  rpavfia  (a  wound)  and  0-qpiov  (a  wild  animal). 
The    synonyms   are  Morsus    and    Rostro    et   Unguibus  'dilacera- 

tio    (Latin);    8-qy/xa,    Sr^is,    Siacnraa-fios  ;    KOWTOWS,    (nrapay/xos    (Greek); 

Morsures,   Dechirements   musculaires,  Dilacerations,  Deplecement 

H7 


148  SOME  TROPICAL  TRAUMATISMS 

des  chairs,  Myalgies  traumatherigenes  (French).  Under  the  defini- 
tion '  Traumatisms  caused  by  the  larger  Carnivora  '  we  refer  especi- 
ally to  the  injuries  inflicted  by  the  bites,  rends,  and  scratches  pro- 
duced by  the  teeth  and  claws  of  species  belonging  to  the  families 
Felidse  and  Ursidae. 

In  the  Felidse  are  Felis  ho  Linnaeus,  whose  habitat  is  Africa  and 
Asia;  F.  tigris  Linnaeus,  habitat  Asia;  F.  pardus  Linnaeus,  habitat 
India;  F.  leopardus,  habitat  Africa;  F.  onca  Linnaeus,  habitat  South 
America;   F.   partialis   Linnaeus,   habitat   South   America.     These 

3    i    3    i 
cats  have  a  general  dental  formula,  '  giving  thirty  teeth 

for  the  whole  mouth,  which  include  the  most  perfect  types  of  carnas- 
sial  teeth  capable  of  producing  exceedingly  severe  lacerations. 
These  animals  feed  not  merely  on  the  fresh  prey  which  they  have 
recently  slain,  but  also  on  its  body  for  a  day  or  so  after  its  death. 
Their  maws  and  claws,  therefore,  become  exceedingly  foul,  being 
infected  with  micro-organisms  and  their  toxins,  and  hence  the  great 
danger  of  septic  intoxication  and  infection,  which  markedly  increases, 
the  gravity  of  the  injuries  inflicted. 

The  other  family,  Ursidae,  includes  the  bears  which  are  found  in 
India  and  Ceylon — e.g.,   Ursus  torquatus,  of  the  Himalayas,  and 

U.   malayanus.       Their  dental  formula  is  ^*     '  J'      =  forty-two 

teeth  in  the  mouth,  but  these  do  not  include  carnassial  teeth,  which, 
added  to  the  facts  that  they  are  not  as  a  rule  such  foul  feeders  and 
often  eat  vegetal  foods,  causes  their  bites  to  be  not  quite  so  serious 
from  a  septic  point  of  view  as  those  of  the  Felidae.  Their  claws, 
however,  may  produce  most  serious  effects  of  both  a  traumatic  and 
of  a  septic  nature. 

The  importance  of  the  septicity  of  these  wounds  has  been  well 
appreciated  from  the  earliest  times,  for  in  the  fifth  book  of  his 
'  De  Medicina  '  Celsus  remarks  with  regard  to  the  bites  of  men, 
apes,  dogs,  and  ferocious  animals,  '  Omnis  autem  fere  morsus  habet 
quoddam  virus,'  and  on  this  he  based  his  treatment.  This  state- 
ment has  been  quoted  again  and  again  in  the  centuries  which  have 
passed  since  the  days  of  Celsus:  for  example,  by  Morgagni,  when 
investigating  the  serious  illness  produced  in  a  young  lady  by  the 
peck  of  a  sparrow  inflicted  on  a  finger,  and  by  Heister,  of  Helmstadt, 
in  the  section  on  bites  in  his  '  System  of  Surgery,'  published  in  1739. 

It  is  of  course  possible  for  any  person  of  any  age  and  either  sex 
to  be  the  victim  of  wounds  inflicted  by  these  animals,  but  the 
persons  most  frequently  injured  are  hunters  (shikaris)  and  sports- 
men, while  the  district  postmen  in  jungle  regions  run  great  risk,  as 
do  shepherds  and,  to  a  less  extent,  herdsmen,  and  to  a  still  less  extent 
cultivators  and  villagers  living  in  lonely  places  in  the  bush  or  jungle. 
The  present  writers  have  also  encountered  wild  animals  under  un- 
expected circumstances  during  their  journeys  into  the  interior  of 
Africa;  but  the  risk  which  an  ordinary  traveller  with  his  gang  of 
porters  runs  is  relatively  small,  particularly  if  he  has  some  slight 


TRAUMATISMS  BROUGHT  ABOUT  BY  ANIMAL  AGENCIES     149 

knowledge  of  the  habits  of  these  animals.  The  most  dangerous 
region  to  travel  through  is  tall  grass,  as  the  hunter  or  traveller  and 
the  wild  beast  may  meet  suddenly,  and  it  is  here  that  an  accident 
is  more  likely  to  occur  than  in  more  open  scrub  country.  Another 
prevalent  cause  of  accidents  is  the  beating  by  means  of  men  on  foot 
of  jungle  or  bush  into  which  a  wounded  animal  has  retreated.  The 
especially  dangerous  animal  under  such  circumstances  is  the  tiger, 
and  as  eminent  as  authority  as  Sir  Samuel  Baker  has  especially 
drawn  attention  to  this  fact,  and  has  stated  that  if  no  elephants  are 
available  then  a  herd  of  buffaloes  should  be  driven  through  the 
jungle,  as  they  will  quickly  dislodge  the  tiger.  The  possible  presence 
in  the  vicinity  of  the  mate  of  the  attacked  animal  should  always  be 
borne  in  mind,  as  the  omission  to  remember  this  simple  fact  has  often 
led  to  unpleasant  accidents. 

The  physical  signs  and  symptoms  produced  by  these  bites  and 
mauls  may  be  divided  into  general  and  local.  With  regard  to  the 
former,  immediately  after  being  bitten  or  mauled  the  victim,  if 
able  to  stand,  feels  giddy,  turns  pale,  becomes  unable  to  stand, 
and,  if  the  injury  is  at  all  severe,  quickly  passes  into  a  condition  of 
shock  with  a  weak  pulse,  cold  extremities,  pinched  and  drawn  face, 
and  weak  voice,  and  may  become  insensible,  which,  indeed,  is  often 
his  condition  when  first  rescued  in  the  severer  cases.  As  a  rule  he 
remains  in  a  more  or  less  torpid  condition,  sleeping  day  and  night, 
and  suffering  severely,  when  aroused,  from  thirst  and  pain.  All 
these  symptoms  are  more  accentuated  in  Europeans  than  in  natives. 
Usually  reaction  sets  in  fairly  quickly,  the  temperature  rising 
to  1010  to  1020  F.  or  even  more,  while  the  pulse  is  generally  quick, 
ranging  about  no  to  120  beats  per  minute.  Usually  the  torpor 
continues  for  some  time,  but  delirium  may  intervene.  The  mouth 
and  throat  continue  to  be  dry,  and  thirst  is  still  a  marked  symptom. 
Locally  the  injured  region  may  show  rends  and  tears  in  the  skin, 
lacerations  of  the  muscles,  tendons  exposed  and  torn,  vessels  and 
nerves  injured,  and  perhaps  torn  across,  with  more  or  less  haemor- 
rhage, bones  may  be  exposed,  bruised,  broken,  or  dislocated,  joints 
may  be  exposed,  opened,  and  injured.  Around  the  injured  regions 
the  parts  are  bluish  or  red  in  colour,  and  swollen,  and  quickly 
become  cedematous,  firm,  and  hot  to  the  touch. 

If  the  wounds  are  but  slight,  the  inflammation  may  remain  super- 
ficial, but  usually  the  great  danger  is  a  cellulitis  associated  with  pus 
formation  and  intermittent  fever.  A  more  serious  complication 
is  spreading  or  acute  traumatic  gangrene.  Later,  as  the  patient 
recovers,  there  is  the  liability  of  sinus  formation  and  of  stiffness  in 
joints. 

It  is  very  important  to  remember  that  malaria  can  occur  as  a 
complication,  and  that  therefore  some  of  the  intermittent  tempera- 
ture may  at  times  be  due  to  this  cause.  There  is  no  difficulty  with 
regard  to  the  diagnosis  as  a  rule,  as  there  is  generally  a  history  to 
be  obtained,  while  the  local  signs  are  sufficiently  indicative  of  the 
condition,  but  the  prognosis  with  regard  to  even  slight  wounds 


I5Q  SOME  TROPICAL  TRAUMATISMS 

must  at  first  be  guarded,  especially  in  Europeans,  as  it  is  impossible 
to  foretell  how  serious  the  intercurrent  septic  infection  may  prove 
to  be. 

The  treatment  resolves  itself  into  two  distinct  categories:  first, 
the  first  aid  when  the  rescue  is  effected;  and,  secondly,  the  usual 
surgical  treatment. 

With  regard  to  the  first  aid,  the  usual  methods  for  arresting 
haemorrhage,  combating  shock,  and  carrying  the  victim  are  too 
well  known  to  require  repetition,  but  the  thorough  washing  of  the 
wound  with  water,  even  jungle  water,  would  appear  preferable  to 
leaving  the  poisons  from  the  animal's  teeth  and  claws  in  the  wound. 
We  consider  that  a  small  first-aid  surgical  case  containing  antiseptics, 
bandages,  etc.,  should  form  part  of  the  outfit  of  every  sportsman, 
and  that  antiseptics  should  be  added  to  the  water  used  to  wash  the 
wound. 

As  a  rule  the  haemorrhage  has  more  or  less  abated  by  the  time 
the  man  reaches  a  hospital,  but  any  possible  source  of  bleeding 
must  be  at  once  attended  to,  and  the  wound  thoroughly  washed 
and  syringed  with  warm  iodine  lotion.  Pieces  of  dead  or  sloughing 
tissue  may  be  removed,  but  it  is  better  to  defer  any  serious  operative 
treatment  for  twenty-four  hours  if  possible,  as  it  is  very  dangerous 
to  perform  anything  of  this  nature  in  the  condition  of  shock  usually 
exhibited  by  the  patient.  The  parts  may  be  drawn  together  by  a 
suture  if  necessary,  but  very  few  of  these  should  be  inserted,  and  as 
free  drainage  as  possible  allowed.  Repeated  and  carefully  applied 
antiseptic  dressings  must  be  carried  out.  Antitetanic  serum  should 
always  be  administered  with  the  view  of  preventing  possible  tetanus. 

As  soon  as  there  is  any  suspicion  that  cellulitis  has  supervened, 
free  incisions  must  be  made,  and  hot  antiseptic  baths,  hot  fomenta- 
tions, or  Bier's  treatment  must  be  applied. 

Amputation  is  necessary  if  spreading  traumatic  gangrene  super- 
venes, when  it  must  be  performed  as  high  up  the  limb  as  reasonable, 
as  it  is  useless  to  do  repeated  operations  first  at  low  and  then  at 
higher  levels,  while  all  the  time  the  disease  is  spreading.  Sinuses 
require  to  be  scraped  and  plugged  with  antiseptic  gauze. 

When  recovery  is  proceeding  and  the  septic  infections  have 
ceased,  plastic  operations  are  necessary  to  close  the  large  wounds 
left  by  the  destruction  of  the  tissues,  while  massage  and  douches 
may  be  required  to  prevent  joints  from  becoming  stiff. 

As  regards  general  treatment,  the  first  requirement  of  the  patient 
is  usually  plenty  of  water  to  drink  to  relieve  the  urgent  thirst  from 
which  he  suffers,  and  to  dilute  the  toxins  of  the  possible  intoxication. 

At  first  the  food  should  be  of  the  lightest  description — broths, 
soups,  and  milk  diet— and  later  the  ordinary  hospital  diets  may  be 
gradually  introduced. 

With  regard  to  prophylaxis,  the  natives  often  adopt  simple 
protective  remedies,  such  as  a  bell  and  spear,  or  a  stick  and  a  small 
axe,  the  latter  being  in  use  in  districts  infested  by  small  bears. 
For  a  sportsman  it  is  important  to  thoroughly  understand  the  habits 


TRAUMATISMS  BROUGHT  ABOUT  BY  ANIMAL  AGENCIES     151 

of  the  ferocious  creatures  which  he  is  hunting,  and  especially  to 
know  what  they  usually  do  when  wounded.  In  travelling  in  the 
African  bush,  a  zareba  with  a  fire  is  usually  a  good  protection  during 
the  night. 

Traumatisms  caused  by  the  Smaller  Carnivora. —  Under  this 
heading  come  the  traumatisms  caused  by  members  of  the  family 
Canidse,  of  which  Canis  lupus  Linnaeus,  the  wolf,  C.  aureus,  the 
jackal,  and  C.  familiaris,  the  dog,  may  be  quoted.     Their  general 

dental  formula  is  3"     '-Ai     —  forty-two  teeth.     A  wolf  bite  resembles 

3-  i-  4.  3 
that  of  the  larger  Carnivora,  while  jackals  generally  attack 
children,  inflicting  severe  wounds,  often  of  a  septic  nature.  The 
jackal  is  often  infected  with  hydrophobia,  which  he  spreads  to  the 
village  dogs,  and  in  this  way  the  disease  is  kept  up  in  tropical 
countries.  There  can  be  no  doubt  that,  at  the  present  time,  hydro- 
phobia is  one  of  the  real  dangers  of  a  tropical  town  or  village,  where 
a  large  number  of  pariah  dogs  are,  as  a  rule,  allowed  to  run  freely 
about  the  streets  and  make  themselves  as  objectionable  as  they 
like.  The  result  is  that  a  number  of  children  and  adults  are  bitten 
every  now  and  again,  and  are  compelled  to  seek  protection  against 
possible  infection  by  treatment  at  one  of  the  now  numerous  Pasteur 
Institutes.  In  our  opinion,  some  attempt  should  be  made  by 
muzzling  dogs  for  a  period  of  at  least  two  years  throughout  a  country, 
and  the  destruction  of  all  dogs  not  so  protected,  to  diminish  this 
danger.  We  also  consider  that  the  destruction  of  all  ownerless 
dogs — i.e.,  dogs  without  a  collar  on  which  a  name  is  engraved — 
should  be  conducted  by  a  systematic  organization. 

The  parasite  of   hydrophobia  is  described  in  Chapter  XXII., 

P-  535" 

One  of  the  most  important  forms  in  which  rabies  attacks  dogs 

is  that  called  '  dumb  rabies,'  in  which  the  lower  jaw  early  becomes 
paralyzed;  this  is  a  form  often  overlooked  for  some  time  by  non- 
medical people,  and  is  a  source  of  great  danger. 

Anyone  interested  in  this  subject  must,  however,  consult  a  book 
on  general  medicine,  as  this  is  hardly  the  place  for  a  description  of 
rabies. 

Rat  and  cat  bite  diseases  are  described  in  Chapter  LI  I.,  p.  1356. 

Traumatisms  caused  by  the  Ungulata.— Among  the  Herbivora 
there  are  two  families  which  are  celebrated  for  vicious  attacks  upon 
man,  and  these  are   he  Camelidae  and  the  Bovidae. 

Camelus  bractrianus  Linnaeus  may  at  times  have  a  bad  temper, 
and  it  is  often  dangerous  for  a  stranger  to  approach  a  camel,  for  its 
bite  is,  as  a  rule,  a  serious  injury,  the  deep  tissues  being  crushed 
and  lacerated,  while  the  bones  may  be  crushed,  broken,  or  dis- 
located, and  tendons,  bursae,  and  joints  may  be  laid  bare  or  opened, 
and  last,  and  by  no  means  least,  because  of  the  possibility  of  gan- 
grene and  severe  septic  infection.  The  bites  generally?  occur  on 
the  upper ^or  lower  limb,  but  are  also  well  known^onjthe  head  and 
face.     The  shock  from  such  severe  injuries  is  naturally  very  great, 


15* 


SOME  TROPICAL  TRAUMATISMS 


but  the  symptoms,  signs,  and  treatment  resemble  those  already 
mentioned  under  the  heading  of  traumatisms  caused  by  the  Car- 
nivora,  and  need  not  be  repeated. 

Among  the  Bovidae,  the  buffalo  is  very  dangerous — e.g.,  Buffelus 
indiats  in  India  and  Ceylon,  and  Bubalus  brachyceros  in  Central 
Africa — the  danger  being  deep,  penetrating  wounds  of  the  limbs, 
chest,  or  abdomen,  as  well  as  severe  punctured,  lacerated,  and 
contused  wounds  in  any  part  of  the  body. 


Fig.  8. — Camel  Bite. 
(From^a  photograph  pwen  to  us  by  Christopherson.) 

Here  attention  may  be  drawn  to  the  fact  that  horses  may  become 
affected  with  hydrophobia,  which,  in  animals  treated  as  family 
pets,  is  a  serious  danger.  The  animal  appears  to  be  in  great  pain, 
and  is  often  thought  to  have  colic ;  it  froths  at  the  mouth  and  becomes 
very  savage,  biting  articles  in  its  stable  and  kicking  the  wall  in  a 
furious  manner  until  weakness  sets  in. 

Kicks  may  produce  serious  contusions  and  wounds,  as  well  as 
injuries  to  internal  organs. 

The  Rhinoceri — Rh.  indicus,  Rh.  javavicus,  Rh.  sumatrensis,  Rh.  africanus 
— produce  most  serious  punctured  and  lacerated  wounds. 

Hippopotami  are  common  in  the  rivers  and  lakes  of  Africa — e.g.,  H.  am- 
phibius  and  H.  liberiensis.  As  a  rule  they  are  quite  peaceful  animals  when 
left  alone,  but,  once  attacked,  they  become  dangerous,  seizing  the  boat  or 
the  persons  in  their  huge  jaws  and  crushing  wood  or  flesh  and  bones  into 
shapeless  masses.  They  are  very  courageous,  and  nothing  but  death  will 
stop  the  charge  of  one  of  these  brutes.  They  will  quickly  stamp  the  life  out 
of  any  victim  they  catch  on  land. 


TRAUMATISMS  BROUGHT  ABOUT  BY  ANIMAL  AGENCIES     153 

The  Suidas,  or  pigs,  are  commonly  met  with  in  tropical  jungles, 
and  are  of  importance  because  of  the  way  in  which  they  eat  the 
remains  of  persons  who  have  been  lost  in  the  jungle.  All  the  soft 
parts  are  completely  destroyed,  while  the  bones  are  broken, 
so  that  it  is  impossible  to  say  whether  the  unfortunate  people 
died  or  were  killed,  whether  they  met  with  an  accident  or  simply 
lost  their  way,  whether  the  pigs  ate  them  while  dying  or  only 
after  death. 

Severe  lacerated  wounds  can  be  inflicted  by  the  tusks  of  an 
enraged  boar. 

Proboscidae. — The  elephants — E.  africanus  and  E.  indicus — usually  kill 
their  victim  by  stamping  upon  him  until  the  soft  parts  are  terribly  crushed, 
lacerated,  and  bruised,  while  bones  are  broken.  They  also  seize  people  by 
means  of  their  trunks  and  dash  them  against  surrounding  objects  or  the 
ground. 

Traumatism  caused  by  the  Larger  Reptilia. — The  crocodiles, 
gavials,  and  alligators  are  a  constant  source  of  danger  in  the  tropics, 
especially  to  natives,  while  bathing  in  rivers.  The  names  '  croco- 
dile '  and  '  alligator  '  are  often  used  as  though  they  were  synonyms, 
but  this  is  by  no  means  so.  Some  twelve  species  of  crocodile  are 
well  known.     They  possess  a   most   formidable   array   of  teeth, 

expressed,  as  a  rule,  by  the  formula  — ,  of  which  the  third  and  ninth 

in  the  upper  jaw  are  longer  than  the  others,  and  are  respectively 
lodged  between  the  second  and  third  and  the  eighth  and  ninth  teeth 
in  the  lower  jaw,  in  which  the  first,  fourth,  and  eleventh  teeth  are 
the  strongest.  The  muzzle  of  the  crocodile  is  longer  than  that  of 
the  alligator.  The  muzzle  of  the  alligator  is  relatively  short  and 
broad. 

The  muzzle  of  the  gavial  is  very  long.  The  two  species  of  im- 
portance are  Gavialis  schlegeli  of  Java  and  Borneo  and  G.  gangeticus 

28   20 

of  the  Ganges.     The  latter  has  a  dental  formula  ^  teeth. 

The  following  list,  modified  from  Ditmar,  gives  the  names  and 
habitats  of  these  formidable  reptiles : — 

A.  Snout  extremely  long  and  slender — ■ 

Gavialis   gangeticus,    India;    Tomistoma  schlegeli,    Borneo 
and  Sumatra. 

B.  Snout  very  sharp,  slender,  and  triangular — 

Crocodilus   cataphr  actus,  West  Africa;  C.  johnstoni,   Aus- 
tralia; ('.  intermedins,  Orinoco. 

C.  Snout  moderately  sharp  and  triangular — 

Crocodilus  americanus,  Mexico,  Central  and  South  America; 
C.  siamensis,  Siam  and  Java;  C.  niloticus,  Africa; 
C.  porosus,  India  and  Malaysia. 

D.  Snout  oval,  bluntly  triangular — j 

Crocodilus  robustus,  Madagascar;  C.  thombifer,  Cuba; 
C.  morelatti,  Guatemala  and  Honduras. 


154  SOME  TROPICAL  TRAUMATISMS 

E.  Snout  short  and  broad — 

Crocodilus    palustris,    India    and    Malaysia;    Osteolcemus 
tetraspis,  West  Africa. 

F.  Canine  teeth  of  lower  jaw  fit  into  a  pit  in  upper  jaw— 

I.  Snout  as  in  D:  Caiman  trigonotus,  Upper  Amazon; 
C.  sclerops,  Central  and  Southern  America;  C.  pal- 
pelrosus,  Tropical  South  America.  II.  Snout  very  broad 
and  rounded:  C.  later  ostris,  Tropical  South  America; 
C.  niger,  Tropical  South  America;  Alligator  mississi- 
piensis,  U.S.A. ;  A.  sinensis,  China. 
The  celebrated  man-eating  species  are — 

Crocodilus  niloticus,  the  Nile  crocodile;    C.  porosus,  the 
salt-water  crocodile. 

The  American  species  are  said  to  be  inoffensive,  as  there  are  no 
records  of  attacks  upon  man. 

Another  important  anatomical  feature  of  these  reptiles  is  the 
length  and  strength  of  the  tail,  by  means  of  which  they  can  strike 
a  man  standing  on  the  low  bank  of  a  river  such  a  powerful  blow 
that  he  may  be  knocked  into  the  water. 

Accidents  are  commonly  met  with  while  people  are  crossing 
streams,  or  bathing  therein,  or  while  women  are  washing  clothes 
or  filling  vessels  with  water  at  a  river  or  lake.  Anyone  sitting  on 
a  steamer  or  other  craft  on  a  lake  or  river  with  his  feet  hanging  over 
the  side,  or  leaning  over  with  his  hand  in  the  water,  simply  provides 
bait  for  any  crocodile  in  the  vicinity. 

As  a  rule,  if  the  victim  is  rescued,  it  is  found  that  a  portion  of  a 
limb  has  been  bitten  off,  but  we  have  met  with  a  case  in  which  only 
a  large  portion  of  the  pectoralis  major  was  removed.  In  this  case 
the  victim  attributed  his  escape  to  driving  his  thumbs  into  the 
crocodile's  eyes.  The  wound  healed  excellently,  though  of  course 
there  was  practically  no  pectoralis  major  left  on  the  side  in  question, 
and  in  its  place  an  area  of  scar  tissue.  Crocodile  bites,  in  our  ex- 
perience, are  not  nearly  so  liable  to  septic  infection  as  the  bites  of 
the  Carnivora. 

Traumatisms  caused  by  the  Larger  Selachii.— By  far  the  greatest 
number  of  sharks  live  in  the  seas  of  warm  climates,  and  are  well 
known  because  of  the  great  danger  of  their  bite,  which  is  often 
fatal.  The  greatest  risk  is  to  bathers  or  fishermen,  but  it  is  a  curious 
fact  that  divers  for  pearls  appear  to  incur  little  risk.  It  is  probable 
that  the  noise  of  the  large  number  of  people  employed  in  this  work 
frightens  the  sharks,  which  keep  away. 

Carcharias  gangeticus  was  for  a  number  of  years  a  source  of  great 
danger  to  the  crowds  at  the  bathing  ghats  of  Calcutta.  Sir  Joseph 
Fayrer  says  that  they  used  to  feed  upon  the  partially  burned  bodies 
which  were  formerly  thrown  into  the  river,  but  when  this  custom 
was  discontinued  they  began  to  attack  the  people  at  the  bathing 
ghats,  especially  in  the  months  of  April  and  May,  when  the  river 
contains  much  salt  water.  He  says  that  they  would  dash  into  the 
crowd  at  the  bathing  ghat  and  inflict  dangerous  and,  at  times, 


TRAUMATISMS  BROUGHT  ABOUT  BY  ANIMAL  AGENCIES     155 

mortal  wounds,  though  they  seldom  were  able  to  get  away  with 
their  victim  because  of  the  numerous  people  at  the  ghat. 

The  patient  is  brought  to  the  hospital  suffering  from  the  effects 
of  shock  and  haemorrhage,  with  a  limb  either  snapped  off  or  partially 
torn  off,  or  with  larger  or  smaller  lacerated  wounds,  in  which  the 
bone  may  or  majr  not  be  exposed  and  grooved  by  the  sharks'  teeth, 
and  with  blood  dripping  from  the  ragged  surfaces  of  the  wound. 
Usually  the  patient  is  in  a  state  of  extreme  prostration,  covered  with 
a  cold  sweat,  and  having  a  hardly  perceptible  pulse. 

More  rarely  there  are  only  a  few  triangular  or  irregular  lacerated 
wounds,  showing  that  the  shark  did  not  obtain  a  proper  hold  of  the 
victim. 

The  great  danger  is  death,  either  immediately  or  in  a  few  hours, 
from  shock  or  haemorrhage.  If  this  is  avoided,  the  wounds  appear 
to  heal  readily  if  the  patient  is  otherwise  in  fair  health,  but  of  course 
amputation  is  often  necessary. 

Man. — The  bites  inflicted  by  the  Kru  men  on  the  West  Coast  of  Africa  in 
quarrels  are,  or  were,  of  not  uncommon  occurrence,  and  it  was  also  fairly 
common  to  meet  with  injuries  on  the  knuckles  caused  by  scratches  from 
their  teeth. 

These  wounds  were  usually  considered  to  be  serious,  for,  although  the  teeth 
of  the  African  appear  to  be  in  excellent  condition  of  repair  and  cleanliness, 
still  the  slightest  scratch  may  lead  to  exceedingly  severe  inflammations,  as 
the  present  writers  well  know.  The  most  careful  antiseptic  treatment  must 
be  applied  at  once. 

TRAUMATISMS  DUE  TO  PHYSICAL  AGENCIES. 

Foot-binding. — The  bandaging  of  the  feet  of  young  female  children 
began  in  the  imperial  harem  of  the  T'ang  Dynasty  in  China  some 
1,400  years  after  Confucius,  the  idea  probably  being  to  reproduce 
as  nearly  as  possible  a  club-foot.  As  a  matter  of  fact,  the  result  of 
pressure  of  the  short,  heavy  bandage  commonly  used,  neatly  and 
tightly  applied  to  the  growing  feet  of  young  girls  aged  three  to  four 
years,  is  to  produce  a  very  small  foot  in  the  condition  of  a  pes  cavus, 
with  the  outer  three  toes  in  a  varoid  and  the  inner  two  toes  in  a 
valgoid  position. 

On  examining  one  of  these  feet  it  is  noted  that  it  is  very  short, 
and  that  the  plantar  surface  has  a  deep  groove  dividing  this  aspect 
of  the  foot  into  posterior  and  anterior  portions.  The  posterior 
portion  contains  the  os  calcis,  which,  when  examined  radioscopically, 
presents  a  very  different  appearance  from  and  position  to  that  in  a 
normal  foot. 

Notwithstanding  objections  to  the  contrary,  we  are  of  the  opinion 
that  the  person  walks  upon  the  posterior  aspect  of  the  os  calcis, 
and  we  further  draw  attention  to  the  great  alteration  in  the  lines 
of  pressure  and  stress,  as  compared  with  those  in  a  normal  os  calcis. 
The  anterior  portion  consists  of  the  four  small  toes  bent  under  the 
foot,  so  that  the  dorsal  aspect  is  placed  ventrally,  while  toes  them- 
selves are  much  atrophied.  By  radiographs  it  is  seen  that  the  heads 
of  the  metatarsals  are  approximated  towards  the  os  calcis.     The 


156  SOME  TROPICAL  TRAUMATISMS 

first  toe  is  only  compressed.  The  weight  of  the  body  is  then 
supported  by  the  posterior  aspect  of  the  os  calcis  and  by  the  distal 
end  of  the  first  metatarsal,  and  the  plantar  aspect  of  the  great  toe, 
while  the  dorsal  aspect  of  the  other  toes  may  assist  a  little.  The 
distance  from  the  end  of  the  os  calcis  to  the  big  toe  may  be  only 
three  inches. 

Such  a  compressed,  deformed,  stunted  foot  may  easily  become 
the  site  of  disease.  In  the  first  instance,  there  is  danger  of  gan- 
grene, necrosis  (especially  of  the  phalanges),  and  synovitis  of  the 
knee-joint  during  the  active  bandaging,  while  the  immediate  result 
may  be  total  lameness.  As  a  later  complication,  tuberculosis  of 
the  bones  of  the  deformed  foot  is  liable  to  occur. 

Fortunately  this  horrible  proceeding,  like  many  other  horrible 
fashions,  is  dying  a  natural  death  under  the  influence  of  increased 
feminine  education  and  common  sense  first  produced  among  Euro- 
pean women,  and  by  them  introduced  into  China.  Naturally  no 
cure  can  be  effected  in  a  foot  which  has  become  fully  deformed. 

Heavy  Fruits. — The  fruits  of  the  coconut  (Cocos  nucifera  Linnaeus)  and  of 
the  jak-tree  (Artocarpus  integrifolia  Linnaeus)  are  heavy  and  fairly  hard, 
and  injuries  may  be  caused  by  the  fall  of  one  of  these  fruits  from  the  tree 
on  to  the  head  or  other  part  of  the  body.  When  the  blow  is  received  by  the 
head,  the  symptoms  produced  may  be  those  of  concussion  or  compression, 
or  there  may  be  signs  of  fracture  of  the  vault  or  base  of  the  skull. 

Electrical  Fans. — In  the  more  civilized  tropical  towns  it  is  common  to 
use  small,  movable,  quickly  running  electric  fans  in  order  to  obtain  a  cooling 
breeze.  These  are  brought  into  use  specially  in  the  bedroom  and  dressing- 
room,  but  are  also  frequently  seen  in  the  dining-room,  and  sometimes  in  the 
office.  Being  easily  movable,  they  are  apt  to  have  their  position  slightly 
altered  when  running  at  full  speed,  and  in  doing  this  quite  a  number  of  acci- 
dents have  taken  place.  Sometimes  during  the  condition  between  sleeping 
and  waking,  people,  stretching  out  then  arms  while  still  in  bed,  catch  their 
ringers  in  the  fans.  The  most  common  traumatism  is  for  the  fingers  to  be 
caught  by  the  blades,  and  to  sustain  contused  and  lacerated  wounds,  the 
danger  of  which  is  tetanus,  as  the  blades  of  the  fan  are  generally  thickly 
covered  with  the  dust  brought  by  the  current  of  air. 

Another  and  far  less  serious  but  most  awkward  accident  sometimes  happens 
in  a  lady's  dressing-room.  The  fan  is  placed  on  or  near  the  dressing-table, 
and  is  so  arranged  that  the  back  of  the  fan  is  towards  the  person  at  the  dressing- 
table.  The  current  of  air  passes  from  the  person  towards  the  back  of  the  fan. 
If  the  lady  has  long  hair  and  is  dressing  it,  the  current  of  air  may  carry  it  into 
the  back  of  the  fan  and  between  the  blades,  which,  still  revolving,  causes  the 
hair  to  be  twisted  into  a  tangle.  Usually  the  lady  or  her  attendant  has  suffi- 
cient nerve  to  switch  off  the  fan,  and  no  very  serious  injury  is  done,  but  it  is 
difficult  to  extract  the  hair  from  the  tangle  in  the  fan. 

Powdered  Glass.-  -In  certain  parts  of  the  tropics,  especially  in  the 
East,  powdered  glass  is  used  for  suicidal  and  homicidal  purposes. 
The  injury  caused  is,  of  course,  purely  mechanical,  and  the  more 
finely  it  is  powdered,  the  less  likely  it  is  to  cause  serious  injury, 
owing  to  mucus  surrounding  the  particles.  The  glass  is  administered 
in  food— e.g.,  bread,  spinach,  sweetmeat,  etc.  The  symptoms  are 
those  of  irritant  poisoning — retching,  violent  vomiting,  spasms, 
convulsions,  and  racking  pain.  The  most  evident  post-mortem 
feature  is  acute  gastritis.     The  mucosa  is  covered  with  a  layer  of 


TRAUMATISMS  DUE  TO  PHYSICAL  AGENCIES  157 

thick  mucus,  under  which  it  is  found  to  be  hyperaemic  and  lacerated. 
In  this  mucus  or  on  the  mucosa  the^minute  pieces'of  glass  may  be 
found.  No  other  pathological  signs  need  be  present.  The  treat- 
ment is  to  administer  any  bulky  food  at  hand,  and  then,  if  vomiting 
has  ceased,  to  give  an  emetic,  and  finally  a  laxative. 

Bamboo  Hairs. — Dendrocalamus  strictus  Nees.  We  have  met 
with  a  case  from  Malaya  in  which  the  fine  hairs  shaved  off  the 
bamboo  sheaths  were  administered  in  food  with  the  intent  to  kill. 
They  produced  a  severe  form  of  enteritis  very  like  chronic  dysentery. 
We  are  therefore  in  a  position  to  confirm  Ridley's  earlier  statements 
that  these  hairs  act  as  mechanical  irritants. 


REFERENCES. 

Armstrong  (1801).     Duncan  Anuales.     (1808).  Salzberg  Med.  Chir.  Zeitung, 

i.  143.     (Human  Bite.) 
Baker,   S.   W.   (1891).     Wild  Beasts  and  their  Ways.     London.     (A  most 

fascinating  book.) 
Baldwin,  A.  E.  (1892).     Pacific  Medical  Journal,  xxxv.  32.     (Boars.)     San 

Francisco. 
Dudgeon,     J.     (1874).      Medical    Reports,     Customs    Gazette.      Shanghai. 

No.  6,  12.     (Bear  and  Camel.) 
Ensor,    F.    (1886).     Lancet,    June   19,    p.    1160.     London.     (Shark   Bite  in 

South  Africa.) 
Fairchild,  W.  F.  (1896-97).     Louisville  Medical  Monthly,  iii.  182.     (Boar.) 
Fayrer,    J,    (1869).       Medical    Times   and   Gazette.      (1873).    Clinical   and 

Pathological  Observations  in  India.     London.     (Shark,  Wolf,  and  Jackal 

Bites.) 
Gleeson  (191 1).     Indian  Medical  Gazette,  p.  99.     London.     (Tigers,  Pan- 
thers, and  Bears.) 
Grieve  (1909).     United  States  Naval  Medical  Bulletin,  iii.  132.     Washing- 
ton.    (Bears.) 
Henning  (1810).     Huseland  and  Hemly's  Journal  der  Pratischen  Heilkunde, 

August,  xxxi.  62.     Berlin.     (Man's  Bite.) 
Jeans,  F.  (1908-09).     Annals  of  Tropical  Medicine  and  Parasitology,  ii.  299. 

Liverpool.     (Foot- binding;  radiographs.) 
Kastagir,  A.  G.  (1881).     Indian  Medical  Gazette,  xvi.  105.     (Shark.) 
Maison,  M.  (1906).     Archives  de  Medecine  et  de  Pharmacia  Militaire,  p.  213. 

Paris.     (Camel's  Bite.) 
Matthew,  R.  G.  (1872).     Indian  Medical  Gazette,  vii.  88.     (Leopard.) 
McLeod,  K.  (1866).     Indian  Medical  Gazette,  i.  116.     (Jackal.) 
Mitra,  N.  C.  (1895).     Medical  Reports,  Calcutta,  v.  138.     (Tiger.) 
Morgan,  C.  (1878).     Austral  Practitioner,  Melbourne,  p.  89.     (Shark.) 
Orme  (1899).     British  Medical  Journal.     (Shark's  Bite.) 
Playfair,  L.  (1889).     British  Medical  Journal,  March  2,  p.  489.     London. 

(Distinguished  Men  damaged  by  Wild  Animals.) 
Raspail,  F.  V.  (i860.)     Histoire  Naturelle  de  la  Sante  et  de  la  Maladk  chez 

l'Homme.     Paris.     (A  general  account.) 
Renxer  (1903).     Journal  of  Tropical  Medicine  and  Hygiene,  p.  119.     London. 

(Sword  Fish.) 
Sircar,  M.  L.  (1871).     Calcutta  Journal  of  Medicine,  iv.  302.     (Crocodile.) 
Toussaint,  H.  (1894).     Revue  Generale  de  Clinique  et  de  Therapu-,  viii.  -^>>- 
£*      Paris. 

Umachigi,  V.  S.  (1905).     Lancet,  February  25,  p.  494.     London. 
Wellman,   F.  C.   (1904).     Journal  of  Tropical  Medicine,  p.   124.     London. 

(Leopard's  Bite.) 
Wietzel,  J.  C.  (1776).     De  morsibus  et  puncturis  animalium. 
Yahoub  (1904-05).     Gazette  Medicale  d'Oricnt,  v.  269. 


SECTION   B 
CHEMICAL  CAUSES 

POISONS 

ARROW  POISONS 

POISONS  USED  IN  FISHING,  HUNTING, 

AND  TRADE 
POISONOUS  FOOD 
VENOMOUS  ANIMALS 


159 


POISONS 

I.  Criminal  Poisoning, 
i.  Homicide. 

2.  Suicide. 

3.  Infanticide. 

4.  Abortion. 

5.  Robbery. 

6.  Pseudotherapy. 

7.  Mimicry. 

8.  Aphrodisiac. 

II.  Accidental  Poisoning. 

III.  Stimulant  and  Sedative  Poisoning. 

IV.  Ordeal  Poisoning. 


i$o 


CHAPTER   X 
POISONS 

Preliminary  —  Definition  —  Classification  —  Criminal  poisoning  —  Accidental 
poisoning — Stimulant  and  sedative  poisoning — Poisons  used  in  trial  by 
ordeal — References. 

PRELIMINARY. 

Tin:  chemical  causes  of  tropical  disease  or  the  tropical  intoxica- 
tions are  numerous,  and  it  is  impossible  in  a  book  of  this  size  to  do 
more  than  give  an  account,  in  condensed  form,  of  the  more  common, 
and  to  provide  means,  by  the  references,  whereby  the  reader  may 
extend  his  information  if  he  so  desires. 

In  the  present  work  we  shall  divide  these  chemical  causes  into 
Poisons  and  Venomous  Animals  ;  and  as  we  begin  the  study  of 
these  matters  in  the  present  chapter,  it  is  as  well  to  state  what  we 
mean  by  a  poison. 

DEFINITION. 

A  poison  is  any  chemical  substance  which,  when  introduced  in 
sufficient  quantity  into,  or  brought  in  contact  with,  the  living 
organism,  is  capable  of  producing  a  variation  in  the  structure,  the 
chemical  composition,  or  the  functions,  of  the  whole  or  any  part  of 
that  organism,  which  exceeds  the  limits  of  physiological  variation. 

Such  a  definition  includes  a  large  number  of  substances,  and 
therefore  some  arrangement  is  necessary  in  order  that  they  may  be 
considered  systematically. 

CLASSIFICATION. 

Poisons  have  been  classified  into  mineral,  vegetal,  and  animal, 
or  according  to  their  action  on  the  human  economy;  but  we  have 
departed  from  these  proposals,  and  have  attempted  to  arrange  them 
according  to  the  purposes  for  which  they  are  used,  as  we  consider 
that  this  method  will  be  of  greater  service  to  the  tropical  practitioner. 

With  this  end  in  view,  we  divide  them  into  the  chemical  substances 
which  occur  in — 

I.  Criminal  Poisoning. 
II.  Accidental  Poisoning. 
III.   Stimulant  and  Sedative  Poisoning. 
IV.  Trial  by  Ordeal. 

161  ii 


i62  POISONS 

We  leave  to  future  chapters  the  consideration  of  poisons  used  in 
war,  fishing,  hunting,  and  trade,  as  well  as  poisonous  food  and  the 
effects  of  venomous  animals. 

I.  CRIMINAL  POISONING. 

Criminal  poisoning  has  been  in  existence  from  the  earliest  and 
most  primitive  ages,  and  as  it  requires  a  highly  and  specially  trained 
chemist  with  a  well-equipped  and  up-to-date  laboratory  to  detect 
many  of  the  tropical  vegetal  poisons,  the  reader  will  not  be  :  urprised 
to  note  that  criminal  poisoning  is  more  frequently  met  with  in  the 
tropics  than  in  the  Temperate  Zone. 

It  seems  to  us  that  it  is  more  commonly  met  with  in  the  East  than 
in  Africa,  and  we  are  inclined  to  think  that  the  reason  for  this  is 
that  in  Africa  only  the  fetish-man  knows  how  to  present  virulent 
poisons  in  acceptable  forms  to  his  victims,  whereas  persons  with  an 
elementary  knowledge  of  poisons  are  common  in  the  East. 

The  poisons  of  different  tropical  countries  vary  according  to 
custom  and  tradition,  and  also  according  to  the  plants  which 
happen  to  grow  in  the  vicinity.  It  is  said  that  arsenic  in  the  East 
is  the  cause  of  as  many  criminal  poisonings  as  all  the  organic  poisons 
put  together.  This  may  be  so,  but  we  are  not  certain  that  anyone 
is  qualified  to  make  this  statement,  as  it  came  as  a  great  surprise  to 
us  to  find  that  in  Ceylon  a  number  of  the  poisonings  at  one  time 
attributable  to  arsenic  were  found  by  advanced  chemical  research 
under  an  exceedingly  able  chemist  to  be  due  to  Cerbera  odollam. 

We  are  therefore  of  the  opinion  that  every  tropical  country 
requires  a  well-equipped  toxicological  laboratory,  with  well-trained 
research  chemists,  whose  business,  inter  alia,  should  be  to  make 
themselves  acquainted  with  the  poisons  of  the  land  in  which  they 
are  residing,  with  the  view  to  discovering  tests  whereby  these  poisons 
may  be  detected  and  so  justice  done  in  criminal  cases.  This  is 
important,  for  the  native  soon  learns  that  methods  of  bringing  the 
criminal  to  justice  exist,  and  therefore  becomes  less  inclined  to  use 
this  method  for  the  removal  of  his  enemy. 

The  poisons  used  criminally  against  man  may  be  divided  into 
{a)  Inorganic  Poisons,  (b)  Organic  Poisons. 

Inorganic  Poisons. 

The  most  common  poison  is  arsenic  in  some  form,  and  the  next  is 
per  chloride  of  mercury,  followed  closely  by  the  mineral  acids.  Salts 
of  copper  have  been  used  for  homicidal  purposes,  but  generally 
poisoning  from  this  source  is  accidental,  and  due  to  the  use  of  copper 
cooking  utensils,whilc  the  preparations  of  antimony  are  seldom  used. 

Organic  Poisons. 

These  may  be  derived  from  animal  or  vegetal  sources,  but  the 
latter  are  far  more  en  evidence,  and  are  largely  derived  from  plants 


CRIMINAL  POISONING  163 

belonging  to  the  natural  orders  Apocynaeeae,  Loganiacea:,  Euphorbi- 
aceae,  Liliaceae,  and  Leguminosae. 

It  would  doubtless  be  more  scientific  to  classify  these  poisons  by 
the  natural  orders  to  which  the  poisonous  plants  belong,  but,  follow- 
ing our  original  proposals,  we  divide  them  as  follows: — 

1 .  Poisons  used  for  homicidal  purposes. 

2.  Poisons  used  for  suicidal  purposes. 

3.  Poisons  used  for  purposes  of  infanticide. 

4.  Poisons  used  for  procuring  abortion. 

5.  Poisons  used  with  the  intent  to  rob. 

6.  Poisons  used  with  the  intent  to  cure  disease. 

7.  Poisons  used  with  the  intent  to  simulate  injuries. 

8.  Aphrodisiacs. 

1.  Homicide. 

Animal  and  vegetal  substances  are  used  for  this  purpose,  but  of 
the  former  the  best  known  is  viperine  venom,  which  is  said  to  cause 
gastritis,  gastro-intestinal  haemorrhages,  and  even  death.  It  is 
known  to  Ceylon  natives  that  the  venom  of  Vipera  riissellii  Shaw, 
locally  called  the  tic  polonga,  is  supposed  to  be  poisonous  when 
administered  by  the  mouth,  and  we  were  informed  that  this  was 
usually  given  in  toddy,  an  alcoholic  drink  prepared  from  the  coconut 
and  from  the  Palmyra  palm.  We  once  met  with  a  case  in  which  we 
suspected  the  possibility  of  this  being  used,  but  an  experiment  in 
which  the  recent  venom  administered  orally  by  means  of  toddy  to  a 
monkey  proving  a  complete  failure,  we  were  left  in  doubt  as  to  the 
possibility  of  such  poisoning. 

The  venom  of  the  Colubrkhe  is  harmless  when  taken  by  the  mouth, 
provided  that  there  are  no  cracks  or  abrasions.  Its  virulence  is 
destroyed  by  saliva  and  by  pancreatic  juice. 

Vegetal  substances  are  sufficiently  numerous,  but  unfortunately, 
as  far  as  we  know,  few  are  on  record.  The  table  given  on  p.  164 
is  an  imperfect  list. 

With  reference  to  the  table,  a  few  notes,  arranged  in  alphabetical 
order,  may  with  advantage  be  given: — 

Aconite. — Aconite  (Ranunculaceae)  is  so  poisonous  that  in  India 
it  is  known  as  '  bish  '  or  '  bikh,'  which  means  '  the  poison,'  which 
generally  refers  to  Aconitum  ferox  Wall  (Himalayas),  A.  napellus 
L.  (Himalayas),  A.  luridume  Aorte  (Sikkim),  A.  lycoctonum  L. 
(Kashmir);  whilst  A.  heterophyllum  Wall  and  A.  palmatum  Don  are 
said  to  be  less  poisonous. 

The  root  is  the  principal  source  of  the  poison,  which,  however, 
also  exists  in  the  leaves  and  stem. 

Aconite  is  used  for  homicidal  purposes,  as  a  cattle  poison,  and 
may  at  times  be  taken  accidentally.  The  fatal  dose  is  said  to  be 
30  grains  of  the  root,  and  the  fatal  period  usually  three  to  six 
hours. 

The  symptoms  are  tingling  ui  the  lips,  tongue,  mouth,  and  fauces, 
followed  by  numbness  and  anaesthesia,  burning  pains  in  the  stomach. 


164 


POISONS 


Country. 


Natural  (  rder. 


Genus  and  Species. 


India  RanunculacecB 

and  De  Candolle,  181 S. 

Ceylon. 

Apocynacect 
Lindley,  1836. 


1  LiliacecB 

Linnaeus,  1751. 

Euphorbiacece 

A.  de  Jussieu,  1824. 
Loganiacece 

Auctores. 


A  con  Hum  Tournefort  with  A.  ferox  Wall 
and  A.  napellus  Linnaeus  in  the  Hima- 
layas, A.  luridume  Aorte  in  Sikkim, 
and  A .  lycoctonum  Linnaeus  in  Kashmir. 

Cerbeva  Linnaeus,  1753,  with  C.  odollam 
Gaertner  and  C.  thevetia  Linnaeus. 
Nerium  Linnaeus  has  N.  odorum 
Solander,  1729.  Urechites  is  repre- 
sented by  U.  suberecta  Mucker. 

Gloriosa  Linnaeus  with  species  G.  superba 
Linnaeus. 

Jatropha  Kunth  with  one  species,  /.  cur- 
cas  Linnaeus,  1753. 

Strychnos  Linnaeus  with  S.  mix  vomica 
Linnaeus,  S.  ignatii  Bergmann  S.  colu- 
brina  Linnaeus. 


Dutch 
Indies. 


Leguminostz 

de  Jussieu,  1789. 


Milletia      Wight      and      Arnott 
M.  seriacea  Wight  and  Arnott. 


with 


Pacific         Myrtacecs 
Islands.  R.  Brown,  1 8 1 . t . 

!  ApocynacecB 

Lindley,  1836. 


Barringtonia    Forskal    with    B.    speciosa 

Linnaeus  and  B.  raratonga. 
Cerbera     Linnaeus       with        C.     lactaria 
.    Hamilton. 


Brazil.         Sapindacece 

de  Jussieu,  181 1. 
EuphorbiacecB 

A.  de  Jussieu,  1824. 
Loganiacece 
Auctores. 


Paullinia    Linnaeus     with     P.     pinnata 

Linnaeus. 
Hura  Linnaeus  with  H.  crepitans  Linnaeus. 

Spigelia  Linnaeus  with  S.  anthelmia 
Linnaeus.  Thevetia  Linnaeus  with 
T.  ahovai  Linnaeus. 


British 
Guiana. 


Sapindacece 

de  Jussieu,  181 1. 


Melicocca    Linnaeus,    1763,    with   species 
not  mentioned. 


West 
Africa . 


Solanacece 

Lindley,  1836. 
Iridacecs 

Lindley,  1836. 
Cactacece 

Lindley,  1836. 


Hyoscyamus  Tournefort  with  H.  falezlez 

Cosson. 
Morcea  Linnaeus  with  M.  collina  Wald- 

tulpe. 
The '  Oro  '  of  Sierra  Leone. 


Sou  tli        Iridacecs 
Africa.  Lindley,  1836. 

Zygophyllacecs 
Lindley,  1836. 


Morcea  Linnaeus  with  M.  collina  Wald- 

tulpe. 
Melianthus    Linnaeus     with    M.     major 

Linnaeus  and  other  species. 


and  vomiting,  muscular  and  cardiac  weakness,  and  finally  death 
takes  place  from  failure  of  the  heart  or  respiration. 

Barringtonia  Forster,  1776  (Myrtaceae),  with  the  species B.  speciosa 
Linnaeus  and  B.  raratonga,  is  said  to  be  used  for  criminal  poisoning 
in  Oceania. 


CRIMINAL  POISONING  165 

Cerbera  odollam.- — C.  odollant  Gaertner  (Apocynacea;)  is  a  very 
common  plant  in  Ceylon,  and  is  similar  to  C.  thevetia.  Its  correct 
name  is  probably  C.  manghas  Linmeus,  1753.  Its  chemical  properties 
have  not  yet  been  properly  worked  out,  and  it  is  said  that  it 
probably  contains  the  same  poisonous  principle  as  C.  thevetia — viz., 
thevetin.  Thesymptoms  are  nearly  the  same — i.e.,  gastro-intestinal 
irritation,  followed  by  cardiac  poisoning.  These  symptoms  are  easily 
mistaken  for  arsenical  poisoning.  The  treatment  is  the  same  a^>  for 
irritant  poisoning  in  general. 


Fig.  9. — Cerbera  odollam  Gaertner. 

Cerbera  thevetia.- — C.  thevetia,  the  common  yellow  oleander  of 
India,  is  a  shrub  about  6  to  12  feet  in  height,  with  yellow  bell-shaped 
flowers  and  globular  green  fruit.  It  is  highly  poisonous,  its  action 
being  due  to  a  glucoside,  thevetin,  which  exists  in  the  milky  juice 
pervading  all  parts  of  the  plant.  It  is  supposed  that  three  seeds 
are  sufficient  to  kill  a  man  in  twelve  to  fifteen  hours,  the  symptoms 
being  gastro-intestinal  irritation,  headache,  dizziness,  and  pain  in 
the  throat.  The  pulse  is  very  soft  and  slow — thirty  to  forty  beats 
a  minute,  which  Windsor  says  is  characteristic;  later  it  becomes 
weak,  very  rapid,  and  irregular.  Death  results  from  cardiac  failure. 
The  treatment  is  the  same  as  for  ordinary  irritant  poisoning. 

Gloriosa  Superba.- — G.  superba  (Liliaceae)  is  a  well-known  poison  in 
India  and  Ceylon,  while  in  Burma  it  is  said  to  be  used  for  suicidal 
purposes.     Its  active  principle,  superbine,  is  said  to  be  allied  to,  or 


1 66 


POISONS 


identical  with,  the  scillitine  of  squills,  and  therefore  the  action  of 
G.  superba  is  not  unlike  that  of  squills.  The  symptoms,  which  may 
appear  in  half  an  hour,  are  retching,  violent  vomiting,  spasms,  with 
contortions  of  the  body  and  racking  pains,  with  short  intervals  of 
relief  from  time  to  time.  Death  may  take  place  in  four  hours. 
The  post-mortem  reveals  congestion  of  the  brain  and  membranes, 
with  extravasations  of  blood,  congestion  of  the  lungs,  liver,  and 
kidneys  and  inflammation  of  the  mucous  membrane  of  the  stomach. 

The  treatment  is  that  for  irritant  poisoning  in  general. 

Hyoscyamus  falezlez.- — -The  Tuaregs  are  said  to  use  H.  falezlez  to 
kill  travellers. 


Fig.  10. -—Gloriosa  superba  Linnaeus. 


Jatropha  curcas.-  ] .  curcas  Linnaeus  (Kuphorbiacea;),  the  jura- 
tree  of  India,  has  a  seed  which  is  called  the  '  physic  nut,'  from  which 
the  oil  can  be  expressed  which  is  an  irritant  to  the  skin  and  a  purga- 
tive. 

The  symptoms  of  poisoning  are  vomiting,  purging,  abdominal 
pain,  derangements  of  the  special  senses,  muscular  twitchings,  and 
loss  of  memory.  The  treatment,  after  getting  rid  of  as  much  of 
the  poison  as  possible,  is  lime-juice  and  stimulants. 

Melianthus  (Melianthaceae).- — Various  species  of  Melianthus  are 
said  to  be  very  poisonous  by  Grey,  who  suspects  the  possibility  of 
their  use  by  South  African  Bushmen. 

Melicocca  (Sapindaceas)  occurs  in  British  Guiana,  where  it  is  called 
Kinnup.     In  a  two-year-old  child  it  caused  convulsive  twitching 


CRIMINAL  POISONING 


167 


of  the  hands  and  feet,  fixed  gaze,  vivid  flush  on  skin,  distension  of 
abdomen,  suppression  of  urine,  rise  of  temperature  to  1010  F. 
The  poisoning  was  said  to  resemble  that  produced  by  belladonna. 
Other  species  are  said  to  stupefy  fish  and  also  to  be  used  as  arrow 
poisons. 

We  may  perhaps  mention  here  that  in  this  order  are  many  excellent 
and  edible  fruits;  thus,  Melicocca  bijuga,  a  West  Indian  tree,  is 
cultivated  in  Brazil  because  of  its  agreeable,  slightly  acid  berries, 
but,  on  the  other  hand,  the  leaves  and  branches  of  other  species  are 
poisonous. 


Milldia  seriacea  (Legumi- 
nosae)  is  a  poison  of  the  Dutch 
Indies,  causing  severe  diarrhoea, 
collapse,  and  death. 

Morea  collina. — M.  collina 
(Iridaceae),  the  wild  tulip  of 
South  Africa,  is  said  by  Grey  to 
have  been  used  by  a  Bushwoman 
to  poison  a  number  of  people, 
two  of  whom  died. 

The  symptoms  were  severe 
vomiting  and  a  feeling  of  con- 
striction across  the  chest,  feeble 
and  intermitting  heart,  and  a 
tendency  to  coma  for  hours 
before  death.  The  post-mortem 
showed  no  rigor  and  no  inflam- 
mation of  the  stomach.  The 
heart  musculature  was  flaccid, 
and  the  right  side  full  of  blood. 

Nerium  odorum,  synonym 
N.  indecium  Mill,  1768  (Apo- 
cynaceae),  is  the  white  oleander, 
and  grows  commonly  in  India, 
where     it     is     a     well-known 

poison.      It    is   rarely    used    for    homicidal   purposes,    but   more 
generally  for  suicide,  abortion,  and  accidental  poisoning. 

The  root  is  the  portion  used,  but  all  parts  are  poisonous.  The 
active  principles  are  neriodorin,  a  powerful  cardiac  poison  acting 
something  like  digitalis;  karabin,  a  cardiac  poison,  with  also  a 
strychnine-like  action  on  the  spinal  cord. 

The  symptoms  are  therefore  (1)  those  of  gastric  irritat'on — viz., 
vomiting,  pain  in  the  stomach,  frothing  at  the  mouth  from  saliva- 
tion, but  as  a  rule  without  diarrhoea ;  (2)  cardiac  symptoms,  produc- 
ing at  first  a  slow  pulse,  which  finally  becomes  quick  and  weak — the 
respirations  are  rapid  from  the  first;  (3)  strychnine-like  symptoms 
of  twitching  of  the  muscles,  tetanic  spasms,  with  cramps  and,  at 
times,  lockjaw. 

Towards  the  end  the  patient  becomes  drowsy,  then  insensible, 


Fig.  11. — Nerium  odorum  Solander. 


1 68  POISONS 

and  finally  dies  from  cardiac  failure.  The  post-mortem  reveals 
dilatation  of  the  right  side  of  the  heart,  which  is  full  of  blood,  while 
the  left  side  is  empty,  with  subendocardial  haemorrhage,  congestion 
of  the  liver,  spleen,  kidneys,  and  lungs,  mucosa  of  the  stomach  and 
small  intestine,  while  the  large  intestine  and  brain  are  normal.  The 
patient  must  be  treated  on  the  same  lines  as  for  digitalis  and  strych- 
nine poisoning. 

The  Uro. — The  oro  (a  cactus)  of  Sierra  Leone  is  a  gastro-intestinal 
irritant,  causing  vomiting,  diarrhoea,  collapse,  and  death. 

Paullinia  pinnaia  (Sapindaceae)  is  said  by  Rho  to  be  used  by 
negro  slaves  in  Brazil  to  poison  their  masters,  and  to  depend  upon 
an  alkaloid,  timboin,  for  its  action.  Adverting  to  our  remarks  on 
Melicocca,  we  may  note  that  the  seeds  of  P.  sorbilis  are  the  source 
of  the  '  Guarana  '  bread  of  Brazilian  aborigines,  used  when  travelling 
and  as  a  remedy,  being  said  to  be  a  stomachic,  febrifuge  and  aphro- 
disiac. 

Sablier  crepitans  Linnaeus,  also  named  Hura  crepitans  (Euphorbi- 
aceae),  grows  in  the  Antilles,  and  has  been  imported  into  tropical 
Africa.  Its  fruit  is  purgative,  and  is  believed  to  be  used  frequently 
for  criminal  purposes,  being  said  to  produce  violent  vomiting  and 
purging,  with  tenesmus,  constriction  of  the  throat,  and  syncope. 
Rufz,  however,  has  thrown  doubt  on  the  possibility  of  its  really 
being  the  cause  of  these  criminal  poisonings.  It  is  to  be  noted 
that  the  same  symptoms  are  produced  by  Croton  tiglium  Linnaeus 
(Euphorbiaceae),  which  is  found  in  India,  Cochin  China,  tropical 
America,  and  Africa. 

Spigelia  anthdmia  Linnaeus  (Loganiaceae)  has  the  reputation  of 
being  very  poisonous,  and  has  been  used  criminally  in  tropical 
America,  in  Brazil,  and  the  Antilles,  where  it  is  still  used  as  an 
anthelmintic.  It  is  said  to  produce  somnolence,  convulsions,  and 
death. 

Strychnos.- — Strychnos  (Loganiaceae)  is  a  genus  with  several 
poisonous  species,  among  which  may  be  mentioned  :■ — 

Strychnos  mix  vomica  Linnaeus. 
Strychnos  ignatii  Bergmann. 
Strychnos  colubrina  Linnaeus. 

Poisoning  by  the  alkaloid  strychnine  is  frequently  met  with  in 
India,  but  is  usually  accidental.  The  symptoms  of  strychnine 
poisoning  are  bitter  taste  in  the  mouth,  tetanic  spasms,  opistho- 
tonus, risus  sardonicus,  and  death  from  asphyxia  or  collapse.  There 
are  no  characteristic  post-mortem  appearances,  except  conges- 
tion of  the  brain  and  spinal  cord.  The  treatment  is  to  empty  the 
stomach  by  emetics,  and  to  administer  chloroform  or  chloral 
hydrate,  and,  when  asphyxia  threatens,  to  perform  artificial 
respiration. 

Thevelia  ahovai. — T.  ahovai  (Apocynaceae)  is  allied  to  the  oleanders 
mentioned  above,  and  has  an  alkaloid,  thevetosin.^said  to  cause 
gastric  irritation  and  difficulty  of  breathing. 


CRIMINAL  POISONING  t6g 

Urechite  suberecta  (Apocynaccse)  is  the  Savannah  flower  of 
Jamaica  and  other  West  Indian  Islands,  which  was  so  celebrated  in 
the  days  of  the  '  Obeah  Man,'  and  about  which  so  many  talcs  were 
told.  The  truth  is  that  there  are  two  glucosides,  urechitin  and 
urcchitoson,  of  which  the  former  is  like  digitalis,  and  hence  it  has 
an  accumulative  action  in  small  doses,  which,  if  given  to  a  person 
for  a  long  time,  will  not  cause  any  deterioration  of  health,  but  will 
cause,  eventually,  sudden  death  owing  to  the  action  on  the  heart. 
A  full  lethal  dose,  on  the  other  hand,  will  kill  in  a  few  hours  or  a  day 
or  so. 

2.  Suicide. 

Of  all  the  poisons  used  for  suicidal  purposes,  opium  is  by  far  the 
most  usual,  though  Neriitm  odorum,  Cerbera  odollam,  and  Gloriosa 
superb'a  are  also  at  times  employed,  the  former  especially  by  women 
in  India.  Rarer  poisons  are  Calotrofis  procera,  Cerbera  thevetia, 
aconite,  prussic  acid,  and  veratrine  (meeta  bish).  The  action  of  all 
these  poisons  is  described  either  in  ordinary  works  on  toxicology  or 
has  already  been  mentioned, 

3.  Infanticide. 

Infanticide  exists  in  the  tropics  in  two  forms — the  first  irrespec- 
tive of  sex,  and  said  to  be  due  in  India  (Waddell)  to  the  high-caste 
Hindu  prohibiting  remarriage  of  widows;  and,  secondly,  female 
infanticides,  to  prevent  too  many  daughters  growing  up.  A  few 
of  the  more  commonly  used  drugs  may  be  briefly  mentioned. 

Opium  is  used  in  India  by  smearing  the  mother's  nipples  with  the 
drug.  There  is  little  necessity  here  to  describe  the  action  of  opium. 
All  that  need  be  said  is  to  warn  the  practitioner  that  ayahs  (native 
nurses)  are  apt  to  soothe  a  baby  to  sleep  by  dipping  the  finger  in 
laudanum,  and  giving  it  to  the  baby  to  suck.  Such  treatment  is 
highly  deleterious  to  the  child,  and  the  intensely  contracted  pupils 
should  make  the  practitioner  suspect  its  use  in  an  obscure  case  of 
illness. 

Calotropis  gigantea  Robert  Brown  and  C.  procera  Robert  Brown 
(Asclepiadacese),  called  '  mador  '  in  Hindustani  and  '  erukam '  in 
Tamil,  have  been  used  in  India  for  infanticide  and  abortion,  rarely 
for  suicide,  and  more  rarely  for  homicide.  The  symptoms  are 
vomiting,  profuse  salivation,  severe  tetanic  spasms,  extremely  slow 
and  stertorous  breathing,  and  dilatation  of  the  pupils.  The  active 
principle  is  a  yellow  bitter  resinr  but  there  is  no  alkaloid.  The 
treatment  is  the  same  as  for  irritant  poisoning. 

Tobacco  is  also  used  as  an  infant  poison. 

4.  Abortion. 

Criminal  abortion  is  very  common  in  the  tropics.  In  India  it  ia 
sa'd  to  be  common  among  Hindu  widows,  because  they  are  not 
allowed  to  remarry. 


t  70  POISONS 

The  drugs  commonly  used  are : — 

(a)   Reputed  Emmenagogues. — 

Ncrium  odorum  Solander. 
■     Cerbera  thevetia  Linnams. 

Carica  papaya  Linnaeus  (seeds). 
Daucus  carota  Linnseus  (carrot  seeds). 

(ft)  Purgatives  (Cucurbitacece). — 

Cucumis  trigonus  Roxburgh. 
Momordica  charanta  Linnaeus. 
Momordica  cymbalaria  Fenzl. 

(c)  Irritants. — Several  inorganic  irritants  are  used — arsenic,  lead, 
mercury,  copper,  and  quicklime.  Browning  informs  us  that  copper 
sulphate  has  been  used  of  late  in  Ceylon  for  this  purpose,  as  well  as 
tartar  emetic,  corrosive  sublimate,  large  doses  of  quinine,  and  very 
large  doses  of  Epsom  salts  and  an  aloes  (socotrine)  iron  pill,  in 
which  the  quantity  of  the  aloes  is  very  considerable. 

Plumbago  rosea  Linnaeus. 

Plumbago  zeylanica  Linnaeus. 

Calotropis  procera  R.  Brown. 

Piper  nigrum  Linnaeus  (black  pepper). 

Ananas  Tournciort,  1735  (unripe  pine-apple). 

Moringa  pterygosperma  Gaertner  (bark). 

Lasiosiphon  speciosus  Decaisne. 

(d)  Supposed  Ecbolics.— 

Bambusa  sp.?  juice  of  bamboo-leaves.     The  fruit  is 

used. 
Randia  dumetorum  Linnaeus. 
Cuscuta  reflexa  Roxburgh.     (A  decoction  is  used  which 

also  acts  as  an  irritant.) 
Seeds  of  Celastrus  paniculatus  Wight. 
Seeds  of  Anethum  graveolens  Linnaeus. 

Plumbago  zeylanica  Linnaeus  and  P.  rosea  Linnaeus  are  evergreen 
shrubs  about  2  to  5  feet  high,  in  the  root  of  which  there  is  an  active 
principle,  plumbagin,  which  acts  externally  as  a  vesicant,  and 
internally  as  an  irritant  and  narcotic.  It  is  used  as  a  paste,  or 
spread  on  wool  on  an  abortion  stick. 

The  abortifacients  which  were  commonly  used  in  Ceylon  were 
Gloriosa  superb  a  L.,  violent  purgatives  (including  large  doses  of 
magnesium  sulphate),  and  the  twigs  of  the  castor-oil  plant,  the 
last  named  being  a  mechanical  irritant. 

5.  Stupefying  with  Intent  to  Rob. 

Two  drugs  are  much  used  in  India  and  Ceylon  for  the  purpose 
of  stupefying  with  intent  to  rob — viz.,  Datu  a  fastuo.a  Linnaeus 
and  Cannabis  sativa  Linnaeus. 


CRIMINAL  POISONING 


171 


Datura  fastuosa  (Solanaceae). — Poisoning  by  datura  is  common 

m  India,  having  been  used  by  the  Thugs.  The  seeds  are  usually 
mixed  with  food  or  drink,  and  the  symptoms,  which  develop 
rapidly,  depend  upon  the  dose,  being  generally  those  of  a  cerebral 
poison.  First  there  is  delirium,  and  later  coma,  but  in  both 
conditions  the  pupils  are  widely  dilated.     The  delirium  is  peculiar; 


Fig.   12. — Datura  fastuosa  Linn;eus. 

for  example,  the  people  affected  may  be  found  searching  their 
bedding  most  vigorously  for  some  lost  article.  When  death  occurs, 
t  is  due  to  cardiac  failure.  The  fatal  dose  is  not  actually  known, 
but  may  be  about  10  to  15  grains  of  the  seeds.  Waddcll  puts  the 
mortality  at  about  i8£  per  cent.  The  post-mortem  charac  er- 
istics are  wide  dilatation  of  the  pupils,  congestion  of  the  brain, 
meninges,  and  the  lungs  and  other  viscera. 

6.  Poisons  used  with  Intent  to  Cure  Disease. 
Decoctions  of  bark  Tfianthema  pentandra  Linnaeus  are  used  in  the 
Sudan  for  the  purpose  of  curing  gonorrhoea ;  unfortunately,  sometimes 
this  remedy  is  worse  than  the  disease,  causing  enteritis  and  death. 

7.  Poisons   used  to  Simulate  1 11  Junes. 
Plumbago  rosea  Linnaeus  (Plumbaginaceae)  and  Anacardium  occi- 
dentale  Linnaeus  (Anacardiaceae)  are  used  to  simulate  bruises  and 
other  injuries  in  order  to  get  innocent  people  into  trouble. 

8.  Aphrodisiacs. 
The  aphrodisiacs,  which  are  much  in  demand  by  tropical  natives, 
may  be  divided  into  those  of  animal  and  those  of  vegetal  origin. 


172  POISONS 

Those  of  animal  origin  are  Meloe  vesicatorius  (Cantharis  vesi- 
catoria,  Lytta  vesicatoria,  Musca  hispaniola  are  synonyms),  which 
is  well  known,  and  Mylabris  cichorii,  a  beetle  called  Pan-mao  by 
the  Chinese  and  containing  i  per  cent,  of  cantharidine.  In  China 
and  the  Far  East  generally  the  testicles,  spinal  cords,  etc.,  of 
animals,  pounded  and  mixed  with  rice  water,  are  eaten  as 
aphrodisiacs. 

Those  of  vegetal  origin  are  numerous,  and  include  Panax  quinque- 
folium  Linnaeus  (Araliaceae),  the  powdered  root  of  which,  called 
by  the  Chinese  Jeun-Chenn,  is  used;  Populus  spinosa  (Amentaceae), 
the  Sen-iang-hoa  of  the  Chinese,  of  which  the  buds  are  used; 
Psorala  corylifolia  Roxburgh  (Leguminosae),  the  fruit  of  which  is 
used  by  the  Chinese  and  Annamese;  Psorala  glandulosa  Linnaeus 
in  Chili;  Amomum  zingiber,  the  ginger  (Zingiberaceae) ;  Caryophyllus 
aromaticus  Linnaeus  (Cantbosa  aromatica  Miquel — Myrtaceae); 
Pausinystalia  yohimba  Karl  Schumann,  the  celebrated  yohimbehe 
or  yumbehoa  bark,  from  which  the  alkaloid  yohimbine  hydro- 
chloride, used  in  i  per  cent,  solution,  dose  5  to  15  minims,  or 
tablets  with  ,'..  grain  taken  one  three  times  a  day,  may  be  men- 
tioned. The  last  is  sometimes  named  Corynanthe  yohimbi,  but 
this  is  merely  a  synonym.  P.  trilh  sii  Pierre  is  also  considered 
to  contain  yohimbine.  These  trees  grow  in  the  Kameruns  and 
the  Congo. 

Cordiceps  sinensis  is  the  mushroom  called  Tch'ovtngtis'ao  by  the 
Chinese,  and  is  used  as  an  aphrodisiac. 


II.  ACCIDENTAL  POISONING. 

Accidental  poisoning  happens  fairly  frequently;  therefore  a  few 
examples  may  be  given. 

Certain  common  articles  of  food  are  poisonous  until  properly 
prepared;  e.g.,  tapioca  is  the  starch  obtained  from  the  root  of 
Manihot  utilissima  Pohl  1821  (Jafropha  manihot  Linnaeus — Euphor- 
biaceae),  commonly  called  the  cassava,  of  which  there  are  two 
varieties,  the  sweet  and  the  bitter.  The  latter  contains  hydro- 
cyanic acid  in  its  milky  juice,  and  is,  therefore,  poisonous  until  it 
is  roasted,  when  the  volatile  acid  is  driven  off,  and  the  bitter 
cassava  can  then  be  used  for  food  after  squeezing  out  the  juice 
and  cooking  the  root.  Waddell  reports  two  cases  of  death  from 
accidental  poisoning  by  this  root  in  1898  in  Madras. 

Ariscema. — Vogt  has  reported  the  accidental  poisoning  of  a 
Chinese  woman  by  an  unknown  species  of  the  genus  Arisamia 
Martius,  belonging  to  the  family  Araccce  Schott,  1832.  She  ate 
a  small  piece  of  the  tuber,  and  in  ten  minutes  became  stuporous, 
and  despite  prompt  and  vigorous  treatment,  which  included  the 
washing  out  of  the  stomach,  her  abdomen  became  distended  and 
she  suffered  from  paralysis  of  the  limbs,  but  eventually  recovered. 

The  members  of  the  Araceae  are  well  known  to  be  poisonous, 
and   Diffenbachia  sequina,   the  dumb  cane,   which  grows  in  the 


ACCIDENTAL  POISONING  173 

West  Indies  and  South  America,  will  cause  a  painful  swelling  of 
the  tongue  if  chewed. 

The  emanations  from  the  flowers  of  Arum  dracunculus  cause 
dizziness,  headache,  and  vomiting  in  some  people. 

Blighia.— -The  succulent  aril  of  the  akee  tree,  which  belongs  to 
the  genus  Blighia  Koenig,  synonym  Cupania  Plumer  (Sapindaceae), 
and  called  B.  sapida,  is  used  as  an  article  of  food  in  the  West  Indies. 

It  is,  however,  known  that  if  eat'  n  in  an  unsound  condition  it 
is  poisonous,  and  recently  Scott  has  shown  that  this  is  the  cause 
of  the  vomiting  sickness  of  Jamaica,  as  will  be  detailed  in 
Chapter  LXXIL,  p.  1695  of  this  book. 

Capsicums  (C.  annum  Linnaeus,  1775— Solanaceae),  it'  taken  in 
large  quantities,  may  cause  burning  in  the  mouth  and  throat, 
vomiting,  colic,  diarrhoea,  and  even  death.  C.  frutescens  Linnaeus, 
1753,  may  also  be  mentioned. 

Cinn  wtonum  zeylanicum  Nees.  -Lewin  states  that  cinnamon-bark 
may  be  poisonous,  while  nutmegs  (Myristica  fragrans  Houtt)  are 
well  known  to  be  poisonous  if  taken  in  large  doses. 

Calotropis  gigantea  R.  Brown  (Asclepiadacese)  has  been  known 
to  cause  fatal  effects  by  administration  non-maliciously  of  two 
dessertspoonfuls  of  its  milk  in  a  quantity  of  cow's  milk.  This 
plant  is  variously  named  '  mudar  '  in  Bengal,  '  yercumby  '  by 
Tamils,  and  '  warra  '  by  the  Sinhalese. 

Chailletia  toxicaria  Don  (Chailletiaceae ;  native  name  '  magberi '  or 
'  manuch  '),  the  powdered  fruit  of  which  is  used  for  killing  rats, 
has  been  described  by  Renner  in  Sierra  Leone  as  the  cause,  of 
'poisoning  in  a  Mendi  carrier. 

The  symptoms  were  mainly  vomiting,  diarrhoea,  trembling, 
general  weakness,  and  inability  to  walk  because  the  legs  were 
paralyzed,  the  tendon  reflexes  having  disappeared.  Hyperesthesia 
was  present  over  the  inner  side  of  the  thighs  and  legs,  and  pressure 
on  the  calf  muscle  gave  severe  pain.  The  bladder,  rectum,  and 
pupils  were  normal.     The  man  recovered  in  about  two  months. 

Renner  remarks  that  this  case  is  probably  the  clue  to  attacks 
of  sudden  paralysis  of  the  lower  limbs  in  young  persons  (twenty 
to  forty  years)  of  both  sexes  in  Sierra  Leone.  When  death  ensues, 
it  is  from  paralysis  of  the  muscles  of  respiration. 

Dioscorea. — Guerreras  and  de  la  Paz  say  that  this  genus,  as 
well  as  Jatropha,  Anamista,  Strychnos,  and  Datura  are  the  cause  "I 
poisoning  in  the  Philippine  Islands. 

Fungi. — -The  presence  of  poisonous  as  well  as  edible  fungi  should 
be  remembered  in  the  tropics;  although  there  is  no  literature 
known  to  us  on  the  subject,  still  we  have  had  the  matter  forcibly 
brought  to  our  notice. 

The  fruit  of  Hippomanc  mancinclla  Linnaeus  (Euphorbiaceae),  the 
manchineel  tree  of  the  Grenadine  Islands,  which  has  a  delicious 
fragrance,  is  said  to  have  been  the  cause  of  many  sailors  meeting 
their  deaths,  for  it  looks  like  an  apple.  The  active  principle  is 
not  known. 


1 74  POISONS 

The  symptoms  are  severe  pain  in  the  mouth  and  stomach, 
followed  by  collapse.  The  lips  and  tongue  become  swollen  and 
blistered,  the  abdomen  tender,  the  pupils  widely  dilated,  while 
bullae  appear  on  the  skin. 

The  treatment  consists  of  stimulants  and  intramuscular  injections 
of  ether,  with  mouth-washes.  Internally  opium,  bromides,  chlorate 
of  potash,  bicarbonate  of  soda,  or  bismuth,  made  into  an  emulsion, 
may  be  given. 

Fontainea  pancheri,  Heckel,  1870  (Euphorbiaceae),  is  a  tree 
growing  in  New  Caledonia,  the  ingestion  of  the  fruit  of  which 
causes  symptoms  analogous  to  those  produced  by  Hippomane 
mancinella, 

Illicium.- — Guerreras  and  de  la  Paz  have  also  drawn  atten- 
tion to  poisoning  from  a  decoction  of  sanki,  which  is  the  fruit 
Illicium  religiosum  v.  Siebold,  which  belongs  to  the  genus  Illicium 
Linnaeus,  of  the  family  Magnoliaece  De  Candolle,  1818.  Montel 
in  Indo-China  has  also  found  it  to  be  poisonous.  The  symptoms 
appear  to  resemble  cholera,  but  diagnosis  has  to  be  made  from 
strychnine-poisoning,  tetanus,  and  cerebro-spinal  meningitis.  The 
symptoms  were  vomiting,  diarrhoea,  thirst,  unconsciousness, 
convulsions,  cramps,  profuse  sweating,  oliguria  and  anuria,  small 
rapid  pulse,  cold  extremities,  paresis  of  the  lower  limbs,  and  ex- 
haustion. The  head  is  retracted,  the  eyeballs  bulge,  and  the  face 
becomes  cyanotic  when  the  respiration  stops.  In  China  and  Japan 
it  and  its  related  species  /.  anisatum,  the  star  anise,  which  is 
harmless,  are  called  badiane. 

The  seeds  of  Ricinus  communis  Linnaeus  (Euphorbiaceae),  the 
castor-oil  plant,  are  poisonous,  causing  burning  in  the  throat  and 
abdomen,  vomiting,  purging  (may  be  absent),  and  collapse.  The 
fatal  dose  appears  to  be  three  seeds,  and  to  kill  in  about  forty-six 
hours.  Post-mortem  the  principal  feature  is  gastro-intestinal 
inflammation. 

The  treatment  is  emetics,  stimulants,  and  hypodermics  of 
morphia. 

III.  STIMULANT  AND  SEDATIVE  POISONING. 

Many  drugs  are  employed  all  over  the  world  to  stimulate  or 
to  deaden  the  nervous  system.  These  stimulants  and  sedatives 
have  been  used  by  man  from  time  immemorable  to  whip  up  a 
ilagging  nervous  system,  or  to  deaden  the  effects  of  mental  01 
bodily  suffering. 

Used  judiciously  and  in  a  proper  manner  there  can  be  no  doubt 
that  they  alleviate  human  suffering,  but  if  used  injudiciously  or 
immoderately,  and  especially  if  they  are  constantly  taken,  they 
become  '  habit  poisons,'  and  as  such  affect  the  cells  of  the  body 
injuriously,  and  by  so  doing  some  of  them  become  true  '  racial 
poisons,'  and  as  such  have  been  mentioned  in  the  section  on 
Eugenics  (see  p.  118). 


STIMULANT  AND  SEDATIVE  POISONING  175 

It  is  not  our  intent  to  write,  except  in  the  briefest  manner,  upon 
these;  poisons,  as  their  effects  arc  fully  considered  in  special  works 
and  are  also  contained  in  all  the  ordinary  textbooks  dealing  with 
general  medicine.  Notwithstanding  this,  we  feel  that  a  few 
remarks  dealing  with  these  drugs  in  the  tropics  are  necessary. 

Alcohol. — We  have  already  referred  to  our  belief  that  this  is 
a  personal  and  a  racial  poison,  and  we  would  warn  our  readers 
not  to  be  misled  by  statistics  on  this  point,  and  if  they  wish  further 
information  to  refer  to  Adami  on  Karl  Pearson  {vide  references). 
Alcoholism  is  unfortunately  on  the  increase  among  tropical  natives, 
and  is  doing  great  harm  in  the  form  of  indigenous  stimulants  such 
as  arrack,  which  is  almost  directly  the  cause  of  a  large  percentage 
of  the  violent  crime  in  Ceylon,  as  was  shown  by  the  fact  that  the 
accident  wards  of  the  hospitals  were  nearly  empty  in  the  pro- 
scribed regions  during  the  period  of  a  social  prohibition. 

More  dangerous,  in  our  opinion,  are  the  imported  cheaper 
alcoholic  drinks,  such  as  the  cheap  whiskies,  gins,  and  rums,  which, 
being  cheap,  are  drunk  in  quantity  and  greatly  deteriorate  native 
races.  These  bad  effects  are  not  due  to  fusel  oil,  which  is  not 
present  in  these  cheap  forms  of  spirit,  which  in  many  ways  are 
the  purest  form  of  alcohol  to  be  obtained,  and  hence  their  effect 
is  truly  due  to  alcohol  and  to  alcohol  only,  and  their  real  danger 
is  simply  because  they  are  cheap.  Methyl  alcohol  is  a  direct 
poison  to  man,  a  fact  but  little  understood  at  the  present  time. 

Opium  is  eaten  in  Persia,  India,  and  Africa,  and  smoked  in 
Malaya,  Indo-China,  and  China,  but  for  the  latter  process  it  has 
to  be  specially  prepared.  On  the  Eastern  mind  opium  is  said  to 
have  two  possible  effects:  either  it  produces  a  sense  of  absolute 
blank,  or  it  produces  fancy  dreams  and  visions.  The  effects  of 
chronic  morphinism  are  loss  of  appetite,  emaciation,  and  exhaus- 
tion, and  hence  inability  to  think  or  work. 

It  is,  however,  probable  that  the  effects  of  opium  are  not  as 
had  as  those  of  alcohol,  and,  used  in  moderation,  it  may  not  he 
more  harmful  than  the  use  of  tobacco. 

Cocaine  has  been  used  much  of  late  in  India  as  an  intoxicant 
or  stimulant,  to  counteract  the  effects,  or  in  lieu,  of  opium,  owing 
to  the  restrictions  on  the  sale  of  opium.  Unfortunately,  children 
have  begun  habitually  to  use  the  drug.  The  cocaine  is  chewed 
with  betel  and  chunam  (slaked  lime),  and  produces  at  first  loss 
of  sensation  in  the  tongue  and  lips,  followed  by  dryness  of  the 
mouth  and  fauces.  The  temperature  does  not  rise,  but  the  pulse 
becomes  full  and  quick,  and  at  this  stage  the  inebriate  likes  to 
be  left  alone,  and  firmly  closes  his  lips  lest  the  saliva  should  How 
out.  His  ears  become  hot  and  red,  his  cheeks  pale,  and  the  tip 
of  his  nose  cold.  Perspiration  breaks  out,  and  the  maximum 
amount  of  the  so-called  hilarity  or  exaltation,  due  to  overstimula- 
tion of  the  nervous  system,  now  appears,  but  is  speedily  followed 
by  depression,  which  induces  the  victim  to  take  another  dose. 
The  teeth  and  tongue    of   the  confirmed   cocaine-eater  turn  jet- 


i7' 


POISONS 


black,  probably  due  to  some  chemical  change  produced  by  the 
action  of  lime  and  saliva  on  cocaine.  Pernicious  symptoms  in  the 
form  of  emaciation  accompanied  by  insomnia,  digestive  disturbance, 
diarrhoea,  deafness,  diminution  of  urine,  delusions  and  hallucina- 
tions, and  even  at  times  acute  mania,  may  appear. 

Indian  hemp  (Cannabis  sativa)  is  used  in  India,  Arabia,  Persia, 
and  elsewhere  as  a  narcotic.  It  must  be  remembered  that  C.  sativa 
grown  in  India  has  quite  different  properties  from  the  same  plant 
grown  in  Europe.  In  India  there  are  four  varieties  sold:  bhang, 
consisting  of  the  dried  leaves  and  stalks  reduced  to  a  powder; 
ganja,  the  flowering  tops;  charas,  the  resin  from  the  leaves;  and 
majun,  a  sweetmeat  prepared  with  hemp.  In  Central  Asia  the 
resin  is  called  haschisch. 

Its  action  on  man  is  first  to  produce  a  pleasurable  excitement 
and  later  narcotism.  In  moderate  doses  it  temporarily  increases 
the  feeling  of  strength  and  power.  As  an  intoxicant  it  is  much 
used,  being  eaten  or  smoked,  and  is  said  to  be  one  potent  cause 
of  insanity  in  India.  Waddell  says  that  about  38-4  per  cent,  of 
Bengal  lunacy  can  be  traced  to  this  source.  It  is  asserted  to  be 
one  of  the  causes  of  the  strange  phenomenon  called  '  running 
amok,'  but  this  will  be  dealt  with  in  detail  later  on,  under  diseases 
of  the  nervous  system. 

Kawa  is  an  intoxicating  drink  prepared  from  the  root  of 
Piper  methysticum  Forster  (Piperaceae),  which  grows  throughout 
Polynesia. 

According  to  Lewin,  kawa  contains  starch,  flour,  two  inactive 
substances — kawain  and  yangonin — and  2  per  cent,  of  resin,  which 
is  believed  to  be  the  active  principle.  But  this  resin,  by  treatment 
with  ether,  can  be  resolved  into  two  separate  substances,  one  of 
which  has  a  weak,  and  the  other  a  strong  action  on  man.  The 
drink  causes  a  feeling  of  bien-etre,  but  too  much  has  an  evil  effect, 
with  symptoms  of  inco-ordination  and  headache,  and  a  desire  for 
sleep,  and  may  induce  liver  disease,  dermatitis,  and  general  debility. 
Taken  in  moderation  it  is  said  to  be  harmless,  and  also  to  be  a 
cure  for  gonorrhoea,  and,  as  such,  was  introduced  into  Europe. 

Peyotll  (pellote)  is  a  narcotic  used  in  Mexico,  and  derived  from 
the  cactus,  Anhaloniiim  lewinii  Henn.  It  causes  sleep  with 
hallucinations. 

Coriaria    species— -C.    ruscifolia    Linnaeus,    the    poison-foot    of 

New  Zealand,  and  C.  myrtifolia  Linmeus  (a  native  of  Europe) — 

considered  to  be  intoxicant  or  poisonous,   according  to  the 

The  symptoms  are  coma,  convulsions,  and  dilated  pupils. 

From  C.   ruscifolia  the   Maoris   are   said  to  prepare  a  wine   and 

jelly. 

Pituri  (Duboisia  hopwoodi  F.  Mueller- — Solanacea;)  is  a  shrub 
growing  in  Australia  and  New  Caledonia.  In  the  former  it  is 
found  in  the  neighbourhood  of  Carlo  or  Mungerebar  on  the  Upper 
Mulligan,  and  from  this  in  scattered  patches  eastwards.  At  Carlo 
live  the  Ulaolinga  tribes,   from  whom  the  other  tribes  purchase 


STIMULANT  AND  SEDATIVE  POISONING  177 

the  pituri  by  barter  with  spears,  boomerangs,  etc.  About  the 
beginning  of  March  the  pituri  leaf  is  gathered  and  is  sold  in  the 
form  of  half-green,  half-yellow  tea  mixed  with  plenty  of  chips. 
The  preparation  is  complex :  it  is  first  roasted  in  ashes,  then  wetted 
with  water,  then  teased  with  the  fingers,  and  all  larger  pieces 
removed.  Then  leaves  of  a  species  of  wattle  or  gigeon  are  heated 
over  a  fire  and  finally  burnt,  the  ashes  being  retained  and  mixed 
with  the  moist  pituri  on  a  '  pituri  plate  ' — i.e.,  a  smooth  surface— 
and  finally  manipulated  by  the  fingers  into  small  rolls,  2\  inches 
long  by  -i*-  inch  thick.  These  rolls  are  chewed  by  the  natives,  and 
are  in  great  demand  as  a  narcotic.  Reserve  rolls  are  carried  at 
the  top  of  the  ear.  The  Australian  native  names  are:  '  Maja  ' 
(Walookera),  '  ne-em-pa  '  (Yaroinga),  '  un-da-kor-a  '  (Undekere- 
bina),  '  pi-tu-ri '  (Ul-aolinga),  '  ti-rum-bol-a  '  (Karanga),  '  ta-rem- 
b6-la  '  (Pitta-Pitta),  '  moda  '  (Kalkadoon).  The  alkaloid  piturine 
is  identical  with  hyoscyamine. 

Betel. — The  chewing  of  betel  is  an  extremely  common  practice 
in  the  East,  where  the  leaves  of  Chavica  beile  (piper  betel)  are 
chewed  with  slices  of  the  nut  of  Areca  oberacca  (Pinang  or  areca- 
nut  palm)  and  mixed  with  lime.  Betel  stimulates  the  salivary 
glands,  and,  it  is  said,  those  of  the  digestive  organs.  It  diminishes 
the  perspiration,  and  should  be  spat  out  and  should  not  be  swal- 
lowed. The  irritation  may  be  the  cause  of  the  commonest  cancer 
of  old  people  in  these  parts.  In  the  young  it  may  possibly  be 
the  cause  of  heart  and  nerve  diseases. 

Kola.- — The  kola  nut  so  much  used  as  a  stimulant  by  the  African 
native  is  the  produce  of  several  species  of  the  genus  Sterculia 
Linnaeus,  of  which  the  principal  are  5/.  tomentosa  Thunberg  and 
St.  acuminata  Beaver,  while  St.  nitida  Vent,  St.  ballayi,  St.  verti- 
cellata  Thorne,  and  St.  sphcerocarpa  may  also  be  noted.  This  nut 
has  been  known  since  the  days  of  Leo  Africanus  in  1556,  when  it 
was  known  in  the  Sudan  as  '  goro.' 

It  is  supposed  to  be  a  nervous  system  and  cardiac  stimulant, 
it  raises  the  blood-pressure  and  increases  muscular  power,  and 
certainly  with  kola  nut  and  water  a  Haussa  can  travel  far  and 
work  hard,  as  we  know  personally. 

Analyses  have  been  made  and  a  glucoside,  '  kolamin,'  has  been 
obtained  by  Hilger  and  Knebel. 

Guarana. — This  substance,  which  is  made  into  oblong  or  round 
cakes,  is  sold  in  Brazil  as  guarana  bread,  being  considered  an 
indispensable  requisite  for  travellers.  It  is  made  from  the  seeds 
of  Paullinia  sorbilis  Martins  (Sapindaceas),  which  are  pounded 
and  sweetened.  It  is  said  to  contain  a  white  crystalline  substance 
which  Theodore  Martius  called  '  guaranene.'  The  Brazilians 
consider  guarana  to  be  a  stomachic,  a  febrifuge,  and  an  aphrodisiac. 

Mate.— Paraguay  tea  is  called  '  mate  '  from  the  cup  out  of  which 
it  is  drunk,  or  better  '  yerba,'  meaning  herb  or  plant.  St.  Hilaire 
was  the  first  to  find  and  name  the  Ilex  paraguariensis,  which 
Lambert  in  1824  changed  to  Paraguay ensis,  and  this  is  accepted 


178  POISONS 

because  St.  Hilaire  cancelled  his  original  name.  It  is  prepared 
by  slightly  scorching  the  leaves,  which  are  then  broken  down  and 
subjected  to  a  strong  pressure.  A  handful  of  this  pressed  foliage 
is  infused  in  a  small  spouted  vessel  called  a  '  mate.'  It  is  then 
sucked  hot  through  the  spout  or  bombilla,  which  is  perforated  on 
its  lower  side  with  small  holes,  which,  while  allowing  the  escape 
of  the  liquid,  prevent  the  pieces  of  leaf  following.  It  is  drunk 
freshly  infused,  and  is  said  to  be  an  aperient  and  diuretic,  and  to 
become  a  habit  with  those  who  drink  it. 

Mate  is  much  used  in  Paraguay,  Uruguay,  the  Argentine,  and 
Southern  Brazil,  but  in  the  last-named  Ilex  gongonha  Martius,  and 
Ilex  thecezans  Martius  are  employed. 

Coffee. — The  deleterious  effects  of  excessive  tea-drinking  are 
well  known  and  need  not  be  repeated,  but  it  may  perhaps  be  as 
well  to  invite  attention  to  the  excessive  amount  of  Turkish  coffee 
which  is  drunk  in  the  Middle  East. 

Other  Poisons.-—  In  Malacca  the  leaves  of  Mitragyna  speciosa 
Korth  (Rubiacese)  are  said  to  be  used  in  place  of  opium.  From 
the  leaves  of  Bassia  latifolia  Roxburgh  and  B.  longifolia  Linnaeus 
(Sapotaceae)  intoxicating  drinks  are  made.  Hyoscyamus  muticus  is 
used  as  an  intoxicant  by  the  Baluches,  and  makes  them  dance  like 
lunatics. 

The  juice  of  the  fruit  of  Anacardium  occidentale  (Anacardiaceae) 
is  used  after  distillation  in  Goa  as  a  drink. 


IV.  POISONS  USED  IN  TRIAL  BY  ORDEAL. 

POISONS  D'EPREUVE  (FRENCH). 

Curious  customs  exist  in  savage  lands  of  trial  by  ordeal,  in 
which  the  patient  is  given  a  drug  and  then  ordered  to  perform 
some  act.  Waddell  records  the  history  of  an  old  Hindu  woman 
who  was  supposed  to  be  a  witch.  She  was  tried  by  ordeal,  being 
given  a  poisonous  drug  (datura)  in  treacle,  as  it  is  a  native  belief 
that  a  witch  can  withstand  poison.  The  result  of  the  ordeal  was 
that'  the  poor  woman  died. 

In  Africa  the  greater  part  of  these  poisons  belong  to  the 
Loganiaceae,  Apocynaceae,  Leguminosae,  and  Solanaceae,  but  the 
plant  employed  varies  in  the  different  regions,  and  many  are  still 
undetermined — e.g.,  M'Faug  may  be  a  strophanthus,  while 
M'Boundou  is  undetermined. 

Rho  gives  an  account  of  trial  in  West  Africa  by  '  imbundi,'  the 
sliced  roof  bark  of  Strychnos  icaja  (Baillon),  which  is  said  to  con- 
tain strychnine.  The  accused,  after  drinking  a  concoction  of  the 
root,  is  made  to  jump  over  a  stick,  and  is  pronounced  guilty  unless 
he  is  able  to  do  this,  or  to  pass  urine  on  to  a  banana-leaf,  both 
of  which  feats  are  usually  impossible. 

Christison  mentions  the  Calabar  bean  of  West  Africa,  Physostigma 
venenosum  Balfour  (Leguminosae),  as  being  used  in  trial  by  ordeal, 


REFERENCES  179 

the  belief  being  that  the  innocent  vomit  and  are  safe,  while  the 
guilty  retain  the  poison  and  die.  Its  antidote  is  atropine,  ad- 
ministered hypodermically. 

ErythrophlcBum  judiciale  Procter;  Tanghinia  venenifera  Poiret. 
(which  contains  a  toxic  base  with  an  action  like  digitalin),  and 
Menabca  venenata  Baillon,  are  used  in  Madagascar,  and  Adenium 
soma!  use  Poiret  in  Somaliland,  for  purposes  of  trial  by  ordeal. 


REFERENCES. 

For  a  description  of  the  families  and  their  species,  see  Engler  and  Prantl, 
'Die  Natiirlichen  Pflanzenfamilien,'  Leipzig — Apocynaceae,  iv.  2,  109; 
Loganiaceae,  iv.  2,  19;  Euphorbiacese,  iii.  5,  1;  Liliaceae,  i.  5,  10;  Legu- 
minosae,  ii.  1,  153.     See  also  Bentley  and  Trimen,  '  Medicinal  Plants.' 

For  the  nomenclature  see  Hooker  and  Jackson's  '  Index  Kewensis.' 

Bancroft,   J.   (1 859-1 872).     Pituri  Poison  in  Transactions  of  Philosophical 

Society,  Queensland  (42nd  article) . 
Bose  (1902).     Indian  Medical  Gazette  (Cocaine  Habit). 
Caddy  (1S95).     British  Medical  Journal,  i.  136  (Hippomane  mancinella). 
Cleland  (1914).     Australasian  Med.  Gazette,  June. 
Dymock,  Warden  and  Hooper  (1890).     Pharmacographia  Indica.     3  vol  . 

Calcutta.     (A  standard  work.) 
Fluckeger  and  Hanbury  (1879).     Pharmacographia.     London. 
Grall  et  Clarac  (1911).     Pathologie  Exotique.     Vol.  v.,  Empoisonnements. 

Paris. 
Grey  (1874).     British  Medical  Journal,  168  (Bushmen  Poisons). 
Heckel  (1870).     These  (Montpellier) . 
Kermorgant    (1909).     Bulletin  de   la   Societe  de   Pathologie   Exotique,    ii. 

330-340  (valuable  paper  on  Alcoholism).     Paris. 
Kobert  (1906).     Lehrbuch  der  Intoxikationen,  2  Auff. 
Lindsay  (1903).    Journal  of  Tropical  Medicine  and  Hygiene,  October  1,  303 

(Yerba-Mate.  with  illustration  of  apparatus). 
Liversedge,  A.  (18S1).     The  Alkaloid  from  Pituri.     Journal  of  Royal  Society, 

New  South  Wales,  for  1880,  123. 
Malone,  A.  (1904).     Botanique  Pharmaceutique.     2  vols.     Paris.     (A  most 

valuable  reference  book.) 
M.vno  (1842).     London  Journal  of  Botany,  i.  2nd  series,  30.     London. 
Ondaatjie,  W.  C.  (1865-66).     Journal  of  Ceylon  Branch  of  the  Royal  Asiatic 

Society,  157  (Calotropis  gigantea).     Colombo. 
Perrot  and  Vogt  (1913).     Poisons  de  Fleches  et  Poisons  d'Epreuve.     (The 

only  book  that  we  know  of  which  deals  with  Poisons  d'Epreuve). 
Renner  (1904).  British  Medical  Journal,  i.  1314  (Chailletia  toxicaria). 
Rho  (191 4) .     Die  Tropischen  Intoxekationskrankheiten  in  Mense's  Handbuch. 

Leipzig.     (Many  references.) 
Rodrigues  (1903).     L'Uiraery  ou  Curare.     (Interesting  account.)     Bruxelles. 
Smith  (1905).     Taylor's  Principles  and  Practice  of  Medical  Jurisprudence,  ii. 

852-882.    Chapter  on  Medical  J  urisprudence  in  India,  by  Major  Buchanan, 

I. M.S.     (An  excellent  summary  of  the  subject.) 
Smith  (1905).     Poisonous  Plants  of  all  Countries.     Bristol. 
Staff  (1905).     The  Aconites  of  India.     Calcutta. 
Stockman  "(1893 ).     Laboratory  Reports  of  the  Royal  College  of  Physicians 

of  Edinburgh,  iv.  (Urechitcs).     Edinburgh. 
Waddell   (1904).     Lyon's   Medical   Jurisprudence  for   India.     3rd  edition. 

Calcutta.     (A  most  valuable  book.) 
Windsor  (1906).     Indian  Toxicology.     (A  most  useful  small  book,  and  gives 

many  useful  tests.) 
Witthaus  (1912).     Manual  of  Toxicology.     (Most  useful  general  work.) 


CHAPTER  XI 
ARROW  POISONS 

Preliminary — Africa — Asia —  Philippine  Islands — Australasia  — 
America — References. 

PRELIMINARY. 

From  time  immemorable  peoples  have  used  poisons  to  accentuate 
wound,  made  by  weapons,  especially  arrows.  In  1857  Fontau 
discovered  some  arrow-points  in  the  Pyrenees  which  were  grooved 
to  receive  poisons.  These  discoveries  are  said  to  date  as  far  back 
as  the  Old  Stone  Age. 

The  arrows  of  primitive  peoples  produce  wounds  which  are  by 
no  means  usually  fatal,  and  therefore,  in  attacking  big  game  or  in 
warfare,  it  is  obvious  that  some  poison  which  will  insure  the  death 
of  the  victim  fairly  quickly  will  be  valuable. 

Usually  these  poisons,  or  the  more  potent  of  them,  are  only 
known  to  the  fetish  priests  or  chiefs,  and  are  generally  mixed  with 
all  sorts  of  animal  extracts,  the  whole  being  made  into  a  paste, 
and  painted  on  the  arrow-heads. 

If  a  special  poison  is  prepared,  as  a  rule  some  sort  of  precaution 
is  also  taken,  so  that  the  owner  of  the  arrow  may  not  be  accidentally 
wounded.  Thus,  the  Fra-Fra  people,  when  preparing  against  the 
invasion  of  their  country,  obtained  a  very  potent  poison,  which, 
however,  they  handled  with  great  caution,  though  they  boasted 
that  they  had  an  antidote.  They  kept  these  arrows,  as  a  rule,  in 
special  quivers,  and  each  arrow  had  a  tiny  stick  tied  to  its  shaft, 
so  that  it  could  be  carefully  lifted  out  of  the  quiver.  Moreover, 
a  tuft  of  red  material  was  tied  to  the  base  of  each  of  these  sticks, 
so  that  there  could  be  no  mistake  as  to  which  were  the  specially 
poisoned  arrows. 

Arrow-poisons  may  be  classified  into  those  of  animal  origin  and 
those  of  vegetal  origin.  The  most  common  animal  arrow-poisons  are 
snake-venom,  scorpions,  spiders,  red  ants,  and  beetles,  crushed  and 
mixed  with  vegetal  poisons.  The  Bushmen  of  South  Africa  and  the 
natives  of  Togoland  make  an  arrow-poison  by  burning  and  powdering 
the  heads  of  adders  and  vipers,  regardless  of  the  fact  that  the  burning 
must  destroy  the  venom.  The  Bushmen  of  the  Kalahari  Desert 
make  a  poison  from  the  larva?  of  Diamphidia  simplex  Paringuey, 
which  is  thought  to  be  really  a  toxin  due  to  some  micro-organism 

180 


PRELIMINARY  181 

growing  in  the  decomposing  larva.  But  animal  poisons  are  not 
nearly  so  common  as  vegetal  poisons. 

The  most  important  natural  orders  containing  vegetal  arrow- 
poisons  are,  firstly,  the  Apocynaceae,  which  contains  the  genera 
Acocanthera,  Strophanthus,  and  Adenium,  all  of  which  are  common 
African  poisons;  secondly,  the  Loganiaceae,  with  the  genus  Strych- 
nos,  which  is  of  great  importance  in  Asian  poisons;  thirdly,  the 
Urticaceae,  with  the  important  ipoh  poison  of  Sumatra,  Borneo, 
and  Indo-China;  and  fourthly,  the  less  important  orders  of  the 
Ranunculaceae,  containing  Aconitum  ferox  (Wall),  used  in  India, 
the  Leguminosae,  and  the  Euphorbiaceae,  containing  some  African 
poisons. 

The  actions  of  arrow-poisons  are  very  varied,  and  may  be  classified 
nto — 

i.  An  acti®n  on  the  heart  and  muscles  like  that  of  digitalis. 

2.  An  action  on  the  peripheral  nerve-endings  like  that  of  curari. 

3.  An  action  on  the  nervous  system  and  heart  like  that  of  aconite. 

4.  An  action  on  the  nervous  system  like  that  of  strychnine. 

5.  An  action  resembling  snake-venoms. 

The  general  treatment  of  a  poisoned  arrow  wound  is  as  follows: 

1.  Tie  a  tight  band  on  the  heart  side  of  the  wound,  if  on  a  limb, 
to  prevent  absorption  of  the  poison. 

2.  Remove  the  arrow  as  quickly  as  possible. 

The  difficulty  in  withdrawing  the  arrow-head  is  the  presence  of 
barbs,  which  can  be  prevented  from  doing  mischief  by  thrusting 
the  head  through  the  skin  on  the  far  side  of  the  limb — there  is  no 
necessity  to  fear  about  the  bloodvessels,  for  they  will  slip  away 
from  the  arrow — then  cutting  the  shaft  off,  and  drawing  the  head 
through  on  the  far  side,  and  the  shaft  on  the  near.  If  it  is  in  the 
body,  a  good  plan  is  to  enlarge  the  wound  and  pass  down  some 
sort  of  a  cannula — e.g.,  a  hollow  bamboo — over  the  head,  and  then 
withdraw  the  whole  arrow. 

3.  Wash  the  wound  with  permanganate  of  potash. 

Having  withdrawn  the  arrow,  wash  the  wound  out  thoroughly 
with  a  3  per  cent,  solution  of  permanganate  of  potash  (if  this 
cannot  be  done,  cup  the  wound  or  suck  it),  in  order  to  neutralize 
any  snake-venom,  and,  indeed,  any  other  poison  capable  of  being 
oxidized. 

4.  Keep  the  heart  working. 

Give  stimulants — e.g.,  hypodermics  of  strychnine- -alter  the 
arrow  is  removed  and  the  wound  washed. 

5.  After-treatment. 

Treat  the  hurt  as  a  poisoned  wound.  A  dose  of  antitetanic  serum 
would  be  good,  if  available. 

Some  of  the  principal  arrow-poisons  require  to  be  described  in 
more  detail. 

Africa. — The  natural  order  Apocynaceae  contains,  as  already 
stated,  several  genera  of  plants  which  provide  celebrated  arrow- 
poisons  much  used  by  native  peoples  in  Africa. 


1 82  ARROW  POT  SONS 

These  genera  are  Acocanthera,  Strophanthus,  and  Adenium. 

Acocanthera  Arrow-Poison.- — The  genus  Acocanthera  supplies  the 
most  important  arrow-poisons  of  East,  Central,  West,  and  South 
Africa.  The#  poison,  which  is  called  waba,  wabajo,  or  ouabaio, 
was  first  fully  described  by  Burton  in  1856.  It  is  prepared  from 
the  tree  A.  schimperi  (Dec)  in  Abyssinia  and  throughout  the  greater 
part  of  East  Africa,  being  used  by  the  Wataita,  the  Wakamba,  and 
probably  other  tribes.  The  special  Fra-Fra  arrow-poison  of  the 
Gold  Coast  is  probably  derived  from  some  species  of  Acocanthera. 
In  Erythrsea  and  Yemen  A.  deflersii  Schweinfurth  is  used,  and  in 
Somaliland  A.  ouabaio  Cathelineau.  These  trees  are  4  to  5  metres 
in  height,  with  dark  green  foliage,  white  or  red  flowers,  and  violet- 
red  fruit.  The  poison  is  usually  prepared  by  making  a  decoction  of 
the  wood,  and  evaporating  it  down  until  it  becomes  a  thick  tar- 
like extract,  which  contains  the  active  principle.  This  principle, 
which  is  a  glucoside  called  ouabain,  acocantherin,  or  wabain,  is  a 
powerful  cardiac  poison.  In  addition,  the  natives  generally  add 
snakes'  heads  and  gall-bladders  to  the  tar-like  mass;  but  it  is 
doubtful  whether  these  really  increase  its  virulence,  though  it  must 
be  admitted  that  sometimes  there  are  symptoms  analogous  to 
snake-poisoning. 

The  thick  extract  of  the  wood  containing  any  other  additions, 
which  individual  peculiarity  may  consider  necessary,  is  now  painted 
upon  the  arrow-heads. 

The  action  of  the  freshly  prepared  poison  is  very  rapid,  death 
taking  place  in  a  few  minutes  through  stoppage  of  the  heart,  after 
a  preliminary  quickening  of  the  respirations  and  convulsions. 
Sometimes  pain  is  complained  of  in  the  lumbar  region.  The 
symptoms  can  be  readily  prevented  by  a  3  per  cent,  solution  of 
permanganate  of  potassium.  The  native  remedy  is  believed  to 
consist  in  eating  some  of  the  poison. 

Another  important  Acocanthera  poison  is  A.  venenata  Thunberg, 
which  is  employed  by  the  South  African  Bushmen,  and  is  said  to  be 
made  from  a  decoction  of  the  bark.  The  symptoms  are  rigors, 
without  convulsions,  and  loss  of  muscular  power,  followed  by  death 
in  a  few  minutes. 

Strophanthus  Arrow-Poison. — Livingstone  was  probably  the  first 
to  draw  attention  to  a  Strophanthus  arrow-poison  called  kombi, 
used  in  Central  Africa.  Strophanthus  hispidus  De  Candolle  is  a 
very  common  plant  in  many  parts  of  West  and  Central  Africa,  and 
is  a  common  arrow-poison,  but  not  nearly  so  deadly  as  that  of 
Acocanthera.  The  other  varieties  used  are  S.  glabris,  S.  kambe, 
S.  lanosus,  S.  ciabe,  S.  barika. 

The  poison  is  obtained  by  cooking  the  seeds  in  water,  and  adding 
snakes'  heads  .and  leaves  and  roots  of  other  plants.  The  injured 
man  falls  to  the  ground,  and  his  breathing  and  pulse  become 
gradually  slower  and  slower,  until  the  heart-beats  suddenly  cease, 
and  death  ensues,  preceded  by  a  convulsion  in  about  ten  to  fifteen 
minutes.     The  heart  stops  in  systole,  and  will  not  contract  on 


AFRICA  183 

stimulation.  Strophanthus  is  used  on  the  Congo,  Lake  Nyassa, 
Zambesi,  Gaboon,  Guinea  Coast,  Gold  Coast,  Cameroons,  and 
Senegambia  as  an  arrow-poison. 

Adenium  Arrow-Poison. — There  are  two  species  of  Adenium 
used  in  Africa — viz.,  A.  boelxmianum  Schinz  and  A.  somalensc  Oliver. 

A.  boehmianum,  which  is  a  shrub  about  i|  to  2  metres  in  height, 
is  used  by  the  Ovambo  of  German  South-West  Africa  to  prepare 
an  arrow-poison  called  echuja.  The  thickest  branches  or  roots  are 
cut  across  and  held  over  a  lire,  when  the  thick,  viscid  sap  exudes 
in  threads,  and  is  collected  by  winding  it  round  small  pieces  of 
wood.  The  arrow-heads  arc  now  moistened  by  spitting  upon  them, 
and  then  smeared  with  the  sap. 

The  active  principle  is  echujin,  which  is  a  very  virulent  cardiac 
poison.     The  Somaliland  species  is  equally  virulent. 

Erythrophlceum  judiciale  Proct. — -Its  active  principle  is  an 
alkaloid,  erythrophloem,  which  causes  dyspnoea,  first  slowing  and 
then  quickening  of  the  heart,  and  finally  death  from  stoppage  of 
breathing.  It  is  used  by  the  Pigmies  of  Central  Africa;  but  the 
principal  Pigmy  arrow-poison  is  a  mixture  of  this  with  strychnine, 
which  will  kill  an  elephant.  Prompt  treatment,  however,  is  said 
to  be  able  to  save  a  man's  life  when  wounded  by  one  of  these 
arrows. 

Munchi  Arrow-Poison. — The  Munchi  arrow-poison,  which  is  used 
by  the  Backorana  clan  in  Northern  Nyeni,  is  said  to  be  nearly 
always  fatal  to  man  in  about  half  an  hour.  The  method  of  pre- 
paration is  not  known,  but  the  poison  is  plastered  in  a  thick  layer 
on  the  long  point  of  the  barb.  Tt  is  brittle,  of  a  dark  brown  colour, 
with  slightly  aromatic  odour,  and  is  insoluble  in  cold  or  warm 
water,  in  normal  saline  or  acidulated  solution,  but  dissolves  easily 
in  alkalis — e.g.,  1  per  cent.  Na2C03  solution.  It  has  no  alkaloidal 
properties,  and  does  not  reduce  copper  sulphate  in  alkaline  solution. 
No  fluorescence  occurs  with  H2S04,  and  there  is  only  slight  reducing 
power  after  prolonged  boiling  with  mixed  acids.  It  acts  by  paralyz- 
ing the  heart  and  the  striated  skeletal  muscles,  but  no  distinct 
action  on  the  muscle  plasm  can  be  detected.  The  toxic  substance 
is  thought  to  belong  to  the  class  of  resinous  acids. 

Euphorbia  candelabrum. — -This  is  supposed  to  be  one  of  the  in- 
gredients of  the  poison  '  uciunga  '  (meaning  poison),  used  by  the 
Wafiomi,  Wagogo,  of  late  German  East  Africa.  The  other  in- 
gredients are  not  known.  According  to  Bneger,  t  h  active  principle 
is  exactly  the  same  as  in  Acocanthera.  Rho  says  the  Wakamba  use 
a  similar  poison. 

Less  important  African  arrow-poisons  are: — 
(a)   Used  by  the  Monbattn  Divarfs — 

1.  Erythrophlceum  guineense  G.  Don.,  belonging  to  the  Lcguminosae, 

of  which  the  bark  is  used. 

2.  Palisota  barteri  Bentham. 

-     3.  Combretum  gramliflorum  G.  Don. 
4.  Strychnos  icaja  Baillon. 


1 84  ARROW  POISONS 

(b)   Used  by  the  Hottentots  and  South  African  Bushmen — 

5.  Haemanthus  toxicarius  (Linnaeus). 

6.  Euphorbia  cerelformis  (Linnaeus). 

7.  Euphorbia  virosa  (Wight) . 

8.  Euphorbia  heptagona  (Linnaeus). 

9.  Euphorbia  arborescens  (Boissier). 
10.  Hyaenanche  globosa  (Lamb). 

Nigerian  Arrow-Poisons. — Parsons  finds  that  the  common  arrow- 
poisons  are  either  strophanthus  or  strychnos. 

Asia.- — The  best  known  of  these  poisons  are  those  used  in  Malaya 
Sumatra,  and  Borneo,  and  prepared  from  the  following: — 
Ranunculacece — • 

Aconite  (various  species). 
UrticacecB — 

Antiaris  toxicaria  Leschenault. 
Leguminosce — 

Derris  elliptica  Bentham. 
Loganiacea — 

Strychnos  tieute  Leschenault. 

Strychnos  wallichiana  Bentham. 

Strychnos  maingayi  Clarke. 
Rubiacece — 

Lasianthus  flavescens  Korthals. 
DioscoreacecB — 

Dioscorea  hirsuta  Blume. 
Aroidece — 

Amorphophallus  campanulatus  Blume. 
ApocynacecB — 

Tabernaemontana  malaccensis  Hooker. 

Aconite. — The  Mishmi  arrow-poison  of  North-East  India  is  derived 
from  some  species  of  aconite,  perhaps  A .  ferox  or  A .  heterophylloide. 

Aconitum  ferox  Wall,  belonging  to  the  natural  order  of  the  Ranun- 
culaceae,  is  used  by  the  Himalayan  tribes  from  Assam  to  Kashmir 
as  an  arrow-poison,  and  several  Sepoys  have  been  mortally  wounded 
in  expeditions. 

The  poison  is  applied  as  a  paste  to  the  arrow,  and  is  said  to  be 
mixed  with  septic  blood  to  increase  its  effects  (Waddell).  It  is  also 
said  to  be  used  along  the  French  and  Chinese  frontiers  of  the  Indian 
Empire,  and  by  the  Ainos  in  Japan,  but  the  latter  are  believed  to 
mix  it  with  tobacco. 

Antiaris  toxicaria. — A.  toxicaria  (Lesch)  is  a  tree  growing  in 
Malaya,  the  sap  of  which  provides  the  arrow-poison  known  as  ipuh, 
ipo,  ipoh,  ternek,  kyass,  poon,  upas,  etc.  It  is  used  by  the  Sakais 
of  Malacca,  the  Battaks  of  Sumatra,  the  Dyaks  of  Borneo,  and  the 
Mois  of  Cochin  China.  Brandwood's  dart-poison,  dajaksch,  from 
Borneo,  appears  to  be  from  the  juice  of  A.  toxicaria. 


ASIA  185 

The  earlier  travellers  in  Malaya  gave  wonderful  accounts  of  the 
upas-tree  and  its  action,  which  were  purely  imaginary.  Delisle 
and  Magendie  appear  to  have  been  the  first  to  make  experiments 
with  the  poison  in  1810,  and  they  were  followed  by  Brodie  in  1811, 
who  showed  that  the  heart-beats  became  weak  and  irregular  before 
respiration  or  the  mental  faculties  were  impaired. 

There  appears  to  have  arisen  a  confusion  between  the  juice  of 
A.  toxicaria  and  Strychnos  tieute,  which  explains  the  finding  by 
Hedbon  and  Welting  of  strychnine  in  upas  antiar.  Pelletier  and 
Cayentou,  the  discoverers  of  quinine,  studied  the  chemistry  of  the 
poison,  and  in  1838  Mulder  isolated  the  active  principle  as  a  crystal- 
line body,  which  he  called  antiarin,  which  in  1868  Deirij  and  Ludwig 
showed  to  be  a  glucoside 

Kiliani  in  1896  investigated  antiarin,  and  found  its  formula  to 
be  C27H42O10.  The  physiological  action  of  the  poison  has  been 
investigated  by  a  large  number  of  observers,  notably  by  Hedbon. 
Kiliani,  and  Seligmann,  the  last-named  observer  giving  a  most 
excellent  account  of  ipoh  as  u-ed  by  the  Kenyans  of  the  Baram 
district  of  Sarawak. 

The  poison  is  prepared  from  the  inspissated  juice  of  the  tree, 
and  is  either  used  alone  or  is  mixed  with  5.  tieute,  snakes'  heads, 
or  other  substances.  The  whole  concoction  is  made  into  a  paste 
with  water,  and  applied  to  the  heads  of  the  arrows,  which  are  then 
dried  before  a  slow  fire. 

The  poison  acts  on  the  ventricles  of  the  heart,  behaving  like 
digitalis,  and,  in  addition,  causes  paralysis  of  the  cerebral  nervous 
system  and  passing  clonic  spasms  of  the  voluntary  muscles. 

Croton  tiglium.- — Fraser  considers  that  this  is  one  of  the  Abors' 
arrow-poison,  while  the  other  is  probably  aconite,  possible  A.  ferox 
and  A.  heterophyllum. 

The  Strychnos  Arrow-Poisons. — Strychnos  tieute  Leschenault  is 
the  upas  tieute  of  Borneo,  5.  walhchiana  Bentham  is  the  ipoh 
aker,  and  S.  maingayi  the  aker  lampong  of  the  natives  of  Malacca. 

The  poisons  obtained  from  these  plants  are  said  to  contain 
strychnine  and  curari.  The  symptoms  are  said  to  be  paralysis  of 
the  muscles,  abolition  of  the  reflexes,  and  stoppage  of  the  heart 
and  respiration.  The  urine  contains  a  substance  which  reduces 
Fehling's  solution. 

Manbhum  Arrow-Poisons  — Anderson  thinks  that  these  poisons 
may  possibly  be  manufactured  in  the  following  ways: — 

1.  By  dipping  the  arrow-heads  into  rotten  fish  or  meat,  or  into 
the  highly  decomposed  human  body,  or  into  animal  secretions 
equally  decomposed. 

2.  By  coating  them  with  nux  vomica  and  sulphide  of  arsenic. 

3.  By  coating  them  with  snake  venom. 

4.  By  dipping  them  in  mud,  so  that  they  acquire  the  organism 
of  tetanus 

Less  important  Asian  arrow-poisons  are : — Guatteria  veneficum  Mart,  Cocculus 
toxiferus  Mart,  C.  amazonum  Mart,  which  are  also  used  in  India  as  arrow- 
poisons,  the  active  principle  being  curari. 


1 86  ARROW  POISONS 

Philippine  Islands.- — The  arrow-poison  used  by  the  Negritos  of 
the  Philippine  Islands  is  Rabelaisia  fthilipfiinensis  Planch,  which 
causes  paralysis  of  the  extremities,  dyspnoea,  convulsions,  and 
cessation  of  the  heart's  action. 

Australasia. — Le  Dantec,  quoted  by  Vaughan  and  Novy,  says 
that  the  poisonous  arrows  of  the  natives^of  theiNew  Hebrides  are 
prepared  by  smearing  the  points,  which  are  usually  made  from 
human  bones,  with,  first,  a  vegetable  resin,  and  then  with  slime 
taken  from  marshy  places. 

America. — The  important  American  arrow-poisons  used  in  the 
valleys  of  the  Amazon  and  Orinoco  belong  to  the  Loganiaceae,  and 
are  Strychnos  toxifera  Schomb,  S.  crevauxii  Planchon,-  5.  castelniceana 
Baillon. 

The  active  principle  is  curari,  and,  it  is  said,  curin.  Curari,  or 
ourari,  was  first  brought  to  Europe  by  Sir  Walter  Raleigh  in  1595. 
The  drug  paralyses  the  motor  end-plates,  and  causes  death  from 
failure  of  the  respiration. 

Less  important  American  arrow-poisons  are: — 

(a)  Paitllinia  pinnaia  (Linnaeus),  used  by  native  Indians  of  Brazil. 

(b)  Piscidia  erythrina  (Linnaeus),  used  in  Brazil  and  Central  America. 

REFERENCES. 

Poisons  used  on  Weapons. 

Anderson  (191  i).     Indian  Medical  Gazette,  January.     (Arrows  and  Arrow 

Wounds  in  Monbhum.) 
Burton  (1856).     First  Footsteps  in  East  Africa. 
Chalmers    (1905).     A   Further   Report   of   Expei'iments   upon  the   Fra-Fra 

Arrow-Poisons.     Journal  Royal  Army  Medical  Corps,  August. 
Fraser   (191 4).     Royal  Society  of  Edinburgh,   December   21.     (Abors  and 

Mishmi  Poisons.) 
Frohlich  (1905).     Munchi  Arrow-Poison.     Journal  of  Physiology,  319. 
Grey  (1874).     British  Medical  Journal,  August,  169. 
Krause  (1907).     Archiv  fur  Schirfs  u.  Tropenk. 
Lewin,   L.   (1894).     Die  Pfeilgifte.     Histrionische  u.  experimentelle  Unter- 

suchungen.     Berlin. 
Lewin,  L.  (1903).     Traite  dc  Toxicologic.     Paris. 

Livingstone  (about  1865).     Expedition  to  the  Zambesi,  pp.  465-467. 
Parsons    (1909).     British  Medical  Journal,   January.      (Arrows   and   Arrow 

Wounds  in  Northern  Nigeria.) 
Perrot  and  Vogt  (1913).     Poisons  dc  Fldch.es  ct  Poisons  d'Epreuve.     (This 

is  an  excellent  book,  and  the  most  complete  which  wc  know,  though  it 

omits  one  of  the  arrow  poisons  with  which  we  are  acquainted.)     Paris. 
Rno,    F.    (1914).     Mense's   Handbuch   der   Tropenkrankheiten,   ii.   520-533. 

Leipzig. 
Rodrigues  (1903).     L'Uirarry.     Bruxelles. 
Seligmann  (1903).     Action  of  the  Kenyah  Dart  Poison  Ipoh  and  its  Active 

Principle  Antiarin.     Journal  of  Physiology,  xxix.  39.     (Complete  litera- 
ture of  Ipoh  poison.) 
Smith  (1905).     Taylor's  Medical  Jurisprudence,  ii.  696-698. 
Stephenson  (1832).     Medical  Zoology.     (A  very  interesting  work.)     London. 
Stockman  (1898).     Pharmaceutical  Journal,  pp.  550-585. 
Vaughan  and  Novy  (1903).     Cellular  Toxins,  p.  68. 

Waddell  (1904).     Lyon's  Medical  Jurisprudence  for  India,  pp.  589,  617. 
Windsor  (191 2).     British  Medical  journal,  January  6. 


CHAPTER  XII 

POISONS   USED  IN   FISHING,   HUNTING, 
AND  TRADE 

Preliminary — Fish  poisons — Poisons  used  in  hunting — Cattle  poisoning — 
Rat  poisoning — Locust  poisoning — Poisoning  of  birds — Trade  poisoning 
— References. 

PRELIMINARY. 

In  this  chapter  we  consider  in  the  briefest  possible  manner  the 
use  of  poisons  to  kill  fish,  lug  game,  cattle,  rat^,  birds,  and  trade 
poisoning. 

FISH  POISONS. 

Every  now  and  again  we  have  been  appealed  to  for  the  purpose 
of  explaining  why  a  large  number  of  fish  have  been  found  dead 
in  a  river  or  lake,  and  certainly  in  those  which  we  have  been  able 
to  investigate  personally  the  causal  agent  has  been  poisoning  of 
the  waters. 

It  is  a  common  practice  all  over  the  world  to  throw  pieces  of 
bark  or  leaves  of  trees  and  shrubs  on  to  the  water,  in  order  to 
stupefy  fish,  and  thus  enable  them  to  be  easily  caught. 

The  number  of  plants  used  for  this  purpose  is  very  great,  and 
though  we  have  not  thought  it  necessary  to  give  a  detailed  list 
in  this  book,  still,  we  consider  that  it  is  useful  to  give  a  few 
examples,  as  a  knowledge  of  the  subject  is  at  times  required. 

The  plants  used  in  Ceylon  for  the  purpose  of  intoxicating  or 
killing  fish  are  given  in  the  following  list  supplied  to  us  by  Mr. 
Drieberg : — 

i.  Anarmirta  paniculata  {A.  cocculus  Wight  and  Arnott). 

2.  Barringtonia  acutangula  Gacrtner. 

3.  Euphorbia  tirucalli  Linnaeus. 

4.  Lasiosiphon  criocephalus  Decaisne. 

5.  Mcesa  indica  Wall. 

6.  Mundulea  suberosa  Bentham. 

7.  Randia  dumetorum  Lamarck. 

8.  Strychnos  nux  vomica  Linnajus. 

9.  Walsura  piscidia  Roxburgh. 
10.  Derris  uliginosa  Bentham. 

Hvdnocarpus  venenatus  Gacrtner  is  also  said  to  be  used,  and  to  be 
poisonous  on  account  of  the  hydrocyanic  acid  it  contains. 

187 


1 88      POISONS  USED  IN  FISHING,  HUNTING,  AND  TRADE 

In  India  the  following  are  used : — 

Anamirta  cocculus  Wight  (Menispermaceae). 
Dolichandrone  falcata  Seemann  (Bignoniaceae). 

In  Java  and  Sumatra  :— 

Pittosporum  densifiorum  Putterlick  (Pittosporeae). 
Tephrosia  toxicaria  Persoon. 
Tephrosia  piscatoria  Persoon. 

In  the  Philippine  Islands:— 

Sapindus  rarak  De  Candolle  (Sapindaceae). 
Harpulia  arbor ea  Radlkofer  (Sapindaceae). 

In  the  Dutch  East  Indies : — 

Derris  elliptica  Bentham  (Leguminosae). 
Pachyrhizus  angidatus  Richard. 

Both  of  these  plants  contain  a  non-nitrogenous  substance,  called 
respectively   derrid   and    pachyrhizid,    highly   poisonous    to    fish. 
Derris-root  will  kill  fish  in  a  dilution  of  i  to  25,000  of  water,  and 
derrid  in  1  to  5,000,000. 
In  the  Comoro  Islands: — 

Tephrosia  vogelii  Hooker  (Leguminosae). 
In  the  West  Indies : — ■ 

Piscidia  erythrina  Linnaeus. 

This  plant,  called  the  Jamaica  dogwood,  is  used  by  throwing 
the  leaves  and  entire  branches  into  the  water,  when  the  active 
principle,  piscidin,  dissolves  out  and  paralyzes  the  fish,  which  are 
easily  caught  floating  on  the  surface. 

In  Guyana: — 

Tapura  guyanensis  Aublet. 

I  cldhy other e  cunabi  Martius. 

In  South  America: — 

Grewia  asiatica  Linnaeus. 

Dichapetalum  toxicarium  Baillon. 

Serjania  ichthyoctova  Radlk  (the  Timba  of  the  Amazon). 

Serjania  lethalis  St.  Hillaire  (the  Timba  of  the  Amazon). 

Serjania  piscatoria  Radlk  (the  Timba  of  the  Amazon). 

I I  vdrocotyle  javenica  Ehrenberg. 
C/ibadium  asperum  Dc  Candolle. 
Jacquinia  armillaris  Linnaeus. 

In  Africa: — 

Kiggelia  africana  Linnaeus. 
Paulowilhelmia  speciosa  R.  Brown. 
Tephrosia  vogelii  Hooker. 

In  Sardinia: — 

(Enanthe  crocata  Linnaeus. 
Daphne  guidium  Linnaeus. 


CATTLE  POISONING 


rs„ 


POISONS  USED  IN  HUNTING. 

In  India  the  root  of  Arum  montanum  Roxburgh  is  said  to  be 
used  to  poison  tigers,  while  aconite  is  employed  for  the  same  pur- 
pose against  elephants,  especially  A.  ferox  Wall.  In  San  Salvador 
the  '  Cangoura,'  Ronrea  oblongifolia  Hooker,  is  employed. 

CATTLE  POISONING. 

Cattle  poisoning  is  a  frequent  method  of  revenge  in  India,  and 
the  drugs  most  commonly  used  are: — Arsenious  oxide,  arsenious 
oxide  with  sulphite,  arsenious  oxide  with  oxides  of  lead,  sulphides 
of  arsenic  only,  oxides  of  lead  only,  sulphate  of  copper,  mix  vomica, 
Cocculus  indicus,  mercury,  and  sulphate  of  iron. 

But,  in  addition,  Abrus  precatorius  Linnaeus,  Cerbera  thevetia 
Linnaeus,  Calotropis  procera  R.  Brown,  aconite,  chopped  hair,  and 
snake-venom  have  been  used.  The  list  of  Ceylon  plants  poisonous 
to  man  and  cattle  will  be  given  below.  It  is  important  to  remember 
that  rinderpest  and  dysentery  resemble  arsenical  poisoning,  while 
poisoning  with  nux  vomica  may  resemble  tetanus. 


Fig.  i 


-Abrus  precatorius  Linn^us. 


Grey  says  that  Lessertia  annularis,  the  t'neuta  of  the  Karroo 
of  South  Africa,  produces  cerebro-spinal  paralysis  in  sheep  and 
goats,  like  Gastro-obium,  the  poison-pea  of  Australia.  Only  Abrus 
precatorius  need  be  discussed  here. 

Abrus  precatorius  Linnaeus. — The  juice  of  this  plant,  which 
belongs  to  the  Lcguminosae,  is  most  irritating,  and  if  injected 
under  the  skin  of  cattle  proves  rapidly  fatal,  by  producing  general 
depression,  drowsiness,  fall  of  temperature,  and  haemorrhagic 
Lesions  somewhat  like  those  of  snake-venom. 


rgo      POISONS  USED  IN  FISHING,  HUNTING,   AND  TRADE 

The  decorticated  seeds  are  made  into  a  paste,  which  is  worked 
into  sharp-pointed  little  needles,  and  hardened  in  the  sun.  Two 
of  these  are  inserted  by  their  bases  into  a  wooden  handle,  and 
then  driven  with  great  force  into  the  animal's  flesh. 

The  active  principle  is  abrin,  a  tox-albumin  resembling  snake- 
venom,  which  causes  thrombosis  and  death  in  from  eighteen  to 
twenty-four  hours. 

Omithoglossum  glaucum  Salisbury,  1806. — This  plant  is  the  cause 
of  accidental  cattle  poisoning  in  South  Africa. 

Much  has  been  written  of  late  years  with  regard  to  stock  poisoning 
in  Australia  and  elsewhere,  but  it  is  rather  outside  the  work  of 
this  book  to  deal  further  with  this  matter,  to  which  we  give  refer- 
ences at  the  end  of  this  chapter.  We,  however,  give  a  list,  which 
we  owe  to  the  kindness  of  Mr.  Drieberg,  of  Ceylon  plants  known 
to  be  poisonous  to  cattle : — 

1.  Ammannia  baccifcra  Linnaeus. 

2.  Anamirta  paniculata  (A.  cocculus)  Wight  and  Arnott. 

3.  Arisccma  curvatum  Thwaites. 

4.  Chrozophora  plicata  A.  de  Jussieu. 

5.  Croton  tiglium  Linnaeus. 

6.  Diospyros  montana  Roxburgh. 

7.  Elcedendron  glaucum  Persoon. 

8.  Euphorbia  tirucalli  Linnaeus. 

9.  Exccecaria  agallocha  Linnaeus. 
10.  Datura  fastuosa  Linnaeus. 

ri.  Lagenaria  vulgaris  Seringe. 

12.  Lasiodphon  eriocephalus  Decaisnc 

13.  Lobelia  nicotiancejolia  Heyne. 

14.  Manihot  utilissima  Pohl. 

15.  Paspalum  scrobiculatum  Linmeus. 

16.  Plumbago  zeylanica  Linnaeus. 

1 7.  Rauwolfia  serpentina  Bentham. 

18.  Rhododendron  arboreuui  Smith. 

19.  Ricinus  communis  Linnaeus. 

20.  Sapium  insigne  Trimen. 

21.  Tylophora  fasciculata  Buch-Ham. 

22.  Withania  somnifera  Dunald. 

RAT  POISONING. 

This  is  generally  carried  out  by  means  ot  yellow  phosphorus 
or  arsenic. 

I  he  phosphorus  is  mixed  with  glucose  to  prevent  spontaneous 
combustion,  and  then  made  into  a  paste  with  a  fatty  base  such  as 
Lard;  but  it  is  advisable  to  vary,  from  time  to  time,  the  atty  base, 
as  rats  are  very  knowing  and  begin  to  suspect  that  something  is 
wrong. 

The  poison  is  then  spread  on  bread  or  made  into  bread  pills, 
but  it  is  often  advised  that  people  who  do  this  should  have  their 


LOCUST  POISONING—TRADE  POISONING  191 

hands  smeared  with  an  ointment  containing  oil  of  aniseed,  with 
which  all  utensils  used  for  the  poison  should  also  be  smeared. 

Arsenic  is  often  preferable  to  phosphorus,  which  is  difficult  to 
obtain  and  dangerous  to  work  with.  It  should  be  treated  in  the 
same  way  as  phosphorus,  but  it  is  as  well  to  find  the  minimal 
lethal  dose  for  the  local  rat  before  commencing  rat  poisoning  on 
a  large  scale,  and  also  to  be  ready  with  an  antidote  in  case  any 
person  indulges  in  a  d< 

Many  rat  poisons  are  known  to  natives,  especially  Tylophora 
fasciculata  Buch-Ham  (Asclepiadeas),  Chaillciia  toxicaria  Don 
(Dichapetalaceas),  both  of  which  are  used  in  Africa,  and  Diauella 
nemorosa  Linnaeus  (Liliaeeae)  in  Malacca. 

LOCUST  POISONING. 

Arsenic  has  been  used  with  success  by  Mr.  King,  Government 
entomologist  in  the  Sudan,  and  others  as  a  poison  for  killing  locusts 
in  the  '  hopper  stage.'  The  arsenic  is  prepared  in  concentrated 
form  in  treacle  and  is  diluted  locally.  Into  the  solution  so  made 
chopped  fodder  is  placed,  and,  after  soaking,  is  spread  out  for  the 
hoppers  to  eat  in  desert  parts.  Spraying  has  also  been  used  in 
cultivated  areas.  Mustard  and  the  usual  iron  antidote  are  handy 
in  case  anyone  takes  a  dose  of  the  poison. 

POISONING  OF  BIRDS. 

Attempts  have  been  made  from  time  to  time  to  diminish  the 
sparrow  pest  in  cultivated  areas  by  poisons — e.g.,  strychnine — 
but  with  doubtful  success. 

Palicourea  marcgravii  (Rubiacece)  St.  Hilaire  is  said  to  be  used 
for  poisoning  pigeons. 

TRADE  POISONING. 

The  trade  poisonings  are  more  fully  dealt  with  in  the  chapter 
on  Dermatitis  venenata,  but  we  may  mention  the  following  here:— 

Vanilla  Poisoning. 

Vanillismus  is  poisoning  by  the  dried  fruit  of  Vanilla  pi  ani folia 
(Andrews),  which  causes  colic,  vomiting,  and  pains  in  the  head 
and  muscles.  Men  working  with  it  may  suffer  from  conjunctivitis, 
fits  of  sneezing,  and  a  skin  eruption  called  vanilla  itch,  charac- 
terized by  swelling,  followed  in  a  few  days  by  scaling.  There  is, 
however,  greal  -  to  what  is  the  real  cause  of  these  symptoms. 

Probably  some  of  them  arc  due  to  a  mite  in  the  vanilla. 

Lacquer  Poisoning. 

I  acquer  is  obtained  Erom  .1  brown  treacle-like  balsam,  which 
exudes  when  incisions  are  made  into  the  lacquer- tree,  Rhus  verni- 
cifera  De  Candolle. 


1 92      POISONS   USED  IN  FISHING,  HUNTING,  AND  TRADE 

The  disease  is  acquired  in  two  ways:  either  by  direct  contact 
with  the  lacquer,  or  through  the  fumes  arising  from  it  by  evapora- 
tion, but  only  as  long  as  the  lacquer  is  not  dry,  for  the  poison, 
whatever  it  is,  disappears  on  drying. 

The  symptoms,  which  develop  in  a  few  hours,  are  fever,  with 
tension  and  oedema  of  the  skin  of  the  face,  limbs,  and  generative 
organs,  nasal  and  conjunctival  catarrh,  while  a  papular  eruption 
appears  on  the  cedematous  skin  of  the  legs  and  forearms. 

The  treatment  consists  in  washing  the  skin  thoroughly  with 
soap  and  water,  and  applying  soothing  applications,  such  as  cold 
lotions,  or  Lotto  Plumbi  subacetatis. 

As  prophylaxis  the  Chinese  rub  the  hands  and  face  with  rape- 
seed  oil  in  which  a  ham  has  been  boiled,  and  wear  a  linen  mask 
for  the  face  and  a  leather  apron  for  the  body.  After  work  the 
exposed  parts  are  rubbed  with  a  decoction  of  chestnut,  pine-bark, 
saltpetre,  and  amaranth. 

The  above  precautions  are  taken  in  China,  but  in  Japan  no 
such  prophylaxis  exists. 

Note. — Camel  poisoning  caused  by  the  hydrocyanic  acid   contained  in 
immuture  dura  is  well  known  in  the  Sudan. 


REFERENCES. 

The  best  account  of  these  poisons  is  given  by  Rho  (191 4)  in  the  second 
edition  of  Mense's  '  Handbuch  der  Tropenkrankheiten,'  517-615.  For  the 
definition  of  genera,  species,  etc.,  see  Bent  ham  and  Hooker  (1867-1883), 
'  Genera  Plantarum' ;  Oliver  and  Dyer, '  Flora  of  Tropical  Africa  ' ;  and  Thonncr 
(1915),  'The  Flowering  Plants  of  Africa.' 

Poisons  used  in  Fishing  and  Hunting. 

Vaccari  (1906).     Annali  di  Medicina  Navale,  XII.,  i.  iii.     Roma. 
Vaughan  (189S).     Twentieth-Century  Practice  of  Medicine,  pp.  38,  39. 
Vaughan  and  Now  (1903).     Cellular  Toxins,  p.  198.     London. 
Waddell  (1906).     Lyon's  Medical  Jurisprudence  for  India. 

Cattle  Poisoning. 

Cleland  (1912).     Third  Report,  Bureau  of  Microbiology.     Australia. 
Long  (191 7).     Plants  Poisonous  to  Live  Stock.     Cambridge. 

Trade  Poisoning. 

Crocker  (1903).     Diseases  of  the  Skin,  third  edition,  i.  418-420. 

Scheube  (1903).     Diseases  of  Warm  Climates,  p.  331.     (English  translation.) 


CHAPTER  XIII 
POISONOUS  FOOD 

Preliminary — Animal  food  poisoning — Products  normally  present — Fuguismus 
— Post-mortem  decomposition — -Vegetal  food  poisoning- — Lathyrismus — 
Loliismus  —  Paspalismus  —  Atriplicismus —  Fabismus — Fagopyrismus — 
References. 

PRELIMINARY. 

Food  poisoning,  technically  called  bromatoxismus,  may  be  divided 
into  two  classes: — 

1.  Animlal  food  poisoning. 

2.  Vegetal  food  poisoning. 

i.  ANIMAL  FOOD  POISONING. 

Animal  food  poisoning  is  called  zootrophotoxismus,  and  may  be 
due  to — 

(a)  Products  normally  present  in  certain  animals,  but  poisonous 

to  man. 

(b)  Poisonous  food  having  been  eaten  by  an  animal  prior  to 

its  being  killed  for  food. 

(c)  Products  abnormally  produced  in  the  living  animal. 
{d)  Post-mortem  decomposition. 

But  of  these  we  need  only  concern  ourselves  with  the  first  and 
the  last. 

Products  Normally  Present. — Poisoning  by  products  normally 
present  in  the  animal  is  called  '  siguatera,'  and  is  generally  due 
to  fish,  though  it  may  also  be  caused  by  Molluscs,  Crustaceans, 
and  Ccelenterates. 

The  most  dangeious  fish  are  those  living  among  coral  reefs,  and 
particularly  those  which  are  bright-coloured.  It  is  possible  that 
the  poisonous  properties  may  be  due  not  so  much  to  the  fish  itself 
as  to  the  fact  that  it  has  eaten  decomposing  food,  such  as  dead 
medusae,  corals,  etc. 

Fretz  and  Branch  have  noted  fish  poisoning  in  1915  in  St. 
Christopher  and  Nevis,  and  think  that  it  is  due  to  the  Barraconda 
[Sphyrcena),  while  McNaughton  reports  similar  poisoning  from  the 
Gilbert  and  Ellice  Islands. 

Certain  species  of  the  genus  Clupea  (Cuvier),  particularly  C.  tlinssa 
(Osbeck)    are  noted   as  being  very  poisonous,  but   there  is  con- 

193  J3 


i94 


POISONOUS  FOOD 


siderable  doubt  about  this  matter,  as  no  scientific  work  has  been 
done  on  the  subject.  The  £  symptoms  are  gastro-intestinal  irrita- 
tion, which  may  lead  to  collapse  and  death.  Another  fish  which 
is  only  poisonous  at  certain  seasons  is  a  so-called  sardine  Clupea 


14. — Clupea  longiceps  (Sardinella  neohowii) 


longiceps  (Sardinella  neohowii  Val),  found  off  the  coasts  of  Ceylon, 

and  which,  according  to  Tennent,  caused  much  sickness  years  ago. 

Other  poisonous  fish  are  Tetrodon  hispidus,  the  '  muki-muki '  or 

death-fish  of  Hawaii,  and  the  file  fishes,  of  which  Stephanolepsis 


Fig.  15. — Tetrodon  vermicularis  Schlegel. 
(From  Savtselicnko's  '  Atlas  of  Poisonous  Fish.') 

hispidus  L.  may  be  mentioned  as  an  example.  Poisoning  with 
Tetrodon  has,  however,  been  more  accurately  studied,  and  may 
be  referred  to  at  greater  length  under  the  term  Fuguismus. 

Fuguismus. 

The  Japanese  term  '  fugu  '  includes  several  species  of  fish  belong- 
ing to  the  genus  Tetrodon,  of  which  the  important  species  are 
T.  vermicidaris,  T.  nibnpes,  T.  Icevigalus,  T.  chrysops,  T.  rivulatus, 
T.  lunaris,  T.  pardalis,  T.  porphyreus,  T.  poicelonotus,  T.  stellatus, 
and  T.  sticonotus,  which  are  said  by  Scheube  to  be  often  used  for 
suicidal  purposes.  T.  pennantii  has  also  been  found  to  be  the 
cause  of  poisoning  in  a  case  in  Burmah. 

The  poison  appears  to  lie  in  the  ovaries  and  testicles,  which, 
according  to  Tabara,  contain — 1.  Tetrodin — a  crystalline  base; 
2.  Tetrodonic  acid- — a  white,  waxy  body.  Both  are  poisonous,  but 
the  acid  is  said  to  be  more  so  than  the  base. 

The  symptoms,  which  begin  in  three  to  fifteen  minutes  after 
eating  one  roe,  are,  according  to  Scheube,  an  unpleasant  sensation 


VEGETAL  FOOD  POISONING  195 

in  the  stomach,  abdominal  pains,  burning  in  the  fauces,  nausea, 
severe  headache,  collapse,  and  fainting.  Death  may  occur  in  a  few 
hours  from  paralysis  of  the  heart  or  respirations.  The  mortality  is 
high,  being  said  to  be  more  than  68  per  cent. 

The  treatment  is  to  empty  the  stomach  with  an  emetic  and  to 
give  stimulants,  especially  hypodermics  of  strychnine. 

Post-Mortem  Decomposition. 

Post-mortem  changes  arc  much  more  rapid  in  the  tropics  than  in 
the  Temperate  Zone,  and,  therefore,  food  is  quickly  apt  to  become 
poisonous.  Meat  is  especially  liable  to  become  infected  with 
saprophytic  or  pathogenic  micro-organisms,  especially  Bacillus  para- 
typhosus  B  (Schotmuller)  and  the  bacillus  of  Gaertner,  more  rarely 
B.  paratyphosus  A  (Schotmuller).  These  micro-organisms  give  rise 
to  ptomaines,  which  cause  symptoms  of  irritant  poisoning  (kreo- 
toxismus),  which  may  be  so  severe  as  to  resemble  those  of  cholera. 
The  treatment  is  to  remove  the  poison  by  emetics  if  necessary  and 
purgatives,  in  the  meanwhile  keeping  up  the  heart's  action  by 
means  of  warm  applications,  stimulants,  and  cardiac  tonics.  When 
collapse  sets  in,  saline  hypodermic  injections  should  be  given.  As 
soon  as  the  acute  symptoms  subside,  the  bowel  should  be  disinfected 
with  small  doses  of  calomel,  salol,  or  naphthol. 

2.  VEGETAL  FOOD  POISONING. 

Sitotoxismus,  or  vegetal  food  poisoning,  is  caused  by  many  kinds 
of  vegetal  food,  and  ought  to  be  well  known,  but,  unfortunately,  is 
by  no  means  on  a  scientific  basis  in  the  tropics. 

Ergotism,  well  known  in  the  temperate  regions,  is  not  important 
in  the  tropics ;  but,  on  the  other  hand,  there  is  lathyrism,  believed 
t<>  he  due  to  Lathyrus  sativus,  and  other  species  of  the  same  genus — 
loliismus,  due  to  Lolium  tcmulentum ;  and  paspalismus,  due  to 
J'aspalum  scrobiculatum — which  are  known  to  occur  in  India.  Less 
known  is  atriplicismus,  which  is  described  in  China. 

Kirke  has  drawn  attention  to  poisoning  by  Cystisus  cadjan,  by 
which  he  probably  means  Dolichus  catjana  (Linne),  named  Vigna 
Catjang  (Walp)  by  Dragendorff,  and  also  by  Dolichos  filosa  (Klein), 
which  is  the  same  as  Vigna  filosa  (Savi),  both  of  which  are  used  as 
foods.  With  regard  to  the  former,  the  native  name  of  which  is  urhur 
or  toar,  he  says  it  mainly  affects  the  poorer  classes,  as  they  do  not 
remove  the  outer  skin  before  eating  it.  The  symptoms  in  the  order 
of  appearance  are  as  follows: — Urticaria,  sense  of  heat  in  the 
stomach,  redness  of  the  lining  membrane  of  the  mouth,  apparent 
elongation  of  the  teeth  (by  this  must  be  meant  shrinking  of  the 
gums),  discoloration,  bronzing  of  the  skin,  sponginess  of  the  nails, 
burning  of  the  hands  and  feet,  a  dry,  harsh,  cracked  condition  of 
the  cuticle  of  the  hands  and  feet,  and  dec})  longitudinal  cracks  in 
the  heels.  Rheumatic  pains,  with  thickening  of  the  periosteum, 
especially  of  the  shins,  and  changes  in  the  joints  are  also  noticed. 


ig6  POISONOUS  FOOD 

Dolichos  filosa,  called  'oordh  dal,'  is  said  by  Kirke  to  be  poisonous 
only  if  eaten  with  the  husks,  when  it  causes  colic,  indigestion,  and 
as  secondary  results  rheumatic  pains,  harshness  and  dryness  of  the 
skin,  with  cracks.  It  is  said  to  be  a  staple  article  of  food  among 
all  classes,  except  the  highest  and  the  lowest. 

Lathyrismus. 

Synonyms. — Platterbsenkrankheit  (Ger.) ;  Meurd  Djilben  (Algeria) ; 
Latirismo  (It.). 

Definition. — Lathyrismus  is  an  intoxication  caused  by  the  inges- 
tion of  Lathyrus  sativus  Linnaeus  and  other  species  of  the  same 
genus,  and  characterized  by  symptoms  of  spastic  paraplegia. 

History. — It  is  believed  that  Hippocrates  was  acquainted  with 
the  disease,  because  he  mentions  that  people  at  Amos  who  fed  con- 
tinually on  pulse  suffered  from  weakness  in  the  legs.  In  1671  the 
Grand-Duke  of  Wiirtemberg  issued  an  edict  forbidding  the  eating  of 
bread  made  from  vetch-seeds,  as  it  had  been  noticed  that  those 
who  ate  such  bread  suffered  from  a  peculiar  stiffness  of  their  legs, 
although  they  seldom  died.  In  1784  an  epidemic  was  recorded  in 
Tuscany,  when,  through  scarcity  of  food,  the  people  were  compelled 
to  eat  chick-peas.  Tozzetti,  while  studying  this  epidemic,  came 
to  the  conclusion  that  only  the  people  who  had  for  at  least  three 
months  eaten  bread  made  of  two  parts  chick-pea  to  one  part  of  rye 
or  wheat  became  ill.  He  then  planted  some  of  the  chick-pea  seeds, 
and,  when  they  grew  up,  identified  them  as  Lathyrus  sativus  (L.). 
In  1824  Desparanches  came  to  the  conclusion  that  the  seat  of  the 
lesion  was  in  the  lumbar  cord.  In  1833  the  disease  was  first 
recognized  in  India  in  the  Sangor  territories,  where,  on  account  of 
three  successive  famines  in  1829-31,  the  people  were  compelled  to 
eat  vetches,  which  are  called  kesari  dal,  or  teori.  Outbreaks  took 
place  in  Sind,  Chota  Nagpur,  the  Central  Provinces,  and  in  the 
Himalayas.  It  apparently  became  very  prevalent,  for  Irving  says 
that  in  one  district  6  per  cent.,  and  in  another  3-19  per  cent.,  of 
the  inhabitants  were  affected.     It  still  exists  in  India. 

Climatology. — The  disease  depends  upon  social  rather  than 
climatic  conditions,  for  people  will  not  eat  the  vetches  unless  com- 
pelled by  famine.     It  is  known  in  India,  Algiers,  Italy,  and  France. 

etiology. — There  appears  to  be  a  consensus  of  opinion  that  the 
disease  is  due  to  eating  bread  composed  largely  of  flour  obtained 
from  seeds  of  some  species  of  Lathyrus  belonging  to  the  natural 
order  Leguminosae.  The  species  most  commonly  suspected  is 
Lathyrus  sativus  Linne,  which  grows  in  India;  but  L.  cicera  L.  (red 
vetch),  L.  clymenum  L.  (Spanish  vetch),  L.  tuberosus,  and  L.  aphaca 
have  all  been  regarded  as  possible  causes.  It  is,  however,  by  no 
means  evident  what  substance  or  substances  in  these  plants  cause 
the  symptoms.  Teilleux  obtained  a  resin  which  caused  tetanic 
spasms  and  paralysis  of  the  posterior  limbs  in  rabbits.  Bourlier 
obtained  an  extract  which  killed  birds  and  frogs.  Asher  obtained 
from  L.  cicera  a  volatile  alkaloid,  which  he  called  lathyrin,  which 


LATHYRISMUS  107 

was  doughy  in  consistence,  alkaline,  insoluble  in  water,  slightly 
soluble  in  ether,  soluble  in  chloroform,  and  which  on  evaporation 
formed  needles;  but  he  did  not  perform  any  experiments  with 
the  substance,  the  action  of  which  is  therefore  unknown.  It  is 
believed  by  some  that  Lathyrus  is  not  poisonous  unless  the  seeds 
are  decomposed  or  contain  some  parasitic  growth,  while  others 
hold  that  the  symptoms  are  not  due  to  Lathyrus  at  all,  but  to 
Agrostcmma  githago  (the  corn-cockle)  or  Loliitm  tcmulentum  (the 
darnel).  In  1883  Astier  separated  out  an  alkaloid,  lathyrin,  which 
Stockman  in  1917  showed  to  be  the  poisonous  principle,  which  is 
present  in  only  small  amount  and  only  in  the  seed  itself. 

Animals  are  by  no  means  immune  from  the  baneful  effects  of  the 
plants,  for  ducks  become  paralyzed  and  may  die  after  eating  the 
seeds;  while  pigs  and  horses  also  suffer,  the  latter  showing  acute  or 
chronic  symptoms  which  are  said  more  or  less  to  correspond  to 
lathyrismus.  On  the  other  hand,  bullocks  and  buffaloes  are  con- 
sidered to  be  immune. 

The  great  predisposing  cause  in  man  is  scarcity  of  food,  whether 
due  to  famine  or  poverty,  both  of  which  compel  the  unfortunate 
people  to  eat  vetches  instead  of  ordinary  food.  If  the  disease  is 
brought  about  by  famine,  it  may  assume  epidemic  proportions;  if 
by  poverty,  it  may  be  simply  endemic.  Young  people  are  more 
liable  to  be  poisoned  than  old  persons,  and  men  more  than  women, 
perhaps  because  they  eat  more  food. 

Morbid  Anatomy. — The  pathology  and  morbid  anatomy  need 
investigation.  When  this  isdone,  it  is  probable  that  some  lesion  of  the 
pyramidal  tracts — i.e.,  of  the  upper  motor  neurones — will  be  found. 

Symptomatology. — The  incubation  period  is  not  known,  and  the 
disease  comes  on  so  insidiously  that  the  patient  often  attributes  it 
to  a  chill  which  he  may  have  experienced  a  day  or  so  previously. 

Prodromata  are  often  said  to  be  absent,  though  it  is  more  prob- 
able that  digestive  disturbances,  colicky  pains,  and  diarrhoea  do 
occur,  but  pass  unnoticed. 

One  of  the  first  symptoms  to  arise  is  pain  in  the  back  and  weak- 
ness in  the  legs,  which  increase  until  symptoms  of  spastic  paraplegia 
appear.  The  patient  now  complains  of  girdle  sensations,  and  walks 
with  difficulty.  The  gait  is  characteristic,  for  the  feet  are  turned 
slightly  inwards,  and  are  dragged  or  raised  with  difficulty  from  the 
ground.  The  joints  appear  so  weak  that  it  is  difficult  to  proceed 
any  distance  without  falling,  while  the  body  has  a  peculiar  up  and 
down  motion.  There  is  no  ataxy,  and  no  vasomotor  phenomena, 
but  the  legs  waste  very  much.  The  arms  are  not,  as  a  rule,  in- 
volved, though  the  hands  may  tremble.  The  superficial  and  deep 
reflexes  are  increased,  and  ankle  clonus  is  present.  The  electrical 
excitability  of  the  affected  muscles  is  diminished,  but  the  reaction 
of  degeneration  is  absent.  Incontinence  of  urine  and  impotence 
are  early  and  common  symptoms.     The  mind  is  unaffected. 

The  disease  does  not  itself  end  fatally,  but  a  definite  improve- 
ment is  seldom  seen  except  in  incipient  cases. 


icfi  POISONOUS  FOOD 

Diagnosis. — Lathyrism  must  be  distinguished  from  ergotism  by 
the  absence  of  gangrene,  from  beri-beri  by  the  absence  of  implica- 
tion of  the  peripheral  nerves  and  the  heart,  and  the  absence  of 
dropsy. 

Prognosis. — The  disease  itself  is  not  fatal. 

Treatment. — Mild  cases  may  be  considerably  benefited  by  being 
given  good  food  and  warm  clothing,  together  with  counter-irrita- 
tion to  the  spine,  and  bromide  of  potassium  internally  in  15-grain 
doses  three  times  a  day.     Strychnine  is  harmful. 

Prophylaxis. — The  only  possible  prophylaxis  is  the  distribution 
of  good  food  to  the  poor  in  times  of  famine. 

Loliismus. 

Loliismus  is  an  intoxication  caused  by  the  ingestion  of  the  seeds 
of  Lolium  temulentum  Linnaeus  in  bread. 

History. — Loliismus  has  been  known  since  Roman  times,  and  is 
said  by  Orfila  to  have  occurred  in  Genoa  during  the  blockade  of 
the  year  1800.  Kingsley  of  Roscrea  described  an  outbreak  in 
1854,  in  which  thirty  persons  suffered  severely.  Similar  cases 
have  been  reported  in  India  from  the  Punjaub,  where  the  herb 
is  called  '  mostaki,'  and  from  the  North-West  Provinces,  where  it  is 
called  '  moschni.' 

/Etiology. — The  exact  method  by  which  Lolium  temulentum 
causes  disease  is  not  known.  Dr.  Cordier  experimented  on  himself 
by  taking  6  drachms  of  the  seeds  early  one  morning,  and  asserts 
that  the  result  was  inability  to  think,  indistinct  vision,  torpor, 
debility,  and  drowsiness,  followed  by  efforts  to  vomit,  and  later  by 
tremors  of  the  limbs,  great  depression,  difficulty  of  speech,  and 
vomiting.  Bley  separated  a  bitter  principle,  which  he  called  loliin, 
but  the  action  of  this  does  not  appear  to  have  been  investigated 
properly.  Freeman  states  that  the  seeds  owe  their  poisonous  pro- 
perties to  an  associated  symbiotic  fungus,  which  he  carefully 
describes,  and  says  that  it  is  probably  identical  with  that  found 
in  other  species  of  Lolium.  He  says  that  it  is  a  disputed  point 
how  far  ergot  and  other  fungi  may  be  concerned  in  the  production 
of  the  disease. 

Climatology. — It  occurs  in  the  Punjaub  and  the  North-West 
Provinces  of  India,  and  in  Europe. 

Pathology  and  Morbid  Anatomy. — Not  known. 

Symptomatology. — -The  affected  persons  become  very  giddy,  and 
stagger  about  as  though  drunk,  and  at  the  same  time  suffer  from 
violent  tremblings  in  the  arms,  legs,  and  tongue,  impairment  of 
vision  with  dilated  pupils,  green  vision,  great  prostration,  and  in 
some  cases  vomiting.  Sometimes  there  is  a  sense  of  burning  heat 
in  the  mouth  and  throat,  and  a  small  irregular  pulse. 

Diagnosis. — The  diagnosis  may  be  effected  by  considering  the 
symptoms  and  examining  the  bread,  when  the  starch  granules  of 
Lolium  may  be  seen. 

Prognosis. — The  disease  does  not  end  fatally. 


PASPALTSMUS 


TOO 


Treatment. — Castor  oil  must  be  given  to  remove  the  poison,  and  at 
the  same  time  stimulants  must  be  used  to  counteract  the  collapse. 

Prophylaxis. — Breadjshould  not  be  made  with  the  seeds  of  Lolium 
temulentum. 

Paspalismus. 

Paspalismus  is  an  intoxication  caused  by  eating  bread  made  from 
flour  derived  in  part  from  the  seeds  of  P  asp  alum  scrobiculatum 
Linnaeus. 


Fig.  16. — Paspalum  scrobiculatum  Linnaeus. 
Seeds  show  separately  at  the  top  of  the  illustration. 


History, — Poisoning  by  Paspalum  scrobiculatum  occurs  in  India, 
where  it  was  reported  as  far  back  as  1879,  and  probably  was  known 
earlier. 

^Etiology. — Some  authorities  doubt  the  genuineness  of  this 
disease,  for,  as  Waddell  points  out,  the  symptoms  are  so  like 
loliismus  that  it  is  quite  possible  that  some  mistake  may  be  made 
as  to  the  causation. 


2oo  POISONOUS  FOOD 

Two  varieties  of  Paspalum  scrobiculatum  are  known  in  India — 
viz.,  the  sweet,  which  is  called  '  pechadi,'  or  '  goraharik/  and  is  said 
to  be  wholesome;  and  the  bitter,  which  is  called  '  dhome,  majara 
harik  '  or  '  mana  kodra,'  and  is  considered  to  be  poisonous.  The 
poison  appears  to  reside  for  the  most  part  in  the  testa,  but  the 
exact  poisonous  principle  is  not  known.  Barry  points  out  that 
the  seed  is  liable  to  the  attacks  of  fungi,  and  that  perhaps  the 
poisoning  is  really  due  to  these  parasites.  It  is  clear  that  the 
whole  subject  requires  revision. 

Symptomatology. — The  symptoms  are  vertigo,  impairment  of 
vision,  apparent  intoxication,  muscular  tremors,  feeble  pulse,  cold 
clammy  skin,  dysphagia,  delirium,  narcosis,  ending  at  times  in  death. 

Diagnosis. — This  must  be  mainly  from  poisoning  due  to  Lolium, 
which  can  only  be  done  by  making  inquiries  as  to  the  seeds  from 
which  the  flour  is  prepared. 

Prognosis. — This  appears  to  be  on  the  whole  good,  though  fatal 
cases  have  been  recorded. 

Treatment. — Similar  to  loliismus. 

Prophylaxis.- — Avoid  the  seeds  of  the  grass  in  making  flour. 

Atriplicismus. 

Atriplicismus  (Matignon,  1898)  is  an  intoxication  said  to  be  caused 
by  the  ingestion  of  certain  species  of  Atriplex  (Linnaeus),  especially 
Atriplex  littoralis  L.  and  A.  angustissima  vel  serrata. 

History. — Atriplicismus  was  first  described  by  Matignon  in  North 
China  (Pekin)  in  1898,  but  he  leaves  the  subject  open  to  some  doubt. 

Climatology.- — The  disease  is,  as  far  as  is  known,  confined  to  China. 

/Etiology.- — In  some  way  the  disease  is  connected  with  Atriplex 
serrata  (Chenopodiaceae),  which  grows  as  a  weed  in  the  courts, 
gardens,  and  along  the  walls  of  the  houses  of  Pekin,  and  is  eaten 
by  very  poor  people  either  uncooked  or  as  a  pancake. 

It  is  said  never  to  be  poisonous  if  well  washed,  and  if  the  red 
leaves  are  picked  out.  But  Matignon  drew  attention  to  the  fact 
that  a  small  insect  of  a  greenish-yellow  colour  is  found  on  the  plant. 
It  is  possible  that  the  disease  may  be  due  to  this  insect,  because 
Megnin  found  that  Holothyrus  coccinella  Gervais,  a  mite  found  in 
Mauritius  and  the  Malay  Archipelago,  causes  severe  inflammation  of 
the  part  touched.  This  insect  may  be  carried  by  the  hand  to  the 
mouth.  Laveran  thinks  that  the  people  get  the  thumb  and  forefinger 
infected  while  plucking  the  herb,  and  that  it  is  by  the  hand  that  the 
disease  is  carried  to  the  mouth.  The  aetiology  is,  therefore,  extremely 
doubtful,  and  it  may  be  either  an  animal  or  a  vegetal  poisoning. 

The  predisposing  cause  is  scarcity  of  food,  which  compels  the 
poorer  classes  to  use  some  substitute  for  the  usual  cereals.  Hence 
in  Pekin  in  1895,  while  the  Japanese  War  was  proceeding,  there 
were  a  number  of  cases  among  beggars.  Women  suffer  more  than 
men,  and  the  young  and  the  old  are  specially  attacked. 

Morbid  Anatomy.— The  pathology  and  morbid  anatomy  are  quite 
unknown. 


ATRIPLTCTSMUS  201 

Symptomatology. — The  disease  begins  suddenly  without  prodro- 
mata,  some  ten  to  twenty  hours  after  the  plant  has  been  eaten. 
The  tips  of  the  fingers  and  the  back  of  the  hands  begin  to  itch, 
though  sometimes  the  irritation  may  be  at  first  limited  to  the  thumb 
and  forefinger.  The  affected  parts  soon  become  painful,  swollen, 
cyanosed,  and  cold,  while  the  pain  and  swelling  spreads  up  the 
hands  on  to  the  forearms.  The  face  and  eyelids  itch,  and  in  due 
course  become  swollen,  and  the  nose  becomes  cyanosed  and  cold. 
Sensibility  to  touch  is  diminished  in  the  affected  parts,  but  much 
increased  to  heat  and  to  the  sun's  rays.  Bullae  and  ulcers  may 
appear  on  the  affected  parts,  the  latter  often  giving  rise  to  keloid 
scars.  There  is  considerable  itching.  Ecchymoses  may  appear  in 
various  parts  of  the  body.  Gangrene  of  the  fingers  may  also  occur. 
The  general  health  of  the  patient  is  not  much  affected. 

Diagnosis. — Atriplicismus  may  require  to  be  diagnosed  from 
Raynaud's  disease  and  erythromelalgia,  but  there  should  be  no 
difficulty,  because  in  the  former  there  is  no  oedema,  and  in  the 
latter  there  is  redness  as  well  as  oedema. 

Treatment. — The  treatment  is  symptomatic,  and  consists  in 
applying  anodynes  and  cold  compresses  locally,  and  giving  purga- 
tives and  disinfectants,  such  as  salol,  internally.  Good  food  and 
good  hygiene  are  also  requisite. 

Prophylaxis. — The  aetiology  must  be  settled  before  definite  rules 
for  prophylaxis  can  be  given. 

Fabismus. 

Synonyms. — Favism,  II  Favismo,  Bohnenkrankeit. 

Definition. —Fabismus  is  a  disease  attributed  to  the  eating  of 
fresh  beans  (Vicia  faba)  or  to  the  scent  of  the  flowers  thereof  when 
in  blossom. 

Historical. — It  has  been  known  for  many  years  in  Sardinia,  and 
has  been  carefully  studied  by  Fermi  in  1905,  and  then  by  Frongia 
in  1907,  followed  by  Zoja  in  1914,  and  Gasparrini  in  1915. 

/Etiology. — The  actual  cause  is  unknown,  but  it  is  associated 
with  the  period  of  the  year  when  the  bean  is  ripening.  It  seems 
to  appear  only  in  certain  families,  and  there  is  a  personal  idio- 
syncrasy, and  no  immunity  is  confirmed  by  an  attack  in  sus- 
ceptible persons,  who  may  have  repeated  seizures.  It  occurs  in 
Sardinia,  and  it  is  suggested  that  it  may  be  found  in  other  Mediter- 
ranean countries. 

Symptomatology. — Within  a  few  hours  of  eating  the  beans  or 
of  being  exposed  to  the  scent  of  the  flowers  an  acute  febrile  attack 
associated  with  marked  blood  destruction  sets  in.  The  red  cells 
fall  to  2,000,000  per  cubic  millimetre,  and  the  haemoglobin  to 
20  per  cent.,  and  icterus  sets  in,  with  liver  tenderness,  but  no 
enlargement  of  that  organ  or  of  the  spleen.  Bile  may  be  vomited 
and  passed  in  the  motions,  while  haemoglobin,  urobilin,  and  indican 
are  found  in  the  urine.  Children  die  in  a  few  days,  but  adults 
recover  quickly. 


202  POISONOUS  FOOD 

Diagnosis. — This  is  made  by  noting  the  period  of  the  year  and 
by  tracing  the  history  of  the  ingestion  of  beans  or  the  smelling  of 
the  flowers,  and  also  by  the  family  and  geographical  incidence. 

From  malaria  it  is  diagnosed  by  the  absence  of  the  parasites  and 
the  negative  reaction  as  regards  complement  deviation  with  malarial 
antigen. 

From  quinine  hemoglobinuria  it  may  be  recognized  by  the  absence 
of  a  history  of  the  drug  being  taken. 

Treatment. — Apparently  there  is  little  known  under  this  heading, 
which  obviously  calls  for  the  administration  of  calcium  salts  (see 
Chapter  XLL,  p.  1213). 

Prophylaxis. — Avoid  eating  raw  or  cooked  fresh  beans  in  Sardinia, 
and  avoid  the  scent  of  the  flowers.  As  the  attacks  recur  it  would 
be  interesting  if  someone  would  try  the  administration  of  calcium 
salts  to  susceptible  people  living  in  Sardinia  during  the  dangerous 
period  of  the  year. 

Fagopyrismus. 

White  animals  fed  upon  buckwheat  and  exposed  to  the  sun 
develop  erythematous  lesions  of  the  skin  and  nervous  symptoms. 

REFERENCES. 

Dieudonne  and  Boldnan  (1909),  'Food  Poisoning,'  New  York,  and  Jordan 
(191 7),  '  Food  Poisoning,'  Chicago,  are  useful  small  books  with  references. 

Fuguismus. 

Scheube     (1903).     Diseases     of     Warm     Climates.     (English     translation.) 
(1915)  Indian  Medical  Gazette. 

Lathyrismus. 

Buchanan  (1898  and  1899).     Journal  of  Tropical  Medicine. 

Irving  (1857).     Indian  Annals  of  Medical  Science,  vi.  424-434. 

Kirk  (1858).     Ibid.,  vii.  144-152. 

Rho  (1914).     Mense's  Tropenkrankheiten,  ii.     Leipzig. 

Scheube  (1903).     Loc.  cit. 

Sheeman  (1837).     Rambles  and  Recollections  of  an  Indian  Official,  i.  134. 

Vaughan  (1898).     Twentieth-Century  Practice  of  Medicine,  xiii.  72-76. 

Loliismus. 

Cordier  (1820).     London  Medical  Repository,  xiii.  260. 
Freeman  (1903).     Proceedings  of  the  Royal  Society,  Ixxi.  27. 
Smith  (1905).     Taylor's  Medical  Jurisprudence,  ii.  765. 
Waddell  (1904).     Lyon's  Medical  Jurisprudence  for  India    p.  585. 

Paspalismus. 

Waddell  (1904).     Loc.  cit.,  pp.  586-587. 
Watt  (1895).     Indian  Medical  Gazette. 

Atriplicismus. 
Dragendorf  (189S).     Heilpflanze,  pp.  196-197. 
Scheube  (1903).     Loc.  cit.,  pp.  328-330. 

Fabismus. 

Frongia  (1907).     Gazctta  degli  Ospedale,  22,  vii. 
Gasbarrini  (1915).     Malaria,  vi.,  January  to  Februarv. 
Zoja  (1914).     Ibid.,  v.,  January  to  February. 


CHAPTER  XIV 

VENOMOUS  ANIMALS:  PROTOZOA  TO 
ARTHROPODA 

Protozoa — Coelenterata — Echinodermata — Platyhelmia — Nemathelminthes — 
Arthropoda  —  Arachnida  —  Scorpionidea  —  Aranea — Acarina — Chilopoda 
— Hexapoda  —  Anopleura  —  Hemiptera  —  Hymenoptera  —  Lepidoptera 
— Diptera — Coleoptera — Mollusca — References. 

VENOMOUS  ANIMALS. 

Many  species  belonging  to  the  various  classes  and  orders  of  the 
animal  kingdom  possess  glands  which  secrete  chemical  substances 
injurious  to  man  and  the  higher  animals.  The  exact  nature  of 
these  chemical  substances  is  but  little  understood  at  present, 
though  of  late  years  much  advance  has  been  made  in  the  knowledge 
of  their  action,  which  seems  to  be  of  a  nature  similar  to  that  of 
bacterial  toxins. 

It  will  be  best  to  consider  these  venomous  animals  i  the  order 
of  their  zoological  classification. 

PROTOZOA. 

Rosenau  and  his  collaborators  have  succeeded  in  produc- 
ing a  malarial  paroxysm  in  a  healthy  man  by  injecting  blood- 
scrum  taken  from  a  malarial  patient  during  the  cold  stage  of  the 
fever,  and  previously  filtered  through  a  Pasteur-Chamberland 
filter.  Casagrandi  and  De  Blasi  have  also  described  a  hemo- 
lytic toxin,  concerning  which  more  will  be  said  when  malaria 
is  discussed. 

Laveran  and  Mesnil  have  shown  that  Sarcocystis  tenella  produces 
a  toxin,  sarcocystin,  of  which  o-l  milligramme  will  kill  i  kilogramme 
of  rabbit  with  choleraic  symptoms,  while  a  less  dose  will  produce 
fatal  cachexia.     It  is,  however,  less  toxic  to  other  animals. 

CCELENTERATA. 

The  Coelenterata  include  anemones,  corals,  and  jelly-fishes,  which 
are  capable  of  stinging  by  means  of  certain  special  cells  called  cnido- 
blasts,  which  enclose  nematocysts — i.e.,  little  sacs— the  invaginatcd 
neck  of  which  is  continued  into  a  long,  hollow,  spirally  coiled  fila- 
ment, surrounded  with  poisonous  fluid.     When  stimulated,  these 

203 


204  VENOMOUS  ANIMALS:  PROTOZOA   TO  ARTHROPOD  A 

cysts  explode,  and  the  filament  is  ejected  and  pierces  the  skin  of 
the  animal  attacked,  and  so  introduces  the  poison. 

Zoantharia.-  -Stings  from  anemones  cause  itching  and  burning  and 
skin  eruptions.  In  its  worst  form  this  is  exhibited  in  la  maladie  des 
plongeurs  (pecheurs  d'eponges)  of  the  Mediterranean.  According  to 
Dr.  Skevos  Zervos,  the  first  symptoms  are  itching  and  intense  burn- 
ing in  the  place  where  contact  with  the  anemone  has  taken  place. 
A  papule  then  appears,  surrounded  by  an  area  which  at  first  is 
red,  but  may  become  blue  and  finally  black,  and  may  spread  over 
the  surrounding  skin  to  a  distance  proportional  to  the  virulence  of 
the  poisoning.  The  skin  sloughs,  and  leaves  a  suppurating  ulcer. 
Dr.  Zervos  has  produced  the  symptoms  of  this  disease  in  a  dog 
by  rubbing  an  actinia,  held  in  forceps,  along  its  abdomen. 

C.  Richet  has  separated  two  poisonous  principles  from  Anemone 
scultatus — viz.,  thalassin  and  congestine.  Thalassin  is  not  very 
toxic,  producing  cutaneous  redness,  intense  congestion  of  mucous 
membranes,  pruritus,  and  sneezing.  Congestine  is  much  more  viru- 
lent than  thalassin,  for  a  dose  of  2  milligrammes  per  kilogramme 
will  kill  a  dog  in  twenty-four  hours.  Thalassin  is,  however,  antago- 
nistic to  congestine,  for  a  dog  inoculated  with  the  former  will  resist 
an  otherwise  mortal  dose  of  the  latter. 

The  application  of  fat  to  the  skin  is  said  to  be  a  preventative  to 
the  venomous  action  of  the  anemone. 

Millepora. — Jones  has  described  an  acute  erythema,  with  severe 
pain,  followed  by  papules,  pustules,  and  desquamation,  as  the 
result  of  stings  by  the  hydroids  of  the  hydrocoralline  millepores 
{Millepora  alcicornis,  M.  complanata,  and  M.  verrucosa)  in  Malaya, 
where  the  corals  are  known  as  '  Karang  gatal,'  or  itchy  corals. 

Trachymedusae. — The  jelly-fishes  of  European  waters,  such  as 
Rhizosloma  pulini  of  the  Mediterranean  and  R.  cuvieri  of  the 
English  Channel,  are  well  known  to  cause  local  redness,  swelling, 
and  urticarial  eruptions. 

The  jelly-fishes  of  the  tropics  produce  the  same  symptoms,  but 
with  1  reater  severity.  The  pain  is  agonizing,  and  there  is  collapse, 
with  local  swelling  and  redness. 

The  treatment  is  to  give  stimulants  internally,  and  to  apply 
alkalis,  such  as  dilute  ammonia,  to  the  affected  area.  Usually 
recovery  is  (puck,  and  there  are  no  after-effects. 

Meyer  describes  a  case  of  poisoning  due  to  the  well-known 
Physalia  pelagica  (the  Portuguese  man-of-war),  in  which  there  was 
severe  inflammation  and  fever.  A  similar  ease  caused  by  Cyanea 
capillata  has  been  recorded  by  Forbes. 

Porter  and  Richet  obtained  a  liquid  from  Physalia  containing  an 
active  principle,  hypnotoxin,  which,  when  injected  into  animals, 
caused  somnolence  and  finally  death,  due  t<>  cessation  of  respiration. 


NEMATHELMINTHES  205 

ECHINODERMATA. 

The  Echinodermata  possess  poison  glands  which  supply  a  venom  to  certain 
modified  spines,  but  this  only  affects  small  animals. 

The  Cuvierian  organs  of  certain  Polynesian  species  of  the  holothurians 
(allied  to  Holothuria  avgus)  are  said  to  cause  inflammation  of  the  skin,  and,  ii 
any  of  the  secretion  gets  into  the  eye,  even  blindness. 

The  spines  of  the  common  sea  urchin  of  the  Red  Sea  are  poisonous,  causing 
painful  wounds,  which  require  a  long  time  to  heal. 

PLATYHELMIA. 

Dibothriocephalus  lotus,  which  causes  a  profound  anaemia,  is  sus- 
pected to  secrete  some  form  of  poison,  and,  indeed,  this  theory  is 
supported  by  certain  experiments  of  Sehaummn  and  Tallquist. 
These  investigators  found  that  if  the  worms  were  subjected  to 
tryptic  digestion,  and  then  mixed  with  food  and  given  to  dogs  by 
the  mouth,  or  extracted  with  normal  salt  solution  and  injected 
hypodermically,  an  exhaustion  which  ended  in  death  was  some- 
times produced.  In  one  case  there  was  a  great  reduction  of  the 
red  blood-corpuscles.     Rabbits,  however,  were  not  affected. 

Tcvnia  saginata  has  been  investigated  by  Messineo  and  Calamida, 
who  consider  that  they  have  found  evidence  of  the  presence  of 
a  poison  which  can  be  obtained  by  pulverizing  the  taenia  with  sand 
and  extracting  with  normal  saline  solution.  This  extract  was  then 
filtered  and  injected  into  animals,  but  the  symptoms  were  not 
characteristic.  Picou  and  Ramond  consider  that  the  extracts  they 
obtained  showed  a  decided  bactericidal  action. 

On  the  other  hand,  the  rupture  of  an  echinococcus  cyst  is  well 
known  to  produce  symptoms  of  po:soning,  but  the  chemical  nature 
of  the  poison  is  not  known.  The  symptoms  in  man  are  urticaria, 
if  the  dose  is  small;  peritonitis  and  severe  cardiac  symptoms, 
leading  to  fatal  collapse,  if  the  dose  is  large.  Injected  into  animals, 
the  liquid  acts  as  a  cardiac  poison  causing  death  by  stoppage  of 
the  heart  in  diastole,  together  with  various  other  symptoms,  such 
as  a  fall  of  the  blood-pressure  and  temperature. 

NEMATHELMINTHES. 
"  Ascarides  produce  a  volatile  body  with  a  peculiar  and  disagreeable 
odour,  very  irritating  to  the  mucous  membranes,  especially  to  the 
conjunctiva.  This  odour  is  most  noticeable  in  making  post-mortems 
upon  persons  suffering  severely  from  these  worms.  Arthus  and 
Chanson  have  injected  rabbits  with  the  liquid  squeezed  out  of  living 
human  ascarides,  and  produced  collapse  and  death  within  ten 
minutes  of  a  dose  of  2  c.c. 

Cattaneo  obtained  a  substance  toxic  to  guinea-pigs  by  allowing 
ascarides  to  live  in  sterile  broth.  Cao,  J  amines.  Mandoul,  and 
Boycott,  however,  failed  to  obtain  any  evidence  of  the  toxicity  "l 
ascarides. 

With   regard   to   Ancylostoma  duodenale,  there   has  been   much 


2o6       VENOMOUS  ANIMALS  :  PROTOZOA   TO  ARTHROPOD  A 

discussion  as  to  whether  it  produces  a  toxin  or  not.  The  experi- 
ments of  Whipple  and  Preti  seem  to  establish  the  presence  of  a 
hemolytic  principle  in  the  alimentary  canal  of  the  worm,  and  those 
of  Loeb  and  Smith  of  a  principle  inhibiting  the  coagulation  of  the 
blood  and  secreted  by  the  cephalic  glands,  but  these  substances 
appear  to  be  of  importance  to  the  worm  for  the  purposes  of  digestion, 
and  not  to  be  of  sufficient  strength  to  act  upon  the  host.  According 
to  Alessandrini,  however,  the  cephalic  glands  secrete  a  true  toxin. 
The  evidence  which  has  been  gathered  together  points  also  to  the 
possibilitv  of  the  toxicity  of  the  ankylostomes  being  partly  due  to 
the  absorption  of  bacteria  or  their  products  into  the  circulation  of 
the  host  through  lesions  in  the  intestinal  mucosae  caused  by  the 
bites  of  the  worms. 

ARTHROPODA. 

The  Phylum  Arthropoda  includes  a  number  of  types,  which  are 
characterized  by  their  capability  of  stinging.  The  forms  which 
we  are  about  to  describe  occur  in  Class  III.,  Arachnida,  Class  V., 
Chilopoda,  and  Class  VI.,  Hexapoda,  of  the  classification  given  in 
Chapter  XXVIII. 

Class  III.  The  Arachnida. 

As  the  definition  and  classification  of  this  class  is  given  in 
Chapter  XXVIII.,  we  have  only  to  consider  the  recognition  of 
the  three  orders  with  which  we  are  concerned  here : — 

I.  Abdomen  segmented — 

Tail  stout  and  armed  at  the  end  with  a  sting.     (Scor- 
pionidea.) 

II.  Abdomen  unsegmented — 

(a)  Abdomen  connected  with   the   cephalothorax   by   a 

short  narrow  stalk.     (Aranea.) 
(/>)  Abdomen  fused  with  the  cephalothorax.     (Acarina.) 

i.  Scorpionidea. 

Scorpions  abound  in  the  tropics,  where  they  grow  to  a  large  size, 
and  are  much  feared  because  of  the  poisonous  properties  of  their 
sting.  The  method  of  striking  is  to  bring  the  tail  forward  over  the 
body  of  the  scorpion,  so  that  the  curved  spine  on  the  last  segment 
(telson)  of  the  tail  penetrates  into  the  skin  and  inflicts  the  wound. 
On  either  side  of  this  curved  barb  is  an  opening  through  which  the 
duct  from  a  poison  gland  discharges  the  venom. 

It  is  probable  that  the  poison  of  different  kinds  of  scorpions 
differ  qualitatively  and  quantitatively,  but  on  this  subject  little  is 
known.  Certainly  the  sting  of  the  small  European  scorpion 
(Euscorpius  europceus)  has  but  slight  action,  causing  only  local  pain, 
redness,  and  swelling,  while  the  larger  one  of  South  Europe  {Buthus 
occitanus)  causes  severe  pain  and  phlegmonous  swelling  of  the  whole 
extremity,  and  such  remote  symptoms  as  vomiting,  faintness, 
tremors,  and  cramps  in  muscles,  while  the  larger  tropical  species 


SCORPIONIDEA  207 

kill  not  merely  children,  but  even  adults.  According  to  Cararoz, 
as  many  as  200  persons  die  annually  from  scorpion-sting  in  the 
neighbourhood  of  Durango  in  Mexico.  In  Africa  scorpion-stings 
are  of  frequent  occurrence,  but  death  is  rare. 

Historical  -  -Maupertuis  in  1731  and  Redi  in  1779  appear  to  have 
been  the  first  to  study  the  effects  of  scorpion-venom  by  experiments, 
though  the  ancients  were  well  acquainted  with  the  sting  and  its 
effects,  and  had  woven  wonderful  legends  as  to  the  origin  of  these 
animals.  Redi  experimented  upon  a  pigeon  and  a  dog,  but  the  real 
study  of  the  venom  began  with  Guyon  1864,  Paul  Bert  1865, 
Delange  1866,  and  Valentin  in  1876,  and  was  followed  up  by 
Joyeaux-Lanine  in  1883  and  many  others.  A  full  literature  is 
given  in  Faust's  '  Die  Tierischen  Gifte.' 

Classification. — This  is  unsettled,  but  Pocock  gives  the  fol- 
lowing : — 

I.  Pentagonal  cephalothoracic  sternum — 

(a)  Single  pedal  spur.     (Pandinoidae  Thorell,  1876.) 
{b)  Two  pedal  spurs.     (Vejovidae  Thorell,  187!).) 

II.  Triangular  cephalothoracic  sternum — • 

With  two  pedal  spurs,  of  which  the  anterior  is  bifur- 
cated.    (Buthidse  Simon,  1879.) 

III.  Short,  wide,  antero-posteriorly  compressed  cephalothoracic 
sternum — 
Two  pedal  spurs.     (Bothriuridse  Simon,  1880.) 

Geographical. — Scorpions  occur  a  1  over  the  world,  but  the  largest 
and  most  dreaded  are  found  in  the  tropics.  They  live  under  stones, 
under  the  bark  of  tries,  in  sand,  and  also  in  nouses,  which  they 
leave  at  dusk.     Some  of  the  best  known  are: — 

t.  Euscorftius  carpathicus  Linnaeus,  Vejovidae  (3  to  3-5  centi- 
metres long) :  Italy,  Tyrol,  South  France. 

2.  Buthus  occitanus  Amoreux,  Buthidse  (8-5  centimetres  long): 
Italy,  Greece,  Spain,  North  Africa. 

3.  Buthus  afer  Linnaeus,  1764(16  centimetres  long):  Africa,  Asia. 

4.  Buthus  quinquestriatus  Hemprich  and  Ehrenbcrg,  1828:  Upper 
Egypt  and  the  Sudan. 

5.  Scorpio  maurus  Linnaeus,  1758:  Egypt,  Tunis. 

(>    Prionurus  citrinus  Hye,  1828:  Desert  nearCairoand  Alexandria. 

7.  Prionurus  amoureuxi  Savigny:  Sudan. 

8.  Androctonus  funestus  Hemprich  and  Fhrenberg,  1828  (9  centi- 
metres long):  North  and  Middle  Africa. 

g.  Heterornetrus  in-ius  Geer,  1778:  Ceylon. 

Anatomical. — The  body  of  the  scorpion  is  divided  into  a  cephalo- 
thorax  or  prosoma,  behind  which  comes  an  abdomen  subdivisible 
into  a  broader  portion,  or  mesosoma,  and  a  narrower,  metasoma, 
with  five  segments,  which  is  popularly  called  the  tail.  At  the 
end  of  this  metasoma  there  is  a  postanal  carved  spine,  called  the 
telson,  inside  which  lies  the  paired  poison  gland.     The  appendages 


2o8       VENOMOUS  ANIMALS:  PROTOZOA   TO  ARTHROPODA 


of  the  scorpion  are:  I.  Small  three-jointed  chelicerae,  which  are  used 
for  hold'ng  prey.  2.  Large  six-jointed  pedipalpi,  which  are  used 
for  seizing  prey.     3-6.  Four  pairs  of  seven-jointed  walking  legs. 

Scorpions  seize  their  prey  with  the  pedipalpi,  hold  them  close  to 
the  mouth  by  means  of  the  chelicerae,  and  sting  them,  if  necessary, 
by  bringing  the  metasoma  forwards  over  the  mesosoma  and  cephalo- 
thorax,  and  inserting  the  tip  of  the  telson  well  into  the  animal's 
body,  and  allowing  it  to  remain  there  until  the  poison  has  had  time 
to  act.  The  telson  consists  of  two  portions — -a  broad  swollen  part 
(the  ampulla)  and  a  narrow  portion  (the  spine),  near  the  extremity 
of  which  are  two  small  openings  for  the  escape  of  the  venom. 

The  two  poison  glands  lie 
inside  the  ampulla,  one  on 
each  side  of  the  middle  line. 
Each  gland  is  covered  with 
a  sheet  of  muscle  on  its 
mesial  and  dorsal  aspects. 
This  muscle,  which  is  called 
by  Wilson  '  the  compressor,' 
is  inserted  by  its  edge 
mesially  along  the  ventral 
inner  surface  of  the  wall  of 
the  telson,  and  by  a  broader 
insertion  laterally.  The 
compressor  muscle  squeezes 
the  poison  out  of  the  gland, 
along  the  duct,  and  through 
the  opening  in  the  spine  into 
the  victim.  The  epithelium 
of  the  gland  shows  three 
distinct  types  of  cells — the 
mucous  cell,  the  fine  oxy- 
phile  granular  cell,  and  the 
cell  with  very  large  granules. 
The  Venom.  —  Scorpion- 
venom  is  a  clear,  faintly 
acid  fluid  of  a  somewhat 
thick  or  oily  consistence,  and  possessed  of  an  extremely  faint 
yellowish  colour.  It  contains  no  structural  elements,  but  crystals 
form  in  it  if  evaporation  takes  place.  On  an  average  it  contains 
about  28  per  cent,  of  solids. 

Wilson  gives  the  following  figures  for  the  venom  of  Buthus  quiii- 
q  uc  st  rial  us  : — 

Spei  iii.   gravity  .  .  .  .  .  .  . .  .  .      1092 

Solids       ..  ..  ..  ..  ..  ..  20*3  per  cent. 

Ash  8-4 

Protcids  form  part  of  the  solids,  and  it  is  believed  that  the  active 
principle  is  either  a  nucleo-proteid,  acid  albumin,  or  a  primary  pro- 
teose.    The  ciiccts  described  by  various  authors  would,  however, 


Fig.  17. — Heteromelrus  indus  (Beer). 
(A  scorpion  commonly  found  in  Ceylon.) 


SCORPIONIDEA  209 

indicate  the  presence  of  toxins,  one  resembling  the  neurotoxin  of 
snake-venom,  and  another  a  haemolysin,  for  Kyes  has  described  a 
typical  lec.ithide  producing  haemolysis  like  the  lecithides  of  cobra- 
venom.  Calmctte  has  also  shown  that  the  venom  of  Buthus  occi- 
tanus  is  neutralized  by  cobra  antivenene.  There  would,  therefore, 
appear  to  be  some  resemblance  between  scorpion-venom  (or,  at  all 
events,  the  venom  of  Buthus  occitanus)  and  cobra-venom.  It  is, 
however,  impossible  to  make  any  definite  statements,  as  the 
condition  of  our  knowledge  with  regard  to  this  poison  is  most 
unsatisfactory. 

Iwano  says  that  the  poison  is  a  protein,  of  which  there  are  two 
kinds,  one  soluble  in  water  and  the  other  in  dilute  acids,  and  from 
these  crystalline  bodies  can  be  prepared.  Lecithin  and  cholesterin 
are  also  present  in  the  venoms,  which  can  be  destroyed  by  pepsin 
and  trypsin,  permanganate  of  potash,  and  calcium  hypochlorite. 
It  seems  to  be  very  like  snake-venom,  and  it  is  time  that  researches 
on  modem  lines  were  made. 

Joyeux-Laffine  thought  that  the  venom  first  increased  reflex 
action,  and  then  caused  paralysis  of  the  nervous  system,  and  that 
death  was  due  to  a  curari-like  poisoning  of  the  end-plates  of  the 
respiratory  muscles;  but  Valentin  found  these  were  quite  intact, 
and  that  the  muscles  contracted  well  when  their  nerves  were 
stimulated  by  electrical  or  mechanical  stimuli. 

As  regards  the  action  on  the  blood,  coagulation,  haemorrhage  due 
to  change  in  the  capillary  walls,  and  haemolysis  have  been  observed, 
as  well  as  agglutination  of  the  red  corpuscles,  which  are  said  to  form 
viscous  masses,  and  thus  to  block  the  bloodvessels  by  embolism. 

These  observations  were  made  by  Jousset  de  Bellesme  on  Lilla 
viridis,  a  frog  remarkable  for  its  lack  of  pigment,  and  therefore 
specially  suitable  for  such  a  purpose.  If  confirmed,  they  would 
show  the  presence  of  fibrin  ferment,  haemorrhagins,  haemolysins,. 
and  agglutinins  in  scorpion-venom,  and  would  make  it  resemble 
very  closely  snake-venoms.  Sanarelli,  however,  was  not  able  to 
observe  any  change  in  the  red  cells  beyond  haemolysis,  which  he 
saw  in  the  blood  of  fishes,  amphibia,  and  birds. 

In  conclusion,  we  may  therefore  assume  the  presence  of  a  neuro- 
toxin acting  on  the  central  nervous  system,  and  the  presence  of 
haemolysins ,  until  further  experiments  give  us  more  exact  information. 

Minimum  Lethal  Dose. — The  minimum  lethal  doses  for  dry 
Buthus  afer  venom  is,  according  to  Calmette,  0-05  milligramme  for 
white  mice,  and  0-5  milligramme  for  rabbits. 

That  the  venom  must  be  very  toxic  for  small  animals  is  shown 
by  the  fact  that  the  minimum  lethal  dose  for  a  guinea-pig  is  0-3 
milligramme  per  kilogramme,  which  gives  a  toxic  value  of  10,000,000 
for  Buthus  quinquestriatus  /  but,  as  may  be  imagined,  the  toxicity 
of  different  venoms  varies  considerably,  and  the  difference  may  be 
not  merely  quantitative,  but  qualitative. 

Effects  of  the  Venom.— It  must  be  remembered  that  the  venom 
is  not  merely  a  means  of  defence  for  the  scorpion,  but  it  is  also  the 

M 


210       VENOMOUS  ANIMALS  :  PROTOZOA   TO  ARTHROPODA 

method  by  which  it  kills  its  prey,  which  usually  consists  of  small 
animals;  and,  further,  that,  in  order  to  be  toxic,  the  venom  must 
be  injected  subcutaneously  or  intravenously,  for  by  the  mouth  it 
is  harmless. 

When  experiments  are  performed  on  animals,  the  following 
symptoms  appear: — • 

i.  Local  irritation  and  pain. 

2.  Muscular  twitchings,  chiefly  of  the  head  and  neck. 

3.  Jumping  movements. 

4.  Lachrymation. 

5.  Increased  orbital,  nasal,  and  salivary  secretions. 

6.  Muscular  spasms,  especially  of  the  hinddimbs,  but  also  in  all 
muscles. 

7.  Erection  of  the  hairs. 

8.  Passage  of  liquid  faeces  (often  absent). 

9.  Erection  of  penis  and  emission  of  semen. 

The  venom  of  Scorpio  maurus  causes  death  in  small  birds  within 
two  minutes  to  half  an  hour  from  failure  of  the  respiration.  If 
the  venom  of  a  scorpion  is  placed  on  the  conjunctiva  of  a  rabbit, 
violent  ophthalmia  results. 

In  man,  the  symptoms  depend  upon  the  size  and  nature  of  the 
scorpion.  Thus,  the  sting  of  the  small  (3!  centimetres)  Euscorpius 
eiiropcens  causes  only  pain,  redness,  and  local  swelling,  whereas 
the  larger  tropical  scorpions  cause  very  intense  pain  of  a  burning 
character  radiating  from  the  skin,  associated  often  with  violent  con- 
vulsions, mental  disturbance,  and  hallucinations,  profuse  perspira- 
tion, and  secretion  of  saliva,  and  perhaps  vomiting.  The  pulse  is 
weak  and  quick,  and  the  respirations  hurried  and  shallow.  These 
symptoms  gradually  diminish  in  three  to  eight  hours,  and  by  about 
nineteen  to  twenty-four  hours  the  person  is  usually  normal.  This, 
however,  is  not  always  so,  for  death  may  ensue  due  to  collapse 
or  stoppage  of  the  respiration,  effects  which  are  more  likely  to 
happen  in  small  children  than  in  adults.  Thus,  Wilson  states 
that  the  mortality  in  children  under  five  is  60  per  cent,  for  Buthus 
qmnquestriatus,  but  the  mortality  diminishes  as  the  age  increases. 
Of  course  this  is  simply  due  to  the  greater  dilution  of  the  poison  in 
the  body  of  the  adult. 

In  addition  to  the  above  symptoms,  some  authors  have  described 
trismus,  but  it  is  probably  due  to  infection  with  the  bacillus  of 
tetanus.  The  erection  of  the  penis  noted  in  experiments  on  animals 
has  been  seen  in  man  by  Delange  and  Guyon  in  Algeria.  A  paralysis 
of  the  lingual  and  hypoglossal  nerves  has  been  noted  by  Posada- 
Arango.  Lymphangitis  and  adenitis  are  described  as  part  of  the 
local  effect  of  the  sting. 

The  above  symptoms  would  indicate  the  action  of  a  neurotoxin 
acting  upon  the  nervous  system,  and  causing  first  of  all  increased 
reflex  action  and  convulsions,  and  later  paralysis  of  the  medullary 
nuclei;  for  if  Valentin's  observations  are  correct,  there  are  no 
paralyses  of  the  motor  nerve-endings. 


ARAN  E  A  211 

Effect  on  the  Scorpion. — At  the  present  time  it  is  not  believed 
that  a  scorpion  commits  suicide  when  in  difficulties  by  stinging 
itself  in  the  head  with  its  own  sting,  because,  though  not  absolutely 
immune  to  its  own  venom,  it  possesses  a  high  degree  of  immunity 
against  it.  Accidental  but  not  intentional  wounding  of  an  indi- 
vidual by  its  own  sting  is  said  to  be  known. 

Immunity. — A  natural  immunity  exists  in  the  jerboa  (Jaculus 
jaculus  L.)  and  in  the  desert  rat  (Gerbillns  pyramidum  Geoffr.),  and 
a  partial  immunity  in  the  zerilla  (let onyx  libyca  Ehrenberg). 

According  to  Balfour,  fakirs  at  times  possess  an  acquired  im- 
munity, but  this  has  not  so  far  been  obtained  in  any  animal.  Cal- 
mette  has  reported  that  the  serum  of  a  horse  immunized  against 
cobra-venom  can  neutralize  the  venom  of  Buthus  occitanus — a  fact 
which  Metchnikoff  has  confirmed ;  but  Nicolle  and  Catouillard  have 
found  this  serum  useless  against  the  venom  of  the  Tunis  scorpion 
(Scorpio  maurus). 

Diagnosis. — The  history  of  the  case  and  the  single  puncture  on 
the  affected  part  makes  the  diagnosis  generally  easy. 

Prognosis. — If  an  adult  is  stung,  the  prognosis  is  good,  as  death 
is  known  to  be  rare,  but  not  so  in  children.  The  prognosis,  there- 
fore, varies  with  the  age,  and  can  be  judged  by  the  following  table 
from  Bray,  quoted  by  Wilson,  which  gives  the  deaths  at  Omdurman 
in  1902  as  follows: — 

Under  one  year  . .  .  .  .  .  .  .  .  .        5 

One  to  five  years        .  .  .  .  .  .        9 

Five  to  fifteen  years  .  .  .  .  .  .  .  .  . .        7 

Total        .  .  . .  ...  . .  ..21 

Deaths  of  adults,  however,  are  known,  but  generally  take  place 
in  a  few  days,  not  quickly. 

Treatment.— In  the  treatment,  the  first  thing  to  do  is  to  give 
a  full  dose  of  the  serum,  and  then  to  apply  a  proximal  ligature 
and  to  treat  the  wound  with  permanganate  of  potash,  as  described 
under  the  heading  of  Snake-Bite. 

Washing  and  bathing  with  a  weak  solution  of  ammonia  may  also 
be  tried,  and  stimulants  should  be  given. 

Colonel  Duke  recommends  that  5  to  10  minims  of  a  5  per  cent, 
solution  of  cocaine  be  injected  subcutaneously  close  to  the  sting  in 
an  adult,  and  1  to  5  minims  in  infants  and  children.  Eucaine  or 
stovaine  might  be  preferable,  and  can  be  imported  from  any 
chemist  in  sterile  capsules  ready  for  hypodermic  injection.  Simpson 
recommends  the  local  application  of  a  paste  of  ipecacuanha. 

2.  Aranea. 

The  Aranea,  or  spiders,  are  found  all  over  the  world,  but  by  far 
the  largest  are  in  the  tropics,  and  their  peculiarly  repulsive  appear- 
ance has  given  rise  to  numerous  fables,  both  ancient  and  modern, 
with  regard  to  their  poisonous  properties. 


212       VENOMOUS  ANIMALS:  PROTOZOA   TO  ARTHROPODA 

Historical.— The  study  of  spider-stings  may  be  said  to  be  modern, 
and  to  begin  with  Blackwell  in  1855,  but  it  was  Robert  in  1893  who 
gave  the  fundamental  data  concerning  these  poisons.  He  main- 
tains that,  in  addition  to  the  secretion  of  the  poison  gland,  there 
is  a  toxalbumin  which  permeates  every  portion  of  the  body  of  the 
animal,  and  in  some  species  of  animals  is  mixed  with  the  venom. 
He  considers  that  the  secretion  of  the  poison  gland  only  gives 
rise  to  local  symptoms,  and  that  the  general  symptoms  are  due  to 
this  toxalbumin,  and  that  it  is  because  of  this  admixture  in  Latro- 
dectus  that  the  bite  may  cause  severe  symptoms  and  even  death 
in  human  beings.  The  common  European  garden  spider  (Epeira 
diadema)  only  causes  local  irritation,  because  the  toxalbumin, 
though  present  in  the  body,  is  not  mixed  with  the  poison  of  the 
poison  gland.  He  also  describes  a  haemolytic  action  in  both  Epeira 
and  Latrodectus. 

Sachs  has  contributed  a  paper  in  which  he  carefully  studies  this 
hasmolysin,  which  he  calls  araclmolysin,  and  Wilson  has  recently 
written  an  excellent  monograph  on  the  spider-bites. 

Classification. — -Spiders  are  divided  into  two  suborders  as 
follows : — ■ 

I.  Spinning  organs  situate  far  anterior  to  the  anus.     Eleven 
tergal  plates  on  the  dorsal  surface.     (Mesothelae.) 
II.  Spinning  organs  situate  just  in  front  of  the  anus.     No 
tergal  plates  visible.     (Opisthothelae.) 

The  Opisthothelae  are  the  only  forms  which  concern  us,  and  they 
are  divided  into  tribes  as  follows : — ■ 

A.  Only  anterior  pair  of  spinning  organs  present.     (Megalo- 

morphse.) 

B.  Two  pairs  of  viramous  spinning  organs  present.     (Arachno- 

morphae.) 

The  Megalomorphae  include — 

I.  Without  large  maxillary  process  on  the  base  of  the  palp — 

1.  Feet  furnished  with  apical  tufts  or  pads  of  hair. 

(Aviculariidae.) 

2.  Feet  not  so  furnished.     (Ctenizidae.) 

II.  With  large  maxillary  process  on   the  base   of   the   palp. 
(Atypidae.) 
The  bird-eating  spiders  '  Mygale  '  come  under  the  Aviculariidae. 
The  Arachnomorphse  include: — 

The    Epeiridae    with    Epeira    diadema,    the    Theridiidae    with 
Latrodectus,  the  Lycosidae  with  the  Tarantula  spider. 

Geographical. — All  genera  of  spiders  appear  to  be  poisonous,  but 
the  most  important  are:  Latrodectus  mactans,  Chili;  L.  scelio, 
the  katipo  of  New  Zealand;  Theraphosa  avicidaria  L.,  South 
America;  T.  blondi  Latr. ;  T.  javanensis  Walck.;  Chiracanthum 
nutrix  Walck.;  Theridium  tredecim  guttatwm  F.,  France  and  Italy; 


A  RAN  E  A  213 

T.  lugubre  Koch,  Kara  kist  of  Russia ;  Segestria  perfida  St. ;  Chceto- 
pelina  olivacea ;  Lycosa  tarantula  L. ;  L.  singoriensis  Laxman; 
Kpeira  diadema  Walck. 

Anatomical. — The  body  of  the  spider  is  sharply  divided  into 
cephalothorax  and  abdomen.  The  pairs  of  appendages  are  six  in 
number: — (1)  The  two-jointed  chelicerae;  (2)  the  six-jointed  leg- 
like pedipalpi;  (3-6)  the  seven-jointed  legs.  The  poison  gland 
usually  lies  in  the  basal  joint  of  the  chelicera,  ensheathed  in  con- 
nective tissue,  inside  which  there  are  two  spirally  arranged  layers 
of  non-striped  muscle  surrounding  a  basement  membrane  which 
benrs  two  to  three  layers  of  polyhedral  cells,  surrounding  the  lumen 
of  the  acinus.  From  the  gland  the  duct  runs  forwards  into  the 
distal  hook-shaped  joint,  upon  the  apex  of  which  it  opens. 

The  Venom. — The  venom,  which  is  useful  to  the  spider,  enabling 
it  to  kill  the  small  animals  upon  which  it  lives,  is  an  oily,  trans- 
lucent, lemon-yellow-coloured  liquid,  with  an  acid  reaction  and  a 
hot,  bitter  taste.     It  has  proteid  reactions,  and  gives  the  xantho- 
proteic reaction.     It  is  difficult  to  obtain  it  in  any  quantity.     Wilson 
recommends  triturating  the  gland  with  distilled  water  (0-5  c.c.  being 
used  for  each  gland),  and  then  filtering,  when  an  extract  suitable  for 
experimental  purposes  is  obtained.     These  extracts  are  rendered 
harmless  by  heating  to  900  C,  and  the  active  principles  are  said 
not  to  dialyze.     The  chemical  peculiarities  and  the  active  principles 
of   the   venom  are  little   known.     Kobert,    as   has   already   been 
pointed  out,  considers  that  there  are  two  poisons: — (1)  A  toxin 
secreted  by  the  poison  gland,  and  only  causing  local  symptoms; 
(2)  a  toxalbumin  distributed    through  the  body  (not  originating 
from  the  poison  gland),  and  causing  general  symptoms.     The  first 
exists  alone  in  Lycosa  tarantula,  L.  singoriensis.     The  second  largely 
predominates  in  Latrodectus . 

Kobert  and  Sachs  have  found  and  studied  a  hsemolysin,  arachno- 
lysin,  in  the  venom  of  several  kinds  of  spiders,  and  Sachs  has  been 
able  to  immunize  a  guinea-pig  against  this  toxin,  and  produce  an 
active  serum.  Arachnolysin  acts  upon  the  red  cells  of  man,  rabbit, 
ox,  mouse,  and  goose,  but  not  on  those  of  the  horse,  dog,  sheep, 
and  guinea-pig. 

Spider-venom  is  also  said  to  increase  the  coagulability  of  the 
blood.  The  venom  of  Theridium  lugubre  is  believed  to  act  in- 
juriously on  the  isolated  frog's  heart,  even  when  diluted  to  1  in 
100,000,  but  it  is  not  known  whether  this  is  due  to  action  directly 
upon  the  heart-muscle  or  upon  the  local  nervous  apparatus.  The 
walls  of  the  capillaries  are  also  said  to  be  damaged  by  spider- 
venom,  and  to  allow  an  increased  amount  of  transudation,  and 
hence  the  hemorrhages  and  oedema  seen  about  the  wound.  It  is 
asserted  that  the  venom  acts  deleteriously  upon  the  mucous 
membrane  of  the  stomach  and  intestines,  causing  redness  and 
swelling,  and  even  haemorrhages,  which  perhaps  are  due  to  some 
attempt  at  excretion  of  the  poison  by  these  organs.  It  is  also 
thought  that  the  venom  acts  upon  the  central  nervous  system,  but 


2i4       VENOMOUS  ANIMALS  :  PROTOZOA   TO  ARTHROPODA 

whether  the  cramps  and  convulsions  are  really  due  to  action  of  the 
poison  upon  the  nerve  cells,  or  merely  to  the  altered  blood  con- 
ditions, has  not  been  decided. 

The  reader  is  particularly  asked  to  compare  these  actions  on  the 
nervous  system  (neurotoxin  ?),  on  the  mucosa  of  the  stomach,  on 
the  capillary  wall,  on  the  blood  and  red  cells,  with  the  venoms  of 
the  scorpion  and  of  the  snakes,  which  they  strongly  resemble. 

Acquired  immunity  can  be  produced  in  animals  by  injections  of 
non-lethal  quantities  of  venom. 

Minimum  Lethal  Dose.— The  minimum  lethal  dose  for  cats  is 
o-20  to  0-35  milligramme  of  the  dry  venom  per  kilogramme  of  the 
body-weight.  Dogs  are  less  sensitive,  and  hedgehogs  still  less, 
while  frogs  require  fifty  times  the  quantity  of  poison  which  will 
affect  warm-blooded  animals. 

Effects  of  the  Venom. — In  general,  the  symptoms  of  spider-bite 
rather  resemble  those  of  the  scorpion,  and  are  divisible  into  (1)  local, 
(2)  general.  Local  inflammation  is  generally  present,  but  may  be 
absent,  and  severe  pain  is  felt  at  the  site  of  the  wound.  The  general 
symptoms  are  those  of  collapse  coming  on  gradually,  with  some- 
times convulsions,  or  rarely  a  typhoidal  condition  ensues,  which  may 
remain  for  weeks.  Many  other  symptoms  may  also  be  noted,  such 
as  nausea,  rigors,  cold  sweats,  dyspncea,  fever,  delirium,  paralysis, 
and  coma  terminating  in  death.  Inflammation  of  the  stomach  and 
intestines,  coagulation  of  the  blood,  and  local  haemorrhages  and 
oedema,  are  the  principal  features  of  a  post-mortem  examination. 
The  symptoms  of  the  bites  of  the  different  spiders  will  now  be 
briefly  described. 

Bite  of  Latrodectus  mactans. — The  symptoms  of  this  bite  are  local 
pain,  which  does  not  appear  till  some  little  time  after  the  bite,  but 
becomes  agonizing,  and  may  last  for  a  couple  of  days.  In  addition, 
tetanoid  symptoms  may  set  in,  but  usually  end  in  recovery  in 
about  ten  days. 

Bite  of  Latrodectus  scelio. — This  is  the  katipo  spider  of  New 
Zealand.  The  symptoms  begin  in  about  thirty  minutes  with  the 
formation  of  a  white  vesicle  surrounded  by  a  red  halo,  and  severe 
pain  at  the  site  of  the  bite.  The  general  symptoms  include,  first, 
stiffness  of  the  muscles  about  the  mouth  and  jaw,  so  that  it  is 
difficult  to  open  the  mouth  or  to  speak,  and  impossible  to  swallow. 
The  pulse  becomes  very  slow  (12  to  14  to  the  minute),  and  there 
is  extreme  pallor  of  the  face  and  body,  with  coldness  of  the  ex- 
tremities, which  are  quite  flaccid.  Respiration  becomes  slower  and 
slower,  and  death  may  take  place  at  this  stage,  or  an  illness  lasting 
about  six  weeks,  and  somewhat  resembling  typhoid,  may  ensue, 
which  may  end  either  in  death  or  recovery. 

Bite  of  Theridiutn  lugubre.- — -This  bite  is  characterized  by  smart- 
ing pains,  no  redness  or  swelling,  cold  sweats,  restlessness,  dizziness, 
mental  anxiety,  depression,  vomiting,  cyanosis,  convulsions,  status 
typhosus,  and,  unless  improvement  sets  in,  death  in  three  days. 

Bite  of  Theraphosa  avicularia. — The  Theraphosae  come  under  the 


A  CARINA  215 

commoner  heading  of  Mygale,  and  cause  prolonged  inflammation 
and  extensive  cicatrization.  Theraphosa  javanensis  is  reported  to 
kill  men. 

Bite  of  Chcetopelina  olivacea.- — The  local  symptoms  are  great 
pain,  redness,  swelling,  but  whether  a  g  neral  effect  (curari-like 
poisoning  of  the  voluntary  muscles  and  death  from  stoppage  of 
respiration)  takes  place  is  very  doubtful. 

Bite  of  Lycosa  tarantula. — The  bite  of  this  spider  produces  wheals 
surrounded  by  a  red  areola,  but  no  general  symptoms  result,  and 
tarantismus  only  exists  in  popular  imagination.  The  tarantula 
dance  was  probably  introduced  as  a  cure,  with  the  purpose  of 
keeping  the  patient  on  the  move,  so  that  he  should  perspire,  and 
thus  get  rid  of  the  poison.  The  tradition  of  the  Middle  Ages  was 
that  the  bite  caused  the  dance  frenzy,  Chorea  saltatoria,  or  taran- 
tismus, which  was  supposed  to  lead  to  such  violent  exertion  that 
death  resulted  unless  the  victim  was  soothed  by  music. 

The  Bite  of  Epcira  diadema. — The  bite  of  the  common  garden  spider  has 
been  recently  proved  l>v  Robert  and  Sachs  to  be  poisonous. 

The  Bite  of  (i  Bengal  Spider. — Fink  has  recently  described  a  herpetic  eruption 
on  the  face  of  Bengalee  children  due  to  a  spider-bite;  for  this  he  recommends 
fumigating  the  face  with  the  smoke  evolved  when  lumps  of  mustard-oil  cake, 
burned  in  a  charcoal  fire,  arc  dropped  into  a  basin  of  cold  water. 

Diagnosis. — Bee-stings,  scorpion-bites,  and  ordinary  skin  bacterial 
infections  must,  of  course,  be  distinguished  from  spider-bites,  with 
which,  without  doubt,  they  have  been  often  confounded.  The 
local  symptoms  and  the  history  ought  to  be  some  guide. 

Prognosis. — This  is  generally  good. 

Treatment.- — Prevent  absorption  by  the  proximal  ligature,  open 
the  wound  by  an  incision,  and  apply  alkaline  solutions — e.g.,  weak 
solutions  of  ammonia  or  carbonate  of  potash,  or  equal  parts  of 
spirit  of  ammonia  and  water  as  a  wet  dressing.  It  appears  to  us 
that  a  strong  permanganate  of  potash  solution  ought  to  be  given 
a  trial. 

3.  Acarina. 

The  Ixodoidea,  or  ticks,  are  well  known  to  cause  severe  symptoms 
by  their  bites,  apart  from  the  introduction  of  any  parasite  such  as  a 
Ptroplasma  or  Spirochcvta. 

The  anatomy  of  these  arthropods  is  given  in  detail  in 
Chapter  XXVIII.,  p.  689,  to  which  reference  should  be  made,  but 
a  few  remarks  are  necessary  concerning  the  act  of  biting,  which 
has  been  studied  by  Nuttall. 

The  tick  pierces  the  skin  by  means  of  the  teeth  on  the  digits  of 
its  chelicerae.  The  digit  is  capable  of  being  extended  by  an  internal 
muscle,  and  turned  outward  by  an  external  muscle.  These  move- 
ments, occurring  alternately,  cause  the  teeth  to  cut  the  skin,  and 
as  the  chelicerae  work  deeper  and  deeper,  the  hypostoinc  is  dr 
into  the  wound,  and  by  its  recurved  teeth  keeps  the  tick  in  position. 
The  palps  but  rarely  enter  the  wound.  During  this  act  of  biting 
it  is  believed  that  the  salivary  glands  pour  a  considerable  amount 


216      VENOMOUS  ANIMALS:  PROTOZOA    TO  ARTHROPODA 


of  secretion  into  the  victim,  but  the  nature  of  this  fluid  and  its 
action  requires  further  investigation.  Nuttall,  drawing  attention 
to  the  immunity  following  bites,  says  that  it  is  probable  that  this 
secretion  is  toxic  in  its  action. 

The  Effects  of  the  Venom. — With  regard  to  the  Argasidae,  Argas 
persicus  Oken  has  an  evil  reputation  in  Persia,  where  its  bite  is  said 
to  cause  severe  pain,  fever,  lassitude,  delirium,  convulsions,  and 
even  at  times  death  in  new-comers,  while  natives  are  immune. 

Bordier  considers  that  these  symptoms  are  due  to  the  injection 
of  a  poison,  but  this  would  hardly  appear  to  be  likely,  as  Louns- 
bury    found    in    his    own    case    in    South    Africa   that  the   bite 

caused  only  slight  itching. 
If  the  symptoms  are  properly 
described  in  Persia,  it  would 
indicate  that  the  tick  intro- 
duced some  parasite  into 
the  new-comer  which  caused 
a  definite  disease  to  which 
the  native  had  acquired  an 
immunity. 


Fig.i8. — Ventral  Aspect  of  the  Mouth- 
Parts  of  a  Tick  (Hcemaphysalis  punc- 
tata Canestrini  and  Fanzago). 

(Alter  Nuttall,  Cooper,  and  Robinson, 
Journal  of  Parasitology.) 

1,  Chelicerae,  showing  teeth;  2,  hypostome, 
showing  rows  of  recurved  teeth;  3,  palp. 


Fig.  19. — Chelicera  from  the 
Same  Tick. 

(After  Nuttall,  Cooper,  and 
Robinson,  Journal  of  Parasi- 
tology.) 

1,  Internal  digit;  2,  external 
digit. 


Argas  reflexus  Fabricius  may  cause  local  pain  and  swelling,  with 
sometimes  an  erythematous  eruption,  while  the  site  of  the  bite  is 
marked  for  years  by  a  cicatrix.  The  bite  of  A .  brumpti  Neumann 
is  also  severe. 

Ornithodoros  moubata  Murray  inflicts  a  very  painful  bite,  with 
much  swelling  and  the  formation  of  raised  hard  wheals,  in  Euro- 
peans, which  may  last  several  days. 

Ornithodoros  iuricata  Dugcs  may  cause  swelling  and  numbness 
all  over  the  body,  with  vomiting  and  diarrhoea,  accompanied  by 
an  urticarial  eruption  and  profuse  perspiration,  with  rigors,  fever, 


CHILOPODA 


ixq 


headache,  and  backache  if  the  poisons  enter  a  vein.  Locally,  an 
ulcer  may  form  at  the  site  of  the  bite.  0.  talaje  Guerin  Meneyille 
causes  severe  itching  and  pain. 

With  regard  to  the  Ixodidae,  Ixodes  ricinus  causes  severe  der- 
matitis, which  may  be  followed  by  pustules  and  abscesses,  with 
oedema,  lymphangitis,  and  lymphadenitis,  associated  with  fever. 

Treatment. — The  treatment  of  tick-bites  is  first  to  detach  the 
tick,  which  is  by  no  means  easy,  as  the  recurved  teeth  of  the 
hypostome  hold  on  to  the  wound  very  firmly.  The  best  plan  is 
to  rub  any  oil  into  the  ventral  surface  of  the  tick,  thus  interfering 
with  its  respiration,  and  compelling  it  to  detach  itself  from  the  host. 
With  regard  to  0.  turicata,  it  is  advised  to  apply  the  actual  cautery, 
as  the  effects  of  the  bite  are  so  severe.  According  to  Wellmari, 
Ornithodoros  bites  should  be  treated  by  bathing  in  very  hot  water, 
after  which  bicarbonate  of  soda  should  be  applied  in  strong  solution. 
Itching  may  be  allayed  by  a  menthol  ointment  (i  to  2  per  cent.). 


Fig.  20. — Scolopendva  movsikins  Linnaeus. 


As  regards  prophylaxis,  badly  infected  native  huts  should  be 
burnt,  while  ordinary  houses  may  be  fumigated  with  sulphur  or 
carbon  bisulphide,  or  sprayed  with  kerosene  or  boiling  water. 
Beds  must  always  be  raised  from  the  ground,  and  the  feet  of  the 
bedstead  placed  in  water  containing  kerosene,  while  pyrethrum 
powder  may  be  dusted  between  the  coverings  of  the  bed.  Wellman 
insists  that  natives  should  not  be  allowed  to  sleep  in  or  near  the 
quarters  of  Europeans. 

2.  Chilopoda. 

The  class  Chilopoda  includes  the  Scolopen<lri(l;e.  or  centipedes, 
which  are  animals  with  a  head  and  a  uniformly  segmented  trunk, 
possessing  numerous  legs.  They  are  very  common  all  over  the 
world,  but  the  tropical  species  are  much  larger  than  those  which 
inhabit  the  Temperate  Zone.     They  live  under  stones  in  shady 


218       VENOMOUS  ANIMALS  :  PROTOZOA   TO  ARTHROPOD  A 

places,  especially  in  woods.  The  poison  apparatus  of  the  centipedes 
is  formed  by  the  appendages  of  the  first  trunk  segment  being 
modified  so  as  to  form  a  large  pair  of  jaws,  at  the  base  of  which 
the  poison  gland  lies.  The  duct  of  this  gland  opens  on  the  apex  of 
the  claw,  and  therefore,  as  there  are  two  jaws,  a  centipede-bite  will 
show  two  minute  punctures  or  drops  of  blood. 

The  venom  is  primarily  intended  to  kill  their  prey,  which  consists 
of  small  insects  and  larvae. 

Geographical. — The  most  noted  species  are  Scolopendra  cingulata, 
France,  Spain,  Italy;  5.  gigantea  Koch,  S.  morsitans  L.,  5.  heros, 
Africa,  India,  Indo-China,  Equatorial  America;  Geophilus  longicornis 
Leach,  Mid-Europe. 

The  Venom. — The  venom  is  an  acid  opalescent  liquid,  but  little 
miscible  with  water.  For  experimental  purposes  it  can  be  obtained 
by  treating  the  lower  lip  and  the  hooks  with  normal  saline  solution. 

When  injected  into  the  veins  of  rabbits,  it  causes  an  immediate 
paralysis,  with  coagulation  of  the  blood,  while  under  the  skin  it 
forms  a  large  abscess. 

Effects  of  the  Venom. — The  poison  causes  local  and  general 
symptoms.  At  first  there  is  itching,  but  this  is  quickly  followed 
by  intense  pain,  which  extends  all  over  the  limb.  A  red  spot 
appears  at  the  site  of  the  bite,  which  enlarges  and  becomes  black 
in  the  centre,  and  sometimes  there  are  lymphangitis  and  lymph- 
adenitis. The  general  symptoms  are  great  mental  anxiety,  vomit- 
ing, irregular  pulse,  dizziness,  and  headache. 

Diagnosis. — -The  diagnosis  is  obtained  by  the  history  and  the 
presence  of  the  two  minute  punctures. 

Prognosis.— The  prognosis  is  good,  though  small  children  have 
been  known  to  die  from  the  effects  of  a  sting.  Adults,  as  a  rule, 
recover  in  about  twenty-four  hours  at  the  most. 

Treatment.— Bathe  the  part  well  with  a  solution  of  ammonia 
(i  in  5  or  i  in  io).  After  bathing,  apply  a  dressing  of  the  same 
alkali,  or  if  there  is  much  swelling  and  redness,  an  ice-bag. 

If  necessary,  give  hypodermic  injections  of  morphia  to  relieve  the 
pain.  At  a  later  period,  fomentations  may  be  required  to  reduce 
the  local  inflammation. 

3.  Hexapoda. 

The  Hcxopoda,  or  insects,  contain  many  species  injurious  to  man. 

The  orders  to  which  the  principal  venomous  species  belong  arc: 
(1)  Anopleura;  (2)  Hemiptera;  (3)  Hymenoptera;  (4)  Lepidoptera; 
(5)  Diptera;  and  (6)  Coleoptera. 

1.  Anopleura. 

This  order  includes  the  lice,  which  cause  much  irritation  by  their 
bites.  The  nature  of  the  venom,  however,  is  not  known,  and  the 
lice  are  of  more  importance  as  carriers  of  disease,  and  will  therefore 
be  dealt  with  more  fully  in  Chapters  XXX.  (p.  749)  and  XXXV. 
(p.  872). 


APT  DM  219 

2.  Hemiptera. 

The  Hemiptera  (Chapter  XXXI.,  p.  761)  include  the  families  of 
the  Clinocoridae,  or  bugs,  and  the  Reduvidae,  or  cone  noses.  In  the 
latter  family  is  classified  Phonergates  bicoloripes  Stal,  which,  accord- 
ing to  Wellman,  produces  a  very  painful  bite  in  man  in  Angola. 
Another  member  of  this  family,  as  yet  not  named,  has  been  described 
by  King  in  the  Sudan,  where  it  bites  human  beings  on  the  hands 
and  wrists,  producing  small  red  lumps,  which,  however,  soon  dis- 
appear.    It  is  said  to  be  closely  related  to  Phonergates  bicoloripes. 

Bugs. — These  hemipterons  secrete  a  strongly  alkaline  poisonous 
secretion  in  their  salivary  glands.  This  poison  flows  down  the 
ducts  of  the  stylets,  and  passing  into  the  wound  made  by  the  bite, 
dilates  the  capillaries,  causing  an  increase  of  blood  in  the  area 
bitten.  This,  of  course,  is  advantageous  to  the  insect,  allowing  it 
to  obtain  a  quantity  of  blood  in  a  short  space  of  time.  Clinically 
the  poison  causes  red  blotches  and  local  swellings. 

It  is,  however,  more  convenient  to  discuss  these  venomous  insects 
along  with  other  parasites  in  Chapter  XXXI.,  p.  761,  as  it  enables 
a  more  systematic  description  to  be  given,  especially  as  the  nature 
of  the  venom  is  quite  unknown. 

3.  Hymenoptera. 

In  this  order  come  the  bees,  wasps,  and  ants. 

APIDiE. 

The  members  of  this  family  which  sting  are  well  known,  and  it 
is  by  no  means  infrequent  to  hear  of  animals  and  even  at  times 
human  beings  in  the  tropics  suffering  severely  from  bee-stings,  and 
more  rarely  dying  from  the  effects. 

The  species  generally  credited  with  evil  effects  are:  Apis  mellifica 
L.,  the  hive-bee;  Vespa  vulgaris  L.,  the  wasp;  V.  germania  Fabr. ; 
V.  crabo  L.,  the  hornet;  V.  orientalis,  the  hornet ;  Bombus  hortorum 
L.,  the  bumble-bee;  B.  lafidarius  L.,  and  Xylocopa  violacea,  the 
wood- bee. 

Historical. — The  venom  of  the  bee  was  first^studied  by  Brandt 
and  Ratzeburg  in  1833,  then  by  Paul  Bert  in  1865  and  Carle  t  in 
1884,  but  the  chemical  nature  was  first  investigated  carefully  by  Josef 
Langer  in  1897,  and  in  1904  Phisalix  made  experiments  on  sparrows. 

Anatomical. — The  body  of  the  bee  is  divided  into  head,  thorax, 
and  abdomen,  from  the  posterior  end  of  the  last  of  which  project.. 
the  sting  in  the  form  of  a  chitinous  sheath,  narrow  posteriorly  and 
wider  anteriorly.  This  sheath  contains  two  barbed  darts,  and  into 
its  wider  portion  (which  possesses  a  cleft  by  which  air  can  penetrate 
into  it)  two  or  three  ducts  from  glands  open.  The  principal 
opening  belongs  to  the  duct  of  the  '  acid  gland,'  and  opens  an- 
teriorly into  a  sac — the  poison  reservoir- — which  leads  into  a 
long,  slender,  coiled  tubular  gland,  either  bifid  anteriorly  or  sub- 
divided into  two  glands.     This  long  gland  ramifies  amongst  the 


220       VENOMOUS  ANIMALS  :  PROTOZOA   TO  ARTHROPOD  A 

contents  of  the  abdomen.  The  second  opening,  which  lies  along- 
side the  first,  belongs  to  a  small,  irregular,  tubular  gland  called  the 
alkaline  gland,  or  gland  of  Dufour.  The  third  opening,  when 
present,  leads  into  a  lanceolate  or  ovoid  accessory  poisonous  gland. 
The  Venom. — The  venom  freshly  extruded  from  the  bee's  body 
weighs  from  o-2  to  0-3  milligramme,  and  is  a  transparent  acid  fluid 
with  a  bitter  taste,  a  peculiar  aromatic  smell,  and  a  specific  gravity 
of  1-1313.  It  contains  about  30  per  cent,  of  solid  matter  when 
dried  at  the  room  temperature. 

The  acid  reaction  is  believed  to  be  due  to  formic  acid,  and  the 
smell  to  volatile  substances,  but  neither  of  these  have  any  connec- 
tion with  the  poisonous  properties  of  the  venom. 

The  preparation  of  venom  in  quantity  was  carried  out  by  Langer 
as  follows:  Several  thousand  fresh  stings  with  their  venom-sacs 
were  placed  in  96  per  cent,  alcohol,  which  was  in  due  course  filtered 
off,  when  the  stings  were  dried  at  400  C,  then  pulverized  and 
extracted  with  water.  The  resulting  extract,  which,  when  filtered, 
was  a  clear  yellowish-brown  fluid,  was  then  precipitated  by  96  per 
cent,  alcohol.  The  precipitate,  after  washing  with  alcohol  and 
ether,  was  dissolved  either  in  ordinary  water  or  in  the  same  acidu- 
lated slightly  with  acetic  acid.  From  this  solution  Langer  obtained 
an  albumin-free  active  body  after  repeatedly  precipitating  with 
a  few  drops  of  concentrated  ammonia  and  again  dissolving  as 
above.  The  active  principle  is,  therefore,  not  albuminous,  and 
is  thought  to  be  an  organic  base,  the  nature  of  which,  however, 
is  not  known.  This  poison  is  destroyed  or  its  activity  lessened 
by  oxidizing  agents,  such  as  potassium  permanganate,  and  also 
by  ferments,  such  as  pepsin  and  rennin. 

Subcutaneously  injected,  the  venom  produces  great  local  irrita- 
tion, but  heating  to  ioo°  C.  for  fifteen  minutes  destroys  this  effect. 
Intravenous  injections  into  dogs  produce  convulsions,  trismus, 
nystagmus,  emprosthotonos,  and  death  from  respiratory  failure. 
This  action  is  believed  by  some  authors  to  be  due  to  a  neurotoxin, 
but  the  blood  after  death  is  very  fluid,  and  the  red  corpuscles  are 
destroyed,  indicating  a  marked  haemolysis,  while  all  the  organs 
except  the  spleen  show  haemorrhages  and  hyperaemia;  so  that  the 
effects  may  not  be  due  so  much  to  the  action  on  the  nervous  system 
as  to  that  on  the  blood.  The  convulsive  effects  can  be  destroyed 
by  heating  to  ioo°  C.  for  thirty  minutes,  when  the  poison  becomes 
merely  narcotic.  All  effects  are  annulled  by  heating  to  1500  C. 
for  fifteen  minutes. 
The  venom,  therefore,  contains: — 

1.  Inflammatory  poisons,  which  are  thought  to  come  from  the 
acid  gland. 

2.  Neurotoxins: — 

(1)  Convulsive,  thought  to  be  derived  from  the  alkaline 

gland. 

(2)  Narcotic,  secreted  by  the  acid  gland. 

3.  Haemolysins. 


APIDM  221 

With  regard  to  the  last,  Morgenroth  and  Carpi  have  shown  that 
a  lecithide  is  formed  which  is  200  to  500  times  more  haemolytic 
than  the  venom  alone.  There  is,  therefore,  a  similarity  between 
this  poison  and  cobra-venom. 

The  only  marked  features  recorded  in  human  post-mortems  are 
hyperemia  of  the  meninges  and  bloody  exudation  into  the  ventricles 
of  the  brain. 

Immunity. — There  appears  to  be  no  doubt  that  bee-keepers 
often  attain  a  considerable  amount  of  immunity  against  the 
venom. 

Thus,  Langer  says:  Out  of  164  bee-keepers,  11  were  immune 
from  the  first;  while  of  the  153  at  first  sensitive,  126  became  more 
or  less  immune,  and  27  did  not.  Of  the  126  more  or  less  immune 
persons,  14  said  that  they  were  not  affected  even  when  several 
stings  were  inflicted  quickly  one  after  the  other. 

Bee  immunity,  however,  is  only  passing,  and  does  not  last,  and 
the  keepers  say  that  the  first  sting  in  the  early  part  of  the  year  may 
produce  a  strong  effect. 

Calmette  has  immunized  a  mouse,  so  that  it  could  resist  doses  of 
the  venom  which  would  surely  have  been  mortal  otherwise. 

The  Effects  of  the  Venom. — Usually  the  symptoms  are  merely 
local,  and  limited  to  pain  in  the  part,  redness,  and  swelling  of  the 
skin,  and  disappear  in  a  few  hours.  Suppuration  is  rare,  and  blood- 
poisoning  very  rare,  only  taking  place  occasionally  if  the  sting  is 
on  the  eyes,  ears,  lips,  or  in  feeble  old  people. 

Slight  fever  may  result  in  sensitive  people,  and  sometimes  general 
constitutional  symptoms,  such  as  nausea,  faintness,  great  weakness, 
vomiting,  precordial  distress,  difficulty  in  breathing,  coldness  of 
the  extremities,  with  an  eruption  on  the  skin  like  measles,  or  with 
wheals.  These  symptoms  may  pass  on  to  delirium,  unconscious- 
ness, and  more  rarely  death. 

Vespa  orientalis  causes  semi-unconsciousness,  the  face  becoming 
pale  and  cyanosed,  the  skin  of  the  extremities  cold  with  a  clammy 
sweat;  respiration  becomes  shallow  and  sighing;  the  pulse  quick 
(130  to  140),  irregular,  and  barely  perceptible.  On  recovery  from 
this  state  of  shock,  the  patient  complains  of  a  sensation  of  tightness 
in  the  throat,  and  oedema  may  develop  in  the  neck  and  face,  as 
well  as  slight  fever  (ioo°  to  1020  F.),  all  symptoms  disappearing  in 
twenty-four  hours. 

The  ordinary  bee  may  at  times  cause  seven-  symptoms,  of  which 
the  following  is  an  example:  a  lady  was  stung  in  the  forehead, 
and  in  four  minutes  swelling  of  the  eyelids  and  lips  began,  which 
rapidly  spread  to  the  arms,  and  was  associated  with  acute  abdominal 
pain.  The  hands  became  rigid  in  the  position  of  main  en  grijfe, 
and  pain  and  stiffness  was  felt  in  the  throat,  together  with  difficulty 
in  speaking.  There  was  also  vomiting  and  a  sense  of  chilliness, 
followed  by  exhaustion.     Recovery  was  rapid. 

Diagnosis.  -There  is  usually  no  difficulty  in  this,  the  history 
being  clear. 


222       VENOMOUS  ANIMALS  :  PROTOZOA   TO  ARTHROPODA 

Prognosis. — Usually  the  prognosis  is  very  good ;  the  only  dangers 
are  in  children  and  old  feeble  persons,  and  in  multiple  stings. 

Treatment.- — The  usual  treatment  is  by  applications  of  weak 
solutions  of  ammonia,  which  answers  well.  Carbolic  acid  (i  in  20 
or  1  in  10)  is  satisfactory  if  applied  immediately  after  the  sting. 
Potassium  permanganate  may  be  tried. 

Calmette  advises  a  solution  of  calcium  hypochlorate  (1  in  60) 
or  eau  de  Javel  (1  in  100).  When  there  is  much  swelling,  apply 
iced  compresses  or  an  ice-bag.  When  general  symptoms  develop, 
strychnine  injections  may  be  used. 

FORMICID/E. 

Ants  may  appear  rather  insignificant  in  the  Temperate  Zone,  but 
in  the  tropics  they  are  most  active,  and  their  bites  are  vety  painful. 

Many  ants — e.g.,  Myrmica  and Ponera — have  a  poison  apparatus 
analogous  to  that  of  the  bees,,  which  has  just  been  described. 

The  Venom. — The  venom  is  well  known  to  contain  formic  acid, 
but  there  must  be  more  than  this  in  the  venoms  of  the  tropical 
species,  though  nothing  is  known  on  the  subject. 

The  Effects  of  the  Venom. — The  symptoms  are  usually  only  local 
■ — that  is  to  say,  pain,  inflammation,  and  swelling  at  the  site  of  the 
bite- — but  in  the  case  of  the  large  tropical  ants  general  symptoms 
of  faintness,  shivering,  and  temporary  paralysis  may  be  produced. 
Indeed,  dried  red  ants  made  into  a  paste  have  already  been  noted 
as  an  arrow-poison  (Chapter  XL,  p.  180). 

In  Ceylon  there  is  a  species  of  very  small  ants  which  infest  the 
beds  and  bite  people  while  asleep,  producing  urticarial  pomphi. 

Treatment. — Apply  weak  solutions  of  ammonia,  carbolic  solution 
(1  in  20),  or  camphorated  alcohol,  to  the  part.  As  a  preventive 
measure  against  the  ants  infecting  beds,  spread  some  powdered 
camphor  in  the  beds  and  sheets. 

4.  Lepidoptera. 

Caterpillars  of  many  butterflies  are  well  known  to  be  venomous 
in  the  tropics,  causing  marked  skin  eruptions,  and  even  a  feeling  of 
illness  associated  with  a  slight  rise  of  temperature. 

Wellman  reports  that  in  Angola  the  most  common  stinging  cater- 
pillar is  that  of  the  tiger-moth  (Archidse),  called  locally  '  ochipia  ' 
—that  which  burns — which  produces  an  angry  eruption  associated 
with  much  pain.  Another  belonging  to  the  Limacodidse,  called 
'  Epuvi,'  he  describes  as  causing  urticaria.  A  third,  belonging  to 
the  Liparidse,  also  causes  severe  local,  and  at  times  reflex  nervous 
symptoms.  We  are  acquainted  with  stinging  caterpillars  in  Ceylon 
and  the  Gold  Coast,  but  we  have  not  determined  the  species.  In 
the:  former,  a  bombyx  larva  living  on  the  Hibiscus  plant  is  apt  to 
cause  skin  irritation.  In  India,  the  '  komlah  '  of  the  Tend  is  liable 
to  cause  intense  irritation  if  it  touches  the  skin.  According  to 
Brooke,  the  larvae  of  Necera  lepida  and  Adolia  are  known  to  be 


LEPIDOPTERA 


223 


venomous.  Recently  Bleyer  has  described  caterpillars  belonging 
to  the  Bombycidae  of  Brazil  which  possess  peculiar  stinging  organs, 
the  venom  from  which  produces  locally  urticaria  and  dermatitis,  as 
well  as  general  symptoms,  which  are  best  treated  by  the  local  appli- 
cation of  a  2  per  cent,  solution  of  menthol  in  aether,  chloroform, 
and  rectified  spirits,  and  by  the  administration  of  a  mixture  con- 
taining liquor  ammonias  acetatis. 

Porthesia  Chrysorrhoea.- — The  caterpillar  of  this  brown-tailed  moth 
is  reported  from  America  (Massachusetts  and  New  Hampshire)  as 
causing  a  peculiar  skin  eruption,  which  Tyzzer  says  is  caused  by 
the  penetration  into  the  epidermis  of  peculiarly  modified  micro- 
scopic hairs  called  the  nettling  hairs,  which  are  sharply  pointed  and 
barbed.  These  hairs  are  specially  arranged  for  penetration,  and 
possess  an  irritating  substance  which  can  be  destroyed  at  1150  C. 
The  other  hairs  are  innocuous.  The  poison  causes  necrosis  of  the 
cells  of  the  epidermis,  together  with  the  formation  of  small  vesicles 
and  inflammation  of  the  corium. 

The  Symptoms,  which  are  generally  those  of  an  urticarial  der- 
matitis, but  occasionally  erysipelatous-like,  may  be  divided  into 
two  groups:  (1)  severe,  due  to  contact  with  the  caterpillar;  (2)  mild, 
due  to  hairs  blown  into  the  air  and  lodging  in  skin  or  under-gar- 
ments.  But  it  must  be  remembered  that  some  people  are  very 
sensitive  and  others  almost  immune. 

Treatment. — The  best  treatment  is  to  clear  away  the  hairs  with 
a  little  alkaline  lotion  (bicarbonate  of  soda  2  per  cent.),  and  then 
to  apply  an  ointment  of  ichthyol  (10  per  cent.). 

5.  Diptera. 

The  classification  of  the  Diptera  is  given  in  Chapter  XXXII. ,  p.  775, 
to  which  reference  should  be  made. 

Culicidce. — The  irritation  of  mosquito-bites  is  most  noticed  by 
the  new-comer  to  the  tropics,  for  as  years  go  by  a  kind  of  partial 
immunity  is  acquired,  and  the  bites  are  much  less  noticed.  Some 
people  appear  to  have  a  partial  natural  immunity  to  the  bites,  but 
this  is  uncommon. 

Only  the  female  mosquito  bites  and  sucks  blood,  which  is  sup- 
posed to  be  required  for  the  nutrition  of  the  eggs.  When  the 
female  mosquito  alights  upon  the  skin,  it  does  not  always  bite  at 
once,  but  may  move  from  one  part  to  another,  apparently  testing 
the  different  parts  of  the  skin  by  its  labellae.* 

Having  selected  a  given  area  of  skin,  it  moves  the  palpi  away 
from  the  proboscis  dorsally,  and  at  the  same  time  rotates  the 
labellae  on  their  hinge-joints  outwards. 

The  labium  is  now  pressed  against  the  skin,  and  is  bent  into  the 
form  of  a  bow,  convex  posteriorly.  An  opening  in  the  skin  is  then 
made,  in  which  the  mandibles  and  maxillae  work  like  saws,  while 
the  head  of  the  mosquito  can  be  seen  rocking  from  side  to  side. 

*  For  the  anatomy  of  the  proboscis  see  Chapter  XXXII.,  p.  776. 


224       VENOMOUS  ANIMALS:  PROTOZOA   TO  ARTHROPODA 


During  this  process  respiration  is  going  on  quietly,  but  at  times, 

according  to  Schaudinn,  a  violent  contraction  of  the  abdomen  is 

noticed,  which  is  said  to 
be  due  to  the  carbonic 
acid  in  the  superficial 
layers  of  the  skin,  for  he 
found  that  when  carbon 
dioxide  gas  acted  upon 
mosquitoes  a  like  contrac- 
tion was  produced. 

As  this  process  is  pro- 
ceeding, an  irritating  sub- 
stance, the  chemical 
nature  of  which  is  not 
known,  is  injected  under 
the  skin,  and  it  is  evident 
that  this  happens  before 
the  mosquito  begins  to 
suck  blood  for  the  irrita- 
tion is  present  when  the 

insect  ceases  to  bite  before  drawing  up  the  blood. 
There  has  been  much  dispute  as  to  where  this  substance  comes 

from,  but  this  appears  to  have  been  settled  by  Schaudinn,  who 


Fig.  2 1 . — An  Anopheline  Mosquito  (A  .macii- 
lipennis  Meigen)  in  the  Act  of  Biting. 

(After  Nuttall  and  Shipley,  Journal  of 
Hygiene.) 

Note  that  the  proboscis  does  not  enter  the 
wound,  and  that  it  is  bent  convex  posteriorly. 
Note  the  distension  of  the  abdomen  as  seen  by 
the  space  between  the  terga  and  the  sterna. 
In  the  natural  condition  this  space  would  be 
bright  red  from  the  blood  in  the  abdomen. 


Fig.  22. — Head  of  Anopheles  maculipennis  Meigen. 

(After  Nuttall  and  Shipley,  Journal  oj  Hygiene.) 

I,  Labium;  2,  maxillae;  3,  hypopharynx;  4,  mandibles;  5,  labrum ; 
6,  palpi;  7,  antennae;  8,  occiput;  9,  eye;  10,  clypcus. 


triturated  the  isolated  salivary  glands  in  salt  solution,  which  he 
applied  to  a  wound  with  negative  result.     On  the  other  hand,  when 


DIPT ERA 


225 


he  applied  the  isolated  oesophageal  diverticula  to  a  scratch,  he 
obtained  the  characteristic  irritation  and  redness.  These  oeso- 
phageal diverticula  contain  gas-bubbles  and  bacteria  or  moulds. 
The  bubbles  were  shown  by  Schaudinn  to  contain  carbon  dioxide 
by  applying  baryta-water  to  the  diverticula,  when  a  precipitate 
was  obtained.  The  fungi  need  further  investigation,  but  they  or 
their  products  appear  to  be  the  real  cause  of  the  irritation,  for 


Fig.  23.  -Anterior  End  of 
a  Mandible. 

(After    Nuttall    and    Shipley. 
Journal  of  Hygiene.) 


Fig.  24. — Anterior  End  of 
a  Maxilla. 

(After  Nuttall  and  Shipley, 
Journal  of  Hygiene.) 


when  Schaudinn  pressed  the  carbon  dioxide  out  of  the  sac  the  signs 
characteristic  of  the  bite  were  still  produced.  It  appears  probable, 
therefore,  that  the  powerful  abdominal  contraction  mentioned 
above  expels  the  gas,  bacteria,  and  fungi  from  the  oesophageal 
diverticula  and  the  saliva  from  the  salivary  glands. 

It  is  possible  that  the  chemical  products  of  the  fungi,  by  causing 
local  irritation,  bring  more  blood  into  the  particular  area  of  skin 


Fig.   25. — The  Alimentary  Canal  of  Anopheles  maculipennis 
Meigen. 

(After  Nuttall  and  Shipley,  Journal  of  Hygiene.) 

1,  Mouth  and  buceal  cavity;  2,  pharynx;  3,  oesophagus;  4,  dorsal  and 
ventral  oesophageal  diverticula ;  5,  proventriculus ;  6,  salivary  glands ;  7,  narrow 
portion  of  ventriculus;  8,  so-called  stomach;  9,  malpighian  tubules;  10,  intes- 
tine; 11,  rectum;  12,  anus. 


affected,  and  thus  enable  the  mosquito  to  get  her  supply  quickly, 
for  feeding  only  takes  two  to  three  minutes,  during  which  time  some 
mosquitoes  will  so  overfill  themselves  with  blood  that  it  may  be 
ejected  per  anum.  The  use  of  the  carbonic  acid  is  probably  to 
prevent  the  coagulation  of  the  blood,  which  is  drawn  up  the  large 
blood-tube  formed  by  the  labrum  epipharynx  and  hypopharynx 
by  the  suctorial  action  of  the  pump-like  pharynx. 

15 


226      VENOMOUS  ANIMALS:  PROTOZOA   TO  ARTHROPODA 

Symptoms.  —  Shortly  after  a  mosquito  has  bitten  a  person,  a 
sensation  of  itching  is  experienced  in  the  affected  part,  which  on 
examination  is  seen  to  be  inflamed  and  reddish,  while  a  wheal  not 
unusually  develops,  especially  in  persons  new  to  the  tropics.  Some- 
times a  papule  or  even  a  nodule  may  form  on  the  site  of  the  bite, 
while  more  rarely  scratching  leads  to  secondary  infection  and  the 
formation  of  boils,  lymphangitis,  or  lymphadenitis. 

Treatment. — The  itching  may  be  relieved  by  dilute  solutions  of 
ammonia  (Scrubb's  Ammonia  is  a  favourite  remedy),  or  by  a  5  per 
cent,  solution  of  carbolic  acid,  or  1  per  cent,  alcoholic  lotion  of 
menthol.  Inflamed  bites  may  be  cleaned  with  1  in  40  carbolic 
lotion,  and  afterwards  dressed  with  boracic  ointment.  Local  septic 
poisoning  should  be  treated  by  boracic  or  carbolic  fomentations, 
while  boils  and  abscesses  must  be  opened. 

Prophylaxis. — The  prevention  of  mosquito-bites  will  be  discussed 
in  the  chapter  on  Malaria  (Chapter  XL.). 

Other  Diptera. — Numerous  flies  other  than  the  Culicidae  cause 
irritation  by  their  bites,  such  as  fleas,  but  the  nature  of  the  venom 
not  being  well  known,  they  will  be  considered  together  in  Chapters 
XXXII.,  p.  771,  XXXIII.,  p.  814,  and  XXXIV.,  p.  857. 

In  Cape  Colony  there  is  a  superstition  that  the  '  bee  moth  ' — 
i.e.,  death's-head  moth,  Acherontia  atropos  Linnaeus — is  poisonous. 
This  is  not  so. 

6.  Coleoptera. 

Beetles  and  their  larvae  are  capable  of  inflicting  severe  bites  or 
wounds  by  means  of  stiff  hairs.  Silvanus  surinarnensis  L.,  the 
saw-toothed  grain-beetle,  is  said  to  bite  people.  Wellman  describes 
the  larva  of  a  beetle,  which  the  natives  of  Angola  call  '  ochisia/ 
which  means  '  to  be  left  alone,'  whose  bristles  will  even  penetrate 
the  skin  of  the  sole  of  the  foot,  causing  pain,  inflammation,  and 
even  sloughing,  when  trodden  upon. 

Blister  Beetles. — Chalmers  and  King  in  19 17  have  drawn 
attention  to  the  beetles  Epicauta  sapphirina  Maeklin,  1845,  and 
Epicautat  omentosa  Maeklin,  1845,  as  the  cause  of  '  seasonal  vesic- 
ular dermatitis  '  in  Khartoum,  while  P.  H.  Ross  had  studied  in 
1910  the  same  complaint  in  Nairobi,  where  it  was  caused  by  Pcederus 
cribi  punctata  Epp  (sic),  and  P.  da  Silva  had  traced  in  1912  similar 
outbreaks  in  Brazil  to  Pcederus  columbinus  de  Laporte,  1832;  Eyscll 
to  Pcederus  peregrinus  Fabricius,  1801,  in  Malaysia;  and  Rodhain 
and  Houssian  to  a  species  of  the  genus  P cedents  Fabricius,  1775. 
Finally,  Roubaud  has  stated  that  Epicauta  flavicomis  Dujardin, 
1838,  is  the  cause  of  the  same  complaint  in  Senegal. 

The  whole  subject,  however,  belongs  to  Chapter  XCYL,  the 
Dermatozoiascs,  and  is  only  mentioned  here  foi  the  purposes  of 
reference. 

It  will  be  noted  that  the  various  authors  only  mention  two 
genera — viz.,  Epicauta  Dejean,  1803,  which  belongs  to  the  family 
Cantharidce  Leach,  1817,  and  Pcederus  Fabricius,  1775,  belong- 
ing to  the  family  Staphylinidce,  which  latter  lack  the  appendage 


COLEOPTERA 


227 


on  the  ventral  aspect  of  the  claws  which  is  so  characteristic  of  the 
former. 

The  life-history  of  these  beetles  is  very  complicated,  and  much 
of  it  is  spent  under  the  ground,  hence  the  seasonal  factor  in  the 
eruption  caused  by  cantharidin,  which  is  present  in  the  fluid 
exuding  from  the  insect,  and  especially  from  what  may  be  termed 
the  knee-joint,  when  irritated. 


Fk 


26. — Blister  Beetles. 


1,  Upper  and  smaller  Epicauta  tomentosa  Maeklin,  1845,  and  the  lower  and 
larger  Epicauta  sapphirina  Maeklin,  1845;  2,  Mylabris  nubica  de  Marseul, 
1857;  3,  a  claw  of  E.  ■iapphivina,  to  show  the  long  appendage  which  is  usually 
closely  applied  to  it. 

MOLLUSCA. 

A  venomous  snail  of  unknown  genus  and  species  is  described 
in  the  Solomon  Islands.  These  snails  possess  radulae  provided 
with  pointed  tubular  teeth,  armed  anteriorly  with  a  barb.  These 
teeth  are  connected  with  a  poison  gland,  and  arc  capable  of  injuring 
men  and  producing  severe  wounds.  Bites  of  the  cones  and  augers 
(Terebrida^)  are  said  to  be  poisonous. 


REFERENCES. 

The  best  general  references  are: 

Calmette  (1907).     Les  Venins.     Paris. 

Faust  (1906).     Die  tierischen  Gifte.     Braunschweig. 

Wells  (1907).     Chemical  Pathology,  pp.  181.  182. 

Protozoa. 
Laveran  and  Mesnil  (1899).     Compt.  Rendus  Soc.  Biol.,  xi.  245-248.     Paris. 
Rosenau,   Parker,   Francis,   and  Bayer  (1904).     Bull.   14,   Yellow  Fever 
Institute.     Public  Health  and  Mar.  Hospital  Scrv.     Washington. 


228       VENOMOUS  ANIMALS:  PROTOZOA    TO  ARTHROPOD  A 

Coelenterata. 

Forbes  (1848).     Monograph  of  the  British  Naked-Eye  Medusae. 
Richet  (1902,  1903,  1904).     Compt.  Rendus  de  la  Soc.  de  Biologie. 
Schmidt  and  W.  Marshall  (1893).     Brehms  Tierleben.     3  Aufi.,  S.  552  and 

553- 
Zervos  (1903).     Semaine  Medicale. 

Echinodermata. 
Saville  Kent  (1893).     The  Great  Barrier  Reef  of  Australia,  p.  293. 

Platyhelmia  and  Nemathelminthes. 

Achard  (1887).     Archive  Generate  de  Medecine. 
Boycott  (1905).     Journal  of  Pathology  and  Bacteriology,  x.  383. 
Messineo  und  Calamida  (1901).     Centralblatt  f.  Bakteriologie,  p.  346. 
Picou  et  Ramond  (1899).     Compt.  Rendus  de  la  Societe  de  Biologie. 
Schaumann  und  Tallquist  (1898).   Deutsche  Medicin.  Wochenschrift,  p.  312. 
Whipple  (1909).     Journal  of  Experimental  Medicine,  xi.  2,  331. 

Arachnid*—  Scorpio  nidea. 

Bert,  Paul  (1885).     Soc.  de  Biolog.,  p.  574. 

Bourne  (1885).     Proceedings  of  the  Royal  Society,  xlii.  17. 

Calmette  (1895).     Annales  de  l'lnstitut  Pasteur,  p.  232. 

Cavaroz  (1865).     tiber  den  Biss  des  Scorpio  von  Durango.     Rec.  de  Mem. 

de  Med.  Milit.,  series  xiii.,  327. 
Balance  (1866).     Rec.  de  Mem.  de  Med.  Milit.,  p.  136. 
Guyon  (1867).     Comptes  Rendus,  vol.  lxiv.,  p.  1001. 
Heinzel  (1866).     Ueber  Scorpionstich.  Wochen.  der  Gesellschaft  der  Wiener 

Aertste. 
Iwano  (191 7).     Kyoto  Igaku  Zassi,  xiv.,  No.  4,  May. 
Jousset  (1870).     Comptes  Rendus,  lxxi.  407. 
Joyeux,  Laffine  (1882).     Comptes  Rendus  des  Sciences. 
Kobert  (1893).     Lehrbuch  der  Intoxicationen,  325. 
Kraepelin  (1899).     Scorpions.     Das  Tierreich,  viii.     Berlin. 
Kyes  (1903).     Beit.  Klin.  Woch. 

Posada  Arango  (1871).     Archive  de  Med.  Naval.,  xvi.  213. 
Posada  Arango  (1871).     Gazette  des  Hopit.,  No.  121. 
Redi  (1731).     Hist,  de  l'Acad.  des  Sciences. 
Sanarelli  (1888).     Boll,  dei  Cult,  delle  Scienze  Med.,  p.  202. 
Valenta  (1876).     Zeit.  fur  Biologie,  xii.  190. 
Werner     (1911).     Scorpions    of    the    Anglo-Egyptian     Sudan.     Wellcome 

Tropical  Research  Laboratories.     London. 
Wilson  (1904).     Records  of  the  Egyptian  Government  School  of  Medicine, 

PP-  7"43-     (Full  account,  with  considerable  literature.) 

Aranea. 

Blackwell  (1855).     Transactions  of  the  Linnsean  Society  of  London,  p.  31. 

Comstock  (1912).     The  Spider  Book.     New  York. 

Frantzuis,   V.  A.   (1869).     Vergiftete  Wunden  bei  Thieren  und  Menschen 

durch  den  Biss  der  in  Costa  Rica  verkommenden  Mininspinne.     Virchow's 

Archiv  f.  Path.,  xlvii.  335. 
Fink  (1906).     Journal  of  Tropical  Medicine  and  Hygiene,  ix.,  December  1. 
Gaubert  (1893).     La  Naturaliste,  p.  24. 
Hassatt  (1896).     Lcs  Venins  des  Araignees  Tijdsch.       Entom.,  xxxix.  (and 

1882). 
Heinzel  (1866).     Ueber  Tarantelbiss.  Wochenb.  der  Gesellschaft  der  Wiener 

Aerzte,  255. 
Kobert  (1901).     Beitrage  zur  Kenntniss  d.  Giftspinnen. 
Kobert  (1906).     Lehrbuch  der  Intoxicationen  (2  vols.). 
Ozanam  (1856).     Etude  sur  le  Venin  des  Aiachnides.     Paris. 


REFERENCES  229 

Panceri  and  Gasco  (1874).     Institut  tigyptien,  July  4. 

S\chs  (1902).  Zur  Kenntniss  des  Kreuz  Spinnengiftes.  Hoffmann  Beitrage, 
ii.  125. 

Ucke  (1870).  Vergiftungen  durch  Spinnenbisse  in  der  Kirgisensteppe  in 
Sommer  1869.     Petersb.  hed.  Zeitschrift,  54. 

Weigenberger  (1878).  Caso  fatal  par  lo  Mordedura  de  Una  Arancnea  Cor- 
dova.    South.  America. 

Wilson  (1901).  Poison  of  Spiders.  Records  of  the  Egyptian  Government 
School  of  Medicine,  pp.  143-150. 

Wright  (1870).     The  Katipo.     Medical  Times  and  Gazette,  November  12, 

P-  57°- 

Ixodoidea. 

Nuttall  (1899).     Johns  Hopkins  Reports,  viii.  1899. 

Nuttall  (1908).     Ticks.     London. 

Nuttall  (1908).     Journal  of  the  Royal  Institute  of  Public  Health,  xvi.  385. 

Chilopoda. 

Bachelier  (1887).     La  Scolopendre  et  sa  Piqflre.     These,  Paris. 

Saulie   (1885).     Appareil  Venemeux  et   Venin  de  la   Scolopendre.     These, 

Montpellier. 
Skbastianv  (1870).     Piqure  de  la  Scolopendre  mordante.     Gaz.  des  Hopit., 

No.  91. 
Siriot  (1904).     Soc.  de  Biologie,  November  15. 
Wood  (1866).     American  Journal  of  Medical  Sciences,  (52),  575. 

Apidse. 

Bordas  (1897).     Description  Anatomique  et  Etude  Histologique  des  glands. 

A.  Venin  des  Insectes  Hymenopteres.     Paris. 
Ewens  (i860).     Death  from  Bee-Sting.     Medical  Times  and  Gazette. 
Mac  Walters  (1908).     Indian  Medical  Gazette,  xliii.  236. 
Morgenroth  and  Carpi  (1906).     Berlin.  Klin.  Wochen.,  xliii.  1424. 
Neuberg  and  Rosenberg  (1907).     Berlin.  Klin.  Woch.,  xliv.  457. 
Nivison  (1857).     Fatal  Results  of  a  Bee-Sting.     New  York  Journal,  May. 
O'Donnell  (1867).     New  York  Medical  Record. 

Phisalix  (1890).     Comptes  Rendus  Academie  des  Sciences.     July  23. 
Steffen  (1866).     Infection  durch  Insectenstich.  Deutsches  Archiv.  f  jr  Klin. 

Medicin.,  ii.  192. 
Thompson  (1869).     British  Medical  Journal,  p.  374. 

Formicidae. 

Fabre  (1898).     Annal.  des  Sciences  Natur. 

Tyzzer  (1907).     Journal  of  Medical  Research.     Boston. 

Culicidae. 

Schaudinn    (1904).     Arbeiten   aus   der   Kaiserlichen   Gesundheitsamte,    xx. 
417-421. 

Lepidoptera. 
Brooke  (1908).     Tropical  Medicine,  pp.  121,  122. 

Fkacker  (1915).    Classification  of  Lcpidopterous  Larvae.     Illinois  Monographs. 
Wellman  (1907).     Journal  of  Tropical  Medicine,  x.  185. 

Coleoptera. 
Beauregard  (1890).     Les  Insects  Vesicants.     Paris. 

Chalmers  and  King  (1917).     New  Orleans  Medical  and  Surgical  Gazette. 
(Blister  Beetles  as  a  Public  Nuisance).     New  Orleans. 

Mollusca. 
Schnee  (1908).     Archiv  f.  Schiff.  u.  Tropen  Hyg.,  171. 


CHAPTER  XV 

VENOMOUS  ANIMALS  [continued)— PISCES 
AND  AMPHIBIA 

Pisces — Zoological  classification — Geographical  distribution — Poison  by 
bite — Poison  by  stings — Amphibia — References. 

PISCES. 

All  over  the  world,  but  especially  in  tropical  seas,  there  are  fish 
which  for  purposes  of  defence  secrete  poisonous  fluids  from  special 
glands.  These  fish  have  been  but  little  studied,  and  still  less  is 
known  about  the  nature  of  their  venom  and  its  physiological  action. 
A  great  deal,  however,  is  known  by  residents  in  the  tropics  about 
wounds  inflicted  by  these  fish,  and  the  doctor  practising  therein  is 
bound  sooner  or  later  to  come  across  not  merely  persons  who  know 
a  good  deal  in  a  general  way  about  the  subject,  but  those  who 
either  are  suffering  or  have  suffered  from  the  poisoning.  It  is 
therefore  necessary  that  the  tropical  practitioner  should  have  some 
knowledge  of  venomous  fish. 

The  subject  might  be  studied  by  classifying  the  fish  zoologically, 
and  then  taking  them  seriatim  and  describing  their  poison  and  its 
effects;  but  though  a  zoological  list  will  be  given,  this  does  not 
seem  so  satisfactory  as  to  follow  Bottard  in  his  special  classification 
based  on  the  manner  in  which  the  fish  inflicts  the  poison. 

Venomous  fish  may  be  classified  into : — 

Class  I.  Fish  which  poison  by  their  bite. 

("lass  II.  Fish  which  poison  by  barbs  (spines)  connected 
with  special  glands. 

Class  III.  Fish  which  poison  by  a  secretion  prepared  by  the 
skin  glands.  This  class  is  illustrated  by  the  lamprey, 
which  is  only  known  to  produce  poisoning  when  eaten. 

It  will  be  understood  from  the  above  classification  that  venomous 
fish  are  to  be  distinguished  from  poisonous  fish — i.e.,  from  fish 
which  cause  symptoms  of  poisoning  when  their  flesh  is  eaten — 
for  the  flesh  of  venomous  fish  can  be  eaten  with  impunity.  The 
poisonous  fish  and  their  effects  have  been  briefly  described  in 
Chapter  XIII.,  p.  193,  under  the  heading  Poisonous  Food. 

During  the  spawning  season  the  quantity  and  the  virulence  of 
the  poison  of  venomous  fish  generally  increase,  and,  indeed,  some 

230 


VENOMOUS  FISH  231 

genera — e.g.,  Cottus — are  only  venomous  at  that  time.  Poisonous 
glands,  being  protective,  occur  more  commonly  in  weak  and  small 
rather  than  in  large  fish,  hence  they  are  more  frequent  in  bony 
than  in  cartilaginous  fish,  which  latter  are  usually  of  large  size. 
Venomous  fish  are  often  conspicuous  by  form  or  colour. 

Historical. — The  history  of  our  knowledge  of  venomous  fish  has 
been  Well  written  by  Faust,  who  points  out  that  it  was  Aristotle, 
the  Father  of  Ichthyology,  who  first  established  the  fact  that  fish 
could  produce  poisoned  wounds,  and  that  after  his  day  informa- 
tion on  this  subject  appears  to  have  been  very  uncertain,  and 
doubts  were  cast  upon  the  facts  ascertained  by  him.  Modern 
knowledge  began  in  1841  by  Allman  writing  a  paper  on  the  stinging 
properties  of  the  lesser  weaver  (Trachinus  vipera),  which,  he  said 
with  all  reservation,  was  probably  due  to  a  poison-gland  at  the 
base  of  the  opercular  valve.  Further  researches  were  made  by 
Byerley  in  1849,  Gunther  from  1864  to  1881,  Corre  1865-81,  Gressin 
1SS4,  and  Savtschenko,  who  produced  his  excellent  atlas  in  1886. 
It  is,  however,  Bottard,  in  his  thesis  on  '  Les  Poissons  Venimeux  ' 
in  1889,  who  first  gave  a  clear  account  of  these  fish,  and  he  has  been 
followed  by  Courtiere  in  1899,  Briot  in  1902-04,  and  Evans  in  1907. 
The  nature  of  the  poison  or  poisons,  and  its  or  their  physiological 
effects,  still  require  considerable  research. 

Effects  of  the  Poison. — As  far  as  investigations  have  gone,  it 
appears  as  though  the  venoms  of  the  different  fish  only  varied 
quantitatively,  and  not  qualitatively.  The  effects  are  local  and 
general.  The  local  effects  consist  in  painful  sensations,  swelling  of 
the  part,  which  may  spread  over  the  whole  limb,  suppuration,  and 
even  gangrene.  The  general  symptoms  appear  to  be  due  in  the 
first  instance  to  the  action  of  the  venom  on  the  central  nervous 
system,  which  shows  itself  in  excitation,  and  later  insensibility  and 
paralysis.  An  action  on  cardiac  muscle  has  also  been  recorded. 
In  man  death  has  been  known  to  occur  from  wounds  of  Synanceia 
brachio. 

Persons  Chiefly  Affected. — The  persons  chiefly  affected  by  the 
venom  are  cooks  and  fishermen,  but  the  latter  are  well  aware  of  the 
danger. 

Diagnosis. — Diagnosis  is  to  be  obtained  by  the  history  of  the 
injury.  . 

Prognosis. — This  is  usually  good,  but  prompt  treatment  is 
needed. 

Treatment.- — The  treatment  of  a  poisonous  wound  due  to  a  fish 
must  be  based  upon  the  following  principles: — 

1.  Prevent  as  far  as  possible  the  poison  entering  the  general 

circulation. 

2.  Neutralize  the  poison  as  far  as  possible  locally. 

3.  Treat  the  general  symptoms. 

1.  Prevent  the  Poison  entering  the  General  Circulation. — The  wound 
will  usually  be  on  an  arm  or  a  leg,  and  therefore  it  will  be  quite 


232  VENOMOUS  ANTMALS 

easy  to  apply  proximally  a  tight  bandage  with  the  same  precautions 
as  mentioned  under  Snake-Bite  (see  p.  274). 

2.  Neutralize  the  Poison  Locally. — This  should  be  done  by  opening 
the  wound  and  letting  it  bleed  while  washing  it  with  1  per  cent, 
solution  of  permanganate  of  potash,  or  by  rubbing  in  crystals  of 
the  same  substance,  and  then  applying  fomentations  and  aseptic 
dressings. 

3.  General  Treatment. — The  pain  must  be  relieved  by  hypodermics 
of  morphia,  and  nervous  symptoms  by  bromides;  syncopal  attacks 
by  stimulants  and  hypodermics  of  strychnine ;  failure  of  respiration 
by  artificial  respiration. 

Zoological  Classification. 

The  venomous  fish  may  be  classified  as  follows:  — 
Subclass  I.  Elasmobranchii. 
Order  3.  Selachii. 

Suborder  3.  Raii. 

Family  Myliobatidae. 

Myliobatis  aquila  Linnaeus. 

Aetobatis  narinari  Euphrasen. 

Family  Trygonidae. 

Trygon  pastinaca  Cuvier  and  other  species. 

Subclass  V.  Teleostei. 

Grade  A.  Physostomi. 

Suborder  2.  Cyprini  siluriformes  (Ostariophysi) . 

Family  Siluridae. 

Plotosus  anguillaris  Bloch,  1793. 
Saccobranchus  fossilis  Bloch. 

Suborder  4.  Anguilliformes  (Apodes). 
Family  Muraenidas. 

Muraena  helena  Linnaeus. 

Grade  B.  Physoclisti. 

Suborder  10.  Acanthopterygii. 

Division  1.  PerciJ'ormes. 

Family  Acanthuridae. 

Acanthurus  luridus. 

Division  7.  Trigliformcs  (Scleroparei) . 
Family  Triglidae. 

Trigla  hirundo  Linnaeus. 

Family  Scorpaenida\ 

Synanceia  brachio  Cuvier  and  Valenciennes,  1826. 

,,  verrucosa  Schneider. 

Scorpaena  gramlicornis  Cuvier  and  Valenciennes, 
[826. 
diabolus  Cuvier  and  Valenciennes,  1826. 
,,  porcus  Linnaeus. 

I  'tcniis  antennata  Bloch. 
Pelor  filamentosum  Cuvier  and  Valenciennes,  1826. 

Family  Cottidae. 

Cottus  scorpius  Linnaeus. 


VENOMOUS  FISH  233 

Division  8.  Blenniformes. 

Family  Trachinidae. 

Trachinus  draco  Linnaeus. 

,,  vipera  Cuvier  and  Valenciennes,  1826. 

,,  radiatusCuvier  and  Valenciennes,  1826. 

araneus  Riss. 

Family  Uranoscopidos. 

Uranoscopus  scabcr  Linnaeus. 

Family  Callionymidae. 

Callionymus  lyra  Linnaeus. 

Family  Batrachidae. 

Batrachus  tau. 

grunniens  Bloch. 
Thalassophryne  reticulata  Giinther. 
„  maculosa  Giinther. 

Addendum. — Serranus  outabili  (Cuv.  and  Val.)  and  Holocanthus  imperator 
(Bl.)  are  looked  upon  as  possibly  poisonous,  but  there  is  no  definite  evidence. 
The  Siluridae  are  believed  to  be  poisonous,  because  some  of  them  possess  sac* 
like  organs  opening  into  the  axillae  of  the  pectoral  fins,  on  which  there  are 
powerful  spines. 

Geographical  Distribution. 
The  geographical  distribution  of  venomous  fish  is  in  temperate  and  tropical 
seas: — 

Tel  cost  omi. 
Plotosus  anguillaris  .  .      Indian  Ocean. 

Murasna  helena       .  .  .  .      Mediterranean. 

Acanthurus  luridus  .  .      Tropical  Atlantic. 

Trigla  hirundo         .  .  .  .      English  Channel. 

Svnanceia  brachio  .  .  .  .      Tropical  Pacific. 

verrucosa  .  .      Indian  Ocean. 

Scorpaena  grandicornis     .  .      Waters  of  the  Antilles. 

,,  diabolus  .  .      Indian  Ocean  and  Tropical  Pacific. 

,,  porcus  .  .  .  .      Mediterranean. 

Pterois  antennata  .  .  .  .      Seas  of  the  Indies  and  Equatorial  Pacific. 

Pelor  filamentosum  .  .      Waters  of  ITsle-de-France. 

Cottus  scorpius       .  .  .  .      Seas  of  Europe,  Asia,  and  North  America. 

Trachinidae.  .  .  .  .  .      Waters  of  Europe. 

Uranoscopus  scaber  .  .      Mediterranean. 

Callionymus  lyra    .  .  .  .      Waters  of  France. 

Batrachidae..  ..  ..      Waters  of  Tropical  America  and  India. 

Leaving,  however,  the  zoological  classification,  we  will  consider 
'he  venomous  fish  according  to  Bottard's  classification,  excluding 
Class  III. 

CLASS  I. 

Fish  which  Poison  by  their  Bite. 

The  type  of  this  class  is  the  genus  Murcena,  all  of  which  possess 
powerful  teeth  capable  of  inflicting  severe  bites.  According  to 
Calmettc,  there  are  more  than  one  hundred  species  in  tropical  and 
subtropical  seas.  Murcena  helena  L.  is  found  in  the  Mediterranean, 
and  Murcena  moringa  Cuv.  in  the  tropical  Atlantic. 

The  poison  apparatus  consists  of  a  pouch  lying  above  the  cover 
ing  of  the  palate  lined  with  epithelial  cells,  secreting  the  venom. 
This  pouch  is  capable  in  larger  species  of  holding  about  h  c.c.  of 


234  VENOMOUS  ANIMALS 

poison,  and  possesses  three  or  four  strong  conical  teeth  curved  with 
an  anterior  convexity.  These  teeth  are  not  grooved  or  channelled, 
but  are  easily  moved  and  erected,  and  are  enclosed  in  a  sheath 
formed  by  the  mucosa  of  the  palate.  The  poison  collects  between 
the  teeth,  and  simply  flows  down  them  into  the  wound. 

The  venom  has  not  been  studied,  except  so  far  as  to  show  that  it 
has  some  digestive  action.  The  effect  on  man  is  not  certainly 
known,  but  is  supposed  to  lead  to  syncope. 

Another  fish,  the  bite  of  which  is  much  dreaded,  is  Tetrodon 
fluviatilis,  which  is  found  in  the  waters  of  Indo-China,  and  fre- 
quently attacks  the  natives,  especially  children. 

CLASS  II. 

Fish  which  Poison  by  Means  of  Stings  associated  with 
Poison  Glands. 

Bottard  classifies  the  poison  apparatus  of  this  class  into  three 
groups : — 

1.  Apparatus  entirely  closed,  and  therefore  before  the  poison  can  escape 

a  membrane  must  be  ruptured : — ■ 

Synanceia  brachio. 
,,  verrucosa. 

Plotosus  anguillaris. 

2.  Apparatus  partially  closed  :  — 

Thalassophryne  reticulata. 
,,  maculosa. 

3.  Apparatus  in  more  or  less  direct  communication  with  the  exterior: — 

I'niclunus    vipera. 
,,  draco. 

radiatus. 
arancus. 
Cottus  scorpius. 
bubalis. 
,,     gobio. 
'  ;illionymus  lyra. 
Scorpaena  porcus. 
,,         scrofa. 
I  'terois  antennata. 
Pclor  fdamentosum. 
Acanthurus  luri&ns. 
Uranoscopus  scaber. 
Trigla  hirundo. 

The  poison  glands  are  generally  placed  at  the  base  of  the  dorsal 
or  anal  tins,  or  under  spines  on  the  operculum.  The  gland  com- 
municates with  one  or  more  rays  of  the  fins.     The  barbs  may  be: — 

1.  Grooved,  but  having  the  groove  converted  into  a  canal  by  a 
membrane,  which  must  be  raptured  for  the  poison  to  escape. 

2.  Canalized  by  channels  which  lead  t"  apertures  near  its  tip. 
This  arrangement  of  the  rays  agrees  with  the  types  of  poison 

apparatus  mentioned  above. 


VENOMOUS  FISH  235 

Section  i.  -Poison  Apparatus  Entirely  Closed. 

The  apparatus  is  connected  with  the  dorsal  tin,  and  is  passively 
defensive— that  is  to  say,  the  fish  cannot  eject  the  poison  unless 
the  barb  is  broken. 

Examples. — Synanceja  (hrachio  and  many  other  species) ;  Plotosus 
arah. 

Synanceia  (brachio  and  many  other  species).- — This  fish,  called 
'  rapau  de  mer  '  in  Reunion,  '  lafte  '  in  Mauritius,  '  ikan  Satan  '  in 
Java,  and  '  nohu  '  in  Tahiti,  is  distributed  through  the  waters  of 
the  Indies,  Cochin  China,  New  Caledonia,  and  the  Pacific  Ocean. 

Its  poison  apparatus  is  connected  with  the  dorsal  fin,  which  has 
thirteen  barbs,  each  of  which  is  supplied  with  two  poison  reservoirs, 
to  which  belong  ten  or  twelve  tubular  glands.  It  cannot  eject  the 
poison  itself,  but  if  trodden  upon  by  the  naked  foot,  the  barbs 
enter  the  skin,  and  the  poison  is  pressed  mechanically  into  the 
wound.     The   venom   is   limpid,   bluish,    and   slightly   acid.     The 


Fig.  27. — -Synanceia  verrucosa  Schneider. 
(From  Savtschenko's  '  Atlas  of  Poisonous  Fish.') 

symptoms  are  severe  pain,  spreading  up  the  limb.  The  sufferer 
becomes  violent,  throwing  himself  from  side  to  side,  and  even 
a>king  to  have  his  foot  cut  off.  Sometimes  syncope  and  death 
may  take  place.  In  other  cases  abscesses  and  symptoms  of  blood- 
poisoning  may  be  noted.  The  skin  surrounding  the  wound  becomes 
bluish,  and  may  slough,  in  which  case  repair  takes  a  very  long  time 
to  be  completed. 

Plotosus  angtiillaris.— This  fish,  called  '  machoira  '  in  Reunion  and 
Mauritius,  '  sanbilang  '  in  Malay,  '  koormat  '  in  Abyssinia,  is  found 
in  the  waters  of  India,  of  the  Seychelles,  and  other  places  men- 
tioned above.  The  poison  apparatus  is  connected  with  the  dorsal 
fin,  and  the  conditions  which  bring  about  the  wound,  together  with 
the  symptoms,  resemble  those  of  Synanceia. 

Saccobranchus  fossilis. — This  fish  is  found  in  the  waters  of  India 
and  Ceylon,  and  wounds  caused  by  its  pectoral  tins  are  much 
dreaded  by  the  natives,  as  they  produce  severe  inflammation  and 
even  tetanic  symptoms. 


236  VENOMOUS  ANIMALS 

Section  2. — Poison  Apparatus  Partially  Closed. 

The  types  of  this  section  are  Thalassophryne  reticulata  Giinther, 
which  is  found  near  Panama,  and  T.  maculosa  Giinther.  which  is 
chiefly  found  in  the  Gulf  of  Bahia  (Brazil). 

In  these  fish  the  poison  apparatus  is  double,  there  being  hollow 
barbs  on  the  gill  covers  and  on  the  back  close  behind  the  head. 
The  barb  on  the  gill  cover,  which  is  bent  somewhat  upwards,  is 
conical  in  shape  and  pierced  by  a  central  canal,  which  is  connected 
with  a  poison  reservoir  situated  at  the  base  of  the  barb.  The  cells 
lining  this  sac  are  probably  those  which  secrete  the  poison.  The 
venom,  therefore,  is  capable  of  flowing  along  this  canal  without 
being  forced  by  muscular  exertion.  The  barbs  on  the  dorsum  of  the 
fish  consist  of  two  spines  pierced,  as  in  the  case  of  the  opercular 
spine,  by  canals  which  communicate  with  poison  reservoirs.  When 
the  barbs  are  erected,  the  poison  flows  out  of  the  peripheral  openings 
of  the  central  canals,  and  thus  can  enter  any  wound  caused  by  them. 
The  nature  of  the  venom  and  its  physiological  action  are  not  known, 
but  it  is  supposed  that  it  will  be  like  Synanceja  and  Trachinus, 
'.  hough  there  is  no  ground  for  this  supposition. 

The  poison  apparatus  of  Batrachus  tan  of  the  waters  of  North 
America  and  B.  grunniens  of  those  of  the  Antilles  are  said  to  be 
identical  (Calmette)  with  that  just  described  for  Thalassophryne. 

Section  3. — Poison  Apparatus  in  more   or  less  Direct  Com- 
munication with  the  Exterior. 

This  section  contains  a  number  of  fish,  the  best  studied  of  which 
is  Trachinus  draco, 

Trachinus  draco. — This  fish  possesses  two  sets  of  poison  appa- 
ratus, the  one  a  barb  on  the  operculum,  and  the  other  connected 
with  the  dorsal  fin.  The  barb  on  the  operculum  possesses  a  groove 
which  is  converted  into  a  canal  by  a  fine  membrane,  which  leaves 
an  opening  near  the  point  of  the  spine.  This  barb,  which  is  slightly 
erectile,  pierces  the  operculum.  At  its  base  lies  the  poison  gland, 
partly  covered  by  an  adductor  muscle,  which  helps  to  press  the 
poison  into  the  canal  and  to  erect  the  spine.  When  the  barb  enters 
the  flesh  of  another  animal,  the  above-mentioned  membrane  is 
stripped  off  and  the  poison  enters  the  wound. 

The  dorsal  apparatus  consists  of  from  five  to  seven  spines  joined 
together  by  a  membrane,  which  is  adherent  almost  to  their  tips. 
Each  barb  has  a  deep  double  channel,  the  two  grooves  of  which 
join  towards  the  base  of  the  spine,  and  form  a  conical  space,  of 
which  the  walls  are  covered  with  cells  which  secrete  the  poison. 

The  first  symptoms  are  very  severe  pain  of  a  burning  or  lancinat- 
ing character.  The  part  then  tingles  and  becomes  painfully  numb, 
and  this  may  spread  along  the  limb,  and  appears  to  travel  along 
the  nerves,  though  the  joints  are  particularly  tender.  This  is 
followed  by  palpitation,  lever,  delirium,  vomiting,  and  syncope. 
The  area  affected  becomes  swollen  and  inflamed,  and  if  neglected 


TRACHINUS  DRACO  237 

may  suppurate  or  even  turn  to  gangrene.     The  symptoms  may 
last  from  two  to  three  hours  to  several  days. 

The  venom  has  been  studied  by  Gunther.  Gressin,  Bottard,  Briot, 
and  Phisalix.  It  has  also  been  studied  by  Evans,  who,  after 
washing  the  fish,  collected  it  by  means  of  an  aseptic  hypodermic 
syringe,  then  dried  it  in  vacuo,  reduced  it  to  a  fine  powder,  and 
finally  dissolved  it  in  normal  saline  or  in  water.  He  collected 
the  poison  from  about  2,000  fish.  The  venom  is  clear,  trans- 
parent, and  very  slightly  acid.  Hypodermically  injected,  it 
causes  mortification  and  local  paresis,  necrosis,  and  haemorrhage. 
Intravenously  injected,  it  causes  failure  of  the  heart  and  respira- 
tory paralysis,  associated  with  first  a  rise  in  the  blood-pressure, 
which  is  followed  later  by  a  marked  fall.  It  also  appears  to  have 
a  hemolytic  effect,  which  is  supposed  to  be  due  to  its  amboceptors 
uniting  with  endocomplements  (lecithin)  in  the  red  cell.  It  will 
thus  be  seen  that  the  poison  in  some  respects  resembles  snake- 
venom.  The  venom  is  lethal  to  fish,  frogs,  and  mammals.  Thus, 
0-015  gramme  of  dried  venom  killed  a  frog,  and  0-02  gramme  a 
mouse. 


Tfct^ 


Fig.  28. — Trachinus  draco  Linnaeus. 

According  to  Briot,  who  has  succeeded  in  immunizing  rabbits, 
the  venom  contains  a  ferment  capable  of  digesting  proteid. 

Trachinus  radiatus.- — Pohl  has  studied  the  poison  of  this  fish, 
and  finds  that  it  stops  the  heart  in  diastole.  The  effect  of  applying 
the  poison  to  the  heart  of  the  frog  is  to  first  produce  strong  con- 
tractions, which  gradually  become  weaker  and  weaker,  until  they 
cease  and  the  heart  stands  still  in  diastole.  The  poison  has,  how- 
ever, no  effect  on  skeletal  muscle. 

Coitus. — The  genus  Coitus,  widespread  in  the  Northern  Hemi- 
sphere, possesses  a  poison  apparatus  which  resembles  that  of  the 
genus  Trachinus,  but  is  less  developed,  and  consists  of  poison 
glands  lying  in  culs-de-sac  in  the  opercular  spines.  The  cells  of  the 
gland  only  secrete  the  venom  during  the  spawning  season,  from 
November  to  the  end  of  January. 

Callionymus. — In  Callionymus  the  operculum  terminates  in  three 
conical  spines  like  a  trident,  and  in  addition  possesses  another  spine 
directed  upwards,  and  these  are  supplied  in  the  spawning  season 
with  a  small  quantity  of  venom  from  the  gill  membrane,  which, 
according  to  Bottard,  has  little  effect  on  man. 


}8 


VENOMOUS  ANIMALS 


Scorpcena  scropha. — In  this  fish  the  poison  apparatus  is  said  to 
exist  not  merely  in  the  dorsal  fin,  but  also  in  the  operculum. 

In  the  dorsal  fin,  the  first  three  rays,  which  project  about  one- 
third  of  their  length  beyond  the  membrane  of  the  fin,  are  grooved 
posteriorly  by  three  channels,  which  are  converted  into  canals  by 
a  fine  membrane,  and  communicate  with  the  poison  gland. 

On  the  operculum  there  are  three  small  spines,  of  which  the 
longest  alone  is  connected  with  a  poison  gland. 

When  handled  incautiously,  a  poisoned  wound  may  result  from 
one  of  these  poison  spines  entering  the  skin.  The  action  of  the 
poison  has  been  studied  by  Pohl,  Brunton,  and  Briot.  Brunton 
describes  the  effects  of  the  poison  as  being  exactly  the  same  as 
that  of  Trachinus  draco,  and  Pohl  thinks  that  the  poison  acts  on 
the  heart  in  the  same  manner  as  he  describes  for  Trachinus. 


Fig.  29. — Cottus  scoypius  Linnaeus. 
(From  Savtschenko's  'Atlas  of  Poisonous  Fish.') 


On  the  other  hand,  Briot  thinks  that  it  is  quite  different  from 
Trachinus,  and  that  the  effects  produced  arc  by  secondary  infection 
of  the  mechanical  wound  caused  by  the  spines.  Brunton's  descrip- 
tion of  the  symptoms  in  man  might  possibly  be  due  to  Trachinus 
only,  as  he  does  not  mention  specifically  whether  it  was  Trachinus 
or  Scorpcena  which  affected  the  person.  His  experiments  on 
animals  with  both  fish  appear,  however,  to  have  caused  the  same 
symptoms.  He  pressed  the  spines  of  the  poison  organs  against 
the  hind-limb  of  a  guinea-pig  or  a  rat.  In  a  few  minutes  the 
animal  began  to  suffer  pain  and  twitching  in  the  injured  limb, 
followed  by  tremors  and  convulsions  (if  disturbed),  and  later  by 
death  from  collapse. 

The  description  which  he  gives  of  the  symptoms  in  human  beings 
lor  cither  Scorpcena  or  Trachinus  is  given  below,  but  reference  to 
his  original  paper  will,  we  think,  convince  the  reader  that  he  is 
really  dealing  with  a  Trachinus  sting. 


SCORPJENA  239 

The  symptoms  of  an  attack  may  be  described  thus: — 
A  sharp  prick  is  felt  as  the  spine  enters  the  skin,  and  this  is 
followed  in  a  few  minutes  by  burning  and  itching,  which  shortly 
become  stabbing  pains,  increasing  in  violence  and  passing  up  the 
limb.  The  sufferer  now  lies  down  and  writhes  and  cries  in  agony, 
while  sweat  breaks  out  on  his  brow,  and  flashes  of  light  pass  in 
front  of  his  eyes.  He  begins  to  feel  a  sensation  of  suffocation,  and 
puts  his  hand  to  his  throat  and  heart,  while  the  pulse  is  felt  to  be 
intermittent.  Presently  he  loses  sight  of  the  bystanders,  and  in  a 
little  becomes  delirious,  crying  out  and  suffering  from  convulsions. 
This  condition  may  lead  to  collapse  and  death,  or,  after  lasting 
several  hours,  may  gradually  subside;  but  the  convalescence  is 
slow,  and  the  patient  may  take  several  months  to  recover. 


1'iG     T,o.-  —  Scoypcena  diabolus  Cuvxer  and  Valenciennks. 
(From  Savtschenko's  '  Atlas  of  Poisonous  Fish.') 

The  local  conditions  show  at  first  merely  the  prick  of  the  .  pine, 
but  tin-  aperture  may  be  pigmented  by  the  covering  membrane 
already  alluded  to.  The  puncture  does  not  bleed,  but  the  skin 
around  for  about  \  inch  is  whiter  than  usual,  and  outside  this  red- 
ness appears,  but  soon  all  the  surrounding  skin  is  red,  turning  as 
time  passes  darker  and  darker,  till  it  becomes  black  and  cedematous. 
The  prick  now  discharges  fluid.  In  a  day  or  so  the  affected  area 
sloughs  and  separates,  leaving  a  deep  wound.  Sometimes  a  spread- 
ing gangrene  ensues,  which  necessitates  amputation.  In  milder 
cases  the  part  remains  painful  and  swollen  for  about  three  days 
before  recovery. 

Pterois  automata. — The  poison  apparatus  is  connected  with  the 
dorsal  I'm,  and  is  said  to  resemble  that  of  the  Scorpaenidae. 

Pelor  filamentosum.-  In  this  fish  the  poison  apparatus  is  con- 
Dected  with  the  dorsal  fin,  and  resembles  that  of  Pterois  ami  Scor- 
pesna.  With  regard  toPclor  japonicum  Cu.  and  Val.,  Sdieube  says 
that  he  knew  of  a  case  in  which  a  sting  on  the  thumb  resulted  in 


240  VENOMOUS  ANIMALS 

phlegmonous  and  gangrenous  symptoms  so  severe  that  the  arm 
had  to  be  amputated. 

Acanthurus  luridus. — Acanthurus  lurid  us  possesses  a  poison 
apparatus  connected  with  the  dorsal  and  anal  fins  like  that  of 
Scorftcena. 

Elasmobranchii.— Associated  with  the  poisonous  fish  of  the  Tele- 
ostei  must  be  placed  those  of  the  Elasmobranchii ,  of  which  the 
sting  rays  (Trygonidse)  and  eagle  rays  (Myliobatidae)  alone  produce 
toxic  symptoms  by  blows  with  the  tail,  which  carries  a  spine. 
These  Rays  are  found  all  over  the  world,  and  we  have  received 
information  as  to  their  effects  from  persons  who  have  been  in 
British  Guiana,  in  Australia,  and  in  Ceylon,  in  which  island  stings 
are  well  known  on  the  west  coast,  particularly  about  Dutch  Bay. 

Dr.  Crevaux  has  studied  Rays  from  the  Orinoco,  and  has  shown 
that  their  barbs  are  canalized  and  the  canals  connected  with  poison 
reservoirs.  This  poison  is  said  to  be  so  severe  as  to  be  able  to  kill 
a  man  in  forty-eight  hours.  The  symptoms  of  Aetobatis  narinari, 
called  the  Bishop  ray,  and  of  Trygon  -pastinaca  (from  Japan),  are 
violent  pain,  a  tendency  to  syncope,  with  locally  a  rapidly  forming 
swelling,  which  soon  becomes  the  seat  of  a  violent  inflammation 
and  even  at  times  gangrene.  The  symptoms  of  the  sting,  as 
observed  by  us  in  Ceylon,  are  local  pain  and  swelling.  The  general 
symptoms  are  not  severe.  Trygon  sephen  and  T.  walga  Mull,  and 
Hen.  are  known  in  Indian  waters. 

A  large  number  of  these  Elasmobranchii  have  not  got  special 
poison  glands,  and  the  venom  must  come  from  the  ordinary  skin 
glands. 

Amphibia. 

Toads  and  salamanders  have  been  celebrated  for  ages  as  venomous 
animals,  the  poison  being  found  in  their  parotid  glands  and  skin. 
In  toads  Faust  has  shown  that  there  are  two  poisons — (i)  an 
acid,  bufotalin,  and  (2)  a  neutral  body,  bufonin,  the  former  being 
the  more  active.  It  is,  as  a  rule,  scarcely  toxic  to  man,  only 
irritating  the  mucous  membranes,  especially  the  conjunctiva;  but 
to  small  animals  it  is  toxic. 

In  salamanders  Zalesky  and  Faust  have  found  two  bodies,  one  an 
inorganic  base- — salamandarin — and  another  an  alkaloid — salaman- 
daridin;  but  this  poison  and  the  digitalis-like  poison  of  Bert  and 
Dulartre  in  frogs  are  not  of  sufficient  practical  interest  to  concern 
11s  here. 

According  to  Vulpian  and  Caparelli,  Triton  cristatus  (Laur)  gives 
a  creamy  secretion  from  the  glands  of  the  skin  at  times  which  is 
poisonous  to  many  animals,  but  the  chemical  nature  of  which  is 
not  known. 


REFERENCES  241 

REFERENCES. 

Pisces. 

Bottard  (1S89).     Lcs  Poissons  Venimeux.     These.     Paris. 

Briot  (1902  and  1904).     Societe  de  Biologie,  p.  6tn>. 

Briot  (1903).     journal  de  Physiologic.      .March. 

Calmette  (1907).     Lcs  Vetdns,  pp.  301-327.     English  edition  (1908)  trans- 
lated by  Austen. 

Corre  (1872).     Archive  de  Physiologic    May  (1865).    Archives  de  Medecine 
Navale.     February  (1881).     Ibid.     January  (18S1). 

Coutieke  (1899).     Poissons  Venimeux  et  Poissons  Veneneux.     These.     Paris. 

Cuvier  et  Valenciennes  (1828-49).     Histoire  Nat.  des  Poissons.      Paris. 

Disiz  Gonsai.ves,  A.  (1907).     Gazeta  Medica  da  Bahia,  No.  10-n. 

Dissaku  et  Noe  (1895).     Societe  de  Biologie,  p.  86. 

Dunbar,  Brunton  (1896).     Lancet,  ii.  600. 

EVANS   (1907).     Observations  011   the   Poisoned  Spines  of  the   Weever  Fish 
(Trachinus  draco).     British  Medical  Journal,  December  1. 

Faust  (1900).     Tierischen  Gifte,  p.  1 34. 

Gressin  (1884).     These.     Paris. 

Jordan  (1905).     The  Study  of  Fishes.     London. 

Nogue  (1897).     Archives  de  Med.  Naval.,  lxviii.  439. 

Phisalix  (1899).     Bulletin  Museum  d'Hist.  Nat. 

Poul  (1893).     Prague  Med.  Wochen.  (18),  31. 

Rho  (1900).     Malattie  dei  Paesi  caldi. 

i:r  (1895).     Traite  de  Pathologie  Generale,  i.  751-755. 

Savtschenko  (1886).     Atlas  des  Poissons  Venimeux.     St.  Petersburg. 

Vaughan  and  Now.     Cellular  Toxins,  pp.  193-195. 

Wells  (1907).     Chemical  Pathology,  pp.  184-185. 

Amphibia. 

Calmette  (1907).  Les  Venins,  pp.  328-332. 
Faust  (1906).  Die  Tierischen  Gifte,  p.  210. 
WELLS  (1906).     Chemical  Pathology,  pp.  182-183. 


1  . 


CHAPTER  XVI 

VENOMOUS  ANIMALS  {concluded)— 
REPTILIA  AND  MAMMALIA 

Reptilia:  Ophidia — Historical — Classification— Geographical  distribution — 
The  act  of  striking — The  venom—  Entry  of  the  venom  into  the  body — 
Minimum  lethal  dose — Effects  of  the  venom — Excretion  of  the  poison 
—  Immunity  —  Diagnosis —  Prognosis  —  Treatment  —  Prophylaxis  — 
Lacertilia- — Mammalia.- — References. 

REPTILIA. 

The  Reptilia  include  two  groups  which  are  of  interest  to  medical 
men  in  the  tropics- — viz.,  the  Ophidia  and  the  Lacertilia;  but  the 
former  is  infinitely  more  important,  as  it  includes  the  venomous 
snakes. 

OPHIDIA. 

Definition. — Reptilia  with  limbs  absent  or  vestigial;  without 
movable  eyelids,  or  ear  openings;  with  retractile  elongated  forked 
tongue,  transverse  anus,  paired  copulatory  organs,  and  elastic  liga- 
ment in  place  of  symphysis  menti. 

Remarks.- — The  bite  of  certain  snakes  causes  ophidismus,  or  snake 
poisoning. 

Historical. 

The  history  of  the  study  of  snake-bite;  and  their  effects  may  be  divided 
into  three  periods: — 

1.  Period  of  ancient  theories. 

2.  Period  of  one  venom. 

3.  Period  of  more  than  one  venom. 

1 .  Period  of  Ancient  Theories. — The  ancients  were  acquainted  with  a  number 
of  snakes,  which  they  described  under  the  terms  Echis  and  Cohtbra,  but  it 
is  not  known  definitely  to  what  species  these  referred.  Echidna  was  a  term 
used  to  denote  the  female  viper. 

They  were  acquainted  with  the  main  symptoms  of  a  snake-bite,  and  had 
many  remedies,  including  the  tying  of  a  ligature  around  the  part,  followed 
by  cupping  alter  suirification,  and  the  administration  of  wine  and  theriac, 
the  last  mentioned  being  a  <  elebrated  remedy  winch,  among  other  substances 
contained  the  burnt  body  of  the  viper.  Celsus  recommends  the  sucking  of 
the  wound,  but  only  if  tin  re  are  no  ulcers  on  the  gums,  palate,  and  other 
parts  of  the  mouth. 

2.  Period  of  One  Venom.  In  [664  Redi  studied  the  effects  of  viper-bites 
by  experiments  on  animals,  and  Morse  Charas,  in  1669,  noted  the  important 
fact  that  the  blood  of  animals  bitten  by  vipers  was  coagulated,  and  came  to 
the  conclusion  that  the  symptoms  and  death  were  due  to  this  coagulation. 

24; 


REPTILIA  243 

In  1767  Abb6  Felix  Fontana  made  a  number  of  obseivations  on  animals 
bitten  by  vipers,  and  in  1796  Russell  published  an  account  of  his  experiments 
on  Indian  snakes.  In  1821  Davy  gave  an  account  of  the  effects  on  animals 
of  the  bites  of  three  Ceylon  snakes. 

In  1843  Prince  Lucien  Bonaparte  published  his  important  discovery  that 
1  he  venom  of  the  adder  contained  an  active  substance,  which  he  called  viperine, 
or  echidnine,  capable  of  being  precipitated  by  alcohol. 

In  1845  Brainard  showed  that  if  an  animal  dies  at  once  after  the  bite  of  a 
rattlesnake,  the  blood  will  be  found  to  be  clotted,  but  if  it  lives  for  some 
time  it  will  be  fluid. 

In  [860  Weir  Mitchell  laid  the  foundations  of  modern  investigations  into 
snake-venom  in  his  classical  paper  on  the  poison  of  Crotalus  durissus. 

In  1867  Sir  Joseph  Fayrer  began  his  work  on  Indian  snakes,  which  resulted 
in  the  publication  of  Ins  magnificent  atlas  on  the  Thanatophidia  of  India 
in  1S72,  and  several  papers  by  himself  and  Sir  Lauder  Brunton  in  1873-75. 

About  the  same  time  Vincent  Richards  published  some  valuable  remarks 
on  snake  poisons  and  their  antidotes. 

In  1883  Wall  wrote  a  most  excellent  little  book  on  the  colubrine  and 
viperine  snakes  of  India. 

In  1886  appeared  a  most  masterly  paper  by  Weir  Mitchell  ana  Reichert,  in 
which  they  state  that  the  active  principles  are  globulins  and  peptones 
(proteoses).  These  researches  indicating  a  proteid  nature  for  the  venom  were 
confirmed  by  Wolf  end  en  and  Karlbach,  and  did  away  with  Gautier  and 
Blyth's  ideas  as  to  their  alkaloidal  nature. 

In  1892  Martin  alone  and  with  Smith  studied  the  venom  of  Australian 
snakes  (Hoplocephalus  and  Psendechis),  and  concluded  that  the  venom  con- 
tained three  proteids — an  albumin  and  two  proteoses  (proto  and  hetero), 
the  latter,  however,  being  alone  virulent. 

In  the  meanwhile  observers  had  not  been  backward  in  making  attempts 
to  find  the  physiological  antidote  suggested  by  Weir  Mitchell  and  Reichert, 
for  in  1887  Sewall  showed  that  by  repeated  injections  of  the  venom  of  Crotalus, 
pigeons  could  be  gradually  rendered  resistant  against  strong  doses  of  that 
poison;  and  a  little  later  Reichert  obtained  the  same  result  with  regard  to 
the  venom  of  the  French  viper.  In  1892  Calmette  published  the  first  of  his 
celebrated  series  of  investigations,  showing  that  successive  inoculations  of 
heated  venom  produced  in  animals  a  certain  degree  of  resistance  to  quantities 
of  the  poison  otherwise  surely  fatal.  Calmette  worked  largely  with  the 
cobra,  and  produced  in  rabbits  and  guinea-pigs  a  true  immunity.  He  further 
concluded  that  animals  vaccinated  against  the  cobra  also  withstood  with 
impunity  mortal  doses  of  the  venom  of  the  viper  and  other  snakes  (Bungarus, 
Cerastes,  Naja  haje,  and  Pseudechis) . 

Phisalix  and  Bcrtrand  also  studied  the  question  of  obtaining  an  immunity 
against  the  bite  of  the  viper.  Fraser  of  Edinburgh,  in  1895,  confirmed  these 
results  of  Calmette.  Since  then  there  has  not  been  the  slightest  doubt  that 
Calmette's  serum  is  of  the  greatest  value  in  certain  cases,  especially  against 
cobra-venom. 

In  1 88 1  permanganate  of  potash  was  recommended  as  an  antidote  by 
Professor  de  Lacerda,  of  Rio  de  Janeiro,  and  by  Badaloni  in  Italy  in  1882-84, 
and  lately  this  remedy  has  again  been  strongly  recommended  by  Rogers,  of 
Calcutta,  and  there  appears  to  be  no  doubt  as  to  its  efficiency;  but  the  question 
of  remedies  will  be  dealt  with  in  their  proper  place. 

It  will  thus  be  seen  that  at  the  close  of  this  period  there  is  a  general  belief 
that  the  venom  of  all  snakes  has  virtually  the  same  active  principles,  which 
are  thought  to  be  proteids,  and  that,  though  they  may  differ  in  amount,  and 
hence  their  effects  be  different,  still,  it  is  only  a  quantitative,  and  not  a  qualita- 
tive, difference;  and,  further,  that  one  antivenene  is  effectual  against  all 
kinds  of  venom. 

3.  Period  ol  more  than  One  Venom. — The  third  period,  extending  up  to  the 
present,  is  that  in  which  there  is  the  conception  that  there  are  at  least  two 
definitely  separate  types  of  venom,  one  of  which  may  be  called  the  colubrine 
type,  having  as  its  example  Naja  tripudians  ;  and  the  other  the  viperine  type. 


244  VENOMOUS  ANIMALS 

which  may  be  exemplified  by  the  Vipera  russellii.  In  addition,  however, 
there  are  venoms  which  show  characters  belonging  to  both  types. 

W  eir  Mitchell  alone  and  with  Reichert  indicated  that  there  was  a  difference 
between  viperine  and  colubrine  poisons;  and  C.  J.  Martin,  working  on 
•Pseudechis ,  a  colubrine  snake,  discovered  the  intravascular  clotting,  and 
suggested  that  the  sudden  death  caused  by  Vipera  russellii  might  be  due 
to  this  cause,  which  hypothesis  Lamb  and  Hanna  confirmed. 

The  difference  in  the  working  of  these  two  classes  of  venoms  is  still  further 
accentuated  by  the  researches  of  Rogers,  and  later  by  those  of  Lamb,  which 
clearly  prove  that  Calmette's  antivenene  will  neutralize  the  colubrine,  but 
not  the  viperine,  venom. 

In  1902  a  most  valuable  paper  appeared,  by  Flexner  and  Noguchi,  showing 
that,  in  addition  to  the  neurotropic  principles,  the  venom  contained  agglutinins 
for  the  erythrocytes  and  for  the  leucocytes  which  were  probably  identical, 
and  lysins  for  erythrocytes  and  leucocytes  which  were  separate. 

They  also  pointed  out  that  venom  contained  hsemorrhagins,  and  lessened 
the  bactericidal  powers  of  the  blood.  They  showed  that  antivenene  neu- 
tralizes venom  by  removing  the  hsemolytic  and  antibacteriolytic  actions.  These 
results  have  been  confirmed  and  extended  by  Kyes,  Sachs,  Lamb,  and  others. 

The  position  at  the  present  time  is  that,  though  snake-venom  is  extremely 
complex,  still,  three  kinds  of  venom  may  be  recognized : — the  colubrine  type, 
the  viperine  type,  and  the  mixed  type.  In  this  last  both  colubrine  and  viperine 
types  are  represented,  but  one  is  predominant.  It  is  probable  that  the  main 
action  of  both  types  is  on  the  nervous  system,  but  that  other  principles  in  the 
venom  may  mask  this  important  action. 

With  regard  to  treatment,  there  is  no  doubt  as  to  the  value  of  Calmette's 
serum  in  cobra-poisoning,  and  Lamb's  serum  in  cobra  and  Vipera  russellii 
poisoning,  though  the  old  method  of  ligature  and  incision,  together  with  the 
application  of  permanganate  of  potash,  is  still  the  most  practically  useful 
method  of  treatment. 

Classification. 

The  order  Ophidia  includes  a  large  number  of  families,  of  which 
only  two  are  of  importance  to  the  tropical  practitioner- — viz.,  Colu- 
bridas  and  Viperidse. 

FAMILY  COLUBRIDAE  Boulenger,  1890. 

Definition. — Ophidia  with  ectopterygoids  (transpalatines)  and 
supratemporals  present  with  teeth  in  both  jaws,  but  without  coro- 
noids,  while  the  prefrontals  are  not  in  contact  with  the  nasal  bones. 

The  Colubridae  are  divided,  in  works  on  snake  poisons,  into  the 
non- venomous  and  the  venomous,  and  the  latter  are  joined  with 
the  vipers  to  form  a  subclass  of  the  order  Ophidia  called  Thana- 
tophidia,  or  poisonous  snakes;  but  this  classification  is  by  no  means 
satisfactory,  as  will  presently  be  shown.  There  is  no  external 
character,  easily  ascertainable,  by  means  of  which  every  poisonous 
snake  can  be  recognized  and  distinguished  from  a  harmless  snake.  All 
rules  given  to  the  contrary  break  down  sooner  or  later,  but  the  mouth 
can  be  opened  and  the  poison-fangs  can  usually  be  easily  seen. 

The  usual  classification  of  the  Colubridae  is  into  three  series:  — 

1.  Aglypha-  Poisonous  Colubridae  possessing  solid  ungrooved 
teeth.- — The  Aglypha  are  usually  stated  to  be  non-poisonous,  but 
the  observations  of  Phisalix  and  Bertrand  on  Tropidonotus  (sp.  ?), 
and  Alcock  and  Rogers  on  Zamenis  mucosus  and  Tropidonotus 
piscator,  prove  that  the  saliva  of  these  species  is  poisonous  to  rats, 


COLUBRID/E 


245 


Fig.  31. 


Skull  of  Tropidonotus  natrix 

LlNNJEUS. 


All  the  teeth  are  solid,  there  are  no  grooved 
or  perforated  fangs,  hence  the  name  Aglypha. 
but  the  saliva  may  be  poisonous, 
length  of  the  maxilla. 


Note  the 


mice,  and  guinea-pigs.     Thus  hypodermic  injections  of  the  saliva  of 

the  two  last-named  snakes  will  cause  convulsions  and  death  from 

failure  of  respiration  in  rats  and  mice. 
Therefore  the  saliva,  though  it  may  not  be  known  to  have  affected 

even  a  child,  must  be  looked  upon  as  poisonous,  and  the  Aglypha 

must  be  grouped  with  the 

other  Colubridae  and  the 

Viperidae  under  the  head 

Thanatophidia. 

The  Aglypha  are  divi 

ded      into      three      sub- 
families:    Acrochordinae, 

Colubrinae      (rat-snakes), 

and  Dasypeltinae  (African 

egg-eating  snakes). 

Some  of  the  important 

species  are  Tropidonotus 

natrix,  the  common  British 

snake,  and  Coronella  aits 

triaca,  a  rare  snake  found 

in  South  England. 

Tropidonotus   fasciatus 

is  the  North  American  water  moccasin,  Zamenis  mucosas  the  Indian 

rat-snake,  and  Dasypeltis  scabra  is  the  African  egg-eating  snake. 
2.  Opisthoglypha— Poisonous   Colubridae   with   one   or   more   of 

the  hinder  teeth  oi  the  upper  jaw  grooved.— Early  last  century 

there  was  a  great  controversy  as  to  whether  these  snakes  were 

poisonous  or  not,  and  it  is  generally  stated  nowadays  that,  though 

poisonous,  their  venom  is 
weak,  and  that  the  posi- 
tion of  the  poison-fangs 
at  the  back  of  the  mouth 
prevents  the  bite  from 
lmrting  man.  Quelch  has, 
however,  recorded  cases 
in  which  bites  on  the 
lingers  from  Erythrolam- 
prus  cesculapii  L.  and 
Xenodon  severus  have 
caused  severe  inflamma- 
tion. 
The  following  list  is  given  by  Faust  of  those  known  to  be  poisonous 

to  animals:  Cwlopeltis  monspessulans  Herm.,  Trimorphodonbiscutatus 

D.  and  B.,  Tarbophis  savignyi  Descr.,  Dryophis  prasinus  Russl.,  and 

Leptodira  annulata  L. 

The  Opisthoglypha  are  divided  into  three  subfamilies:— 

(1)  Dihsadomorphince — Opisthoglyphida  with  well-developed  mouth, 

and  nostrils  situated  at  the  side  of  the  head. — They  include  the  Indian 

tin  -snakes. 


Fig.  32. — Skull  of  Ccelopeltis  monspessuLim 
Hermann. 

Note  the  fangs  in  the  rear  of  the  upper  jaw; 
hence  the  name  Opisthoglypha.  These  fangs 
are  grooved. 


246 


VENOMOUS  ANIMALS 


(2)  Elachistodontince — Opisthoglyphida  with  rudimentary  teeth  on 
the  palatine  and  pterygoid  bones. — Their  venom  is  said  to  be  so 
weak  and  their  poison-fangs  so  unfavourably  situated  that  they 
are  not  to  be  considered  as  dangerous  to  man.  They  include  the 
Indian  egg-eating  snakes. 

(3)  Homalop since — Opisthoglyphida  with  nostrils  valvular  and 
situated  on  the  upper  part  of  the  snout. — They  are  all  water-snakes. 

3.  Proteroglypha — Poisonous  Colubridse  with  the  front  teeth  in 
the  upper  jaw  well  developed  to  form  fan  s,  and  grooved  anteriorly. 
The  bases  of  these  fangs  are  connected  with  ducts  which  lead  from 
well-developed  poison  glands, — These  snakes  are  well  known  to 
be  highly  dangerous  to  man  and  animals.  They  are  divided  into 
three  subfamilies — Elapinae  and  Hydrophinse. 


Fig.  33. — Skull  of  Naja  tripudians  Merrem. 
Note  the  pair  of  short  rigidly  attached  fangs  situate  in  the  front  of  the  upper 
jaw;   hence  the  name  Proteroglypha.     These  fangs  are  grooved.     Note  the 
shortening;  of  the  maxilla. 


Elapince — Proteroglypha  living  on  land,  and  possessing  a  cylindrical 
tail. — Among  these  are  classed  the  cobras,  whose  proper  name  is 
cobra-di-capello — i.e.,  the  snake  with  the  hood,  so  called  because, 
when  excited,  it  expands  the  skin  behind  the  head  by  throwing 
outwards  the  cervical  ribs. 

Buddhists  regard  these  snakes  with  reverence,  because  one  with 
seven  heads  is  said  to  have  placed  its  expanded  hoods  over  Buddha's 
head,  and  thus  to  have  protected  him  from  the  glare  of  the  mid- 
day sun. 

The  genera  of  the  Elapina;  (Boulenger)  arc:  -Naja  Laurent;  Bunqarus 
Daudin;  H  emibungarus  Peters;  Callophis  Giinther;  Doliophis  Girard; 
Boulengerina  Dollo;  Elapechis  Boulenger;  Aspidelaps  Fitzinger;  W  alter  in- 
nesia  Latastc;  Dendraspis  Schlegel;  Ogmodon  Peters;  Glyphodon  Giinther; 
Pseudelaps  Dumeril  and  Bibron;  Dicmcnia  Gray;  Pseudcchis  Wagler; 
Denisonia  Krefft;  Tropidechis  Giinther;  Notechis  Boulenger;  Rhinoploce- 
phahis  F.  Midler;  Brachyaspis  Boulenger;  Acanthophis  Daudin;  Elapognathus 
Boulenger;  Ixhynchelaps  Jan;  Furma  Dumeril  and  Bibron;  Elaps  Schneider; 
Sepedon  Merrem;  Micropechis  Boulenger;  II oplocephalus  Cuvier. 

Naja  tripudians  Merrem,  the  cobra  with  one  spot,  or  a  pair  of 
spectacles  on  its  hood,  is  common  in  India  and  Ceylon.     N.  bungarus 


THE    VENOM 


247 


Schlegel.,  the  king  cobra,  or  hamadryad,  is  not  so  common,  but  is 
feared  because  of  its  size,  and  because  it  is  said  to  attack  people. 
N.  haje  L.  is  Cleopatra's  asp,  and  is  well  known  as  a  resident  of 
Egypt  and  North  Africa.  AT.  regalis  Schl.,  is  found  on  the  Gold 
Coast.  N.  nigricollis  Reinhart  is  found  on  the  Gold  Coast  and  in 
Sierra  Leone. 


Fig.  34. — Naja  tripudians  Merrem,  1781.     The  Cobra. 
Note  the  pair  of  spectacles  on  the  hood. 

The  kraits  are  also  included  in  this  family,  and  are: — Bungarus 
candidus  L.,  the  true  krait,  and  B.  fasciatus  Schn.,  the  banded 
krait,  with  yellow  and  black  bands,  both  of  which  are  common  in 


Fig. 


-Side  View  on  the  Head  of  the  Copra. 


India,  while  B.  ceylonicus  Gthr.  is  the  carawalla  of  Ceylon.  The 
Elapinae  are  the  only  poisonous  snakes  of  Australia,  and  include 
Noiechis  scutatus  Ptrs.  and  N.  pseudechis,  and  Acaiithophis  ant- 
arcticus  Shaw,  the  death  adder,  recognized  by  the  spines  on  its  tail. 


248  VENOMOUS  ANIMALS 

Elaps  corallinns  Wied,  the  coral  snake,  with  black  and  red  bands 
separated  by  narrow  rings  of  a  yellow  colour,  is  found  in  Columbia, 
British  Guiana,  Venezuela,  and  Brazil. 


Fig.  36. — Bungarus  ceylonicus  Gunthek. 
This  is  the  Carawalla  of  Ceylon. 

The  Sepedons  are  hooded  snakes  like  cobras  (Sepedon  hceniachates 
Lacep.  of  South  Africa),  and  are  supposed  to  throw  their  venom 


Fig.  37. — Hydrus  platurus  Linn^us. 
This  is  a  typical  sea-snake.     Note  the  flattened  spotted  tail. 

so  far  that  there  is  a  danger  of  it  getting  into  the  eyes  of  animals 
and  human  beings,  and  causing  severe  conjunctivitis. 


THE   VENOM  249 

None  of  these  snakes  are  found  in  Europe  or  America. 

Hxdrophince—Proteroglyphce  living  in  the  sea,  and  possessing  a 
flat  tail.— -These  snakes'  can  be  seen  swimming  ?in  families  far  out 
.n  the  Indian  Ocean,  but  are  also  found  in  all  Eastern  tropical  seas. 


Fig.  38. — Vipera  russeilii  Shaw. 

This   is   the    Tic    Polonga   of   Ceylon. 

The  genera  of  the  Hydrophinre  (Boulenger)  are: — Distera  Lacepede;  Aca- 
lyptus  Dumeril  and  Bibron;  Hydrophis  Dandin;  Enhydrina  Gray;  Hydreiaps 
Boulenger;  Hydrus  Schneider;  Thalassophis  Schmidt;  Enhydvis  Merrem; 
Flatiinis  Latreille;  Aipysurus  Lacepede. 

The  best-studied  species  is  Enhydrina  valakadien  Boie.  Another 
species,  Distera  semperi  Garm.,  lives  in  fresh  water  in  the  Philippine 
IslaiuR     It  is,  of  course,  dangerous  to  fishermen. 


FAMILY   Vll'l'Kin.E   Bonaparte,  1840. 

Definition.-— The  vipers  are  characterized  by  their  triangular  head 
and  their  tubular  poison-fangs  (hence  the  name  Solenoglypha), 
with  are  situated  anteriorly  in  the  mouth,  and  are  provided  with 
a  wide  foramen,  piercing  the  base  anteriorly  for  connection  with 
the  duct  of  the  poison  gland.  They  possess  a  stout  body  and  short 
tail,  and  are  all  viviparous. 

The  Viperidie  are  divided  into: — 

Crotalinse  Boulenger.— Vipers  with  a  deep  pit,  probably 
sensory  in  function,  situated  between  the  nostril  and 
the  eye  on  each  side  of  the  head. 

Viperinae  Boulenger. — -Vipers  without  such  a  pit. 

Crotalinae. — The  Crotalirue  include  the  rattlesnakes,  so  called 
because  they  have  a  number  of  horny  rings  which  lit  into  one 
another  at  the  end  of  the  tail. 


25  o 


VENOMOUS  ANIMALS 


^  The  genera  of  the  Crotalinse  (Boulenger)  are: — Crotalus  Linnaeus;  Sislrurus 
Garman;  Ancistrodon  Beauvois;  Lachesis  Daudin. 

There  are  two  divisions  of  rattlesnakes  in  America — Crotalus  and 
Sistrurus — distinguished  by  the  former  having  many  small,  and  the 
latter  only  nine  large,  scales  on  the  top  of  the  head. 

The  best-known  rattlesnakes  are  Crotalus  horridus  L.,  C.  scutu- 
latus  Kenn,  of  Texas,  C.  confluent  us  Say,  of  the  Pacific,  C.  durissus 
L.,  and  C'cerastes  Hallow. 


Fig.   39. — Skull  of  Crotalus  horridus  Linnjeus. 

Note  that  in  place  of  the  long  horizontal  maxilla  of  the  other  three  skulls 
there  is  only  a  small  vertical  movable  maxilla  on  each  side  of  the  anterior 
part  of  the  skull.  It  can  be  recognized  by  carrying  the  enormously  developed 
fang  which  is  canalized  and  is  virtually  a  hypodermic  needle  for  the  injection 
of  the  venom.     Note  the  reserve  fangs,  which  should  lie  up  against  the  skull. 


Fig.  40. — Side  View  of  the  Head 
of  a  Rattlesnake  (C.  horridus). 


Fie,.     41. — End    of     the    Tail    of 
C.  horridus  to  show  the  Rattle. 


Other  genera  are  Ancistrodon,  with  Ancistrodon  piscivorus  Lacep., 
the  water  moccasin,  and  A.  contortrix  L.,  the  copper-head;  Lachesis, 
with  Lachesis  lanceolatus  Laccp.,  the  celebrated  fer-de-lance  of  Mar- 
tinique; L.  anamallcnsis  Gthr.  and  Sistrurus,  with  Sistrurus  ravus 
Cope  and  5.  miliarius  L. 

Viperinae. — The  true  vipers  include:  Viper  a  berus  L.,  the  adder 
of  England;  V.  russellii  Shaw,  the  handsome  viper  of  India  and 
Ceylon;  Bitis  arietans  Merr.,  the  puff-adder  of  the  Gold  Coast; 
Cerastes  cornuius  Forskal,  the  horned  viper  of  North  Africa;  and 
Echis  carinatus  Sim.,  the  viper  of  the  Pyramids,  called  '  eta.' 

'1  he  genera  of  the  Viperinae  (Boulenger)  are" —  Vipera  Laurent;  Causns 
Wagler;  Bitis  Gray;  Pseudoccrastes  Boulenger;  Cerastes  Wagler;  Echis 
Merrem;  Atheris  Cope;  Atractaspis  Smith. 


THE  ACT  OF  STRIKING  251 

Geographical  Distribution. 

Asia. — Ei-apin^e:  Naja  tripudians,  N.  samarensis,  N.  bungarus  ;  Bungay  us 
fasciatus,  B.  candidus,  B.  ceylonicus  ;  Hemibungayus,  Callophis,  Doliophis. 

HyDROPHiNiE:  Enhydyina  valakadien,  Hydyus  platuyus,  Enhydyis  cuytus, 
Hydyophis  obscurus,  and  many  others. 

Viperin^e:  Vipera  berus,  V.  renavdii,  V.  raddii,  V.  lebetina,  V.  russellii  ; 
Pseudocerastes  peysicus  ;  Ceyastes  cornutus  ;  Echis  carinatus. 

Crotalin^e:  Ancistrodon  halys,  A.  himalayanus,  A.  hypnale,  and  others; 
Lachesis  flavoviridis,  L.  sumatranus,  L.  borneensis,  etc. 

Africa. — Elapin^::  Naja  haje,  N.  flava,  N.  melanoleuca,  N.  nigficollis,  N. 
anhietcB,  N .  goldii  ;  Sepedon  heemachates  ;  Boulengeyina  stoymsi  ;  Elapechis guen- 
theri,  etc.;  Aspidelaps  scutatus,  Walterinnesia  cegyptica,  Dendraspis  viyidis,  etc. 

ViPERiNiE:  Causus  rhombeatus,  etc.;  Vip:ra  ammodytes,  etc.;  Bit  is  arietans, 
B.  coynuta,  B.  gabonica,  B.  caudalis,  B.  atyopos,  B.  nasicornis,  B.  peyingueyi, 

B.  inornate;  Cerastes  cornutus,  Echis  carinata,  Atheris  chlor echis,  Atractaspis 
congica,  etc. 

Australia  and  Oceania. — Elapin^:  Ogmodon  vitianus  ;  Glvphodon  tyistis  ; 
Pseudelaps  muelleri,  etc.;  Diemenia  psammophis,  etc.;  Pseudechis  poyphyria- 
cus,  etc.;  Dcnisonia  supcrba,  etc.;  Micyopechis  elapoides,  Hoplocephalus 
vayiegatus,  etc.;  Tyopidechis  carinata  ;  Notechis  scutatus  ;  Bvachyaspis  cuyta  ; 
Elapognathits  minor;  Acanthophis  anterciicus,  Rhynchelaps  austyalis  ;  Furina 
calonota,  etc. 

Hydrophin'.e:  Hydyus,  Thalassophis,  Hydyelaps,  Hydyophis,  Disteva,  Enhy- 
dyis, Enhydyina,  Aipysuyus  ;  Platuyus. 

America. — Elapin^e:  Elaps,  many  species;  Micyopechis  elapoides  ;  Ancis- 
trodon piscivoyus,  A.  bilineatus,  A.  contovtyix,  Lachesis  mutus,  L.  lanceolatus, 
and  many  others;  Sistyuyus  miliarias,  S.  catynatus,  S.  ravus  ;  Crotalus  adaman- 
teus,  C.  horridus,  C.  confluentus,  C.  atyox,  C.  oyegonus,  C.  ceyastes,  C.  mitchelli, 

C.  terrificus,  and  others. 

The  Act  of  Striking. 

The  poison  is  secreted  by  glands,  which  are  either  modified  upper 
labial  glands  or  a  pair  of  glands  occupying  the  sides  of  the  head 
behind  the  eyes,  and  which  are  the  homologues  of  the  parotid  gland 
of  other  animals.  (An  account  of  the  structure  of  the  glands  can 
be  found  in  '  Spolia  Zeylanica/  1913.)  The  duct  usually  begins  as 
a  receptacle  which  runs  the  whole  length  of  the  gland.  This 
receptacle  is  of  importance,  as  it  enables  the  reptile  to  store  the 
venom.  Into  this  receptacle  the  smaller  ducts  of  the  gland  open, 
and  from  it  the  main  duct  runs  forward  just  above  the  line  of  the 
lip,  to  a  point  below  the  eye.  It  is  now  bent  backwards,  and  ends 
'in  a  small  papilla  on  the  anterior  wall  of  the  sheath  of  mucous 
membrane,  which  embraces  the  base  of  the  fang. 

Weir  Mitchell  describes  a  sphincter  muscle  of  reddish  appearance, 
and  composed  of  non-striated  muscle,  on  the  course  of  the  duct  of 
Crotalus,  but  no  such  sphincter  has  been  described  in  the  other 
snakes. 

The  poison  from  the  duct  either  runs  along  a  groove  on  the 
anterior  surface  of  a  long  tooth  called  the  fang,  or  else  along  a  canal 
formed  by  the  sides  of  the  groove  meeting  and  coalescing  by  the 
binding  of  the  developing  dentine.  It  should  be  clearly  understood 
that  the  venom  duct  does  not  directly  communicate  with  the  groove 
or  canal  in  the  tooth,  but  ends  close  to  it,  the  venom  being  con- 
ducted into  the  groove  by  a  fold  of  mucous  membrane.  The  vipers 
have  the  longest  fangs,  measuring  nearly  1  inch. 


252  VENOMOUS  ANIMALS 

The  poison-fang  projects  downwards  and  backwards  in  the  closed 
mouth,  being  firmly  attached  to  the  alveolar  process,  and  it  is  en- 
tirely due  to  the  free  mobility  of  the  cranial  bones  one  on  the  other 
that  the  fang  can  be  placed  in  such  a  position  as  to  be  able  to  enter 
the  skin  of  the  victim. 

The  act  of  striking,  as  described  by  Weir  Mitchell  in  Crotalus, 
is  as  follows:— In  preparing  to  strike,  the  snake  first  of  all  throws 
itself  into  its  well-known  characteristic  attitude,  with  the  lower 
part  of  the  body  coiled,  the  tail  slightly  projecting,  and  the  head 
raised  a  few  inches. 

The  tongue  now  darts  backwards  and  forwards,  and  the  air  of 
expiration,  in  passing  through  the  narrow  glottis,  produces  the 
characteristic  hissing.  The  muscles  on  the  convexity  of  the  coils 
now  contract  and  straighten  the  snake,  so  that  the  head  is  thrust 
suddenly  upwards,  forwards,  or  downwards,  as  required.  The 
maximum  thrust  is  half  of  the  body-length,  the  usual  one-third; 
but  the  reptile  judges  this  for  itself,  and  sometimes  makes  mistakes. 
The  jaws  are  widely  separated,  and  the  head  is  bent  back  on  the 
cervical  vertebrae,  and  a  muscle  called  the  spheno-pterygoid,  which, 
passing  from  the  basal  orbito-sphenoid  region,  backwards,  to  be 
inserted  into  the  inner  dorsal  surface  of  the  pterygoid,  contracts, 
and  draws  forward  the  pterygoid,  thus  pushing  upwards  the  ecto- 
pterygoid  (transversum),  and  causing  the  superior  maxillary  bone 
to  rotate  forward  on  its  lachrymal  articulation,  and  thus  to  erect 
the  fang.  This  motion,  when  it  reaches  its  limit,  is  checked  by 
ligaments,  and  now  the  lachrymal  yields  a  little  to  the  force  applied 
to  the  maxilla,  with  the  result  that  the  whole  muzzle  of  the  snake 
is  elevated,  and  produces  the  curious  appearance  which  it  has 
when  preparing  to  strike.  The  fang  now  enters  the  flesh  of  the 
victim,  and  the  head  of  the  snake  is  drawn  violently  backwards, 
too  much  action  being  prevented  by  the  muscles  of  the  spine.  In 
the  meanwhile  the  spheno-pterygoid,  acting  from  the  pterygoid, 
and  together  with  the  external  pterygoid,  rotates  the  maxilla  and 
pulls  the  fang  backwards,  and  so  drives  it  deeply  into  the  flesh. 

The  lower  jaw  now  closes  on  the  bitten  part,  and  this  act  squeezes 
the  fluids  from  all  parts  of  the  glands  forward  into  the  duct,  and 
not  merely  deepens  the  wound,  but  injects  the  venom  forcibly 
into  it. 

The  snake  then  has  to  disentangle  itself,  and  in  so  doing  may 
lose  its  fang.  But  this  is  of  no  moment,  for  fangs  are  shed  naturally, 
and  there  are  a  number  of  tooth-germs  in  different  stages  of  develop- 
ment ready  to  take  the  place  of  the  lost  tooth. 

Sometimes  the  fangs  have  not  been  properly  erected,  and  there- 
fore only  their  convex  borders  touch  the  skin  of  the  victim,  in 
which  case  the  venom  will  flow  on  to  the  skin,  but  the  fangs  will 
not  penetrate. 

The  Venom. 

Collection. — -The  venom  can  be  collected  by  making  the  snake 
strike  a  watchglass  covered  with  a  thin,  tightly  stretched  piece  of 


THE   VENOM  253 

indiarubber  sheeting,  or  by  chloroforming  the  snake  and  squeezing 
the  poison  out  of  the  glands  into  a  vessel. 

In  order  to  preserve  this  venom,  it  must  be  quickly  dried  over 
calcium  chloride  or  sulphuric  acid  in  a  desiccator,  when  it  will  keep 
for  years — e.g.,  Weir  Mitchell  kept  his  Crotalus  venom  for  twenty- 
three  years,  and  then  found  it  acti\ 

Physical  Characters. — The  quantity  of  the  venom  obtained 
depends  upon  many  factors,  such  as  the  general  condition  and  size 
of  the  snake,  whether  it  has  previously  ejected  venom,  and  whether 
it  has  been  long  in  captivity — -a  condition  in  which  the  secretion 
diminishes. 

An  adult  cobra  in  good  condition  is  said  by  Martin  to  give  from  o-6  c.c. 
to  i*  1  ex.,  and  this  should  yield  from  200  to  370  milligrammes  of  solids. 
Calmette  gives  124  milligrammes  of  liquid  venom,  yielding  35  milligrammes 
of  dry  venom  for  Naja  haje  Linnaeus. 

The  water-snake,  Enhydrina  valakadien  Boie,  gives  only  9-4  to  2-3  milli- 
grammes of  dry  venom,  according  to  Rogers. 

A  Vipcra  russellii  Shaw  gives  from  0*6  c.c.  to  i*o  c.c.  of  liquid,  which  yields 
150  to  250  milligrammes  of  solids. 

According  to  C.  J.  Martin,  Notechis  scutatus  Ptrs.  gives  205  milligrammes  of 
liquid,  containing  73  milligrammes  of  solids,  Notechis  pseudectis  160  milli- 
grammes of  liquid  and  94  milligrammes  of  solids. 

According  to  Calmette,  Lachesis  lanceolatus  Lacep.  gives  320  milligrammes 
of  liquid  venom,  containing  127  milligrammes  of  solids.  Cerastes  coriuitux 
Forsk.  from  Egypt  gave  123  milligrammes  of  liquid  and  27  milligrammes  of 
solids,  and  Crotalus  confluentus  Say  gave  370  milligrammes  of  liquid  and 
105  milligrammes  of  solids;  while  Crotalus  durissus  L.,  according  to  Flexner 
and  Noguchi,  yields  from  309  to  179  milligrammes  of  dry  venom;  and 
Ancistrodon  piscivorus  Lacep.  from  180  to  125  milligrammes. 

The  different  venoms  vary  in  physical  characters,  as  may  be 
judged  by  a  few  descriptions. 

Cobra-venom,  when  fresh,  is  a  transparent,  almost  colourless 
fluid,  with  a  syrupy  consistence  and  a  disagreeable  bitter  taste. 
When  dried,  it  becomes  yellowish-brown,  and  may  be  kept  for 
months.  It  can  decompose  and  become  of  a  dark  brown  colour, 
possessing  a  disagreeable  odour. 

Crotalus-venom,  according  to  Mitchell,  may  vary  from  a  pale 
emerald-green  to  an  orange  or  straw  colour,  and  when  dried  re- 
sembles dried  albumin.     It  has  no  taste  or  smell. 

The  poison  varies,  being  clear  and  limpid  or  pale  straw  or  yellow 
in  colour,  which  is  said  to  vary  with  the  degree  of  pigmentation 
of  the  snake  and  the  concentration  of  the  venom.  The  specific 
gravity  varies  from  1030  to  1044  (Weir  Mitchell)  for  Crotalus, 
1110  for  Cobra,  and  1077  for  Vipera  russellii.  Microscopic;*  !1\ . 
there  may  be  only  a  few  epithelial  cells  and  salivary  corpuscles 
and  bacteria,  all  due  to  contamination  with  fluids  from  the  mouth. 

Chemical  Analysis.- — The  reaction  of  pure  venom  is  acid. 

The  ultimate  analysis  was  made  by  Armstrong  for  Sir  Joseph 
Fayrer,  and  is  as  follows: — 

Crude  Dried  Poison. 
Carbon     .  .  .  .  . .  .  .  . .  .  .      43"55 

Nitrogen 13-43 


45'76 
i4'30 

6-6o 

2-50 
Traces. 


254  VENOMOUS  ANIMALS 

Alcoholic  Extract. 
Carbon     .  . 
Nitrogen.  . 
Hydrogen 
Sulphur   .  . 
Ash 

These  figures  merely  indicate  the  presence  of  proteid  in  some 
form,  and,  as  a  matter  of  fact,  Armstrong  found  reactions  indicating 
the  presence  of  albumin;  but  it  must  be  remembered  that  Prince 
Charles  Lucien  Bonaparte  had  already  shown  that  a  proteid  existed 
in  the  venom  of  the  viper,  and  that  the  toxicity  was  carried  down 
with  this  when  precipitated,  and,  further,  that  Weir  Mitchell  had 
corroborated  his  statements  while  examining  Crotalus-venom. 

Weir  Mitchell  and  Reich  ert  went  further,  and  discovered  tox- 
albumins  of  the  nature  of  globulins  (which  must  be  considered  to 
include  the  more  modern  proteoses)  in  venom.  They  considered 
these  proteids,  which  they  found  to  be  poisonous,  to  be  the  true 
active  principles  of  the  venom.  In  this  they  have  received  support 
from  Phisalix  and  Bertrand,  who  separated  from  viper-venom  two 
toxalbumins — echidin,  which  acts  locally;  and  echitoxin,  which 
acts  generally — and  also  from  C.  J.  Martin  and  Smith,  who  showed 
that  the  proteoses  consisted  of  proto-  and  heteroproteose,  with 
perhaps  a  little  deuteroproteose,  and  that  true  peptones  were 
absent. 

The  reader  will,  therefore,  not  be  surprised  to  hear  that  venom 
gives  proteid  reactions — e.g.,  Millon's,  the  xanthoproteic  and  the 
biuret — and  that  precipitates  appear  on  the  addition  of  picric  acid, 
copper  sulphate,  and  alcohol,  and  on  saturation  with  sodium 
chloride,  magnesium  chloride,  or  ammonium  chloride,  and,  lastly, 
that  it  coagulates  on  heating. 

With  regard  to  heat,  it  is  found  that  viperine  venoms  more 
readily  lose  their  toxicity  than  colubrine — e.g.,  8o°  to  850  C.  will 
destroy  most  of  the  former  venoms,  while  it  takes  1200  C.  to  do 
the  same  to  those  of  the  latter  with  certainty. 

If  venom  is  only  heated  to  the  temperature  of  first  coagulation, 
and  then  filtered,  it  will  be  found  that  the  filtrate  still  gives  a 
precipitate  with  alcohol,  and  is  still  active,  though  its  virulence 
is  diminished,  and  that  this  action  is  mostly  on  the  nervous 
system. 

The  analysis  of  venom,  however,  does  not  stop  with  toxalbumins, 
for,  as  Ewing  pointed  out  long  ago,  they  contain  true  toxins  allied 
to  those  produced  by  bacteria,  and  recently  Faust  has  separated 
from  the  toxalbumins  a  very  poisonous  non-nitrogenous  substance 
called  ophiotoxin. 

The,  knowledge  of  these  toxins  is  principally  due  to  the  work  of 
Flexner  and  Noguchi  on  the  venoms  of  Crotalus  durissus,  Ancis- 
trodon  piscivorus,  A.  contortrix,  and  Naja  tripudians. 

The  work  of  these  investigators,  coupled  with  that  of  C.  J. 
Martin,  Calmctte,  Lamb,  Weir  Mitchell,  Reichert,  Stewart,  Rogers, 
and  others, [have  shown  that  snake-venoms  are  very  complex  liquids 


THE   VENOM  255 

containing  some,  but  not  in  any  one  venom  all,  of  the  following 
active  principles : — 

1.  Neurotoxins. 

(1)  Acting  principally  on  the  respiratory  centre. 

(2)  Acting  principally  on  the  vasomotor  centre. 

(3)  Acting  upon  nerve  end-plates  in  striated  muscle,  par- 

ticularly on  those  of  the  phrenics. 

2.  Agglutinins. 
3    Cytolysins. 

(a)  Hemolysins. 
(6)  Leucolysins. 

(c)  Haemorrhagins. 

[d)  Other  cytolysins. 

4.  A  ntihcemolysins. 

5.  Antibactericidal  substances. 

6.  A  fibrin  ferment. 

7.  An  anti fibrin  ferment. 

8.  A  proteolytic  ferment. 

(.).  A  cardiac  and  vascular  tonic. 

Of  these  principles,  the  most  important  are  the  neurotoxins,  the 
cytolysins,  and  the  fibrin  ferment. 

The  analysis  of  the  venom,  according  to  Martin,  may  be  effected  by : 

(1)  Dialyzing  and  filtering  the  venom  through  a  gelatin  filter 
supported  in  the  pores  of  a  Pasteur-Chamberland  filter.  Fibrin 
ferments  and  heemorrhagins  d>  not  dialyze. 

(2)  Heating  from  70"  to  ioo°  C,  when  some  neurotoxins  and 
S<  >me  hemolysins  will  not  be  affected. 

(3)  Haemolysins  can  be  separated  from  neurotoxins  by  digestion 
with  red  blood  cells  mixed  with  serum  which  has  previously  been 
heated  to  560  C. 

Neurotoxins  and  other  cytolysins  can  be  separated  by  the  method 
of  Flexner  and  Noguchi,  which  will  be  described  later.  It  must  be 
clearly  understood  that  the  venom  of  any  one  snake  does  not 
contain  all  these  principles. 

1.  Neurotoxins. — The  neurotoxins  are  the  most  important 
active  principles  of  the  venom  of  many  snakes,  especially  the 
colubrine  snakes.  They  have  been  studied  in  Ancistrodon  con- 
tortrix  by  Flexner  and  Noguchi,  who  tested  the  anchoring  power 
of  the  various  tissues  of  the  body  for  the  principles  in  venom  in 
the  following  manner: — They  took  a  definite  weight  of  tissue 
washed  in  tepid,  sterile,  normal  saline  solution,  and  after  triturat- 
ing it  in  a  sterile  mortar,  mixed  it  in  test-tubes  with  a  given  number 
of  minimal  lethal  doses  1  M.L.I).)  of  the  venom.  The  mixture,  alter 
being  placed  in  a  thermostat  for  one  hour,  was  centrifugalized, 
and  the  supernatant  fluid  injected  into  guinea-pigs.  They  first 
took  2  grammes  of  the  organs,  and  mixed  them  with  three  times 
M.L.D.,  calculating  that  after  centrifugalizing  there  should  be  le/' 
at  least  two  M.L.D. 


256  VENOMOUS  ANIMALS 

The  results  were  as  follows : — 

Control  guinea-pig  died  in  45  minutes. 
Brain-injection  guinea-pig  died  in  19  hours. 
Blood-injection  guinea-pig  died  in  3  hours  50  minutes. 
Adrenals-injection  guinea-pig  died  in  2  hours  35  minutes. 
Spleen-injection  guinea-pig  died  in  2  hours  10  minutes. 
Liver-injection  guinea-pig  died  in  1  hour  30  minutes. 
Kidney-injection  guinea-pig  died  in  1  hour  55  minutes. 
Muscles- injection  guinea-pig  died  in  1  hour  30  minutes. 

Next  they  tried  two  M.L.D.,  with  the  following  results: — 
Brain-injection  guinea-pig  survived. 
Blood-injection  guinea-pig  died  in  28  hours. 
Liver-injection  guinea-pig  died  in  19  hours. 

From  these  experiments  they  conclude  that  snake-venom  con- 
tains a  neurotoxic  principle,  which  is  the  chief  poison,  and  which 
unites  in  multiple  minimal  doses  with  the  nerve  cells,  but  that,  even 
if  this  chief  toxic  principle  be  removed,  there  is  still  left  sufficient 
haemolysin  to  cause  death.' 

This  neurotoxic  substance  has  been  shown  by  Rogers  in  the 
cobra  and  the  Hydrophidse  to  attack  the  respiratory  centre  in  the 
medulla,  the  respirations  becoming  both  fewer  in  number  and  less 
in  amplitude  minute  by  minute,  until  they  cease  if  sufficiently  large 
doses  are  administered,  but  when  smaller  doses  are  given  there  is  at 
first  a  temporary  stimulation. 

Further,  he  shows  that  the  neurotoxic  substance  can  paralyze 
the  end-plates  of  the  phrenic  nerves  in  the  diaphragm  shortly  after 
the  failure  of  the  respiratory  centre  in  the  medulla. 

The  blood-pressure  does  not  appear  to  be  affected  by  the  poison, 
and,  in  fact,  the  circulation  can  be  kept  going  for  a  long  time  after 
cessation  of  breathing  if  artificial  respiration  is  resorted  to— a  fact 
first  shown  by  Brunton  and  Fayrer. 

On  the  other  hand,  with  regard  to  viperine  snakes — e.g.,  Vipera 
russellii,  Bitis  arietans,  Crotalus  horridus,  and  Lachesis  anamallensis 
— Rogers  concluded  that  the  neurotoxin  acted  upon  the  vasomotor 
centre  in  the  medulla — a  point  which  was  noted  by  Weir  Mitchell 
and  Reichert  as  a  cause  of  the  variation  of  the  blood-pressure  in 
Crotalus  poisoning. 

There  are  thus  several  neurotoxic  elements  in  snake-venom,  of 
which  two  great  groups  can  at  present  be  provisionally  described: 

(r)  Colubrine  neurotoxic  element,  acting  upon  the — (1)  Respira- 
tory centre  in  the  medulla;  (2)  the  end-plates  of  the  phrenic  nerve. 

(2)  Viperine  neurotoxic  element,  acting  upon  the  vasomotor 
centre  in  the  medulla. 

Kilvington  has  studied  the  effects  of  the  venom  of  H 'otocephalus 
curtus  Giinther  (Brachyaspis  curia  Schleg.)  on  nerve  cells,  and 
found  that  the  nerve  cells  of  the  central  part  of  the  cervical  enlarge- 
ment showed  a  breaking-up  of  the  Nissl  granules  into  a  fine  dust- 
like deposit.     The  nucleus  may  become  indistinct,  but  it  remains 


THE   VENOM  257 

in  the  centre  of  the  cell.  The  cells  are  unequally  attacked.  Those 
around  the  central  canal  are  most  severely  injured,  while  the 
motor  cells  are  little  affected.  In  sudden  death  no  change  is  noted. 
He  says  that  the  character  of  the  changes  are  of  the  same  order 
as  those  described  by  Marinesco  as  toxic  degeneration,  and  are 
very  like  those  following  the  fatal  dose  of  abrin.  Inflammatory 
and  vascular  changes  are  absent. 

As  to  the  cause  of  this  cytolysis,  it  would  appear  from  the  re- 
searches of  Flexner  and  Noguchi  that  it  is  probably  due  to  the 
union  of  an  endocomplement  (capable  of  being  neutralized  by 
calcium  chloride,  and  therefore  not  lecithin)  in  the  nerve  cell  with 
an  amboceptor  in  the  venom.  This  neurotoxin,  according  to 
Ehrlich's  denomination,  is  neurotropic — i.e.,  unites  only  with  nerve 
cells — and  monotropic — i.e.,  has  affinities  for  one  tissue  only. 

These  facts  have  been  demonstrated  by  Flexner  and  Noguchi  in 
cobra-venom  by  first  treating  it  with  erythrocytes  to  remove  the 
hemolysin,  and  then  heating  it  to  destroy  the  haemorrhagin,  thus 
Leaving  only  the  neurotoxic  principle  to  act  on  the  animal. 

They  found  that  after  cerebral  injection  the  appearance  of  the 
nervous  symptoms  was  almost  immediate,  while  with  other  methods 
of  injection  the  development  was  more  gradual. 

The  first  effect  of  the  neurotoxin  was  irritation  (convulsions), 
and  the  final  paralysis.  By  cobra- venom,  death  was  caused  by 
respiratory  paralysis.  Intracerebral  injection  of  a  viperine  venom 
like  that  of  Crotalus,  however,  caused  but  slight  symptoms. 

They  further  found  that  the  venoms  of  Ancistrcdon  piscivorus 
Lacep.  and  .1.  contortrix  L.  occupied  an  intermediate  position 
between  the  colubrine  and  viperine  venom-,  containing  both  neuro- 
toxins and  haemolysins  in  considerable  quantities.  From  these 
experiments  it  was  possible  to  classify  venoms  into  the  three  classes 
given  above. 

2.  Agglutinins. — Agglutination  of  the  red  cells  was  first  de- 
scribed bv  Weir  Mitchell  and  Reichert,  and  that  of  the  leucocytes 
by  Halford  and  Ralf. 

The  reaction  can  be  studied  by  adding  a  o-oi  per  cent,  to  10  per 
cent,  solution  of  dried  venom  in  normal  saline  to  washed  corpuscles 
suspended  in  normal  saline. 

The  time  required  for  agglutination  depends  upon  the  strength 
of  the  solution  of  venom,  and  the  effect  upon  the  corpuscles  depends 
upon  whether  they  come  together  quickly  or  slowly.  In  the  former 
case  they  are  not  damaged,  while  in  the  latter  their  shape  is  con- 
siderably altered.  Agglutinins  are  destroyed  by  heating  the  venom 
to  75°-8o°  C. 

The  agglutinins  for  the  red  cells  appear  to  be  the  same  sub- 
stances as  those  for  the  white,  and  in  both  cases  they  appear  to 
act  prior  to  the  cytolysis  of  the  cells. 

3.  The  Cytolysins. — {a)  Hemolysins. — Fontana  many  years  ago 
noted  that  the  blood  of  animals  bitten  by  vipers  was  fluid,  and  Weir 
-Mitchell  and  Reichert  described  the  haemoglobin  dissolving  out  of 

17 


258  VENOMOUS     ANIMALS 

the  agglutinated  red  corpuscles,  which  finally  became  invisible  when 
treated  with  Crotalus-venom.  Feoktistow  showed  that  a  2  per 
cent,  solution  of  the  venom  of  Viper  a  berus  destroyed  red  corpuscles 
in  eighteen  to  twenty-four  hours.  Martin  has  demonstrated  also 
that  the  venom  of  Pseudechis  in  o-i  per  cent,  solution  destroyed 
the  red  corpuscle. 

Flexner  and  Noguchi  showed  that  these  haemolysins  must  be 
looked  upon  as  amboceptors,  which  require  a  complement,  and  this 
they  obtain  in  the  bactericidal  principles  found  in  the  serum  of  the 
victim.  Hence,  when  they  join  with  the  erythrocytes  and  the 
complement,  they  not  merely  produce  haemolysis,  but  they  take 
away  the  bactericidal  powers  from  the  blood.  If,  as  was  found  to 
be  the  case  in  Necturus,  they  are  incapable  of  uniting  with  the 
complements,  they  are  incapable  of  damaging  the  bactericidal 
properties  of  the  serum;  for  it  was  found  that  haemolysis  was  but 
slightly  produced  in  the  blood  of  Necturus,  and  then  only  after 
long  periods,  and  at  the  same  time  the  serum  of  Necturus  did 
not  lose  its  bactericidal  effects  to  Bacillus  colt  communis  and 
B.  typhosus. 

The  haemolysins  have  been  further  studied  by  Kyes,  who  showed 
that  in  some  animals  the  venom  alone  could  haemolyze  the  washed 
red  cells,  whereas  in  others  it  could  not  do  so  until  some  fresh  serum 
was  added.  In  the  first  class  came  man,  dog,  rabbit,  guinea-pig, 
and  horse,  and  with  reference  to  these  he  came  to  the  conclusion 
that  the  complement  was  contained  in  the  red  blood  cell  itself 
— i.e.,  was  an  endocomplement.  In  a  further  research  with  Sachs, 
he  shows  that  this  endocomplement  is  attached  to  the  stroma  of 
the  red  cells.  Further,  they  conclude  that  it  is  the  lecithin  of  the 
stroma  which  acts  as  the  complement,  and  support  this  by  experi- 
ments showing  that  lecithin  prepared  from  the  yolk  of  an  egg 
can  act  as  a  complement  for  the  venom,  and  dissolve  cells  which 
are  not  affected  by  the  venom  alone.  They  look  upon  the 
fatty  acid  radical  of  the  lecithin  as  being  probably  the  active 
agent. 

In  the  second  class — viz.,  those  animals  whose  erythrocytes  are 
not  affected  by  venom  alone  without  the  presence  of  serum — come 
the  ox,  sheep,  and  the  goat ;  but  Kyes  found  it  very  easy  to  produce 
solution  by  the  addition  of  foreign  sera — e.g.,  ox  blood  by  venom 
and  guinea-pig  serum;  sheep  blood  by  venom  and  guinea-pig 
serum — which  clearly  showed  that  the  venom  was  an  amboceptor, 
and  agreed  with  the  results  of  Flexner  and  Noguchi. 

Further,  he  showed  that  by  heating  the  serum  to  560  C.  for  half 
an  hour  this  action  was  destroyed,  but  if  heated  to  650  C.  for  half 
an  hour  haemolysis  took  place.  In  other  words,  serum  contained 
two  possible  complements:  (1)  free  in  the  serum,  and  destroyed  by 
heat;  (2)  only  in  heated  serum.  Kyes  and  Sachs  consider  (1)  to  be 
complements  in  the  restricted  sense  of  the  term,  and  that  there  are 
differences  in  their  workings  from  that  of  the  lecithin  complement. 
More  recently,  however,  they  have  doubted  this,  and  begun  to 


THE  VENOM  259 

believe  that  tne  serum  merely  trees  the  lecithin,  which  acts  as  the 
true  complement. 

In  (2)  the  lecithin,  being  free,  is  able  to  combine  with  the  ambo- 
ceptor and  cause  the  haemolysis.  They  further  show  that  if  a 
blood  solution  is  heated  to  620  C,  it  is  inactivated,  owing  to  the 
union  at  this  temperature  of  the  lecithin  directly  to  the  haemoglobin. 

They  therefore  came  to  the  conclusion  that  the  reason  why  there 
was  a  difference  in  the  action  of  the  venom  on  red  cells  was  that  in 
the  rirst  class — e.g.,  man,  etc. — -the  lecithin  was  so  loosely  bound  to 
the  cell  that  it  was  available  as  a  complement  for  the  venom  ambo- 
ceptor, whereas  in  the  other  cases  it  was  more  closely  bound,  and 
therefore  was  not  available. 

Kyes  then  went  a  step  further,  and  mixed  40  c.c.  of  a  1  per  cent, 
solution  of  cobra-venom  in  a  0*75  per  cent,  salt  solution,  with 
20  c.c.  of  20  per  cent,  solution  of  lecithin  in  chloroform,  and  then 
centrifugalized  the  mixture.  The  result  was  the  separation  of 
chloroform  and  water  into  two  layers;  from  the  former  the  cobra- 
venom  Lecithin  could  be  precipitated  by  the  addition  of  pure  ether. 
This  body  possessed  haemolytic  but  no  neurotoxic  properties,  which 
entirely  remained  in  the  water.  Thus  Kyes  clearly  supports  the 
fact  first  pointed  out  by  the  late  Dr.  Myers  that  the  neurotoxic 
and  haemolytic  actions  are  quite  separate. 

This  cobra-venom  lecithin  differs  in  many  of  its  properties  from 
cobra-venom  and  from  lecithin- — e.g.,  it  is  soluble  in  water,  which 
lecithin  is  not ;  it  is  soluble  in  alcohol,  chloroform,  and  toluol,  which 
the  cobra-venom  amboceptor  is  not. 

Kyes  found  that  the  lecithin  was  active  with  the  blood  cells  of  all 
the  species  he  examined,  and  that  the  absolute  quantity  necessary 
for  haemolysis  was  the  same  for  the  blood  cells  of  different  species. 
Thus  lecithin  corresponding  to  0*003  milligramme  of  the  dry  cobra- 
venom  was  capable  of  haemolyzing  1  c.c.  of  a  5  per  cent,  suspension 
of  the  erythrocytes  of  guinea-pig,  rabbit,  man,  or  ox. 

The  lecithide  acts  very  quickly  on  the  red  cells  (twenty-four  times 
more  quickly  than  the  venom),  which  is  due  to  the  fact  that  no  time 
is  spent  in  developing  the  real  toxic  agent — i.e.,  the  lecithide. 

The  lecithide  is  not  destroyed  by  heating  to  ioo°  C.  for  six  hours, 
and  is  little  affected  by  Calmette's  serum. 

Kyes  went  further,  and  studied  the  lecithides  of — (1)  Lachesis 
anamallensis  Gunther;  (2)  L.  lanceolatus  Lacep.;  (3)  L.  flavoviridis 
Hallow;  (4)  Crotalus  durissus  L.;  (5)  Vipera  russellii  Shaw  (6)  Naja 
bungarus  Schleg.;  (j)Bungarus  candidus  L.;  (8)  B .  fascial  us  Schn. 

All  these  poisons,  on  the  addition  of  sufficient  lecithin,  destroy 
blood  cells,  and,  except  in  the  first  and  the  third,  the  absolute 
quantity  ol  the  poison  is  the  same  as  that  mentioned  just 
above. 

That  of  Lachesis  anamallensis  Gunther  is,  however,  twenty-live 
times  weaker,  and  L.  lanceolatus  Lacep.  ten  times  weaker,  this 
being  due  to  the  fact  that  the  former  forms  only  one-twenty-rifth 
and  the  latter  one-tenth  the  usual  quantity  of  lecithide. 


260  VENOMOUS  ANIMALS 

Hence  Kyes  concludes  that  the  hemolytic  element  of  all  snakes 
is  an  amboceptor  possessed  of  a  haptophore  group  for  the  erythro- 
cyte, and  a  toxophore  group  for  lecithin,  which  contains  the  active 
element  for  ■  the  haemolysis.  The  haptophore  group,  however, 
probably  differs  in  different  poisons,  for  Lamb  has  shown  that, 
while  cobra-venom  will  unite  with  Calmette's  antitoxin,  poison  of 
Viper  a  nissellii  will  not.  Bungarus  and  Naja  bungarus  act  like 
the  cobra,  and  Lachesis  and  Crotalus  do  not. 

Noguchi  investigated  lecithin,  and  found  it  to  be  by  no  means 
an  inert  substance,  and,  further,  that  certain  oleic  compounds  and 
oleic  acid  itself  would  act  as  venom  activators. 

He  found  that  the  addition  of  oleic  acid  or  its  soluble  soaps  to 
a  non-activating  serum  in  the  ratio  which  corresponds  to  the  per- 
centages of  fatty  acids  and  soaps  contained  in  some  of  the  easily 
activating  sera  makes  it  highly  active  to  venom.  In  the  normal 
serum  of  a  dog,  however,  he  found  that  there  was  a  lecithin  com- 
pound acting  like  free  lecithin.  He  further  found  that  these  two 
classes  of  activators  could  be  differentiated  from  one  another  by 
calcium  chloride,  which  annulled  the  first  group,  but  was  powerless 
against  the  lecithide.  Non-activating  sera  do  not  contain  this 
lecithin  compound,  and  other  lecithides — e.g.,  lecith  albumin — are 
powerless. 

When  serum  is  heated,  the  non-coagulated  portions  contain  a 
lecithin  activator,  as  described  by  Kyes,  which  is  identical  with 
Chabrie's  albumon;  but  this  does  not  exist  preformed  in  unheated 
sera,  and  is  due  to  the  high  temperature  altering  other  proteid 
lecithides  into  albumon. 

He  further  found  ovovitellin  to  be  one  of  the  best  lecithin  proteid 
activators.  He  finally  came  to  the  conclusion  that  the  reason  why 
some  red  corpuscles  (man,  etc.)  are  acted  upon  by  venom,  while 
others  (ox,  etc.)  are  not,  depends  solely  upon  the  amount  of  fatty 
acids,  and  perhaps  also  of  soaps  and  fats,  contained  in  the  cor- 
puscles, to  the  stroma  of  which  they  are  attached.  They  exist 
plentifully  in  corpuscles  easily  affected,  and  in  small  amount  in 
those  not  easily  affected. 

The  position  at  the  present  moment  is,  therefore,  that  snake- 
venom  produces  haemolysis  by  its  amboceptors  uniting  with  com- 
plements contained  in  the  sera  of  the  majority  of  mammals  and 
birds  investigated,  and  that  these  complements  are  fatty  acids  and 
soaps  (belonging  principally  to  the  oleic  series). 

Further,  there  are  endocomplcments  in  the  erythrocytes  of  certain 
species,  and  these  are  of  +he  same  nature  as  those  in  normal  sera, 
and  are  attached  to  the  stroma  of  the  corpuscle. 

Finally,  the  reason  why  heated  sera  become  active  at  high  tem- 
peratures after  losing  their  activity  at  lower  temperatures  is  because 
of  the  conversion  of  the  proteid  lecithides  into  another  form  of 
lecithide  called  albumon,  which  is  an  activator. 

For  the  controversy  between  von  Dungern,  Coca,  supported  by 
Mainwaring  on  the  one  side  and  Kyes  on  the  other,  reference  must 


THE  r/:Ynu  261 

be  made  to  the  original  papers  given  in  our  list  at  the  end  of  this 
chapter. 

(6)  The  Leucolysins.  -Weir  Mitchell  and  Reichert  hud  noticed  in 
their  researches  that  the  mobility  of  leucocytes  absolutely  ceased 
in  crotalus  poisoning.  Martin  studied  this  carefully  with  Pseu- 
dechis  venom,  and  says  that  for  the  first  fifteen  minutes  he  could 
see  no  change  in  the  white  cells,  but  they  exhibited  no  amoeboid 
movements.  At  the  end  of  this  time  the  nuclei  in  some  of  them 
wen-  very  distinct,  as  if  fixed  by  acetic  acid.  They  then  became 
intensely  granular,  and  soon  began  to  swell,  and  their  outlines  to 
gJUW  less  distinct,  until  they  disappeared,  leaving  only  a  small 
heap  of  granules. 

Flexner  and  Noguchi  studied  this  phenomenon,  and  found  that 
leucocytes  with  large  coarse  granules  were  most  quickly  affected; 
next  came  the  fine  granular  varieties;  and  last  of  all  the  lympho- 
cytes. They  found  cobra  poison  much  more  vigorous  than  that 
of  crotalus.  As  to  the  leucolysins,  they  proved  that  they  were 
separate  from  the  hemolysins  by  treating  washed  red  corpuscles 
with  copperhead  venom  until  the  supernatant  fluid,  after  centri- 
lugalization,  ceased  to  have  any  effect  on  red  cells.  This  fluid  was 
then  brought  into  contact  with  leucocytes,  when  lysis  without 
agglutination  took  place.  If,  however,  washed  leucocytes  were 
treated  first,  the  supernatant  fluid  was  found  to  be  actively  haemo- 
lytic.  They  therefore  concluded  that  the  haemolysins  were  distinct 
from  the  leucolysins,  but  that  the  agglutinins  were  probably  the 
same. 

We  are  not  aware  of  further  researches  as  to  the  nature  of  the 
leucolysins,  though  obviously  such  researches  are  required. 

(c)  Hamorrhagin.-  Weir  Mitchell  and  Reichert,  by  observing  a 
mesentery  moistened  with  crotalus-venom,  came  to  the  conclusion 
that  the  blood  escaped  from  the  vessel  owing  to  damage  to  the  wall. 

Flexner  and  Noguchi  found  that  by  heating  crotalus-venom  to 
75°  C.  for  thirty  minutes,  this  haemorrhagic  power  was  lost,  and 
along  with  it  most  of  the  toxicity,  as  ten  or  twenty  M.L.D.  were 
required  to  cause  death  with  symptoms  resembling  cobra-venom. 
They  conclude  that  this  death  must  be  due  to  the  neurotoxic  or 
haematoxic  properties  (haemolysins  and  agglutinins)  in  the  venom, 
md  that,  as  the  latter  can  be  eliminated  without  any  apparent  loss 
oi  toxicity,  it  must  be  due  to  the  neurotoxins. 

The  toxic  principle  lost  by  heating  to  75  '  ('.,  Flexner  and  Noguchi 
called  haemorrhagin.  They  studied  its  action  in  the  mesentery  by 
injecting  the  venom  into  the  peritoneal  cavity,  or  placing  a  minute 
particle  of  the  dried  poison  on  the  exposed  mesentery,  and  then 
removing  specimens,  which  they  fixed  in  Zenker's  fluid,  cut  into 
sections,  and  stained  with  haematoxylin  and  eosin.  They  found 
that  the  extravasation  of  blood  took  place  not  by  diapedesis,  but 
through  actual  rents  in  the  walls.  These  rents  are  not  simple 
ruptures,  but  are  apparently  due  to  a  cytolytic  action  upon  the 
endothelial  cells  of  the  capillaries  and  the  walls  of  the  small  veins. 


262  VENOMOUS  ANIMALS 

(d)  Other  Cytolysins. — Flexner  and  Noguchi  have  found  that  the 
amboceptors  in  venom  can  act  upon  a  number  of  the  cells  of  the 
body — e.g.,  liver,  kidney,  testicle,  and  ovary — causing  lysis,  the 
complement  being  probably  either  endocellular  or  in  the  lymph- 
stream.  The  nature  of  the  complement  is,  however,  quite  unknown 
at  present,  but  is  probably  different  from  the  complement  acting 
on  the  red  cells,  as  its  activity  is  destroyed  by  heating  to  6o°  C.  for 
some  time.  The  histological  effects  of  these  toxins  can  be  noted 
particularly  in  the  microscopical  appearances  in  the  liver  and 
kidney.  The  liver  shows  necrosis  and  fatty  degeneration  of  its 
cells,  and,  as  a  reactionary  process,  leucocytic  infiltration  around 
the  bile-passages.  In  the  kidney,  the  glomeruli  show  intense  con- 
gestion of  their  capillaries,  often  associated  with  ruptures  of  their 
walls  and  haemorrhage  into  Bowman's  capsule.  The  cells  of  the 
tubules  are  necrotic  and  detached,  filling  the  lumen.  The  whole 
organ  is  congested,  and  there  may  be  interstitial  haemorrhages. 
The  spleen  is  but  slightly  affected. 

4.  Antih^emolysins. — Weir  Mitchell  and  Stewart  have  shown 
that  if  crotalus-venom  is  added  to  red  corpuscles  in  a  certain 
degree  of  concentration,  no  haemolysis  takes  place.  This  fact  has 
been  confirmed  by  Myers  and  Stephens  for  the  cobra,  and  Lamb 
for  Viper  a  russellii. 

Noguchi  believes  that  the  action  is  due  to  venom  having  the 
power  in  certain  cases  of  precipitating  the  outer  layer  of  the  haemo- 
globin, while  in  other  cases  this  does  not  take  place. 

5.  Antibactericidal  Substances. — Weir  Mitchell  drew  atten- 
tion to  the  fact  that  bodies  of  animals  dead  from  crotalus  poisoning 
rapidly  decomposed,  while  Ewing  found  that  the  normal  germicidal 
power  of  the  serum  was  destroyed— a  fact  confirmed  by  Martin. 

Flexner  and  Noguchi  also  investigated  this  action,  and  came  to 
the  conclusion  that  :— 

(1)  All  venoms,  when  used  in  suitable  quantities,  destroy  the 
bactericidal  properties  of  many  normal  sera. 

(2)  The  manner  of  this  destruction  consists  in  the  fixation  of  the 
serum  complements  by  the  venoms. 

(3)  Venoms  have  no  action  upon  the  intermediary  bodies  of  the 
serum. 

6.  Fibrin  Ferment.— A  fibrin  ferment  has  been  shown  by  Martin 
to  be  present  in  the  venoms  of  the  viperidse  and  also  of  some  of  the 
colubridae.  In  the  former  it  is  the  active  agent  which  causes  the 
vascular  clotting  in  small  animals,  with  convulsions  and  sudden 
death.  This  coagulative  substance  has  been  shown  by  Barratt  to 
be  a  thrombin. 

7.  Antifibrin  Ferment. — An  antifibrin  ferment — that  is  to 
say,  a  substance  which  in  minute  quantities  is  able  to  prevent  the 
coagulation  of  the  blood — is  found  in  cobra  and  allied  venoms. 

8.  Proteolytic  Ferment. — Venom  contains  a  body  of  some 
description,  probably  a  ferment,  which  is  capable  of  transforming 
proteid. 


ENTRY  OF  THE  VENOM  INTO  THE  BODY  26.^ 

Thus,  Mitchell  and  Reichert  long  ago  showed  that  muscle-fibres 
at  the  site  of  the  bite  were  quickly  softened  by  crotalus-venom, 
and  Flexner  and  Noguchi  have  shown  that  gelatin  is  liquefied  by 
both  crotalus-  and  cobra-venoms,  but  that  coagulated  proteids  are 
not  acted  upon.  Microscopically  the  muscular  fibres  at  the  site 
of  the  bite  are  seen  to  have  undergone  necrosis  and  degenera- 
tion, and  later  a  polymorphonuclear  leucocytic  infiltration  may  be 
noted. 

9.  Cardiac  and  Vascular  Tonic. — Sir  Lauder  Brunton  and  Sir 
Joseph  Fayrer  showed  that  the  poisons  of  the  cobra  had  a  stimulant 
effect  on  the  heart,  and  that  the  circulation  could  be  kept  going 
tor  a  long  time  after  complete  failure  of  breatning  if  artificial 
respiration  is  kept  up — -a  fact  of  considerable  importance  if  any 
antidotal  treatment  is  available. 

It  is  not  clear  whether  this  is  due  to  direct  action  on  the  muscles 
of  the  heart,  but  it  appears  from  Rogers'  experiments  that  the 
effect  on  the  bloodvessels  is  clue  to  local  action  on  the  arterioles. 
This  effect  is  produced  by  the  cobra  and  Vipera  russellii  venom. 

Entry  of  the  Venom  into  the  Body. 

The  poison,  the  characters  of  which  have  been  described,  is  intro- 
duced into  the  body  of  man  or  that  of  an  animal  usually  by  the 
snake  biting  the  skin  and  injecting  the  poison  either  subcutaneously 
or  into  a  vessel.  In  the  former  case  it  will  soon  reach  the  blood- 
stream, and  be  distributed  to  the  different  parts  of  the  body. 

The  effect  of  entry  into  a  bloodvessel  is  to  produce  immediately 
the  signs  of  the  poisoning,  whereas  in  the  subcutaneous  tissue  it 
may  take  some  time,  and  even  be  modified,  especially  in  the  viperine 
type. 

The  quantity  injected  by  a  cobra,  according  to  Acton  and 
Knowles,  during  the  first  strike,  is  0-172  gramme  (i.e.,  -{"  of  total 
venom  in  gland);  during  the  second  0-1215;  after  which  it  steadily 
diminishes  until  it  is  not  fatal  to  man  (probably)  about  the  seventh 
or  eighth  strike.  Echis  injects  {'(  of  total  venom  during  first 
strike. 

If  the  venom  falls  on  the  conjunctiva  it  is  readily  absorbed,  and 
symptoms  of  poisoning  will  ensue,  or  an  acute  inflammation  be 
set  up. 

Taken  by  the  mouth,  the  venom  of  the  colubridae  is  harmless, 
provided  there  arc  no  cracks  or  abrasions,  and  is  destroyed  by  the 
saliva  and  pancreatic  juice.  Viperine  venom,  on  the  other  hand, 
causes  gastritis,  gastro-intestinal  haemorrhage,  and  even  death, 
without  the  appearance  of  the  usual  symptoms,  a  fact  known  to 
the  natives  of  Ceylon  with  regard  to  the  venom  of  Vipera  russellii. 

Minimum  Lethal  Dose  (M.L.D.). 

The  minimum  lethal  dose  varies  with  the  species  of  snake,  the 
condition  of  the  snake,  and  with  the  species  of  the  victim. 


264  VENOMOUS  ANIMALS 

Tables  are  given  by  Calmette,  and  Martin  and  Lamb,  showing 
the  amount  for  different  snakes  and  animals.  Thus,  the  quantity 
of  cobra-venom  required  to  kill  a  kilogramme  of  a  dog  is  o-ooo8 
gramme,  and  of  a  rabbit  0-0005;  an(l  that  of  Bungarus  Candidas 
for  a  rabbit  is  0-0008  gramme,  and  that  of  Enhydrina  valakadien 
for  a  rabbit  is  0 -00006  gramme,  while  the  same  for  a  cat  is  0-0002. 
Putting  it  in  another  way,  1  gramme  of  cobra-venom  will  kill 
1,250  kilogrammes  in  weight  of  a  dog,  2,000  of  rabbit,  2,500  of 
guinea-pig,  1,500  of  rat,  and  8,333  °f  mouse,  and  20,000  grammes 
of  horse. 

Calmette  calculates  that,  taking  a  man  of  average  size,  the 
minimum  lethal  dose  might  be  halfway  between  the  dog  and  the 
horse — i.e.,  would  be  0-015  gramme  of  cobra-venom — and  1  gramme 
will  kill  10,000  kilogrammes  of  man,  or  165  persons  of  the  weight 
of  60  kilogrammes;  but,  of  course,  this  is  only  a  very  approximate 
guess.  Lamb  calculates  the  M.L.D.  for  man  to  be  0-015  gramme 
of  cobra -venom,  and  Fraser  puts  the  same  at  0-031  gramme,  while 
other  authors  give  cobra  M.L.D.  for  man  o-oio  gramme  and  echis 
M.L.D.  the  same  figure. 

Lamb  gives  a  number  of  minimum  lethal  doses  for  snakes  cal- 
culated per  kilogramme  of  rabbit  and  injected  intravenously,  which 

are: — 

Bungarus  eandidus    .  .  .  .  .  .  0*00004  gramme. 

Enhydrina  valakadien  .  .  .  .  0*00005 

Vipera  russellii  .  .  .  .  .  .  o-oooi 

Naja  tripudians  and  N.  bungarus  .  .  0*00035  ,, 

Bungarus  fasciatus    ..  ..  ..  0-0007 

Effects  of  the  Venom. 

The  effects  of  the  venom  have  been  carefully  studied  on  warm 
and  cold  blooded  animals  by  many  observers  for  a  long  series  of 
years,  but  there  is  a  distinct  difference  in  the  action  of  different 
kinds  of  venom,  and  therefore  it  is  as  well  to  discuss  the  effect  of 
each  separately. 

In  doing  this  it  will  be  noted  that  it  is  difficult  to  obtain  un- 
doubted cases  of  bites  by  definitely  known  snakes  in  man,  and 
even  when  these  are  obtained  the  urgent  necessity  for  treatment 
causes  the  symptoms  to  be  little  noted.  Therefore  it  is  necessary 
to  detail  first  the  experiments  on  animals,  and  then  the  symptoms 
found  in  man. 

Colubrine  Venom — Naja  tripudians  Merrem. — The  experiments  of 
numerous  observers  show  that  the  effects  of  this  venom  on  animals 
are : — 

1.  Paralysis  of  voluntary  movement. 

2.  Salivation. 

3.  Marked  effect  on  the  respiration,  which  ceases  before  the  heart. 
In  smaller  quantities  the  paralysis  becomes  more  marked,  and 

in  cases  of  longer  duration  several  features  are  added: — 

1.  Local  inflammation  where  the  bite  was  inflicted. 

2.  Lachrymation. 


EFFECTS  OF  THE   VENOM  263 

3.  Mucous  discharges  from  the  nose,  respiratory  organs,  and 
stomach. 

4.  Very  occasionally  the  mucous  discharges  arc  stained  with 
blood. 

Beyond  obvious  pain,  the  local  effects  are  engorgement  of  the 
vessels  with  blood,  and  effusion  into  the  tissues.  If  the  animal 
recovers,  there  may  be  suppuration  and  sloughing  of  the  affected 
part.  The  effects  on  the  nervous  system  seem  to  be  due  to  the 
action  of  the  poison  on  the  brain  and  spinal  cord,  and  pari  passu 
on  the  motor  nerve  endings.  The  most  evident  paralysis  is  that 
of  the  tongue,  larynx,  and  pharynx,  as  evinced  by  the  inability 
to  retain  the  saliva  within  the  mouth,  to  move  the  tongue,  or  to 
swallow.     This  is  due  to  the  action  of  the  poison  on  the  medulla. 

There  is  also,  as  indicated  above,  clear  evidence  of  action  upon 
the  respiratory  centre,  which  has  been  carefully  studied  by  Wall 
and  others,  who  show  that  in  large  doses  there  is  a  progressive  slow- 
ing, and  in  smaller  doses  first  acceleration  and  then  slowing  of  the 
respirations.  There  appears  to  be  but  little  effect  upon  the  heart 
and  circulation  or  temperature. 

The  effect  on  the  blood  in  causing  haemolysis  was  first  demon- 
strated by  Cunningham,  who  considered  it  the  main  feature.  Not 
merely  are  the  corpuscles  dissolved,  but  the  coagulability  is  re- 
duced, and  hence  the  blood-staining  of  the  tissues  and  the  urine 
in  experiments  on  animals,  provided  that  artificial  respiration  is 
kept  up. 

The  effects  of  the  venom  on  man  are  local  pain  in  the  neighbour- 
hood of  the  bite,  which  appears  as  two  small  punctures  about  J  inch 
apart,  usually  exuding  a  blood-stained  fluid.  The  pain  increases  in 
severity,  and  spreads  up  the  limb  on  to  the  body.  In  a  short  time 
the  victim  feels  intoxicated,  and  presently  loses  control  of  his  legs, 
which  become  paralyzed,  as  may  other  muscles,  including  those  of 
the  jaw.  There  is  often  profuse  salivation,  and  inability  to  speak 
or  swallow.  The  pulse  and  respirations  increase  for  a  time,  and 
then  the  breathing  becomes  slower,  and  death  occurs  from  failure 
of  the  respiration,  while  the  heart  continues  to  beat  for  a  short 
time  after  the  respirations  have  ceased. 

If  recovery  takes  place,  the  urgent  symptoms  abate,  some  slight 
fever  and  local  swelling  occurs,  while  a  large  amount  of  urine  is 
passed. 

When  examined  post  mortem,  it  will  he  found  that  the  rigor 
mortis  is  well  marked,  while  the  blood,  is  fluid  in  man,  but  coagulated 
m  animals.  If  the  corpuscles  are  examined  soon  after  death,  no 
change  will  be  noted,  but  later  they  alter,  and  blood-crystals, 
indicating  haemolysis,  may  form.  The  parotids  may  be  swollen. 
The  brain  is  normal,  but  the  pia  mater  is  gorged  with  blood.  The 
muscles  are  often  of  a  dirty  red  colour.  The  lungs  in  human  beings 
are  generally  congested,  and  the  bronchi  and  smaller  tubes  filled 
with  thin  frothy  fluid  and  intensely  congested.  Particles  of  food 
or  remedies  are  to  be  found  in  the  air-tubes  because  of  the  paralysis 


26f>  VENOMOUS  ANIMALS 

of  the  larynx.  The  right  heart  is  distended  with  blood.  The  liver 
is  congested  and  dark.  The  kidneys  may  be  normal  or  intensely 
congested.  The  intestines  show  nothing  in  particular.  The  bladder 
is  contracted 

Microscopically,  fatty  degeneration  of  the  liver  and  kidney,  and 
necrosis  of  hepatic  and  renal  epithelium,  are  to  be  seen,  as  well  as 
round-celled  infiltration  along  bile-ducts,  which  is  probably  due  to 
excretion  of  poison. 

Turning  now  to  the  colubrine  snakes,  which  resemble  the  cobra, 
there  are  observations  upon  Naja  haje,  N.  bungarus,  Bungarus 
candidus,  B.  fasciatus,  and  the  Hydrophidce. 

Naja  haje  Linnaeus.- — Calmette  records  that  Dr.  Deschamps 
observed  a  case  of  this  bite  in  Senegal  in  which  the  snake  bit  the 
patient  in  the  forehead.  Almost  immediately  great  weakness, 
accompanied  by  nausea  and  pains  in  the  head  and  neck,  set  in. 
Locally  two  raised  areas  were  seen,  around  which  the  tissue  was 
cedematous.  Cold  sweats  occurred.  The  oedema  spread  to  the 
face,  dyspnoea  appeared,  and  the  pulse  became  small  and  inter- 
mittent, paralysis  set  in,  and  the  patient  became  comatose,  but 
recovered  on  treatment  with  antivenene. 

Naja  bungarus  Schlegel. — N .  bungarus,  the  hamadryad,  is  by  far 
the  biggest  of  the  Indian  poisonous  snakes.  Rogers  rinds  its 
venom  very  like  that  of  the  cobra,  producing  paralysis  and  death 
from  failure  of  respiration,  while  the  heart  continues  to  beat  for  a 
time. 

There  is  no  intravascular  clotting,  and  the  haemolytic  action  is 
very  slight,  but  the  phrenic  nerve-plates  are  paralyzed.  If  small 
doses  are  given,  the  respirations  are  increased. 

We  are  not  acquainted  with  the  symptoms  exhibited  by  an 
undoubted  case  of  this  bite  in  a  human  being. 

Bungarus  candidus  Linnaeus.— As  to  B.  candidus  L.,  the  com- 
monest of  all  Indian  snakes,  there  is  not  much  to  say,  except  that 
all  researches  (Fayrer,  Wall,  and  Rogers)  indicate  that  its  venom 
is  almost  exactly  the  same  as  that  of  the  cobra,  but  is  slightly 
more  virulent. 

Cases  of  this  bite  are  common.  In  brief,  the  symptoms  are: — a 
sense  of  tightness  across  the  chest,  with  paralysis,  particularly  of 
the  muscles  of  the  face,  deglutition,  and  phonation.  The  con- 
junctival' are  suffused,  the  pupils  dilated,  the  pulse  and  respirations 
quickened;  the  temperature  is  normal,  and  the  local  signs  are  not 
ma  iked. 

Coma  and  convulsions  precede  death,  which  is  due  to  failure  of 
respiration.  Cong<  st ion  of  the  meninges  and  brain  and  liquid  blood 
arc  the  principal  signs  found  post  mortem. 

Bungarus  ceylonicus  (Gunther).— B.  ceylonicus,  the  Ceylon  krait 
or  carawalla,  has  been  reported  by  Green  to  have  killed  a  man  in 
twelve  hours.  The  man  was  bitten  on  the  left  foot  at  4  a.m.,  and 
felt  quite  well  till  5.30  a.m.,  when  he  felt  drowsiness,  which  in- 
creased till  10  a.m.,  when  he  could  hardly  swallow  and  was  very 


EFFECTS  OF  THE   VENOM  267 

sick.  Paralysis  affected  his  legs,  and  he  became  cold.  Artificial 
respiration  was  now  resorted  to,  but  at  2  p.m.  he  became  very 
feverish  and  insensible,  and  died  at  4  p.m. 

Bungarus  fasciatus  Schneider. — -The  effects  of  the  poison  of 
B.fasciatus  have  been  carefully  studied  by  Wall,  Lamb,  and  Rogers. 

In  acute  rases  death  takes  place  quickly  from  failure  of  respira- 
tion; the  blood  is  coagulated,  and  there  is  paralysis,  and  sometimes 
convulsions. 

Chronic  cases,  on  the  other  hand,  last  for  days,  during  which 
there  is  loss  of  weight  and  emaciation,  and  perhaps  some  paralysis. 

Microscopical  examination  of  the  cortex  of  the  brain,  medulla, 
and  spinal  cord  shows  diffuse  chromatolysis,  affecting  a  very  con- 
siderable portion  of  the  ganglion  cells,  being  most  marked  in  the 
cortex,  next  in  the  cord,  least  in  the  medulla.  The  cells  show  a 
rather  deeply  stained  plasma,  in  which  are  scattered  dust-like 
granules,  the  remnants  of  the  Nissl  bodies;  many  cells  show  vacuo- 
lation  of  the  plasma,  and  some  are  reduced  to  mere  outlines  (ghost 
cells). 

Rogers'  experiments  tend  to  show  that  even  in  injecting  large 
doses  the  blood  may  not  clot,  and  that  the  animal  may  be  killed, 
as  in  cobra-venom,  by  direct  action  of  the  poison  on  the  respiratory 
centre,  and  also  on  the  nerve-endings  of  the  phrenics,  so  that  the 
venom  appears  to  be  a  mixture  of  a  viperine  with  a  colubrine 
poison. 

The  only  authentic  case  of  human  poisoning  by  B.  fasciatus  is 
mentioned  by  Fayrer,  in  which  there  was  tingling  sensation  and 
later  pain  at  the  seat  of  the  punctures,  with  some  swelling,  all  of 
which  disappeared  in  less  than  twenty-four  hours. 

Australian  Snakes. — -The  symptoms  produced  by  the  bite  of  the 
Elapinae  in  Australia  are  local  swelling  and  pain,  followed  in  from 
fifteen  minutes  to  two  hours  by  constitutional  symptoms.  The 
patient  becomes  unable  to  stand,  signs  of  prostration,  accompanied 
by  vomiting,  appear.  The  circulation  begins  to  fail,  the  heart's 
action  becomes  weak,  the  extremities  cold,  and  the  skin  blanched, 
while  the  respiration,  after  a  preliminary  excitation,  becomes 
slowed.  Coma  now  intervenes,  the  sensations  being  diminished 
and  the  pupils  dilated,  and  death  results  from  failure  of  the  respira- 
tion, preceded  sometimes  by  convulsions.  The  heart  continues  to 
beat  after  the  circulation  has  ceased. 

Elaps  fulvius,  the  harlequin  snake,  which  is  found  in  the  eastern 
parts  of  the  Southern  United  States,  causes  great  local  pain,  fol- 
lowed in  one  hour  by  drowsiness,  unconsciousness,  and  collapse, 
lasting  until  death,  or  for  a  day  or  so  if  the  patient  recovers.  Death 
usually  ensues  in  about  twenty-four  hours  after  a  bite,  and  in 
persons  tending  to  recovery  the  danger  of  death  is  not  escaped  until 
three  to  four  days  have  passed  away,  as  the  symptoms  tend  to 
recur  periodically. 

Spitting  Snakes. — The  known  spitting  snakes — i.e.,  snakes  which 
can  project  their  venom  to  a  distance — are  Sepedon  hcBmochates, 


268  VENOMOUS  ANT  MAIS 

Naja  flava,  and  N.  nigricollis,  N .  tripudians,  Echis  cariuata,  with 
perhaps  the  addition  of  Naja  melanoleuca  and  Vipera  ritssellii ;  and 
it  is  possible  that  further  observations  will  show  that  all  the  Colu- 
bridse  and  Viperidae  have  this  power  to  a  greater  or  lesser  extent. 
Of  course  the  action  is  not  spitting  in  the  correct  sense  of  the  word, 
but  merely  projection  of  venom,  which  causes  conjunctivitis  if  it 
enters  the  eyes,  and  a  saltish  taste  if  it  enters  the  mouth. 

The  Hydrophidce. — -Rogers  experimented  with  Enhydrina  vala- 
kadien  Boie,  Distera  cyanocincta  Daud.,  and  Hydrophis  cantoris  (ithr., 
and  came  to  the  conclusion  that  their  venom  only  differed  from 
that  of  the  cobra  in  the  following  points: — 

1.  They  were  more  toxic. 

2.  They  were  much  less  hemolytic,  and  hence  caused  no  blood- 
stained effusion  at  the  site  of  the  injecti  n. 

3.  They  did  not  affect  the  coagulability  of  the  blood;  therefore 
the  poison  is  almost  purely  neurotoxic. 

There  is  at  first  an  excitation  of  the  nervous  system,  leading  to 
a  feeling  of  activity  and  vivacity,  which,  however,  soon  passes  off. 
The  earliest  signs  of  distress  begin  with  difficulty  of  articulation 
and  feeling  of  stiffness  in  the  body  and  of  suffocation.  The  stiffness 
in  the  muscles  increases,  and  occasional  spasms  occur,  while  signs 
of  gastric  irritation,  with  vomiting,  appear.  Convulsions  and  death 
may  ensue  after  a  day  or  so.     The  local  signs  may  be  slight. 

Viperine  Venom.  — ■  Vipera  russellii  Shaw,  the  tic  polonga  of 
Ceylon,  is  a  good  example  of  this  type  of  venom.  Wall's  experi- 
ments show  that  a  dog  bitten  by  one  of  these  vipers  will  become 
convulsed,  and  die  within  five  minutes.  The  cause  of  this  sudden 
death  has  been  shown  by  Rogers  to  be  intravascular  clotting,  which 
is  best  marked  in  the  portal  vein,  and  then  only  in  small  animals. 
Post  mortem,  there  are  haemorrhages  into  the  area  of  the  bite,  and 
into  kidney  and  intestine. 

In  addition  to  these  acute  cases,  there  are  also  chronic  cases,  in 
which  the  local  symptoms  are  more  or  less  extensive  subcutaneous 
haemorrhages,  around  which  there  is  much  oedema.  This  haemor- 
rhage may  be  absorbed,  or  the  area  may  slough,  or  an  abscess,  or 
even  a  spreading  gangrene,  may  ensue 

The  general  symptoms  are  rapid  emaciation,  profound  anaemia 
and  lethargy,  and  in  sonic  cases  hematuria  and  a  discharge  of  blood 
from  the  bowel. 

Rogers  has  carefully  investigated  these  symptoms,  and  has 
pointed  out  that  there  is  a  remarkable  fall  of  blood-pressure  due  to 
vaso-dilatation  of  the  portal  system,  caused  by  action  of  the  poison 
on  the  central,  and  not  the  peripheral  vasomotor  apparatus,  the 
heart  muscle  being  unaffected.  Lamb  and  Hanni  showed  that  in 
chronic  cases  there  is  deficiency  in  the  blood  coagulability. 

In  man  there  are  the  two  small  punctured  wounds  caused  by  the 
fangs,  around  which  the  skin  is  swollen  and  livid  and  painful,  The 
swelling  and  discoloration  spreads,  and  in  the  course  of  twenty-four 
hours  the  patient  becomes  at  first  excited,  with  thready  pulse  and 


EFFECTS  OF  THE  VENOM  269 

hurried  respirations,  and  later  stuporous.  The  skin  is  clammy  and 
covered  with  a  cold  sweat,  while  the  swelling  and  discoloration 
spreads  considerably,  reaching  the  trunk.  In  due  course  convul- 
sions set  in,  and  death  ensues  from  failure  of  the  circulation.  The 
post-mortem  reveals  congestion  of  the  meninges  and  lungs  with 
fluid  blood,  and  nothing  else  of  importance. 

Bitis  arietans. — The  puff-adder  poison  was  found  by  Rogers  to 
work  in  much  the  same  manner  as  that  of  Vipera  russcllii,  but  not 
to  be  so  poisonous. 

Echis  carinaia. — This  is  a  very  poisonous  snake,  and  the  effects 
of  its  bite  resemble  that  of  the  cobra. 

Wall  records  a  case  in  which  there  was  much  local  swelling, 
passage  of  blood  in  the  urine,  faeces,  and  vomit,  elevation  of  tem- 
perature, and  death  from  exhaustion,  due  to  loss  of  blood,  on  the 
ninth  day.  Martin  and  Lamb  record  another  case  in  which  there 
was  much  swelling  of  the  bitten  part,  due  to  exudation  of  liquid 
blood.  Pain  and  tenderness  were  felt  along  the  nerves,  together 
with  anaesthesia,  extreme  restlessness,  with  cold  and  clammy  ex- 
tremities, but  no  haemorrhages.  Loss  of  consciousness,  with  de- 
lirium, set  in  only  a  short  time  before  death,  which  took  place  at 
the  twenty-fifth  hour. 

Fayrer  gives  a  good  account  of  a  chronic  case,  in  which  there  was 
depression  and  faintness,  coldness  of  the  extremities,  with  swelling 
of  the  affected  part,  and  marked  haemorrhages  from  eyes,  gums, 
throat,  nose,  vagina,  and  under  the  nails. 

The  Crolalidce  are  typically  represented  by  Crotalus  horridus  of 
America,  which  has  been  carefully  studied  by  Weir  Mitchell  and 
Reichert,  and  by  Lachesis,  which  latter  has  been  studied  by  Rogers 
in  India. 

Crotalus  horridus. — The  local  effects  are: — -oedema,  swelling,  dark- 
ening of  the  parts  with  infiltration  of  incoagulable  blood,  breaking 
down  of  the  tissues,  putrefaction,  and  sloughing.  There  is  no  clot- 
ting of  the  blood,  which,  on  the  other  hand,  is  fluid  and  incoagulable. 
There  is  a  marked  fall  of  blood-pressure,  and  respiration  gradually 
ceases,  due  to  the  failure  of  the  circulation,  but  there  is  no  direct 
effect  on  the  respiratory  centre,  and  the  phrenics  are  not  paralyzed. 
The  heart  goes  on  beating  after  respiration  ceases,  but  is  slightly 
weakened.  Post-mortem  examination  shows  haemorrhages  into  the 
peri-  and  endo-cardium,  and  into  the  peritoneum  and  pleura,  but 
not  in  the  brain  or  the  medulla,  while  the  whole  portal  system  is 
much  congested. 

Rogers  placed  a  loop  of  small  intestine  in  an  oncometer,  and  found 
that  fall  of  blood-pressure  was  associated  with  a  vaso-dilatation  of 
the  portal  system,  in  which  the  blood  was  not  clotted.  This  vaso- 
dilatation he  considers  may  possibly  be  due  to  the  action  of  the 
venom  on  the  vasomotor  centre  in  the  medulla,  and  thinks  that 
he  is  supported  in  his  theory  by  the  appearance  of  Traube-Hering 
curves  in  his  blood-pressure  tracings.  Pearce  notes  acute  glomeru- 
lar lesions  due  to  the  eiidothelialytic  body. 


270  VENOMOUS  ANIMALS 

Weir  Mitchell  and  others  have  carefully  collected  the  symptoms 
following  this  bite.  In  most  instances  the  bite  is  painful,  and 
the  part  becomes  swollen  and  discoloured,  while  both  the  pain 
and  the  swelling  increase  steadily.  The  swelling  is  due  to  the 
effusion  of  blood.  Very  seldom  is  there  any  lymphangitis  or 
enlargement  of  the  lymphatic  glands.  Vesication,  sloughing,  and 
gangrene  may  result  if  life  is  prolonged  and  the  dose  considerable. 
If,  on  the  other  hand,  the  amount  of  poison  injected  is  inconsider- 
able, the  swelling  declines,  and  the  pain  disappears  very  quickly. 
Constitutional  symptoms  are  said  by  some  people  to  begin  directly 
after  the  bite,  but  this  is  hardly  likely,  as  man  is  a  relatively  large 
animal.  Under  exceptional  circumstances  it  is  recorded  that  the 
symptoms  did  not  begin  till  about  thirty  minutes  after  the  bite, 
but  usually  the  length  of  time  is  only  a  few  minutes.  The  person 
feels  extremely  faint,  or  complains  that  his  lower  limbs  are  not 
able  to  support  him.  There  is  no  primary  stimulating  effect  like 
that  mentioned  in  other  venoms.  The  patient  staggers  or  falls, 
cold  sweats  bathe  the  surface  of  the  skin,  and  nausea  and  vomiting 
occur.  The  pulse  is  rapid  and  feeble,  the  expression  anxious,  and, 
according  to  Mitchell,  in  a  few  cases  the  mind  may  be  slightly  dis- 
turbed, but  this  may  be  largely  due  to  fear.  If  the  patient  does 
not  die  at  this  stage,  the  local  symptoms  mentioned  above  become 
very  pronounced,  and  signs  of  general  blood-poisoning  show  them- 
selves, and  often  lead  to  death. 

The  post-mortem  reveals  that  the  brain  is  normal,  but  congested 
and  somewhat  cedematous ;  the  trachea  and  bronchi  are  congested, 
and  full  of  red  frothy  mucus;  while  the  lungs  are  healthy,  but 
somewhat  congested.  The  peritoneum  may  contain  a  little  fluid, 
and  the  mucosa  of  the  stomach  and  small  intestines  may  be  in- 
tensely congested  and  infiltrated  with  serum.  In  some  cases  the 
blood  is  coagulated,  in  some  it  is  fluid.  The  local  swelling  is  due 
to  serous  exudation.  The  chief  features  of  the  post-mortem  are 
vaso-dilatation  of  the  portal  system  and  fluidity  of  the  blood. 

Lachesis.- — -This  snake  shows  the  same  symptoms  as  Crotalus,  but 
it  has  some  effect  upon  the  respiratory  centre,  causing  quickening 
of  respiration  before  the  slowing  begins.  The  phrenics  arc  not 
paralyzed.  Moreover,  it  is  possible  that  the  first  quick  fall  of 
blood-pressure  observed  is  due  to  action  of  the  poison  on  the  heart, 
but  the  subsequent  steady  fall  is  due  to  the  action  on  the  vasomotor 
centres,  as  in  Crotalus. 

Kitajima  says  that  the  region  of  the  bite  becomes  dark  purple 
in  colour  and  swells;  that  the  pain  is  severe  and  burning;  and  that 
the  lymph  glands  become  enlarged  and  tender.  The  face  is  pale, 
the  pulse  feeble  and  rapid.-  Respiration  is  normal;  a  slight  fever 
is  not  infrequent.  Coldness  of  the  extremities,  with  dyspnoea  and 
cold  sweats,  come  on  just  before  death.  Blood  has  been  observed 
in  the  urine  and  faeces. 


IMMUNITY  271 

Excretion  of  the  Poison. 

It  is  believed  that  the  poison  leaves  the  body  principally  by  the 
kidney,  and  to  a  less  extent  by  the  mucosa  of  the  stomach,  the 
salivary  and  mammary  glands. 

With  regard  to  the  kidney,  there  is  some  direct  proof  of  the 
excretion,  because  the  urine  of  a  dog  poisoned  by  Enhydrina  vala- 
kadien,  when  injected  hypodermically  into  a  pigeon,  caused  death 
in  twenty-two  hours. 

It  is  also  stated  that*i  drachm  of  the  saliva  of  a  dog  poisoned  by 
a  cobra  was  capable  of  causing  death  in  two  hours. 

With  regard  to  excretion  by  the  mammary  glands,  an  infant  is 
said  to  have  died  after  sucking  the  breast  of  a  woman  bitten  by  a 
poisonous  snake. 

Immunity. 

Having  considered  the  chemical  composition  and  physiological 
action  of  the  venom,  the  next  point  to  be  discussed  is  immunity  to 
its  action. 

Ancient  and  modern  peoples  have  equally  held  the  belief  that  a  person  who 
has  been  bitten  by  a  poisonous  snake  and  survived  obtains  some  sort  of 
immunity;  generally  the  belief  has  been  that  this  immunity  is  capable  of 
protecting  the  individual  against  all  kinds  of  snakes. 

Ancient  fables  credited  the  Psylli  of  Africa,  the  Marsi  of  Italy,  and  Gouni 
of  India,  with  immunity,  on  the  ground  that  they  had  snake's  blood  in  then 
veins. 

The  pig  was  long  thought  to  be  naturally  immune;  but  this  is  a  mistake, 
for  the  relatively  slight  effect  of  snake-venom  is  due  to  the  presence  of  the 
thick  layer  of  but  slightly  vascular  fat  which  surrounds  the  animal's  body. 
The  mongoose  (Htrpestes  ichneumon)  is  believed  to  be  naturally  immune  to 
cobra-bite. 

Acquired  immunity  is  said  to  occur  among  natives,  especially  snake- 
charmers,  and  Europeans  who  have  been  bitten  several  times  by  snakes. 
The  Eisowy  of  Western  Barbary  are  said  to  have  acquired  such  an  immunity, 
and  to  allow  themselves  to  be  bitten  by  snakes  proved  afterwards  to  be 
poisonous  by  killing  a  fowl.  The  natives  of  Bushmanland,  Namaqualand, 
and  Damaraland  are  said  to  drink  the  venom  of  snakes  as  a  protection. 
In  Ceylon  a  cobra  is  said  to  have  bitten  a  snake-charmer,  and  shortly  after- 
wards a  bystander.  The  snake-charmer  escaped  without  symptoms,  the 
bystander  died. 

The  first  scientific  attempt  to  produce  an  artificial  immunity  was  made  by 
Sewall  in  1887,  when  by  repeated  small  injections  he  raised  the  resistance  of 
pigeons  so  high  that  they  were  able  to  resist  ten  times  the  minimum  lethal 
dose  of  the  venom  of  a  Crotalus.  Kanthack  also  produced  a  partial  immunity 
to  cobra-venom  in  1891.  Kaufmann,  a  little  later,  obtained  a  similar  result 
with  the  French  viper. 

In  1892  Calmette  showed  that  by  repeated  inoculation  of  venom 
heated  to  8o°  C.  a  certain  amount  of  resistance  was  produced  in 
animals.  In  1894  he  made  researches  on  the  venom  of  the  cobra, 
and  about  the  same  time  Phisalix  and  Bertrand  investigated  that 
of  the  viper,  and  showed  that  animals  vaccinated  with  venom 
developed  a  true  immunity,  and  those  inoculated  against  the 
cobra-venom  were  able  to  resist  mortal  doses  of  Viftera,  Bungarus, 
Cerastes,  Naja  haje,  and  Pseudechis  venoms.     Later  they  showed 


272  VENOMOUS  ANIMALS 

that  the  serum  of  an  animal  vaccinated  by  snake-venom  contained 
antitoxins  capable  of  producing  an  immunity  in  new  animals. 

Calmette  obtained  his  serum  from  horses,  but  with  great  diffi- 
cui.'y,  as  many  of  the  animals  died  in  the  course  of  treatment  from 
endocarditis  and  acute  nephritis,  while  in  others  abscesses  formed. 

He  found  that  in  a  fresh  horse  0-025  gramme  of  cobra-venom 
was  sufficient  to  kill  the  animal  in  twelve  to  twenty-four  hours, 
but  on  vaccinating  the  animals  for  sixteen  months,  it  was  found 
that  a  horse  could  stand  without  reaction  the  injection  of  2  grammes 
of  cobra-venom — i.e.,  eighty  times  the  M.L.D. 

From  such  a  horse  it  was  found  possible  to  withdraw  as  much  as 
20  litres  of  blood  in  three  bleedings  spread  over  ten  days,  the  serum 
being  considered  to  be  ready  for  use  when  1  cc.  mixed  with  o-ooi 
gramme  of  cobra-venom  produced  no  sign  of  intoxication  when 
injected  subcutaneously  into  a  rabbit,  and  when,  after  injecting 
2  cc.  of  the  serum  into  a  rabbit  of  2  kilogrammes  weight,  two 
hours  later  1  milligramme  of  venom  could  be  injected  without 
results.  This  serum  was  said  to  preserve  intact  its  antitoxic  value 
in  all  climates.  The  venom  used  for  these  injections  was  principally 
that  of  the  cobra,  with  a  slight  admixture  of  other  venoms. 

In  1895-96  Fraser  of  Edinburgh  confirmed  Calmette's  results,  and 
believed  that  if  an  animal  was  so  successfully  vaccinated  that  it 
could  resist  the  minimum  lethal  dose  of  one  venom,  it  would  also 
be  able  to  resist  that  of  other  venoms.  He  believed  that  venom 
introduced  into  the  stomach  conferred  immunity. 

In  1897  C.  J.  Martin  showed  that  Calmette's  serum  did  not 
preserve  animals  against  the  venom  of  Notechis  scutatus. 

From  1901  onwards  Lamb  in  India  studied  carefully  the  effects 
of  snake-venoms,  and  came  to  the  conclusion  that  Calmette's  serum 
is  active  against  cobra-venom,  but  is  not  useful  against  that  of 
Vifiera  russellii,  Btingarus  fasciatus,  or  of  Echis  carinatus. 

In  1902  Tidswell  showed  that  serum  prepared  from  the  venom 
of  Notechis  scutatus  did  not  neutralize  the  venoms  of  the  cobra, 
Bungarus  fasciatus,  or  Viper  a  russellii,  and,  further,  had  no  effect 
on  the  venoms  of  the  brown  and  black  snakes  and  death-adder  of 
Australia. 

In  the  same  year  Lamb  pointed  out  that  there  was  a  precipitin 
id  venom-immune  sera,  and  this  point  being  further  investigated  by 
Hunter,  the  deduction  was  made  that  these  precipitins  were  specific, 
and  due  to  the  coagulable  proteids. 

The  following  pure  sera  have  been  prepared : — 

1.  Lamb's  Pure  Naja  tripudians  Merrem  Serum.- — This  serum 
is  strongly  antitoxic  for  cobra  -  venom,  and  in  large  doses  1<  >r 
Enhydrina  valakadien  Boie,  but  has  no  effect  upon  Bungarus  can- 
did us  L.,  Brachyasfiis  curia  Schleg.,  Echis  carinatus  Schn.,  Lachesis 
gramineus  Shaw,  Vij>era  russellii  Shaw. 

It  delays  death  in  Bungarus  fasciatus  Schn.,  Naja  bungarus 
Schleg.,  Crotalus  durissus  L. 

2.  Lamb's  Pure    Vipera    russellii    Shaw    Serum.  —  This    serum 


IMMUNITY  275 

neutralizes  the  venom  of  Vipera  russellii  and  Crotalus  durissus,  but 
has  no  action  upon — Colubridae:  Naja  tripudians  Merrem,  N .  bun- 
garus  Schleg.,  Bungarus  candidus  L.,  B.  fasciatus  Schn.,  Enhydrina 
valakadien  Boie;  Viperidss:  Echis  carinatus  Schn.,  Lachesis  gramineiis 
Shaw. 

3.  Tidswell's  Pure  Notcchis  scutatus  Ptrs.  Serum. — -This  serum 
has  a  strong  antitoxic  effect  upon  the  venom  of  Notcchis  scutatus, 
but  has  no  effect  upon  that  of — Colubridae :  Naja  tripudians  Merrem, 
N.  bungarus  Schleg.,  Bungarus  candidus  L.,  B.  fasciatus  Schn., 
Enhydrina  valakadien  Boie;  Viperidse:  Vipera  russellii  Shaw,  Echis 
carinatus  Schn.,  Lachesis  gramineus  Shaw,  Crotalus  durissus  L. 

4.  Noguchi's  Pure  Crotalus  Serum. — It  has  a  strong  effect  upon 
Crotalus  venom,  and  a  slight  effect  upon  Ancistrodon  piscivorus 
Lacep.,  and  none  on  the  cobra. 

5.  Noguchi's  Pure  Ancistrodon  piscivorus  Lacep.  Serum. — -This  has 
a  marked  effect  upon  moccasin- venom,  and  medium  effect  upon 
Crotalus,  and  none  on  cobra-venom. 

6.  Brazil's  Pure  Crotalus  horridus  L.  Serum. — This  serum  is 
equally  efficient  for  the  venoms  of  Crotalus  horridus  or  C.  durissus, 
but  is  useless  for  cobra-venom. 

The  Caracas  Commission  reports  that  this  serum  is  more  effica- 
cious against  the  venom  of  Crotalus  than  that  of  Calmette,  which 
fails  to  neutralize  the  haemorrhagins. 

7.  Kitajima's  Pure  Lachesis  flavoviridis  Hallow  Serum. — This 
serum  is  specific  for  Lachesis  venom,  against  which  Calmette's 
serum  is  useless. 

It  is  clear  that  the  antisera  mentioned  above  are  very  nearly 
specific,  for  they  neutralize  principally  the  venom  of  the  species 
employed,  and  sometimes,  in  larger  doses,  that  of  some  allied 
species. 

It  is  obvious  that  this  is  of  great  importance  in  considering  the 
serum  treatment  of  snake-bite. 

8.  Polyvalent  Sera.— Polyvalent  sera  prepared  for  more  than  two 
venoms  are  not  very  efficacious. 

Diagnosis. 

It  might  be  thought  that  the  diagnosis  of  snake-bite  would  be 
obvious,  and  that  nothing  need  be  written  on  the  subject,  but  this 
is  not  always  so,  because  snake-bite  often  takes  place  in  the  dark, 
and  the  nature  of  the  snake  is  unknown. 

The  diagnosis  may  be  divided  into  two  heads: — -(1)  Has  a  snake 
bitten  the  person  ?     (2)  Was  the  snake  a  poisonous  one  ? 

The  first  thing  to  do  is  to  tie  a  proximal  ligature  on  the  limo, 
and  then  to  examine  the  area  of  the  supposed  bite.  If  there  are 
absolutely  no  fang-marks  and  no  venom  on  the  skin,  then  obviously 
there  is  no  danger;  but  fang-marks  on  the  skin,  or  venom  on  mucous 
m>  mbranes  (which,  of  course,  may  have  cracks),  or  on  skin  with 
scratches,  may  be  dangerous. 

If  there  are  no  fang-marks,  and  the  snake  is  forthcoming,  examine 

IS 


274  VENOMOUS  ANIMALS 

it  to  see  whether  it  is  poisonous  or  not,  especially  to  see  whether 
there  are  fangs,  and  if  non-poisonous,  the  patient's  mind  can  be 
relieved  at  once. 

Prognosis. 

It  appears  that  only  a  relatively  small  percentage  of  persons 
bitten  by  snakes  (supposed  to  be  poisonous)  die.  C.  J.  Martin  and 
Lamb  place  it  about  30  per  cent.,  but  much  depends  upon  the 
quantity  of  venom  injected  and  the  rapidity  with  which  symptoms 
develop.  The  recoveries  from  full  doses  of  echis-venom  in  un- 
treated cases  is  about  40  per  cent.,  and  of  cobra-venom  only  3  to 
4  per  cent.  Personally,  we  believe  that  ir>  most  cases  if  treatment 
has  been  prompt,  and  the  symptoms  appear  slowly,  the  outlook  is 
by  no  means  hopeless. 

Treatment. 

Snake-poisoning  consists  in  the  hypodermic  or  intravascular 
injection  of  a  series  of  poisonous  principles  which  act  chiefly  upon 
the  nervous  system  and  the  blood. 

The  virulence  of  the  poisoning  depends  upon  the  ratio  of  the 
quantity  of  the  poison  injected  to  the  size  of  the  animal.  The 
same  quantity  of  poison  will  therefore  have  a  more  serious  effect 
upon  a  child  than  upon  an  adult.  The  less  the  quantity  of  poison 
which  gets  into  the  general  circulation,  the  less  the  symptoms; 
hence  the  first  indication  for  treatment  is  to  prevent  the  passage 
of  the  poison,  as  far  as  possible,  into  the  circulation. 

The  second  indication  for  treatment  is  to  neutralize  the  poison 
which  has  got  into  the  system,  and  the  third  indication  is  to  treat 
special  symptoms  as  they  appear. 

1.  Prevent  the  Poison  getting  into  the  General  Circulation. — In 
order  to  prevent  the  poison  getting  into  the  general  circulation, 
three  points  must  be  attended  to : — ■ 

(1)  Stoppage  of  the   flow  of  blood  and  lymph   from  the 

affected  area. 

(2)  Free  opening  of  the  poisoned  area. 

(3)  The  neutralization  of  the  poison  locally. 

(1)  Stoppage  of  the  Flow  of  Blood  and  Lymph  from  the  Affected 
Area.- — A  person  is  usually  bitten  in  the  arm  or  leg,  and  in  such  a 
case  the  old  treatment  advised  by  Celsus  should  be  carried  out  by 
applying  a  tight  ligature  round  the  affected  limb  on  the  proximal 
side  of  the  wound,  so  as  to  compress  the  blood  and  lymphatic  vessels. 
In  order  to  do  this  successfully,  the  ligature  must  be  applied  to  the 
arm  or  the  thigh — i.e.,  where  there  is  one  bone — and  not  the  fore- 
arm or  leg. 

Such  a  ligature  cannot  be  left  in  position  indefinitely,  otherwise 
gangrene  will  result;  and  after  some  attempts  at  neutralization  of 
the  poison  have  been  made,  it  must  be  loosened  for  a  couple  of 
seconds  and  reapplied,  and  this  must  be  repeated.  It  must  be  kept 
on  for  at  least  twenty  or  thirty  minutes. 


TREA  TMENT  275 

The  advantages  of  the  ligature  or  tourniquet  have  been  known 
since  ancient  times,  but  C.  J.  Martin  has  shown  that  its  principal 
action  with  colubrine  poison  is  not  merely  to  delay  the  absorption 
of  the  poison,  but  also  to  give  time  for  any  already  absorbed  to  be 
excreted.  In  the  viperine  poisons,  which  coagulate  the  blood  by 
fibrin  ferment,  it  is  most  beneficial;  for  the  blood,  in  coagulating 
locally,  retains  the  poison,  which  therefore  but  slowly  passes  into 
the  general  circulation,  and  may,  as  Martin  and  Lamb  suggest, 
unite  with  the  cells  near  the  bite. 

There  is  therefore  no  doubt  that  the  correct  immediate  treatment 
in  a  bite  due  to  any  kind  of  poisonous  snake  on  a  limb  is  the  applica- 
tion of  a  proximal  tourniquet. 

(2)  Free  Opening  into  the  Poisoned  Area. — It  will  be  obvious  that 
the  two  minute  punctures  caused  by  the  fangs  are  not  sufficiently 
large  openings  into  the  area  of  the  bite  for  the  application  of  anti- 
dotes. 

Therefore  the  next  step  is  to  cut,  not  merely  round  the  apertures 
of  the  fangs,  but  also  to  extend  the  incision  along  the  course  of  the 
veins  and  lymphatics,  and  in  some  cases  to  remove  the  piece 
of  skin  marked  out.  In  this  way  the  area  of  inoculation  is 
freely  opened. 

(3)  Neutralization  of  the  Poison  Locally. — The  next  indication  is 
to  diminish  the  toxicity  of  the  poison  as  much  as  possible,  and  to 
do  this  the  best  remedy  we  at  present  possess  is  permanganate  of 
potash,  though  recent  laboratory  experiments  have  thrown  some 
doubt  upon  its  efficacy. 

This  should  be  used  in  strong  solution,  and  not  as  a  solid,  as  the 
liquid  penetrates  better  into  the  interstices  of  the  wound,  which 
should  be  well  washed  with  it.  For  carrying  out  this  treatment  a 
most  useful  little  case  has  been  devised  containing  a  little  lancet  for 
making  the  wound,  and  permanganate  crystals  for  making  a  solu- 
tion. This  little  case  only  costs  a  few  pence,  and  can  be  carried 
without  any  inconvenience  in  the  waistcoat  pocket,  and  therefore 
should  be  carried  by  everyone  in  countries  where  poisonous  snakes 
abound,  especially  when  on  business  or  pleasure  in  jungles  or  grassy 
places.  Should  there  be  no  water  available  to  make  a  solution, 
then  the  crystals  can  be  rubbed  into  the  wound. 

If  the  bite  is  on  the  head  or  trunk,  the  incision  should  be  made 
as  above,  and  the  resulting  wound  thoroughly  soaked  with  per- 
manganate of  potash  solution  (3  per  cent.).  The  subcutaneous 
tissue  must  be  freely  opened,  otherwise  the  permanganate  may  be 
prevented  from  doing  its  work  properly. 

The  after-treatment  should  be  boric  fomentations,  frequently 
repeated  at  first;  but  if  there  is  no  marked  swelling  of  the  part, 
these  may  be  gradually,  not  quickly,  diminished  in  number,  and 
finally  a  mild  antiseptic  dressing  should  be  applied  until  the  wound 
heals. 

2.  Neutralization  of  the  Poison  in  the  System. — We  have  already 
endeavoured  to  impress  on  the  reader  the  following  facts: — ■ 


276  VENOMOUS  ANIMALS 

(i)  The  specificity  of  snake-venom. 

(2)  The  inutility  of  an  antiserum  prepared  for  one  venom  against 
another  venom. 

It  now  remains  to  consider  these  subjects  from  a  practical  point 
of  view. 

The  serum  most  readily  obtained  is  Calmette's,  in  20  c.c.  and 
50  c.c.  phials  standardized  against  cobra  and  Viper  a  russellii 
venoms,  and  prepared  by  the  immunization  of  horses  against  these 
venoms,  as  well  as  those  of  Bungarus  (krait)  and  Enhydrina  (sea- 
snake).  Reliable  sera  are  also  prepared  by  the  Indian  Pasteur 
Institute  of  Kasauli  for  the  venoms  of  the  cobra  and  Russell's  viper. 

All  these  sera,  unfortunately,  deteriorate  quickly  unless  kept  in 
a  dark  and  cool  place,  and,  further,  must  be  used  in  large  doses, 
for  even  when  fresh,  1  c.c.  will  only  neutralize  I  milligramme  of 
cobra-venom.  A  healthy  cobra  when  it  bites  may  inject  from  250 
to  350  milligrammes  of  venom,  of  which  the  minimum  lethal  dose 
may  be  estimated  at  15  to  17-5  milligrammes  for  a  person  weighing 
60  to  70  kilogrammes;  therefore  at  least  350  c.c.  of  the  antivenene 
must  be  injected  intravenously,  or  ten  to  twenty  times  that  amount 
must  be  injected  subcutaneously — i.e.,  from  3,500  to  7,000  c.c. 

The  antivenene,  of  course,  will  succeed  in  much  smaller  doses 
if  a  small  quantity  of  venom  has  been  injected,  and  will  fail  if  the 
quantity  be  large.  Therefore  the  obvious  indication  is  to  begin 
with  100  c.c.  of  antivenene,  injected  hypodermically,  or  far  better 
intravenously,  and  to  repeat  this  several  times  if  necessary.  The 
technique  for  the  intravenous  injection  is  as  follows: — 

An  all-glass  syringe  should  be  carefully  sterilized  by  boiling,  and 
the  skin  over  the  vein  must  be  cleansed  witn  1  in  40  carbolic  and 
with  absolute  alcohol;  a  band  should  be  tied  round  the  arm,  so 
that  the  vein  shows  up  clearly,  and  the  needle  should  be  irserted 
with  the  aperture  pointing  proximally — i.e.,  towards  the  heart — 
and  should  De  felt  free  in  the  vein.  The  ligature  should  then  be 
removed  and  the  serum  slowly  injected.  On  removal  of  the  needle, 
an  antiseptic  pad  and  bandage  should  be  applied. 

If,  on  the  other  hand,  the  species  of  snake  which  inflicted  the 
wound  is  known,  and  the  particular  serum  for  that  animal's  venom 
happens  to  be  available  in  good  condition,  then  it  should  be  used 
intravenously. 

3.  Treatment  of  Special  Symptoms — (1)  Failure  of  the  Respira- 
tion. -The  experiments  of  Fayrer,  Brunton,  and  Rogers  seem  lo 
indicate  that  in  cases  of  poisoning  due  to  cobra  and  sea-snake 
venoms  artificial  respiration  should  be  resorted  to  when  natural 
respiration  is  failing  and  medical  aid  or  remedies  are  being  sent  for. 

(2)  Failure  of  Circulation. — In  poisoning  due  to  viper- venoms, 
which  produce,  according  to  Rogers,  a  paralysis  of  the  central  vaso- 
motor centre,  he  recommends  that: — 

(a)  A  binder  should  be  applied  to  the  abdomen  and  bandages  to 
the  legs,  so  that  as  much  blood  as  possible  may  be  available  for 
maintaining  the  circulation  of  the  brain  and  medulla. 


OTHER   METHODS  OF  TREATMENT  277 

(b)  That  hypodermic  injections  of  adrenalin  be  used  to  constrict 
the  peripheral  vessels  and  to  stimulate  the  vasomotor  centre. 

In  both  colubrine  and  viperine  poisons  it  is  obvious  that  the  cir- 
culation should  also  be  maintained  by  the  applications  of  warmth, 
by  stimulants,  either  alcoholic  or  ammoniacal,  or  by  strychnine 
hypodermically. 

Summary.— i.  Apply  proximal  ligature. 

2.  Freely  open  the  cellular  tissue  in  the  vicinity  of  the  bite. 

3.  Wash  the  wound  well  with  a  strong  solution  of  permanganate 
of  potash  (3  per  cent.),  or  apply  crystals. 

4.  Inject  100  c.c.  of  fresh  antivenene  intravenously. 

5.  Artificial  respiration,  if  necessary. 

6.  Keep  up  the  circulation  by  binders  to  abdomen,  bandages  to 
legs,  stimulants,  and  hypodermic  injections  of  strychnine. 

Other  Methods  of  Treatment. 

<  >ther  methods  of  treatment  which  may  be  briefly  mentioned  are: — 

Snake-Stones. — The  cure  which  is  strongly  believed  in  by  the  native  is  the 
snake-stone.  These  stones  are  smooth,  highly  polished,  very  light,  black 
bodies,  said  to  consist  of  calcined  animal  bone  soaked  several  times  with  blood, 
and  calcined  after  each  soaking.  It  is  easy  to  understand  that  these  stones  are 
very  hygroscopic,  and  when  applied  to  a  wound,  cling  tightly,  and  suck  up 
fluids,  and  perhaps  some  poison.  There  are  supposed  to  be  three  kinds  of 
stones: — (1)  Those  composed  of  burnt  bone;  (2)  those  composed  of  chalk; 
(3)  those  composed  of  burnt  vegetal  substance.  Of  these  three  only  the  first 
is  considered  of  value. 

The  method  of  use  is  as  follows: — Puncture  the  wounds  of  the  snake-bite 
slightly,  and  apply  the  stone,  which  adheres  for  about  two  minutes,  and 
should  then  drop  off  into  a  vessel  of  water,  after  which  it  should  be  dried  by 
a  cloth,  and  applied  again  to  the  wound,  when  it  will  adhere  for  about  a 
minute.  It  should  be  applied  a  third  time.  During  application  the  limb 
should  be  nibbed  towards  the  stone.  The  stones  are  used  principally  in  India 
and  Ceylon,  but  they  are  also  known  in  Mexico  as  '  piedra  ponsona.'  It  is 
hardly  necessary  to  say  that  from  the  days  of  Redi  it  has  been  shown  how 
useless  these  stones  are. 

Exorcism  of  the  poison  by  shouting  charmed  verses  is  used  in  India. 
Numerous  plants,  seeds,  earth  moistened  with  urine,  etc.,  have  been  extolled 
as  cures. 

Ammonia. — Of  all  the  old  remedies  ammonia  has  lived  the  longest,  and  it 
is  almost  incredible  that  Fontana  settled  the  question  as  to  its  lack  of  utility 
by  his  experiments  on  vipers  more  than  130  years  ago.  Whether  given  by 
the  mouth,  injected  subcutaneously,  or  into  a  vein,  it  is  useless,  except  as  a 
stimulant,  when  it  is  certainly  of  no  more  use  than  alcohol.  Fayrer  has  shown 
that  if  liquor  ammoniae  is  mixed  in  more  than  equal  parts  with  venom,  it  does 
not  destroy  the  poison. 

Oils. — It  is  extraordinary  how  the  remedies  of  the  Middle  Ages  are  clung 
to,  and  oil  is  still  used,  though  known  to  be  useless  since  the  days  of  Morgagni. 

Strychnine. — Many  years  ago  Duncan  recommended  strychnine  as  a  remedy 
lor  East  Indian  snake-bites.  Recently  Muller  of  Victoria,  Australia,  has 
strongly  recommended  the  hypodermic  injection  of  this  drug.  He  says  that 
never  less  than  ,',,  grain  is  to  be  used,  and  this  must  be  increased  in  urgent 
cases  to  ]  or  J,  and  repeated  every  fifteen  or  twenty  minutes,  until  the  symp- 
toms of  snake-poisoning  are  removed.  If  a  fang  has  perforated  a  vein,  he 
recommends  intravenous  injection  instead  of  subcutaneous.  The  patient 
must  be  watched  for  twenty-four  hours  after  the  disappearance  of  the  last 
symptoms,  in  order  to  combat  a  sudden  relapse.  Colonel  Duke,  in  1895, 
highly  recommends  this  remedy. 


278  VENOMOUS  ANIMALS 

Arsenic. — Arsenic  is  principally  famous  as  the  Tanjore  pill,  which  was  said 
to  contain  white  arsenic  and  many  other  substances,  but  is  quite  useless. 

Iodine. — Brainard's  remedy  was  the  injection  of  a  solution  of  10  grains  of 
iodine  and  30  grains  of  iodide  of  potassium,  dissolved  in  1  ounce  of  water,  and 
probably  owed  its  reputation  to  its  caustic  action. 

Bromine  was  at  one  time  considered  a  specific. 

Caustics. — Fontana  strongly  advised  caustics,  which  he  considered  to  be 
useful,  but  long  experience  has  shown  their  inutility. 

Stimulants. — Brandy  and  whisky  have  been  repeatedly  vaunted,  and  so 
have  sinapisms,  warmth  to  the  precordial  region,  and  electricity  along  the 
spine,  but  all  these  are  useless. 

Energetic  Movements. — Energetic  movements,  such  as  walking  the  patient 
about,  flogging  him,  pinching  him,  have  been  advised,  but  are  contra-indicated , 
as  tending  to  exhaustion  and  to  hasten  the  end. 

Prophylaxis. 

In  the  tropics  Europeans  and  better-class  natives  seldom  suffer 
from  snake-bite,  because  they  do  not  sleep  on  the  ground,  in  the 
open  or  in  small  huts,  like  the  lower-class  native.  Among  the 
latter,  however,  any  prophylaxis  is  difficult  in  regions  such  as 
India,  because  they  reverence  the  cobra,  and  encourage  it  to  take 
up  its  abode  in  their  huts. 

Gardens  should  be  kept  free  from  jungle  or  long  grass,  and 
gratings  should  be  placed  on  the  drains  from  bath-rooms,  as  snakes 
have  often  been  found  in  these  rooms. 

Good  strong  boots  and  the  puttee  pattern  of  legging  should  be 
worn  when  going  shooting  or  into  the  jungle.  A  lantern  should 
be  used  when  walking  after  dark,  and  the  small  permanganate  case 
already  mentioned  should  be  carried  in  the  waistcoat  pocket  in  case 
of  accidents. 

LACERTILIA. 

FAMILY  HELODERMIDiE  Gray,  1838. 

Synonym.- — Helodermatidce  Fitz,  1843. 

In  the  Helodermidas  there  are  two  celebrated  lizards — Heloderma  horridum 
Wiegmann  and  H.  suspectum  Cope — which  were  placed  by  Sumichrast  in 
the  family  Varanidae,  and  though  this  may  be  disputed,  still,  it  is  probable 
that  they  are  allied  closely  to  that  family. 

GENUS    HELODERMA    Wiegmann,   1834. 
Heloderma  horridum  Wiegmann,  1834. 

Synonym. — Trachyderma  korridum  Wiegm.,  1829. 

This  lizard  lives  exclusively  in  Mexico  in  the  hot  zone  which  extends  from 
the  western  slope  of  the  Cordilleras  to  the  Pacific.  It  inhabits  the  hot,  dry 
districts  of  Jamiltepec,  Juchitan,  and  Tehuantepec,  where  it  lives  in  holes 
dug  at  the  roots  of  trees  or  under  vegetable  debris.  It  is  called  '  escorpion  ' 
by  the  Creoles,  and  '  tala-chini '  by  the  Zapotec  Indians;  and  in  1651  Fer- 
nandez says  it  was  called  '  acastetepon  '  by  the  Mexicans. 

Wlien  irritated,  there  escapes  from  its  mouth  a  white,  glutinous  fluid,  which 
is  secreted  by  the  large  salivary  glands.  Its  bite  is  much  dreaded  by  the 
natives,  who  say  that  ill-effects  are  produced  thereby  and  by  eating  its  flesh. 
It  may  reach  to  a  length  of  nearly  five  feet  when  old.  We  are  not  aware  of 
observations  on  the  bite  or  venom  of  this  reptile. 


MAMMALIA  279 

Heloderma  suspectum  Cope,  1869. 

Cope  gave  the  lizard  the  name  suspectum,  because  he  suspected  that  its 
bite  would  be  found  to  be  poisonous.  This  lizard  is  found  in  the  United 
States — in  Arizona,  Texas,  Utah,  New  Mexico,  and  Southern  California — 
where  it  is  called  the  '  gila  monster.'  The  poison  apparatus  consists  of 
glands  under  the  lower  jaw  and  teeth  in  that  jaw. 

The  poison  gland  in  this  species  lies  on  either  side  of  the  lower  jaw,  and 
from  its  mesial  aspect  four  ducts  pass  upwards,  each  towards  its  opening  on 
the  outer  surface  of  the  mandible,  through  which  it  passes  obliquely  upwards 
and  inwards,  to  end  at  the  base  of  a  tooth  near  the  termination  of  a  groove. 

The  upper  teeth  are  also  grooved,  but  Schufeldt  failed  to  find  any  gland 
wherewith  they  could  be  supplied  with  poison. 

There  appears  to  be  no  doubt  as  to  the  poisonous  nature  of  the  secretion 
from  the  glands  above  mentioned,  for  Bonberger  records  that  a  bite  in  the 
leg  of  a  guinea-pig  caused  convulsions  and  death  in  three  minutes. 

Venom. — The  venom  was  obtained  by  Mitchell  and  Reichert  by  making 
the  lizard  bite  a  saucer.  It  was  found  to  be  alkaline,  with  a  weak  smell,  and 
to  kill  frogs,  pigeons,  and  rabbits. 

The  effects  of  gila  poison  have  been  most  carefully  investigated  by  Weir 
Mitchell  and  Reichert,  and  by  Van  Denburgh  and  Wight. 

The  latter  consider  that  it  differs  in  no  important  respect  from  snake- 
venoms,  causing  death  by  acting  rapidly  upon  the  respiratory  centre  in  the 
medulla,  and  causing  paralysis  of  respiration.  Its  other  actions  are  to  first 
Stimulate  and  then  paralyze  the  heart  by  poisoning  its  muscular  fibres. 
On  inoculation,  there  is  an  immediate  great  fall  of  blood -pressure,  but  whether 
this  is  due  to  action  on  the  vasomotor  centre  or  not  is  not  clearly  known. 
There  is  a  secondary  gradual  fall  due  to  cardiac  failure.  The  motor  nerves 
and  1  ills  are  not  affected,  but  the  sensory  apparatus  is  at  first  rendered  more 
irritable  and  then  paralyzed.  Coagulation  of  the  blood  is  at  first  accelerated 
and  then  retarded,  so  that  it  may  become  incoagulable.  Haemolysis  may 
occur.  Local  signs  arc  almost  nil,  as  a  rule  a  little  cedema  and  slight  extrava- 
sation being  present. 

Symptoms. — Very  -even'  pains  radiating  from  the  part,  rapid  swelling, 
faintness,  profuse  perspiration,  may  be  noted. 

Treatment. — A  proximal  ligature  should  be  applied  if  on  a  limb,  and  per- 
ni  inganate  of  potash,  1-3  in  100,  should  be  used  to  bathe  the  wound,  which, 
finally,  should  be  dressed  aseptically. 

FAMILY  LANTHANOTID^E  Steindachner,  1S77. 

This  family  was  formed  for  Lanthanotus  Steindachner,  1877,  which  is  the 
type  genus.     It  is  closely  related  to  Helodermidae. 

Lanthanotus  borneensis  Steindachner,  1877. 
I  his  lizard,  which  is  closely  allied  to  Heloderma,  is  suspected  of  being 
poisonous,  but  there  are  as  yet  no  proofs  of  this,  especially  as  the  teeth  are 
not  grooved,  and  there  is  doubt  as  to  the  presence  of  poison  glands.  Its 
habitat  is  Borneo,  but  it  requires  reinvestigation,  as  but  few  specimens  are 
known . 

MAMMALIA  Linnaeus. 
The  mammal  suspected  of  causing  poisoning  is  Omithorhynchus  paradoxus, 
belonging  to  the  Monotremata . 

MONOTREMATA   Bonaparte,  1837. 

Omithorhynchus  paradoxus  Blumenbach,  1800. 

As  is  well  known,  the  males  of  this  animal,  which  is  only  found  in  Australia, 

have  large  spurs  projecting  backwards  from  their  hind-limbs.     Thesespursare 

hollow,  and  into  them  open  the  ducts  of  poison  glands.     The  venom  is  an 

albuminous  fluid  containing  albumoses. 


280  VENOMOUS  ANIMALS 

Injected  subcutaneously,  it  only  causes  local  swelling,  and  the  animal 
recovers  in  a  few  days.  Injected  intravenously,  it  causes  fall  in  the  blood- 
pressure  and  death  from  respiratory  failure,  the  heart  appears  to  be  un- 
affected, but  the  blood  in  the  venous  system  is  found  coagulated  after  death, 
which  takes  place  in  twenty-five  to  thirty  minutes.  The  venom  has  no 
haemolytic  or  proteolytic  action. 

The  difference  between  the  slight  effect  of  the  subcutaneous  and  the  serious 
effect  of  the  intravenous  injection  is  thought  to  be  due  to  the  fact  that  the 
poison  is  but  slowly  absorbed. 

In  a  man  who  was  stung  on  the  hand  the  symptoms  were  very  severe  pain, 
swelling  in  the  hand,  which  rapidly  spread  up  the  arm,  difficulty  in  opening 
the  mouth,  cold  sweats,  with  severe  sickness.  Recovery  took  place  in  a 
few  days  as  far  as  the  general  symptoms  were  concerned,  but  it  was  several 
weeks  before  the  hand  quite  recovered. 

The  treatment  has  generally  been  ammonia,  but  the  symptoms  and  the 
experiments  point  to  a  venom  closely  related  to  viperine  poison,  and  we 
should  recommend  the  proximal  ligature  and  permanganate  of  potash — in 
fact,  the  treatment  advocated  for  snake-bite. 

O.  paradoxus  is  often  called  O.  anatinus  Shaw,  1799. 

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Weir  Mitchell.     On  the  Venom   of   the  Rattlesnake.     Smithsonian  Con- 
tributions to  Knowledge,  xii. 
Weir  Mitchell  and  Reichert.     Researches  upon  the  Venoms  of  Poisonous 

Serpents.     Smithsonian   Contributions   to    Knowledge,    xxvi.     (Copious 

literature.) 
West  (1895).     Proceedings  of  the  Zoological  Society,  p.  313. 
Willson  (1908).     Snake  Poisoning. 

Lacertilia. 

Faust  (1906).     Die  Tierischen  Gifte.     Braunschweig. . 

Fayrer,  Sir  Joseph  (1S82).  Proceedings  of  the  Zoological  Society  of  London, 
p.  632. 

Jamieson,  Sir  J.  (1818).  Transactions  of  the  Linnean  Society  of  London, 
xii.  584. 

Loeb  (191 3).  The  Venom  of  Heloderma.  Carnegie  Institution,  Wash- 
ington. 

Martin,  J.  C,  and  Tidswell  (1894).  Proceedings  of  the  Linnean  Society 
of  New  South  Wales. 

Packard,  A.  S.  (1882).     The  American  Naturalist,  p.  842.     Philadelphia. 

Shufeldt,  R.  W.  (1890).  Proceedings  of  the  Zoological  Society  of  London, 
p.  148.     (Full  literature  up  to  1890.) 

Shufeldt,  R.  W.  (1882).  The  American  Naturalist,  pp.  907-908.  Phila- 
delphia. 

Sumichrast,  F.  (1864).     Annals  and  Magazine  of  Natural  History,  xiii.  497. 

Weir  Mitchell  and  Reichert,  E.  T.  (1883).  Medical  News,  February, 
1883.  Science  I.,  13,  372.  (Celebrated  paper  on  the  poisonous  effects 
of  the  bite.) 

Mammalia. 

Waikrhouse  (1846).     Mammalia,  vol.  i.     Marsupiata,  pp.  25-39.     London. 


SECTION  C 
PARASITES 

ANIMAL    PARASITES 
VEGETAL    PARASITES 


DIVISION  I.:  ANIMAL  PARASITES. 

Protozoa. 

Plasmodromata : — 

Sarcodina. 

Mastigophora. 

Telosporidia. 

Neosporidia. 
Heterokaryota : — 

Ciliata. 
Metazoa. 

Trematoda. 

Cestoid  ea. 

Nematoda. 

Hirudinea. 

Arthropoda,. 
Animal  Carriers. 

DIVISION  II.:  VEGETAL  PARASITES. 

Schizomycetes. 
Fungaceae. 


284 


CHAPTER  XVII 
PLASMODROMATA  AND  SARCODINA 

Preliminary — Animal  parasites — Nomenclature — Classification — Protozoa — 
Classification  —  Plasmodromata — Sarcodina — Gymnamcebida  —  Loeschia 
— Vahlkamfia — Dientamceba  —  Craigia — Thecamcebida — Chlamydoplirys 
— References. 

PRELIMINARY. 

In  tropical  medicine  the  parasitic  causes  of  disease  are  extremely 
important,  and  it  is  well  to  be  clear  as  to  the  meaning  of  the  term 
'  parasite.'  A  parasite  is  defined  to  be  a  living  organism,  animal 
or  vegetal,  which  takes  up  its  abode  temporarily  or  permanently  on 
or  within  other  living  organisms  (called  the  hosts)  for  the  purpose 
of  obtaining  food.  Parasites  may  be  divided  into  animal  parasites 
and  vegetal  parasites,  and  it  is  with  the  former  that  we  are  con- 
cerned in  this  chapter. 

ANIMAL  PARASITES. 

Animal  parasites  (zooparasites),  in  the  process  of  obtaining  their 
food,  may  cause  disease  by  their  mechanical  action  and  chemical 
products,  or  by  introducing  into  the  host  pathogenic  micro- 
organisms. 

As  examples  of  the  latter  may  be  mentioned  the  transmission  of 
the  animal  organism  which  causes  malaria  by  certain  members  of  a 
family  of  the  mosquitoes,  or  that  of  the  vegetal  organism  which  is 
the  cause  of  plague  by  certain  fleas.  Intestinal  worms  probably 
cause  many  of  the  symptoms  of  the  disease  with  which  they  are 
associated  by  the  introduction  into  the  body  of  poisons  through 
their  bites,  or,  according  to  Sambon  and  other  observers,  by  their 
active  migrations  before  attaining  maturity  and  reaching  their 
selective  anatomical  habitat. 

A  well-known  example  of  the  irritation  caused  by  the  introduction 
of  chemical  poisons  is  the  ordinary  mosquito-bite  alread3'  described, 
while  Trichinella  spiralis  Owen,  1835,  produces  severe  disturbance 
during  its  wanderings  through  the  body. 

Mechanically  the  jigger  (Dermatophilits  penetrans  Guerin,  1 
causes  much  irritation  to  the  foot,  andLofl  loa  (Guiyot,  177s)  to  the 
eye. 

Animals  ma}-  be  only  '  temporary  parasites  ' — i.e.,  they  may  only 
temporarily  affect  the  host,  as,  for  example,  mosquitoes — or  they 
may  be/  stationary  parasites,'  such  as  the  malarial  organism  which 

285 


286  PLASMODROMATA   AND  SARCODINA 

lives  in  the  red  cells  of  the  blood.  These  latter  may  be  subdivided 
into  '  periodical  parasites,'  which  only  spend  a  portion  of  their 
life-history  within  a  host,  and  '  permanent,'  which  are  parasitic 
throughout  the  whole  life-cycle.  As  an  example  of  the  former 
may  be  mentioned  the  larvae  of  certain  flies  which  are  parasitic, 
while  the  fly  itself  is  not,  and  of  the  latter  Oxyuris  vermicularis 
(Linnaeus,  1767)  is  a  good  example. 

Animal  parasites  may  be  classified  into  ectoparasites  or  epizoa, 
affecting  the  skin  and  exterior  of  the  host;  and  eudoparasites  or 
entozoa,  affecting  the  internal  organs  or  cavities  of  the  host. 

Until  recent  years  the  greatest  confusion  existed  as  to  the  nature 
of  parasites.  With  our  present  knowledge  it  appears  that  parasites, 
however  altered  in  structure  some  of  them  may  have  become  during 
their  parasitic  existence,  have  been  originally  derived  from  free- 
living  forms.  It  will,  however,  be  noted  that  there  are  great 
differences  in  the  structure  and  appearance  between  some  of  the 
permanent  parasites  and  their  nearest  free-living  affinities.  This 
difference  has  been  brought  about  mainly  by  environment. 

The  permanent  parasite,  particularly  if  an  entozoon,  has  food 
prepared  for  it  by  its  host  in  an  easily  assimilated  form;  hence 
there  is  no  necessity  for  a  complicated  digestive  apparatus,  which 
in  certain  cases  has  entirely  disappeared. 

Further,  certain  parasites,  having  reached  an  organ  which  supplies 
them  with  suitable  food,  do  not  require  organs  of  locomotion,  for 
they  have  only  to  remain  where  they  are,  and  the  tissues  of  the 
host  will  subserve  their  purpose.  Some  of  them  have  no  necessity, 
as  a  rule,  for  locomotion  for  sexual  purposes,  because  hermaphro- 
ditism is  common,  and  even  in  cases  where  this  is  not  found  para- 
sites often  live  in  couples  (male  and  female).  Being  enclosed  in 
the  body  of  the  host,  there  is  no  necessity  for  sense  organs;  therefore 
these  are  much  reduced,  or  are  absent. 

On  the  other  hand,  the  parasite  requires  something  to  enable  it 
to  fix  itself  firmly  to  the  tissues  of  the  host;  hence  suckers  and 
hooks  are  often  found,  and  also  clasping  and  clinging  organs. 

The  chance  of  a  parasite,  locked  up  inside  a  host,  successfully 
reproducing  its  species  is  small;  hence  reproduction  assumes  im- 
portant features  associated  with  the  production  of  large  numbers  of 
new  forms,  which  are  often  protected  by  shells  or  other  coverings. 

Reproduction  may  be  asexual,  especially  in  the  protozoa,  or 
sexual.  vSexual  reproduction  in  parasites  is  generally  complicated, 
ending  in  the  production  of  large  quantities  of  eggs  or  spores;  and 
very  often  the  spores  of  the  protozoa  or  the  corresponding  larval 
forms  of  the  metazoa  may  travel  through  one  or  more  intermediary 
hosts  before  they  infect  another  definitive  host — that  is,  one  in 
which  the  sexual  life-history  is  gone  through. 

With  regard  to  the  sexual  process,  it  may  be  noted  that  often  the 
male  is  smaller  than  the  female,  and  in  fewer  numbers,  but  there 
are  exceptions. 

Usually  parasites  keep  strictly  to  certain  hosts  called  '  normal 


ANIMAL  PARASITES  287 

hosts,'  but  at  times  they  are  found  in  unusual  hosts — for  exampl ■•. 
Echinorhynchus  gigas  (Goeze,  1782),  which  is  usually  found  in  pigs, 
may  infect  man.      Such  a  parasite  is  called  a  'chance  paraph, 
while   objects    mistaken    for    parasites    are    known    as   '  pseudo- 
parasites.' 

The  above  are  examples  of  simple  parasitism;  but  there  are  para- 
sites which  are  parasitic  upon  other  parasites — a  condition  called 
'  hyperparasitism.'  These  hyperparasites  may  be  secondary, 
tertiary,  or  quaternary,  and  their  importance  in  disease  has  been 
emphasized  by  Sambon,  who  has  shown  that  it  may  be  one  of  the 
causes  of  the  disappearance  of  malaria  from  a  district,  for  the 
black  spores  found  by  Ross  in  mosquitoes  infected  with  malaria  are 
now  known  to  be  hyperparasites  of  the  genus  Nosema. 

For  further  remarks  see  the  article  on  Metazoan  Parasites. 

Nomenclature. — Medical  men  in  the  tropics  are  at  present  almost  daily 
discovering  new,  or  what  are  thought  to  be  new,  parasites,  and  are  generally 
desirous  of  giving  them  definite  names,  but  before  doing  so  it  behoves  the 
discoverer  to  know  and  obey  the  international  code  laid  down  by  zoologists, 
for  which  purpose  they  should  study  Stiles's  pamphlet  in  the  bulletins  of  the 
United  States  Public  Health  and  Marine  Hospitals  Service. 

Four  rules  may  be  mentioned  here: — 

1 .  Language  Rule. — The  name  given  to  the  parasite  must  be  in  Latin,  and 
not  in  any  vernacular. 

2.  Rule  of  Priority. — The  valid  name  for  a  genus  or  species  is  the  oldest 
available  name.  Therefore,  in  describing  a  species  or  genus,  give  not  merely 
the  name  of  the  authority  who  invented  the  term,  but  the  date  also. 

3.  Rule  of  Homonyms. — When  two  distinct  genera  or  species  of  animals 
receive  the  same  name,  that  applied  earliest  alone  must  stand. 

4.  Rule  of  Appropriateness. — No  name  is  allowed  to  be  changed  simply 
because  it  is  inappropriate. 

With  regard  to  disease  there  is  no  fixed  rule,  but  we  feel  sure  that  if  medical 
men  would  attempt  to  evolve  a  fixed  method  of  nomenclature,  much  confusion 
would  be  avoided. 

When  an  animal  parasite  causes  a  series  of  symptoms  in  a  man  or  an 
animal,  it  is  usual  to  name  the  affection  by  that  of  the  animal  causing  the 
disease,  together  with  the  suffix '  iasis.'  Thus,  Loeschia  histolytica  (Schaudinn, 
1903)  causes  loeschial  dysentery  and  liver  abscess,  etc.,  which  may  be 
classed  together  under  the  term  '  Loeschiasis ' ;  or  Paragon  imus  ringeri 
(Cobbold,  1890)  causes  a  varied  number  of  symptoms,  which  can  all  be 
■  lassed  together  as  '  Paragonimiasis.' 

The  drawback  to  this  nomenclature  is  that,  parasites  being  very  often 
changed  from  genus  to  genus,  such  terms  are  not  permanent.  For  instance, 
the  same  pathological  condition  may  be  indicated  by  various  authorities 
with  the  terms  '  Amcebiasis,'  '  Entamcebiasis,'  '  Loeschiasis.'  We  therefore 
prefer,  wherever  possible,  to  use  common  names  for  diseases — e.g.,  '  Kala- 
azar.' 

Classification. — The  animals  which  cause  and  convey  the  diseases 
of  man  may  be  classified  into  the  following  subkingdoms:  Sub- 
kingdom  I.,  Protozoa;  Subkingdom  II.,  Metazoa. 


288  PLASMODROMATA  AND  SARC0D1NA 

SUBDIVISION  A.  PROTOZOAN  PARASITES. 

SUBKINGDOM  I.     PROTOZOA  Goldfuss,  1S17. 

Definition.— Protozoa  are  unicellular  animals,  solitary  or  united 
into  colonies,  free-living  or  parasitic,  with  asexual  reproduction 
(schizogony)  by  binary  fission,  budding  or  fragmentation  and  sexual 
reproduction  (sporogony),  or  merely  rejuvenescence  by  conjugation. 

Remarks. — The  border-line  between  unicellular  animals  and  uni- 
cellular plants  is  very  vague,  and  hence  at  present  it  is  uncertain 
whether  some  forms  should  be  classed  with  the  bacteria  and  con- 
sidered to  be  plants,  or  with  the  protozoa  and  considered  to  be 
animals.     Therefore  it  is  not  unusual  to  call  both  '  protists.' 

Phylogenesis. — There  can  be  little  doubt  that  the  primitive  form 
of  protozoon  must  have  been  an  animal  with  some  of  the  charac- 
teristics of  the  amoeba,  and  would  most  likely  be  free-living,  most 
probably  in  water.  This  simple  form,  taken  into  the  alimentary 
canal  of  higher  animals,  possibly  benefited  by  the  ease  with  which 
food  was  obtained  and  by  the  protection  afforded  by  the  new 
position,  and  thus  became  modified  to  suit  its  environment.  The 
most  important  modification  would  be  some  protection  for  the 
earliest  stages  of  its  life-history,  which  would  enable  it  to  live  in 
the  outside  world  until  taken  up  by  a  suitable  host,  and  associated 
with  this  would  be  the  necessity  to  produce  large  numbers  of  such 
protected  spores,  as  the  chance  of  one  finding  a  suitable  host  must 
be  relatively  small.  Such  a  type  would  be  represented  by  the 
Loeschia  coli  Loesch,  which  is  a  parasite  of  man.  Such  a  parasite 
may  cause  no  harm  to  its  host,  which  is  fairly  indifferent  to  its 
existence.  On  the  other  hand,  a  parasite  may  not  find  sufficient 
nutriment  in  the  alimentary  canal,  and  be  compelled  to  seek  better 
food,  and  perhaps  more  protection,  by  entering  the  glands  of 
Lieberkiihn,  or  even  the  sub  mucosa  of  the  bowel.  Such  a  parasite 
might  cause  disease  in  its  host,  and  would  be  illustrated  by  the 
Loeschia  histolytica  Schaudinn  of  man. 

Such  a  process,  however,  took  place  not  merely  in  man,  but  in 
many  other  kinds  of  animals,  among  which  may  be  mentioned 
insects,  in  the  alimentary  canal  of  many  of  which  protozoan  para- 
sites are  found.  In  these  insects  the  sexual  process  occurs,  and 
therefore  they  are  the  definitive  hosts,  and  may  also  be  considered 
the  primary  hosts. 

If  these  primary  hosts  become  predatory,  biting  and  sucking  the 
blood  of  other  animals — e.g.,  vertebrates — then,  during  this  process, 
they  might  pass  the  spores  of  their  parasites  into  the  blood  of  the. 
vertebrata,  and  if  these  are  not  killed  off  (for  some  animals  are 
repellent)  by  chemical  substances,  or  destroyed  by  leucocytes,  they 
might  develop  in  the  blood  of  some  vertebrate  (called  tolerant), 
which  thus  becomes  the  secondary  host. 

It  is,  of  course,  possible  that  some  of  these  blood  protozoa  may 


PROTOZOAN  PARASITES  289 

have  been  derived  from  parasites  originally  intestinal  in  the  verte- 
brate, which  found  their  way  not  merely  into  the  mucosa  of  the 
bowel,  but  later  into  the  blood-stream,  in  which  they  would  be 
fairly  well  protected,  and  from  which  they  would  at  first  escape 
by  becoming  encysted  in  the  intestinal  wall,  and  then,  bursting  into 
the  bowel,  make  their  way  to  the  exterior  with  the  hecal  matter 
and  so  infect  a  new  host.  When  blood-sucking  animals  became 
evolved,  a  new  cycle  would  be  open  for  them — viz.,  from  the  verte- 
brate through  the  blood-sucker  back  to  the  vertebrate — and  thus 
the  old  method  by  way  of  the  alimentary  canal  would  be  lost. 

The  origin  of  the  protozoan  blood-parasites  of  man  may  therefore 
be  twofold:  (a)  from  man's  intestine  into  the  blood;  (6)  from  an 
invertebrate's  alimentary  canal  into  the  blood  of  man. 

The  result  of  one  or  other  of  these  methods  is  well  illustrated  by 
the  malarial  parasite,  which  passes  through  its  sexual  cycle  in  an 
Anopheline  mosquito,  which  is  its  definitive  and  according  to  the 
view  adopted,  its  primary  or  secondary  host.  When  the  infected 
Anopheline  bites  a  man,  the  parasite  enters  into  the  blood-sti-eam, 
in  the  red  cells  of  which  it  develops  and  undergoes  its  asexual 
cycle'.  Man  is  therefore  the  intermediary,  and  either  the  primary 
or  secondary,  host  of  the  malarial  parasite,  as  mentioned  above. 

The  blood-stream  of  man  contains  two  different  elements — ■ 
(1)  licmor  sanguinis;  (2)  cells- — (a)  red,  (b)  white.  Therefore  the 
parasite  has  two  possibilities  before  it — -either  to  live  in  the  liquor 
or  in  a  cell,  or  partially  in  one  and  partially  in  the  other;  and  this 
last  is  what  generally  happens — i.e.,  the  parasite  lives  so  much  of 
its  cycle  in  a  cell  and  so  much  in  the  blood-stream.  It  would,  how- 
ever, appear  that  there  is  a  great  phylogenetic  tendency  for  pro- 
tozoan  parasites  to  leave  the  liquor  sanguinis  and  to  reside  in  red 
cells  (the  malarial  parasite)  or  in  white  cells  or  in  endothelial  cells 
(the  Leishman-Donovan  parasite). 

Infection  of  the  Embryo.— Protozoan  blood  parasites  apparently 
can  In-  arranged  in  two  categories  as  regards  the  infection  of  the 
foetus,  I <ir  some,  like  the  malarial  parasite  (which  is  generally  con- 
sidered  to  be  incapable),  do  not  traverse  the  placenta,  while  others, 
like  the  Spirochetes  and  Treponemata,  can  do  so.  With  regard  to 
the  infection  of  invertebrate  eggs  the  matter  is  quite  different,  for 
many  of  these  parasites  infect  the  eggs,  thus  carrying  the  germs  of 
disease  into  a  new  generation  of  blood-suckers. 

It  would  appear  as  though  the  intracellular  stage  enabled  the 
parasite  to  grow  (e.g.,  consider  Schaudinn's  history  of  the  develop- 
ment of  Hcemoproteus  noctuce  in  the  little  owl)  and  to  multiply 
note  the  development  and  multiplicat  on  of  the  malarial 
parasite). 

In  the  evolution  of  such  haunatozoan  types  some  authorities 
(Woodcock)  hold  that  the  flagellate  form-,  living  in  the  blood- 
stream are  to  be  considered  the  mosl  primitive,  ami  that  the  more 
truly  cellular  the  parasite  becomes  the  more  it  ha-,  evolved.  Hence 
the  H cento flagellata,  or  parasites  Freely  moving  in  the  liquor  san- 

10 


290  PLASMODROMATA  AND  SARCODINA 

guinis,  are  with  difficulty  separated  from  the  Hcemosporidia,  or 
parasites  which  mostly  live  in  blood  cells.  For  many  reasons  some 
of  these  two  groups  of  parasites  were  united  together  into  one 
order  of  the  flagellates  by  Hartmann, 

Morphology. — Protozoan  parasites  vary  in  size  from  the  large 
SarcocystidcB  in  muscle  to  most  minute  forms  in  the  blood  {Hcemo- 
protozoa).  In  fact,  it  is  possible  that  some  forms  may  exist  which 
we  have  not  yet  recognized,  because  their  minute  size  prevents  their 
being  visible  to  the  human  eye,  even  when  aided  by  the  highest 
powers  of  the  microscope. 

The  parasites  themselves  consist  of  protoplasm,  which  in  some 
instances  shows  a  modification  into  ectoplasm  and  endoplasm,  the 
former  being  clear  and  hyaline  and  the  latter  dark  and  granular. 
In  the  protoplasm  are  to  be  found — (i)  one  or  more  nuclei, 
(2)  chromidiosomes  and  chromidia,  (3)  metachromatic  granules, 
(4)  volutine  granules,  (5)  metaplastic  granules,  (6)  centrosomes, 
(7)  archoplasm,  (8)  rhizoplast,  (9)  vacuoli. 

(1)  The  nucleus  in  its  simplest  form  is  merely  a  collection  of 
smaller  or  larger  particles  of  chromatin  (chromidiosomes  or  chro- 
midia). A  very  simple  form  is  that  termed  Protokary on,  in  which 
one  large  chromidial  mass  (the  Karyosome)  lies  in  a  delicate  achro- 
matic network  of  linin  inside  a  vacuole  filled  with  nuclear  sap, 
called  enchylema.  Some  chromidia  may  or  may  not  be  situated 
peripherally  as  well  as  more  centrally.  There  is  no  definite  mem- 
brane. The  next  advance  is  the  vesicular  nucleus,  which  consists 
of  a  definite  nuclear  membrane  separating  it  from  the  cytoplasm. 
Inside  this  membrane  there  is  an  achromatic  framework  made  of 
linin;  a  nuclear  fluid  or  enchylema,  lumps  of  a  substance  called 
plastin  giving  rise  to  the  nucleolus,  so  common  in  the  Metozoa  and 
so  rare  in  the  Protozoa,  and  in  association  with  chromatin  to  the 
karyosome,  which  in  this  instance  is  called  the  endosome,  or  Binnen- 
korper.  The  granular  nucleus  is  a  further  evolution,  and  is  pro- 
duced by  a  more  scattered  condition  of  the  chromatin. 

The  nucleus  is  therefore  a  complex  body  composed  of  chromatic 
and  achromatic  substances.  It  may  be  single,  or  divided  into  two 
principal  masses — -trophonucleus  or  nutrition-nucleus  and  kineto- 
nucleus  or  motion-nucleus,  or  into  macronucleus  and  micronucleus. 
The  latter  are  quite  different  from  the  tropho-  and  kinetonuclei,  for 
the  macronucleus  is  trophic  and  kinetic,  while  the  micronucleus  is 
purely  reproductive.  The  former  is  typically  seen  in  the  trypano- 
somidae  and  the  latter  in  the  heterokaryota. 

(2)  Chromidiosomes  are  the  smallest  particles  of  chromatin 
which,  when  massed  together,  give  rise  to  the  chromidia  which  may 
be  intranuclear  or  extranuclear.  (3)  The  metachromatic  granules 
or  chromatoid  grains  represent  stages  in  the  anabolism  or  katabolism 
of  chromatin.  (4)  Volutine  granules  stain  like  chromatin.  They 
are  composed  of  nucleic  acid  in  combination,  and  represent  reserve 
food  material  for  the  nucleus.  (5)  Metaplastic  granules  are  products 
of    cytoplastic    anabolism    or    katabolism.      (6)  Centrosome    is    a 


PROTOZOAN  PARASITES  291 

minute  grain  or  pair  of  granules  (diplosome)  lying  typically  outside 
the  nucleus  close  to  the  membrane.  (7)  The  archoplasm  is  the  clear 
protoplasm  which  sometimes  surrounds  the  centrosome.  (8)  The 
rhizoplast  is  the  portion  of  the  flagellum  (when  present)  which 
penetrates  into  the  cytoplasm.  The  flagellar  apparatus  is  described 
under  the  heading  '  Mastigophora  '  in  the  next  chapter.  (9)  The 
vacuoli  may  be  either  contractile  vacuoles  which  are  considered 
to  be  respiratory  and  excretory  in  function,  or  the  food  vacuoles, 
which  begin  with  a  globule  of  water  taken  in  with  the  food.  Into 
this  vacuole  an  acid  is  secreted  from  the  cytoplasm  and  digests  the 
fond,  which  is  then  absorbed.  Then  the  vacuole  with  the  undigested 
food  travels  to  the  periphery,  and  the  waste  product  is  extruded. 

Protozoa  generally  have  some  power  of  movement  by  pseudo- 
podia,  cilia,  or  flagella,  but  under  unfavourable  circumstances  they 
may  lose  this  power,  and,  becoming  quiescent,  surround  them- 
selves with  an  envelope  and  become  encysted.  Unfavourable 
circumstances  are  lack  of  food,  desiccation,  irritating  chemical 
substances,  and  unusual  surroundings. 

Life-History. — Reproduction  in  the  protozoa  takes  place  asexually 
or  sexually.  As  long  as  conditions  are  favourable — i.e.,  there  is 
abundance  of  food— protozoa  reproduce  asexually  by  one  of  the 
following  methods:  (1)  binary  fission;  (2)  gemmation;  and  (3)  spore- 
formation. 

1.  Binary  Fission.- — -In  binary  fission  there  is  first  division  of  the 
nucleus,  which  sometimes  takes  place  by  amitosis,  followed  by  that 
of  the  cytoplasm.  Then  the  parasite  divides  into  two  more  or  less 
equal  halves  (Fig.  42).  The  other  methods  of  nuclear  division  are 
bv  chromidial  fragmentation  or  by  mitosis,  of  which  there  are  three 
types — (a)  Promitosis,  (b)  Mesomitosis,  (c)  Metamitosis.  In  chro- 
midial fragmentation  the  nucleus  breaks  up  into  minute  chromidia, 
which  eventually  collect  into  two  new  nuclei.  In  Promitosis  a  pro- 
karyon  type  of  nucleus  divides  by  the  centrosome  splitting  into  two, 
and  giving  rise  to  the  central  thread  (centrodesmose)  of  the  spindle. 
Then  the  karyosome  divides  by  constriction,  and  the  achromatic 
spindle  is  formed  from  the  framework  of  the  nucleus,  and  lies 
between  the  two  separating  karyosomes,  with  the  centrodesmose  in 
the  middle.  Then  the  chromosomes  appear  formed  from  the  peri- 
pheral chromatin  as  well  as  from  that  of  the  karyosome. 

There  are  two  types  of  Promitosis — the  simpler,  in  which  no 
equatorial  plate  is  formed,  and  the  chromosomes  are  merely  scat- 
tered along  the  spindle,  and  finally  gather  at  opposite  poles  to  form 
the  daughter  nuclei;  and  the  more  advanced,  with  an  equatorial 
plate  of  chromosomes  which  may  divide  by  either  an  equating  or 
a  reducing  division.  In  Promitosis  the  nuclear  membrane  is  neg- 
ligible, while  the  whole  process  is  confined  to  the  nuclear  area.  In 
mesomitosis,  which  takes  place  in  a  nucleus  in  which  the  karyosome 
is  reduced  and  in  which  there  are  more  chromatic  particles  in  the 
body  of  the  nucleus,  perfect  karyomitotic  figures  are  formed,  but 
the  whole  process  takes  place  inside  the  nuclear  membrane.     In 


292 


PLASMODROMATA  AND  SARCODINA 


metamitosis  the  polar  caps  of  archoplasm  situate  in  the  cytoplasm 
assist  in  the  mitosis. 

2.  Gemmation. — In  gemmation  the  nucleus  divides  usually  by 
mitosis  into  two  or  more  nuclei,  which  either  travel  to  the  peri- 
phery, and  become  surrounded  by  small  masses  of  protoplasm, 
which  separate  from  the  parent  parasite- — ectogenous  gemmation— 
or  remain  in  the  cytoplasm,  a  portion  of  which  becomes  differ- 
entiated around  each  nucleus- — endogenous  gemmation. 

The  explanation  of  the  two  methods  is  that  in  ectogenous  gemma- 
tion the  buds  are  separated  from  the  mother  cell  externally,  while 


Fig.  42. — Diagram  of  the  Life-Cycles  of  Loeschia  coli  Loesch,  emendavit 

SCHAUDINN,   1903,  SHOWING    HARTMANN   AND   WhITMORe'S  VlEWS   AS    TO 

Zygosis. 
1,  Loeschia  coli;  a-e,  stages  in  the  process  of  binary  fission  by  promitosis; 
A-D,  schizogony  by  repeated  division;  2-12,  sexual  reproduction  or  sporogony; 
11  are  the  gametes,  12  the  zygote,  but  these  stages  are  not  definitely  known. 

in  endogenous  gemmation  the  localized  budding  area  sinks  into  the 
body  substance  of  the  mother  cell,  with  the  result  that  the  buds  are 
contained  in  a  brood  sac.  This  localized  endogenous  area  is  called 
a  Pansporoblast,  though  in  some  the  entire  organism  forms  a  pan- 
sporoblast, which  is  considered  to  be  phylogenetically  derived  from 
the  localized  condition — i.e.,  the  whole  cell  represents  only  the 
pansporoblast. 


PROTOZOAN  PARASITES 


293 


Plasmotomy. — Plasmotomy  is  the  term  applied  to  the  inter- 
mediate division  of  the  cytoplasm  of  multinuclear  parasites  into 
two  or  more  masses,  which  afterwards  may  or  may  not  reproduce 
by  spore-formation. 

3.  Spore-Formation. — Instead  of  being  considered  a  process  of 
internal  gemmation,  the  formation  of  pansporoblasts  may  be 
looked  upon  as  a  process  of  spore-formation  proceeding  while  the 
organism  grows,  as  is  typically  seen  in  the  Neosporidia. 

The  typical  asexual  spore-formation  or  schizogony  is,  however, 
met  with  in  the  Telosporidia,  in  which  the  early  stages  absorb 
nutriment  and  increase  in  size,  being  therefore  called  trophozoites. 
When  fully  grown  they  form  a  quiescent  body,  the  schizont, 
whose  nucleus  and  cytoplasm  divide  into  a  number  of  small 
forms  called  asexual  spores  or  merozoites,  generally,  however, 
leaving  a  little  undivided  cytoplasm  laden  with  effete  matter, 
which  is  called  a  nucleus  de  reliquat,  or  '  rest  body.' 


Fig.  43. — Schizogony  of  Plasmodium  vivax  Grassi  and  Feletti. 
(After  Schaudinn.) 

1,  Young  trophozoite;  2,  ring  form;  3,  ring  form  showing  haemozoin; 
.(,  parasite  with  pseudopodia;  5,  old  trophozoite;  6,  schizont  showing  com- 
mencement of  first  division;  7,  schizont  with  four  nuclei;  8,  schizont  with 
several  nuclei  (the  corpuscle  shows  Schuffner's  dots) ;  9,  schizont  divided  into 
merozoites;  10,  merozoites  and  haemozoin  free. 

These  merozoites  are  the  forms  by  which  the  parasite  multiplies 
in  the  given  host,  and  are  not  the  means  by  which  new  hosts  are 
infected.  The}'  therefore  enter  new  cells  in  the  host  in  which 
they  are  formed,  and,  growing  into  a  trophozoite,  complete  an 
asexual  life-cycle,  which  is  called  the  cycle  of  schizogony,  or  simply 
schizogony  (Fig.  43). 

A  time  arrives  in  the  infection  of  every  host  when  the  food 
material  for  the  given  parasite  is  diminished  by  the  numbers  of 
forms  produced  by  asexual  reproduction,  or  when  the  tissues  of  the 
host  react  against  the  parasite  by  chemical  substances,  or  phago- 
cytosis, or  by  both  methods  combined. 

When  these  adverse  circumstances  become  sufficiently  severe, 
changes  take  place  in  the  parasite  which  produce  forms  capable  of 
leaving  the  given  host  and  existing  outside  it,  either  in  a  different 
species  of  animal  or  simply  in  the  exterior,  until  an  entry  is  made 


2<H 


PLASMODROMATA   AND  SARCODINA 


into  a  new  host  of  the  same  species  as  before,  when  schizogony 
begins  again. 

The  changes  which  the  parasite  has  to  undergo  in  spreading 
from  one  host  to  another  are  generally  associated  with  sexual 
reproduction,  and  the  whole  cycle  from  a  given  host  of  a  certain 
species  to  another  host  of  the  same  species  is  called  the  cycle  of 
sporogony,  or,  more  simply,  sporogony  (Figs.  44,  45,  and  46). 


m 

Fig.  44.— Sporogony  of  Plasmodium  vivax  Grassi  and  Feletti. 
Development  of  the  Microgamete.     (After  Schaudinn.) 

1,  Young  microgametocy te ;  2,  3,  older  forms;  4,  fully  grown  microgameto- 
cyte,  as  seen  in  the  blood  of  man;  5,  division  of  the  nucleus  (reduction)  in  the 
stomach  of  an  anopheline ;  6,  nuclei  have  travelled  to  the  periphery,  which  has 
grown  out  to  form  the  commencement  of  a  microgamete;  7,  microgametocy  te 
with  three  microgametes ;  8,  a  free  microgamete. 

In  adverse  or  changed  circumstances,  therefore,  the  merozoites 
develop  into  more  resisting  forms,  which  are  called  gametocytes, 
in  which,  by  reduction  of  the  nuclear  material,  the  male  and  female 
elements  in  the  nucleus  are  separated;  the  two  elements  may  exist 
in  the  same  cell  or  in  separate  cells,  but  usually  the  male  element  of 
one  cell  fuses  (zygosis)  with  the  female  element  of  another  cell, 
and  forms  a  new  individual  .with  a  new  nucleus  or  synkaryon. 


Fig.  45.— Sporogony  of  Plasmodium  vivax   Grassi  and  Feletti. 
Development  of  the  Macrogamete.     (After  Schaudinn.) 
1-2,    Young  macrogametocytes ;    3,   fully   developed   macrogametocyte  in 
the  blood  of  man;  4,  reduction  and  formation  of  a  polar  body  in  the  stomach 
of  an  anopheline  mosquito;  5,  macrogamete  and  one  polar  body. 

This  new  individual  proceeds  to  reproduce  itself  rapidly  by  either 
binary  fission  or  spore-formation.  In  the  latter  case,  in  order  to 
prevent  confusion,  the  terms  employed  are  different  from  those 
used  in  asexual  reproduction.  The  parasite  is  called  a  sporont,  the 
spores  sporozoites.     The  sexual   reproduction  takes  place  in  the 


PROTOZOAN  PARASITES 


295 


definitive  host,  which  may  be  different  from  the  intermediary  host 
in  which  the  asexual  reproduction  is  found. 

Parthenogenesis  and  Etheogenesis. — Reproduction  is  said  to  take 
place  from  a  female  type  of  parasite  (parthenogenesis)  or  more 
rarely  from  a  male  type  of  parasite  (etheogenesis),  without  any 
completion  of  the  sexual  process  (Fig.  47). 

An  example  of  parthenogenesis  is  found  in  the  malarial  parasite,  in  which 
the  female  gametocyte  is  capable  of  resisting  both  the  action  of  the  chemicals 
of  the  body  and  drugs,  and  is  therefore  capable  of  lying  dormant  for  some 
time.  When  given  an  opportunity  for  development,  its  nucleus  and  proto- 
plasm divide  into  two  portions,  one  of  which  degenerates  and  disappears, 
while  the  other  forms  merozoites  and  starts  the  cycle  of  schizogony  anew. 
Another  is  described  by  Prowazek  in  Herpetomonas  muscce- domestics ,  but 
neither  example  has  been  definitely  proved;  and,  indeed,  of  late  grave  doubts 
have  arisen  as  to  its  truth.  Nevertheless,  we  feel  that  it  is  necessary  to  keep 
some  remarks  upon  the  subject,  as  we  feel  that  the  last  word  has  not  yet  been 
said,  as  we  have  seen  once  bodies  very  like  those  described  by  Schaudinn. 


Fig.  47. — Parthenogenesis  of  Plasmodium 

vivax  Gkassi  and  Feletti. 

(After  Schaudinn.) 

1,    Macrogametocyte;    2,    division    of    the 

nucleus;   3-6,   formation  of  merozoites  from 

one   portion  of  the   nucleus,    and  separation 

of  the  other  portion  with  the  hasmozoin. 


Fig.     46. — Sporogony     of 
Plasmodium,  vivax  Grassi 
and    Feletti  :     Zygosis. 
(After  Schaudinn.) 

1,  Zygosis  of  one  micro- 
gamete  with  the  macro- 
gamete;  2,  ookinete  and 
degenerate  microgametes. 

Etheogenesis,  a  term  introduced  by  Prowazek,  is  the  much  rarer 
change  in  the  male  parasite  whereby  asexual  reproduction  begins 
again.  He  described  it  in  Herpetomonas  muscce-domesticcz,  but  Flu 
says  that  an  error  was  made,  and  that  the  objects  believed  to  be 
male  elements  were  really  stages  in  the  life-cycle  of  a  Microsporidian 
— Octosporea  muscce- domestic ce. 

Pathogenicity.— The  pathogenicity  of  the  Protozoa  is  of  the 
highest  importance,  as  they  are  the  causes  of  a  large  number  of 
endemic  and  epidemic  diseases  in  man  and  animals,  as  will  be 
described  in  the  following  pages.  They  produce  toxins;  but  these 
have  not  been  well  studied,  with  the  exception  of  the  Sarcosporidio- 
toxin,  which  is  only  toxic  for  rabbits  and  not  for  other  animals. 
The  toxins  produced  by  the  malarial  parasites  have  been  referred 
to  on  p.  203. 


296  PLASMODROMATA  AND  SARCODINA 

Classification. — The  classification  of  the  subkingdom  Protozoa  is 
by  no  means  satisfactory  at  present,  but  for  remarks  upon  this 
subject  we  refer  the  reader  to  Poche's  article  thereon  written  in 
the  Archiv  fur  Protistenkunde,  vol.  30,  in  191 3. 

The  old  classification  was  into  four  classes:  (1)  sarcodina;  (2)  mas- 
tigophora; (3)  sporozoa;  (4)  infusoria. 

The  sarcodina  move  and  capture  food  by  pseudopodia;  the 
mastigophora  by  flagella ;  the  sporozoa  are  parasites  without  motile 
organs;  and  the  infusoria  move  by  means  of  cilia.  When  this 
classification  was  brought  into  use,  practically  nothing  was  known 
about  the  life-history  of  the  protozoa,  a  more  complete  knowledge 
of  which  is  still  required. 

Schaudinn's  work  with  regard  to  the  life-history  of  flagellates 
having  failed  to  be  confirmed,  and  Hartmann's  binucleate  theory 
having  fallen  into  disuse,  we  have  returned  to  Doflein's  classification 
as  set  forth  below. 

Among  the  blood  parasites  of  man  and  other  animals  there  are 
found  some  wavy,  thread-like  organisms  (Spirochetes  and  Tre-> 
ponemata),  with  which  must  be  classed  some  free-living  forms  whose 
position,  even  in  the  animal  kingdom,  has  been  disputed. 

Most  authorities  believe  that  these  forms  are  protozoa  with  a 
low  type  of  nucleus,  but  so  different  are  they  from  the  ordinary 
phyla  of  protozoa  that,  following  Doflein's  and  Fantham's  sugges- 
tions, we  shall  place  them  in  a  separate  section  making  them  an 
Appendix  to  the  Mastigophora,  though  Calkins  thinks  it  better  to 
leave  them  in  their  old  position  at  present. 

Further,  the  old  group  of  the  Sporozoa  Leuckart,  1879,  contains 
two  such  different  groups  of  animals  in  its  subdivisions  into  Telo- 
sporidia  and  Neosporidia  that  it  is  justifiable  to  do  away  with  this 
combination,  and  to  raise  the  two  divisions  to  the  rank  of  separate 
phyla. 

Finally,  the  two  nuclei  of  the  infusoria  are  so  totally  different 
in  function  from  the  nucleus  or  nuclei  of  the  rest  of  the  protozoa 
that  the  Subkingdom  is  capable  of  being  divided  into  two  divisions  :— 
the  Heterokaryota  or  infusoria;  and  the  Plasmodromata,  under 
which  heading  come  the  other  phyla. 

In  the  present  work  the  following  classification  is  adopted : — 

DIVISION  A.  PLASMODROMATA  Doflein,  1901. 

Phylum  I. — Sarcodina  Hertwig  and  Lesser,  1874. 
Phylum  11.— Mastigophora  Diesing,  1866. 
Phylum  III. — Telosporidia  Schaudinn,  1900. 
Phylum  IV. — Neosporidia  Schaudinn,  1900. 

DIVISION  B.  HETEROKARYOTA  Hickson,  1903. 

Phylum  V.—CMata  Pcrty,  1852. 
Phylum  Vl.—Acinetaria  Lankester,  1885. 


PLASMODROMATA  297 

Species. — Before  commencing  the  systematic  description  of  the 
Protozoa  it  may  perhaps  be  as  well  to  remind  the  reader  that  in 
the  higher  animals  the  distinctness  of  a  species  depends  upon  the 
fertility  of  its  members  inter  se,  but  not  usually  with  members  of 
other  species. 

In  protozoology  and  bacteriology  many  mere  varieties  have  been 
called  species,  but  such  variants  lack  any  morphologically  specific 
character,  and  are  merely  separated  from  one  another  by  physio- 
logical characters,  which,  as  we  have  seen  in  the  section  on  evolution 
of  disease,  can  be  made  to  alter  by  change  of  environment. 

It  is  convenient  and  useful  for  purposes  of  identification  and 
reference  to  give  them  names  as  though  they  were  true  species, 
and  this  does  no  harm  so  long  as  the  reader  does  not  expect  to 
find  morphologically  specific  differences  in  these  forms,  which  can 
only  be  separated  biologically  and  physiologically. 


DIVISION  A:  PLASMODROMATA  Doflein,  1901. 

Synonym. — Cytomorpha  Hatschek,  1888. 

Definition. — -Protozoa  in  which  the  nucleus  is  not  separated  into 
reproductive  (micronucleus)  and  non-reproductive  (macronucleus) 
portions. 

Classification. — The  Plasmodromata  may  be  divided  into  phyla 
according  to  the  following  scheme: — 

(a)  With  motile  organs  in  adult  stage  : — - 

I.  Move  and  capture  food  by  pseudopodia — Sarcodina. 
II.  Move  and  capture  food  by  flagella — Mastigophora. 

(b)  Without  motile  organs  in  adult  stage  : — 

I.  Spore  formation  distinct  from  and  takes  place  after 
the  trophic  phase — Teleosporidia. 
II.  Spore    formation    and    trophic    stage   proceed    simul- 
taneously— Neosporidia. 

PHYLUM:  SARCODINA  Hertwig  and  Lesser,  1874. 

Definition. — -Plasmodromata  which  move  and  capture  their  food 
by  n ica  11s  of  pseudopodia. 
Classification.— The  Sarcodina  may  be  classified  as  follows: — 

(a)  Without  axial  filaments  in  the  lobose,  filose,  or  reticulose 

pseudopodia — -Rhizopoda. 

(b)  With  central  axial  filaments  in  line  ray-like  pseudopodia — 

Heliozoa  Haeckel,  1866;  Radiolaria  Haeckel,  1861. 

Remarks. — -Only  the  Rhizopoda  concern  us  at  present. 

CLASS:  RHIZOPODA  von  Siebold,  1845. 
Definition. — -Sarcodina,    parasitic    or    free-living,    without    axial 
filaments  in  their  lobose,  filose,  or  reticulose  pseudopodia. 


298  PLASMODROMATA   AND  SARCODINA 

Classification. — This  class  may  be  divided  into  subclasses  as 
follows : — 

(a)  With  blunt  loose  pseudopodia  which  do  not  anastomose— 

Amoeba. 

(b)  With    fine    branching    and    anastomosing    pseudopodia- — • 

Foraminifera. 

Remarks. — Only  the  Amcebae  concern  us. 

SUBCLASS:  AMCEBCE  Ehrenberg,    1830. 

Synonyms.- — Amcebina  Auctores  (a  misprint);  Chaidea  Poche, 
1913;  Amoelidce  Brown,  1859. 

Definition. — Rhizopoda,  parasitic  or  free-living,  with  blunt,  loose 
pseudopodia  which  do  not  anastomose. 

Classification. — The  subclass  Amcebae  may  be  divided  into  two 
orders  as  follows : — 

(a)  Without  a  shell- — Gymnamoebida. 

(b)  Witn  a  shell — Thecamoebida. 

ORDER  I.  GYMNAMCEBIDA  Delage  Herouard,  1896. 

Synonym. — Lobosa  Carpenter,  1861;  Amcebidce  Broun,  1859; 
Chaidce  Poche,  1913. 

Definition.- — Amcebae  without  a  shell,  but  with  a  tendency  of  the 
peripheral  plasm  to  harden  into  a  membrane-like  zone. 

Type  Genus. — Amoeba  Bory  de  St.  Vincent,  1822. 

Remarks.— The  genera  of  this  order  are  in  a  wild  state  of  con- 
fusion. Calkins  in  1912  gave  a  large  number  of  genera — Amoeba, 
Vahlkamfia,  Naegleria,  Craigia,  Trimastigamoeba,  Entamoeba, 
Paramceba,  Trichospherium,  Hyalodiscus,  Chromaletta,  Pelomyxa, 
Dactylosphera,  Nucleophaga.  In  the  same  year  Alexeieff  created 
the  genera  Naegleria  and  Hartmannia  for  Amcebae  of  the  limax 
type,  and  also  Proctamceba  for  Amcebae  parasitic  in  vertebrates, 
but  the  two  last  names  have  not  come  into  general  use.  Doubtless 
many  more  exist. 

Classification. — Those  found  in  man  up  to  the  present  may  be 
classified  into : — 

1.  Loeschia  Chatton  and  Lalung-Bonnaire,  1912. 

2.  Vahlkamfia  Chatton  and  Lalung-Bonnaire,  1912. 

3.  Craigia  Calkins,  191 2. 

4.  Dientamoeba  Jepps  and  Dobell,  1918. 

They  may  be  differentiated  as  follows: — ■ 
A.  Without  uniflagellate  stage  : — 
I.  Typically  uninucleate: — 

Ecto-  and  endoplasm  distinct  when  moving.  Nucleus 
with  or  without  visible  karyosome  and  centriole. 
Contractile  vacuoles  generally  absent.  Division 
by  mesomitosis — Loeschia. 


PLASMODROMATA  299 

Ectoplasm  only  seen  in  outbursts.  Nucleus  with 
finely  divided  chromatin  forming  a  membrane-like 
contour  and  with  definite  karyosome.  Division 
by  promitosis — Vahlkamfia. 

II.  Typically  binucleate,  the  two  nuclei  having  the  same 
size  and  structure. 
Ecto-  and  endoplasm  distinct — Dientanueba. 

B.  With  uniflagellate  stage  : — 

Ectoplasm  visible  on  movement.      Endoplasm   with  or 
without  a  body  like  a  Nebenkorper — Craigia. 

THE  GENUS  AMOEBA. 

The  old  original  genus  Amoeba  seems  to  have  been  first  described 
by  Rosel  von  Rosenhof  in  1775,  under  the  heading  the  Small 
Proteus,  and  to  this  organism  Linnaeus  gave  the  name  Volvox  chaos, 
which  Pallas  in  1766  turned  into  Volvox  proteus.  In  1822  Baron 
Bory  de  Saint  Vincent,  in  the  '  Dictionnaire  Classique  d'Histoire 
Naturelle,'  vol.  i.,  pp.  260-262,  established  the  genus  Amiba,  calling 
Volvox  proteus  by  the  name  Amiba  divergens,  which  Ehrenberg  in 
1 83 1  altered  to  Amceba  princeps  and  Leidy  in  1878  to  Amoeba 
proteus. 

This  original  genus  is  now  divided  into  the  following  genera : — 

A.  Usually  free  living  : — 

I.  Without  a  flagellate  stage  in  the  life-cycle: — 
{a)  Usually  uninucleate. 

1.  Large  forms  reaching  to  1  millimetre  in  diameter, 

free  living,  with  well  differentiated  ecto-  and 
endoplasm  and  well  developed  pseud opodia. 
One  or  many  large  nuclei  with  doubly  refracting 
membrane  and  chromatin  concentrated  into  a 
single  large  karyosome  or  as  granules  diffused 
through  nucleus.  One  or  more  contractile 
vacuoles — Genus  1,  Amceba  Bory  de  St.  Vincent, 
1822. 

2.  Minute  forms,  free  living  or  commensal,  ectoplasm 

not  well  differentiated  from  endoplasm,  moving 
as  a  fingei -formed  single  pseudopodium  or  with 
irregular  ectoplasmic  bursts  to  form  a  general  or 
local  ectoplasm.  Nucleus  single  or  double,  with 
finely  divided  chromatin,  forming  a  membrane- 
like structure  and  a  definite  karyosome.  One 
contractile  vacuole  present  as  a  rule — Genus  2, 
Vahlkamfia  Chatton  and  Lalung-Bonnaire,  1911; 
emendavit  Calkins,  1912. 
(■'»)  Usuallv  binucleate.  Genus  3,  Dientamtvba  Jeffs 
and  Dobell,  1918. 


3oo 


PLASMODROMATA  AND  SARCODINA 


I. 

2. 

3- 


II.  With  a  flagellate  stage  in  the  life-cycle: — 

(a)  Flagellate    forms    divide — Genus    4,    Parameeba 
Schaudinn,  1896. 

(b)  Flagellate  forms  do  not  divide: — 

Uniflagellate- — Genus  5,  Craigia  Calkins,  1912. 

Biflagellate  —  Genus  6,  Naegleria  Alexeieff, 
1912;  emendavit  Calkins,  1912. 

Triflagellate — Genus  7,  Trimastigamcela  Whit- 
more,  191 1. 

B.  Parasitic,  commensal,  or  pathogenic  : — 

I.  Contractile    vacuoles    numerous;    cysts    give    rise    to 

gametes — Genus  8,  Entamoeba  Leidy,  1879. 

II.  Contractile  vacuoles  absent;  cysts  not  known  to  give 

rise    to    gametes — Genus   9,    Loeschia   Chatton    and 
Lalung-Bonnaire,  1912. 

The  principal  species  of  the  genus  Amoeba  are  the  type  A .  proteus 
(Pallas,  1766),  A.  vespertilio  Penard,  1902,  A.  verrucosa  Ehrenberg, 

1838,  and  A.  terricola  Greeff,  1892, 
but  the  last  two  may  be  the 
same  species. 

The  type  species  of  Naegleria 
is  A',  punctata  Dangeard,  1910, 
found  in  pond  water  and  infusions. 
Trimastigamceba  has  only  one 
species,  T.  philippinensis  Whit- 
more,  found  in  tap  water  in 
Manila. 

Entamoeba  has  as  its  type 
species  E.  blattce  Butschli,  1878, 
described  in  detail  by  Mercier  in 
1909  and  1910,  who  says  that  the 
gamete-forming  cysts  give  rise 
to  minute  uninucleate  gametes, 
which  conjugate  outside  the  cyst,  while  the  copula  develops  directly 
into  the  trophozoite.  This  is  very  different  from  what  is  known 
concerning  the  life-history  of  Loeschia. 

As  the  type  genus  is  Amoeba,  and  its  type  species  Anucba  proteus 
1  Pallas,  1766),  it  is  interesting  to  know  its  life-cycle,  which  is  but 
little  understood  at  present. 

Miss  Carter  has,  however,  studied  encystment,  while  simple  division  is 
lulK  established  and  schizogony  is  doubtful. 

The  precystic  stage  is  characterized  by  the  Amoeba  becoming  sluggish, 
clearing  its  body  of  debris,  and  exuding  a  slimy  mucus,  which  causes  surround- 
ing detritus  to  adhere  to  it,  and  so  to  form  an  outer  protecting  covering,  inside 
which  two  membranous  cyst  walls,  separated  by  fluid,  are  formed.  The  cysts 
measure  70  to  140  microns  in  diameter,  and  are  found  in  England  from  late 
December  to  the  middle  of  March.  They  are  spherical  and  without  means  of 
attachment. 


Fig.  48. — Cyst  of  Amoeba  proteus 
(Pallas,  1766).     (After  Carter  ) 


LOESCHTA  301 

Inside  the  cyst  the  nucleus  breaks  down  and  the  chromatin  and  plastin  are 
distributed  throughout  the  cytoplasm,  in  which  they  form  secondary  nuclei 
of  the  protokaryon  type,  and  finally  some  75  to  100  young  nucleated  amoebae, 
which  apparently  do  not  become  flagellate,  and  so  far  as  is  known  do  not  form 
gametes,  but  this  and  the  further  development  require  investigation. 

Metcalf  has,  however,  observed  zygosis  in  mimite  gametes  of  Amccba 
profens. 


Genus  Loeschia  Chatton  and  Lalung-Bonnaire,  1912. 

Synonyms. — -Amceba  Ehrenberg,  1830,  pro  parte;  Entamceba 
Casagrandi  and  Barbagallo,  1897;  nee  Endamoeba  Leidy,  1879. 

Definition. — Gymnamoebida,  with  a  vesicular  nucleus  containing 
a  small  karyosome  (as  a  rule)  and  abundant  peripheral  chromatin, 
and  dividing  by  mesomitosis,  and  with  cysts  containing  four  to 
eight  nuclei,  which  form  young  amoebae  which  are  not  known  to 
be  gametes. 

Nomenclature. — The  name  Amoeba  was  applied  by  St.  Vincent 
in  1822  and  by  Ehrenberg  in  1830  to  free  living  forms,  of  which 
the  type  is  Amoeba  proteus,  which  Poche  thinks  is  the  Volvox  chaos 
of  Linnaeus;  and  the  term  Endamoeba  was  given  by  Leidy  in  1879 
to  the  parasitic  E.  blatta  Biitschli,  but  this  name  cannot  be  applied 
to  the  human  parasites,  because  Mercier's  researches  have  shown 
that  it  may  be  different,  and  therefore  it  is  necessary  to  use  Chatton 
and  Lalung-Bonnaire's  term. 

Remarks. — The  genus  is  composed  of  amoeba-like  forms  varying 
in  size  from  5  to  80  microns,  and  possessing  distinct  ectoplasm  and 
endoplasm,  which,  however,  may  be  only  visible  during  motion. 
The  ectoplasm  is  clear  and  hyaline,  while  the  endoplasm  may  be 
either  clear  or  finely  granular.  The  nucleus  usually  has  a  karyo- 
some and  centriole.  Reproduction  is  by  simple  division,  schizogony, 
and  cyst  formation. 

The  species  live  in  the  alimentary  canal  of  man  and  animals, 
but  may  enter  other  tissues  and  organs,  and  may  be  pathogenic 
or  non-pathogenic. 

It  is  still  doubtful  whether  artificial  cultivation  has  been  per- 
formed successfully. 

Type  Species. — The  type  species  is  Loeschia  coli  Loesch,  1875, 
found  in  man,  but  used  in  the  sense  of  the  term  as  defined  by 
Schaudinn  in  1903,  an  1  not  as  defined  by  Loesch  in  1875. 

Classification. — Chatton  and  Lalung-Bonnaire  suggested  the 
formation  of  two  subgenera — viz.,  Loeschia,  characterized  by  cysts 
with  eight  nuclei,  and  Viereckia,  distinguished  by  cysts  with  four 
nuclei,  but  this  has  not  been  adopted  so  far. 

As  there  are  a  very  large  number  of  species  described,  we  will 
kri\v  a  list  classified  according  to  the  part  of  the  body  in  which 
tlav  were  discovered,  but  Schaudinn's  statement  made  in  1903 
should  be  remembered,  '  The  knowledge  of  the  development  is  the 
first  postulate  of  protozoan  research  ;'  and  because  this  knowledge  is 
lacking  so  much  confusion  exists. 


3o2  PLASMODROMATA  AND  SARCODINA 

I .  Intestinal : — 

1.  L.  coli  Loesch,  1875. 

2.  L.  histolytica  Schaudinn,  1903. 

3.  L.  tetragena  Viereck,  1907. 

4.  L.  tropicalis  Lesage,  1908. 

5.  L.  minuta  Elmassian,  1909. 

6.  L.  nipponica  Koidzumi,  1909. 

7.  L.  undulans  Castellani,  1905. 

8.  L.  williamsi  Prowazek,  1911. 

9.  L.  hartmanni  Prowazek,  1912. 

10.  L.  biitschli  Prowazek,  1912. 

11.  L.  brasiliensis  Baurepaire-Aragao,  1912. 

12.  L.  dysentericc  europaece  Popper,  1917. 

13.  L.  nana  Wenyon  and  O'Connor,  1917.     (This  is  con- 

sidered under  Vahlkamfia  (see    p.  323.) 

14.  L.  minutissima  Brug,  1917. 

The  researches  of  Hartmann,  Whitmore,  Wenyon,  Craig,  Calkins, 
and  James,  have  demonstrated  that  only  two  of  these  are  good 
species,  viz. : — 

Loeschia  coli  Loesch,  1875. 
Loeschia  histolytica  Schaudinn,  1903. 

II.  Hepatic  and  renal  :■ — ■ 

L.  mortinatalium  Smith  and  Weidman,  1910. 

This  species  was  found  originally  in  the  liver  and  kidneys  of 
a  fcetus  born  dead. 

III.  Buccal : — 

1.  L.  gingivalis  Gros,  1849. 

2.  L.  buccalis  Sternberg,  1862. 

3.  L.  dentalis  Grassi,  1879. 

4.  L.  dentalis  Braun,  1883. 

5.  L.  buccalis  Prowazek,  1904. 

6.  L.  maxillaris  Kartulis,  1901. 

There  is  only  one  good  species,  viz.: — 

Loeschia  gingivalis  Gros,  1849. 

IV.  Genito-urinary :  — 

L.  urogenitalis  Baelz,  1883,  which  may  be  the  same  as 
Amoeba  urince  granulata  Ward,  Coles  and  Friel,  which 
the  latter  suggests  comes  from  an  organism  like  a 
protococcus  taken  into  the  alimentary  canal. 
Chalmers  and  O'Farrell  consider  it  to  be  L.  histolytica 
in  all  probability. 

V.  Pulmonary : — 

L.  pulmonalis  Artault,  1898. 

This  may  be  the  same  organism  as  L.  mortinatalium  Smith  and 
Weidman,  1910,  and  both  may  be  L.  histolytica,  as  Chalmers  and 
Atkey  have  reasons  for  believing  that  L.  pulmonalis  is  very  like 
L.  histolytica. 


LOESCHIA  303 

VI.  In  Abscesses  : — 

L.  kartulisi  Doflein,  1901. 

VII.  In  serous  exudations  : — 
L.  miurai  Ijima,  1898. 

All  the  above,  except  the  last,  are  probably  either  L.  coli  or 
L.  histolytica,  while  the  last  may  be  the  Leydenia  stage  of  Chlamy- 
dophrys  enchelys  Ehrenberg,  which  is  often  classified  in  the 
Foraminifera. 

If  this  is  accepted,  we  have  only  three  species  to  consider- 
viz.:— 

L.  coli  Loesch,  1875,  emendavit  Schaudinn,  1903. 
L.  histolytica  Schaudinn,  1903. 
L.  gingivalis  Gros,  1849. 

And  these  may,  with  difficulty,  be  distinguished  as  follows: — 

(a)  Size  small — average  12-20  microns  : — 

Endoplasm  often  contains  red  blood-corpuscles,  cvsts 
with  one  nucleus — -1.  Gingivalis. 

(b)  Size  larger — average  25-35  microns : — 

1.  Endoplasm  does  not  normally  contain  red  blood- 

corpuscles.     Cysts  usually  contain  eight  nuclei,  but 
may  have  sixteen — 2.  Coli. 

2.  Endoplasm  normally  contains  red  blood-corpuscles. 

Cysts  contain  one  to  four  nuclei  and  characteristic 
chromidial  bodies — 3.  Histolytica. 

Amcebje  in  Animals. — -A  full  list  of  Amoebae  according  to  hosts 
was  given  by  Hassall  in  1913  (see  references),  and  therefore  we 
omit  the  full  list  given  in  previous  editions,  only  a  short  list  being 
given  on  p.  321  but  we  may  say  that  in  vertebrates  and  inverte 
brates  a  very  large  number  of  species  have  been  described,  but 
many  of  these  will  probably  be  found  to  be  the  same. 

Type  Species. — The  type  species  in  Loeschia  coli  (Loesch,  1875) 
Schaudinn,  1903,  which  we  will  now  describe. 

Loeschia  coli  Loesch  1875,  emendavit  Schaudinn,  1903. 
Synonyms. — Amceba  coli  Loesch,   1875;  Entamceba  coli  Loesch, 

i875- 

Probable  Synonyms. — Entamoeba  tropicalis  Lesage,  1908;  E.  nip- 
ponica  Koidzumi,  1909;  E.  williamsi  Prowazek,  1911;  E.  muris 
Grassi;  and  perhaps  others  (vide  supra). 

Definition. — Loeschia  with  cysts  containing  eight  nuclei,  cyto- 
plasm almost  always  without  red  blood-corpuscles,  ectoplasm  in- 
visible except  when  a  pseud opodium  is  being  protruded.  Nucleus 
subcentral,  vesicular,  with  cyclic  changes  not  well  marked.  Karyo- 
some  often  with  two  granules. 

Nomenclature. — The  correct  name  is  Loeschia  hominis  Casagrandi 
and  Barbagallo,  1897.  The  name  L.  coli  was  originally  applied  by 
Loesch  to  the  pathogenic  amceba  which  caused  dysentery,  but  the 


3<>4  PLASMODROMATA  AND  SARCODINA 

nomenclature  was  reversed  by  Schaudinn  (as  Dobell  has  pointed 

out)  in  1903,  and  it  is  most  difficult  to  alter  it  at  the  present  time. 

History.- — In   1859   Lambl   published   a   note   referring   to   the 

presence   of  an  amoeba,   associated  with   other  protozoa,   in  the 

motions  of  a  case  of  dysentery,  and  this  was  followed  by  an  account 

by  Loesch  in  1875  in  which  he  states  that  he  considers  these  amoebae 

to  be  the  cause  of  dysentery.     Grassi,  in  1879,  was  the  first  observer 

to  demonstrate  the  presence  of  amoebae  in  the  motions  of  healthy 

people,   and   alone    or   with    Calandruccio   described    encystment, 

while  Calandruccio  infected  himself  per  os  with  the  cysts.     They 

both  noted  its  non-path ogenicity.     Lewis  and  Cunningham  in  1881 

saw  them  in  the  motions  of  persons  suffering  from  cholera.     In 

1894  Colli  and  Fiocca  described  and  named£six|species  of  amoeba 

occurring  in  man,  but  it  is  doubtful  what  these  really  are;  probably 

some  of  them  belong  to  L.  coli.     Grassi's  findings  were  confirmed 

by   Koch  and   Kartulis,   but   Kruse  and  Pasquale  in  a  classical 

investigation  demonstrated  that  there  were  two  kinds  of  amoebae, 

one  harmless  and  the  other  the  cause  of  dysentery.     It  was  not, 

however,  until  Casagrandi  and  Barbagallo  investigated  and  defined 

L.  coli,  which  is  harmless,  that  it  was  possible  for  Jiirgens  to  make 

his  researches,  which,  extended  by  Schaudinn,  ended  in  defining 

a  second  amoeba  named  L.  histolytica,  which  was  considered  to  be 

the  cause  of  amoebic  dysentery.     It  has  been  studied  in  detail  in 

1912  by  Hartmann  and  Whitmore  with  important  results,  and  in 

an  important  memoir  by  James  in  1914. 

It  seems  to  us  that  Wenyon's  researches  into  L.  muris  are  so 
important  with  regard  to  the  opposing  opinions  of  Schaudinn  and 
Werner  on  the  one  hand,  and  Hartmann  and  Whitmore  on  the 
other,  that  we  give  this  in  detail. 

Loeschia  muris  Grassi,  1881. 

The  life-history  of  this  amoeba  has  been  carefully  studied  by  Wenyon  in 
1907.  L.  muris  lives  in  the  caecum  of  mice  and  rats,  either  freely  amongst 
the  contents,  or  upon  the  epithelial  surface,  or  in  the  glands  to  then  ends. 
It  measures  up  to  30  to  40  microns  in  diameter. 

The  food  appears  to  be  anything  at  hand — bacteria,  flagellates  and  their 
cysts,  yeast  cells,  and  cast-off  epithelial  cells. 

The  Trophozoite. — The  narrow  ectoplasm  is  only  distinctly  visible  in  the 
formation  of  the  pseudopodia,  while  the  granular  endoplasm  contains  the  food 
vacuoles  and  the  nucleus,  which  latter  is  distinctly  visible  as  a  clear  vesicle 
with  a  distinct  nucleolus. 

When  stained,  the  nucleus  is  seen  to  have  a  definite  fairly  thick  membrane, 
with  chromatinic  lumps  at  one  or  two  points.  The  nucleolus  or  karyosome 
is  chromatinic,  and  between  it  and  the  nuclear  membrane  is  the  linin  network 
with  scanty  granules  of  chromatin  scattered  over  it.  This  is  the  type  of 
nucleus  found  in  L.  coli. 

Mnliiphi  ation  takes  place  by  binary  division  and  by  encystment.     In  the 

former  a  nuclear  spindle  is  formed  without  chromosomes  or  an  equatorial 

plate,  as  the  chromatin  gathers  at  the  poles,  and  the  nucleus  after  elongation 

■  mes  indented  and  then  divided  in  the  middle,  and  after  some  length  of  time 

the  cytoplasm  divides. 

The  precystic  stage  is  distinguished  by  having  its  endoplasm  cleared  of  all 
large  inclusions,  and  is  surrounded  by  a  soft  gelatinous  wall,  through  which 
the  remains  of  food  materials  can  be  cast  out. 


LOESCHIA 


3°5 


Cystic  Stage.— A  cyst  is  spherical  or  slightly  oval,  12  to  14  microns  in  dia- 
meter, and  contains  a  cytoplasm  free  from  food  particles,  and  may  or  may  not 
contain  a  retractile  body,  while  the  nucleus  is  large  and  contains  much 
chromatin.  This  nucleus  divides,  by  simple  division,  forming  two  daughter 
nuclei,  and  this  binucleate  stage,  which  is  of  long  duration,  is  characterized 
by  the  throwing  out  of  chromatin  from  the  nuclei. 

Autogamy. — Each  nucleus  now  gives  off  reduction  bodies  which  are  dis- 
solved in  the  cytoplasm.  These  two  nuclei  are  slightly  different:  in  one  it  is 
evenly  distributed,  while  in  the-  other  it  is  concentrated  at  one  end ;  the  former 
migrates  towards  the  latter,  and  both  become  alike  and  throw  out  chromatin. 
The  nuclei  were  not  seen  to  fuse,  but  they  elongate  greatly,  spindles  are 
formed,  and  they  divide,  giving  rise  to  four  nuclei — i.e.,  two  pairs  at  opposite 
poles  of  the  cysts,  composed  of  one  nucleus  from  each  of  the  original  forms 
extending  to  the  opposite  pole  of  the  cysts. 


Fig.  49. — Diagram  of  the  Life-Cycles  of  L.  mavis  Grassi  (con- 

STRUCTED    FROM    WeNYON'S    DRAWINGS). 


Each  pair  then  fused  to  form  one  nucleus,  and  then  almost  immediately 
divided  to  form  four  nuclei,  and  these  again  to  form  eight  nuclei. 

During  this  process  the  soft  gelatinous  cyst  wall  of  the  precystic  stage  is 
converted  in  a  tough  resistant  envelope,  inside  which  an  inner  membrane 
is  formed  (compare  Amoeba  proteus).  The  outer  cyst  wall  becomes  tough  and 
irregular  in  the  faeces. 

Method  of  Infection.— The  cysts  now  escape  from  the  intestine  in  the  normal 

fasces,  in  which  the  amoeba?  are  not  seen,  these  being  only  found  in  diarrhoea! 

motions.     Cysts  wen'  used  to  infect  b]   feeding  a  mouse,  which  was  apparently 

-Mm  infection,  and  in  about  three  to  lour  weeks  cysts  appeared  for  the 

lirst  time  in  the  faeces. 

20 


306  PLASMODROMATA  AND  SARCODINA 

Wenyon  did  not  see  the  cysts  burst  and  the  amoebae  escape. 

Wenyon  says: '  When  we  take  into  account  the  striking  similarity  oi  these 
two  amoebas  (L.  muris  and  L.  coli),  both  in  the  free  condition  and  in  their  encyst- 
ing process,  it  is  difficult  to  avoid  the  conclusion  that  they  are  identical.' 

In  1917  Wenyon  and  O'Connor  published  exceedingly  valuable 
researches  on  the  diagnosis  of  L.  coli  and  on  the  house-fly  as  a 
carrier  of  the  cysts. 

We  therefore  see  that  while  a  great  deal  is  known  as  to  the 
structure,  life-history,  and  method  of  infection,  there  is  still  much 
to  be  observed.  Are  Schaudinn  and  Wenyon  correct  in  their 
description  of  autogamy,  or  does  L.  coli  really  form  gametes  like 
Entamoeba  blattce  ?     Is  there  any  true  schizogony  ? 

After  this  rather  long  history,  we  will  not  enter  fully  into  the 
structure  of  L.coli,  but  will  only  present  a  very  condensed  account. 

Morphology. — In  diameter  it  measures  as  a  rule  20  to  40  /jl, 
although  forms  as  small  as  10  /u  and  even  5  ju  have  been  described. 
The  cytoplasm  is  vacuolated  and  contains  bacteria,  and  extremely 
rarely  one  red  corpuscle.  The  ectoplasm  is  not  visible  until  a 
pseudopodium  is  about  to  be  protruded.  The  vesicular  nucleus 
resembles  that  of  the  tetragena  stage  of  L.  histolytica,  an  account 
of  which  is  given  below,  but  the  cyclic  changes  are  not  so  well 
defined.  The  karyosome  when  present  is  small,  and  is  composed 
of  two  chromidia  united  by  a  chromatic  substance.  At  the  com- 
mencement of  a  cycle  this  karyosome  is  a  round  compact  mass  of 
chromatin  connected  with  the  periphery  by  a  linin  network  with 
few  chromatinic  granules.  This  karyosome  breaks  up,  its  chromatin 
increasing  in  amount,  the  linin  network  becomes  thicker,  and 
there  are  more  chromatin  granules  at  its  nodes,  and  this  goes 
on  until  all  the  chromatin  is  collected  as  blocks  under  the  nuclear 
membrane  and  only  a  small  granule  is  left  in  the  centre,  and  then 
the  cycle  begins  again  by  the  growth  of  the  granule  into  a  large 
karyosome. 

Life-History. — The  life-cycle  comprises  two  phases:  a  binary 
division  by  promitosis  takes  place  (and  not  by  amitosis,  as  de- 
scribed by  Schaudinn).  The  process  of  schizogony  is  described  to 
take  place  by  repeated  division  into  two,  forming  two,  four,  and 
eight  nuclei  (vide  Fig.  42,  p.  292),  which  form  eight  little  Loeschire 
which  begin  the  asexual  cycle  again,  but  this  is  very  doubtful. 
Encystment  takes  place,  followed  by  division  of  the  nucleus  into 
two,  four,  and  finally  eight  nuclei.  During  this  stage  a  large 
vacuole  exists  in  the  cytoplasm,  which  disappears  in  the  eight- 
nuclei  stage.  Contrary  to  Schaudinn,  Hartmann  and  Whitmore 
believe  that  no  zygosis  takes  place  in  the  cyst,  but  that  eight 
little  amoebae  are  formed  which,  on  escaping  from  the  cyst,  they 
think  may  conjugate  in  pairs  and  form  the  synkaryon  or  zygote 
from  which  the  vegetative  forms  arise  after  the  manner  described 
by  Mercier  in  1909  for  E.  blattce.  Sometimes  the  cysts  have  more 
than  eight  nuclei — e.g.,  ten  or  twelve— which  must  be  considered 
to  be  abnormal. 


LOESCHIA  307 

Bionomics. — L.  coli  lives  in  the  lumen  of  the  intestine,  and  feeds 
upon  the  contents  of  the  bowel. 

Diagnosis. — Amoebae  moving  slowly  with  pale  non-refractile 
pseudopodia,  with  a  thin  rim  of  ectoplasm  and  with  an  endoplasm 
containing  all  sorts  of  organisms  and  no  red  cells,  and  with  a  large 
distinct  nucleus,  are  L.  coli,  and  this  diagnosis  should  be  confirmed 
by  the  discovery  of  the  cyst  because — - 

1.  The  typical  characters  are  liable  to  considerable  changes, 
and  the  amoeba  may  be  very  like  L.  histolytica,  as  will  be 
emphasized  below. 

2.  Wenyon  and  O'Connor's  researches  confirm  that  L.  coli 
will  not,  as  a  rule  at  all  events,  ingest  red  blood-corpuscles. 

With  regard  to  the  cysts,  they  measure  from  13-38  microns,  but 
the  average  is  over  25  microns;  the  typical  cyst  has  eight  nuclei 
and  the  very  large  cysts  sixteen.  At  times  chromidial  bodies  may 
be  present,  making  them  look  like  L.  histolytica  cysts,  from  which 
they  are  to  be  distinguished  by  the  number  of  nuclei,  which  in  the 
motions  is  generally^eight. 


Fig.  50. — Loeschia  coli  Schaltdinn,   Vegetative 'Form,  stained. 
(  x  1950  Diameters.) 

(After  James.) 

Carriage  by  House-Flies. — Wenyon  and  O'Connor,  working  in 
Egypt,  have  shown  that  L.  coli  and  L.  histolytica  cysts  can  be  in- 
l  by  house-flies  (Musca,  Fannia,  Calliphora,  and  Lucilia)  which 
have  fed  on  faeces  containing  such  cysts.  These  cysts  can  live  in 
the  gut  of  the  fly  so  long  as  any  faecal  matter  remains  there,  but 
die  after  all  the  faecal  matter  has  been  expelled,  which  takes  place 
some  twenty-four  hours  after  the  faecal  feed.  The  cysts  may  be 
seen  in  the  droppings  of  the  fly  as  early  as  five  minutes  and  as  late 

twenty-four  hours  after  the  faecal  feed. 

As  to  the  conveyance  of  cysts  on  the  exterior  of  the  fly,  the 
observations  of  Kuenen  and  Swellengrebel  and  Nicol  show  that 
flies  do  not  move  far  until  they  have  cleaned  themselves,  so  that 
but  little  faecal  matter  is  left,  and  as  this  dries  the  cysts  perish. 

Method  of  Infection. — -The  experiments  of  Calandruccio  and  of 
Wenyon  and  O'Connor  have  proved  that  infection  takes  place 
Per  os,  ;n>l  is  due  to  the  cysts;  and  that,  further,  these  are  intro- 
duced most  probably  by  food  contaminated  by  the  cyst-laden 
faecal  matter  of  house-flies. 

Distribution.— L.  coli  is  found  in  both  the  tropics  and  the  Tern- 


3o8  PLASMODROMATA  AND  SARCODINA 

perate  Zone.     In  the  former  it  is  especially  common  in  the  fseces  of 
natives. 

Pathogenicity.- — L.  coli  is  a  non-pathogenic  commensal  found  in 
man,  and  possibly  in  rats  and  mice,  and  perhaps  in  other  animals. 
Views  as  to  its  pathogenicity  have  probably  arisen  through  mis- 
taking the  tetragena  phase  of  L.  histolytica  for  L.  coli.  An  Amoeba 
resembling  L.  coli  is  found  in  monkeys  in  which  an  Amoeba  resem- 
bling L.  histolytica,  and  called/,,  nuttalli,  is  also  found. 

Loeschia  histolytica  Schaudinn,  1903. 

Synonyms.- — Amoeba  coli  Loesch,  1875;  Entamoeba  histolytica 
Schaudinn,  1903;  Entamoeba  tetragena  Viereck,  1907;  E.  africana 
Hartmann  and  Prowazek,  1907;  E.  minuta  Elmassian,  1909;  and 
Amoeba  dysenteries  Councilman  and  Lafleur,  1891.  Among  the 
many  doubtful  species  of  Amoebae  found  in  man  there  must  be 
many  names  which  are  synonyms  of  L.  histolytica,  but  comparisons 
are  very  difficult,  as  descriptions  are  often  incomplete — e.g.,  Amoeba 
urogenitalis  Baelz,  and  Amoeba  pulmonalis  Artault. 

Nomenclature.- — The  correct  name  is  Loeschia  coli  (Loesch,  1875), 
as  will  be  explained  below. 

Definition. — Loeschia  with  cytoplasm  often  containing  red 
corpuscles  and  with  four-nucleate  cysts. 

Historical — Early  Observations.- — Loesch  discovered  the  amoeba 
which  he  named  Amoeba  coli  in  motions  from  a  case  of  dysentery, 
and  considered  it  to  be  pathogenic.  It  was  by  this  name  that 
Ouinke  and  Roos  in  1893  called  the  organisms  found  by  them  in 
dysentery.  As  already  stated,  Councilman  and  Lafleur  called  an 
amoeba  found  in  cases  of  dysentery  Amoeba  dy sentence,  and  it  is 
certain  that  this  was  Loesch's  Amoeba  coli.  An  amoeba  somewhat 
similar  to  the  '  tetragena  stage  '  of  L.  histolytica  was  seen  by  Kruse 
and  Pasquale  in  1893. 

We  thus  see  that  the  correct  name  for  the  dysenteric  amoeba 
is  Loeschia  coli,  as  Dobell  has  pointed  out,  and  that  the  correct 
name  for  the  harmless  amoeba  is  L.  hominis,  because  Casagrandi 
and  Barbagallo  called  it  Entamoeba  hominis  in  1897,  when  it  really 
had  no  name.  Unfortunately  Schaudinn  did  not  utilize  this  name, 
and  in  his  revision  applied  the  term  '  coli '  to  the  non-pathogenic 
form,  and  invented  the  name  histolytica  for  the  pathogenic  amoeba, 
which  is  difficult  to  change  at  the  present  time,  as  there  is  no 
certainty  that  there  is  at  present  finality  in  this  nomenclature. 

Differentiation.- — In  1902  Jiirgens  for  the  first  time  clearly 
differentiated  the  pathogenic  amoeba,  and  in  the  following  year 
(1903)  Schaudinn  studied  and  compared  the  morphology  and  the 
life-cycles  of  his/,,  coli  and  hisL.  histolytica,  and  thus  established 
their  characters,  and  gave  the  following  account : — 

Morphology. — Its  average  measurement  is  25  to  50  /j,  in  diameter,  and 
therefore  the  average  is  greater  than  thai  of  /..  coli.  It  consists  of  clear 
hyaline  ectoplasm  and  granular  endoplasm,  in  which  can  be  seen  red  blood- 
corpuscles,   vacuoles,   bacteria,  and   other  matters,   but  the  nucleus  is  not 


LOESCHIA 


3°9 


clearly  visible  unless  coloured  by  some  preparation.  When  resting  it  is  oval 
pr  spherical,  but  during  movement  it  alters  its  appearance  repeatedly,  throwing 
out  pseudopodia  and  creeping  about.  The  nucleus  is  small,  about  5  /li  in 
diameter,  and  is  poor  in  chromatin,  and  placed  excentrically  sometimes  close 
to  the  periphery.  The  limiting  membrane  is  difficult  to  define,  and  the 
amount  of  chromatin  is  relatively  very  small.  A  small  karyosome  can  some- 
times be  seen  in  the  centre  of  the  nucleus. 

Life-History. — It  reproduces  in  three  ways:    (1)   binary  fission;   (2)   gem- 
mation; and  (3)  sporogony. 


Fig. 


-Diagram  of  the  Life-Cycles  of  Loeschia  histolytica 

ACCORDING    TO    SCHAUDINN'S    VlEWS. 


(Constructed  from  Craig's  drawings  in  the  Journal  of  Infectious  Diseases.) 
A,  B,  Binary  fission;  1-8,  spore-formation. 


1.  Binary  Fission. — This  method  was  only  discovered  by  Schaudinn  on 
examining  fresh  specimens  of  the  infected  alimentary  canal. 

The  nucleus  divides  by  amitosis  into  two,  and  then  the  cytoplasm  splits 
into  two  equal  daughter  i  ells. 

2.  Gemmation.  —Gemmation,  found  more  commonly  than  binary  fission 
by  Schaudinn,  consists  of  the  division  of  the  nucleus  by  amitosis  into  two  or 
more  daughter  nuclei,  which,  together  with  small  portions  of  the  cytoplasm, 
separate  off  from  the  mother  cell,  the  daughter  cell  being  smaller  than  the 
mother  cell. 

3.  Spore-Formation. — In  spore-formation,  which  only  takes  place  under 
favourable  circumstances,  such  as  when  recovery  is  taking  place  after  an 


31o  PLASMODROMATA  AND  SARCODINA 

attack  of  dysentery,  the  chromatin  in  and  around  the  nucleus  becomes 
diffused  into  the  cytoplasm,  and  finally  collects  near  the  periphery,  and  the 
remains  of  the  nucleus  disappear,  being  either  pushed  out  or  absorbed.  The 
ectoplasm  forms  small  knobs,  containing  several  chromidia  in  each.  These 
knobs  and  their  chromidia  become  separated  off  as  rounded  bodies,  which, 
becoming  surrounded  with  a  yellowish-brown  envelope,  form  the  spores  for 
the  infection  of  a  new  host,  as  has  been  shown  by  Schaudinn's  feeding  experi- 
ments on  cats,  which  developed  typical  dysentery  with  the  amoeba?  in  the 
motions,  in  the  lumen,  and  in  the  wall  of  the  alimentary  canal.  These  experi- 
ments further  proved  that  it  was  only  by  the  spores  that  infection  would  be 
spread .  The  remaining  portion  of  the  amoeba  dies  after  the  formation  of  the 
spores. 

Recent  Work.- — Modern  researches  tend  to  confirm  Schaudinn's 
morphological  description  as  well  as  his  binary  fission,  but  not  the 
amitotic  form  of  division,  while  the  bud  formation  (Fig.  52)  has 
been  proved  by  James  and  others  to  be  artificial,  and  the  spores 
are  regarded  as  not  belonging  to  an  Amoeba,  but  to  some  other 
organism  in  the  faeces. 

In  1905  Craig  in  the  Philippine    Islands  confirmed  Schaudinn's 
morphological  characters,  and  called  attention  to  the  rapid  move- 
ments of  L .  histolytica  and  to  the  greenish 
tint  which  it  often  assumes  in   motions 
containing  much  blood. 

In  1907  Viereck  stated  that  there  were 
more  than  one  pathogenic  amoeba  in  man. 
The   second   one,  which   he   named   Ent- 

F  .       ttt  amoeba  tetragena,  looked  like  L.  coli,  but 

Budding    in    Loesckia     had  only  four-nucleate  cysts,  and  this,  he 

histolytica   Schaudinn,      thinks,  is  the  type  seen  by  Ouinke  and 

in      Moist     Chamber     R0os  and  by  Kruse  and  Pasquale.    In  the 

Preparations.  same  year  Hartmann  and  von  Prowazek 

(After  James.)  found  an  entamoeba  in   patients   coming 

from  Africa,  which  could  be  differentiated 

by  its  nuclear  structure  from  L.  coli  and  L.  histolytica,  and  this 

they  named  E.  africana  ;   but   later   Hartmann,   finding   quadri- 

nucleate  cysts,  concluded  that  it  was  the  same  as  E.  tetragena, 

which  is  an  accepted  fact. 

In  1908  Craig,  drawing  attention  to  variations  in  L.  histolytica 
and  in  L.  coli,  emphasized  the  difficulty  in  differentiation  between 
these  organisms,  and  in  the  same  year  Werner  confirmed  the  exist- 
ence of  L.  histolytica  and  of  E.  tetragena. 

In  1909  Hartmann  states  that  Schaudinn  knew  about  E .  tetragena, 
and  that  of  tho  three,  L.  coli,  L.  histolytica,  and  E.  tetragena, 
L.  histolytica  is  the  smallest,  and  has  ectoplasm  differentiated  from 
endoplasm  even  at  rest.  Its  nucleus  is  excentric,  can  be  distorted, 
and  does  not  possess  a  double  contoured  achromatic  membrane, 
while  its  lack  of  chromatin  is  characteristic,  there  being  only  a 
little  karyosome  and  a  condensed  layer  of  chromatin  at  the  margin 
of  the  nucleus,  while  nuclear  cyclical  changes  are  rare.  In  the 
same  year  Noc  wrote  a  paper  mainly  of  an  epidemiological 
nature,  but  also  dealing  with  this  amoeba,  and  Elmassian  described 


LOESCHIA 


3" 


E.  minula,  which  is  to-day  generally  considered  to  be  a  stage  of 
L.  histolytica. 

In  191 1  there  appeared  a  valuable  paper  by  Walker,  in  which  he 
distinguished  only  L.  coli  and  L.  histolytica,  but  the  latter  was 
considered  to  have  '  a  tetragena  stage,'  a  fact  accepted  to-day. 
He  said  that  L.  histolytica  was  hyaline,  feebly  refrangent,  with  active 
motility,  feebly  staining  cytoplasm,  and  an  indistinct  nucleus, 
with  a  relative  paucity  of  chromatin,  which  was  present  as  a  barely 
perceptible  layer  on  the  inner  surface  of  the  nuclear  membrane, 


Fig.  55. — Diagram  of  the  Life-Cycles  of  Loeschia  histolytica  Schaudinn. 

(Constructed  from  Hartmann's  drawings  in  the  Archiv  fur 
Schiffs-  tind  Tr open-Hygiene.) 

I,  Fully  grown  parasite;  2-6,  stages  in  encystment  and  nuclear  division. 


with  or  without  a  few  fragments  scattered  in  the  nuclear  network 
(histolytica  stage),  or  as  a  more  extensive  but  loose  peripheral 
granular  layer  and  a  loose  central  karyosomc  (tetragena  stage). 
All  cysts  were  quadrinucleate. 

In  the  same  year  Whitmore  and  Akashi  published  contributions. 

In  1912  Hartmann  came  to  the  conclusion  that  there  really  was 
only  one  pathogenic  amoeba  in  man,  and  that  this  was  E.  tetragena, 
the  morphology  and  development  of  which  he  studied. 

This  was  the  view  which  we  adopted  in  our  second  edition,  and 
Hartmann's  observations  may  be  gathered  from  the  following 
account: — 


312  PLASMODROMATA  AND  SARCODINA 

Morphology.- — It  is  usually  about  25  to  40  ju  in  diameter,  but  may 
be  as  small  as  20  /li,  10  ju,  or  even  5  ju.  When  at  rest  it  is  spherical, 
but  varies  in  shape  when  in  motion.  The  ectoplasm  is  usually 
well  defined,  and  in  pseudopodia  is  seen  to  consist  of  hyaline  highly 
refractive  protoplasm,  but  this  differentiation  is  sometimes  difficult 
to  define.  The  endoplasm  is  greyish  in  colour,  and  usually  contains 
red  blood-corpuscles  as  well  as  other  matters.  The  vesicular 
nucleus  is  clearly  visible,  and  has  a  well-defined  membrane  on  which 
chromatic  granules  are  distributed.  In  the  centre  there  is  a  karyo- 
some  surrounded  by  a  clear  area,  and  containing  a  centrosome. 
A  cycle  of  changes  is  constantly  proceeding  in  the  nucleus:  first 
chromidia  break  away  from  the  karyosome  and  pass  outwards  into 
the  nucleus,  and  this  proceeds  until  little  but  the  centrosome  is 
left,  when  it  ceases,  and  chromatin  begins  to  accumulate  again 
around  the  centrosome,  until  the  karyosome  is  re-formed,  when  the 
cycle  begins  again. 

L  ife  History.- — Asexual  reproduction  is  by  promitosis.  Sporogony 
is  rare,  and  when  it  occurs  tends  to  cyst  formation,  before  which 
the  amoebae  become  small,  and  their  chromidia  form  three  to  six 
masses.  The  cyst  sometimes  contains  a  large  vacuole.  Nuclear 
division  takes  place  until  four  nuclei  are  formed.  The  further 
life-history  is  unknown. 

In  1912  Calkins  gave  his  account  of  the  Genera  and  Species  of 
Amoebae,  Hassall  his  valuable  bibliography,  Crawley  his  list  of 
Parasitic  Amoebae,  Craig  his  relationship  of  Parasitic  Amoebae  to 
Disease,  Darling  his  identification  of  Pathogenic  Panama  Amoebae, 
and  von  Prowazek  the  structure  of  the  nucleus  of  parasitic  Amoebae, 
while  James  contributed  two  papers  on  the  clinical  identification 
of  the  Entamoebas  and  on  infection  with  E.  tetragena.  In  the  latter 
of  these  papers  it  is  stated  that  the  histolytica  phase  is  found  in 
infections  with  acute  symptoms,  while  the  tetragena  phase  is  found 
in  more  chronic  infections.  Craig  formulates  a  life-history  for 
L.  histolytica  as  follows: — ■ 

1.  Vegetative   Stage :    Histolytica-phase   in    acute   dysentery; 

tetragena-phase  in  chronic  dysentery. 

2.  Precystic  Stage  :  Amoebae  decrease  in  size  (minuta-phase), 

and  the  nucleus  is  intermediate  in  type  between  the  other 
two  phases. 

3.  Cystic  Stage  :  Cysts  7-20  microns  quadrinucleate. 

In  1913  Whitmore  gives  an  account  of  his  own  and  the  work  of 
\  tereck,  Hartmann,  and  Huber.  In  1914  there  appeared  a  most 
important  paper  by  James  detailing  historical  matter,  morphology, 
and  classification  and  technique,  with  regard  to  the  Entamcebae  of 
man.  In  1917  Craig  gave  an  excellent  summary  of  the  Amoebae 
parasitic  in  man. 

\\  e  thus  see  that  although  L.  coli  and  L.  histolytica  are  distinct, 
it  is  difficult  to  effect  a  diagnosis  in  the  trophozoite  phase,  and  that 
histolytica,  tetragena,  and  perhaps  minuta,  are  phases  of  one  and 
tin-  same  organism. 


LOESCHIA  313 

In  the  same  year  there  appeared  papers  by  Wenyon  and  O'Connor 
on  the  '  Human  Intestinal  Protozoa  in  the  Near  East,'  detailing 
the  characters  of  E.  histolytica,  and  by  Chalmers  and  O'Farrall 
with  regard  to  its  presence  in  the  urinary  tract,  which  brings  in 
the  synonym  Amceba  urogenitalis  Baelz,  1883. 

Wenyon  and  O'Connor  consider  that  no  infection  can  be  ascribed 
to  L.  histolytica  unless  some  amoebae  with  included  red  corpuscles 
are  present  or  unless  typical  cysts  are  present  in  the  stool.  An 
amceba  with  retractile  ectoplasm,  and  indistinct  nucleus  and  active 
movement,  is  most  likely  to  be  L.  histolytica,  but  these  characters 
alone  will  not  distinguish  the  organism. 

For  the  diagnosis  of  Amoebae  they  lay  down  the  following  rules:— 

1.  Amoebae  containing  red  blood-corpuscles  are  L.  histolytica, 

whether  the  stool  is  dysenteric  or  not;  and,  further,  they 
indicate  an  active  dysentery.  These  cases  urgently 
require  emetine  treatment. 

2.  Amoebae,    none    of    which    contain    red    blood-corpuscles, 

occurring  in  a  dysenteric  motion  are  indicative  of  L.  coli 
or  of  L.  histolytica  in  a  carrier,  while  the  cause  of  the 
dysentery  is  not  an  amceba;  and  these  cases  should  be 
watched  for  a  few  days,  without  treatment,  with  a  view 
to  finding  the  cysts. 

3.  Amoebae,    none    of    which    contain    red    blood-corpuscles, 

occurring  in  non-dysenteric  motions  may  be  L.  coli  or 
L.  histolytica,  and  diagnosis  has  to  be  made  by  finding 
the  quadrinucleate  cysts,  perhaps,  after  several  days' 
observation. 

In  1918  Dobell  showed,  by  experimental  infection  of  tadpoles, 
that  L.  histolytica  and  L.  ranarum  were  distinct  species,  and  with 
Jepps  drew  attention  to  the  existence  of  diverse  races  of  L.  histo- 
lytica, which  could  be  distinguished  by  the  dimensions  of  the 
cysts. 

The  above  does  not  complete  the  history,  but  is  as  full  as  space 
permits,  and  we  will  now  turn  to  the  morphology. 

Morphology — Vegetative  Stage  :  Young  Trophozoite  Phase. — This 
phase  may  also  be  termed  the  histolytica  phase,  as  defined  above. 

It  occurs  when  active  dysenteric  processes  are  proceeding  in  the 
bowel,  and  is  represented  as  a  rule  in  the  fresh  condition  by  large 
amoebae  measuring  from  30-go  microns  in  diameter,  but  exception- 
ally being  present  in  small  size.  As  a  rule  its  motility  is  very  marked, 
often  starting  with  such  a  rapid 'action  as  to  be  worthy  of  the  name 
explosive.  The  pseud opodia  are  broad,  and  may  be  solely  ecto- 
plastic,  or  be  composed  of  endoplasm  as  well.  The  ectoplasm  may 
be  clearly  distinguishable  from  the  endoplasm  even  when  the  amoeba 
is  at  rest,  but  often  there  is  no  such  distinction. 

The  cytoplasm  may  have  a  well-defined  light  green  colour,  or 
more  usually  this  colour  is  wanting.  It  may  contain  a  number 
of  vacuoles,  or  it  may  not.     It  often  possesses  a  number  of  ingested 


314  PLASMODROMATA  AND  SARCODINA 

red  blood  cells,  but  at  times  these  are  wanting.  It  may  be  vacuo- 
lated, or  it  may  be  granular. 

The  nucleus  in  the  fresh  specimen  is  usually  difficult  to  see.  It  is 
excentric,  poor  in  chromatin,  and  easily  altered  by  internal  pressure. 
It  possesses  a  very  delicate  membrane,  with  a  few  peripherally 
arranged  grains  of  chromatin. 

In  stained  specimens  there  is  rarely  any  differentiation  of  the 
ectoplasm  from  the  endoplasm.  The  cytoplasm  may  contain 
vacuoles,  erythrocytes,  and  perhaps  the  phagocyted  nuclei  of  other 
cells.  The  nucleus,  unless  distorted,  is  roundish,  possesses  a  delicate 
nuclear  membrane,  under  which  a  thin  band  or  a  few  grains  of 
chromatin  may  lie.     The  centre  of  the  nucleus  is  occupied  by  a 


Fig.  54. — Photomicrograph  of  the  Livixg  and  Rapidly  Moving 
Loeschia  histolytica  Schaudinn,  in  the  Young  Trophozoite  Stage  of 
Acute  Dysentery,     (x   1,500  Diameters.) 

(From  the  Journal  of  Tropical  Medicine.) 

karyosome,  which  may  contain  a  very  minute  centriole.  The  space 
between  the  karyosome  and  the  nuclear  membrane  sometimes  shows 
a  delicate,  poorly  staining  network,  at  the  nodes  of  which  lie  fine 
granules  of  chromatin.  The  cyclical  changes  described  by  Hart- 
mann  for  the  next  stage  are  not  visible. 

James  has  pointed  out  that  when  stained  by  Hastings'  and 
Giemsa's  method  the  nucleus  takes  on  a  light  blue  colour,  and  con- 
tains  a  delicate  network  of  blue  threads,  and  a  number  of  fine  red 
coloured  threads  and  bars  scattered  irregularly  over  this  network, 
composed  of  a  substance  which  he  calls  erythrochromatin,  to 
distinguish  it  from  the  true  chromatin. 

Old  Trophozoite  Phase- — This  is  the  phase  so  carefully  described 


LOESCHIA 


3*5 


by  Hartmann  under  the  heading  E.  tetragena,  and  often  called  the 
tetragena  phase.  It  resembles  the  histolytica  phase  in  many  par- 
ticulars, but  differs  therefrom  in  the  fact  that  the  nucleus  is  usually 
clearly  visible  as  a  well-rounded  globular  vesicle  plainly  set  off  from 
the  cytoplasm  by  a  stout  double  contoured  membrane  and  showing 
in  the  middle  a  small  karyosome,  surrounded  by  a  clear  structure- 
less zone,  between  which  and  the  nuclear  membrane  there  is  a  linin 
network  on  which  granules  of  chromatin  are  distributed. 


Fig.  55. — Loeschia  histolytica  Schau- 
dinn,  Young  Trophozoite  Fixed 
and  Stained,  showing  Nucleus 
and  Phagocyted  Red  Blood 
Cells,      (x    1,950  Diameters.) 


Fig.  56. — Loeschia  histolytica  Schau- 
dinn,  Old  Trophozoite  or 
Tetragena  Phase.  Stained 
Preparation,  (x  1,950  Diam- 
eters.) 


(After  James.) 

This  nucleus  undergoes  cyclical  changes,  but  in  a  given  prepara- 
tion, as  a  rule,  all  the  amoebae  show  the  same  appearance.  The 
cyclical  changes  are: — 

1.  Large  blocks  of  chromatin  under  the  nuclear  membrane,  a  very 
definite  karyosome  containing  a  centriole  (Fig.  57,  a,  and  58,  a). 

2.  Many  small  granules  of  chromatin  scattered  under  the  mem- 
brane and  at  the  margin  of  the  karyosome  (Fig.  57,  b). 


^.^       c 


Fig.  57. — Nucleus   of  Loeschia  histolytica  Schaudinn,  Old  Trophozoite 

Phase.     Stained  Preparations,  (x    1,950  Diameters.) 

(After   James.) 

Note  the  cyclical  changes  described  in  the  text. 

3.  Chromatin  more  concentrated  under  the  nuclear  membrane 
and  at  the  karyosome  margin,  while  a  clear  zone  is  appearing  around 
the  centriole  (Fig.  57,  c). 

4.  Chromatin  under  the  membrane  and  at  the  karyosome  margin 
(Fig.  57,  d). 


316  PLASMODROMATA  AND  SARCODINA 

5.  Chromatin  has  left  the  karyosome  margin  and  passed  over  the 
limn  network  towards  the  nuclear  membrane  (Fig.  57,  e). 

6.  The  centriole  swells  and  re-forms  the  karyosome,  and  so  the 
cycle  begins  again  or  the  amoeba  divides  (Fig.  58,  b). 

Life-History.—- L .  histolytica  may  reproduce  by  binary  fission 
during  the  vegetative  stage,  or  it  may  encyst. 

The  first  is  the  method  by  which  it  increases  its  numbers  in  a  given 
host,  and  the  second  is  for  the  purpose  of  passing  from  one  host  to 
another. 

There  is  no  sure  evidence  of  schizogony. 

Simple  Division. — The  centriole  divides  into  two  parts,  each  of 
which  travels  to  opposite  sides  of  the  karyosome  and  are  connected 
by  a  thread,  the  centrodesmose.     The  further  stages  require  study. 

Encystment — Precystic  Phase. — All  the  amoebae  present  in  a  given 
case  reduce  in  size  (L.  viinuta),  but  their  numbers  are  augmented. 
The  amoebae  become  sluggish  and  have  a  clear  ectoplasm,  but  the 
nucleus  is  not  easy  to  see,  and  chromidia  may  or  may  not  be  present 
in  the  cytoplasm.  The  nucleus  is  spherical,  with  a  thick  regular 
membrane  and  with  chromatin  granules  near  the  periphery.  The 
karyosome  shows  no  centriole. 


Fig.  58. — Loeschia  histolytica  Schaudinn:  Old  Trophozoite  Phase  showing 
the  First  and  Last  Stages  of  the  Cyclical  Nuclear  Changes. 
(x   1,950  Diameters.)     (After  James.) 

Cystic  Phase. — Different  strains  produce  cysts  of  different  sizes — 
e.g.,  small  cysts  7-10,  medium  9-12,  large  12-18  microns  in  diameter. 
Chromidia  are  formed  in  the  cytoplasm,  and  may  be  derived  from 
the  nucleus,  and  may  function  as  food  material.  The  cytoplasm 
becomes  granular  and  the  nucleus  swollen  and  elongated.  An 
intranuclear  spindle  is  formed  between  two  centrioles  situate  at 
each  end.  The  chromatin  forms  rows  of  granules  extending  from 
pole  to  pole.  The  nucleus  divides  and  the  daughter  nuclei  entei  the 
resting  stage,  in  which  they  remain  for  a  long  time.  Each  of  these 
subsequently  again  divide,  giving  rise  to  the  typical  quadrinucleate 
cysts.  Tenfold,  Woodcock,  and  Drew  have  brought  evidence  to 
show  that,  as  a  rule,  the  amoeba  escapes  undivided  from  the  cyst. 
No  one  has  so  far  seen  any  flagellate  forms  or  any  gametes. 

Infection.— Darling  in  1913  showed  that  only  the  cysts  were  in- 
fective, and  that  they  are  ingested  with  food,  and  must  not  have 
been  passed  out  of  the  original  host  longer  than  two  or  three  days. 

Wenyon  and  O'Connor  in  1916  have  proved  that,  as  in  the  case 
of  L.  colt,  house-flies  can  ingest  the  cysts,  which  are  subsequently 
passed  on  to  human  food,  and  so  the  infection  carried  from  man  to 
man. 


LOESCHIA  317 

These  researches  clearly  prove  that  the  method  of  infection  is  by 
cysts  passed  in  faecal  matter  entering  the  flies,  and  so  reaching  human 
food,  as  direct  faecal  contamination  is  not  so  likely,  though,  of  course, 
it  may  also  be  a  method  of  infection. 

Further,  these  cysts  are  spread  abroad  by  the  faecal  matter  of 
human  carriers — i.e.,  persons  who  have  recovered  from  amoebic 
dysentery,  and  even  those  who  have  never  suffered  in  this  manner. 
These  carriers  are  the  human  reservoir  of  the  parasite. 

Diagnosis. — Amoebae  present  in  human  faeces  and  containing  red 
blood-corpuscles  are,  as  a  rule,  L.  histolytica.  Amoebae  without 
red  corpuscles  require  differentiation  by  the  cysts,  which  must  be 
sought  during  several  days.  Quadrinucleate  cysts  belong  to 
L.  histolytica,  others  are  doubtful  or  definitely  negative. 

Cultivation.— Since  the  days  of  Auerbach  in  1856  attempts  have 
been  made  to  cultivate  pathogenic  amoebae  in  pure  or  contaminated 
cultures.  With  regard  to  L.  histolytica  all  such  attempts  were 
failures  until  Cutler  apparently  succeeded,  in  1918,  on  Dean  and 
Monat's  egg  medium,  to  which  a  few  drops  of  blood  had  been  added, 
and  on  blood-clot  medium.  The  media  were  inoculated  with  blood 
and  mucus  from  motions  passed  not  longer  than  three  hours,  and 
were  incubated  at  28°-30°  C.  In  culture  the  amoebae  varied  from 
8-30  microns  in  size,  with  homogeneous  but  often  vacuolated  cyto- 
plasm containing  ingested  red  blood  cells  and  moving  typically  like 
L.  histolytica.  Uninucleate  and  binucleate  forms  were  seen.  Cysts 
were  obtained  by  ceasing  to  subculture  for  two  to  three  days  and 
then  placing  the  culture  for  two  hours  in  an  ice-chest. 

Cysts  from  the  culture  produced  typical  dysenteric  lesions  in 
cats  by  feeding  and  by  inoculation  high  into  the  rectum  by  means  of 
a  catheter. 

Strains. —  Vide  historical  section  (p.  313). 

Pathogenicity. — L.  histolytica  is  the  cause  of  amoebiasis  in  man 
and  animals,  causing  amoebic  dysentery  and  amoebic  abscesses  in 
the  liver  and  other  parts  of  the  body. 

Loeschia  gingivalis  Gros,  1849. 

Synonyms. — -Amoeba  gingivalis  Gros,  1849;  A.  buccalis  Sternberg, 
1862;  A.  dentalis  Grassi,  1879;  A.  dentalis  Braun,  1883;  Entamoeba 
buccalis  Prowazek,  1904;  A.  maxillaris  Kartulis,  1906. 

Definition. — -Loeschia  with  cysts  containing  only  one  nucleus, 
cytoplasm  often  containing  red  blood-corpuscles,  ectoplasm  only 
visible  during  motion  as  a  clear  highly  refractive  layer.  Nucleus 
as  a  rule  not  visible.     Reproduction  only  by  simple  fission. 

History. — This  amoeba,  which  occurs  in  the  mouth  in  healthy 
and  diseased  conditions,  was  first  described  by  Gros  in  1849,  and 
was  afterwards  studied  by  Sternberg,  Grassi,  Prowazek,  and  men- 
tioned by  Braun,  and  is  probably  the  same  as  Kartulis'  organism. 

Morphology. — Its  size  varies  from  7-35  microns,  tin-  average 
being  12-20  microns. 

The  ectoplasm  is  only  well  defined  during  movement,  which  is 


3i8 


PLASMODROMATA  AND  SARCODINA 


quite  active,  and  takes  place  by  short  blunt  or  long  tapering  pseudo- 
podia.  The  endoplasm  is  granular,  containing  non-contractile 
food  vacuoles  and  often  red  blood-corpuscles.  The  nucleus  as  a 
rule  is  not  distinct. 

Life-History.- — Reproduction  apparently  only  takes  place  by 
simple  fission,  while  cyst  formation,  which  has  been  observed,  is 
believed  to  be  purely  protective,  as  they  contain  only  one  nucleus. 
The  cysts  may  measure  from  8-10  or  more  microns. 

Animal  Experiments. — All  attempts  to  produce  dysentery  in 
animals  by  means  of  this  amoeba  have  so  far  been  failures. 

Pathogenicity. — It  has  been  accused,  without  sufficient  proof,  of 
being  the  cause  of  pyorrhoea  alveolaris. 

Doubtful  Species. 

The  species  to  be  now  described  are  not  considered  as  '  good  '  by 
many  authorities,  but  we  give  a  brief  account  of  them  for  the  sake 
of  completeness. 

Loeschia  tropicalis  Lesage,  1908. 

Lesage,  from  his  studies  of  tropical  dysentery,  has  come  to  the  conclusion 
that,  just  as  there  is  a  Loeschia  coli  Loesch  parasitic,  but  non-pathogenic,  in 
the  intestine  of  man  in  warm  and  temperate  countries,  so  there  is  another 
amoeba  parasitic,  but  non-pathogenic,  in  the  intestine  of  man  in  the  tropics. 
This  parasite  he  names  L.  tropicalis. 


Fig.  59. — Loeschia  tropicalis  Lesage,  1908  :  Diagram  of  the  Life-Cycles 

CONSTRUCTED   FROM    LESAGE'S    DRAWINGS. 

(Constructed  from  Lesage's  drawings  in  the  Bulletin  de  la  Society  de  Pathology 
Exotique,  showing  binary  fission  and  spore  formation.) 


It  resembles  L.  coli  by  having  a  nucleus  which  contains  much  chromatin 
and  by  becoming  encysted,  but  it  differs  from  _the  same  in  having  a  clearly 
visible  ectoplasm,  by  the  small  size  of  its  cysts,  and  by  the  fact  that  the  nucleus 
of  the  cysts  breaks  up  into  a  number  of  nuclei,  which  are  from  three  to  several 
(he  draws  thirteen  in  one  cyst) .  This  entamoeba  can  be  cultivated  along  with 
bacteria,  but  is  non-pathogenic  to  animals. 

Lesage  considers  this  to  be  the  same  amoeba  which  was  studied  and  culti- 
vated by  Musgrave  and  Clegg,  and  thinks  that  the  production  of  dysenteric 
symptoms  in  their  experiments  was  due  to  contamination  with  the  minute 
of  Loeschia  histolytica.  Walker  in  1908  describes  as  a  new  species, 
E.  hominis,  whii  b  may  perhaps  be  the  same  asL.  tropicalis. 

Pathogenicity.      1 1  is  a  harmless  1  ommensa]  in  the  alimentary  canal  of  man. 

Culture. — It  can  be  cultivated  in  symbiosis  with  bacteria. 


DOUBTFUL  SPECIES  319 

Loeschia  undulans  Castellani,  1905. 

Synonym. — Entamoeba  undulans  Castellani,  1905. 

This  amoeba  was  found  in  faeces  from  persons  suffering  from  diarrhoea  in 
Ceylon,  together  with  other  intestinal  protozoa — e.g.,  Cercomonata  and  Tricho 
monata.     A  somewhat  similar  amoeba  has  been  found  by  Gauducheau  in  dogs. 

It  varies  in  size,  being  from  12  to  30  /;  in  diameter,  but  there  may  be  much 
smaller  individuals.     It  has  no  fiagella,  but  possesses  an  undulating  membrane, 


(? 


Q 


■;■■ 


Fig.  60.— Loeschia  undulans  Castellani,  1905. 

and  long  straight  pseudopodia,  which  are  rapidly  emitted  and  retracted,  only 
one  pseudopodium  being  protruded  at  a  time.  There  is  no  marked  differenti- 
ation into  ectoplasm  and  endoplasm,  and  a  non-contractile  vacuole  is  usually 
to  be  seen.  The  cytoplasm,  which  is  finely  granular,  often  contains  bacteria. 
Castellani  is  inclined  to  consider  this  parasite  as  a  developmental  stage  of 
Cercomonas  hominis,  as  was  his  original  opinion.  Perroncito  long  ago  de- 
scribed an  amoeboid  stage  of  Cercomonas  hominis.  Wenyon  considers  it  to  be 
a  stage  of  a  Cercomonas. 

Loeschia  phagocytoides  Gauducheau,  1908. 

Synonym. — Entamoeba  phagocytoides  Gauducheau,  1908. 

Loeschia  phagocytoides  was  discovered  by  Gauducheau  in  Indo-China  in  a 
case  of  dysentery.  It  is  very  small — only  2  to  1 5  /<  in  diameter — very  actively 
motile,  and  possessing  a  well-developed  ectoplasm.  It  can  be  easily  cultivated 
or  ordinary  agar-agar  inoculated  with  Bacillus  typhosus  or  other  bacteria, 
which  it  readily  engulfs  and  digests.  Some  individuals  show  in  their  cytoplasm 
peculiar  spirochaete-like  bodies. 

Loeschia  minuta  Elmassian,    1909. 

Synonym. — Entamoeba  minuta  Elmassian,  1909. 

This  amoeba,  found  by  Elmassian  in  a  case  of  chronic  dysentery  in  South 
America,  resembles  L.  tetragena,  but  is  much  smaller,  rarely  exceeding  14  /« 
in  diameter.  There  is  no  differentiation  between  the  ecto-  and  endo-plasm. 
The  nucleus  is  invisible  in  fresh  preparations,  and  when  stained  is  rich  in 
chromatin.     Encysted  forms  contain  four  nuclei. 

Loeschia  nipponica  Koidzumi,  1909. 

Synonym. — Entamoeba  nipponica  Koidzumi,  1909. 

This  entamoeba  was  found  by  Koidzumi  in  the  motions  of  cases  of  dysentery 
and  in  healthy  people  in  Japan.  In  the  former  case  it  is  associated  with 
L.  histolytica,  which  it  resembles  in  size  (1 5  to  30  /<)  and  in  the  marked  difference 
between  the  ecto-  and  endo-plasm.  The  pseudopodia  are  never  spinose;  the 
endoplasm  is  vacuolated,  and  more  granular  than  in  L.  histolytica.  The 
nucleus  is  well  defined  (5  to  7  ju),  and  rich  in  chromatin.  This  amceba  repro- 
duces by  fission,  schizogony,  and  sporogony. 

Loeschia  hartmanni  Prowazek,  1912. 
Found  in  man  in  Savaii.     It  is  4  to  13  /t  in  diameter;  nucleus  vesicular, 
2  t°  3'3  t* '.  cysts  small,  quadrinucleate,  characterized  by  a  thin,  bacteria-like 
arrangement  of  chromidia. 


320  PLASMODROMATA  AND  SARCODINA 

Loeschia  williamsi  Prowazek,  191 1. 
This  Loeschia  is  considered  to  be  identical  withL.  coli  Loesch. 

Loeschia  brasiliensis  H.  Baurepaire  Aragao,  1912. 
Resembles  L.  coli.     Cysts  7  to  15  /<  in  diameter,  with  eight  nuclei  and  a 
double  contour  membrane.     The  cysts  are  characterized  by  the  presence  of 
a  certain  amount  of  siderophile  siibstance  which  divides  the  cysts  into  two 
portions  of  nearly  equal  size. 

Loeschia  butschlii  Prowazek,  1912. 

Synonym. — Entamoeba  butschlii  Prowazek  1912. 

Found  in  a  boy  in  the  Caroline  Islands.  It  varies  in  size  from  10  to  24  //  ; 
coarse  alveolar  cytoplasm;  nucleus  vesicular;  round  karyosome  and  centriole; 
cysts  roundish,  said  to  differ  from  those  of  L.  coli. 

Loeschia  mortinatalium  Smith  and  Weidman,  1910. 

Synonym. — -Endamceba  mortinatalium  Smith  and  Weidman,  1910, 
and  perhaps  Amoeba  pulmonalis  Artault,  1898. 

Definition. — Loeschia  of  large  size,  22-38  x  20-25  microns,  with 
nucleus  10  microns  in  diameter,  with  well-defined  membrane,  large 
karyosome,  and  occasionally  a  centriole. 

Remarks. — Somewhere  about  1890  Ribber+  found  amcebae  in  the 
kidneys  and  parotid  glands  of  infants.  In  1898  Artault  observed 
amcebae  with  a  nucleus  and  a  vacuole  in  a  lung  cavity.  Brumpt 
has  seen  similar  amoebae  and  R.  Blanchard  has  found  some  in  the 
lungs  of  sheep,  which  may  or  may  not  be  the  same  as  the  Entamoeba 
ovis  Swellengrebel,  1914,  found  in  the  gut  of  sheep.  This  latter 
measures  12-14  x  11-12  microns.  Its  cysts  are  8  microns  in 
diameter,  uninucleate,  with  a  glycogen  vacuole.  In  1904  Jesionek 
and  Kiolemengolou  found  amoebae  in  the  kidnej's,  liver,  and  lungs 
of  an  eight  months  syphilitic  foetus.  In  1910  Smith  and  Weidman 
found  an  amoeba  in  the  kidneys,  liver,  and  lungs  of  stillborn  full- 
term  foetus,  and  in  1914  they  found  their  L.  mortinatalium  again  in 
the  lungs  of  a  two-months-old  child  which  was  syphilitic  and  died  of 
pneumonia.  Atkey  and  Chalmers  have  observed  amoebae  in  the 
sputum  and  in  the  lungs  of  a  case  of  pneumonia  in  the  Anglo- 
Egyptian  Sudan,  unassociated  with  any  known  history  of  dysentery, 
which  they  thought  were  possibly  L.  histolytica.  Time  must  show 
what  these  amcebae  really  are. 

Loeschia  minutissima  Brug,  1917. 

Synonym. — E.  minutissima  Brug,  1917. 

A  very  small  amoeba,  4-11x4-8  microns.  Usually  6-5-7x5-6 
microns. 

Loeschia  tenuis  Kuenen  and  Swellengrebel,  1917. 

This  amoeba,  which  was  described  as  Entamoeba  tenuis,  measures 
6-9  microns  in  diameter,  with  cysts  6-8  microns,  and  one  to  four 
nucleated,  is  very  like  E.  nana  of  Wenyon  and  O'Connor  and  the 
/:'.  minuta  of  Woodcock  and  Penfold,  which  latter,  however,  is  said 
to  he  the  same  as  E.  histolytica. 


VAHLKAMFIA 


321 


Loeschia  in  Animals.— Though  somewhat  beyond  the  bounds  of 
the  present  work,  we  may  mention  that  amoeba;,  believed  to  belong 
to  the  genus  Loeschia,  but  re- 


ii 


genus 
quiring  restudy  in  the  light  of 
recent  researches,  occur  in 
several  vertebrates — e.g.,  L .  nut- 
talli  Castellani,  1908,  found 
in  liver  abscesses  and  dysentery 
in  monkeys  in  Ceylon;  L.  cobayce 
in  guinea-pigs,  L.  enterica  in 
cats,  etc.,  L.  muris  Grassi  in 
mice,  considered  by  Wenyon 
to  be  L.  colt,  L.  fecalis  in 
several  animals,  L.  intestinalis 

in  horses,  etc.,  L.  galloparvce  Fig.  61. — Loeschia  nuttalli  Castellani, 
in  turkeys,  L.  ranarum  Grassi  I9°8  containing  Red  Blood  Cells. 
in  frogs,  and  many  more. 

Genus  Vahlkamfia  Chatton  and  Lalung-Bonnaire,  1912. 

Definition. — Gymnamcebida,  with  vesicular  nucleus  (protokaryon) 
having  one  large  karyosome  with  or  without  a  centrosome,  with  little 
peripheral  chromatin,  with  division  by  promitosis.  Cysts  typically 
uninuclear. 

Remarks. — Practically  all  cultivable  amoeba?  isolated  from  human 
stools  and  potable  water  by  various  observers  belong  to  this  genus. 
Cropper  has  grown  a  peculiar  amceba  belonging  to  this  genus  in 
citrate  solution. 

Type. —  Vahlkamfia  Umax  Dujardin,  1841,  emendavit  Vahlkamf, 
1904. 

Vahlkamfia  punctata  Dangeard,  1910. 

This  amceba  was  found  in  Indo-China  in  the  motions  of  a  case  of 
diarrhoea.     The  ectoplasm  is  rarely  visible,  and  the  endoplasm  is 


X 


Fig.  62. — Amoiba  and  Cyst  found  in  Human  Faeces  and  possessing 
the  Limax  Type  of  Nucleus,  (a)  Trophozoite,  (b)  Cyst,  (x  1,950 
Diameters.) 

(After  James,  from  the  Annals  of  Tropical  Medicine  and  Parasitology.) 

very  basophile,  while  the  method  of  division  is  by  promitosis.  The 
cysts  are  8  to  12  /li  in  diameter,  with  a  thin  wall  showing  a  double 
contour  ornamented  with  punctations,  and  always  uninucleate. 

21 


322  PLASMODROMATA  AND  SARCODINA 

Vahlkamfia  lobospinosa  Craig,  1912. 

Synonym. — Amoeba  lobospinosa  Craig,  1912;  V.  withmorei 
Hartmann,  1912. 

This  amoeba  was  cultivated  from  a  dysenteric  stool  from  a  patient 
in  Manila  in  1905,  and  first  described  by  Musgrave  and  Clegg.  In 
IQ12  it  was  studied  by  Craig  and  called  Amoeba  lobospinosa,  also  by 
Williams  and  Calkins,  by  James,  by  Liston,  and  by  Wells. 

James,  in  the  Canal  Zone,  obtained  this  amoeba  for  a  considerable 
period  from  the  faeces  of  a  patient  which  were  guarded  against  con- 
tamination, and  hence  it  must  be  admitted  that  it  can  live  for  a 
time  in  the  intestine  of  man,  but  it  is  probably  non-pathogenic. 

On  the  other  hand,  in  all  the  other  reported  cases  it  has  occurred 
as  an  aerial  contamination  of  the  faeces  or  pus  in  which  it  has  been 
found.     It  was  first  cultivated  by  Musgrave  and  Clegg. 

Other  Species. 
In  1917  Kuenen  and  Swellengrebel  divided  the  species  of  Limax 
amoeba  into  three  types,  the  Limax,  the  Endolimax,  and  the  Pseudo- 
Umax  ;  but  taking  V .Umax  Dujardin,  1841,  emendavit  Vahlkamf, 
1904,  as  the  type  species,  and  allowing  that  V.  lacustris  Naegler, 
1909,  is  the  same  species,  the  following  are  known: 
A    Small  forms,  3-15  microns  :— 

Cysts  1-5   microns  in  diameter- — V.  limax  Dujardin, 

1841,  emendavit  Vahlkamf,  1904. 
Cysts  over  7  microns  in  diameter. 

(a)  Karyosome  surrounded  by  a  peripheral  row  of 

chromatin  granules — V.  lacertcc  Hartmann,  1907. 

(b)  Karyosome  not  so  surrounded — V .  froschi  Hart- 

mann and  Prowazek,  1907. 

B.  Medium-sized  forms,  15-30  microns  :— 

(a)  Trophozoite  binucleate — V.  diploidea  Hartmann 

and  Naegler,  1908. 
(&)  Trophozoite  uninucleate  : — • 

1.  Contractile    vacuole    present- — V.  tachypodia 

Glaeser,  1912. 

2.  Contractile     vacuole     absent — V.     polypodia 

Schutze,  1875. 

C.  Large  forms  reaching  to  50  microns  : — 

(a)  Trophozoite    binucleate—  V.    binucleata    Gruber, 

1884. 
(6)  Trophozoite  uninucleate  : — 

1.  Ectoplasm   like    a    lamella—  V.    lamellipoda 

Glaeser,  1912. 

2.  Ectoplasm  not  so  distinct  :■ — ■ 

(1)  Nuclear  division  promitotic — V.  albida 

Naegler,  1909. 

(2)  Nuclear  division  mesomitotic — V.  guttula 

Dujardin,  1912. 


VAHLKAMFIA   NANA  323 

V.  binucleata  may  be  a  stage  in  the  development  of  Pelomyxa, 
which  appears  to  be  impossible  to  Jepps  and  Dobell,  while  Alexeieif 
places  it  in  a  genus  Hartmannella  with  a  type  H.  hyalima  Dangeard, 
which  Jepps  and  Dobell  say  is  quite  different.  It  probably  requires 
a  new  genus  creating  for  itself.  V .  diploidea  was  obtained  by 
Hartmann  and  Naegler  in  cultures  from  lizard  faeces,  and  has  been 
found  by  Jepps  and  Dobell  in  human  faeces  which  had  been  kept  for 
some  time.  Alexeieff  proposes  to  place  it  in  Sappinia  Dangeard,  1896. 
V.  pcedophthora  Caullery,  1910,  is  like  V.  Umax,  but  is  parasitic  in  the 
eggs  and  embryos  of  a  crab,  belonging  to  the  genus  Peltogaster. 

Vahlkamfia  nana  Wenyon  and  O'Connor,  1917. 

Synonym. — Entamoeba  nana  Wenyon  and  O'Connor,  1917; 
Vahlkamfia  nana  Brug,  1917. 

Definition. — -Vahlkamfia  of  small  size  (5-10  microns),  moving 
slowly,  with  blunt  ectoplasmic  pseudopodia,  nucleus  with  membrane 
and  large  central  karyosome,  cysts  7-8  x  8-10  (when  elongated) 
microns  with^one  to  four  nuclei,  without  chromidial  bodies. 


a  b  c 

Fig.  63. — Vahlkamfia  nana  (Wenyon  and  O'Connor,  1916). 
(a)  Trophozoite,  fresh  conditions ;    (b)  trophozoite  stained  preparation ; 

(c)  cyst  with  two  nuclei. 

(After  Wenyon  and  O'Connor,  from  the  publications  of  the  Wellcome 

Bureau  of  Scientific  Research.) 

Remarks. — -This  amoeba  was  found  by  Wenyon  and  O'Connor  in 
Egypt,  and  we  have  seen  it  in  the  Anglo-Egyptian  Sudan  and 
Southern  Italy.  It  has  been  confused  with  L.  colt,  L.  histolytica, 
and  V.  Umax.     V.  nana  has  not  been  cultivated. 

Time  will  be  required  to  show  definitely  its  generic  position. 
Provisionally  we  have  placed  it  under  Vahlkamfia,  though  its  cyst 
is  binucleate. 

Genus  Dientamoeba  Jepps  and  Dobell,  1918. 

Definition. — Gymnamcebida  of  small  size,  without  a  known  flagel- 
late stage,  and  typically  binucleate,  with  both  nuclei  of  the  same 
size  and  structure. 

Type  Species.— Dientanuvba  fragilis  Jepps  and  Dobeli,  1918, 
found  in  man.     It  is  the  only  known  species  at  present. 

Dientamoeba  fragilis  Jepps  and  Dobell,  1918. 
Definition. — Dientamoeba  with  the  generic  characters. 
Historical. — -This  amoeba  was  first  detected  by  Jepps  and  Dobell 
in  1917  in  a  native  of  the  British  Isles  who  had  never  been  abroad, 


324  PLASMODROMATA  AND  SARCODINA 

but  was  suffering  from  slight  diarrhoea,  attributed  to  a  chill.  It  was 
found  in  British  soldiers  who  had  been  to  Salonika,  and  in  natives 
of  New  Zealand  serving  as  soldiers.  In  all  it  has  been  seen  in  seven 
cases. 

Morphology.- — It  is  a  very  small  active  organism,  measuring  when 
rounded  some  3-5-8-10-12  microns  in  diameter,  and  moving  about 
by  means  of  extremely  thin,  hyaline,  leaf-like  pseudopodia  composed 
of  sharply  defined  ectoplasm.  The  rest  of  the  body  is  often  rounded, 
and  consists  of  granular  endoplasm,  and  is  situate  posterior  to  the 
pseudopodia,  thus  giving  a  snail-like  appearance  during  active 
movement. 

The  cytoplasm  is  alveolar  and  contains  bacilli  and  cocci.  There 
is  no  contractile  vacuole,  but  there  are  diffuse  brown-stained 
patches  indicative  of  glycogen  in  iodine- stained  preparations. 
The  amoeba  is  binucleate  in  about  80  per  cent,  of  the  forms  ex- 
amined, and  these  nuclei  are  usually  invisible  in  the  living  organism. 
In  stained  preparations  they  are  2  microns  in  diameter,  and  ec.ch 
contains  a  large  central  karyosome  surrounded  by  a  clear  zone,  which 
is  traversed  by  a  few  very  fine  radiating  linin  threads,  and  which 
separates  the  kaiyosome  from  the  extremely  delicate  nuclear  mem- 
brane, on  which  there  is  no  chromatin.  There  is  sometimes  a 
separate  granule  to  be  seen  lying  in  the  centre  of  the  karyosome, 
which  is  the  centriole  of  many  authors. 

Life-History. — No  signs  of  division  or  cyst  formation  have  been 
observed. 

Habitat. — The  intestine  of  man,  probably  in  the  colon. 

Food. — Small  bacteria  and  yeasts  living  in  the  intestinal  contents. 

Pathogenicity. — It  is  believed  to  be  non-pathogenic. 

Cultivation.— So  far  all  attempts  at  cultivation  have  failed. 

Binucleate  Amoebae. — -We  have  already  noted  under  the  genus 
Vahlkamfia  two  binucleate  amoebae  in  addition  to  V.  nana — viz., 
V .  diploidea  Hartmann  and  Naegler,  1908,  with  occasional  uni- 
nucleate forms,  and  V.  binucleata  Gruber,  1884,  and  have  shown 
that  they  probably  are  not  Vahlkamfia  and  equally  they  are  not 
Dientamccba.  Another  binucleate  form  ma}-  be  Amoeba  mira  Glaeser, 
1912,  about  which  there  appears  to  be  much  doubt  as  to  whether 
the  name  was  given  to  a  binucleate  or  uninucleate  form.  Schau- 
dinn' sParanurba  is  a  marine  binucleate  amoeba,  and  forms  a  genus 
in  which  Janiclei  in  1912  placed  some  of  Grassi's  parasitic  amoebae 
found  in  Sagitta.  In  these  amoebae  the  two  nuclei  are  dissimilar, 
one  being  a  nucleus  and  the  other  a  Nebenk*  erper.  Craigia  (vide 
infra)  may  also  possess  two  dissimilar  bodies,  one  a  nucleus  and 
the  other  like  a  Nebenkoerper. 

Genus  Craigia  Calkins,  191 2. 

Definition. — Gymnamcebida,  free  swimming  or  parasitic,  with  a  uniflagellate 
swarm  stage,  and  with  or  without  an  extranuclear  Nebenkoerper-like  body 
in  the  endoplasm.     Ectoplasm  seen  on  movement;  size  10-25  microns. 

History. — In  1896  Schaudinn  described  the  life-history  of  Paramccba  eilhardi 
Schaudinn,  1896,  which  possessed  a  cytoplastic  extranuclear  body,  which  he 


CRAIGIA  325 

called  a  '  Nebenkoerper.'  Reproduction  was  by  simple  fission  and  by  cyst 
formation,  in  which  the  parasite  broke  up  into  a  number  of  spores,  each  of 
which  contained  a  piece  of  the  nucleus  and  a  piece  of  the  Nebenkoerper.  Each 
of  these  spores  develops  two  flagella,  and  breaking  out  of  the  cyst  forms  the 
swarm  stage.  Finally  the  flagella  are  lost,  after  longitudinal  division,  and  the 
spores  become  small  amoebae. 

In  1906  Craig  found  a  parasite  resembling  that  described  by  Schaudinn 
in  the  faeces  of  patients  suffering  from  chronic  dvsentery  in  the  Philippine 
Islands.  He  considered  that  they  were  the  pathogenic  agent  of  the  symptoms 
from  which  the  patients  sintered,  and  because  of  their  similarity  to  Schaudinn  s 
organism  called  them  Paramceba  hominis  Craig,  1906,  and  as  such  we  described 
them  in  the  first  two  editions  of  this  work. 

In  1912  Calkins  considered  that  Craig's  parasite  could  not  be  classified  111 
the  genus  Paramceba,  because  its  swarm  spores  have  only  one  and  not  two 
flagella,  while  its  extranuclear  body  is  apparently  different  from  that  in 
Par?mreba.  He  therefore  gave  it  the  name  Craigia  hominis  (Craig,  1906), 
which  Jepps  and  Dobell  consider  a  non-existent  organism  and  the  genus  a 
nomen  nudum. 

In  1915  Barlow  discovered  a  new  species,  which  he  called  Craigia  migrans 
in  Honduras. 

Craig  thinks  that  probably  infections  with  this  parasite  are  widespread, 
and  that  they  may  be  often  confounded  with  Cercomonads,  etc. 

Species. — There  are  four  known  species — viz.,  two  parasitic  in  marine  worms 
and  two  parasitic  in  man.     The  latter  are  distinguished  as  follows : — 

A.  Small  accessory  extranuclear  body  present  in  larger  forms.     Flagellate 

forms  multiply  by  longitudinal  division — Hominis. 

B.  Small  accessory  extranuclear  body  absent.     Flagellate  forms  do  not 

divide — Migrans. 

Craigia  hominis  Craig,  1906. 

Synonym. — Paramceba  hominis  Craig,  1906. 

Definition. — Craigia  in  which  the  accessory  nuclear  body  is  present  in  the 
larger  forms,  and  the  swarm  spores  divide  longitudinally,  the  accessory  body 
ami  the  motile  organ  participating  in  this  division. 

History.— It  was  discovered  in  1906  by  Craig,  in  the  Philippine  Islands,  in 
cases  of  chronic  diarrhoea,  and  in  191 5  by  Barlow,  in  Honduras,  where  it  not 
only  causes  a  form  of  chronic  diarrhoea,  but  also  severe  ulcerative  conditions 
of  the  intestine,  resembling  those  of  amoebic  dysentery.  Barlow  fully  con- 
firmed Craig's  observations. 

Morphology. — In  the  amoeba  stage  it  measures  from  15-25  microns,  ami 
possesses  an  ectoplasm  which  is  clearly  visible  during  motion,  but  not  while 
at  rest.  The  endoplasm  is  granular,  and  contains  a  nucleus  which  is  distinct 
and  composed  almost  entirely  of  chromatin.  There  is  also  an  extranuclear 
body  which  is  of  an  accessory  nature. 

Life-History.— The  amoeba  can  reproduce  by  binary  division  for  some  time, 
at  the  end  of  which  it  encysts,  surrounding  itself  with  a  double  contoured 
envelope,  and  divides  into  a  number  of  small,  spherical  bodies,  each  of  which 
contains  a  piece  of  the  nucleus  and  a  portion  of  the  accessory  body.  I  he  cyst 
now  ruptures  and  the  spores  escape  as  uniflagellate  swarm  spores,  some  3-20 
microns  in  length.  This  is  the  flagellate  stage.  These  little  pear-shaped 
flagellates  divide  by  longitudinal  fission,  in  which  the  accessory  body  and  the 
tiagellum  take  part.  Later  the  flagellates  cease  to  move,  lose  their  flagella, 
and  become  amoebae,  thus  completing  the  cycle  of  the  life-history. 

Cultivation. — We  are  not  aware  of  any  attempts  at  artificial  cultivation. 

Pathogenicity. — It  causes  chronic  diarrhoea  and  dysentery  in  man. 

Craigia  migrans  Barlow,  1915. 
Definition. — Craigia  in  which  the  accessory  nuclear  body  is  absent,  ami  in 
which  the  swarm  spores  do  not  divide  longitudinally  before  becoming  amoebae. 
History. — It  was  discovered  by  Barlow  in  fifty-one  infections  in  Honduras, 


326 


PLASMODROMATA  AND  SARCODINA 


where  it  caused  a  severe  dysenteric  condition  in  the  lower  bowel  and  sometimes 
liver  abscess.  Barlow  notes  that  it  may  be  necessary  to  place  this  species  in 
a  genus  distinct  from  Craigia. 

Morphology. — The  amoeba  measures  some  12-30  microns,  the  average  being 
20  microns.  The  endoplasm  is  granular  and  contains  a  nucleus,  but  no 
accessory  nuclear  body. 

Life-History. — The  cysts  measure  18  microns,  and  the  flagellates,  of  which 
there  are  forty  or  more  in  a  cyst,  about  3-5  microns.  These  flagellates  do  not 
divide,  but  pass  directly  into  the  amoeba  stage. 

Pathogenicity. — It  causes  severe  dysenteric  lesions  and  liver  abscess  in  man 


Fig.  64. — Diagram  of  the  Life-Cycles  of  Craigia  hominis  Craig. 
(After  Craig,  from  the  American  Journal  of  Medical  Sciences.) 

ORDER  II.  THECAMCEBIDA. 

Synonyms. — Filosa  Leidy,  1879;  Testacea. 

Definition. — Amoebae  with  a  shell  composed  of  different  materials  cemented 
on  a  chitinous  base.  Through  the  single  opening  in  this  shell  pseudopodia, 
which  may  be  lobose  or  branched,  but  which  never  anastomose,  project. 

Family  Gromiid;e  Eimer  and  Fickert,  1899. 

Definition. — Thecamcebida  with  simple  shell,  composed  for  the  most  part 
of  chitin,  without  calcareous  deposits  and  single-chambered. 


Type  Species. 


Genus  Chlamydophrys  Ehrenberg. 
-Chlamydophrys  enchelys  Ehrenberg. 


Chlamydophrys  enchelys  Ehrenberg. 

Synonym. — Chlamydophrys  stercovea  Cienkowsky,  1876;  Leydenia  gemmipara 
Schaudinn,  1896. 

This  rhizopod  (Fig.  66),  winch  is  believed  to  be  parasitic  in  man  in  one  stage 
of  its  life-history,  can  be  found  growing  in  human  faeces,  as  well  as  in  those 
of  the  cow,  the  rabbit,  the  mouse,  and  the  lizard.  It  is  oval  in  form,  enclosed 
by  a  shell,  except  anteriorly,  where  the  filiform  pseudopodia  project.  The 
body  of  the  parasite  is  divisible  into  an  anterior  portion,  in  which  lie  the 


THECAMCEBIDA 


327 


contractile  and  food  vacuoles,  and  a  posterior,  with  the  nucleus.  Reproduc- 
tion is  by  '  bud-fission,'  by  which  is  meant  that  half  the  protoplasm  protrudes 
at  the  mouth  and  forms  a  new  shell,  and  then  separates  from  the  other  half, 
which  retains  the  old  shell.  If 
two  forms  reproduce  by  '  bud- 
fission  '  close  together,  the 
daughter  cells  may  partially 
coalesce  (plasmogamy) ,  forming 
large  colonies  of  twenty  or  more 
individuals.  The  parasites  may 
become  encysted. 

The  sexual  process  starts  by 
the  extrusion  of  all  foreign  sub- 
stances and  the  collection  of  the 
remainder  of  the  plasma  and 
the    chromidia   into    the   shell. 


'X9 


Fig.     65. — Chlamydophrys   enchelys 

(Leydenia  Stage)  Ehrenberg. 

(After  Schaudinn.) 


Fig.  66. — Chlamydophrys    enchelys 
Ehrenberg. 

(After  Cienkowsky.) 


The  chromidial  mass  breaks  up  into  a  number  of  nuclei,  never  more  than 
eight,  around  which  the  plasma  divides,  forming  swarm  cells,  which,  developing 
two  flagella  at  one  pole  and  escaping  from  the  cell,  conjugate  with  the  swarm 
cells  of  another  individual,  and  then  become  encysted.  When  the  cyst 
ruptures  under  favourable  circumstances,  a  little  amoeba  escapes,  which 
speedily  forms  a  shell,  and  becomes  in  due  course  an  adult  Chlamydophrys. 
If,  however,  it  enters  man  it  may  remain  in  the  amoeboid  stage,  and  as  such  was 
formerly  called  Leydenia  gemmipara  by  Schaudinn.  They  were,  however, 
originally  observed  by  Lieberkuhn  in  ascitic  fluid  taken  from  persons  suffering 
from  a  malignant  growth,  but  he  did  not  determine  their  true  nature.  Leyden, 
again  observing  these  cells  in  two  similar  cases,  caused  them  to  be  examined  by 
Schaudinn.     Lauenstein  and  Behla  have  also  seen  them  in  a  case  of  cancer. 

They  are  spherical  or  irregularly  polygonal,  3  to  36  n  in  diameter,  with 
knobs  projecting  from  the  surface.  They  possess  a  distinct  ectoplasm  with 
hyaline  pseudopodia  and  a  large  vascular  nucleus.  Development  takes  place 
by  binary  fission  and  gemmation  (Fig.  65). 

Classification. — We  have  retained  the  old  classification  for  the  organism, 
and  have  not  placed  it  in  the  Foraminifera,  as  is  done  by  many  authors. 


328  PLASMODROMATA  AND  SARCODINA 

REFERENCES. 

Protozoa. 

Doflein  (191 1).     Lehrbuch  der  Protozoenkunde.     3rd  Auflage.      Jena. 
Doflein  and   Koehler   (1912).     Kolle  and  Wassermann's   Handbuch  der 

Pathogenen  Mikro-Organismen.     2nd  Auflage.     Lieferung  16-19.     Jena. 
Minchin  (1912).     Study  of  the  Protozoa.     London. 
Prowazek,     v.    S.     (1911-14).       Handbuch     der     Pathogenen     Protozoen. 

Leipzig. 

Amoeba. 
Carter  (191 5).     Proceedings  of  the  Royal  Physical  Society  of  Edinburgh. 

xix.,  No.  8,  204.     Edinburgh. 

Loeschia. 

The  bibliography  of  Parasitic  Amoebae  can  be  found  in  Hassall  (1913),  Trans 
actions  of   Fifteenth  International  Congress  on  Hygiene  and  Demography, 
ii.  198-286.     Washington.     The  genera  and  species  in  Calkins  (see  below) ;  the 
list  of  parasitic  amoebae,  Crawley,  ibid.,  179-185;  the  morphology,  James  (see 
below) . 

Castellani  (1905).  Centralblatt  fur  Bakteriologie  (1908).  Journal  of  Para- 
sitology, vol.  i.,  No    2  (L.  nuttalli). 

Chalmers  and  Archibald  (1915).  Journal  of  Tropical  Medicine  and  Hygiene 
(L.  histolytica) . 

Chalmers  and  O'Farrell  (1917).  Journal  of  Tropical  Medicine  and  Hygiene 
(L.  urogenitalis) . 

Chatton  and  Lalung-Bonnaire  (1912).  Bulletin  de  la  Societe  de  Patho- 
logic Exotique  (Loeschia).     Paris. 

Craig  (191  i).  The  Parasitic  Amoebae  of  Man  (Paramceba  hominis).  (19 17). 
Journal  of  Medical  Research,  xxxv.  425-442.     Boston. 

Darling  (191 3).     Archives  of  Internal  Medicine. 

Deeks  (1914)-     Annals  of  Tropical  Medicine  and  Parasitology,  viii.  321. 

Dobell  (1918).  Parasitology,  x.  2.  (1918).  With  Jepps,  ibid.  (Races  and 
Dientamoeba). 

Elmassian  (1909).     Centralblatt  fur  Bakteriologie  (E.  minuta). 

Gauducheau  (1909).  Bulletin  de  la  Societe  de  Pathologie  Exotique  (E. 
phagocytoides) . 

Hartmann  and  Prowazek  (1907).     Archiv  fur  Protistenkunde  (E.  tetragena). 

Hartmann  (1909-12).  Archiv  fur  Protistenkunde  (several  papers  on  L. 
histolytica  and  L .  tetragena) . 

Hartmann  and  Whitmore  (1911).     Archiv  fur  Protistenkunde  (L.  coli). 

James  (1914).     Annals  of  Tropical  Medicine  and  Parasitology,  viii.  133-320. 

Koidzumi  (1909).     Centralblatt  far  Bakteriologie  (E.  nipponica). 

Lesage  (1908).  Bulletin  de  la  Societe  de  Pathologie  Exotique  (E.  tropicalis), 
vol.  i.,  No.  2.     Paris. 

Prowazek  (1912).     Archiv  fi'ir  Protistenkunde. 

Schaudinn  (191  i).  Arbeiten  (E.  coli,  E.  histolytica,  Paramceba  eilhardi, 
Leydenia  gemmipara,  and  Chlamydophrys  stercorea) .     Hamburg. 

Wenyon,  C.  M.  (1912).  Journal  of  the  London  School  of  Tropical  Medicine, 
London  (Experimental  Amoebic  Dysentery  and  Liver  Abscess  in  Cats). 

Wenyon  and  O'Connor  (1917).  Human  Intestinal  Protozoa  in  the  Near 
East.     London. 

Whitmore  (1911).     Archiv  fiir  Protistenkunde. 

Woodcock  (1918).     British  Medical  Journal,  December  28. 

Vahlkampfia. 

Calkins  (1912).  Transactions  of  the  Fifteenth  International  Congress  of 
Hygiene  and  Demography,  i.  51. 

Chatton  and  Lalung-Bonnaire  (1912).  Bulletin  de  la  Societe  de  Patho- 
logie Exotique,  xv.  135-143.     Paris. 

Craig  (1914).     Archives  for  Internal  Medicine,  xiii.  737. 


REFERENCES  329 


Dientamoeba. 

Jepps  and  Dobell  (1918).     Parasitology,  x.  3.     Cambridge. 

Craigia. 

Barlow  (1915).     American  Journal  of  Tropical  Diseases,  ii.  680. 

Calkins    (191 2).     Transactions  of  the   Fifteenth  International  Congress   of 

Hygiene,  i  51. 
Craig  (1917).     Journal  of  Medical  Research,  xxxv.  425-442.     Boston. 

Chlamydophyrs. 

Ciknkowsky  (1876).  Archiv  f.  Mikroskop.  Anatomie,  Bd.  xii.  39. 
IJobell  (1909).  Quarterly  Journal  Microscopical  Science,  iii.  255. 
Schaudinn  (1902).     Arbeit,  aus  Kaiserlich  Gesundheits,  xix.,  Bd.  iii.,  p.  560. 


CHAPTER  XVIII 
MASTIGOPHORA  AND  PROTOMONADINA 

Mastigophora — Euflagellata — Protomonadina — Monozoa — Oicomonadidae 
Bodonidae — Cercomonadidas — Tetramitidse — References. 

MASTIGOPHORA  Diesing,  1866. 

Definition.- — Plasmodromata  with  one  or  more  permanent  flagella 
which  serve  as  organs  of  locomotion,  and  at  times  for  the  capture 
of  food. 

Morphology.- — The  Mastigophora  are  usually  microscopical  in  size, 
but  have  a  tendency  to  colony  formation. 

The  ectoplasm  is  present  in  the  form  of  a  sheath  called  the  peri- 
plast, a  term  which  is  really  botanical  in  its  meaning.  The  peri- 
plast contains  contractile  elements  called  myonemes.  The  flagellum 
may  be  situate  anteriorly  (tractellum)  or  posteriorly  (pulsellum); 
there  may  be  but  one  (monomastigote),  two,  or  four  of  equal  length 
(isomastigote),  one  long  and  one  short  (paramastigote);  one  anterior 
and  one  posterior  (heteromastigote);  several  flagella  placed  together 
(polymastigote),  or  numerous  flagella  scattered  over  the  body 
(holomastigote). 

The  typical  flagellum  consists  of  an  elastic  axial  core  more  or  less 
enclosed  in  a  contractile  sheath  from  which  the  '  end-piece  '  projects. 
It  takes  its  origin  from  a  granule  situated  in  the  cytoplasm,  and 
apparently  forming  only  a  swelling  at  its  base.  The  swelling  is, 
however,  a  centrosome,  to  which  various  names  have  been  applied, 
such  as  basal  granule  or  blepharoplast.  Sometimes  this  centro- 
some is  contained  in  a  special  nucleus  which  is  called  a  kineto- 
nucleus.  The  centrosome-blepharoplast  may  be  single,  when  there 
is  only  one  flagellum;  or  multiple,  when  there  are  many  flagella. 
The  flagellum  may,  however,  penetrate  deeper  into  the  cytoplasm, 
until  it  reaches  the  nucleus.  This  prolongation  is  called  the  rhizo- 
plast,  which  may  represent  the  central  spindle  (centrodesmose)  of 
the  achromatic  elements  of  the  dividing  nucleus,  and  which  connects 
the  divided  portions  of  the  original  centrosome;  or  it  may  have 
arisen  simply  as  an  outgrowth  from  the  blepharoplast.  Thus,  the 
various  parts  of  the  flagellum  may  be  rhizoplast,  blepharoplast, 
sheath  or  envelope,  and  end-piece. 

If  the  centrosome  is  single,  it  may  be  intra-  or  extra-nuclear, 
and  in  either  case  is  a  centrosome-blepharoplast;  if  multiple,  the 
portion  connected  with  the  nucleus  is  the  centrosome,  and  that 
connected  with  the  flagellum  is  the  blepharoplast. 

330 


MASTIGOPHORA 


33i 


The  periplast  in  the  heteromastigotes  may  be  drawn  out  into  an 
undulating  membrane  which  helps  locomotion. 

When  the  periplast  is  thin  or  absent  the  body-form  may  still 
be  preserved  by  an  internal  stiff  rod — as,  for  example,  the  axostyle 
of  Trichomonas. 

There  is  a  difference  of  opinion  as  to  which  is  the  anterior  end  of 
the  mastigote.  We  believe,  with  Sambon,  that  the  non-flagellate 
end  should  correctly  be  considered  as  the  anterior  end,  but  several 
authorities  hold  quite  different 
views,  and  our  anterior  end 
will  correspond  with  mam' 
other  writers'  posterior.  Very 
often  there  is  a  depression 
somewhere  on  the  surface  of 
the  animal,  generally  near  the 
base  of  the  flagellum,  which  is 
intended  for  the  reception  of 
food,  and  is  called  the  mouth 
or  cytostome;  more  rarely  there 
is  an  oesophagus  leading  into 
the  interior  of  the  cell.  Nutri- 
tion may  be  holozoic  or  holo- 
phytic,  but  this  hardly  concerns 
us,  as  the  forms  to  be  described 
are  all  parasitic,  and  live  in 
fluids  from  which  they  absorb 
nourishment  by  their  whole 
surface. 

In  the  cytoplasm  there  is  a 
nucleus,  and  in  certain  forms 
two  nuclei:  a  trophonucleus  for 
nutrition,  and  a  kinetonucleus 
for  movement.  The  character 
of  these  nuclei  will  be  dealt 
with  in  detail  in  the  section 
Trypanosomida?.  The  cyto- 
plasm may  also  contain  food 
vacuoles,  contractile  vacuoles, 
chromatin  particles,  and  meta- 
plastic granules. 

Life-History.— Reproduction  takes  place  asexually  by  simple 
division.     Latent  or  encysted  forms  are  also  known. 

The  whole  subject  of  the  structure  and  life-history  of  the  parasitic 
Mastigophora  requires  much  further  research,  which,  indeed,  is 
being  rapidly  carried  out  all  over  the  world — in  fact,  so  rapidly  that 
it  is  hardly  possible  to  write  anything  on  the  subject  as  a  whole  which 
will  not  quickly  be  out  of  date. 

Classification. — The  Mastigophora  may  be  divided  into  subclasses 
as  follows: — 


Fig.  67. — Diagram  of  the  Life- 
Cycles  of  a  Mastigote  {Copro- 
monas  subtilis  Dobell)  . 

The  upper  cycle  demonstrates  simple 
fission  and  the  lower  sporogony. 

(After  Dobell,  from  the  Quarterly 
Journal  of  Microscopical  Science.) 


332  MASTIGOPHORA  AND  PROTOMONADINA 

A.  Body  inflated  with  gelatinous  substance — Subclass  i,  Cysto- 

flagellata  Haeckel,  1873. 

B.  Body  not  so  inflated  : — 

I.  Periplast  markedly  thickened,  with  two  flagella  arising 
in  the  middle  of  the  body,  one  trailing  and  one  lying 
in  the  transverse  groove- — Subclass  2,  Dinoflagellata 
Biitschli,  1885. 
II.  Periplast  thin,  with  a  variable  number  and  arrangement 
of  flagella- — Subclass  3,  Euflagellata  Cohn,  1887. 
Only  the  third  subclass  concerns  us. 

SUBCLASS  EUFLAGELLATA  Cohn,  1887. 

Definition. — Mastigophora  without  body  inflated  with  gelatinous 
substance,  and  possessing  a  thin  periplast  and  a  variable  number 
and  arrangement  of  flagella. 

Classification. — -The  Euflagellata  may  be  classified  into  orders  as 
follows: — 

A.  Chromatophores  often  present : — 

I.  With    cellulose    envelope — Order    i,    Phytomonadina 

Blochmann,  1895. 
II.  Without  cellulose  envelope— 

A.  Small  forms  without  oesophagus  or  vacuole  system 

— Order  2,  Chromomonadina  Klebs,  1872. 

B.  Large  forms  with  oesophagus  and  vacuole  system- — ■ 

Order  3,  Euglenoidina  Biitschli,  1884. 

B.  Chromatophores  absent : — 

I.  Amoeboid  forms  in  which  the  food  is  captured  by 
pseudopodia- — Order  4,  Rhizomastigina  Biitschli, 
1884. 
II.  Non-amoeboid  forms  in  which  the  food  is  usually 
captured  by  flagella— Order  5,Protomonadina  Bloch- 
mann, 1895. 

We  are  only  concerned  with  Order  5,  Protomonadina . 

ORDER  V.  PROTOMONADINA  Blochmann,  1895. 

Definition.-— Euflagellata  in  which  chromatophores  are  absent  and 
in  which  the  individuals  are  non-amoeboid  and  usually  capture  their 
food  by  flagella. 

Remarks.-  -As  defined  above,  the  Protomonadina  is  a  large  order, 
and  includes  the  Polymastigina  of  Biitschli  and  Blochmann,  as  well 
as  the  Binucleata  of  Hartmann,  both  of  which  were  treated  as 
separate  orders  in  our  previous  editions.  We,  however,  fore- 
shadowed a  return  to  Doflcin's  method  of  classification,  and  dis- 
cussed the  whole  subject  on  pp.  282  and  283  of  the  second  edition. 

Classification. — So  large  is  this  order  that,  for  convenience'  sake 
as  well  as  for  morphological  reasons,  it  may  advantageously  be 


SUBCLASS  EUFLAGELLAt'A  333 

divided  into  two  suborders  after  the  method  of  Hartmann  and 
Chagas,  which  is  as  follows: — 

A.  No  tendency  to  bilateral  symmetry  in  undividing  forms- 

Suborder  i,  Monozoa  Hartmann  and  Chagas,  1911. 

B.  More  or  less  tendency  to  bilateral  symmetry  in  undividing 

forms- — Suborder  2,  Diplozoa  Hartmann  and  Chagas,  1911. 

Suborder  I.  Monozoa  Hartmann  and  Chagas,  191 1. 

Definition. — Protomonadina  without  tendency  to  bilateral  sym- 
metry in  undividing  forms.  The  anterior  flagella  vary  from  one  to 
many,  in  addition  to  which  a  trailing  flagellum  or  undulating  mem- 
brane may  be  present. 

Classification, — -This  suborder  can  be  divided  into  some  ten 
families  as  follows:- — - 

Diagnostic  Table  of  the  Monozoa. 

A.  One  flagellum  present : — 

I.  With  a  collar — Family  1,  Craspedomonadidce  Stein,  1878. 
II.  Without  a  collar : — 

(a)  Kinetonucleus  not  separate  from  the  nucleus — ■ 

Family  2,  Oicomonadidce  Senn,  1900. 

(b)  Kinetonucleus  separate  from  the  nucleus — 

Family  3,  Trypanosomidce  Doflein,  1901. 

B.  Two  flagella  present : — ■ 

I.  Both  anterior:- — ■ 

(a)  Unequal — Family  4,  Monadidce  Stein,  1878,  emen- 

davit Senn,  1900. 

(b)  Equal- — Family  5,   Amphimonadidce   Kent,    1880, 

emendavit  Biitschli,  1884. 

II.  One  anterior  and  one  trailing  flagellum: — ■ 

(a)  Trailing  flagellum  free  :■ — ■ 

1.  In  horny  sheath  and  with  lip  or  proboscis-like 

process — Family  6,  Bikcecidce  Stein,  1878. 

2.  Without  sheath  or  process — Family  7,  Bodo- 

nidce  Biitschli,  1884. 
(Jo)  Trailing  flagellum  in  part  attached  to  the  body — 
Family  8,  C  ercomonadidce  Kent,  1880,  emendavit 
Biitschli,  1884. 

C.  Three  to  six  anterior  flagella,  with  or  without  one  trailing 

flagellum  (except  Enibadomonas  with  one  anterior  and  one 
cytostomic  flagellum) — -Family  9,  Tetramitidce  Kent,  1880. 

D.  Numerous  anterior   flagella- — Family  io,  Callimastigidce  da 

Fonseca,  1915. 
Of  these  ten  families  we  are  concerned  with  only  five,  of  which  one, 
the  Trypanosomids,  because  of  its  importance,  we  shall  leave  till 
tnc  next  chapter;  so  that  at  present  we  will  consider  the  following 
families  only: — 


334  MASTIGOPHORA  AND  PROTOMONADINA 


Family  2.  Oicomonadidse. 
Family  7.  Bodonidae. 
Family  8.  Cercomonadidse. 
Family  [g.  Tetramitidae. 


Family  Oicomonadid^;  Senn,  190c. 

Synonym.— C ercomonadina  Saville  Kent,  1880,  pro  parte. 

Definition. — Monozoa  with  a  single  flagellum,  no  collar  and  no 
kinetonucleus. 

Remarks. — -This  family  was  formed  by  Senn  for  Oi-  omonas,  several 
allied  forms  of  which  are  to-day  classified  in  the  Trypanosomidae. 

Type  Genus.— Oicomonas  Saville  Kent,  1880. 

Classification. — The  various  genera  of  this  family  may  be  differ- 
entiated as  follows:- — ■ 

A.  Without  definite  nucleus.    Chromatin  diffuse — Selenomonas 

(Selenomastix) . 

B.  With  definite  nucleus: — 

lr  Rhizostyle:  not  known  to  be  present : — 
{a)  Flagellum?anteriorly  directed : — 

Body  oval  or  roundish — Oicomonas. 
(b)  Flagellum  trailing  or  posterior: — ■ 

1.  Body  long  spindle-shaped — Ancyromonas . 

2.  Body    three-cornered    bowed    leaf- shaped — 

Phyllomonas. 
II.   Rhizostyle  present : — 

Body  6-11  x  3-5    microns.       Flagellum    springs 
from  a  small  basal  granule,  and  is  continued 
backwards  into  the  body  by  a  dark  staining 
filament,  the  rhizostyle—  Rhizomastix . 
Only  the  first  genus  concerns  us. 

Genus  Oicomonas  Saville  Kent,  1880. 

Synonym. — Cercomonas  Davaine,  i860,  pro  parte  nee  Dujardin, 
1S41. 

Definition. — Oicomonadidae,  with  oval  or  roundish  body  and  one 
anteriorly  directed  flagellum. 

Remarks. — In  1841  Dujardin  formulated  the  genus  Cercomonas, 
which  WTenyon  has  placed  upon  a  firm  basis. 

In  i860  Davaine  described  two  varieties  of  flagellates  which  he 
found  in  cholera  motions.  The  first  and  larger  of  these,  which  he 
calls  A,  is  without  doubt  Chilomastix  mesnili,  while  the  second  and 
smaller  is  an  Oicomonas.  Unfortunately  Davaine  called  both  these 
parasites  Cercomonas  hominis,  but  the  genus  was  one  of  his  own 
construction,  and  most  assuredly  was  not  the  Cercomonas  of 
Dujardin. 

In  1880  Saville  Kent  formed  the  genus  for  uniflagellate  free- 
swimming  forms,  which  are  capable  of  temporarily  fixing  themselves 
to  any  object  by  extending  a  sarcode  thread,  which  can  be  withdrawn 
when  they  start  to  swim. 


OICOMONAS  535 

This  sarcode  thread  was  the  only  point  of  distinction  from  the 
genus  which  Saville  Kent  called  Monas,  but  which  Stein  in  1878 
had  improved,  so  that  it  came  to  be  defined  as  possessing  two  anterior 
flagella,  one  long  and  one  short,  while  the  posterior  end  was  capable 
of  forming  a  filiform  pseudopodium.  In  view  of  this,  and  as  the 
filiform  pseudopodium  is  not  an  essential  character,  Oicomonas 
came  to  be  looked  upon  as  including  forms  with  a  single  anteriorly 
directed  flagellum,  and  as  such  requires  investigation  by  modern 
cyt.ological  methods.  In  this  genus  must  come  all  those  organisms 
which  resemble  Form  B  of  Davaine's  Cercomonas  hominis,  as  this 
is  not  a  Cercomonas,  and  they  must  include  Monas  pyophila 
Blanchard. 

With  regard  to  the  flagellate  called  Monas  lens  Miiller,  1786,  and 
reported  as  being  present  in  man,  it  is  not  a  Monas,  but  was  classified 
by  Saville  Kent  as  a  Heteromita.    It  may  be  a  Bodo  or  a  Prowazekia. 

Type  Species. — -Oicomonas  mutabilis  Saville  Kent,  1880,  found  in 
vegetable  infusions. 

The  more  important  parasitic  species  which  concern  us  are: — 

Oicomonas  pyophila  R.  Blanchard,  1895, 

Oicomonas  hominis  Davaine,  1854, 

Oicomonas  vaginalis  Castellani  and  Chalmers,  1909, 

and  these  may  be  differentiated  as  follows: — 

A.  With  thick  cuticle — Pyophila. 

B.  Without  thick  cuticle,  in  human  intestine — Hominis. 

C.  Without  thick  cuticle,  in  vaginal  mucus —  Vaginalis. 

Oicomonas  pyophila  R.  Blanchard,  1895. 

Synonym. — Monas  pyophila  R.  Blanchard,  1895. 

Definition.- — -Oicomonas  with  a  thick  cuticle. 

Historical. — Grimm  found  this  flagellate  in  the  sputum  and  pus 
of  a  pulmonary  and  of  a  hepatic  abscess  occurring  in  a  Japanese 
woman  living  in  Sappho.  The  organism  requires  reinvestigation 
by  modern  methods. 

Morphology. — The  flagellate  measures  30-60  microns  in  length 
and  is  heart-shaped,  being  enclosed  in  a  thick  cuticle  which  extends 
into  the  cytoplasm,  dividing  it  into  three  parts,  and  is  continued 
along  the  flagellum  for  a  considerable  distance.  At  its  tip  the  flagel- 
lum is  free. 

Life-History. — Nothing  is  known  as  to  this. 

Oicomonas  hominis  (Davaine,  1854),  emeiulavit  Castellani  and 
Chalmers,  1918. 

Synonyms. — Cercomonas  hominis  Davaine,  1854,  pro  parte — 
i.e.,  Form  B. 

Definition.— Oicomonas  with  a  thin  cuticle. 

History.— In  1854  Davaine  described  two  forms,  A  and  B,  under 
the  heading  Cercomonas  hominis.  Form  A  is  Chilomastix  mesnili, 
while  Form  B  is  Oicomonas  hominis. 


MASTIGOPHORA   AND  PROTOMONADINA 


4 

Fig.  68. — Oicomonas  hominis 
(Davaine)  . 

1-3,  and  5,  Flagellate  forms; 
4,  encysted  form. 


Morphology.— 0.  hominis  is  a  round  or  pear-shaped  parasite 
averaging  from  8  to  10  ix  in  diameter,  with  a  long  flagellum  projecting 

from  the  more  pointed  end. 
There  is  no  undulating  mem- 
brane. The  nucleus  is  small, 
indistinct,  and  usually  situated 
near  the  flagellar  extremity. 

Life-History. — Reproduction  is 
by  binary  fission,  and  Perroncitc 
and  Piccardi  have  described  en- 
cyst ment. 

Habitat. — According  to  our 
experience  at  autopsies,  the 
parasite  may  live  not  only  in 
the  small  intestine,  as  generally 
stated,  but  also  in  some  cases  in 
the  large  intestine.  Oicomonas 
is  readily  killed,  as  observed  by 
Castellani  and  Willey,  by  a  solu- 
tion of  methylene  blue  (1  in  3,000). 

Oicomonas  vaginalis  Castellani  and  Chalmers,   1909. 

Synonym.- — Cercomonas  vaginalis  Castellani  and  Chalmers,  1909. 

This  is  a  pear-shaped  or  rounded  parasite,  measuring  5  to  12  ^  in 
its  maximum  diameter,  and  provided  with  one  flagellum,  a  small 
nucleus,  and  food  vacuoles,  but  without  a  pulsating  vacuole.  It  is 
not  uncommon  in  the  vagina  of  native  women  in  Ceylon. 

Oicomonas  perryi  Castellani,  1907. 
Synonym.— Cercomonas  perryi  Castellani,  1907. 

Found  by  Castellani  in  Ceylon  in  monkeys  (Macacus  pileatus  and  Semno- 
pithecus  priamus)  suffering  from  diarrhoea.  It  is  morphologically  extremely 
similar  to  0.  hominis,  being  roundish  or  pear-shaped,  8  to  12  /t  in  diameter. 
There  is  one  flagellum  originating  from  the  pointed  end.  The  nucleus  is 
situated  near  the  flagellar  end.  Reproduction  seems  to  be  by  binary  fission, 
but  cysts  can  be  seen. 

Other  Species. — 0.  anatis  Davaine,  in  the  alimentary  canal  of  ducks; 
0.  cants  Gruby  and  Dclafond,  in  dogs;  (J.  gallinarum  Davaine,  in  fowls. 

Bodonidse  Biitschli,  1884,  emcndavit  Doflein,  1901. 
Definition. — Monozoa,  free  living  or  parasitic,  with  one  anterior 
and  one  posterior  (or  trailing)  flagellum,  with  or  without  a  kineto- 
nucleus  and  an  undulating  membrane. 

Nomenclature. — In  part,  at  all  events,  this  family  represent  the 
Heteromitkke  of  Saville  Kent,  as  Heteromita  Dujardin,  1841,  is  in 
part  Bodo  and  in  part  Cercomonas. 
Type  genus. — Bodo  Stein,  1878. 

Classification. — The  following  is  a  poor  attempt  to  differentiate 
the  genera  of  the  Bodonida:  known  to  us : — 
A.  With  an  undulating  membrane: — 

I.  Kinetonuclcus  well  marked — Trypanoplasma. 
1 1 .  Kinetonuclcus  poorly  marked — Trypanophis. 


TR  YPA  NOPLA  SMA  3  37 

B.  Without  an  undulating  membrane,  but  a  kinetonucleus  may 
or  may  not  be  present  :— 
I.  While  swimming  all  flagella  are  posterior.     (Genera 
with  which  we  are  not  concerned,  as  yet  not  found 
in  man.) 
II.  While  swimming  all  flagella  are  not  posterior: — 

{a)  Body  with  antero-posterior  groove — Colponcma. 
(b)  Body  without  such  a  groove : — • 

i .  Food  believed  to  enter  anteriorly : — 
(i)  Kinetonucleus  absent — Bodo. 
(2)  Kinetonucleus  present — Prowazekia. 
2.  Food  believed  not  to  enter  anteriorly.  (Genera 
with  which  we  are  not  concerned,  as  not 
yet  found  in  man.) 

Trypanoplasma  Laveran  and  Mesnil,  1901,  emendavit,  1904. 

Definition. — Bodonidae  living  in  the  blood  and  alimentary  canal  of  vertebrates 
with  two  flagella — one  projecting  anteriorly  and  the  other  running  posteriorly, 
and  raising  the  periplast  into  an  undulating  membrane.  Kinetonucleus 
almost  as  large  as  the  trophonucleus.     Sporogony  in  the  Hirudinea. 

Remarks. — This  genus,  which  was  first  described  by  Laveran  and  Mesnil,  is 
interesting,  first,  because  it  shows  definitely  an  anterior  flageHum,  which  has 
disappeared  in  most  trypanosomes,  and  a  posterior  flagellum,  which,  like  all 
trypanosomes,  carries  the  undulating  membrane;  secondly,  because,  according 
to  Leger  and  Keysselitz,  members  of  this  genus  are  parasitic  in  the  alimentary 
canal  of  fish,  and  not  in  the  blood. 

Morphology. — The  body  of  a  trypanoplasma  is  flattened,  and  often  curved, 
with  a  concave  side  thicker  than  the  convex,  to  which  the  undulating  mem- 
brane is  attached.  The  body  is  soft  and  of  changing  form.  At  the  junction 
of  the  anterior  and  middle  thirds  of  the  body  can  be  seen  two  masses  of  chro- 
matin. The  one  on  the  convex  side  is  the  trophonucleus,  and  the  other  on  the 
concave  side  the  elongated  kinetonucleus,  in  front  of  which  are  two  small 
chromatic  granules,  one  of  which  gives  rise  to  an  anterior  flagellum  which  be- 
comes free  at  once,  and  the  other  to  a  posterior,  which,  turning  backwards, 
runs  the  whole  length  of  the  cytoplasm,  raising  the  periplast  into  an  un- 
dulating membrane. 

Life-History. — Division  is  longitudinal,  the  kinetonucleus  dividing  first,  and 
then  the  flagella. 

Often  Trypanoplasmata  show  seasonable  variation,  the  infection  being  more 
intense  in  hot  weather.  They  are  evidently  pathogenic,  producing  anaemia 
associated  with  serous  fluid  in  the  peritoneum,  pericardium,  and  oedema  of 
the  organs. 

The  parasite  appears  to  be  spread  by  leeches,  in  which  the  sexual  forms 
conjugate  by  a  fusion  of  nuclei,  after  reduction,  and  of  the  cytoplasm,  from 
which  results  an  ookinete  possessing  a  trophonucleus  and  a  kinetonucleus. 

These  ookinetes  give  rise  to  male,  female,  and  indifferent  forms,  which 
multiply  abundantly.     Parthenogenesis  may  occur. 

Brumpt  infected  fish  by  the  bite  of  leeches,  but  Keysselitz  failed  witli 
Pisciola  gcometra,  and  it  is  hardly  surprising,  for  he  describes  the  lee<  h.  as 
becoming  ill,  with  swelling  of  the  clitellar  region,  alteration  in  colour  ami 
activity,  and  finally  death,  thus  showing  that  tins  leech  could  hardly  be  the 
usual  definitive  host.  He  has  already  noted  the  initial  stages  in  }Iini>/>> 
medicinalis.  Another  genus  of  leech  which  spreads  these  parasites  is  Ucmi- 
<  lepsis. 

Classification. — Crawly  considers  that  the  generic  name  should  be  Cryptobia 
Leidy,  but  the  diagnosis  of  this  genus  is  vague.     With  regard  to  classification, 


338  MASTIGOPHORA   AND  PROTOMONADINA 

Keysselitz  is  of  the  opinion  that  all  so  far  described  species  should  be  con- 
sidered to  belong  to  one  species — Trypanoplasma  borreli  L.  and  M. 
Type  Species. — Trypanoplasma  borreli  Laveran  and  Mesnil,  190 1 . 

Trypanoplasma  borreli  Laveran  and  Mesnil,  190 1. 
In  the  blood  of  Leuciscus  erythrophthalmus  (the  rudd)  and  PJioximis  Icsvis 
(the  minnow),  and  in  the  alimentary  canal  of  the  leech  Pisciola  geometra,  and 
perhaps  in  Hirudo  medici nalis . 

Trypanoplasma  cyprini  Plehn,  19.  >3. 
In  Cyprinus  carpis. 

Trypanoplasma  (Cryptobia)  dendrocoeli  Fantham  and  Porter,  1910. 

This  parasite  measured  20  to  40  ji  in  length,  with  a  large  and  often  curved 
kinetonucleus.  It  lives  in  the  alimentary  canal  of  Dendroccehtm  lacteum,  and 
was  the  first  trypanoplasma  to  be  found  in  the  Platyhelminthes. 

Trypanoplasma  intestinalis  Leger,  1905. 

This  trypanoplasma  is  very  important,  because  it  was  found  in  the  oesophagus 
and  anterior  part  of  the  stomach  of  Box  boiips,  a  salt-water  fish. 

It  is  the  first  trypanoplasma  described  as  existing  outside  the  blood.  In 
addition  to  typical  forms,  Leger  describes  globular  parasites  with  three  anterior 
flagella  and  a  rudimentary  undulating  membrane,  which  reminds  one  of 
Trichomonas. 

These  he  considers  to  be  female  forms,  and  says  that  he  has  seen  conjugation 
with  male  forms. 

Trypanoplasma  ventriculi  Keysselitz,  1906. 

Synonyms.— Heteromita  dahlii  apstena  =  Diplomasti.x  dahlii. 

This  is  found  in  the  intestine  of  Cyclopterus  lumpus,  and  is  apparently  a 
typical  trypanoplasma.     Discovered  by  Dahlin  1887. 

Trypanoplasma  varium  Leger,  1904. 
In  Cobitis  barbatula  (loach),  and  in  Hemiclepsis  marginata. 

Trypanoplasma  guernei  Brumpt,  1905. 
In  Coitus  globio,  and  develops  in  Pisciola. 

Trypanoplasma  barbi  Brumpt,  1905. 
In  Barbus  fluviatilis,  and  in  the  leech  {Pisciola) . 

Trypanoplasma  abramidis  Brumpt,  1905. 
In  the  bream  [A  bramis  brama)  and  the  leech  {Hemiclepsis) . 

Trypanoplasma  truttse  Brumpt,  1905. 
In  Salmo  fario,  and  perhaps  in  Pisciola. 

Other  Species. 

T.  keysselitzi  Minchin,  1909,  in  the  tench;  T.  gumeyorum  Minchin,  1909,  in 
the  pike;  T.  claries Mathis  and  Leger,  191 1,  in  Clarias  macrocephalus,  T.  congri. 

Trypanophis  Keysselitz,  1904. 

Bodonidae  in  C  celentcrata ,  with  two  flagella,  an  anterior  and  a  posterior. 

The  kinetonucleus  is  situated  anteriorly,  and  is  much  smaller  than  the 
trophonucleus.  According  to  Floyd,  a  blepharoplastic  granule  gives  rise 
to  the  free  flagellum.  The  attached  flagellum  arises  near  the  basal  granule 
of  the  free  flagellum,  and  gives  rise  to  a  narrow  undulating  membrane. 

Trypanophis  grobbeni  Poche,  1903. 
In  the  gastro-vascular  system  of  different  Siphonophora — -e.g.,  Halistemma 
ergestnntui.     The  parasite  is  curved  somewhat,  like  a  trypanosome. 


PROWAZEKIA  339 

Genus  Prowazekia  Hartmann  and  Chagas,  1910. 

Definition.— Bodonidce  with  a  kinetonucleus. 

Type. — Prowazekia  cruzi  Hartmann  and  Chagas,  1910. 

The  separation  of  the  old  genus  Bodo  sensu  lato  into  Bodo  sens// 
stricto  and  Prowazekia  is  not  at  present  generally  accepted;  for 
example,  Alexeieff  and  others  oppose  it,  stating  that  the  generic 
name  for  all  the  species  included  under  Prowazekia  should  be  Bodo, 
while,  that  for  the  only  species  at  present  under  Bodo — viz., 
B.  lacertce  Grassi,  1881— should  be  Prowazekella  (new  genus)  lacertce 
Grassi,  1881.  Nor  is  this  the  only  confusion  with  regard  to  Prowa- 
zekia, for  one  species — P.  urinaria  Hassall,  1859 — -has  been  found  in 
urine  which  has  been  passed  for  six  hours  or  more  in  the  Temperate 
Zone;  and  three  species — P.asiatica  Castellani  and  Chalmers,  1910, 
<  Y\  Ion;  P.  cruzi  Hartmann  and  Chagas,  1910,  Brazil;  P.  weinbergi 
Mathis  and  Leger,  1910,  Indo-China — -are  found  in  faeces;  while  one 
form — P.  ftarva  Naegler,  1910 — lives  in  slime  on  stones  at  Lunz. 

All  observers  are  agreed  that  these  flagellates  are  non-pathogenic, 
but  the  question  which  is  debated  is  whether  they  are  accidental 
contaminations  of  the  urine  and  faeces  after  being  passed  out  of  the 
body,  and  the  urine  problem  is  further  complicated  by  the  question 
as  to  whether  it  was  contaminated  by  the  faeces. 

With  regard  to  the  urinary  species,  it  has  been  found  by  Hassall 
in  1859,  Salisbury  in  1868,  Kunstler  in  1883,  and  Stinton  in  1912. 
He  obtained  it  only  twice  from  the  same  patient,  who  was  in  a  hos- 
pital ward  in  Liverpool,  and  in  none  of  the  other  patients  in  the 
ward ;  it  was  not  found  in  the  faeces,  nor  in  a  vessel  of  water  exposed 
to  the  air  of  the  ward,  nor  in  the  water-supply.  It  was  not  present 
in  later  observations  taken  aseptically,  and  cultures  died  rapidly  at 
370  C.     It  is  therefore  concluded  to  be  an  accidental  contamination. 

The  intestinal  forms  are  not  so  easily  dismissed,  as  we  have  found 
them  in  stools  collected  in  sterile  petri-dishes,  and  Mathis  and 
Leger  found  their  species  in  the  faeces  of  persons  in  good  health  and 
suffering  from  diarrhoea,  even  when  taken  with  aseptic  precautions. 
It  is  possible,  therefore,  that  some,  at  all  events,  of  the  intestinal 
forms  are  harmless  occasional  parasites  of  man. 

Classification. — The  species  may  be  differentiated  as  follows: — 

A.  Posterior  flagellum  free: — 

I .  Large  forms .     More  than  8  microns  in  length  as  a  rule : — 
{a)  Shape  oval : — 

1.  Rhizoplast  present: — 

(1)  Cytostonro  present — Urinaria. 

(2)  Cytostome  absent — Asiatica  and  vaginalis. 

2.  Rhizoplast  absent — Cruzi. 
{b)  Shape  pyriform:— 

Apex  sharp — Weinbergi. 
II.  Small  forms.   Not  exceeding  8  microns  in  length — Parva. 

B.  Posterior  flagellum  attached  to  the  body  for  a  short  distance 

— Javanensis. 


34°  MASTIGOPHORA   AND  PROTOMONADINA 

Prowazekia  urinaria  Hassall,  1859. 

This  species  has  several  times  been  found  in  human  urine  which 
has  been  passed  some  hours. 

Morphology. — The  flagellate  appears  in  three  forms — a  sausage- 
shaped  form,  10  to  25  ju  in  length  by  2-5  to  6  /u  in  breadth ;  a  round 
or  oval  form,  varying  from  4^  in  diameter  to  15  by  10  ju  in  measure- 
ment; a  carrot-shaped  form,  varying  from  6  by  3  /i  to  25  by  4  ju. 
The  cytoplasm  contains  a  large  number  of  small,  highly  refractile 
granules,  and  contains  a  trophonucleus  and  a  kinetonucleus,  which 
latter  is  a  relatively  large  pear-shaped  body.  The  body  is  enclosed 
by  a  thin  periplast,  and  possesses  two  flagella,  a  shorter  anterior 
and  a  longer  lateral,  which  arise  fromblepharoplasts  (basal  granules), 
which  are  connected  by  rhizoplasts  to  the  kinetonucleus.  There, 
is  a  cytostome  situate  near  the  root  of  the  short  flagellum. 

Bionomics. — It  moves  in  a  jerky  manner,  with  the  short  flagellum 
directed  forwards  and  the  long  flagellum  backwards.  The  small 
flagellum  is  also  useful  in  capturing  food,  such  as  bacteria.  Food 
enters  by  means  of  the  cytostome  and  forms  the  usual  food  vacuoles, 
which  accumulate  at  the  aflagellar  end.  A  contractile  vacuole  is 
seen  in  large  flagellates,  and  may  measure  1  to  3  ju  in  diameter. 
It  is  situate  near  the  base  of  the  cytostome,  to  which  it  is  joined  by  a 
minute  canal.  It  contracts  every  15  to  30  seconds  at  a  temperature 
of  20°  C.  It  is  thought  to  be  the  dilated  fundus  of  the  cyto- 
stome. 

Life-History. — It  divides  in  two  by  binary  fission,  the  blepharo- 
plast  apparently  dividing  first  and  forming  two  new  flagella,  after 
which  the  cell  nuclei  and  the  cell  divide.  It  can  lose  its  flagella, 
and  can  form  round  or  oval  cysts  5  to  7  /u  in  diameter,  inside  from 
which  after  a  time  it  again  becomes  flagellate,  and  escapes  in  its 
typical  form. 

Cultivation. — In  association  with  bacteria  it  grows  well  in  urine, 
on  salt  agar,  nutrient  agar,  serum  agar,  blood  agar,  peptone,  salt 
solution,  nutrient  broth,  and  diluted  blood-serum  at  a  temperature 
of  200  C,  but  is  killed  by  a  temperature  of  370  C.  in  one  or  two  hours. 
It  has  not  been  cultivated  free  from  bacteria. 

Prowazekia  asiatica  Castellani  and  Chalmers,  1910. 

Synonym. — Bodo  asiaticus  Castellani  and  Chalmers,  1910. 

This  flagellate  was  found  in  1909  by  Castellani  and  Chalmers  in 
the  stools  of  cases  of  ankylostomiasis  suffering  from  diarrhoea  in 
Ceylon.  It  was  studied  in  detail  by  Whitmore  in  191 1,  and  assigned 
to  the  new  genus  Prowazekia,  which  Hartmann  and  Chagas  had 
differentiated  from  the  old  genus  Bodo. 

Morphology.  —P.  asiatica  is  found  in  the  motions  in  two  forms — 
either  as  a  long,  slender  flagellate  measuring  10  to  16  jjl  in  length  by 
5  to  8  fjb  in  breadth  or  as  a  more  rounded  form,  which  has  a  trans- 
verse diameter  of  8  to  10 /u.    The  cytoplasm  is  alveolar  in  structure, 


PROWAZEKIA   A  STATIC  A 


34i 


containing  iuod  vacuoles,  but  no  contractile  vacuole.     The  tropho- 
nucleus  is  usually  situate  in  the  flagellar  third  of  the  cytoplasm, 
and  consists  of  a  nuclear  membrane,  a  widish  space  for  the  enchylema, 
and  a  central  karyosome,  with  usually  a  centrosome.     The  kineto- 
nucleus    is    situate  nearer   the  flagellar 
extremity,  and  is  connected  by  a  long 
strand  with  a  small  piece  of  chromatin 
situate  near  the  aflagellar  extremity,  and 
by  another  strand  with  one  of  the  two 
blepharoplasts  which  lie  adjacent  to  the 
flagellar    extremity.     These     blepharo- 
plasts are  united  together,  and,  as  already 
stated,  to  the  kinetonucleus  by  strands. 
I'sually   there   are   two,  which  may  lie 
side  by  side  or  one  over  the  other.    From 
these  blepharoplasts  the  two  flagella  take 
origin,  and  quickly  pass  to  the  exterior. 

Reproduction. — -Asexual  reproduction 
lakes  place  by  metamitosis,  but  sexual 
reproduction  is  unknown.  Cyst  formation 
has  been  observed,  resulting  in  rounded 
bodies  6  to  7  fx  in  transverse  diameter, 
possessing  tropho-  and  kineto-nuclei,  and 
enclosing  the  remains  of  the  flagella. 

Culture. — P.  asiatica  is  readily  cultivated  in  liquid  and  in  the 
water  of  condensation  of  solid  media  in  symbiosis  with  bacteria. 
The  most  suitable  medium  is  the  condensation  water  of  nutrose 
agar  (2  to  4  per  cent.),  or  maltose  agar,  on  which  a  few  drops  of 


Fig.  69. — Prowazekia  asi- 
atica Castellani  and 
Chalmers:  From  F^ces. 


&  I 


'/  1  '•.-;  '  2 

Fig.  70. — Prowazekia  asiatica  Castellani  and  Chalmers:  From  Cultures. 

(After  Whitmore.) 


albumin-water  have  been  placed,  when  it  can  be  subcultured  and 
grown  indefinitely  if  the  tubes  are  kept  uncapped  and  subcultures 
are  made  twice  a  week. 

Pathogenicity. — Probably  nil. 


342  MASTIGOPHORA   AND  PROTOMONADINA 

Prowazekia  cruzi  Hartmann  and  Chagas,  1910. 
Oval  to  pear-shaped  forms;  length  8  to  12  /^;  breadth,  5  to  6  fj,, 
with  the  flagella  at  the  narrow  end.  Found  in  Brazil.  Differs 
from  P.  asiatica  by  the  absence  of  the  strand  which  originates  from 
the  kinetonucleus  and  terminates  into  a  chromatin  granule.  Martin 
has  found  in  human  stools  in  Tsingtau  a  Prowazekia  which  he 
believes  to  be  identical  with  P.  cruzi. 

Prowazekia  weinbergi  Mathis  and  Leger,  1910. 
Pear-shaped,  but  rather  drawn  out  into  a  point ;  length,  8  to  15  /j, ; 
breadth,  4  to  6-5  /n.     Flagella  at  broad  end.     Found  frequently  in 
the  motions  of  men  in  Tonkin. 

Prowazekia  parva  Naegler,  1910. 
Characterized  by  its  small  size,  the  longest  forms  being  5  to  8  /*. 
The  cysts  do  not  contain  flagella. 

Prowazekia  javanensis  Flu,  1912. 

Definition. — Prowazekia  in  which  the  posterior  flagellum  is 
attached  to  the  body  for  a  short  distance. 

Remarks. — -Flu  believes  that  there  is  only  one  species  of  Prowa- 
zekia. He  obtained  his  variety  from  an  agar  culture  of  human 
faeces  in  the  Dutch  East  Indies. 

Prowazekia  vaginalis  Castellani  and  Chalmers,  1918. 

Definition. — Prowazekia  living  in  the  vaginal  mucus. 

Remarks. — Morphologically  identical  with  P.  asiatica  found  in 

motions,  but  the  investigated  strains  of  the  latter  will  not  live  in 

vaginal  mucus.  _  _    ,    _,   .        0 

Genus  Bodo  Stem,  1875. 

Definition.- — Bodonidae  without  undulating  membrane  or  kineto- 
nucleus, but  with  a  rhizoplast.  While  swimming  one  flagellum  is 
anterior  and  the  other  trailing,  without  antero-posterior  groove. 

Bodo  stereoralis  Porter,  191S. 
Discovered  in  human  faeces  by  Miss  Porter.     Body  measures  from  14  u  to 
lung  and  is  from  6  fj.  to  9  fj.  broad,  with  large  nucleus. 

Bodo  lens  Muller,  1786. 
Synonyms. — Monas  lens,  Heteromita  lens. 

Remarks. — Usually  free  living,  but  said  to  be  found  in  man  once  (vide 
■  Animal  Parasites  of  Man,'  by  Fantham,  Stephens,  and  Theobald). 

Genus  Toxobcdo  Sangiorgi,  1917. 
Definition. — Bodonidge  of  semilunar  shape. 
Type  and  only  Genus. — Toxobodo  intestinalis  Sangiorgi,  1917. 

Toxobodo  intestinalis  Sangiorgi,  1917. 
A  flagellate  organism  semilunar  in  shape,  6-9-6  x  1-6-4-8  microns, 
found  in  the  human  intestine  and  grown  for  ten  generations  in 
culture  media  (peptone  water).     It  has  two  flagella,  and  resembles 
a  Bodo,  except  in  shape. 


ORDER  CERCOMONADIDsE  343 

Genus  Heteromita  Dujardin,  1841. 
15odonidae  round  or  oval,  with  two  rlagella,  one  at  each  pole. 

Heteromita  zeylanica  Castellani  and  Chalmers,  19 10. 

This  flagellate  is  elongated,  8  to  15  fi  in  length  by  3  to  4  /x  in  breadth,  with 
single  flagellum  at  each  pole,  and  a  nucleus  fairly  rich  in  chromatin.  No 
undulating  membrane  or  pulsating  vacuole,  but  with  chromidia  in  the  cyto- 
plasm. It  is  not  cultivable.  This  flagellate  we  classify  provisionally  under 
the  genus  Heteromita.  It  was  found  in  the  stools  of  persons  suffering  from 
ankylostomiasis  in  Ceylon. 

ORDER  CERCOMONADIDffi  Saville  Kent,  1880,  emendavit  Biitschli. 

Definition.-  -Monozoa  with  elongate  or  oval  forms,  possessing 
one  free  anterior  flagellum  and  one  trailing  flagellum. 

Type  Genus.— Cercomonas  Dujardin,  1841,  emendavit  Wenyon, 
[910. 

Remarks. — It  appears  to  us  that  this  is  the  only  genus  which 
can  be  classified  in  this  family  at  the  present  moment. 

Genus  Cercomonas  Dujardin,  1841,  emendavit  Wenyon,  1910. 

Synonyms.- — -Heteromita  Dujardin,  1841,  pro  parte  nee  Cercomonas 
Davaine,  i860,  nee  Oicomonas  Saville  Kent,  1880. 

Definition.— Cercomonadidae,  pear-shaped,  with  a  protokaryon 
type  of  nucleus  situate  near  the  flagellar  extremity,  with  a  basal 
granule  or  blepharoplast  from  which  a  sort  of  rhizoplast  may  run 
to  the  margin  of  the  cytoplasm,  at  which  it  divides  into  the  two 
nagella,  one  of  which  is  anterior,  while  the  other  is  posterior  and 
closely  attached  to  one  side  of  the  body,  at  the  posterior  end  of 
which  it  becomes  free. 

Type  Species. — The  type  species  of  the  properly  defined  family 
is  certainly  Cercomonas  longicauda  Dujardin,  1841,  emendavit 
Wenyon,  1910,  even  though  the  first  species  in  Dujardin's  descrip- 
tion is  C.  detracta,  because  this  latter  has  never  again  been  described, 
and  has  therefore  never  been  examined  by  modern  methods. 

Certainly  Dujardin's  genus  Heteromita  agrees  in  description  and 
illustration  with  many  of  the  features  of  C.  longicauda,  and  therefore 
we  consider  it  to  be  a  synonym. 

There  are  a  number  of  species  described  by  Dujardin,  but  until 
they  have  been  examined  by  modern  methods  it  is  impossible  to 
define  them.     They  are  all  free-living  forms. 

Cercomonas  longicauda  Dujardin,  1841,  emendavit  Wenyon,  1910. 

Synonyms. — Cercomonas  parva  Hartmann  and  Chagas,  1910. 

Definition. — Cercomonas  elongate  8-15x3-4  microns,  with  very 
marked  long  posterior  flagellum. 

History.- — This  flagellate  was  first  discovered  by  Dujardin  in 
1841  in  an  old  infusion,  and  was  next  described  by  Wenyon  in  1910, 
being  found  in  cultures  made  from  human  faeces.     In  the  same  year 


344 


MASTIGOPHORA  AND  PROTOMONADINA 


Hartmann  and  Chagas  met  with  it  in  Brazil.     Since  then  it  has  only 
been  recorded  once. 

Morphology.- — The  body  is  pear-shaped,  measuring  on  an  average 
8-15  microns  in  length  by  3-4  microns  in  breadth,  but  Wenyon  has 
met  with  small  forms  measuring  only  some  2-3  microns  in  greatest 
length. 


Fig.  71. — -Cercomonas  longicauda  Dujardin,  1841. 

Type  with  granules  around  the  nucleus  ;  compare  this  with  Fig.  74. 

(After  Wenyon,  from  the  Quarterly  Journal  of  Microscopical  Science.) 

The  cytoplasm  is  alveolar  and  contains  a  large  anteriorly  situate 
nucleus,  which  has  a  nuclear  membrane  enclosing  a  clear  space,  in 
which  lies  a  large  karyosome.  The  nuclear  membrane  may  be 
drawn  out  into  a  cone,  at  the  apex  of  which  lies  the  granule — - 
blepharoplast— from  which  either  the  flagella  spring  directly  or  a 
single  rhizoplast  passes  to  the  periphery  and  then  divides  into  the 
two  flagella .  In  any  case,  the  flagella  arise  from  the  anterior  broader 
end,  and  while  one  is  directed  forwards,  the  other  passes  posteriorly 
over  the  surface  of  the  body,  to  which  it  is  attached  until  it  reaches 
the  posterior  end,  when  it  becomes  a  free  posterior  flagellum.  The 
cytoplasm  also  contains  a^number  of  bright  retractile  granules. 


Fig.   72. — Cercomonas  longicauda  Dujardin, 
Type  without  granules  and  Cyst. 
(After  Wenyon.) 


1841. 


Life-History. — Simple  fission,  with  division  of  the  nucleus  by 
promitosis,  takes  place,  while  cyst  formation  is  also  known. 

The  cysts  measure  some  6-7  microns  in  diameter.  They  are 
slightly  brownish  spherical  bodies  containing  a  spherical  central 
nucleus  surrounded  by  bright  retractile  granules. 

Pathogenicity. — It  is  believed  to  be  non-pathogenic,  and  to  be 
accidentally  present  in  the  faeces. 


FAMILY  TETRAMITIDM  345 

Cercomonas  parva  Hartmann  and  Ctiagas,  1910. 
This  is  probably  the  same  as  C.  longicauda. 

Family  Tetramitid.e  Kent,  1880,  emendavit  Chalmers  and  Pekkola, 

1917. 

Definition. — -Monozoa  with  three  to  six  anterior  flagella  (with  the 
exception  of  Embadomonas,  which  has  only  two  visible  flagella, 
one  anterior  and  one  posterior),  with  or  without  a  rhizoplast,  with 
or  without  a  posterior  or  trailing  flagellum,  which  may,  or  may  not, 
form  an  undulating  membrane,  with  or  without  an  axostyle  or  a 
cytostome.     Habitat,  free  living  and  parasitic. 

Type  Genus. — Tetramitus  Perty,  1852. 

Classification. — The  family  may  be  divided  into  three  subfamilies 
as  follows: — ■ 

A.  Without  an  axostyle  : — 

(a)  With  three  flagella — -Subfamily  I.,  Embadomonadince 

Chalmers  and  Pekkola,  1918. 

(b)  With  four  to  six  flagella — -Subfamily  II.,  TetmmitidincB 

Chalmers  and  Pekkola,  1917,  emendavit  1918 

B.  With  an  axostyle — Subfamily  III.,  Trichomonadince  Chalmers 

and  Pekkola,  1917. 

Subfamily  Embadomoxadix.e  Chalmers  and  Pekkola,  1918. 

Definition. — Tetramitida?  with  or  without  a  cytostome,  but  with- 
out an  axostyle  and  with  three  flagella  only.  (Only  two  are  visible 
in  Embadomonas.) 

Classification. — The  known  genera  of  the  subfamily  Embadomo- 
nadinae  may  be  recognized  as  follows : 

A.  Without  cytostome  : — 

I.  With    three    anterior    flagella— (1)    Enteromonas    da 
Fonseca,  1915. 
II.  With    one    anterior    and    two    posterior    flagella — 
(2)  Dallengeria  Saville  Kent,  1S80. 
III.  With  two  anterior  and  one  posterior  flagella— (3)  Di- 
cercomonas  Chalmers  and  Pekkola,  1919 

B.  Cytostome  present  or  probably  present  (as  a  groove)  : — 

I  With  one  anterior,  one  cytostomic  and  then  free,  and 
one  free  trailing  flagellum— (4)  Trimastix  Saville 
Kent,  1880. 
II.  With  one  anterior  and  one  posterior  flagellum  which 
is  generally  cytostomic,  and  with  a  large  cytostome 
with  siderophilous,  often  folded,  border—  (5)  Emba- 
domonas Mackinnon,  1911. 

The  genera  in  which  we  are  interested  are  Enteromonas,   Di- 
cercomonas  and  Embadomonas. 


346 


MASTIGOPHORA   AND  PROTOMONADINA 


Genus  Enteromonas  da  Fonseca,  1915. 

Definition.- — Embadomonadinae  without  a  cytostome  or  trailing 
flagellum  and  with  three  anterior  flagella. 

Type  and  only  Species.- — Enteromonas  hominis  da  Fonseca,  found 
in  Brazil. 

Enteromonas  hominis  da  Fonseca,  1915. 

Definition.- — Enteromonas  with  the  characters  of  the  genus. 
Remarks.- — This  parasite  was  first  found  by  da  Fonseca  in  Brazil 
in   1915,    and   subsequently   by   Chalmers    and    Pekkola,    in   the 
Anglo-Egyptian    Sudan,   in   Europeans  and 
natives. 

Morphology. — The  parasite  is  roundish  or 
oval,  without  a  tail,  and  with  a  diameter 
varying  from  5-6  microns.  The  periplast  is 
not  rigid,  and  encloses  an  endoplasm,  often 
with  inclusions  such  as  bacteria.  Situate 
anteriorly  lies  the  protokaryon  type  of 
nucleus,  from  which  a  rhizoplast  runs  to  a 
blepharoplast,  from  which  three  anterior 
flagella  arise. 

Life-History.- — Da  Fonseca  records  longi- 
tudinal division. 

Pathogenicity. — The  flagellate  probably 
causes  diarrhoea. 


Fig.  73. — Enteromonas 
hominis  da  Fonseca, 
1915. 


Genus  Embadomonas  Mackinnon,  1911. 

Synonym. — Waskia  Wenyon  and  O'Connor,  1916. 
Definition.- — Embadomonadinae,    with     a     cytostome    and    one 
anterior    and    one   posterior  flagellum,  and  with  a  siderophilous, 
often  folded,  cytostomic  margin. 

Type  Species. — Embadomonas  agilis 
Mackinnon,  1911. 

Other  Species.- — The  type  and  the 
other  species  may  be  recognized  as 
follows : — 

A.  Habitat:  intestine  of  Tricho- 
pterous  and  Tifttda 
Larvce  in  British  Isles: — 
{a)  Cytostomic  borders  feebly 
siderophilous,  cytosto- 
mic flagellum  exceed- 
ingly delicate  and  in- 
conspicuous-— ■ 
Size:  4-11  x  1*5-3  microns.    Cysts:  about  4x3  microns. 

(1)  Agilis. 
Cytostomic  borders  markedly  siderophilous,  cytostomic 
flagellum  well  developed.     Size:  7-16  x  5-9  microns. 
Cysts:  5-6  X4-5  microns.     (2)  Alexeieffi. 


Fig. 


74. — Embadomonas 
Mackinnon,  1911. 


agilis 


(After  Mackinnon,  from  the 
Quarterly  Journal  of  Microscop- 
ical Science.) 


{b) 


EMBADOMONAS  347 

B.  Habitat:  intestine  of  Man  in  Alexandria  : — 

Anterior  flagellum  long  and  thin,  cytostomic   flagellum 

shorter  and  stouter. 
Size:  4-9  microns  long,  but  with  variable  width  2-4  microns 
in  narrow  forms.     Cysts:  4-5-6  microns  in  length.     (3) 
Intestinalis. 
Only  Embadomonas    intestinalis  Wenyon  and  O'Connor,   1916, 
concerns  us. 

Embadomonas  intestinalis  Wenyon  and  O'Connor,  1916. 

Synonym.— Waskia  intestinalis  Wenyon  and  O'Connor,  1916. 

Definition.— Embadomonas  found  in  the  intestine  of  man  in 
Alexandria.  Size  4-9  microns  in  length,  but  with  variable  width, 
some  3-4  microns  in  narrow  forms.  Cysts  4*5-6  microns  in 
length. 

Remarks. — This  flagellate  was  found  by  Wenyon  and  O'Connor 
in  two  cases  in  the  Orwa-el-Waskia  section  of  the  19th  General 
Hospital  in  Alexandria. 

Morphology.— The  flagellate  is  pear-shaped,  with  a  cytostome 
at  the  anterior  end,  from  which  (or  slightly  nearer  the  cytostome) 
a  thin  anterior  flagellum  takes  origin,  while  a  second  stouter  and 
shorter  arises  from  the  inner  part  of  the  anterior  wall  of  the  cyto- 
stome, from  which  it  projects  for  a  considerable  distance. 


Fig.  75. — Embadomonas  intestinalis  (Wenyon  and  O'Connor,   191 6). 
Showing  dividing  form,  flagellate,  and  cyst. 
(After  Wenyon  and  O'Connor.) 

The  cytoplasm  is  pale,  frequently  vacuolated  with  an  anteriorly 
situate  nucleus,  which  has  a  nuclear  membrane  and  a  central  karyo- 
some.  On  the  surface  of  the  nuclear  membrane  there  are  two 
granules  from  which  the  flagella  arise. 

Life-History. — Forms  with  two  cytostomes  and  four  flagella  have 
been  seen,  indicative  of  division. 

The  cysts  are  pear-shaped  bodies  of  a  pearly-white  appearance, 
and  quite  structureless  unless  stained,  when  certain  nuclear  struc- 
tures can  be  made  out. 

Pathogenicity. — There  is  no  evidence  that  it  is  pathogenic. 

Subfamily  Tetramitidinze  Chalmers  and  Pekkola,  1918. 

Definition. — Tetramitidse  with  or  without  a  cytostome,  with  four 
to  six  flagella,  but  without  an  axostyle. 

Classification. — Tight  genera  belong  to  the  subfamily— viz:- — 


348  MASTIGOPHORA   AND  PROTOMONADINA 

Tetramitus  Perty,  1852. 
Callodictyon  Carter,  1865. 
Costiopsis  Senn,  igoo. 
Chilomastix  Alexeieff,  191 1. 
Tetrachilomastix  da  Fonseca,  1915. 
Copromastix  Aragao,  1916. 
Tricercomonas  Wenyon  and  O'Connor,  191 7. 
Protetramitus  Chalmers  and  Pekkola,  1918. 

And  they  may  be  differentiated  as  follows  :— 

A.  Without  cytostome  :■ — ■ 

1.  With     rhizoplast.       (1)    Protetramitus    Chalmers    and 

Pekkola,  1918. 

2.  Without    rhizoplast — (2)    Copromastix    Aragao,    1916. 

(3)  Tricercomonis  Wenyon  and  O'Connor,  1917. 

B.  Cytostome  probably  present : — ■ 

At  all  events,  there  is  a  deep  ventral  longitudinal  furrow — 
(3)  Callodictyon  Carter,  1865. 

C.  Cytostome  present  :■ — ■ 

I .  Trailing  flagellum  is  free : — 

{a)  Body  dorso-ventrally  compressed,  ventral  surface 
with  deep  depression  which  serves  as  a  sucker 
and  contains  the  cytostome  and  two  short  free 
flagella ;  the  two  thick  long  trailing  flagella  issue 
from  this  depression— (4)  Costiopsis  Senn,  1900. 

(b)  Body  more  or  less  symmetrical  and  not  compressed 
or  arranged  as  above,  with  three  anterior  and 
one  free  trailing  flagellum— (5)  Tetramitus  Perty, 
1852. 
II.  Free  trailing  flagellum  absent:— 

(a)  Three  anterior  flagella — (6)  Chilomastix  Alexeieff, 
1911. 

{b)  Four  anterior — (7)  Tetrachilomastix  da  Fonseca, 

Of  these  genera  we  are  only  concerned  with  Copromastix,  Tri- 
cercomonas,  Chilomastix,  and  Tetrachilomastix. 

Genus  Copromastix  De  Beaurepaire  Aragao,    1916. 
Definition. — Tetramitidinae  without  cytostome  and  rhizoplast. 

Copromastix  prowazeki  Aragao,  19 16. 
Found  in  cultures  of  human  faeces  in  Brazil. 

Genus  Tricercomonas  Wenyon  and  O'Connor,  1916. 

Definition. — Tetramitidinae  without  cytostome  and  with  three 
anterior  and  one  trailing  flagellum. 

Remarks. — This  genus  is  like  Cercomonas  in  many  ways,  but 
cannot  be  classified  in  the  family  Cercomonadidae ;  and  as  it  shows  a 
resemblance  to  Protetramitus,  we  place  it  here. 


TRICERCOMONA  S  3  49 

Type  Species.— The  type  and  only  species  is  Tricercomonas  hominis 
Wenyon  and  O'Connor,  1916. 

Tricercomonas  hominis  Wenyon  and  O'Connor,  1916. 

Definition. — Tricercomonas  of  small  size  and  active  movements, 
with  spherical  or  ovoid  body  distinctly  flattened  on  one  side  and 
with  the  posterior  end  drawn  out  and  terminating  in  a  flagellum, 
which  can  be  traced  forwards  along  the  flattened  side  to  the  anterior 
end  of  the  body,  where  three  anterior  long  flagella  take  origin. 
Habitat,  the  intestine  of  man  in  Egypt. 

Morphology. — In  addition  to  the  characters  given  above,  the  body, 
which  measured  4-8  microns  in  length,  is  seen  to  be  somewhat 
grooved  along  the  course  of  the  posterior  flagellum.  No  definite 
cytostome  could  be  seen.  The  cytoplasm  contains  bacilli  and  cocci, 
a  nucleus  with  a  central  karyosome,  and  a  nuclear  membrane,  which 
is  drawn  out  into  a  cone-like  elevation,  from  the  summit  of  which 
the  flagella  take  their  origin. 

Life-History. — As  forms  with  two  nuclei  have  been  seen,  it  is 
presumed  that  binary  division  may  take  place.  The  cysts  are  oval, 
6-8  microns  in  length  and  about  half  this  breadth,  containing  one 
to  four  nuclei  of  the  same  type  as  the  flagellate. 

Pathogenicity.- — It  is  believed  to  be  non-pathogenic. 


Fig.  76. — Tricercomonas  intestinalis  Wenyon  and  O'Connor,  1915. 

Two  flagellate  forms  (compare  side  view  with  Fig.  71)  and  one  cyst. 

(After  Wenyon  and  O'Connor,  from  the  publications  of  the  Wellcome  Bureau 
of  Scientific  Research.) 

Genus  Chilomastix  Alexeieff,  1911. 

Synonyms. — (i)  Cercomonas  Davaine,  1880,  pro  parte  •//•«;  Dujardin, 
1841;  (2)  Trichomonas  Roos,  1893,  nee  Donne,  1837;  (3)  Monocerco- 
monas  Epstein,  1893,  nee  Grassi,  1879  >  (4)  Macrostoma  Alexeieff,  1909, 
nee  Latreille,  1825;  (5)  Fanapepea  Prowazek,  1911;  (6)  Tetramitus 
Brumpt,  1912,  nee  Perty,  1852;  (7)  Difamus  Gabel,  1914;  (8)  Cyatho- 
mastix  Prowazek  and  Werner,  1914. 

Definition. — Tetramitidinae  with  large  cytostome,  three  anterior 
flagella,  but  no  free  trailing  flagellum. 

Type  Species. — Chilomastix  caulleryi  Alexeieff,  1909.  Synonym  : 
Macrostoma  caulleryi  found  in  the  intestine  of  tadpoles. 

Other  Species.- — C.  mesnili  Wenyon,  1910;  C.  motella  Alexeieff, 
1912;  C.  bittencourti  da  Fonseca,  1915;  C.  caprce  da  Fonseca,  1915; 
C.  cuniculi  da  Fonseca,  1915. 


35° 


MASTIGOPHORA   AND  PROTOMONADINA 


These  species  may  be  differentiated  as  follows : — 

A.  Characters  known  to  us  : — 

I.  Size  large  ;  20-25  microns  in  length  : — 

Flagella  easily  seen  in  cysts  which  resemble  C.  mesnili 
cysts  in  size  and  appearance — (1)  Caulleryi. 
II.  Size  medium  ;  n-18  microns  in  length  : — ■ 

(a)  Cytostome  long;  cysts  about  7x5-6  microns  in 

which  the  anterior  flagella  are  difficult  to  see— 
(2)  Mesnili. 

(b)  Cytostome  very  short;  cysts  large,   about   8x6 

microns,  in  which  the  anterior  flagella  are  very 
distinct — -(3)  Bitten  court  i. 
III.  Size  small  ;  7-12  microns  in  length  : — ■ 

(a)  Nucleus  with  a  central  karyosome  connected  to  the 

blepharoplast  by  a  rhizoplast;  size  9-12  microns 
in  length — (4)  Caprce. 

(b)  Nucleus  without  a  central  karyosome  and  without 

a    rhizoplast;    size    7-9    microns    in    length — 
(5)  Cuniculi. 

B.  Characters  unknown  to  us  : — 

Found  in  species  of  Motella—(6)  Motellce. 

Chilomastix  mesnili  Wenyon,   1910. 

Synonyms. — {a)  Cercomonas  hominis  Davaine,  1869,   pro  parte ; 

(b)  Monocercomonas  hominis  Epstein,  1893,  nee  Grassi,  1879;  (c)  ^n" 

chomonas  intestinalis  Roos,   1893,   pro  parte  nee  Leuckart,   1879; 

(d)  Macrostoma   mesnili   Wenyon,    1910;   (e) 

Fanapepea   intestinalis   Prowazek,   191 1;   (/) 

Tetramitus  mesnili  Brumpt,  1912 ;  (g)  Difamus 

tiaieiisisGabel,  1914;  {h)  C yathomastix  hominis 

Prowazek  and  Werner,   1914;   (i)  Tetramitus 

bocis  Brumpt,  1912 ;  {k)  Chilomastix  intestinalis 

Kuczynski,  1914. 

Definition.— Chilomastix  of  medium  size, 
with  long  cytostome  and  with  cysts  about 
7  x  5-6  microns,  in  which  the  anterior  flagella 
are  difficult  to  see. 

Historical. — This  flagellate  appears  to  have 
been  first  noted  by  Davaine  in  i860,  being 
called  Form  A  of  Cercomonas  hominis.  Alter 
this  it  was  noted  by  Roos  in  1893,  and  by 
Epstein  in  the  same  year.  It  was  rediscovered 
and  properly  described  by  Wenyon  in  1910, 
and  later  noted  by  Prowazek  in  1911,  Nattan- 
Larrier  in  1912,  Brumpt  in  1912,  Gaebel  in 
1914,  Chatterjee  in  1915,  Wenyon  in  1915,  Da  Fonseca  in  1915  and 
1916,  Fantham  and  Porter  in  1915,  Archibald,  Hadfield  Logan,  and 
Campbell  in  1916,  Wenyon  and  O'Connor  in  1917,  Castellani  in  1917, 
and  Chalmers  and  Pekkola  in  1918. 


Fig.  77. — Chilomastix 
nicsnili  Wenyon 
1910. 

Note  the  membrane 
raised  by  the  cyto- 
stomic  flagellum. 


SUBFAMILY  TRICHOMONADINJE  351 

Remarks. — The  parasite  is  widely  distributed  all  over  the  world. 

Morphology. — -Its  shape  varies,  but  it  is  generally  pear-shaped, 
measuring  some  11-18  microns  in  length  if  the  caudal  appendage  is 
included,  and  some  1-6-4-0  microns  less  if  this  is  excluded.  There 
is  a  large  cytostome  situate  anteriorly.  The  cytoplasm  contains 
a  large,  roundish,  oval  or  slightly  irregular  chromatic  nucleus, 
anterior  to  which  lies  two  or  three  granules,  from  which  the  three 
anterior  flagella  take  their  origin.  No  rhizoplast  can  be  seen.  The 
margins  of  the  cytostome  are  thickened,  and  appear  to  contain  a 
fourth  or  posteriorly  directed  flagellum  in  the  inner  siderophilous  rim, 
while  the  outer  rim  appears  to  be  homologous  with  a  parabasal. 

Life-History. — Reproduction  takes  place  by  binary  fission  and 
cyst  formation.  The  cysts  are  usually  egg-shaped,  measuring 
7  x  5-6  microns.  The  cyst  wall  is  separated  from  the  parasite  by  a 
clear  space,  while  the  cytoplasm  contains  a  nucleus,  a  blepharo- 
plastic  mass,  and  at  times  the  mouth  margins  can  be  seen.  Division 
forms  with  two  nuclei  have  been  noted. 

Pathogenicity. — -There  is  a  difference  of  opinion.  Some  observers 
consider  it  to  be  non-pathogenic,  while  others  hold  that  it  is  may 
cause  diarrhoea. 

Subfamily  Trichomonadin^e  Chalmers  and  Pekkola,  1917. 

Definition. — Tetramitidse  with  an  axostyle. 

Classification. — -The  ten  genera  belonging  to  this  subfamily  may 
be  differentiated  as  follows: — - 

Diagnostic  Table  of  the  Trichomonadin.e. 

A.  Cytostome  absent : — 

I.  Three  anterior  flagella — (1)  Protrichomonas  Alexeieff, 

1911. 

II.  Four   anterior  flagella— (2)    Monocercomonas    Grassi, 
1879. 

B.  Cytostome  present : — ■ 

I.  Without  undulating  membrane: — 

(a)  Without  trailing  flagellum  :— 

1.  Periplast   thickened   in  places;   four  anterior 

flagella — (3)  Polymastix  Biitschli,  1884. 

2.  Periplast  not  thickened;  six  anterior  flagella 

— (4)  Hexamastix  Alexeieff,  1912. 

(b)  With  trailing  flagellum  : — 

1 .  Three    anterior    flagella : — 

(1)  Without   parabasal— (5)    Eutrichomastix 

Kofoid  and  Swezy,  1915. 

(2)  With  parabasal  wound  around  the  axo- 

style— (6)  Devescovina  Foj,  1905. 

2.  Four   anterior   flagella — (7)    Tetratrichomastix 

Mackinnon,  1914. 


352 


MASTIGOPHORA   AND  PROTOMONADINA 


II.  With   undulating  membrane: — 

i.  Three  anterior  flagella— (8)   Trichomonas  Donne, 

1837- 

2.  Four  anterior  flagella^ — (9)  1  etratrichomonas  Parisi, 

1910. 

3.  Five  anterior  flagella — (10)  Pentatrichomonas  Chat- 

terjee,  1915. 

Of  these  genera,  Trichomonas,  Tetratrichomonas,  and  Pentatri- 
chomonas concern  us. 

Genus  Trichomonas  Donne,  1837. 
Definition.- — Trichomonadinae  with  a  cytostome,  an  undulating 
membrane,  and  three  anterior  flagella. 

Remarks.— In  his  work  '  Recherches  microscopiques  sur  la  nature 
du  mucus,'  Donne  (1837)  described  and  figured  an  organism  which 
he  found  in  innumerable  quantities  in  vaginal  mucus. 

He  considered  that  it  possessed  a  single  flagellum  which  at  times 
was  bifurcated  distally,  a  series  of  three  to  five  cilia  with  very  rapid 
rotatory  movement,  and  that  at  times  it  was 
elongated  posteriorly  into  a  tail.  The  name  Was 
first  spelt  Tricomonas,  but  afterwards  altered  to 
Trichomonas. 

Dujardin  (1841)  described  T.  Umacis  from 
Limax  agrestis  in  much  the  same  terms,  and  so 
did  Perty  (1852)  with  regard  to  T.  batrachorum, 
though  he  depicted  the  axostyle,  but  Stein's 
figures  of  Perty 's  organism  show  clearly  the  three 
anterior  flagella,  the  undulating  membrane,  the 
posterior  free  flagellum,  the  axostyle,  the  nucleus, 
and  the  cytostome,  and  in  this  way  was  laid  the 
foundations  upon  which  the  main  features  of  the 
genus  were  placed. 

Returning  now  to  the  type  T.  vaginalis,  this 
was  restudied  in  1884  by  Blochmann,  who  illus- 
trated the  three  anterior  flagella,  the  undulating 
membrane,  the  axostyle.  and  the  nucleus,  but  in 
the  same  year  Kunstler  produced  a.  much  better 
illustration  showing  four  anterior  flagella  taking 
their  origin  from  a  blepharoplast  from  which  the 
undulating  membrane  also  arose,  while  this  shows 
a  trace  of  a  parabasal.  The  nucleus  is  also  represented,  while  the 
axostyle  shows  exceedingly  clearly.  He  also  saw  the  cytostome. 
Benson  (1910)  figured  two  blepharoplasts,  one  of  which  is  connected 
with  the  nucleus  by  means  of  a  rhizoplast,  and  he  also  gave  an 
illustration  of  a  cyst.  Thus  the  type  species  T.  vaginalis  was 
brought  into  line  with  the  results  of  researches  upon  the  species 
found  in  animals,  of  which  a  number  have  been  carefully  described 
and  drawn  by  Dobell,  Alexeieff,  Martin  and  Robertson,  Kuczynski, 
and  by  Kofoid  and  Swezy. 


Fig.  78. —  Tetra- 
trichomonas gal- 
linariim  (Martin 
and  Robertson, 
1912).  (x  2,000 
Diameters.) 


TRICHOMONAS  353 

The  only  difficulty  is  with  the  type  T.  vaginalis.  Does  it 
possess  three  anterior  flagella  or  four  ?  If  the  latter,  then  the  genus 
Trichomonas  has  as  a  synonym  Tetratrichomonas,  and  a  new  name 
must  be  found  for  the  forms  with  three  anterior  flagella. 

Type  Species.— Trichomonas  vaginalis  Donne,  1837. 

Morphology. — -The  essential  points  in  the  general  morphology  are 
the  pear-shaped  body,  the  small  anterior  and  ventrally  situate  cyto- 
stome  without  siderophilous  lips,  and  the  three  anteriorly  springing 
flagella  arising  (according  to  Wenyon)  from  the  anterior  of  the  two 
granules  into  which  the  blepharoplast  is  divided.  From  the  pos- 
terior granule  arises  a  posterior  flagellum,  which,  passing  backwards, 
forms  the  undulating  membrane  and  finally  terminates  in  a  free 
posterior  portion.  From  the  same  granule  arises  another  stiff  rod- 
like structure,  the  parabasal,  which  serves  as  a  support  for  the  un- 
dulating membrane,  and  often  there  is  a  row  of  granules  lying  parallel 
to  this  rod.  Springing  from  the  blepharoplast  and  directed  pos- 
teriorly over  the  nucleus  is  a  peculiar  body,  clear,  with  bounding 
lines,  which  projects  from  the  posterior  end  as  a  spine  and  often 
contains  chromatinic  granules.  Th:s  organella  is  the  axostyle,  called 
also  the  baguette  interne.  It  may  be  a  supporting  structure,  but 
it  may  also  be  concerned  in  movement.  It  does  not  stain  with 
nuclear  stains,  and  therefore  appears  clear,  while  in  the  living 
organism  it  is  a  refractile  rod. 

The  nucleus  is  usually  more  or  less  oval,  and  possesses  a  membrane, 
inside  which  the  chromatin  is  distributed  in  the  form  of  granules. 

Two  chromatinic  granules  (axoplasts)  are  often  found  where  the 
axostyle  leaves  the  cytoplasm. 

Life-History. — -Binary  division  with  its  nuclear  changes  have  been 
carefully  studied  by  Kofoid  and  Swezy .  Multiple  fission  has  also  been 
described.     Transference  from  host  "to  host  is  by  the  typical  cysts. 

Classification.— A  very  large  and  increasing  number  of  species 
of  doubtful  value  are  in  existence — -e.g.,  T .  bactrachorum  Perty,  1852, 
in  frogs;  T.  suis  Gruby  and  Delafond,  in  pigs;  T.  limacis  Dujardin, 
in  snails;  T.  lacertce  Blochmann,  in  lizards;  T.  cavice  Davaine,  in 
guinea-pigs;  T.  perronciti  Castellani,  1907,  in  monkeys;  T.  col  mil- 
itant >n,  in  pigeons.  Plimmer  and  others  have  also  recorded  a 
Tetratrichomonas  in  the  blood  of  snakes  (Fig.  79),  and  this  probably 
came  as  an  infection  from  the  alimentary  canal.  Martin  and 
Robertson  have  also  described  forms  in  fowls,  and  Kuczynski  has 
contributed  an  elaborate  paper  on  the  morphology  of  the  genus. 

Four  spscies  are  said  to  occur  in  man — T.  vaginalis,  T.  hominis, 
T.  dxscnterice,  and  T .  pulmonalis. 

While  some  differences  do  exist  in  the  animal  forms,  still  there  is 
nothing  of  a  specific  nature  to  be  found  in  the  human  and  it  is 
quite  possible  that  they  are  all  one  species,  and  that  they  are  the 
same  as  that  found  in  the  rat — viz.,  T.  intestinalis,  with  three  anterior 
flagella,  unless,  indeed,  T.  vaginalis  really  possesses  four  flagella, 
but  on  this  point  we  are  not  certain;  moreover,  Kiinstler  was  often 
wrong  with  regard  to  the  number  of  flagella  {vide  Polymastix  melo- 

23 


354  MASTIGOPHORA  AND  PROTOMONADINA 

donthcB,  which  he  said  had  six  flagella,  and  T.  intestinalis,  which  he 
depicted  with  four  flagella). 

There  is,  however,  a  peculiar  matter  which  must  be  referred  to. 
Schaudinn  stated  that  trichomonas  becomes  an  amoeba,  and  that 
two  of  these  amoebae,  after  giving  off  reduction  bodies,  became  en- 
cysted together  and  conjugated.  The  zygote  divided  into  several 
portions,  leaving  a  considerable  nucleus  de  reliquat.  Gauducheau 
has  described  amoeboid  forms  becoming  a  trichomonas,  but  such 
observations  have  failed  to  meet  with  confirmation  so  far,  and  are 
therefore  sub  judice. 

Trichomonas  vaginalis  Donne,  1837. 

Synonym. — Trichomonas  irregularis  Salisbury,  1868. 

This  parasite  lives  in  the  vagina  when  the  reaction  of  the  mucus  is 
acid.  It  is  found  in  Europe,  and  we  have  observed  it  in  Ceylon  and 
in  equatorial  Africa.  It  has  also  been  reported  to  occur  in  the 
urethra  in  men,  after  cohabitation  with  women  infected  with  the 
parasite. 

It  is  not  transferable  to  rabbits,  guinea-pigs,  or  dogs.  It  has 
not  been  cultivated,  nor  is  it  understood  how  women  become 
infected. 

T.  vaginalis  is  fusiform  or  pear-shaped  in  appearance,  length 
from  15  to  25  /li,  and  breadth  from  7  to  12  //.  The  non-flagellate 
extremity  is  pointed  and  the  flagellate  extremity  rounded.  The 
parasite  is  generally  considered  to  be  harmless,  but  we  have,  how- 
ever, found  it  much  more  frequently  in  women  suffering  from 
vaginitis  than  in  normal  women. 

Trichomonas  hominis  Davaine,  1854. 

Synonyms. — Cercomonas  hominis  Davaine,  1854;  C.  intestinalis 
Lambl,i875;  T.  intestinalis  Leuckart,  1879;  Monocercomonas  hominis 
Grassi,  1882;  Cimcenomonas  hominis  Grassi,  1883. 

The  utmost  confusion  has  existed  between  this  species,  Oicomonas 
hominis  and  T.  vaginalis.  It  has  been  found  in  cases  of  diarrhoea  in 
Europe,  India,  and  Ceylon,  but  in  small  numbers  may  be  found  also 
in  the  intestine  of  individuals  apparently  healthy ;  it  has  also  been 
reported  from  the  mouth  cavity  and  stomach.  It  seems  to  prefer 
to  live  in  alkaline  mucus. 

T.  hominis  is  pear-shaped,  with  a  breadth  of  from  18  to  25  ju, 
with  three  flagella  at  its  broadest  end,  and  an  undulating  membrane. 
The  cytoplasm  contains  a  rather  indistinct  nucleus,  and  one  or 
several  non-pulsating  vacuoles. 

It  has  not  been  transmitted  to  animals,  nor  has  it  been  cultivated. 
It  can  reproduce  by  longitudinal  division,  but  forms  are  to  be  seen 
indicating  encystment  and  conjugation.  Alexeieff  considered  at 
one  time  the  bodies  described  as  trichomonas  cysts  to  be  in  reality  an 
ascomycetes  fungus,  which  he  called  Blastocystis  enterocola  and 
Brumpt  used  the  term  Blastocystis  hominis. 


TRICHOMONAS  PULMONALIS 


355 


Trichomonas  dysenterige  Billet,  1907. 
This  Trichomonas  was  first  found  by  Billet  in  the  faeces,  and  later 
in  1912  by  Gaiiducheau,  who  believes  that  it  becomes  an  amoeba 
in  one  stage  of  its  life-history.  The  latter  observer  divides  the 
life-history  of  a  Loeschia  into — -(1)  Stage  of  parasitism  in  the  tissues; 
(2)  stage  of  saprophytism  in  the  lumen  of  the  bowel  or  in  -cultures 
when  it  lives  on  bacteria;  (3)  stage  of  free  existence  when  it  is  a 
flagellate.  He  considers  that  Loeschia  undulans  Castellani,  1904, 
is  allied  to  this  species,  although  Castellani  is  inclined  to  behe\  e 
that  it  is  a  stage  of  an  Oicomonas. 


Trichomonas  pulmonalis  Schmidt,  1895. 

This  form  has  been  found  by  Schmidt  and  St.  Artault,  Ley  den 
and  Jaffe,  in  the  sputum  and  lungs  of  persons  suffering  from  phthisis, 
gangrene,  and  putrid  bronchitis. 

Other  Species. — T.  batrachorum  Perty,  1852,  in  the  cloaca  "of 
Rana  temporaria,  R.  esculenta,  Bufo  vulgaris,  and  Hyla  arborea,  in 
Germany  and  Italy;  T.  suis  Gruby  and  Delafond,  in  the  alimentary 
canal  of  pigs;  T.  limacis  Dujardin,  in  the  gut  of  Limax  agrestis  ; 
T.  lacertce  Blochmann.  in  the  cloaca  of  Lacerta  agilis,  T.  cavice 
Davaine,  in  the  large  ^  bowel  of 
guinea-pigs;  but  this  last  may 
perhaps  be  separated  off  into  a 
separate  genus,  Trichomastix, 
with  one  long  flagellum  directed 
across  the  body.  T.  perronciti 
Castellani,  1907,  in  monkeys 
su tiering  from  diarrhoea,  is  very 
similar  morphologically  to  T. 
hominis.  T.  columbarum  Pro- 
wazek  and  Aragao  1909,  is  found 
in  the  buccal  mucosa  of  pigeons. 
Plimmer  has  shown  that  flagel- 
lates of  the  type  of  Trichomonas 
can  be  found  in  the  blood  of 
snakes.  Fxg     7Q__flagellate    of   Tricho- 

monas Type  found  in  the  Blood 
Tetratrichomonas  Parisi,  1910.  of  a  Leopardine  Snake. 

Definition. — Trichomonadinae  (After  Plimmer.) 

with  a  cytostome,  an  undulating 
membrane,  and  four  anterior  flagella. 

Type  Species. — T.  prowazeki  Alexcieff,  1909,  found  in  salamanders 
and  tritons. 

Remarks.— Alexeieff  (1909)  found  a  trichomonas-like  parasite  in 
the  terminal  intestine  of  Salamandra  maculosa,  Triton  cristatus.  and' 
Alytes  obstetricans,  and  subsequently  in  Hcemopis  sanguisuga.  This 
parasite,  measuring  to  to  14  by  4  to  7  microns,  possessed  four  free 
unequal  anterior  flagella  and  an  undulating  membrane  thrown  into 


356  MASTIGOPHORA  AND  PROTOMONADINA 

long  loose  folds,  as  well  as  a  thinnish  axostyle  and  a  nucleus  rich  in 
chromatin  and  bounded  by  a  very  definite  membrane.  He  named 
this  organism  Trichomonas  prowazeki,  but  as  it  possesses  four  and 
not  three  anterior  unequal  flagella,  Parisi  created  a  new  genus  with 
it  as  the  type. 

Tetratrichomonas  vaginalis  Castellani  and  Chalmers,  191 9. 
Kiinstler  described  Trichomonas  vaginalis  with  four  flagella,  and 
we  have  seen  forms  in  the  human  vagina  with  four  flagella. 

Tetratrichomonas  intestinalis  Chalmers  and  Pekkola,  191 9. 
Found  in  human  fasces  in  Egypt  by  Wenyon  and  O'Connor,  and 
later  by  Chalmers  and  Pekkola  in  the  Sudan. 

Genus  Pentatrichomonas  Chatterjee,  1915. 

Definition. — Trkhomonadinae  with  a  cytostome,  an  undulating 
membrane,  and  five  anterior  flagella. 

Type  Species.— Pentatrichomonas  ardindelteili  Derrieu  and  Ray- 
naud, 1914,  found  in  the  intestine  of  man  in  Africa  and  India. 

Remarks. — Chatter jee  instituted  this  genus  for  a  flagellate  which 
he  found  in  the  intestine  of  man  in  Bengal,  and  which  at  the  time 
he  called  P.  bengalensis.  This  organism  agrees  in  most  particulars 
except  measurement  with  that  mentioned  above  under  the  heading 
Hexamastix  Derrieu  and  Raynaud,  and  therefore  Chatterjee's 
generic  name  takes  the  place  of  this  Hexamastix,  but  Derrieu  and 
Raynaud's  specific  name  has  priority,  and  the  parasite  becomes 
known  as  Pentatrichomonas  ardindelteili  Derrieu  and  Raynaud,  1914, 
until  some  definite  difference  between  the  two  is  established. 

More  recently  Chatterjee  states  that  he  has  found  this  organism 
to  be  present  in  thirty-two  cases  of  chronic  dysentery. 

Pentatrichomonas  ardindelteili  (Derrieu  and  Raynaud,  1914). 
This  is  the  only  species'  and  hence  also  the  type,  and  has  the  char- 
acters of  the  genus.     It  is  found  in  man. 

REFERENCES. 

There  is  no  one  paper  or  book  which  deals  at  all  adequately  with  the  Mas- 
tigophora;  the  best  we  can  recommend  is  Saville  Kent's  'Infusoria,'  Doflein's 
latest  edition,  and  Fantham,  Stephens,  and  Theobald's  (1916)  '  Animal  Para- 
sites of  Man.'  But  none  of  these  are  any  use  without  Dujardin,  Davaine, 
and  Stein,  combined  with  Biitschli,  Kiinstler,  Klebs,  Wenyon,  Dobell,  Kofoid, 
and  Swezy,  etc.  Chalmers  and  Pekkola  have  attempted  statements  with 
regard  to  the  Tetramitidae,  with  a  view  to  clearing  up  the  existing  confusion. 

For  references,  see  Field,  H.  H.  (1912),  'Bibliographia  Protozoologica,'  Archiv 
fitr  Protistenhunde,  xxvi.,  p,  444.     Jena. 

Doflein   and   Koehler  (1912).      Ueberblick  liber   Stamm.  der  Protozoen. 

Kolle  and  Wassermann's  Handbuch  der  Pathogenen  Mikroorganismen. 

Jena. 
Minchin  (191 2).     An  Introducton  to  the  Study  of  the  Protozoa.     London. 
Prowazek  (1911-12).     Handbuch  der  Pathogenen  Protozoen.     Leipzig. 


REFERENCES  357 

Classification  :  Tetramitidae  and  Chilomastix. 

Chalmers  and  Pekkola  (1918).  Annals  of  Tropical  Medicine  and  Para- 
sitology (references),  xi.  3,  213-262.     Liverpool. 

Oicomonas. 

Saville  Kent  (1880-81).     Manual  of  the  Infusoria. 

Senn   (1900).    Engler  and  Prantl.     Pflanzenfamiliar  I..  1a,   141-147.    Leipzig. 

Prowazekia. 

Castellani  and  Chalmers   (1910).     Annual   Meeting   of   the   Far   Eastern 

Association. 
Whitmore  (191  i).     Archiv  fur  Protistenkunde,  xxii.  370:     Jena. 

Enteromonas. 

Chalmers  and  Pekkola  (191 8).  Journal  of  Tropical  Medicine  and  Hygiene, 
July  15  (references). 

Embadomonas. 

Mackinnon  (1910).  Parasitology,  vol.  iii.,  pp.  245-253;  (1911)  ibid.,  vol.  iv., 
pp.  28-38;  (1912)  ibid.,  vol.  v.,  pp.  175-189;  (1913)  Quarterly  Journal  of 
Microscopical  Science,  vol.  lix.,  pp.  297-308;  (1914)  ibid.,  vol.  lx.,  pp.  459- 
470;  (1915)  ibid.,  vol.  lxi.,  pp.  105-118.     London. 

Cercomonadidae. 

Dujardin  (1841).     Histoire  Naturelle  des  Zoophytes-Infusoires.     Paris. 
Porter  (191 8).     Publications  South  African  Institute  for  Medica.l  Research, 

No.  xi.      (Entozoa  observed  among  natives  in  Johannesburg.) 
Wenyon  (1910).     Quarterly  Journal  of  Microscopical  Science,  vol.  Iv. 
\\  1  won  and  O'Connor  (1916).     Journal  Royal  Army  Medical  Corps. 


CHAPTER  XIX 

TRYPANOSOMIDAE 

Preliminary'-  remarks — Trypanosomidae — Herpetomoninae — Trypanosominae— - 
Incertae  sedis — Leucocytozoon — Spirochaetacea- — References. 

PRELIMINARY  REMARKS. 

In  this  chapter  we  complete  the  study  of  the  Monozoa  by  considering 
the  forms  allied  to  Herpetomonas  and  to  Trypanosoma,  which 
have  been  gathered  together  into  one  family,  the  Trypanosomidae 
of  Doflein,  and  follow  this  by  a  description  of  Leucocytozoon  and 
the  Spirochetes,  of  which  the  classification  is  uncertain. 

FAMILY  TRYPANOSOMIDAE  Doflein,  190 1. 

Definition. — Monozoa  possessing  one  flagellum,  without  a  collar 
and  with  the  kinetonucleus  separate  from  the  nucleus. 

Classification. — This  family  may  conveniently  be  divided  into 
two  subfamilies  as  follows : — 

(a)  Undulating  membrane  absent  or  rudimentary  and  the  kine- 

tonucleus on  the  flagellar  side  of  the  trophonucleus — 
Subfamily  I,  Herpetomonince  Castellani  and  Chalmers, 
1919. 

(b)  Undulating   membrane   well   developed   and   the   kineto- 

nucleus on  the  aflagellar  side  of  the  trophonucleus — 
Subfamily  2,  Trvpanosomifke  Castellani) and  Chalmers, 
1919. 

SUBFAMILY  HERPETOMONIN^  Castellani  and  Chalmers, 

1919. 

Definition.- — Trypanosomidae  in  which  the  undulating  membrane 
is  cither  rudimentary  or  absent,  and  in  which  the  kinetonucleus  is 
situate  on  the  flagellar  side  of  the  trophonucleus  and  remains  there. 

Type  Genus. — Herpetomonas  Saville  Kent,  1881. 

Classification. — The  various  genera  which  used  to  be  gathered 
together  in  the  family  Herpetominidae  were — 

1.  Herpetomonas  Kent,  1881. 

2.  Leptomonas  Kent,  1881. 

3.  Crithidia  Leger  1902,  emendavit  Patton,  1908. 

4.  Leishmania  R.  Ross,rTQ03. 

358 


SUBFAMILY  HERPETOMONINM  359 

5.  Toxoplasma  Nicolle  and  Manceaux,  1908. 

6.  Piroplasma  Patton.  1895. 

7.  Achromatic  us  Dionisi,  1898. 

8.  Histo  plasma  Darling,  1906. 

Unfortunately,  there  has  been  11  inch  contusion  with  regard  to 
these  genera,  due  to  lack  of  certain  knowledge  with  regard  to  the 
morphology  and  life-histories  of  the  type  species.  The  controversy 
was  keenest  with  regard  to  the  points  as  to  whether  Herpetomonas 
and  Leptomonas  were  or  were  not  the  same  genus ;  whether  Herpeto- 
monas  and  Crithidia  are  good  genera,  or  simply  stages  in  the  life- 
cycle  of  a  trypanosome.  Briefly,  the  position  is  this:  In  1851 
Burnett  discovered  a  flagellate  in  the  house-fly,  and  called  it  Bodo 
miiscce-domesticce,  for  which  Kent  created  the  genus  Herpetomonas  in 
1881;  but  two  pages  earlier  in  his  book  Kent  created  the  genus 
Leptomonas  for  a  flagellate  which  Biitschli  had  found  in  the  intes- 
tine of  Trilobius  gracilis  in  1876.  The  only  distinguishing  features 
between  these  two  genera  are  the  presence  of  a  contractile  vacuole 
and  the  flexibility  of  the  body  in  Herpetomonas,  but  modern  research 
fails  to  confirm  the  presence  of  this  contractile  vacuole  in  Herpeto- 
monas, and  flexibility  per  se  is  insufficient  to  separate  the  two 
genera.  Prowazek,  however,  in  1904,  emended  Herpetomonas, 
describing  H.  muscce-domesticce  as  possessing  two  flagella  united  by 
a  membrane,  and  arising  from  a  flagellar-situated  diplosome;  but 
Patton,  in  1909,  and  Mackinnon,  in  1910,  have  demonstrated 
that  this  is  merely  a  stage  in  the  division  of  H.  muscce-domesticce  ; 
and  Chatton  and  Leger,  in  1911,  demonstrated  that  there  was  an 
axostyle  present  in  Leptomonas  drosophilce;  and  Chatton  later  showed 
that  the  diplosome  of  H.  muscce-domesticce  was  merely  the  remains  of 
this  axostyle.  Therefore  it  would  appear  that  the  two  genera  are 
indistinguishable,  and  might  therefore  be  united,  and,  if  so,  the  older 
name  Leptomonas  would  by  the  law  of  priority  come  into  use,  to  the 
exclusion  of  the  name  Herpetomonas  ;  and  this  may  happen,  but  it 
cannot  be  adopted  at  present,  because  the  type  species  of  the  genus 
l.rhtomonas — namely,  L.  Uitschlii  Kent,  1881 — has,  as  yet,  been 
incompletely  studied,  and  may  eventually  be  found  to  be  the  same 
as,  or  different  from,  Herpetomonas  /therefore  we  continue  to  retain 
the  two  genera  Herpetomonas  and  L.eptomonas  in  the  same  condition 
as  in  our  last  edit  inn  -that  is  to  sav,  indistinguishable  from  one 
another. 

With  regard  to  the  controversy  as  to  whether  there  is  a  genus 
Crithidia  or  not,  the  answer  is  much  simpler .  There  can  be  no  doubt 
that  crithidia-like  forms  exist  in  the  life-cycle  of  many  trypano- 
somes;  but  the  work  of  Patton,  Porter,  and  Swingle  has  clearly 
shown  that  there  is  a  separate  genus,  Crithidia  Leger,  1902,  emended 
Patton.  Further,  we  believe  that  Miss  Porter  is  correct  when 
she  states  that  Crithidia  should  be  placed  in  the  family  Trypanoso- 
midae  on  account  of  the  presence  of  an  undulating  membrane. 

With  regard  to  Leishmania,  a  better  knowledge  of  the  life-history 


360  TRYPANOSOMIDJE 

has  shown  that  this  is  merely  a  Herpetomonas  or  Leptomonas,  but 
at  the  present  time  we  retain  it  as  a  separate  genus,  as  the  full  life- 
cycle  has  never  been  completely  traced. 

So  far  we  have  been  considering  genera  in  which  there  is  no 
doubt  that  one  stage  of  the  life-cycle  is  flagellate;  now  we  turn  to 
the  other  genera,  concerning  which  doubt  is  freely  expressed  as  to 
whether  they  belong  to  the  Mastigophora  at  all. 

With  regard  to  Toxoplasma,  it  was  considered  by  some  observers 
to  be  allied  to  Leishmania,  but  it  contains  only  a  single  nucleus, 
without  evidence  of  a  kinetonucleus,  and  without  the  appearance  of 
a  flagellate  stage  on  cultivation;  and  its  life-cycle  is  little  known, 
as  is  that  of  an  apparently  allied  genus,  ElleipsisomaFra.n(;a,  1911, 
while  the  relationship  is  further  complicated  by  the  genus  Toddia 
Franca,  191 1,  which  is  said  to  arise  from  the  infective  granule. 
There  appears  to  be  more  flagellate  evidence  for  the  genus  Globidium 
Neumann,  1909.  The  so-called LeucocytozoonpiroplasmoidesThivoux 
and  Teppaz  appears  to  be  allied  to  Toxoplasma,  having  only  one 
nucleus,  and  not  developing  any  flagellate  forms  on  cultivation. 
Finally,  the  work  of  Yakimoff  and  Kohl-Yakimoff  indicates  that 
Toxoplasma  is  related  to  the  Hsemogregarines,  especially  as  Splen- 
dore's  flagellate  stage  has  not  been  confirmed  by  Laveran's 
work. 

The  genus  Piroplasma  used  to  be  classed  with  Herpetomonas 
because  flagellate  forms  had  been  found  by  several  observers,  but 
these  findings  have  been  discredited  because  (1)  they  were  discovered 
in  the  old  faulty  air-dried  smears;  (2)  the  possibility  of  their  being 
intestinal  flagellates  of  the  genus  Prowazekia,  which  entered  the 
blood  before  death  in  diseased  animals;  (3)  they  are  really  trypano- 
somes,  and  not  development  stages  of  Piroplasma  ;  (4)  the  careful 
work  of  Nuttall  and  his  collaborators  have  failed  to  demonstrate 
a  flagellate  stage. 

Achromaticus  was  placed  with  the  Herpetomoninae  because, 
according  to  Gonder,  it  always  has  a  trophonucleus  and  a  kineto- 
nucleus, while  Neumann  maintains  that  it  becomes  flagellate  in 
the  bat  mite,  Pteropus  vespertilionis.  On  the  other  hand,  Yakimoff, 
Stolnikoff,  and  Kohl-Yakimoff  deny  the  presence  of  the  double 
nucleus,  and  consider  the  parasite  to  be  a  typical  Piroplasma. 

According  to  Darling,  Histoplasma  becomes  flagellated  in  the 
lungs,  and  therefore  belongs  to  the  Herpetomoninae,  though  Rocha- 
Lima  considers  it  to  be  a  yeast,  a  view  which  we  adopt. 

Rhynchoidomonas  belongs  to  the  Trypanosominse. 

We  therefore  recognize  the  following  as  definitely  belonging  to 
the  Herpetomoninae : — 

1.  Herpetomonas  Kent,  1881. 

2.  Leptomonas  Kent,  1881. 

3.  Crithidia  Leger,  1902,  emendavit  Patton,  1908. 

4.  Leishmania  Ross,  1903. 

5.  Hcemocystozoon  Franchini,  1913. 


SUBFAMILY  HERPETOMONINJE 


361 


These  five  genera  may  be  differentiated  as  follows : — 

(a)  Undulating  membrane  absent : — 

Genera:  Herpetomonas,  Leptomonas,  Leishmania,  Hcemo- 
cystozoon.  (Probably  all  belong  to  one  and  the  same 
genus,  Herpetomonas.) 

(b)  Rudimentary     undulating     membrane     present.  ■ — Genus 

Crithidia. 
Morphology. — The  flagellate  stage  of  the  Herpetomoninae  is 
usually  an  elongated  spindle-shaped  mass  of  cytoplasm  composed 
of  an  inner  granular  endoplasm  surrounded  by  a  periplast  (ecto- 
plasm). In  the  cytoplasm  lies  a  chromatinic  mass,  the  tropho- 
nucleus,  which,  when  properly  treated,  appears  to  be  of  the  nature 
of  a  protokaryon.  On  the  flagellar  side  of  this  lies  another  mass  of 
chromatin  called  the  kinetonucleus,  and  further  back  on  the  same 
side  a  minute  bead — -the  blepharoplast — from  which  the  flagellum 


Fig.  80. — The  Life-History  of  a  Herpetomonas.     (After  Fantham.) 

passes  through  the  cytoplasm,  either  directly,  and  so  forming  no 
undulating  membrane  and  becoming  a  free  flagellum,  or  it  carries 
the  cytoplasm  with  it,  forming  a  rudimentary  undulating  membrane . 

Life-History. — The  flagellate  forms  are  usually  the  inhabitants 
of  the  intestine  of  the  arthropoda,  but  some  live  in  plants. 

They  can  multiply  in  their  arthropodal  host  by  longitudinal 
division  of  the  flagellate  stage,  but  this  may  become  rounded  binu- 
cleate  cysts,  which,  passing  from  one  host  with  the  faeces,  can  infect 
a  new  host. 

In  the  new  host  it  appears  as  a  non-flagellate  binucleate  rounded 
form,  often  called  a  Leishmania-like  body,  or  the  Leishmaniform 
stage,  which  develops  in  due  course  into  the  flagellate  stage  again. 

Thus  in  the  life-cycle  there  are  the  following  stages: — 

1.  The  flagellate  stage. 

2.  The  post-flagellate  or  encysted  stage. 

3.  The  Leishmaniform  stage. 

4.  The  flagellate  stage  again. 


362 


TR  YPA  NOSOMIDJE 


The  Herpetomoninse  are  distinct  forms,  and  are  not  stages  in 
the  life-cycle  of  a  trypanosome. 

Hereditary  Infection. — In  an  important  paper  O'Farrell  in  1913 
traced  the  infection  of  the  ovum  of ;  the  tick  Hyahmma  cegypiium 
by  Crithidia  hyalommce.    'Usually  the  flagellate  stage  is  passed  in 


T    O    O 


MEXT      OEMER/CKTIOrsI 

Fig.  81. — The  Life-Cycle  of  Crithidia  hyalommce  O'Farrell,   1913. 
(After  O'Farrell.) 

It  demonstrates  hereditary  infection.  The  arrows  in  the  infection  of  the 
ovum,  except  the  two  on  the  right-hand  side,  are  wrong.  The  left  upper 
arrow  should  run  from  the  adult  to  the  ovum;  the  other  two  arrows  should 
be  omitted. 

haemoccelic  fluid  of  the  tick,  but  about  the  time  of  and  during 
ovoposition  a  considerable  number  of  the  flagellates  enter  the  ovary, 
and  some  penetrate  by  their  aflagellar  extremity  into  the  ova,  where 
they  become  the  Leishmaniforin  stage,  which  may  form  large  plas- 
modial  masses  which  break  up  into  small  resting  forms.  This  flagel- 
late  is  therefore  strictly  parasitic  in  the  tick,  and  its  life-history 


HEREDITARY  IXFECTION  363 

resembles  that  described  by  Porter  for  Crithidia  melophagia  in  the 
fly  Melophagus  ovinus. 

Pathogenicity.  In  an  able  paper  published  in  1916  Fantham 
.1  n<  1  Porter  have  shown  that  by  feeding  and  by  inoculation  of  various 
forms  of  herpetomonads  and  crithidias  acute  and  chronic  attacks 
of  herpetomoniasis  can  be  induced  in  vertebrates.  Thus  Herpeto- 
monas jaculum,  from  Nepa  cinerea,  by  feeding,  produced  the  disease 
in  mice,  birds,  a  snake,  frogs,  newts,  and  fish;  H.  stratiomyice  from 
Stratiomvia  chameleon  in  a  mouse;  H.  pediculi  from  Pediculus 
corporis  in  mice;  H.  culicis  from  Citlex  pipiens  in  birds; 
H.  ctenocephali  from  a  flea  in  a  dog;  Crithidia  gerridis  from  Gerris 
pabulum  in  dogs,  lizards,  mice,  and  frogs.  In  the  infected  animals 
both  flagellate  and  Leishmaniform  parasites  were  present. 

These  experiments  are  of  great  importance,  and  support  the  views 
expressed  by  Archibald  that  the  method  of  infection  of  kala-azar 
in  man  is  from  aquatic  insects  and  per  os.  Experimental  herpeto- 
moniasis is  characterized  by  insidious  onset  followed  by  rapid  illness, 
splenic  and  often  hepatic  enlargement,  attacks  of  fever,  emaciation, 
and  often  death. 

Evolution  of  Herpetomoniasis. — -As  a  result  of  the  above-mentioned 
experimental  work,  Fantham  and  Porter  have  deduced  the  view 
that,  in  the  case  of  the  herpetomonads,  disease  is  in  the  making  to- 
day, and  that  as  the  result  of  change  of  habitat  (brought  about  by 
ingestion  or  insect-faecal  contamination  of  a  bite),  a  herpetomonas 
may  iind  itself  in  a  vertebrate  host,  and  there,  taking  on  its  Leish- 
maniform stage,  becomes  pathogenic,  producing  the  disease  herpeto- 
moniasis,  which  may  be  acute  or  chronic.  In  the  acute  disease  the 
flagellate  forms  abound,  while  in  the  chronic  there  are  many  more 
Leishmania-like  forms. 

Vertebrate  Reservoir. — As  a  variety  of  the  chronic  infection  may 
be  mentioned  the  vertebrate  reservoir. 

In  1914  Sergent.  Lemaire,  and  Sanevet  found  herpetomonad 
flagellates  in  the  blood  and  organs  of  a  gecko  in  areas  in  Algeria  in 
which  Oriental  sore  was  endemic,  and  suggested  that  the  possible 
carrier  was  a  phlebotomus.  In  the  same  year  Chatton  and  Le 
Blanc  found  Leishmania-like  forms  in  the  red  blood-cells  of  geckos 
in  Tunis. 

In  1915  Bayon  found  herpetomonas  in  the  alimentary  canal  of 
Chameleon  pumilus  at  Robbin  Island,  and  also  in  a  fly,  Scatophaga 
hotlentota,  and  suggested  the  possibility  of  infection  of  the  verte- 
brate by  swallowing  a  fly. 

In  1914  Lindsey  suggested  that  the  oral  Leishmaniasis  of  Paraguay 
might  have  its  reservoir  in  rattlesnakes  and  its  carrier  in  ticks  or 
Simulium  flies. 

On  the  other  hand,  the  very  careful  work  carried  out  by  Archibald 
in  the  Sudan  has  apparently  excluded  domestic  animals  as  possible 
reservoirs  of  kala-azar  in  that  region,  where  dogs  are  not  readily 
susceptible  to  the  virus,  a  fact  which  rather  tends  to  differentiate 
the  parasites  of  Sudan  kala-azar  from  those  of  the  Mediterranean. 


364  TRYPANOSOMIDM 

Method  of  Infection. — As  indicated  above,  the  method  of  infection 
would  be  by  swallowing  the  arthropod  or  some  of  its  faecal  matter 
containing  cysts,  or  by  faecal  contamination  of  its  cutaneous  bite, 
or  by  both  methods. 

Archibald's  evidence  is  against  an  insect  as  the  infective  agent  of 
kala-azar  in  the  Sudan,  which  he  suggests  is  water-borne,  in  which 
case  it  might  come  from  the  fasces  of  insect  larvae  or  an  aquatic 
arthropod. 

Treatment  of  Infections. — Preparations  of  arsenic  and  of  antimony 
are  of  great  benefit  in  treating  cases  of  herpetomoniasis  or  Leish- 
maniasis. 

Prevention. — Dodds,  Price,  and  Young  seem  to  have  had  some 
success  in  segregating  the  infected  human  cases  and  removing  the 
healthy  to  new  abodes,  and  on  theoretical  grounds  it  would  appear 
that  if  herpetomoniasis  was  endemic  in  any  region,  this  should  be 
examined  for — 

{a)  Possible  vertebrate  reservoir; 
(6)   Possible  arthropod  carrier; 

and  if  these  are  found,  even  if  they  are  only  possible,  steps  should 
be  taken  to  protect  the  inhabitants  from  them. 

Genus  Herpetomonas  Kent,  1881. 

Synonyms. — Bodo  Stein,  pro  parte  ;  Cercomonas  Dujardin,  pro  parte  ;  and 
perhaps  Leptomonas  Kent. 

Definition. — Herpetomoninae  elongated,  rod-like,  with  a  single  flagellum. 
The  kinetonucleus  is  situated  near  the  posterior  end,  so  that  the  flagellum  is 
not  attached  to  the  side  of  the  body,  but  becomes  free  at  once  and  projects 
posteriorly.  There  is  no  undulating  membrane.  The  contractile  vacuole 
is  situate  quite  close  to  the  posterior  extremity.  The  trophonucleus  lies  about 
the  middle  of  the  parasite,  and  possesses  an  achromatic  substance  with 
chromatic  granules  interspersed.     The  anterior  end  is  tapering. 

Type  Species. — Herpetomonas  musca-domesticce  Burnett,  1851. 

History. — The  genus  Herpetomonas  was  created  in  1881  by  Saville  Kent  for 
Burnett's  Bodo  muscce-domseticce,  and  since  then  many  flagellates  have,  rightly 


Fig.   82. — Diagram  of  a  Herpetomonas. 

or  wrongly,  been  classified  under  this  genus.  The  life-cycles  have  been  studied 
by  Leger  in  1903;  Prowazek,  1904;  Patton,  1907-08;  Berliner,  1909;  and  Miss 
Porter,  191 1.  At  the  present  time  there  are  two  different  views  concerning 
the  characters  of  the  genus:  (a)  Prowazek's  view,  supported  by  Chatton, 
Alilaire,  and  Berliner,  that  it  is  biflagellate;  {b)  Patton's  view,  supported  by 
Miss  Porter  and  others,  that  it  is  uniflagellate  (a  view  which  our  observations 
support). 

Remarks. — The  species  of  Herpetomonas,  though  not  parasitic  in  human 
beings,  are  important  to  the  student  of  tropical  medicine,  as  they  are  parasitic 
in  insects.  Thus,  Herpetomonas  muscce-domestica  Burnett  is  parasitic  in  the 
intestinal  canal  of  8  per  cent,  of  the  house-flies  (Prowazek),  while  others  are 
found  in  fleas  and  bugs. 


HERPETOMONA  S  M  USCJE-DOMESTICM 


365 


As  already  stated,  there  is  considerable  difference  of  opinion  concerning  the 
status  of  the  Herpetomoninae  at  the  present  moment.  A  number  of  observers, 
including  Leger  and  Sambon,  look  upon  them  as  merely  stages  in  the  life-history 
oi  ti  vpanosomes;  while  others,  such  as  Now,  McXeal,  Ross,  and  Patton,  hold 
that  they  are  probably  distinct  from  the  blood  trypanosomes.  Woodcock,  how- 
ever, is  correct  when  he  says  that  those  with  trypaniform  characters  will 
probably  be  found  to  be  stages  in  the  life-cycle  of  trypanosomes,  while  the 
more  typical  herpetomonads  will  be  found  to  be  separate  and  distinct  from 
these  parasites. 

In  other  words,  some  of  the  forms  found  in  blood-sucking  flies,  leeches,  etc., 
may  be  stages  in  the  life-cycle  of  trypanosomes,  while  other  forms,  together, 
with  thosefound  in  non-blood-sucking  flies,  and  perhaps  those  found  in  larvae, 
may  (though  it  is  open  to  question  in  the  larvae  of  blood-suckers)  belong  to  a 
truly  separate  genus.  The  life-history  of  these  forms  has  been  mainly  studied 
by  Prowazek  and  Patton,  whose  results  differ  remarkably. 


Herpetomonas  muscae-domesticae  Burnett,  1851. 

Synonyms. — Bodo    musccs-domesticce    Burnett,     1851;    Cercomonas    musca- 
domesticcB  Burnett,  1851  ;  Leptomonas  muse  (B-domest  ices  Burnett,  1851. 

This  flagellate  is  found  in  Musca  domestica  L.,  Homalomyia  scalaris 
Fabricius,  Pollcnia  rudis  F.,  Theicom\~t<  fusca  Macquart,  Lucilia  sp.  ?,  Pycno- 
soma  pulorum,  Scatophaga  lutaria 
F.,  Neuroctena  anilis  Fallen,  and 
Homalomyia  corvina  Verrall. 

Miss  Mackinnon  has  given  a 
careful  account  of  the  morpho- 
logy and  life-history  of  Herpeto- 
monas muse a- domestic ce  which 
is  found  in  the  house-fly  Musca 
domestica  Linnaeus. 

Morphology. — The  preflagel- 
late  stage  takes  place  in  the  mid- 
gut, or  more  rarely  the  hind-gut, 
of  the  fly  in  the  form  of  small 
round  or  oval  bodies,  3  to  4  ti  by 
2-5  f.t,  which  possess  a  circular  tro- 
phonucleusand  a  rod-shaped  kine- 
tonucleus,  while  a  rose-pink  area 
in  specimens  stained  by  Giemsa, 
running  from  the  kinetonucleus 
to  the  end  of  the  cell,  indicates 
the  position  of  the  future  flagel- 
lum.  This  stage  passes  into  the 
flagellate  stage  which  takes  place 
in  the  mid-gut  when  theHerpeto- 
monad  appears  as  a  rather  elon- 
gated (25  /u,  by  2-5  f£)  body,  which 
is  blunt  at  the  aflagellar  end, 
and  furnished  with  a  flagellum 
which  measures  30  ji,  and  arises 
from  a  blepharoplast  situate  near 
the  kinetonucleus.  The  rhizo- 
plast  measures  4  /i,  and  is  mark- 
edly thickened.  The  rod-shaped  kinetonucleus  is  situate  6  /.i  from  the  flagellar 
extremity,  and  measures  2  /u,  by  o-8  /a.  The  trophonucleus  is  situate  almost 
centrally,  and  measures  3  \i  by  2  /.i.  The  Doppelfaden  of  Prowazek  is  present 
as  a  line  from  the  kinetonucleus  via  the  trophonucleus  far  into  the  aflagellar 
end  of  the  body. 

Life-History.  —Herpetomonas    mitsca-domesticee   multiplies   by   longitudinal 
division,  in  which  the  rhizoplast  divides  first,  and  each  half  is  seen  to  have  a 


Fig.    83. — The    Life-Cycle   of   Herpeto- 
monas musccB-domesticcB  Burnett. 

(After  Patton.) 

i,  Fully  developed  parasite;  2-5,  stages 
of  encystment ;  6,  encysted  or  preflagellate 
form;  ya-Sa,  multiplication  of  the  pre- 
flagellate form  by  simple  division;  76-86, 
multiple  division;  9,  young  flagellate 
stage;  10,  other  form;  11,  longitudinal 
division  commencing. 


366  TRYPANOSOMID&. 

separate  blepharoplast;  but  there  does  not  appear  to  be  a  splitting  of  the 
flagellum;  on  the  contrary,  Miss  Mackhinon  believes  that  the  new  flagelluni 
grows  out  from  one  of  the  blepharoplasts,  but  for  some  time  the  two  flagella 
lie  close  together,  and  this  may  last  until  the  new  flagellum  has  reached  the 
length  of  the  old  flagellum.  It  is  in  this  stage  that  the  deceptive  appearances 
of  a  bi  flagellate  organism  is  produced.  The  kihetonucleus  divides,  and  the 
trop  ho  nucleus  also  divides  amitotically,  the  karyosome  dividing  first;  after 
this  the  cytoplasm  divides.  Division  takes  place  so  rapidly  that  the  organisms 
become  smaller  and  smaller,  and,  attaching  themselves  to  the  epithelium  of 
the  hind-gut,  encyst — -i.e. .pass  into  the  post- flagellate  stage  of  aflagellar  cysts 
(3  to  4  fi  by  3*5  to  2-5  fjC),  possessing  tropho-  and  kineto-nuclei.  These  cysts 
pass  out  in  the  faeces,  and  are  accidentally  ingested  by  the  fly  along  with  food. 

Hereditary  Infection. — No  sign  of  hereditary  infection  could  be  found,  nor 
of  sexual  reproduction. 

Other  Observations. — Prowazek  describes  asexual  reproduction  by  longi- 
tudinal division,  m  which  the  trophonucleus  divides  first,  then  the  kineto- 
nucleus,  and  lastly  the  flagellum;  while  Patton  fails  to  find  the  division  of  the 
flagellum,  and  states  that  the  second  flagellum  is  developed  as  an  outgrowth 
from  the  kinetonucleus.  Prowazek  has  seen  sexual  conjugation,  which  Patton 
fails  to  find.  Prowazek  describes  encystment,  and  considers  that  the  infection 
is  carried  by  the  fasces,  with  which  latter  statement  Patton  agrees,  Prowazek 
finds  that  the  male  and  female  parasites  penetrate  into  the  eggs  of  the  fly,  and 
undergo  therein  an  autogamy  by  etheogenesis,  in  which  the  kinetonucleus 
carries  out  the  development;  by  parthenogenesis,  in  which  the  trophonucleus 
is  active;  and  by  an  indifferent  type,  in  which  both  nuclei  participate.  There 
are,  however,  many  transitional  forms  between  these  stages.  Patton's 
description  of  the  life-cycle  is  quite  different,  and  resembles  that  which  he  has 
given  for  Crithidia  gerridis  {vide  p.  367).  He  further  supports  this  life-cycle 
by  his  previous  description  of  a  Herpetomonas  in  Culex  pipiens. 

Herpetomonas  jaculum  Leger,  1902. 

This  parasite,  which  was  found  in  the  alimentary  canal  of  Nepa  cinerea  by 
Leger,  has  been  studied  in  detail  by  Miss  Porter. 

Morphology. — This  Herpetomonas  in  the  flagellate  stage  measures  13  to  33  fi 
in  length  by  1  to  4  /j,  in  breadth,  and  is  surrounded  by  a  clear,  flexible  ectoplasm 
provided  with  myonemes,  inside  which  is  a  granular  endoplasm  with  granules 
arranged  in  such  a  way  as  to  suggest  a  cytopharynx.  The  trophonucleus  is 
oval,  the  kinetonucleus  is  fairly  large,  and  chromidia  are  found  widely  separate 
lrom  one  another.     A  blepharoplast  lies  close  to  the  well-developed  flagellum. 

Life-History. — The  flagellate  attaches  itself  to  the  wall  of  the  gut  or  to  debris, 
and  divides  until  small  motionless  forms  result,  which,  shortening  and  encyst- 
ing, form  the '  post-flagellate  stage.'  It  now  escapes  from  its  host  as  minute 
cysts  in  the  faeces,  which  are  deposited  on  the  leaves  of  water-plants.  The 
fasces  are  eaten  by  the  young  Nepa — i.e.,  there  is  contaminative  or  casual  in- 
fection, and  now  the  ingested  cysts,  which  are  small  oval  bodies,  with  tropho- 
and  kineto-nuclei,  form  the  preflagellate  stage  of  the  life-cycle,  which  passes 
into  the  flagellate  adult  stage. 

Hereditary  Infection. — In  addition,  Miss  Porter  has  seen  flagellate  forms 
pass  through  the  wall  of  the  gut  near  the  ovaries,  into  which  they  penetrate 
and  encyst,  all  of  which  is  suggestive  of  hereditary  infection. 

H.  btltschlii  Saville  Kent,  1881. 
In  Trilobiiis  gracilis,  but  it  has  not  been  perfectly  studied . 

H.  pyenosomae  Roubaud,  1904. 
In  Pycnosotna  putorium  Wiedmann,  in  Africa. 

H.  davidi  La  font,  1909. 
Described  in  Euphorbia  pilulifcra   by   Lafont,  in  Mauritius,    Ceylon,    and 
Reunion,  East  and  West  Africa,  West  Indies,  Portugal,  and  India.     We  have 


CRITHIDIA 


367 


often  found  this  species  in  Ceylon.  The  parts  of  the  plants  affected  are 
not  healthy,  and  the  disease  is  called  '  ilagellosis.'  Miss  Robertson  has  found 
a  similar  parasite  in  cotton  plants  in  Uganda.  It  measures  io^-iO'SX  1*5 
microns. 

Other  Species. — H.  gracilis  Leger,  1902,  in  the  Malpighian  tubules  of  the 
larvae  of  Tanypus  ;  H.  Icsnci  Leger,  1903,  in  the  mid-gut,  near  the  Malpighian 
tubules  of  Dasvphora  pratovum  ;  H.  subalata  Leger,  1903,  in  the  gut  of  Tabanus 
glaucopis  and  Hcsmatopota  italica  Meigen;  H.  sarcophagce  Prowazek,  1904,  in 
the  gut  of  Sarcophaga  hcsmorrhoidalis  ;  H.  bombycis  Levaditi,  1905;  H.  vespcs 
Porter,  191 1,  in  the  gut  of  Vespa  cvabro  ;  H.  ctenophthalmi  Mackinnon,  1909, 
in  Ctenophthalmns  argyrtes  ;  H.  drosophilce  Chatton  and  Alilaire,  1908,  in 
Drosophila  confusa. 

Genus  Crithidia  Leger,  1902,  emendavit  Patton,  1907. 

Definition. — Herpetomoninae,  in  which  the  schizont  is  characterized  by  an 
attenuated  posterior  end,  to  which  the  flagellum  is  attached  by  a  rudimentary 
undulating  membrane.  The  kinetonucleus  is  situated  close  to  the  tropho- 
nucleus, either  on  the  flagellar  sides  or  slightly  and  rarely  a  little  on  the 
aflagellar  aspect  of  this  structure. 


Diagram  of  a  Crithidia. 


Remarks. — In  1902  Leger  created  this  genus  for  a  flagellate  organism  which 
he  found  in  the  alimentary  canal  of  Anopheles  maculipennis,  and  in  1907  Patton 
worked  out  the  life-history  of  Crithidia  gerridis. 

Crithidia  gerridis  Patton,  1908. 

This  flagellate  is  a  parasite  in  Gt  rris  fossarum  b'abricius  and  in  a  species  of 
Microvelia,  and  in  a  water-bug  allied  to  Perillopus  found  in  Madras.  The 
flagellate  is  found  in  the  crop  of  the  insect  as  a  round,  oval,  or  pear-shaped 
body,  4  to  6  ja  in  length  and  3  to  4  /j,  in  breadth,  in  which  lie  a  circular  tropho- 
nucleus  and  a  rod-shaped  kinetonucleus. 

The  parasite  grows  and  becomes  vacuolated,  showing,  when  coloured,  a 
small  pink  staining  area  between  the  kinetonucleus  and  the  periphery,  which 
later  becomes  a  distinct  pink  rod,  and  is  a  rudimentary  flagellum  attached  by  a 
rudimentary  undulating  membrane  to  the  cell.  This  membrane  shows  as  a 
faint  pink  band  between  the  flagellum  and  the  body  of  the  parasite. 

Later  the  flagellum  can  be  seen  arising  from  an  achromatic  area,  the  blepharo- 
plast,  close  to  the  kinetonucleus,  and  running  along  the  periphery  of  the  para- 
site. 

The  kinetonucleus  increases  in  size,  and  the  trophonucleus  shows  its  chromo- 
somes, while  chromatic  particles  appear  in  the  cytoplasm. 

The  kinetonucleus  now  approaches  the  trophonucleus,  and  elongates  and 
divides,  while  the  flagellum  thickens  and  splits  longitudinally,  so  that  there 
are  two  kinetonuclei  and  two  fiagella. 

The  trophonucleus  and  the  cytoplasm  now  divide,  so  that  two  daughter 
cells  are  formed,  which  in  turn  divide,  forming  rosettes  of  eight  to  forty  or 
more  cells,  measuring  6  to  10  fi  in  length  by  4  to  8  11  in  breadth. 

Eventually  the  rosettes  break  up,  and  the  rounded  parasite  has  a  central 
nucleus  and  a  kinetonucleus  at  one  side,  and  from  a  point  close  to  this  a  flagel- 
lum passes  round  its  circumference,  giving  it  an  undulating  contour.     The 


368 


TRY  PA  NOSOMIDJE 


parasite  elongates,  and  the  posterior  end  is  drawn  out  along  the  flagellum;  the 
length  is  now  15  to  45  fx  and  the  breadth  2  to  4  /x.  They  are  often  found 
agglomerated  together. 

Longitudinal  division  now  takes  place  rapidly,  and  the  parasites  pass  down 
the  intestinal  tract  and  shorten,  until  they  become  round  bodies  with  long 
llagella.     A  change  then  takes  place,  the  flagellum  becoming  absorbed  and 


Fig.  85. — The  Life-Cycle  of  Crithidia  gerridis  Patton. 
(This  is  a  diagram  constructed  from  Patton's  drawings.) 

14,  Crithidial  form;  15,  very  slender  forms;  16-18,  rounded  forms  losing 
their  flagella;  19-3,  preflagellate  round  forms,  gradually  increasing  in  size; 
4,  5,  formation  of  the  flagellum;  6-8,  division;  10,  agglomeration;  11-13, 
division. 


finally  detachul,  and  the  parasite  appearing  as  a  rounded  body  with  a  tropho- 
and  a,  kineto-nucleus.  The  life-history  is  completed  by  the  bodies  being 
discharged  with  the  faeces  into  the  water,  and  so  taken  up  by  a  new  host. 
The  ovaries  and  eggs  were  not  infected.  This  is  an  excellent  example  of 
MincMn's  contaminative  method  of  infection. 

Miss  Porter  has  fully  traced  out  the  life-history  of  C .  gerridis  found  in  Gerris 
pallidum  in  England,  and  confirms  Patton's  researches. 


LEISHMANIA  369 

Crithidia  melophagia  Flu,  1908. 

Flu  has  described  Crithidia  melophagia  in  Melophagus  ovinus,  a  parasite  of 
the  sheep.  He  gives  an  account  of  asexual  and  sexual  reproduction.  The 
latter  is  characterized  by  a  process  of  reduction,  followed  by  conjugation  with 
the  formation  of  an  ookinete  and  the  infection  of  the  eggs  of  the  insect,  which 
may  cause  a  second  generation  of  flies  to  carry  the  organism  (Fig.  90) . 

Other  Species. — C.  fasciculata  Leger,  1902,  in  the  intestines  of  females  of  the 
species  Anopheles  maciilipcnnis  and  in  Culex  fatigans  Wied.;  C.  campanulata 
Leger,  1903,  in  the  intestine  of  Chironomus  plumosus  ;  C.  minuta  Leger,  1903; 
this  parasite  is  found  in  Tabanus  tergestinus,  and  is  characterized  by  having 
a  thick  rounded  end;  C.  cleti  Hiiidle  and  Lewis,  1912,  in  Cletus  varius  Dall, 
C  pulicis  Porter,  191 1,  in  Pulex  irritans  L.,  C.  hystrichopsylles  Mackinnon, 
1909,  in  Hystrichopsylla  talpce,  and  a  number  unnamed  by  Miss  Robertson 
in  Hemiptera  in  Uganda;  Crithidia  hyalommcs  O'Farrell,  1913. 

Genus  Leishmania  R.  Ross,  1903. 

Synonyms.— Piro  plasma  Laveran  and  Mesnil,  1903,  Helcosoma 
Wright,  1903,  Herpetomonas  Rogers,  1904. 

Definition. — Herpetomoninae,  living  principally  in  endothelial 
cells,  but  also  found  in  leucocytes  and  in  the  peripheral  blood  of 
mammals  as  small,  oval,  cytoplasmic  masses  with  tropho-  and 
kineto-nuclei,  and  developing  into  flagellate  bodies  in  cultures. 

Remarks. — -Three  species  are  known  in  man,  morphologically 
similar,  but  pathogenetically  different:  Leishmania  donovani 
Laveran  and  Mesnil,  1903,  L.  infantum  Nicolle,  1908,  and  L.  tropica 
Wright,  1903,  and  probably  there  are  other  varieties. 

With  regard  to  these  species  there  is  a  general  consensus  of  opinion 
that!,,  tropica,  with  its  variety  americana,  is  distinct  from  L.  dono- 
vani and  L.  infantum.  In  respect  to  the  two  last-named  forms  it 
has  been  argued  that  they  are  identical  because : — 

I.  Both  attack  adults  and  children. 
II.  A  monkey  immunized  against  L.  infantum  is  refractory  to 
L.  donovani. 

On  the  other  hand,  there  are  some  differences,  viz.: — 

I.  It  is  true  that  both  attack  adults  and  children,  but  the  latter 

are  much  more  easily  infected  by  L.  infantum. 
II.  L.  infantum  infects  dogs  readily,  while  these  are  more 
refractory  to  L.  donovani. 
III.  L.  infantum,  according  to  one  experiment  by  Nicolle  and 
Manceaux,  only  produces  a  local  cutaneous  lesion  when 
inoculated  under  the  skin  of  a  monkey,  while  L.  donovani, 
under  similar  conditions,  according  to  Row  and  Korke, 
produces  a  local  cutaneous  lesion,  with  or  without  a 
general  infection,  when  inoculated  into  or  under  the  skin. 

For  the  present  we  shall  treat  L.  donovani  and  L.  infantum  as 
separate  parasites. 

The  Sudan  parasite  is  considered  by  Archibald  to  be  distinct 
from  L .  infantum  because : — 

24 


37°  TRYPANOSOMID2E 

I.  It  behaves  like  L.  donovani  in  that  it  does  not  readily  infect  dogs 
experimental!}'. 
II.  It  behaves  like  L.  donovani  in  that  it  produces  a  local  cutaneous 
lesion,  with  or  without  a  general  infection,  when  inoculated  into 
the  skin  of  a  monkey. 

He  further  believes  that  it  is  a  special  variety  of  L.  donovani 
because : — 

I.  It  has  signs  of  a  coccal  stage  in  its  life-history.  This  has  been 
objected  to  by  Wenyon  and  Laveran,  but  has  been  confirmed  by 
Smallman  in  two  cases  from  Malta  and  by  Stathan  and  Butler  in 
Sierra  Leone. 
II.  Experimental  evidence  is  not  in  favour  of  its  being  insect-borne. 
On  the  contrary,  careful  feeding  experiments  suggest  that  the 
method  of  infection  is  oral,  while  a  study  of  the  epidemiology  and 
other  facts  make  it  probable  that  it  is  water-borne.  The  feeding 
experiments  have  been  confirmed  by  Basile,  though  objected  to  by 
Laveran,  while  the  epidemiology  supports  facts  noticed  by  Bous- 
field,  Thomson,  and  Marshall. 
III.  The  local  lesion  produced  by  intracutaneous  inoculations  into 
monkeys  does  not  exhibit  any  eosinophile  leucocytes,  which  is 
different  from  the  lesions  produced  by  L.  tropica,  but  it  is  not 
known  whether  this  occurs  or  not  in  those  due  to  L.  donovani  and 
L.  infantum. 

We  therefore  recognize  it  as  L.  donovani  varietas  archibaldi. 

Leishmania  donovani  Laveran  and  Mesnil,  1903. 

Definition. — Leishmania,  producing  in  man  the  signs  and  symp- 
toms of  tropical  kala-azar,  in  experimental  monkeys  general  and 
local  infections,  but  not  readily  infecting  dogs. 

History. — The  history  is  fully  given  in  Chapter  XLVII.,  p.  1289, 
and  it  need  only  be  remarked  that  the  parasite  discovered  by  Leish- 
man  in  1900  was  described  by  himself  and  by  Donovan  in  1903; 
while  Rogers,  in  1904,  cultivated  the  parasite  at  220  C.  and  discovered 
the  flagellate  stage. 

Christophers,  in  1904,  considerably  added  to  our  knowledge  of 
these  parasites,  and  Patton,  in  1906  and  1907,  showed  that  they  were 
not  merely  found  more  commonly  in  the  leucocytes  of  the  peripheral 
blood  than  had  been  previously  believed,  but  that  they  could  develop 
into  typical  flagellates  in  the  bed-bug,  Clinocoris  rotundatns  Signoret, 
1852  (which  is  the  same  as  C.  macrocephalus  Fieb),  but  this  is 
apparently  more  in  the  form  of  a  natural  culture  than  of  a  cyclic 
development. 

Development  in  the  Bug. — According  to  Patton,  the  parasites  are  ingested 
by  the  bug  enclosed  in  the  large  cells  or  leucocytes,  as  just  mentioned,  and 
develop  into  fully  flagellated  forms  without  reference  to  the  temperature  of 
the  external  air. 

The  first  change  begins  usually  by  an  increase  in  size  up  to  4  to  7  fi  and  a 
vacuolation  of  the  cytoplasm  on  the  second  day,  but  may  be  deferred  for 
several  days. 

The  single  parasite  may  proceed  directly  to  flagellation  by  the  appearance 
of  an  area  stained  bright  pink  by  Giemsa,  and  called  '  the  flagellar  vacuole.' 
This  vacuole,  which  has  a  dark  centre,  rapidly  increases  in  size  up  to  1  to  3  /n, 
and,  passing  to  the  surface,  sends  out  a  small  pink  brush,  which  forms  the 
flagellum  by  merely  growing  longer.     There  appears  to  be  no  doubt  that  the 


LEISHMANIA 


37i 


flagellum  forms  in  this  vacuole   anrl  is  not  directly  connected  with  the  kineto- 
nucleus. 

The  flagellate  form  has  a  dark  blue,  granular  cytoplasm  with  a  circular 
t  rophonucleus,  which  stains  deeply  in  the  centre,  and  a  kinetonucleus  lying 


Fig.  86. — Leishmania  donovani  Laveran  and  Mesnil. 


1,  Free  binucleate  forms  (after  Christophers);  2,  endothelial  cell  and  leuco- 
cytes containing  parasites  (after  Christophers);  3,  capillary  in  the  liver, 
showing  endothelial  cells  containing  parasites  (after  Christophers) ;  4,  two 
parasites  escaping  from  a  leucocyte  in  the  alimentary  canal  of  the  bug  (after 
Patton) ;  5,  further  development  in  the  bug  (after  Patton) ;  6,  flagellate  forms 
in  the  bug  (after  Patton);  7-11,  culture  forms  (after  Leishman);  7,  8,  9  show 
the  development  of  the  flagellum. 

across  the  long  diameter,  and  situated  near  the  trophonucleuf-,  and  possessing 
a  long  flagellum  consisting  of  a  number  of  filaments  adhering  closely  together, 
inserted  into  a  pale  area  near  the  kinetonucleus.  These  parasites  may  divide 
into  two  equal  or  unequal  flagellate  forms,  and  apparently  may  go  on  so 
dividing  for  a  length  o£  time. 


372  TR  YPA  NO  SOMID& 

Instead  of  proceeding  directly  to  flagellation,  the  parasite  may  show  a 
division  of  its  nuclei  into  two,  with  the  formation  of  two  flagella,  and  then 
division  into  two  flagellate  parasites,  or  the  nuclei  may  multiply  without 
division  of  the  cytoplasm,  so  that  forms  containing  four  to  eight  nuclei  may 
be  found  together,  which  eventually  break  up  into  separate  flagellate  forms. 
Patton  has  traced  the  development  into  the  post- flagellate  stage,  and 
believes  that  if  the  bug  is  fed  upon  human  or  monkey's  blood  the  flagellates 
are  quickly  destroyed,  but  if  not  so  fed  the  cycle  of  development  is  completed 
in  ten  to  twelve  days  after  a  single  feed.  He  believes  that  this  destruction  of 
the  flagellates  by  warm  blood  is  the  cause  of  the  endemicity  of  the  disease. 

Donovan  suggests  that  the  true  host  may  be  Conorhinus  rubro- 
fasciatus,  but  Patton  finds  that  the  parasite  in  this  bug  degenerates 
and  never  flagellates. 

Further,  the  evidence  so  far  collected  does  not  support  the  possi- 
bility of  the  bug,  the  flea,  the  mosquito,  the  phlebotomus,  the 
domestic  fly,  the  louse,  or  the  tick  as  being  the  causal  agent.  It  will 
be  remembered  that  all  these  arthropods  possess  flagellates  of  their 
own,  which  the  researches  of  Fantham  and  Porter,  and  Laveran 
and  Franchini,  have  shown  to  be  capable  of  producing  disease  and 
death  in  mammals  when  injected  (vide  p.  363). 

As  examples  of  flagellates  occurring  in  bugs  we  may  quote: — 
Herpetomonas  lygcei  in  Lygcsus  militaris,  found  in  the  Sudan  and 
investigated  by  Archibald ;  H.  hospei  in  Lygceus  hospes  ;  H.  aspongopi 
Aders  in  Aspongopus  viduatus  (Sudan);  H .  pyrrhocori  in  Pyrrhocoris 
aptera  ;  also  Crithidia  in  Cletus  varius,  Gerris  fossorum,  Conorhinus 
rubrofasciatus,  Leptocoris  trivittatus  ;  also  a  trypanosome  in  Neotoma 
fuscipes.  It  is  therefore  possible  that  the  last  word  has  not  yet 
been  said  with  regard  to  arthropods  and  their  flagellates  as  the 
causal  agent  of  kala-azar. 

Archibald's  experiments  with  the  Sudan  variety  are  very  sugges- 
tive that  the  infection  may  be  per  os.  The  cycle  may  possibly  be 
from  man  via  the  faeces  to  some  water  arthropod,  from  which  it  may 
escape  also  via  the  faeces  into  water,  and  so  via  the  mouth  into 
the  alimentary  tract  and  system  of  man,  but  this  is  not  yet  proved. 
With  reference  to  this  it  should  be  remembered  that  Fantham  and 
Porter  infected  young  rats  by  feeding  with  Nepea  cinerea  containing 
Herpetomonas  jaculum. 

The  present  state  of  our  knowledge  with  regard  to  this  parasite  is  that  it  is 
the  cause  of  the  disease  called  kala-azar;  and  that  it  is  probably  spread  by 
means  of  some  arthropod,  but  the  particular  carrier  is  not  known. 

Geographical. — The  parasite  is  known  to  occur  in  India,  Ceylon,  China, 
Arabia,  Egypt,  and  the  Sudan,  and  many  parts  of  Africa. 

Morphology. — The  parasite  is  round,  oval,  or  pyriform  in  shape,  measuring 
2  to  3*5  fx  in  length  by  1-5  to  2  /x  in  breadth,  with  a  granular  cytoplasm  con- 
taining two  chromatic  masses:  the  larger,  more  rounded,  stains  slightly;  the 
smaller,  rod-shaped,  stains  deeply.  From  the  latter  a  linear  structure  (Mesnil 
and  Novy's  rhizoplast)  runs  to  the  acute  end.     A  vacuole  is  also  often  present. 

Distribution  in  the  Body. — The  parasites  are  found  sometimes  in  large 
numbers  in  endothelial  cells  in  the  capillaries  of  the  liver,  spleen,  bone-marrow, 
lymphatic  glands,  and  mucosa  of  the  intestine,  in  the  blood  from  the  femoral, 
portal,  and  hepatic  veins,  and  more  rarely  in  the  circulating  blood  shortly 
before  death. 

Parasites  liberated  from  the  large  cells  are  apparently  taken  up  by  mono- 


LEI  SUM  AN  I A   INFANTUM  *73 

nuclear,  polynuclear,  and  rarely  eosinophile  leucocytes,  and  may  be  occasion- 
ally seen  in  films  obtained  from  the  finger  even  in  early  stages  of  the  disease, 
though  more  frequently  near  the  end. 

Treutlein  has  stated  that  the  parasite  is  to  be  also  found  in  red  blood  cells, 
but  probably  the}'  are  merely  lying  in  the  concavity  of  the  red  corpuscle. 

Lite-History. — Multiplication  in  man  takes  place  by  simple  binary  fission 
and  by  multiple  division  into  three  or  more  bodies.  Division  begins  at  the 
broad  end,  but  cytological  details  are  still  wanting,  and  the  rest  of  the  life- 
cvcle  is  unknown. 

Cultivation.— Cultures  are  obtained  by  adding  the  spleen-juice  to  a  sterile 
sodium  citrate  solution  and  incubating"  at  220  C,  as  done  by  Rogers,  or  the 
N.N.N,  medium  may  be  used  (p.  377). 

Inoculation. — Monkeys,  rats,  and  less  readily  dogs  can  be  infected. 

Pathogenicity. — Leishmania  donovani  is  the  cause  of  Indian  kala-azar. 

Archibald's  Variety  of  Leishmania  donovani. 

Definition. — Leishmania  donovani,  which  does  not  readily  infect  dogs  experi- 
mentally, with  signs  of  a  coccal  stage  in  its  life-history.  There  is  evidence 
that  intection  is  by  means  of  water.     Habitat,  Anglo-Egyptian  Sudan. 

Remarks. — This  parasite  has  been  investigated  by  Bousfield,  who  reported 
also  a  natural  canine  infection  therewith  (this,  however,  has  not  been  confirmed 
by  Archibald's  many  investigations),  and  also  by  Marshall,  who  infected 
monkeys  and  performed  many  careful  experiments.  Archibald's  reasons 
for  believing  that  this  parasite  is  a  variety  of  L.  donovani  are : — 

1.  Coccal  Bodies. — Certain  coccal  bodies  have  been  noted  by  Archibald  in 
liver  smears  obtained  from  a  case  clinically  simulating  kala-azar.  Material 
obtained  by  liver  puncture  from  this  case  produced  kala-azar  when  inoculated 
into  a  monkey,  and  Archibald  suggests  the  hypothesis  that  these  coccal  bodies 
represent  a  stage  in  the  life-history  of  the  Leishman-Donovan  parasite. 

2.  Epidemiology. — In  the  Sudan  the  evidence  collected  by  Archibald  does 
not  suggest  that  the  disease  is  insect-borne.  This  observer  produced  the 
disease  in  monkeys  by  carrying  out  careful  feeding  experiments,  and  suggests 
that  the  disease  may  be  water-borne,  a  point  which  agrees  with  the  observations 
of  Bousfield,  Thomson,  and  Marshall,  that  the  disease  exists  more  commonly 
in  villages  situate  near  water  than  in  those  farther  away.  A  large  number  of 
domestic  animals  have  been  examined  by  Archibald,  and  none  have  been 
found  to  act  as  natural  hosts  of  the  virus;  even  experimental  evidence  shows 
that  dogs  are  not  readily  susceptible  to  the  virus — a  fact  which  tends  to 
differentiate  the  parasites  of  Sudan  kala-azar  from  those  of  the  Mediterranean. 

Clinically  the  disease  resembles  that  met  with  in  other  countries.  As  an  aid 
to  its  diagnosis  and  as  indication  for  splenic  puncture  being  carried  out, 
Archibald  records  the  fact  that  peripheral  blood  films  from  suspected  cases 
show  evidence  of  blood  destruction,  lcucopenia,  and  increase  of  large  mono- 
nuclears and  large  lymphocytes,  together  with  an  absence  of  eosinophiles. 
The  comparative  or  total  absence  of  eosinophiles  are  suggestive  of  the 
disease;  further,  during  the  course  of  the  disease  an  increase  or  diminution 
of  the  eosinophiles  in  the  peripheral  blood  is  some  criterion  as  to  whether 
recovery  from  kala-azar  is  likely  to  result. 

Leishmania  infantum  Nicolle,  1908. 

Synonym. — -Leishmania  donovani  Laveran  and  "Mesnil,  1903,  pro 
■parte. 

History.— In  1904  Cathoirc  observed  peculiar  bodies  in  films 
from  the  spleen  of  a  child  who  had  died  of  an  ill-defined  malady  in 
Goulette,  in  Tunisia.  These  bodies  Laveran  recognized  as  L. 
donovani.  In  1905  Pianese  announced  his  discovery  of  Leishmania 
bodies  in  large  mononuclear  cells  in  the  smears  from  the  liver  and 
spleen  of  children  dying  from  a  type  of  infantile  splenic  anaemia, 
which  he  proposed  to  call  infantile  Leishmania  anaemia  in  order  to 


374  TRYPANOSOMIDJE 

distinguish  it  from  other  forms  of  infantile  splenic  anaemia.  In  1907 
Nicolle  and  Cassuto  observed  the  parasites  in  the  spleen  of  a  child 
in  Tunisia  suffering  from  irregular  fever,  splenomegaly,  etc.,  and 
Xicolle  named  this  disease  infantile  kala-azar,  which  is  a  most 
suitable  name.  After  this  it  was  described  in  Crete  in  1907  by 
Archer;  in  Sicily,  Stromboli,  and  Calabria  by  Gabbi  and  Feletti;  in 
1910  it  was  found  in  Malta  by  Critien,  in  Lisbon  by  Alvares,  while 
Gabbi  proved  that  the  disease  '  ponos,'  as  seen  in  Spezzia,  was  the 
same  disease;  and  Christomanos,  Aravandinos,  and  Michaelides 
found  it  in  the  Grecian  islands  and  Greece  itself.  In  1911  Christo- 
monas  found  it  in  several  places  in  Greece  and  Asia  Minor,  while 
Batinos  found  it  in  Corfu,  Kefalinos  in  Paris,  and  it  was  found  to  be 
widely  distributed  in  Southern  Italy  and  Sicily;  Martzinowsky  has 
observed  cases  in  Moscow,  Tashim  Ibrahim  in  Tripoli,  Lemaire  in 
Algiers,  and  Sluka  and  Zarfl  in  Tashkent  in  Turkestan.  Marshall 
reports  the  disease  among  children  of  about  twelve  years  of  age  in 
the  Sennar  province  of  the  Sudan. 

_____^  It  is  thus  seen  that  L.  infantum  is 

mainly  found  around  the  Mediterranean 

,  basin,  but  may  extend  to  Moscow  and 

to  Turkestan ;  probably  its  geographical 

,  \      distribution    is    but    little    known    at 

^|*  -\      present. 

The  study  of  the  life-history  began 
*j  by  the  experiments  of  Xicolle,  who  in 
1908  successfully  inoculated  a  dog  in 
Tunis  intrahepatically  and  intraperi- 
toneally  with  splenic  blood  from  a  case 
of  infantile  kala-azar;  monkeys  were 
Fig.    87.— Leishmania [inf an-     a]s0  inoculated  successfully. 

turn    Nicolle,    from    the  later     Manmiix     fomte     Laveran 

Liver  of  a  Dog  experi-     _  ^ater    luanceaux,    l  omu .    L,a\  eran, 

mentally  infected.  Pettit,   Jemma,    Di   Cnstma,  Cannata, 

(From  a  microphotograph       Alvares,    da     Silva,      Pulvirenti,    and 

by  Basile.)  Tomaselli,  successfully  inoculated  dogs, 

monkeys,  and  guinea-pigs,  and  Yolpino 

produced  a   purely   local   lesion   somewhat   analogous  to  Oriental 

sor(   by  inoculating  the  cornea  of  a  rabbit  from  an  infected  dog. 

In  1908  Nicolle  and  Comte  recorded  the  discovery  of  spontaneous 
kala-azar  in  dogs  in  Tunis,  and  eventually  found  i-8  per  cent,  to 
be  infected  in  the  spring,  but  this  percentage  was  raised  by  the 
Sergents  to  7-2  per  cent,  in  the  summer  in  Algiers,  and  Sevenet  has 
found  that  in  Algiers  1-6  per  cent,  show  infection  in  the  spring  and 
8-8  per  cent,  in  the  summer.  Basile,  in  an  endemic  region,  Bordo- 
naro,  near  Messina,  found  twenty-seven  infected  dogs  out  of  thirty- 
three  examined  by  trephining  the  head  of  the  femur  and  making 
smears  of  the  bone-marrow ;  and  he  obtained  also  a  very  important 
fact  when  he  found  infected  dogs  in  every  house  where  kala-azar 
had  been  found  by  Gabbi ;  and  still  more  interesting  is  the  observa- 
tion that  infected  dogs  were  found  in  houses  without  cases  of  kala- 


LEI  SH  MAN  I A   INFANTUM  375 

azar,  but  subsequently  a  case  has  already  occurred  in  one  of  these 
houses.  Canine  kala-azar  has  also  been  found  in  Catania,  slightly 
in  Rome,  in  6«6o,  per  cent,  of  dogs  in  Greece  by  Cardamatis,  in  2*66 
per  cent,  in  Lisbon,  also  in  Malta  by  Critien  and  Babington,  and  in 
a  few  dogs  in  Colombo  by  Castellani  in  1911.  It  must  be  noted, 
however,  that  Colombo,  being  one  of  the  greatest  harbours  of  the 
world,  some  of  the  dogs  found  are  in  reality  imported  dogs.  Negative 
results  are  reported  by  Donovan  in  Madras  in  1,150  dogs,  by 
Fiilleborn  in  Hamburg  in  50  dogs,  by  Wenyon  in  Bagdad  in  no  dogs, 
by  Jemma,  Cristina,  and  Cannata  in  Palermo  in  127  dogs,  and  by 
Archibald  in  the  Sudan.  For  a  long  time  cats  were  examined  with 
negative  results,  but  recently  Ed.  and  Et.  Sergent,  Lombard,  and 
Quillchini,  have  found  a  four-month-old  kitten  to  be  infected  in 
Algeria.  It  will  thus  be  seen  that  of  all  the  endemic  centres  of 
infantile  kala-azar,  Palermo  alone  affords  no  evidence  of  natural 
canine  kala-azar. 

As  the  result  of  his  work  Basile,  supporting  Nicolle,  has  come  to 
the  conclusion  that  infantile  and  canine  kala-azar  are  one  and  the 
same  disease.  He  reared  a  number  of  dogs  in  the  laboratory  in 
Rome  (where  canine  kala-azar  is  rare),  and  some  of  these  he  took  to 
Bordonaro,  where  they  contracted  canine  kala-azar  and  died. 
The  parasites  were  found  in  the  bone-marrow,  spleen,  and  liver 
(Fig.  87),  and  also  in  Pulex  serraticeps,  taken  from  them  during 
the  last  stages  of  the  disease.  The  dogs  in  Rome  were  sub- 
sequently killed,  and  found  to  be  free  from  L.  infantum.  P. 
serraticeps  from  a  laboratory  dog  whose  bone-marrow  contained  no 
Leishmania  were  isolated  and  kept  at  220  C.  in  two  glass  vessels, 
and  eventually  one  lot  was  fed  on  spleen- juice  from  a  case  of  canine 
kala-azar,  while  the  others  were  kept  as  controls.  After  a  time  the 
intestines  of  the  fleas  were  dissected  out  and  divided  into  two 
portions — -one  Was  used  for  smears,  and  the  other  was  made  into 
an  emulsion  and  injected  subcutaneously  into  a  young  dog  one 
month  old,  the  bone-marrow  of  which  had  been  shown  to  be  free 
from  Leishmania,  while  another  dog  was  used  as  a  control. 

The  smears  from  the  infected  fleas  showed  numerous  specimens 
of  Leishmania  in  a  state  of  multiplication,  while  the  control  fleas 
were  free.  After  fifteen  days  the  dog  became  ill  with  fever  and 
loss  of  appetite  and  dejection,  and  showed  the  parasites  in  the  peri- 
pheral blood.  In  twenty-nine  days  the  dog  died,  probably  as  a 
result  of  art  operation  to  obtain  bone-marrow  from  the  tibia. 
Natural  infection  by  flea-bites  was  effected  by  introducing  a  sick 
dog  covered  with  fleas  into  a  cage  containing  a  bitch  and  two  thirty - 
day-old  puppies,  whose  bone-marrow  had  been  found  free  from 
infection.  In  thirty  days  these  dogs  were  found  to  be  infected, 
and  subsequently  the  puppies  died,  but  the  other  dogs  lived, 
Controls  were  not  infected.  Basile  found  P.  serraticeps  in  the  bed- 
clothes and  mattresses  of  families  who  kept  dogs  in  the  house,  and 
some  of  these  fleas  were  brought  to  Rome  from  dogs  or  mattresses 
of  people  living  in  Bordonaro,  and  were  fed  upon  laboratory-reared 


376  TRYPANOSOMIDJE 

marrow-examined,  clean  dogs,  whose  peripheral  blood  and  liver  had 
also  been  examined  for  parasites  with  negative  result.  The  dogs  be- 
came ill  and  died,  and  the  parasites  were  found  in  the  bone-marrow, 
liver,  and  spleen.  Control  dogs  were  then  killed  and  found  healthy. 
Basile  concludes  that  P.  serraticeps  is  the  carrier  of  the  disease. 
In  Bordonaro  he  examined  1,000  fleas  from  dogs  and  the  beds  of 
families,  but  found  only  four  infected  with  Leishmania.  With 
regard  to  P.  irritans,  Basile  finds  that  it  is  frequently  a  parasite  of 
the  dog,  and  that  among  specimens  caught  in  the  bed  of  a  child 
suffering  from  kala-azar  one  was  found  to  contain  Leishmania. 
From  experiments  he  believes  that  fleas  are  infective  from  December 
to  March.  There  is  one  curious  point  noted,  that  Leishmania  was 
found  in  spleen,  liver,  and  bone-marrow  only  a  few  days  before 
death,  though  the  fleas  had  bitten  the  dogs  three  months  earlier. 

With  regard  to  the  objections  to  this  work,  Gabbi  has  pointed  out — 

i.  Canine  and  human  fleas  placed  in  contact  with  pure  cultures  of 
Leishmania  on  Nicolle's  blood-agar  show  blood  in  the  gut,  but 
no  Leishmania. 

2.  Leishmania  in  culture  with  intestinal  bacteria  from  the  flea  or  in 

culture  with  the  juice  from  the  same  do  not  develop. 

3.  Starving  fleas  placed  in  contact  with  spleen-juice  obtained  by  puncture 

from  a  child  with  kala-azar  do  not  become  infected  with  Leishmania. 
Mazocchi  in  Piedmont  finds  that  the  fleas  of  dogs  possess  flagellate  bodies 
of  a  crithidia-like  nature,  distinct  from  Basile's  description  of  the  Leishmania 
bodies  found  by  him. 

Alvares  and  Pereira  da  Silva's  experiments  with  Ctenocephalus  serraticeps 
support  Basile,  and  they  believe  the  infection  to  be  contaminative  via  the 
faeces. 

The  main  objection  to  Basile's  experiments  is  that  they  were  conducted  in 
Rome,  in  which  place  dogs  may  acquire  natural  canine  kala-azar;  secondly, 
the  question  has  to  be  solved  as  to  whether  the  bodies  seen  in  the  flea  are  or  are 
not  Leishmania,  and  if  not,  whether  they  are  some  parasite  naturally  occurring 
in  the  flea. 

Basile  describes  the  forms  found  in  the  flea  as  follows: — 
In  the  mid-gut  Leishmania-like  forms  as  oval,  rounded,  or  pyriform  bodies, 
2  to  3  fz  in  length,  with  an  excentrically-placed  trophonucleus,  and  generally 
a  kinetonucleus.  Large  forms,  4  to  6  ft,  by  2  to  3*5  jx,  are  also  seen,  and  more 
posteriorly  pyriform  bodies,  6  to  8  /j,  by  1*5  to  2-3  /j,,  which  latter  are  provided 
with  flagella  measuring  about  3  /x  in  length.' 

Basile  concludes  that  there  is  a  cycle  of  development  with  preflagellate, 
flagellate,  and  post-flagellate  forms.  But  a  number  of  fleas  have  been  found 
to  possess  natural  parasites  belonging  to  the  genera  Herpetomonas  and  Crithidia, 
and  Miss  Porter  has  definitely  proved  that  Crithidia  pulicis  is  a  true  parasite 
of  P.  irritans.     The  list  of  known  flea  parasites  is: — 

Crithidia  pulicis  Wenyon,  1908,  in  Xenopsylla  cleopatrce. 

Crithidia  ctenophthalmi  Patton   and    Strickland,   1908,  in   Ptenophthalmus 

csgyrtes. 
Crithidia  hystrichopsyllce  Mackinnon,  1909,  in  Hystrichopsylla  talpce. 
Crithidia  pulicis  Porter,  191 1,  in  Pulex  irritans. 
Herpetomonas  ctenophthalmi  Mackinnon,  1909,  in  Ptenophthalmus  agyrtes. 

There  are  also  a  number  of  unnamed  flagellates  recorded — e.g.,  a  species  of 
Herpetomonas  by  Balfour  in  1906  in  LcBtnopsylla  cleopatra,  which  may  be 
the  same  as  Wenyon's  Crithidia.  It  does  not  appear  certain  that  Miss  Porter's 
Crithidia  and  Wenyon's  Crithidia  are  the  same,  and  if  they  are  not,  then  Miss 
Porter's  Crithidia  must  be  given  a  different  name. 


LEI SH MANIA   INFANTUM  1?7 

The  identity  of  infantile  kala-azar  and  canine  kala-azar  is  supported  also 
by  Bandi's  experiments  on  agglutination.  Animals  inoculated  by  him  with 
cultures  of  L.  infantum  developed  agglutinins  for  this  species,  and  nearly 
in  the  same  amount  also  for  the  Leishmania  isolated  from  dogs,  and  vice  versd. 

Franchini  states  that  Anopheles  maculipennis  can  be  infected  with  cultural 
forms  of  Leishmania.  Gabbi  inculpated  at  one  time  Musca  domestica  as  a 
carrier. 

Morphology.— L.  infantum  so  closely  resembles  L.  donovani  as 
to  be  indistinguishable  morphologically. 

Life-History. — It  exists  in  the  peripheral  blood,  bone-marrow, 
spleen,  and  liver  in  children,  and  suspicion  is  aroused  that  it  may  be 
spread  by  fleas,  and  that  aflagellate  and  flagellate  organisms  seen  in 
these  parasites  may  be  stages  in  the  life-cycle. 

Culture.— It  is  easily  cultivated  upon  the  Nicolle,  Novy,  MacNeal 
(or  N.N.N.)  medium,  as  was  first  shown  by  Nicolle.  The  organisms 
develop  in  the  condensation  liquid  and  on  the  moist  surface  of  the 
agar.  It  can  be  subcultured  indefinitely.  No  distinct  differences 
can  be  discerned  between  the  three  species  of  Leishmania  in  culture. 
L.  infantum  can  to  a  certain  extent  be  distinguished  from L.  donovani 
by  the  fact  that  the  latter  is  less  easily  inoculable  with  success 
into  dogs. 

Pathogenicity. — It  is  the  cause  of  infantile  kala-azar,  and  at  one 
time  was  considered  to  be  the  cause  of  canine  kala-azar,  which  we 
will  now  describe. 

Canine  Kala-Azar. — There  are  two  types  of  canine  kala-azar- — an 
acute  and  a  chronic. 

Acute  canine  kala-azar,  usually  appears  in  young  dogs,  when  it  is 
associated  with  fever  (390  to  400  C.)  of  a  remittent  type,  followed  by 
loss  of  appetite,  wasting,  tremors,  motor  disturbance  in  the  hind- 
limbs,  and  rarely  diarrhoea.  The  animal  finally  dies  in  a  comatose 
condition  at  the  end  of  three  to  five  months. 

Chronic  canine  kala-azar  begins  without  any  apparent  symptoms, 
except,  perhaps,  loss  in  weight,  but  as  it  progresses  anaemia  sets  in, 
and  tremors,  together  with  motor  disturbances  of  the  hind-limbs, 
may  be  noticed.  It  is  therefore  milder  than  the  preceding,  is  very 
chronic,  and  associated  with  considerable  enlargement  of  the  spleen. 
The  inoculated  dogs  have  several  times  been  reported  to  exhibit 
symptoms  resembling  dumb  rabies.  Post-mortem  examination 
exhibits  that  the  spleen  has  a  thickened  capsule,  with  hypertrophy 
of  the  lymphoid  elements;  the  epithelium  of  the  blood-lacuna?  are 
much  hypertrophied,  and  full  of  parasites.  The  liver  cells  show 
fatty  degeneration;  parasites  are  found  in  the  liver  cells  and  in  the 
endothelium  of  the  lymphatics.  The  interstitial  tissue  of  the  kidney 
is  increased,  and  parasites  occur  in  the  endothelial  cells.  Parasites 
may  be  found  in  the  round-celled  infiltration  under  the  capsule  of 
the  kidney.  The  suprarenal  bodies  show  cloudy  swelling  of  the 
cortical  cells,  infarcts  in  the  medulla,  and  vacuolation  of  the  cells, 
which  may  be  invaded  in  patches  by  the  parasites.  The  pancreas 
showed  a  hypertrophy  of  the  connective  tissue,  with  the  presence 
of  the  parasites  in  the  endothelium  of  the  lymphatics.     The  bone- 


378  TRYPANOSOMIDM 

marrow  showed  large  numbers  of  mononuclear  cells  with  parasites. 
The  heart  muscle  showed  cloudy  swelling.  No  parasites  are  found 
in  the  lungs. 

There  is  a  growing  suspicion  that  this  is  quite  distinct  from  any  human 
disease,  because- — 

i .  Canine  Leishmaniasis  exists  in  places  like  Marseilles,  where  there  is  no 
Mediterranean  kala-azar,  and  this  disease  exists  in  Palermo,  where 
Canine  Leishmaniasis,  according  to  Caronia  and  di  Giorgio,  is  absent. 

2.  Spagnolio  says  that  in  Bordonaro,  in  1910,  Basile  found  Canine  Leish- 
maniasis in  70  per  cent,  of  dogs  examined.  From  1910  onwards 
a  number  of  dogs  were  destroyed,  and  in  1914  a  very  large  number 
were  killed  because  of  threatened  rabies.  In  19 15  some  seventeen 
dogs  were  examined  for  Leishmania  and  found  negative,  and  yet 
the  human  endemic  disease  had  not  diminished. 

It  is  known  to  occur  in  Africa,  Europe,  and  Asia,  but  not  in  America  or 
Oceania. 

The  formation  of  a  local  sore  on  the  cornea  of  a  rabbit  must  be 
remembered  as  indicating  the  possibility  of  a  local  disease  like  that 
caused  by  L.  tropica. 

Leishmania  tropica  Wright,  1903. 

Synonyms. — Helcosoma  tropicumWright,  1903;  Crithidia  cunning- 
hami  Carter,  1909;  Sporozoon  furunculosum  Firth,  1891. 

History. — This  parasite  was  described  by  Wright  in  a  case  of 
Oriental  sore,  and  later  Martinowski  and  Bognoff  found  the  same 
parasites  in  Bouton  d'Alep.  It  is  believed  by  some  that  this  para- 
site was  first  described  by  Cunningham  in  1885,  and  more  completely 
studied  by  Firth,  who  called  it  Sporozoon  furunculosum  Firth,  1891; 
if  this  is  so,  the  correct  name  of  the  parasite  should  be  L.  furun- 
culosa  Firth,  1891. 

It  was  specially  investigated  in  1905  by  James  in  Delhi  sore, 
Lahore  sore,  and  Frontier  sore.  Nicolle  has  obtained  cultures  of 
the  parasite  on  the  McNeal-Novy  medium,  and  Carter  describes 
sexual  forms.  Carter,  Balfour,  and  Nattan-Larrier  believe,  in  our 
opinion  correctly,  that  there  are  several  varieties  or  species  included 
under  the  term  L.  tropica  ;  thus  Carter  maintains  that  the  Cambay 
sore  is  different  from  the  'clou  de  Gafsa '  of  Africa.  Werner, 
Carini,  and  Splendore  have  shown  that  the  sore  may  spread  to  or 
begin  on  mucous  membranes. 

Distribution. — It  is  found  principally  in  Asia,  in  India,  China, 
Asia  Minor,  Persia,  etc.,  but  also  occurs  in  Africa,  Algeria.  Tunisia, 
on  the  Niger  and  in  the  Egyptian  Sudan,  in  Mexico,  Panama,  and 
South  America. 

Morphology. — It  differs  in  no  morphological  respect  from  Leish- 
mania donovani  in  the  human  body,  though  certain  minor  differences 
have  been  described  in  the  flagellate  forms  in  cultures. 

Cultivation. — In  1908  Nicolle  first  cultivated  the  parasite  on  blood- 
agar  and  on  the  modified  Nicolle,  Novy,  McNeal  medium  often  called 
'  N.N.N.'     It  grew  slowly  both  in  the  liquor  of  condensation  and 


LEI SH MANIA   TROPICA  379 

on  the  agar  at  20°  to  22°  C,  producing  flagellato  and  division  forms 
on  the  fourth  day,  which  increased  in  numbers  by  the  eighth  to  tenth 
day,  when  rosettes  appeared  and  increased  in  such  numbers  that  the 
masses  were  visible  to  the  naked  eye.  After  this  a  tendency  to 
agglutination  develops  and  increases  until  after  one  or  two  months 
the  parasites  die.  The  typical  flagellate  of  these  cultures  is  herpc- 
tomad-like,  measuring  with  the  flagellum  40  to  45  fi,  with  a  breadth  of 
2  to  4  [i,  but  the  flagellum  alone  measures  16  to  20  fj,.  There  is  no 
undulating  membrane,  but  a  trophonucleus  and  kinetonucleus  can 
be  seen.  Three  types  of  flagellates  can  be  seen  in  cultures- — viz., 
one  almost  spherical,  a  second  short  and  stumpy,  and  a  third  long 
and  narrow.  Subcultures  are  best  made  from  the  tenth  to  the 
fifteenth  day,  and  these  can  be  repeated  apparently  indefinitely. 
Forty-five  generations  have  been  recorded  during  aperiod  of  eighteen 
months. 

It  is  usual  to  state  that  there  are  no  differences  between  the 
cultural  forms  of  L.  tropica  and  L.  donovani,  but  Row  considers 
that  there  are  several  points  of  difference — viz.,  that  the  flagellate 
forms  of  L.  tropica  are  longer  and  larger,  that  the  flagellum  is 
longer,  while  the  growth  is  quicker  and  may  take  place  at  higher 
temperatures  than  in  L.  donovani. 

Inoculation. — Martzinowsky,  Wenyon,  and  Patton  have  success- 
fully inoculated  themselves,  and  other  people  have  also  been  suc- 
cessfully inoculated  from  cases  of  Oriental  sore.  The  incubation 
period  varies  from  sixteen  days  to  six  and  a  half  months,  and  the 
papule  is  generally  ushered  in  with  febrile  symptoms  lasting  several 
days.  The  inoculated  sore  begins  as  a  papule,  and  becomes  a 
nodule;  when  excised  and  examined  it  presents  the  typical  ap- 
pearances of  Oriental  sore,  and  contains  L.  tropica. 

Successful  inoculations  are  recorded  from  man  to  monkeys  and 
dogs,  from  monkeys  to  man,  other  monkeys  and  dogs,  from  dogs 
to  dogs,  and  from  cultures  to  man,  monkeys,  and  dogs. 

Immunity.-  Infection  confers  immunity  if  the  cure  is  complete, 
and  if  a  sufficient  interval  has  elapsed  between  the  cure  and  the 
reinfection;  if  not,  a  condition  of  hypersensibility  is  produced,  as 
demonstrated  by  a  shortened  incubation  period.  Kala-azar  infec- 
tion ir  dogs  affords  immunity  against  /. .  tropica  during  and  after  the 
attack;  Oriental  sore  protects  monkeys  partially  or  completeby 
against  L.  donovani. 

Insect  Carriers. — No  insect  at  present  has  been  demonstrated  to 
be  the  true  host  of  L.  tropica.  Mitsca  domestica  may  possibly  be  a 
carrier  because  the  parasites  can  retain  their  vitality  therein,  and 
may  be  transferred  to  any  raw  surface,  and  thus  induce  infection; 
but  it  is  not  a  true  host,  though  Row  has  found  the  contents  of  the 
gut  to  be  infective,  and  believes  that  infection  can  be  spread  by  its 
faeces.  There  can  be  no  doubt  that  a  natural  culture  producing 
flagellates  and,  according  to  Patton,  even  post-flagellate  forms,  can 
take  place  injthe  bed-bug  Clinocoris  rotundatus,  but  all  attempts  at 
transmission  have  failed,  and  the  same  condition  of  affairs  holds 


380  TRYPANOSOMIDJE 

good  for  Stegomyia  fasciata.  Phlebotomus  is  suspected,  but  there 
is  no  experimental  evidence.  Flu  suspects  ticks  as  being  the 
possible  carriers  in  Dutch  Guiana.  Pediculi  have  no  supporters, 
and  Stomoxys  is  not  regarded  as  a  likely  carrier.  As  Patton  has 
recorded  the  presence  of  L.  tropica  in  the  peripheral  blood,  it  might 
not  be  necessary  for  a  blood-sucker  to  ingest  juices  from  the  local  sore . 
Pathogenicity. — It  is  the  cause  of  specific  sores  found  in  the  skin 
and  on  mucous  membranes  in  Asia,  Africa,  and  America,  and  which 
are  commonly  known  as  Oriental  sore,  but  which  also  have  a  large 
number  of  local  names,  such  as  pian-bois,  espundia,  Delhi  sore, 
Bagdad  button,  clou  de  Gafsa,  ulcer  of  Bauru,  etc. 

Laveran  and  Nattan-Larrier  have  created  the  variety  americana  (L.  tropica 
Wright  var.  americana  Laveran  and  Nattan-Larrier)  for  the  Leishmania  found 
in  Espundia,  characterized  by  a  flattened  nucleus.  Vianna  has  created  a  new 
species,  L.  braziliensis,  for  a  Leishmania  observed  by  him  in  cases  of  ulcer,  but 
Marchoux  doubts  whether  this  new  species  is  justifiable,  as  it  has  no  distinc- 
tive characters. 

SUBFAMILY  TRYPANOSOMINiE  Castellani  and  Chalmers, 

1919. 

Definition. — Trypanosomidae  in  which  the  kinetonucleus  is 
situate  in  certain  stages  of  the  life-cycle  between  the  trophonucleus 
and  the  aflagellar  extremity  of  the  body .  A  well-developed  undulat- 
ing membrane  is  present. 

Type  Genus. — Trypanosoma  Gruby,  1843,  emend avit  Laveran  and 
Mesnil,  1901. 

Classification.- — -A  brief  history  of  the  discovery  of  the  more 
important  species  of  this  family  has  been  given  in  Chapter  I.  The 
genera  which  have  been  described  are : — 

Trypanosoma  Gruby,  1843,  emendavit  Laveran  and  Mesnil,  1901. 
Trypanoplasma  Laveran  and  Mesnil,  1901,  emendavit  1904. 
TrypanopJiis  Keysselitz,  1904. 
Endotrypanum  Mesnil  and  Brimont,  1908. 
Schizotrypanum  Chagas,  1909. 
Rhynchoidomonas  Patton,  1912. 

But  Trypanoplasma  and  Trypanophis  belong  to  the  Bodonidae, 
and  not  to  the  Trypanosomidae  {vide  p.  337). 

Endotrypanum  would  appear  to  be  an  immature  trypanosome, 
without  an  undulating  membrane,  and  parasitic  in  red  corpuscles. 
In  1905  Nissle  drew  attention  to  the  occasional  invasion  of  red  cells 
by  trypanosomes,  and  in  1904  Moore  found  peg-shaped  bodies  in 
the  red  blood-corpuscles  of  cattle  suffering  from  trypanosomiasis  in 
Southern  Nigeria. 

With  regard  to  Schizotrypanum,  it  was  at  first  classified  as  a 
trypanosome,  but  when  its  peculiar  schizogony  became  known,  it 
was  thought  necessary  to  separate  it  therefrom  under  a  separate 
generic  name,  and  to  this  we  now  adhere. 

The  subfamily  therefore  contains  the  genus  Trypanosoma,  of 


SUBFAMILY  TRYPANOSOMINM  381 

which  we  shall  presently  suggest  a  classification  {vide  p.  395), 
and  the  genera  Endotrypanum,  Schizotrypanum,  and  Rhynchoido- 
monas. 

Trypanosoma  Gruby,  1843. 

Synonyms. — Amoeba  Mayer,  1843;  Paramecium  Mayer,  1843; 
Globularia  Wedl,  1850;  Undidina  Lankester,  1871;  Herpetomonas 
Kent,  1878;  Hcematomonas  Mitrophan,  1883;  Trypanosomonas 
Danilewsky,  1885;  Trypanozoon  Luehe,  1906. 

Definition. — Trypanosominae,  with  the  periplast  raised  into  a 
longitudinal  undulating  membrane,  along  which  the  single  flagellum 
runs. 

Historical. — The  history  of  the  genus  has  been  largely  detailed 
in  Chapter  I.,  and  we  need  only  remind  the  reader  it  commenced 
by  Valentin,  in  1841,  reporting  minute  bodies  in  the  blood  of 
Salmofario  Linnaeus,  the  brown  trout,  which  induced  Gluge  to  bring 
forward  his  discovery  of  Trypanosoma  sanguinis  in  frog's  blood, 
while  Gros,  in  1845,  found  them  in  mice  and  moles.  Later,  in  1850, 
Wedl  found  the  same  parasites  in  the  blood  of  birds  and  mammals, 
while  Chaussat  in  the  same  year  and  Lewis  in  1879  found  them  in 
rats,  and  Danilewsky  studied  their  structure  and  started  interest  in 
them. 

Morphology. — The  usual  form  in  which  trypanosomes  are  found 
in  vertebrate  blood  is  that  of  an  elongated,  spindle-shaped  mass  of 
cytoplasm  composed  of  an  inner  granular  endoplasm,  and  surrounded 
by  ectoplasm  (periplast).  The  shape  of  the  parasite  is,  however, 
by  no  means  always  a  spindle,  but,  on  the  contrary,  varies  con- 
siderably in  different  species,  and  may  even  be  rounded. 

In  the  endoplasm  is  situated  a  trophonucleus,  often  called  the 
'  nucleus,'  concerning  the  structure  of  which  there  is  considerable 
difference  of  opinion.  Some  authorities — e.g.,  Prowazek,  etc. — 
with  regard  to  the  nucleus  of  T.  lewisi  and  T.  brucei,  and  Miss 
Robertson,  with  regard  to  T.  raice,  say  that  the  nucleus  is  complex 
and  resembles  the  description  already  given  for  that  of  Hcemoproteus 
noctuce,  that  of  T.  lewisi  having  eight  chromosomes  and  a  centrosome 
connected  by  a  strand. 

Other  authorities,  like  Ross  and  Moore,  Breinl  and  Hindle,  con- 
sider that  observers  have  been  led  astray  by  using  dried  films;  for, 
according  to  them,  though  pretty  pictures  of  the  parasite  are  pro- 
duced by  this  method,  still,  such  delicate  structures  as  the  details 
of  the  nucleus  are  ruined;  and  therefore,  in  order  to  study  these 
bodies  accurately,  the  films  must  be  fixed  while  wet  in  such  a  reagent 
as  Fleming's  fluid,  and  suitably  stained.  If  this  is  done  properly, 
according  to  them,  it  is  seen  that  the  nucleus  is  a  vesicle  bounded  by 
a  nuclear  membrane,  and  having  in  its  centre  one  small  chromatin 
sphere,  called  by  some  the  intranuclear  centrosome. 

Situated  somewhere  in  the  cytoplasm,  and  generally  near  the 
aflagellar  extremity,  is  another  mass  of  chromatin,  the  kinetonuclcus. 
From  this  kinetonucleus  a  faint  strand — the  rhizoplast — proceeds, 


382 


TR  YPA  NO  SO  MI  DM 


which  ends  in  a  little  bead — the  blepharoplast — from  which  the 
flagellum,  which  is  also  composed  of  chromatin,  arises.  A  more 
primitive  arrangement  is  for  the  kinetonucleus  to  contain  the  blepha- 
roplast, which  is  really  only  a  centrosome.  Under  these  circum- 
stances the  flagellum  will  arise  from  the  kinetonucleus.  When  the 
blepharoplast  is  separate  from  the  kinetonucleus  it  is  a  moot  point 
as  to  whether  there  is.  or  there  is  not  another  centrosome  in  that 
nucleus. 

The  flagellum  runs  outwards  through  the  endoplasm  to  the  ecto- 
plasm, which  it  raises  into  a  membrane,  the  undulating  membrane, 
and  turns,  and  runs  along  the  remaining  length  of  the  cytoplasm,  in 
which  it  may  end,  or  it  may  project  as  a  free  lash  beyond  the  cyto- 
plasm. In  this  course  it  presents  three  portions:  (i)  The  root  in 
the  endoplasm;  (2)  the  undulating  portion  in  the  ectoplasm,  and 
(3)  the  free  portion.  In  some  stages  of  the  life-history  the  flagellum, 
instead  of  turning  along  the  undulating  membrane,  projects  from 
its  blepharoplast  through  the  endo-  and  ecto-plasm  to  the  outside 
of  the  parasite. 


anterior  end 
vacuole 


undulating  membrane 


flagellum 


kinetonucleus 


trophonucleus  chromatoid   granules 


Fig. 


-Diagram  showing  the  Structure  and  Polarity  of  a 
Trypanosome. 


The  undulating  membrane,  therefore,  is  the  layer  of  ectoplasm 
(periplast)  raised  from  the  surface  of  the  parasite  by  the  second 
portion  of  the  flagellum  along  a  line  sometimes  called  dorsal,  and 
ma}'  be  prolonged  a  certain  distance  along  what  is  generally  con- 
sidered to  be  its  free  portion.  The  membrane  is  variously  described 
as  being  homogeneous  or  strengthened  by  myonemes  as  in  Hcemo- 
proteus  noctuce. 

Besides  these  structures  the  endoplasm  often  contains  a  vacuole, 
looked  upon  by  some  observers  as  a  contractile  vacuole,  while  others 
deny  its  existence.  There  is  no  doubt  about  its  existence  in  Try- 
panosoma castellanii.  Chromatoid  granules  can  also  be  seen  in 
the  cytoplasm. 

Before  leaving  this  part  of  the  subject  it  must  be  noted  that 
many  authors  have  given  various  names  to  the  trophonucleus, 
kinetonucleus,  centrosome,  and  blepharoplast.  We  use  the  terms 
in  the  same  sense  in  which  they  have  been  used  by  Minchin  and 
Woodcock — viz.,  the  principal  nucleus  is  a  trophonucleus,  because 
it  is  believed  to  be  largely  concerned  in  nutrition;  it  contains  an 
achromatic  body,  which  is  the  centrosome.  The  smaller  nucleus 
is  a  kinetonucleus,  because  it  is  mainly  concerned  in  motion ;  while 
the  little  bead  connected  with  the  flagellum  is  looked  upon  as  a 


TRYPANOSOMA  383 

blepharoplast,  because  it  is  an  achromatic  body  connected  with  a 
cilium  or  a  flagellum . 

We  now  come  to  a  point  on  which  there  is  a  great  difference  of 
opinion — viz.,  the  polarity  of  the  parasite.  There  can  be  no  doubt, 
in  our  opinion,  that,  as  a  rule,  the  anterior  end  of  a  parasite  should  be 
the  non- flagellate  end,  as  first  suggested  by  Sambon,  because,  in 
wending  its  way  through  the  blood,  that  end  goes  first,  and  the 
undulating  membrane  and  flagellum  follow,  and  blood  being  the 
natural  habitat  of  the  parasite,  this  method  of  propulsion  must  be 
considered  to  be  normal.  Moreover,  morphologists  (Woodcock) 
support  this  view.  There  is,  however,  no  doubt  that,  at  times,  the 
flagellate  end  can  be  in  front. 

Movement  is  largely  caused  by  the  undulating  membrane,  while 
the  flagellum  assists;  but  creeping  or  gregarinoid  movements  have 
been  noted  by  Leger,  and  zigzag  movements  by  Gray  and  Tulloch, 
and  in  both  of  these  the  non- flagellate  ends  go  first.  In  this  work 
anterior,  therefore,  means  the  non-flagellate  end  of  the  trypanosome 
and  posterior  the  flagellate  end. 

The  anterior  end  is  very  variable,  and  may  be  even  amoeboid, 
while  the  posterior  end  is  generally  tapering,  because  the  cytoplasm 
extends  some  way  along  the  flagellum. 

It  has  already  been  noted  that  the  body  of  the  parasite  is  slightly 
compressed  laterally,  and  the  edge  with  the  undulating  membrane 
is  considered  to  be  dorsal.  In  some  species  a  supporting  structure 
somewhat  of  the  nature  of  an  axostyle  has  been  described. 

The  measurements  of  the  parasite  are  from  the  non-flagellate 
extremity  to  the  kinetonucleus,  from  that  to  the  anterior  end  of 
the  trophonucleus,  from  that  to  the  posterior  end  of  the  tropho- 
nucleus,  from  that  to  the  tip  of  the  flagellum,  the  sum  of  these 
giving  the  length;  while  the  width  is  taken  in  the  region  of  the 
trophonucleus. 

Stephens'  method  of  measurement  is,  after  outlining  the  parasite,  to  draw 
a  straight  line  on  a  piece  of  transparent  paper,  and  to  mark  one  end,  which  is 
made  to  coincide  with  one  extremity  of  the  outlined  trypanosome  and  then 
transfixed  by  a  vertical  needle.  The  transparent  paper  is  now  rotated  so  that 
the  line  runs  in  the  long  axis  of  the  parasite.  Where  it  deviates  another  pin  is 
inserted  and  the  first  removed.  The  transparent  paper  is  again  rotated  to 
take  in  another  portion  of  the  axis  of  the  parasite,  and  this  is  repeated  until 
all  the  deviations  of  the  parasite  have  been  followed  and  the  distal  extremity 
reached. 

The  results  of  careful  measurements  have  been  to  show  that  some  trypano- 
somes  are  polymorphic  and  others  are  not. 

Food  is  absorbed  by  osmosis  from  the  liquid  in  which  the  parasite 
is  living. 

Life-History. — -The  life-history  of  a  trypanosome  is  not  as  yet 
fully  known,  but  it  is  recognized  that  it  has  an  alternation  of  genera- 
tions associated  with  an  alteration  of  hosts,  one  generation  being 
usually  completed  in  the  blood  of  a  vertebrate,  and  the  other  in  the 
alimentary  canal  and  its  appendages  of  some  blood-sucking  in- 
vertebrate. 


3«4 


TR  YPA  NO  SO  MI  DM 


In  the  Vertebrate. — If  an  uninfected  or  clean  non-immune  is  in- 
fected by  the  bites  of  infective  invertebrates,  at  first  no  parasites 
are  to  be  found  in  the  peripheral  blood,  and  some  days  must  elapse 
before  they  appear.  This  interval  is  the  incubation  period.  What 
takes  place  during  this  period  is  but  little  known,  the  only  observa- 
tions being  those  by  Fantham,  who  saw  a  few  rounded  forms  fifteen 


Fig.  89. — Diagram  of  the  Life-Cycle  of  Trypanosoma  lewisi  Saville  Kent, 
1S80,  in  the  Body  of  the  Rat. 

1,   Trypanosoma  lewisi;   2-10,  stages  in  rosette  formation;   11-13,   develop 

ment  of  a  small  flagellate  form  into  a  trypanosome ;  14,  binary  fission. 

(Constructed  from  drawings  by  Moore,  Breinl,  and  Hindle  in  the  Annals  of 

Tropical  Medicine  and  Parasitology .) 


to  eighteen  hours  after  inoculating  T.  castellanii  and  T.  rhodesiense 
into  rats;  and  those  by  Franca,  who  reports  the  presence  of  similar 
forms  at  a  later  stage  of  incubation.  These  are  probably  multiplica- 
tion forms,  which  are  the  parent  forms  of  the  trypanosomes  presently 
to  be  seen  in  increasing  numbers  in  the  blood. 


TRYPANOSOMA  385 

When  the  parasites  are  present  in  the  peripheral  blood,  they 
usually  show  a  marked  pleomorphism.  Thus,  in  T '.  cast ell 'ami  Miss 
Robertson  finds  short  forms  14  to  20  /*  in  length,  medium  forms 
20  to  24  //■  in  length,  and  long  forms  23  to  33  /a  in  length.  Until 
recently  it  was  usual  to  consider  these  variations  as  being  probably 
indicative  of  sexual  differentiation,  but  she  concludes  that  this  is  not 
so,  but  that  they  are  variations  due  to  different  stages  of  growth 
and  subsequent  division.  The  multiplication  of  the  trypanosome 
in  the  blood  is  usually  by  longitudinal  fission,  but  it  may  also  take 
place  by  schizogony,  with  or  without  entering  an  endothelial  or 
other  cell.  The  number  of  trypanosomes  in  the  blood  varies  con- 
siderably from  time  to  time,  apparently  in  more  or  less  regular 
cycles;  and  their  disappearance  appears  to  be  associated  with  the 
encystment  in  the  lungs,  spleen,  bone-marrow,  etc.,  in  the  form  of 
the  latent  bodies  described  by  Breinl,  Fantham,  and  others.  During 
their  life  in  the  vertebrate  it  was,  at  one  time,  thought  that  they 
could  propagate  their  species — -in  part,  at  all  events — by  granules, 
which  are  comparable  to  the  '  infective  granule  '  described  by 
Balfour  for  spirochetes,  because  Fry  demonstrated  that  T.  britcei 
could  throw  off  granules,  and  his  observations  had  been  confirmed 
by  Ranken.  This  granule-shedding  was  described  as  taking  place 
in  the  liver,  spleen,  lungs,  and  lymphatic  glands.  At  first  the 
granule  was  simply  a  free  pyriform  body,  but  later  it  developed  a 
flagellum  and  became  actively  motile.  Its  further  history  was,  how- 
ever, untraced  in  trypanosomes. 

There  can  be  no  doubt  that  there  is  a  reaction  on  the  part  of  the 
cells  of  the  vertebrate  against  the  trypanosomes  with  the  formation 
of  antibodies  in  the  form  of  trypanolysins,  etc.,  but  more  will  be 
said  on  this  subject  later. 

Binary  Fission. — A  binary  fission  takes  place  with  or  without 
growth.  This  is  brought  about  by  amitotic  division  of  the  kine- 
tonucleus  and  trophonucleus,  followed  by  the  formation  of  a 
new  flagellum  in  the  daughter  parasite  and  the  division  of  the 
cytoplasm. 

The  details  of  the  division  are  as  follows : — 

1.  The  kinetonucleus  swells  up  and  forms  a  vesicle  through  which 
the  chromatin  is  evenly  distributed. 

2.  The  chromatin  forms  a  band  across  the  middle  of  the  vesicle. 

3.  The  band  elongates  and  divides  into  two  portions. 

4.  The  two  portions  move  apart,  all  trace  of  the  vesicle  disappears, 
and  the  two  new  kinetonuclei  are  formed. 

5.  The  blepharoplast  divides  at  the  same  time  as  the  kineto- 
nucleus. 

6.  Either  the  old  flagellum  divides  or  a  new  flagellum  develops 
from  one  of  the  new  blepharoplasts.  The  process  varies  in  different 
species. 

7.  The  central  karyosome  of  the  trophonucleus  either  divides 
and  the  two  portions  move  to  opposite  poles  of  the  nucleus,  but  are 
connected  by  a  fine  line,  or  the  chromatin  forms  an  equatorial  plate, 

25 


386 


TRY  PA  NOSOMIDM 


which  divides  transversely,  and  each  half  goes  to  an  opposite  pole, 
or  the  chromatin  gathers  around  opposite  poles. 

8.  The  connecting  line  disappears  and  two  new  trophonuclei  are 
formed. 

Rosette  Formation. — The  medium-sized  parasite,  according  to 
Moore,  Breinl,  and  Hindle,  grows  into  large  forms,  which  pass  through 
the  following  development : — 

i.  The  trophonucleus  undergoes  reduction  by  amitosis,  the  re- 
duction body  disappearing. 

2.  The  kinetonucleus  gives  off  a  body,  which  travels — increasing 
in  size  as  it  proceeds— to  the  trophonucleus,  with  which  it  perhaps 
fuses,  but  this  is  not  definitely  known. 

In  T.  castellanii  a  strand  forms  between  the  kineto-  and  tropho- 
nuclei, instead  of  this  travelling  body,  which  is  seen  in  T.  lewisi 
and  T.  equip erdum. 


Fig.  90. — Crithidia  melophagia  Flu. 

(After  Flu.) 

1,  Microgamete;  2,  macro  gamete;  3,  zygosis;  4,  ookinete  and  degenerating 
microgamete;  5-8,  ookinete  in  the  alimentary  canal  and  ovary. 

3.  The  tropho-  and  kineto-nuclei  divide  to  form  fusion  masses  con- 
sisting of  two,  four,  seven,  or  more  small  parasites,  which  at  first 
possess  only  the  old  flagellum,  but  in  which  later  new  flagella  form 
(the  rosette  formation).  This  stage  is  not  definitely  known  in 
T.  castellanii. 

4.  The  small  parasites,  which  must  be  looked  upon  as  representing 
latent  phases,  separate  from  the  fusion  mass.  These  small  parasites 
grow  into  medium-sized  parasites,  thus  completing  the  cycle. 

All  observers  are  agreed  as  to  the  rosette  formation,  and  with 
regard  to  the  process  from  the  kinetonucleus,  this  was  first  pointed 
out  by  Miss  Robertson,  whose  work  is  therefore  confirmed.  The 
band  is  said  to  be  composed  of  volutine.  As  to  the  latent  phases, 
we  believe  that  they  are  the  same  as  the  peculiar  aflagellate  round 
and  oval  forms  described  several  years  ago  by  Castellani,  in  the 
cerebro-spinal  fluid  of  sleeping-sickness  patients,  and  which  he  com- 
pared to  the  amoeboid  forms  found  by  Plimmer  in  the  brains  of 
animals  infected  with  nagana. 


TRYPANOSOMA  3  §7 

The  development  of  Schizotrypanum  differs  in  many  points  from 
this  description,  for  the  trypanosome  enters  an  endothelial  cell  in 
the  lung,  or  a  cardiac  muscle  fibre,  or  a  neuroglia  cell  of  the  central 
nervous  system,  or  a  striped  muscular  fibre.  In  these  situations  it 
becomes  simply  a  rounded  body,  which  possesses  trophonucleus  and 
kinetonucleus,  but  has  lost  its  flagellum  and  undulating  membrane. 
This  body  undergoes  repeated  divisions,  and  each  division  eventua- 
ally  becomes  a  trypanosome. 

In  the  Invertebrate  Host. — -Theoretically,  it  would  be  expected 
that  sexual  forms,  male  and  female,  would  be  found  in  the  blood  of 
the  vertebrate,  and  that  these,  taken  into  the  alimentary  canal  of  the 
blood-sucker,  would  conjugate  and  produce  ookinetes,  and  perhaps 
oocysts,  from  which  forms  would  be  produced  which  might  infect 
the  proboscis  of  the  same  individual,  or,  by  entering  into  the  eggs, 
infect  a  new  generation,  which  alone  might  be  the  means  of  dissemi- 
nation of  the  parasite.  But  these  theoretical  views  have  so  far  not 
been  confirmed  by  actual  observations,  which  must  now  be  discussed 
seriatim. 

So-called  Sexual  Forms.— According  to  Prowazek,  T.  lewisi  can 
be  differentiated  into  three  forms — (i)  male,  (2)  female,  (3)  in- 
different; and,  according  to  Prowazek,  Liihe,  Nocht,  and  Mayer, 
the  same  can  be  seen  in  T.  castellanii ;  but  according  to  Holmes,  only 
males,  females,  and  young  females  can  be  seen  in  T.  evansi. 

Male  Forms. — 'These  are  defined  to  be  very  slender  trypanosomes, 
actively  motile,  with  an  elongated  nucleus,  which  stains  well. 

Female  Forms. — Broad,  sluggish  trypanosomes,  with  reticulated 
protoplasm  and  a  round  nucleus,  both  of  which  stain  poorly.  They 
possess  a  slender,  undulating  membrane  and  a  short  flagellum. 

Indifferent  Forms. — -These  are  the  forms  most  commonly  met  with, 
possessing  granular  cytoplasm  and  a  not  very  well-defined  nucleus. 
It  must  be  admitted  that  between  these  there  are  all  stages  of 
intermediary  forms,  so  that  they  are  not  sharply  defined ;  and  some 
of  these  may  be  simply  the  ordinary  trypanosome  in  various  stages 
of  growth  and  division,  as  described  above. 

Miss  Robertson  has  probably  arrived  at  the  truth  when  she  says 
that  the  short  forms  (13-20  microns)  of  T.  castellanii,  the  so-called 
female  forms,  are  really  the  adults,  which  by  growth  become  the 
indifferent  forms  which  are  merely  steps  in  the  formation  of  the 
slender  forms,  so-called  male  forms,  which  are  the  dividing  stage 
of  this  trypanosome. 

Chagas  has  shown  that  Schizotrypanum  cruzi  in  the  lungs  may 
lose  its  flagellum  and  become  curved  into  an  arc,  the  extremities 
of  which  fuse,  forming  at  first  a  ring,  which  subsequently  becomes 
a  sphere,  with  a  trophonucleus  and  a  kinetonucleus,  the  latter  of 
which  is  expelled  in  female  forms,  while  it  is  retained  in  male  forms. 
In  this  manner  the  macrogametocytes  and  the  microgametocytes 
arise.  Each  of  these  divides  into  eight  macrogametes,  which  are 
uninuclear,  and  eight  microgametes,  which  have  a  trophonucleus 
and  kinetonucleus  united  by  a  filament.    These  gametes  escape  from 


388  TRYPANOSOMIDJE 

the  cyst  which  is  formed  by  the  periplast  of  the  original  trypanosome, 
and  enter  red  blood-cells,  in  which  they  develop  into  sexually  differ- 
entiated trypanosomes— i.e.,  females  with  one  and  males  with  two 
nuclei.  These  are  the  forms  which  infect  the Lamus,  or  invertebrate 
host,  and  do  not  multiply  in  the  vertebrate  host. 

Method  of  Transmission. — The  blood  of  the  infected  vertebrate  is 
not  always  infective  for  the  invertebrate  host .  Thus  Miss  Robertson 
has  shown,  with  regard  to  T.  castellanii,  that  the  tsetse-fly  cannot 
be  infected  by  feeding  just  before  an  outburst  of  multiplication  in 
the  vertebrate  host,  or  during  the  period  of  destruction  which 
precedes  a  paucity  period,  or  at  the  summit  of  an  exalted  period, 
or  during  certain  periods  of  rapid  multiplication,  when  the  absolute 
and  relative  numbers  of  the  short  forms  mentioned  above  are 
diminished. 

Immediately  after  infection  the  invertebrate  host  can  mechani- 
cally convey  the  infection  to  a  clean  host,  and  this  power  persists 
for  about  twenty-four  hours,  after  which  the  invertebrate  host 
becomes  non-infective,  and  remains  so  for  a  varying  period,  which 
was  found  by  Kleine  not  to  be  less  than  eighteen  days  as  regards 
Glossina  palp  alts  and  T.  castellanii,  and  by  Kinghorn  and  Yorke 
to  be  about  fourteen  days  in  G.  morsitans  infected  with  T.  rhodesiense, 
after  which  the  flies  become  again  infective,  and  apparently  remain 
so  for  a  very  long  period,  probably  for  the  rest  of  their  lives.  These 
facts  prove  definitely  that  the  parasites  undergo  some  changes  of  an 
important  nature  in  the  flies  in  question,  and  that  the  second  in- 
fective period  cannot  possibly  be  classed  as  mechanical.  The  fact 
that  Lamus  megistus  remains  infective  ten  to  twenty-five  days  after 
feeding  on  a  host  infected  with  S.  cruzi  also  proves  that  the  infection 
is  not  mechanical.  We  therefore  draw  the  conclusion  that  the 
trypanosome  undergoes  part  of  its  life-cycle  in  the  invertebrate  host, 
and  the  first  question  which  naturally  arises  is  the  fate  of  the  so-called 
'  male  '  and  '  female  '  forms  found  in  the  blood  of  the  vertebrate. 
Are  they  true  male  and  female  forms,  and  do  they  conjugate  and 
form  an  ookinete  or  zygote  or  do  they  not  ? 

Conjugation. — -It  is  difficult  to  be  certain  that  conjugation  has 
been  seen,  and  not  division.  It  has  been  described  by  Keysselitz 
as  occurring  in  leeches  fed  on  a  carp  infected  with  Trypanoplasma 
borreli,  by  Prowazek  in  lice  fed  on  rats  infected  with  T.  lewisi, 
and  by  Flu  in  Crithidia  melophagia,  to  which  reference  will  be  made 
under  the  heading  of  Crithidia. 

On  the  other  hand,  careful  observers  like  Miss  Robertson  and 
Captain  Patton  have  quite  failed  to  set-  this  process  in  their  studies 
of  trypanosomes  and  herpetomonads.  The  conclusion  is  that 
conjugation  has  not  been  proved  to  be  present  in  trypanosomes 
so  far. 

Development  without  Conjugation.  According  to  most  observers, 
there  is  no  conjugation,  but  development  takes  place  asexually  in 
the  invertebrate  host.  This  development  varies  in  different  species, 
and  ma}7  be  classified  as  follows : — 


TRYPANOSOMA 


389 


A    Development  in  the  proboscis. 

B.  Development  in  the  anterior  portions  of  the  alimentary  canal. 

C.  Development  in  the  whole  alimentary  canal. 

D.  Development  associated  with  infection  of  the  salivary  glands. 

E.  Rectal  encystment — faecal  infection. 

F.  Ovum  infection. 

A.  Proboscian  Development. — Roubaud  has  described  a  form  of 
asexual  development  of  T.  castellanii  and  T.  brucei  in  the  proboscis 
of  Glossina  palpalis  in  which  the  undulating  membrane  disappears; 
the  flagellum  is  shortened,  and  the  kinetonucleus  approaches  the 
trophonucleus,  while  the  parasite  becomes  attached  to  the  wall 
of  the  proboscis,  and  multiplies,  forming  masses  of  parasites,  the 
whole  process  occupying  only  a  few  minutes. 

Though  he  thinks  that  this  method  of  development  explains  the 
infection  of  man  and  animals  by  tsetse-flies  in  Africa,  he  was  unable 
to  produce  infection  of  susceptible  animals  by  inoculation  of  these 
forms. 

This  form  of  development  occurs 
in  T.  vivax  and  in  T.  cazalboui. 

B.  Anterior  Development. — Miss 
Robertson  has  shown  that  the 
trypanosomes  of  fresh -water  fish, 
when  ingested  by  the  leech  Hemi- 
clepsis  marginata,  first  of  all  undergo 
rapid  multiplication  by  unequal 
binary  fission,  giving  rise  to  small 
crithidial-like  individuals,  which 
also  multiply  in  the  crop,  and  then 
towards  the  end  of  digestion  pass 
forward  as  long,  slender  trypano- 
somes into  the  proboscis  sheath, 
and  are  capable  of  infecting  a  new 
host;  while  the  crithidial  tonus 
which  remain  in  the  crop  become 

Leishmania-likc  bodies  which  multiply  again  when  fresh  blood  is 
ingested.  The  development  of  T .  vittaice  of  the  milk  tortoise  Emxda 
vittata,  takes  place  in  a  somewhat  similar  manner  in  the  leech 
Glossiphonia  sp.  (?). 

C.  Entire  Canal  Development.— This  form  of  development  is  ex- 
emplified by  T.  rajce  in  the  Leech Pontodella  muricata,  but  in  this  case 
the  trypanosomes  in  the  crop  give  rise  to  binucleate,  rounded, 
Leishmania-like  forms  without  locomotor  apparatus,  which  pass  into 
the  intestine,  where  they  become  flagellate,  and  appear  as  crithidial 
forms  and  multiply  rapidly.  During  hunger  periods  they  become 
Leishmania-like  bodies,  only  to  revert  to  the  crithidial  form  when 
food  is  ingested.  These  crithidial-like  forms  become  long,  slender 
trypanosomes,  which  pass  forward  into  the  proboscis  and  are  the 
infective  agents. 


Fig.  91. — Proboscian  Develop- 
ment.    (After  Roubaud.) 


39o 


TR  YPA  NO  SO  MI  DM 


D.  Salivary  Gland  Infection. — According  to  Bruce  and  his  col- 
laborators, if  G.  palpalis  is  fed  with  T.  castellanii,  the  proboscis  is 
not  involved  in  the  further  development.  The  fly  now  becomes 
non-infective  for  some  twenty-eight  days  on  an  average.  The 
trypanosomes  in  five  to  seven  days  disappear  (possibly  become  intra- 
cellular), but  later  return  in  a  small  percentage  of  flies,  and  multiply 
in  the  fore,  mid,  and  hind  guts,  generally  as  long,  moderately  broad 
forms,  with  protoplasm  which  stains  well,  and  contains  an  oval 
central  nucleus,  a  small  micronucleus,  undulating  membrane,  and  a 
flagellum  with  a  blepharoplast .  After  twenty -eight  days  it  is  found 
that  the  salivaiy  glands  become  infected  with  the  short,  stumpy 
forms  already  mentioned  above,  and  now  the  fly  is  found  to  be 
infective  and  to  remain  so  for  long  periods.  These  short  stumpy 
forms  have  been  noted  by  Kleine  in  the  intestine.  Miss  Robertson 
finds  that  the  trypanosomes  infect  the  salivary  glands  from  the  gut 
via  the  proboscis  and  the  salivary  ducts. 

1  2  3 


Fig.  92. — Development  of  T.  castellanii  Kruse,   1903. 

1,  In  the  vertebrate  blood;  2  and  3,  in  the  mid-gut;  4  and  5,  in  the 

hind-gut;  6,  in  the  salivary  glands  of  the  tsetse-fly. 

(After  Bruce,  Hamerton,  Bateman,  and  Mackie.) 

Kinghorn  and  Yorke  have  shown  that  the  salivary  glands  of 
Glossina  morsitans  become  infected  in  a  somewhat  similar  manner 
with  T.  rhodesiense. 

Chagas  has  seen  trypanosomes  in  the  body  cavity  and  salivary 
glands  of  Lamus  megistus,  which  are  without  doubt  the  forms 
which  are  inoculated  in  infections. 

E.  Rectal  Eticystment.—Tslmchin  finds  that  the  crithidial  forms  of 
T.  grayi  become  encysted  in  the  rectum  of  G.  palpalis. 

F.  Ovum  Infection. — This  has  not  been  proved  to  take  place. 
Conditions  influencing  Development.— Kinghorn  and  Yorke  have 

shown  that  the  development  of  T.  rhodesiense  in  G.  morsitans  is 
markedly  influenced  by  the  temperature  of  the  air,  750  to  85  °  F. 
being  more  favourable  than  6o°  to  700  F.,  and,  under  favourable 
conditions,  the  first  stage  of  development  can  take  place,  but  not  the 
later  stages,  and  flies  may  remain  with  the  parasites  incompletely 


TR  YPA  NO  SO  MA  391 

developed  for  eighty  days.  Humidity  is  without  effect.  Another 
important  matter,  as  we  shall  see  later,  is  the  effect  of  the  next 
following  clean  feed  after  an  infected  feed. 

Methods  of  Infection. — Tn  nature  there  can  be  no  doubt  that  infec- 
tion can  take  place  in  more  than  one  way,  and  Minchin  has  pointed 
out  that  the  different  methods  may  be — 

1.  Contaminative. — This  is  the  infection  of  the  host  by  swallow- 
ing encysted  parasites.  At  present  there  is  no  proof  that  this  exists 
in  trypanosomes.  But  Minchin  has  shown  that  T.  grayi  becomes 
encysted  while  lying  in  the  proctodeum  of  Glossina  fialpalis,  by  a 
shortening  of  the  flagellum  and  an  excretion  of  a  cyst-wall,  which, 
beginning  at  the  anterior  extremity,  gradually  spreads  round  the 
shortening  parasite  while  the  flagellum  is  being  absorbed.  The 
cysts  which  lie  quite  free  from  the  proctodeum  are  first  pear-shaped 
and  then  oval,  and  the  trophonuclei  and  kinetonuclei  break  up  into 
chromidia.  Minchin  believes  that  these  cysts  will  be  found  to  infect 
some  vertebrate,  but  there  is  no  proof  of  this  at  present. 

2.  Inoculative. — The  spread  of  a  trypanosome  from  one  verte- 
brate host  to  another  was  demonstrated  by  Bruce  while  studying 
T.  brucei.  and  also  by  the  same  observer,  Nabarro,  and  Kleine,  for 
T .  castellanii ,  both  diseases  being  spread  by  tsetse-flies,  though  with 
regard  to  the  fonner  it  had  long  been  known  that  the  tsetse-fly  was 
the  carrier  of  the  disease. 

There  are,  however,  two  ways  in  which  a  blood-sucker  can  spread 
an  infection:  (a)  the  direct;  (b)  the  indirect. 

(a)  The  Direct. — In  this  the  blood-sucker  simply  transmits  the 
parasite  unchanged. 

(b)  The  Indirect. — In  this  method  the  parasite  undergoes  a  cycle 
of  development  in  the  blood-sucker,  the  nature  of  which  has  been 
fully  discussed  already. 

It  would  appear  probable  that  it  is  only  in  the  natural  hosts  that 
forms  develop  which  are  infective  for  the  invertebrate. 

Effects  upon  the  Vertebrate  Host. — Trypanosomes  may  produce 
pathological  effects  on  their  vertebrate  host,  or  may  apparently  be 
harmless,  and  certain  harmless  trypanosomes  will  only  live  in  some 
particular  vertebrate  and  die  when  injected  into  others,  but  no 
pathogenic  trypanosome  is  restricted  to  one  host. 

The  best  known  of  the  former  are  T.  gambiense,  T.  castellanii  and 
T.  rhodesiense,  the  causes  of  sleeping  sickness;  S.  cruzi,  of  American 
trvpanosomiasis;  T.  evansi,  of  surra  in  horses,  etc.,  in  India  and 
elsewhere;  T.  brucei,  of  nagana  in  cattle  and  horses,  etc.;  T.  vivax, 
of  disease  in  cattle,  sheep,  and  goats,  in  the  Cameroons;  T.  nanum, 
of  cattle  sickness  in  the  Anglo-Egyptian  Sudan;  T.  dimorphon,  of 
the  Gambia  horse  sickness;  T.  cazalboui,  of  souma.  a  disease  of 
cattle  in  the  French  Sudan,  and  T.pecaudi,  of  sheep  in  the  same  place ; 
T.equinumoi  mal  dc  caderas  in  South  America;  T.  cquiperdum,  of 
dourine  in  horses  in  Europe  and  Africa. 

Symptoms. — The  pathogenic  effects  of  the  parasites  show  them- 
selves in  the  production  of  fever,  skin  eruptions,  emaciation,  local 


392  TRYPANOSOMIDJE 

or  general  oedema,  and  disease  of  the  nervous  system.     Secondary 
bacterial  affections  are  also  common.    The  mortality  is  often  high. 

Mordid  Anatomy. — The  lesions  are  often  insignificant,  but  in- 
flammation and  enlargement  of  the  lymphatic  glands  is  character- 
istic, and  dropsy  and  inflammation  of  the  meninges  are  also  found, 
which  in  human  trypanosomiasis  takes  the  form  of  meningo- 
encephalitis, as  will  be  described  later. 

Inoculations.- — The  parasites  can  be  spread  from  one  animal 
and  from  one  species  to  another  by  inoculation  of  infected  blood. 

Agglutinins/ — While  in  the  body  of  the  host  agglutinins  are 
formed,  for  if  blood  containing  trypanosomes  is  treated  with  the 
serum  of  an  animal  which  has  had  one  or  more  injections  of  blood 
containing  the  same  parasite,  a  rapid  massing  of  the  parasites  into 
rosettes,  with  the  anterior  ends  pointing  inwards  and  the  flagella 
outwards,  takes  place. 

This  is  called  agglomeration,  and  may  last  a  few  minutes,  the 
parasites  being  unaffected,  or  may  persist  till  they  die. 

Reducing  Power. — Trypanosomes  have  been  shown  by  Nauss 
and  Yorke  to  have  a  marked  reducing  power  on  haemoglobin. 

Precipitins. — Mayer  has  shown  that  the  serum  of  a  dog  infected 
by  T.  brucei  is  precipitated  by  a  salt  extract  of  the  same  parasite, 
but  not  by  that  of  T.  equinum,  thus  proving  the  presence  of  specific 
precipitins. 

Immunity.- — Active  immunity,  due  to  the  action  of  the  leucocytes 
(Laveran  and  Mesnil)  or  to  cytolysins  (McNeal),  can  be  produced 
in  certain  cases,  but  it  is  not  carried  from  mother  to  young.  Leger 
and  Ringenbach  have  shown  that  the  serum  of  animals  affected  with 
nagana  and  surra,  also  T.  equinum,  T.  castellanii,  and  T.  congolense, 
is  trypanolytic  for  homologous  and  allied  trypanosomes,  but  not  for 
others. 

Chalmers  and  O'Farrell  have  shown  that  T.  castellanii  can  be 
separated  from  T.  rhodesiense  by  immune  serum  reactions  in  vitro 
and  in  vivo. 

Involution  Forms. — Degenerated,  vacuolated  involution  forms 
may  be  seen  as  a  result  of  immunity  coming  on  or  of  treatment  by 
drugs.  Advanced  forms  after  treatment  with  immune  serum  have 
been  noted  by  Chalmers  and  O'Farrell. 

Toxins. — Uhlenhuth,  Hiibcner,  and  Worthe  have  demonstrated 
the  presence  of  endotoxins  in  T.  equiperdum,  which  observation 
supports  McNeal's  suggestion  as  to  their  presence,  and  also  the 
work  of  Martin,  Darre,  and  Leber.  Free  toxins  do  not  exist,  but 
endotoxins  can  be  set  free  by  trypanolysis. 

Local  Reservoirs.- — The  long-continued  infectivity  of  Glossina 
palpalis  after  the  removal  of  man  from  a  district  points  to  either 
long  duration  of  infectivity  in  the  fly  or  to  a  local  reservoir,  which 
may  perhaps  be  found  in  antelopes,  and  perhaps  other  animals  in 
the  case  of  T.  castellani. 

Cultivation. — McNeal  and  Novy  cultivated  T.  lewisi  in  the  water 
of  condensation  of  blood-agar  tubes  in  1903,  and  obtained,  at  370  C. 


TRYPANOSOMA  393 

and  also  at  the  room  temperature,  good  cultures,  in  which  T.  lewisi 
varied  in  size  from  minute  forms  i  to  2  microns  in  length  up  to  50 
to  60  microns,  and  colonies  of  rosettes  were  seen  with  all  the  flagella 
turned  inwards.  The  flagellum  in  cultivated  forms  projects  directly 
from  the  kinetonuclear  end  of  the  parasite. 

The  following  have  been  cultivated :  S.  cruzi,  by  Chagas;  T.  britcei, 
by  McNeal  and  Novy,  and  by  Laveran  and  Mesnil;  T.  equinum,  by 
R.  Thomas  and  Breinl,  T.  equifterdum,  by  Thomas  and  Breinl, 
with  slight  success;  T.  castellanii,  by  Thomas,  Breinl,  Gray,  and 
Tulloch,  with  partial  success;  T.  evansi,  by  Novy,  McNeal,  and  Hare, 
and  by  Thomas  and  Breinl,  but  were  found  to  be  non-virulent, 
and  subcultures  could  not  be  obtained. 

Effects  upon  the  Invertebrate  Host. — The  effects  of  trypanosome 
infection  upon  the  invertebrate  host  has  been  but  little  studied, 
except  with  reference  to  T.  castellanii  and  Glossina  palpalis,  and 
the  result  may  be  tabulated  as  follows:- — • 

A.  Non-Infection  of  the  Fly. — 1.  The  trypanosomes  intro- 
duced by  the  infective  feed  may  entirely  disappear,  being  digested 
in  some  fifty  to  seventy  hours. 

2.  The  trypanosomes  may  multiply  in  the  crop,  but  disappear 
after  the  next  feed  if  non-infective. 

3.  The  trypanosomes  may  grow  and  multiply  in  the  gut,  and  yet 
be  all  swept  out  by  the  next  feed  if  clean. 

4.  The  trypanosomes  may  survive  and  develop  in  the  crop  for 
twelve  days,  providing  that  blood  is  always  present,  but  no  trypano- 
somes appear  in  the  gut,  and  the  infection  dies  out. 

B.  Infection  of  the  Fly  Doubtful. — In  the  third  instance 
quoted  above  infection  may  take  place;  everything  depends  upon 
the  effects  of  the  second  feed. 

C.  Infection  of  the  Fly. — The  trypanosomes  persist  after  the 
clean  feed  has  displaced  the  blood  from  the  gut,  but  the  infection 
also  depends  upon  the  strain  of  trypanosome,  as  there  is  undoubtedly 
a  struggle  for  existence  between  the  trypanosome  and  the  chemical 
defences  of  the  fly  against  T.  castellanii . 

Type  Species. — Trypanosoma  rotatorium  Mayer,  1843. 
it    is  necessary,  for  purposes  of  classification,  that   the  reader 
should  clearly  understand  the  nature  of  the  type  species. 

Trypanosoma  rotatorium  Mayer,  1843. 

Synonyms. — Paramcecium  loricatum,  sen  costatum  Mayer,  1843,  Amceba 
rotatoria  Mayer,  1843,  Trypanosoma  sanguinis  Gruby,  1843,  Monas  rotatorium 
Lieberkiihn,  1870,  Undulina  ranarum  Ray  Lankestcr  1871,  Paramaecioides 
costatus  Grassi,  1872. 

History. — Gluge  in  1842  discovered  in  the  blood  of  frogs  an  organism  re- 
sembling that  which  had  been  discovered  by  Valentin  in  the  previous  year  in 
Salmofario,  the  brown  trout,  and  which  was  thought  to  be  related  to  the  genus 
Amceba  of  Ehrenberg,  but  which  from  his  description  and  from  his  figures  is 
more  probably  a  trypanosome.  Gluge's  description  is  also  very  short,  and  he 
is  followed  by  Mayer,  in  1843,  who  describes  two  forms — an  Amceba  rotatoria 
and  a  Paramcecium  loricatum,  or  costatum — but  in  November  of  the  same 
year  Gruby  gave  a  clear  description  of  the  organism,  and  applied  the  generic 


394  TRYPANOSOMIDM 

term  '  Trypanosoma  '  to  it,  so  that  it  becomes  the  type  species  of  the  genus, 
from  which  any  variation  in  the  classification  of  the  species  must  be  made. 

Ogawa  has  studied  this  parasite  in  the  frog  in  191 3,  as  well  as  Doflein  and 
Mendeleeff-Goldberg. 

Gruby's  Original  Description. — '  Its  elongated  body  is  flattened,  transparent, 
curved  like  a  centre-bit;  the  cephalic  end  is  terminated  in  a  thin,  elongated 
filament;  the  caudal  end  is  terminated  also  in  a  pointed  filament.  The  length 
of  the  animal  is  40  to  80  fi,  its  breadth  is  5  to  10  n,  the  filamentous  pointed 
cephalic  end  has  the  greatest  mobility,  the  length  of  the  cephalic  filament 
is  10  to  12  /t;  its  body  is  elongated,  flat,  and  toothed  like  the  blade  of  a  saw 
all  along  the  length  of  one  of  its  margins;  it  is,  as  I  have  above  mentioned, 
supple  and  twisted  two  or  three  times  around  its  axis,  like  an  auger  or  a 
corkscrew,  which  is  the  reason  why  I  propose  to  name  this  haematozoon 

Trypanosoma."  ' 

Zoological  Distribution. — It  has  been  found  in  Rana  esculenta  Linnaeus,  in 
R.  temporaria  Linnaeus  in  Europe;  in  R.  speciosa  in  the  Congo;  in  R.  trinodis 
in  the  Gambia.  Whether  the  species  found  in  Hyla  arborea  are  truly  T.  rota- 
tor inm  or  not  is  uncertain. 

Morphology. — The  pleomorphism  exhibited  by 
this  form  is  so  varied  that  it  requires  classification, 
for,  as  Chalachnikov  has  shown,  the  following 
varieties  exist: 

1.  Flattened  Forms. — (a)  Simple  plain  forms; 
(b)  plain  forms  rolled  on  themselves;  (c)  spiral 
forms. 

2.  Pectinated  Forms. — (a)  Pectinated  spiral  forms; 
(b)  cornucopial  forms.  In  all  these  forms  the 
undulating  membrane  is  much  folded,  and  has  a 
thickened  edge.  The  fiagellum,  which  is  short, 
starts  from  the  kinetonucleus,  which  is  situate  at 
a  variable  distance  from  the  afiagellar  extremity. 
The  trophonucleus  is  round  or  oval.  The  usual 
length  varies  from  40  to  80  ^i,  the  breadth  from 
5  to  40  fi,  and  the  fiagellum  is  about  10  to  12  (i  long. 

Doflein   finds    that   in    the   blood    and   internal 
ig    93.— -    rypa  organs  forms   intermediate  between  the  flagellate 

rotatonum  mayer.         and   ^    non.flagellate  organisms  are  found.    The 

(After  Dutton  and         latter  cannot  divide. 

Todd.)  Life-History.  —  The    life-history    is    but    little 

known.  Asexual  multiplication  takes  place  by 
the  trypanosome  becoming  round  and  losing  its  locomotor  apparatus, 
and  dividing  by  mitosis.  It  is  but  rarely  inoculable  into  other  frogs, 
but  it  grows  in  cultures,  especially  upon  Novy-McNeal's  medium,  but 
the  cultures  are  not  inoculable.  In  the  cultures  leptomonas  and  rosette  forms 
are  seen.  The  researches  of  Franca  show  that  it  is  capable  of  developing  in 
the  leech  (Helobdella  algira),  in  which  it  gives  rise  to  leptomonas-like  forms, 
which  are  to  be  seen  located  against  the  walls  of  the  gastric  intestinal  pouches. 
Frogs  can  be  infected  by  the  bites  of  infected  leeches  or  by  the  inoculation 
of  the  intestinal  contents. 

Cultivation. — It  has  been  cultivated  in  acid  bouillon  -  blood  media  by 
Pouselle  in  19 17. 

Classification. — The  question  is  unsettled  as  to  whether  there  are  more  than 
one  species  included  under  the  term  T.  rotatorium. 

Pathogenicity. — It  is  believed  to  be  non-pathogenic.  This  immunity  of 
the  frog  has  been  studied  by  Doflein  and  others. 

Classification. — If  the  section  on  evolution  contained  in  Chapter  V. 
be  read,  it  will  be  seen  that  we  believe  that  new  diseases  can  arise 
at  the  present  time;  that  organisms  usually  harmless  in  a  given 
environment  may  become  so  altered  under  certain  circumstances 


TRYPANOSOMA  395 

that  they  may  become  pathogenic;  and  that  this  change,  though 
merely  at  first  chemical,  may  subsequently  become  structural. 

The  researches  of  O'Farrell,  Fantham,  and  Porter,  already  referred 
to  under  the  Herpetomoninae,  seem  to  indicate  that  the  original  try- 
panosomes  were  parasites  of  such  invertebrates  as  Annulates, 
Arachnids,  and  Hexapoda,  from  which  they  spread  to  vertebrates. 

With  regard  to  man,  it  would  appear  as  though  his  infection  was  of 
comparatively  recent  date,  and  that  in  him  and  in  the  tsetse-flies 
which  infect  him  the  adaptation  of  the  trypanosomes  to  the  new 
environments  is  not  yet  complete,  and  therefore  the  differential 
characters  of  the  various  species  infecting  him  have  not  yet  become 
completely  crystallized. 

It  therefore  appears  to  us  that  a  natural  division  of  the  numerous 
species  of  trypanosomes  would  be  into — 

A.  Trypanosomes  infecting  invertebrata : — 

I.  Trypanosomes  of  Hirudinea. 

II.  Trypanosomes  of  Arachnida. 

III.  Trypanosomes  of  Hexapoda. 

B.  Trypanosomes  infecting  cold-blooded  vertebrates: — 

I.  Trypanosomes  of  Pisces. 
II.  Trypanosomes  of  Amphibia. 
III.  Trypanosomes  of  Reptilia. 

C.  Trypanosomes  infecting  warm-blooded  vertebrates:' — 

I.  Trypanosomes  of  Aves. 
II.  Trypanosomes  of  Mammalia. 

It  is  not  our  purpose  to  write  accounts  of  all  known  trypanosomes, 
but  merely  those  which  infect  man,  and  to  sketchily  describe  some 
of  those  which  produce  disease  in  the  mammalia,  and  to  draw  atten- 
tion to  others  which  can  be  classified  in  the  series  of  divisions  given 
above. 

With  regard  to  the  trypanosomes  of  mammals,  it  appears  to  us, 
from  an  evolutionary  point  of  view,  to  be  correct  to  divide  them  into 
two  sections — viz. : — 

A.  Non-pathogenic  mammalian  trypanosomes. 

B.  Pathogenic  mammalian  trypanosomes. 

As  it  is  the  last  section  only  with  which  tropical  medicine  is  con- 
cerned, we  shall  restrict  our  further  remarks  on  classification  until 
we  come  to  these  organisms. 

A  New  Classification. — Although,  for  purposes  of  general  infor- 
mation, we  have  given  the  usual  classification,  still,  it  must  be 
obvious  even  to  the  casual  reader  that  the  genus  Trypanosoma  com- 
prises an  enormous  number  of  species,  some  of  which  arc  of  very 
diverse  form. 

We  feel  that  the  time  has  arrived  in  which  to  bring  forward  a  fuller 
and  more  useful  classification,  based  upon  morphological  and 
physiological   characters,    especially   as   classifications   have   been 


396  TRYPANOSOMIDJE 

outlined  by  Noller,  while  Minchin,  had  he  lived,  would  probably 
have  brought  forward  one. 

In  the  Tiypanosominae  the  definitive,  and  hence  primitive,  host 
is  the  invertebrate,  and  we  should  expect  to  find  some  trypanosomes 
which  were  solely  denizens  of  these  animals,  and  apparently  this 
is  so.  Unfortunately,  their  full  life-history  still  requires  much 
elucidation,  but  such  forms  as  Cystotrypanosoma  intestinale 
Roubaud,  1911,  are  worthy  of  more  consideration;  and  it  is 
obvious  that  such  forms  deserve  separate  classifications,  and 
should  form  part  of  a  tribe — Cystotrypanece,  with  Cystotry panosoma 
as  type  genus  and  C.  intestinale  as  type  species. 

As  evolution  proceeds  so  life-histories  tend  to  become  compli- 
cated. In  this  case  the  complication  is  the  introduction  of  a  verte- 
brate intermediary  host,  and  with  the  change  in  environment  one 
meets  with  the  large,  relatively  slow-moving,  trypanosome  of  the 
cold-blooded  vertebrate  and  the  smaller,  quicker-moving,  trypano- 
some of  the  warm-blooded  vertebrate .  They  appear  to  us  to  deserve 
to  be  ranked  into  tribes  and  to  merit  more  study.  The  type  of 
the  first  is  obviously  Gluge's  parasite,  and  of  the  second  the  organism 
found,  by  one  of  us,  to  be  the  cause  of  sleeping  sickness. 

These  various  ideas  may  be  crystallized  as  follows : — 

A.  Live  only  in  a  definitive  invertebrate  host:— 

Type  genus:  Cystotrypanosoma  Roubaud,  ign— Tribe  I, 

Cystotry panece  Chalmers,  1918. 
Type  species :  C.  intestinale  Roubaud,  1911. 

B.  Live  in  a  definitive  invertebrate  host  and  in  a  cold-blooded 

intermediate  vertebrate  host : — 
Type  genus:- — Trypanosoma  Gruby,  1843— Tribe  2,   Try- 

panosomece  Chalmers,  191S. 
Type  species: — T.  rotatorium  Gruby,  1843. 

C.  Live  in  a  definitive  invertebrate  host  and  in  a  warm-blooded 

intermediate  vertebrate  host  :— 
Type  genus:  Castellanella  Chalmers,  iqi8 — Tribe  3,  Try- 

pocastellanellcce  Chalmers,  1918. 
Co-type  species:  C.  gambiensis  (Dutton,  1902). 
C.  castellanii  (Kruse,  1903). 

In  the  present  work  we  are  chiefly  concerned  with  the  third  tribe, 
'  TrypocastellanelleiB.' 


SERIES  A:  TRYPANOSOMES  INFECTING  INVERTEBRATA. 

TRIBE  1:    CYSTOTRYPANECE. 

This  tribe  has  not  yet  been  fully  studied,  but  provisionally  it 
can  be  classified  as  follows: — 


CYSTOTRYPANEM  397 

A.  Forms  carefully  studied  : — 

Snout  long,  no  free  flagellum  forms  like  T.  dimorphon  : — 

1.  Trophonucleus  round- — Rhynchoidomonas   Patton, 

1910. 

2.  Trophonucleus   elongate — Cystotrypanosoma   Rou- 

baud,  1911. 

B.  Forms  not  yet  fully  studied: — 

We  still   retain   the  old  term  Trypanosoma  sensu  lato  for  these 
forms,  pending  further  investigation,  and  divide  them  into: — 
I.  Trypanosomes  of  Hirudin ea. 
II.  Trypanosomes  of  Arachnida. 
III.  Trypanosomes  of  Hexapoda. 

Forms  Carefully  Studied. 
Genus  Rhynchoidomonas  Patton,  1910. 

Definition. — CystotrypanecB  with  large  kinetonucleus  situated  on 
the  aflagellar  side  of  the  rounded  trophonucleus,  with  distinct 
undulating  membrane  and  with  the  aflagellar  end  drawn  out 
considerably. 

Rhynchoidomonas  lucilise  Patton,  1910. 

This  parasite  is  found  in  the  Malpighian  tubes  of  Lucilia  serenis- 
sima  Walker,  and  Musca  nebula  Fabricius,  in  India.  It  moves  by 
sharp  jerking  movements,  and  has  no  free  flagellum,  but  a  pointed 
flagellar  extremity  and  a  pointed  aflagellar  extremity.  The  kineto- 
nucleus is  large  and  circular,  while  the  trophonucleus  is  also  large. 
Tlir  cytoplasm  contains  many  chromatoid  granules. 

Genus  Cystotrypanosoma  Roubaud,  191 1. 

Definition.- Cystotvypancce  with    small   terminal   kinetonucleus 

situate    on    the   aflagellar    side   of    an    elongated   trophonucleus. 
There  is  no  free  flagellum.     It  gives  rise  to  pyriform  cysts. 

Cystotrypanosoma  intestinale  Roubaud,  191 1. 

This  parasite  is  found  in  the  intestine  of  a  species  of  Lucilia  at 
Bamako  in  French  West  Africa. 

Forms  not  yet  Fully  Studied. 
Trvpanosomes  belonging  to  the  invertebrate  and  not  due  to  the 
sucking  of  contaminated  blood  have  been  found  in  the  tsetse-fly,  in 
mosquitoes,  in  ticks,  and  perhaps  in  leeches,  but  it  is  doubtful  about 
the  last  named. 

The  presence  of  the  Herpetomoiias,  Crithidia,  and  Trypano- 
soma in  bloods-sucking  Arthropods  may,  therefore,  be  peculiar 
to  those  animals,  or  only  acquired  from  their  hosts.  Hence  it  is 
quite  possible  f  or  serious  errors  to  arise  in  working  out  the  life-history 
of  these  parasites,  especially  as  infection  of  the  blood-sucker  may 
come  from  the  eg.^s. 


398  TRYPANOSOMID& 

Section  I.:  Trypanosomes  of  Hirudinea. 

Trypanosoma  inopinatum  is  believed  to  be  a  true  parasite  of  the 
leech  Helobdella  agira,  though,  according  to  some  observers,  it  is  the 
same  as  the  parasite  of  the  frog. 

Section  II.:  Trypanosomes  of  Arachnida. 

T.  christophersi  Novy,  1907,  found  in  Rhipicephalus  sanguineus, 
fed  on  dogs. 

Section  III.:  Trypanosomes  of  Hexapoda. 

Trypanosoma  boylei  Lafont,  1902,  has  been  found  in  Conorhinus 
rubrofasciatus,  an  insect  which  attacks  man  in  Mauritius  and 
Reunion. 

Trypanosoma  tullochi  Minchin,  1907. — This  parasite  closely  resembles  C. 
castellanii,  from  which  it  can  be  differentiated  by  the  central  round  nucleus 
and  the  small  centrosome.     It  is  found  in  G.  palpalis. 

T.  culicis  Novy,  190  7,  is  found  in  various  Cuficinae.  Novy  strongly  advocated 
the  view  that  the  trypanosomes  found  in  mosquitoes  which  Schaudinn  had 
fed  on  Athene  noctuce  infected  with  halteridium  should  be  defined  as  T.  noctuce 
Schaudinn,  1904,  a  parasite  of  Culex  pipiens,  and  the  same  for  T.  ziemanni 
Schaudinn,  1904,  also  in  Culex  pipiens  ;  and,  further,  that  the  trypanosome 
found  by  Durham  in  Stegomyia  fasciata,  which  had  been  fed  on  bats,  should 
be  looked  upon  as  belonging  to  the  mosquito. 

T.  triatomce.  Kofoid  and  McCulloch,  1916,  is  a  parasite  of  Triatoma 
protracta,  found  in  nests  of  the  wood-rat  N eotoma  fuscipes . 


SERIES  B:  TRYPANOSOMES  INFECTING  COLD-BLOODED 
VERTEBRATES. 

TRIBE  2:  TRYPANOSOMES. 

At  present  this  tribe  contains  one  genus — viz.,  Trypanosoma 
sensfi  stricto,  as  defined  above,  and  with  T.  rotatorium  Mayer,  1843, 
as  the  type. 

It  is  probable  that,  as  constituted,  the  genus  still  contains  a 
number  of  non-defined  genera,  but  these  require  further  investiga- 
tion, and  we  therefore  divide  the  species  into: — 

Section  I.  :  Trypanosomes  of  Fish. 
Section  II.  :  Trypanosomes  of  Amphibia. 
Section  III.  :  Trypanosomes  of  Reptilia. 

Section  I. :  Trypanosomes  of  Fish. 

In  1 84 1  the  first  known  trypanosome  was  found  by  Valentin  in  the  blood  of 
Salmo  fario,  the  brown  trout. 

Since  that  time  a  considerable  number  have  been  found  in  fresh-  and  salt- 
water fish  all  over  the  world.  As  examples  may  be  mentioned  T.  remaki 
Laveran  and  Mesnil,  1901,  which  exists  in  two  varieties — parva  and  magna — 
and  is  found  in  pike;  T.  raja:  Laveran  and  Mesnil,  1902,  in  Raja  punctata. 


Fig.    94  —  Trypanosoma 
leschenaultii  Robertson. 


Fig.  95. — Trypanosoma rajce. 
Round  Form,  in  the  Le  ech 


.>.-■>■- 


Fig.  97. — Trypanosoma 
raja:  Young  Try- 
panosome  in  the 
Leech. 


Fig.  96. — Trypanosomayyajce: 
Round  Form,  Older  Stage. 


Fig.  98. — Trypanosoma 
rajce :  Possibly  a 
Female  Form,  in 
the  Leech. 


/ 

Fig.  99. —  Trypano- 
soma rajce :  (Possi- 
bly a  Male  Form 
in  the  Leech. 


Fig.  100. — Trypanosoma  Fig.  ioi. — Trypanosoma  rajce 

rajce:  Slender  Form,  Fully  developed  Trypano- 

from  the  Proboscis  some  in  the  Skate. 
of  the  Leech. 

(All  after  Miss  Robertson.) 


4QO  TRYPANOSOMIDJE 

and  is  thought  to  be  spread  by  a  leech — Pontobdella  muricata  ;  T.  sacco- 
branchi  Castellani  and  Willey,  1905,  in  Saccobranchus  fossilis  in  the  Lake  of 
Colombo,  Ceylon. 

Trypanosomes  have  been  found  in  eels.  Brumpt  in  1906  described  a 
number  of  new  species  in  different  kinds  of  fish,  and  Zupitza,  in  1909,  made 
a  valuable  addition  to  the  knowledge  of  this  subject. 

Some  trypanosomes  found  in  fish  are  T.  danilewskyi  Laveran  and  Mesnil, 
1904,  in  Cvprinus  carpis  ;  T.  carassii  Mitrophanov,  1883,  in  Zarassius  vulgaris  ; 
T.  tincce  Laveran  and  Mesnil,  1904,  in  Tinea  tinea  ;  T.  barbcB  Brumpt,  1906,  in 
Barbus  fluviatilis  ;  T.  elegans  Brumpt,  1906,  in  Gobio  fluviatalis  ;  T.  phoxini 
Brumpt,  1906,  in  Phoxinius  Icevis  ;  T.  abramidis  Laveran  and  Mesnil,  1904,  in 
Abramis  brama  ;  T.  leucisci  Brumpt,  1906,  in  Leuciscus  sp.  (?)  ;  T.  scardini 
Brumpt,  1906,  in  Scardinius  erythrophthaltnus  ;  T.  squalii  Brumpt,  1906,  in 
Squalius  cephalis  ;  T.  cobitis  Mitrophanov,  1883,  in  Cobitis  fossilis.  There  are, 
however,  many  others  described.  T.  roulei  Mathis  et  Leger,  191 1,  in 
Monopteres  javanensis  ;  T.  pellegrini  Mathis  et  Leger,  191 1,  in  Macropodus 
viridi  auratus  ;  T.  chagasi  Horta  and  Machado,  191 1;  T.  dovhni  Yakimon, 
1912,  in  Solea;  T.  yakimoffi  in  Syngnatis. 

Section  II. :  Trypanosomes  of  Amphibia. 

The  trypanosomes  of  frogs  were  discovered  by  Gluge  as  far  back  as  1842 
in  the  form  of  the  largest  trypanosome  known — i.e.,  T.  rotatorium. 
It  seems  probable  that  leeches  are  the  carriers  of  these  parasites. 


r^^^ 


J 


\- 


Fig.    102.  —  Trypanosoma    pertenue       Fig.     103.  —  Trypanosoma      vittatce 
Robertson.  Robertson.     Shows    the    Try- 

panosome rolling  up  Prior  to 
Division. 
(From  drawing  by  Miss  Robertson.) 

Trypanosoma  inopinatum  Ed.  and  Et.  Sergent,  1904. 

Synonyms. — T.  elegans  Franca  and  Athias ;  T.  undulans  Franca ;  T.  henderson 
Patton. 

Found  in  R.  esculenta  L.  in  Algeria,  in  R.  hexodactyla  and  R.  tigrana  in 
India.  It  is  very  like  L.  lewisi,  but  is  more  stumpy.  It  is  spread  by  the  leech, 
Helobdella  algira.  It  gives  rise  to  herpetomonas  and  crithidial  forms  and 
Brumpt  has  been  able  to  infect  frogs  by  the  bite  of  the  infected  leeches,  and 
has  shown  that  the  infection  can  be  spread  by  the  second  generation  also — 
i.e.,  that  it  is  hereditary.  It  is  also  inoculable.  The  crithidial  forms  are  said 
to  be  the  infective  agent  by  Franca. 

Trypanosoma  nelspruitense  Laveran,  1904. 
Discovered  by  Theiler  in  R.  avgolensis  Bocage  and  in  7?.  theileri  Macquart  . 

Trypanosoma  somalense  Brumpt,  1906. 
In  Bufo  reticulatus  from  Somaliland. 


TRYPOCASTELLANELLEJE  401 

Trypanosoma  sp.  (?). 
Found  by  Tobey  in  the  American  newt,  Dienycleihis  viridescens. 

Section  III.:  Trypanosomes  of  Reptilia. 

Tortoises.— Trypanosoma  damoniee  Laveran  and  Mesnil,  1902,  in  Damonia 
ivcvcsi,  an  Asiatic  tortoise;  T.  vittatcs  Robertson,  1907,  in  Emyda  vittata  in 
Ceylon,  the  intermediate  host  being  a  leech. 

Crocodilia. — Trypanosoma  grayi  Novy. — This  parasite,  which  was  thought 
to  be  part  of  the  life-cycle  of  the  Trypanosoma  of  the  crocodile,  is  now  known 
to  be  a  Crithidia. 

Lizards. — T.boueti  Martin,  1907,  in  Mabuia  raddonii  ;  T .  leschenaidtii  Robert- 
son, 1 90 7,  in  Hemidactylusleschenaultii,  in  Ceylon;  T.  pertenne  Robertson,  1907, 
in  Hemidactylns  triedri  leschenaulti,  in  Ceylon. 

Ophidia. — T.  pythonis  Robertson ;  Mesnil  is  doubtful  whether  this  is 
not  a  haemoproteus,  while  Sambon  considers  that  it  is  a  hsemogregarine, 
(H.ro'oerisoni).  T.  erythrolampri  Wenyon,  1909,  in  Erythrolampns  cssculapii, 
T.  primeti  Mathis  et  L6ger  in  H.  piscator,  T.  najce  Wenyon,  1909,  in 
Naja  nigricollis. 

SERIES  C  :  TRYPANOSOMES  INFECTING  WARM-BLOODED 

ANIMALS. 

TRIBE  3:  TRYPOCASTELLANELLE^. 

This  tribe  may  be  divided  into: — 

Section  I . :  Trypanosomes  of  Aves. — These  are  but  little  known, 
and,  pending  further  study,  we  must  retain  the  old  genus  Trypano- 
soma scns.ii  lalo. 

Section  II.:  Trypanosomes  of  Mammalia. — They  may  be 
classified  as  follows: — 

Series  (a). — Non-Pathogenic. 

1.  Classifiable  : — 

Genus  Lewisonella. 
Genus  Endotrypanum. 

2.  Unclassijiable  : — 

Old  genus  Trypanosoma  sens/1  lato  pending  further  work. 

Series  (b).- — Pathogenic. 

1.  Classifiable  : — 

Genus  Schizotrypanum . 
Genus  Castcllanella. 
Genus  Duttonella. 

2.  Unclassijiable  : — 

Old  genus  Trypanosoma  sensit  lato  pending  more  research. 

3.  Little  known. 

The  classifiable  mammalian  trypanosomes  may  be  recognized  by 
the  characters  given  in  the  following  table: — 

A.  With  schizogony  in  the  vertebrate  host — Schizotrypanum 
Chagas,  1909. 

26 


402  TR  YPA  NO  SO  MID  JE 

B.  Without  schizogony  in  the  vertebrate  host: — 

I.  Enters   red    blood-corpuscles-  ■Endotrypanum   Mesnil 

and  Brimont,  1908. 
II.  Does  not  enter  red  blood-corpuscles. 

(a)  Final  stage  of  development  in  the  definitive  host  is' 
in  the  hind  gut.  Infection  is  contaminative. 
Aflagellar  extremity  long  drawn  out  and  pointed. 
Cytoplasm  free  from  granules- — Lewisonella 
Chalmers,  191 8. 
{b)  Final  stage  of  development  in  the  definitive  host 
■is  in  the  salivary  glands,  proboscis,  or  hypo- 
pharynx.     Infection  inoculative. 

1.  Polymorphic,  with  granular  cytoplasm,  small 

kinetonucleus,  and  well-developed  undulating 
membrane.  Final  stage  in  the  definitive 
host  takes  place  in  the  salivary  glands — 
Castellanella  Chalmers,  1918. 

2.  Monomorphic,  with  non-granular  cytoplasm, 

large  kinetonucleus,  and  with  or  without 
well  -  developed  undulating  membrane . 
Final  stage  of  development  anterior,  but 
not  in  the  salivary  glands — DuttoneUa 
Chalmers,  191 8. 

The  type  species  of  these  genera  are  as  follows : — 
Schizotrypanum  cruzi,  synonym  Trypanosoma  cruzi  Chagas,  1909. 
Endotrypanum  schaudinni  Mesnil  and  Brimont,  1908. 
Lewisonella  lewisi,  synonym  Trypanosoma  lewisi  Kent,  1879. 
C astellanella  gambi  en  sis  Dutton,  1902  (co-type  species:  Castellanella 
castellanii   Kruse,  1903,  synonym  Trypanosoma  castellanii  Kruse, 

I9°3)- 

DuttoneUa  vivax,  synonym  Trypanosoma  vivax  Ziemann,  1905. 

Section  I. :  Trypanosomes  of  Aves. 

In  1845  Gros  found  trypanosomes  in  the  blood  of  goat-suckers  and  cranes 
which  are  now  known  to  be  very  common  in  birds;  but  the  detection  in  blood- 
films  is  not  easy,  as  the  parasites  are  few  and  far  between.  According  to 
Novy  and  McNeal,  the  cultivation  method  is  much  better. 

Laveran  and  Mesnil  summarize  them  into  three  types : — (1)  Trypanosomes  of 
type  of  T.  lewisi  in  rats  (T.  avium  minus) ;  (2)  trypanosomes  of  type  of  T.  rota- 
torium  of  the  frog;  (3)  long  thin  trypanosomes  without  free  flagellum — 
distinct  type. 

A  few  examples  may  be  mentioned: — T.  avium  Laveran,  1903,  in  Syrnium 
aluco  L.,  the  wood-owl;  T.  confusum  Liihe,  1906,  in  Agelaius  phceniceus  L., 
and  other  North  American  birds;  T.  laverani  Novy  and  McNeal,  1905,  in 
Astragalinus  tristis  L., North  America;  T.  paddts  L.  and  Mesnil,  1904,  in  Padda 
oryzivora,  the  Java  sparrow. 

Also  T.  lagonostictcB  Maiullaz,  1914,  from  Lagonosticta  se negala  ;  and  T. 
Leothricis,  from  the  Japanese  nightingale,  Leothrix  luteus. 

Section  II.:  The  Trypanosomes  of  the  Mammalia 
Mammalian  trypanosomes  may  be  classified  according  to  Laveran 
and  Mesnil,  into: — 


THE  NON-PATHOGENIC  MAMMALIAN  TRYPANOSOMES     403 

Series  (a). — The  non-pathogenic  mammalian  trypanosomes. 
Series  (b). — The  pathogenic  mammalian  trypanosomes. 
This  classification  is,  in  our  opinion,  in  accord  with  evolutionary 
knowledge. 


SERIES  A:  THE  NON-PATHOGENIC  MAMMALIAN 
TRYPANOSOMES. 

It  is  quite  beyond  the  limits  of  this  book  to  give  detailed  accounts 
of  these  trypanosomes,  and  all  that  we  can  do  is  to  attach  a  list  of 
the  more  common  with  an  account  of  a  few. 

Classifiable. 
Two  genera  are  known— viz.: — 

A.  Endoglobular  forms  known — Endotryfamtm. 

B.  Endoglobular  fonns  unknown — Lewisonella. 

Unclassifiable. 

C.  Little  known  forms — Trypanosoma  sensil  lato. 

Genus  Lewisonella  Chalmers,  1918. 
Definition. — Trypocastellanellese,  found  in  mammals,  non-patho- 
genic, without  endoglobular  forms. 

Type  Species. — Lewisonella  lewisi  Saville  Kent,  1880. 
We  will  describe  the  type  species  L.  lewisi  Saville  Kent,  1880,  in 
greater  detail. 

Lewisonella  lewisi  (Saville  Kent,  1880). 

Synonyms. — Herpetomonas  lewisi  Kent,  1880;  Trichomonas lewisiCrookshank, 
1886;  Trypavomonas  lewisi  Labbe,  1891;  Trypanosoma  sanguinis  Kanthack, 
Durham,  and  Blandford,  1898;  T.  rattorum  Borner,  1901;  Trypanomonas 
murium'Ds.nW,  1899;  Trypanozoon  lewisi  Liihe,  1906;  Trypanosoma  lewisi  Kent, 
1880. 

Remarks. — L.  lewisi  was  the  first  mammalian  trypanosome  to  be  discovered, 
for  it  was  seen  by  Chussat  in  1 850  in  Epimys  rattns  (probably  not  by  Gros  in 
1845),  who  thought  it  was  a  young  nematode,  while  Lewis,  in  Calcutta,  in 
1877,  rediscovered  it,  and  recognized  that  it  was  a  protozoon.  It  is  a  typical 
Lewisonella,  and  is  found  in  Epimys  rattus  L.,  E.  norvegicus  Pall,  and  E. 
rufescens  Gray  all  over  the  world — in  Asia  (India,  Ceylon,  Java,  Philippines, 
Japan),  in  Europe  (England,  Ireland,  France,  Holland,  Germany,  Russia), 
in  Africa  (Uganda,  Abyssinia,  Gambia,  and  Cameroons),  and  in  America 
(United  States  and  Brazil).  It  is  non-pathogenic  and  restricted  to  rats, 
among  which  it  is  spread  by  Ceratophyllus  fasciatits,  the  rat-flea. 

Morphology. — It  is  a  very  active,  worm-like  little  parasite  darting  about 
among  the  corpuscles.  It  is  24  to  25  /x  in  length  and  1-5  fx  in  breadth.  The 
anterior  end  is  very  pointed,  and  the  whole  parasite  is  thin,  the  tropho- 
nucleus  is  situated  near  the  junction  of  the  middle  and  posterior  thirds  of  the 
body,  and  the  kinetonucleus,  which  is  rod-shaped,  is  situated  anteriorly. 
There  are  eight  myonemes  in  the  ectoplasm  (periplast) .  Prowazek  distinguishes 
small  male  forms  with  a  nucleus  rich  in  chromatin,  large  female  forms  with 
clear  cytoplasm,  and  indifferent  forms  with  many  granules  and  poorly  defined 
nucleus. 

Life-History — In  the  Vertebrate. — The  life-history  in  the  rat  has  been 
worked  out    by  Breinl  and    Hindle  (Fig.  89,  p.  384).      The   filament   they 


4o4  TRYPANOSOMID/E 

mention  as  occurring  between  the  kinetonucleus  and  the  trophonucleus 
appears  to  have  been  also  seen  by  Prowazek.  Asexual  reproduction  may  be 
summarized  into  reproduction  with  longitudinal  division  and  reproduction 
with  rosette  formation  and  encystment  after  some  interchange  between  the 
kineto-  and  tropho-nuclei,  followed  in  due  course  by  increased  power  for 
longitudinal  division.  Battaglia  describes  a  process  of  sporogony  with  the 
formation  of  macro-  and  micro-gametocytes,  and  of  macrogametes  and  micro- 
gametes,  and  a  similar  reproduction  has  been  described  by  Pricolo.  Carini's 
cyst-like  bodies  in  the  lungs  are  considered  by  Delinois  to  be  a  coccidium, 
Pneumocystis  carinii. 

In  the  Invertebrate. — The  rat-flea,  Ceratophyllus  fasciatus,  is  the  true  carrier 
of  L.  lewisi,  as  was  first  demonstrated  by  Nuttall,  and  the  rare  development 
which  may  take  place  in  louse  Polyplax  spinulosa  is  more  of  the  nature  of  a 
natural  culture  than  a  proper  development.  The  development  in  the  flea 
has  been  studied  by  Swellengrebel  and  Strickland,  and  more  recently  by 
Minchin  and  Thompson. 

When  the  flea  ingests  blood  containing  the  flagellates,  they  pass  directly  to 
the  mid-gut,  where  they  enter  the  epithelial  cells,  inside  which  they  attain 
a  large  size  and  undergo  multiplication  in  a  peculiar  manner  by  forming  a 
large  spherical  body  containing  a  number  of  tropho-  and  kineto-nuclei,  and 
developing  flagella,  while  the  original  flagellum  still  remains  attached,  but  is 
subsequently  lost;  and  then  the  cytoplasm  divides  into  the  daughter  trypano- 
somes,  which  are  now  set  free,  and,  passing  into  the  rectum,  become  crithidial 
forms  by  the  kinetonucleus  travelling  past  the  trophonucleus  towards  the 
flagellum.  These  crithidial  forms  attach  themselves  to  the  wall  of  the  rectum, 
and  shorten  into  Leishmania-like  forms  without  flagella  or  without  free  flagella. 
These  in  their  turn  develop  into  trypanosome  forms,  which  pass  forwards 
into  the  mid-gut. 

The  intracellular  stage  is  at  its  height  about  the  end  of  the  first  day  after 
infection ;  the  rectal  stage  begins  during  the  second  day,  the  trypaniform  types 
pass  into  the  mid-gut  towards  the  end  of  the  fifth  day;  and  the  flea  is  infective 
in  about  six  days  after  its  own  infective  meal. 

The  191 5  work  of  Minchin  and  Thompson  may  be  summarized  as  follows: — 

L.  leivisi  is  transmitted  from  rat  to  rat  by  the  rat-flea  Ceratophyllus  fasciatus, 
but  infection  does  not  occur  by  the  flea-bites,  but  is  contaminative  by  the  rat 
licking  from  its  fur  or  skin  the  moist  faeces  of  infective  fleas  containing  the 
final  propagative  form,  or  by  eating  the  fleas. 

The  cycle  of  development  is  as  follows: — The  flea  sucks  the  blood  of  an 
infected  rat,  and  so  acquires  the  trypanosomes,  which  require  a  minimum 
of  five  days  to  attain  the  infective  stage,  which  is  a  small  trypanosome  which 
does  not  penetrate  the  salivary  glands,  but  remains  in  the  digestive  tract, 
from  which  it  escapes  in  the  faeces,  which  are  taken  into  the  mouth  of  the  rat 
while  licking  the  fur.  The  flea  remains  infective  for  a  long  time,  but  does  not 
pass  the  germ  on  to  the  next  generation.  After  infection  some  five  to  seven 
days  elapse  before  the  trypanosome  appears  in  the  rat's  blood,  in  which  it 
multiplies  till  the  eleventh  to  thirteenth  day  after  infection. 

In  the  louse,  Polyplax  spinulosa,  the  life-cycle  has  been  studied  by  Prowazek, 
who  finds  that  the  micro-  and  macro-gametocytes  undergo  first  a  reduction 
of  the  trophonucleus  from  sixteen  chromosomes  to  four,  and  that  then  the 
microgamctocyte  gives  rise  to  only  one  microgamete,  which  fuses  with  the 
macrogamete,  forming  an  ookinete.  This  becomes  a  trypanosome  by  the 
separation  of  the  kinetonucleus  from  the  synkaryon.  The  flagellum  projects 
from  the  posterior  end,  which  the  kinetonucleus  now  leaves,  and,  taking  the 
flagellum  with  it,  proceeds  towards  the  anterior  end,  thus  forming  the  undu- 
lating membrane.  Gregariniform  non-flagellate  forms  also  appear,  which 
penetrate  between  the  epithelial  cells.  Prowazek  failed  to  infect  rats  by 
the  bite  of  the  louse,  but  this  has  been  done  successfully  since.  Swellengrebel 
and  Strickland  find  that  the  development  in  the  louse  is  very  irregular  and 
not  to  be  compared  with  that  in  the  flea. 

Cultivation. — Cultural  experiments  have  been  carried  out  successfully  by 
Novy  and  McNeal  on  a  medium  prepared  by  mixing  agar  and  defibrinated 


THE  NON-PATHOGEXIC  MAMMALIAN  TRYPANOSOME     405 

rabbit's  blood  in  equal  parts,  when  forms  from  1 J  to  60  /x  in  length  may  be 
found,  and  also  rosettes,  but  the  forms  are  herpetomoniform,  with  the  kine- 
tonucleus  at  the  flagellar  end. 

Pathogenicity. — Inoculation  can  only  be  carried  out  successfully  in  rats,  in 
which  it  is  generally  non-pathogenic,  though  some  observers  have  described 
the  rare  occurrence  of  dyspnoea,  oedema,  and  subcutaneous  haemorrhages  in 
intense  infections.  Some  strains  may  become  very  pathogenic  for  rats. 
These  strains  show  morphological  and  developmental  anomalies — e.g.,  forms 
without  a  blepharoplast — and  there  is  a  correlation  between  virulence  and 
these  changes. 

Immunity. — Immunity  is  gamed  when  a  rat  becomes  free  from  the  parasites, 
and  hyperimmunity  can  be  obtained  by  inoculations.  It  is  thought  that  the 
immunity  is  largely  due  to  phagocytosis,  but  this  is  being  questioned  in  many 
species  of  trypanosomes.  A  protective  serum  is  obtainable  from  hyperimmune 
rats.     Immune  serum  will  agglomerate  the  trypanosomes. 

Hereditary  Infection. — -The  parasites  cannot  be  transmitted  from  the  mother 
to  young,  as  it  appears  that  they  cannot  traverse  the  placenta. 

Genus  Endotrypanum  Mesnil  and  Brimont,  1908. 
Definition. — Trypocastellanelleae,  found  in  mammals,  non-pathogenic,  and 
with  endoglobular  forms. 

Type  Species. — Endotrvpanum  schaudinni  Mesnil  and  Brimont,  1908. 

Endotrypanum  schaudinni  Mesnil  and  Brimont,  1908. 

This  trypanosome,  1 3*4  X  3*5  microns,  is  only  known  in  the  endoglobular  form 
in  the  red  blood  cells  of  the  sloth,  in  which  it  appears  as  a  peg- top-shaped  try- 
panosome with  a  short  nagellum  possessing  trophonucleus  and  kinetonucleus. 
This  must  be  only  one  stage  in  its  life-history,  and  as  yet  the  other  stages  are 
unknown ;  and  though  a  free  trypanosome  was  seen  in  the  same  animal  as  the 
encysted  forms,  it  was  considered  to  be  different  from  the  endoglobular  forms. 
In  1914  Darling  confirmed  these  researches,  finding  the  organism  in  Cholcepus 
didactyhis  in  Panama.  No  free  trypanosomes  were  seen  in  the  sloth.  Free 
forms  only  occur  after  fresh  preparations  have  stood  some  time. 

Unclassifiable. 

The  following  is  a  list  of  the  unclassified  species,  divided 
according  to  the  classification  of  the  host  and  arranged  according 
to  known  importance : — ■ 

Trypanosomes  found  in  Monkeys.- — America  :  T.  minasense  Chagas, 
1909;  T.  prowazeki  Gossler,  1908.  Asia:  T.  rhesii  Terry,  1911; 
T.  vickerscB  Brumpt,  1900.  Africa :  A  number  of  unnamed  trypano- 
somes are  reported  in  chimpanzees  and  species  of  Cercopithecus. 

Trypanosomes  of  U  ngulata  .—Trypanosoma  theileri  Bruce,  1902. 

Trypanosomes  of  Rodents. — T.  duttoni  Thiroux,  1905;  T.  mnscitli 
Kendall,  1906;  T.  grosi  Laveran  and  Pettit,  1909;  T.  microti 
Laveran  and  Pettit,  1909;  T.  blanchardi  Brumpt,  1905  (  =  7\  myoxi 
Blanchard);  T.  evotomys  Hadwen;  T.  peromysci  Watson;  T.  criceti 
Liihe,  1906;  T.  cuniculi  R.  Blanchard,  1906;  T.  bandicotti  Lingard, 
1904;  T.  nabiasi  Railliet;  T.  leporis  sylvatici  Watson;  T.  acouchii 
Brimont;  T.  indicum  Liihe;  T.  citelli  Watson;  T.  spermophili 
Laveran;  T.  otospermophili  Wellman  and  Wherry;  T  petrodronn 
Bruce,  1915. 

Trypanosomes  of  Bats. — T.  vespertilionis  Battaglia.  1904;  T.  mega- 
derma  Wenyon,  1908:  T.  nicolleoram  Ed.  and  Et.  Sergent,  1905; 
T.  limeatus  Iturbe  and  Gonzalez.  1916. 


4o6  TRYPANOSOMID&. 

Trypanosomes  of  Insectivora. — T.  talpc?  Nabarro;  T  soricis 
Hadwen. 

Trypanosomes  of  Edentata. — T.  legeri  Mesnil  and  Brimont,  1910. 

Trypanosomes  of  Carnivora. — T.pestanai  Bettencourt  and Fran9a, 
1905. 

Trypanosoma  duttoni  Thiroux,  1905. 

Dutton  and  Todd  in  1903  saw  a  flagellate  organism  in  the  blood  of  mice 
obtained  in  a  house  in  McCarthy  Island  on  the  Gambia  River,  but  they  con- 
sidered it  to  be  of  the  type  of  a  Herpetomonas  ;  but  in  1905  Thiroux  described 
a  definite  trypanosome  in  Mas  musculus  L.  in  Senegal  which  will  only  infect 
mice  of  all  kinds — e.g.,  M.  minutus  L.  (the  harvest-mouse) — and  it  is  possible 
that  Dutton  and  Todd  saw  one  stage  of  its  development. 

A  number  of  interesting  researches  have  taken  place  with  this  trypano- 
some. Pricolo  found  that  it  could  pass  through  the  placenta  and  multiply 
in  the  foetus,  in  which  he  describes  latent  forms  very  like  those  already  men- 
tioned in  T.  lewisi — i.e.,  which  resembled  Leishmania — having  only  a  rod- 
shaped  kinetonucleus  and  tropho nucleus. 

Trypanosomes  were  found  in  fleas  caught  on  infected  animals,  but  they 
did  not  show  any  development. 

Trypanosoma  musculi  Kendall,  1906. 
This  parasite  was  found  in  8  per  cent,  of  the  mice  examined  by  Kendall 
in  Panama.     It  was  non-pathogenic,  and  resembled  T.  duttoni. 

Trypanosoma  microti  Laveran  and  Pettit,  1909. 
Found  in  Microtus  arvalis  Pallas.     It  is  25  to  30  jli  by  1*5  fx. 

Trypanosoma  blanchardi  Brumpt,  1905. 
In  Myoxis  glis,  the  common  dormouse.     Like  T.  lewisi,  but  not  inoculable 
into  rats. 

Trypanosoma  myoxi  R.  Blanchard,  1906. 
Found  by  Galli-Valerio  in  Muscardium  {Myoxis)  avellanarius  L.,  but  nothing 
much  is  known  about  the  parasite. 

Trypanosoma  aivicanthidis  Delanoe,  191 5,  from  species  of  Arvicanthus  and 
T.  eburnense  Delanoe,  1915,  from  Musconcha  are  varieties  of  T.  lewisi. 

Trypanosoma  criceti  Liihe,  1906. 

Synonyms. — T.  rabinowitschi  Brumpt,  1906. 

This  trypanosome,  which  is  very  like  T.  lewisi,  but  distinguished  by  not 
being  transferable  to  the  rat,  was  found  in  the  hamster  (Cricetus  cricetus  L.) 
by  Koch  in  1881.  A  blood-sucking  louse  has  not  been  found  on  the  hamster, 
but  Ceratophyllus  fasciatus  Bosc  is  common. 

Trypanosoma  cuniculi  R.  Blanchard,  1906. 

This  trypanosome  was  found  by  Jobjet  and  Nabois  in  1891  in  the  rabbit 
(Lepus  cuniculus  L.),  in  which  it  causes  emaciation  and  perhaps  diarrhoea.  It 
is  very  similar  to  T.  lewisi,  but  smaller.  It  will  not  infect  white  rats  and  guinea- 
pigs,  but  it  can  be  cultivated.  It  is  suspected  that  Hcematopinus  ventricosus 
Denny  and  Pulex  goniocephalus  Taschenberg  may  perhaps  have  something 
to  do  with  its  life-history. 

Trypanosoma  bandicotti  Lingard,  1904. 

This  trypanosome  is  probably  not  the  same  as  T.  lewisi,  which  it  resembles 
in  being  pathogenic  to  guinea-pigs.  It  is  found  in  Nesokia  bandicotti  Bechst 
in  Bombay  and  the  Deccan. 


THE  PATHOGENIC  MAMMALIAN  TRYPANOSOMES         407 


Trypanosoma  indie  urn  Liihe,  1906. 
T.  indicum  is  found  in  the  Indian  squirrel  (Funambulus  palmarum  L.)  in 
Madras.     It  is  very  like  T.  lewisi,  and  only  slight  morphological  differences 
can  be  found. 

Trypanosoma  vespertilionis  Battaglia,  1905. 

Synonym. —  Trypanosoma  dionisii  lvttcncourtand  Franca,  1908. 

Dionisi  found  a  trypanosome  in  the  Italian  bat  (Miniopterus  schrenbersii) 
in  1899,  and  since  then  numerous  bats  have  been  found  to  carry  trypanosomes, 
and  also  they  can  be  inoculated  with  the  parasites  of  surra  and  mibori,  which 
produce  pathogenic  effects. 

T. vespertilionis  has  been  found  in  bats  from  South  Italy  (Battaglia),  Roman 
Campagna  (Sambon),  Brazil  (Durham),  India  (Donovan),  North  Africa  (Ser- 
gents),  and  from  Portugal  (Bettencourt  and  Franca).  This  parasite  has  been 
investigated  by  Battaglia,  who  has  described  a  process  of  sporogony,  and  has 
shown  that  the  blood  filtered  through  a  Kitasato  filter  is  still  infectious. 

According  to  Pringault,  T.  vespertilionis  is  spread  by  Cimex  pipestrelli. 

Trypanosoma  nicolleorum  Ed.  and  Et.  Sergent,  1905. 

In  the  blood  of  Vespertilio  kuhli  Natt  and  V.  myotis  Bechst  in  Algeria;  not 
transmissible  to  mice,  rats,  or  rabbits. 

The  carrier  of  the  infection  is  not  known.  Durham  saw  trypanosomes  in 
Stegomyia  fasciata  which  had  fed  on  a  bat,  but  they  might  have  belonged  to 
the  mosquito.     Fleas  have  been  examined  without  success. 

Trypanosoma  theileri  Bruce,  1902. 

Synonym. — T.  transvaaliense  Laveran,  1902. 

T.  theileri  is  found  in  the  Transvaal,  in  Togoland,  East  Africa,  Trans- 
caucasia, and  in  India.  It  is  of  large  size,  60  to  70  /j,  in  length  and  4  to  5  (/, 
in  breadth.  A  small  form  is  known,  25  to  53  /j,  in  length  and  2  to  3  /x  in 
breadth.  It  moves  very  rapidly,  and  has  a  long  rlagellum,  while  the  anterior 
end  is  pointed  and  the  kinetonucleus  is  oval.  Multiplication  is  by  simple 
longitudinal  fission.  A  female  form  has  been  described  by  Liihe.  It  is 
believed  to  be  spread  by  species  of  Hippobosca,  and  is  specific  for  bovines,  not 
being  inoculable  into  other  animals.  According  to  Nocht  and  Mayer,  it  is 
not  the  cause  of  gall-sickness  or  galziekte  in  cattle  in  Africa. 

Carrier:  Hippobosca  rufipes  (Fig.  447,  p.  854).  An  allied  species  is  T.  uru- 
blewskii  Wladimiroff  and  Takimofl,  1909. 

Similar  species  are  T.  himalayanum,  T.  indicum,  T.  muktesauri  Lingeard, 
1904;  T.  franki  Frosch,  1909;  T.  americanum  Crawley,  1909;  T.  rutherfordi 
Had  wen,  19 12. 


SERIES  B:  THE  PATHOGENIC  MAMMALIAN 
TRYPANOSOMES. 

Bra*  e  has  classified  pathogenic  mammalian  trypanosomes  into 


groups  as  follows : — 


Polymorphic  trypanosomes  with  granular  cytoplasm,  active 
movements,  well-developed  undulating  membrane,  small 
kinetonucleus.  Spread  by  tsetse-flies,  which  are  the 
definitive  hosts  in  which  development  is  completed  in 
the  salivary  glands — T.  gambiense,  T.  brucei,  T.  rhode- 
siense,  T.  evansi,  T.  equiperdum.  (This  group  corre- 
sponds with  the  genus  Castellanella.) 


4o8  TRYPANOSOMIDJE 

B.  Monomorphic  trypanosomes  with  non-granular  cytoplasm. 
Spread  by  tsetse-flies,  in  which  development  is  confined 
to  the  proboscis  and  hypopharynx.  (This  group  agrees 
with  the  genus  Duttonella.) 

I.  Kinetonucleus  large  and  terminal.    Undulating  mem- 
brane poorly  developed  and  simple.     Movements 
very    rapid — T.    vivax,'  T.   caprce,    T.    uniforme. 
(Vivax  sub-group.) 
II.  Kinetonucleus  prominent  and  subterminal.  Undulat- 
ing membrane  well  developed .  Movements  active- 
ly, pecorum  and  T.  simice.     (Pecorum  sub-group.) 
Taking  into  consideration  the  above,  we  may  arrange  the  patho- 
genic mammalian  trypanosomes  as  follows: — 
A.  Classifiable: — 

I.  Genus  Castellanella. 

Genus  Castellanella  Chalmers,  1918. 

Definition. — Trypocastellanelles  with  the  definitive  host  a  fly  and 
the  intermediate  host  in  a  warm-blooded  vertebrate.  Without 
reproduction  by  schizogony  in  the  vertebrate  host,  in  which  it  is 
polymorphic,  with  granular  cytoplasm,  small  kinetonucleus,  and 
well-developed  undulating  membrane.  Final  stage  in  the  definitive 
host  is  in  the  salivary  glands.  Infection  is  inoculative  and  trans- 
mission is  ingestive  (see  Chapter  XXXV.,  p.  878). 

Co-Type  Species. — Castellanella  gambiensis  (Dutton,  1902)  and  Castellanella 
castellanii  (Kruse,  1903). 

Other  Species. — The  species  of  the  genus  may  be  differentiated  as  follows: — ■ 

A.  Posteriorly  nucleate  in  rats  : — 

I.  Will    not    infect    man.     Kills    an    animal    immunized    against 
C.  rhodesiensis — C.  brucei. 
II.    Infects  man.     Kills  an  animal  immunized  against  C.  brucei — 
C.  rhodesiensis. 

B.  Not  posteriorly  nucleate  in  rats  ■' — 

1.   Infection  direct  from  vertebrate  host  to  vertebrate  host  during 
coitus — C.  equiperdum. 
IT.   Infection  by  means  of  a  definitive  host: — 

(a)  Definitive  host  not  a  tsetse-fly— C.  evansi. 

(b)  Definitive  host  a  tsetse-fly:  — 

1 .  Causes   chronic   and    often    mild    infections   in    man — 

C.  gambiensis. 

2.  Causes  acute  and  severe  infections  in  man — C.  castellanii. 

II.  Genus  Duttonella. 

Genus  Duttonella  Chalmers,  1918. 

Definition, — Trypocastellanellece  with  definitive  host  in  a  fly  and 
intermediate  host  in  a  warm-blooded  vertebrate.  Without  repro- 
duction by  schizogony  in  the  vertebrate  host,  in  which  it  is  mono- 
morphic, with  non-granular  cytoplasm,  a  large  kinetonucleus, 
which  may  be  terminal  or  subterminal,  with  or  without  a  well- 


TRYPANOSOMES  OF  ANIMALS  4°9 

developed  undulating  membrane.     Movements  active.     Final  stage 
in  the  definitive  host  is  confined  to  the  proboscis  and  hypopharynx. 

Type  Species. — Bruce's  Uganda  strain  of  vivax,  which  is  probably  the  same 
as  cazalboui. 

Other  Species. — The  other  species  may  be  recognized  as  follows: — 

(a)  Kinetonucleus  large  and  terminal.     Undulating  membrane 

well  developed  and  simple.  Invertebrate  host  a  glossina : — 
i.   Rats  refractory — Uniformis. 

2.  Rats  susceptible — Vivax. 

3.  Only  equidae  and  ruminants  susceptible — Caprte. 

(b)  Kinetonucleus    prominent    and     subterminal.     Undulating 

membrane  poorly  developed : — 

1.  Small,  8-18  microns;  found  in  cattle — Pecorum. 

2.  Larger,  14-24  microns;  found  in  monkeys — Simice. 

B.  Unclassifiable : — 

Genus  Trypanosoma  sensu  lato  : — 

Group  1 :  Part  of  the  flagellum  always  free. 

Group  2:  No  part  of  the  flagellum  free. 

Group  3 :  Part  of  the  flagellum  may  or  may  not  be 

free. 
Group  4:  Little-known  forms. 

TRYPANOSOMES  OF  ANIMALS. 
FORMS  CLASSIFIABLE. 

Genus  Castellanella  Chalmers,  1918. 

Castellanella  evansi  Steel,  1885. 

Synonyms. — Spirochtzta  evansi  Steel,  1885;  Heematomonas  evansi  Crook- 
shank,  1886;  and  Trichomonas  evansi  Crookshank,  1886.  According  to  Yorke 
and  Blacklock,  T.  soudanense  and  T.  venezuelense  ;  according  to  Bruce, 
T.  soudanense  Laveran. 

Castellanella  evansi,  discovered  by  Evans  in  India  in  1880,  is  the  cause 
of  a  disease  called  surra,  which  occurs  in  horses,  mules,  camels,  and  cattle  in 
India,  Burma,  Indo-China,  Java,  Philippines,  Mauritius,  and  North  Africa. 
With  regard  to  cattle,  they  were  supposed  to  be  immune  until  the  outbreak  in 
Mauritius  in  1902,  which  killed  from  25  to  100  per  cent,  of  the  infected  cattle. 

Morphology. — Thistrypanosome,  25  jx  in  length  and  1*5  /x  in  breadth,  has  a 
pointed  anterior  extremity,  a  long  flagellum,  and  is  actively  motile.  It  repro- 
duces asexually  by  simple  division. 

Walker  finds  that  a  schizogony  takes  place  in  the  spleen  of  the  vertebrate 
host.  The  trypanosome  in  the  capillary  bends  round  until  its  two  ends  meet 
and  fuse,  forming  a  ring,  which  may  become  a  disc  with  the  llagellum  at  first 
attached,  but  subsequently  lost.  These  bodies  measure  2-5  /x  in  diameter,  and 
possess  a  kinetonucleus  and  a  trophonucleus.  They  grow,  and  their  nuclei 
divide  until  they  reach  a  size  of  10  to  1 5  fx  in  diameter,  and  divide  into  four  to 
sixteen  kineto-  and  tropho-nuclei,  and  eventually  form  mesozoitcs  inside  a 
thin  cyst  wall.  Each  mesozoite  is  6  to  10  //,  in  length  and  1  to  1*5  fx  in  width, 
with  two  nuclei,  but  no  flagellum  or  undulating  membrane.  These  mesozoites 
are  believed  to  develop  into  trypanosomes.  No  dimorphism  in  these  bodies 
has  been  seen. 

Life-History. — Holmes  recognizes  male  and  female  forms,  which  he  considers 
conjugate  by  the  anterior  extremities  only,  after  which  the  female  divides, 
forming  four  amoeboid  bodies,  which,  in  the  liver,  spleen,  and  bone-marrow, 
develop  into  trypanosomes.  This  appears  to  somewhat  resemble  the  descrip- 
tions of  Breinl  and  Hindle  of  latent  forms  in  C.  castellanii.      C.  evansi  can  be 


4io  TRYPANOSOMIDJE 

cultivated,  and  appears  to  develop  in  certain  flies — for  example,  Tabanus 
tropicus,  T.  lineola,  Stomoxys  calcitrans,  S.  geniculatus,  in  the  stomach  of  the 
last  of  which  it  has  been  found.  Certainly  it  can  be  transmitted  to  healthy 
animals  by  the  bites  of  flies  and  fleas.  It  is  said  that  it  can  also  be  contracted 
by  eating  infected  meat. 

T.  striatus  Fabricius,  according  to  Mitzmain,  can  mechanically  transmit 
surra. 

Pathogenicity. — The  symptoms  are  fever,  remittent  or  intermittent,  emacia- 
tion, cedema  of  the  limbs  and  ventral  surfaces,  frequently  lesions  of  the  eyes 
and  eyelids,  great  muscular  weakness,,  paralysis,  and  death.  The  treatment  is 
by  arsenic.  A  variety,  C.  evansi  var.  niborii  Laveran,  1905,  is  the  cause  of  the 
disease  mbori  in  dromedaries  in  Africa. 

Castellanella  brucei  Plimmer  and  Bradford,  1889. 

Synonyms. — Perhaps  T.  equi  Blacklock  and  Yorke,  1913.  According  to 
Bruce,  T.  rhodesiense  and  T.  ugand.ce. 

This  parasite  was  discovered  by  Sir  David  and  Lady  Bruce  in  1 895  in  animals 
suffering  from  the  tsetse-fly  disease  or  nagana  (which  means  '  weakness  ')  in 
Zululand.  At  the  same  time  they  showed  that  the  tsetse-fly  (Glossina  morsi- 
tans)  disseminated  the  disease. 

The  parasite  is  widespread  throughout  Africa,  especially  in  Zululand, 
Northern  Transvaal,  and  its  surrounding  countries;  also  from  Pretoria  to 
Lake  Nyassa  in  the  basin  of  the  Limpopo,  in  the  basin  of  the  Zambesi,  in 
East  Africa,  where  it  causes  nagana  or  the  fly  disease,  and  in  Uganda, 
where  it  is  called  '  jinja.' 

Morphology. — The  appearance  of  the  parasite  is  worm-like,  being  28  to  33  (x 
in  length  in  horses  and  donkeys.  The  length  is  constant  for  the  given  animal, 
but  varies  in  different  hosts,  being  26  to  27^  in  rats,  mice,  guinea-pigs,  rabbits, 
and  dogs.  The  anterior  end  (non-flagellate)  is  a  truncated  cone,  behind  which 
lies  the  kinetonucleus  as  a  well-marked  rounded  mass,  posterior  to  which  the 
flagellum  arises.  The  trophonucleus  lies  in  the  middle  of  the  body,  and 
many  chromatoid  granules  may  be  seen  posterior  to  it,  while  still  further 
posterior  the  free  whip  of  the  flagellum  may  be  noted.  Koch  considers  C. 
brucei  to  be  identical  with  C.  evansi,  but  the  animal  reactions  clearly  show 
them  to  be  different  species. 

Life-History. — The  life-cycle  in  the  vertebrate  host  has  not  been  very  fully 
worked  out,  but  the  longitudinal  division  is  well  known.  The  kinetonucleus 
divides  first,  then  the  flagellum,  then  the  trophonucleus,  and  finally  the 
cytoplasm,  but,  according  to  Prowazek,  division  is  really  a  very  complicated 
process.  First  the  blepharoplast  becomes  thickened,  elongated,  and  dumb- 
bell-shaped, and  then  divides.  In  the  trophonucleus  the  chromosomes  behave 
like  the  kinetonucleus  and  the  centrosome,  and,  having  divided,  the  whole 
nucleus  divides.  The  chromatin  granides  in  the  cytoplasm  are  also  said  to 
undergo  fission,  while  a  new  flagellum  develops  from  the  new  kinetonucleus. 
Parasites  resembling  the  latent  forms  of  Breinl  and  Hindle  are  known,  and  are 
called  involution  forms. 

It  is  believed  by  some  authorities  that  the  parasite  lives  in  nature  in  the 
wildebeeste  (Catoblepus  gnu),  the  koodoo  (Strepsiceros  capensis),  the  bush-buck 
{Tragelaphus  scriptus  sylvaticus),  and  the  hyena,  without  causing  disease. 
These  may  form  a  reserve  from  which  the  tsetse-flies  G.  morsitans,  G.  pallidipes, 
and  G.  fusca  can  obtain  parasites  which  undergo  development  in  their  alimen- 
tary canal,  during  which  time  they  are  non-pathogenic,  and  when  fully 
developed  are  found  in  the  proboscis,  and  are  again  capable  of  being  inoculated 
into  animals,  in  some  of  which  they  are  pathogenic.  Kleine  has  proved  that 
the  transmission  of  the  trypanosome  is  not  merely  mechanical,  as  suggested 
by  Bruce  and  others,  but  also  takes  place  after  the  trypanosome  has  undergone 
development  in  the  fly,  which  is  its  true  host.  Thus,  freshly  caught  G.  morsi- 
tans for  the  first  three  days  infected  cattle,  and  then,  from  the  fourth  to  the 
tenth  day  the  flies  were  non-infective,  but  from  the  eleventh  to  the  forty- 
fourth  day  they  were  very  infective.  This  shows  that  the  parasite  must 
undergo  a  development  in  the  fly. 


CASTELLAN  ELLA  BRUCEI  jii 

Cultivation. — Novy  and  McNeal  have  cultivated  C.  brucei  in  the  same 
manner  as  Lewisonella  lewisi,  and  found  some  evidence  of  a  toxin,  but  it  only 
grows  exceptionally  in  the  water  of  condensation  from  the  agar  medium  which 
contains  half  or  less  than  half  its  volume  of  blood.  Agglomeration  takes 
place  under  various  circumstances — e.g.,  mixture  with  immune  blood  or  a  few 
drops  of  dilute  acetic  acid,  etc. 

Pathogenicity. — The  disease  can  therefore  be  spread  by  the  bites  of  certain 
tsetse-flies,  particularly  G.  morsitans  and  perhaps  the  others  mentioned  above. 

It  can,  however,  be  also  spread  by  inoculation  and  by  eating  the  blood  of 
animals  recently  dead  from  the  disease.  The  incubation  period  is  about  ten 
days,  and  the  effects  produced  in  animals  vary  considerably  in  the  following 
manner: — 

i.  It  is  an  acute  disease  in  mice,  rats,  dogs,  monkeys,  cats,  etc.,  dogs  dying 
in  two  to  six  days,  rats  in  three  to  six  days. 

2.  It  is  a  subacute  disease  in  rabbits,  guinea-pigs,  equines,  and  pigs,  a 
horse  dying  in  fifteen  to  nineteen  days. 

3.  It  is  a  chronic  disease  in  cattle,  goats,  geese,  and  fowls.  In  cattle  it 
lasts  from  one  week  to  six  months. 

Battaglia  has  succeeded  in  inoculating  bitches  by  injecting  some  infected 
blood  in  vaginam.  He  has  also  infected  rabbits  by  inoculating  blood  on  the 
penis,  when  a  hard,  granulomatous  nodule,  very  similar  to  a  human  syphilitic 
primary  sore,  developed. 

Nagana  is  invariably  fatal  to  the  horse,  the  ass,  and  the  dog,  but  a  small 
percentage  of  bovines  recover.  In  these  animals  it  is  characterized  by  fever; 
by  an  infiltration  of  coagulable  lymph  in  the  subcutaneous  tissue  of  the  neck, 
of  the  abdomen,  or  of  the  extremities,  giving  a  swollen  appearance  to  those 
parts;  by  a  destruction  more  or  less  rapid  of  the  red  corpuscles  of  the  blood, 
with  an  extreme  emaciation,  often  blindness ;  and  by  the  presence  constantly 
in  the  blood  of  C.  brucei. 

Very  few  lesions  are  found  at  the  autopsy,  the  most  characteristic  being:  — 

1 .  Enlargement  of  the  spleen. 

2.  Trypanosomes  in  the  blood. 

3.  Hypertrophy  of  the  lymphatic  glands,  but  apparently  not  associated 
with  a  development  of  the  parasites  in  these  organs. 

4.  In  horses,  the  liver  and  spleen  are  hypertrophied,  and  there  is  yellow 
serous  infiltration  under  the  skin  and  mucosa  and  between  the  muscles,  as 
well  as  some  pleural  and  pericardial  exudations  and  subpericardial  ecchymoses. 
A  gelatinous  substance  is  found  at  times  around  the  spinal  cord. 

According  to  Bradford,  Plimmer,  Yakimoff,  Lanfranchi,  Rondoni,  Goretti 
and  others,  the  spleen  has  a  trypanolytic  action,  but  this  is  denied  by  Laveran, 
Thiroux,  Massaglia,  and  others. 

The  best  treatment  is  arsenic  in  some  form.  Trypanroth,  a  benzine  colour, 
and  serum  treatment  have  not  proved  of  great  service. 

Castellanella  equiperdum  Dollein,  1901. 

Synonym. — T.  rougeti  Laveran  and  Mesnil. 

C.  equiperdum  is  the  cause  of  the  disease  called  dourine  or  mal  du  coit  in 
horses  in  Europe,  India,  North  Africa  (Algeria),  and  North  America. 

Morphology. — It  is  about  25  to  28  fi  in  length,  and  has  no  chromatic  granules 
in  the  cytoplasm.  It  is  difficult  to  find  in  naturally  infected  animals,  being 
best  obtained  from  the  plaques  of  the  eruption.  Salvin-Moore  and  Breinl 
reported  the  presence  of  latent  bodies  in  inoculated  rats. 

Life-History. — It  does  not  appear  to  be  spread  by  a  fly,  but  by  coitus  between 
stallion  and  mare.  Hence  the  disease  resembles  syphilis,  and  proves  that  a 
trypanosome  is  capable  of  penetrating  a  mucous  membrane.  The  incubation 
is  from  eleven  to  twenty  days. 

Stage  1,  or  the  Period  of  (Edema. — The  genital  organs  begin  to  show  signs 
of  oedema,  generally  painless  and  not  inflammatory,  though  there  is  some  fever. 
In  about  a  month  the  oedema  disappears,  and  weakness  and  emaciation  begin. 

Stage  2,  or  the  Period  of  Eruption,  is  characterized  by  the  appearance  in 
about  forty  to  forty-five  days  (or  two  months)  after  infection  of  an  eruption. 


4i2  TRYPANOSOMIDM 

characterized  by  circular  cedematous  areas  about  the  size  of  a  two-shilling 
piece,  generally  under  the  skin  of  the  sides  and  hind-quarters,  but  sometimes 
also  under  that  of  the  neck,  shoulders,  and  thighs.  This  eruption  is  very 
variable,  and  may  appear  in  the  morning  and  disappear  at  night,  but  generally 
it  lasts  a  week,  and  leaves  the  animal  in  a  feeble  condition.  There  is  also 
synovial  engorgement  of  the  joints  and  tendon-sheaths,  and  enlargement  of 
the  lymphatic  glands,  particularly  the  inguinal.  The  temperature  is  often 
raised  to  390  C.  (102-2°  F.)  in  the  evening,  and  falls  to  38'5°  C.  (10 1-4°  F.)  in 
the  morning. 

Stage  3,  or  the  Period  of  Ancemia  and  Paralysis. — The  animal  now  becomes 
very  anaemic,  with  pale  mucosas,  and  emaciation  is  marked.  There  are  often 
superficial  abscesses  which  do  not  heal,  and  some  conjunctivitis  and  ulcerative 
keratitis.  Micturition  is  difficult,  and  the  urine  is  thick.  Sensibility  is 
diminished,  and  paralysis  comes  on,  due  to  softening  of  the  cord,  and  in  from 
two  to  eighteen  months  the  animal  dies.     The  disease  is  said  to  be  always  fatal. 

The  above  is  the  usual  type  of  the  disease,  and  may  be  called  chronic 
dourine,  but  in  addition  there  is  an  acute  type,  in  which  the  animal  dies  after 
the  first  stage  from  acute  paralysis,  which  comes  on  suddenly  a  few  days 
after  the  appearance  of  the  eruption. 

The  post-mortem  lesions  are  in  the  spinal  cord  and  the  lymphatic  glands. 
In  the  cord  there  is  gelatinous  exudation  around  the  lumbar  area,  and  cervical 
enlargement  with  intense  chronic  inflammation  of  the  posterior  spinal  ganglia, 
with  degeneration  of  the  perikarya  and  their  associated  neurones,  causing 
degeneration  of  the  posterior  roots  and  columns,  as  in  tabes  dorsalis. 

The  grey  matter  of  the  cord  also  shows  chromolytic  changes,  with  capillary 
haemorrhages  due  to  chronic  inflammation.  Mott  says  that  the  infiltration 
and  thickening  of  the  septa  of  the  cord,  the  infiltration  of  the  nerve  roots  and 
the  vessel  walls  with  lymphocytes,  is  like  a  syphilitic  meningitis.  The  mem- 
branes at  the  base  of  the  brain  may  also  be  affected.  The  lymphatic  glands  are 
enlarged,  congested,  and  softened.  The  disease  appears  to  begin  by  inocula- 
tion, and  then  to  spread  to  the  inguinal  glands,  and  then  to  the  pelvic  lympha- 
tics, and  from  them  to  the  posterior  lumbo-sacral  roots,  and  thus  the  cord 
becomes  affected.  Other  lesions  are  gelatinous  exudation  under  the  skin, 
serous  effusions  into  the  pleural  and  peritoneal  cavities,  wasting  and  pallor 
of  muscles,  with  fatty  degeneration  and  an  interstitial  keratitis. 

Genus  Duttonella  Chalmers,  1918. 

Duttonella  vivax  Ziemann,  1905. 

Synonym. — Trypanosoma  vivax  Ziemann,  1905. 

This  trypanosome  was  found  by  Ziemann  in  1905  in  the  blood  of  cattle, 
sheep,  and  goats,  suffering  from  '  souma  '  in  the  Cameroons.  Morphologically 
it  closely  resembles  T.  cazalboui,  but  it  differs  in  the  following : — 

1 .  Rats  are  susceptible  to  T.  vivax,  but  not  to  T.  cazalboui. 

2.  Cross  immunity  experiments  indicate  distinct  differences. 

Bruce's  T.  vivax  is  T.  cazalboui,  because  rats  are  not  susceptible  to  Bruce's 
Uganda  strain.  It  is  possible  that  a  strain  allied  to  D.  vivax  has  been  found 
by  Macfie  in  human  blood  {vide  p.  430.). 

The  flagellate  is  very  rapid  in  its  movements.  A  large  kinetonucleus  and 
clear  cytoplasm  are  present.  It  measures  16-31X2-3  microns,  and  has  its 
flagellum  always  free.  It  is  pathogenic  for  equidae  and  ruminants.  The 
d<  \ dopment  is  anterior  in  the  tsetse-fly,  being  confined  to  the  proboscis. 

Duttonella  caprae  Kleine,  1910. 

Synonym. — Trypanosoma  caprce  Kleine,  1910. 

Found  in  sick  goats  near  Tanganyika,  it  is  capable  of  passing  through  its 
cycle  of  development  in  G.  morsitans  in  some  nineteen  days  after  infection. 
Development  only  takes  place  in  the  proboscis.  The  final  stage  is  in  the 
hypopharynx,  where  the  trypanosomes  revert  to  the  blood  form  and  become 
infective. 

1 1  is  a  heavily  built  trypanosome,  with  very  rapid  movements,  measuring 


GENUS  TRYPANOSOMA  '  SENSU  LATO'  413 

1 8-32 X  i'75-4"25  microns,  and  having  the  flagellum  always  free.     It  is  patho- 
genic for  equidae  and  ruminants  only. 

Duttonella  uniformis  Bruce,  Hamerton,  Bateman,  and  Mackay,  1911. 

Synonym. —  Trypanosoma  uniforme  Bruce,  Hamerton,  Bateman,  Mackie. 

It  is  very  like  T .  cazalboui,  but  smaller,  and  causes  a  very  fatal  disease  in 
cattle.  It  is  a  small  active  trypanosome  16X  1  •5-2*5  microns,  with  the  free 
part  of  the  flagellum  some  1-5  microns  in  length.  There  is  no  narrowing 
opposite  the  trophonucleus.  It  is  spread  by  Glossina  palpalis,  which  becomes 
infective  in  twenty-seven  to  thirty-seven  days.  The  development  is  anterior, 
being  confined  to  the  proboscis. 

Duttonella  pecorum  Bruce,  Hamerton,  Bateman,  Mackie,  19 10. 

Synonym. — Trypanosoma  pecorum. 

This  term  probably  includes  Trypanosoma  dimorphon,  T.  congolcnse,  and 
T.  confusum,  Dr.  Edington's  Zanzibar  trypanosome,  the  trypanosomes  from 
Chai-Chai  and  from  Southern  Rhodesia. 

It  is  found  in  cattle.  It  measures  80-180  microns,  and  is  capable  of 
passing  through  a  cycle  of  development  in  G.  morsitans,  which  becomes 
infective  after  twenty  days.  Development  takes  place  like  T .  simice  first  in 
the  gut,  then  in  the  labial  cavity,  and  finally  in  the  hypopharynx,  where  it 
becomes  infective. 

Duttonella  simiae  Bruce,  Harvey,  Hamerton,  Davey,  and  Lady  Bruce,  1912. 

Synonym. — Trypanosoma  ignotum  Kinghorn  and  Yorke,  1902. 

It  causes  a  rapidly  fatal  disease  in  monkeys  and  a  chronic  disease  in  goats. 
It  is  abundantly  present  in  Glossina  morsitans  in  Nyassaland  and  North- 
Eastern  Rhodesia.  It  measures  14-24X  1-2*75  microns,  and  is  monomorphic. 
Its  natural  host  appears  to  be  G.  morsitans,  and  the  monkey  seems  to  be  a 
new  host.     The  development  is  completed  in  the  proboscis  and  hypopharynx. 

FORMS  UNCLASSIFIABLE. 

Genus  Trypanosoma  sensu  lato. 
Group  i  :  Part  of  the  Flagellum  always  Free. 

They  may  be  separated  from  one  another  according  to  the  follow- 
ing scheme,  based  upon  the  invertebrate  host,  the  pathogenicity, 
and  the  serum  reactions: — ■ 

A.  No  invertebrate  host,  spread  directly  from  male  to  female 

by  coitus : — 
Kinetonucleus     near    aflagellar     end    and     easily    seen. 
Habitat  America — Hippicum. 

B.  Invertebrate  host  not  a  Glossina  : — 

I.  Kinetonucleus    very    insignificant.     Habitat,     South 

America — Equinum. 
II.  Kinetonucleus      ordinary.      Parasite     monomorphic. 
Habitat,  various.    Animal  immune  to  C.  evansi 
becomes    infected    with    T.    togolense    and    T. 
soudanense. 

(a)  Animal  immune  to  T.  togolense,  infective  by  C. 

evansi  and  T.  soudanense — Togolense. 

(b)  Animal  immune  to  T.  soudanense  becomes  infec- 

tive by  C .  evansi  and  T.  togolense — Soudanense. 


4i4  TRYPANOSOMIDJE 

C.  Invertebrate  host  a  Glossina  : — 

Rats  refractory.     Large  forms,  24  microns — Cazalbom. 

D.  Invertebrate  host  unknown: — ■ 

I.  Attacks  horses: — 

(a)  In  Venezuela—  V  enezuelense . 

(b)  InMorocco. separated bycross immunity  —Marocamtm. 

(c)  In  Algeria,  separated  by  cross  immunity — Berberum. 
II.  Attacks  horses  and  cattle: — 

In  Annam — Annamense. 
III.  Attacks  cattle :— 

In  Italian  Somaliland- — Cellii. 

Trypanosoma  equinum  Vosges,  1901. 

Synonym. — T.  elmassiani  Lignieres. 

T.  equinum,  discovered  by  Elmassian,  is  the  cause  of  mal  de  caderas  in 
horses  and  dogs  in  South  America. 

Morphology. — This  parasite  closely  resembles  T.  brucei  and  T.  evansi.  In 
length  it  is  22  to  24  /n,  and  in  breadth  1-5  /jt,  and  it  has  the  same  measurements 
in  different  species  of  animals.  It  is  very  active,  but  its  principal  characteristic 
is  that  the  kinetonucleus  is  very  insignificant. 

Life-History. — Multiplication  is  by  equal  binary  division.  It  agglomerates, 
and  has  been  cultivated  by  Thomas  and  Breinl  on  a  rabbit's  blood  and  chicken- 
broth  agar  medium. 

It  can  be  inoculated  into  the  ordinary  laboratory  animals.  Its  mode  of 
propagation  is  not  well  known,  but  Migone  has  shown  that  it  is  the  cause  of  a 
disease  which  kills  the  capybara  (Hydrochcerus  capybara),  which  appears  to  be 
the  reservoir  for  the  parasite,  as  monkeys  inoculated  from  a  sick  Hydrochcerus 
died  in  seventeen  days.  How  the  disease  spreads  from  the  Carpinchos  {Hydro- 
chcerus) to  the  horses  is  not  clear.  Dogs  may  be  infected  by  eating  diseased 
animals,  and  then  from  the  dog  the  infection  may  be  spread  to  the  horse  by 
fleas,  because  they  have  been  found  to  infect  rats.  Some  authorities  consider 
that  it  may  be  spread  by  members  of  the  Tabanidae  (Chrysops  ?)  and  by 
Stomoxys,  but  Neiva  has  infected  Triatoma  infeslans  Klug,  and  its  faeces 
produced  the  disease  in  guinea-pigs  when  placed  on  the  conjunctiva. 

Pathogenicity. — Mal  de  caderas  is  a  very  fatal  disease  among  the  horses  of 
South  America.  The  first  sign  of  the  disease  is  weakness,  which  makes  rapid 
progress,  though  the  appetite  remains  good.  The  temperature  is  febrile,  and 
after  a  variable  period  the  hind-quarters  become  paralyzed  and  the  horse  drags 
its  limbs,  the  hoofs  scraping  the  ground.  As  it  walks  it  staggers,  the  hind- 
quarters oscillating  from  right  to  left,  which  characteristic  gives  the  disease 
its  name  of  mal  de  caderas,  the  disease  of  the  hind-quarters.  In  the  stable 
it  can  support  itself  against  the  walls,  but  in  the  open  air  it  staggers  and  falls. 
There  may  be  albuminuria  and  haematuria,  and  an  eruption  on  the  neck, 
shoulders,  and  hind-quarters.  The  eyelids  show  conjunctivitis  and  chemosis. 
The  horse  lives  about  two  months  after  the  paralysis  sets  in. 

Congestion  and  enlargement  of  the  spleen  and  mesenteric  glands  are  seen 
in  post-mortems.  The  kidneys  are  affected,  nephritis  and  interstitial  haemor- 
rhages being  noted.  There  are  also  serous  exudations  into  the  peritoneum, 
the  pleura,  the  pericardium,  and  the  spinal  <  anal. 

Trypanosoma  soudanense  Laveran,  1907. 
Type  of  Trypanosoma  evansi  causing  tahaga  in  dromedaries  in  the  Upper 
Niger,  el  debab  in  Southern  Algeria,  and  the  zousfana  in  horses  in  Southern 
Algeria.     Carriers:  Tabanidae.     Yorke  and  Blacklock  consider  this  to  be  the 
same  as  Castellavella  evansi. 

Trypanosoma  togolense  Mesnil  and  Brimont,  1909. 
Type  of  Castellanella  evansi,  parasitic  in  horses  and  cattle,  and  the  cause  of 
nagana  in  Togoland . 


TRYPANOSOMA   CAZALBOUI  415 

Trypanosoma  (Duttonella)  cazalboui  Laveran,  1906. 
This  organism,  which  should  be  placed  in  the  genus  Duttonella,  was  found 
by  Cazalbou  in  1904  in '  souma,'  a  form  of  cattle  trypanosomiasis  in  Upper 
Nigeria.  The  disease  is  known  in  West  Africa,  in  Uganda,  the  French 
Congo,  the  Congo,  and  Rhodesia.  It  affects  cattle,  horses,  mules,  and 
donkeys,  the  incubation  being  seven  days  and  the  disease  acute,  subacute, 
or  chronic.  Cattle  may  die  in  eight  days,  two  months,  or  more  than  twelve 
months.  It  is  monomorphic,  24  X  i'5-2  microns,  with  an  oval  trophonucleus 
situate  about  the  middle  of  the  body,  and  a  spherical  kinetonucleus  lying 
near  the  aflagellar  extremity.  The  undulating  membrane  is  not  markedly 
folded,  and  the  flagellum  always  becomes  free.  In  the  vertebrate  there  is 
the  usual  longitudinal  division.  Trautmann  records  the  successful  inocula- 
tion of  Cercopithecus  patas.  It  may  develop  in  G.  palpalis,  G.  tachinoides,  G. 
longipalpis,  or  G.  morsitans,  and  may  be  directly  conveyed  by  stomoxys. 
G.  palpalis  is  the  usual  carrier.  The  development  is  anterior,  being  restricted 
to  the  proboscis.  The  first  three  carriers  become  infective  in  six  to  seven  days, 
and  G.  morsitans  in  eight  to  ten  days,  but  in  Uganda  it  may  require  eleven  to 
thirty-five  days  to  become  infective  in  a  fly,  which  difference  may  be  due  to 
climate.  In  the  proboscis  the  trypanosome  passes  through  leptomonas  or 
critbidial  forms,  and  becomes  attached  to  the  walls  of  the  labium  and  multiplies. 
Under  the  influence  of  the  salivary  secretion  these  forms  become  small,  actively 
motile  trypanosomes,  which  are  the  infective  agent,  and  apparently  remain 
in  the  fly  for  the  remainder  of  its  life. 

Trypanosoma  hippicum  Darling,  1910. 
This  trypanosome  causes  a  disease  called  murrina  among  mules,  and  was  first 
described  in  some  animals  imported  from  the  United  States  via  New  Orleans 
to  Panama.  The  trypanosome  resembles  Castellanella  evansi,  being  18  to  28^ 
in  length,  with  a  width  of  1*5  to  3  ju.  The  trophonucleus  is  oval  and  median. 
The  kinetonucleus,  which  is  near  the  aflagellar  end,  is  very  easily  seen,  which 
is  a  characteristic  feature  of  the  parasite.  The  undulating  membrane  is  not 
much  folded.  It  divides  longitudinally  in  the  blood.  It  is  spread  by  coitus, 
and  can  also  be  spread  mechanically  by  species  of  Musca,  Compsomyia,  and 
Sarcophaga  sucking  wounds  in  the  diseased  and  the  healthy.  The  essential 
pathology  of  murrina  is  an  intoxication  resulting  in  cellular  degeneration  and 
necrosis.  These  toxins  produce  endothelialysis,  lymphocytosis,  auto-haema- 
glutination,  phagocytosis  of  erythrocytes  and  trypanosomes,  hyperplasia  of 
the  spleen,  bone-marrow,  and  lymph  glands,  and  cellular  exudations  into  the 
kidney,  liver,  etc.  Owing  to  the  destruction  of  the  endothelium  there  is  con- 
siderable amount  of  ecchymosis  in  various  regions. 

Trypanosoma  venezuelense  Mesnil,  1910. 
Type  of  Castellanella  evansi,  and  considered  by  Yorke  and  Blacklock  to  be 
identical.     Attacks  horses  in  Venezuela;  carrier  unknown. 

Trypanosoma  annamense  Laveran,  191 1. 

Type  of  Castellanella  evansi  ;  causes  disease  in  horses  and  cattle  in  Annam. 
Carriers:  Tabanidae  and  Hippoboscidae. 

Trypanosoma  cellii  Marfoglio,  191  r. 

This  trypanosome  is  pathogenic  for  1  attle  in  Italian  Somaliland,  causing  a 
disease  called  '  gobiat.'     Pathogenic  for  dogs,  rabbits,  rats,  and  mi<  e. 

In  bovines  there  are  the  following  types: — (1)  Irregularly  rounded,  with 
short  fiagella  inside  some;  (2)  Lcishmania-like  forms;  (3)  Trypanosomes. 

Trypanosoma  marocanum  Sergent,  Lheritier,  and  Belleval,  1915  (16-24X  i*5- 
2-5  microns),  is  the  cause  of  a  disease  of  horses  at  Casablanca  in  Morocco. 
Morphologically  it  is  identical  with  T.  berberum,  the  cause  oi  debab,  but 
crossed  immunity  experiments  separate  it  from  this  organism  and  from  T. 
equiperdum  and  T.  soudanense.  Laveran  says  that  there  are  two  trypanosomes 
at  work  on  Moroccan  horses,  one  monomorphic  and  one  polymorphic. 

Trypanosoma  berberum  Edmond  and  Et.  Sergent,  and  Lheritier,  1912,  is 
the  cause  of  debab  in  Algerian  horses. 


4T6  TRYPANOSOMID&. 

Group  2  :  No  Part  of  the  Flagellum  Free. 

Trypanosoma  congolense  Broden,  1904. 

Synonyms. — According  to  Blacklock  and  Yorke,  T.  dimorphon  (sensu 
Laveran  and  Mesnil) ;  T.  ccmfusum  (Montgomery  and  Kinghorn) ;  T.  pecorum 
(Bruce) ;  T.  nanum  (Laveran). 

This  trypanosome  causes  disease  among  horses,  cattle,  sheep,  and  drome- 
daries in  the  French  and  Belgian  Congos  and  in  North-East  Rhodesia.  It  is 
10  to  17  /n  long  and  1  to  2  /j,  broad.  Carrier:  Glossina  morsitans,  winch  is  in- 
fective twenty-three  days  after  a  feed  thereon.  The  alimentary  canal  is  full 
of  parasites,  and  the  labrum  contains  the  Leptomonas  type,  while  the  small 
infective  trypanosomes  are  in  the  hypopharynx. 

Trypanosoma  dimorphon  Laveran  and  Mesnil,  1904. 

This  trypanosome  was  discovered  by  Dutton  and  Todd  in  1904  in  horses 
on  the  Gambia,  and  is  now  known  to  exist  in  several  parts  of  Africa,  where 
perhaps  a  wide  equatorial  belt  across  the  continent  is  affected.  It  is  also 
found  in  cattle,  dogs,  pigs,  sheep,  and  goats. 

Morphology. — It  exists  in  three  forms: 

1.  Tadpole  Form. — Found  in  the  early  stage  of  the  disease,  11  to  13  /j,  long 
and  o-i8  /u  broad. 


Fig.   104. — Trypanosoma  dimorphon  Laveran  and  Mesnil. 
(After  Dutton  and  Todd.) 

2.  Stumpy  Form. — Seen  when  the  disease  is  not  too  far  advanced,  and 
characterized  by  a  short  thick  body  and  a  short  flagellum.  Length  16  to  19  [x, 
breadth  3^4  to  3-5  fx. 

3.  Long  Form. — With  long  thin  body  and  long  flagellum,  found  a  few  days 
before  death.     Length,  26  to  30  /a,;  breadth,  i-6  to  2  /x. 

These  may  be  respectively  indifferent,  female,  and  male  forms  of  the  para- 
site, a  view  supported  by  Hindle. 

It  has  been  cultivated,  and  it  can  be  inoculated  into  rats,  mice,  guinea-pigs, 
and  rabbits,  as  well  as  horses. 

Life-History. — Hindle's  observations  show  that  the  indifferent  forms  give 
rise  to  latent  bodies  or  cysts  which  gather  in  the  spleen,  where  they  lie  dormant 
for  a  time,  and  finally  develop  again  in  trypanosomes.  It  apparently  can 
undergo  development  in  Glossina  palpalis,  as  Bruce  and  Hamerton  have 
shown  that  it  is  a  carrier,  while  Bouet  and  Roubaud  have  shown  thatG.  tachi- 
noides  and  G.  longipalpis  can  also  transmit  the  parasite  as  in  G.  morsitans. 
The  development  is  by  multiplication  in  the  intestine,  and  then  in  the  form  of 
Leptomonas  or  Crithidia  in  the  proboscis,  after  which  the  fly  becomes  infective 
in  about  eighteen  days  from  the  date  of  the  infective  feed. 


THE  TRYPANOSOMES  OF  MAN  4i7 

Pathogenicity.  —The  symptoms  in  the  horse  begin  with  loss  of  vigour, 
followed  in  two  to  three  weeks  by  fever.  During  the  next  month  the  weakness 
is  more  marked  and  the  abdomen  swells,  the  testicles  hang  down  and  arc 
(edematous,  the  coat  becomes  staring,  the  animal  looks  apathetic,  and  death 
ensues  in  about  a  year. 

The  post-mortem  shows  oedema  of  the  abdominal  wall  and  a  coloured  fluid 
in  the  pleura  and  pericardium,  with  hypertrophy  of  the  lymphatic  glands, 
fatty  liver,  and  congestion  of  the  lungs.     The  spleen  is  normal. 

Trypanosoma  frobeniusi  Weissenborn,  191 1. 
Allied  to  T.  dimorphon  and  T.  congolense,  and  found  in  horses  in  Togoland. 

Trypanosoma  nanum  Laveran,  1905. 

Balfour  in  1904  discovered  this  parasite  in  cattle,  which  appeared  to  be  ill, 
on  the  While  Nile.  The  parasites  are  small  (10  to  14  /u,  by  1-5  to  2  /j),  with  no 
free  fiagellum,  and  are  non-pathogenic  for  dogs,  rabbits,  and  monkeys. 
Amoeboid  forms  were  found  in  the  cerebro-spinal  fluid.  Duke  in  19 12  showed 
that  it  was  transmitted  by  Glossina  palpalis,  in  which  it  developed  in  the  hind- 
gut,  and  from  thenceforwards  to  the  oesophagus,  but  did  not  infect  the  salivary 
glands.  Development,  according  to  Miss  Robertson,  takes  place  in  G.  palpalis, 
and  is  like  CasteHanella  castellanii,  but  with  crithidial  phase  in  proboscis,  not  in 
salivary  glands.  The  parasite  develops  in  the  hind  intestine  and  reaches  the 
proventriculus  on  the  twentieth  day,  and  the  proboscis  on  the  twenty-fifth, 
where  they  become  crithidial  forms,  and  finally  trypanosomes,  which,  however, 
may  only  be  developed  in  the  hypopharynx. 


Group  3 :  Part  of  the  Flagellum  may  or  may  not 
be  Free. 

Trypanosoma  pecaudi  Laveran,  1907. 

In  the  French  Sudan,  in  addition  to  rn'bori  and  souma,  there  is  a  third 
disease — baleri,  in  EquidaB — caused  by  T.  pecaudi,  with  two  forms  like 
T.  dimorphon — (1)  long  and  slender  (25  to  35  yu  by  1*5  /j),  (2)  short  and  broad 
(14  to  20  ft  by  3  to  4  /j.).  Carriers:  Glossina  longipalpis,  rarely  G.  palpalis 
and  G.  tachinotdes. 

The  incubation  in  G.  longipalpis  is  about  twenty-three  days.  The  trypano- 
somes multiply  in  the  intestine,  and  in  seven  to  nine  days  invade  the  whole 
intestine  and  pharynx.  The  parasites  now  eiter  the  proboscis  and  pass 
through  crithidial  and  leptomonas  stages.  Finally,  some  reach  the  hypo- 
pharynx,  where  they  assume  the  '  salivary  trypanosome  form  '  and  become 
infective. 

LITTLE-KNOWN  TRYPANOSOMES. 

Trypanosoma  elephantis  Bruce,  Hamerton,  and  Mackie,  1909,  has  been  found 
in  the  elephant  in  Uganda;  it  resembles  T.  soudanense. 

Trypanosoma  ingens  Bruce,  Hamerton,  and  Mackie,  1909,  has  been  found 
in  the  reed  buck  and  ox  in  Uganda ;  it  is  of  large  size  (72  to  122  /a  by  7  to  10  /j)  . 

Trypanosoma  giganteum  Lingard  was  found  twice  in  cattle  suffering  from 
symptoms  similar  to  those  found  in  surra. 

Trypanosoma  bovis  Kleine  was  found  in  sick  cattle  near  Tanganyika. 


THE  TRYPANOSOMES  OF  MAX. 

There  is  evidence  that  man  is  infected  with  a  variety  of  trypano- 
somes, the  number  of  which  is  likely  to  be  increased  in  the  near 
future.     Those  described  in  man  are: — 

27 


4iS  TRYPANOSOMIDM 

i.  Trypanosoma  gambiense  Dutton,  1902. 

2.  Trypanosoma  castellanii  Kruse,  1903. 

3.  Trypanosoma  vivax  Ziemann,  1905,  varietas  macfiense. 

4.  Trypanosoma  critzi  Chagas,  1909. 

5.  Trypanosoma  rhodesiense  Stephens  and  Fantham,  1910. 

6.  Trypanosoma  nigeriense  Macfie,  1913. 

7.  Trypanosoma  gambiense  varietas  longum  Da  Costa,  St.  Anna, 
Dos  Santos,  and  Alvares,  1915. 

When  a  classification  is  desired  it  is  always  necessary  to  attempt 
to  discover  the  characters  of  the  original  species,  which  in  this  case 
is  T.  gambiense  Dutton,  1902.  Sixteen  years  have  passed  since  the 
slides  containing  the  original  specimens  of  Dutton  and  Todd  were 
made,  and,  therefore,  as  the  original  strain  has  long  been  lost,  the 
only  method  of  comparing  other  organisms  with  the  original  speci- 
mens is  morphological.  Chalmers  and  O'Farrell  have  made  this 
comparison  by  measuring  one  thousand  non-dividing  forms  in  the 
original  slides.  As  far  as  measurements  go,  these  strains  are  very 
similar,  but,  as  we  have  repeatedly  insisted,  morphology  often  may 
not  help  in  separating  closely  related  but  perhaps  quite  distinct 
species,  which  require  to  be  studied  serologically  and  with  regard  to 
animal  pathogenicity,  and,  in  cases  of  human  infection,  with  regard 
to  the  nature  of  the  disease  in  man.  Thus  Stephens  has  pointed 
out  that  T.  lewisi  and  T.  rabinowitschi,  T.  brucei  and  T.  evansi,  T. 
pecaudi  and  T.  ugandce,  T.  rhodesiense  and  T.  pecaudi  are  indis- 
tinguishable morphologically,  but  are  distinct  biologically. 

We  mention  these  points  in  order  to  make  clear  to  the  reader  the 
necessity  of  comparing  human  trypanosomes  by  means  of  the  clinical 
features  of  the  disease  in  man,  the  serum  reactions  and  animal 
experiments,  as  well  as  hy  morphological  characters,  and  we 
have  suggested  for  years  that  the  name  T.  gambiense  covered  a 
number  of  different  forms,  which  at  the  present  time  is  generally 
admitted  with  regard  to  T.  rhodesiense.  And  why  not  ?  Are  there 
not  a  number  of  different  trypanosomes  in  wild  animals  in  Africa, 
and  is  it  impossible  that  man  should  from  time  to  time  become 
infected  by  one  of  these,  even  if  it  does  not  appear  in  epidemic  form 
in  the  human  race  ?  To  exemplify  we  draw  attention  to  an  organism 
resembling  T.  vivax  found  by  Macfie  in  man. 

SirDavid  Brucebelieves  that  T  .rhodesiense  Stephens  andFantham, 
1910,  is  the  same  as  T.  brucei  Plimmer  and  Bradford,  1899,  but  this 
can  hardly  be  so,  because  Laveran  and  Nattan-Larrier  have  im- 
munized a  ram  against  T .  brucei,  and  then  infected  it  with  T.  rhode- 
siense, an  acutely  lethal  infection  ensuing.  The  serological  experi- 
ments of  Chalmers  and  O'Farrell  in  vitro  and  in  vivo  also  show 
the  same  marked  differences  between  T.  rhodesiense  and  another 
posterier  nucleate  trypanosome.  These  experiments,  to  our  mind, 
are  more  important  than  measurements,  and  more  important  than 
finding  that  the  development  in  Glossina  morsitans  is  very  similar 
in  both  variants.     T.  rhodesiense  may  have  been  derived  in  recent 


THE  TRYPANOSOMES  OF  MAN  419 

times  from  T.  brucci,  but  its  altered  environment  in  man  has 
changed  its  physiological  characters.  As  the  fly  remains  the  same, 
one  would  expect  this  portion  of  the  life-cycle  to  be  similar  in  the 
two  trypanosomes. 

We  look  upon  T.  nigeriense  and  T.  gambiense  var.  longum  as 
belonging  to  T.  gambiense,  because,  apart  from  the  morphological 
similarity,  to  which  we  do  not  assign  importance,  their  pathological 
action  in  man  and  the  lower  animals  appears  to  be  identical. 

As  a  result  of  these  considerations,  and  changing  the  names  so  as 
to  agree  with  the  new  nomenclature,  we  recognize  the  following 
parasites  of  man : — 

A.  Belonging  to  the  genus  Castellanella  : — 

1.  Castellanella  gambiensis  (Dutton,  1902). 

2.  Castellanella  castellanii  (Kruse,  1903). 

3.  Castellanella  rhodesiensis  (Stephens  and  Fantham,  1910). 

B.  Belonging  to  the  genus  Duttonella  : — ■ 

4.  Duttonella    vivax    (Ziemann,    1905),     var.    Macfieusis 

(Castellani  and  Chalmers,  1918). 

C.  Belonging  to  the  genus  Schizotrypanum  : — 

5.  Schizotrypanum  cruzi  Chagas,  1909. 

These  five  species  may  be  differentiated  as  follows: — - 

A.  With  schizogony — S.  cruzi. 

B.  Without  schizogony: — 

I.  Monomorphic — D.  vivax. 
II.  Polymorphic:—- 

(a)  Posteriorly  nucleate — C.  rhodesiensis. 
(&)  Not  posteriorly  nucleate : — ■ 

1.  Animal  infections  chronic  and  comparatively 

mild.        Common      North-West     Africa — 
C.  gambiensis. 

2.  Animal  infections  severe.    Common  Equatorial 

Africa — C.  castellanii. 

Castellanella  gambiensis  (Dutton,  1902). 

Usual  old  name  Trypanosoma  gambiense  Dutton,  1902. 

Synonyms. — T.  nepveui  Sambon,  1903;  T.  hominis  Manson,  1903; 
T.fordii  Maxwell,  1903;  T.  nigeriense  Macfie,  1913;  T.  gambiense 
var.  longum  Da  Costa,  St.  Anna,  Dos  Santos,  and  Alvares,  1915. 

Definition. — Castellanella  without  schizogony,  polymorphic,  tro- 
phonucleus  not  situate  close  to  aflagellar  end.     Infections  chronic. 

History. — This  trypanosome  was  first  noticed  by  Ford  in  a  ease 
of  peculiar  fever  on  the  Gambia.  He  showed  the  parasite  to  Dutton, 
who,  recognizing  it  to  be  a  trypanosome,  described  and  named  it; 
and  they  considered  it  to  be  the  cause  of  Gambia  fever,  which  was 
never  thought  by  them  to  be  connected  with  sleeping  sickness. 
The  organism  had,  however,  been  previously  seen  in  the  blood  of 
man  and  imperfectly  described  byNcpvcu.     We  consider  it  to  be 


420 


TR  YPA  NOSOMID.E 


the  same  organism  as  that  described  by  Scott  Macfie  in  1913  as 
T.  nigeriense.  Yorke  and  Blacklock  in  1915  consider  that  man 
is  the  chief  reservoir  of  this  parasite  in  Sierra  Leone,  where  sleeping 


Fig.  105. — Castellanella  gambiensis  (Dutton,  1902).     (X  1,200  Diameters.) 

Long  form  from  the  original  Gambia  fever  case  (Mr.  K.)  discovered  by 

Dutton.    (Photomicrograph.) 

sickness  is  very  chronic  and  difficult  to  recognize.  A  secondary 
reservoir  is  in  cattle.  They  record  two  cases  with  very  mild 
symptoms.     Sartory,  Lasseur,  and  Brissaud  record  C.  gambiensis 


Fig.  106.— Castellanella  gambiensis  (Dutton,   1902).     (X    1,200  Diameters.) 
Original  Gambia  specimens  from  a  rat  inoculated  from  the  second  case  of 
Gambia  fever,   showing  polymorphism — i.e.,  long,   intermediate,   and  short 
forms. 

trypanosomiasis  in  a  French  soldier  who  had  left  Africa  for  eight 
years,  and  had  never  been  in  a  tsetse-fly  area.     In  Africa  he  lived 


12 
II 

.0 

9 

5 7 
|6 

3 

2 

1 
0 

"is 

"el 

17  ha 

19 

'-" 

?! 

iJ 

23 

Z* 

't\A 

17 

26 

29 

:-o 

31 

32 

33 

34- 

35 

36 

j 

V 

/ 

1 

0«l 

J 

~r 

-•-' 

../- 

Fig.  107. — Castellanella  gambiensis  (Dutton).     Chart  of  Lengths. 

in  Algiers,  at  El  Golca,  and  went  to  Timimoun.  Bagshawe  draws 
attention  to  Nepveu's  1888  and  1890  observations,  which  have 
never  been  explained, 


CASTELLANELLA    CASTELLAXIt  421 

Morphology.  -It  is  a  polymorphic  trypanosomc,  and  morphologi- 
cally does  not  differ  essentially  from  C.  castellanii,  of  which  a 
detailed  description  is  given  below. 

Life-History. — This  has  not  been  fully  studied,  and  it  is  not 
definitely  known  whether  it  takes  place  in  Glossina  palpalis  or  in 
some  allied  tsetse-fly. 

Serum  Reactions. — -These  reactions  require  to  be  studied  in  detail. 

Pathogenicity.- — It  causes  a  form  of  sleeping  sickness,  which  appar- 
ently is  more  chronic  than  that  produced  by  C.  castellanii,  while  the 
symptoms  are  often  less  severe,  though  the  termination  is  fatal 
without  treatment,  to  which  it  appears  to  be  more  amenable. 

Castellanella  castellanii  (Kruse,  1903). 

Usual  old  name  Trypanosoma  castellanii  Kruse,  1903. 

Synonym. — T.  ugandense  Castellani,  1903. 

C.  castellanii  was  first  seen  in  the  cerebro-spinal  fluid  of  cases  of 
sleeping  sickness  by  Castellani  in  1902,  and  reported  by  him   as 
the  cause  of  the  disease  in  1903;  he  asserted 
also  the  probable  plurality  of  species  of  the 
trypanosomes    affecting  man,    in   analogy  to 
what  takes  place  in  the  lower  animals,  such  as 
horses  and  cattle.   Bruce  and  Nabarro  demon- 
strated the  fact  first  suggested  by  Sambon  and 
Brumpt  that  it  could  be  spread  by  a  tsetse-fly, 
Glossina  palpalis  ;  and  Kleine  has  demonstrated 
that  the  transmission  is  not  merely  mechanical, 
but  also  takes  place  after  a  period  during  which 
the  fly  is  non-infective,  the  deduction  being    pIG    I0s.  —  Castella- 
that  the  trypanosome  must  undergo  a  develop-        nella        castellanii 
ment  in  the  fly  which  acts  as  a  true  host.  Finally        (Kruse,  1903). 
Miss  Robertson  worked  out  the  life-cycle  in  the        The  original  trypa- 
tsetse-flv  nosome      found      by 

'  Morphology.-C.  Castellanii  measures  from  ^SS^hM^ 
J4  to  33  [*  m  length  and  from  2  to  2-5  /j,  in  a  case  of  sleeping 
breadth  (Laveran  and  Mesnil  give  17  to  28  f.i  sickness  in  Uganda. 
in  length  and  1-4  to  2  fi  in  breadth);  but,  as  (Photomicrograph.) 
already  stated,  it  is  very  polymorphic,  having 
short  forms  14  to  20  /ii,  medium  forms  20  to  24  f.i,  and  long  forms 
23  to  33  [j,.  The  anterior  end  is  variabL  and  sometimes  rounded; 
the  kinetonucleus  is  an  oval  body,  behind  which  is  often  seen  a 
vacuole.  The  trophonucleus  is  oval  in  shape,  and  situated  about 
the  middle  of  the  body,  behind  which  there  may  be  some  chro- 
matic granules  in  the  cytoplasm,  which  at  the  posterior  end  runs 
along  the  flagcllum  for  a  considerable  distance. 

Asexual  Reproduction.— The  life-history  of  the  parasite  in  the 
human  body  is  not  accurately  known.  It  can  often  be  obtained 
from  the  peripheral  blood,  but  sometimes  the  most  prolonged  search 
fails  to  demonstrate  it.     It  can  then  be  found  by  puncturing  the 


422 


TR  YPA  NOSOMIDJE 


enlarged  lymphatic  glands,  by  scarification  of  the  eruption,  or  by 
puncture  of  the  spinal  canal,  if  the  case  is  one  of  sleeping  sickness. 

Salvin,  Moore,  and  Breinl  have,  however,  investigated  the  life- 
cycle  in  the  rat,  in  which,  after  inoculation,  the  parasites  increase 
to  a  maximum  in  the  peripheral  blood,  and  then  decline  gradually 
to  nil,  at  which  they  remain  for  a  period — the  latent  period — and 
then  increase  again  in  numbers  and  reappear  in  the  peripheral  blood. 

Their  investigations  give  the  following  results :  The  parasite  may 
grow  to  a  fair  size,  and  then  divide  into  two  by  simple  fission,  and 
this  may  be  repeated  till  the  blood  is  swarming  with  them.  When 
this  is  the  case,  a  relatively  thick  band,  said  by  Swellengrebel  to  be 
composed  of  metachromatic  or  volutine  granules  (axial  filament), 
such  as  that  described  by  Miss  Robertson  in  T.  rajcs  and  by 
Prowazek  in  T.  lewisi,  grows  from  the  kinetonucleus  down  the 
endoplasm  till  it  reaches  or  even  passes  the  nucleus,  or  it  may 
coil  on  itself,  but  eventually  is  connected  with  the  trophonucleus. 


12 
II 

10 
9 

*    8 

h 

|6 

s 

3 

2 

1 
0 

14 

16 

1 

ia 

19 

20  |2I 

■-■• 

21 

■" 

25 

26  127 

23 

29 

3d 

31 

32 

•-- 

34 

US 

-f 

Fig.  109. — Castellanella  castellanii.     Chart  of  Lengths. 

The  trypanosomes  now  decrease  in  numbers  in  the  peripheral 
blood,  and  are  found  in  the  lungs,  spleen,  and  bone-marrow.  In 
these  organs  the  protoplasm  becomes  detached  from  the  periphery 
of  the  nucleus,  which  lies  in  a  clear  space.  The  nucleus  contracts, 
and  a  large  clear  vesicle  forms  in  connection  with  it,  and  around 
both  a  cytoplasmic  sheath  is  formed.  The  rest  of  the  cell  body 
now  disintegrates,  and  the  flagellum  with  the  kinetonucleus  may 
be  seen  lying  detached.  These  bodies  now  become  lodged  in  the 
spleen  and  bone-marrow,  where  they  remain  intact  for  a  period  of 
ten  days  or  more — through  the  whole  of  the  negative  or  latent  period 
when  the  trypanosomes  are  missing  from  the  blood  of  the  infected 
rat.  Moore  and  Breinl,  therefore,  call  them  latent  bodies.  They 
consist  of  a  flattened  nucleus,  containing  a  centrosome,  and  attached 
to  a  vesicle,  the  whole  being  surrounded  by  a  ring  of  cytoplasm. 
This  latent  phase  has  been  confirmed  by  Fantham. 

Just  before  the  reappearance  of  the  trypanosomes  in  the  peri- 


CASTELLAN  ELLA   CASTELLANII 


423 


Fig.   1 10. — Castellanella  castellanii  (Kruse,   1903). 

(Forms  found  in  the  cerebro-spinal  fluid.) 

The  figures  in  the  top  row  show  the  ordinary  forms;  in  the  second  row  the 
stumpy  forms;  in  the  third  and  fourth  rows  longitudinal  division,  ihc 
lowest  row  shows  multinucleate  and  polyflagcllate  forms  (Rabinowitsch- 
Kempner  forms)  and  small  round  Hagellate  and  non-flagellate  '.onus  (Phmmer- 
Bradiord  and  Castellani's  forms).  (From  Castellani's  report  in  Reports  ol  the 
Royal  Society  on  Sleeping  Sickness.) 


424 


TR  YPA  NO  SO  MI  DM 


pheral  blood  the  centrosome  inside  the  nucleus  divides,  and  the  new 
eentrosome,  escaping  from  the  nucleus,  becomes  the  kinetonut  leus, 
and  lies  in  the  cytoplasm,  which  has  now  increased  in  amount.  The 
vesicle  has  gradually  disappeared.  A  new  flagellum  now  appears, 
and  gradually  the  latent  body  becomes  a  trypanosome.  The 
rounded  bodies  with  one  or  two  nuclei,  with  or  without  the  small 
flagella,  are  probably  identical  with  the  forms  found  by  Castellani 
several  years  ago  in  the  cerebro-spinal  fluid  of  cases  of  sleeping 
sickness,  and  described  by  him  under  the  term  '  amoeboid  forms.' 


Fig.   hi. — Castellanella  castellanii.     Life-Cycle. 

Reproduction  in  the  Fly. — The  researches  of  Kleine,  Taute,  Bruce, 
Hamerton,  Bateman,  and  Mackie  have  shown  that,  after  ingestion 
at  a  correct  period  (as  demonstrated  by  Miss  Robertson),  the  try- 
panosomes  enter  the  stomach  of  the  fly,  and  in  twenty-four  hours 
lose  their  infectivity,  as  demonstrated  by  inoculation.  According 
to  Miss  Robertson,  the  trypanosomes  multiply  in  the  posterior  part 
of  the  mid-gut,  and  after  the  tenth  or  twelfth  day  give  rise  to  long 
forms  which  move  forwards  into  the  proventriculus  between  the 


CASTELLANELLA   RHODESIENSIS  425 

twelfth  and  twentieth  day,  after  which  they  pass  along  the  hypo- 
pharynx  into  the  salivary  glands.  Here  they  become  attached  to 
tlu  walls  and  are  converted  into  crithidial  forms,  which  divide,  form- 
ing small  trypanosomes  similar  to  those  found  in  the  blood  of  the 
vertebrate.  The  salivary  gland  development  requires  two  to  five 
days  before  the  fly  becomes  infective,  which  only  happens  in  about 
8  per  cent,  of  flies.  The  duration  of  the  life-cycle  in  the  fly  depends 
upon  the  air  temperature. 

Vertebrate  Reservoir. — Duke  considers  that  he  has  proved  that 
the  Sitatunga  antelope  is  a  reservoir  for  this  trypanosome,  and 
considers  that  the  infection  of  two  boys  working  on  the  uninhabited 
islands  of  Victoria  Nyanza  and  constantly  exposed  to  bites  of  G 
palpalis  is  confirmatory. 

Pathogenicity. — It  is  the  cause  of  one  form  of  sleeping  sickness. 

Castellanella  rhodesiensis  (Stephens  and  Fantham,  1910). 

Synonym. — Trypanosoma  rhodesiense  Stephens  and  Fantham,  1910. 

History. — In  1910  Stephens  and  Fantham  advanced  the  view  that 
the  trypanosomes  found  in  cases  of  sleeping  sickness  in  the  Luangeva 
Valley  in  Rhodesia  belonged  to  a  new  species,  because  the  tropho- 
nucleus  of  a  certain  percentage  of  short  forms  was  situate  either  close 
to  or  even  on  the  aflagellar  side  of  the  kinetonucleus.  This  view 
is  at  the  present  time  accepted  by  the  majority  of  authorities, 
although  there  are  some  who  maintain  that  it  is  a  variety  of  C.  brucei, 
in  which  similar  forms  have  also  been  seen.  The  animal  reactions 
of  the  new  trypanosome  were  studied  by  Yorke  in  1910,  Bevan  in 
1911,  and  more  recently  by  other  observers.  In  1912  Kinghorn 
and  Yorke  showed  that  this  trypanosome  was  transmissible  by 
Glossina  morsitans,  in  which  it  underwent  development.  They 
demonstrated  that  it  occurred  in  waterbuck,  hartebeest,  impala, 
and  wart-hogs,  as  well  as  in  native  dogs,  and  they  further  showed 
the  importance  of  atmospheric  temperature  on  the  length  of  time 
required  for  the  cycle  of  development  in  the  fly. 

Morphology. — C.  rhodesiensis  closely  resembles  C.  castellanii  in 
general  appearance.  It  has  a  length  varying  from  12  to  31  fj,, 
with  an  average  of  21-5  /j,,  and  shows  the  usual  pleomorphic 
forms — e.g.,  short  stumpy  forms  varying  from  13  to  21  /u,  in  length; 
intermediate  forms,  22  to  24  fj,  in  length;  and  long,  slender  forms 
25  jli  or  more  in  length.  The  most  common  are  the  long,  slender 
forms.  The  position  of  the  trophonucleus  is  variable,  but  it  is 
usually  situate'  towards  the  aflagellar  end  of  the  parasite,  and  in 
the  short  stumpy  forms  is  often  close  to  the  kinetonucleus,  or  even 
on  its  aflagellar  side. 

Life-History. — (a)  In  the  Vertebrate  longitudinal  division  can 
take  place  as  in  C.  castellanii.  About  the  time  that  trypanosomes 
are  most  numerous  in  the  blood  the  researches  of  Fantham  show 
that  some  forms  in  the  lungs  become  converted  into  latent  bodies 
by  disintegration  and  loss  of  the  flagellar  end.  followed  by  a  migra- 
tion of  the  kinetonucleus  towards  the  trophonucleus,  and  a  sub- 


426 


TR  YPA  NO  SO  MID  IE 


sequent  casting  off  of  the  aflagellar  end  with  the  remains  of  the 
flagellum.  The  result  of  this  posterior  and  anterior  reduction  in 
length  is  to  produce  a  rounded  body,  with  a  trophonucleus  and  a 
kinetonucleus,  which  surrounds  itself  with  a  capsule  and  forms  the 
latent  body  or  the  post- flagellate  stage  of  the  life-cycle.  These  cysts 
are  about  2  to  4  fj,  in  diameter. 

After  a  time  these  bodies  become  the  preflagellate  stage,  increase 
in  size  and  length,  and  eventually  a  flagellum  grows  out  from  the 
kinetonucleus  and  gives  rise  to  the  undulating  membrane,  and 
thus  again  forms  the  usual  flagellate  stage. 

(b)  In  the  Invertebrate.— Glossina  morsitans,  when  fed  upon  in- 
fected animals,  is  capable  of  spreading  the  infection  mechanically 
for  about  twenty-four  hours,  after  which  period  it  ceases  to  be 
infective,  and  remains  non-infective  for  at  least  fourteen  days, 
after  which  about  5  per  cent,  of  flies  become  again  infective,  when 
trypanosomes  can  be  demonstrated  in  its  alimentary  canal  and  in 
its  salivary  glands. 


Fig.  112. — Castellanella  rhodesiensis  (Stephens  and  Fantham). 
(After  Stephens  and  Fantham.) 
1,  Long  narrow  form;  2-4,  nucleus  passing  to  aflagellar  end;  5,  nucleus  at 
the  aflagellar  end. 

Zoological  Distribution. — As  mentioned  above,  this  parasite  occurs 
not  merely  in  man  and  domestic  animals,  but  also  in  big  game. 

Specificity. — The  question  now  arises,  Is  it  a  good  species  or  not  ? 
First  of  all,  is  it  T.  castellanii  ? 

(a)  Sero-Diagnosis. — -(1)  Attachment  experiments  are  very  in- 
constant, and  do  not  distinguish  between  the  two. 

(2)  Trypanolysis  does  not  help,  being  also  inconstant. 

(3)  C.  castellanii  is  resistant  to  human  serum.  C.  rhodesiensis  is 
less  resistant. 

(b)  Crossed  Immunity. — An  animal  having  an  immunity  against 
C.  castellanii  can  be  infected  by  C.  rhodesiensis.  The  reverse  experi- 
ment has  not  yet  been  conducted. 

We  may  therefore  conclude  that  C.  castellanii  and  C .  rhodesiensis 
are  different  species. 

Is  C.  rhodesiensis  a  variety  of  C.  brucei  ?  The  answer  is  No, 
because    Laveran    has    shown    that    animals    immunized    against 


SCHIZOTRYPANUM  CRUZ  I 


427 


C.  brucei  are  susceptible  to  ('.  rhodesiensis..  Is  C.  rkodesiensis  a 
variety  of  T.  pecaudi  ?  No,  because  the  former  is  more  virulent  tha  n 
the  latter  to  animals,  and  because  sleeping  sickness  is  unknown  in  the 
region  where  '  baleri '  is  intense,  and,  finally,  because  an  animal 
immunized  against  C.  rhodesiensis  is  not  immune  against  T.  pecaudi. 

We  may  therefore  conclude  that  C.  rhodesiensis  Stephens  and 
Fantham,  1910,  is  a  good  species. 

Cultures. — Thomson  has  cultured  it  with  partial  success  on  a 
modification  of  the  Novy-McNeal-Nicolle  medium. 

Vertebrate  Reservoir.— It  is  claimed  that  the  larger  game  animals 
are  the  reservoir  of  this  trypanosome. 

Pathogenicity.— C.  rhodesiensis  is  the  cause  of  one  form  of  sleeping 
sickness. 

Schizotrypanum  cruzi  Chagas,  1909. 

Synonym. — Trypanosoma  cruzi  Chagas,  1909. 

History. — -This  trypanosome  was  discovered  by  Chagas  in  the 
intestine  of  Lamus  megistus  Burmeister  in  Brazil,  and  later  it  was 
found  in  the  blood  of  a  child  suffering  from  irregular  fever,  pro- 
gressive anamiia,  and  enlargement  of  various  groups  of  lymphatic 


Fig.   113. — Schizogony  of  Schizotvypanum  cruzi  Chagas. 
(After  Chagas.) 

1,  Merozoite  in  red  blood  cell;  2,  parasite  totally  enclosed  in  red  cell,  no 
flagellum  or  undulating  membrane;  3-5,  parasites  partially  enclosed  in  red  cell ; 
6,  7,  parasites  in  human  blood;  8-n,  parasites  in  the  lungs  of  Callithrix; 
12,  13,  initial  forms  of  schizogony;  14,  15,  schizogony  in  the  lungs  of  Callithrix. 

glands.  The  trypanosome  was  characterized  by  the  presence  of  a 
large  kinetonucleus,  and  by  the  facility  with  which  it  could  be 
cultivated  on  blood  agar.  In  1910-n  Chagas  published  a  series 
of  papers  upon  the  life-history  of  the  parasite  and  the  symptoma- 
tology of  the  disease  which  it  produces.  In  1911  Vianna  studied 
the  pathological  anatomy,  while  further  studies  on  the  parasite 
were  made  by  Brumpt,  Martin  Mayer,  Rocha-Lima.  and  othe 

Morphology. — In  the  peripheral  blood  of  man  S.  cruzi  appears  in 
two  forms — either  free  or  in  the  red  blood-corpuscles. 


428  TRYPANOSOMIDM 

The  free  forms  are  also  differentiated  into  two  forms — -viz.,  one 

with  a  large  egg-shaped  kinetonueleus,  with  a  chromatic  appendage, 

and  with  an  oval  or  band-like  trophonucleus  with  a  centrosome. 

The  flagellum  starts  from  the  kinetonueleus  or  from  its  chromatic 

appendage. 

In  the  second  free  form  the  kinetonueleus  is  round  and  smaller 

than  the  first,  and  has,  as  a  rule,  no  chromatic  appendage.     This 

form  is  broader  than  the  one  previously  described.     Whether  this 

is  a  sexual  differentiation  or  not  is  unknown. 

The  intraglobular  forms  may  be  completely  or  partially  enclosed 

in  the  red  cell,  or  merely  attached  by  the  aflagellar  end. 

Measurements  of  these  forms  were  not  originally  given  by  Chagas, 

but  it  would  appear  as  though  the  average  length  was  20  /n,  with  a 

certain  amount  of  variation. 

Life-History — Schizogony. — S.  cruzi  is  remarkable  in  that  it  is 

not  known  to  undergo  longitudinal  division  either  in  the  peripheral 

blood  or  the  internal  organs  of  its  host. 

According  to  Chagas,  there  is  a  regular 

cyclic  development,  the  parasite  entering 

the  capillaries  of  the  lungs,  where  it  loses 

its  flagellum  and  undulating  membrane, 

while   the    trophonucleus    moves    nearer 

the  flagellar  end,  and  the  whole  parasite 

becomes  curved,  first  into  a   half-moon, 

and   finally  so  much  that  the  two  ends 

fuse,    forming  a  ring  and  finally  a  disc. 

Fl£'™tTJf^fx!^     In  some  instances  the  kinetonueleus  dis- 
Section  of  a  Striated  .  .  . 

Muscle,  containing  S.  appears,  while  m  others  it  fuses  with  the 
cruzi  Chagas  in  the  trophonucleus,  after  which  the  nucleus 
Central  Portion,  divides  into  eight,  and  eventually  gives 
(X  1,363-)  rise  to  eight  merozoites  lying  inside  the 

(After  Vianna.)  periplast,  which   acts   like  a   cyst   wall. 

The  merozoites  with  kinetonuclei  are  con- 
sidered to  be  microgametes,  and  those  without  kinetonuclei  to  be 
macrogametes.  The  merozoites  escape  from  the  periplast  wall 
singly,  and,  entering  the  red  blood  cells,  become  flagellates,  and, 
finally  leaving  the  red  cell,  become  free  in  the  liquor  sanguinis, 
thus  completing  the  cycle  of  gametogony,  or  differentiation  and 
multiplication  of  gametes. 

Agamogony,  or  asexual  reproduction,  takes  place  in  the  cells  of 
various  organs — i.e.,  in  hypertrophied  endothelial  cells  in  the  lungs, 
in  the  cardiac  muscle,  in  the  neuroglia  of  the  central  nervous  system, 
and  in  striped  muscle.  In  these  situations  the  parasite  appears 
as  a  rounded  body  with  trophonucleus  and  kinetonueleus,  but  with- 
out flagellum  or  undulating  membrane.  Agamogony  increases  the 
number  of  parasites  in  the  host,  and  is  responsible  for  the  production 
of  the  symptoms,  while  gametogony  differentiates  the  sexual  forms, 
and  presumably  lays  the  basis  for  the  infection  of  the  invertebrate 
host.     This  form  of  development  is  confirmed  by  Brumpt. 


SCHIZOTRYPA  N  UM  Cli  '  Zl 


429 


In  the  Invertebrate.— The  further  development  takes  place  in  the 
bug  Lamus  megistus  {Triatoma  megista)  and  allied  forms,  in  which 
Chagas  notes  two  forms  of  development :  the  first  is  considered  to  be 
sexual,  and  the  second  to  be  asexual. 

The  sexual  method  is  as  follows : — In  about  six  hours  after  the 
ingestion  of  blood  the  kinetonucleus  moves  close  to  the  tropho- 
nucleus,  with  which  it  possibly  blends;  the  flagellum  and  undulating 


jzm 


Fig.   115. — Schizotry •panum  cvuzi  Chagas:  Development  in  Lamus  inegisins 

(Triatoma  megista). 

(After  Chagas.) 

i-6,    Forms   found  in  the  mid-gut  of  Lamus  megistus;   7,   flagellate  forms 
found  in  the  posterior  gut  of  L.  megistus. 

membrane  are  now  usually  lost,  but  some  forms  retain  the  flagellum. 
The  parasite  now  becomes  rounded,  and  multiplies  rapidly  by  divi- 
sion, but  after  this  has  ceased  it  becomes  pear-shaped,  develops  a 
flagellum,  and  becomes  a  crithidial  form,  and  then  passes  into  the 
cylindrical  portion  of  the  intestine,  in  which  it  can  be  seen  in  about 
twenty-five  hours  after  the  ingestion  of  blood.  These  crithidial 
forms  can  also  be  found  in  the  rectum  and  in  the  faeces.     The  final 


Fig.  116. — Schizotrypanum  cruzi  Chagas. 

(After  Chagas.) 

Forms  found  in  the  salivary  glands  of  Lamus  megistus  (Triatoma  megista). 

stage  is  a  small  trypaniform  type— i.e.,  long,  slim  forms,  with  band- 
like trophonucleus  and  large  kinetonucleus.  These  are  found  in 
the  hind-gut  in  the  body  cavity,  and  in  the  salivary  glands,  and 
are  the  forms  by  which  the  parasite  is  transmitted  to  a  new  verte- 
brate host.  The  development  in  the  bug  requires  at  least  eight  days 
for  its  completion. 

The  asexual  method  is  a  constant  process,  and  resembles  the 
growth  seen  in  artificial  cultures,  and  is  a  simple  multiplication, 
giving  rise  to  crithidial  forms  which  are  found  principally  in  the 
hind-gut. 


430  TR  YPA  NO  SOMIDJE 

Brumpt  finds  that  the  parasite  lives  well  in  Clinocoris  lectularius, 
C.  rotundaius,  Clinocoris  boueli,  and  Ornithodorus  moubata.  His 
account  of  the  cycle  of  development  is  as  follows: — Starting  with  the 
trvpancsome  in  the  posterior  part  of  the  intestine,  when  this  is 
inoculated  into  the  vertebrate,  it  enters  the  cells  of  the  body,  and 
becomes  Leishmania-like  bodies,  which  eventually  develop  into 
free-swimming  trypanosomes,  from  which  the  form  capable  of 
continuing  the  infection  in  the  vertebrate  or  invertebrate  is  pro- 
duced. In  the  invertebrate  these  become  crithidia-like  forms,  and 
eventually  trypanosomes  capable  of  infecting  vertebrates,  and  thus 
completing  the  cycle  of  life-history. 

Brumpt  and  Gonzalez-Lugo  have  found  the  parasite  in  the  faeces 
of  Rhodnius  prolixus  two  months  after  infection.  Triaioma  vitticeps 
and  T.  diminuata  are  also  carriers,  as  is  T.  sordida  Stal  and  Rhipi- 
cephalus  sanguineus . 

Culture.— S.  cruzi  is  easily  cultivated  upon  the  Novy-McNeal 
medium,  when  the  first  changes  begin  in  about  six  hours,  and  closely 
resemble  these  already  described  in  the  bug. 

Pathogenicity. — Two  to  three  days  after  an  infective  feed  the 
larvae  of  Lamus  cease  to  be  infective  to  vertebrates,  and  first 
become  so  on  the  eighth  to  the  tenth  day,  after  which  they  remain 
infective  for  a  long  period.  The  parasites  so  introduced  into  man 
give  rise  to  American  trypanosomiasis. 

Reduction  in  Virulence.— 5.  cruzi,  when  repeatedly  passed  through 
animals  of  the  same  species,  become  weakened  in  virulence,  but 
regain  this  when  transmitted  to  a  fresh  species. 

Infectivity. — The  infected  monkey  is  infective  for  the  bug,  while 
the  infected  guinea-pig  is  not. 

Duttonella  vivax  Ziemann,  1905,  var.  macfiensis. 

Synonym. — Trypanosoma  vivax  (Ziemann,  1905)  pro  parte. 

In  1917  Macfie  described  a  monomorphic  trypanosome  very 
closely  resembling  T.  vivax,  but  slightly  smaller,  with  the  crest  in 
curves  of  measurements  at  21  instead  of  at  23  microns.  It  is  said 
to  be  intermediate  between  T.  unijorme  and  T.  vivax. 

It  was  found  in  the  blood  of  a  man  suffering  from  trypanosomiasis 
on  the  Gold  Coast,  where  T.  vivax  is  common  in  the  humpbacked 
cattle  at  Accra.  The  maximum  length  was  24  microns,  the  minimum 
iS  microns,  and  the  average  207  microns. 

It  is  monomorphic,  with  abrupt  narrowing  of  the  body  immediately 
anterior  to  the  trophonucleus.  The  posterior  (aflagellar)  end  is  blunt, 
and  the  large  rounded  kinetonucleus  is  terminal  or  nearly  so.  The 
undulating  membrane  is  narrow,  and  there  is  always  a  long  free 
flagellum. 

Castellaneila  nigeriensis  Macfie,  1913. 

This  trypanosome  was  found  in  cases  of  human  trypanosomiasis  from  the 
Eket  district  of  Southern  Nigeria,  by  Macfie,  where  it  was  common  in  young 
pi  ople.  It  appears  to  give  rise  to  a  nol  very  virulent,  non-epidemic  form  of 
trypanosomiasis.     It  is  polymorphic,  and  in  our  opinion  is  the  same  parasite 


LEUCOCYTOZOON  431 

as  the  original  (".  gdmbiensis,  of  which  it  appears  to  be  merely  a  variant.     We 
have  placed  it  as  a  synonym  of  C.  gambiensis. 

Castellanella  lanfranchii  Lanfranchi,  1915- 
It  approximates  to  C.  evansi,  and  is  the  organism  with  which  Lanfranchi 
accidentally  inoculated  himself.     As  regards  precipitating  and  complemen! 
fixation  power  is  very  similar  to  C.  evansi,  but  as  regards  trypanolytic  action 
of  the  serum  it  approximates  more  C.  castellanii. 

APPENDIX:  INCERT.E  SEDIS. 

In  this  addendum  to  the  Trypanosomidse  we  include  the  genus  Leucocytozoon 
and  the  Spirochsetacea .  With  regard  to  the  former — Leucocytozoon  Danilewsky, 
1889 — a  number  of  species  have  been  described  of  which  the  life-history  is 
but  imperfectly  known,  except  in  the  case  of  L.  ziemanni,  which  has  been 
studied  by  Schaudinn,  and  partly  in  L.  lovati,  which  has  been  carefully  studied 
by  Fantham.  They  are  only  definitely  known  to  occur  in  birds,  and  must  be 
distinguished  from  the  Hsemogregarines  of  mammals. 

Leucocytozoon  Danilewsky,  1889. 

Synonyms.  —  Hcemamceba  Lavcran,  1903;  Spirochceta  Schaudinn,  1904; 
Trypanomovpha  Woodcock,  1906. 

The  leucocytozoa  were  first  described  by  Danilewsky  between  18S4  and 
1886  in  the  blood  of  the  wood-owl  (Syrnicum  aluco)  and  other  Strigidae. 


Fig.  117. — Leucocytozoon  damlewskyi  Ziemann. 
(After  Schaudinn.) 
From  the  left  to  the  right,  a  macrogametocyte  free,  same  attached  to  a 
blood   cell,  same  enclosed   in  a  blood   cell;  a  free  microgametocyte,  same 
enclosed  in  a  blood  cell. 

He  described  them  as  spherical  or  oval,  slightly  granular  bodies  contained 
in  a  delicate  transparent  homogeneous  capsule,  which  possessed  a  large 
elongated  nucleus,  compressed  in  the  middle,  and  broadened  at  the  ex- 
tremities. This  capsule  he  believed  to  be  a  degenerated  leucocyte,  but  later 
he  held  it  to  be  an  erythrocyte.  He  also  described  macrogametes  and  motile 
ookinetes,  and  later  he  described  the  microgametocytes.  In  1893  Sakharoff 
confirmed  these  observations  and  described  new  species  in  ravens,  rooks,  and 
lies.  In  1895  Theobald  Smith  discovered  a  leucocytozoon  in  Meleagris 
gallapavo  domestica  (the  turkey);  and  in  1898  Ziemann  described  another 
specimen  in  Glaucidium  noctucB  (the  little  owl)  from  Crema,  in  Italy.  In  1902 
and  1963  Laveran  desi  ribed  forms  in  birds  with  mixed  infections,  and  stated 
that   he  considered   that   they  were  contained  in  red  blood  cells.     In   1904 


432 


TR  YPA  NOSOMIDM 


Berestneff  described  several  forms  in  owls,  ravens,  and  magpies,  but  noted 
that  they  were  in  leucocytes;  and  in  the  same  year  came  Schaudinn's  paper 
on  the  development  of  Leucocytozoon  ziemanni,  which  is  given  in  detail  later  on. 
The  Sergents,  in  studying  the  parasite  in  the  little  owl  in  Algeria,  supported 
Schaudinn.  In  1905  Laveran  and  Lucet  studied  Theobald  Smith's  parasite, 
and  concluded  that  it  was  enclosed  in  a  leucocyte.  In  1906  Neave  described 
a  parasite  in  Numidia  ptilorhynca;  and  in  1907  Sambon  and  Seligmann 
described  one  in  Lagopus  scoticus  (the  red  grouse) ;  and  Dutton,  Todd,  and 
Tobey  another  in  Asturinula  monogrammica  (the  Congo  grey  hawk) ;  and 
lastly  Sambon  has  reviewed  the  whole  genus  in  a  singularly  able  manner,  and 
has  described  species  from  the  capercailzie  (Tetrao  urogallus)  and  the  pheasant 
(Phasianus  colchicus).  Important  work  has  been  clone  by  Fantham,  who 
demonstrated  a  schizogony  in  L.  lovati  Sambon  and  Seligmann,  1907.  E.  H. 
Ross  has  suggested  that  Kurloff's  bodies  may  be  Leucocytozoa,  and  may 
produce  spirochaete-like  organisms. 

Leucocytozoon  danilewskyi  Ziemann,  1898. 

Synonyms. — Hmmamceba    ziemanni    Laveran,    1902;    Spiroclueta    ziemanni 
Schaudinn,    1904;    Plasmodium    ziemanni    Blanchard,     1905;    Leucocytozoon 


Fig.  118. — Intracellular  Form  of  Leucocytozoon  lovati. 
(After  Sambon.) 


Fig.   1 19. —Intracellular  Microgametocyte  of  Leucocytozoon  lovati. 
(After  Seligmann  and  Sambon.) 


Fig.  120. — Intracellular  Macrogametocyte  of  Leucocytozoon  lovati. 
(After  Seligmann  and  Sambon.) 


- u  manni  Liihe,  1906.     L.  danilewskyi  is  found  as  a  parasite  in  the  hsematoblasts 
1  in  ling  to  other  authors,  in  the  leucocytes)  of  the  little  owl,  Glav.cidium 
noctuce  {Athene  noctuce  Retz),  and  the  wood-owl,  Syrnicum  aluco  L. 

The  history  of  the  life-cycle,  according  to  Schaudinn,  may  be  begun  with 


LEUCOCYTOZOON  DANILEWSKYI 


433 


the  biting  of  the  owl  by  Culex  pipiens  L.,  and  the  sucking  of  blood  containing 
micro-  and  macro-gametocytes. 

Microgametoeyte. — -The  microgametoeyte^  may  attain  dimensions  much 
larger  than  a  leucocyte,  and  exists  in  the  blood  of  the  owl  in  two  conditions : 
(i)  a  free  active  stage  in  the  liquor  sanguinis;  (2)  endocellular  resting  stage  in  a 
blood  cell ;  and,  later,  when  the  parasite  has  become  too  large  to  penetrate  a  host 
cell,  free  in  the  blood  stream.  In  this  condition  the  parasite  may  engulf  the 
cells  which  formerly  served  it  for  food  and  shelter. 

(1)  Free  Active  Stage. — This  is  the  trypanosome  stage  (T.  ziemanni).  The 
anterior  end  is  sharp-pointed,  with  a  kinetonucleus  just  at  its  base,  from 
which  the  flagellum  arises,  passing  posteriorly  along  the  body  and  projecting 
some  distance  from  the  posterior  end.  There  is  a  well-defined  undulating 
membrane,  with  sixteen  myoncmes  arranged  in  four  double  rows  or  pairs  on 
each  side.  The  trophonucleus  is  well  developed,  and  situate  near  the  centre 
of  the  trypanosome. 


Fig.    121. — Leucocytozoon  danilewskyi 

Ziemann:  Microgamete. 

(After  Schaudinn.) 


Fig.  122. — Leucocytozoon  dani- 
lewskyi Ziemann  :  Macro- 
gamete. 

(After  Schaudinn.) 


Fig.  123. — Leucocytozoim  danilewskyi  Ziemann:  The  Development  of  the 
Ookinete  and  the  Formation  of  Small  Trypaniform  Bodies. 
(After  Schaudinn.) 


(2)  Endocellular  Resting  Stage. — In  the  intracellular  stage  the  parasite  is 
quite  spindle-shaped,  the  ends  being  composed  of  ectoplasm,  while  the 
endoplasm  forms  a  dark  oval  central  mass  containing  the  trophonucleus,  close 
to  which  the  kinetonucleus  is  situated.  The  flagellum  has  disappeared,  but 
the  myonemes  of  the  ectoplasm  can  still  be  seen. 

Macrogametocyte. — This  has  also  two  stages — (1)  free,  (2)  endocellular. 

(1)  Free  Active  Stage. — The  free  stage  differs  from  the  microgametoeyte  in 
being  larger,  in  having  no  free  projection  of  the  flagellum,  and  in  having 
smaller  tropho-  and  kineto-nuclei,  and  in  the  myonemes  not  being  arranged 
in  pairs. 

(2)  Resting  Stage. — This  differs  from  the  microgametoeyte  in  being  large, 
with  smaller  nuclei. 

These  gametocytes,  called  '  leucocytozoon  '  by  Danilewsky  and  '  haem- 
amceba  '  by  Laveran,  being  found  in  the  peripheral  blood  of  the  owl,  are  sucked 
into  the  stomach  of  Culex  pipiens,  and  then  proceed  to  conjugation. 

28 


434  TRYPANOSOMIDM 

Microgamete.— The  microgametocyte  escapes  from  the  capsule-like  peri- 
plast, and  its  nucleus  breaks  up  into  eight  double  chromosomes,  which  are 
reduced  to  eight  single  chromosomes.  These  travel  to  the  periphery,  and 
form  microgametes  in  the  manner  described  for  Hcemoproteus  noctuce,  micro- 
gametes  which  they  are  said  to  resemble. 

Macrogamete. — The  macrogametocyte  escapes  from  its  enclosing  cell,  and 
the  process  of  development  of  the  macrogamete  is  the  same  as  in  Hcsmo- 
proteus. 

Fertilization. — This  is  the  same  as  in  Hcemoproteus. 

Ookinete. — There  are  the  same  three  kinds  of  ookinetes  as  in  Hcemoproteus — 
viz.,  the  indifferent,  the  male,  the  female. 

The  ookinete,  however,  differs  by  growing  in  size  and  multiplication  of  its 
nuclei,  and  at  the  same  time  coiling  upon  itself  so  as  to  form  a  skein.  This 
skein  contains  a  large  number  of  nuclei  uniformly  distributed. 

Around  each  of  these,  small  portions  of  protoplasm  gather,  and  become 
finally  separated  off,  to  form  small  indifferent  trypanosomes  in  the  case  of 
the  indifferent  ookinete,  male  trypanosomes  from  the  male  ookinete,  female 
trypanosomes  from  the  female  ookinete.  A  large  mass  of  residual  protoplasm 
is  left. 

These  trypanosomes,  especially  the  male,  are  very  minute,  and  reproduce 
by  longitudinal  division,  during  which  they  do  not  separate  at  once,  but 
remain  attached  posteriorly.  Couples  attached  to  one  another  may  extend 
into  the  same  straight  line,  thus  giving  rise  to  a  spirochaete-hke  form,  and 
while  in  this  position  may  undergo  longitudinal  division.  The  spirochsete 
forms  may  become  pear-shaped  resting  forms. 

In  the  Owl. — On  entering  into  the  owl,  the  indifferent  forms  pass  through 
alternate  endocellular  and  free  stages.  In  the  former  there  is  growth,  and 
in  the  latter  there  is  division  into  smaller  forms.  After  some  time  micro-  and 
macro-gametocytes  are  formed  in  increasing  numbers. 

This  life-history  has  been  doubted,  but  Sambon  has  seen  forms  in  which 
a  coiled  trypanosome  body  can  be  detected  in  the  blood  cells. 

The  Enclosing  Cell. — There  has  been  great  doubt  as  to  the  character  of  the 
body  enclosing  a  leucocytozoon. 

i.  Ziemann,  Schaudinn,  Dutton,  Todd,  and  Tobey  believe  that  it  is  a 
portion  of  the  parasite  itself — i.e.,  the  periplast — and  that  it  may  enclose  a 
red  blood  cell. 

2.  Danilewsky  considers  it  to  be  a  leucocyte,  but  derived  his  red  cells  from 
leucocytes.  In  considering  it  to  be  a  leucocyte,  he  is  supported  by  Laveran, 
Lucet,  Sakharoff ,  and  Berestneff ,  and  most  recent  observers. 

3.  Laveran  in  his  earlier  observations  believes  it  to  be  a  red  cell,  and  this 
Sambon  supports,  as  do  Keysselitz  and  Mayer. 

It  may  be  taken  to  be  a  much-enlarged  dehaemoglobinized  haematoblast 
or  red  cell,  the  spindle  shape  of  which  may  be  explained  by  the  fusiform 
shape  of  the  haematoblasts,  and  by  the  pseudopodia  of  the  young  parasites 
protruding  into  the  long  ends  of  the  host  cell.  When  the  parasite  contracts, 
these  ends  shrivel  up,  giving  rise  to  the  usual  appearance. 

The  Spirochaetes. — At  first  Schaudinn,  after  tracing  out  the  life-history 
described  above,  thought  that  all  spirochaetes  would  be  found  to  be  allied  to 
true  trypanosomes;  but  in  1905  he  stated  that  the  spirochaete-like  forms  which 
he  found  in  the  little  owl  were  far  removed  from  true  spirochaetes,  and  that 
the  relationship  was  only  phylogenetic,  and  very  distant  at  that. 

E.  H.  Ross  has  brought  evidence  to  show  that  Kurloff's  bodies  (i.e., 
clear  spherical  vacuoles  in  the  large  lymphocytes  of  guinea-pigs)  are 
intracorpuscular  stages  in  the  life-history  of  a  Leucocytozoon  (Lymphocyto- 
zo'&n  cobayce  E.  H.  Ross,  1912)  which  ultimately  give  rise  to  spirochaete-like 
bodies,  the  development  of  which  he  traces,  and  which  he  considers  to  be 
the  gametes.  Later  he  and  McDonagh  described  a  similar  origin  for  Treponema 
pallidum. 

Recent  work  has  tended  to  confirm  the  doubts  thrown  on  Schaudinn's 
work,  but  the  general  appearance  of  a  Leucocytozoon  in  its  cell  is  sometimes 
remarkably  similar  to  a   trypanosome.     It  is  possible  that  there  may  be 


LEUCOCYTOZOON  LOVATI  435 

different  parasites  confused  under  the  term  Leucocytozoon,  and  their  life- 
histories  may  be  different,  as  Fantham's  work,  presently  to  be  described,  is 
opposed  to  Schaudinn's  work. 

Leucocytozoon  lovati  Sambon  and  Seligmann,  1907. 

This  leucocytozoon  was  discovered  by  Sambon  and  Seligmann  in  the  red 
grouse  (Lagopus  scoticus),  and  has  been  recently  restudied  by  Fantham. 
The  microgametocyte  and  macrogametocyte  are  depicted  in  Figs.  119  and  120 
6n  p.  1  52,  and  were  till  recently  the  only  forms  known,  but  Fantham  has  now 
found  the  schizonts,  and  described  the  process  of  schizogony. 

Sporogony. — The  microgametocytes  measure  i3to  17 //in  length  by  6  to  12  /j, 
in  breadth,  and  possess  hyaline  pale  staining  cytoplasm  with  a  large,  rather 
granular  nucleus.  The  macrogametocyte  measures  14  to.  20  /j,  in  length  by 
10  to  16  fx  in  breadth,  and  has  a  granular  somewhat  alveolar  cytoplasm  with 
ral  nucleus  with  a  karyosome.  Their  further  development  is  unknown, 
but  Fantham  has  found  vermicides  in  Omithomyia  lagopodis,  the  grouse-fly, 
whit  h  may  be  the  agent  of  transmission. 

Schizogony. — The  schizont  is  found  in  the  spleen  in  cells  which  they  almost 
till  and  absorb,  and  which  they  do  not  elongate  in  the  way  in  which  the  game- 
tocytes  deform  their  host  cells.  The  schizont  measures  11  to  14  fj,  by  8  to  11  fx, 
and  is  therefore  of  an  oval  shape,  with  a  nucleus  resembling  that  of  the  micro- 
gametocyte, and  a  cytoplasm  like  that  of  the  macrogametocyte. 

I  he  nucleus  divides  by  rapid  binary  fission  into  some  12  to  20  small  nuclei 
and  then  the  cytoplasm  divides,  giving  rise  to  12  to  20  merozoites,  which  are 
small  vermicules  measuring  7  to  8  j«  by  1  to  1-5  /1.  There  is  some  residual 
cytoplasm  after  division.  The  merozoites  now  escape  from  the  parasite  and 
cell,  and  for  a  very  brief  period  become  free,  swimming  in  the  liquor  san- 
guinis, and  then  quickly  re-enter  leucocytes  or  immature  erythrocytes,  and 
ultimately  differentiate  into  gametocytes  or  schizonts. 

Remarks. — -This  process  of  schizogony  may  explain  the  periodical  increase  in 
the  gametocytes  in  the  blood  noted  by  Mathis  and  Leger  in  L.  caulleryi  in 
Tonkin.  Fantham  very  carefully  points  out  that  the  above  life-history  may 
not  take  place  in  all  Leucocytozoidae,  but,  notwithstanding  this,  Fantham's 
results  do  not  support  Schaudinn's  researches. 

Species.— Some  of  the  species  described  are:  Leucocytozoon  majoris  Laveran, 
m  the  great  tit  (Pants  major):  L.  sahharoffi  Sambon,  1908,  in  the  raven 
(Corvus  corax);  L.  berestneffi  Sambon,  190S,  in  the  magpie  (Pica  pica) ;  L.  dani- 
Icwskyi  Ziemann,  1898,  in  the  little  owl  (Athene  noctuce) ;  L.  toddi  Sambon,  1907, 
in  the  Congo  grey  hawk  (Asturinula  monogrammica) ;  L.  mansoni  Sambon,  1908, 
in  the  capercailzie  (Tetrao  urogalhts) ;  L.  lovati  Sambon  and  Seligmann,  in  the 
red  grouse  (Lagopus  scoticus);  L.  macleani  Sambon,  1908,  in  the  common 
pheasant  (Phasianus  colchicus);  L.  smithi  Laveran  and  Lucet,  1905,  in  the 
domestic  turkey  (Mclcagris  gallopavo  domestica)  ;  L.  neavi  Balfour,  1906,  in  the 
\1>\  ssinian  guinea-fowl  (Numidia  pi ilorhynca) ;  L.  caulleryi  Mathis  and  Leger, 
191  1 ,  L.  sabrazesi  in  Gallus  ferrugintus  ;  L.  martini  Mathis  and  Leger  in  Pavo 
eristatus ;  L.  marchouxi  Mathis  and  Leger  in  Turtur  humilis,  and  L.  lebceufi 
Mathis  anfl  Leger  in  Querquedula  crecca. 

Spiroehaetacea  Fantham,  1908. 

Synonyms.— Proflagellata  Doflein;  Spiroschaudinnidce  Sambon, 
1907;  Spiroftagellata  Krzysztalowicz  and  Siedlecki,  1907. 

Definition.— Plasmodromata,  generally  parasitic,  in  form  narrow, 
wavy,  and  thread-like,  with  or  without  an  undulating  membrane. 
The  <  ytoplasm  is  divided  into  endoplasm  and  ectoplasm,  and  is 
bounded  by  a  flexible,  chitinous  periplast.  The  nucleus  consists  of 
a  spiral  achromatic  filament,  on  which  are  arranged  transverse  bars 
or  rodlets  of  deeply  staining  chromatin. 


4  3  6  TR  YPA  NO  SO  MID  M 

Remarks. — -The  Spirochaetacea  are  closely  related  to  the  Binu- 
cleata,  and  especially  to  the  Trypanosomidae. 

The  Treponemata  are  joined  to  the  spiroehaetes  because  of  their 
general  resemblance,  though  it  must  be  admitted  that  no  nucleus 
of  the  nature  of  the  spirochete  nucleus  has  yet  been  described,  and 
the  spirals  are  apparently  not  due  to  movement. 

The  Spirochaetacea  are  potent  factors  in  the  production  of  disease, 
for  S.  recunentis  is  the  cause  of  one  type  of  relapsing  fever,  S.  carteri 
of  another,  S.  duttoni  of  another,  and  5.  novyi  of  yet  another,  while 
the  Treponemata  are  the  cause  of  syphilis  and  yaws. 

The  Spirochaetacea  may  be  divided  into  two  families: — • 

i.  With  undulating  membrane:  Spirochaetidae. 

2 .  Without  undulating  membrane :  Treponemidae. 

Spirochaetidae  Ehrenberg,  1883. 

Definition. — Spirochaetacea  with  an  undulating  membrane.  Body 
may  be  ribbon-shaped  on  transverse  section. 

Type  Species. — Spirocluzta  plicatilis  Ehrenberg,  1833. 

Remarks. — -There  is  a  difference  of  opinion  as  to  whether  these 
organisms  are  protozoa  or  bacteria.  At  first  they  Were  universally 
regarded  as  bacteria,  but  in  1904  Schaudinn's  paper  on  the  leuco- 
cytozoon  in  the  little  owl  indicated  that  this  body,  after  fertiliza- 
tion in  the  gut  of  Culex  pipiens  and  subsequent  asexual  division, 
produced  a  large  number  of  minute  forms  which  he  at  the  time 
considered  to  be  spiroehaetes,  and  he  further  concluded  that  in  all 
probability  all  spiroehaetes  were  stages  in  the  life-history  of  intra- 
cellular parasites.  In  1905,  however,  he  came  to  the  conclusion  that 
the  spirochaete  forms  which  he  had  seen  develop  from  T.  ziemanni 
Were  trypanosomes.  In  fact,  there  is  one  great  point  of  difference 
— the  forms  which  he  described  possess  a  distinctly  consolidated 
nucleus,  whereas  spiroehaetes  do  not.  After  this  the  view  that 
spiroehaetes  were  bacteria  was  revived,  particularly  by  Novy  and 
Knapp,  on  the  following  grounds:— 

1 .  Absence  of  trophonucleus. 

2.  Transverse  division. 

3.  Rapid  multiplication. 

4.  Absence  of  plasmolysis  with  distilled  water. 

5.  Persistence  of  form  when  acted  upon  by  heat. 

6.  The  production  of  active  immunity. 

7.  The  absence  of  aerotropism — i.e.,  the  tendency  to  mass  round 
a  bubble  of  air. 

Dobell,  as  a  result  of  his  prolonged  inquiries,  ca-  3  to  the  con- 
clusion that  they  are  Schiophyta  (bacteria  +  Cyanophyceae),  and 
not  protozoa.  He  also  concludes  that  they  belong  to  the  bacteria, 
and  probably  constitute  a  group  of  the  same  systematic  status  as 
the  cocci,  the  bacilli,  and  the  spirilla. 

On  the  other  hand,  there  is  a  growing  feeling  among  biologists  that 
spiroehaetes  are  really  protozoa — e.g.,  Doflein,  Minchin,  Sambon, 
Nuttall,  Fantham,  and  Krzysztalowicz  and  Sisdlecki.     Fantham 


SPJROCHJETIDm  437 

points  out  that  the  strongest  arguments  in  favour  of  their  being 
bacteria  are: — 

i.  Diffuse  character  of  nucleus  somewhat  like  Bacillus  biitschilii. 

2.  The  possible  occurrence  of  transverse  fission. 

3.  The  absence  of  a  typical  kinetonucleus. 

While  the  points  in  favour  of  their  belonging  to  the  protozoa  are : — 

1.  The  possession  of  an  undulating  membrane. 

2.  The  occurrence  of  longitudinal  division  (denied  by  Schellach). 

3.  The  non-plasmolysis. 

4.  Difficulty  to  find  artificial  media  on  which  they  can  grow. 

We  consider  that  they  are  protozoa,  and,  further,  that  they  are 
related  to  the  trypanosomes.  Spirochetes  are,  however,  distinctly 
peculiar,  particularly  with  regard  to  their  diffuse  nucleus;  but 
there  appears  to  be  almost  a  series  from  the  diffuse  nucleus  of  the 
bacteria  through  the  achromatic  spiral,  with  its  attached  chromo- 
somes of  the  spirochetes,  to  the  condensed  nucleus  of  the  higher 
protozoa.  Schellach  derives  them  phylogenetically  from  the  oscilla- 
tory cyanophees,  genus  Spirulina. 

Morphology. — Spirochsetes  vary  much  in  size,  from  Spiroschau- 
dinnia  recurrentis,  which  is  8  /j,  in  length,  to  Cristispira  balbianii, 
which  may  be  150  fj,  in  length  and  2  to  3  jli  in  thickness.  The  type 
species  Spirochceta  plicatilis  was  found  in  muddy  Water  by  Ehren- 
berg  in  1833,  and  was  said  by  Schaudinn  in  1905  to  possess  an 
undulating  membrane.  Sambon,  however,  considers  that  this  so- 
called  type  species  is  quite  different  from  5.  recurrentis,  and  should  be 
placed  in  a  different  group  therefrom.  The  most  carefully  studied 
types  are  Cristispira  balbianii  Certes,  1882,  found  in  oysters,  and 
Cristispira  anodonta  Keysselitz,  1906,  emended  Schellach,  1909,  both 
of  which  have  been  the  subject  of  research  by  Fantham,  whose  results 
are  here  followed.  These  organisms  are  long,  Wavy,  and  thread- 
like, composed  of  cytoplasm,  which  can  be  differentiated  into  an 
ectoplasm,  which  is  generally  converted  into  a  thin,  flexible,  chitin- 
ous  membrane,  the  periplast.  This  is  continued  laterally  into  a 
spirally  arranged  membrane,  the  crista,  containing  longitudinally 
arranged  fibrillse,  and  having  a  thickened  border  composed  of 
chromatin.  The  longitudinal  fibrillas  are  composed  of  eight  to  nine 
principal  and  numerous  secondary  fibrillar  which  are  contractile, 
and  are  called  '  the  myoneme  fibrillae  '  (Fig.  124).  The  membrane, 
or  crista,  which  does  not  markedly  undulate,  helps  in  locomotion, 
which  is  rapid,  and  takes  place  by  a  wave-like  flexion  of  the  body, 
which  causes  forward  movement,  and  a  corkscrew  motion,  produced 
by  the  spiral  winding  of  the  membrane,  enabling  the  parasite  to  bore 
its  Way  through  the  debris  amidst  which  it  may  be  living.  A  spiro- 
chete can  move  backwards  or  forwards  indifferently. 

The  endoplasm  is  slightly  more  granular  than  the  ectoplasm,  and 
contains  a  diffuse  nucleus,  which  appears  to  consist  of  an  achromatic 
filament  with  bars  of  chromatin. 

In  addition  to  this  nucleus  there  is  a  dot  of  chromatin  (basal 
granules)  at  each  end  of  the  periplast  inC.  balbianii,  and  only  at  one 


433 


TRYPANOSOMID/E 


end  in  C.  anodontce  ;  in  the  latter  a  short,  stiff  process  of  periplast 
projects  from  it,  which  is  considered  by  some  observers  to  be  a 


flagellum. 


Fig.  124. — Spirochetes. 

1,  Cristispira  anodoniee,  showing  the  undulatingTmembraneJand  chromatic 
bars  (after  Fantham,  Quarterly  Journal  of  Microscopical  Science);  2,  C.  balbi- 
anii,  showing  fibrillae  in  undulating  membrane  (after  Fantham);  3-7,  Spiro- 
scha'udinnia  duttoni  (after  Breinl,  Annals  of  Tropical  Medicine  and  Parasitology) ; 
4,  shows  the  uncoloured  transverse  band;  5,  longitudinal  division;  6,  possible 
male  and  female  forms;  7,  encystment. 


SPIROSCHA  UDTNNIA  439 

Reproduction  takes  place  by  both  longitudinal  and  transverse 
divisions;  it  has  been  described  by  Fantham  and  Porter  in  C.  ano- 
donta Keysselitz,  1906,  and  C.  balbianii.  The  basal  granule  first 
divides,  and  then  the  membrane,  followed  by  the  cytoplasm,  as 
far  as  one  end,  which  does  not  divide  at  once,  but  later,  thus  com- 
pleting the  act  of  asexual  reproduction. 

Dobell  gives  a  very  different  description  of  C.  anodonta,  which  he  states  has 
a  chambered  structure,  and  divides  only  by  transverse  division. 

Bosanquet  has  observed  the  formation  of  coccoid  bodies  in  Cristi- 
spira  analogous  to  those  presently  to  be  described  in  Spiroschaudinnia . 
Classification. — The  following  genera  are  recognized: — ■ 

Spirochczta  Ehrcnberg  1838,  sensu  stricto. 

Cristispira  Gross,  1910. 

Saprospira  Gross,  igir. 

Pseudospira  Dobell,  1912. 

Spiroschaudinnia  Sambon,  1907. 
But  it  is  only  the  last  genus  which  contains  the  forms  of  importance 
in  tropical  medicine. 

juchi  has  created  the  genus  Leptospira  Noguchi,  19 17,  for  the  spiros- 
chaudinnia  found  in  Weil's  disease  and  the  spiroschaudinnia  he  has  observed 
in  yellow  fever.  Characteristic  features  would  be  the  true  elicoid  structure 
with  persistent  spirals,  and  the  resistance  to  the  action  of  saponin. 

Cristispira  balbianii  Certes,  1882. 

This  spirochaete  is  found  in  the  crystalline  style  of  oysters.  The  oysters 
are  apparently  affected;  at  all  events,  they  are  poorly  developed.  It  has  a 
well  denned,  undulating  membrane,  strengthened  by  myonemes,  and  also  a 
diffuse  nucleus  of  rodlets  of  chromatin  on  an  achromatic  spiral,  as  has  already 
been  described.    . 

Cristispira  anodontze  Keysselitz,  1906. 

Synonym. —  Spivochizta  anodontce  Keysselitz,  1906,  emendavit  Schellach,  1909. 

>'.  anodonta  was  found  in  the  crystalline  style  of  Anodonta  mutabilis  by 
Keysselitz  in  1906,  and  in  that  of  A  .  cygnea  by  Fantham  in  1908. 


Fig.    1 25. — Diagram   of   S.   duttoni,    showing   Chromatin   Granules, 
Pointed  Ends,  and  Slight  Membrane  Edge.      (After  Fantham.) 

1 1  is  40  /t  in  length  by  0-7  /i  in  breadth,  with  pointed  ends  and  a  spirally 
wound  undulating  membrane.  The  nucleus  is  diffuse,  consisting  of  chromatin 
rodlets  on  a  more  faintly  staining  spiral. 

S.  plicatilis  Ehrenberg,  1833,  found  in  pond-water. 

Spiroschaudinnia  Sambon,  1907. 

Spirochaetidse  parasitic  in  the  blood  and  tissues  of  vertebrates 
and  in  some  blood-sucking  invertebrates. 

Remarks. — This  genus,  as  we  believed  would  happen,  is  now 
recognized  by  many  authorities,  and  therefore  we  adopt  it,  though 
\\.  had  hesitated  to  do  so  in  the  previous  edition. 

Type  Species. — Spiroschaudinnia  recurrentis  Lebert,  1874. 


44° 


TRYPANOSOMIDM 


Morphology.— This  has  been  most  carefully  studied  by  Fantham 
in  5.  recurrentis,  S.  duttoni,  and  S.  marchouxi,  and  he  finds  that  they 
have  long,  narrow  bodies,  bent  into  many  spiral  coils,  enclosed  in 
a  firm  periplast,  with  a  very  tenuous  membrane,  which  is  often  in- 
visible. The  nucleus  consists  of  granules  of  chromatin  distributed 
along  the  body. 

Life-History.— Multiplication  can  take  place  by  longitudinal  and  by 
transverse  division,  and  also  by  multiple  transverse  fission,  in  which 
case  the  protoplasm  concentrates  around  the  chromatin  masses, 
giving  rise  to  a  number  of  round  or  oval  granules,  probably  the 

same  as  the  infective  granules 
of  Fry  and  Balfour,  which  are 
known  to  escape  from  one  end 
or  the  other  of  the  periplastic 
sheath  when  in  the  internal 
organs.  These  infective 
granules  enter  the  red  cells, 
and  divide  into  a  number  of 
merozoites,  which  escape  from 
the  red  cell  and  enter  the 
liquor  sanguinis;  but  their 
further  development  is  un- 
known, though  it  is  possible 
that  they  become  spirochaetes. 
Fantham's  observations 
have  confirmed  this  granule 
stage  of  the  life-history,  but 
it  must  not  be  forgotten 
that  every  granule  seen  in  a 
spirochete  is  not  an  infective 
granule,  which  our  own  ob- 
servations support. 

Minchin  regarded  these  granules 
as  true  endogenous  chromidial 
buds,  and  considered  therefore 
that  the  term  infective  granule 
should  be  replaced  by  the 
term  '  endogenous  '  bud  forma- 
tion. 

The  life-history  of  a  spiroschaudinnia  in  the  invertebrate  has  been  traced  by 
Leishman  for  S.  duttoni  in  the  tick,  Ornithodoros  moubata,  and  his  account  has 
been  confirmed  by  Balfour,  Hindle,  Blanc,  Fantham,  and  others. 

The  Spiroschaudinnia,  on  entering  the  tick,  penetrate  the  gut  wall,  and  on 
reaching  the  body  cavity  divide  by  multiple  transverse  fission  into  minute 
ovoid  or  rod-like  bodies,  which  reach  the  ovary  and  become  incorporated 
with  some  of  the  ova.  In  this  situation  they  are  not  often  infective.  When 
laid,  the  egg  only  contains  a  few  ovoid  bodies,  but  in  three  to  five  days'  in- 
cubation, when  the  Malpighian  tubes  have  begun  to  develop,  ovoid  and  more 
elongate  bodies  may  be  seen  therein.  In  six  to  seven  days'  incubation  these 
bodies  have  elongated  and  become  bacillary,  and  may  rupture  the  cell  and 
appear  in  the  lumen  of  the  tube.  It  is  believed  that  these  bacillary  forms  give 
rise  to  spirochaetes  either  by  elongation  and  growth,  or  by  fusion  of  rods.  The 
recently  hatched  tick  contains  ovoid  bodies,  bacillary  forms,  and  a  very  few 


Fig.  126. — Life-Cycle  of    Spiroschau- 
dinnia marchouxi  Nuttall. 

(After  Hindle,  from  the  Journal 
of  Parasitology .) 


SPIROSCHA  UDINNIA 


44i 


fully  developed  spirochaetes.  Infection  takes  place  towards  the  end  of  feeding 
by  the  excretion  from  the  Malpighian  tubules,  which  contains  the  spirochaetes, 
passing  into  the  wound  caused  by  the  bite. 

Some  of  the  Spiroschaudinnia ,  on  entering  the  tick,  pass  into  the  cells  by 
the  alimentary  canal,  and  undergo  multiple  transverse  division,  while  others 
may  live  for  some  weeks  in  the  gut. 

Cultivation. — -Noguchi  has  successfully  cultivated  S.  duttoni  in 
sterile  ascitic  or  hydrocele  fluid,  to  which  a  piece  of  fresh  rabbit's 


Fig.   127. — Schizogony  of  S piroschaudinnia  marchouxi  Nuttall. 
(After  Sambon.) 

kidney  has  been  added.  For  inoculation  of  this  medium  he  uses  a 
few  drops  of  the  citrated  heart  blood  from  a  mouse  forty-eight  to 
seventy-two  hours  after  infection. 


Fig.   128. — Development  of  S. 
Duttoni.     (X   1,000.) 

The  small  dots  are  chromatin  bodies 
and  the  large  granules  are  digested 
blood,  while  the  pale  outlines  are 
spirochaetes  in  the  contents  of  the 
intestinal  sac  of  a  tick  two  days  after 
an  infective  feed.  (From  a  micro- 
photograph  by  Sir  William  Leishman.) 


Fig.  129. — Chromatin  Granules  in 
the  Malpighian  Tubule  of  a 
Tick  Six  Days  after  Infective 
Feed.     (X  1,000.) 

(From  a  microphotograph  by  Sir 
William  Leishman.) 


At  a  temperature  of  370  C.  the  maximum  growth  is  found  about 
the  eighth  to  ninth  day,  after  which  disintegration  sets  in,  resulting 
in  total  disappearance  about  the  fifteenth  day.  Subcultures  are 
best  made  from  the  fourth  to  the  ninth  day,  but  after  that  date 


44- 


TR  YPA  NO  SO  MI  DM 


the  virulence  diminishes.  The  subcultures  do  not  lose  their  viru- 
lence even  after  the  ninth  passage. 

He  has  also  cultivated  in  this  way  S.  recurrentis  Lebert,  1874, 
when  the  maximum  growth  occurs  on  the  seventh  day;  5".  rossi 
Nuttall,  1905,  with  a  maximum  on  the  ninth  day;  and  S.  novyi, 
which  is  the  most  difficult,  with  a  maximum  on  the  seventh  day. 
5.  marchouxi  has  also  been  cultivated.  Bronfenbrenner  in  1914 
simplified  this  method  of  cultivation. 

Carriers, — -The  Spiroschaudinnice  are  spread  by  the  agency  of  ticks 
and  lice. 

Method  of  Infection, — The  Spiroschaudinnice  infect  the  ova  of  the 
tick,  and  so  pass  into  the  second  generation,  from  which  they 
escape  in  the  faeces  and  enter  the  wounds  made  by  the  tick  when 
it  bites,   and  so  infect  the  vertebrate  host.     Whether  the  same 


\ 


Fig.  130.- — Granules  in  an  Infected 
Egg. 

(From  a  micropkotograpb.  by  Sir 
William  Leishman.) 


Fig.  131. — Masses  of  Granules  in 
Malpighian  Tubule  of  a  Young 
Unfed  Nymph.     (X  1,000.) 

(From   a   microphotograph   by   Sir 
William  Leishman.) 


method  of  development  takes  place  in  the  louse  is  not  known,  but 
the  method  of  infection  is  thought  to  be  due  to  the  irritation  of  the 
louse-bite  causing  the  vertebrate  host  to  scratch,  and  thus  to  crush 
the  louse  and  at  the  same  time  to  cause  abrasions  of  the  host's 
own  skin.  The  Spiroschaudinnice,  escaping  from  the  crushed  louse, 
enter  the  vertebrate  host  through  the  abrasions  caused  by  the 
scratches.  Both  these  are  contaminative  methods  of  infection. 
It  is  believed  that  Spiroschaudinnia  in  the  vertebrate  can  pass 
from  the  mother  via  the  placenta  to  the  fcetus,  thus  giving  rise  to 
an  hereditary  method  of  infection,  in  contradistinction  to  the  con- 
taminative methods  mentioned  above. 


HUMAN  SPIROCHETES 


443 


I.  HUMAN  SPIROCHETES. 
A.  Blood  Spirochetes. 

Spiroschaudinnia  recurrentis  Lebert,  1874. 

Synonyms. — Spirochete   recurrentis  Lebert,  1874;   5.   obermeyeri 
Cohn,  1875. 

This  spirochete  Was  discovered  by  Obermeyer  in  cases  of  relapsing 
fever  in  Berlin. 

Morphology. — It  exists  in  the  blood  in  short  and  long  forms. 
The  short  forms,  which  are  from  7  to  9  jj,  in  length,  are  probably 
early  stages.  The  long  forms,  16  to  19  fi,  result  from  multiplica- 
tion or  agglutination.  The  latter  condition  in  a  hyperimmune  blood 
may  lend  to  forms  18  to  100  fi  in  length,  brought  about  by  agglutina- 
tion of  two  or  more  cells  end  to  end.  The  width  is  0-25  /*.  The 
number  of  spirals  in  the  short 
form,  which  is  considered  to  be 
one  cell,  is  two  to  three. 

The  short  form  is  said  by 
Novy  and  Knapp  to  have  a 
long  rlagellum  at  one  end, 
while  the  other  has  a  faint 
appendage.  The  presence  of 
Ha-ella  in  this  as  well  as  in 
other  spirochetes  is  denied  by 
Nuttall. 

Life-History.  — ■  This  spiro- 
chaete is  pathogenic  to  man, 
monkeys,  rats,  and  mice;  but 
these  latter  have  to  be  infected 
from  a  monkey.  Rabbits  or 
guinea-pigs  are  not  susceptible. 
It  is  found  in  the  peripheral 
blood  during  the  attacks  and 
relapses,  but  not  in  the  inter- 
mission, unless  occasionally 
after  very  protracted  search.  It  can  also  live  in  the  bed-bug — 
Clinocoris  lectularius — for  some  days,  and  Nuttall  has  succeeded  on 
one  occasion  in  transmitting  5.  recurrentis  from  mouse  to  mouse 
by  the  bites  of  the  same  bug.  Positive  results  have  also  been 
obtained  by  Sikul  in  Odessa.  Most  authorities  consider  lice  to  be 
the  carriers. 

Immunity. — The  blood  serum  of  animals  immunized  to  5.  recur- 
rentis is  without  effect  upon  S.  duttoni  and  5.  novyi. 

Pathogenicity. — It  is  the  cause  of  European  relapsing  fever. 


Fig.  1  52. — Spiroschaudinnia  from 
Case  of  Asiatic  Relapsing  Fever. 

(From  a  micro pho tograph  by 
J.  J.  Bell.) 


/        444  TRYPANOSOMID& 

v  r 

V&  V/  Spiroschaudinnia  duttoni  Novy  and  Knapp,  igo6. 

Synonyms.— Spirillum  duttoni  Novy  and  Knapp,  1906;  Spiro- 
ch-ata  duttoni  Todd,  1906. 

This  spirochete  is  the  cause  of  the  West  African  and  the  Colombian 
tick  fever. 

Morphology  .—Its  length  is  variously  described;  thus  Novy  and 
Knapp  say  that  the  young  forms  are  16  ju  in  length,  while  Breinl 
and  Kinghorn  make  them  24  f.i  in  length  and  0-45  /j,  in  width  when 
fully  grown.  The  number  of  spirals  varies  from  two  to  three  to 
eight  to  ten,  with  a  width  of  2-2  /j,.  The  parasite  is  ribbon-shaped 
on  transverse  section,  and  though  it  is  often  in  spirals,  may  be 
simply  waved.     The  two  ends  are  pointed  (vide  Fig.  125). 

The  central  core  is  seen  to  consist  of  lighter  and  darker  portions, 
which  correspond  to  the  chromatic  and  the  achromatic  portions  of 
the  nucleus.  The  chromatic  portion  can  break  up  into  granules, 
when  the  parasites  begin  to  disappear  from  the  circulation. 

The  periplast  is  well  marked,  but  there  is  great  doubt  as  to  the 
presence  of  an  undulating  membrane.  Breinl,  who  has  studied 
the  subject  carefully,  could  not  definitely  define  one,  but  Dutton 
and  Todd  have  seen  it  in  blood  taken  directly  from  the  circulation 
in  man,  or  animals,  or  from  the  gut  of  Ornithodoros  moubata.  A 
small  uncoloured  transverse  band  is  often  to  be  seen  in  specimens 
stained  by  Giemsa  lying  across  the  parasite,  about  one-third  its 
length  from  one  end. 

Life- History  .—Reproduction  can  take  place  by  longitudinal  and 
transverse  division.  In  the  former  the  parasite  thickens  and  then 
divides  from  one  end,  while  in  the  latter  the  parasite  increases  in 
length  and  divides  in  the  middle.  Some  authors  deny  the  occur- 
rence of  transverse  division,  but  this  is  untenable  after  Fantham 
and  Porter's  experiments. 

There  is,  however,  another  and  but  little  known  method  of  repro- 
duction, which  appears  to  be  analogous  to  spore-formation. 

Just  before  the  crisis,  when  the  blood  is  swarming  with  parasites, 
they  can  be  seen,  according  to  Breinl,  in  the  spleen  and  bone-marrow, 
and  more  rarely  in  the  liver,  coiling  themselves  up,  and  either  show- 
ing a  swollen  appearance,  or  becoming  thinner  and  rolling  themselves 
into  more  and  more  complicated  skein-like  forms,  which  may  be 
engulfed  by  phagocytes  in  the  spleen,  but  in  other  organs  become 
more  regular  and  surrounded  by  a  thin  cyst-wall,  the  interior  of 
which  is  tilled  with  faintly  blue-staining  plasma. 

In  this  cyst  the  parasite  becomes  more  and  more  indistinct,  and 
at  a  later  stage  small  red  granules  are  to  be  seen,  which  are  thought 
to  be  the  cause  of  the  infection  in  the  blood  when  filtered  through 
a  Pasteur-Chamberland  filter.  Therefore,  according  to  the  investiga- 
tions by  Breinl,  the  life-history  of  the  parasite  has  two  well-defined 
stages  in  the  vertebrate.  In  the  first  it  is  found  free  in  the  liquor 
sanguinis  in  its  typical  form ;  in  the  second  it  enters  a  cell,  and, 
becoming  coiled,  its  chromatin  breaks  up  into  a  number  of  granules, 
each  of  which  is  believed  to  become  a  new  spirochete. 


SPIROSCHAUDINNIA   NOVYI  445 

The  stage  in  the  liquor  sanguinis  is  associated  with  the  febrile 
attacks,  and  that  in  the  cells  with  the  apyrexial  intervals. 

Carriers. — -It  is  spread  by  the  agency  of  Omithodoros  moubata  in 
Africa,  and  by  Argas  americanus  (chinche)  in  Colombia. 

In  the  Tick. — S.  duttoni  in  Africa  is  conveyed  to  man  and  animals 
by  faecal  infection  of  the  bites  of  a  tick,  Omithodoros  moubata. 
Leishman  has  demonstrated  that  when  S.  duttoni  enters  the  intes- 
tinal sac  of  the  tick  it  loses  its  mobility  and  characteristic  appear- 
ance, and  chromatic  masses  escape  into  the  lumen  of  the  gut  in  the 
form  of  small  rods  or  rounded  bodies  resembling  micrococci.  These 
multiply  and  pass  into  the  cells  of  the  Malpighian  tubules,  and  also 
into  the  immature  eggs  in  the  ovary.  They  can  be  followed  through 
all  the  stages  of  the  egg  into  the  adult  tick,  as  small  chromatin 
bodies  lying  in  the  cells  of  the  Malpighian  tubules.  These  bodies 
are  voided  with  the  fasces,  and  when  the  tick  feeds  are  capable  of 
entering  the  wound  produced  by  the  bite,  and  in  this  manner  in- 
fecting the  host. 

The  tick  remains  infective  for  a  very  long  time — according  to 
Moller  as  long  as  eighteen  months — and  the  infection  can  be  passed 
not  merely  through  the  eggs  into  a  new  generation  of  ticks,  as  has 
been  demonstrated  by  Button,  Todd,  Leishman,  and  others,  but 
also  according  to  Moller  into  the  third  generation,  even  if  the 
second  generation  have  only  fed  on  clean  animals. 

Pathogenicity.— It  is  the  cause  of  West  African  and  Colombian 
relapsing  fever. 

Spiroschaudinnia  rossi  Nuttall,  1908. 

This  spirochaete  is  distinguished  from  S.  duttoni  by  its  biological 
reactions,  though  some  authorities  consider  it  identical  with  S. 
duttoni.  It  is  the  cause  of  East  African  relapsing  fever,  and  is 
conveyed  by  Omithodoros  moubata. 

Spiroschaudinnia  novyi  Schellach,  1907. 

History. — In  1907  Professor  Manteufel,  while  investigating  an 
accidental  laboratory  infection  of  relapsing  fever,  found  that  the 
serum  of  the  patient  agglutinated  a  spirochaete  found  by  Novy  in 
a  case  of  relapsing  fever  in  America  in  a  dilution  of  1  in  100,  but 
showed  no  such  power  over  the  spirochete  of  the  European  disease. 
Moreover,  it  gave  Pfeiffer's  reaction,  being  active  in  doses  of  0-05  c.c. 
in  experimentally  infected  mice.  Schellach  has  investigated  this 
spirochaete,  and  given  it  the  specific  name  used  above. 

Morphology. — It  is  17  to  20  yt,  in  length,  with  six  to  eight  undula- 
tions and  a  thickness  of  0-31  fj,.  He  gives  the  dimensions  for  the 
S.  recurrentis  as  19  to  29  /lc,  with  eight  to  ten  undulations  and  a 
thickness  of  0-39  [/,,  and  S.  duttoni  as  24  fi  at  the  most,  with  eight 
to  ten  undulations  and  a  thickness  of  0-45  /t;  which  appear  to  be 
very  different  from  Novy's  table  given  under  S.  carteri. 

The  spirochaete  appears  to  have  great  flexibility  and  activity 
of  movement.     One  end  has  a  filiform  prolongation  about  5  p,  in 


446 


TR  YPA  NO  SO  MI  DM 


length,  while  the  other  is  merely  pointed.  No  undulating  mem- 
brane could  be  differentiated;  but  he  states  that  he  was  able  to 
demonstrate  lateral  cilia,  which  he  considers  to  be  artificial;  but 
this,  in  our  opinion,  is  highly  suggestive  of  the  presence  of  an 
undulating  membrane.  Coloured  granules  could  be  made  out 
when  stained  by  Giemsa.  Reproduction  was  usually  by  transverse 
division. 

Life-History. — -The  spirochetes  are  found  in  the  blood  during 
the  attacks  of  fever,  and  equally  distributed  in  the  organs  in  the 
apyrexial  interval. 

Inoculation. — -It  can  be  inoculated  into  monkeys,  but  small  rodents 
are  especially  susceptible.  Subinoculations  can  be  made  from 
monkey  to  monkey  and  from  mouse  to  mouse. 

Immunity. — -Serum  of  animals  immunized  for  S.  novyi  is  without 
effect  upon  5.  rccurrentis,  S.  duttoni,  or  S.  carteri. 

Cultivation. — It  has  been  cultivated  by  Noguchi  as  mentioned 
above  (see  p.  441 1 . 

Pathogenicity. — It  is  the  cause  of  North  American  relapsing 
fever. 

Spiroschaudinnia  carteri  Manson,  1907. 

«.  VX\    5.  carteri  has  a  minimal  length  of  12  /j,,  with  open  flexures.     It  is 

y"^\  thinner  than  5.  novyi,  and  it  is  not  agglutinated  by  serum  of  animals 

/w\0  immunized  against  5.  novyi.     It  can  be  inoculated  into  monkeys 

W       and  with  difficulty  into  mice,  and  can  be  subinoculated  from  monkey 

f  x       to  monkey  or  mouse  to  mouse. 

Novy  and  Knapp  give  the  following  differences  between  5.  carteri, 
S.  duttoni,  and  5.  novyi  : — • 


Character. 

Spiroschau- 
dinnia novyi. 

Spiroschau- 
dinnia duttoni. 

Spiroschau- 
dinnia carteri. 

Length  of  simple  cell 
Length  of  double  cell 

Width 

Number  of  turns  in  a  single 

cell 

Distance  between  the  turns    .  . 

Movement 

Number  in  peripheral  blood  .  . 

8  jx 

16-20^ 
0-25  /.i 

2-3  ^ 

Vigorous 

Many 

16  fX 

0'2  /U, 

2'5  A* 
4-5 /< 
Little 
Few 

8/4, 

16-20 /i 

0-2  /4 

2-3  li 
2-3^ 

Many 

According  to  Strong's  experiments,  rats  immunized  against  S.  recurrcntis 
and  S.  novyi  are  immune  to  S.  carteri.  He  therefore  believes  these  three 
strains  to  be  closely  allied,  if  not  identical. 

They  can  also  be  distinguished  by  agglutination,  immunization 
by  Pfeiffer's  reaction,  and  by'  certain  animals  being  suscep- 
tible to  some  species  and  not  to  others.  Mackie  has  suggested  that 
S.  carteri  may  be  transmitted  by  a  pediculus.  It  is  the  cause  of 
Asiatic  relapsing  fever. 


SPIROSCHAUDINNIA   BEKBERA  447 

Spiroschaudinnia  berbera  Sergent  and  Foley,  1910. 

Spiroschaudinnia  with  minimal  length  of  12  /u  and  irregular  open 
spirals  or  flexures.  It  can  be  inoculated  into  monkeys  {Macacus 
cynocephahis)  and  with  difficulty  into  rats  and  mice.  Subinocula- 
tions  can  be  made  with  difficulty  from  rat  to  rat  and  from  mouse 
to  mouse.  The  immune  serum  is  without  effect  upon  5.  recurrentis. 
It  produces  a  mild  infection  in  animals,  but  a  severe  one  in  man, 
for  whom  it  is  the  cause  of  North  African  and  possibly  Egyptian 
relapsing  fever.     Probably  it  is  spread  by  the  agency  of  lice. 

Spiroschaudinnia  morsusmuris  Futaki,  Takaki,  Taniguchi,  and 
Osumi,  1917. 

Synonym.- -Spirochuia  morsusmuris. 

This  spirochaete  was  found  in  the  blood,  skin,  and  lymph  glands 
of  six  patients  suffering  from  rat-bite  disease. 

The  spirochaete  is  mobile  and  shows  a  single  flageilum  at  each  pole, 
but  no  undulating  membrane,  and  has  generally  three  or  four  curves, 
but  may  have  two  to  nineteen.  The  smaller  forms  occur  in  the 
blood  and  the  larger  in  the  tissues. 

Mice  and  white  rats  become  affected,  but  guinea-pigs  and  monkeys 
fail  to  do  so. 

Spiroschaudinnia  icteroheemorrhagiae  Inada,   Ido,   Hoki,    Kaneko, 

and  Ito,  1915. 

Synonyms.  —  Spirochete  icterohcemorrhagice  Inada,  etc.,  1915: 
S.  icterogenes  Uhlenhuth  and  Fromme;  5.  nodosa  Huebener  and 
Reiter.  ' 

Nomenclature.— Noguchi  has  created  a  new  genus  (see  p.  439) 
for  this  parasite,  calling  it  Leptospira  icterohcemorrhagice ,  and  this 
will  probably  be  generally  accepted. 


l'IG-  i^SS- — Spiroschaudinnia  icterohesmorrhagi  a  Inada.  etc. 

This  spirochete  is  found  during  the  first  four  weeks  in  the  blood 
and  urine  ot  patients  suffering  from  infective  jaundice  (Weil's  disease) 
of  the  spirochaetal  type,  and  can  be  inoculated  into  animals,  produc- 
ing jaundice.     These  observations  have  been  confirmed  by  French, 


448  TRYPANOSOMIDM 

Italian,  and  German  workers.  The  spirochaetes  found  in  Japan  and 
Belgium  have  been  shown  by  Noguchi  to  be  identical  morphologically 
and  serologically.  The  parasite  seems  to  occur  in  the  kidneys  and 
urine  of  wild  rats  in  Japan,  in  the  rats  in  the  trenches  in  Belgium, 
in  those  in  France,  where  the  disease  in  unknown,  and  in  America, 
where  it  is  rare. 

The  organism  can  enter  through  the  alimentary  canal,  via 
abrasions  on  and  even  through  the  healthy  skin,  and,  as  it  can  live 
in  water,  this  is  thought  to  be  the  principal  means  of  infection — i.e., 
by  Walking  barefoot  or  in  sandals  on  wet  earth  or  in  stagnant 
water. 

The  spirochaetes  are  6-9  microns  long  on  an  average,  but  may 
reach  to  20  microns  and  about  02-5  micron  in  breadth,  with  two  to 
three  large  or  four  to  five  small  waves.  It  often  contains  refractile 
granules,  to  the  number  of  twenty-five  to  forty  (these  may  in  reality 
represent  small  waves,  as  shown  by  Dobell). 

Guinea-pigs  may  be  infected  orally,  subcutaneously,  or  intra- 
peritoneally,  with  the  blood  of  patients  up  to  the  seventh  day  of  the 
illness,  but  usually  not  later,  though  there  are  exceptions  to  this. 
The  incubation  period  in  these  animals  is  seven  to  eight  days,  and 
the  symptoms  resemble  those  produced  in  man.  Rabbits  cannot  be 
infected.  Ito  and  Matsuzaki  obtained  it  in  pure  culture  from  the 
heart  blood  of  subinoculated  guinea-pigs,  by  sowing  this  on  blood 
agar  or  blood  gelatine  and  incubating  from  20°-25°  C,  though  it  can 
grow  from  i5°-37°  C.  It  produces  neither  odour,  gas,  nor  lique- 
faction of  the  medium.  The  organism  so  cultivated  remains  patho- 
genic for  guinea-pigs.  A  good  medium  is  a  mixture  of  rabbit 
blood-serum  and  085  per  cent,  saline  in  the  proportion  of  1  to  5. 

Spiroschaudinnia  hebdomadis  Ido,  Ito,  and  Wani,  19 18. 

Morphologically  similar  to  S.  icterohcemorrhagice,  differs  serologically. 
Found  by  Ido,  Ito,  and  Wani  in  cases  of  a  seven-day  fever  called  Nanukayami, 
which  somewhat  resembles  atypical  Weil's  disease. 

The  field  mouse  (Microtus  montebelli)  seems  to  be  the  normal  host  of  the 
spirochete. 

Spiroschaudinnia  in  Yellow  Fever. 

Stimson  in  1909  described  a  spirochaete  in  the  organs  of  persons  who  had 
died  of  yellow  fever  (S.  interrogans  Stimson  1909),  but  little  importance  was 
given  to  this  observation.  In  19 18  Noguchi  cultivated  from  the  blood  of 
several  vellow  iever  patients  a  spirochaete  similar  to  S.  icier  ohamorrhagi ce 
(Leptospira  ictcroh&morrhagicB),  and  by  inoculating  cultures  of  the  organism 
he  produced  in  monkeys  the  same  haemorrhagic  lesions  as  seen  after  the 
successful  incculation  of  blood  of  yellow  fever  patients. 

B.  Cutaneous  Spirochetes. 
Spiroschaudinnia  vincenti  Blanchard,  1906. 

Synonym. — Spiroschaudinnia  schaudinni  Prowazek,  1907. 

This  is  a  very  active  motile  spirochaete  10  to  20  /j,  in  length,  with  a  well- 
marked  undulating  membrane  and  one  rather  short  flagelhim.  Male  and 
female  forms  can  be  seen,  according  to  Prowazek.     Division  is  longitudinal. 


SPIROSCHAUDINNIA   BRONCHIA  LIS  449 

It  is,  according  to  Prowazek,  the  cause  of  ulcus  tropicum,  and  is  possibly 
transmitted  by  a  leech.     Induces  formation  of  pseudo-membranes. 

It  is  often  associated  -with  the  so-called  fusiform  bacilli  causing  angina 
Vincenti  and,  according  to  certain  authors,  hospital  pha.gedaena  and  noma. 

Spiroschaudinnia  aboriginalis  Cleland,  1909. 

This  spirochaete  was  found  by  Wise  in  British  Guiana  in  1906,  and  by 
Cleland  in  West  Australia  in  1909  in  cases  of  granuloma  inguinale.  Its  length 
is  6  to  18  /ut,  and  it  possesses  but  few  coils,  which  vary  in  depth.  The  extremities, 
aci  o riling  to  Cleland,  are  blunt.  Similar  spirochaetes  have  been  found  by  Wise 
and  others  in  a  peculiar  granulomatous  affection,  which  attacks  the  genital 
organs  of  dogs  and  bitches.  It  is  believed  at  the  present  time  that  this 
Spirosch .tudium'a  is  not  the  cause  of  granuloma  inguinale,  but  merely  a 
saprophyte. 

Spiroschaudinnia  phagedenis  Noguchi,  19 12. 

Noguchi  discovered  this  spirochaete  in  an  indurated  and  ulcerated  swelling 
of  the  labium  which  had  lasted  ten  days.  It  has  been  cultivated  by  him  on 
ascitic  agar  medium,  and  is  a  strict  anaerobe.  Length  varies  from  4  to  30  fi, 
and  the  curves  from  1  to  8  Ju,  while  young  forms  may  be  quite  straight.  Inoc- 
ulated into  monkeys  and  rabbits  it  causes  transient  inflammation. 

S.  acuminata  Castellani,  1905,  and  S.  obtusa  Castellani,  1905. 
Found  in  the  open  sores  of  yaws. 

S.  pseudopallida  Mulzer,  1905. 

Found  in  ulcerating  carcinomata. 

Unnamed  forms  of  cutaneous  spirochaetes  have  been  seen  by  von  Prowazek 
in  cases  of  psoriasis. 

C.  Respiratory  Spirochetes. 
Spiroschaudinnia  bronchialis  Castellani,  1907. 

The  presence  of  this  spirochaete  and  the  disease  which  it  causes 
was  first  described  by  Castellani  in  1906.  They  have  been  confirmed 
by  Branch  in  the  West  Indies,  by  Chalmers  and  O'Farrell  in  the  Sudan, 


J 


Figs.  134  and  135. — Spiroschaudinnia  bronchialis  Castellani. 

29 


45o  TRYPANOSOMID&: 

by  Macfie  in  West  Africa,  by  Castellani  and  Jackson  in  the  Balkans, 
by  Toro  Villa  in  Colombia  and  South  America,  by  Ragazzi  in  Bengazi, 
'by  Galli-Valerio  in  Switzerland,  by  Lurie  in  Serbia,  by  Violle  in 
France,  and  by  Brought  on -Alcock  in  North  Italy  (see  p.  1882)7 

It  was  originally  found  by  Castellani  in  cases  of  bronchitis  in 
Ceylon,  and  its  morphology  lias  been  carefully  studied  by  Fantham 
in  the  Anglo-Egyptian  Sudan. 

S.  bronchialis  is  an  organism  with  marked  polymorphism,  varying 
in  length  from  5-25  microns  and  in  breadth  from  0-2-0-3  micron. 
The  variations  indicate  different  stages  of  growth  and  division. 
As  a  rule  the  ends,  though  varying  considerably,  are  acuminate. 
Its  movements  are  active,  but  cease  shortly  after  removal  from  the 
body,  and  are  succeeded  by  a  granule  stage,  as  described  by  Fantham, 
and  from  these  granules  new  spirochetes  are  believed  to  be  formed. 

The  granules  are  probably  the  infective  agent,  and  spread  the  in- 
fection from  man  to  man  by  the  air. 

It  is  believed  to  be  different  from  S.  dentium  and  S.  buccalis, 
the  mouth  spirochetes,  of  which  the  former  measures  4-10  and  the 
latter  9-22  microns  in  length. 

Chalmers  and  O'Farrell's  experiments  tend  to  show  that  monkeys 
can  be  infected. 

Spiroschaudinnia  minuta  Castellani,  1916. 

Found  in  cases  of  rhinopharyngitis  (p.  18S1).  With  Romanosky 
it  stains  a  pinkish  red,  and  has  very  few  spirals.  Length  3-10-12 
microns. 


f 

— \ 
Fig.  136. — Spirochaudinnia  minuta  Castellani. 

D.  Alimentary  Canal  Spirochetes. 

Spiroschaudinnia  subtilis  Castellani,  1907. 
Found  in  scrapings  from  oral  mucosa  and  in  intestinal  contents. 


URINARY  SPIROCHETES  451 

Spiroschaudinnia  eurygyrata  Werner,  1909,  emendavit  Fantham, 

1916. 

Synonyms.— Spirillum hachaizce  Kowalski  (perhaps);  5.  eurygyrata 
Werner,  1909. 

The  spirochete  Was  first  noted  under  the  name  spirillum  in  cholera 
motions  in  1884-86  and  1893-94.  In  1903  Le  Dantec  saw  them  in 
cases  of  so-called  spirochetal  dysentery.  In  1909  Werner  gave  them 
the  two  names  mentioned  above,  which  Fantham  in  his  1916  re- 
searches considers  to  be  the  same. 

The  spirochetes  were  found  by  Fantham  in  the  feces  of  soldiers 
suffering  from  diarrhoea  or  dysentery  in  Gallipoli  and  Flanders,  and 
also  in  healthy  people.  It  has  pointed  ends,  and  varies  from  3-15 
microns  in  length  by  about  0-25  micron  in  breadth.  The  number 
of  Waves  is  from  two  to  nine,  while  chromatin  granules  can  be  seen 
along  the  body.  It  is  actively  motile,  and  has  been  seen  to  enter  the 
shed  epithelial  cells  found  in  the  feces,  where  it  produces  coccoid 
bodies. 

Note. — It  is  essential  not  to  confuse  true  spirochetes  found  in 
the  feces  with  vegetal  organisms  with  pseudo-spirochetal  shapes, 
as  has  occurred — e.g.,  Spirobacillus  (Bacillus)  zeylanicus  Castellani, 
19 10,  has  often  been  mistaken  for  a  true  spirochete  (see  p.  1838). 

E.  Urinary  Spirochetes. 

Spiroschaudinnia  urethrae  Macfie,  1917. 

These  spirochetes  have  been  seen  by  Macfie  in  urine  in  natives 
on  the  Gold  Coast,  where  it  caused  an  acute  urethritis. 

The  parasite  was  found  free  in  large  quantities  in  the  pus  and  also 
in  the  pus  cells.     It  measured  from  5-20  microns  in  length,  and 

Fig.  137. — Spiroschaudinnia  mitis  Castellani. 

showed  a  membrane  or  crest.  The  cytoplasm,  which  was  homo- 
geneous, contained  chromatin  granules  or  rodlets  at  intervals. 
Some  pus  cells  contained  coccoid  granules. 

Spirochetes  have  been  found  in  the  normal  urethra  by  various  authors— e  g 
Menaelson.  "  ' 

S.  mitis  was  found  by  Castellani  in  the  centrifuged  urine  of  certain  cases 
ot  camp  jaundice  of  mdd  type.  It  is  thicker  than  S.  icterohamorrhagia.  and 
has  larger  and  better  defined  waves.     Of  doubtful  pathogenicity. 


452 


TRYPANOSOMID& 


THE  DIFFERENTIATION  OF  HUMAN  SPIROCHETES. 

The  differentiation  of  spirochetes  is  exceedingly  difficult,  as 
morphological  characters  seldom  help,  and  measurements  with  wave 
formations  are  useless  for  this  purpose. 

As  many  of  the  so-called  species  are  probably  only  variants  pro- 
duced by  environment,  it  seems  correct  to  classify  them  according 
to  site  in  the  human  body,  according  to  their  action  on  man  and 
animals,  and  according  to  immunity  experiments. 

The  following  is  an  attempt  on  these  lines : — ■ 

A .  Found  in  the  blood  :— 

I.  In  cases  of  relapsing  fever  :— 

(a)  Clinical  symptoms  in  man  mild,  but  in  animals  severe 

— S.  novyi. 

(b)  Clinical  symptoms  in  man  severe: — 

1.  In  animals  severe — S.  duttoni. 

2 .  In  animals  mild : — 

(i)  Berbera  immune  serum  protective — 5.  berbera. 
(2)  Berbera  immune  serum  ineffective  and  re- 
currentis  immune  serum  protective;  closely 
allied  forms: — 
(a)  Found  in  Europe — S.  recurrentis. 
{b)  Found  in  India — '5.  carted. 
II.  In  cases  of  infectious  jaundice— S.  icterohcemorrhagica. 
III.  In  cases  of  rat-bite  disease — S.  morsusmuris. 

B.  Found  in  the  skin  : — 

I.  In  ulcus  tropicum : — ■ 

Not  cultivated,  with    undulating   membrane   and   short 
flagellum — 5.  vincenti. 
II.  In  granuloma  inguinale: — 

Not  cultivated  without  undulating  membrane  or  flagellum 
— S.  aboriginalis. 
III.  In  cutaneous  inflammation: — 

(a)  Cultivated,   strictly  anaerobic;   causes    transient    in- 

flammation in  animals — S.  phagedenis. 

(b)  Not  cultivated;  found  in  open  yaws  ulcers: — 

1.  Acuminate — S.  acuminata. 

2.  Obtuse — S.  obtusa. 

(c)  Not   cultivated;   found   in   ulcerating   carcinomata — 

S.  pseudopallida. 

C.  Found  in  the  respiratory  passages  : — 

I.  In  bronchial  spirochetosis — 5.  bronchialis. 
II.  In  rhinopharyngitis — S.  minuta. 

D.  Found  in  the  alimentary  canal  and  skin  lesions  : — 

I.  In  the  mouth: — 

{a)  Produces  pseudo-membranes.     In  cases  of  angina  and 

ulcus  tropicum — S.  vincenti. 
(b)  Non-pathogenic: — 


ANIMAL  SPIROCHETES 


453 


1.  Short  forms — S.  dentium. 

2.  Long  forms — S.  bnccalis. 
II.  In  vomit: — - 

Rather  doubtful   forms   in   vomit   of   Belyando   spew  in 
Queensland — Unnamed. 
III.  In  faeces: — 

In  health  and  disease — -S.  eurygyrata. 

E.  Found  in  the  urethra  : — 

I.  In  free  and  in  coccoid  form  in  pus  cells  from  urethritis. 

With  crest  or  membrane — S.  urethrce. 
II.  In  urine  from  cases  of  mild  camp  jaundice.     With  well- 
marked  waves — S.  mitis. 


ANIMAL  SPIROCHETES. 
Spiroschaudinnia  macaci  Castellani  and  Chalmers,  1910. 

Synonym. — Spirochceta  macaci  Casttllani  and  Chalmers,  1910. 

This  spirochaete  was  found  by  us  in  monkeys  in  Ceylon  in  1906. 
In  length  it  measures  about  12  jjl,  and  closely  resembles  5.  carteri 
Manson,  1907.  It  can  be  easily  inocu- 
lated from  monkey  to  monkey.  Spiro- 
chaetes  which  may  be  of  a  different  species 
have  also  been  found  by  Leishman, 
Balfour,  and  by  Plimmer  in  Cerco- 
pithecus  sebcB  from  Sierra  Leone. 

Spiroschaudinnia  anserina  Saccharoff, 
1 89 1. 

Found  in  enormous  numbers  in  the  blood 
of  geese  in  the  Caucasus  and  Tunis.  It  causes 
fever,  diarrhoea,  tenderness  of  the  feet,  and 
death  in  about  a  week,  the  mortality  being 
80  per  cent.  It  can  be  inoculated  into  other 
geese. 

Spiroschaudinnia  marchouxi  Nuttall, 
1904. 

Synonym.—  Spirochceta  gallinarum  R.  Blan- 
chard,  1  g<  >  5 . 

This  spirochaete,  which  has  been  discovered 
by  Marcnoux  and  Salirabeni,  and  studied  by 
Balfour,  is  about  10  to  20  /t  in  length,  causes 
disease  in  fowls  in  many  countries — e.g.,  Brazil, 
the  Sudan,  Egypt,  Tunisia,  and  Serbia.     The 

symptoms  are  lever,  diarrhoea,  anemia,  somnolence,  convulsions,  and  death  in 
four  to  five  clays,  or  in  chronic  cases  cachexia  and  death  in  fourteen  days. 
As  first  observed  by  Sambon,  it  appears  to  enter  the  red  corpuscle,  and  to  break 
up  within  it  in  a  way  which  reminds  one  of  the  description  already  given  for 
S.  duttoni.  Balfour  has  made  an  important  investigation  on  granules  spread- 
ing and  the  infective  granules.  It  is  spread  by  Argas  persicus  and  other 
Ldae,  as  Fulleborn  has  shown  with  Ornithodoros  moubata.  Balfour  has 
made  the  important  observation  that  in  the  infected  ticks  chromatic  granules 
are  present  as  described  by  Leishman  in  S.  duttoni. 


Fig.  138. — Spirochetes  in 
the  Blood  of  Cercopi- 
thecus  sebcens  from  Sierra 
Leone.      (X   1,000.) 

\From  a  microphotograph 
by  H.  G.  Plimmer.) 


454 


TR  YPA  NO  SO  MI  DM 


Recent  researches  by  Balfour  tend  to  show  that  the  Sudan  strain  is  a 
separate  species:  5.  granulosa  Balfour,  1910.  Aragao  has  attempted  to 
obtain  a  serum  and  a  vaccine  with  a  certain  degree  of  success. 

Spiroschaudinnia  neveuxii  Brumpt,  1909. 
Brumpt    describes    this    spirochaete    as    morphologically    identical    with 
5.  marchouxi,  but  cross  immunization  shows  that  the  two  species  are  different. 
It  is  the  cause  of  fowl  spirochaetosis  in  Senegal,  and  is  spread  by  Argas  pcrsicus. 

Spiroschaudinnia  theileri  Laveran,  1904. 

This  spirochaete,  discovered  by  Theiler  in  1902,  is  found  in  cattle  in  Africa 
about  Pretoria,  in  the  Cameroons,  and  in  East  Africa.  The  symptoms  are  not 
clear,  as  babesia  has  also  been  seen  in  the  same  animals.  It  is  spread  by 
Margaropus  decoloratus,  the  blue  tick. 

Spiroschaudinnia  ovina  R.  Blanchard,  1906. 

This  spirochaete  may  be  the  same  as  S.  theileri.  It  was  found  by  Marfoglio 
and  Carpano  in  sheep  in  Erythraea,  on  the  Red  Sea,  and  by  Theiler  in  the 
Transvaal. 

Spiroschaudinnia  equi  Novy  and  Knapp,  1906. 

Found  by  Theiler  in  the  Transvaal,  and  by  Martin  in  French  Guinea,  and 
may  be  the  same  as  S.  theileri. 

Other  Spirochetes. — 5.  vespertilionis  Novy  and  Knapp,  found  by  Nicolle 
and  Confine  in  1905,  in  Vespertilio  kuhli. 

S.  gracilis  Levaditi  and  Stanesco,  1909,  very  like  Treponema  pallidum. 

S.  culicis  Jaffe,  1907,  found  in  the  gut  and  Malpighian  tubules  of  Culex 
pipiens  and  the  larva  of  Anopheles  maculipennis. 

S.  muris  Wenyon  and  S.  laverani  Breinl  and  Kinghorn,  in  mice. 

S.  bufonis  Dobell,  1908,  found  in  the  rectum  of  a  frog. 

S.  glossince  Novy  and  Knapp,  1906,  in  the  stomach  of  tsetse-flies. 

5.  microgyrata  Gaylord  and  Calkins,  1907,  in  cancer  of  the  breast  in  mice. 

5.  balanitidis  Hoffmann  and  Prowazek,  1906,  found  by  Hoffmann  and 
Prowazek  in  balanitis. 

S.  hi  res  Prowazek,  1907,  found  by  Prowazek  in  the  otter. 

Sambon  has  found  spirochaetes  in  scrapings  from  gastric  ulcers  in  a  fox. 

Various  spirochaetes  have  also  been  observed  in  the  stomach  of  normal  cats, 
dogs,  and  rats  (Bizzozzero,  Salomon),  in  the  intestinal  ulcers  of  dogs  and 
monkeys  affected  with  trypanosomiasis  (Balfour),  in  the  intestine  of  normal 
mice  (Wenyon)  and  birds  (Kent). 

Treponemidae  Schaudinn,  1905. 

Definition. — Spirochsetacea  with  a  minute  thread-like  body- 
twisted  into  numerous  fine  coils,  with  pointed  tapering  extremities. 
The  body  is  cylindrical  on  section,  and  not  flattened,  and  the  spirals 
appear  preformed.  There  is  no  undulating  membrane.  Trans- 
verse and  longitudinal  division  have  been  observed,  the  latter  type 
being  the  only  one  found  in  cultures. 

Classification. — Only  one  genus. 

Treponema  Schaudinn,  1905. 

Synonym. — Spirodiceta  Ehrenberg pro  parte;  Spironema  Vuillemin, 
1905,  von  Klebs,  1892. 

Treponemidae  with  the  characters  of  the  family. 
Type  Species. — Treponema  pallidum  Schaudinn,  1905. 


TREPONEMA  PALLIDUM  455 

Treponema  pallidum  Schaudinn,  1905. 

Synonyms. — -Spirochceta  pallida  Schaudinn,  1905 ;  Spironema  pal- 
lidum Vuillcmin,  1905;  Microspironema  pallidum  Stiles  and  Pfander, 
1905;  Trypanosoma  luis  Krzysztalowicz  and  Siedlecki,  1905. 

History.— This  treponema  was  discovered  by  Schaudinn  in  syphilis 
in  1905 .  The  history  of  the  finding  of  parasites  in  syphilis  is  interest- 
ing, for  as  long  ago  as  1546  Frascastorius  considered  syphilis  to  be 
a  parasitic  disease.  In  1879  Klebs,  and,  later,  Losdorfer  and 
Dohle  in  1901,  described  parasites,  and  saw  cell  inclusions  in  the 
disease,  and  in  1905  Siegel  described  an  organism,  Cytoryctes  luis, 
in  which  there  are  flagellate  bodies  very  closely  resembling  spiro- 
chetes.    In   1905    Schaudinn,    after   investigating   and   reporting 


Fig.   139. — Treponema   pallidum    Schaudinn,    1905. 
(From  a  microphotograph  by  J.  J.  Bell.) 

ui\t;i.vourably  on  Siegel's  work,  found  the  Treponema  pallidum, 
which  is  accepted  as  the  cause  of  the  disease.  Korte  in  1906  described 
free  round  bodies  and  cysts  with  threads  in  primary  sores.  E.  H.  Ross 
has  described  an  intracellular  formation  allied  to  his  Lymphocytozoon 
cobayce,  which  develops  into  spirochetes,  and  these  researches  have 
in  part  been  confirmed  by  Jennings.  McDonagh  also  has  described 
a  complicated  life-cycle. 

Morphology.  -It  varies  from  4  to  10  pi,  in  length,  average  7  /*, 
witli  a  width  up  to  0-5  pi.  It  is  twisted  into  spirals,  which  vary 
from  six  to  twelve  and  more  in  number,  the  average  being  eight 
to  ten,  and  are  to  a  certain  extent  preformed — i.e.,  not  due  to  the 
pamsite's  movements.  It  moves  by  rotation  on  a  long  axis  by 
gliding  movements,  forwards  and  backwards,  and  also  by  flexion 


456  TRYPANOSOMIDM 

of  the  whole  body.  The  periplast  is  continued  as  long  delicate 
processes  at  each  end,  which  are  considered  by  some  to  be  flagella. 

Krzysztalowicz  and  Siedlecki  say  that  not  far  from  the  middle 
the  body  may  be  nearly  straight,  and  a  clear  spot  can  be  observed 
which  they  think  is  a  nucleus ;  but  it  might  correspond  to  the  similar 
area  in  S.  duttoni.  They  also  describe  male  and  female  gametes 
and  conjugation,  which  they  think  leads  to  the  formation  of  a  cyst 
or  spore,  which  may  be  carried  via  the  blood  stream  to  different 
parts  of  the  body,  and  there  develop  into  Treponemata. 

The  parasite  is  found  in  the  primary  sores  and  in  the  secondary 
lesions,  but  is  very  difficult  to  detect  in  tertiary  eruptions,  though 
it  is  abundantly  present  in  the  liver,  spleen,  decidua,  the  placental 
villi,  the  umbilical  cord  of  syphilitic  foetuses,  and  infants. 

It  is  distinguished  from  other  spirochetes  (S.  refringens)  which 
may  be  met  with  on  ulcerated  surfaces  by  difficulty  in  staining; 
number,  character,  and  permanence  of  the  spirals;  the  terminal 
prolongations;  absence  of  an  undulating  membrane;  minute  size 
and  delicacy. 

Inoculation.- — -Syphilis  can  be  inoculated  into  chimpanzees  (as 
shown  by  Metchnikoff  and  Roux)  and  other  monkeys,  and 
T.  pallidum  can  be  found  in  the  lesions  so  caused,  the  incubation 
being  fifteen  to  forty-nine  days,  average  thirty  days,  for  the  primary 
sore;  and  nineteen  to  sixty-one  days,  average  thirty-three  da}'s,  for 
the  secondary  eruption  after  the  primary  have  appeared.  In  the  lower 
monkeys  the  lesion  remains  localized  to  the  seat  of  the  inoculation. 

Cultivation. — Schereschewsky  has  cultivated,  with  a  certain  degree 
of  success,  T.  pallidum  on  a  medium  of  horse  serum,  brought  to  a 
gelatinous  consistence  by  heating  to  6o°  C,  and  partly  autolyzed  by 
keeping  in  an  incubator  at  370  C.  for  three  days.  Later  Miihlens 
and  Hartmann  also  cultivated  it,  Hartmann  inoculating  a  pure 
culture  with  success  in  the  testicles  of  a  rabbit,  and  more  recently  it 
was  grown  by  Noguchi  quite  successfully,  as  described  above  for 
Spiroschaudinnia,  and  he  has  also  been  successful  in  reproducing  the 
disease  in  monkeys  by  inoculation  of  the  pure  culture.  The  monkeys 
present  a  positive  Wassermann  reaction  two  weeks  after  inoculation. 
Noguchi  has  made  the  important  observation  that  there  are  several 
varieties  of  T.  pallidum  ;  he  distinguishes  a  normal  type  of  medium 
thickness,  a  thick  type,  and  a  thin  type.  Inoculated  in  the  testicles 
of  rabbits,  the  normal  type  gives  rise  to  a  diffuse  induration,  which 
develops  the  third  Week  after  inoculation;  the  thick  type  gives  rise 
to  several  small  hard  nodules,  which  develop  slowly;  the  thin  type 
induces  a  diffuse  swelling,  which  develops  veiy  quickly,  ten  to 
fourteen  days  after  inoculation.  It  is  interesting  to  note  that  Mott, 
several  years  ago,  suggested — on  clinical  and  pathological  grounds — 
that  there  might  be  more  than  one  variety  of  T.  pallidum. 

Biological  Reactions. — By  heating  the  cultures  to  6p°  C.  Noguchi 
has  produced  a  product  which  he  calls  luetine,  by  means  of  which 
a  cutaneous  reaction  can  be  obtained  in  syphilitic  patients. 

Life-History.— Unknown . 


TREPONEMA   PERTENUE  457 

E.  H.  Ross  found  cellular  inclusions  resembling  Kurlofl's  bodies  in  mono- 
nuclears in  non-ulcerated  Hunterian  chancres,  and  examined  them  in  detail 
by  placing  the  blood  from  such  a  chancre  upon  H.  C.  Ross's  coefficient  jelly. 

Similar  bodies  have  been  described  by  McDonagh,  who  has  given  an  account 
of  a  complicated  life-cycle  for  T.  pallidum  (see  second  edition  of  this  book, 
p.  409). 

Pathogenicity. — T.  pallidum  is  the  cause  of  syphilis. 

Treponema  pertenue  Castellani,  1905. 

Synonyms. — Spirochata  pertenuis  Castellani,  June,  1905;  Sfiiro- 
chceta  pallidula  Castellani,  November,  1905. 

History.— It  was  discovered  by  Castellani  in  1905  in  the  scrapings 
from  yaws  papules. 

Morphology. — Treponema  pertenue  is  an  extremely  delicate  spiral- 
shaped  organism,  varying  in  length  from  a  few  microns  to  18 
and  20  [x  and  even  more.  It  is  very  slender.  Some  individuals 
are,  however,  thicker  than  others.  It  does  not  stain  easily,  but 
good  results  may  be  obtained  with  Giemsa's  method,  and  also  with 
Irishman's  stain,  provided  the  alcoholic  solution  is  allowed  to  act 
for  five  minutes,  and  the  subsequent  admixture  With  distilled  Water 
for  from  one  half-hour  to  several  hours.  Using  either  of  these 
methods,  the  Treponemata  stain  purplish.  Occasionally  a  few 
deeply  stained  granules  may  be  seen  in  the  body  of  the 
organism.  The  extremities  of  the  parasite  are  often  pointed,  but 
forms  may  be  met  with  presenting  blunt  extremities,  or  one  ex- 
tremity pointed  and  the  other  blunt.  In  some  individuals  one  of 
the  extremities  may  present  a  large  pear-shaped  expansion  or  a 
loop-like  formation.  The  number  of  coils  varies  from  six  to  twenty 
or  more,  but  they  are,  as  a  rule,  numerous,  uniform,  and  of  small 
dimensions.  Occasionally  a  portion  of  the  Treponema  shows 
numerous  close  uniform  coils,  while  the  rest  of  its  body  shows  no 
coils  at  all.  Sometimes  two  Treponemata  may  be  attached  end 
to  end,  or  apparently  twisted  together.^  Castellani  has  not  been 
able  to  detect  any  undulating  membrane,  though  its  presence  has 
been  asserted  by  other  observers  (Blanchard).  Occasionally,  in 
preparations  stained  by  Loffler's  method  of  flagella  staining,  it  has 
seemed  to  several  observers  that  some  of  the  organisms  present  an 
extremely  delicate  flagellum  at  one  end.  Prowazek  has  described 
a  resting  form,  oval  or  round,  produced  by  a  coiling  up  of  the  spiral. 
Ranken,  by  means  of  the  dark-ground  illumination,  has  been  able 
to  observe  the  extrusion  from  the  parasite  of  small,  highly-refractile 
granules,  which  are  apparently  shot  out  by  free  lateral  motion. 
These  granules  immediately  after  extrusion  remain  stationary,  then 
begin  to  rotate  and  move  about,  though  apparently  not  supplied 
with  flagella. 

Intracellular  Stage. — Castellani  in  1905  described  some  peculiar 
bodies,  free  and  intracellular,  in  leucocytes,  which  possessed  an  oval 
or  roundish  shape,  and  contained  chromatin  dots.  At  the  time  he 
Was  inclined  to  consider  them  to  be  stages  in  the  development  of 
the  parasite,  but  later  he  held  that  they  were  cell  inclusions  of  non- 


458 


TR  YPA  NO  SO  MI DM 


parasitic  origin.  In  view,  however,  of  the  work  of  E.  H.  Ross 
and  McDonagh  on  the  organism  of  syphilis,  it  is  possible  that  they 
are  in  reality  a  stage  in  the  development  of  T.  pertenue. 

Comparison  with  T.  pallidum. — From  the  above  description  it 
is  evident  that  the  frambcesia  organism  is  morphologically  very 
similar  to  that  of  syphilis.  Blanchard,  Martin,  Prowazek,  and 
others  seem  to  have  been  able  to  make  out  some  slight  morphological 
differences  between  the  two.  Martin  states  that  the  frambcesia 
Treponema  is  even  more  slender  and  more  difficult  to  stain  than  the 
T.  pallidum  of  Schaudinn.  On  the  other  hand,  some  authorities 
consider  it  to  be  thicker.  Rivas  states  that  it  has  closer  coils. 
Prowazek,  Levaditi,  and  Nattan-Larrier  state  that  T.  pertenue  shows 
less  regularly  shaped  coils,  and  one  extremity  terminates  in  a  loop 
much  more  frequently  than  in  T.  pallidum.  Moreover,  according 
to  LevadUi  and  Nattan-Larrier,  in  fresh  preparations  T.  pertenue 


Fig.  i  40.- -Treponema  per- 
tenue Castellani. 


Fig.   141. — Basophile  Cell,  with  Chro 
matin  Dots,  in  a  Case  of  Frambcesia. 


displays  whip-like  lateral  movements  rather  than  translator}^ 
ones.  Russell  and  Archibald  consider  that  T.  pertenue  is  slightly 
thicker  than  T.  pallidum  ;  the  distance  from  crest  to  crest  of  the 
waves  and  the  dip  from  the  crest  to  the  hollow  is  greater;  the 
parasite  has  greater  tendency  to  curl  up  into  a  loop  at  one  end. 
Ranken  states  that  the  parasite  does  not  show  any  corkscrew-like 
motion,  nor  any  progressive  motion.  We  believe  that  the  differentia- 
tion of  the  two  organisms,  and  in  general  of  spirochetes  and  Trypano- 
somata,  is  to  be  based  more  on  the  results  of  the  biological  tests 
than  on  slight  morphological  differences.  The  animal  tests  clearly 
show  that  T.  pertenue  and  T.  pallidum  are  two  different  species, 
inasmuch  as  monkeys  immunized  with  T.  pertenue  do  not  become 
immune  for  T.  pallidum. 

Incidence  of  the  T.  pertenue  in  Frambcvsia  Lesions. — The  presence 
of  the  Treponema  is  constant  in  the  primary  lesion  and  in  the  un- 
broken papules  of  the  general  eruption.     It  may  be  found  in  the 


TREPONEMA   PERTENUE  459 

spleen,  lymphatic  glands,  and  bone-marrow.  In  the  blood  it  has 
not  yet  been  demonstrated  microscopically,  though  there  is  no 
doubt  that  the  blood  of  the  general  circulation  is  infectious,  inas- 
much as  monkeys  inoculated  with  it  develop  typical  yaws  lesions, 
in  which  the  Treponema  is  abundantly  present.  The  Treponema  is 
absent  in  the  cerebro-spinal  fluid,  and  generally  in  the  tertiary 
lesions. 

Bacteriological  Flora  found  in  Open  Sores  of  Frambcesia. — While 
T.  pertenue  is  the  only  germ  found  in  the  non-ulcerated  lesions,  the 
ulcerated  lesions  of  framboesia  are  soon  invaded  by  all  kinds  of 
germs.  Apart  from  innumerable  bacteria,  various  kinds  of  spiro- 
chetes are  present.  One  form  is  rather  thick,  and  takes  up  the 
staiu  easily.  It  is  morphologically  similar  to  the  Spiroschaudinnia 
refringens  of  Schaudinn.  Another  form  is  thin,  delicate,  with  coils 
varying  in  size  and  number,  and  with  blunt  extremities — S.  obtusa 
Castellani.  A  third  form  is  likewise  thin  and  delicate,  but  tapers  at 
both  ends — 5.  acuminata  Castellani;  T.  pertenue  is  also  present  in 
many  cases. 

Inoculation  Experiments  of  Framboesia  in  Man.- — -Paulet,  in  1848, 
inoculated  fourteen  negroes  with  the  secretion  taken  from  fram- 
boetic  granulomata.  All  of  them  developed  framboesia,  the  inocu- 
lation period  varying  from  twelve  to  twenty  days,  when  at  the  seat 
of  inoculation  in  ten  cases  the  first  nodule  appeared,  soon  followed 
by  a  typical  general  eruption.  In  two  cases  apparently  the  erup- 
tion did  not  start  from  the  seat  of  inoculation. 

Charlouis,  in  1881,  inoculated  thirty- two  Chinese  prisoners,  who 
had  never  suffered  from  the  disease,  with  crusts  and  scrapings  from 
a  case  of  yaws.  The  disease  developed  in  twenty-eight  of  them, 
beginning  invariably  at  the  seat  of  inoculation.  Moreover,  he 
inoculated  a  native  suffering  from  typical  yaws  with  syphilis.  The 
inoculation  was  quite  successful,  a  primary  syphilitic  sore  develop- 
ing, followed  by  all  the  usual  types  of  secondary  eruption.  That 
yaws  patients  are  not  immune  against  syphilis  is  proved  also  by 
Powell  and  Nicolas  and  others,  who  have  described  several  cases  of 
syphilis  supervening  on  yaws.  Syphilitic  patients  may  contract 
framboesia  naturally  and  experimentally. 

Inoculation  Experiments  in  Monkeys. — Neisser,  ProWazek,  Hal- 
berstadter  in  Java,  and  shortly  afterwards  Castellani  in  Ceylon,  have 
shown  that  monkeys  are  susceptible  to  framboesia.  According  to 
their  experiments,  the  inoculation  period  varies  from  a  minimum 
of  sixteen  days  to  a  maximum  of  ninety-two.  The  appearance  of 
the  lesions  developing  at  the  seat  of  inoculation  is  practically  the 
same  in  all  cases— viz.,  an  infiltrated  spot  slowly  increasing  in  size, 
and  soon  becoming  moist,  the  secretion  drying  into  a  thick  crust. 
Removal  of  the  crust  exposes  a  raw,  granulating,  red  surface. 

In  the  monkeys  of  a  low  class  (genus  Macacus,  genus  Semnopi- 
thecus)  tlie  eruption  is,  as  a  rule,  localized  to  the  seat  of  inoculation. 
The  infection,  however,  is  general,  as  is  proved  by  the  presence  of 
T.  pertenue  in  the  spleen  and  lymphatic  glands  besides  the  local 


460  TRYPANOSOMIDM 

lesions.  Halberstadter  has  obtained  a  general  eruption  in  ourang- 
outangs.  According  to  Castellani's  experiments,  splenic  blood,  ob- 
tained by  puncturing  the  spleen  of  a  patient  affected  with  fram- 
bcesia,  can  reproduce  the  disease  in  monke}^.  The  inoculation  of 
the  blood  of  the  general  circulation  also  may  occasionally  produce 
the  disease.  The  inoculation  of  cerebro-spinal  fluid  into  normal 
monkeys  has  always  proved  negative. 

Neisser,  Halberstadter,  J.  Prowazek  in  Java,  and  later  Castellani 
in  Ceylon,  have  proved  that  monkeys  successfully  inoculated  with 
frambcesia  do  not  thereby  become  immune  to  syphilis,  and,  viu 
versa,  monkeys  successfully  inoculated  with  syphilis  do  not  thereby 
become  immune  to  frambcesia.  According  to  Levaditi,  monkeys 
immunized  for  frambcesia  do  not  acquire  any  immunity  for  syphilis, 


Fig.  i  42.  —Monkey  inoculated  with 
Frambcesia. 

but  monkeys  immunized  for  syphilis  may  acquire  a  partial  immunity 
for  framboesia.  According  to  Ashburn  and  Craig,  monkeys  of  the 
species  Cynomolgus  philippinensis  are  susceptible  to  frambcesia,  but 
not  to  syphilis. 

The  following  facts  are  in  favour  of  the  T.  pertenue  being  the 
specific  cause  of  frambcesia:- — ■ 

1.  In  the  non-ulcerated  papules,  in  the  spleen,  in  the  lymphatic 
glands  of  frambcesia  patients,  as  well  as  in  inoculated  monkeys,  the 
T.  pertenue  is  the  only  organism  present.  No  other  germ  can  be 
demonstrated,  either  microscopically  or  by  cultural  methods. 

2.  The  extract  of  frambcesia  material  containing  the  T .  pertenue— 
but,  so  far  as  our  present  methods  of  investigation  permit  us  to  say, 
no  other  germs— is  effective  when  inoculated  into  monkeys. 

3.  The  extract  of  frambcesia  material  from  which  the  T.  pertenue 


TREPONEMA   MUCOSUM  461 

has  been  removed  by  nitration  becomes  inert,  and  monkeys  inocu- 
lated with  it  do  not  contract  the  disease. 

Inoculation  Experiments  in  Rabbits. — Nichols  has  inoculated 
rabbits  successfully,  and  finds  that  the  incubation  period  is  shorter 
than  that  for  T.  pallidum  in  the  same  animal.  He  finds  that  4-5 
milligrammes  of  salvarsan  per  kilogramme  of  the  animal's  weight 
injected  intravenously  will  effect  a  cure,  which  is  less  than  for 
T.  pallidum.  Complement  fixation  is  positive  by  the  fourteenth 
day,  but  after  administration  of  salvarsan  it  becomes  negative. 
He  has  not  been  able  to  produce  immunity,  and  he  finds  that  if 
reinoculation  is  unsuccessful  it  is  because  the  animal  is  still  infected; 
whereas,  if  it  is  cured,  reinoculation  can  be  successfully  performed. 
It  is  possible  to  demonstrate  the  difference  between  syphilis  and 
frambcesia  by  the  reinoculation  of  rabbits  after  treatment  by  sal- 
varsan. Castelli  has  inoculated  rabbits  intravenously,  and  states 
that  the  general  clinical  symptoms,  papules,  etc.,  are  so  different 
from  those  obtained  after  a  similar  injection  of  T.  pallidum  that 
this  method  may  be  of  use  for  differentiating  them. 

Cultivation.— T.  pertenue  has  Ken  successfully  cultivated  by 
Noguchi,  as  described  for  Spiroschaudinnia  (p.  441). 

Pathogenicity. — It  is  the  cause  of  frambcesia  tropica  (vide  Chap- 
ter LXI.,  p.  1535). 

Treponema  mucosum  Noguchi,  1912. 

This  Treponema  Was  isolated  from  the  pus  of  a  case  of  pyorrhoea 
by  Noguchi.  It  closely  resembles  T.  pallidum  and  T.  micro  dentium, 
but  differs  in  certain  biological  properties.  It  can  be  cultivated  in 
citrate  dilutior  of  ascitic  agar.  Cultures  have  a  strong  foetid  odour, 
and  mucin  is  produced  in  the  medium,  but  this  property  is  lost  by 
repeated  subcultures.  It  is  a  strict  anaerobe.  Inoculated  into 
monkeys  or  rabbits  it  causes  transitory  local  inflammation. 

Treponema  calligyrum  Noguchi,  1913. 

Found  by  Noguchi  in  condylomata — cultivated  by  the  same  observer.  It 
shows  deep,  regular  curves,  not  so  closely  set  as  in  T.  pallidum.  It  is  also 
thicker. 

Other  species  are:  T.  microdentium,  T.  refringens,  T.  terminii  Leidy,  1881,  in 
Calotermes  militaris  ;  T.  minei  Prowazek,  19 10 ;  T.  vivax  Dobell,  191 1 ,  in  Oscitta- 
torice;  T .  stytopygce  Dobell,  1911,  in  Sty topyga  orientalis ;  T.  parvum .Dobell,  191 1  ; 
T.  minutum  Dobell,  191 1;  T.  dentium  Koch,  1877;  T.  triccale  Cohn,  1872; 
T.  intermedium  Dobell,  191 1,  in  the  human  mouth. 

A  rather  doubtful  Treponema  has  been  described  by  Dobell  in  the  intestine 
of  Bufo  vulgaris  L. 

T.  urethrale  Castellani,  191 5,  found  in  the  mucopurulent  discharge  from 
the  urethra.  It  is  very  delicate  and  has  numerous  spirals  all  equal.  Length, 
6-12  microns.     The  patient  had  no  sign  of  gonorrhoea  or  syphilis. 


462  TRYPANOSOMIDM 

REFERENCES. 

The  most  valuable  publications  for  references  with  regard  to  this  chapter  are 
Archiv  fiir  Protistenkunde,  Annals  of  Tropical  Medicine  and  Parasitology,  and 
the  Journal  of  Parasitology. 

Herpetomonidae. 

Mackinnon  (1909-10).     Several  papers  in  Parasitology. 

Fatton,  W.  S.  (1907-12).  Numerous  papers  in  the  British  Medical  Journal 
(1907),  Archiv  fur  Protistenkunde  (1908-12),  Lancet  (1909).  Parasito- 
logy (1909-12). 

Porter,  A.  (1 909-1  >).     Numerous  papers  in  Parasitology. 

Leishmania. 

A  most  complete  account  of  the  recent  literature  on  this  subject  is  con- 
tained in  the  Kala-Azar  Bulletin,  now  the  Tropical  Diseases  Bulletin,  and  in 
Laveran  (191 7)  Leishmanioses,  Paris. 

Archibald,  R.  G.  (May,  191 3).  An  Interesting  Case  of  Kala-Azar,  Journal 
of  the  Royal  Army  Medical  Corps.  (November,  19 14).  A  Preliminary 
Report  on  some  Further  Investigation  of  Kala-Azar  in  the  Sudan 
Journal  of  the  Royal  Army  Medical  Corps. 

Trypanosomidae. 

The  most  important  literature  will  be  found  in:— Laveran  and  Mcsnil 
Trypanosomes  et  Trypanosomiases,  Paris  (English  Translation,  with  numerous 
additions,  by  Nabarro) ;  Reports  of  the  Sleeping  Sickness  Commission  of  the 
Roval  Society  I.,  II.,  III.,  IV.  (1903);  V.,  VI.  (1905);  VII.  (1906);  VIII.  (1907); 
IX'  (1908);  X.  (1910);  XI.  (1911);  XII.  (1912);  XIII.,  XIV.  (1913);  XV. 
(1914);  XVI.  (1915);  Memorias  de  Instituto  Oswaldo  Cruz  (1909-1919). 
Sleeping  Sickness  Bulletin  (1909-1912),  Tropical  Diseases  Bulletin  (1912-1919). 

Castellani  (1903-1904).  Royal  Society  Reports,  Journal  of  Tropical  Medicine, 

Centr.  fiir  Bakt. 
Chalmers  and  O'Farrell  (1914).     Journal  of  Tropical  Medicine. 
Chalmers  (1918).     Journal  of  Tropical  Medicine  (Classification). 

Spirochaetacea — General. 

Fantham  (1908).     Quarterly  Journal  of  Microscopical  Science,  January. 

Keysselitz,  G.  (1907).     Arch.  f.  Protisten.,  Bd.  x.,  Heft  1,  p.  127. 

Leishman  (1908).     Journal  of  the  Royal  Army  Medical  Corps,  vol.  x.,  April. 

Lowenthal  (1905).     Biolog.  Centralb.,  Bd.  i. 

Minchin  (1915).     Annales  Institut  Pasteur,  November. 

Now  and  Knapp  (1906).     Journal  of  Infectious  Diseases,  vol.  iii.,  No.  3. 

Prowazek  (1906-07).     Arb.  a.  d.  Kaiserl.  Gesundheits.,  Bd.  xxiii.  and  xxvi.. 

Heft  1. 
Schaudinn  (1904).     Arb.  a.  d.  Kaiserl.  Gesundheits.,  Bd.  xx. 
Schaudinn  (1907).     Arb.  a.  d.  Kaiserl.  Gesund.,  Bd.  xxvi.,  Heft  1. 
Schaudinn  (October  19,  1905).     Deutsche  Med.  Wochensch. 
Siebert  (1908).     Archiv  fiir  Protistenk.,  Bd.  ii.,  p.  362. 

Spiroschaudinnia  recurrentls. 

Manteufel  (1907).     Arb.  a.  d.  Kaiserl.  Gesundh.,  Bd.  xxvii.,  Heft  2,  326. 

Obermeyer  (1873).     Centralb.  f.  die  Med.  Wiss. 

Schellach  (1909).     Arbeiten  aus  dem  Kais.  Gesundheitsamte. 

Spiroschaudinnia  duttoni. 

Breinl  (1907).     Annals  of  Tropical  Medicine  and  Parasitology,  No.  3. 
Breinl  and  Kinghorn  (1906).     Memoir  XXI.     Liverpool  School  of  Tropical 
Medicine. 


REFERENCES  463 

Dutton  and  Todd.     Memoir  XVII.     Liverpool  School  of  Tropical  Medicine. 
Dutton  and  Todd  (1907).     Journal  of  Tropical  Medicine. 
Levaditi  and  Manonelian  (1907).     Annals  de  lTnstitut  Pasteur,  xxi 
Ross  and  Milne  (1904).     British  Medical  Journal,  vol.  ii.,  p.  1453. 

Spiroschaudinnia  carteri. 

Carter  (1882).     Spirillum  Fever.     London. 

Mackie  (1907).     Lancet,  ii.,  September  21  and  December  14. 

Spiroschaudinnia  bronchialis. 

Castellani  (1906).     Lancet,  May  19,  1906. 

m  wi  (1909).     British  Medical  Journal;  (1917)  Presse  Medicale ;  (1917) 

Journal  of  Tropical  Medicine,  September  15. 
Chalmers  and  O'Farrell     (1913).     Journal    of    Tropical    Medicine    and 

Hygiene,  November  1. 
I   in  1  ham  (1915).     Journal  of  Tropical  Medicine  and  Parasitology,  xix.  391. 
Macfie  (1915).     Ibid.,  xviii.  63. 
VlOLLE  (1918).     Bull.  Path.  Exot.  and  Lancet. 
Violle  (1918).      Bronchite  sanglante  (Spirochetose  broncho-pulmonaire  de 

Castellani).     Presse  Medicale,  No.  39. 

Spiroschaudinnia  in  Yellow  Fever. 
Noguchi  (1919).     Journal  American  Medical  Association,  January  18. 

Spiroschaudinnia  icterohaemorrhagiae. 

Inada,  Ido,  Hoki,  Kaneko,  Ito  (1916).    Journal  of  Experimental  Medicine, 

xxxiii.  p.  377. 
Martin  and  Pettit  (1917).     Comptes  Rendus  Soc.  Biol. 
Stokes  and  Ryt.e  (1916).     Journal  Royal  Army  Medical  Corps. 

Treponema  pallidum. 

Krzysztalowicz  and  Siedlecki  (1906).     Bull.  Inst.  Past.,  vol.  iv.,  p.  204 
(Abstract.) 

1  m  (1910-191S).     Several  important  papers  in  the  Journal  of  Experi- 
mental Medicine. 

Schaudinn  and  Hoffmann  (1905-06).     Deutsch.  Med.  Wochens.     Selected 
Essay  New  Sydenham  Society. 

Schereschewsky  (1909).     Deutsche  Medizinische  Wochenschrift,  p.  1260. 

Treponema  pertenue. 
Ashburn  and  Craig  (1907).     Philippine  Journal  of  Science,  vol.  ii.,  p.  441. 
Castellani  (June,  1905).    Journal  Ceylon  Branch  British  Medical  Association. 
Castellani  (November,  1905).     British  Medical  Journal. 
Castellani  (1905-1914).     Journal  Tropical  Medicine.     Several  papers. 
Castellani  (1906).     Deutsche  Med.  Woch.,  xxxii.  132-134. 
Castellani  (1907)/    Trans.  Dermatological  Congress. 
Castelli  (1912).     Zeitschrift  fur  Chemotherapie. 
IIaitm  ann  (191 1).      Deutsche  Medizinische  Wochenschrift. 

an  (1906).     British  Medical  Journal,  ii.  995. 
Nichols    (1910-1916).      Several   important   publications   in   the    Journal   of 

Experimental  Medicine,  etc. 
Noguchi  (1911-1912).     Journal  of  Experimental  Medicine. 
Ranken  (1912).     British  Medical  Journal. 
\\  1  i.lman  (1905).     Journal  of  Tropical  Medicine. 


CHAPTER  XX 
DIPLOZOA  AND  OCTOMITID^E 

Preliminary — Diplozoa — Octornitida^ — Octomitus — Giardia — References, 

PRELIMINARY. 

We  now  return  to  the  classification  of  the  Protomonadina  given 
on  p.  332,  where  the  order  is  divided  into  two  suborders..  Monozoa 
and  Diplozoa.  The  Monozoa  we  have  just  considered,  and  in  the 
present  chapter  the  Diplozoa  are  described. 

SUBORDER  2.  DIPLOZOA  Hartmann  and  Chagas,  1911. 
Definition. — Protomonadina  with  more  or  less  tendency  to  bilateral 
symmetry  in  undividing  forms,  as  shown  by  the  arrangement  of  the 
flagella,  by  the  duplication  of  the  axostyle,  with  sometimes  the 
nucleus  and  more  rarely  of  the  cytostome.  An  undulating  mem- 
brane is  absent. 

^Classification. — This  suborder  may  be  divided  into  two  families, 
of  which  one  is  of  importance  in  tropical  medicine. 

A.  Cytostome  single  or  absant;   flagella  eight  in  number-- 

Family  1,  Octomitidce  Minchin,  1912. 

B.  Cytostome  double;  flagella  variable  in  number — -Family  2, 

DistomatidcB  Senn,  1900. 

Only  the  first  of  these  families  concerns  us. 

FAMILY  1.  OCTOMITIDCE  Minchin,  1912. 

Definition.— Diplozoa  with  eight  flagella  and  with  or  without  a 
cytostome. 

Type  Genus. — Octomitus  Prowazek,  1904. 

Classification. — The  family  is  divisible  into  several  genera  as 
follows : — ■ 

A.  Anteriorly  three  pairs  and  posteriorly  on<>  pair  of  flagella; 

nucleus  single,  bilaterally  lobed    or  doubled;    sucker 
absent. 
I.  Parasitic— Octomitus. 
II.  Free  living — Hexamita. 

B.  Antero-laterally  one  pair,  mesially  two  pairs,  and  posteriorly 

one  pair  of  flagella ;  nucleus  usually  double ;  sucker  present 
— Giardia. 

Octomitus  and  Giardia  concern  us;  Hexamita  does  not. 

464 


OCTOMITUS  HOMINIS 


46; 


Genus  i.  Octomitus  Prowazek,  1904. 

Definition.  -Octomitidse,  parasitic  with  anteriorly  three  pairs 
and  posteriorly  one  pair  of  flagella;  nucleus  single,  bilaterally  lobed 
or  doubled;  sucker  absent. 

Type  Species.— 0.  intestinalis  Prowazek,  1904,  found  in  rats. 

Classification. — The  known  species  of  Octomitus  may  be  recog- 
nized as  follows: — ■ 

A.  Nucleus  situate  close  to  the  anterior  end: — 

I.  Nucleus  often  bilobed — Dnjardini. 
II.  Nucleus  double: — 

{a)  Measurements  8-12  x  5-7  microns — Intestinalis. 
(b)  Measurements  4-6  x  2  microns — Muris. 

B.  Nucleus  not  situate  close  to  the  anterior  end: — ■ 

Nucleus  single  and  rounded;  size  6x3  microns — Hominis. 


Fig.   143. — Octomitus  hominis   CHAL- 
MERS     AND      PEKKOLA,      I916. 

(X  2,000.) 


Fig.  144. — Octomitus  hominis  Chal- 
mers and  Pekkola,  191 6. 
(X  2,000.) 


Octomitus  hominis  Chalmers  and  Pekkola,  1916. 

Definition.— Octomitus  with  single  rounded  nucleus,  not  situate 
close  to  anterior  end. 

Morphology. — Small  fusiform  or  pear-shaped  flagellates,  in  size 
5-6-6-0  x  2-8-3-0  microns. 

When  examined  in  the  stained  condition  it  showed  a  circular 
clearly  defined  nucleus  (Figs.  143  and  144),  measuring  about 
1-4  microns  in  transverse  diameter,  and  lying  near  the  junction  of 
the  anterior  third  with  the  posterior  two-thirds  of  the  body.  This 
nucleus  is  bounded  by  a  well-marked  membrane,  which  limits  the 
homogeneous  dark  staining  contents,  in  which  there  is  often  a 
centrally  or  excentrically  placed  karyosome. 

3° 


job  DIPLOZOA  AND  OCTOMITIDM 

In  front  of  the  nucleus  and  closely  approximated  to  the  anterior 
end  of  the  body  is  a  well-defined  blepharoplast,  which,  though 
typically  single,  may  have  a  secondary  smaller  blepharoplast 
associated  with  it.     No  sign  of  a  rhizoplast  could  be  seen. 

From  this  blepharoplast  there  arise  six  anteriorly  directed  flagella, 
though  occasionally  one  accidentally  appears  as  though  directed 
backwards.  When  there  are  two  blepharoplasts,  then  three  flagella 
arise  from  each. 

These  flagella  vary  considerably  in  length,  being  generally  much 
longer  than  the  body,  but  it  is  exceedingly  difficult  to  be  certain 
where  they  end,  and  in  the  specimens  drawn  only  such  portions  as 
could  be  clearly  seen  are  portrayed,  though  in  other  specimens  the 
length  was  clearly  much  greater,  in  some  instances  quite  three 
times  the  length  of  the  parasite. 

Directed  backwards,  and  also  arising  from  the  blepharoplast  or 
LFpharoplasts,  there  are  two  chromatic  lines,  which,  diverging  and 
running  on  either  side  of  the  nucleus,  may  or  may  not  converge, 
but  in  either  case  end  near  the  posterior  margir.  of  the  body  in  very 
minute  chromatic  particles,  which  are  generally  very  difficult  to 
see.  From  each  of  these  chromatic  particles  there  arises  a  posteriorly 
directed  flagellum. 

The  chromatic  rods  are  obviously  axostyles,  and  the  little  particles 
in  which  they  end  may  be  termed  axoplasts. 

It  is  not  often  that  the  axostyles  are  seen  together,  as  the  parasite 
usually  lies  so  that  only  one  is  visible,  while  the  other  is  almost 
invisible;  but  at  times  they  are  seen  as  described  above,  or  at  other 
times  when  the  parasite  has  shrunk  into  a  rounded  mass  they  may 
be  observed  crossing  one  another. 

No  cytostome  has  been  observed,  while  the  periplast  is  thin  and 
without  markings. 

The  cytoplasm  is  vacuolated  with  food  vacuoles. 

Life-History.— Nothing  is  known  of  the  life-history. 

Pathogenicity.— Belie\  ed  to  cause  diarrhoea. 

Genus  Giardia  Kiinstler,  1882. 

Synonyms. — Lamblia  R.  Blanchard,  1888;  Dimorphus  Grassi, 
1879,  nee  Haller,  187S;  Megastoma  Grassi,  1881,  nee  de  Blainville. 

Definition. — Octomitidae  with  one  antero-mesial  pair,  two  pairs 
of  mesial  and  one  pair  of  posterior  flagella ;  nucleus  usually  double ; 
sucker  present. 

Type  Species. — Giardia  intestinalis  (Lambl,  1859). 

Giardia  intestinalis  (Lambl,  1859). 

Synonyms. — Lamblia  intestinalis  Lambl,  1859;  Cercomonas  intes- 
tinalis Lambl,  1S54;  Hexamitus duodenalis Davaine,  1875;  Dimorphns 
muris  Grassi,  1879;  Megastoma  entericnm  Grassi,  1881;  Megastoma 
intestinale  Blanchard,   1886;  Lamblia  intestinalis  Blanchard,  18S8. 

This  parasite  lives  in  the  intestine  of  different  species  of  the 


GIARDIA  INTESTINALIS 


46? 


genera  Mus  and  Epimys  {M.  nut  satins,  E.  ratlus,  E.  norvegictts, 
M.  silvestris) ;  also  in  species  of  Arvicola  (A .  arvensis  and  A .  amphi- 
bius);  also  in  the  rabbit,  the  cat,  the  dog,  the  sheep,  and  man. 

It  was  first  observed  by  Lambl  in  the  mucous  intestinal  evacuations 
of  children  in  Russia ;  then  by  Grassi  in  Italy,  who  made  a  complete 
study  of  the  parasite;  by  Moritz  in  Germany;  by  Jaksch  in  Austria; 
by  Kruse  in  Egypt;  and  we  have  observed  it  several  times  in  Ceylon; 
While  it  has  been  carefully  studied  by  Werner  in  1901,  and  more 
especially  by  Wenyon  in  1907  and  1916,  and  his  account  is  classical. 
It  is  common  in  the  Anglo-Egyptian  Sudan. 

It  occurs  in  the  small  bowel  of  man,  and  it  and  its  cysts  can  be 
found  in  the  faeces.  Infection  is  brought  about  by  swallowing  the 
encysted  forms.  This  has  been  proved  experimentally  by  Grassi, 
and  as  it  occurs  in  mice,  it  is  quite,  easy  to  see  how  infection  of 
foodstuffs  is  possible. 

G.  intestinalis  is  an  actively  motile  organism 
about  12  to  21  [X  in  length,  and  about  5  to  12  /u 
in  breadth .  It  is  pear-shaped,  being  surrounded 
by  a  thin  periplast  (ectoplasm),  which  keeps 
its  form.  The  under  surface  (when  attached) 
is  excavated  with  a  well-defined  border,  which 
is  interrupted  at  the  site  of  the  cytostome. 
This  hollow  is  probably  a  kind  of  peristome, 
and  is  useful  in  fixing  the  parasite  to  the 
intestinal  epithelium.  ■...,.,■■      .: 

There  are  two  oval  nuclei,  with  definite 
nuclear  membranes  and  with  large  irregular 
karyosomes  in  their  centres.  There  is  no 
connection  between  these  nuclei,  but  between 
them  lie  two  darkly  staining  rods  with  ex- 
panded ends,  and  which  posteriorly  are  con- 
tinuous with  the  prolongations  of  the  posterior 
flagella  into  the  body.  From  the  thickened 
posterior  ends  of  the  two  rods  spring  the  mesial  pair  of  flagella, 
while  at  their  anterior  ends  is  a  small  granule,  from  which  arises 
the  anterior  pair  of  flagella,  which,  running  forwards  and  inwards, 
cross  one  another  and  pass  across  the  peristome,  or  sucking  disc 
or  sucker,  to  its  raised  margin,  around  which  they  run,  forming  a 
kind  of  membrane,  till  nearly  at  the  level  of  the  nucleus  they 
become  free  on  each  side. 

From  the  same  anterior  pair  of  granules  there  arise  the  second 
and  finer  pair  of  mesial  flagella,  running  down  on  the  mesial  aspect 
of  the  nuclei,  behind  which  they  turn  outwards  along  the  margin  of 
the  sucker  and  finally  become  free. 

Sometimes  there  is  a  row  of  granules  extending  from  the  anterior 
granules  to  the  nucleus  on  the  same  side. 

Behind  the  two  nuclei  there  is  a  triangular  area,  which  forms  a 
groove  running  towards  the  tail.  Dorsal  to  this  groove  lie  two  darkly 
staining  masses. 


Fig.    145.  —  Giardia 
intestinalis  (Lambl, 
1859). 
(After  Wenyon.) 


468  DIPLOZOA  AND  OCTOMITIDJE 

In  addition  in  the  living  animal  retractile  granules  can  be  seen 
lying  in  the  anterior  part  of  the  animal  on  each  side  of  the  mesial 
line.  From  each  of  these  granules  a  fine  line  runs  posteriorly,  and 
all  these  lines  converging,  as  it  were,  into  the  handle  of  a  fan,  end 
in  the  tail,  with  the  movements  of  which  they  may  be  concerned. 

Life-History. — Reproduction  may  take  place  by  binary  fission. 
The  process  is  very  complicated,  the  whole  system  of  sucking  disc 
and  flagella  being  reproduced  dorsally,  and  then  the  flagellate  splits 
longitudinally,  the  fissure  passing  from  before  backwards  between 
the  sucking  discs. 

Kofoid  and  Christiansen  have  described  multiple  fission  in  the 
lamblia  of  mice,  but  this  has  not  been  seen  in  those  in  man. 

Encystment  begins  by  a  thin  wall  being  excreted,  inside  which  the 
flagellate  can  be  seen  moving.  Later  the  cyst  becomes  ovoid  and 
the  wall  tougher,  and  the  contained  lamblia  may  or  may  not  have 
undergone  division.     Conjugation  is  not  known  to  occur. 

The  cysts  are  oval  and  measure  13-14x6-7  microns;  the  Wall  is 
smooth  and  transparent.  Later  the  nuclei  divide,  giving  rise  to 
four  nuclei  in  all,  which  are  crowded  together. 

Method  of  Infection. — The  cysts  escape  in  faecal  matter  and  are 
taken  into  house-flies,  Musca  and  Fannia,  etc.,  and  passing  into  the 
intestine,  eventually  escape  in  the  flies'  droppings,  and  so  can 
infect  human  food. 

Pathogenicity. — It  is  usually  believed  to  be  the  cause  of  the 
diarrhcea  with  which  it  is  associated. 


REFERENCES. 

Oetomitus  hominis. 
Chalmers  and  Pekkola  (191 7).     Journal  of  Tropical  Medicine  and  Hygiene. 
June  15,  142-146.     London. 

Giardiaintestinalis. 

Castellani  (1906).     Ceylon  Medical  Reports. 

Wenyon  (1907) .     Festband  zum  25  jahringen  Professoren  Jubilaum  des  Herrn. 

Geheimen  Hofrat  Prof.  Dr.  Richard  Hertweg.     Jena. 
Wenyon  and  O'Connor  (191 7).     Human  Intestinal  Protozoa  in  the  Near 

East.     London. 


CHAPTER  XXI 
TELOSPORIDIA 

Telosporidia — -Gregarinida — Coccidiidea — Haemosporidia — Haemogregarinidae 
Toxoplasmic^  —  Piroplasmidae  —  Plasmodidse —  Haemoproteidae  — . 
References. 

PHYLUM  III.  TELOSPORIDIA  Schaudinn,  1900. 

Synonym. — Eimerioinea  Poche,  1913. 

Definition. — Parasitic  ftlasmodromata  without  motile  organs,  in 
which  the  reproductive  phase  of  the  life-cycle,  which  produces  spores, 
is  distinct  from  and  follows  after  the  trophic  phase. 

Remarks. — All  the  Telosporidia  are  parasitic,  and  usually  begin 
their  life-cycle  as  small  amceboid  bodies,  with  a  single  nucleus,  called 
trophozoites,  which  absorb  nutriment  and  grow,  and  when  fully 
developed  show  a  cuticle,  an  ectoplasm,  and  an  endoplasm.  The 
endoplasm  is  granular,  and  contains  a  vesicular  nucleus  with  chro- 
matin karyosomes.  The  nucleus  of  the  fully-grown  trophozoite 
now  begins  to  divide,  and  the  parasite  is  known  as  a  schizont, 
which  reproduces  by  spore-formation.  These  spores,  called  mero- 
zoites,  complete  the  cycle  of  asexual  reproduction  called  schizogony. 
At  some  stage  in  the  life-history  of  the  parasite,  generally  when 
conditions  of  life  are  not  favourable,  some  merozoites  are  produced, 
which,  instead  of  developing  into  trophozoites,  become  sexual 
garnet ocytes,  male  and  female.  These  forms,  which  are  often  resis- 
tant, are  the  means  of  transmitting  the  given  species  from  one  host 
to  another.  They  produce  gametes,  which  conjugate  and  form 
bodies  called  sporoblasts,  and,  lastly,  spores  called  sporozoites. 

Classification. — The  Telosporidia  are  divided  into  three  orders: 
Gregarinida,  Coccidiidea,  and  Haemosporidia,  while  the  two  latter 
are  often  put  together  into  the  Coccidiomorpha. 

These  may  be  recognized  as  follows : — 

A.  Only  young  trophozoites  intracellular — Gregarinida. 

B.  Full  trophozoite  stage  intracellular — Coccidiomorpha. 

'■  I.  With  resistant  spores  in  the  sporocysts — Coccidiidea. 
■   II.  Without  resistant  spores  in  sporocysts — ■Hcemosporidia. 

ORDER  I.  GREGARINIDA  Lankester,  1866. 

^Synonyms.  —Gregarinidea  Lankester,  1885;  Grcgarince  Haeckel,  1866. 

Definition. — Telosporidia,  in  which  only  the  young  trophozoites  are  intra- 
cellular, the  fully-grown  forms  being  extracellular. ' 

469 


470  TELOSPORIDIA 

Reproduction  by  Schizogony  or  Sporogony. — The  gregarines  are  essentially 
parasites  of  the  invertebrata,  not  being  found  in  true  vertebrates,  though 
known  in  Amphioxus  and  Ascidians.  They  are  generally  found  in  the  Arthro- 
poda  and  worms,  and  appear  to  be  non-pathogenic. 

Their  life-history  may  be  briefly  described  as  follows: — -The  young  tropho- 
zoite enters  a  cell,  generally  of  the  alimentary  canal,  in  which  it  grows,  appar- 
ently causing  considerable  damage,  for  the  cell  first  swells  and  afterwards 
degenerates. 

In  the  meanwhile  the  parasite  has  found  its  way  either  wholly  or  partially 
out  of  the  cell,  to  the  remains  of  which,  however,  it  is  attached  until  all 
nourishment  is  extracted,  when  it  becomes  ccelozoic — i.e.,  it  leaves  the  remains 
of  the  cell,  and  dwells  either  in  the  alimentary  canal,  the  ccelome,  or  the 
blood  stream.  The  young  parasite  is  unicellular,  having  its  cytoplasm  divided 
into  ectoplasm  and  endoplasm.  The  ectoplasm  is  hyaline,  and  when  fully 
developed  has  three  layers:  (i)  external  epicyte,  (2)  middle  sarcocyte,  (3)  in- 
ternal myocyte. 

The  last-named  contains  contractile  fibrils  called  myonemes.  The  endo- 
plasm is  granular,  and  contains  a  well-developed  vesicular  nucleus.  A  uni- 
cellular gregarine,  such  as  this,  belongs  to  the  suborder  Acephala,  and  is 
illustrated  by  Monocystis  agilis  Stein,  which  is  found  in  the  vesicular  seminales 
of  Lumbricus  terrestris. 

On  the  other  hand,  in  such  a  gregarine  as  Pyxinia  frenzeli  Laveran  and 
Mesnil,  a  part  of  the  sporozoite  grows  out  from  the  cell,  and  into  this  external 
portion  the  nucleus  travels.  The  portion  left  in  the  cell  is  known  as  the 
'  epimerite,'  while  the  external  portion,  growing  considerably,  is  divided  by  a 
septum  into  a '  protomerite  '  near  the  cell,  and  a '  deutomerite  '  away  from  the 
cell. 

The  parasite  in  this  condition  is  called  a  cephalont,  and  belongs  to  the  sub- 
order Cephalina. 

In  due  course  the  trophozoite,  whether  entirely  or  partially  in  the  cell,  is  set 
free,  either  by  bursting  its  way  out,  or  by  a  separation  between  the  epi-  and 
proto-merite.  The  cell  now  degenerates,  and  the  parasite  may  be  called  a 
sporont.  Sporogony  takes  place  by  two  sporonts  or  gametocytes  lying  side 
by  side  becoming  enclosed  in  a  cyst  with  two  walls — an  external  epicyst  and 
internal  endocyst. 

The  karyosomes  of  the  nuclei  of  the  gametocytes  now  break  up  into 
chromidia,  which  collect  to  form  the  generative  nucleus.  This  divides  by 
mitosis  to  form  a  large  number  of  nuclei,  which,  travelling  to  the  surface  and 
surrounding  themselves  with  cytoplasm,  become  detached  as  gametes,  the  rest 
of  the  cell  forming  a  nucleus  de  reliquat  or  residual  mass.  Thus,  inside  the  cyst- 
walls  there  are  gametes  from  two  separate  parasites  and  two  residual  masses. 

Gametes  presumably  from  different  individuals  fuse  and  form  a  true  zygote 
with  a  synkaryon.  Each  zygote  represents  a  sporoblast,  and  each  sporoblast 
becomes  a  single  spore  by  the  secretion  of  a  chitinous  cuticle  and  the  contrac- 
tion of  its  protoplasm  (called  by  Minchin  the'  sporoplasm  ') .  This  sporoplasm 
divides  by  amitosis  into  eight  sporozoites  and  a  residual  mass.  During  this 
process  the  two  residual  masses  of  the  original  cyst  disappear.  The  cyst  now 
contains  only  the  spores  which  used  to  be  called  pseudonavicellae.  These 
spores  are  intended  to  convey  infection  to  a  new  host,  in  the  intestine  of  which 
they  set  free  the  sporozoites,  which  promptly  attack  either  the  cells  of  the 
intestine  or  some  other  organ,  thus  completing  the  cycle  of  sporogony. 

Schizogony. — This  is  uncommon  in  the  gregarines,  being  only  found  in  the 
Schizogregarinidae.  It  is  typically  seen  in  Schizocystis,  in  which  the  tropho- 
zoite grows  into  a  schizont,  whose  nucleus  divides  into  a  large  number  of 
daughter  nuclei,  round  each  of  which  a  portion  of  cytoplasm  gathers,  forming 
a  merozoite.  This,  escaping  from  the  schizont,  infects  another  cell,  thus  com- 
pleting the  cycle  of  schizogony.  Some  of  the  merozoites  may  develop  by 
sporogony. 

Classification, — The  gregarines  are  classified  as  follows: 


COCCIDIIDEA  I7i 

SUBORDER  I.  SCHIZOGREGARINARIA  Doflcin,    1909. 

Synonyms. — Schizogregarina  Minchin,  1903;  Schizocystina  Poche,  1913. 
Reproduction  by  schizogony  and  sporogony. 

Genera. — Schizocystis  Leger,  1900,  in  the  intestine  of  Ceratopogon  ;  Ophryo* 
cystis  Schneider,  1884,  in  the  Malpighian  tubules  of  beetles. 

SUBORDER  II.  EUGREGARINARIA  Doflein,  1901. 
Reproduction  as  usual  by  sporogony.     Schizogony  very  rare,  if  present  at 
all,  and  only  in  the  earliest  cytozoic  stages.     The  Eugregarinida  are  divided 
into  two  tribes. 

Tribe  i.  Acephalina  Delage  Herouard,  1896. 

Synonym. — Monocystidea  Haeckel,  1866.     No  epimerite  and  no  septa. 

Genera  (eighteen  described  by  Minchin). — Monocystis  Stein,  1848,  parasitic 
in  the  vesicuke  seminales  and  body  cavities  of  the  Oligochaetse  and  Gyclopidae; 
Zygocystis  Stein,  1848,  in  Lumbricus  agricola  ;  Zygosoma  Labbe,  1S99;  Laiikes* 
tcria  Mingazzini,  1891,  in  Ascidians. 

Tribe  2.  Cephalina  Delage  Herouard,   1896. 

Synonym. — Polycystidea  Haeckel,  1866.  With  epimerite,  and  with  or  with' 
out  a  septum  in  the  body. 

Subtribe   1 :      Gymnosporea   Leger. — Cyst    with   naked   sporozoites 

(gymnospores) . 
Family  i  :  Aggregation  Labbe,  1S99. 
Genus. — Aggregata  Frenzel,  1885.     Sporozoites  grouped  about  residual 

masses. 
Family  2:  Porosporidn  Labbe,  1899. — Each  sporoblast  giving  rise  to 

numerous  sporozoites  grouped  round  a  residual  mass. 
Genus. — Porospora  Schneider,  1875.     P.  gigantea  in  the  lobster. 
Subtribe  2:  Angiosporea. — Spores  well  developed. 
Family    i:    Gregarinimj    Greene,    1859.-  Trophozoites  with  simple 

epimerites. 

Genera. — ■GregarinaDuiour,  1828.  Epimerite  conical  or  knobbed.  Species 
found  in  cockroaches,  earwigs,  meal-worms,  and  in  the  intestines  of  other 
insects.  Gamocystis  in  the  cockroach;  also  Eirmocystis,  Hyalospora,  Euspora, 
Sphcerocystes,  Cnemidospora,  Stenophora. 

Other  families  are  Didymophyidae,  Dactylophoridae,  Actinocephalidae, 
Acanthosporidae,  Monosporidae,  Stylorhynchidae,  and  Doliocystidae. 

ORDER  II.  COCCIDIIDEA. 

Synonyms. — Coccidiomorpha    Doflein,    1901;    Eimcridea    Po^he, 

I9T3- 

Definition. — -Telosporidia,  parasitic,  as  a  rule,  in  epithelial  cells 
of  vertebrates  and  invertebrates.  Reproduction  always  by  both 
schizogony  and  sporogony. 

Remarks. — -The  Coccidiidea  Were  recognized  as  long  ago  as  1839 
by  Hake,  who  did  not  know  that  they  Were  animals,  that  discovery 
being  made  by  Rcmak  (1845) ;  while  Lieberkiihn  in  1854  showed  that 
they  were  allied  to  Gregarines.  Leuckart  (1876)  gave  them  the 
name  Coccidium,  while  Schaudinn  in  1900  first  described  a  full  and 
complete  life-history  of  Coccidinm  schubergi,  which  will  be  taken  a? 
the  type. 


47^ 


TELOSPORIDIA 


Coceidium  schubergi  Schaudinn,  1900. 

Coccidium  schubergi  begins  its  life-history  in  the  intestinal  cell  of  the  centi- 
pede (Lithobius  forficatus  L.)  by  a  sporozoite  pressing  its  anterior  end  against 
an  intestinal  cell,  and  thus  forcing  a  way  into  its  interior. 

Inside  this  cell  it  becomes  the  young  trophozoite,  an  oval  body  which  grows 
rapidly  at  the  expense  of  the  protoplasm  of  the  cell,  and  in  twenty-four  hours 
attains  its  full  size. 


FlG.   146. — Diagram  of  the  Life-History  of  Coccidium 
schubergi  Schaudinn.     (After  Schaudinn.) 

1,  Sporozoite  entering  an  intestinal  canal;  2-3,  trophozoites;  4-5,  schizonts; 
6-8,  merozoites;  9,  young  gametocyte;  ioa-na,  microgametocyte ;  iob-i\b, 
macrogametocyte;  12a,  microgametes;  126,  maciogamete;  13-16,  oocyst; 
17,  sporocysts;  18,  sporozoites. 


It  is  now  called  a  schizont,  because  its  nucleus  divides  into  a  number  of 
daughter  nuclei,  which  are  formed  into  merozoites  in  the  usual  way.  These 
merozoites,  set  free  by  the  breaking  up  of  the  schizont,  attack  new  intestinal 
cells,  thus  increasing  the  infection  of  the  host. 

This  process  cannot,  of  course,  go  on  for  any  length  of  time,  for  a  limit  to 
the  nutritive  power  of  the  host  is  reached  in  five  days,  when  the  parasite  must 
attempt  to  infect  a  new  host,  and  this  is  done  by  sporogony. 


TETRA  SPOROC  YSTID.  E  .,73 

Some  merozoites  now  become  differentiated  into  micro-  and  macro-ga- 
metocytes.  The  former  consist  of  finely  granular  cytoplasm,  with  little 
reserve  material,  while  the  latter  are  bean-shaped  and  have  much  food- 
material.  The  microgametocyte  forms  the  microgametes  by  its  nucleus 
becoming  irregular,  and  forming  fine  achromatic  paths  through  the  cytoplasm 
to  the  periphery  of  the  parasite,  along  which  chromidia  travel  from  the  nucleus. 

At  first,  scattered  evenly  along  the  periphery,  these  chromidia  gather  into 
patches,  and  finally  fuse  into  masses,  enclosing  in  each  a  vacuole.  The 
masses  of  chromatin  lengthen,  and  by  bending  project  from  the  cytoplasm, 
which  now  forms  two  flagella,  whose  active  movements  set  free  the  micro- 
gamt  I 

In  the  meanwhile  the  macrogametocyte  becomes  a  macrogamete  by  expul- 
sion of  the  karyosome  of  the  nucleus. 

Micro-  and  macro-gametes  now  fuse  and  form  a  zygote  with  a  synkaryon. 
The  oocyst,  as  it  may  be  called,  now  passes  out  of  the  body  of  the  host,  and 
divides  into  four  sporoblasts.  Each  sporoblast  now  develops  two  vacuoles 
and  a  cyst-wall,  the  sporocyst,  so  that  the  sporoblast  is  often  called  the  spore. 
The  nucleus  of  the  spore  divides  into  two,  while  the  two  vacuoles  fuse  and  the 
cytoplasm  divides,  forming  two  sporozoites  which  are  capable  of  infecting  a 
new  host,  being  set  free  by  the  acid  of  the  digestive  juices.  ( 

Sporogony  takes  about  two  to  three  days  for  completion. 

It  may  be  as  well  at  the  present  time,  when  so  much  disputation  is  taking 
place  re  Schaud  inn's  work  on  trypanosomes,  to  mention  that  he  worked  out 
this  life-history,  which  has  never  been  refuted,  though  the  parasite  was  found 
in  company  with  C.  lacazei  Labbe  and  Adelea  ovata  H.  Schneider. 

Classification  of  the  Coccidiidea. — The  usual  classification  is  that  by  Leger  in 
1900,  and  is  based  upon  the  number  of  sporozoites  in  each  cyst. 

Family  i.  Asporocystid^. — Sporozoites  naked,  no  sporocysts  inside  the 
oocyst. 

Family  2.  Disporocystid^e. — Oocyst  has  two  spores. 

Family  3.  Tetrasporocystid^. — Oocyst  has  four  spores. 

Family  4.  Polysporocystid^e. — Oocyst  has  many  spores. 

Family  Asporocystid^e  Leger,  1900. 

The  genus  included  in  this  family  is  Eimeriella  Stiles,  1902,  of  which  there 
is  only  one  species.  Eimeriella  nova  Schneider,  18 19  in  the  Malpighian  tubules 
of  Glomeris. 

Family  Disporocystid^;  Leger,  1900. 

The  genera  of  this  family  are:  Cyclospora  A.  Schneider,  18S1  (spores  dizoic)  ; 
Diplospora  Labbe,  1893  (spores  tetrazoic) ;  Isospora  A.  Schneider,  1881  (spores 
poly  zoic). 

Isospora  A.  Schneider,  1881. 

Definition. — Disporocystidae  with  polyzoic  spores. 

Isospora  bigemina  Stiles,  1891. 

Synonym. — Cytospermium  villorum  intestinalium  cants  et  felis  Rivolta,  1874. 

This  parasite  lives  in  the  intestinal  villi  of  dogs  and  cats,  and  is  distinguished 
because  it  is  small  and  because  it  is  in  pairs,  the  oocyst  dividing  into  two  equal 
portions,  which  become  encysted  and  form  two  spores  {vide  Coccidiosis  in 
man  infra). 

Family  Tetrasporocystid^e  Leger,   1900. 

Type  Genus.— Eimcria  A.  Schneider,  1874. 

Synonym.—  Coccidium  Leuckart,  1879  (the  dizoic  spores  are  spherical  or 
oval).  Other  Genus:  Crystallospora  Labbe,  1896  (the  dizoic  spores  have  the 
form  of  a  double  pyramid). 


474  TELOSPORIDIA 

Eimeria  A.  Schneider,  1875. 

7 '  etvasporocystidce  with  the  formation  of  an  oocyst  after  fecundation ;  sporo- 
blasts  in  the  form  of  a  pyramid ;  spores  globular  or  oval,  provided  with  a 
micropyle. 

Eimeria  stiedse  Lindemann,  1865. 

Synonyms. — Psovospermium  cuniculi  Rivolta,  1878;  Coccidiiim  oviforme 
Leuckart,  1879;  C.  perfomns  Leuckart;  Pfeifferia  princeps  Labbe,  1896. 

This  is  the  common  species  found  in  the  liver  of  rabbits.  The  spores 
swallowed  by  the  rabbit  are  opened  by  the  action  of  the  acid  of  the  gastric 
juice,  and  the  sporozoites  set  free  ascend  the  bile-duct,  and  pass  into  the  cells 
lining  the  small  bile-ducts.  Here  they  propagate  vigorously  by  schizogony, 
causing  proliferation  of  the  epithelium  and  connective  tissue  of  the  ducts,  so 
that  thick-walled  nodules,  more  or  less  isolated  and  containing  caseous  material 
(consisting  of  detritus,  pus,  epithelial  cells,  and  coccidia),  are  formed.  The 
inflammation  may  be  severe  enough  to  kill  the  rabbit. 

Sporogony  proceeds  with  the  formation  of  macrogametocytes  with  macro- 
gametes,  and  the  microgametocytes  with  microgametes,  which  conjugate  and 
form  zygote, sporoblast, spores,  and  sporozoites  (vide  Coccidiosisinman,  infra). 


Family  Polysporocystid^e  Leger. 

Comprises  a  large  number  of  genera:  Adelea  A.  Schneider,  1875  (dizoic) ; 
Klossia  (tetrazoic)  A.  Schneider,  1875;  Minchinia  Labbe,  1896;  Klossiella 
Smith  and  Johnstone,  1902 ;  Barronsia  (monozoic) ;  Benedenia  (trizoic). 

Coccidiosis  in  Man. 

The  utmost  confusion  has  existed  as  to  this  infection  of  man, 
but  now,  thanks  to  the  labours  of  Dobell,  whose  writings  we  have 
followed,  the  subject  is  more  defined. 

In  1841  Johannes  Miiller  introduced  the  name  '  psorosperms '  for 
the  spores  of  the  myxosporidia,  and  as  the  coccidia  were  believed  to 
resemble  these  bodies,  they  were  called  '  oviform  psorosperms  ' 
until  Leuckart  in  1879  gave  them  the  name  coccidiiim.  The  various 
diseases  and  cases  rightly  or  wrongly  called  coccidiosis  at  any  time 
in  man  may  be  considered  as  follows : — ■ 

Diseases  now  known  not  to  be  Coccidiosis. — These  are  (1)  a  form 
of  blastomycosis  (granuloma  coccidoides) ;  (2)  rhinosporidiosis; 
(3)  Darier's  disease;  (4)  molluscum  contagiosum. 

Cases  wrongly  diagnosed  as  Coccidiosis.  — These  are  the  cases 
described  by  Virchow  (i860),  Rivolta  (1873  and  1878),  Grassi  (1879), 
Podwyssoki  (1889),  Giles  (1890),  Jurgens  (1895),  Quincke  (1899), 
Thomas  (1899),  Grunow  (1901),  and  probably  by  Kiinstler  and 
Pitres  (1884). 

Cases  correctly  recognized  as  Coccidiosis.— Dobell  considers  that 
over  seventy  cases,  mostly  from  the  Near  East,  have  recently 
been  recognized  as  coccidiosis.     The  earlier  cases  are : — 

Hepatic. — Grubler  in  Paris  (1858),  Dressier  in  Prague  (recorded 
by  Leuckart  in  1863),  Sattler  in  Vienna  (recorded  by  Leuckart  in 
1879),  Perls  in  Giessen  (recorded  by  Leuckart  in  1879);  Perls  and 
von  S6mmering(?)  (recorded  by  Leuckart  in  1879),  and  Silcock  in 
London  (1890). 


COCCIDIOSIS  IN  MAN  475 

Intestinal. — Kjellberg  (recorded  by  VirchoW  in  i860)  and  two 
cases  by  Eimer  (1870). 

Fcecal. — These  are  numerous.  The  earliest  are  Woodcock  (1915), 
Low  (1915),  Wenyon  (1915),  Woodcock  and  Penfold  (1916),  Dobell 
(1916),  Roche  (1917),  Cragg  (1917),  Wenyon  and  O'Connor  (1917), 
Savage  and  Young  (1917),  Castellani  and  Richards  (1917),  Martin, 
Kellaway,  and  Williams  (1918),  Boney,  Crossman,  and  Boulenger 
(1918),  while  Dobell  (1918)  has  found  a  new  form. 

Coccidia  found  in  Man.— The  coccidia  found  in  the  above  cases 
may  be  classified  as: — (1)  Isospora  hominis  Rivolta,  1878,  emendavit 
Dobell,  1918;  (2)  Eimeria  wenyoni  DobzW,  1918;  (3)  Eimeria  oxyspora 
Dobell,  1918 ;  (4)  the  hepatic  coccidium  of  man.  These  species  may 
be  described  as  follows : — 

Isospora  hominis  Rivolta,  1878,  emendavit  Dobell,  1913. 

Synonyms. — Psorospevmien  Virchow.  i860,  Leuckart,  1863,  Eimer,  1870; 
Cytospermium  hominis  Rivolta,  1878;  Coccidium  perforans  Leuckart,  1879; 
Coccidium  bigeminum  var.  hominis  Railliet  and  Lucet,  1891;  Coccidium  per- 
forates var.  kjellberg  Labbe,  1899;  Coccidium  hominis  Rivolta,  1878,  emendavit 
Labbe,  1896;  Eimeria  stiedce  Lindemann,  pro  parte  Liihe,  1906;  Isospora 
bigemina  Stiles,  1891,  pro  parte  Liihe,  1906. 

Definition. — Isospora  with  oocysts  elongate,  ovoid  in  form, 
narrow  end  drawn  out  into  a  neck,  25-33  x  12-5-16  microns,  with  clear, 
colourless,  and  porcellaneous  Wall,  with  two  or  more  layers  and  an 
inconspicuous  micropyle  at  narrow  end.  Development  of  spores 
takes  place  outside  of  host,  and  requires  several  days  for  completion. 
Oocyst  forms  two  round  sporoblasts,  from  Which  arise  two  sporocysts, 
which  form  four  vermiform  sporozoites  and  leave  a  large  granular 
sporocystic  residue.     Habitat,  man. 

History. — i".  hominis  was  discovered  by  Kjellberg  about  i860,  in 
the  villi  of  the  small  intestine;  it  Was  seen  in  1870  by  Eimer,  and 
Was  named  in  1878  by  Rivolta.  Its  oocysts  were  probably  first 
found  in  human  faeces  by  Railliet  and  Lucet  in  1890,  but  the  first 
clearly  recognizable  account  is  that  given  by  Wenyon  in  1915,  since 
when  some  fifty  cases  of  infection  have  been  recorded,  making  in 
all,  with  the  cases  seen  by  Castellani  and  Richards  in  the  Balkans, 
about  seventy  infections. 

Distribution.— It  has  been  found  in  people  coming  from  Gallipoli, 
Salonika,  Egypt,  Mesopotamia,  and  in  the  Balkans. 

Pathogenicity.— This  is  believed  to  be  nil,  as  most  cases  showed 
merely  a  small  and  transitory  infection.  Animals  have  so  far  not 
been  infected  with  this  parasite. 

Eimeria  wenyoni  Dobell,  1918. 

Synonyms. — Eimeria  (Coccidium)  Wenyon,  1915;  Coccidium 
(Eimeria)  Wenyon,  1916;  Eimeria  sp.  Dobell,  1917. 

Definition. — Eimeria  with  a  spherical  oocyst,  20  microns  in 
diameter,  with  outer  surface  rough  and  rugose,  inner  smooth  and 
lined  by  a  delicate  membrane.     Four  oval  spores  measuring  10  x  7 


476  TELOSPORIDIA 

microns.  External  surface  of  sporocyst  rough.  No  oocystic 
residual  body.  Each  spore  contains  two  typical  sporozoitcs  and 
one  or  two  sporocystic  residua.     Habitat,  man. 

History. — This  parasite  was  found  by  Woodcock  and  Wenj^on, 
in  1915,  in  the  faeces  of  a  British  soldier  from  Gallipoli.  It  Was 
again  found  by  Roche  in  1917  in  three  cases  at  Salonika,  so  that 
the  total  infections  up  to  date  (1918)  are  four. 

Distribution.— Shores  of  the  Eastern  Mediterranean. 

Pathogenicity.- — -Unknown,  and  no  attempts  so  far  made  to  infect 
animals. 

Eimeria  oxyspora  Dobell,  1918. 

Definition. — Eimeria  with  spherical  oocyst  36  microns  in  diameter, 
with  faintly  yellow  transparent  wall,  composed  of  at  least  two  dis- 
tinct layers,  containing  four  dizoic  spores  and  a  small  oocystic 
residue.  Spores  long,  sharply  pointed  at  both  ends,  30-32  x  7-5 
microns.  Sporocyst  has  a  tough  endospore  and  deciduous  epispore, 
the  remains  of  which  give  the  spore  a  frilled  appearance.  There  are 
two  sporozoites  in  each  spore,  with  pointed  anterior  and  rounded 
posterior  ends,  which  contain  the  nucleus. 

History.— The  parasite  was  found  by  Dobell  in  a  young  man  Who 
had  been  in  South  Africa,  Ceylon,  and  India. 

Distribution.— Unknown. 

Pathogenicity. — Infection  small,  but  pathogenicity  not  certainly 
known,  because  the  patient  was  infected  with  L.  histolytica  and 
Ancylostoma.    Believed  not  to  be  pathogenic. 

The  Hepatic  Coccidium  of  Man. 

Synonyms.- — Cellules  ovoides  (?)  ceufs  d'helminthes  Gubler,  1858; 
Corps  ooiformes  Davaine,  i860;  Psorospermien  Leuckart,  1863; 
Psorospermi  Rivolta,  1873;  Coccidium  oviforme  Leuckart,  1879; 
Coccidien  leberpsorospermien  Biitschli,  1882;  Coccidium  cuniculi 
(Rivolta)  Blanchard,  1896;  Eimeria  stiedce  (Lindemann)  Liihe,  1906; 
Eimeria  (?)  sp.  Dobell,  1918. 

Definition. — Not  at  present  capable  of  definition. 

History. — It  was  first  recorded  by  Gubler  in  1858,  in  a  quarryman, 
aged  forty-five,  in  Paris.  This  man  is  said  to  have  died  from 
peritonitis.  He  suffered  from  digestive  troubles,  anaemia,  and  had 
an  enlarged  liver.  Post-mortem  the  liver  contained  many  tumours 
of  a  cancerous  appearance,  in  which  were  numerous  ovoid  cells 
or  eggs  of  helminthes,  at  least  four  times  the  size  of  the  largest  cells 
of  the  surrounding  tissue.  Some  had  a  distinct  double  contour,  and 
Were  completely  filled  with  granular  contents.  One  end  was  rather 
blunter  than  the  other,  which  showed  a  slight  constriction,  and  had 
a  small  depressed  surface,  as  though  an  operculum  or  micropyle 
were  present. 

The  second  case  was  found  by  Dressier  of  Prague,  and  consisted 
of  three  small  nodules  in  the  margin  of  a  human  liver.  These  nodules 
contained  a  whitish  pulp,  which  surrounded  oval  bodies  18-20  microns 


H/EMOSPORIDIA  477 

in  length,  and  his  drawings  show  four  oocysts.  The  third  case  was 
discovered  by  Sattler  of  Vienna  in  a  pathological  preparation.  It 
showed  a  dilated  bile-duct  with  greatly  proliferated  epithelium 
and  coccidia. 

The  fourth  case  is  by  Perls;  it  was  from  a  preparation  made  by 
von  Sommering,  and  is  said  by  Leuckart  to  have  contained  coccidia. 

The  fifth  and  last  case  is  that  described  by  Silcock  in  1890  at 
St.  Mary's  Hospital,  London.  A  woman  aged  fifty  had  enlargement 
of  the  liver  and  spleen,  with  fever  and  slight  diarrhoea.  At  the 
post-mortem  the  liver  was  much  enlarged  and  showed  a  number  of 
caseous  foci.  The  ileum  contained  six  papule-like  elevations 
surrounded  by  an  inflammatory  zone,  and  the  large  intestine  had 
deeply  congested  patches  of  mucosa. 

In  the  caseous  nodules  were  agglomerations  of  small  oval,  egg- 
like bodies,  v>  ith  granular  contents  and  a  well-marked  capsule,  and 
Were  considered  to  be  identical  with  Leuckart 's  coccidia.  They  were 
kept  in  water,  and  psorosperms  freely  developed.  He  considered 
them  to  be  Coccidivim  oviforme,  and  to  be  present  in  the  spleen, 
but  does  not  state  anything  definite  as  to  the  intestine. 

In  all,  therefore,  up  to  1918,  five  cases  have  been  recorded. 

Dobell  does  not  consider  this  parasite  to  be  Eimeria  stiedce, 
judging  from  Dressier 's  drawings. 

Gubler's  case  Was  considered  to  be  a  hydatid  cyst.  Dobell's 
conclusions  are  that  there  is  a  coccidial  parasite  which  very  rarely 
occurs  in  the  human  liver,  and  resembles  E.  stiedce,  but  is  consider- 
ably smaller  and  is  probably  a  distinct  species,  though  perhaps 
belonging  to  the  same  genus. 

Distribution. — Europe. 

Pathogenicity. — It  causes  cyst-like  swellings  of  the  liver,  with 
enlargement  of  that  organ. 

ORDER  III.  H/EMOSPORIDIA  Doflein,  1901. 

Synonym.— Hcemocytozoa  Mesnil,  1915. 

Definition. — Telosporidia,  Coccidiomorpha  without  resistant  spores 
in  the  sporocysts  and  with  the  trophozoite  stage  intracellular. 
With  alternations  of  generation,  schizogony  in  a  vertebrate  and 
sporogony  in  a  blood-sucking  arthropod  or  leech. 

Remarks. — -Mesnil  considers  that  the  family  Haernogregarinidae 
is  related  to  Leger's  Adeleidea  division  of  the  Coccidiidea,  and  the 
Plasmodidae  to  the  Eimeridea  division,  and  that  they  should  find 
their  places  in  that  group.  He  considers  that  the  genus  Leucocyto- 
zoon  should  come  into  the  Haemosporidia,  and  that  the  Piroplas- 
midae  require  more  study  in  the  invertebrate  before  being  classified. 
There  is  no  doubt  that  Haemosporidia  is  merely  a  temporary  order 
in  which  to  place  forms  pending  a  fuller  classification,  which  will 
probably  be  on  the  lines  indicated  by  Mesnil. 

Classification. — -The  following  families  may  be  temporarily  placed 
in  this  order  for  convenience,  and  can  be  differentiated  as  follows : — ■ 


478  TELOSPORIDIA 

A.  Without  hcemozoin  : — 

I.  Live  in  red  and  white  blood  cells  in  the  peripheral 
blood— Hcemogregarinidce . 
II.  Live  in  white  cells  in  the  organs — -Toxoplasmidce. 
III.  Live  in  red  cells  in  the  peripheral  blood — Piroplas- 
midce. 

B.  With  hcemozoin  : — 

$i  I.  Ookinete  encysts  and  forms  an  oocyst — Plasmodidce. 
II.  Ookinete  is  not  known  to  encyst — -HcemoproteidcB. 

Family  ILemogregarinid^e  Neveu-Lemaire,  1901* 

Synonyms. — Hamosporidia  Labbe,  1894;  H&mosporea  Minchin,  1903. 
Definition. — Telosporidia,  in  which  either  the  gametocytes  or  the  schizonts, 
or  both,  are  present  in  red  or  white  cells  in  the  peripheral  blood  of  vertebrates, 
and  in  which  schizogony  takes  place  either  in  the  cells  of  the  peripheral  blood, 
or  in  those  of  some  organ,  while  sporogony  takes  place  in  the  body  of  some 
blood-sucking  invertebrate,  such  as  a  leech,  a  tick,  a  mite,  or  an  insect. 
Neither  schizonts  nor  sporonts  contain  haemozoin. 

History. — Although  the  first  haemogregarine  was  dis- 
covered in  a  frog  as  far  back  as  1850  by  Chaussat,  who 
thought  it  was  a  nematode,  it  is  only  quite  recently,  owing 
to  the  labours  of  Sambon,  Miller,  Miss  Robertson,  Christo- 
phers, and  others,  that  any  accurate  knowledge  has  been 
obtained. 

The  evolution  of  the  knowledge  concerning  these  para- 
sites may  be  briefly  stated. 

Discovered,  as  mentioned  above,  by  Chaussat,  they  were 
next  seen  by  Ray  Lankester  in  1871,  and  thought  to  be  a 
stage  in  the  life-history  ot  the  frog  trypanosome,  T.  (Un- 

Fig    147  • Hcb-    dulina)  rotatontm,  and  then  by  Gaule  in  1880,  who  mistook 

mogreearina  them  for  cell  inclusions.  In  1885  Danilewsky  first  applied 
cantlei  Sambon  ^e  name  '  Haemogregarina '  to  the  parasites  he  found  in  the 
blood  of  tortoises  and  lizards.  In  1894  Labbe  classified  them, 
(After  Sambon.)  according  to  the  relationship  between  the  length  of  the 
parasite  and  that  of  the  blood  cell,  into  (1)  Drepanidium, 
parasite  not  more  than  three-quarters  of  the  length  of  the  host  cell;  (2)  Karyo- 
lysus,  parasite  not  exceeding  host  cell  in  length,  and  destroying  the  nucleus; 

(3)  Danilewskya,  parasite  exceeding  the  host  cell  in  length,  and  bent  upon 
itself. 

The  term  Drepanidium  having  been  previously  employed  for  one  of  the 
Heterokaryota,  it  was  necessary  to  alter  it  to  Lankester ella,  and  the  term 
Danilewskya  was  also  altered  by  Danilewsky  in  1897  to  '  Haemogregarina  ' 
(sensu  stricto) ;  but  since  Sambon  and  others  have  described  so  many  new 
species  this  classification  no  longer  stands,  nor  can  a  natural  arrangement  be 
proposed  until  the  life-histories  of  the  various  species  are  fully  known;  there- 
fore the  suggestion  of  Laveran  is  being  universally  adopted,  which  consists  of 
arranging  them  according  to  the  classes,  orders,  and  genera  of  the  hosts,  and 
distinguishing  only  one  genus,  Hcemogregarina  Danilewsky,  1885,  the  various 
species  of  which  are  arranged  into  four  groups:  (1)  Haemogregarinida  of 
mammals;  (2)  Hasmogregarinida  of  reptiles;  (3)  Haemogregarinida  ot  amphibia; 

(4)  Haemogregarinida  of  fish.  With  regard  to  the  Haemogregarinida  of  mam- 
mals, they  were  first  discovered  by  Bentley  in  the  blood  of  a  pariah  dog  (Canis 
familiaris)  in  Assam,  and  confirmed  by  James  in  1905.  In  1905  Balfour 
discovered  Hcemogregarina  jaculi  Balfour,  1905,  in  Jaculus  gordoni  in 
Khartoum,  and  described  the  cycle  of  schizogony;  but  though  numerous  ex- 
periments were  conducted  with  Xenopsylla  clcopatvcB,  species  of  Dermanyssus 
(mites),  and  Clinocoris  rotundatus,  only  the  liberated  gametocytes  have  been 


Hmmogregarinidje 


479 


traced .     A  danger  is  to  mistake  Crithidia  p ulicis  of  the  flea  for  a  developmental 
stage  of  the  H.jaculi. 

In  1905  Christophers  discovered  H.  gerbilli  in  the  Indian  field-rat  (Gerbillus 
indicus),  and  traced  its  schizogony  and  later  cyst-formation  in  a  louse 
{Hcematopimis  stephensi) ;  but  he  did  not  observe  conjugation,  nor  did  he 
reinfect  rats  from  the  louse,  and  finally  in  1907  he  appears  to  think  it  probable 
that  the  cysts  he  described  may  have  nothing  to  do  with  the  haemogregarine. 


Fig.  148.— Life-Cycle  of  Hcemogregarina  muris  Balfour. 
(After  Miller.) 
1,  2,  Free  sporozoites  in  the  intestine  of  the  rat  penetrating  the  villus  and 
entering  the  blood;  3,  entering  the  liver  cells;  4-8,  schizogony  in  the  liver; 
9,  merozoite  about  to  reinfect  a  liver  cell;  10-11,  merozoite  infecting  a  white 
blood  cell;  12,  free  vermicules  in  the  stomach  of  the  louse;  13,  conjugation; 
i\,  the  zygote;  15,  ookinete  in  the  stomach;  16,  ookinete  in  the  wall  of 
the  stomach;  17,  ookinete;  18-19,  oocyst;  20,  sporoblasts  appearing ;  21,  early 
sporoblasts;  22,  sporoblasts;  23,  late  sporoblasts;  24,  formation  of  sporozoites. 

In  1906  Adie  discovered  a  haemogregarine  in  Epimys  rattus,  Balfour  one  in 
E.  norvegicus,  Christophers  another  in  Felis  domestica,  Patton  another  in 
Funambulus  pennantii. 

In  1907  Christophers  traced  the  sporogony  of  H.  canis  in  Rhipicephalus 
sanguineus.  In  1908  Miller  contributes  a  most  valuable  paper  on  H.  muris 
Balfour,  1905,  under  the  term  Hepatozoon  perniciosum  Miller,  1908,  in  which  he 


480  TELOSPORIDIA 

not  merely  traced  out  the  cycle  of  schizogony,  but  also  fully  that  of  sporogony. 
This  was  the  first  description  of  the  full  life-history  of  a  haemogregarine  ever 
given.  This  paper  is  also  of  the  greatest  importance  in  arranging  the  classifi- 
cation of  the  Hsemogregarinida,  for,  as  already  stated,  Ray  Lankester  in  1871 
believed  that  H.  minima  might  be  a  stage  of  Trypanosoma  rotatorium,  and  in 
this  was  supported  by  Billet  in  1904,  who  considered  that  he  could  infect 
clean  frogs  with  haemogregarines  by  the  bites  of  leeches  containing  trypano- 
somes. 

Brumpt's  experiments  in  1904  on  the  sporogony  of  H.  bagenesis  in  the  leech 
(Placobdella  catenigera)  also  supports  this  theory  by  finding  a  binucleate 
condition  in  the  ookinetes.  Miss  Robertson  believes  that  haemogregarines  have 
a  trypanosoma  stage.  These  observers  would  therefore  classify  the  Haemo- 
gregarinida  with  the  Binucleata;  but  against  this  Brnmpt  in  1907  has  shown 
that  Billet  was  probably  mistaken,  for  if  leeches  infected  with  T.  inopinatum 
are  placed  on  a  '  clean '  frog  a  trypanosomiasis  results,  and  the  fact  that 
though  Sambon  has  often  seen  haemogregarines  in  snakes  and  lizards,  trypano- 
somes  are  absent  or  rare. 

The  life-history  of  H.  muris  as  worked  out  by  Miller  shows  no  trypanosome 
stage,  and  clearly  indicates  that  the  Haemogregarinida  belong  to  the  Telo- 
sporidia,  and  are  related  to  the  Gregarinida  and  Coccidiidea,  as  was  pointed 
out  by  Laveran  in  1898. 

With  regard  to  the  Haemogregarinida  of  reptiles,  a  very  complete  work 
is  that  of  Sambon  in  1908  on  the  parasites  in  snakes,  where  a  full  history 
will  be  found.  Those  which  occur  in  tortoises  and  crocodiles  have  been 
studied  by  Danilewsky,  Castellani  and  Willey,  Miss  Robertson,  Dobell,  and 
others,  while  Siegel  has  worked  out  fully  the  schizogony  and  sporogony  of 
H.  stepanovi  in  the  leech. 

The  Haemogregarinida  of  lizards  have  been  studied  by  Danilewsky,  Laveran, 
Minchin,  C.  Franca,  and  others,  and  those  of  amphibia  by  Chaussat,  Lankester, 
Billet,  Durham,  Brumpt,  Labbe,  Lesage,  and  others. 

Life-History. — The  most  accurately  known  life-history  is  that  given  for 
H.  muris  Balfour  by  Miller. 

Schizogony. — The  asexual  reproduction  takes  place  in  the  cells  of  the  liver, 
in  which  the  young  trophozoite  appears  as  a  small  spherical  organism  with  a 
large  vesicular  nucleus  containing  a  well-defined  karyosome.  The  trophozoite 
grows  at  the  expense  of  the  liver  cell,  the  nucleus  of  which  is  pushed  to  one 
side,  and  in  due  course  becomes  a  schizont,  which  divides  into  twelve  to  twenty 
merozoites,  and  a '  rest '  body. 

Some  of  these  merozoites  on  liberation  enter  fresh  liver  cells,  and  continue 
the  cycle  of  schizogony,  while  others  enter  mononuclear  leucocytes,  in  which 
they  become  encysted,  and  develop  into  gametocytes. 

Sporogony. — Sexual  reproduction  takes  place  in  a  mite  belonging  to  the 
Gamasidae  called  Lelaps  echidninus  Berlese,  which  lives  on  the  blood  of  the  rat. 

The  gametocytes,  liberated  from  the  leucocytes  by  the  digestive  action  of 
the  juices  of  the  mite's  gut,  arrange  themselves  in  couples,  which  are  at  first 
exactly  similar,  but  which  later  differentiate  into  a  large  encircling  form, 
which  is  more  granular,  and  which  is  probably  the  macrogamete,  and  a  smaller, 
more  rounded,  and  less  granular  microgamete.  Zygosis  now  takes  place, 
forming  an  ookinete,  which  grows,  and  leaving  the  gut  by  piercing  the  wall, 
forces  its  way  into  the  body  cavity,  which  consists  of  a  series  of  small  spaces 
between  the  organs,  and  further  into  the  sheaths  of  the  muscles,  and  into  the 
investing  membrane  of  the  salivary  glands. 

In  the  tissues  the  ookinete  encysts  and  becomes  the  oocyst,  which  grows 
rapidly  in  size,  and  undergoes  nuclear  division. 

The  daughter  nuclei  migrate  to  the  periphery,  which  becomes  covered  with 
50  to  100  bud-like  projections,  in  each  of  which  a  nucleus  is  to  be  found.  These 
buds  break  off  from  the  central  mass,  and  form  the  sporoblasts,  the  nuclei  of 
which  divide,  forming  daughter  nuclei,  which  gather  at  the  poles,  while  the 
whole  sporoblast  encysts.  Short  rod-like  processes  of  cytoplasm,  each  con- 
taining a  nucleus,  now  break  off  from  the  sporoblasts,  each  of  which  becomes 
a  sporozoite,  of  which  there  are  on  an  average  sixteen  to  each  sporoblast. 


HJEMOGREGA  RINID& 


Infection  of  the  rat  takes  place  by  ingestion  of  the  mite,  when  the  sporozoites 
are  liberated  by  the  juices  of  the  duodenum,  and  become  actively  motile 
striated  vermicules,  which  penetrate  the  intestinal  villi,  enter  the  blood  stream, 
and  are  carried  to  the  liver,  into  the  cells  of  which  they  penetrate,  and  start 
the  cycle  of  schizogony. 

As  the  mites  leave  the  rats  during  the  day-time,  and  only  feed  on  them 
during  the  night,  it  is  easy  to  understand  the  manner  in  which  the  disease 
spreads  from  the  sick  to  the  healthy. 

Variations  in  the  Life-Cycle. — 
The  life-history  of  H.  muris  is 
peculiarly  interesting,  because  it 
is  fully  known,  but  it  is  not  quite 
typical  for  all  haemogregarines, 
for  in  it  the  gametocytes  alone 
are  found  in  the  peripheral  blood, 
and  they  are  enclosed  in  leu- 
cocytes. 

Other  species,  however,  show 
marked  differences  from  H.  maris, 
for  the  majority  are  found  in  red, 


Fig.  149. — Hcemogregarina  vittatcs 
Robertson,  showing  Schizo- 
gony. 

(After  Miss  Robertson.) 


Fig.  150. — Hcemogregavina  rarefaciens 
Sambon,  showing  Male  and 
Female  Schizonts. 

(After  Sambon.) 


not  white,  corpuscles,  while  in  some  the  whole  process  of  schizogony  is 
completed  in  the  blood  stream;  therefore  a  few  more  general  remarks  are 
necessary  to  supplement  the  life-history  given  above. 


Fig.  151. — Hcsmogregarina  rarefaciens 
Sambon:    Young  Gametocyte. 

(After  Sambon.) 


Fig.  152. — Hcsmogregarina  seligmanni 
Sambon,  showing  Capsule  and 
Cleavage  Lines. 

(After  Sambon.) 


The  peripheral  blood  of  the  vertebrate  can  contain  trophozoites,  schizonts, 
and  gametocytes  lying  either  in  red  or  white  corpuscles,  the  two  latter  being 
contained  in  a  double  capsule,  which  is  probably  formed  by  the  parasite, 
and  which  is  always  in  close  attachment  to  the  nucleus  of  the  host  cell. 

Schizogony  begins  with  the  young  trophozoite  lying  free  m  the  enclosing 


482 


TELOSPORIDIA 


cell,  as  an  oval,  fusiform,  or  club-shaped  mass  of  cytoplasm  with  a  large, 
homogeneous  nucleus.  As  this  trophozoite  grows  it  becomes  encapsuled, 
and  forms  the  schizont,  which,  when  fully  grown,  is  a  large  oval  or  rounded 
body,  with  a  central  nucleus,  and  with  the  cytoplasm  filled  with  spherules. 
This  schizont  usually  lies  in  an  enlarged  and  dehsemoglobinized  cell,  in  which 
it  is  seen  to  be  surrounded  by  a  thick;  capsule,  which  shows  three  definite 
cleavage  lines,  of  which  two  cross  it  transversely  a  short  distance  from  either 
pole,  while  the  third  is  longitudinal. 

There  are  two  varieties  of  schizonts,  one  which  gives  rise  to  relatively  few 
large  merozoites  called  '  macro merozoites,'  while  the  other  breaks  up  into 
relatively  many  small  micromerozoites. 


Fig.   153. 


-Hcemogvegarina    mirabilis    Castellani    and    Willey,    showing 
the  Escape  of  the  Gametocyte  from  its  Capsule. 

(After  Gastellani  and  Willey.) 


This  differentiation  is  considered  to  be  a  prelude  to  the  formation  of  macro- 
and  micro-gametocytes.  Usually  the  schizont  divides  into  eight,  twelve,  or 
sixteen  merozoites,  which  may  escape  from  the  enclosing  cell  in  the  peripheral 
blood,  but  more  generally  do  so  in  an  organ,  such  as  the  liver,  lung,  or  bone- 
marrow.  Other  haemogregarines,  like  H.  jaculi  and  H.  muris,  undergo  seg- 
mentation in  the  cells  of  an  organ  such  as  the  liver. 

The  gametocytes  are  easily  recognizable  from  the  schizonts,  as  they  He  bent 
up  in  the  capsule,  and  because  the  enclosing  cell  is  not  affected  by  the  para- 
site. It  is  not  possible  at  present  to  differentiate  between  the  macro-  and 
the  micro-gametocyte. 


Fig.  154. — H&mogregarina  seligmanni 
Sambon  :  Free  Sporont. 

(After  Sambon.) 


Fig.  155. — Hcsmogregarina  seligmanni 
Sambon. 
According  to   Sambon,  this    figure 
probably  represents  conjugation. 

(After  Sambon.) 


In  shed  blood  they  quickly  escape  from  the  capsule,  which  may  be  seen  to  be 
double,  for  Sambon  depicts  a  gametocyte  which  has  escaped  from  the  outer 
wall  of  the  capsule,  but  has  the  inner  wall  still  adherent. 

When  free,  they  are  seen  to  be  of  an  elongated,  club-shaped  form.  At  the 
thicker  end,  which  is  anterior,  there  projects  a  small  retractile  rostrum  or 
beak,  from  which  a  clear  line,  probably  a  cytostome  or  pharynx,  runs  back- 
wards through  the  cytoplasm,  and  ends  near  the  nucleus. 

The  ectoplasm  shows  at  times  a  differentiation  into  three  layers — epicyte, 
sarcocyte,  and  myocyte — while  the  endoplasm  is  granular,  and  about  its 
middle  is  found  the  round  or  oval  nucleus. 

According  to  Sambon,  conjugation  can  be  seen  taking  place  in  blood  spread 


HAEMOGREGARINES  OF  THE  MAMMALIA  483 

on  an  ordinary  slide.  The  further  history  of  the  cycle  of  sporogony  is  only 
known  in  H.  muris  and  H.  cants  ;  the  former  has  already  been  described,  and 
the  latter  will  be  mentioned  later. 

Recently  Henry  has  shown  that  Balfour's  infective  granule  is  a  phase  in 
the  life-history  of  H.  simondi.  Haemogregarines  can  be  cultivated  in  Nicolle's 
blood-agar  medium. 

No  haemogregarines  are  at  present  known  in  birds  nor,  until  recently,  in 
man,  but  some  peculiar  parasites  have  been  seen  by  Castellani  and  Willey  and 
others  in  the  peripheral  blood  of  man  (p.  53S);  whether  these  will  prove 
to  be  haemogregarines,  or  whether  they  belong  to  some  other  order  of  the 
protozoa,  remains  to  be  seen.  Krempf  has  recently  described  a  haemogregarina 
in  the  spleen  of  a  Chinese. 

Classification. — As  already  mentioned,  the  species  of  the  genus  Hcemogrega- 
n'ttaDanilewsky,  1885,  will  be  arranged  according  to  their  hosts.  Some  authors 
recognize  Hepatozoon  Miller,  1908,  with  H.  muris  Balfour,  1905,  as  a  type, 
and  distinguish  it  by  living  in  leucocytes,  and  sometimes  undergoing  schizo- 
gony in  the  cells  of  the  internal  organs. 

HAEMOGREGARINES  OF  THE  MAMMALIA. 
Haemogregarina  hominis  Krempf,  191 7. 

Definition. — Hamogregarina  found  only  in  the  spleen  of  man  suffering  from 
splenomegaly,  in  China. 

Remarks. — The  infection  appears  to  have  been  acquired  in  China. 

Morphology. — The  parasite  lives  in  red  cells  which  increase  in  size.  Inside 
the  red  cells  the  organism  lies  in  a  capsule,  10 X  5  microns,  and  is  vermicular 
in  shape,  being  bent  or  twisted.  There  is  a  granular  nucleus,  mostly  central 
in  position.  Parasites  which  have  escaped  from  the  red  cells  and  lie  free  in 
the  plasma  are  identical  with  those  found  in  the  cells. 

Life-History. — Unknown. 

Pathogenicity. — -Believed  to  cause  splenomegaly. 

Haemogregarina  muris  Balfour,  1905. 

Synonyms. — Leucocytozoon  muris  Balfour,  1905;  Hepatozoon  perniciosum 
Miller,  1908. 

H.  muris  is  found  in  the  mononuclear  leucocytes  of  Epimys  norvegicus  in 
Khartoum,  and  in  white  rats  in  Washington,  D.C.  Its  schizogony  and 
sporogony  in  Lelaps  echidninus  have  already  been  described  (p.  479).  It 
caused  anaemia,  severe  illness,  and  death  in  the  rats. 

Haemogregarina  canis  James,  1905. 

Synonym. — Leucocytozoon  canis  James,  1905. 

Hcemogregarina  canis  was  discovered  by  Bentley  in  the  blood  of  a  pariah  dog, 
Canis  familiaris,  in  Assam,  and  this  discovery  was  fully  confirmed  by  James 
in  1905.  Christophers  was  the  first  investigator  to  trace  out  its  full  liie- 
history  in  1906-07. 

It  appears  to  be  common  in  pariah  dogs  in  Assam  and  Madras,  but  more 
particularly  in  the  puppies  and  less  common  in  the  adults.  It  is  also  found 
in  Ceylon,  and,  according  to  Dutton,  Todd,  and  Tobey,  it  probably  occurs  in 
dogs  in  the  Gambia. 

Morphology.-  -The  parasite  is  seen  in  the  white  corpuscle  of  the  peripheral 
blood  as  an  oval,  unpigmented  mass  which  is  difficult  to  stain,  and  which  lies 
in  two  envelopes — an  outer  formed  from  the  cytoplasm  of  the  corpuscle,  and 
an  inner  formed  by  itself.  The  cell  in  which  it  lies  is  not  typical  of  any 
corpuscle,  though  at  first  sight  it  resembles  a  polymorphonuclear  leucocyte. 
When  stained,  it  is  seen  to  possess  a  nucleus  in  the  shape  of  amassol  chromatin 
stretching  across  the  body  at  one  end . 

Schizogony. — Schizogony  appears  to  take  place  only  in  the  bone-marrow, 
and  has  not  been  seen  in  the  liver  or  spleen.     It  begins  by  the  parasite  gathering 


484 


TELOSPORIDIA 


itself  on  one  side  of  the  cyst-walljwhile  the  nucleus  comes  more  into  the  middle. 
The  cyst  becomes  more  swollen  and  rounder,  and  is  most  difficult  to  stain, 
being  brilliantly  clear  and  refractile,  but  as  it  grows  older  it  becomes  filled  with 
round  or  oval,  clear,  refractile  granules  of  large  size.  No  details  are  given  of  the 
action  of  the  nucleus  or  of  the  cytoplasm  during  the  stages,  which,  of  course, 
marks  a  gap  in  the  life-history.  As  the  cyst  matures  the  granules  become  less 
in  number,  and  merozoites  are  seen  lying  among  them,  and,  later,  the  granules 
having  disappeared,  only  merozoites,  which  number  about  thirty,  are  seen 
lying,  along  with  a  little  granular  matter,  in  the  oval  or  circular  cyst,  which 
may  be  48  /j,  in  diameter. 


Fig.  156. — Diagram  of  the  Life-Cycle  of  Hcemogregarina  cants  James. 
(Constructed  from  drawings  by  Christophers.) 


1 1  does  not  appear  clear  what  happens  to  these  merozoites,  but  from  Christo- 
phers' description  one  is  led  to  infer  that  they  infect  other  cells  in  the  bone- 
marrow  of  the  dog,  and  thus  become  young  trophozoites. 

Trophozoite. — By  inference  one  is  led  to  believe  that  the  trophozoite 
probably  appears  in  the  bone-marrow  as  a  small,  round,  or  egg-shaped  body, 
possessing  no  capsule,  and  having  a  chromatin  mass  of  isolated,  rod-shaped 
granules  arranged  loosely  in  a  circle.  These  trophozoites  lie  in  a  mono- 
nuclear cell,  which  are  the  parents  of  the  transitional  cells,  which  are  looked 
upon  as  the  parents  of  the  polymorphonuclear  leucocytes,  but  when  infected 
by  the  parasite  the  proper  development  is  not  completed,  and  hence  the 
appearance  in  the  peripheral  blood  of  a  peculiar  type  of  cell  containing  the 
encapsuled  parasite.  The  young  trophozoite  is  seen  in  the  liver  and  spleen  as 
well  as  in  the  bone-marrow,  but  is  rare  in  the  peripheral  blood.     This  tropho- 


HMMOGEEGARINA   CAN  IS  485 

zoite  grows  into  the  encapsuled  form  just  described,  all  stages  between  the 
two  having  been  seen  by  Christophers,  and  in  this  way  the  cycle  of  schizogony 
is  completed. 

Sporogony. — The  tick  Eitrhipicephalus  sanguineus  Latreille  is  very  common 
on  the  dogs  in  Madras.  The  female  takes  from  two  to  four  days  to  suck 
the  blood,  which  it  only  does  once  in  its  lifetime,  but  most  of  the  blood  is 
taken  in  the  last  twenty-four  hours.  After  sucking  the  blood  it  drops  off, 
and  when  examined  at  different  periods  the  following  sporogony  can  be 
made  out: — 

The  encapsulated  forms  already  described  as  existing  in  the  blood  pass 
into  the  stomach,  and  the  parasite  escapes  from  the  corpuscle,  but  is  still 
inside  its  own  envelope. 

By  elongation  and  passage  of  the  protoplasm  behind  the  nucleus,  the  oval 
parasite  becomes  a  vermicule.  These  vermicules  must  probably  be  looked 
Qpon  as  macrogametocytes  and  microgametocytes.  In  any  case  they  enter 
young  epithelial  cells  lining  the  lumen  of  the  gut,  in  whose  cytoplasm  they 
divide  by  fission,  which  in  many  cases  takes  place  several  times,  resulting  in 
tin  secondary  formation  of  four  to  eight  vermicules  lying  in  a  pocket  in  the 
cytoplasm  of  the  cell.  Two  of  these  secondary  vermicules,  which  apparently, 
as  a  rule,  do  not  differ  in  appearance,  conjugate,  and  the  nuclei  fuse,  and  then 
follows  a  throwing  out  of  two  large  masses  of  chromatin  from  the  nucleus 
and  the  separation  of  a  portion  of  cytoplasm.  The  former  may  represent 
reduction,  and  the  latter  the  separation  of  the  body  of  the  microgamete. 
Anyway,  as  the  result  of  this  process  there  is  formed  an  oocyst  with  a  syn- 
karyon,  and  therefore  the  conjugation  results  in  a  true  zygosis.  The  oocyst, 
still  embedded  in  the  epithelial  cell,  grows  rapidly,  and  has  a  central  clear  area 
and  outer  rim  of  protoplasm,  with  chromatin  diffused  in  irregular  masses 
near  the  periphery.  When  about  14  //  in  diameter,  the  oocyst  divides  into 
twelve  to  fourteen  sporozoites  (or  sporoblasts),  which  rather  resemble  vermi- 
cules, but  differ  by  being  more  globular  and  having  a  short  oval  nucleus. 
These  sporozoites  escape  into  the  lumen  of  the  gut  of  the  tick. 

Whether  these  bodies  are  sporozoites  or  sporoblasts  is  not  known;  neither 
is  it  known  how  they  get  into  the  dog  so  as  to  complete  the  cycle  of  sporogony. 
In  other  words,  there  is  a  great  gap  in  the  cycle  of  sporogony  at  this  point. 

Haemogregarina  bovis  Marfoglioand  Carpano,  1906. 

lti  Bos  taunts  in  Abyssinia.  The  parasites  are  7  to  10  /n  in  length,  and 
1-5  to  2  fj.  in  breadth,  and  possess  rounded  ends. 

Haemogregarina  gerbilli  Christophers,  1905. 

Found  in  the  Indian  field-rat,  Gerbillus  indicus,  in  which  it  produces  only  a 
little  anaemia.  It  lies  in  cysts  in  enlarged  pale  blood  corpuscles  as  a  vermicule 
with  a  bent  tail,  and  has  a  median  nucleus  and  some  chromatin  dots.  In  the 
louse  Hcematopinus  s'.ephensi,  the  parasite  has  been  described  as  escaping  from 
its  "cyst  and  becoming  a  free  vermicule,  which  gets  in  the  ccelome,  and  there 
in.  j  sts  and  becomes  a  large  oocyst,  growing  up  to  350  fx  in  diameter.  This 
oocyst  divides  into  numerous  sporoblasts,  which  contain  six  to  eight  crescentic 
sporozoites.  These,  when  free,  appear  as  sausage-like  bodies,  15  by  4  fi 
with  a  distinct  nucleus. 

There  is,  however,  some  doubt  as  to  whether  these  cysts  are  really  developed 
from  the  haemogregarine. 

Haemogregarina  jaculi  Balfour,  1905. 

Synonym. — H.  balfouri  Laveran,  1905. 

This  parasite  has  been  found  in  the  jerboa  (Jaculus  gordoni)  at  Khar- 
toum, and  in  /.  orientalis  in  Tunis.  It  appears  as  a  pale  hyaline,  homo- 
geneous body,  with  the  narrower  end  bent  on  itself,  lying  in  a  decolourized 
erythrocyte. 

The  trophozoite  is  found  in  a  liver  cell  as  an  oblong  parasite  lying  in  a  cavity. 
This  body  can  divide  into  three  young  forms,  which  presumably  can  grow 


486  TELOSPORIDIA 

into  schizonts  in  liver  cells.     The  schizont  divides  into  a  large  number  of 
merozoites,  leaving  no  residual  mass  of  undivided  cytoplasm.     The  mero- 
zoites  probably  infect  the  red  blood  cells,  and  after  a  time  can  escape  into 
the  liquor  sanguinis  as  free  trophozoites,  and  invade  the  liver  cells. 
What  happens  to  the  free  vermicule  is  not  known. 

Haemogregarina  funambuli  Patton,  1906. 

Synonym. — Leucocytozoon  funambuli  Patton,  1906. 

This  parasite  was  found  by  Patton  in  the  large  mononuclear  leucocytes  of 
Funambulus  pennatii  (the  Kathiawar  palm-squirrel) . 

It  is  found  in  cysts  in  the  leucocytes,  and  as  free  forms  in  the  plasma.  No 
evidence  of  schizogony  could  be  found.  In  the  gut  of  the  louse  (H&niato- 
pinus  sp.)  parasitic  on  these  squirrels  vermicules  could  be  found,  and  also  in 
the  coelome,  but  no  further  development  took  place. 

Haemogregarina  ratti  Adie,  1906. 
This  is  a  haemogregarine  found  in  the  leucocytes  of  Epimys  rattus. 

Haemogregarina  felis  Christophers,  1906. 
Like  H.  canis,  only  found  in  cats.     It  was  discovered  by  Patton.     Schizo- 
gony and  sporogony  unknown. 

HiEMOGREGARINES  OF  REPTILIA. 

Haemogregarines  of  the  Crocodilia. 

H.  hankini  Simond,  100 1,  in  Gavialis  gangeticus  Gmel. ;  H.  crocodilinorum 
Borner,  1901,  in  Osteotcsmus  tetraspis  Cope,  and  in  C.  cataphoractes  Cuv. 

Haemogregarines  0!  the  Chelonia. 

A  very  large  number  of  haemogregarines  are  known  in  Chelonia,  but  the 
best-studied  life-history  is  that  of  H.  stepanovi. 

Haemogregarina  stepanovi  Danilewsky,  1889. 

H.  stepanovi  is  a  parasite  in  the  red  blood-corpuscles  of  tortoises— e.g., 
Emys  orbicularis  L.  and  Cistudo. 

It  appears  in  two  forms — one  kidney-shaped,  and  the  other  long  and  thin, 
and  bent  upon  itself. 

The  young  trophozoite  is  club-shaped,  and  grows  into  the  broad  kidney 
form,  which  in  the  bone-marrow,  liver,  or  spleen  breaks  up  into  merozoites, 
which,  escaping  from  the  red  cell,  complete  the  cycle  by  entering  new  cells. 

The  trophozoite  grows  into  a  large  oval  form,  which  elongates  until  it  gives 
rise  to  the  long  thin  form  which  is  bent  upon  itself.  If  blood  containing  this 
form  is  sucked  by  a  leech  (Placobdella  catenigera  Moqu.-Tand),  it  escapes  from 
the  corpuscle  in  the  intestine,  and,  entering  between  the  epithelial  cells, 
develops  into  a  macrogamete  or  a  microgamete,  and  forms  an  ookinete,  which 
wanders  into  the  bloodvessels  around  the  intestine,  and  so  gets  to  the  pharyn- 
geal glands,  in  which  it  becomes  an  oocyst  forming  numerous  sporoblasts  and 
sporozoites,  which  complete  the  cycle  of  sporogony  by  entering  the  tortoise, 
when  it  is  again  bitten  by  the  leech.  There  is  also  evidence  of  the  infection 
of  the  ova  of  the  leech  in  the  finding  of  sporozoites  in  the  pharyngeal  glands 
of  immature  embryo  leeches. 

Haemogregarina  nicoriae  Castellani  and  Willey,  1904. 
This  parasite  is  common  in  the  tortoises  (Nicoria  trijaga  Schweigg)  which 
are  found  in  the  ditches  and  marshy  lands  round  Colombo,  and  also  in  Colombo 
Lake.     The  young  trophozoite  grows  into  the  schizont,  which  divides  into 
merozoites. 


H.EMOGREGARTNES  OF  REPTILTA 


487 


Other  parasites  a  re :  H.  laverani  Simond ,'  1  o<>  1 ,  in  Emyda  granosa  Schoepff ; 
//.  mesnili  Simond,  1901,  in  Kachuga  tectum  Gray;  H.  billeti  Simond,  1901, 
in  Trionyx  cartilagineus  Boddert;  H.  stepanoviana  Laveran  and  Mesnil,  1902, 
ni  Damonia  recvesii ;  H.  vara  Laveran  and  Mesnil,  1902,  in  Damonia  reevesii ; 
H.  mauretania  Sergent,  1904,  in  Testudo  ibera  Pall.;  H.  bagenesis  Ducloux, 
1904,  in  Clemmys  leprosa  Schweigg.  Its  sporogony  is  said  to  occur  in  Placob- 
della  catenigera  Moqu.-Tand .  H.  vitiate  Robertson  is  Emyda  vittata  (Figs.  149, 
157,  and  158). 

Haemogregarines  of  the  Ophidia. 

The  haemogregarines  of  Ophidia  are  numerous,  but  their  life-history  has  not 
been  properly  studied.     They  have  mostly  been  described  by  Sambon. 

Haemogregarina  mirabilis  Castellani  and  Willey,  1904  (Fig.  153). 

//.  mirabilis  is  a  parasite  in  the  red  cells  of  Tropidonotus  piscator  Schn. 

The  trophozoite  is  vermicular  and  large  (12  fi),  and  stains  uniformly  blue, 
leaving  no  clear  pole.  The  nucleus  is  dense,  and  placed  near  the  anterior 
end,  and  is  enclosed  in  a  well-developed  cytocyst,  which  is  stippled  [with 
Schiiffner's  dots. 

Other  forms  are  :  — H.  pythonis 
Billet,  1895,  in  Python  reticularis 
Schn.;  H.  pococki  Sambon  and  Selig- 
mann,  1907,  in  P.  molurus  L. ;  H.  schat- 
tocki  Sambon  and  Seligmann,  1907,  in 
P.  spilotes  Lacep.;  H.  najce  Laveran. 


Fig.  157. — Hcemogregarina  vittata 
Robertson:  a  Broad  Form,  show- 
ing Peculiar  Red  Bodies. 


Fir, 


158. — Hamogregarina      vitiates 
Robertson:  Gametocyte. 


(After  Miss  Robertson.) 

m  Naja  tripiidicuis  Merr.;  H.  mocassini  Laveran,  1902,  in  Aucistrodon 
piscivorus  Pal.;  H.  crotali  Laveran,  190 1,  in  Crotalus  confluentus  ;  H.  seligmanni 
Sambon,  1907,  in  Lachesis  mutus  ;  H.  zamenis  Laveran,  1902,  in  Zamenis 
hippocrepis  L.;  H.  mansoni  Sambon  and  Seligmann,  1907,  in  Zamenis  flagelli- 
formis  L.;  //.  refringens  Sambon  and  Seligmann,  1907,  in  Pseudaspis  cana  L. ; 
Jf.  rarcfaciens  Sambon  and  Seligmann.  1907,  in  Coluber  corais  Holb.;  H.  cant- 
liei  Sambon,  1907,  in  Eryx  conicus  ;  H.  terzii  Sambon,  1907,  in  the  boa- 
constrictor;  and  many  others. 

Haemogregarines  of  the  Sauna. 

I  he  best  known  of  these  is  H .  lacertarum.  Danilewsky,  1885,  in  the  red  cells 
ol  Laccrta  muralis  Laur.,  L.  viridis  Laur.,  L.  agilis  L.,  and  L.  ocellata  Daud. 

I  In  young  trophozoite  grows  into  a  schizont,  which  is  enclosed  in  a  cyto- 
cyst,  and  which  breaks  up  into  merozoitcs  in  the  liver,  spleen,  or  kidney. 

Among  the  merozoites  there  mav  be  macromerozoites  or  micromerozoites, 

1  are  thought  to  be  precursors  of  the  macro- and  micro-gametocytcs  which 

develop  in  Ixodes  victims  L.     This  tick  mav  infect  the  lizard  in  the  adult  stage, 

though  this  must  br  rare,  as  it  usually  attacks  mammals,  and  then  only  by  its 

nymphae  and  larvae. 

A  number  are  described:  H.  thomsoni  Minchin,  1907,  in  the  Himalayan 
lizard  (Agama  tuberculata) ;  H.  schaudinni  C.  Franca,  in  Lacerta  ocellata  Daud. 


488  TELOSPORIDIA 

H.EMOGREGARINES  OF  THE  AMPHIBIA. 

The  best  studied  of  these  is  Hamogregarina  minima  Chaussat. 

Synonyms. — Drepanidium  ranarum  Lankester,  Laverania  ranarum  Grassi, 
H.  ranarum  Kruse,  Lankesterella  ranarum  Labbe. 

This  parasite  is  found  in  the  red  cells,  leucocytes,  and  tissue  cells  of  Rana 
esculenta  L. 

Schizogony  takes  place  in  the  spleen,  liver,  kidney,  and  bone-marrow,  where 
the  cytocysts  containing  round  schizonts,  which  break  up  into  five  to  eight 
macromerozoites  (5  to  8  fi)  or  numerous  micromerozoites  (3  to  4  jx). 

The  sporont  is  club-shaped,  and  sporogony  takes  place,  according  to  Billet, 
in  the  leech  (Helobdella),  but  his  account  is  very  doubtful,  and  will  require 
confirmation. 

Hintze  gives  a  quite  different  development  in  the  intestine  of  the  frog, 
but  it  is  possible  that  he  mistook  a  coccidial  parasite  for  the  sporogenic 
stages. 

Durham  notes  a  Drepanidium  (haemogregarine)  in  the  blood  of  a  toad  in 
Para,  and  a  Dactylosoma  (Labbe)  in  the  internal  organs — the  former  is  the 
schizont,  and  the  latter  the  sporont — and  found  evidences  of  conjugation  and 
cyst-formation  in  ticks  fed  on  these  toads. 

H.  splendens  Labbe,  1908,  is  found  in  Rana  esculenta  in  Portugal.  H.  lepto- 
dactyli  Lesage,  1908,  is  found  in  Leptodactylus  ocellatus  in  Argentina;  Lankes- 
terella tritonis  Fantham,  1905,  in  Triton  cris'alus. 

HiEMOGREGARINES  OF  THE  PISCES. 

Fish  of  all  kinds  and  in  all  parts  of  the  world  appear  to  contain  these  para- 
sites. 

Haemogregarina  simondi  Laveran  and  Mesnil,  190 1. 

H.  simondi  is  a  parasite  in  Solea  vulgaris  (the  sole).  Schizogony  takes 
place  in  the  red  corpuscles,  the  schizont  dividing  longitudinally  into  two,  four, 
or  eight  merozoites.  Sporogony  takes  place  in  Platybdella  solece  Kroger,  a 
leech  found  on  the  sole  in  which  ookinetes  have  been  found. 

HaBmogregarina  anarrhichadis  Henry,  1912. 

H.  anarrhichadis  is  found  in  the  catfish  Anarrhichas  lupus. 

Other  fish  heemogregarines  are:  H.  bigemina  Laveran  and  Mesnil,  190 1,  in 
Blennius  pholis,  H.  quadrigemina  in  Callionymus  lyra,  H.  platessce  Lebailly, 
19C4,  in  Pleuronectes  platessa,  H.  rovignensis  Minchin  and  Woodcock,  1910,  in 
Trigla  linen ta. 

Family  Toxoplasmidce  Franca,  1917. 

Definition. — Haemosporidia  without  haemozoin  generally  living 
in  white  cells  in  the  organs  of  vertebrates. 

Type  Genus. — Toxoplasma  Nicolle  and  Manceaux,  1908. 

Remarks. — Only  two  genera.  It  is  possible  that  some  authors 
might  place  Elleipsisoma  Franca,  1911,  and  some  allied  genera 
tin  rein.  At  present  we  have  classified  these  with  the  Piroplasmidae, 
Ovoplasma  may  also  come  here. 

Classification. — The  genera  of  the  Toxoplasmidse  may  be  recog- 
nised as  follows:— 

A.  With  a  definite  nucleus—  Toxoplasma. 

B.  Without  a  nucleus — Ovoplasma. 

Genus  Toxoplasma  Nicolle  and  Manceaux,  1908. 
Definition. — Toxoplasmidae  of  oval  or  reniform  shape,  reproducing 
by  longitudinal  division  or  by  multiple  division  inside  cells.     Live 


TOXOPLASMA 


,89 


usually  in  mononuclear  and  polymorphonuclear  cells  in  the  spleen 
an.  1  internal  organs.     Rarely  seen  in  the  blood. 

Type  Species.— Toxoplasma  gondii  Nicolle  and  Manceaux,  190S. 

Other  Species.— T.  cuniculi  Splendore,  1909,  found  in  Oryctolagus 


• 


Fig.  159. — Toxoplasma  pyrogenes  Castellani,  1913. 

cunicukts  in  Brazil,  and  T.  canis  Mello,  1910,  found  in  the  dog  in 
Italy,  Germany,  and  Brazil.  These  two  forms  and  T.  pyrogenes 
Castellani,  1913,  found  in  man  are  all  pathogenic. 

T.  talpce  Prowazek,  1910,  in  Japan;  T.  muscidi  Sangiorgi,  1913, 
in  M its  musculus  in  Italy;  T.  sciuri  Coles,  1914,  in  England;  T.  ratti 


Figs.   160-162. — Toxoplasma  pyrogenes  Castellani,  1913. 

Sangiorgi,  1915,  in  Mus  rattus  in  Italy;  T.  sp.  (?)  Plimmer,  1915,  in 
Cryptoprocta  ferox ;  T.  cavice  Carini  and  Migliano,  1916;  T.  sp.  (?) 
Theze,  1916,  in  Myceles  seniculus  arc  mammalian  parasites. 

A  number  of  forms  are  known  in  birds — e.g.,  T.  avium  Adie,  1909; 
T.  sfiorophila  (Aragao,  1911);  T.  neophrontis  Todd  and  Nolbach, 


4go  TELOSPORTDTA 

1912 ;  and  T.  franm  de  Melo,  1915 ;  with  two  unnamed  species  by 
Plimmer,  1916,  and  five  by  Carini  and  Maeiel  in  1916.  In  snakes 
one  species  unnamed  Was  found  by  Plimmer  in  1916. 

Toxoplasma  gondii  Nicolle  and  Manceaux,  1908. 

Endoleucocytic  crescentic  parasites  6  to  7  fx  by  3  to  4  fi,  found  in  the  spleen 
and  other  organs  of  Ctenodactylus  gondii. 

Toxoplasma  euniculi  Splendore,  1909. 

Found  by  Splendore  in  the  spleen  and  other  organs  of  the  rabbit,  in  which  it 
produces  lesions  resembling  kala-azar.  Shape,  oval  or  reniform;  length 
5  to  8  ju;  breadth,  2-5  to  4  fx. 

Toxoplasma  pyrogenes  Castellani,  1913. 

Definition. — -Toxoplasma  pathogenic  to  man. 

History. — Found  by  Castellani  in  1913  in  a  case  of  splenomegaly  in 
the  tropics.  In  1916  a  similar  parasite  was  found  by  Fedorovitch 
in  the  peripheral  blood  of  a  case  of  splenomegaly  in  a  child  on  the 
Black  Sea  coast,  and  also  in  the  blood  of  a  dog  from  the  same 
neighbourhood. 

Morphology. — Roundish  oval  or  crescentic  bodies  2-5-6-0  microns 
in  diameter,  with  blue  staining  cytoplasm,  and  with  one  large 
roundish  mass  of  chromatin  at  one  pole  or  in  the  centre.  In  one 
instance  the  faintest  appearance  of  a  fiagellum  seemed  to  be  present. 
Occasionally  the  bodies  Were  larger,  roundish  or  pear-shaped,  and 
possessed  two  chromatin  masses,  one  at  each  pole  or  close  together. 
The  bodies  were  generally  free,  and  only  in  one  specimen  were  a  few 
found  in  a  leucocyte. 

While  in  the  spleen  numerous  bodies  of  this  description  were  found  in  this 
case,  in  the  peripheral  blood  they  were  absent.  In  the  peripheral  blood  some 
peculiar  structures  were  observed  of  roundish  or  pyriform  appearance. 
They  were  mostly  vacuolated,  and  took  a  pale  blue  colour  with  Romanowsky, 
and  showed  several  large  masses  of  chromatin.  Castellani  at  first  thought 
that  these  might  be  related  to  Koch's  bodies  or  plasniakugd,  which  are 
roundish,  oval,  or  irregularly  shaped  cells,  8-12  microns  in  diameter,  found  by 
Koch  in  African  cattle  suffering  from  East  Coast  fever.  Koch's  bodies  were 
later  classified  under  Piroplasma  by  Gonder.  who  believed  them  to  represent 
a  stage  in  the  life-cycle  oi  Theilcria.  parva. 

Against  this  hypothesis  Castellani  observed  that  they  were  only  present  in 
the  blood  and  not  in  the  spleen,  and  the  chromatin  masses  were  much  larger 
than  those  in  typical  Koch's  bodies.  Castellani  was  inclined  to  believe  that 
these  bodies  found  in  the  blood  were  related  to  Toxoplasma  found  in  the 
spleen  in  some  similar  manner  to  that  by  which  Koch's  bodies  are  related  to 
Theilcria.  It  must  be  remembered  that  Castellani's  slides  were  examined 
by  a  number  of  protozoologists  and  medical  men,  all  of  whom  agreed 
as  to  the  parasitic  and  protozoal  nature  of  the  bodies;  but  while  the  majority 
regarded  them  to  be  Toxoplasma,  others  held  the  view  that  they  might 
represent  a  new  genus  between  Toxoplasma  and  Leishmania,  and  a  few 
thought  that  they  might  be  a  mixture  of  Toxoplasma  with  Theilcria  and 
Ann  plasma. 

Life-History. — Unknown. 

Cultivation.— So  far  not  cultivated. 

Pathogenicity. — Probably  the  eause  of  a  splenomegaly  in  man. 


OVOPLASMA  ANUCLEATUM  49t 

Genus  Ovoplasma  De  Raadt,  1913. 
Definition. — Toxoplasmic^  without  definite  nucleus. 
Remarks. — Some  doubt  has  been  thrown  upon  this  genus  and 
its  species. 

Type  Species.— Ovoplasma  anucleatum  De  Raadt,  1913. 

Ovoplasma  anucleatum  De  Raadt,  1913. 

Definition. — Ovoplasma  ring-like,  with  large  vacuole,  found  in 
man. 

History.  -This  parasite  Was  found  in  Borneo  in  the  spleen  of  a 
Madurese  with  splenomegaly,  who  was  born  in  Java. 

Morphology. — -The  organisms  were  generally  found  in  mononuclear 
leucocytes,  though  rarely  they  Were  in  the  red  cells.  They  were 
ring-like,  with  large  vacuoles  and  without  any  nucleus,  but  the 
cytoplasm  collects  on  one  side  of  the  vacuole.  Sometimes  it  was 
pyriform . 

Life-Cycle. — It   reproduces   by   budding  and   by  binary  fission. 

Pathogenicity.— May  be  harmless,  but  in  certain  cases  pathogenic. 

Family  Piroplasmidce  Franca,  1909. 

Definition. — Haemosporidia  without  haemozoin  living  in  red  blood- 
corpuscles. 

Classification. — Paraplasma  Seidelin,  1911,  is  the  resultant  of 
certain  blood  conditions,  and  is  not  a  parasite.  Globidium  Neumann, 
1909,  and  Immanoplasma  Neumann,  1909,  require  further  investi- 
gation. 

The  following  genera  can  be  differentiated: — 

1.  Piro plasma  Patton,  1895. 

2.  Smithia  Franca,  1909. 

3.  Nuttattia  Franca,  1909. 

4.  Theileria  Bettencourt,  Franca,  and  Borges,  1907. 

5.  Achromaticus  Dionisi,  1900. 

6.  Rangelia  Carini  and  Maciel,  1914. 

7.  Rossiella  Nuttall,  1910. 

8.  Elleipsisoma  Franca,  1910. 

9.  Nicollia  Nuttall. 

10.  Anaplasma  Theiler,  1910. 

11.  Bartonella  Strong,  Tyzzer,  Brues,  Sellards,  and  Gastia- 

buru,  1915. 

A.  Cytoplasm  voluminous  : — 

I.  Rounded  forms  in  red  cells  with  circular  nucleus. 
Schizogony  by  binary  division  inside  red  cells. 
Division  may  continue  and  form  a  number  of  large 
merozoites — -Rossiella. 
II.  Oval  forms  in  red  cells,  which  they  dehaemoglobinize. 
Nucleus  large  at  one  side  of  parasite.  Schizogony  in 
the  lung — Elleipsisoma. 


4M2  TELOSPORIDIA 

B.  Cytoplasm  easily  visible  : — -    - 

I.  Schizogony  known:— 

(a)  Large    pear-shaped    solitary    forms.     Numerous 

merozoites — Achromaticus. 

(b)  Small  oval  or  pear-shaped  forms,  often  in  pairs, 

30-100  merozoites — Rangelia. 
II.  Schizogony  unknown: — 

(a)  Division  in  pairs — Piroplasma. 
(6)  Division  in  fours: — 

r.  Nucleus  without  dimorphism — 

(a)  Pear-shaped  swollen  parasites  occupying 

the  whole  breadth  of  the  corpuscle — 
Smithia . 

(b)  Small  oval  forms,  no  bacillary  forms — - 

Nuttallia. 

(c)  Bacillary  forms — Theileria. 

2.  Nucleus  with  dimorphism — Nicollia. 

C.  Cytoplasm  usually  invisible  :—  . 

'  I.  Coccus-like  bodies  found  in  animals — -Anaplasma. 
II.  Rounded  and  rod-like  bodies:— 

Extremity  small,  and  found  in  man  in  Oroya  fever — 
Bartonella. 

Genus  Piroplasma  Patton,  1895. 

Synonyms. — Hcematococcus  Babes,  1888  {non  Agardh) ;  Pyrosoma 
Smith  and  Kilborne,  1893  {non  Peron);  Ixodioplasma  Schmidt,  1904; 
Apiosoma  Von  Wandollek,  1875  {non  Blanchard,^i855);  Babesia 
Starcovici,  1893;  Amxbosporidium  Bonome,  1895. 

Definition.— Piroplasmidse  living  inside  red  cells,  without  volu- 
minous, but  with  easily  visible,  cytoplasm,  not  possessing  any  pig- 
ment, and  multiplying  by  division. 

Type  Species. — Piroplasma  bovis  (Babes,  1888). 

Classification. — There  are  a  number  of  species. 

A.  In  bovines  : — 

1.  P.  bovis  (Babes,  1888),  spread  by  Bodphilus  annulatus, 

B.  australis,  and  B.  decoloratus — America,  Australia, 
Asia,  and  Africa. 

2.  P.   divergens  MacFadyean  and   Stockman,   spread   by 

Ixodes  ricinus — Europe. 

B.  In  sheep  :■ — 

3.  P.  ovis  Starcovici,  1893,  spread  by  Rhipicephalus  bursa — 

Europe. 

C.  In  dogs  :— 

4.  P.    canis   Piana    and    Galli-Valerio,   1895,    spread   by 

Rhipicephalus  sanguineus — everywhere . 

D.  In  horses  : — 

5.  P.  caballi  Nuttall,  1910 — Europe. 


PIROPLASMA   CAN  IS  493 

E .  In  rodents  : — 

6.  P.  muris  Fantham,  1905 — -England. 

7.  P.  aviculavis  Wenyon,  1908— Sudan. 

F.  In  monkeys  : — - 

8.  P.  pithed  P.  H.  Ross,  1905 — -Uganda. 

Piroplasma  canis  Piana  and  Galli  Valerio,  1895. 

Synonym. — Babesia  canis  Piana  and  Galli  Valerio,  1895. 

In  1895  Piana  and  Galli  Valerio  found  a  characteristic  haematozoon  in  the 
red  blood -corpuscles  of  a  dog  which  was  infested  by  ticks  (Ixodes  reduv'.us  L.), 
and  which  was  suffering  from  fever,  weakness,  and  slight  jaundice,  after 
having  hunted  in  marshy  localities.  This  haematozoon  occupied  3  to  4  per 
cent,  of  the  corpuscles,  and  also  occurred  free  in  the  plasma.  In  the  cor- 
puscles the  parasites  appeared  as  pyriform  bodies,  as  many  as  two,  three,  four, 
or  five  in  one  corpuscle,  and  showed  amoeboid  movement.  The  dog  in  question 
recovered,  but  in  other  dogs  the  post-mortem  showed  fluid  blood,  congested 
liver  and  spleen,  with  icteric  staining  of  the  tissues  and  necrotic  foci  in  the 
omentum  near  the  pancreas.  Other  symptoms  noted  by  them  in  dogs 
were  haemoglobinuria,  anorexia,  prostration,  and  emaciation. 

In  1899  Hutcheon  described  the  disease  caused  by  this  parasite  as  '  malig- 
nant jaundice  '  or  '  bilious  fever  '  in  dogs.  It  is  also  known  as  '  malignant 
malaria,'  '  hondziekte,'  and  '  malarial  fever,'  and  is  said  to  have  often  been 
mistaken  for  distemper.  The  disease  is  by  no  means  uncommon  in  dogs  in 
the  tropics,  and  should  be  called  '  cannie  piroplasmosis.' 

Geography. — It  is  known  in  Europe,  especially  in  Lombardy  and  other 
parts  of  Italy;  also  in  France.  In  Africa  it  is  found  in  South  Africa,  East 
Africa,  Senegal,  and  other  parts  of  West  Africa,  and  also  in  North  Africa, 
including  Egypt.  Nuttall  suggests,  however,  that  the  African  Piroplasma  may 
be  different  from  the  European.     In  Asia  it  is  found  in  India  and  Ceylon. 

Place  and  Season. — It  appears  to  be  more  common  in  coast  towns  and 
districts,  and  less  common  in  higher  inland  places.  It  seems  to  have  a 
seasonal  variation,  but  this  is  not  properly  understood. 

The  Parasite. — The  life-cycle  in  the  dog  has  been  most  carefully  studied  by 
Nuttall  and  Graham-Smith. 

In  the  fresh  blood  it  is  noted  that  the  infected  corpuscles  are  pale  and 
enlarged,  and  contain  irregular,  dark-coloured,  pear-shaped  bodies,  possessing 
a  central  refractive  portion.  Amoeboid  or  globular  non-motile  bodies  may 
be  noted,  and  also  many  free  forms. 

In  specimens  stained  by  Leishman's  method  the  parasites  seem  to  consist 
of  a  blue-coloured  cytoplasm,  with  a  delicate  vacuolated  or  trabecular  struc- 
ture centrally,  but  more  condensed  around  the  periphery.  This  cytoplasm 
may  <  ontain  a  single  homogeneous  nucleus,  which  has  a  vivid  red  colour,  and 
is  often  connected  by  a  thin  strand  with  a  loose  mass  of  chromatin,  which  is 
situated  near  the  blunt  end.     The  parasite  contains  a  vacuole. 

Schizogony. — A  free  pyriform  parasite  (pyriform  stage)  enters  a  normal 
red  blood-corpuscle  and  becomes  rounded  (ring  stage)  in  shape,  while  the 
loose  mass  of  chromatin  is  drawn  near  to  the  original  nucleus,  where  it  con- 
denses.    Finally  it  fuses  with  that  nucleus,  forming  a  single  chromatin  mass. 

The  x^arasite  now  throws  out  pscudopodia  and  appears  as  an  amoeba 
(amoeboid  stage),  and  the  chromatin  subdivides  into  two  unequal  masses, 
connected  with  a  thin  strand. 

This  amoeboid  stage  lasts  for  a  long  time,  at  the  end  of  which  the  parasite 
enters  upon  a  quiescent  stage,  in  which  the  vacuole  appears  in  a  subcentral 
position,  and  the  chromatin,  which  lies  along  its  margin,  has  its  two  masses 
widely  separated,  though  still  connected  by  the  thin  strand  already  referred 
to.  The  smaller  mass  has  divided  into  two,  malting  in  all  three  masses  of 
chromatin  connected  together  by  chromatin  strands. 

Two  small  symmetrical  processes  of  cytoplasm  protrude  from  the  parasite 


494 


TELOSPORIDIA 


in  the  neighbourhood  of  the  two  small  chromatin  masses,  which  they  carry 
with  them. 

The  processes  enlarge  at  the  expense  of  the  rest  of  the  cytoplasm,  and  the 
vacuole  divides,  and  the  so-called  trefoil  stage  is  reached,  in  which  the  main 
mass  of  the  chromatin,  much  reduced  in  size,  lies  at  the  base  of  the  two 
processes. 


Fig.  163. — Diagram  of  the  Life-Cycles  of  Piroplasma  canis. 
(After  Nuttall  and  Graham-Smith,  Christophers,  and  Breinl  and  Kinghorn.) 
1-12*,    Reproduction  by  simple  division;   a-a,   reproduction   by  multiple 
division;  A-F,  development  of  a  flagellate  form;   12V-25,  sporogony  in  the 
tick. 


The  single  strand  connecting  the  two  smaller  chromatin  particles  has 
shortened  and  disappeared,  so  that  the  strand  of  each  small  mass  now  rises 
directly  from  the  principal  chromatin  mass.  This  now  divides  into  two 
nuclei,  connected  by  a  strand,  while  the  cytoplasmic  processes  become  large. 
Finallv,  the  cytoplasm  divides,  and  two  pyriform  parasites  are  found  lying 
side  by  side  in  one  corpuscle,  an  arrangement  considered  typical  of  a  piroplasma. 

In  each  parasite  is  a  vacuole,  and  a  principal  chromatic  nucleus  situated 


PIROPLASMA    CAN  IS  495 

near  the  pointed  extremity,  from  which  a  tail  of  loose  chromatin  runs  along- 
side the  vacuole  towards  the  blunt  extremity. 

The  corpuscle  now  ruptures  and  liberates  the  two  parasites  and  some 
granules,  representing  residual  matter,  from  the  parasite  or  the  corpuscle, 
or  both. 

Two  slight  variations  of  the  process  have  been  described  by  Nuttall  and 
Graham-Smith;  in  one  the  two  nuclei  and  their  strands  form  an  hourglass- 
shaped  mass,  and  in  the  other  the  strand  and  second  nucleus  form  a  reticular 
mass;  but  both  develop  into  the  stage  depicted  in  the  diagram.  Four 
pyriform  parasites  may  be  found  in  a  corpuscle  instead  of  two,  and  this  may 
come  about  by  an  invasion  of  the  corpuscle  by  two  pyriform  shapes,  which 
proceed  to  division,  or  by  the  division  of  the  uninuclear  shape  into  two, 
both  of  which  proceed  to  develop  regularly.  Reproduction  by  gemmation 
with  the  formation  of  one  or  two  buds  has  been  described  by  Breinl  and 
H  indie,  and  of  many  buds  by  Kinoshita. 

Flagellate  Forms. — Nuttall  and  Graham-Smith  in  1905  described  large  forms 
in  the  blood  of  the  first  dog  which  they  infected  in  Cambridge  by  ticks  from 
South  Africa.  These  forms  were  found  on  the  fourth,  fifth,  and  tenth  days, 
and  occurred  in  the  peripheral  blood  and  in  that  from  a  kidney.  They 
wen-  sausage-shaped,  with  rounded  or  tapering  extremities.  In  some  the 
chromatin  was  almost  entirely  concentrated  in  the  middle,  while  in  others  it 
appeared  to  be  of  loose  texture.  Kinoshita  has  seen  similar  parasites  in 
blood  from  the  heart,  the  pancreas,  and  the  lungs  after  death.  The  significance 
of  these  parasites  is  not  yet  understood. 

Free  parasites  with  flagella-like  processes  have  been  seen  by  Pound,  Bowhill, 
Le  Doux,  Nuttall  and  Graham-Smith,  Kinoshita,  Fulleborn,  and  Breinl  and 
Hindle,  the  last-mentioned  observers  describing  the  development  of  large 
biflagellate  forms  from  the  normal  intracellular  parasite. 

The  significance  of  these  forms  is  not  understood,  Breinl  and  Hindle 
considering  that  they  are  such  very  transient  stages  in  the  life-history  that 
they  may  easily  be  overlooked. 

The  development  as  given  by  Breinl  and  Hindle  is  associated  with  a 
binuc  leafed  form. 

Cultivation. — Kleine,  Nuttall,  and  Graham-Smith  have  attempted  to  culti- 
va.te Babesia  cams  in  defibrinated  blood.  Kleine  has  observed  elongated  forms 
with  radiating  processes,  similar  to  those  found  by  Koch  in  ticks. 

Nuttall  and  Graham-Smith  have  observed  the  same  forms,  but  consider 
them  to  be  intracellular,  the  haemoglobin  having  nearly  disappeared  from 
the  red  cells. 

Inoculation. — It  was  first  shown  by  Dr.  Corrington  Purvis  in  1900  that  the 
disease  could  be  spread  from  dog  to  dog  by  blood  inoculation. 

Infection  from  Tick-Bites. — Piana  and  Galli  Valerio,  when  they  discovered 
the  parasite  in  1895  in  Italy,  suspected  that  it  was  transmitted  by  the  tick 
Ixodes  rcduvius  L.,  but  the  first  actual  demonstration  that  this  really  took 
place  was  by  Loundsbury  in  190 1,  by  the  bites  of  the  tick  Hcemophy •salts 
Icacln  Audouin,  in  South  Africa. 

Dermacentor  reticularis  Fabr.  is  suspected  as  the  spreader  of  the  disease  in 
France. 

This  subject  has  been  carefully  investigated  by  Loundsbury,  who  finds 
that  the  parent  tick,  having  gorged  with  blood,  falls  to  the  ground  and  lays 
her  eggs,  which  develop  into  six-legged  larvae. 

These  larvae  do  not  infect  the  dog,  which  they  attack  as  soon  as  possible, 
and  on  whom  they  remain  two  days  sucking  blood.  After  dropping  off, 
thej  in  due  time  shed  their  larval  skin,  and  become  eight-legged  nymphs, 
ir  bit<   1  he  dog,  but  do  not  infect  it. 

rhe  nymph,  alter  dropping  off,  undergoes  metamorphosis,  and  sheds  its 
nymphal  skin  and  becomes  the  sexually  mature  tick,  which  is  the  only  form 
that  spreads  the  infection,  a  fact  confirmed  by  Nuttall. 

Christophers  has  traced  out  the  development  in  Eurhipicephalus  sanguineus 
Latrcille,  thus  finally  confirming  the  idea  of  the  transmission  through  the 
tick. 


496  TELOSPORIDIA 

Development  in  the  Tick. — When  an  adult  tick  or  a  nymph  bites  a  dog 
and  takes  in  blood  containing  the  oval  parasites  already  described,  these 
parasites  develop  in  the  gut  into  round  or  oval  bodies,  4  to  5  fj.  in  diameter, 
the  chromatin  remaining  undisturbed . 

The  cytoplasm  now  partially  divides  into  a  portion  with  and  a  portion 
without  chromatin,  the  latter  turning  round  to  form  a  tail  to  the  former, 
thus  constituting  a  club-shaped  body,  which  gradually  becomes  an  ookinete. 

In  the  adult  these  wander  into  the  ova,  while  in  the  nymph  they  simply  pass 
into  the  embryonic  tissue. 

In  either  case  they  become  rounded,  and  form  the  zygote,  which  breaks 
up  into  sporoblasts,  and  these,  again,  into  sporozoites,  which  infect  the  salivary 
glands  of  the  nymph  and  the  adult  of  the  second  generation .  This  development 
explains  Loundsbury's  experiments. 

Pathogenicity. — The  pathological  effects  are  divided  by  Nocard  and  Le- 
clainche  into  two  types — the  acute,  always  fatal,  and  the  subacute,  ending  in 
recovery. 

Acute  Form. — In  the  severe  attack  the  dog  quickly  becomes  ill  with  high 
fever  (400  C),  accompanied  with  great  weakness.  After  the  attack  of  fever 
comes  a  stage  of  subnormal  temperatures.  The  mucous  membrane  becomes 
pallid,  bluish,  or  icteric.  Respiration  is  laboured,  and  the  movements  of  the 
animal  are  shaky.  Vomiting  is  frequent.  The  spleen  is  enlarged,  the  urine 
albuminous,  and  in  3*5  per  cent,  of  cases  there  is  haemoglobinuria.  The  blood 
is  pale  and  watery,  and  the  serum  stained  with  haemoglobin  or  bile  pigments ; 
the  red  corpuscles  are  reduced  (in  one  dog,  according  to  Wright,  from 
5,800,000  to  1,000,000)  and  altered,  some  becoming  larger,  others  smaller, 
than  normal,  and  often  nucleated.  The  haemoglobin  is  diminished,  the 
smallest  amount  observed  being  17  per  cent.  Usually  the  leucocytes  are 
increased  up  to  even  60,000,  but  in  some  cases  they  are  reduced.  Poly- 
morphonuclear and  mononuclear  leucocytes  share  the  general  increase. 
Phagocytosis  is  not  energetic,  being  rarely  met  with.  The  animal  dies  in 
from  three  to  six  days. 

Subacute  Form. — This  is  characterized  by  progressive  anaemia  and  feeble- 
ness, with  sometimes  a  little  haemoglobinuria  or  a  little  icterus.  Fever  may 
at  first  be  high,  but  generally  falls  to  normal.  The  anaemia  is  very  pro- 
nounced, and  is  accompanied  with  paralysis,  etc. 

The  attack  lasts  six  weeks,  and  the  convalescence  takes  three  months. 

Post-Mortem  Appearances. — The  mucous  membranes  are  pale,  and  there  is 
icteric  staining  of  the  tissues.  Congestion  and  enlargement  of  the  spleen, 
more  rarely  of  the  liver,  oedema  of  the  lungs,  congestion  of  the  kidneys, 
and  inflammation  of  the  stomach  and  intestines  may  be  noted,  but  some- 
times no  macroscopical  lesions  are  to  be  seen. 

Histological. — The  capillaries  of  the  alveoli  are  dilated,  and  their  walls 
show  some  proliferation  of  the  cells,  and  there  may  be  leucocytes  and  red 
corpuscles  in  the  lumen  of  the  air  cell. 

In  the  heart  the  capillaries  are  dilated,  and  there  may  be  slight  haemorrhages. 
There  is  no  change  in  the  skeletal  muscles.  The  liver  has  the  central  vein 
and  the  interlobular  capillaries  much  dilated,  as  are  the  intralobular  vessels. 
The  fibrous  tissue  is  normal,  but  the  liver  cells  are  distorted,  and  in  many 
cases  destroyed.  The  spleen  contains  a  large  quantity  of  blood  in  its  pulp. 
The  kidneys  only  show  dilatation  of  the  bloodvessels,  especially  those  of  the 
glomeruli.  The  suprarenal  capsules  have  all  the  capillaries  (cortex  and 
medulla)  dilated,  as  has  the  pancreas.  In  the  brain  and  spinal  cord  there  is 
only  slight  dilatation  of  the  capillaries,  and  slight  excess  of  cerebro-spinal 
fluid.  In  the  small  intestine  the  vessels  of  the  villi  are  congested  and  crowded 
with  infected  corpuscles,  as  are  those  of  the  mesentery  and  omentum.  The 
lymphatic  glands  are  normal,  except  dilatation  of  their  smaller  vessels.  The 
general  histological  condition  is  engorgement  of  the  organs  by  dilatation  of  the 
capillaries. 

Treatment. — Quinine,  benzoate  of  soda,  calomel,  etc.,  have  all  been  advised. 
Nuttall  and  Hadwen  have  introduced  Trypanbleu  treatment  with  success. 


PIROPLASMA  BIGEMINUM  497 


Piroplasma  gibsoni  Pattern,  1910. 

This  Piroplasma  has  been  found  in  dogs  and  in  the  jackal  (Cants  aureus)  in 
India  by  Patton. 

Morphology. — In  films  from  the  peripheral  blood  it  is  seen  as  small  rings 
<>*i  f.i  in  diameter,  with  one  or  two  chromatin  masses,  of  which  the  second 
is  much  smaller  than  the  first,  to  which  it  is  often  joined  by  a  pink  thread. 
(  hal  parasites,  with  a  long  amoeboid  process,  are  also  seen. 

Division. — Division  is  by  binary  fission,  giving  rise  to  a  number  of  forms 
enclosed  in  one  leucocyte. 

Pathogenicity.  —It  causes  one  variety  of  canine  piroplasmosis. 

Piroplasma  bigeminum  Smith  and  Kilborne,  1893. 

Synonyms. — Pyrosoma  bigeminum  Smith  and  Kilborne,  1893;  Apiosoma 
bigeminum  W&ndollek;  Babesia  bovis  Chauvelot;  Ixodioplasma  specificum  bovum 
Schmidt. 

P.  bigeminum  is  the  cause  of  Texas  fever  in  oxen,  and  appears  as  pyriform, 
round,  or  amoeboid  cells,  and  also  as  flagellate  forms.  It  can  be  cultivated 
on  artificial  media. 

Koch  has  traced  the  development  in  the  tick,  in  whose  gut  the  parasites 
leave  the  red  cell  and  become  long  and  club-shaped,  at  the  broad  end  of  which 
is  found  a  round  chromatin  mass.     From  the  club  pseudopodia  project. 

This  club  then  becomes  spherical,  and  immense  numbers  of  amceba-like 
forms  appear,  which  are  said  to  grow  into  clubs. 

Pathogenesis. — The  disease  may  exist  in  two  forms,  a  grave  and  a  benign. 

The  usual  symptoms  of  high  fever,  haenioglobinuria,  icterus,  anaemia, 
paralysis,  constipation,  and  death  in  a  week  or  less,  are  exhibited  in  the  grave 
form,  in  which  the  mortality  is  60  to  80  per  cent. 

In  the  benign  form  there  is  anaemia  Avithout  haemoglobinuria  as  a  rule, 
and  the  duration  is  about  fourteen  days. 

The  disease  can  be  spread  by  inoculation  or  naturally  by  the  bites  of  in- 
fected ticks — Margaropus  australis  Fuller  in  South  America,  Cuba,  Porto 
Rico,  Australia,  and  the  Philippines,  and  by  M.  decoloratus  Koch  in  South 
Africa. 

Post-Mortem. — The  usual  post-mortem  signs  are  visible. 

Treatment. — There  is  no  specific  treatment.  Kragerud  advises  intravenous 
injections  of  1  in  100  of  protargol  or  formol,  and  afterwards  a  beverage  of 
10  grammes  of  lysol  and  carbolic  acid  in  500  grammes  of  distilled  water. 

Lignieres  recommends  chloride  of  sodium  and  purgatives.  Quinine  has 
also  been  advised.     Nuttall  and  Hadwen's  treatment  should  be  tried. 

Piroplasma  bovis  Babes,  1888. 

Synonyms. — Piroplasma  annulatum  Dschunkowsky  and  Liihe,  1888,  Piro- 
plasma bigeminum  Babes,  Hcematococcus  bovis  Babes. 

P.  bovis  is  the  cause  of  red  water  or  hsemoglobinuric  fever  in  European  cattle 
and  in  red  deer  (Cervus  elaphus  L.),  and  is  spread  by  the  tick  Ixodes  reduvius  L. 
and  Margaropus  annulalus  Say. 

The  disease  produced  may  be  acute  or  chronic.  In  the  acute  form  about 
90  per  cent,  of  the  red  cells  are  infected  by  bacillary  or  ring-like  parasites, 
which  cause  high  fever,  quick  pulse  and  respirations,  seldom  haemoglobinuria, 
with  convulsions  and  death  in  one  or  two  weeks;  or  a  chronic  form,  with 
minute  coccus-like  parasites  in  10  to  40  per  cent,  of  the  red  cells,  producing 
weakness,  jaundice,  and  anaemia.  The  post-mortem  shows  haemorrhages 
into  many  organs. 

Piroplasma  ovis  Babes,  1880. 

Synonyms. — Il&matococcus  ovis  Babes,  Piroplasma  ovis  Law-ran,  Amoeba- 
sporidium  polyp hagam  Bonome. 

P.  ovis  is  found  in  sheep  in  Europe,  Africa,  and  the  West  Indies,  as  large 
intracorpuscular  and  extracorpuscular  forms,  and  causes  anaemia,  haemoglo- 

32 


4q8  TELOSPORIDIA 

binuria,  hematuria,  and  bile  in  the  urine,  and  also  blood  in  the  motions.     The 
mortality  is  50  per  cent. 

The  post-mortem  shows  oedema  of  the  tissues,  enlargement  of  the  spleen, 
inflammation  of  the  liver,  kidney,  and  bowels,  in  the  last  of  which  there  may 
be  ulcers. 

The  Piroplasma  is  spread  by  the  daughter  adult  tick  developed  from  the 
Eurhipicephalus  bursa,  which  sucked  the  infected  blood.  It  is  inoculable 
into  other  sheep. 

Piroplasma  pitheci  P.  H.  Ross,  1905. 

This  organism  caused  piroplasmosis  in  a  species  of  Cercopithecus  from  Kikuga, 
in  Uganda. 

The  parasite  is  a  non-pigmented ,  pear-shaped,  oval,  or  round  endocor- 
puscular  body,  being  1*5  /n  in  diameter  when  round,  and  3  by  2  fi  to  2*5  by 
1*5  [X  in  the  pyriform  shapes.  It  may  be  single,  double,  or  in  multiples  of  two, 
four,  eight,  or  sixteen. 

Nuttall  and  Graham-Smith  have  investigated  the  parasite  carefully,  and 
conclude  that  it  is  a  true  Piroplasma,  and  multiplies  in  the  same  manner  as 
P.  canis  ;  and  they  figure  one  body  in  a  corpuscle  very  like  the  peculiar  free 
forms  noted  in  P.  canis. 

Ross  tried  inoculation  into  dogs  twice,  but  though  one  of  the  dogs  showed 
a  temporary  rise  of  temperature,  the  experiment  failed.  No  ticks  were  found 
on  the  monkeys,  or  in  the  box  in  which  they  lived.  The  disease  causes  fever, 
and  killed  four  out  of  twelve  monkeys. 

Piroplasma  muris  Fantham,  1906. 
P.  muris  causes  a  chronic  disease  in  mice,  in  which  it  exists  as  pyriform 
intracorpuscular  parasites,  singly  and  in  pairs  (as  many  as  four  and  six  have 
been  seen).     The  secondary  mass  of  chromatin  has  not  been  observed,  and 
no  typical  dividing  forms  have  yet  been  seen. 

Piroplasma  cervi  Franca  and  Borges,  1907. 
This  Piroplasma  is  found  as  bacillary  and  cross  forms  in  the  blood  of  Cervus 
darna  L.     Its  development  is  not  known. 

Piroplasma  minense  Yakimoff,  1909. 
Found  in  Russia  in  hedgehogs,  and  spread  by  Dermatocentor  reticnlatus  (?). 

Piroplasma  aristotelis  Denier,  1907. 
This  parasite  is  found  in  Cervus  aristotelis  in  Annam. 

Genus  Theileria  Bettencourt,  Franca,  and  Borges,  1907. 

Synonym. — Lymphohcematocytozoon  Meyer,  1913. 

Definition. — Bacilliform  or  rod-shaped  forms  arranged  at  times  in  the  form  of 
a  cross. 

Type  Species. — Theileria  parva  Theiler,  1903. 

Theileria  parva  Theiler,  1903. 

Synonyms. — Piroplasma  theileri,  Babesia  parva  Theiler,  1903 ;  Lympholicemato- 
cytozobn  parvum  Meyer,  1913. 

This  is  the  cause  of  East  Coast  fever  in  cattle  in  Rhodesia,  and  is  also  found 
in  India  and  Japan. 

Parasite. — The  parasite  appears  in  the  blood  as  minute  bacillary  forms 
or  as  small  rings,  which  later  become  larger,  and  give  the  typical  pyriform 
appearance,  being  frequently  arranged  in  the  form  of  a  cross.  Very  large 
forms,  consisting  of  protoplasmic  masses  containing  numerous  chromatin 
particles,  may  be  found  in  the  endothelial  cells  of  the  spleen  and  lymphatic 
glands. 

Schizogony.— According  to  Gonder,  the  large  multinucleated  plasmodial 
masses  divide  into  minute  merozoites,  and  lead  to  the  breaking  up  of  the 
enclosing  lymphocyte.     The  merozoites  penetrate  into  another  lymphocyte 


THEJLERTA    PARVA 


499 


in  the  spleen  or  lymphatic  glands,  in  which  they  grow  and  become  the  multi- 
nucleated masses,  and  so  complete  the  process  of  schizogony. 

Sporogony. — After  a  time  merozoites  are  produced  with  a  different  nuclear 
structure;  these  multiply  and  produce  the  gametocytes,  which,  penetrating 
into  the  red  blood  cells,  appear  in  the  peripheral  circulation.  The  micro- 
gametocytes  are  the  bacillary  forms,  and  the  rounded  or  pear-shaped  forms 
are  the  macrogametocytes.  In  Eurhipicephalus  these  come  out  of  the 
corpuscles,  and  the  male  forms  creep  about  like  little  amoeba?,  while  the 
nucleus  undergoes  reduction,  forming  the  microgamete.  In  a  similar  manner 
the  macrogamete  is  formed.  Copulation  takes  place,  and  a  zygote  in  the 
form  of  an  active  ookinete  is  formed,  which  enters  the  salivary  glands  and 
breaks  up  into  sporozoites. 


Fig.  164. — -Life-Cycle  of  Theileria  parva  (Theiler,  1903). 
(After  Gonder,  from  the  Report  of  the  First  Expedition  of  the  Harvard  School 
of  Tropical  Medicine  to  South  America  in  1913.) 

It  is  spread  by  Eurhipicephalus  append iculatus  Neumann,  by  the  nymphs 
and  the  adults. 

Cultivation. — Miyajima  states  that  he  has  cultivated  the  parasite  in  broth, 
producing  trypanosome-like  bodies,  but  this  has  not  been  confirmed. 

Inoculation. —  It  cannot  be  inoculated  successfully. 

Incubation. — Fourteen  days. 

Symptoms.— The  symptoms  produced  arc  very  similar  to  those  caused  by 
mil  but  there  is  very  little  anaemia  and  no  haemoglobinuria. 

Mortality.— The  mortality  is  about  90  per  cent. 

Post-Mortem. — The  autopsy  shows  oedema  of  the  lungs,  inflammation  of 
the  lymphatic  glands,  and  infarcts  in  the  lungs,  liver,  and  kidneys. 

Theileria  mutans  Theiler,  1907. 

Synonym. —  Piroplasma  mutans  Theiler,  1907. 

This  Piroplasma  is  found  along  with  P.  bigemina,  in  cattle  in  the  Transvaal, 
and  produces  forms  like  Theileria  parva,  but  distinguished  by  being  inoculable, 
It  is  not  known  how  it  is  spread. 


500  TELOSPORIDIA 

Theileria  cellii  Castellani  and  Chalmers,  1910. 
This  parasite  is  found  in  Macacus  pileatus  in  Ceylon,  in  bacillary  and  pear- 
shaped  forms,  lying  side  by  side  in  the  same  erythrocyte.     The  development 
has  not  been  traced. 

Theileria  buffali  Neveu-Lemaire,  191 2. 
This  parasite  was  discovered  by  Shein  in  1908  in  the  buffalo  in  Nha-Trang 
in  Indo-China,  and  is  seen  in  two  forms— an  ovoidal,  which  is  most  frequently 
met  with,  and  a  bacillary.     Its  mode  ol  transmission  is  unknown. 

Genus   Nieollia  Nuttall. 

Definition. — Oval  or  pear-shaped  parasites,  with  an  oval  nucleus  with  two 
karyosomes,  one  near  the  centre  and  another  close  to  the  surface  of  the  body, 
with  quadruple  division. 

Nieollia  quadrigemina  Nicolle,  1907. 
This  parasite  is  found  in  Ctenodactylns  gondii  in  North  Africa,  and  Nuttall 
and  Graham-Smith  point  out  that  its  method  of  division  and  its  chromatin  are 
so  peculiar  that  its  position  is  doubtful. 

Genus   Nuttallia  Franca,  1909. 
Definition. — Oval  or  pear-shaped  parasites  with  multiplication  in  the  form 
of  a  cross. 

Type  Species. — Nuttallia  equi  Laveran,  1899. 

Nuttallia  herpetedis  Franca,   1908. 
N.  herpetedis  is  found  in  considerable  numbers  in  Herpestes  ichneumon  L., 
the  mongoose,  as  small  spheres,  with  the  chromatin  arranged  as  a  cross,  or 
as  pyriform  shapes,  or  in  fours  arranged  in  cross  form. 

Nuttallia  equi  Laveran,   1899. 

Synonym. — Piroplasma  equi  Laveran,  1899. 

Nuttallia  equi  is  the  parasite  of  piroplasmosis  in  horses,  mules,  donkeys,  and 
zebras  in  Africa,  Germany,  Italy,  and  Venezuela. 

The  disease  appears  to  have  been  first  differentiated  by  Wiltshire,  in  1883, 
as  anthrax  fever,  which  name  was  changed  to  biliary  fever  by  Hutcheon. 
The  parasite  was  first  seen  by  Guglielmi,  in  Italy,  in  1899. 

It  differs  from  P.  canis  in  existing  in  large  and  small  spherical  forms,  in 
large  and  small  pyriform  shapes,  in  large  and  small  rod-like  bodies,  in  rosettes 
of  four,  and  sometimes  as  free  flagellate  forms.  Koch  believes  that  this  list 
includes  two  different  types  of  parasite — one  of  parasites  arranged  in  groups 
of  four,  and  the  other  like  P.  canis. 

It  is  very  difficult  to  inoculate,  and  is  believed  to  be  spread  by  the  blue 
tick  (Eurhipicephalus  decolor atus) . 

The  incubation  period  is  not  known.  The  disease  begins  with  high  fever, 
but  becomes  subnormal  before  death.  The  appetite  varies.  The  animal  is 
very  weak,  and  in  the  later  stages  becomes  paralytic  and  comatose.  Anaemia 
and  jaundice  are  noted.  The  pulse  varies,  being  often  weak  and  irregular. 
The  respirations  are  accelerated.  Bowels  often  constipated;  urine  is  highly 
coloured,  and  haemoglobinuria  may  occur.  The  disease  may  be  acute  or 
chronic. 

In  acute  cases  death  may  take  place  in  from  two  to  five  days,  but  the 
mortality  is  not  high.     Secondary  and  terminal  infections  may  take  place. 

The  post-mortem  reveals  emaciation  and  icteric  staining,  and  anaemia  of 
the  tissues,  enormous  enlargement  of  the  spleen,  and  thin,  watery  blood. 
The  liver  is  yellow  and  congested;  the  kidneys  are  enlarged  and  anaemic; 
the  lymphatic  glands  are  haemorrhagic,  as  may  be  the  mucosa  of  the  intes- 
tines,     the  heart  is  sometimes  enlarged.     The  lungs  are  usually  normal. 

Other  species  are  N .  ninensis  Yakimoff,  1910,  in  Erinaceus  curopceus;  N.  muris 
Coles,  1914;  N .  decumani  Macfie,  1915;  A',  microti  Coles,  191  \. 


ANAPLASMA  501 

Genus  Smithia  Franca,  19m. 

Definition. —  Pear-shaped  forms,  not  in  pairs,  occupying  the  whole  diameter 
of  the  corpuscles.     Forms  crosses. 

Type  Species. — Smithia  microti  Franca,  1910. 

Other  Species.  —  In  addition  to  Smithia  microti  Franca,  iqio,  found  in 
Microtus  arvalis,  there  is  5.  talpce  Galli-Valerio,  1913,  in  Talpa  europaa. 

Genus  Anaplasma  Theiler,  1910. 
Definition. — Coccus-like  parasites,  round  or  oval  in  form,  apparently  con- 
sisting  wholly  of  chromatin,  and  devoid  of  cytoplasm.     Flagellate  forms  said  to 
exist. 
-Dias  and  Axagao  consider  these  organisms  to  be  degenerations  of  red  cells. 
Type  Species. — Anaplasma  marginale. 

Anaplasma  marginale  Theiler,  1910. 

Coccus-like  parasites  situated  near  the  margin  of  the  corpuscles. 

Morphology. — -Round  or  oval  parasites  consisting  only  of  chromatin  sub- 
stance, sometimes  situated  in  a  paler  zone  of  the  corpuscle.  Multiply  rapidly, 
and  invade  40  to  50  per  cent,  of  the  corpuscles. 

Life-History. —It  is  spread  by  the  ticks  Eurhipicephalus  decoloratus  and 
/■'.  simns,  and  possibly  passes  through  the  egg. 

Cultivation.— Vegha  claims  to  have  cultivated  this  organism  on  defibrinated 
blood  media. 

Pathogenicity.— It  causes  a  disease  like  red  water,  but  different  therefrom 
in  that  animals  immune  against  red  water  are  susceptible  to  it.  Clinically, 
it  causes  a  severe  type  of  illness,  with  fever,  anaemia,  and  diarrhoea,  with 
yellow  faeces  and  urine.  The  blood  shows  anisocytosis,  poikilocytosis,  poly- 
chromasia,  and  basophilia.  The  post-mortem  appearances  are  anaemia  with 
jaundice,  enlarged  and  yellow  liver,  inspissated  bile,  and  enlarged  spleen. 

Anaplasma  marginale  var.  centrale  Theiler,  1912. 
Like  A.  marginale,  but  situate  towards  the  centre  of  the  cell.     Type  of 
illness  milder  than  the  above  form. 

Anaplasma  canis  Basile,   1912. 

Cocci-like  forms  and  crescent-shaped  bodies  free  and  enclosed  in  cor- 
puscles found  in  peripheral  blood,  liver,  spleen,  and  lungs  of  dogs  around 
Messina.  Large  form  4-9  by  2-3  fi  observed,  provided  with  a  flagellum 
measuring  5  (x. 

Pathogenicity. — Causes  canine  anaplasmosis. 

Genus  Aehromaticus  Dionisi,  1898. 

Definition. — Piroplasmidtz  with  easily  visible  but  not  voluminous  cytoplasm, 
sickle  shaped,  pyriform  or  rounded.  Schizogony  in  red  cells.  Many  mero- 
zoites.     Large  solitary  parasites. 

Type  Species. — A.  vesperuginis  Dionisi,  1898. 

Aehromaticus  vesperuginis  Dionisi,  1898. 
This  parasite  was  found  by  Dionisi  in  the  nocrule  in  189S.  Sambon  classifies 
it  as  a  Piroplasma,  but  this  is  doubted  by  Nuttall  and  Graham-Smith,  as  well  as 
by  I » lonisi,  though  they  report  pyriform  endocellular  parasites  from  blood  films 
trom  hats  of  the  genus  Vesperugo,  and  Nuttall  and  Graham-Smith  report  four 
pyrifonn  parasites  in  a  corpuscle.  Gonder,  however,  believes  that  it  is  in  some 
intermediate  position  between  thePlasmodidaeand  the  Piroplasma,  and  Nuttall 
and  Graham -Smith  consider  that  further  investigations  are  necessary  before 
it  can  be  classified.  We  agree  with  Gonder,  and  consider  the  parasite  to 
be  neither  a  Piroplasma  nor  a  plasmodium,  and  therefore  return  to  Dionisi's 
original  idea  of  a  separate  genus.  Recently  it  has  been  studied  by  YakimofI, 
Stolnikolf,  and  Kohl- YakimofI,  who  believe  that  it  is  a  true  Piroplasma. 
Another  species  is  A .  gibsoni  Patton,  1910. 


502  TELOSPORIDIA 

Genus  Rangelia  Carini  ancbMaciel,  1914. 

Definition. — Piroplasmidse,  often  in  pairs,  \Vith  rounded,  oval,  or 
pyriform  appearance,  with  easily  visible  cytoplasm.  Schizogony  in 
endothelial  cells  in  internal  organs.     Merozoites  very  numerous. 

Type  Species,— Rangelia  vitalli  Pestana,  1910. 

Rangelia  vitalli  Pestana,  1910. 
This  is  the  cause  of  a  disease  in  dogs  in  Brazil  called  nambiavii. 

Genus  Rossiella  Nuttall,  1910. 

Definition.- — Piroplasmidse  of  unusual  type,  with  voluminous 
cytoplasm,  not  pigmented;  rounded  form  and  rounded  nucleus, 
which  is  not  peripherally  placed.  Schizogony  in  red  cells,  division 
first  into  two  and  subsequently  in  more  merozoites. 

Type  Species. — Rossiella  rossi  Nuttall,  1910. 

Rossiella  rossi  Nuttall,  1910. 
Parasite  of  Canis  adustus  in  Africa. 

Genus   Elleipsisoma  Franca,  1910. 

Definition.-  -Piroplasmidse  of  unusual  type,  with  voluminous 
cytoplasm,  not  pigmented;  living  in  red  blood  cells  which  become 
dehsemoglobinized.     Schizogony  in  the  lungs. 

Type  Species. — Elleipsisoma  thomsoni  Franca,  1910. 

Elleipsisoma  thomsoni  Franca,  1910. 
Parasite  of  Talpa  euro  pee  a  and  T.  cceca. 

Genus  Bartonella  Strong,  Tyzzer,  Brues,  Sellards,  and  Gastiaburu, 

I9I5- 

Definition. — -Piroplasmidse  with  rounded  or  rod-shaped  dividing 
forms,  sometimes  in  chains;  reproduction  by  binary  division, 
cytoplasm  and  chromatinic  substance  often  differentiated  with 
difficulty.     Motile.     Habitat,  red  blood-corpuscles. 

Type  and  Only  Species. — Bartonella  bacillifonnis  Strong,  Tyzzer, 
Brues,  Sellards,  and  Gastiaburu,  1915. 

Bartonella  bacilliformis  Strong,  Tyzzer,  Brues,  Sellards,  and 
Gastiaburu,  1915. 

Definition. — Bartonella  with  the  characters  of  the  genus. 

History. — In  1901  and  1902  Barton  found  an  organism  in  Oroya 
fever  which  Tamayo  and  Gastiaburu  identified  as  belonging  to  the 
paratyphoid  group. 

In  1905  Barton  described  bacillary-like  bodies  in  the  red  cells  of 
persons  suffering  from  malignant  fever.  In  1909  he  noted  these 
bodies  in  fourteen  additional  cases,   and  stated   that  they  Were 


BARTONELLA  BACILLI  FORM  IS 


5o3 


protozoa,  and  probably  the  cause  of  the  disease.  In  the  same  year 
Gastiaburu  and  Rebagliati  confirmed  these  findings  and  regarded 
the  organism  as  the  cause  of  Oroya  or  Carrion's  fever.  In  1915 
Strong,  Tyzzer,  Brues,  Sellards,  and  Gastiaburu,  confirmed  and 
enlarged  these  discoveries  and  named  the  parasite. 

Morphology. — -In  fresh  blood-films  the  parasite  appears  as  a 
rounded  or  rod-shaped  body,  0-5-1-0  microns  in  diameter  in  the 
former  case,  and  1-5-2-5  microns  in  length  in  the  latter.  They  are 
very  abundant  in  severe  cases,  and  are  endowed  with  a  definite 
motility  which  is  totally  distinct  from  pedesis.  They  glide  slowly 
about  the  cell.  Sometimes  a  dot  or  bead-like  body  can  be  seen  at 
the  two  poles. 


Fig.   165. — Life-Cycle  of  Bartonella  baccilliformis  Strong,  Tyzzer,  Brues, 
Sellards,  and  Gastiaburu,   1915. 

(Constructed  from  the  illustrations  in  the  Report  of  the  First  Expedition  of  the 
Harvard  School  of  Tropical  Medicine  to  South  America  in  191 3.) 

When  stained  they  are  seen  to  be  slightly  curved,  and  to  be 
present  as  single  individuals,  pairs,  or  in  chains  of  three  to  five. 
V  and  Y  forms  are  not  uncommon,  and  are  considered  to  represent 
dividing  forms.  Cross  forms  are  rare,  and  due  to  organisms  being 
superimposed. 

The  ends  of  the  rods  are  more  intensely  coloured  than  the  rest 
of  the  organism. 

Some  forms  are  rounded,  oval,  or  almost  pyriform.  As  many  as 
ten  parasites  may  be  found  in  a  single  cell,  which  they  apparently 
destroy. 

Life-Cycle.— They  are  also  to  be  found  in  large  swollen  endothelial 
cells,  free  or  attached  to  the  vessel  Wall,  in  the  spleen  and  the  lymph 
glands.  An  endothelial  cell  may  be  so  distended  with  rounded  and 
rod-shaped  parasites  as  to  occlude  a  vessel.  In  these  cells  the  para- 
site, when  coloured  by  Giemsa's  stain,  appears  as  rounded  bodies, 
composed  of  bluish  cytoplasm  and  containing  small  granules  of 
chromatin,  which  vary  in  number  from  one  to  many,  and  it  is  sug- 


5<H 


TELOSPORIDIA 


gested  that  the  parasite  breaks  up  into  a  large  number  of  minute 
elements,  each  of  which  possesses  a  chromatin  granule.  These 
elements  grow  and  become  rods,  which  are  set  free  by  rupture  of 
the  enclosing  sphere,  and  so  fill  the  endothelial  cells,  from  which 
they  escape  also  by  rupture.  The  rods  are  looked  upon  as  gameto- 
cytes,  rather  than  merozoites,  and  are  considered  to  be  the  forms 
seen  in  the  red  cells. 

Comparison.— The  organism  is  believed  to  resemble  Theileria 
parva. 

Inoculations.— Attempts  to  transmit  the  parasite  to  inoculated 
animals  failed.     The  animals  used  were  rabbits  and  monkeys. 

Cultivation. — So  far  the  organism  has  not  been  cultivated. 

Transmission  by  Insects.— Experiments  have  been  performed  with 
the  mosquito  Phalangomyia  debilis  Dyar  and  Knab,  but  no  evidence 
of  the  presence  of  the  parasites  in  the  stomach  or  salivary  glands 
could  be  obtained. 

Pathogenicity. — -It  is  believed  to  be  the  causal  agent  of  Oroya  fever. 

Family  Plasmodidae  Luhe,  1906. 

Synonyms. — Gymnosporidia  Labbe,  1894;  Acytosporidia  Wasie- 
lewski,  1896;  HcemammbidcB  Ross,  1899;  Acytosporea  Minchin,  1903. 

Definition.- — Haemosporidia  with  haemozoin.  The  trophozoite 
grows  into  the  schizont,  containing  haemozoin,  which  breaks  up  into 
a  number  of  merozoites,  which  are  usually  said  never  to  be  flagellate. 
The  ookinete  encysts  and  forms  a  typical  oocyst,  which  breaks 
up  eventually  into  sporozoites. 

Classification. — The  genera  of  the  Plasmodidae  are :  Plasmodium 
Marchiafava  and  Celli,  1885;  Laverania  Grassi  and  Feletti,  1889; 
Hcemocystidium  Castellani  and  Willey,  1904. 

These  genera  may  be  distinguished  as  follows: — 

A.  Size  large.     Schizogony  binary  or  at  times  quaternary,  in 

general  circulation — Hcemocystidium. 

B.  Size  small.     Schizogony  into  more  than  four  merozoites- — 

I.  Without  crescent  bodies— Plasmodium. 
II.  With  crescent  bodies — Laverania. 

Genus  Plasmodium  Marchiafava  and  Celli,  1885. 

Synonyms. — Oscillaria  Laveran,  1881 ;  Hcematomonas  Osier,  1887 ; 
Hcematophyllum  Metchnikoff,  1887;  Hamamceba  Grassi  and  Feletti, 
1889;  Laverania  Grassi  and  Feletti,  1889;  Cytamccba,  DanileWski, 
1890;  Proteosoma  Labbe,  1894;  Hamosporidium  Lewkowicz,  1897; 
Cytosporon  Wasielewski,  1901. 

Definition. — Plasmodidae,  in  which  the  gametocytes  resemble  more 
or  less  the  schizonts  by  being  round  in  shape.  Schizogony  in  the 
peripheral  blood. 

Nomenclature. — Some  remarks  are  perhaps  necessary  on  the 
nomenclature.  Laveran  first  used  the  term  Oscillaria  because  he 
saw  the  flagellate  form,  which  at  that  time  was  thought  to  be  a 


PLASMODIUM  505 

Polymitus  form  because  of  its  flagella.  Later  Laveran  repudiated 
this  term,  which,  indeed,  could  not  be  used,  because  it  had  already 
been  applied  to  a  plant.  He  then  suggested  the  term  '  hgematozoon,' 
but  this  is  objectionable,  because  the  haematozoa  are  a  group  of 
parasites,  and  not  a  single  genus.  Metchnikoff  suggested  the  term 
HcematophvUum  malaria,  which  is  equally  impossible;  therefore  the 
earliest  distinctive  term  is  '  plasmodium'  which  Was  used  by 
Marchiafava  and  Celli  in  1885. 

It  is  not  a  good  term,  because  a  plasmodium  is  generally  con- 
sidered to  be  a  mass  of  protoplasm  with  several  nuclei  representing, 
not  one  single  animal,  but  several. 

General  Account. — -The  malarial  parasites  may  be  taken  as  the 
typical  examples  of  the  Plasm odidae. 

The  malarial  parasite  exists  in  nature  outside  the  human  body 
in  certain  species  of  different  genera  of  the  family  Anophelinas, 
a  type  of  mosquito  which  is  somewhat  easily  identified  by  its 
habit  of  projecting  at  almost  right  angles  from  the  surface  on  which 
it  stands.  In  the  salivary  glands  of  infected  insects  the  malarial 
parasites  are  found  as  fine  fusiform  bodies,  about  10  to  20  f.i  in  length, 
and  1  to  2  fi  in  breadth,  lying  in  the  cells  or  in  the  duct.  These 
fusiform  bodies  are  called  sporozoites,  and  consist  of  cytoplasm 
containing  a  central  nucleus  composed  of  chromatin. 

The  ends  of  the  parasite  are  pointed,  one  being  sharper  than  the 
other.  They  are  capable  of  movement  forwards,  and  of  flexion  into 
loops  or  curves.  It  may  be  that  the  sporozoites  represent  male, 
female,  and  indifferent  parasites,  or  they  may  not;  the  question 
is  still  undecided. 

When  inoculated  into  man  by  a  mosquito,  they  penetrate  into  the 
red  blood  cells,  and  develop  into  small  endo-corpuscular  parasites 
called  the  trophozoites,  which  at  first  are  composed  of  cytoplasm  and 
a  nucleus. 

This  young  trophozoite  grows,  throwing  out  pseudopodia  for  the 
purposes  of  nutrition,  and  presently  a  vacuole  appears,  converting 
the  small  parasite  into  a  ring  form,  which,  according  to  Schaudiim, 
is  of  benefit  in  enabling  it  to  absorb  nutriment  quickly. 

The  vacuole  does  not  keep  pace  with  tlie  growth  of  the  parasite, 
and  finally  in  the  old  form  disappears.  Early  in  the  ring  forms 
there  appear  granules  of  a  black  pigment,  which  used  to  be  called 
melanin,  but  which  has  by  no  means  the  chemical  characteristics 
"i  true  melanin,  as  will  be  described  under  Malaria.  This  pigment 
has  been  named  by  Sambon  '  haemozoin  ' — a  name  which  appears  to 
us  to  be  peculiarly  suitable,  and  will  therefore  be  used  in  this  work. 
It  is  really  of  an  excrementitious  nature.  The  fully-grown  tropho- 
zoite now  ceases  to  be  amoeboid,  and,  becoming  rounded  off  and 
lull  of  pigment  granules,  is  called  the  schizont,  which  has  a  subcentral 
nucleus.  This  nucleus  now  divides,  so  that  parasites  may  be  seen 
with  two,  three,  four,  five,  six,  up  to  twenty-four  nuclei.  The 
cytoplasm  around  these  nuclei  segments  into  small  bodies  called 
merozoites,   each   with   a   nucleus,   but   an  unsegmented  portion 


506  TELOSPORIDIA 

containing  the  hsemozoin,  and  called  the  residual  mass,  or  nucleus 
de  reliquat,  is  always  left  unsegmented. 

The  blood-corpuscle  now  breaks  up,  and  the  merozoites,  residual 
protoplasm,  and  pigment  are  liberated  into  the  blood  stream, 
where  the  effete  matter  and  some  merozoites  are  taken  up  by  the 
leucocytes  and  destroyed. 

The  merozoite  usually  tries  to  enter  a  red  blood  cell  and  to  start 
again  as  a  trophozoite,  thus  completing  a  cycle  in  the  blood  of  the 
human  being  who  is  acting  as  host.  This  cycle  is  called  the  cycle 
of  Golgi,  or  schizogony.  Sometimes  more  than  one  merozoite  will 
enter  a  cell,  thus  giving  rise  to  multiple  infection.  In  such  a  case 
they  are  generally  of  the  same  age,  but  this  is  not  invariable.  In 
the  red  cell,  under  these  conditions  of  multiple  infection,  some 
observers  have  thought  that  the  young  trophozoites  might  con- 
jugate; but  this,  together  with  the  suggestion  of  further  division 
of  the  merozoite,  We  believe  to  be  incorrect,  though  it  must  be 
admitted  that  forms  with  a  double  nucleus  can  be  seen.  When 
such  a  binucleate  form  is  seen  nowadays,  it  makes  the  observer 
think  seriously  of  a  possible  flagellate  origin,  and  inclines  him  to 
support  Sambon  and  Hartmann's  classification,  but  never,  as  far 
as  We  know,  has  anyone  seen  a  flagellate  merozoite  in  human 
malaria. 

.  It  will  be  seen  that  in  going  through  the  process  of  schizogony 
one  sporozoite  becomes  several  merozoites,  and  that  each  of  these 
may  again  become  several  merozoites,  so  that  the  infection  grows 
unless  kept  in  check  by  phagocytosis,  and  perhaps  chemical  action 
cr  quinine  treatment. 

Each  parasite  means  a  red  cell  destroyed  and  so  much  toxin 
liberated  into  the  blood  stream.  Hence  in  a  certain  number  of 
days  (eight  to  twelve,  as  a  rule)  the  parasites  will  have  increased  to 
such  a  degree  that  their  collective  toxins,  acting  upon  the  organs  of 
the  body,  upset  the  metabolism  and  produce  an  attack  of  fever. 
This  period  of  eight  to  twelve  days  is  the  incubation  period  of  the 
disease. 

It  is  possible  that  all  the  sporozoitcs  develop  into  schizonts,  and 
there  is  at  present  no  evidence  that  they  develop  into  male  or 
female  forms  directly.  If  they  do  not  do  this,  then  the  merozoites 
must  differentiate  sexually;  for  in  about  a  Week  male  and  female 
fonns  can  be  seen  in  the  blood  stream,  and,  moreover,  very  young 
stages  can  be  observed. 

The  earliest  form  of  a  sexual  parasite  is  like  an  ordinary  merozoite, 
but  it  grows  very  slowly,  and  it  never  possesses  a  vacuole,  and  as  it 
grows  its  protoplasm  becomes  heavily  pigmented  and  granulated  in 
the  female,  and  lighter  and  clear  in  the  male.  The  result  is  to  produce 
a  female  type  of  parasite  called  the  macrogametocyte,  or  a  male 
type  of  parasite,  the  microgamctocyte.  So  that  there  are  three 
types  of  parasite — the  indifferent  or  schizont,  the  female,  and 
the  male. 

The  macrogametocyte  is  characterized  by  possessing  a  small, 


PLASMODIUM 


507 


more  or  less  rounded  nucleus  excentrically  placed  and  poor  in 
chromatin,  and  a  cytoplasm  full  of  granules  and  pigment. 

The  microgametocyte  is  characterized  by  having  a  large  nucleus 
extending  like  a  band  across  the  cytoplasm,  and  much  chromatin, 
a  clear  protoplasm,  and  less  pigment. 

The  macrogametocyte  and  microgametocyte  are  the  means  of 
propagating  the  parasite  in  the  mosquito,  and  if  they  fail  to  reach 
the  gut  of  this  insect  the  microgametocytes  die  off. 

The  macrogametocytes,  on  the  other  hand,  are  extremely  per- 
sistent, and  can  wait  in  the  body  for  a  long  time  until  some  chill 
or  accident  lowers  its  resistance,  when  they  become  active  and 
develop  merozoites  by  parthenogenesis,  thus  accounting  for  the 
relapses  and  the  recurrences  of  malaria,  even  months  and  years 


Fig.  166. — Schizogony  in  Plasmodium 
vivax  (Grassi  and  Feletti,  1890). 
(X  1,000  Diameters.) 

(By  Norman;  given  us  by  J.J.  Bell.) 


Fig.  167.— Oocyst  in  Stomach  of 
Anopheline  Mosquito.  (X  1,000 
Diameters.) 

(By  Norman,  from  a  preparation 
by  James.) 


after  having  left  a  tropical  country.  Hence  in  malaria  there  is  a 
latent  phase  which  is  capable  of  lasting  an  unknown  time — -at  least 
one  to  three  years,  perhaps  longer;  but  upon  this  subject  more 
will  be  said  later,  and,  indeed,  more  information  is  urgently  needed. 

In  developing  parthenogenetically,  the  nucleus  of  the  macro- 
gametocyte divides  into  two  portions,  one  rich  and  the  other  poor 
in  "chromatin.  The  pigment  granules  gather  round  the  pale  nucleus, 
and  with  it  the  surrounding  cytoplasm  and  haemozoin  form  a  sort 
of  nucleus  de  rcHqitat.  The  rest  of  the  protoplasm,  rendered  clearer 
by  loss  of  its  haemozoin,  contains  the  nucleus  rich  in  chromatin, 
which  now  divides  like  the  nucleus  of  a  schizont,  and  forms  mero- 
zoites, which,  escaping  from  the  red  cell,  infect  red  corpuscles,  and 
start  the  cycle  of  schizogony  anew. 

Etheogenesis  is  unknown  in  the  malarial  parasite. 

If  a  female  mosquito  (the  male  does  not  suck  blood)  belonging  to 


5o8 


TELOSPORIDIA 


certain  of  the  genera  of  the  Anophelinae  sucks  the  blood  of  a 
person  in  whom  both  macro-  and  micro-garnet ocytes  are  to  be 
found,  a  new  cycle  is  started  in  that  mosquito.  This  cycle  is 
sporogony,  which  is  characterized  by  being  a  sexual  process. 
Changes  now  appear  in  the  macro-  and  micro-gametocyte,  which 
are  thought  by  Schaudinn  to  be  brought  about  by  the  alteration  in 
temperature. 

The  macrogametocyte,  escaping  from  its  red  cell,  undergoes 
reduction  by  division  of  its  nucleus  once  or  twice,  forming  polar 
bodies.     The  reduced  garnet ocyte  is  now  called  the  macrogamete. 

Similarly  the  microgametocyte  Undergoes  changes,  for  chromidial 
masses  separate  from  its  nucleus  and  travel  to  the  periphery  of 
the  parasite,  from  which  thin  threads  of  protoplasm  now  project. 


-•  "* 


«• 


T~-i«*L*fej 


Fig.  168. — Sporocysts  in   Stomach  of  Anopheline  Mosquito.     (X  1,000 

Diameters.) 

(By  Norman,  from  a  preparation  by  James.) 

These  threads,  which  vary  from  four  to  six  in  number,  lash  about 
vigorously,  moving  the  whole  parasite,  which  therefore  whirls  about, 
and  it  and  its  processes,  called  flagella,  were  looked  upon  as  a 
polymitus;  hence  this  stage  is  often  called  the  polymitus  stage. 

The  threads  break  off,  and  are  now  called  microgametes.  Each 
microgamete  is  composed  of  a  long,  tapering  thread  of  protoplasm 
capable  of  bending  and  moving  rapidly.  Its  chromatin  is  spread 
along  it  in  dots  or  bars,  and  hence  the  whole  structure  somewhat 
resembles  a  spirochete,  but  there  is  no  undulating  membrane. 

A  microgamete  now  conjugates  with  a  macrogamete,  the  male 


PLASMODIUM 


509 


and  female  pronuclei  fusing  to  form  a  synkaryon,  and  the  resulting 
zygote  is  called  an  ookinete.  This  zygote  elongates,  and  its  anterior 
extremity,  which  is  more  or  less  clear  of  hamozoin,  becomes  pointed; 
the  nucleus  lies  in  the  middle,  and  the  posterior  end  contains  most 
of  the  pigment,  which  may  be  largely  cast  off  or  may  be  retained. 

It  now  pierces  the  epithelium  of  the  mosquito's  stomach,  below 
which  it  comes  to  rest,  and  forms  a  thin  cyst-wall,  and  is  called  the 
oocyst.     This  now  grows  rapidly,  and  its  nucleus  divides  into  a  large 


Fig.  169. — Diagram  of  the  Life-Cycle  of  Plasmodium  vivax  (Grassi 

AND    FELETTl),    IN   MAN  AND    THE    ANOPHELINE    MOSQUITO. 


number  of  daughter  nuclei,  around  each  of  which  the  protoplasm 
gathers,  forming  the  sporoblasts,  which  are  somewhat  connected 
together  (Fig.  169). 

The  nucleus  of  each  sporoblast  now  divides  into  several  small 
nuclei.  These  travel  to  the  periphery,  which  grows  out  into  a  series 
of  small  projections,  each  of  which  takes  a  chromatin  particle  with 
it.  Each  of  these  projections  is  a  sporozoite,  so  that  each  sporoblast 
forms  a  large  number  of  sporozoites,  and  leaves  a  residual  mass  of 


5i° 


TELOSPORIDIA 


pigment  and  cytoplasm  undivided.  The  cyst,  now  enormously  en- 
larged, bursts,  and  the  sporozoites  escape  into  the  ccelome  of  the 
insect,  which  in  this  case  is  a  haemoccele.  and  therefore  they  enter 
the  blood,  and  are  carried  by  it  probably  all  over  the  insect's  body. 
Certainly  they  are  seen  in  the  thoracic  muscles,  but  finally  they 
find  their  way  to  the  salivary  glands,  and  so  to  a  new  host,  or 
according  to  Schaudinn  to  the  eggs,  and  so  probably  to  a  new 
generation  of  mosquitoes. 

Sporogony  takes  about  ten  to  twelve  days,  during  which  the 
mosquito  will  have  sucked  blood  three  or  four  times. 

Abnormal  Forms.— In  mosquitoes,  whether  infected  by  malarial 
parasites  or  by  Proteosoma,  peculiar  bodies,  called  '  black  spores  ' 
by  Ross,  are  sometimes  found  in  the  stomach  wall,  which  are  now 
known  to  be  protozoal  parasites  of  the  genus  Nosema,  Which  have 
invaded  the  oocysts,  and  are  therefore  hyperparasites. 

Cultivation. — Plasmodium  malarice,  P.  vivax,  and  Laverania 
malaria  were  first  cultivated  by  Bass, 
alone  and  with  John.  They  grow  anae- 
robically  in  blood  mixed  with  dextrose 
at  41  °  C,  but  the  blood  must  have  no 
leucocytes  if  more  than  one  generation 
is  to  be  cultivated.  The  whole  asexual 
cycle  of  P.  vivax  and  L.  malarice  has  been 
completed  in  vitro  in  the  corpuscles  of 
human  blood.  Forms  suggesting  par- 
thenogenesis were  seen. 

Animal  Hosts.  —  Although  species  of 
Plasmodium  exist  in  animals,  still  there  is 
no  evidence  that  the  human  parasites  live 
in  any  other  animal  than  man.  Fermi 
and  Lumbau  in  1912  have  tested  this 
sparrows,   owls,   quails,    and    frogs,     with 


Fig.  170.  —  An  Oocyst 
showing  Ross's  '  Black 
Spores,'  now  known  to 
be  Protozoa  belonging 
to  the  Genus  Nosema. 

(After  Grassi.) 


with    regard   to   bats, 
negative  results. 

Classification. — -A  number  of  species,  increasing  gradually,  belong 
to  this  genus,  among  which  are  two  of  the  malarial  parasites,  P.  vivax 
and  P.  malarice. 


Plasmodium  vivax  Grassi  and  Feletti,  1890  (Plate  I.). 

Synonyms. — Hcemanuxba  vivax  Grassi  and  Feletti,  1890;  H.  mala- 
rice var.  magna  Laveran,  1900;  H.  malarice  var.  tertiance  Laveran, 
1901;  Plasmodium  malarice  var.  tertiance  Celli  and  Sanfelice,  1891; 
P.  malarice  tertianum  Labbe,  1899;  Hcemosporidium  tertian um 
Lewkowicz,  1887. 

Plasmodium  vivax  is  the  parasite  of  tertian  malarial  fever,  and 
derives  its  specific  name  from  its  energetic  amoeboid  movements, 
which  probably  take  place  lor  purposes  of  nutrition. 

Its  schizogony  has  been  Well  studied  by  Golgi  and  Schaudinn. 
and  its  sporogony  by  Grassi,  Bignami,  and  Bastianelli. 

The  whole  process  of  the  schizogony  of  P.  vivax  can  be  sum- 


PLASMODIUM   VIVAX  511 

marized  as  follows: — -During  the  first  twenty-four  hours  after  the 
entry  of  the  sporozoite  or  merozoitc  into  the  red  cell  the  little 
trophozoite,  which  at  the  beginning  is  about  one-third  the  size  of 
the  erythrocyte,  grows  rapidly,  absorbing  nutriment  from  the  red 
cell  by  its  pseudopodia  and  by  the  large  surface  of  cytoplasm  ex- 
posed, owing  to  the  size  of  the  vacuole. 

Hence,  not  merely  does  it  increase  in  size,  but  it  acts  deleteriously 
upon  the  enclosing  cell,  which  loses  its  haemoglobin,  turns  pale  and 
degenerates,  as  is  evident  by  its  becoming  swollen  owing  to  the 
absorption  of  fluid,  and  by  showing,  on  staining  with  any  modifica- 
tion of  Romanowsky,  a  dotted  appearance  due  to  red  granules 
called  Schiiffner's  dots.  These  dots  can  be  seon  in  red  cells  affected 
by  other  plasmodia — e.g.,  P.  cards  in  the  dog.  In  growing,  it  gives 
rise  to  a  quantity  of  haemozoin,  which  appears  as  fine,  reddish- 
brown  granules,  often  seen  in  active  movements  due  to  currents  in 
the  cytoplasm  of  the  parasite.  In  about  thirty  hours  it  becomes 
rounded  off  as  the  schizont  (Fig.  44,  p.  294),  8-5  ^  in  diameter. 

From  the  thirtieth  to  the  forty-eighth  hour  the  fully-grown 
schizont  undergoes  sporulation,  when  it  will  be  noticed  that  fifteen 
to  twenty  merozoites  are  formed,  while  the  haemozoin  granules  are 
packed  together,  either  into  the  centre  or  towards  the  periphery  of 
the  parasite.  It  will  also  be  noted  that  the  red  cell  is  now  con- 
siderably swollen  and  almost  colourless. 

About  the  forty-eighth  hour  the  remains  of  the  corpuscle  dis- 
integrate, and  the  merozoites  (size  1-5  ^t),  haemozoin,  etc.,  escape. 

So  that  P.  vivax  occupies  forty-eight  hours  in  the  process 
of  schizogony.  As  curiosities,  it  may  be  mentioned  that  a 
trophozoite  or  a  schizont  may  be  seen  in  the  same  fed  cell  as  a 
gametocyte. 

Sporogony. — The  development  in  the  mosquito  was  first  worked 
out  in  A  nopheles  claviger. 

The  development  of  the  gametes,  and  the  fertilization  of  the 
macrogamete,  and  the  structure  of  the  ookinete,  have  been  carefully 
described  and  figured  by  Schaudinn  {vide  Figs.  45,  46,  and  47,  p.  294). 
In  about  forty  hours  after  the  mosquito  has  been  fed,  the  oocyst  can 
be  found  as  a  round  transparent  body  with  strands  of  yellowish 
haemozoin  scattered  throughout  it,  lying  in  the  stomach  wall  beneath 
the  epithelium,  and  covered  over  by  the  musculo-elastic  layer  of  the 
gut.  Its  wall  is  seen  to  be  Well  defined — -i.e.,  the  ookinete  has  become 
encysted.  By  this  time  the  chromatin  will  have  divided  into  small 
masses. 

On  the  third  day  it  will  have  become  from  one-third  to  one-fourth 
larger,  and  the  cyst- wall  will  be  more  distinct,  and  the  imperfect 
segmentation  of  the  protoplasm  around  the  nuclei  can  be  seen. 
The  haemozoin  is  seen  gathered  into  little  masses  lying  between  the 
segments  of  the  cytoplasm,  which  are  the  sporoblasts.  The  fust 
stages  of  the  formation  of  sporozoites  may  also  be  observed. 

During  the  fourth  day  the  size  increases  about  a  fourth,  and  the 
nuclei  and  their  surrounding  protoplasm  will  have  formed  some 


512  TELOSPORIDIA 

twenty  to  thirty  sporoblasts,  whose  periphery  will  be  marked  by  a 
palisade  of  forming  sporozoites. 

Between  the  fourth  and  fifth  day  the  cysts  (50  pi  in  diameter) 
full  of  sporozoites  (size  14  jy,)  will  be  seen  to  be  projecting  into  the 
ocelome. 

After  the  seventh  day  the  oocyst  ruptures,  and  the  sporozoites 
escape  and  find  their  Way  to  the  salivary  glands,  in  the  cells  of 
which  they  lie,  mainly  in  those  of  the  mid  or  poison  gland.  Thus, 
about  the  tenth  to  the  twelfth  day  after  infection  the  mosquito  is 
ready  to  spread  the  disease  by  its  bite,  and  the  cycle  of  sporogony 
is  complete.  It  must  be  remembered  that  Schaudinn  observed 
infection  of  the  mosquito's  egg,  but  whether  the  parasite  penetrates 
into  the  larva,  and  from  that  to  the  pupa,  and  thus  into  a  second 
generation,  is  not  known. 

Plasmodium  malariae  Laveran,  1881  (Plate  1.1. 

Synonyms.— Hcemamceba  malarice  Grassi  and  Feletti,  1890; 
H.  laverani  var.  quartana  Labbe,  1894;  H.  malarice  var.  magna 
Laveran,  1900;  H.  malarice  var.  quartana  Laveran,  igoi ;  Plasmo- 
dium malarice  var.  quartan-ce  Celli  and  Sanfelice,  1891;  Hcemospor- 
idium  quartance  Lewkowicz,  1897;  Plasmodium  ma'arice  quartanum 
Labbe,  1899;  P.  golgii  Sambon,  1902;  Laverania  malarice  Jannesco, 
1905"  and  Oscillaria  malarice  Laveran,  1881. 

Schizogony.— The  young  trophozoite,  which  is  smaller  than 
P.  vivax,  forms  a  compact  ring,  which  lies  in  an  unaltered  erythro- 
cyte, and  shows,  as  a  rule,  but  little  pseudopodial  activity.  Very 
soon  haemozoin  appears  in  the  form  of  dark  rodlets. 

After  the  first  twenty-four  hours  the  parasite  is  found  to  be  much 
larger,  and  the  haemozoin  more  abundant.  The  granules  of  pig- 
ment will  be  noticed  to  be  gathered  at  the  periphery,  and  to  be 
very  dark  in  colour,  and  non-motile.  The  red  cell  tends,  if  any- 
thing, to  become  smaller  and  darker.  In  about  sixty  hours  the 
trophozoite  will  have  become  the  full-grown  schizont,  which  is  a 
large,  round,  pigmented  body  surrounded  b}\a  rim  belonging  to 
the  corpuscle.  During  the  next  twelve  hours  its  nucleus  divides  up 
into  six  or  twelve  nuclei,  around  which  the  cytoplasm  gathers,  while 
the  haemozoin  is  driven  into  the  centre,  and  the  appearance  of  a 
daisy  is  produced  by  the  central  block  of  haemozoin  and  the  regular 
arrangement  of  the  merozoites  around  it  (size  6  /n). 

The  merozoites  (size  175  /li)  are  now  set  free,  and,  as  a  rule,  many 
of  them  appear  to  be  killed  off,  and  not  to  be  able  to  affect  the  red 
cells.  More  rarely  they  go  on  increasing  in  number,  and  recently 
have  been  said  to  cause  death  in  a  case  (Leislunan),  but  a  severe 
infection  is  not  usual. 

The  whole  schizogony  takes  place  in  the  peripheral  blood,  and 
occupies  seventy-two  hours. 

Sporogony. — Gametocytes  are  very  rarely  seen,  and  only  after 
the  disease  has  lasted  a  long  time,  but  Vida  has  recently  described 
all  stages  of  their  development  as  seen  in  the  peripheral  blood. 


PLASMODIUM  DANILEWSKYI  513 

They  begin  as  small  forms,  with  a  central  nucleus  but  no  vacuole, 
and  soon  become  pigmented,  the  fully-grown  macrogametocyte 
being  a  little  larger  than  a  normal  corpuscle.  Its  dark  cytoplasm  is 
heavily  pigmented,  especially  at  the  periphery,  at  which  the  nucleus 
is  also  placed.  The  corpuscle  forms  but  a  small  rim  around  the 
parasite. 

The  microgametocyte  shows  the  usual  structure  already  described, 
but  is  less  pigmented,  and  has  a  clearer  cytoplasm.  The  corpuscle 
is  not  enlarged,  as  in  the  case  of  the  macrogametocyte,  and  much 
more  of  it  is  visible  around  the  parasite.  The  formation  of  the 
microgametes  has  been  observed,  but  the  infection  of  the  mosquito 
is  difficult  to  bring  about,  though  the  development  in  the  mosquito 
has  been  traced  by  Bignami  and  Bastianelli.  The  oocyst  is  charac- 
terized by  the  pigment,  which  is  black,  coarse,  and  gathered  into  a 
clump.  The  cycle  of  development  is  the  same  as  in  P.  vivax,  but 
takes  about  eighteen  to  twenty-one  days  to  be  completed  after 
infection  in  mosquitoes  which  were  kept  at  a  temperature  of  about 
22°  C.  This  appears  to  be  the  degree  of  heat  at  Which  the  process 
takes  place  best.  At  the  end  of  that  time  the  completely  developed 
sporozoites  can  be  seen. 

Pathogenicity. — Causes  quartan  fever. 

Plasmodium  tenae  Stephens,.  1914,  is  an  extremely  amoeboid  form,  with 
scanty  cytoplasm  and  much  chromatin,  found  first  in  blood-films  from  India, 
but  known  also  in  Africa.  It  may  be  Laverania  malarice.  Plasmodium 
caucasicum  Marzinowsky,  1916,  found  on  the  Black  Sea  littoral,  may  also  be 
Laverania  malarice. 

Plasmodium  danilewskyi  Grassland  Feletti,  1890. 

Synonyms. — Laverania  danilewskyi  Grassi  and  Feletti,  1890;  Hcemamceba 
relicta  Grassi  and  Feletti,  1891 ;  Cytosporon  malarice  avium  Danilewskyi,  1891 ', 
Proteosoma  grassii  Labbe,  1894;  Plasmodium  relictum  Sergent,  1907. 

This  parasite  was  discovered  by  Grassi  in  the  blood  of  birds  in  Italy,  and 
causes  death  in  partridges  in  Hungary.  It  affects  sparrows  in  India,  and  is 
the  form  in  which  Ross  first  traced  the  development  of  a  Plasmodium  in  a 
mosquito.     It  occurs  in  Ceylon,  and  is  common  in  Africa. 

The  young  trophozoite  becomes  pigmented,  and,  displacing  the  nucleus, 
grows  into  the  schizont,  which  forms  about  nine  merozoites. 

The  macrogametocyte  has  but  little  chromatin  in  its  nucleus,  which  is 
rounded,  while  the  microgametocyte  has  an  elongated,  darkly  -  staining 
nucleus. 

These  develop  in  Culex  fatigans,  C.  nemorosus,  or  some  other  species,  when 
in  about  twelve  to  fifteen  hours  ookinetes  are  seen,  and  in  about  one  to  two 
days  well-developed  oocysts  are  present  in  the  stomach  in  the  form  of  round, 
transparent  cysts,  with  haemozoin  scattered  through  them. 

In  three  to  four  days  the  oocysts  have  increased  in  size,  and  sporoblasts 
have  appeared,  and  even  sporozoites  are  forming. 

In  nine  to  ten  days  the  oocyst  has  become  fully  developed  and  bursts, 
and  the  sporozoites  can  first  be  seen  in  the  muscles  of  the  thorax,  and  then  in 
the  salivary  glands,  in  which  they  lie  principally  in  the  central  or  poison  lobe. 
The  black  spores  already  mentioned  can  be  noted  in  the  stomach,  and,  accord- 
ing to  Stephens  and  Christophers,  in  either  the  thoracic  muscles  or  in  the 
salivary  glands. 

No  traces  of  parasites  have  been  found  in  the  larva;  or  second  generation  of 
Culex. 

33 


PLATE  I. 

THE  MALARIAL  PARASITES. 

[Coloured  by  Leishman's  Slain. 

ia — 4a.  Plasmodium  Malaria. 

icf .  Young  Trophozoite. 
2a.  Older  Trophozoite. 
3«.  Schizont. 
4«.  Sporulation. 

it — 86.  Plasmodium  Vivax. 

i b.  Young  Trophozoite. 

2b.  Older  Trophozoite,  showing  Amoeboid  Movement. 

36.  Schizont  with  single  Chromatin  Mass. 

46.  Schizont  with  three  Chromatin  Masses. 

56.  Sporulation. 

6b.  Young  Sporont. 

jb.  Microgametocyte. 

8b.  Macrogametocyte. 


ic — 4c'  Laverania  Malaria. 

ic.  Two  Young  Trophozoites. 

2c.   Sporulation. 

3c.   Macrogametocyte. 

4c.   Microgametocyte. 


PLATE    I. 


0  0"*  m    * 


* 


3« 


4a 


I* 


2b 


3* 


4^ 


* 


N  ,J*  '>-;.  1' 


*  » *         * 

'V'    ,,*     ,„, 


» »     i»» » 


5* 


6/- 


^ 


7* 


8/' 


OejWiuntcn*  Sons.  Ltd  Edirt 


MALARIAL   PARASITES. 
(Coloured  by  Leishman"s  stain.) 


4<r 


To  face  pagt  si* 


PLASMODIUM  CAN  IS 


515 


Plasmodium  kochi  Laveran,  1899. 
This   plasmodium  is   found  in  chimpanzees    (Anthropopifhecas  troglodytes 
Gm.),  and  in  monkeys  in  Africa  and  in  Ceylon;  in  the  latter  it  causes  illness 
and  death.     The  spleen  and  bone-marrow  are  found  pigmented.     It  is  said 
not  to  be  inoculable. 

Plasmodium  pitheci  Halberstaedter  and  Prowazek,  1907. 
Found  in  the  ourang-outang  {Simla  satyrus)  and  the  chimpanzee,  in  which 
the  trophozoites  resemble  P.  vivax  and  the  gametes  P.  malaria.     Schiiffner's 
dots  can  be  seen. 

Plasmodium  inui  Halberstaedter  and  Prowazek,  1907. 

In  Macacus  cynomolgus  L.  and  M.  nemestrinus  L.  It  is  like  P.  pitheci, 
but  the  haemozoin  is  in  the  form  of  fine  yellow  granules.  Merozoites,  twelve 
to  sixteen  in  number.     Schiiffner's  dots  absent. 

Plasmodium  cynomolgi  Mayer,  1907. 

In  M.  cynomolgus  L.  Merozoites,  eight  to  thirteen.  Schiiffner's  dots 
present. 

Plasmodium  bovis  Kolle,  1898. 

In  cattle  in  South  Africa,  in  which  they  produce  remittent  fever  and  severe 
anaemia. 

Plasmodium  canis  Castellani  and  Chalmers,  1910. 

This  parasite,  which  is  very  common  in  pariah  dogs  in  Ceylon,  was  discovered 
by  us  in  1908.  It  resembles  P.  vivax,  entering  the  red  cell  as  a  small  round 
merozoite,  and  growing  into  a  pigmented  plasmodium,  and  finally  dividing  into 


Fig.  171. — Plasmodium  canis  Castellani  and'Chalmers. 

i-2,  Merozoite  entering  the  corpuscle;  3,  young  trophozoite  (the  red  cell 
shows  Shiitfner's  dots) ;  4-6,  trophozoites,  enclosing  cells  showing  Shiiffner's 
dots;  7-10,  schizonts  showing  various  stages  of  nuclear  division  prior  to  the 
formation  of  the  merozoites. 

a  number  of  merozoites.  Schiiffner's  dots  are  also  present.  Fig.  171  shows 
the  schizogony  of  this  parasite,  and  Fig.  172  the  gametocytes.  The  macro- 
gametocyte  has  a  small  rounded  nucleus  and  the  microgametocyte  an  elongated 
narrowish  nucleus  extending  across  the  parasite. 


5i6 


TELOSPORIDIA 


Plasmodium  equi  Castellani  and  Chalmers,  1913. 
Found  by  us  in  a  horse  in  Ceylon.     It  closely  resembles  P.  canis. 

Plasmodium  brasilianum  Gonder  and  Gossler,  1908. 
Resembles  the  human  quartan  parasite,  but  found  in  Brachyurus  calvus  in 
Brazil. 

Plasmodium  vassali  Laveran,  1905. 

Synonym. — P.  vassali  Sambon,  1907. 

Found  by  Vassal  in  a  squirrel — Sciurus  griseimanus. 


m 

Fig.   172. — Plasmodium  canis  Castellani  and  Chalmers. 
Young  gametocyte;   2,   Macrogametocyte ;   3,   Microgametocyte. 


in    Myotis   myotis; 


Other  Forms. 

In    Mammals. — Plasmodium  murinum    Dionisi,    1 
P.  monosoma  Vassal,  1907,  in  Vesperugo  abramus. 

In  Birds. — P.  majoris,  in  Pavus  major;  P.vaughani  Novyand  MacNeal,  1904, 
in  Merula  migratoria. 

In  Lizards. — P.  diploglossi  Aragao  and  Neiva,  1900,  in  Diploglossus  jasciatus  ; 
P.  tropiduri  Aragao  and  Neiva,  1909,  in  Tropidurus  torquatus  Wied.  in  Brazil. 

Genus  Haemocystidium  Castellani  and  Willey,  1904. 

The  characters  of  this  genus  resemble  those  of  the  genus  Plasmodium,  but 
the  parasites  are  generally  larger,  and,  according  to  Dobell,  the  schizogony  is 
very  simple,  there  being  as  a  rule  binary  and  occasionally  quarternary  division, 
which  takes  place  in  the  general  circulation.  Woodcock,  however,  considers 
the  forms  which  Dobell  describes  as  binary  fission  to  be  fusion  forms  of  the 
parasites.     Pigment  present. 


Fig.  173. — Hcemocystidium  simondi  Castellani  and  Willey. 
(After  Castellani  and  Willey.) 

Haemocystidium  simondi  Castellani  and  Willey,  1904. 

1  his  parasite  was  found  in  Hemidactylus  leschenaultii  Gray  in  Ceylon. 

Other  species:  //.  metschnikowi  Simond  in  Chitrao  indica  Gray  in  India; 
H  mesnili  Bonet  in  Naja  sp.  (?)  in  West  Africa;  H.  roumei  Bonet  in  Cinnyxis 
belliana  Gray  in  Wesl  Africa;  H.  tesfudinis  Laveran  in  Testudo  partialis  in 
South  Africa;  //.  naja  Wenyon  in  Naja  haje ;  and  in  Naja  nigricollis  in 
Khartoum. 


LAVERANIA   MALA  RIM 


5i7 


Genus  Laverania  Grassi  and  Feletti,  1890. 

Definition. — Plasmodidae,  in  which  the  gametocyte  is  dissimilar 
from  the  schizont,  appearing  in  the  form  of  a  crescent.  Schizogony 
in  the  red  blood  cells  in  internal  organs. 

Laverania  malariae  Grassi  and  Feletti,  1890  (Plate  I.). 

Synonyms. — -Hcemctmceba  malaria  Laveran,  1890;  H.  prcBcox 
Grassi  and  Feletti,  1890;  H.  laverani  Labbe,  1894;  //.  immaculala 
Grassi  and  Feletti,  1891;  Plasmodium  malaria  var.  quotidians 
Celli  and  Sanfelice,  1890;  P.  precox  Doflein,  1901 ;  P.  immaculatum 
Schaudinn,  1902  ;  P.  falciparum  Blanchard,  1905 ;  Hcemomonas  prcecox 
Ross,  1899;  Hcemosporidium  undecimance  Lewkowicz,  1892;  H.  sede- 
ciiuainv  Lewkowicz,  1S92;  H.  vigesimotertiance  Lewkowicz,  1892, 
Hamatozoon  falciparum  Welch,  1897. 


C 


Fig.  i  71 . — Male  Crescent  of  Laver- 
ania malaria  (Grassi  and  Feletti 
1890).     (X  1,000  Diameters.) 

(By  Norman,  through  the  kindness  of  J.  J.  Bell.) 


Fig.  175.  —  Female  Crescent  of 
Laverania  malaria.  (X  1,000 
Diameters.) 


The  young  trophozoite  begins  as  a  very  small  parasite,  which 
quickly  forms  a  ring,  of  which  the  size  is  only  one-sixth  to  one- 
seventh  of  the  diameter  of  the  enclosing  red  cell.  This  quickly 
grows  into  an  oval  form,  which  becomes  pigmented,  while  the  en- 
dosing  crvthrocyte  in  stained  preparations  may  show  the  so-called 
Maurer's  dots,  the  significance  of  which  is  not  understood. 

The  fnlly-grown  schizont  (size  4-5  /n)  is  but  rarely  seen  in  the 
peripheral  blood,  and  the  segmentation  into  merozoites  (size  07  //,) 
—  always  takes  place  in  the  internal  organs,  when  eight  to  ten 
or  fifteen  are  formed.  When  this  is  in  progress  there  is  a  great 
tendency  for  the  red  corpuscles  to  cling  together  and  to  the  wall 
of  the  vessel,  and  hence  to  give  rise  to  obstruction  of  the  circula- 
tion, which  produces  the  perniciousness  of  the  fevers  due  to  this 
parasite. 


518  TELOSPORIDIA 

Differential  Characters  of  the  Malarial  Parasites. 


Character. 


P.  malarice. 


Schizogony 


Young  tropho- 
zoite 


Hacmozoin 

Schizont 
Merozoites 

Gametocytes 
Erythrocytes 


Completion  in 
seve  nty-two 
hours. 

Young  tropho- 
zoite, smaller 
than  P.  vivax, 
larger  than  L. 
malarice;  move- 
ments rather 
slow;  pseudo- 
podia  not 
marked  or  long. 

Granules  coarse, 
sluggish ;  peri- 
pherally  ar- 
ranged; dark 
brown. 

Smaller  than  red 
corpuscle. 

Six  to  twelve, 
regularly    ar- 
ranged   in     a 
rosette. 
Resemble  sporonts, 
but  larger. 

Almost  normal. 


P.  vivax. 


Completion  in 
forty-eight 
hours. 

Young  tropho- 
zoite, large; 
very  actively 
motile;  long 
pseudopodia. 


Granules  fine; 
m  ovement 
marked. 


Larger  than  red 
corpuscle. 

Fifteen  to  twenty, 
regularly  ar- 
ranged. 

Resemble  sporonts, 

but  larger. 
Pale  and  swollen. 


L.  malarice. 


Completion  in 
forty-eight 
hours  or  less. 

Young  tropho- 
zoite, small; 
actively  motile. 


Granules  fine  and 
scanty;  often 
motionless. 


Much  smaller 
than  red  cor- 
puscle. 

Eight  to  fifteen, 
arranged  irre- 
gularly. 

Crescentic     in 

shape. 
May  be  small  and 

dark. 


Schizogony  takes  from  thirty-six  to  forty-eight  hours  to  be 
completed. 

The  gametocytes  are  characterized  by  being  crescent-shaped  and 
large,  with  the  remains  of  the  red  cell  stretched  round  them.  The 
haemoglobin  of  the  cell  is  often  seen  lying  in  juxtaposition  to  the 
parasite,  \Vhile  the  remaining  portion  of  the  corpuscle  is  almost 
colourless. 

The  macrogametocyte  is  characterized  by  its  long  thin  shape. 

Family  H^emoproteid^e  Sambon  1906. 

Definition. — Ha?mosporidia  with  haemozoin,  but  with  ookinete  which  does 
not  encyst. 

Genus  Haemoproteus  Kruse,  1890. 

Synonyms. — Hatteridium  Labbe,  1894;  Laverania  Laveran,  1899;  Trypano- 
oma  Schaudinn,  1904;  Trypanomorpha  Leger,  1906. 

Historical. — These  parasites  were  first  described  by  Grassi  and  Feletti  in 
the  blood  of  birds  in  1890  as  Laverania,  a  term  altered  by  Labbe  in  1894  to 
Hatteridium  danilewskyi.  In  190.1  came  Schaudinn's  paper  showing  that 
they  were  stages  in  the  life-history  of  trypanosomes,  which  has  been  sup- 
ported by  the  work  of  the  Sergents,  and  has  been  severely  criticized  by  Novy. 
Mi  Neal,  Ross,  and  Thiroux,  who  believe  that  Schaudinn  made  a  mistake,  and 
that  the  flagellates  and  intracorpuscular  parasites  are  quite  distinct.     In  1908 


HAEMOPROTEUS  NOCTV.T, 


5io 


a  paper  by  Aragao  appeared  on  H.  columbce,  which  certainly  docs  not  suppi 
Schaudinn's  views;  but  in  1909  Woodcock's  researches,  as  already  mentioned, 
strongly  support  that  distinguished  protozoologist;  however,  later  researches 
have  all  tended  to  indicate  that  Schaudinn  was  wrong  and  that  his  now  cele- 
brated life-cycle  for  Hcemoproteus  noctuce  is  a  mixture  of  the  life-cycles  of  a 
haemoproteus  and  a  trypanosome.  We,  however,  at  present  still  give  Schau- 
dinn's account,  pending  confirmation  of  the  recent  work  on  the  subject. 
At  all  events,  the  question  as  to  whether  Schaudinn  was  right  or  wrong 
cannot,  impartially,  be  said  to  be  settled  one  way  or  the  other. 

Haemoproteus  noctuae  Celli  and  Sanfelice  1901. 

H.  noctnee  goes  through  the  cycle  of  schizogony  in  Glaucidium  noctuce  Retz, 
the  little  owl,  and  its  sporogony  in  Culex  pipiens  Linnaeus. 


Fig.  176. — Hcemoproteus  mansoni  Sambon,  showing  the  Development  of 

THE    GAMETOCYTES. 

(After  Sambon.) 

When  this  gnat  sucks  the  blood  of  a  little  owl  infected  with  haemoproteus, 
two  halteridial  forms  in  the  owl's  corpuscles  are  seen  to  undergo  development 
in  its  stomach.  These  two  forms  are  the  microgametocytes  and  the  macro- 
gametocytes. 

Microgametocyte.  —  The  microgametocyte  ap- 
pears as  a  typical  halteridium  parasite  enclosed 
in  an  erythrocyte,  and  possessing  pale  clear  cyto- 
plasm, with  coarse  haemozoin  granules  and  a  large 
single  nucleus,  which  is  composed  of  eight  groups, 
each  containing  trophic  and  kinetic  elements. 

Macrogametocyte. — The  macrogametocyte  as  a 
typical  halteridium,  laden  with  food  granules, 
lying  in  a  pale,  disorganized  erythrocyte.  It  has 
a  rather  small  trophonucleus,  alongside  of  which 
is  a  small  kinetonucleus. 

In  the  Mosquito. — When  these  gametocytes 
reach  the  alimentary  canal  of  Culex  pipiens,  they 
escape  from  the  erythrocytes,  and  appear  free  in 
the  lumen  of  that  canal,  and  proceed  first  to 
1  eduction  and  then  to  zygosis,  with  the  formation 
of  a  zygote. 

The  whole  process  has  been  carefully  worked 
out  by  Macallum  in  another  species  of  halteri- 
dium, and  is  confirmed  by  Schaudinn  in  the 
present  species. 

Formation  of  the  Microgametocyte. — The  micro- 
gametocyte is  a  clear  hyaline  body,  which,  on 
escaping  from  the  red  blood-corpuscles,  throws 
out  active  flagella,  which,  after  beating  about 
a  little,  break  loose,  forming  the  free  micro- 
gametes.  Schaudinn  studied  the  cytological  pro- 
cesses underlying  these  grosser  changes,  and  found 
that  the  trophonuclei  were  reduced  to  four  chro- 
mosomes, while  the  eight  kinetonuclei  remain, 
and,  separating  from  the  parent  nucleus,  form  microgametes  in  the  way 
presently  to  be  described  for  the  development  of  a  male  ookinete  into  a  male 
trypanosome. 


Fig.  177.  —  Hcemoproteus 
noctuce  Celli  and  San- 
felice. 

(After  Schaudinn.) 

On  the  left  is  the  micro- 
gamete,  and  on  the  right 
a  scheme  showing  the 
arrangement  of  the  nuclei, 
centrosomes,  undulating 
membrane,  and  myo- 
nemes. 


520 


TELOSPORIDIA 


The  Microgamete. — The  microgamete  is  very  thin,  and  tapering  at  the 
posterior  extremity,  where  it  ends  in  a  tail-like  prolongation  of  the  cytoplasm 
containing  a  portion  of  the  trophonucleus.     The  anterior  end  is  acutely  conical. 

The  trophonucleus  is  elongated  into  a  long  thread,  extending  from  the 
anterior  to  the  posterior  end  of  the  body,  and  carrying  four  chromosomes  in 
the  form  of  dots  at  regular  intervals. 


Fig.  178. — HcemopYoteus 
noclucB  Celli  and  San- 
felice:  The  Ookinete. 


Fig.   179. — Hcemoproteus  nociuce  Celli  and 
Sanfelice:  Maturation  of  the  Ookinete. 


(After  Schaudinn.) 

The  kinetonucleus  is  situate  in  the  posterior  third  of  the  cytoplasm,  and 
consists  of  a  rather  elongated  mass,  with  eight  chromosomes  and  one  intra- 
nuclear centrosome. 

In  addition  to  this  centrosome  there  are  two  others:  an  anterior,  situate 
just  at  the  base  of  the  anterior  conical  projection,  and  a  posterior,  situate 
just  anterior  to  the  tail,  being  connected  with  the  trophonucleus  by  a  chro- 
matin bar.  The  undulating  membrane  runs  from  the  anterior  to  the  posterior 
centrosome,  and  is  strengthened  by  eight  myonemes. 


Fig.  180. — Hamoproteus  noctuee  Celli  and  Sanfelice. 

(After  Schaudinn.) 

Formation  of  the  indifferent  ookinete  and  its  development  into  the 
indifferent  trypanosome. 

Formation  of  the  Macrogamete. — The  macrogametocyte  becomes  rounded 
and  ruptures  the  remains  of  the  erythrocyte,  and  is  set  free.  The  centrosome 
of  the  trophonucleus  disappears,  and  the  chromatin  forms  a  spiral  thread, 
which  separates  by  longitudinal  and  transverse  divisions  into  four  tetrads. 
The  kinetonucleus  first  forms  a  spindle,"  and  then  divides,  causing  the  first 


HMMOPROTEUS  NOCTUJE 


521 


reduction,  which  results  in  four  dyads,  and  then  a  second  division  follows, 
leaving  four  monads  or  single  chromosomes.  The  kinetonucleus  now  returns 
to  its  old  position  outside  and  close  to  the  trophonucleus,  and  the  macro- 
gamete  is  fully  developed. 

Schaudinn  was  not  able  to  trace  out  the  reduction  of  the  kinetonucleus, 
but  it  ultimately  consists  of  four  chromosomes  and  a  centrosome,  which, 
Woodcock  points  out,  are  not  wholly  sexual. 


Fig.  181. — Hcemoproteus  noctuce  Celli  and  Sanfelice. 
(After  Schaudinn.) 

Formation  of  the  male  ookinete,  and  its  development  into  the  male 
trypanosome. 

Zygosis. — This  consists  in  the  penetration  of  a  microgamete  into  a  receptive 
cone,  which  has  arisen  from  the  cytoplasm  of  the  macrogamete^on  the  side 
where  the  nuclei  are  situated. 

The  only  parts  which  enter  are  the  male  trophonucleus,  which  is  reduced, 
and  the  male  kinetonucleus,  which  is  not  reduced,  but  which  now  undergoes 
two  divisions.  The  trophonuclei  of  the  male 
and  female  elements  fuse,  and  form  the  fusion 
spindle,  at  either  end  of  which  the  kineto- 
nuclei  take  up  positions,  and  thus  the  zygote 
is  formed. 

Ookinete. — While  zygosis  is  proceeding,  and 
even  before  the  complete  formation  of  the 
synkaryon.  the  zygote  becomes  vermiform 
and  motile,  and  is  therefore  called  an  ookinete. 
It  consists  of  an  anterior,  hyaline,  change- 
able end,  which  is  followed  by  a  region  of  cyto- 
plasm with  vacuoles,  then  by  a  denser  region 
with  the  nuclear  spindle  just  described,  and 
finally  a  rounded  posterior  end,  full  of  granules 
and  hannozoin.  From  this  posterior  end  a 
portion  of  cytoplasm  enclosing  granules  and 
hacmozoin,  etc.,  is  cut  off,  thus  freeing  the 
ookinete  of  waste  material.  The  spindle  of 
the  synkaryon  now  consolidates  to  form  eight 
chromosomes,  which  will  constitute  the  tropho- 
nucleus, while  the  two  kinetonuclci  at  either 
end  of  the  spindle,  meeting  together,  form  a 
single  kinetonucleus,  which  takes  up  a  central 
position  inside  the  trophonucleus,  and  divides 
into   eight   chromosomes,    with  a   centrosome 

in  its  centre.  The  nucleus  of  the  ookinete,  therefore,  consists  of  a  central 
centrosome,  with  eight  surrounding  chromosomes,  around  which  lie  another 
eight  chromosomes,  bordering  the  periphery. 

But  ookinetes  are  not  all  alike.  On  the  contrary,  Schaudinn  describes  three 
kinds: — - 

1.  Indifferent  Ookinete. — Cytoplasm  clear,  and  staining  faintly,  with  one  or 
two  large  vacuoles  anteriorly,  and  having  some  granular  material  and  luemozoin 
still  left. 


i% 


Fig.  1S2. — H&moproteus  noc- 
tiHz  Celli  and  Sanfelice: 
Development  of  the 
Female  Ookinete  and 
the  Female  Trypano- 
some. 

(After  Schaudinn.) 


522 


TEL0SP0R1D1A 
<S7 


Fig.  183. — Diagram   showing  the   Life-Cycle   of   Hcemoproleus 

noctucB  Celli  and  Sanfelice. 

(After  Sambon  and  Terzi.) 

Many  authorities  consider  this  life-cycle  to  be  made  up  of  the  cycles  of  a 

haltendium  and  a  trypanosome,  which  are  believed  to  be  quite  distinct. 


HMMOPROTEUS  NOCTURE 


523 


2.  Male  Ookinete. — Smaller  than  the  indifferent  or  female  forms,  with 
cytoplasm  almost  hyaline,  and  much  clearer  than  that  of  the  indifferent  form, 
with  granular  material  completely  lacking,  nucleus  large,  and  rich  in  chromatin. 

3.  Female  Ookinete. — Cytoplasm  fairly  dense,  with  plenty  of  granules,  with 
a  nucleus  smaller  than  in  the  indifferent  form. 

The  Indifferent  Ookinete. — The  indifferent  ookinete  starts  its  development 
by  expelling  for  a  second  time  a  quantity  of  haemozoin,  while  its  kinetonucleus 
unites  with  the  trophonucleus,  so  that  the  nucleus  now  possesses  eight  com- 
pound chromosomes. 

The  centrosome  becomes  dumb-bell  shaped,  and  forms  an  axial  spindle, 
around  which  the  chromosomes  are  arranged.  These  now  divide,  and  form  a 
diaster  by  the  different  portions  passing  to  either  end  of  the  spindle,  which  is 
heteropolar,  the  smaller  half  being  kinetic  in  function.  The  nucleus  now 
divides  into  a  larger  portion,  the  trophonucleus,  and  a  smaller,  the  kineto- 
nucleus. The  former  enters  on  a  resting  stage,  while  the  latter  proceeds  to 
the  periphery,  and  forming  another  axial  spindle  at  right  angles  to  the  length 


Fig.  184. — Heemoproteus  noctuce  Celli  and  Sanfelice. 
(After  Schaudinn.) 

On  the  left  a  small  trypanosome  is  seen  entering  a  red  corpuscle  in  the 
blood  of  the  little  owl,  and  in  the  corpuscle  is  seen  the  first  endocellular 
stage.  The  second  corpuscle  shows  a  more  advanced  endocellular  stage 
and  the  act  of  liberation  into  the  liquor  sanguinis.  Farther  to  the  right  is 
seen  a  medium-sized  trypanosome.  The  third  corpuscle  shows  the  fully-grown 
halteridial  form,  while  on  the  extreme  right  a  fully-grown  trypanosome  is 
depicted. 


of  the  parasite,  divides  into  two  portions  by  its  centrosome  forming  the  axial 
spindle  and  the  chromosomes  the  two  ends  of  a  diaster.  One  of  these  daughter 
kinetonuclei  lying  in  the  ectoplasm  is  attached  to  the  other,  lying  in  the  endo- 
plasm,  by  means  of  the  axial  spindle.  The  ectoplasmic  kinetonucleus  forms 
another  spindle,  with  a  longitudinal  axis,  which  grows  backwards  along  a 
fold  of  the  ectoplasm,  expanding  it  as  it  goes,  to  the  hinder  end  of  the  body. 
In  this  way  an  undulating  membrane  is  formed,  which,  therefore ,  contains 
eight  chromosomes — the  myonemes— on  each  side  of  the  folded  ectoplasm, 
while  the  axial  spindle,  becoming  excentric,  forms  the  flagellum.  At  the 
posterior  end  of  the  undulating  membrane  the  flagellum  joins  with  the 
chromosomes,  and  grows  out  of  the  body  to  form  the  free  flagellum,  along 
which  the  ectoplasm  is  drawn  for  a  short  distance. 

Of  the  two  centrosomes  of  this  spindle,  the  distal  one  disappears,  while  the 
proximal  one  forms  the  blepharoplast  at  the  root  of  the  flagellum. 

The  endoplasmic  daughter  kinetonucleus  becomes-  the  kinetonucleus  of  the 
rypanosome,  and  thus   is  formed  the  indifferent  Lrypanosome,  which  now 


524  TELOSPORIDIA 

multiplies  by  binary  division.  After  some  time  it  takes  on  a  gregariniform 
phase,  and  becomes  attracted  to  an  epithelial  cell  in  the  stomach  of  the 
mosquito  by  its  flagellum,  which  is  reduced  to  a  short  rod.  While  so  attached 
it  may  multiply  by  binary  division,  and  may  also  penetrate  in  between  the 
cells  of  the  stomach  and  encyst,  losing  its  flagellum. 

After  a  period  of  rest  the  trypanosome  can  become  active  again,  but  after 
a  time  it  must  either  (i)  pass  into  the  blood  of  the  little  owl;  (2)  become  a 
male  or  female  form;  (3)  die  out. 

The  Male  Ookinete. — The  male  ookinete  forms  a  heteropolar  diaster,  but 
with  a  subdivision  of  the  elements  into  male  and  female  instead  of  into  kinetic 
and  trophic. 

The  larger  or  female  portion  disappears,  while  the  smaller  or  male  portion 
forms  eight  double  nuclei,  with  kinetic  and  trophic  elements,  which  are  dis- 
tributed throughout  the  cytoplasm. 

The  ookinete  now  becomes  rounded,  while  the  eight  double  nuclei  travel 
to  the  periphery,  which  grows  out  into  little  elevations,  each  with  a  double 
nucleus.  Each  little  elevation  grows  into  a  little  male  trypanosome  in  the 
same  manner  as  in  the  indifferent  form,  and  breaks  off  from  the  '  rest  body  ', 
(nucleus  de  reliquat)  of  the  parent  cell.  These  male  trypanosomes,  according 
to  Schaudinn,  simply  die  off. 

The  Female  Ookinete. — In  this  form  the  same  changes  take  place  as  in  the 
male  ookinete,  but  it  is  the  small  male  nucleus  which  degenerates,  after  divid- 
ing into  a  number  of  forms,  while  the  large  female  nucleus,  which  consists 
of  the  trophic  and  kinetic  elements,  remains,  and  forms  a  trypanosome  in  the 
same  manner  as  in  the  indifferent  form. 

The  female  trypanosome  is  slow  moving,  and  does  not  divide,  but  can 
become  gregariniform,  and  lie  quiescent  between  the  epithelial  cells  for  a 
time.  It  can  also  pass  into  the  ovaries  and  eggs,  and  lie  dormant  during  the 
winter. 

The  female  ookinete,  however,  undergoes  parthenogenesis  by  losing  its 
flagellar  apparatus  and  developing  a  trophonucleus  with  a  kinetonucleus  in 
contact  with  it.  The  kinetonucleus  now  divides,  and  undergoes  reduction, 
while  the  trophonucleus  also  divides,  one  portion  being  lost.  The  reduced 
kinetonucleus,  which  has  divided  into  two,  now  enters  the  trophonucleus  from 
opposite  sides,  and  fusing,  forms  the  synkaryon  of  an  ookinete,  which  may 
become  an  indifferent,  a  male,  or  a  female  trypanosome. 

In  the  Owl. — The  male,  female,  and  indifferent  trypanosomes  may  be 
injected  into  the  owl  during  the  process  of  biting  by  the  mosquito,  but  the 
majority  are  of  the  indifferent  type.  The  male  trypanosomes,  if  they  enter, 
die  off.  The  indifferent  trypanosomes  divide  in  the  blood  until  a  small  size 
is  reached,  when  they  enter  the  erythrocytes,  and  become  a  young  halter- 
idium  by  the  flagellar  apparatus  disappearing  and  the  kinetonucleus  approach- 
ing the  trophonucleus. 

In  twenty-four  hours  this  parasite,  which  now  contains  haemozoin,  becomes 
active,  and,  re-forming  its  flagellar  apparatus,  leaves  the  blood  cell  usually  at 
night  as  a  typical  Trypanosoma  noctucs.  After  a  short  period  of  activity  it 
inters  .mother  erythrocyte,  and  grows  till  the  next  night,  when  it  again 
becomes  free.  This  process  takes  place  six  times  before  the  trypanosome 
attains  its  full  size,  when  it  undergoes  repeated  division  until  again  small, 
thus  completing  the  cycle  of  schizogony.  The  small  extracellular  forms  may 
be  looked  upon  as  the  mcrozoites,  and  the  intracellular  forms  as  trophozoites, 
and  the  Large  extracellular  form  as  a  schizont.  The  sexual  forms  are  developed 
from  the  merozoites — i.e.,  the  very  young  indifferent  trypanosomes — which 
•  nter  tlie  red  nils,  and  become  microgametocytes  and  macrogametocytes,  thus 
completing  the  cycle  of  sporogony. 

Remarks. — Xovy  and  many  others  are  convinced  that  Schaudinn  is  entirely 
wronf,',  and  that  he  was  dealing  with  a  double  infection  of  a  halteridium  and  a 
trypanosome,  both  of  which  probably  develop  in  entirely  different  ways.  We 
are  also  convinced  thai  these  parasites  are  Hremosporidia. 


HJEMOPROTEUS  COLUMBM 


525 


Haemoproteus  columbae  Celli  and  Sanfelice,  1891. 
Hesmoproteus  columbes  is  the  halteridium  of  Columba  livia  L.  Its  life- 
history  is  not  exactly  known  at  present,  but  has  been  studied  by  Ed.  and  Et. 
Sergent  and  by  Aragao.  According  to  the  latter  observer,  it  would  seem  to 
have  the  usual  two  life-cycles  of  schizogony  and  sporogony  joined  into  one, 
taking  place  in  Columba  livia  and  in  Lynchia  maura  or  L.  brunea  (lividicolor) 
Oliv. 


/2. 


Fig.  185. — The  Life-Cycle  of  Hcsmoproteus  columbcB~Q,v.\JL\  and 
Sanfelice. 

(According  to  the  researches  of  Aragao.     After  Aragito,  from  Archiv 
f.  Protistenkunde.) 


Starting  with  the  macro-  and  micro-gametocytes,  which  are  of  the  same 
appearance  as  in  H.  nociucB,  and  which  enter  the  gut  of  the  Lynchia  along 
with  the  blood  sucked  from  the  pigeon,  the  usual  processes  of  reduction,  with 
the  formation  of  microgametes  and  macrogametes  and  ookinetes,  and  the 
clearance  of  waste  matter  from  these  latter,  are  gone  through.  The  further 
changes  undergone  by  the  ookinete  are  at  present  unknown. 

After  the  Lynchia  bites  a  pigeon,  a  small  binuclear  parasite  is  to  be  found  in 
a  leucocyte,  first  at  the  site  of  the  bite  and  later  in  the  lungs,  where  the 
further  development  takes  place.  First  the  small  parasite  divides  into  a 
number  of  mononuclear  forms,  which,  along  with  the  leucocyte,  grow 
enormously,  and  form  large  parasites,   at  first  full  of  nuclei,  and  later  of 


526 


TELOSPORTDIA 


mononucleated  merozoites,  the  whole  process  taking  some  twenty-six  or  more 
days.  The  minute  merozoites  now  enter  the  red  corpuscles  and  grow  into 
typical  Halteridia.  It  appears  that  there  are  no  trypanosome  stages  and, 
indeed,  the  only  form  of  that  nature  met  with  was  Trypanosoma  avium  ISovy 
and  McNeal. 

This  is  quite  a  different  history  from  that  of  Schaudinn  for  H.  noctuce,  but 
it  must  be  observed  that  it  is  incomplete,  and,  therefore,  deductions  cannot 
safely  be  drawn  from  it.  ,    . 

Other  Species. — A  large  number  of  species  are  described  by  Celliand  Sanielice, 
Novy  and  McNeal,  and  others,  which  have  been  found  in  birds  as  well  as  in 
some  reptiles. 


Fig.  i  86. — Hcemoproteus  columbce  Celli  and  Sanfelice. 
(After  Sambon.) 

Sambon  has  described,  under  the  name  of  HcBmoproteus  mansoni  (Fig.  176), 
a  new  species  found  in  the  red  grouse  (Lagopus  scoticus),  the  gametocytes  of 
which  are  not  closely  adherent  to  the  nucleus  of  the  erythrocyte,  as  is  usually 
the  case,  and  sporogony  takes  place  in  a  parasitic  fly  of  the  grouse  (Ornithomyia 
lagopodis),  in  the  stomach  of  which  ookinetes  were  found. 

Anschutz  has  described  a  schizogony  of  H.  oryzivorce  taking  place  in  the 
circulating  blood  of  Padda  oryzivora. 


REFERENCES. 

Telosporidia  in  General. 

Minchin  (1903).      Lankester's  Treatise  on  Zoology,  I.,  ii.  150-360.     (1912). 
An  Introduction  to  the  Study  of  the  Protozoa.     London. 


Gregarinida. 

Castellani  and  Willey  (1904).  Spolia  Zeylanica,  II.,  vi.  78-92.  (i9°5)« 
Quarterly  Journal  of  Microscopical  Science. 

Christophers  (1905).     Scientific  Mem.  India,  No.  18. 

Christophers  (1907).     Scientific  Mem.  India,  No.  28. 

James  (1905).     Scientific  Mem.  India,  No.  14. 

Ltjhe  (1906).     Mense's  Tropenkrankheiten,  iii. 

Robertson  (1906).  Proceedings  of  the  Royal  Physiological  Society  of  Edin- 
burgh, xvi.  232-247. 

Sambon  and  Seligmann  (1907).  Transactions  of  the  Pathological  Society  of 
London,  LVIII.,  iii.  310. 


REFERENCES  5*1 

Coccidiidea. 
Dobell  (19 1 9).     Parasitology. 

Toxoplasmidae. 
Castellani  (1914).     Journal  of  Tropical  Medicine  and  Hygiene,  April  15. 
Nicolle  and  Manceaux  (1908).     Comp.  Rendus  Acad.  Sciences,  cxlvii. 
Nicolle  and  Manceaux  (1909).     Ibid.,  cxlviii. 
Splendore  (1908).     Rivista  du  Soc.  Scient.  de  Sao  Paulo,  pp.  109-112. 

Piroplasmidae. 

Aragao  and  Neiva  (1909).     Memorias  do  Institute  Oswaldo  Cruz. 

Bignami  e  Bastianelli  (1893-94).     Bollet.  R.  Acad.  Med.,  xx. 

Grassi  (1901).     Die  Malaria.     Jena. 

Laveran  (1899).     Les  Hematozaires  Endoglobulaires.     Paris. 

Manson  (1896).     Lancet,  i.  695,  751,  831. 

Ross   (1896).     British  Medical   Journal,   February;    (1897),   op.  cit.,  i.   251, 

ii.  1786;  (1898),  op.  cit.,  i.  21;  Lancet,  ii.  488;  (1899),  Nature,  lx.  322; 

(1900),  Nature,  lxi.  522;  (1901),  Thompson- Yates  Reports,  iii.  2. 
Schaudinn  (1904).     Arbeit,  a.  d.  Kaiser.  Gesundheitsamte,  xix.  2    169. 

Plasmodidae. 

The  most  complete  account  of  this  order  is  Franca  (191 7),  '  Snr  la  Classifica- 
tion des  hemosporidies.'     Lisbon. 

Christophers  (1907).     Scientific  Memoirs  of  India,  29.     (B.  canis.) 

Gonder  (1906).  Arb.  a.  d.  Kais.  Gesundheitsamte,  xxiv.  220-226.  (Achro- 
maticus.)  (1910).  Journal  of  Comparative  Pathology,  xxiii.  328. 
(Theileria  parua.) 

Koch  (1906).     Zeitschrift  f.  Hygiene  u.  Inf.,  1. 

Nuttall  (1904-08).  Journal  of  Hygiene  and  Journal  of  Parasitology. 
(Various  papers  on  P.  canis,  P.  bovis.) 

Strong,  Tyzzer,  Brues,  Sellards,  and  Gastiaburt  (1915).  First  Expedi- 
tion Harvard  School  to  South  America.     Cambridge,  U.S.A. 

Theiler  (1904).     Journal  of  the  Royal  Army  Medical  Corps.     London. 

Wilson  and  Chowning  (1904).     Journal  of  Infectious  Diseases,  pp.  31-57. 

Haemopioteidae. 

Beaurepaire-Aragao    (1908).      Arch.   f.   Protistenkunde,  vol.   xii.,   p.   154. 

{HcBmoproteus  columbce.) 
Schaudinn  (1904).    Arbeitenaus  dem  Kaiserlichen  Gesundheitsamte,  vol.  xx., 

P-  3«9- 


CHAPTER  XXII 
NEOSPORIDIA 

Neosporidia  —  Myxosporidia — Actinomyxidia — Sarcosporidia — Haplosporidia 
— Protozoa  incerta?  sedis — Chlamydozoa- — Filterable  viruses — References. 

NEOSPORIDIA  Schaudinn,  1900. 

Definition. — Parasitic  plasmodromata,  without  motile  organs,  in 
which  spore-formation  and  trophic  growth  proceed  simultaneously. 

Remarks. — The  Neosporidia  are  protozoa  in  which  reproduction 
and  growth  go  on  together.  In  the  Telosporidia  the  trophozoite 
grows  into  the  schizont,  which  divides  into  spores;  in  the  Neosporidia 
growth  and  spore-formation  go  on  together;  but,  as  in  the  case  of  all 
attempts  at  classification,  there  are  exceptions,  for  the  trophozoite 
may  grow  into  the  schizont,  and  then  divide. 

It  appears  as  though  the  Neosporidia  Were  evolved  from  a  sarco- 
dinal  ancestor. 

They  are  divided  into  four  orders:  (1)  Myxosporidia,  (2)  Actino- 
myxidia, (3)  Sarcosporidia,  (4)  Haplosporidia;  and,  in  addition, 
there  are  a  number  of  parasites  belonging  evidently  to  the  protozoa, 
which  cannot  easily  be  classified,  and  are  therefore  placed  in  an 
addendum  to  the  Neosporidia  as  Protozoa  incertce  sedis. 

ORDER  I.  MYXOSPORIDIA  Biitschli,  1881. 

Neosporidia  with  spore-formation  commencing  early  in  the  amceboid  tropho- 
zoite.    Each  spore  has  one  or  more  polar  capsules. 

The  Myxosporidia  are  subdivided  into: — 

Suborder  I.  Phaenocystes  Gurley,  1893,  Synonym. — Myxosporidia  (sensii 
striclo).     Spores  with  two  to  four  large,  clearly  visible  polar  capsules. 

Suborder  II.  Cryptocystes  Gurley,  1893.  Synonym. — -Microsporidia  (Bal- 
biani) .  Spores  with  one  minute  polar  capsule,  which  is  only  rendered  visible 
by  treatment  with  reagents. 

SUBORDER  I.  PHiENOCYSTES  Gurley,  1893. 

Phaenocystes  comprise  the  true  Myxosporidia,  being  usually  found  in 
Teleostean  fish,  though  they  may  occur  in  clasmobranchs,  amphibia,  and 
reptiles. 

In  fish  they  have  long  been  known  as  psorosperms,  being  found  in  the  bile- 
passages,  the  urinary  organs,  the  muscles,  and  the  nervous  sj'stem. 

The  amceboid  trophozoite  has  a  differentiation  of  its  cytoplasm  into  endo- 
and  ecto-plasm,  and  moves  about  by  pscudopodia.  Spore-formation  begins 
early  by  a  concentration  of  the  cytoplasm  around  one  of  the  nuclei  of  the 
trophozoite.     This  concentrated  area  is  marked  off  by  a  capsule,  and  is  the 

528 


ACTINOMYXIDIA  529 

pansporoblast.  The  nucleus  of  the  pansporoblast  divides  repeatedly,  after 
which  the  cytoplasm  splits  into  two  masses — the  sporoblasts — each  of  which 
is  covered  by  a  cuticle  and  contains  three  nuclei. 

The  cytoplasm  of  the  sporoblast  now  divides  into  three  areas  around  the 
nuclei.  One  of  these  areas  is  large,  and  is  called  the  sporoplasm,  while  the 
other  two  are  small,  and  form  the  polar  capsules.  Each  spore,  therefore, 
contains  two  polar  capsules  and  one  mass  of  sporoplasm,  which  represents  a 
single  sporozoite.  Each  polar  capsule  develops  a  spirally  coiled  thread.  A 
spore  escapes  when  the  parent  trophozoite  dies,  and  then  finds  its  way  out  of 
its  host  by  the  bile  or  urine,  or  through  the  tissues  into  the  alimentary  canal. 
For  further  development  it  must  be  swallowed  by  another  host,  in  whose  ali- 
mentary canal  the  threads  of  the  polar  capsules  are  extruded,  fixing  the  little 
spore,  which  bursts  and  allows  the  amoeboid  sporozoite  to  escape  and  go  on 
"its  travels  in  search  of  a  suitable  tissue.  Perhaps  en  route  it  conjugates  with 
another  sporozoite;  if  so,  this  is  not  known.  While  sporogony  is  preparing, 
schizogony  may  take  place  by  plasmotomy,  which  is  the  division  of  the  multi- 
nuclear  trophozoite  into  two  or  more  forms. 

It   will  thus  be  seen  that  growth,   plasmotomy  (schizogony),  and  spore- 
iormation  (sporogony)  go  on  simultaneously. 

Classification. — Disporea  Dofiein,  1899. — Phaenocystes  with  two  spores. 

Family.- — Ceratowyxida  Dofiein,  1901. 

Genera. — Ceratomyxia,  Leptolheca. — Parasitic  in  fish  and  frogs. 
Polysporea  Dofiein,  1899. — Phaenocystes  with  more  than  two  spores. 

Family  i. — MyxidUdte  Auerbach,  1910. 
Genera. — Spharospora,  Myxidium . 

Family  2.- — ChloromyxidcB  Thelohan. 

Family  3. — Myxobolidce  Gurley,  1893. 


SUBORDER  II.  CRYPTOCYSTES. 

This  order  is  divided  by  Dofiein  and  Perez  into : — 

Tribe  1.  Monosporogenea  Perez.: — Trophozoite  becomes  a  single  pansporo- 
blast (sporont),  which  produces  a  single  spore. 

Tribe  2.  Oligosporogenea  Dofiein,  1899. — Trophozoite  becomes  a  single 
pansporoblast  (sporont),  which  produces  four  to  eight  spores. 

Tribe  3.  Polysporogenea  Dofiein,  1899. — Trophozoite  becomes  numerous 
pansporoblasts  (sporont),  which  produce  many  spores. 

Tribe  i.    Monosporogenea. 

This  tribe  includes  Nosema  bombycis  Nageli,  1857,  which  is  the  cause  of 
pebrine,  the  silkworm  disease.  N.  apis  Zander,  1909,  was  shown  to  be  the 
cause  of  microsporidiosis  in  bees  in  England  by  Fantham  and  Porter. 

Tribe  2.    Oligosporogenea  Dofiein,  1899. 

This  includes  the  genera  Gurleya  Dofiein,  Thilohania  Henneguy,  and  Pleisto- 
phora  Gurley. 

Tribe  3.    Polysporogenea  Dofiein,  1899. 

This  includes  the  genera  of  Glugea  Thelohan,  and  Myxocysles  Mrazck,  of 
which  Glugea  anomala  Moniez  is  a  parasite  of  the  stickleback. 

Microsporidium  polyedricum  liolle.  a  doubtful  species,  is  said  by  Perroncito 
to  occur  in  man. 


ORDER  II.  ACTINOMYXIDIA  Stole,  1899. 

These  are  parasites  in  the  Tubificidae  of  the  oligochaete  worms,  and  need  not 
concern  us. 

34 


53° 


NEOSPORIDIA 


ORDER  III.  SARCOSPORIDIA  Biitschli,  1882. 

Definition. — Neosporidia  in  which  the  young  trophozoite  is,  with 
rare  exceptions,  found  in  the  muscle-fibre  of  warm-blooded  animals. 
Spore-formation  commences  early,  and  proceeds  during  the  whole 
growth  of  the  trophozoite,  which  may  attain  a  very  large  size,  when 
it  is  covered  by  two  coats,  the  inner  of  which  is  prolonged  internally 
through  the  parasite,  dividing  it  into  a  series  of  chambers. 

Remarks. — The  Sarcosporidia,  discovered  by  Miescher  in  1843, 
are  very  common  parasites,  and  in  the  form  of  Sarcocystis  tenella 
may  be  seen  by  the  practitioner  in  the  tropics  in  meat  sent  as  food 
to  gaols  and  hospitals. 

Two  families  are  known:  (1)  Sarcocystidce,  (2)  Rhinosporidiidce. 

1.  Sareocystidse  Poche,  1913. 
Definition. — Sarcosporidia  found  in  muscle  fibres,  and  divided 
into  chambers  by  septa. 

Sarcocystis  Lankester,  1882. 

Synonym. — Gastrocystis  Chatton,  1910. 

Definition. — Sarcocystidae  with  outer  radially  striated  and  inner 
homogeneous  coat  and  poles  of  undifferentiated  protoplasm. 

Type  Species. — Sarcocystis  miescheriana  Kuhn,  1865. 

Though  a  common  parasite,  its  life-history  is  by  no  means  well 
known.  The  youngest  form  is  the  trophozoite  described  by 
Bertram,  which  lies  in  a  muscle-fibre,  and  consists  of  cytoplasm 
united  by  a  cuticle,  and  containing  several  mononuclear  pansporo- 
blasts. The  next  stage  is  more  advanced,  for  in  this  the  troph  )zoite 
has  grown  considerably,  and  now  consists  of  two  coats — an  outer, 
radially  striated,  and  an  inner,  homogeneous,  which  is  prolonged 
externally  into  filaments  and  internally  into  a  series  of  septa, 
marking  out  chambers,  each  of  which  contains  one  pansporoblast. 
Internal  to  this  coat  is  a  layer  of  cytoplasm  forming  the  endoplasm 
of  thejDarasite. 


— ■ ■ — '         -— '-'-" — ' ■■  ■  ■■fflfcjj 

Fig.  187. — Sarcocystis  tenella  bubali:  Young  Form. 

The  poles  of  the  parasite  consist  of  undifferentiated  endoplasm, 
and  form  the  areas  of  growth  of  the  young  trophozoite.  The  pan- 
sporoblast breaks  up  into  a  large  number  of  spores. 

The  third  stage  is  reached  when  the  parasite  has  grown  so  much 
that  it  has  stretched  the  muscle-fibre,  in  which  it  is  lying,  into  a  thin 
sheath  covering  it,  and  therefore  now  appears  to  lie  between  the 
muscle-fibres.  The  endoplasmic  layer  extends  all  round  the  interior 
of  the  parasite,  so  that  the  pansporoblasts  are  formed  from  the  whole 
periphery,  and  therefore  the  youngest  forms  are  in  this  position, 


SARCOSPORIDIA 


531 


while,  farther  in,  chambers  with  the  fully-developed  pansporoblasts 
are  found,  and,  still  farther  in,  is  the  centre  of  the  parasite,  filled 
by  a  granular  substance  formed  from  broken-down  and  dead  spores 
which  have  been  too  long  in  existence. 

As  to  the  spores,  a  curious  point  to  be  noted  is  that  some  observers 
only  describe  gymnospores,  while  others  only  describe  chlamydo- 
spores.  Minchin  suggests  that  this  is  because  parasites  in  different 
stages  of  their  life-history  have  been  examined,  and  he  looks  upon 
the  gymnospores  as  merozoites  and  the  chlamydospores  as  spores, 
and  these  views  are  strongly  supported  by  Korte's  description  of  a 
form  in  Macacus  rhesus. 

The  merozoites  are  crescent-shaped,  naked  spores,  from  1  to  21  jj, 
in  length,  according  to  the  species,  consisting  of  a  finely  granular 

protoplasm  with  a  nucleus, 
some  granules,  and  one  or 
two      vacuoles.       They      are 


-Sarcocystis   tenellce  bubali 
ix  Meat. 


Fig.     189.  —  Sarcocystis     Spores 

FOUND    IN    THE  BLOOD  OF  B OS  indl- 
CUS  BY  CASTELLANI  AND   STURGESS. 


thought  to  be  the  means  by  which  the  parasite  spreads  itself  jn 
its  host,  especially  as  they  are  motile  by  gliding,  corkscrew,  or 
amoeboid  movements. 

The  spores  are  from  3  to  14  fj,  long  in  Sarcocystis  tenella,  with  one 
extremity  rounded  and  the  other  pointed.  They  are  curved,  and 
surrounded  by  a  thin  membrane.  The  pointed  third  of  the  spore  is 
spiially  striated,  due  to  fine  folds  in  the  outer  capsule,  while  the 
blunt  third  contains  a  nucleus.  It  is  obvious  that  this  resembles 
the  spore  of  a  myxosporidian,  and,  in  fact,  Van  Eecke  says  that 
(me,  two,  or  even  three  filaments  issue  from  a  spore.  The  spores  can 
be  seen  in  the  peripheral  blood  at  times. 

It  is  thought  that  these  spores  spread  the  infection  to  another 
host,  but  in  what  manner  is  not  clear.     Perrin  has  recently  sug- 


532  NEOSPORIDIA 

gested  that  the  parasite  may  be  transmitted  by  the  larvae  and 
imagines  of  the  blow-fly  (Calliphora)  or  the  flesh-fly  (Sarcophaga). 

It  is  true  that  Smith  has  infected  (after  a  long  incubation)  mice 
by  feeding  them  on  the  flesh  of  infected  mice,  but  that,  of  course, 
might  simply  be  by  the  merozoites,  and  would  in  any  case  not 
explain  how  herbivorous  animals  are  infected.  Our  feeding  experi- 
ments with  a  dog  were  not  successful. 

Erdmann  says  that  the  spore  germinates  in  the  intestine  of  the 
host,  and  liberating  the  toxin — sarcocystin — which  may  come  from 
the  polar  capsule,  causes  the  epithelium  to  be  shed,  while  the  little 
amoeba  coming  out  from  the  spore  is  able  to  penetrate  the  denuded 
area  and  to  get  into  the  lymph  spaces  of  the  intestine,  Where  it  lives 
about  a  month  and  then  passes  on  to  the  muscles. 

Crawley  considers  that  the  spore  bores  its  Way  into  the  intestinal 
cells  where  it  appears  to  undergo  some  form  of  schizogony.  At  all 
events,  it  disappears  in  twenty -four  hours,  but  later  he  thought  that 
he  had  noted  sexual  differentiation  in  these  spores  in  the  cells, 
and  the  formation  of  a  zygote. 

Pathogenicity. — Sarcocystis  tenellce  bubali  is  very  common  in  the 
buffalo-meat  in  Ceylon,  and  frequently  causes  inquiries  to  be  made. 
It  appears  as  white  particles,  called  by  the  native  butchers  '  milk 
nerves,'  lying  among  the  muscular  fibres  of  tongue,  larynx, 
diaphragm,  and  skeletal  muscles.  This  ingestion  of  infected  meat 
has  apparently  no  deleterious  effect  on  man,  but  the  spores  may  be 
the  cause  of  irregular  tever. 

Classification. — A  number  of  species  are  recognized: — 
i.  Sarcocystis  miescheriana  Kiihn,  1865,  found  in  the  pig. 

2.  S.  bertrami  Dofiein,  1901,  in  the  horse. 

3.  S.  tcnellcB  Railliet,  18S6,  in  the  sheep.  5.  tenellce  bubali,  in  the  Ceylon 
buffalo.     Yuillemin  has  described  a  case  of  this  infection  in  man. 

4.  S.  blanchardi  Dofiein,  1901,  in  cattle. 

5.  S.  lindemanni  Bivolta,  1878. — This  species  has  been  found  in  man. 
They  were  first  described  indefinitely  by  Lindemann  in  1868,  in  the  myo- 
cardium and  on  the  valves  of  the  heart  of  a  person  who  had  died  of  dropsy. 
They  were  said  to  be  3  millimetres  in  length  and  1-5  millimetres  in  breadth, 
but  it  is  very  doubtful  what  these  really  were. 

Rosenberg,  in  1902,  reports  a  most  doubtful  case  of  a  cyst  in  a  papillary 
muscle  in  a  person  who  died  from  pleuritis  and  endocarditis.  Kartulis 
described  them  in  the  muscular  system  and  liver  (most  doubtful)  of  a  person 
who  died  from  multiple  abscesses  in  the  liver  and  muscles.  The  man  was  a 
Sudanese.     Koch,  in  1887,  described  an  undoubted  case  in  Egypt. 

Baraban  and  St.  lvemy,  in  1S94,  described  them  in  the  laryngeal  muscles 
of  a  man  who  had  been  executed.  This  description  is  not  to  be  doubted. 
J  he  parasite  is  described  as  being  16  millimetres  long,  and  about  0-17  milli- 
metre in  width.  Yuillemin  in  Nancy  and  Darling  (1909)  in  Barbados  have 
recorded  cases. 

6.  5.  hueti  Blanchard,  1885,  in  the  seal. 

7.  S.  kortei  Castellani  and  Chalmers,  1909. — This  parasite,  found  by  Korte 
in  the  thigh  muscles  of  Macacus  rhesus,  is  peculiar  in  that  the  inner  coat  was 
not  continued  into  the  cytoplasm  of  the  trophozoite,  and  the  endoplasm 
contained  only  gymnospores  (merozoites),  and  no  pansporoblasts  or  alveolar 
network.  The  spores  contained  nothing  but  a  nucleus,  no  cell  membrane 
or  other  structure  being  visible.  There  were  no  signs  of  any  reaction  on  the 
part  of  the  tissues. 


RHINOSPORIDI I  'M   SEEDER  I 


53  3 


8.  S.  aramidis  Splendore,  1907. — Parasite  in  Aramidis  saracura,  a  Brazilian 
bird. 

9.  5.  ammodromi  Splendore,  1907. — Miescheria  ammodromi  Splendore,  1007. 
Mcsnil  says  it  is  not  generic,  and  perhaps  not  specific.  It  is  found  in  a 
Brazilian  bird,  Ammodromus  manimbe. 

10.  S.  lepomm  Crawley,  1914,  in  American  rabbits. 
U.S.  setophaga  Crawley,  1914,  in  American  redstarts. 
12.  5.  muris  Blanchard,  in  rats. 

2.  Rhinosporidiidse  Poche,  1913. 
D3finition, — Sarcosporidia   found  in  connective  tissue  and  not 
divided  into  chambers  by  septa. 

Rhinosporidium  Minchin  and  Fantham,  1905. 
Definition.— Rhinosporidiidas  with  well-defined  sporoblast. 
Type  Species. — Rhinosporidium  seeberi  (Wernicke,  1900). 

Rhinosporidium  seeberi  Wernicke,  1900. 

Synonym. — Rhinosporidium  kineaiyi  Minchin  and  Fantham,  1905. 

Rhinosporidium  was  discovered  in ^1896  by  Dr.  Guillermo  Seeber 
in  Buenos  Ayres  in  a  nasal  polypi  in  'a  young'man  of^nineteen  years 
of  age.  In  1900  he  published  a  description  of  the  parasite,  and  in 
the  same  year  Wernicke  gave  it  the  name  of  Coccidium  seeberi. 

Kinealy,  in  1903,  reported  to  the 
Laryngological  Society  a  peculiar 
case  of  polypus  growing  from  the 
septum  of  the  nose  of  an  Indian  in 
Calcutta  as  a  pedunculated  vascular 
growth  resembling  a  raspberry  in 
appearance  by  having  whitish  spots 
on  the  general  red  surface.  On 
section,  this  tumour  was  found  to 
have  peculiar  bodies  embedded  in  it. 

It  was  then  carefully  examined 
and  described  by  Minchin  and  Fan- 
tham, who  came  to  the  conclusion 
that  it  was  a  haplosporidian,  and 
named  it  Rhinosporidium  kineaiyi. 

In  1905  Nair  of  Madras  came 
across  a  similar  polypus  in  several  people  who  all  came  from  the 
small  native  State  of  Cochin  on  the  west  coast  of  India.  These 
polypi  have  been  carefully  described  by  Beattie  in  1906.  Castellani 
and  Chalmers  have  found  it  in  polypi  in  Ceylon. 

Morphology.— On  cutting  into  the  polypus  it  is  noticed  that  there 
are  minute  dots  visible  to  the  naked  eye,  and  capable  of  bein^  dis- 
sected out.     These  dots  are  cysts. 

When  examined  with  the  microscope,  it  is  seen  that  the  growth 
is  covered  by  stratified  pavement  epithelium,  which  shows  signs  of 
proliferation  and  invasion  by  polymorphonuclear  leucocytes.  Under 
this  epithelium  there  is  a  stroma  formed  of  delicate  fibrous  tissue, 


Fig.   190. — Rhinosporidium 

seeberi  Wernicke. 
(From  a  nasal  polypus  in  a  case 
in  Ceylon;  schematic,  and  highly 
magnified.) 


534  NEOSPORIDIA 

myxomatous  in  places,  and  cellular  at  other  spots.  The  cysts  were 
found  to  be  oval,  round,  tubular,  branched  or  irregular  bodies,  hang 
below  the  epithelium  principally,  but  also  found  in  haemorrhages 
and  in  cell  collections.  The  wall  of  the  cyst  is  generally  thin,  and 
has  either  an  opening  or  a  conical  elevation  at  one  point.  It  con- 
sists of  two  layers — a  thinner  external  and  thicker  internal  coat. 
The  smaller  cj'sts,  from  10  to  30  fx  in  diameter,  contained  undiffer- 
entiated protoplasm  with  a  vesicular  nucleus  containing  a  nucleolus. 
The  larger  cysts  had  one  or  more  definite  chromatic  masses.  A 
fully-developed  cyst  is  lined  with  protoplasm,  in  which  }7oung  pan- 
sporoblasts are  forming,  while  the  centre  of  the  parasite  is  full  of 
old  pansporoblasts,  separated  from  one  another  by  an  indefinite 
framework  continuous  with  the  capsule.  A  young  pansporoblast 
is  seen  to  be  a  small  oval  or  rounded  mass  of  cj'toplasm  with  a 
single  nucleus.  This  body  grows,  and  becomes  surrounded  by  a 
membrane,  while  its  nucleus  divides  by  amitosis  into  four  to  sixteen 
spores,  each  of  which  has  a  very  thin  wall  and  a  central  nucleus. 
The  pansporoblasts  and  spores  are  set  free  by  rupture  of  the  cyst, 
and  may  be  surrounded  by  polymorphonuclear  leucocytes,  thus 
forming  minute  abscesses,  -or  may  be  engulfed  by  mononuclear 
leucocytes,  or  may  grow  into  parasites,  or  escape  from  the  host  in 
the  nasal  secretion.     The  method  of  infection  is  not  known. 

The  framework  inside  the  cyst  separating  the  pansporoblasts 
indicates  that  Rhino sp or idium  belongs  to  the  Sarcosporidia,  and  not 
to  the  Haplosporidia. 

Pathogenicity. — The  pathology  appears  to  be  a  proliferation  of 
the  submucosa  and  mucosa  of  the  nose,  brought  about  by  the 
irritation  of  the  parasite  (see  p.  1578). 

ORDER  IV.  HAPLOSPORIDIA  Caullery  and  Mesnil,  1899. 

Synonym. — Haplosporidiidea  Poche,  1913. 

Neosporidia  with  very  simple  life-history  and  undifferentiated  cell-plasma, 
without  septum  and  with  spores  of  simple  structure,  with  one  nucleus,  and 
no  polar  capsules. 

The  Haplosporidia  are  characterized  by  the  simplicity  of  their  life-cycle, 
which  begins  with  a  mononuclear  or  binuclear  trophozoite,  which  may  encyst, 
and  in  any  case  grows  larger  and  larger,  while  its  nucleus  divides  into  several 
nuclei,  so  that  a  multinucleated  mass  or  schizont  is  formed.  This  escapes  from 
its  cyst  and  divides  up  into  merozoites,  either  directly  or  after  plasmotomy, 
each  of  which  becomes  a  trophozoite,  thus  completing  schizogony.  Sporogony 
is  unknown. 

They  are  parasites  of  fishes  and  invertebrates. 

Classification. — Family  i.  Haplosporidia  Caullery  and  Mesnil. — Spores 
with  double  envelope  and  opening. 

Genus  1.  Haplosporidinm. — Spores  closed  by  a  valve.     In  annelids. 
Genus  2.   Urosporidinm. — Spores  open.     In  annelids. 

FAMILY  2.  Bertramiida. — Spore  envelope  without  opening. 
Genus  1.  Bertramia. — Stomach  of  fish. 
Genus  2.  Ichfhyosporidium.—In  tumours  of  fish  (Figs.  191-196). 

Family  3.  Coilosporidiid/f.. — Spores  nude. 
Genus  1.  Polagarynum. 
Genus  2.  Blastnlidium. 


PROTOZOA   INCERTM  SEDIS  535 

Protozoa    Incertae   Sedis. 

Cytoryctes  variola  Guarnieri,  1892. 

Synonym. — Slrombodcs  jeuneri  Sjobrung,  1902. 

In  1892  Guarnieri  described  peculiar  parasitic  bodies  in  lesions  of  smallpox, 
and  in  those  produced  by  vaccination  of  the  cornea  of  rabbits,  etc.  Pfeiffer, 
in  1893,  confirmed  these  findings,  as  did  Jackson  Clarke  in  1894,  and 
Wasielewski  in  1897.  Councilman,  Magrath,  and  Calkins,  in  1903,  published 
the  full  account  of  the  life-history  of  the  parasite,  and  their  findings  have 
been  confirmed — in  part,  at  least — by  De  Korte  in  1905. 

In  its  youngest  form  Cytoryctes  variolce  is  seen  in  the  cells  of  the  skin  as  a 
minute  spherical  homogeneous  body,  0*7  /j,  in  size.  No  differentiation  into 
nucleus  and  cytoplasm  is  possible,  as  the  organism  appears  to  be  all  nucleus. 
The  parasite  grows  to  3  fx,  and  then  shows  a  vacuolization  in  the  centre, 
with  sometimes  a  central  dot.  The  periphery  next  shows  minute  unstained 
dots,  which,  when  they  become  larger,  take  on  the  green  of  a  Borrel's  stain. 
The  red  staining  material  is  called  by  Calkins  protogonoplasm. 

The  organism  can  now  change  its  shape  and  throw  out  pseudopodia,  and 
lives  in  a  vacuole  near  the  nucleus;  there  is  no  ectoplasm  or  endoplasm,  no 
vacuoles,  but  only  chromatin  granules  of  protogonoplasm.  Volpino  has 
described  minute  motile  granules  in  the  epithelial  cells,  which  he  considers 
to  be  the  true  parasites. 

Auto-Infection. — In  a  large  parasite  (10  to  14  fx)  the  protogonoplasm  is  dis- 
tributed through  the  body  in  minute  spherical  granules  lying  in  a  minute 
vesicle,  forming  granules  from  0*7  to  1  [X  in  diameter,  which  are  liberated  by 
disintegration  of  the  framework  of  the  host  cell,  while  the  rest  of  the  cyto- 
plasm form  a  nucleus  de  reliquat. 

Sexual  Development. — The  homogeneous  granules  or  gemmules  may  start 
the  cycle  of  cytoplasmic  organisms  again,  or  may  become  germ-cells  in  the 
nucleus.  The  gemmules  reach  the  nucleus,  but  they  now  stain  uniformly 
and  become  minute,  clearly-defined,  homogeneous  bodies — female  gameto- 
cytes.  Sometimes  they  fail  to  reach  the  nucleus  and  remain  in  the  cytoplasm, 
in  which  they  can  only  partially  develop.  Within  the  nucleus  Calkins  thinks 
they  form  male  and  female  gametocytes,  homogeneous  granules,  or  the 
gemmules  become  spherical,  with  central  red  masses,  and  later  red  masses 
at  the  periphery — the  male  gametes.     No  conjugation  has  been  observed. 

The  zygote  is  an  amoeboid  body  lying  in  the  nucleus,  and  staining  deeply, 
This  zygote  becomes  a  pansporoblast  and  the  mother-cell  of  the  sporoblasts. 
The  spore  is  very  minute,  and  contains  a  vacuole ;  it  migrates,  and  may  travel 
into  the  nucleus  and  form  secondary  sporoblasts. 

Cytoryctes  (Doubtful  Species). 

This  organism  can  be  found  as  corroid  bodies  in  the  smears  taken  from  the 
heart  muscle  of  animals  suffering  from  foot  and  mouth  disease. 

Neuroryctes  hydrophobiae  Calkins,  1907. 

Nettrqryctes  hydrophobia,  better  known  as  the  Negri  bodies,  because  they 
were  discovered  by  Negri  in  1903  as  round  or  oval  bodies,  1  to  23  [A,  in  length, 
in  the  nerve-cell  of  the  brain,  especially  the  Cornu  ammonis,  of  animals 
su tiering  from  hydrophobia,  are  now  generally  accepted  as  the  cause  of  the 
disease.  Hydrophobia  is  so  common  in  India  and  Ceylon  that  a  knowledge 
of  its  parasite  is  necessary  to  the  practitioner  in  that  part  of  the  tropics. 

S.une  authorities  consider  these  bodies  to  be  cell-structures,  but  in  our 
opinion  there  cannot  be  any  doubt  that  they  are  parasites,  especially  after 
the  further  investigation  of  Negri,  amply  confirmed  by  Williams,  Lowden, 
and  Calkins,  who  named  it  Neuroryctes  hydrophobics  Calkins,  1907.  Prowazek 
es  them  to  be  Chlamydozoa.  When  stained  by  Giemsa  the  protoplasm 
takes  on  a  bluish  tinge  like  the  malarial  organism,  while  there  is  a  central 


Fig.  191 . — A  Series  of  Small  Ichthyosporidia 

ENCLOSED  IN  CONNECTIVE  TISSUE. 


Fig.  192. — A  Medium-sized 
ichthyosporidium  in  a 
Nest  of  Connective 
Tissue. 


Fig.  194.  —  Breaking- 
up  of  an  ichthyo- 
SPORIDIUM into  Re- 
productive Bodies. 


Fig.  193. — Escape  of  the  Ichthyosporidium 
from  its  Cyst. 


•  ' 


-\ 


Fig.  195. — Large  Ichthyosporidia,  one 
of  which  (on  the  Right)  is  under- 
going Plasmotomy. 


Fig.  196. — Young  Forms 
developed  from  the 
Breaking  -  up  of  a 
Large  Parasite. 


(From  drawings  by  Miss  Robertson.) 


SERGENTELLA   HOMINIS 


53; 


body  like  a  nucleus,  composed  of  a  periphery  of  chromatin,  and  containing 
a  central  chromatic  particle  staining  red.  Negri,  Williams,  and  Lowden  give 
drawings  indicating  the  rapid  division  and  growth  of  the  organism,  which 
apparently  as  it  grows  divides,  until  finally  large  forms  result  whose  chromatin 
breaks  up  into  minute  masses. 

They  consider  that  the  parasite  reaches  the  nervous  system  by  spreading 
along  the  nerves,  which  it  does  more  quickly  than  travelling  by  the  blood. 

Cyclasterella  scarlatinalis  Mallory  (Doubtful  Species). 

In  1904  Mallory  described  round  and  elongated  bodies,  sharply  stained 
with  methylene  blue,  2  to  7  /i  in  size,  lying  in  the  epithelium  of  the  epidermis, 
together  with  radiate  bodies,  composed  of  a  central  spherical  body  with  ten 
to  eighteen  segments  radiating  away  from  it,  in  epithelial  cells  and  lymph- 
spaces  of  the  epidermis  of  people  suffering  from  scarlet  fever. 

This  discovery  has  since  been  confirmed  by  Field  and  Duval,  both  during 
life  and  in  post-mortems. 

Further  research  is  needed  before  the  nature  of  these  bodies  can  be  definitely 
settled. 


Fig.  197. — Sergentella  hominis 
Brumpt. 


Fig.  198.  —  Sarcocystis  Spores 
found  in  the  blood  of  man  by 
castellani  and  wllley. 


Coccidioides  immitis  Rixford  and  Gilchrist,  1897  (A  Fungus). 

Synonyms. — C.  pyogenes  Rixford  and  Gilchrist,  1897;  Coccidiitm  posades 
Caxton  (?),  1898. 

These  parasites  were  first  seen  by  Wernicke  and  Possadas  in  Buenos  Ayres, 
and  later  in  the  United  States  by  Rixford  and  Gilchrist,  Montgomery,  Moffit, 
and  Ophiils,  where  they  cause  an  infection  producing  nodules  in  the  skin, 
liver,  kidney,  genitalia,  and  lymphatic  glands. 

This  so-called  protozoon  is  a  fungus  (see  p.  985). 

The  Bodies  of  Ureteritis  Cystica  (Doubtful). 

In  this  disease  the  kidney  is  hydronephritic  and  the  ureter  and  bladder 
are  cystic. 

The  cysts  contain  large  and  small  oval  and  irregular  cells  with  bright 
globules,  variously  interpreted  as  Coccidia,  Myxosporidia,  and  cell  inclusions. 

Sergentella  hominis  Brumpt,  1910. 
Ft.  and  Ed.  Sergent  in  1903  reported  a  vermiform  body,  40  fx  long  by  1  to 
i'5  A'  broad,  pointed  at  each  end,  with  a  nucleus  in  the  middle,  in  the  blood 
of  a  person  suffering  from  night-sweats  and  nausea. 


538 


NEOSPORIDIA 


Bodies  found  by  Sambon  in  Pseudochirus  peregrinus. 

Sambon  has  found  bodies  in  a  lemur  which  may  have  some  relationship 
to  the  spores  of  Sarcocystis,  but  this  is  doubtful. 

Bodies  described  in  Man  by  Castellani  and  Willey. 

These  bodies  were  found  and  described  in  1905  in  two  patients  suffering 
from  irregular  fever.  They  generally  have  a  crescentic  shape,  10  to  30  /j,  in 
length,  and  1-5  to  4  /n  in  breadth.  They  often  present  vacuoles,  and  a  nucleus 
may  be  seen  in  some  specimens,  but  not  in  all.  The  whole  body  stains  bluish, 
while  here  and  there  granules  of  chromatin  can  be  seen.  They  cannot  be 
compared  with  malarial  crescents,  as  they  never  contain  pigment.  These 
bodies  may  be  spores  of  Sarcocystis. 

Protozoal  Bodies  found  in  Dysentery. 

In  1914  Castellani  described  a  peculiar  protozoal  organism  (Entoplasma 
Castellanii  Paul,  1914)  which  he  found  in  three  cases  of  dysenteric  colitis,  in 
which  amoebae  and  dysenteric  bacilli  were  absent.  One  of  the  cases  had  been 
infected  in  Burma,  and  the  other  two  probably  in  Ceylon. 

In  fresh  preparations  the  organisms 
appeared  as  large  pear-shaped  or  flask- 
shaped  bodies,  60-80  microns  in  diam- 
eter, actively  motile,  and  showing  only 
slight  changes  of  shape  while  moving, 
and  no  pseudopodia. 

The  anterior  portion  at  its  upper  part 
was  shaken  by  very  rapid  vibratile 
movements,  as  though  produced  by  a 
fiagellum.  No  such  organella  could  be 
seen  in  fresh  or  stained  preparations 
by  Castellani  or  any  other  observer. 
The  cytoplasm  was  very  vacuolated. 
In  stained  preparations  a  group  of 
granular  bodies  could  be  seen,  and  were 
thought  by  Mesnil  to  be  a  diffuse  nucleus. 


Fig.  199. —  Entoplasma  Castellanii 
Paul,  191 4. 


Chlamydozoa  Prowazek,  1907. 

Definition.— The  Chlamydozoa 
are  a  collective  group  of  minute 
parasites,  which  either  live  extra- 
cellularly,  when  they  are  capable  of  passing  through  the  usual 
filters,  or  intracellularly,  when  they  excite  a  reaction  upon  the 
part  of  the  enclosing  cell  which  produces  a  substance  which  encloses 
them  as  it  were  with  a  mantle,  thus  forming  a  cell  inclusion. 

Remarks. — This  collective  group  was  formed  by  Prowazek  to 
embrace  a  number  of  minute  parasitic  forms  which  become  en- 
dosed  in  a  cellular  product  as  with  a  mantle.  The  general 
tendency  is  to  range  these  forms  among  the  Protozoa.  The  minute 
granules  are  the  parasites,  and  the  surrounding  substance  is  either 
plastin  or  chromatin  from  the  nucleus,  or  a  fatty  substance.  The 
name  Chlamydozoa  is  derived  from  the  Greek  fwoV,  an  animal,  and 
Xkafivs,  a  mantle.  At  the  present  time  doubt  is  expressed  as  to 
causal  action  of  the  Chlamydozoa  as  well  as  to  their  parasitic  nature. 
History. — In  1907  Prowazek  and  Halberstaedter,  on  examining 
trachoma  smears  stained  by  Giemsa's  method,  found  dark  blue 


CHLAMYDOZOA  539 

granular  inclusions  in  the  protoplasm  of  the  epithelial  cells.  These 
granules  were  at  first  round  or  oval,  and  increased  in  size,  at  the  same 
time  becoming  less  dark,  while  minute  red  dots  appeared,  which 
increased  rapidly  in  numbers,  while  the  blue  masses  gradually  dis- 
appeared. The  granules  formed  cell  inclusions,  and  the  blue  masses 
weir  considered  to  be  a  reaction  product  on  the  part  of  the  cell,  and 
were  thought  to  be  composed  of  plastin,  while  the  minute  red  dots 
were  considered  to  be  the  virus.  The  reason  why  they  considered 
the  blue  granules  to  be  distinct  from  the  red  points  was  because 
the  blue  gradually  disappeared,  while  the  red  points,  or  elementary 
bodies,  could  be  seen  extracellularly  situated.  They  inoculated 
anthropoid  apes  successfully  with  trachoma,  and  found  the  same 
bodies  in  this  infection.  These  researches  were  confirmed  by  Greef 
in  the  same  year,  and  were  extended  in  1908  by  Stargardt  and 
Schmeichler  in  1909,  who  described  a  conjunctivitis  neonatorum 
non-gonorrhoica  with  typical  Chlamydozoa.  In  1909  Heymann 
found  the  same  bodies  in  four  cases  of  gonorrhceal  conjunctivitis  in 
new! y -born  infants.  This  discovery  was  of  the  greatest  importance, 
because  since  the  days  of  Kroner  it  had  been  known  that  the  con- 
junctivitis of  the  new-born  was  not  always  due  to  the  gonococcus. 
Linder,  in  1909,  and  Wolfrum,  in  1910,  showed  that  there  were  two 
forms  of  blennorrhcea— viz.,  a  conjunctivitis  neonatorum  caused 
by  the  gonococcus,  and  a  second  caused  by  Chlamydozoa,  this  latter 
disease  being  termed  by  Linder  '  inclusion-blennorrhcea  '  in  contra- 
distinction to  gonoblennorrhoea.  Linder  maintains  that  the  same 
virus  produced  trachoma,  inclusion-blennorrhcea,  and  that  this 
virus  can  be  found  in  the  male  and  female  genital  passages,  and  he 
bases  his  opinion  on  the  facts  that  he  has  been  able  to  produce 
trachoma  in  monkeys  inoculated  from  a  case  of  non-gonorrhceal 
urethritis  in  a  man,  from  two  such  cases  in  women,  and  from  several 
cases  of  inclusion-blennorrhcea  in  infants.  Further  investigations 
have  shown  that  inclusion-blennorrhcea  is  histologically  similar  to 
trachoma. 

Later,  Leber  and  Prowazek  in  1911  found  a  similar  organism, 
Lyozoon  atrophicans  in  epitheliosis  desquamativa,  and  in  the  same 
I  rhlenhuth  found  inclusions  in  swine  pest,  and  Botteri  in  spring 
catarrh. 

In  the  meanwhile  Halberstaedter  and  Prowazek  had  in  their  first 
paper  grouped  with  these  cell  inclusions  the  forms  described  in 
smallpox,  hydrophobia,  molluscum  contagiosum,  epithelioma  con- 
11m,  and  Lipschiitz  grouped  the  causes  of  dermotropismus,  or 
human  dermatoses,  under  the  subhead  Strongyloplasmata.  Finally 
the  Whole  subject  was  gathered  together  and  reviewed  by  Prowazek 
in  191 1  in  his  '  Handbuch  der  Pathogenen  Protozoen.'  Somewhat 
similar  bodies  have  been  seen  by  Castellani  in  sprue  in  cells  from  the 
oral  mucosa,  although  most  of  these  inclusions  are  non-granular,  and 
he  doubts  their  parasitic  nature.  He  has  observed  somewhat  similar 
l)i  >dies  in  conjunctivitis  and  in  urethritis  of  a  non-gonorrhceal  nature. 

Morphology.— On  examining  the  cells  from  a  case  of  urethral 


54°  XEOSPORIDIA 

discharge  of  non-gonorrhceal  origin,  or  the  cells  from  the  discharge 
in  certain  forms  of  conjunctivitis,  they  can  be  seen  to  contain 
peculiar  masses  of  granules  which  are  grouped  into  oval  or  roundish 
bodies,  measuring  2  to  6  /j,  in  transverse  or  maximum  diameter. 
The  individual  granules  measure  0  -5  to  1  /lo  in  diameter,  and  stain  a 
purplish-red  colour  with  Giemsa  or  Leishman's  preparations.  These 
granules  appear  to  be  embedded  in  a  pale  bluish  matrix. 

Life-History. — The  smallest  form  or  elementary  body  is  merely  a 
minute  speck  of  chromatin,  apparently  without  any  cytoplarm, 
which  lives  extracellularly,  but  may  enter  a  cell.  This  entry  into 
the  cell  is  not  a  process  of  phagocytosis,  as  may  be  shown  by  the 
absence  of  the  usual  vacuole,  and  by  the  fact  that  they  do  not  show 
the  usual  yellow  coloration  when  stained  by  neutral  red.  Inside 
the  cell  the  elementary  body  grows  in  size,  and  becomes  the  initial- 
body,  which  becomes  surrounded  by  the  mantle,  and  thus  forms  the 
cell  inclusion.  This  body  now  breaks  up  into  a  number  of  small 
bodies  called  initial  corpuscles,  which  divide  by  simple  division — - 
i.e.,  by  the  formation  of  dumb-bell  forms,  the  two  ends  of  which 
simply  move  apart  until  the  connecting  thread  is  broken.  The 
result  of  the  division  of  the  initial  corpuscles  is  the  elementary  body. 
In  this  way  the  life-cycle  is  completed. 

Comparison. — -It  will  thus  be  seen  that  the  Chlamydozoa  are  the 
granules  inside  the  bod}>'  of  the  Cytoryctes  variolce  or  the  Neuroryctes 
hydrophobia,  and  that  the  whole  organism  of  these  two  forms  corre- 
sponds to  the  mantle  and  parasite  of  the  chlamydozoon. 

Pathogenicity. — -They  are  believed  to  be  the  cause  of  smallpox, 
vaccinia,  trachoma,  Samoan  epitheliosis,  hydrophobia,  scarlet 
fever,  etc. 

Classification. — The  Chlamydozoa  are  classified  into : — ■ 

A.  Chlamydozoa  vera. 

Chlamydozoa,  which  commences  as  elementary  bodies 
from  cell  inclusions. 

1.  Cytoryctes  group — cause  destruction  of  the  cell. 

2.  Cytooikon  group — eause  proliferation  of  the  cell. 

3.  Gelbsucht  group — cause  gelbsucht  in  the  Lepidoptera. 

B.  Chlamydozoa  strongylo plasmata . 

Chlamydozoa,  which  always  remain  as  elementary  bodie? 
— e.g.,  the  forms  in  the  peripneumonia  of  cattle  and 
the  diphtheria  in  birds. 

Only  the  Cytoryctes  and  Cytooikon  groups  concern  us. 

The  Cytoryctes  Group. 

It  is  important  to  distinguish  between  the  Chlamydozoon  of  such 
.1  disease  as  smallpox  and  the  parasite  Cytoryctes  variolce.  The 
Chlamydozoon  is  one  of  the  chromatic  particles  of  C.  variol<e,  the 
protoplasm  of  which  forms  the  mantle.  The  Cytoryctes  group  in- 
cludes the  parasites  of : — 


FILTERABLE    VIRUSES  541 

1.  Vaccinia. 

2.  Variola. 

3.  Scarlet  fever. 

4.  Hydrophobia. 

The  Cytooikon  Group. 

The  Cytooikon  group  includes:— 

1    Lyozoon  atrophicans  Leber  and  P'"owazek. 
2.  Trachoma  bodies. 

The  former  group  have  been  described  above,  and  the  latter  group 
will  be  dealt  with  in  the  chapter  dealing  with  the  diseases  of  the 
special  senses. 

The  Filterable  Viruses. 

By  the  term  '  filterable  virus '  is  meant  micro-organisms  so  small 
that  they  will  pass  through  the  pores  of  filters  which  are  too  small  to 
allow  the  passage  of  bacteria.  The  term  '  ultramicroscopic  '  is 
also  used  for  filterable  viruses,  but  is  not  free  from  objection. 

History. — In  1892  Iwanowski  demonstrated  the  filterability  of  the 
mosaic  disease  of  the  tobacco  plant,  and  in  1S98  Loffler  and  Frosch 
discovered  that  the  virus  of  foot  and  mouth  disease  would  pass 
through  the  pores  of  the  finest  porcelain  filter.  Shortly  after- 
wards Beijerinck  confirmed  Iwanowski's  observations,  and  since 
then  numerous  observations  have  been  made. 

In  Max.— Yellow  fever  virus  by  Reed  and  Carroll  in  1901, 
destroyed  if  heated  to  53°  C.  for  ten  minutes;  Molluscum  con- 
tagiosum,  by  Julius  Very  in  1905;  Dengue  fever  by  Ashburn  and 
Craig  in  1907;  Three  days'  fever  by  Doerr  in  1908;  Poliomyelitis 
by  Lentz,  Landsteiner,  Levaditi,  Flexner,  and  Lewis  in  1909; 
Typhus  by  Nicolle  in  1910;  Measles  by  Goldberger  and  Anderson 
in  1911,  as  well  as  Trachoma,  Scarlatina,  Verruca  vulgaris,  and, 
according  to  Nicolle,  Influenza. 

Animals  and  Man. — Foot  and  Mouth  Disease  by  Loffler  and 
Frosch  in  1898;  Vaccinia  by  Siegel  in  1905,  Variola  and  Rabies. 

Besides  these  filterable  viruses  others  have  been  found  in  diseases 
of  birds  and  one  in  plants. 

Cultivation. — The  virus  of  pleuro-pneumonia  of  cattle,  of  fowl  pest, 
fowl  diphtheria,  epithelioma  contagiosum,  and  of  Novy's  rat  disease 
have  been  cultivated.  The  organism  of  pleuro-pneumonia  is  a  very 
small  spirochete,  but  the  organisms  of  the  other  disease  are  only 
evident  by  the  fact  of  their  infectivity  in  subcultures  carried  beyond 
any  reasonable  limit  of  dilution  from  the  original. 

Immunity.— In  nearly  every  case  the  immunity  produced  by  a 
filterable  virus  is  complete  and  of  long  duration. 

Secondary  Infections. — Secondary  infections  with  bacteria  are 
common,  and  it  is  thought  that  many  of  the  so-called  typical 
symptoms  of  the  disease  may  be  due  to  the  secondary  agent. 

Methods  of  Infection. — The  methods  of  infection  are  various: 
(1)  By  blood-sucking  insects — e.g.,  Stegomyia  calopus  and  yellow 


542  NEOSPORIDIA 

fever,  etc.;  (2)  by  entry  through  an  abrasion — e.g.,  Molluscum  con- 
tagiosum  ;  (3)  by  contact — e.g.,  fowl  pest;  (4)  by  unknown  methods 
■ — e.g.,  Novy's  rat  disease. 

Nature. — The  nature  of  the  viruses  is  unknown;  some,  especially 
those  spread  by  blood-sucking  agents,  are  probably  protozoal,  but 
others  may  be  bacterial. 

Classification. — The  filterable  viruses  may  be  divided  into— 

1.  Filterable  viruses  associated  with  no  known  organism. 

2.  Filterable  viruses  associated  with  some  known  organism. 

1.  Filterable  Viruses  associated  with  No  Known  Organism. 

Under  this  heading  come  the  viruses  of  several  diseases  of  im- 
portance in  tropical  medicine— e.g.,  the  virus  of  yellow  fever,  of 
dengue  fever,  of  pappataci  fever,  of  typhus  fever. 

Yellow  Fever. — The  virus  is  found  in  the  blood  only  during  the 
first  three  days  of  the  fever.  It  can  pass  through  Berkefeld  and 
Chamberland  B  filters,  and  can  be  destroyed  by  heating  to  550  C. 
for  ten  minutes,  or  by  a  temperature  of  240  to  300  C.  for  forty-eight 
hours.  It  is  conveyed  by  Stegomyia  calopus  after  an  interval  of 
twelve  days  from  the  time  of  the  infective  feed. 

Dengue  Fever. — The  virus  is  in  the  blood  during  the  fever,  and 
can  be  filtered  through  Berkefeld  filters  impermeable  to  Micrococcus 
melitensis.     It  is  spread  by  Culex  fatigans. 

Pappataci  Fever.' — The  virus  exists  in  the  blood  during  the  first 
day  of  the  fever,  and  can  be  filtered  through  Berkefeld  filters,  and 
is  spread  by  Phlebotomus  papatasii  after  an  interval  of  seven  days 
from  the  date  of  the  infective  feed. 

Typhus  Fever.- — The  virus  exists  in  the  blood,  and  can  be  filtered 
through  the  coarser  Berkefeld  filters.  It  is  destroyed  by  a  tempera- 
ture of  520  to  550  C;  it  is  spread  by  Pediculus  vestimentorum  L. 

Verruga  Peruviana.— The  experiments  of  Strong,  Tyzzer,  Brues, 
Sellards,  and  Gastiaburu  tend  to  show  that  the  virus  of  this  disease 
is  a  filterable  virus,  and  distinct  from  that  of  Oroya  fever.  It 
appears  to  be  similar  in  many  respects  to  the  virus  of  smallpox.  It 
can  be  inoculated  successfully  into  monkeys,  but  only  a  modified 
form  of  the  disease  appears,  the  lesions  regressing  in  four  to  five 
weeks  (analogy  with  inoculated  smallpox).  It  has  also  been 
transmitted  to  rabbits  and  dogs.  It  has  not  yet  been  demonstrated 
that  Phlebotomus  verrucarium  or  an}7  other  insect  does  transmit  the 
disease,  but  it  is  believed  that  some  arthropod  is  the  carrier. 

2.  Filterable   Viruses  associated  with  Some  Known  Organism. 

Borrel  has  clearly  shown  that  a  minute  flagellated  organism 
(Micromonas  mesnili)  exists  in  the  filtrates  of  sheep-pox,  and  it  is 
quite  possible  that  all  filtrates  contain  these  minute  organisms,  and, 
further,  there  is  reason  to  suppose  that  certain  larger  organisms 
possess  these  minute  forms  in  some  stage  of  their  life-cycle — e.g.,  the 
organisms  of  trachoma,  variola,  and  vaccinia. 

Bradford,  Bashford  and  Wilson  have  described  minute  bodies 


REFERENCES  543 

which  they  state  to  have  cultivated,  using  Noguchi's  method,  from 
cases  of  acute  infective  polyneuritis,  influenza,  trench  fever,  typhus, 
and  other  conditions. 

Trachoma.— The  virus  passes  through  the  Berkefeld  filters,  and 
can  be  successfully  inoculated  into  monkeys. 

Variola  and  Vaccinia. — The  virus  passes  through  Berkefeld  and 
the  coarser  Chamberland  filters,  and  is  destroyed  by  heating  to 
570  to  580  C.  in  fifteen  minutes,  or  by  almost  any  disinfectant,  by 
saponin,  vicin,  bile,  taurocholic  acid,  and  sodium  oleate. 

REFERENCES. 

Neosporidia  in  General. 

Minchin  (1903).     Lankester's  Treatise  on  Zoology,  I.,  ii.  150-360.     (1912).  An 
Introduction  to  the  Study  of  the  Protozoa.     London. 

Sarcocystis. 

Crawley  (1914).     Proc.  Acad.  Nat.  Sciences,  Philadelphia,  p.  432. 
Erdmann  (1910).     Sitzb.  d.  Gesellsch.  Naturf.  Fr.  zu  Bed. 
Splendore  (1907).     Rev.  d.  Soc.  Sci.  de  San  Paulo,  pp.  115-120. 
Willey,  Chalmers,  and  Philip  (1904).     Spolia  Zeylanica,  II.,  vi.  65. 

Rhinosporidium. 

Beattie  (1906).     Journal  of  Pathology,  270. 

Kixealy  (1903).     Proceedings  of  the  Laryngological  Society,  x.  109;  xi.  43. 

Minchin  and  Fantham  (1905).     Quarterly  Journal  of  Microscopical  Science, 

xlix.  521. 

Haplosporidia. 
Caullery  and  Mesnil  (1905).     Archiv.  de  Zoologie  Experiment.,  101. 
Robertson  (1907,  1908).     Proceedings  of  the  Royal  Physiological  Society  of 

Edinburgh,  XVII.,  v.  175. 

Protozoa  Incertse  Sedis. 

Calkins.     New  Sydenham  Society  (Cytoryctes) . 

Castellani  and  Willey  (1905).     Quart.  Jour.  Micr.  Science. 

Darling  (1909).     Journal  of  Experimental  Medicine. 

Duval  (1905).     Virchow's  Archiv,  clxxix.  485-488  (Cyclasterella). 

Keysselitz  and  Mayer  (1908).     Archiv  fur  Protistenkunde,  p.  113. 

Luzzani  (1904).     Archivi  Scienze  Mediche. 

Mallory  (1904).     Journal  of  Medical  Research,  x.  4  (Cyclasterella). 

Negri    (1903-04).     Boll.    Soc.    Med.    Pa  via.     ^1909).  Reale   Accademia   dei 

Lincei. 
Prowazek  (1907).     Archiv  f.  Protistenkunde,  X.,  ii.  336-364  (Chlamydozoa). 
Prowazek  and  Aragao  (1909).     Munch.  Med.  Wochenschrift. 

Chlamydozoa. 

Castellani  (1912).     Journal  of  Tropical  Medicine  and  Hygiene.     London. 

Linder  (1912).     Archives  of  Ophthalmology. 

Prowazek  (191 1).     Handbuch  der  Pathogcnen  Protozoen.    Leipzig. 

Filterable  Viruses. 

Bradford,    Bashford   and   Wilson    (1919).      Br.   Med.   Jour,    and   Quart 

Journ.  of  Medicine. 
Strung,  1'\zzer,  Brues,  Sf.llards,  and  Gastiaburu  (1915).    Report  of  the 

First  Expedition  to  South  America  (Harvard  School  of  Tropical  Medicine). 

Cambridge,  U.S.A. 
Wolbach  (1912).     Boston  Medical  and  Surgical  Journal.     Boston. 


CHAPTER  XXIII 
HETEROKARYOTA 

Preliminary — Heterokaryota — Ciliata — Balantidium — Nyctotherus — 

References. 

DIVISION  B.  HETEROKARYOTA  Hickson,  1903. 

PHYLUM  V.  CILIATA  Perty,  1852. 

The  Ciliata  are  free-living  or  parasitic  Heterokaryota,  found 
principally  in  water,  where  they  exist  upon  small  animal  and 
vegetal  organisms  and  the  debris  of  decomposing  plants  and 
animals.  Some  of  them  can  live  in  the  alimentary  canal  of  man 
and  animals,  obtaining  their  food  from  its  contents,  and  increasing 
to  such  numbers  as  to  cause  irritation  of  the  intestine. 

Their  movement  is  by  cilia,  but  always  with  one  end,  the  anterior, 
in  front.  They  turn  round  when  desiring  to  progress  in  a  different 
direction.  This  anterior  end  may  be  similar  morphologically  to 
the  posterior,  or  may  be  characterized  by  being  more  pointed,  by 
having  a  mouth,  or  by  peculiar  sensory  cilia  (Hypotricha),  or  by 
a  peristome  of  long  cilia  (Heterotiicha).  The  body,  which  may  be 
spherical  or  flattened,  is  divided  into  an  ectoplasm  (the  cortex) 
and  endoplasm  (the  medulla).  The  ectoplasm  may  simply  be  a  clear 
outer  layer  of  the  protoplasm,  or  it  may  be  differentiated  into  three 
layers.  The  first  is  very  thick  and  very  tough;  the  next,  called 
the  alveolar  sheath,  is  marked  by  vertical  parallel  lines,  which  are 
the  contractile  myoneme  threads;  while  the  innermost  layer  next 
to  the  endoplasm  consists  of  clear  transparent  ectoplasm. 

The  semifluid  endoplasm  is  in  constant  rotatory  motion,  con- 
taining food  vacuoles,  contractile  vacuoles,  nuclei,  pigment  granules, 
colourless  granules,  crystalline  bodies,  and  smaller  particles.  The 
cytostome  or  mouth  is  present  in  all  except  the  parasitic  Opalinas. 
It  is  a  slit  in  the  cortex  at  the  anterior  end  of  the  body,  which  can 
be  opened  for  the  reception  of  food,  but  is  usually  kept  closed.  It 
may  be  on  the  surface  or  may  be  carried  inwards  by  a  funnel-shaped 
depression  in  the  ectoplasm  called  the  vestibule,  which  may  be 
lined  by  cilia  specialized  for  the  capture  of  food. 

A  cytopyge,  or  cell  anus,  occurs  in  Nyctotherus,  but  as  a  rule  no 
definite  opening  appears,  and  the  undigested  food  is  simply  pushed 
through  the  cortex. 

544 


PHYLUM   V.  CI  LI  AT  A  545 

Two  wholly  distinct  nuclei  exist  in  the  Heterokaryota,  a  mega-  or 
macro-nucleus  and  a  micronucleus.  They  are  not  merely  different 
in  size,  form,  structure,  and  appearance,  but  also  in  function;  for 
the  macronucleus  is  somatic  and  trophic  in  its  function,  while  the 
micronucleus  is  purely  sexual.  They  are  not  comparable  to  the 
tropho-  and  kineto-nuclei  of  the  trypanosomes. 

The  macronucleus  is  generally  well  marked,  but  breaks  down 
into  granules  before  or  after  conjugation.  It  consists  of  an  achro- 
matic portion,  with  a  chromatic  portion  in  the  form  of  a  close- 
meshed  network  of  fibrils,  but  whether  there  is  a  definite  surrounding 
membrane  or  not  is  doubtful. 

The  micronucleus,  when  at  rest,  is  a  minute  irregular  granule  of 
chromatin  lying  in  the  centre  of  a  perfectly  clear  achromatic  area. 
Probably  there  is  only  one  in  each  animal,  and  the  appearance  of 
two  or  more  is  due  to  reproductive  phases  which  are  just  finishing. 

The  Ciliata  are  characterized  by  the  presence  of  protoplasmic  pro- 
cesses projecting  all  over  the  body.  These  are  fine,  short  whips, 
called  cilia,  which  in  places  are  transformed  into  thick  processes 
called  cirri  or  flat  membranes  in  certain  species.  The  cilia  are  pro- 
cesses of  the  pellicle,  but  they  appear  to  be  supported  by  a  thread 
of  specialized  ectoplasm.  The  short,  fine  cilia  are  for  motion,  and 
the  long,  motionless  cirri  for  the  purpose  of  entangling  food-particles. 
The  membranes  are  supposed  to  be  formed  of  fused  cilia.  Tricho- 
cysts  exist  in  the  Holotricha,  and  an  excretory  organ  has  recently 
been  described  by  Metcalfe  in  certain  species  of  Opalina,  parasitic 
in  frogs,  while  other  Ciliata  have  a  contractile  vacuole. 

Reproduction  may  take  place  asexually  by  (i)  transverse  or 
longitudinal  division;  (2)  gemmation,  simple  or  multiple;  (3)  en- 
cystment  and  spore-formation,  or  sexually  by  conjugation. 

1 .  Fission.- — There  is  no  morphological  distinction  between  longi- 
tudinal and  transverse  fission,  in  which  the  following  changes  take 
place:  (r)  A  second  mouth  is  formed;  then  comes  (2)  enlargement 
and  division  of  the  micronucleus;  followed  by  (3)  enlargement  and 
division  of  the  macronucleus;  and,  finally,  (4)  division  of  the 
cytoplasm. 

2.  Encystment  and  Spore-Formation.— The  animal  encysts  and 
breaks  up  into  a  number  of  small  individuals. 

3.  Conjugation.-  Conjugation  has  been  best  described  by  Calkins 
and  Caullery  mPararncecium  aurelia.  Two  conjugating  cells  about 
1  In  same  size  are  placed  so  that  the  mouths  are  directly  opposed. 
Tin  micronucleus  swells,  its  chromatin  becomes  granular,  elongated, 
crescentic,  fusiform,  and  finally  forms  two  nuclei,  each  of  which  at 
once  divides  mto  two.  Of  these,  two  degenerate,  while  the  other  two 
divide  to  form  a  migratory,  or  male,  and  a  stationary,  or  female,  pro- 
nucleus The  male  interchange  and  fuse  with  the  opposite  female 
nuclei,  and  then  the  organisms  separate.  The  macronucleus  frag- 
ments and  disappears,  and  the  synkaryon  breaks  up  into  eight 
micronuclei. 

Four  of  these  swell,  and  are  changed  into  macronudei;  so  that 


54b  HETEROKARYOTA 

four  micro-  and  four  macro-nuclei  are  in  the  same  cell,  which  divides 
into  two  very  small  cells  with  two  macro-  and  micro-nuclei  each. 
These  cells  grow  to  nearly  full  size,  and  then  divide,  giving  rise  to 
the  typical  protozoon,  with  one  macronucleus  and  one  micronucleus. 

Parasitism. — A  great  many  species  of  the  Ciliata  are  parasitic  in 
the  intestine  or  bladder  of  other  animals,  and  some  are  epizoic. 

The  latter  will  often  be  met  with  as  Vorticellce,  living  on  Anopheles 
and  Culex  larvae.  The  former  are  found  largely  in  the  Orthoptera, 
the  Amphibia,  and  in  herbivorous  mammals — e.g.,  horse  and  cow. 

In  man  a  few  have  been  recorded:  Chilodon  dentatus  Dujardin, 
1842;  C.  uncindtus,  Colpoda  cucullus  Schutz,  1889;  Balantidium  coli 
Malmsten,  1857;  B.  minutum  Jakobi  and  Schaudinn,  1898;  Nycto- 
therus  faba  Jakobi  and  Schaudinn,  1898;  N.  giganteus  Krause,  1906; 
N.  africanus  Castellani,  1905. 

Parasitism  does  not  appear  to  affect  the  structure  of  the  animal, 
unless  the  loss  of  the  cytostome  in  Opalina,  parasitic  in  frogs,  is 
considered  to  be  due  to  this  cause. 

Pathogenicity. — The  ciliate  parasites,  as  a  rule,  appear  to  cause 
but  little  effect,  unless  they  are  present  in  large  numbers,  when 
diarrhoea,  often  severe  and  long-persisting,  may  result. 

Classification. — -The  Ciliata  are  classified  into  four  orders: — 

Order  I.  Holotricha  Stein,  1859. — Mobile  Ciliata  without  special 
oral  cirri  {Chilodon,  Colpoda). 

Order  II.  Heterotricha  Stein,  1859.— Mobile  Ciliata  with  special 
oral  cirri  (Balantidium,  Nyctotherus). 

Order  III.  Hypotricha  Stein,  1859.— Mobile  Ciliata  with  well- 
developed  dorsal  and  ventral  surfaces.  Not  known  to  be  parasitic 
in  man. 

Order  I V .  Peritricha  Stein,  1859. — Fixed  Ciliata.  Not  known  to 
be  parasitic  in  man. 

ORDER  I.  HOLOTRICHA  Stein,  1859. 

Definition. — The  Holotricha  are  free-moving  Ciliata,  in  which 
all  the  cilia  are  of  approximately  equal  length  and  thickness,  and 
never  possessing  cirri. 

Remarks. — It  is  divided  into  two  suborders: — 

Suborder  1,  Gymnostomata.— Mouth  closed  when  ingesting  food. 

Suborder  2,  Hymenostomata. — Mouth  always  open,  and  provided 
with  an  undulating  membrane. 

SUBORDER  GYMNOSTOMATA  BiitschH.  1889 
Family  Chlamydodontid^e  Stein. — In  this  family  there  is  a 
genus  Chilodon  Ehrenberg,  1833,  which  includes  oval,  strongly  dorso- 
ventrally  compressed  Chlamydodontidae,  commonly  found  in 
infusions,  of  which  one  species,  C.  dentatus  Dujardin,  1842,  was 
found  in  great  abundance  by  Guiart  in  the  motions  of  a  woman 
suffering  from  severe  dysentery  in  Paris.  Manson  and  Sambon 
have  described  a  case  of  chance-parasitism  due  to  another  species, 
C.  uncinatus  Blochmann,  in  a  patient  from  tropical  South  Africa. 


HETEROTRICHA  547 

They  noted  that  the  parasites  were  only  found  in  th«-  mucus,  never 
in  the  faecal  masses.  They  were  present  in  very  large  numbers, 
and  were  found  to  be  all  gametes,  some  of  which  were  conjugating. 
It  appears  probable  that  Guiart's  parasites  may  really  have  been 
C.  uncituitus,  and  notC.  dentatus. 

SUBORDER  HYMENOSTOMATA  llickson,  1903. 
FAMU  v  Cffl]  [FER1D  E  B  .tschli.-  -The  genus  Cotyodd  Muller.  1773, 
includes  the  kidney-shaped  Chilifera,  with  rows  of  cilia  twisted  from 
left  to  right,  commonly  found  in  hay  infusions,  of  which  one  specie;-. 
Colhoda  cucullus  Schutz,  tSqq,  commonly  found  in  the  water  of 
marshes,  was  noticed  in  a  brickmaker  attacked  with  dysentery  in 
Berlin.  Uromma  caudatum  Dujardin,  1841,  has  been  found  in  the 
motions  of  cases  of  diarrhoea  in  man. 


ORDER  II.  HETEROTRICHA  Stem.  1859. 

The  Heterotricha  are  free-moving  Ciliata,  with  strong  cirri  or 
membranellae,  forming  an  adoral  ring  enclosing  a  space,  the  peri- 
stome, at  one  part  of  which  the  mouth  opens.  The  order  is  divided 
into  Polytrichia,  Oligotricha. 

Polytricha  Hickson,  1903. — -Heterotricha  in  which  the  surface  of 
the  body  is  covered  with  rows  of  short  cilia. 

Families. — Plagiostoniinida-  Claparede  and  Lachmann,  Bursa- 
rinute  Butschli,  Stentorinida  Stein,  Gyrocoryna  Stein. 

Family  Bursarhd^  Kent,  iv 

Synonym. — BursarinitUe  Butschli. 

This  family  includes  the  genus  Balantidium. 

Genus  Balantidium  Claparede  and  Lachmann.  1858. 

Definition.— 5 ursarinidu  with  a  large  peristome  and  a  well- 
marked  anal  aperture. 

Remarks. — Balantidium  is  common  in  the  rectum  of  pigs,  and 
is  sometimes  found  in  the  intestines  of  man.  Cyst  80-100  p  in 
diameter. 

Balantidium  coli  Malmsten.  1857. 

Synonyms.— Parametrium  coli  Malmsten,  1857;  Plagiosioma  coli 

Claparede  and  Lachmann.  185S :  Lcucophrys  coli  Stein.  1800;  Balan- 
tidium coli  Stein,  1867;  Holophrya  coli  Leuckart.  1863. 

Balantidium  coli  is  constantly  found  in  pigs,  and  has  been  found 
in  the  colon  and  the  dejecta  of  man  in  cases  of  cholera  and  diarrhoea. 

In  shape  it  is  oval,  slightly  pointed  anteriorly,  but  this  depends 
upon  whether  the  peristome  is  funnel-shaped  or  contracted.  It  is 
covered  with  cilia  arranged  in  parallel  rows,  which  give  it  a  striated 
appearance. 

It  is  006  to  <  -i  millimetre  in  length  by  0-05  to  007  millimetre  in 
breadth,  and  possesses  a  bean-  or  kidney-shaped  macronucleus,  and 


54» 


HETEROKARYOTA 


a  globular  micronucleus  situated  near  it.  It  develops  asexually  by 
transverse  division  or  by  conjugation.  It  can  encyst,  and  in  this 
condition  pass  from  pigs  to  man.  B.  coli  li\  es  in  the  rectum  of  pigs, 
and  is  transferred  by  its  cysts  to  man. 

It  was  discovered  by  Malmsten  in  a  man  who  had  had  cholera, 
and  was  suffering  from  diarrhoea  and  ulcer  of  the  rectum.  The 
ulcer  had  nothing  to  do  with  the  disease,  as  it  healed,  while  the 
diarrhoea  was  probably  due  to  the  parasites. 

Casagrandi  and  Barbagallo  produced  catarrhal  enterocolitis  in 
young  cats  by  means  of  this  parasite. 

Strong  nas  investigated,  in  a  masterly  manner,  the  enterocolitis 
produced  X>yB.  coli  in  the  Philippine  Islands. 

Balantidium  minutum  Schaudinn,  1899. 

The  body  is  shortly  oval,  with  a  pointed  anterior  extremity. 
Length,  20  to  32  /j,;  breadth,  14  to  20  pi. 

The  peristome  extends  into  the  centre  of  the  body,  and  has  the 
right  lateral  border  fringed  with  cilia,  and  the  left  lateral  border 


^ 

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V 

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-itiii-r^ 

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Fig.  200. — Balantidium  coli  Malmsten. 

(After  Hartmann.     From  the  Archiv  fi/r  Schiffs- 
u.  Tropenhygiene.) 


Fig.  201.  —  Balantidium 
minutum  Schaudinn. 

(After  Hartmann.  From 
the  Archiv  fi'tr  Schiffs- 
u.  Tropenhygiene.) 


terminates  in  a  hyaline  membrane  which  can  pass  over  to  the 
right  side,  and  has  a  row  of  cirri.     The  cysts  are  oval. 

This  parasite  (along  with  Nyctotherus  faba)  was  found  by 
Schaudinn  in  a  German  who  had  often  stayed  in  North  America. 
The  symptoms  were  constipation  alternating  with  diarrhoea  asso- 
ciated with  abdominal  pain. 

Balantidium  minutum  vai .  italicum  Sangiorgi  and  Ugdulena,  1917. 

This  parasite,  which  was  found  by  Sangiorgi  and  Ugdulena  in 
human  faeces,  differs  fronijB.  minutum  in  that  the  nucleus  is  excentric, 
and  in  the  peculiar  orientation  of  the  micronucleus. 


UF.TEROTRICIlA 


549 


Genus  Nyctotherus  Leidy,  1849. 

Definition.  -Body  bean-  or  kidney-shaped,  with  a  large  peristome 
on  the  concave  side  extending  from  the  anterior  end  up  to  the  middle 
of  the  body,  from  where  a  curved  cytopharynx  or  oesophagus  extends 
inwards.  The  macronucleus  is  large,  and  situated  almost  in  the 
cen  re. 

Remarks.— The  species  are  mostly  parasitic  in  the  intestine  of 
Amphibia,  Insect  a,  and  Myriapoda. 

Species  known  in  man:  Nyctotherus  faba  Schaudinn,  1899; 
N.  giganteus  Krause,  E906;  N.  africanus  Castellani,  1905. 


Nyctotherus  faba  Schaudinn,  1899. 

N.  faba  is  flattened  dorso-ventrally,  and  is  26  to  28  /j,  in  length, 
and  ro  to  18  ^  in  breadth,  and  12  fj,  in  thickness 
peristome  are  of  two  kinds,  those 
on  the  right  side,  of  the  size  of 

the  body,    being   true   cilia,   and  W-'-'    '■'    il 

those  on  the  left  side  being  cirri.  W-:::':";'''-'% 


The  cilia  on  the 


Fig.  20Z. —  Xyctothcrus  faba 
Schaudinn. 

(After  Hartmann.     From  the  Archiv 
fiiy  Schiffs-  it.  Tropenhygiene.) 


Fig.  203. — Xyctotherus  africanus 
Castellani. 


The  contractile  vacuole  is  large,  and  situated  posteriorly.  The 
macro  nucleus  is  in  the  centre,  and  is  peculiar  in  having  four  or 
five  large  collections  of  chromatin  at  its  periphery.  The  micro- 
nucleus  lies  close  by.     The  cysts  are  oval. 

This  species  was  discovered  by  Schaudinn  in  the  same  patient 
as  Balantidium  minutum. 


Nyctotherus  giganteus  P.  Krause,  1906. 

Synonym.    Balantidium  giganteum  P.  Krause,  1906. 

rhis  organism,  along  with  Trichomonas  intestinalis,  was  found  by 
Krause  in  the  dejecta  of  persons  suffering  from  typhoid  in  Breslau. 

It  is  shaped  like  a  truncated  cone,  with  the  anterior  end  narrowed, 
and  the  posterior  broad.  Lengtu,  90  to  400  [j,;  breadth,  60  to  150  (/,. 
Surface  covered  with  cilia.  The  peristome  is  situated  laterally, 
and  from  it  a  cytopharynx  leads  inwards. 


55o  HETEROKARYOTA 

The  macronucleus  is  large  and  bean-shaped,  while  the  micro- 
nucleus  is  small  and  round.  One  or  two  vacuoles  can  be  seen.  The 
cytopyge  is  situated  posteriorly. 

In  the  faeces  the  parasite  becomes  rounded  off  and  encysted, 
and  then  divides  into  four. 

Nyctotherus  africanus  Castellani,  1905. 

Found  by  Castellani  in  a  Baganda  native.  N.  africanus  is  hour- 
glass shaped,  with  the  anterior  portion  much  less  developed  than 
the  posterior.  Length,  40  to  50  ^;  breadth,  30  to  40  u.  The 
surface  is  covered  with  very  minute  cilia,  which  are  generally  more 
evident  on  the  posterior  portion,  being  almost  invisible  on  the 
anterior. 

The  peristome  is  short.  The  cytoplasm  is  finely  granular  through- 
out. The  nucleus  is  situate  far  posteriorly,  near  the  contractile 
vacuole.  The  micro  nucleus  is  very  small,  and  situated  close  to  the 
macronucleus.     No  food  vacuoles  are  to  be  seen. 

Neither  division,  conjugation,  nor  encystment  are  known. 

The  patient,  who  had  diarrhoea  alternately  with  long  periods  of 
constipation,  was  suffering  from  sleeping  sicknesr . 

The  caecum  contained  many  parasites,  as  did  other  parts  of  the 
bowel.  The  mucosa  of  the  caecum,  colon,  and  rectum  were  slightly 
congested,  but  not  ulcerated.  Castellani  originally  considered  this 
parasite  to  belong  to  the  genus  Nyctotherus,  but  more  complete 
investigations  will  probably  show  that  it  constitutes  a  new  genus. 

SUBORDER  HYMENOSTOMATA  Biitschli,    1889. 
Genus  Uronema  Dujardin.  1841. 
Definition. — Hymenostomata  ovate  or  elongate  with  one  or  more  caudal 
setae. 

Type  Species. —  Uronema,  marinum  Dujardin,  1841. 

Uronema  caudatum. 

Found  in  a  case  of  diarrhoea. 

REFERENCES. 

Heterokaryota. 

Fantham,  Stephens  and  Theobald  (1916).     The  Animal  Parasites  of  Man. 

London. 
Hickson.     Treatise  on  Zoology,  E.  Ray  Lankester,  Part  I..  Second  Fascicle, 

1903.  P-  361. 
Calkins  and  Caullery.     Archiv  f.  Protistenkunde,  1907,  vol.  x.,  2  and  3, 

P-  375- 
Metcalfe.     Arch,  f .  Protistenkunde,  1907,  vol.  x.,  2  and  3,  pp.  183,  365. 

Chilodon  dentatus. 
Guiart,  M.  J.  (1903).     Comptes  Rendus  des  Seances  de  la  Societe  de  Biologie 

Balantidium  coli. 

Bensen  (1908).     Archiv  f.  Schiffs-  u.  Tropenhygiene,  xii.  672. 
Manslove  (1917).     Philippine  Journal  of  Science,  xii.,  Sec.  B. 


REFERENCES  55i 

Balantidium  minutum. 

Bensen    1908).     Op.  cit.,  673. 

Nyctotherus  faba. 

Jakoby  and  Schaudinn.     Centralblatt  fur  Bakteriol.  u.  Parasitol.,  I     xxv., 
1899,  4S7. 

Nyctotherus  giganteus. 
Krause,  P.     Deutsche  Archiv  fiir  Klin.  Med.,  lxxxvi.  442. 

Nyctotherus  africanus. 
Castellani.     Centralblatt  fiir  Bakteriol.  11.  Parasitol.,  1905,  xxxviii.  66,  67 


CHAPTER  XXIV 
"l REM A TOD A 

Metazoan  parasites — Platyhelmia — Trematoda — Classification — Malacotylea 
— Digenea — Prostomata — •  Paramphistomoidea — Fascioloidea —  Schisto- 
somidre — References. 

SUBKINGDOM  II.  METAZOA. 

Definition. — Metazoa  are  free-living  or  parasitic,  multicellular 
animals,  characterized  by  a  physiological  division  of  labour  among 
their  cells. 

Remarks. — Tropical  medicine  is  only  concerned  with  parasitic 
IMetazoa,  and  chiefly  with  those  which  affect  man.  Parasitic  Metazoa 
may  be  ectoparasites — as,  for  example,  many  species  of  the  Insecta — 
or  endoparasites — -as,  for  example,  many  worms.  The  ectoparasites 
can  cause  disease  by  introducing  toxins,  protozoa,  or  bacteria  into 
the  tissues,  and  in  this  way  they  are  of  the  utmost  importance  as 
the  spreaders  of  disease,  for,  as  is  generally  recognized,  a  disease 
is  very  often  limited  by  the  special  cecological  conditions  of  the 
animal  which  spreads  its  germ.  Many  of  the  ectoparasites,  such 
as  mosquitoes,  are  temporary;  or,  like  "ticks,  periodic;  while  others, 
like  lice,  are  permanent  parasites. 

With  regard  to  the  endoparasites,  their  ill  effects  on  the  host 
depend  upon  many  factors  which  have  been  recently  studied  in 
considerable  detail. 

The  effects  of  metazoan  parasites  on  their  hosts  depend  upon  the 
species  of  the  parasites,  their  condition,  the  number  present,  their 
presence  in  certain  organs,  bacterial  infection,  their  migration  in 
the  1»  kIv,  the  loss  to  the  host  in  feeding  them,  the  damage  caused 
by  their  toxins,  and  the  condition  of  the  host. 

1.  The  Species  of  Parasite. — Filaria  may  exist  in  a  host  without 
apparent  ill  effect,  but  A  .•  cylostoma  will  produce  anaemia,  oedema, 
and  perhaps  death. 

2.  The  Condition  of  the  Parasite. — The  dead  eggs  of  Filaria  are 
believed  to  block  the  lymph  channels,  and  give  rise  to  swelling  and 
rupture  of  these  vessels,  thus  bringing  about  lymphangitis  and 
elephantiasis,  while  the  Living  larvae  apparently  do  no  harm. 

3.  The  Number  of  Parasites. — A  few  Ascarides  may  cause  no 
symptoms,  while  a  large  number  may  lead  to  serious  disease. 

4.  The  Organ  Affected. — Asca  rides  in  the  alimentary  canal  are  not 
nearly  so  virulent  as  in  the  liver,  while  Paragonimus  ringeri 
in  the  lungs  will  cause  a  disease  somewhat  resembling  phthisis. 

552 


METAZOA  553 

Ascarides  may  cause  serious  mischief  in  the  pancreas,  as  observed  by 
Chalmers;  and  may  cause  appendicitis,  as  noted  by  Blanchard, 
Mctchnikoff.  Castellani,  and  others. 

5.  Bacterial  Infection  caused  by  the  Parasite. — Trichuris  trichiura 
may  be  a  harmless  parasite  in  itself,  but  it  is  quite  capable  of  intro- 
ducing bacteria  into  the  mucosa  of  the  vermiform  appendix  and 
causing  appendicitis,  for,  as  is  well  known,  it  burrows  in  the  mucosa. 
The  fever  so  often  found  in  patients  suffering  from  ankylostomiasis 
is  probably  caused  by  intestinal  bacteria  entering  the  small  wound 
produced  by  the  ancylostome. 

This  method  of  producing  ill  effects  upon  the  host  appears  to  us 
to  be  of  the  greatest  importance  in  the  tropics,  and  is,  we  fear,  often 
overlooked. 

6.  Migration  of  the  Parasite  in  the  Body. — The  larvae  of  A  ncylo- 
stoma  as  they  enter  the  skin  cause  a  dermatitis  known  as  Cooly  itch, 
sore  feet,  ground  itch,  etc.,  which  may  be  primarily  due  to  the 
irritation  of  the  worm,  or  secondarily  to  bacteria  introduced  into 
the  skin  by  its  agency.  The  wanderings  of  the  larvae  of  Trichinella 
spiralis  through  the  muscles  cause  the  severe  symptoms  of  trichiniasis. 

Sambon  has  pointed  out  that  much  that  is  obscure  in  the  patho- 
genesis of  various  forms  of  helminthiasis  might  be  elucidated  by  a 
better  knowledge  of  the  migrations  of  the  entozoa  in  their  immature 
stages  from  the  time  they  attack  the  host  to  that  of  their  settlement 
in  their  selective  anatomical  habitat.  He  believes  that  many  forms 
do  not  go  directly  to  the  part  in  which  they  are  usually  found,  but 
may  take  a  very  different  route  from  that  generally  accepted,  and 
may  even  live  for  a  length  of  time  in  other  structures  before  reaching 
such  organs  as  the  alimentary  canal  or  nasal  fossae,  which  are  only 
s<  mght  in  order  to  enable  the  young  to  escape  from  the  host.  During 
these  wanderings  mechanical  injury  may  be  caused  to  the  host,  and 
pathogenic  micro-organisms  may  be  carried  from  one  part  of  the 
body  to  another. 

7.  The  Absorption  of  Food. — Leuckart  estimates  that  a  Dibothrio- 
cephalus  latus  gives  off  in  a  year  proglottides  to  the  weight  Oi 
r[i)  grammes;  Tcenia  saginata,  550  grammes;  and  Ascaris  lumbri- 
coides,  42  grammes  of  eggs  in  the  same  period. 

If  the  number  of  these  parasites  is  great,  the  drain  on  the  host 
must  be  considerable,  especially  in  children  who  need  food  for  growth. 

8.  Toxins.  -This  subject  has  already  been  dealt  with  (p.  205). 

9.  The  Condition  of  the  Host. — The  condition  of  the  host  is  also  a 
factor  in  the  diseases  produced  by  these  parasites,  for  though 
Ascarides  may  be  harmless  in  a  healthy  intestine,  they  may  per- 
forate a  typhoid  or  dysenteric  ulcer,  or  a  traumatic  lesion  of  the 
bowel,  and  cause  fatal  peritonitis. 

With  regard  to  the  question  as  to  whether  parasites  ever  benefit 
human  beings,  reference  can  be  made  to  the  belief  that  the  develop- 
ment of  the  Bacillus  tuberculosis  Koch  is  delayed  by  the  presence  of 
entozoa  in  the  bowels,  a  view  which,  with  our  Eastern  experience, 
we  are  unable  to  support. 


554  TREMATODA 

The  old  idea  that  worms  were  good  for  children  has  died  out  long 
ago,  and  we  know  of  no  eases  of  mutualism,  or  benefit  to  parasite 
and  host,  in  the  animal  parasites  of  man. 

True  parasitism  is  found  in  those  cases  in  which  the  parasite 
benefits  and  the  host  is  injured.  Chance  parasites  are  animals 
which  accidentally  and  temporarily  become  parasites. 

The  life-history  of  a  parasite  may  be  simple,  being  carried  out  in 
one  host,  or  it  may  be  complex,  with  one  or  more  hosts  for  its  larval 
stages  and  another  for  its  adult  condition. 

Generally  these  hosts  bear  a  direct  relationship  to  one  another, 
the  intermediary  host  often  being  herbivorous,  and  thus  becoming 
infected  through  eating  faecally  contaminated  food,  and  the  definitive 
host  being  carnivorous  or  omnivorous,  becoming  infected  through 
eating  the  herbivorous  host  of  the  larva. 

Some  parasites,  particularly  the  Microfilariae  in  the  blood,  show 
a  remarkable  periodicity  in  their  habits,  which  appears  to  be  asso- 
ciated with  the  means  of  escape  from  the  definitive  host  by  some 
intermediary  host,  such  as  a  mosquito  or  a  tick,  whose  habits  agree 
with  the  periodicity  of  the  parasite.  Such  correlations  are  very 
numerous  in  Nature — as,  for  example,  the  opening,  or  emitting  of 
strong  odours,  by  certain  flowers  at  definite  times  of  the  day  or 
night,  which  accords  with  the  habits  of  insects  which  help  on  their 
fertilization. 

Tropical  countries  are  the  home  par  excellence  for  parasites,  as 
the  means  of  infection  by  bad  sanitation,  biting  flies,  etc.,  are  easily 
available.  It  is  therefore  obvious  that,  as  there  may  be  many 
methods  of  infection  by  the  mouth,  the  skin,  and  the  nose,  preven- 
tion is  not  an  easy  matter.  It  depends  upon  two  factors — -personal 
and  public  hygiene.  The  question  of  personal  hygiene  is  the  more 
important  and  more  easily  applied,  as  only  one  person  is  concerned, 
while  that  of  public  hygiene  is  more  expensive  and  not  so  easy  to 
apply,  as  many  people  have  to  act  in  unison  in  order  to  produce  any 
effect. 

Personal  hygiene  includes  such  matters  as  personal  and  domestic 
cleanliness;  protection  of  the  skin  against  infection,  by  the  use  of 
mosquito  curtains  and  boots;  avoidance  of  infection  from  domestic 
pets,  such  as  dogs  and  cats,  by  not  too  close  association  with  them; 
the  protection  of  articles  of  food  against  flies  and  vermin ;  and  the 
careful  cooking  of  food  and  filtering  of  water. 

With  regard  to  public  rules,  the  first  is  the  proper  disposal  of 
waste,  particularly  of  faecal  matter;  careful  cattle  and  meat  inspec- 
tion in  well-kept  slaughter-houses ;  and  the  destruction  of  ownerless 
dogs  by  means  of  a  lethal  chamber,  in  which  they  are  killed  by  gas. 

Classification.— The  mctazoan  parasites  of  man  can  be  arranged 
into  phyla  as  follows: — 

Phylum       I.  Platyhelmia. 
Phylum     II.  Nemathelmia. 
Phylum  III.  Annulata. 
Phylum    IV.  Arthropoda. 


PL  A  T  Y  HELM  I A  555 

PHYLUM  I.  PLATYHELMIA  Vogt,  185 1. 

Synonyms. — Platodes  Leuckart,  1854;  Platyhelminthes  Gegenbaur, 
1859;  Platyhelminthes  Minot,  1877. 

Definition. — Platyhelmia  are  bilaterally  symmetrical  Metazoa, 
with  dorso-ventrally  flattened  bodies,  and  without  a  true  ccelom. 

Morphology. — -The  Platyhelmia  are  flat-worms,  with  an  oval  or 
tape-like  body,  which  is  either  covered  by  a  ciliated  epithelium,  as  in 
the  free-living  Turbellaria,  or  with  a  cuticle  under  which  the  surface 
epithelium  has  sunk  into  the  parenchyma,  forming  the  so-called 
subcuticular  layer  in  the  parasitic  Trematoda  and  Cestoda.  A  well- 
developed  musculo-dermal  layer  is  present,  but  there  is  no  ccelom. 

The  mouth  is  generally  situated  at  the  anterior  end,  when  present, 
but  it  may  be  moved  to  the  inferior  surface,  and  opens,  via  a 
pharynx,  into  a  forked  or  branched  gut,  which  has  no  anal  aperture. 
The  alimentary  canal  may,  however,  be  wanting  (Cestoda).  The 
excretory  system  begins  in  the  so-called  flame  cells — i.e.,  cells 
provided  with  a  leash  of  cilia  from  which  fine  channels  run,  uniting 
together  to  form  larger  channels.  These  ultimately  empty  into  a 
pair  of  laterally  placed  canals,  opening  to  the  exterior  separately 
or  together,  often  through  an  excretory  vesicle. 

The  nervous  system  consists  of  a  large,  bi-lobed,  cerebral  gan- 
glion, with  nerves  running  forwards  and  backwards. 

The  Platyhelmia  are  mostly  hermaphrodite,  but  may  rarely  be 
unisexual ;  the  ova  are  produced  in  the  ovary,  near  which  they  are 
fertilized,  and  then,  after  obtaining  food-yolk  from  the  yolk  reservoir, 
which  has  received  it  via  the  vitelline  ducts  from  the  yolk  glands, 
they  acquire  a  shell  in  a  shell  gland,  and  then  enter  a  uterus,  through 
which  they  slowly  pass  to  the  exterior. 

The  male  organs  consist  of  testes,  vasa  deferentia,  vesicula 
seminalis,  and  a  cirrus  pouch,  with  a  cirrus  and  a  so-called  prostate 
gland. 

Classification. — The  Platyhelmia  are  classified  into : — 

Class  I.  Turbellaria.— Free-living  flat-worms,  covered  with  cilia. 

(lass  II.  Trematoda. — Parasitic  flat-worms  with  an  alimentary 
canal ;  cuticle  non-ciliate. 

Class  III .  Cestoidea. — Parasitic  flat-worms  without  an  alimentary 
canal;  cuticle  non-ciliate. 

Class  I.  does  not  enter  into  the  subject  under  discussion. 

CLASS  II.  TREMATODA  Rudolphi,  1808. 

Synonyms.— Sucking  Worms. 

Definition. — -The  Trematoda  are  parasitic  Platyhelmia,  which  re- 
tain the  mouth  and  alimentary  canal,  but  in  which  the  epidermis 
not  merely  loses  its  cilia  during  development,  but  is  sunk  into  the 
mesoblast  after  secreting  the  chitinous  cuticle.  Suckers  are  de- 
veloped in  the  region  of  the  mouth,  and  also  on  the  ventral  surface. 

Remarks.— The  knowledge  of  the  Trematoda  began  in  1379,  when 


Fig.  2oj — Fascioh 
(x  250.) 


S3 

Fig.   206. — Opistorchis  sinensis 
(  X250.) 


Fig.  207. — Schistosoma  japonicwn. 
(x  250.) 


Fig.  208. — Schistosoma  hccma-  Fig.  209. — Schistosoma  mansoni. 

tobium.     1x35°-)  (x35°-) 

Figs.  204-209. — Eggs  of  Various   Trematodes  found  in  Human  Faeces 
(From  photomicrographs  by  J.  J.   Bell.) 


TREMATODA 


557 


Jehan  de  Brie  discovered  the  liver-fluke  in  the  sheep,  which  was  sub- 
sequently described  by  Gabucinus  in  1547;  but  it  was  not  till  the 
time  of  O.F.  Midler,  in  1777,  that  any  accurate  idea  of  their  form  was 
obtained.  Zeder  in  1  voo  made  the  first  attempt  to  classify  parasitic 
worms,  calling  the  Trematodes  '  sucking-worms  ' ;  while  in  1808 
Rudolphi  invented  the  name  of  the  class,  deriving  it  from  the  Greek 
rprj/uarojSy]^  which  means,  '  pierced  by  holes.'  After  this  date  come 
many  observers,  among  whom  may  be  mentioned  Laurer  (whose 

"  canal  still  bears  his  name)  in 
1830,  van  Beneden  in  T858,  and 
Leuckart  in  1867  (who  divided 
them  into  Distomea  and  Poly- 
stomea),  and  Thomas  in  1883, 


Fig.  210. — Diagram  of  a  Type  of 
the  Female  Generative  Appar- 
atus of  a  Trematode. 

(After  Stiles.) 
1,  Ovary;  z.  uterus;  3,  shell  gland; 
4,  ootype;  5,  ovarian  tluct ;  6,  Lau- 
rer's  canal;  7,  vitellarian  duct. 


Fig.  211. — Diagram  of  Another 
Type  of  the  Female  Genera 
tive  Apparatus  of  a  Trematode. 

1,  Ovary;  2,  ovarian  duct;  3,  shell 
gland ;  4,  ootype ;  5,  uterus ;  6, 
Laurer's  canal ;  7,  vitellarian  duct  ; 
8,  receptaculum  seminis. 


who  worked  out  the  development  of  Fascicla  hepatica.  In  1892 
Monticelli  revived  an  older  classification  of  the  group  by  Burmeister 
into  three  orders. 

In  1899  Looss  completely  revolutionized  the  whole  classification. 
His  work  has  since  been  extended  by  Leiper,  Odhner,  Liihe,  and 
others.  Of  recent  years  our  knowledge  of  the  life-history  of  these 
parasites  has  been  extended  in  a  remarkable  manner  by  Leiper  and 
numerous  Japanese  observers. 

Morphology.— In  shape  the  Trematoda  are  generally  leaf-like  or  tongue- 
shaped,  and  but  rarely  cylindrical.  They  are  provided  with  a  cuticle,  which 
may  have  spine-like  scales,  and  with  one  or  two  suckers,  oral  and  ventral 
(often  called  the  '  acetabulum  '),  which  are  capable  of  fixing  the  parasites  by 
the  action  of  their  equatorial,  meridional,  and  radial  muscular  fibres  to  the 
lining  of  the  alimentary  canal,  or  such  other  organ  as  they  may  inhabit. 

The  mouth  lies  in  the  oral  sucker,  and  leads  to  a  pharynx.  The  oesophagus 
may  be  short  or  long,  with  or  without  a  sphincter  muscle,  and  is  often  pro- 
vided with  unicellular  salivary  glands.  The  intestinal  tubules,  which  may 
be  branched  or  simple,  end  blindly,  there  being  no  anal  aperture.  The  food 
is  composed  oi  epithelial  eel  Is  and  blood. 

The  excretory  system  is  well  developed,  commencing  in  special  cells  pro- 
vided with  cilia  (flame  cells),  which  communicate  with  excretory  capillaries. 
These  open  into  canals,  which  anastomose  freely,  and  then  join  the  gathering 
tubes,  which  open  into  an  excretory  vesicle.     This  vesicle,  which  may  be  long 


558  TREMATODA 

or  short,  pear-shaped  or  Y-shaped,  generally  opens  posteriorly,  but  may 
open  dorsally  above  the  acetabulum. 

The  sexes  are  but  rarely  separate,  hermaphroditism  being  usual.  The 
male  organs  consist  of  testes,  which  may  be  simple  or  branched,  and  are, 
as  a  rule,  situated  posteriorly.  The  vas  deferens  leads  forwards  sometimes 
through  a  vesicula  seminalis  to  the  genital  opening,  below  which  a  cirrus 
enclosed  in  a  muscular  pouch  provided  with  glands,  called  the  '  prostate,' 
may  be  found. 

The  female  organs  consist  of  an  ovary,  which  may  be  branched  and  is 
usually  situated  in  front  of  the  testes,  and  an  ovarian  duct,  which  joins  with 
the  vitellarian  duct  from  the  yolk  glands,  making  a  tube,  called  the  '  ootype,' 
surrounded  by  the  shell  gland,  in  which  the  egg  is  formed  (Fig.  210). 

A  curious  little  canal,  Laurer's  canal,  joins  by  its  inner  aperture  the  ootype 
near  the  uterine  tube,  while  its  outer  aperture  is  found  on  the  dorsal  surface. 
The  homology  of  this  little  canal  is  not  quite  clear ;  it  may  be  a  vagina.  Some- 
times a  receptaculum  seminis  is  present.  The  ootype  opens  into  the  uterine 
tube,  which  is  usually  much  coiled,  and  has  its  anterior  portion  thickened,  to 
form   the  metatrema  or  vulva,  which  opens  into  the  genital  orifice  (Fig.  211). 

The  genital  pore  varies  in  position,  being  situated  in  the  mid-line  in  front 
of  or  behind  the  ventral  sucker  as  a  rule.  Rarely  it  opens  rather  laterally 
and  has  a  muscular  depression  of  its  own. 

Life-History. — -The  full  life-history  of  a  number  of  forms  has  been 
worked  out  by  Leuckart  and  Thomas  for  Fasciola  heftatica,  under 
which  heading  details  will  be  given,  by  Looss  for  various  amphi- 
stomes,  by  Leiper  for  the  genus  Schistosoma,  and  by  numerous 
Japanese  observers  for  other  forms. 

Typically  there  is  an  alternation  of  generations  where  one  sexual 
generation  is  followed  by  two  asexual  generations.  Two  hosts  are 
required  for  the  whole  life-cycle. 

Leiper  has  given  the  following  scheme  for  the  development  of  a 
digenetic  trematode: — 

1.  Definitive  host         .  .  .  .  .  .  . .     Egg. 

2.  First  transition        ..  ..  ..  ..     Miracidium. 

'  Sporocyst 
S    Intermediate     Sporocyst  and  daughter  cysts 

host  Sporocyst  and  Rediae  Cercance. 

Sporocyst,  Rediag,  and  daugh- 
I      ter  Rediae 

4.  Second  transition    ..     Free-swimming  or  encysted  Cercarice. 

5.  Definitive  host        Adults. 

Luhe  has  provided  the  following  classification  of  Cercariae  (slightly 
modified  for  convenience  of  reference) : — 

A.  Body  without  internal    differentiation.     With  cuticular  ala— 

Lophocercarice. 

B.  Body  with  internal  differentiation.     Tails  may  or  may  not  be 

forked  :— 

I.  Acetabulum  absent — Monostomes. 
II.  Acetabulum  present:— 

(a)  Posteriorly  situate — Amphistomes. 

(b)  Ventrally  situate : — 

1.  Mouth  central — Gasterostomes. 

2.  Mouth  terminal — Distcmes. 


TREMA  TOD  A  559 

The  Distome  cercarice  may  be  identified  as  follows: — 

A.  Tails  absent — Cercarice. 

B.  Tails  present : — 

I.  Tails  stumpy — Monocercous. 
II.  Tails  well  developed: — 

(a)  Tails  joined,  forming  colony — Rattenkonig  cercarice. 

(b)  Tails  not  so  joined: — 

1.  Tails  set  with  spines — -Trichocercous. 

2 .  Tails  not  set  with  spines  :— 

(a)  Tails  forked  at  end — Furcocercous. 

(b)  Tails  not  so  forked: — • 

(c)  Base  of  tail  forms  space Jn to  which  body 

can  be  drawn- — Cystocercous. 

(d)  Base  of  tail  forms  no  such  space: — 

(e)  Tail  as  wide  or  wider  than  body— 

Rhopalocercous . 

(f)  Tail   narrower   than   body— Lepto- 

cercous. 
The   Leptocercous    cercarice    may    be    further    differentiated    as 
follows : — 

A.  Body  armed  anteriorly : — 

I.  With  collar  and  crown  of  thorns — Echinostomes. 
II.  With  a  stylet — Xiphidiocercarice. 

B.  Body  unarmed  anteriorly — Gymnocephalous  cercarice. 

Habitat. — -These  parasites  are  found  in  all  classes  of  the  verte- 
brates, and  may  occur  in  any  of  the  organs,  but  the  most  common 
in  man  are  those  of  the  liver,  the  intestinal  tract,  the  lungs,  and  the 
urinary  bladder.  It  is  important  to  remember  that  the  adult 
parasites  may  live  in  domestic  animals,  especially  in  cats,  that 
they  may  affect  pigs  and  cattle,  that  development  takes  place  in 
snails,  and  that  the  cercaria  are  free-swimming,  but  encystment  on 
grass,  water-weeds,  etc.,  must  be  borne  in  mind. 

Pathogenicity. — -Apparently  the  smaller  forms  can  live  in  human 
beings  without  being  suspected,  but  irritation  of  the  bladder,  liver, 
intestine,  and  lungs  may  result  either  as  the  effect  of  the  eggs  or  of 
the  parasite. 

Diagnosis. — -The  systematic  examination  by  the  microscope  of 
the  faeces  after  centrifuging,  especially  in  cases  of  diarrhoea,  and  of 
t  he  urine  and  sputum,  is  the  only  certain  method  of  diagnosis. 

Treatment.— The  treatment  of  infections  by  these  animals  is 
little  studied,  but  Christopherson  has  lately  recommended  Tartar 
ic  [vide  Chapter  LXXIX.,  and  more  especially  Chapter 
LXXXII.).  One  may  try  to  kill  or  expel  the  intestinal  forms  by 
chloroform  mixed  with  eucalyptol  "or  Chenopodium  followed  by 
purgation,  as  described  in  Chapter  LXXV.  (Ankylostomiasis),  or  by 
extract  of  male  fern  all  in  the  same  chapter  (Taeniasis). 

Prophylaxis. — We  do  not  know  enough  about  the  life-cycles  to 
lay  down  general  rules  about  prophylaxis,  but  it  will  be  obvious 


560  TREMA  TOD  A 

that  the  cat,  the  dog,  the  pig,  and  cattle  are  indirect  sources 
of  infection,  while  bathing,  wading  and  drinking  water  as  well  as 
green  vegetables,  particularly  those  not  cooked,  must  be  regarded 
as  definite  sources  of  infection,  and  so  must  that  delicacy  the  edible 
snail,  which  may  not  be  properly  cooked. 

Classification. — The  classification  of  the  Trematoda  is  as  follows : — 

SUBCLASS  I.  HETEROCOTYLEA  Monticelli. 

Synonyms.— Polystomea  Leuckart,  Peciobothrii  Burmeister,  and 
Monogenea  van  Beneden. 

These  Trematodes  are  generally  ectoparasitic,  but  may  be  endo- 
parasitic  in  amphibia  and  tortoises. 

SUBCLASS  II.  ASPIDOCOTYLEA  Monticelli. 

Synonym. — Aspidobothrii  Burmeister. 

These  are  lowly  organized  endoparasitic  trematodes,  with  one 
large  sucker  occupying  the  whole  ventral  surface,  found  in  tortoises, 
marine  fish,  and  shellfish . 

SUBCLASS  III.  MALACOCOTYLEA  Monticelli. 

Synonyms. — Distomea  Leuckart,  Malacobothrii  Burmeister,  and 
Digenea  van  Beneden,  1858. 

Definition. — Typical  endoparasitic  trematodes,  with  never  more 
than  two  sucking-discs,  oral  and  ventral,  and  a  Laurer's  canal. 

Remarks. — The  Malacocotylea  include  all  the  human  trematode 
parasites. 

Classification. — -The  Malacocotylea  may  be  divided  into  orders 
as  follows : — 

A.  Development  without  alternation  of  generations—  Order  i, 

Monogenea  van  Beneden,  1858. 

B.  Development  with  alternation  of  generations — Order  2, 

Digenea  van  Beneden,  1858. 

We  are  only  concerned  with  Order  2. 

ORDER  DIGENEA  van  Beneden,  1858. 

Definition.-  -Malacocotylea  with  a  single  median  anterior  sucker, 
a  vagina,  and  few  eggs  which  develop  by  alternation  of  generations. 

Classification. — This  order  is  divided  into  several  suborders,  of 
which Prostomata  concerns  us. 

Mouth    surrounded    by   the  anterior  sucker— Suborder  Pro- 
stomata Odhnei,  1905. 

Suborder  Prostomata  Odhner,  1905. 

Definition.-  Digenea,  in  which  the  mouth  is  surrounded  by  the 
anterior  sucker. 

Classification.— The  Prostomata  are  divided  into  superfamilies 
in  the  following  manner: — 


CLADORCHIINM  561 

A.  Acetabulum  or  posterior  sucker  caudoterminal,  subterminal, 

or  ventroterminal,  and  behind  the  genitalia  or  at  the 
most  embraced  by  the  vitellaria— Super-family  i.Param- 
phistomoidea  Stiles  and  Goldberger,  1910. 

B.  Acetabulum  or  posterior  sucker  ventral  and  separated  from 

the  posterior  extremity  by,  at  least,  a  part  of  the  genitalia 
— Super-family  2,  Fascioloidea  Stiles  and  Goldberger,  1910. 

Super-Family  Paramphistomoidea  Stiles  and  Goldberger, 

1910. 

Synonym.— A  mphistomata  Rudolphi,;_i8oi. 

Definition. — Prostomata  with  acetabulum,  caudoterminal  or  sub- 
terminal,  or  ventral  close  to  the  caudal  end.  Oral  sucker  and 
oesophagus  present.  Caeca  two  in  number.  Hermaphrodites  with 
genital  pore  ventro-median,  prae-equatorial,  praetesticular,  and  prae- 
ovarial,  and  with  one  or  two  prae-ovarial  testes.  Vitellaria  paired. 
j&Type  Family. — Paramphistomidce  Fischoeder,  1901,  restricted. 

Classification. — Paramphistomidce  Fischoeder,  1901  restricted; 
Gastrodiscidce  Stiles  and  Goldberger,  1910;  Gastrothylacidce  Stiles  and 
Goldberger,  1910.  The  last-named  family  does  not  contain  any 
human  parasites. 

Family  I.  Paramphistomidae  Fischoeder,  1901,  restricted. 

Definition.— Pyriform  paramphistomoidea  with  ventral  pouches 
absent. 

Type  Genus. — Paramphistom  ion  Fischoeder,  1901. 

Classification. — The  Paramphistomidae  are  classified  into  the 
following  subfamilies  -.Paramphistomince  Fischoeder,  1910,  restricted ; 
Cladorchiince  Fischoeder,  1901 ;  and  Diplodiscince  Cohn,  1904;  but 
of  these  only  the  second  concerns  us. 

These  suborders  may  be  recognized  as  follows:— 

A.  Oral  sucker  without  evaginations — Paramphistomince. 

B.  Oral  sucker  with  evaginations — Cladorchiince. 

Subfamily  Cladorchiince  Fischoeder,  1901. 

Definition. — -Paramphistomidae  with  oral  sucker  with  evagination. 

Classification. — The  Cladorchiinae  can  be  subdivided  into  the 
Stephanopharyngince  Stiles  and  Goldberger,  19m,  with  circular 
evagination,  and  Cladorchiince  sens/i  stricto  Fischoeder,  1910,  with 
paired  evagination.  This  last  subdivision  contains  the  following 
genera :  Cladorchis  Fischoeder,  1901,  which  is  the  type  genus  ;P  sen  do  > 
discus  Sonsino,  1895;  Chiorchis  Fischoeder,  1901;  Tasiorchis 
Fischoeder,  1901 ;  Pseudocladorchis  Daday,  1907;  Microrchis  Daday, 
1907;  Pfenderius  Stiles  and  Goldberger,  1910;  and  Watsonius  Stiles 
and  Goldberger,  1910;  of  which  the  last  is  of  importance  in  tropical 
medicine. 

It  may  be  remarked  that  this  subfamily  will  probably  soon  be 
made  a  family,  and  its  divisions  subfamilies. 

36 


562 


TREMA  TOD  A 


Watsonius  Stiles  and  Goldberger,  1910. 

Definition.- — Cladorchiinse  without  genital  sucker,  with  lobate 
or  lobulate  testes,  without  cirrus  pouch,  and  with  each  oral  invagina- 
tion single. 

Species. — Watsonius  watsoni  (Conyngham,  1904)  Stiles  and  Gold- 
berger, 1910. 

Watsonius  watsoni  (Conyngham,  1904)  Stiles  and  Goldberger,  1910. 
Synonyms. — Cladorchis  watsoni  (Conyngham,  1904),  Amphistomum 
watsoni  (Conyngham,  1904),  Par  amphistomum  watsoni  (Conyngham, 
1904). 

Definition. — Watsonius  with  the  characters  of  the  genus. 
History. — Watsonius  watsoni  was  first  discovered  in  the  duodenum 
and  upper  part  of  the  jejunum  of  a  negro  who  had  come  from 

Adamawa,  in  late  German  West 
-^=a^     a  Africa,  to  Northern  Nigeria.    Since 

its  discovery  it  has  been  reported 
near  Lake  Chad.     The  type  was 
kY\  first    described    by    Conyngham, 

later  by  Shipley,  and  in  1910  by 
Stiles  and  Goldberger. 

Morphology. — The  parasite  is  red- 
dish-yellow when  fresh,  8  to  10  milli- 
metres in  length  by  4  to  5  millimetres 
in  breadth.  In  shape  it  is  oval  or 
pyriform.  The  ventral  sucker  is  large 
and  situated  posteriorly  and  subter- 
minally,  while  the  oral  sucker  is  so 
small  as  to  be  hardly  worthy  of  being 
considered  a  true  sucker.  It  has  a 
pair  of  lateral  caudal  irregularly 
globular  suctional  pouches.  The 
pharynx  is  spherical,  with  two  lateral 
diverticula,  called  the  '  pharnygeal 
pouches.'  The  oesophagus  divides 
into  two  long  intestinal  caeca  about 
the  level  of  the  junction  of  the  anterior 
third  with  the  posterior  two-thirds  of 
the  body,  and  is  here  surrounded  by  a 
sphincter  muscle.  The  excretory  pore 
opens  slightly  to  the  left  of  the  middle 
line  dorsal  to  the  posterior  sucker. 
The  excretory  vesicle  is  relatively 
small,  and  lies  over  that  sucker.  The 
genital  papilla  is  situated  in  the  mid- 
ventral  line,  about  the  junction  of  the 
anterior  quarter  with  the  posterior  three-quarters  of  the  body,  and  on  it  open 
the  canal  of  the  cirrus  and  the  metatrema.  The  testes,  which  lie  one  behind 
the  other,  are  deeply  lobulated.  The  vas  deferens  runs  into  a  vesicula  semi- 
nalis,  which  opens  into  the  cirrus  canal,  but  has  no  true  cirrus  pouch.' 

The  ovary  lies  close  behind  the  testes,  and  rather  to  the  right  of  the  body. 
The  ovarian  duct  curves  backwards,  and  is  almost  at  once  surrounded  by 
the  shell  gland,  when  it  may  be  called  the  '  ootype,'  which  just  behind  the 
shell  gland  receives  the  vitellarian  duct  and  the  inner  end  of  Laurer's  canal. 
The  uterus,  full  of  eggs,  coils  over  the  testes  and  runs  as  far  forwards  as  their 


Fig.  212.- — Watsonius  watsoni. 

(After  Shipley;  emended  by  Leiper.) 

a,  Schematic;  b,  natural  size. 


GA STRODI SCUS  HOMINIS  563 

anterior  border,  where  it  becomes  thick  and  muscular,  and  is  called  the 
'metatrema.'  The  eggs  are  large  (122  to  130  /n  in  length  by  75  to  80  /j,  in 
breadth). 

Life-History.- — The  life-cycle  is  not  known,  but  it  is  believed  that 
the  usual  host  is  a  herbivorous  animal. 

Pathogenicity. — It  may  perhaps  cause  diarrhoea  and  anaemia.  A 
post-mortem  showed  the  mucosa  slightly  congested. 

Diagnosis. — -By  recognition  of  the  eggs  or  adults  in  the  faeces. 

Treatment. — The  eucalyptus  and  chloroform  mixture  advised  for 
ankylostomiasis  (Chapter  LXXV.). 

Family  II.    Gastrod'iscid^e  Stiles  and  Goldberger,  1910. 

Definition. — Paramphistomoidea  with  rather  discoidal  bodies 
divided  by  a  transverse  constriction  into  cephalic  and  caudal 
portions.  Ventral  pouch  absent.  Venter  with  many  large  papillae. 
Acetabulum  ventral  at  caudal  end. 

Type  Genus.- — Gastrodiscus  Leuckart,  1877;  the  other  genus  is 
Homalogaster  Poirier,  1883, 

Gastrodiscus  Leuckart,  1877. 

Definition. — -Gastrodiscidae  with  bodies  slender  anteriorly  and 
broadened  posteriorly.  The  latter  contains  the  genital  glands. 
The  acetabulum  is  small.  The  ventral  pouch  is  absent.  The  oral 
sucker  has  paired  evaginations,  and  leads  into  an  oesophagus  with 
muscular  thickening.  The  caeca  are  long,  not  wavy,  and  end  post- 
testicularly.  Male  organs: — These  are  two  branched  testes,  and 
a  cirrus  pouch  which  is  not  completely  closed.  Female  organs: — 
(  hurv  and  shell  gland  are  post-testicular;  vitellaria  are  extracaecal ; 
and  the  uterus  intercaecal.     Laurer's  canal  is  prevesicular. 

Type. — Gastrodiscus  (Bgyptiacus  Cobbold,  1876,  in  the  horse. 

Other  Species. — G.  hominis  in  man;G.  secundus  Looss,  1907,  in 
the  horse;  G.  minor  Lciper,  1913,  in  the  pig  in  Uganda  and  Nigeria. 

Gastrodiscus  hominis  Lewis  and  McConnell,  1876. 

Synonym. — Amphistomum  hominis  Lewis  and  McConnell. 

Definition.— Gastrodiscus  5-8  mm.  in  length  and  3-4  mm.  broad. 

History. — It  was  lirst  described  in  1876  by  Lewis  and  McConnell, 
who  found  it  in  hundreds  attached  by  its  posterior  sucker  to  the 
mucosa  of  the  caecum,  vermiform  appendix,  and  ascending  colon  of 
an  Assamese.  Since  then  it  has  been  reported  in  natives  of  India, 
and  perhaps  it  may  be  common.  We  have  not  met  with  it  in 
Ceylon,  though  there  was  a  small  jar  in  the  Medical  College  Museum 
labelled  Amphistomum  hominis,  but  without  a  history. 

per  has  made  G.  hominis  the  type  of  a  new  genus  Gastrodiscoides, distill- 
ed from  Gastrodiscus  by  the  absence  of  papillae  on  the  venter  and  the 
position  "I  the  genital  pore  on  the  cone. 

Morphology. — The  parasite  is  reddish-coloured,  8  to  10  millimetres  in  length 
and  4  to  5  millimetres  in  greatest  breadth,  tapering  to  2-5  millimetres  in  front. 
The  thickness  is  about  4  millimetres.     The  posterior  end  of  the  body  presents 


564  TREMATODA 

a  larger  disc,  on  the  hinder  border  of  which  lies  the  acetabulum.  The  rest  of 
the  body  is  thin,  tapering  to  the  mouth.  The  genital  pore  is  at  a  level  with 
the  bifurcation  of  the  intestine.  The  testes  are  double,  with  a  sinuous  vas 
deferens.  The  uterus  and  the  yolk  glands  are  situated  laterally.  The  eggs 
are  oval,  0-15  millimetre  in  length  and  0072  millimetre  in  breadth. 

Pathogenicity.— It  is  not  known  whether  these  parasites  cause 
any  disease.     It  occurs  in  5%  of  the  pigs  in  French  Indo-China. 

Super-Family  Fascioloidea  Stiles  and  Goldberger,  1910. 

Synonym.— Distomata  Retzius,  1782. 

Definition. — -Prostomata  with  acetabulum  ventral  and  always 
separated  from  the  posterior  extremity  by  some  part  of  the  genital 
apparatus.  Oral  sucker  present;  cae^a  two  in  number.  [Hermaphro- 
dites or  with  separate  sexes. 

Type  Family. — Fasciolidce  Railliet,  1895. 

Classification. — -The  super-family  may  be  classified  into  the  follow- 
ing families  as  follows : — 

A.  Hermaphrodites : — 

I.  Oral  sucker  without  collar  of  strong  pointed  spines: — 
{a)  Ovary  in  front  of  testes  :— 

1.  Genital  pore  in  front  of  ventral  sucker— Fasciolidce. 

2.  Genital  pore  not  in  front  of  ventral  sucker: — 

(a)  Genital  pore  surrounded  by  a  pseudo-sucker — 

Heterophyiidce. 

(b)  Genital  pore  not  so  surrounded: — 

(c)  Cuticle  with     pointed     spines — Troglo  - 

tremidcB. 

(d)  Cuticle   without   pointed    spines — Opis- 

thorchiidce. 
(b)  Ovary  behind  testes — Dicrocceliidte . 
II.  Oral  sucker  with  a  dorsal  and  lateral,  but  not  ventral, 
fold  or  collar  bearing  pointed  spines—  Echinostomidce. 

B.  Sexes  separate — Schistosomidce. 

FAMILY  FASCIOLIM)  Railliet,  1895. 

Definition. — Fascioloidea,  hermaphrodites  with  oral  sucker  with- 
out spiny  collar,  with  ovary  in  front  of  the  testes  and  genital  pore 
behind  the  ventral  sucker.  Vitellaria  well  developed,  extending 
dorsally  and  ventrally.  Cirrus  and  vagina  without  spines.  Uterus 
poorly  developed      Excretory  vesicle  much  branched      Eggs  large. 

Classification. — The  Fasciolidae  are  divided  into  two  subfamilies 
as  follows : — 

A.  Body  with  shoulder;  receptaculum  seminis  absent;  intestine 

branched — Fasciolin<e . 

B.  Body    without  shoulder;    receptaculum    seminis    present; 

intestine  not  branched — Fasciolopsinw. 


FASCIOLA 


565 


Suborder  Fasciolin^e  Odhner,  1910. 

Definition.— Fasciolidae  with  a  shoulder  separating  the  head  from 
the  body,  with  a  much  branched  intestine,  without  a  receptaculum 
seminis. 

Remarks. — This  subfamily  contains  the  genus  Fasciola,  which 
concerns  us. 

Fasciola  Linnaeus,  1758. 

Definition. — -Large.  Fascioloidea  with  leaf-like  bodies,  with  the 
anterior  end  shaped  into  a  conical  head  and  with  the  ventral  sucker 
situated  near  the  mouth.     Cuticle  covered  with  spines 

Type  Species. — Fasciola  hepatica  Linnaeus,  1758. 

Fasciola  hepatica  Linnaeus,  1758. 

Synonyms. — Distomum  hepaticum  Retz,  1786;  Fasciola  humana  Gmel,  1789; 
D.  cavice  Sons,  1890;  Cladoccelium  hepaticum  Stoss,  1892. 

Definition. — Fasciola  with  long  cephalic  cone,  converging 
sides,  small  acetabulum  situate  some  distance  behind  the 
oral  sucker.     Eggs  I30-I45X  70-90  microns. 


Fig.  213.  —  Egg 
of  Fasciola  he- 
patica. 


Fig.  214.  —  The 
Miracidium  OF 
Fasciola  hepa- 
tica. 


Fig.  215.  —  The 
Larva  of  Fas- 
ciola hepatica. 


Fig.  216.  —  The 
Sporocyst  of 
Fasciola  hepa- 
tica. 


\iicr  Thomas,  from  the  Quarterly  Journal  of  Microscopical  Science.) 


History. —  Fasciola  hepatica,  the  liver-fluke,  is  a  parasite  of  sheep,  oxen, 
goats,  horses,  and  many  other  herbivorous  animals,  in  Europe,  North  Africa, 
North  and  South  America,  Australia,  Tasmania,  Japan,  China,  Burma,  and 
India.     It  is  said  to  be  extremely  common  in  Burma  and  Egypt. 

It  has  been  found  in  man  several  times,  and  apparently  usually  in  the 
liver,  but  it  has  been  recorded  in  the  bloodvessels,  in  a  swelling  on  the  sole 
of  the  foot,  in  abscesses  about  the  head,  and  in  a  swelling  in  the  right  hypo- 
chondriac region.  It  is  probable  that  Distomum  oculi  humani  Ammon,  1833, 
and  Monostomum  lentis  Von  Nordmann,  1832,  may  have  been  young  liver- 
flukes. 

Morphology. —  Fasciola  hepatica  is  a  flat,  oval  animal,  with  an  anterior 
triangular  projection.  Length,  20  to  30  millimetres;  breadth,  8  to  13  milli- 
metres.    The  cuticle  is  covered  with  minute  pointed  scales  directed  backwards. 


566 


TREMA  TOD  A 


There  are  two  suckers — an  oral,  which  is  situated  at  the  anterior  end  of  the 
animal  and  surrounds  the  mouth  opening,  and  a  ventral,  the  acetabulum, 
which  is  a  muscular  cap  situated  in  the  median  line  near  the  junction  of  the 
anterior  projection  with  the  rest  of  the  body.  The  mouth  leads  into  a  mus- 
cular pharynx,  which  passes  via  a  short  oesophagus  into  the  intestine,  which 
divides  just  in  front  of  the  genital  aperture  into  two  tubes  running  to  the 
posterior  end  of  the  body,  giving  off  numerous  branched  caeca. 

The  excretory  system  starts  with  dilated  tubules,  into  which  project  the 
cilia  of  the  so-called  flame  cells.  The  ducts,  which  freely  anastomose,  open 
into  a  main  duct,  which  runs  directly  backwards  to  open  at  a  median  pore 
at  the  posterior  end  of  the  body. 

The  two  testes  are  much-branched  tubes,  lying  in  the  middle  of  the  body, 
of  equal  size,  one  lying  in  front  of  the  other;  from  each  a  vas  deferens  runs 
as  far  as  the  ventral  sucker,  where  it  opens  into  an  elongated  sac,  the  vesicula 
seminalis,  from  which  the  ductus  ejaculatorius  runs  to  the  end  of  a  large 
muscular  organ,  called  the  cirrus,  which  lies  in  a  sac  situate  just  in  front  of 
the  ventral  sucker.  The  genital'  opening  through  which  the  cirrus  can  be 
protruded  is  situated  between  the  two  suckers  on  the  ventral  surface. 


Fig.  217. — The  Redia  of  Fig.  218.— The  Cercaria  of 

Fasciola  hepatica.  Fasciola  hepatica. 

( After  Thomas,  from  the  Quarterly  Journal  of  Microscopical  Science.) 


The  branched  and  tubular  ovary  lies  on  the  right,  in  front  of  the  anterior 
testes.  The  ovarian  ducts  run  backwards  to  join  the  middle  line  with  the 
median  vitellarian  duct  from  the  yolk  reservoir,  into  which  open  the  vitcl- 
larian  ducts  from  the  large  branched  yolk  glands  lying  on  either  side  of  the 
body,  from  the  level  of  the  ventral  sucker  to  the  posterior  extremity. 

The  junction  of  these  two  ducts  is  surrounded  by  the  shell  gland,  and  forms 
a  much-convoluted  tube,  the  uterus,  which  is  joined  close  to  its  commence- 
ment by  a  little  tube,  Laurer's  canal,  opening  on  to  the  dorsal  surface.  The 
uterus,  which  is  generally  full  of  eggs,  opens  on  the  left  side  of  the  base  of 
the  cirrus. 

The  nervous  system  consists  of  a  nerve  collar  around  the  pharynx,  from 
which  two  nerve  cords  run  backwards  along  the  sides  of  the  body. 

Life-History. — The  ovum  starts  from  the  ovary  and  travels  along  the 
ovarian  duct,  where  it  is  fertilized,  after  which  it  is  surrounded  by  a  large 
number  of  yolk  cells,  and  then  by  a  shell  formed  from  the  secretion  of  the 


FASCIOLA  HEPATIC  A  567 

shell  gland.  The  egg  now  passes  forwards  into  the  uterus,  and  is  evidently 
deposited  in  the  bile-passages  and  escapes  in  the  faeces.  It  is  oval,  yellowish- 
brown,  with  a  cap-like  lid  013  to  01 45  millimetre  in  length  by  007  to  0-09 
millimetre  in  breadth,  and  is  seen  to  enclose  a  mass  of  yolk  cells  with  one 
ovum,  which  now  segments  and  grows,  using  up  the  yolk  cells,  forming  a 
young  form,  called  a  '  miracidium,'  013  by  0027  millimetre,  which  in  a 
few  weeks  escapes  by  the  opercular  opening  if  the  egg  is  in  water,  and,  being 
ciliated,  swims  about  as  a  conical  larva,  with  a  little  anterior  papilla  and 
two  eye-spots.  It  has  a  cuticular  epithelium,  under  which  are  muscular 
layers,  and  contains  a  simple  sac,  like  an  alimentary  canal,  a  cerebral  gan- 
glion, and  an  excretory  system.  There  is  a  segmentation  cavity  (forming  a 
body  cavity)  between  the  alimentary  canal  and  the  body-wall. 

It  now  bores  its  way  into  the  pulmonary  cavity  of  some  snail  by  means 
of  its  anterior  papilla;  otherwise  it  dies  in  about  eight  hours.  The  varieties 
of  snail  hosts  are:  Lunncea  trimcatula  Midler,  in  Europe,  Asia,  Africa;  L. 
oahnensis  in  the  Sandwich  Islands;  L.  viator  Orb  in  South  America;  L.  kumilis 
Say  in  North  America,  in  which  it  loses  all  its  organs,  and  increases  in  size 
rapidly,  while  cells  grow  from  the  wall  into  the  primary  body  cavity,  so  that  a 
cyst  is  formed,  called  the  '  sporocyst.'  This  has  an  external  cuticle,  a  thin 
muscular  layer,  and  an  epithelial  lined  cavity,  containing  collections  of  cells, 
which  develop  into  cylindrical  forms,  possessing  a  simple,  short,  tube-like 
alimentary  canal,  with  a  pharynx,  glands,  and  intestine,  and  a  genital  pore 
near  the  anterior  end.  These  forms,  which  are  called  Redice,  after  the  cele- 
brated biologist  Redi,  force  their  way  out  of  the  sporocyst  by  making  a  wound, 
which  heals  readily,  and  then  wander  about  the  snail,  being  especially  abundant 
in  the  liver.  When  fully  formed  they  have  a  ridge  running  round  the  anterior 
end,  and  a  pair  of  blunt  processes  for  locomotion  posteriorly. 


Fig.  219. — LimncBa  truncatula  Muller. 

Inside  the  Redice  cells  bud  off  from  the  body-wall  and  form  the  Cercarice 
which  arc  not  unlike  a  young  Fasciola  with  a  tail. 

The  <  ercaria  possess  cutaneous  glands  for  the  purpose  of  secreting  the 
cyst-wall  of  the  next  stage.  They  escape  from  the  Redice  by  means  of  the 
genital  pore,  and,  leaving  the  snail,  swim  about  in  the  water  for  some  time, 
finally  becoming  encysted  on  grass  or  water-weeds,  and  are  then  eaten  by 
inside  which  they  escape  from  the  cyst,  and,  working  their  way  along 
the  bile-ducts,  develop  in  six  weeks  into  sexually  mature  flukes. 

Habitat. —  The  liver-fluke  usually  lives  in  the  sheep,  in  which  it  causes  the 
e  called  '  sheep-rot  ';  but  infection  can  spread  to  man. 

Pathogenicity.  It  causes  the  disease  '  Halzoun  '  in  North  Lebanon  by 
entering  the  pharynx.  It  is  probably  Hexathyridmm  venarum  Treutler,  found 
in  the  anterior  tibial  vein,  and  the  worms  found  in  the  portal  vein  by  Duval 
at  Rennes  in  1  s  j 2 ;  by  Vital  from  Constan;.ia  in  1874,  by  Giesler,  in  1850, 
in  a  foot;  by  Harris,  in  Liverpool,  in  an  abscess.  It  may'  be  Distonum  oculi 
kutnani  Amnion.  1833;  Monostomum  lentis  Von  Nordmann,  1832;  and  the 
■  niiDi  ophthalmicum  Diesing,  1830. 

Fasciola  gigantica  Cobbold,  1856. 
Synonyms.-    Fasciola  angusta  Railliet,  1895;  F.  giganlea  Cobbold, 
1858. 
Definition.— Fasciola  with  short  cephalic  cone,  almost  parallel 


568  TREMATODA 

sides,  large  acetabulum  situate  close  behind  oral  sucker.      Eggs 
150-190  x  75-90  microns. 

Remarks.- — F.  gigantica,  which  is  nearly  allied  to  F.  hepatica,  is 
found  in  herbivora  in  Africa,  and  is  believed  to  have  occurred  in  a 
man,  for  a  parasite  somewhat  resembling  it  was  expelled  from  the 
lung  during  a  fit  of  coughing  associated  with  haemoptysis,  but  there 
is  some  doubt  as  to  whether  it  was  not  different  from  Cobbold's 
species.  Its  length  was  26  to  28  millimetres  and  its  breadth  6  to 
8  millimetres,  but  it  was  contracted.  It  caused  fever,  cough,  and 
slight  haemoptysis. 

Subfamily  Fasciolopsusle  Odhner,  1910. 

Definition. — Fasciolidae    without    shoulder    between    head    and 
body,  with  simple  zigzag  intestines,  and  with  a  receptaculum  seminis. 
Type  Genus. — Fasciolopsis  Looss,  1896. 

Fasciolopsis  Looss,  1896. 

Definition.- — Fasciolinae  with  large  ventral  sucker  elongated 
posteriorly  to  form  a  sac.  Cirrus  pouch,  long  and  cylindrical. 
Laurer's  canal' present. 

Type  Species. — Fasciolopsis  buski  Lankester,  1857. 

Classification. — Four  species  are  known  to  occur  in  man,  and  they 
can  be  recognized  as  follows  :— 

A.  Spines  present  on  cuticle  : — 

I.  Vitelline  acini  very  large- — Goddardi. 
II.  Vitelline  acini  not  large — Kwan's  fluke  (?). 

B.  No  spines  on  cuticle  : — 

I .  Cirrus  sac  conspicuous : — 

(a)  Cirrus  pouch  very  long,  broad,  convoluted,  power- 

fully built — Fulleborni. 

(b)  Cirrus  pouch  not  so  long,  narrow,  straight,  not 

powerfully  built— Buski. 
II.  Cirrus  sac  inconspicuous—  Rathouisi  (?). 

Fasciolopsis  buski  Lankester,  1857. 

Synonyms. — Distomum  buski  Lankester,  1857;  D.  crassum  Busk, 
1859;  nec  v-  Siebold,  1836;  Distomum  rathouisi  Poirier,  1887. 

History. — Fasciolopsis  buski  is  a  very  large  trematode,  which  was 
first  discovered  by  Busk  in  the  duodenum  of  a  Lascar  who  died 
in  the  Seamen's  Hospital  in  1843.  In  1857  it  was  named  by  Lan- 
kester, and  in  1859  described  by  Cobbold. 

It  appears  to  be  by  no  means  uncommon  in  man  and  pigs  in 
South  China,  and  is  known  in  Borneo,  the  Straits  Settlements, 
Assam,  and  India.  In  1910  F.  rathouisi  Poirier,  1887,  was  regarded 
as  the  same  as  F .  buski  Lankester,  1898,  but  at  the  present  time  some 
authorities  go  back  to  the  older  view  that  they  are  separate  species 
— e.g.,  Odhner  says  they  are  the  same,  and  Ward  that  they  are 
separate,  because  the  cirrus  sac  is  convoluted  and  not  conspicuous 
while  that  of  F   buski  is  straight  and  conspicuous. 


FASCIOLOPSIS  FULLEBORNI 


569 


Morphology. — It  is  a  large,  thick,  brown,  smooth  trematode,  24  to  70  milli- 
metres in  length  and  5*5  to  14  millimetres  in  breadth.  The  oral  sucker  and 
acetabulum  are  in  the  proportion  of  0-5:  2-0.  The  pharynx  is  globular,  and 
there  is  a  prepharynx,  with  a  sphincter.  The  oesophagus  is  short,  and  the 
intestinal  caeca  are  not  branched,  and  extend  ^ 

to  the  posterior  border.  The  genital  pore  is 
situated  anteriorly  to  the  acetabulum,  but  the 
most  remarkable  feature  is  the  very  long 
cirrus,  about  one-fourth  the  length  of  the 
body.  The  testes  lie  posteriorly,  with  the 
ovary  and  the  uterus  in  front.  The  yolk  glands 
are  extensive,  like  those  in  F.  hepaiica. 

Life- History. — The  eggs  are  0-12  to  0-13 
millimetre  in  length  and  0*077  to  o-oS  in 
breadth,  and  the  larval  stages  are  said  to 
occur  in  shrimps. 

Habitat. — The  intestine  of  the  pig  and 
man. 

Pathogenicity. — -It  is  believed  to  cause 
dysenteric  diarrhoea,  wasting,  and  jaun- 
dice at  times. 


Fasciolopsis  fulleborni  Rodenwaldt, 
1909. 

History. — -This  worm  was  discovered 
and  described  by  Rodenwaldt  in  1909, 
being  found  in  the  motions  of  an  Indian 
in  Hamburg. 

Morphology. — The  parasite  is  very  large, 
measuring  from  30  to  50  millimetres  in  length 
and  from  14  to  16  millimetres  in  breadth. 
The  oral  sucker  and  acetabulum  are  in  the 
proportion  of  0-75  to  o-6.  There  is  a  prepharynx 
and  pharynx,  but  no  oesophagus. 


Fig.  220. — Fasciolopsis  buski. 
(After  Odhner,  from  the 
"The  intestinal  cae'ea  are^longand  wavy,  and    Centralblatt  fur  Bakteriologie.) 
extend  to  the  posterior  end.  The  genital  aper-    a,  Schematic;  b,  natural  size, 
tures  lie  in  front  of  the  acetabulum. 

The  cirrus  sac  is  very  long  and  well  developed,  and  the  testes  lie  behind  the 
ovary  and  the  ootype.  The  latter  is  much  larger  than  in  F.  buski.  and  is  oval 
instead  of  being  round.  The  yolk  glands  extend  from  the  acetabulum  to  the 
posterior  end  of  the  body,  being  situated  laterally.  The  excretory  vesicle 
is  well  developed. 

The  eggs  measure  o-i  millimetre  in  length  by  0-073  millimetre  in  breadth. 

Habitat. — Intestine  of  man. 

Pathogenicity. — The  patient  harbouring  it  was  suffering  from 
fever,  which  had  been  diagnosed  as  typhoid. 


Kwan's  Fluke  (  =  F.  goddardi  ?). 

Under  this  term  Heanley  has  described  a  trematode  found  by  Dr.  Kwan 
King  Hung  in  a  child  in  the  island  of  Hong  Kong. 

Morphology.  -In  length  it  is  2  inches,  in  breadth  £  inch.  The  cuticle  pos- 
sessed spines.  The  intestine  was  not  clearly  seen,  but  the  caeca  were  un- 
orauched.     The  testes  were  large  and  placed  one   behind  the  other.     The 


57°  TREMA  TOD  A 

ovary  was  branched,  and  it — the  shell  gland  and  the  yolk  glands  (which  met 
each  other  posteriorly) — resembled  those  of  F.  buski. 

Pathogenicity. — The  patient  suffered  from  vomiting,  which  resulted  in  the 
expulsion  of  the  flat-worms. 

Fasciolopsis  goddardi  Ward,  1910. 

Definition. — Fasciolopsis  with  spines  and  very  large  vitellaria. 
Remarks. — This  fluke,  which  is  imperfectly  known,  was  found 
in  Shanghai,  China,  and  measures  22  x  9  mm. 

FAMILY  HETEROPHYIED^  Odhner,  igi-j. 

Definition. — Fascioloidea,  hermaphroditic,  with  the  ovary  in 
front  of  the  testes,  genital  pore  behind  the  ventral  sucker,  and 
surrounded  by  a  pseudo-sucker,  which  is  behind  or  on  a  level 
with  the  acetabulum,  and  has  its  muscles  blended  with  the  body 
musculature  and  not  sharply  differentiated  therefrom. 

Type  Genus. — Heterophyes  Cobbold,  1866. 

Classification. — The  two  genera  which  concern  us  can  be  differen- 
tiated as  follows : — 

A.  Acetabulum    and    genital    suckers    ventrally    situate    and 

separate- — Heterophyes. 

B.  Acetabulum   and   genital   suckers   dextro-laterally   situate 

and  surrounded  by  a  complex  musculature — M  etagonimus . 

Genus:  Heterophyes  Cobbold,  1866. 

Synonyms. — Cotylogonimus  Liihe,  1899;  Canogonimns  Looss,  1899. 

Definition. — Heterophyiidse  with  suckers  ventrally  situate, 
with  a  narrow,  movable,  anterior  portion,  and  a  broader,  less 
movable,  posterior  portion,  which  contains  the  genitalia.  Cuticle 
with  scale-like  spines;  suckers  widely  separated;  oesophagus  long. 
Genital  pore  placed  laterally,  behind  the  ventral  sucker,  and 
surrounded  by  a  genital  prominence  with  chitinous  rodlets.  No 
cirrus  pouch.  The  testes  are  at  the  posterior  end,  and  the  ovary  in 
a  median  position  between  them.  Yolk  glands  are  small,  and 
situated  at  the  sides  posteriorly. 

Type  Species.—  Heterophyes  heterophyes  v.  Siebold,  1852. 

Heterophyes  heterophyes  v.  Siebold,  1852. 

Synonyms.- — Distomnm  heterophyes  v.  Siebold,  1852;  Mesogonimus 
heterophyes  Railliet,  189c;  Ccvnogonimus  heterophyes  Looss,  1900; 
Cotylogonimus  heterophyes,  Braun,  1901. 

Definition. — Heterophyes  with  ventrally  situate  and  separate 
acetabular  and  genital  suckers. 

History. — This  minute  parasite  was  discovered  by  Bilharz  in  the 
intestine  of  a  boy  in  Cairo  in  1851,  and  again  a  little  later,  but  the 
third  observation  was  not  till  1891  by  R.  Blanchard;  since,  then  Looss 
has  found  it  in  Alexandria  and  Cairo,  where  he  says  it  is  not  un- 
common.    Leiper  has  recorded  several  cases  in  Chinese  seamen. 


HETF.ROPHYES 


57i 


It  is  also  found  in  dogs  and  cats  in  Egypt,  Japan,  and  Formosa; 
in  man  in  Khartoum  (eggs  0-026  x 0-013  mm.),  also  adults;  and  in 
dogs  in  the  same  town. 

Morphology.  //< icrophyes  heterophyes  is  pear-shaped,  very  narrow  in 
front,  broad  behind;  2  millimetres  in  length  by  1  millimetre  in  breadth,  but 
can  stretch  to  quite  double  this  length.  Cuticle  with  rectangular  scales,  and 
with  numerous  glands  on  the  anterior  ventral  surface.  Oral  sucker  01  milli- 
metre ami  ventral  0*35  millimetre  in  diameter.  (Esophagus  relatively  long. 
Intestinal  caeca  end  posteriorly  near  each  other.  Testes  situated  posteriorly, 
not  quite  on  the  same  level  on  each  side  of  the  excretory  vesicle;  ducts  join 
in  a  large  vesicula  seminalis,  from  which  a  canal  unites  with  the  metatrema, 
and  then  discharges  into  the  genital  cavity,  the  pore 
of  which  is  placed  laterally,  surrounded  by  an  annular 
muscular  elevation,  provided  with  seventy-five  to 
eighty  branched  chitinous  spines,  probably  intended 
to  help  in  sexual  intercourse. 

The  ovary  lies  medianly,  and  its  duct  passes 
backwards  to  join  the  receptaculum  seminis,  which 
is  just  in  front  of  the  testes. 

Here  also  joins  the  vitellarian  duct  of  the  yolk 
glands,  which  also  lie  laterally  in  the  posterior  third 
of  the  body.  The  uterus  is  coiled  throughout  the 
posterior  part  of  the  body.  The  canal  of  Laurer  is 
present.  The  eggs  have  thick  shells,  and  are  0-03 
millimetre  in  length  and  0*017  millimetre  in  breadth, 
containing  a  miracidium. 

Habitat. — -Small  intestine. 

Life-History. — Unknown. 

Pathogenicity.  — ■  Perhaps  nil,  but  the 
parasite  is  very  small,  and  may  therefore 
be  overlooked. 

Genus  Metagonimus  Katsurada,  1913. 

Synonym. — Yokogawa  Leiper,  1913.  fig.     221  .—Heterophyes 

Definition. — Heterophyiid?e    with    suckers  heterophyes. 

dextro-laterally  situate.  (After     Looss,     from 

Type    Species. — ■  Met 'agoni mus     vokogawai  Braun's 

Katsurada,  1913. 


Animal   Para- 
Man,'    English 


sites     of 
edition.) 

a,  Schematic  x  35;  b. 
natural  size;  c,  eggs  x 
250;  d,  spine  X  700. 


Metagonimus  yokogawai  Katsurada  1913. 

Synonym. — Yokogawa    yokogaivai    Leiper, 
i'ii.',-     Leiper  now  believes  that  this  fluke  is 

nno  as  one  pit  \  iously  described  by  Kobayashi  ;  s  Loxjotrema 
ooatum.  n.g.,  n.sp. 

Definition.  -  Metagonimus  1-5-2-5  x  0-4-0-7  mm.,  with  body 
covered  with  nail-shaped  spines  about  10  microns  in  length,  with  a 
characteristic  sac-like  acetabulum  placed  deeply  in  the  body,  and 
not  opening  on  the  ventral  surface,  but  dextro-laterally. 

History.-  -It  was  found  in  Japan  in  the  upper  or  middle  part  of  the 
jejunum,  rarely  thecaxum,  of  man  and  mammals.  'I  hey  enter  and 
destroy  the  solitary  glands. 

Morphology. — Mctago)nmus  yokogawai  is  a  small  fluke  possessing 
the  characters  given  above.     The  oral  sucker  is  77-85  microns  in 


57^  TREMATODA 

diameter.  The  testes  are  elliptical  and  situate  posteriorly.  The 
ejaculatory  ducts  open  with  the  uterus  into  a  genital  sinus,  which 
opens  into  a  pit  at  the  front  of  the  ventral  sucker. 

The  ovary  is  spherical,  and  lies  in  the  middle  of  the  posterior  part 
of  the  body.  A  receptaculum  seminis  and  a  Laurer's  canal  are 
present.  The  vitellarian  acini  lie  on  each  side  in  the  posterior  part 
of  the  body.     The  uterus  forms  three  to  four  transverse  coils. 

Life-History. — The  eggs  are  elliptical,  28  x  16  microns,  double 
contoured  and  yellowish  brown,  with  an  operculum,  but  no  shoulder, 
and  a  knob  at  the  narrower  end. 

Muto  found  cercaria  in  the  liver  of  Melania  libertUia,  in  Kaishu, 
Korea,  where  metagonimiasis  is  common.  On  breaking  up  the  liver 
in  water,  it  was  found  that  the  cercaria  became  encysted  under  the 
scales  of  uninfected  goldfish  kept  in  the  water.  Kittens  fed  with 
these  fish  became  infected  in  twelve  to  fifteen  days. 

The  cercariae  also  live  in  a  trout,  Plecoglossus  altivelis,  rarely  in 
other  fish.  Infection  takes  place  by  eating  raw  fish,  and  the  period, 
judging  by  dogs,  is  seven  to  sixteen  days  for  the  eggs  to  appear 
in  the  faeces. 

Pathogenicity. — -It  causes  chronic  diarrhoea  in  man. 

FAMILY  TROGLOTREMIM:  Odhnef,  1914. 

Definition. — Fascioloidea  hermaphroditic,  with  ovary  in  front 
of  testes,  genital  pore  just  in  front  or  just  behind  rim  of 
acetabulum,  but  not  surrounded  by  a  pseudo-sucker,  and  with  the 
cuticle  completely  covered  with  pointed  spines.  Yitellaria  well 
developed  and  for  the  most  part  dorsally  situate.  More  or  less 
flattened  worms  2-3  mm.  in  length,  with  extreme  posterior  end 
prolonged  into  a  small  appendage,  with  ventral  surface  flat  or  some- 
what hollowed,  and  dorsal  surface  vaulted.  Musculature  in  forms 
living  in  cysts  poorly  developed.  Pharynx  present.  Gut  diverti- 
cula terminal  e  a  short  distance  from  the  posterior  end.  Genital  pore 
immediately  in  front  or  immediately  behind  the  rim  of  the  aceta- 
bulum in  the  middle  fine  or  slightly  to  the  left.  Cirrus  usually 
absent.  Pars  prostatica  and  seminal  ^vesicle  present.  ..  Testes 
symmetrical.  Ovary  in  front  of  the  testes.  Vitellaria  well 
developed.  Uterus  long  and  much  coiled,  with  small  eggs,  or  short 
and  kinked  with  large  eggs. 

Remarks. — Odhner  formulated  this  family  in  Zoologiska  Bidrag 
frah  Uppsala  in  1914  for  Distomum  acutum,  in  the  frontal  sinuses  of 
Mu stela  putoria  ;  D.  gastrophilum  from  cysts  in  the  pylorus  of 
Phoccena  communis  ;  for  C oily ri chum  f aba  from  Sylvia  hortensis  and 
for Paragonimus  ringeri,  etc. 

Type  Species.— Troglotrema  Odhner,  19 14. 

Gents  Paragonimus  Braun,  1899. 
Definition. — Troglotremid;e  with  thick,  oval,  or  broad,  fusiform 
bodies,   almost  circular  on  transverse  section.     Cuticle,  with  sac- 
like spines.     Suckers  separated  by  half  the  length  of  the  body. 


PARAGONIMUS  RINGER  I 


573 


The  intestinal  caeca  are  wavy,  and  run  to  the  posterior  end  of  the 
body,  but  are  unbranched.  The  excretory  vesicle  runs  from  the 
pharynx  backwards  to  its  aperture  on  the  posterior  margin  of  the 
body.  The  genital  pore  is  just  behind  the  ventral  sucker.  There 
is  no  cirrus  pouch,  and  no  receptaculum  seminis. 

Type  Species. — Paragonimus  westermanii  Kerbert,  1878. 
Classification.— There  are  five  species,  but  P.  rudis  Diesing,  1850, 
from  a  Brazilian  otter,  and  P.  compactus  Cobbold,  from  an  Indian 
ichneumon,  are  not  well  known.  According  to  Ward  the  other 
three  may  be  distinguished  as  follows,  but  Japanese  workers  do  not 
accept  these  characters  as  of  specific  value: — - 
A.  Chisel-shaped  spines: — 

I.  Arranged  in  circular  rows  in  groups — Ringeri. 
II.  Arranged  in  circular  rows  singly — Kellicolti. 
Lancet-shaped  spines: — ■ 
Arranged  in  circular  rows  in  groups — -Wesiermani. 


B. 


Fig.  222. — Paragonimus  ringeri. 

(After  Looss,  from  Mensc's  '  Tropenkrankheiten.') 

a,  Schematic  x8;  b,  eggs  x  300;  c,  natural  size. 

Paragonimus  ringeri  Cobbold,  1880. 

Synonyms, — Distoma  ringeri  Cobbold,  1880;  D.  hepaticum  Miura, 
I),  pulmonale  Baelz,  1883;  D.  pulmonis  Suga,  1883;  D.  cerebrate 
1889;  Yamagiwa,  1890;  Mesogonimus  westermani  Railliet,  1890 ; 
.]f.  pulmona  c  Stossich,  1892. 

History.— Paragonimus  westermani  was  discovered  by  Kerbert 
in  1878  in  the  lungs  of  two  Bengal  tigers,  which  died  respectively 
in  the  Zoological  Gardens  of  Amsterdam  and  Hamburg. 


574  TREMATODA 

In  1880  Baelz  found  in  the  sputum  of  cases  of  haemoptysis  bodies 
which  he  took  to  be  psorosperms,  and  therefore  called  the  disease 
gregarinosis  pulmonum,  but  when  these  were  referred  to  Leuckart 
he  said  that  they  were  eggs  of  a  Distomum.  In  the  same  year 
Manson  found  what  he  took  to  be  eggs  of  some  parasite  in  a  case 
of  haemoptysis,  in  a  Chinaman  from  Northern  Formosa,  and  later 
he  saw  a  Portuguese  with  haemoptysis  and  obscure  thoracic  symp- 
toms, who  lived  in  Tamsui  in  North  Formosa. 

This  man  died  in  Formosa,  and  Dr.  Ringer,  who  performed  the 
post-mortem,  discovered  in  the  lungs  a  minute,  fleshy,  slightly 
flattened,  oval  body,  grey  in  colour,  and  about  a  quarter  of  an  inch 
in  length,  which  expelled  some  brownish  material  from  a  minute 
orifice  near  one  end. 

This  specimen  was  sent  to  Manson,  who  noted  the  same  eggs  as  he 
had  found  in  the  Chinaman  already  mentioned,  and  then  forwarded 
the  parasite  to  Cobbold,  who,  rightly  thinking  it  new  to  science, 
named  it  Distomum  ringeri,  the  name  now  in  use.  In  1883  Baelz, 
having  found  specimens  in  the  lungs,  named  it  D.  pulmonale.  In 
1890  Otani  and  Yamagiwa  proved  that  it  could  occur  in  other  parts 
of  the  body  besides  the  lungs  by  finding  it  in  the  brain,  where  it 
produced  symptoms  of  J  acksonian  epilepsy.  Stiles  and  Looss  defined 
its  zoological  position ;  Ward  found  it  in  cats,  Railliet  in  dogs,  and 
Stiles  in  hogs;  while  the  best  description  of  the  lesions  caused  by 
it  is  that  by  Musgrave  in  1907,  who  found  it  in  the  Philippine 
Islands. 

It  is  very  common  in  Japan,  and  is  found  in  China,  Korea,  and 
North  America,  a  human  case  being  reported  from  Mexico  by 
Naunyn. 

In  1908  Ward  found  P.  kellicotti  in  pigs,  dogs,  and  cats  in  North 
America. 

Morphology. — -The  parasite  varies  from  a  reddish-brown  to  a  light  slate 
colour  when  first  removed  from  the  body,  but  soon  becomes  greyish  on 
exposure  to  the  air.  In  shape  it  is  oval,  with  a  somewhat  flattened  ventral 
surface,  and  is  capable  of  slight  alterations  of  its  appearance  by  protruding 
and  retracting  its  head,  and  by  altering  its  ventral  sucker  so  that  it  may  appear 
terminal.  The  cuticle  is  covered  with  scale-like  spines,  which  may  be  capable 
of  being  moved.  The  oral  sucker  is  spherical  and  terminal,  0-63  to  0-97 
millimetre  in  diameter.  The  ventral  sucker  is  situated  in  the  anterior  half 
of  the  body,  and  is  0-76  to  1*31  millimetres  in  diameter.  The  oesophagus  is 
short,  and  divides  into  the  two  wavy  caeca.  The  genital  pore  may  be  in- 
distinct, and  is  always  small,  lying  close  to  and  behind  the  ventral  sucker. 
The  testes  lie  about,  but  not  quite  on,  the  same  level  on  each  side  of  the  median 
line  just  behind  the  uterus.  There  is  neither  a  cirrus  nor  a  cirrus  pouch.  The 
ovary  is  opposite  and  slightly  posterior  to  the  uterus,  which  is  visible  just 
posterior  to  the  ventral  sucker.  The  yolk  glands  lie  at  the  sides,  and  their 
branches  almost  meet  dorsally,  while  ventrally  they  only  extend  to  the 
intestinal  caeca.  Laurer's  canal  is  present.  The  eggs  are  oval  in  shape,  of 
a  reddish-brown  to  a  light  yellow  in  colour,  with  a  length  from  0-08  to  o-i  milli- 
metre, and  a  breadth  from  0-052  to  0-075  millimetre.  They  possess  an  oper- 
culum, and  contain  the  ovum  and  yolk  cells. 

The  excretory  vesicle  is  well  developed,  and  extends  from  the  pharynx 
backwards. 


OPISTHORCHIID.r.  575 

Life-History. — -According  to  Nakagawa,  the  miracidia  infect  the 
snails  Melctnia  libertina  and  Melania  obliquegrctnosa. 

Nagakawa  in  Formosa  found  encysted  larvae  in  fresh-water 
crabs: — i.  Geothelphusa  obtusipes.  Synonyms. — Potamon  obtusipes, 
Thelphusa  rubra.  2.  Geothelphusa  dehaanii.  Synonyms. — Potamon 
dehaanii,  Thelphusa  berardi,  and  perhaps— 3.  Eriocheir  japonicus. 
Synonym. — E.formosa. 

According  to  Sadao  Yoshida,  in  the  first  two,  the  larvae  are  found 
in  the  liver,  rarely  in  the  gills  or  muscles,  and  in  the  last  chiefly  in  the 
gills,  muscles,  and  hypoderm,  and  rarely  in  the  liver. 

Dogs  and  cats  have  been  infected  by  these  observers  from  the 
crabs,  when  the  larva,  escaping  from  the  cyst  in  the  intestine,  pene- 
trates the  wall  near  the  jejunum  and  enters  the  abdominal  cavity, 
perforates  the  diaphragm,  and,  entering  the  subpleural  tissue, 
may  pierce  its  way  into  the  lung  and  encyst  or  pass  into  the  neck 
(and  perhaps  so  to  the  brain,  etc.).  The  lungs  are  their  favourite 
seat,  and  the  only  one  in  which  they  attain  maturity. 

Kakami,  on  the  other  hand,  says  that  cercariae  may  be  found  in 
Melania  libertina,  and  that  they  get  into  drinking-water  and  so 
infect  people  directly. 

Pathogenicity. — It  causes  paragonimiasis  in  man. 


FAMILY  OPISTHORCHIID.E  Braun,  1901,  emendavit 
Stephens,  1916. 

Definition. — Fascioloidea,  hermaphroditic,  with  oral  sucker  with- 
out collar  of  spines.  Ovary  in  front  of  testes.  Genital  pore  behind 
ventral  sucker.  Cuticle  without  pointed  spines.  Small  to  medium 
flukes  tapering  anteriorly.  Cirrus  absent,  but  receptaculum  seminis 
and  Laurer's  canal  present.     Eggs  small. 

Classification. — -The  family  is  divided  into  subfamilies  as  follows : — 

A.  Excretory     pore     terminal  ;     bladder     long,     dorsal     to 

testes. 
Uterine  coils   not   overlapping   intestinal   caeca — Opisthor- 
chiince. 

B.  Excretory  pore  ventral;  bladder  short,  ventral  to  testes. 
Uterine  coils  overlapping  intestinal  caeca — ■Metorchiince. 

Subfamily  Opisthorchiin^;  Looss,  1899,  emendavit 
Stephens,  1916. 

Definition. — As  above. 

Classification. — The  genera  important  to  us  can  be  distinguished 
as  follows : — 

.  I .  Testes  lobed : — 

(  I.  With  long  retractile  process  projecting  from  ventral 
surface  and  carrying  out  its  apex  the  acetabulum  and 
the  genital  pore-  -Par opisthorclus. 


576  TREMATODA 

II.  Without  such  process: — 

Vitellaria    from    acetabulum     to    ovary    in     one 

mass- — Opistorchis. 
Vitellaria  divided  into  one  mass  in  front  of  and 
another  behind  the  ovary— Amphimerus . 
B.  Testes  branched  :■ — 

Branches  cover  intestinal  caeca  ventrally — Clonorchis. 
Type  genus. — Opistorchis  R.  Blanchard,  184^ . 

Opisth orchis  R.  Blanchard,  1845. 

Definition. — Opisthorchiinse  with  long  flattened  body  and  some- 
what pointed  anterior  extremity,  suckers  small,  intestinal  case  a 
unbranched,  yolk  glands  situate  laterally  and  not  extending  beyond 
the  ventral  sucker  in  front,  testes  in  the  posterior  part  of  the  body, 
one  behind  the  other. 

Type  Species. — Opistorchis  felineus  Rivolta,  1885. 

Classification. — The  species  of  this  genus  are  separated  from 
one  another  with  great  difficulty. 

The  following  are  found  in  man:  Opisthorchis  felineus  Rivolta, 
1885;  Opisthorchis  viverrini  Poirier,  1866. 

These  two  species  are  distinguished  as  follows  :■ — 

A.  Cuticle  without  spines — Felineus. 

B.  Cuticle  with  minute  spines — Viverrini. 

Opisthorchis  felineus  Rivolta,  1885. 

Synonyms. — Distoma  conus  Gurlt,  1831,  nee  Creplin,  1825;  D. 
lanceolatum  v.  Siebold,  1836,  nee  Mehlis,  1825;  D.  sibiricum 
Winogradoff,  1892;  D.  tenuicolle  Miihl,  1896,  p.p. 

Definition.— Opisthorchis  with  cuticle  without  spines. 

Remarks. — Opisthorchis  felineus  lives  in  the  gall-bladder  and 
bile-ducts  of  the  domestic  cat,  and  is  also  found  in  dogs  in  Europe. 
The  North  American  species  is  different  (0.  pseudo-felineus). 

In  human  beings  it  is  apparently  a  common  parasite  in  Siberia, 
where  it  was  first  found  by  Winogradoff  in  Tomsk. 

Morphology. — It  is  reddish-yellow  in  colour,  with  a  conical  neck  at  the 
level  of  the  ventral  sucker,  marked  by  a  shallow  constriction. 

The  length  is  from  8  to  11  millimetres  and  the  breadth  1-5  to  2  millimetres. 
The  testes  lie  in  the  posterior  part  of  the  body,  one  behind  the  other.  The  yolk 
glands  are  situate  on  either  side  of  the  middle  third  of  the  body,  beginning 
behind  the  ventral  sucker  and  terminating  about  the  level  of  the  ovary. 

The  genital  pore  is  close  in  front  of  the  ventral  sucker. 

The  eggs  are  oval,  with  a  well-defined  operculum  (30  /j,  by  n  /*). 

Life-History. — The  parasites  live  in  the  bile-duct,  and  the  eggs, 
containing  a  ciliated  miracidium,  escape  in  the  faeces.  Complete 
development  is  not  known,  but  cercaria  have  been  found  in  fish 
which  infect  men  and  cats. 

Pathogenicity.— It  causes  inflammation,  dilatation  of  the  bile 
ducts  in  man,  with  atrophy  of  the  liver  substance,  ascites,  and 
icterus. 


PAROPTSTHOHCnTS  CANINUS  577 

Opistorchis  viverrini  Poirier,  1886. 

Definition. — Opisthorchis  with  cuticle  covered  with  minute 
acicular  spines.  Ovary  multilocular.  Branches  of  intestine  almost 
reach  the  hinder  end  of  the  body,  and  the  ovary  and  testes  are 

deeply  lobed. 

Remarks.  -This  trematode,  which  belongs  to  the  Indian  civet-cat, 
was  obtained  by  Kerr  from  prisoners  at  Chiengmai,  and  recognized 
by  Lei  per. 

Infection. — Infection  is  probably  by  eating  raw  or  partially  cooked 
fresh-water  fish. 

Paropisthorchis  Stephens,  1912. 

Definition. — Opisthorchiime  with  lobed  testes  and  with  ventral 
process  on  which  are  situate  the  ventral  sucker  and  the  genital  pore. 
Type  Species. — Paropisthorchis  caninus  Barker,  1912. 

Paropisthorchis  caninus  Barker,  1912. 

Definition. — -Paropisthorchis  with  the  generic  characters. 

Remarks. — Cobbold  in  1858  found  a  little  fluke,  Distomum  con- 
)  nudum,  in  the  bile-ducts  of  Cants  fiilvus  Lewis,  the  American  fox. 

Fourteen  years  later  Lewis  and  Cunningham  found  the  same 
fluke  in  Indian  pariah  dogs,  and  in  1874  McConnell  found  what 
was  thought  to  be  the  same  fluke  in  human  beings  in  Calcutta. 
In  1903  Braun  pointed  out  that  the  American  and  Indian  flukes 
were  different,  and  named  the  latter  Opisthorchis  noverca  (vide  infra, 
Amphimerus) . 

In  1 91 2  Barker  separated  the  parasite  of  the  Indian  pariah  dog 
from  the  human,  calling  the  former  0.  caninus  ;  and  in  the  same 
year  Stephens  created  a  separate  genus  for  it.  Leiper  still  main- 
tains, however,  that  these  two  forms,  in  man  and  dog,  are  identical. 

It  is  not  known  to  occur  in  man. 

Amphimerus  Barker,  1912. 

Definition. — Opisthorchiinae  without  ventral  process,  but  with 
lobed  testes  and  vitellaria  divided  by  the  position  of  the  ovary  into 
anterior  and  posterior  lobes. 

Type  Species. — Amphinterus  noverca  Braun,  1903. 

Remarks. — -This  genus  was  created  for  Braun's  Opisthorchis  noverca, 
which,  as  explained  above  according  to  Stephens,  only  applies  to 
McConnelTs  flukes,  found  in  two  Mohammedans  in  Calcutta. 

Amphimerus  noverca  (Braun,  1903). 
Definition. — Amphimerus  with  the  characters  of  the  genus. 

Morphology. — It  is  lancet-shaped,  with  anterior  and  posterior  extremities, 
pointed  body,  covered  with  spines;  9-5  to  12-7  millimetres  in  length  and 
2*5  millimetres  in  breadth,  with  two  suckers  very  close  together,  the  anterior 
being  larger  than  the  posterior.  The  genital  pore  opens  just  in  front  of  the 
ventral  sucker.  The  pharynx  is  spheroidal,  and  the  intestinal  caeca  extend 
far  back.     The  two  testes  are  very  distinct,  the  anterior  rounded  and  the 

37 


578 


TREMATODA 


posterior  lobate.  The  ovary  is  slightly  lobate,  and  it  and  the  uterus  are 
situated  medianly.  The  yolk  glands  lie  laterally  in  the  middle  third,  extend- 
ing from  behind  the  ventral  sucker  to  the  back  of  the  testes.  There  is  no 
cirrus  pouch.     The  eggs  are  oval  (0-034  by  0-021  millimetre). 

Habitat. — The  dog  and  man. 
Pathogenicity.— Not  known. 

Clonorchis  Looss,  1907. 

Definition. — Opisthorchiinae  characterized  by  the   fact  that   the 

testes  are  not  notched  or  lobate,  but  distinctly  ramified,  the  branches 

crossing  the  intestinal  caeca  on  their  ventral  side  and  extending  very 

near  the  body  margin.     The  excretory  vesicle  is  simply  an  unpaired 

cab  tube,  which  becomes  somewhat 

widened  at  its  anterior  end, 
assuming  sometimes  the  shape 
of  an  irregular  triangle. 


Fig.  223. — Clonorchis  sinensis. 

(After  Looss,   from  the  Annals  of 

Tropical  Medicine  and  Parasitology.) 

a,  Schematic;  b,  natural  size;  c,  egg 

X5°°- 


Fig.  224. — Clonorchis  endemicus. 

(After  Looss,  from  the  Annals  of 
Tropical  Medicine  and  Parasitology.) 

a,  Schematic;  b,  natural  size;  c,  egg 
X5°°- 


"■  Speeies.— Clonorchis  sinensis  Cobbold,  1875;  Clonorchis  endemicus 
Baelz,  1883;  but  the  work  of  Kobayashi  in  1917  tends  to  show 
that  they  are  one  and  the  same  species, 

Clonorchis  sinensis  Cobbold,  1875, 

Synonyms. — Distoma    sinense    Cobbold,    1875;    D.    spathulatum 
Leuckart,  1876;  Distomum  hepatis  innocunm  Baelz,  1883. 
Definition.  -Clonorchis  with  the  generic  characters. 


CLONORCHIS  SINENSIS  579 

History. — Clonorchis  sinensis  was  first  discovered  by  McConnell 
in  1874  in  the  liver  of  a  Chinaman.  It  was  believed  to  be  an 
<)  pi  sth  orchis,  but  in  1907  Looss  gave  reasons  why  it  should  be 
placed  in  the  new  genus  Clonorchis.  As  far  as  is  known  it  occurs 
principally  in  China  and  Japan,  and  has  not  yet  been  found  in 
animals. 

Remarks. — -It  may  be  the  same  as  Clonorchis  endemicus  Baelz, 
1883;  Distoma  hepatis  endemicum  sive  perniciosum  Baelz,  1883; 
Distotna  japonicum  R.  Blanchard,  1886.  In  1883  flukes  were 
first  described  in  the  liver  of  human  beings  in  Japan  by  Kiyono, 
Nakahama,  Suga,  and  Yamagata,  and  a  little  later  in  the  same 
year  Baelz  reported  the  occurrence  of  two  hepatic  distoma  in 
Japan. 

1.  Distoma  hepatis  innoaium,  up  to  20  millimetres  in  length,  with 
a  lighter-coloured  uterus  of  larger  volume,  with  slightly  larger  ova, 
21  to  36  [jl  in  length  by  18  to  20  p  in  breadth,  and  with  a  black  granu- 
lar pigment  in  its  excretory  apparatus  and  body  parenchyma.  It 
caused  little  or  no  symptoms  in  human  beings,  and  was  found  acci- 
dentally in  post-mortems. 

2.  Distoma  hepatis  endemic um  sive  perniciosum,  which  was  smaller, 
8  to  11  millimetres  in  length,  and  did  not  possess  the  above  char- 
acters, while  its  eggs  were  only  20  to  30  ^in  length  by  i5]to  17  [jl  in 
breadth. 

Kobayashi  finds  that  Looss's  differences  between  C.  sinensis  and 
C.  endemicus  do  not  hold  good.  They  were  (1)  size;  (2)  discontinuity 
of  the  vitellaria;  (3)  pigmentation;  (4)  size  and  shape  of  the  egg. 
In  the  experimentally  reared  forms  there  are  no  such  constant 
differences. 

It  is  found  in  Japan,  where  it  is  common,  and  in  Annam  and 
Tonkin,  in  man,  cats,  dogs,  and  pigs. 

Morphology. — Clonorchis  sinensis  is  a  white,  or  yellowish-red,  or  brownish, 
narrow  trematode,  13  to  19  millimetres  in  length  and  3  to  4  millimetres  in 
breadth.  The  pigmentation  is  due  to  the  deposit  of  fine  yellowish  or  brown 
granules  in  the  body  parenchyma.  The  ramifications  of  the  testes  are  long, 
the  anterior  arising  from  four  and  the  posterior  from  five  main  stems,  with 
sometimes  ventral  bulgings.  The  ovary  is  trilobate,  but  may  show  three  to 
six  smaller  lobules.  The  yolk  glands  reach  from  the  ventral  sucker  to  the 
level  of  the  ovary,  and  are  peculiar  in  that  certain  groups  of  follicles  remain 
undeveloped.  In  perfectly  mature  specimens  the  seminal  vesicle  extends  back 
as  far  as  the  middle  of  the  uterus.  The  eggs  are  generally  narrowed  towards 
the  anterior  end,  and  have  a  rather  high  lid,  with  a  sharply  projecting  brim 
(these  peculiarities  may  be  absent.)  The  egg  is  29  fx  in  length  and  16  //.  in 
breadth. 

Life-History. — Kobayashi  has  found  the  cysts  in  the  muscles  of 
fish — Pseudorasbora  parva,  Leucogobio  giintheri,  Leucogobio  maycdce, 
and  Carassins  auratus — -and  was  able  to  infect  cats  by  feeding  with 
the  infected  flesh.  He  also  found  cysts  in  other  fish — Acheilogna- 
thus  lanceolatus,  A.  limbatus,  A.  cyanostigmus ,  Paracheilognathus 
rhombeus,  Pseudoperclampus  typiis,  Abbottina  psegma,  Biwia  zezera, 
and  Sarcocherlichthys  variegalus.     These  fish  are  the  second  inter- 


58o 


TREMA  TOD  A 


mediate  host.     The   first  intermediate  host   and   the  method   ot 
infection  of  the  fish  are  unknown,  but  Melania  libertina  is  suspected. 

Habitat. — It  is  found  in  cats,  dogs,  hogs,  and  men. 

Pathogenicity.— Enlargement  of  the  liver,  and  diarrhoea. 

A  Possible  Feline  Clonorchis  (or  Opisthorchis). 

Looss  draws  attention  to  the  fact  that  Ijima,  in  1886,  describes  a  Distomum 
from  the  liver  of  a  cat  in  Japan,  with  fine  spines,  and  smaller  than  C.  endemicus, 

which  is  to  be  looked  upon  as  a  normal  parasite 
C  3  b  of  the  cat.     It  is  only  4-5  millimetres  in  length 

by  0-9  millimetre  in  breadth.     It   may  be   a 
Clonorchis  or  an  Opisthorchis. 

Katsurada,  in  1900,  published  a  paper  based 
upon  seventy-six  post-mortems  with  an 
enormous  number  of  parasites,  among  which 
he  mentioned  three  fqund  in  a  man  from  the 
province  of  Saga,  with  an  average  length  of 
5-16  millimetres  and  breadth  of  0-96  milli- 
metre, which  Looss  considers  can  only  be 
explained  as  an  infection  with  a  feline  species. 

Habitat. — Cats  and  man  (?). 

FAMILY  DICROCCELIIM) 
Odhner,  1910. 

Definition. — -Fascioloidea,  hermaphro- 
ditic, without  spiny  collar  around  the 
oral  sucker,  and  with  the  ovary  behind 
the  testes. 

Type  Genus. — Dicroccelium  Dujardin, 
1845. 

Dicroccelium  Dujardin,  1845. 

Definition. — Dicrocceliidae  with  lancet- 
shaped  bodies,  without  spines,  and  with 
suckers  placed  close  together.  Intestine 
does  not  reach  the  posterior  end.  Genital 
pore  close  behind  the  pharynx,  with  a 
cirrus  pouch  in  front  of  the  ventral 
sucker,  just  behind  which  the  testes  lie 
with  the  ovary  in  the  median  line 
behind  them.  The  uterus  lies  behind 
the  ovary  and  testes,  extending  as  far  back  as  the  posterior 
border.  The  yolk  glands  are  small,  and  situated  in  the  middle 
quarter  of  the  lateral  areas  of  the  body.  The  excretory  vesicle 
is  tubular.  Ova  dark  brown.  Worms  live  in  the  liver  and  gall- 
bladder, rarely  in  the  intestine. 
Type  Species. — Dicroccelium  dendriticum  Rudolphi,  1819. 

Dicroccelium  dendriticum  Rudolphi,  1819. 

Synonyms.— Fasciola  lanceolata  Rudolphi,  1803,  nee  Schrank, 
1790;  Distomum  lanceolatum  Mehlis,  1825;  Dicroccelium  lanceolatum 
Dujardin,  1845;  Dicroccelium  lanceatum  Stiles  and  Hassall,  1896. 


Fig.  225. — Dicroccelium 
dendriticum  Rudolphi. 

(After  Looss,  from  Mense's 
'  Tropenkrankheiten.') 

a,  SchematicX6;  b,  natural 
size;  c,  eggs  X  250. 


DICROCCELIUM  DENDRITICUM  581 

History. — Bucholz  appears  to  have  been  the  first  to  discover 
these  worms  in  the  gall-bladder  in  Weimar,  and,  later,  Chabert  in 
the  intestines  of  a  girl  in  France,  and  Kiichner  in  Weimar.  Since 
then  they  have  been  noted  in  Italy  and  Egypt.  They  are  found  in 
the  bile-ducts  of  herbivorous  and  omnivorous  animals  in  Europe, 
North  Africa,  Asia,  and  North  and  South  America. 

Morphology. —Dicrocoelium  dendriticum  is  a  small  trematode,  measuring 
8  to  10  millimetres  in  length  by  1*5  to  2*5  millimetres  in  breadth.  It  is  pointed 
in  front  and  narrow  behind,  so  that  the  widest  point  is  just  behind  the  yolk 
glands.  Cuticle  is  smooth;  the  oral  sucker  is  terminal,  and  about  the  same 
size  as  the  ventral  (0-5  to  o-6  millimetre).  The  intestine  bifurcates  just  in 
front  of  the  genital  pore,  which  is  situate  in  the  median  line  in  front  of  the 
ventral  sucker,  behind  which  the  two  testes  lie,  from  which  the  vasa  deferentia 
run  forwards  to  form  a  cirrus  lying  in  a  cirrus  sac. 

The  ovary  lies  behind  the  posterior  testis;  there  is  a  receptaculum  seminis 
and  a  Laurer's  canal.  The  yolk  glands  lie  in  the  lateral  portion  of  the  middle 
fifth  of  the  body,  the  posterior  portion  of  which  is  filled  up  by  the  large  coiled 
uterus.  The  eggs  are  thick-shelled,  and  yellowish  to  brown  in  colour,  with  a 
length  of  38  to  45  fi  and  a  breadth  of  22  to  30  fjb. 

Life-History. — -Not  known,  but  suspicion  rests  on  Planorbis  mar- 
ginatum and  land-snails. 

Pathogenicity. — No  special  symptoms. 


FAMILY  ECHINOSTOMID/E  Looss,  1902. 

Definition. — Fascioloidea,  hermaphroditic,  with  a  fold  or  collar 
bearing  a  row  or  rows  of  pointed  spines  on  the  dorsal  and  lateral 
aspects  of  the  oral  sucker.  The  rows  of  spines  are  continued  laterally 
on  to  the  ventral  corners,  and  the  number  of  spines  is  constant  for 
each  species.     The  corner  spines  are  large  or  specialized. 

Classification. — -The  family  is  divided  into  two  subfamilies  as 
follows : — 

A.  Cirrus  sac  does  not  reach  beyond  acetabulum.     Without 

strong  rosethorn  hooks — Echinostomince. 

B.  Cirrus  sac  reaches  beyond  acetabulum.     With  strong  rose- 

thorn  hooks — ■HimastlilincB. 

Subfamily  Echinostomince  Looss,  1899. 

Definition. — As  above. 

Type  Genus. — Echinostoma  Rudolphi,  1809. 

Classification. — E.  malayanum  Leiper,  1911,  has  been  placed  by 
Odhner  in  the  genus  Euparyphium  Odhner,  so  that  it  now  becomes 
Euparyphi urn  malayanum,  as,  according  to  Leiper,  it  is  probably 
the  same  as  Artyfechinostomum  sufrartyfex  Lane,  1915,  which  Lane 
found  in  a  girl  of  eight  years  of  age  on  the  Ragnik  Tea  Estate  in 
Assam.  In  1916  Stephens  pointed  out  that  Lane's  genus  did  not 
possess  the  strong  rosethorn  hooks  of  the  Himasthlinae.  In  191 7 
Lane  pointed  out  that  as  Odhner's  principal  character  of  the 
Echinostominae  was  that  the  cirrus  sac  usually  reaches  to  the  centre 


582  TREMA  TOD  A 

of  the  acetabulum,  but  not  beyond  it,  while  that  of  .4 .  sufrartyfex 
reaches  0-75  mm.,  therefore  it  is  not  a  member  of  the  Echino- 
stominae. 

Genus  Echinostoma  Rudolphi  18C9. 

Synonym. — -Fascioletta  Garrison,  1908. 

Definition. — Echinostominae,  with  small  elongated  bodies,  broader 
anteriorly  than  posteriorly,  with  characteristic  circumoral  ring  of 
spines  and  with  other  spines  on  the  body,  and  with  large  prominent 
acetabulum.  (Esophagus  short,  intestinal  caeca  unbranched.  Ex- 
cretory vesicle  tubular.  Genital  pores  anterior  to  the  acetabulum. 
Testes  compact,  situate  in  the  median  line  one  behind  the  other. 
Cirrus  and  pouch  well  developed.  Ovary  compact ;  no  receptaculum 
seminis;  Laurer's  canal  present.  Yolk  glands  well  developed  in 
the  posterior  fifth  of  the  body;  well-developed  shell  gland  and  uterus, 
which  lies  between  the  ovary  behind  and  the  acetabulum  in  front. 
Ova  large  and  operculated. 

Remarks. — With  regard  to  the  position  of  Echinostoma,  it  should 
be  observed  that  some  authorities  do  not  classify  it  under  the  Fas- 
ciolidx,  but  in  a  special  family  Echinostomidae  which  we  adopt. 

Type  Species, — The  type  species  is  Echinostoma  revolutum  (Eroe- 
lich,  1802),  of  which  the  synonym  is  Distoma  echinatum  Zeder, 
1803.  Another  species  of  importance  in  tropical  medicine  is 
E.  ilocanum  (Garrison,  1908), 

Echinostoma  ilocanum  Garrison,  1908. 

Synonym. — Fascioletta  ilocana  Garrison,  1908. 

History.— Echinostoma  ilocana  was  discovered  and  described  by 
Garrison,  who  in  1907  noticed  peculiar  eggs  in  the  faeces  of  Philip- 
pine prisoners  in  Bilibid  Prison  in  Manila,  and  subsequently,  after 
treatment  with  male-fern,  obtained  a  small  number  of  trematodes. 
Quite  recently  Odhner  has  shown  that  it  belongs  to  the  genus 
Echinostoma,  family  Echinostomidae. 

Morphology. — Echinostoma  ilocana  is  a  very  small  trematode,  measuring 
4  to  6  millimetres  in  length  by  0-75  to  1-35  millimetres  in  breadth  and  0-5  to  1 
millimetre  in  thickness.  Posteriorly  it  is  attenuated.  The  acetabulum  is 
about  three  times  the  size  of  the  oral  sucker,  which  is  either  terminal  or  slightly 
ventro-subterminal.  The  prepharynx  is  long,  the  pharynx  globular;  the 
oesophagus  short,  bifurcating  just  anterior  to  the  genital  pore  into  the  intes- 
tinal caeca.  The  genital  pores  open  separately  a  little  behind  the  halfway 
point  between  the  pharynx  and  the  acetabulum. 

The  cirrus  pouch  is  well  developed,  and  contains  posteriorly  the  vesicula 
seminalis,  into  which  open  the  vasa  deferentia,  and  which  gives  rise  to  the 
long  coiled  cirrus.  Each  testis  shows  an  anterior  and  a  posterior  lobe.  The 
ovary  is  globular,  the  yolk  glands  well  developed,  and  the  uterus  fairly 
developed.     Ova  88-8  to  ii4'7  ju.  long  by  53-5  to  81-9  /u  broad. 

Life-History. — Nothing  is  known  of  the  life-history  beyond  the 
fact  that  a  miracidium  hatches  in  about  ten  days  after  the  eggs 
have  left  the  host. 

Habitat.— The  intestine  of  man  in  Luzon,  in  the  Philippine 
Islands. 

Pathogenicity. — It  is  probable  that  the  worm  is  non-pathogenic. 


EUPARYPHIUM  MALAY ANUM  583 

Genus  Euparyphium  Odhner. 
Euparyphium  malayanum  Lciper,  191 1. 

Synonym. — Echinostoma  malayanum  Leiper,  ign. 

History. — In  1911  Leiper  received  two  consignments  of  flukes 
from  Dr.  Macaulay  of  Singapore  and  from  Dr.  Stanton  of  Kuala 
Lumpur  which  had  been  collected  from  the  intestine  of  a  Tamil 
in  the  Malay  States. 

Merphology. —  It  is  a  thick,  fleshy  trematode,  light  brown  in  colour,  12  milli- 
metres in  length,  3  millimetres  in  breadth,  and  1-3  millimetres  in  thickness. 
The  oral  sucker  is  situated  on  a  kidney-shaped  anterior  portion,  which  is 
somewhat  detached  from  the  rest  of  the  parasite  by  a  furrow  on  either  side. 
This  circumoral  disc  is  surrounded  by  a  row  of  forty-two  stout  spines.  The 
cuticle  of  the  body  is  unevenly  furnished  with  spines.  The  acetabulum  is 
several  times  larger  than  the  oral  sucker.  The  oral  sucker  lies  in  the  middle 
third  of  the  circumoral  disc,  and  leads  into  a  spheroid  muscular  pharynx, 
and  so  into  the  oesophagus,  which  bifurcates  immediately  behind  the  pharynx 
into  two  branches,  which  are  simple  and  end  blindly  at  the  posterior  end  of 
the  body. 

The  deeply  lobed  testes  lie  one  behind  the  other  behind  the  acetabulum; 
there  is  a  well-developed  cirrus  pouch  and  a  long,  thick  cirrus.  The  ovary  is 
smooth,  and  lies  immediately  in  front  of  the  anterior  testis  and  just  behind 
the  acetabulum.  The  yolk  glands  are  numerous,  extending  from  the  aceta- 
bulum to  the  posterior  end  of  the  body.  The  brown  eggs  are  few  in  number 
and  large  in  size. 

Habitat. — Leiper  does  not  think  that  this  worm  is  a  normal 
parasite  of  man,  and  considers  that  domesticated  animals,  especially 
cats  and  dogs,  should  be  investigated  for  it. 

Pathogenicity. — Not  stated. 

Subfamily  Himasthlin^e  Odhner,  1910. 

Definition. — E chinos tomidae  in  which  the  cirrus  sac  extends 
caudad  to  the  acetabulum. 

Remarks. — The  only  genus  with  which  we  are  concerned  is  :■ — 

Genus  Artyfechinostomum  Clayton-Lane,  1915. 

Definition.— Himasthlinge  without  strong  rosethorn  hooks. 
Remarks. — -There  has  been  much  dispute  as  to  whether  this  is  a 
good  genus  or  not. 
Type  Species. — Artyfechinostomum  sujrartyfex  Clayton-Lane,  1915. 

Artyfechinostomum  sufrartyfex  Clayton-Lane,  1915. 

Nomenclature. — -Leiper  has  pointed  out  that  this  name  clashes 
with  the  recommendations  of  the  International  Rules :  '  The  use  of 
proper  names  in  the  formation  of  compound  generic  names  is 
objectionable.'     However,  the  name  cannot  now  be  changed. 

History. — The  worm  was  found  in  a  girl,  aged  eight  years,  on  the 
Ragnik  Tea  Estate  in  Assam,  and  was  thought  by  Leiper  to  be 
probably  the  same  as  Euparyphium  malayanum ;  but  in  1917 
Clayton-Lane  showed  that  the  cirrus  sac  extended  0*75  mm.  caudad 
to  the  acetabulum,  a  fact  agreeing  with  the  definition  of  the  sub- 
family. 


584  TREMATODA 

FAMILY  SCHISTOSOMID^E  Looss,  1899. 

Definition. — Fascioloidea  with  separate  sexes,  and  with  genital 
pore  posterior  to  the  elevated  acetabulum.  No  pharynx.  In- 
testinal caecare  unite  to  form  a  single  intestine. 

Type  Genus. — -Schistosoma  Weinland,  1858. 

Schistosoma  Weinland,  1858. 

Synonyms. — G\nicecophorus  Diesing,  1858;  Bilkarzia  Cobbold, 
1859;  Thecosoma  Moquin-Tandon,  i860. 

Definition. — Schistosomidae  with  long  filiform  females  and  shorter 
males,  with  body  considerably  widened  behind  the  acetabulum.  In 
this  part  the  lateral  walls  can  curve  ventrally  to  form  an  almost 
closed  canalis  gyntecophorus,  within  which  the  female  is  enclosed. 
No  cirrus  pouch.  No  pharynx.  No  Laurer's  canal.  Eggs  with 
spines  and  no  lids.  Miracidia  ciliated  with  large  glandular  cells 
discharging  anteriorly  beside  gastric  sac.  Development  in  various 
snails.  Cercariae  with  forked  tails  and  no  eye  spots.  Enter 
vertebrate  hosts  through  skin  or  mucosa,  and  pass  into  blood 
vessels. 

Classification. — The  species  known  to  occur  in  man  may  be 
recognized  as  follows  (S.  magna  Cobbold,  1852,  found  in  a  monkey — 
Cercocebus  fuliginosus — is  represented  to-day  by  only  a  piece  of  a 
male,  which  Leiper  says  cannot  be  recognized  as  belonging  to  a 
human  species) : — 

A.  Cuticle  with  spines: — 

I .  Male,  four  to  five  large  testes ;  female,  ovary  posteriorly 
situate.  Eggs,  terminal  spined.  Development  in 
subgenera  and  species  oiBullinus — Haematobium. 
1 1 .  Male,  eight  small  testes ;  female,  ovary  anteriorly  situate . 
Eggs,  lateral  spined.  Development  in  species  of 
Planorbis — Mansoni . 

B.  Cuticle  nearly  smooth,  only  a  few  spines  seen  in  fresh  con- 

dition along  margin  of  canal. 
Male,  six  to  eight  testes;  female,  ovary  almost  in  middle 
of  body.     Eggs  with  small  lateral  spines  or  thickenings. 
Development  in  species  oiBlanfordia — Japoniatm. 

Schistosoma  haematobium  Bilharz,  1852. 

Synonyms. — ■Distomum  haematobium  Bilharz,  1852;  D.  capense 
Harley,  iS()^.;Bilharzia  hcematobia  Cobbold,  1859. 

Definition. — -Schistosoma  with  spiny  cuticle.  Males  with  four  to 
five  large  testes  and  with  intestinal  caeca  uniting  late  to  form  a 
short  single  intestine.  Females  with  ovary  in  the  posterior  half  of 
the  body.  Uterus  very  long,  with  many  terminal  spined  eggs. 
ViteUaria  in  posterior  fourth  of  the  body.  Development  of  eerearise 
in  subgenera  and  species  oiBullinus. 

History.— Schistosoma  haematobium  was  discovered  in  the  portal 
vein  of  a  man  in  1851  by  Bilharz  in  Cairo,  and  later  by  Harley  in 


SCHISTOSOMA  HAEMATOBIUM 


585 


C864  in  a  patient  from  the  Cape  of  Good  Hope.  Since  then  it  has 
been  found  widely  distributed  through  Africa  (Egypt,  Sudan,  Tunis, 
Algiers,  West  Coast,  including  the  Gold  Coast,  East  Coast,  and 
South  and  Central  Africa),  which  is  its  endemic  centre,  and  in  Asia, 
in  Syria,  Arabia,  Mauritius,  Persia,  India.  Only  imported  cases 
occur  in  Ceylon. 

Other  species  are  known  in  sheep,  horses,  oxen,  etc. 

In  1915  Leiper  discovered  its  complete  life-history  in  the  snail 
and  its  method  of  entry  into  the  vertebrate. 

Morphology— Male.— The  male  is 
whitish  in  colour,  and  from  12  to 
14  millimetres  in  length,  with  a 
greatest  width  behind  the  ventral 
sucker  of  1  millimetre.  It  is  really 
thin  and  flat,  though  it  may  look 
cylindrical,  because  the  lateral 
margins  are  turned  ventrally  inwards, 
enclosing  a  canal,  called  the  '  gyna?- 
cophoric  canal,'  in  which  the  female 
lies.      The    whole    body   is    covered 


Fig.  226.- — Schistosoma  hesmatobium. 

(After  Looss,  from  Mense's  '  Tropen- 
krankheiten.') 

This  drawing  shows  the  female 
worm  enclosed  in  the  gynaecophoric 
canal  of  the  male. 


Fig.  227. — Egg  of  Schistosoma 
hesmatobium  (X250). 

(After  Looss,  from  Mense's 
'  Tropenkrankheiten.') 


with  projections  tipped  with  short  spines,  which  enable  it  to  cling  to  the  wall 
of  the  bloodvessel.  The  oral  sucker  looks  ventrally.  The  ventral  sucker  is 
situate  near  to  it.  There  is  no  pharynx,  but  the  oesophagus  is  long  and 
covered  with  numerous  glands,  and  bifurcates  just  in  front  of  the  ventral 
sucker  into  the  intestinal  caeca,  which  unite  behind  the  testes  into  a  median 
trunk.  The  excretory  pore  is  at  the  posterior  end,  situated  a  little  dorsally. 
There  are  four  to  five  testes,  from  which  the  vas  deferens  runs  to  a  vesicula 
seminalis,  from  which  an  ejaculatory  duct  proceeds  to  the  genital  pore, 
situated  behind  the  \entral  sucker  at  the  beginning  of  the  gynaecophoric 
canal. 

Female.  -The  female  worm  is  long,  thin,  being  20  millimetres  in  length 
[i.e.,  longer  than  the  male)  and  0-25  millimetre  in  breadth  (much  thinner 
than  the  male).  Posteriorly  it  is  coloured  dark  brown,  because  of  the  colour 
of  the  contents  of  the  intestine.  The  cuticle  is  smooth,  except  in  the  sucker 
and  at  the  tail  end,  where  there  are  large  spines.  The  alimentary  canal  is 
much  the  same  as  in  the  male.     The  ovary  is  median,  and  the  ovarian  duct, 


586  TREMATODA 

taking  origin  at  the  posterior  end,  runs  forward  to  join  with  the  vitellarian 
duct  from  the  single  yolk  gland,  which  lies  about  the  middle  of  the  body. 
The  junction  of  the  two  ducts  is  at  first  narrow  and  surrounded  by  the  shell 
gland,  but  it  soon  dilates  into  the  uterus,  which  runs  forwards  to  end  in  the 
genital  pore,  just  behind  the  ventral  sucker.  The  eggs  are  bluntly  spindle- 
shaped,  yellowish  in  colour,  slightly  transparent,  and  provided  with  a  thin 
shell,  without  a  lid,  but  possessing  a  terminal  spine,  which  may  be  absent 
at  the  posterior  end.  They  measure  from  0-12  to  0-19  millimetre  in  length 
and  0-05  to  0-073  millimetre  in  breadth,  but  vary  considerably. 

Life-History. — -The  young  immature  and  mature  males  and 
females  are  found  in  the  portal  system. 

Looss  notes  that  it  is  not  uncommon  to  find  males  alone  in  the 
portal  vein,  and,  further,  that  they  are  all  of  the  same  age. 
Eventually  they  pair,  and  now  the  male  carries  the  female  along 
that  vein  down  the  inferior  mesenteric  vein  to  the  bladder,  which 
is  a  fairly  direct  route,  but  Looss  considers  that  they  may  be 
chemically  attracted  to  the  bladder,  for  their  journey  is  against 
the  blood-stream,  and  they  are  enabled  to  perform  it  by  means 
of  the  bristles  on  the  male  cuticle. 


Fig.  228. — Bullinus  contortus  Fig.  229. — Bullinus  dybowskii 

Michaud,  1829.  Fischer,  1891. 

The  length  of  time  occupied  by  the  journey  is  not  known,  and 
probably  varies  considerably.  Arrived  in  the  veins  of  the  bladder, 
the  real  oviposition  begins,  and  Looss  is  inclined  to  think  that  the 
female  can  push  the  head  (close  to  which  is  the  genital  opening)  into 
the  capillaries,  and  thus  lay  the  eggs  directly  into  these  channels, 
where  they  are  held  in  position  by  contraction  of  the  capillary  upon 
them.  Looss  thinks  that  it  is  probable  that  the  worms  may  live 
three  years  in  these  vessels,  producing  during  that  period  large 
numbers  of  eggs,  which  work  their  way  like  any  other  foreign  body 
into  the  lumen  of  the  bladder,  probably  by  means  of  the  con- 
tractions of  that  organ. 

Leiper  finds  that  in  experimentally  infected  monkeys  eggs  begin 
to  appear  about  ten  weeks  after  infection. 

Egg.— During  their  journey  through  the  tissues  the  eggs  increase 
in  size  from  0-08  to  0-09  fx  in  length  and  0-03  to  0-04,0.  in  breadth 
in  the  06 type  to  0-13  to  0-15  p.  in  length  and  0-04  to  0-06  ix  in  breadth 
in  the  urine,  while  the  embryo  develops,  so  that  when  they  are 
voided  in  the  urine  they  contain  a  well-developed  miracidium;  but 
during  this  journey  many  die  and  become  calcified.  It  is  not 
known  how  long  an  egg  must  take  before  it  escapes  in  the  urine, 


SCHISTOSOMA   MANSONI  587 

but  Looss  points  out  that  even  the  presence  of  an  egg  with  a  true 
miracidium  is  no  evidence  that  the  parent  worms  are  alive. 

Miracidium. — These  eggs  will  simply  die,  unless  they  gain  access 
to  water,  in  which  they  hatch,  and  the  ciliated  miracidium  escapes 
and  swims  about.  In  the  so-called  body  cavity  of  this  miracidium 
there  are  germinal  cells. 

Intermediate  Hosts.— When  miracidia  are  allowed  to  hatch  out 
in  water  containing  suitable  and  unsuitable  snails,  they  crowd 
round  and  enter  the  former,  while  they  neglect  the  others.  In  a 
short  time  all  the  miracidia  have  disappeared  from  the  water  con- 
taining suitable  snails. 

The  snails  which  are  suitable  are  those  in  which  Leiper  found  the 
development  to  proceed — viz.,  Bullinus  contortus  Michaud,  1829; 
B.  dybowskii  Fischer,  1891;  and  B.innesi  Bourguignat.  In  South 
Africa  Becker  has  experimentally  implicated  Bullinus  (Phy sops-is) 
africanus  as  an  intermediary. 

Within  these  molluscs  the  miracidium  makes  its  way  into  the 
liver  and  becomes  changed  into  a  smooth-walled  sac — the  sporocyst 
— from  which  are  formed  daughter  sporocysts,  and  from  these 
cercariae.  In  any  case  the  cercaria  is  the  end  of  this  stage,  and  is 
alone  the  infective  organism . 

In  some  of  our  experiments  we  so  heavily  infected  our  snails 
that  they  died,  but  in  nature  this  does  not  take  place. 

Cercarice.— If  an  infected  snail  is  allowed  to  remain  in  clear  water 
it  is  amazing  the  quantities  of  cercariae  which  may  escape  therefrom 
into  the  water  and  swim  about. 

Infection. — -Leiper  has  shown  that  these  cercariae  may  penetrate 
the  skin  and  infect  animals.  They  may  also  penetrate  the  mucosa 
of  the  mouth  and  throat ;  and  then  by  gradual  growth  and  differ- 
entiation of  the  organs  become  male  or  female  adult  worms. 

Pathogenicity. — -It  is  usually  the  cause  of  urinary  schistosomiasis, 
or,  as  it  is  better  known,  vesical  Bilharziosis,  but  occasionally  it 
may  give  rise  to  Bilharzial  Dysentery. 

Schistosoma  mansoni  Sambon,  1907. 

Definition. — Schistosomum  with  spiny  cuticle.  Male  with  eight 
small  testes.  The  gut  forks  unite  early,  and  hence  the  straight 
intestine  is  long.  Female  with  ovary  in  the  anterior  half  of  the 
body.  Uterus  very  short,  with  only  one  lateral-spined  egg  present 
at  a  time.  Vitellaria  in  posterior  two-thirds  of  body.  Development 
of  cercaria  in  Planorbis  boissyi  in  Egypt  and  the  Sudan,  and  P 
olivaceus  Spixin  Brazil,  and  P.  "itadeliipensism  Venezuela. 

Historical. — In  1851  Bilharz  in  Egypt  noted  that  certain  female 
worms  possessed  uteri  containing  lateral-spined  eggs,  and  later 
Sonsino  considered  that  these  worms  should  be  made  into  a  species 
separate  from  those  with  terminal-spined  eggs,  but  nothing  came 
of  it.  In  1902  Castellani  in  Uganda  noted  that  some  patients  had 
only  lateral-spined  eggs  in  the  faeces  and  no  ova  in  the  urine.     In 


588  TREMA  TOD  A 

1903  Manson  observed  the  same  fact  in  a  patient  from  the  West 
Indies.  In  1907  Sambon  created  a  new  species,  Schistosoma 
mansoni,  for  the  following  reasons : — ■ 

1.  Lateral-spin  ed  eggs  are  never  found  in  the  urine,  but  only  in 
the  faeces,  and  never  occur  in  the  bladder,  only  in  the  rectum 
and  liver. 

2.  The  egg  is  oval  in  shape,  with  a  lateral  spine,  while  that  of 
5.  hcematobium  is  oblong  and  lanceolar  in  shape,  with  a 
terminal  spine,  and  that  of  5.  japonicum  oval  or  roundish, 
with  a  lateral  very  small  spine  in  about  75  per  cent,  of  those 
examined  by  Looss. 

The  lengths  and  breadths  are  different :  S.  mansoni,  112  to  162  /j,  by 
60  to  70  {j,;  S.  hcematobium,  no  to  120  fj,  by  46  to  50  /i; 
S.  japonicum,  75  to  90  fj,  by  53  to  75  fj,. 

3.  The  males  are  apparently  similar,  but  the  females  have  a  differ- 
ence in  the  genital  tract,  which  has  been  described  by 
Fritsch,  and  when  mature  contain  lateral-spined  ova  in  the 
uterus. 

4.  The  geographical  distribution  of  5.  mansoni  and  S.  hcematobium 
is  different.  5.  hcematobium  is  alone  found  in  the  Cape; 
S.  mansoni  is  the  only  species  in  the  West  Indies  and  in  South 
America. 

Looss  in  Egypt  immediately  challenged  Sambon's  statements,  but 
the  history  of  this  polemic  will  be  found  in  the  earlier  editions  of  this 
book.  We  have  all  through  felt  that  Bilharz,  Sonsino,  Manson, 
and  Sambon,  were  right,  and  Ward  always  supported  Sambon,  and 
now  this  has  been  proved  experimentally  by  Leiper  to  be  correct. 

In  1909  Da  Silva  described  the  adult  worms  as  follows: — 

Males. — The  male  measures  12  millimetres  in  length  by  0-448  millimetre 
in  breadth  in  the  middle.  The  ventral  sucker  is  0-540  millimetre  behind 
the  oral  sucker. 

The  anterior  end  shows  six  sexual  masses  composed  of  testes  and  seminal 
vesicles.  The  posterior  end  is  tapering.  The  spinous  papilla;  are  not 
so  marked  as  in  5.  hcematobium. 

Females. — The  female  worms  measure  14-5  to  15  millimetres  in  length  by 
0-168  millimetre  in  breadth  in  the  middle.  The  distance  between  the 
two  suckers  is  0-224  to  0-252  millimetre.  It  is  thickest  in  the  middle, 
and  tapers  to  each  extremity.  The  anus  opens  0-336  millimetre  in 
front  of  the  tip  of  the  tail.  The  oviduct  is  much  shorter  than  in 
S.  hcematobium,  and  enters  the  vitelline  ducts  after  only  a  short  turn. 
The  uterus  contains  laterally  spined  eggs.  The  eggs  measure  146  /j,  by 
62  [x,  with  18  ft  as  the  length  of  the  spiculum.  The  miracidium  escapes 
by  a  transverse  rupture  of  the  shell,  and  measures  153  ft  by  72  fi. 

In  191 1  Flu,  in  studying  the  Bilharziosis  in  Surinam,  concluded  that  5. 
mansoni  is  distinct  from  S.  hcematobium  because:  (1)  5.  hcematobium  has  eggs 
differently  shaped  from  those  of  S.  mansoni;  (2)  the  anterior  border  of  the 
lateral  folds  in  the  male  S.  hcematobium  forms  almost  a  right  angle  with  the 
anterior  portion  of  the  body,  while  in  S.  mansoni  the  transition  is  more 
gradual;  (3)  the  ovaries  of  5.  mansoni  have  always  a  more  or  less  winding 
course,  a  character  not  described  for  any  other  species  of  Schistosoma  ;  (4)  the 
ootype  is  asymmetrical  in  relation  to  the  long  axis  of  the  worm;  the  oviduct 
opens  laterally  on  the  ventral  side  where  the  shell  gland  is  situate;  (5)  S. 
mansoni  lives  in  the  region  of  the  mesenteric  veins,  and  S.  hcematobium  pre- 


SCHISTOSOMUM  MANSONI 


5  So 


dominates  in  the  pelvic  veins;  (6)  S.  mansoni gives  rise  to  an  illness  likekata- 
yama  disease,  and  never  to  the  bladder  symptoms  produced  by  S.  hcematobiuiu; 
(7)  the  morbid  anatomy  of  cases  invaded  by  5.  mansoni  agrees  with  those 
invaded  by  S.  japonicum,  and  differs  considerably  from  those  caused  by  5. 
hcsmatobium  ;  (8)  the  geographical  distribution  is  in  opposition  to  Looss's 
view  that  the  lateral-spined  eggs  are  unfertilized  because  they  are  the  only 
eggs  found  in  Brazil,  the  Antilles,  and  Surinam. 

He  also  found  a  single  type  of  egg  with  lateral  spine  in  the  uterus  and 
ootype  of  sixty  females. 

In  1915  Leiper's  work  in  Egypt  proved  that  the  miracidium 
developed  in  a  special  snail,  Planorbis  boisseyi,  and  that  the 
vertebrate  could  be  infected  by  the  skin  or  oral  mucosa. 

In  1917  Chalmers  and  Pekkola 
in  the  Anglo-Egyptian  Sudan 
have  experimentally  infected  the 
same  snail  with  the  miracidia, 
and  obtained  cercariae,  and  in 
the  same  year  Lutz  carried  out 
similar  experiments  in  Brazil 
with  P.  olivaceus. 

In  1917  Iturbe,  working  in 
Caracas,  Venezuela,  found  that 
the  miracidia  could  infect  Pla- 
norbis cultratus  and  P.  guaJclu- 
pensis,  but  the  latter  was  more 
easily  infected,  and  showed 
typical  cercariae  by  the  end  of 
the  sixth  week.  He  considers  it 
to  be  the  true  carrier  of  the  in- 
fection there.  He  noted  that  it 
was  easier  to  infect  animals  per 


Fig.  230. — Outlines  of  the  Eggs 
of  (1)  5.  japonicum  (without 
spine);  (2)  5.  hesmatobiwm;  (3) 
S.  mansoni.     (After  Sambon.) 


Fig.  231. — -Schistosoma  mansoni. 

(After  Holcomb.) 

a,  Male;  b,  egg;  c,  larva. 


os  than  by  the  skin.  He  found  no  less  than  120  out  of  400 
specimens  of  P.  guadelupensis  to  be  naturally  infected  around 
Caracas.  The  '  rediac '  described  by  him  have  since  been  recognized 
as  immature  stages  of  a  new  species  of  Tetracotyle. 

Morphology. — Sufficiently  described  above. 

Life-History. — -The  adults  live  chiefly  in  the  mesenteric  veins. 
and  the  ova  pass  into  the  submucosa  of  the  large  bowel,  and  through 
this  into  the  faeces,  and  so  escape  from  the  body.  The  egg  is 
oval,  112-162  x  6070  microns,  and  possesses  a  well-defined  lateral 
spine. 


590 


TREMA  TOD  A 


The  miracidia  quickly  hatch  when  placed  in  water  in  the  tropics, 
and  swarm  around  Planorbis  boissyi,  into  which  they  disappear 
so  rapidly  that  in  twenty  minutes  none  will  be  visible  in  the  water. 


Fig.  232. — Planorbis  boissyi  Potiez  and  Michaud,   1838. 

They  pass  to  the  liver  of  the  mollusc  and  form  sporocysts,  redise. 
and  cercarise,  and  finally  end  in  cercarise,  which,  leaving  the  snail 
and  swimming  about  the  water,  enter  the  skin  or  mucosa  of  the 
mouth  or  throat  and  so  infect 
man. 

Pathogenicity. — -S.  mansoni  is 
the  cause  of  intestinal  schisto- 
somiasis (Chapter  LXX1X.). 


Fig.  233. — Sporocysts  of  Schisto- 
soma mansoni  Sambon,  1907,  still 
Partially  Embedded  in  Tissue 
from  the  Liver ofthe  Planorbis. 

(After  Lei  per,  from  '  Researches 
on  Egyptian  Bilharziosis.') 


Fig.  234. — Cercaria  of  Schistosoma 
mansoni  Sambon,  1907. 

(After  Lei  per.) 


Schistosoma  japonicum  Katsurada,  1904. 

Synonym. — Schhtosomum  cattoi  Blanchard,  1905. 

Definition. — Schistosoma  with  a  nearly  smooth  cuticle.  Male 
with  a  few  spines  or  protuberances  along  the  margins  of  the  gynae- 
cophoric  canal  in  the  fresh  condition.  Testes  six  to  eight,  irregularly 
elliptical.  Intestinal  caeca  unite  very  late  and  form  a  very  short 
intestine.  Female  with  ovary  almost  in  the  middle  of  the  body. 
Vitellaria  do  not  reach  the  posterior  extremity.  Uterus  long,  with 
many  eggs,  showing  small  lateral  spines  or  thickenings.  Develop- 
ment of  cercaricB  in  species  df  Blanfordia. 

History.-  -For  several  years  an  endemic  disease,  characterized  by 
enlargement  of  the  liver  and  spleen,  fever,  diarrhoea  with  mucus 
and  blood  in  the  motions,  associated  with  ascites  and  cachexia  and 
extreme  weakness,  had  been  observed  in  the  provinces  of  Yamanashi 


SCHISTOSOMA  JAPONICUM 


591 


and  Hiroshima  of  Central  Japan  and  Saga  of  Kinshu.  Eggs  con- 
taining a  miracidium  were  to  be  found  in  the  liver  and  other  organs. 
Katsurada  then  examined  cats  in  the  neighbourhood,  and  found 
numerous  Schistosoma  in  the  portal  veins  of  two  cats  in  the  province 
of  Yamanashi,  in  which  there  were  eggs  exactly  similar  to  those 
found  in  the  above-mentioned  disease.  Catto  a  little  later  found  the 
same  parasite  in  a  Chinaman  from  the  province  of  Fukien.  Logan 
and  others  have  found  it  in  Chinamen  in  the  province  of  Hunan, 
Nicols  in  a  case  from  the  Philippines,  and  Manson  and  Sambon  in 
cases  from  China. 


Fig.  235. — Schistosoma  japonicum  Katsurada,   1904.     Male  and 
Female.     (From  a  photograph  by  J.  J.  Bell.) 

With  regard  to  the  life-history,  in  1908  Fujinami  and  Nakamura 
immersed  cattle,  cats,  and  dogs  in  water  containing  many  miracidia 
from  S .  japonicum,  but  no  infections  followed.  They  then  immersed 
a  second  series  in  rice-fields,  ditches,  and  streams,  reputed  to  be 
sources  of  infection,  and  heavy  infections  with  5.  japonicum  resulted, 
the  young  parasites,  0-15  mm.  in  length,  being  found'in  the  portal 
system  on  the  third  day  afterjimmersion. 


Fig.  236. — -Schistosoma  japonicum  Katsurada,   1904.     Female. 
(From  a  photograph  by  J.  J.  Bell.) 

In  1911  Miyagawa  described  smaller  forms  as  seen  in  the  cutaneous 
tissues  and  peripheral  vessels  in  two  to  twenty-four  hours  after 
immersion. 

In  1913  Miyairi,  experimenting  with  local  snails,  found  a  sporo- 
cyst  in  an  unidentified  snail. 

In  1914  Miyairi  and  Sudzuki  found  a  snail  with  a  dark  shell  with 
seven  spirals  to  be  heavily  and  naturally  infected  with  cercariae, 
and,  taking  non-infected  young  samples,  were  able  to  find  that  the 
miracidia  penetrated  the  cuticle  of  the  snail,  and  found  their  way 


592 


TREMATODA 


to  the  gills  and  the  wall  of  the  alimentary  canal,  where  in  twelve 
days  the  first  rediae  appeared  and  gradually  concentrated  in  the  bile- 
ducts,  where  they  grew  and  formed  second 
redise.  Mice  were  immersed  in  the  water  in 
which  the  full-grown  snails  were  kept,  and 
after  three  weeks  many  5.  japonicum  speci- 
mens were  found  in  their  livers. 

In  1914  Leiper  confirmed  this  work  in  Japan, 
having   recognized   morphologically   the   cer- 
cariaa    originating   in   sporocysts,    mistermed 
"^t?,-      ^     rediae    by    the    Japanese    authorities.      The 

til,.      237. t.GG     OF  j  j  .  r 

Schistosoma   japoni-     mollusc  in   question   was   named   Katayama 

cum.  (After Leiper.)  nosophora.  Katayama  is  a  synonym  of 
Blanfordia. 

In  1916  Narabayashi  showed  that  man,  cattle,  horses,  goats,  pigs, 
cats,  and  dogs,  are  naturally  infected  by  5.  japonicum,  which  con- 
tains ferments  which  can  digest  albumen  in  an  alkaline  medium. 
He  also  found  that  in  dogs  and  guinea-pigs,  after  penetrating  the 
skin,  most  of  the  parasites  enter  the  venous  blood- stream,  though 
some  few  enter  arteries  or  lymphatics.  Eventually  they  all  enter 
the  right  side  of  the  heart  and  are  scattered  all  over  the  lungs,  at 
the  bases  of  which  they  collect  and  then  migrate  through  the 
mediastinum,  diaphragm,  and  liver  into  the  portal  system,  while 
a  few  re-enter  the  circulation  and  reach  the  rectum. 

Morphology. — In  general  it  resembles  5.  hcvmatobhim,  but  the 
cuticle  of  the  female  is  smooth  and  that  of  the  male  has  only  the 
few  spines  mentioned  above.     There  are  no  '  bosses.' 

Male.—  8-19  millimetres  in  length,  0-53  millimetre  in  breadth,  with 
acetabulum  larger  than  oral  sucker.  (Esophagus  with  two  bulbs. 
Junction  of  intestinal  caeca  far  back,  and  united  intestine  only  one- 
fifth  to  one-sixth  of  body  length.  The  lateral  excretory  canals  open 
into  a  dorsal  pore.  Testes  six  to  eight  in  anterior  part  of  hind  body, 
from  which  the  vasa  efferentia  unite  into  a  common  vas  deferens, 
which  opens  just  behind  the  acetabulum.     Seminal  vessels  present. 

Female.- — -8-26  millimetres  in  length  and  about  0-4  millimetre 
in  breadth.  Suckers  armed  with  fine  spines.  Body  thicker  behind 
ovary,  behind  which  gut  forks  unite.  Ovary  elliptical,  dilated 
behind,  where  the  oviduct  arises,  and  running  forwards  joins  the 
vitellarian  duct.  Vitellaria  well  developed,  lying  behind  the 
ovary,  but  not  quite  reaching  the  posterior  end  of  the  body. 
Shell  gland  at  the  junction  of  the  oviduct  with  the  vitellarian  duct. 
Canal  forms  an  ootype,  and  then  becomes  the  uterus,  which  opens 
just  behind  the  acetabulum. 

Life-History. — The  eggs  vary  from  50  to  300,  and  in  utero  are  soft, 
and  so  can  form  various  shapes.  Ex  utero  they  are  oval,  faintly 
yellow,  and  double-contoured,  83-5  x  62-5  microns,  and  have  small 
lateral  spines  or  thickenings,  and  at  the  opposite  side  cap-like 
thickenings. 

The  miracidia  hatch  out  quickly  and  develop  into  cercarise  in 


SCHISTOSOMA  JAPONICUM  593 

Blanfordia  nosophora.  The  cercaria  is  barrel-shaped,  tapering 
towards  the  anterior  end,  mouth  with  two  short  lancet-shaped 
bristles.  Small  ventral  sucker  at  posterior  one-sixth  of  body. 
Hinder  end  with  three  pairs  of  poison  glands,  from  each  of 
which  a  duct  runs  forwards  to  open  into  the  mouth.  Two  pairs 
of  laterally  placed  flame  cells  with  vessels.  In  the  middle  of 
this  body  there  is  an  oval  light  brown  body  with  a  small  anterior 
canal.  The  cercaria?  penetrate  the  skin,  pass  via  the  veins  to 
the  heart,  and  so  to  the  lungs,  from  the  bases  of  which  they 
penetrate  the  mediastinum,  diaphragm,  liver,  and  so  enter  the 
portal  vein,  from  which  the  eggs  pass  to  the  submucosa  and  mucosa 
of  the  colon  and  cause  growths.  The  adult  worms  can  live  at  least 
two  years  in  the  vertebrate. 

Pathogenicity. — -The  cercaria;,  while  entering  the  skin,  cause  the 
disease  kabure,  and  in  the  body  katayama  disease. 

Christophers  and  Stephens'  Schistosoma. 

Christophers  and  Stephens  in  1905  described  a  Schistosoma  egg  which 
differs  from  the  usual  descriptions,  and  may  belong  to  a  new  and  as  yet 
unknown  species  or  genus;  but  it  was  found  with  ordinary  5.  hesmatobium 
eggs,  and  may  therefore  be  an  abnormality.  The  egg  was  found  in 
Madras;  it  was  of  an  elongated,  spindle  shape,  with  a  long  snout-like 
process  extending  from  the  broader  end  (205-2  fi  by  53-2  //). 

New  Schistosoma. 

In  1904  Salomone  and  Belli  found  portions  of  a  worm  which  they  think  may 
be  a  new  Schistosoma  in  a  patient  suffering  from  haematuria  contracted  in 
Brazil.  It  may,  however,  have  been  a  S.  mansoni,  which  very  occasionally 
occurs  in  the  bladder  wall  and  is  a  common  infection  in  Brazil. 

REFERENCES. 

The  most  useful  textbook  is  Fantham,  Stephens,  and  Theobald  (1916),  'The 
Animal  Parasites  of  Man,'  London. 

Entozoa. 

Blanchard  (1889).     Traite  de  Zoologie  Medicale.     Paris. 

Braun  (1892).      Klassen  und  Ordnungen  des  Tierreichs,  vol.  iv.,  pp.  1  and  2. 

Braun  (1908).     Die  tierischen  Parasiten  des  Menschen.     Fourth  edition. 

Cobbold  (1864).     Entozoa.     London. 

Davaine  (1877).     Traite  des  Entozoa. 

Dujardin  (1845).     Histoire  Naturelle  des  Helminthes.     Paris. 

Kuchenmeister  (1867).     Parasitology.     London. 

Leuckart  (1879-?).     Die  Parasiten  des  Menschen.     Second  edition. 

Platyhelmia. 

Benham  (i«joi).     Treatise  on  Zoology,  Ray  Lankester,  part  iv. 

Trematoda. 

In  addition  to  the  books  already  mentioned: — 
Stiles.  Illustrated  Key  to  the  Trematode  Parasites  of  Man.  Bulletin  17, 
Hygienic  Laboratory  of  the  United  States  Public  Health  and  Marine 
Hospital  Service,  Washington. 
Ward  (1903-08).  Data  for  the  Determination  of  Human  Entozoa.  I,, 
Studies  for  th.  Zoological  Laboratory  of  the  University  of  Nebraska. 
No.  49;  II.,  ibid.,  No.  86. 

38 


594  TREMA  TO  DA 

Paramphistomoidea. 

Stiles  and  Goldberger  (1910).     Bulletin  6o,  Hygienic  Laboratory,  Public 
Health  and  Marine  Hospital  Service,  United  States.     Washington. 

Paramphistomidae. 

Fischoeder   (1903).      Zool.  Aiiz.,  xxiv.  367.     (iyoi).  Zool.   Jahrbuch  Syst. 

xvii.  485. 

Watsonius  watsoni. 
Conyngham    (1904).     British   Medical    Journal,    No.    2,281,    September    17, 

p.  663. 
Shipley  (1905).     Report  of  Thompson  Yates  and  Johnston  Laboratory,  VI., 

i.  129. 
Stiles  and  Goldberger  (1910).     hoc.  cit. 

Gastrodiseus  hominis. 

Lewis    and    McConnell    (1876).     Proceedings    of   the    Asiatic    Society    of 

Bengal,  p.  182. 

Fasciola  hepatica. 
Thomas,  P.  (1883).     The  T  ife-History  of  the  Liver-Fluke.     Quarterly  Journal 

of  the  Medical  Society,  xxiii.  99. 

Fasciola  gigantica. 

Gouvea  (1895).     La  distomatose  Pulm.  par  la  Douve  du  Foie.     These,  Paris. 
Railliet,  A.  (1895).     Comptes  Rendus  de  la  Soc.  de  Biologie,  X.,  ii.  388. 
Paris. 

Echinostoma  ilocanum. 
Garrison  (1908).     Philippine  Journal  of  Science,  B.iii.,  5,  385. 
Odhner  (1911).     Zoologischer  Anzeiger,  August. 

Agamodistomum  ophthalmobium. 

Gescheidt  and  Ammon  (1833).     Die  Entozoa  des  Auges,  Zeitsch.  f.  Ophth., 

iii.  405. 

Fasciolopsis  buski. 
Ludd,   G.   (1852).     Diseases  of  the  Liver.     Second  edition  (first  reference). 

London. 
Cobbold  (i860).     Proceedings  of  the  Linnaean  Society:  Zool.,  vol.  v.,  p.  5. 

(Original  description.) 
Cobbold  (1879).     Parasites,  p.  20.     London. 
Poirier,  P.  (1887).     Archiv.  Zool.  Exp.  et  Gen.,  V.,  ii.203. 

Fasciolopsis  fulleborni. 

Rodenwaldt  (1909).     Centralb.  f.  Bakt.,  Parasit.  u.  Infect.,  451.     Jena. 

Kwan's  Fluke. 

Heanley  (1908).     Journal  of  Tropical  Medicine,  April  15,  p.  122. 

Opistorchis  felineus. 

Looss  (1907).     Annal.  Trop.  Med.  and  Parasit.,  pp.  123-154. 
Verdum  and  Brugant  (1908).     Arch,  de  Parasitologie,  xii.  125. 

Clonorchis. 
Looss  (1907).     Annal.  Trop.  Med.  and  Parasit.,  pp.  123-154. 
Verdum  and  Brugant  (1908).     Arch,  de  Parasitologie,  xii.  99. 


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Opistorchis  noverca. 

Barker,    F.    D.    (1911).     Archives    de    Parasitologie,     xiv.     13-61.      Paris. 

(Deals  with  the  whole  genus.) 
Cobbold  (1859).     Journal  of  the  Linnsan  Society  of  London:  Zool.,  vol.  v., 

p.  8. 
Cobbold  (1862).     Transactions  of  the  Linnaean  Society  of  London,  xxiii.  349. 
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Commission  of  the  Government  of  India.     Appendix  C,  p.  168. 
MacConnell  (1876).     Lancet,  i.  343;  (1878),  i.  476. 

Paragonimus  westermani. 

Baelz  (1880).     C  f.  Med.  Wiss.,  p.  721.     Berlin. 
Baelz  (1883).     Klin.  Woch.,  p.  23  [. 
Kebert  (1881).     Arch.  f.  Mik.  An.,  xix.  519. 

Manson  (1882).     Medical  Times  and  Gazette  (1881),  ii.  8;  (1882),  ii.  42. 
Musgrave  (1907).     Philip.  Journal  of  Science,  Book  II.,  p.  16. 
Stiles    (1889).     Sixteenth  Ann.     Rep.    Bur.    of    Anim.    Industry,    p.    559. 
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Monostomum  lentis. 
Nordmann  (1853).     Mik.  Beitr.  z.  Naturg.  d.  Wirbellos  Thiere,  ii.  9.  Berlin. 

Heterophyes  heteropbyes. 

Blanchard,  R.  (1891).     Comptes  Rendus  de  la  Soc.  de  Biologie,  IX.,  iii.  792. 

Paris. 
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Orig.,  xxxii.  886. 
Sandwith  (1899).     Lancet,  ii.  888. 
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Dicrocoelium  lanceatum. 

Aschoff,  L.  (1892).     Archiv  f.  Path.  Anat.,  cxxx.  493. 
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Christophers  and  Stephens  (1905).     Tropical  Medicine,  p.  259. 

Leiper  (1916).     British  Medical  Journal,  vol.  i. 

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Sambon  (1908).     Journal  of  Tropical  Medicine,  p.  29;  (1909).    No.  1,  p.  1. 
Da  Silva  (1909).     Archives  de  Parasitologie,  xiii.  2,  p.  281. 

Schistosoma  japonicum. 

Catto,  J.  (1905).     British  Medical  Journal,  p.  11. 

Katsurada  (1904).     Annot.  Zool.  Japon.,  V.,  iii.  147. 

Leiper  and  Atkinson   (191 5).     British  Medical  Journal,  January. 

Looss  (1905).     Centralblatt  f.  Bakteriologie  u.  Parasit.,  Orig.,  xxxix.  280. 

Woollev  (1906).     Philippine  Journal  of  Sci.,  B.  i.  83. 


CHAPTER  XXV 
CESTOIDEA 

Cestoidea — -History — Morphology — Life-History — Habitat — Classification — 
Cestodes  in  man — References. 

CESTOIDEA  Rudolphi,  1808. 

Definition. — Platyhelmia  without  alimentary  canal  in  any  stage 
of  the  life-cycle,  with  segmented  body,  in  which  the  epidermis,  which 
has  sunk  into  the  parenchyma,  secretes  a  thick  cuticle.  Lime- 
secreting  cells  are  developed  in  greater  or  less  number,  and  form 
calcareous  concretions.  Organs  of  fixation  of  a  variable  character  are 
developed.  The  habitat  of  the  adult  worm  is  typically  the  intestine, 
and  that  of  the  larval  form  some  other  part  of  the  body,  normally 
that  of  another  host. 

History. — It  is  believed  that  cestodes  were  known  to  the  ancients, 
and  that  the  reason  wh}7  Moses,  who  figures  largely  in  the  history 
of  Tropical  Medicine,  forbade  the  Israelites  to  eat  pigs  and  such 
animals,  was  because  of  the  parasites  known  to  exist  in  their  flesh. 

Aristotle  knew  the  proglottides  of  tapeworms,  and  as  early  as 
1592  Tcenia  was  distinguished  from  Bothriocephalus.  Tyson  (1683) 
discovered  the  head  of  the  tapeworm  of  a  dog.  Redi  (1687-1.705) 
came  to  the  conclusion  that  Cysticerci  were  animals,  and  Zeder 
(1800)  formed  them  into  a  separate  group,  Cystici  ;  but  Kuchen- 
meistcr  in  1851  proved  by  feeding  experiments  that  these  were  only 
the  larvae  of  tapeworms,  and  that,  as  a  rule,  two  different  kinds  of 
animals  were  required  as  hosts  in  order  that  the  life-cycle  might 
take  place. 

Leuckart,  Braun,  Fuhrmann,  Looss,  Sonsino,  Grassi.  Blanchard, 
von  Linstow,  Lithe,  Stiles,  Leiper,  and  Sambon  may  be  mentioned 
as  investigators  who  have  greatly  improved  our  knowledge  of  these 
parasites. 

Morphology. — There  are  two  groups  of  cestodes,  one  called  the  Cestodaria 
containing  genera  with  only  a  single  segment,  and  another  Cestoda,  in  the 
restricted  sense  of  the  word,  which  includes  all  forms  possessing  a  scolex  and 
segments.     It  is  with  this  latter  group  that  we  are  now  concerned. 

The  true  cestodes  are  easily  recognized  by  their  band-like  segmented  body, 
which  is  usually  of  a  white  colour.  They'  are  broad  and  large  posteriorly, 
becoming  narrower  and  narrower  till  the  place  is  reached  where  they  are 
attached  to  the  intestinal  wall.  This  anterior  end  is  called  the  '  scolex,'  while 
the  segments  are  called  '  proglottides.'  The  scolex  is  divisible  into  a  broader 
anterior  portion  called  the  head,  and  a  narrower  posterior  portion,  the  neck. 

596 


CESTOIDEA 


597 


The  head  is  provided  with  muscular  suckers,  which  keep  it  attached  to  the 
mucous  membrane  of  the  bowel.  Often  there  are  also  hooks  present  on  some 
part  of  the  head,  not  infrequently  on  an  anterior  pro- 
jection called  the  rostrum.  The  neck  is  constricted, 
and  shows  posteriorly  faint  rings  indicating  the  com- 
mencement of  new  segments,  which  are  always  formed 
from  the  neck. 

Behind  the  head  come  the  proglottides,  the  youngest 
being  those  situated  anteriorly,  and  the  most  fully 
developed  posteriorly.  Their  number  is  very  variable, 
and  their  size  increases  from  before  backwards.  They 
tain  the  male  and  female  sexual  organs. 

The  whole  surface  of  the  worm  is  covered  by  a  thick, 
non-chitinous  cuticle.said  to  contain  a  quantity  of  lime 
salts,  under  which  lies  a  basal  membrane;  beneath  this 
come  the  cuticular  muscles,  and  then  the  cortical 
parenchyma,  in  which  lie  the  sunken  epithelial  cells, 
nerve  cells,  sense  organs,  excretory  cells,  etc.  Among 
these  cells  are  peculiar  calcareous  corpuscles,  varying 
from  3  to  30  /t  in  diameter,  and  having  essentially  the 
structure  of  a  fat  cell — -that  is  to  say,  they  are  composed 

of  concentrically  deposited  calcareous  material  enclosed  in  a  cell  with  a  nucleus 
at  one  side.  These  corpuscles  are  highly  characteristic  of  a  Cestode.  The 
calcareous  matter  is  composed  of  79  per  cent,  organic  matter  and  21  per  cent. 
of  lime  salts,  in  the  form  principally  of  the  carbonate,  but  also  of  an  albuminate 
and  a  urate.  Their  function  is  not  understood;  perhaps  it  is  skeletal,  perhaps 
protective. 


Fig.  2  }8.— 1  Ikad  of 

Tesnia  solium. 

(After  Leuckart.) 


Fig.  239. — Mature  Segment  of  Tcenia  saginata  Goeze,   1782. 
(After  Leuckart.) 

In  the  cortex  come  the  longitudinal  muscles,  beneath  which  are  the  trans- 
verse muscles,  which  enclose  a  central  area  of  the  parenchyma  called  the 
medullary  layer,  and  therefore  separate  cortical  from  medullary  layers. 

There  is  no  alimentary  canal,  and  the  excretory  system  with  its  flame  cell 
terminations  consists  of  anastomosing  capillaries  emptying  into  a  dorsal  and 
ventral  collecting  tube  on  each  side  of  the  body,  winch  run  from  the  scolex  to 


598 


CESTOIDEA 


the  last  proglottis,  where  they  open  to  the  exterior.  In  the  originally  pos- 
terior proglottis  there  is  a  pear-shaped  excretory  vesicle  in  the  middle  of  the 
posterior  edge,  but  this  arrangement  is  lost  when  this  proglottis  drops  off,  and 
then  the  tubes  open  as  a  rule  separately  on  the  last  proglottis.  The  nervous 
system  consists  of  one  ganglion  in  the  scolex  and  two  nerve  cords.  The 
generative  organs  gradually  develop  in  the  proglottides  as  they  grow  older, 
the  youngest  having  no  trace  of  them.  With  the  exception  of  the  end  por- 
tions, these  organs  lie  in  the  medullary  layer  of  the  body. 

The  male  organs,  which  are  the  first  to  reach  maturity,  usually  consist  of 
numerous  follicular  testes  scattered  over  the  dorsal  portion  of  the  medullary 
layer,  but  may  be  consolidated  into  one  to  three  glands.  The  efferent  ducts 
from  these  unite  about  the  middle  of  the  proglottis  into  a  vas  deferens,  which, 
after  a  wavy  convoluted  course,  enters  a  cirrus  pouch  and  terminates  in  the 
genital  atrium  near  the  vaginal  orifice. 

The  female  reproductive  organs  consist  usually  of  two  ovaries,  which  lie 
near  the  ventral  surface  of  the  medullary  layer,  from  which  a  common  oviduct 
runs  to  join  with  the  spermatic  duct,  which,  after  travelling  a  certain  distance, 
is  dilated  to  form  a  eceptaculum  seminis,  and  continued  as  the  vagina  to  the 
female  opening  in  the  genital  atrium.  After  the  junction  with  the  spermatic 
duct,  the  oviduct  is  joined  by  the  common  duct  of  the  yolk  or  vitellogene 
gland  or  glands,  and  then,  forming  the  ootype,  receives  the  ducts  of  the  shell 
gland,  and  passes  on  to  enter  the  uterus.  This  is  usually  a  blind  tube,  but 
may  open  by  a  special  aperture  on  the  same  or  the  opposite  surface  to  that  on 
which  the  genital  atrium  is  found. 

When  the  uterus  becomes  laden  with  eggs,  it  is  apt  to  alter  its  appearance 
and  become  branched,  and  grows,  filling  up  the  proglottis,  while  the  male 
generative  organs  atrophy  and  disappear  (vide  Fig.  253,  p.  614). 

Life-History. — -The  proglottis  can  fertilize  itself  with  or  without 
the  use  of  the  cirrus,  or  different  proglottides  may  fertilize  one 
another.  In  any  case,  the  receptaculum  seminis  receives  the  sper- 
matozoa, which  travel  down  the  spermatic  duct,  and,  meeting  the 


Fig.  240. — Uterine  Egg  of  Tcenia 
saginata.    (X375-) 
(After  Leuckart.) 


Fig.  241. — Ovum 
of  Dibothrio- 
cephalus  latus. 

(After  Leuckart.) 


Fig.  242. — 

F/Ecal  Egg  of 

Tcenia  solium. 

(X3°°)- 
(After  Leuc- 
kart.) 


ovum,  fertilize  it.  The  fertilized  ovum  now  obtains  its  yolk 
(vitellus)  and  its  shell,  and  then  passes  into  the  uterus,  from  which 
it  may  escape  by  the  uterine  [orifice  when  there  is  one,  or  not  until 
the  proglottis  is  destroyed. 

Development  usually  begins  in  the  uterus.  An  egg  is  as  a  rule 
oval  in  form,  enclosed  in  a  brown  or  yellow  shell  with  or  without 
an  operculum.  This  shell  contains  food  yolk  and  the  developing 
embryo,  whose  cells  form  two  membranes — an  outer  in  contact  with 
the  shell,  and  an  inner  in  contact  with  the  embryo. 


CESTQIDEA 


599 


The  outer  envelope  and  the  shell  are  soon  lost,  and  when  the 
embryo  appears  in  the  faeces  it  is  surrounded  by  its  inner  envelope, 
the  embryophore,  and  has  developed  six  hooks.  In  this  stage  of 
development  it  is  called  an  onchosphere. 

It  will  therefore  be  evident  that  the  so-called  egg  as  seen  in  the 
faeces  is  not  an  egg  at  all,  but  the  onchosphere  with|its  embryonic 
envelope,  which  in  certain  species  may  be  ciliated. 

When  the  onchosphere  enters 
the  alimentary  canal  of  a  new 
host,  generally  of  a  different 
class  from  the  original  host  it 


0 


Fig.  243.— Free  Ciliated  Embryo 
of  Dibothriocephalus  laius. 

(After  Leuckart.) 


Fig.  244.- — Cysticercus  of  T&nia 
saginata  Goeze,  1782. 

(After  Leuckart.) 


throws  off  its  envelope,  and  works  its  way  into  the  tissues  by  its 
hooks  until  it  arrives  in  some  suitable  organ,  when  it  throws  off  its 
hooks,  encysts,  and  forms  either  a  little  bladder-like  cyst,  from 
the  wall  of  which  the  scolex  develops  (the  whole  being  called  a 
'  Cysticercus  ';  if  the  cyst  is  small,  it  is  called  a  '  cysticercoid  ' ;  and 
if  in  addition  it  has  a  caudal  appendix,  a  '  cercocystis  '),  or  it 
develops  directly  into  the  scolex  without  the  intervention  of  a 
cyst,  forming  a  plerocercoid  (-Xijpip,  full;  Kep/<os,  a  tail).  These 
wanderings  of  the  onchosphere  in  search  of  a  suitable  resting-place 


Fig.   245. — Plerocercoid  of  Dibothriocephalus  latus. 
(After  Leuckart.) 

may  produce  unpleasant  symptoms  if  there  are  a  number  of 
parasites.  The  time  occupied  in  the  transformation  of  an 
onchosphere  into  a  Cysticercus  varies,  being  from  two  to  six 
months,  or  longer. 

With  but  rare  exceptions  the    Cysticercus    does    not    develop 
further   until  it  enters  another  and  different  host,  though  some, 


600  CEST01DEA 

like  Hymenolepis  murina,  which  is  said  to  have  its  larvae  in 
the  villi  and  its  adults  in  the  intestine  of  the  rat,  infest  only 
one  host. 

Often  the  Cysticercus  is  found  in  a  herbivorous  animal,  while  the 
tapeworm  occurs  in  a  carnivorous  or  omnivorous  animal.  Infection 
is  direct  by  feeding,  for  in  the  alimentary  canal  the  cyst  dies  off,  and 
leaves  the  scolex,  which  develops  in  the  course  of  a  few  weeks  into 
an  adult  tapeworm,  whose  span  of  life  appears  to  be  about  a  year, 
but  may  be  much  more  or  much  less.  An  example  is  Cysticercus 
fasciolaris  of  the  mouse,  which  becomes  Tcenia  crassicollis  in  the  cat. 
Abnormalities  are  often  met  with  in  the  segments. 

Habitat.— As  a  rule  the  adult  lives  in  the  alimentary  canal  usually 
of  a  vertebrate,  but  they  may  be  found  in  the  liver  and  pancreas. 
They  are  capable  of  active  movements  during  life.  Food  is  obtained 
by  osmosis  from  the  contents  of  the  alimentary  canal. 

Classification. — The  classification  followed  is  that  of  Monti- 
celli, given  by  Braun  in  Bronn's  '  Klassen  und  Ordnung  des 
Thierreichs.' 

The  Cestoidea  Rudolphi,  1808,  are  divided  into  Cestoidaria  Monti- 
celli,  1892,  which  are  Cestodes  consisting  of  a  single  segment  con- 
taining a  single  set  of  reproductive  organs,  and  Cestoda  sens/7  stricto 
Monticelli,  1892,  which  are  the  typical  cestodes  with  a  scolex' and 
segments.     The  subclass  Cestoda  are  divided  into  orders  as  follows : — 

Cestoda  Sensu  Stricto  Monticelli,  1892. 

Synonyms. — Pollaplasiogonei  E.  Blanchard,  Cestodes  digeneses  van 
Beneden,  C.  polyzoa  Lang. 

Definition.— Cestodes  in  which  the  adult  worm  consists  of  a 
scolex  and  proglottides. 

Order  I.  Pseudophyllidea  Cams,  1863.— Synonyms. — Bothrio- 
cephaloidea.— Scolex  armed  or  unarmed,  with  two  usually  slightly 
developed,  groove-like  suckers,  with  three  genital  orifices.  Vitel- 
laria  situated  laterally.     Eggs  with  or  without  a  lid. 

Order  II.  Tetraphyllidea  Cams. — Scolex  armed  or  unarmed, 
with  four  very  motile  pedunculated  or  sessile  bothridia,  or  with 
four  round  suckers;  no  uterine  orifice;  cirrus  and  vagina  open  at 
the  sides.     Vitellaria  situated  laterally. 

Order  III.  Cyclophyllidea  van  Beneden. — Scolex  with  four 
suckers,  between  which  there  is  an  apical  rostellum  with  or  without 
hooks;  segmentation  distinct;  no  uterine  orifice;  vitellogene  gland 
single,  placed  behind  the  ovary.     Eggs  without  lids. 

Order  IV.  Diphyllidea  Cams. — Head  stalk  armed  with  hook- 
lets,  with  solex,  rostellum,  and  two  bothridia. 

Order  V.  Trypanorhyncea  Diesing. — Scolex  with  two  or  four 
bothridia,  and  four  retractile  armed  rostella. 

The  only  orders  which  contain  parasites  found  in  man  are  I. 
and  III. 


CESTODA 


601 


CESTODES  IN  MAN. 
The  cestodes  which  are  found  in  man  may  be  classified  as  follows  :- 


Order  and 
Family. 


Subfamily. 


id 

">» 

a, 


a, 


Dibothrio- 
cephalinae 


g    g  I  Ligulinae 


Genus  and  Subgenus. 

j   Dibothriocephalus 
Diplogonoporus 

I   Sp.irganum 

.    Braunia 
/Dipylidium 


U 


Dipylidiinae     Hymena- 
ls     lepis 

Davaineinae    Davainea 


i  Hymenolepis 
-.  Drepanido- 
[      taenia  (?) 


Taeniinae 


Taenia 


Taenia 


Taeniarhvnchus 


Echinococcus 


Species. 

(    i.  D.  latus. 
-     2.  D.  cordatus. 
I    3.D.  parvus. 
/   4.  D.  grandis. 
I    5.   D.  brauni. 
T  6.  S   mansoni. 
1    7-  S   prolifer. 
(    8.  S.  baxteri. 

9.  B.  jassyensis. 
10.  D.  caninum. 
f  11.  H.  nana. 
V  12.   H.  diminuta. 

13.    LT.  lanceolata  (?). 
[  14.  D.  madagascarien- 

sis. 
{  15.  D.  asiatica. 

16.  T.  solium. 
r  17.  T.  saginata. 

18.  T.  africana. 

19.  T.  hominis. 

20.  T.  philippina. 

21.  T.  confusa. 

k  22.  T.  bremneri. 
f  23.  E.  granulosus. 
^  24.  E.  multilocularis. 


Two  tapeworms  are  not  included  in  this  list — -Tcsnia  (Tcsnia)  tenieeformis 
Bloch,  1750,  a  tapeworm  found  in  cats,  and  T.  (TcBnia)  pisiformis  Bloch,  1780, 
a  tapeworm  found  in  rabbits — -because  no  definite  evidence  exists  that  man 
has  ever  been  infected  by  them. 

At  the  time  of  writing,  man  alone  is  known  to  be  the  host  of  the 
adults  of  the  following  worms: — -Tcenia  solium,  T.  saginata  (there  is 
probably  no  doubt  about  this),  T.  africana,  T.  hominis,  T.  philippina, 
T.  confusa,  T.  bremneri,  Dibothriocephalus  parvus,  Hymenolepis 
nana  (?),  Davainea  madagascariensis,  D.  asiatica.  Other  hosts  may 
yet  be  found. 

The  following  are  only  occasional  parasites  in  man:— Dibothrio- 
cephalus latus  (true  host  may  perhaps  be  the  dog  ?),  D.  cordatus 
(true  host,  the  seal  and  walrus),  Hymenolepis  diminuta  (true  host, 
the  rat  and  mouse),  Drepanidotcenia  lanceolata  (true  host,  ducks  and 
geese). 

Therefore  in  man  there  is  the  question  of  intestinal  taeniiases  to 
be  considered.  But  cysts  may  also  develop  in  man  from  T.  solium 
and  Echinococcus  granulosus  and  multilocularis.  From  the  species 
of  Sparganum  larval  forms  give  rise  to  somatic  taeniiases.  These 
affections,  with  their  treatment,  will  be  considered  later,  as  will  the 
treatment. 

It  must  be  noted  that  the  cysticercus  of  T.  saginata  is  not  included, 
as  it  is  very  doubtful  whether  it  has  ever  been  found  in  man. 

Cysticercus  acanthotrias  Weinland,  1858,  is  the  same  as  C.  ^lluloscz 
— i.e.,  the  larva  of  T.  solium. 


602  CESTOIDEA 

The  following  tables,  modified  from  Stiles,  may  be  of  help,  as 
they  give  the  names  of  recognition  of  the  genera,  and  the  species  of 
Tarda,  as  determined  by  the  head  or  the  segment,  and  also  a  scheme 
for  recognizing  the  eggs. 

Table  of  Genera. 

A.  Head  with  two  elongated  or  slit-like  suckers;  uterus  forms  a  rosette; 

genital  pores  ventral- — Dibothrioccphalidcs. 

I.   Tapeworms.— Single  set  of  genital  and  uterine  pores  present  in 
medium  ventral  line — Dibothrioce pluilus. 

Double  set  of  uterine  and  genital  pores  present  in  ventro- 
submedium  lines — Diplogonoporus. 

II.  Plerocercoids  (Sparganum). — Probably  larval  forms  of  this  group. 

B.  Head  with  four  cup-shaped  suckers;  uterus  does  not  form  a  rosette; 

genital  pores  lateral — Tceniida. 

I.  Large  forms,   ripe  segments  9  to   35   millimetres  long.     Uterus 
median,  with  lateral  branches — Teenia. 

II.  Smaller  forms,  ripe  segments  up  to  7  millimetres  long. 

(a)  Genital  pores  single,  rostellum  with  no  more  than  two  hooks. 

(1)  Suckers  not  armed.     Three  testes  in  each  segment — 

Hymenolepis. 

(2)  Suckers   armed  with  hooks,    15  to   50  testes  in  each 

segment — Davainea. 

(b)  Genital  pores  double,  rostellum  with  several  rows  of  hooks — 

Dipylidium. 

Table  of  the  Species  of  Taenia  found  in  Man. 

A.  Specimen  is  a  Tapeworm. 

Head  Characters. 

I.  Head  armed  with  hooks.     Subgenus:  Teenia.     Species:  T.  solium. 
II.   Head  unarmed.     Subgenus:  Taniarhynchus. 

(1)  Circular  ring  around  head  behind  the  suckers,   which  are 

directed  posterio-anteriorly — T.  hominis. 

(2)  Without  circular  ring. 

(a)  Head  cuboid,  1*5  to  2  millimetres  in  diameter;  suckers 

o«7   to    o-8    millimetre     in    transverse    diameter — 
T.  saginata. 

(b)  Head  small,    1-38  millimetres   broad,    1*03   millimetres 

thick,  0'47  millimetre  long;  suckers  0-63  millimetre 
in  transverse  diameter — T.  africana. 
(c)  Head  small  cuboid,  1  to  1-5  millimetres  in  diameter, 
0-75  millimetre  thick,  and  1  millimetre  long;  suckers 
0-34  to  0*37  millimetre  in  transverse  diameter — 
T.  philippina. 

III.  Head  not  known — T.  confusa,  T.  bremneri. 

Segment  Characters. 

I.   Segment  Longer  than  Broad. 

(a)  Only  in  the  last  100  segments— 1\  saginata. 

(b)  In  the  last  half  of  the  worm — T.  solium. 

(c)  In  nearly  the  entiiv  worm—  T.  confusa. 

(d)  In  the  entire  worm-    T.  africana. 

(e)  Known  segments  very  large,  28-6  by  8-5  millimetres  on  an  average — 

T.  bremneri. 
(/)  Unknown.- — T.  hominis. 


TABLE  OF  GENERA 


603 


II.  Segment  Broader  than  Long. 

Except  in  the  terminal  segments,  which  are  equilateral  or  slightly  longer 
than  broad — T.  philippina. 

B.  Specimen  is  a  Cysticercus. 

I.  Small  bladder-worm  with  one  scolex — Tcsnia. 

(a)  Head  armed — T.  solium. 

(b)  Head  unarmed  (very  rare,  if  ever  present)- — T.  saginata. 

II.  Large  bladder-worm  with  brood  capsules,  inside  which  are  the 
si  1  dices — Echinococcus. 

C.  Specimen  is  an  Egg. 

I.   With  an  operculum — Dibothriocephalidce. 
68  to  71  fi  X  45  to  50  fi — D.  latits. 
75  to  So  /x  X  50  ft — D.  cord  a  tits. 
63    <  48  ft  to  50  jjl,  brownish — D.  grandis. 


Fig. 


247. —  Tcenia 
solium. 


Fi£ 


248. — Dipylidium 
caninum. 


Fig.  246.  —  Dibothrio- 
cephalus  latus. 

Figs.  246-248. — Eggs  ofCestode  Worms  from  Human  Faeces 
(From  photographs  by  J.  J.  Bell.) 


II.  Without  an  operculum  and  with  a  six-hooked  embryo — Tceniida. 

(a)  Egg  with  a  thick,   radially-striated,  inner  shell  or  embryo- 

phore — Teeniinte. 

(a)  Embryophore    round    or    oval,    39X33    ix.      Africa — 

T.  africana. 

(b)  Embryophore    oval,    whitish    to    yellow,    39  X  30    //. 

America — T.  confusa. 

(c)  Embryophore,  38  X  30*4  fi.     Africa — T.  bremneri. 

(d)  Embryophore  oval,  55  to  41,  [X  X  26  to  35  /n.     Philip- 

pines— T.  philippina. 

(e)  Embryophore,  ovoid,  rusty  brown,  35  to  40  fi  X  20  to 

30  fi,.     Cosmopolitan  and  common — T.  saginata. 

(f)  Embryophore  almost  round;  brown;  31  to  36  fi.     Not 

uncommon  in  the  tropics — T.  solium. 

(g)  Egg    and    embryophore  unknown.       Asiatic    Russia — 

T.  hominis. 

(b)  Egg  with  a  thin,  membranous  inner  shell. 

(1)   Xot  in  Capsules — Hymenolepis. 

(a)  Egg  oval  or  globular,  with  two  distinct  membranes — 
outer  30  to  60  fi.  inner,  16  to  34  fx — mammillate 
projection  at  each  pole—//,  nana. 


6o4  CESTOIDEA 

(b)  Egg  round  or  oval;  outer  membrane,  54  to  86  li; 
yellowish;  may  be  radially  striated;  inner 
membrane,  24  to  40  li  X  20  to  35  fx,  with  not 
very  evident  mammillate  projection  at  each 
pole — H.  diminuta. 
(c)  Egg  oval  or  spherical;  outer  membrane,  50  to 
100  fju  X  35  to  100  ft;  inner  membrane,  30  to  40  li 
X  25  li;  occasionally  polar  papillae;  very  rare 
in  man — H.  lanceolata. 

(2)   Egg  in  Capsules. 

(a)  Eight  to  twenty  eggs  in  a  capsule;  egg  spherical,  43 

to  50  [x — Dipylidium  caninum. 

(b)  One  to  three  eggs  in  a  capsule,   with  calcareous 

corpuscles.  Eggs  with  two  shells  and  two 
mammillate  projections;  onchosphere,  8  /n — 
Davaiuea  madagascariensis. 

(c)  Egg  capsules  without  calcareous  corpuscles ;  mature 

eggs  not  observed — D.  asiatica. 

ORDER  I.  PSEUDOPHYLLIDEA  Cams 

This  order  has  three  families:  (1)  Dibothriocephalidae ;  (2)  Ptychobothriidae; 
(3)  Amphitretidae.     The  first  only  contains  human  parasites. 

Family  Dibothriocephalidje. — Pseudophyllidae,  with  variously  developed 
suckers,  and  a  uterus  which  forms  a  rosette.  Eggs  with  opercula.  There 
are  two  subfamilies  with  species  found  in  man:  (1)  Dibothriocephalinae ; 
(2)  Ligulinae. 

Subfamily  i.  Dibothriocephalinae. — The  suckers  or  bothria  are  more  or 
less  definite  slit-like  furrows.  Proglottides  distinct,  and  drop  off  in  groups. 
Genus  1.  Dibothriocephalus  ;  Genus  2.  Diplogonoporus  ;  Genus  3.  Sparganum. 

Dibothriocephalus  Liihe,  1S99. 

Synonyms.- — Diphyllobothrium  Cobbold,  1858  (considered  to  be  correct  name 
by  some  authors);  Bothriocephahts  pro  parte  Rudolphi,  1819;  Dibothrius  pro 
parte  Rudolphi,  1819;  Dibothrium  pro  parte  Diesing,  1850. 

Dibothriocephalina?,  with  a  more  or  less  elongated,  unarmed  scolex  with 
flat  suckers  cutting  deeply  into  the  head.  Single  genitalia  in  each  proglottis. 
(1)  Dibothriocephalus  latus  ;  (2)  D.  cordatus  ;  (3)  D.  cristatus  ;  (4)  D.  parvus. 

Dibothriocephalus  latus  Linnaeus,  1748. 

Synonyms. — TamalataL..,  1748;  T. vulgaris L.,  1748;  T '. membraneacea ~P&\\a.s, 
1 781;  T.  tenella  Pallas,  1781;  T.  dentata  Batsch,  1786;  T.grisea  Pallas,  1796; 
Bothriocephahts  lalus  Bremser,  1819;  Dibothrium  latus  Diesing,  1830;  B.  balticus 
Kuchenmeister,  1855;  B.  cristatus  Davaine,  1874;  B.  latissimus  Bugn,  1886. 

History. — This  tapeworm  has  long  been  known  in  Europe,  especially  in 
French  Switzerland  and  the  Baltic  provinces,  Germany,  and  in  many  other 
parts.  It  is,  however,  well  known  in  Asia,  Turkestan,  and  Japan;  in  Africa 
about  the  Lake  N'gami,  in  Madagascar,  and  in  North  America. 

It  occurs  in  man,  and  dogs  and  cats. 

Morphology.— It  is  about  9  metres  in  length,  with  some  3,000  to  4,200  seg- 
ments; colour  yellowish-grey.  Scolex  elongated,  almond-shaped;  2-5  milli- 
metres in  length,  with  two  deep  laterally  place  suckers.  Neck  very  narrow, 
and  of  variable  length. 

Proglottides  very  broad  (10  to  20  millimetres),  breadth  being  greater  than 
the  length;  postero-lateral  angles  project.  Testes  situated  dorsally;  vas 
deferens  has  a  vesicula  seminalis  and  a  cirrus  sac  which  opens  dorsally. 
Vaginal  opening  directly  behind  this,  leading  into  a  receptaculum  seminis. 
Yolk  glands  in  pairs,  shell  gland  behind,  ovaries  on  each  side  of  the  median 
line  behind.     Uterus  is  arranged  in  a  rosette,  with  four  to  six  convolutions, 


PSEUDOPHYLLIDEA   CARUS  605 

and  possesses  its  own  separate  opening.  The  genital  orifices  are  two  in 
number:  a  transverse  slit  for  the  cirrus  pouch  and  the  vagina,  and  a  posterior 
roundish  opening  for  the  uterus.  Calcareous  bodies  present.  The  brown  eggs 
are  oval,  68  to  71  [x  in  length,  and  45  /n  in  breadth,  with  an  operculum. 

Life-History. — The  egg  remains  undeveloped  for  a  longer  or  shorter  time, 
and  eventually  a  six-hooked  onchosphere,  enclosed  in  a  ciliated  embryophore, 
escapes  through  the  lid  opening,  after  undergoing  a  preliminary  development 
in  a  species  <>i  Cyclops;  then  gets  into  certain  fish,  particularly  Esox  lucius 
(pike),  Lola  vulgaris  (Miller's  thumb),  Perca  fluvialilis,  Salmo  umbla,  Trutta 
vulgaris,  T.  lacustris,  Thymalis  vulgaris,  Corcgonus  lavaretus,  C.  albula,  and 
Onchorhynchus  perryi,  in  the  muscles  of  which  it  becomes  a  plerocercoid. 

When  these  fish  are  eaten,  the  plerocercoids  quicldy  develop  into  the  tape- 
worm, eggs  appearing  in  the  fasces  in  some  twenty-one  to  twenty-four  days. 

Habitat. — Man,  dog,  cat,  and  fox. 

Pathogenicity. — It  produces  a  severe  forrn  of  anaemia,  together  with  fever 
(990  to  1040  F.)  in  some  cases,  and  a  quick  pulse,  which  is  supposed  to  be  due 
to  the  action  of  a  toxin. 

Dibothriocephalus  cordatus  R.  Leuckart,  1863. 

Synonym.- — Bothriocephalus  cordatus  R.  Leuckart,  1863. 

The  parasite  is  commonly  found  in  the  seal,  the  walrus,  and  the  dog  in 
Greenland  and  Iceland.     It  may  infect  man. 

Morphology. — The  principal  features  are  the  short,  broad,  heart-shaped 
head  with  the  grooves  on  the  flat  surface,  the  absence  of  the  neck,  and  the 
length  only  1  to  i\  metres.  Uterine  rosette,  with  six  to  eight  loops.  Eggs 
with  lids  75  /li  in  length  by  50  /j,  in  breadth. 

Dibothriocephalus  parvus  Stephens,  1907. 

This  parasite  was  found  by  Elkington  in  Tasmania  in  1906  in  a  Syrian,  aged 
thirty-seven,  who  had  not  long  arrived  from  his  native  country. 

Morphology. — Scolex  not  known.  Proglottides  with  clearly-defined,  central, 
uterine  rosette,  with  four  to  five  loops  on  each  side  of  the  median  line ;  largest 
segment,  5  by  3  millimetres.  Genital  atrium  0-4  to  0*5  millimetre  behind 
the  anterior  margin;  uterine  opening  same  distance  behind  the  genital  atrium. 
Calcareous  bodies  were  not  seen.     Eggs,  59  by  40  [x. 

Diplogonoporus  Lonnberg,  1892. 

Synonym. — Krabbea  R.  Blanchard,  1894. 

Bothriocephalinas  with  short  scolex,  powerful  suckers,  no  neck,  and  two 
sets  of  genitalia  side  by  side  in  each  proglottis. 

Type  Species. — Diplogonoporus  balanoptera  Lonnberg,  1892. 

Diplogonoporus  grandis  R.  Blanchard,  1894. 

Synonym. — Krabbea  grandis  R.  Blanchard. 

So  far  this  parasite  has  only  been  observed  twice  in  Japanese — in  Hioyo, 
Japan. 

Morphology. — Scolex  unknown.  Proglottis,  1-5  millimetres  broad  in  front 
and  2-5  millimetres  broad  behind;  very  short,  only  0-45  millimetre.  Two 
ventral  grooves  on  either  side  of  tin/  median  line  with  the  genital  pores.  Uterus 
with  few  loops.  Eggs  brown;  thick  shells,  63  to  48  [i  in  length  and  50  fx  in 
breadth,  with  opercula. 

Diplogonoporus  brauni  Leon,  1907. 

Two  specimens  of  this  worm  have  been  found  in  Roumania. 

Morphology. — The  worm  presents  the  appearance  of  a  thick,  opaque, 
greyish  ribbon  12  centimetres  in  length,  marked  by  slight  transverse  rings  and 
with  a  dorsal  and  ventral  sucker,  which  mark  a  division  of  the  head  into 
two  unequal  parts.  There  is  no  neck.  The  genital  orifices  are  double,  with 
a  double  genital  apparatus  in  each  ring.  The  vitellogene  glands  are  situate 
peripherally.     No  genital  sinus,  no  calcareous  corpuscles. 


606  CESTOIDEA 

Sparganum  Diesing,  1850. 

A  collective  group  of  larval  stages  of  Dibothriocephalidse  which 
have  not  reached  a  stage  in  their  development  at  which  they 
can  be  determined  generically:  Sparganum  mansoni,  S.  prolifer, 
S.  baxteri. 

Sparganum  mansoni  Cobbold,  1883. 

Synonyms. — Ligula  mansoni  Cobbold,  1883;  Bothriocephalus  ligu- 
loides  R.  Leuckart,  1886;  Dibothrium  mansoni  Ariola,  1900. 

This  larva  was  found  by  Manson  while  making  a  post-mortem  on 
a  Chinaman  in  Amoy,  lying  under  the  peritoneum  near  the  kidneys 
and  over  the  iliac  fossae;  he  also  found  one  free  in  the  pleural 
cavity.  Scheube  discovered  another  specimen  in  the  urethra  of  a 
Japanese,  and  Sonsino  a  third  in  an  Egyptian  jackal. 

Morphology.— Long,  white,  ribbon-shaped  parasites,  with  feeble 
movements.  No  head  or  definite  structure  visible.  Length,  30  to 
35  centimetres;  breadth,  3  to  12  millimetres.  At  the  broader  end 
there  is  a  sort  of  papilla.     There  is  no  reproduction  by  fission. 

Sparganum  prolifer  Ijima,  1905. 

Synonym. — Plerocercus  prolifer  Ijima,  1905. 

In  1905  Ijima  found  this  worm  in  a  woman  living  near  Tokio, 
and  in  1907  Gates  found  the  same  or  a  similar  worm  in  a  man  in 
Manatee,  U.S.A. 

Morphology. — -The  larva,  which  lies  enclosed  in  a  cyst,  may  attain 
1  to  12  millimetres  in  length  by  2-5  millimetres  in  breadth.  The 
head  at  the  narrow  end  is  motile,  and  capable  of  evagination  and 
invagination.  It  shows  an  apical  depression,  which  perhaps  serves 
as  a  sucker,  but  there  are  no  true  suckers 
or  other  organs  of  attachment . 

Calcareous   spherical   corpuscles   can    be 
found  anywhere,  except  in  the  head.     No 
genitalia  are  to  be  seen,  but  there  is  a  good 
muscular  and  excretory  system  and  food- 
reserve  bodies.     It  can  multiply  by  trans- 
Fir    2       —Sbe  verse   division,    and   supernumerary  heads 
prolifer Ijima.    (After     maY  become  independent,  and  may  assume 
Stiles.)                            bizarre  and  irregular  shapes.     The  adult  is 

unknown. 
Habitat. — -It  lives  in  the  subcutaneous  tissue  and  elsewhere  in 
man. 

Pathogenicity. — -It  produces  nodules  in  the  skin  and  fascia  be- 
tween the  inusck'S  and  in  the  abdominal  cavity.  Associated  with 
these  nodules  there  may  be  considerable  swelling  of  the  integument, 
and,  in  fact,  a  condition  not  unlike  elephantiasis  may  arise.  Also 
there  may  be  acne-like  spots  all  over  the  body  causing  itching, 
which  may  lead  to  the  escape  of  a  worm  from  the  spot.  When  a 
nodule  is  cut  open,  a  cyst  is  found  containing  one  or  two  worms, 
either  filled  with  a  watery  fluid,  or  with  a  jelly  or  slime-like  sub- 


SlJAli(rANUM 


607 


stance.  Apparently  after  weeks  or  months  the  cyst-wall  may 
become  firm  and  thick,  and  encapsulate  the  worms.  This  condi- 
tion may  last  for  years,  and  apparently  can  kill  the  victim,  who 
may  be  literally  '  eaten  up  of  worms.' 

Sparganum  baxteri  Sambon,  1907. 

This  Dibothriocephalid  larva  was  found  by  Baxter  in  an  abscess 
in  the  thigh  of  a  Masai  in  late  German  East  Africa. 


Fig.  250. — Sparganum  baxteri  Sambon. 
(After  Sambon.) 

Morphology. — -It  has  a  long  unsegmented  body,  15  centimetres  in 
length  and  I  millimetre  in  breadth,  with  numerous  irregular  trans- 
verse folds,  and  a  distinct  longitudinal  groove  on  the  ventral  sur- 
face. Anterior  extremity  is  2  millimetres  broad,  with  a  completely 
invaginated  head;  posterior  extremity,  1-2  millimetres  broad,  with 
a  shallow  medium  slit. 

Leon  has  described  a  new  tapeworm  in  man  which  is  referred  to  the  Ligulina;, 
in  which  it  requires  a  new  genus,  called  Braunia  jassyensis  Leon,  1908. 


ORDER  III.  CYCLOPHYLLIDEA  van  Beneden. 
There  is  only  one  family  with  human  parasites. 

Family  Tmuiidje  Ludwig,  1886. 

Scolex  globular  or  pyriform,  with  unarmed  suckers,  and  an  armed 
or  unarmed  rostellum.  Vagina  posterior  to  the  cirrus.  Mostly 
parasitic  in  mammals.  Larval  stage  a  cysticercus  or  cysticercoid. 
Subfamily  1.  Dipylidiinge ;  Subfamily  2.  Davaineiinae ;  Subfamily  3. 
Tieniinse. 

Subfamily  i.    Dipylidiin^e  Stiles,  1896. 

Definition. — Tseniidas,  with  armed  rostellum  and  unarmed 
suckers.     Genital    pores   marginal.     Genitalia    simple    or    double. 


6o8 


CESTOIDEA 


Uterus   becomes  divided  into  ovarium  follicles,  or  entirely   atro- 
phied, and  the  eggs  are  set  free  into  the  parenchyma.     Eggs  with 
thin  transparent  shells,  with  or  without  appendages. 
Genera. — (i)  Dipylidium  ;  (2)  Hymenolepis. 

Dipylidium  R.  Leuckart,  1863. 

Definition. —  Dipylidimae  of  medium  or  small  size,  with  retractile 
rostellum  armed  with  several  rings  of  alternating  hooks,  which 
have  a  broad  basis.  Genitalia  duplicated,  with  pores  on  each  side 
of  a  proglottis.    Eggs  with  a  double  shell. 

Dipylidium  caninum  Linnaeus,  1758. 

Synonyms. — Tcvnia  canina  Leuckart,  1758;  Aloiiilijormis  Pallas, 
1781;  T.  cucumerina  Blochmann,  1782;  T.  elliptica  Batsch,  1786; 
Dipylidium  cucumerinum  Leuckart,  1863. 

Dipylidium  is  frequently  found  in  the  dog  and  the  cat,  which  are 
its  proper  hosts;  in  man  it  is  only  an  accidental  and  rare  parasite, 
having  been  first  found  by  Dubois,  a  pupil  of  Linnaeus,  in  1751. 
Melnikow  showed  that  the  scolex  was  to  be  found  in  the  dog-louse 
(Trichodectes  canis)  and  in  that  of  the  cat  (T.  subrostratus),  as  well 
as  in  the  dog- flea  (Ctenocephalus  canis  Curtis),  the  cat-flea  (C.felinis 
Boyche),  and  in  that  of  man  (P.  irritans),  but  how  the  infection 

reaches  man  is  not  definitely 
proved.  Recently  Blanchard 
has  summarized  sixty  cases  in 
man  up  to  the  year  1907,  most 
of  which  occur  among  young 
children. 

Morphology.  —  It  measures 
*5  to  35  and  even  to  40  centi- 
metres in  length,  and  the  seg- 
ments are  from  1-5  to  3  milli- 
metres in  breadth. 

The  scolex  has  the  typical 
rostellum,  with  three  to  four 
rings  of  hooks,  diminishing  in 
size  from  the  first  circle,  where 
they  are  12  to  15  y,,  to  the  last, 
where  they  art  only  5  to  (>  fi  in  length,  and  four  suckers,  which 
are  unarmed. 

The  genitalia  are  double,  with  spores  on  each  side.  The  eggs  are 
round,  from  43  to  50  [j,  in  diameter,  with  a  thin  shell. 

Life-History.— The  ripe  proglottides  by  their  own  movement  pass 
through  the  host's  anus,  and  get  into  the  fur,  where  the  eggs  infect 
the  clog  and  cat  louse,  or  flea,  in  which  they  develop  into  cysti- 
cercoids  (Cryptocystis  trichodectis  Villot,  1882). 

The  dog  bites  the  louse  or  flea,  and  infects  itself,  and  may  pass 
on  the  cysticercoids  to  man  by  licking.  The  cat  licks  its  fur,  and 
gets  infected  in  that  manner. 


Fig.  251. — Dipylidium  caninum 

Nkst  or  Eggs.     (X  250.) 

( I  rein  u  photograph  by  J.  J.  Bell.) 


HYMENOLEPSIS  609 

Blanchard  thinks  that  the  cat  spreads  the  parasite  by  infecting 
milk  with  the  cysticercoids  when  it  steals  a  drink  from  a  bowl,  the 
contents  of  which  are  afterwards  given  to  children. 

Hymen olepis  Weinland,  1858. 

Synonym,-  -Diplacanthus  Weinland,  1858,  nee  L.  Agassiz,  1842. 

Definition.  Dipylinidiince  with  small  head,  with  armed,  well- 
developed,  or  unarmed,  rudimentary  rostellum.  Neck  long.  Pro- 
glottides serrated,  longer  than  broad.  Genital  pores  always  on  the 
left.     Three  testes.     Eggs  with  three  shells. 

Type. — H.  diminuta.  The  genus  possesses  two  subgenera, 
Hymenolepis  and  Drepanidotcenia. 

Subgenus  1.  Hymenolepis  Sensu  Stricto. 

With  the  characters  of  the  genus,  but  the  hooks  have  the  dorsal 
root  much  longer  than  the  ventral,  and  number  twenty-four  to 
thirty. 

Proglottis  narrow,  female  genitalia  ventral  to  or  between  testes. 

Hymenolepis  (Hymenolepis)  diminuta  Rudolphi,  1819. 

Synonyms. — -Tcenia  diminuta  Rudolphi,  1819;  T.  leptocephala 
(Teptlin,  1825;  T.  fiavo punctata  Weinland,  1858;  T.  varesina  Parona, 
1884;  T.  minima  Grassi,  1886, 

It  is  a  parasite  of  Epimxs  norvegicus,  E.  musculus,  and  E.  rattus 
alexandrinus,  being  not  uncommon  in  rats  in  Ceylon. 

The  first  human  specimen  was  discharged  by  a  child  aged  nineteen 
months,  and  was  presented  to  the  Boston  Medical  Improvement 
Society  by  Dr.  Ezra  Palmer  in  1842.  Since  then  a  number  of  cases 
have  been  recorded  in  Philadelphia,  Sicily,  Italy,  France,  South 
America,  and  the  West  Indies. 

Morphology. — -The  worm  measures  20  to  60  centimetres  in  length, 
and  up  to  3-5  millimetres  in  breadth.  The  head  is  very  small,  only 
o-2  to  0-5  millimetre  in  diameter,  club-shaped,  and  has  a  rudi- 
mentary, unarmed  rostellum  and  four  elliptical  suckers.  The 
segments  measure  o-66  millimetre  in  length  by  3-5  millimetres  in 
breadth.  The  anterior  proglottides  show  a  yellow  spot  (hence  the 
name  T.  flavopunctata),  caused  by  the  distended  receptaculum 
seminis.  The  posterior  proglottides  show  a  brownish-grey  colour, 
due  to  the  mature  uterus.  The  genital  pore  is  situated  laterally. 
The  eggs  are  oval,  with  a  diameter  of  about  Co  yb. 

Life-History. — It  is  a  common  parasite  in  rats  and  mice,  while  the 
cysticercus  is  said  to  live  in  the  larva  and  imago  of  the  meal-moth 
{Asopia  arinalis),  in  an  earwig  (Anisolabis  annulipes),  and  in  the 
beetles  Acts  spinosa  and  Scaurus  si  rial  its.  it  is  not  likely  that  rat 
fleas  are  important,  as  the  cysticercus  has  been  found  in  Cerato- 
phyllus  fasaatus  by  Nicoll  and  Minchin,  and  Johnston  in  Australia 
has  found  it  in  Xenopsylla  cheopis. 

The  infection  in  man  is  mostly  among  infants  and  children. 

J9 


610  CESTOIDEA 

Hymenolepis  (Hymenolepis)  nana  von  Siebold,  1852. 

Synonyms. — Tcenia  marina  Dujardin,  1845,  nee  Gmelin,  1790; 
T.  nana  von  Siebold,  1852,  nee  van  Beneden,  1867;  T.  cegyptiaca 
Bilharz,  1852 ;  Diplacanthus  nanus  Weinland,  1858. 

This  is  the  dwarf  tapeworm  of  man,  and  was  discovered  by 
Bilharz  in  the  ileum  of  a  boy  who  died  of  meningitis  in  Cairo.  It 
is  found  in  Egypt,  Europe,  North  and  South  America,  Siam,  and 
Japan,  and  is  by  no  means  a  rare  parasite  in  man.  Calandruccio 
estimates  that  10  per  cent,  of  the  children  in  Sicily  are  affected.  Stiles 
reports  4-8  per  cent,  for  125  children  in  Washington.  The  number 
found  varies  from  one  or  two  to  several  thousands  in  one  individual. 

There  is  doubt  as  to  whether  this  worm  is  or  is  not  identical  with 
Hymenolepis  nana  var .  jraterna  Stiles,  1906,  which  is  common  in  rats 
and  mice.  Probably  it  is  distinct  from  this  parasite,  because  Grassi 
and  Looss  were  unable  to  transmit  it  to  mice. 

Morphology. — It  is  the  smallest  tapeworm  in  man,  measuring 
only  10  to  15  millimetres  in  length,  and  from  0-5  to  0-7  millimetre 
in  breadth. 

The  head  is  globular,  and  provided  with  a  rostellum  with  one  ring 
of  twenty-four  to  thirty  hooks,  which  are  very  small,  14  to  18  fi  in 
length.     The  neck  is  relatively  long. 

There  are  about  150  proglottides,  0-4  to  0-9  millimetre  in  breadth 
and  0-014  to  0-030  millimetre  in  length.  The  genital  pore  is 
marginal.  The  mature  uterus  contains  about  thirty  or  more  eggs, 
which  are  oval,  and  measure  30  to  48  /j,,  and  contain  onchospheres 
measuring  16  to  19  /j,  in  diameter. 

Life-History. — It  is  believed  that  the  cysticercus  will  be  found  in 
some  insect. 

The  nearly  related  T .  nana  var.  jraterna  completes  its  development 
entirely  in  the  rat,  for  the  cysticercus  develops  in  the  villus,  while 
the  adult  lies  in  the  lumen  of  the  intestine. 

Pathogenicity. — Owing  to  its  small  size  it  is  apt  to  be  overlooked, 
but  there  is  no  doubt  that  it  spreads  in  crowded  institutions  and 
poorer  families.  Apparently,  when  the  parasite  occurs  in  small 
numbers  no  symptoms  result,  but  in  considerable  numbers  dis- 
turbance may  occur,  which  has  been  assigned  by  Mingazzini  to  the 
effects  of  toxins. 

Treatment— Male-fern  is  the  best  treatment  [vide Chapter  LXXV.). 

Prophylaxis. — While  it  is  doubtful  whether  T.  nana  and  T.  nana 
var.  jraterna  are  the  same  or  different  species,  it  will  be  necessary  to 
guard  against  the  contamination  of  food  by  rats  and  mice.  More- 
over, it  must  be  remembered  that  the  infection  spreads  in  crowded 
dwellings,  and  therefore  isolation  of  the  infected  child  should  be 
insisted  upon, 

Subgenus  2.  Drepanidotaenia  Railliet,  1892. 

With  the  characters  of  the  genus,  but  the  hooks  have  a  dorsal  root  much 
larger  than  the  ventral,  and  are  only  eight  to  twenty  in  number.  Proglottis 
broad,  testes  three,  alongside  which  lies  female  genitalia. 


DAVAINEA   MADAGASCARIENSIS  611 

Hymenolepis  i  Drepanidotaenial  lanceolata  Blochmann,  1782. 

Synonyms. — Tmnia  lanceolata  Blochmann,  1782;  T.  anserum  Frisch,  1727; 
T.  acutissima  Pallas,  1781;  T.  anseris  Blochmann,  1779;  T.  lanceola  Batsch, 
1786;  Halysis  lanceolata  Blochmann,  1803. 

It  is  common  in  ducks,  geese,  and  other  birds,  including  the  flamingo,  and 
has  been  found  in  man  in  Europe,  but  the  record  is  considered  to  be  very 
doubtful;  probably  the  worm  should  not  be  included  among  human  parasites. 

Morphology. — It  is  about  30  to  130  millimetres  in  length  and  5  to  18  milli- 
metres in  breadth,  with  a  very  small  globular  head.  Eggs,  with  three  enve- 
lopes, oval  (50  by  35  n). 

Life-History. — The  cysticercoid  lives  in  a  cyclops,  which  is  eaten  by  ducks 
and  geese. 

Subfamily  2.  DavaineiNuE  Braun,  1900. 

Definition.  -Tteniidce.  Rostellum  and  suckers  armed.  Eggs 
mostly  encapsuled. 

Genus. — Davainea  R.  Blanchard. 

Davainea  R.  Blanchard,  1891. 

Definition. — Davaineinae,  with  a  globular  head,  armed  with 
two  rings  of  hammer- like  hooks  and  four  suckers,  surrounded 
by  several  rings  of  hooks. 

Species. — D.  madagascariensis  ;  D.  asiatica. 

Davainea  madagascariensis  Davaine,  1869. 

Synonyms. — Tcenia  madagascariensis  Davaine,  1869;  T.  demara- 
riensis  Daniels,  1895. 

This  worm  was  first  discovered  by  Grenet  in  children  at  Mayotte 
(Comores).  Over  ten  infections  have  been  recorded:  by  Davaine 
from  the  Comoro  Islands,  Leuckart  from  Siam,  Daniels  from 
British  Guiana,  Blanchard  from  Nossi-Be,  four  by  Cherreau  from 
Mauritius,  and  two  by  Garrison  from  the  Philippines. 

Morphology. — The  worm  is  25  to  30  centimetres  in  length,  with 
a  maximum  breadth  of  1-4  millimetres.  The  scolex  has  four  large 
suckers  and  a  rostellum,  with  ninety  hooks  (18  (j,  long).  The  pro- 
glottides number  from  500  to  700,  being  2  millimetres  long  by 
1 -4  millimetres  broad.  Genital  pores  are  unilateral,  and  near  the 
proximal  corner.  Testes  number  about  fifty,  with  a  long  vas  deferens 
and  a  fusiform  cirrus  pouch.  The  receptaculum  seminis  is  long 
and  broad.  The  uterus  is  composed  of  a  number  of  tubes,  rolled 
up  on  each  side  into  an  almost  spherical  coil.  When  mature,  these 
windings  uncoil  and  fill  the  proglottides;  then  they  lose  their  walls, 
and  the  eggs,  lying  free  in  the  parenchyma,  become  surrounded  by 
proliferating  cells,  which  form  capsules  for  them. 

As  many  as  300  to  400  of  these  capsules  may  exist  in  one  pro- 
glottis, arranged  in  transverse  rows. 

The  egg  consists  of  the  usual  two  membranes  and  an  onchosphere, 
which  is  8  by  15  fj,. 

Life-History. — The  life-history  is  unknown,  but  it  is  suggested 


612  CESTOIDEA 

that  the  cysticercus  may  be  found  in  the  cockroach  {Peripianeta 
orientalis  or  P.  americand). 

Allied  genera  are  common  in  rats,  hares,  fowls,  pigeons,  turkeys, 
pheasants,  partridges,  grouse,  and  other  birds. 

Davainea  asiatica  von  Linstow,  1901. 

Synonym. — Tcenia  asiatica  von  Linstow,  1901 . 

This  worn  was  found  in  a  person  in  Aschabad,  near  the  northern 
frontier  of  Persia,  and  consists  of  750  proglottides  without  a  head. 
The  genital  pores  all  lie  on  the  same  lateral  border.  The  testes  are 
globular,  the  cirrus  pouch  pyriform.  The  female  organs  lie  an- 
teriorly, with  a  large  ovary  and  a  small  vitellogene  gland.  There 
is  a  large  receptaculum  seminis.  The  uterus  breaks  into  sixty  to 
seventy  large  egg  follicles.  Nothing  is  known  about  the  appearance 
of  the  mature  egg,  or  about  the  life-history. 

Subfamily  3.    T.eniin^e  Stiles,  1896. 

Definition.  —  Tceniidce,  usually  of  considerable,  length,  with 
segments  longer  than  they  are  broad.  Scolex  with  either  a 
rostellum  armed  or  unarmed,  or  an  apical  sucker.  Genital  pores 
irregularly  arranged  on  the  lateral  borders.  Genitalia  single. 
Testes  numerous,  placed  laterally.  Ovary  shell  and  vitellogene 
gland  situated  posteriorly.  Uterus,  a  single  median  trunk,  from 
which  lateral  branches  develop  later.  Eggshell  thin;  embryonic 
envelope  (embryophore)  thick,  with  radial  stripes.  Cysticercus 
generally  in  herbivora,  adults  in  carnivora. 

Taenia  Linnaeus,  1758.  / 

Definition. — Taeniinae  with  the  characters  of  the  subfamily.  The 
genus  Tcenia  is  subdivided  into  three  subgenera : 

Subgenus  1.  Tcenia  Linnaeus,  1758.     Type:  T.  {Tcenia)  solium. 

Subgenus  2.  Tceniarhynchiis  Weinland,  1858.  Type:  T.  (Tcenia- 
rhynchus)  saginata. 

Subgenus  3.  MuUiceps  Goeze,  1782.  Type:  T.  (Multiceps) 
ccenurus.     This,  however,  is  not  a  human  parasite. 

Taenia  (Taenia)  solium  Linnaeus,  1758. 

Synonyms. —  T.  cucurbitina  Pallas,  1 766 ;  T.  pellucida  Goeze,  1 782 ;  T.  vulgaris 
Werner,  1782;  T.  dentata  Batsch,  1786;  Halysis  solium  Zeder,  1803;  T.  armata 
humana  Brcra,  1808. 

The  name  '  solium  '  is  derived  from  a  Syrian  term  schuschl,  meaning  a  chain, 
which  has  arrived  at  its  present  form  by  being  first  turned  into  Arabic  and 
finally  into  Latin.     It  is  often  called  the  armed  tapeworm. 

This  worm  is  cosmopolitan  in  its  distribution,  for  it  can  be  found  wherever 
a  pig  and  a  man  can  live,  for  the  cysticercus  lives  in  the  pig,  man,  and  rarely 
in  sheep  and  dogs,  while  the  tapeworm  only  lives  in  man.  Even  monkeys 
appear  not  to  be  capable  of  infection. 

It  seems  to  be  more  widespread  in  the  tropics  than  in  the  Temperate  Zone. 
It  is  not  uncommon  in  Ceylon,  and  it  is  apparently  common  in  Panama. 


TMNIA   SOLIUM 


6i3 


Fig. 


Morphology.— Length  usually  2  to  3  metres,  but  may  reach  8  metres. 
Mature  segments  measure  5  to  6  millimetres  in  breadth.  Scolex  provided 
with  a  rostellum,  which  may  be  pigmented  and  is  armed  with  a  double  row  of 
alternately  large  and  small  hooks,  which  number  from  twenty-two  to  thirty- 
two,  and  with  four  hemispherical  suckers.  The  neck  is  long.  Proglottides 
number  from  Soo  to  900,  with  a  length  of  10  to  12  millimetres  in  mature 
segments.  Genital  pore  lateral  and  irregularly  alternate.  The  mature  uterus 
has  seven  to  ten  ramified  lateral  branches,  and  contains  three  ovaries,  the 
third  being  formed  by  subdivision  of  the  one  on  the  side  of  the  genital  pore. 
Eggs  globular,  pale  yellow  in  colour,  from  31  to  38  a  in  diameter. 

Life-History. —  The  adult 
worms  live  solely  in  the  human 
intestines,  from  which  the  oncho- 
spheres  with  their  envelopes 
escape  in  the  faeces,  and  are  apt 
to  be  eaten  by  pigs,  or  these  may 
be  infected  by  contaminated  food 
or  water.  The  cysticercus,  often 
called  Cysticercus  celluloses 
(synonym,  C.  acanthotrias),  de- 
velop in  the  flesh  of  the  pig.  If 
this  flesh  is  eaten  in  an  under- 
cooked condition,  the  cysticercus 
infects  the  human  being  and 
forms  the  tapeworm.  Occasion- 
ally man  becomes  infected  with 
Cysticercus  cellulose,  most  com- 
monly in  the  brain,  then  the  eye, 
the  muscles,  liver,  lungs,  etc., 
where  they  are  sometimes  few, 
sometimes  numerous.  This  infection  must 
or  water. 

The  tapeworm  can  live  for  years  in  the  intestine  of  man.  A  variety  called 
T.  solium,  var.  abietina  Weinland,  originally  found  in  a  Chippewa  Indian, 
belongs  probably  to  this  species. 

Pathogenicity. — The  intestinal  symptoms  are  not  severe,  but  colicky  pains 
and  diarrhoea  alternate  with  constipation.  The  patient  may  slowly  emaciate. 
The  danger  of  this  infection  is  the  entry  of  eggs  into  the  human  being  and  the 
formation  of  cysticerci  in  the  organs. 

Treatment. — Warn  the  person  affected  to  be  v-ery  careful  to  keep  his  hands 
clean,  and  to  avoid  infecting  himself  and  other  people  with  the  eggs.  Kill 
the  tapeworm  with  extract  of  male-fern  given  in  capsules  (four  to  eight  of 
10  minims  each),  or  in  emulsion  on  an  empty  stomach,  and  followed  after 
four  to  six  hours  by  a  saline  purgative. 

Prophylaxis. — Fasces  should  be  so  treated  as  not  to  infect  pigs,  and  the  flesh 
of  these  animals  should  be  carefully  cooked. 

Taenia  (Taeniarhynchus)  saginata  Goeze,  1782. 

Synonyms. — T.  solium  Linnaeus,  1767,  pro  part. ;  T.  cucurbitina  Pallas,  1781, 
pro  parte  ;  T.  mermis  Brera,  1802;  T.  dentata  Nicolai,  1830;  T.  lata  Pruncr,  1847  ; 
Bothriocephalus  tropicus  Schmidtmuller,  1847;  T.  mediocanellata  Kuchen- 
meister,  1855;  T.  zillavensis  Kuchenmcister,  1855;  T.  tropica  Moquin-Tandon, 
i860. 

This  is  the  unarmed  beef-worm  or  the  fat  tapeworm,  which  has  a  cosmo- 
politan distribution,  the  adult  being  known  only  in  man  and  the  cysticercus 
in  cattle,  though  it  can  be  produced  experimentally  in  a  number  of  animals. 
It  is  very  common  in  the  tropics,  especially  in  Africa,  and  particularly 
Abyssinia,  the  Sudan,  and  Asia. 

Morphology. — It  measures  4  to  8  to  10  metres  in  length,  and  has  been  said 
to  attain  much  greater  length.  A  mature  segment  is  4-7  millimetres  in  breadth. 
The  head  possesses  four  hemispherical,  often  pigmented,  suckers,  and  a  sucker 


252. — Proglottis  of  Tcenia  solium 
Linnaeus.     (After  Stiles.) 

be  due  to  contaminated  food 


6i4  CESTOIDEA 

in  place  of  a  rostellum.  The  neck  is  long.  The  proglottides  number  about 
1,000  segments,  with  a  length  of  about  16  to  20  millimetres  when  mature, 
The  genital  spores  are  arranged  irregularly  at  the  sides,  and  the  median  uterus 
produces  twenty  to  thirty-five  ramified  lateral  branches.  Malformations  of 
the  segments  are  not  uncommon.  Eggs  globular,  often  with  the  original  shell, 
to  which  may  be  attached  one  to  two  filaments  and  the  two  embryonic 
envelopes,  as  well  as  the  onchosphere.  The  inner  embryonic  envelope  is  oval, 
striated,  measures  30  to  40  /j,  in  length  by  20  to  30  /j,  in  breadth.  Segments 
can  escape  per  anum  by  their  own  action. 

Life-History. — The  adult  worm  lives  in  man,  the  cysticercus  requiring  some 
fifty-four  days  (Perroncito  quoted  Leuckart)  to  develop,  so  that  proglottides  are 
seen,  and  the  embryophore,  escaping  in  the  faeces,  enters  cattle  by  means  of 
contaminated  food  or  water,  and  develops  in  their  muscles  into  the  Cysticercus 


Fig.  253. — Proglottis  of  Tcenia  saginata  Goeze. 
(After  Stiles.) 

bovis,  which  is  rather  small — only  7-5  to  9  millimetres  in  length  and  5*5  milli- 
metres in  breadth.  The  tongue  and  the  muscles  of  mastication,  especialy  the 
pterygoids,  are  chiefly  affected. 

Man  becomes  infected  by  eating  under-cooked  meat.  It  can  live  in  him 
for  a  number  of  years.     The  cysticercus  very  rarely  occurs  in  man. 

Pathogenicity. — It  is  believed  to  be  more  difficult  to  kill  medicinally  than 
T.  solium,  and  to  produce  more  severe  anaemia. 

Treatment. — As  for  T.  solium. 

Prophylaxis. — Prevent  human  faeces  contaminating  the  food  of  cattle,  and 
have  the  meat,  especially  the  tongue  and  the  pterygoid  muscles,  inspected  in 
the  slaughter-house.  In  African  beef  animals  also  common  in  the  muscles  of 
the  shoulder,  foreleg,  back,  rump,  and  hindquarters.  Only  in  extensive 
infections  and  exceptionally  in  slight  invasions,  it  is  found  in  the  lymph 
glands,  lungs,  liver,  brain,  and  oesophagus  which,  therefore,  ought  also  to  be 
inspected. 

Taenia  (Taeniarhynehus)  africana  von  Linstow,  1900. 

Two  specimens  of  this  worm  were  found  in  a  negro  in  late 
German  East  Africa,  at  Langenburg,  near  Lake  Nyassa. 

Morphology. — It  is  about  1-4  metres  in  length.  The  scolex  is 
provided  with  an  apical  sucker  in  place  of  a  rostellum,  and  also  with 
four  ordinary  suckers.  The  neck  is  very  short.  The  proglottides 
vary  in  length  and  breadth,  according  to  position,  but  always 
broader  than  long,  in  the  portion  discovered.  This  species  is  as 
yet  not  clearly  denned  from  T.  saginata. 

The  ripe  segments  are  9  millimetres  broad  by  1-20  millimetres 
thick.  Their  number  is  about  600.  The  genital  pore  is  irregularly 
alternate  on  the  lateral  border.  The  testes  are  very  numerous,  and 
the  vas  deferens  much  convoluted,  with  a  thick,  pear-shaped  cirrus 
pouch.  The  cirrus  is  beset  with  bristles,  as  is  the  vagina.  The 
receptaculum  seminis  is  large.  The  ovary  is  large  and  double,  and 
the  vitellogene  gland  is  situated  at  the  posterior  border.     The 


TMNIA   PHILIPPINA  615 

mature  uterus  consists  of  a  median  portion  with  fifteen  to  twenty- 
four  non-ramified  lateral  branches. 
The  embryophore  is  thick,  with  radial  markings,  round  or  oval 

(39  by  33  A*)-  .    . 

Life-History.— The  life-history  is  not  known,  but  it  is  suggested 
that  the  cysticercus  may  live  in  Bos  indicus,  the  hump-backed 
cow,  the  flesh  of  which  the  natives  of  East  Africa  eat  raw. 

Taenia  (Taeniarhynchus)  hominis  von  Linstow,  1902. 

This  worm  was  found  by  Anger  in  a  man  in  Aschabad  in  Siberia. 

The  length  was  70  millimetres.  The  scolex  had  a  rudimentary  rostellum 
without  hooks.  There  were  four  unpigmented  suckers,  behind  which  there 
was  a  ring-shaped  swelling.     Nothing  further  is  known  about  this  parasite. 

Taenia  (Taeniarhynchus)  philippina  Garrison,  1907. 

This  specimen  was  found  by  Hare  in  a  prisoner  in  Bilibid  Prison, 
in  the  Philippine  Islands,  in  1905. 

Morphology. — The  length  is  80  to  100  centimetres;  maximum 
breadth,  1  centimetre.  Head  cuboid,  with  an  unarmed  retractile 
rostellum  and  four  suckers.  Neck  segmental.  Proglottides 
number  about  800,  being  sexually  mature  about  the  470th.  Mature 
proglottides  4  to  5  millimetres  in  width  and  o-8  to  1  millimetre  in 
length.  Surfaces  and  margins  extend  posteriorly  in  an  elongated 
cuff-like  projection  over  the  succeeding  segment.  Testes  130  to 
160  [j,  in  length,  and  from  60  to  80  /j,  in  breadth.  Vas  deferens 
without  vesicula  seminalis;  cirrus  and  pouch  present.  Genital 
pore  situated  irregularly  on  the  lateral  borders.  Ovaries,  with 
two  unequal  transversely  elongated  lobes,  close  against  the  vitello- 
gene  gland.  Vagina  without  setae  and  with  two  coils.  Uterus 
stem  with  a  V-shaped  course  posteriorly,  and  with  four  to  six 
distinct  coils  anteriorly.  Mature  uterus  very  compact,  with  a 
median  stem  and  numerous  long,  slender  dichotomous  branches. 

Embryophore  oval,  35  to  41  fi  long,  and  26  to  35  yt,  broad. 

Life-Cycle.— Life-history  not  known. 

Taenia  (?)  confusaWard,  1896. 

This  worm  has  so  far  only  been  found  in  Lincoln,  Nebraska,  U.S.A. 

Morphology. — Length  about  8£  metres,  breadth  5  millimetres,  scolex 
unknown.  Segments  much  longer  than  they  are  broad,  27  to  35  millimetres 
long  by  3-5  to  5  millimetres  broad.  Genital  pore  irregularly  placed  behind  the 
middle  of  the  lateral  border.  Testes  numerous,  vas  deferens  not  much  coiled, 
cirrus  pouch  thick-walled.  Cirrus  beset  with  little  hairs.  Receptaculum 
seminis  globular;  ovary  small  and  double,  bean-shaped.  Vitellogene  gland 
narrow  and  triangular;  shell  gland  globular.  Uterus,  when  mature,  consists 
of  a  median  trunk,  and  fourteen  to  eighteen  short  dichotomous  branches  on 
each  side.     Embryophores  are  oval,  thick,  and  striated  (39  by  30  /n). 

Life-Cycle. — Nothing  is  known. 

Taenia  (?)  bremneri  Stephens,  1907. 
This  worm  was  found  by  Dr.  Bremner  in  a  Fullani  woman  in 
Northern  Nigeria. 

Morphology. — The  head  is  not  known.     The  segments  examined 


6i6 


CESTOIDEA 


measured,  on  an  average,  28-6  by  8-5  millimetres,  but  ranged  from 
21  by  6  millimetres  to  32  by  29  millimetres  in  size.  The  central 
uterine  axis  has  twenty- two  to  twenty-four  ramified  lateral  branches, 
and  one  terminal  branch  with  four  to  five  ramifications.  The  genital 
pore  is  prominent,  and  lies  behind  the  middle  of  the  segment.  Eggs 
measure  on  an  average  38  by  30-4  fi. 

Leiper  considers  that  these  large  segments  are  relaxed  Tcenia  saginaia. 

Life-Cycle. — Nothing  is  known  at  present  about  the  life-history. 

Echinococcus  Rudolphi,  1801. 

Synonym. — Acephalocystis  Laennec,  1804. 

Species. — Echinococcus  granulosus  Batsch,   1786;  E.  muHilocularis  Huber 
1896. 

Echinococcus  granulosus  Batsch,  1786. 
Synonyms. — Tcenia  echinococcus  Zeder,   1803,  Siebold,   1853;    T.  nana  van 
Beneden,  1861,  nee  Siebold,  1853;  Echinococcifer  echinococcus  Weinland,  1861. 

Hydatid  disease  appears  to  have 


been  known  since  the  days  of  Hippo- 
crates. In  1684  Redi  suggested 
that  the  cysts  were  animal  in  origin, 
and  in  1760-67  Pallas  clearly  showed 
their  relationship  to  tapeworms 
(Tee nia  hydatigena). 

It  appears  doubtful  whether  there 
are  two  species  of  worms  associated 
with  hydatid  disease,  but  the  ap- 
pearance of  the  larvae  and  the 
geographical  distribution  tend  to 
separate  the  genus  into  two  species. 
Echinococcus  granulosus  causes 
the  cystic  form  of  hydatid  disease, 
which  is  found  most  markedly  in 
Iceland  and  Australia,  but  also 
exists  all  over  Europe,  and  is  known 
in  New  Zealand.  It  is  rare  in  India, 
and  the  only  case  we  have  seen  in 
Ceylon  came  from  South  Africa, 
where  it  occurs;  but  Begbie  has 
recently  described  another  case  in 
Ceylon.  It  is  known  in  the  Philip- 
pine Islands,  and  is  not  uncommon 
in  Egypt  and  Algeria,  and  we  have 
seen  it  in  the  Sudan.  The  mature  worm,  which  is  very  small,  lives  in  the 
small  bowel  of  the  dog,  the  jackal,  and  the  wolf  in  large  numbers,  while  the 
cysticercus  is  found  in  man,  sheep,  ox,  and  pig. 

Morphology. — It  is  very  small,  only  2-5  to  5  to  6  millimetres  in  length,  and 
is  composed  only  of  a  scolex  and  three  to  four  segments.  The  scolex  has  four 
suckers  and  a  rostellum  armed  with  a  double  row  of  twenty-eight  to  fifty  hooks, 
which  vary  in  size,  the  larger  being  40  to  45  /x  in  length,  and  the  smaller  30  to 
38  ju  in  length.     The  genital  pores  alternate. 

The  testes  are  numerous,  the  vas  deferens  spirally  coiled,  the  vitellogene 
gland  double,   the  shell  round.     The   mature  uterus  has   only  lateral  pro- 
tuberances, no  true  branches,  and  the  eggs  may  form  heaps. 
The  egg  is  globular,  30  to  36  //.  in  diameter. 

Life-Cycle. — The  dog  infects  man  with  the  onchospheres,  usually  directly 
when  being  petted.  Infection  may,  however,  be  brought  about  by  contami- 
nated food. 

On  arrival  in  the  stomach,  the  onchosphere  escapes  from  its  embryophore 


Fig.  254. — Cyst  of  Echinococcus 
granulosus  (Batsch,   1786). 

(From  a  photomicrograph  by  J.  J.  Bell.) 


ECHINOCOCCUS  GRANULOSUS  617 

and  bores  its  way  into  the  liver  or  some  other  organ.  Here  it  grows,  and 
forms  a  cyst  with  a  thick  outer  cuticle,  inside  which  is  fluid  enclosed  by  a  layer 
of  parenchyma,  the  endocyst,  composed  of  two  layers  of  cells.  The  irritation 
caused  by  the  growth  of  this  cyst  produces  a  connective-tissue  coat,  formed 
by  the  organ  in  which  the  cyst  is  growing.  The  cyst  in  this  condition  is  called 
an  acephalocyst  (Echinococcus  cysticus  sterilis),  and  is  often  found  in  cattle. 

The  next  stage  is  the  formation  of  the  brood  capsule.  The  inner  layer  of 
the  endocyst  grows  inwards,  forming  large  numbers  of  small  hollow  capsules 
(brood  capsules) ,  which  have  the  endocyst  externally  and  the  cuticle  internally. 
On  these  capsules  heads  develop.  The  cyst  now  forms  the  Echinococcus 
cysticus  fertilis,  found  in  domestic  animals. 

In  man,  however,  daughter-cysts  appear  between  the  strata  of  the  cuticle, 
into  which  cells  belonging  to  the  endocyst  have  found  their  way  and  formed 
cysts,  with  an  external  cuticular  and  an  internal  parenchymal  layer.  These 
cysts  may,  of  course,  bulge,  and  escape  externally  or  internally.  If  exter- 
nally, they  then  lie  between  the  capsule  and  the  mother-cyst  and  form  Echino- 
coccus hydatidosus  var.  exogenus,  or  if  internally,  they  fall  into  the  interior  of  the 
mother-cyst  and  form  Echinococcus  hydatidosus  var.  endogenus.  These 
daughter-cysts  may  remain  sterile  or  produce  brood  capsules  and  heads. 
Granddaughter-cysts  may  be  formed  in  the  same  way.  The  wall  of  the 
mother-cyst  may  disappear,  leaving  the  daughter-cysts  free. 

Of  all  these  varieties,  the  endogenous  cyst  is  the  most  common.  It  may 
reach  several  pounds  in  weight,  with  hundreds  of  daughter-cysts. 

In  Khartoum  cysts  fed  into  dog  developed  in  fourteen  days  into  worms, 
but  not  quite  sexually  mature. 

It  is  believed  that  the  usual  cycle  of  life-history  takes  place  in  the  dog  and 
the  sheep.  Manson  suspects  the  jackal  in  India  as  a  spreader  of  the  disease 
to  man.  Stirling  and  Verco  lay  down  the  following  factors  as  necessary  for 
the  spread  of  the  disease : — ■ 

1.  Sufficiency  of  infected  dogs. 

2.  Domestic  herbivora,  especially  sheep,  as  intermediary  hosts. 

3.  Conditions  favourable  for  the  transmission  of  the  parasite  from  the  dog 
to  man. 

4.  Facility  of  access  to  dogs  of  infected  carcasses. 

Perhaps,  however,  the  egg  gains  access  to  the  human  body  through  con- 
taminated food  and  dust. 

Pathogenicity. — The  cysts  grow  but  slowly,  consequently  organs  adapt 
themselves  to  the  pressure,  so  that  the  symptoms  may  be  wanting  and  depend 
entirely  upon  whether  the  organ  can  or  cannot  expand. 

If,  however,  fluid  escapes  from  a  cyst,  urticarial  eruptions,  or  even  rigors, 
with  local  pain  and  tenderness,  may  result. 

Prophylaxis. — Prophylaxis  must  be  on  the  lines  indicated  by  the  factors 
above  mentioned — viz.,  registration  of  dogs,  destruction  of  pariah  dogs,  non- 
feeding  of  dogs  with  raw  meat,  clean  kennels,  non-handling  of  dogs. 

Echinococcus  multilocularis  Leuckart,  1863. 

Synonym. — Echinococcus  osteoklaster  Iluber,  1896. 

This  is  the  parasite  which  causes  the  alveolar  or  multilocular  form  of 
hydatid  disease,  which  is  very  different  from  the  ordinary  form.  The  disease 
was  first  observed  by  Ruysch  in  1721,  and  was  generally  looked  upon  as  .1 
colloid  cancer,  until  Virehow  in  1856  showed  that  it  had  its  origin  in  a  worm. 
Mangold  and  Muller  consider  that  by  feeding  experiments  they  obtained  from 
it  a  Tcenia  different  from  E.  granulosus  in  the  hooks  and  the  distribution  of 
the  ova. 

Melnikow-Raswedenkow  gives  quite  a  different  life-history  for  this  parasite, 
which,  if  correct,  will  make  it  a  new  species.  Further,  there  is  the  support  of 
Stiles,  Stirling,  Verco,  and  others  for  the  differentiation  of  the  parasites  from 
one  another. 

This  form  of  hydatids  occurs  in  man,  sheep,  and  pigs,  but  principally  in 
large  cattle. 


618  CESTOIDEA 

The  geographical  distribution  is  interesting,  it  being  mostly  found  in  South 
Germany,  Switzerland,  the  Austrian  Alpine  region,  Russia,  and  East  Siberia, 
in  which  districts  it  occurs  in  large  cattle  and  man,  whereas  it  is  absent  from 
Iceland  and  Australia  and  European  districts  where  sheep  are  common  and 
where  the  other  form  is  frequently  met  with. 

Morphology. — Melnikow-Raswedenkow  says  that  the  cysts  are  composed 
of  parenchyma  internally  and  externally,  the  latter  being  in  direct  contact 
with  the  tissue  of  the  host,  and  producing,  it  is  said,  not  merely  scolices,  but 
immature  amoeboid  embryos,  which  spread  the  cyst  by  continuity,  or  may 
enter  the  blood-stream  and  form  metastases. 

An  amoeboid  embryo  develops  into  a  much-folded  chitinous  vesicle,  having 
parenchyma  both  internally  and  externally.  This  parenchyma  produces 
poisons  which  act  upon  the  host.  The  cyst  is  looked  upon  as  the  homologue 
of  a  ripe  proglottis,  because  it  can  produce  living  embryos,  for  the  parenchyma 
can  form  scolices,  immature  embryos  without  a  capsule,  and  mature  ovoid 
embryos  enclosed  in  a  chitinous  capsule. 

The  scolices,  however,  are  frequently  destroyed  by  phagocytosis,  because 
they  are  situated  in  direct  contact  with  the  host's  tissue.  Hence  the  failure 
of  feeding  experiments,  as  the  scolices  arrive  in  the  intestine  damaged. 

The  result  of  this  development  is  to  produce  a  collection  of  cysts,  measuring 
from  o-i  to  5  millimetres  in  diameter,  embedded  in  connective  tissue.  Dis- 
integration may  begin  in  the  centre  of  the  masses  of  the  cysts.  Whether  the 
Teenies  obtained  by  feeding  experiments  are  the  same  as  T.  echinococcus  or 
not  is  uncertain. 

Pathogenicity. — It  produces  a  primary  tumour  in  the  liver,  brain,  spleen, 
kidney,  or  adrenals,  with  metastases  in  different  parts  of  the  body.  The 
symptoms  produced  vary  with  the  region  affected,  but  eventually,  perhaps 
after  years,  lead  to  anaemia,  emaciation,  and  weakness,  which  cause  death. 


REFERENCES. 

The  most  useful  general  reference  is  '  Die  Susswasserfauna  Deutschlands 
eine  Exkursionsfauna,'  Heft  18.  Parasitische  Plattwiirmer.  II.  Cestodes. 
Fischer,  Jena,  1910. 

General. 

Blanchard  (1889).     Traite  de  Zoologie  Medicale.     Paris,  I. 

Braun   (1 894-1900).     Bronn's  Thierreich,  vol.  iv.,  ab  1   b.     Leipzig.     (This 

gives  a  full  literature  up  to  1895.) 
Braun  (1908).     Die  thierischen  Parasiten  des  Menschen,  4th  ed.     Wiirzburg. 
Letjckart  (1886).     Parasites  of  Man.     English  translation.     Edinburgh. 
Looss  (1905) •     Mense's  Handbuch  d.  Tropenkrankheiten,  vol.  i. 
Stiles  (1906).     Bull.  25,  Hyg.  Lab.,  U.S.  Pub.  Health  and  Mar.  Hosp.  Serv. 

(Key  and  specific  diagnosis  of  tapeworms  of  man.) 
Ward   (1903).      Studies  for  the   Zoological  Laboratory  University,   lv.  49. 

Nebraska,  also  No.  54  of  1902. 

Dibothriocephalus  latus. 
Stiles  (1906).     Loc.  cit. 
Ward  (1901).     Circulars  on  Tropical  Diseases,  i.  22. 

Dibothriocephalus  cordatus. 
Leuckart  (1886).     Loc.  cit. 

Diplogonoporus  grandis. 
Stiles  and  Tailor.     Bull.  29,  U.S.  Bureau  Animal  Industry. 

Diplogonoporus  brauni. 

Leon,  N.  (1907).     Zoologischer  Anzeiger,  xxxii.  376. 
Leon,  N.  (1908).     Ibid. 


REFERENCES  619 

Sparganum  mansoni. 

Cobbold  (1883).     J.  Linn.  Soc.  Lond.  (Zool.),  xvii.  78. 
Ijima  and  Murata  (1888).     J.  Coll.  Sci.  Imp.  Univ.  Jap.,  ii.  149.     Tokio. 
Sambon  (1907).     Journal  Tropical  Medicine. 

Stiles  and  Ray  (1902).     Bull.  35,  Bureau  of  Animal  Industry,  U.S.  Dept. 
Agric,  pp.  47-56.     Washington. 

Sparganum  prolifer. 

Ijima  (1905).     J.  Coll.  Sci.  Imp.  Univ.  Jap.,  xx.  7.     Tokio. 
Stilus  (1907).      Bull.  39,  Hygienic  Lab.  U.S.  Pub.  Health  and  Marine  Hosp. 
Service.     Washington. 

Sparganum  baxteri. 

Sambon  (1907).     Journal  Tropical  Medicine  and  Hygiene. 

Ligulinae. 

Lkon  (1908).      Zool.  Anzeig.,  xxxiii.  359. 

Dipylidium  caninum. 

Blanchard  (1907).     Archiv.  de  Parasit.,  xi.  439.      (Summaries  of  sixty  cases 

up  to  1907.) 
Diamare    (189s).      II   genere    Dipylidium.      Atti    Reale   Accademia    Scienze 

Fische  e  Matematiche  Napoli,  ii.,  Ser.  2,  No.  7. 
Zschokke  (1905).     Centralb.  f.  Bakt.  u.  Par. 

Hymenolepis  nana,  H.  diminuta,  Drepanidotaenia  lanceolata., 

Blanchard  (1891).     Hist.  Zool.  et  Med.  d.  T.  du  Genre  Hymenale.     Paris. 

Grassi  (1887).     Centralb.  Bakt.  u.  Par.,  i.  97;  ii.  282,  305. 

Grassi  and  Rovelli  (1892).     Atti  Ac.  Sci.  Nat.  Catania,  iv.  4. 

Linstow  (1896).     Zeits.  f.  d.  ges.  Naturw.,  p.  571. 

Ransom   (1904).     Bull.   18,   Hygienic  Lab.  Pub.   Health  and  Marine   Hosp. 

Service,  U.S.A. 
Ransom  (1888).     Lancet,  ii. 
Stiles,  Ch.,  Wardell,  and  Garrison  (1906).     Bull.    24,  Hyg.   Lab.   Pub. 

Health  and  Marine  Hosp.  Service.     Washington. 

Davainea  madagascariensis. 

Blanchard,  R.  (1891).     C.  R.  de  Soc.  Biolog.,  (9),  iii.  604.     Paris. 

Blanchard,  R.  (1899).     Archiv.  Parasit.,  ii.  200. 

Daniels,  C.  W.  (1896).     Lancet,  ii.  1455. 

Grenet  et  Davaine  (1869).     Mem.  Soc.  Biolog.,  (5),  i.  233.     Paris. 

Taenia  solium  and  saginata. 
Stiles  and  Hassall  (1898).     Bull.  19,  U.S.  Dept.  Agric.  B.  Animal  Industry. 

Taenia  afrieana. 
Von  Linstow  (1900).     Centralb.  f.  Bakt.  u.  Par.,  1.  AM.,  xxviii.  185. 

Taenia  hominis. 

Von  Linstow  (1902).     C.  f.  B.  Pu.  I.,  I.  xxxi.  770. 

Taenia  philippina. 

Garrison  (1907).     Phil.  J.  of  Sci.,  ii.  542.     Manila. 

Taenia  co  nf  us  a. 

Ward   (1895-96  and   1896-97).     Ann.   Rep.   Nebraska   Bd.    Agric,    1895-96, 
p.  257;  1896-97,  p.  178. 


620  CESTOIDEA 

Taenia  bremneri. 

Stephens  (1907).     Annals  of  Tropical  Medicine,  i.  551. 

Echinococcus. 

Begbie  (1908).     Journ.  Roy.  Army  Med.  Corps.     (Echinococcus  in  Ceylon.) 

Bremser.     Lebende  Wurmer  im  lebenden  Menschen.  Wien. 

Christopherson.     J.  Trop.  Med.  and  Hygiene. 

Coulet  (1729).     Tractatus  de  Ascaribus  et  Lumbrio  lato  Lugd.  Bat. 

Goeze  (1786).     Naturgeschichte  de  Bandwurmgaltung.     Halle. 

Neisser  (1877).     Die  Echinococcenkrankheit. 

Raswedexkow  (1901).     Studien  ii.  d.  Ech.  alveolaris. 

Rogers  and  Wilson  (1906).     British  Medical  Journal,  i.  1397. 

Seeger  (1852).     Die  Bandwiirmer.     Stuttgart. 

Stiles.     Bulletin  25,  loc.  cit. 

Stirling  and  Verco  (1907).     System  of  Medicine,  II.  ii.  976.     Allbutt  and 

Rolleston. 
Wawruch  (1841).     Praktische  Monographie  de  Bandwurmkrankheit. 
Weinland  (1858).     Essay  on  the  Tapeworms  of  man.     Cambridge,  U.S.A. 


CHAPTER  XXVI 
NEMATHELMINTHES 

Nemathelminthcs  —  Nematoda  —  Anguillulidae  ■ —  Angiostomidae  —  Gnatho- 
stomidae  —  Physalopteridae  —  Filariidae  —  Dracunculidae  — ■  Mermithidae — 
Ascaridaj  —  Oxyuridae  —  Strongylidae  —  Metastrongylidae — Trichostrongy- 
lidae  —  Ankylostomidae  —  Eustrongylidae  —  Trichinellidae — Trichurineae — 
Gordiacea — -Acanthocephala — References. 

PHYLUM  II.  NEMATHELMINTHES. 

Metazoa,  worm-like  in  form,  tubular,  or  filiform,  unsegmented,  but 
covered  with  a  cuticle  which  may  be  ringed.  Without  appendages 
or  limbs,  but  usually  with  bristles,  hooks,  papillae,  or,  rarely,  suckers. 
Usually  with  an  alimentary  canal,  but  without  any  closed  vascular 
system,  and  without  respiratory  organs.  With  a  complete  absence 
of  cilia.  Sexes  are  separate.  Usually  parasitic  through  some  part 
of  the  life-cycle,  in  which  the  larvae  develop  in  a  different  host  or 
organ  from  that  occupied  by  the  adult.  The  larva?  may  be  free 
and  the  adult  parasitic,  or  vice  versa. 

Remarks. — The  Nemathelminthes  are  extremely  important  to  the 
student  of  tropical  medicine,  for  they  include  some  of  the  most 
potent  agents  of  disease — e.g.,  An:ylostoma  duodenale  and  the 
Filayiidce.  Recent  researches  have  shown  that,  no  matter  how 
common  the  worm  may  appear  to  be,  it  is  advisable  to  carefully 
study  it,  as  it  has  been  found  that  several  species  and  genera 
have  been  included  in  an  old  species  which  was  thought  to  be 
so  well  known,  that  nothing  new  could  be  discovered  concerning 
it — e.g.,  Ascaris,  in  examining  specimens  of  which  Leiper  has 
separated  two  new  genera. 

Classification. — -The  Nemathelminthes  can  be  divided  into  two 
classes : — 

Class  I. — Anterior  end  not  provided  with  an  armed  proboscis; 
intestine  present  either  complete  or  in  part  rudimentary. 

This  class  includes  two  orders:- — 

Order  I.    Nematoda. 
Order  II.  Gordiacea. 

Class  II. — -Anterior  end  provided  with  an  armed  proboscis; 
intestine  absent. 

Order  III.  Acanthocephala. 
621 


622  NEMA  THELMINTHES 

CLASS  I. 
ORDER  I.  NEMATODA. 

Definition. — Nemathelminthes  with  white  filiform  bodies,  with 
usually  a  complete  alimentary  canal  in  the  adults,  but  sometimes 
this  may  be  represented  by  only  an  oesophagus  and  a  rudimentary 
intestine;  with  papillae  on  the  head.  The  male  with  one  testis,  a 
strongly  recurved  posterior  extremity,  and  usually  spicules.  The 
female  with  a  vulvar  opening  always  distinct  from  the  anus.  Egg 
contains  ovum  only- 
Morphology. — The  Nematoda  are  parasitic,  as  a  rule,  but 
minute  sexually  mature  forms  can  be  met  with  in  moist  soil  all  over 
the  world.  The  body  is  enclosed  in  a  thick,  transparent,  smooth, 
or  ringed  cuticle,  which  may  form  hooks,  spines,  or  lateral  fins. 

Under  the  cuticle  comes  a  syncytium  called  the  epidermis,  under 
which  is  the  peculiar  muscular  layer  cut  into  four  quadrants  by 
thickenings  of  the  epidermis,  which  project  inwards,  surrounding 
dorsally  and  ventrally  a  nerve  cord,  and  laterally  excretory  canals. 
Under  the  skin  comes  the  large  undivided  body  cavity,  which  is  not 
of  the  nature  of  a  true  ccelom,  as  it  is  not  between  the  two  layers 
of  the  mesoblast,  but  between  mesoblast  externally  and  hypoblast 
internally,  and  contains  a  fluid  which  may  represent  the  hsemolymph 
fluids  of  higher  animals. 

The  digestive  system  consists  of  a  mouth  situated  at  the  anterior 
end,  and  surrounded  by  two  to  six  lips,  which  opens  into  a  thick 
suctorial  oesophagus  lined  with  chitin. 

The  oesophagus  opens  into  the  intestine,  which  is  a  thin-walled 
tube  lined  by  a  simple  layer  of  endothelial  cells,  and  leads  to  the 
short  chitinous  rectum,  which  ends  in  the  anus. 

The  excretory  system  consists  of  two  longitudinal  tubes  lying  in 
the  lateral  line,  and  uniting  anteriorly  by  a  transverse  '  bridge  '  to 
open  in  a  pore  situated  in  the  mid-ventral  line  just  behind  the  mouth 
in  the  region  of  the  nerve  ring. 

The  nervous  system  consists  of  a  circumcesophageal  ring,  with  six 
anterior  and  six  posterior  nerve  trunks. 

The  sexes  are  separate.  The  male  reproductive  organs  consist 
of  one  tube  divisible  into  testis,  vas  deferens,  vesicula  seminalis, 
and  ductus  ejaculatorius,  which  opens  on  the  ventral  surface  of  the 
rectum  close  to  the  anus,  while  the  posterior  end  of  the  body  is 
modified  j  for  sexual  purpose  with  alae  and  papillae.  The  female 
reproductive  organs  consist  of  two  much-coiled  tubes  divisible  into 
ovary,  oviduct,  and  uterus,  which  join  together  to  form  the  simple 
vagina,  which  opens  about  the  middle  of  the  body  in  the  mid- ventral 
line;  in  some  instances  just  in  front  of  the  anus,  in  others,  as  in  the 
iilaria  worms,  quite  near  the  head. 

Biology. — They  appear  to  live  upon  the  juices  of  the  part  of  the 
body  in  which  they  are  found.  Generally  this  is  the  intestine,  the 
contents  of  which  supply  them  with  ample  food.  But  some  of  them 
are  capable  of  entering  the  villi  of  the  intestine. 


NEMA  TOD  A 


623 


Life-History. — -Sometimes  the  life-history  is  fairly  simple,  or  is 
supposed  to  be  so,  for  it  is  possible  that  we  are  not  well  acquainted 
with  details. 

Other  life-histories  are  most  complicated,  and  must  be  dealt  with 
in  detail. 

Pathogenicity. — Some  of  the  worms  are  markedly  pathogenic, 
while  others  usually  produce  but  slight  effects. 

Classification. — The  Nematoda  are  classified  into — The  Non- 
Bursata,  comprising  the  families:  (1)  Enoplidae,  (2)  Anguillulidae, 
(3)  Angiostomidae,  (4)  Gnathostomidse,  (5)  Physalopteridse,  (6)  Fila- 
riidae,  (7)  Dracunculidae,  (8)  Mermithidae,  (9)  Ascaridae,  and  (10) 
Oxyuridae;  and  the  Bursata,  which  are  subdivided  into  the  Stron- 
gyles,  comprising  the  families  (11)  Strongylidae,  (12)  Metastrongy- 
lidae,  (13)  Trichostrongylidae,  (14)  Ancylostomidae,  and  the  Pseudo- 
strongyles,  comprising  the  families  (15)  Eustrongylidae,  (16)  Trichi- 
nellidae,  and  (17)  Trichosomidae. 

The  Enoplidae  are  free-living,  and  do  not  concern  us. 

The  following  table  gives  the  parasites  known  in  man,  excluding 
a  number  of  doubtful  Filariidae: — 


Division. 


Family. 


'  AnguillulidEe 

Angiostomidae  . 
Gnathostomidae 

Physalopteridae 


Filariidae 


Dracunculidae 


Ascaridae 


Oxyuridae 
Eustrongylididae 

Trichosomidae .  . 


Filaria 


(Microfilaria) 


(Agaraofilaria) 


1  icnus. 

Anguillula 
Anguillulina 
Rhabditis 
Leptodera 
Strongyloides    .  . 
Gnathostoma    .  . 

Physaloptera     .  . 

f    9- 

10. 

I  11. 

r  12. 
1 13. 

(14- 
1  I5- 
,16. 

I  17- 
Acanthocheiloneraa  18. 
Dirofilaria 
Loa 

Hamularia 
Onchocerca 
Dracunculus 

f  Ascaris  . . 

-    Toxuscaris 
Belascaris 
\_  Lagocheil.i  51   iri! 
Oxyuris .  . 
Dioctophyni'- 
I  Trichinella 
\  Trichuris 


Species. 

i.  A.  aceti. 

2.  A.  putrefaciens. 

3.  R.  niellyi. 

4.  L.  pellio. 

5.  S.  intestinalis. 

6.  G.  spinigerum. 

7.  P.  caucasica. 

8.  P.  mordens. 
F.  bancrofti. 
F.  ozzarJi. 
(F.  inermis.) 
(M).  powelli. 
(M.)  philippinensis. 
(Agm.)  conjunctivae. 
(Agm.)  labialis. 
(Agm.)  oculi. 
(Agm.)  georgiana. 
A.  perstans. 

19.  D.  magalhaesi. 

20.  L.  loa. 

21.  H.  equi. 

22.  O.  volvulus. 

23.  D.  medinensis. 
f  24.  A.  lumbricoides. 

25.  A.  maritima. 
[  26.  (A.  texana.) 

27.  T.  cams. 

28.  B.  mystax. 

29.  L.  minor. 

30.  O.  vermicularis. 

31.  D.  renale. 

32.  T.  spiralis. 

33.  T.  trichiura. 


624 


NEMA  THELMINTHES 


Division. 

r 


Family. 


Strongylidce 


Genus. 
r  Triodontophorus 


34- 
f  35- 


'     I  CEsophagostomum     •*£' 


Metastrongylida?        Metastrongylus 
(  Nematodirus 
I  Haemonchus 

Trichostrongylidael 


Ancylostomidae        I   Ancylostoma 
1  \  Necator 


37- 
38. 
39- 


I  Trichostrongylus    -    41- 
42. 

Us. 

44- 
\  45. 


Species. 
T.  deminutus. 
CE.  brumpti. 
CE.  stephanostomum 

var.  thomasi. 
M.  apri. 
N.  gibsoni. 
H.  contortus. 
T.  colubriformis. 
T.  probolurus. 
T.  vitrinus. 
T.  orientalis. 
A.  duodenale. 
A.  ceylaiicum. 
N.  americanus. 


It  is  not  possible  at  the  present  moment  to  give  a  scientific  and 
easily  workable  classification  of  the  Nematoda,  because  the  type 
genera  require  revision.  We  group  the  various  families  under  the 
following  divisions: — 

A.  Nematoda  in  which  the  bursa  copulatrix  is  merely  a  cuti- 

cular  expansion  not  supported  by  true  fleshy  rays  in  the 
males — Non-Bur  sat  a . 

B.  Nematoda  with  true  bursa  copulatrix — i.e. ,  supported  by 

fleshy  rays  in  the  males — Bur  sat  a. 


DIVISION  NON-BURSATA. 

Leiper  gives  the  following  table  for  differentiation  of  the  non- 
bursate  families  which  are  represented  in  the  parasitic  nematodes 
of  man: — 

A.  (Esophagus  a  simple  cellular  tube—  Trichosomidce. 

B.  (Esophagus  a  simple  muscular  bulb : — 

(a)  Mouth  surrounded  by  several  protuberances.     Male 

with  one  spicule;  female  with  one  uterus — Eustror,- 
gylidida. 

(b)  Mouth  guarded  by  large  fleshy  jaws.     Male  with  two 

spicules;  female  with  two  uteri :- — 

(t)  Jaws   two    in    number:    skin    smooth—  Physalof- 

teridce. 
Jaws    two    in    number:    skin    spinous — Gnatho- 

stomidcs. 
(2)  Jaws  three  in  number:  skin  striated — Ascaridcr. 

if)    Mouth  a  simple  pore  without  buccal  capsule:- — 

(1)  Female  without  vagina:  embryos  striated.     Male 
with  two  equal  spicules — Dracuncnlidce. 


NEMATODE  EGGS 


625 


NEMATODE  EGGS. 


Fig.  255.  —  Oxyuris 
vermicularis  Egg. 
IX250.) 


Fig.   256. — Tvkhuris         Fig.    257. — T.    irichiura. 
trichiura      Egg.  Egg     with     Larva. 

(X250.)  (X250.) 


. 


gHHanHn 


Fjt».  258. — Ascaris  lum-     F'g.    259. — A.    lumbri-     Fig.     260. — A.    htmbri- 
bficoidesTlGG.  (X  250.)         coides  Egg  segment-         coides  Egg  unferti- 

ING.       (X25O.)  LIZED. 


Fig.     261.  —  Aiuylostoma        Fig.     262.  —  Ancylostoma 
dnodcnale  Egg.    (X  250.)  duodenule  Egg  segment- 

ing.    (X250.) 

Figs    255-262. — Nematode  Eggs  from  Human  Faeces. 
(From  photographs  by  J.  J.  Bell.) 


40 


626 


NBMA  THELMINTHES 


(2)  Female  with  vagina  opening  near  mouth;  uteri 

convergent:  embryos  not  striated.  Male  with 
spicules  dissimilar — -FilariiiUs. 

(3)  Female  with  vagina  in  posterior  third  of  body: 

uteri  divergent.  Parasitic  parthenogenetic 
adult  of  Slrongyloides.  [For  free-living  adults 
seeC  (1).] 

C.    (Esophagus  with  a  double  muscular  bulb:- — 

(1)   Skm  smooth ;  male  with  t  wo  spicules  and  accessory 
piece;  female  viviparous — Free-living  adults  of 
A  ngiostomidce. 
Skin    deeply    striated :    male   Math    one    spicule: 
female  oviparous— Oxyuridce. 


(<2) 


EGGS  OF  DOUBTFUL  IDENTIFICATION. 


Fig.  267. 


Fig.  264. 


Fig.  265. 


266. 

Figs.   263-266. — Eggs  of  Doubtful  Idkmification  fko.v 
Human  F^ces. 

(From   preparations  and  photographs  by   J.J.  Bell.) 

1  is.   .63   and  265.—  Abnormal  Eggs    probably  of  Ascaris  luwbricoides. 


DIVISION  NON-BURSATA  627 

NON-BURSATA. 

Family  2.    Anguillulidae. 

Very  small  Nematoda,  mostly  free-living,  rarely  parasitic,  with 
an  oral  cavity  armed  with  a  tooth  or  spine,  and  an  oesophagus  with 
a  double  dilatation.  Male  with  two  spicules,  and  sometimes  a 
bursa  copulatrix.  Female  with  a  pointed  tail,  and  a  vulva  situated 
in  the  middle  of  the  body. 

Genera. — (1)  Anguillula,  (2)  Anguillulina,  (3)  Rhabditis,  (4)  Lef- 
t  oder  a. 

Anguillula  Ehrenberg,  1826. 

Anguillulidae  with  small  mouth,  oesophagus  with  two  dilatations,  of  which 
the  posterior  has  valves.  Male  without  bursa,  spicules  with  accessory  pieces 
feather-shaped.  Female  with  the  vulva  in  the  hinder  portion  of  the  body; 
uterus  asymmetrical. 

Anguillula  aceti  Miiller,  1783. 

Anguillula  aceli  is  the  common  vinegar  eel,  which  has  several  times  been 
reported  as  occurring  in  the  human  bladder,  but  the  method  of  infection  is 
unknown. 

Morphology. — Cuticle  not  striated,  body  cylindrical,  tapering  a  little  to 
the  anterior,  but  considerably  to  the  posterior  end.  Male  1  to  2  millimetres 
long  and  24  to  40  fi  broad,  with  two  pre-anal  and  one  post-anal  papillae.  Two 
equal  spicules  38  /n  long.  Female,  2-4  millimetres  long  and  40  to  72  [x  broad. 
Vulva  near  the  equator.     Embryos  222  by  12  \x. 

Pathoge  nieity . — Nil . 

Anguillulina  Gervais  and  van  Beneden,  1859. 

Synonym. — Tyienchus  Bastian,  1864. 

Anguillulidae  possessing  a  spine  on  the  oral  cavity.  Male  bursa  without 
papilla;  uterus  asymmetrical. 

Species. — Anguillulina  putrefaciens  Kiihn,  1879. 

Anguillulina  putrefaciens  Kiihn,  1879. 

Synonyms. — Tyienchus  putrefaciens  Kiihn,  1879;  Trichina  contorta  'Botkin, 
1883. 

This  small  nematode  lives  in  onions,  and  it  or  other  varieties  may  at  times 
iind  access  to  the  stomach  with  the  food,  and  be  rejected  by  vomiting,  as 
reported  by  Botkin  in  1883. 

Rhabditis  Dujardin,  1845. 

Small  Anguillulidae  with  no  teeth  in  the  oral  cavity,  with  accessory 
pieces  to  the  two  male  spicules,  and  without  lateral  ridges' 

Rhabditis  niellyi  Blanchard,  1885. 

Synonym. — -Leptodera  niellyi  Blanchard,  1885. 
This  parasite  was  described  by  Nielly  in  1882  in  a  boy  who  suffered 
from  an  itching  papular  eruption  in  Brest,  which  he  had  never  left. 

Morphology. — The  parasites  measured  0*33  by  0-03  millimetre  in  width, 
and  possessed  a  cuticle  with  delicate  transverse  striation,  a  double-bulbed 
oesophagus,  and  an  intestine,  but  no  genital  organs. 


628  NEMATHELMINTHES 

Pathogenicity. — The  specimens  were  found  in  the  papules,  and 
also  in  the  blood  at  the  beginning  of  the  illness,  but  not  in  the  faeces, 
urine,  or  sputum. 

Life-History.— Unknown. 

LeptoderaDujardin,  1845. 

Anguillulidae  with  mouth  guarded  by  two,  three,  or  six  lips.  Male  with 
or  without  bursa,  which,  when  present,  never  surrounds  the  point  of  the  tail. 
Two  equal  spicules,  and  three  pre-anal  papilla?.  Female  with  the  tail  pro- 
longed into  a  long  unsymmetrical  point. 

Leptodera  pellio  Schneider,  1866. 

Synonyms. — Pelodera  pellio  Schneider,  1866;  Rhabditis  genitalis  Scheiber, 
1880. 

Leptodera  pellio  is  merely  an  occasional  parasite  in  man.  Infection  arises 
in  rather  a  peculiar  manner.  The  larva  lives  in  the  earthworm  (Lumbricus 
terrestris),  while  the  adults  exist  in  decomposing  matter  in  the  soil. 

The  Hungarian  peasants  use  soil  for  making  poultices,  from  which  the 
little  worms  apparently  make  their  way  into  the  vaginae  of  women  and  live 
there.  Oerley  has  shown  experimentally  that  they  will  live  in  the  vagina 
of  a  mouse. 

Morphology.— Male,  o-8  to  1-05  millimetres  in  length,  with  a  bursa  supported 
by  seven  to  ten  ribs  on  each  side.  Spicules,  which  are  not  quite  alike,  measur- 
ing 27  to  33  [x  in  length.  Female,  0-9  to  1*3  millimetres  in  length,  with  a  vulva 
slightly  posterior  to  the  middle  of  the  body. 

Pathogenicity. — Nil. 

Family  3.  Angiostomid^. 

Nematoda  characterized  by  heterogony,  each  species  having  a 
free-living  bisexual  rhabdite  form  and  a  parasitic  hermaphrodite 
filarial  form. 

Strongyloides  Grassi,  1879. 

Synonyms. — Pseudorhabditis  Perroncito,  1881 ;  Rhabdonema  Leuc- 
kart,  1882. 

The  parasitic  form  has  an  unarmed  mouth,  long  cylindrical 
oesophagus,  which  reaches  nearly  to  the  middle  of  the  body.  The 
free-living  stage  has  a  small  mouth,  short  oesophagus  with  a  double 
dilatation,  in  the  hinder  part  of  which  are  small  teeth.  The  male 
spicules  are  of  equal  size. 

Strongyloides  stercoralis  Bavay,  1877. 

Synonyms. — Anguillula  intestinctlis  et  stercoralis  Bavay,  1877; 
Leptodera  intestinalis  et  stercoralis  Cobbold ;  Pseudorhabditis  stercoralis 
Perroncito,  1881;  Rhabdonema  strongyloides  Leuckart,  1883; 
R.  intestinale  Blanchard,  1886. 

History.  — This  little  worm,  which  is  not  uncommonly  met  with 
in  faeces,  was  first  described  in  1876  by  Normand  in  the  faeces  and 
the  intestine  of  French  soldiers  just  returned  to  Toulon  from  Cochin 
China. 

At  first  it  was  thought  that  there  were  two  species- — one  in  the 
faeces  (Anguillula  stercoralis)  and  the  other  in  the  bowel  (^4.  intes- 


STRONGYLOIDES  STERCORALTS 


629 


tinalis)—b\\t  Leuckart  showed  that  they  were  but  succeeding  stages 
of  one  life-cycle.  It  is  found  in  Europe,  Africa,  India,  Ceylon, 
Indo-China,  China,  the  Philippines,  Oceania,  the  United  States, 
the  West  Indies,  and  Brazil. 

The  fully-developed  worm  is  found  in  the  duodenum  and  jejunum, 
into  the  mucosa  of  which  it  has  bored  its  way  deeply. 

Morphology. — The  parasitic  adult  worm  is  very  small — 2-2  millimetres 
long  and  34  /*  bread — -with  a  finely  striated  cuticle,  and  a  mouth  surrounded 
by  four  lips,  leading  into  a  cylindrical  oesophagus,  equal  in  length  to  one- 
quarter  of  the  whole  body.  The  anus  is  just  in  front  of 
the  tip  of  the  tail.  Inside  this  parasite  can  be  seen  ellip- 
soidal eggs.  The  sex  of  this  parasite  is  doubtful.  Is  it  a 
hermaphrodite,  in  which  the  male  organs,  after  serving 
their  purpose,  have  degenerated,  or  is  it  a  parthenogenetic 
female  ?  At  present  these  questions  cannot  be  answered 
definitely.  Most  probably  it  is  a  hermaphrodite.  The 
eggs  measure  50  to  58  /.i  in  length  by  30  to  34  jx  in  breadth, 
and  are  arranged  in  strings  surrounded  by  a  delicate 
tubular  structure.  They  occur  in  the  faeces  only  during 
attacks  of  diarrhoea. 

Life-History. — -The  eggs  are  oviposited  into  the 
mucosa  of  the  host's  intestine,  and  the  embryos 
hatch  and  find  their  way  into  the  lumen,  and  are 
evacuated  with  the  faeces.  On  reaching  water  or 
moist  earth  these  embryos  grow  into  adult  male 
and  female  forms,  which  conjugate,  and  then  the 
female  lays  eggs.  The  eggs  produce  free-living 
rhabditiform  embryos,  which  moult  and  turn  into 
filariform  embryos,  which  have  been  shown  by 
Mozocchi  and  van  Durne  to  penetrate  the  skin, 
not  through  the  hair-follicles,  but  through  the 
horny  layer  into  the  rete  Malpighii,  and  so  into 
the  corium.  The  experiments  of  Fulleborn  and 
V.  Schilling-Torgau  in  infecting  tracheotomized 
dogs  or  dogs  with  the  oesophagus  cut  and  fixed  to  the  skin  with 
larvae  of  Strongyloides  stercoralis  Bavay,  1877,  have  shoWn  that 
the  more  important  route  is  from  the  skin  to  the  lungs  and  so  via 
the  trachea  and  oesophagus  to  the  bowels,  while  a  less  important 
route  from  the  skin  via  the  blood-stream  directly  to  the  bowel 
can  also  take  place  [vide  the  life-history  of  Ancylostoma  duodenale, 
p.  663).  On  arrival  in  the  intestine  they  burrow  into  Lieberkiihn's 
follicles,  and  begin  to  lay  their  eggs. 

Pathogenicity. — The  parasite  is  generally  believed  to  cause  a 
catarrh  of  the  small  intestine,  though  many  believe  it  to  be  non- 
pathogenic. 

Family  4.  GxathostomidjE. 

Nematoda,  with  two  large  lips  and  the  whole  or  only  the  anterior 
part  of  the  body  covered  with  minute  ramified  spines.  They  live 
often  in  the  tumours  in  the  gut  wall  of  vertebrates,  especially 
mammals. 

Two  genera:  Gnathostoma  Owen,  1836,  and  Tanqua. 


Fig.  267. — Rhab- 
ditiform 
Embryo  of 
Strongyloides 
intestinalis 

B AV  AY  AS 

FOUND         IN 

Human  Faeces. 
(After  Looss.) 


630  NEMA  THELMINTHES 

Gnathostoma  Owen,  1837. 
Synonyms. — Cheiracanthus  Diesing,  1839;  Liorhynchus  Rudolphi. 
Definition. — With  the  characters  of  the  family. 
Remarks. — The  genus  comprises  only  intestinal  parasites,    of 
which  nine  species  are  known  in  man,  alligators,  cats,  tigers,  pigs,  etc. 

Gnathostoma  spinigerum  Owen,  1837. 

Synonyms. — -Cheiracanthus  siamensis  Levinsen,  1889;  Gnathostoma 
siamense  Levinsen,  1889;  Cheiracanthus  robustum  Diesing,  1839. 

Remarks. — Only  two  specimens  are  known,  one  a  female,  which 
was  obtained  by  Deuntzer  from  a  young  Siamese  woman  in  whose 
breast  a  hard  painful  swelling  had  formed,  accompanied  with  slight 
fever,  and  another  a  male  described  by  Leiper.  Nodules  the  size 
of  beans  appeared  in  the  skin,  from  one  of  which  the  worms  were 
extracted.  Two  other  similar  cases  have  recently  been  reported. 
Leiper  has  recently  compared  a  male  specimen  from  man  with 
typical  specimens  of  G.  spinigerum  of  the  tiger,  and  declares  them 
to  be  identical. 

Morphology — Male. — 10*55  millimetres  long  by  o*6  millimetre  broad,  with 
the  anterior  half  of  the  body  quite  straight  and  terminating  in  a  globular 
swelling,  which  carries  two  large  fleshy  lips  which  guard  the  mouth.  Neck 
only  0-3  millimetre  in  diameter.  In  front  of  the  neck  the  cuticle  is  provided 
with  eight  transversed  rows  of  chitinous  hooks  with  their  points  directed 
backwards.  Behind  the  neck  the  cuticle  has  many  cuticular  laminae,  but 
the  posterior  half  of  the  body  is  without  armature. 

The  mouth  is  simple,  without  a  vestibule.  The  paired  labial  glands  open 
on  the  lips  already  mentioned.  The  oesophagus  is  2*4  millimetres  long  and 
very  muscular,  and  opens  into  the  chyle  intestine,  which,  being  uniformly 
0*25  millimetre  broad,  is  with  difficulty  separated  from  the  rectum,  which 
leads  to  the  cloaca. 

There  are  two  pre-anal  and  two  post-anal  large  nipple-like  genital  papillae 
around  the  cloaca,  and  though  the  cuticle  is  folded  there  is  no  bursal  forma- 
tion; but  there  are  two  unequal  spicules,  i«i  millimetres  and  0-4  millimetre 
long.     There  is  a  distinct  muscular  ejaculatory  duct,  1-5  millimetres  long. 

Female. — Nine  millimetres  long  by  1  millimetre  broad,  with  eight  rows  of 
bristles  around  the  head,  and  spines  covering  the  anterior  third  of  the  body. 
Each  spine  ramifies  into  three  points,  of  which  the  middle  is  the  longest. 
The  anterior  end  was  narrow,  and  the  mouth  appeared  to  be  bordered  by 
two  lips.  The  posterior  end  had  a  three-lobed  prominence,  at  the  base  of 
which  the  anus  opened. 

Habitat. — Subcutaneous  tumours  in  man  in  Siam.  Allied  species 
live  in  the  stomach  of  pigs  and  oxen.  The  species  is  said  to  occur 
in  the  pariah  dogs  ol  Calcutta. 

Pathogenicity. — Man  is  apparently  an  aberrant  host,  for  in  man 
only  do  the  worms  wander  into  the  connective  tissue  and  form 
subcutaneous  tumours.  The  species  normally  lives  in  the  stomach 
of  animals,  causing  fibrous  thickenings. 

Family  5.  PhysalopteridjE. 
Physaloptera  Rudolphi,  1819. 
Physalopteridae  possessing  mouth  with  usually  two  lips,  each  with 
papillae  and  teeth.     Posterior  end  of  the  male  lancet-shaped,  owing 


FILARIIDJE  631 

to  a  widening  of  the  cuticle.  The  ventral  aspect  is  here  covered 
with  cuticular  plates,  and  there  are  four  pairs  of  pedunculated 
external  papillae  and  a  number  of  sessile  internal  papillae  and  unequal 
spicules.  Female:  vulva  situated  anteriorly.  Eggs  thick-shelled 
and  smooth. 

Physaloptera  caucasica  von  Linstow,  1902. 

This  has  only  been  found  once  by  Menetries  in  the  alimentary  canal  of 
man  in  the  Caucasus. 

Male  1-42  millimetres  long  by  0-71  millimetre  broad.  Female  27  millimetres 
long  by  1-14  millimetres  broad.     Eggs  57  by  39  fi. 

Physaloptera  mordens  Leiper,  1907. 
Leiper  has  recently  described  a  large  number  of  cases  of  infection 
with  Physaloptera  in  natives  of  tropical  Africa,  which  differed  from 
P.  caucasica  not  only  in  size,  but  in  the  length  of  the  spicules  in 
the  male. 

Family  6.    Filariid^e  Claus,  1885. 

Synonyms.— Filaridea  Cams,  1863;  Filariadea  Leuckart,  1876; 
Filaridce  Cobbold;  Filarides  Assenova,  1899. 

Definition. — Long  filiform  nematodes  with  uniform  diameter,  and 
a  straight  head  provided  with  two  latero-median  and  four  submedian 
papillae.  Mouth  terminal,  with  two  lips,  and  occasionally  a  more 
or  less  distinct  buccal  capsule.  (Esophagus  slender,  elongated, 
and  may  be  divided  into  two  portions,  but  has  no  posterior  bulb. 
Mid-gut  present,  rectum  present,  anus  subterminal. 

Males  with  one  or  two  unequal  spicules  and  a  spirally  recurved 
tail,  provided  with  papillae,  and  in  some  cases  with  lateral  alae. 
Females  larger  than  the  males,  with  or  without  a  vulva  in  the 
gravid  worms,  which,  when  present,  is  situate  anteriorly.  Uterus 
usually  double.  All  species  parasitic  and  ovoviviparous,  with  a 
change  of  host  in  at  least  certain  species. 

Type  Genus. — Filaria  Miiller,  1787. 

The  genus  Filaria  was  created  by  Miiller  in  1787,  unfortunately 
without  naming  a  particular  type,  which  Stiles  suggests  should 
be  Filaria  martis  Gmelin,  1790  (F.  perforans).  This  rs  found  in 
Mustela  martes  L.,  the  pine-marten  of  Europe,  and  was  one  of  the 
parasites  originally  described  by  Miiller.  This  parasite  requires  to 
be  restudied  before  definite  characters  can  be  given  for  the  genus. 

Classification. — The  subfamilies  are  Filariina  and  0 nchocercincv . 

Subfamily  Filariin^e  Stiles,  1907. 
Filaria  Miiller,  1787. 
Definition.— This  is  doubtful.  Filariidae  with  long  slender  fili- 
form bodies;  anterior  extremity  attenuated,  obtuse;  posterior  very 
attenuated,  more  so  than  the  head.  Cuticle  without  transverse 
striation,  and  without  bosses.  Male  shorter  than  the  female,  with 
spirally  bent  tail  provided  with  lateral  cuticular  alae,  pre-  and  post- 


623  NEMATHELMINTHES 

anal  papillae,  and  unequal  spicules.  Females  longer  than  males, 
with  vulva  situate  anteriorly  near  the  mouth . 

Synonyms. — Filer  aria  Rudolphi,  1809;  Filaire  Lee,  1840 ;  and  some 
misprints. 

Type. — F.  mart  is  Gmelin,  1790. 

Species.— F.  bancrofti  Cobbold,  1877;  (?)  F-  demarquayi  Manson, 
1895. 

Some  years  ago  the  genus  Filaria  contained  a  large  number  of 
species  parasitic  in  man,  but  the  following  genera  have  definitely 
been  separated  from  Filaria:  Acanthocheilonema,  Dirofilaria, 
Dracunculus,  Onchocerca,  and  Hamularia.  At  the  present  time 
there  are  only  three  species  known  to  be  human  parasites,  which 
are  referred  to  the  genus  Filaria — viz.,  F.  bancrofti  Cobbold, 
1877;  F.  ozzardi  Manson,  1897;  and  F.  inermis  Grassi,  188S;  in 
addition  to  the  embryonic  forms  included  in  the  collective  group 
(Microfilaria)  and  the  immature  forms  in  the  collective  group 
{A gamo filaria).  There  are,  however,  a  number  of  spurious  or 
doubtful  forms  scattered  throughout  medical  literature  and  de- 
scribed as  human  parasites  which  must  be  eliminated  from  the 
genus,  and  these  are: — ■ 

1.  Filaria  (?)  hominis  oris  Leidy,  1850. — This  probably  belongs  to  the 
Mermithidae,  and  may  have  been  a  mermis  accidentally  taken  into  the  child's 
mouth  while  eating,  say,  an  apple,  because  it  had  an  obtuse  posterior 
extremity  with  a  recurved  hook. 

2.  Filaria  (?)  gigas  Prout,  1902. — Two  embryonic  filarial  structures  220  to 
340  /u,  by  8  to  12  fi,  found  with  rounded  head  and  tapering  tail  ending  bluntly, 
no  sheath;  stained  readily  with  fuchsin.  Low  thinks  that  these  might  be 
contaminations- — i.e.,  insect  hairs;  Looss  thinks  that  they  may  be  cast  skins, 
and  as  Stiles  has  also  adopted  this  view,  the  parasite  may  perhaps  be  elimin- 
ated.    Recently  Leiper  has  considered  it  to  be  a  stained  fungoid  growth. 

3.  Nematoideum  tracheale  Cobbold,  1864. 
The  following  can  certainly  be  eliminated: — 

4.  Filaria  (?)  restiformis  Leidy,  1880,  as  this  is  Agamomeris  restiformis, 
and  belongs  to  the  Mermithidae. 

5.  bilana  (?)  cystica.  Sti^s  1  elieves  this  (o  bemerelv  Oxw.ris  vermieulavis ; 
it  nay  be  the  embrvo  of  a  Filaria. 

6.  Filaria  (?)  niellyi  is  Rhabditis  niellyi. 

7.  Filaria  (?)  zebra  Mon  Grand,  1852,  is  said  to  be  a  fibrinous  clot,  and 
therefore  a  species  fictitia. 

The  following  may  have  to  be  eliminated: — 

8.  Filaria  (?)  kilimarce  Kolb,  1898. — These  consist  of  several  female  speci- 
mens once  found  free  in  the  abdominal  cavity  of  a  fallen  Kitu  warrior.  Oral 
papillae  are  said  to  have  been  like  Dracunculus  medinensis. 

They  were  10  to  20  centimetres  in  length,  and  0-5  to  1  millimetre  in  diameter, 
white,  and  resembled  Gordius  aquaticus  in  general  appearance. 

With  these  Kolb  classified  free-living  worms,  and  therefore  doubts  are  held 
as  to  the  exact  zoological  determinations  of  the  species  recorded. 

9.  Filaria  (?)  romanorum  orientalis  Sarcani,  1888. — Observed  in  the  blood  of 
a  Roumanian  woman ;  1  millimetre  long  by  0-3  millimetre  broad,  with  intestine 
and  generative  apparatus  developed;  believed  by  some  to  be  an  adult  thread- 
worm . 

The  uncertain  species  are: — 

1 .  Filaria  Species  (?)  Cholodkowsky,  1896. — Found  in  whitlow-like  tumours 
on  the  fingers  of  peasants  in  the  Twer  Government. 

2.  Filaria  Species  (?)  Prout,  1902. 


FILARTA   BANCROFTI  633 

3.  There  was  a  parasite  called  Spiroptera  hominis  Rudolphi,  18 19,  which 
appears  to  have  been  spurious,  being  really  Filaria  communis,  of  which  Filaria 
piscium  is  a  synonym. 

Filaria  bancrofti  Cobbold,  1877. 

Synonyms. — Trichina  cystica  Salisbury,  1868,  nee  Rudolphi,  1819; 
F.  sanguinis  hominis  Lewis,  1872 ;  F  sanguinis  hominis  cegyptiaca 
Sonsino,  1874;  F.  dermatemica  da  Silva  Araiyo,  1875;  F.  wuchereri 
da  Silva  Lima,  1877;  F.  sanguinis  hominum  Hall,  1885;  F.  sanguinis 
hominum  nocturna  Manson,  1891;  F.  noctuma  Manson,  1891. 

History. — The  Microfilaria  was  discovered  in  Paris  by  Demarquay 
in  August,  1863,  in  the  chylocele  fluid  of  a  patient  from  Havana. 
In  1866  Wucherer  found  it  in  Brazil  in  the  urine  of  patients  suffering 
from  chyluria.  In  1872  Lewis  made  the  important  observation 
that  its  true  anatomical  habitat  is  the  blood.  Bancroft,  in  1876, 
discovered  the  adult  female  form;  Borne,  in  1888,  discovered  the 
adult  male.  In  1899  Manson  discovered  that  the  Microfilaria,  on 
disappearing  from  the  peripheral  circulation,  resorted  to  the  lungs 
during  the  day-time.  The  parasite  is  spread  by  mosquitoes,  as 
discovered  by  Manson  in  1878,  who  thought  that  the  Filarice 
escaped  from  their  insect  hosts  into  water,  and  reached  man  by 
this  means.  Later  Bancroft  conjectured  that  Filarice  might  be 
inoculated  directly  into  man,  and  about  this  time  sent  infected 
mosquitoes  to  Manson  in  London.  Bancroft's  material  was 
investigated,  at  Manson' s  request,  by  Low,  who  discovered 
that  the  Filarice  migrate  to  the  mouth-parts  of  their  insect  hosts 
after  a  period  of  growth  within  the  musculature.  A  little  later, 
independently,  James  made  the  same  discovery  in  India.  In 
the  meantime  Grassi  and  No;;  investigated  the  life-history  of  a 
corresponding  Filaria  of  the  dog  (D.  immitis),  and  demonstrated 
that  it  undergoes  a  similar  development  also  in  mosquitoes,  choosing, 
however,  the  Malpighian  tubes  instead  of  the  thoracic  muscles  as 
the  seat  of  their  development.  Moreover,  Grassi  and  Noe  were 
successful  in  inoculating  normal  dogs  by  means  of  mosquitoes  fed 
on  infected  dogs.  Fiilleborn  and  Bahr  have  most  carefully  re- 
studied  the  subject. 

Morphology — General  Characters. — The  worms  are  whitish  in 
colour,  long,  and  filiform,  with  a  smooth  cuticle,  and  a  globular 
head  terminating  in  a  simple,  circular,  unarmed,  lipless  mouth. 
The  tail  is  rounded. 

Sexual  Characters. — The  male  is  smaller  than  the  female,  and  a 
complete  specimen  measures  on  the  average  38  millimetres  in  length 
and  0-12  millimetre  in  thickness.  In  the  dead  worm  the  tail  is  spiral 
or  much  incurved,  but  may  be  straight  during  life,  according  to  Mait- 
land.  The  anus,  which  is  0-13  millimetre  from  the  posterior 
extremity,  is  guarded  by  two  projecting  lips.  The  anal  papillae 
are  not  easily  defined,  but  are  said  to  consist  of  three  pairs  of  pre- 
anal  and  three  of  post-anal  papillae.  Leiper  has  recently  figured 
fourteen  pairs. 


634  NEMATHELMINTHES 

There  are  two  unequal  curved  retractile  spicules.  The  larger 
measures  o-6  millimetre  and  the  smaller  o-2  millimetre  in  length. 
They  consist  of  a  basal  portion,  which  is  broad,  rigid,  and  chiti- 
nous,  measuring  0-17  millimetre  in  the  larger'and  0-12  millimetre 
in  the  smaller  spicule,  and  a  long,  thin,  colourless,  cylindrical, 
slightly  undulating  terminal  portion. 

The  female,  while  more  or  less  transparent,  is  longer  and  thicker 
than  the  male,  and  measuring  76  to  100  millimetres  in  length,  with 
a  thickness  of  0-185  millimetre. 

The  mouth  is  situated  at  the  anterior  extremity,  being  8  jli  in 
diameter,  and  leading  into  an  oesophagus  which  passes  insensibly 
into  the  intestine.  This  terminates  in  the  anus,  situated  0-28  milli- 
metre from  the  incurved  posterior  end. 

The  vulva,  situate  t-2  millimetres  from  the  anterior  extremity, 
opens  into  a  single  vagina,  from  which  two  uterine  tubules  run 
along  most  of  the  length  of  the  body.  These  tubules  contain  the 
eggs  and  embryos  in  various  stages  of  development. 

Cobb's  formula  is  :— 

-0-36,  3-64  (?),  1-22,  99-5 
-0-145,  0-377  (?),  0-254,  0-147 

The  numerator  indicates  lengths  from  the  anterior  extremity  to  {1)  base 
of  oesophagus;  (2)  nerve  ring;  (3)  posterior  pharyngeal  constriction;  (4)  vulva 
in  females  or  middle  in  males;  (5)  anus.  The  denominator  represents  trans- 
verse measurements  at  the  same  levels.  All  measurements  are  expressed  as 
percentages  of  the  total  length.  At  the  present  time  Cobb's  formula  is  not 
accepted  as  a  reliable  guide  to  the  parasitic  species. 

Life-History. — The  males  and  females  may  be  found  coiled  to- 
gether in  the  lymphatics  of  the  scrotum,  the  arm,  the  leg,  hydro- 
celes of  the  cord,  epididymis,  or  testicle,  and  more  rarely  in  those 
of  the  pelvis  and  abdomen.  The  males  are  less  numerous  than  the 
females. 

When  placed  in  saline  solutions,  they  show  active  movements, 
coiling  and  uncoiling  themselves  for  several  hours. 

In  the  uterus  of  the  female,  as  has  already  been  stated,  eggs  may 
be  noted  in  all  stages  of  development. 

At  first  nearly  round,  measuring  50  by  34  y,  and  containing  a 
coiled-up  embryo,  the  eggs  become  more  and  more  elongated  by 
the  movements  of  the  embryo,  until  in  the  anterior  part  of  the 
uterus  they  are  much  longer  than  broad.  Finally,  they  escape 
through  the  genital  pore,  and  enter  the  lymph-stream,  along  which 
they  travel  through  lymphatic  vessels  and  glands,  the  thoracic  duct, 
the  right  side  of  the  heart,  and  the  lungs,  to  reach  the  peripheral 
circulation,  where  they  are  best  seen  at  night;  hence  the  name 
Microfilaria  nocturna.  In  the  blood  they  appear  as  little  wriggling 
filiform  bodies,  knocking  the  corpuscles  about,  but  not  moving 
from  the  position  in  which  they  are  lying.  The  Microfilaria  in  the 
blood  are  said  to  be  a  little  larger  than  those  in  the  uterus,  which 
is  thought  by  Penel  to  be  due,  not  to  growth,  but  to  inhibition  of 
fluid  by  osmosis. 


FILAR!  A   BANCROFT  I 


635 


They  measure  from  290  to  320  ju  in  length  and  from  7-5  to  8-4  u  in 
breadth  (Low),  and  are  seen  to  be  long,  slender,  cylindrical  organisms 
with  a  rounded  anterior  and  a  tapering  posterior  end,  enclosed  in 
a  sheath— the  vitelline  or  egg  membrane — inside  which  they  are 
capable  of  darting  backwards  and  forwards,  because  it  is  longer 
than  they  are,  the  empty  portion  being  noted  either  in  front  of 
the  anterior  or  behind  the  posterior  end  of  the  Microfilaria.  Manson 
considers  that  this  sheath  is  of  vital  importance  to  the  little  parasite, 
as  it  prevents  its  using  its  anterior  spine  to  escape  out  of  the  blood- 
vessel, and  so  losing  the  chance  of  its  invading  a  mosquito. 

The  anterior  rounded  extremity  is  said  to  possess  a  thick  hemi- 
spherical proboscis,  carrying  a  minute  apical  spine,  which  is  capable 
of  being  covered  by  a  retractile  and  protractile  six-lipped  prepuce, 
but  this  observation  requires  confirmal  ion. 

Behind  the  anterior  end,  the  body  can  be  seen  to  be  composed 
of  a  transversely  striated  dermo-muscular  layer,  inside  which  are  a 
number  of  closely  packed  cells  whose  nuclei  show  up  clearly  on 


l®§§§ 


Fig.  268. — Diagram  of  the  Development  of  a  Microfilaria 
(Loa  loa  Stiles). 

(After  Penel.) 

staining.  Unstained,  the  central  mass  appears  granular,  but  the 
granules  are,  however,  wanting  at  certain  spots,  which,  following 
Annett,  Dutton,  and  Elliot,  may  be  defined  as:  (1)  A  clear  anterior 
area  from  the  front  to  the  first  nuclei;  (2)  an  irregular  transverse 
spot  situated  21-5  per  cent,  of  the  length  of  the  body  from  the 
anterior  end;  (3)  a  V-shaped  or  transverse  irregular  spot  at  30  per 
cent,  of  the  length,  called  V-spot  by  Manson;  (4)  a  median  line,  the 
central  viscus  of  Manson,  whose  centre  is  at  63  per  cent,  of  the 
length;  (5)  an  irregular  oval  spot  often  present  at  85  per  cent., 
called  the  tail-spot  by  Manson;  (6)  a  small  central  spot  only  occa- 
sionally present  at  917  per  cent.;  (7)  the^clear  posterior  area 
behind  the  last  nucleus. 

Leiper  points  out  that  these  areas  are  not  peculiar  to  the  Filaria 

embryos,  but"  occur  also  in  other  forms.    The  V-spot  is  the  excretory 

vesicle  and  the  tail-spot  the  proctodeum.     The  morphology  of  the 

worm  has  been   studied  in  detail  by   Fiilleborn,   whose  diagram 

s  reproduced  on  p.  637. 


636 


NEMA  THELMINTHES 


These  Microfilaria  occur  in  the  peripheral  blood  at  night,  as 
has  just  been  stated,  beginning  about  5  to  7  p.m.,  and  increasing 
in  numbers  till  midnight,  and  then  diminishing  till  about  7  to  8  a.m., 
when  only  a  stray  one  may  be  met  with,  as,  indeed,  can  be  observed 
all  through  the  day  until  the  evening  increase  begins.  There  is, 
therefore,  a  definite  periodicity — at  night  the  Microfilaria  abound 
in  the  blood,  while  in  the  day-time  they  do  not. 

In  the  day  it  appears  that  they  live  mostly  in  the  lungs  and  in 
the  large  vessels  of  the  thorax.  This  was  shown  by  Manson  by  the 
careful  examination  of  films  and  sections  taken  from  the  different 
organs  of  a  man  who  had  Microfilaria  bancrofti  in  his  peripheral 
blood,  as  well  as  a  lymph  scrotum  and  varicose  groin  glands. 
The  post-mortem  was  made  six  hours  after  death,  which  took  place 
almost  instantaneously  at  8.30  a.m.,  being  due  to  drinking  hydro- 
cyanic acid.  By  far  the  largest  number  of  parasites  were  to  be 
found  in  the  lungs  and  carotid  artery,  and  then  in  the  heart  muscle, 
while  a  few  were  found  elsewhere,  especialty  in  the  kidney. 


Fig.  269. — Microfilaria  bancrofti  Cobbold. 

These  facts  have  been  confirmed,  but  the  question  as  to  what 
induces  the  parasites  to  live  in  the  peripheral  blood  in  the  night 
and  the  thoracic  organs  in  the  day  is  not  clear.  True,  it  enables 
the  Microfilaria  to  enter  the  mosquito,  but  that  does  not  explain 
the  problem.  Neither  variations  in  atmospheric  temperature  nor  in 
pressure,  in  light,  or  in  darkness  seem  to  have  any  effect.  Nor  does 
the  pulse-rate  or  the  individual's  temperature  make  much  differ- 
ence; but  there  is  one  factor,  first  shown  by  Mackenzie  and  since 
confirmed  by  Manson  and  others,  that  it  is  in  some  way  connected 
with  sleep;  for  if  a  person  with  Microfilaria  in  his  blood  stays 
awake  all  night  and  sleeps  during  the  day,  the  parasites  will 
abound  in  his  blood  in  the  day,  and  not  at  night.  Penel  remarks 
that  the  problem  of  the  periodicity  of  the  Microfilaria  and  the 
periodicity  of  sleep  in  man  are  connected,  and  that  when  one  is 
properly  solved  the  other  will  also  be  elucidated . 

Recently  Bahr  has  shown  that  the  microfilaria  of  F.  bancrofti 


FILARIA  BANCROFTI 


637 


in  Fiji  does  not  develop  so  well  in  Culex  fatigans  as  it  does  in 
Stegomyia  pseudoscutellaris  Theobald,  1910. 

This  latter  mosquito  feeds  only  b>  day,  and  in  Fiji  Bahr  has  found  that  the 
microfilaria  occur  in  the  peripheral  blood  both  during  the  day  and  during 
the  night,  and  believes  that  the  periodicity  usually  observed  in  the  micro- 
filaria is  dependent  upon  the  habits  of  the  insect  host. 


Fig.  270. — Scheme  of  the  Structure  of  a  Microfilaria,  showing 
(1)  the  Excretory  Pore;  (2)  the  Cells,  which  will  form  the 
Excretory  Apparatus;  (3)  the  Subcuticular  Cells;  (4)  the  Genital 
Cells;  (5)  Anus. 

(After  Fiilleborn.) 


The  number  of  Microfilaria  in  the  blood  varies  from  very  few 
up  to  quite  considerable  numbers,  reaching,  according  to  Manson, 
up  to  500  in  a  single  film,  which  gives  some  40,000,000  to  50,000,000 
in  an  average-sized  man.  This 
naturally  raises  the  question  of,  How 
many  adults  do  these  come  from  ? 
How  long  does  an  adult  live  ?  How 
long  does  a  Microfilaria  live  ?  What 
finally  happens  to  the  Microfilaria  ? 

It  would  seem  probable  that  a  given 
Filaria  can  live  several  years  in  the 
human  body,  and,  of  course,  give 
rise  to  many  embryos.  Further, 
numbers  of  Filaria  can  be  met  with  in  one  individual. 

Fiilleborn  has  shown  that  Microfilaria  ran  live  in  the  blood  for 
several  months,  and  observers  have  thought  that  they  may  be 
destroyed  by  leucocytes  and  endothelial  cells.  It  is,  however, 
evident  that  they  develop  no  further  in  the  human  body,  and 
require  to  be  taken  into  the  body  of  a  mosquito  before  further 
development  is  possible. 

In  the  Mosquito. — Abounding  as  they  do  in  the  peripheral  blood 


Fig.  271. — Early  Stage  of  the 
Development  of  Filaria 
bancrojti  Cobbold  in  the 
Muscles  of  Culex  fatigans. 

(After  Looss,  from  Mense's 
'  Tropenkrankheiten.') 


638 


NEMA  THELMINTHES 


at  night,  there  is  no  difficulty  for  the  Microfilaria  to  reach  the 
stomach  of  a  mosquito  in  the  tropics,  and  here  and  in  its  thorax 
development  proceeds. 

The  mosquitoes  known  to  be  capable  of  serving  as  efficient  hosts 
for  this  development  are:  Culex  fatigans  Wied  in  the  West  Indies, 
Myzomyia  rossii  Giles  in  India, Pyretophorus  costalis  Loew  in  Nigeria, 
Panoplites  africanus  in  Central  Africa. 


Fig.  272. — Late  Stage  of  the  Development  of  Filaria  bancrofti 
Cobbold  in  Culex  fatigans. 

(After  Looss,  from  Mense's  '  Tropenkranklieiten.') 

Incomplete  results  have  been  obtained  with  Culex  microannu- 
latus,  C.  albopictus,  C.  taniatus,  Cellia  albimana ;  and  negative 
results  in  C.  notoscriptus,  C.  annulirostris,  C.  hispidosus,  C.  vigilax, 
C.  nigrithorax,  C.  procax,  A.  musivus,  Myzomyia  funesta,  A.  maculi- 
pennis,Pulex  serraticeps,  Stomoxys  (?),  Clinocoris  lectularius. 


Fig.  273. — Diagram  of  the  Development  of  Filaria  bancrofti  Cobbold 
in  the  Thorax,  Head,  and  Labium  of  a  Mosquito. 

The  Microfilaria  enter  with  the  blood  into  the  mosquito's  stomach, 
and  there  escape  from  the  sheath  by  rupturing  it  at  the  anterior 
extremity. 

*  They  then  pierce  the  wall  of  the  stomach,  and  find  their  way 
into  the  muscles  of  the  thorax,  where  they  grow  considerably  till 
1*5  millimetres  long  and  0-25  millimetre  broad. 


FILARIA  OZZARDI  639 

They  also  undergo  development,  obtaining  an  alimentary  canal 
and  a  three-lobed  tail.  When  so  far  developed,  they  leave  the 
thorax  and  pass  through  the  prothorax  and  head  into  the  labium, 
where  they  remain  until  the  mosquito  bites  [a  man,  when  they 
escape  into  the  skin  by  making  their  way  through  Dutton's 
membrane,  which  is  a  thin^  membrane  between  the  labella  and  the 
chitinous  skeleton  of  the  labium,  as  was  demonstrated  byLebredo. 
(For  further  details  see  Chapter  I  XV I .) 

Their  further  development  in  man  is  not  known,  but  in  due  course 
they  become  adults. 

Pathogenicity. — Usually  non-pathogenic,  these  worms  under 
certain  circumstances  can  cause  elephantoid  fever,  elephantiasis, 
lymph  scrotum,  etc.,  or,  in  other  words,  nlariasis. 

Filaria  taniguchi  Penel,  1905. 

This  Filaria  was  found  in  a  lymphatic  gland  from  a  person  living 
in  Ama  Kusha  in  Japan.  Only  the  female  and  the  microfilaria  are 
known. 

The  former  measured  68  millimetres  in  length  and  0-2  milli- 
metre in  breadth,  and  had  a  non-striated  cuticle,  a  terminal  mouth 
with  two  pairs  of  papillae,  an  anus  0-23  millimetre  in  front  of  the 
posterior  extremity,  and  a  vulva  1-3  millimetres  behind  the 
mouth. 

The  latter  measured  164  [i  long  by  8  fi  broad,  possessed  a  sheath 
and  a  truncated  tail,  and  showed  a  nocturnal  periodicity.  Leiper 
regards  this  species  as  the  same  as  F.  bancrofti. 

Life-History.— Not  known. 

Pathogenicity. — Not  known. 

Filaria  ozzardi  Manson,  1897. 

Synonyms.—  Filaria  ozzanfo' Manson,  1897 ;  F.  juncea  Railliet,  1908. 

in  1895  Manson  discovered  a  microfilaria  in  blood-films  from 
natives  of  St.  Vincent  in  the  West  Indies,  which  he  named  Filaria 
demarquayi,  after  the  discoverer  of  the  microfilaria  of  F.  bancrofti. 
In  1897  he  found  in  blood-films  from  Carib  Indians  of  British 
Guiana  another  microfilaria,  which  is  the  same  as  that  called 
F.  demarquayi,  but  which  he  provisionally  considered  to  be  a 
different  species,  and  called  F.  ozzardi.  The  name  demarquayi 
is  preoccupied. 

Lately  Penel  and  Manson  have  come  to  regard  them  as  identical. 
Galgey  found  the  adult  females  in  the  West  Indies. 

It  is  found  in  St.  Vincent,  Dominica,  Trinidad,  St.  Lucia,  in  the 
West  Indies,  and  in  British  Guiana,  where  it  is  found  in  jungly 
districts.  The  adults  live  in  the  connective  tissue  at  the  root  of 
the  mesentery  and  elsewhere. 

Morphology.— The  male  has  not  yet  been  described,  and  only  a 
fragment  of  a  posterior  end  has  been  found.  The  female  measures 
65  to  80  millimetres  in  length  and  0-21  to  0-25  millimetre  in  breadth, 


640  NEMA  THELMINTHES 

with  a  bulbous  cuticular  expansion  at  the  tip  of  the  tail.  Anus 
0-25  millimetre  in  front  of  the  posterior  extremity,  vulva  0-71  milli- 
metre behind  the  anterior  end. 

Life-History. — -The  egg  develops  into  a  microfilaria  which  has 
no  sheath,  shows  no  periodicity,  and  measures  200  /j,  by  5  u.  Its 
tail  is  tapering  and  sharp  pointed,  and  it  moves  actively.  Nothing 
further  is  known  as  to  the  life-history. 

Pathogenicity. — Nil. 

Filaria  inermis  Grassi. 

Synonyms.-  -(?)  Hamularia  lymphatica  Treutler;  (?)  Filaria 
palpebralis  Pace,  1867;  (?)  Filaria  labialis,  etc. 

Several  female  filaria  worms  have  been  described  from  Southern 
Europe  as  occurring  in  subcutaneous  swellings  in  various  parts  of 
the  body  in  man  and  horses.  These  resemble  the  forms  recorded  by 
Addario  and  Alessandrini  under  the  name  Filaria  conjunctives,  but 
differ,  however,  in  the  position  of  the  vulva. 

(Microfilaria)  Le  Dantec,  1904. 

A  collective  group  of  the  larvae  of  unknown  adult  Filariidae  found 
in  the  blood  of  man  and  other  vertebrates. 

(Microfilaria)  powelli  Penel.  1905. 

This  microfilaria  was  found  by  Powell  in  1903  in  the  blood  of  a 
Bombay  policeman. 

It  showed  a  nocturnal  periodicity  (?),  was  provided  with  a  sheath, 
measured  131  /j,  by  5-3  [x,  and  had  a  truncated  tail. 

(Microfilaria)  philippinensis  Ashburn  and  Craig,  1906. 

Ashburn  and  Craig  described  this  blood  filaria  in  May,  1906.  It  measures 
0-29  to  0*335  millimetre  in  length,  has  no  periodicity,  is  actively  and  pro- 
gressively motile,  and  is  enclosed  in  a  tight-fitting  sheath,  within  which  it 
cannot  slip  backwards  and  forwards,  and  which  is  only  clearly  seen  at  the 
extremities.  The  anterior  extremity  is  broad,  with  a  serrated  prepuce,  and 
supports  a  small  retractile  spicule.  The  body  has  an  outer  striated  musculo 
cutaneous  coat  and  an  inner  clear  portion,  with  an  anterior  V-spot  situate 
0-105  millimetre  from  the  anterior  end,  and  piercing  the  outer  coat  by  its 
apex,  and  opening  on  the  surface. 

The  central  viscus  is  seen  as  a  convoluted  or  spiral  tube  in  the  posterior 
part  of  the  middle  third  of  the  body.  The  tail-spot  is  in  the  centre  of  the 
posterior  third  of  the  body,  and  opens  by  the  apex  of  its  V  on  the  surface, 
where  there  is  a  distinct  papilla.  The  tail  begins  to  taper  at  a  point  midway 
between  the  tail-spot  and  the  posterior  end,  and  ends  in  a  fine  threadlike 
point.     It  is  thought  that  this  end  disappears  during  later  development. 

The  column  of  nuclei  runs  the  whole  length  of  the  worm,  being  broken  by 
unstained  areas  here  and  there.  In  stained  species  the  V-spots  and  central 
viscus  are  not  seen. 

Life-History. — This  microfilaria  develops  in  Culex  fatigans  Wied.  On 
entering  the  stomach  of  the  mosquito  it  escapes  from  its  sheath  within  twenty- 
four  hours,  and  has  pierced  the  stomach-wall  and  appeared  free  in  the  ccelom, 
where  many  die,  but  others  develop  rapidly,  and  complete  their  mosquito 
eye  e.     Generally  by  the  third  day  they  have  left  this  position  and  travelled 


AGAMOFILARTA   CONJUNCTIVAE  641 

into  the  thoracic  muscles,  where  they  develop.  At  first  there  is  a  decrease 
in  length  from  0-32  to  0-21  millimetre,  but  an  increase  in  breadth  from  0-0065 
to  o-oi  millimetre. 

By  the  eighth  day  the  Filaria  has  increased  in  length  and  breadth,  and 
shows  an  alimentary  canal  along  its  whole  length. 

From  this  till  the  eleventh  day  the  development  is  rapid,  and  the  worm 
now  measures  from  1-2  to  i-6  millimetres  in  length  by  0-04  to  o>o2  milli- 
metre in  breadth,  and  has  a  mouth,  oesophagus,  chyle  intestine,  and  an  anus, 
and  the  tail  has  three  well-defined  papilla?. 

From  the  eleventh  to  twelfth  day  the  worms  are  found  in  the  head,  and 
by  the  fourteenth  to  fifteenth  day  in  the  labium,  lying  side  by  side,  with 
their  heads  pointing  forwards. 

Remarks. — There  appears  to  be  every  reason  to  consider  this 
microfilaria  as  merely  the  microfilaria  of  F.  bancrofti  Cobbold, 
1877,  because,  as  Low  and  Bahr  have  pointed  out,  they  are 
morphologically  identical,  while  both  nematodes  live  in  the  tissues 
and  are  associated  with  the  same  pathological  signs.  Finally,  the 
same  mosquito,  Stegomyia  pseudoscutellaris  Theobald,  1910,  is  an 
efficient  host  for  both.  Bahr  suggests  that  the  loss  of  periodicity  is, 
probably,  a  partial  adaptation  to  the  habits  of  the  intermediary 
host,  S.  pseudoscutellaris,  which  only  feeds  by  day.  This  cor- 
relationship  between  parasite  and  host  Sambon  has  long  insisted 
upon. 

(Agamofilaria)  Stiles,  1906. 

A  purely  collective  group,  made  to  contain  agamic  forms  of 
Filariidte  which  have  not  yet  reached  a  stage  in  their  development 
permitting  their  generic  determination. 

Species. — {Agamofilaria)  conjunctiva  Addario,  1885;  {A),  labialis 
Pane,  1864;  (A.)  georgiana  Stiles,  1906;  {A.)  oculi  Diesing,  1851; 
(.4.)  palpebralisYo.ee,  1867. 

(Agamofilaria)  conjunctivae  Addario,  1885. 

Synonyms. — E.  peritonei  hominis  Babes,  1880;  E.  inermis  Grassi,  1887; 
F.  apapillocephala  Condorelli  Francaviglia,  1892. 

Remarks. — This  worm  was  first  discovered  by  Dubini  in  the  eye  of  a  man 
in  Milan,  then  by  Babes  in  the  gastro-splenic  omentum  of  a  woman  in  Buda- 
pest, then  by  Vadela  in  the  conjunctiva  of  a  woman  in  Sicily.  Perhaps 
F.  palpebralis  Pace,  1867,  and  F.  oculi  humani  van  Nordmann  belong  to  this 
group.  It  is  possible  that  the  L.  loa  described  in  India  was  one  ol  ih<  c 
parasites. 

Morphology. — Several  females  are  known.  It  is  white  in  colour,  and 
measures  16  to  20  centimetres  in  length  and  0-5  millimetre  in  breadth.  The 
cuticle  is  striated  except  just  around  the  mouth,  but  there  are  neither  papilla? 
nor  lips.  The  anus  is  subterminal,  and  the  vulva  close  behind  the  mouth. 
There  is  a  single  vagina  and  a  double  uterus  containing  eggs  and  embryos. 

Graham  Forbes  lias  recently  recorded  a  male  specimen  from  a  soldier  in 
Macedonia. 

Life-History  and  Pathogenicity. — Intermediary  is  unknown.  The  worms 
produce  subcutaneous  tumours. 

(Agamofilaria)  labialis  Pane,  1864. 
This  parasite  was  extracted  from  a  small  pustule  on  the  inner 
surface  of  the  upper  lip  of  a  person  in  Naples  in  1864,  and  was  not 
again  described  until  Pierantoni,  in  1908,  again  found  it  occurring 

n 


6 12  NEMA  THELMINTHES 

in  Naples.  In  both  cases  the  female  has  been  found,  varying  from 
130  to  30  millimetres  in  length,  with  a  whitish-yellow  body,  and  a 
pointed  anterior  extremity,  on  which  the  terminal  mouth,  guarded 
by  four  papillae,  opens.  The  anus  opens  150  fj,  anterior  to  the 
posterior  end,  and  the  vulva  opens  3  millimetres  behind  the  anterior 
extremity.    The  uterus  bifurcates  into  two  branches. 

(Agamofilaria)  georgiana  Stiles,  1906. 

These  immature  Filarice  were  obtained  by  Graham  from  a  sore  on 
the  leg  of  a  negress  at  Darien. 

They  were  cylindrical  in  shape,  with  a  more  or  less  uniform 
diameter,  gradually  attenuating  towards  both  extremities.  Mouth 
terminal,  central,  circular,  small,  unarmed,  and  surrounded  by 
six  papillae,  four  of  which  were  prominent  and  sub-median;  two 
were  smaller  and  latero-median.  Anus  a  transverse  slit,  situated 
from  64  to  128  ju,  from  the  posterior  end.  Tip  of  the  tail,  with 
conical  projections,  8  to  13  /j,  in  length  by  4  //  in  breadth.  Excre- 
tory pore  0-432  to  0-520  millimetre  from  anterior  end. 

Cuticle  without  striation,  except  some  very  fine  transverse  lines 
near  the  anus.  Median  lines  visible  in  glycerine  specimens.  Lateral 
bands  rather  prominent,  with  longitudinal,  sinuous  ridges  hang- 
ing into  the  body  cavity,  and  with  longitudinal  canal  emptying 
into  excretory  pore.  (Esophagus  simple,  2-5  to  2-9  millimetres  in 
length,  triradiate  on  section.  Chyle  intestine  straight.  Rectum 
200  fj,  long.  Body-cavity  almost  completely  occupied  by  the 
intestine,  lateral  longitudinal  glands,  and  reticular  formation, 
which  is  probably  the  primordium  (Anlage)  of  the  genital  apparatus. 

(Agamofilaria)  oculi  von  Nordmann,  1832. 

Synonyms. — Filaria  oculi  humani  von  Nordmann,  1882;  E.  lentis  Diesing, 
1851. 

These  are  immature  filarial  worms,  found  in  cataracts  by  von  Nordmann, 
Gescheidt,  and  Kiihnt.  Braun  rejects  those  by  Quadri,  Fano.  Schoeler,  and 
Everbusch.  The  common  error  here  appears  to  be  to  mistake  the  remains  of 
the  hyaloid  artery  for  a  parasite.  The  worms  measured  from  0-38  millimetre 
up  to  12-6  millimetres  in  length. 

(Agamofilaria)  palpebralis  Pace,  1867,  nee  Wilson,  1844. 
This  Filaria  was  removed  from  a  tumour  in  the  upper  eyelid  of  a  boy. 

Acanthocheilonema  Cobbold,  1870. 

Filariidce  with  thin  filiform  bodies  provided  with  smooth  cuticle, 
which  is  only  striated  longitudinally.  Mouth  unarmed.  Posterior 
extremity  in  both  sexes  provided  with  two  short  conical  cut  iculai 
terminal  appendages  situate  near  the. terminal  point.  Males  with 
four  pairs  of  pre-anal  and  one  pair  of  poSt-anal  papillae  and  two 
unequal  rod-like  spicules.  Female  viviparous;  vulva  situate  in 
the  oesophageal  region.  Parasites  in  serous  cavities  of  Carnivora 
and  Primates.     Embryos  in  general  circulation. 


A  ( '.  1 NTH0CHE1L0NEMA  PERSTA  NS 


643 


Type. — Acanthocheilonema  dracunculoides  Cobbold,  1870. 
Other  species  are  A .  Persians  Manson,  1891  (A .  recondita  Grassi, 
1890;  and  A.  grassii  Noe,  1907.) 

Acanthocheilonema  perstans  Manson,  1891. 

Synonyms. — Filaria  perstans  Manson,  1891 ;  F.  sanguinis  hominis 
minor  Manson,  1891;  F.  sanguinis  hominis  perstans  Manson,  1891; 
F.  ozzardi  (variety  truncated)  Manson,  1897. 

History. — The  microfilaria  was  first  found  by  Manson  in  the 
blood  of  negroes  from  the  Congo.  Daniels  found  the  adults  in 
British  Guiana.  The  geographical  distribution  known  at  present 
is  Tropical  Africa  and  British  Guiana. 

Morphology. — The  adults  are  found,  as  a  rule,  free  in  the  con- 
nective tissue  at  the  base  of  the  mesentery,  around  the  pancreas, 
behind  the  pericardium,  and  behind  the  abdominal  aorta  and  the 
suprarenal  capsules.  The  body  is  cylindrical,  uniform,  except 
towards  both  ends,  when  it  tapers  a  little. 


Fig.  274. — Embryo  of  Acanthocheilonema  perstans  Manson. 

The  male,  rarely  met  with,  is  45  millimetres  in  length  by  o-6  milli- 
metre broad,  with  a  greatly  curved  tail,  which  ends  in  a  bifid  pro- 
longation  of  the  cuticle.  Low  describes  two  unequal  spicules  and 
four  pairs  of  pre-anal  and  one  of  post-anal  papillae,  all  of  which  are 
verv  small.     According  to  Leiper  there  are  two  pairs  of  post-anals. 

The  female  is  70  to  80  millimetres  in  length  and  0-12  millimetre 
in  breadth,  with  a  rounded  head  and  a  long  neck.  The  incurved 
tail  ends  in  two  triangular  cuticular  lobes.  The  mouth  is  simple 
and  small,  and  the  alimentary  canal  shows  no  differentiation  into 
oesophagus  or  intestine.  The  anus  opens  upon  a  papilla  0-145  milli- 
metre in  front  of  the  tip  of  the  tail.  The  uterus  is  double,  and, 
when  full  of  eggs  and  embryos  in  various  stages  of  development, 
nearly  fills  the  body.  The  vulva  is  o-6  millimetre  behind  the  anterior 
extremity. 

Life-History. — The  egg  undergoes  its  development  in  the  uterus, 
and  the  microfilaria  escapes  from  its  egg  membrane  and  appears 
in  the  peripheral  circulation  without  a  sheath,  and,  consequently, 
can  move  about  on  a  slide.  It  measures  190  to  210  [j,  in  length  and 
4'5  t°  5  /*  in  breadth.  It  is  covered  with  a  finely  striated  cuticle, 
and  has  a  retractile  spine,  situated  (apparently)  upon  a  papilla  at 
the  anterior  end  of  the  body.  The  posterior  two-thirds  of  the  body 
tapers  to  the  tip  of  the  tail,  which  is  abruptly  rounded  off. 


6-J4  NEMATHELMINTHES 

It  does  not  appear  to  have  the  central  viscus  seen  in  microfilaria 
of  F.  bancrofti.  In  stained  specimens  there  is  an  area  free  from 
nuclei  anteriorly,  a  transverse  break  at  34  jj,,  a  V-spot  at  49  yb,  and 
the  tail-spot  at  125  /u. 

A  short  type,  measuring  90  to  100  jj,,  has  been  noted.  There 
is  no  periodicity  in  its  appearance  in  the  peripheral  blood.  It 
never  occurs  in  large  numbers,  but  it  is  always  there  day  and  night. 

Many  unsuccessful  attempts  have  been  made  to  trace  its  life- 
history.  Its  larvae  are  said  to  have  been  found  in  the  thorax  in 
Panoplites  (africanus  ?),  Stegomyia  fasciata,  and  Ticniorhynchus 
fuscopennatus.  It  will  not  develop  in  a  large  number  of  blood- 
suckers— e.g.,  species  of  Anopheles,  Cnlex,  Puhx,  Pediculus,  and 
Urano  tenia.  Wellman  and  Feldham  claim  to  have  found  its 
development  in  a  tick  (Omithodoros  moubata),  as  first  suggested 
by  Christy.  According  to  Leiper,  however,  these  are  spermato- 
phores ! 

It  is  to  be  noted  that  it  only  occurs  in  areas  covered  with  dense 
forest  and  possessing  swamps,  which  indicates  that  the  host  prob- 
ably requires  shade  in  the  day  and  water  to  lay  its  eggs  in. 

Pathogenicity.— Nil. 

Dirofilaria  Railliet  and  Henry,  1911. 

Filariidae  with  very  long  filiform  body,  with  a  striated  cuticle 
unprovided  with  bosses,  mouth  unarmed,  with  six  cephalic  papillae. 
Males  with  a  spiral  tail.  Female  with  vulva  in  anterior  hundredth 
of  body.     Viviparous. 

Type.- — Dirofilaria  immitis  Leidy,  1856. 

Dirofilaria  magalhaesi  Blanchard,  1895. 

Synonyrn. — F.  bancrofti  Magalhaes,  1892,  nee  Cobbold,  1877. 

In  1887  Magalhaes  described  male  and  female  forms  of  a  Filaria 
found  by  Figeira  de  Saboia  in  the  left  ventricle  of  the  heart  of  a 
child  in  Rio  de  Janeiro. 

For  a  time  it  was  mistaken  for  F.  bancrofti,  but  in  1894  Manson 
pointed  out  that  it  was  a  different  species,  and  in  1895  Blanchard 
gave.it  the  present  name. 

Morphology.- — The  worms  were  white,  opalescent,  and  trans- 
versely striated,  the  head  club-shaped  and  simple,  mouth  terminal, 
oesophagus  with  a  bulb,  and  there  was  a  rounded  tail.  The  male 
measured  83  millimetres  in  length  and  0-28  to  0-4  millimetre  in 
breadth,  and  possessed  a  rounded  tail,  with  a  cloaca  g-ii  milli- 
metre from  its  tip,  with  two  spicules  and  four  pre-anal  and  three 
post-anal  pairs  of  papillae. 

The  female  was  155  millimetres  in  length,  and  o-6  to  o-8  milli- 
"metre  in  breadth,  with  a  vulval  opening  2-56  millimetres  behind  the 
mouth,  and  an  anal  opening  0-13  millimetre  in  front  of  the  tip  of 
the  tail. 
Lif  e-History  and  Pathogenicity.— Unknown, 


DIROFILARIA  IMMIT1S  645 

Dirofilaria  immitis  Leidy,   1856. 

This  worm  lives  in  the  right  heart  and  in  the  veins  of  the  dog,  and  also  of 
the  wolf  and  the  fox,  in  Europe  and  tropical  regions.  It  is  very  common  in 
China  and  Japan. 

Bowlby  is  commonly  reported  to  have  found  it  in  the  portal  vein,  kidneys, 
bladder,  ureters,  and  lungs  of  an  Arab,  and  also  in  a  rectal  tumour  in  a  youth, 
but  this  is  quite  erroneous,  as  he  never  made  any  such  statement,  for  the 
eggs  in  the  bladder  and  rectum,  and  the  parasites  in  the  portal  vein  of  the 
Arab,  were  Schistosoma  hcematobium,  as  he  carefully  reported,  never  mentioning 
D.  immitis.  Braun,  however,  seems  to  think  it  possible  that  this  worm  may 
occur  in  man. 

Morphology. — The  worm  is  long,  measuring  12  to  18  centimetres  by  0-7  to 
0*9  millimetre  in  the  male  and  25  to  30  centimetres  by  i-o  to  1*3  millimetres 
in  the  female,  and  filiform,  with  a  smooth  rounded  cuticle  and  a  rounded 
anterior  extremity,  on  which  is  situated  the  terminal  mouth  with  six  small 
papillae.     The  anus  is  subterminal,  and  the  posterior  extremity  pointed. 

The  male  has  a  twisted  tail  with  a  cuticular  fold  on  each  side,  and  four  pre- 
anal  and  post-anal  papillae.  In  the  female  the  vulva  is  7  millimetres  from  the 
anterior  extremity.     Viviparous. 

Life-History.— The  young  larvae,  285  to  295  [i  by  5  /u,  are  not  enclosed  in 
an  egg-case,  and  have  a  tapering  posterior  extremity.  They  appear  in  the 
peripheral  blood  particularly  at  night,  when  they  may  enter  a  mosquito  if  it 
bites  the  dog. 

They  enter  the  Malpighian  tubules  or  their  epithelial  cells,  where  they 
moult  and  grow,  eventually  passing  via  the  body  cavity  to  the  labium. 

They  escape  through  button's  membrane  on  to  the  sun  when  the 
mosquito  bites,  and  so  enter  the  dog. 

Loa  Stiles,  1905. 
Filariidse  with  bosses  on  the  cuticle  and  with  large  caudal  papillae. 
Species. — Loa  loa  Guiyot,  1778. 

Loa  loa  Guyot,  1778. 

Synonyms.— Filaria  oculi  Gervais  and  van  Beneden,  1859; 
Dracunctdus  oculi  Diesing,  i860;  D.  loa  Cobbold,  1864;  F.  subcon- 
junclivalis  Guyon,  1864. 

The  larval  names  are:—  F.  sanguinis  hominis  vox. major  Manson, 
1891;  F.  diurna  Manson,  1891. 

History.— That  a  Filaria  occurred  in  the  eye  appears  to  have  been 
known  since  the  end  of  the  sixteenth  century  in  Europe,  and  prob- 
ably in  Africa,  especially  in  Angola,  where  it  was  called  '  loa.'  That 
knowledge  must  have  been  very  ancient.  Mongin  in  1770  appears 
to  have  been  the  first  person  to  record  the  presence  of  a  worm 
in  the  eye.  Guyot,  in  1778  and  1805,  thought  it  was  a  Strongylus, 
and  used  the  term  '  loa '  for  the  first  time  in  European  literature. 
In  1891  Manson  found  a  microfilaria  in  the  blood  of  several  negroes 
from  the  Congo  which  differed  from  those  already  described,  and 
which  he  named  Filaria  diurna,  and  further  suggested  that  it 
might  be  the  larva  of  L.  loa.  Since  then  this  hypothesis  has  been 
proved  to  be  correct  by  the  observations  of  Penel,  Prout,  Henly, 
Brumpt,  Wurtz,  and  Kerr.  L.  loa  and  Microfilaria  diurna  are, 
therefore,  simply  different  stages  in  the  life- history  of  the  same 
parasite. 


646 


XEMA  THELMINTHES 


L.  loa  is  a  parasite  of  the  superficial  connective  tissue — the 
conjunctiva,  the  subcutaneous  fat,  and  the  superficial  aponeuroses 
in  all  parts  of  the  body.  It  probably  only  occurs  in  man,  for 
its  alleged  existence  in  sheep  and  goats  in  the  Cameroons  requires 
further  investigation.  Its  endemic  area  is  on  the  West  Coast  of 
Africa  from  Sierra  Leone  to  Benguela,  being  most  common  in  Old 
Calabar,  the  Cameroons,  and  the  Ogome  River.  It  is,  however, 
by  no  means  confined  to  the  coast,  for  it  is  known  to  penetrate  at 
least  600  miles  into  the  interior  of  Africa. 

The  cases  reported  from  India  are  of  doubtful  validity,  and  the 
cases  from  the  West  Indies  and  South  America  appear  to  have  all 
been  imported  from  the  West  Coast  of  Africa. 

The  parasite  appears  to  have  never  become  endemic  outside  a 
given  area,  which  means  that  the  animal  by  which  it  is  spread  has 
a  restricted  geographical  range. 

Morphology. — -The  male  is  a 
thin,  white,  almost  transparent 


A« 


a 

Fig.     275. — Loa      loa      Cobbold.       Fig.     276. — Loa      loa      Cobbold. 
Posterior   Extremity   of  the  Posterior   Extremity   of  the 

Male.  Female. 

(After  Looss.) 

worm,  with  a  body  tapering  to  each  extremity,  and  measuring 
25  to  34  millimetres  in  length  and  0-273  to  0-430  millimetre  in 
breadth.  The  head  is  like  a  truncated  cone;  the  neck  is  but 
feebly  indicated.  The  tail,  more  or  less  incurved,  has  a  rounded 
tip,  from  which  the  anus  is  distant  74  to  82  jj,.  There  are  three 
pairs  of  well-marked  pre-anal  and  two  pairs  of  post-anal  papillae, 
with  sometimes  a  little  tubercle  on  each  side  of  the  middle  line  far 
posteriorly. 

The  spicules  are  two  in  number  and  unequal,  and  are  usually 
stated  to  differ  but  little  in  length.  Penel  says  that  the  larger  is 
traversed  by  a  fine  canal,  opening  laterally  a  little  distance  from  the 
free  extremity. 

The  cuticle  consists  of  a  superficial,  thin,  translucent  layer  and 
a  deeper  perpendicularly  striated  layer.  Scattered  over  this 
cuticle  there  are  rounded  thickenings,  or  bosses,  the  smaller  being 
g  to  11  jj,  and  the  larger  14  to  16  /j,  in  height.  The  thickness  at  the 
posterior  extremity  is  variable,  as  also  is  the  constriction  correspond- 


LOA  LOA 


647 


ing  to  the  neck.  The  viscera  are  enclosed  in  a  cylindrical  musculo- 
cutaneous tube.  The  mouth  is  terminal,  small,  unarmed,  and  sur- 
rounded by  a  powerful  muscular  cone;  the  oesophagus  is  short,  and 
without  a  bulb;  the  intestine  opens  via  the  rectum  at  the  anus, 
near  the  posterior  extremity.  The  excretory  pore  is  0*65  milli- 
metre from  the  anterior  end  of  the  body. 

The  genital  apparatus  consists  of  a  tubular  testis  and  vas  deferens, 
filled  with  spherical  spermatozoa,  which  terminates  in  a  vesicula 
seminalis  situate  in  the  neighbourhood  of  the  bases  of  the  spicules. 

The  female  is  larger  and  thicker  than  the  male,  measuring  in 
the  fresh  condition  44  to  63  millimetres  (may  be  from  32  to  57  milli- 
metres in  different  conditions  of  preservation)  in  length,  and  from 
0-38  to  0-49  millimetre  in  thickness.  The  cuticle  and  anterior 
extremity  resemble  those  of  the  male. 

The  genital  system  consists  of  a  vulva  situated  on  a  little  eleva- 
tion 23  [i  in  height,  and  distant  some  2-5  millimetres  from  the 
anterior, extremity.  This  vulva  leads  into  a  thick-walled  canal- — 
the  vagina — from  which  the  two  uterine  tubes  full  of  embryos  and 
eggs  diverge, ^and  end  in  the  ovaries. 


Fig.  277. — Embryo  of  Loa  loa  Guyot. 

Life-History.— The  life-history,  unfortunately,  is  not  well  known. 
The  unsegmented  egg,  starting  in  the  uterus  with  a  length  of  32  /j, 
and  a  breadth  of  17  p,,  grows  into  40  by  25  /j,  in  the  morula  stage, 
and  50  by  25  /^  in  the  stage  when  a  twisted  and  rolled- up  embryo 
can  be  seen.  It  now  approaches  the  vulva,  and  the  embryo  unrolls 
and  elongates  itself  inside  the  egg  membrane,  which  is  now  con- 
siderably lengthened,  measuring  250  to  260  p,  in  length  by  5-5  to 
6-6  yt,  in  breadth.  The  embryo  now  escapes  from  the  mother,  and 
passes  via  the  lymph-stream  into  the  blood,  where  it  is  known  as 
Microfilaria  diurna,  and  is  noticed  to  have  increased  somewhat  in 
size,  which  Penel  considers  is  due  to  imbibition  of  fluid  by  osmosis, 
and  now  measures  298  by  7-5  p.  It  will  be  noted,  however,  that 
it  does  not  quite  fill  up  its  sheath,  which  is  generally  empty  in  front 
and  behind  for  a  short  space.  These  embryos  are  only  to  be  found 
in  the  peripheral  blood  during  the  day,  and  not  at  night,  but  they 
have  no  relation  to  sleep  in  the  host  like  M.  bancrofti,  as  they 
are  unaffected  by  altering  the  habits  of  the  host,  and  making  him 
sleep  in  the  day  and  work  at  night.  When  examined  under  the 
microscope,  they  can  be  seen  in  irregular  curves,  which  are  different 


6i8 


NEMA  THELM1NTHES 


from  the  graceful  curves  of  M.  bancrofti.  The  anterior  V-spot 
can  be  seen,  and  probably  opens  at  the  apex  to  the  exterior,  as 
Penel  has  observed  that  the  stain  penetrated  easily  at  that  spot; 
probably  there  is  also  an  opening  at  the  tail-spot.  In  stained 
specimens  the  first  8  jj,  is  clear,  without  nuclei;  at  62  ^uthe  column 
of  nuclei  is  broken  by  an  irregular  transverse  spot;  at  99  p  by  a 
triangular  spot;  at  253  ^  by  a  large  and  at  267  fj,  by  a  small  spot. 
The  last  nuclei  are  arranged  in  single  file.  One  noticeable  thing 
about  these  embryos  is  the  scarcity  with  which  they  are  met  with 
in  the  peripheral  blood  as  compared  with  those  of  F.  bancrofti. 
No  explanation  of  this  is  forthcoming  at  present. 

It  has  been  thought  by  Manson  that  the  further  stages  of  the 
life-history  will  be  found  in  a  mango-fly  (Chrysofts  dimidialus),  and 
this  has  been  shown  to  be  the  case  by  Leiper,  who  also  finds  a 
development  in  C.  silacea,  but  the  method  of  infection  of  man  is 
unknown. 

After  entering  the  human  body,  it  would  appear  probable  that 
the  worm  takes  some  three  to  four  years  to  reach  sexual  maturity, 
and  that  it  is  long-lived — i.e.,  fifteen  or  more  years.  The  reason  for 
believing  this  is  the  fact  that  immature  forms  may  be  noted  in 
children  and  the  fully  grown  worm  found  in  the  adult.  When  the 
worm  dies,  it  may  become  cretified. 

Table   showing   the   Differences   between   the    Embryos    of    Filaria 
b  ir.crofti  and  Loa  loa.     (Modified  from  Dr.  G.  C.  Low.) 


Average  length 
Average  breadth 

Break  in  cells  from  head 
V-spot  from  head 
Eggs  (average) 

Character  of  curves  in 
dried  specimens  on 
slides 

Periodicity 


Periodicity  when  habits 
of  sleeping  and  wak- 
ing changed 


Filaria  bancrofti 
Embryos. 


0-317  millimetre 

0-0084-0-0075  millime- 
tre 

0-050  millimetre 

0-090  millimetre 

0-050  X  0-033  millime- 
tre 

Spiral  coils 


In  blood  at  night  (or 
in  equal  numbers  in 
blood  by  day   and 
night,  Fiji,  etc.) 
Inverted 


Loa  loa  Embryos. 


0-245  millimetre 

0-0075-0-0070     millime- 
tre 

0-042  millimetre 

0-060  millimetre 

0-042  X  0-033    millime- 
tre 
In  wavy  lines 


In  blood  by  day 


No  change 


Pathogenicity.— It  may  be  noted  under  the  skin  of  the  finger,  the 
back,  the  breast,  the  scrotum  and  penis,  the  eyelid,  under  the 
conjunctiva,  the  mucosa  of  the  tongue.     It  moves  quickly,  and 


OtiCHOCERCINJE  649 

may  cause  itching,  creeping  sensations,  so-called  Calabar  swellings, 
irritation  of  the  eyes  and  of  the  glottis  (see  Chapter  LXXXVI1I.). 

Setaria  Viborg,  1795. 
Synonyms. — Hamularia  Treutzler,  1793;  Tentacularia  Zcder,  1800,  ncc  Bosc, 
1797. 

Definition. — Filariidts  with  chitinous  ring  (and  papillae  around  the  mouth) 
which  is  deeply  notched  laterally  and  less  so  dorsally  and  ventrally.  Tail 
in  both  sexes  with  caudal  appendages.  Parasitic  in  serous  cavities  of 
ruminants. 

Setaria  equi  Gmelin,  1789. 

Synonyms. — Gordius  equimis  Abbild,  1 789 ;  Filaria  equi  Gmelin,  1 789 ;  Hamu- 
laria lymphatica  Treutzler;  Tentacularia,  subcompressa  Zeder,  1800;  Filaria 
papulosa  Rudolphi,  1802;  F.  hominis  bronchialis  Rudolphi,  1829;  E.  hominis 
Diesing,  1851;  Strongylus  bronchialis  Cobbold,  1879. 

History. — -Setana  equi  is  frequently  found  in  horses  and  asses,  generally 
in  the  abdominal  cavity,  but  also  in  the  liver,  female  genitalia,  and  cranium. 

It  is  doubtful  whether  the  immature  FilaricB,  so  commonly  met  with  in 
horses'  eyes  in  India  and  Ceylon,  belong  to  this  species.  Railliet  has  recently 
put  forth  the  view  that  they  are  due  to  the  cattle  filaria  F.  labiato papulosa. 
Other  cases  have  been  noticed  by  Blanchard,  Brera,  and  von  Linstow. 

Morphology. — Whitish  filiform  body,  pointed  posteriorly.  Cuticle  with 
delicate  transverse  striata,  and  mouth  small,  round,  with  chitinous  ring  and 
two  lips,  and  papilliform  processes  dorsally  and  ventrally,  and  two  sub- 
median  papilla?. 

Male  6  to  8  centimetres  in  length,  with  posterior  extremity  spiral,  with 
four  pre-anal  and  four  post-anal  papillae,  and  two  unequal  spicules. 

Female  9  to  12  centimetres. 

Pathogenicity. — Nil. 

Subfamily  Onchocercin^e  Leiper,  191 1. 

Onchocerca  Diesing,  1841. 

Synonym. — -Oncocerca  Creplin,  1846. 

Filariidae  with  thick  cuticle  possessing  spiroid  thickenings.  Male 
with  always  four  pre-anal  papillae;  female  very  long,  with  vulva 
situated  anteriorly.  Viviparous.  Name  derived  from  6'yKos  ('  a 
hook  ')  and  xepxos  ('  a  tail '). 

Species. — -Onchocerca  volvulus  Leuckart,  1893. 

Other  species  are  common  in  cattle — -e.g.,  0.  gibsoni  Cleland  and 
Johnston,  191 0.  in  Australia,  0.  gutturosa  Neumann,  1910,  in  Algeria 
and  Tunis.  They  cause  onchocerciasis.  Cleland  and  Johnston 
suspect  that  0.  gibsoni  is  spread  by  lice,  especially  Hcematopinus 
vituli.  They  report  finding  a  Protozoal  parasite  somewhat  like 
a  Herpetomonas  or  a  Crithidia  in  0.  gibsoni. 

Onchocerca  volvulus  Leuckart,  1893. 
This  worm  was  discovered  by  a  German  medical  missionary  in 
two  tumours  on  the  scalp  and  chest  of  negroes  in  the  Gold  Coast 
Colony,  West  Africa.  Labadie,  Lagrave,  and  Deguy  found  another 
specimen  in  a  small  swelling  in  the  arm  of  a  soldier  from  Dahomey. 
Prout  next  described  two  cases  in  Sierra  Leone,  and  Bnunpt  a 
number  of  cases  in  his  tour  in  West  Africa,  and  Fulleborn  has 
thoroughly  studied  the  condition. 


650  NEMA  THELMINTHES 

It  is  found  in  Sierra  Leone,  Gold  Coast,  and  Dahomey;  but  on 
the  Welle,  between  Dongon  and  M'Bini,  it  is  said  to  occur  in  5  per 
cent.,  and  on  the  Itumburi,  between  Bonta  and  Idembo,  in  1  per 
cent,  of  the  population.  It  has  not  been  recorded  as  far  south  as 
the  Congo.  Theze  has  recorded  three  cases  from  Dutch  Guiana, 
and  Leiper  has  recently  confirmed  its  occurrence  in  Guatemala, 
where,  according  to  Robles,  the  infection  is  very  common, 

Morphology. — The  male  worm  has  a  white  filiform  body,  slightly 
attenuated  at  the  ends,  covered  with  a  transversely  striated  cuticle, 
measuring  30  to  35  millimetres  in  length  and  0-14  millimetre  in 
breadth. 

The  head  is  rounded,  the  mouth  unarmed,  the  alimentary  canal 
straight  and  undifferentiated,  the  anus  subterminal  0-049  milli- 
metre in  front  of  the  posterior  end.  Other  canals  are  reported, 
which  probably  belong  to  the  generative  and  extretory  systems. 

The  tail  is  strongly  recurved,  and  somewhat  flattened  on  its 
concave  aspect.  Brumpt  reports  three  pairs  of  papillae  on  each  side 
of  the  anus  and  three  pairs  of  post-anal  papillae.  There  are  two 
unequal  spicules,  the  larger  177  /u  and  the  smaller  82  p,  in  length. 


^X 


Fig.  278. — -Microfilaria  of  Onchocerca  volvulus  Leuckart. 
(After  Fiilleborn.) 

The  female  is  longer  and  thicker  than  the  male,  measuring  60  to 
70  millimetres  in  length  and  0-36  millimetre  in  breadth.  The 
cuticular  striations  are  ring-like  and  well  marked.  The  tail  is 
recurved.  The  uterus  is  seen  full  of  eggs  and  larvae,  and  the  vulva 
is  0-76  millimetre  from  the  anterior  end. 

Life-History. — -The  worm  is  said  to  lie  in  a  lymphatic,  which 
becomes  inflamed,  and  a  perilymphangitis  causes  a  condensation 
of  connective  tissue,  in  which  males  and  females  are  embedded, 
leaving  the  posterior  end  of  the  male  and  the  anterior  end  of  the 
female  free  in  the  lymph  space.  The  embryos  pass  out  of  the  uterus 
into  this  space,  where  they  can  be  found  250  to  300  [i  in  length,  and 
5  to  6  [i  in  breadth,  with  a  rounded  head  and  a  body  which  tapers 
during  the  last  fifth,  and  terminates  in  a  pointed  tail.  There  is  no 
sheath.  The  anterior  V-spot  is  clearly  seen.  The  microfilaria  have 
not  been  seen  in  the  blood,  and  their  further  development  is  quite 
unknown. 

The  embryos  have  recently  been  found  in  the  blood,  and  Brumpt 
is  inclined  to  think  that  the  further  development  will  be  in  a  tsetse- 
fly.     The  adults  live  for  years  in  the  human  body. 


DRA(  i  NCULID/E 


65i 


Pathogenicity. — Lymphangitis,  perilymphangitis,  sometimes  acute 
and  with  fever,  and  resulting  in  small  tumours,  are  their  pathological 
signs. 

Family  7.    Dracunculid^e  Leiper,  1912. 

Dracunculus  Kniphoff,  1759. 

Nematodes  with  small  males  and  long  females.  In  the  latter 
a  vagina  is  wholly  absent ;  the  embryos  being  discharged  by  rupture 
of  the  gravid  female. 

Dracunculus  medinensis  (Linnaeus,  1758). 

Synonyms. — Dracunculus  vcterum  Velsch,  1674;  Vena  medinensis 
Velsch,  1674;  Dracunculus  fersaruni  Kampfer,  1691;  Gordius  medi- 
nensis Linnaeus,  1758;  Filaria  dracunculus  Bremser,  1819;  F.cethi- 
opica  Valenciennes,  1856;  Dracunculus  medinensis  Cobbold,  1864. 

Dracuncuhts  medinensis,  commonly  called  the  guinea-worm,  the 
dracunculus,  Beinwurm,  Brachwasserwurm,  tankworm,  or  dragon- 
neau,  is  endemic  in  tropical  Africa,  India,  Persia,  Turkestan, 
Arabia,  and  some  places  in  South  America,  to  which  it  was  imported 
from  Africa. 


Fig.  279. — Dracunculus  medinensis  Linn^us. 

It  has  been  known  since  the  most  remote  periods,  and  it  was 
probably  the  fiery  serpent  mentioned  by  Moses,  who  apparently 
knew  the  method  of  twisting  the  worm  out  on  a  stick,  as  he  appears 
to  have  made  a  model  of  this  method  of  extraction.  Galen  called 
the  disease  caused  by  these  worms  dracontiasis. 

The  anatomy  of  the  worm  was  carefully  studied  by  Bastian  in 
1863,  and  the  infection  of  Cyclops  with  the  larva  was  observed  by 
Fedschenko  in  1870,  and  confirmed  later  by  Manson.  Charles 
found  a  calcified  guinea-worm  in  1892,  which  he  described  as  the 
male. 

Leiper,  1907,  has  repeated  these  experiments,  and  has  further 
proved  that  when  monkeys  arc  fed  on  infected  Cyclops  the  males 
and  females  can  be  found. 

Morphology.— The  female  is  a  long  white  filiform  worm  50  to 
80  centimetres  in  length  and  0-5  to  17  millimetres  in  diameter. 

The  anterior  end  is  bluntly  rounded,  and  carries  the  small  terminal 
mouth,  which  has  two  lips  and  two  lateral  and  four  submedian 
papillae.  It  leads  into  a  straight  alimentary  canal,  which  atrophies 
considerably  in  the  fully  developed  condition.     The  large  uterus, 


652  NEMATHELMINTHES 

which  occupies  the  whole  length  of  the  body  when  filled  with 
embryos,  evacuates  its  contents  by  a  rupture  close  to  the  mouth 
and  just  external  to  the  papillae.  The  tail  is  rounded  off,  and 
carries  a  small  bent  chitinous  hook. 

Leiper  states  that  the  male  is  only  22  millimetres  in  length,  and 
has  five  pairs  of  papillae. 

Life-History.— The  males  and  females  live  in  the  connective 
tissue  about  the  mesentery,  and  after  copulation  probably  the  males 
die  off.  When  the  female  is  gravid,  she  moves,  head  first,  appar- 
ently in  search  of  water,  usually  downwards  towards  the  leg  or 
foot;  more  rarely  she  moves  to  the  hand  or  arm,  and  very  rarely 
to  the  head.  Arrived  under  the  epidermis,  she  bores  her  way 
through  the  deep  layers,  while  a  little  bulla  on  the  surface  marks 
her  presence. 

When  this  bulla  bursts,  a  small  hole  is  seen,  at  the  bottom  of 
which  lies  the  vulva,  through  which  the  tube  of  the  uterus  has 
prolapsed,  bending  the  head  to  one  side.  Clear  fluid  can  be  seen 
escaping  from  this  tube,  which,  when  examined,  is  found  to  be  full 
of  embryos. 


Fig.  280. — Larva  of  Dracunculus  medinensis  Linn^us. 
(After  Looss,  from  Mense's  '  Tropenkrankheiten.') 

The  segmentation  of  the  egg  takes  place  in  the  uterus,  and  the 
embryos  are  born  alive.  They  are  flat,  pointed  little  bodies. 
o-6  millimetre  in  length  and  17-5  ft  in  breadth,  with  a  narrow,  very 
pointed  tail.  The  mouth  is  at  the  anterior  end,  and  leads  into  an 
alimentary  canal  with  an  anus.  There  is  a  little  sac  on  each  side 
of  the  root  of  the  tail.  According  to  Leiper,  these  little  larvae  cannot 
swim,  but  either  die  or  are  swallowed  by  a  Cyclops.  In  this  crusta- 
cean they  pass  from  the  stomach  into  the  coelom,  where  they  develop 
for  four  weeks.  Leiper  describes  the  first  ecdysis  as  taking  place 
about  the  seventh  to  ninth  day,  and  the  second  between  the  tenth 
and  eleventh  day,  after  which  progressive  histological  changes  occur. 
After  the  fourth  week  no  further  change  takes  place,  though  they 
can  live  for  forty-one  days  in  the  Cyclops.  When  placed  in  0-22  per 
cent,  solution  of  hydrochloric  acid,  the  Cyclops  is  promptly  killed, 
while  the  larva  appears  to  be  stimulated,  undergoing  ecdysis,  and 
escaping  from  the  Cyclops  by  boring  its  way  through  the  chitinous 
cuticle.  In  a  monkey  fed  with  infected  Cyclops,  three  females  and 
two  males  were  found.  It  is,  therefore,  correct  to  assume  that  man 
is  infected  by  ingesting  infected  Cyclops  with  his  drinking-water, 
and  it  is  probable  that,  set  free  in  the  stomach,  the  larvae  enter  the 
connective  tissue  by  boring  their  way  through  the  stomach-wall. 

Pathogenicity.-  The  worm  causes  dracontiasis  (see  Chapter 
LXXXVIII.). 


ASCARID/E  653 

Family  8.  Mermithid-e. 

Nematoda  with  a  diagonal  fibre  system  in  the  cuticle,  without  anus,  and 
with  six  mouth  papillae. 

The  male  has  two  spicules  and  three  rows  of  numerous  papillae 
Genus. — Mertnis  Dujardin. 

Mermis  Dujardin,  1845. 
Mermithidae  possessing  the  characters  of  the  family. 

Subgenus  (Ag-amomermis)  Stiles,  1903. 
A  purely  collective  group,  which  contains  forms  sexually  immature  and 
not  capable  of  being  definitely  placed. 

(Agamomermis)  restiformis  Leidy,  1880. 

Synonym.— Filaria  resliformis  Leidy,  1880. 

In  1880  Leidy  received  from  Woodward  a  worm  which  was  supposed  to 
have  come  from  the  urethra  of  a  man  living  in  America.  Stiles  has  re- 
examined this  specimen,  and  concludes  that  it  is  an  Agamomermis. 

The  cuticle  is  32  to  4S  /a  thick,  with  a  diagonal  fibre  system.  The  headend 
is  attenuated,  and  possesses  a  very  small  terminal  mouth  without  lips,  behind 
which  are  six  papillae.  The  excretory  pore  (?)  is  0-442  millimetre  behind  the 
mouth.  The  pharynx  is  straight,  and  opens  into  the  cylindrical  intestine, 
which  is  a  dark  caecal  structure;  but  there  is  no  anus  and  no  caudal  papilla?. 
The  tail  is  curved  ventrally  and  bluntly  rounded. 

On  one  side  of  the  oesophagus  there  is  a  blind  sac,  which  probably  represents 
the  fat  body. 

Filaria  (?)  hominis  oris  Leidy,  1850. — Perhaps  this  worm  ought  to  be 
classified  here  instead  of  under  Filaria. 

Family  9.    Ascarid^e  Cobbold,  1864. 

Definition. — Nematoda  with  three  lips,  one  median  dorsal  and 
two  submedian  ventral,  touching  one  another  in  ventral  median 
line;  oesophagus  with  a  bulb.  Male  with  (one  or)  two  spicules; 
female  with  two  ovaries.  Oviparous.  Development  believed  to 
be  direct. 

Genera.— .4 scans,  Toxascaris,  Belascaris,  and  Lagochilascaris. 

Ascaris  Linnaeus,  1758. 

Synonyms. — Stomachida  Pereboom,  1870;  Fusaria  Zeder,  icoo. 

Definition —Ascaridae  in  which  the  oral  cavity  is  surrounded  by 
three  large  lips  provided  generally  with  denticulated  borders,  one 
placed  dorsally  and  two  ventrally.  Male  with  two  equal  spicules  and 
numerous  pre-anal  and  post-anal  papillje.  Vulva  in  front  of  the 
middle  of  the  body.  Shell  of  egg  thick,  with  outer  albuminous 
layer  often  raised  into  numerous  projections. 

Species.— .4 scaris  litmbricoides,  A.  texana,  A.  maritima. 

Ascaris  lumbricoides  Linnaeus,  1758. 
Definition. — Ascaris  with  reddish-yellow  colour  in  fresh  condition. 
Oral  papillae  finely  toothed,  without  interlabia. 


654 


NEMA  THELMINTHES 


Remarks.— This  is  one  of  the  most  common  parasites  in  the  tropics. 
It  is,  however,  possible  that  other  species  escape  recognition  by  being 
casually  considered  to  be  Ascaris  lumbricoides.  It  is  usually  met 
with  in  the  small  bowel,  but  may  be  found  post  mortem  in  the 


Fig.   281. — Development  of  Ascaris  lumbricoides. 
(After  Stiles.) 


stomach,  oesophagus,  mouth,  nose,  larynx,  trachea,  or  bronchi.  It 
may  also  be  found  escaping  from  the  anus.  More  rarely  it  has  been 
seen  in  the  liver,  causing  abscesses,  in  the  pancreatic  duct,  and  in 
the  vermiform  appendix,  and  in  worm  abscesses  in  the  body-wall. 

Usually  it  gives  rise  to 
no  symptoms,  but  at 
times,  when  in  large 
numbers,  it  may  cause 
pathological  effects. 

Morphology. — It  is  yel- 
lowish in  colour,  with 
often  a  faint  trace  of  a 
reddish  tinge.  In  form 
it  is  spindle-shaped.  Male 
is  15  to  25  centimetres  in 
length  and  3  millimetres 
in  diameter.  The  pos- 
terior extremity  is  conical, 
and  bent  ventrally,  with 
two  spicules  2  millimetres 
in  length,  and  broader  at 
the  tips.  On  each  side 
of  the  cloaca  there  are 
seventy  to  seventy-five 
papillae,  of  which  seven 
pairs  are  post-anal. 
Female  is  20  to  40  centimetres  [in  f  length  by  5  millimetres  in 
bread tli.  The  vulva  is  at  the  junction  of  the  anterior  and  middle 
thirds  of  the  body. 

Life-History.— The  eggs  arc  laid  in  the  small  intestine,  and  appear 
unsegmented  in  the  faeces.  They  measure  50  to  70  p,  in  length  by 
40  to  50  n  in  breadth,  surrounded  by  a  thick  transparent  shell, 


Fig.  282. — Ascaris  lumbricoides  newly 

HATCHED. 

(Microphotograph.  by  J.   J.  Bell.) 


ASCARIS  LUMBRICOIDES  655 

which  has  an  externally  irregular  coating  of  albumin,  which  is 
stained  brownish-yellow  by  the  stercobilin  of  the  fseces.  These  eggs 
can  stand  alteration  in  temperature  and  moisture.  In  warm,  moist 
earth  the  embryo  appears  in  about  a  month  in  the  form  of  a  spiral 
roll,  but  does  not  hatch  until  it  reaches  the  interior  of  man,  when  it 
develops  into  an  adult,  as  was  shown  by  the  experiments  of  Davaine, 
Grassi,  Calandruccio,  Liitz,  and  Epstein. 

Leuckart  and  von  Linstow  believed  that  an  intermediate  host  was 
necessary.  Stewart  has  shown  that  the  larval  forms  after  hatching 
from  the  eggs  pass  into  the  liver  and  thence  by  the  blood-stream  to 
the  lungs,  whence  they  reach  the  stomach  by  migrating  up  the 
bronchii  and  trachea. 

Stiles  found  that  the  house-fly  could  carry  the  egg,  which  passed 
through  its  alimentary  canal  unaltered.  The  worm  matures,  and 
deposits  ova  in  one  month  from  entering  the  body. 

Pathogenicity. — -It  is  only  pathogenic  in  large  numbers,  or  when 
it  invades  the  liver,  causing  abscess,  or  the  appendix,  causing 
appendicitis.  The  larvse  in  the  lungs  apparently  cause  bronchitic 
symptoms. 

Animals. — Monkeys,  dogs,  and  perhaps  pigs. 

Ascaris  (?)  maritima  Leuckart,  1876. 
An  immature  worm,  possibly  accidentally  swallowed  in  food,  was 
vomited  by  a  child  in  North  Greenland  in  1865,  and  was  supposed 
to  be  an  immature  female  Ascaris. 

Ascaris  (?)  texana  Smith  and  Goethe,  1904. 

Stiles  appears  very  doubtful  as  to  whether  this  worm  is  an 
Ascaris.  The  female  only  is  known,  measuring  58  to  60  millimetres 
in  length.    Uterine  eggs  60  by  40^.    It  was  found  in  a  man  in  Texas. 

Toxascaris  Leiper,  1907. 

Definition. — Ascarida?  with  the  anterior  end  of  the  body  bent 
dorsally,  cuticle  finely  striated,  oesophagus  simple,  without  a  bulbous 
portion.  Palpi  of  lips  club-shaped.  Male  with  a  tapering,  acicular 
tail,  and  without  ventral  protuberance  behind  anus.  Six  pairs  of 
post-anal  papilhe  in  two  groups,  the  ventral  pairs  continuous,  with 
a  pre-anal  row  on  each  side  of  the  body,  and  three  lateral  pairs  on 
the  outer  aspect  of  the  tail.  Testis  lies  in  the  anterior  part  of  the 
posterior  half  of  the  body.  Seminal  vesicle  long  and  tubular. 
Ejaculatory  duct  short.  Female  with  vulva  about  the  centre  of 
the  body.     Egg  oval  and  smooth. 

Species. — Of  the  species  belonging  to  this  genus,  only  one, 
Toxascaris  canis  Werner,  1782,  is  known  in  man. 

Toxascaris  canis  Werner,  1782. 

Synonyms. — Luntbricus  canis  Werner,  1782;  Ascaris  canis  Gmelin, 
1789;  A.  marginata  Rudolphi,  1802;  Toxascaris  limiuila  Railliet 
and  Henry,  1911. 


656  NEMATHELMINTHES 

Remarks. — Toxascctris  canis  is  the  common  A  scans  of  dogs,  which 
used  to  be  called  A .  canis,  but  recently  Leiper,  when  examining  a 
number  of  specimens  of  ,4 .  lumbricoides  in  Egypt,  found  among  them 
several  smaller  and  apparently  younger  forms.  On  examining  these 
he  found  that  they  had  winged  expansions  on  either  side  of  the  head, 
which  indicated  that  they  were  not  A.  lumbricoides.  On  further 
examination  they  proved  to  be  the  same  species  as  that  found  in 
dogs,  but  differed  from  that  found  in  cats.  Up  to  that  time  A .  canis 
in  the  dog  and  A .  mystax  in  the  cat  were  supposed  to  be  identical. 
Finally,  on  careful  anatomical  examination,  it  was  found  that  the 
two  not  merely  differed  considerably  from  one  another,  but  also 
from  A.  lumbricoides.  He  therefore  formed  two  new  genera — 
Toxascaris  and  Belascaris.  So  far,  Toxascaris  has  only  been 
recorded  once  in  man. 

Morphology. — -Body  white  or  reddish,  head  curved  dorsally,  with 
two  membranous  lateral  expanisons,  broader  behind  than  in  front. 
Male  5  to  10  centimetres  in  length,  with  curved  tail,  possessing  two 
small  lateral  membranous  wings  and  twenty-six  papillae.  Female 
9  to  12  centimetres  in  length,  with  an  obtuse  tail.  Eggs  75  to  80  {i 
in  diameter. 

Life-History. — -Development  is  similar  to  A.  lumbricoides. 

Pathogenicity. — It  often  causes  intestinal  and  nerve  symptoms  in 
dogs.  Post  mortem  the  mucosa  of  the  intestine  is  tumefied  and 
catarrhal. 

Belascaris  Leiper,  1907. 

Definition.— Ascaridae  with  the  anterior  end  of  the  body  bent 
ventrally,  cuticle  coarsely  striated,  oesophagus  with  a  distinct 
bulbous  portion.  Male  with  a  probular  tail — i.e.,  like  a  closed  fist, 
with  forefinger  semi-extended.  Immediately  behind  the  anus  there 
is  a  protuberance,  with  a  pair  of  papillse.  On  the  tail  there  are 
two  ventral  and  two  lateral  pairs  of  papillae,  the  tips  of  which 
support  a  slight  expansion  of  the  cuticle.  The  testis  is  situate  in 
the  anterior  half  of  the  body.  The  vesicula  seminalis  is  remarkably 
long,  and  there  is  a  short  ejaculatory  duct.  Female  with  vulva 
situated  in  the  anterior  part  of  the  body.  Egg  with  a  honey- 
combed shell. 

Type. — Belascaris  cati  Schrank,  1788. 

Belascaris  cati  Schrank,  1788. 

Synonyms. — Fusaria  mystax  Zeder,  1800;  Ascaris  alata  Belling- 
ham,  1839. 

This  Ascaris  is  common  in  cats,  and  has  been  recorded  nine  times 
in  man. 

Morphology. — -Head  curved  ventrally,  with  two  membranous 
lateral  expansions.  Male  4  to  6  centimetres  in  length;  female 
4  to  10  centimetres  in  length. 

Life-History. — Similar  to  A.  lumbricoides. 

Pathogenicity. — It  rarely  causes  any  symptoms. 


OXYURIDM  657 

Genus  Lagochilascaris  Leiper,  1909. 

Definition. — Ascarida  with  dense  cuticular  lips  and  interlabia 
surrounded  by  a  ridge  and  furrow,  separating  the  lips  from  the  rest 
of  the  body.  (Esophagus  simple.  Shallow  ledge-like  cuticular  alae 
extend  along  either  side  of  the  body  to  near  the  tail.     Eggs  mosaic. 

Type  Species. — Lagochilascaris,  major  Leiper,  1909,  in  the  lion. 

Lagochilascaris  minor  Leiper,  1910. 

This  species  has  been  found  in  the  pus  of  subcutaneous  abscess 
in  man  in  Trinidad. 

Morphology. — Males  9  millimetres  in  length  by  0-5  millimetre 
in  breadth,  with  bent  posterior  part  of  body.  Female  15  millimetres 
in  length,  straight  posteriorly.  The  vulva,  with  two  projecting  lips, 
opens  6  millimetres  from  the  anterior  end. 

Hosts. — Possibly  one  of  the  Carnivora.     Man  is  an  accidental  host. 

Habitat. — Probably  intestinal  in  its  normal  host.  The  specimens 
were  found  in  abscesses  under  the  skin  in  man.  An  allied  species, 
A.  major,  occurs  in  the  intestine  of  the  lion  in  East  Africa. 

Family  10.    Oxyurid^e  Dujardin. 

Genus  Oxyuris  Rudolphi,  1803. 

Definition.— Nematoda  in  which  the  three  labial  papillae  are  not 

very  distinct.     (Esophagus  long,  with  a  double  dilatation.     Skin 

markedly  striated.     Male  with  curved  posterior  end,  one  spicule, 

and  two  pairs  of  pre-anal  papille.     Female  with  straight  posterior 

end,  which  tapers  to  a  point.     Vulva  in  the  anterior  part  of  the  body. 

Type. — Oxyuris  vermicularis  Linnaeus,  1767. 

Oxyuris  vermicularis  Linnaeus,  1767. 

Synonyms.- — Ascaris  vermicularis  Linnaeus,  1767;  Fusiaria  ver- 
micularis Zeder,  1803. 

Remarks. — Oxvuris  vermicularis  is  the  pin  or  thread  worm,  and 
occurs,  as  far  as  is  known,  only  in  man  and  all  over  the  world.  It 
is  believed  to  live  in  the  lower  part  of  the  small  intestine  at  first, 
and  then  the  gravid  females  travel  to  the  large  bowel.  It  has  been 
known  from  the  earliest  times. 

Morphology.— It  is  a  minute  white  round  worm,  with  transversally 
striated  cuticle,  which  forms  two  ridges  along  the  ventral  and  dorsal 
surfaces  corresponding  to  the  lateral  ridges. 

Male  is  3  to  5  millimetres  in  length,  with  a  spirally  rolled  posterior 
extremity,  with  one  spicule  and  six  papillae.  Female  is  10  milli- 
metres in  length  and  o-6  millimetre  in  breadth,  with  a  long  pointed 
tail. 

Life-History. — The  egg,  when  deposited  from  the  uterus,  measures 
50  to  52  [a  by  16  to  24  p.  with  a  thin  shell  and  a  fairly  well-developed 
embryo.  The  dorsal  surface  of  the  egg  is  more  convex  than  the 
ventral.     These  eggs  escape  in  the  faeces.     They  are  then  reintro- 

4^ 


Fig.  283. — Oxyuris  vermicularis  Fig.  2S4. — Oxyuris  vermicular  is 

(Linnjeus,   1767):     Male.  (Linnaeus,   1767):     Female. 

(From  a  photograph  by  J-   J«  Bell.) 


Fig.  285. — Oxyuris  vermicularis 

(LiNNiEUS,  1767):     Head. 

(From  a  photograph  by  J.J.  Bell.) 


Fig.  286. — Oxyuris  vermicularis. 
The  male  is  to  the  left,  the  female 

to  the  right. 

(After  Claus.) 


DIVISION  BURS  ATA  659 

duced  into  the  mouth  or  nose  by  self-infection,  fruits,  vegetables, 

etc.,  hatch,  and  grow  in  the  small  intestine  into  male  and  females. 

After  fertilization  the  males  die  off  and  the  females  travel  into 

the  caecum,  and  later  into  the  colon,  and  have  a  great  tendency  to 


Fig.  287. — -Development  of  Oxyuris  vermicularis 
(After  Leuckart,  from  Stiles.) 

wander  through  the  anus  to  the  outside.     The  duration  of  life  of 
0.  vermicularis  in  the  human  body  is  not  known. 

Pathogenicity. — In  large  numbers  may  set  up  enterocolitis;  in 
small  numbers  it  causes  only  irritation. 

DIVISION  BURSATA. 

Definition. — Nematoda  with  true  cuticular  bursa  in  the  male. 
Classification. — Leiper  gives  the  following  table  for  the  differentia- 
tion of  the  various  bursate  families  represented  by  species  in  man :  — 

A.  Mouth  with  simple  pore ;  no  buccal  capsule : — 

(a)  Male  with   large  bursa   and   elongated  rays;    female 

oviparous,  uteri  divergent,  oviject or s present.     Intes- 
tinal parasites — Trichoslrongylidce. 

(b)  Male  with  short  bursa  and  stunted  rays;  female  ovip- 

arous,   uteri   convergent,    ovijectors   absent.     Lung 
parasites     Metastrongylidce. 

B.  Mouth  a  simple  opening,  leading  into  a  large  buccal  capsule 

guarded  by  chitinous  structures: — 
(a)  Mouth  capsule  bent  dorsally  and  guarded  by  paired 
bilaterally  arranged  plates — Ancylostomidee. 
Plates  with  smooth  edge — Necator. 
Plates  with  toothed  edge — Ancylostoma. 
(h)   Mouth  capsule  terminal  guarded  by  ring  of  setae — 
Strongylidce. 

BURSATA. 

Family  ii.    Strongylid^:  Cobbold,  1864. 

Nematoda  with  cylindroid,  rarely  filiform  bodies,  mouth  usually 
with  wide  buccal  capsule,  with  ring  of  chitinous  armature,  and  an 
(esophagus  more  or  less  enlarged  posteriorly.  Male  with  a  bursa 
copulatrix  and  two  equal  spicules.  Female  with  two  ovaries; 
vulva  situated  medially  or  posteriorly.  As  a  rule,  the  specie^  are 
small.     Oviparous. 

Type  Genus.— Strongylus  Mueller,  1780 . 

Other  Genera.— Triodontophorus  Looss,  190 1;  Uisophagostoinuni 
Molin,  i860. 


660  XEMATHELMINTHES 

Triodontophorus  Looss,  1901. 

Synonyms. — Triodontus  Looss,  1901,  nee  Westwood,  1845 ;  Terni- 
dens  Railliet  and  Henry,  1909. 

Strongylidee  with  small,  almost  spherical,  thick-walled  oral 
cavity,  arising  from  the  floor  of  which  three  teeth  are  found,  each 
of  which  consists  of  two  surfaces  joined  together  at  an  acute  angle. 
Male  bursa  is  finely  serrated  at  the  edge.  The  female  genital  orifice 
is  situate  a  short  distance  in  front  of  the  tip  of  the  tail. 

Found  in  horses  and  men. 

Triodontophorus  deminutus  Railliet  and  Henry,  1905. 

Synonym.- — Ternidens  deminutus  (Railliet  and  Henry,  1905). 

Railliet  and  Henry  in  1905  discovered  that  a  male  and  female 
parasite  presented  in  1865  by  Monestier  to  the  Paris  Natural 
History  Museum,  and  collected  post-mortem  from  an  American 
negro  who  died  in  Mayotte,  were  not  ankylostomes,  but  belonged 
to  Looss's  genus  Triodontophorus.  They  named  them  deminutus 
because  of  their  small  size.  Leiper  also  met  with  some  specimens 
of  the  same  species  collected  in  Nyassaland  and  Lorenco  Marques. 
It  has  now  been  recorded  in  a  number  of  cases.  It  is  also  found  in 
monkeys.     Their  normal  habitat  is  the  large  intestine. 

Morphology. — To  the  naked  eye  their  size  and  general  appearance  resemble 
those  of  ankylostomes.  The  body  is  white,  cylindrical,  tapering  towards 
the  end.  Cuticle  transversely  striated,  and  forms  an  overhanging  transverse 
fold  across  the  ventral  surface  of  the  body  at  the  level  of  the  excretory  pore. 

The  mouth-collar  is  moderately  developed,  with  a  depth  of  0*04  millimetre. 
The  anterior  surface  carries  four  small  knob-like  submedian  papillae,  and  the 
edge  surrounds  the  entrance  to  the  mouth  with  a  double  series  of  delicate 
fringes  composed  of  cuticle.  These  two  rows  constitute  the  external  and 
internal  crowns  of  the  corona  radiata. 

The  buccal  capsule  is  a  barrel-shaped  chitinous  structure,  capped  and 
covered  in  by  the  mouth-collar  and  the  corona  radiata.  Posteriorly  it  touches 
the  dilated  end  of  the  oesophagus,  whose  chitinous  lining  expands  into  a 
funnel,  uniting  with  the  cuticle  on  the  outside  of  the  oesophagus,  and  coming 
near  the  cuticle  of  the  buccal  cavity.  It  shows  three  cuticular  edges  project- 
ing into  the  lumen,  which  are  continued  forwards  as  three  stout  chitinous 
prongs  or  teeth,  one  dorsal  and  two  ventral.  The  characters  of  these  teeth 
are  specifically  important.  They  are  formed  of  two  plates  curved  longi- 
tudinally, and  meet  to  form  a  keel.  The  oesophagus  is  muscular,  o«8  milli- 
metre long,  with  three  fleshy  valves  guarding  its  entrance  into  the  chyle 
intestine.  The  rectum  is  short,  and  ends  in  the  anus,  which  is  0*24  millimetre 
from  the  tip  of  the  tail.  The  excretory  system  opens  on  the  ventral  surface 
halfway  between  the  posterior  limit  of  the  buccal  cavity  and  the  nerve  ring. 

The  male  is  9-5  millimetres  long  by  0-56  millimetre  in  breadth,  with  a 
spicule  0-9  millimetre  long.  Female  is  14  to  16  millimetres  in  length,  and 
0-73  millimetre  in  breadth,  with  a  tapering  posterior  extremity.  The  vulva 
is  nearly  0-48  millimetre  from  the  hinder  end.  The  vagina  is  short,  and  opens 
into  two  uterine  tubules.  The  uterine  eggs  are  60  to  80  [i  by  40  yi,  with  a 
delicate  shell  and  often  a  morula. 

Life-History  and  Pathogenicity.-    Unknown. 


OSSOPHA  GOSTOM  UM  661 

GEsophagostomum  Molin,  1861. 

Strongylidae  in  which  the  mouth  is  small  and  circular,  with  a 
chitinous  ring,  which  carries  a  fold  and  six  papillae.  There  is  a 
marked  swelling  just  behind  the  anterior  extremity.  Male  bursa 
with  two  equal  spicules;  female  with  two  ovaries,  and  the  vulva 
opening  situate  near  the  anus. 

Type  Species.— CE.  subulatum^lolm,  1861 ;  CE .  dentatnm  (Rudolphi, 
1803). 

Species. — 'Esophagostomum  apiostomum  and  CE.  stephanostomum, 
var.  thomasi  Railliet  and  Henry,  1909,  are  known  in  man,  but  other 
species  are  found  in  the  gorilla,  chimpanzee,  and  other  monkeys. 

(Esophagostomum  apiostomum  Willach. 

Synonym. — -(Esophagostomum  brumpti  Railliet  and  Henry,  1905. 

This  worm  was  found  by  Brumpt  in  cyst-like  nodules  in  the  caecum 
and  colon  of  a  negro  on  the  Omo  River,  near  Rudolph's  Sea  in  East 
Africa.     Found  also  in  monkeys. 

According  to  Leiper,  this  parasite  occurs  in  5  per  cent,  of  the 
natives  of  Northern  Nigeria. 

Morphology. — Female  8-5  to  10-2  millimetres  long  by  0-295  to  0-325  milli- 
metre broad,  white  and  cylindrical,  tapering  towards  the  posterior  end, 
Cuticle  transversely  striated.  There  is  a  distension  behind  the  oral  cavity 
which  is  formed  of  a  cuticular  band  with  a  crown  with  twelve  spines;  on  the 
front  and  inner  side  lamella?;  six  head  papillae  (two  lateral,  four  submedian). 
Posterior  end  rounded  off  with  three  broad  undulations. 

Life-History.— Outside  the  body  similar  to  that  of  the  Anky- 
lostomes. 

Pathogenicity. — The  young  form  cyst -like  nodules  in  the  large 
intestine. 

(Esophagostomum  stephanostomum  var.  thomasi  Railliet  and 

Henry,  1909. 

This  species  was  found  by  Wolferston  Thomas  in  tumours, 
numbering  187,  in  the  large  and  small  intestines  of  a  man  in  Brazil. 
The  tumours  were  in  some  instances -large  enough  to  diminish  the 
lumen  of  the  bowel.  Each  tumour  contained  a  male  and  a  female 
worm.  The  species  CE.  stephanostomum  Stossich,  1904,  was  found 
in  the  large  intestine  of  the  gorilla,  and  a  variety  (E .  stephanostomum 
var.  dentigera  Railliet  and  Henry,  1909,  is  foundin  the  chimpanzee. 

Morphology. — Body  cylindrical,  thick,  only  attenuated  towards  the  ex- 
tremities. Buccal  capsule  with  an  external  crown  of  38  lamellae.  Male 
17  to  22  millimetres  in  length  and  0-75  millimetre  broad.  Bursa  thick  at 
the  sides,  with  one  spicule  1-38  to  1-475  millimetres  long.  Female  16  to  20 
millimetres  long  by  0-9  millimetre  broad.  Vulva  in  front  of  the  anus,  0-5  to 
0-525  millimetre  from  the  posterior  end. 

Life-History. — Not  known. 

Pathogenicity.- — Forms  tumours  in  the  wall  of  the  small  and 
large  intestines. 


662  NEMATHELMINTHES 

Family  12 :  Metastrongylid.e:  Leiper,  1912. 

Nematoda  with  simple  mouth,  very  small  cavity,  and  not  enlarged 
to  form  a  buccal  capsule,  and  a  bursa  in  the  male  with  true  but 
stunted  rays.     Two  spicules. 

This  family  includes  a  number  of  genera,  parasitic  in  the  lungs  of 
domesticated  animals. 

Metastrongylinse  Leiper,  1908. 

Metastrongylus  Molin,  1861. 

Metastrongylidae  with  mouth  surrounded  by  six  small  papillae.  Male  with 
a  bursa  copulatrix  and  two  spicules.  Female  with  two  ovaries  and  a  tapering 
posterior  end;  vulva  situate  in  the  hinder  half  of  the  body.  Embryos  without 
teeth,  and  with  slightly  developed  oesophageal  bulb. 

Metastrongylus  apri  Gmelin,  1789. 

Synonyms. — Gordius  pulmonalis  apri  Ebel,  1777;  Ascaris  apri  Gmelin,  1789; 
Strongylus  suis  Rudolphi,  1809;  S.  paradoxus  Mehlis,  1831;  S.  elongatus  Du- 
jardin,  1845;  S.  longevaginatits  Diesing,  1851. 

Metastrongylus  apri  is  not  uncommonly  found  in  the  bronchial  tubes  of  pigs 
in  Germany  (60  per  cent.  Berlin,  15  to  52  per  cent.  Leipzig);  occasionally  it 
infects  other  animals,  including  man.  Filaria  tracheal  is  Rainey,  1855,  found 
by  Rainey  and  by  Bristowe,  may  be  infection  of  man  with  this  parasite. 
Diesing  recognized  the  worm  in  the  lung  of  a  boy  aged  six  in  Klausenberg  in 
1845.  It  is  said  to  also  occur  in  the  intestine,  but  this  is  looked  upon  as 
accidental,  as  its  usual  habitat  is  the  lung,  where  it  may  cause  pneumonia  and 
bronchitis. 

Morphology. — Bod y  relatively  short;  colour,  white  or  brown;  mouth  with 
six  lips,  of  which  the  two  lateral  are  the  largest.  Male:  12  to  25  millimetres 
in  length,  with  bilobed  bursa  -with  five  ribs  in  each  lobe,  and  thin  spicules 
about  4  millimetres  in  length.  Female:  20  to  40  millimetres  in  length,  with  a 
curved  posterior  end,  close  in  front  of  which  is  the  anus,  while  the  vulva  opens 
on  a  papilla  just  in  front  of  this.  Eggs  elliptical,  50  to  100  /x  by  39  to  72  /x; 
when  oviposited,  they  already  contain  an  embryo. 

Life-History. — Only  the  embryonic  and  larval  development  appear  to  have 
been  studied.  From  analogy  with  Ankylostoma  a  skin  infection  would  be 
presumed  nowadays,  and,  further,  the  fact  that  the  worms  have  been  noted 
in  the  alimentary  canal  bears  quite  a  different  significance  from  what  it  did 
'years  ago,  as  it  may  be  natural  for  the  worms  at  times  to  travel  from  the  lungs 
to  the  bowel  like  the  Ankylostoma.  It  is  interesting  to  note  that  Leuckart 
failed  to  infect  sheep  by  feeding  them  with  bronchial  mucus  full  of  embryos. 

Pathogenicity. — This  subject  has  recently  been  studied  by  Santiocchi,  and 
consists  essentially  of  bronchitis,  broncho-pneumonia,  and  pneumonia. 

Family  13:   Trichostrongylid^e  Leiper,  1912. 

Nematoda  with  filiform  bodies;  cuticle  markedly  striated  trans- 
versely or  longitudinally;  mouth  without  buccal  capsule  or  tooth 
armature;  bursa  large,  with  well-developed  rays;  genital  pore  in 
posterior  half  of  body;  ovijectors  present;  oviparous.  Intestinal 
parasites. 

NematOdirus  Ransom,  1907. 

Trichostrongylidae  with  bursa  provided  with  double  ventral  median  ribs, 
two  dorsal  ribs,  spicules  long  and  filiform,  without  accessory  piece.  Head 
50  microns  in  diameter;  cuticle  with  eighteen  distinct  longitudinal  ridges. 
Cervical  papillae  absent. 


HMMONCHUS  663 

Type  Species. — Nematodirus  filicollis  Rudolphi,  1802. 

Remarks. — The  subgenus  Mecistocirrus  Railliet,  1912,  with  distinct  cervical 
papillae  and  cuticular  ridges  little  apparent,  contains  the  human  parasite. 

Mecistocirrus  fordi  Daniels,  1908. 

Synonym. — Nematodirus  gibsoni  Stephens,  1909. 

This  worm  was  discovered  by  Bell  in  the  faeces  of  a  Chinaman  in  Hong 
Kong,  and  described  by  Stephens. 

Morphology. — The  male  measures  21  millimetres  by  0-4  millimetre,  and 
possesses  an  attenuated  head  with  two  cervical  papillae,  and  a  mouth  with 
two  lateral  papillae.  The  bursa  shows  two  well-marked  lobes,  continued 
dorsally  on  to  the  body  as  a  V-shaped  slit.  There  is  one  pair  of  ventral  rays 
and  six  pairs  of  dorsal  rays — an  anterior,  two  middle,  and  two  posterior, 
which  last  arise  from  a  common  stem.  The  spicules  are  very  long  (7  milli- 
metres) and  delicate. 

The  female  measures  25  millimetres  long,  and  possesses  a  pointed  tail,  on 
which  the  anus  opens  0*2  millimetre  from  the  tip,  while  the  genital  pore  is 
0-5  millimetre  from  the  same  extremity.  The  uterine  egg  measures  110  [a 
by  53  H- 

Life-History. — Nothing  is  known  as  to  the  life-history. 

Pathogenicity. —  It  is  not  stated  whether  it  is  01  is  not  pathogenic. 

Hseraonchus  Cobb,  1898. 

Synonyms. — Hcentonchus  Stiles,  1903 ;  Strongyles  O.  F.  Miiller,  pro 
parte. 

Strongylidae  with  unarmed  mouth.  Male  bursa  trilobed.  with 
median  lobe  asymmetrical,  spicules  short  with  an  accessory  piece; 
female  with  vulva  situate  posteriorly  and  protected  by  some  tegu- 
mentary  appendages. 

Type  Species. — Hcentonchus  contortus  Rudolphi,  18c  3. 

Hsemonchus  contortus  Rudolphi,  1803. 

Synonyms.— S^o«gy/«s  contortus  Rudolphi,  1803;  5.  filicollis 
Molin,  1861;  S.  placet  Place,  1893. 

This  worm  was  found  by  de  Magalhaes  in  a  case  of  anaemia  sup- 
posed to  be  due  to  Ankylostorna  duodenale,  and  from  which  the 
specimens  were  obtained  by  treatment  with  thymol,  after  which 
treatment  the  patient  rapidly  recovered. 

Morphology. — Body  red  or  white,  filiform,  with  attenuated  extremities 
Anterior  extremity  with  two  cervical  papillae  in  the  form  of  teeth  directed, 
backwards.  Cuticle  finely  striated.  Male:  10  to  20  millimetres  in  length, 
with  bursa  provided  with  two  lobes,  of  which  the  right  carries  an  asymmetrical 
median  lobe.  The  two  spicules  measure  0*3  to  0-5  millimetre  in  length,  and 
are  each  furnished  with  an  accessory  portion.  Female:  20  to  30  millimetres 
in  length,  with  caudal  extremity  pointed.  Vulva  situated  in  the  posterior 
fifth  of  the  body.     Eggs  are  ellipsoidal,  70  to  95  fx  long  by  43  to  54  /x  broad. 

Life-History.— The  eggs  quickly  develop  when  placed  in  pure  or 
muddy  water,  producing  rhabdite  embryos;  the  latter  undergo 
ecdysis. 

Habitat. — -The  intestine  of  the  goat,  sheep,  etc. 

Pathogenicity. — Produces  anaemia,  resembling  that  of  ankylo- 
stomiasis, and  has  a  haemolytic  toxin. 


664  NEMATHELMINTHES 

Trichostrongylus  Looss,  1905. 

Trichostrongylidae  with  body  tapering  gradually  from  the  genital 
opening  anteriorly.  Head  with  three  small  lips  and  blunt  or 
pointed  papillae,  without  cuticular  protuberances  or  neck  papillae. 
Cuticle  transversely  striated;  oesophagus  long.  Male  with  the 
bursa  closed  round  by  large  side-flaps,  without  evident  median 
folds;  spicules  spoon-like,  with  a  boat-shaped  accessory  piece. 
Female  with  the  genital  opening  in  the  posterior  half  of  the  body. 
Tail  short,  with  two  small  papillae  near  the  tip.     Egg  thin-shelled. 

Type  Species. —  Trichostrongylus  retortceformis  Zeder. 

Four  species  of  interest  in  tropical  pathology :  Trichostrongylus 
colubriformis,  T.  probolurus,  T.  vitrinus,  and  T.  orientalis. 

Trichostrongylus  colubriformis  Giles,  1892. 

Synonyms. — Strongyles  colubriformis  Giles,  1892;  S.  instabilis 
Railliet,  1893;  5.  subtilis  Looss,  1895. 

This  species  was  found  by  Looss  in  post-mortems  on  fellahs  in 
Alexandria  and  Cairo,  and  also  by  Ijima  in  a  woman  in  Japan.  In 
man,  however,  it  is  only  an  accidental  parasite,  being  usually  found 
in  the  duodenum,  rarely  in  the  stomach,  of  sheep,  antelopes,  drome- 
daries in  Egypt,  monkeys  in  North  America,  and  sheep  in  India. 

Morphology. — Male  4  to  5  millimetres  in  length,  and  0-08  milli- 
metre in  thickness  just  in  front  of  the  bursa.  Spicule  135  to  145  p 
in  length,  and  the  accessory  portion  70  /j,  in  length,  with  a  long 
muscular  oesophagus.  Bursa  with  two  lateral  semicircular  wings 
connected  by  a  cross-bridge.  Ribs  arranged  asymmetrically. 
Female  5  to  6  millimetres  in  length,  and  about  0-09  millimetre  in 
breadth.  Posterior  extremity  tapers  to  a  pointed  tail,  in  front  of 
which  the  anus  is  situated,  0-055  to  0-07  millimetre,  and  the  vulva 
1-05  to  i-2  millimetres.  Eggs  72  to  80  fjb  by  40  to  43  ji;  when 
oviposited,  generally  contain  eight  to  twelve  celled  embryo. 

Life-History.- — -Resembles  that  of  Ancylostoma  duodenale  outside 
the  body,  according  to  Leiper. 

Pathogenicity. — -Believed  to  be  unimportant. 

Trichostrongylus  orientalis. 

Synonym. — Triclwslrongylus  subtilis  Looss,  1895. 

Trichostrongylus  eggs  nave  recently  been  found  in  the  faea>  of 
a  considerable  percentage  of  the  agricultural  population  of  certain 
districts  in  Japan,  and  is  probably  the  same  as  that  recorded  pre- 
viously from  Japan  by  Ijima  and  Looss  as  Trichostrongylus  subtilis 
(vide  T.  colubriformis,  supra).  This  species  differs  slightly  in  details 
of  ray-disposition  in  the  bursa  and  in  configuration  of  the  spicules. 

Trichostrongylus  probolurus  Railliet,  1896. 

Synonym. — Strongylus  probolurus  Railliet,  1896. 
This  parasite  lives  in  the  duodenum  of  sheep,   antelopes,   and 
dromedaries  in  Egypt,  and  has  also  been  found  in  man  in  Egypt. 


TRICHOSTKOAGYLUS  665 

Morphology. — Male  4-5  to  5-5  millimetres  in  length,  0-08  milli- 
metre in  breadth  just  in  front  of  the  bursa.  Spicule  126  to  134  /x, 
accessory  piece  75  to  80  /j,  in  length. 

Female  4-5  to  6  millimetres  in  length,  anus  0-04  to  0-05  milli- 
metre, and  vulva  1-08  to  1-25  millimetres  in  front  of  the  tip  of  the 
tail,  which  is  short.     Egg  76  to  80  /*  by  43  to  46  jj,. 

Life-History. — -This  is  unknown. 

Pathogenicity. — -Believed  to  be  unimportant. 

Trichostrongylus  vitrinus  Looss,  1905. 

T.  vitrinus  is  found  in  the  duodenum  of  sheep  and  dromedaries, 
and  also  in  man  in  Egypt. 

Male  4  to  5-5  millimetres  in  length  by  0-085  millimetre  in  breadth 
in  front  of  the  bursa,  which  is  larger  than  in  the  other  two  species. 
Spicule  160  to  170  fi  accessory  piece  85  to  95  jli  in  length. 

Female  5  to  6-5  millimetres  long;  vulva  1-15  to  1-25  millimetres 
in  front  of  the  tip  of  the  tail;  egg  84  to  90  tu  by  46  to  50  jjl. 

Life-History. — This  is  not  known. 

Pathogenicity. — Believed  to  be  unimportant. 


Family  14:   Ancylostomid^e  Looss,  1911. 

Strongyles  with  armed  mouth  and  bursa  copulatrix  provided 
with  ribs. 

Subfamilies.- — -Ancylostominae  and  Bunostominse. 

Subfamily  Ancylostomin^e  Looss,  1911. 

Ankylostomidae  with  more  or  less  funnel-shaped  mouth  capsule, 
its  walls  on  the  ventral  side,  and,  especially  towards  the  anterior 
edge,  provided  on  each  side  with  two  longitudinal  thickenings 
projecting  outwards  like  ridges.  In  the  gutter-like  depressions 
between  the  ridges  lie  the  terminations  of  the  dorsal  and  lateral 
papillary  nerves.  Floor  of  the  mouth  cavity  with  one  pair  of 
inner  ventral  teeth,  otherwise  free  from  tooth-like  structures. 
Aperture  of  the  dorsal  oesophageal  gland  situated  in  the  wall  of  the 
mouth  capsule.  Bursa  of  the  male  closed  all  round.  Only  one- 
third  of  the  dorsal  ray  is  cleft.  The  course  of  the  genital  tubes  is 
longitudinal. 

Type  Genus. — Ancylostoma  Dubini,  1843.  Other  genus:  I' mi- 
liaria Frolich,  1789. 

Ancylostoma  Dubini,  1843. 

Synonym. — Dochmius  Dujardin,  1845,  pro  parte. 

AncylostornincB  with  the  head  end,  where  the  mouth  is  situated, 
abruptly  truncated.  Mouth  large,  round,  with  its  ventral  margin 
armed  with  two  pairs  of  strong  hook-like  teeth,  the  points  of  which 
are  bent  backwards,  while  the  bases  are  continuous  posteriorly  with 
longitudinal   rib-like   thickenings   of  the   external  surface   of  the 


666 


NEMA  THELMINTHES 


capsule  wall.  The  aperture  of  the  dorsal  oesophageal  gland  can 
be  seen  in  the  dorsal  wall  of  the  mouth  capsule. 

Male  with  a  three-lobed  bursa,  broader  than  long,  with  two 
spicules.     Female  with  vulva  behind  the  middle  of  the  body. 

Species. — A  number  of  species  are  known  in  man,  dogs,  bears, 
civet  cats,  and  other  carnivora. 

Ancylostoma  duodenale  Dubini,  1843.* 

Synonyms. — Strongylus  quadridentatus  von  Siebold,  1851 ;  Doch- 
mius  ancylostomum  Molin,  i860;  Sclerostoma  duodenale  Cobbold; 
Strongylus  duodenale  Schneider,  1866 ;  Dochmius  duodenalis  Leuc- 
kart,  1876,  pro  parte. 


Fig.  289. 


Fig.  288.  —  AncyloJoma 
duodenale  Dubini,  1843: 
Male. 

(From  photographs  by  J.   J.  Bell. 


■Ancylostoma  duodenale  Dubini, 
1843:  Male  Bursa. 


This  worm,  which  is  the  great  cause  of  tropical  anaemia,  was  per- 
haps known  to  the  ancient  Egyptians  under  the  term  '  Heltu,'  men- 
tioned in  the  '  Ebers  Papyrus,'  which  is  supposed  to  have  been 
written  some  1550  years  b.c.  the  disease  being  called  A.A.A.,  and 
a  remedy  being  advised.  Perhaps  the  same  anaemia  is  referred  to  in 
the  '  Harita  Samhita '  under  the  term  '  pandu  roga,'  which  was 
said  to  be  caused  by  swallowing  clay.  If  this  is  correct,  then 
knowledge  of  anaemia  due  to  geophagy  is  very  old  indeed.  If  the 
ancients  did  really  know  about  this  worm,  and  the  disease  caused 
thereby,  the  knowledge  was  totally  lost,  and  it  was  not  till  Dubini 
in  1838  discovered  the  worm  in  a  peasant  woman  in  Milan  that 
modern  medicine  knew  anything  about  its  existence.  Pruner,  in 
r.8  [6,  found  the  parasites  in  Egypt,  and  Griesinger,  in  1851,  showed 


ANCYLOSTOMA  667 

that  it  was  the  cause  of  Egyptian  anaemia.  Wucherer,  in  1872, 
found  that  it  was  the  cause  of  tropical  anaemia  in  Brazil  (called 
'  oppilacao  ' ) .  Pcrroncito  found  that  it  was  the  cause  of  the  anaemia 
which  badly  affected  the  miners  employed  in  the  St.  Gothard  tunnel. 
Grassi  and  Parona  in  1878  discovered  the  eggs  in  the  faeces,  thus 
enabling  a  diagnosis  to  be  made  during  life.  The  wide  geographical 
distribution  of  the  parasite,  and  the  amount  of  disease  which  it 
causes,  is  slowly  being  realized,  and  the  deaths  from  anaemia, 
general  dropsy,  and  so-called  beri-beri,  etc.,  in  different  tropical 
regions  are  being  found  to  be  due  to  this  animal. 

The  development  and  method  of  infection  have  been  completely 
traced  out  by  Looss  in  Egypt  in  a  most  masterly  manner. 


Fig.  290. — Copulation  of  Ancylostoma. 
(From  a  photograph  by  J.   J.   Bell.) 

In  1902  Stiles  found  that  under  the  term  Ancylostoma  two  dif- 
ferent parasites  were  being  confused,  one  corresponding  to  Dubini's 
Ancylostoma  duodenale,  and  the  other  new,  which  he  named 
Necator  americanus.  Leiper  has  shown  how  widespread  this  latter 
parasite  is  in  the  Old  World. 

The  geographical  distribution  is  probably  not  fully  known, 
because  in  many  places  it  is  confounded  with  Necator.  It  is  sup- 
posed to  be  cosmopolitan  in  tropical  regions,  and  in  mines  and 
tunnels  in  colder  climates,  in  which,  of  course,  the  air-temperature 
is  higher  than  that  of  the  outside. 

Morphology.— The  body  is  cylindrical,  tapering  from  back  to 
front  in  both  sexes.  During  life  it  is  flesh-coloured.  The  cuticle 
is  ringed.  The  mouth  is  terminal,  with  a  chitinous  wall,  which 
ventrally  carries  two  pairs  of  hook-like  teeth,  and  dorsally  one  pair. 
Close  to  the  base  of  the  outer  ventral  tooth  opens  the  single-celled 


663 


NEMA  T  HELM  IN  THE  S 


head  gland,  which  runs  through  nearly  half  the  length  of  the  body. 
In  the  floor  of  the  mouth  there  are  two  ventral  chitinous  plates,  and 
the  prominent  opening  of  the  dorsal  head  gland  (often  called  a  tooth). 
Male  measures  about  10  millimetres  in  length  by  0*4  to  0-5  milli- 
metre in  breadth,  and  possesses  a  bursa  copulatrix  at  the  posterior 
end,  which  is  umbrella-shaped  and  supported  by 
chitinous  rods,  which  are  arranged  as  follows:  In 
the  median  dorsal  line  is  the  costa  dorsalis,  which 
divides  dorsally  into  two  small  branches,  which 
are  ramified  at  their  tips.  Postero-laterally  there 
is  one  root  on  each  side — the  single  costa  dorsalis 
externa,  in  front  of  which  is  a  single  broad  lateral 
root,  which  divides  into  the  costa  lateralis  posterior, 
the  costa  lateralis  media,  and  the  costa  lateralis 
externa;  while  anteriorly  also  on  each  side  is  the 
costa  ventralis.  Through  the  opening  of  this  bursa 
project  the  two  spicules,  unless  they  are  retracted, 
which  are  long  and  slender,  and  measure  about  2 
millimetres  in  length.  The  male  generative  appar- 
atus consists  of  a  testis  in  the  form  of  a  tube,  an 
oval  vesicula  seminalis,  and  a  long  cement  gland, 
whose  secretion  fixes  the  male  to  the  female  during 
conjugation,  and  a  spicule  sac. 

The  female  measures  12  to  13  millimetres  in  length, 
and  has  the  vulva  at  the  junction  of  the  middle 
and  hinder  parts  of  the  body,  from  which  a  short 
vagina  opens  into  two  tubes,  which  are  divisible  into 
ovijector,  uterus,  receptaculum  seminis,  and  an 
ovary. 

Life-History. — The  adult  worms  live  chiefly  in  the 
jejunum  of  the  host,  where 
they  feed  upon  the  villi. 
Blood  is  only  accidentally 
found  in  a  worm.  Here 
the  females  lay  the  eggs, 
which  are  oval  in  form, 
with  broad  rounded  poles, 
surrounded  by  a  colourless 
shell,  which  is  really 
double,  but  looks  single, 
inside  which  lies  an  oval 
granular  mass  separated 
from  the  shell  by  a  con- 
siderable space.  As  the 
egg  travels  down  the  alimentary  canal  the  granular  mass  divides 
into  two,  and  finally  into  four  segments,  in  which  condition  the 
egg  is  usually  found  in  the  faeces.  Development  proceeds  in  the 
faeces,  depending  upon  the  temperature  of  the  atmospheric  air.  In 
twenty- four  hours,  if  supplied  with  air  water,  and  heat,  the  embryo 


Fig.  291. — An- 
(ylostoma  duo- 
denale  Dubini: 
Male. 

(After  Looss.) 


Fig.  292. — Anterior  End 
of  Ancylostoma  duoden- 
ale  Dubini. 

(After  Looss,  from  Mense's 
'  Tropenkrankheiten.') 


AN  CYLO  STOMA 


669 


can  be  seen  coiled  up  in  the  egg,  from  which  it  escapes  as 
and  feeds  on  the  fsecal  material.  The  larva  is  needle-shaped, 
posteriorly,  and  measures  200  to  250  ft  in  length 
by  15  to  17  jj,  in  breadth,  and  is  rhabdite  in 
form,  with  a  long  cylindrical  terminal  mouth, 
opening  into  an  oesophagus,  which,  after  narrow- 
ing, swells  out  into  a  bulb  with  three  valves.  The 
straight  intestine  surrounded  by  granular 
material  opens  into  an  anus  situate  some  dis- 
tance in  front  of  the  tip  of  the  tail.  This  larva 
undergoes  a  first  ecdysis  when  it  becomes 
narrower,  and  the  oesophagus  and  mouth  lose 
their  characteristic  appearance,  while  it  forms 
a  new  skin  inside  the  chitinous  cuticle,  so  that 
(at  the  end  of  five  days  in]  the  tropics)  it  now 
ceases  to  grow  and  feed,  and  takes  to  water  or 
moist  earth,  where  it  can  remain  unchanged  for 
months,  living  on  the  food-material  enclosed  in 
its  own  cells  (stage  of  encystment).  During  this 
condition  it  may  be  quite  active,  and  can  swim 
and  climb  up  any  surface  which  is  wet.  This  is 
an  important  factor  in  explaining  the  production 
of  certain  kinds  of  skin  eruptions.  It  is  now 
ready  to  infect  man,  which  it  does  through  the 
hair-follicles  of  the  skin,  causing  eruptions  or 
sores — -e.g.,  ground-itch. 

From  the  hair-follicles  it  forces  its  way  via  the 


a  larva, 
pointed 


The    Median    and   External    Caudal     Fig.    294. — Ancyic 

stoma      duodenal' 
Dubini:  Female. 


Fig.-'  293 
1  "*  Bursa  of  Ancylostoma  duodenale  Dubini.]| g| 

1,  Costa  dorsalis;  2,  costa  dorsalis  externa;   3,  costa 


lateralis     posterior      et     externa;  14,      costa  -lateralis  (After  Looss.) 

media;  5,  costa  ventralis. 

(After  Railliet,  from  Stiles's  Report.) 

subcutaneous  tissue  into  the  venous  bloodvessels  and  lymphatics.  In 
the   former  it  reaches  the  right  heart  and  the  lungs  easily;  in  the 


670 


NEMA  THELMINT  HES 


latter  many  are  killed  in  the  lymphatic  glands,  but  some  get  through 
to  the  blood,  and  in  this  way  are  carried  to  the  lungs.  They  now 
work  their  way  out  of  the  capillaries  into  the  lumen  of  the  air  cells,  and 
travel  up  the  bronchi,  trachea,  and  larynx  into  the  oesophagus  (they 
might  by  chance  get  into  the  mouth),  and  so  through  the  stomach  to 


Fig. 


295 


Ar.cylostoiua  duodenale  Dubini:  Development  of  the 
Rhabditiform  Embryo. 


•  ■  I  ** 


(After  Looss,  except  the  last  figure,  which  is  after  Perroncito.) 

the  intestine.  The  time  occupied  by  this  journey  is  believed  to  be 
from  seven  to  ten  days.  In  the  skin  they  undergo  their  second 
ecdysis,  and  later  a  third  and  fourth  ecdysis  takes  place  in  the  alimen- 
tary canal,  the  third  in  four  to  five  days  and  the  fourth  from  four  to 
six  days  after  their  arrival.     They  now  measure  3  to  5  millimetres  in 

length,  and  eight  days  later 
the  generative  organs  begin 
to  attain  maturity,  and  the 
first  copulations  take  place, 
and  a  few  days  later  the  first 
eggs  appear  in  the  faeces,  thus 
completing  the  cycle  of  de- 
velopment, of  which  the  por- 
tion after  infection  occupies 
four  to  six  weeks. 

The  more  important  morpho- 
logical changes  which  take  place 
in  the  human  body  may  be  briefly 
recapitulated. 

On  entering  the  skin  the  third 
stage     of     development     begins, 
during     which     the      provisional 
buccal     capsule    is     formed.      A 
third  ecdysis  ushers  in  the  fourth 
stage,   characterized  by  the   pro- 
visional   buccal     capsule     armed 
with  a  dorsal  and  a  ventral  pair 
of  teeth.    During  this  stage  the  sexes  become  dilferentiated  and  the  permanent 
buccal  capsule  is    formed.      The  fourth  ecdysis  results  in  the  appearance  of 
the  adult  worms. 

The  number  of  females  can  be  calculated  from  the  number  of 

eggs  in  the  faeces  by  the  formula  X= — ,  where  X  is  the  number 

47 
of  females  and  .4  the  number  of  eggs  in  a  gramme  of  faeces. 


Fig.  296. — -Hatching  of  Egg  of  Ancylo- 
stoma  duodenale  Dubini,    1843. 

(From  a  photograph  by  J.  J.  Bell.) 


ANCYLOSTOMA 


671 


This  history  has  been  pieced  together  by  Looss  from  observations 
on  the  infection  of  Ancylostoma  duodenale  in  man  and  A.  caninum 
in  dogs. 

These  discoveries  of  Looss  have  been  confirmed  by  Lambinet.  Sambon, 
while  agreeing  with  the  view  that  the  worms  penetrate  the  skin  and  work 
their  way  to  the  lungs,  considers  that  they  pass  from  the  pulmonary  artery 
to  the  pulmonary  veins,  and  in  this  way  reach  the  general  blood-stream,  and 
in  due  course  the  jejunum,  the  mucosa  of  which  they  pierce,  and  enter  the 
lumen  of  the  bowel.  He  believes  that  the  worms  seen  in  the  trachea,  larynx, 
and  stomach  by  Looss  are  merely  stray  specimens  which  have  escaped  in  the 
air  cells  from  the  vessels  of  the  lungs.     His  reasons  for  this  belief  are: — 


n 

Fig.  297.         Fig.  298.  Fig.  299.  Fig.  300.         Fig.  301. 

Figs.  297-301. — Development  of  Ancylostoma  duodenale  Dubini. 

(After  Looss,  from  Mense.) 

1 .  The  larval  forms  of  A .  duodenale  have  seldom  been  found  in  the  stomach, 
and  when  found  in  this  organ  are  lodged  beneath  the  epithelium. 

2.  They  are  invariably  absent  from  the  duodenum. 

3.  They  have  been  found  in  the  left  heart,  in  the  pulmonary  and  azygos 
veins,  in  the  thoracic  duct,  in  the  peritoneum,  in  the  kidneys,  in  the  lymph 
glands,  and  in  the  connective  tissue  of  various  regions. 

4.  At  the  beginning  of  the  infection  there  is  always  an  intense  haemorrhagic 
inflammation  of  the  jejunum,  which  entirely  subsides  later  on,  notwithstand- 
ing the  presence  of  enormous  numbers  of  parasites  in  the  intestine. 


672  NEMATHELMINTHES 

5.  Immature  forms  have  been  found  again  and  again  in  blood-filled  spaces 
beneath  the  intestinal  mucosa  by  Bilharz,  Griesinger,  Sonsino,  Grassi,  and 
many  other  competent  investigators. 

6.  A  number  of  other  worms  which  inhabit  the  intestinal  cavity  at  maturity, 
such  as  CEsophagostomum,  Sclerostomum,  Ascaris,  Gnathostoma,  etc.,  in  an 
earlier  developmental  stage  are  usually  found  either  free  or  encysted  beneath 
the  intestinal  mucosa. 

He  also  considers  that  when  the  larvae  are  taken  in  by  way  of  the  mouth 
they  probably  pierce  through  the  walls  of  the  oesophagus  like  the  larvae  of 
Hypoderma  bovis  (see  Chapter  XXXIII.),  and  reach  their  intestinal  habitat  by 
way  of  the  vessels  in  exactly  the  same  way  as  those  which  penetrate  the  hair 
follicle. 

Fiilleborn  and  von  Schilling-Torgau  have  re-investigated  the 
subject  by  tracheotomizing  dogs  and  inserting  a  cannula  in  such  a 
way  that  the  larvae  could  not  pass  from  the  lungs  to  the  oesophagus, 
but  only  to  the  exterior.  The  dogs  were  then  infected  with 
Ancylostoma  caninum.  (Ercolani,  1859),  and  after  some  time  the 
secretion  from  the  cannula  in  the  trachea  swarmed  with  larvae.  In 
other  dogs  the  oesophagus,  not  the  trachea,  was  cut  across  and  its 
ends  separately  stitched  to  the  skin,  and  after  a  time  the  secretion 
from  the  upper  cut  end  contained  larvae.  In  both  sets  of  experi- 
ments the  dogs  became  infected  intestinally  with  only  a  very  small 
number  of  parasites. 

It  is  thus  seen  that  Sambon's  hypothesis  is  theoretically  correct, 
but  Looss's  route  is  the  one  by  which  the  vast  majority  of  the  larvae 
enter  the  body. 

Pathogenicity.— It  causes  ankylostomiasis  in  man. 

Subfamily  Bunostomiinle  Looss,  191  i. 

Ancylostornidce  with  small  mouth  capsule,  with  aperture  nar- 
rowed anteriorly  by  plates  with  cutting  edges  springing  from  the 
sides,  and  more  or  less  covering  the  ventral  half  of  the  aperture. 
At  the  base  of  the  cone  which  carries  the  opening  of  the  dorsal 
oesophageal  gland  there  is  on  each  side  one  tooth-like  plate  with 
smooth  edges.  Coils  of  the  genital  tubes  very  numerous  and  close. 
Externo-dorsal  ray  thin,  more  especially  at  the  root.  Spicule  of 
the  male  barbed  at  the  end. 

Type  Genus. — Necator  Stiles,  1903. 

There  are  seven  genera  in  the  subfamily — viz.,  Bunostomum 
Railliet,  1902 ;  Necator  Stiles,  1902  ;By  achy  clonus  Railliet  and  Henry, 
1910 ;  Gaigeria  Railliet  and  Henry,  1910 ;  Euntonodontus  Molin  emend. 
Railliet  and  Henry;  Bathmostomum  Railliet  and  Henry,  1909; 
and  Grammocephahis  Railliet  andVHenry,  1910;  but  only  Necator 
Stiles,  1903,  concerns  us. 

Necator  Stiles,  1903. 

Bunostominae  closely  resembling  Ancylostoma,  but  distinguished 
thereform  by  the  small  mouth  capsule,  which  is  armed  only  by 
semilunar  plates.    The  head  is  strongly  bent  dorsally.     In  the  male 


NEC  A  TOR 


673 


the  bursa  is  bilobed.     In  the  female  the  vulva  lies  in  the  anterior 
part  of  the  body. 
Type  Species.— Necator  americanus  Stiles,  1902.     Other  species: 

N.  africanits  Looss,  191 1,  in  the  chimpanzee. 

Necator  americanus  Stiles,  1902. 

Synonyms. — -Dochmius  duodenalis  R.  Leuckart,  pro  parte;  U uri- 
naria americana  Stiles,  1902 ;  Ancylosloma  americanum  von  Linstow, 
1903,  pro  parte. 

In  1902  Stiles  discovered  that  two  distinct  genera  were  being 
confused  under  the  term  Ancylostoma,  and  eventually  called  the 
new  genus  Necator.  Leiper  has  recently  shown  that  this  new  genus 
is  very  widely  distributed  over  the  world,  and  is  the  common  cause 
of  ankylostomiasis  in  Ceylon;  while  it  occurs  in   India,   Assam, 

7\ 


Fig.     302.  —  The 
Mouth  Capsule 
of  Necator  ameri- 
canus Stiles. 
(After  Looss, 
from  Mense.) 


Fig.  303. — The  Bursa  Copulatrix  of  a  Male 

Necator  americanus  Stiles, 
i,  Spicules;  2,  costa  ventralis;  3,  costa  lateralis  pos- 
terior; 4,  costa  lateralis  externa  et  costa  lateralis  media; 
5,   costa  dorsalis  externa;  6,   costa  dorsalis;    7,   dorsal 
lobe;  8,  lateral  lobe;  9,  ventral  lobe. 
(After  Stiles.) 


Burma,  the  Philippine  Islands,  Fiji,  Japan,  America,  and  has  been 
found  in  West  and  Central  Africa  and  in  North-West  Rhodesia. 
In  due  course,  no  doubt,  it  will  be  reported  in  other  places. 

Morphology. — The  body  is  cylindrical,  and  somewhat  attenuated 
anteriorly.  Head  acutely  bent  dorsally.  Mouth  with  a  ventral 
pair  of  prominent  semilunar  chitinous  plates  and  a  dorsal  pair  of 
slightly  developed  plates.  Into  the  floor  of  the  mouth  projects  the 
opening  of  the  dorsal  head  gland,  which  appears  like  a  dorsal  conical 
tooth,  while  deep  in  the  cavity  appear  one  pair  of  dorsal  and  one 
pair  of  ventral  submedian  lancets.  Excretory  pore  0-5  millimetre 
behind  the  mouth,  with  cervical  papillae  on  either  side. 

Male  7  to  9  millimetres  in  length  and  0-3  to  0-35  millimetre  in 
breadth.  The  bursa  consists  of  two  large  lateral  lobes  joined  to  a 
dorsal  median  lobe,  which  appears  as  if  divided  into  two,  and  to 

43 


6  74  NEM'A  THELMIN  THES 

an  indistinct  ventral  lobe.  There  is  a  slight  ventral  enlargement 
just  posterior  to  the  point  at  which  the  bursa  joins  the  body-wall. 
The  costa  dorsalis  is  divided  at  its  base  into  two  diverging  branches, 
which  are  bipartite.  The  common  base  of  the  costa  dorsalis  and 
costa  dorsalis  externa  is  very  short,  while  the  latter  ray  is  long, 
slender,  and  clavate.  The  costa  lateralis  externa  is  closely  joined 
to  the  costa  lateralis  media.  Two  small  precaudal  papilla?  can  be 
seen  anterior  to  the  ventral  rays.  The  spicules  are  long  and  slender, 
0*92  millimetre  in  length,  and  terminate  in  barbed  points. 

Female  is  9  to  12-6  millimetres  in  length;  vulva  in  the  anterior 
half  of  the  body,  but  near  the  equator.  Eggs  57-7  to  80  /<«  by  35 
to  52-5  (jl ;  average,  66  by  40  ^i. 

Life-History . — This  is  the  same  as  Ancylostoma  daodenale. 

Zoological  Distribution.— Man  and  the  gorilla. 

Pathogenicity. — It  causes  ankylostomiasis  in  certain  regions. 

Ancylostoma  ceylanicum  Looss,  1911. 

Synonym. — (?)  Ancylostoma  braziliense  Gomez  de  Faria,  1910. 

Definition. — Ancylostoma  with  one  large  tooth  at  the  anterior 
edge  of  the  mouth  capsule,  and  below  and  behind  this  a  very  small 
tooth  towards  the  middle  line.  Lobes  of  bursa  almost  as  broad  as 
long. 

Remarks. — This  worm  was  found  in  cats  and  dogs  in  India,  and 
is  the  same  as  that  found  in  the  civet  cat  in  Ceylon,  and  in  man 
in  Bengal  by  Clayton-Lane,  and  called  A.  ceylanicum. 

It  has  also  been  found  by  Darling  in  a  Tamil  and  a  Chinese  in 
Kuala  Lumpur,  and  also  in  dogs,  in  which  they  were  frequently 
found. 

Clayton-Lane  suggests  that  the  genus  Ancylostoma  should  be 
divided  into  two  subgenera- — viz  :— 

c  ,  Ail        (A.  duodenale. 

Subgenus  Ancylostoma^   cmimm^ 

Subgenus  Ceylancylostoma[A/  ceylamcum- 
'        J  [A.  malayanum. 

G.  de  Faria  maintains  that  A.  braziliense  and  A.  ceylanicum  are 
probably  not  the  same,  because  of  the  character  of  the  oral  capsule 
and  bursal  rays. 

PSEUDOSTRONGYLES  Leiper,  1912. 

Ncmatoda  with  simple  mouth,  and  a  cuticular  bursa  in  the  male 
without  rays.     One  spicule. 

Family  15:  Eustrongylidid^e  Leiper,  1912. 
Subfamily  Dioctophymin^e  Railliet. 

Eustrongylidae  with  unarmed  mouth;  bursa  copulatrix  without  ribs  or 
bands.     Genus:  Dioctophytne  Collet- Megret,  1802. 


PSFAJDOSTRONGYLES  675 

Dioctophyme  Collet-Megret,  1802. 
Very  Large  Strongylidae  with  cylindrical  bodies;   mouth  with  six  papillae. 
Male  with  collar-like  bursa  and  one  spicule.     Female  with  one  ovary;  vulva 
in  the  anterior  half  of  the  body. 

Dioctophyme  renale  (Goeze,  1782). 

Synonyms. — A  scar  is  can  is  et  martis  Schrenk,  1788;  A.  visceralis  et  renalis 
Gmelin,  1789;  Strongylus  gigas  Rudolphi,  1802;  Euslrongylus  gigas  Diesing, 
1 851;  Strongylus  renalis  Moquin-Tandon,  i860;  Enstrongylus  visceralis  Railliet, 
1885. 

This  worm  lives  in  South  America  in  the  pelvis  of  the  kidney  in  the  dog, 
seal,  otter,  and  wolf.  It  has  been  recorded  twelve  times  in  man,  if  the 
records  really  refer  to  this  worm. 

Morphology. — The  worm  is  blood-red  in  colour,  but  otherwise  very  like  a 
large  A  scar  is  htmbricoides.  Along  the  lateral  lines  there  are  about  150  papillae. 
The  submedian  ridges  are  well  developed,  and  the  anterior  extremity  some- 
what attenuated.     Cuticle  finely  striated  transversely. 

Male  40  centimetres  long  by  4  to  6  millimetres  broad;  bursa  without  rays, 
and  with  one  very  long,  slender  spicule  5  to  6  millimetres  in  length.  Female 
100  centimetres  in  length  and  12  millimetres  in  thickness,  with  an  obtuse, 
slightly  curved  posterior  end,  a  single  ovary,  and  a  vulva  situate  50  to  70  milli- 
metres behind  the  anterior  extremity.  Eggs  ovoid,  with  thick,  brownish 
shell  68  to  80  fi  by  40  to  43  /.t,  with  numerous  depressions. 

Life-History. — Development  begins  in  the  uterus  of  the  female,  but  stops 
at  a  certain  stage,  and  does  not  continue  (Balbiani)  until  brought  into  contact 
with  water  or  damp  soil,  when  the  egg  hatches.  The  embryo  is  240  n  by  14  /j,, 
cylindrical,  and  gradually  tapering  posteriorly.  The  head  is  pointed,  with  a 
terminal  mouth  without  papillae,  but  which  is  thought  to  be  provided  with  a 
small  protractile  dart.  The  further  development  is  not  known;  it  has  been 
thought  that  it  takes  place  in  fish,  but  experiments  have  failed  to  justify 
this  view. 

Pathogenicity. — -It  is  usually  found  in  the  kidney,  which  it  destroys.  In 
animals  it  has  also  been  found  in  mammary  and  perineal  tumours.  Symp- 
toms appear  to  be  haematuria,  and  the  diagnosis  is  made  by  the  discovery  of 
the  eggs. 


Family  16:    Trichosomid^;. 

Nematoda  with  the  anterior  portion  of  the  body  thin  and  whip- 
like; posterior  portion  thick  with  genitalia.  Mouth  small,  without 
papillae.     (Esophagus  very  long,   traversing  a  peculiar  strand  of 

cells. 

Trichinellin»  Ransom,  1911. 

Male  without  spicule.     Female  producing  embryos. 

Trichurinae. 
Male  with  spicule.     Female  producing  barrel-shaped  eggs. 

Genus  Trichinella  Railliet,  1895. 

Trichineila  Railliet,  1895. 

Synonym.— Trichina  Owen,  1835,  nee  Meigen,  1830. 

Very  small  Trichinellidae,  with  thin,  hair-like  bodies.  Posterior  end  of  the 
male  with  two  cone-like  appendages,  between  which  the  cloaca  is  situate. 
Vulva  placed  far  forwards. 


676  XEMATHELMINTHES 

Trichinella  spiralis  Owen,  1835. 

Synonym. — Trichina  spiralis  Owen,  1835. 

T.  spiralis,  though  discovered  by  Paget  in  1835  and  described  by  Owen, 
had  been  previously  seen  by  Peacock  in  1828  and  by  Hilton  in  1833. 

It  is  really  a  parasite  of  the  black  rat  (Epimys  rattus)  and  the  sewer  rat 
(E.  norvegicus),  in  which  the  rate  of  infection  is  placed  from  8-3  to  100  per 
cent.,  according  to  the  locality,  but  it  spreads  from  the  rat  to  pigs,  dogs, 
cats,  and  many  other  animals. 

Man  becomes  infected  from  the  pig  as  a  rule,  for  that  animal  is  particularly 
liable  to  the  disease,  because  it  is  apt  to  be  fed  upon  scraps  of  raw  meat. 
Further,  the  larva  in  the  flesh  of  the  pig  is  very  difficult  to  kill,  for  it  will 
resist  a  temperature  of  8o°  C,  pickling,  smoking,  and  freezing.  Hence,  though 
ham  be  well  boiled,  it  does  not  follow  that  the  larvae  in  its  centre  are  killed. 
Sausages,  however,  are  the  greatest  danger,  for  in  them  the  larva?  can  live  well 
protected. 

In  order  to  infect  man,  there  must  be  a  source  of  infection  for  the  pig, 
and  tins,  in  the  first  instance,  can  come  from  the  rat,  and  afterwards  be  kept 
up  in  the  pig,  and  then  the  transmission  to  man  is  easy. 

As  rats,  pigs,  and  men  are  cosmopolitan,  so  trichiniasis  is  also  cosmopolitan. 
It  is  not  uncommon  in  certain  parts  of  India,  and  is  known  in  China.  In 
considering  the  endemicity  of  the  disease,  it  must  not  be  forgotten  that  the 
wild  boar  (Sus  scrofa  ferox)  is  susceptible.  The  disease  is  supposed  to  have 
been  introduced  into  Europe  from  Asia,  either  by  Epimys  norvegicus  at  the 
end  of  the  eighteenth  century,  or  by  the  Chinese  pig  from  1820  to  1830.  At 
present  it  is  common  also  in  America. 

Morphology  and  Life-History. — It  is  usually  found  in  human  or  pig's 
muscles,  where  it  appears  as  minute  white  specks,  which,  when  magnified, 
are  found  to  be  encysted  larva?.  These  cysts  are  oval,  with  their  long  axis 
in  the  same  direction  as  that  of  the  muscular  fibres,  measuring  400  by  250  fi. 
The  cyst  membrane  is  formed  from  inflamed  connective  tissue,  which  has 
invaded  the  infected  muscular  fibre.  Inside  the  cyst  is  the  coiled-up  worm. 
In  this  condition  the  larva?  may  live  for  years,  but  may  be  killed  by  calcifica- 
tion. They  are  mostly  found  in  the  diaphragm,  the  larynx,  tongue,  abdo- 
minal and  intercostal  muscles. 

When  these  cysts  reach  the  stomach  of  a  man  or  animal,  the  gastric  juice 
dissolves  the  cyst-wall,  and  the  parasites  escape,  and,  entering  the  duodenum 
and  jejunum,  they  grow  into  adult  males  3  to  4  millimetres  long  by  60  fj,  in 
diameter,  and  females  1-4  to  i-6  millimetres  long  by  40  /j,  in  diameter,  which 
copulate.  The  males  now  die  off,  and  the  females,  increasing  in  size,  penetrate 
the  mucosa  of  the  bowel  until  they  reach  a  lymph-channel,  where  they  de- 
posit their  larva?,  which  are  born  alive.  Leuckart  says  one  female  gives  rise 
to  1,500  larva?,  which  are  carried  by  the  lymph  and  blood  streams  all  over  the 
body.  The  larva?  now  leave  the  capillaries  and  work  their  way  into  the 
tissues,  and  in  about  nine  to  ten  days  encapsule  in  the  muscles,  the  attacked 
fibres  of  which  degenerate  and  become  inflamed,  and  the  cyst  already  described 
is  formed. 

Pathogenicity. — When  the  female  pierces  the  mucosa,  and  during  the  wan- 
dering through  the  lymph  and  blood  of  the  larva?,  very  severe  symptoms 
called  trichinosis  or  trichiniasis  are  produced. 


Subfamily  Trichurin^;  Ransom,  1911. 
Type  Genus.- — Trichuris;  also  Capillaria  Zeder,  1800. 

Trichuris  Roederer  and  Wagler,  1761. 

Trichosomidge,  with  the  anterior  part  of  the  body  very  long 
and  thread-like,  and  the  posterior  thicker  portion  sharply  trun- 


TRICHURIS 


677 


cated,  with  a  terminal  anus.  Male  with  a  spirally  rolled  posterior 
end  and  one  spicule;  female  with  one  ovary,  and  the  vulva  situated 
at  the  junction  of  the  thinner  and  thicker  parts  of  the  body. 

Species  in  man :  Trichuris  trichiura 
Linnaeus,  1761. 


Fig.  304. — Trichuris  trichiura  (Linnaeus,         Fig.  305.—  Trichuris  trichiura 
1761):  Male.  (Linn.eus,    1761):  Female. 

(From  a  photograph  by  J.   J.  Bell.) 

Trichuris  trichiura  Linnaeus,  1761. 

Synonyms.- — Ascaris  trichiura  L.,  1771;  Trichocephalits  hominis 
Schrank,  1788;  T.  dispar  Rudolphi,  1801. 

This  worm  is  very  commonly  met  with  in  the  tropics.  Its  eggs 
appear  in  the  faeces,  and  it  is  met  with  in  the  caecum  and  sometimes 


Figs.  306  and  307. — Trichuris  trichiura  Linn^us:  Female  and  Male. 

(After  Claus.) 

in  the  vermiform  appendix  during  post-mortems.  Its  anterior 
end  is  frequently  found  buried  in  the  mucous  membrane,  and  while 
in  this  position  it  is  possible  for  bacteria  to  enter  and  cause  disease 
— e.g.,  appendicitis. 


678  NEMATHELMINTHES 

It  is  commonly  called  the  whip-worm,  and  is  cosmopolitan  in  its 
distribution. 

Morphology. — The  male  measures  40  to  45  millimetres  in  length, 
and  is  easily  recognized  by  the  spirally  coiled  posterior  end.  Its 
spicule,  which  lies  in  a  retractile  pouch,  measures  2-5  millimetres. 
The  female  measures  45  to  50  millimetres  in  length.  The  ova  are 
oval,  brown,  thick-shelled,  with  a  pale,  clear  body  at  each  pole, 
where  the  shell  is  deficient.     They  measure  50  to  54  by  23  /x. 

Life-History. — When  the  egg  appears  in  the  faeces,  it  is  unseg- 
mented,  and  is  said  to  take  eighteen  months  before  the  embryo  is 


Fig.  308. — Development  of  the  Egg  of  Trichuris  trichiura. 
(After  Stiles.) 

fully  developed.  The  egg  with  the  enclosed  embryo  is  then  taken 
in  through  the  mouth  in  contaminated  food  or  water,  there  being 
no  intermediate  host.  The  shell  is  dissolved  by  the  gastric  juice, 
and  the  embryo  reaches  maturity  in  the  intestine  in  about  four  to 
five  weeks. 

Pathogenicity.- — Usually  harmless,  but  may  give  rise  to  intestinal 
disturbance  and  at  times  appendicitis. 

Syngamus  von  Siebold,  1836. 

Strongyles  with  broad  head,  mouth  with  a  chitinous  capsule.  Male  with 
two  spicules.  Female  with  two  ovaries  and  a  vulva,  situate  in  the  anterior 
part  of  the  body. 

Syngamus  kingi  Leiper,  191 3. 
King  forwarded  quite  recently  a  pair  of  specimens  to  Leiper  purporting  to 
come  from  a  woman  living  in  St.  Lucia  who  suffered  from  chronic  cough,  when 
the  worms  were  expectorated  with  blood.  Leiper  thinks  that  this  may  be  an 
accidental  infection  of  man  with  a  parasite  which  is  harboured  possibly  by  a 
carnivore.  It  differs  from  S.  trachealis,  the  common  nematode  of  poultry,  in 
the  buccal  capsules;  these  in  the  male  and  female  are  on  the  same  kvel, 
whereas  in  S.  trachealis  that  of  the  male  is  more  anterior.  Mouth  capsules 
terminal.     Tail  of  female  bluntly  pointed. 

ORDER  II.     GORDIACEA. 

Nemathelminthes  with  the  intestinal  canal  always  atrophied  anteriorly 
in  the  adult;  head  without  papilla?;  two  testes,  but  never  spicules  in  the 
male;  vulva  always  united  with  the  posterior  portion  of  the  intestine  to  form 
a  cloaca;  rare  in  man;  only  accidental  parasites. 

These  worms  are  popularly  known  as  horsehairs,  and  are  supposed  to 
cause  serious  and  even  fatal  disease  in  man  or  animals  if  swallowed.  Their 
pathogenicity  has  recently  been  studied  by  Stiles,  who  is  unable  to  support 
the  popular  belief  as  to  the  serious  nature  of  these  parasites  in  man.  They 
are  very  long,  thin  worms,  like  Filaria,  which  can  be  found  in  ditch-water 
swimming  freely  or  twining  round  water-plants. 

The  body  is  covered  with  a  well-developed  two-layered  cuticle.  The  mouth 
and  the  anterior  part  of  the  intestine  is  obliterated.  The  posterior  end  of 
the  male  is  lobed,  and  without  spicules.     In  the  female  there  are  two  ovaries 


GORDIACEA  &79 

and  the  egg-sacs,  which  open  by  means  of  oviducts  into  a  uterus.  The  males 
are  often  blackish  brown,  and  the  females  light  clay  brown. 

The  life-history  of  Parachord.od.es  tolosanus  is  very  complicated:  the  first 
larva  enters  the  larva  of  the  alder-fly  (Sialis  luiaria  L.),  where  it  lives  during 
the  winter,  and  passes  over  to  the  imago  of  the  same  insect,  which  is  eaten  by 
a  beetle  (Pterosiichus  niger) .  The  first  larva  changes,  becoming  a  second  larva, 
which  lives  in  the  beetle  during  the  second  winter,  and  finally  escapes  into  the 
water  about  twenty  months  after  hatching.  In  the  water  it  soon  becomes 
adult  Gordiidae. 

The  Gordiacea  includes  the  family  Gordiidae,  which  is  divided  by  Camerano 
into  four  genera:  Gordius  Linnseus,  1758;  Paragordius  Camerano,  1879;  Para- 
chordodes  Camerano,  1897;  Chordodes. 

Without  going  into  details,  it  may  be  said  that  the  following  species  have 
been  reported  as  parasitic  in  man: — 

Gordius  aquaticusL..,  1758. — Tour  recorded  cases  in  Europe  with  abdominal 
symptoms,  pain,  vomiting,  etc.,  and  nervous  symptoms,  hysteria,  and  neu- 
ralgia. 

G.  chiliensis  E.  Blanchard,  1849. — This  is  simply  based  on  the  legends  of 
Chilian  Indians,  who  fear  the  worm. 

Paragordius  varius  Leidy,  1851. — Four  cases  of  infection  in  North  America. 
Worms  were  expelled  per  anum  or  by  vomiting.     Symptoms:  unimportant. 

P.  tricuspidatus  Dufour,  1828. — One  case  in  France.  Symptoms:  slight 
colic.     Worm  extracted  from  the  throat. 

P.  cinctus  von  Linstow,  1906. — From  a  man  in  Leydenburg  in  the  Transvaal. 

Parachordodes  tolosanus  Dujardin,  1842.- — Four  cases,  in  one  of  which  it  is 
accused  of  causing  epileptiform  fits.     Cases  occurred  in  France  and  Italy. 

P.  pustulosis  Baird,  1853. — One  case  in  Italy  caused  anal  pruritus  and 
discharge. 

P.  violaceus  Baird,  1853. — One  case  in  France;  it  lodged  in  the  throat 
before  expulsion. 

P.  alpestris  Villot,  1884.— One  case  in  France. 

Undetermined. — Ward,  in  1903,  published  the  account  of  a  case  in  which  the 
genus  of  the  worm  was  not  determined. 

CLASS  II. 

ORDER  III.     ACANTHOCEPHALA  Rudolphi. 

Nemathelminthes  with  a  retractile  proboscis  armed  with  several  rows  of 
spines  or  hooks;  intestine  absent;  parasitic  in  the  intestine  of  vertebrates. 

The  Acanthocephala  are  elongated  cylindrical  worms,  in  which  the  body 
can  be  divided  into  proboscis,  neck,  and  trunk.  The  proboscis  is  a  hollow, 
finger-shaped,  retractile  process,  covered  with  a  thin  cuticle,  and  armed  with 
rings  of  hooks  arranged  in  longitudinal  rows.  The  neck  is  not  always  dis- 
cernible. The  trunk  has  a  rounded  posterior  end,  and  consists  of  a  body-wall 
with  muscular  layers,  covered  by  a  thin  cuticle,  enclosing  the  excretory  and 
reproductive  organs.  The  sexes  are  separate.  The  male  organs  are  two  oval 
testes,  whose  vasa  efferentia  unite  into  a  vas  deferens,  which  opens  into  a  cirrus 
contained  in  a  pouch  or  bursa,  and  provided  with  a  prostate  gland. 

The  female  organs  consist  of  two  ovaries,  which  break  down  into  masses  of 
cells  which  escape  into  the  ccelom.  Here  the  ova  are  fertilized  and  the  embryo 
is  formed,  and  escapes  through  a  funnel-shaped  structure  called  '  the  bell  ' 
into  the  uterus,  and  so  through  the  vagina  and  the  genital  orifice  at  the 
posterior  end  of  the  body  into  the  lumen  of  the  host's  intestine. 

The  embryo  leaves  the  host  with  the  faeces,  and,  getting  into  water,  enters 
the  alimentary  canal  of  a  crustacean,  water-insect,  or  fish,  inside  which  it 
hatches.  It  now  bores  its  way  through  the  intestinal  wall  into  the  ccelom, 
where  it  develops  all  its  organs  except  the  reproductive. 

The  crustacean,  water-insect,  or  fish  must  now  be  eaten  by  a  vertebrate, 
when  the  acanthocephalid  becomes  sexually  mature  in  the  intestine.  They 
are  very  rarely  found  in  man. 


6  So  NEMA  T  HELM  I N  THES 

Classification. — The  Acanthocephala  are  divided  into  four  families  by 
Hamann  and  Shipley : — Echinorhynchidae,  Gigantorhynchidae,  Neorhynchidae, 
and  Arhynchidae.  Human  parasites,  which  are  very  rare,  are  only  found  in 
the  first  two  families. 

ECHINORHYNCHIDiE. 

Acanthocephala  with  elongated,  smooth  body;  proboscis  can  be  retracted 
into  a  sheath  with  double  walls. 

Genus. — Echinorhynchus  M  tiller,  1776. 

Echinorhynchus  (Mailer,  1776). 
Echinorhynchus  hominis  Lambl,  1859. 
This  parasite  was  found  in  the  intestine  of  a  boy  who  died  of  leukaemia; 
it  was  5-6  millimetres  long.     There  appears  to  be  much  doubt  as  to  whether  this 
really  was  Echinorhynchus. 

Gigantorhynchidae. 

Gigantorhynehus  Hamann,  1892. 
Large  Acanthocephala  with  ringed,  flat,  taeniform  bodies. 

Gigantorhynehus  gigas  (Goeze,  1782). 
This  parasite  was  alleged  by  Lindemann  to  occur  in  man  in  South  Russia, 
where  Schneider  says  Melolontha  is  eaten  raw.  It  is  10  to  15  centimetres  long ; 
eggs  80  to  100  fi  long,  with  three  shells.  Its  usual  life-history  is  that  the 
adult  is  found  in  pigs,  and  the  larva  in  Melolontha  vulgaris,  Cetonia  aurata, 
or  Lachnosterna  arenata. 

Gigantorhynehus  moniliformis  (Bremser,  191 1). 

Synonym. — Echinorhynchus  moniliformis  Bremser,  191 1. 

Leiper  records  a  parasite  found  in  a  Sudanese  by  Christopherson  as  probably 
belonging  to  this  species.  It  has  also  been  seen  in  man  by  Grassi  and  Calan- 
druccio.     The  worm  is  found  in  Europe,  Africa,  and  Brazil. 

Morphology. — White  body  with  attenuated  ends  with  many  rings,  making 
it  closely  resemble  a  Porocephalus.  Male  4  to  5  centimetres  in  length,  with  a 
bursa  visible  to  the  naked  eye.  Female  7  to  10  centimetres  long.  Eggs  ellip- 
soidal, 85  jx  by  45  ix. 

Life-History. — The  intermediate  host  is  Blaps  mucronata.  Calandruccio  has 
shown  experimentally  that  it  can  develop  in  the  human  body. 


REFERENCES. 
Nemathelminthes. 

Hamann  (1891).     Die  Nemathelminthen.     Jena. 
Schneider  (1866).     Monographic  der  Nematoden.     Berlin. 
Shipley  (1896).     Cambridge  Natural  History,  ii.  123. 

NEMATODA. 
Anguillula  aceti. 

Marocchi  (1907).     Gior.  R.  A.  Med.  Torino,  lxx.  1-2,  p.  3. 
Orley  (1880).     Monographie  der  Anguilluliden.     Budapest. 
Stiles   and  Frankland  (1902).     Bur.  Anim.  Industry,  United   States  De- 
partment of  Agriculture,  Bull.  No.  35,  p.  35.     Washington. 

Anguillulina  putrefaciens. 

Botkin  (1883).     Vet.  Kl.  Wochenschrift. 


REFERENCES  68 1 


Rhabditis  niellyi. 

Nielly  (1883).     Archiv.  Med.  Nav.,  xxxvii.  337,  488. 

Leptodera  pellio. 

Peiper  and  Westphal  (1888).     Centralblatt  fur  Klin.  Med.,  ix.  145. 

Strongyloides  intestinalis. 
Golgi  e  Monti  (1885).  Sulla  Storia  naturale  delle  Anguillule  Intestinali  e 

Stercorali. 
Strong  (1901).     Johns  Hopkins  Reports  (Bibliography). 

Gnathostoma  spinigerum. 

Leiper  (1909).     Parasitology. 

Leiper  (1913).     Trans.  Soc.  Trop.  Med.  and  Hyg.,  vi.,  No.  8. 

Levinsen  (1890).     Centralblatt  fi'ir  Bakteriologie,  viii.  182. 

Filariidae. 

Bahr  (191 2).     Filariasis  and  Elephantiasis  in  Fiji.     London. 

Blanchard  (1890).     Traite  de  Zoologie  Medicale,    Paris,  ii.   1-61.     (Biblio- 
graphy up  to  1890.) 

Manson  (1883).     The  Filaria  Sanguinis  Hominis.     London. 

Penel  (1905).     Les  Filaires  du  Sang  de  1' Homme.     Paris.     (Bibliography. 
1890-95.) 

Physaloptera. 

Leiper   (1908).     Report  of  the  Advisory  Committee  of  Tropical  Diseases. 

London. 
Leiper  (1913).     Trans.  Soc.  Trop.  Med.  and  Hyg.,  vi..  No.  8. 

Microfilaria. 

Le  Dantec  (1904).     Maladies  des  Pays  Chauds,  p.  1000.     Paris. 

Agamofilaria. 

Stiles  (1907).     Bulletin  34,  Hygiene  Laboratory,  U.S.  Public  Health    and 
Marine  Hospital  Service.     Washington. 

Acanthocheilonema. 

Leiper  (1910).     Proceedings  of  the  Zoological  Society.     London. 
Railliet  and  Henry  (1912).     Bulletin  de  la  Societe  de  Pathologie  Exotique, 

p.  392.     Paris. 

Dirofilaria  magalhaesi. 
Magalhaes  (1892).   Centralblatt  far  Bakteriologie  u.  Parasitenkunde,  xii.  512. 
Railliet  and  Henry  (191  i).     Bulletin  de  la  Societe  de  Pathologie  Exotique, 

iv.  285. 

Loa  loa. 
Leiper  (1913).     Trans.  Soc.  Trop.  Med.  and  Hyg.,  vi.,  pp.  272-3. 
Ward  (1906).     Zool.  Annals,  p.  376. 

Onchocerca. 

Gilruth  and  Sweet  (1911).     Onchocerca  gibsoni.     Sydney.     (Bibliography 

of  genus.) 
Railliet  and  Henry  (1910).     Comptes  Rendus  de  la  Societe  de  Biologie, 

lxviii.  248-251.     Paris. 


682  XEMATHELMINTHES 


Dracunculus. 

Charles  (1892).     Life-History  of  the  Male  Filaria  medinensis. 

Inglis  and  Leiper  (191 2).     Bibliography  of  Dracontiasis,  Journal  of  London 

School  of  Tropical  Medicine.     London. 
Leiper  (1908).      Report  of  the    Advisory  Committee  of  Tropical  Diseases. 

London. 
Leiper  (1907).      Brit.  Med.  J. 
Leiper  (1910).     Journ.  Trop.  Med. 

Ascaris  lumbricoides. 

Chalmers  (1904).     Spolia  Zeylanica. 
Castellani  (1907).     British  Medical  Journal. 
Davaine  (1877).     Traite  des  Entozaires.     Paris. 
Epstein  (1892).     Jahrb.  f.  Kinderheilk. ,  N.F.,  xxx.,  iii.  3. 
Grassi  (1887-88).     C.  f.  B.  u.  P.,  1887,  p.  131;  and  1888,  p.  74S. 
Guiart  (1900).     Archiv.  de  Paras.,  p.  70. 
Sick  (1901).      liber  Spuhviirmer  Tubingen. 
Stewart  (1916-17).      Parasitology. 

Ascaris  texana. 

Smith  and  Goethe  (1904).     Journal  of  the  American  Medical  Association, 
P-  542. 

Toxascaris  canis. 

Leiper  (1907).     British  Medical  Journal. 

Belasearis  mystax. 

Bellingham  (1839).     Dublin  Medical  Press,  p.  104. 

Cobbold  (1863).     Lancet,  i.  31. 

Leiper  (1907).     British  Medical  Journal. 

Lagocheilascaris. 

Leiper  (1909).     Proceedings  Zoological  Society.    London. 
Leiper  (1913).     Trans.  Soc.  Trop.  Med.  and  Hyg.,  vi.,  p.  267. 

Oxyuris  vermicularis. 

Blanch ard  (1906).     Archives  de  Paras.,  x.  404. 
Edens  (1905).     C.  f.  B.  u.  P.,  xl.  499. 

CEsophagostomum. 

Weinberg  (1909).     Archives  de  Parasitologie,  xiii.  2. 
Leiper  (1911).     Journ.  Trop.  Med.,  April. 
Leiper  (1915).     Journ.  R.A.M.C. 

Nematoderus  gibsoni. 
Stephens  (1907).     Annals  Trop.  Med.  and  Parasit.,  ii.  4,  315. 

Trichostrongylus. 

Ijima  (1896).     Zoological  Magazine,  p.  155. 
Looss  (1895).     C.  f.  B.  u.  P.,  xviii.  161. 

Ancylostoma. 

Bentley  (1902).     British  Medical  Journal,  p.  1900. 

Boycott  (1905).     Journal  of  Hygiene,  p.  280. 

Dubini  (1843).     Annal.  Univ.  Med.  d'Omodei,  cvi.  51. 


CHAPTER  XXVII 
ANNULATA  AND  HIRUDINEA 

Annulata — Hirudinea — Classification — Gnathobdellidae — -Hirudinae — 
Haemadipsinae — -Remaining  orders — References . 

PHYLUM  ANNULATA  AUCTORES. 

Metazoa  with  elongated  bodies  divided  externally  into  a  number 
of  rings  which  represent  a  division  of  the  internal  parts  into  seg- 
ments or  somites  (metameres),  usually  with  an  extensive  ecelom. 
Nervous  system  consists  of  a  cerebral  ganglion,  with  double  com- 
missure and  ventral  nerve  cord.  Organs  of  excretion  in  the  form 
of  metamerically  arranged  pairs  of  nephridia. 

The  only  class  of  this  phylum  which  contains  animals  of  impor- 
tance in  tropical  medicine  is  the  Hirudinea  or  Discophora — i.e., 
the  leeches. 

CLASS  HIRUDINEA  Savigny,  1817. 

Annulata  with  oval  bodies,  showing  a  dorso-ventral  flattening 
and  two  suckers,  one  at  each  end. 

Remarks. — Teeches  are  of  interest  in  the  tropics,  first  because 
they  may  be  a  considerable  nuisance  as  ectoparasites— e.g.,  land 
leeches  or  Hcsmadipsa  ;  and,  secondly,  they  may  be  of  considerable 
danger  to  the  health  and  even  the  life  of  a  person  as  endoparasites 
— e.g.,  the  water  leeches,  particularly  Limnatis. 

As  ectoparasites  they  are  apt  to  fasten  on  the  legs  of  persons 
going  through  grass  or  jungle.  In  fact,  in  Ceylon,  while  standing 
on  a  piece  of  grass  in  certain  parts  of  the  low  country,  the  leeches 
can  be  watched  converging  from  all  quarters  of  the  compass  towards 
the  observer. 

Very  often  the  bite  is  not  noticed,  and  the  leech  or  leeches  may 
have  sucked  a  considerable  amount  of  blood  before  any  attention 
is  paid  to  them,  and  tales  are  told  of  persons  feeling  faint  before 
noticing  that  they  were  being  attacked  by  these  creatures. 

They  are  apt  to  get  into  the  nose,  naso-pharynx,  or  larynx  with 
drinking-water,  and  in  this  endoparasitic  condition  they  may  suck 
blood  and  cause  epistaxis  or  haemoptysis,  and  this  may  go  on  to 
such  an  extent  that  ansemia  and  even  death  may  result. 

It  is  hardly  possible  to  believe  that  they  can  live  in  the  stomach, 
for  it  is  much  more  likely  that  they  are  at  once  killed  by  the  gastric 
juice  and  digested. 

683 


684  ANNULATA  AND  HIRUDINEA 

A  great  many  tropical  countries  appear  to  be  plagued  with  leeches 
which  affect  men  and  animals  as  indicated  above,  but  it  is  prob- 
able that  Algeria,  Palestine,  and  Ceylon  are  the  most  infested. 
Among  the  other  places  in  which  they  are  troublesome  may  be 
mentioned  the  Philippines,  Java,  Sumatra,  Australia,  Japan,  and 
Chili.  In  Algeria  and  Palestine  the  leech  lives  in  the  pools  of 
drinking-water,  and  here  the  endoparasitic  form  may  be  met  with ; 
whereas  in  Ceylon  it  is  usually  a  land  leech  which  attacks  the 
individual,  and  therefore  the  ectoparasitic  condition  is  common, 
while  the  endoparasitic  is  more  rare,  being  due  to  Hirudo  multi- 
striata. 

Morphology. — Leeches  have  an  elongated,  more  or  less  oval  body,  which 
is  very  retractile  and  extensile,  and  is  marked  by  annuli  or  rings,  of  which 
several — usually  five — form  a  somite.  The  number  of  rings  to  a  somite  is, 
however,  reduced  anteriorly  and  posteriorly,  being  abbreviated.  At  the 
anterior  extremity  is  the  oral  sucker,  and  at  the  posterior  the  acetabulum. 
The  skin  possesses  many  unicellular  dermal  glands.  The  mouth-opening  is 
situate  in  the  anterior  sucker,  and  the  anus  either  in  or  just  in  front  of  the 
constriction  which  separates  the  posterior  sucker  from  the  body. 

The  male  genital  opening  is  placed  on  the  twenty-fourth  annulus,  and  the 
female  five  annuli  behind  it  in  H.  medicinalis  ;  but  the  female  orifice  may 
vary  with  regard  to  the  male  in  other  genera.  A  number  of  nephridial 
orifices  can  be  seen  as  paired  openings  on  the  posterior  annuli  of  many  of  the 
somites.  Eyes  exist  as  small,  dark  dots  on  the  dorsum  of  the  body,  behind 
the  anterior  sucker.  The  mouth  may  be  armed  or  unarmed.  In  the  former 
condition  it  possesses  three  jaws — one  dorsal  and  two  ventro-lateral — each 
with  a  thickened  free  edge  notched  with  teeth.  In  the  latter  there  may  be 
only  a  proboscis.  Into  the  mouth  open  the  salivary  glands,  which  secrete  a 
fluid  which  prevents  the  coagulation  of  the  blood.  The  pharynx  is  an  oval 
sac,  with  strong  muscular  walls  and  radial  muscles,  which  can  alternately 
contract  and  dilate  the  cavity,  thus  forming  a  sucking-pump.  From  the 
pharynx  an  oesophagus  leads  to  the  crop,  which  is  a  straight,  thin-walled  tube 
with  lateral  diverticula. 

Behind  the  crop  comes  the  small  stomach,  which  opens  into  a  narrow 
straight  tube — the  intestine — which  runs  to  the  anus.  The  ccelom  consists 
of  a  series  of  tubes  containing  red  blood.  The  excretory  system  consists  of 
the  nephridia.  There  is  a  supra-cesophageal  ganglion,  a  nerve  collar,  and  a 
ventral  nerve  chain.  The  male  reproductive  organs  are  a  number  of  testes, 
with  vasa  efferentia  opening  into  two  vasa  deferentia,  which,  after  coiling 
into  epididymes,  run  to  the  single  penis.  The  female  organs  are  a  pair  of 
ovaries  and  oviducts  opening  into  a  single  vagina. 

Biology. — Leeches  appear  to  be  essentially  water  animals,  and 
though  certain  genera  can  live  on  land,  still,  they  require  a  great 
deal  of  moisture.  Hence  land  leeches  retire  into  moist  places  under 
stones,  earth,  etc.,  and  only  come  out  when  requiring  food.  In 
dry  weather  not  a  leech  can  be  seen,  while  in  damp  weather  they 
may  be  very  abundant. 

Any  disturbance  of  the  air  appears  to  affect  them.  Hence  they 
are  quickly  aroused  from  their  retreats  when  a  human  being  or 
animal  approaches,  and  set  forth  at  once,  often  with  considerable 
speed,  to  the  attack. 

The  bite  is  not  always  painful  at  first,  and  may  not  be  noted 
until  the  flow  of  blood  is  observed.  The  leech,  while  biting,  keeps 
itself  and  the  skin  of  the  victim  moist  by  liquid  excreted  by  the 


MRU  DIN  EA  685 

nephridia  and  the  dermal  glands.  When  it  has  gorged  itself  with 
blood  it  drops  off,  but  its  salivary  secretion  prevents  the  coagulation 
of  the  blood,  and  hence  the  site  of  the  leech-bite  bleeds  considerably 
for  some  time.  The  blood  is  stored  up  in  the  crop  and  its  caecal 
diverticula,  and  only  a  little  is  used  day  by  day  for  food. 

Pathogenicity.— Leeches  are  hosts  of  trypanosomes  and  other 
parasites,  and  their  bite  may  possibly  introduce  these  parasites 
into  the  skin  of  the  human  victim  as  well  as  into  that  of  animals. 

The  marked  feature  of  the  pathogenesis  is  loss  of  blood,  not 
merely  caused  by  the  sucking  of  the  leech,  but  also  by  the  bleeding 
from  the  wound  caused  by  the  bite.  Further,  the  punctures 
caused  by  Hcemadipsa  zcylanica  are  extremely  liable  to  become 
ulcers,  which,  according  to  Marshall  and  Davy,  caused  a  high  rate 
of  mortality  among  the  Madras  sepoys  and  coolies  during  the 
Kandyan  rebellion  of  1818  in  Ceylon.  Short  of  death,  amputa- 
tion of  the  limb  was  necessary  in  those  days.  We  are  not  inclined 
to  consider  these  old  statements  as  erroneous,  because  it  is  quite 
possible  that  some  organism  is  often  introduced  into  the  affected 
part  by  the  leech-bite.  For  a  further  discussion  of  the  pathogeni- 
city, see  the  chapters  on  Diseases  of  the  Respiratory  Organs  and 
of  the  Skin. 

Classification. — The  class  Hirudinea  may  be  divided  into  several  orders: — 

Order  I.:  Rhynchobdellida. — -Hirudinea  without  jaws,  with  an  extensile  pro- 
boscis and  with  colourless  blood,  living  in  salt  and  fresh  water. 

The  Rhynchobdellida  are  divided  into  two  families : 

Family  1 :  IchthyobdellidcB. — Rhynchobdellida  with  the  anterior  narrower 
part  of  the  body  distinct  from  the  posterior,  and  with  both  suckers  distinct 
from  the  body. 

To  this  family  belong  the  genera  Pisciola  de  Blainville,  1818,  and  Pontobdella 
Leach,  181 5,  mentioned  in  the  chapter  on  Protozoa. 

Family  2 :  Glossiphoniidts.- — Rhynchobdella  with  the  anterior  sucker  fused 
to  the  body,  while  the  posterior  is  distinct. 

Among  the  genera  of  this  family  is  Hcementaria  de  Filippi,  1849,  of  which 
H.  officinalis  de  Filippi  is  found  in  Mexico,  and  is  alleged  to  cause  drowsiness, 
buzzing  in  the  ears,  and  a  painful  rash,  when  it  bites  a  person.  The  causation 
of  these  symptoms  is  obscure.     Another  species  is  H.  ghiilanii  de  Filippi,  1849. 

Other  genera  are  Glossiphonia  Johnson,  1816 ;  Hemiclepsis  Vejdovsky,  1883 ; 
and  Placobdella  R.  Blanchard,  1893. 

Order  II.  :  Arhynchobdellida. — Hirudinea  usually  with  jaws,  without  a 
proboscis,  and  with  red  blood,  living  in  fresh  water  or  on  land.  There  are 
two  families,  Gnathobdellidae  and  Herpobdellidae,  of  which  only  the  first 
concerns  us. 

Family  Gnathobdellidae. 

Arhynchobdellidae  with  five  or  more,  rarely  four,  pairs  of  eyes,  and,  except 
in  the  Semiscolinae,  with  three  denticulate  jaws.  Eggs  enclosed  in  a  spongy 
cocoon,  which  is  deposited  above  water-line. 

The  Gnathobdellidae  are  classified  into  the  following  subfamilies:  Hirudi- 
ninae,  Hagmadipsinae,  and  Semiscolecinae,  which  last  is  not  of  interest  to  us. 

Subfamily  Hirudinin^e  R.  Blanchard,  1894. 

Aquatic  Gnathobdellidae  with  ten  eyes,  and  with  an  eyeless  ring  between 
the  third  and  fourth  pair  of  eyes,  with  denticulate  jaws.  Complete  somite 
formed  of  five  rings.  The  nephridial  pores  open  near  the  margins  of  the  body 
on  the  ventral  surface. 


686  ANNUL  AT  A  AND  HIRUDINEA 

In  1896  Blanchard  divided  this  subfamily  into  two  series:  (1)  Monosticho- 
donta — jaws  armed  with  one  row  of  teeth;  (2)  Distichodonta — jaws  armed 
with  two  rows  of  teeth. 

The  genera  are:  Hirudo,  Limnatis,  Hcemopis,  Hirudinaria,  Limnobdella, 
Macrobdella,  and  Whitmania,  which  are  divided  into  two  series. 

Series  1:  Monostichodonta. 

Hirudininae  with  jaws  with  or  without  papillae,  and  armed  with  a  single  row 
of  numerous  sharp  teeth. 

Hirudo  Linnaeus,  1758. 

Synonyms. — Sanguisuga  Savigny,  1832;  Iatrobdella  de  Blainville,  1827. 

Hirudininae  with  twenty-six  somites,  of  which  the  1st  and  2nd  have  each 
one  ring;  3rd,  two  rings;  4th,  5th,  and  6th,  each  three  rings;  7th  to  22nd, 
each  five  rings;  23rd,  three  rings;  24th,  25th,  and  26th,  each  two  rings;  making 
in  all  102  rings. 

Eyes  are  carried  on  the  1st,  2nd,  3rd,  5th,  and  8th  rings.  The  buccals  are 
the  5th  and  6th,  and  the  post-buccals  the  7th  and  8th.  The  first  pair  of 
nephridia  is  on  the  13th,  and  the  last  (the  17th)  pair  on  the  93rd  ring. 

The  male  orifice  is  between  the  30th  and  31st  rings,  which  are  the  2nd  and 
3rd  of  the  10th  somite. 


Fig.  309. — Hirudo  multistriata  Schmarda. 
The  common  water  leech  of  Ceylon. 

The  female  orifice  is  five  rings  behind  that  of  the  male — i.e.,  between  the 
35th  and  36th  rings.  The  anus  is  situate  on  the  102nd  ring,  or  between  the 
101st  and  102nd. 

Hirudo  medicinalis  Linnaeus,  1 758,  is  found  principally  in  Hungary.  Variety 
officinalis. 

H.  troctina  Johnston,  1816,  is  the  medicinal  leech  of  England,  France,  Spain, 
and  Algeria. 

H.  nipponia  Whitman,  1886.     Japan. 

H.  sinica  de  Blainville,  1827.     China. 

H.  quinqtiestriata  Schmarda.     Australia. 

H.  saigonensis.     Cochin-China. 

H.  asiatica  R.  Blanchard.     Afghanistan  and  Persia. 

H.  timorensis  R.  Blanchard.     Timor. 

H.  septemstriata  Grube.     South  Africa. 

H.  hildebrandti  R.  Blanchard.     East  Africa,  Victoria  Nyanza. 

H.  multistriata  Schmarda.     Ceylon. 

Series  2:  Distichodonta. 

Hirudininae  with  jaws  without  papillae,  and  armed  with  two  rows  of  in- 
frequent, blunt,  irregular  teeth. 

Haemopis  Savigny,  181 7. 

Synonym. — Aulastoma  Moquin-Tandon,  1826. 

Hirudininae  with  3  rings  on  the  23rd  somite,  and  two  rings  to  the  24th, 
25th,  and  26th  somites.  Crop  with  one  pair  of  elongate  lateral  caeca  reflected 
posteriorly.  Genital  openings  usually  separated  by  five  rings.  Upper  lip 
of  anterior  sucker  not  divided  interiorly  by  a  longitudinal  groove.  H. 
sanguisuga  Linnaeus,  1758,  found  in  Europe,  and  H.  lacustre  Leidy  in  America. 

Limnatis  Moquin-Tandon,  1826. 

Hirudinin33  with  a  longitudinal  groove  on  the  inner  surface  of  the  upper 
lip  of  the  anterior  sucker.     Jaws  with  more  than  100  teeth. 


HMMADIPSINM  687 

Limnatis  nilotica  Savigny,  1820.  This  leech  is  8  to  10  centimetres  in  length, 
and  is  common  in  North  Africa,  the  Canaries,  South  Europe,  and  Asia  Minor, 
while  it,  or  some  other  species,  is  found  on  the  West  Coast  of  Africa. 

Limnatis  mysomelas  Serulias  and  Virey,  1829,  is  found  in  Senegambia,  and 
L.  granulosa  Savigny,  1820,  in  India. 

These  leeches  are  of  importance,  because  they  are  apt  to  get  into  the  nose, 
naso-pharynx,  pharynx,  and  larynx  of  persons  drinking  at  pools  of  water, 
and  to  cause  serious  symptoms.  Other  species  are  L.  africana  R.  Blanchard  in 
Senegal  and  the  Congo,  L.  maculosa  Grube,  1859,  in  Singapore,  L.  mysomelas 
in  Senegal,  and  L  granulosa  in  India. 

Hirudinaria  Whitman,   1886. 

Hirudininae  with  the  sexual  pores  separated  by  several  rings.  Acetabulum 
very  large. 

H.  javanica  Wahlberg,  1855.     In  Batavia,  Sumatra,  and  Burma. 

Limnobdella  R.  Blanchard. 

Hirudininae  with  103  to  104  rings.  Jaws  without  papillae.  The  6th  somite 
with  three  rings,  the  23rd  with  five  rings. 

L.  grandis  R.  Blanchard.     Timor,  Sumatra,  and  Ceylon. 
L.  australis  Besisto,  1859.     Sydney  and  New  South  Wales. 
L.  mexicana  R.  Blanchard.     Mexico. 

Macrobdella  Verrill,  1872. 

Hirudininae,  jaws  without  sensory  papillae;  teeth  not  numerous;  103  body 
rings.     Both  genital  openings  on  the  nth  somite. 
M.  sestertia  Whitman,  1886.     America. 

Whitmania  R.  Blanchard,  1884. 
Hirudininae  with  105  to  107  rings;  6th  segment  with  five  rings;  23rd  has 
always  more  than  three  rings.     Teeth  more  or  less  rudimentary. 

W.  ferox  R.  Blanchard,  1896.     London  Zoological  Gardens  and  in  Asia. 

Subfamily  H^madipsin^e  R.  Blanchard,    1894. 

Gnathobdellidae,  small  leeches,  living  on  land,  with  ten  eyes,  and  no  eyeless 
ring  between  the  3rd  and  4th  eyes.  The  three  last  body  somites  (twenty- 
three  to  twenty-six)  with  only  one  ring  each.     Dentition  simple  and  complete. 

Remarks.  —  The  Haemadipsinae  were  monographed  by  Blanchard  in  July, 
191 7,  in  his  usual  masterly  style. 

Type  Genus. — Hcemadipsa  Tennent,  1861. 

Haemadipsa  Tennent,  1861. 

Synonyms. — Hcsmofis  Schmarda,  1861;  Chthonobdella  Grube,  1865. 

Haemadipsinae,  terrestrial  in  habit,  2  to  3  centimetres  in  length;  sub- 
cylindrical,  tapering  slightly  forwards,  cephalic  lobe,  rounded  when  at  rest, 
but  pointed  in  extension  ;  acetabulum  moderately  large,  round,  or  oval, 
centrally  attached,  separated  from  the  body  only  by  a  feeble  constriction. 

Eyes  in  five  pairs,  the  rings  bearing  the  3rd  and  4th  pair,  not  separated  by 
an  intervening  ring,  the  rings  bearing  the  4th  and  5th  pairs,  separated  by 
two  rings.  Qisophagus  with  three  plications — -one  dorsal  and  two  latero- 
ventral.  The  three  maxillae  covered  with  teeth,  which  increase  in  size  towards 
the  converging  anterior  ends  of  the  jaws.  Clitellum  includes  three  somites 
and  fifteen  rings.  Genital  orifices  separated  by  five  rings;  nephridial  pores  at 
the  margin  of  the  body,  the  last  pair  opening  in  the  constriction  between  the 
body  and  the  acetabulum. 

Remarks. — The  land  leeches  of  Ceylon  were  separated  from  the  genus 
Hirudo  by  Tennent  in  1861,  under  the  name  of  Hamadipsa  ;  and  those  of 


688  AN NU LATA  AND  HIRUDINEA 

Australia  by  Whitman  in  1886,  under  the  term  Geobdella,  altered  to  Moquinia 
by  Blanchard. 

Land  leeches  are  mostly  tropical,  living  in  the  area  denned  by  the  parallels 
400  N.  and  400  S.  of  the  Equator,  for  they  appear  to  prefer  a  warm,  moist 
climate.  In  the  Himalayas  they  ascend  to  a  height  of  11,000  feet;  but  in 
Ceylon  they  diminish  in  numbers  above  4,000  feet.  They  are  to  be  found 
in  Ceylon,  India,  Java,  Sumatra,  Luzon,  Mindanao,  Pelew  Islands,  Japan, 
New  Guinea,  Celebes,  New  South  Wales,  Queensland,  and  the  southern 
provinces  of  Chili  and  Trinidad.  They  live  under  damp  leaves  and  loose 
rubbish,  and  appear  when  the  air  is  disturbed  by  the  approach  of  man  or 
beast,  and  so  quickly  do  they  rush  to  the  attack  that  they  have  earned  the 
name  of  the  '  jumping  leech.'  As  a  rule  they  bite  gently,  but  make  a  deep 
wound,  the  scar  of  which  may  take  months  to  disappear.  They  fill  them- 
selves with  blood  in  about  thirty  minutes,  and  then  drop  off. 

Classification, — Some  of  the  species  are  as  follows: — 

H.  zeylanica  de  Blainville,  1827.  Ceylon.     H.  vagans  R.  Blanchard.      Mada- 
gascar. 
H.  ttmbata  Grube.     Sydney.  H .javatiica  Wahlberg.     Java. 

H.fallax  R.  Blanchard.    Madagascar.         H .  ialagalla  Meyen.     Philippines. 
H.  morsitans  R.  Blanchard.        ,,  H.japonica  Whitman.     Japan. 

Other  Genera. 

Mesobdella  R.  Blanchard,  1893.— With  three  rings  to  a  somite. 

M.  gemmata  R.  Blanchard,   1894. 
Philcemon  R.  Blanchard,  1893. — With  four  rings  to  a  somite. 

P.  pungens  R.   Blanchard.     Java  and   Australia. 

P.  grandidieri  R.  Blanchard.     Madagascar. 
PhytobdeUa  R.  Blanchard,  1893. — With  six  rings  to  a  somite. 

P.  meyeri  R.  Blanchard.     Luzon. 

P.  moluccensis  R.  Blanchard.     Salawati. 
Planobdella  R.  Blanchard,  1894. — With  seven  rings  to  a  somite. 

P.  quoyi  R.  Blanchard.     North  Celebes. 

P.  molesta  R.  Blanchard.     Celebes. 
Moquinia  R.  Blanchard,  1881. — With  seven  and  a  half  rings  between  genital 
apertures. 

Remaining  Orders. 

The  remaining  orders,  Histriobdellida,  Acanthobdellida,  and  Branchio- 
bdellida,  do  not  concern  us. 


REFERENCES. 

Hirudinea. 

Blanchard,  R.  (1888).     Dictionnaire  Encyclop.  de  Science  Med.,  vol.  xiv. 

(A  most  valuable  account.) 
Blanchard,  R.  (1893-94).     Bull.  Mus.  Zool.  d.  R.  Un.  di  Torino,  viii.  145,  146; 

ix. 192. 
Blanchard,  R.  (1917).     Bulletin  de  la  Societe  de  Pathologie  Exotique,  x.  7, 

640-675. 
Harding    (1908).     Journal   of   Parasitology,    i.    186;     (1910)    ibid.,    p.    130. 

Cambridge. 
Knox,  R.  (1861).     Historical  Relation  of  the  Island  of  Ceylon,  pp.  48,  49. 

1861. 
Moquin-Tandon  (1846).     Monographic  de  la  Famille  des  Hirudinees.     Paris. 
Tennent  (1859).     Ceylon,  pp.  302-305.     London,  1859.     Natural  History  of 

Ceylon,  pp.  479-483.     London,  1861. 
Whitman  (1886).     Quarterly  Journal  of  Microscopical  Science,  xxvi.  315. 


CHAPTER   XXVIII 
ARTHROPODA 

Arthropoda — Diplopoda — Acarina— Gamasoidea — Ixodoidea  —  Trombidoidea 
— Eupopoidea — -Sarcoptoidea — Vermiformia  —  Linguatulida  —  Crustacea 
— Chilopoda — References . 

PHYLUM  ARTHROPODA  v.  Siebold  and  Stannius,  1845. 

Bilaterally  symmetrical  metazoa,  with  well-developed  body  cavity 
and  heteronomously  segmented  body  with  hollow  segmental  appen- 
dages, moved  by  intrinsic  muscles  and  penetrated  by  blood  spaces. 
One  or  more  pairs  of  appendages  behind  the  mouth  are  densely 
chitinized  and  turned  inwards  so  as  to  act  as  jaws. 

The  phylum  Arthropoda  is  divided  into  the  following  grades  and 
classes  by  Ray  Lankester: — 

Grade  A:  Protarthropoda. 
Class  I.  Onchophora. 

•  trade  B:  Euarthropoda  Lankester. 

Class  II.  Diplopoda. 
Class  III.  Arachnida. 
Class  IV.  Crustacea. 
Class  V.  Chilopoda. 
Class  VI.  Hexapoda. 

The  Onchophora,  which  includes  the  genus  Peripatiis,  does  not 
concern  us,  but  the  other  classes  all  contain  species  of  importance  in 
medicine. 

CLASS  II.  DIPLOPODA  Ray  Lankester,  1904. 

Synonym.— Chilognatha. 

Euarthropoda,  in  which  the  somites  generally  fuse  after  early  development, 
forming  double  somites,  with  two  pairs  of  appendages,  or  present  legless  and 
leg-bearing  somites  alternately.     They  are  terrestrial,  breathing  by  tracheae. 

The  following  orders  are  recognized: — (1)  Juliformia;  (2)  Symphyla;  and 
(3)  Pauropoda.     We  shall  only  consider  the  first. 

Order  I.  Juliformia — Diplopoda  with  two  pairs  of  appendages  on  each 
somite. — Two  families  of  the  Juliformia  need  be  mentioned: — 

Family  ]vi.iDM—fulifor»iia  with  large  free  head,  without  broad  dorsal 
plates. — Two  species  of  Julus — viz.,  /.  terrestris  L.  and  /.  londinenensis  Leach 
— have  been  found  as  occasional  parasites  (accidental)  in  the  human  alimentary 
canal  in  Europe. 

689  44 


69o  ARTHROPOD  A 

Family  PoLYDESMiDiE — Juliformia  with  large  free  head  and  laterally  ex- 
tended dorsal  plates. — Polydesmus  complanatus  has  once  been  recorded  as  an 
accidental  parasite  in  the  human  alimentary  canal  in  Europe. 

Pathogenicity. — These  parasites  give  rise  to  symptoms  both  direct  and 
reflex. 

CLASS  III.  ARACHNIDA  Lamarck,  1815. 

Euarthropoda  with  two  pre-oral  segments,  the  first  bearing 
typical  eyes,  and  the  second  antennae  or  cheliceras,  and  six  post- 
oral  appendages,  modified  so  as  to  function  as  jaws,  but  possessing 
also  a  well-developed  ramus,  which  may  be  a  leg,  palpus,  or  chela. 
The  primitive  forms  have  branchial  respiratory  processes,  and  the 
higher  pulmonary  organs. 

The  Arachnida  are  classified  by  Lankester  into  :- — 

Grade  A:  Anomomeristica. 
Grade  B:  Nomomeristica. 

Subclass  I.  Pantapoda. 
Subclass  II.  Euarachnida. 

Grade  a:  Hydropneusta. 
Grade  b:  Aeropneusta. 

Section  A:  Pectinifera. 
Order  Scorpionidea. 

Section  B:  Epectinata. 
Order  I.  Pedipalpi. 
Order  II.  Aranea. 
Order  III.  Palpigrada. 
Order  IV.  Solifuga. 
Order  V.  Pseudoscorpions. 
Order  VI.  Podogona. 
Order  VII.  Opiliones. 
Order  VIII.  Acarina. 
Order  IX.  Linguatulida  (Incertae  sedis). 

Details  with  regard  to  this  classification  may  be  obtained  by 
reference  to  Ray  Lankester's  paper  in  the  Quarterly  Journal  of 
Microscopical  Science,  1904,  vol.  xlviii.,  p.  165. 

We  have  already  considered  the  effects  of  the  bites  of  the  Scor- 
pionidea, the  Aranea,  and  some  of  the  Acarina,  and  now  it  is  neces- 
sary to  consider  more  particularly  those  which  are  parasitic,  and 
cause  or  spread  disease. 

Two  orders  must  be  dealt  with  in  some  detail— viz.,  the  Acarina 
and  the  Linguatulida. 

ORDER  ACARINA  Nitzsch,  181S. 

Synonym. — Rhynchostomi . 

Definition.— Degenerate  Arachnida  with  the  basal  segments  of  the 
second  pair  of  appendages  united  in  the  middle  line  behind  the 
mouth,  while  those  of  the  third,  fourth,  fifth,  and  sixth  appendages 
are  widely  separated,  and  take  no  part  in  mastication.      The  re- 


ACARINA  691 

spiratory  stigmata  usually  belong  to  the  prosoma,  and  the  primitive 
segmentation  of  the  opisthosoma  has  either  entirely  or  almost 
entirely  disappeared. 

Remarks. — -The  Acarina  include  the  mites  and  ticks  which  have 
long  been  known  to  be  human  parasites,  but  it  is  only  recently  that 
the  latter  have  come  into  notice  as  carriers  of  disease. 

It  is  true  that  a  mite,  or  rather  its  larva,  has  long  been  suspected 
to  be  the  cause  of  Tsutsugamushi  disease,  but  it  is  probable  that 
at  present  we  are  not  fully  aware  of  the  disease  carrying  and  pro- 
ducing effects  of  these  small  arachnids. 

The  Acarina  are  cosmopolitan  in  their  distribution,  and  are 
said  to  be  most  numerous  in  temperate  regions.  They  are  abundant 
at  high  altitudes.  Banks  remarks  that  the  parasites  follow  the 
distribution  of  the  host — i.e.,  of  the  food- — a  remark  the  importance 
of  which  has  already  been  appreciated.  The  observer  will  find 
that  a  parasitic  disease  is  often  bounded  by  the  distribution  of 
the  food  of  the  insect,  which  spreads  the  real  cause  of  the  disease. 

Morphology. — -The  morphology  is  described  under  the  heading 
Ixodoidea. 

Life-History. — The  female  lays  eggs  covered  by  a  shell  and  an 
inner 'membrane  called  the  deutovum.  A  six-legged  larva  hatches 
out  from  the  egg,  and  after  a  time,  during  which  it  may  be  active 
or  quiescent,  moults  and  produces  the  nympha,  which  is  eight- 
legged,  and  resembles  the  adult,  except  in  the  non-development  of 
the  sexual  organs  and  apertures.  The  leg  which  is  added  to  the 
nympha  is  the  fourth,  or  posterior.  The  nymph  is  usually  energetic, 
and  feeds  on  some  host;  eventually  passing  into  a  quiescent  stage 
and  undergoing  considerable  histological  changes,  it  moults  and 
becomes  the  adult  male  or  female.  The  males  are  usually  smaller 
and  more  active  than  the  females.  Both  sexes  suck  fluid  nourish- 
ment from  the  host,  whether  animal  or  plant.  Their  life-history 
will  be  found  to  vary  with  the  different  families  and  species. 

Pathogenicity. — The  Acarina  are  important  in  the  dissemination 
of  disease  both  among  men  and  animals.  In  men  they  are  respon- 
sible for  the  spread  of  such  fevers  as  Dutton's  relapsing  fever,  the 
tick  fever  of  the  Rocky  Mountains,  Tsutsugamushi  disease,  and  the 
disease  associated  with  the  Miana  bug  in  Persia;  also  they  are 
responsible  for  a  number  of  skin  diseases,  among  which  may  be 
mentioned  scabies.  In  animals  they  are  responsible  for  the  spread 
of  the  Babesiases,  and  of  some  Spirochsetiases,  as  well  as  causing 
some  forms  of  dermatitis.  Incidentally  it  may  be  mentioned  that 
they  also  cause  disease  in  plants,  producing  galls,  etc. 

Enemies. — Hurtful  as  they  are  themselves,  they  are  not,  however, 
free  from  persecution  on  the  part  of  other  animals.  Blood-sucking 
insects,  particularly  the  Reduviidae,  prey  on  some  arachnids, 
sucking  their  blood.  Wellman  has  reported  that  he  has  caught 
Phonergates  bicoloripes  Stal  in  the  act  of  sucking  the  juices  of 
Ornithodoros  moubata,  the  tick  responsible  for  the  spread  of  Dutton's 
relapsing  fever. 


692  ARTHROPOD  A 

Classification. — The  order  Acarina  is  divided  into  the  following 
suborders: — 

Suborder  Notostigmata. — Acarina  in  which  the  opisthosoma 
is  segmented  by  ten  integumental  grooves,  of  which  the  anterior 
four  are  furnished  with  a  single  pair  of  dorsally  placed  spiracles. 
(Family :  Opilioacaridae.)     This  suborder  does  not  concern  us. 

Suborder  II.  Cryptostigmata.  —  Acarina  with  a  hard  integu- 
ment strengthened  by  chitinized  dorsal  and  ventral  sclerites. 
Stigmata  on  the  acetabula  of  the  third,  fourth,  fifth,  and  sixth 
pairs  of  appendages.  (Family:  Oribatidae.)  This  also  does  not 
concern  us. 

Suborder  III.  Metastigmata.  — Acarina  with  a  hard  integument 
like  the  Cryptostigmata.     One  pair  of  stigmata  above  and  behind 
the  base  of  the  fourth,  fifth,  or  sixth  pair  of  appendages. 
Superfamily  A :  Gamasoidea. 
Superfamily  B :  Ixodoidea. 

Suborder  IV.  Prostigmata. — Acarina  with  soft  integument 
strengthened  by  special  sclerites,  those  on  the  ventral  surface  of 
the  prosoma  apparently  representing  the  basal  segments  of  the 
legs  embedded  in  the  skin.  Except  in  the  aquatic  species,  there 
is  a  pair  of  stigmata  close  to  or  above  the  first  pair  of  appendages. 
Superfamily  A :  Trombidoidea. 
Superfamily  B :  Eupopoidea. 

Suborder  V.Astigmata. — Degenerate  Acarina,  mostly  parasitic, 
like  Prostigmata  in  the  development  of  integumental  sclerites  and 
the  softness  of  the  skin,  but  with  the  respiratory  system  absent. 
(Superfamily:  Sarcoptoidea.) 

Suborder  VI.  Vermiformia. — Degenerate  parasitic  Acarina 
without  respiratory  system,  and  with  the  body  produced  posteriorly 
into  an  annulated  caudal  prolongation.  With  the  third,  fourth, 
fifth,  and  sixth  pairs  of  appendages  short,  and  only  three  jointed. 
(Family:  Demodicidae.) 

Suborder  VII.  Tetrapoda. — Degenerate  atracheatc  Acarina 
with  body  as  in  the  Vermiformia,  but  with  the  third  and  fourth  pairs 
of  appendages  long  and  normally  segmented,  and  the  fifth  and 
sixth  entirely  absent.  (Family:  Eriophyidae.)  This  suborder, 
however,  need  not  concern  us. 

SUBORDER  III.   METASTIGMATA. 

The  parasites  included  in  this  suborder  would  in  popular  language 
all  be  called  ticks. 

It  is  divided  into  two  superfamilies: — 

A.  Gamasoidea. — With  a  small  hypostome  without  teeth. 

B.  Ixodoidea. — With  a  large  hypostome  armed  with  many 
recurved  teeth. 

SUPERFAMILY  A:  GAMASOIDEA. 

The  superfamily  Gamasoidea  is  divided  into  three  families: — (i)  Dermanys- 
sid^e,  (2)  Uropodida?.  (3)  Gamasidae. 


GAMASID/E  693 

Family  i  :  Dermanyssid^e. 

Gamasoidea  parasitic  on  vertebrates,  with  mandibles  fitted  for  piercing, 
with  the  body  sometimes  constricted,  with  soft  integuments  finely  striated. 

The  Dermanyssidse  are  divided  into  two  subfamilies: — Dermanyssinae,  with 
an  anal  plate;  Halarachninae,  without  an  anal  plate. 

Subfamily  Dermanyssin^;. 
Dermanyssus  Duges,  1834. 
Dermanyssinae  with  a  long  body  not  distinctly  constricted;  peritreme  on 
the  venter,  with  chelate  mandibles  in  the  male  and  long  stiliform  mandibles 
in  the  female.     Parasitic  on  birds. 

Dermanyssus  gallinae  Redi,  1674. 

Synonyms. — Pulex  gallincB  Redi,  1674;  Acarus  galli-ncB  de  Geer,  1778;  Der- 
m&nyssus  avium  Dugds,  1836. 

This  parasite  lives  in  cracks,  etc.,  in  the  hen-house  during  the  day,  and 
attacks  the  fowls  at  night,  sucking  the  blood.  It  is  also  found  on  many  other 
birds  and  mammals,  and  occasionally  on  man,  generally  on  poultry-men,  in 
whom  it  produces  a  papular  eczematous  dermatitis  on  the  back  of  the  hands 
and  forearms.  D.  hirudinis  Hermann,  1804,  which  is  probably  only  a  variety 
of  this  species,  can  also  be  found  on  man. 

Morphology.- — Body  egg-shaped,  posterior  end  wider  than  anterior,  abdo- 
men with  short,  marginal,  widely  separated  bristles. 

Male,  0'6  millimetre  by  0-32  millimetre;  female,  0-7  millimetre  by  0*4  milli- 
metre. 

Holothyrus  Gervais,  1842. 

Holothyrus  coccinella  Gervais,  1842. 

This  arachnid  is  found  on  ducks  and  geese  in  Mauritius,  and  is  said  to  attack 
human  beings,  causing  swelling  of  the  affected  part,  which,  if  the  lips  or  tongue 
of  a  child,  may  be  dangerous.  Some  authorities  consider  that  this  arachnid 
should  form  a  separate  family  of  its  own — Holothyryidae. 

Family  2 :  Gamasid^e. 

In  this  family  comes  the  genus  Lcelaps  Koch,  1842,  with  its  species  L.  echid- 
ninus  Berlese,  mentioned  in  the  chapter  on  Protozoa,  because  Miller  has 
traced  the  life-cycle  of  Hcemogregarina  muris  Balfour,  1905,  in  it  and  in  the 
rat  Mas  decumanus. 

SUIT.kl  AMILY  B:  IXODOIDEA    Banks,   1894. 

Synonyms.-  Acarus  Linnaeus,  17 46,  pro  parte;  Ricinice  Latreille, 
Is"),  pro  parte;  Ixodides  Leach,  1815;  Ixodea  Burmeister,  1837; 
Ricini  Koch,  [8  |f  and  1847;  Ixodes  Gervais,  1844;  Ixodida  Kiichen- 
meister,  1855;  Ixodida  Leach,  1863;  Ixodides  Donnadicu,  1875,  and 
Mtegnin,  1876;  Ixoda  Wagner,  1876;  Metastigmata Canestrini,  1892; 
Cynorhastea  Marx,  1892;  Arpagostoma  Lahille,  1905. 

The  term  Cynorhastea  is  derived  from  Aristotle,  who  speaks  of 
these  arachnids  as  Kvvopaiarrjs  (the  dog-tormentors),  because  ticks 
were  well  known  in  his  day  to  attack  hunting-dogs. 

The  Exodoidea  are  the  ticks,  which  have  become  of  importance  in 
tropical  medicine  not  merely  because  of  their  unpleasant  bite,  but 
because  of  the  spread  of  disease  by  their  agency — as,  for  example, 


694 


ARTHROPOD  A 


the  tick  fever  of  Africa,  Tsutsugamushi  disease,  the  tick  fever  of 
the  Rocky  Mountains,  etc.  They  are  parasitic  on  mammals,  birds, 
and  reptiles,  but  are  not  strictly  confined  to  one  host.  The  Arga- 
sidas,  one  of  the  two  families  included  in  the  superfamily,  are  now 
nocturnal  in  habits,  and  do  not  become  greatly  distended  with  blood : 
while  the  other  family,  Ixodidae,  or  true  ticks,  are  very  common 
in  tropical  countries. 

Morphology. — A  tick  is  divisible  into  a  head,  rostrum,  or  capitulum,  and  a 
body.  The  capitulum  is  the  small  anterior  structure  with  the  mouth  parts, 
and  is  easily  visible  from  above  in  the  Ixodidae  (vide  Fig.  313),  but  must  be 
viewed  from  below  in  the  Argasidae  (Fig.  321).  It  joins  the  rest  of  the  body 
at  the  camerostome.     The  capitulum  consists  of  the  following  parts: — 

1.  Neck. — This  is  the  junction  of  the  rostrum  with  the  rest  of  the  body. 

2.  Base.— This  is  the  hard  basal  portion,  and  is  usually  quadrangular,  but 
its  outline  varies. 

In  females  of  the  Ixodidae  there  are  two  porose  areas  on  the  upper  surface 
(vide  Fig.  31 1).     Attached  behind  the  base  is  the  neck;  in  front,  in  the  middle 

line,  is  the  haustellum,  composed  of  the 
hypostome  and  the  mandibles  and  their 
sheaths,  on  each  side  of  which  lie  the 
palpi. 

3.  The  hypostome  is  an  elongated 
structure  composed  of  two  symmetrical 
halves,  with  numerous  minute  teeth, 
called  denticles,  on  its  ventral  surface. 

4.  The  chelicera3,  or  mandibles,  are 
two  in  number — -one  on  each  side  of  the 
median  line,  lying  dorsal  to  the  hypo- 
stome. The  posterior  portion  enclosed 
in  the  body  is  swollen  for  the  attachment 
of  muscles,  while  the  anterior  is  flat  and 
narrow,  and  terminated  by  a  hook-like 
digit,  which  has  two  or  three  processes 
— the  apophyses — an  internal,  an  ex- 
ternal, and  a  middle,  with  hook-like 
teeth. 

5.  The  mandibular  sheath  lies  dorsal 
to  the  mandibles. 

6.  The  palpi  are  composed  of  four 
segments    or    articles — basal,    antepen- 

They  are  of  importance  in  classification 
into  genera,  as  they  possess  hairs,  bristles,  edges,  angles,  and  spines,  varying 
in  different  species.  There  is  sometimes  a  group  of  long  hairs  on  the  internal 
aspect  of  the  palpi,  which  are  probably  sensory. 

The  body  varies  greatly  in  form,  colour,  outline,  and  structure.  It  is 
divided  into: — (1)  Dorsal  surface;  (2)  ventral  surface;  (3)  to  (5)  anterior, 
posterior,  and  lateral  margins. 

1 .  Dorsal  Surface. — On  the  dorsal  surface  may  be  noted  (Figs .  3 1 3  and  318): — ■ 

(a)  The  scutum,  found  in  the  Ixodida,  and  well  marked  in  the  adult 

male,  but  much  smaller  in  the  adult  female.     It  is  a  hard,  chitin- 
ous  plate,  with  two  longitudinal  grooves  (cervical  grooves). 

(b)  The  eyes,  only  sometimes  present  on  each  lateral  margin  of  the 

scutum  in  Ixodidae,  or  near  the  first  coxa  in  Argasidaa. 

(c)  The  dorso-submedian  porose  plates  are  small,   circular,   or  oval 

chitinous  structures  on  each  side  of  the  median  line,  near  the 
third  and  fourth  legs. 

(d)  The   postero-marginal   festoons,    when   present,   are  eleven   areas 


Fig.  310. — Margaropus  annnlatus 
var.  auslralis  Say:  Dorsal  View 
of  the  Male. 

ultimate,  penultimate,  and  apical. 


IXODOIDHA 


69; 


marked  out  by  grooves  lying  along  the  posterior  margin  of  the 

body  between  the  stigmata. 
(e)  The  dorsal  grooves  are  usually  longitudinal,  and  not  always  distinct, 

as  they  are  due  to  muscular  contractions. 
(/)  Pits,  hairs,  spines,  etc.,  may  be  visible  on  the  dorsal  surface. 

Ventral  Surface. — The  ventral  surface  exhibits  (Fig.  324): — 

(a)  The  genital  pore,  situated  in  the  ventro-median  line,  between  the 

coxae  of  the  first  three  pairs  of  legs. 

(b)  The  anus,  situate  in  the  ventro-median  line,  behind  the  posterior 

pair  of  legs.     It  is  surrounded  by  a  valve,  and  in  the  male  of 
certain  genera  has  laterally  the  clypea  or  anal  valves. 

(c)  The  ventral  shields  of  chitin  are  small  sclerites  covering  the  surface 

in  the  male. 


0 
Fig.   311. — Dorsal   View   of  the  Capitulum 
of  a  Tick:  Female  {Hcemaphysalis  punctata 
C.  and  F.). 
I,  Cheliceras;  2,  hypostome;  3,  palp;  4,  porose  area. 

(After  Nuttall,   Cooper,  and  Robinson,  Journal  of  Parasitology.) 


Fig.  312.  —  Chelicera 
of  H.  punctata  :  Male 
(C.  and  F.). 


(d)  The  stigmata  lie  one  on  each  side  of  the  body,  between  the  3rd 

and   4th  pairs   of  legs  in  the  Argasidae,  and  behind  the  fourth 
in  the  Ixodidae. 

(e)  There  are  often  to  be  seen  a  pair  of  genital  furrows  and  an  anal 

furrow. 
(/)  Pits,  pores,  hairs,  and  punctations  are  to  be  found  as  on  the  dorsal 
surface. 

3.  Anterior  Margin. — -This  varies  as  compared  with  the  posterior,  being 
sometimes  straighter,  sometimes  emarginate,  and  receiving  at  the  camero- 
some  the  rostrum. 

4.  Posterior  Margin. — This  is  generally  rounded,  and  often  marked  by  the 
festoons  already  mentioned  on  the  dorsal  surface. 

5.  Lateral  Margins. — They  vary  as  to  their  straightness  or  degree  of  cur- 
vature. 


6g6 


ARTHROPODA 


The  legs  are  segmented  into  trie  following  articles :  coxa,  trochanter,  femur, 
patella,  tibia,  and  tarsus. 

Internal  Anatomy. — The  internal  anatomy  has  been  studied  by  Christo- 
phers in  Omithodoros  savignyi,  and  most  elaborately  by  Bonnet  in  eight 
Ixodidae  and  three  Argasidae,  males  and  females. 

The  tegument  consists  of  chitinous  layers,  under  which  lies  the  epidermis. 
On  the  surface  are  the  openings  of  numerous  glands.  A  large  cephalic  gland 
is  present  in  some  species,  opening  dorsally  at  the  junction  of  the  rostrum 
with  the  body. 

The  mouth,  which  is  lined  with  chitin,  is  situated  anteriorly  between  the 
mandibular  sheath  dorsally  and  the  hypostome  ventrally.  In  this  position 
it  is  merely  a  horizontal  slit,  with  open  sides,  but  farther  back  these  are  closed 
by  the  junction  of  the  hypostome  with  the  mandibular  sheaths.     The  cavity 


Fig.  313. — Margaropus  annulatus  var,  australis  Say:  Distended  Female. 


extends  backwards  some  little  distance,  and  ends  blindly.  Into  its  postero- 
lateral angles  open  the  ducts  of  the  salivary  glands,  two  large  racemose  glands 
lying  over  the  bases  of  the  first  pair  of  legs.  The  acini  are  globular,  and  their 
walls  consist  of  large  cells,  as  a  rule  laden  with  refractile  granules  staining 
deeply,  or  with  indistinct  granules  staining  less  deeply. 

In  addition  to  the  ordinary  acini,  there  are  groups  of  four  or  five  cells, 
forming  pear-shaped  masses,  which  have  a  peculiar  affinity  for  acid  stains  like 
eosin.  These  elements  are  really  unicellular  glands,  which  open  into  the 
principal  salivary  ducts,  not  into  the  small  ductules.  These  glands,  which  are 
numerous  in  the  Argasidae,  are  probably  poison  glands. 

On  the  floor  of  the  mouth  is  a  V-shaped  opening,  apex  pointing  forwards, 
which  leads  into  the  pharynx.  This  is  a  fusiform  organ,  narrow  in  front, 
where  it  turns  upwards  to  open  into  the  mouth,  while  behind  it  ends  in  the 
oesophagus.  Its  walls  consist  of  chitinous  plates  arranged  ventrally  and 
laterally,  so  that  the  lumen  is  triradiate  on  transverse  section.  At  the  angles 
the  chitinous  plates  are  united  together  by  double  folds,  allowing  expansion 


IXODOIDEA 


697 


and  contraction,  and  brought  about  by  the  contraction  and  relaxation  of 
muscles  taking  origin  in  the  sclerites  forming  the  endoskeleton  of  the  head, 
and  inserted  into  these  plates.  It  ends  posteriorly  in  a  narrow  oesophagus, 
which  is  without  chitinous  support,  and  therefore  soft.  This  oesophagus 
runs  backward,  perforating  a  large  ganglionic  mass,  and  ends  in  the  mid-gut. 
Its  walls  are  composed  of  a  layer  of  columnar  cells  internally  and  by  muscular 
fibres  externally.  Just  before  it  joins  the  mid-gut  its  wall  thickens  and  forms  a 
fold,  the  homologue  of  the  proventriculus,  which  projects  into  that  passage. 

The  oesophagus  opens  on  the  floor  of  the  large  central  food  reservoir  or 
mid-gut,  the  main  canal  of  which  runs  forward  a  little  distance  in  front  of 
this  opening,  and  backwards  to  the  neighbourhood  of  the  rectum. 

The  central  canal  gives  off  diverticula,  which  may  be  classed  into  an  anterior 
set,  consisting  of  a  single  diverticulum;  a  lateral  set,  consisting  of  an  antero- 


FlG.  314. — Copulation  of  the  Male  and  Female  Tick. 
(After  Sambon.) 


lateral  diverticulum,  subdivided  into  three  branches — a  medio-lateral,  into 
two  or  three,  a  postero-lateral,  which  is  single,  and  a  posterior  set,  which  is 
also  single. 

The  walls  of  the  central  tube  and  the  diverticula  consist  of  a  single  layer  of 
large  cells  lying  upon  a  thin  basement  membrane,  external  to  which  are  large 
single  muscular  fibres  arranged  longitudinally  and  transversely  in  an  open 
network.  Digestion  is  assisted  by  free  cells  mingling  with  the  coagulated 
blood  filling  the  diverticula. 

Posteriorly  the  central  canal  is  connected  with  the  rectum  by  means  of  a 
very  fine  canal,  which  appears  to  represent  a  functionless  rudimentary  intestine. 
This  communication  is  not  admitted  by  Bonnet. 

Into  the  rectum  open  also  two  long,  fine,  much-convoluted  tubules  —  the 
Malpighian  tubes,  which  are  composed  of  a  single  layer  of  large  cells  placed 
on  a  basement  membrane.  In  females  they  may  contain  spherical  corpuscles, 
which,  though  present  in  males,  are  much  smaller.  Berlese  and  Bonnet 
consider  that  these  bodies  are  composed  of  guanine. 

The  rectum  is  a  sacculated  tube,  with  a  wall  composed  of  a  single  layer  of 
Il.ntcned  cells  leading  to  the  anus.     Bonnet   objects  to  the  term   'anus,' 


698 


ARTHROPOD A 


considering  the  tubules  as  renal,  the  rectum  as  a  bladder,  and  the  opening  as 
an  excretory  pore;  but  this  term  must  be  kept  for  morphological  reasons. 
Further,  he  states  that  this  excretory  matter  is  only  expelled  during  moulting, 
collecting  at  other  times  in  the  rectum.  The  anus  is  a  slit-like  aperture, 
guarded  by  two  lateral  semicircular  chitinous  plates. 

The  male  reproductive  organs  consist  of  a  thin,  transparent  tubule — the 
testes — ending  at  either  end  in  a  vas  deferens,  which,  after  coiling  upon  itself, 
enters  a  tabulated  structure — the  white  gland.  The  ejaculatory  duct  ends 
in  the  chitinous  penis.  The  female  reproductive  organs  consist  of  a  single 
ovary,  which  lies  across  the  abdomen,  just  behind  the  central  alimentary  sac. 
This  ends  in  two  coiled  oviducts,  which  open  into  a  large  spermatheca  with 
thick  walls,  and  from  which  a  duct  leads  to  the  genital  opening. 

The  tick  breathes  by  a  means  of  a  system  of  tubes,  lined  by  a  spiral  thread  of 
chitin.  These  tubes  are  called  tracheae,  and  radiate,  from  the  opening  on 
the  stigma  called  the  '  spiracle,'  all  over  the  body.     The  circulatory  system 

consists  of  a  median  heart  and  dis- 
tributing vessels.     The  fat  body  is 
well  marked. 
™ -*»  There   are  a  number   of   dermal 

glands,  a  coxal  gland  in  the  second 
coxal  joints  and  opening  on  the  first 
coxal  joints  by  a  minute  pore,  and 
a  cephalic  gland  in  the  head. 

Life-History. — While  on  the 
host  sucking  blood,  the  male 
and  female  parasites  copulate, 
and  the  latter,  growing  to  a 
large  size,  drops  to  the  ground 
and  lays  a  number  of  eggs. 
The  egg  consists  of  a  shell  with 
an  inner  membrane,  enclosing 
food-yolk  and  embryo,  which 
eventually  hatches  as  a  six- 
legged  larva,  without  sexual 
organs  or  stigmata.  The 
digestive  organs  are,  however, 
present,  and  the  little  larva,  becoming  parasitic  on  some  animal,  sucks 
its  blood,  drops  off  and  moults,  giving  rise  to  the  nympha.  The 
nympha  has  eight  legs  and  a  pair  of  large  stigmata,  but  is  without 
reproductive  openings  or  organs.  The  nympha?  now  become  para- 
sitic, and  feed,  after  which  they  drop  off,  moult,  and  become  males 
or  females  with  fully-developed  generative  organs. 

The  adults  now  become  parasitic  and  moult,  and  the  young 
female,  fixing  itself  to  the  host,  grows  considerably,  but  rarely 
changes  her  place;  while  the  male,  remaining  small,  wanders  about 
looking  for  the  female. 

The  life-history  and  the  habits  of  the  different  divisions  of  the 
Ixodidce  are  so  various  that  they  will  be  described  under  their 
separate  heads.  One  example  may,  however,  be  mentioned  here 
— viz.,  Margaropus  decolor  atus — whose  life-history  has  been  studied 
by  Lounsbury.  In  this  species  the  female,  dropping  off  the  host, 
completes  oviposition  in  a  time  varying,  according  to  the  temperature 
of  the  air,  from  five  days  to  four  weeks,  while  the  incubation  of  the 


Fig.  :i5. — A  Tick  laying  Eggs. 
(After  Sambon.) 


IXODOIDEA 


699 


egg  varies  from  three  weeks  to  three  months.  The  larvae,  which  are 
capable  of  remaining  on  grass  without  food  for  months,  must  obtain 
access  to  cattle,  on  which  they  feed,  and  grow  for  three  days,  after 


Fig.  316. — The  Larva  of  Hcsmaphysalis        Fig.  317. — The  Nymph  of  Hesma- 
punctata  C.  and  F.   (X  40.)  physalis  punctata  C.  and  F. 

After  Nuttall,  Cooper,  and  Robinson,  Journal  of  Parasitology .) 


Fig.  318. — Adult  Female  of  Hcemaphysalis  punctata  C.  and  F. 
(After  Nuttall,  Cooper,  and  Robinson,  Journal  of  Parasitology.) 

which  they  moult  and  form  nymphs  on  the  sixth  day  of  their  para- 
sitic existence — i.e.,  without  leaving  the  host.  The  nymph  sucks 
blood  and  grows  till  the  eleventh  day,  and  the  adult  is  hatched  on  the 
thirteenth  to  sixteenth  day  without  the  nymph  leaving  the  host. 

Pairing  takes  place  on  the  seventeenth  to  twentieth  day,  and  the 
fertilized  gorged  female  drops  off  the  host  on  the  twenty-fourth  to 


700 


ARTHROPODA 


thirty-first  day.     Thus,  in  this  case  the  larva  and  nymph  remain 

parasitic  on  the  host,  and  do  not  drop  off  as  described  above. 

Parasitic  on  Man. — The  ticks  known  to  be  parasitic  on  man 

are: — (i)  Argas  reflexus  Fabricius; 
(2)  A.  persicus  Oken;  (3)  Orni- 
thodoros  savignyi  Audouin;  (4) 
0.  moubata  Murray;  (5)  0.  megnini 
Duges;  (6)  0.  turicata  Duges;  (7) 
0.  tholozani  Laboulbene  and  Megnin; 
(8)  Alectorobius  talaje  Guerin-Mene- 
ville;  (9)  Eurhipicephalus  sanguineus 
Latreille;  (10)  Mar  gar  opus  annulatus 
Say;  (11)  Rhipicentor  bicornis  Nut- 
tall  and  Warburt  on;  (12)  Dermacen- 
tor  reticulatus  Fabricius;  (13)  D.  an- 
tler soni  Stiles;  (14)  D.  electus  Koch; 
(15)  D.  modestus  Banks;  (16)  Ixodes 
ricinus  Linnaeus;  (17)  I.  hexagonus 
Leach;  (18)  Amblyomma  americanum 
Koch;  (19)  A.  dissimile  Koch; 
(20)  Hyalomma  cegyptium  Linnaeus. 

Pathogenicity. — Ticks  are  spreaders 
of    disease    in    man    and    animals. 

They  may  be  classified  into  spreaders  of  SpirochcetidcB,  spreaders 

of  Babesia,  and  into  spreaders  of  unknown  germs. 


Fig.  319. — Fully  replete  Fe- 
male of  Hcemaphysalis  punc- 
tata C.   AND   F. 

(After    Nuttall, 
Robinson,  Journal 

ogy-) 

(a)  Magnified;  (b)  natural  size. 


Cooper,    and 
of  Parasitol- 


1.  Spreaders  of  Spirochaetidse. 

1.  Ornithodoros  moubata  carries  Spiroschaudinnia  duttoni  Novy 
and  Knapp,  1906,  and  causes  African  tick  fever  or  Dutton's 
relapsing  fever  in  man. 

2.  Argas  persicus  carries  Spiroschaudinnia  marchouxi  Nuttall, 

x9°4- 

3.  Margaropus     annulatus     carries     Spiroschaudinnia      theileri 

Laveran,  1904. 

2.  Spreaders  of  Piroplasma. 

Eurhipicephalus  appendiculatus  carries  P.  bigeminum. 


1. 

2. 
3- 
4- 
5- 
6. 

/• 


E.  simus — P.  bigeminum. 

E.  evertsi — P.  equi. 

E.  sanguineus — P.  canis. 

E.  bursa — P.  ovis. 

Margaropus  annulatus — P.  annulalum. 

Hcemaphysalis  leachi — P.  canis. 


3.  Spreaders  of  Unknown  Germs. 

1.  Argas  persicus  causes   a  disease   in   Persia.     2.  Dermacentor 
venustus  (sec  D.  andersoni)  causes  Rocky  Mountain  fever. 

Experimentally,  the  nymphs  of  D.  marginatus  and  Amblyomma 


UNKNOWN  GERMS 


701 


americamis  and  the  nymphs  and  adults  of  D.  variabilis  can  transmit 
the  virus  of  Rocky  Mountain  fever. 

Enemies. — The  enemies  of  ticks  are  numerous,  and  among  them  may  be 
mentioned  fowls  and  blackbirds. 

Prophylaxis. — The  prevention  of  ticks  in  cattle  is  a  difficult  proceeding. 
The  following  are  some  of  the  methods  in  use  (from  Balfour  and  Archibald)  :— 

Cattle  Washes  and  Dips. — Arsenic  used  to  be  employed  (Cooper's  Dip 
Powder),  but  was  found  to  be  dangerous.  A  useful  oil  is  crude  petroleum, 
2  gallons;  hard  soap,  £  pound;  and  water,  £  gallon.  The  soap  is  dissolved 
in  the  hot  water  and  the  petroleum  gradually  added.  Five  days'  spraying  is 
advocated  in  place  of  the  usual  fortnightly  dip. 

Rotation  of  Crops. — This  is  said  to  be  useful  in  the  United  States. 

Burning  of  Pastures. — Not  a  good  plan. 

Immunization. — Immunization  by  inoculation  against  babesia,  etc.  It  is 
not  very  useful. 

Quarantine. — Quarantine  of  cattle  and  control  over  their  movements  is 
important. 

There  are,  however,  a  good  many  practical  points  to  be  attended  to  in 
spraying  or  dipping  cattle.  Reference  may  be  made  to  Cooper's  paper  in  the 
Journal  of  Agricultural  Science,  vol.  iii.,  or  to  Newstead's  Report  of  Twenty- 
first  Expedition  of  the  Liverpool  School  of  Tropical  Medicine. 

Classification. — The  Ixodoidea  are  divided  into  two  families: — 
Family  i:    Argasid^e  Canestrini,  1890. — -Ixodoidea  without   a 

scutum;  mouth  parts  of  adult  not  prominent  from  above;  no  pul- 

villus  attached  to  tarsus  in  adults. 
Family  2  :  Ixodid^;  Murray,  1877. — Ixodoidea  with  a  scutum ; 

mouth  parts  prominent  from  above;  pulvillus  present,   attached 

to  the  tarsus  in  adults. 

Remarks. — Neumann's  classification  is  very  different  from  the  one  used  in  this 
book.  He  recognizes  ixodidae  (=ixodoidea)  divided  into  Ixodinae  (  =  Argasidae 
and  Ixodidae)  and  Spelaeorhynchinae,  these  last  being  parasites  on  bats.  Other 
classifications  are  those  by  Lahille  and  by  Banks. 

Family  I:  ArgasId^;. 

These  arachnids  are  more  like  bugs  than  ticks  in  their  habits. 
During  the  day  they  are  concealed  in  cracks  in  walls  or  floors,  or  in 
gravel,  but  at  night  they  come  out  and  run  about.  Christophers 
says  that  if  handled  they  sham  death,  and  that  when  running  about 
they  have  a  curious  habit  of  raising  the  first  pair  of  legs  as  though 
to  receive  information  about  their  surroundings.  They  can  live 
for  a  long  time  (three  to  four  years)  without  food.  They  generally 
feed  after  dark,  being  gorged  in  about  fifteen  minutes. 

Donovan  states  that  while  feeding  fluid  is  secreted  by  the  coxal 
glands,  and  lies  between  the  parasite  and  the  skin  of  the  host. 
This  fluid  is  alkaline,  and  prevents  coagulation  of  blood.  After 
feeding,  the  tick  drops  to  the  ground,  and,  being  wet  with  secretion, 
becomes  covered  with  dust  and  dirt.  At  first  they  are  much  swollen, 
but  in  a  few  days  this  diminishes,  though  they  may  remain  dis- 
tended for  weeks.  Soon  after  feeding,  the  tick  moults,  and  then 
becomes  active  again,  and  is  ready  for  another  feed. 

The  Argasidae  pair  at  various  times,  one  female  being  fertilized 


702 


ARTHROPODA 


by  several  males.  The  female  now  becomes  quiescent,  and  passes 
out  its  ova,  a  process  requiring  a  week  or  more  to  be  completed. 
During  this  process  the  head  is  forcibly  flexed  on  the  body,  so  that 
the  palpi  lie  on  each  side  of  the  body,  while  above  the  head  is  the 
prolapsed  duct  of  the  cephalic  gland,  forming  a  protuberant  mass. 
The  ova  are  not  as  numerous  as  those  of  the  cattle  ticks,  and  are 
generally  laid  in  a  loosely  adherent  mass. 

The  six-legged  larva  hatches  in  less  than  a  week.  In  Ornitho- 
doros  it  appears  to  be  quiescent,  making  no  attempt  to  obtain  food, 
and  in  0.  moubata  does  not  leave  the  egg.  In  three  or  four  days 
it  moults,  and  becomes  the  eight-legged  nymph,  which  is  an  active 
little  creature,  feeding  readily.  In  Argas  the  larva  is  more  vigorous, 
and  feeds.  It  appears  as  though  there  were  great  differences  in  the 
life-history  of  the  different  species  of  the  Argasidae. 


Fig.  320. — Argas  persicus  Latreille:     Fig.  321. — Argas  persicus  Latreille: 
Female,  Dorsal  Aspect.  Female,  Ventral  Aspect. 


The  adult  Argasidse  appear  to  moult  many  times  as  they  grow 
larger.     They  are  preyed  upon  by  insects. 

Genera. — The  Argasidae  are  divided  into  four  genera: — Argas, 
Caris,  Ornithodoros,  Alectorobius. 

The  diagnosis  of  these  genera  is  as  follows : — 

1.  Eyes  absent,  body  usually  flat,  with  thin  borders,  without 
deep  ventral  grooves:  (a)  No  groove  behind  anus — Argas  ;  (b)  trans- 
verse groove  behind  anus — Caris. 

2.  Eyes  present  or  absent;  body  more  or  less  distended,  with 
deep  ventral  grooves:  (a)  Without  a  fold  of  skin  (sclerite)  on  each 
side  of  palpi — Ornithodoros  ;  (b)  with  such  a  fold — Alectorobius. 


ARGAS  703 

There  is,  however,  some  doubt  as  to  whether  Caris  is  really 
entitled  to  be  a  separate  genus. 

Argas  Latreille,  1796. 

Synonyms. — Nee  Argas  Seoul,  1835;  Carols  Latreille,  1796; 
Rhynchoporion  Hermann,  1804;  Caris  Latreille,  1806. 

Definition. — Argasidae  with  oval  or  flattened  bodies,  in  which  the 
rostrum  is  at  least  its  own  length  from  the  anterior  margin,  which 
is  less  bluntly  rounded  than  the  posterior  margin.  No  fold  present 
around  the  base  of  the  rostrum  ventrally.  Tegument  roughened 
by  wrinkles  and  folds,  and  marked  by  circular  pits.     Without  eyes. 

Type. — Argas  reflexus  Fabricius,  1794. 

The  number  of  species  known  is  steadily  increasing.  The  more 
important  can  be  defined  by  the  following  table,  modified  from 
Neumann:— 

A.  Posterior  margin  with  rectangular  festoons — A.  persicus. 

B.  Posterior  margin  with  narrow  festoons: — 

I.  Tegument  with  fine  folds,  body  long,  swollen — A.  her- 

manni. 
II.  Tegument  with  large  folds,  body  flat : — 
(a)  Body  narrower  in  front : — 

(1)  Anterior  extremity  flat  and  rounded — A.  re- 

flexus. 

(2)  Anterior  extremity  pointed: — 

(a)  With    deep    camerostome    and    dorsal 

hexagonal  markings — A .  brumpti. 

(b)  Without  these — A.  c&qualis. 

(/?)  Body  almost  as  large  in  front  as  behind : — 

(1)  Body   short,    a   little   longer   than    broad — 

A.  transgariepinus. 

(2)  Body  twice  as  long  as  broad — A .  cucumerinus. 

Argas  reflexus  Fabricius,  1794. 

Synonyms. — Acarus  reflexus  Fabricius,  1794;  A.  marginatus 
Fabricius,  1794 ;  Rhynchoporion  columba  Hermann,  1804. 

Argas  with  yellowish  body;  male  4  by  3  millimetres,  female 
6  to  8  by  4  millimetres.  Its  distribution  is  mainly  in  Europe  and 
America,  where  it  lives  in  dovecots;  but  it  can  and  does  attack  man, 
producing  the  symptoms  already  described. 

Argas  persicus  Oken,  1818. 

Synonyms. — Rhynchoporion  persicum  Oken,  1818;  Argas  persicus 
Fischer  de  Waldheim,  1820;  A.  mauritianus  Guerin-Meneville ;  A. 
miniatus  Koch,  1844;  A.  americanus  Packard,  1872;  A.  sanchezi 
Duges,  1891;  A.  chinche  Gondet. 

Argas  with  oval,  brownish-red  body.  Male,  4  to  5  by  3  milli- 
metres; female,  7  to  10  by  5  to  6  millimetres.  Dorsal  and  ventral 
surfaces  with  pits  in  rows,  and  irregularly  placed. 


7'M 


ARTHROPOD  A 


This  Areas  is  widely  distributed,  being  found  in  Asia,  where, 
lindei  the  term  '  garib  gucz  '  (fiunaise  de  Miana),  it  has  long  had 
;m  evil  reputai  ion  for  causing  sickness.  It  is  also  known  in  Quetta. 
In  South  Africa  it  occurs  as  a  parasite  oi  fowls  and  ducks,  and  is 

also  known   in  tin:  Sudan,  Egypi ,  Turkestan,  and   J'ekin.      Undel 

t  he  name  oi  I .  minialus  it  w;is  desci  ibed  in  I  he  form  ol  I  he  chicken 
t  icfc  ol  the  United  States  and  the  adobe  tick  oi  Mexico  and  Arizona. 
According  to  Balfour,  it  spreads  the  Spirochata  marchouxi  in 
Sudanese  fowls.  Nuttall  and  Strickland  have  demonstrated  the 
pr<  ience  oi  an  anticoagulin  in  the  salivary  glands  and  intesl  ine  oi 
the  ti(  I 

Argas  brumpti  Neumann,  C907. 

I  In  .  I  k.I:  was  diseovei  cd  by  J>ruui]>1  in  Somaliland.     The  dorsum 

i,  marked  by  symmetrica]  hexagonal  depressed  areas.  Female, 
20  by  [3  millimetres.  Nuttall  says  that,  according  to  Brumpt, 
the  bite  is  very  painful,  and  causes  pruritus  lasting  several  days, 
and  the  site  may  remain  indurated  aftei  seven  years 

Argas  cucumerinus  Neumann,  r.901. 

Only  the  male  oi  this  tick  is  known,  li  has  an  oval  elongated 
body,  brownish  red  in  Colour,  [O  by  5  millimetres.  It  is  found  in 
Lima  in  Peru.     Possibly  this  is  merely  a  variety  of  A.  reflcxus. 

Argas  hermanni  Audouin,  1827. 
Argas  With  Very  line  skin  folds  and  sin.'dl  rostrum.      It    is  found 

in  Abyssinia  and  Egypt.  Possibly  this  :dso  is  only  n  variety  oi 
A .  reflex  11 . 

Argas  sequalis  Neumann,  [908. 

Synonym.    Ornithodoros  aqualis  Neumann,  C901. 

Nuttall  places  this  species  with  the  Argasidae.  II  was  found  in 
German  Easl  Africa  by  FttUeborn.  In  size  ii  is  5  by  2-5  milli- 
metres,  with  folded  finely  granulated  integument. 

Argas  transgariepinus  White,  [846. 

Synonym.     Argas kochi  Neumann,  [901. 

Argas  with  very  compressed  body,  not  much  longer  than  broad 
7-5  by  6  millimetres.    M.-irgin  with  irregular  folds.    Found  in 
Sont  h  Africa. 

Caris  Latreille,  1804. 

Argasidae  with  almosi  circulai  body,  a  little  larger  in  front  than 
b.  lund,  wit  1 1  a  conspicuous  tram    erse  groove  behind  the  anus. 

Caris  vespertilionis  Latreille,  170b. 
Synonyms.  -  (  arios  vespertilionis  Latreille,  C796;  Argas  pulchella 
( reorge,  1K70. 
p. 11. 1  it  ic  on  bats. 


0RN1  THODOROS  7":> 

Ornlthodoros  Koch,  1844. 

\i  ga  .i.l.i-  wit  h  in  uiiliiiiii  eyes.     Rostrum  surrounded  ventrallj 
by  a  1  amero  .tome.     I  ips  oi  the  palpi  v  i  ible  from  above.     I  at  era! 

borders  ol   the  body  straight,  sometimes  < ave      Integumenl 

111.11111111ll.il  t -<  1 .  with  hemispherical  elevations,  Two  longitudinal 
coxal  folds,  1  paii  oi  raprai  "v-.il  folds,  one  1  rans>  ei  s<  pi  e  anal  and 
oneposl  anal  groove,  and  one  longitudinal  anal  groove  running  from 
1  he  ,11111 .  to  the  posl  anal  gi  oove. 

Type.    Omithodoros  savignyi  Audouin,  [827. 

Eleven  species  are  re led:  (1)  Omithodoros  savignyi  Audouin, 

(2)  O.moubata  Murray,  [875     (3)  0. turicatus  Duges,  [876; 
1 1)  0,  megnim  Dugi  >,  1883;  (5)  0.  lahorensis  Neumann,  [908;  (6)  0 
tholozam  l  aooulbene  and  Megnin,  [882    (7)0   pavimmtosus  Neu 
in. inn.  [901 ;  (8)  0.  furcosus  Neumann,  [908;  (9)  0.  erraticus  I  in  1 
[849;  (i")  0.  ooriai bus  Koch,  c8  14;  (11)  0. 1  anestrinh  Birula,  L895. 

I  )l  \«. Mr, I  l<       I   \i:i  I-  . 

A.  k\  es  presenl : — 

rhree  knobs  on  the  lasl  segmenl  ol  the  fourth  leg : 
[a)  Tegumenl  wn  h  hemispherical  protuberances 

( 1 )  Eyes  <il  equal  size  (Afi  ica  and  India)     0,  savignyi. 
f  ■)  Anit-i  lor  eyes  largei  (Amei  ica)    0. < 01  iaceus 
(A)  Tegumenl    with    flattened    protuberances    (Africa) 
0  pavitnentosus. 
I '.,   E  \  es  abi  enl  : — 

I .  Subrei  tangulai  body  nearly  square  (Mexico)     0.  turicatus 
II.  Body  more  0]  lei     .1 1  icl  ed  behind  1  he  foui  th  pah  ol 

(a)  W it  li  in  oad  antei  ioi  end  (Me  ci<  0)     0.  megnim. 
i/m  With  narrow  anterior  end  (Lahore)    0.  lahorensi  ■. 
III.  Ovoid  body,  wil  li  In  oadei  posl  ei  ior  end ! 

\ni  ei  ior  end  broad  and  rounded  (1  entral  Africa) 
0.  moubata. 
[b     \m  1 1  M.i  end  1  apei  ing 

( 1 1    l  .11  1  iin  I . .  1 1  distally  (Ecuadoi  I     0.  fun  osus 

■1    1 .11  1  lighl  ly  knobbed  (Algei  ia)     0  erraticus, 

<  -,i    1 .11  .1   set  ond   1 0   foui  1  h   mai  kedly   knobbed 

i  Pel  sia)    0,  tholozam. 
(4)   l  .11  si  in  si  wil  li  1  In  ee  dorsal  knobs,  e<  ond  to 
1. mm  1  h   wit  h   one  knob   (Pei  ia)     <>    1  ant 

si  I' I  111  I 

Ornlthodoros  savignyi  Audouin,  tl 
Synonyms,      irgas  savignyi   Vudouin,  L827 ;  Omithodoros  morbil 
lotus ( ri  1  tftcker,  1873;   1/  ■■<■.  s<  kin  >ii  Bei  l<  •    1 

This  is  1  he  t  ype  Bpei  ii  s  ol  1  h<  g s,  and  has  been  si  udied  In 

detail  by  Neumann  and  <  hi  istophei 

1  • 


7o6  ARTHROPOD  A 

It  is  common  in  Africa,  India,  and  Aden,  and  perhaps  else- 
where. 

Morphology. — Omithodoros,  with  two  pairs  of  eyes  appearing  as 
circular,  smooth,  convex  elevations,  situated  on  the  supracoxal  fold 
above  the  bases  of  the  first  pair  of  legs,  and  between  those  of  the 
second  and  third  pairs.  Body  oval,  constricted  slightly  between  the 
third  and  fourth  pairs  of  legs,  yellow  in  colour  when  young,  and 
blackish-brown  when  old.  Integument  covered  with  irregular  hemi- 
spherical prominences  pointed  at  their  summits,  between  which  are 
narrow  depressions  with  hairs.  Capitulum  embedded  in  an  infundi- 
buliform  camerostome,  from  which  it  is  separated  by  a  deep  groove, 
in  the  dorsal  portion  of  which  can  be  seen  the  opening  of  the  cephalic 
gland.  Mandibles  with  a  simple  claw-like  internal  apophysis,  and 
without  middle  apophysis.  Teeth  of  the  hypostome  arranged  in 
three  longitudinal  parallel  rows.  Two  spines  at  the  base  of  the 
hyposome,  which  is  large. 

Dorsum  of  the  body  marked  by  two  transverse  furrows,  one  just 
in  front  of  the  posterior  border,  and  the  other  situate  farther 
forward,  marking  off  a  median  elevation  with  a  central  depression, 
and  seven  similar  depressions,  each  of  which  becomes  a  deep  sulcus 
posteriorly. 

The  ventral  surface  shows  a  well-marked  pre-anal  furrow,  which 
laterally  meets  the  supracoxal  sulcus,  which  runs  round  the  anterior 
aspect  of  the  body  as  a  well-marked  groove,  defining  the  supra- 
coxal fold,  on  which  the  eyes  are  situate.  Behind  the  anus  are 
three  symmetrical  longitudinal  grooves,  while  a  short  V-shaped 
depression  abuts  on  the  anus.  The  genital  papilla  is  well  marked, 
and  surrounds  the  wide  transverse  opening. 

The  fourth  pair  of  legs  is  one  and  a  half  times  as  long  as  the  first. 
The  coxae  are  contiguous,  and  diminish  in  size  from  the  first  to 
the  fourth,  and  the  first  has  the  opening  of  the  coxal  gland. 
Christophers  has  observed  that  the  fluid  from  this  gland  is  alkaline 
and  prevents  coagulation  of  the  blood.  The  stigmata  are  placed 
behind  and  above  the  supracoxal  folds.  The  fifth  joints  of  the 
first  three  pairs  of  legs  with  three  teeth,  the  two  proximal  quad- 
rangular, and  the  distal  conical. 

This  tick  is  very  hardy,  and  is  said  to  be  able  to  live  for  many 
months  without  food  or  moisture.  It  attacks  human  beings,  and 
is  found  in  Afnca  and  India. 

Pathogenicity. — Not  known. 

Omithodoros  moubata  Murray,  1877. 

Synonyms. — Argas  moubata  Murray,  1877 ;  Ixodes  moubata  Cobbold, 
1882;  Omithodoros  savignyi  var.  ueca  Neumann,  1901. 

0.  moubata  is  of  importance  as  the  spreader  of  Spiroschaudinnia 
duttoni,  the  cause  of  Djr^ton^s^lap_singfever,  or  African  tick  fever. 
The  tick  is  distributed^vri^el^TmAlHcaTwhere  it  is  called  bibo  in 
Uganda,  moubata  in  Angola,  and  tampan  in  Zambesi.  Christy  has 
described  a  similar  tick  in  Brazil. 


ORNITHODOROS 


707 


Morphology. —  Omithodoros  without  eyes,  body  oval,  a  little  wider  behind 
than  in  front,  with  a  slight  constriction  between  the  third  and  fourth  legs; 
colour  varies  with  age  from  yellow-brown  to  dusky  brown.  Integument 
covered  with  irregular  hemispherical  prominences.  Capitulum  embedded  in 
an  infundibuliform  camerostome.  Mandible  with  external  apophyses,  with 
two  widely  separated  teeth,  and  an  internal  apophysis,  which  is  bidentate. 
Hypostome  not  much  ^\ider  at  the  base  than  at  the  anterior  third.  Dorsum 
of  the  body  marked  by  two  short  transverse  grooves  posteriorly  and  three 
pairs  of  pits,  from  each  of  which  a  sulcus  runs  backwards  and  inwards. 

The  \  entral  surface  shows  a  well-marked  pre-anal  sulcus,  which  joins  the 
sugracoxal  groove,  as  in  5.  savignyi  ;  behind  the  anus  are  three  pairs  of 
longitudinal  grooves.  The  stigmata  are  semilunar,  situate  above  the  snpra- 
coxal  groove.  The  last  segment  of  the  fourth  pair  of  legs  is  stout  and  com- 
pressed, with  three  knobs,  the  distance  between  the  first  and  second  bring 
equal  to  that  between  the  second  and  third. 

Tibiae  and  tarsi  of  the  first  three  pairs  of  legs,  with  three  teeth — proximal, 
submedian,  and  distal,  the  last  being  conical. 


Fig.  322. — Omithodoros  moabata 
Murray  :  Female,  Dorsal  As- 
pect.    (X  4-) 


Fig.  323. — Omithodoros  moubata 
Murray  :  Female,  Ventral 
Aspect.     (X  4-) 


Life-History.— The  female  lays  a  variable  number  of  eggs,  from 
70  to  139,  which  adhere  together,  and  are  golden-brown  in  colour; 
881  by  776  /jb.  Inside  these  eggs  the  larvae  develop  and  moult, 
becoming  nymphse,  which  hatch  about  the  twentieth  day  at  a 
temperature  of  200  to  300  C.  and  a  humidity  of  71  to  77  per  cent. 
After  three  or  four  days  these  nymphae  suck  blood.  At  first  the 
position  of  the  stigma  is  marked  by  only  a  small  white  spot  and 
pit,  but  after  the  first  moult  this  becomes  clear.  The  genital  pore 
is  always  absent  until  after  the  second  moult. 

The  adult  tick  moults  after  each  feed  of  blood,  and  may  live 
about  a  year.  They  are  night  feeders,  and  rather  resemble  bugs 
in  their  habits.  Leishman  observed  that  the  fluid  secreted  by  the 
coxal  glands  prevents  coagulation  of  the  blood. 

Pathogenicity. — -It  is  the  spreader  of  Spiroschaudinnia  duttoni, 
and  according  to  Wellman  andFeldmann  possibly  of  Acanthocheilo- 
iicaia  herstdns. 


708  ARTHROPOD A 


Ornithodorcs  turicatus  Dugts,  1876. 

Synonyms.- — Arg<is  titricata  Duges,  1876;  Ornithodorcs  americanus 
Marx,  1895. 

Ornithodoros  without  eyes;  anteriorly  the  body  is  much  narrowed. 
Tibiae  and  tarsi  with  three  small  tubercles. 

Habitat. — Mexico  and  Central  America.  Attacks  men  and 
fowls. 

Ornithodoros  megnini  Duges,  1883. 

Synonyms. — Argas  megnini  Duges,  1883;  A.  americanmn  Packard, 
1893;  Rhynchoporion  spinosam  Marx,  1895. 

Ornithodoros  with  phial-shaped  body;  attenuated  anteriorly. 
Females  5  to  6  millimetres  by  3  to  4  millimetres.  Males  somewhat 
smaller. 

This  is  the  ear  tick  of  American  cattle,  and  has  been  found  in 
the  ear  of  man. 

Ornithodoros  lahorensis  Neumann,  1908. 

Ornithodoros  without  eyes.  Male  8  by  4-5  millimetres.  Female 
10  by  5*6  millimetres.     Found  at  Lahore,  India.    Parasitic  on  sheep. 

Ornithodoros  tholozani  Laboulbene  and  Megnin,  1882. 

Synonyms. — A .  tholozani  Laboulbene  and  Megnin,  1882 ;  A .  papil- 
lipes  Birula,  1895. 

Ornithodoros  without  eyes.  Males  4  to  6  millimetres  in  length 
and  2  to  4  millimetres  in  breadth.  Females  8  to  10  millimetres  by 
4  to  5  millimetres. 

It  is  specially  a  parasite  of  sheep  in  Caucasia  and  Persia,  but  is 
very  dangerous  to  man. 

Ornithodoros  pavimentosus  Neumann,  1901. 

Ornithodoros  with  ej^es.  Body  covered  with  flat  warts  forming 
a  pavement.  South  Africa.  Only  female  known.  12  by  8  milli- 
metres. 

Ornithodoros  furcosus  Neumann,  1908. 

Found  in  Ecuador.     Female  10  by  5  millimetres. 

Ornithodoros  erraticus  Lucas,  1849. 

Synonyms.- — Argas  erraticus  Lucas,  1849;  0.  miliaris  Karsch,  1880. 
Found  in  Algeria  and  Bengal.     Length,  5  millimetres;  breadth, 
3  millimetres. 

Ornithodoros  coriaceus  Koch,  1844. 

Ornithodoros  with  eyes.  Only  one  knob  on  the  hind  tarsus. 
America.  Male  6-4  to  8-6  by  3-4  to  46  millimetres;  female  9-5  to 
x3"8  by  5-3  to  8-2  millimetres- 


ALECTOROBTUS  709 

Ornithodoros  canestrinii  Birula,  1895. 

Synonym.  -Argas  canestrinii  Birula,  1895. 

Found  in  Persia.  Male  10  by  5  millimetres;  female  14  by  S 
millimetres. 

Alectorobius  Pocock,  1907. 

Argasichu  with  folds  of  integument  capable  of  being  folded  under 
the  palpi.  This  genus  is  not  recognized  by  Nuttall,  as  he  considers 
it  a  synonym  of  Ornithodoros. 

Type. — A .  talajc  Guerin-Meneville,  1849. 

Alectorobius  talaje  Guerin-Meneville,  1849. 

Synonyms. — 0.  talajc  Guerin  and  Meneville,  1849 ;  0.  rndis  Karsch. 
1880;  Alectorobius  talije  Pocock,  1907. 

This  is  the  chinch  of  South  America  and  Mexico,  where  it  is  a 
great  pest.  A.  coniceps  of  South  Europe  and  A.  capensis  of  South 
Africa  are  varieties  of  this  species. 

Family  2  :    Ixodid^e  Murray,  1877. 

Synonyms. — Ixodei  Duges,  1834;  Ixcdiden  Koch,  1844;  Ixodides 
Gervais  and  van  Beneden,  1859;  Ixodini  Canestrini  and  Fanzago, 
rS/7;  Ixodince  Trouessart,  1892;  Anistomata  Marx,  1892. 

lxodoidea  with  a  dorsal  scutum  and  a  terminal  capitulum.  The 
digit  of  the  mandible  has  two  apophyses,  and  the  palpi  are  free. 

Most  of  the  ticks  belong  to  this  family,  which  has  the  following 
features : — 

Morphology.— There  is  a  dorsal  scutum  and  a  terminal  capitulum. 
The  mandible  has  a  digit  with  two  apophyses,  of  which  the  internal 
is  short  with  one  to  four  teeth,  and  the  external  long,  with  two 
to  five  teeth.  The  palpi  are  free.  The  second  pair  of  legs  is  the 
shortest,  and  the  fourth  pair  the  longest.  The  tarsus  has  a  pul- 
villnm.  The  stigmata  are  situate  posterior  to  the  coxa  of  the  fourth 
Leg.  The  male  is  smaller  and  fatter  than  the  female.  The  scutum 
covers  the  whole  dorsum  except  a  marginal  region,  the  posterior 
portion  of  which,  between  the  two  stigmata,  is  generally  divided 
into  eleven  festoons.  The  female  has  but  a  small  scutum,  situated 
anteriorly,  and  the  capitulum  has  two  symmetrical  porose  areas  on 
its  basal  piece. 

Type  Genus.— Ixodes  Latreille,  1796. 

Life-History  of  the  Ixodidae. — When  the  pregnant  female  tick 
drops  off  the  host,  it  at  first  appears  to  seek  for  a  suitable  place  to 
lay  its  eggs.  When  this  is  found,  it  becomes  quiescent,  and  the 
anterior  part  of  the  ventral  surface  between  the  first  pair  of  legs 
becomes  depressed,  and  forms  a  hollow,  in  which  the  head  and 
genital  orifice  are  situated.  When  an  ovum  passes  out  of  the  orifice, 
the  tick  moves  slightly  backwards.  This  oviposition  takes  about 
fifteen  to  twenty  days.     While  it  is  proceeding  the  tick  begins  to 


710  ARTHROPOD  A 

shrive!  and  to  show  yellow  areas,  due  to  the  distencion  of  the 
Malpighian  tubes  with  guanine.  At  the  end  of  oviposition  the 
tick  dies. 

From  the  egg  comes  a  six-legged  larva,  which  generally  climbs 
into  some  grass  or  bushes  and  waits  to  get  on  to  a  host.  While 
so  doing  it  may  remain  for  months  without  food. 

It  now  sucks  blood,  and  drops  off  this  first  host  and  moults  on 
the  ground,  becoming  an  eight-legged  nymph,  like  an  adult,  but 
without  generative  apparatus,  which  again  has  to  go  in  search  of 
a  second  host  and  obtain  a  feed  of  blood,  when  it  drops  off  and 
undergoes  a  second  moult,  turning  this  time  into  the  sexually 
mature  adult,  which  goes  in  search  of  a  third  host.  Before  feeding, 
the  adult  female  is  small,  flat,  and  thin.  When  she  arrives  on  the 
third  host  she  drives  her  rostrum  perpendicularly  into  the  skin 
as  far  as  its  base,  a  hole  being  made  by  the  mandibles. 

The  palpi  do  not  enter  the  hole  in  the  skin,  but  lie  on  each  side. 

The  recurved  hooks  on  the  hypostome  keep  the  tick  in  position, 
and  can  only  with  difficulty  be  detached.  The  tick  now  sucks  the 
blood,  and  at  the  same  time  becomes  fertilized  and  increases  enor- 
mously in  size  by  the  addition  of  blood  and  the  development  of  the 
eggs.  She  then  drops  off  this  third  host  and  proceeds  to  lay  her 
eggs. 

The  male  does  not  gorge  and  does  not  increase  so  much  in  size, 
but  sucks  blood,  which  it  requires  for  its  fertilizing  work. 

The  Ixodidce  are  divided  into  two  subfamilies:— 

Subfamily  i:    Rhipicephalin/E  Salmon  and  Stiles,  1901. 

Synonyms. — Rhipistomidea  Koch,  1844;  Conipalpi  Canestrini, 
1890;  Rhipicephalce  Neumann,  1897;  Rhipistomidce  Marx,  1896. 

Ixodidce  in  which  the  palpi  are  no  longer  than  broad.  Anterior 
portion  of  the  body  emarginate. 

Type  Genus.- — Eurhipicephahts  Neumann,  1904. 

Genera. — Eitrhipicephahis  Margaropus,  Hcemaphysalis,  Derma- 
centor,  Rhipicentor. 

Subfamily  2:    Ixodusle  Salmon  and  Stiles,  1901. 

Synonyms.— Ixodidea  Koch,  1844;  CuUripalpi  Canestrini,  1890; 
Ixodidce  Marx,  1892:  Hcematustoridce  Marx,  1892;  EschatocephaUd.ee 
Marx,  1892;  Ixodes  Neumann,  1899. 

Ixodidce  with  palpi  longer  than  broad;  rostrum  long.  Anterior 
portion  of  the  body  straight  or  emarginate. 

Type  Genus. — Ixodes. 

Genera. — Ixodes,  Escha/occphaltis,  Ceratixodes,  Aponomma, 
Amblyomma,  Hyalomma. 


RHIPICEPHALINM  711 

Diagnostic  Table  of  Genera,  from  Salmon  and  Stiles. 

rhipicephalinm. 
A.  Eyes  present: — 

I.  Dorsal  surface  of  capitulum  hexagonal,  sides  drawn  out 

laterally  into  sharp  points. 

(a)  Males  with  anal  plates. 

1.  Second  and  third  palpal  segments  straight; 

stigmata  comma-shaped — Eitrhipicephahts. 

2.  Second  and  third  palpal  segments  drawn  out 

laterally  into  sharp  points;  stigmata  round 
— Margaropns. 

[b)  Males  with  rudimentary  anal  plates — Rhipicentor. 

II.  Dorsal  surface  of  capitulum  rectangular,  sides  straight ; 

male  without  anal  plate — Dermacentor. 
B.  Eyes  absent — Hcemaphysalis. 

Nuttall  and  Warburton's  new  classification  of  the  Ixodidae  is  as  follows  :— 
Prostriata. — Ixodidae  with  anal  grooves  surrounding  the  anus  in  front — 

Ixodes. 
Metastriata. — Ixodidae  with  anal  groove  contouring  the  anus  behind,  but 

this  groove  may  be  faint  or  obsolete. 

Brevirostrata. — 

Group  I. :  Inornate  without  eyes,  but  with  festoons — Hcemaphysalis. 
Group  II.:  Ornate  or  inornate  with  eyes,  and  with  or  without  festoons 

Anal  grooves  marked. 
Ornate  with  festoons. 

Basis  capituli  rectangular  dorsally — Dermacentor. 
Basis  capituli  hexagonal  dorsally — Rhipicentor. 
Usually  inornate  with  festoons. 

Basis  capituli  usually  hexagonal  dorsally — Rhipicephalns. 
Anal  grooves  obsolete. 

With  short  palpes — Mar  gar  opus. 

With  very  short  compressed  palpes  ridged  dorsally  and 
laterally — B  oOphilus . 
Longirostrata. — 

Group  I.:  Ornate  or  inornate,  with  eyes  and  with  or  without  festoons 
basis  capituli  subtriangular  dorsallv.     Male  with  a  pair  of 
adanal  shields — Hyalomma. 
Group  II.:  Generally  ornate,  with  eyes  and  with  festoons,  basis  capituli 
variable.     Without  adanal  shields— Amblyomma. 

Subgenus  Aponomma  chiefly  found  on  reptiles  with  poorly- 
developed  or  no  eyes. 
It  will  be  observed  that  the  genera  Eschatocephalus  and  Ceratixodes  are 
rejected  and  referred  to  the  genus  Ixodes.     Another  genus,   Neumanniella 
Lahille,  1905.  is  also  rejected,  and  it  is  referred  to  Aponomma. 

Subfamily  Rhipicephalinm. 

Eurhipicephalus  Neumann,  1904. 

Synonyms. —  Rhipicephaltts  Koch,  1844  ;  Phauloixodes  Berlese, 
1889. 

Rhipicephalinae  with  distinct  eyes;  base  of  the  capitulum  broader 
than  long;  hexagonal,  or  dorsal  surface  forming  a  projecting  angle 


7i2  ARTHROPODA 

at  each  side.     Palpi  short  and  broad.     First  coxa  with  two  large 
teeth.     Male  with  one  or  two  pairs  of  anal  shield.     (Fig.  324.) 
Type  Species. — Eurhipicephalus  sanguineus  Latreille,  1804. 

Eurhipicephalus  appendiculatus  Neumann,  1901. 

This  is  the  brown  tick  of  South  Africa,  where  it  spreads  Theileria 
parva  among  cattle  and  buffaloes,  causing  '  coast  fever.' 

Morphology. — Male,  scutum  does  not  quite  cover  the  dorsum; 
festoons  narrow;  the  median  is  prolonged  into  a  caudal  process. 
In  front  of  the  festoons,  three  wide  longitudinal  grooves.  Size, 
4  by  2-6  millimetres.  Female,  dorsal  plate  oval;  porose  area 
small. 

Life-History. — The  eggs  are  laid  in  thousands  on  the  grass,  and 
hatch  in  about  twenty-eight  days  into  six-legged  larvae,  which  pass 
from  the  grass  on  to  cattle,  suck  blood,  and  drop  off  replete  in  about 
three  to  four  days. 

They  now  remain  dormant  for  about  twenty-one  days,  and  finally 
moult,  giving  rise  to  the  eight-legged  nymph. 

The  nymph  proceeds  to  attack  cattle  and  suck  blood,  taking  the 
same  length  of  time  as  the  larva.  It  then  drops  off  replete,  and 
in  about  eighteen  days  moults  and  becomes  an  adult  male  or  female 
tick,  which  again  infests  cattle.  The  female  settles  down  quickly, 
and  is  joined  by  the  male.  In  about  four  days  the  female,  which 
has  become  fertilized  and  full  of  blood,  drops  off,  and  completes  the 
life-cycle  by  laying  the  eggs,  after  which  she  dies. 

What  becomes  of  the  male  is  not  known. 

Pathogenicity.— It  spreads  Theileria  parva,  the  cause  of  coast 
fever  in  cattle,  by  the  bites  of  the  infected  nymphs'  only — i.e., 
infected  larvae  and  adults  do  not  spread  the  disease,  but  the  larva 
can  hand  the  infection  over  to  the  nymph,  which  is  the  spreader. 

Eurhipicephalus  bursa  Canestrini  and  Fanzago,  1878. 

Synonym. — Rhipicephalus  bilenus  Pavesi,  1883. 

This  species  is  widespread  through  Southern  Europe,  and  is  also 
known  in  Africa,  West  Indies,  and  Malaga,  as  a  sheep,  horse,  cattle, 
and  dog  tick. 

Morphology. — Male,  scutum  half  as  long  as  wide;  narrow  anteri- 
orly, with  many  punctations.  Eleven  festoons.  Size  4-5  by  3  milli- 
metres. 

Female,  when  newly  hatched,  flat ;  when  distended  with  blood, 
ovoid.  Scutum  oval;  eyes  about  the  middle  of  the  length.  Tegu- 
ment with  numerous  punctations  dorsally  when  young. 

Life-History. — The  female  lays  the  eggs  on  grass,  and  these  develop 
into  larvae,  which  attack  a  sheep,  and  moult  on  it  in  about  eight 
days,  forming  nymphae,  which  grow  for  twenty-one  days,  fall 
off  on  to  the  ground,  moult,  and  become  adults,  which  again 
infest  sheep. 


EURHIPICEPHALUS 


7i3 


Pathogenicity. — It  spreads  Piroplasma  ovis,  which  causes  '  heart- 
water  '  in  sheep,  the  infection  being  carried  from  an  adult  female 
through  the  eggs  to  the  adult  ticks  of  the  next  generation,  which 
alone  are  capable  of  transmitting  the  disease. 


Figs.  324-326. — Eurhipicephalus  pulchellus  Gerstacker,   1873: 
Ventral  Aspect. 

a,  Male  (X  10) ;  b,  mouth  parts  (more  highly  magnified) ;  c,  female  (X  10). 

Eurhipicephalus  simus  Koch,  1844. 

Synonym's. —  Rliipicephalus  sencgalensis  Koch,  1844;  Rh.  pmten- 
tatus  Gerstacker,  1893. 

This  tick  is  found  in  various  parts  of  Africa — viz.,  Egypt,  late 
German  East  Africa,  and  the  Cape.  It  has  several  varieties — e.g., 
E.  simus  erlangeri,  E.  simus  hilgerti,  E.  simus  shipleyi.  In  South 
Africa  it  is  called  the  black -pitted  tick,  because  of  its  punctations, 
and  causes  '  coast  fever  '  by  spreading  Theileria  parva.  Male  oval, 
rounded  posteriorly;  4  by  2-2  millimetres.  Scutum  brown-red. 
Female  oval,  6  by  3  millimetres. 

Eurhipicephalus  sanguineus  Latreille,  1804. 

Synonyms. — Ixodes  sanguineus  Latreille,  1804 ;  /.  rufus  Koch,  1844. 

Synonym  of  Nymph. — Phauloixodes  rufus  Berlese,  1889. 

This  is  the  common  dog  tick,  by  which  Piroplasma  canis  is  spread, 
which  it  acquires  as  an  adult,  and  transmits  in  the  succeeding 
nymphal  and  adult  stages.  It  also  spreads  Htemogregarina  cams. 
It  is  practically  cosmopolitan. 

The  female  has  an  elliptical  body,  wider  in  front  than  behind: 
11  by  7  millimetres,  reddish-brown  in  colour.  Scutum  very  small; 
integument  nearly  or  completely  without  hairs.  The  mandibles 
have  an  internal  apophysis  with  three  teeth,  arranged  one  internally 
and  two  externally;  and  an  external  apophysis  with  three  teeth, 
arranged  in  series. 


7i4  ARTHROPOD  A 

The  male  is  3-35  by  1-55  millimetres,  with  a  scutum  covering  the 
dorsal  surface,  except  at  the  sides  and  back.  External  apophysis 
with  only  two  teeth. 

Eurhipicephalus  evertsi  Neumann,  1897. 

This  is  the  red-leg  tick,  which  spreads  Nuttall ia  equi,  and  is  found 
in  Europe,  Africa,  and  Asia.  The  life-history  resembles  Eurhipi- 
cephalus  appendiculatus  in  the  changes  of  host  by  larva  and  nymph. 
The  infection  is  acquired  in  the  nymphal  stage,  and  transmitted 
by  the  adult.  Size:  male,  5  to  6  by  3  to  4  millimetres;  female, 
14  By  9  millimetres. 

Margaropus  Karen,  1879. 

Synonyms. — Boophilus  Curtice,  1891;  Rhipicephalus  Neumann, 
1897. 

Rhipicephalince  with  eyes,  though  often  indistinct;  base  and 
capitulum  broader  than  long.  Palpi  short  and  broad;  second 
and  third  segment  thicker  in  the  middle,  and  forming  a  sharp  angle 
externally.  Posterior  margin  of  the  first  coxa  slightly  bidentate; 
stigmal  plate  round.  Body  without  marginal  festoons;  anal 
groove  absent.     Male  with  two  pairs  of  anal  plates. 

Type. — Margaropus  annulatus  Say,  1821. 

Only  three  or,  according  to  Neumann,  two  species,  of  which  two 
species  (M.  annulatus,  M.  decoloratus)  may  be  one,  the  third  being 
.1/.  lounsburyi  Neumann,  1907. 

Margaropus  annulatus  Say,  1821. 

Synonyms. — Ixodes  annulatus  Say,  1821;  Hcemaphysalis  rosea 
Koch,  1844;  Ixodes  bovis  Riley,  1869;  Margaropus  winthemi  Karsch, 
1879;  Boophilus  bovis  Curtice,  1880;  and  several  others. 

Female  with  elliptical  body,  as  wide  in  front  as  behind.  Scutum 
very  small.  Eyes  small.  Dorsal  surface,  with  two  antero-posterior 
grooves,  interrupted  towards  their  middle.  Ventral  surface  with 
small  sexual  aperture  and  sexual  furrows.  Stigmata  oval.  Capi- 
tutum  very  short.  Internal  apophysis  of  mandible  conical;  the 
external  with  three  teeth.  Hypostome  broad.  Palpi  very  short. 
Legs  short  (vide  Fig.  313). 

Male  with  body  oval,  2-15  by  2-35  millimetres,  narrow  anteriorly; 
widest  opposite  stigmata.  Scutum  brown-red,  covering  the  whole 
dorsal  surface  with  large  punctata.  Sexual  orifice  large,  a  little 
in  front  of  the  level  of  the  second  pair  of  legs.  Festoons  hardly 
marked.  Two  pairs  of  clypeal  shields.  Internal  apophysis  of  the 
mandibles  with  bifid  point ;  the  external  has  two  teeth.  Coxa  of 
first  leg  with  a  blunt  anterior  process  and  bifid  posteriorly. 

This  tick  has  a  very  wide  geographical  distribution,  being  found  in 
North  and  South  America,  the  West  Indies,  Africa,  Europe,  Japan, 
and  Australia;  but  the  different  countries  show  certain  variations 
in  the  tick,  and  hence  the  species  receive  a  little  change  in 
the  name. 


MARGAROPUS  715 

Life-History. — Margaropus  annulatus  begins  its  life  with  the  egg 
on  the  ground,  from  which  the  larva  emerges,  and,  gaining  access  to 
I  he  host,  undergoes  its  development  into  nymph  and  adult  without 
the  changes  of  host  described  in  Eurhipicephalus. 

When  the  adult  female  has  gorged  with  blood,  she  drops  off  the 
host  and  lays  her  eggs. 

Pathogenicity.— It  is  the  spreader  of  Piro plasma  bigeminum,  the 
cause  of  Texas  or  red-water  fever  in  cattle.  The  adult  female 
acquires  the  Piroplasma  and  passes  it  on  to  the  larva,  which  infects 
the  host.     It  is  also  the  carrier  of  Spiroschaudinnia  theileri. 

Varieties.— The  names  of  the  varieties  are:  (1)  M.  dugesi  Megnin, 
1880,  in  North  Africa;  (2)  M.  microphilus  Canestrini,  1887,  in 
South  America;  (3)  M.  austral  is  Fuller,  1899,  in  Australia,  Asia, 
Africa;  (4)  M.  calcaratus  Birula,  1895,  in  the  Caucasus;  (5)  M.  cau- 
datus  Neumann,  1901,  in  Japan;  (6)  M.  argentinus  Neumann,  iqoi, 
in  Buenos  Ayres. 

Margaropus  decoloratus  Koch,  1844. 

This  is  looked  upon  as  a  variety  of  Margaropus  annulatus  Say 
by  some  authors.     It  is  the  blue  tick  of  South  Africa. 

Morphology. — The  clypeal  plates  in  the  male  end  in  sharp  points, 
and  a  caudal  appendage  is  present.  The  hypostome  has  six  rows 
of  teeth. 

Life-History. — It  lives  from  the  larval  stage  to  the  adult  on  the 
same  host.  The  adult,  when  fully  fed,  drops  off  and  lays  the  eggs 
on  the  ground. 

Pathogenicity. — It  is  a  spreader  oi  Piroplasma  bigeminum. 

Rhipicentor  Nuttall  and  Warburton,  1908. 

Rhipicephalinae  with  eyes,  inornate,  with  festoons.  Basis  capituli 
hexagonal  dorsally,  and  having  very  prominent  lateral  angles  with 
short  palps.  Coxa  I.  bifid  in  both  sexes.  The  male  resembles 
Eurhipicephalus  dorsally  and  Dermacentor  ventrally.  Coxa  IV.  is 
much  the  largest.  There  are  no  ventral  shields  or  plates.  Spiracles 
subtriangular  or  comma-shaped. 

Type. —  Rhipicentor  bicomis  Nuttall  and  Warburton,  1908. 

Rhipicentor  bicornis  Nuttall  and  Warburton,  1908. 

Synonym. —  Rhipicephalus  gladiger  Neumann,  1908. 

This  is  an  African  species  living  on  the  horse  in  the  Congo  and 
Central  Africa.  It  attacks  and  can  live  on  man.  Another  species  is 
Rh.  vicinus  Nuttall,  1908. 

Dermacentor  Koch,  1844. 

Rhipicephalinae  with  eyes;  base  of  capitulum  rectangular,  broader 
than  long.  Dorso-submedian  porose  plate  present ;  palpi  short  and 
thick;  stigmata  comma-shaped.     Male  without  anal  shields.     The 


7*6  ARTHROPODA 

coxa  of  the  fourth  leg  much  larger  than  those  of  the  others.     Scutum 
ornamented. 
Type, — Dermacentor  reticulatus  Fabricius,  1794. 

In  19 10  Stiles  classified  the  species  of  Dermacentor  into  four  groups,  accord- 
ing to  the  microscopical  structure  of  the  stigmal  plates  in  the  adult. 

A.  Adults  with  four  longitudinal  rows  of  large  denticles  on  each  half  of 

hypostome,    stigmal    plate    nearly    circular   without    dorso-lateral 
prolongation,  goblets  very  large — D.  nitens. 

B.  Adults  with  three  longitudinal  rows  of  large  denticles  on  each  half  of 

hypostome,  goblets  small,  medium,  or  large. 
Dorso-lateral  prolongation  of  stigmal  plate  absent — Salmoni  group. 
Dorso-lateral  prolongation  of  stigmal  plate  distinct. 

Goblets  of  medium  size — Andersoni  group. 

Goblets  small — Reticulatus  group. 

The  Salmoni  group  includes  D.  albipictus  Packard,  1869;  D.  salmoni  Stiles, 
1910;  and  D.  nigrolineatus  Packard,  1869. 

The  Andersoni  group  includes  D.  occidentalis  Marx,  1892;  D.  parumapertus 
Neumann,  1901;  D.  venustus  Marx,  1897;  -D-  andersoni  Stiles,  1905. 

The  Reticulatus  group  includes  D .  reticulatus  Fabricius,  1794!  D.  variabilis 
Say,  1 82 1. 

Remarks. — There  has  been  the  greatest  confusion  as  to  the  tick 
which  causes  Rocky  Mountain  fever.  This  was  called  Dermacentor 
occidentalis  because  Stiles  considered  that  D.  andersoni  Stiles,  1905, 
was  identical  with  D.  occidentalis  Marx,  1892,  but  the  two  forms 
have  since  been  shown  by  him  to  be  quite  distinct.  Therefore  in 
any  reference  to  a  tick  causing  Rocky  Mountain  fever,  no  matter 
what  name  is  used,  it  is  important  to  understand  that  D.  andersoni 
Stiles,  1905,  is  the  species  really  referred  to. 

Dermacentor  reticulatus  Fabricius,  1794. 

Synonyms.1— Acarus  reticulatus  Fabricius,  1794;  Ixodes  reticulatus 
Fabricius,  1805;  I.  marmoratus  Risso,  1826;  Dermacentor  albicollis 
Koch,  1844;  D.  pordalinus  Koch,  1844;  D.  ferrugineits  Koch,  1844; 
HcemapJiysalis  marmorata  Berlese,  1887. 

Dermacentor  with  coarsely  punctate  stigmal  plate. 

This  tick  gains  its  importance  from  the  fact  that  for  some  time 
it  was  considered  to  be  the  cause  of  the  spread  of  Rocky  Mountain 
fever,  which  was  really  due  to  the  nearly  related  D.  andersoni,  with 
which  it  was  long  confused.  It  probably  does  not  occur  in  America. 
It  is  widely  distributed  through  Europe  and  Asia. 

Dermacentor  occidentalis  Marx,  1892. 
This  tick  was  received  by  Marx  from  Occidental  in  California,  and  was  first 
described   by  Neumann.      It    is  found  in  the  north-western  portion  of  the 
United  Stales  from  California  to  Montana. 

Morphology.— Male:  Oval,  narrow  in  front,  broad  behind;  scutum  varie- 
gated brown  and  white.  Anteriorly  there  is  an  elliptical  area,  the  pseudo- 
scutum,  closely  representing  the  form  and  colour  of  the  female  scutum,  and 
limited  by  a  white  border,  and  possessing  two  lateral  brown  stripes,  with  a 
median  brown  stripe  or  spots  between  them.  Behind  this  there  are  four 
brown  stripes  arranged  in  a  curve,  open  anteriorly.  Posterior  to  these  usually 
five  brown  stripes ;  one  central  and  two  lateral.     Between  these  areas  the  whole 


DERMACENTOR 


717 


dorsum  is  speckled  with  brown  pu notations,  The  eleven  festoons  are  some- 
what quadrangular,  each  composed  of  a  white  area  with  one  brown  spot,  and 
speckled  with  brown  punctations.  Ventral  surface  with  the  first  coxa  biden- 
tate,  and  the  others  with  a  single  spine.  Fourth  coxa  very  large;  about 
twice  as  large  as  the  third.  Generative  aperture  on  a  level  with  the  second 
pair  of  legs.  Stigma  comma-shaped;  hypostome  with  three  rows  of  teeth  on 
each  side.     Palpi  longer  than  hypostome.     Size,  5  by  2-5  millimetres. 

Young  female:  Oval  depressed  body,  broader  posteriorly  than  anteriorly; 
reddish-brown  in  colour;  about  the  same  size  as  the  male — -5  by  2-5  milli- 
metres. Scutum  very  large,  and  marked  like  the  anterior  part  of  the  male, 
extending  as  far  back  as  the  third  pair  of  legs,  with  eyes  in  the  anterior 
part  of  the  Literal  border.  Dorsal  surface  of  abdomen  with  a  marginal 
groove  beginning  behind  the  eyes,  and  three  longitudinal  grooves  running 
backwards,  the  two  lateral  beginning  just  behind  the  scutum,  and  the  median 
about  the  centre  of  the  bodv.  l'<  sterior  margin  with  eleven  festoons.  Ventrai 
surface  with  tine  hairs.  Genital  aperture  at  the  level  of  the  second  coxa; 
genital  grooves  close  to- 
gether at  first,  but  diver- 
ging laterally  behind  the 
fourth  coxa,  and  ending 
between  the  second  and 
third  external  festoons. 
Anus  with  short  anomar- 
ginal  groove.  Stigma 
comma-shaped . 

Capitulum  with  the 
posterior  lateral  angle 
prolonged  into  a  sharp 
point.  Porose  areas  cir- 
cular. Internal  apo- 
physis of  the  mandible 
with  strong  posterior 
tooth;  external  with 
three  successive  teeth. 
First  coxa  bidentate, 
other  three  with  spines. 
Replete  female :  Swollen 
body  laterally  con- 
stricted at  the  stigmata ; 
of  deep  brown  or  slate 
colour;  size,  16  by  10 
millimetres. 

Life-History. — The  egg 
hatches  in  seven  to  ten  days,  and  produces  a  larva  which  feeds  on  some 
animal  for  several  days,  and  then,  becoming  swollen  and  of  a  uniform  slate- 
colour,  drops  off,  and,  becoming  quiescent,  moults  and  gives  rise  to  the  nymph. 
This  nymph  again  attacks  an  animal,  and  when  fed  drops  off,  and  in  ten 
days  moults  and  becomes  the  adult.  The  nymph,  however,  can  hibernate. 
If  the  adults  do  not  obtain  a  host  they  die  off  quickly. 

Pathogenicity.  —Nil. 


Fig.  327. — Dermacentor  salmoni  Stiles,   1909; 
Male,  Dorsal  Aspect. 


Dermacentor  andersoni  Stiles,  1905. 

Synonyms. — Dermacentor  occidentalis  of  all  writings  on  Rocky 
Mountain  spotted  fever  until  some  time  after  1910;  D.  venustus 
Marx  (iu  part  only) ;  D.  andersoni  Kieffer,  1907. 

Dermacentor  with  caudal  margin  nearly  or  quite  semicircular. 
Colour,  greyish  to  red  or  deep  red-brown.  Eyes  not  prominent. 
Scutum  with  whitish  rust,  and  with  large  or  small  punctations. 


718 


ARTHROPOD A 


Genital  pore  surrounded  by  hairs.  Anal  ring  nearly  circular. 
Stigmal  plates  with  prominent  dorso-lateral  prolongation,  aperture 
and  chamber  large  and  elongate,  goblets  of  medium  size.  Postero- 
lateral projections  of  plate  small.  Capitulum  with  short  postero- 
lateral projections  of  base.  External  article  with  large  recurved 
tooth,  a  smaller  subapical,  and  a  very  small  apical  tooth.  Hypo- 
stome  with  three  rows  of  strong  denticles.  Palpi  with  lateral  margin 
convex;  first  article  with  four  or  five  bristles;  third  article  rather 
triangular  dorsally.  Legs:  outer  spur  of  coxa  I.  longer  than  inner 
spur;  trochanter  I.  with  retrograde  curved  blade. 

Male. — Length,  4  by  2-5  millimetres  broad.  Body  oval.  Scutum 
covers  dorsum  except  capitulum;  deep  reddish-brown,  marked  by 

four  elongate 
spots  arranged  in 
semicircle;  two 
elongated  reni- 
form  spots  behind 
these,  one  elon- 
gated median  spot , 
and  two  shorter 
elongate  subme- 
dian  spots,  and  an 
indistinct  forked 
spot. 

Female.  —  Scu- 
tum, 1-56  to  1-62 
millimetres  in 
length  by  1  -9  milli- 
metres broad;  very 
conspicuous  b  e- 
cause  of  it  s 
whitish  colour. 
Cervical  grooves 
well  developed. 
Venter  with  punc- 
tation  and  fine 
hairs.     Genital  grooves  running  parallel  caudad. 

Young  Female. — This  is  the  form  most  commonly  found.  Length, 
4-5  to  7  millimetres.  Breadth,  2-3  to  2-6  millimetres.  Body  oval. 
Scutum  covers  about  0-43  of  the  length  of  the  body.  Eyes  not 
very  distinct.     Vulva  between  coxae  II. 

Replete  Female. — Length  about  16  millimetres,  and  6  millimetres 
to  Q'5  millimetres  thick.  Eyes  more  distinct  than  in  young  female. 
Vulva  may  shift  to  level  of  first  and  second  intercoxal  space, 
and  a  radial  groove  may  appear  on  each  side  between  the  anal 
and  the  genital  grooves.  Coxae  naturally  farther  apart  than  in 
young  female  owing  to  repletion. 

Hexapodc  Larva. — 0-656  millimetre  in  length  by  0-316  millimetre 
in  breadth,  with  the  caudal  end  broader  than  anterior  end. 


Fig.  328. — Dermacentor  salmoni  Stiles,   1909: 
Male,  Ventral  Aspect. 


DERMACENTOR 


719 


Fig.  329. — Devmacentor  salmoni  Stiles,  1909: 
Replete  Female,  Dorsal  Aspect. 


Hosts. — Man,  cattle,  horses,  dogs,  rabbits,  ground  squirrels,  and 
other  squirrels. 

Distribution. — Montana,  Washington  State,  Colorado,  and  Idaho 

Pathogenicity.  —  It  is 
the  carrier  of  the  virus 
of  Rocky  Mountain  fever, 
and  also  causes  Tick 
Paralysis. 


HaemaphysalisKoch,  1844 
(vide  Figs.  316-319). 

Rhipicephalime  w  i  t  h- 
out  eyes,  with  the  base 
of  the  capitulum  rectan- 
gular; twice  as  broad  as 
long.  Palpi  triangular  or 
crescentic.  Stigmata 
circular  or  comma-shaped. 
Anal  shields  absent.  Tegu- 
ment brownish. 

Type.  —  Hesmaphysalis 
concinna  Koch,  1844. 

Species. — The  most  important  species  are:  H.  concinna,  H.  leachi, 
H.  flavii,  H.  punctata,  the  life-history  of  the  last  named  having 
been  studied  in  detail  by  Nuttall,  Cooper,  and  Robinson,  while 
according  to  Stockmann  it  transmit sPiroplasma  ovis. 

Haemaphysalis  leachi 

Audouin,  1827. 

Synonyms.  —  Ixodes 
leachi  Audouin,  1827; 
Rhipistoma  leachi  C.  L. 
Koch,  1844;  Rhipicepha- 
lus  ellipticum  C.  L.  Koch, 
1844;  Rhipidosiomaleaclii 
Karsch,  1878 ;  Hcemaphy- 
salis  leachi  Neumann, 
1897. 

This  species  is  found 
in  Africa,  Sumatra,  and 
New  South  Wales.  It  is 
the  South  African  dog 
tick. 

The  male  is  3  by  1*5 
millimetres,  with  yellow- 
ish-red  scutum,  finely  punctated   dorsum,  with  eleven  marginal 
festoons.     Palpi  longer  than  hypostome.     Coxa?  of  all  legs,  with  a 
short  spine. 


Fig.  330. — Dermacentor  salmoni  Stiles,  1909: 
Replete  Female,   Ventral  Aspect. 


720  ARTHROPODA 

The  replete  female  is  9  by  5  millimetres;  scutum  oval,  larger  than 
wide.     Second  segment  of  palpi  long  and  spiny. 

Life-History. — The  larva,  after  feeding,  drops  off  the'  dog,  and 
moults.  The  nymph  attacks  another  dog,  feeds,  drops  off,  and 
moults.  The  adult  attacks  a  third  dog,  feeds,  drops  off.  and  lays 
eggs  which  develop  larvae. 

Pathogenicity. — It  is  the  spreader  oiPiroplasma  cants  among  dogs, 
causing  their  biliary  fever.  Nuttall  and  Hadwen  have  shown  that 
this  canine  piroplasmosis  can  be  successfully  treated  by  hypodermic 
injections  of  6  c.c.  of  a  1  per  cent,  solution  of  trypanrot,  or  4-5  to 
5*5  c.c.  of  a  saturated  solution  of  trypanblau. 

Subfamily  Ixopin.l. 

The  following  diagnostic  table,  modified  slightly  from  Salmon 
and  Stiles,  will  indicate  the  genera: — 

A.  Eyes  absent:- — 

I.  Pre-anal  crescentic  groove  opens  posteriorly: — 
(a)  Palpi  valvate — Ixodes  (Fig.  331). 
(.&)   Palpi  clavate — Eschatocephalus. 
II.  Post-anal   crescentic   groove   open   anteriorly — A-po- 

nomma.     (Fig.  333). 
III.  Without  anal  groove  in  the  female;  one  anal  shield  in 
the  male — Ceratixodes. 

B.  Eyes  present: — 

I.  Anal  plates  absent- — Amblyomma  (Fig.  336). 
II.  Anal  plates  present  on  males — Hyalomma  (Fig.  339). 

Ixodes  Latreille,  1796. 

Synonyms. — Cynorhcestes  Hermann,  1804;  Crotonus  Dumeril,  1822. 

Ixodinae  without  eyes,  and  with  long  palpi  hollowed  on  the  internal 
surface.  Tarsi  without  terminal  spurs.  Pre-anal  groove  open 
posteriorly. 

Male  with  scutum  not  covering  the  lateral  and  posterior  margins: 
no  festoons;  stigmata  oval.  Ventral  shields  seven  in  number; 
one  pregenital,  one  median,  two  epimeral,  one  anal,  and  two 
adanal. 

Female  with  three  dorsal  longitudinal  grooves  and  two  longi- 
tudinal genital  grooves  ventral,  and  the  anal  crescentic  groove 
already  mentioned. 

Type  Species. — Ixodes  ricinus  Linnaeus,  1758. 

Ixodes  ricinus  Linnaeus,  1758.' 

Synonyms. — A  cams  reduvius  Linnaeus,  1758;  A.  ricinus  Linnaeus, 

1758. 

This  is  the  castor-oil  tick,  and  is  found  in  Europe,  North  Africa, 
and  North  America  on  man,  sheep,  goats,  cattle,  horses,  dogs,  cats, 
rabbits,  bats,  birds,  etc. 


IXODES 


721 


The  male  has  an  oval  body,  broader  posteriorly,  2-5  by  1-5  milli- 
metres. Scutum  convex,  deep  red-brown.  Genital  pore  on  a  plane 
with  the  third  coxa.  Pregenital  and  anal  shields  well  marked. 
Capitulum  long. 


a  b 

Figs.  331-332. — Ixodes  pilosus  Koch,  1844:  Ventral  Aspect. 
a,  Male  (X  10)  and  mouth  parts;  b,  mouth  parts  and  female  (X  10). 

The  female,  when  young,  has  a  flat,  oval  body.  Replete  female 
is  like  a  castor-oil  bean,  10  to  11  by  6  to  7  millimetres,  of  ashy 
colour.  Tegument  covered  with  fine,  short  hairs.  Dorsal  surface 
with  three  well-marked  posterior  grooves^and  two  anterior. 


Figs.  333-335. — Aponomma  gervaisi  Lucas,   1847:  Ventral  Aspect. 
a,  Male  (X  15) ;  b,  mouth  parts  (more  highly  magnified) ;  c,  female  (X  15)- 


Genital  pore  at  the  level  of  the  fourth  coxae.  Genital  grooves 
unite  in  front  of  the  vulva.  Well-marked  pre-anal  crescentic 
groove,  open  posteriorly.     Stigmata  whitish.     Porose  areas  elon- 

46 


■jzi  ARTHROPOD  A 

gated   transversely.     Mandibles  with   two   teeth   on   the  internal 
apophysis,  and  external  with  five  teeth. 

Life-History. — The  female  lays  about  1,000  eggs  in  about  one  to 
two  weeks;  the  eggs  take  six  weeks  to  hatch  into  a  larva,  which 
remain  one  week  on  the  first  host  and  then  four  weeks  on  the 
earth  before  it  becomes  a  nymph.  This  stage  requires  one  week  on 
the  second  host  and  eight  weeks  on  the  earth  before  it  becomes  the 
adult,  which  seeks  the  third  host,  copulates,  sucks  blood,  and  drops 
off  to  lay  eggs. 

Pathogenicity,— It  acquires  Piroplasma  bigeminum  from  infected 
cattle  in  the  adult  stage,  and  spreads  it  to  fresh  cattle  in  the  larval 
and  nymph al  stages. 

Ixodes  hexagonus  Leach,  1815. 

Synonyms. — Ixodes  autumnalis  Leach,  1815;  /.  erinacei  Audouin, 
1832;  /.  reduvius  Audouin,  1832;  i".  sexpunctatus  Koch,  1847. 

This  is  the  European  dog  tick. 

Pathogenicity. — According  to  Blanchard,  the  tick  can  transmit 
Piroplasma  cams  Piana  and  Galli  Valerio,  1895. 

Eschatocephalus  Frauenfeld,  1853. 

Synonyms. — Sarconissus  Kolenati,  1857;  Hcemalastor  Neumann, 
1889. 

Ixodinae  without  eyes,  and  with  a  long  rostrum.  Palpi  pyriform 
in  the  male  and  claviform  in  the  female.  Pre-anal  groove  opening 
posteriorly.     Stigmata  circular.     Legs  long. 

Male  with  dorsal  and  ventral  irregular  chitinous  thickenings. 

Female  with  very  fine  parallel  grooves. 

Type  Species. — E.  vespertilionisC.  L.  Koch,  1844. 

There  are  over  seven  species  found  on  bats  and  in  caves. 

Aponomma  Neumann,  1899. 

Synonym. — Ophiodes  Murray,  1877. 

Ixodinse  without  eyes,  and  with  the  base  of  capitulum  usually 
pentagonal,  with  dorso-lateral  border  very  short;  palpi  long.  Post- 
anal groove.     V entral  sexual  grooves. 

Male  nearly  as  broad  as  long,  with  a  scutum  marked  with  green 
spots  covering  the  whole  dorsal  surface. 

Female  scutum  shorter  than  broad. 

Type  Species.— Aponomma  gervaisi  Lucas,  1847. 

These  ticks  are  found  chiefly  on  reptiles,  but  are  also  found  on 
other  animals. 

Ceratixodes  Neumann,  1904. 

Ixodinae  with  long  palpi,  without  eyes,  and  without  anal  groove 
in  female.  Stigmata  circular.  One  anal  and  two  adanal  shields  in 
the  male. 

Type  Species. — Ceratixodes  pnUis  Cambridge,  1879.  It  lives  on 
sea-birds,  and  is  found  on  cliffs,  while  C.  signatus  Banks,  1908,  is 
known  in  North  America. 


AMBLYOMMA 


72  3 


Amblyomma  Koch,  1844. 

Ixodinse  with  flat  eyes;  rostrum  long,  with  valvate  palpi.  Anal 
groove  semicircular,  opening  anteriorly.  No  median  ano-marginal 
groove;  no  anal  plates  in  the  male.  Stigmata  triangular.  Nearly 
always  eleven  festoons. 

Type  Species.— A mblyomma  cajennense  Koch,  1844. 


Figs.  336-338. — Amblyomma  hebrceum  C.  L.  Koch,  1844:  Ventral  Aspect. 
a,  Male  (X  7);  b,  mouth  parts  (more  highly  magnified);  c,  female  (X  7). 

Amblyomma  hebraeum  C.  L.  Koch,  1844. 

Synonyms. — -A.  annulipes  C.  L.  Koch,  1844;  Ixodes  ftoorlmani 
Lucas,  1850;  A.  hassalli  Marx  and  Neumann,  1899. 

This  tick  is  found  in  Africa,  especially  in  Cape  Colony,  where  it  is 
called  the  '  bont '  or  variegated  tick,  and  is  the  spreader  of  '  heart 
water  '  in  sheep  and  goats. 

Morphology. — 'Male  {vide  Fig.  336)  with  sulphur-yellow-coloured 
scutum,  variegated  with  brown,  and  finely  punctated  and  marked 
with  longitudinal  grooves.  Marginal  festoons  light-coloured  except 
the  two  extreme  festoons.  Female  with  brown  and  white  scutum,  as 
broad  as  long;  body  of  a  fully  replete  female,  24  by  15  millimetres. 

Life-History. — The  usual  life-history  for  Ixodidse. 

Pathogenicity. — Transmits '  heart-water '  in  sheep. 

Hocyalomma  Koch,  1844. 

Ixodinae  with  eyes,  rostrum  long,  palpi  valvate,  anal  groove 
semicircular,  opening  forwards,  uniting  sexual  grooves,  and  followed 
by  a  median  ano-marginal  groove.  Male  with  two  pairs  of  ventral 
shields,  two  adanal  and  two  lateral.  Female  with  triangular  stig- 
mata. 

Type  Species.— Hyalomma  agyptium  Linnaeus,  1758. 

Only  a  few  species: — H.  csgyptium,  H.  crassitarsus,  H.  affme,  H. 
syrictcum,  H.  rhipicephaloides,  H.  hippopotamense,  H.  monstrosuni. 


724 


ARTHROPOD A 


Hyalomma  segyptium  Linnaeus,  1758. 

Synonyms.- — -Acarus  cegyptus  L.,  1758;  Ixodes  camelinus  Fischer, 

l823- 

This  tick  is  found  in  Africa,  particularly  in  Egypt  and  South 

Africa;  in  Asia,  particularly  in  Southern  India;  in  Europe,  espe- 
cially in  France  and  Italy.  The  adults  attack  cattle,  especially 
sheep  and  goats,  and^also  at  times  man.  The  larvae  and  nymphae 
are  supposed  to  attack  birds,  not  cattle. 


a  b  c 

Figs.  339-341.— Hyalomma  eegyptium  Linn^us,  1758  (X  3) :  Ventral  Aspect 
a,  Male  (X  8);  b,  mouth  parts  (more  highly  magnified);  c,  female  (X  8). 

The  male  is  almost  black,  with  a  pale  marginal  stripe,  with  a 
small,  triangular,  often  white,  median  festoon. 

The  female  is  brown,  with  light  blue  stripes.  Scutum,  which 
as  a  rule  is  as  broad  as  long,  possesses  numerous  punctations,  and  is 
indentated  behind  the  eyes. 

Life-History. — This  appears  to  require  further  investigation. 

Pathogenicity.- — -Can  transmit Piropla^ma  bovis  to  oxen. 


SUBORDER  IV.    PROSTIGMATA. 

The  suborder  Prostigmata  contains  two  superfamilies,  which  are 
of  importance  in  medicine. 

Superfamily  A:  Trombidoidea. — Prostigmata  in  which  the  last 
joint  of  the  palpi  is  bent  down  towards  the  penultimate  joint,  which 
usually  ends  in  a  claw.     Body  often  with  many  hairs. 

Superfamily  B :  Eupopoidea. — Prostigmata  with  simple  palpi, 
in  which  the  last  joint  of  the  palpi  is  not  bent  down  towards  the 
penultimate  joint.     Body  with  few  hairs. 


TROMBIDOIDEA 


725 


SUPERFAMILY  A:  TROMBIDOIDEA. 

The  Trombidoidea  include  the  following  families,  which  are  of 
importance  in  medicine: — (i)  Trombididae;  (2)  Tetranychidae ; 
(3)  Cheyletidae. 

Family  Trombididae. 

Trombidoidea  with  soft  skins,  and  chelate  mandibles  adapted  for 
biting. 

There  are  two  important  genera,  which  may  be  differentiated 
as  follows  :■ — ■ 

A.  Distal  segment  of  palp  with  single  claw — Trombidium. 

B.  Distal  segment  of  palp  with  two  claws— Microtrombidium. 

Trombidium  Latreille,  1795. 

The  larvae  of  this  genus  are  the  harvest-mites,  and  are  widely 
distributed.  Leptus  ctmericanus  Riley  and  L.  irritans  Riley  are 
American  species,  being  found  in  the  United  States  and  Mexico. 
Trombidium  tlalsahuate  Le- 
maire,  1867,  is  the  Tlalsahuate 
of  Mexico.  The  zoological 
names  of  the  '  pou  d'agouti ' 
of  Guiana,  the  '  niaibi '  of  New 
Granada,  the  '  Colorado '  of 
Cuba,  the  '  mouqui '  of  Para, 
the  '  bete  rouge  '  of  Martinique 
and  Honduras,  are  not  known. 
It  must  be  confessed  that  there 
is  a  great  deal  of  uncertainty 
about  the  genus  and  species  of 
these  larvae,  and  the  subject 
evidently  requires  revision. 

Morphology.— They  are  six- 
legged  larvae  with  prominent 
claws  on  the  tips  of  their  legs,  provided  with  a  powerful  hypostome, 
which  they  drive  through  the  skin.  Around  this  hypostome  the 
tissues  of  the  host  are  supposed  to  form  a  tube. 

Life-History. — -Only  the  larvae  appear  to  be  parasitic;  the  adults 
apparently  arc  not. 

Pathogenicity.— They  cause  itching,  redness,  and  swelling  of  the 
affected  part,  which,  if  scratched,  may  become  eczematous,  and 
even  at  times  suppurate. 

Treatment.— Sulphur  ointment  kills  them. 

Genus  Microtrombidium  Haller,  1882. 

Definition.— Trombididae  in  which  the  distal  segment  of  the  palpus 
terminates  with  two  stout  claws. 

Remarks.  -These  mites  arc  quite  common.  Thus  Microtrom- 
bidium dutumnalis  Shaw,  1790,  is  the  harvest  bug  of  England,  and 


Fig.  342. — Microtrombidium  akamnshi 
Brumpt,   1910. 

(After  Tanaka,  from  Centralb.  fur 
Bakteriologie  Par.  unci  Inf.) 


726  ARTHROPODA 

is  commonly  found  in  the  South  of  England  during  August  and 
September.  It  is  also  common  in  France  during  the  hot  and  dry 
months.  Bruyant  raised  a  nymph  in  1910  which  was  thought  at 
first  to  be  M .  pusillum  Hermann,  but  this  is  now  thought  to  be 
doubtful.  It  is  also  found  in  Germany.  It  generally  attacks  small 
mammals,  such  as  dogs  and  cats.  Acarus  batatas  Linnaeus  of 
Surinam  perhaps  belongs  here.  M.  wichmanni  Oudemans  is  found 
in  New  Guinea  and  Celebes. 

Microtrombidium  akamushi  Brumpt,  1910. 

Synonyms. — -Akamushi  (red  mite);  Kedani  (hairy  mite);  Shashitsu 
(sand  mite);  Shimamushi  (island  mite);  T  suisugamushi  (dangerous 
mite);  Yochubia. 

Definition.- — -Microtrombidium  of  various  characters,  probably 
covering  several  distinct  species,  with  and  without  all  dorsal  hairs 
of  the  palp  feathered.  Hair  on  galea  of  maxilla  always  strongly 
feathered.  Hairs  on  dorsum  of  palp  not  feathered,  except  that  on 
the  tibia.  Tarsal  claw  trifurcate.  Last  tarsus  without  long  fine 
tactile  hair. 

Remarks. — -The  form  shown  in  Fig.  342  may  be  a  distinct  species 
from  M.  akamushi,  because  all  the  dorsal  hairs  on  the  palp  are 
feathered.  This  may  be  called  Microtrombidium  brumpti  Hirst, 
1915. 

These  are  the  mites  which  cause  Japanese  river  fever,  called 
tsutsugamushi  fever. 

Morphology. — The  larva  is  orange  red  in  colour,  0-16-0-24  milli- 
metre in  length,  by  0-10-0-24  millimetre  in  breadth.  The  palpi 
are  leg-like,  and  the  body  and  legs  are  veiy  hirsute. 

The  scutum  is  oblong,  not  wide,  with  straight  posterior  margin  and 
usually  seven  hairs.  The  pseudostigmata  are  nearer  the  posterior 
than  the  anterior  margin. 

Eyes  are  well  developed. 

Dorsal  hairs  are  2,  8,  6,  8-10,  8,  with  a  few  posterior  hairs. 

The  first  coxa  has  two  hairs.  The  hair  on  the  galea  of  the  maxilla 
is  strongly  feathered,  while  those  on  the  dorsal  surface  of  the  palp 
are  plain,  except  the  one  on  the  tibia,  which  is  feathered.  Tarsus 
with  seven  feathered  hairs  and  a  blunt  rod-like  hair.  Legs  slender 
and  moderately  long,  with  strongly  feathered  hairs. 

Life-History.- — -The  akamushi  does  not  attack  insects  nor  spiders, 
but  will  attach  itself  to  man  and  to  small  mammals- — monkey,  dog, 
cat,  rat,  mouse,  rabbit,  and  guinea-pig. 

The  mite  remains  on  its  host  for  three  to  four  days,  during  which 
it  swells  up  and  turns  pale.  It  then  drops  off  and  finds  shelter 
under  the  ground,  where  a  metamorphosis  takes  place  in  some  five 
to  six  days,  during  which  a  nymph  forms  under  the  larval  skin,  and 
from  which  it  escapes. 

The  newly  hatched  nymph,  0-4-0-57  x  0-25-0-285  mm.,  is  a  minute 
eight-legged  creature,  which,  though  it  crawls  about,  is  neither  para- 
sitic nor  predaceous,  but  it  feeds  upon  the  juice  of  potatoes,  melons, 


MICROTROMBIDIUM  727 

and  other  vegetables.  After  some  growth  the  nymphs  seek  shelter 
under  the  earth  and  become  pupae. 

The  pupa  is  formed  from  the  elongated  body  of  the  nymph,  inside 
which  the  adult  form  develops,  and  which  in  a  few  days  emerges. 

The  imago  is  at  first  without  sexual  organs,  which  begin  to  de- 
velop. Meanwhile  the  adult  grows  and  undergoes  more  than  one 
ecdysis,  and  in  about  ten  weeks  arrives  at  sexual  maturity. 

The  eggs  are  laid  singly  in  earth,  but  oviposition  has  not  been 
observed,  and  the  earliest  egg  known  is  the  dentovum,  0-21-0-24  x 
0-17-0-22  mm.,  inside  which  the  chorion,  having  split  the  pale 
vitelline  membrane,  could  be  seen  containing  the  red  akamushi, 
which  hatched  out  after  three  weeks'  incubation. 

Microtrombidium  wichmanniOudemans,  1905. 
Its  larva  attacks  man  and  animals  in  Celebes. 

Microtrombidium  vandersandei  Oudemans,  1905. 

Synonym. — Microtrombidium  Van  der  Sander. 

The  larva  of  this  Trombidium  occurs  in  New  Guinea,  and  attacks  man 
and  animals.     Its  local  name  is  '  Gonone.' 

Metatrombidium  Oudemans,  1909. 
Metatrombidium  poriceps  Heim  and  Oudemans,  1904,  has  been  found  on 
fowls,  dogs,  and  men. 

Family  Tetranychid^. 

Trombidoidea  with  first  and  second  pairs  of  legs  without  spines;  skin  with 
few  shields ;  palpi  not  much  thickened  on  base,  moving  vertically ;  eyes  usually 
present.  First  pair  of  legs  do  not  end  in  long  hairs.  Coxa;  more  or  less  in 
two  groups.  Body  with  fewer  longer  hairs.  No  dorsal  groove;  often  spinning 
threads;  tarsi  never  swollen.     Mandibles  styliform. 

Genus  Tetranychus  Dufour. 
Definition. — Tetranychidae  without   cephalothoracic  tubercles.     Few   legs, 
slightly  longer  than  body,  which  is  not  twice  as  long  as  broad.     Legs  slender. 
Integument  not  tessellated  dorsally.     Palpi  ending  in  a  distinct  thumb. 

Tetranychus  molestissimus  Weyenbergh,  1886. 
This  mite  is  found  in  the  Argentine  and  Uruguay.  It  is  small  and  of  red 
colour,  living  in  a  web  on  the  inferior  surface  of  the  leaves  of  Xanthum  macro- 
carpum.  From  December  to  February  it  attacks  mammals  and  man,  thrust- 
ing its  hypostome  into  the  skin  and  causing  severe  itching.  Another  species — 
T.  telarius  (var.  russeolus)  L.,  1758 — may  attack  human  beings. 

Family  Cheyletid^e. 

Trombidoidea  without  spinous  processes  on  the  legs;  skin  with  few  if  any 
shields;  palpi  much  thickened  at  the  base,  moving  laterally;  last  joint  often 
with  two  pectinate  bristles  without  eyes.  First  leg  ending  in  several  long 
hairs. 

Cheyletus  Latreille,  1796. 

These  are  very  small  mites,  distinguished  by  having  enormous  palpi,  with 
pectinate  bristles.  Cheyletus  eruditus  has  been  described  in  the  external 
auditory  meatus  of  a  man. 


7-« 


ARTHROPOD  A 


Acaropsis  Moquin-Tandon,  1863. 

Acaropsis  mericourti  Laboulbene  has  been  found  in  the  human  external 
auditory  meatus. 

SUPERFAMILY  B.  EUPOPOIDEA. 

Family  Bdellid^e. 

No  specialized  seta  on  cephalothorax ;  integument  not  chitinized  or  leathery; 
palpi  composed  of  four  or  five  segments;  cephalothorax  large  and  clearly 
separated  from  abdomen;  palpi  large,  geniculate,  and  bearing  distally  long 
tactile  bristles ;  mandibles  chelate. 

Tydeus  molestus  Moniez,  1889. 

This  mite  was  imported  into  Belgium  in  Peruvian  guano,  and  caused  much 
trouble  to  man  and  beast. 

Family  Tarsonemid^e. 

With  marked  sexual  dimorphism  and  tracheae.     No  ventral  suckers. 
Tarsonemus  hominis  Dahl,  found  in  cancerous  tissues  in  man,  is  probably 
an  accidental  contamination  of  the  preserving  fluids. 


Figs.  343-3/j. — Pediculoides  ventricosus  Newport. 
a,  Male  (X  35°);  b,  female  (X  220);  c,  distended  female  (X  60). 

Genus  Pediculoides  Targioni-Tozzetti. 
Pediculoides  ventricosus  Newport,  1850. 

Synonyms. — Hitcropus  ventricosus  Newport,  1850;  Acarus  tvitici  Lagreze- 
Fossot  and  Montane,  1851;  Physogaster  larvarum  Lichtenstein,  1868;  Pedi- 
culoides tritici  Targioni-Tozzetti,  1878;  Spharogyna  ventricosa  Laboulbene  and 
Megnin,  1885;  Tarsonemus  monougniculosus. 

This  mite  causes  severe  itching  and  urticarial  eruptions  on  the  breast, 
arms,  face,  neck,  and  shoulders  of  persons  handling  corn  and  barley,  which 
contains  it,  in  India,  Algeria,  and  Europe. 

Morphology. — Males  are  oval,  0-12  by  0-08  millimetre,  with  six  pairs  of 
dorsal  hairs  and  a  lyre-shaped  lamella. 


XEPHRUPHAGES 


729 


Female  cylindrical,  0-2  by  0-07  millimetre;  becomes  much  distended  pos- 
teriorly when  gravid. 

Life-History. — They  live  on  the  stalks  of  cereals,  and  feed  on  animal  and 
vegetal  juices.     The  adult  hatches  directly  from  the  egg. 

Pathogenicity. — They  cause  diffuse  erythema,  urticaria,  and  itching. 

Nephrophages  Miyake  and  Scriba,  1893. 

Nephrophages  sanguinarius  Miyake  and  Scriba,  1893.  It  is  a  very  doubtful 
parasite  of  man;  it  was  found  in  bloody  urine  passed  by  a  man  in  Japan. 

SUBORDER  V.  ASTIGMATA. 

This  suborder  includes  the  superfamily  Sarcoptoidea. 

SUPERFAMILY  SARCOPTOIDEA. 

Astigmata  with  small  three-pointed  palpi  adhering  for  some  distance  to 
the  hypostome,  with  usually  ventral  suckers.  Two  families  concern  us — 
(1)  Tyroglyphidae,  (2)  Sarcoptidae.  '} 


FxG.  346. —  Tyroglyphus  longiov 
var.  castellanii  Hirst,  1912; 
Dorsal  Aspect. 


Fig.  347.  —  Tyroglyphus  longiov 
var.  castellanii  Hirst  191 2: 
Ventral  Aspect. 


Family  i  :    Tyroglyphidae. 

Very  small  mites  without  eyes;  only  accidental  parasites  being  found  in 
flour,  sugar,  cheese,  etc. 

Tyroglyphus  Latreille,  1796. — With  smooth  dorsum;  cephalo thorax  with 
four  long  bristles  and  no  stout  spines  on  tarsi ;  with  claws  and  suckers.  Aleuro- 
bius  farincB  (De  Geer)  in  corn  may  get  into  the  skin.  They  are  the  cause 
of  so-called  vanillismus.  According  to  Theobald,  Linnaeus  reported  a  case  of 
dysentery  as  being  due  to  this  species  (Acarus  dysenterice). 

Tyroglyphus  siro  Linnasus,  1758,  is  supposed  to  be  the  cause  of  vanillismus, 
and  T.  longior  Gervais,  1844,  is  found  accidentally  in  faeces,  urine,  or  pus. 

T.  longior  var.  castellanii  Hirst,  1912,  was  found  by  Castellani  in  copra  and 
on  people  affected  by  copra  itch  in  Ceylon.  In  this  variety,  in  contrast  to 
T.  longior,  there  is  no  pair  of  short  hairs  on  the  ventral  surface,  behind  the  anal 
suckers. 

Glyciphagus  Hering,  1838. — With  dorsum  covered  with  hairs. 

G.  prunorum  Hermann  (synonym,  G.  domesticus  de  Geer,  1808)  is  the  cause 
of  grocer's  itch. 

Rhizog'yphus  Claparide,  1869 — R.  parasiticus  Dalgetty,  1 90 1.— With  short 
legs,  armed  with  spines.     Tarsi  end  in  a  claw.     Live  on  plants. 


73° 


ARTHROPOD  A 


Fig.  348. — Rhizoglyphus  parasiticus  Dalgetty,   1901. 
(From  a  photograph  by  J.  J.  Bell.) 

This  is  the  species  which  causes  trouble  in  the  feet  of  Indian  coolies.  Bell 
described  a  large  circular,  superficial  sore  on  the  sole  of  the  foot,  caused  by 
many  of  these  parasites  invading  the  skin  (see  Chapter  XCVI.). 


Fig.  349. — Sarcoptes  scabiei  var.  hominis  Linnaeus,  1758:  Female 
(X125.) 


SARCOPTin.il 


73i 


Histiogaster  Berlese,  1883 — H.  spermaticus  Trouessart,  1900. — This  mite, 
which  feeds  on  vegetables,  appears  to  have  been  introduced  into  a  patient  by 
means  of  a  catheter,  and  to  have  formed  a  cyst  in  the  testis  in  a  man  in  India. 

Carpoglyphus  Robin,  1869. — C.  alienus  Banks  has  been  found  in  purulent 
urine  passed  by  a  man.     Probably  it  was  a  contamination. 

Family  2:    Sarcoptidae. 

Sarcoptoidea  without  genital  suckers,  without  clinging  apparatus,  with 
transverse  vulva.     Lines  in  skin. 

Sarcoptes  Latreille,  1806. — Sarcoptidae  with  round  or  slightly  oval  bodies; 
posterior  two  pairs  of  legs  concealed  beneath  the'body;  tarsi  end  in  simple 
long  pedicles  with  ambulatory  suckers. 

Sarcoptes  scabiei  var.  hominis  Lin- 
naeus, 1758. — Female  lives  in  furrows 
in  the  epidermis,  in  which  it  lays  its 
eggs.  Posterior  legs  end  in  spines. 
Males  occur  on  the  surface  and  die 
after  copulation.  Posterior  legs  end 
in  suckers.  Six-legged  larva  hatches  in 
four  to  eight  days. 

Sarcoptes  minor  Fiirstenberg,  1 86 1. 
— Usually  a  parasite  of  cats;  has  been 
found  on  man. 

Sarcoptidae  as  Internal  Parasites. — 
Sarcoptidae  have  been  described  by 
Newstead  and  Todd  as  internal  para- 
sites in  monkeys.  An  Acarid-like 
parasite  was  found  by  Castellani  in  the 
omentum  of  a  negro  in  Uganda.  This 
parasite  somewhat  resembled  Cyto- 
leichus  sarcoptoides  Heguin,  which 
lives  in  the  air  sacs,  and  at  times  the 
liver  and  kidneys,  of  fowls. 

Notcedres  Railliet,  1893 — N.  cati 
Railliet,  1893. — Cause  of  the  itch  in 
the  cat,  and  transmissible  to  man. 

Cytoleichus    sarcoptoides    Megnin.  —  Synonym 
1868),  in  fowls  in  the  Sudan. 

Cytoleichus   hominis 


Fig.  350.  —  Savcoptes  scabiei  var. 
hominis  Linnaeus,  1758:  Male. 
(X  125.) 


Cytodites    nudus    (Vizioli, 


Hirst, 
Castellani,  in    1902,    embedded 
omentum  of  a  negro  in  Uganda. 

Chorioptes  bovis  Gerlach  and 
Gervais  are  stated  by  Ziirn  and 
man. 


191 7. — Found     by 
in    the  fat  of   the 

Psoroptes    equi 

Hirst  to  attack 


VERMIFORMIA. 

with  abdomen   elongated 


SUBORDER  VI 

Very  minute  Acarina 
and  annulated,  without  tracheae,  and  with  epimeres 
on  the  legs. 

This  suborder  contains  only  one  family. 


Fig.  351. — Cytoleichus 
hominis  Hirst,  1917. 


Family  Demodicid^j. 


Vermiformia  with  eight  legs,  living  on  animals. 
This  family  includes  only  one  genus — Demodex  Owen,  1843. 

Demodex  Owen,  1843. 
With  the  family  characters.     This  genus  has  been  recently  revised  by  Hirst. 
The  species  of  Demodex  live  in  the  sebaceous  glands   and   hair-follicles  of 
mammals  and  man.     The  mouth  consists  of  a  rostrum,  which  is  arranged  for 


73? 


ARTHROPOD  A 


sucking.  The  palpi  are  three-jointed,  and  pressed  to  the  under  surface  of 
the  rostrum.  The  legs  are  eight  in  number,  short,  and  consist  of  three  segments 
with  small  terminal  ungues.  The  abdomen  is  tapering,  striated  dorsally  and 
ventrally,  and  rounded  at  the  tip.  The  anus  is  situated  at  the  anterior  end 
of  the  abdomen. 

Demodex  folliculorum  Simon,  1842. 

Synonyms. — -A carus  folliculorum  Simon,  1842;  D .  folliculorum  Owen,  1843; 
Macrogaster  platypus  Miescher,  1843;  Simonea  folliculorum  P.  Gervais,  1844; 
Steal ozoon  folliculorum  Wilson,  1847. 

This  parasite  was  first  discovered  by  G.  Simon,  of  Berlin,  in  1842,  in  the 
contents  of^pustules  of  Acne  sebacea. 

About  the  same  time  Heme  had  found  them  in  hair- 
follicles  in  the  external  auditory  meatus,  and  Topping 
a  variety  in  the  dog.  Two  other  species  are  known: 
D.  phylloides  Cook  in  pigs  and  D.  bovis  Stiles  in  cattle. 
D.  folliculorum  hominis  is  cosmopolitan,  living  in  the 
sebaceous  follicles  of  the  face. 

Male  measures  300  /x  by  40  /x,  and  the  female  380  fx 
by  45  /x. 

Life-History. — The  eggs  are  60  to  90  /x  in  length  by 
20  to  50/x  in  breadth,  and  heart-shaped  or  fusiform.  The 
egg  hatches  out  a  six-legged  larva,  which  develops  into 
an  eight-legged  nymph,  from  which  the  adult  appears. 
Pathogenicity. — Usually  said  to  be  nil,  but  a  few 
authorities  suspect  the  parasites  to  produce  acne-like 
eruptions,  and  Borrel  considers  they  play  a  part  in  the 
spread  of  cancer  and  leprosy. 

ARACHNIDS  INCERT.E  SEDIS. 
LlNGUATULIDA. 

Parasitic  Arachnoidea  with  ringed,  elongated, 
vermiform  bodies,  possessing  two  pairs  of  hooks 
in  the  neighbourhood  of  the  jawless  mouth. 

Remarks. — The Lingnatulidahzve  been  found 
parasitic  in  man  both  in  the  adult  and  larval 
conditions,  but  the  adult  is  much  rarer  than  the 
larva.  They  have  been  found  in  Europe  and 
Africa,  and  reported  from  the  West  Indies,  but 
this  was  in  a  negro  from  West  Africa.  It  is  not 
impossible  that  they  will  be  found  to  be  far 
from  uncommon  parasites  when  the  medical 
history  of  the  West  Coast  of  Africa  is  better 
known.  When  dealing  with  cases  showing  obscure  abdominal  or 
pulmonary  symptoms  in  that  part  of  the  world,  the  medical  man 
should  remember  these  parasites. 

Morphology. — -The  body  is  white  in  colour  and  vermiform  in 
appearance,  and,  indeed,  they  were  long  mistaken  for  worms. 

It  is  elongated,  flattened,  or  cylindrical,  and  marked  by  a  variable 
number  of  rings,  and  is  usually  divisible  into  two  regions — an 
anterior  broader  portion  called  the  cephalothorax,  and  a  posterior, 
more  attenuated,  called  the  abdomen.  It  is  covered  with  a  chitinous 
cuticle  pierced  by  pores,  called  stigmata,  which  have  nothing  to 
do  with  respiration,  being  merely  the  orifices  of  epidermal  glands. 


Fig.  352. — Demoicx 
folliculorum  Simon, 
1842.     (X  I5°0 

(Partly  after  Berlese.) 


LINGUATULIDA  733 

The  mouth  is  situated  anteriorly,  and  is  either  terminal  or  sub- 
terminal,  with  a  chitinous  ring.  Two  pairs  of  chitinous  hooks, 
retractile  into  grooves,  are  situate  on  either  side  of  the  mouth,  and 
are  looked  upon  by  Stiles  as  antennas  and  palpi.  There  are  no  legs. 
The  anus  is  terminal  at  the  posterior  end  of  the  abdomen,  with  the 
female  aperture  situate  just  in  front.  The  male  generative  pore 
is  on  the  ventral  surface,  near  the  anterior  end  of  the  abdomen. 
The  sexes  are  distinct.  The  mouth  leads  into  a  simple  straight 
alimentary  canal,  which  ends  in  the  anus.  There  are  no  circula- 
tory or  respiratory  organs.  The  nervous  system  consists  of  a  ventral 
mass  and  a  circum oesophageal  commissure. 

Life-History.— The  female  produces  eggs,  which,  escaping  from 
the  definitive  host,  pass  into  the  intermediary  host,  and  there  hatch 
out  a  four-legged  larva,  not  unlike  an  embyro  Acctrus.  This  embryo 
undergoes  complete  metamorphosis,  and  forms  a  nymph  resembling 
the  adult,  which  does  not,  as  a  rule,  mature,  until  it  reaches  its 
definitive  host  again. 

Genera.— Linguatula Frolich,  iy8g;Porocephalus Humboldt,  1811 ; 
ReighardiaWard,  1899;  and  Raillietiella  Sambon,  1909;  but  only  the 
first  two  contain  species  parasitic  in  man. 

Linguatula  Frolich,  1789. 

Linguatulida  with  depressed  body,  rounded  dorsum,  and  crenate 
margins.  Body  cavity  forming  diverticuli  into  the  lateral  parts 
of  the  rings. 

Species. — -Linguatula  serrata  Frolich,  1879. 

Linguatula  serrata  Frolich,  1789. 

Synonyms. — -Tcenia  rhinaria  Pilger,  1802;  Polystoma  tcenioides 
Rudolphi,  1810;  Linguatula  tcenioides  Lambinet,  1816 ;  Pentastoma 
tcenioides  Rudolphi,  1819.     Nymph.— Pentastoma  denticulatum. 

The  adult  lives  in  the  nasal  cavity  and  frontal  sinus  of  the  dog, 
wolf,  fox,  and  rarely  in  the  horse,  mule,  sheep,  goat,  and  man  in 
Europe;  while  the  larva  exists  in  sheep,  oxen,  horses,  rarely  in  cats 
and  dogs.     Its  real  host  appears  to  be  the  dog,  especially  sheep-dogs. 

Habitat.— Europe,  especially  Central  France. 

Morphology. — The  male  is  white  in  colour,  18  to  20  millimetres 
in  length,  and  3  millimetres  broad.  The  female  is  greyish-white 
or  brownish,  owing  to  the  contained  ova. 

Life-History. — -The  eggs,  which  are  ovoid,  90  by  70  fju,  are  laid  in 
the  nasal  cavities  of  the  dog,  and  expelled  by  sneezing.  If  they 
fall  on  grass,  they  may  enter  the  alimentary  canal  of  a  herbivorous 
animal,  in  whose  intestine  the  embryo  hatches.  This  embryo 
measures  130  by  60  /j,,  and  possesses  two  pairs  of  legs  and  an  anterior 
perforating  apparatus  composed  of  a  stylet  and  two  hooks. 

It  now  bores  its  way  into  the  liver,  lungs,  or  some  other  organ, 
and  in  about  eight  weeks  becomes  encysted,  losing  all  its  appendages 
and  measuring  275  by  180  (x. 


734  ARTHROPOD  A 

A  succession  of  ecdyses  results  in  the  formation  of  the  nymph, 
which  resembles  the  adult,  except  that  it  possesses  numerous 
chitinous  spicules  on  its  skin,  and  by  the  sixth  to  the  seventh  month 
is  about  6  to  8  millimetres  in  length. 

These  nymphae  now  wander  about  the  host,  and  are  supposed  to 
reach  the  bronchi,  and  thus  to  leave  the  herbivorous  host  and 
reach  the  dog  either  by  the  nose  or  mouth,  in  the  nasal  cavities  of 
which  they  moult  and  become  sexually  mature,  copulating  about 
the  sixth  to  seventh  week  after  infection. 

Pathogenicity.— Both  the  larva  and  the  adult  may  be  found  in 
man,  the  former  in  the  lung,  rarely  in  the  liver,  spleen,  or  intestinal 
wall.  The  latter  has  but  rarely  been  met  with,  and  then  appears  to 
be  due  to  embryos  wandering  into  the  nose  and  developing  directly. 
Hitherto  it  has  only  been  found  in  man  in  Europe  and^Central 
America. 

Porocephalus  Humboldt,  1811. 

Linguatulida  with  cylindrical  body  and  continuous  coelom. 

Type  Species.— Porocephalus  armillatus  Wyman,  1847. 

Species. — There  are  about  twenty  known  species,  of  which  P. 

rmillatus  and  P.  moniliformis  are  known  to  occur  in  man,  and  will 

be  described  below,  but  Sambon  suspects  thatP.  crotali,P.  clavatus, 

P.  stilesi,  and  P.  najcB  will  probably  also  be  found  in  man  as  scientific 

work  in  parasitology  extends. 

Pathogenicity.— They  cause  porocephalosis  in  man  and  animals. 

Porocephalus  armillatus  Wyman,  1847. 

Synonyms— Adult.— Linguatulida  armillata  Wyman,  1847  >  Penta- 
stomum  polyzonum  Harley.  1856;  Porocephalus  moniliformis  Neu- 
mann, 1899,  pro  parte.  Nymph. — Pentastonum  diesingi  Beneden, 
1849;  P.  euryzonum  Diesing,  1850;  P.  leonis  Weddell,  1863;  P.  con- 
strictum  von  Siebold,  1852;  P.  protelis  Hoyle,  1883;  Linguatulida 
constricta  Kuchenmeister,  1855. 

Porocephalus  with  cylindrical  body,  slightly  flattened  on  its 
anterior  face,  and  surrounded  by  about  sixteen  to  twenty-two  dis- 
tinct rings,  separated  from  one  another  by  a  wide  interval.  The 
body  tapers  from  the  middle  backwards. 

Remarks. — The  larva  of  this  parasite  was  discovered  by  Pruner  in 
the  liver  of  two  negroes  in  Cairo  in  1847,  and  subsequently  by  Bilharz, 
Fenger,  Kearney,  Crawford,  Marchoux,  Chalmers,  and  others;  while 
the  adult  was  discovered  by  Wyman  in  1848  in  the  lungs  of  the 
African  python.  The  adult  was  discovered  by  Savage  in  Python 
sebce  and  described  by  Wyman  in  1845.  Sambon  has  recently 
studied  both  adult  and  larva. 

The  adult  lives  in  African  pythons  and  snakes  (Python  sebce, 
P.  regius,  Bitis  nasicornis,  and  B.  arietans).  The  larval  forms 
usually  occur  in  Proteles  cristatus,  Cynocephalus  maimon,  and  other 
monkeys;  in  Erinaceus  czthiopicus,  the  African  hedgehog;  and  in 
Felis  leo,  the  Hon. 


POROCEPHALUS 


735 


Morphology.— Female  9  to  12  centimetres  in  length  and  5  to  9 
millimetres  in  breadth,  with  eighteen  to  twenty-two  rings,  each  1  to 
2  millimetres  in  width.  The 
cephalothorax  extends  from  the 
anterior  end  of  the  body  to  the 
first  body-ring,  which  is  often  very 
indistinct.  Dorsally  this  region 
is  convex,  while  ventrally  it  is 
concave,  and  carries  the  mouth, 
in  front  of  which  there  are  two 


Fig.  353. — Porocephahts  armillatus        Fig.    354. — Porocephalus  armillatus 

Wyman:  Male,   Natural  Size,  Wyman:  Female,  Natural  Size. 

(After    Sambon.) 

papillae,  and  on  either  side  of  which  there  are  two  hooks.  Genital 
opening  about  I  millimetre  in  front  of  the  anus,  which  is  terminal. 
Male  3  to  4-5  centimetres  in  length 
and  3  to  4  millimetres  in  breadth, 
with  sixteen  to  seventeen  rings. 
Genital   opening   in    the   middle 


Fig.     355.  —  Lateral    Aspect     of         Fig.     356. — 'Ventral     Aspect     of 
the    Cephalothorax    of    Poro-  the    Cephalothorax     of    Poro- 

cephalusarmillalusWYMAW.    (X5-)  cephalns  armillatus  Wyman.  (X5-) 

(After  Sambon.) 

of  the  ventral  surface  at  the  anterior  end  of  the  abdomen. 

Life-History.— Probably  this  resembles  that  of  Lingiiatula  serrata, 
with  the  difference  of  hosts.     In  man  the  nymph  oe  are  found  not 


736  ARTHROPODA 

merely  encysted  in  the  lungs  and  liver,  but  moving  freely  through  the 
peritoneal  cavity  and  in  the  small  intestine.  Sambon  considers  that 
the  eggs  pass  from  the  snake  into  water,  and  thence  into    animals 


V> 


^,:-U«F 


Fig.     357.  —  Posterior     End  Fig.  358.— Nymph  of  Porocephalus 

of     Porocephalus     armillatus  armillatus    Wyman,    encysted 

Wyman.     (X  5.)  in  the  Liver. 

(After  Sambon.)  (After  Sambon,  from  our  West 

African  case.) 

and  man  while  drinking,  and  become  larvae  and  nymphae,  which 
later  gain  access  to  the  snake  when  the  host  is  killed  and  eaten. 
Pathogenicity.— This  will  be  described  later  (Chapter  LXXXIII.). 

Porocephalus  moniliformis  Diesing,  1836. 

Synonyms — -Adult. — Pentast&ma  moniliforme  Diesing,  1835;  P. 
moniliforme  Leuckart,  i860;  Linguatule  moniliforme  Megnin,  1880; 
Porocephalus  moniliformis  Stiles,  1893.  Nymphs — Pentaslomum 
tornatum  Creplin,  1849,  pro  parte;  P.  aonycis  Macalister,  1874; 
Porocephalus  armillatus  Stiles,  pro  parte. 

Porocephalus  with  twenty-six  to  thirty-one  rings. 

Remarks. — This  parasite,  which  was  discovered  by  Czermak  in 
the  lung  of  Python  molurus  Linnaeus  in  1828,  and  was  first  described 
by  Diesing  in  1835,  has  been  carefully  studied  by  Sambon,  who 
remarks  that  it  so  strikingly  resembles  P.  armillatus  in  general  ap- 
pearance and  structure  that  at  first  sight  it  may  be  easily  mistaken 
for  it. 

Morphology. — -It  is  more  slender,  tapers  more  caudad;  with 
twenty-six  rings  in  the  male  and  twenty-eight  to  thirty-one  rings 
in  the  female.  In  fresh  specimens  it  is  bright  lemon  yellow  in  colour, 
with  genital  opening  on  the  mid-ventral  surface  of  the  first  body- 
ring  in  the  male,  and  on  the  mid-ventral  surface  of  the  terminal 
body-cone  I  millimetre  in  front  of  the  anus  in  the  female.  The  anus 
is  terminal. 

Life-History.— The  life-history  is  unknown. 

Hosts. — The  hosts  of  the  adult  are  Python  molurus  Linnaeus  (the 
Indian  python), Python  reticulatus  Schneider  (the  reticulated  python), 
in  which  it  lives  in  the  lungs;  while  the  hosts  of  the  nymph  are  man, 
monkeys,  tigers,  leopards  (?),  civets,  otters,  and  dogs  (?). 

Distribution. — India,  Indo-China,  Southern  China,  the  Philippines. 
Sumatra,  Java. 


POROCEPHALUS 


737 


Pathogenicity. — So  far  only  two  cases  have  been  recorded  in  man 
—one  at  Djambi  in  Sumatra  in  1906,  when  a  nymph  was  found  en- 
cysted beneath  the  serous  coat 
of  the  small  intestine  of  a 
Djambi  native  who  died  of 
dysentery,  and  the  other  was 
found  in  the  liver  of  a  native 
Filippino  who  died  of  tubercu- 
losis. The  liver  in  this  latter 
case  showed  signs  of  atrophic 
cirrhosis. 


Fig.    359. — Ventral   Aspect   of 

THE    CEPHALOTHORAX     OF   Poi'O- 

cephalus   moniliformis  Diesing, 
1836.     (X  5-) 

(After  Sambon.) 


Fig.  360. — Porocephalus  monili- 
formis Diesing,  1836:  Female, 
Natural  Size. 


Species  imperfectly  described  in  Man. 

In  addition  to  the  well-known  cases  of  porocephalosis  due  to 
Porocephalus  armillatus  and  P.  moniliformis,  thert  are  the  following 
cases  to  be  discussed — viz.,  Welch's  parasite,  Osier's  parasite,  and 
Flint's  parasite.  Osier's  parasite  is  considered  to  be  doubtful,  as 
it  was  passed  per  urethram,  and  might,  according  to  Sambon,  have 
been  a  sparganum. 

Welch's  Parasite. 

In  the  Lancet  of  November  16,  1872,  F.  H.  Welch  had  an  article 
on  '  The  Presence  of  an  Encysted  Echinorhynchus  in  Man.'  This 
parasite  was  damaged  in  extraction,  and  his  drawing  was  not  very 
instructive,  but  was  sufficient  to  convince  Cobbold,  R.  Blanchard, 
and  Sambon  that  it  represented  a  Linguatulid,  and  it  shows  two 
sets  of  hooks.  The  last-named  observer  comes  to  the  conclusion 
that  it  may  be  either  a  very  early  nymph  of  Porocephalus  monilifoi  mis 
(provided  with  caducous  accessory  hooks),  or  it  may  be  P.  najcc 
Leuckart,  i860  (which  is  found  in  the  abdominal  muscles  and  peri- 
toneum of  the  cobra),  or  P.  crocidurce  Parona,  1890  (found  in 
Crocidura  fuliginosa,  a  musk-shrew) ,  or  it  may  be  a  new  spec  ies. 

47 


73S  ARTHROPOD  A 

Porocephalus  najse  Leuckart,  i860. 

Synonym. — P.  najcs  sputatricis  Leuckart,  i860. 

Morphology. — Body  imperfectly  cylindrical,  with  about  fifty 
rings.     Length,  4-5  millimetres  long  by  o-6  millimetre  broad. 

Distribution.— Found  in  cysts  in  the  abdominal  muscles  and  peri- 
toneum of  the  cobra. 

Flint's  Parasite. 

Flint  described  the  parasite  at  a  meeting  of  the  New  York  Patho- 
logical Society  on  December  12,  1876,  as  occurring  in  a  man  from 
Albany,  Gentry  County,  Montana.  This  man  had  cavities  in  his 
lungs,  and  coughed  up  75  to  100  parasites,  which  could  crawl  about 
the  floor  and  could  live  for  ten  days  in  a  bottle ;  moreover,  they  could 
resist  freezing. 

With  regard  to  these  parasites,  which  at  the  time  were  considered 
to  bePorocephalus  armillatus  (i.e. ,  Pentastomum  constrictum) ,  Sambon 
points  out  that,  if  genuine  Linguatulida,  they  can  hardly  belong  to 
an  African  species,  as  the  case  occurred  in  America,  and  therefore  he 
is  inclined  to  believe  that  they  must  belong  to  P.  crotali  Humboldt, 
1808,  which  are  found  as  adults  in  Crotalus  adar.'.anteus  Beauvois, 
C.  liorridus  Linnaeus,  and  C.  terrificus  Laurent,  while  the  nymphae 
have  been  found  in  Marmosa  murina  Linnaeus,  the  murine  opossum. 

Porocephalus  crotali  Humboldt,  1808. 

Synonyms. — Echinorhynchus  crotali  Humboldt,  1808;  Distoma 
crotali  Humboldt,  1808;  Distoma  crotali  durissi  Rudolphi,  1809; 
Porocephalus  crotali  Humboldt,  1811 ;  Polystoma  proboscideum  Ru- 
dolphi, 1814;  Pentastoma  proboscideum  Rudolphi,  1819;  Linguatula 
proboscidea  van  Beneden,  1849,  pro  parte;  Porocephalus  humboldti 
Mayer,  1852;  Linguatula  quadriuncinata  Mayer,  1852;  Porocephalus 
moniliformis  Megnin,  1880,  pro  parte.  Nymph. — Pentastoma  sub- 
cylindricum  Diesing,  1836. 

Remarks. — This  porocephalus  was  discovered  by  Humboldt  in 
the  lungs  of  the  tropical  rattlesnake. 

Morphology. — When  fresh,  it  is  of  a  bright  yellowish  colour,  with 
elongate,  incurved,  cylindrical  body,  somewhat  flattened  ventrally 
and  club-shaped  anteriorly,  and  is  transversely  encircled  by  over 
eighty  flat  bands.  It  is  said  to  have  an  ovoid-shaped  mouth  on  a 
line  with  the  hooks,  and  two  prominent  papillae. 

Distribution.— It  is  thought  to  be  coextensive  in  its  distribution 
with  the  genus  Crotalus — i.e.,  the  United  States,  Mexico,  and 
Brazil. 

Pathogenicity. — Possibly  it  is  the  cause  of  one  form  of  poro- 
cephalosis in  man. 


COPEPODA  739 


CLASS  IV.    CRUSTACEA  Lamarck,  1815. 

Aquatic  Arthropoda  which  breathe  by  means  of  gills. 

Crustaceans  can  hardly  be  considered  as  human  parasites,  for  they  have 
very  rarely  occurred  as  such — e.g.,  Caligits  curtus  in  the  cornea,  and  Gammarus 
pulex  in  the  stomach. 

ORDER  COPEPODA  Latreille,  1831. 

It  must,  however,  be  remembered  that  the  Copepoda  are  of  importance, 
because  a  species  of  Cyclops  has  been  found  to  be  the  intermediary  host  of 
Dracunculus  medinensis.  the  guinea-worm.  An  excellent  paper  on  the  species 
found  on  the  Gold  Coast  is  contributed  by  Graham  to  vol.  i.  of  the  '  Annals  of 
Tropical  Medicine  and  Parasitology.'  The  Cyclops  live  in  fresh  water  in  any 
ditch,  pond,  or  well. 

Prophylaxis. — It  is  recommended  to  treat  a  well  with  sufficient  quick- 
lime to  render  the  water  suddenly  hot  in  order  to  kill  these  crustaceans.  The 
well  must,  of  course,  be  closed  for  some  time  after  this  proceeding,  until  the 
percentage  of  lime  has  diminished  to  reasonable  proportions.  A  simpler 
remedy  is  to  boil  all  water  before  drinking.  It  has  been  also  suggested  to  add 
1  pound  of  caustic  soda  to  180  gallons  of  water  =  0-07  per  cent,  for  the  same 
purpose.     Leiper's  recommendation  is,  however,  the  best,  and  this  is  to  raise 


Fig.  361. 


of  the  well-water  lo  650  C.  by  blowing  in  steam,  as  he  finds 
clops  die  if  the  water  is  raised  to  350  C.  He  calculates  that  it 
requires  87  gallons  of  water  as  steam  to  raise  1,000  gallons  of  water  from  15° 
to  650  C,  and  that  this  requires  1  pound  of  coal  or  its  equivalent  in  oil  per 
gallon  of  water,  and  that  for  every  square  foot  of  grate  15  pounds  of  coal  can 
be  burnt  per  hour,  so  that  if  the  grate  is  1  square  foot  it  will  require  \ :,  6 
hours  to  raise  87  gallons  of  water  as  steam — -i.e.,  12  square  feet  of  grate  give 
90  gallons  of  water  as  steam  in  half  an  hour. 

CLASS  V.  CHILOPODA  Latreille,  1837. 

Arthropoda  with  three  prosLhomeres.  The  first  post-oral  somite  is  the 
mandibular;  the  second  and  third  post-oral  somites  carry  the  maxillae,  while 
the  fourth  has  its  appendages  converted  into  very  large  powerful  jaws,  which 
are.  provided  with  poison  glands.     The  remaining  somites  carry  single-clawed 


74° 


ARTHROPODA 


walking-legs,  one  pair  to  each  somite.  Body  anomomeristic,  showing  from 
17  to  175  somites  behind  that  which  carries  the  poison  glands.  They  breathe 
by  tracheae,  and  the  genital  ducts  open  on  the  penultimate  somites. 

Family  1 :   Scolopendridae. 
Family  2 :  Lithobiidae. 
Family  3 :  Scutigeridae. 

Family  i:    Scolopendrid^  Leach,  1812. 

Chilopoda  with  antennae,  possessing  few  joints,  and  with  few  ocelli. 

Geophilus  carpophagns  Leach,  G.  electricus  Linnaeus,  G.  cephalicus  'Wood, 
G.  sunilis  Leach,  have  been  found  as  accidental  parasites  about  nineteen  times 
in  the  nasal  cavities  and  their  neighbouring  sinuses  in  man  in  Europe.  G.  elec- 
tricus Linnaeus  has  been  found  in  the  alimentary  canal  about  four  times. 

Family  2 :    Lithobiidae  Newport,  1844. 

Chilopoda  with  many-jointed  antennae;  numerous  ocelli. 
Lithobius  fortificatus  L.  and  L.  melanops  have    been  found  in   the  nasal 
cavities  in  three  cases  in  man. 

Family  3:    Scutigeridae  Gervais,  1837. 

Chilopoda  with  antennae  at  least  as  long  as  the  body,  and  faceted  eyes 
instead  of  ocelli. 

Scutigera  coleoptrata  has  been  found  in  the  alimentary  canal. 

Other  species  found  in  the  alimentary  canal  are:  Chcetechelyne  vesuviana 
Newport  (found  also  in  the  nasal  cavities),  Himantavium  gervaisi,  Stigmatogaster 
subterraneus. 

Pathogenicity. — In  the  nose  these  parasites  cause  inflammation  with,  at 
times,  no  flow  of  mucus,  and  at  others  a  large  discharge  of  it,  associated  with 
headache,  which  is  generally  more  or  less  continuous,  but  may  show  remis- 
sions. In  addition  to  these  local  symptoms,  general  symptoms  such  as  con- 
vulsions, anginiform  attacks,  dyspnoea,  etc.,  may  be  induced  through  irritation 
of  the  fifth  nerve.     There  is  no  evidence  that  these  parasites  cause  any  of  the 


Fig.  362. — Scolopendra  Species  (?) 
(This  is  a  very  common  species  in  Ceylon.) 

symptoms  by  their  venom.  They  are  generally  expelled  in  attacks  of  sneezing, 
or  spontaneously.  The  best  methods  of  making  them  leave  the  nostrils  are 
applications  of  snuff,  eau-de-Cologne,  or  turpentine;  but  in  some  instances 
it  will  be  necessary  to  open  a  sinus — e.g.,  the  frontal  sinus — by  surgical  means 
in  order  to  remove  the  parasite. 

In  the  alimentary  canal  the  symptoms  will  give  rise  to  the  suspicion  of 
helminthiasis.  They  are — pain  in  the  abdomen,  cramp,  nausea,  vomiting, 
and  reflex  nervous  symptoms. 

Treatment  does  not  appear  very  satisfactory. 


REFERENCES  741 


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Blanchard,  R.  (1902).     Archiv.  de  Parasit.,  1898,  i.  452;  vi.  245. 
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A  carina. 

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Blanchard,  R.  (1909).     LTnsecte  et  LTnfection.     Paris. 

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Akamushi. 

Miyajima  and  Okumura  (1917).  Kitasato's  Archives  of  Experimenta 
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Tyroglyphidse. 

Hirst  (1915).     Journal  of  Economic  Biology,  x.,  4.    (The  Harvest  Bug  and 

the  Akamushi.) 
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742  ARTHROPODA 

Sareoptidae. 

Castellani  (1906).     Centralblatt  fiir  Bakteriologie. 

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Leuckart     (i860).     Bau     und     Entwicklungsgeschi elite   der   Pentastomen. 

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Sambon  (1910-1912).     Journal  of  Tropical  Medicine  and  Hygiene.     London. 

(A  very  excellent  account  of  the  parasites  found  in  man  and  animals.) 
Shipley  (1898).     Archives  de  Parasitologie,  i.  52. 

Chiiopoda. 

Blanchard  (1898).     Archives  de  Parasitologie.     (1910).  Archives  de  Para- 
sitologie. 
Laveran  and  Roubaud   (1916).     Bull.  Pathol.  Exot.,  vol.  ix.,  p.  64 
Verdun  and  Bruyant  (1912).     C.  R.  Soc.  Biol.,  p.  236. 


CHAPTER  XXIX 
THE   HEXAPODA 

Synonym — -Remarks — Morphology — Internal  anatomy — Life-history — Habits 
— Enemies — Pathogenicity— Collection — Classification — References. 

Synonym — Insecta. — Arthropoda  breathing  by  means  of  tracheae, 
with  antennas  on  the  head,  three  pairs  of  legs,  and  usually  two  pairs 
of  wings  on  the  thorax,  which  is  composed  of  three  segments. 
Abdomen  with  generally  nine  apparent  segments. 

Remarks, — The  Hexapoda,  or  insects,  are  known  to  be  of  the 
utmost  importance  in  the  spread  of  disease,  for  the  researches  of 
Manson,  Ross,  Grassi,  and  others  have  shown  that  they  are  agents 
in  the  propagation  of  the  parasites  of  filariasis,  mabria,  and'other 
diseases. 


Fig.   363. — Culicoides  brucei,  a  Typical  Dipterous  Insect. 
(From  a  photograph  by  J.  J.  Bell.) 

Morphology. — The  body  is  distinctly  divided  into  head,  thorax,  and  abdo- 
men. The  head  is  composed  of  the  fusion  of  about  six  segments,  which  are 
the  ocular,  antennal,  intercalary  (probably  homologous  with  the  second 
antennal  segment  of  the  Crustacea),  mandibular,  maxillary,  and  labial;  but 
whether  the  hypopharynx  represents  a  seventh  segment  or  not  is  doubtful. 
The  head  carries,  in  addition  to  the  ■eyes,  four  pairs  o^  appendages,  one  for 
each  somite  or  segment,  except  the  intercalary  segment,  which  is  pre-man- 
dibular.  These  appendages  are  the  antennae,  the  mandibles,  the  maxillae, 
to  which  are  attached  palpi  called  the  maxillary  palps,  and  a  second  pair  of 
maxilla?  usually  fused  to  form  the  lower  lip  or  labium,  which  generally  carries 
a  pair  of  labial  palps. 

743 


744  THE  HEX  A  POD  A 

The  exoskeleton  of  the  head  is  composed  of  sclerites — that  is  to  say,  more 
densely  chitinized  regions  of  the  integument — which  are:  (i)  The  clypeus; 
(2)  the  epicranium;  (3)  the  gula. 

The  clypeus  is  the  sclerite  situate  on  the  anterior  portion  of  the  dorsal  sur- 
face, and  carrying  the  labrum;  in  flies  it  is  often  called  the  face. 

The  epicranium  is  the  larger  part  of  the  head,  and  may  be  subdivided 
into  an  anterior  frons  and  a  posterior  occiput.  The  genaa  form  the  sides  of 
the  head,  meeting  the  epicranium  and  the  gula  at  the  occipital  foramen. 

The  gula  is  the  sclerite  in  the  median  ventral  line  which  carries  the  basal 
part  of  the  labium  called  the  submentum.  There  is  no  exoskeleton  at  the 
posterior  part  of  the  head  ventral  to  the  occipital  region,  which  thus  forms  a 
foramen  in  the  hard  tissues  called  the  occipital  foramen,  through  which  the 
soft  structures  of  the  head  communicate  with  those  of  the  thorax. 

The  antennae  appear  to  be  sensory  organs,  and  the  mandibles  to  vary  in 
structure  according  as  to  whether  the  mouth  is  to  be  used  for  biting  or  sucking. 
In  the  former  case  they  are  broad  and  strong,  while  in  the  latter  they  are 
styliform.  The  first  pair  of  maxillae,  similarly,  may  be  broad,  strong  organs  or 
stvliform  organs. 


Fig.  364. — Wing  of  a  Mosquito  to  illustrate  the  Venation. 
(From  a  photograph  by  j.  J.  Bell.) 

In  addition  to  these  appendages,  the  mouth  shows  an  upper  lip  or  labrum, 
which  is  simply  a  sclerite  attached  to  the  cephalic  shield,  and  may  have  a 
median  projection  from  its  internal  surface  called  the  epipharynx,  while  the 
labium  has  a  similar  one  called  the  hypopharynx.  Thus  the  mouth  parts  of 
an  insect  may  be  very  complicated,  with  labrum  and  epipharynx,  mandibles, 
maxillae,  and  maxillary  palps,  labium,  and  hypopharynx. 

The  thorax  is  joined  to  the  head  by  a  neck,  and  is  subdivided  into  three 
segments — prothorax,  mesothorax,  and  metathorax.  These  somites  are  by 
no  means  simple  horny  rings,  but  have  their  chitinous  exoskeleton  split  up 
into  hard  pieces  joined  together  by  soft  material.  The  hard  pieces  are  a  dorsal 
plate  called  '  the  notum,'  a  ventral  plate  called  '  the  sternum,'  and  lateral 
plates  called  '  pleura.'  Further,  the  terms,  '  pro,'  '  meso,'  and  '  meta,'  are 
applied  to  these,  indicating  the  region  to  which  they  belong — '  pronotum,' 
'  mesonotum,'  and  '  metanotum  ' ;  'pro-,'  'meso-,'  and  '  metasternum  ' — 
while  each  pleuron  is  divided  into  an  anterior  episternum  and  a  posterior 
epimeron.  According  to  Audouin,  a  typical  thoracic  segment  should  have 
a  notum  composed  of  praescutum,  scutum,  scutellum,  and  post-scutellum, 
but  all  these  parts  are  seldom  seen. 

Each  somite  of  the  thorax  carries  a  pair  of  jointed  walking-legs,  in  which 
the  segments  or  articles  are  named  coxa,  trochanter,  femur,  tibia,  and  tarsus 
(consisting  of  several  joints,  the  first  joint  of  which  is  sometimes  called  the 


MORPHOLOGY  745 

metatarsus) ;  some  authorities  have  caused  much  confusion  by  calling  the 
first  tarsal  joint  the  metatarsus,  and  the  real  second  tarsal  joint  the  first 
tarsal  joint,  and  so  on.  The  last  tarsal  joint  is  terminated  by  claws  or  ungues, 
between  which  other  appendages  called  empodia  and  pulvilli  are  to  be  found, 
as  will  be  explained  later. 

Typically,  the  mesothorax  and  the  metathorax  should  each  carry  a  pair  of 
wings.  These  are  transparent  and  strengthened  by  nervures,  ribs,  or  veins, 
which  are  chitinous  canals  containing  blood-spaces,  nerves,  and  trachea;. 
The  areas  between  the  nervures  are  called  cells.  The  wings,  however,  become 
much  modified  in  the  different  orders,  and  may  be  entirely  absent.  The 
arrangement  of  the  nervures  in  the  wing  is  called  the  '  venation,'  and  has 
been  restudied  by  Comstock  and  Needham,  who  find  that  the  primitive  type 
is  composed  of  two  main  tracheal  branches,  an  anterior  and  a  posterior. 
The  anterior  breaks  up  at  the  base  of  the  wing  into  four  longitudinal  branches 
— the  costa,  subcosta,  radius,  and  media — while  the  posterior  has  also  four 
branches,  of  which  the  first  is  called  the  cubitus,  and  may  be  subdivided  into 
two ;  and  the  other  three  are  simple,  and  are  called  the  anal  veins — first,  second, 
and  third.  The  costal  vein  is  unbranched,  and  runs  along  the  anterior  margin 
of  the  wing.  The  subcostal  vein  typically  divides  into  two  branches,  the 
radial  vein  into  five  branches,  and  the  median  into  four. 

This  primitive  type  is  altered  by  atrophy  or  coalescence,  leading  to  the 
reduction  of  the  veins.  The  latter  may  take  place  from  the  base  towards  the 
tip,  or  from  the  tip  towards  the  base  of  the  wing,  called  outward  and  inward 
coalescence  respectively.     The  wing  cells  may  be  named  as  follows : — 

i.  Costal  Cell,  between  the  Costa  and  the  Subcosta. 

2.  Mediastinal,  between  the  Subcosta  and  the  Radius. 

3.  Marginal,  between  Radius  1  and  Radius  2. 

4.  First  Submarginal,  between  Radius  2  and  Radius  3. 

5.  Second  Submarginal,  between  Radius  3  and  Radius  4. 

6.  Third  Submarginal,  between  Radius  4  and  Radius  5. 

7.  First  Posterior,  between  Radius  5  and  Media  1. 

8.  Second  Posterior,  between  Media  1  and  Media  2. 

9.  Third  Posterior,  between  Media  2  and  Media  3. 

10.  Fourth  Posterior,  between  Media  3  and  Media  4. 

11.  Fifth  Posterior,  between  Media  4  and  Media  5. 

12.  Sixth  Posterior,  between  Media  5  and  Cubitus  1. 

13.  Seventh  Posterior,  between  Cubitus  1  and  Cubitus  2. 

14.  First  Anal,  between  Cubitus  2  and  Anal  1. 

15.  Second  Anal,  between  Anal  1  and  Anal  2. 

16.  Axillary,  between  Anal  2  and  Anal  3. 

17.  Spurious  Cell,  behind  Anal  3. 

But  all  these  cells  are  not  present  in  any  one  given  type  of  wing,  owing  to 
coalescence  of  the  nervures,  and  hence  the  arrangement  of  the  cells  is  different. 
Besides  this,  the  venation  is  complicated  by  the  presence  of  transverse  veins, 
as  will  be  explained  later;  moreover,  wings  may  be  absent,  as  in  the  lice. 

The  abdomen  usually  consists  of  ten  somites,  without  appendages,  com- 
posed of  dorsal  and  ventral  plates  connected  together  and  to  preceding  and 
succeeding  segments  by  soft  membranes.  The  posterior  segments  are  often 
modified  with  reference  to  reproduction,  possessing  claspers  in  the  male,  and 
ovipositors  in  the  female.  The  anal  opening  is  on  the  last  abdominal  segment , 
and  the  reproductive  aperture  on  the  penultimate  segment. 

Internal  Anatomy.  —The  mouth  lies  between  the  labrum  above  and  the 
labium  below,  and  leads  into  an  oral  cavity. 

The  salivary  glands  in  most  of  the  genera  which  we  have  to  consider  are  well 
developed,  and  are,  as  a  rule,  not  connected  with  the  mouth,  but  open  into 
a  common  duct  which  communicates  with  a  groove  or  canal  on  the  hypo- 
pharynx,  and  so  opens  near  the  tip  of  the  proboscis. 

From  the  mouth  a  pharynx  leads  through  an  oesophagus,  with  a  dilatation 
called  the  crop,  into  a  proventriculus  or  masticatory  stomach,  which  latter 
communicates  with  the  mesenteron  or  chylific  ventricle,  whose  juncture  with 


746  THE  HEX  APOD  A 

the  intestine  is  denned  by  the  openings  of  the  csecal  Malpighian  tubules. 
This  is  an  important  landmark,  defining  where  the  stomach  ends  and  the 
intestine  begins.  The  intestine  is  subdivided  into  small  intestine,  colon  or 
large  intestine,  and  rectum.  The  last-mentioned  may  possess  rectal  glands, 
while  anal  glands  may  open  into  the  rectum  just  in  front  of  the  anus,  and  are 
useful  to  the  insect  by  forming  the  secretion  which  gives  rise  to  repulsive  odours. 
With  regard  to  the  proventriculus,  it  should  really  be  a  powerful  muscular 
organ  lined  with  chitin,  and  possessing  teeth,  bristles,  etc.,  but  in  the  Diptera 
it  will  be  found  to  be  much  degenerated.  The  Malpighian  tubules,  which 
number  from  four  to  six,  are  excretory  in  function.  The  alimentary  canal 
possesses  longitudinal  and  transverse  muscular  coats  and  a  llining'of  epithelial 
cells. 


Fig.  365. — Phlhirius  pubis  Linnaeus,   1758,  to  illustrate  an  Insect 

without  Wings. 

(From  a  photograph  by  J.  J.  Bell.) 

The  stigmata  or  openings  of  the  respiratory  system  are  situate  on  the 
membranes,  on  the  side  of  the  body,  in  the  thorax  and  abdomen,  and  are  very 
varied  in  number.  They  are  never  to  be  found  on  the  head  or  on  the  last 
abdominal  segment.  From  the  stigmata  the  tracheae,  or  air-tubes,  ramify  all 
over  the  body.  These  trachea;  are  kept  open  by  spiral  thickenings  of  the 
chitinous  lining  membrane. 

The  fat-bodies  are  lobulated  masses  packed  beneath  the  skin  and  between 
the  organs,  and  are  supposed  not  merely  to  represent  reserve  material,  but  to 
be  of  great  importance  in  metabolism. 

The  circulatory  system  consists  of  a  dorsal  longitudinal  vessel  divided  into 
chambers,  which  pulsate,  and  an  anterior  aorta,  from  which  blood  flows  freely 
into  the  ccelom  or  body  cavity.  From  this  it  returns  to  -the  heart  by  two 
lateral  vessels  and  one  dorsal  and  one  ventral  vessel.  The  blood  is  colourless, 
and  contains  amoeboid  cells. 

As  already  mentioned,  some  insects  possess  poison  glands. 

The  nervous  system  and  sense  organs  will  not  be  described  here,  as  they  are 
not  of  importance  in  tropical  medicine. 

The  male  reproductive  organs  consist  of  testes,  vasa  deferentia,  ductus 
ejaculatorius,  and  an  external  copulatory  organ.  The  female  reproductive 
organs  are  two  ovaries,  which  consist  of  a  series  of  egg-tubes,  and  oviducts, 
which  are  united  together  to  form  the  single  oviduct,  the  lower  portion  of 


INTERNAL  ANATOMY  747 

which  is  a  vagina.  This  receives  the  cement  glands  and  the  sebaceous  glands, 
which  provide  the  secretion  for  gluing  the  eggs  together,  and  the  receptaculum 
seminis,  beneath  winch  is  the  bursa  copulatrix,  which  is  sometimes  separated 
irom  the  vagina. 

Life-History. — -This  is  very  varied.  In  general  terms  the  sperma- 
tozoa, bound  into  bundles  of  spermatophores,  are  introduced  by 
the  external  copulatory  organ,  which,  when  protruded,  is  surrounded 
by  the  claspers  in  the  form  of  a  sheath,  into  the  bursa  copulatrix. 
The  ovum,  starting  from  the  terminal  portion  of  the  ovarian  tube, 
obtains,  as  it  passes  downwards,  its  food-yolk  and  its  shell  or  mem- 
brane, the  chorion,  which  has  a  small  gap,  the  micropyle.  On  arrival 
at  the  junction  of  the  oviduct  and  the  spermatheca,  or  receptaculum 
seminis,  the  spermatozoa  enter  via  the  micropyle,  and  fertilize  the 
egg.  These  eggs  may  be  strung  together,  as  they  are  laid,  into  masses 
by  means  of  the  sebaceous  secretion  mentioned  above.  The  egg  may 
develop  directly  into  the  adult,  but  this  is  only  in  the  lowest  forms. 
Usually  the  egg  develops  into  a  larva,  which  becomes  a  nymph  or 
pupa,  and  this  into  an  adult,  often  called. the  '  imago.'  This  series 
of  changes  is  called  a  metamorphosis.  The  pupa  may  present 
three  forms: 

1.  The  free  pupa,  with  appendages  free. 

2.  The  obtect  pupa,  with  appendages  and  body  bound  together. 

3.  The  coarctate  pupa,  in  which  the  pupa  is  contained  in  a  pupa- 
rium  formed  from  the  larval  skin. 

The  larva  is  a  most  vigorous  feeder,  but  the  pupa  does  not  take 
nourishment  as  a  rule,  though  there  are  marked  exceptions,  espe- 
cially among  the  Rhynchota  and  Siphunculata. 

Habits.— We  are  mainly  concerned  with  the  predatory  or  blood- 
sucking insects.  As  a  rule,  only  the  female  sucks  blood,  which, 
apparently,  it  does  with  a  view  of  obtaining  rich  nourishment  for 
its  eggs.  It  is  this  habit  which  makes  these  insects  of  importance 
in  tropical  medicine,  because  not  merely  does  it  cause  irritation 
by  the  introduction  of  secretions  from  the  insects'  salivary  glands 
and  mouth  (alimentary  canal),  but  also  leads  to  the  introduction 
into  the  victim  of  the  germs  of  disease.  Again,  as  we  shall  see  later, 
larvae  are  apt  to  become  parasitic  in  man  and  animals,  and  in  this 
way  cause  disease. 

Enemies. — Insects  and  their  larvae  have  many  enemies  in  birds, 
reptiles,  fish,  and  other  insects.  Cannibalism  is  also  met  with, 
especially  among  mosquito  larvae. 

Pathogenicity. — The  principal  disease-spreading  insects  are  the 
Diptera — -for  example,  the  Anophelince  disseminate  malaria,  the 
genus  Stegomyia  yellow  fever,  and  the  genus  Culex  filariasis,  and 
perhaps  dengue  fever.  Some  species  of  Glossina  are  responsible  for 
the  African  trypanosomiases,  while  they  and  other  flies  spread  the 
animal  trypanosomiases. 

In  addition,  the  common  house-fly  is  an  important  factor  in  the 
dissemination  of  typhoid  and  perhaps  dysentery  in  tropical 
countries.     Fleas  are  now  known  to  be  the  spreaders  of  plague, 


748  THE  HEX  A  POD  A 

and  bugs  perhaps  of  some  of  the  relapsing  fevers.  This  is  a  suffi- 
cient list  of  ills  to  commend  insects  and  their  habits  to  the  serious 
notice  of  the  medical  practitioner  of  the  tropics. 

How  to  Colleet  Blood-Susking  Flies. — Mr.  Austen,  of  the  British.  Museum. 
(Natural  History),  has  informed  us  that  he  will  be  pleased  to  send  anyone, 
on  application,  a  pamphlet  giving  full  directions  as  to  the  collection  and 
preservation  of  blood-sucking  flies. 

Classification. — The  Hexapoda  are  classified  into  the  following 
orders: — 

i.  Apt  era. 


Neuroptera. 

3.  Orthoptera. 

4.  Mallophaga. 

5.  Thysanoptera. 

6.  Hemiptera. 


7.  Anoplura. 

8.  Diptera. 

9.  Lepidoptera. 

10.  Hymenoptera. 

11.  Siphonaptera. 

12.  Coleoptera. 


But  the  only  orders  which  contain  species  important  as  spreaders 
of  disease  or  as  human  parasites  are: — 


1.  Anoplura. 

2.  Mallophaga. 

3.  Hemiptera. 


4.  Diptera. 

5.  Siphonaptera. 

6.  Coleoptera. 


REFERENCES. 

RECENT  LITERATURE. 

Summaries  of  recent  literature  are  given  in:  Journal  of  Royal  Microscopical 
Society,  Zoologisches  Centralblatt  und  Jahresbericht,  and  the  Entomological 
News  of  Philadelphia. 

A  most  useful  series  is  the  Bulletins  of  the  United  States  Department  of 
Agriculture,  Bureau  of  Entomology,  Washington;  and  the  Bulletin  of  Ento- 
mological Research,  London. 

The  Annals  and  Magazine  of  Natural  History,  Parasitology,  and  the  Journal 
of  Parasitology,  Deutsche  Entomologische  Zeitschrift,  Transactions  of  the  Ento- 
mological Society  of  London,  Entomologische  Zeitung,  Entomologische 
Nachrichten,  Entomologists'  Annual,  Entomologists'  Monthly  Magazine,  Bulletino 
della  Societa  Entomologica  Italiana,  Annates  de  la  Societi  Entomologique  de 
France.  Wystsman's  '  Genera  Insectorum  '  is  perhaps  the  most  useful;  it 
started  in  1902,  and  is  still  being  reproduced.  See  also  the  Tijdschrift  voor 
Entomologie  and  the  Revue  Entomologique. 

Hexapoda. 

Alcock,  A.  (1911).     Entomology  for  Medical  Officers.      London. 

Folsom,  J.  W.  (1906).     Entomology  with  Reference  to  its  Economic  Aspects. 

London. 
Henneguy,  L.  F.  (1904).     Les  Insectes,  Morphologie,  Reproduction,  Embryo- 
genie.     Paris. 
Howard,  L.  O.  (1901).     The  Insect  Book.     New  York. 
Kellogg,  V.  L.  (1905).     American  Insects.     New  York. 
Packard  (1889).     Guide  to  the  Study  of  Insects.     New  York. 
Packard  (1898).     Textbook  of  Entomology.     New  York  and  London. 
Patton  and  Craig.     Entomology. 

Sergent  (1909).     Les  Insectes  Piqueurs  et  Suceurs.     Paris. 
Sharp,  D.  (1895-1901).     Cambridge  Natural  History,  vols.  v.  and  vi.    London. 
Theobald  (1899).     Textbook  of  Agricultural  Zoology.     London. 
Theobald.     Also  in  Fantham,  Stephens,   and  Theobald's  Parasites  of  Man. 
London. 


CHAPTER  XXX 
MALLOPHAGA  AND  ANOPLURA   (LICE) 

General    remarks  —  Mallophaga  —  Anoplura- — Pediculidas —  Pediculina? — 
Haematopinidae — References. 

GENERAL  REMARKS 

The  wingless  insects  which  occur  as  ectoparasites  on  mammals 
belong  as  a  rule  to  the  Mallophaga  and  the  Anoplura,  when  they  are 
generally  called  '  lice,'  or  to  the  Siphonaptera,  when  they  are 
called  fleas,  while  some  few  belong  to  the Pupipara. 

The  Mallophaga  (biting  lice)  and  Anoplura  (sucking  lice),  however, 
differ  from  the  Siphonaptera  (fleas),  in  that  in  the  former  the  whole 
of  the  life-history  is  spent  upon  the  vertebrate  host,  while  in  the 
latter  the  larvae  live  in  soil  or  in  protected  areas  in  houses.  More- 
over, the  fleas  can  change  from  one  host  species  to  another,  while  the 
lice  have  an  extraordinary  limitation,  as  they  may  spend  genera- 
tions on  individual  hosts,  and  generally  only  change  from  one  host 
to  another  of  the  same  species  by  actual  contact,  and  as  a  rule  die 
in  a  few  days  if  separated  from  a  host  or  if  a  host  dies. 

This  limitation  to  one  given  species  of  host  has  been  ably 
demonstrated  by  Kellogg,  who  has  pointed  out  that  it  explains 
many  of  the  curious  features  of  their  evolution. 

Kellogg  and  Mjoberg  believe  that  the  Mallophaga  and  the  Anoplura  are 
fairly  closely  related  to  one  another.  They  think  that  it  is  possible  that  the 
Mallophaga  are  the  more  primitive,  especially  as  no  Anoplura  are  known  on 
marsupials,  while  Mallophaga  are  present,  which  they  think  points  to  the 
possibility  of  these  mammals  being  older  than  the  sucking  lice,  especially  as 
the  known  genera  of  two-clawed  Mallophaga  found  on  mammals  are  limited 
to  marsupials,  while  the  two-clawed  condition  is  common  to  the  Hexapoda 
generally,  while  all  the  Anoplura  found  on  mammals  are  one-clawed. 

It  is  possible  that  the  ancestors  of  the  Mallophaga  may  have  been  related 
to  the  ancestors  of  the  book  louse  [Atropos  divinatoria) ,  which  belongs  to  the 
Psocidae,  a  family  of  the  Neuroptera,  there  being  perhaps  a  common  psocid- 
mallophagan  ancestor,  from  which,  by  process  of  evolution,  the  Psocidae  and 
he  Mallophaga,  and  later  the  Anoplura,  were  evolved.  The  difference  in  the 
nouth  parts  of  the  Mallophaga  and  Anoplura  is  looked  upon  as  being  adoptive 
r.ther  than  palegenetic  in  character. 

'The  relationship  of  the  Psocidae  to  the  Mallophaga  lies  in  the  common 
ex£rnal  and  internal  characters,  as  well  as  in  their  habits,  and  more  especially 
jn  avery  curious  pharyngeal  sclerite,  which  is  thought  to  be  a  modified  hypo- 
pharx'nx'  which  is   found  in   both   these   groups   and   nowhere   else   in  the 

Hexa?odii-  .    a 

Once  slarted   on   their  evolution,   the  Mallophaga   have   been  influenced 
mainly  by  the  fact  that  they  live  in  a  sort  of  '  island  isolation  '  on  given 

749 


75Q  MALLOPHAGA   AND  ANOPLURA    (LICE) 

species.  This  condition  of  life,  which  is  exactly  similar  for  many  different 
species,  is  suitable  for  the  production  of  many  varieties  of  one  and  the  same 
species,  and  hence  the  description  of  a  given  species  has  to  be  of  a  very  flexible 
character,  but  it  is  opposed  to  the  production  of  those  more  distinctive 
differences  which  are  utilized  to  make  genera  and  families. 

Hence,  although  in  these  orders  the  varieties  and  species  may  be  many, 
the  genera  and  families  are  but  few  in  number.  Thus,  for  example,  in  the 
Mallophaga  there  are  about  1,500  known  species  grouped  into  27  genera, 
4  families,  and  2  suborders. 

The  important  difference  between  the  Mallophaga  and  tho 
Anoplura  is  that  the  forma-  have  a  masticatory  mouth,  while  the 
latter  have  a  sucking  mouth. 

ORDER  MALLOPHAGA  Nitzsch,  1818. 

Synonyms. — Mandibulata  De  Geer,  1783;  Ricinida. 

Nomenclature. — The  name  Mallophaga  is  derived  from  /xa\\6s,  wool,  and 

(pay elu,  to  eat. 

Definition. — Hexapoda  usually  of  small  size,  wingless,  provided  with 
biting  mouth  parts  and  with  simple  incomplete  metamorphosis.  Habitat, 
epizoic  parasites  on  birds  and  mammals. 

Historical. — The  first  descriptions  and  illustrations  of  these  animals  are 
to  be  found  in  Redi's  '  Esperienze  intorno  alia  Generazione  degl'  Insetti,' 
published  in  Florence  in  1668,  where  the  illustration  on  Plate  2,  called  '  Pollino 
de  Piccion  Grosso,'  is  the  same  as  Linnaeus'  Pediculus  columbce,  or  pigeon 
louse,  and  Nitzsch's  Lipurus  baculus,  a  name  by  which  it  is  still  known ;  while 
the  figure  termed  '  Pollino  dell'  Arzavola  o  Forquetola  '  on  Plate  12  is  the  same 
as  Nitzsch's  Tnnoton  luridum,  the  duck  louse.  Linnaeus  classified  all  these 
bird  lice  under  the  generic  term  of  '  Pedicums,'  from  which  they  were 
separated  by  De  Geer,  in  1783,  under  the  term  '  Ricinus,'  because  their  masti- 
catory mouth,  enabling  them  to  eat  pieces  of  skin,  hairs,  and  feathers,  distin- 
guished them  from  the  blood-sucking  species,  for  which  the  name  '  Pediculus  ' 
was  retained. 

The  name  '  Ricinus  '  was  changed  into  '  Nirmus  '  by  Hermann  in  1804, 
while  the  whole  of  the  species  known  at  the  time  were  classified  and  named 
by  Nitzsch  in  1818,  since  which  date  our  knowledge  of  these  parasites  has  been 
increased  by  Denny  in  1842,  Giebel  in  1874,  Piaget  in  1880  and  1885,  Taschen- 
berg  in  1882,  Kellogg  in  1908,  191 3,  and  1914,  as  well  as  by  many  other 
observers  whose  papers  may  be  found  in  the  Bvilletin  of  Entomological  Research 
and  in  the  Annals  and  Magazine  of  Natural  History.  To  all  these  works  the 
reader  is  referred  for  a  fuller  knowledge  of  these  interesting  parasites  than  that 
which  can  be  given  in  the  present  work. 

Morphology. — The  Mallophaga  vary  in  size  from  1*5  to  10  mm.,  and  from 
1-2  mm.  in  breadth,  but  the  majority  are  small,  about  2*5  millimetres  in  length. 
The  body  is  strongly  chitinized,  smooth,  wingless,  and  flattenened  dorso- 
ventrally.  The  mouth  parts  are  of  the  biting  type,  with  well-developed 
mandibles,  and  in  some  species  the  labial  palps  are  easily  seen.  The  eyes 
are  represented  by  a  single  pair  of  ocelli  placed  at  the  lateral  margins  of  the 
head.  The  antenna;  are  3-5  segmented,  and  may  be  concealed  in  a  groove, 
or  the  ventral  aspect  of  the  cheeks,  or  may  be  exposed. 

The  prothorax  is  distinct,  but  the  meso-  and  meta-thoraces  are  sometime? 
united,  and  may  also  be  with  difficulty  differentiated  from  the  abdominq 
segments.  The  legs  are  flattened,  long,  and  strong,  and  end  in  one  or  tvvj 
claws. 

The  body  varies  in  colour,  being  whitish,  pale  brownish,  or  dark  brown  in 
colour,  and  marked  by  darker  spots  and  bands,  which  are  caused  by  chitiriza- 
tion. 

The  pharyngeal  sclerite  may  be  present  or  absent,  as  may  be  the  accompany- 
ing glands;  the  crop  may  be  simple  or  have  a  sac-like  diverticulum.     In^iuvial 


ORDER  MALLOPHAGA  751 

glands  may  be  present  or  absent,  and  the  testes  may  number  four  to  six  and 
the  egg  tubes  three  to  five. 

Life-History. — Owing  to  the  fact  that  these  parasites  die  in  a  few  hours 
to  seven  days  if  removed  from  the  body  of  the  host,  and  also  in  a  few  days  if 
the  host  which  they  do  not  leave  is  killed  or  dies,  the  life-story  of  not  a  single 
species  has  so  far  been  completely  worked  out.  It  is,  however,  known  that 
the  eggs  are  fastened  to  the  hairs  or  feathers  of  the  host,  and  that  the  young 
when  hatched  are  like  the  parents,  but  smaller,  paler,  and  without  characteristic 
skin  markings ;  they  attain  their  adult  characters  without  metamorphosis. 

They  run  freely  about  the  host,  feed  upon  hairs  and  feathers,  and  very  rarely 
upon  dried  blood,  and  usually  pass  from  bird  to  bird  or  animal  to  animal  by 
contact,  being  rarely  found  away  from  the  host,  which  they  probably  slightly 
irritate,  because  birds  are  seen  to  be  constantly  cleaning  their  feathers.  They 
have  been  found  to  be  parasitic  on  about  100  species  of  mammals,  representing 
48  genera,  24  families,  and  5  orders,  and  1,100  bird  species,  or  55  orders  of 
birds  out  of  a  total  of  35  orders. 

Classification. — The  principal  factor  which  has  influenced  the  evolution 
of  this  curious  group  of  animals  is  isolation,  each  host  being,  according  to 
Kellogg,  like  a  small  island,  so  that  each  species  is  made  up  of  many  dislocated 
small  groups,  and  this  is  why  each  species  has  to  be  given  a  very  flexible 
description,  and  why  many  varieties  might  be  made  from  one  species.  This 
condition  of  life  is  opposed  to  producing  larger  variations,  which  might  be 
used  to  make  genera  and  families,  and  the  life  conditions  of  many  of  the  species 
are  very  similar.  Hence  varietal  specific  distinctions  are  many,  and  generic 
and  family  few. 

Hence  some  1,500  species  are  known,  which  can  be  divided  into  two  sub- 
orders, each  4  families  and  27  genera.  The  mammalia-infesting  families  are 
only  two  in  number,  the  Gyopididae  and  Trichodechitidae,  characterized  by 
having  two-clawed  members,  and  each  of  those  families  by  only  one  genus. 
The  bird-infesting  families  are  also  two  in  number,  and  have  respectively  15 
and  10  genera. 

The  following  table  gives  the  differentiation  of  the  suborders'  families: — - 

SUBORDER  1:  ISCHNOCERA  Kellogg,   1896. 

Antennae  exposed,  filiform,  three-  or  five-segmented,  no  maxillary  palpi, 
mandibles  vertical,  crop  with  sac-like  diverticula,  ingluvial  glands  present, 
testes  four,  egg  tubes  five. 

A.  Antenna;    three-jointed,     tarsi     one     claw.      Habitat,     mammals — 

TrichodectidcB. 

B.  Antennae  five-jointed,  tarsi  two  claws .     Habitat,  birds — Philopteridcs. 

SUBORDER  2;  AMBYCERA  Kellogg,   1896. 

Antenna?  concealed,  clavate  or  capitate,  four-segmented,  maxillary  palpi 
present,  mandibles  horizontal,  crop  single,  ingluvial  glands  absent,  testes 
six,  egg  tubes  three  to  five. 

A.  Tarsi  with  one  claw.     Habitat,  mammals — Gyropidce.  . 

B.  Tarsi  with  two  claws.     Habitat,  birds — Liotheidce. 

The  genera  parasitic  on  mammals  may  be  recognized  as  follows: — 

SUBORDER  ISCHNOCERA  Kellogg,   1896. 
Family  TrichodectidjE  Burmeister,   1835. 
This  family  contains  only  one  genus,  Trichodectes  Nitzsch,  181 8,  which  is 
parasitic  on  mammals  and  has  tarsi  with  only  one  claw. 

SUBORDER  AMBYCERA  Kellogg,   1896. 
Family  Gyropidce  Burmeister,   1835. 
This  family  contains  only  one  genus,  Gyropus  Nitzsch,  1818,  parasitic  on 
mammals  and  with  tarsi  armed  with  only  one  claw. 


752  MALLOPHAGA   AND  ANOPLURA   (LICE) 

ORDER  ANOPLURA  Leach,  1815. 

Synonyms. — Pediculina  Burmeister,  1835;  Siphunculata  Meinert, 
1891 ;  Pseudorhynchota  Cholodkowsky,  1903 ;  Lipognatha  Borner, 
1904;  Ellipoptera  Shipley,  1904. 

Definition. — Hexapoda  with  labrum  and  labium  joined  together 
to  form  a  rostrum  or  proboscis,  which  is  armed  with  recurved 
hooklets,  and  contains  a  hollow  extensile  sucker  formed  by  the 
mandibles  and  maxilke.  Eyes  without  facets.  Antennae  five- 
jointed.  Thorax  with  little  traces  of  segmentation.  Wings  absent. 
Legs  with  hook-like  terminal  joints,  suitable  for  clinging.  Last 
abdominal  segment  rounded  in  male,  notched  in  female.  Meta- 
morphosis incomplete.     Habitat,  epizoic  on  mammals. 

Historical. — The  sucking  lice  were  known  to  the  ancients,  for  Aristotle 
was  acquainted  with  the  pubic  louse,  while  references  can  be  found  in  the  works 
of  Theophrastus,  Dioscurides,  Galen,  and  Pliny. 

The  more  modern  writers  are  Moffat,  1634,  Camerarius,  1652,  Redi,  1668, 
Leuwenhoek,  1697,  and  Swammerdamm  in  1737,  several  of  whom  give  excel- 
lent figures  of  these  parasites. 

In  1758  Linnaeus,  in  his  '  Systema  Naturae,'  gathered  a  heterogeneous  collec- 
tion of  species,  including  some  of  Mallophaga  and  Anoplura,  in  his  genus 
Pediculus;  and  in  1815  Leach  gave  the  more  commonly  used  name  to  the  order, 
which  included  the  Mallophaga  as  well  as  the  sucking  lice. 

We  have  already  seen  how  the  species  of  Mallophaga  were  separated  from 
this  composite  genus  Pediculus,  and  it  now  remains  to  point  out  that  Leach 
in  1 81 5  created  the  genera  Phthirius  for  Pediculus  pubis  and  Hcsmatopinus 
for  Pediculus  vituli,  P.  asini,  and  P.  suis. 

Later  important  investigations  were  made  by  Nitzsch,  1818,  Burmeister, 
1835,  Denny,  1842,  Giebel,  1874,  Piaget,  1880,  and  especially  by  Enderlein 
in  his  '  Lause  Studien,'  published  in  1904,  and  by  Delia  Torre  in  1908. 

We  have  seen  that  Mjoberg  and  Kellogg  consider  that  the  Anoplura  are 
derived  from  ancestors  common  to  them  and  the  Mallophaga,  being  separated 
by  the  alterations  induced  by  sucking  blood. 

Morphology. — The  anatomy  will  be  dealt  with  under  the  heading 
Pediculidae,  and  need  not  detain  us  here,  except  to  invite  atten- 
tion to  the  characters  of  the  mouth  parts,  which  are  so  modified 
as  to  form  a  sucking  mouth,  while  the  pharynx  performs  the  role 
of  a  sucking  pump. 

Classification. — The  order  is  divided  into  four  families,  some  of 
which  are  capable  of  being  subdivided  into  subfamilies.  The  number 
of  genera  is  15,  and  the  known  species  are  about  100,  which  are  all 
parasitic  on  mammals. 

The  following  table,  taken  from  Delia  Torre,  enables  the  families 
to  be  differentiated: — 

A.  Head  not  prolonged  into  a  nozzle-like  projection.     Antennae 

three  to  five  segments.     Tibia  with  a  thumb-like  process. 

Tibia  and  tarsus  very  short  and  thick.     Legs  clinging 

in  character. 

I.  Body  flattened.  Mesothorax  and  three  to  eight 
abdominal  segments,  with  stigmata.  Antenna  three 
to  five  segments.     Tibia  with  thumb-like  process. 


ANOPLURA  753 

(a)  Head    broader    than    thorax.     Eyes    large    pig- 

mented. Pharynx  short  and  broad.  Proboscis 
short  and  pressed  against  thorax — Pediculidcd 
Leach,  1815. 

(b)  Eyes  very  small  or  absent.     Pharynx  long  and 

narrow.     Proboscis  very   long — Hcematopinidce 
Enderlein,  1904. 
II.  Body   thick    and    heavy.     Mesothorax,    metathorax, 
and  two  to  eight  abdominal  segments,  with  stigmata. 
Eyes  absent.     Back  part  of  the  head  widened  back- 
wards.    Antennae    four    to    five    segments.     Tibia 
with  short  strong  thumb-like  process.     Thick  short 
spines  on  the  body.     Female  gonopodia  elongated 
and  narrow — Echinophthiridce  Enderlein,  1904. 
B.  Head  prolonged  into  a  nozzle-like  projection,  at  the  anterior 
end  of  which  lies  the  mouth  opening.     Antennae  five 
segments.     Tibia    without    thumb-like   process.     Tibia 
and  tarsus  very  long  and  thin.     Legs  not  clinging  in 
character — Hcematomyzidce  Enderlein,  1904. 


Family  i:  Pediculid^;  Leach,  1815. 

Definition. — Anoplura  with  flattened  body,  and  head  not  pro- 
longed anteriorly  into  a  nozzle-like  projection,  with  large  prominent , 
pigmented  eyes,  three  to  five  jointed  antennae,  and  short  proboscis. 
Pharynx  short  and  broad.  Paroglossae  (fulturae)  very  strong  and 
broad,  with  broad  arms.  Stigmata  on  mesothorax  and  third  to 
eighth  abdominal  segments.  Legs  suitable  for  clinging.  Tibia  and 
tarsus  thick.     Tibia  with  a  thumb-like  process. 

Remarks. — The  Pediculidae  are  found  all  over  the  world,  on  man  as  well  as 
on  animals.  They  cause  much  irritation  by  their  bites,  which  may  become 
infected,  causing  impetigo.  Apart  from  this,  however,  they  have  recently 
been  suspected  of  spreading  blood-parasites — e.g.,  Trypanosoma  lewisi  and 
H&mogregarina  gerbilli — which  are  believed  to  undergo  development  in  them ; 
and,  in  addition,  they  contain  parasites  peculiar  to  themselves — e.g.,  Herpeto- 
monas  pediculi. 

Morphology. — The  head  is  usually  clearly  defined,  but  the  thorax  may  or 
may  not  be  so  well  defined  from  the  abdomen.  Eyes  may  be  present  or 
absent — a  fact  which  appears  to  depend  upon  whether  the  host  is  nocturnal 
or  not  in  its  habits.  The  antennae  are  usually  five-jointed.  The  mouth  con- 
sists of  a  proboscis,  composed  of  labrum  and  labium,  which  is  armed  with  re- 
recurved  hooklets,  and  contains  the  maxillae  and  mandibles,  which  take  the 
form  of  a  suctorial  tube.  The  thoracic  segments  are  fused  together.  The 
thorax  may  be  as  broad  as  the  abdomen,  or  narrower.  There  are  no  wings. 
The  legs  have  four  segments,  of  which  the  terminal  one  carries  a  strongly 
curved  claw.  The  abdomen  has,  if  statements  can  be  trusted,  a  various  number 
of  segments,  differing  in  the  different  genera. 

The  last  segment  in  the  female  has  a  slit-like  opening  guarded  by  two 
chitinous  plates,  while  in  the  male  there  is  in  the  same  situation  a  horny 
papilla  surrounded  by  spines. 

Internal  Anatomy. — Christophers  and  Newstead  have  studied  the  anatomy 
of  H cematopinus  stephensi  Christophers  and  Newstead,  1906,  parasitic  on 
Gerbillus  i adieus  (the  Indian  field-rat).! 

a6 


754 


MALLOPHAGA  AND  ANOPLURA    {LICE) 


The  alimentary  canal  consists  of  a  mouth  followed  by  a  chitinous  pharyngeal 
pump,  into  which  the  ducts  of  the  salivary  glands  open,  and  an  oesophagus 
which  leads  into  the  mid-gut.  This  second  part  of  the  canal  consists  of  two 
portions,  of  which  the  first  appears  to  be  a  crop  and  the  second  a  chylific 
ventricle.  There  are  four  Malpighian  tubules.  The  intestine  shows  no  differ- 
entiation into  small  and  large.  The  rectum  is  globular,  with  a  distended 
posterior  portion  containing  the  rectal  papillae.  The  fat-body  is  well  developed . 
The  female  generative  organs  consist  of  two  ovaries  with  oviducts.  Each 
ovary  consists  of  five  to  six  follicular  tubes.  The  two  oviducts  unite  into  a 
common  duct,  and  there  is  a  spermatheca.  The  male  organs  are  testes, 
vasa  deferentia,  vesiculae  seminales,  and  penis. 

Life-History. — The  ova,  which  are  attached  to  the  hairs  of  the  host,  give  rise 

larvae,  which  closely  resemble  the  adults. 


Fig.  366. — Pediculu*  humanus 
L.:  Male,     (x  25.) 


Fig. 


367.  —  Pediculus   humanUs 
L. :  Female.     (X  25.) 


Pathogenicity. — Lice  are  important  carriers  of  disease,  being 
vectors  in  certain  forms  of  relapsing  fever,  in  typhus,  and  in  trench 
fever,  etc. 

Classification.- — The  Pediculidae  are  subdivided  into  two  sub- 
families, which  may  be  recognized  as  follows : — 

A.  Pediculidce  with  five-jointed  antennae— Pediadince. 

B.  Pediculidce  with  three-jointed  antennae — Pedicince. 

Subfamily  A:  Pediculin.e  Enderlein,  1904. 

Definition. — Pediculiche  with  five-jointed  antennae. 
Classification. — The  Pediculinae  contain  two  genera,  both  of  which 
are  parasitic  on  man,  and  which  may  be  differentiated  as  follows: — 

(a)  All  legs  strong,  distinct  neck,  thorax  narrower  than 

abdomen — Pediculus. 
{b)  Forelegs  long,   slender,  with  three  claws;   no  neck; 

thorax  broader  than  abdomen — Phthirius. 


PEDICULUS 


755 


Genus  Pediculus  Linnaeus,  1758. 

Definition. — Pediculinae  with  distinct  neck  and  thorax  narrower 
than  abdomen.  Legs  all  strong  with  strong  claws.  Thumb-like 
projection  of  the  tibia  long,  thin,  and  covered  with  bristles.  Abdo- 
men long  and  narrow,  with  segments  not  compressed  together,  and 
without  lateral  hook-like  processes  on  the  fifth  to  eighth  segments. 
Two-jointed  telson  carries  ventrally  a  pair  of  cone-like  processes. 
Female  gonopodia  clamp-like  and  bent  inwards. 

Classification, — Only  four  species  are  at  present  assigned  to  the 
genus  Pediculus: — 

P.  humanus  Linnaeus,  1758,  found  on  man. 

P.  corporis  de  Geer,  1778,  found  on  man. 

P.  punctatus  Rudow,  1869,  found  on  Bos  grunniens. 

P.  consobrinus  Piaget,  1880,  found  on  Ateles  pentadactylus. 

There  is  a  doubt  as  to  whether P .  punctatus  is  really  a  pediculus,  and 
P.  consobrinus  is  said  by  Neumann  to 
be  indistinguishable  from  P.  humanus, 
therefore  the  species  are  reduced  to 
two: — 

P.  humanus  Linnaeus,  1758. 
P.  corporis  de  Geer,  1778. 

These  are  very  alike,  and  have  been 
thought  to  be  only  varieties  of  one 
another.  Interbreeding  seems  to  be 
possible.  The  following  points  may 
help  to  differentiate  them : — 

1.  Found   on    the   human   head, 

with  well-defined  abdominal 
segments  marked  by  a  fes- 
tooned lateral  border — 
P.  humanus. 

2.  Found  in  the  clothing,  larger 

than  P.  humanus,  with 
broader  thorax  and  lateral 
borders  of  abdomen  less 
festooned,  and  segments  not 
quite  so  distinctly  indicated 
— P.  corporis. 


1 

1 

Fig.  368. — Egg  of  Pediculus 
humanus  Linn^us,  1758, 
attached  to  a  hair.  (x  35 
Diameters.) 


(From  a  photograph  by 
J     J-  Bell.) 


Pediculus  humanus  Linnaeus,  1758. 

Synonyms.  -Pediculus  humanus  var.  1  Linnaeus,  1766; P.  humanus 
var.  capitis  de  Geer,  1778;  P.  cervicalis  Leach,  1817;  P.  capitis 
Nitzsch,  1818;  P.  humanus  Csiki,  1904;  P.  nigritarum  Latreille. 

Definition. — Pediculus  often  varying  in  colour  somewhat  accord- 
ing to  the  human  race,  on  which  it  is  parasitic,  with  thorax  often 
narrowing  distinctly  anteriorly,  well-defined  abdominal  segments 


756 


MALLOPHAGA   AND  ANOPLURA    (LICE) 


marked  by  lateral  festoons.      Thumb-like  projection  on  the  tibia 
armed  with  a  spine.     Habitat,  homo. 

Remarks. — This  is  the  head-louse,  which  is  cosmopolitan  in  distribution, 
but  varies  in  colour  on  the  different  races,  as  was  pointed  out  by  Murray, 
being  very  dark  on  African  negroes  and  Tamils,  and  said  to  be  yellow  on  Chinese 
and  Japanese,  and  orange  on  Hottentots. 

On  Europeans  it  is  light  grey  in  colour.  Daniels  says  that  the  pediculi  of 
Chinese  do  not  pass  readily  to  Tamils ;  though  in  our  experience  the  pediculi  of 
native  servants,  Sinhalese  and  Tamils,  will  pass  to  Europeans. 

These  pediculi  are  extremely  common  in  the  tropics,  and  it  is  an  every- 
day scene  to  witness  natives  busy  at  work  killing  them  on  their  friends'  heads. 

Morphology. — The  head-louse  is  about  2  millimetres  in  length  by  1  milli- 
metre in  breadth.  The  female  is  larger  than  the  male,  and  exists  in  greater 
numbers.  The  head  is  triangular,  the  thorax  ^-oad  with  short  leg'*,  and  the 
margins  of  the  abdomen  are  dark. 


Fig.   369. — Pediculus    corporis 
Geer:  Male.  (X25.) 


Fig.    370. — Pediculus     corporis     de 
Geer:  Female.  (X25.) 


Male. — The  posterior  somite  is  rounded  oft  and  prominent,  with  a  circular 
opening  dorsally,  which  is  the  common  aperture  of  the  genital  and  alimentary 
caual.  The  penis  is  simple,  wedge-shaped,  and  is  usually  seen  protruding 
dorsally. 

Female. — The  last  abdominal  segment  is  deeply  notched  at  the  apex,  where 
the  anus  is  situated.     The  vagina  opens  on  the  ventral  surface. 

Life-History.— The  female  lays  fifty  to  sixty  eggs,  which  are  attached  firmly 
tci  the  hairs  by  the  secretion  of  the  cement  gland.  In  about  six  days  these 
eggs  hatch.     The  young  pediculi  become  fully  developed  in  fourteen  to  twenty 

Pathogenicity. — It  can  carry  typhus  and  produce  a  form  of  impetigo. 
Treatment. — White  precipitate  ointment  or  common  paraffin  oil  may  be 


PEDICULUS 


757 


Pediculus  corporis  de  Geer,  1778. 

Synonyms. — P.  humanus  Linnaeus,  1758;  P.  humanus  var.  2 
Linnaeus,  1766 ;  P.  humanus  var.  corporis  de  Geer,  1778 ;  P.  vesti- 
menti  Nitzsch,  1818;  P.  corporis  Csiki,  1904. 

Definition. — Pediculus  usually  dirty-white  in  colour,  thorax 
only  slightly  narrowed  anteriorly,  abdominal  segments  not  very 
distinctly  defined  and  not  well  festooned  laterally.  Thumb-like 
projection  on  the  tibia  without  a  spine.     Habitat,  homo. 

Remarks. — This  louse  lives  in  the  folds  and  seams  of  the  clothes. 

Morphology. — It  is  larger  than  P.  humanus,  and  has  an  oval, 
elongated  head,  with  large  antennae.  The  thorax  is  more  segmented 
than  inP.  humanus,  and  the  legs  more  developed,  with  larger  claws. 

Life- History. — It  lays  seventy  to  eighty  eggs,  measuring  07  to 
0-9  millimetre,  in  the  seams  of  the  clothing,  which  hatch  in  three  to 
four  days,  and  become  mature  in  fifteen  to  eighteen  days. 

Pathogenicity. — It  is  a  carrier  of  typhus  fever,  trench  fever, 
and  certain  forms  of  relapsing  fever. 

Treatment. — Boil  or  steam  the  clothes  in  a  sterilizer  at  2120  F. 

Genus  Phthirius  Leach,  1815. 

Pediculidae  with  the  anterior  legs  weak,  armed  with  large  short 
claws;  abdomen  broad  and  short',  with  first  to  fifth  segment  so 
strongly  compressed  that 
the  stigmata  appear  to  lie 
in  one  segment.  Fifth 
to  eighth  segments  with 
lateral  tooth-like  pro- 
cess, of  which  thet  wo  last 
are  long.  Habitat,  homo. 

Phthirius  pubis  Lin- 
naeus, 1758. 

Synonyms. — Pediculus 
pubis  Linnaeus,  1758; 
P.  inguinalis  Reichard, 
1759;  Phthirius  inguina- 
lis Leach,  1815;  P.  tube-  fig.  371. 
seen!  i  um  Ab  ,  lSlS;P.  pu- 
bis Kiichenmeister,  1855. 

Remarks. — P.  pubis  is  the  pubic  or  crab-louse,  and  is  more  common 
on  men  than  on  women.  It  usually  infests  the  pubic  hairs,  but  may 
also  be  found  on  the  eyelashes  and  on  the  eyebrows. 

Morphology  .—The  body  in  general  is  flat  and  broad,  with  a 
rounded  head  bearing  antennae  with  five  segments,  and  two  small 
eyes.  There  is  a  neck.  The  broad,  flat  thorax  is  merged  into  the 
abdomen,  and  carries  three  pairs  of  legs,  of  which  the  anterior  pair 
is  slender,  and  possesses  a  straight  claw  suitable  for  walking,  and 
the  two  posterior  pairs  have  claws  suitable  for  clinging. 


—Phthirius  pubis  Linnaeus: 
Female.    (X2.5.) 


758 


MALLOPHAGA  AND  ANOPLURA   {LICE) 


The  female  measures  i-2  to  2  millimetres  in  length  by  1-5  milli- 
metres in  breadth.     The  male  is  half  the  size  of  the  female. 

Life-History. — The  female  lays  ten  to  fifteen  eggs,  which  it 
attaches  to  hairs.  These  hatch  in  seven  days,  and  the  resulting 
pediculi  become  mature  in  about  two  weeks. 

Pathogenicity.- — It  produces  often  a  dermatitis,  with  itching 
and  a  greyish  discoloration  of  the  skin,  said  by  Dugnet  to  be  caused 

by  a  pigment  produced  by  the  parasite. 
Erasmus  Wilson  says  that  reddish  de- 
posits may  be  seen  on  the  hairs,  due  to 
the  fsecal  matter  of  the  parasite. 

Treatment. — White  precipitate  oint- 
ment or  some  other  mercurial  prepara- 
tion. 

Subfamily  B:  Pedicinin^e 
Enderlein,  1904. 

Definition. — Pediculidas  with  three-jointed 
antennae. 

Remarks. — Only  one  genus,  Pediciuits 
Gervais,  1847,  is  known,  and  there  are  three 
known  species  found  on  monkeys — viz., 
P.  euvygastes  Burmeister,  1835  (synonym. 
P.  micvops  Nitzsch  and  Giebel,  1S64),  found 
on  Pithecus  sinicus  (Linnaeus,  1771);  P.  longi- 
ceps  Piaget,  1880,  found  on  Lasiopyga  mono. 
(Schreber,  1775) ;  and  P.  piazeti  Strobelt,  1881 
on  Pithecus  brevicaudis  (Elliot,  1909). 

Family  2:  H.ematopinid^; 
Enderlein,  1904. 

Definition. — Anoplura  with  head  broadest 
behind,  and  not  prolonged  anteriorly  into  a 
nozzle-like  projection.  Eyes  rudimentary  or 
absent.  Antennae  three  to  five  segments. 
Proboscis  very  long.  Pharynx  long  and 
narrow.  Paraglossae  very  small.  Mesothorax  and  third  to  eighth  abdominal 
segments  with  stigmata.  Row  of  hairs  on  each  abdominal  tergite  and 
sternite.  I  egs  suitable  for  clinging.  Tibia  and  tarsus  very  short  and  thick. 
Tibia  with  a  thumb-like  projection.    Pretarsal  sclerite  sometimes  present. 

Classification. — Enderlein  has  divided  the  family  into  three  subfamilies, 
which  may  be  recognized  as  follows: — 
A.  Antenna?  with  five  segments: — 

I.  Eyes  rudimentary,  situate  on  the  extremity  of  a  forwardly 
directed  fork-like  lateral  process  from  the  posterior  aspect  of 
the  head.  .Mandibles  well  developed.  Forelegs  larger  and 
stronger  than  other  legs.  Pretarsal  sclerite  present — 
H&matopinincB. 
II.  Eyes  and  eye  process  absent,  mandibles  rudimentary.  Fore- 
legs smaller  than  other  legs.  Pretarsal  sclerite  absent — 
I.inosnathince. 
Antennae  with  three  segments — Enhcematopinince . 


Fig.  372. — Polyplax spinulosa 
Burmeister:  Female. 


B. 


Subfamily  H^matopixin.e  Enderlein,  1904. 
This   subfamily  contains  only  the  genus  Hesmatopinus  Leach.   1817,  with 
some  twenty  known  species,  of  which  the  type  H.  suis  (Linmeus,  1758)  Leach, 


L1N0GNATHINJE  739 

1 817,  is  found  on  Sus  scrofa  Linnreus;  other  species  are  found  on  equines, 
bovines,  camels,  antelopes,  deer,  conies,  and  monkeys. 

Subfamily  Linognathiinle  Enderlein,  1904. 

This  subfamily  contains  five  genera,  which  may  be  recognized  as  follows: — 

A.  Abdomen  with  strongly  chitinized  tergites,  sternites,    and    pleurites. 

Tergites  and  sternites  partly  subdivided.  Pleurites  extended  back- 
wards and  outwards,  making  sides  of  abdomen  segmented.  Hind 
legs  stronger  than  middle  legs.  Claw  of  hind  leg  short  and  much 
compressed,  and  fittable  into  tarsus. 

I.  Abdomen  elongated;  4-7  sternites  and  2-7  tergites,  divided  into 
two  plates  lying  one  behind  the  other.  Each  plate  with  a 
transverse  row  of  strong  long  hairs.  Pleura  without  serrated 
process  on  the  inner  side.  Stigmata  small — Polyplax  Ender- 
lein, 1904. 
II.  Abdomen  more  or  less  elongated.  Pleura  two  to  six,  provided 
with  a  dorsal  and  ventral  long  knife-like  pointed  process. 
Four  to  seven  tergites  and  sternites,  composed  of  three 
secondary  segments,  each  with  a  transverse  row  of  long  broad 
scale-like  hairs:  third  tergite  and  sternite  composed  of  two 
rings  each.  Anterior  ring  is  broader  than  posterior — Hoplo- 
pleura  Enderlein,   1904. 

B.  Abdomen  without  sclerites,   with  smooth  border,     Hind  legs  same 

size  as  middle  leg  :— 
I.  Each  sternite  and  tergite  of  the  abdomen  with  two  or  three 
transverse  rows   of  very  long  closely  set  hairs — Linognatkus 
Enderlein,    190.1. 
II.  Each  sternite  and  tergite  of  the  abdomen  with  one  transverse 
row  of  hairs : — ■ 

(a)  Stigmata   large,    and   those    on   the   abdomen   raised   like 

tubercles  and  standing  out  above  the  hinder  border  of 
that  segmented — Solenopoles  Enderlein,  1904. 

(b)  Stigmata  very  small,  and  not  raised  as  tubercles—  Hamo 

dipsus  Enderlein.  1904. 
The  genus  Polyplax  contains  a  rapidly  increasing  number  of  species.     The 
one  illustrated  in*  Fig.  372  is  P.  spinulosa  (Burmeister,  1839),  which  is  found 
on  Epimys  norve^icus  Erxleben,  1777,  in  Europe. 

Subfamily  C:  Euh^matopinin^;  Enderlein,  1904. 

This  subfamil-/  has  two  genera,  with  one  species,  and  this  can  be  recognized 
as  follows: — ■ 

A.  Hind  legs  with  femur  and  tibia  armed  with  projecting  rectangular, 

stalked,  sheath-like  appendages — Enhamialobinus  Osborn,  1896. 
Species:  E.  abnormis  Osborn,   1896,  on  Scalops  ar^entatus  in  North 
America. 

B.  Hind  legs  normal — HcBmatopinoid.es  Osborn,  1891. 

Species:  H.  sqnamosus  Osborn,  1891,  on  Geomys  luvsanus  in  North 
America. 

Remaining  Families. 

The  family  Echinobthiyiudce  Enderlein,  1904,  contains  three  genera — 
viz.,  Antarctophthirius  Enderlein,  1904 — with  two  species,  Echinophthirius 
Giebel,  1871,  with  three  species,  and  Lepidothivius  Enderlein,  1904.  with  only 
L.  macrorhiui  Enderlein,  1904. 

The  family  Hcematomyzidce  Enderlein,  1904,  contains  one  genus,  Hcema- 
iomyzus  Piaget,  1869,  and  one  species,  H.  elephantis,  on  the  Ceylon  elephant 


76o  MALLOPHAGA  AND  ANOPLURA  (LICE) 

REFERENCES. 

Mallophaga. 

Dknny  (1842).     Anoplurorum  Britanniae.     London. 

Kellogg  (1908).     Wytsman's  Genera  Insectorum,  66'»e  Fascicule.      Brussels. 
(1913).  American  Naturalist,  129.     (1914).   Ibid.,  257,  Lancaster,  P.  A. 

Anoplura. 

Bacot.  (1917).      Tropical  Diseases   Bull.,   vol.  ix.,   p.  371    (Interbreeding  of 

P.humauus  and  P.  corporis). 
Burmeister  (1835).     Handbook  Eivtomology,  vol.  2. 

Christophers  and  Newstead  (1906).     Thompson,  Yates,  Reports,  vii.  13. 
Enderi.ein  (1904).     Zoologische  Anzeiger,  vol.  28. 
Gervais  (1847).     Histoire  Naturelle  Insectes  Apteres. 
Landois  (1865).     Zeitschrift  fur  Zoologie,  xiv.  1864;  xv.  1865. 
Leach    .(1815).     Brewster's     Edinburgh     Encycl.,     vol.     9     (1817).      Zool. 

Miscellany,  vol.  3 
Linnaeus  (17.58).     Systema  Natura,  ed.  x. 
Martini  (1918).     Miinch.  Med.  Woch. 
Osborn  (1891).     Bulletin  United  States  Department  of  Agriculture.  Mo.  7. 

Washington. 
Piaget  (1869).     Tydschriften  voor  Entomologie,  vol.  12. 
Piaget  (1880-188.5).     Les  Pediculines  Leide.     Supplement.  Leide. 
Von    Della    Torre    (1908).     Anoplura — -Wytsman's    Genera    Insectorum, 

Fascicule  81. 


CHAPTER  XXXI 
HEMIPTERA 

Hemiptera  —  Gymnocerata  —  Clmocorida^ —  Reduviida^ —  Hydrometrida?  — 
Aradi  dne — References . 

ORDER  HEMIPTERA  Linnaeus,  1742. 

Synonyms.  - R hyngota  Fabricius;  Rhynchota  Burmeister. 

Definition.— Hexapoda  with  four  wings,  the  front  pair  being 
either  membranous  or  half  horny  and  half  membranous,  but  both 
pairs  may  be  wanting  in  the  parasitic  species.  Mouth  suctorial. 
Metamorphosis  complete. 

Remarks. — The  Hemiptera  include  the  cochineal  insect,  Coccus 
cacti ;  the  Aphidae,  plant-lice;  and,  in  particular,  the  cicadas,  whose 
shrill  notes  wake  the  quiet  of  an  African  forest.  The  anterior  wings 
are  called  hemelytra,  and  usually  consist  of  three  portions: — 

1.  The  clavus— the  hard,  coriaceous  portion  next  to  the 
scutellum. 

2.  The  corium— hard,  coriaceous  portion  occupying  the  whole  of 
the  area  between  the  clavus  and  the  membrane. 

3.  The  membrane— apical  portion. 
The  posterior  pair  are  the  true  wings. 

In  the  Clinocoridae  the  corium  is  divided  into  three  portions: — 

1.  Internal — corium  proper. 

2.  External  and  basal — embolium. 

3.  External  and  apical — cuneus. 

Classification. — The  order  is  divided  into  two  suborders: — 

Suborder  I.:  Homoptera. — With  both  pairs  of  wings  mem- 
branaceous. 

Suborder  II. :  Heteroptera. — -With  the  front  pair  of  wings  half 
horny. 

The  first  will  not  be  considered  here. 

HETEROPTERA. 

This  suborder  has  two  series: — 

Scries  1,  Gymnocerata  Fieber. — Antennae  conspicuous. 
Series  2,  Cryptocerata  Fieber. — Antennae  hidden. 

761 


762  HEMIPTERA 

GYMNOCERATA  Fieber. 

The  families  of  importance  to  us  are: — 

Clinocoridae. 
Reduviidae  Stephens. 
Aradidae. 
Hydrometridae. 

These  families  can  be  diagnosed,  according  to  Distant,  in  the 
following  manner: — 

A.  Species  not  aquatic;  abdomen  not  clothed  beneath  with  a 

silvery,  velvety  pubescence;  scutellum  not  reaching  to  the 
base  of  the  membrane  nor  to  the  middle  of  the  abdomen. 
(i)  Mesopleurae  and  metapleurae  composed  of  one  piece; 
hemelytra  without  cuneus. 

(a)  Tarsi  three-jointed.     Rostrum  short,  stout,  bent 

at  the  base,  so  that  in  repose  it  does  not  lie 
against  under-surface  of  the  head ;  ocelli  behind 
eyes;  hemelytra  complete  with  distinct  mem- 
brane— ReduviidcB. 

(b)  Tarsi  two-jointed,  anterior  legs  normal  and  in- 

serted on  the  disc  of  the  prosternum.     Hemelytra 
neither  reticulate  nor  cellular — Aradidce. 
(2)  Mesopleurae  and  metapleurae  composed  of  seven  pieces; 

hemelytra  with  a  cuneus  and  an  embolium;  ocelli 

absent — Clinocoridce. 

B.  Species  aquatic  or  semi-aquatic;  abdomen  clothed  beneath 

with  a  silvery  velvety  pubescence;  antennae  four-jointed — 
Hydrometridce. 

Family  Clinocorid^. 

Synonym. — Acanthiadce. 

Definition. — Gymnocerata  without  ocelli,  with  elytra  so  short 
that  the  abdomen  is  left  uncovered.     Tarsi  three-jointed. 

Remarks. — This  family  contains  the  bugs  as  so  called  in  medical 
literature.  There  are  eight  genera — Clinocoris  Petersonn,  1829; 
CEciacus  Stal,  1873 ;  Loxaspis  Rothschild,  1912 ;  Cacodnws  Stal,  1873 ; 
Aphramia  Champion,  1900 ;  Hcematosiphon  Champion,  1900 ;  Bertilia 
and  Leptocimex  Roubaud,  1913 — and  by  some  authorities  these  are 
gathered  into  two  subfamilies,  Clinocorince  and  H&matosiphonince, 
with  about  twenty  species  in  all,  of  which  twelve  are  parasitic 
on  bats. 

Clinocorin^. 
Clinocoris  Petersonn,  1829. 

Synonyms. — Cirncx  Linnaeus,  1758;  Acanthias  Fabricius,  1803; 
Klinophilos  Kirk,  1899. 

Nomenclature. — Koris  Aristotle;  Cimex  Pliny. 


CLINOCORIS  763 

Definition. — Clinocoridae  with  the  anterior  margin  of  the  thorax 
strongly  excavated  and  with  prominent  lateral  angles. 

Remarks. — There  can  be  no  doubt  that  originally  bugs  fed  upon 
vegetable  juices,  and  that  it  is  only  within  geologically  recent  periods 
that  they  have  taken  to  blood.  Thus  the  field  bug,  Lyctocoris 
campestris,  which  is  found  under  stacks  of  corn  in  Europe,  may  find 
its  way  into  barns  and  stables,  and  will  then  attack  horses  and 
cattle,  though  under  normal  circumstances  it  would  merely  suck 
vegetal  juices.  The  relationship  to  bats  is  interesting,  as  apparently 
the  family  is  essentially  a  family  of  bat  parasites. 

Type  Species. — Clinocoris  lectularius  (Linnaeus,  1758). 

Other  Species.— C.  rotundatus  Signoret,  1852;  C.  ciliatius  Evers- 
mann,  1841 ;  C.  pipistrelli  Jenyns,  1839  (spreads  Trypanosoma  vesper- 
tilionis);  C-  columbarius  Jenyns,  1839;  C.  fcedus  (vary  rare); 
C.  dissimilis  ;  C-  improviso  (very  rare) ;  C.  pelosellus  (America) ; 
C.  peristerce. 

C.  boneti  Brumpt,  1910,  of  our  previous  editions  becomes  Lepto- 
cimex  boneti  (Brumpt,  1910),  and  C.  inodorus  of  previous  editions 
becomes  Hcematosiphon  inodorum,  which  is  found  on  fowls  and  may 
enter  dwellings. 

Clinocoris  lectularius  Linnaeus,  1758.  ^~ 

Synonyms. — C.  lectularius  Merrett,  1667;  Cimex  lectularius 
Linnaeus,  1758;  Acanthia  lectularius  Fabricius,  1794. 

Definition. — Clinocoris  with  short,  broad  head,  with  two  promi- 
nent eyes,  but  no  ocelli;  antennae  four-jointed,  apical  joints  slender; 
elytra  rudimentary  and  lie  over  the  metathorax;  prothorax  semi- 
lunar, with  extended  anterior  angles;  abdomen  uncovered,  with  seven 
segments  and  an  eighth  anal  appendage;  legs  slender,  anterior  tibia 
twice  as  long,  and  posterior  three  times  as  long  as  the  tarsi,  which 
are  three-jointed;  proboscis  flexed  into  a  groove  beneath  the  head 
and  prothorax. 

Historical. — The  bed  bug  was  well-known  to  the  ancient  peoples 
of  Asia  and  also  to  the  Romans,  who  called  it  Cimex.  It  seems  to 
have  come  to  Europe  from  the  East,  and  to  have  reached  Germany 
in  the  twelfth  century,  England  about  1500,  while  Thomas  Moffat 
says  it  was  recognized  in  London  in  1503 — but  then  he  was  writing 
one  hundred  years  after  the  event.  Originally  it  was  known  as 
the  wall-louse  or  chinch,  and  the  term  '  bed-bug  '  is  apparently  of 
recent  origin.  Both  males  and  females  suck  blood,  and  are  suspected 
of  spreading  Obermeyer's  relapsing  fever. 

Morphology. — It  is  reddish-brown  in  colour,  with  short,  broad 
head  carrying  two  eyes,  two  antennae  composed  of  four  segments, 
of  which  the  first  and  second  are  stout,  and  the  third  and  fourth 
slender.  The  mouth  consists  of  a  proboscis,  which  is  composed  of 
an  upper  part — the  labrum — which  is  small,  and  a  lower  curved 
portion.  This  is  large  and  jointed — the  labium — inside  which 
are  four  stylets,  the  two  outer  being  the  mandibles,  and  the  two 
inner  the  maxillae.     There  are  no  palpi.     The  prothorax  is  semi- 


764 


HEMIPTERA 


lunar,  with  two  rounded  horns.  The  dorsum  is  raised  in  the  median 
line.  The  mesothorax  is  triangular,  with  the  apex  posteriorly. 
The  metathorax  is  covered  dorsally  by  the  elytra,  which  are  two 
small  chitinous  plates  belonging  to  the  mesothorax,  but  consist  of 
clavus,  corium,  empodium,  cuneus,  and  membrane.  The  abdomen, 
which  is  rounded  in  shape,  with  seven  segments  and  an  eighth  anal 
appendage,  is  broadest  opposite  the  third  segment.  Posteriorly  it 
is  covered  with  round  hairs.  Length,  5  to  6  millimetres.  Male 
smaller  than  female,  with  penis  flexed  into  a  notch  between  seventh 
and  eighth  segments. 

Internal  Anatomy. — The  mouth  leads  into  the  pharynx,  beneath 
which  is  a  syringe  organ  or  salivary  pump,  into  which  the  salivary 
glands  open.  The  pharynx  leads  via  the  oesophagus  into  a  large 
crop.     There  is  the  usual  mid-gut,  intestine,  and  rectum. 


Fig.  373. — Clinocoris    leclularhis 
L.:  Male.     (X  10.) 


Fig.  374. — Clinocoris    lectularius 
L.:  Female.    (X  10.) 


Life-History.— They  live  in  cracks  in  floors,  walls,  and  furniture 
during  the  day,  and  issue  forth  at  night  to  suck  blood  from  human 
beings.  They  are  capable  of  emigration  from  house  to  house. 
The  female  lays  some  fifty  eggs  three  or  four  times  a  year.  Com- 
plete development  is  said  to  require  eleven  weeks,  but  may  be 
completed  in  as  short  a  time  as  seven  weeks. 

The  eggs,  which  are  oval,  I-I2  millimetres  in  length,  and  white  in 
colour,  take  about  seven  to  ten  days  to  hatch.  The  larva  grows 
slowly,  moulting  about  five  times,  at  intervals  of  about  eight  days, 
after  which  the  wing-pad  appears,  showing  that,  the  adult  stage 
is  reached.     They  feed  only  upon  blood. 

Bionomics— Bite.— In  biting,  they  extend  the  proboscis,  and  feel 
about,  testing  the  skin  with  the  delicate  hairs,  then  pierce  it  by 
the  stylets,  and  inject  saliva  by  the  syringe,  causing  congestion  of 
the  area,  when  the  blood  runs  up  the  grooves  in  the  stylets  by 
capillary  attraction  into  the  pharynx. 


CLINOCORIS 


7&5 


Smell. — The  peculiar  odour  is  due  to  the  secretion  of  sac-like 
glands  situated  at  the  base  of  the  abdomen,  and  opening  on  each 
side  of  the  metasternum.  The  secretion  is  a  .clear,  oily,  volatile 
liquid,  which  is  supposed  to  be  protective  in  function. 

Pathogenicity. — It  is  quite  possible  that  they  spread  Spiroschau- 
dinnia  recurrentis,  the  cause  of  Obermeyer's  relapsing  fever.  The 
effects  of  their  venom  have  already  been  described. 

Prophylaxis. — Bugs  are  by  no  means  without  their  enemies,  of 
which  the  most  marked  is  the  common  red  house-ant  (Monomorium 
pharaonis),  while  another  enemy  is  the  common  cockroach;  but, 
despite  these  foes,  bugs  are  extremely  common  in  tropical  hospitals. 


Fig.  375. — Clinocoris   rotundatus 
Signoret:  Male.     (X  i°-) 


Fig.    376. — Clinocoris    rotundatus 
Signoret:  Female.     (X 10.) 


The  first  step  in  prophylaxis  is,  of  course,  strict  cleanliness,  and  the 
use  of  painted  iron  bedsteads  which  can  be  easily  taken  to  pieces 
and  washed.  Another  good  means  is  to  make  use  of  mattresses 
and  pillows  covered  with  Willesden  canvas,  which  can  easily  be 
washed.  The  mattress  should  be  in  sections,  and  not  all  in  one 
piece,  as  otherwise  it  is  difficult  to  manipulate.  The  most  useful 
substances  for  killing  bugs  are  acetic  acid,  camphor,  and  carbolic 
acid.  Acetic  acid  poured  into  the  joints  of  a  bedstead  is  said  to  kill 
the  bugs  rapidly.  Kerosene  is  often  used,  but  does  not  appear  to 
be  very  effective.  P3rrethrum  is  also  used.  Apart  from  bedsteads, 
the  whole  room  may  be  infected,  in  which" case  fumigation  with 
sulphur  is  quite  the  best  remedy,  4  ounces  being  burnt  for  each 
1,000  cubic  feet  of  space,  and  the  room  left  closed  for  four  or  five 
hours,  in  order  that  the"gas"may  act  thoroughly. 


766  HEMIPTERA 

Clinocoris  rotundatus  Signoret,  1852. 

Synonyms. — Cimex.  rotundatus  Signoret,  1S52:  Cimex  macro- 
cephalus  Fieber,  1861.  This  is  the  Indian  bed-bug,  which  is  found 
in  India,  Ceylon,  Burma,  Assam,  and  Malaya  in  Asia,  and  also  in 
Sierra  Leone,  Mauritius,  Reunion,  St.  Vincent,  and  Porto  Rico. 

Morphology ,—C.  rotundatus  differs  from  C.  lectularius  by  being 
darker  in  colour,  with  a  shorter,  narrower  head,  with  a  prothorax 
with  rounded  borders,  and  with  a  longer,  narrower  abdomen. 

Pathogenicity, — According  to  Patton  it  spreads  Leishmania 
donovani ,  the  parasite  of  kala-azar  or  tropical  febrile  splenomegaly. 

Clinocoris  ciHatus  Eversmann,  1841. 

Synonym. — Cimex  ciliatus  Eversmann,  1841. 

This  bug  is  found  in  Kasan,  in  Russia.     It  requires  reinvestigation. 
Morphology. — It  is  smaller  than  C.  lectularius,  yellowish-red  in  colour,  and 
thickly  covered  with  hairs.     Length,  3-3  millimetres. 
Pathogenicity. — Not  known. 

Genus  GEciacus  Stal,  1873. 

ClinocoridcB  with  the  anterior  margin  of  the  thorax  slightly  excavated,  and 
with  only  slightly  projecting  lateral  angles. 

Type  Species. — CEciacus  hirudinis  Jenyns,  1839;  also  CEciacus  vicarius  in 
martin  and  swallow  nests  in  North  America. 

Loxaspis  Rothschild,  19 12. 

ClinocoridcB  with  anterior  margin  of  thorax  very  narrow,  scutellum  trans- 
versely oblong,  with  posterior  margin  produced  centrally  into  a  point. 

Type  Species. — L.  mirandus  Rothschild,  found  on  a  bat  in  Uganda,  and  found 
in  1 91 3  by  Marshall  on  bats  in  Sennaar,  Anglo-Egyptian  Sudan;  also  L. 
seminiteus  on  bats  in  Java,  L.  barborus  Roubaud,  1913,  on  bats,  and  bites  man. 

Genus  Cacodmus  Stal,  1873. 

C.  villosus  on  Natal,  Transvaal,  and  Nyassaland  bats;  C.  is;notus  on  African 
bats;  C.  indicus  on  Indian  bats. 

Genus  Aphraraia  Champion,  1900. 
Aphramia  barys. 

Genus  Hsematosiphon  Champion,  1900. 
H.  inodorum,  usually  found  on  fowls,  but  ma}-  enter  dwellings. 

Genus  Bertilia. 

B.  valdiviana  under  the  bark  of  trees  in  Chili. 

Genus  Leptocimex  Roubaud,  19 13. 

L.  boneti,  synonym  Cimex  boneti  Brumpt,  1901,  found  on  man  in  the  higher 
regions  of  the  Ivory  Coast  and  in  Haute-Guinec. 

Family  Anthocorid^e. 

Gymnocerala  with  embolium,  membrane  with  one  to  four  nerves,  which 
arise  at  the  tip  and  along  the  side  of  a  triangular  basal  cell.  Antennae  cylin- 
drical. 

Genera.- -Antkocoris  Fallen,  1829,  and  Lyctocoris  Hahn,  1835. 


RED!TVIID.Z  767 

Anthocoris  Fallen,  1829. 
Two  species  of  importance — A.  kingi  Brumpt,  1910,  in  the  Egyptian  Sudan, 
and  A.  congolensis  Brumpt,  1910,  in  the  Belgian  Congo. 

Lyctocoris  Hahn,  1835. 
Lyctocoris  campestris  Fabricius  is  said  to  attack  man. 

Family  REDUviiDiE. 

Gymnocerata  with  long,  narrow  heads  and  distinct  neck.  Eyes 
large  and  prominent;  proboscis  short,  thick",  and  curved;  antennae 
long,  slender  at  the  tip;  legs  long;  elytra  with  three  divisions  when 
present;  tarsus  three-jointed. 

The  genera  which  will  be  noted  here  are:  Reduvius,  Conorhinns, 
Lamus,  Reduviolus,  Rasahus,  Melanolestes,  but  Harpactoy,  Eulyes, 
Arilus,  Prionotus  also  bite  man  and  animals. 

In  addition,  it  may  be  mentioned  that  Wellman  found  Phonergates  bi- 
coloripes  Stal,  which  is  locally  known  as  '  ochindundu,'  in  the  act  of  sucking 
the  juices  of  Omithodoros  monbata.  It  is  well  known  that  the  Reduviidae 
attack  other  insects  and  ticks.  He  also  mentions  that  the  same  insect  pro- 
duces a  more  painful  effect  upon  man  than  the  bite  of  the  tick  O.  moubata. 

Reduvius  Fabricius,  1803. 

Body  moderately  elongate,  head  oblong,  ante-ocular  portion  of  head  larger 
than  post-ocular  portion;  eyes  large,  completely  extending  across  the  lateral 
parts  of  the  head;  rostrum  with  second  joint  much  larger  than  first;  pro- 
notum  transversely  constricted  before  the  middle  anterior  lobe  with  a  strong 
central  sulcus  or  fissure,  which  is  broadly  extended  to  the  disc  of  the  posterior 
lobe.  Anterior  much  shorter  than  posterior  lobe.  Scutellum  with  apical 
spines;  legs  moderately  long  and  slender;  anterior  femora  normal;  anterior 
tibire  furrowed. 

Reduvius  personatus  Linnaeus,  1758. 

This  is  the  wheel  or  masked  bug  found  in  Europe  and  the  United  States, 
and  known  for  the  severity  of  its  bite;  for  it  causes  pain,  swelling,  and 
irritation  in  the  affected  area  which  may  last  as  long  as  a  week. 

Conorhinus  Laporte,  1832. 

Synonym. — Triatoma  Wolf,  1802. 

Reduviidce  with  head  long,  porrect,  and  more  or  less  distinctly  im- 
pressed behind  eyes;  rostrum  with  first  joint  very  much  shorter 
than  second;  antennae  inserted  on  the  sides  of  the  head  about  mid- 
way between  eyes  and  apex ;  ocelli  placed  very  far  apart ;  prosternum 
broadly  sulcated;  abdomen  frequently  with  the  disc  flattened; 
posterior  tibiae  longer  than  the  femora. 

The  species  of  Conorhinus  are  mostly  found  in  South  America, 
and  live  on  the  blood  of  mammals  and  of  insects,  including  bed-bugs. 
Some  of  the  more  important  are: — C.  sanguisugus,  C.  rubrofasaatus 
de  Geer,  C  renggeri  Herrich-Schaeffer,  C.  nigrovarius,  C.  protract  us, 
and  C.  variegatus. 

Conorhinus  sanguisugus  Lccontc,  1855. 

This  is  the  blood-sucking  cone  nose  of  America,  which  feeds  upon  the  blood 
of  insects,  including  bed-bugs,  and  of  mammals,  including  man.     The  bite  is 


768 


HEMIPTERA 


very  severe,  and  causes  much  swelling  and  irritation.     It  is  a  night-flier,  and 
has  an  odour  like  that  produced  by  bugs. 

Morphology.— It  is  a  large  dark  brown  insect,  with  pink  markings  and  a 
flattened  body  and  very  narrow  pointed  head,  with  a  strong,  thick,  long 
proboscis.     The  thorax  is  provided  with  wings. 

Life-History. — The  eggs  when 
first  laid  are  white,  but  later 
change  to  yellow,  and  finally  to 
pink.  The  larva  hatches  in 
about  twenty  days,  and  is  very 
active.  It  moults  twice  and 
becomes  the  pupa,  which  also 
moults  twice,  the  last  stage  show  - 
ing  wing  pads.  The  pupa  is  also 
active. 

Habits. — In  addition  to  feed- 
ing upon  blood,  these  insects 
may  suck  the  juices  of  decom- 
posing flesh. 

Pathogenicity. — Its  bite  at 
times  is  followed  by  severe 
general  symptoms,  such  as  swell- 
ing in  different  parts  of  the  body, 
nausea,  etc.,  as  well  as  local  pain. 
Remedy. — Sweet  oil  is  advised 
as  a  remedy  for  the  local  pain. 

Conorhinus  rubrofasciatus  de 
Geer.  This  is  the  Malay  bug, 
found  in  Africa  (Sierra  Leone 
and  Madagascar),  in  Asia  (Cey- 
lon, India,  Malaya,  China,  and  the 
Philippine  Islands).  It  is  said  to 
produce  a  very  severe  bite.  Con- 
orhinus renggeri  Herrich-Schaeffer  is  the  black  bug  of  the  Pampas.  Conorhinus 
nigrovarius  is  the  '  bichugue  '  of  South  America,  and  bites  severely.  Cono- 
rhinus proiractus  is  the  big  bed  bug  of  Utah. 


Fig.  377. — Conorhinus  sanguisugus 
Leconte,  1855:  Female.     (X2.) 


Lamus  Stal,  1859. 

Reduviidce  with  the  head  much  shorter  than  the  thorax,  with  a 
conical  preocular  portion,  with  the  basal  segment  of  the  rostrum 
longer  than  the  apical.  Antennae,  which  are  inserted  a  little  in 
front  of  the  eyes,  are  more  than  twice  as  long  as  the  head,  ocelli 
present.  Scutellum  unarmed;  legs  rather  slender;  anterior  femora 
slightly  thinner  than  the  posterior,  and  armed  with  spines. 


Lamus  megistus  Burmeister. 

Synonym. — Conorhinus  megistus  Burmeister;  Triatoma  megista. 

Chagas  has  demonstrated  that  Lamus  megistus  is  the  carrier  of 
Trypanosoma  cruzi.  This  Reduvid  attacks  men  and  animals,  and, 
owing  to  its  habit  of  biting  the  face,  is  called  '  Barbeiro  '  by  the 
indigenous  population. 

Morphology. — L.  megistus  Burm.  is  a  large  black  insect  with 
numerous  regularly  arranged  red  markings,  and  differs  from  C.  rubro- 
fasciatus de  Geer,  whi~h  is  closely  allied  to  it,  by  the  fact  that 


LAM  US  MEGISTUS 


'/'"> 


C.  rubrofdsciatus  is  of  a  dull  dark  brown  colour  with  markings  on 
the  pronotum,  and  with  dusky  yellow  or  brick-red  elytra  and 
connexivum. 

Pathogenicity. — It  is   the    cause   of    South   American   trypano 
somiasis. 


Fig.  378. — Lamus  megistus  13urmeister:  Female.     (X2.) 

Reduviolus  Kirby,  1837. 

Reduviolus  subcolcoptratus  Kirby,  1837,  has  once  been  recorded  as  a  human 
blood-sucker  in  the  United  States. 

Rasahus  Amyot  and  Serville,  1843. 

Rasahus  biguttatus  Say,  1831,  is  found  in  the  houses  in  Cuba,  Panama,  and 
Para,  where  it  really  seeks  the  bed-bug,  but  bites  man  also. 

Melanolestes  Stal,  1866. 
Melanolestes  morio  Erichson,  1848.     Found  under  stones  during  the  day  in 
Guiana.  Mexico,  and  the  United  States  of  America.     Bites  man. 

M.  abdominal  is  Herrich-Schaeffer,  1848,  in  the  same  regions  as  M.  morio. 


Family  HYDROMETRiDiE. 

The  Hydrometridae,  or  water-bugs,  are  interesting  to  the  student  of  tropical 
medicine,  because  Patton  has  traced  out  the  development  of  a  Crithidia 
resembling  Leishuiania  donovani  in  one  of  them,  as  has  been  described  in  the 
chapter  on  Protozoa,  p.  567 

49 


770  HEMIPTERA 

Family  Aradid.e. 

Broad,  very  flat  bugs,  with  lour  segments  in  the  antenna  and  three  in  the 
proboscis.     No  cuneus.     Tarsus  two  segments. 

Dysodips  luwaius  Fabricius  is  the  '  Pito  '  bug  of  South  American  houses, 
which  bites  severely. 


REFERENCES. 

The  older  literature  can  be  found  in  Denny  (1842),  '  Monographia  Anopluro- 
rum  Britannia;.'     London. 

Hemiptera. 

Burmeister.     Rhyncota. 

Distant.     Fauna  of  British  India,  vols.  i.  and  ii. 

Eversmann  (1841).     Bull.  Soc.  Imp.  d.  Natur.  Moscou,  p.  351. 

Fierer.     Die  Europaischen  Hemiptera. 

Howard    and    Mari.att    (1896).     U.S.    Department    of   Agriculture.     Bur. 

Ent.,  Bull.  No.  4  (New  Series). 
Jenyns  (1893).     Annals  and  Magazine  of  Natural  History,  vol.  iii.,  p.  241. 
Landois  (1869).     Zeits.  f.  w.  Zoologie,  xviii.,  186S;  xix. 
Patton  (1907).     Scientific  Memoirs,  India,  No.  31. 
Signoret  (1852).     Ann.  Soc.  Ent.  de  France,  x.  539. 
Southall.     A  Treatise  of  Bugges. 

Reduviidae. 

Chagas  (1909).     Bulletin  de  la  Societe  de  Pathologie  Exotique. 

Darwin  (1888).     Voyage  of  the  Beagle,  p.  330. 

Darwin  (1S98).     U.S.  Department  of  Agriculture,  B.  Entomology,  Bull.  iS 

(New  Series). 
Darwin    (1900).     U.S.   Department   of   Agriculture,    B.    Entomology,    Bull. 

No.  22. 
Howard  and  Marlatt  (1896).     Household   Insects.     U.S.  Department  of 

Agriculture,  Bureau  Ent.,  No.  4  (New  Series). 
King  (1900).     U.S.  Department   of   Agriculture,  Bureau  Entomology,  Bull. 

No.  22. 
Theobald  (1903).     First  Report  Economic  Zoology. 
Wfllman  (1900).     Journal  of  Tropical  Medicine,  ix.  373. 


CHAPTER  XXXII 

THE    DIPTERA 

CULICID^E  AND  THEIR  ALLIED  FAMILIES 

Diptera  :     Morphology — -Classification — Culicidae — Corethridae — Chironomida? 
— Psychodidae — Simulida; — References. 

DIPTERA. 

Definition.- — Hexapoda  with  two  well-developed  transparent  wings 
and  two  rudimentary  wings  in  the  form  of  halteres.  Mouth  parts 
well  developed,  adapted  for  piercing  and  sucking  or  for  suction. 
Mesonotum  forms  by  far  the  larger  portion  of  the  thorax.  Meta- 
morphosis is  complete. 

Remarks. — The  Diptera  are  by  far  the  most  important  order  of 
the  Hexapoda  as  regards  tropical  medicine,  for  they  include  the 
blood-sucking  flies,  which  are  capable  of  carrying  disease;  also 
certain  flies  which  cause  disease  by  depositing  their  eggs  in  cavities 
or  on  the  surface  of  the  body,  with  the  result  that  the  larvae  enter  the 
nose,  and  cause  disease  by  gnawing  away  mucous  membrane, 
cartilage,  and  even  bone,  or  the  alimentary  canal,  in  which  they  may 
cause  serious  symptoms.  Apart  from  these,  it  must  be  remembered 
that  flies,  particularly  the  common  house-fly,  may  mechanically, 
either  externally  or  by  its  alimentary  canal,  carry  and  deposit  germs 
on  food,  by  which  means  human  beings  become  infected  with  disease. 

Morphology. — The  most  important  points  in  the  morphology  of  the  Diptera 
in  general  may  be  briefly  mentioned. 

Head. — The  head  in  certain  families  shows  an  anterior  depressed  area, 
the  lunula,  bounded  by  an  arched  suture,  which  passes  over  the  base  of  the 
antenna?.  This  is  the  invaginated  '  ptilinum,'  or  vesicle,  by  which  the  imago 
breaks  its  way  out  of  the  pupa.  With  regard  to  the  antenna,  it  is  of  great 
importance  whether  it  is  many-  or  few-jointed.  In  the  latter  case  it  often 
carries  an  arista  on  the  third  joint,  which  may  be  looked  upon  as  represent- 
ing the  remainder  of  the  larger  antennas  of  other  species. 

The  mouth  parts,  though  composed  of  the  typical  labrum,  epipharynx, 
maxillae,  mandibles,  hypopharynx,  and  labium,  will  be  found  to  be  very 
different  in  the  various  species  of  biting  flies.  More  especially  are  the  labial 
palps  altered  in  Glossina  and  Sfomo.vvs,  becoming  armed  with  teeth  and 
ile  ol  making  the  hole  in  the  skin  which  is  necessary  for  the  sucking  of 
the  blood. 

Thorax.—  In  many  <  ,is<-s  the  thorax  is  largely  composed  of  mesothorax, 
the  pro-  and  mcta-thoraces  being  much  reduced.  The  wings  arc  of  impor- 
tance. Some  genera  possess  a  prolongation  backwards,  called  the  squama, 
which  conceals  the  halter.     The  venation  of  the  wing  has  a  peculiar  nomen- 

771 


772  THE  DIPT  ERA 

clature,  which  will  be  more  fully  explained  under  the  heading  Culicids,  but 
which  may  here  be  compared  with  the  typical  arrangement  of  Comstock  and 
Xeedham,  from  which  it  differs  mainly  by  the  form  of  coalescence  called 
'  inward,'  which  means  that  two  veins  have  coalesced  from  the  tip  towards 
the  base  of  the  wing. 

Typical  Names.  Dipteral  Names. 

Costa      .  .  .  .  .  .  .  .        Costa. 

Subcosta  . .  . .  .  .        Subcosta. 

Radius  i  .  .  . .  . .        First  Longitudinal. 

•n>   a-       Z     Coalesced  .  .  .  .        Second  Longitudinal. 

Radius  3  J  a 

a  m  Coalesced  .  .  .  .        Third  Longitudinal. 

Radius  5  J  ° 

Media  i  "| 

Media  2  |  Coalesced    more   or  ~\    r,       ,,    T         -,     ,.      . 

Media  3  |        less        .  .  .  .  )   Fourth  Longitudinal. 

Media  4  J 

Cubitus  O         Fifth  Longitudinal. 

Cubitus  2  J  ° 

^na!   r      \ Sixth  Longitudinal. 

Anal  2      J  ° 

Anal  3  . .  . .  . .  . .        Seventh  Longitudinal. 

The  above  table  shows  the  two  ordinary  systems  of  nomenclature  for  the 
wing-veins  of  the  Diptera  at  present  in  use.  The  terms  in  the  right-hand 
column  are  older  than  the  other  series,  and  are  generally  employed  by  English 
writers.  In  addition  to  the  longitudinal  veins  there  are  several  transverse 
veins,  viz. : — 

1.  The  Humeral  from  the  Costa  to  Subcosta. 

2.  The  Radio-medial  or  anterior  from  the  Radius  to  the  Media. 

3.  The  distal  Medio-cubital  or  posterior  from  the  Media  to  the  Cubitus. 

4.  The  proximal  Medio-cubital  or  anterior  Basal. 

5.  The  Cubito-anal  or  posterior  Basal. 

The  wing  shows  a  costal  cell,  generally  subdivided  by  the  humeral  vein,  a 
subcostal,  a  marginal,  a  variable  number  of  submarginal,  a  posterior,  and  an 
anal  cell.  The  second  anal  vein  is  often  wanting,  and  represented  by  merely 
an  incrassation.  In  addition  there  are  generally  an  anterior  or  radial,  a 
posterior  medial,  and  an  anal  or  cubital  basal  cell.  In  the  Oulicidac  the  first 
submarginal  and  the  second  posterior  cells  are  often  called  the  fork  cells.  In 
the  first  posterior  cell  it  is  important  to  note  whether  it  is  closed,  and  does  not 
reach  the  margin  of  the  wing  owing  to  the  junction  of  the  media  with  the 
radius,  or  open,  or  partially  open,  and  does  reach  the  margin  of  the  wing.  A 
distal  cell  in  the  middle  of  the  wing  is  present  in  some  genera.  It  is  bounded 
either  by  the  media  or  by  that  vein  and  the  cubitus. 

The  legs  possess  the  usual  number  of  segments,  but  with  regard  to  the 
nomenclature  of  these  segments  there  is  a  certain  amount  of  confusion.  The 
fifth  tarsal  segment  carries  two  claws  and  usually  two  pulvilli  or  pads,  while 
between  them  lies  the  empodium  in  the  form  of  a  bristle  or  third  pad,  which 
may  be  looked  upon  as  a  sixth  tarsal  or  claw  segment. 

Abdomen. — Tins  has  usually  nine  segments,  which  may  be  reduced  by  the 
fusion  of  segments,  especially  in  connection  with  the  male  and  female  genera- 
tive organs.  The  genitalia,  especially  the  male,  are  of  importance  in  ciassifica- 
lion,  and  will  be  mentioned  in  detail  under  the  heading  Culicidae. 

The  body  is  adorned  by  s<  ales  and  hairs.  The  former  have  been  made  use 
01  by  Theobald  to  classify  the  Cnliddae,  while  the  latter  may  be  strongly 
ped  in  places,  and  1  ]  in  flies  as  a  help  in  classification, 

and  are  of  the  utmost  importance  in  fleas. 

Flies  are  usually  modest  in  colour,  being  often  yellowish,   brownish,  or 


ORTHORRHAPHA  773 

blackish,  but  some  of  the  Cuhcidsc- — e.g.,  Megarhina — are  brilliantly  coloured. 
The  colours  depend  partly  upon  pigments  and  partly  upon  interference  with 
or  reflection  of  light. 

Life-History.— The  female  generally  lays  eggs;  more  rarely  a 
larva  is  produced  directly,  as  in  Glossina.  The  eggs  are  laid  in 
some  material  which  will  be  useful  to  the  larvae— e.g.,  the  eggs  of 
Culicidae  in  water  and  the  eggs  of  Muscidae  often  in  decomposing 
matter.  The  larva  is  generally  a  very  active,  vigorously  feeding 
little  grub,  which  may  or  may  not  have  a  distinct  head.  The  pupa 
may  either  remain  in  the  old  larval  skin  which  forms  the  puparium— 
such  a  pupa,  as  seen  in  the  Muscidae,  belongs  to  the  coarctate  type 
—or  it  may  not  be  so  enclosed,  but  the  body  and  appendages  being 
closely  united,  it  forms  the  obtectate  type.  The  imago  escapes 
from  its  pupal  skin  by  a  T-shaped  slit  (Orthorrhapha),  or  by  a 
circular  opening  (Cj'clorrhapha). 

Collection  of  Flies. — Air.  Austen  has  asked  us  to  invite  the  reader's  attention 
to  certain  remarks  of  his  taken  from  the  second  report  of  the  Wellcome 
Research  Laboratories,  which  are  as  follows: — 

1.  Specimens  of  blood-sucking  and  other  Diptera  intended  for  determina- 
tion should  be  in  the  most  perfect  possible  condition. 

2.  Specimens  collected  by  natives  seldom  fulfil  this  condition. 

3.  Flies  should,  if  possible,  always  be  transfixed  by  a  pin  through  the  thorax 
and  pinned  to  a  small  piece  of  cardboard,  and  should  be  drawn  up  near  the 
head  of  the  pin,  and  not  left  close  to  the  point. 

4.  If  pinning  is  impossible,  specimens  are  best  placed  in  three-cornered 
envelopes  of  soft  paper. 

5.  Flies  should  never  be  placed  in  contact  with  dry  cotton-wool . 

6.  A  plug  of  soft  paper  must  always  be  pressed  down  on  top  of  specimens 
placed  in  spirit,  in  order  to  fix  them  in  the  tube. 

7.  Several  specimens  of  both  sexes  should  be  sent  if  identification  is  desired. 

8.  Specimens  should  always  be  legibly  labelled,  with  the  name  of  locality, 
and  date  of  capture,  and  notes  of  interest  forwarded  at  the  same  time. 

Classification. — -The  Diptera  may  be  classified  as  follows,  according 
to  the  characters  of  the  pupa,  larva,  and  antennae  :— 

SUBORDER  I.  ORTHORRHAPHA. 

Definition. — 'Diptera  without  lunula  or  ptilinum.  Larva  with  a 
distinct  head.  Pupa  obtectate.  Imago  escapes  by  T-shapcd 
opening. 

Section  1:  Meraatocera. — -Orthorrhapha  with  antennae  composed 
of  more  than  six  joints,  with  the  joints,  except  the  first  two,  similar; 
without  arista.     Palpi  four-  or  five-jointed. 

Families. — Culicidae,  Corethridae,  Chironomidae,  Psycho- 
didae,  Simuliidae,  Blepharoceridae,  etc. 

Section  2:  Brachycera. — -Orthorrhapha  with  antennae  in  which 
the  joints  differ  from  one  another,  with  or  without  arista,  which, 
when  present,  is  usually  terminal. 

Tribe  i  :  Brachycera  homeeodactyla.- — Orthorrhapha  brachy- 
cera with  three  well-developed  pulvilli.  Larva  with  a 
projecting  posterior  stigma. 

Families. — Tabanidae,  Leptidae. 


774  THE  DIPTERA 

Tribe  2 :  Brachycera  heterodactyla. — Orthorrhapha  brachy- 
cera  with  two  or  three  pulvilli.  In  the  last  case  the 
middle  is  different  from  the  two  other  pulvilli.  Some 
species  without  pulvilli.  Posterior  stigma  of  the  larva 
in  front  of  the  body-end. 

Families. — Asilidse,  Empidae. 

SUBORDER  II.    CYCLORRHAPHA. 

Definition. — -Diptera  with  a  lunula  and  usually  a  ptilinum. 
Antenna  with  always  three  joints  and  an  arista.  Palpi  one-jointed. 
Mandibles  absent.  Maxillae  rudimentary.  Discoidal  cell  bounded 
by  the  media  and  cubitus.  Abdomen  with  seven  segments  at  the 
most,  often  with  less. 

Section  1:  Aschiza. — -Cyclorrhapha  with  a  clearly  defined  lunula, 
but  a  rudimentary  ptilinum.     Arista  poorly  developed. 

Families. — -Not  of  interest  in  tropical  medicine. 

Section  2:  Schizophora. — Cyclorrhapha  with  lunula;  at  times 
absent,  but  the  arched  suture  over  the  antennae  is  well  defined. 
Ptilinum  usually  well  developed.  Antennae  lie  in  separated  hollows. 
Arista  well  developed. 

Tribes:  Muscidce  acaly pirates  and  Muscidce  calyptratce. 

SUBORDER  III.    PUPIPARA. 

Definition. — Diptera  with  well-developed  rudimentary  or  no  wings ; 
parasitic  on  vertebrates.  The  fully-developed  larvae  are  passed 
directly  from  the  body  of* the  imago  without  a  free-living  egg  stage. 

SUBORDER   ORTHORRHAPHA. 

section  nematocera. 

Family  Culicid^e. 

Definition. — Orthorrhapha  nematocera  with  a  long  piercing  pro- 
boscis, and  a  body  more  or  less  clothed  with  scales  and  hairs. 
Antennae  with  whorls  of  hairs  or  plumes,  which  may  be  dense  and 
long  in  the  male,  though  scanty  in  the  female.  Wings  with  six  to 
seven  longitudinal  veins,  with  scales  and  two  distinct  fork  cells. 
The  costa  passes  all  round  the  wing,  and  carries  scales,  which  form 
a  fringe.     Metamorphosis  complete. 

The  Culicidae  include  the  flies  which  we  call  mosquitoes,  a  word 
which  is  derived  from  the  Spanish,  meaning  little  flies,  and  are  the 
same  as  gallinippers  in  America.  The  genus  Ctilex  was  formed  by 
Linnaeus  in  1790  for  the  gnat  Culex  pipiens  ;  the  genus  Anopheles, 
from  a  Greek  word  meaning  harmful,  by  Meigcn  in  1818;  the  genus 
Stegomyia  by  Theobald  in  1901.  A  great  many  other  genera  have 
also  been  described,  but  are  not  so  important  in  tropical  medicine 


CULICID.E 


775 


as  these  three.  Among  the  early  workers  in  this  held  of  research 
special  prominence  must  be  given  to  the  names  of  Arribalzaga  and 
Ficalbi. 


ITo.  379.— Diagram  of  a.  Mosquito. 

(After  Theobald,  from  '  The  Culicidae  of  the  World.') 

Pr.,  proboscis;  P.,  palp;  An.  antenna;  E.,  eye;  Oc,  occiput;  Pro.,  prothorax; 
Mes.,  mesothorax;  Scu.,  scutellum,  behind  which  is  seen  (Met.)  the  shield-like 
post-scutellum;  //.,  halter;  Abd.,  abdomen;  Ovp.,  ovipositor;  Wi.,  wing;  Fe., 
femur;  Ti.,  tibia;  1//..  metatarsus;  Ts.,  tarsus — -the  line  indicating  the  tarsus 
is  made  to  include  the  metatarsus,  which  is  sometimes  regarded  as  the  first 
tarsal  joint. 


In  onr  description  of  the  classification  of  the  Culicidae  we  have 
follouvtl  Theobald,  but  a  simpler  system  is  urgently  required  and 


776 


THE  DIPTERA 


mav  be  evolved  during  the  next  few  years,  as  there  are  already  signs 
that  such  a  system  may  be  possible. 

Careful  dissections  of  Anopheles  have  been  made  by  ISiuttall  and 
Shipley,  and  of  Culex  by  Christophers,  while  the  larva  and  pupa  of 
A  nopheles  have  been  studied  in  detail  by  Tmms. 

As  the  Anopheles  is,  without  doubt,  of  the  greatest  importance 
to  medical  men,  its  anatomy  will  be  described. 


Fig.  381. — Distal  End  of  the  Proboscis 
of  Ancpheles  macuhj-ennis  Meigen. 

1,  Labium;  2,  labeilae;  3,  labrum- 
epi pharynx;  4,  maxillae;  5,  mandibles; 
6,  skin  line.  (The  labeilae  should  be  diver- 
gent to  the  plane  of  the  paper.) 


Fig.  380. — Transverse Section 
of  the  Proboscis  of  Ano- 
pheles maculipennis  Meigen. 

(After  Nuttall  and  Shipley,  from 
the  Journal  of  Hygiene.) 

1,  Labium;  2,  maxilla;  3, 
hypopharynx,  with  salivary 
duct;  4,  mandible;  5,  labrum- 
epipharynx  with  the  figure  (5) 
placed  in  the  blood-tube. 

Morphology.— A  nopheles  maculipennis  Meigen  has  been  studied  by  Nuttall 
and  Shipley,  whose  account  is  followed  in  the  description  given  below. 

The  body  of  a  mosquito  is  divided  into  (a)  head,  (/>)  thorax,  (c)  abdomen. 

Head.- — The  most  conspicuous  objects  on  the  head  are  the  two  large 
reniform,  often  brilliantly  coloured  eyes,  which  lie  on  a  piece  of  exoskeleton, 
called  the  '  epieranium,'  which  covers  the  whole  head,  except  in  the  ventral 
median  line,  where  the  gula  can  be  seen.  Dorsally  the  eyes  nearly  meet,  being 
separated  by  a  space  called  the  '  vertex,'  in  front  of  which  is  the  frons,  which 
carries  a  pair  of  antennae,  different  in  male  and  female.  The  male  antenna 
has  sixteen  segments,  of  which  the  first  segment  is  very  small;  the  second  is 
globular,  and  contains  an  auditory  organ;  the  third  is  long,  and  the  fourth 
to  the  fifteenth  carry  twenty- five  to  thirty  hairs  in  whorls  at  the  proximal  end 
of  each  segment.  The  sixteenth  segment  is  about  half  as  long  as  the  penulti- 
mate. So  dense  are  the  whorls  of  verticillate  hairs  in  the  male  that  the  term 
'  plumose  '  is  applied  to  the  whole  antenna.  The  base  of  the  sixteenth  seg- 
ment carries  six  hairs,  and  the  tip  is  rounded.  The  female  antenna  consists 
of  fifteen  segments.  The  first  is  very  small,  merely  a  ring  of  chitin  ;  the  second 
is  deeply  hollowed  for  the  third  segment,  which  is  the  longest.  The  proximal 
ends  of  the  fourth  to  the  fifteenth  carry  six  large  hairs.  The  tip  of  the 
i  segmenl  bears  fine  hairs.  These  few  hairs  produce  quite  a  different 
appearance  in  the  antennae,  which  are  called  '  pilose,' 

In  front  of  the  frons  a  sclerite  called  the  '  clypens,'  belonging  to  the  exo- 


PLATE    I 


ANOPHELES    MACULIPENNIS    MEIGEN. 
Male. 


r.ta  Wai.riton  A  Son«  Lid  Edin 


To  face  Plate  111. 


PLATE    III. 


ANOPHELES   MACULIPENNIS  MEIGEN. 
Female. 

(After  Austen,  by  kind  permission  of  the  Trustees  of  the  British  Museum. ) 


GeoWaterston  &  Son«  Ltd  Edii\ 


To  /cue  fia^e  77« 


CULICID.E 


777 


ma  ine   more   ventral,  conuiiuuua   wmi   me  ummuuo  mmi0  ^*   .— ~   -*~ 

;avity,  is  the  epipharynx;   the  part  in  the  proboscis  forms  a  deep  groove, 
jpen  ventrally.     In  the  female  its  free  end  is  sharp  and  pointed;  in  the  male 


skeleton  of  the  head,  projects  forwards,  under  cover  of  which  the  mouth 
appendages  appear  as  a  median  proboscis  and  two  lateral  palpi. 

These  mouth  parts  are  made  up  of  the  following  [vide  Fig.  22,  p.  224): — 

1 .  Labrum,  or  upper  lip,  with  which  is  combined  the  epipharynx  to  form 
the  labrum  epipharynx. 

2.  The  mandibles. 

3.  The  first  pair  of  maxilke.  to  which  the  palpi  beiong. 

4.  The  hypopharynx. 

5.  The  second  pair  of  maxilla?,  which  have  united  together  to  form  the 
lower  lip  or  labium. 

The  labrum-epipharynx  commences  at  the  head  end  as  two  separate  chitin- 
ous  structures:  the  more  dorsal,  continuous  with  the  clypeus,  is  the  labrum, 
and  the  more  ventral,  continuous  with  the  chitinous  lining  of  the  mout 
c&\ 

open  ventrally. 
it  is  truncated. 

The  mandibles  are  absent 
in  the  males,  while  in  the 
female  they  appear  as  yellow 
delicate  chitinous  blades,  the 
base  of  which  is  attached  to 
the  sides  01  the  labrum,  and 
the  apex  is  knife-shaped,  with 
its  edge  serrated  by  thirty- 
one  fine  teeth  (vide  Fig.  23). 

The  first  maxillae  are  chiti- 
nous rods  attached  posteriorly 
to  the  side  of  the  base  of  the 
labium,  which  is  here  swollen, 
and  carries  on  its  outer  angle 
the  palp.  It  is  continuous 
posteriorly  with  a  chitinous 
bar,  which  runs  backwards 
into  the  head,  and  affords 
attachment  to  several  mus- 
cles. The  free  extremity  of 
the  maxilla  has  thirteen  teeth 
(vide  Fig.  24,  p.  225). 

The  maxillary  palps  pro- 
ject on  either  side  of,  and 
dorsal  to,  the  proboscis.  They 
are  five-jointed,  and  covered 
with  scales.  In  the  male  the 
distal  end  of  the  third  segment 

is  broadened,  and  the  whole  fourth  and  fifth  segments  are  broad  and  flat, 
giving  a  spatulate  appearance  to  the  tip.  The  length  of  these  palpi  varies  in 
the  different  genera  of  the  Culicidre,  as  will  be  mentioned  under  the  heading 
of  Classification. 

The  hypopharynx  takes  its  origin  just  above  the  base  of  the  labium  in  a 
solid  mass  of  chitin,  which  is  pierced  by  the  salivary  duct,  which  is  a  canal  35 
to  36  p.  in  diameter.     In  the  male  the  hypopharynx  is  fused  with  the  labium. 

The  second  maxilla;  arc  united  together  to  form  a  lower  lip.  or  labium, 
which  is  curved  dorsally  so  as  to  form  a  deep  groove,  in  which  the  first  maxilla; 
lie  ventrally  and  laterally,  with  the  hypopharynx  situated  dorsally  and 
mesially,  and  the  labrum-epipharynx  dorsally  with  the  mandibles  on  either 
side.  The  distal  end  carries  two  short  segments  called  '  labelke.'  which  are 
movable  on  hinge-joints.  Between  these  labelke  there  is  a  projection  of 
the  labium  connected  with  them  by  a  thin  membrane — Dutton's  membrane 
—  •which  is  stretched  during  the  act  of  biting.  Through  this  membrane 
filarial  embryos  escape  from  the  interior  of  the  labium.     The  labium  itself 


Fig.  382. — The  Occiput  and  Scutelu'm  of 
an  Anopheline  Mosquito,  to  show  the 
Scale  Characters. 

At  the  side  is  seen  the  lateral  aspect  of 
the  vertical  scale1;. 

(After  Theobald,  from  '  The  Culicida;  of 
the  World.') 


778 


THE  DIPTERA 


is  composed  of  a  double  cuticnlar  wall  carrying  scales  on  its  exterior,  and 
enclosing  internally  a  cavity  containing  muscles,  etc.,  among  which  the 
filarial  embryos  can  lie.  There  are,  therefore,  two  tubes  in  the  proboscis: 
the  first,  large,  formed  by  the  labrum-epipharynx  and  the  hypopharynx,  is 
the  blood-tube,  up  which  the  blood  is  sucked  into  the  pharynx;  while  the 
other,  small,  lying  in  the  hypopharynx,  is  the  salivary  duct.  The  first  is 
afferent,  the  second  efferent. 

Behind  the  eyes  there  is  an  area  of  the  head  called  the  'occiput,*  which 
carries  different  kinds  of  scales  in  different  genera,  as  is  seen  by  the  following 
diagram  (Fig.  383).  These  scales  may  be  differentiated  into  "narrow  curved 
scales,  upright  forked  scales,  and  flat  scales,  the  presence  and  character  of 
which  have  been  made  the  means  of  classification.     The  upright  forked  and 


Fig.  383. — Various  Forms  of  Scales  found  on  Different  Parts  of  a 

Mosquito. 

(After  Theobald,  from  '  The  Culicidse  of  the  World.') 

a,  Flat  scale  from  abdomen;  b,  broad  wing  scale;  c,  another  broad  wing 
scale;  d,  curved  hair-like  scale;  e,  narrow  curved  scale;  /,  flat  spindle-shaped 
scale;  ?,  small  form  of/;  h  and  i,  upright  forked  scales;  j,  twisted  upright 
scale;  k,  inflated  scale. 


the  curved  scales  occupy  the  middle  area  of  the  occiput,  and  alone  are  met 
with  in  this  species;  but  quite  different  arrangements  are  met  with  in  other 
genera.  The  extreme  posterior  area  of  the  head  is  the  nape.  Below  the  eye 
laterally  is  the  area  of  the  head  called  the  '  gena.'  At  the  back  of  the  head  is 
the  occipital  foramen,  through  which  the  soft  structures  pass  to  the  neck. 

Neck. — The  neck  is  the  soft  connection  of  the  head  with  the  thorax.  It  is 
strengthened  with  chitinous  rods. 

Thorax. — The  thorax  shows  the  usual  three  divisions  into  pro-,  meso-,  and 
meta-thorax,  but  of  these  the  mesothorax  is  much  the  largest,  and  is  often 
called  '  the  thorax  ' ;  in  fact,  the  pro-  and  meta-thorax  are  hard  to  see.  It  will 
be  remembered  that  a  typical  thoracic  segment  should  show  dorsally  a  notum, 
composed  of  pra-scutum,  scutum,  scutellum,  and  post-scutcllum;  ventrally 
a  sternum,  and  laterally  a  pleuron,  consisting  of  episternum  and  epimerum. 


CULICID.E  779 

On  the  posterior  portion  of  each  side  of  the  neck  may  be  seen  a  small  sausage- 
shaped  sclerite,  called  the  patagium,  in  front  of  which  is  the  neck  sclerite, 
while  posteriorly  there  is  another  sclerite  reaching  as  far  as  the  hrst  thoracic 
spiracle.  Below  these,  and  reaching  to  the  coxa  ot  the  first  leg,  is  still  another 
sclerite.  These  four  sclerites  make  up  the  prothorax.  The  patagium  may 
represent  a  pronotum,  the  neck  sclerite  an  eoisternite,  and  the  posterior 
sclerite  an  epimerum,  while  the  sclerite  connected  with  the  coxa  of  the  first 
leg  is  undoubtedly  a  prosternum.  This  segment  of  the  thorax  carries  the 
first  pair  of  legs,  and  perhaps  the  first  spiracle. 

The  interpretation  of  the  parts  of  the  prothorax  presents  considerable 
difficulty.  Some  authorities  believe  that  there  is  no  pronotum.  The  meso- 
thorax  is  well  developed,  and  presents  dorsally  a  praescutum  and  scutum 
fused  together,  behind  which  is  a  trilobed  area,  the  '  scutellum.'  Behind  this, 
again,  is  a  shield-shaped  area,  looked  upon  by  some  observers  as  a  metanotum. 
but  more  probably  representing  the  post-scutellum  of  the  mesothorax. 
Laterally  behind  the  first  spiracle  lies  the  episternum  of  the  mesothorax, 
below  and  behind  which  is  the  mesosternum,  wedged  in  between  the  second 
and  third  legs  on  each  side.  The  two  mesosterna  are  bound  together  by  a 
chitinous  bar. 

Between  the  post-scutellum  and  the  first  abdominal  segment  lies  the  minute 
true  metanotum.  The  metasternurn  is  easily  seen  between  the  second  and 
third  pairs  of  legs,  and  the  episternum  of  that  segment  lies  just  dorsal  to 
the  third  coxa,  and  contains  the  second  thoracic  spiracle  as  well  as  carrying 


Fig.  384. — Lateral  View  of  Anopheles  maculipennis  Meigen. 
(After  Nuttall  and  Shipley,  Journal  of  Hygiene.) 
1,  Labium;  2,  labrum-epipharynx;  3,  palp;  4,  antenna;  5,  occiput;  6,  meso- 
thorax   (praescutum  and   scutum);   7,   prothorax;    8,   mesosternum;   9,   first 
thoracic  spiracle;  10,  metasternurn;  11,  second  thoracic  spiracle;  12,  scutellum; 
13,  post-scutellum;  14,  wing;  15,  tergum;  16,  pleural  membrane;  17,  sternum. 

the  halter.  The  thorax  is  covered  with  hair-like  curved  scales,  and  its 
appendages  are  the  legs  and  wings.  There  are  three  pairs  of  legs,  one  for 
each  division  of  the  thorax,  which  have  the  usual  number  of  segments — 
coxa,  trochanter,  femur,  tibia,  metatarsus,  and  tarsus,  the  latter  being  four- 
jointed.  The  last  joint  of  the  tarsus  carries  the  two  claws  or  ungues,  which 
may  be  toothed.  In  the  first  leg  in  the  male  the  claw  is  single,  and  the  first 
terminal  tarsal  segment  is  hollowed  out.  In  the  female  all  the  legs  terminate 
in  a  double  hook,  and  the  first  tarsal  segment  is  not  hollow.  The  empodium, 
a  median  process  projecting  between  the  ungues,  is  in  Anopheles  maculipennis 
reduced  to  a  tuft  of  hairs.  The  arrangements  of  the  ungues,  however,  vary 
very  much  in  different  genera  and  species. 

The  wings  arise  by  their  bases  from  the  side  of  the  mesothorax,  between 
the  scutum  and  the  episternum.  The  anterior  border  of  the  wing  is  straight 
and  thick,  while  the  posterior  is  curved,  and  near  the  base  is  folded  or  indented 
twice  to  form  squama  and  alula.  The  area  of  the  wing,  bounded  by  the 
squama  and  alula,  is  broken  up  by  a  series  of  thickenings  and  ridges  from 
which  the  nerves  take  their  origin.  The  base  of  the  wing  has  a  socket  which 
fits  on  to  a  knob  on  the  episternum.     The  veins  of  the  wings  are: — 

1.  The  Costa. 

2.  The  Subcosta,  which  joins  the  Costa  some  distance  from  the  apex  of  the 
wing. 

3.  The  Radius  1  [First  Longitudinal). — Runs  from  base  to  apex  of  the 
wing- 


780  THE  DIPTERA 

4.  The  Radius  24-3  (Second  Longitudinal). — Commences  in  the  middle  of 
the  wing,  and  shortly  divides  into  two  branches  (Radius  2+3),  enclosing  a 
piece  of  the  wing  called  the  first  submarginal  cell. 

5.  The  Radius  4+5  {Third  Longitudinal  Vein). — Commences  in  the  middle 
of  the  wing  and  runs  to  the  margin. 

6.  The  Media  (Fourth  Longitudinal  Vein). — Runs  from  the  base' of  the 
wing  to  the  margin,  but  forks  (Media  1  +  2)  to  enclose  the  second  posterior  cell. 

7.  The  Cubitus  (Fifth  Longitudinal  Vein). — -Runs  from  the  base  and  forks 
(Cubitus  1  +  2)  to  enclose  the  third  posterior  cell. 

8.  The  Anal  1  +  2  (Sixth  Longitudinal  Vein).- — Runs  a  curved  course  from 
its  margin. 

In  some  mosquitoes  there  is  a  second  anal  vein  (seventh  longitudinal  vein) , 
but  more  often  this  is  only  indicated  by  a  fold  or  incrassation.  There  may 
be  a  vena  spuria  or  marking  between  the  cubitus  and  the  anal  vein. 

9.  Transverse  or  Cross  Veins. 

(a)  The  Humeral,  between  the  Costa  and  Subcosta. 

(b)  The  Radial,  between  Radius  2+3  and  Radius  4+5  (second  +  third 

longitudinal  veins) . 

(c)  The  Radio-medial,  between  the  Radius  and  Media  (third  +  fourth 

longitudinal  veins). 

(d)  The  Medio-cubital,  between  the  Media  and  the  Cubitus  (fourth  4- 

fifth  longitudinal  veins). 

These  veins  mark  out  the  following  cells : — 

1.  The  Costal  cell,  between  Costa  and  Subcosta,  but  subdivided  by  the 
humeral  vein. 

2.  Subcostal  (Mediastinal)  cell,  between  Subcosta  and  Radius  1. 

3.  Marginal  cell,  between  Radius  1  and  Radius  24-3. 

4.  First  Submarginal  cell,  between  Radius  24-3. 

5.  Second  Submarginal  cell,  between  Radius  2+3  and  Radius  24-5. 

6.  First  Posterior  cell,  between  Radius  44-  5  and  Media. 

7.  Second  Posterior  cell,  between  Media  14-2. 

8.  Third  Posterior  cell,  between  Media  and  Cubitus. 

9.  Fourth  Posterior  cell,  between  Cubitus  14-2. 

10.  Anal  cell,  between  Cubitus  and  Anal  1. 

11.  Axillary  cell,  between  Anal  14-2  and  Anal  3,  when  present. 

12.  Spurious  cell,  behind  Anal  3,  when  present. 

13.  Anterior  Basal  cell,  bounded  anteriorly  by  the  Radius  1,  posteriorly 
by  the  Media,  and  externally  by  the  Radial  transverse  vein. 

14.  Posterior  Basal  cell,  bounded  anteriorly  by  the  Media,  and  posteriorly 
by  the  Cubitus,  and  externally  by  the  Medio-cubital  vein. 

The  wing  has  scales  on  all  its  veins,  except  the  cross  and  the  spurious  veins, 
which  are  arranged  in  two  ways:  (1)  Two  rows  of  flat  scales  on  each  vein; 
(2)  lateral  scales  along  each  vein. 

Generally  these  scales  in  the  Anophelinae  are  lanceolate,  or  long  and  narrow, 
but  one  genus,  Cycloleppteron,  has  large  inflated  scales.  It  will  be  found  that 
scales  vary  much  in  the  different  genera  and  species,  the  principal  forms  of 
which  may  be  gathered  from  the  following:  The  posterior  margin  of  the 
wing  carries  a  fringe  consisting  of  scales  arranged  as  follows:  (1)  Flat  scales; 
(2)  long  lanceolate  scales;  (3)  short  lanceolate  scales  alternating  with  the 
long  lanceolate  scales. 

Abdomen. — There  are  eight  segments  in  the  abdomen,  each  of  which  consists 
of  a  dorsal  plate,  the  tergum,  and  a  ventral  plate,  the  sternum,  joined  together 
by  a  pleural  membrane,  on  which  lie  the  abdominal  spiracles,  said  to  number 
six  or  eight  by  different  observers. 

On  the  posterior  end  of  the  terminal  segment  are  the  external  genital 
organs.  In  the  male  these  consist  of  a  pair  of  large  basal  lobes,  each  termin- 
ating in  a  clasp  segment  armed  with  a  claw,  thus  forming  the  clasper.  The 
arrangements  of  the  male  genitalia  vary  so  much  that  they  have  been  used  as 
a  method  of  classification.  Therefore  it  is  necessary  to  explain  in  a  general 
way  the  terms  used  with  regard  to  the  various  parts  which  may  be  found. 


CULICID.E 


781 


On  the  ventral  surface  of  the  basal  lobe  is  the  tubercle  or  lobe,  called  the 
claspette,  while  from  their  inner  margin,  near  the  base,  a  pair  of  claspers 
called  harpagones,  and  more  distally  another  pair,  the  harpes,  project.  Just 
at  the  junction  of  the  two  basal  lobes  are  another  pair  of  lobes — the  setaceous 
lobes  -which  are  believed  to  be  the  rudimentary  ninth  segment.  The  unci 
are  absent  in  the  Anophelinae,  but  present  as  a  pair  of  ventral  processes  in  the 
Culicinae.     In  the  female  there  are  the  flap-like  ovipositors. 

The  flat  abdominal  scales  of  the  other  Culicidae  are  absent  in  the  Anophelinae, 
except  in  one  genus. 

Internal  Anatomy. — A  few  points  with  regard  to  the  internal  anatomy  of 
the  mosquito  may  be  mentioned. 

Alimentary  Canal.- — -The  alimentary  canal  consists  of:  (1)  Mouth; 
(2)  buccal  cavity;  (3)  pharynx,  or  pumping  organ;  (4)  oesophagus  and  its 
pouches;  (5)  oesophageal  valve,  or  proventriculus;  (6)  mid-gut;  (7)  ileum; 
(8)  colon;  (9)  rectum;  (10)  anus  (vide  Fig.  385). 


Fig.  385. — The  Alimentary  Canal  of  Anopheles  maculipennis  Meigen. 

(After  Xuttall  and  Shipley,  Journal  of  Hygiene.) 

1,  Mouth  and  buccal  cavity;  2,  pharynx;  3,  oesophagus;  4,  dorsal  and  ventral 
oesophageal  diverticula;  5,  proventriculus;  6,  salivary  glands;  7,  narrow 
portion  of  ventriculus;  8,  so-called  stomach;  9,  Malpighian  tubules;  10,  intes- 
tine; 11,  rectum;  12,  anus. 


1.  Mouth. — The  mouth  is  the  place  where  the  maxillae,  mandibles,  labrum- 
epipharynx,  hypopharynx,  and  palps  fuse  together. 

2.  Buccal  Cavity.- — This  extends  from  the  mouth  to  the  valve  between  it 
and  the  pharynx,  and  is  lined  with  chitin,  and  has  an  upward  and  backward 
direction  until  it  approaches  the  pharynx,  when  it  turns  suddenly  upward. 
There  is  a  portion  of  its  roof  which  possesses  a  thinner  cuticle  than  the  rest 
of  the  buccal  cavity,  and  has  been  called  the  soft  palate.  This  structure 
possesses  two  spines  directed  downwards  into  the  lumen  of  the  cavity,  and  has 
attached  to  it  five  pairs  of  palatal  muscles.  It  is  thought  that  as  this  mem- 
brane is  wrinkled,  and  has  muscles  attached  to  it,  it  may  indicate  that  it  is 
used  for  suctorial  purposes.  Posteriorly  there  is  a  valve  between  the  buccal 
cavity  and  the  pharynx,  lying  on  a  level  just  behind  the  posterior  end  of  the 
clypeus.  This  prevents  the  return  of  fluids  to  the  mouth  during  pumping. 
Annett  and  Dutton  described  a  complicated  sense-organ  at  the  junction  of  the 
buccal  cavity  and  the  pharynx,  but  this  has  not  been  confirmed. 

3.  Pharynx. — The  pharynx  extends  from  the  posterior  end  of  the  buccal 
cavity  to  nearly  the  posterior  end  of  the  head,  where  it  ends  in  the  oesophagus. 
It  is  considerably  larger  in  the  female  than  in  the  male,  because  the  former 
sucks  blood,  while  the  latter  does  not.  The  anterior  portion  is  tubular,  and 
passes  through  the  nerve  ring  between  the  supra-  and  in  Ira -oesophageal 
ganglia.  The  posterior  portion  is  triangular,  and  has  a  chitinous  wall  arranged 
into  three  plates,  one  dorsal  and  two  latero- ventral. 

Posteriorly,  near  the  oesophagus,  the  triradiate  pharynx  is  surrounded  by 
a  sphincter  muscle,  and  the  chitin  oi  this  portion  is  marked  by  ridges  which 
end  in  very  line  spines,  making  a  comb-like  appearance,  and  possibly  acting 
as  a  strainer.     The  three  chitinous  plates  have  powerful  muscles  attached 


782 


THE  DIPTERA 


to  them,  of  which  the  two  posterior  dorsal  dilators  run  from  the  occiput  to 
the  dorsal  plate ;  the  two  anterior  dilators  (two  pairs  in  the  female)  taking 
their  origin  from  the  vertex  are  inserted  also  into  the  dorsal  plate,  and  the 
five-paired  latero-ventral  dilators  arising  from  the  lateral  posterior  angle  of 
the  head  pass  upwards  and  a  little  forwards  to  the  latero-ventral  plates. 
When  these  muscles  contract  the  triradiate  pharynx  becomes  nearly  circular, 
and  when  they  relax  the  walls  come  together. 

In  this  way  the  pharynx  pumps  the  blood  from  the  victim  up  the  blood 
tube  in  the  proboscis  into  the  alimentary  canal. 

4.  OEsophagus. — The  short  oesophagus  runs  from  the  pharynx  to  the  oeso- 
phageal valve.  Anteriorly  it  is  narrow,  but  posteriorly  it  expands  so  much 
that  this  portion  is  sometimes  called  the  crop.  It  is  lined  with  thin  chitin, 
and  has  many  bands  of  muscles  attached  to  it.  Its  posterior  end  lies  on  a 
level  with  the  origin  of  the  first  pair  of  legs,  and  at  this  situation  it  gives  off 
three  pouches,  two  dorsal  and  one  ventral.  The  large  ventral  pouch  opens 
into  the  oesophagus  by  a  single  opening  in  the  middle  line,  and  extends  back- 
wards under  the  alimentary  canal  to  the  level  of  the  fifth,  sixth,  or  seventh 
abdominal  segment,  when  fully  distended.  In  shape  it  is  fusiform.  The 
two  small  latero-dorsally  placed  pouches  open  into  the  sides  of  the  oesophagus. 
All  these  sacs  are  lined  with  thin  chitin,  and  have  some  slight  musculature. 


Fig.  386. — The  Alimentary  Canal  of  Anopheles  utaculipennis  in  situ. 

(After  Nuttall  and  Shipley,  Journal  of  Hygiene.) 

1,  Proboscis;  2,  buccal  cavity;  3,  pharynx;  4,  oesophagus;  5,  oesophageal 
pouches;  6,  salivary  glands;  7,  proventriculus;  8  and  9,  mid-gut;  10,  Mal- 
pighian  tubes;  11,  ileum;  12,  colon;  13,  rectum;  14,  rectal  papilla?;  15,  anus. 

5.  The  (Esophageal  Valve  or  Proventriculus.- — The  oesophageal  valve  is  an 
annular  thickening  of  the  intestinal  wall,  due  partly  to  circular  muscles,  which 
are  capable  of  closing  the  lumen  of  the  gut  when  they  contract,  and  partly 
to  an  invagination  of  the  more  anterior  portion  of  the  gut  into  the  more 
posterior,  thus  forming  a  valve.  Projecting  from  it  are  six  small  protuber- 
ances, more  marked  in  the  larva  than  in  the  adult  insect.  Christophers 
considers  that  this  portion  of  the  alimentary  canal  is  the  proventriculus  of 
other  insects.     It  is  not  lined  with  chitin. 

6.  Mid-Gut  or  Chylific  Ventricle. — The  mid-gut  is  a  straight  tube  running 
from  the  oesophageal  valve  at  the  level  of  the  first  pair  of  legs  to  the  posterior 
limit  of  the  sixth  abdominal  segment ;  but  this  varies  as  to  whether  it  is  filled 
with  food  or  not.  It  consists  of  two  parts :  an  anterior  narrow,  and  a  posterior 
more  distended,  often  called  the  '  stomach,'  which  begins  on  a  level  with  the 
second  abdominal  segment,  and  is  the  receptacle  for  the  food.  The  wall  of 
the  stomach  is  composed  of  the  following  layers : — 

(1)  A  delicate  internal  cuticle. 

(2)  A  single  layer  of  large  cylindrical  or  cubical  epithelial  cells  with  large 
nuclei ;  their  condition  varies  with  the  state  of  distension  of  the  stomach. 

(3)  An  elastic  basement  membrane. 

|  |i    Muscular  fibres,  circular  and  longitudinal,  forming  a  loose  network. 
In  this  last  layer  there  are  numerous  air-tubes  or  tracheae,  which  probably 
help  to  keep  the  gut  in  position  in  the  ccelom. 


CULKin.l 


783 


7-10.   Hind-Gut. — This  runs  from  the  end  of  the  mid-gut  to  the  anus,  being 
divided  into  the  following  regions: — 

(1)  A  dorsally  bent  portion,  the  ileum,  lined  by  flattened  epithelium. 

(2)  A  ventrally  bent  portion,  the  colon,  lined  by  cubical  epithelium. 

(3)  A  dilated  portion,  the  rectum,  which  has  six  large  ovoid  papilla:. 

The  rectum  narrows  just  before  the  anus,  which  opens  on  the  last  segment 
of  the  body. 

Malpighian  Tubes.- — -There  are  five  Malpighian  tubes  opening  at  the  junction 
of  the  mid-  and  hind-gut. 

Salivary  Glands. — The  salivary  glands  consist  of  two  groups,  each  con- 
taining three  acini,  lying  on  each  side  of  the  body,  in  the  anterior  portion  of 
the  thorax,  close  against  the  presternum,  and  extending  almost  as  far  back 
as  the  proventriculus.  The  ducts  from  each 
of  these  acini  unite  together  to  form  a 
single  duct  on  each  side,  which  passes  for- 
wards through  the  neck  into  the  head,  where 
it  unites  beneath  the  subcesophageal  ganglion, 
with  its  fellow  of  the  opposite  side,  to  form 
a  common  salivary  duct.  This  duct  passes 
forwards  to  end  in  the  salivary  pump,  which 
is  continuous  with  the  salivary  groove  or 
canal  of  the  hypopharynx.  The  duct  of  the 
salivary  gland,  therefore,  is  not  in  any  way 
connected  with  the  alimentary  canal.  These 
glands,  which  are  much  larger  in  the  female 
than  in  the  male,  are  composed  of  acini, 
surrounded  by  a  basement  membrane  which 
is  very  delicate  and  structureless,  and  upon 
which  rests  a  single  layer  of  epithelial  cells 
surrounding  a  central  lumen.  The  whole 
acinus  lies  in  a  cleft  in  the  fat-body. 

Space  does  not  permit  of  descriptions  of  the 
vascular,  nervous,  and  muscular  systems  being 
included. 

Reproductive  Organs. — The    female   repro- 
ductive organs  consist  of  ovaries,  oviducts,  and  a  common  oviduct,  a  mucous 
gland  and  its  duct,  and  a  spermatheca  and  duct ;  while  the  male  organs  are 
testes  and  vasa  deferentia,  which,  after  receiving  the  ducts  of  the  receptacula 
seminis,  run  to  an  ejaculatory  duct,  which  ends  in  a  short  penis. 

Life-History. — A  mosquito  passes  through  a  complicated  life 
cycle,  consisting  of  an  egg,  a  larval,  and  a  pupal  stage,  the  last- 
named  giving  rise  to  the  perfect  insect  or  imago. 

Soon  after  a  female  insect  is  hatched  it  probably  becomes  fertilized, 
though  some  authorities  believe  that  this  does  not  take  place  until 
after  the  first  meal  of  blood,  which  in  any  case  precedes  the  ovi- 
position,  which  takes  place  in  the  early  morning. 

The  eggs,  which  number  about  one  hundred,  are  laid  upon  the 
surface  of  the  water,  on  which  they  may  be  seen  arranged  in  stars, 
rows,  or  triangles. 

The  eggs  of  A.  niaculipennis  are  boat-shaped,  about  0-5  to  1 
millimetre  in  length,  with  a  flat  upper  and  convex  lower  surface, 
and  with  one  end  somewhat  broader  than  the  other.  The  head  of 
tlu1  larva  will  be  found  at  this  broader  anterior  end.  The  upper 
surface  is  granular  and  reticulated,  while  the  lower  is  smooth. 
On  each  side  of  the  middle  third  the  chitinous  capsule  is  thrown  into 
folds,  called  floats,  while  the  margin  projects  as  a  chitinous  frill. 


Fig.  387. — Egg  of  Anopheks 
niaculipennis. 

(After  Nuttall  and  Shipley.) 

On  the  left  the  egg  is  seen 
from  above,  and  on  the  right 
from  the  side. 


784 


THE  DIPTERA 


The  duration  of  the  egg  stage  has  not  been  well  defined.  Nuttall 
and  Shipley  give  two  to  three  days  for  Anopheles  maculipennis,  but 
it  is  probable  that  it  is  shorter  in  the 
tropics.  The  appearance  and  grouping  of 
the  eggs  are  quite  different  in  the  Culic'nae, 
as  will  be  mentioned  later. 

The  larva  escaping  from  the  blunt 
anterior  end  of  the  egg  by  the  shifting  off 
of  a  piece  like  a  cap  from  the  rest  of  the 
shell  is  seen  to  consist  of  head,  neck,  and 
abdomen. 

When  first  hatched  the  head  is  very  black, 
but  later  on  it  becomes  lighter  in  colour,  and 
shows  characteristic  markings.  At  the  back  of 
the  head  there  is  a  little  notch,  and  from  this  a 
V-shaped  dark  line  opens  forwards,  formed  by 
two  diverging  bands  of  chitin,  arranged  along 
which  are  patches  of  pigment,  which  give  rise 
to  the  characteristic  markings.  There  are  two 
large  compound  eyes,  behind  each  of  which  lies 
a  single  eye-spot,  or  ocellus. 

The  antennae  are  conspicuous  rod-like  bodies 
ending  in  two  leaf-shaped  appendages,  between 
which  is  a  branched  hair,  while  another  hair  of 
specific  importance  arises  from  a  papilla  situated 
at  the  junction  of  the  proximal  and  middle 
thirds. 

Between  the  roots  of  the  antenna  and  projecting 
forwards  there  is  a  smooth,  shield-like  area,  the 
clypeus,  which  carries  four  or  six  hairs,  which  are 
also  of  specific  importance.  Two  of  these  hairs 
(internal  clypeal  hairs)  arise  anteriorly  near  the 
middle  line;  external  to  these  lie  the  external 
clypeal  hairs,  which  arise  from  the  outer  angle 
of  the  clypeus ;  and  behind  them  lie  the  posterior 
clypeal  hairs.  Sometimes  there  is  a  basal  hair 
external  to  the  antennae. 

The  mouth  parts  consist  of  two  large  feeding- 
brushes,  two  maxillary  palps,  two  mandibles,  and 
on  the  ventral  median  line  the  under  lip  of 
Meinert,  a  conical  chitinous  structure,  and  a 
snout-like  process  covered  with  hairs  projecting 
between  the  brushes. 

The  thorax  is  large,  increasing  in  size  as  the 
larva  grows  older.  It  has  numerous  hairs,  and 
sometimes  a  pair  of  the  palmate  hairs  presently 
to  be  described. 

There  are  nine  segments  in  the  abdomen,  of  which  the  eighth  is  characterized 
by  possessing  the  openings  of  the  tracheae,  and  the  ninth  by  possessing  four 
large  papillae,  and  hairs  projecting  downwards  and  backwards.  The  first  two 
segments  possess  a  pair  of  large  feathered  hairs  on  each  side,  the  third  a  single 
hair  on  each  side.  The  others  do  not  possess  these  hairs.  Certain  of  the 
abdominal  segments  have  small,  fan-shaped  hairs,  called  '  palmate  hairs,'  fixed 
by  .1  short  stalk  on  the  outerside  of  the  dorsum  of  the  segment.  Each  of  these 
consists  oi  nineteen  to  twenty  Leafli  ts,  which  are  capable  of  closing  and  opening 
ilk  like  a  fan.  These  hairs  are  rudimentary  in  the  freshly  hatched 
larva,  but  in  the  adult  they  are  well  marked,  and  have  been  used  for  purposes 
of  classification,  according  to  the  variations  in  their  number  and  position,  and 


Fig.  388. — Larva  of 
Anopheles  maculipennis. 

(Alter  Nuttall  and  Shipley, 

Journal  of  Hygiene.) 

1 ,  Internal  clypeal  hairs ; 

2,  external  clypeal  hairs ; 

3,  antennae;  4,  head  mark- 
ings; 5,  thorax;  6,  abdo- 
men; 7,  palmate  hair;  8, 
stigmatic  siphon;  9,  last 
segment. 


CU  LI  CI  DM 


785 


the  characters  of  the  leaflets  and  their  terminal  hairs,  if  present.  These  hairs 
are  of  use  in  helping  to  keep  the  larva  in  its  horizontal  position  when  it  comes 
up  to  breathe  on  the  surface  of  the  water. 

The  stigmatic  siphon  is  placed,  as  already  mentioned,  on  the  eighth  seg- 
ment, forming  by  means  of  raised,  toothed,  chitinous  processes  a  quadrilateral 
space. 


>  -^^--^vv-v^-^-— Hr 


Fig.  389. — Larva  of  an  Anopheline  Mosquito  lying  Parallel  to 
the  Water. 

(Modified  after  Howard.) 


Fig.  390. — Larva  of  a  Culicine  Mosquito  hanging  down  from  the 
Surface  of  the  Water. 

(After  Howard.) 


The  teeth  are  of  great  importance,  being  capable  of  being  approximated  so 
as  to  close  the  cavity,  and  thus  protect  the  two  openings  of  the  tracheae  which 
lie  in  the  anterior  portion  of  the  siphon.  From  these  openings  the  long 
tracheae  can  be  seen  running  from  back  to  front  along  the  larva. 

The  duration  of  the  larval  stage  varies  with  food  and  tempera- 
ture, being  longer  in  the  temperate  zone  than  in  the  tropics. 
According  to  Stephens,  it  is  twelve  days  in  Cellia  argyrotarsis  and 

50 


786 


THE  DIPTERA 


eleven  days  in  Myzomyia  rossi,  while  it  may  be  eighteen  to  twenty- 
one  days  in  Anopheles  maculipennis  in  the  temperate  zone.  The 
larva  grows  by  moulting  several  times. 

Culicine  larvae  are  easily  distinguished  from  Anopheline  larvae 
by  the  fact  that  the  spiracles  are  carried  on  a  long  respiratory 
siphon,  formed  by  a  prolongation  of  the  dorsum  of  the  eighth 
abdominal  segment,  which  has  been  used  to  distinguish  the  different 
species  (Fig.  390). 

Below  the  siphon  on  the  eighth  segment  there  are  spines,  forming 
a  comb,  while  along  the  length  of  the  siphon  there  is  another  comb, 
distal  to  which  is  a  tuft  of  hairs.  The  variations  in  these  structures, 
together  with  those  in  the  length  and  breadth  of  the  siphon,  asso- 
ciated with  those  of  the  antennae  and  clypeus,  afford  means  of  classi- 
fying the  Culicine  larvae.     For  further  information,  consult  either 

Theobald's  Monograph,  vol.  iv., 
p.  6,  or  Felt's  paper,  Bulletin  97 
of  the  Division  of  Entomology 
of  the  New  York  State  Museum. 
The  Megarhininae,  ^Edinae,  and 
Uranotaeninae  possess  larvae  be- 
longing to  the  Culicine  type. 

The  pupal  stage  lasts  about 
forty- eight  hours.  Towards  the 
end  of  an  afternoon  the  pupa 
comes  up  to  the  surface,  and  the 
dorsal  portion  of  the  thorax  splits 
with  a  T-shaped  fissure,  and  the 
adult  insect  or  imago  emerges. 
Pupae  do  not  eat. 

Differences  between  the  Ano- 
phelinae and  Culicinae. — The  differ- 
ence between  these  two  important 
families  may  popularly  be  de- 
scribed as  follows: 

The  Anophelinae,  as  a  rule, 
project  from  any  plane  surface  on 
which  they  may  be  resting  at  a  sharply  defined  angle,  owing  to 
their  head,  thorax,  and  abdomen  forming  a  more  or  less  straight 
line;  while  the  Culicinae,  on  the  other  hand,  do  not  make  such  a 
well-defined  angle,  owing  to  the  fact  that  the  abdomen  is  not  in 
the  same  straight  line  as  the  long  axis  of  the  thorax.  The  eggs  of 
the  Anophelinae  are  laid  singly,  while  those  of  the  Culicinae  are  laid 
in  rafts.  The  larvae  of  the  Anophelinae  have  no  drawn-out  siphons, 
and  therefore  lie  more  or  less  parallel  to  the  surface  of  the  water, 
while  the  larvae  of  the  Culicinae  hang  downwards.  There  are, 
however,  exceptions  to  these  rules — thus,  e.g.,  Myzomyia  culicifacies 
rests  on  a  surface  like  a  Culex,  not  like  an  Anopheles. 

Bionomics. — The  imago  emerges  from  the  pupa  during  the  late 
afternoon,  after  which  the  females  are  ready  for  fertilization  by  the 


Fig.  391. — Pupa  of  Anopheles 
maculipennis. 

(After  Nuttall  and  Shipley,  Journal 
of  Hygiene.) 


CULICID.'E 


787 


males.  These  latter  can  sometimes  be  seen  in  large  numbers,  while 
but  few  females  are  observed,  which  is  supposed  to  be  characterist  ic 
of  the  breeding  period. 

The  female  alone  bites  man  and  animals,  apparently  for  the  pur- 
pose of  obtaining  rich  food  for  the  eggs,  while  the  male  feeds  on  the 
juices  of  plants  and  fruits.  The  female  can  also  be  seen  feeding 
upon  vegetable  juices,  though  this  is  more  common  in  the  females 
of  the  Culiciiue  than  in  those  of  the  Anophelime.     It  is  believed 


Fig.  392. — -Diagram  to 
show  the  Posture 
of  an  anopheline 
Mosquito  on  a  Wall. 


Fig.  393. — Diagram  to 
show  the  Posture  of 
Another  Anopheline 
Mosquito  on  a  Wall. 


Fig.  394. — Diagram 
to  show  the  Pos- 
ture of  Citlex  pi- 
biens  on  a  Wall. 


(After  Sambon,  from  the  British  Medical  Journal.) 

that  a  female  feeds  on  blood  once  a  day  in  nature,  but  this  is 
a  difficult  matter  to  be  certain  about.  The  mechanism  of  the 
bite  has  already  been  described  in  page  223,  to  which  reference 
should  be  made.  It  will  also  be  noted  that  the  structure  of  the 
female  mouth-parts  is  adapted  for  piercing,  while  that  of  the 
male  is  not.  It  will  also  be  remembered  that  only  the  stylets 
pierce  the  skin,  and  that  the  labium  never  does  so.  Infection  of 
the  victim  by  the  malarial  germ  takes  place  during  the  act  of 

biting,  as  the  sporozoites 
pass  down  the  hypopharyn- 
geal  or  salivary  tube,  while 
the  infection  of  the  mosquito 
is  effected  by  the  blood, 
which  passes  from  the  victim 
along  the  labial  or  blood- 
tube  into  the  mouth.  So 
much  blood  may  be  sucked  that  it  may  appear  per  anitm. 

Usually  the  mosquitoes  bite  at  night,  and  preferably  in  the  dark, 
.is,  for  example,  they  will  attack  the  ankles  of  people  while  sitting 
a1  dinner  at  night. 

A  i  1 «  1  feeding,  the  mosquitoes  usually  retire  to  a  dark  portion  of 
the  room  to  digest  the  food.  It  is  noticeable  that  they  avoid 
white  areas  during  the  daytime,  and  prefer  dark-coloured  regions 
away  from  the  light,  and  hence  are  very  difficult  to  find  in  ill- 
lighted  native  huts. 


Fig.  395- 


-Raft  of  Culicine  Eggs. 
(After  Sambon.) 


788  THE  DIPTERA 

In  the  early  morning  the  female  flies  to  the  nearest  water  and 
lays  her  eggs.  Usually  she  does  not  travel  far,  but  is  believed  to 
be  capable  of  going  at  least  half  a  mile  in  case  of  need. 
;/;  The  females  of  the  Culicinae  do  not  appear  to  concern  themselves 
as  to  the  nature  of  the  water  in  which  they  lay  their  eggs,  but  the 
female  Anophelinae  prefer  clean  water  with  a  certain  amount  of 
weed.  This  water  may  be  the  back  eddies  of  a  river,  where  there 
is  the  protection  of  weeds,  or  the  margins  of  large  lakes,  where 
dense  surface  vegetation  is  to  be  found,  or  any  collection  of  water 
which  contains  green  vegetal  matter,  or,  failing  these,  any  collec- 
tion of  fresh  or  moderately  salt  water.  Small  and  large  wells  are  a 
prolific  source  of  mosquitoes,  as  are  puddles,  and  water  in  broken 
bottles,  shells,  and  especially  in  plants  like  bamboos,  etc.  Having 
laid  the  eggs,  they  retire  to  some  dark  corner  during  the  daylight, 
and  emerge  at  night  for  another  feed  of  blood.  How  long  they  live 
is  not  known  with  certainty,  and  will  be  discussed,  together  with 
other  features  of  their  bionomics,  in  Chapter  XL.,  under  Malaria. 
^Mosquitoes  can  hibernate  during  the  cold  weather  of  the  tem- 
perate zone,  and  sestivate  during  the  dry  hot  weather  of  the  tropics. 


Fig.  396. — Girardinus  pceciloides  de  Filippi. 
(The  tail  should  have  been  drawn  expanded.) 

In  this  latter  condition  they  bite  and  suck  blood,  but  apparently 
do  not  lay  eggs,  even  if  water  is  provided.  The  eggs  are  kept  afloat 
on  the  surface  of  the  water  by  their  structure,  and  in  due  course 
give  rise  to  the  larvae,  which  are  great  eaters,  living  not  merely 
upon  unicellular  organisms,  such  as  algae  and  diatoms,  but  also 
upon  their  fellows.  For  purposes  of  obtaining  air  they  are  com- 
pelled to  come  to  the  surface  of  the  water.  The  Anopheline  larva, 
not  possessing  a  siphon,  has  to  lie  more  or  less  parallel  with  the 
surface  of  the  water  in  order  to  enable  the  air  to  enter  the  spiracles, 
and  this  it  is  able  to  do  by  the  aid  of  the  palmate  hairs  already 
mentioned;  while  the  Culicine  larva  have  merely  to  bring  the 
apex  of  the  siphon  to  the  surface  of  the  water,  from  which  they 
apparently  hang  downwards.  Larvae  are  certainly  able  to  hiber- 
nate, and  perhaps  eggs  also.     The  pupa  does  not  feed. 

Mosquitoes  have  many  enemies  and  parasites,  but  the  most 
important  from  a  point  of  view  of  the  prophylaxis  of  malaria  are 
those  which  eat  the  eggs,  the  larvae,  and  the  pupae,  of  which  fish 
are  the  most  import  ant . 

In. 1905  C.  K.  Gibbons  pointed  out  that  a  small  fish,  popularly 


CVLICIDJE  789 

termed  '  millions,'  which  lived  in  shallow  water,  was  a  voracious 
feeder  on  eggs,  Larvae,  and  pupae  of  mosquitoes.  These  fish,  which 
belong  to  the  species  Girardinus  pceciloides  de  Filippi,  are  found  in 
Barbados,  which  is  very  free  from  malaria.  .They  are  very  small, 
the  full-grown  female  only  measuring  ij  inches  in  length,  while 
the  male  is  smaller.  The  female  is  dull  in  colour,  while  the  male 
is  distinguished  by  red  splashes  and  a  black  circular  dot  on  its 
sides.  The  great  importance  of  these  little  fish  is  that  they  are 
able  to  live  in  very  shallow  water,  and  to  work  their  way  in  among 
dense  surface  vegetation,  and  thus  to  gain  access  to  the  larvae,  etc., 
of  the  mosquitoes,  which  otherwise  are  protected  by  the  weeds 
from  attacks  by  the  larger  fish.  Their  classification  is  Teleostei, 
Haplomi,  Cyprinodontidae,  genus  Haplochihts  McClelland,  1839.  a  c  j 
The  family  contains  220  species,  of  which  only  50  live  out  of  Qr  J^/ 
America.  Haplochilus  has  24  species  in  Africa  and  35  in  Asia  ^^%k(f\\^r 
America.  There  is  no  doubt  that  these  small  fish  should  be  intro-  ^ 
(lueed  into  malarious  places  as  a  prophylactic  measure  against  the 
disease.  Other  closely  allied  species  are  G.  versicolor  Giinther,  ^jL 
found  in  St.  Domingo,  and  G.  formosus,  found  in  Florida  and  South  *  ^ 
Carolina.  With  regard  to  other  species,  Gambusea  molliensia  is  said 
to  be  of  great  value  in  consuming  larvae,  especially  when  protected 
by  dense  surface  vegetation.  Recently  Graham  has  reported  that 
Haplochilus  grahami  Boulenger,  191 1,  and  H.  bifasciatus  Stein- 
dachner,  1881,  of  the  Cyprinodontidae,  eat  larvae  greedily,  while 
Gowdey  finds  the  same  for  Fundatus  tcaniopygus  and  Haplochilus 
pumilus  Boulenger,  1906,  in  Uganda. 

Certain  plants,  as  is  well  known,  collect  water,  especially  the 
bromelias,  the  bamboos,  and  the  pitcher-plants.  In  this  water 
Culicine  and  sometimes  Anopheline  larvae  can  be  found.  E.  E. 
Green,  of  Ceylon,  has  shown  that  the  flowers  of  the  lobster-claw 
plant  (Heliconea  brasiliensis)  can  hold  a  considerable  amount  of 
water,  in  which  he  found  Stegomyia  and  Desvoidea  larvae  in  large 
numbers. 

Classification. — Various  methods  of  classifying  mosquitoes  have 
been  brought  forward.  The  earliest  were  based  upon  the  characters 
of  the  palpi,  but  in  1901  Theobald  showed  that  they  were  useless 
for  anything  but  specific  characteristics,  and  based  his  larger  divi- 
sions on  the  variations  of  the  scales  on  the  head,  body,  and  wings. 
Fell  brought  forward  a  classification  based  upon  the  male  genitalia 
and  the  wing  veins,  but,  as  Theobald  remarks,  the  majority  of 
known  mosquitoes  being  female,  it  is  most  undesirable  to  take  only 
male  characters  for  the  classification.  Recently  Dyar  and  Knab 
have  issued  a  classification  of  the  Culicidae  by  larval  characters, 
and  Eysell  has  advanced  matters  considerably  by  separating  the 
Corethrinae  from  the  Cidicidae  under  the  term  Corethridae,  because 
the  Corethridae  have  an  entire  absence  of  the  long  piercing  proboscis 
Hid  oi  scales  in  the  adults,  both  of  which  are  marked  features  of 
the  Culicidae.  It  will  be  evident  that  this  is  useful.  Lutz  has 
brought  forward  a  classification  based  upon  larval  and  adult  forms, 


79° 


THE  DIPTERA 


Fig.     397. — Head     and     Scutellum     of 
Megarhinus,  to  show  the  Scales. 

On  the  right  a  profile  view  of  the  scales. 

(After  Theobald,  '  Culicida?  of  the  World.') 


which  Theobald  has  modified  and  brought  into  accord  with  one 
based  upon  scales  as  generic  characters,  and  this  classification  is 
followed  below. 

Theobald's  Classifica 
tion. — The  Culicidae  may 
be  divided  into  subfamilies, 
according  to  the  characters 
of  the  scales  on  the  head, 
body,  legs,  and  wings. 

A.  Scutellum  simple, 
never  trilobed ;  pro- 
boscis straight, 
palpi  long  in  male 
and  female  —  Ano- 
phelincB. 

B.  Scutellum  trilobed: — 
I.  Proboscis     strongly 

recurved  ;  first 
submarginal  cell 
very  small — Me- 
garhinince. 
II.  Proboscis  straight; 
post-scutellum 
nude: — 

1.  Wings  with  six  longitudinal  scaled  veins: — 

(1)  Antenna  with  second  joint  normal  in  length:- — 

(a)  First  submarginal  cell  as  long  as  or  longer 

than  the  second  posterior  cell. 

Palpi   in   the   female    shorter   than   the 

proboscis;  long  in  male — Culicince. 
Palpi  short  in  both  sexes — Mdince. 

(b)  First   submarginal  cell  very   small;    smaller 

than  second  posterior — Uranotcenince. 

(2)  Antennae   with    second   joint    very   long — Deino- 

ceratince. 

2.  Wings  with   seven   longitudinal   scaled   veins — Hepta- 

phlebomyince. 

III.  Proboscis  straight ;  post-scutellum  with  scales  or  chaetae : — 

1.  Palpi    long    in    male,    short    in    female — Trichoproso- 

ponincs. 

2.  Palpi  short  in  both  sexes. — Dendromyince. 

IV.  Proboscis  elbowed — Limatina. 

Of  these,  only  the  Anophelinae  and  the  Culicinae,  and  possibly 
the  iEdinae,  contain  species  of  importance  in  tropical  medicine, 
and  concerning  these  subfamilies  a  few  details  must  be  given. 


anopheltnje  791 

Anophelin^. 

Definition. — Culicidre  with  straight  proboscis;  palpi  long  in  both 
sexes;  occiput  mostly  with  upright  forked  scales,  never  with  flat 
lateral  scales.  Thorax  with  scales  or  hairs,  scutellum  never  trilobed, 
with  scales  or  hairs.  Post  scutellum  nude.  Abdomen  with  hairs  or 
scales.  Eggs  laid  singly,  and  not  in  rafts.  Larvae  without  respira- 
torv  siphon. 

This  is  a  most  important  subfamily,  because  it  contains  the  species 
which  are  known  to  carry  malaria.  The  list  of  known  carriers 
will  be  found  in  Chapter  XXXV.  (p.  883). 

It  is  important  for  the  student  of  tropical  medicine  to  be  able 
to  recognize  the  genera  and  species  of  the  more  important  Anophe- 
linae.  For  this  purpose  we  give  the  following  tables  taken  from 
Theobald's  'Manual  of  the  Culicidre,'  vol.  v.,  1910.  For  fuller 
information  the  original  work  must  be  consulted,  but  it  must  be 
admitted  that  there  is  a  growing  opinion  that  Theobald's  genera 
imperceptibly  merge  with  one  another,  and  are  not  founded  on 
essential  points;  and  Edwards  has  returned  to  two  genera,  Anopheles 
and  Bironella,  therefore  in  Chapter  XXXV.  (p.  883)  we  will  give 
another  classification  when  considering  the  anophelines which  carry 
malaria. 

Subfamily  Anopheliisle  Theobald,  1901. 
Table  of  Genera. 

A.  First  submarginal  cell  very  small — Bironella  Theobald. 

B.  First  submarginal  cell  large: — 

I.  Antennal  segments  with  dense  lateral  scale-tufts — Chagasia  Cruz. 
II.  Antennal  segments  with  outstanding  scales  on  the  second  segment 
and  more  appressed  ones  on  the  first.     At  least  one  abdominal 
segment  with  long  flat  more  or  less  spatulate  scales — Calvertina 
Ludlow. 
III.  Antennal  segments  without  dense  lateral  scale-tufts: — 

1.  Thorax  and  abdomen  with  hair-like  curved  scales  :^ — 

\r<>  flat  scales  on  head,  but  upright  forked  ones. 

(a)  Basal  lobe  of  male  genitalia  of  one  segment. 

(1)  Wing  scales  large,  lanceolate — Anopheles  Meigen. 

(2)  Wing  scales  mostly  small,  or  narrow,  or  slightly 

lanceolate,  costa  spotted — Myzomyia  Blanchard. 

(3)  Wings  similar  to  (2),  but  with  fourth  longitudinal 

vein  very  near  base  of  third.  Prothoracic  lobes 
with  outstanding  scales — Neomvzomyia  Theo- 
bald. 

(4)  Wings    with    patches    of    large    inflated    scales — 

Cycloleppteron  Theobald. 

(b)  Basal  lobe  of  two  segments: — 

Prothoracic  lobes  with  dense  outstanding  scales — 
Feltinella  Theobald. 
(b)  Median   area   of    head  with  some  flat    scales;  prothoracic 
lobes  mammillated.     Wing  scales  lanceolate — Stethomyia 
Theobald. 

2.  Thorax  with  narrow  curved  scales;  abdomen  hairy: — 

(a)  Wing  scales  small  and  lanceolate;  head  with  normal  forked 

scales — Pyretophorus  Blanchard. 

(b)  Wing  scales  broad  and  lanceolate;  head  with  broad  scales 

not   closely  appressed,  but   not.  forked   or   fimbriated — 
Myzorhynchella  Theobald. 


792  THE  DIPTERA 

3.  Thorax  with  hair-like,  curved  scales,  and  some  narrow  curved 

ones  in  front ;  abdomen  with  apical  lateral  scale-tufts  and  scaly 
venter;  no  ventral  tuft.  Wing  scales  lanceolate — Arribalzagia 
Theobald. 

4.  Thorax  with  hair-like,  curved  scales;  no  lateral  abdominal  tufts; 

distinct  apical  ventral  tuft.  Palpi  densely  scaly.  Wing  with 
dense,  large,  lanceolate  scales— Myzorhynchus  Blanchard. 

5.  Thorax  with  hair-like,  curved  scales,  and  some  narrow,  curved 

lateral  ones ;  abdomen  hairy,  with  dense,  long,  hair-like,  lateral, 
apical,  scaly  tufts.  Wing  scales  short,  dense,  lanceolate;  fork 
cells  short — Christy  a  Theobald. 

6.  Thorax  with  very  long,  hair-like,  curved  scales;  abdomen  with 

hairs,  except  last  two  segments,  which  are  scaly.  Dense 
scale-tufts  to  hind  femora.  Wings  with  broadish,  blunt,  lanceo- 
late scales- — Lophoscelomyia  Theobald. 

7.  Thorax  and  abdomen  with  scales : — 

(a)  Thoracic    scales    narrow-curved   or    spindle-shaped;    abdo- 

minal scales  as  lateral  tufts  and  small  dorsal  patches  of 
flat  scales — Nyssorhynchus  Blanchard. 

(b)  Abdomen   nearly   completely   scaled,    with   long,    irregular 

scales,  and  with  lateral  scale-tufts — Cellia  Theobald. 

(c)  Similar    to    above,    but    no    lateral    scale-tufts — -Neocellia 

Theobald. 

(d)  Abdomen  completely  scaled  with  large  flat  scales,   as  in 

Culex — Aldrichinella  Theobald. 

(e)  Thoracic  scales  hair-like,  except  a  few  narrow-curved  ones 

in  front;  abdominal  scales  long,  broad,   and  irregular — - 
Kertiszia  Theobald. 
(/)    Thorax  with  narrow,  hair-like,  curved  scales,  some  broad 
straight  scales,  and  some  spatulate  laterally.     Abdomen 
with  fine  hairs  except  last  three  segments,  which  have 
scales.     Tufts   of   scales  on   hind  femora.     Wing  scales 
lanceolate — Manguinhosia  Cruz. 
Note. — The  genus  Ccelodiazesis  Dyar  and  Knab  is  said  by  Theobald  to  be 
invalid,  being  based  on  Anopheles  barberi,  which  is  a  true  Anopheles. 

Anopheles  Meigen,  1818. 
Essentially  Anopheles  are  temperate  zone  or  hill-station  Anophelinae,  of 
which  the  type  Anopheles  maculipennis  Meigen.    181 8,   has    been    already 
described. 

Eighteen  species  are  definitely  known,  but  in  addition  there  are  the  uncertain 
species  of  A.  ferrnginiensis  Wiedemann;  A.  martini  Laveran;  A.  pursati 
Laveran ;  A .  vincenti  Laveran ;  A .  vestitipennis  Dyar  and  Knab,  1906 ;  A .  strigi- 
macula  Dyar  and  Knab,  1906;  A.  apicumacula  Dyar  and  Knab,  1906;  A. 
punctimacula  Dyar  and  Knab,  1906;  etc. 

Theobald  gives  the  following  table  by  means  of  which  the  species  may  be 
recognized: — 

Anopheles. 
A.  Wings  spotted:- — 

I.  Legs  unhanded: — ■ 

1.  Wings  with  spots  formed  of  collections  of  scales  on  the  wing 

field;  no  costal  spots — maculipennis  Meigen. 

2.  Wings  with  light  and  dark  costal  markings. 

(1)  Costa  with  two  yellow  spots: — 

(a)  Large  species: — 

(a)  No  fringe-spots — pnnctipennis  Say. 

(b)  Fringe-spots    present— -pseudopunctipennis    Theo- 

bald. 

(b)  Small    species.       Wings    much    spotted — franciscanus 

McCracken. 

(2)  Costa  with  one  spot — perplexus  Ludlow. 


ANOPHELES  793 

II.  Legs  with  basal  pale  bands: — 

i.  Costa  with  two  large  dark  spots — gigas  Giles. 
2.  Two  large  and  two  small  basal  spots — formosus  Ludlow, 
III.  Legs  with  narrow  apical  bands : — 

Costa  dark,   with  two  small  pale  yellow  spots — ■wellconui  Theo- 
bald. 

B.    Wings  unspotted: — 

I.  Legs  unhanded: — 

i .  Thorax  adorned  as  in  Corethra — corethroides  Theobald. 
2.  Thorax  normal  ornamentation. 

(a)  Second  fork  cell  much  more  than  half  the  length  of  the  first. 

(i)   Palpi  unhanded. 

(a)  Petiole  of  first  fork  cell  more  than  one-third  length 

of  cell. 
Abdomen  with  golden  hairs — bijitrcatus  Linnaeus. 
Abdomen  with  brown  hairs — algeriensis  Theobald. 

(b)  Petiole  of  first  fork  cell  one-third  length  of  cell — 

barberi  Coquillett. 
(2)   Palpi  banded.     Dark  species.     Wing  scales  very  dense 
—smithi  Theobald. 
Wing  scales  not  so  dense — nigripes  Staeger. 

(b)  Second  fork  cell  not  more  than  half  the  length  of  the  first 

— aitkeni±Ih.eoba]d. 
II.  Legs  banded: — 

1.  Hind  femora  only  with  broad  white  band — lindsayi  Giles. 

2.  Apices  of  hind  tarsi  pale — immaculatus  Theobald. 

Myzomyia  Blanchard,  1902. 

This  Myzomyia  includes  some  important  mosquitoes  found  in  West  Africa, 
and  in  India  and  Ceylon,  which  are  carriers  of  malaria. 
The  diagnostic  table  given  by  Theobald  is  as  follows: — 

Myzomyia. 
A.  Proboscis  unhanded: — 
1.  Legs  banded: — 

(a)  Palpi  with  three  white  rings. 

(1)  Legs  with  faint  apical  pale  bands. 
Wing  fringe  spotted — funesta  Giles. 

(2)  Legs  with  prominent  apical  pale  bands,  and  a  broad,  pale, 

median  band  to  fore-  and  mid-metatarsi — lutzi  Theobald. 

(3)  Legs  (hind)  with  apical  and  basal  pale  bands. 

Wings  with  five  to  six  pale  costal  spots,   the  largest  T- 

shaped — rossi  Giles. 
Wings  with  three  yellow  costal  spots — longipalpis  Theobald. 

(b)  Palpi  with  two  white  rings: — 

(1)  Apex  white — aconita  Donitz. 

(2)  Apex  black — d'thali  Patton. 

(c)  Palpi  with  four  white  rings — jehafi  Patton. 
1.   Legs  spotted  and  banded: — 

(a)  Supernumerary    cross-vein    straight.     Palpi    with   three    white 

bands.     Apical  and  basal  pale  leg  banding. 

(1)  Third  large  costal  spot  with  two  spots   beneath  on   first 

vein — ludlowi  Theobald. 

(2)  Similar,  but  much  smaller — mangy  ana  Banks. 

(3)  Third  costal  spot  T-shaped,  as  in  rossi — indefinata  Ludlow. 

(4)  Thorax   with    two   ocelli;    wings    much   spotted — tessellata 

Theobald. 

(b)  Supernumerary    cross-vein     markedly    curved — pyretophoroides 

Theobald. 


794  THE  DIPTERA 

3.  Legs  unhanded: — 

(a)  Apex  of  palpi  white  and  ringed.     Three  pale  palpal  bands. 

(a)  Third  long  vein  mostly  yellow — listoni  List  on. 

(b)  Third  long  vein  dark. 

(1)  Several  fringe-spots — leptomeres  Theobald. 

(2)  Two  fringe-spots — culicifacies  Giles. 

(3)  No  fringe  spots — rhodesiensis  Theobald. 

(b)  Apex  of  palpi  white  only — nili  Theobald. 

(c)  Apex  of  palpi  black. 

(1)  Black  apex  narrow — turkhudi  Liston. 

(2)  Black  apex  broad — hispaniola  Theobald. 

4.  Legs  with  spots  only  at  joints.     Palpi  with  three  bands;  apex  black 

— azriki  Patton. 

B.  Proboscis  banded: — 

I.  Legs  unspotted — albirostris  Theobald. 
II.  Legs  spotted — thorntoni  Ludlow. 

Neomyzomyia  Theobald,  1912. 

This  genus  includes  only  one  species,  Neomyzomyia  elegans  James,  1903.     It 
is  found  in  India. 

Pyretophorus  Blanchard,  1902. 

The  important  species  is  Pyretophorus  costalis,  the  spreader  of  malaria  in 
West  Africa  and  Mauritius. 

Pyretophorus. 

A.  Legs  unhanded : — 

I.  Palpi  with  three  pale  bands;  apex  black — nigrifasciatus  Theobald. 

II.  Palpi  with  three  pale  bands;  apex  white: — ■ 

(a)  Wings  with  four  large  and  two  small  black  costal  spots;  mid 

cross- vein  very  long — nursei  Theobald. 

(b)  Wings  with  four  large   black  spots;   mid  cross-vein  normal — 

minimus  Theobald. 

(c)  Wings  with  five  large  black  costal  spots : — 

(1)  First  fork  cell  much  longer  than  the  second  posterior — 

ser genii  Theobald. 

(2)  First  fork  cell  about  as  long  as  the  second  cell — palesti- 

nensis  Theobald. 

B.  Legs  banded: — ■ 

I.  Legs  with  apical  banding.     Hind-legs  only  banded.     Palpi,  black 
apex,  and  three  pale  bands. 

(a)  Three  dark  lines  on  post-scutellum — myzomyfacies  Theobald. 

(b)  Two  dark  lines  on  post-scutellum — chaudoyei  Theobald. 

II.  All  legs  with  apical  pale  bands.     Palpi  with  three  white  bands. 

(a)  Wings  with  four  black  costal  spots;  fringe  unspotted — super- 

pictus  Grassi. 

(b)  Wings  with  four  large  and  two  small  costal  spots ;  fringe  spotted. 

(a)  Apical   palpal   band   broad;    other   two   small — jeyporensis 

Theobald. 

(b)  Apical   and   median   palpal    bands    broad — austeni    Theo- 

bald. 

(c)  Thoracic  scales  creamy — pitchfordi  Power. 

III.  Fore  and  hind  legs  with  apical  pale  bands. 

Four  white  palpal  bands — cinereus  Theobald. 

C.  Legs  spotted  and  banded : — 

I.  Last  three  hind  tarsals  all  white. 

Thorax  golden  scaled — aureosquamiger  Theobald. 

II.  Last  hind  tarsal  not  white: — 

(a)  Femora  and  tibiae  spotted.     Tarsal  bands  apical.     Three  palpal 
bands. 


MYZORHYNCHUS  795 

(a)  Apical  one  broad ;  others  narrow : — 

(1)  Fringe-spots  narrow — costalis  Loew. 

(2)  Fringe-spots  broad — merits  Donitz. 

(b)  Apical  and  median  ones  broad — marshalli  Theobald. 

(b)  No  spots  on  femora — -pseudocostalis  Theobald. 

(c)  Femora,  tibiae,  and  first  tarsals  spotted.     Tarsal  bands  apical. 

Four  palpal  bands   -ardensis  Theobald. 

Myzorhynchus  Blanchard,  1902. 

These  mosquitoes  are  usually  said  to  only  occur  in  the  open,  but  we  have 
repeatedly  found  Myzorhynchus  barbirostris  in  houses.  M.  sinensis  is  known 
to  carry  the  parasite  of  malaria  in  Japan.  No  species  have  so  far  been 
reported  from  America. 

The  thirteen  species  can  be  recognized  as  follows  (it  has  been  asserted  that 
Anopheles  coustani,  which  has  never  been  correctly  placed,  is  M.  coustani 
Laveran,  but  see  Chapter  XXXV.  on  this  point) : — 

Myzorhynchus. 

A.  Palpi  unhanded: — 

I.  Last  hind  tarsals  brown.     Legs  with  pale  apical  tarsal  bands : — 

(a)  One  fringe-spot. 

(1)  Legs  not  spotted — barbirostris  van  der  Wulp. 

(2)  Legs  with  speckled  femora  and  tibiae,  and  more  numerous 

'  round-ended  '    scales   on    the    wing — pseudobarbirostris 
Ludlow. 

(b)  Several  fringe-spots — bancrofti  Giles. 

(c)  No  fringe-spot. 

(1)  One  pale  costal  spot;  wings  with  light  and  dark  scales — 

umbrosus  Theobald. 

(2)  Two  pale  costal  spots;  wings  mostly  dark  scaled — strachani 

Theobald. 

II.  Last  hind  tarsal  white — albotesniatus  Theobald. 

B.  Palpi  banded: — 

I.  Last  hind  tarsal  brown: — 

(a)  Wing-fringe  with  one  pale  spot — sinensis  Wiedemann. 

(b)  Wing-fringe  unspotted. 

(a)  Palpi  with  four  pale  bands;  apex  white. 

1.  Wings  with  two  yellow  costal  spots. 

(1)  Wings  distinctly  spotted — vanus  Walker. 

(2)  Wings     without     prominent     spots — psendopictus 

Grassi. 

2.  Wings  with  two  white  costal  spots — minutus  Theobald. 

(b)  Apex  of  palpi  black — nigerrimus  Giles. 

I  I .   Last  two  hind  tarsals  white — mauritianus  Grandpre. 

III.  Last  three  hind  tarsals  white—  paludis  Theobald. 

Nyssorhynchus  Blanchard,  1902. 
The  important  member  is  Nyssorhynchus  fuliginosus  Giles,  1900,  which  is 
without  doubt  a  malarial  carrier.     Theobald's  diagnostic  table  is  as  follows: — 

Nyssorhynchus. 

A.  Last  hind  tarsals  brown: — 
Legs  spotted : — 

(a)   Apical  pale  bands  to  legs. 

(1)  Proboscis  dark — stephensi  Liston. 

(2)  Proboscis  pale  on  apical  half — master  i  Skuse. 
{b)  Apical  and  basal  pale  banding — annulipes  Walker. 


796  THE  DIPTERA 

B.  Last  hind  tarsal  white : — 

I.  Legs  spotted  with  white : — 

(a)  Palpi  with  three  white  bands — willmori  James. 

(b)  Palpi  with  four  white  bands — maculatus  Theobald. 
II.  Legs  not  spotted;  four  palpal  bands — karwari  James. 

C.  Last  two  hind  tarsals  white.     Legs  with  mottled  femora,  tibiae,  and  tarsi; 

three  white  palpal  bands : — 

(a)  Two  apical  palpal  bands  close  together — theobaldi  Giles. 

(b)  Two  apical  palpal  bands  far  apart — -pretoriensis  Theobald. 

D.  Last  two  and  a  half  to  two  and  three-quarters  tarsals  white — tibani  Patton. 

E.  Last  three  hind  tarsals  white: — 

I.  Palpi  with  three  white  bands: — ■ 

(a)  Palpi  spotted;  legs  spotted- — macnlipalpis  Giles. 

(b)  Palpi  spotted;  hind  legs  not  banded — indiensis  Theobald. 

(c)  Palpi  not  spotted;  legs  spotted — -jamesii  Theobald. 

(d)  Palpi  and  legs  not  spotted. 

(i)   Wings  with  four  white  costal  spots — ■fuliginosus  Giles. 
(2)  Wings  with  five  white  costal  spots — nivipes  Theobald. 
II.  Palpi  with  four  white  bands — philippinensis  Ludlow. 

F.  Legs  uniformly  brown — brunnipes  Theobald. 

Cellia  Theobald,  1902. 

This  genus,  which  is  widely  distributed  throughout  the  tropics,  has  two 
malarial  carriers,  Cellia  argyrotarsis  and  C.  albimana,  the  latter  being  also 
known  as  a  filarial  carrier. 

Cellia. 

A.  Legs  with  last  three  hind  tarsals  white: — 

I.  Dark  species — argyrotarsis  Robineau-Desvoidy. 
II.  Dark  species,  but  with  whitish-grey  apex  to  abdomen — braziliensis 
Chagas. 
III.  Yellowish  species — pulcherrima  Theobald. 

B.  Legs  with  last  hind  tarsals  white : — ■ 

I.  Femora  and  tibia?  mottled;  apical  foot-bands — pharcensis  Theobald. 
II.  Femora  and  tibiae  not  mottled — bigoti  Theobald. 

C.  Legs  with  last  hind  tarsal  white,  except  base;  second  and  third  white — 

albimana  Wiedemann. 

D.  Legs  with  last  hind  tarsal  dark. 

I.  Dark  species;   three   white   long  lateral  thoracic   lines — squamosa 
Theobald. 
II.  Pale  species: — • 

(a)  Thorax  with  two  eye-like  spots;  pleurae  pale  with  large  black 

spots— kochi  Donitz. 

(b)  Similar,  but  with  wings  more  spotted — punctulata  Donitz. 

Subfamily  Culicinjs  Theobald,  1901. 

Definition. — Culicidae  with  straight  proboscis,  long  palpi  in  the  male,  short 
in  the  female.  Post-scutellum  nude ;  wings  with  a  long  first  submarginal  cell , 
and  without  a  third  anal  vein.     Larvae  with  respiratory  siphons. 

Remarks. — There  are  upwards  of  sixty-three  known  genera,  but  of  these  only 
Stegomyia,  Culex,  and  perhaps  Mansonia,  are  of  importance  to  medical  men 
at  present. 

Stegomyia  Theobald,  1901. 

Definition. — Culicinae  with  the  head  and  scutellum  clothed  with  flat  scales. 

Remarks. — The  important  species  is  Stegomyia  fasciata,  the  tiger  mosquito, 
which  spreads  yellow  fever.  It  is  peculiar  in  that  it  bites  chiefly  in  the  after- 
noon. It  is  found  all  over  the  world,  which  is  due  to  the  fact  that  it  can  live  on 
board  ship  easily. 


STEGOMYIA  797 

Unfortunately  its  name  is  about  to  be  changed  either  to  S.  calopus  Meigen, 
or  S.  frater  Desvoidy.  Theobald  at  present  is  not  certain  which  will  prove 
to  be  the  correct  term.     The  name  as  it  stands   at   present   is  S.  fasciaia 


Fig.  398. — Head  and  Scutellum  of  Stegomyia,  to  show  Scales. 
(After  Theobald,  '  The  Culicida?  of  the  World.') 

Fabricius,  1805  (non  O.  F.  Miiller,  1764)  (synonyms:  Culex  calopus  Meigen, 
1818  (?),  C.  frater  Desvoidy,  1827).  O.  F.  Miiller,  it  appears,  used  the  term 
'  fasciata  '  for  a  Culex  in  1764. 

A.  Proboscis  banded: — 

I.  Legs  basally  banded : — 

(a)  Thorax    brown,    with    scattered,    creamy-white    scales — annuli- 

rostris  Theobald. 

(b)  Thorax  black,  with  narrow,   curved,   golden  scales — periskelata 

Giles. 
II.  Legs  with  basal  and  apical  banding.     Fore-legs  with  no  bands;  mid 
with  apical  and  basal  bands  on  first  tarsal  and  second  tarsal;  hind 
with  basal  bands. 
Thorax  white  in  front,  with  a  brown  eye-like  spot  on  each  side — 
thomsoni  Theobald. 

B.  Proboscis  unbanded: — 

I.  Legs  basally  banded:  — 
(a)   Abdomen  basally  banded. 

(a)  Thorax    with    one    median    silvery    white    line — sculellaris 

Walker. 

(b)  Thorax  similar,  but  with  two  white  spots  near  where  the 

line  ends. 

(c)  Thorax  with  two  median  yellow  lines,  and  lateral  curved 

silvery  lines — fasciata  Fabricius. 

(d)  Thorax  with  two  short  median  pale  lines  and  a  white  patch 

on  each  side — nigeria  Theobald. 

(e)  Thorax   with   large   lateral   white   spots   in   front,    smaller 

ones  by  the  wings,  two  narrow  median  yellow  lines,  and 
two  posterior  submedian  white  lines — lilii  Theobald. 

(f)  Thorax  with  a  white  W-shaped  area  in  front,  a  prolonga- 

tion  curved   on   each   side  enclosing   a   brown,   eye-like 
spot — alba  Theobald. 


798  THE  DIPTERA 

(g)  Thorax  with  white  frontal  median  spot,  two  large  lateral 
spots,  one  small  spot  on  front  of  wings,  one  narrow 
median  white  line  and  narrow  submedian  lines  on 
posterior  half.  Last  two  hind  tarsi  white — welhnani 
Theobald. 

(h)  Thorax  brown,  with  broad  white  line  in  front,  extending 
laterally  towards  the  wings,  where  they  swell  into  a 
large  patch,  a  white  line  just  behind  wings.  Last  two 
hind  tarsi  white — albipes  Theobald. 

(i)  Thorax  with  silvery  white  spot  on  each  side  in  front,  small 
spot  over  root  of  wings,  and  a  white  spot  over  the  base 
of  the  wings — pseudonigeria  Theobald. 

(j)  Thorax  with  two  lateral  white  spots,  the  front  one  the 
largest;  a  small  median  one  near  the  head;  two  yellow 
median  lines  and  a  short  silvery  one  on  each  side  before 
the  scutellum — simpsoni  Theobald. 

(k)  Thorax  with  a  silvery  white  scaled  area  in  front,  and 
another  on  each  side  in  front  of  wings — argenteomaculaia 
Theobald. 

(1)  Thorax  with  a  median,  yellowish-white  line,  a  silvery  patch 

on  each  side  in  front  of  the  wings,  extending  as  a  fine 

yellow  line  to  scutellum,  and  another  silvery  spot  before 

base  of  each  wing — power i  Theobald. 
(m)  Thorax  with  small  grey-scaled  area  in  front  of  roots  of 

wings,    and    three    short    creamy    lines    behind — minn- 

tissima  Theobald. 
(n)  Abdomen   black,   fifth   segment    with  yellow   basal   band, 

sixth  unbanded,  (seventh)  two  medio-lateral  white  spots, 

(eighth)  two  baso-lateral  white  spots;  second  hind  tarsi 

nearly  white — dubia  Theobald. 
(b)   Abdomen  unbanded. 

(i)   Third  hind  tarsal  nearly  all  white. 

Thorax  with  two  lateral  white  marks  directed  upwards — 

africana  Theobald. 

(2)  First  bind  tarsal  all  white. 

Thorax  with  one  white  spot  anteriorly,  and  one  in  front 

of  each  wing — apicoargentea  Theobald. 
Thorax  chestnut  brown — terrens  Walker. 
II.  Legs  with  white  lines  as  well  as  basal  bands. 

Thorax  brown,  with  white  lines ;  abdomen  with  basal  bands — granti 
Theobald. 

III.  Fore  and  mid  legs  with  apical  bands;  hind  basal. 

Fourth    tarsal    of     hind-legs     nearly     all    white  —  medio  punctata 

Theobald. 
Base  of  mid-metatarsi,   base  and  apex  of  hind,   and  base  of  first 

tarsal  with  pale  banding — assamensis  Theobald. 

IV.  Legs  unbanded: — 

(a)  Abdomen  basally  banded. 

(1)  Thorax  with   front   half  silvery  white,  remainder   bronzy- 

brown — pseudonivea  Theobald. 

(2)  Thorax    deep    brown  with  scattered    golden    scales — albo- 

cephala  Theobald. 

(3)  Thorax  brown  with  golden  stripes — auriostriata  Banks. 

(b)  Abdomen  banding  indistinct. 

Thorax  with  broad  silvery  white  patch  on  each  side  anteriorly — 
albolateralis  Theobald. 

(c)  Abdomen  unbanded. 

Thorax  with  six  silvery  spots — argenteopunctata  Theobald. 

(d)  Abdomen  with  apical  white  lateral  spots. 

Thorax    unadorned,    except    for    pale    scaled    lines    laterally — ■ 
punctolateralis  Theobald. 


PLATE    IV. 


STEGOMYIA   CALOPUS    MEIGEN. 

Female. 


G«oWatarstot\*  Sons. Ltd  Edir 


To  /ace  page  79s 


CVLEX 


799 


(e)  Abdomen  with  basal  white  lateral  spots. 

(i)   Thorax  with  two  pale,  indistinct,  median,  parallel  lines,  and 

two  silvery  lateral  spots — miniita  Theobald. 
(2)   Thorax  unadorned. 

White  spot  mid-head — tripunctata  Theobald. 

No  white  spot — amesii  Ludlow. 

C.   Proboscis  yellow  basally,  dark  apically. 

Abdomen  with  apical  pale  bands — crassipes  van  der  Wulp. 

1).   Proboscis  with  median  interrupted  white  line  on  basal  half. 
Head  black  with  grey  margin — albomarginata  Newstead. 

Note. — -5.  lamberti  Ventbrillon;  S.  leucomeres,  S.  desmotes  Giles;  S.  striocrura 
Giles,  of  uncertain  position. 


Culex  Linnaeus,  1758. 

Definition. — Cu Ik  id 32  with  head  covered  with  narrow,  curved  scales  above, 
fiat  scales  at  the  sides,  and  upright  forked  scales.     Male  palpi  long,  acuminate. 
Female,  short.    Thorax  with  hair- 
scales    or    narrow 
Linear  lateral  vein- 


like, curved 
curved  scales 
scales. 

Remarks.  —  The  important 
species  are  Culex  pipiens  Lin- 
naeus and  C.  fatigans  Wiedemann. 

Culex  pipiens  Linnaeus,  1758. 

Synonyms.  —  Culex  vulgaris 
Linnaeus,  1767;  C.  alpinus  Lin- 
naeus, 1767;  C.  agilis  Bigot;  C. 
ciliaris  Linnaeus,  1767;  C.  com- 
munis de  Geer;  C.  rufus  Meigen, 
1 81 8  ;  C.  phytophagus  Ficalbi, 
1889. 

C.  pipiens  is  widely  distributed 
in  Europe,  North  Africa,  and 
North  America,  where  it  is  the 
common  brown  mosquito. 

Its  general  appearance  is  well 
shown  in  the  illustration,  in 
which  the  head  is  brownish  from 
the  golden-brown  scales,  as  are 
the  proboscis,  palpi,  and  antennae. 

The  thorax  is  dark  brown,  with  golden-brown  curved  scales,  and  with  three 
black  lines  due  to  black  bristles.  Abdomen  brown,  with  basal  yellow  bands. 
Legs  are  brown  and  unbanded. 


^m^^oooo.:^ 


\      V 


Fig. 


1   \ 


399. — Head  and   Scutellum 
Culex,  to  show  Scales. 


(After  Theobald,  '  Culicidse  of  the  World.') 


Culex  fatigans  Wiedemann,  1S28. 

Synonyms. — Culex cestuans  Wiedemann,  1828;  C.  pungens  Wiedemann,  1828; 
C.  pallipes  Meigen,  1838;  Heteronychia  dolosa  Arribalzaga,  1896. 

This  is  the  common  brown  house-mosquito  of  the  tropics,  which  is  believed 
to  spread  dengue  fever. 

It  resembles  the  above,  but  has  only  two  dark  lines  on  the  thorax  as  a  rule, 
while  the  basal  abdominal  bands  are  white  or  pale  cream  colour,  and  the  first 
fork  cell  is  longer. 

.ZEdin^e  Theobald. 

Culicklae  with  straight  proboscis,   short  palpi  in  both  sexes, 


Definition. 

usually  plumose  antennae  in  the  male,  pilose  in  the  female. 


Wings  with  six 


8oo 


THE  DIPTERA 


scaled  longitudinal  veins,  and  with  the  first  submarginal  cell  as  long  as  or 
longer  than  the  second  posterior.     Post-scutellum  nude. 


Fig.  400. — Culex  pipiens  Linnaeus. 

The   mosquitoes  included  in   this   subfamily  are   generally  found  in  the 
jungle,  and  not  in  habitations. 

Daniels  thinks  that  perhaps  they  may  be  proved  to  be  malarial  carriers  (see 


CHIRONOMIDM 


8oi 


Chapter  XXXV.).     Loew  suspects  some  of  them"  (H&mogogus  ?)  as  possible 
carriers  of  Filaria  (especially  F.  perstans) . 

The  eggs  are  laid  in  rafts,  and  the  larvae  have  respiratory  siphons.  A 
number  of  genera  are  described  by  Theobald,  whose  work  should  be  consulted 
if  further  information  is  desired. 


Limatin,e  Theobald. 


Definition. — Culieidae  with  elbow- 
bent  proboscis  and  squamae  on  post- 
scutellum.  Palpi  short  in  both  sexes. 
First  fork  cell  longer  than  second. 

Genus. — Limatus. 


Family  Corethrid^e 
Eysell,  1905. 

Definition. — Orthorrhapha  ne- 
mocera  with  short  proboscis  not 
formed  for  piercing,  without 
scales  in  the  adult  condition, 
with  transparent  larvae  rather 
resembling  those  of  Chiro- 
nomits. 

Remarks. — The  only  reason 
why  this  family,  which  includes 
the  genera  Corethra  and  Mo- 
chlonyx,  is  mentioned  here  is 
separated  from  the  Culieidae,  of 
Culicimorphae. 


[Fig.  401. — Head  and  Scutellum 
of  yedes,  to  show  scales. 

(After  Theobald,   '  Culieidae  of 
the  World.') 

that   it   has  only  recently  been 
which  it  formed  a  subfamily — 


Family  CmRONOMiDiB. 

Synonyms. — Tipularice  culijormis,  Cidicites  Newman,  TipiladcB 
Leach,  Chironomii  Zelt,  Chironomince  Rondani. 

Definition. — Orthorrhapha  nematocera  with  head  small,  often 
retracted  under  and  covered  by  the  thorax.  Ocelli  absent.  No 
transverse  suture  on  thorax;  eyes  reniform.  Antennae  from  six  to 
fifteen  joints:  pectinate  in  male,  simple  and  composed  of  fewer 
joints  in  female.  Wings  without  veins  along  the  posterior  margin; 
costal  vein  ending  near  the  tip  of  the  wing. 

Remarks.- — The  Chironomidse  include  over  800  species  of  very 
delicate  and  often  quite  minute  flies,  popularly  called  '  midges,' 
which  are  found  all  over  the  world,  especially  near  water. 

Kieffer  classifies  the  family  into  three  subfamilies,  as  follows: — 

A.  Media  and  cubitus  united  by  a  cross  vein — Tanypince. 

B.  Media  and  cubitus  united  only  at  the  base. 

I.  Thorax  humped  over  the  head — Chironomince. 
II.  Thorax  not  humped  over  the  head — Ceratopogonince. 

Of  these  three  subfamilies  only  the  last  concerns  us. 


5* 


8o2  THE  DIPTEUA 

Subfamily  Ceratopogoniisle  Kieffer,  1899. 

Definition. — Chironomidae  with  the  thorax  not  prolonged  over 
the  head,  antennae  with  fourteen,  rarely  thirteen,  joints  in  both 
sexes,  and  the  last  joint  never  longer  than  the  two  preceding  taken 
together,  while  the  last  five  are  longer  or  almost  the  same  as  the 
preceding  joint. 

Life-History. — The  eggs  may  be  laid  on  land  or  water.  If  they 
are  laid  on  land  the  larvae  and  pupae  resemble  those  oiPhlebotomits, 
presently  to  be  described;  while  ii  they  are  laid  in  water  they  occur 
in  small  clusters  of  thirty  to  sixty  eggs.  The  larva  is  snake-like 
and  transparent,  and  lives  on  the  surface  of  stagnant  water,  or 
slowly  flowing  streams,  along  which  it  wriggles  and  finally  develops 
Jnto  a  dark-coloured  inactive  pupa,  with  usually  breathing  organs 
on  the  thorax,  which  floats  on  the  surface  of  the  water. 

Genera. — The  subfamily  has  been  especially  studied  by  J.  J. 
Kieffer,  who  recognizes  the  following  genera:  Leptoconops  Skuse, 
1889;  Cevatopogon  sensu  stricto  Kieffer,  1899;  Culicoides  Latieille, 
1809;  CEcacta  Poey,  1851  ;Bezzia  Kieffer,  1899 ;  Brachypogon  Kieffer, 
1899;  Ceratolophus  Kieffer,  1899 \Palpomyia  Mergele,  1818.  Of  the 
other  genera  usually  mentioned  he  considers  Tersesthes  Townsend, 
1893,  and  Mycterotypus  Noe,  1905,  to  be  simply  synonyms  of  Lepto- 
conops Skuse,  1889;  and  Psychopkcena  Phillipi,  1865,  Tetraphora 
Phillipi,  1865,  and  Didymorphleps  Weyenbergh,  1883,  to  be  identical 
with  either  Certopogon  or  Culicoides,  but  which  it  is  impossible  to 
say,  as  the  descriptions  are  too  imperfect. 

Key  of  Genera, 
(a)  Wings  absent  or  rudimentary. 
(an)   Wings  present. 

(b)  Median-cubital  cross  vein  present  (i.e.,  cell  enclosed  by  a  vein). 
(bb)  Median-cubital  cross  vein  absent. 

(c)  Wing  with  four  to  five  very  indistinct  longitudinal  veins, 
wing  club-shaped,  the  anterior   margin    with  a   long, 
curved  seta;  the  antennae  with  about  twelve  joints. 
(cc)  Wing  margin  without  long,  curved  seta. 
(d)  Proboscis  and  palpi  rudimentary. 
(dd)  Palpi  not  rudimentary. 

(e)  Antennas  with  not  more  than  ten  joints. 
(ee)  Antennas  with  thirteen  to  fifteen  joints. 
(/)   Antennas  fifteen  jointed  (European  and  tropical  genera). 
(g)  Wings  hyaline. 
(gg)  Wings  spotted — (i)   CEcacta. 
(fj)  Antennae  fourteen  or  less  joints. 

(g)  Thorax  rounded  and  not  produced   over  the  head.      Antennae 
thirteen  to  fourteen  joints,  legs  of  moderate  length. 
(Ji)  Antennas  thirteen  joints — (2)  Leptoconops. 
(h/i)  Antennas  fourteen  joints,   plumose  in  the   male,   sparsely 
paired  in  female.     Typical  wing  venation. 
(i)  Wings  hairy;  last  joint  of  tarsus  with  an  empodium. 

(_/')  Empodium  well  developed,  almost  as  long  as  the  claws,  which 

arc  without  setae- — (3)  Ceraiopogon. 
(jj)  Empodium  not  so  distinct,  less  than  half  as  long  as  the  claws, 
which  have  setae  on  the  underside — (4)  Culicoides. 


LEPTOCONOPS  803 

(ii)  Wings  bare;  pulvilli  and  empodium  wanting. 

(;')  Wing  with  R,  distinctly  separated  from  R2+  3,  and  not  connc< 

with  it  by  the  cross  vein  like  R> — (5)  Bezzia. 
[jj)  Wing  with  R._,  present,  cells  sometimes  indistinct. 
(k)  Media  wanting — (6)  Brachypogon. 
(kk)  Media  present. 

(I)  Femora  unarmed — (7)   Ceratolophus. 
(ll)  Some  of  the  femora  spinose  beneath — (8)  Palpomyia. 

Leptoconops  Skuse,  1889. 

Synonyms. — Tersesthes  Townsend,  1893;  Mycterotypits  Noe,  1905. 

The  flies  of  the  genus  are  found  in  Egypt,  Australia,  New  Mexico, 
and  Italy. 

The  various  species  are  L.  kerteszi  Kieffer,  1908;  L.  stygius  Skuse, 
r.889;  L.  torrms  Townsend,  1893;  L.  bezzii  Noe,  1905;  aiidJL  irriians 
Noe,  and  they  can  be  recognized  as  follows: — 

A.  Antennae  of  the  female,  twelve  joints,  with  verticillates  twice  as 
long  as  the  thickness  of  the  joint.  Palpi  three-jointed.  Costal 
nervure  stops  at  the  cubitus.  Legs  without  spines,  except  four 
anterior;  metatarsi-tarsal  hooks  simple  (Egypt— L.  kerteszi  Kieffer). 

B.  Antennas  of  the  female  thirteen  articles. 

I.  Palpi  with  four  joints,  legs  without  spines,  tarsal  hooks 
simple,   costal  nervure  stops  at  the  cubitus,  flagellum 
with  dense  verticillates  (Australia — L.  stygius  Skuse). 
II.  Palpi  with  three  joints. 

(a)  Legs  without    spinules,   tarsal  hooks   simple,   costal 

nervure  nearly  to  the  extremity  of  the  wing,  verticil- 
lates of  flagelli  a  little  shorter  than  thickness  of 
joints  (New  Mexico — L.  ton  ens  Townsend). 

(b)  Legs  armed  with  spinules,  especially  the  tibias. 

(1)  Tarsal  hooklets  of  the  female  with  one  large  basal 

tooth;  those  of  the  male  unequal;  the  anterior 
with  one  long,  curved,  S-shaped  tooth;  the  pos- 
terior with  a  short,  arched  tooth  (Italy — L.  bezzii 
Noe). 

(2)  Tarsal  hooklets  of  the  female  with  one  strong  basal 

tooth,  flagellum  with  some  verticillates,  spinose, 
and  stronger  than  in  L.  bezzii  (Italy — L.  initans 
Xoe). 

New  species  are  L.  laurce  Weiss,  1912,  Tunisia;  and  L.  intermptus  Enderlein, 
1907,  South  Africa. 

Ceratopogon  sensu  stricto  Meigen,  1803. 

Definition. — Ceratopogoninse,  with  long-haired  wings,  especially 
in  the  female,  and  with  a  very  apparent  and  hair}-  empodium  on 
the  last  joint  of  the  tarsus. 

Type.- -Ceratopogon  bipunctatus  Linnaeus. 

Kieffer  has  subdivided  this  genus  into  the  subgenera  Ceratopogon, 
Atrichopogon,  and  Forcipomyia,  but  none  of  the  species  of  these 
genera  are  definitely  known  to  suck  the  blood  of  vertebrates, 


804  THE  DIPTERA 

although  Austen  states  that  in  the  type  specimen  of  the  species 
C.  castaneus  Walker,  1848,  the  abdomen  is  apparently  distended 
with  blood  as  far  as  can  be  judged  by  external  examination. 

Culicoides  Latreille,  1809. 

Synonyms. — Ceratopogon  Meigen,  1803,  pro  parte-  Cheironomus 
Fabricius. 

Definition. — Ceratopogoninae  with  body  small,  pilose,  or  bare. 
Head  depressed  in  front,  prolonged  into  a  short  rostrum.  Proboscis, 
which  is  markedly  longer  than  the  head,  with  fleshy  labium ;  labrum 
horny,  seated  on  base  of  labium.  Maxilla?  long  and  horny.  Antennae 
filiform,  fourteen-jointed,  hairy,  with  the  second  to  eighth  joints 
cylindrical,  ovate,  and  the  next  four  or  five  more  elongate  and  sub- 
cylindrical,  and  the  last  joint  ovate  and  cylindrical.  Subcostal 
vein  ending  much  beyond  half  the  length  of  wing;  radial  ending 


Fig.  402. — Culicoides  pulicaris:  Female. 
(After  Austen,  '  British  Blood-Sucking  Flies.') 

near  tip;  cubital  ending  by  the  tip.  Abdomen  composed  of  eight 
segments.  Legs  almost  equal  in  length ;  femora  armed  beneath  with 
spines. 

Type. — Culicoides  pulicaris  Linnaeus. 

There  are  over  one  hundred  known  species  of  this  genus  (and 
many  more  have  been  described  since  this  statement  was  first 
written),  in  which  only  the  females  suck  blood,  which  they  do  most 
viciously,  and  though  they  are  not  known  to  cause  disease,  still 
they  give  rise  to  much  irritation,  especially  as,  being  very  small, 
they  can  get  through  any  ordinary  mosquito-netting.     The  eggs 


CULICOIDES  GRAHAM  I  805 

of  the  naked  species  are  laid  in  water,  attached  to  floating  algae, 
and  give  rise  \o  white  worm-like  larvae  and  small  pupae,  with 
prominent  respiratory  horns.  The  eggs  of  the  hairy  species  are  laid 
in  decaying  vegetal  matter,  and  give  rise  to  small  larvae. 

Culicoides  grahami  Austen,  1909. 

Synonyms. — Culicoides  habereri  Becker,  1909;  (Ecacta  hoslilissima 
Pittaluga,  1910. 

This  minute  fly  appears  to  be  extremely  common,  and  to  be 
almost  the  most  troublesome  of  these  blood-thirsty  insects  in 
tropical  Africa.  It  is  known  in  the  Spanish  Guinea,  Ashanti, 
Congo  Free  State,  Uganda,  Kamerun,  Southern  Nigeria,  Angola. 
For  fuller  particulars  see  Austen's  '  African  Blood-Sucking  Flies,' 
p.  7,  Plate  I.,  Fig.  3,  and  Pittaluga's  works. 

Culicoides  varius  Winnertz,  1867. 
This  is  the  blood-thirsty  species  in  Europe. 

(Ecacta  Poey,  1851. 

This  genus  is  closely  related  to  Ceratopogon  and  Culicoides.  The  antennae 
have  fifteen  and  the  palpi  five  joints.  Ocelli  are  present.  The  wings  have 
few  cells.  The  tibial  spurs  and  the  pulvilli  are  absent.  The  sexes  are  similar, 
but  the  antennae  of  the  male  are  more  hairy  than  those  of  the  female. 

Species. — CEcacta  furens  Poey,  1851,  found  in  America,  but  according  to 
Austen  CEcacta  hoslilissima  Pittaluga,  191 2,  is  the  same  as  Culicoides 
grahami  Austen,  191 2. 

(Ecacta  furens  Poey,  1851. 
This  is  the  jejen  of  Cuba,  which  is  said  to  be  very  irritating.  Its  length  is 
2  millimetres  from  the  head  to  the  end  of  the  abdomen.  Frons  and  antennae 
rufous.  Thorax  bronze-coloured  with  fuscous  spots;  abdomen  fuscous;  legs 
with  whitish  articulations  and  a  ring  upon  each  femur;  tibia  fuscous.  Wings 
broad,  whitish,  with  fuscous  spots.  They  are  covered  with  minute  scales  and 
possess  conspicuous  marginal  fringes. 

Bezzia  Kieffer,  1899. 

Synonym. — Ceratopogon    Meigen,    1803,    pro   parte.     CeratopogonincB   with 
bare  wings  and  tarsi  without  empodia.     Radius  with  three  branches. 
Type. — Bezzia  ornata  Meigen,  1803. 

Brachypogon  Kieffer,  1899. 
CeratopogonincB  with  bare   wings,   media  coalescent   with   R4+  5,    pulvilli 
absent. 

Type. — Brachypogon  vitiosus  Winnertz,  1852  (?)  1846  (?). 

Ceratolophus  Kieffer,  1899. 

Synonym. — Johannseniella  Williston.  CeratopogonincB  with  bare  wings, 
simple  K    .nul  Ra  connected  by  cross  vein,  tarsal  claws  without  teeth. 

Type.  Ceratolophus  femoratus  Fabricius.  C.fitlcithora.x  Austen,  1912,  isthe 
first  Ccrololophus  to  be  described  in  Africa. 


8o6  THE  DIPTERA 

Palpomyia  Mergele. 

Synonym. — Xylocrypta  Kiefter. 

Ceratopogonince  with  bare  wings  and  five  radial  cells.  R2  present;  media 
simple;  some  or  all  the  femora  spinose  underneath;  pulvilli  and  empodia 
wanting. 

Four  subgenera:  Alasion  Rondani,  1857;  Spheeromyas  Stephens,  1829, 
Serromyia  Mergele,  181 8;  Heteromyia  Say,  1825. 

Family  Psychodidae. 

Definition. — Orthorrhapha  nematoceta  without  ocelli,  and  with 
body  densely  covered  with  coarse  hairs.  Thorax  without  trans- 
verse suture.  Antennae  long,  sixteen- jointed.  Wings  very  broad 
and  hairy.     No  discoidal  cell.     Legs  long,  tibiae  without  spurs. 

Remarks. — The  members  of  this  family  are  small,  sometimes  very 
small  midges,  with  the  bodies  and  wings  thickly  covered  with  hairs 
and  scales,  which  give  them  a  most  characteristic  appearance.  They 
are  found  all  over  the  world,  and  have  a  preference  for  damp, 
shady  places,  while  their  larvae  have  been  found  in  damp  places— 
in  cracks  in  rocks,  old  walls,  etc. ;  in  rotting  vegetation,  liquid  filth, 
and  water.  The  blood-sucking  genera  are:  Phlebolomns  and 
Sycorax  belonging  to  the  Phlebotominae,  and  possibly  one  in  the 
Psychodinae. 

The  Psychodidae  are  classified  into  two  subfamilies: — 

(1)  PsychoMncB. — Psychodidae,  in  which  the  second  longitudinal 
vein  gives  off  its  first  branch  in  the  root  of  the  wing.  The  female 
has  a  horny  ovipositor,  while  the  male  has  two  claspers. 

(2)  Phlebotomince.— Psychodidae,  in  which  the  second  longi- 
tudinal vein  branches  after  it  has  passed  well  into  the  body  of  the 
wing.  The  female  has  not  got  a  horny  ovipositor,  while  the  male 
has  three  claspers. 

Subfamily  Psychodinae. 

The  genera Pevicoma  and  Psychoda  and  their  allies  belong  to  this 
subfamily.  As  a  rule  it  is  stated  that  these  flies  are  not  blood- 
suckers, but  Howlett  states  that  an  Indian  species  occasionally 
sucks  blood. 

Subfamily  Phlebotominae. 

Tli is  subfamily  is  of  importance  not  merely  because  it  contains 
blood-sucking  flies,  but  because  the  genus  Phleboiomiis  is  accused 
of  spreading  the  'Three  Days'  Fever.'  The  two  blood-sucking 
genera  may  be  distinguished  as  follows:— 

(1)  Two  simple  veins  between  the  forks  of  the  second  and  fourth 
longitudinal  veins — PJiIcbotomus. 

(2)  One  simple  vein  between  the  forks  of  the  second  and  fourth 
longitudinal  veins.    Seventh  longitudinal  vein  very  short — Sycorax. 

Phleboiomiis  Rondani,  1840. 

Morphology. — Phlebotominae,  with  mouth-parts  formed  for  pierc- 
ing and  sucking,  palpi  of  five  joints,  antenna:  long,  filiform,  composed 


PHLEBOTOMUS  807 

normally  of  sixteen  segments.  The  thorax  is  mainly  mesothorax, 
the  prothorax  being  very  diminutive,  but  the  scutelium  and  post- 
scutellum  are  well  developed.  Wings  hairy,  narrow,  with  second 
longitudinal  vein  twice  forked,  thus  forming  one  of  the  two  simple 
veins  between  the  forks  of  the  second  and  fourth  longitudinal 
veins,  the  other  simple  vein  being  the  third  longitudinal.  The 
cross  veins  are  placed  near  the  basal  fourth  of  the  wing.  Legs  very 
long  and  slender,  and  densely  clothed  with  scales.  Ungues  simple. 
The  abdomen  has  ten  segments,  the  last  being  modified  for  the 
genitalia,  which  in  the  female  are  flattened,  leaf-like  structures,  and 
in  the  male  very  complex  structures  composed  of  superior  claspers, 
inferior  claspers,  submedian  lamellae,  and  intermediate  appendages, 
and  a  penis. 

The  buccal  cavity  is  wide  in  front  and  narrow  behind,  where  it 
leads  via  the  pharynx  into  the  oesophagus,  which  divides  posteriorly 


Fig.  403. — Phlebotomus  duboscquii  Neveu-Lemaire,  1906. 
(From  a  photograph  by  J.  J.  Bell.) 

into  two  tubes,  one  leading  to  the  sucking  and  the  other  to  the 
mid-gut,  at  the  posterior  extremity  of  which  are  situate  the  four 
Malpighian  tubules,  after  which  come  the  small  and  large  intestines. 
Attention  is  invited  to  the  presence  of  the  sucking  stomach,  and 
to  the  number  of  the  Malpighian  tubules. 

The  female  organs  consist  of  ovaries,  from  which  the  tubular 
oviducts  pass  to  unite  before  reaching  the  base  of  the  inferior 
claspers.     There  are  two  spermathecae. 

The  male  organs  are  testes,  seminal  vesicles,  ejaculatory  duct, 
pompetta  or  little  pump — which  regulates  the  exit  of  the  sper- 
matozoa— and  penis. 

Life-History. — After  fertilization  the  female  takes  a  meal  of 
blood,  even  though  she  may  have  previously  sucked  blood.  She 
then  lays  some  thirty  to  eighty  eggs  in  damp  places,  usually  cracks 
in  rocks,  stones,  or  bricks,  and  in  doing  so  is  apparently  much 


808  THE  DIPTERA 

exhausted,  and  in  captivity  may  soon  die.  The  eggs  vary  in  size 
in  different  species  from  0*15  to  0-5  millimetre  in  length.  They 
are  elongate  oval  in  shape,  marked  with  longitudinal  dark  marks, 
connected  at  places  by  means  of  cross  lines.  The  eggs  are  laid 
singly,  and  require  four  to  six  days  in  warm,  and  fourteen  days  in 
cold,  weather  before  hatching.  The  larvae  measure  some  2  to 
5  millimetres  in  length,  and  are  composed  of  a  head  without  eyes, 
but  with  well-developed  mouth-parts  and  a  Y-shaped  mark,  and 
cylindrical  body  of  twelve  segments,  each  with  a  transverse  row 
of  spinous  hairs,  and  with  spiracles  on  the  first  and  penultimate 
segments.  The  characteristic  point  about  the  larvae  is  the  presence 
of  two  very  long  bristles  situate  on  two  tubercles  on  the  ultimate 
segment.  These  bristles  may  be  as  long  as  the  head  and  body 
taken  together.  The  length  of  the  larval  stages  depends  upon  the 
air  temperature,  and  may  last  from  two  to  fourteen  days. 

The  pupa,  2  to  5  millimetres  in  length,  is  motionless,  lying  in  the 
wrinkled,  brownish  larval  skin  which  envelops  its  last  three  seg- 
ments, and  by  which  it  is  attached  to  the  stone  on  which  it  lives. 
The  duration  of  the  pupal  stage  varies  from  eight  or  nine  to  twenty- 
eight  days.  The  whole  development,  therefore,  requires  about  one 
month  in  warm  and  two  months  in  cold  weather. 

Habits. — These  little  flies  are  essentially  nocturnal  in  their  habits, 
but  are  attracted  by  light.  During  the  day  they  lie  up  in  cool, 
shady  places  in  houses,  etc.,  under  bricks,  in  hollow  trees,  behind 
shutters,  books,  pictures,  etc.,  often  in  bathrooms,  and  more  often 
in  latrines.  They  are  very  small,  and  can  easily  pass  through  the 
meshes  of  an  ordinary  mosquito  curtain  and  fill  themselves  with 
human  blood;  or,  failing  this,  they  will  content  themselves  with 
animal  blood — e.g.,  that  of  cattle,  dogs,  frogs,  geckos,  serpents, 
lizards,  etc.  They  fly  quite  silently,  and  only  the  female  bites, 
and  that  only  at  night.  She  appears  to  be  stimulated  in  her  biting 
propensities  by  an  increase  of  humidity  and  temperature,  and  will 
even  crawl  under  the  bed-clothes  to  get  at  her  victim.  During  the 
act  of  biting  the  posterior  end  of  the  abdomen  is  raised,  while  the 
whole  abdomen  becomes  much  distended  with  blood  and  reddish 
in  colour,  except  at  the  posterior  tip. 

The  originally  replete  female  becomes  half  empty  in  sixteen, 
and  quite  empty  of  blood  in  thirty-six  to  forty  hours.  When  first 
gorged,  she  cannot  fly  easily,  and  may  be  unable  to  escape  from 
the  mosquito  curtain,  where  she  may  be  caught  while  quietly 
digesting  her  enormous  meal.  During  the  day,  as  already  stated,  the 
flies  remain  resting  in  cool,  shady  places  in  houses  and  other  buildings, 
under  bricks,  in  hollow  trees,  behind  shutters,  pictures,  books,  etc., 
and  are  often  found  in  bathrooms,  and  more  often  in  latrines. 

The  larvae  are  very  difficult  to  find,  because  they  are  so  small, 
while  the  pupae  are  even  more  difficult  to  see,  because  not  merely 
are  they  small,  but  they  are  also  of  a  colour  similar  to  the  stones 
to  which  they  are  attached.  Hence  the  habits  of  larvae  and  pupae 
are  not  well  known,  and  require  to  be  restudied.     Their  presence 


PHLEBO  TOM  US  809 

may  be  determined,  even  when  they  cannot  be  found,  by  placing 
the  stones  in  a  glass  case  or  under  fine  netting,  when  the  adult  flies 
will  appear  in  due  course  if  any  pupa  are  present. 

Pathogenicity. — Phlebofomus papatasii  Scopoli,  1786,  is  the  carrier 
of  the  virus  of  '  Pappataci  fever,'  and  the  whole  genus  is  composed 
of  virulent  blood-suckers,  whose  bite  is  generally  severe,  and  may 
be  quite  painful  to  non-immune,  new  arrivals,  when  the  sensations 
produced  by  the  bite  is  stated  to  resemble  that  which  people  imagine 
ought  to  be  experienced  by  the  application  of  a  red-hot  needle. 
The  area  of  the  bite  becomes  a  small  rose-red  papule,  surrounded 
by  a  reddish  macula,  the  total  result  being  a  maculo-papule,  which 
may  persist  for  several  days,  and  is  associated  for  a  day  or  so  with 
a  sensation  of  itching.     Children  are  especially  liable  to  be  attacked. 

Prophylaxis. — Newstead  classifies  the  possible  means  of  prophy- 
laxis into — (1)  Repellents,  (2)  fumigation,  (3)  light,  (4)  artificial 
air  movements,  (5)  traps,  (6)  nets,  (7)  destruction  of  breeding- 
grounds,  and  of  all  these  he  thinks  that  very  fine  spraying  with  a 
1  per  cent,  solution  of  formalin  is  the  most  effective,  especially  if 
performed  during  the  day  into  the  dark  portions  and  angles  of  the 
sleeping-chamber,  while  the  mosquito  curtain  might  be  sprayed 
towards  night.  He  thinks  that  an  electric  fan  and  a  modified 
biscuit -box  trap  lined  with  dark  cloth  and  placed  high  up  in  dark 
places  of  the  sleeping-chamber  would  be  useful.  Major  Crawford 
recommends  the  following  ointment  for  personal  use:  Oleum  anisi, 
1  drachm ;  oleum  eucalypti,  1  drachm ;  oleum  terebinthinse,  J  drachm ; 
and  unguentum  acidi  borici,  1  ounce. 

Species.— The  species  are  fairly  numerous,  and  may  be  grouped  geographic- 
ally as  follows : — 

Europe. — Phlebotomus  papatasii  Scopoli,  1786  (type  species);  P.  minutus 
Rondani,  1840;  P.  mascitii  Grassi,  1908;  P.nigerrimus  Newstead,  1911 ;  P.  per- 
niciosus  Newstead,  191 1. 

Africa. — P.  duboscquii  Neveu-Lemaire,  1906,  found  in  Timbuktu. 

Asia. — P.  papatasii  Scopoli,  I786(?) ;  P.  argentipes  Annandale,  1910;  P.  major 
Annandale,  1910;  P.malabaricus  Annandale,  1910;  P.  babu  Annandale,  1910; 
P.  himalayensis  Annandale,  1910;  P.  perturbans  Meijere;  P.  angustipennis 
Meijere. 

America. — P.  vexator  Coquillett,  1906;  P.  cruciatus  Coquillett,  1906;  P.  ros- 
trans  Summers,  1912. 

Newstead  gives  the  following  table  for  the  purpose  of  recognizing  the 
Phlebotomi  of  Malta: — 

A.  Abdominal  Hairs  Recumbent: — 

(a)  Integument  black.     Large  species.     Palpi  with  second  segment 

slightly  longer  than  the  third — P.  nigerrimus. 

(b)  Integument   ochreous.     Small   species.     Palpi   with  second  seg- 

ment   one-half    the    length    of    the    third — P.    minutus   and 
P.  minutus  var.  africanus  Newstead. 

B.  Abdominal  Hairs  more  or  less  Erect  :— 

(a)  Legs  in  both  sexes  relatively  short ;  average  length  of  hind-leg 

3  millimetres — P.  perniciosus. 

{b)  Legs  in   both  sexes  relatively  long;   average  length  of  hind-leg 

4  millimetres — P.  papatasii. 

Other  species  are: — P.  squamiplairis  in  Khartoum;  P.  antennatus,  Gold 
Coast;  P.  vexator,  P.  legeri  Mansion,  1914,  Corsica;  P.  duboscquii,  Mauritania. 


810  THE  DIPT  ERA 

Phlebotomus  verrucarum  Townsend,  1913,  is  believed  by  Townsend 
to  be  the  carrier  of  Verruga  peruviana,  but  Strong,  Tyzzer,  Brues, 
Sellards,  and  Gastiaburu  consider  that  the  observations  need  con- 
firmation before  they  can  be  accepted. 

Phlebotomus  papatasii  Scopoli,  1786. 

Synonyms. — Cyniphes  molestus  Costa,  1840;  Hermasson  minuius 
Loew,  1844. 

Newstead  reports  that  there  are  two  distinct  colour  varieties  of 
this  insect — viz. :  (1)  A  uniformly  pale  variety  which  is  to  be  con- 
sidered typical;  and  (2)  a  variety  with  a  dark  fringe  to  the  costa 
and  hind  margin  of  wing.  These  two  varieties  he  distinguishes 
as  the  pale  variety  and  the  dark  variety. 

Pale  Variety. — Almost  uniformly  pale,  translucent,  ochreous; 
thorax  with  a  long,  dull,  red-brown  median  stripe  and  a  single  spot 
of  the  same  colour  on  either  side  near  the  front;  wing  fringe  not 
markedly  darker  than  the  hairs  on  the  disc  of  the  wing. 

Dark  Variety. — Female  with  general  colour  of  pale  form,  but 
with  wing  fringes  smoky  grey,  and  some  of  the  hairs  on  the  veins 
also  dark  grey  or  smoky  grey.     The  male  was  not  observed. 

Life-History. — Ovum  when  first  expelled  shows  the  oolemma 
(interior)  and  a  micropyle  at  anterior  end.  The  first  instar  of  the 
larva  is  caterpillar-like.  Two  pairs  of  caudal  bristles,  one  much 
longer  than  the  other,  the  other  pair  very  short.  Length,  2  to 
3*28  millimetres.  Pupa  with  abdomen  curved  upwards  in  varying 
degree.  The  eggs  hatch  in  six  to  nine  days,  and  the  larvae,  which 
live  in  the  earth,  become  pupae  in  about  eight  weeks.  The  total 
item  of  development  is  about  ten  to  eleven  weeks,  and  the  life  of  the 
fly  is  about  eight  days. 

Pathogenicity. — It  is  the  carrier  of  Pappataci  fever. 

Family  Simuliid^e. 

Synonyms. — Melusinidce,  Tipularice  Meigen,  Simtdides  Zelt, 
Sinuilitcs  Newman,  Simulince  Rondani. 

Ortliorrhapha  nematocerawithout  ocelli;  without  transverse  suture 
on  the  thorax;  with  short  legs,  in  which  the  posterior  tibiae  and  the 
first  joint  of  the  hind  tarsi  are  dilated;  with  short,  straight,  cylin- 
drical, eleven-jointed  antennae  without  setae.  Eyes  of  the  male 
are  large,  and  meet  in  the  middle  line,  while  those  of  the  female  are 
smaller  and  separate.     Size,  1  -5  to  4  millimetres  in  length. 

The  Simidiidce  or  Melusinidce  are  the  sand-flies,  also  called 
'  brulots  '  or  '  potu  '  flies,  and  have  a  wide  distribution,  being  par- 
ticularly found  in  the  tropics,  but  are  also  well  known  in  Europe. 
Though  small  in  size,  they  are  great  blood-suckers,  attacking  man 
and  beast,  and  also  other  insects,  but  only  the  females  suck  blood. 

Though  there  is  only. one  genus,  Mehtsina  Meigen,  1800,  more 
correctly  known  as  SimuUum  Latreille,  1802,  there  are  very  many 
species — i.e.,  about  seventy — of  which  SimuUum  reptans  Latreille 


SIMULIIDM 


8ti 


and  S.  hirtipes  Fries  arc  known  in  Scotland.  S.  colwnbaczense 
Schonberg,  locally  known  as  the  '  banat,'  is  the  cause  of  much 
destruction  of  cattle  in  South  Hungary.  S.  indicum  Becher  is 
the  '  dam  din  '  of  Assam,  which  is  a  cause  of  irritation  to  tea- 
coolies.  5.  damnosnm  Theobald  in  Uganda,  where  it  is  called 
'mbwa,'  and  in  the  Sudan,  where  it  is  called  'kunteb';  and 
S.  griscicollis  Becker,  of  Dongola,  locally  called  '  nimetta,'  are  very 
virulent.  Austen  says  that  the  '  potu  '  flies  were  accused  of  having 
caused  the  death  of  coolies  while  constructing  an  Indian  road. 
The  effects  of  the  bite  of  these  small  insects  is  most  irritating,  and 
the  appearance  of  a  person  after  a  severe  attack  is  most  peculiar, 
the  face  and  hands — i.e.,  the  exposed  parts — being  covered  with 
papules. 

Life-History. — -The  eggs  are  deposited  on  stones  or  plants  in 
running  water.  The  larva  is  broad  posteriorly,  where  it  possesses 
a  sucker,  capable  of  attaching  it  to  any  convenient  object.  An- 
teriorly it  has  two  fan-like  organs.     It  moves  about  in  the  water 


Fig.  404. — Simuliiim  reptans  Latreille:  Female. 


after  the  manner  of  a  leech,  and  also  by  the  aid  of  a  silken  thread 
which  it  spins.  It  feeds  on  water  plants.  The  larval  stage  lasts 
about  a  month,  when  a  cocoon  is  spun,  inside  which  the  pupa  is 
formed.  The  pupa  breathes  by  means  of  branched  filaments,  and 
at  the  end  of  a  week  becomes  the  imago,  which  is  carried  to  the 
surface  of  the  water  in  an  air-bubble. 

Habits. — -The  Simuliidce  live  in  the  open  country,  and  very 
rarely  enter  houses.  They  can  be  found  in  the  early  morning,  or, 
better,  in  the  late  afternoon,  flying  in  clouds.  During  the  day- 
time they  can  be  found  on  trees,  grasses,  etc.  It  is  common  to 
find  the  males  quite  close  to  the  streams  in  which  the  eggs,  larvae, 
and  pupae  abound ;  but  the  female  can  apparently  travel  for  con- 
siderable distances  in  search  of  food,  and  can  quite  easily  be  caught 
on  the  wing.  They  may  also  be  found  in  the  ears  of  cattle,  donkeys, 
etc.,  where  they  feed.  They  are  not  all  vicious,  blood-thirsty 
insects.  Thus,  for  example,  5.  venustum  Say  is  said  to  be  quite 
peaceably  disposed.     It  is  quite  possible  that  in  some  instances 


812 


THE  DIPTERA 


mistakes  have  been  made  with  regard  to  the  blood-thirsty  pro- 
pensities of  some  species,  and  it  is  possible  that  the  real  culprit 
was  one  of  the  Ceratopogoninae,  and  therefore  it  is  necessary  to  be 
quite  certain  that  the  insect  in  question  is  really  a  Simulium,  and 
this  can  only  be  done  by  careful  examination.  For  purpose  of 
quick  field  examination,  it  is  as  well  to  inspect  the  antennae  care- 
fully, as  they  are  fairly  characteristic. 

Enemies. — 'The  Simuliidce  have  many  enemies,  among  which 
may  be  mentioned  the  larvae  of  the  May-  and  that  of  the  Caddis-fly, 
and  many  kinds  of  fish  which  prey  upon  the  larvae,  pupae,  or  flies. 


-H, 


Fig.  405. 


-Simulium  Larva. 
(X8.) 


Fig.  406. — Simulium  Pupa. 
(X8.) 


Classification. — The  genus  has  been  divided  into  two  subgenera 
by  Roubaud — i.e.,Prosimulium  and  Eusimulium,  but  the  differenti- 
ation of  the  species  is  very  difficult.  In  fact,  the  family  urgently 
requires  revision. 

Pathogenicity. — Although  sand-flies  are  very  irritating,  and  cause 
the  death  of  cattle,  it  is  not  known  whether  they  are  the  carriers  of 
any  definite  disease  of  cattle  or  man,  though  it  seems' possible 
that  they  may  be  associated  with  the  spread  of  pellagra,  as  Sambon 


REFERENCES  813 

has  suggested;  but  more  will  be  said  on  this  subject  when  dis- 
cussing pellagra  in'Chapter  LXXHI. 

Marchoux  and  Borret  have  suggested  that  sand-flies  may  play  a 
role  in  the  transmission  of  leprosy. 

Family  Blepharocerid,e  Loew,  i860. 

Orthorrhapha  nematocera,  without  discal  cell  and  with  a  secondary  set  of 
crease-like  lines  on  the  wings. 

In  this  family  the  genus  Curupira  Osten-Sacken  is  said  to  contain  species 
which  suck  blood.  The  larvae  live  in  rapid  streams.  C.  torrentium  (Mtiller) 
is  found  in  Brazil. 

REFERENCES. 

Blepharoceridae. 

Kellogg  (1903).     The  Net- winged  Midges. 

Diptera. 

Williston  (1908).     North  American  Diptera.     London  (a  most  useful  book). 

Culicidae. 

Blanchard,  R.  (1905).     Les  Moustiques.     Paris. 

Christophers  (1901).     Royal  Society  Reports  to  Malarial  Committee,  No.  4. 

Ficalbi,    E.    (1896).     Revisione    sistematica    della   famiglia    delle   Culicide 

Europee.     Firenze. 
Giles  (1904).     Gnats  or  Mosquitoes.     Second  edition,  1902;  supplemented. 
Innes  (1908).     Journal  of  Parasitology,  vol.  i.,  No.  2. 
James  and  Liston  (1904).     Anopheles  Mosquitoes  of  India. 
Leicester    (1908).     Studies   from   Institute   for   Medical   Research,    Malay 

States,  III.,  Part  3,  168. 
Nuttall  and  Shipley  (1901).     Journal  of  Hygiene,  vol.  i.,  1901,  4.  451: 

1907,  ibid.,  297. 
Theobald  (1901-10).     The  Culicidae  of  the  World,  vols.  i.-v. 

Chironomidae. 

Miall  and  Hammond  (1900).     The  Harlequin  Fly.     Oxford. 
Theobald  (1892).     British  Flies,  vol.  i.     London. 

Psychodidae. 

Austen  (1909).     Trans.  Society  Trop.  Medicine  and  Hygiene. 

Blanchard,   R.   (1909).     Archives  de  Parasitologic,  XIII. ,  No.  2   (Phlebo- 

tomus) . 
Scopoli,  A.  (1786-88).     Deliciae  Florae  et  Faunas  Insulricae.    Ticino. 
Walker  (1856).     Insecta  Britannica:  Diptera.     London. 

Simuliidae. 

Ballon  (1908).  Imperial  Department  of  Agriculture,  West  Indies.  Pam- 
phlet Series,  No.  55. 

Christy  (1908).     Sleeping  Sickness  Report,  Royal  Society,  London.     No.  3. 

Leon  (1909).  Centralblatt  fur  Bakteriologie.  Bd.  51,  Heft  6,  S.  659  (S. 
columbaczense) . 

Theobald  (1903).     Ibid.,  No.  2. 


CHAPTER  XXXIII 

DIPTERA  (concluded) 

MUSCID^E  AND  ALLIED   FAMILIES 

Flies — Orthorrhapha — Brachycera — Tabanidse — Leptidae — Asilidae  —  Phoridae 
— Scenopinidae — Empidae- — ■  Cyclorrhapha  —  (Estridae  —  Sarcophagidae  — 
Muscidae — Anthomyidae— Pupipara — References. 

BITING  AND  PARASITIC  FLIES. 

This  chapter  deals  with  all  those  insects  which  come  under  the 
term  '  biting  and  parasitic  flies.'  In  medicine  they  are  of  importance 
because  of  their  blood-sucking  habits,  through  which  they  are  able 
to  disseminate  animal  parasites.  Further,  the  larvae  of  certain 
species  may  enter  the  skin  or  the  alimentary  canal,  and  cause 
irritation  and  disease  in  this  way  (Myiasis  Hope,  1837). 

Continuing  the  classification  of  the  Diptera  already  given,  the 
first  section  included  in  this  chapter  is  that  known  as  the  Brachy- 
cera. 

SUBORDER  I.    ORTHORRHAPHA. 

SECTION  BRACHYCERA. 

The  principal  Orthorrhapha  Brachycera  may  be  divided  into  two 
groups : — ■ 

Group  i:  Brachycera  Homceodactyla.- — Imago  with  pulvilliform 
empodia.  Larvae  with  a  terminal  posterior  stigma.  Families: 
Tabanidae,  Leptidae,  Stratiomyidae. 

Group  2:  Brachycera  Heterodactyla.- — Imago  with  empodia  un- 
developed or  bristle-like.  Posterior  stigma  of  the  larva  not  ter- 
minal.    Families:  Asilidae,  Empididae. 

BRACHYCERA  HOMCEODACTYLA. 

The  families  with  which  we  are  concerned  may  be  recognized  as 
follows: — ■ 

A.  Antennae  composed  of  more  than  five  joints,  or  third  joint 

complex. 
I.  Squamae  large — Tabanidce. 
II.  Squamae  small. 

Tibia  with  spurs — LepHdce  in  part. 

B.  Antennae  composed  of  three  joints  or  third  joint  simple— 

Leptidce  in  part. 

814 


TAB  AN  I  DM 


815 


Family  Tabanid^e. 

Orthorrhapha  Brachycera  with  bulky  bodies  and  often  large 
heads.  The  eyes  usually  meet  in  the  males,  but  are  separate  in 
the  females.  Antennae  with  third  joint  marked  by  four  to  eight 
annuli,  but  without  a  terminal  bristle.  Proboscis  strong  and 
prominent.  Thorax  narrower  than  the  head.  Wings  with  large 
basal  cells  and  five  posterior  cells.  Third  longitudinal  vein  bifur- 
cate.    Legs  moderately  stout.     Empodia  large. 


Fig.  407. — Tabanns  bovinus  Linnaeus:  Female. 


Remarks. — The  Tabanidge  are  blood-sucking  flies,  of  which  some 
2,000  species  are  known.  The  blood-sucking  habit  is  confined  to 
the  females,  while  the  males  live  on  the  juices  of  plants.  They 
are  variously  known  as  horse-flies,  breeze-flies,  gad-flies,  serut-flies 
(Nile),  and  mangrove-flies  (West  Africa),  and  are  distributed  widely 
over  the  world.  They  are  in  the  habit  of  coming  to  water  for 
drinking  purposes,  and  this  has  enabled  them  to  be  killed  in  large 
numbers  by  sprinkling  the  water  with  kerosene,  which  probably 
prevents  them  escaping  from  the  surface  of  the  water,  and  partially 
kills  them  by  its  poisonous  effects. 

Morphology. — As  a  rule  the  head  is  as  wide  or  wider  than  the  thorax,  convex 
anteriorly,  and  concave  posteriorly,  with  very  large,  brilliantly  coloured  eyes, 
with  golden-green  or  purple  markings. 

The  antenna?  are  very  distinct,  but  the  proboscis  varies,  being  very  short 
in  some  genera  and  enormously  long  in  others.  In  the  genera  in  which  it  is 
short  it  hangs  vertically  downwards  from  the  head.  It  consists  of  a  labrum, 
two  maxillae  with  palps,  two  mandibles,  a  hypopharynx,  and  a  thick  labium 


8i6 


THE  DIPTERA 


with  well-marked  labial  palps  (labella).  The  wings  have  a  large  discoidal 
cell  and  very  elongate  basal  cells.  When  at  rest  the  wings  diverge  at  the 
tips.  They  may  be  mottled.  The  legs  are  large  and  strong.  The  body  is 
brown,  whitish,  or  yellowish  in  colour,  but  there  may  be  markings  on  the 
abdomen. 


Fig.  408. — Antennae  of  the  Tabanidje. 

a,  a',  a",  Silvius;  b,  b',  Chrysops;  c,  Rhinomyza;  d,  d' ,  Cadicera;  e,  Dorca- 
loemus;  /,  Pangonia;  g,  Erephopsis;  h,  Lepidoselaga;  i,  V,  Tabanus;  j,  j', 
Hsematopota;  k,  k',  Hippocentrum. 

Life-History.— The  eggs,  which  are  spindle-shaped,  and  whitish 
in  colour,  are  laid  in  raft-  or  flask-shaped  masses  attached  to 
water-plants.  The  larvae  live  either  in  water  or  damp  earth,  and 
feed  upon  small  animal  organisms.  They  are  spindle-shaped  and 
segmented,  with  knobs  or  protuberances  on  the  rings,  either  all 
round  or  only  ventrally.  The  pupa,  which  is  free,  is  found  in  water 
or  damp  rubbish. 


r?-** 


-^^^3>f0£ 


Fig.  409.— Larva  of  a  Tabanus.     (X2J.)  * 

Pathogenicity. — It  is  possible  that  they  may  disseminate  try- 
panosomes.  The  diseases  m'bori  in  dromedaries  in  Timbuktu  and 
souma  in  Segon  are  believed  to  be  spread  by  Tabanus  ditceniatus, 
while  the  dromedary  disease  of  Algeria  is  spread  by  T.  nemoralis 
Meigen  and  T.  nigritus  Fabricius.  T.  glaucopis  Meigen  is  infected 
with  Herpetomonas  subulata.  According  to  Leiper,  Chrysops  is  the 
carrier  oiLoa  loa  Cobbold,  1864. 


TABANINJE  817 

Prophylaxis. — -Kerosene  spread  on  water  appears  to  be  the  best 
method  of  dealing  with  these  pests. 

Classification.— The  family  is  divided  into  two  subfamilies: 
Tabanime  and  Pangoninae. 


Fig.  410. — Pupa  of  Tabanus  kingi  Austen.     (After  King.) 

(From  the  Fourth  Report  of  the  Wellcome  Tropical  Research  Laboratories, 

Khartoum.) 

TABANIN.E. 

Tabanidae  without  spurs  on  the  hind  tibia . 

The  important  genera  of  the  Tabanime  may  be  recognized  by  the 
following  table  :— 

I.  Thorax  and  abdomen  with  iridescent  torn  en  turn- — -Lepido- 
selaga. 
II.  Thorax  and  abdomen  without  iridescent  tomentum. 
1.  Eyes  bare. 

(a)  Third  joint  of  the  antenna  without  basal  tooth  :• — ■ 

(1)  Antennae  extremity  slender,   and  first  joint 

elongate — Hippo  centrum  (Fig.  408,  k,  k'). 

(2)  Antennae   not   remarkably  slender  and   first 

joint     not     remarkably    elongate — Hamct- 
topota  (Fig.  408,  /,  /'). 

(b)  Third  joint  of  the  antenna  with  well-developed 

basal  tooth — Tabanus  (Fig.  408,  *",  i'). 

Lepidoselaga  Macquart,  1838. 

Synonym. — Hadrus  Perty. 

Lepidoselaga  lepidota  Wiedemann,  1828,  the  motiica  fly  of  Brazil, 
is  a  well-known  biter.     (Antennae:  vide  Fig.  408,  h.) 

Haematopota  Meigen,  1803. 

Synonym. — Chrysozona  Meigen,  1800. 

The  number  of  species  comprised  in  this  genus  is  rapidly  in- 
creasing. About  130  have  already  been  described,  and  Austen 
informs  us  that  many  more  still  await  description  from  Africa  alone. 
The  characteristics  of  a  species  belonging  to  this  genus  are- — The 
elongate  antennae,  the  peculiar  wing-markings  (Fig.  412),  and  the 
peculiar  arrangement  of  the  wings  when  at  rest,  when  the  bases 
meet  together,  while  the  rest  of  the  wings  diverge  slightly  and 
slope  backwards  and  outwards.    The  species  of  Hamettopota  are 

52 


8i8 


THE  DIPTERA 


very  blood-thirsty,  and  are  a  terrible  pest  in  the  wet  season  to  man 
and  beast  alike.  Thev  are  said  never  to  bite  in  the  early  morning 
or  after  sunset,  but,  on  the  contrary,  Mayer  states  that  H.  decora 
is  most  troublesome  in  the  early  morning  and  late  evening.     Neave 


Fig.  411. —Lcpidosela§a  lepidola  Wiedemann:  Female.     (Xt>.) 


Fig.  412. — Hcematopota  vittata  Loew.     (X4O 

states  that  the  females  bite  in  rather  dull,  damp  weather,  and 
rarely  in  the  heat  of  the  sun,  being  mostly  in1  evidence  from  about 
8  to  10  a.m.  and  from  4  p.m.  to  sunset  in  sunny  weather,  but  in 
the  shady,  damp  forest  they  may  be  troublesome  all  day.    The 


HIPPOCEN'IRUM  819 

life-history  of  the  tropical  species  is  but  little  known,  but  Neave 
thinks  that  the  majority  of  the  species  may  have  two  broods.  The 
life-history  of  H.  pluvialis  Linnaeus  is  partially  known.  The  egg 
stage  has  not,  so  far  as  we  know,  been  observed.  The  larva  and 
pupa  are  of  the  Tabanid  type,  as  described  above.  With  regard 
to  pathogenicity,  Balfour  reports  El  Takasha  ('  the  attacking  fly  '), 
probably  H.  tacituma  Austen,  is  believed  to  cause  swelling  of  the 
lungs  in  sheep  and  goats. 

With  regard  to  individual  species,  H.  pluvialis  Linnaeus  is  common 
in  Europe,  while  H.  grahami  Austen,  1912;  H.  daveyi  Austen,  1912; 
H.  rubens  Austen,  1912 ;  H.  beringeri  Austen,  1912 ;  H.  crudelis  Austen, 
1912;  are  some  new  species  recently  described  by  Austen  from 
tropical  Africa.  Other  species  are  H.  obscura  Loew,  1875,  in  South 
Africa;  H.  vittata  Loew  in  tropical  Africa;  and  H.  bullalifrons 
Austen  in  Northern  Nigeria. 

Hippocentrum  Austen,  1908. 

This  genus  is  nearly  allied  to  Hcematopota  Meigen,  1S03,  but  is, 
according  to  Austen,  distinguished  by  the  fact  that  the  head  is 
for  the  most  part  shining,  the  antennas  extremely  slender,  and  the 
first  joint  elongate  (Fig.  40S,  k,  ft'),  and  the  terminal  joint  of  the 
palpi  in  the  female  very  large  and  shining  on  the  outer  side,  which 
is  strongly  convex,  while  the  inner  side  is  flattened;  the  wings  are 
more  or  less  suffused  with  dark  colour,  interrupted  with  pale  streaks 
or  blotches  without  the  peculiar  light  markings  of  Hcematopota. 

Species. — H.  versicolor  Austen,  1908,  in  Uganda  and  the  Lado, 
H.  trimaculatum  Newstead  in  West  Africa,  H.  strigipennis  Karsch, 
which  may  be  identical  with  H.  trimaculatum,  has  only  been  found 
in  Gaboon,  and  H .  murphyi  Austen,  1912,  in  West  Africa.  The 
females  bite  man  and  animals.    The  life-history  is  unknown. 

Tabanus  Linnaeus,  1761. 

There  are  over  900  known  species  of  Tabanus,  of  which  Tabanus 
bovinus  Linnaeus,  1761,  is  found  in  Europe,  Asia,  and  South  Africa. 
In  the  Sudan  these  flies  are  called  serut-flies:  T.diiceniatus  Macquart, 
T.  grains  Loew.T.  /<#m'o/«PalisotdeBeauvois,  T.fasciatus  Fabricius, 
T.  africanus  Gray,  may  be  noted.  In  West  Africa  they  are  known 
as  mangrove  flies.  Recently  Patton  has  described  the  life-cycle 
of  a  Crithidia  (C.  tabani  Patton,  1909),  which  is  a  true  parasite  of 
T.  hilarius  and  another  species. 

Subgenus  Therioplectes  Zcller,  1842. 

A  number  of  species  of  this  genus  are  known  in  Europe.  Therioplectes 
micans  Meigen,  T.  borealis  Meigen,  T.  montanus  Meigen,  and  T.  tropicus,  may 
be  mentioned. 

Subgenus  Atylotus  Osten  Sacken,  1876. 
Atylotus  fulvus  Meigen  $nd  A-  msticus  FabriQius  are  met  with  in  Europe, 


820 


THE  DIPTERA 


Other  Genera. 

In  1906  Griinberg  described  three  genera,  with  one  species  in  each,  as 
belonging  to  the  Tabaninse — viz.,  Thaumastocera — T.  akiva — in  West  Africa; 
Holoceria — H.  iiobilis — in  Tropical  East  Africa;  Parhcematopota — P.cognata — 
in  Tropical  East  Africa  and  Zanzibar;  while  other  genera  are  Hexatoma  Meigen 
in  Europe,  Dasybasis  Macquart  in  South  America  and  Australia,  Bolbodimyia 
Bigot  in  South  America,  Udenocera  Ricardo  in  Ceylon,  Diachlorus  Osten 
Sacken  in  America,  Stibasoma  Schiner  in  South  America,  Acanthocera  Mac- 
quart  in  South  America,  Dichelacera  Macquart  in  South  America,  and  Selasoma 
Macquart  in  South  America. 

PANGONIINiE. 

Tabanidae  with  hind  tibias  armed  at  the  tips  with  spurs. 

I.  Prosboscis  short. 

1.  Antennae  longer  than  the  head — Chrysops. 

2.  Antennas  shorter  than  the  head — Silvias. 
II.  Proboscis  long. 

1.  Proboscis  little  longer  than  the  head — Cadiccra. 

2.  Proboscis  usually  much  longer  than  the  head,   often 

longer  than  the  body— Pangonia. 

Chrysops  Meigen,  1803. 

This  genus  has  become  of  greater  importance  since  Leiper  has 
shown  that  it  includes  the  carrier  of  Loa  loa  Cobbold,  1864,  which 
in  its  turn  is  suspected  to  be  the  cause  of  Calabar  swellings. 

The  genus  is  world-wide  in  its  distribution,  and  is  said  to  contain 
more  than  160  species,  of  which  some  seventeen  or  more  have  been 

J 


Fig.  413. — Chrysops  wellmani  Austen:  Female.      (X4^-) 

found  in  the  Ethiopian  region.  The  African  flies  belonging  to  the 
genus  are  of  medium  size,  not  exceeding  10-5  millimetres  in  length 
according  to  Austen.  The  wings  of  the  majority  show  a  conspicuous 
black  band  (Fig.  413)  running  across  the  surface.  There  are  three 
ocelli  on  the  crown  of  the  head.  The  characters  of  the  antennae  are 
shown  in  Pig.  408,  b,  b';  in  the  latter  the  first  joint  is  shown  to  be 
conspicuously  swollen.     During  life  the  eyes  are  of  a  golden-green 


CHRYSOPS 


821 


colour,  and  are  marked  with  purplish  spots  and  streaks,  which 
Austen  considers  presenl  useful  specific  characters.  Whenresting, 
the  wings  are  kept  half  open. 

The  females  inflict  a  very  severe!  bite,  which  causes  pain,  in- 
flammation, and  even  at  times  <  edema  and  fever. 

The  eggs,  which  at  first  arc  white  and  later  turn  brown  or  black, 
are  deposited  upright  in  a  single  layer  upon  leaves  and  stems  of 
plants  near  water,  in  which,  or  in  the  mud  in  the  vicinity,  the  larvae 
live.  The  larvae  and  pupae  resemble  those  of  Tabanus,  but  in  the  larva 
the  last  antennal  joint  is  longer  than  the  penultimate,  and  in  the 
pupae  the  antennae  project  beyond  the  head.  With  regard  to  patho- 
genicity, the  genus  is  now  known  to  contain  the  carrier  of  Loa  loa. 


Fig.  414. — Cadicera  chvysostigma  Wiedemann:  Female.     (X  2j.) 

As  examples  the  following  species  may  be  mentioned:  C.  dimi- 
diate van  der  Wulp,  1885,  in  West  Africa;  C.  distinctipennis  Austen, 
1906,  in  tropical  Africa  generally ;  C.  bicolor  Cordier,  1907,  in  Tropical 
East  Africa;  C.  silacca  Austen,  1907,  in  West  Africa;  C.  magnified 
Austen,  1911,  in  Tropical  East  Africa;  C.  centurionis  Austen,  1911, 
in  Uganda;  C.  cana  Austen,  1911,  in  East  Africa;  and  C.  dispar 
Fabricius  in  the  Oriental  region. 

Silvius  Meigen,  1S20. 

This  widely  distributed  genus  may  be  exemplified  by  Silvius 
fallax  Austen,  1912,  found  in  North-Eastern  Rhodesia,  and  S. 
decipiens  Loew.  The  characters  of  the  antennae  are  illustrated 
in  Fig.  408,  a,  a',  and  a". 

Cadicera  Macquart,  1854. 
Over  a  dozen  species  of  this  genus  are  now  known  in  the  Ethiopian 
region,  of  which  the  following  may  be  mentioned:  C.  tnelanopyga 


822 


THE  DIPTERA 


Wiedemann,  1819;  C.  chrysostigma  Wiedemann,  182S;  C.  rubra- 
mzrginata  Macquart,  1885;  C.  quinquemaciilata  Austen,  1908;  C. 
biclausa  Loew,  i860;  C.  chrysophila  Macquart,  1834;  C.  distant* 
Austen,  1912;  C.  speciosa  Austen,  1912;  C.  flavicoma  Austen,  1912; 
and  C.  obscura  Ricardo,  1908.  The  females  have  been  observed 
to  bite  man,  but  very  little  is  known  as  to  the  habits  or  life-history 
of  the  species  of  this  genus. 

Pangonia  Latreille,  1802. 
This  widely  distributed  genus  used  to  contain  a  very  large  number 
of  species,  but  has  of  late  been  split  up  into  several  subgenera, 


TERZi. 

Fig.  415. — Pangonia  ruppellii  Jaennicke,  1867:  Female.     (X3-) 


as  may  be  shown  in  the  following  table  taken  from  Miss  Ricardo's 
paper  in  The  Annals  and  Magazine  of  Natural  History,  Series  7, 
vol.  v.,  January,  1900: — 

I.  Wings  with  first  posterior  cell  closed. 

(a)  Eyes  bare — Pangonia  Latreille  (subgenus Pangonia). 

(b)  Eyes  hairy — Pangonia  Latreille  (subgenus  Erephopsis 

Rondani). 

II.  Wings  with  first  posterior  cell  open. 

(a)  Eyes  hairy — Diatomineiira  Rondani  (subgenus  Dialo- 

mineura). 

(b)  Eyes  bare — Dialomineura  Rondani  (subgenus  Corizo- 

neura  Rondani). 


RHINOMYZA  823 

The  characteristic  of  the  genus  is  the  extremely  long  proboscis. 
The  antennal  characters  of  Pangonia  are  shown  in  Fig.  408,  /, 
and  of  Erephopsis  at  g  in  the  same  figure.  The  females  arc  known 
to  be  very  blood-thirsty  and  to  bite  while  on  the  wing,  a  feat  which 
they  can  "readily  perform  owing  to  the  length  of  the  proboscis.  At 
the  present  time  the  life-history  is  unknown,  and  the  pathogenicity 
is  also  unknown. 

As  examples  the  following  may  be  mentioned : P.  ro strata  Linnaeus, 
1764;  P.  varicolor  Wiedemann,  1828;  P.  gulosa  Wiedemann,  1828, 
in  Africa;  P.  beckeri  Bezzi,  1900,  in  Somaliland;  P.  rilppellii  Jaen- 
nicke,  1867,  in  the  Anglo-Egyptian  Sudan  and  British  East  Africa; 
P.  comata  Austen,  1912,  in  East  Africa;  Diatomineura  snavis  Loew, 
1858,  in  South  Africa;  D.  (Corizoneura)  lineatithorax  Austen,  1912,  in 
Northern  Rhodesia;  D.  (Corizoneura)  penetrabilis  Austen,  1912, 
in  Northern  Rhodesia;  and  D.  (Corizoneura)  hasta  Austen,  1912, 
in  Portuguese  East  Africa. 

Rhinomyza  Wiedemann,  1820. 
In  this  genus  the  first  and  second  segments  of  the  antenna  are 
short,  while  the  third  segment  is  composed  of  five  rings  (Fig.  408,  c). 
Moreover,  the  third  segment  has  a  well-marked  tooth.  The  pro- 
boscis is  short.  R.  fusca  Wiedemann,  1820,  is  known  in  Java, 
and  R.  denticornis  Wiedemann,  1828,  in  South  Africa.  R.  costata 
Loew,  R.  edentula  Wiedemann,  and  R.  pusilla  Schiner  may  also 
be  noted,  as  may  R.  umbraticola  Austen,  1911,  in  North-Eastern 
Rhodesia  and  Kalanga,  while  R.  maculata  Surcouf  is  found  in 
Madagascar. 

Other  Genera. 

Other  genera  of  the  Pangoniinse  are  Dicrania  Macquart  in  Brazil,  Apo- 
campta  Schiner  in  Australia,  Pityocera  Tos  in  Central  America,  Goniops 
Aldrich  in  North  America,  Pelecorhynchus  Macquart  in  Australia  and  South 
America,  Apatolestes  Williston  in  California,  Dorcalcemus  Austen  in  South 
Africa,  Scione  Walker  in  South  America,  Pronopes  Loew  in  South  Africa, 
Gastroxides  Saunders  in  India,  and  Subpangonia  Surcouf  in  West  Africa. 

Family  Leptid^e. 

Orlhorrhapha  brachycera  with  brownish,  medium-sized,  or  long  narrow 
bodies  and  small  heads.  The  third  antennal  joint  is  short,  and  carries  either 
a  terminal  brush  or  bristle.  The  proboscis  resembles  that  of  the  Tabanidas, 
as  does  the  wing  venation. 

Three  genera  are  accused  of  blood-sucking:  Leptis,  Symphoromyia,  and 
Trichopalpus . 

With  regard  to  Leptis,  the  species  L.  scolopacea  Linnaeus  and  L.  strigosa 
Meigen  are  said  to  bite  persons  in  France,  but  this  is  rare.  Symphoromyia 
(species  uncertain),  characterized  by  a  single  spur  on  the  hind  tibia  and  a 
kidney-shaped  third  antennal  joint,  is  found  in  California.  Trichopalpus 
obscurus  Phil,  is  known  in  Chili. 

The  life-history  of  the  blood-sucking  species  is  not  known,  but  the  other 
larvae  of  the  Leptidae  live  upon  decaying  vegetable  matter. 


824  THE  DIPTERA 

BRACHYCERA  HETERODACTYLA. 

A.  Antenna  apparently  two-jointed  with  a  three-jointed  arista. 

Small  hunch-backed,  quick-running  flies — Phoridce. 

B.  Antenna  always  three-jointed. 
Empodia  wanting,  vestigial  or  linear. 

I.  Radial  4  and  5  separate. 

(a)  Arista  dorsal — Empidce  (in  part). 

(b)  Arista  terminal. 

(1)  Front  hollowed  out  between  the  eyes.     Males 

never  holoptic.  Proboscis  without  fleshy 
labellae  at  tip — Asilidce. 

(2)  Front      plane      or      convex.     Males      often 

holoptic.  Not  more  than  four  posterior 
cells.  Third  antennal  joint  without  bristle 
or  style — Scenopinidce. 

II.  Radial  4  and  5  not  separate. 

Wings  not  lanceolate,  anal  cell  short ;  second  basal  cell 
confluent  with  distal  cell.  Not  brilliantly  coloured 
— Empidce  (in  part) . 

The  orders  Therevidse,  Midasidae,  and  Dolichopodidae,  while  containing 
species  predatory  on  other  insects,  do  not  appear  to  attack  man. 

Family  Asilim:. 

Orthorrhapha  brachycera  with  long  narrow  body,  short  broad  head,  prom- 
inent eyes,  third  joint  of  the  antennae  simple.  Thorax  narrow  in  front. 
Wings  with  elongate  basal  cells,  third  longitudinal  vein  bifurcate,  two  inter- 
calary veins  present.     Empodium  with  a  horny  bristle. 

It  is  not  known  whether  the  Asilidae  are  really  blood-sucking  flies  or  not. 
It  is  suspected  that  they  bite  in  the  tropics,  but  there  is  no  definite  informa- 
tion. 

Family  Phorid;e. 

Phora  femorata  occurs  occasionally  in  houses.  Aphiochcsla  ferruginea  Brun- 
ner  causes  intestinal  myiasis. 

Family  Scenopinidce. 

Scenopinus  feneslralis  Linnaeus  is  the  so-called  window  fly,  winch  is  prob- 
ably the  only  household  fly  which  is  not  injurious  to  health. 

Family  Empid.e. 

Orthorrhapha  brachycera  with  medium  or  small  bodies  and  small  heads. 
Antennae  with  the  first  two  joints  very  small  and  hardly  distinct,  the  third 
joint  annulated,  often  with  terminal  bristle.  Wings  with  three  large  complete 
basal  cells,  of  which  the  third  is  shorter  than  the  second.  The  posterior  basal 
transverse  vein  is  parallel  to  the  border  of  the  wing.  Empodium  membrana- 
ceous. 

It  is  doubtful  whether  these  insects  attack  man.  As  a  rule  they  live  on  the 
juices  of  other  insects  and  plants. 


CYCLORRHAPHA  825 

SUBORDER   II.  CYCLORRHAPHA. 

Section  1:  Aschiza. — This  group  includes  the  family  Syrphidae, 

of  which  no  species  is  known  to  bite  man. 

Section  2:  Schizophora. — This  group  includes  the  true  flies 
characterized  by  a  distinct  frontal  lunula  and  a  frontal  suture; 
antennae  with  three  simple  segments,  and  an  arista  which,  is  generally 
dorsal.     They  may  be  classified  into — ■ 

Muscoidea. 
Synonym. — Eumyidea. 

This  superfamily  is  divided  into: — 

Tribe  i:  Muscoidea  acalyptratce,  without  squamae  covering  the 
halteres  (see  Chapter  XXXV.). 

Tribe  2:  Muscoidea.  calyptratce,  with  squamae  covering  the 
halteres. 

MUSCOIDEA  CALYPTRAT^. 

i.  CEstridae. 

2.  Sarcophagidae. 

3.  Muscidae.  v 

4.  Ant  homy  idae. 

Diagnostic  Table. 

A.  First  posterior  cell  of  the  wings  not  widely  open. 

I.  Antennae  small,  more  or  less  hidden  in  round  pits; 
arista     single     or     plumose;     body    very    hairy — 
(EstridcB. 
II.  Antennae  well  marked,  not  hidden;  arista  more  or  less 
plumose ;  body  not  very  hairy. 
{a)  Arista    plumose    for  only  half  its  length,    bare 
in    the    terminal    half,    which    is    hair-like — 
Sarcophagi  dee. 
(b)  Arista  plumose  or  pectinate  along  its  whole  length 
— Muscidce. 

B.  First  posterior  cell  widely  open — Anthomyidce. 

Family  CEstridae. 

Muscoidea  calyplraice  with  very  hairy  bodies,  which  cause  them 
to  resemble  bees.  Antennae  inserted  into  round  pits,  with  a  terminal 
bristle  on  the  third  joint.     Mouth-parts  rudimentary. 

Remarks. — The  CEstridae  are  commonly  known  as  the  bottle  or 
warble  Hies,  and  are  of  interest  because  the  larvae  become  parasitic, 
either  under  the  skin,  in  the  nasal  or  pharyngeal  cavities,  or  in 
the  alimentary  canal. 

Classification. — The  genera  may  be  grouped  into  two  subfamilies — 
[a)  (Estrince  with  rudimentary  proboscis,  including  the  genera  Gastro- 


S26 


THE  DIPTERA 


philus,  (Estrus,  Hypoderma,  etc. ;  and  (b)  Cuter  ebrince ,  with  a  well- 
developed  retractile  proboscis,  including  Dermatobia,  etc.  The 
four  genera  of  interest  to  us  may  be  recognized  as  follows: — 


P^h 


-Hypoderma  bovis  de    Geer.      (X  2  J.) 

I.  Wing  without  posterior  transverse  vein;  the  media  runs  towards 
the  posterior  border.  First  posterior  cell  is  partly  open. 
Arista  naked — Gastrophilus  Leach,  1817. 
II.  Wing  with  posterior  transverse  vein.  The 
media  at  its  end  is  bent  towards  the 
radius,  and  the  first  posterior  cell  is 
either  open,  partially  open,  or  closed. 

A.  Facial  grooves  approximated  below.  First 
posterior  cell  closed  and  petiolate  body 
nearly  bare — (Estrus  Linnaeus,  1758. 

B.  Facial  grooves  remote. 

(a)  Proboscis  straight,  capable  of  being 
extended,  or  entirely  rudimentary. 
Antennal  groove  with  small  angular 
dividing  wall.  Palpi  absent — Hypo- 
derma Latreille,  1825. 

(b)  Proboscis  bent  and  capable  of  being 
drawn  into  a  deep  cavity  on  the  under 
surface  of  the  head,  and  generally 
hidden  therein.     Arista  with  hairs  on 

the     upper     side.        Third     antennal 
¥lHyfo7deVL^lZ  Joint  much  longer  than  the  first  two- 

de  Geer.    (X2J.)  Dermatobia  Brauer,  i860. 


(ESTRIDM 


827 


Hypodcrma. — A  good  example  of  dermal  infection  is  Hypo- 
derma  bovis  de  Geer,  which  infests  cattle.  The  eggs  are  laid  on 
the  skin  of  the  animal,  and  arc  probably  transferred  to  the  mouth 


Fig.  41S. — "Estrus  ovis  Ltnn.eus:   Female.  *(X4-) 


by  licking,  whence  they  pass  via  the  oesophagus  to  the  skin,  in 
which  they  form  tumours.  It  is  found  in  Europe  and  America, 
and  Peiper  has  gathered  together  histories  of  several  cases  in 
which  Hypoderma  bovis  and  H.  diana  Brauer 
have  occurred  in  man,  but  this  is  very  rare. 
The  larva  which  is  commonly  found  in  man 
belongs  to  Dermatobia  cyaniventris,  which  is 
described  below. 

(Estrus. — -Rhinal  myiasis  is  exemplified  by 
(Estrus  ovis  Linnaeus,  1761,  which  has  been 
found  several  times  in  the  nasal  cavities  of 
man,  though  usually  found  in  sheep.  The  egg 
is  laid  in  the  nasal  cavity,  in  which  the  larvae 
live  until  they  become  pupae. 

Gastrophilus. — Intestinal  myiasis  is  exem- 
plified by  Gastrophilus  equi  Fabricius.  The 
eggs  are  laid  on  the  skin,  often  about  the  knees, 
and  transferred  to  the  mouth,  and  so  to  the 
stomach,  by  licking.  In  this  organ  they  live 
on  the  secretions  and  contents;  but  though 
they  do  not  bite  the  mucosa,  they  cause 
irritation.     In  due  course  they  pass  out  of  the    FlS'E-479-—LARVtT°F 

v  i  1         -,i      ,i         r  j     x-l  (Estrus    OVIS    LlN- 

ahmentary   canal   with   the   faeces,    and    then       N^us.    (x  4-) 


THE  DIPTERA 


proceed  to  pupation.     G.  pccorum   Fabricius,   1794,  is   stated  to 
frequently  attack  man  in  Siberia. 


Fig.  420. — Gastrophilus  equi  Fabricius.     (X  3|-) 


Dermatobia  Brauer,  i860. 

Dermatobia  cyaniventris  Macquart,  1843. 

Synonyms. — Cuterebra  noxialis  Goudot,  1845; 
Dermatobia  noxialis  Brauer,  i860;  Dermatobia 
hominis  Say,  1822 ;  (Estnts  hominis  Gmelin,  1788. 
There  appears  to  have  been  great  doubt  as  to 
whether  D.  noxialis  is  the  same  as  or  different 
from  D.  cyaniventris.  At  present,  on  the  strength 
of  R.  Blanchard's  observations,  it  is  usual  to 
look  upon  them  as  the  same.  The  larva  of  this 
species  is  found  in  the  skin  of  man  in  tropical 
America  at  times,  and  is  known  by  various  local 
names:  '  Ver  moyoquil '  in  Mexico; '  ver  macaque  ' 
in  Cayenne;  '  torcel '  in  Venezuela;  '  nuche  '  in 
Colombia;  '  ura  '  and  'berne'  in  Brazil;  '  cor- 
mollote  '  and  '  anal  coshol '  in  British  Guiana; 
'  nuche  '  or  '  gusano  '  in  New  Granada. 
The  fly,  which  has  a  yellowish  head  and  dark 
blue  abdomen,  is  supposed  to  lay  its  eggs  on  the  skin  of  domestic 
and  wild  animals  and  man.  The  larvae  from  these  eggs  are  supposed 
to  enter  the  skin.     The  usual  areas  affected  are  the  head  or  trunk. 


Fig.  421 . — Larva 
of  Gastrophilus 
equi  Fabri- 
cius.   (X3-) 


DERMA  r  OBI  A 


829 


The  larva  presents  two  quite  different  appearances.     In  the  first 
they  are  club-shaped,  white  in  colour,  with  a  thick  anterior  and  a 


Fig.  422. — Dermatobia  cyaniventris  Macquart.     (X3-) 


Fig.  423. — Young  Larva  of 
Dermatobia  cyaniventris . 
(X3-)    (After  Blanchard.) 


Fig.  424. — Older  Larva  of 

Dermatobia      cyaniventris 
Macquart.     (X2J.) 


thin  posterior  end.  The  anterior  portion  is  besot  with  booklets, 
and  has  two  strong  oral  hooks.  The  posterior  end  carries  the 
stigmata. 

If  left  to  themselves,  the  larvae  will  remain  in  the  skin  for  some 


83o 


THE  DIPTERA 


time,  after  which  an  abscess  forms,  and  they  are  thrown  out,  drop 
on  to  the  ground,  and  become  pupse,  and  finally  imagos. 

We  have  seen  larvae  resembling  these  in  the  skins  of  Europeans 
in  Africa,  and  similar  observations  have  been  made  by  Plehn, 
Strahan,  Kolb,  Nagal,  Arnold,  and  Smith  and  others,  but  whether 
these  are  D.  cyaniventris  or  some  other  species  has  not  been 
determined. 

Pathogenicity. — -They  cause  pain  and  itching  at  the  infected  spot, 
with  swelling  and  oedema  of  the  surrounding  region,  giving  rise  to 
a  boil-like  swelling,  rather  hard,  of  a  deep  red  colour,  with  a  central 
opening.     Berne  or  ura  of  Brazil  is  the  disease. 

Treatments — On  inspecting  the  region,  a  small  opening  will  be 
seen,  and  the  larva  may  be  noted,  showing  its  stigmata  at  times, 
and  at  other  times  disappearing  and  reappearing  like  a  jack-in-the- 
box.  There  is  no  difficulty  in  seizing  this  parasite  with  a  pair  of 
forceps  and  forcibly  removing  it,  and  then  treating  the  wound 
antiseptically.  The  Brazilians  try  to  asphyxiate  the  larva  by 
tobacco-smoke,  or  apply  some  animal  fat  to  the  opening  in  the 
little  tumour.  The  fat  is  said  to  act  by  preventing  the  larva  from 
breathing  and  compelling  it  to  leave  the  tumour.  Some  authors 
advise  the  application  of  calomel  to  the  opening. 

Dermatobia  (?)  kenise  Kolb. 

Kolb  described  a  reddish-brown  fly  in  East  Africa  under  this 
term. 

The  fly  behaved  like  D.  cyaniventris  in  laying  its  eggs  on  the 
skin  of  people  when  bathing.  The  larvae  entered  the  skin,  forming 
nodules.  The  natives  called  the  fly  '  ngumba.'  It  is,  however, 
possible  that  this  is  not  a  true  Dermatobia,  which  is  a  New  World 
genus,  but  a  Cordylobia. 

Family  Sarcophagid^e. 

Muscoidea  calyptratce  with  large  bodies,  and  antennal  bristles 
feathery  at  the  base,  but  hair-like  and  very  fine  at  the  tip.  Legs 
stout.     First  posterior  cell  closed  or  only  slightly  open. 

The  Sarcophagidae  are  the  blow-flies,  of  which  5.  carnaria  is 
common. 

Genera. — Sarcophaga,  Wohlfahrtia,  Sarcophila,  Cynomyia. 

Sarcophaga  Meigen,  1826. 

It  is  by  no  means  uncommon  in  the  tropics  to  find  ulcers,  and 
especially  syphilitic  erosions  of  the  nose,  infected  with  larvae  of  flies, 
which  may  belong  to  5.  carnaria  Linnaeus,  1758.  The  larvae  have 
also  been  found  in  several  cavities  of  the  human  body,  and  those  of 
the  former  in  the  alimentary  canal.  The  following  are  causes  of 
intestinal  myiasis:  S.  affmis,  S.  carnaria  Linnaeus,  1761;  5,  h(emor~ 


SARCOPHAGA  831 

rhoidalis  Fallen,  1810;  5.  luematodes  andS.  chrysostotna  Wiedemann, 
1830.  S.  lambens  and  S.  ruficomis  cause  cutaneous  myiasis  in 
South  America.  S.  plinthopya  and  5.  lambens  have  been  found  in 
ulcers. 


Fig.  425. — Sarcophaga  carnaria  Linnaeus:  Female.      (X3.) 


Wohlfahrtia  Brauer  and  Bergenstamm,  1889. 

The  larvae  of  Wohlfahrtia  magnified  Schiner, 
1862,  have  been  found  in  cavities  in  man's  body, 
and  also  in  cattle,  sheep,  dogs,  and  domestic 
fowls. 

Sarcophila  Rondani,  1856. 

The  larvae  of  species  of  this  genus — e.g., 
S.  meigeni  Schiner,  S.  latifrons  Fall.,  and  S.  nivalis 
Fall. — may  also  be  found  in  ulcers,  etc.,  in 
Germany,  Austria-Hungary,  and  France. 

Cynomyia  Robineau-Desvoidy,  1830. 

Cynomyia  mortuorum  Linnaeus,  1761,  is  believed 
to  infect  ulcers  with  its  larvae. 


Family  Muscid^e. 

Muscoidea  calyptratce  with  stout  bodies  and 
short  thoraces.  Arista  either  entirely  plumose 
or  pectinated.  The  first  posterior  cell  is  either 
only  slightly  opened,  or  else  closed  at  the 
border  of  the  wing. 

The  Muscidae  include  a  number  of  important  genera,  which  may 
be  recognized  by  the  following  table  ;• — ■ 


Fig.  426. — 

Lakva     of 

Sarcophaga  sp. 


32  THE  DIPT  ERA 

A.  Proboscis  long,  adapted  for  biting — Philcematomyina. 

I.  Proboscis    partly    chitinous,    partly    fleshy,    with    large 
fleshy  labellse — Philcematvmyia. 
II.  Proboscis   entirely   chitinous,  with    attenuated    labellse — 
StomoxyMnce. 

(a)  Arista  feathered  dorsally  only. 

(a)  Palpi   thin,    much    shorter    than   the    proboscis. 

Third    longitudinal    vein   with    bristles    proxi- 
mally;  first  posterior  cell  open — Stomoxys. 

(b)  Palpi  thickened,  as  long  as  or  nearly  as  long  as 

the  proboscis. 

(i)  Proboscis  long  and  tapering;  first  posterior 
cell  widely  open;  third  longitudinal  vein 
without  bristles — Lyperosia. 

(2)  Proboscis  short  and  stumpy;  first  posterior 
cell  narrowly  open;  third  longitudinal  vein 
with  bristles  proximally — Stygeromyia. 

(c)  Palpi  strongly  built  everywhere,  not  thickened. 

Proboscis  thin,  more  than  twice  the  head 
length,  swollen  at  the  base.  Arista  with 
many  branched  hairs.  Media  (fourth  longi- 
tudinal) with  two  sharp  bends — Glossina. 

(b)  Arista  feathered  dorsally  and  ventrally. 

(a)  First  posterior  cell  narrowly  open;  third  longi- 

tudinal vein  without  bristles — Hcematobosca. 

(b)  First  posterior  cell  widely  open. 

(1)  Third  longitudinal  vein  with  bristles  proxi- 

mally— Hcemato  b  ia . 

(2)  Third    longitudinal    vein    without     bristles 

proximally — Bdellolarynx. 

B.  Proboscis  short,  not  adapted  for  biting — Mitscince. 

(a)  Mid-tibia  without  bristle  on  inner  side — Musca. 

(b)  Mid-tibia  with  bristles  on  inner  side. 

(1)  Thorax    and    abdomen   bluish-black,    not    lustrous — 

Calliphora. 

(2)  Thorax  and  abdomen  green  or  greenish,  lustrous. 

(a)  Scutum  longitudinally  marked — Chrysomyia. 

(b)  Scutum  not  so  marked. 

(a)  Thorax    metallic    green    or    bluish-green — 

Luc  ilia. 

(b)  Thorax    brassy    green    or    purplish-blue — 

Pycnosoma. 

(3)  Thorax  and  abdomen  dirty  brownish-yellow. 

(a)  Eyes  wide  apart  in  both  sexes,  second  abdominal 

segment  of  the  female  more  than  half  the  length 
of  the.  abdomen—  Auchmeromyia. 

(b)  Eyes  of  male  not  wide  apart,  and  second  abdo- 

minal segment  without  the  above  character — 
Cordylobia, 


PHILAEMATOMYIA  833 

Ph  yi.^m  atom  YIN  m. . 
Philaematomyia  Austen,  1909. 

Stomoxydinae  resembling  Musca  domestica  Linnaeus,  being  grey 
flies  with  remarkable  proboscis.  Front  in  male  narrow,  its  width 
in  centre  being  from  one-eleventh  to  one-fifteenth  of  total  width  of 
head;  width  of  the  front  in  the  female,  one-third  of  total  width 
of  head.  Proximal  portion  of  proboscis  shows  a  swollen  chitinous 
bulb,  distal  portion  soft  and  fleshy,  and  folded  back  under  distal 
end  of  bulb  when  not  in  use,  but  when  extended  there  is  a  tubular 
extension  furnished  with  a  circle  of  chitinous  teeth.  Distribution : 
India,  Ceylon  (very  common),  Cyprus,  Senegal,  and  the  Congo. 

Type  Species. — Philcematomyia  insignis  Austen,  1909. 

Philaematomyia  insignis  Austen,  1909. 

Smoke  grey  or  yellowish-grey  in  colour,  with  dorsum  of  thorax 
with  four  dark  longitudinal  stripes.  The  eggs  are  laid  in  batches  of 
fifty  to  sixty  in  cracks  in  dry  cow's-dung.  Egg  is  2  to  2  -2  millimetres 
in  length  by  0-4  millimetre  in  breadth.  Larvae  hatch  in  eight  to 
nine  hours,  and  when  mature  measure  about  1-25  centimetres. 
They  are  bright  lemon  yellow  in  colour.  They  burrow  under  the 
ground  on  the  evening  of  the  second  day,  and  pupate.  The  puparium 
resembles  that  of  Musca,  0-5  centimetre  long  by  0-18  centimetre 
broad.  It  is  of  a  light  mahogany  colour,  and  has  eleven  segments. 
The  life-history  may  be  summarized :  Egg-laying,  five  to  ten  minutes ; 
egg,  eight  to  ten  hours;  larvae,  two  days;  pupa,  three  and  a  half  to 
four  and  a  half  days;  total,  six  to  seven  days.  The  fly  is  ready  to 
feed  eight  hours  after  hatching.  Feeds  usually  on  cattle;  only  occa- 
sionally bites  man .  They  pass  out  a  clear  watery  fluid  from  the 
anus  while  feeding  (common  in  a  blood-sucking  fly). 

Enemies. — Hymenoptera,  spiders,  tachinids. 

Other  Species.— Ph.  lineata  Brunetti.  1910  (synonym,  Pristirrhyn- 
chomyia  lineata  Brunetti,  1910),  and  Ph.  gurnet  Patton  and  Cragg, 
1912,  both  in  India. 

Stomoxydinae. 

Stomoxys  Geoffry,  1764 . 

Arista  of  three  segments,  feathered  dorsally  only;  proboscis  long, 
tapering,  chitinized  in  all  its  extent,  non-retractile;  palpi  slender, 
very  short,  less  than  half  the  length  of  the  proboscis.  Fourth 
longitudinal  vein  curved  so  as  to  merely  narrow  the  first  posterior 
cell  distally;  third  longitudinal  vein  bristly  at  its  proximal  end. 
Front  narrower  in  the  male  than  in  the  female. 

Type  Species. — ■Stomoxvs  calcitrans  Linnaeus,  1758. 

The  genus  Stomoxys  is  cosmopolitan  in  its  distribution.  The 
principal  species  are — 

European  Species. — S.  calcitrans  L.,  1758. 

Asiatic  Species. — Twelve  species  known  and  two  synonyms:  S.  brunnipes 
Grunberg,  S.  calcitrans  L.,  S.  pluvinotata  Bigot,  S.  dacnusa  Speiser,  S.  indica 

53 


834  THE  DIPT  ERA 

Picard,  S.  limbata  Austen,  5.  nigra  Macquart,  S.  bengalensis  Picard,  S.  oblongo- 
punctata  Brunetti,  5.  pratlii  Summers,  S.  pulla  Austen,  S.  siliens  Rondani, 
S.  triangularis  Brunetti. 

African  Species. — Fourteen  species  and  four  probable  synonyms  are  known  : 
S.  calcitrans  L.  (S.  korogwensis  Griinberg),  S.  sitiens  Rondani,  S.  griseiceps 
Becker,  S.  nigra  Macquart  (S.  glauca  Griinberg  and  5.  lafonti  Picard),  S.  bon- 
vieri  var.  clara  Roubaud,  S.  inornata  Griinberg,  S.  omega  Newstead,  S.  varipes 
Bezzi,  S.  intermedia  Roubaud,  S.  bouffardi  Picard,  5.  bilineata  Griinberg,  S. 
brunnipes  Griinberg  (5.  stellata  Griinberg),  5.  tcsniatus  Bigot,  S.  ochrosoma 
Speiser. 

American  Species. — S.  calcitrans  L. 

Australian  Species. — S.  calcitrans  L. 

For  the  methods  of  diagnosis  of  these  species,  vide  Summers,  L.  M.  (1912), 
Journal  of  London  School  of  Tropical  Medicine,  July,  p.  184;  London. 

The  following  table,  modified  from  Griinberg,  gives  the  diagnosis  of  a  few 
of  the  species: — 

A.  Legs  entirely  yellow.     Wings  yellowish — -S.  tcsniatus  Bigot,  1887. 

B.  Legs  either  entirely  black  or  largely  black  or  blackish-brown.     Wings 

clear  or  darkish  coloured. 
I.  Venter  brilliantly  white — S.  sitiens  Rondani.  1873. 
II.  Venter  pale  dusky  brown,  with  characteristic  omega  mark  on  the 
thorax — 5.  omega  Newstead,  1907. 
III.  Venter  grey  or  yellow. 

1.  Thorax  without  clear  black  stripes.     Hinder  part  black  without 

any  markings — S.  inornata  Griinberg,  1906. 

2.  Thorax  with  clear  black  stripes.     Abdomen  with  regular  dark 

marks  or  spots. 

(a)  Knee,  tibia,  and  tarsus — at  all  events,  on  the  two  anterior 

pairs  of  legs — entirely  brown. 

(1)  Tibia  and  tarsus  on  the  anterior  and  middle  legs  light 

brown,  on  the  hind  legs  dark  brown.  Thorax  with 
two  small  brown  longitudinal  median  lines  —  S. 
bilineata  Griinberg,  1906. 

(2)  Tibia  and  tarsus  brown  on  all  three  legs.     Thorax  with 

broad  black  longitudinal  stripes. 

Wings  blackish,  head  and  thorax  brown-yellow — 
S.  brunnipes  Griinberg,  1906. 

Wings  glassy,  head  and  thorax  grey — S.  stellata 
Griinberg,  1906. 

(b)  Legs  black,  with  light  brown  knees  or  decidedly  dark  brown 

spots. 

(1)  Wing  brushes  yellowish-brown,  with  black  tips.     Abdo- 

men with  dark  middle  longitudinal  line.  Second 
and  third  segments  with  dark  anterior  and  posterior 
borders — S.  glauca  Griinberg,   1906. 

(2)  Wing    brushes    black.     Abdomen  grey.     Both    middle 

segments  with  regularly  arranged  dark  spots  without 
dark  median  longitudinal  line. 

Second  and  third  abdominal  segments  with  one 
middle  basal,  one  side  apical  dark  spot,  and  dark 
anterior  border,  with  which  the  basal  spot  unites — 
5.  korogwensis  Griinberg,  1906. 

Second  and  third  abdominal  segments  with  the 
same  dark  spots,  but  without  anterior  border-lines — 
S.  calcitrans  Linnaeus,  1761. 

Stomoxys  calcitrans  Linnaeus,  1758. 

S.  calcitrans  is  the  common  stable-fly,  found  in  houses,  stables, 
and  in  the  open  near  cattle.     It  bites  all  classes  of  mammals,  and 


STOMOXYS  CALCITR.  I  X S 


835 


in  so  doing  is  suspected  of  spreading  trypanosomes,  especially 
T.  evansi.  Manders  considered  5.  nigra  Macquart,  1850,  to  be  the 
cause  of  the  spread  of  surra  in  Mauritius. 

It  is  rather  like  the  common  house-fly,  but  is  easily  recognized 
by  the  head  being  raised  in  the  resting  position,  by  the  projecting 
proboscis,  and  by  the  closed  wings,  touching  one  another  at  their 
bases,  and  diverging  behind. 


Fig.  4-7- — Stomoxys  calcitrans  :  Female. 


Morphology. — The  mouth-parts  consist  of  a  proboscis,  composed  oi  rostrum, 
haustellum,  and  labellse,  which  are  bent  posteriorly,  forming  an  elbow-shaped 
joint.  The  posterior  portion  can  be  retracted  or  projected  forwards,  and 
carries  the  chitinous  fulcrum  of  the  pharyngeal  wall,  the  maxillae,  and  their 
palps.     It  is  cone-shaped,  and  is  called  the  rostrum. 

The  structure  of  the  haustellum,  or  proboscis  proper,  is  very  complex.  It 
consists  essentially  of  a  labrum,  hypopharynx,  and  labium.  The  labrum  is  a 
sharp-pointed  stylet,  which  near  its  apex  bears  a  ventral  ridge  with .  four 
sensory  hairs.  Posteriorly  it  is  attached  to  the  head,  where  it  forms  a  chitinous 
projection.  It  is  horseshoe-shaped  on  transverse  section,  the  ventral  opening 
being  closed  by  the  hypopharynx,  while  laterally  its  walls,  which  expand  and 
enclose  a  cavity  containing  muscles,  articulate  with  the  labium,  thus  keeping 
the  hypopharynx  in  its  place.  The  hypopharynx,  which  contains  the  salivary 
tube,  starts  from  the  labium  and  runs  forwards,  expanding  laterally  and 
closing  in  the  labial,  pharyngeal,  or  blood-tube  mentioned  above.  Its  lateral 
expansions  contain  a  cavity.  At  its  tip  it  appears  to  be  membranous,  which 
Stephens  and  Newstead  think  by  its  flaccid  condition  prevents  ingress  of  fluid 
during  blood-sucking,  while  freely  permitting  the  egress  of  saliva.  The 
labium  is  stout  and  thick,  with  a  swollen  basal  portion,  gradually  tapering 
towards  the  proximal  and  distal  extremities,  but  less  so  basally.  Posteriorly 
it  encloses  the  labrum  and  hypopharynx,  which  it  carries  on  a  sclerite,  which 
farther  forwards  forms  the  boundary  of  the  labial  gutter,  and  is  joined  dorsally 
by  another  dorsal  hooked  sclerite.  These  sclerites  stop  at  the  base  of  the 
labell  33.     Ventral   to   the   dorsal   sclerites   are   two   ventral   sclerites,    which 


836 


THE  DIPTERA 


anteriorly  articulate  with  a  transverse  forked  sclerite  whose  arms  run  forwards. 
To  these  arms  the  tendons  of  longitudinal  muscles  are  attached,  which  are 
capable  of  rotating  them,  causing  the  eversion  of  the  labellae.  Farther 
forward  the  two  labellae  are  strengthened  internally  by  dorsal  and  ventral 
sclerites,  while  a  pear-shaped  axial  apophysis  projects  forwards  freely  from 
the  labium. 

The  ventral  plate  is  obliquely  placed,  and  carries — (i)  five  teeth;  (2)  nine 
sets  of  petiolated  blades ;  (3)  six  sets  of  rod-like  hairs ;  (4)  five  sets  of  opercu- 
late  hairs;  (5)  six  sets  of  bifurcated  hairs;  (6)  an  anterior  dorsal  fringe  of 
hairs;  (7)  a  posterior  ventral  set  of  hairs;  (8)  ventral  phalanges  or  lips  with 
ventral  hairs;  (9)  dorsal  external  set  of  hairs;  and  (10)  latero-external  set  of 
hairs. 

Internal  Anatomy.— The  pharyngeal  tube  leads  into  the  pharynx,  whose 
wall  is  formed  by  the  chitinous  fulcrum.  The  oesophagus,  at  first  flattened, 
afterwards  cylindrical,  passes  into  the  thorax  and  opens  into  the  ventral 
surface  of  the  proventriculus.  At  this  point  it  is  joined  by  the  duct  from  the 
crop  or  sucking-stomach,  which  is  a  large  hollow  blood-reservoir  lying  in  the 
abdomen.  The  chylific  ventricle  has  three  coils.  The  usual  Malpighian 
tubules,  small  and  large  intestine,  and  rectum  are  present.  The  salivary 
glands  resemble  those  of  Musca  and  Glossina. 

Method  of  Biting. — Stomoxys 
carefully  inspects  the  skin,  and 
having  selected  a  spot,  everts 
the  labellae,  and  by  a  rotatory 
motion  cuts  a  hole  through  the 
epidermis  by  means  of  its  teeth, 
and  then,  inserting  the  proboscis 
into  the  wound,  sucks  the  blood. 
Life-History. — -The  life-history 
has  been  studied  by  Newstead, 
who  finds  that  the  incubation 
period  of  the  egg  is  two  to  three 
days,  the  life  of  the  larva  four- 
teen to  twenty-one  days,  the 
pupa  1  stage  nine  to  thirteen  days, 
making  the  total  life-cycle 
twenty  -  five  to  thirty  -  seven 
days,  but  this  may  be  consider- 
ably prolonged  by  the  incubation  and  larval  stages  being  lengthened 
in  the  absence  of  moisture,  or  the  presence  of  a  low  temperature. 

The  eggs  are  1  millimetre  in  length,  white,  turning  later  to  a 
cream  colour;  coriaceous  and  reticulated;  curved  on  one  side  and 
straight  on  the  other,  where  there  is  a  broad  deep  groove,  wider 
anteriorly,  where  the  larva  escapes.  The  number  of  eggs  varies 
from  forty-eight  to  seventy  one,  and  they  arc:  laid  in  warm  dung 
and  fermenting  grass. 

The  larva  is  11  millimetres  long,  and  tapering,  yellowish  in  colour, 
with  blackish  mouth-pa  its.  The  segmentation  is  not  well  marked. 
The  head  has  two  large  diverging  processes,  which  carry  the  four- 
jointed  antennas.  The  mouth  is  armed  with  a  hook-like  mandible, 
which  carries  a  ventral  tooth,  and  is  attached  by  means  of  a  hypo- 
stomal  sclerite  to  two  large  cephalo-pharyngeal  sclerites,  in  front  of 


Fig.  428. — Head  of  Stomoxys 
calcitrans  :  Female. 


LYPEROSIA  837 

the  upper  arms  of  which  is  a  small  perforated  sclerite.  The  pos- 
terior stigmata  are  two  in  number.  The  mouth-hook  is  used  for 
locomotion. 

Pupation  is  brought  about  in  two  hours  by  the  larva  shortening 
itself  and  becoming  barrel-shaped,  the  colour  turning  to  red.  The 
pupa  measures  5  to  5-5  millimetres  in  length,  and  possesses  eleven 
visible  segments.  In  a  few  days  the  pupal  skin  is  split  along  lateral 
and  median  lines  anteriorly,  and  at  the  fourth  segment  transversely, 
and  the  imago  escapes. 

Lyperosh  Rondani,  1862. 

Synonym. — Glossinella  Grimberg,  1906. 

Stomoxydinae  resembling  Stomoxys,  but  with  palpi  as  long  as  the 
long  slender  proboscis,  around  which,  as  they  are  broad,  they  form 
almost  a  sheath,  with  no  bristles  on  the  third  longitudinal  vein. 
Distribution:  Europe,  Asia,  Africa,  North  America,  and  Australia. 

Type. — Lyfierosia  irritans  Linnaeus,  1761. 

They  are  dirty  brown  or  dirty  yellowish-grey,  very  small  blood- 
sucking flies,  with  inconspicuous  markings,  and  usually  only  attack 
animals,  and  do  not  come  into  houses. 

European  Species. — L.  irritans  L.,  1758;  L.  titillans  Bezzi,  191 1. 

Asiatic  Species. — L.  minuta  Bezzi,  1892;  L.  schillingsi  Grunberg,  1906; 
L.  exigua  de  Meijere,  1903;  L.  flavoherta  Brunetti,  1910;  L.  rufipalpis  Becker, 
1910  (probably  =  Stygeromyia  maculosa  Austen,  1907). 

African  Species. — L.  minuta  Bezzi,  1892;  L.  longipalpis  Roubaud,  1906 
(=L.  pallidipes  Roubaud,  1907);  L.  schillingsi  Grunberg,  1906  (  =  St.  Macu- 
losa ?);  L.  potans  Bezzi,  1908;  L.  punctigera  Austen,  1909;  L.  exigua  (Meijere, 
1903);  L.  thirouxi  Roubaud,  1903. 

American  Species. — L.  irritans  L.,  1758;  L.  aids  Snow,  1891  (synonym: 
Hcsmatobia  alcis  Snow,  1891). 

Australian  Species. — L.  exigua  Meijere,  1903. 

(For  details  see  Summer's  paper,  vide  infra.) 

Stygeromyia  Austen,  1907. 

Stomoxydinae  with  general  appearance  and  body  like  Stomoxys, 
proboscis  and  palpi  like  HceniatoUa,  arista  feathered  dorsally  only. 
Head  flattened  from  front  to  rear;  proboscis  short,  stout,  shiny, 
chitinous.  not  tapering;  palpi  as  long  as  the  proboscis;  clavate  at 
tips,  curving  upwards.  Cell  opening  as  in  Stomoxys.  Apical  por- 
tion of  fourth  vein  straight  beyond  bend— -i.e.,  not  bent  inwards 
as  in  Stomoxys  and  Hcematohia.  Distribution :  Africa  and  Southern 
Arabia. 

Type.— -Stygeromyia  maculosa  Austen,  1907. 

Stygeromyia  sdnguinaria  Austen,  1909,  is  stated  by  Yale  Massey 
to  be  a  blood-sucker  in  the  Congo  Free  State,  while  S.  maculosa' 
Austen,  1907,  found  in  Little  Aden,  is  inferred  to  be  also  a  blood- 
sucker, and  S.  woosnami  Austen,  1912,  in  East  Africa. 

Glossina  Wiedemann,  1830. 

Synonym. — Nentorhina,  Robineau-Desvoidy,  1830. 

Narrow  bodied,  elongate,  greyish-brown  or  yellowish-brown,  dull- 


838 


THE  DIPT  ERA 


coloured  flies,  with  the  wings  closed  flat  over  one  another,  and 
projecting  considerably  beyond  the  abdomen  when  at  rest,  with  an 
anterior  projecting  proboscis,  beyond  which  the  palpi  slightly  extend, 
and  in  which  they  are  ensheathed.     Base  of  proboscis  bulbous. 

This  is  the  genus  of  the  tsetse-flies,  a  name  probably  derived 
from  the  noise  which  they  make  when  flying,  and  now  used  in  a 
generic  sense.  They  were  first  named  by  Wiedemann  from  G.  longi- 
palftis,  brought  from  Sierra  Leone  by  Adam  Afzelius,  and  in  the  same 
year  Robineau-Desvoidy  named  another  species  from  the  Congo 
Xemorhina  palpalis.  Their  bites  have  been  long  known  to  be 
dangerous  to  animals,  but  it  was  not  till  Bruce  showed  that  they 


Fig.  429. — Glossiiia  palpalis  :  Female. 

were  the  spreaders  of  Trypanosoma  brucei  and  the  cause  of  the 
disease  nagana  in  horses,  etc.,  that  they  received  much  attention. 
The  interest  in  them  became  vastly  greater  when  in  1903  Bruce 
and  Nabarro  showed  that  they  were  the  spreaders  of  T.  castellan*  i 
and  especially  when  Kleine  showed  that  the  transmission  was  not 
mechanical. 

The  genus  is  confined  to  tropical  Africa  and  Arabia. 

Morphology. — The  points  in  the  morphology  to  which  attention 
should  be  paid  are  as  follows : — 

The  eyes  are  large  and  bare,  and  between  them  the  vertex  is 
depressed,  and  at  its  back  carries  ocelli.     In  front  a  deep  facial  pit 


GLOSSTNA 


839 


is  separated  by  a  transverse  impression  from  the  gena.  The  pro- 
boscis projects  horizontally  forwards,  while  its  bulbous  posterior 
portion  is  enclosed  in  a  fold  of  skin.  Palpi  are  rod-like,  and  clothed 
with  short  black  hairs,  and  enclose  the  proboscis.  The  antennse  are 
three- join  ted,  the  first  two  being  small  and  the  third  large,  with  its 
anterior  external  angle  prominent  and  directed  forwards  and 
outwards.  At  its  base  is  attached  a  two-jointed  arista,  of  which  the 
first  segment  is  small,  and  the  second  long  and  tapering,  bearing 
some  twenty- two  fine,  curving,  branched  hairs  on  its  upper  surface 
only.     Bristles  are  frontal,  vertical,  ocellar,  and  post-medial. 

With  regard  to  the  thorax,  the  most  important  feature  is  the  wing, 
which  is  brownish,  with  a  peculiar  venation.     The  costal  vein  is 


Fig 


This  figure  shows  the  proboscis 
being  lowered  previously  to  piercing 
the  skin  to  suck  blood. 


This    figure    shows  the  proboscis 
ready  for  sucking. 


well  marked,  and  the  subcostal  vein  (auxil;ary)  joins  it  about  the 
junction  of  the  inner  with  the  outer  third  in  the  extended  position 
of  the  wing,  thus  enclosing  the  costal  cell,  which  is  divided  into  two 
portions  by  the  humeral  transverse  vein.  The  radius  1  (first 
longitudinal)  curves  forwards,  joining  the  costa  about  the  junction 
of  the  inner  two-thirds  with  the  outer  one-third,  thus  forming  a 
very  narrow  subcostal  cell.  The  radius  2  and  3  (second  longi- 
tudinal) also  curves  forwards,  meeting  the  costal  margin  before  the 
tip  of  the  wing  is  reached,  as  does  the  radius  4  and  5  (third  longitudi- 
nal) ;  hence  the  marginal  and  submarginal  cells  are  long  and  narrow. 
The  media  (fourth  longitudinal)  is  highly  characteristic.  It  starts 
separately  from  the  preceding,  and  running  outwards,  after  meeting 
with  the  anterior  basal  vein,  curves  forwards  to  join  with  the  anterior 
transverse  vein,  when  it  bends  at  right  angles,  turning  backwards 


8*o 


THE  DIPT  ERA 


mi 


Fig.  432. — Diagram  of  a  Tsetse-Fly. 
(Modified  after  Austen,  from  '  Monograph  of  Tsetse-Flies.') 


He.,  head;  Th.,  thorax;  Ab.,  abdomen;  Fr.  I.,  front  leg;  Mi.  I.,  middle 
leg;  Hi.  I.,  hind  leg;  Pr.,  proboscis  ensheathed  by  the  palpi;  Ay.,  arista; 
Fr.,  frons;  Oc,  occiput;  Ey.,  eye;  Sc,  scutellum;  Ha.,  haltere;  S-/.,  squama; 
Wi..  wing;  Fe.,  femur;  Ti.,  tibia;  Ta.,  tarsus. 

Venation  of  Wing. — la,  Subcostal  or  auxiliary  vein;  \a,  ib,  two  portions 
of  the  costal  cell  divided  by  the  humeral  transverse  vein;  ic,  subcostal  cell; 
/,  radius  1,  or  first  longitudinal;  2,  marginal  cell;  II,  radius  2  and  3,  or  second 
longitudinal;  3,  submarginal  cell;  III,  radius  4  and  5,  or  third  longitudinal; 
8,  first  basal  cell;  5,  first  posterior  cell;  A,  anterior  transverse  vein;  IV,  media 
or  fourth  longitudinal;  9,  posterior  basal  cell;  4,  discoidal  cell,  external  to 
which  is  the  second  posterior  cell,  without  a  number;  B,  posterior  transverse 
vein;  C,  anterior  basal  vein;  V,  cubitus  1  and  2,  or  fifth  longitudinal; 
D,  posterior  basal  transverse  vein;  10,  posterior  basal  cell;  7,  third  posterior 
cell;  VI,  anal  or  sixth  longitudinal. 


and  outwards  to  join  with  the  posterior  transverse  vein,  when  it 
again  turns  and  runs  obliquely  forwards  to  join  the  costal  vein  Justin 
front  of  the  tip  of  the  wing.     Between  it  and  the  radius  4  and  5  (third 


GLOSSTNA 


841 


longitudinal)  lie  internally  the  first  (anterior)  basal  cell,  and  exter- 
nally the  first  posterior  cell,  separated  by  the  anterior  transverse 
vein,  which  is  very  oblique.  The  cubitus  1  and  2  (fifth  longitu- 
dinal) joins  the  anterior  basal  vein,  marking  out  the  posterior  basal 
cell,  and  then  runs  forwards  to  join  the  posterior  transverse  vein, 
marking  out  the  discoidal  cell,  which  is  hatchet-shaped,  with  the 
handle  running  up  to  the  anterior  basal  transverse  vein.  After 
this  the  vein  turns  backwards  to  join  the  margin  of  the  wing, 
delineating  the  large  second  posterior  cell.  The  anal  (sixth  longi- 
tudinal) is  very  short,  being  unchitinized  after  meeting  with  the 
posterior  transverse  basal  vein,  with  which  it  marks  out  the  posterior 
basal  cell.  The  third  posterior  cell  is,  however,  shown  by  its  un- 
chitinized trace.  The  posterior  part  of  the  wing  shows  an  incrassation 
corresponding  to  anal  2  and  3. 

The  legs  are  simple,  rather  long,  with  long  claws  and  pulvilli. 

The  abdomen  is  flattened, 
tapering  to  the  apex,  and  clothed 
with  short  black  hairs.  The  male 
genitalia  are  characteristic.  The 
ventral  plate  of  the  sixth  segment 
carries  a  patch  of  dark  hairs  on 
each  side  of  the  middle  line,  behind 
which  is  the  hypopygium,  which 
is  oval,  tumid,  and  marked  by  a 
vulviform  median  groove,  the 
anus,  running  from  its  anterior 
margin  backwards  to  beyond  the 
middle. 

The  proboscis  shows  the  usual 
rostrum  or  conical  head  projec- 
tion, the  haustellum,  or  proboscis 
proper,  and  the  labellse. 

The  proboscis  proper  is  com- 
posed  of   labrum,   hypopharynx, 

and  labium.  The  labrum  arises  from  the  basal  bulb  of  the  proboscis 
in  the  form  of  a  tube,  which  is  continuous  posteriorly  with  the 
pharynx,  while  anteriorly  it  runs  forwards,  forming  the  dorsal  wall  of 
the  proboscis.  In  this  position  it  articulates  by  means  of  interlocking 
teeth  with  the  labium,  while,  opening  ventrally,  it  articulates  with 
the  hypopharynx,  which  closes  the  potential  ventral  opening. 
Farther  forwards  it  separates  from  the  labium,  and  ends  in  a  point. 
The  tube  composed  by  the  hypopharynx  and  the  labrum  is  the 
afferent  blood  or  pharyngeal  tube.  The  hypopharynx  starts  below 
the  pharynx  surrounding  the  salivary  efferent  duct,  and  pierces 
the  bulb  of  the  proboscis,  appearing  on  its  dorsal  aspect.  Farther 
forward  it  lies  in  a  groove  on  the  labium,  articulating  laterally  with 
the  labrum.  Finally  it  ends  as  a  delicate  chitinous  tube  just  pos- 
terior to  the  labellse.  Its  canal  is  the  salivary  tube  or  hypo- 
pharyngeal  canal. 


Fig. 433. — Antenna  of  a  Glossina, 
showing  the  arista. 

(Alter  Austen,  from  '  Tsetse-Flies.') 


842 


THE  DIPTERA 


The  labium,  or  second  maxilla,  starts  from  the  ventral  area  of 
the  head,  and  is  first  swollen  to  form  the  bulb.  Anteriorly  it  is 
grooved  dorsally  to  hold  the  hypopharynx  and  the  labrum,  while 
farther  anteriorly  it  ends  in  the  labellae.  These  structures  (labelke) 
are  joined  together  in  the  ventral  line,  except 
anteriorly,  where  there  is  a  V-shaped  notch, 
while  dorsally  they  possess  teeth  which 
interlock. 

In  the  ventral  line  the  chitinous  floor  of 
the  labium  is  prolonged  forwards  in  the  form 
of  a  fork,  in  front  of  which  is  a  membranous 
area,  anteriorly  to  which  the  inner  wall  of 
each  labellum  becomes  divided  into  dorsal, 
median,  and  ventral  segments.  Each  segment 
is  armed  with  a  series  of  about  ten  rasps, 
composed  of  some  thirty  minute  bars,  in  front 
of  which  are  two  pairs  of  teeth.  Between  the 
bases  of  the  anterior  pairs  of  teeth  there 
projects  a  fan-shaped  mass  of  spine-like  scales. 
The  segments  are  capable  of  e version, 
when  the  muscles  pull  backwards  the  external 
walls  of  the  labellse.  In  this  way  the  teeth 
would  be  brought  in  contact  with  the  skin, 
and  the  wound  necessary  for  blood-sucking 
made,  probably  by  rotatory  movements. 

Internal  Anatomy. — The  internal  anatomy 
has  been  carefully  studied  by  Minehin,  and 
does  not  materially  differ  from  that  of 
Stomoxys. 

The  pharyngeal  tube  opens  into  the 
pharynx,  which  is  situated  mainly  in  the 
rostrum.  Its  walls  are  strongl}'  chitinized, 
forming  the  fulcrum.  The  oesophagus  runs 
upwards  and  then  backwards  to  open  into 
the  proventriculus,  and  to  be  continuous  via 
a  long  ventral  duct  with  the  crop,  which  lies 


Fig.  434.  —  Anatomy 
of  a  Tsetse-Fly. 

(After  Minehin,  from 
Reports  of  the  Royal 
Society.)    ■ 

1,  Pharynx;  2,  oeso- 
phagus; 3,  proventri- 
culus; 4,  thoracic  intes- 
tine; 5,  duct  of  sucking- 
stomach  ;  6,  salivary 
duct ;  7,  salivary  gland ; 
8,  sucking-stomach;  9, 
abdominal  intestine  ; 
10,  rectum. 


in  the  first  two  segments  of  the  abdomen. 


The  chylific  ventricle  is  narrow  at  first  in  the 
thorax,  but  bee  >mes  wider  in  the  abdomen, 
where  it  coils  several  times.  There  are  the  usual  ileum,  colon, 
rectum,  and  Malpighian  tubules. 

The  salivary  glands  are  two  long  coiled  tubes  lying  first  in 
the  abdomen,  and  then  passing  into  the  thorax,  and  probably 
opening  finally  on  the  hypopharynx,  though  this  has  not  yet  been 
worked  out. 

Life-History.— The  species  of  Glossina  live  in  jungles  or  bush, 
along  the  banks  of  streams  or  lakes.  They  appear  to  live  principally 
upon  the  blood  derived  from  big  game,  but  Koch  believed  that 
G.  palpalis  lives  on  that  of  crocodiles,  and  Hodges,  on  that  of  hippo- 


GLOSSINA 


«43 


potami.  According  to  Kinghorn,  copulation  in  G.  morsitans  lasts 
for  several  hours.  The  female  in  due  course  produces  a  single  larva, 
and  may  produce  a  second  after  fourteen  to  fifteen  days.  At  the 
completion  of  intra-uterine  life  the  larva  almost  completely  rills 
the  abdomen  of  the  mother.  Its  extrusion  takes  place'very  rapidly, 
and  it  commences  to  crawl  at  once.     The  larvae,  which  are  yellow  - 


FlG. 


435- 


-A  Glossina  in  the  Act  of  giving  Birth  to  a  Larva. 
(Modified  after  Newstead.) 


coloured,  are  to  be  found  as  a  rule  near  the  roots  of  banana-trees. 
These  larvae  are  composed  of  twelve  segments,  the  anterior  of  which 
carries  the  two  minute  mouth-hooks,  and  the  posterior  a  dark  hood 
or  anal  segment.  The  larvae  retire  to  some  hole,  and  in  a  few  hours 
become  jet-black  pupae,  from  which  the  fully  developed  insects 
issue  in  about  six  weeks. 

The  pupa  is  5-53  (5  to  6)  millimetres  long,  a  b 

and  3-2  (3  to  3*75)  broad,  according  to  an 
average  of  twenty  measurements  by  Kinghorn, 
with  twelve  segments.  The  anterior  four 
show  the  longitudinal  seam,  which  bifurcates 
at  the  fourth  segment,  forming  an  opening 
through  which  the  imago  escapes.  The  first 
segment  carries  the  mouth,  and  the  twelfth 
two  lateral  tumid,  tuberculated  lips,  con- 
nected by  dorsal  and  ventral  ridges  enclosing 
a  pit,  in  which  the  posterior  stigmata  can  be 
seen. 

The  larvae  of  G.  palpalis  measure  4-5  by  1-75 
millimetres,  and  the  pupae  5  to  5-75  by  3 
millimetres. 

According  to  Kinghorn,  forty-seven  to 
fifty-three  days  elapse  from  the  birth  of  the 
larva  to  the  escape  of  the  imago  in  G. morsitans. 

Bionomics.— As  G.  palpalis  is  most  prob 
ably  the  sole  means  of  propagation  of  human 

trypanosomiasis,  it  is  important  to  have  some  idea  of  what  is 
known  as  to  its  bionomics,  which  have  been  carefully  studied  by 
Hodges  and  Bagshawe. 

The  main  resort  of  the  fly  is  to  be  found  in  bush  near  water, 
especially  in  the  undergrowth  composed  of  shrubs,  bushes,  vines, 


Fig. 


436. — Pupa 
Tsetse-Fly. 


(After  Austen,  from 
'  Tsetse-Flies.') 

a,  Magnified;  b, 
natural  size. 


844  THE  DIPTERA 

creepers,  tall  grass,  cane-break  tangle,  and  herbaceous  plants.  Tall 
trees  alone  will  not  afford  the  protection  necessary  for  the  fly  unless 
they  overhang  the  water,  or  their  foliage  "reaches  so  low  as  to  mix 
with  the  undergrowth. 

The  fly  is,  however,  not  met  with  behind  a  wide  strip  of  papyrus, 
though  it  may  be  found  on  its  water  edge.  This  is  explained  by 
Bagshawe  on  the  grounds  that  papyrus  grows  best  in  shallow  water, 
which  means  that  the  ground  is  swampy,  a  condition  which  prevents 
the  fly  from  depositing  its  larva.  From  a  resort  such  as  this  a  fly 
can  travel  for  feeding  purposes,  or  be  carried  by  attraction  or 
artificial  means.  It  appears  probable  from  Bagshawe's  experiments 
that  a  single  flight  will  not  reach  70  to  80  yards,  but  flies  can  be 
carried  to  almost  any  distance  by  the  agency  of  boats  and  floating 
islands  of  papyrus.  Human  traffic  also  increases  the  dissemination 
of  the  fly,  as  it  is  apt  to  pursue  human  beings  for  considerable 
distances. 

Female  flies  appear  to  travel  farther  in  search  of  food  than  males, 
probably  because  they  more  urgently  require  it.  Bagshawe  suggests 
that  this  can  be  made  use  of  in  finding  the  breeding-grounds,  where 
he  says  plenty  of  males  as  well  as  females  are  to  be  found,  while 
females  alone  may  be  met  with  at  some  distance  therefrom.  The 
feeding  range,  therefore,  varies  considerabty. 

Flies  bite  mostly  during  the  middle  part  of  the  day,  and  not  so 
much  at  dawn  or  in  the  late  afternoon. 

According  to  Hodges,  the  chief  conditions  required  for  a  breeding- 
ground  are  loose,  dry,  friable  earth,  situate  not  more  than  20  yards 
away  from  the  high-water  mark  of  a  stream,  and  protected  from  sun 
and  rain  by  the  shade  of  trees  and  undergrowth. 

Such  conditions  are  found  on  steep  banks  along  lakes,  rivers, 
watercourses,  etc.,  and  the  larvae  are  to  be  looked  for  at  the  bases 
of  shrubs  and  trees,  in  the  undergrowth,  and  in  earth-filled  hollows 
in  tree-trunks  and  branches  at  no  great  distance  from  the  ground. 
Bagshawe  found  the  larvae  principally  at  the  roots  of  bananas 
with  scrub  and  water  in  the  immediate  neighbourhood:  at  the  roots 
of  a  shrub  called  Allophylliis ,  belonging  to  the  Sapindaceae,  especi- 
ally in  the  dry  season ;  at  the  roots  of  large  figs  and  of  the  wild  date- 
palm  {PJuznix  rccliuata) ;  while  he  also  found  a  few  pupae  in  dry  earth 
sheltered  by  overhanging  rocks  on  wooded  banks. 

The  breeding  season  appears  to  be  at  the  commencement  of  the 
rains,  as  Bagshawe  generally  found  empty  pupal  cases  in  the  dry 
season. 

The  pupae  apparently  have  their  enemies  which  eat  them.  These 
are  minute  winged  insects  probably  belonging  to  the  Chalcididse, 
though  this  is  not  definitely  known. 

Pathogenicity.— Glossina  palpalis  is  the  carrier  of  Trypanosoma 
castellanii,  and  G.  morsitans  of  T.  rhodesiense,  both  of  which  are 
the  causes  of  sleeping  sickness  in  Africa. 

Classification. — Newstead  in  191.1  revised  the  genus  Glossina,  and  published 
a  classification  based  on  the  male  genital  armature.     This  is  a  very  excellent 


GLOSSINA  845 

classification,  but  requires  the  addition  of  female  characters  to  complete  it. 
We  have,  therefore,  kept  Austen's  revised  classification  in  1911,  which,  slightly 
modified,  is  as  follows: — - 

A.  Hind  tarsi  entirely  dark  (female  of  Glossina  tachinoides) ,  basal  half  of 

firsi  and  extreme  bases  of  succeeding  joints  pale,  Glossina  palpalis 
group. 
I.  Ground  colour  of  abdomen  ochraceous  buff,  with  interrupted  dark 
brown  deep  transverse  bands  and  sharply  defined  pale  hind  borders 
to  segments.     A  very  conspicuous  square  or  oblong  pale  area  in  the 
centre  of  the  second  segment.     Small  species:  Body  length  7  milli- 
metres-— G.  tachinoides  Westwood,  1850. 
II.  Abdomen  not  so  marked. 

1.  Third  joint  of  the  antenna  dusky  brown  to  cinereous  black. 

(a)  Dorsum  of  abdomen  dark  sepia  brown,  median  paler  area 
on  second  segment,  broad,  more  or  less  quadrate  or 
irregular,  hypopygium  of  male  buff  or  ochraceous  buff — 
G.  caliginea  Austen,  191 1. 

(/;)  Dorsum  of  abdomen  blackish-brown,  median  paler  area 
triangular,  hypopygium  of  male  grey — G.  palpalis 
Robineau-Desvoidy,  1830. 

2.  Third  joint  of  antenna  pale — G.  pallicera  Bigot,  1891. 

B.  Hind  tarsi  not  entirely  dark  (except  in  G.  austeni). 

I.  Upper  surface  of  abdomen  with  pale  ground  colour,  drab  grey,  buff, 
or  ochraceous  buff,  marked  with  very  conspicuous  dark  brown 
or  clove  brown  transverse  bands  interrupted  in  the  middle 
line — Glossina  morsitans  group. 

(a)  Last  two  joints  of  front  and  middle  tarsi  with  sharply  defined 

dark  brown  or  black  tips. 

(1)  Large   species:   Wide  head,    darker   anteriorly;   abdominal 

bands  deep — G.  longipalpis  Wiedemann,  1830. 

(2)  Smaller  species:   Narrower  head — G.   morsitans  Westwood, 

1850. 

(b)  Last  two  joints  of  fore  and  middle  tarsi  very  narrowly  darker, 

and  sometimes  the  colour  is  absent  in  the  former — G.  austeni 
Newstead,  1912. 

(c)  Last  two  joints  of  fore  and  middle  tarsi  pale.     Body  length  8  to 

10  millimetres — G.  pallidipes  Austen,  1903. 
II.  Upper  surface  of  abdomen  not  so  banded. 

(a)  Wings   dull   sepia   coloured,    palpi    (except  in   G.   tabaniformis) 
long  and  slender — Glossina  fusca  group. 

1.  Third  joint  of  antenna  fringed  anteriorly  and  posteriorly 

with  hairs  conspicuous  when  magnified  15  diameters. 

(a)  Longest  hairs  in  front  of  third  joint  equal  in  length  from 

one-quarter  to  one-third  of  width  of  third  joint; 
palpi  moderately  long — G.  tabaniformis  Westwood, 
1850. 

(b)  Longest  hairs  in  front  of  third  joint  equal  in  length 

from  one-half  to  one-third  of  width  of  third  joint; 
palpi  noticeably  long  and  slender — G.  nigrofusca 
Newstead,   I9IO. 

2.  Third  joint  antennae  fringed  anteriorly  with  five  short  hairs, 

1   inr]y  noticeable  when  magnified  15  diameters. 

(a)  Pleura   drab   grey,   hind   coxae  buff  or   greyish-buff — 

G.  fusca  Walker,  1849. 

(b)  Pleura   dark  grey,   hind   coxae   mouse   grey — G.  fusci- 

pleuris  Austen,  191 1. 


846  THE  DIPTERA 

(b)  Wings  pale,  palpi  short — Glossina  brevipalpis  group. 

(1)  Dorsum  of  thorax  with  four  sharply  defined   dark  brown 

oval  or  elongate  spots,  arranged  in  a  parallelogram,  two 
in  front  and  two  behind  the  transverse  suture  proboscis 
bulb,  with  brown  or  dark  brown  tip — G.  longipennis 
Corti,  1895. 

(2)  Dorsum  of  thorax  without  such  spots,  and  proboscis  bulb 

not  brown  or  dark  brown  at  the  tip. 
(i.)  Wings    with    upper    thickened    portion    of    anterior 
transverse   vein   dark  and   distinct — G.   brevipalpis 
Newstead,  1910. 
(ii.)  Wings  with  anterior  transverse  vein — G.  medicorum 
Austen,  1911. 

Recently  Griinberg  has  described  a  new  species,  G.  ziemanni  Grunberg, 
1912,  but  its  position  at  present  is  not  quite  certain. 

Haematobosca  Bezzi,  1911. 

Stomoxydinae  resembling  Hcematobia,  but  with  no  bristles  on  the 
first  and  third  longitudinal  veins,  and  with  fourth  longitudinal  vein 
almost  as  strongly  bent  as  in  Musca  ;  therefore  first  posterior  cell 
only  very  narrowly  opens.  Distribution:  Southern  Europe  and 
China. 

Type. — Hcematobosca  atripalpis  Bezzi,  1895. 

European  Species. — H.  atripalpis  Bezzi,  1895. 

Asiatic  Species. — H.  perturbans  Bezzi,  1907,  found  at  Tang-San,  China. 

Haematobia  Robineau-Desvoidy,  1830. 

Sy  nony  m—Siphona  Meigen,  1824. 

Stomoxydinae  resembling  Stomoxys,  but  with  spatulate  maxillary 
palps  nearly  as  long  as  the  proboscis;  arista  feathered  dorsally  and 
ventrally,  and  third  longitudinal  vein  bristly  proximally.  Body 
robust,  head  broad  and  squat.     Distribution:  Europe,  India,  etc. 

Type. — Hcsmatobia  stimulans  Meigen,  1824. 

European  Species. — H.  stimulans  Meigen. 

Asiatic  Species. — H.  sanguisugeus  Austen,  1909;  H.  ntfipes  Brunetti,  1910, 
in  India. 

Bdellolarynx  Austen,  1909. 

Flies  like  Hcsmatobia,  but  without  sexual  colour  dimorphism. 
Arista  with  long  hairs  above  and  with  six  fairly  long  hairs  below. 
No  bristles  on  first  and  third  longitudinal  veins. 

B.  sanguinolentns  Austen,  1909,  is  a  blood-sucker  found  in  India 
and  Ceylon. 

Muscin^e. 
Musca  Linnaeus,  1761. 
Musca  putrida  is  the  cause  of  Myriase  do  Sero  in  San  Paulo. 

Calliphora  Robineau-Desvoidy,  1830. 

These  are  the  blow-flies  or  bluebottles,  of  which  C.  erythrocephala  Meigen  is 
the  common  species.  It  and  the  following  have  been  found  in  the  human  intes- 
tine: C.  azurea,  C.  vomitoria.     C.  limeus  is  a  common  cause  of  nasal  myiasis. 


CHRYSOMYIA 

Chrysomyia  Robineau-Desvoidy,  1830. 


847 


Chrysomyia  macellaria  Fabricius,  1794. 

SynDnyms. — Musca  macellaria  Fabricius,  1794;  Lucilia  macellaria 
Robineau-Desvoidy,  1830 ; L.  hominivorax  Coquerel,  1858 ;  Calliphora 
infesta  Philippi,  1861;  C.  macellaria  Jorge,  1878;  C.  anthropophaga 
Conil,  187S :  Compsomyia  rubrifrons  Macquart ;  Somomyia  monteri- 
clensis  Bigot. 


Fig.  437. — Chrysomyia  macellaria  :  Female.     (X  4-) 

In  all  this  fly  has  twenty-six  synonyms,  largely  due  to  Walker, 
Macquart,  and  Robineau-Desvoidy,  but  these  were  all  carefully 
consolidated  by  Arribalzaga. 

Muscina?  with  blue  bodies,  red  front  to  the  head,  and  three  black 
lines  on  the  thorax.  The  body,  which  is  less  than  10  millimetres 
in  length,  is  covered  with  stiff  black  hairs. 

Life-History. — The    fe- 
male deposits  some  three 
10  four  hundred  eggs  in  a 
space  of  a  few  moments  in 
some  wound  or  decaying 
matter,  but  as  the  same 
fry  may  oviposit  in  differ- 
ent   places    at    different 
times,  the  total  number  of 
eggs  laid  by  one  fly  must 
number  some  hundreds,  or 
perhaps  even  thousands. 
The  eggs  are  white  and  cylindrical,  1  millimetre  in  length,  and 
marked  by  a  prominent  unilateral  ridge.    They  hatch  in  from  one  to 
nine  hours,  and  produce  a  whitish  footless  larva,  rather  slender, 


Fig.   438. 


-Chrysomyia    macellaria  :   Larva. 
(X4-) 
(After  Blanchard.) 


848  THE  DIPTERA 

with  twelve  segments,  armed  with  minute  spines.  It  is  most 
active,  and  burrows  into  the  tissues  of  the  affected  animals  or  into 
the  mass  of  putrid  flesh  or  decaying  matter.  It  grows  rapidly 
and  matures  in  from  five  to  seven  days,  when  it  endeavours  to 
escape  from  the  wound  or  cavity  on  to  the  ground,  when  it 
wriggles  off  and  buries  itself  in  the  ground  at  a  suitable  place,  and 
becomes  the  brown  cylindrical  pupa  with  rounded  ends.  The  pupa 
is  about  §-  inch  in  length,  and  matures  in  some  nine  to  fourteen 
days. 

Habits. — It  is  a  pest  to  man  and  animals. 

Distribution.— America,  from  Canada  to  Patagonia,  but  most 
common  in  the  tropical  and  subtropical  belts.  It  is  killed  by  cold 
winds.  In  the  Southern  United  States  it  occurs  from  July  to  October . 
It  is  also  found  in  the  West  Indies. 

Pathogenicity. — It  attacks  cattle  after  castration,  spaying, 
branching,  dehorning,  and  when  wounded  by  ticks  or  barbed  wire. 
It  will  enter  the  uterus  if  there  is  placental  retention,  and  will  attack 
the  navels  and  mouths  of  young  calves.  Horses  and  mules  may 
be  attacked  in  the  sheaths  and  vaginae,  and  in  the  navel  in  colts. 
Hogs  are  especially  liable  to  be  attacked,  but  sheep  rarely,  unless 
after  being  worried  by  dogs.  Man  is  attacked  when  sleeping  in 
the  open  air,  and  more  rarely  when  driving.  The  symptoms  pro- 
duced in  man  will  be  detailed  later  under  Nasal  Myiasis  in 
Chapter  LXVII. 

Treatment.- — Injections  of  chloroform  water  are  the  best  means  of 
getting  rid  of  the  larvae,  but  the  frontal  and  other  sinuses  may  have 
to  be  opened  to  remove  them  if  in  large  numbers. 

Prophylaxis. — The  use  of  mosquito  curtains  and  protection  to 
the  nose  by  handkerchiefs  are  important  in  man.  Wounds  of 
animals  should  be  washed  with  weak  carbolic  lotion  and  dressed 
with  pine  tar  or  oakum  and  tar. 

Chrysomyia  viridula. 

Causes  nasal  myiasis  in  Central  America,  and  will  attack  ulcers. 

Pycnosoma  Brauer  and  Bergenstamm,  1893. 

The  larvae  of  Pycnosoma  putorium  Wiedemann,  1830,  are  said  to 
be  parasitic  in  man  and  the  domestic  animals  in  Abyssinia,  the 
Belgian  Congo,  and  Lorenzo  Marques. 

This  fly  resembles  Chrysomyia,  but  the  three  dark  stripes  on  the 
dorsum  of  the  thorax  are  wanting. 

Pathogenicity. — It  causes  nasal  myiasis  in  man,  while  other 
species — e.g.,  P.  megacephala  and  P.  marginale,  etc.— are  found  in 
cattle. 

Lucilia  Robin eau-Desvokly,  1830. 

Flies  of  this  genus — e.g.,  L.  ccesar  Linnaeus  and  L.  sericata — deposit  their 
eggs  on  ulcers.  L.  nobilis  Meigen  has  been  found  in  the  auditory  meatus. 
According  to  Peiper,  L.  ctssar  Linnaeus  and  L.  regimi  Macy  have  been  recog- 
nized as  causes  of  intestinal  myiasis. 


CORDYLOBIA 


849 


Cordylobia  Griinberg,  1903. 
Cordylobia  anthropophaga  E.  Blanchard. 
Synonyms. — Ochromyia    anthropophaga   E.   Blanchard,  Glossina 
grunbergi  Donitz. 


Fig.  439. — Cordylobia  anthropophaga  Blanchard:  Female.    (X4-) 

The  larva  of  this  fly,  which  is  called  '  ver  du  Cayor,'  because  it 
was  first  noticed  in  Cayor,  in  Senegambia,  burrows  into  the  skin  and 
causes  a  painful  swelling.     It  extends  from  Senegal  to  Natal. 

Life-History  and  Morphology. — It  is  not 
certain  whether  the  fly  lays  its  eggs  upon  the 
ground  or  upon  the  clothing  of  people  and  the 
skin  of  animals.  Hence  it  is  not  known 
whether  the  larva  creeps  from  the  ground  on 
to  the  human  being  or  animal,  or  hatches  in 
the  clothing  and  simply  enters  the  skin. 

The  larva,  which  measures  about  12  milli- 
metres, is  composed  of  twelve  segments,  of 
which  the  anterior  or  cephalic  is  bluntly 
pointed  in  front  and  truncated  behind,  and 
carries  two  black  mouth  hooklets  on  its 
ventral  surface.  External  to  these  hooklets 
lie  the  antennal  protuberances.  On  the 
third  to  the  eleventh  segments  there  are 
minute,  rather  characteristic,  brownish,  chiti- 
nous,  recurved  spines.  The  greatest  breadth 
is  at  the  level  of  the  sixth  to  seventh  seg- 
ments, while  the  last  segment  has  a  flattened 
posterior  surface  which  carries  the  posterior  stigmata.  It  is 
parasitic  in  men,  monkeys,  and  dogs.  The  pupa  measures  10-3 
by  4-6  millimetres,  and  looks  like  an  ordinary  muscid  pupa. 

The  fly  measures  9-5  millimetres,  and  has  a  yellowish-coloured 

54 


® 


Fig.  4-1 


Larva    of- 

Cordylobia       anthro- 
pophaga.   (X  4-) 
(After  Austen.) 


8so 


THE  DIPTERA 


head,  body,  and  wing.  The  thorax  is  marked  dorsally  by  longi- 
tudinal dark  stripes,  while  the  abdomen  has  also  blackish  markings, 
and  the  wings  are  of  a  brownish  tinge.  The  female  is  distinguished 
from  the  male  by  the  eyes  being  separated  by  a  broad  frontal  stripe; 
in  the  black  colour  of  the  third  and  fourth  abdominal  (except  the 
margin)  segments;  and  in  the  blackish  quadrangular  median  patch 
on  the  second  abdominal  segment.     In  the  male  the  eyes  join. 

Cordylobia  rodhaini  Gedoelst,  1905. 

Synonym. — Lund's  larva. 

Under  this  term  a  larva  is  described  as  occurring  in  the  Congo 
Free  State  which  possesses  habits  similar  to  those  of  Cordylobia 
anthropophaga. 

The  larva  of  this  species  also  occurs  at  times  under  the  skin  of 
man  in  the  Belgian  Congo. 

Auchmeromyia  Schiner  and  Brauer  Bergenstamm,  18 19. 
Auchmeromyia  luteola  Fabricius,  1805. 

Synonym.-^MMsca  luteola  Fabricius,  1805,  Ver  de  Case. 

The  larva  of  this  fly  is  called  the  '  Congo  floor-maggot.'  It  was 
found  by  Dutton,  Todd,  and  Christy,  living  in  the  floor  of  native 
huts  to  the  depth  of  3  inches.  At  night  these  larvae  came  out,  and 
sucked  the  blood  of  persons  sleeping  on  the  ground,  or  on  beds  but 
little  raised  therefrom,  but  not  on  high  beds. 


Fig.  441. — Auchmeromyia  luteola  Fabricius:  Female.     (X3-) 

The  native  names  for  the  larvae  are,  '  Mabinzu,'  '  Nchichi,' 
'  Ntunga,' '  Mvidi,'  and  '  Kiso.' 

Morphology. — The  fly  is  widely  distributed  in  tropical  and  sub- 
tropical Africa.  It  is  10  to  12  millimetres  in  length,  tawny  in 
colour,  with  small  black  hairs  giving  it  a  smoky  appearance.  The 
head  is  large,  as  broad  as  the  thorax.     The  eyes  are  separated  by  a 


AUCHMEROMYIA  LUTEOLA  851 

considerable  space.  The  proboscis  is  folded  beneath  the  head  into 
a  deep  groove.  The  palpi  are  club-shaped,  with  a  long,  yellow, 
flattened  third  joint,  which  carries  an  arista  with  black  hairs  on  its 
upper  and  lower  borders. 

The  dorsum  of  the  thorax  is  marked  by  longitudinal  black  and 
brown  stripes,  and  shows  a  well-marked  transverse  suture.     The 
squamae  are  large,  yellow 
in  colour,  and  cover  the     ''  -^O 

halteres.     The  first  abdo-  ^/\      ^     '  ]  ;    ' 

minal      segment      has     a  /  >    : 

narrow     dark     line    pos-      (^ 
teriorly,    the      second     a  '&  .  ,    t 

central  median  dark  line,      ^jJF8^  -— *^r- 

which  joins  with  a  pos-        ^* 

terior  dark  line.  The  third       Fig.  442. — Auchmeromyialuieola:  Larva. 
segment   is   dark    brown,  (X3-) 

except  for  a  narrow  yellow 

anterior  streak.  The  fourth  segment  is  dark-coloured,  with  a 
posterior  light  brown  band.  The  fifth  segment  is  small,  and  con- 
tains the  genital  apparatus. 

The  legs  are  buff-coloured,  with  black  hair  and  bristles.  The 
fifth  tarsal  joint  is  jet  black,  and  has  a  large  cream-white  pulvillus. 

Life-History. — The  fly  deposits  its  eggs  on  the  ground  of  the  hut, 
especially  on  spots  on  which  urine  has  been  voided.  The  larva  is 
semitranslucent,  of  dirty  white  colour,  acephalous  and  amphi- 
pneustic,  and  has  eleven  distinct  segments.  The  first  segment  is 
divisible  into  two  portions,  of  which  the  anterior  carries  the  mouth- 
parts.  The  broadest  segments  are  the  ninth  and  tenth.  There  are 
distinct  dorsal  and  ventral  surfaces,  at  the  junction  of  which  in  each 
segment  there  are  protuberances,  with  a  spine  and  a  pit.  The 
ventral  surface  is  flattened,  and  has  three  footpads  transversely 
arranged  at  the  posterior  margin  of  each  segment.  The  last  seg- 
ment is  large,  and  carries  the  posterior  spiracles  and  the  anus. 

The  mouth,  which  is  provided  with  teeth,  leads  into  an  oeso- 
phagus, which  ends  in  a  proventriculus,  and  has  a  dorsal  diverticu- 
lum. The  ventriculus  is  short.  Malpighian  tubules  mark  the 
commencement  of  the  intestine.  The  hind  gut  is  coiled.  The 
salivary  glands  are  well  marked. 

The  larva  becomes  a  dark  brown  or  black  pupa,  9  to  10*5  by 
4  to  5  millimetres,  with  an  anterior  conical  and  a  posterior  rounded 
end,  and  marked  by  annular  ridges.  The  pupal  stage  lasts  two  to 
three  weeks. 

Habits.— The  fly  does  not  bite  man.  The  larva,  as  described 
above,  attacks  man  and  fills  its  dorsal  oesophageal  pouch  with  blood, 
and  thus  acquires  a  red  colour. 

Pathogenicity. — As  far  as  is  known  it  is  non-pathogenic. 

In  191 1  Roubaud  described  a  new  genus,  Chceromyia  Roubaud.  191 1,  of 
which  the  larvae  of  two  species,  C.  boueti  Roubaud,  191 1,  and  C.  chcsrophaga 
Roubaud,  1911,  were  blood-suckers  attacking  African  wart-hogs  and  African 
ant-eaters. 


852 


THE  DIPTERA 


Auchmeromyia  praegrandis  Austen,  1910. 

A  saffron-yellow  fly.     It  occurs  in  South  Africa. 

Pollenia  Robineau-Desvoidy,  1830. 

The  larvae  of  Pollenia  rudis  Robineau-Desvoidy  have  been  found 
in  a  case  of  gastric  myiasis  in  man. 

Bengalia  depressa  Walker. 

By  an  error  this  fly  was  said  to  cause  cutaneous  myiasis  in  Natal, 
Rhodesia,  British  Central  Africa,  Uganda,  and  the  Sudan,  the  true 
causal  agent  being  Cordylobia  anthropophaga  Grunberg.  The  life- 
history  of  B.  depressa  is  unknown. 


Family  Anthomyid^e  Latreille. 

Diptera  with  arista  naked  or  pectinate.  Thorax  with  complete  transverse 
suture.  First  posterior  cell  completely  open.  Abdominal  bristles  often 
absent . 

This  family  includes  a  number  of  genera  known  to  be  troublesome  to  man — 
Fannia  Robineau-Desvoidy,  Hylemyia  Macquart,  Hydrotcea  Robineau-Des- 
voidy— which  may  be  recognized  by  the  following  characters:  (a)  Arista  bare 
— Fannia  ;  (b)  arista  plumose — Hylemyia  ;  (c)  arista  pubescent — Hydrotcsa. 

Fannia  Robineau-Desvoidy,  1830. 

Fannia  canicularis  Linnaeus,  1761. 
Synonyms. — Homalomyia  canicularis  Linnaeus,  Anthomyia  canicularis  Lin- 
naeus. 

This  species  has  frequently  been  reported  as  being  passed  in  human  faeces. 


Fig.  443. — Fannia  canicularis  Linnaeus:  Female.     (X8-) 


FANNIA   CANICULARIS 


853 


The  fly  is  commonly  found  in  houses  in  Europe  and  North  America.     The 
larvae  normally  live  in  vegetables,  by  means  of  which  they  enter  the  human 
digestive  tract.     They  are  provided  with  branched  pro- 
cesses on  the  segments. 

Pathogenicity. — Blankmeyer  gives  an  account  of  a 
case  of  this  infection  which  is  said  to  have  lasted  some 
twelve  years,  being  associated  at  first  with  abdominal 
pain,  blood}'-  diarrhoea,  severe  pains  in  the  region  of 
the  liver.  After  the  initial  attack  the  pains  continued, 
but  instead  of  diarrhcea,  constipation  resulted,  with 
severe  headaches.     The  abdomen  was  distended. 

The  patient  was  treated  with  raw  pumpkin  seeds  and 
then  given  a  saline  purge,  and  passed  1,000  to  1,500 
Fannia  larvae.  After  this  he  still  passed  a  few  larvae  for 
some  days,  but  eventually  recovered.  This  is  a  curious 
case,  in  that  the  larvae  lived  for  years  inside  the  man, 
and  because  it  is  not  clear  how  such  an  enormous  infection 
was  possible.  Chevrel  has  collected  and  described  seven 
authentic  cases  of  myiasis  of  the  urinary  passages  caused 
by  the  larva  of  this  fly. 


Fannia  desjardensii  Macquart. 

Synonyms.- -Homalomyia  desjardensii  Macquart,  An- 
thomyia  desjardensii  Macquart. 

Wellman  describes  cases  of  this  myiasis  in  the  alimen- 
tary canal  of  human  beings  in  Angola  who  showed 
dysenteric  symptoms,  and  which  he  successfully  treated 
with  castor-oil,  then  santonin,  and  then  castor-oil  again. 

The  disease  is  locally  known  as  '  ovaenyo, '  a  term  which  signifies  maggots. 
The  editors  of  the  Journal  of  Tropical  Medicine  in  1907  asked  for  information 


Fig.  444. ■ — Larva 
of  Fannia  can- 
icular is. 


Fig.   445. — Penicillidia  dufouri  Westwood  from  a  Bat:  Female.    (X8.) 


«54 


THE  DIPTERA 


with  regard  to  an  African  myiasis  called  '  muculo,'  but  as  far  as  we  know 
this  disease  has  not  been  traced.  Wellman  says  that  the  term  is  not  used  in 
Angola.  In  F.  desjardensii  the  larvae  become  pupa?  in  seven  to'nine  days, 
and  the  pupae  insects  in  another  thirteen  to  fifteen  days. 

Other    Species. — Peiper  also  lists  F.  scalaris,   F.  incisurata,  F.  manicuta, 
F.  saltatrix  as  being  causes  of  intestinal  myiasis. 


Hydrotsea  Robineau-Desvoidy,  1830. 
HydrolcBa   meteorica   Linnaeus,   which   usually  attacks   animals'   eyes   and 


nostrils,  is  said  to  attack  man  also. 


SUBORDER  III.   PUPIPARA. 


Synonym.— Epvoboscida . 
The  Pupipara  are  flies  which  appear  to 
have  become  altered  owing  to  their  parasitic 
life.  They  possess  a  well-defined  proboscis, 
which  is  said  by  Austen  to  resemble  that  of 
the  Glossince  by  being  armed  at  its  tip  with 
teeth.  Wings  have  been  lost  in  several 
species,  either  entirely  or  after  the  imago 
has  become  parasitic,  though  they  may  exist 
throughout  life  in  other  species.  Their 
feet  are  provided  with  extra  ungues  to  enable 
them  to  cling  to  the  hairs,  etc.,  of  the  host. 
They  do  not  lay  eggs,  but  produce  a  larva, 
which  soon  becomes  a  pupa. 

The  suborder  is  divided  into  four  families : 

(1)  Hippoboscidae;  (2)  Nycteribidae;  (3)  Brau- 

lidae;  (4)  Streblidae. 

The  Nycteribidae  are  parasitic  on  birds  and  bats.     In  this  family  comes 

Penicillidia  dufouri  Westwood,  which  is  the  carrier  of  Achromaticus  vesperu- 

ginis  Dionisi,  1898.     The  Braulidae  are  parasitic  on  bees,  and  the  Streblidae 

on  bats,  and  therefore  will  not  be  considered  further. 


Fig.  446. — Nycteribia  sp.  (?).       ,} 


Fig.   447. — Hippobosca  rufipes  von  Olfers:  Female      (X  4-) 


HIPPOBOSCIDM 


Family  Hippoboscid^e. 

Pupipara  with  horny  flattened  heads  and  bodies,  and  with  one  jointed 
antenna  furnished  with  a  terminal  arista.  The  first  joint  of  the  tarsus  is 
usually  abbreviated  in  all,  but  certainly  in  the  first  two  legs. 

Wings  may  be  well  developed,  or  rudimentary, 
or  entirely  absent. 

This  family  is  composed  of  forms  parasitic 
on  mammals,  and  includes  the  following  genera : 
Hippobosca  Linnaeus,  1761;  Allobosca  Speiser, 
1902;  Olfersia  Wiedemann,  1830;  Ortholfersia ; 
Pseudolfersia  Coquillett;  Lipoptena  Nitzsch, 
1 81 8;  Melophagus  Latreille,  1802;  Ornithoctona 
Speiser,  1902;  Lynchia  Weyenberg,  1881;  and 
Ornithomyia  Latreille,  1802. 

Hippobosca  is  parasitic  on  cattle,  horses, 
dogs,  etc.,  all  over  the  world;  Allobosca  is 
parasitic  on  lemurs  in  Madagascar;  Ortholfersia 
on  kangaroos  in  Australia;  Lipoptena  on  deer 
all  over  the  world;  and  Melophagus  on  sheep. 

Hippobosca  rufipes  von  Olfers  is  thought  to 
be  capable  of  transmitting  Trypanosoma  theileri. 


Fig.  448.-  -Larva   and   Pupa   of   Hippobosca     Fig.  449. — Head  of  Hip- 
rufipes  von  Olfers.     (X4-)  pobosca  rufipes  :  Female. 

Hippobosca  equina  Linnaeus  is  known  on  horses  in  the  New  Forest,  England ; 
Hippobosca  capensis  Leach  on  dogs  in  Africa,  India,  Persia,  and  South  Europe; 
H .  camelina  Leach  and  H.  maculata  Leach  are  found  in  the  Sudan  and  Egypt ; 
and  in  addition  to  these  Melophagus  ovinus  Linnaeus  is  found  all  over  the  world. 

REFERENCES. 

General. 

Austen  (1906).     British  Blood-Sucking  Flies. 

Austen  (1907).     Blood-Sucking  Flies,  Ticks,  etc. 

Austen  (1909).     Annals  and  Magazine  of  Natural  History,  series  viii.,  iii.  285 . 

(Descriptions    of    Lyperosia,    Stygeromyia,    Haematobia,    Bdellolarynx, 

Stomoxys,  Philaematomyia.) 
Austen  (1909).     African  Blood-Sucking  Flies. 
Cluss  (1902).     Myiasis  Tubingen. 

Cluss(i903).  Sitzung.  Ges.  Nat.  Frde.  Berlin,  400.   (Parasitic  Muscid  larvae.) 
Grunberg  (1907).     Die  Blutsaugenden  Dipteren.     Jena. 
Huber  (1899).     Bibliographic  d.  klin.  Entomologie.     Miinchen. 
Meigen   (1818-1838).     Syst.  Beschr.  d.  bek.  Europ.  zweifl.  Insect.     7  vols. 

Hamm. 
Peiper  (1900).     Fliegenlarven  als  gelegentliche  Parasiten  des  Menschen. 
Schiner  (i860).     Fauna  Austriaca.     Die  Fliegen.     Wien,  i860. 
Sergent  (1909).     Les  Insects  Piqueurs  et  Suceurs. 
Theobald.     British  Flies,  vol.  i. 

Verrall  (1901  and  1909).     British  Flies.     Vols.  i.  and  v.  only  published. 
Walker  (1851).     Insecta  Britann.  Diptera.     London. 
Wersung  (1906).     Zeitschrift  fur  Klin.  Med.,  lx.  122. 


856  THE  DIPTERA 

(Estridae. 

Brauer  (1863).     Die  CEstriden.     Wien. 

Dermatobia. 

Oliva  (1909).     Annali  Med.  Naval.,  p.  183. 

Peiper  (1906).     Loc.cit. 

Cordylobia. 

Austen   (1907).     Proceedings  of  the  Entomological  Society.     (A  very  im- 
portant paper.) 

Austen  (1908).     Journal  Royal  Army  Medical  Corps. 

Fuller  (1914).     The  Skin  Maggot  of  Man.     Agricultural  Journal  of   South 
Africa. 

Tabanidae. 

Hart  (1895).    Bulletin  Illinois  State  Laboratory  of  Natural  History,  vol.  iv., 

1895- 
Hine  (1906).     U.S.  Dep.  Agriculture  Bureau,  Entomology,  No.  12    Part  II. 

(habits  and  life-histories). 
Patton  (1909).     Archiv  f.  Protistenkunde,  p.  333. 

Auchmeromyia  luteola. 
Dutton,  Todd,  and  Christy.     Liverp.  Sch.  Trop.  Med.      Memoir  XIII. 

Bengalia  depressa. 

Theobald  (1906).     Second  Report,  Wellcome  Research  Laboratories,  London. 

Storaoxys. 

Stephens  and  Newstead  (1907).     Annals  Trop.  Med.  and  Parasitology. 
Tulloch  (1906).     Proceedings  of  the  Royal  Society.     1906. 

Glossina. 

Austen  (1903).     Monograph  of  the  Tsetse-Flies.     London. 

Austen  (1904).     Liverp.  Sch.  Trop.  Med.   Memoir  XIII. 

Austen  (191  i).     Handbook  of  the  Tsetse-Flies.     London. 

Hodges    (1909).     The    Distribution    and    Bionomics    of    Glossina    palpalis. 

Sleeping  Sickness  Bureau,  London. 
Minchin  (1905).     Proceedings  of  the  Royal  Society,  vol.  lxxv. 
Stephens  and  Newstead  (1906).    Liverp.  Sch.  Trop.  Med.    Memoir  XVIII. 

Chrysomyia. 

Peiper  (1900).     Loc.  cit. 

Oscinidae. 
Perry  and  Castellani  (1907).     Journal  of  Tropical  Medicine. 

Fannia. 

Blankmeyer  (1907).     Journ.  American  Med.  Assoc,  vol.  xlviii.,  p.  1505. 
Chevrel  (1909).     Archives  de  Parasitologic,  xii.  369. 

Pupipara. 
Austen  (1903).     Ann.  Natur.  History,  series  vii.,  vol.  xii. 
Bigot  (1885).     Ann.  Soc.  Ent.  Franc,  series  vi.,  tome  v.,  1885. 

Sepsidae. 

Alessandrini  (1900).     Archives  de   Parasitologic,  xiii.  3,  337  (Myiasis  due 
to  Piophila  casei). 


CHAPTER  XXXIV 
SIPHONAPTERA   AND   COLEOPTERA 

Siphonaptera — Sarcopsyllidae — Dermatophilus  penetrans — Pulicidae — Pulicinae 
—  Pulex  irritans  —  Xenopsylla  cheopis  — •  Coleoptera  —  Orthoptera  — 
References. 

SIPHONAPTERA  Latreille,  1825. 

Synonyms. —  Roplwteira  Schellenberg,  1798;  Aptera  Lamarck,  1801; 
Afihanipt&ra  Kirby  and  Spence,  1826; Pulicidce  Stephens,  1829. 

Definition. — Hexapoda  with  laterally  compressed  bodies  and  dis- 
tinctly separated  thoracic  rings.  Wings  absent,  except  for  two 
lateral  plate-like  appendages  on  the  meso-  and  meta-thorax. 

The  antennae  are  three-jointed,  and  embedded  in  grooves.  The 
third  joint  has  nine  more  or  less  separated  pseudo-joints. 

Remarks. — Fleas  have  come  into  considerable  prominence, 
owing  to  the  work  of  the  Indian  Plague  Commission  and  that  of 
Dr.  Verjbitski,  of  St.  Petersburg,  who  have  shown  that  they  are  to 
be  looked  upon  as  the  main  agents  by  which  plague  is  spread  from 
rat  to  rat,  and  from  rat  to  man. 

Fleas  may  also  carry  blood-parasites- — as,  for  example,  Trypano- 
soma lewisi — and,  again,  they  may  serve  as  intermediary  hosts  for 
the  cysticercus  of  tapeworms,  as  in  the  case  of  Dipyiidium  caninnm. 

History. — The  knowledge  concerning  fleas  is  of  recent  date.  In 
1758  Linnaeus  started  with  one  genus  and  species,  Pulex  irritans  ; 
the  second  genus  was  that  of  the  Chigoe  in  1815,  under  the  term 
Rhynchoprion  penetrans  ;  and  the  third  genus  was  created  by  Curtis 
in  1832  under  the  heading  Ceratophyllus.  The  first  general  syste- 
matic treatise  was  by  Kolenati  in  1863,  the  second  by  Taschen- 
berg  in  1880,  and  the  third  by  Baker  in  1904. 

Recently  much  work  has  been  done  on  these  parasites  by 
Rothschild  and  Jordan. 

Morphology. — The  head  is  small,  and  may  or  may  not  possess  eyes,  which, 
when  present,  are  onlv  simple  pigment  masses.  Directly  behind  the  head  is 
the  antennal  groove,  in  which  the  antennas,  which  are  important  organs  to 
the  flea,  lie  protected  from  harm.  This  groove  is  continued  upwards  to  the 
mid-line  of  the  vertex  by  an  incrassation  which  divides  the  frons  from  the 
occiput.     The  groove  may  be  open  or  closed  by  a  process  of  the  gena. 

The  antennae  are  composed  of  three  joints,  of  which  the  third,  often  called 
the  club,  may  be  unsegmented,  segmented  on  the  posterior  border  only,  or 
completely  segmented  into  nine  more  or  less  separate  pseudo-segments. 

The  frons  may  carry  a  tubercle  or  notch,  situate  rather  nearer  the  mouth 
than  the  centre  of  the  head,  while  laterally  the  eyes,  when  present,  are  to  be 
seen.     The  area  of  the  head  below  the  eyes  and  extending  from  the  perioral 

&57 


858 


SIPHONAPTERA   AND  COLEOPTERA 


ring  to  the  antennal  groove  is  the  gena.  A  process  of  this  area  may  be  pro- 
longed backwards,  so  as  to  meet  the  hind  edge  of  the  post-antennal  part  of 
the  head,  and  so  to  close  the  antennal  groove  below  in  those  species  which 
possess  a' closed  antennal  groove.  -      _ 

The  occipital  area  carries  usually  three  rows  of  bristles,  the  first  near  the 
base  of  the  antennae,  the  second  in  the  middle,  and  the  third  near  the  hinder 
ed<*e  of  the  head,  which  are  continued  forwards  on  to  the  frons,  and  probably 
defineate  the  four  segments  of  which  the  head  is  composed. 

Anterior  and  ventral  to  the  frons  and  gena  lies  the  perioral  ring,  winch 
carries   the   mouth   appendages,   which   consist    of   a  labrum   (epipharynx) , 

mandibles,  maxillae,  and  palps,  hypo- 
pharynx,  and  labium  with  palps. 
There  does  not  appear  to  be  a 
separate  clypeus. 

The  labrum  (variously  known  as 
epipharynx,  hypopharynx,  and  by 
other  names)  is  a  hollow  prolonga- 
tion of  the  dorsal  wall  of  head  and 
pharynx.  In  front  it  is  closed,  while 
behind  it  opens  into  the  coelom. 
Ventrally  it  shows  a  groove,  con- 
verted into  a  canal  when  it  is  articu- 
lated with  the  mandibles  laterally. 
The  mandibles  consist  of  basal  seg- 
ments attached  to  the  sides  of  the 
mouth,  and  an  anterior  portion  which 
projects  freely  forwards,  and  shows 
fine  serrations  anteriorly.  The  inner 
aspect  of  the  mandibles  possesses  a 
groove,  converted  into  a  trilobed 
channel  by  articulation  with  the 
Fig.  450. — Xenopsylla  cheopis :  Male,  fellow  of  the  opposite  side  and  the 
(After  Tordan  and  Rothschild,  Journal    hypopharynx 


of  Parasitology .) 
1,  Labrum,  mandibles,  and  labial 
palps  (at  the  junction  of  the  last  named 
with  the  head  is  seen  the  triangular 
maxilla) ;  2,  maxillary  palpi ;  3,  antenna; 
4,  pronotum;  5,  mesonotum;  6,  meta- 
notum;  7-12,  ordinary  abdominal  ter- 
gites;  13,  seventh  tergite  with  bristle 
(behind  this  is  seen  the  small  eighth 
tergite) ;  14,  ninth  tergite,  with  sensory 
plate;  15,  tenth  tergite ;  16-24,  sternites 
of  abdominal  segments;  25-27,  meta- 
sternite;  28,  mesosternite ;  29,  pro- 
sternite. 


The  maxillae  are  triangular  chiti- 
nous  plates,  each  possessing  a  four- 
jointed  maxillary  palp.  The  labium 
(which,  of  course,  represents  the 
second  maxillae  with  their  palps)  is 
single  posteriorly ,  where  it  is  attached 
to  the  perioral  ring,  while  in  front  it 
is  divided  into  two  one-to-thirteen 
jointed  palps  (labial  palps),  which 
form  a  sheath  or  rostrum  for  the 
other  mouth-parts. 

The  hypopharynx  consists  of  a 
basal  portion,  which  is  a  chitinous 
plate  concave  ventrally,  extending 
forwards  in  the  head  from  the  infra- 


oesophageal  ganglion  to  the  mandi- 
bulo-basal  articulation,  and  an  anterior  portion,  which  projects  from  the 
basal  portion  forwards,  and  contains  the  canal  from  the  salivary  pump. 

This  anterior  portion  of  the  hypopharynx  articulates  laterally  with  the 
mandibles,  and  its  canal,  opening  ventrally,  fo.ms  the  triradiate  canal  men- 
tioned above,  which  is  continuous  with  the  salivary  groove  on  the  mandibles. 

The  thorax  is  composed  of  the  usual  three  divisions,  but  there  are  no  signs 
of  scutellum  or  post-scutellum.  There  is  generally  one,  but  there  may  be 
two  or  three  rows  of  bristles  on  each  segment.  The  pronotum  may  have  a 
comb.  The  metanotum  may  be  dentate  or  serrate  apically.  Laterally  the 
metathorax  is  typical,  showing  a  sternite,  episternite,  and  epimerite,  while  the 
mesothorax  shows  a  sclerite,  divided  into  two  by  an  internal  incrassation 
running  from  the  coxa  upwards.     These  two  divisions  represent  the  episternite 


SIPHON  A  PTERA 


859 


and  the  epimerite.  The  episternite  has  the  anterior  and  ventral  portion 
separated  off  by  an  oblique  incrassation  to  form  a  sternite.  The  prosternite, 
or  sternite  of  the  prothorax,  is  not  divided.  Generally  these  various  sclerites 
show  bristles. 

With  regard  to  the  abdomen,  the  first  to  seventh  segments  are  more  or  less 
normal,  but  the  eighth  to  tenth  are  modified  sexually.  The  tergites  of  the 
second  to  the  seventh  segments  are  normal,  carrying  bristles  and  combs  in 
different  species.  The  seventh  tergite  has  a  subapical  bristle.  The  first 
segment  has  no  sternal  sclerite,  hence  the  first  visible  sternite  belongs  to  the 
second  segment.  The  third  to  the  sixth  sternites  carry  a  ventral  row  of 
bristles.  The  seventh  has  a  considerable  number  of  bristles.  The  sexually 
different  segments  must  be  considered  according  to  sex.  In  the  female  the 
eighth  tergite  is  very  broad  ventrally,  but  the  sternite  is  reduced  to  an 
elongated  plate  lying  between  the  ventral  edges  of  the  tergite. 

The  ninth  tergite  carries  the  sensory  plate,  with  usually  fourteen  (there 
may  be  more)  setiferous  grooves.  The  ninth  sternite  is  membranaceous 
laterally,  and  extends  far  ventrally,  where  it  is  strongly  chitinized,  and  lies 


1,   Mouth;  2, 


Fig.  451. — Anatomy  of  a  Flea. 

(From  the  Journal  of  Hygiene,   1906.) 

pharynx;  3,  salivary  glands;  4,  stomach;  5,   Malpighian 
tubes;  6,  intestine;  7,  rectum. 


inside  the  seventh  or  eighth  segment.  It  forms  the  ventral  wall  of  the  vagina, 
which  is  joined  just  anterior  to  it  by  the  duct  of  the  receptaculum  seminis. 

The  tenth  tergite  carries  a  short  conical  stylet,  while  the  sternite,  which  is 
triangular,  carries  a  long  bristle  ventrally  before  the  apex  and  shorter  bristles 
at  the  apex. 

The  eighth  tergite  of  the  male  is  small,  while  its  sternite  is  large,  and  from 
its  cavity  the  copulatory  organs  project.  The  accessory  genital  organs 
belong  to  the  ninth  segment,  the  sides  of  whose  tergite  form  the  clasping 
organ  laterally.  The  internal  ventral  angle  of  the  clasper  is  prolonged  into 
a  manubrium,  above  which  is  a  tubercle-like  projection.  The  outer  side  of  the 
clasper  has  three  processes,  which  are  different  in  Pulex  and  Lcemopsylla. 
The  ninth  sternite  has  an  internal  vertical  arm  and  a  ventral  horizontal  arm. 
The  latter  appears  beyond  the  eighth  sternite.  The  penis  can  be  seen  between 
the  ninth  sternite  and  the  claspers. 

Internal  Anatomy. — The  mouth,  which  is  situate  below  the  base  of  the 
labrum,  opens  into  the  aspiratory  pharynx,  which  communicates,  via  a  long 
oesophagus,  with  the  stomach.  Just  before  this  organ  the  oesophagus  is 
swollen  into  a  bulb.'which  represents  the  proventriculus. 

At  the  junction  of  the  stomach  with  the  intestine  are  the  openings  of  the 


86o 


SIPHONAPTERA   AND  COLEOPTERA 


four  Malpighian  tubes.  The  intestine  is  divided  into  small  intestine,  colon, 
and  rectum,  the  last  mentioned  opening  at  the  anus. 

The  salivary  apparatus  is,  as  usual,  separate  from  the  alimentary  canal. 
It  consists  of  two  glands,  on  each  side  of  the  body,  lying  in  the  fat-body  in 
front  of  the  stomach.  The  duct  from  each  gland  joins,  forming  a  common 
duct  on  each  side,  which  runs  forward  to  open  into  the  salivary  pump.  This 
i  a  hollow,  chitinous  organ,  supplied  with  powerful  muscles,  situated  at  the 
anterior  end  of  the  ventral  surface  of  the  hypopharynx. 

The  duct  of  this  pump,  running  forwards  through  the  hypopharynx,  opens 
via  the  triradiate  canal  already  mentioned  as  formed  by  the  junction  of  the 
hypopharynx  with  the  mandibles,  into  the  groove  of  these  organs. 

The  Act  of  Biting. — -The  flea  apparently  carefully  selects  the  spot 
at  which  it  is  to  bite,  and  thenpierc.es  a  hole  by  means  of  thelabrum. 
This  hole  is  then  enlarged  by  the  mandibles,  through  whose  grooves 

salivary  secretion  is 
pumped  into  the  skin. 
This  secretion  irritates 
the  vessels,  causing  a 
local  rush  of  blood  to 
the  part,  and  this  blood 
is  drawn  by  the  suction 
of  the  pharynx  up  a  tube 
formed  by  articulation 
of  the  labrum  with  the 
mandibles.  This  tube, 
of  course,  is  embedded 
in  -the  skin,  which  is 
pierced  by  its  two  com- 
ponent parts. 

There  are  therefore 
two  tubes  in  the  mouth- 
parts  of  a  flea  —  an 
efferent,  carrying  the 
salivary  secretion,  and 
an  afferent,  carrying  the 
blood,  which  is  taken 
to  the  stomach,  and 
luemolyzed  and  digested.  It  appears  that  the  black  residual  mass 
is  capable  of  further  digestion  by  the  rectal  glands.  Further 
bionomics  will  be  given  under  Xenopsylla  cheopis.  In  some  people 
flea-bites  may  cause  a  local  papular  eruption — e.g.,  ceratophyllus 
fasciatus. 

Life-History. — The  egg  is  oval,  waxy  white  or  opaque  porcelain  in 
appearance,  smooth,  and  with  a  length  of  about  0*5  millimetre. 
It  is  generally  deposited  between  the  hairs  of  the  host,  and  falls 
off  on  to  the  ground.  In  two  to  four  days  the  larva  is  hatched. 
This  larva  is  an  elongated  worm-like  little  creature  with  fourteen 
segments.  The  head  is  well  developed,  and  has  strong  mandibles 
suitable  for  biting.  It  lives  on  dead  organic  matter,  and  moults 
three  times  as  a  rule — i.e.,  three  to  four  days,  and  again  six  days, 
and  again  seven  to  fourteen  days  after  hatching.     It  then  spins  a 


Fig.  452. — Egg  of  the  Dog  Flea. 

(X  50  Diameters.) 
(From  a  photograph  by  J.  J. 


Bell.) 


SARCOPSYLLIDJE  86 1 

cocoon,  inside  which  the  pupa  becomes  the  imago  in  about  [five 
days,  the  whole  time  required  for  development  being  fourteen  to 
thirty-three  days. 

Dispersal. — Fleas  are  dispersed  mainly  by  their  host  travelling 
about.  Such  a  host  as  a  rat  may,  of  course,  be  carried  by  merchan- 
dise, and,  again,  merchandise  itself  can  spread  fleas. 

Capture  of  Fleas. — If  it  is  desired  to  capture  fleas,  allow  a  suitable 
animal  to  remain  in  the  place,  when  the  fleas  will  gather  on  it. 
Then  chloroform  the  animal,  and  comb  the  stupefied  or  dead  fleas 
on  to  white  paper. 

Remedies. — The  remedies  for  fleas  are,  first  and  best,  a  clean 
house — i.e.,  plenty  of  soap  and  water  applied  to  the  floors,  etc.  Other- 
wise naphthalene,  pyrethrum  powders,  tobacco  leaves  and  infusions, 
and  benzene  may  be  used. 

A  flea  cannot  jump  more  than  4  inches — an  important  fact  to  be 
noted. 

Flea  larvae  are  delicate  little  things,  and  cannot  stand  disturbance ; 
hence  fleas  will  not  be  found  in  houses  kept  well  swept  and  dusted, 
but  will  abound  in  infected  empty  houses. 

Classification. — The  Siphonaptera  are  classified  by  Rothschild  into 
three  families:  (1)  Sarcopsyllidae,  (2)  Pulicidae,  (3)  Ceratopsyllidae. 

Only  the  first  two  are  of  importance,  the  last  named  being  found 
on  bats. 

Family  Sarcopsyllid^  Taschenberg,  1880. 

Synonym. — -Rhynchoprionidce  et  Hectopsyllidce  Baker,  1905. 

Siphonaptera  without  ctenidia.  Labial  palps  rather  long,  but 
very  weak  and  fragile;  pale,  slightly  chitinized,  formed  of  one  or 
two  segments.  Small  maxillae  little  prominent.  Piercing  apparatus 
very  developed;  mandibles  large  and  strong.  Genal  extremity 
always  prolonged  below  and  in  front  into  a  process,  placed  behind 
the  insertion  of  the  mandibles.  Nota  of  thoracic  segments  shorter 
than  that  of  the  first  abdominal. 

Genera.— Echidnophaga  Olliff,  1886;  Hectopsylla  Fra.nenield,  i860; 
Dermatophilus  Guerin,  1838  or  1839,  which,  according  to  Jordan 
and  Rothschild,  may  be  recognized  in  the  following  manner: — 

I.  Hind  coxa  with  patch  of  spines  on  inner  side — Echidnophaga. 
II.  Hind  coxa  without  such  a  patch  of  spines: — 

(a)  Hind  femur  with  large  basal  tooth-like  projection — 

Hectopsylla. 

(b)  Hind  femur  simple — Dermatophilus. 
We  need  only  consider  Dermatophilus. 

Dermatophilus  Guerin,  1838. 

Synonyms. —  Rhynchoprion  Oken,  1815,  nee  Hermann,  1804; 
Surcopsylla  Westwood,  1836. 

This  genus  contains  the  species  Dermatophilus  penetrans  Guerin, 
distinguished  by  having  a  distinct  eye,  and  D.  ccecata  Enderlein, 
190 1,  with  a  rudimentary  eye.  The  latter  species  was  found  behind 
the  car  of  Epimys  rattus  in  Brazil. 


862 


SIPHON  APT  ERA   AND  COLEOPTERA 


Fig.  453. 


-Dermatophilus  penetrans :  Male. 

(MlCROPHOTOGRAPH.) 


Dermatophilus  penetrans  Guerin,  1838. 

Synonyms. — Pulex  minimus  cutem  penetrans  Catesby,  1743 ;  Pulex 
minutissimus  nigricans  Barrere,    1743;   Acarus  fuscus   sub  cutem 

nidulans  proboscice  aculiorc 
P.  Brown,  17  56;  Pulex  pene- 
trans Linnaeus,  1767 ;  Rhyn- 
clioprion  penetrans  Oken, 
1815. 

This  is  the  insect  vari- 
ously known  as  the  Chigoe, 
or  jigger,  and  believed  to 
have  been  discovered  by 
Oviedo  in  1551.  The  home 
of  this  little  insect  appears 
to  be  South  America, 
especially  Brazil,  from 
which  it  was  conveyed  to 
West  Africa  about  the 
middle  of  last  century, 
arriving  on  the  West  Coast 
at  Loanda  from  Rio  Janeiro 
by  a  ship,  the  Thomas 
Mitchell,  in  1872,  whose 
crew  was  suffering  from  jiggers,  it  was  probably  noted  on  the 
Gold  Coast  for  the  first  time  in  the  early  seventies.  It  appears 
to  have  spread  across 
Africa  by  Stanley's  Expe- 
dition and  by  trade  routes, 
arriving  in  East  Africa  in 
1895,  and  from  East  Africa 
it  spread  to  India  in  1899 
by  the  4th  Bombay  In- 
fantry, but  luckily  the 
infection  did  not  spread 
beyond  Bombay.  In  1900 
it  reached  Madagascar.  It 
affects  not  merety  man, 
but  domestic  and  wild 
animals.  Perhaps  the  most 
noted  feature  is  the  way  in 
which  it  attacks  pigs.  On 
the  Gold  Coast  it  appeared 
to  be  largely  kept  in  exist- 
ence by  these  animals.  It 
is  very  easily  captured  in 
the  free  state  by  taking  a  little  pig  with  a  pale  abdomen,  and 
placing  it  on  its  back  on  the  ground  on  which  infected  pigs  are 
living.     After  watching  a  few  moments,  a  black  speck  will  appear 


Fig.  454. — Dermatophilus  penetrans  : 
Female.      (Microphotograph.) 


DERM ATO PHI LUS  PENETRANS 


863 


on  the  pig's  abdomen,  and  quickly  another  and  another.  These 
black  specks  are  jiggers,  which  can  easily  be  transferred  to  a  test- 
tube.  On  examination,  they  will  be  found  to  be  males  and  females 
in  about  equal  numbers.  It  appears  likely  that  a  number  of  different 
species,  if  not  genera,  are  included  under  the  term  D.  penetrans, 
and  there  is  without  doubt  room  for  investigation  into  jiggers  taken 
from  wild  and  domestic  animals  and  man. 

If  the  reader  will  look  at  the  list  of  synonyms,  it  will  be  clear 
that,  by  the  law  of  priority,  the  name  of  this  little  insect  should 
be  Rhynchoprion  penetrans,  and  not  D.  penetrans,  as  the  name 
Rhync'ho prion  Oken  is  dated  1815;  but  Rothschild  has  recently 
pointed  out  that  Rhynchoprion  was  applied  in  1804  by  Hermann 
to  a  tick,  and  also  by  Oken  to  other  ticks  in  1815. 

Geographical  Distribution.— It  occurs  in  Mexico,  West  Indies, 
Central  and  Squth  America,  through 
the  whole  ot  tropical  Africa,  and  as 
far  south  as  Mashona — i.e.,  300  N. 
to  300  S.  In  Asia  it  does  not  appear 
to  flourish;  it  has  only  infected  Bom- 
bay,   and  will  probably  not  become 


Fxg. 


455. — Dermatophilus   penetrans  : 
Pregnant  Female. 


Fig.  456. — Dermatophilus  penetrans  . 

(After  Newstead,  Annals  of  Tropical 

Medicine  and  Parasitology.) 

a,     Larva;    b,    younger    larva; 

c,  empty  cuticles  of  eggs. 

naturalized,  as  the  monsoon  conditions  do  not  appear  good  for  it, 
lor  it  flourishes  in  a  warm,  dry,  sandy  soil. 

The  female  only  becomes  endoparasitic,  and  when  it  first  arrives 
in  a  place,  and  is  unknown,  may  cripple  people,  and  cause  loss  of  one 
or  more  toes. 

Morphology.— The  general  account  already  given  of  the  morpho- 
logy of  fleas  and  the  special  characters  indicate  the  morphology 
sufficiently  for  the  purposes  of  this  book. 

Life-History. — -The  males  and  females  live  in  dry,  sandy  soil  as 
reddish-brown  little  insects  about  1  millimetre  in  length,  and  are 
very  active.  They  live  by  sucking  the  blood  of  warm-blooded 
animals.  When  impregnated,  the  female  burrows  into  the  skin  of 
a  warm-blooded  animal,  whether  bird  or  mammal.  The  abdomen 
now  swells  enormously  into  the  size  and  appearance  of  a  small 
pea.  If  one  of  these  small  peas  is  examined,  it  will  be  seen  to 
show  the  head  and  thorax  anteriorly,  and  the  two  last  abdominal 


864 


SIPHONAPTERA  AND  COLEOPTERA 


segments  posteriorly.  The  head  is  in  the  bottom  of  the  burrow 
in  the  skin,  and  the  posterior  abdominal  segments  block  the  opening. 
The  eggs  are  expelled  through  the  opening  in  the  skin,  after  which 
the  female  jigger  is  expelled  by  ulceration.  The  egg  develops  into 
a  larva  with  thirteen  segments.  This  larva  spins  a  cocoon,  inside 
which  is  the  pupa,  which  gives  rise  to  the  imago  in  about  eight  to 
ten  da  vs. 

Pathogenicity.— This  will  be  described  later  (Chapter  XC  VI.),  but 
it  may  be  mentioned  that  it  includes  irritation,   pus  formation, 

ulceration,  and  forma- 
tion of  a  sore,  which 
/-^Jpc:^-^- —  | — -  ~~^\~r-^       may  become  infected 

^^^^4r^Pt-yT '  I  o'/   "^^-5  wit^     bacteria-     and 

cause  loss  of  a  toe  or 

a  leg,  or  even  tetanus 

may  develop. 

Family  Pulicim: 
Stephens,  1829. 

Siphonaptera  with 
body  compressed  or 
elongated,  always 
larger  than  in  the 
preceding  family. 
Head,  in  comparison 
to  the  rest  of  the 
body,  small;  top 
round ;  venter  pro- 
tected with  hairs; 
often  no  eyes.  The  antennal  groove  is  at  times  covered  by  a  chitinous 
plate.  The  end  segment  of  the  antenna  is  either  segmented  or  un- 
segmented.  Thorax  wide;  pronotum  often  with  ctenidia.  Abdo- 
men never  so  swollen  that  the  original  form  is  lost.  Female  never 
endoparasitic. 

There  are  three  subfamilies:  Pulicince  Tiraboschi,  Typlopsyllince 
Tiraboschi,  Hystrichopsyllince  Tiraboschi. 


Fig.  457. — Ctenocephalns  felis  Bouche. 

This  drawing  shows  the  combs  on  the  head  and 
prothorax. 


Subfamily  Pulicince. 
Pulicidce  with  eyes. 

The  more  important  genera  of  the  Pulicina?  may  be  arranged  as 
follows  (modified  after  Jordan  and  Rothschild)  :— 

A.  Ctenidia  on  prothorax  and  head — Ctenocephalus. 

B    Ctenidia  on  prothorax,  and  only  two  teeth  on  cheek  at  genal  angle — 

Chiasiopsylla . 
C.  Ctenidia  on  prothorax  only. 

I.  Pygidium  freely  projecting  behind — -Pygiopsylla. 
II.   Pygidium  not  freely  projecting  behind. 

(1)  Club  of  antenna  completely  segmented — Ceratophyllus. 

(2)  Club  of  antenna  incompletely  segmented — Hoptopsyllus. 


PULICINM  865 

D.  Ctenidia  absent  on  prothorax  and  head. 

I.  Terminal   segment   of   antennae   short,    only   distinctly   segmented 
posteriorly.     Hind  coxa    with  a  comb;   fifth  tarsal  segment 
with  four  lateral  and  one  subapical  bristle, 
(i)   Forms  with  small  mesial  tubercle — Mccopsylla. 
(2)   Forms  without  small  mesial  tubercle: — 

(a)  Mesosternite  with  internal  rod-like  incrassation  from  inser- 

tion of  the  coxa  upward. 

(a)  Anterior  angle  of  genal  edge  prolonged  backwards  into 

a  triangular  lobe ;  pronotum  stronger  than  metanotum 
— Pariodontis. 

(b)  Anterior   angle  of   genal  edge   not   produced  into   tri- 

angular lobe — Xenopsylla. 

(b)  Mesosternite    without    internal   rod-like   incrassation   from 

insertion  of  the  coxa  upward — Pulex. 
II.  Terminal  segment  of  antennae  segmented  all  round;  hind  coxa  with- 
out a  comb;  fifth  tarsal  segment  with  four  lateral  bristles  and 
one  subapical  hair. 

(1)  Terminal  segment  of  antennae  symmetrical;  genal  process  with 

a  number  of  bristles — Parapsylhis. 

(2)  Terminal  segment  of  antennae  asymmetrical;  proximal  segments 

sloping    backwards.     Genal    process    with   only   one   to    two 

bristles- — Phopalopsylla. 
III.  Terminal  segment  of  antennae  segmented  all  round;  symmetrical. 
Hind   coxa   without   comb.   Fifth  tarsal   segment   with  five 
lateral  bristles  at  least,  and  subapical  hair. 

(1)  Antenna!  groove  open  behind. 

(a)  Abdominal  tergites  with  one  row  of  bristles,  except  first, 
which  bears  two.  First  hind  tarsal  segment  shorter  than 
second — Coptopsylla. 

(I))  Abdominal  sternites  with  very  numerous  short  bristles. 
First  mid-tarsal  segment  longer  than  second- — Goniopsyllus , 

(2)  Antennal  groove  closed  behind. 

Abdominal  tergites  with  one  row  of  bristles — Lycopsylla. 

Subfamily  Typhlopsyllusle. 

Pulicidfe  with  eyes  absent  or  very  rudimentary.  Head  rounded 
in  front.     Body  thin. 

Genera. — Ctenopsylla  Kolenati;  Ctenophthalmas  Kolenati,  1857; 
TyphlopsyUa  Wagner;  Neopsylla  Wagner-;  Typhloceras  Wagner. 
Ctenophthalmus  can  be  recognized  by  having  movable  ctenidia 
in  front  of  the  ocelli,  and  the  rest  can  be  differentiated  as  follows : — 

I.  Third  tarsal  with  five  lateral  bristles  on  each  side — Typhloceras. 

II.  Third  tarsal  with  four  lateral  and  two  accessory  bristles — Ctenopsylla. 

III.  Third  tarsal  with  four  lateral  and  no  accessory  bristles — Neopsylla. 

I V .  Third  tarsal  with  three  lateral  and  two  accessory  bristles — TyphlopsyUa. 

Subfamily  Hystrichopsyllin^. 

Abdominal  tergites  with  one  or  more  ctenidia;  posterior  tibial 
spines  in  numerous  short,  close-set,  transverse  rows  on  posterior 
border,  with  about  four  spines  in  each  row;  female  with  four 
antepygidial  bristles  on  each  side. 

Genera.-- Hystrichopsyttct  Taschenberg,  Mctcropsylla. 

THE  FLEAS  OF  RATS  AND  MICE. 
The  following  table  gives  the  fleas  observed  on  rats,  mice,  and 
field-mice,  by  Tiraboschi  and  Rothschild. 

55 


866 


SIPHONAPTERA   AND  COLEPTERA 


'Pulicinae 


Puiicidae  < 


Typhlopsy  Hi  nae 


Pulex.  . 
Xenopsylla     .  . 
Hoplopsyllus  . 
Ctenocephalus 


P.  irritans  L. 

f  X.  cheopis  Roth. 
\X.  brasiliensis  Baker. 

H.  anomalus  Baker. 


^  Hystrichopsyllinae 


Sarcopsyllinae 


Ceratophyllus 


Odontopsyllus 
v  Pygiopsylla.     . 


Ctenopsylla     .  . 

Stephanocircus 
Ctenophthalmus 

Typhlopsylla   .  . 
Chiastopsylla  .  . 

Neopsylla 

Typhloceras    .  . 

Hystrichopsylla 

Macropsylla     . . 
|  1  >ermatophilus 


fCt. 
\Ct. 

Cer. 
Cer. 
Cer. 
Cer. 
Cer. 
Cer. 
Cer. 
Cer, 
Cer. 
Cer, 
Cer. 
Cer. 
I,  Cer. 

rod. 

\.Od. 

I  p. 
(p. 

,'Ct 

ct 


felis  Bouche. 
canis  Duges. 

fasciatus  Bosc. 
londiniensis  Roth, 
anisus  Roth, 
niger  Fox. 
penicilliger  Grube. 
walked  Roth, 
pinnatus  Wag. 
gallinse  Sch. 
abantis  Roth, 
lucifer  Roth, 
pollionis  Roth, 
agilis  Roth, 
calif ornicus  Baker. 

charlottensis  Baker, 
telegoni  Roth. 

colossus  Roth, 
hilli  Roth, 
rainbowi  Roth. 


u 


Echidnophaga 


musculi  Duges. 

spectabilis  Roth. 
Ct.  taschenbergi  Wag. 
Ct.  aganifhes  Roth. 
Ct.  ellobius  Roth. 
Ct.  pectuniceps  Wag. 
Ct.  selenis  Roth. 

i'St.  thomasi  Roth. 
4  St.  dasyuri  Skuse. 
(St.  simpsoni  Roth. 

(Ct.  aegyrtes  Heller. 
\Ct.  assimilis  Tasch. 

/Typhi,  pseudogyrtes  Baker. 
^Typhl.  prosuma  Wag. 
Ch.  rossii  Waterst. 

(N.  bidentatiformis  Wag. 
N.  pentacanthus  Roth. 
N.  isacanthus  Roth. 

Typhi,  poppei  Wag. 

(Hystr.  tripectinata  Tirab. 
Hystr.  talpae  Curtis. 
Hystr.  narbeli  Galli-V. 

Macr.  hercules  Roth. 

(D.  penetrans  L. 
\D.  ca3cata  Enderlein. 

/"Ech.  murina  Tirab. 
J  Ech.  gallinacea  Westw. 
j  Ech.  myrinecobis  Roth. 
\.Ech.  lispus  Roth. 


EPIMYS  RATTUS  867 

Epimys  norvegicus  Erxleben,  1777. 

Pulex  irritans  Linnaeus,  Xenopsylla  cheopis  Rothschild,  Cteno- 
cephahis  felis  Bouche,  C.  canis  Curtis,  Ceratophyllus  fascial  us  Bosc, 
C.  londiniensis  Rothschild,  C.  penicilliger  Grube,  Ctenocephalus 
musculi  Duges,  Neopsylla  bidentaliformis  Wagner. 

Epimvs  norvegicus  is  the  true  host  of  Ceratophyllus  fasciatus. 

Mus  musculus  Linnaeus,  1758. 
Ceratophyllus  fasciatus  Bosc,  C.  londiniensis  Rothschild,  C.  walkeri 
Rothschild,  Odontopsyllus  charlottensis  Baker  (?),  Ctenocephalus 
serraticeps  Taschenberg,  C.  musculi  Duges,  Typhlopsylla  assimilis 
Taschenberg,  T.  agyrtes  Heller,  Hystrichobsylla  tripectinata  Tira-- 
boschi. 

Epimys  rattus  Linnaeus,  1758. 

Pulex  irritans  Linnaeus,  Xenopsylla  cheopis  Rothschild,  Cteno- 
cephalus felis  Bouche,  C.  canis  Curtis,  Ceratophyllus  fasciatus  Bosc, 
C.  londiniensis  Rothschild,  Ctenopsylla  musculi  Duges.  Dermato- 
philus  ccecata  Enderlein,  Echidnophaga  rhynchopsylla  Tiraboschi, 
E.  gallinacea  West  wood. 

Of  all  these  fleas,  the  most  important  with  regard  to  plague  are  :— 

A.  Spreading  the  disease  from  rat  to  rat — -Xenopsylla  cheopis 
Rothschild  and  its  allies;  Ceratophyllus  fasciatus  Bosc  and  its 
allies;  Ctenopsylla  musculi  Duges;  Ctenocephalus  felis  Bouche; 
C.  canis  Curtis. 

B.  Spreading  the  disease  from  rat  to  man — Pulex  irritans 
Linnaeus,  Xenopsylla  cheopis  Rothschild,  Ctenocephalus  felis  Bouche, 
C.  canis  Curtis,  Ceratophyllus  fasciatus  Bosc. 

Of  all  these,  the  most  important  is  Xenopsylla  cheopis  Roths- 
child and  it  is  believed  that  its  true  host  is  Epimys  rattus. 

Citellus  beecheyi  Richardson. 

This  is  the  ground  squirrel  of  California,  which  has  been  proved 
to  play  an  important  part  in  the  plague  infection  of  that  country, 
and  its  fleas  have  been  recently  studied,  and  it  has  been  found  that 
Hoplopsyllus  anomaius  Baker  is  capable  of  carrying  the  bacillus, 
and  according  to  McCoy  Ceratophyllus  acutus  Baker  can  also  convey 
the  disease  from  squirrel  to  squirrel. 

Arctomys  bobae  Schreb. 
This  is  the  tarbagan,  and  its  common  flea  is  Ceratophyllus  silvan 
tieri  Wagner,  1898. 

Pulex;  Linnaeus,  175S. 

Pulicince  with  head  without  notch  on  the  frons ;  antennal  groove 
closed  behind  by  a  genal  process.  Strong  incrassation  separating 
occiput  and  frons.  Eye  large,  a  little  pointed  below,  with  two 
bristles  beneath  it,  and  one  on  the  oral  edge.  Anterior  angle  of 
genal  process  projecting  somewhat  downwards,  and  usually  bearing 


868 


SIPHONAPTERA   AND  COLEOPTERA 


-a  small  tooth  (remains  of  a  comb).  Anal  coxa  is  pear-shaped, 
carrying  a  number  of  hairs  on  the  inner  posterior  portion,  as  well 
as  in  front,  and  carrying  a  row  or  patch  of  short  spines  near  apex. 
Greatly  reduced  thorax,  the  tergites  being  short,  each  with  a  row 
of  bristles,  but  without  subapical  spines  on  the  mesonotum. 
Mesosternite  characteristic,  very  narrow,  with  ventral  edge  close 
before  apex,  stigmata  not  being  entirely  covered.  No  internal  rod- 
like or  cariniform  incrassation  from  the  insertion  of  the  coxa  to 
the  dorsal  edge. 

Male  with  eighth  tergite  with  small  manubrium;  clasper  with 
very  large  flap,  on  inside  of  which  are  two  processes,  forming  a  kind 
of  claw.  Manubrium  of  clasper  large,  curved.  Ninth  stemite 
boomerang-shaped,  with  its  upper  end  pointed.  Internal  wire 
like  spring  of  ninth  sternite  and  penis  making  several  coils. 

Female.— No  hairs  above  stigma  of  eighth  stergite.  Stylet  with 
long  apical  bristle  and  short  bristle  near  apex.  Anal  sternite 
truncate;  bristles  confined  to  the  apical  edge. 

Species:  P.  irritans  Linnaeus. 

Pulex  irritans  Linnaeus,  1758. 

Synonyms,  —Pulex  vulgaris  Raius,  iyio:P.  ater  Linnaeus,  1746; 
P.  hominis  Duges,  1832;  P.  simulans  Baker,  1895:  P.  dugesi 
Baker,  1904. 

This,  in  a  much  restricted  sense,  is  the  P.  irriians  of  Linnaeus, 
which  included  all  fleas,  but  now  the  term  is  restricted  to  the 
parasite  of  man.  It  is  essentially  an  Old-World  flea,  those  of 
America   being   but    distantly   connected,   but    has  become   now 


Fig.  458. — Pulex  irritans  :  Male.         Fig.  459. — Pulex  irritans:  Female. 

cosmopolitan  through  trade.  It  appears  to  have  been  introduced 
into  the  eastern  tropics  by  European  trade.  It  is  absent  from 
the  Sahara  and  the  Haussa  countries  south  of  it,  but  it  abounds  all 
through  Africa  where  there  are  European  settlements. 

The  question  whether  there  are  different  varieties  on  the  different 
races  of  mankind  is  not  settled.     Baker  described  a  Pulex  dugesi 


XENOPSYLLA  869 

or  P.  irritans  dugesi  from  West  Mexico  on  Citellus  macrourus  and 
man,  but  is  the  only  person  who  indicates  this. 

P.  irritans  is  also  found  on  animals,  particularly  the  badger 
(Meles  taxus)  in  England;  on  dogs,  cats,  rats,  and  other  animals  in 
various  parts  of  the  world. 

Xenopsylla  Glinkkewicz,  1907. 

Synonym. — Lamopsylla  Jordan  and  Rothschild,  1908. 

PulicincB  with  third  segment  of  antennae  distinctly  segmented 
only  on  posterior  side.  Eye  round;  one  bristle  below,  one  in  front 
of  eye,  third  at  oral  edge.  Frons  without  tubercle;  four-segmented 
labial  palpus;  closed  antennal  groove.  Pleura  of  the  mesosternitc 
divided  by  a  suture  into  an  episternite  and  an  epimerite,  with  the 
dorsal  apical  bristle  of  the  seventh  abdominal  tergite  remote  from 
the  edge  of  the  segment,  with  short  spines  on  the  inner  surface  of 
che  coxa  of  the  third  leg,  with  a  rod-like  incrassation  on  the  inside 
of  the  coxa  of  the  second  leg;  fifth  tarsal  segment  with  four  lateral 
bristles  besides  the  subapical  hair. 

Male  with  clasper  provided  with  two  or  three  small  processes; 
manubrium  narrow;  upper  internal  portion  of  the  ninth  sternite 
not  very  sharply  defined. 

Female  with  the  stylet  bearing,  besides  the  long  apical  bristle, 
a  short  bristle  situated  in  a  notch  before  apex. 

Type.— Xenopsylla  cheopis  Rothschild.  This  genus  is  found  in 
Africa  and  Central  Asia  in  particular. 

At  the  time  of  writing  there  are  some  twenty-four  species  known. 

Xenopsylla  cheopis  Rothschild,  1903. 

Synonyms. — Lcemopsylla  cheopis  Rothschild,  1903;  Pu i 'ex  cheopis 
Rothschild,  1903;  P.  brasiliensis  Baker,  1904;  P.  murinits  Tira- 
boschi,  1904;  P.  ph.il ippinensis  Herzog,  1904. 

This  is  the  rat -flea  in  all  parts  of  the  tropics,  and  is  believed  to 
be  the  principal  transmitter  of  bubonic  plague  from  the  rat  to  man. 
Its  home  is  believed  to  be  the  Nile  Valley,  where  it  lives  on  various 
hosts,  but  it  has  spread  from  there  by  the  agency  of  the  rats. 

It  is  often  referred  to  in  literature  by  the  name  P.  pallidas 
Taschenberg,  which  is  really  a  different  species. 

Jordan  and  Rothschild  report  it  on  man  or  animals  from  the 
Egyptian  Sudan.,  Pretoria,  Beira  in  East  Africa,  Entebbe,  Uganda, 
Benguella,  Angola,  Reunion.  Marseilles,  Plymouth,  Aden,  Bombay, 
Agra,  Arabia,  Japan,  West  Australia,  New  South  Wales,  Colombia, 
Paraguay. 

They  have  found  it  on  man,  Epimys  norvegicus,  E.  rattus,  Mas 
chrysophilus,  and  several  other  animals. 

Morphology. — Episternum  of  metathorax  separated  from  ster- 
num. The  latter  carries  a  bristle  as  long  as  that  on  the  former. 
Hind  femur  angulate  ventrally  at  the  widest  part.  Fifth  segment 
of  fore-  and  mid-tarsi,  with  three  spine-like  bristles,  ventrally  at 
apex:  lateral  ones  very  stout  in  male.  Clasper  with  two  distinct 
free  processes;  manubrium  long.     Penis  without  a  brush  near  apex. 


87°  SIPHONAPTERA    AND  COLEOPTERA 

Life-History. — The  eggs  are  round,  waxy-white  or  pearly  in 
colour,  and  number  one  to  five  at  each  oviposition.  They  hatch 
in  Bombay  in  two  days,  and  produce  the  little  larvae,  which  at  once 
hide  themselves  away  from  the  light.  In  about  a  week's  time  these 
larvae,  which  at  first  are  very  active,  become  sluggish,  and,  ceasing 
to  eat,  spin  cocoons  composed  of  fine  white  silk-like  fibres.  The 
cocoon  becomes  covered  with  rubbish,  and  is  hard  to  see.  In  about 
seven  to  fourteen  days  the  imago  escapes  from  the  cocoon.  The 
total  development,  therefore,  requires  about  twenty-one  to  twentv- 
two  days. 

Bionomics. — The  young  flea  is  capable  of  living  without  a  feed 
of  blood  for  some  seven  to  fourteen  days,  but  if  not  fed  then  it  dies. 
The  length  of  life  of  a  flea  is  difficult  to  ascertain,  but  Xenopsylla 
cheopis  will  live  forty-one  days  on  a  rat  and  twenty-seven  days  on  a 
man.  Therefore,  the  whole  life  of  a  rat -flea  from  birth  to  death  is 
about  sixty-three  days.  A  rat-flea  is  more  readily  attracted  by  a 
rat  than  by  a  man.  It  breeds  at  all  temperatures,  but  has  one 
optimum  temperature  above  and  below  which  it  does  not  thrive 
so  well.  Dampness  is  injurious  to  the  flea,  killing  the  larvae  and 
hindering  development. 

X.  cheopis  is  the  commonest  rat -flea,  being  probably  the  flea  of 
Epimys  norvegicas  in  India,  while  in  Western  Europe  CeratopJiylh  s 
Jasciatus  is  the  flea  of  the  same  rodent.  It  is  found  on  E.  norvegicus, 
E.  r.attus,  and  Nesokia  bengaliensis  ;  also  on  musk-rats,  guinea- 
pigs,  cats,  rabbits,  antelopes,  kangaroos,  and  men. 

The  infection  with  plague  bacilli  does  not  appear  to  affect  the 
flea  s  health,  for  it  has  an  immunity  dependent,  apparently,  on 
phagocytosis. 

Hoplopsyllus  Baker. 
Closely  related  toPulex,  but  distinguished  at  once  by  the  ctenidia 
on  the  prothorax.   Hoplopsvlliis  anomahts  Baker  is  the  plague  carrier 
of  the  Californian  ground  squirrel. 

Family  Ceratopsyllid^;  Baker,  1905. 

Siphonaptera  with  ctenidia  present  on  the  metathorax  and  abdomen ;  eyes 
rudimentary  or  absent. 

Genus.— Ceratopsvllns  Kolenati. 

The  species  of  this  genus  are  found  on  bats. 


Jffi 

i 

i     I 

P* 

t^r'S- 

*&.>* 

i^.«Vk-/^ 

V-  '  ^    v. 

lria.  460. — Larva  of  a   Beetle  passed  per  Urethram. 
(Alter  King.) 


REFERENCES  871 

COLEOPTERA. 

Hexapoda  with  biting  mouth-parts.  Anterior  wings  altered  to  form  cases 
for  the  thin  posterior  wings. 

Remarks. — The  larvae  of  beetles  have  rarely  been  recorded  as  parasites  of 
the  alimentary  canal,  or  found  in  abscesses  in  man  in  the  temperate  and 
tropical  regions.     Silvanus  surinamensis  Linnaeus  bites  people  at  night. 

ORTHOPTERA. 

The  bite  of  Enyaliopsis  durandi  Lucet  causes  a  nasty  eruption 
(according  to  Wiggins,  1910,  in  man  in  Uganda),  with  high  fever 
and  general  illness,  and  finally  sloughing  at  the  site  of  the  bite. 

E.  petersi  Schaum,  the  nantundua  of  Nyassaland,  according  to 
Stannius,  ean  cause  ulceration  by  the  action  of  a  yellow  fluid  which 
it  emits. 

The  Phasmidce,  or  stick  insects,  are  said  to  eject  a  fluid  which 
may  cause  blindness  if  it  gets  on  to  the  conjunctiva. 


REFERENCES. 

Siphonaptera. 

Advisory  Committee  Reports  on  Plague  in  India  (1907-1908).  J.  Hygiene. 
Bacot     (1914).     Journal    of     Hygiene,     Plague    Supplement,     III.       (Flea 

Bionomics).     Cambridge. 
Baker,  C.  (1904).     Proc.  U.S.  Nat.  Mus.,  xxvii.;  xxix.,  1905. 
Baker,  C.  (1905).     Entomologica,  xx. 
Jordan  and  Rothschild  (1906).     Thompson  Yates  and  Johnston  Laboratory 

Reports,  vii.  1. 
Jordan  and  Rothschild  (1908).     J.  Parasitol.,  i.  1.     (Full  literature.) 
Kolenati  (1863).     Horae  Soc.  Entomol.  Rossicae,  ii. 
Rothschild  (1906).     Entomologist,  xxxix. 
Rothschild.     Journal  of  Hygiene,  vi.,  1906. 
Sharp.     Cambridge  Natural  History:  Insects,  II. 
Taschenberg  (1S80).     Die  Flohe. 

Tiraboschi  (1904).     Archiv.  de  Parasitologic,  viii.;  xi.,  1907. 
Tyrrel  (1884).     Trans.  Ottawa  Natural  Club.     (Anatomy.) 
Wagner  (1893).     Horae  Soc.  Entomol.  Rossicae,  xxvii.;  xxviii.,  1894;  xxix., 

1895;  xxxi.,  1898;  xxxv.,  1902;  xxxvi.,  1903. 

Coleoptera. 

Fantham,  Stephens  and  Theobald  (1916).     Parasites  of  Man.     Londom. 
Wellman  (1907).     Journal  of  Tropical  Medicine,  vol.  x.,  p.  185. 


CHAPTER  XXXV 
THE  ANIMAL  CARRIERS  OF    DISEASES 

Preliminary —  Historical  —  Protozoal  diseases  —  Helminthiasis  —  Myiasis — 
Bacterial  diseases — Diseases  of  unknown  causation — Chance  trans- 
mission— Imperfect  carriage  of  parasites — Terms — References. 

PRELIMINARY. 

The  present  chapter  is  an  attempt  to  put  in  concrete  form  the  role 
of  the  '  animal  carrier  '  of  disease. 

Animals  can  produce  traumatisms  by  their  bites,  and  can  cause 
disease  by  injecting  chemical  substances  manufactured  in  their 
bodies — e.g.,  American  and  Australian  tick  paralysis — but  these 
questions  do  not  now  concern  us.  The  problems  which  we  are 
about  to  consider  are  those  associated  with  the  spread  of  diseases 
known  or  suspected  to  be  parasitic.  Such  diseases  are  divisible  into 
those  caused  by  animal  and  those  caused  by  vegetal  parasites.  The 
latter  are  the  simpler,  as  their  carriage  does  not  involve  any  great 
morphological  changes  in  the  parasite,  such  as  often  accompanies  the 
carriage  of  an  animal  parasite,  which,  as  it  is  the  more  complex, 
we  will  consider  first. 

A  given  animal  parasite  apparently  has  some  form  of  sexual 
generation  in  some  stage  of  its  life-history,  and  it  is  probably  merely 
our  lack  of  knowledge  which  prevents  us  from  acknowledging 
this  as  a  proven  fact. 

The  host  in  which  the  sexual  generation  takes  place  is  called  the 
definitive  host,  and  is  probably  the  original  host,  in  which,  as  a  rule, 
the  parasite  does  not  produce  severe  forms  of  disease  and  may 
produce  no  ill  effects  at  all.  This  shows  that  it  and  its  host  have 
become  so  adjusted  that  it  does  not  overproduce  itself  in  the 
host,  which  on  its  part  does  not  poison  or  otherwise  attack  the 
parasite. 

It  is  certainly  not  the  object  of  the  parasite  to  kill  its  definitive 
host,  but  to  leave  it  by  some  route  which  causes  no  great  disturb- 
ance of  its  tissues  or  functions.  Hence  intestinal  parasites  leave 
by  means  of  the  faeces,  but  in  so  doing  they  areflung  into  new  dangers, 
and  therefore  require  protection  by  encystment.  These  cysts  may 
be  eaten  by  another  individual  of  the  same  species  as  the  original 
definitive  host,  and  the  cycle  may  begin  again;  but  the  dangers 
of  the  outer  world  may  be  guarded  against  by  eni  ering  some  animal's 
body  in  which  no  development  occurs.     Such  an  animal  would  be 

872 


THE  DEFINITIVE  HOST 


873 


a  protective  intermediary  host,  and  such  a  cycle  can  be  exemplified 
by  the  amoeba  of  dysentery  and  house-flies. 

This  extremely  simple  carriage  is  also  shown  by  animals  which 
convey  bacteria,  but  some  of  these  undergo  multiplication  in  the 
gut  of  the  intermediary  host — as,  for  example,  the  plague  bacillus — ■ 
and  may  even  have  their  virulence  raised— as,  for  example,  Eberth's 
bacillus.  Returning  again  to  the  animal  parasite,  this  may  grow 
and  multiply  in  this  second  host,  and  may  invade  its  tissues  and 
dwell  therein  for  a  length  of  time.  This  is  quite  different  from  the 
short  passage  of  an  amoebic  cyst  in  the  flies'  intestines.  The  second 
host  now  becomes  a  true  intermediate  host,  but  it  is  something 
relatively  new  interposed  in  the  life-cycle  of  the  parasite,  which 
has  not  yet  adjusted  itself  to  its  new  host,  nor  has  this  host  adjusted 
itself  to  the  parasite;  and  the  result  is  that  the  parasite  almost 
invariably  causes  disease  in  the  intermediate  host,  which  may  be  a 
vertebrate  or  an  invertebrate—^.: — 


The  Definitive  Host. 


Parasite. 

Definitive  Host.         Intermediate  Host.              n         ...  •* 

'                                                                            Parasitism. 

Filar  ia 
bancrofti. 

Man     but     little      Culex    and     Stego-      True  parasitism  of 
affected  patho-          myia  mosquitoes          the  vertebrate, 
logically.                      severely  affected   i 
by  infection. 

Plasmodium 
malaria. 

Anopheline  mos-  \  Man    suffers    from 
quitoes     unaf-        malarial  fever, 
fected     patho- 
logically. 

True  parasitism  of 
the  mosquito. 

It  is  therefore  obvious  that  these  two  diseases,  from  the  point 
of  view  of  evolution,  have  two  quite  different  origins.  The  first 
is  originally  a  parasite  of  man,  and,  as  Hindle  has  pointed  out, 
Manson's  original  idea  of  water  infection  may  be  the  true  method, 
and  that  ah  initio  the  '  Larvofilaria  '  lived  in  water  and  pierced  the 
human  skin,  as  it  does  to-day  on  leaving  the  mosquito,  and  requires, 
as  Bahr  has  shown,  dampness  in  order  to  live  while  it  pierces  the 
skin.  The  mosquito  carrier  is  therefore  a  relatively  new  acquisition, 
and  the  mosquito,  not  having  adjusted  itself  to  these  conditions, 
often  dies,  as  Bahr  has  shown.  On  the  other  hand,  Filar  ia  bancrofti, 
barring  accidents,  causes  no  symptoms  in  man,  but  if  there  are 
accidents  the  disease  ensues. 

It  is  quite  otherwise  with  the  malarial  parasites,  in  which  the 
anopheline  mosquito  is  the  definitive  host  and  man  the  intermediate 
host.  Here  the  mosquito  is  not  affected  pathologically,  but  man 
suffers  from  malarial  fever.  Here  the  malarial  parasite  must  have 
been  originally  a  sort  of  coccidioform  parasite  of  the  mid-gut  of 


874 


THE  ANIMAL  CARRIERS  OF  DISEASES 


the  mosquito,  and  may  have  spread  from  mosquito  to  mosquito 
by  hereditary  infection,  as  Schaudinn  suggested,  the  sporozoites — 
i.e.,  the  infective  agent — going  all  over  the  body,  and  so  entering 
the  salivary  glands,  and  subsequently,  when  the  evolution  of  warm- 
blood  animals  took  place,  becoming  blood  parasites,  at  first 
accidentally. 

The  passage  from  the  intermediate  host  to  the  definitive  host  we  call 
transmission. 

It  is  never  directly  inoculative,  like  infection,  but  it  may  be — 

i.  Ingestive,  via  the  alimentary  canal. 

2.  Penetrative,  via  the  unbroken  skin  and  mucous  membranes. 

In  the  first  it  is  the  arthropod  which  ingests  the  parasite;  in  the 
second  the  parasites  come  in  contact  with  the  unbroken  skin  or 
mucosa,  through  which  they  force  their  own  way,  and  so  enter 
the  body  of  the  intermediate  host,  which  is  usually  the  vertebrate 
in  this  case. 

Following  our  life-cycle,  we  come  to  the  passage  from  the  de- 
finitive to  the  intermediate  host,  and  this  may  be  called  '  infection,' 
because  it  is  so  often  followed  by  disease  in  the  intermediate  host. 
This  generally  takes  place  by  the  agency  of  the  product  of  the  sexual 
generation — i.e.,  some  descendant  of  the  zygote,  using  this  term  in 
the  widest  sense  to  mean  the  product  of  the  fusion  of  male  and  female 
elements. 

Infection  of  the  vertebrate  is  usually  inoculative,  and  may  be 
performed  in  two  ways: — 

(a)  The  Direct. — In  this  the  blood-sucker  simply  transmits  the 
parasite  unchanged  after  holding  it  for  a  short  time. 

(b)  The  Indirect. — In  this  the  parasite  undergoes  development 
in  the  blood-sucker. 

Infection  and  Transmission. 


n         ..             Definitive 
Parasite.              w     . 
Host. 

Infection . 

1 

Intermediate       ^            ■     ■ 
TT     .               Transmission. 
Host. 

Plasmodium 
malaricB. 

Anopheline 
mosquitoes. 

Sporozoites 
from  zygote. 

Inoculative. 

Man.                Micro-  and 
macro-game- 
tocytes. 

Ingestive. 

Filaria               Man. 
bancrofti. 

Microfilaria 
from  egg. 

Ingestive. 

Culicine  mos-       Larvofilaria?. 
quitoes.                       — 

Penetrative. 

The  direct  is  unusual,  as  a  blood-sucker  as  a  rule  takes  a  full 
meal  from  one  individual,  and  does  not  feed  again  for  a  day  or  so, 
but  it  may  take  place — as  Edmond  and  Ktienne  Sergent  have  shown 
to  be  the  case  of  the  tabanid  flies,  which  bite  camels  in  North  Africa, 


INFECTION  AND  TRANSMISSION  875 

and  which  spread  the  trypanosome  disease,  '  el  debab  ' — by  this 
method,  because  they  acquire  a  full  meal  from  several  individuals, 
and  because  the  camels  resent  their  attentions. 

Infection  may  also  be  contaminative.  In  this  method  the  parasite, 
escaping  with  the  carrier's  fasces,  enters  the  new  host  via  wounds, 
either  pre-existing  or  caused  by  the  carrier  itself. 

In  the  case  of  the  Arthropoda  infection  is  generally  ingestive,  as 
it  sucks  the  blood  of  the  vertebrate  and  so  obtains  the  blood  parasite. 

Finally,  just  as  the  fly  is  an  intermediary  or  temporary  host  for  the 
amoeba  of  dysentery,  so  blood-sucking  flies  may  take  up  some 
blood-containing  parasites  and  immediately  pass  them  on  to  a 
healthy  animal  in  a  second  feed;  but  while  biting  through  the  skin 
they  inject  this  second  animal  with  the  parasite,  and  infection 
results. 

We  will  now  assume  that  the  definitive  and  intermediate  hosts 
have  been  living  together  for  long  periods  undisturbed,  and  that 
they  have  adjusted  themselves  to  the  parasite  and  the  parasites 
to  them.  Under  circumstances  such  as  these  there  will  be  little  or 
no  sign  of  disease  in  the  intermediate  host,  which  has  now  become 
a  '  reservoir  '  for  the  parasite. 

Assuming  that  the  definitive  host  is  a  blood-sucking  arthropod, 
and  that  man  enters  such  an  area  as  a  new-comer,  and  is  bitten  by 
the  blood-sucker,  then  several  things  may  happen  to  the  parasite. 

A.  It  may  be  killed  off  and  no  infection  follow. 

B.  It  may  find  in  man  a  suitable  intermediate  host,  and  cause— 

(1)  Acute  epidemic  disease. 

(2)  Chronic  endemic  disease. 

(3)  No  disease,  only  infection. 

The  second  is  obviously  better  for  the  parasite  than  the  first, 
and  the  third  than  the  second. 

Therefore,  in  studying  the  carriage  of  an  animal  parasite  of  man 
by  some  other  animal,  we  must  know — 

1.  The  parasite. 

2.  The  definitive  hosts: — 

(a)  Reservoirs. 

(b)  Non-reservoirs. 

3.  The  method  of  infection. 

4.  The  intermediate  hosts: — 

(a)  Reservoirs. 

(b)  Non-reservoirs. 

5.  The  method  of  transmission. 

But  there  is  another  question  which  it  is  necessary  to  consider 
when  man  is  the  definitive  host.  This  question  is  whether  the  inter- 
mediate host  is  new,  and  if  so,  whether  any  trace  of  the  old  original 
life-cycle  still  persists.  It  should  be  remembered  that  man  evolved 
later  than  blood-sucking  insects,  as  evidenced  by  tsetse-flies  found 
in  geological  formations  in  America— so  Sambun  informs  the  writers. 


8 ;6  THE  ANIMAL  CARRIERS  OF  DISEASES 

Therefore,  in  order  that  man  may  be  the  definitive  host  and  the 
blood-sucker  a  pathologically  affected  intermediate  host  means  a 
comparatively  recent  evolutionary  change.  Therefore  an  old 
original  life-cycle  may  still  be  discoverable,  if  sought  for,  and 
may  be  of  value  in  prophylaxis,  which  is  the  end  and  aim  of  ihe 
study  of  the  animal  carrier. 

With  these  preliminary  remarks  we  may  now  turn  to  the  history 
of  the  subject. 

Historical. — The  history  of  the  animal  carrier  of  disease  may  be  divided  into 
three  periods  by  the  dates  1878  and  1898 — i.e.,  by  Hanson's  and  by  Ross's 
discoveries — and  these  periods  will  be : — 

I.  Early  views. 
II.  Manson's  period. 
III.  Ross's  period. 

I.  Early  Views. — This  period  is  characterized  by  gropings  in  search  of 
truth,  mainly  by  suggestions  and  by  theories,  but  also  by  the  first  experi- 
ments with  bacteria. 

In  1577  Mercurialis  suggested  that  plague  might  be  spread  by  house-flies, 
and  in  1666  Sydenham  opined  that  the  autumnal  diseases  of  England  were 
due  to  the  flies  of  summer.  In  1769  Bancroft  advanced  the  theory  that 
Frambcesia  tropica  was  a  fly-borne  disease,  and  in  1808  Crawford  believed 
insects  to  be  carriers  of  infection.  In  1848  Nott  of  Alabama  brought  forward 
reasons  to  support  the  insect  origin  of  yellow  J ever.  In  1853  -\I00re  referred 
to  flies  as  possible  carriers  of  cholera,  typhoid,  tuberculosis,  anthrax,  and  leprosy, 
to  the  last  named  of  which  Linnaeus  had  already  invited  attention,  while 
Raimbert  in  1869  performed  the  first  actual  experiments  to  try  to  prove  that 
flies  carried  anthrax. 

In  1853  Beauperthuy  argued  that  mosquitoes  spread  yellow  fever. 

II.  Manson's  Period. — This  opens  with  the  publication  of  Manson's  epoch- 
making  discoveries  of  the  carriage  of  Filaria  bancrofti  by  mosquitoes,  and  it 
must  never  be  forgotten  that  he  grasped  at  once  that  this  was  a  new  infection 
of  the  mosquito,  and  that  water  was  the  original  method;  and  thus  he  dis- 
covered two  great  truths,  of  which  so  far  only  one  has  been  properly  appreci- 
ated, because  the  insect-carriage  laid  the  foundation  of  Ross's  great  work. 

In  1 881  Findlay  definitely  accused  mosquitoes  as  being  the  transmitters  of 
yellow  fever,  and  conducted  experiments  in  which  he  is  considered  to  have 
been  successful  in  transmitting  the  disease  experimentally  by  their  bites. 

In  1883  King  formulated  the  theory  that  malaria  was  spread  by  mosquitoes, 
and  in  the  same  year  Thomas  demonstrated  the  carriage  of  Fasciola  hepatica 
by  snails,  while  Grassi  and  Stiles  showed  that  parasitic  worms  were  carried 
by  arthropods. 

In  1895  Bruce  discovered  that  Trypanosoma  brucei  was  spread  by  a  tsetse- 
fly,  a  fact  which  led  eventually  to  clearing  up  of  the  carriers  of  trypanosome 
diseases. 

During  the  closing  years  of  this  period  Ross  in  India  was  hard  at  work 
dissecting  mosquitoes  in  the  face  of  much  difficulty,  thus  opening  the  way  for 
the  last  period  of  our  history. 

III.  Ross's  Period. — Just  twenty  years  ago  (1898)  the  new  stage  of  research 
into  the  animal  carrier  in  disease  was  opened  by  Ross's  most  important, 
careful,  and  laborious  work  into  the  causation  of  malaria,  and  the  carriage 
of  its  parasites  by  the  anopheline  mosquitoes. 

This  discovery  was  followed  in  1899  by  the  classical  paper  by  Nuttall,  on 
'  Insects  as  Carriers  of  Disease,'  while  in  1900  Reed,  Carroll,  and  Agramontc 
showed  that  Stegomyia  (cedes)  calopus  was  the  carrier  of  yellow  fever. 

The  resv  of  this  period  has  been  referred  to  in  the  opening  chapter  of  this 
book,  and  need  not  be  recapitulated,  and  we  will  now  pass  on  to  study  the 
results  of  this  work,  by  considering  the  parasites  in  the  zoological  order 
followed  in  the  preceding  chapters. 


PROTOZOAL  DISEASES 


877 


A.  PROTOZOAL  DISEASES. 

Amoebic  Dysentery. — We  have  already  seen  that  amoebiasis  in 
man  is  principally  caused  by  Loeschia  histolytica,  which,  escaping 
as  cysts  in  the  faeces,  is  taken  up  by  house-flies — that  is  to  say,  flies 
belonging  to  the  genera  Mitsca,  Fannia,  Calliphora,  etc. 

The  cysts  do  not  undergo  development  in  the  fly,  which  serves 
merely  as  a  carrier  and  protector  for  them,  which,  escaping  with 
the  flies'  faeces  on  to  human  food,  afford  a  means  of  infection. 

This  carriage  is  interesting,  indicating  that  the  environment  of 
the  alimentary  canal  of  the  fly  is  not  suitable  for  the  development 
of  this  amoeba,  though  it  is  known  that  there  are  amoebae  passing 
their  whole  life-cycle  in  insects — e.g.,  Endamceba  Uattce. 

With  regard  ot  L.  histolytica,  it  is  believed  that  the  sexual  life- 
cycle  occurs  in  man,  but  it  is  not  definitely  known  whether  gametes 
are  formed  in  the  human  intestine,  or  whether  autogamy  takes  place 
in  the  cyst,  which  is  improbable,  but  in  either  case  the  life-cycle 
does  not  require  more  than  one  host,  and  infection  can  take  place 
by  direct  contamination  of  the  food,  without  passing  through 
the  fly. 

Animals  can  be  infected  with  amoebic  dysentery,  but  there  is  no 
evidence  at  present  of  any  animal,  other  than  man,  acting  as  a 
reservoir,  but  tins  does  occur  in  human  carriers. 

To  demonstrate  what  we  mean  we  give  the  following  table: — 

Amcep.ic  Dysentery. 


Parasite. 


Defini- 

Host. 


Reser- 
voir. 


Trans- 
mission. 


Loeschia 

Man  in 

histoly- 

carrier 

tica. 

stage. 

Cysts. 


Man  in 
>  airier 
stage.     Ingestive. 


Inter- 
mediary 

Host. 


Flies. 


Tnft  ction. 


Intermediate 

Host. 


Cysts        in- Man  in  acute 
gestedfrom      and  chronic 
contami-      infections, 
nated   food 
or  drink. 


Flagellate  Diarrhoea  and  Dysentery. — Whatever  may  be  the  views 
of  zoologists,  medical  men  have  little  doubt  that  some  of  the  flagel- 
lates, such  as  Giardia  intestinalis ,  produce  diarrhoea;  and  Wenyon 
and  O'Connor  have  shown  that  their  cysts  have  been  found  in  flies, 
and  thai  in  g<  anal  the  process  of  infection  is  much  the  same  as  in 
man,  but  the  reservoir  is  different.  There  is  little  doubt  in  our 
minds  that  man  is  more  or  less  accidentally  infected  with  many  of 
these  parasites,  and  certainly  with  Giardia  intestinalis,  which 
appears  to  us  to  be  a  true  parasite  of  the  rat. 

If  there  is  a  sexual  cycle,  it  takes  place  either  in  the  cyst  or  in 
the  vertebrate. 


878  THE  ANIMAL  CARRIERS  OF  DISEASES 

Flagellate  Diarrhcea  and  Dysentery. 


Parasites. 


Definitive     j  Reser- 
Host.         '   voir. 


Inter-  Inter- 

mediary      Infection.       mediate 
Host.  Host. 


Giardia 
intestinalis 
and  others. 


Man  in 
chronic  cases 

and  as 

carriers,  and 

rats. 


Rats.      Cysts 
ingested. 


Flies. 


Cysts  in-      j  Man  in 
gested  with  \    acute 
contaminated;    cases, 
food  or 
drink. 


Sleeping  Sickness.— We  have  already  indicated  that  we  think 
that  there  are  several  forms  of  this  disease — viz.,  that  caused  by — 
i.  Trypanosoma  gambiense. — Synonym:  T.  nigeriense. 

2.  Trypanosoma  castellanii. — Synonyms:  T.  ugandense,  T.  gam- 
biense pro  parte. 

3.  Trypanosoma  rhodesiensc. 

4.  Other  Forms  of  Trypanosomes. — (a)  Some  type  of  T.  brucei 
in  the  laboratory  infection  of  Professor  Lanfranchi;  {b)  some  type 
of  T.  vivax  found  by  Macfie. 


Fig.  461.  —  Glossina    palpalis   Robineau-Desvoidy,    1830:    The    Carrier 
of  the  Trypanosome  of  the  Castellani  Type  of  Sleeping  Sickness. 

(From  a  photograph  by  J.J-  Bell.) 

The  carrier  of  the  first  (T.  gambiense)  has  never  been  properlv 
studied.  Possibly  it  is  not  Glossina  palpalis,  and  as  nothing  can 
be  said  definitely,  we  will  not  pursue  this  subject  further,  except 
to  say  that  Yorke  and  Blacklock  consider  man  to  be  the  principal 
reservoir,  with  domestic  cattle  as  a  secondary  reservoir. 

With  regard  to  T.  castellanii,  we  have  noted  that  Miss  Robertson's 
researches  have  shown  that  it  never  multiplied  in  the  vertebrate 
in  cells  of  the  liver,  spleen,  or  lungs,  and  that  there  was  no  schizo- 


SLEEPING  SICKNESS 


879 


gony,  and  that  division  was  simple  and  longitudinal,  taking  place 
always  in  the  circulating  blood  and  producing  transmission  forms, 
which  are  her  short  blood  forms. 

These  forms  can  be  ingested  by  Glossina  palpalis  (but  one  has  to 
be  sure  that  it  is  really  palpalis,  as  flies  apparently  of  this  species 
have  been  found  by  King,  using  Newstead's  more  accurate  methods 
of  classification,  not  to  be  this  species),  first  establishing  themselves 
in  the  posterior  part  of  the  mid-gut  and  then  multiplying  and  form- 
ing many  types  therein,  but  moving  on  the  tenth  to  twelfth  day  to 
the  proventriculus  in  the  form  of  long,  slender,  non-infective  trypano- 
somes,  from  which  they  find  their  way  via  the  hypopharynx  to  the 
salivary  glands  after  the  sixteenth  day.  In  these  glands  they 
assume  a  crithidial  form,  from  which  after  multiplication  small 
infective  trypanosomes  appear  after  the  eighteenth  to  twenty-first 
day — i.e.,  some  two  to  five  days  after  infection  of  the  salivary 
glands. 

Miss  Robertson  never  saw  any  signs  of  conjugation  or  of  sexual 
forms,  as  described  by  Minchin,  Gray,  and  Tulloch,  but  considers 
the  cycle  in  the  fly  has  this  significance,  and  if  so  the  fly  is  the 
definitive  host,  and  susceptible  animals  can  be  infected  by  its  bite. 

Is  there  hereditary  infection  of  the  fly  via  the  ova,  as  shown  by 
O'Farrell  to  take  place  with  a  crithidia  in  a  tick  ?  This  question  is 
so  far  answered  in  the  negative. 

Is  there  an  animal  reservoir  for  T.  castellanii  ?  Perhaps  there  is, 
but  notwithstanding  Duke's  experiment  with  an  antelope,  we  believe 
that  no  such  reservoir  has  been  proven;  and  this  is  supported  by 
the  very  small  numbers  of  wild  glossime  which  have  been  found 
to  contain  T.  castellanii.  One  suspects  that  if  there  is  a  reservoir, 
it  must  be  in  man  himself  when  he  becomes  more  or  less  immune 
to  the  disease. 

The  possibility  of  direct  infection  during  sexual  intercourse 
must  be  remembered,  in  addition  to  insect  carriage. 

There  appears  to  be  no  doubt  that  the  fly  at  present  labelled 
Glossina  palpalis  is  the  carrier  of  the  disease,  as  all  experiments 
tend  to  show. 

Castellani  Type  of  Sleeping  Sickness. 


Parasite. 

Definitive 
Host. 

Definitive 
Reser- 
voir. 

Infection. 

Inter- 
mediate 
Host. 

Inter- 
mediate 
Reser- 
voir. 

Trans- 
mission. 

Trypano- 
soma 
castellanii. 

Glossina 
palpalis. 

Heredita  re- 
infection 
of  tsetse- 
flies  (?). 

Short 
salivary 
trypano- 

somes. 

Inocula- 
tive. 

Man. 

Game 
ani- 
mals (?). 

^horr 

blood 
trypano- 
somes. 

lngestive. 

88o  THE  ANIMAL  CARRIERS  OF  DISEASES 

Rhodesiense  Type  of  Sleeping  Sickness. — Kinghorn  and  Yorke 
have  described  short  blood  trypanosomes  in  man,  and,  judging 
bv  Miss  Robertson's  Castellanii  experiments,  these  must  be  the 
transmission  agents  which  infect  Glossina  morsitans,  in  the  salivary 
glands  of  which  short  trypanosomes  occur,  which  infect  the  verte- 
brate, which  is  the  intermediate  host. 

We  now  come  to  the  very  important  question  of  the  intermediate 
reservoir  of  this  trypanosome.  Bruce  says  that  T.  brncei  and  T. 
rhodesiense  are  one  and  the  same  parasite.  Assuming  this  to  be 
true,  the  intermediate  reservoir  would  be  the  African  antelopes 
— e.g.,  Catoblepas  guv,  the  wildebeest;  Strepsiceros  capensis,  the 
koodoo;  Tragelaphus  scriptus  var.  sylvaiicus,  the  bush-buck.  But 
there  are  doubts  about  this,  because — 


Fig.  462. Glossina    morsitans    Westwood,    1850:    The    Carrier    of   the 

Trypanosome   of  the  Stephens  and  Fantham   Type   of  Sleeping 
Sickness. 

(From  a  photograph  by  J.  J.  Bell.) 

1.  Stephens  and  Blacklock  have  shown  that  two  distinct  trypano- 
somes have  been  called  T.  bntcei — viz.  :— 

(a)  Moiiomorphic. — This  is  the  original  strain  of  brucei  discovered 
by  Bruce  in  cattle  suffering  from  nagana  in  Zululand. 

"  (b)  Polymorphic. — This  is  a  posterior  nucleated  form  from  Uganda, 
where  the  Rhodesiense  form  of  sleeping  sickness  is  unknown. 

2.  Chalmers  and  O'Farrell,  working  with  a  posterior  nucleated 
trypanosome,  sent  to  them  in  dogs  inoculated  from  a  case  of  sleeping 
sickness  in  the  Bahr-el-Ghazal  province  of  the  Anglo-Egyptian 
Sudan,  found  it  to  differ  markedly  in  serological  experiments  and 
animal  inoculations  from  the  original  strain  of  T.  rhodesiense. 
This  shows  that  merely  obtaining  a  posterior  nucleated  trypanosome 
in  a  sleeping  sickness  area  does  not  prove  that  it  is  T.  rhodesiense, 
or,  indeed,  has  anything  to  do  with  sleeping  sickness. 


SLEEPING  SICKNESS 


3.  Laveran's  cross  immunity  experiments  mentioned  in  Chapter 
XIX.  show  that  T.  brucei  and  T.  rhodesiense  are  quite  different  from 
an  immunity  point  of  view. 

4.  Taute  has  injected  himself  with  2  c.c.  of  blood  from  a  dog 
infected  with  T.  brucei.  He  did  not  become  infected,  and  suffered 
no  bad  effects. 

5.  Taute  fed  Glossina  morsitans  upon  animals  infected  with 
T.  brucei,  and  after  waiting  the  necessary  time  these  flies  were 
allowed  to  feed  upon  two  men,  with  negative  results,  although 
control  animals  became  infected  and  died. 

Thus  the  chain  of  evidence  is  strengthening  which  tends  to  show 
that  T.  brucei  is  not  T.  rhodesiense,  and  if  this  is  so,  then  we  do  not 
know  the  intermediate  reservoir  of  this  trypanosome,  and  its  chart 
becomes: — 

Stephens  and  Fantham  Type  oe  Sleeping  Sickness. 


Parasite. 

Definitive 
Host. 

Definitive 
Reser- 
voir. 

Infection. 

Inter- 
mediate 
Host. 

Inter- 
mediate 
Reser- 
voir. 

Trans- 
mission. 

Trypano- 

Glossina 

Hereditary- 

Short 

Man. 

Game 

Short 

soma 

morsitans. 

infection 

salivary 

ani- 

blood 

rhodesiense. 

of  tsetse- 
flies!?). 

trypano- 
somes. 

Inocula- 
tive. 

mals  (?). 

trypano- 
somes. 

Ingestive. 

With  regard  to  the  other  forms  of  sleeping  sickness  due  to  trypano- 
somes  allied  to  T.  vivax,  etc.  (vide  p.  1280),  too  little  is  known  about 
them  and  their  carriers,  and  therefore  it  is  impossible  for  us  to 
discuss  the  means  of  infection  and  transmission.  G.  tachinoides  is 
suggested  as  a  possible  carrier. 

Chagas'  Disease. — Chagas  has  shown  that  Trypanosoma  cruzi 
in  the  vertebrate  intermediate  host  finally  enters  the  lungs,  where 
it  loses  its  flagellum,  while  its  two  extremities  join,  and  it  becomes 
a  sphere,  inside  which  eight  daughter  spheres  arise,  which,  elongating 
and  entering  red  blood  cells,  become  male  and  female  trypano- 
somes.  These  are  the  transmission  agents  which  carry  on  the  life- 
cycle  of  the  parasite  in  Lamus  megistus  (Triatoma  megista)  when 
it  sucks  infected  blood. 

In  this  insect  the  trypanosome  lives  and  multiplies  in  the  gut  of 
the  insect,  and  gives  rise  to  crithidial  forms  in  the  mid-gut.  These 
eventually  develop  into  small  trypanosomes,  which  pass  into  the 
salivary  glands,  and  from  there  are  injected  into  the  intermediate 
host  when  the  insect  bites. 

He  considers  that  the  armadillo,  Dasypus  novemcinctus,  may  be 
the  intermediate  reservoir,  and  that  Lamus  geniculates,  which  lives 

56 


882  THE  ANIMAL  CARRIERS  OF  DISEASES 

with  this  animal,  may  also  be  a  definitive  host,  as  may  Latnus 
infest ans  and  L.  sordida  ;  while  Brumpt  has  shown  that  T.  cruzi 
can  develop  in  Clinocoris  lectularius  and  in  Leptocimex  boneti.  (It 
must  be  remembered  that  Triatomacanbe  infected  naturally  with  a 
trypanosome.) 

There  is  no  evidence  of  hereditary  infection  in  these  insects, 
but  there  is  some  evidence  that  at  times  infection  may  be  contamina- 
tive  from  the  insect  faeces  via  the  bite,  but  this  requires  more  in- 
vestigation. 

The  chart  of  this  disease  would  be:- — 


Chagas'  Disease. 


Parasite. 


Definitive 
Host. 


Infection . 


Inter- 
mediate- 
Host  . 


Intermediate 
Reservoir. 


Trans- 
mission. 


Trypanosoma       Lamus  Short  sali- 
cruzi.            megistus         vary  try- 

j  (synonym,  panosomes. 
I    Triatoma  — 

j    megista).  Inoculative. 


Man.     '      Dasypus      I   Male  and 
novemcinctus.  female  try- 
panosomes. 


Ingestive. 


Leishmaniasis. — The  nature  of  the  carrier  and  the  reservoir  is 
very  uncertain  at  the  present  moment.  Judging  by  the  more 
marked  resistance  of  the  dog  to  experimental  infection  in  India  and 
the  Sudan,  we  may  assume  that  there  are  at  least  two  kinds  of 
kala-azar.  It  is  believed  by  certain  authorities  that  a  flea  is  the 
transmitter  of  the  Mediterranean  type,  whereas  the  Indian  and 
Sudan  type  are  not  so  transmitted.  Patton's  incrimination  of  the 
bug  has  not  stood  the  test  of  time.  Archibald  has  suggested  and 
brought  forward  evidence  that,  at  least  in  regard  to  the  Sudan, 
infection  is  probably  due  to  the  ingestion  of  cysts  from  water 
arthropods. 

The  development  of  generalized  kala-azar  in  Archibald's  monkeys, 
after  the  successful  inoculation  of  Oriental  sore,  points  to  a  close 
relationship  between  the  two  diseases,  as  suggested  long  ago  by 
Manson. 

There  is  no  complete  evidence  at  present  that  the  espundia 
parasite  is  essentially  different  from  that  of  kala-azar,  but  it  may 
prove  in  the  long  run  to  be  different,  because  of  its  marked  different 
clinical  results. 

The  present  state  of  our  knowledge,  which  is  unsatisfactory,  may 
be  summarized  as  follows: — 


tropical  kala-azar 
Tropical  Kala-Azar. 


883 


Parasite. 


Inter- 
mediate 
Host. 


Intermediate 
Reservoir. 


Trans- 
mission. 


Definitive 
Host. 


Method  of 
Infection . 


Leishmania 
donovani. 


Man. 


(?) 


Parasites 

passed  in 

faeces. 

Ingestive  (?). 


Water 
insect  (?). 

Biting 
insects  (?). 


Cysts  in 
drinking- 
water  (?). 

Ingestive  (?). 
Inocula- 
tive (?). 


Mediterranean  Kala-Azar. 


Inter-            Inter-             Trans- 
Parasite,           mediate        mediate 

TT     .           r,            .           mission. 
Host.         Reservoir. 

1 

Host 

Nature 
Doubtful. 

Method  of 
Infection. 

Leishmania 
infantum. 

Man. 

Dogs  (?). 

Blood-suck- 
ing insect  (?). 

Inocula- 
tive (?). 

Fleas  (?). 

Blood-sucking 
insect  (?). 

Inoculative  (?). 

Contamina- 

tive  (?). 

Coccidiosis. — The  discovery  of  a  coccidial  oocyst  in  a  fly's  intestine 
by  Wenyon  and  O'Connor  suggests  that  possibly  this  is  the  method 
of  infection  of  man  by  these  parasites,  the  fly  only  acting  as  an 
intermediary  host,  as  in  the  case  of  Loeschia.  Perhaps  this  ought  to 
be  included  with  chance  infections. 

Malaria. — The  three  well-recognized  malarial  parasites  have  as 
their  definitive  host  various  species  of  anopheline  mosquitoes.  The 
classification  of  the  Anophelinse  is  as  follows: — 


-Protoanopheles. 


A.  Costa  with  less  than  four  main  dark  spots- 

B.  Costa  with  four  main  dark  spots : — 

I.  Sixth  vein  with  not  more  than  three  dark  spots — Deuteroano- 
pheles. 
II.  Sixth  vein  with  more  than  three  dark  spots — Neoanopheles. 
The  Neoanopheles  have  no  malarial  carriers. 

DIVISION  I.:  PROTOANOPHELES  Christophers,  191  i. 
The  division  contains  the  following  genera: — 
A.  Costa  without  pale  areas  : — 

I.  Female  palps   with  second  segment  disproportionately  long — 

Stethomyia. 
II.  Female  palps  with  second  segment  not  disproportionately  long — 
Anopheles. 


THE  ANIMAL  CARRIERS  OF  DISEASES 

B.  Costa  with  at  least  one  pale  area  : — 
I.  Mesothorax  without  true  scales. 

(a)  Wing  scales  mixed  dark  and  light — Patagiamvia. 

(b)  Wing  scales  not  so  mixed : — 

i.  Wing  scales  not  inflated — Myzorhynchus. 
2.   Wing  scales  inflated — Cycloleppteron. 
11.  Mesothorax  with  true  scales — Arribalzasia. 


Fig.  463.  —  Anopheles  maculipennis 
Meigen,  1818.  A  Carrier  of  the 
Malarial  Germs. 

(From  a  photograph  by  J.  J.  Bell.) 


James  distinguishes  between 
true  scales,  which  are  broad  and 
have  distinct  striations,  and  false 
scales,  which  are  hair-like  and 
have  indistinct  striations. 

The  question  whether  any  of 
these  serve  as  definitive  reservoirs 
by  infection  of  the  ova,  as  sug- 
gested by  Schaudinn,  has  never 
been  proved,  but  we  doubt  whether 
much  research  has  been  attempted 
in  this  direction. 

The  anopheline  mosquitoes 
known  definitely  to  transmit 
malaria,  arranged  according 
to  recent  methods  of  classifi- 
cation and  following  Hindle 
and  our  previous  lists,  are  as 
follows: — 

I.  Anophelines  definitely 
known  to  be  able  to 
carry  the  malarial 
parasit  es  through 
the  complete  cycle 
of  quartan,  tertian, 
or  subtertian  infec- 
tions, or  only  as  far 
as  zygotes: — 


(a)  Anopheles  Carriers. 


Number. 

Mosquito. 

Observer. 

Observation. 

Habitat. 

1 

A .  algeriensis 
Theobald,  1903. 

A .  bifurcatus 
Linnaeus,  1758. 

The 
Sergents. 

To  sporozoites. 

North  Africa. 

2 

Grassi. 

Tertian. 

England . 

3 

A .  maculipsnnis 
Meigen,  181 8. 

Many. 

Quartan,  tertian, 
malignant  tertian. 

Europe. 

PATAGIAMYIA   CARRIER 


88  5 


(b)   PATAGIAMYIA   CARRIER. 


Number. 

Mosquito. 

Observer. 

Observation. 

Habitat. 

4 

P.  pseudopuncti- 
pennis  Theobald. 

Darling. 

Malignant  tertian. 

Panama 
Canal  Zone. 

(c)  Cycloleppteron  Carriers. 

Number. 

Mosquito. 

Observer. 

Observation. 

Habitat. 

5 

i    C.  mediopuncta- 
tum  Theobald. 

Cruz. 

Tertian. 

Brazil. 

6 

C.  nototrichum  =   ,       Cruz. 
y2 .  intermedius 
Chagas. 

Tertian . 

Brazil. 

(</)  Arribalzagia  Carrier. 

/Vwrnfeey. 

1 

Mosquito.               Observer. 

Observation. 

Habitat. 

7 

A.  pseudo-                Cruz. 
maculipes  Chagas. 

Tertian. 

Brazil. 

DIVISION  II.:  DEUTERO ANOPHELES  Christophers,   i9ii. 

This  division  may  be  classified  as  follows : — 

A.  Terminal  segment  of  female  palpi  less  than  half  length  of  penultimate. 

Tarsi  not  broadly  banded: — 
I.  Mesothorax  without  true  scales— Myzomyia. 
II.  Mesothorax  with  true  scales — Pyretophorus. 

B.  Terminal  segment  of  female  palpi  at  least  half  length  of  penultimate. 

Tarsi  broadly  banded: — 
I.   Mesothorax  not  completely  covered  with  true  scales — Pseudo- 

myzomyia. 
II.  Thorax  completely  covered  with  true  scales: — 

(a)  Abdomen  without  lateral  scale  tufts : — 

i.   Palpi  moderately  shaggy — Nyssorhynchus. 
2.  Palpi  markedly  shaggy — Myzorhynchella. 

(b)  Abdomen  with  lateral  scale  tufts — Cellia. 

Most  of  these  genera  possess  malarial  carriers. 


886  THE  ANIMAL  CARRIERS  OF  DISEASES 

(e)  Myzomyia  Carriers. 


Number. 

Mosquito.                Observer. 

Observation. 

Habitat. 

8 

i 
M.  albirostris 
Theobald. 

Staunton. 

Malignant  tertian 
zygote. 

Malaysia. 

9 

M .  culicifacies 
Giles. 

Stephens  and 
Christophers. 

All  forms. 

India  and 
Ceylon. 

10 

M.  formoscensis 
I.  and  II.  Tsuguki 

=  M.  aconita 
D6nitz=^  nopheles 

kochii  Donitz. 

Tsuguki. 

Malignant  tertian. 

Formosa. 

1 1 

M.  funesta  Giles= 

M.  kumassi 

Chalmers. 

Many,  includ- 
ing Chalmers 
in  Kumassi. 

Malignant  tertian, 

including 

Kumassi  zygote 

and  sporozoites. 

Tropical 
Africa. 

12 

M.  hispamola 
Theobald. 

Sergents. 

Tertian. 

North  Africa, 
South  Spain. 

13 

M.  listoni  Lis  ton. 

Kimoshita, 
Stephens,  and 
Christophers. 

Tertian. 

India. 

14 

M.  turkhudi 
Liston. 

Stephens  and 
Christophers. 

Malignant  tertian. 

India. 

(/)  Pyretophorus 

Carriers. 

Number. 

Mosquito. 

Observer. 

Observation. 

Habitat. 

15 

P.  costalis  Loew. 

Many. 

All  forms. 

Tropical 
Africa. 

16 

P.  myzomyfacies 
Theobald. 

Sergent. 

Sporozoites. 

Algeria. 

17 

P.  superpictus 
Grassi. 

Grassi, 

Bignami,  and 

Bastienelli. 

Tertian. 

Europe. 

(?)    PSEUDOMYZOMY 

i a  Carrier. 

.V  umber 

Mosquito.                Observer. 

Observation. 

Habitat. 

lS 

P.  ludlowi            Christophers. 
Theobald. 

Malignant  tertian 
zygote. 

Malaysia, 
Andamans. 

NYSSORHYNCHUS  CARRIERS 
(h)   NYSSORHYNCHUS   CARRIERS. 


887 


Number. 

Mosquito. 

Observer. 

Observation. 

Habitat. 

ig 

N.  annulipes 
Walker. 

Kimoshita. 

Malignant  tertian. 

Australia. 

20 

N.  fuliginosus 
Giles. 

Stephens, 

Christophers, 

and  Addie. 

Quartan, 
malignant  tertian. 

India. 

21 

N.  maculatus 
Theobald. 

Staunton. 

Malignant  tertian. 

India. 

22 

N.  maculipalpis 

var.  indiensis 

Theobald. 

Stephens  and 
Christophers. 

Malignant  tertian. 

India. 

23 

N.  stephensi 

Liston=  Neocellia 

stephensi 

Theobald. 

Stephens, 

Cliristophers, 

Liston,  and 

Bentley. 

Tertian. 

India. 

-4 

N .  theobaldi 
Giles. 

Stephens  and 
Christophers. 

Quartan, 
malignant  tertian. 

India. 

25 

N.  willmori 
James. 

Addie. 

Sporozoites. 

India. 

(i) 

Cellia  Carriers. 

Number. 

Mosquito. 

Observer. 

Observation. 

Habitat. 

26 

C.  albimana 
Weidemann. 

Darling. 

All  forms. 

Central  and 
Tropical 
America. 

27 

C.  argyrotarsis 
Desvoidy. 

Darling. 

Malignant  tertian. 

West  Indies, 

South 

America. 

28 

C.  pharcensis 
Theobald. 

Newstead, 

Dutton,  and 

Todd. 

Tertian. 

Egypt. 

2Q 

C.  tarsimaculata 
Goeldi. 

Darling. 

Tertian, 
malignant  tertian. 

South. 
America . 

(/)  Myzorhynchella  Carrier. 

Number. 

Mosquito. 

Observer. 

Observation. 

Habitat. 

30 

M.  arabiensis. 

Patton. 

Sporozoites. 

Aden 
Hinterland. 

888 


THE  ANIMAL  CARRIERS  OF  DISEASES 


II.  Anophelines  believed  to  be  malarial  carriers  for  epidem- 
iological reasons : — 


Number. 

Mosquito. 

Observer. 

Habitat. 

3i 

Stethomyia  aitkeni 
James. 

Daniels, 
Christophers. 

Billet. 

Malaysia,  India. 

32 

yyretophorus  chaudoyei 
Theobald . 

Algerian  Oases 
(saline  waters). 

33 

Mysomyia  d'thali 
Pattern. 

Patton. 

Aden. 

34 

Myzomyia  kochi  Donitz 
=M.  aconita= 
M.  formoscBnsis. 

Daniels. 

Malaysia. 

35 

Myzomyia  lutzi 
Theobald. 

Lutz. 

Brazil. 

36 

Nyssorkynchus  karwari 
James  and  Liston. 

Staunton. 

Malaysia,  India. 

37 

Anopheles  (?)  martini 
Laveran. 

Laveran. 

Cambodia. 

38 

Myzorhynchus 

mauritianus  Grand  pre 

(?=M.  paludis— 

M.  aconita). 

Ross. 

Mauritius, 
Madagascar. 

39 

Anopheles  (?)  pursati 
Laveran. 

Laveran. 

Cambodia. 

III.  Malarial  carriers  in  Lists  I.  and  II.  under  synonym  names.     (The 

nomenclature  is  in  such  confusion  that  it  is  quite  impossible 
to  be  certain  whether  these  synonyms  are  correct) : — 

(a)  Myzomiafunesta  (Giles,  1 900) ;  A nopheles  kumassii  Chalmers,  1 900. 

(b)  Myzomia  formoscBnsis  : — 

1.  Anopheles  Constance  Laveran,  Madagascar. 

2.  Anopheles  jamesi  Theobald,  India. 

3.  Anopheles  jeporensis  James,  India. 

4.  Anopheles  kochii  Donitz,  Malaysia. 

5.  Anopheles  mauritianus  Grandpre,  Mauritius. 

6.  Anopheles  paludis  Theobald,  West  Africa. 

(c)  Stethomyia  atkeni  : — 

Anopheles  vincenti  Laveran,  Tonkin. 

(d)  Myzomia  listoni  : — 

Anopheles  cohczsus,  Doune  Japan. 

IV.  Probably  not  carriers : — 

(a)  Myzorhynchus  barbirostris  Van  der  Walp,  India,  Ceylon,  Malaysia, 

China. 

(b)  Myzomia  rossi  Giles,  India,  Ceylon,  China. 

(c)  Pyretophorus  sergenti  Theobald,  Algeria. 

(d)  Myzomia  sinensis  Wiedemann,  India,  Malaysia,  China. 
V.  Said  to  be  a  carrier,  but  reason  unknown  to  us: — 

Cyclolepptcron  grabbami  Theobald,  West  Indies,  South  America. 


HELMINTHIASIS 


889 


An  infective  mosquito,  when  biting  a  man,  injects  the  salivary 
sporozoites  into  his  blood  and  gives  him  the  infection. 

When  a  mosquito  bites  a  suitable  human  carrier  it  receives  the 
macrogametocytes  and  microgametocytes,  which  enable  the  para- 
sites to  undergo  sexual  development  in  its  body. 

The  scheme  is: — 

Malaria. 


Parasites. 

Definitive- 
Hosts. 

Definitive 
Reservoir. 

Infection. 

Inter- 
mediate 
Host. 

Inter- 
mediate '       Trans- 
Reser-  \     mission, 
voir.    | 

1 

Plasmodium 

malaricB, 

Plasmodium 

vivax, 

Laverania 

malaria. 

Anopheline 
mosquitoes. 

Unknown. 

Salivary 
sporo- 
zoites. 

Inocula- 
tive. 

Man. 

Human  Macrogame- 
carriers.  tocytes  and 

microgame- 
tocytes 

from  blood. 

lngestive. 

B.  HELMINTHIASIS. 

Trematode  Infections. — The  trematode  infections  of  man  have  as 
their  intermediate  host  a  mollusc.  The  definitive  host  is  a  verte- 
brate, from  whom  the  eggs  escape  in  the  urine,  the  faeces,  or  the 
respiratory  secretions.  These  eggs  hatch  in  water,  producing  a 
ciliated,  actively  swimming  miracidium,  which  will  enter  and 
develop  in  some  definite  genus  of  mollusc.  Chalmers  and  Pekkola, 
watching  the  miracidia  of  schistosoma,  noted  that  they  rapidly 
entered  the  known  susceptible  molluscs,  rejecting  other  genera. 

It  would  appear  that  the  mollusc  is  liable  to  disease  and  death 
if  too  heavily  infected. 

It  is  therefore  necessary  to  note  the  classification  and  method 
of  recognition  of  the  known  carriers. 


PHYLUM  MOLLUSCA  Cuvier. 

Synonyms. — Palliata  Latreille;  Malacozoa  de  Blainville. 

Definition. — Metazoa  with  no  sign  of  primitive  segmentation,  with  well- 
developed  distinct  ccelom  (gonad  and  pericardial),  enteron,  and  haemoccel, 
with  (or  has  lost)  a  radular  sac,  with  peri  oesophageal  ring;  dorsal  moiety  is 
the  cerebral  commissure,  and  the  ventral  the  labial  commissure;  and  with  a 
dorsal  and  a  ventral  nerve  trunk.  Body  wall  differentiated  into  an  antero- 
dorsal,  cephalic  portion,  with  the  sense  organs,  a  postero-dorsal,  the  pallium 
or  mantle,  which  secretes  externally  a  calcified  cuticle,  the  shell,  and  develops 
the  ctenidia,  or  respiratory  organs,  on  its  lower  surface,  and  a  ventral  portion, 
the  foot,  or  organ  of  locomotion.  A  veliger,  or  free  trochospere  larva,  is  nearly 
always  present. 

Classification. — The  phylum  so  defined  is  divided  into  three  grades  as 
follows : — 


890  THE  ANIMAL  CARRIERS  OF  DISEASES 

A.  Gonadial    and    reno-pericardial    cavities    communicate — Isopleura, 

Sipkonopoda. 

B.  Gonadial   and   reno-pericardial   cavities   separate — Prorhipidoglossa- 

tnorpha. 
The  Isopleura  contains  the  '  Chitons',  and  the  Siphonopoda  the  '  Gepha- 
lopods,  with  which  we  are  not  concerned. 

Grade  Prorhipidoglossomorpha  Grobben. 

Definition. — Mollusca  in  which  the  gonadial  and  reno-pericardial  cavities 
are  separate,  the  foot  is  wholly  posterior  to  the  head,  and  a  visceral  commissure 
is  present. 

Classification. — The  Prorhipidoglossomorpha  are  divided  into  three  classes 
as  follows : — 

A.  Body  bilaterally  symmetrical  : — 

I.  Mantle  united  ventrally  to  form  a  tube.     No  ctenidia — Class  I., 
Scaphopoda  Bronn. 
II.  Mantle  not  so  united;  ctenidia  present — Class  II.,  Lamellibranchia 
de  Blainville. 

B.  Body  asymmetrical — Class  III.,  Gastropoda  Cuvier. 
We  are  only  concerned  with  the  third  class. 

Class  Gastropoda  Cuvier. 

Definition. — Prorhipidoglossomorpha  with  asymmetrical  organization,  with 
well-developed  head,  with  shell  formed  in  one  piece  and  spirally  coiled,  at 
least  in  the  larva. 

Classification. — The  class  may  be  divided  into  two  subclasses: — 

A.  Visceral  commissure  twisted  into  a  figure  of  eight,  mostly  dioecious — 

Streptoneura. 

B.  Visceral  commissure  not  so  twisted,   with  shortened  visceral  com- 

missure monoecious — Euthyneura. 

Subclass  I.:  Streptoneura  Spengel. 

Definition. — Gastropoda,  dioecious,  with  a  few  aberrant  genera;  maximum 
torsion  of  visceral  mass  and  commissure.  Head  with  only  one  pair  of  ten- 
tacles. 

Classification. — The  Streptoneura  are  divided  into  two  orders: — 

A.  Nervous    system    not    concentrated.     Infra  oesophageal    commissure 

present.    Ctenidia    bipectinate    and    free    at    their    distal    ends — 
Aspidobranchia . 

B.  Nervous    system   somewhat    concentrated.      Infracesophageal    com- 

missure   present.     Ctenidium    monopectinate    and    attached    to 
mantle  along  its  whole  length — Peclinibranchia. 
Only  the  last  concerns  us. 

Order  Pectinibranehia. 

Definition. — Streptoneura  as  defined  above. 

Classification. — The  Pectinibranehia  are  divided  into  two  suborders: — 

A.  Without  proboscis,  pallial  siphon,  or  Leibleim's  unpaired  oesophageal 

poison  gland — Tcenioglossa. 

B.  With  proboscis,  pallial  siphon,  and  Leibleim's  poison  gland — Steno- 

glossa. 
Only  the  Tsenioglossa  are  of  importance  to  us. 

Suborder  Taenioglossa. 

Definition.— Pectinibranehia  with  the  characters  given  above,  with  three 
teeth,  one  lateral  and  two  marginals,  on  each  side  of  the  median  tooth  ot  the 
radula. 


M  ELAN  I A 


Classification. — There  are  two  tribes: — 

A.  Creeping  forms,  with  foot  flattened  ventrally — Platypoda. 

B.  Free-swimming  forms,  with  foot  flattened  laterally — Heteropoda. 
We  are  concerned  with  the  Platypoda. 

Tribe  Platypoda. 
Definition. — Taenioglossa  with  the  characters  given  above. 
Classification. — There  are  some  fifty-five  families,  of  wliich  we  are  interested 
in  the  Melaniidae  only. 

Family  Melaniidae  Gray. 

Definition. — Platypoda  with  spiral  shell  and  elongated  spire. 
Operculum  horny.  Foot  short.  Mantle  border  fringed.  Vivi- 
parous.    Fluviatile. 

Classification. — Several  genera. 

A.  Shell  long : — 

I.  Shell     turriculated,    aperture    enlarged     anteriorly — 

Melania. 
II.  Spiral  very  long,  aperture  notched  anteriorly — F annus. 

B.  Shell  short,  thick,  and  aperture  rounded — Other  genera. 

Melania  Lamarck. 

Synonyms. — Thiara  Mergele;  Pyrgula  Crist. 

Definition. — Melaniidae  with  turreted  shell,  acute  apex,  whorls 
ornamented  with  striae  or  spires;  aperture 
oval,    pointed    above ;   outer     lip     sharp, 
sinuous.     Operculum  subspiral. 

Type  Species. — Melania  hastula  Leach. 

Remarks. — Some  400  or  more  species 
distributed  throughout  Southern  Europe, 
India,  the  Philippines,  Japan,  and  the 
Pacific  Islands.  Distinct  groups  in  the 
Southern  United  States. 

According  to  Nakagawa,  Melania  obliquogranosa  Smith  and  M • 
libertina  Gould  are  intermediate  hosts  of  Paragonimus  ringeri 
Cobbold,  but  Kobayashi  believes  that  the  cercariae  seen  by  Naka- 
gawa in  these  molluscs  are  not' those  of  P.  ringeri. 

Blandfordia  Adams,  1863. 

Definition. — Melaniidae  with  ovate  conical 
shell,  apex .  truncated.  Aperture  elliptical, 
peristome  continuous,  operculum  subspiral. 
Rostrum  elongated.  Tentacles  very  short, 
eyes  sessile.  Foot  large;  divided  into  two 
parts  by  a  transverse  sulcus. 

Type. — Blandfordia  striatitla  Menke. 

Other  Species. — B.  bensoni  Adams;  B.  japo- 
nica  Adams;  B.  pyrrhostona  Cox;  B.    viri- 
descens  Carpenter. 
We  arc  only  concerned  with  B.  japonica,  which  is  the  carrier  of 
Schistosomum  japonic um. 


Fig. 464. — Bulinus 
contovtus  (p.  S93). 


Fig.  465. — Blandfordia 
japonica  Adams, 
1861.  The  Carrier 
of  Schistoso  in  a 
Japonicum. 


892  THE  ANIMAL  CARRIERS  OF  DISEASES 

Subclass  II.:  Euthyneura  Spengel. 

Synonym. — -Platymalakia  von  Jhering. 

Definition. — Gastropoda  moncecius  with  radula  possessing  uniform  teeth 
on  each  side  of  the  median  tooth.  Head  usually  with  two  pairs  of  tentacles. 
Detorsion  of  organization  when  adult. 

Classification. — 

A.  Marine  forms  with  aquatic  respiration — Opisthobranchiala. 

B.  Aerial  or  fresh-water  (exceptionally  marine)  forms,  with  pallial  cavity, 

but  no  ctenidium.     No  free  larval  form — Pulmonata. 

Order  Pulmonata  Cuvier. 
This  order  is  divided  into  two  suborders : — ■ 

A.  Aquatic  forms,  with  a  single  pair  of  tentacles — Basommatophora. 

B.  Terrestrial  forms,  with  two  pairs  of  tentacles — Stylommatophora. 

Suborder  Basommatophora. 

Definition. — Pulmonata  with  an  external  shell  and  a  single  pair  of  welJ- 
developed  contractile  but  not  invaginable  tentacles,  at  the  bases  of  which  lie 
the  eyes. 

Classification. — There  are  some  eleven  families,  but  only  the  following 
concern  us: — 

A.  Shell  thin,  dextral;  no  inferior  pallial  lobe — Limnceidce. 

B.  Shell  sinistral;  inferior  pallial  lobe  prominent — Planorbida. 

Family  Limnaeidse  Broderip. 

Definition. — Basommatophora  with  shell  thin,  horn  coloured,  and  capable 
of  retaining  the  whole  animal  when  retracted.  Aperture  single;  Up  sharp, 
No  inferior  pallial  lobes.     Tentacles  angular  and  flat. 

Remarks. —These  molluscs  are  found  in  fresh  water  all  over  the  world. 

Type  Genus — Limnesa  Lamarck. 

Genus  Limnaea  Lamarck. 

Definition. — Limnaeida?  with  spiral  shell,  more  or  less  elongated,  thin  pointed 
spire  translucent;  body  whorl  large;  aperture  rounded;  columella  obliquely 
twisted. 

Type  Species. — Limncea  stagnalis  Linnaeus. 

Other  Species. — The  hosts  of  Fasciola  hepatica  are  : — L.  truncatula  Muller, 
Europe,  Asia,  Africa;  L.  onhonensis,  Eyd,  Sandwich  Isles;  L.  viator, 
D'Orbigny,  South  America;  L.  humilis,  Say,  North  America. 


Family  Planorbidse  Adams. 

Definition. — Basommatophora  with  sinistrally  coiled  shell.  In- 
ferior pallial  lobe  very  prominent,  transformed  into  a  branchia; 
tentacles  tapering. 

Classification. — 

A.  Shell  discoid,  branchia  not  folded — Planorbis. 

B.  Shell  ovoid,  with  prominent  spire.     Branchia  not  folded — 

Bulinus. 


PLANORBIS 


893 


Genus  Planorbis  Guettard. 

Definition. — As  above.  Shell  discoidal,  dextral,  many  whorled; 
aperture  crescentic.  Peristome  thin,  incomplete;  upper  margin 
projects. 

Type. — Planorbis  comeus  Linnaeus. 

Planorbis  boissyi  Potiez  and  Michaud,  1838. 

Synonym. — P.  laurenti  Bourguignat. 

Remarks. — This  is  the  intermediate  host  of  Schistosoma  mansoni 
in  Egypt  and  the  Sudan,  ab  discovered  by  Leiper. 

Planorbis  olivaceus  Spix. 
This  is  the  carrier  of  S.  mansoni  in  Brazil. 


Fig.  466. — Planorbis  olivaceus.     The  Carrier  of  Schistosoma  mansoni 

in  Brazil. 


Genus  Bulinus  Adamson. 

Synonyms. — Naufa  Leach ;  Aplexa  Fleming.     Often  spelt Bullinus. 

Definition. — Planorbidae  with  ovoid  shell,  prominent  spire, 
branchia  folded. 

Type. — Bulinus  hypnorum  Linnaeus. 

Classification. — The  species  of  importance  to  us  are: — Bui  inns 
contortus  Michaud,  1829;  Bulinus  dybowski  Fischer,  1891;  Bulinus 
alexandrina  Innes;  Bulinus  innesi  Bourguignat. 

The  above  are  the  hosts  of  Schistosoma  hczmatobium  in  Egypt. 


Fig.  467.' — Physa 


(Physopsis)    africanus    Krauss, 
Schistosoma  Hcematobium. 


A  Carrier  of 


894 


THE  ANIMAL  CARRIERS  OF  DISEASES 


Family  Physidse  Dall. 

Definition. — Basommatophora  with  visceral  mass  and  shell 
sinistrally  coiled.  Shell  thin,  with  a  narrow  aperture;  tentacles 
cylindrical.     No  inferior  pallial  lobe. 

Type  Genus. — Physa  Draparnaud. 

Remarks. — Physopsis  is  distinguished  from  Physa  by  the  spire 
not  being  at  all  exserted,  and  having  the  columella  truncated  at  the 
end. 

Phya  or  Physopsis  africanus  is  the  carrier  of  5.  hcematobium  in 
Brazil. 

Trematode  Infections. 


Trematode. 

Defini- 
tive 
Host. 

Defini- 
tive 

Reser- 
voir. 

Trans- 
mission. 

Intermediate- 
Host. 

Infection. 

Fasciola 
hepatica. 

Man. 

Sheep. 

Miracklium 
in  water. 

Penetrative. 

Species  of 
Limnaea. 

Cercaria  encysted 
on  weeds. 

Ingestive. 

Fasciolopsis 
buski. 

Man. 

Pig. 

Miracidia 
in  water. 

Shrimps  (?). 

(?) 
Ingestive  (?). 

Metagonimus 
yokogawai. 

Man. 

Un- 
known. 

Ditto. 

Melcenia 
libertina. 

Cercaria  under 
scales  of  fish. 

Ingestive. 

Paragonimus 
ringer  i. 

Man. 

Car 
nivora. 

Ditto. 

Ditto. 

Cercaria  in 
water. 

Penetrative, 
or  in  crabs 
ingestive. 

Clonorchis 
sinensis. 

Man. 

Cats, 

dogs, 
pigs. 

Ditto. 

Ditto. 

Cercaria  encysted 
in  muscles  of  fish. 

Ingestive. 

Schistosoma 
hcematobium. 

Man.       Man. 

Ditto. 

Subgenera 
and  species 
of  Bulinus. 

Cercaria  in  water. 
Penetrative. 

Schistosoma 
mansoni. 

Man.       Man. 

Ditto. 

Species  of 
Planorbis. 

Cercaria  in  water. 
Penetrative. 

Schistosoma 
japonicum. 

Man. 

;    Cats. 

Ditto. 

Blandfordia 

nosophora 

vel  japonica. 

Cercaria  in  water. 
Penetrative. 

CESTODE  INFECTIONS 


Cestode  Infections. 
[These  are  on  the  same  lines  as  the  trematode  infections.) 


Cestode. 

Defini- 
tive 
Host. 

Defini- 
tive 

Reser- 
voir. 

Infection. 

Intermediate. 
Hosts. 

Transmission. 

Dibothrio- 

cephalus 

latus. 

Man. 

Dogs, 
cats. 

Eggs    in 
water. 

Cyclops, 
fish. 

Plerocercoid 
in  muscles. 

Ingestive. 

Dipylidium 
caninum. 

Man. 

Dogs, 
cats. 

Eggs  on 
iur. 

Dog  and  cat, 
louse  or  flea. 

Dog  licking 
cysticerci. 
Cat  milk 
cysticerci. 

Ingestive. 

Hymenolepis 
diminuta. 

Man. 

Rats, 
mice. 

Eggs  on 
fur. 

Meal  broth 
beetles, 
rat  flea. 

Food  cysticerci. 
Ingestive. 

Taenia 

solium. 

Man. 

Man. 

Eggs  in 
faeces. 

Pigs. 

Cysticerci  in 
muscles. 

Ingestive. 

TcBnia 

saginata. 

Man. 

Man. 

Eggs  in 
faeces. 

Cattle. 

Cysticerci  in 
muscles. 

Ingestive. 

Echinococcus. 

Dog, 
jackal. 

Dog, 
jackal. 

Eggs  on 
fur. 

Man,  sheep. 

Cysticerci  in 
muscles. 

Ingestive. 

C.  MYIASIS. 

Myiasis  comprises  the  infestation  of  the  vertebrate  body  with 
the  larva  of  diptera,  and  the  disorders  which  arise  in  the  body  of  the 
host  therefrom. 

The  vertebrate  is  an  intermediate  host,  because  not  merely  is  it 
protective  to  the  fly  larva,  but  in  it  the  larva  grows  and  develops 
until  it  is  about  to  pupate. 

There  is  no  doubt  that  this  is  an  advantage  to  the  fly,  and  that 
this  method  of  protection  is  in  process  of  evolution.  In  Chapter 
XXXIII.  we  have  written  upon  the  change  in  habits  of  flies,  and  will 
merely  remind  the  reader  that  there  is  ample  evidence  that  within 
quite  recent  years  a  scatophilous  fly  has  so  changed  its  habits  that 


S96 


THE  ANIMAL  CARRIERS  OF  DISEASES 


Nematode  Infections. 
{These  are  on  the  same  lines  as  trematode  and  cestode  as  a  rule.) 


Defini-    Deftni- 
Nematode.        tL        iive  Injection,     /"^mediate     Transmission. 

Host.  I    Reser-   !  HosL 

voir. 


Filaria 

Mar.. 

Man. 

Microfilaria 

Culex  and 

Larvofilaria. 

bancrofti. 

in  blood. 

. 

Ingestive. 

Stegomyia. 

Penetrative. 

Loa  loa. 

Man. 

Goat  (?), 

Microfilaria. 

Species  of 

(?) 

sheep  (?). 

— 

chrysops. 

Ingestive. 

Dracunculus 

Man. 

Man. 

Larvae  in 

Species  of 

Water. 

medinensis. 

water. 

cyclops. 

Ingestive. 

Ingestive. 

A  scaris 

.Man. 

Pig. 

Eggs. 

Rats. 

Larvae  on  food . 

lumbricoides. 

Ingestive. 

Ingestive. 

it  has  deposited  its  larvae  on  the  skin  of  sheep  and  become  a  pro- 
ducer of  myiasis  thereon. 

Myiasis  will  form  the  subject-matter  of  Chapter  LXVII.  (p.  1619), 
and  here  it  is  only  necessary  to  say  that  the  larvae  may  be  deposited 
in  the  natural  cavities  of  the  body,  placed  in  neglected  wounds,  live 
in  the  subcutaneous  tissue,  or  pass  through  the  alimentary  canal. 

In  this  chapter  we  are  merely  concerned  with  the  method  by 
which  the  larva  reaches  man,  and  it  would  appear  that  it  is  always, 
or  nearly  always,  due  to  the  direct  action  of  the  mother  fly;  but 
there  is  a  curious  observation,  which  is  that  an  intermediary  animal 
carrier  exists,  at  all  events,  in  the  case  of  Dermatobia  cyaniventris, 
which  has  been  studied  by  Blanchard,  Surcouf,  Rincones,  Tovar, 
Zepeda,  and  Sambon. 

According  to  the  last-named  observer,  D.  cyaniventris  lives  in 
Trinidad  and  Central  and  South  America,  and  its  young  produce 
cutaneous  myiasis  in  man,  monkeys  (the  brown  howler  and  the 
capuchin),  pumas,  agoutis,  cattle,  goats,  pigs,  and  birds  (the  toucan 
and  the  turkey). 

Man  is  most  liable  to  be  infected  while  working  in  the  mahogany 
forests  of  Honduras  and  Columbia,  as  many  as  a  hundred  maggots 
being  found  in  a  single  patient.  These  maggots  are  called  by  the 
natives  '  mosquito  worms,'  because  they  are  deposited  by  a 
culicine  mosquito,  Janthinosoma  lutzi. 


BACTERIAL  DISEASES 


897 


The  history  is  as  follows: — 

The  female/,  lutzi  lays  its  eggs  in  water;  these  hatch  and  produce 
the  imago,  which  is  then  seized  by  the  D.  cyaniventris  (according 
to  Kudi),  and  some  eight  to  eighteen  long,  pale,  yellow  eggs  are  glued 
one  after  the  other  to  the  velvet  surface  of  the  gnat's  first  second  to 
third  abdominal  segments. 

The  eggs'  are  quite  ready  to  hatch,  and  Sambon  says  that  some 
of  them  quickly  become  uncapped,  and  that  the  anterior  part  of  the 
larva  is  protruding.  The  mosquito  now  goes  off  to  get  a  meal  of 
warm  vertebrate  blood,  and  while  it  is  so  doing  the  larvae  drop  out 
of  their  shells  and  enter  the  skin  via  the  hole  made  by  the  mosquito. 
This  much  is  known,  but  we  may  well  ask  whether  this  happens 
with  any  other  insects.  Sambon  says  that  the  common  house-fly 
spreads  the  book-scorpion,  Chermes  modosus,  in  this  way,  and  says 
that  he  has  seen Pedicukts  capitis  do  the  same  thing.  If  this  be  so, 
then  the  study  of  entomology,  applied  to  man  and  animals,  has  still 
much  work  in  front  of  it . 

Restricting  our  attention  to  Dermatobia  cyaniventris,  the  chart 
of  its  carriage  is  as  follows: — 

Dermatobia  Myiasis. 


Parasite. 

Intermediary 
Hosts. 

Infection. 

Inter- 
mediate 
Host. 

Inter- 
mediate 
Reser- 
voir. 

Trans- 
mission. 

Dcfini- 
j  tive] 
Stage. 

Larva  of 
D.  cyani- 
ventris. 

Janthinsoma 

lutzi. 
Carries  eggs. 
Only  female. 

Mosquito  sucks 
blood  ;  larva 
enters  wound. 

Penetrative. 

Man. 

Warm- 
blooded 
verte- 
brates. 

Larva 

escapes 

from 

skin. 

Free 
living. 

D.  BACTERIAL  DISEASES. 

The  spores  of  bacteria  enable  them  to  spread  from  host  to  host 
with  a  degree  of  protection  during  the  passage,  but  non-sporing 
forms  will  be  benefited  by  the  aid  of  a  carrier,  which  not  merely 
affords  protection,  but  also  a  means  of  dissemination.  We  will 
divide  the  discussion  into  flies,  fleas,  and  lice. 

1.  FLIES. 
This  '  intermediary  host  '  is  often  a  non-blood-sucking  fly  of  the 
nature  of  the  '  common  house-fly,'  which  is  a  potential  carrier  of 
disease,  because  it  and  its  kind  frequent  decaying  matter  and 
excreta  for  the  purpose  of  laying  the  eggs,  while  both  it  and  its 
larvae  are  filth  feeders. 

If  it  and  its  allies  only  fed  upon  filth,  there  would  be  but  little 
harm,  but,  unfortunately,  they  are  attracted  to  many  articles  of 

57 


898  THE  ANIMAL  CARRIERS  OF  DISEASES 

human  food,  cooked  and  raw,  such  as  milk,  meat,  butter,  sweets, 
etc. ;  and  the  distances  within  reason  to  which  flies  travel  is  limited 
by  the  necessities  of  food  and  shelter,  but  they  go  to  the  nearest 
place,  and  if  both  exist  at  hand  they  do  not  travel. 

Nicholls,  working  in  St.  Lucia,  has  shown  that  the  fly  Limosina 
piiiuiipennis  Wiedemann  lives  and  breeds  almost  exclusively  upon 
human  excrement,  and  that  it  is  a  carrier  of  Bacillus  coli  communis. 
In  Africa  flies  belonging  to  the  genusPycnosoma — e.g.,  P.  marginale 
— do  the  same  as  do  other  species  in  India  and  China. 

These  flies  one  and  all  are  great  feeders,  and  are  accustomed  to 
vomit  frequently,  while  they  pass  a  considerable  amount  of  excre- 
ment. Graham  Smith  records  1,102  vomit  marks  and  nine  faecal 
deposits  on  an  area  of  a  cupboard  window  6  inches  square. 
Bearing  this  in  mind,  it  can  readily  be  appreciated  how  well  they 
contaminate  food  and  what  efficient  disseminators  of  geims  they 
may  be. 

Graham  Smith  describes  faecal  deposits  as  round,  opaque,  often 
raised,  spots  of  a  yellowish,  brownish,  or  whitish  colour,  while  vomit 
spots  have  an  opaque  centre  and  a  clear  periphery  bounded  by  a 
darker  zone. 

But  the  body  of  the  fly  is  thickly  clothed  with  hairs  or  setae,  and 
as  it  walks  over  filth,  particles  containing  bacteria  are  apt  to  cling 
to  these  hairs. 

Wo  therefore  have  to  consider: — 

A.  The  external  carriage  of  germs. 

B.  The  internal  carriage  of  germs. 

With  regard  to  the  former,  Graham  Smith's  experiments  with 
B.  prodigiosus  show  that  this  bacillus  can  be  cultivated  frcm  the 
legs  and  wings  of  infected  flies  for  eighteen  hours  after  infection. 
It  must  be  remembered  that  flies  are  everlastingly  cleaning  them- 
selves, and  it  is  a  matter  of  common  knowledge  how  the  proboscis 
is  rubbed  by  the  anterior  pair  of  legs,  which  become  contaminated 
therefrom. 

Therefore  the  external  carriage  of  germs  from  filth  to  food  is 
possible,  provided  that  it  takes  place  within  a  relatively  short  time. 

With  regard  to  the  internal  carriage,  the  same  observer  has  shown 
that,  though  there  is  no  evidence  that  B.  prodigiosus  multiplies 
therein,  it  can  live  in  the  alimentary  canal  of  flies  for  four  to  five 
days. 

The  investigation  of  the  presence  of  B.  typhosus  in  a  fly  is  most 
difficult,  because  there  are  non-lactose  ferment ers  present  as  normal 
denizens  of  the  fly.  Faichnie  has  shown  that  it  tends  to  be  present 
in  the  intestine,  and  not  on  the  legs,  but  Cochrane's  experiments 
show  that  it  may  be  recovered  from  the  external  washings  of  flies. 
The  bacilli  so  obtained  were  tested  with  typhoid  serum,  and  gave 
positive  reactions,  and  even  by  immunizing  animals  therewith 
and  testing  the  serum  so  obtained  against  stock  B.  typhosus, 
positive  results  were  obtained. 


FLIES  899 

With  regard  to  the  spread  of  B.  typhosus  and  B.  paraiyphosts 
A  and  B  via  the  larva  to  the  fly,  the  only  experiments  of  real 
moment  are  those  of  Faichnie,  who  worked  with  uncultivated 
germs,  the  flies  being  bred  in  infected  faeces.  He  showed  that 
this  was  highly  probable,  though  other  workers  have  failed  with 
cultivated  material.  Faichnie,  however,  did  not  say  that  he 
separated  the  larvae  which  had  fed  upon  the  excrement  therefrom, 
and  therefore  did  not  say  that  he  had  excluded  the  possibility  of 
the  newly  hatched  flies  feeding  upon  the  excrement.  Hence  the 
subject  of  the  carriage  from  the  larva  to  the  imago  is  sub  judice  at 
present. 

Finally,  as  far  as  is  known,  flies  do  not  suffer  in  health  from  the 
carriage  of  germs  pathogenic  to  man. 

Is  the  fly,  with  its  non-lactose  fermenters,  the  original  home  of  the 
enteric  fevers  of  man  ?  We  have  not  sufficient  knowledge  at  present 
to  discuss  this  subject,  but  we  have  said  enough  to  demonstrate  its 
importance. 

For  epidemiological  reasons,  supported  by  bacteriology,  it  appears 
probable  that  '  epidemic  or  summer  diarrhoea  '  is  due  to  Morgan's 
bacillus  spread  by  flies. 

For  epidemiological  reasons  it  seems  possible  that  flies  may  infect 
food  with  the  germs  of  the  choleras. 

There  is  no  doubt  that  flies  can  obtain  the  tubercle  bacillus 
from  sputum,  keep  it  alive  in  the  crop  for  three  days,  and  in  the 
intestine  for  twelve  or  more  days,  and  thus  can  contaminate  food 
by  the  faeces  up  to  the  fifth  day,  and  sometimes  up  to  the  sixth  to 
fourteenth  day. 

Anthrax  spores  remain  infective  in  flies  for  twenty  days,  being 
found  in  the  faeces,  while  in  dead  flies  the  period  is  indefinite; 
moreover,  they  can  pass  via  the  larva  to  the  imago. 

At  this  stage  we  may  point  out  that  the  infection  of  wounds 
produced  by  biting  flies  may  be  carried  out  by  the  agency  of  non- 
biting  flies.  Patton  was  the  first  to  point  out  that  non-biting  flies 
— e.g.,  Muse  a  pattoni — suck  the  blood  which  exudes  from  the  bites 
made  by  tabanids,  stomoxys,  etc.  As  M.  pattoni  breeds  in  bovine 
excrement,  the  possibility  of  bacterial  infection  of  the  wound  is  to 
be  remembered. 

The  possibility  of  the  Klebs-Loeffler  bacillus  and  allied  organisms 
being  spread  by  flies  must  not  be  forgotten,  though  there  is  no 
evidence  that  this  is  the  usual  form  of  infection;  still,  judging  from 
a  case  of  conjunctival  diphtheria  seen  in  Khartoum  by  Chalmers, 
it  is  possible  that  it  may  occur  as  the  means  of  infection  of  unusual 
sites,  as  Graham  Smith  has  shown  that  the  germ  can  live  in  the  crop 
and  intestine  for  twenty-four  hours  and  longer,  and,  further,  that 
the  vitality  may  be  under-estimated. 

Ophthalmia,  for  epidemiological  reasons,  especially  the  Egyptian 
ophthalmia,  is  believed  to  be  spread  by  flies,  and  Perry  and  Cast*  1- 
lani  have  shown  that  Microneurum  funicolum  de  Mcijere,  1905 — 
the  eye-fly  of  Ceylon  and  Java — is  a  possible  carrier  of  the  Koch- 


900  THE  ANIMAL  CARRIERS  OF  DISEASES 

Weeks  bacillus  and  a  spreader  of  the  severe  forms  of  ophthalmia 
found  therein. 

Flies  can  also  carry  the  plague  bacillus  in  living  virulent  form  in 
their  alimentary  canal  for  forty-eight  hours,  but  they  do  not  play 
any  great  part  in  the  dissemination  of  the  disease. 

They  also  may  be  regarded  with  suspicion  as  spreaders  of  coccal 
infections,  as  these  germs  have  been  found  in  their  alimentary  tracts, 
as  well  as  externally. 

Flies  are  therefore  of  great  importance  as  intermediary  hosts  of 
bacteria,  and  as  such  are  worthy  of  study. 

We  require  to  know  the  house-flies  of  the  tropics,  but  these  are  little  investi- 
gated, though  Nicholls  at  St. Lucia  has  found  the  following  breeding  in  human 
faeces  :— 

Drosophila  melanogaster  Meigen. 

Limosina  punctipennis  Wiedemann. 

Sepsis  species. 

Sarcophaga  aurifinis  Walker. 

Sarcophaga  species. 

Sarcophagula  species. 

In  Africa  and  the  East  generally: — 

Pycnosoma  marginale  Wiedemann. 
Pycnosoma  chloropyga  Wiedemann. 

In  India  by  Patton  i — 

Musca  domestica  Linnaeus. 

Musca  domestica  var.  determinata  Walker. 

Musca  nebulo  Fabricius. 

Musca  pattoni  Austen. 

In  England  the  investigation  is  much  more  complete — e.g.: — 

Musca  domestica  Linnaeus.  Fannia  scalaris  Fabricius. 

Musca  corvina  Fabricius.  Anthomyia  radicum. 

Calliphora  erythroce,phala  Meigen.  Sarcophaga  camaria  Linnaeus. 

Calliphora  vomitoria  Linnaeus.  Sepsis  punctum  Meigen. 

Lucilia  cesser  Linnaeus.  Piophila  casei  Linnaeus. 

Pollenia  rudis  Fabricius.  Scatophaga  stercoria  Linnaeus. 

Fannia  canicularis  Linnaeus.  Drosophila  fenestrarum . 

Also  Scenopinus  fenestralis  and  species  of  Stomoxys  and  of  Psychoda;  but 
these  two  last  have  already  been  described,  and  now  it  behoves  us  to  look 
at  the  classification  and  structure  of  the  non-biting  flies. 

We  have  already  given  the  classification  of  the  Dipt  era  in  Chapte1' 
XXXIII.,  and  need  only  consider  that  of  the  families. 

Family  Phorid.e. 

Phora  femorata  occurs  occasionally  in  houses.  Aphiochceta  femtginea 
Brunner  causes  intestinal  myiasis. 

Family  Scexopixid.e. 

Scenopinus  fenestralis  Linnaeus  is  the  so-called  window  fly,  which  is  prob- 
ably the  only  household  fly  which  is  not  injurious  to  health. 


CYCLORRHAPII.l  901 

Family  Empidie. 

Orthorrhapha  brachycera  with  medium  or  small  bodies  and  small  heads. 
Antennae  with  the  first  two  joints  very  small  and  hardly  distinct,  the  third 
joint  annulated,  often  with  terminal  bristle.  Wings  with  three  large  complete 
basal  cells,  of  which  the  third  is  shorter  than  the  second.  The  posterior  basal 
transverse  vein  is  parallel  to  the  border  of  the  wing.  Empodium  membrana- 
ceous. 

It  is  doubtful  whether  these  insects  attack  man.  As  a  rule  they  live  on  the 
juices  of  other  insects  and  plants. 

SUBORDER  II.  CYCLORRHAPHA. 

Section  1 :  Aschiza. — This  group  includes  the  family  Syrphkke, 
of  which  no  species  is  known  to  bite  man. 

Section  2:  Schizophora. — This  group  includes  the  true  flies 
characterized  by  a  distinct  frontal  lunula  and  a  frontal  suture; 
antennae  with  three  simple  segments,  and  an  arista  which  isgenerally 
dorsal.     They  may  be  classified  into— 

Muscoidea. 
Synonym. — Eumyidea. 
This  superfamily  is  divided  into: — 

Tribe  i:  Muscoidea  acalyptrata,  without  squamae  covering  the 
halteres. 

Tribe  2:  Muscoidea  calyptratce,  with  squamae  covering  the 
halteres. 

MUSCOIDEA  ACALYPTRATIE. 

A  huge  number  of  families  are  grouped  together  under  this 
division,  of  which  the  most  important  for  our  purposes  are — 

1.  Sepsidae. 

2.  Oscinidae. 

3.  Urosophilidae. 

4.  Borborkke. 

These  families  can  be  recognized  as  follows: — 

A.  Subcostal   (auxiliary)   vein  present.     Radial  1  (first  longi- 

tudinal) terminates  near  or  beyond  the  middle  of  the 
wing. 
I.  With  a  distinct  bristle  on  each  side  of  the  face.near  the 
oral  margin. 
Front  never  bristly  near  antennae;  abdomen  some- 
what elongate,  cylindrical,  usually  narrowed  near 
base.     Small    black    flics    found    about    decaying 
matter — Sepsidce. 

B.  Subcostal  vein  absent,  vestigial,  or  incomplete.     Radial  1 

usually  ends  in  the  costa  before  the  middle  of  the 
wing.     Head  not  produced  into  lateral  processes. 
I.  Hind  metatarsi  incrassate  and  usually  slimier  than  the 
second  joint — Borboridce. 


9Q2  THE  ANIMAL  CARRIERS  OF  DISEASES 

II.  Hind  metatarsi  not  incrassate  and  always  longer  than 
the  following  joint. 

(a)  Discal  and  basal  cells  united;  anal  cell  absent; 

front  bare,  or  at  most  bristly  above;  small, 
usually  light-coloured  flies — Oscinidce. 

(b)  Discal  and  second  basal  cells  separated;  anal  cell 

complete,  though  small.  Scutellum  not  elongate 
and  triangular,  and  without  spines  on  margin. 
Oral  vibrissse  present.  Arista  long  plumose — 
Drosophilidce. 

Family  Sepsidje. 

The  Sepsidae  includes  the  genus  Piophila,  of  which  the  species 
Piophila  casei  Linnaeus  may  cause  intestinal  myiasis.  Sepsis 
violacea  is  a  dung-fly  often  found  in  houses. 

Family  Oscinid.e  Latreille,  1804. 

Muscoidea  acalyptrata  with  front  without  bristles;  crown  with 
only  a  few  short  bristles;  border  of  mouth  without  vibrissas. 
Middle  tibia  with  small  spurs;  costa  of  wings  without  bristles. 
Subcostal  vein  absent.  Anterior  of  two  small  basal  cells  united 
with  discal  cell;  posterior  wanting. 

The  genera  with  which  we  are  concerned  are — Microneurum 
Becker,  1903,  and  Hippelates  Loew,  1863. 

Microneurum  Becker,  1903. 
Microneurum  f  unicola  de  Meijere,  1905. 

Synonym. — Sipkonella  f unicola  de  Meijere,  1905. 

This  little  fly  is  the  common  '  eye-fly  '  of  Ceylon  and  Java,  which 
causes  great  annoyance  by  hovering  in  front  of  the  eyes,  especially 
when  reading  or  writing  indoors. 

It  is  said  to  suck  blood,  but  our  experience  is  quite  opposed  to 
this.  It  chiefly  attacks  the  eyelids  and  the  ears,  and  since  the 
experiments  performed  by  Sir  Allan  Perry  and  Castellani  it  has  been 
suspected  as  a  possible  carrier  of  the  Koch-Weeks  bacillus,  which 
is  the  cause  of  severe  attacks  of  conjunctivitis.  It  objects  to  the 
•  odour  of  such  substances  as  Odol,  which  may  be  used  to  drive  it 
away. 

Hippelates  Loew,  1863. 

Some  authorities  consider  this  genus  not  well  founded,  and  state 

a  revision  of  the  genera  of  the  Oscindise  is  urgently  required. 
The  species  Hippelates  flavipes  Loew,  H.  plebejus  Loew,  and  H. 
pitsio  Loew,  attack  men  and  domestic  animals  by  darting  at  the 
eyes  and  other  parts  of  the  body  in  search  of  moisture  or  perspira- 
tion. They  also  attack  wounds,  sores,  scratches,  ulcers.  Their 
life-history  is  unknown.  In  habits  they  are  diurnal,  frequenting 
open  and  sunny  places.  They  are  found  in  the  southern  United 
in  Florida,  Alabama,  and  Texas.     Veils  can  be  used  as  a 


MUSCINM 


'•■  ■' 


protection,  and  eucalyptus  oil  or  a  menthol  spirit  lotion  can  be 
sprinkled  on  the  coat  collar  to  drive  them  away. 

Family  Drosophilidte. 

This  family  includes  the  species  Drosophila  ampelophila  Loew, 
commonly  called  the  fruit-fly,  and  found  hovering  over  fruit  in 
houses;  and  as  it  is  attracted  by  excrementum  it  must  be  regarded 
as  dangerous.  There  are  a  large  number  of  species  of  Drosophila 
known. 

Family  Borborid^e. 

This  family  includes  Borborus  equinus,  a  small  fly  sometimes 
found  in  houses. 

MUSCOIDEA   CALYPTRAT7E. 

MUSCINJ2. 

Musca  Linnaeus,  1761. 

Musca  domestica  Linnaeus,  1761. 

Musca  :  face  in  its  lower  part  silky  yellow;  shot  with  blackish- 
brown.     Median  stripe  black ;  antennae  brown ;  palpi  black. 

Thorax  dusty  grey,  with  four  equally  broad  longitudinal  stripes. 


Fig.  468. — Musca  domestica  Linnaeus.     (X6.) 

Scutellum  grey,  with  black  sides.  Wings  tinged  pale  grey  with 
yellowish  base.  Legs  blackish-brown.  Abdomen  yellowish,  with 
dorsal  blackish-brown  line,  except  the  last  segment,  which  is  entirely 
blackish-brown.  Eyes  separated  by  a  wide  frontal  stripe  in  the 
female,  and  near  together  in  the  male.  Length,  6  to  7  millimetres: 
wing  breadth,  13  to  15  millimetres. 


904 


THE  ANIMAL  CARRIERS  OF  DISEASES 


Remarks.— It  has  been  known  for  many  years  that  flies  can 
carry  micro-organisms  on  their  legs.  In  1888  Celli  proved  that 
flies,  fed  upon  pure  cultures  of  typhoid  bacilli,  were  able  to  transmit 
virulent  bacilli  with  their  excrement.  Early  observations  also 
proved  that  flies  were  capable  of  transmitting  cholera.  In  the 
Spanish-American  War,  in  the  Army  Concentration  Camps  of  1898, 
flies  were  found  to  be  spreaders  of  typhoid.  Lime  was  sprinkled 
on  the  fecal  pits,  and  the  flies  on  the  soldiers'  mess-table  were 
noticed  to  have  their  legs  whitened  with  the  lime. 


Fig.  469. — Head  of  Musca  domestica 
Linnaeus:  Female. 
(After  C.  J.  Martin.) 
ch.,  Pseudo-tracheae. 


Fig.  470. — Leg  of  Musca 

domestica. 

(After  C.  J.  Martin.) 


The  flies  which  breed  in  human  excrement  in  America  are: 
(1)  Musca  domestica,  house-fly;  (2)  Drosophila  ampelopliita,  fruit- 
fly;  (3)  Fannia  canicularis ,  little  house-fly;  (4)  F.  brevis,  little 
house-fly;  (5)  Stomoxys  calcitrans,  stable-fly;  (6)  Phora  femorata  ; 
(7)  Sarcophaga  trivialis. 

Of  these  the  most  common  are  the  house  and  the  stable  flies. 
The  house-fly  is  98  per  cent,  of  all  flies  infesting  houses. 

In  the  Boer  War  of  1900-02  flies  were  held  to  be  great  spreaders 
of  typhoid.  In  1902  a  paper,  entitled'  An  Inquiry  into  the  Influence 
of  Soil,  Fabrics,  and  Flies  in  the  Dissemination  of  Enteric  Infec- 
tion,' was  published  by  Firth  and  Horrocks  in  the  British  Medical 
Journal,  and  they  showed  that  the  ordinary  house-fly  {Musca 
domestica)  can  convey  enteric  infective  matter  from  excreta  or 
polluVl  materials,  or  objects  on  which  they  may  walk,  rest,  or 


MUSCINM 


905 


feed.  Such  infective  matter  appears  to  be  attached  to  their  heads 
(mandibles),  legs,  wings,  and  bodies.  Klein  has  grown  the 
typhoid  bacilli  from  flies  caught  in  an  infected  area. 

Flies  have  long  been  accused  of  being  the  spreaders  of  dysentery, 
and  recently  this  view  has  been  experimentally  proved  by  several 
authors,  including  one  of  us.  Other  diseases,  including  intestinal 
myiasis,  are  said  to  be  spread  by  flies. 

The  flies  found  by  Newstead  in  houses  in  Liverpool,  or  bred  from 
refuse  and  excreta,  were  Musca  domestica  in  quite  90  per  cent,  of 
all  flies,  while  the  other  species  met  with  were — Calliphora  erythro- 
cephala,  the  blow-fly;  Scatophaga  stercoraria,  the  dung-fly;  Bor- 
borus  equinus,  a  small  fly;  Stomoxys  calcitrant,  the  stable-fly ;  Fannia 
canicular  is  ;  F.  scalaris  ;  Anfhomyia  radicum,  the  root -fly;  Psy- 
clio.la  plialcenoides,  the  owl-midge. 

Morphology. — The  vertex  shows  three  ocelli,  situated  on  a  slightly  raised 
ocellar  triangle,  which  is  surrounded  by  another  triangle,  the  vertical  triangle. 

Between  the  upper  and  lateral  edges  of  the  clypeus  (face)  and  the  lower  edge 
of  the  epicraniura  can  be  seen  the  crescentic  opening  of  the  ptilinum. 


Fig.  471. — Anatomy  of  Musca  domestica. 

(After  C.   J.   Martin.) 

/.,  Labella;  P.,  proboscis;  S.D.,  near  salivary  duct;  g.,  gullet;  S,  mid-gut; 
i.,  intestine;  C,  sucking  stomach;  T,  rectum. 

The  proboscis  consists  of  the  rostrum,  the  haustellum  (proboscis  proper), 
and  the  labellae.  The  rostrum  is  a  truncated  cone  containing  the  pharynx; 
the  haustellum  is  grooved  anteriorly  to  contain  the  labrum,  epipharynx,  and 
the  hypopharynx.  Posteriorly  it  is  strengthened  by  a  sclerite  called  the 
'  theca,'  which  distally  carries  the  fork  (furca). 

The  labrum  and  the  epipharynx,  with  the  hypopharynx,  as  is  usual,  form 
the  pharyngeal  tube,  while  the  hypopharynx  contains  the  salivary  or  hypo- 
pharyngeal  tube.  The  labellae  are  complicated  organs  with  a  number  of 
channels  (pseudo-tracheae)  on  their  distal  surface. 

Each  labella  has  lobes  anterior,  middle,  and  posterior,  with  respectively 
twelve,  twenty-one,  and  three  channels,  which  eventually  run  to  the  oral 
aperture,  which  lies  at  the  base  of  the  oral  pit.  This  pit  is  kept  open  by  two 
discal  sclerites.  In  the  oral  pit  the  pseudo-tracheae  cease,  and  the  sides  of  the 
channels  are  covered  by  overlapping  teeth. 

The  pro-  and  meta-thoraces  are  much  reduced,  while  the  mesothorax  is  well 
developed,  and  shows  a  typical  structure.  The  venation  of  the  wings  may  be 
briefly  described  by  saying  that  the  costa  and  subcosta  are  well  marked,  and 
the  usual  costal  and  first  costal  cells  are  present.  Radius  1  cuts  off  the  sub- 
costal cell;  R.  2  and  3  the  first  radial,  and  R.  4  and  6  the  third  radial;  while 


906 


THE  ANIMAL  CARRIERS  OF  DISEASES 


media  i  and  2  bound  the  radial  and  fifth  radial  cells,  which  are  separated  by 
the  radio-median  nerve.  Median  3  and  cubitus  1  cut  off  the  median  and 
second  median  cells,  which  are  separated  by  the  medio-cubital  vein.  The 
anal  vein  is  incomplete,  and  therefore  does  not  separate  the  cubital  and  anal 
cells. 

The  abdomen  consists  of  eight  segments  in  the  male,  and  nine  in  the  female. 
The  first  segment  in  both  sexes  is  rudimentary,  and  fused  with  the  second. 
The  second,  third,  fourth,  and  fifth  are  well  developed.  The  sixth,  seventh, 
and  eighth  in  the  male  are  atrophied,  and  surround  the  anal  and  genital 
orifices.  The  sixth,  seventh,  eighth,  and  ninth  in  the  female  form  the  long 
ovipositor,  which  can  be  retracted  into  the  abdomen. 

The  pharyngeal  tube  mentioned  above  ends  in  the  pharynx,  which  has  a 
chitinous  wall,  the  fulcrum.  The  oesophagus  runs  into  the  thorax,  where  it 
opens  into  the  proventriculus,  and  sends  a  long  duct  to  the  trilobed  crop  which 
lies  in  the  abdomen.  The  proventriculus  is  really  a  valve  which  leads  to  the 
chylific  ventricle.  This  tube  is  narrow  in  front  and  wide  behind,  and  much 
coiled.  At  the  junction  with  the  Malpighian  tubes  it  becomes  the  intestine, 
which  runs  to  the  rectum.     There  are  the  four  usual  rectal  glands. 

The  salivary  glands  are  two  long  tubes  whose  ducts  unite  in  the  head  and 
open  into  the  salivary  duct  of  the  hypopharynx.  The  labial  glands  lie  in  the 
proboscis  at  the  base  of  the  labellse,  and  by  their  secretion  keep  the  tip  moist. 

The  reproductive  organs  consist  in  the  female  of  ovaries,  spermathecse, 
accessory  glands  and  ducts,  and  the  ovipositor.  In  the  male  they  consist  of 
testes,  vasa  deferentia,  an  ejaculatory  duct,  and  penis. 

Life-History. — This  was  first  studied  by  de  Geer  in  1752-78, 
next  by  Bouche  in  1834,  Packard,  junior,  in  1873,  and  more  recently 

by  ourselves  and  a 
number  of  other  people. 
The  most  recent  works 
are  those  by  New  stead 
in  Liverpool  and  Hewitt 
in  Manchester. 

The  house-flies  lay 
their  eggs  by  preference 
in  human  faecal  matter 
when  somewhat  decom- 
posed, in  horse-manure, 
goat -manure,  cow-dung, 
and  in  fermenting  vege- 
table substance,  on 
which  the  larvae  can 
feed  when  hatched. 

But  these  grubs  can 
eat  textile  fabrics  and 
paper  when  in  need  of 
nourishment.  Usually 
the  fly  works  its  way 
into  the  rubbish-heap 
or  loose  earth  to  lay  its  eggs,  but  this  is  not  invariable. 

The  time  required  for  the  development  to  be  gone  through 
depends  upon  the  temperature  of  the  air,  being  most  rapid  from 
22°  to  35°  C;  upon  the  food,  being  more  rapid  when  animal  food 
is  available;  on  moisture,  which  is  most  necessary;  and  upon  fer- 


Fig.  472. 


-Egg,  Larva,  and  Pupa  of 
Musca  domestica. 

(After  C.  J.  Martin.) 


MUSCINM  907 

mentation,  which  is  also  necessary.  The  egg  takes  from  one  to  three 
days  to  hatch  into  the  larva,  which  lives  rather  less  than  a  week, 
and  then  turns  into  the  pupa,  which  produces  the  imago. 

The  whole  time  required  is  usually  twelve  to  twenty  days,  and 
never  less  than  eight  days. 

Aldridge  gives  the  following  table  for  India : — 


Stage. 

Hot  weather. 

Cold  weather. 

Eggs 

Larvae 

Pupae 

One  day 
Five  days 
Three  days 

Two  days. 
Fourteen  days. 
Five  days. 

In  Colombo,  Ceylon,  we  found  the  development  to  be  quick,  and 
to  resemble  the  times  given  in  Aldridge's  hot -weather  table. 

Egg. — The  imago  becomes  sexually  mature  in  ten  to  fourteen  days, 
and  eggs  are  laid  as  soon  as  the  fourth  day  after  fertilization,  usually 
120  to  150  eggs  laid  being  in  a  batch.  The  egg  is  cylindrically  oval, 
being  broader  posteriorly,  and  has  two  curved  ribs  along  its  dorsal 
aspect.  It  hatchesby  splitting  at  the  dorsal  portion  of  the  anterior  end. 

Larva. — The  larval  life  is  divided  into  periods  or  instars  by  the 
ecdyses. 

First  Instar. — The  larva  is  2  millimetres  in  length,  with  a  slender 
body,  the  head  being  at  the  narrow  end,  with  a  spiny  area  on  the 
anterior  ventral  edge  of  each  segment,  and  posteriorly  two  stigmatal 
openings.     This  stage  lasts  twenty-four  to  thirty-six  hours. 

Second  Instar. — The  larva  develops  a  pair  of  anterior  spiracles. 
This  stage  lasts  twenty-four  hours. 

Third  Instar. — The  larva  eats  vigorously  for  the  first  two  days, 
and  then,  ceasing  to  feed,  still  increases  in  size.  This  stage  lasts 
three  to  four  days,  and  ends  in  pupation.  The  larva  has  a  well- 
developed  alimentary  canal. 

Pupation. — Pupation  takes  place  in  three  to  four  hours,  and 
consists  of  the  larva  contracting  (especially  anteriorly)  inside  its 
own  skin,  from  which  a  puparium  with  rounded  ends  is  formed. 
Length  about  6-3  millimetres,  which  is  at  first  creamy-yellow,  but 
later  becomes  dark  brown.  This  is  a  typical  coarctate  pupa, 
around  which  the  spiral  locomotory  pads  may  be  seen. 

Pupa. — The  pupal  stage  lasts  about  three  to  five  days,  when  the 
imago,  dilating  its  frontal  sac,  ruptures  the  anterior  end  into  dorsal 
and  ventral  portions,  the  whole  separating  by  a  circular  split  at  the 
sixth  segment. 

Fly. — The  young  fly  is  at  first  underground  or  in  the  middle  of  a 
rubbish-heap,  through  the  interstices  of  which  it  makes  its  way  to 
the  surface  by  the  aid  of  its  ptilinum  or  frontal  sac.  When  first 
hatched  it  is  rather  grey  in  colour,  and  has  to  allow  its  wings  to 
dry  before  it  is  able  to  fly. 

Habits. — After  hatching  the  fly  sets  about  to  obtain  food,  and 
on  this  point  it  is  not  particular  as  to  the  kind,  as  anything,  from 
typhoid  faeces  and  dysenteric  fpeces  to  a  pudding,  are  quite  agreeable 
to  its  oral  lobes.     It  also  has  a  liking  for  human  sweat,  much  to  the 


goS 


THE  ANIMAL  CARRIERS  OF  DISEASES 


annoyance  of  a  person  desiring  a  rest  on  a  tropical  afternoon.  It 
works  all  day,  but  rests  at  night  in  any  place  which  is  dark.  It  is 
not  known  whether  it  has  a  particular  preference  for  the  spots  on 
wThich  to  defalcate,  as  fly-specks  are  abundant.  It  is  believed  to 
defalcate  about  fifty  times  in  twenty-four  hours.  A  number  of 
experiments  have  been  performed  to  see  how  far  Muse  a  domestica 
can  fly,  but  they  are  not  satisfactory.  It  is  believed  that  a  female 
fly  becomes  sexually  mature  and  deposits  ova  in  ten  days  after 
leaving  the  pupal  case,  that  she  lays  four  batches  of  eggs  at  intervals 
of  ten  to  fourteen  days,  and  that  then  she  dies,  but  these  figures 
must  be  received  with  great  caution.  Jephson  believes  that  the 
limit  of  life  of  an  adult  fly  is  three  weeks,  but  a  hibernating  or 
activating  fly  must  live  much  longer.  Indeed,  a  fly  has  been  known 
to  live  sixteen  weeks. 

Enemies. — -The  enemies  of  the  house-fly  are  numerous,  and 
include  fungi  {e.g.,  Empusa  muscce),  protozoa  (?),  nematode  worms 
(?),  mites  {i.e.,  larvae  of  Trombidium  muscantm  Riley,  T.  musccB 
Oudemans,  the  genus  Pigmeophorus,  nymphs  of  Tyroglyplms) , 
spiders,  pseudo-scorpions,  centipedes,  larvae  of  beetles,  ants,  wasps; 
also  members  of  Cynipidae,  insects  which  produce  galls  on  plants 
{e.g.,  Figites  anthomyiarum  and  F.  scuiellaris  attack  the  maggots, 
while  Spalangia  niger  of  the  Pteromalidae  lays  its  eggs  in  the  pupae) ; 
and  Stenomalits  muscarum  is  also  a  pupal  parasite,  as  is  Nasonia 
brevicomis,  Pachycrepoideus  dubius,  and  Mitscidifiirax  raptor. 
Toads,  lizards,  and  rats  are  expert  fly-catchers. 

Pathogenicity. — It  is  a  carrier  of  the  bacilli  of  enteric  fever, 
dysentery,  cholera,  infantile  diarrhoea,  frambcesia  tropica,  anthrax, 
tuberculosis,  ophthalmia,  oriental  sore,  and  parasitic  worms  {e.g., 
Ascaris  lumhric aides). 

Calliphora  Robineau-Desvoidy,  1830. 

These  are  the  blow-flies  or  bluebottles,  of  which  C.  erythrocephala  Meigen  is 
the  common  species. 

Enteric  Fevers. 


Organism. 

Infected 
Host. 

Infected 
Reservoir. 

Trans- 
mission. 

Protective 
Host. 

Infection. 

Bacillus 
typhosus. 

Man. 

Man. 

Typhoid 
carriers. 

Bacilli  in 

urine  and 

faeces. 

Ingestive. 

Flies. 

Bacilli  on  to 
human  food. 

Contaminative. 

2.  FLEAS. 

These  insects  have  been  accused  of  spreading  leprosy  and  tuber- 
culosis, but  only  one  bacterial  disease  of  man  has  really^beenjproved 
to  be  carried  by  them,  and  this  is  the  plague. 


FLEA  S  <  09 

The  Plague. — The  aetiology  of  plague  has  been  placed  on  a  sure 
footing  by  the  labours  of  Kitasato,  Yersin,  Cantlie,  Simpson, 
Thompson,  Kolle,  Martini,  and  the  Special  Committee  already 
mentioned,  together  with  the  Second  Indian  Commission. 

It  is  caused  by  the  Bacillus  pestis  of  Kitasato  and  Yersin,  which 
is  found  in  the  fluid  of  the  initial  cutaneous  vesicle,  the  buboes,  the 
spleen,  the  blood,  and  the  sputum  in  cases  of  pneumonia.  When 
inoculated  into  monkeys,  cats,  rats,  guinea-pigs,  squirrels,  mon- 
gooses, bats,  jerboas,  etc.,  it  causes  the  typical  disease,  while  in 
bovines  and  equincs  it  only  causes  local  reactions.  Canines,  birds, 
and  reptiles  appear  to  be  immune.  It  causes  a  natural  epizootic  in 
rats,  which  apparently  is  the  true  disease,  from  which  that  of  man 


Fig.  473. — Rat  Flea. 

must  be  looked  upon  as  an  offshoot.  In  rats  it  produces  either  as 
acute  or  a  chronic  attack,  the  post-mortem  appearances  of  which 
are  different. 

In  the  acute  type  a  bubo  is  found  in  85  per  cent,  of  infected  rats, 
being  present  usually  in  the  neck  or  axilla.  If  the  bubo  is  absent , 
a  plague  rat  can  be  recognized  by  the  subcutaneous  congestion,  the 
purplish-red  appearance  of  the  muscles,  the  waxy,  mottled,  or 
finely  granular  appearance  of  the  liver,  the  haemorrhages,  and  the 
pleural  effusions.  The  diagnosis  can  be  confirmed  by  finding  the 
bacilli  in  the  bubo,  the  spleen,  or  the  blood. 

The  chronic  type  of  the  disease  consists  of  encapsuled  caseous 
foci,  or  abscesses  containing  bacilli,  and  found  in  the  spleen  and 
other  organs.     This  form  plays  no  part  in  the  spread  of  the  disease. 

The  epizootic  does  not  continue  with  equal  virulence  all  the  year 


9io  THE  ANIMAL  CARRIERS  OF  DISEASES 

round,  for  it  appears  to  be  profoundly  altered  by  the  temperature, 
being  diminished  in  the  hot  weather  of  the  tropics  and  the  cold 
weather  of  the  Temperate  Zone.  Thus  in  Bombay  the  Plague 
Commission  found  1,766  plague-infected  rats  in  one  week  in  the 
season  December  to  May,  and  only  20  to  30  in  the  season  June  to 
November.     The  cause  of  this  variation  has  already  been  given. 

But  all  rats  are  not  equally  infected,  for  it  was  found  in  Bombay 
that  there  were  two  principal  species,  Epimys  norvegicus  and  E. 
rattus,  and  that  during  the  epizootic  period  no  less  than  1,334  of  tne 
1,766  belonged  to  the  former  species,  while  in  the  non-epizootic 
period  it  alone  carried  on  the  disease.  The  reason  assigned  for  this 
difference  was  that  the  numbers  of  the  flea  population  of  the  two 
rats  were  very  different,  E.  norvegicus  possessing  about  double  the 
number  of  E.  rattus.  Further,  it  was  noticed  that  the  curve  of 
E.  norvegicus  infection  began  to  rise  about  ten  days  before  that 
of  E.  rattus,  which  points  to  the  origin  of  the  infection  of  the  latter 
from  the  former  in  the  first  instance. 

E.  norvegicus,  which  is  not  nearly  so  numerous  in  Bombay  as 
E.  rattus,  lives  outside  houses,  for  the  most  part  in  sewers,  drains, 
and  stables,  and  has  a  great  facility  for  burrowing,  and  is  a  good 
climber.  It,  however,  has  never  been  found  above  the  third  floor 
of  a  house.  It  forms  its  nest  in  one  of  its  burrows,  and  breeds  all 
the  year  round,  but  has  two  special  seasons,  one  in  March  and  one 
from  June  to  October,  the  average  family  being  eight. 

E.  rattus  is  more  common  in  Bombay  than  E.  norvegicus,  especially 
in  houses,  where  it  increases,  relatively  to  the  other,  up  to  the  third 
floor,  but  above  that  level  it  alone  infects  the  house.  It  is  not  so 
common  in  gullies,  compounds,  stables,  go-downs,  and  food  and  tea 
shops  as  E.  norvegicus.  The  common  meeting-ground  of  the  two 
species  appears  to  be  the  lower  floors  of  houses,  gullies,  and  go- 
downs.  Though  a  domesticated  rat,  it  can  climb  and  burrow.  It 
forms  its  nest  in  cupboards,  heaps  of  firewood,  etc.,  and  breeds 
all  the  year  round,  but  especially  from  June  to  October,  the  average 
family  being  five. 

The  spread  of  the  plague  from  E.  norvegicus  to  E.  rattus,  accord- 
ing to  the  experiments  of  the  Commission,  is  neither  by  direct  con- 
tact nor  by  air,  soil,  or  food,  but  solely  by  the  flea.  Contact  was 
excluded  by  placing  healthy  rats  in  the  same  room  with  plague- 
infected  animals  from  which  the  fleas  had  been  removed,  when  it 
was  found  that  none  of  them  developed  plague.  The  experiment 
was  kept  up  for  a  long  time,  replacing  dead  infected  rats  with 
freshly  infected  rats,  and,  further,  the  room  was  never  cleaned  out, 
so  that  the  healthy  animals  lived  in  contact  with  the  infected 
urine  and  faeces,  and  even  ate  food  polluted  therewith,  and  yet  not 
one  contracted  plague,  thus  excluding  transmission  by  contact,  soil, 
and  food. 

Again,  when  healthy  animals  were  suspended  in  cages  2  feet 
from  the  ground,  so  that  the  fleas  could  not  get  to  them,  or  placed 
on  the  ground,  and  surrounded  by  6  inches  of  tangle-foot,  over 


FLEAS  9ii 

which  a  flea  cannot  pass,  as  it  is  said  to  be  incapable  of  jumping 
more  than  4  inches,  or  surrounded  by  a  curtain  of  wire  gauze  so 
fine  that  a  flea  could  not  penetrate  it,  and  exposed  to  infection, 
they  escaped,  though  others  not  so  protected  became  infected,  thus 
disproving  aerial  infection.  Further,  the  transmission  by  the  rat- 
tle,1  was  proved  by  constructing  a  glass  box,  inside  which  two  wire 
c  iges  were  placed  at  a  little  distance,  but  side  by  side,  each  standing 
111  a  t  ray  tilled  with  sand.  Each  cage  had  a  lid,  through  which  rats, 
food,  water,  etc.,  could  be  introduced,  and  the  whole  apparatus 
was  covered  in  with  fine  muslin  to  prevent  the  escape  of  the  fleas. 
A  plague-infected  rat  and  a  number  of  rat-fleas  were  placed  in  one 
cage.  When  this  rat  died,  a  healthy  rat  was  placed  in  the  other 
cage,  and  after  some  time  the  dead  body  of  the  infected  rat  was 
removed,  when  it  was  found  that  the  new  rat  became  infected  with 
plague,  and  fleas  containing  plague  bacilli  were  found  upon  it. 
This  experiment  was  repeated  many  times,  45  per  cent,  of  the 
exposed  rats  taking  the  disease.  Further,  fleas  infected  by  biting 
plague  rats,  when  placed  upon  healthy  rats,  produced  the  disease  in 
55  per  cent,  of  the  experiments. 

The  Commission  calculated  that  the  blood  of  an  ordinary  plague 
rat  in  two-thirds  of  the  cases  contains  more  than  100,000,000  bacilli 
per  cubic  centimetre,  and  that  a  flea's  stomach  could  hold  0-5  cubic 
millimetre  of  blood.  Therefore,  when  the  flea  gorged  itself  on  the 
average  plague-stricken  rat  it  received  at  least  5,000  bacilli.  These 
bacilli  are  found  only  in  the  stomach  and  in  the  alimentary  canal 
posterior  to  that  viscus,  especially  the  rectum,  and  escape  from  the 
flea  solely  with  the  fseces.  It  was  proved,  however,  that  the  bacilli 
multiplied  in  the  body  of  the  flea  by  allowing  infected  fleas  to  feed 
solely  on  uninfected  rats,  a  fresh  one  being  supplied  each  day,  when 
abundant  bacilli  were  found  up  to  the  twelfth,  and  once  to  the 
twentieth  day,  thus  proving  that  multiplication  must  have  taken 
place,  otherwise  the  original  number  of  bacilli  would  have  become 
much  diluted  by  the  feeds  with  fresh  blood.  Further,  it  was  dis- 
covered that  the  proportion  of  fleas  in  whose  stomach  multiplication 
took  place  was  six  times  greater  in  the  epidemic  than  in  the  non- 
epidemic  season.  In  the  former  season  the  bacilli  could  be  found 
easily  up  to  the  fourth  and  even  to  the  twelfth  day,  while  in  the 
latter  never  after  the  seventh  day.  Infected  fleas  were  found  to 
transmit  the  disease  for  seven  to  fifteen  days. 

The  method  of  infection  probably  is  in  one  of  two  ways — either 
Leeal  pollution  of  the  proboscis,  or  else  frecal  pollution  of  the  wound 
made  by  the  proboscis,  which  was  found  quite  large  enough  for  the 
purpose  of  introducing  the  bacilli  into  the  skin.  Both  males  and 
females  can  transmit  the  disease,  but  it  was  found  that  one  infected 
Ilea  alone  was  unlikely  to  do  so.  The  flea  most  commonly  found 
on  rats,  and  the  one  by  which  the  infection  in  these  experiments 
was  usually  spread,  was Xenopsylla  cheopis,  but  others — e.g.,Cerato- 
pliyllus  fasciatus  and  Piriex  irritans — were  found  also  capable  of 
causing  the  disease. 


912  THE  ANIMAL  CARRIERS  OF  DISEASES 

Bacot  and  Martin  have  proved  the  inoculative  method  of  infection 
in  Ceratophylhts  Jasciatus,  \\hich,  when  blood-sucking,  injects  the 
bacilli,  when  the)-'  are  present  in  its  stomach  in  such  numbers  as 
to  cause  temporary  obstruction  at  the  entrance  to  that  organ. 

With  regard  to  the  spread  of  the  disease  to  man,  the  Commission 
believes  that  the  infection  generally  comes  from  Epimys  rattus, 
because  the  habits  of  that  rodent  bring  it  into  close  relationship 
with  man,  and  because  the  curve  of  its  epizootic  begins  to  rise  ten 
to  fourteen  days  before  that  of  the  epidemic.  This  period  is  calcu- 
lated to  be  made  up  of  three  days,  during  which  the  flea  leaves 
the  dead  rat,  to  which  is  added  another  three  days,  which  is  the 
incubation  period  of  plague  in  man,  and  five  and  a  half  days,  which 
is  the  average  duration  of  the  fatal  illness  in  man. 

Xenopsylla  cheopis  appears  to  be  the  flea  by  which  plague  is 
spread  from  Epimys  rattus  to  man.  This  rat -flea  will  not  merely  bite 
man  when  it  cannot  get  rat's  blood,  but  is  capable  of  living  for 
three  to  four  weeks  on  man's  blood,  and  is  often  found  on  human 
beings  after  inspection  of  plague-stricken  houses. 

Further,  it  is  believed  that  the  spread  of  plague  is  due,  not  to 
migration  of  rats,  but  to  the  carriage  of  infected  rats  on  ships,  and 
of  fleas  in  merchandise  or  on  human  beings.  The  Commission 
apparently  consider  the  last  to  be  the  most  important  method. 

Pneumonic  plague,  which  occurs  only  in  2-5  per  cent,  of  cases 
during  bubonic  epidemics,  spreads  from  man  to  man  by  bacilli 
carried  by  the  air,  for  Strong  and  Teague  demonstrated  that  the 
sputum  in  invisible  droplets  containing  viable  plague  bacilli  was 
frequently  to  be  found  ir  the  air  near  a  patient.  Teague  and  Barber 
have  shown  that  the  fine  droplets  of  sputum  disappear  very  quickly 
unless  there  is  a  considerable  amount  of  aqueous  vapour  in  the 
atmosphere,  as  is  found  in  very  cold  climates,  and  hence  the  ten- 
dency for  pneumonic  plague  to  spread  in  those  rather  than  in  warm 
climates.  On  the  other  hand,  the  bubonic  or  septicsemic  is  not 
spread  from  man  to  man,  but  from  rats  to  man.  The  epizootic 
is  the  real  disease,  and  the  epidemic  is  only  an  offshoot. 

The  above  aetiology  explains  fully  the  predisposing  causes  of  sex, 
women  staying  more  in  the  house  than  men;  of  house,  of  season,  of 
climate,  and  also  the  carriage  of  the  disease  from  one  place  to 
another  by  people,  fodder,  grain,  bales  of  cotton  and  clothing, 
rags,  etc. 

Verjbitski  in  1908  showed  that  bugs  could  act  as  carriers  of  the 
bacilli,  and  this  has  been  confirmed  by  Jordansky  and  Kladnitsky, 
while  Walker  considers Clinocoris  rotundalus  to  be  one  of  the  carriers 
of  plague  in  India,  having  found  22  per  cent,  infected  with£>.  pestis 
when  collected  from  infected  native  huts.  Moreover,  he  successfully 
transmitted  the  disease  from  man  to  the  rat  by  means  of  C.  rotun- 
da t us. 

In  California,  Wherry,  McCay,  and  others  have  shown  that  the 
ground-squirrel  (Citellus  beecheyi)  is  subject  to  plague,  and  that  its 
commonest  flea,  Ceratophylhts  acutus  Baker,  is  the  vector  from 


MAMMALIA  913 

squirrel  to  squirrel,  and,  further,  that  this  flea  will  bite  man 
Further,  they  record  a  subacute  case  of  plague  in  a  boy  where  the 
infection  was  believed  to  be  acquired  by  contact  with  ground 
squirrels.  With  regard  to  the  outbreak  in  Manchuria  and  North 
China,  Gray  suggested  that  it  started  among  men  who  handled  the 
tarbagan  (Arctomys  bobcs  Schreb),  which  is  susceptible  to  epizootic 
plague,  and  that  these  men  on  returning  to  their  homes  introduced 
the  disease  into  three  provinces,  as  pneumonic  and  septicemic 
plague,  while  it  was  spread  by  the  agency  of  the  breath  and  personal 
contact  of  clothes  and  belongings  by  coolies  travelling  in  parties 
and  sleeping  together  in  overcrowded  insanitary  inns,  especially 
as  the  cold  of  the  winter  induced  an  indoor  existence.  These 
travelling  parties  infected  adult  males  who  stayed  at  the  inns  or 
were  travelling,  and  so  it  spread  to  the  ordinary  population.  No 
infected  rats  could  be  found,  in  20,000  examined,  while  isolation  of 
the  patients  and  their  contacts,  together  with  efficient  disinfection, 
were  sufficient  to  diminish  the  death-rate.  Further  researches, 
however,  tended  to  show  that,  though  the  tarbagan  suffers  at  times 
from  plague,  the  epizootic  is  not  extensive,  and  its  direct  relationship 
to  human  plague  negligible.  The  pneumonic  form  of  plague  may 
be  in  epidemics,  especially  in  cold  weather,  but  it  is  also  to  be  noted 
that,  although  it  starts  from  association  with  an  epizootic,  it  tends 
to  die  out  without  being  succeeded  by  a  bubonic  outbreak,  but  it 
may  infect  rats  and  so  cause  a  bubonic  outbreak.  The  marmot 
(Spermophilus  citelkis) ,  which  is  common  around  Mukden,  was  sus- 
ceptible to  the  infection.  There  has  been  an  epizootic  in  Suffolk, 
and  a  few  cases  of  bubonic  plague  in  man. 

We  therefore  have  to  consider  the  role  of  the  flea  and  the  role  of 
the  vertebrate  in  plague,  and  with  regard  to  the  latter  there  does 
appear  to  be  some  such  sequence  asthis : — The  enzootic,  the  epizootic  ; 
and  these  become  in  man : — The  endemic,  the  epidemic,  the  pandemic. 

The  fleas  we  have  described  in  Chapter  XXXIV.  (p.  857),  but  it 
is  necessary  to  say  a  few  words  with  regard  to  the  rats. 


CLASS  MAMMALIA. 

SUBCLASS  EUTHERIA. 

Order  Glires  Linnaeus,  1758. 

Definition. — Eutheria  with  toes  armed  with  claws.  Size  usually  small  or 
medium.  Front  teeth  chisel-shaped  and  separated  from  the  grinding  teeth 
by  a  wide  space. 

Classification. — This  classification  is  taken  from  Swenk: — 

A.  Upper  front  teeth  two,  both  large  (suborder  Simplicidentata) . 

I.  Fur  not  sprinkled  with  quills. 

(a)  Tail  very  broad,   flat,   scaled;  hind  feet  webbed;  size  large— 

Castoridce. 
(6)   Tail  round  or  compressed;  hind  feet  not  webbed;  size  small  to 
medium. 

58 


9i4  THE  ANIMAL  CARRIERS  OF  DISEASES 

i.  Fore  feet  modified  for  digging,  their  claws  very  large;  eyes 
and  ears  very  small;  form  stout  and  short;  large  external 
cheek  pouches — Geomyidce. 

2.  Fore  feet  not  modified  for  digging;  their  claws  normal;  eyes 
and  ears  generally  large;  form  slender. 

(a)  Grinding  teeth  at  least  four  in  each  jaw;  tail  long- 

haired, generally  bushy,  not  scaled — Schiridcs. 

(b)  Grinding  teeth  not  more  than  three  in  each  jaw,  or  if 

four  (Perognathus  and  Zapus) ;  the  tail  closely  haired, 
sometimes  scaly. 

(c)  With  large  external  cheek  pouches — Heteromyidce. 

(d)  Without  external  cheek  pouches: — 

(i)  Hind  feet  not  greatly  elongated,  little  if  any  longer 

than  front  feet ;  tail  not  longer  than  rest  of  body 

— Muridce. 
(2)   Hind  feet   greatly  elongated,    much  longer   than 

front  feet ;  tail  much  longer  than  rest  of  body — 

— Zapodidce. 
II.  Fur  thickly  sprinkled  with  sharp,  stiff,  spine-like  quills — Erethizontidce. 

B.  Upper  front  teeth  four,  the  second  pair  minute  and  placed  directly  behind 
the  first  pair;  hind  legs  much  longer  than  front  legs;  ears  very  large; 
tail  very  short  (suborder  Duplicidentata) — Leporida. 

Family  Sciuru  ,e  Gray,  1821. 

Squirrels  and  Marine ts. 
The  genera  of  the  Sciuridae,  which  concern  us,  may  be  recognized  by  the 
following  table  taken  from  Swenk: — 

A.  Sides  without  a  furred  membrane  (subfamily  Sciurines,  true  squirrels  and 

marmots) . 
I.  Tail  long,   much   over  one-half  of   length  of    body;   form  slender; 
coloration  usually  spotted  or  streaked. 

(a)  Cheek  pouches  absent ;  tail  bushy,  the  hairs  growing  outward ; 

arboreal  (squirrels)— Sciurus. 

(b)  Cheek  pouches  present,  large;  tail  well  haired,  but  not  bushy; 

mainly  terrestrial. 

1.  Nail  of  thumb  well  developed;  back  conspicuously  striped 

lengthwise  with  five   dark  and  two   or  four  white 
stripes. 

(a)  Premolars  in  upper  jaw  one  on  each  side;  back  with  two 

white  stripes;  rump  rufous;  tail  with  hairs  shorter 
than  rest  of  body  (eastern  chipmunks)- — Tamias. 

(b)  Premolars  in  upper  jaw  two  on  each  side;  back  with 

four  white  stripes;  rump  greyish;  tail  with  hairs  as 
long  as  rest  of  body  (western  chipmunks) — Eulamias. 

2.  Nail  of  thumb  rudimentary;  back  striped   lengthwise  with 

seven  lines  alternating  with  six  rows  of  spots,  or  irregularly 

and  indistinctly  spotted  with  whitish,   or  plain   without 

either  distinct  spots  or  streaks  (ground  squirrels)- — Citellus. 

II.  Tail  short,  less  than  one-half  of  length  of  body;  form  stout;  coloration 

always  plain. 

(a)  Skull  highly  arched,  causing  the  head  to  appear  convex  above ; 

tail  very  short,  flattened;  thumb-nail  well  developed,  normal; 
fur  short  and  full  (prairie  dogs)- — Cynomys. 

(b)  Skull  nearly  straight,  causing  the  head  to  appear  flat  above;  tail 

short,  bushy,  not  flattened;  thumb-nail  broad   and  flat;  fur 
long,  coarse,  and  heavy  (woodchucks) — Marmotta. 

B.  Sides  with  a  densely  furred  membrane  joining  front  and  hind  legs  (sub- 

family Pteromyinae,  flying  squirrels) — Sciuropierus. 


MURIDJE  9T5 

Genus  Citellus  Oken,  1816. 

Synonym. — -Spermophilus  F.  Cuvier,  1825;    Citellus  Lichtenstein. 

Definition.— As  above. 

Type  Species. — Citellus  citellus  Linnaeus,  1 766. 

We  are,  however,  concerned  with  C.  beecheyi  and  with  M.  bobak. 

Citellus  beecheyi  Richard,  1829. 

Definition. — Citellus  of  large  size  with  large  prominent  ears.  Tail  more 
than  two-thirds  of  body-length.  Colour  above  mixed  black  and  pale  yellowish 
brown. 

Remarks. — This  is  the  ground  squirrel  of  California  mentioned  above. 

Genus  Marmotta  Blumenbach,  1779. 

Synonym. — Arctomys  Storr,  1780. 

Definition. — As  above. 

Type  Species. — Marmotta  marmota  Linnseus,  1758. 

Marmotta  bobak  Muller,  1776. 
Definition. — Marmotta  of  medium  size  resembling  the  type,  but  of  uniform 
colour,  being  above  yellowish-brown,  overlaid  with  black. 

Remarks. — This  is  the  tarbagan  of  Mongolia  and  Central  Asia. 

Family  Murip^e  Gray,  1821. 

Rats  and  Mice. 
The  genera  of  the  Muridae,  which  concern  us,  may  be  recognized  as  follows : — ■ 

A.  Crowns  of  grinding  teeth,  with  tubercles  arranged  in  transverse  rows. 

I.   Rows  of  tubercles  in  grinding  teeth  three,  very  distinct  in  upper 
jaw;  tail  long  and  scaly.     Subfamily  MurincB  (Old  World  rats 
and  mice). 
II.   Rows  of  tubercles  in  grinding  teeth  two;  tail  generally  hairy 
Subfamily  Cricetince  (American  rats  and  mice). 

B.  Crowns  of  grinding  teeth  divided  into  raised  loops  or  triangles  of 

enamel,  not  tubercular. 
I.  Upper  front  teeth  narrow,  compressed,  each  one  thicker  than 
wide  at  base;  body  not  clumsy;  tail  always  long;  eyes  and 
ears  large  and  prominent.  Subfamily  Neotomince  (wood  rats 
and  cave  rats) — Neotoma. 
II.  Upper  front  teeth  broad,  each  one  wider  than  thick  at  base; 
body  clumsy;  tail  short;  eyes  and  ears  small  andinconspicuous. 
Subfamily  Microtincs  (voles  and  lemmings). 

Subfamily  Murinae  Blaird,  1857. 

Definition. — As  above. 

Remarks. — The  Murinae  comprise  the  genus  Epimys  Trouessart,  1857,  to 
which  belong  the  rats  and  mice,  of  which  two  are  of  great  importance  in  the 
spread  of  plague — viz.,  Epimys  rattus  and  E.  norvegicus. 

Genus  Epimys  Trouessart,  1857. 

Definition. — Murinae  with  first  and  second  upper  molars,  with  two  tubercles 
on  inner  side.     Upper  incisors  with  outer  cutting  edge  entro. 

Epimys  rattus  Linnasus,  1758. 

Synonym. — Mus  rattus  Linnaeus. 

Slender  rats  with  very  pointed  muzzles  and  large  out-standing  ears,  large 
prominent  eyes,  long  tail,  and  greyish-black  fur. 


9*6 


THE  ANIMAL  CARRIERS  OF  DISEASES 


The  tail,  which  is  25  per  cent,  longer  than  the  length  of  the  head  and  body- 
together,  is  brown  and  regularly  annulated.  Feet  medium-sized,  but  compara- 
tively long  and  slender. 

Body  variable,  14  to  19  centimetres  in  length.  Colour  variable:  light 
rufescent,  brown  on  the  dorsum,  white  or  grey  on  the  venter,  but  may  be 

darker  or  lighter.     Mammae  two  to 
three. 

There  are  two  varieties  of  this 
rat:  alexandrinus ,  which  is  larger 
and  heavier;  and  rufescens,  which 
is  smaller  and  redder;  but  there 
are  any  number  of  intermediate 
species.  It  breeds  frequently 
throughout  the  year. 

It  is  essentially  a  house  rat, 
living  in  the  tiles  or  thatch  of  the 
roof,  or  in  holes  and  recesses  in 
the  floor,  but  it  will  live  in  the 
crowns  of  cocoanut  trees. 

Its  pathogenicity  is  important, 
for  it  is  the  plague  rat  of  Upper 
India.  It  is  supposed  to  have 
entered  Europe  with  the  Asiatic 
invasion. 

Epimys  norvegieus  Erxleben,  1777. 

Synonym.  —  Mus  decumanus 
Pallas,  1778. 

Large,  heavy  rats,  with  heavy, 
uniformly  tapering  tails;  dark 
coloured  dorsally,  lighter  coloured 
ventrally;  only  89  per  cent,  of  the 
length  of .  the  head  and  body. 
Heavy,  flesh-coloured  feet,  short 
round  ears,  and  broad  heavy 
snout. 

Colour  brown  on  the  dorsum  and 
dirty  white  on  the  venter.  Foot- 
pads large;  heart-shaped  mammae 
Fig.  474. — Rat:  Plague  Reservoir.       ten  to  twelve  in  number. 


Fig.  475. — Head  of  Epimys 

rattus. 

(After  Hossack.) 


Fig.  476.— Head  of  Epimys 
norvegieus. 
(After  Hossack.) 


LICE 


017 


This  is  the  brown  sewer  or  ship  rat,  which  is  supposed  to  have  come  from 
China  to  Europe,  and  from  Europe  to  India.  It  is  the  plague  rat  of  Bombay. 
It  is  very  prolific,  producing  several  litters  of  eight  to  ten  young  per  annum. 

The  chart  of  plague  is  as  follows: — 

Plague. 


n         .          Infected 
Organism.      ^ 

Infected 
Reser-       Transmission, 
voir. 

Propa- 
gative 
Host. 

Infection. 

Bacillus         Man. 
pestis. 

Murinae.            Bacilli 

obtained  by 
blood-sucking. 

Ingestive. 

Fleas. 

Bacilli  in  faeces 
into  wound  by  bite. 

Contaminative. 
More  rarely 
inoculative. 

3.  LICE. 

Relapsing  Fevers. — With  the  downfall  of  Schaudinn's  views  many- 
authorities  consider  spirochetes  to  be  bacteria — e.g.,  Dobell  con- 
siders them  to  be  such  because  the  longitudinal  division  is  said  to  be 
based  on  imperfect  observation,  and  hereditary  transmission  can 
occur  with  Bacillus  cuenoti  in  the  germ  cells  of  the  cockroach. 


••   f 


Fig.  477. — Pediculus 
Geer,  1778:  Male. 
Typhus,  etc. 


corporis     de        [Fig.    478. — Pediculus    corporis    de 

Carrier  of  Geer,    1778:    Female.     Carrier 

of  Typhus,  etc. 


(From  a  photograph  by  J.  J.  Bell.) 

Many  of  them  are  said  to  be  flagellate;  their  nucleus  is  diffuse,  like 
bacteria,  and  there  is  no  conjugation,  sex  formation,  or  encystment 
known,  and  it  would  appear  as  though  a  coccoid-like  infective 
granule  was  the  important  method  of  their  infection  of  the  host. 


gi8 


THE  ANIMAL  CARRIERS  OF  DISEASES 


They  therefore  behave  more  like  the  bacteria  than  like  animal 
parasites  in  the  carrier. 

For  our  present  purpose  relapsing  fevers  may  be  divided  into 
two  groups  as  follows: — 

I.  The  Louse  Group,  which  is  characterized  by  being  carried  by 
the  louse.  These  are  the  European,  the  North  African,  the  Indian, 
and  the  American  types. 

From  the  infective  blood  the  spirochaetes  pass  into  the  alimentary 
canal  of  the  louse,  and  from  thence  into  its  ccelom,  where  they 
remain,  and  from  there  they  find  their  way  into  the  eggs,  which  are 
infective,  as  are  their  larvae. 

Infection  of  man  is  brought  about  by  contaminative  means — i.e., 
the  louse  in  biting  causes  irritation,  the  man  scratches  his  skin, 
causing  abrasions,  and  at  the  same  time  kills  a  louse,  crushes  it, 
and  rubs  it  into  the  abrasions,  which  become  infected.  Nicolle 
and  Blaizot  believe  that  the  organisms  which  are  infective  are 
granules  just  before  they  reappear  as  spirochaetes.  Sergent  and 
Foley  have  stated  that  there  were  very  small  virulent  forms  in  man 
during  apyrexia. 

In  this  life-cycle  there  is  no  definitive  host,  merely  two  hosts 
of  equal  value.  Only  the  insect  is  the  preservative  host  and  the  verte- 
brate the  intermediary  host. 

I.  The  Louse  Group  of  Relapsing  Fevers. 


Parasites. 


Preservative 
Host. 


S.  recurrentis,     Pediculus 
5.  berbera,        corporis. 
S.  cartcri, 
S.  novyi. 


Preservative 
Reservoir. 


Lice  by 

hereditary 

transmission, 


Infect  ion . 


Inter- 
mediate 
Host. 


Small  forms  in 
body  cavity. 

Contaminative. 


Man. 


Trans- 
mission. 


Small 
blood 
forms. 

Ingestive. 


Spirochetal  Epidemic  Jaundice. — This  is  caused  by  Spiroscliau- 
dinnia  icterohcemorrhagice,  which  may  have  its  reservoir  in  rats, 
from  which  it  probably  escapes  in  the  urine,  and  after  living  in 
water  enters  via  the  alimentary  canal  or  the  skin.  It  is  believed  to 
have  been  caused,  but  very  rarely,  as  the  result  of  a  rat -bite.  It  is 
introduced  here  as  a  convenient  place,  though  not  known  to  be  due 
to  lice. 


Parasite.                     Host. 

Reservoir.           Method  of  Infection. 

Spirosch.iudinnia               Man. 
icterohesmorrhagiee . 

Rats  (?).        Contaminated  water  (?). 

THE  TICK  GROUP  OF  RELAPSING  FEVERS 


919 


II.  The  Tick  Group,  which  is  characterized  by  being  spread  by 
the  genus  Ornithodorus.  The  known  forms  are  the  African  (perhaps 
a  separate  East  African),  the  Persian,  the  Colombian,  with  the 
Panamanian. 

This  group  differs  from  the  louse  group  in  the  pre-eminence  of 
the  infective  granule,  which,  according  to  many  authorities,  is  in 
itself  doubtful. 

Spirochaetes  enter  the  tick  with  the  infective  feed,  bore  their  way 
into  the  cells  of  various  organs,  and  break  up  into  coccoid  bodies, 
the  infective  granules.  These  granules  pass  into  the  second  genera- 
tion, and  so  the  tick  is  a  preservative  reservoir.  They  also  pass  into 
the  Malpighian  tubules,  from  which  they  escape  when  the 
thick  white  Malpighian  excrement  is  passed,  which  only  takes 
place  towards  the  end  of  a  feed.  The  spirochaetes  now  enter 
the  new  host  via  the  hole  made  in  the  skin  by  the  tick  for  its 
meal  of  blood. 

II.  The  Tick  Group  of  Relapsing  Fevers. 


Parasite. 


Preservative 
Host. 


Preserva- 
tive 
Reservoir. 


Infection. 


Inter- 
mediate 
Host. 


Trans- 
mission. 


Forms  allied  to 
5.  duttoni  and 


Species  of 
Ornithodorus- 


found  in  Aid-  e.g.,  0.  moubata, 


ca.  East  Afri- 
ca, Colombia, 
Panama,  am! 
perhaps  m 
Persia . 


0.  turicata, 

O.  talagce, 

and  perhaps 

O.  savignyi. 


The  ticks  The 

by  infective 

hereditary  granules(P). 
trans-  — 

Contami- 
native. 


Man. 


Blood 
spiro- 
chetes. 

Ingestive. 


We  have  followed  Balfour's  suggestion  that  the  Persian  relapsing 
fever  is  not  caused  by  Argas  persicus,  but  by  a  species  of  Ornitho- 
dorus, probably  0.  savignyi.  It  must  be  admitted  that  many 
authorities  disbelieve  in  the  infective  granule. 


4.  PHLEBOTOMUS  FLIES. 

Verruga  Peruviana. — It  has  been  suggested  that  the  carrier  of  this 
disease  may  be  P/ilebotomus  vcrrucarum  Townsend,  1913,  but  this 
appears  to  be  very  doubtful. 


920 


THE  ANIMAL  CARRIERS  OF  DISEASES 


E.   DISEASES  OF  UNKNOWN  CAUSATION. 

The  evidence  in  favour  of  pellagra  being  an  insect -borne  disease 
has  not  increased,  and  many  authorities  believe  it  to  be  a  deficiency- 
disorder.  The  insects  which  were  accused  were  species  of  Simulium 
and  some  Chironomid  biting  flies.  There  are  suggestions  that 
Rocky  Mountain  fever  and  tsutsugamushi  disease  are  bacterial 
infections,  and  Noguchi  has  found  a  spirochete  in  yellow  fever. 


Disease. 

Host. 

Reservoir. 

Transmission . 

Carrier. 

Infection. 

Pappataci 
fever. 

Man. 

— 

Blood-sucking. 
Ingestive. 

Species  of 
phlebotomus. 

Bites. 
Inoculative. 

Dengue 
fever. 

Man. 

— 

Blood-sucking. 
Ingestive. 

Stegomyia 
culex  (?). 

Bites. 
Inoculative. 

Yellow 
fever. 

Man . 

Man  in 

mild 
attacks. 

Mon- 
keys (?). 

Blood-sucking. 
Ingestive. 

Stegomyia 
calopus. 

Bites. 
Inoculative. 

Rocky 

Mountain 

fever. 

Man. 

— 

Blood- sucking. 
Ingestive. 

Dermacentor 

venustus  = 

D.  andersoni. 

Bites. 
(?) 

Tsutsuga- 
mushi 
disease. 

Man. 

A  rvicola 
nataned- 
zunni  (?). 

Blood-sucking. 
Ingestive. 

Microtrom- 
bidium 

akamushi. 

Bites. 
(?) 

Trench  fever 

spiro- 

chaete  (?). 

Man. 

Blood-sucking. 
Ingestive. 

Lice. 

Bites. 
Contaminative. 

Typhus. 

Man. 

— 

Blood-sucking. 
Ingestive. 

Lice. 

Bites. 
(?) 

Acute 

anterior 

poliomyelitis. 

Man. 

Blood-sucking. 
Ingestive. 

Stomoxys 
calcitrans. 

Bites. 
Inoculative. 

F.  CHANCE  TRANSMISSION. 

Numerous  blood-sucking  and  non-blood-sucking  insects  may  bjr 
chance  obtain  an  organism  and  carry  it  in  their  proboscis,  and 
directly  infect  an  open  sore — e.g.,  flies  and  yaws,  which,  according 
to  Castellani's  observations  and  experiments,  is  far  from  a  rare 
occurrence. 


TERMS 


921 


G.  IMPERFECT  CARRIAGE  OF  PARASITES. 

Parasites  may  develop  up  to  a  certain  point  in  the  alimentary 
canal  of  insects  in  which  they  are  unable  to  complete  their  life- 
cycles — e.g.,  the  malarial  germ  in  many  anophelines  only  proceeds 
as  far  as  the  zygote. 

H.  TERMS. 

Terms  for  Animal  Parasites. 

Host    with    sexual     life     of 
parasites. 


Definitive  host 
Intermediate  host 
Intermediary  host 
Definitive  reservoir   . 
Intermediate  reservoir 
Transmission 
Infection 
Cont  ami-native 
Inoculative     . . 
Ingestive 

Infected  host  .  . 

Infected  reservoir 
Protective  host 

Propagative  host 

Transmission^ 
Infection         ) 


Host    with    asexual    life    of 

parasites. 
No  development  of  parasite. 

Merely  carriage. 
Natural  supply  of  infection  of 

intermediate  host. 
Natural   supply   of   infection 

for  definitive  host. 
Passage  from  intermediate  to 

definitive  host. 
Passage    from    definitive    to 

intermediate  host. 
Abrasions  or  bites  contami- 
nated by  faeces,  etc. 
Parasites  injected  by   insect 

during  biting. 
Parasites  taken  into  alimen- 
tary canal  -per  os. 

Terms  for  Bacteria. 

Vertebrate  infected  by  bac- 
terium. 

Vertebrate  carrier. 

Arthropod  carrier  without 
germ  increasing  in  number. 

Arthropod  carrier  with  germ 
increasing  in  number. 

As  in  animal  parasites. 

REFERENCES. 

Graham-Smith  (191 4).     Non-Blood-Sucking  Flies.     Cambridge. 

Hindle  (1914).     Blood-Sucking  Flies.     Cambridge. 

Leiper    (1915-1918).      Jour.    Royal    Army    Med.    Corps    (Transmission    of 

Bilhar  ziosis) . 
MacGregor   (191 7).     Journal  of  Tropical   Medicine  and   Hygiene,   xx.   205 

(Insect  Vectors).     London. 


SECTIOxN   II 
VEGETAL    PARASITES 

CHAPTER  XXXVI 
SCHIZOMYCETES 

Preliminary  —  Thallophy  ta  — .  Schizomycetacea —  Eubacteriales  — Coccaceae — 
Bacillaceae — Spirillaceae — Mycobacteriaceae — References. 

PRELIMINARY. 

In  our  previous  editions  we  drew  attention  to  the  numerous  text- 
books and  easily  available  works  on  bacteriology,  which  we  decided 
not  to  consider,  and  we  hold  to  that  view  still;  but  we  notice  that  the 
works  on  this  subject,  as  supplied  to  the  student  of  medicine,  are 
perhaps  somewhat  lacking  in  systematic  classification. 

To  meet  this  need  we  have  written  the  present  chapter,  which 
merely  considers  those  bacteria  which  are  of  importance  from  the 
point  of  view  of  tropical  medicine;  and  instead  of  giving  descriptions 
of  their  characters,  these  are  merely  indicated  by  tables.  Hence 
it  should  be  used  in  conjunction  with  a  good  textbook  on  bacteri- 
ology, in  which  the  details  with  reference  to  the  species  can  be  found. 

It  is  well  known  that  the  nomenclature  of  the  bacteria  is  in  hope- 
less confusion,  but  an  International  Botanical  Congress  was  to  have 
been  held  in  London  in  1915,  at  which  the  medically  important 
nomenclature  of  the  schizomycetes  would  have  been  considered,  and 
probably  some  such  congress  will  take  place  after  the  war. 

In  the  meanwhile  the  reader  can  find  the  existing  rules  in  '  Regies 
Internationales  de  la  Nomenclature  Botanique,'  published  in  Jena 
in  1912 ;  and  we  may  perhaps  be  permitted  to  remind  him  that  names 
of  orders  should  end  in  -ales,  or  suborders  in  -inece,  and  of  families 
in  -acece,  while  names  of  genera  must  be  in  the  singular  number  and 
written  with  a  capital  letter,  and  those  of  subgenera  and  sections  should 
resemble  that  of  the  genus. 

With  regard  to  species,  it  is  designated  by  a  binomial  name,  the 
first  portion  of  which  is  the  generic  name,  while  the  second  portion 
is  the  specific  name,  and  is  usually  begun  with  a  small  and  not  a 
capital  letter,  and  is,  further,  of  the  nature  of  an  adjective  as  a  rule. 

It  is  difficult  to  say  what  should  be  taken  as  the  standard  for 
bacterial  nomenclature  and  classification,  but  it  appears  to  us  that 
it  is  useless  to  go  further  back  than  Migula;  in  any  case  the  reader 

922 


PHYLUM   THALLOPHYTA  923 

will  realize  that  in  no  instance  can  a  species  be  designated  by  more 
than  two  words — viz.,  the  generic  and  the  specific. 

With  regard  to  the  value  of  bacterial  species  based  upon  biolog- 
ical and  not  upon  morphological  differences,  the  remarks  which 
we  wrote  on  this  subject  in  regard  to  the  Protozoa  hold  good  here, 
and  need  not  be  repeated,  while  we  would  refer  the  reader  again  to 
the  section  on  evolution  in  Chapter  V.,  p.  112. 

The  Regnum  Vegetabile,  or  vegetal  kingdom,  is  usually  divided 
into  four  great  phyla  or  groups — -viz.,  the  Thallophyta,  the 
Briophyta,  the  Pteridophyta,  and  the  Phanerogams,  but  of  all  these 
only  the  first  need  concern  us. 

The  Thallophyta  include  a  great  variety  of  plants  whose  vege- 
tative body  may  consist  of  one  or  many  cells,  forming  a  more  or 
less  branched  structure. 

These  plants  may  be  defined  and  classified  as  follows: — 

PHYLUM  THALLOPHYTA. 

Definition.— Vegetabiles  with  a  cellular  structure,  which  is  gener- 
ally little  differentiated,  and  reproducing  asexually  by  division 
and  by  spore  formation  or  sexually,  after  conjugation,  by  oospores. 

Classification.— The  Thallophyta  may  be  divided  into : — 

A.  Thallophyta    with    chromatophores    and    often    with    chlorophyll — 

Class  I.,  Alga  Roth,  1797. 

B.  Thallophyta    without    chromatophores    or    chlorophyll — Class    II., 

Fungacea  Linnaeus,  1737. 

There  can  be  no  doubt  that  the  Fungaceae  are  descendants  of  the 
Algae,  which,  because  of  a  saprophytic  or  parasitic  environment, 
have  altered  their  food  habits  and  have  adapted  themselves  to  new 
methods  of  nutrition,  and  hence  no  longer  require  chromatophores 
or  chlorophyll,  as  they  no  longer  manufacture  their  food  with  the 
aid  of  sunlight,  but  subsist  on  decaying  animal  or  vegetal  material 
rich  in  organic  substances. 

They  may  be  parasitic  or  saprophytic,  or  a  form  which  is  usually 
parasitic  may  at  times  become  a  saprophyte,  or  vice  versa. 

With  regard  to  their  origin,  the  three  great  divisions  probably 
differed  in  their  evolution;  thus  the  Schizomycetes  are  probably 
derived  from  the  Cyanophyceae,  or  Blue-Green  Algae,  while  the 
Phycomycetes  and  thqEumycetes  stand  in  closer  relationship  with 
the  Chlorophyceae,  or  Green  Algae;  and  it  is  because  of  this  great 
difference  in  origin  that  the  Schizomycetes  are  kept  apart  from  the 
Fungaceae,  and  are'classified  with  the  Algae,  although  they  are 
often  included  in  the  loosely  used  term  Fungi  (auctores). 

Another  less  usual  classification  is  to  divide  the  Thallophyta  into 
two  great  groups,  of  which  the  first  includes  the  Cyanophyceae  and 
the  Schizomycetes,  while  the  second  embraces  the  Myxomycetes, 
the  Peridineae,  the  Conjugatae,  the  Diatomenae,  the  Heterocontae, 
the  Chlorophyceae,  the  Characeae,  the  Phycomycetes,  the  Phaeo- 
phyceae,  the  Rhodophyceae,  the  Eumycetes. 

We  will  now  turn  to  consider  the  Schizomycetes. 


924  SCHIZOMYCETES 

SCHIZOMYCETACEA  Naegeli,  1857. 

Definition. — Thallophyta  without  chlorophyll  and  as  a  rule  with- 
out chromatophores,  with  the  vegetative  body  consisting  of  a 
single  cell,  in  which  the  nucleus  is  not  present  in  the  form  typical 
for  other  thallophytes.     Reproduction  by  fission  or  spore  formation. 

Classification. — The  Schizomycetes  may  be  divided  into  orders 
as  follows: — 

A.  Cells  without  sulphur  or  bacterio-purpurein — Order  I.,  Eubacteriales. 

B.  Cells  containing  sulphur — Order  II.,  Thiobacteriales. 

C.  Motile  rods  in  pseudoplasmodial  masses  embedded  in  a  gelatinous 

matrix  and  forming  highly  developed  cysts— Order  III.,  Myxo- 
bacteviales. 

Only  the  first  order  contains  forms  of  importance  in  tropical 
medicine. 

ORDER  I.  EUBACTERIALES. 

Definition. — Schizomycetes  which  contain  neither  sulphur  nor 
bacterio-purpurein. 

Classification. — The  Eubacteriales  may  be  divided  into  families 
as  follows : — 

A.  Cells,  in  free  condition,  usually  globular,  in  division  somewhat  ellip- 

tical— Family  1,  Coccacece  Zopf,  1885,  emendavit  Migula,  1900. 

B.  Cells,   long  or  short,  cylindrical,  straight;   division  one   direction — 

Family  2,  Bacillicece  Fischer,  1894. 

C.  Cells,  spirally  curved  or  representing  part  of  a  spiral;  division  in  one 

direction — Family  3,  Spirillacece  Migula,  1900. 

D.  Cells,  surrounded  by  a  sheath  and  arranged  in  elongated  filaments — 

Family  4,  Chlamydobacteriacece  Migula,  1900. 

E.  Cells,  short  or  long,  cylindrical  or  filamentous,  often  clavate,  cuneate, 

or  irregular,  with  enclosed  granules.  Filaments  without  a  sheath- — ■ 
Family  5,  Mycobacteriacecs  Chester,  1901. 

The  Chlamydobacteriaceae  do  not  concern  us,  but  the  other 
families  require  some  consideration. 

FAMILY  COCCACEjE  Zopf,  1885,  emendavit  Migula,  1900. 

Definition. — Eubacteriales  in  which  the  free  cells  are  usually 
globular,  though  in  division  they  become  somewhat  elliptical. 

Type  Genus. — Micrococcus  Hallier,  1866,  emendavit  Cohn,  1872, 
and  Winslow  and  Rogers,  1905. 

Classification. — This  family,  which  contains  forms  of  importance 
to  us,  may  be  divided  into  two  tribes  as  follows: — 

A.  Parasitic  on  plants  and    animals,  often  growing  best  anaerobically 

but  frequently  with  difficulty  and  in  small  amount,  or  even  not  at 
all,  on  artificial  media;  in  pairs  or  chains,  generally  but  not  always 
staining  by  Gram,  and  often  producing  acidity  in  glucose  and  lactose 
media,  and  when  pigmented  generally  white  or  orange — Tribe  I., 
StreptococcecB  Trevisan,  1889,  emendavit  Winslow  and  Rogers,  1905. 

B.  Facultative    parasites    or    saprophytes    growing   best   under   aerobic 

conditions  and  well  on  artificial  media;  in  cell  groups,  packets 
or  zooglcoa  masses  and  often  Gram-negative,  and  when  pigmented 
usually  yellow  or  red — Tribe  II.,  Micrococcece  Trevisan,  1889, 
emendavit  Winslow  and  Rogers,  1905. 


COCCACEM 


925 


The  two  tribes  may  be  divided  into  genera  as  set  forth  in  the 
following  table: — 

Diagnostic  Table  of  the  Family  CoccACEiE  Zopf,  1885. 
Growth  and  Carbohydrates. 


Poor  and  fermented 
(Streptococcese) . 

Gram's  stain. 


Good  and  not  fermented 
(Micrococceae). 

Pigment. 


Negative. 
1.  Neisseria. 


Positive.  Red.  Yellow.  Black. 

I  I 

Pigment.       7.  Rhodococcus.       Cells.        10.   Nigvococcus. 


Absent. 
I 
Cells. 


Present. 


Irregular  groups. 
8.  Micrococcus. 


Packets. 
9.  Sarcina. 


In  zooglcea 
masses. 

2.  Ascococcus. 


Not  in  zoogloea 
masses. 

! 

Morphology, 
bile  and  salt. 


Orange.  White. 

5.  Aurococcus.      6.  Albococcus. 


Pairs  or  chains  encap- 
sulated, soluble  in 
bile  and  salt  solu- 
tions. 

3.  Diplococcus. 


Chains,  not  encapsu- 
lated, not  soluble 
in  bile  or  salt  solu- 
tions. 

4.  Streptococcus. 


We  are,  however,  only  concerned  with  certain  genera  of  the 
Streptococcese,  which  are  Neisseria,  Diplococcus,  Streptococcus, 
Aurococcus  and  one  genus  of  the  Micrococceae — viz.,  Nigrococcus. 
As  Micrococcus  melitensis  is  often  elongated  (coccobacillus) ,  we 
propose  to  place  it  under  a  separate  heading,  '  Incerta  Sedis.' 


TRIBE   I. 


STREPTOCOCCE/E  Trevisan 
Rogers,  1905 


1S89,  emendavit  Winslow  and 


Genus  Neisseria  Trevisan,  1885. 

Synonyms. — Micrococcus  Hallier,  1866,  pro  parte ;  Diplococcus 
Weichselbaum,  1887,  pro  parte. 

Definition. — Streptococceae  growing  best,  and  often  only,  aerobi- 
cally,  with  or  without  pigment  formation,  usually  present  in  pairs 
without  a  true  capsule,  and  in  exudates  usually  intracellular,  and 
readily  decolourized  by  Gram's  method  of  staining. 

Primary  cultures  grow  poorly  on  usual  laboratory  media,  but 
best  on  media  containing  glucose  or  blood  serum.  No  lysis  with  bile. 
Ferment  carbohydrates  usually  with  but  slight  acid  production. 

Type  Species. — Neisseria  gonorrJioea  (Bumm,  1885). 


926 


SCHIZOMYCETES 


Classification. — The  genus  Neisseria  includes  the  following  species : 
i.  N.  gonorrhoea  (Bumm,  1885),  which  is  the  cause  of  gonorrhoea. 

2.  N.  intracellularis  (Weichselbaum,  1887),  which  is  one  of  the 
organisms  causing  epidemic  cerebro-spinal  meningitis. 

3.  N.  sicca  (von  Lingelsheim,  1906). 

4.  N.flava  (von  Lingelsheim,  1906). 

5.  N.  pseudomeningitidis  (Elser  and  Huntoon,  1909). 

6.  N  .parameningitidis  (Dopter,  1909). 

7.  A  number  of  heterogeneous  strains,  separable  by  the  agglutina 
tion  and  absorption  tests  of  specific  immune  sera. 

These  various  strains  and  groups  can  be  differentiated  from  one 
another  by  the  tests  set  forth  in  the  following  diagnostic  table: — 

Diagnostic  Table  of  the  Genus  Neisseria  Trevisan,   18S5. 
Glucose  Agar. 


Pigment  absent. 
Glucose  and  maltose. 


Pigment  present 
(Flava  Group). 

Glucose  and  maltose  fermented 
saccharose. 


Only  glucose  fermented 
(Gonorrhoeal  Group). 

In  gonorrhoeal  infections. 
Separable  by  absorp- 
tion test. 
1.  GonorrhcecB. 


Both  fermented. 

Saccaatoseaad 

fructose. 
I 


Fermented. 

7.  E.  and 

H.*  (I). 


Neither  fermented        Both 
(Meningococcal       fermented. 
Group).  6.  Sicca. 

In  epidemic  cerebro- 
spinal infections. 
Separable'by  Castellani's  absorption  test. 

Specific  intracellularis 
agglutinins. 


No  change. 

I 
Fructose. 


Fermented. 
8.  Flava. 


No  change. 

9.  E.  and  H.* 
(HI). 


•  E  and  H.  =  Else 
and  Huntoon. 


Absorbed. 
2.  Intracellularis. 


Not  absorbed. 

Specific  pseudomeningitidis 
agglutinins. 


Absorbed. 


Not  absorbed. 


3.  Pseudomeningitidis.         Specific  parameningitidis 

agglutinins. 


Absorbed.  Not  absorbed. 

4.  Parameningitidis.  5.  Heterogeneous  Group. 


STREPTOCOCCUS  927 

Genus  Diplococcus  Weichselbaum,  1886,  emendavit  Winslow 
and  Rogers,  1905. 

Definition.— Streptococceae  usually  in  encapsulated  pairs,  forming 
acid  in  glucose,  lactose,  saccharose,  and  inulin.  Haemolysis  usually 
absent.  Characteristic  group  serum  reactions.  Soluble  in  bile  salts. 
Undergo  autolysis  in  cultures  and  in  emulsions  of  physiological  saline. 

Type  Species. — Diplococcus  pneumonia  Weichselbaum,  1886. 

Remarks. — The  genus  contains  the  organisms  associated  with 
pneumonia,  of  which  there  are  many  strains  separable  by  serum 
reactions.  The  genus  requires  further  study  before  a  definite 
classification  can  be  given. 

Two  groups  are  recognized — viz.,  those  which  exhibit  a  diplococcal 
form  and  are  usually  oval  or  lanceolate  in  shape  (Pneumonia  group), 
and  those  which  are  in  chains  and  rounded  in  form  (Mucosus  group) . 
These  groups  can  be  further  differentiated  by  seriological  tests  and 
by  complement  fixation. 

Genus  Streptococcus  Rosenbach,  1884,  emendavit  Winslow 
and  Rogers,  1905. 

Definition. — Streptococceae  parasitic  in  short  or  long  chains  or  pairs, 
forming  a  large  quantity  of  acid  in  fermented  sugars.  Haemolysis 
present  or  absent.     Without  characteristic  group  serum  reactions. 

Type  Species. — Streptococcus  erysipelatos  Fehleisen,  1883. 

Remarks. — Streptoccoci  are  frequently  found  in  disease  in  the 
tropics,  as  primary  agents  causing  the  pathological  changes,  and 
as  secondary  or  terminal  infections  in  the  course  of  illnesses  due  to 
other  causes. 

They  are  responsible  for  several  types  of  puerperal  fever,  of 
abscesses,  of  septicaemias  and  of  skin  diseases. 

Natural  Habitat. — Most  streptococci  are  found  as  parasites  (or 
saprophytes)  of  the  nose,  nasopharynx,  and  alimentary  canal  of 
vertebrate  animals,  but  they  can  also  be  found  in  the  alimentary 
tract  of  the  invertebrata,  and  apparently  also,  but  to  a  less  extent, 
living  on  or  in  plants. 

From  these  natural  homes  they  may  pass  to  air,  soil,  milk,  or 
water,  and  so  may  be  conveyed  from  one  animal  to  another,  as  they 
are  extremely  resistant  against  heat  and  drought. 

Thus  S.  salivarius  Andrewes  and  Horder,  1906,  lives  in  normal 
human  saliva;  S.  bovinus  Broadhurst,  1915,  in  bovine  faeces,  and 
is  found  in  the  cow-dung  plastered  on  walls  and  floors  of  native 
huts;  while  5.  versatilis  Broadhurst,  1915,  is  found  in  equine  and 
bovine  faeces. 

Researches  with  regard  to  certain  human  passages  have  shown 
how  quickly  these  become  infected  with  streptococci  after  birth. 

It  would  appear  that  man  quickly  obtained  his  normal  strepto- 
coccal flora  from  the  animals  by  which  he  is  surrounded,  and  that 
so  long  as  they  abide  in  their  natural  habitats  they  do  no  harm,  but 
if  they  depart  therefrom  they  become  pathogenic. 


92S  SCHIZOMYCETES 

Classification. — This  is  difficult,  and  perhaps  should  not  be  carried 
further  than  groups  which  may  be  recognized  as  follows: — 

Diagnostic  Table  of  Streptococcal  Groups. 

A.  Parasitic  on  plants.    Grow  in  broth  but  not  on  agar  or  gelatine — /.  Sphagni 

group. 

B.  Parasitic  in  animals.     Gro  v  in  broth  and  on  agar  and  usually  on  gelatine : — 

I.  Obligatory  anaerobes — II.  Fcetidus  group. 
II.  Aerobes,  facultative  anaerobes: — 

(a)  Pigment  present — III.  Sanguineus  group. 

(b)  Pigment  absent  : — 

i.  Gelatine  actively  liquefied — IV.  Gracilis  group . 
2.  Gelatine  usually  not  or  rarely  slightly  liquefied,  inulin  usually 
not  fermented: — 

(a)  Gas  produced — V.  Gasogenous  group. 

(b)  Gas  not  produced  : — 
Non-Fermenters  : — 

(a)  Glucose    and    other   sugar   media   not  fermented — 
VI.  Non-fermenting  group. 
Monosaccharide  Fermenters — Equine  Fcscal  Type  : — 

{b)  Glucose  usually   and    other  sugar    media   generally 

fermented, 
i.  Glucose    alone    or   with  saccharose   and  salicin,  but 
not  with  lactose,  fermented — VII.  Equine  group. 
Disaccharide  Fermenters — Human  F cecal  Type  .— 

2.  Lactose,   glucose,  saccharose,    and    salicin,    but    not 

mannitol  fermented — VIII.  Er y sip elatos  group. 

3.  Lactose,  glucose,  saccharose,   salicin,  mannitol,   and 

sometimes      raffinose      fermented  - — ■  IX.      Fcecalis 


Trisaccharide  Fermenters — Bovine  Fcecal  Type  : — 

4.  Raffinose,  lactose,  saccharose,  usually  glucose  some- 
times salicin  and  rarely  inulin,  but  not  mannitol 
fermented— X.  Salivarius  group. 

If  desired  the  investigation  can  be  extended,  but  in  our  experience 
only  Groups  II.,  VII.,  VIII.,  IX.,  and  X.  are  of  tropical  import- 
ance, and  therefore  we  shall  limit  our  remarks  to  them : — 

II.  Fcetidus  Group. 
Definition.- — Streptococcus  parasitic  in  animals,  obligatory  anae- 
robes growing  well  at  370  C,  and  poorly  or  not  at  all  at  20°  C.  :■ — 

I.  Foetid  gas  produced;    milk   usually  acidified  and  slowly  clotted — 
S.  fcetidus. 
II.  Foetid  gas  not  produced;  milk  unchanged — S.  anaerobius. 

Both  these  organisms  have  been  known  to  cause  puerperal  fever. 

VII.  Equine  Group. 
Definition. — Streptococcus  parasitic  in  animals,  aerobe  facultative 
anaerobe,  without  pigment,  not  liquefying  gelatine  nor  producing 
gas,  and  being  a  monosaccharide  fermenter.  Glucose,  salicin,  and 
usually  saccharose,  are  fermented,  but  not  lactose,  and  with  feeble 
or  no  growth  at  200  C.     Milk  not  clotted. 


EQUINE  GROUP  929 

Classification. — By  the  action  upon  raffinose  and  inulin  the  group 
may  be  divided  into  two  subgroups — i.e.,  a  typical,  in  which  these 
are  not  fermented,  and  an  atypical,  in  which  one  or  both  are  fer- 
mented. 

A.  Raffinose  and  inulin  not  fermented  and  neutral  red  not  reduced — 
Typical  subgroup. 
I.  Saccharose  fermented — S.  e^uinus. 

II.  Saccharose  not  fermented — Andrewes  and  Horder,  Winslow  and 
Palmer,  Broadhurst  (A),  Fuller  and  Armstrong. 
13.   Raffinose  or  inulin  fermented  or  neutral  red  reduced — Atypical  sub- 
group. 

We  have  found  S.  equinus  Andrewes  and  Horder,  1906,  in  a  case 
of  septicemia  in  the  tropics. 

VIII.  Erysipelatos  Group. 

Definition. — Streptococcus  parasitic  in  animals,  aerobe  facultative 
anaerobe,  without  pigment ;  does  not  liquefy  gelatine  or  produce 
gas;  ferments  lactose,  glucose,  saccharose,  and  salicin,  but  not 
mannitol  or  raffinose. 

Classification. — The  group  may  be  differentiated  into  strains  as 
follows: — ■ 

A.  Colonies  on  agar  large,  white,  and  opaque,  at  the  end  of  forty-eight  hours 

resembling  those  of  an  albococcus;  milk  clotted.     Haemolytic  action 
unknown — S.  puerperalis. 

B.  Colonies  on  agar  small,  translucent,  not  resembling,  at  the  end  of  forty- 

eight  hours,  those  of  an  albococcus: — 
I.  Haemolysis  present: — ■ 
(a)  Milk  clotted : — 

1 .  Some  kind  of  a  capsule  present,  colonies  on  agar  typical 

— S.  epidemicus. 

2.  Capsule  absent,  growth  on  agar  may  be  absent  or  in  the 

form  of  very  fine  or  at  times  watery  colonies,   but 
typical  on  ascitic  agar — S.  equi. 
{b)   Milk  not  clotted:—. 

Capsule  absent,  colonies  on  agar  typical: — 

1 .  Found  in  cases  of  erysipelas — 5.  erysipelatos. 

2.  Found  in  dermatitis  cupoliformis — 5.  tropicalis. 
II.  Haemolysis  absent: — 

(a)  Milk  clotted — S.  mitiov. 

(b)  Milk  not  clotted — S.  mitis. 

S.  puerperalis  Fur neaux- Jordan  and  Mackay,  1912,  was  found  in 
twenty-one  cases  <>t  puerperal  fever  in  England. 

S.  equi  Schutz,  1888,  is  the  same  as  S.  coryzce  contagiosa  equorum 
Eisenberg,  and  as  5.  equi  Capelletti-Vivaldi,  1899,  and  S.  capellettii 
Chester,  1901,  and  causes  strangles,  etc.,  or  adenitis  in  horses. 

S.  erysipelatos  Fehleisen,  1883,  is  the  type  species  of  the  genus 
Streptococcus.  It  is  the  same  as  S.  pyogenes  Rosenbach,  1884,  and 
S.  puerperalis  Arloing,  1884,  and  it  may  be  the  same  as  S.  puerperalis 
Furne.iux- Jordan  and  Mackay,  though  there  are  differences. 

S.  tropicalis  Castellani,  1914,  is  the  cause  of  Dermatitis  cupoli- 
formis, which  is  a  type  of  tropical  ecthyma  (see  p.  2034). 

59 


93°  SCHIZOMYCETES 

It  may  be  that  S.  mitior  Schottmiiller,  1903,  is  the  same  as  S. 
mitis  Andrewes  and  Horder,  iqo6.  It  has  been  found  in  cases  of 
puerperal  fever. 

IX.  Fjecaijs  Group. 

Definition. — -Streptococcus  parasitic  in  man,  facultative  anaerobe, 
growing  in  broth  and  upon  agar  and  blood  serum  without  the  forma- 
tion of  pigment,  and  well  upon  gelatine  at  220  C,  without  producing 
liquefaction;  fermenting  glucose,  saccharose,  lactose,  mannitol, 
and  salicin;  sometimes  raffinose,  but  typically  not  inulin,  and  gener- 
ally, but  not  always,  clotting  milk ;  variable  as  regards  neutral  red 
reduction  and  sulphuretted  hydrogen  formation,  and  usually  pro- 
ducing relatively  large  amount  of  acidity  in  glucose  media  tested 
quantitative^. 

Remarks. — This  is  an  important  pathogenic  group  in  the  tropics, 
being  found  in  all  sorts  of  conditions.  Its  various  strains  may  be 
differentiated  as  follows: — 

A.  Glucose,    saccharose,    lactose,    salicin,    and    mannitol    fermented — 

Typical  subgroup. 
I.  Raffinose  not  fermented- — S.fcecalis  Andrewes  and  Horder,  1906. 
II.  Raffinose  fermented — S.  versatilis  Broadhurst,  1915. 

B.  Suppression  of  one  of  the  characters  of  the  typical  subgroup  or  with 

the  addition  of  the  fermentation  of  inulin — Atypical  subgroup. 
I.  Raffinose  not  fermented — Variants  of  S.  fcecalis. 
II.  Raffinose  fermented — Variants  of  S.  versatilis. 

X.  Salivarius  Group. 

Definition. — Streptococcus  parasitic  in  animals,  facultative  anae- 
robe, growing  in  broth  and  on  agar  without  pigment  or  gas  forma- 
tion, with  slight  or  no  growth  at  22°  C.  in  gelatine  which  is  not 
liquefied,  and  capable  of  fermenting  glucose,  saccharose,  lactose, 
and  raffinose;  may  ferment  inulin,  but  not  mannitol,  and  generally 
capable  of  clotting  milk.  Habitat,  human  saliva,  human  fseces, 
bovine  and  equine  faeces. 

Classification.— -This  group  can  be  divided  into  a  typical  sub- 
group, and  an  atypical  subgroup  containing  varieties  of  the  typical 
group,  in  which  there  is  suppression  of  some  important  character, 
which  is  not  inulin  fermentation. 

Typical  Subgroup. — Glucose,  saccharose,  lactose,  and  raffinose,  and  at 
times  inulin  fermented. 

A.  Salicin  not  fermented: — 

I.  Haemolysis  marked — S.  anginosus. 
II.  Haemolysis  absent — S.  salivarius. 

B.  Salicin  fermented : — 

I.  Haemolysis  marked — S.  acluosus. 
II.  Haemolysis  absent — S.  bovinus. 
Atypical  Subgroup. — Contains  varieties  of  S.  anginosus,  S.  salivarius, 
S.  acluosus,  and  5.  bovinus,  in  which  there  is  suppression  of  some  character 
but  as  these  suppressions  are  generally  only  temporary  it  is  not  necessary  to 
specially  characterize  them. 

Remarks. — These  streptococci  are  frequently  found  in  sore  throat 
and  other  infections  in  the  tropics. 


AUROCOCCUS  93  r 

Shottmuller's  Classification  of  the  Genus  Streptococcus. — This  is 
very  simple,  and  is  based  on  the  characters  of  colonies  on  blood-agar  plates. 

i.  Colonies  surrounded  by  a  clear  zone  of  haemolysis — S.  hamolyticus 
(  =  S.  pyogenes  =  S.  erysipelatos=S.  erysipelatosus). 

2.  Colonies  not  surrounded  by  a  clear  zone  of  haemolysis;  of  a  peculiar 
greenish  colour — S.  viridans  (  =  S.  mitior). 

3.  Colonies  whitish,  slimy,  somewhat  adherent  to  the  medium  (cocci 
capsulated) — S.  mucosus. 

Genus  Aurococcus  Winslow  and  Rogers,  1905. 

Definition. — Streptococceae  parasitic,  producing  pigment,  and  in 
irregular  groups  or  in  non-capsulated  groups  of  four,  or  in  pairs,  but 
never  in  zooglcea  masses.  Growth  good.  Sugars  fermented  with 
formation  of  a  moderate  amount  of  acid,  but  no  gas.  May  or  may 
not  reduce  nitrates  and  liquefy  gelatine. 

Type  Species. — Aurococcus  aureus  (Rosenbach,  1884). 

Classification. — Winslow  and  Rogers,  after  a  long  discussion  of 
synonyms,  have  recognized  only  three  types,  which  may  be  differen- 
tiated as  follows: — 

A.  Nitrates  not  reduced : — 

(1)  Gelatine  strongly  liquefied — Aurococcus  aureus  (Rosenbach,  1884). 

(2)  Gelatine  not  liquefied — Aurococcus  aurantiacus  (Cohn,  1872). 

B.  Nitrates  reduced: — ■ 

(3)  Gelatine  may  or  may  not  be  liquefied — Aurococcus  mollis  (Dyar 

1895). 

Remarks. — This  group  is  of  great  interest  in  the  tropics,  as  its 
members  are  the  cause  of  boils  and  pyosis  in  various  parts — e.g., 
Aurococcus  mollis  causes  Nile  boils  and  pyosis  Corletti. 

With  regard  to  '  pyosis  Mansoni,'  Castellani  in  Ceylon  showed  it 
to  be  caused  by  a  species  of  aurococcus,  which  Clegg  and  Wherry 
in  1906  called  Micrococcus  pemphigicontagiosi,  which  seems  to  be 
the  same  as  that  named  Micrococcus  pemphigineonatorum  by 
Almquist  in  1901,  and  both  may  be  Aurococcus  mollis.  Aurococcus 
tropicus  Chalmers  and  O'Farrell,  1913,  found  in  Castellani's 
'  pyosis  tropica,'  appears  to  be  different,  as  its  vaccine  was  without 
effect  on  a  case  of  Nile  Boils,  but,  unfortunately,  it  was  not  possible 
to  test  it  on  nitrates  and  gelatine. 

TRIBE  II.   MICROCOCCEiE  Trevisan,    1889,   emendavit  Winslow  and 

Rogers,   1905. 

Genus  Rhodococcus  Winslow  and  Rogers,  1905. 

Definition.— Micrococceae,  usually  saprophytes,  rarely  parasites, 
with  cells  in  groups  or  regular  packets.  Generally  more  or  less 
decolourized  by  Gram.  Growth  on  agar  abundant,  with  the 
formation  of  red  pigment.  Very  slight  fermentative  action. 
Gelatine  rarely  liquefied.     Generally  reduce  nitrates  to  nitrites. 

Type. — Rhodococcus  roseus  (Fliigge,  1886),  emendavit  Dyar,  1895. 

Remarks. — Winslow  and  Rogers  recognize,  in  addition  to  the 
type,  R.  fulvus  Cohn,  1875,  and  they  leave  the  rest  in  groups  to 
await  further  investigation. 

We  add   Rhodococcus  castellanii,   discovered  by  Castellani  and 


932  SCHIZOMYCETES 

which  Chalmers  and  O'Farrell  in  1913  named  and  more  fully  de- 
scribed. It  is  found  in  Trichomycosis  rubra,  and  we  differentiate  the 
three  species  as  follows:— 

A.  Does  not  ferment  glucose — Castellanii. 

B.  Produces  slight  acidity  in  glucose: — 

I.  Nitrates  reduced  to  nitrites — Roseus. 
II.  Nitrates  not  reduced — Fulvus. 

Genus  Nigrococcus  Castellani  and  Chalmers,  1918. 

Definition. — Micrococcese  saprophytic,  rarely  parasitic,  produc- 
ing black  or  bluish -black  pigment. 

Type. — Nigrococcus  nigrescens  (Castellani,  191 1). 

Classification.- — -The  type  is  found  in  Trichomycosis  nigra,  along 
with  Cohnistreptothrix  tenuis  Castellani;  other  forms  are  N.  fuscus 
Adametz  (1888),  in  water;  N.  cyaneus  Schroeter,  1870,  in  air 
and  water;  and  they  may  be  differentiated  as  follows:- — 

A.  Gelatine  liquefied — Fuscus. 

B.  Gelatine  not  liquefied: — ■ 

I.  Pigment  indigo  blue — Cyaneus. 
II.  Pigment  black — Nigrescens. 

iNCERTiE    SEDIS. 

The  so-called  Micrococcus  melitensis  Bruce,  1886,  which  is  the 
causal  agent  in  Mediterranean,  Malta,  or  undulant  fever,  is  difficult 
to  classify,  because  elongated  forms  are  seen  at  times  in  cultures, 
and  because  it  seems  to  have  no  affinity  with  the  Gram-negative 
cocci;  but,  on  the  other  hand,  is  very  like  the  typhoid-colon  group  of 
organisms  in  certain  respects.  It  does  not  ferment  sugars,  nor 
produce  indol;  does  not  liquefy  gelatine,  nor  show  polar-staining; 
while  milk  becomes  alkaline. 

FAMILY  BACILLACE^E  Fischer,  1894. 

Definition. — -Eubacteriales  with  cells  long  or  short,  flagellate  or 
non- flagellate,  sporogenous  or  non  sporogenous,  but  always  cylin- 
drical and  straight.     They  divide  in  one  direction  only. 

Type  Genus.— Bacillus  Cohn,  1872. 

Remarks.— The  enormous  numbers  of  species  and  varieties 
gathered  together  under  the  names  Bacterium  and  Bacillus  form 
such  an  unwieldy  mass,  that  we  have  endeavoured  to  simplif}^ 
matters  by  formulating  a  number  of  tribes  with  genera. 

Classification.— The  family  '  Bacill  aceas '  may  be  classified  into 
tribes  as  follows : — ■ 

Growth,  in  ordinary  laboratory  media: — 

A.  Entirely  or  almost  entirely  absent — Tribe  1,  Nitrobacterecz. 

B.  Poor,  Gram-negative,  grow  best  on  blood  media— Tribe  2,  Hamo- 

philea. 

C.  Extremely  slow  and  scanty  growth  on  ordinary  and  blood  media — 

Tribe  3,  Graciloidece. 

D.  Growth  good: — 

I.  Endospores  present — Tribe  4,  Bacilleee. 

II.  Endospores  absent: — 


BACILLACEM  933 

(a)  Fluorescent  or  chromogenic — Tribe  5,  Bacteridiecs. 

(b)  Neither  fluorescent  nor  chromogenic : — 

1.  Obligatory  anaerobes — -Tribe  6,  BacteroidecB. 

2.  Aerobes  often  facultative  anaerobes: — 

(1)  Gelatine  liquefiers- — Tribe  7,  Protecs. 

(2)  Gelatine  non-liquefiers : — 

(i.)  Without  capsules : — ■ 

(a)  With  polar  staining — Tribe  8,  Pasleurellece. 

(b)  Without  polar  staining — Tribe  g,  Eberthece. 
(ii.)  With  capsules — Tribe  10,  Encapsulates. 

THE  TRIBES. 
This  is  obviously  not  the  place  to  enter  into  a  prolonged  discussion 
with  regard  to  these  tribes,  but  in  order  that  there  may  be  no  doubt 
as  to  our  meaning,  we  give  the  following  table  showing  the  type 
genus  and  type  species  which  we  propose  for  each  tribe  : — 


Tribe. 

Type  Genus. 

Type  Species. 

Original  Name  of  Type 
Species. 

Nitro- 
bacterieae. 

Nitrobacterium 
Castellani  and 
Chalmers,  1918. 

Nitrobacterium 

nitrobacter 

(Winogradsky,  1892). 

Nitrobacter 
Winogradsky,  1892. 

Haemo- 
phileae. 

Hemophilus 

Castellani  and 

Chalmers,  191 8. 

Hemophilus 

influenza 

(Pfeiffer,  1892). 

Bacillus  of 

influenza, 

Pfeiffer,  1892. 

Graciloidese. 

Graciloides 
Castellani. 

Graciloides 
albofaciens. 

Bacillus  albofaciens 
Castellani,  1904. 

Bacilleae. 

Bacillus 
Cohn,  1872, 
pro  parte. 

Bacillus  subtilis 
(Ehrenberg,  1833). 

Vibrio  subtilis 
Ehrenberg,  1833. 

Bacteri- 
dieae. 

Bacteridium 

Schroeter, 
1872. 

Bacteridium 

prodigiosum 

(Ehrenberg,  1838). 

Monas  prodigiosa 
Ehrenberg,  1838. 

Bacter- 

oideae. 

Bacteroides 
Castellani  and 
Chalmers,  19 18. 

Bacteroides 

fragilis 

Veillon  and  Zuber. 

Bacillus  fragilis 
Veillon  and  Zuber. 

Pro  tea*. 

Proteus 
Hauser,  1885. 

Proteus  vulgaris 
Hauser,  1885. 

Proteus  vulgaris 
Hauser,  1885. 

Pasteur- 
elleae. 

Pasteurella 

Toni  and 

I'nvisan,  1S89. 

Pasteurella  galling 
Toni  and  Trevisan, 
1889. 

Microbe  du  cholera 

des  Poles, 

Pasteur,  1880. 

Ebertheae. 

Eberthus 
Castellani  and 
Chalmers,  19 18. 

Eberthus  typhosus 
Zopf,  1885. 

Bacillus  of  Eberth 
auctores. 

Encapsu- 
late*. 

Encapsulatus 
Castellani   and 
Chalmers,  191 8. 

Encapsulatus 

pneumonia 

(Friedlaender,   1883). 

Pneu  mo  coccus. 
The  micrococcus  of 

pneumonia. 
Friedlaender,  1883. 

934  SCHIZOMYCETES 

Of  all  these,  the  most  important  from  our  present  point  of  view  is 
Eberthece,  which  contains  many  intestinal  organisms. 

TRIBE  ENCAPSULATED  Castellani  and  Chalmers,   1918. 

Definition. — Bacillaceae  growing  well  on  ordinary  laboratory 
media,  without  endospores;  neither  fluorescent  nor  chromogenic 
aerobes,  not  liquefying  gelatine,  possessing  capsules  in  animal  tissues. 

Type  Genus. — Encapsulahis  Castellani  and  Chalmers,  1918. 

Genus  Encapsulatus  Castellani  and  Chalmers,  1918. 

Definition.— Encapsulates  with  the  tribal  characters. 

Type  Species. — Encapsulatus  pneumonia  (Friedlaender,  1883). 

Remarks.— This  genus  is  the  only  one  at  present  in  the  tribe,  and 
it  includes  the  old  group  of  encapsulated  bacilli  which  have  been 
reviewed  by  Fricke  in  1896,  Clairmont  in  1902,  Perkins  in  1904,  Abel 
and  Hallwacks  in  1912,  and  Fitzgerald  in  1914. 

The  species  are  mostly  short,  non-motile,  Gram-negative,  en- 
capsulated pleomorphic  organisms,  which  ferment  glucose  and 
lactose;  but  as  regards  the  latter  sugar,  they  may  give  rise  to  acid 
only,  though  more  usually  they  form  acid  and  gas. 

Classification. — The  various  species  of  this  genus  may  be  recognized 
as  follows: — ■ 

A.  Glucose  completely  fermented  with  the  formation  of  acid  and  gas; 

lactose  fermented  partially  with  the  formation  of  acid,  but  no  gas. 
Milk  clotted — Pneumoniae. 

B.  Glucose  and  lactose  completely  fermented  with  the  formation  of  acid 

and  gas.     Milk  clotted: — 
I.  Inosite  not  fermented — Acidi  laciici. 
II.  Inosite  fermented  with  the  formation  of  acid  and  gas — Lactis- 
aerogenes. 

TRIBE  EBERTHE.E  Castellani  and  Chalmers    1918. 

Definition. — -Bacillaceae  growing  well  on  ordinary  laboratory 
media;  not  forming  endospores,  aerobes,  and  often  facultative  anae- 
robes; without  fluorescence,  pigment  formation,  or  gelatine  lique- 
faction; without  polar  staining;  Gram-negative,  without  a  capsule. 

Type  Genus.— Eberthus  Castellani  and  Chalmers,  1918. 

Classification. — 'The  tribe  may  be  divided  into  genera,  which  may 
be  recognized  as  follows:— 

A.  Glucose  and  lactose  either  not  at  all  or  only  partially  fer- 
mented with  the  production  of  acid,  but  no  gas : — 

I.  Milk  not  clotted  :— 

(a)  Glucose  and  lactose  not  fermented — Genus   1,   Alcaligenes 

Castellani  and  Chalmers,  1918. 

(b)  Glucose   partially  fermented  with  the   production  of  acid 

and  no  gas ;  lactose  not  fermented : — 

1.  Motile — Genus  2,  Eberthus  Castellani  and  Chalmers,  1918. 

2.  Non-motile — Genus  3,  Shigella  Castellani  and  Chalmers, 

1918. 

(c)  Lactose  and  glucose  partially  fermented  with  the  production 

of  acid,  but  no  gas — Genus  4,  Dysenteroides  Castellani  and 
Chalmers,  1918. 


eiieutuem 


935 


II.  Milk  clotted  ;— 

Glucose  partially  fermented  with  the  production  ot  acid,  but  no 
gas;  lactose  not  fermented  (no  gas  in  any  sugar) — Genus  5, 
Lankoides  Castellani  and  Chalmers,  191 8. 

B.  Glucose  completely  fermented  with  the  production  of  acid  and  gas; 

lactose  not  fermented : — 
I.   Milk    not    clotted — Genus    6,    Salmonella  Lignieres,    emendavit 

Castellani  and  Chalmers,  19 18. 
I  I .  Milk  clotted — Genus  7,  Balhanella  Castellani  and  Chalmers,  191 8. 

C.  Glucose  completely  fermented  with  the  production  of  acid  and  gas; 

lactose  partially  fermented  with  the  production  of  acid  and 
no  gas : — 
I.  Milk  not  clotted — Genus  8,  Wesenbergus  Castellani  and  Chalmers, 
1918. 

D.  Glucose  and  lactose  completely  fermented  with  the   production  of 

acid  and  gas: — 
I.  Milk  not  clotted — Genus  9,  Enteroides  Castellani  and  Chalmers, 
1918. 
II.  Milk  clotted—Genus   10,  Escherichia  Castellani  and  Chalmers, 
1918. 

In  order  to  be  quite  definite,  we  give  the  following  table  showing 
the  type  species  for  each  genus : — 


Genus. 

Type  Species. 

Original  Name  of  the 
Type  Species. 

Alcaligenes. 

A  Icali genes  facalis 
(Petruschky,  1896). 

Bacillus  jcecalis 

alkaligenes 

Petruschky,  1896. 

Eberthus. 

Eberthus  typhosus 
(Zopf,  1885). 

Bacillus  of  Eberth 
auctores. 

Shigella. 

Shigella  dysenteric 
(Kruse,  1899). 

Bacillus  dysenteric 
Kruse,  1899. 

Lankoides. 

Lankoides  pyogenes 
(Passet,  1902). 

Bacillus  pyogenes  fcetidus 
Passet,  1902. 

Dysenteroides. 

Dysenteroides 

metadysenlericus 
(Castellani,  1917). 

Bacillus  metadysenlericus 
Castellani,  1904. 

Salmonella. 

Salmonella  paratyphi 
(Schottmiiller,  1902). 

Bacillus  paratyphosus  A 
Schottmidler,  1902. 

Balkanella. 

Balhanella  coagulans 
(Castellani,  1916). 

Bacillus  coagulans 
Castellani,  19 16. 

Wesenbergus. 

Wesenbergus  wesenbergi 
(Castellani,  191 3). 

Bacillus  ivesenberg 
Castellani,  19 13. 

Enteroides. 

Enteroides  entericus 
(Castellani,  1907). 

Bacillus  entericus 
Castellani,  1907. 

Escherichia. 

Escherichia  colt 
(Escherich,  1886). 

Bacterium  coli  commune 
Escherich,  1886. 

9  3<>  SCHIZOMYCETES 

Genus  Alcaligenes  Castellani  and  Chalmers,  1918. 

Definition. — Ebertheae  which  do  not  ferment  glucose  or  lactose, 
and  are  characterized  by  their  general  lack  of  fermentative  power 
and  by  actually  increasing  the  alkalinity  of  the  media.  Milk  is 
not  clotted,  and  is  rendered  alkaline. 

Type.— Alcaligenes  fcecalis  (Petruschky,  1896),  emendavit  Castel- 
lani and  Chalmers,  1918. 

Here  also  comes  Alcaligenes  vivax  (Archibald,  1918),  which  was 
obtained  from  the  blood  of  a  case  of  enteroideain  the  Anglo-Egyptian 
Sudan,  produced  acidity  in  galactose  and  mannitol  and  was  charac- 
terized by  its  marked  motility. 

Classification. — These  various  organisms  can  be  differentiated 
as  follows : — 

A.  Non-motile — Metalkaligenes. 

B.  Motile: — 

I.  No  acidity  in  any  sugar — Fcecalis. 
II.  Acidity  in  mannitol — Vivax. 

Genus  Eberthus  Castellani  and  Chalmers,  1918. 

Definition.— Bacillacese  motile,  partially  fermenting  glucose  with 
the  production  of  acid  and  no  gas.  Lactose  not  fermented.  Milk 
not  clotted. 

Type  Species. — Eberthus  typhosus  (Zopf,  1885). 

Remarks. — This  genus  has  as  its  type  species  the  organism  which 
causes  that  variety  of  enteric  fever  which  is  called  typhoid  fever, 
as  well  as  a  number  of  species  which  are  the  causal  agents  of  forms 
of  enteroidea. 

Classification. — The  genus  contains  the  following  species,  in 
addition  to  the  type: — -E.  kandiensis  Castellani,  E.  lalavensis 
Castellani,  E.  priztnitzi  Castellani. 

They  may  be  differentiated  biochemically  as  follows,  though  they 
can  be  distinguished,  in  addition,  by  their  serological  reactions  : — 

Mannitol. 


Acid.  No  change. 

I  I 

Maltose.  Saccharose. 


Arid.  No  change.  Acid.  No  change. 

Typhosus.  Kandiensis.  Talavensis.  Priztnitzi. 

Genus  Shigella  Castellani  and  Chalmers,  1918. 

Definition. — -Ebertheae  non-motile,  partially  fermenting  glucose 
with  the  production  of  acid,  but  no  gas;  lactose  not  fermented. 
Milk  not  clotted. 

Types.— Shigella  dysenteric?  (Kruse,  1899). 

Remarks.— This  genus  includes  a  number  of  forms  which  are 
,is<.ociated  with  bacillary  dysentery,  but  in  going  through  those 
which  have  been  described,  we  have  rejected  all  with  very  imperfect 
descriptions  which  will  never  permit  of  their  recognition. 


FLEXNERELLA 


937 


Classification. — -The  species  belonging  to  this  genus  may  be  divided 
for  purposes  of  recognition  into : — ■ 

A.  Mannitol  fermented — Subgenus  Flexnerella  (Flexner  group  sensfi  lata) . 

I.  Maltose  fermented — Flexner  group. 
II.  Maltose  not  fermented — Pseudodysentery  group. 

B.  Mannitol  not  fermented — Subgenus  Shigella. 

The  forms  belonging  to  these  divisions  and  sections  may  be  re- 
cognized by  the  following  tables : — ■ 

Subgenus  Flexnerella  Castellani  and  Chalmers,  1918. 

(Mannitol  Partial  Fermenters.) 
Flexner  Group:  Maltose  Partial  Fermenters. 

Milk. 


Acid  then  alkaline. 

1 
Sorbitol. 

Alkaline  only. 
Fescaloides. 

No  change. 
Flexneri. 

i 
Acid. 

1 
Salicin. 

1 

Acid. 
Tangallensis. 

No  change. 

Dysenteries. 
Strong. 

Subgenus  Flexnerella  Castellani  and  Chalmers,  1918. 

(Mannitol  Partial  Fermenters.) 

Pseudodysentery  Group  :  Maltose  Non-Fermenters. 

Dextrin. 


Acid. 
Salicin. 


No  change. 

I 
Salicin. 


r  1  1  1 

V  nl.  No  change  No  change.  Acid. 

PsendodysentericB       S.  dysenteries  Hiss      P seudodysenterics    Pseudo dysenteries 
var.  Dj.  and  Russell.  var.  D2.  var.  A. 

Shiga- Kruse  Division:  Mannitol  not  Fermented. 

Milk. 


Acid  then  alkaline. 
Arabinose. 


No  change. 

Dysenteries 

Shiga- Kruse. 


Acid. 
Lunavensis. 


Permanently  acid. 

Shiga  serum  agglutination. 

Negative. 
Paradysenteries. 


938  5CHIZ0MYCETES 

Genus  Lankoides  Castellani  and  Chalmers,  1918. 

Definition. — Eberthese  fermenting  glucose  partially  with  the 
production  of  acid,  but  no  gas;  lactose  not  fermented  or  only 
partially,  without  gas  production.     Milk  clotted. 

Type  Species. — Lankoides  pyogenes  (Passet,  1902). 

Classification. — The  species  classified  in  this  genus  may  be  re- 
cognized as  follows : — ■ 

Motility. 


Present.  Absent. 

Pyogenes. 


Mannitol. 


No  change.  Acid. 

Galactose.  Dulcitol. 


No  change.  Acid.  Acid.  No  change. 

Ceylonensis  var.  A.  Gintottensis.  Madampensis. 

Ceylonensis  var.  B. 

Genus  Dysenteroides  Castellani  and  Chalmers,  1918. 

Definition. — -Eberthea?  fermenting  glucose  and  lactose  partially, 
with  the  production  of  acid,  but  no  gas.     Milk  not  clotted. 

Type  Species.— Dysenteroides  ntetadysentericiis  (Castellani,  1917). 

Remarks.— This  genus  contains  the  organisms  of  the  Meta- 
dysenteric  group,  which  may  be  differentiated  as  follows:— 

Mannitol. 


Acid.  No  change. 

Dulcitol.  Indol. 

I  I 

I  III 

Acid.  No  change.  Produced.  Not  produced. 

Metadysentericus  Metadysentericus      Metadysentericus        Metadysentericus 
var.  D.  var.  A.  var.  B.  var.  C. 

Genus  Salmonella  Lignieres,   emendavit  Castellani  and   Chalmers, 

1918. 

Definition.— Ebertheae  which  completely  ferment  glucose,  but 
do  not  ferment  lactose,  and  partially  or  completely  ferment  manni- 
tol, in  addition  to  other  carbohydrates.     Milk  not  clotted. 

Type  Species. — Salmonella  paratyphi  (Schottmuller,  1902). 

Remarks. — 'This  genus  contains  a  large  number  of  species, 
which  may  be  divided  into  groups  as  follows: — 


VEBODA  GROUP  939 

A.  Mannitol  not  fermented — Morgan  group. 

B.  Mannitol  partially  fermented  with  the  production  of  acid,  but  no  gas 

- —  Veboda  group. 

C.  Mannitol  completely  fermented  with  the  production  of  acid  and  gas — 

Paratyphoid- A  siaticus  group. 

The  Morgan  group  only  contains  Salmonella  morgani,  which  is  the 
same  as  Morgan  I.  of  older  nomenclature. 

Veboda  Group. 
This   group   contains    two   organisms- — -viz.,    Salmonella   veboda 
Castellani,  1909,  and  S.  willegoda  Castellani,  1911.     They  may  be 
distinguished  as  follows: — 

Dulcitol. 


Acid  and  gas.  Acid. 

I  I 

Salicin.  Salicin. 

I  I 

No  change.  Acid  and  gas. 

Veboda.  Willegoda. 

Paratyphoid-Asiaticus  Group. 
This  group  contains  a  number  of  forms,  some  of  which  are  of 
tropical  importance.     It  may  be  classified  as  follows: — 

A.  Indol  not  produced — Paratyphoid  division. 

B.  Indol  produced — Asiaticus  division. 

The  first  subgroup  contains  S.  paratyphi  A,  S.  paratyphi  B, 
S.  aertrycke,  S.  wolinice.  The  term  S.  paratyphi  C  has  been  applied 
by  various  authors  to  indicate  different  germs,  one  of  which  is 
identical  serologically  with  5.  enteritidis. 

Paratyphoid  Division  :  Indol  Non-Producers. 
Milk. 


Permanently  acid.  Becomes  alkaline  after  a  time. 

I  I 

Paratyphi  Gaertner  serum. 
—  D.  paratyphosus  A. 

No  agglutination.  Agglutination. 

Castellani 's  absorption  test  Enteritidis  Gaertner 

with  Paratyphosus  B.  serum.  —  B.  danysz. 


Agglutinins  absorbed.  Agglutinins  not  absorbed. 

Paratyphi  B.  \ 

=B.  paratyphosus  B.  Dulcitol. 

_J 

G  is.  No  gas. 

Aertrycke  Woliitics. 

=  Suipestifer 
=  Psittacosis 
—  Typhimurium  (p.p.). 


940  SCHIZOMYCETES 

Asiaticus  Division:  Indol  Formers. 
Saccharose. 


I  I 

No  change.  Acid  and  gas. 

I  I 

Voges-Proskauer.  Salicin. 


Positive.  Negative.  Acid  and  gas.         No  change. 

Atchibaldi  Castellani  Pseudo-asiatica 

and  Chalmers.  Carolina  Castellani.  Motility. 

Castellani. 

Present.  Absent. 

Asiatica  var.  mobilis  Asiatica 

Castellani.  Castellani. 

Genus  Balkanella  Castellani  and  Chalmers,  1918. 

Definition. — Ebertheae  which  ferment  glucose  completely  with  the 
production  of  acid  and  gas;  lactose  not  fermented.     Milk  clotted. 

Type  Species.— Balkanella  coagulans  Castellani,  1916. 

Remarks. — There  are  two  species — -viz.,  the  type  and  B.  caroli- 
noldes  Castellani — -which  may  be  separated  as  follows : — ■ 

Saccharose. 


No  change.  Acid  and  gas. 

Coagulans.  Carolinoides. 

Genus  Wesenbergus  Castellani  and  Chalmers,  1918. 

Definition.— Ebertheae  which  ferment  glucose  completely  and 
lactose  partially,  producing  acid,  but  no  gas.     Milk  not  clotted 

Type  Species. — Wesenbergus  wesenbergi  Castellani,  191 3. 

Remarks. — The  type  described  by  Castellani  is  motile,  and  pro- 
duces acidity  in  litmus  milk.  It  forms  acid  and  gas  in  glucose  and 
saccharose,  but  only  acid  in  lactose,  mannitol,  and  dulcitol.  It  is 
an  indol  producer. 

To  the  same  group  belongs  Wesenbergus  giumai  Castellani,  which 
is  non-motile. 

Archibald  in  the  Anglo-Egyptian  Sudan  obtained  an  organism 
of  this  type  from  the  blood  of  a  case  of  enter oidea  in  Khartoum  on 
the  fifth  day  of  the  illness.  It  was  motile,  formed  acid  and  gas  in 
glucose,  galactose,  and  rhamnose  (iso-dulcite),  dextrin,  starch, 
mannitol,  and  sorbitol,  but  only  acid  in  lactose,  levulose,  maltose, 
and  dulcitol,  while  it  failed  to  ferment  saccharose,  raffinose,  inulin, 
salicin,  glycerol,  erythrol,  or  adonitol.  It  did  not  produce  indol, 
gave  a  negative  Voges-Proskauer  reaction,  but  reduced  nitrates  and 
neutral  red.  Specific  serum  reactions  separated  it  from  Eber thus 
typhosus,  Salmonella  paratyphi,  S.  paratyphosa,  and  5.  gaertneri, 
and  it  was  well  agglutinated  by  the  patient's  serum  during 
convalescence.     We  name  it  Wesenbergus  fermentosus. 

Readers  interested  in  this  group  will  find  some  strains  described 


ENTEROIDES  941 

by  Alexander  in  1914  in  the  supplement  to  the  Annual  Report  of 
the  Local  Government  Board,  which  may  well  be  classified  here. 
The  named  species  may  be  separated  as  follows : — 

A.  Indol  produced  : — 

I.  Dulcitol  fermented — Wesenbergi. 
II.  Dulcitol  not  fermented — Giumai. 

B.  Indol  not  produced — Fermentosus. 

Genus  Enter oides  Castellani  and  Chalmers,  19 18. 

Definition. — Ebertheae  which  ferment  glucose  and  lactose  com- 
pletely with  the  production  of  acid  and  gas.     Milk  not  clotted. 

Type  Species. — Enteroides  entericus  (Castellani,  1907). 

Remarks. — Castellani  isolated  two  organisms  from  cases  of  enter- 
oidea  and  appendicitis  in  Ceylon — viz.,  the  type  and  E.  paraentericus 
— -and  later  found  another,  E.  vekanda,  in  the  Balkans. 

Chalmers  and  Macdonald  obtained  E.  khartoumensis  from  cases 
of  enteroidea  in  the  Anglo-Egyptian  Sudan. 

Classification. — The  various  species  of  the  genus  may  be  recog- 
nized as  follows: — 

Adonitol. 
1 

No  change.  Acid  and  gas. 

I  !  . 

Saccharose.  Salicm. 
I        I 


No  ga-.  Gas.  No  change.         Acid  and  gas. 

Entericus.  Paraentericus.  Vekanda.         Khartoumensis. 

Genus  Escherichia  Castellani  and  Chalmers,  1918. 

Definition. — Ebertheae  which  ferment  glucose  and  lactose  com- 
pletely; milk  clotted. 

Type  Species.— Escherichia  coli  (Escherich,  1886). 

Classification. — The  number  of  species  gathered  together  under 
this  genus,  even  after  the  rejection  of  those  so  imperfectly  described 
that  they  cannot  be  classified,  is  so  large  that  they  require  to  be 
divided  into  groups  and  sections  as  follows:- — 

A.  Indol  produced — Smith's  indol  division. 

I.  Saccharolytic — Communior  section. 
II.  Non-saccharolytic — Communis  section. 

B.  Indol  not  produced — Smith's  non-indol  division. 

We  recognize  the  mistake  which  has  been  made  with  regard 
to  the  organism  called  Coscoroba,  which,  as  originally  described, 
belongs  to  the  genus  Pasteur ella — i.e.,  among  the  hemorrhagic 
septicaemias,  being  a  cause  of  disease  and  death  in  swans.  By  some 
mistake,  years  ago  quite  a  different  organism  belonging  to  the  Colon 
group  received  this  name.  In  order  to  prevent  confusion,  we  pro- 
pose to  call  the  Colon  type  of  Coscoroba  by  the  name  Escherichia 
pseudocoscoroba  Castellani  and  Chalmers,  1918.  The  species  may 
be  recognized  as  follows: — 


942 


SCHIZOMYCETES 


Smith's  Indol-Producing  Division. 

Durham's  Saccharolytic  Commnnior  Section. 

Dulcitol. 


Acid  and  gas.                                          No  change. 

I                                                                 1 
Adonitol.                                                Motility. 

1 

Acid  and  gas. 

1 
Motility. 

No  cr 
Moti 

1                                    1 
tange.               Present.                      Absent. 

Pseudocoscoroba 
lity.                  Inosite. 

Absent.                 Present. 
)xytocus.              Metacoli. 

Acid  and  gas.                  No  change. 
Pseudocoloidella .             Pseudocoloides. 

Present.                                    Absent. 

1                           •                       1 
Pseudocoli  serum.                      Neapoliianus. 

1 

1 

Agglutination. 

Pseudocoli. 

Non-agglutination  (late 

fermentation  of  saccharose). 

Coliformis. 

Smith's  Indol-Producing  Division. 

Durham's  N  on-Saccharolytic  Communis  Section. 

Dulcitol. 


Acid  and  gas. 
Salicin. 


Acid. 
Cavicida. 


I 
Acid  and  gas. 

Motility. 


No  change. 
Metacoloides. 


Absent. 
Inosite. 


Present. 
Coli. 


Absent. 

I 
Maltose. 


No  change. 
Coloidella. 


Acid  and  gas. 
Coloides. 


No  change. 


Motility. 


Present. 
Maltose. 


Acid  and  gas. 
Paragrunthali. 


No  change. 
Griinthali. 


Acid  and  gas. 
Colitropicalis. 


No  change. 
Vesiculosus. 


PASTEURELLA  943 

Smith's  Non-Indol-Producing  Division. 

This  division  contains  only  one  organism,  Escherichia  coli  muta- 
bilis  Massini,  insufficiently  described. 

TRIBE  PASTEURELLEiE  Castellani  and  Chalmers,  1918. 

Definition. — Bacillaceaewith  good  growth  on  ordinary  media,  with- 
out endospores,  aerobic,  without  fluorescence  or  pigment  formation, 
unable  to  liquefy  gelatine,  and  Gram-negative,  but  with  polar  staining. 

Type  Genus. — Pasteurella  Toni  and  Trevisan,  1889. 

Genus  Pasteurella  Toni  and  Trevisan,  1889. 

Definition. — Pasteurelleae  with  the  tribal  characters. 

Type  Species. — Pasteurella  choler&gallinarum  (Zopf,  1885). 

Remarks. — -This  genus  was  formed  by  Toni  and  Trevisan,  and 
includes  all  the  organisms  of  the  hemorrhagic  septicemic  group, 
and  especially  plague.  It  is  to  be  noted  that  Pasteurella  coscoroba 
(Tretrop,  1900)  belongs  to  this  genus,  as  well  as  Pasteur eh 'a  pestis 
Kitasato  and  Yersin,  1894.  The  two  great  divisions,  the  animal 
and  the  human  diseases,  may  be  separated  as  follows: — 

A.  No  growth  on  MacConkey's   medium  containing  glucose,  levulose 

galactose,  or  mannitol — Animal  group. 

B.  Growth  on  MacConkey's  medium  containing  the    above-mentioned 

sugars — Plague . 

This  test  must,  however,  be  confirmed  by  animal  inoculations. 
TRIBE  PROTEGE  Castellani  and  Chalmers,  191 8. 

Definition. — -Bacillaceae  growing  well  on  ordinary  laboratory 
media,  not  forming  endospores,  aerobic,  without  fluorescence  or 
pigment  formation,  but  liquefying  gelatine. 

Type  Species. — Proteus  vulgaris  Hauser,  1885. 

Classification. — The  tribe  may  be  divided  into  genera  as  follows: — 

A.  Rapid  gelatine  liquefiers;  do  not  ferment  lactose;  mostly 

Gram-positive — Proteus. 

B.  Slow  gelatine  liquefiers;  ferment   lactose;   Gram-negative 

— Cloaca. 

Genus  Proteus  Hauser,  1885,  em.  Castellani  and  Chalmers,  1918. 
Type  Species. — Proteus  vulgaris  Hauser,  1885. 
Remarks. — These  organisms  are  of  difficult  classification,  as  the 
serological  reactions  are  not  always  in  accord  with  the  biochemical 
characters.      To  this  group  belongs  Proteus  X19  (see  page  1336). 
Some  species  may  be  separated  as  follows: — 

Saccharose. 
I 

No  change.  Acid  and  gas. 
Glucose.  Maltose. 
I  I 


No  change.  Acid  and  gas.  Acid  and  gas.  No  change. 

Metadiffluens.  Diffluens.  Proteus.  Paradiffluens. 


944 


AEROBIC   ASPOROGENOUS 


Bacteria. 


O 


D.       acidi 
Hiippe 


lactici     O    i    O       O       O      AC    AG      O       O      AG    AG    AG    AG    AG  I  AG 


B.       aertryke       De     -+- 
Nobele 


B.  albofaciens  Cas- 
tellani,  1905 

B.  archibaldiCsLStel- 
lani  and  Chal- 
mers, 191 8 

B.  asiaticus  Cas- 
tellani,  1905 

B.  asiaticus  mobilis 
Castellani,  191 4 

B.  bentotensis  Cas- 
tellani, 1912 

B.  capsulatus 
Pfeiffer 

B.  carolinus  Cas- 
tellani 
B.  cavicida  Briefer 


B.  ceylonensis  A 
Castellani,  1905 

B.  ceylonensis  B 
Castellani,  1905 

B.  cloacte,  Jordan 


O 


+ 


+ 

+ 

O 
O 


0 

0 

+ 

0 

+ 

0 

0 

0 

o 


o 


o 
o 

o 
o 
o 
o 

o 
o 

o 
o 
+ 


o 


o 
o 

o 
o 
o 
o 

o 
o 

o 
o 


A, 
Alk 


AC 

A, 
Alk 

A, 
Alk 

A, 
Alk 

A 

AC 


0 


o 

o 
o 

A 
AG 

O 


A, 
Alk 
AC    AG 


AC 


+      AC 


A 
AG 


O      AG 


O       O 


AC      O       O 


O 

AG 
AG 
A 
AG 

O 
O 


o 

AG 

O 
O 
As 


AG 


O 

AG 


AG 


A 
AG 


AG1  AG 

AG    AG 

O    i   A 


AG      O 


O 
AG 


O 


o 


AG  AG  AG 
AG  AG  AG 
A    I   O      As 


O      AG    AG    AG 


A 
AG 


O 
AG 

O 
A 
O 


A  or  A  or 
AG  I  AG 
AG    AG 


O       A 

A        A 


A  or 
AG 
O 


AG    AG 


AGs 


0 


AG     O 


AG 


AG 


AG 
AG 


OOO 

AAA 


AG 


AG    AG 


AG    AG 


AG 

O 

AG 

AG 
AG 

O 

A 

AG 


O 

O 

AG 

O 

0 

o 
o 


INTESTINAL   BACILLI. 


945 


■r. 


^ 

o 

o 

B 

S 

^ 

«  52 


■us* 

t  i  i 


O      AG    AG    AG 


0      AG    AG    AG 


0 

O 

AG 

O 

0    , 

Remarks. 


oq 


AG     0 


0      — 


O 
O 
O 
O 

O 
O 

O 
0 

o 


AG 
AG 
O 


AG 


AG  AG 
AG  AG 
A       A 


0  —  +  O  Gt  Belongs  to  the  capsulated 
bacilli ;  differs  from  B. 
lactis  aerogenes  in  not 
fermenting  inosite;  dif- 
fers from  B.  coli  tropi- 
calis  in  being  capsu- 
lated and  in  fermenting 
adonite  and  not  fer- 
menting salicin. 
O  or  O  Gt  Identical  culturally  and 
+  s  serologically    with    B. 

suipestifer ;  identical 
culturally  with  B.  en- 
teritidis  Gaertner  (dif- 
ferentiation by  agglu- 
tination tests)  and  B. 
paratyphosus  B  (dif- 
ferentiation by  Castel- 
lani's  absorption  test; 
agglutination  not  suffi- 
cient). 
—  Very  slow  and  scanty 
growth  on  agar. 
+       Gt 


O 
O 

As 


AG  O 
AG  O 
O       O 


AG    AG    AG    AG 

A 

O 


AG 

AG 

AG 

AG 

O 

O 

A 

A 

AG 

AG 

AG 
AG 
A 


A      —     — 


O 

+ 

"+s 
+  s 

+ 

+ 

+ 

+ 


Gt  — 

O       Gt  Differs  from  B.  asiaticus 
only  in  being  motile. 
Gt  — 

Gt  Capsulated,  probably 

identical  with  B.  lactis 
aerogenes. 
O    Gtor  — 

P 

-    Brieger    described    it    at 
first     as     non-motile; 
differs  from  B.  colt  in 
not  fermenting  maltose. 
O       O       O       Gt 

A    |   + 

Gt  Liquefaction  of  gelatine 
very  slow.  The  import- 
ant intestinal  liquefy- 
ing bacilli  may  be 
grouped  as  follows :  ( i ) 
lactose  fermenters  {B. 
cloacce) ;  (2)  lactose  non- 
fermenters,  Gram+(S. 
proteus  vulgaris) ;  (3) 
lactose  not  fermenters, 
Gram  O  {B.  difflnens). 


61 


94^ 


AEROBIC  ASPOROGENOUS 


Bacteria. 

8 

•0 

s 
-r. 

Litmus 
Milk. 

Lactose. 

<o 
O 

e 

Dulcite. 
Mannite. 
Glucose. 

Maltose. 

Dextrin. 

Raffinose. 

A  rabinose. 

s 

0 

B.      coagulans 

0 

O 

0 

O 

AC      O 

O 

—      O     AG 

AG     —     —      — 

Castellani 

B.  coll  Esche- 

+ 

O 

0 

0 

AC    AG 

O 

AG    AG    AG 

AG    AG    AG    AG 

0 

rich 

B.    coll    tnuta- 

0 

O 

0 

0 

AC    AG 

O 

O      — 

0 

bills  Massini 

B.  coloides  var. 

0 

O 

0 

0 

AC    AG 

O 

AG    —     AG 

AG 

_      _ 

A  Castellani 

B.  coloides  var. 

O 

O 

0 

0 

AC    AG 

O 

AG     —     AG 

AG 

—      



B  Castellani 

B.  colotropica- 

O 

O 

0 

0 

AC    AG 

O 

O      AG    AG 

AG 

AG    AG    AG 

0 

lis  C  a  s  t  e  1  - 

lani,  1907 

B.  columbensis 

+ 

O 

0 

0 

Ays, 

O  or 

O 

AG 

AG    AG 

AG 

As     O       AG 

0 

Castellani, 

Alk,  Gvs 

Gs 

1905 

Dor 
A 

B .  coscoroba 

O 

O 

0 

0 

AC    AG 

AG 

O     AG 

AG 

AG 

AG    AG    AG 

0 

(=B.pseudo- 

coscoro ba) 

Castella  ni 

and     Chal- 

mers 

B.  danysz 

B.    diffluens 

+ 

O 

+ 

+ 

Alk,    O 

O 

O 

O  or 

AG 

O 

O 

O 

O  or 

0 

Castellani, 

D 

A 

Ays 

1915 

B.     douglasi 

O 

O 

0 

0 

Alk     O 

O 

A 

A 

A 

A 









Castellani 

and    Chal- 

. 

mers,  191 8 

B.     dysenteric 

O 

0 

0 

0 

A,      O 

O 

O 

A 

A  ' 

A 

A 

A 

A 

0 

Flexner 

Alk 

B.     dysenteries 

O 

O 

0 

0 

A,      O 

O 

O 

A 

A 

O 

A 

A       A 

0 

Hiss    and 

Alk 

Russell 

B.     dysenteric 

O 

O 

0 

0 

A,      O 

O 

O 

O 

A 

O 

0  or 

O       O 

— 

Shiga-Kruse 

Alk 

As 

B.     dysenteric 

O 

0 

0 

0 

AC      O 

A 

A 

A 

A 

0 

O 

A 

A 

0 

Strong 

B  entrricusCas- 

O 

0 

0 

0 

O      AG 

O 

AG 

AG 

AG 

AG 

AGs 

OD 

AG 

0 

tellani,  19^1 

INTESTINAL  BACILLI— Continued. 


947 


>-< 

© 

Galactose. 
Levulose. 

O 
S 

>-< 

! 

1 

o 

s 
s 

"o 

55 

Remarks. 

0 

AG 

AG     — 

— 

o 

AG 

AG    AG 

0 

AG 

o 

AG 

o 

AG 

+   j  o 

Gt 

— 

o 

O 

Incompletely  described  ; 
late  lactose  fermenter 
(after   six   days) ;   said 

not  to  produce  indol. 

— 

— 

—      — 

o 

AG 

— 

— 

— 

— 

— 

— 

— 

— 

— 

— 

. 

AG 

AG 

— 

- 

— 

— 

— 

— 

— 

— 

0 

AG 

AG    AG 

O 

AG 

o 

AG 

o 

AG 

+ 





Differs  from  B.  coli  in  be- 

ing non-motile  and  in 

non-fermentingdulcite ; 

from  B.  neapolitanus  in 

not  fermenting  saccha- 

rose and  dulcite. 

o 

AG    AG 

AG 

O 

-AG 

o 

AG 

o 

AG 

+ 

o 

Gt 

~ 

AG    AG 

A 

o 

Differs  from  B.  coli  tropi- 

calis  in  fermenting  sac- 

charose;      certain 

authors  use  the  term  B. 

coscoroba  to  indicate  a 
different  germ  with  all 
the  characters  of  the 
fowl    cholera    bacillus 

(pasteurella) . 

Culturally  and  serologi- 
cally identical  with  B. 
enteritidis  Gaertner 
(Bainbridge). 

o 

— ■ 

AG  A  or 

AG 

— 

O 

— 

— 

— 

A 

0 

— 

Gt 

See  remarks  on  B.  cloaccs. 
Some  strains  clot  and 

— 

— 

— 

— 

—  i 

— 

— 

— 

+ 

— 

— 

peptonize  milk. 

0 

O 

A        A 



O 

o 

0 

o 

O 

+ 







0 

O 

A        A 

— 

o 

<) 

O 

o 

O 

+  or 
+ 

— 

— 

— 

o 

o 

A        A 

— 

o 

— 

As 

— 

O 

— 

— 

— 

o 

A 

A        A 

— 

0 

o 

A 

o 

o 

+ 

— 

— 

— 

o 

AG 

AG    AG 

+     o 

Gt 
Ps 

— 

94  8 


AEROBIC  ASPOROGENOUS 


Bacteria. 

s 

■a 
00 

to 

<o 
O 

to 
0 

« 

00 

s 

<0 

to 

0 

0 

ta 
to 
O 

3 

.8 

to 

0 

s 

« 

<0 

0 
S 

e 

8 
0 

B.     enteritidis 

+ 

0 

O 

O 

A, 

0 

O 

AG 

AG 

AG 

AG 

AG 

O 

AG 

O 

Gaertner 

Alk 

B.  fescalis   alka- 

+ 

0 

O 

O 

Alk 

0 

O 

O 

O 

O 

O 

O 

O 

O 

O 

li  gen  rs      Pe- 

trushky 

B.      fcepaloides 

+ 

0 

O 

O 

Alk 

0 

O 

O 

A 

A 

A 

A 

Oor 

O 

O 

Cas  t  e  1 1  an  i, 

A 

1915 

B.     gasoformans 

O 

0 

O 

— 

AC 

AG 

AG 

O 

— 

— 

— 

— 

— ■ 

— 

AG 

non  liquefa- 

ciens 

B  .gintotensisCas- 

O 

0 

O 

O 

D, 

O 

O 

O 

O 

A 

O 

O 

O 

A 

O 

tellani,  1910 

AC 

B.   giumai    Cas- 

O 

0 

O 

O 

A,   1   A 

O 

O 

O 

AG 

AG 

AGs 

O 

AG 

O 

tellani,  1910 

Alksi 

B.    grunt  halt 

+ 

0 

O 

O 

AC    AG 

O 

O 

AG 

AG 

— 

AG 

AG 

AG 

O 

Castellani 

■ 

B.       icteroides 

+ 

0 

O 

0 

A,      O 

O 

A  or 

AG 

AG 

AG 

AG 

Oor 

A  or 

— 

Sanarelli 

Alk 

AG 

A 

AG 

B  .kandiensisCsLS- 

+ 

0 

O 

0 

As,      O 

As 

O 

A 

A 

O 

0 

O 

O 

A 

tellani,  1912 

D, 
Alk 

B.  khartoumensis 

O 

0 

O 

0 

A 

AG 

O 

AG 

AG 

AG 

AG 

O 

O 

AG 

— 

Chalmers  and 

Macdonal  d, 

1915 

B.     lactis      aero- 

O 

0 

O 

0 

AC 

AG 

AG 

O 

AG 

AG 

AG 

AG 

AG 

AG 

AG 

genes    Esche- 

rich 

B.    levans   Wolf- 

+ 

0 

+ 

— 

AC    AG 

O 

O 

AG 

AG 

— 

AG 

AG 

AG 

O 

fin 

B .  lunavensisCas- 

O 

0 

O 

0 

As, 

O 

A 

O 

O 

A 

A 

A 

O 

A 

O 

tellani,  1912 

Alk 

B.    madampensis 

O 

0 

O 

0 

AC 

A 

A 

O 

A 

A 

A 

A 

As 

A 

O 

Castellani,  191 1 

B.    meta    alkali- 

O 

0 

O 

0 

Alk   Alk 

Alk 

Alk 

Alk 

Alk 

Alk 

— - 

— 

— 

— 

genes      Castel- 

lani, ^915 

B.       metacoli 

+ 

0 

O 

0 

AC 

AG 

AG 

AG 

AG 

AG 

AG 

AG 

AG 

AG 

O 

Cas  t el 1  an  i 

1915 

INTESTINAL  BACILLI— Continued. 


949 


t/] 


<S 


s 
Is 

u 

--. 


R5 


Remarks. 


O      AG    AG 


O       O       O 


AG 


O       O       O 


O 


O 


O       A       A 


O    !   O       A 
O     AG    AG 
O      AG    AG 


AG 


O      AG 


O       O 


O      AG    AG 


O 

AG 
AG 

AG 


O       O 


—      O 


O       O 


O      —      O 


O       O       O       O 

o 
o 


o 


AG    AG 


AG  AG  AG 

O       O  A 

O  A  A 

—  —  Alk 

O  AG  AG 


AG 

AG 

AG 

A 

A 
Alk 


O 


O 


O     AG     O 


AG    AG     — 


AG  — 
O  O 
O       O 


AG    AG    AG     O 


O       O 

O      As 

O      — 


0 


AG 


—     AG 


O      — 

O    Avs 
O       A 


O     AG 


Gt 


Gt 


O 

+ 
+ 
+ 

o 

+ 

o 

o 

+ 
+ 

+ 


o 


o 


o 


+ 


Gt 


GtP 

Gt 

Gt 

Gt 

or 

GtP 

Gt 


Gt 


+ 
O 


O 


(J 


Identical  culturally  with 
B.  suipestifer  (  =  B. 
atrtryke)  and  B.  para- 
typhosus  B ;  differs  sero- 
logically. 

The  tyj>ica.\B  .facalis  alka- 
ligenes  produces  strong 
alkalinity  in  all  sugar 
broths,  but  certain 
strains  are  said  to  pro- 
duce slight  acidity  in 
glucose  and  maltose. 
Some  strains  peptonize 
milk. 


Incompletely  described. 
It  is  probably  very 
similar  to  B.  colotropi- 
calis,  but  indol  O. 


Considered  to  be  identical 
withB.  suipestifer,  but 
complete  serological 
tests  have  not  been 
carried  out. 


Differs  from  B.  acidi  lac- 
tici  in  fermenting  ino- 
site. 


Gt 

Gt  Differs    from    B.   fetalis 

alkaligenes     in     being 

non-motile. 
Gt  Differs    from  B.  pseudo- 

coli  in  fermenting  ino- 

site. 


95o 


AEROBIC  ASPOROGENOUS 


Bacteria. 

'o 

5 

0 

CO 

u 

3« 

_© 
S3 

Saccharose. 

Dulcite. 

Mannite. 

Glucose. 

O 

Dextrin. 
Raffinose. 
Arabinose. 

§ 

B.      metacoloides 

+ 

0 

O 

O 

AC 

AG 

O       G     AG    AG 

AG 

AG    AG    AG 

0 

Castellani 

B.      metadiffluens 

+ 

0 

+ 

+ 

Alk 

O 

OO       O       O 

O 

O       O    O  or 

0 

Castellani 

As 

B.        tnetadysen- 

0 

0 

O 

O 

A  or 

A       A     O  or    A       A 

A 

—      —      — 

— 

tericus        Cas- 

Alk 

As 

tellani,      1904, 

var.  A 

B.        metadysen- 

0 

0 

O 

O 

A, 

A     OorOorOor     A 

A 

— 

—      — 

— 

tericus        Cas- 

Alk 

Avs  Avs  Avs 

tellani,      1904, 

var.  B 

B.        metadysen- 

0 

0 

O 

O 

A, 

As  O  or  O  or  O  or    A 

As 

— .      —      — ; 

— - 

tericus        Cas- 

Alk, 

Ays  Avs  Avs 

tellani,      1904, 

D 

var.  C 

B.     metady  s  en- 

0 

0 

O 

O 

A,      A 

A       A       A 

A 

A 

— 

— 

— 

— 

ter  icus     Cas- 

Alk 

tellani,       1904, 

var.  D 

B.         morgani 

0 

O 

O 

O 

O, 

O       O 

O       O 

AG 

O  or 

O  or    O     O  or 

0 

Caste  Hani 

Alk. 

A 

A                A 

and  Chalmers, 

or 

1918 

As, 

Alk 

B.     neapolitanus 

0 

O 

O 

O 

AC 

AG    AG 

AG    AG    AG 

AG 

AG    AG    AG 

0 

Emmerich 

B .      negombensis 

0 

O 

O 

O 

O, 

O 

O 

O       O 

A 

O 

O 

O 

O 

0 

Castellani,  1 910 

Alk 

B .    oxytocus    per- 

0 

0 

O 

O 

AC 

AG    AG 

AG    AG    AG 

— 

AG    AG 

AG 

AG 

niciosus  Wys- 

sokowitsch 

B.    para-aertryke 

+ 

0 

O 

O 

A, 

O       O 

AG    AG    AG 

AG 

O     O       AG 

O 

Castellani,  191 4 

Alk 

B.     para  -  asiati- 

0 

0 

O 

O 

O 

O       O 

AG    AG    AG 

AG 

AG    AG    AG 

O 

cus      Castel- 

lani, 1916 

B.    paracoagu- 

O 

0 

O 

O 

AC 

O 

O 

O      AG    AG 

AG 

—    AG 

AG 

lans    Castel- 

lani, 1914 

B.       paracolon 

+ 

0 

O 

O 

A, 

O       O 

A      AG    AG 

AG 

AG    AG 

AG 

— - 

Day 

Alk, 

B.     paradifflu- 

+ 

0 

+ 

+ 

Alk 

O     AG 

O    0  or 

AG 

O 

O 

0 

O 

O 

ens     Castel- 

D or 

A 

lani 

P 

INTESTINAL  BACILLI— Continued. 


951 


O 


O 


0 

8 

5 
u 

0 

s 

'J 

K| 

AG 


AG    AG     O 


—    O  or     (  ) 
\s 
O  As      A 


—       A        A 


—      —      A       A 


—      A       A 


O       O    A  or  A  or 
AGs  AGs 


O     AG    AG    AG 


O 


o     o 

AG    AG 


A 
AG 


O      AG    AG 


As 
AG 


"*3 

P 


AG 


O 


O    AGs 


O       O 
AG    AG 


AG    AG 


O      AG    AG    AG     O 


O       A      AC,     AG 


AG 


AG 


-     AG 


AG 
AG 


-^ 
O 


O      AG  I   + 


O 


O    AGs 


O 
AG 


O 


AG     O 
AG     O 


—      + 


O 


O     AGs 


O 
AG 

AG 
O 


+  + 


+       O 


o 

+ 

o 

+  s 


—  l  Gt 


Gt 


Gt 

Gt 
Gt 

Gt 

Gt 
Gt 


Remarks. 


Differs  from/?,  coll  in  be- 
ing non-motile  and  in 
fermenting  saccharose; 
from  B.  pseudo-coil  in 
being  non-motile;  from 
B.  colotropicalis  in  fer- 
menting dulcite  and 
saccharose. 


Differs  from  B.  asialicus 
in  not  fermenting  sac- 
charose and  in  ferment- 
ing dulcite. 


95 


AEROBIC  ASPOROGENOUS 


>■. 

g 

s 

to 

is 

.0 

<a 
0 

to 
to 

nite. 
■■ose. 

ta 
to 
0 

5» 

to 
to 

0 

S 

<a 
<o 
0 
.8 

2    ' 

Bacteria. 

"0 

s» 

3 

to 

.2  '<s> 

3^ 

^0 

to 

"S 

1        s 

"« 

^ 

«: 

1 

^ 

0 

^ 
0 

O 

to 

to 

Q 

^       O 

S 

Q 

^ 

B.     paradysen- 

O 

0 

O 

0 

A       O 

O       O       O    O  or 

O 

O 

O 

0 

0 

tericus      Cas- 

A 

tellani,  1904 

B.  para-enteri- 

+ 

0 

O 

0 

A 

AG 

AG    AG    AG    AG 

AG 

AGs 

AG 

AG 

0 

c.ts       Castel- 

lani,  1 91 4 

B.     paragriinthali 

+ 

0 

O 

0 

AC    AG 

O       O      AG    AG 

AG 

AG 

AG 

AG 

0 

Castellani 

B.     paratypho- 

+ 

0 

0 

0 

A      O 

O      AG    AG    AG 

AG 

AG 

0 

AG 

0 

shs    A    Schot- 

miillcr 

B.     paratypho- 

+ 

0 

0 

O 

A,       O 

O      AG    AG    AG 

AG 

AG 

O 

AG 

0 

sus    B    Schot- 

Alk 

miiller 

B.     paratypho- 

— 

— 

sits  C 

B.    pneumonia 

O 

0 

0 

O 

AC 

A 

AG    AG    AG    AG 

AG 

AG 

AG 

AG 

AG 

Friedlaender 

B.  pritnitzi    Cas- 

+ 

0 

0 

O 

A 

O 

O 

0 

O       A 

A 

A 

O 

O 

O 

tellani 

B.     proteus     vul- 

+ 

+ 

+ 

+ 

C  or 

O 

AG 

O       O      AG 

AG 

O 

O 

O 

O 

garis  Hauser 

P 

B.  pseudo-asia- 

O 

0 

0 

O 

A, 

O 

AG  AGs 

AG 

AG 

AG 

AG 

AG 

AG 

O 

ticus      Castel- 

Alk 

lani,  1 91 3 

B.  psendo-asia- 

+ 

0 

0 

O 

A  or 

O 

AG 

AG 

AG 

AG 

AG 

AG 

AG 

AG 

O 

ticus    mob  His 

O, 

Cas  tella  n  i, 

Alk 

I9t5 

B.  pseudo-caro- 

0 

0 

0 

O 

0 

O 

O 

0 

AG 

AG 

AG 

— 

AG 

AG 

— 

linus    Castel- 

lani, 1917 

B.     pseudo-coli 

+ 

0 

0 

O 

AC 

AG 

AG 

AG 

AG 

AG 

AG 

AGs 

AG 

AG 

O 

Cas  tell  a  ni, 

1909 

B.  pseudo-coli- 

+ 

0 

0 

O 

AC 

AG 

O. 

AG 

AG 

AG 

AG 

AG 

AG 

AG 

O 

Jormis        Cas- 

AG 

tellani,  1 91 7 

INTESTINAL  BACILLI— Continued. 


953 


8 

H 

•** 

© 

Galactose. 
Ltvulose. 
Inosite. 

.8 

Is 

S 

1 
f 

<0 

o 

3 

hi 

s 

<3 

"o 

s 

IPS 

1  ! 

Remarks. 

— 

— 

Oor    O       O 
As 

o 

o 

o 

O 

o 

+ 

— 

Gt 

Milk     rendered     perma- 
nently acid. 

o 

AG 

AG    AG     — 

+ 

O 

Gt 

B.  bzdullensis  Castellan i, 

Ps 

191 1 ;  culturally  identi- 
cal, differs  serologically . 

o 

AG 

AG    AG 

O 

AG 

o 

AG 

O 

AG 

+ 

— 

Gt 

Differs  from  B.  grunthali 
in  fermenting  maltose. 

o 

AG 

AG    AG 

o 

O 

o 

AG 

o 

O  or 
As 

O 

o 

Gt 

■ 

o 

AG 

AC,    AG 

AG 

0 

0 

AG 

o 

O 

O 

o 

Gt 

Certain  strains,  serologi- 
cally typical,  may  pro- 

duce  at  times  only  A 

instead    of    AG;    some 

strains  do  not  ferment 

inosite(Weissand  Rice). 

Cover  1  several  germs,  one 

identical  with  B.  enter- 

itidis. 

o 

AG 

AG 

AG 

AG 

AG 

— 

— 

o 

— 

o 

o 

— 

— 

A 

O 

A 

A 

O 

A 

o 

O 

o 

o 

o 

— 

Gt 

— 

O 

O 

AG 

A  or 

O 

O 

_ 





O  or 

+ 



Gt 

Cultures  emit  a  disagree- 

AG 

As 

able  odour.        Hauser 
distinguished    at    first 
three  varieties  of  pro- 

teus:P.  vulgaris  (rapid 

liquefaction     of     gela- 

tine), P.  mirabilis  (slow 

liquefaction),  P.  zenkeri 

(no  liquefaction) ;  later 

abandoned  this  differ- 

entiation). 

O 

AG 

AG 

AG 

0 

AG 

o 

AG 

o 

AG 

+ 

o 

Gt 

Differs  from  B.  asiaticus 
in  fermenting  dulcite. 

O 

AG 

AG 

AG 

o 

AG 

o 

AG 

0 

AG 

+ 

o 

Gt 

4 

O 

A 

AG 

AG 

+ 

o 

GtP 

— 

O 

AG 

AG 

AG 

o 

AG 

o 

AG 

o 

AGs 

+ 

o 

Gt 

Ps 

Differs  from  B.  coli  in  fer- 
menting saccharose,  be- 
longing    to   the  group 
Communiorof  coliform 
bacilli. 

0 

AG 

AG 

AG 

o 

AG 

0 

AG 

o 

AG 

+ 

o 

Gt 

Differs  from  B.  pseudo-coli 
serologically     and      in 
fermenting    saccharose 
only  after  several  days . 

954 


AEROBIC  ASPOROGENOUS 


Bacteria. 

0 

5? 

15 

1 

<o 
■5  *** 

0 

8 

<u 
to 
0 

e 

U 

<s 

■^0 

s 

Glucose. 
Maltose. 

to 

0 

s 

<s 

<o 

0 

.g 

s 

B.    pseudo-col- 



O 

oid;s  Castel- 

lani,  1916 

B.    pseudo-col- 

O 

oides,  var.  B, 

Castellani 

B.    pseudo-col- 

0 

O 

0 

O 

O 

O 

0 

AG 

AG 

AG 

AG 

AGs 

O 

AG 

0  i 

u  >n  b  e  n  sis 

Castellani, 

1917 

B.  pscudo-mor- 

+ 

O 

0 

O 

O, 

O 

0 

O 

O 

O 

O 

O 

O 

0 

oani  Castel- 

Alk 

lani 

B.    pseudo-u  e- 

0 

O 

0 

O 

O 

O 

AG 

O 

O 

AG 

senbergi  Cas- 

tellani, iqi8 

B.      psittacosis 

+ 

O 

0 

O 

A, 

O 

O 

AG 

AG    AG    AG    AG 

AG 

AG 

0 

Nocard 

Alk 

B.  pyogenes  foe- 

+ 

O 

0 

O 

AC 

A 

A 

A 

A 

A       A 

A 

A 

A 



tidus  Passet 

B.schaefferi  von 

0 

O 

0 

— 

AC 

AG 

O 

AG 

0 

Freudenreich 

B.      suipestifer 

+ 

O 

0 

O 

A, 

O 

O 

AG 

AG    AG    AG     O 

O 

AGs 

0 

Kruse 

Alk 

B.  talavensis 

+ 

O 

0 

O 

Alk, 

O 

A 

O 

O 

A 

O       O 

O 

O 

0 

Castellani, 

D 

1909 

B.   tangallensis 

0 

O 

O 

O 

As, 

O 

A 

A 

A 

A 

A       A 

A 

A 

0 

Castellani, 

Alk 

1911 

B.  tardus  Cas- 

0 

O 

O 

O 

DP 

O 

O 

O 

O 

As 

O      — 

— 

— 

— 

tellani,  191 7 

B.    typhi   mur- 

+ 

O 

O 

O 

A, 

O 

O 

AG 

AG 

AG 

AG    AG 

O 

AG 

0 

ium  Loeffler 

Alk 

B.     typhosus 

. 

O 

O 

O 

A 

O 

O 

0 

A 

A 

A 

A 

As 

O 

0 

Eberth 

B.  veboda  Cas- 

+ 

O 

O 

O 

A, 

O 

O 

AG 

A 

AG 

AG    AG 

AG 

AG 

O 

tellani,  1909 

Alk 

B.vekanda  Cas- 

+ 

O 

O 

O 

A 

AG 

O 

AG 

AG 

AG 

AG     0 

O 

AG 

AG 

tellani 

B.      vesiculosis 

0 

O 

O 

O 

AC 

AG 

O 

O 

O 

Henrici 

| 

INTESTINAL  BACILLI— Continued. 


955 


« 

s 

«j 

• 

^' 

"a 

© 
1/3 

C5 

C3 

<o 
o 

S 

to 

o 
s 

00 

? 

o 

r 

(5 

IS 

»J     Co 

~3 

Remarks. 

Differs  from/?,  pseudo-coli 
in  not  fermenting  dul- 
cite. 

AG 

Differs  from  B.  pseudo- 
coloides  in  fermenting 
inosite. 

o 

AG 

\<; 

AG 

o 

AG 

o 

o 

AG 

+ 

O 

Gt 

— 

o 

U 

A 

A  or 
AG 

O 

0 

0 

O 

o 

O 

+ 

+ 

o 

Gt 
Gt 

— 

b 

AG 

AG 

AG 

— 

o 

— 

— 

— 

— 

O 

o 

Gt 

Identical  with  B.  a:  rtryke, 
according  to  Bain- 
bridge. 

— 

— - 

A 

A 

— 

— 

— 

— 

— 

+ 

o 

Gt 

— 

0 

O 

— 

— 

O 

— 

— 

— 

+ 

o 

Gt 

Incompletely  described. 

o 

AG 

AG 

AG 

O  or 
AG 

o 

o 

AG 

o 

As 

+  s 

o 

Gt 

Identical  with B.  a  rtryke. 
Other  synonyms  for  B. 

o     o 


o 

O      AG 


O 
AG 


O  or 


O  A 

O  AG 

O  AG 

O  — 


A        A 
AG    AG 
AG    AG 


O 
AG 


A 

0 

o 

o 

A 

0 

A 

o 

O 

— 

— 

O 

° 

o     o 

O       — 


o 
o 

O      AG     O 


A 

+ 

o 

Gt 

A 

+ 

0 

Gt 

— 

O 

— 

— 

O 

o 

o 

Gt 

As 

o 

o 

Gt 

O 

o 

— 

Gt 

AG 

o 

— 

Gt 

— 

+ 

o 

— 

suis,  bacillus  of  hog- 
cholera,  Salmon  and 
T.  Smith,  i88s. 


Very  slow  and  scanty 
growth  on  agar. 

Bainbridge  has  found  out 
that  the  name  is  ap- 
plied to  different  or- 
ganisms, some  strains 
being  serologically  iden- 
tical with  B.  at  rtryke, 
others  with  B.  enteriti- 
dis  Gaertner,  others 
with  B.  paratyphosus  B. 

Certain  strains,  milk  A, 
Alk. 


956 


AEROBIC  ASPOROGENOUS 


~Bacteria. 

■J 
s 

8 

00 

10 

<0 

0 

B 

0 
<0 

8 

Glucose. 
Maltose. 

3 

5 

B.     watareka 

+ 

O 

0 

O 

A 

O 

O 

AG 

AG 

AG 

AG 

O 

AG 

AG 

O 

Castellani 

B.     werahensis 

+ 

0 

0 

O 

A 

O 

O 

AG 

A 

A 

AG 

AG 

AG 

AG 



Castellani 

B.     wesenbergi 

+ 

— 

0 

O 

A 

A 

AG 

A 

A 

AG 

Castellani 

B.    wesev.ber- 

+ 

O 

0 

O 

O 

O 

AG 

O 

0 

AG 

AG 

— 

. — . 



— 

goides     Cas- 

tellani, 1 91 6 

B.       willegodai 

+ 

O 

0 

O 

A, 

O 

O 

A 

A 

AG 

AG 

AG 

AG 

AG 

O 

Castellani 

Alk 

B.  wolinisp  Cas- 

+ 

O 

0 

O 

A  or 

O 

A  or 

O 

AG 

AG    AG 

O 

O 

O 

O 

tellani,  1 91 6 

A, 

Alk 

* 

Alk 

B .      zeyla  nic  us 

+ 

O 

0 

O 

Alk 

Alk 

Alk 

Alk 

Alk 

Alk   Alk 

Alk 

Alk 

Oor 

0  or 

Castellani, 

Alk 

Alk 

1910 

Abbreviations  used  in  the  above  Table. — A=acid;  G=gas;  C=clot;  D  =  decolorized; 
Peptonized  (milk)  pellicle  (broth);  VS  =  very  slight ;  0  =  negative  result — viz.,  neither  acid 
liquefaction  of  gelatin  or  serum  as  the  case  may  be ;  +    =positive  result;   +    =sometimes 

The  new  nomenclature  has  not  been  used  in  this  table. 


INTESTINAL  BACILLI— Continued. 


957 


s 

s 

Sorbite. 
Galactose. 

1-1 

o 

8 

CO 

K 

1 

1 

Erythrite. 

Glycerine. 

Indol. 

3*£ 

1 

Remarks. 

O 

O 

Alk 

AG 

O 

Oor 
Alk 

AG 
O 

AG 

A  or 
AG 

Alk 

AG 
O 

A 
O 

Alk 

AG 

O 

O  or 

Alk 

O 

A 

AG 
O 

Oor 
Alk 

O 

o 
o 

O  or 
Alk 

AG 
AG 

AG 

Oor 
Alk 

O 

O  or 

Alk 

A 
O 

O 
A 

O  or 
Alk 

+ 
+  s 

+ 

+ 

+  s 
O 

O 

o 

Gt 
Gt 
Gt 
Gt 

Gt 
Gt 

Gt 
or  P 

Classification        difficult, 
the   germ   being  poly- 
morphic,    vibrio -like, 
bacillus  -  like,       lepto  - 
thrix-like,   spirilloides- 
like,  hence  its  various 
generic  names :  bacillus, 
vibrio,       spirobacillus, 
vibriothvix,  p.  1068 

Alk=Alkaline;  S=slight;  A,  Alk^Acid  then  alkaline;  Gt  =  general  turbidity;  P  = 
nor  clot  in  milk,  neither  acid  nor  gas  in  sugar  media,  non-production  of  indol,  non- 
positive,  sometimes  negative. 


958  SCHIZOMYCETES 

Genus  Cloaca  Castellani  and  Chalmers,  1918. 

Type  Species. — Cloaca  cloaca  Jordan,  1890. 

Remarks. — Two  species  are  known,  C.  cloaca  Jordan  and  C. 
levans  Wolffin,  but  they  are  not  important  in  tropical  medicine. 
They  may  be  recognized  as  follows: — 

Sacchirose. 


Acid  and  Gas.  No  change. 

Cloicace.  Levans. 

TRIBE  BACTERIDIE.E  Castellani  and  Chalmers. 

Definition. — Bacillaceag  growing  well  on  ordinary  laboratory 
media,  without  endospores,  and  either  fluorescent  or  chromogenic. 

Type  Genus. — Bacteridiitm  Schroeter,  1872. 

Remarks. — Two  distinct  groups  belong  to  this  tribe — viz.,  the 
fluorescent  and  the  chromogenic — but  we  are  only  concerned  with 
the  latter,  to  which  the  type  genus  belongs. 

Genus  Bacteridium  Schroeter,  1872. 

Definition. — Bacteridieas  which  are  chromogenic. 

Type  Species. — Bacteridiitm  prodigiosum  (Ehrenberg,  1838). 

Remarks. — -Although  we  are  not  particularly  concerned  with  this 
genus  as  a  whole  in  the  tropics,  still  there  is  one  species — Bacteridium 
pyocyaneum  Gessard,  1882,  synonym  Bacterium  eeruginosum 
Schroeter,  1872 — which  is  the  organism  of  bluish-green  pus. 

It  is  a  common  intestinal  parasite  in  the  tropics,  and  is  moderately 
common  in  pus  in  Ceylon,  India,  and  the  Anglo-Egyptian  Sudan. 

It  is  a  small  motile  rod,  which  becomes  pleomorphic  if  grown  on 
media  containing  carbolic  or  boric  acids.  It  only  produces  its 
bluish-green  pigment  when  grown  aerobically. 

It  produces  acid,  but  no  gas,  in  glucose,  and  no  change  in  maltose, 
dulcitol,  or  salicin.  Litmus  milk  is  rendered  alkaline  and  not 
clotted. 

TRIBE  GRACILOIDES  Castellani  and  Chalmers,  1918. 

Daflnition. — -Bacillaceae  growing  very  slowly  and  scantihT  on 
ordinary  and  blood  media,  without  endospores  or  capsules,  neither 
fluorescent  nor  chromogenic. 

Type  Genus. — Graciloides  Castellani. 

Genus  Graciloides  Castellani,  1917. 

Definition. — Graciloidea  with  the  tribal  characters. 
Type  Species. — Graciloides  albojaciens  Castellani,  1904. 
Classification. — Two  species  have  been  so  far  described,  which 
may  be  recognized  as  follows: — 

A.  Litmus  milk  rendered  acid  and  clotted — Albojaciens. 

B.  Litmus  milk  decolorized  or  peptonized — Tardus. 


BACTEROIDES  959 

TRIBE  BACTEROIDEJE  Castellani  and  Chalmers. 

Definition. — Bacillaceae  with  good  growth  on  ordinary  laboratory  media, 
without  endospores,  fluorescence,  or  pigment  formation,  and  obligatory 
anaerobes. 

Type  Genus. — Bactcroides  Castellani  and  Chalmers,  191 8. 

Genus  Bacteroides  Castellani  and  Chalmers,  191 8. 

Definition. — Bacteroideae  with  the  tribal  characters. 

Type  Species. — Bacteroides  fragilis  Veillon  and  Zuber. 

The  type  is  found  in  abscesses  from  various  parts  of  the  body.     Another 
species  is  the  well-known  Bacteroides  fusiformii  of  Le  Dantec  and  Vincent, 
found  in  hospital  gangrene,  and  in  Vincent's  angina  and  many  other  conditions, 
as  well  as  in  the  mouths  of  healthy  persons  and  in  the  tartar  on  teeth. 
Some  of  the  intestinal  forms  are  given  on  p.  560. 

TRIBE  BACILLE.E  Castellani  and  Chalmers,  191 8. 

Definition.— Bacillaceae  growing  well  on  ordinary  laboratory  media  and 
possessing  endospores. 

Type  Genus. — Bacillus  Cohn,  1872,  pro  parte. 

Genus  Bacillus  Cohn,  1872. 

Definition. — Bacilleas  with  the  tribal  characters. 

Type  Species. — Bacillus  subtilis  (Ehrenberg,  1833). 

Classification. — The  genus  may  be  divided  into  two  groups  as  follows: — 

A.  Aerobes — Subtilis  group. 

B.  Obligatory  anaerobes — Tetanus  group. 

Only  the  latter  concerns  us  at  present. 

Tetanus  Group. 

The  group  may  be  divided  into  subgroups  as  follows: — 

A.  Gelatine  liquefied: — 

I.  Inspissated  blood  serum  not  liquefied: — 

(a)  Little  or  no  gas  in  milk;  white  of  egg  not  sensibly  affected. 

Usually  motile — Subgroup  Quarter  Evil. 

[b)  Much  gas  in  milk;  white  of  egg  slightly  affected.    Usually 

non-motile — Subgroup  Saccharolytic. 
II.  Inspissated  blood  serum  liquefied: — 

White  of  egg  digested — Subgroup  Proteolytic. 

B.  Gelatine  not  liquefied: — ■ 

Inspissated  blood  serum  not  liquefied.     White  of  egg  not  digested 
— Subgroup  Non-lijuej "active. 

Subgroup  Quarter  Evil. 

Synonym. — Rauschbrand  group. 

Definition. — Tetanus  group  usually  motile,  liquefying  gelatine,  non-proteo- 
ly tic,  and  do  not  liquefy  inspissated  blood  serum.  Clotting  milk  without 
much  shrinkage.     Citron  and  bladder  forms  occur.     Spores  usually  central. 

Classification.— The  organisms  of  this  group  may  be  recognized  as  follows : — 

A.  Long  threads  present — Vibrion  septijue. 
1 i.  Long  threads  absent: — 

I.  Saccharose  fermented — Feseri. 
II.  Saccharose  not  fermented : — 

(a)  Spores  rare  in  animals — Novyi. 

(b)  Oval  end  spores  present — End-sporing  types. 


o6o 


SCHIZOMYCETES 


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SACCHAROLYTIC  961 

Remarks. — Bacillus  feseri  |Trevisan,  1885,  the  causal  organism  of  quarter- 
evil,  is  the  same  asB.  chauvcei  Arloing,  Cornevin,  and  Thomas,  1887;  B.  car- 
bonis  Migula,  1900;  B.  anthracis  symptomatica  Kruse,  1896;  and  theBacillus  of 
Rauschbrand  auctores. 

The  Vibrion  septique  of  Pasteur  is  the  same  as  the  bacillus  of  Ghon  and  Sachs, 
and  has  been  found  in  gas  gangrene ;  it  really  covers  a  group  of  strains  which 
agree  in  morphology  and  in  cultural  characters,  as  well  as  in  pathogenicity, 
but  their  agglutinative  reactions  are  different. 

Subgroup  Saccharolytic. 

Synonyms. — Welchii  subgroup  ;  Perfringens  subgroup. 

Definition. — Tetanus  group,  liquefying  gelatine,  usually  causing  stormy 
fermentation  in  milk,  in  which  spores  are  not  formed.  Do  not  blacken  meat 
or  liquefy  blood  serum. 

Classification. — The  following  organisms  belong  to  this  group: — 

1.  B.   welchii  Migula,    1900.     (Synonyms: — B.  perfringens  Veillon  and 

Zuber,  1898;  B.  aerogenes  capsulatus  Welch  and  Nuttall,  1892;  B. 
phlegmonis  emphysematosi  Fraenkel,  1902;  B.  saccharobutyricus 
immobilis  Schattenfroh  and  Grassberger,  1900;  B.  enteritidis  sporo- 
genes  Klein,  1915,  pro  parte.  This  organism  is  merely  a  mixture  of 
B.  welchii  and  B.  sporogenes,  Achalme's  bacillus.) 

2.  B.  fallax  Weinberg,  1915. 

3.  B.  cedematiens  Weinberg  and  Sequin,  1915. 

4.  B.  aerofelidus  Weinberg,  1916. 
They  may  be  differentiated  as  follows: — - 

A.  Non-motile  : — ■ 

Saccharose   and   lactose   fermented,    but   salicin   not   fermented — ■ 
Welchii. 

B.  Feebly  motile  in  cultures,  more  motile  in  tissues  : — 

I.  Saccharose  and  salicin  fermented,  but  lactose  not  fermented — 

Fallax. 
II.  Saccharose  not  fermented,  but  lactose  and  salicin  fermented — - 
A  erofetidus. 
III.  Saccharose,  lactose,  and  salicin  not  fermented — (Edematiens. 

Subgroup  Proteolytic. 

Definition. — Tetanus  group  liquefying  gelatine  and  inspissated  blood 
serum.  Meat  media  blackened.  Milk  usually  digested  without  forming  a 
clot.     Colonies  grow  out  in  long  tangled  filaments. 

Classification.- — The  following  organisms  belong  to  this  subgroup  : — 

1.  B.  telani  Flugge,  1886. 

2.  B.  sporogenes  Metchnikoff,    1908.     (Synonyms  : — B.  cadaveris  sporo- 

genes Klein,   1901;   B.csdematis  maligni  Koch,   1881;  B .  enteritidis 
sporogenes  Klein,  1895,  pro  parte;  B.  putrificus  coli  Bienstock,  1906.) 

3.  B.  botulinus  van  Ermengem,  1898. 

4.  B.  histolyticus  Weinberg  and  Sequin,  1916. 
They  may  be  differentiated  as  follows  :■ — ■ 

A.  Dense  white  balls  in  four  to  five  days  in  meat  media  : — 

Very  few  large   subterminal   spores   in   culture.     Pathogenic   for 
laboratory  animals — -Histolyticus. 

B.  No  formation  of  white  balls  in  meat  media  : — - 

I.  Non-pathogenic  for  laboratory  animals: — ■ 

Central,  subterminal,   or  terminal  spores  a  marked  feature  in 
cultures — Sporogenes. 

II.  Pathogenic  for  laboratory  animals: — 

(a)  Spores  oval,  central,  or  terminal — Botulinus. 

(b)  Spores  round  and  terminal — Tetani. 

61 


962  SCHIZOMYCETES 


Subgroup  Non-Liquefactive. 

Definition. — Tetanus  group,  motile,  not  liquefying  gelatine  or  inspissated 
blood  serum,  and  do  not  blacken  meat  media. 
Remarks. — This  group  includes: — - 

i.  B.    tertius    Henry,    1917,    found   in    gas    gangrene.     (Synonyms:  — 
B.  Y.  Fleming,  1915;  B.  von  Hibler  IX.;  B.  rodella  III.) 

2.  B.  von  Hibler  VII. 

3.  B.  amylobacter  Gruber,  1887. 

Classification. — These  oiganisms  may  be  recognized  as  follows: — 

A.  Attack  milk  slowly,  forming  a  soft  clot  after  a  long  period : — 

I.  Spores  usually  central — Von  Hibler  VII. 
II.  Spores  typically  terminal — B.  tertius. 

B.  Attack  milk,  forming  tough  clot,  broken  by  gas — Amylobacter. 

FAMILY  3:  SPIRILLACEJE  Migula,  1900. 

Definition.- — Eubacteriales  with  cells  spirally  curved  or  repre- 
senting part  of  a  spiral;  division  in  one  direction. 

Type  Genus. — Spirillum  Ehrenberg,  1838. 

Classification. — The  family  may  be  divided  into  the  following 
genera : — 

A.  Xon-motile,  comma-shaped,  or  spirally  curved  filaments,  rigid,  with- 

out flagella — -Genus  1,  Spirosoma  Migula,   1900. 

B.  Motile,  short,  slightly  curved,  rigid,  comma-like,  sometimes  in  chains, 

with  one,  rarely  more,  flagella  at  one  end,  seldom  at  both  ends — 
Genus  2,  Vibrio  O.  F.  Muller,  1773,  emendavit  Loefrler. 

C.  Motile,  long,  spirally  curved,  usually  with  a  bunch  of  polar  flagella 

composed  of  long  and  short  forms — Genus  3,  Spirillum  Ehrenberg, 
1838,  emendavit  Loefrler. 

Remarks. — We  are  only  concerned  with  the  genus  Vibrio,  which 
contains  the  cholera  and  paracholera  organisms. 

If  the  spirochetes  were  to  be  considered  to  be  bacteria,  they  would  be 
classified  here  under  the  name  Spironema. 

Genus  Vibrio  O.  F.  Muller,  1773. 

Definition. — Spirillaceae  motile,  with  short  comma-like  cells, 
possessing  one,  rarely  more,  flagellum  at  one,  rarely  at  both 
ends. 

Type. — It  is  difficult  to  decide  which  is  the  type  of  this  genus  so 
denned. 

Remarks. — The  important  species  is  the  Vibrio  comma  Koch,  1884, 
which  is  the  cause  of  Asiatic  cholera,  but  there  are  many  other 
which  cause  paracholera — e.g.,  V.  gindha,  Pfeiffer,  1896;  V.  kegal- 
lensis  Castellani,  1913;  V.  insolitus  Castellani,  1913,  etc. 

Classification. — The  genus  may  be  divided  into  aerobic  groups 
as  follows; — 


GENUS  VIBRIO  963 


The  Aerobic  Groups  of  the  Genus  Vibrio  O.  F.  Muller, 

EMENDAVIT    LOEFFLER. 


Phosphorescence. 


Present.  Absent. 

/.  Albensis group. 

Gelatine. 


Liquefied.  Not  liquefied. 

VII.  Terrigenus  group. 
Pigment  formation  in  alkaline. 
Peptone  water. 

!__ 

Absent.  Present. 

VI.  Drennani  group. 
Cholera  immune  serum. 
Dilutions  of,  or  greater  than,  1  in  200. 


Agglutination.  Agglutination  absent  or  unknown. 

II.  Cholera  group. 

Growths  in  gelatine  stabs. 


Resembles  true  cholera.  Does  not  resemble  true  cholera. 

V.  Finkler-Prior  group. 
Pigeon  pathogenicity. 
Small  intramuscular  injections. 

I  I 

Quickly  lethal.  Effect  slight,  negative,  or  unknown. 

III.  Metschnikovi  group.  I V.  Gindha  group. 

Only  the  cholera  and  the  gindha  groups  concern  us. 

Cholera  Group. 
Ruffer  classifies  the  strains  of  the  cholera  group  as  follows: — 

Series  I '.- — A.  Cholera  immune  serum. 

1.  Agglutination  positive. 

2.  Castellani's  saturation  positive. 

3.  Pfeiffer's  reaction  positive. 

4.  Complement  fixation  positive. 

B.  Hannolysis  negative. 
Series  II.,  El  tor  vibrios. — A.  Cholera  immune  serum. 

1.  Agglutination  positive. 

2.  Castellani's  saturation  positive. 

3.  Pfeiffer's  reaction  positive. 

4.  Complement  fixation  negative. 

B.  Haemolysis  strongly  marked. 


964  SCHIZOMYCET.  ES 

Series  III. — A.  Cholera  immune  serum. 

i.  Agglutination  positive. 

2.  Castellani' s  saturation  negative. 

3.  Pfeiffer's  reaction  negative. 

4.  Complement  fixation  positive. 

B.  Haemolysis  feeble  and  late. 

The  bacteriological  characters  of  the  usual  vibrio  are  to  be  found  in 
every  textbook  on  bacteriology. 


Gindha  Group. 
This  group  may  be  divided  into  species  as  follows  :- 

Nitrate  Reduction  and  Indol  Formation. 


Both  present.  One  or  both  absent. 

Blood  serum.  Nitrate  reduction. 

Liquefaction. 


Not  known.  Absent. 

Rapid.  Slow. 

1.  Gindha.      2.   Wieseckensis.         Potato.  .Milk. 

Growth. 


I         Acid  and  clot         Slight  acidity. 

in  forty-eight     Peptonized  above. 
Evident.  Not  evident.  hours.  Clotted  below. 

5.  Striatus. 
Colour.  Potato. 

I                                                Yellowish  growth. 
I                                    J                                 6.   Wolfii. 
Greyish.                       Brown.                                                   Kegallensis  serum. 
3.  Sputigenus.        4.  Liquefaciens.  I 

Agglutination.  No  aggutination. 

7.  Kegallensis.  8.  Insolitus. 

The  names  of  the  eight  species  so  differentiated  are: — 

1.  V.  gindha  (Pfeiffer,  1896). 

2.  V .  liquefaciens  (Migula,  1900). 

3.  V.  wieseckensis  (Migula,  1900). 

4.  V.  striatus  (Migula,  1900). 

5.  V.  wolfii  (Migula,  1900). 

6.  V.  sputigenus  (Migula,  1900). 

7.  V.  kegallensis  vel paracholercz  (Castellani,  1913). 

8.  V.  insolitus  (Castellani,  1913). 

Of  these,  the  first  and  the  last  two  have  been  associated  with  para- 
cholera,  to  the  exclusion  of  other  organisms. 


MYCOBACTERIACEM  965 

FAMILY   MYCOBACTERIACEJE  Chester,  1901. 

Definition.— Eubacteriales  with  short  or  long  cells,  cylindrical 
or  filamentous,  without  a  sheath,  but  often  clavate,  cuneate,  or 
irregular,  and  often  with  enclosed  granules. 

Type  Genus. — Mycobacterium  Lehmann  and  Neumann,  1896. 

Remarks.— Chester  created  this  family  to  hold  such  forms  as  the 
diphtheria  germ,  the  tubercle  bacillus,  and  the  nocardias. 

The  latter  we  classify  with  the  Fungi  Imperfecti,  and  probably  the 
other  organisms,  especially  the  tubercle  bacillus,  should  join  them; 
nevertheless,  for  the  time  being,  we  keep  them  in  Chester's 
family. 

Mycobacterium  becomes  the  only  genus  of  the  family,  as  Chester 
included  with  it  the  Corynebacterium  of  Lehmann  and  Neumann. 

Genus  Mycobacterium  Lehmann  and  Neumann,  1896. 

Definition. — Mycobacteriacese  with  the  characters  of  the 
family. 

Type  Species.— Mycobacterium  lepra  (Hansen,  1874). 

Remarks. — From  our  point  of  view  there  are  two  divisions  of  the 
genus  which  are  of  importance — viz : — 

A.  Acid-fast  when  stained  by  Ziehl-Neelsen's  method. 

B.  Not  acid-fast  when  stained  by  Ziehl-Neelsen's  method. 

The  former  include  the  tubercle  and  the  leprosy  bacilli,  which  may 
be  distinguished  by  the  latter  being  present  in  very  large  numbers 
in  the  leprotic  nodules,  and  being  very  resistant  to  decolourization, 
while  the  former  are  but  few  in  a  cell  and  relatively  easier  to  de- 
colourize. Moreover,  the  leprosy  bacillus  can  be  readily  stained  by 
Gram,  while  the  tubercle  is  difficult  to  stain  properly. 

The  tubercle  bacillus  can  be  cultivated,  but  so  far  there  is  a  doubt 
as  to  the  leprosy  bacillus  ever  having  been  cultivated. 

The  other  group  contains  the  diphtheria  bacillus.  The  names  of 
these  three  organisms  are:  M.  lepra  (Hansen,  1874) ;  M.  diphtherice 
(Klebs,  1883) ;  and  M.  tuberculosis  (Koch,  1882). 

In  addition  the  Mycobacterium  malei  (Loefner,  1886),  the  cause  of 
glanders,  may  be  mentioned,  as  Whitmore  has  described  a  fever  in 
Rangoon  characterized  by  broncho-pneumonic  symptoms  and  often 
multiple  abscesses,  which  is  due  to  a  closely  allied  organism  intro- 
duced into  the  body  while  injecting  morphine  subcutancously. 

REFERENCES. 

The  current  literature  may  be  found  in  the  Bull,  for  Trop.  Diseases,  and 
in  the  Bulletin  de  I'Institut  Pasteur.  A  very  valuable  general  account  of 
anaerobe  bacteria  is  given  by  Weinberg  and  Seguin  in  their  recent  monograph: 
"  Gangrene  Gazeuse"  (Masson  and  Co.,  Paris). 

Anaerobe  Committee  (1918).    Demonstration  of  Anaerobes.    London. 
Archibald  (191 8).     Lancet  (Wesenberg  and  Alcaligen  s). 


966  SCHIZOMYCETES 

Browning  (191 8).     Applied  Bacteriology.     London. 

Castellani  (1905).  Reports  of  Meetings  C.  B.  British  Med.  Ass.  (1905-1914). 
Ceylon  Medical  Reports.  (1912).  Centr.  f.  Bacter.,  Orig.,  Bd.  39,  p.  14 
(Intestinal  organisms.)  (1914).  Journ.  Ceylon  Branch  B.M.A.  (Para- 
cholera).  (1915).  Journ.  Trop.  Med.,  April  15  (Note  on  a  vibrio  isolated 
from  cases  of  Paracholera).  (1916).  Brit.  Med.  Journ.  (Paracholera) . 
(191 6)  Infezioni  paratifosimili  e  miste,  Annali  Med.  Navale.  (191 8). 
Alcune  osservazioni  sulla  etiologia  diagnosi  e  cura  della  dissenteria, 
Annali  di  Medicina  Navale  e  Coloniale  (Intestinal  Organisms).  I.  and  II. 
Roma.  (1917).  Diseases  in  the  Balkans.  Journal  of  Tropical  Medicine, 
August. 

Castellani  and  Chalmers  (1919).  Annales  de  lTnstitut  Pasteur  (Classifica- 
tion of  Intestinal  Bacteria). 

Chalmers  and  Macdonald  (1916).     Lancet,  July  22. 

Chalmers  and  Marshall  (1916).  Ibid.  (Streptococci);  also  (1915)  ibid. 
(Aurococcus). 

Chalmers  and  O'Farrell  (1916).     Ibid.  (Neisseria). 

Chalmers  and  Waterfield  (1916).  Journal  of  Tropical  Medicine  and 
Hygiene  (Paracholera) . 

Chester  (1901).     Determinative  Bacteriology.     New  York. 

Hewlett  (1918).     Manual  of  Bacteriology.     London. 

Lurie  (1916).     Lancet,  February  12  (B.  columbensis). 

McIntosh  (1918).  Medical  Research  Committee.  Special  Report  Series,  No.  12 
(Anaerobic  Bacteria). 

Migula  (1900).     System  der  Bakterien.     Jena. 

Robertson  (1916).  Journal  of  Pathology  and  Bacteriology,  xx.  (Anaerobes). 
(1917).  Transactions  of  the  Royal  Society  of  Medicine,  xi.,  i.  56-68 
(Tetanus).     (1918).     British  Medical  Journal,  May  25  (Vibrion  Septique). 

Smith  (1915).     British  Medical  Journal,  July  3  (Typhoid  Cohn  Group). 

Spaar  (1915).  Journal  of  Tropical  Medicine,  December  15  (B.  columbensis 
Castellani). 

Weinberg  and  Seguin  (1918).  Gangrene  Gazeuse.  Masson  and  Co.,  Paris. 
(Good  general  account  of  anaerobe  bacilli.) 

Winslow  (1908).     The  Coccaceae.     New  York. 


CHAPTER  XXXVII 
FUNGACE/E-PHYCOMYCETES 

Preliminary — Fungaceae — Phycomycetes — -Zygomycetes — Mucorales — 

References. 

PRELIMINARY. 

The  study  of  fungi,  or  mycology,  as  it  is  often  called,  includes 
macroscopic  and  microscopic  forms.  The  microfungi  are  those 
which  principally  cause  disease,  which,  for  this  reason,  is  termed 
a  mycosis.  Thus  '  otomycosis  '  means  a  mycosis  of  the 'ear,  and 
'  mucormycosis  '  a  disease  caused  by  a  mucor,  which  is  a  fungus 
known  to  Malpighi  in  1686. 

The  study  of  the  microfungi  began  in  the  days  of  Charles  II.,  when  Hooke 
in  1 07 7,  made  a  lens  with  which  he  examined  the  blighted  or  yeliow  specks  on 
the  leaves  of  the  damask  rose,  and  made  excellent  drawings  of  the  micro- 
fungi which  he  saw.  His  book  contains  a  chapter  devoted  to  the  '  Blue 
Mold  and  the  First  Principles  of  Vegetation  arising  from  Putrefaction.' 

Malpighi,  in  1686,  has  a  chapter  devoted  to  '  Plantis  qua3  in  alliis  vegetant,' 
in  which  he  refers  to  mucedo. 

Kay,  in  1706,  in  his  '  Historia  Plantarum,'  describes  Pilobolus  crystallinns, 
one  of  the  Mucoraceae,  which  has  beautiful  crystalline  sporangia  on  yellowish 
sporangiophores,  and  of  which  Plukenet  in  1720  gave  the  first  illustration. 

Micheli,  in  1729,  named  and  gave  a  scientific  account  of  the  genus  Mucor, 
as  well  as  of  Aspergillus  and  many  other  fungi. 

Linnaeus,  in  1753,  in  his  '  Species  Plantarum,'  made  a  resume  of  knowledge 
up  to  that  date ;  and  Hudson,  in  1 762,  described  mucors  in  his  '  Flora  Anglica  ' ; 
while  Lightfoot  in  his  '  Scottish  Flora,'  published  in  1777,  mentioned  the 
ascomycete-sphaeria.  Pelham  (1785),  Withering  (1795),  Dickson  (1785-1801), 
and  Hill  (1796),  all  contributed  to  the  knowledge  of  microfungi,  which  was 
slowly  growing,  as  did  Batsch,  in  1783,  in  Germany,  and  Bulliard,  in  1791, 
in  France. 

This  slow  but  sure  progress  now  became  very  rapid,  and  the  only  way  in 
which  we  can  trace  its  evolution  is  by  mentioning  the  great  systematic  works 
which  arc  of  use  for  reference. 

They  are  Persoon  (1801),  '  Synopsis  Methodica  Fungorum';  Link  (1824), 
'  Caroli  Linne  Species  Plantarum,'  Editio  Quarto,  tomus  vi.,  p.  1 ;  Fries  (1821- 
1829),  '  Systema  Mycologicum  ';  Nees  von  Esenbeck  and  Henry  (1837),  '  Das 
System  der  Pilze;  Kiitzing  (1849),  '  Species  Algarum  ';  Charles  Robin  (1853), 
'  Vegetaux  Parasites  ';  Kuchenmeister  (1857),  '  Animal  and  Vegetal  Parasites 
of  Man  ';  Fuckel  (1869-1870),  '  Symbolae  Mycologist  ';  Eidam  (1872),  '  Myco- 
logie  ';  Naegeli  (1877),  '  Die  Niederen  Pilze.' 

In  1 881  Winter,  Rehm,  Fischer,  and  Lindau's  '  Die  Pilze  Deutschlands,' 
etc.,  began  to  appear,  and  in  1886  Saccardo's  great  work  of  reference,  the 
'  Sylloge  Fungorum,'  began.  Both  have  continued  down  to  the  present 
period.  In  1890  Zopf's  oft-quoted  work,  '  Die  Pilze,'  was  published,  and  in 
1900  Engler  and  Prantl's  '  Pflanzenfamilien.'     In  1907  Vuillemin  started  his 

967 


968  FUNGACE&—PHYCOMYCETES 

new  classification  in  his  paper,  '  Les  Bases  actuelles  de  la  Systematique  en 
Mycologie.' 

Leaving  now  the  systematic  study,  we  turn  to  the  discovery  of  forms 
parasitic  in  man,  beginning  with  the  ringworm  discoveries  of  Remak  (1837), 
Schonlein  (1837),  Gruby  (1842),  and  Malmsten  (1845),  and  passing  through 
the  days  of  Carter  and  Manson  to  those  of  Sabouraud,  Brumpt,  De  Beurmann, 
and  Gougerot,  down  to  the  last,  and  by  no  means  least,  Pinoy,  whose  valuable 
researches  are  of  such  use  in  tropical  medicine. 

The  above  rather  dry  account  will  enable  the  reader  of  this  and  the  two  follow- 
ing chapters  to  realize  the  references  and  the  names  of  the  genera  and  species. 

Nomenclature  is,  however,  very  confused,  and  an  author,  before  he  gives 
a  fungus  a  name,  should  read  '  Regies  Internationales  de  la  Nomenclature 
Botanique,'  published  in  1912.  Unfortunately,  it  has  been  decided  that  the 
nomenclature  of  the  Fungi  Imperfecti,  which  are  so  important  in  tropical 
medicine,  should  commence  with  Fries'  work,  while  we  are  in  accord  with 
Vuillemin,  who  says  that  Saccardo's  '  Sylloge  '  should  be  the  basis  for  all  fungi. 

With  this  brief  history  we  will  pass  on  to  consider  the  Fungacece 
Linnaeus,  1737,  which,  as  we  have  already  seen,  belongs  to  the 
Regnum  Vegetabile,  division  Thallophyta. 

SUBDIVISION  FUNGACEjE  Linnaeus,  1737. 

Synonym. — Fungi  auctores. 

Definition. — Thallophyta  thread-like,  with  apical  growth  produc- 
ing cells  (hyphae)  or  rows  of  cells  (hyphae),  which  collectively  are 
termed  a  mycelium,  and  reproducing  by  freely  escaping  spores, 
which  are  formed  either  acrogenously  at  the  end  of  hyphae  or  endo- 
genously  in  special  cells  (sporangia),  situate  either  at  the  apex  of  a 
free  hypha,  or  are  formed  by  sexual  cells,  which  may  be  enclosed 
in  a  fruit  or  perithecium,  formed  by  the  interlacing  of  mycelial 
threads  without  chromatophores  or  chlorophyl. 

Morphology. — Fungi  are  Thallophytes  without  chlorophyl,  and 
do  not  contain  starch  or  chromatophores.  Their  vegetative  body, 
or  thallus,  consists  generally  of  a  mass  of  filaments  or  threads 
termed  the  '  mycelium.'  The  threads  or  filaments  forming  the 
mycelium  are  called  '  hyphae.'  The  mycelial  threads  or  hyphae 
may  be  septate  or  non-septate.  Their  walls  do  not  consist  of  ordinary 
cellulose,  but  of  a  substance  known  as  fungus-cellulose,  which  does 
not  stain  blue  by  iodine  and  sulphuric  acid. 

Nutrition. — The  fungi,  being  unprovided  with  chlorophyl,  cannot 
make  use  of  the  carbon  dioxide  of  the  air,  and  therefore  derive  their 
carbonaceous  food  material  from  complex  organic  compounds,  as, 
for  instance,  decaying  organic  substances. 

Mode  of  Life. — Fungi  live  as  parasites  or  as  saprophytes.  They 
may  live  one  way  or  the  other,  according  to  circumstances.  Fungi 
are  parasites  of  man,  of  the  lower  animals,  and  of  plants. 

Biological  Characters. — Recent  researches  have  shown  the  great 
biological  analogies  between  fungi  and  bacteria  as  regards  produc- 
tion of  toxins,  agglutination,  and  immunization  phenomena,  etc. 
Charrin  and  Ostrowsky,  Concetti,  Roger,  and  others,  have  obtained 
a  soluble  toxin  from  Monilia  albicans.  Auclair  and  Verliac  have 
isolated   from  Nocardia  bovis   a  toxic  product   soluble  in   ether, 


FUNGACEJE  969 

which  they  call  '  actinomycetine.'  They  state  that  the  injection 
of  this  substance  produces  the  same  lesions  as  the  fungus.  Ceni, 
Besta,  Otto,  and  others,  have  obtained  various  toxins  from  fungi 
of  the  genus  Aspergillus. 

Macfadyen,  by  vaccinating  animals  with  cultures  of  a  saccharo- 
myces,  and  G.  H.  Rogers  and  Concetti,  using  Monilia  candidans 
Robin,  have  noticed  a  production  of  specific  agglutinins  and  immune 
bodies.  Similar  results  have  been  obtained  by  Quarelli  using 
Monilia  balcanica  Castellani. 

Plato,  Bloch,  Truth,  and  others  have  prepared  trichophyton 
vaccines  by  killing  with  heat,  and  triturating  cultures  of  these 
fungi.  By  injecting  these  vaccines  into  patients  suffering  from 
trichophytoses,  they  have  observed  a  general  reaction,  with  fever, 
similar  to  the  reaction  obtained  in  tubercular  patients  by  injecting 
tuberculin.  De  Beurmann  has  described  a  cuti-reaction  in  patients 
affected  with  sporotrichosis. 

Widal  and  Abrami  have  introduced  a  general  diagnostic  method, 
'  sporo-agglut ination,'  based  on  the  fact  that  the  blood  of  patients 
suffering  from  diseases  due  to  fungi  contain  specific  agglutinins  for 
the  spores  of  such  fungi.  Non-specific  coagglutinins  ma}^,  however, 
be  present  in  large  amount. 

Other  biological  reactions — complement  fixation,  etc. — have  been 
described. 

Reproduction. — The  seeds  of  the  Phanerogamia  may  be  said 
to  be  represented  in  the  fungi  by  the  roundish  or  oval-shaped 
bodies  called  '  spores.'  The  spores  multiply  by  budding,  producing 
daughter  spores,  identical  with  the  parent  spores.  Under  certain 
conditions  the  spore,  by  a  process  of  germination,  gives  rise  to  a 
true  mycelial  filament,  which  ramifies,  producing  mycelial  hyphse. 
Some  of  the  terminal  hyphse  are  shorter  and  structurally  different 
from  the  other  hyphse,  and  they  become  organs  of  fructification, 
which  produce  spores.  The  formation  of  spores  upon  these  hyphse 
takes  place  in  various  modes,  of  which  five  different  types  may  be 
distinguished. 

1.  Conidia  or  Exospores. — These  are  non-sexual  spores,  which 
take  origin  by  a  process  of  budding  or  septation  from  the  extremity 
of  a  germinal  mycelial  hypha  or  sporophora.  The  spores  may  all 
be  oi  1  he  same  size,  or,  at  other  times,  some  are  much  larger,  macro- 
conidia,  others  smaller,  microconidia.  The  conidia  are  at  first 
always  unicellular,  but  later  they  may  divide  and  become  multi- 
cellular. 

2.  Chlamydospores  or  Endoconidia. — These  are  asexual  globular 
spores  of  great  size,  and  provided  with  a  thick  membrane.  Chlamy- 
dospores are  terminal  or  intramycelial. 

3.  Endospores  or  Gonidia. — These  spores  take  origin  inside  a 
special  spore-case  structure,  ox  sporangium,  which  is  often  terminal 
and  aerial.  Endospores  which  are  free  and  provided  with  organs 
of  locomotion  (cilia  or  flagella)  are  called  zoospores,  and  the  spor- 
angium is  known  under  the  name  of  zoosporangium. 


PLATE  V. 

CULTURES  OF  SOME  TROPICAL  FUNGI. 

i.  Endodermophyton  concentricum  Blanchard,   1901,  emendavit 
Castellani,  191 1. 
Typical  culture  on  glucose  agar  three  weeks  old. 

2.  Endodermophyton  tropicale  C:\stellani,  1914. 

Old  culture  on  glucose  agar. 

3.  Endodermophyton  indicum  Castellani,  1911. 

Fairly  old  culture  on  glucose  agar. 

4.  Endodermophyton  indicum  Castellani,  191 1. 

Young  culture  on  glucose  agar. 

5.  Epidermophyton  rubrum  Castellani,  1909. 

Culture  on  glucose  agar. 

6.  Trichophyton     violaceum     Bodin,     190^;     var.     decalvans 

Castellani,  191 1. 
Culture  on  Sabouraud's  agar. 

7.  Cladosporium  mansoni  Castellani,  1905. 

Culture  on  Sabouraud's  agar. 

8.  Nigrococcus  nigrescens  Castellani,  1910. 

Culture  on  Sabouraud's  agar. 


970 


PLATE    V. 


\ 


678 

CULTURES   OF   SOME     TROPICAL   FUNGI. 
<k.wmn..&»W  Ed.n  To  face  page  9?o 


FUNGACEJE  971 

Ascits  Fructifications,  or  Asci,  are  special  sporangia,  containing 
four  or  eight  or  a  multiple  of  eight  spores  arranged  in  a  single  line. 
These  spores  are  called  ascospores.  Each  ascospore  presents  two 
membranes,  one  internal,  one  external.  The  external  membrane 
frequently  shows  a  pore,  which  is  called  the  germinating  pore. 

Basidia  Fructifications. — Basidia  are  large  elongated  cells,  each  of 
which  supports  at  its  apex  two  or  four  slender  processes  (sterigmata), 
each  terminating  in  a  small  roundish  conidium  or  basidio-spore. 

4.  Zygospores. — -These  are  the  product  of  a  process  of  conjugation 
or  modified  sexual  act  between  two  special  hyphae.  These  hyphae 
give  rise  to  small  club-shaped  branches,  which  come  into  contact 
and  fuse  together,  forming  a  new  large  cell,  which  presents  a  very 
resistant  double  wall.  The  special  branches  {gametes)  which  come 
into  contact  and  unite  to  produce  the  zygospore  do  not  show  any 
apparent  sexual  differentiation. 

5.  Oospores. — These  are  formed  by  a  complete  sexual  act  or 
fertilization,  and  can  therefore  be  compared  with  a  fertilized 
ovum. 

The  female  element  {oosporangium,  oogonium)  contains  one  or 
more  roundish  protoplasmatic  masses  (macrogameles  or  oospheres, 
female  gametes),  and  presents  a  thick  wall  pierced  by  several  pores. 
The  male  gamete  {antheridium),  which  originates  on  a  delicate 
special  hypha,  comes  into  contact  with  the  oosporangium,  sending  a 
protoplasmatic  process  through  it.  In  other  cases  the  antheridium 
divides  into  several  motile  bodies  called  microgametes,  anther ozoids, 
or  spermalozoids,  which  come  into  contact  with  the  oosporangium, 
and  fertilization  takes  place.  In  some  rare  cases  the  transformation 
of  the  oosporangium  into  an  oospore  is  in  reality  a  process  of  parthe- 
nogenesis. 

Classification. — The  Fungacese  may  be  arranged  in  two  divisions, 
viz. : — 

A.  Vegetative  body  a  multinucleate  naked  plasmodium — Myxomycetes. 

B.  Vegetative  body  usually  filamentous' — Eumycetes  Schroeter,  1892. 

We  are  only  concerned  with  the  Eumycetes. 

Eumycetes  Schroeter,  1892. 
The  Eumycetes  may  be  classified  as  follows: — 

A.  Mycelium  continuous  in  the  vegetative  stage— Class  I.,  Phycomycetes 

De  Bary,  1856. 

B.  Mycelium  septate: — 

I.  Spores  in  asci — Class  II.,  Ascomycetes  Berkeley. 
II.  Spores  in  basidia — Class  III.,  Basidiomycetes  De  Bary,  1856. 
III.  Spores  not  in  asci  or  basidia,  but  on  conidiophores,  naked  or 
in  pycnidia  or  unknown — Class  IV.,  Fungi  Iiuperfecti  Fuckel, 
1869. 

The  fungi  parasitic  in  man  are  practically  all  found  among  the 
Phycomycetes,  the  Ascomycetes,  and  the  Fungi  Imperfecti.  Only 
one  species  of  importance  is  found  among  the  Basidiomycetes,  and 
none  among  the  Myxomycetes. 


972  FUNGACEM— PHYCOMYCETES 

CLASS  I.  PHYCOMYCETES  De  Bary,  1856. 

Definition. — Eumycetes  with  nrycelium  continuous  in  the  vege- 
tative stage. 

Type  Genus, — Mucor  Micheli,  1729. 

Classification. — The  Phycomycetes  may  be  divided  into  subclasses 
as  follows : — 

A.  Sexual  spores  when  present  isogamous  (similar  gametes)- — Subclass  1, 

Zygomycetes. 

B.  Sexual   spores   when    present   heterogamous    (dissimilar   gametes) — - 

Subclass  2,  Odmycetes. 

ZYGOMYCETES. 

Definition. — Phycomycetes  with  similar  gametes. 
Classification. — The    Zygomycetes    may    be    divided    into    two 
orders: — 

A.  Several  asexual  spores  in  sporangia — Order  1,  Mucor  ales. 

B.  Solitary  asexual  spore,  a  true  conidium,  on  conidiophore — Order  2, 

Entomophthorales. 

Only  the  first  order  is  of  interest  to  us. 

Order  Mucorales. 

Definition.— Zygomycetes  with  several  asexual  spores  in  a 
sporangium,  which  in  some  genera  are  conidia-like  bodies. 

Type  Genus. — Mucor  Micheli,  1729. 

Classification. — The  Mucorales  may  be  divided  into  the  following 
families: — 

A.  Asexual  spores  in  typical  sporangia,  in  some  genera  few  spored. 

I.  Columella  present,  zygospores  naked  and  thinly  covered — Family 
1,  MucovacecB. 
II.  Columella    absent,    zygospores    closely    covered     by    hyphae — 
Family  2,  Moriierellacece. 

B.  Asexual  spores  not  in  typical  sporangia — Families  Choanephoracece, 

ChcBtocladiacecu,  Pipiccladiacees. 

Only  the  Mucoracea?  are  of  importance  to  us. 

Family  Mucorace^e. 

These  organisms  have  a  ramified  thallus,  branches  taking  origin 
laterally  or  by  dichotomy.  Some  species  are  provided  with  rhizoids, 
root-like  hairs  by  which  they  are  attached  to  the  surface  on  which 
they  grow.  From  the  surface  of  the  mycelium  some  aerial  branches 
called  '  gonidiophores '  take  origin,  each  of  which  supports  on  its 
distal  extremity  a  pear-shaped,  globular,  or  claviform  sporangium 
called  gonidangium.  The  sporangium  is  at  first  separated  from  the 
gonidiophore  by  a  septum,  which  later  protrudes  into  the  lower 
portion  of  the  sporangium  to  form  a  variously  shaped  structure 
termed  the  columella. 

Inside  the  sporangium  or  gonidangium  endospores  or  gonidia 
develop  by  free  cell-formation. 


MUCORACEAE  973 

The  sporangial  protoplasm  not  used  in  the  formation  of  enclo- 
spores  gives  rise  to  a  peculiar  mucilaginous  substance,  which  at  a 
later  period,  by  absorption  of  water,  causes  the  bursting  of  the 
sporangium.  Each  endospore  or  gonidium,  when  it  has  become 
free,  gives  rise  to  a  mycelial  tube  by  germination.  This  mycelial 
tube  ramifies,  and  a  new  mycelium  is  formed. 

In  some  species,  under  certain  conditions,  a  sexual  reproduction 
may  take  place.  This  consists  in  the  conjugation  of  undifferentiated 
non-motile  gametes,  which  leads  to  the  formation  of  zygospores. 

Many  species,  when  vegetating  in  unfavourable  media,  reproduce 
only  by  formation  of  conidia  and  chlamydospores. 

The  Mucoraceae  are  extremely  common  as  parasites  or  saprophytes 
of  plants  and  animals.  A  mycosis  due  to  these  parasites  is  often 
termed  '  mucormycosis.' 

Mucoraceae  can  be  easily  grown  on  sugar  culture  media — for 
instance,  Sabouraud's  maltose  agar — or  even  on  ordinary  agar. 
The  optimum  temperature  for  their  growth  is  between  35°  and 
400  C.  The  Mucoraceae  require  plenty  of  oxygen,  and  therefore 
the  media  tubes  must  never  be  closed  with  rubber  caps.  When 
there  is  not  enough  oxygen,  the  Mucoraceae  lose  their  character- 
istics, and  give  rise  to  monilia-like  or  yeast-like  forms. 

Classification. — Four  genera  of  Mucoraceae  are  found  to  contain 
species  parasitic  on  man: — 

'Mycelium  ramified,  no  rhizoids- — Mucor. 

Mycelium  non-ramified,  with  or  without  rhizoids;  the  peduncle 
Family  supporting  the  sporangium  terminates  in  a  special  forma- 

Mucoraceae  -s        tion  encircling  the  base  of  the  columella — Lichtheimia. 
Mycelium  with  rhizoids;  columella  ovoid— Rhizomucor. 
Mycelium  with  rhizoids ;  columella  hemispheric,  shaped  like  a 
k        mushroom — Rhizopus. 

Genus  Mucor  Micheli,  1729. 
Ramified  mycelium;  absence  of  rhizoids. 

Mucor  mucedo  Linnaeus,  1764. 

Synonyms. — Mucor  vulgaris  Micheli,  1729;  M.  sphcerocephalus 
Bulliard,  1791. 

The  hyphce  carrying  sporangia  (sporangiophores)  are  long  and 
erect;  the  sporangium  is  globular,  100  to  200  ju  in  diameter;  its 
colour  brownish;  its  surface  covered  by  fine,  minute  crystals  of 
oxalate  of  calcium.  The  spores  (gonidia)  are  elliptical,  with  a 
smooth  surface.  The  columella  is  ovoid-shaped,  and  generally 
yellowish.     Occasionally  very  large  zygospores  may  be  observed. 

.1/.  mucedo  L.  is  very  common,  living  in  organic  substances  in 
decomposition — for  instance,  horse-dung.  It  is  the  cause  of  a 
deadly  disease  in  bees — the  so-called  '  mucorine,'  or  May's  disease — 
but  is  seldom  found  in  man.  Furbringer  has  observed  it  twice  in 
cases  of  pulmonary  infarcts.  A  case  of  broncho-pulmonary  mucor- 
mycosis has  been  observed  by  Castellani  in  the  Balcanic  Zone. 


974  FUNGACEJE—PHYCOMYCETES 

Mueor  pusillus  Lindt,  1886. 
Mycelium  at  first  white,  then  yellowish.  The  hyphse  carrying 
sporangia  are  much  shorter  than  in  the  preceding  species.  The 
sporangium  is  globular,  at  first  pale  greyish,  then  dark  greyish. 
Its  diameter  varies  between  50  and  80  /t.  The  columella  is  clavi- 
form,  ovoid  or  spherical,  yellowish  or  brownish.  The  spores  are 
smooth,  spherical,  3  to  3*5  p,  in  diameter. 


Fig.    479. — Mucoy   mucedo  Fig.  480. — Mucor  pusillus  Lindt. 

Linnaeus.  (After  Lindt.) 

M.  pusillus  is  often  found  in  bread  which  has  been  soaked  in 
water.  It  is  very  pathogenic  to  rabbits;  it  has  once  been  found 
in  man  in  a  case  of  otomycosis  by  Jakowski. 

Genus  Lichtheimia  Vuillemin,  1904. 
Non-ramified  mycelium ;  rhizoids  may  be  present  or  not ;  ped- 
uncle supporting  sporangium  terminates  in  a  formation  encircling 
the  base  of  the  columella. 

Lichtheimia  corymbifera  Cohn,  1884. 

Synonym. — Mucor  corymbifer  Cohn,  1884. 

Mycelium  at  first  white,  then  yellowish.  The  sporangia  are  pear- 
shaped,  10  to  70  [i  in  diameter;  columella  conical,  dark  greyish  or 
brownish ;  spores  elliptical,  2  to  3  fi.  The  hyphre  carrying  sporangia 
are  ramified  in  corymbiform  formation.  This  parasite  has  been 
observed  several  times  in  man,  giving  rise  to  a  mycosis  of  the  ear 
(Hiickel,  Siebenmann,  Graham),  of  the  nose  (Siebenmann),  of  the 
Lungs  (Podack).  A  case  of  generalized  infection  has  been  recorded 
by  Paltauf  (see  p.  977). 

Lichtheimia  ramosa  Lindt,  1886. 

Synonyms. — Mucor  ramosus  Lindt,  1886;  Lichtheimia  ramosa 
Vuillemin,  1904. 

Closely  resembles  L.  corymbifera,  but  rhizoids  are  often  present. 
The  spores  are  larger,  ovoidal,  4  to  7  ft  in  length.  The  columella 
is  always  smooth. 

This  species  has  been  observed  in  man  by  Jakowski  in  a  case  of 
otomycosis.  According  to  Vuillemin,  it  is  frequently  found  in  the 
nasal  mucosa  of  horses. 


RHIZOMUCOR  PARASITICUS 


975 


Genus  Rhizomucor  Lucet  and  Costantin,  1900. 
Rhizoids  generally  present,  columella  of  ovoid  shape. 

Rhizomucor  parasiticus  Lucet  and  Costantin,  1900. 
Mycelium  at  first  greyish,  later  brownish.     Sporangium  globular, 
35  to  80  yt,.     Hyph,e  carrying  sporangia  are  often  ramified,  and  are 
between  1  and  2  centimetres  in  length.     They  are  often  provided 
at  their  basal  portion  with  rhizoids. 


Fig.  481. — Lichtheimia  corym- 
bifera  Vuillemin. 

(After  Lichtheim.) 


Fig.  482. — Rhizomucor  parasiti- 
cus Lucet  and  Costantin. 

(After  Lucet  and  Costantin.) 


The  columella  is  ovoid  or  pyriform;  dark  brownish;  spores 
ovoid;  longitudinal  diameter,  4  /*;  transverse  diameter,  2-5  fi. 

R.  parasiticus  is  pathogenic  for  guinea-pigs  and  rabbits.  It  was 
found  in  the  expectoration  of  a  woman  by  Lucet,  Costantin,  and 
Lambry.  The  patient  had  been  considered  at  first  to  be  suffering 
from  tuberculosis.  She  recovered  under  a  potassium  iodide  and 
arsenical  treatment. 

Rhizomucor  septatus  von  Bezold,  1889. 

Synonyms. —Mucor  septatus  von  Bezold;  Rhizomucor  septatus 
Luoei  and  Costantin,  1889. 

Rhizoids  present ;  sporangia  of  a  brownish-greyish  colour,  spheri- 
cal, with  a  smooth;  or  occasionally  slightly  moriform  surface; 
diameter  about  30  to  35  /*  columella  spherical,  brownish;  spores 
roundish  or  slightly  oval,  from  2*5  to  4  fi. 

The  spores  are  of  a  yellowish  or  brownish  colour;  spherical  or 
ovoid,  with  a  smooth  surface. 

Tliis  species  was  found  by  Siebenmann  in  a  case  of  otomycosis. 

Genus  Rhizopus  Ehrenberg,  1820. 

Rhizoids  present;  columella  hemispheric;  mushroom-like. 
This  genus  contains  only  one  species. 

Rhizopus  niger  Ciaglinski  and  Hewelke,  1893. 

Synonym. — Mucor  niger  Ciaglinski  and  Hewelke,  1893. 

The  mycelial  filaments  are  provided  with   abundant   rhizoids 


976 


F  UNGA  CEM—PH  YCOM  YCETES 


forming  a  snow-white  mass.  Sporangia  globular,  of  black  colour 
when  ripe.  Spores  ovoid,  smooth.  Columella  is  at  first  globular, 
but  later  takes  a  cylindrical  shape,  and  when  the  spores  have 
become  detached,  shows  a  peculiar  mushroom-like  appearance. 


Fig. 


483. — Rhizomucor    sepia- 
tus  von  Bezold. 

(After  Siebenmann.) 


Fig.     484.- — Rhizopus      niger 

ClAGLINSKI  AND  HEWELKE. 

(After  Ciaglinski.) 


This  species  was  discovered  by  Ciaglinski  and  Hewelke  in  a  case 
of  black  mvcosis  of  the  tongue. 


General  Remarks  on  Mycoses  due  to  Species  of  the  Family 
Mucoraceae. 

These  mycoses  are  generally  called  mucormycoses.  They  have 
been  recorded  several  times  in  man. 

Mucormycosis  of  the  Nose. — Several  cases  are  on  record  in 
which  species  of  Mucoraceae  (generally  Lichtheimia  corymbifera) 
were  found  in  various  affections  of  the  nose.  Their  pathogenic 
role  in  such  affections  has  not  been  demonstrated  with  certainty. 

Mucormycosis  of  the  Tongue. — Ciaglinski  and  Hewelke,  and 
later  Seniyiak,  have  described  cases  of  so-called  '  black  tongue,' 
due  to  Rhizopus  niger. 

Mucormycosis  of  the  Ear — Otomucormycosis. — Several  cases 
are  found  in  the  literature  (Siebenmann,  Boke,  Hiickel,  etc.). 
Almost  always  Lichtheimia  corymbifera  was  present.  In  the  tropics 
we  have  observed  two  cases  in  which  L.  ramosa  occurred.  When 
the  fungus  is  in  great  quantity,  the  patient  complains  of  tinnitus 
aurium  and  deafness — the  same  symptoms  as  those  produced  by 
a  plug  of  cerumen  in  the  external  auditory  meatus. 

Mucormycosis  of  the  Lungs.— This  condition  is  rare. 
Furbringer  has  described  two  cases  in  which  L.  corymbifera  was 
found  at  the  autopsy  in  some  hemorrhagic  foci  in  the  lungs.  Lucet, 
Costantin,  and  Lambry  described  a  case  of  bronchitis  in  a  woman 
due  to  Rhizomucor  parasiticus.  The  expectoration  was  rather 
scanty  and  mucopurulent,  but  without  blood.  Mycelial  threads 
and  spore-like  bodies  were  present.     Cultures  were  made,  and  the 


REFERENCES  977 

fungus  grown.  The  condition  lasted  several  months.  Potassium 
iodide  was  given,  and  later,  owing  to  the  symptoms  of  iodism,  various 
arsenical  preparations.  Castellani  has  recorded  a  case  of  broncho- 
mucormycosis  due  to  Mucor  mucedo,  in  the  Balcanic  Zone. 

General  Mucormycosis. — One  case  only  is  on  record — that  of  Paltauf. 
The  patient  during  life  presented  fever,  slight  jaundice,  enlargement  of  the 
spleen  and  liver,  with  signs  of  diffuse  bronchitis  and  obscure  nervous  symptoms. 
At  the  post-mortem  the  brain  presented  several  foci  of  a  friable,  yellowish 
substance;  the  other  internal  organs  showed  nodules  of  various  size,  some 
rather  hard ;  others  had  undergone  a  purulent  change.  In  all  these  formations 
mycelial  threads  were  found ;  in  the  lung-nodules  fructifications  (sporangia)  were 
also  present,  which  enabled  Paltauf  to  determine  the  fungus  as  Lichtheimia 
corymbifera.  According  to  him,  the  infection  must  have  originated  from  the 
intestine,  which  showed  several  ulcerative  lesions  containing  the  same  fungus. 


REFERENCES. 

Current  Literature. 

This  is  very  scattered,  but  references  can  usually  be  found  in  the  Bulletin  de 
I'Institut  Pasteur,  while  original  papers  may  be  found  in  the  Archives  de 
Parasitologic,  edited  by  R.  Blanchard;  in  the  Centralblatt  f.  Bakteriologie, 
in  the  principal  journals  of  dermatology,  such  as  the  British  Journal  of  Derma- 
tology, the  Archiv  fi'tr  Dermatologie  und  Syphilis,  the  Annales  de  Dermatologie, 
II  Giornale  Italiano  delle  Malattie  della  Pelle,  and  Lo  Sperimentale. 

Brumpt  (1913).     Parasitologie.     Paris.     (An  excellent  manual.) 
Castellani  (1904-1912).     Various  papers  in  the  Journal  of  Tropical  Medicine 

and  British  Journal  of  Dermatology. 
Castellani  (1917)  Journal  of  Tropical  Medicine.     September  1  and  15. 
Gedoelst  (191  i).     Synopsis  de  Parasitologie.     Bruxelles. 
Guiart  and  Grinbert  (1911).     Precis  de  Diagnostique.     Paris. 
Horta  (1912).     Memorias  Inst.  O.  Cruz. 
Lour,  C.  (1911).     Edinburgh  Medical  Journal. 
Pinoy  (1908-1918).     Numerous  papers  in  the  Bulletin  de  la  Societe  de  Path. 

Exot.,  and  other  journals. 

Important  Old  Publications. 

In  preparing  this  chapter  we  have  used  the  following: — 

Bonorden,  H.  F.  (1851).    Handbuch  der  Allgemeinen  Mykologie.    Stuttgart. 

Busse,  O.  (1897).     Die  Hefen  als  Krankheitserreger.     Berlin. 

Eidam,  E.  (1872).     Mycologie.     Berlin. 

Fries  (1821-1829).     Systema  Mycologicum,  3  vols.  Gryphiswaldiae. 

Fuckel,  L.  (1 869-1 870).     Symbol®  Mycologicae  Beitrage  zur  Kenntniss  der 

rheinischen  Pilze.     Jahrbiicher  des  Nassanischen  Vereins  fur  Naturkunde. 

Wiesbaden.     (1872).  Continuation  of  above.     Wiesbaden. 
Ki  TziNo,  F.  T.  (1849).     Species  Algarum.     Lipsise. 
Micheli,  P.  A.  (1729).     Nova  Plantarum  Genera.     Florentiae. 
Persoon,  D.  C.  H.  (1801).     Synopsis  Methodica  Fungorum.     Gottingae. 
Robin,  Charles  (1853).     Vegetaux  Parasites.     Paris. 

Mucor. 
Castellani  (1903-1914).  Ceylon  Medical  Reports  (Scattered  references). 
Colombo.  (1917).  Journal  of  Tropical  Medicine  and  Hygiene,  September 
(Mucormycosis).  London.  (1918).  Annali  Medicina  Navale,  vol.  i., 
fasc.  iii.,  iv. 
Zimmermann  (1871).  Das  Genus  Mucor.  Chemitz  (History,  Morphology, 
Classification). 

62 


CHAPTER  XXXVIII 
ASCOMYCETES  AND  BASIDIOMYCETES 

Preliminary —  Classification  —  Protoascomycetes  —  Saccharomycetales  —  Sac- 
charomycetaceae— Endomycetaceae — Euascomycetes — Gymnoascaceae — 
Aspergillaceae — Pyrenomycetes — Basidiomycetes — References. 

PRELIMINARY. 

This  chapter  includes  an  account  of  the  fungi  parasitic  on  man 
which  belong  to  the  Ascomycetes.  These  fungi  are  characterized 
by  their  mode  of  reproduction — viz.,  by  spores  originating  inside 
special  cells  called  asci.  The  spores  (ascospores,  endospores, 
gonidia)  inside  the  asci  are  generally  four  or  eight  or  a  multiple  of 
eight.  While  these  fungi  live  a  parasitic  life,  no  asci  are  found, 
and  reproduction  takes  place  by  germination  and  conidia.  The 
fungi  belonging  to  this  order  are  often  pleomorphic,  their  morpho- 
logical characters  changing  according  to  the  medium  on  which  they 
live. 

Classification. — The  Ascomycetes  are  divided  into  subclasses  as 
follows : — 

A.  Asci  with  varying  number  of  spores,  usually  numerous — Hemiasco- 

mycetes. 

B.  Asci  with  a  definite  number  of  spores: — 

I.  Asci  separate  or  scattered- — Protoascomycetes . 
II.  Asci  approximate,  usually  forming  a  hymenium — Euascomycetes. 

SUBCLASS  PROTOASCOMYCETES. 

This  subclass  contains  a  single  order,  the  Saccharomycetales. 

ORDER  SACCHAROMYCETALES. 

This  order  is  divided  into  two  families  as  follows:- — 

A.  Vegetative   cells  single   or  loosely   attached  in  irregular  colonies — 

Saccharomycetacecs. 

B.  Vegetative  cells  forming  a  mycelium — Endomycetaceee. 

FAMILY  SACCHAROMYCETACE^)  Rees,  1870. 

Definition.— Protoascomycetes  with  vegetative  cells  single  or 
loosely  attached  in  irregular  colonies;  mycelium  not  usually 
developed;  asci  isolated,  not  differentiated  from  vegetative  cells. 

Remarks. — These  organisms  are  generally  round  or  ovoid  cells, 
presenting  a  cell  wall  of  single  or  double  contour;  the  internal  proto- 
plasmatic mass  often  shows  granules  and  vacuoles.     During  active 

978 


SACCHAROMYCETACE/E  979 

vegetation  as  parasites  they  reproduce  by  a  budding  process,  hence 
the  name  of  budding  fungi ;  when  living  on  artificial  media,  under 
unfavourable  nutritive  conditions,  or  in  the  absence  of  oxygen,  they 
multiply  also  by  formation  of  endospores  or  ascospores.  Each  cel- 
lular element  may  become  anascus  containing  1-4,  sometimes  more, 
up  to  12  spores  (ascospores). 

The  organisms  are,  as  a  rule,  unicellular  plants,  but  at  times  the 
cells  elongate,  and  a  rudimentary  mycelium  may  be  formed.  This 
occurs,  for  instance,  when  the  organisms  are  cultivated  in  certain 
fluid  culture  media — for  example,  fluid  beer -wort.  In  such  cases 
side-buds,  which  separate  into  conidia-like  bodies,  may  also  develop 
on  the  hyphse. 

Classification. — The  family  contains  thirteen  genera,  of  which  only 
two — Saccharomyces  Meyen,  1837,  and  Willia  Hansen,  1904 — 
contain  species  parasitic  on  man;  while,  in  regard  to  Schizosac- 
charomyces  Beyerinck,  1893,  it  appears  doubtful  to  us  whether 
this  really  should  be  placed  in  this  family,  as  it  reproduces  by  division 
instead  of  by  budding.  The  various  genera  may  be  recognized 
as  follows:— 

A1.  Vegetative    cells    globose,    ovoid,    or    pyriform,    without    lemon-shaped 
extremities : — 
B1.   Vegetative  cells  increase  by  budding  : — 

C1.  Vegetative  cells  without  large  fat  globule;  asci  3-4  spored: — 
D1.  Ascospores  globose  or  ovoid  : — 

E1.  On  germination  spores  form  typical  yeast  cells: — 
F1.  A  sens  formation  not  preceded  by  zygosis  : — 
G1.  Spore  membrane  single: — 

H1.  Spore  membrane  verrucose — Debaryomyces  Klocher. 
H2.  Spore  membrane  verrucose  and  possessing  a  superficial 
elevated  linear  process,  dividing  the  surface  into  two 
unequal  portions — Schionniomyces  Klocher. 
H3.  Spore   membrane   without   verrucosities   or   crest — Sac- 
charomyces Meyen,  1838. 
G2.  Spore  membrane  double — an  inner,   endosporium,  and  an 
outer,  exosporium — Saccharomycopsis  Schionning. 
F2.  Ascus  formation  preceded  by  zygosis: — 

Ascospores  have  a  smooth  membrane — Zygosaccharomyces 
Barker,  1901. 
E2.  On  germination  spores  form  a  poorly  developed  promycelium, 
multiplication  by  a  process  intermediate   between  budding 
and  transverse  division — Saccharomycodes  Hansen,  1904. 
D2.  Ascospores  pileiform  or  limoniform;  costate  with  bowler-hat  shape. 
No  alcoholic  formation,   but  ethers  produced,  with  pleasant 
fruity  odour,  in  sugar  media — Willia  Hansen,  1904. 
D3.  Ascospores  spherical,  hemispherical,  or  irregularly  shaped. 

Thick  pellicle  with  air-bubbles  on  sugar  liquid  media — Pichia 
Hansen,  1904. 
C2.  Vegetative  cells  large,  spherical,  each  containing  a  large  fat  globule 
as  in  torula.     D.  Asci  8-spored— Torulaspora  Linder. 
B2.    Vegetative  cells  increase  by  fission  : — Asci  8-spored — Schizosaccharomyce 
Beyerinck,   1893. 
A2.    Vegetative   cells   oval,    with   one   or   both    extremities     lemon-shaped. 

Asci  1 -spored — Hansenia  Linder. 
A3.  Vegetative  cells  elongate,  cylindrical,  spores  filiform. 
Asci  1 -spored — Monospora  Metchnikoff. 
Asci  S-spored ;  ascospores  flagellate — Nemalospora  Peglion. 


98o 


ASCOMYCETES  AND  BASIDIOMYCETES 


Fig.  485. — Types  of  Yeasts. 

a,    Saccharomyces    cerevisiae;    b,    S.    ellipsoideus;    c,    S.    pastorianus; 

d,  S.  apiculatus;  e,  Saccharomycodes;  /,  Schizosaccharomyces. 

(After  Lindner.) 


9  to 

Fig.  486. —  Zygosis  and   Formation   of  an   Ascus  in   Zygosaccharomyces 

octosporus. 
(After  Guilliermond.) 


O  7  0  0  ® 


5 


<)       C 


} 


I 


9 


Fig.  487. —  Reproduc- 
tion of  Saccharomy- 
codes. 


Fig.  488. — Types  of  Ascospores. 
1,  Saccharomyces;    2-4,    Willia;    5,   Debaryo- 
myces;  6,  Schionniomycts;  7,  Saccharomycopsis ; 
8,  Monospora;  9,  Nematospora. 

(After  Guilliermond.) 


Fig.  489. — Monospora  cuspidata. 
1-7,  Budding  cells;  8-9,  Ascus  formation;   10,  Ascospore  germinating. 
(After  Metchnikoff  and  Guilliermond.} 


SACCHAROMYCES  981 

Genus  Saccharomyces  Meyen,  1838. 

Definition. — No  proper  thallus.  Reproduction  by  budding  and 
ascospores;  fermentation  of  glucose  and  saccharose,  and  often 
of  other  carbohydrates.  Ascospores  with  one  membrane.  No 
trace  of  any  copulative  process.  Occasionally  rudimentary  mycelial 
tubes  present,  with  transverse  septation. 

Remarks. — -As  already  stated,  the  fungi  of  this  genus,  as  well  as 
of  the  genera  Cryptococcus,  Monilia,  Oidium,  and  Coccidioides,  are 
usually  called  Blastomycetes,  and  the  diseases  induced  by  them 
blastomycoses. 

The  fungi  of  the  genera  Saccharomyces,  Cryptococcus,  and  Cocci- 
dioides have  a  great  importance  in  dermatology,  as  they  give  rise 
to  peculiar  ulcerative  affections  of  the  skin,  often  resembling  a 
syphilide  or  a  tuberculide.  The  first  cases  of  blastomycosis  were 
observed  in  America  by  Posadas,  Wernike,  and  others,  who  at  first 
believed  them  to  be  a  protozoal  infection.  Later  Gilchrist,  Ricketts, 
and  others  recognized  the  true  nature  of  the  parasites.  By  some 
authors  (Sanfelice,  Roncali,  etc.),  cancer  has  been  considered  to  be 
of  blastou^cetic  origin. 

Fungi  of  the  genus  Saccharomyces  are  very  important  from  an  industrial 
and  agricultural  standpoint,  being  the  cause  of  alcoholic  fermentation.  The 
best-known  yeast  is  the  brewer's^  yeast,  5.  cerevisice,  which  is  slightly  ovoid, 
8  to  9  ^  in  diameter. 

Saccharomyces  blanchardi  Guiart,  1906. 

Found  at  an  operation  by  Blanchard,  Schwartz,  and  J.  Binot, 
on  a  patient  who  had  been  considered  to  be  suffering  from  tuber- 
cular peritonitis.  The  fungus  had  produced  in  the  peritoneum 
a  large,  whitish,  gelatiniform  mass,  weighing  about  1  kilogramme. 
The  fungus  grew  well  on  all  sugar  media. 

On  maltose  agar  it  produced  crateriform  colonies  of  a  snow-white 
colour.  Presence  of  asci  with  eight  spores.  On  gelatine  mucoid-like, 
of  greyish  colour.  Slow  liquefaction  of  the  medium.  On  potato 
mucoid  growth,  whitish,  darkening  after  a  long  time.  On  carrot 
growth  viscid,  abundant;  pathogenic  to  rabbits,  in  which  it 
induced  a  general  mycosis,  terminating  fatally. 

Saccharomyces  granulatus  Vuillemin  and  Legrain,  1900. 

Observed  by  Vuillemin  and  Legrain  in  a  tumour  of  the  sub- 
maxillary bone.  Cells  ovoid,  4  to  5  ju  in  length,  and  3  to  4  fx  in 
breadth.  Cultures  pinkish  or  pinkish-red;  ascospores  and  chlamy- 
dospores   present.     Gelatine   not    liquefied.     Sugar   reactions   not 

eriven 

Saccharomyces  tumefaciens  Curtis,  1896. 

Synonym. — Saccharomyces  stibcutaneus  tumefaciens  Curtis,  1896. 

Found  by  Curtis  in  a  myxomatous  tumour.  It  appeared  in 
the  tissues  in  the  shape  of  spherical  bodies  16  to  20  ^i  in  diameter, 
each  surrounded  by  a  zone  of  amorphous  substance.  Grows  well  on 
all  sugar  media;  in  very  old  cultures  asci  are  seen,  with  1-4  spores. 


9S2  ASCOMYCETES  AND  BASIDTOMYCETES 

Gelatine  with  surface  growth  whitish;  no  liquefaction.  Said  to 
ferment  saccharose,  but  not  maltose  or  lactose.  Its  action  on 
glucose  is  not  mentioned.     Pathogenic  to  rats  and  dogs. 

Saccharomyces  samboni  Castellani,  1907. 

Cells  roundish — 6  to  8  yu  in  diameter — easily  grown  on  various 
media,  producing  white  colonies,  which  rapidly  coalesce.  Found 
by  Castellani  in  Ceylon  in  a  few  cases  of  intertriginous  dermatitis 
of  the  cruro-scrotal  region.  A  similar  or  identical  organism  has 
been  observed  by  Whitfield  in  England  in  a  case  of  the  same  derma- 
titis. Ferments  glucose,  levulose,  and  maltose.  Gelatine  is  not 
liquefied.     In  very  old  cultures  asci  present. 

Saccharomyces  ellipsoides  Rees,  1870. 

Found  by  Maggiora  and  Gradenigo  in  two  cases  of  chronic  otitis 
media.  The  cells  are  elliptical,  about  6  /j,  in  maximum  diameter; 
presence  of  asci.  Maggiora  and  Gradenigo  do  not  consider  this 
fungus  to  be  pathogenic.  The  yeast  is  found  on  ripe  grapes,  and 
has  been  carefully  described  by  Hansen,  Asci  ellipsoide  containing 
1-4  spores  each.  The  fungus  often  produces  a  pellicle  in  sugar 
fluid  media.     Ferments  glucose,  maltose,  and  saccharose. 

Saccharomyces  hominis  Klein  and  Gordon,  1903. 
Isolated    in   some    cases   of     tonsillitis    clinically   resembling   diphtheria. 
Roundish  or  oval  cells,  5  to  7  jj,  in  diameter.     Pathogenic  to  guinea-pigs  and 
rabbits.     Sugar  reactions  unknown. 

Saccharomyces  anginaB  Achalme  and  Troisier,  1895. 
Found   by  Achalme  and  Troisier  in  a  case  of  tonsillitis  showing  white 
patches;  in  situ  cells  ovoid,  8-15X5-6  microns.     In  cultures  asci,  4-spored, 
present.      On   gelatine,  surface   growth   white.     Ferments   saccharose,    but 
other  reactions  not  given. 

Saccharomyces  balzeri  Balzer,  Burnier,  and  Gougerot,  191 1. 

Synonym. — Parendomyces  balzeri  Balzer,  Burnier,  and  Gougerot,  191 1. 

Grows  on  culture  media  under  the  type  of  oval  or  roundish  yeast-like  cells, 
proliferating  by  budding.  Isolated  by  Balzer,  Burnier,  and  Gougerot  from  a 
gummatous  affection.     Sugar  reactions  unknown. 


190. — Crateriform  Colonies  Fig.  491. — Saccharomyces    angince 

Saccharomyces  hlanchardi  Guiart.  Vuillemin. 

(After  Blanchard.    Schwartz,   and  (After  Trosier  and  Achalme.) 
Binot,  from  Brumpt.) 

Saccharomyces  roseus  Maggiora  and  Gradenigo,  1890. 
Found  by  Maggiora  and  Gradenigo  in  the  Eustachian  tube,  and  considered 
by  them  to  be  non-pathogenic.     Cultures  of  pink  colour.     Sugar  reactions 

unknown. 


ENDOMYCETACEJE  983 

Genus  Willia  Hansen,  1904. 

Definition. — Saccharomycetace?e  with  ascospores  lemon-shaped 
or  hat-shaped  (see  Fig.  492).  As  a  rule  do  not  produce  alcoholic 
fermentation,  but  produce  various  ethers.  Cultures  present  a 
pleasant  fruity  odour. 

Species  in  Man. — Willia  anomala  Hansen,  1904. 


Fig.  492.— Ascospores  of  Willia  anomala  Hansen. 
(After  Guilliermond.) 

Willia  anomala  Hansen,  1904. 

Rather  small  oval  cells.  In  sugar  liquid  media  it  forms  a  well- 
marked  membrane,  containing  air-bubbles.  Asci  with  2-4  spores 
of  the  so-called  hat-like  type.  Glucose  fermented,  but  not  saccha- 
rose or  maltose.  Ferments  beer-wort,  with  production  of  ethers. 
Found  by  Beauverie  and  Lesieur  in  the  sputum  of  a  tubercular 
patient. 

FAMILY  ENDOMYCETACE.E. 

Definition. — Mycelium  usually  well  developed,  multiseptate; 
asci  4-8  spored;  spores  one-celled. 

A.  Mycelium  poorly  developed — Podocapsa. 

B.  Mycelium  well  developed : — 

I.  Asci  formed  after  zygosis — Eremascus. 
II.  Asci  formed  asexually: — 

(a)  Asci  4-spored — Endomyces. 

(b)  Asci  8-spored — Oleina. 

(c)  Asci  with  a  large  number  of  spores — Coccidioides. 

Only  Endomyces  and  Coccidioides  concern  us. 

Genus  Endomyces  Rees,  1870. 

Definition. — Endomycetaceae  with  mycelium  abundant,  ramified 
or  not,  simple  or  septate.  Presence  of  budding  and  asci  with  four 
spores.  Reproduction  by  external  spores,  ascospores,  and  spores 
situated  inside  the  mycelial  tubes. 

Remarks. — Vuillcmin  believed  at  one  time  that  the  thrush  fungus 
belonged  to  this  genus.  Researches  carried  out  by  Castellani 
have  demonstrated  that  the  condition  known  as  thrush  may  be 
caused  by  various  fungi.  These  fungi,  as  a  rule,  do  not  reproduce 
by  ascospores,  and,  as  justly  remarked  by  Pinoy  and  Vuillemin 
himself,  belong  to  the  genus  Monilia  (see  p.  1079).     For  the  fungus 


9M 


ASCOMYCETES  AND  BASIDIOMYCETES 


isolated  once  by  Vuillemin,  which  has  all  the  characteristics  of  the 
genus  Endomyces,  Landrieu  has  suggested  the  term  Endomyces 
vuillemini. 

Endomyces  vuillemini  Landrieu,  1912. 

Synonym. — Endomyces  albicans  Vuillemin,  1898. 
Found  by  Vuillemin  in  1898  in  thrush  patches. 
Parasitic  Life. — This  fungus  forms  white  patches  on  the  tongue 
and  buccal  mucosa.     The  patches  are  easily  detached.     A  particle 
examined  under  the  microscope   shows  septate  mycelial  threads, 
simple  or  ramified,  the  articles  of   which  are   straight   or    some- 
what   bent.     Each    article     or    cell    is 
about  20  /j,  in  length,  and  3  to  5  [i  in 
breadth.   At  the  terminal  portion  of  each 
mycelial  thread  three   or   four    shorter 
ovoid  elements  are  found  which  repro- 
duce by  budding.     Some  similar  ovoid 
or  roundish  globular  refringent  cells  can 
be  observed,  originating  laterally  at  the 
septations    of    the    mycelium.      These 
globular  elements,  which  were  at  first 
considered  to  be  spores,  become  detached, 
and  reproduce  by  germination. 

Saprophytic  Life — Culture  Characters. 
— The  fungus  grows  well  on  slightly 
acid,  Sabouraud's,  and  other  media; 
does  not  grow  abundantly  in  alkaline 
media;  does  not  ferment  lactose  and  is 
Gram-positive. 

In  cultures  the  fungus  appears  under 
two  forms:  (1)  A  filamentous  form, 
showing  the  mycelial  threads  simple  or 
ramified.  (2)  A  globular  form,  morpho- 
logically similar  to  a  typical  yeast,  and 
reproducing  by  budding.  Both  forms 
may  be  found  in  the  same  culture. 

The  fungus  in  cultures  reproduces 
by:— 

1.  Chlamydospores  or  external  spores;  large  globular  cells  10  to 
20  (j,  in  diameter,  with  thick  resistant  walls.  The  chlamydospores 
are  situate  at  the  terminal  extremity  of  some  mycelial  hyphae, 
and  represent  modified  mycelial  articles. 

2.  Asci  containing  four  ascospores. 

3.  Internal  spores.  These  are  oval  cells  with  membrane,  proto- 
plasm, and  nucleus  similar  to  the  external  spores.  The  internal 
spores  are  arranged  in  a  single  string  inside  some  mycelial  tubes. 

Pathogenicity. — The  fungus  was  found  by  Vuillemin  in  a  case 
of  thrush,  a  condition  generally  due  to  fungi  of  the  genus  Monilia 
(see  p.  1079). 


Fig.  493. — -Endomyces  vuille- 
mini Landrieu. 

(From  a  culture.    After 
Vuillemin.) 

I,  Mycelial  threads,  with 
endospores  and  conidia;  2, 
ascus  fructification. 


COCCIDIOIDES  985 

Genus  Coccidioides  Rixford  and  Gilchrist,  1896. 
Definition. — Endomycetacese  with  mycelium  well  developed  and 
asci  containing  a  large  number  of  spores,  with  intermediate  char- 
acters between  Saccharomyces  and  Monilia.     One   species  only: 
Coccidioides  immitis  Rixford  and  Gilchrist,  1896. 

Coccidioides  immitis  Rixford  and  Gilchrist,  1896. 

Synonyms.— Coccidioides  pyogenes  Rixford  and  Gilchrist,  1896; 
Oidiam  coccidioides  Ophiils,  1905;  0.  ftrotozoides  Ophiils,  1905; 
Posadasia  esferiformis  Canton,  1898;  Oidiam  immiie  Verdun,  1907. 

Definition. — Coccidioides  with  a  large  number  of  spores  in  the 
asci. 

Discovered  by  Wernicke  in  1882  in  America  in  a  patient  with 
patches  resembling  a  tuberculide,  and  gummata.  In  the  lesions 
roundish  bodies  are  seen  of  various  sizes,  3  to  80  p,  in  diameter, 
with  a  well-defined  thick  membrane.  Inside  some  of  the  bodies 
numerous  spores  may  be  seen.     This  genus  is  not  well  defined. 

Cultures. — The  fungus  grows  under  two  types:  (1)  a  saccharo- 
myces-like  type,  reproducing  by  budding;  (2)  a  filamentous  type. 

The  colonies  are  roundish,  slightly  elevated,  but  deepening  into 
the  medium.  They  are  grey  or  white,  but  when  old  often  become 
brownish.  In  old  cultures  chlamydospores  may  be  present.  The 
biochemical  properties  of  the  fungus  are  not  known. 

Pathogenicity. — The  fungus  induces  in  man  a  type  of  blasto- 
mycosis (see  p.  2084).  It  is  pathogenic  to  monkeys,  mice,  guinea- 
pigs,  and  rabbits.     It  probably  lives  saprophytic  in  nature. 

SUBCLASS  EUASCOMYCETES. 

Definition. — Ascomycetes  with  asci  not  separate  or  scattered, 
but  approximate,  usually  forming  a  hymenium,  and  with  a  definite 
number  of  spores  in  an  ascus. 

Classification. — According  to  Stevens,  the  following  orders  may  be 
recognized : — 

A.  Asci  approximate,  no  definite  ascoma,  but  an  indefinite  hymenium— 

Protodiscales. 

B.  Asci  grouped  in  a  definite  ascoma: — 

I.  Asci   not  in  a  cylindrical  or   globose   perithecium — -Helvellales, 

Pezizales,  Phacidiales,  Hysteriales,  Tuberales. 
II.  Asci  in  a  cylindrical  or  globose  perithecium: — ■ 

(a)  Perithecium  sessile: — ■ 

1.  Asci  arising  from  a  common  level  in  the  perithecium — 

Perisporiales,    Hypocriales,     Doihidiales,     Sph&riales, 
Pyrenomycetes. 

2.  Asci   arising   at   different   levels   in   the   perithecium — 

Aspergillales. 

(b)  Perithecium  on  a  short  pedicle — Laboulbeniales. 

Only  the  Aspergillales  and  the  Pyrenomycetes  interest  us.  The 
latter  differ  from  the  former  by  having  their  asci  arranged  in  a 
hymenium  within  the  closed  ascocarp. 


9S6  ASCOMYCETES  AND  BASIDIOMYCETES 

ORDER  ASPERGILLALES. 

Definition. — Euascomycetes  with  asci  gathered  into  definite 
cylindrical  or  globose  perithecia. 

Type  Family. — Aspergillaceae. 

Classification.- — The  order  contains  a  number  of  families,  which 
may  be  recognized  as  follows: — 

A.  Peridium  of  loose  floccose  hyphae — Gymnoascacece  Baranetsky,  1872. 

B.  Peridium  compact  :■ — 

I.  Perithecia  small : — 

(a)  Perithecia  mostly  sessile: — 

1.  Peridia  closed — Aspergillacece. 

2.  Peridia  o-pen—Trichocomacetz. 

(b)  Perithecia  mostly  stalked — Oxygenacece. 

II.  Perithecia  large — Elaphomycetacea  and  other  families. 

Only  the  Gymnoascacese  and  the  Aspergillacese  concern  us. 

FAMILY  GYMNOASCACECE  Baranetzky,  1872. 

Definition. — Aspergillales  with  the  peridium  composed  of  loose 
hyphce,  at  the  extremities  of  which  the  asci  are  situate,  or  without 
perithecial  or  ascal  formation,  and  reproducing  (as  far  as  is  known), 
as  a  rule,  by  mycelial  or  conidial  spores. 

Type  Genus.- — Gymnoascus  Baranetzky,  1872. 

Classification.- — From  the  definition  given  above,  it  is  obvious 
that  the  family  is  capable  of  being  divided  into  two  tribes,  as 
follows :- — 

A.  Ascomycetes  type  : — 

With  perithecia  and  asci — Tribe  1,  Gymnoascecs  Castellani  and 
Chalmers,  1918. 

B.  Fungi  Imperfecti  type  : — 

Without  perithecia  or  asci.  Reproduction  asexual  by  mycelial 
and  conidial  spores — Tribe  2,  Trichophytonece  Castellani  and 
Chalmers,  1918. 

The  first  tribe  includes  the  genera  Myxotrichum  Kiinze,  1823; 
Gymnoascus  Baranetzky,  1872;  Ctenomyces  Eidam,  1880;  Amauro- 
ascus  Schroeter,  1893;  Arachniotus  Schroeter,  1893;  and  Eidamella 
Matruchot  and  Dassonville,  1901;  but  these  are  not  directly  con- 
cerned with  tropical  medicine,  and  will  only  receive  a  passing  notice 
as  required  in  the  following  pages. 

The  second  tribe  is,  however,  of  considerable  importance,  and 
must  be  considered  in  some  detail;  but  we  must  first  inquire  why 
the  genus  Trichophyton  and  its  allies,  which  are  included  in  this 
tribe,  should  be  classified  here. 

It  must  be  pointed  out  that  Vuillemin  would  classify  all  these 
genera  as  follows: — Class,  Fungi  Imperfecti;  Order,  Thallosporales; 
Suborder  r,  Blastosporinese ;  Family,  Oosporaceae;  Genus,  Achorion; 
Suborder  2,  Arthrosporineae ;  Genera,  Microsporum,  Trichophyton, 
etc. 


GYMNOASCACEM  987 

We,  however,  classify  them  as  given  above,  and  our  reasons  for 
so  doing  may  be  set  forth  in  a  short  historical  statement-. 

Historical. — In  1844  Gruby  discovered  the  parasite  of  ringworm,  and  this 
was  verified  in  1845  by  Malmsten,  who  proposed  two  generic  names  for  the 
new  fungus — i.e.,  '  Trichophyton  '  or  '  Trychomyces  ' — and  one  specific  name, 
'  Tonsurans.'  The  first  generic  name  has  become  established,  and  the  genus, 
the  systemic  position  of  which  we  are  about  to  review,  is  now  known  as  Tricho- 
phyton Malmsten,  1845;  very  often  the  date  given  is  1848,  which  is  that  of 
the  publication  of  the  German  translation,  and  not  the  date  of  the  original 
Swedish  work,  the  name  being  derived  from  dpi!;,  '  hair,'  and  <pvr6v,  '  a  plant.' 
Malmsten  believed  the  genus  Trichophyton  to  be  closely  related  to  the  genus 
Torula  Persoon,  1801,  and  especially  to  the  species  T.  olivacea  Corda,  1837, 
and  T.  abbreviata  Corda,  1837. 

This  relationship  was  adopted  by  Charles  Robin  in  his  celebrated  work 
'  Histoire  Naturclle  des  V6getaux  Parasites,'  published  in  1853.  His  classifi- 
cation is  as  follows: — Fungi:  Division,  Arthrosporei  /Tribe,  Torulacei ;  Genus, 
Trichophyton  Malmsten. 

In  1886  Hallier  regarded  the  relationship  to  be  closely  allied  to  the  genus 
Penicillium  Link,  1  - 

In  1875  Grawitz  made  a  new  assertion,  claiming  that  the  relationship  was 
with  Oospora  Wallroth,  1833,  a  view  which  was  adopted  by  Baumgarten  in  his 
'  Pathologischen  Mykologie  '  in  1890. 

Later  researches  by  Duclaux  in  1886,  by  Verujsky  in  1887,  and  still  later 
by  Sabouraud,  indicated  that  some  of  the  species  should  be  classified  near  to 
Sporotrichum  Link,  1809,  which  suggestion  has  been  adopted  by  Saccardo  in 
his  '  Sylloge  Fungorum,'  though  he  goes  further,  making  Trichophyton  merely 
a  synonym  of  Sporotrichum. 

Bodin  (1 899-1 902)  brought  forward  views  tending  to  show  that  the  relation- 
ship is  complex,  some  of  the  species  being  allied  to  Endoconidium  Prillieux 
and  Delacroix,  1891  (a  genus  which  lately  disappeared,  having  become  Stroma- 
tinia  Prillieux,  1897),  while  other  species  were  held  to  be  more  closely  related 
to  Acladium  Link,  1809,  and  to  Haplaria  Link,  1809.  These  views  are  based 
upon  a  study  of  the  sporulation,  and  indicate  that  Trichophyton  is  a  genus 
belonging  to  Fuckel's  class  Fungi  Imperfecti,  and,  adopting  the  older  methods 
of  classification,  to  the  subclass  Hyphomycetece  Martius,  181 7,  the  family 
MucedinacecB  Link,  1809,  subfamily  Amerosporecs  Saccardo,  1886,  tribe 
Macronemcs  Saccardo,  1886,  and  subtribe  Botrytidce  Saccardo,  1886. 

In  June,  1899,  Matruchot  and  Dassonville  published  a  paper  entitled  '  Sur 
la  Position  systematique  des  Trichophytons,'  and  followed  it  later  in  the  same 
year  by  another  paper  entitled  '  Sur  le  Ctenomyces  serratus  (Eidam)  compare 
aux  Champignons  des  teignes.'  Briefly  stated,  their  view  is  that  the  genus 
Trichophyton  Malmsten,  1845,  belongs  to  the  Ascomycetes  of  De  Bary,  if  this 
is  taken  to  include  Hemiascomycetes  of  Brefeld.  In  either  case,  whether 
these  classifications  or  Schroeter's  more  detailed  arrangement  of  the  Ascomy- 
cetes be  adopted  does  not  concern  our  present  purpose,  as  both  contain  the 
family  Gymnoascaceae  (often  written  Gymnoasceae) ,  in  which  Matruchot  and 
Dassonville  place  the  genus  Trichophyton. 
Their  reasons  for  this  classification  are : — 

1.  Ctenomyces  serratus  Eidam,  1880,  is  a  fungus  found  on  the  feathers  of 
birds,  which,  when  cultivated  on  Sabouraud's  proof  media,  produces  growths 
strikingly  analogous  to  those  of  species  of  Trichophyton. 

2.  Ctenomyces  serratus,  when  inoculated  into  animals,  gives  rise  to  lesions, 
resembling  a  Trichophyton  eruption,  in  which  it  appears  in  a  filamentous 
form. 

3.  A  fungus  closely  resembling  a  ctenomyces,  which  they  found  in  a  ring- 
worm in  a  dog,  when  cultivated  gave  rise  to  perithecia.  For  this  fungus  they 
created  a  new  genus,  Eidamella  Matruchot  and  Dassonville,  1901,  calling  the 
given  species  Eidamella  spinosa  Matruchot  and  Dassonville,  1901. 

Against  this  view  Sabouraud  has  pointed  out  that  in  the  cultures  of  this 
fungus  they  found  intercalary  cblamydospores.  but  neither  fusiform  bodies 


gSS 


ASCOMYCETES  AND  BASTDIOMYCETES 


nor  the  conidia  usually  seen  in  Trichophyton  cultures,   and  therefore   he 
considers  their  demonstration  to  be  still  incomplete. 

Chalmers  and  Marshall  in  1914  pointed  out  that  they  had  found  oval 
perithecia  in  very  old  cultures  of  Trichophyton  currii.  The  peridium  was 
at  first  loose,  but  hardened  later,  and  contained  a  number  of  asci  situate  at 
different  levels,  but  these  were  degenerate  and  did  not  contain  ascospores. 
The  perithecia  were  judged  to  belong  to  the  Trichophyton,  because  there  was 
no  sign  at  any  time  of  any  other  organism  in  or  on  the  growth,  macroscopically 
or  microscopically,  and  the  perithecia  appeared  at  the  same  time  all  through 
the  culture.  When  very  old  the  peridium  became  compact  and  like  that  of 
the  Aspergillaceae,  but  at  that  stage  they  consisted  of  the  outer  wall  only,  the 
contents  having  all  disappeared.  They  therefore  considered  that  their 
observation  supported  the  views  of  Matruchot  and  Dassonville. 

We  therefore  classify  the  genus  Trichophyton  in  the  Gymnoasca- 
ceae,  but  the  very  large  number  of  species  included  in  that  genus 
exhibit  such  different  characters  that  they  can  easily  be  arranged 
in  groups,  which  appear  to  us  to  be  of  generic  value,  especially  as 
we  know  that  Malmsten  meant  only  the  form  we  now  call  '  endo- 
thrix  '  to  be  designated  by  his  name  Trichophyton,  because  he 
states: — 'The  mould  formation  appears  in  the  root  of  the  hair, 
and  it  occurs  only  inside  of  the  hair,  between  its  fibres,  so  that  the 
epithelial  layer  is  uninfected;  besides,  there  is  no  mould  formation 
to  be  found  among  the  epidermal  cells,  so  that  one  can  say  with 
good  reason  that  the  disease  absolutely  belongs  to  the  hair.' 

We  have  therefore  distinguished  the  other  groups  by  the  generic 
names  Ectotrichophyton ,  Neotrichophyton,  and  Atrichophyton,  given 
below. 


1  2        3        4 

Fig.   494.   — ■    Microsporum    audouini 

Gruby. 

(After  Bodin.) 

1,  Chlamydospores ;  2,  spindle;  3,pluri- 

septate     spindle;     4,     spore-bearing 

hypha ;  type  Acladium. 


Fig.  495. 


Microsporum  audouini 
Gruby. 


(From  cultures.) 
1,  Septate  spindle  body;  2,  mycelium, 
with   denticulated   structures. 


Tribe  Trichophytone^  Castellani  and  Chalmers,  1918. 
Definition— Gymnoascaceae  of  the  Fungi  Imperfecti  type. 
Type  Genus.— Trichophyton  Malmsten,  1845. 


TRICHOPHYTON  EJE  989 

Classification. — The  various  genera  belonging  to  this  tribe  may 
be  recognized  as  follows: — 

A.  In  lesions  only  mycelial  filaments  and  no  spores  present- — Genus  Lopho- 

phyton  Matruchot  and  Dassonville,  1899. 

B.  In  lesions  mycelial  filaments  and  spores  present:— 

I.  In  cultures  no  conidial-bearing  hyphae  found.  Do  not  attack  hairs 
or  hair  follicles,  but  grow  in  the  superficial  or  deep  strata  of  the 
epidermis. 

(a)  Pluriseptate  spindles  present  in  cultures.     Grow  in  the  super- 

ficial strata  of  the  epidermis,  do  not  attack  hairs.     Cultures 
not  faviform — Genus  Epidermophyton  Lang,  1879. 

(b)  Pluriseptate  spindles  unknown  in  cultures.     Grow  between  the 

superficial  and  deep  layers  of  the  epidermis.     Cultures  favi- 
form— Genus  Endodermophyton  Castellani.  1909. 
II.  In  cultures  conidi  d-bearing  hyphae  present.     May  or  may  not  attack 
hairs  or  hair  follicles. 
(a)  Conidia  only  at  the  ends  of  hyphae  ;  large — -Genus  Montoyella 

Castellani,  1907. 
{b)  Conidia  only  at  the  sides  of  hyphae;  not  large — Genus  Pinoyella 
Castellani  and  Chalmers,  1918. 

(c)  Conidia  at  the  ends  and  sides  of  hyphae: — . 

1.  In  cultures  fusiform  bodies  present  as  septate  or  non-septate 
spindles.     Yellow  fa  vie  scutula  not  present  in  lesions: — 

(a)  Conidia  on  short  stalks: — 

(1)  Attack  hairs  or  hair  follicles: — 

(i.)  Grows  in  and  on  the  surface  of  the  hair.  Is 
often  pyogenic  and  of  animal  origin — 
Genus  Ectotrichophyton  Castellani  and 
Chalmers,  1918. 
(ii.)  Grows  mainly  in  the  hair,  but  a  few  mycelial 
filaments  and  spores  can  be  found  out- 
side the  hair.  Not  pyogenic;  of  human 
origin — Genus  Neotrichophyton  Castellani 
and  Chalmers,  191 8. 
(iii.)  Grows  entirely  in  the  hair,  and  filaments  and 
spores  cannot  be  found  outside  it.  Not 
pyogenic,  except  most  rarely.  Of  human 
origin  —  Genus  Trichophyton  Malmsten, 
1845. 

(2)  Do    not  attack    hairs    or    hair   follicles' — Genus 

Airichophyton  Castellani  and  Chalmers,  1918. 

(b)  Conidia  sessile — Genus  Microsporia}!  Gruby,  1843. 

?..  In  cultures  fusiform  bodies  present  in  the  form  of  swollen 
claviform  ends  of  filaments.  Yellow  favic  scutula  present 
in  lesions— Genus  A  chorion  Remak,  1845. 


Fig.  496 .—  Trichophyton  currii,  Chalmers  and  Marshall,  to  show  Fungus 

in  Hair. 


99°  ASCOMYCETES  AND  BASIDWMYCETES 

Genus  Microsporum  Gruby,  1843. 

Definition. — Gymnoascaceae  with  only  Fungi  Imperfecti  forms 
known;  producing  in  the  lesions  mycelial  filaments  and  mycelial 
spores,  which  are  small,  roundish,  and  about  2-3  microns  in  diameter. 
In  cultures  hyphse  bearing  sessile  conidia  may  be  seen  and  septate 
or  non-septate  fusiform  bodies.  The  lesions  in  man  do  not  produce 
yellow  favic  scutula. 

Type  Species. — Microsporum  audouini  Gruby,  1843. 

Remarks. — The  fungi  belonging  to  this  genus  are  generally  para- 
sitic in  the  hairs  and  hair  follicles,  but  may  attack  glabrous  parts. 
When  parasitic  in  the  hairs,  they  are  characterized  by  the  mycelial 
spores  being  roundish,  small  (2  to  3  /x),  and  irregularly  arranged 
in  a  mosaic-like  manner.  They  are  easily  cultivated  on  Sabouraud's 
and  other  sugar  media  (see  Genus  Trichophyton,  p.  996) .  In  cultures 
the  microsporons  proliferate  by  sprouting  with  branching  of  the 
mycelium ;  and  also,  often,  by — 

1.  Spore-Bearing  Hyphz — of  type  Acladium,  the  conidia  being 
oval,  3  to  4  11  in  length,  and  2  to  3  /j  in  breadth.  They  are  not 
supported  by  short  sterigmata,  as  is  the  case  in  the  genus  Tricho- 
phyton. 

2.  Terminal  Septate  or  Non-Septate  Spindles. — These  structures 
are  found  at  the  end  of  certain  filaments,  and  may  be  considered 
to  be  modified  terminal  conidia.  They  are  large  fusiform  struc- 
tures, 30  to  60  fi  in  length,  and  15  to  18  p,  in  breadth.  They  have 
granular  contents,  and  may  be  septate  or  non-septate.  The  surface, 
especially  at  the  apex,  presents  some  peculiar  hair-like  formations 
which  are  not  observed  in  the  spindles  of  the  fungi  of  the  genus 
Trichophyton. 

3.  Chlamy do  spores. — Certain  mycelial  articles  become  expanse, 
ovoid,  or  ampulliform,  22  to  18  /u  in  length,  and  6  to  8  p,  in  breadth. 
Their  protoplasm  may  be  granular,  and  the  membrane  may  become 
much  thicker  and  have  a  double  contour.  These  elements  are 
chlamydospores.  They  are  generally  found  when  the  fungi  vege- 
tate under  unfavourable  conditions.  Another  structure  often 
seen  in  fungi  of  the  genus  Microsporum  are  the  so-called  denticu- 
late or  pectinate  bodies,  which  are  mycelial  segments,  generally 
curved,  showing  on  one  side— the  convex  side  as  a  rule — several 
small  protruding  processes.  Bodin  has  demonstrated  these  pro- 
cesses to  be  mycelial  tubes  arrested  in  their  development. 

Pleomorphism. — After  a  time,  and  often  rapidly,  the  cultures  of 
microsporons  lose  their  characteristics  and  become  pleomorphic. 
This  phenomenon  is  not  very  prominent,  however,  in  the  most 
important  species — viz.,  Microsporum  audouini — while  it  is  very 
accentuated  in  some  microsporons  of  animal  origin,  especially 
M.  minimum,  in  which,  according  to  the  complete  investigation 
carried  out  by  Bodin,  two  types  may  be  met  with: — 

1.  The  downy  type  (Acladium  type). 

2.  The  glabrous  type  {Endoconidium  type). 


Microsporum  Gruby, 
1843 


MICROSPORUM  991 

i.  The  downy  type  is  found  on  the  ordinary  sugar  media  in 
which  there  is  an  abundant  development  of  white  duvet.  Micro- 
scopically, fructifications  of  the  type  Adadium  are  seen,  the  spore- 
bearing  hyphae  presenting  numerous  lateral  sexile  conidia.  Sub- 
cultures will  always  give  rise  to  the  same  downy  type. 

2.  The  glabrous  type  is  observed  on  wort  agar.  The  growth 
has  a  smooth  surface,  without  duvet.  Microscopically,  short 
strings  of  hyaline,  ovoid,  or  cylindrical  conidia  are  seen  inside  the 
terminal  segments  of  the  fertile  hyphae.     Lateral  conidia  are  absent. 

Mode  of  Infection. — Infection  takes  place  from  man  to  man  in 
the  case  of  microsporons  of  human  origin;  from  the  lower  animals 
to  man  in  the  case  of  microsporons  of  animal  origin.  The  human 
microsporons  LM.  audouini,  M.  velveticum,  M.  umbonatum,  M. 
tardum)  do  not  seem  to  be  inoculable  into  the  lower  animals. 

Table  showing  Species  of  Microsporum  Parasitic  on  Man. 

Genus.  Species. 

(M.  audouini  Gruby,  1843. 
•  of  human  origin    -  ^-  velveticum  Sabouraud,  1907. 
I  M.  umbonatum  Sabouraud,  1907. 
^M.  tardum  Sabouraud,  1909. 
'M.  scorteum  Priestley,  1914. 
M.  minimum    Le    Calve    et    Mai- 

herbe,  1898. 
M.  lanosum  Sabouraud,  1907. 
M.  ielineum  C.  Fox  and   BlaxalL 
1896. 
of  animal  origin    ^  m.  fulvum  Uriburu,   1907. 

M.  pubescens  Sabouraud,  1909. 
M.  villosum  Minne,  1907. 
M.  tomentosum  Pelagatti,   1909. 
M.  iris  Pasini,  1912. 
M.  flavescens  Horta,  1912. 
^M.  depauperatum  Gueguen,  1912. 

Some  species  (M.  audouini,  M.  velveticum,  M.  umbonatum, 
M .  tardum)  seem  to  be  parasitic  on  man  only;  others  (M.  lanosum, 
M.  felineum,  M.  minimum,  etc.)  are  parasitic  on  the  lower  animals, 
but  occasionally  infect  man. 

Microsporum  audouini  Gruby,  1843. 

This  parasite  was  described  by  Gruby  in  1843,  but  his  investi- 
gation was  forgotten,  till  Sabouraud,  in  his  classical  researches 
on  ringworm  in  1892,  demonstrated  the  plurality  of  species  of 
the  fungi  found  in  this  affection,  and  showed  that  a  form  of  tinea 
capitis  was  due  to  the  microsporon  described  by  Gruby. 

Parasitic  Life. — Around  the  affected  hairs  the  fungus  forms  by 
means  of  its  mycelial  spores  a  white  opaque  sheath,  extending  2 
or  3  millimetres  above  the  opening  of  the  hair  follicle.  The  sheath 
is  composed  of  a  mosaic  of  small,  roundish,  or  polyhedral  spores, 
the  diameter  of  which  varies  between  2  and  3  ju.  In  the  interior 
of  the  hair  a  few  mycelial  filaments  of  the  fungus  may  be  observed. 
The  fungus  very  seldom  attacks  glabrous  parts  of  the  body. 


992  ASCOMYCETES  AND  BASIDTOMYCETES 

Saprophytic  Life — Cultures. — Microsporum  audouini  grows  well 
on  Sabouraud's  maltose  agar  and  other  media.  The  rate  of  growing 
is  slow.  In  maltose  agar  the  growth  becomes  evident  about  a 
week  after  inoculation  under  the  appearance  of  a  plaque  of  a  so- 
called  '  satiny  aspect,'  beneath  the  surface.  In  a  few  days  more, 
aerial  hyphse  develop,  extending  above  the  surface.  When  the 
development  is  complete — generally  this  takes  about  six  to  eight 
weeks — the  growth  is  roundish,  covered  with  short  greyish  duvet, 
and  presents  often  a  central  knob,  and  some  concentric  rings  of 
a  whitish-greyish  colour.  The  cultural  characters,  however,  are 
variable,  and  pleomorphism  occurs.  The  cultural  characters  have 
been  thoroughly  investigated  by  Sabouraud,  Fox  and  Blaxall,  Bodin, 
and  others.  The  fungus  very  slowly  liquefies  gelatine;  on  potatoes 
it  produces  a  brownish  discoloration  compared  by  Sabouraud  to 
the  colour  of  dried  blood. 

Reproduction. — This  takes  place — 

i.  By  sprouts  from  the  mycelial  tubes. 

2.  By  small  terminal  and  lateral  conidia,  there  being  spore- 
bearing  hyphse  of  type  Acladium  (see  Fig.  494). 

3.  By  large  unilocular  or  multilocular  spindle  conidia.  These 
spindles  are  large  structures  30  to  60  /ll  in  length,  and  15  to  18  (jl  in 
breadth.     They  may  be  septate  or  non-septate. 

4.  By  formation  of  chlamydospores. 

Pathogenicity. — Microsporum  audouini  causes  the  most  obstinate 
form  of  tinea  capitis.  The  patches  affected  are  often  large,  scaly, 
and  present  stumps,  provided  with  an  opaque  whitish  sheath.  It 
seldom  attacks  glabrous  parts  of  the  body.  M.  audouini  is  ex- 
tremely common  in  England;  but  rare  in  the  South  of  Europe 
(Italy),  and  extremely  rare  in  the  tropics.  We  have  never  seen 
cases  of  ringworm  due  to  M.  audouini  in  Equatorial  Africa  or 
Ceylon,  but  a  few  cases  have  been  described  in  Brazil,  in  Mada- 
gascar, and  in  Senegal. 

M.  audouini  seems  to  live  only  on  the  human  subject,  but  closely 
allied  species  have  been  found  by  Fox  in  cats,  by  Bodin  in  dogs, 
and  by  Bodin,  Fox,  and  others,  in  horses. 

Microsporum  velveticum  Sabouraud,  1907. 

Resembles  closely  M.  audouini,  but  the  cultures  are  more  velvety, 
the  duvet  being  white  instead  of  greyish,  and  of  closer  growth. 
Not  inoculable  into  guinea-pigs.  This  species  seems  to  be  fairly 
common  in  North  America. 

Microsporum  umbonatum  Sabouraud,  1907. 

Found  by  Sabouraud  in  two  cases  of  microsporosis  of  the  scalp 
contracted  in  Russia.  The  appearance  of  the  growth  when  it  has 
reached  complete  development  (about  twenty-five  to  thirty  days 
after  inoculation)  has  been  compared  by  Sabouraud  to  the  appear- 
ance of  an  ancient  round  shield,  with  a  central  conical  formation 
representing  the  umbo  of  the  shield.  Not  inoculable  into  guinea- 
pigs. 


MICROSPORUM  TARDUM  993 

Microsporura  tardum  Sabouraud,  1909. 

Found  by  Sabouraud  in  cases  of  microsporosis  capitis  clinically 
identical  with  the  type  caused  by  M.  audouini.  Differs  from 
M.  audouini  by  the  growth  being  much  slower  and  scantier,  and 
the  duvet  being  shorter. 

Microsporum  lanosum  Sabouraud,  1907. 

Synonym. — Microsporon  audouini  var.  canis  Bodin,  1897. 

Commonly  found  in  dogs.  May  affect  man,  causing  a  type  of 
severe  tinea  capitis;  may  also  produce  forms  of  tinea  barbae  and 
tinea  corporis. 

On  Sabouraud's  agar  the  growth  is  at  first  similar  to  M.  audouini, 
only  more  abundant  and  more  downy.  Later — twenty-five  to 
thirty  days  from  inoculation- — the  central  portion  of  the  growth 
becomes  umbilicatcd,  the  depression  being  surrounded  by  a  ring 
of  snow-white  duvet,  which  in  very  old  cultures  may  become 
yellowish.     Pleomorphism  is  common. 

Microsporum  felineum  C.  Fox  and  Blaxall,  1896. 

Common  in  the  cat  in  England,  North  America,  and  Belgium; 
may  infect  man,  attacking  hairy  and  non-hairy  regions  of  the  body. 
On  Sabouraud's  agar  the  growth  is  rather  abundant,  discoid,  with 
flattened  surface,  showing  no  furrows,  and  covered  with  a  large 
amount  of  grey  duvet.  The  fungus  is  easily  inoculable  into  cats, 
dogs,  and  guinea-pigs. 

Microsporum  minimum  Le  Calv«  and  Malherbe,  1898. 

Synonyms. — Microsporon  audouini  var.  equinum  Bodin,  1896: 
Trichophyton  minimum  Le  Calve  and  Malherbe,  1898. 

Very  common  in  foals;  may  infect  man,  giving  rise  to  a  mild 
type  of  tinea  corporis,  which  gets  cured  spontaneously. 

On  Sabouraud's  and  glucose  agar  the  growth  is  deeply  furrowed, 
and,  in  contrast  to  all  other  microsporons,  duvet  is  absent,  or,  when 
present,  is  very  scanty,  very  short,  and  of  a  pinkish  colour. 

Microsporum  fulvum  Uriburu,  1907. 

Found  by  Uriburu  in  cases  of  tinea  capitis  in  the  Argentine. 
It  grows  very  rapidly  on  Sabouraud's  agar,  the  growth  presenting 
a  central  umbo,  or  projection,  surrounded  by  a  brownish  powdery 
ring.     The  peripheral  zone  of  the  growth  is  covered  with  white  duvet. 

Microsporum  pubescens  Sabouraud,  1909. 
Discovered  by  Sabouraud  in  a  case  of  tinea  capitis  contracted 
in  New  York.  It  grows  rapidly  on  Sabouraud's  medium,  the 
culture  being  characterized  by  the  presence  of  abundant  but  very 
delicate  silky  duvet.  At  complete  development — :about  thirty 
days  from  inoculation — the  growth  may  have  a  flattened  surface, 

63 


994  ASCOMYCETES  AND  BASIDIOMYCETES 

or  some  furrows,  radiating  from  the  centre,  may  be  present.  The 
central  portion,  which  is  covered  with  rather  long,  white  duvet, 
is  encircled  by  a  zone  of  powdery  appearance;  outside  this  there 
is  the  peripheral  zone  covered  by  the  extremely  delicate,  character- 
istic, silky-like  duvet. 

Microsporum  villosum  Minne,  1907. 

Found  in  Belgium  by  Minne  in  a  child  suffering  from  ringworm 
of  the  hair  clinically  identical  with  the  type  caused  by  M.  an&ouini. 
On  Sabouraud's  agar  the  growth  at  complete  development  is  i  bout 
6  centimetres  in  diameter;  the  central  portion  is  flattened,  with 
powdery,  slightly  brownish  surface.  This  is  surrounded  by 
mammillary,  downy  formations,  which  decrease  in  size  towards  the 
periphery. 

Microsporum  tomentosum  Pelagatti,  1909. 

Found  by  Pelagatti  in  Sardinia  in  a  case  of  microsporosis  capitis, 
clinically  identical  with  the  usual  type  caused  by  M.  audouini.  It 
grows  rapidly  on  Sabouraud's  agar.  The  growth  at  complete  de- 
velopment has  a  somewhat  flattened  appearance,  but  several 
furrows  are  present,  originating  from  the  central  portion,  which 
may  be  umbilicated.  The  whole  surface  is  covered  by  thin  white 
duvet. 

Microsporum  iris  Pasini,  191 1. 

Discovered  by  Pasini  in  Italy  in  some  cases  of  microsporosis 
capitis,  clinically  somewhat  different  from  the  usual  type.  The 
fungus  grows  well  on  Sabouraud's  agar.  At  complete  develop- 
ment— twenty-two  to  twenty-six  days  from  inoculation — the 
growth  presents  a  central  knob  covered  with  white  duvet,  and 
surrounded  by  white  and  brick-red  rings,  alternating. 

The  microsporosis  capitis  due  to  this  microsporon  is  charac- 
terized by  the  hairs  remaining  nearly  of  normal  length,  and  pre- 
senting a  white-greenish  discoloration. 

Microsporum  flavescens  P.  Horta,  1912. 

Isolated  by  Horta  from  some  circinate  squamous  patches  situate 
on  the  neck  of  a  child  in  Brazil.  Grows  rapidly  on  Sabouraud's  agar : 
the  growth  is  of  a  yellow  colour;  there  is  a  depression  at  the  centre, 
from  which  radiate  four  or  five  shallow  furrows.  Pleomorphic 
duvet  appears  quickly. 

Microsporum  depauperatum  F.  Gueguen,  1912. 

Isolated  by  Gueguen  from  some  circinate,  dry,  squamous  patches. 
In  cultures  the  membrane  of  some  nucleal  filaments  presents 
peculiar  thickenings.  Spore-bearing  hyphae  are  not  so  well  differ- 
entiated as  in  other  species. 


MICROSPORUM  SCORTEUM  995 

Microsporum  scorteum  Priestley,  1914. 

This  parasite  resembles  M.  fulvum  Uriburu,  1909,  both  morpho- 
logically and  culturally,  and  may  be  identical  therewith,  as  the 
descriptions  given  in  Europe  of  Uriburu's  parasite  are  scanty.  It 
was  found  by  Priestley  in  Townsville  in  Tropical  Queensland; 
and  occurred  in  two  circular  inflamed  areas  on  the  calf  of  a  boy's 
leg.  There  was  no  scaliness,  and  the  hairs  were  not  visibly  altered, 
though  microscopically  they  contained  mycelium  and  a  few  spores. 

On  Sabouraud's  maltose  agar  it  grew  rapidly,  producing  a  growth 
like  a  piece  of  chamois  leather.  It  slowly  digested  milk,  which  it 
did  not  clot.  Multiseptate  spores  were  abundant,  but  lateral  conidia 
were  few,  3-4X2-3  microns  in  size,  while  chlamydospores  were  in- 
frequent. Nodular  bodies  like  those  found  by  Sabouraud  in  T. 
lacticolov  were  found.  Spirals  were  frequent  and  pectinate  bodies 
rare.     Duvet  was  formed. 

Genus  Trichophyton  Malmsten,  1845. 

Definition. — Trichophy tones  with  mycelial  filaments  and  spores 
present  in  the  lesions  and  conidial-bearing  hyph?e  in  cultures,  only 

attacking    hairs    and    entirely 

v  of     human     origin.       Almost 

*«**W         jfe*'  never  pyogenic. 

**%»*. fc    #  Type  Species. — Trichophyton 

$  '  *>\    '    64)  tonsurans  Malmsten,  1845. 

$  0  General      Considerations.  — 

~"^  During  their  parasitic  life  the 

*w*^  species    of  the  genus   Tricho- 


*"***», 


4 


Fig.  497. — Trichophyton  currii,  Fig.  498. — Trichophyton  ciirrii, 

to  show  Mycelial  Spores.  to  show  Conidial-bearing  Hypha. 

phyton  vegetate  according  to  two  types:  (1)  mycelial  filaments; 
(2)  mycelial  spores. 

The  mycelial  filaments  consist  of  long  cylindrical  cells,  separated 
by  septa.  The  so-called  mycelial  spores  are  simply  a  modification 
of  the  mycelial  filaments,  due  to  the  septa  being  much  closer,  so 
that  the  cells  limited  by  them  arc  almost  as  broad  as  they  are  long. 
The  term  '  mycelial  spores  '  is  incorrect,  as  they  are  not  organs  of 
reproduction,  but  only  vegetative  organs. 

When  the  shape  of  these  mycelial  spores  or  spoiulating  mycelia 
is  roundish  or  oval,  the  filament  takes  a  moniliform  appearance. 
Moreover,  these  cells  are  easily  dissociated.     Such  a  type  is  called 


996 


ASCOMYCETES  AND  BASIDI0MYCE1 ES 


'  fragile  mycelium. '  To  this  type  belongs,  for  instance,  Trichophyton 
sabouraudi  R.  Blanchard. 

When  the  mycelial  spores  are  square,  the  filament  straight,  and 
its  articles  long,  the  mycelium  is  called  'resistant.'  This  type  is 
observed,  for  example,  in  Trichophyton  tonsurans  Malmsten. 

Cultivation.- — Most  Trichophytons  can  be  cultivated,  some  cannot. 
The  best  medium  is  Sabouraud's  maltose  agar,  the  composition 
of  which  is  the  following: — 


Maltose 

Peptone  Chassaing 

Agar 

Distilled  water 


4  grammes, 
i  gramme. 
1-50  grammes. 
100  c.c. 


On  this  medium,  however,  pleomorphism  is  of  frequent  occur- 
rence. 

Pleomorphism. — Cultures  on  maltose  and  other  sugar  agars  of  all 
Trichophytons,  with  the  single  exception  of  T.  sabouraudi,  becoming 
old,  lose   their    characteristics   and   become 
covered  with  abundant  white  duvet.    In  these 
cultures,  which  can  be  considered  degenerate, 


Fig.  499. — Trichophy- 
ton. 


Fig.  501. — Trichophy- 
ton: Spiral  Bodies. 


Fig.     500.  —  Fructifi- 
cations. 

(Preparation  from         I,  2,  Spore-bearing  hyphae 
cultures,  after  Bodin.)         (Trichophyton) ;  3, spore- 
1,   Chlamydospore;  2  and     bearing  hypha  {Micros- 
3.  septatespindle  bodies,     porum). 

and  are  generally  called  '  pleomorphic,'  organs  of  fructification  are 
usually  absent.  By  transplanting  these  cultures,  the  same  pleo- 
morphic, downy  type  of  growth  will  be  obtained;  never  again  will 
the  growth  show  the  characteristics  of  the  original  young  cultures 
directly  obtained  from  the  lesions.  It  is  impossible  to  return  to 
the  original  type,  even  by  animal  inoculations. 

To    prevent    pleomorphism,    Sabouraud    advises   the    following 
medium: — 

Agar..  ..  ..  ..  ..      i-8  grammes. 

Peptone  Chassaing  . .  . .      3  to  5  grammes. 

Water  . .  . .  . .  . .     100  c.c. 


TRICHOPHYTON 


997 


*&*m 


Fig.  502. — Trichophyton   currii,  to  show 
Ladder-like  Rows  of  Mycelial  Spores. 


On  this  medium  the  growth  of  the  various  Trichophytons  is  much 
less  abundant  than  on  sugar  media,  but  the  cultures  are  fairly 
characteristic,  and  do  not  become  pleomorphic. 

Experimental  Inoculations. — Certain  Trichophytons  can  be  easily 
inoculated  experimentally  into  man  and  many  of  the  laboratory 
animals — guinea-pigs,  rab-  |^^^H^HHB^^^K^^UH 
bits,  etc.  Sabouraud  advises 
the  inoculation  of  portions 
of  the  cultures  to  be  made 
into  a  small  flictena,  arti- 
ficially induced  by  burning, 
such  as  by  applying  to  the 
skin  a  lighted  match. 

The   intravenous   injection   may    induce   generalized    lesions    of 
the  internal  organs. 

The  intraperitoneal  injection  as  done  by  Citron  may  induce  a 
type  of  peritoneal  pseudo-tuberculosis. 

Mode  of  Infection. — Infection  may  take  place  from  man  to  man — 
this  is  generally  the  case  with  Trichophytons  of  the  group  endothrix — 
or  from  the  lower  animals  to 
man.  There  is  also  little  doubt 
that  Trichophytons  may  live 
saprophytically  in  nature,  this 
explaining  sporadic  cases  of 
trichophytoses  in  man. 


Fig.  503.  —  Trichophyton  currii, 
Four  Days'  Growth  on  Sabou- 
raud's  Maltose  Agar  at  340  C, 
to  show  White  Growth  with 
Knob-like  Centre. 


Fig.  504. — Trichophyton  violaceum 
var.  khartoumense. 
(Note  absence  of  acuminate  centre 
and    dark     [violet]     colour    of     the 
growth.) 


Reproduction. — This  takes  place  by— 

1.  Lateral  and  terminal    conidia,   supported    by    short    sterig- 
mata. 

2.  Chlamydospores;  these  are  rare. 

3.  Large  terminal  septate  and  unseptate  spindles. 
Classification.   -The  principal  species  of  the  genus  Trichophyton 

arranged  chronologically  are : — 


o98  ASCOMYCETES  AND  BASIDIOMYCETES 

i.  T  tonsurans  Malmsten,  1845. 

2.  T.  sabouraudi  R.  Blanchard,  1895. 

3.  T.  violaceum  Bodin,  1902. 

4.  T.  sulphureum  C.  Fox,  1908. 

5.  T.  glabrum  Sabouraud,  1909. 

6.  T.  fumatum  Sabouraud,  1909. 

7.  T.  effr actum  Sabouraud,  1909. 

8.  T.  circonvolutum  Sabouraud,  1909. 

9.  T.  regulare  Sabouraud,  1909. 

10.  T.  umbilicatum  Sabouraud,  1909. 

11.  T.  exsiccatum  Uribuni,  1909 

12.  T.  polygonum  Uriburu,  1909. 

13.  T.  soudanense  Joyeux,  1912. 

14.  T.  currii  Chalmers  and  Marshall,  1914. 

These  may  be  recognized  as  follows: — 

A.  Condition  of  mycelium  in  hair  not  definitely  stated,  but  probably  that  of 

the  Crateriform  subdivision  (see  below). 

(1)  In  cultures  very  convoluted — Circonvolutuni. 

B.  Condition  of  mycelium  in  hair  definitely  stated. 

I.  Mycelium  in  hair  resistant  to  caustic  potash,  segments  characteristi- 
cally quadrangular  in  shape,  with  double  contour,  4  to  6  (x  in 
breadth,  arranged  in  fairly  straight  ladder-like  rows — Crateriform 
subdivision. 

(a)  Cultures  coloured  and  with  craters  :  Tonsurans  group  : — 

(2)  Yellow  in  centre,  white  at  periphery — Tonsurans. 

(3)  As  'tonsurans,'  but,  when  old,  cracked  and  dry — Effractum. 

(4)  Orange-red  centre,  remainder  sulphur  coloured — Sulphureum. 

(5)  Golden-yellow    convoluted    centre,    becoming    crateriform 

later — Soudanense. 

(6)  When  old  of  a  yellowish-brown  colour- — Fumatum. 

(b)  Cultures  white  with  craters  :  Umbilicatum  group  : — 

(7)  Deeply  umbilicated  with  aureola — Umbilicatum. 

(8)  Slow  growth,  surface  cracked  with  dry  appearance — Exsic- 

catum. 

(9)  Growth  at  first  roundish  and  then  polygonal — Polygonum. 

(c)  Cultures  white  with  knob-like  centre  :  Currii  group  : — ■ 

(10)  Does  not  form  duvet — Currii. 

II.  Mycelium  in  hair  not  resistant  to  caustic  potash;  segments  rounded, 
47  /x  in  diameter,  not  arranged  as  a  rule  in  rows,  but  if  a  row  is 
visible  it  resembles  a  string  of  beads  and  not  a  ladder — Acuminate 
subdivision, 
(a)    Without  acuminate  centre  :  Violaceum  group: — 

(11)  Primary  growth  violet: — 

(a.)  Most  strains  do  not  melt  gelatine  very  rapidly: — 

(i.)  Ordinary  amount  of  scaling  on  the  head — Viola- 
ceum. 
(ii.)   Enormous  numbers  of  scales,  followed  at  times  by 
permanent  baldness — Var.  decalvans. 
(b)  Melts  strong  gelatine  very  rapidly,  beginning  as  soon  as 
growth  appears — Var.  kharioumense. 

(12)  Primary  growth  white — Glabrum. 

(b)   With  acuminate  centre  :  Sabouraudi  group  : — 

(13)  Without  duvet  when  old — Sabouraudi. 

(14)  With  duvet  when  old — Pilosum. 


Courmont's  parasites  cannot  be  easily  classified. 


TRICHOPHYTON   TONSURANS 


999 


Fig.  505. — Trichophyton  tonsu- 
rans Malmsten. 

(Preparation  of  a  hair  in  liquor 
potasss,  after  Sabouraud.) 


Trichophyton  tonsurans  Malmsten,  1845. 

Synonyms.— Trichomyces  tonsurans  Malmsten,  1845;  Oidium  ton- 
surans Zopf,  1890 ;  Trichophyton  megalospor um  endothrix  Sabouraud, 
1894;  T.  crater  if orme  Bodin,  1902,  which  is  the  term  in  current 
use  in  dermatological  literature. 

Causes  a  type  of  tinea  capitis  some- 
what rare  in  England,  but  common 
on  the  Continent.  The  hairs  are 
broken  2  to  4  millimetres  from  the 
scalp,  and  the  stumps  are  variously 
bent.  The  diseased  hairs  have  a 
powdery,  greyish  appearance,  and 
on  pulling  them  out  the  roots  are 
not  black,  as  in  normal  hairs.  It 
belongs  to  the  type  Endothrix.  The 
mycelial  cells  are  large  (4  to  5  fi), 
quadrangular  (so-called  resistant 
mycelium  type).  Grows  well  on 
maltose  agar  and  other  media;  on 
maltose  agar  colonies  are  white  or 
yellowish,  often  crateriform,  and  present  a  velvety  surface  at 
first,  later  powdery.  In  hanging-drop  cultivations  spore-bearing 
fructifications  can  be  seen. 

T.  tonsurans,  besides  producing  a  type  of  tinea  capitis,  produces 
also  a  form  of  tinea  corporis  and  a  trichophytosis  of  the  nails. 

Trichophyton  sabouraudi  R.  Blanchard,  1895. 

Synonym. — Trichophyton  acuminatum  Bodin,  1902.  This  is  the 
term  commonly  used  in  dermatological  works. 

This  Trichophyton  is  of  the  type  Endothrix.  Mycelial  threads 
have  a  moniliform  appearance,  and  their  articles  become  easily 
dissociated  (so-called  fragile  mycelium).  Grows  well  on  maltose 
agar,  giving  rise  to  conical  white  colonies;  often  acuminate  with 
central  plumes,  and  occasionally  may  present  yellowish  or  pinkish 
rings;  older  cultures  may  present  a  powdery  surface  of  a  dark 
pinkish  colour.  Pleomorphism  always  absent.  In  hanging-drop 
cultures  aerial  filaments  with  lateral  conidia  are  seen. 

T.  sabouraudi  causes  a  form  of  tinea  capitis  called  by  Sabouraud 
'  tondante  peladoide,'  and  also  a  variety  of  tinea  circinata. 

The  tinea  capitis  induced  by  this  fungus  is  also  known  under  the 
name  of  '  black-dotted  ringworm.'  The  hairs  get  broken  lower 
than  in  the  type  of  ringworm  caused  by  T.  tonsurans.  The  stumps 
are  on  the  same  level  as  the  surface  of  the  scalp,  and  appear  as 
black  dots. 

Trichophyton  pilosum  Sabouraud,  1909. 

Very  similar  to  T.  sabouraudi,  from  which  it  differs  only  by  the 
cultures  being  covered,  when  old,  by  a  dense,  short,  white  duvet. 


rooo  ASCOMYCETES  AND  BASIDIOMYCETES 

Trichophyton  soudanense  C.  Joyeux,  1912. 
Endothrix ;  very  similar  to  T.  tonsurans.  In  the  hairs  the  mycelial 
spores  are  generally  rectangular,  arranged  in  long  strings.  On 
Sabouraud's  agar  the  growth  appears  three  to  four  days  after  in- 
oculation as  a  small  yellow  nodule;  later,  the  peripheral  portion 
of  the  growth  appears  white.  It  has  been  found  by  C.  Joyeux  in 
cases  of  tinea  capitis  in  the  Sudan. 

Trichophyton  viclaceum  Bodin,  1902. 

Discovered  by  Sabouraud  in  cases  of  tinea  barbae;  type  Endo- 
thrix. The  growth  on  maltose  agar  is  of  a  light  brownish  or  greyish 
colour,  with  moist  surface,  and  later  becomes  violet. 

This  species  is  common  in  Italy  and  North  Africa.  In  Ceylon 
a  variety  of  this  fungus  produces  a  type  of  very  common  ring- 
worm of  the  scalp  in  children,  with  white  patches  covered  by 
enormous  numbers  of  pityriasic  squamae.  The  patches  often  remain 
permanently  bald.  The  Ceylon  fungus  is  endo-ectothrix,  and 
although  culturally  is  hardly  distinguishable  from  T.  riolaceum, 
is  probably  a  different  variety  (var.  decalvans  Castellani,  1913),  as 
it  produces  lesions  generally  different  from  those  induced  by 
T.  riolaceum.  In  the  Sudan  it  apparently  liquefies  gelatine  more, 
rapidly  (var.  khartoumense  Chalmers  and  Macdonald,  1915). 

Trichophyton  glabrum  Sabouraud,  1909. 

Closely  allied  to  T.  violaceum,  but  shows  a  more  rapid  growth,  and 
no  violet  pigmentation  develops.     Surface  smooth  and  moist. 

Trichophyton  sulphureum  C.  Fox,  1908. 

Described  by  Colcott  Fox  in  some  cases  of  tinea  capitis  in  Eng- 
land. Endothrix  type.  On  Sabouraud's  agar  the  growth  is 
characterized  by  a  central  reddish  nodule,  which  later  becomes 
crateriform,  assuming  a  speckled  appearance.  The  rest  of  the 
culture  has  a  delicate  but  distinct  primrose  or  sulphur  colour. 

Trichophyton  plicatile  Sabouraud,  1909. 
Colonies  closely  resemble  those  of  T.  tonsurans,  but  have  a  creased 
appearance.     Found  by  Sabouraud  in  cases  of  sycosis.     Sequeira 
has  observed  it  in  a  case  of  trichophytic  granuloma.    We  have  placed 
the  fungus  in  the  genus  Neotrichophyton  (p.  100 1). 

Trichophyton  circonvolutum  Sabouraud,  1909. 

Endothrix;  somewhat  similar  to  T.  plicatile  ;  the  growth  has  a 
convoluted  surface.  Found  by  Sabouraud  in  cases  of  trichophytosis 
contracted  in  the  Sudan  and  Dahomy. 

Trichophyton  exsiccatum  Uriburu,  1909. 
Found  in  Argentina  by  Uriburu.     Endothrix;  very  slow  growth; 
crateriform  colonics,  with  surface  finely  cracked,  and  of  a  dry  aspect 


TRICHOPHYTON  POLYGONUM  iooi 

Trichophyton  polygonum  Uriburu,  1909. 
Endothrix.     The  growth  is  at  first  roundish,  then  takes  a  char- 
acteristic polygonal  outline.     The  central  part  is  crateriform. 

Trichophyton  regulare  Sabouraud,  1909. 

Endothrix;  very  similar  to  T.  tonsurans,  the  cultures  being  at 
first  crateriform;  then,  the  edges  of  the  crater  becoming  under- 
mined, the  growth  takes  a  peculiar  pouch-like  shape,  with  several 
radiating  small  sulci.  The  characters  of  the  fungus  show  always 
the  greatest  regularity,  never  changing;  hence  the  name  T.  regulare 
given  to  it  by  Sabouraud.     This  fungus  was  found  by  Dalla  Favera. 

Trichophyton  umbilicatum  Sabouraud,  1909. 

Endothrix;  cultures  are  deeply  umbilicated;  present  at  the 
periphery  fine  radiating"  hyphae,  forming  a  sort  of  aureola. 

Trichophyton  fumatum  Sabouraud,  1909. 

Cultures  crateriform,  taking  when  old  a  yellowish-brownish 
colour,  compared  by  Sabouraud  to  the  colour  of  a  dead  leaf.  This 
Trichophyton  is  fairly  common  in  some  parts  of  Italy. 

Trichophyton  effractum  Sabouraud,  1909. 

Cultures  at  first  very  similar  to  those  of  T.  tonsurans,  being 
crateriform;  when  old,  the  growth  becomes  very  dry,  and  the 
surface  splits  from  the  edge. 

Trichophyton  currii  Chalmers  and  Marshall,  1914. 

This  fungus  was  found  in  an  epidemic  of  ringworm  in  a  Khartoum 
school.  It  is  not  the  common  fungus  of  the  town,  which  appears 
to  be  T.  violaceum  var.  khartoumense.  T.  currii  is  of  the  type 
endothrix,  and  grows  aerobically,  but  not  anaerobically.  It  forms 
ladder-like  rows  of  mycelial  spores  in  the  hairs.  These  spores  are 
usually  4-2  microns  in  breadth,  and  they  and  the  mycelium  resist 
the  action  of  caustic  potash.  It  forms  neither  acid  nor  gas  in  mono- 
saccharids,  disaccharids,  trisaccharids,  polysaccharids,  glucosides, 
or  alcohols.  It  does  not  alter  litmus  milk.  It  does  not  liquefy 
gelatine.  On  Sabouraud's  agars  it  produces  white  growths  with  a 
central  knob,  a  white  plateau  with  a  slight  circular  marking,  and  a 
peripheral  fringe.  It  grows  on  carrot,  potato,  but  was  not  char- 
acteristic on  beetroot,  and  was  poor  on  Buchanan's  and  Loeffier's 
media.  Inoculations  directly  from  the  patients'  heads  failed  in 
monkeys,  cats,  dogs,  and  mice.  In  man  it  gives  rise  to  a  type 
of  tinea  capitis  tropicalis. 

Genus  Neotrichophyton  Castellani  and  Chalmers,  1918. 

Definition. — Trichophytineae  with  mycelium  and  spores  present 
in  the  lesions,  and  conidial-bearing  hyphae  in  cultures,  attacking 
hairs,  but  with  mycelial  spores  and  filaments  outside  the  hair  shaft. 


1002  ASCOMYCETES  AND  BASIDIOMYCETES 

Type  Species.- — Neotrichophyton  flavum  Bodin,  1902. 
Classification. — There  are  only  two  species,  which  may  be  dis- 
tinguished as  follows: — 

A.  Cultures  cerebriform — Flavum. 

B.  Cultures  crateriform  and  creased — Plicatile. 

Neotrichophyton  flavum  Bodin,  1902. 

Synonym. — Trichophyton  cerebriforme  Sabouraud,  1909. 

Differs  from  Trichophyton  tonsurans  by  the  cultures  being  cere- 
briform, and  by  becoming  creamy-white  when  old. 

Pathogenicity. — Induces  a  type  of  tinea  corporis  and  a  form  of 
sycosis.     Inoculable  into  guinea-pigs. 

Neotrichophyton  plicatile  Sabouraud,  1909. 

Synonym. — Tricophyton  plicatile  Sabouraud,  1909. 

Colonies  closely  resemble  those  of  Trichophyton  tonsurans,  but 
have  a  creased  appearance  with  white,  powdery  surface.  Found  by 
Sabouraud  in  cases  of  sycosis.  Sequeira  has  observed  it  in  a  case  of 
trichophytic  granuloma. 

G  enus  Ectotrichophyton  Castellani  and  Chalmers,  1918. 

Definition. — Trichophytoneae  with  mycelium  and  spores  present 
in  the  lesions,  and  conidial-bearing  hypha:  in  cultures;  attack  hairs 
and  hair  follicles,  growing  in  and  on  the  surface  of  the  hairs;  is  often 
pyogenic  and  of  animal  origin. 

Type  Species. — Ectotrichophyton  mentagrophytes  Robin.  1853. 

Classification. — The  genus  is  capable  of  division  into  three  sub- 
genera by  the  following  characters: — 

A.  Ectotrichophyton  : — 

With  small  spores  about  3  to  4  microns  in  diameter,  forming  a  sheath 
outside  the  hair  shaft,  on  dissociation  of  which  they  are  seen  to 
form  chains;  with  sinuous  and  quadrangular  hyphal  segments, 
together  with  spores  of  varying  diameter  and  air-bubbles,  inside 
the  hair  shaft;  with  cultures  easily  obtainable,  of  rapid  growth, 
and  of  considerable  vitality,  characterized  by  plaster-like  or  floury 
centres  surrounded  by  a  fringe,  when  grown  on  Sabouraud's  proof 
media,  and  by  successful  inoculations  into  animals — Subgenus 
Microlrichophyton . 

B.  Ectotrichophyton  : — 

With  large  spores  about  5  to  7  microns  in  diameter,  forming  a  sheath 
outside  the  hair  shaft,  on  dissociation  of  which  they  are  seen  to 
form  chains,  and  with  sinuous  hyphal  segments,   together  with 
large-sized  spores   and  air-bubbles,   inside  the  hair  shaft;   with 
cultures    easily   obtainable,    but   of    slow    growth  in   temperate 
climates,  though  much  more  rapid  in  tropical  climates,  character- 
ized by  their  tendency  to  resemble  (at  all  events  when  old)  those 
of  the  Achorions,  and  capable  of  being  inoculated  into  animals — 
I.  With  early  formation  of  a  duvet — Subgenus  Ectotrichophyton. 
II.  Culture  sooner  or  later  resembles  that  of  A  chorion  schoen- 
leinii— Subgenus  Favotrichophyton. 


ECTOTRICHOPHYTON  (FA  VOTPICHOPHYTON) 


1003 


Ectotrichophyton  (Favotrichophyton)  Castellani  and  Chalmers, 

1918. 

Definition— Ectotrichophyton  with  the  characters  given  ahove 
for  Favotrichophyton. 
Type  Species. — Ectotrichophyton  discoides  Sabouraud,  1909. 


Fig.  506.  —  Ectotrichophyton  dis- 
coides :  Nineteen  Days'  Growth 
on  Sabouraud's  Maltose  Agar 
at  320 C 


Fig.  507.  — ■  Eciotrichophylon  dis- 
coides: Forty-two  Days'  Growth 
on  Sabouraud's  Maltose  Agar 

at    32°C. 


Classification. 

are: — 


-The  Favotrichophyton  species  which  are  known 


E.  verrucosum  Bodin,  1902, 

E.  ochracetim  Sabouraud,  1909, 

E.  album  Sabouraud,  1909, 

E.  discoides  Sabouraud,  1909, 

E.  luxurians  Brault  and  Viguier,  1914. 

which  may  be  differentiated  as  follows: — 

A.  Condition  of  mycelium  in  hair  not  definitely  stated: — • 

I.  Young  cultures  white  in  colour,  and  soon  resembling  those  of 
Achorion  schoenleini,  but  sunk  into  the  medium — -Album. 

B.  Condition  of  mycelium  in  hair  that  of  an  ecto-endothrix: — - 

II.  Cultures  grey  in  colour,  humid,  with  verrucose  surface — Verru- 
cosum 
III.  Young  cultures  of  a  yellow  ochre  colour — Ochraceum. 

IV.  Cultures  yellowish-brown  or  greyish-yellow,  cupola-shaped, 
humid,  with  usually  smooth  surfaces,  and  not  resembling  the 
Achorion  cultures  until  old — Discoides. 

V.  Very  rapid  development — Luxurians. 


Ectotrichophyton  verrucosum  Bodin,  1902. 

Synonym. — Trichophyton  verrucosum  Bodin,  1902. 

Endo-ectothrix,  megalosporon,  faviform.  This  fungus,  though 
producing  typical  trichophytic  lesions  when  parasitic,  shows  cul- 
tural characters  somewhat  similar  to  an  achorion,  the  growth, 
which   is  white,    being    often   convoluted    or    cerebriiorm.     It    is 


ioo4  ASCOMYCETES  AND  BASIDIOMYCETES 

found  in  donkeys,  and  may  infect  man.  The  same  or  similar 
species  are  found  parasitic  on  the  horse  and  on  some  birds,  and  may 
also  infect  man. 

Ectotrichophyton  ochraceum  Sabouraud,  1909. 

Synonym. — Trichophyton  ochraceum  Sabouraud,  1909. 

Type  Ectothrix,  of  animal  origin;  cultures  somewhat  similar  to 
fivus.  On  maltose  and  glucose  agars  the  colonies  are  character- 
ized by  an  ochre-yellow  knob ;  portions  of  the  growth  may  be  covered 
by  an  extremely  short,  almost  invisible,  duvet.  On  ordinary  agar 
the  surface  of  the  colonies  is  cerebriform.  Optimum  temperature, 
250  C.     It  is  easily  inoculated  into  guinea-pigs. 

Ectotrichophyton  album  Sabouraud,  1907. 

Synonym. — Trichophyton  album  Sabouraud,  1907. 

The  cultures  are  extremely  like  favus,  but  are  generally  less 
bulging,  more  deeply  umbilicated,  and  more  regularly  folded; 
the  growth  deepens  in  the  medium;  some  white  duvet  present. 
Optimum  temperature,  250  C.     Can  be  inoculated  into  guinea-pigs. 

Ectotrichophyton  discoides  Sabouraud,  1909. 

Synonym. — Trichophyton  discoides  Sabouraud,  1909. 

Endo-ectothrix,  megalosporon,  faviform.  Somewhat  similar  to 
E.  album,  but  the  growth,  which  is  almost  a  perfect  disc,  has  a 
more  flattened  surface.  There  is  often  a  central  knob.  The  whole 
growth  has  a  brownish-yellowish  colour,  with  a  moist  surface, 
somewhat  resembling  the  non-pigment ed  cultures  of  Trichophyton 
violaceum.  It  occurs  in  Egypt  and  in  the  Anglo-Egyptian  Sudan, 
as  described  by  one  of  us. 

Ectotrichophyton  luxurians  Brault  and  Viguier,  1914. 

Isolated  from  cases  of  kerion  in  Algeria.  Very  rapid  growth  with 
faviform  appearance. 

Ectotrichophyton  (Microtrichophyton)  Castellani  and 
Chalmers,  1918. 

Definition. — Ectotrichophyton  with  small  spores  3-4  microns  in 
diameter. 

Type  Species. — Ectotrichophyton  (Microtrichophyton)  mentagro- 
phytes  Robin,  1853. 

Classification. — The  following  species  are  known: — 

E.  mentagrophytes  Ch.  Robin,  1853. 
E .  farinulentum  Sabouraud,  1910. 
E.  persicolor  Sabouraud,  1910. 
E.  granidosum  Sabouraud,  1908. 
E.  lacticolor  Sabouraud,  1910. 
E.  radiolatum  Sabouraud,  1910. 
E.  felineitm  R.  Blanchard,  1895. 
E.  denticulatitm  Sabouraud,  1910. 


ECTOTRICHOPHYTON  MENTAGROPHYTES  1005 

They  may  be  differentiated  as  follows: — 

A.  Grows  best  on  agar  without  sugars — Persicolor. 

B.  Grow  best  on  agar  with  sugars : — 

I.  Growth    white,  elevated    centre,    powdery    surface,    radiating 
furrows. 
(a)  Furrows  well  marked.     Pure  white — Mentagrophytes. 
\b)  Furrows  poorly  marked.     Not  so  white — Radiolatum. 
II.  Growth  white,  discoid,  umbilicated,  but  later  knob  in  centre; 
white  powdery  surface,  radiating  furrows — Farinulentum. 

III.  Growth  white,  yellowish,    dotted    with  granular    projections — 

Granulosum. 

IV.  Growth  cream  white  to  yellowish,  not  granular — Lacticolor. 

V.  Growth  white,  with  umbilicated  centre,  with  numerous  radiating 
projections  at  periphery. 

(a)  Projections  well  marked — Felineum. 

(b)  Projections  poorly  marked — Denticu  latum. 

Ectotrichophyton  mentagrophytes  Ch.  Robin,  1853. 

Synonyms. — Microsporon  mentagrophytes  Robin,  1853;  Sporo- 
trichnm  mentagrophytes  Saccardo,  1886 ;  Trichophyton gypseum  Bodin, 
1902;  T.  asteroid.es  Sabouraud,  1909;  Trichophyton  mentagrophytes 
Robin,  1853. 

Endo-ectothrix;  mycelial  spores  are  mostly  situated  outside 
the  cuticle  of  the  hair,  while  a  few  are  found  in  the  interior.  The 
latter  are  5  to  6  jj,  in  size;  those  outside,  forming  the  parasitic 
sheath,  are  of  very  unequal  size  (2to  ii/i). 

On  Sabouraud's  agar  the  growth  is  of  white  colour;  the  centre 
is  somewhat  elevated  and  covered  by  duvet ;  the  rest  of  the  growth 
has  a  powdery  surface,  and  often  presents  several  radiating  furrows. 
At  the  periphery  numerous  tapering  projections  are  observed. 
This  Trichophyton  is  of  animal  origin,  being  found  in  horses,  cows, 
dogs,  and,  perhaps,  pigs  and  sheep.  In  man  it  is  pyogenic,  causing 
a  type  of  trichophytic  sycosis,  kerion,  and  also  a  pustular  type  of 
tinea  corporis. 

The  following  five  species  arc  very  closely  allied  to  E.  mentagrophytes: — 

Ectotrichophyton  farinulentum  Sabouraud,  1910. 

Synonyms. — Trichophyton  gypseum  Bodin,  1902,  pro  parte;  Trichophyton 
fari  lulcnlum  Sabouraud,  1910. 

Found  in  cases  of  kerion  by  Sabouraud.  On  maltose  agar  the  growth  is 
at  first  discoid,  umbilicated,  with  a  white  powdery  surface  and  several  radiat- 
ing furrows.  Later,  the  central  part  becomes  raised,  forming  a  knob  covered 
with  white  duvet.  On  agar  media  not  containing  sugars  the  growth  is  at 
first  smooth,  without  any  duvet,  of  moist  appearance  and  yellow  colour; 
while  later  the  central  part  becomes  downy,  and  the  peripheral  portions  take 
a  powdery  aspect. 

Ectotrichophyton  persicolor  Sabouraud,  1910. 

Synonym. — Trichophyton  gypseum  Bodin,  1902,  pro  parte;  Trichophyton 
persicolor  Sabouraud,  19 10. 

Found  by  Sabouraud  in  cases  of  pustular  ringworm  of  the  palms  of  the 
hands  and  of  the  beard.     In  contrast  to  all  other  species  of  Trichophytons,  it 


ioo5  ASCOMYCETES  AND  BASIDIOMYCETES 

grows  better  on  agar  without  sugar  than  on  sugar  media.  The  cultures  are 
of  a  pinkish-reddish  colour.  The  appearance  of  the  colonies  has  been  aptly 
compared  by  Adamson  to  the  skin  of  a  very  ripe  peach. 

Eetotriehophyton  granulosum  Sabouraud,  1908. 

Synonym. — Trichophyton  gypseum  Bodin,  1902,  pro  parte;  Trichophyton 
granulosum  Sabouraud,  1908. 

The  growth  on  Sabouraud's  agar  is  discoid,  often  umbilicated;  powdery 
surface  of  a  white-yellowish  colour,  with  granular  formations  or  prominences 
dotted  all  over. 

This  Trichophyton  is  found  in  the  horse,  in  which  it  produces  a  peculiar  type 
of  trichophytosis,  with  extremely  numerous,  very  small,  patches.  It  has  been 
observed  in  man  in  Italy  by  Dalla  Fa  vera. 

Eetotriehophyton  laeticolor  Sabouraud,  1910. 

Synonym. — Trichophyton  gypseum  Bodin,  pro  parte;  Trichophyton  laeticolor 
Sabouraud,  1910. 

The  cultures  are  discoid,  flattened,  with  shallow  furrows  radiating  from 
the  centre.  The  colour  is  cream-white,  with  occasionally  a  slight  yellow  tinge. 
In  old  cultures  there  is  abundant  pleomorphic  duvet.  Can  easily  be  inocu- 
lated in  guinea-pigs. 

Eetotriehophyton  radiolatum  Sabouraud,  19 10. 

Synonym. — Trichophyton  gypseum  Bodin,  pro  parte;  Trichophyton  radiolatum 
Sabouraud,  19 10. 

Isolated  by  Sabouraud  from  cases  of  kerion.  Very  similar  to  E.  menta- 
grophyte>,  from  which  it  differs  in  culture  by  the  colour  being  of  less  pure 
white,  and  by  the  radiating  projections  being  less  marked  or  absent.  After 
three  to  four  weeks  abundant  white  pleomorphic  duvet  appears. 

Eetotriehophyton  felineum  R.  Blanchard,  1895. 

Synonyms. — Trichophyton  niveum  Sabouraud;  T.  radians  Sabou- 
raud, 1909 ;  T.  felineum  R.  Blanchard,  1895. 

Endo-ectothrix;  causes  often  a  pustular  ringworm  of  the  body; 
less  frequently  attacks  the  hairs.  In  the  pustules  free  spores  and 
a  few  mycelial  elements  are  seen;  in  the  affected  hairs  the  spores 
forming  the  parasitic  sheath  are  of  large  dimensions,  7  to  9  pi  in 
diameter.  The  growth  on  Sabouraud's  medium  is  umbilicated, 
with  a  white  powdery  surface  and  numerous  radiating  projections 
at  the  periphery. 

Pathogenicity. — This  fungus  is  found  in  the  cat,  and  probably 
also  in  horses,  cattle,  dogs,  sheep,  and  pigs.  In  man  it  causes  a  type 
of  kerion  celsi  and  also  a  type  of  vesiculo-pustular  tinea  corporis, 
called  by  Sabouraud  'trichophytosis  circinata  disidriformis,'  and 
'  herpes  iris  vesiculosus  '  by  Biett. 

Eetotriehophyton  denticulatum  Sabouraud,  1910. 

Synonym. — Trichophyton  niveum  Sabouraud,  pro  parte;  T.  denticulatum. 
Almost  identical  with  E.  felinetftn,  but  in  cultures  the  radiating  projections 
are  much  shorter  and  more  pointed. 

Eetotriehophyton  (Eetotriehophyton)  Castellani  and  Chalmers, 

1918. 

Definition. — Eetotriehophyton  with  large  spores  about  5-7 
microns. 


ECTOTRICHOPHYTON  MEGNINI  ic.07 

Type  Species. — Ectotrichophyton  (Eclotrichophytori)  megnini  R. 
Blanchard,  1895. 

Classification. — The  following  species  are  known: — 

E.  megnini  (R.  Blanchard,  1895). 
E.  equinum  (Gedoelst,  1902). 
E.  vinosum  (Sabouraud,  1909). 
E.  nodoformans  (Castellani,  1912). 

They  may  be  distinguished  as  follows: — 

A.  Mycelial  spores  very  large,  8-9  microns  in  diameter: — 

I.  Old  cultures  pinkish — Megnini. 
II.  Old  cultures  deep  wine  red — Vinosum. 

B.  Mycelial  spores  not  large,  2-4  microns  in  breadth: — 

I.  Surface  growth  abundant,  dark  red — Equinum. 
II.  Surface  growth  scanty  and  colourless,  submerged  portion  brick 
red — Nodoformans. 

Ectotrichophyton  megnini  R.  Blanchard,  1895. 

Synonyms. — Trichophyton  roseum  Bodin,  1902;  T.  rosaceitm 
Sabouraud,  1902;   T.  megnini  R.  Blanchard,  1895. 

Endo-ectothrix,  megalosporon,  downy-culture  type.  Mycelial 
spores  found  in  the  hairs  are  very  large,  8  to  9  fi  in  diameter.  On 
maltose  agar  the  growth  is  at  first  white,  with  a  velvety  appear- 
ance; later,  pinkish,  or  of  a  deep  rose  colour.  Duvet  becomes  very 
abundant  in  old  cultures.  It  is  parasitic  in  fowls  and  pigeons: 
may  infect  man,  causing  a  variety  of  tinea  barbse  without  suppura- 
tion. 

Ectotrichophyton  vinosum  Sabouraud,  1909. 

Synonym. — -Trichophyton  vinosum  Sabouraud,  1909. 

Endo-ectothrix,  megalosporon,  of  downy-culture  type.  Is  very 
similar  to  E.  megnini,  but  the  colour  of  old  cultures  is  of  a  deep 
wine-red  colour.  Abundant  duvet.  Found  by  Sabouraud  in  a 
case  of  tinea  circinata. 

Ectotrichophyton  equinum  Gedoelst,  1902. 

Synonym. — Trichophyton  equinum  Gedoelst,  1902. 

Endo-ectothrix,  megalosporon,  downy-culture  type.  Mycelial 
spores  of  oval  shape,  4  to  6  ft  in  length,  2  to  4  /u  in  breadth.  On 
maltose  agar  the  growth  is  orbicular,  with  abundant  duvet;  later 
on,  the  portion  of  the  growth  which  is  in  contact  with  the  medium 
becomes  yellowish  and  afterwards  dark  red.  It  is  parasitic  in 
the  horse,  and  may  infect  man. 

Ectotrichophyton  nodoformans  Castellani,  1912. 

Synonym, — Trichophyton  nodojormans  Castellani,  1912. 

Found  in  Ceylon  in  cases  of  dhobi  itch  and  tinea  barba?;  not 
very  abundant  in  the  lesions.  On  Sabouraud 's  agar  the  growth  is 
white,  with  a  powdery  surface  and  a  central  small  knob.  The 
growth  deepens  in  the  medium,  and  the  submerged  portion  has  a 


i oo 8  ASCOMYCETES  AND  BASIDIOMYCETES 

characteristic  brick-red  colour,  which  generally  disappears  after 
repeated  transplantations.     The  surface  growth  is  whitish. 

Glucose  Agar. — Growth  somewhat  more  abundant  than  in 
Sabouraud's  agar.  Colour  of  the  surface  and  submerged  growth 
white.     Red  pigment  usually  absent. 

Maltose  4  per  cent. — Scanty  growth,  no  pigment. 

Glycerine  Agar. — Growth  fairly  abundant,  no  pigment. 

Agar. — Scanty  growth,  whitish. 

Saccharine. — Same  as  agar. 

Adonite. — Same  as  agar. 

Pathogenicity. — The  fungus  gives  rise  to  a  peculiar  type  of  tinea 
cruris  (p.  2042),  with  very  thick,  elevated  margins  and  deep-seated 
nodules.  It  has  pyogenic  properties,  and  may  spread  to  other  parts 
of  the  body,  in  addition  to  the  inguinal  regions.  It  is  capable  of 
affecting  the  hair  follicles.  In  one  of  our  cases  the  fungus  affected 
the  hairs  of  the  beard,  producing  a  typical  '  kerion  barbae.' 

Genus  Atrichophyton  Castellani  and  Chalmers,  1918. 

Definition. — Trichophytoneae  with  mycelium  and  spores  present 
in  the  lesions  and  conidia  on  short  stalks,  but  they  do  not  attack 
hairs. 

Type  Species. — Atrichophyton  albiscicans  Nieuwenhuis,  1907. 

Classification. — The  following  table  will  indicate  the  characters 
of  the  species: — 

A.  Has  been  cultivated  : — 

I.  Culture  whitish  with  powdery  surface — Albiscicans. 
II.  Culture  brownish  mass  with  deep  furrows— Macfadyeni. 
III.  Cultures  pinkish  with  violet  tinge —  Viannai. 

B.  Has  not  been  cultivated  : — 

I.  Spores  are  numerous  and  of  various  sizes — Blanchardi. 
II.  Spores  are  few  and  about  4  microns  in  diameter — Ceylonense. 

Atrichophyton  albiscicans  Nieuwenhuis,  1907. 

Synonym. —  Trichophyton  albiscicans  Nieuwenhuis,  1907. 

Discovered  by  Nieuwenhuis  in  tinea  albigena.  In  fresh  prepara- 
tions from  scrapings  spores  are  absent;  the  mycelial  tubes  are 
straight,  occasionally  showing  a  double  contour;  they  are  often 
dichotomous.  On  Sabouraud's  agar  the  growth  is  very  slow, 
whitish,  with  a  powdery  surface. 

Atrichophyton  blanchardi  Castellani,  1905. 

Synonym. — Trichophyton  sahouraitdi  Castellani,  1905;  T.  blan- 
chardi Castellani,  1905. 

Temporary  species,  as  the  fungus  has  not  been  grown.  In  fresh 
preparations  from  the  lesions  the  mycelial  tubes  are  not,  as  a  rule, 
quite  straight;  they  are  often  banana-shaped;  do  not  show  a 
double  contour;  the  mycelial  segments  are  separated,  the  mycelial 


ATRICHOPHYTON  VIANNAI  1009 

spores  are  shed  without  forming  a  filament  by  their  union,  and 
are  of  various  sizes.  All  attempts  at  cultivation  have  failed. 
It  is  the  cause  of  tinea  Sabouraudi  tropicalis. 

Atrichophyton  viannai  de  Mello,  1917. 
Synonym. — Trichophyton  viannai  de  Mello,   1917.       Found  by 
F.  de  Mello  in  a  case  of  tinea  corporis.    Colonies  on  Sabouraud's 
maltose-agar  pinkish  with  often  a  violet  tinge. 

Atrichophyton  ceylonense  Castellani,  1908. 

Synonym. — Trichophyton  ceylonense  Castellani,  1908. 

Found  by  Castellani  in  cases  of  tinea  nigro  circinata.  Temporary  species, 
cultivation  having  not  been  obtained ;  possibly  a  variety  of  A .  blanchardi. 
In  fresh  preparations  the  spores  are  very  few  in  number,  roundish,  rather 
large  (4  jj),  showing  a  double  contour.  The  mycelial  tubes  are  about  3 J  fx 
in  breadth,  straight,  or  variously  bent.     It  is  found  in  tinea  nigro  circinata. 

Atrichophyton  macfadyeni 

Castellani,  1905. 

Synonym.  —  Trichophyton  mac- 
fadyeni Castellani,  1905. 

Found  by  Castellani  in  some 
cases  of  tropical  tinea  corporis. 
In  fresh  preparations  mycelium 
and  spores  are  rather  of  small 
dimensions.      The   mycelial   tubes  a-~, 

are  regularly  shaped,  do  not  show  \      * 

swellings,  and  are  about  2\  yi,  in  p\ 

breadth.     The  free  spores  are  very  <£  -  *    ^    gy 

numerous,  and  present   a  peculiar  ^        ~c 

ovoid  shape,  the  maximum  diameter  «^^ 

being  2|  to  3!  /i.  In  stained  Fig.  508.— Atrichophyton  macfad- 
preparations  the  spores  present   a  yeni  Castellani. 

bipolar     staining.       The     fungus  (Stained  with  fuchsin.) 

grows  with  difficulty;  on  the  rare 

occasions  when  the  inoculations  are  successful,  the  growth  is  very 
slow,  the  colonies  coalesce,  forming  a  brownish  mass,  with  deep 
furrows,  and  deeply  rooted  in  the  medium. 


Incert^e  Sedis. 

Trichophyton  balcaneum  Castellani,  1916. 

Found  in  cases  of  peculiar  condition  of  the  scalp  in  the  Balkans, 
which  clinically  resembled  more  a  diffuse  type  of  severe  pityriasis 
sicca  than  a  trichophytic  affection. 

When  grown  on  glucose  agar  from  scales  it  slowly  formed  a 
somewhat  crinkled  growth  of  whitish  colour.  An  interesting 
characteristic  of  this  fungus  is  that  apparently  it  does  not  become 

64 


lOlO 


ASCOMYCETES  AND  BASIDIOMYCETES 


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Motility 
Gram. 

Trichophyton 
balcaneum     .  .     O        O 

«9 

.8 

Day. 
4        8       12 

Oor  Oor  Oor 

Avs  Avs  Avs 

Day. 
4812 

OOO 

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Avs 

Starch. 

Day. 

4     8     12 

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s 

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Trichophyton 
balcaneum     .  . 

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TRICHOPHYTON  BALCANEUM 


pleomorphic,  even  after  very  numerous  transplantations.  Gelatine 
is  rapidly  liquefied.  It  does  not  form  gas  in  any  carbohydrate 
medium. 

Microscopically  the  fungus  shows  features  intermediate  between 
a  trichophyton  sensu  lato,[a.  microsporurrfand  an  achorion. 


Figs.  509  and  510.— Cultures  of 
Trichophyton  balcaneum  Castel- 
lani:  Glucose  Agar. 


Fig.  511 . — Microscopical  Appear- 
ances of  Trichophyton  balcaneum 
Castellani  :  Hanging  -  drop 
Culture. 


Genus  Achorion  Remak,  1845. 

Definition. — -Trichophytoneae  with  mycelial  filaments  and  spores 
in  the  lesions;  in  cultures  conidial-bearing  hyphse  present,  with 
spores  situate  laterally  and  apically.  Fusiform  bodies  in  cultures 
in  the  form  of  swollen  claviform  ends  of  filaments.  Yellow  favic 
scutula  present  in  lesions. 

Type  Species. — Achorion  schoenleinii  Lebert,  1845. 

Remarks. — The  fungi  belonging  to  this  genus  often  show  during 
parasitic  life  much  longer  mycelial  segments  than  Trichophytons 
and  Microsporons  ;  masses  of  them,  developing  in  hair  follicles, 
form  the  well-known  sulphur-coloured  scutula  which  always  develop 
round  a  hair.  In  the  hairs  the  mycelial  tubes  are  frequently  tri- 
chotomous  and  tetrachotomous,  forming  structures  which  have  been 
compared  in  appearance  to  the  skeleton  of  the  human  foot,  and 
called  '  favus  tarsi.' 

Cultures. — Sabouraud  has  noted  that  in  hanging-drop  cultures 
the  spores  sometimes  develop  very  slowly,  sometimes  rapidly. 
When  the  development  is  slow,  there  is  formation  of  numerous 
chlamydospores  of  various  sizes,  with  a  double  contour  membrane. 
When  the  development  is  rapid,  one  notes  that  the  mycelium 
ramifies  quickly  in  every  direction,  with  presence  of  very  few  or 
no  chlamydospores.     The  following  structures  may  be  noted : 

1.  Claviform  Bodies. — The  terminal  portion  of  some  filaments 
becomes  swollen  and  claviform.     These  claviform  filaments  have 


loi2  ASCOMYCETES  AND  BASIDIOMYCETES 

been  compared  by  some  authorities  to  the  '  spindles  '  of  the  Tri- 
chophytons and  Microsporons,  but  they  are  slenderer,  and  not 
septate.  The  French  authors  call  these  formations  '  chandeliers 
faviques,'  on  account  of  their  shape  somewhat  resembling  a  candle- 
stick. 

2.  Fan  us  Yellow  Bodies. — The  protoplasm  of  some  filaments 
collects  itself  at  the  terminal  ends,  the  filaments  becoming  much 
thinner,  and  terminating  in  roundish  or  oval  bodies,  which  must  be 
considered  to  be  terminal  chlamydospores.  It  is  to  be  noted  that 
in  the  typical  Achorions  of  human  origin  conidia-bearing  hyphae  are 
not  seen,  while  these  are  present  in  the  Achorions  of  animal  origin, 
in  which  separate  spindles  may  be  present. 

Media. — Achorions  grow  well  on  all  the  usual  sugar  media, 
especially  Sabouraud's  agar  and  glucose  agar.  They  generally 
liquefy  gelatine  fairly  rapidly. 

Pleomorphism. — Very  common  in  all  Achorions.  If  a  culture 
becomes  pleomorphic,  it  is  impossible  to  make  it  revert  to  the 
original  type. 

Transmission. — In  the  case  of  Achorions  of  human  origin  infection 
takes  place  from  man  to  man;  in  the  case  of  Achorions  of  animal 
origin  infection  takes  place  from  the  lower  animals.  It  is  not 
impossible  thztfA  chorions  may  live  saprophytically  in  nature. 

Table  of  Achorions. 

Genus.  Species* 


f  Of  human  origin  I    .        ,         ,  .    .  T    , 

(typical)  |   A    sckoenleim  Lebert, 

C  A.  quincket 
-J  A.  gypseum 
[  A.  arloingi 


Achorion  Remak.  1845  -|  of  animal  oriirin  f  A'  qninckeamim  Zopf,  1890. 
{      (non-typicaT)     ,  £  S&^ham"7*, 


These  may  be  recognized  as  follows: — 

A.  Whitish-yellow  cerebriform  colonies — Schoenleini. 

B.  White  downy  colonies — Quinckeannm. 

C.  Yellowish  colonies — Gypseum. 

A .  arloingi  has  not  been  properly  described. 

Achorion  schoenleini  Lebert,  1845. 

Synonyms. — Oidium  schoenleini  Lebert,  1845 ;  0.  porriginis  Mon- 
tague; Oospora  porriginis  Saccardo,  1886;  Oidium  schoenleini  Zopf, 
1890. 

Causes  the  well-known  affection  called  favus,  which  is  char- 
acterized by  the  presence  of  peculiar  disc-shaped  crust  formations, 
called  scutula,  of  a  sulphur-yellow  colour,  and  emitting  an  offensive 
odour  which  has  been  compared  to  the  smell  of  mice's  urine. 

The  fungus  may  infect  the  hairs  or  glabrous  parts  of  the  body; 
it  may  attack  the  nails.  In  the  hairs  the  mycelium  is  very  abun- 
dant, the  segments  being  comparatively  long.  Sometimes  the 
mycelial  threads  divide  into  three  or  four  branches,  each  of  which 
terminates  in  a  single  row  of  roundish  spores.  This  is  known  as 
favic  tarsus. 


A  CHORION  SCH0ENLE1NI 


1013 


Cultures. — The  fungus  is  easily  cultivated  on  various  media. 
On  Sabouraud's  agar  and  on  glucose  agar  the  growth,  when  com- 
pletely developed,  is  convoluted  or  cerebriform,  and  somewhat 
bulging.  It  has  been  compared  by  Sabouraud  to  the  appearance 
of  a  sponge.  The  colour  is  white-yellowish,  like  that  of  old  wax. 
After  a  time  cultures  become  pleomorphic  and  abundant;  white 
duvet  is  present.  To  prevent  pleomorphism,  media  not  containing 
sugars  should  be  used  (see  p.  996). 

A.  schoenleinii  liquefies  gelatine  in  between  three  to  four  days, 
while  the  Trichophytons  take  generally  between  fifteen  to  twenty 
days. 

By  inoculation  of  pure  cultures  of  the  fungus  favus  lesions  are 
produced  in  man,  dogs,  mice,  rabbits,  and  fowls.  The  inocula- 
tion in  guinea-pigs  does  not  give 
rise  to  typical  favus  lesions  with 
scutula,  but  to  circinate  tri- 
chophytic-like  lesions. 


Fig.    512.  —  So-called    Yellow 
Bodies  in  Cultures  of  Acho 
rion  schoenleinii  Lebert. 
(After  Bodin.) 


Fig.  513.  —  Claviform  Bodies 
in  Cultures  of  A  chorion 
schoenleini   Lebert. 


Reproduction. — This  takes  place — 

1.  By  sprouting. 

2.  By  elongated  fusiform  structures  analogous,  according  to 
some  authorities,  to  the  so-called  '  spindles  '  of  the  Trichophytons 
and  Microsporons,  but  they  are  slenderer  and  not  septate.  These 
formations  arc  called  by  the  French  authors  'chandeliers  faviques,' 
on  account  of  their  shape  somewhat  resembling  a  candlestick. 

3.  By  so-called  '  favus  '  or  '  yellow  bodies,'  which  are  structures 
8  to  15  fX  in  diameter,  generally  terminal,  showing  a  double  contour, 
and  containing  a  granular  substance.  These  structures  should 
probably  be  considered  to  be  chlamydospores  (see  also  general 
remarks  on  the  genus  Achorion). 

Sabouraud  admits  only  one  species  of  human  Achorion,  but 
Neeb  and  Unna  have  described  as  many  as  nine:  Achorion  cys- 
ticnm,  A.  tarsiferon,  A.  moniliforme,  A.  demergens,  A.  akromegalicnm, 
A.  dikroon,  A.  radians,  A.  euthythrix,  A.  atacton.  Sabouraud's 
opinion  is  the  one  generally  accepted  at  the  present  time. 


ioi4  ASCOMYCETES  AND  BASIDIOMYCETES 

Achorion  quinckeanum  Zopf,  1890. 

The  fungus  appears  in  the  lesions  in  the  shape  of  numerous 
mycelial  filaments  often  dissociated  in  so  many  small  segments 
constituting  so-called  spores.  Grows  readily  on  Sabouraud's  agar, 
producing  white,  downy  colonies. 

This  fungus  botanically  holds  an  intermediate  position  between 
the  typical  Achorions  and  the  Microsporons  and  Trichophytons, 
conidia  bearing  hyphae  of  the  type  Acladium  being  present.  It 
produces,  however,  typical  favus  lesions  with  scutula. 

Pathogenicity.- — Is  the  cause  of  favus  in  mice,  and  may  occa- 
sionally infect  man,  in  whom,  too,  it  induces  typical  favus.  It  can 
be  inoculated  into  guinea-pigs. 

Achorion  gypseum  Bod  in,  1907. 

Found  by  Bodin  in  1907  in  a  typical  case  of  favus.  On  Sabour- 
aud's agar  the  growth,  which  is  roundish,  presents  a  little  white 
duvet  in  the  centre,  while  the  rest  has  a  glabrous  surface  of  yellowish 
colour.  Old  cultures  become  pleomorphic,  with  presence  of  abun- 
dant white  duvet  all  over  the  growth.  Botanically  the  fungus  is 
closely  allied  to  the  Trichophytons  and  Microsporons,  but  gives  rise 
to  typical  favus,  with  scutula,  when  inoculated  in  mice  and  guinea- 
pigs.  The  inoculation  of  pleomorphic  cultures  does  not  cause  any 
eruption. 

Achorion  arloingi  R.  Blanchard,  1891. 

Synonym. — Achorion  arloingi  Busquet,  1891. 

Incompletely  known  species.  Was  isolated  from  a  human  trichophytic- 
like  eruption  by  Desir  de  Fortunet  and  Courmont.  Is  said  to  be  inoculable 
into  mice,  rabbits,  and  man. 

Genus  Lophophyton  Matruchot  and  Dassonville,  1899. 
Mycelial   filaments,   either  tortuous,   very  thin,   or   thick,   with  granular 
protoplasm.     No  spores  present.     One  species  only. 

Lophophyton  gallinae  Megnin,  1881. 

Synonyms. — Epidermophyton  gallines  Megnin,  1881;  Lophophyton  gallincs 
Matruchot  and  Dassonville,  1899;  Achorion  gallince  Sabouraud,  1910. 

In  the  lesions  mycelial  filaments  are  seen,  some  thin  and  tortuous,  without 
practically  any  protoplasm;  others  of  much  larger  dimensions,  with  granular 
protoplasm.  No  spores  observed.  The  fungus  is  easily  cultivated,  and  is 
inoculable  into  rabbits,  mice,  and  fowls,  in  which  it  gives  rise  to  typical 
favus  lesions.  In  man  it  does  not  produce  favus,  but  merely  trichophytic-like 
erythematous,  squamous  patches. 

Genus  Epidermophyton  Lang,  1879,  emendavit  Sabouraud,  1907. 

Definition. — -Trichophytineae  with  mycelial  filaments  and  spores 
present  in  the  lesions  and  with  pluriseptate  spindles  present  in 
the  cultures.  Does  not  attack  the  hairs  or  hair  follicles,  but  grows 
in  the  superficial  layers  of  the  epidermis. 

T/pe  Species. — Epidermophyton  cruris  Castellani,  1905. 

Remarks. — The  fungi  belonging  to  this  genus,  which  has  been 
investigated  by  Sabouraud  and  Castellani,  grow  superficially  on  the 


EPIDERMOPHYTON  1015 

skin  without  invading  the  hairs  and  hair  follicles;  do  not  produce 
suppuration.  Reproduction  takes  place  principally  by  pluriseptate 
spindles,  with,  on  the  average,  four  to  six  cells.  The  septa,  as  noted 
by  Pinoy,  may  not  be  complete,  and  the  cavities  may  communicate. 
Spiral  hyphae,  as  found  in  most  species  of  Trichophyton,  absent; 
pectinate  structures,  as  found  in  the  Microsporons,  absent ;  no  spore- 
bearing  hyphae,  with  lateral  conidia  of  type  Acladinm,  as  noted 
both  in  the  Trichophytons  and  in  the  Microsporons.  The  cultures 
undergo  rapid  degenerative  changes,  losing  their  characteristics,  and 
becoming  covered  with  abundant  uniform,  long,  whitish  duvet 
(pleomorphism).  They  are  not  inoculable  into  guinea-pigs,  except 
Pinoy's  Epidermophyton  simii.  The  species  so  far  known  have 
been  isolated  from  human  lesions,  except  the  Epidermophyton 
discovered  by  Pinoy  in  monkeys. 

Table  of  Epidermophytons. 

Genus.  Species. 

t~.j         .,    .      T      _      o  ,     •.  C  E.  cruris  Gastellani,    190^. 

Epidermophytoses   1879,  emendavitj  R  ,.  Castellani    r^. 

Sabouraud,  1907  [  R    vrubrum  Castellani,  1907. 

These  species  may  be  recognized  by  their  growths  on  Sabouraud's 
agar:— 

A.  Colour  peculiar  yellow — Cruris. 

B.  Colour  pinkish — Perneti. 

C.  Colour  deep  red — Rubrum. 

For  E.  simii  Pinoy,  191 1,  we  have  created  the  genus  Pinoy ella. 

Epidermophyton  cruris  Castellani,  1905. 

Synonyms. — Trichophyton  cruris  Castellani,  1905;  Epidermo- 
phyton inguinalis  Sabouraud,  1907;  T.  castellanii  Brooke,  1908. 

Found  in  cases  of  tinea  cruris  in  Ceylon  by  Castellani,  and  in 
France  by  Sabouraud.  The  fungus  is  very  abundant  in  recent 
cases,  extremely  scarce  in  old  ones.  The  mycelial  tubes  in  recent 
cases  are  generally  straight,  have  often  a  double  contour,  and  the 
segments  are  somewhat  rectangular,  their  breadth  being  3J  to  4^  pi. 
Branching  is  not  rare.  The  spores  are  rather  large  (4  to  7  pi), 
roundish,  and  have  generally  a  double  contour;  they  do  not  collect 
in  clusters.  In  chronic  cases  degeneration  forms  of  the  fungus 
are  met  with;  the  mycelium  may  be  banana-shaped,  may  show 
several  constrictions,  or  long  strings  of  ovoid  elements  may  be 
seen. 

This  Epidermophyton  grows  well,  but  rather  slowly,  on  Sabour- 
aud's agar.  The  growth  begins  to  be  visible  after  four  to  eight 
days,  the  colonies  being  at  first  of  a  peculiar  yellow  colour,  lemon- 
yellowish  or  orange-yellowish,  occasionally  with  a  greenish  tinge. 
Later  they  become  white,  with  pulverulent  surface,  and  may  be 
acuminate  or  crateriform.  Pleomorphism,  with  abundant  white 
duvet,  develops  quickty. 

This  fungus  in  Ceylon  is  the  commonest  species  found  in  cases 


1016  ASCOMYCETES  AND  BASIDIOMYCETES 

of  tinea  cruris.  It  is  not  inoculable  into  guinea-pigs.  Attempts 
at  reproducing  the  eruption  in  man  by  inoculating  pure  cultures 
have  also  failed. 

Epidermophyton  perneti  Castellani,  1907. 

This  fungus  has  been  described  by  Pernet.  It  differs  from 
E.  cruris  by  growing  much  more  rapidly  on  Sabouraud's  agar  and 
by  the  cultures  having  a  delicate  pinkish  colour,  which  is  generally 
lost  in  subcultures.     It  is  very  rare  in  Ceylon. 

Epidermophyton  rubrum  Castellani,  1909. 

Synonym. — Trichophyton  purpureum  Bang,  1910. 

This  fungus  was  described  by  Castellani  in  Ceylon  in  1909,  and 
by  Bang  in  France  in  1910.  On  Sabouraud's  agar  the  growth 
begins  to  appear  four  to  six  days  after  inoculation  as  a  raised  red 
spot,  which  gradually  enlarges.  At  complete  development  the 
growth  is  of  a  deep  red  colour,  either  with  a  central  knob  or  crateri- 
form,  and  is  partly  covered  with  a  white,  delicate  duvet.  In  old 
cultures  the  white  duvet  is  much  more  abundant  and  thicker,  and 
may  hide  the  red  pigmentation  almost  completely. 

On  glucose  agar  (4  per  cent.),  which  is  the  best  medium  for  this 
fungus,  the  growth  is  of  a  very  deep  blood-red  colour,  and  the  red 
pigmentation  may  spread  to  portions  of  the  medium  itself.  In 
old  cultures  abundant  white — occasionally  white-greenish — duvet 
is  present.  This  may  hide  the  pigmentation,  but,  scraping  out 
the  duvet,  the  red  pigmentation  will  be  found  to  be  still  well 
marked.  On  ordinary  agar  and  glycerine  agar  the  fungus  grows 
fairly  well,  but  there  is  no  red  pigmentation. 

Genus  Endodermophyton  Castellani,  1909. 

Definition. — Trichophytonese  with  mycelial  filaments  and  spores 
in  the  lesions,  but  no  conidial  filaments  in  cultures.  Pluriseptate 
spindles  unknown;  grows  between  the  superficial  and  deep  layers 
of  the  epidermis,  and  does  not  attack  the  hairs  or  hair  follicles. 

Remarks. — The  fungi  belonging  to  this  genus  are  characterized 
by  their  growth  between  the  superficial  and  deep  strata  of  the 
epidermis,  forming  an  interlacing  felt  of  mycelia,  which  detaches 
the  horny  and  granular  layers  from  the  rete  Malpighi.  They  do  not 
invade  the  hair  follicles,  and  do  not  cause  suppuration.  They  have 
been  cultivated  by  Castellani. 

Cultures. — Botanically,  these  fungi  are  closely  allied  to  the 
Achorions,  as  remarked  by  Sabouraud  and  Pinoy,  who  have  exam- 
ined Castellani's  cultures.  Attempts  at  cultivation  failed  for  a  long 
time,  as  they  generally  do  not  grow  on  solid  media  direct  from  the 
scales.  These,  after  being  treated  with  alcohol  for  five  to  ten 
minutes,  must  be  placed  in  glucose-broth  tubes,  one  scale  in  each 
tube.  Most  of  the  tubes  become  contaminated  with  bacteria,  but 
in  those  which  remain  clear,  after  a  time  (five  to  ten  days)  a  few 


ENDODERMOPHYTON  1017 

delicate,  short,  white  filaments  will  be  seen  originating  from  the 
scale.  The  growth  slowly  increases  until,  after  three  to  four  weeks, 
it  takes  the  appearance  of  a  small,  white,  fluffy  mass,  with  a  dark 
spot  (the  scale)  in  the  centre.  Portions  of  the  broth  cultures  are 
sown  on  solid  sugar  media,  on  which  growth  takes  place  now  quite 
easily.  Fungi  can  then  be  indefinitely  subcultured  on  solid  media. 
The  fungi  grow  much  more  abundantly  on  glucose  agar,  4  per  cent., 
than  on  Sabouraud  or  any  other  media. 

Reproduction. — In  hanging-drop  cultures  long  mycelial  filaments 
are  seen;  no  conidia-bearing  hyphae  are  present;  reproduction  is 
apparently  by  sprouting,  branching  taking  place;  but  further 
investigation  is  necessary  on  the  subject. 

Pleomorphism. — Pleomorphism  is  much  less  marked  than  in  the 
Trichophytons,  Epidermophytosis ,  and  Achorions,  but  old  cultures 
may  lose  their  characteristics,  becoming  covered  with  duvet. 

Table  showing  Endodermophytons  found  in  Man  in  Order 
of  Frequency. 

E.  tropicale  Castellani. 
E.  indicnm  Castellani. 
E.  concentricum  Blanchard. 
E.  mansoni  Castellani. 

These  may  be  recognized  as  follows: — 

A.  Glucose  agar  cultures  amber  coloured,   no  duvet   or   only   slight — 

Tropicale. 

B.  Glucose  agar  cultures  deep  red: — 

I.  Causes  Tinea  imbricata — Indicum. 
II.  Causes  Tinea  inter secla — Castellanii. 

C.  Glucose  agar  cultures  after  a  time  black: — 

I.   Pigmentation   fairly   slow — Concentricum. 

II.  Pigmentation  very  rapid — Mansoni. 

Endodermophyton  tropicale  Castellani,  1914. 

Remarks. — -Manson,  in  1872,  described  a  trichophyton-like 
organism  in  the  squamae  of  tinea  imbricata  ;  with  the  laboratory 
technique  of  that  time  attempts  at  cultivation  did  not  succeed. 
Blanchard  considered  it  non-cultivable,  and  called  it  Trichophyton 
concentricum;  on  the  other  hand,  Nieuwenhuis  stated  that  it  was 
quite  easily  cultivable,  and  was  characterized  by  the  colonies  being 
crateriform.  His  researches  were  not  confirmed.  In  recent  years 
the  general  opinion  has  been  that  aspergillus-like  fungi  were  the 
real  cause  of  the  disease.  Tribondeau  described  fructifications 
somewhat  similar  to  those  of  an  Aspergillus,  and  created  for  the 
fungus  the  genus  Lepidophyton.  Wehmcr  has  described  it  as  a  true 
Aspergillus — Aspergillus  tokelau.  Castellani,  from  the  investiga- 
tions he  has  carried  out  in  Ceylon,  has  come  to  the  conclusion  that 
Aspergillus  and  aspergillus-like  fungi  have  nothing  to  do  with  the 
disease.  When  they  are  present  in  the  squamae,  they  are  merely 
saprophytes  or  contaminations.  By  using  a  special  technique  he 
has  succeeded  in  growing  what  he  considers  to  be  the  true  fungi 
causing  the  disease.     He  recognized  at  first  two  species,  and  more 


ioiS 


ASCOMYCETES  AND  BASIDIOMYCETES 


recently  four,  further  investigation  having  shown  that  the  term  he 
used  for  one  species  (concentricum)  covered  more  than  one  species. 
Endodermophyton  tropic  a1 e  is  very  abundant  in  the  lesions, 
forming  a  felting  of  interlacing  mycelial  threads  with  mycelial 
articles,  regular  in  shape,  rectangular  or  somewhat  square-shaped, 
and  usually  straight.  If  the  liquor  potassa?  be  left  to  act  some  time, 
the  mycelial  articles,  which  are  of  very  variable  length,  and  i\  to 
3^  fz  in  breadth,  will  be  seen  to  have  a  double  contour.     Aspergillus 


Fig.  514.- — -Endodermophyton 
tropicale  Castellani:  Glucose 
Agar  Culture. 


Fig.  515.—  Endodermophyton 
tropicale  Castellani  :  Old  Glu- 
cose Agar  Culture. 


fructifications,  described  by  so  many  authors,  when  present,  are  due 
to  contaminations;  they  form  no  part  of  the  fungus.  Cultivation 
of  this  fungus  has  been  obtained  by  Castellani,  using  the  method 
mentioned  in  the  paragraph  above  on  the  genus  Endodermophyton. 
The  principal  cultural  characters  on  solid  media,  when  the  growth 
is  fifteen  to  twenty-one  days  old,  are  as  follows: — 

Glucose  Agar  (4  per  cent.). — Growth  abundant;  surface  cerebriform  or 
crinkled.  The  growth  and  the  medium  show  a  slight  amber  colour,  which 
later  on  may  become  of  much  deeper  hur.  Duvet  as  a  rule  absent,  but  in 
old  cultures  which  have  been  transplanted  many  times  and  are  degenerating, 
some  very  scarce,  short,  whitish  duvet  may  appear. 

Sabouraud  Agar. — Growth  comparatively  scanty,  whitish-grey,  mostly 
submerged.     The  colonies  are  whitish,  have  generally  a  small  central  knob  > 


ENDODERMOPHYTON  TROPIC  ALE 


ioiq 


and  never  show  any  duvet.  The  submerged  portion  is  very  firmly  embedded, 
and  often  presents  projections  deepening  in  the  medium.  Colour  of  the 
medium  unchanged. 

Glycerine  Agar. — Similar  growth  to  Sabouraud's  agar.  When  the  colonies 
coalesce,  the  growth  shows  a  knobby  surface.     No  duvet. 

Ordinary  Agar. — Scanty  growth ,  somewhat  similar  to  Sabouraud .    No  duvet . 

Mannite  Agar  (4  per  cent ). — Appearance  somewhat  similar  to  glucose  but 
growth  less  abundant.  The  medium  may  take  a  slight  amber  colour.  No 
duvet. 

Saccharose  Agar  (4  per  cent.). — Growth  rather  scanty,  similar  to  Sabouraud. 
Duvet  absent. 

Nutrose  Agar  (4  per  cent.). — -Very  slow  growth.  Separate  young  colonies 
have  a  central  knob;  they  coalesce  later  into  a  knobby  mass. 


Fig.  516. — Endodermophyton  tropica le 
Castellani:  Agar  Culture. 


Fig.  517. —  Endodermophyion 
tropicale  Castellani:  Mal- 
tose Agar  Culture. 


Maltose  Agar  (Acid). — Similar  to  Sabouraud. 
Maltose  Agar  (Alkaline). — Similar  to  Sabouraud. 
Adonite  Agar. — Not  very  abundant;  cerebriform;  duvet  absent. 
Galactose  Agar. — Knobby  or  cerebriform. 
Levulose  Agar. — Knobby. 
Raffinose  Agar. — Cerebriform. 
Inidin  Agar. — Cerebriform. 

Saccharine  Agar  (4  per  cent.). — Somewhat  knobby  surface;  duvet  absent. 
Lactose  Agar. — Similar  to  Sabouraud,  but  surface  growth  more  abundant. 
Gelatine. — Very  slow  liquefaction  of  the  medium. 

Milk. — Very  scanty  growth.     After  a  time  the  medium  becomes  separated. 
Sugar  Broths  (Maltose,  Lactose,  etc.). — Slight  growth  at  the  bottom  of  the 
tube;  no  production  of  acid  or  gas. 

Hanging-Drop  Cultures. — In  hanging-drop  cultures  (Sabouraud's 
maltose  broth)  long  mycelial  threads  are  seen.  Reproduction  is 
apparently  by  sprouts  from  the  mycelium,  branching  taking  place. 

Pathogenicity. — The  fungus  is  the  cause  of  a  common  type  of 
tinea  imbricata.  Castellani  has  demonstrated  that  the  inocula- 
tions into  human  beings  of  cultures  of  the  fungus  reproduce  a  typical 


loao  ASCOMYCETES  AND  BASIDIOMYCETES 

form  of  tinea  imbricata,  and  that  from  the  scales  of  the  eruption, 
experimentally  induced,  the  same  fungus  is  recoverable.  For 
further  details  see  Chapter  XCII.  on  Tinea  Imbricata  (p.  2509). 

Endodermophyton  indieunr  Castellani,  1911. 
This  fungus  was  found  by  Castellani  in  some  cases  of  tinea  imbri- 
cata.    The  microscopical  appearance  of  the  fungus  in  the  scales  is 
identical  with  E.  tropicale.     The  principal  cultural  characters  on 


Fig.  518.  —  Patch  of  Experi- 
mental Tinea  Imbricata  in  a 
Singhalese  Boy,  obtained  by 
inoculating  a  Culture  of  En- 
dodermophyton indicam. 


Fig.  519.  —  Endodermophyton 
indicum  Castellani  :  Hang- 
ing-Drop Culture. 


solid  media,  when  the  growth  takes  place  in  the  dark,  about  8o° 
to  850  F.,  without  rubber  caps  on  the  tubes,  and  is  between  fifteen 
and  twenty-one  days  old,  are  as  follows: — 

Glucose  Agar  (4  per  cent.). — Growth  fairly  abundant,  with  surface  some- 
what convoluted  or  furrowed.  Portions  of  the  growth,  often  the  central, 
is  of  a  deep  orange,  or  pinkish-orange,  or  red-orange,  occasionally  of  bright 
red  colour.  The  surface  of  the  rest  of  the  growth  often  appears  white  and 
powdery,  being  covered  by  a  very  short  delicate  white  duvet. 

Sabouraud  Agar. — Slow  growth,  with  powdery  surface,  either  with  central 
knob  or  convoluted.  The  growth  does  not  deepen  in  the  medium  so  much 
as  E.  concentricum. 

Glycerine  Agar. — Growth  abundant,  white  or  amber  colour;  delicate  white 
short  duvet  present  on  some  portions  of  the  growth. 

Ordinary  Agar. — Growth  fairly  abundant;  knobby  surface  covered  by 
snow-white  very  short  delicate  duvet. 

Mannite  Agar. — Growth  knobby  or  convoluted,  covered  by  short  white 
duvet. 

Saccharose  Agar. — Cerebriform,  covered  by  white  duvet. 

Saccharine. — Crinkled  surface;  delicate  white  duvet  present. 

Maltose  Agar  (Acid). — Somewhat  similar  to  Sabouraud's,  but  the  surface 
growth  is  more  abundant. 

Maltose  Agar  (Alkaline). — Similar  to  acid  maltose,  but  the  white  duvet  is 
more  abundant. 

Lactose  Agar. — Knobby  surface  covered  by  snow-white  duvet. 

Nulrose  Agar. — Yellowish  crinkled  surface;  short  white  duvet  present. 

Levulose  Agar. — Scanty  growth,  yellow  or  orange;  scarce;  very  short  white 
duvet  present. 

Galactose  Agar. — Fairly  abundant;  surface  convoluted  with  abundant, 
short  snow-white  duvet. 


ENDODERMOPHYTON  INDICUM 


1021 


Raffinose  Agar. — Same  appearance  as  galactose. 

Inulin  Agar.— Same  appearance  as  in  galactose  and  raffinose  agars. 

Adonite  Agar.— Cerebnform;  surface  covered  with  snow-white  duvet. 

Gelatine. — Very  slow  liquefaction. 

Litmus  Milk.— Very  scanty  growth.  After  a  time  the  medium  may  become 
separated. 

Various  Sugar  Broths  {Maltose,  Lactose,  etc.).— Slight  growth  at  the  bottom 
of  the  tube.     No  production  of  acid  or  gas. 

The  annexed  table  shows  at  a  glance  the  different  cultural  characteristics 
of  the  two  fungi  in  the  principal  media. 


Fig. 520. — Endodermophylonindicum       Fig.  521.  —  Endodermophyton  in- 
Castellani:  Agar  Culture.  dicum    Castellani:     Glucose 

Agar  Culture. 


Comparison  between   the   Cultural   Characters   of    Endodermophyton 
tropicale  and  of  Endodermophyton  indicum. 


Media. 


E.  tropicale. 


E.  indicum. 


Glucose  agar 


Sabouraud  agar 


Agar 


Glycerine  agar 


Amber  colour,  duvet  absent 
■in  young  cultures. 


Growth  scanty,  mostly  sub- 
merged, grey  -  whitish 
duvet  absent. 

Scanty,  mostly  submerged ; 
similar  to  Sabouraud 
agar;  no  duvet. 

Growth  mostly  submerged; 
surface  growth  very 
scanty;  similar  to  Sa- 
bouraud agar ;  no  duvet. 


Deep  orange,  at  times, 
pinkish  or  red,  very  short 
white  delicate  duvet 
often  present. 

Surface  growth  more  abun- 
dant, powdery  white. 

Fairly  abundant,  knobby 
well-marked  snow-white 
duvet. 

Surface  growth  very  abun- 
dant; crinkled  appear- 
ance; white  short  duvet 
present. 


The  above  characters  are  based  upon  the  appearance  of  cultures  kept  in 
the  dark  at  a  temperature  8o°  to  900  F.,  and  without  rubber  caps.  If  any  of 
these  conditions  are  altered,  the  cultural  characters  are  changed.     If  rubber 


1022 


ASCOMYCETES  AND  BASIDIOMYCETES 


Fig.    522. — Endodermophyion    indicum    Castel- 
lani  in  the  "Scales. 


caps  are  used,  both  E.  indicum  and  E.  tropicale  may  assume  a  bright  red 
colour.  If,  however,  subcultures  are  made  from  these,  using  tubes  without 
rubber  caps,  the  fungi  again  show  the  characters  given  above. 

Hanging-Drop  Cul- 
tures.— Long  mycelial 
filaments  are  present. 
No  free  spores  are 
seen;  reproduction  is 
apparently  by  sprouts 
from  the  mycelium. 

Pathogenicity. — The 
fungus  is  the  cause  of 
a  certain  number  of 
cases  of  tinea  imbri- 
cata.  The  type  of 
the  disease  caused  by 
this  fungus  seems  to 
be  more  superficial 
than  that  caused  by 
E.  tropicale,  but  fur- 
ther researches  are 
required  on  this  sub- 
ject. Castellani  has  succeeded  in  experimentally  reproducing  the 
disease  by  inoculating  coolies,  who  had  volunteered,  with  pure 
cultures  "of  the  fungus.  The  skin  was  first  scarified  with  a  sterile 
knife;  then  a  certain  amount  of  a  pure  agar  culture  of  E.  indicum 
was  well  rubbed  in.  After 
fifteen  to  twenty-one  days  the 
first  signs  of  the  eruption  ap- 
peared, and  the  typical  patches 
of  tinea  imbricata  developed. 
From  the  scales  of  the  experi- 
mental cases  a  fungus  was 
grown  absolutely  identical  with 
the  strain  of  E.  indicum  with 
which  the  individuals  had  been 
inoculated. 

Endodermophyton  castellanii 

Perry,  1907. 

Found  by  Castellani  in  cases 
of  tinea  intersecta.  In  the  scales 
the  mycelium  is  fairly  abundant ; 
no  free  spores  are  seen.  Mycelial 
segments  uniform,  rather  straight,  and,  provided  the  liquor  potassae 
be  left  to  act  for  sufficient  time,  they  often  show  a  double  contour. 


Fig. 


523. — Endodermophyton 
castellanii  Perry. 


Their  breadth  is  2\  to  3 \ 
roundish    refringent    dots, 


one 


Each    mycelial  segment  has  two 
at    each    extremitv-      Has    been 


PI  NO  YELL  A  1023 

cultivated  only  on  one  occasion,  the  cultures  being  apparently 
similar  to  those  of  E.  indicum.  It  is  the  cause  of  tinea 
intersect  a. 

Endodermophyton  ooncentricum  Blanchard,   1901. 

Cultures  on  glucose  agar  are  at  first  amber  colour,  but  after  four  to  eight 
weeks  become  jet-black  and  covered  with  abundant  duvet. 

Endodermophyton  mansoni  Castellani,   1914. 
Portions  of  the  growth  are  black  from  the  very  first,  scanty  duvet. 

Genus  Pinoyella  Castellani  and  Chalmers,  1908. 

Definition. — Trichophytoneae  with  mycelial  filaments  and  spores 
in  the  lesions,  and  in  cultures  conidial-bearing  hyphae,  with  the  spores 
situate  laterally  only. 

Type  and  only  Species. — Pinoyella  simii  (Pinoy,  191 1);  Epider- 
mophyton  simii  Pinoy,  191 1. 

Discovered  by  Pinoy  in  a  trichophytic-like  eruption  observed 
in  a  monkey.  On  Sabouraud's  agar  the  growth  is  at  first  yellowish- 
orange,  somewhat  similar  to  Epidermophyton  cruris/  later,  the 
growth  is  whitish  and  covered  with  white  duvet. 

Pinoy's  fungus  has  several  interesting  botanical  features,  some 
of  which  are  those  of  the  genera  Microsporon  and  Trichophyton. 
In  contrast  to  the  typical  Epidermophytons ,  it  presents  spore- 
bearing  hyphae  with  lateral  conidia,  and  is  inoculable  into  guinea- 
pigs,  in  which  it  produces  a  trichophytic-like  eruption. 

Genus  Montoyella  Castellani,  1907. 

Definition.— Trichophytoneae  with  mycelial  filaments  and  spores 
in  the  lesions,  in  cultures  conidial-bearing  hyphae  with  only  terminal 
spores. 

Remarks. — -Temporary  genus.  Two  kinds  of  mycelial  threads: 
some  slender,  ramified,  septate;  others  much  thicker,  having 
numerous  intermediate  chlamydospores.  From  the  thicker  fila- 
ments delicate  hyphae  take  origin,  which  terminate  in  large  pear- 
shaped  or  globular  conidia. 

Type  Species. — Montoyella  nigra  Castellani,  1907. 

Classification. — There  are  two  species,  which  maybe  differentiated 
as  follows : — 

A.  Cultures  black — Nigra. 

B.  Cultures  whitish  or  greenish — Bodini. 

Montoyella  nigra  Castellani,  1907. 

Temporary  species.  Colonies  on  maltose  agar  are  black.  If 
glycerine  agar  is  used,  the  medium  takes  a  black  colour.  This 
species,  discovered  by  Montoya,  is  common  in  black  pinta. 

Montoyella  bodini  Castellani,  1907. 
Temporary  species.     Colonies  whitish  or  greenish. 


1024  ASCOMYCETES  AND  BASIDIOMYCETFS 

FAMILY  ASPERGILLACE^:. 

Definition. — Aspergillales  with  compact  peridium,  small  sessile 
closed  perithecia. 

Type  Genus. — Aspergillus  Micheli,  1729. 

Classification. — The  genera  of  the  Aspergillaceae  can  be  recognized 
as  follows: — 

A.  Spores  unicellular  : — 

I.  Perithecium  beaked — Microascus. 
II.  Perithecium  not  beaked:— 

(a)  Perithecia  with  appendages — Cephalotheca 

(b)  Perithecia  without  appendages : — 

1.  Conidiophores  absent — Thelavia. 

2.  Conidiophores  present: — 

(a)  Conidia  solitary — Aphanoascus. 

(b)  Conidia  in  chains: — 

(i.)  Conidiophores  simple — Emencella. 
(ii.)  Conidiophores    enlarged    apically    and     bearing 
sterigmata: — 

(1)  Sterigmata  simple — Aspergillus. 

(2)  Sterigmata  branched — Sterigmatocystis. 
(iii.)  Conidiophores  branched: — 

(1)  Sympodially  branched — Eurotiopsis. 

(2)  Bushy  branched: — • 

(a)  In  bundles,  perithecia  stalked — Penicil- 

liopsis. 

(b)  Not    in     bundles,   perithecia    sessile — 

Penicillium. 

B.  Spores  bicellular — Testudina. 

We  are  concerned  with  the  genera  Penicillium,  Aspergillus,  and 
Sterigmatocystis,  of  which  the  following  species  are  parasitic  in 
man: 

[P.  crustaceum  Linnseus,  1763. 

P.  minimum  Siebenmann,  1889. 

P.  barbce  Castellani,  1907. 

P.  montoyai  Castellani,  1907. 

P.  pruriosum  Salisbury. 

P.  brevicaule   var.    hominis    Brumpt   and 
Langeron,  1910. 


Penicillium  Link,  1809 


0.     .         .        .     n     „„     ,a*n  f  S.  antacustica  Cramer,  1859. 
Stengmatocystis  Cramer,  1869  {  s    nidulans  Eidam    l88J 


Aspergillus  Micheli,  1725 


'  A.  jumigaius  Fresenius,  1775. 
A.  flavus  Link,  1791. 
A.  bronchialis  Bhimentritt,  1901. 
A.  nigrescens  Robin,  1851. 
A.  repens  De  Bary,  1870. 
A.  malignus  Lindt,  1889. 
A.  pictor  R.  Blanchard,  1895. 
A.  barbce  Castellani,  1907. 
A  .  bouffardi  Brumpt,  1905. 
A.  herbariorum  Wiggers,  1780. 
A .  fontoynonli  Gueguen,  1909. 


PENICILLIUM 


1025 


Genus  Penicillium  Link,  1809. 

The  whole  fruit-bearing  hypha  with  its  sterigmata  and  conidia 
resembles  a  hair-pencil,  hence  the  name  of  the  genus  {Penicillium= 
hair-pencil).  The  conidiophore  hypha  shows  verticillate  branches, 
which  give  rise  to  slender  fusiform  formations  (sterigmata)  abstn'ct- 
ing  chains  of  conidia. 

Penicillium  crustaceum  Linnaeus,  1763. 

Synonyms. — Mucor  crusiaceus  albus  Linnaeus,  1763;  Manilla 
digitata  Persoon;  Penicillium  glaucum  Linnaeus,  1809  ;P.  exfiansum 

Linnaeus; P.  crustaceum  Fries,  1829. 

An  extremely  common  saprophyte  found  on  bread,  cheese,  fruits, 
and  various  organic  substances  in  a  state  of  decomposition.  The 
conidia  are  spherical  or  slightly  elliptical,  of  bronze  colour,  with 
smooth  surface;  maximum  diameter  4  fi.  This  fungus  grows  well 
at  any  temperature  between  20  and  350  C,  and  is  very  resistant. 


Fig.  524. — Asper- 
gillus Fructifi- 
cation. 


Fig.    525. —  Sterig- 
matocystis  fruc- 
tification. 
(After  Brumpt.) 


Fig.  526. — Penicil- 
lium Fructifica- 
tion. 


It  has  been  found  by  Maggiora  and  Gradenigo  in  two  cases  of 
otitis  media.  Heinhorn  has  observed  it  in  the  vomiting  of  four 
cases  of  acid  dyspepsia  together  with  Aspergillus  herhariorum. 

WVrtheim  has  observed  that  the  intravenous  inoculation  of  P. 
crustaceum  is  pathogenic  to  rabbits,  dogs,  and  lambs. 

Penicillium  minimum  Siebenmann,  1889. 

Conidia  are  roundish,  smooth,  of  a  brownish-black  colour;  smaller 
than  in  P.  crustaceum,  being  2-5  to  3  fj,  in  diameter.  Was  found  in 
a  case  of  acute  otitis  by  Siebenmann. 

Penicillium  montoyai  Castellani,  1907. 

Synonym.  -  P.  pictor  Neveu-Lemaire,  1908. 

Conidia  roundish  or  slightly  oval,  smooth,  3  to  4^  it  in  diameter. 
Grows  well  on  maltose  agar  and  ordinary  agar;  cultures  of  dark 
greyish  colour.  Discovered  by  Montoya  in  cases  of  pinta,  of  the 
greyish-violet  variety.  Similar  species,  not  yet  well  defined,  are 
found  in  other  varieties  of  pinta. 

65 


1026 


ASCOMYCETES  AND  BASIDIOMYCETES 


Penicillium  brevicaule  var.  hominis  Brumpt  and  Langeron,  iqio. 
Found  by  Brumpt  and  Langeron  in  two  cases  of  onychomycosis. 
In  the  lesions  septate  mycelial  threads  were  seen,  2  to  10  /i  in 
diameter,  and  large  groups  of  chlamydospores,  generally  terminal, 
10  to  30  ft  in  diameter.  The  fungus  is  easily  cultivated  on  Sabou- 
raud's  agar  and  other  sugar  media,  also  on  potatoes  and  carrots. 
Optimum  temperature  250  C,  but  grows  well  also  at  370  C.  Conidia 
spherical  or  occasionally  ovoid,  of  a  chocolate  colour. 


Fig.  527. — Pencillium  brevi- 
caule var.  hominis  Brumpt 
and  Langeron. 

(After  Brumpt.) 


Fig.    528.- — Penicillium    brevicaule   var. 

hominis  Brumpt  and  Langeron. 

(Preparation   from    the   diseased   nails, 

after  Brumpt.) 


Penicillium  barbae  Castellani,  1907. 

Found  by  us  growing  on  the  beard  of  natives  of  equatorial  Africa,  and  in 
natives  of  Ceylon. 

Penicillium  pruriosum  Salisbury. 

Doubtful  species  found  by  Salisbury  in  the  vaginal  mucus  of  a  woman 
suffering  from  intense  vaginal  pruritus. 

Genus  Aspergillus  Micheli,  1725. 

The  conidiophore  hyphse  are  not  ramified,  and  terminate  into 
ovoid  or  roundish  formations,  which  support  numerous  claviform 
elements  (sterigmata),  each  of  which  sup- 
ports a  chain  of  roundish  conidia. 

Aspergilli  are  generally  saprophytes, 
but  they  may  become  parasites.  They 
are  easily  grown  on  acid  media,  liquid  or 
solid,  and  also  on  alkaline  media.  Iron  and 
manganese  have  a  favourable  influence  on 
the  growth  and  sporulation  of  these  fungi. 


Fig.  529. — -Aspergillus 
Fructification. 


A  medium  much  used  is   Raulin's  liquid,  the 

formula  of  which  is:   Cane-sugar,    70    grammes; 

(After  Brumpt.)  tartaric    acid,    4    grammes;    ammonium    nitrate, 

4  grammes;  ammonium  phosphate,  o  60  gramme; 

potassium   carbonate,    o-6o   gramme;  magnesium  carbonate,  0-40  gramme; 

ammonium    sulphate,  0-25  gramme;    zinc  sulphate,  007  gramme;    ferrous 

sulphate,  0-07  gramme;  potassium  silicate,  0-07  gramme. 

Fungi  of  the  genus  Aspergillus,  when  growing  parasitically  in  the 
tissues,  often  lose  their  characteristics;  the  typical  fructifications 


ASPERGILLUS  FUMIGATUS 


1027 


are  absent,  and  only  mycelial  threads  and  roundish  or  oval  yeasl 
like  bodies  are  seen. 

The  various  species  may  be  differentiated  with  difficulty  as  follows, 
or  cannot  be  differentiated: — 

A.  Green  species  : — 

I.  Spores  5  microns  and  more.     Can  hardly  be    differentiated — 
Repens,  h'lavus. 
II.   Spores  less  than  5  microns:— 

(a)  Lives  saprophytically — -Fumigatus. 

(b)  Not  known  to  live  saprophytically: — 

1.  Very  pathogenic  for  rabbits — Malignus. 

2.  Found  in  bronchial  sputum — -Bronchialis. 

B.  Blackish-brown  species — Nigrescens. 

C.  Golden,  brownish,  gold-brown,  or  reddish — Herbariorum. 

Aspergillus  fumigatus  Fresenius,  1775. 
This  is  the  commonest  Aspergillus,  and  is  very  often  found  on 
various  cereals,  straw,  hay,  etc.  On  solid  media  it  produces  a 
brownish-black  culture  if  the  medium  is  alkaline  or  neutral,  greenish 
if  the  medium  is  acid.  The  mycelial  filaments  are  more  or  less 
ramified,  the  breadth  varying  between  2  and  3  /,<;.  The  conidio- 
phore  hyph?e  are  much  thicker  than  the  mycelial  tubes,  being,  on  the 
average,  about  5  ft  in  breadth.  The  sterigmata,  which  are  situated 
very  close  together,  are  6  /t  long;  the  conidia  are  roundish,  2-5  to 
,.>'•-.;•.       «••:..- v  3    I-1   m    diameter,    smooth, 

colourless.  Optimum  tem- 
perature, 370  C. ;  the  growth 
stopsbelow20°  or  above  55°C. 


Fig.  530. 


-A  spergillus  fumigatus 
Fresenius. 


Fig.  531.— Aspergillus  bron- 
chialis Blumentritt. 
(After  Blumentritt.) 


Pathogenicity. — This  Aspergillus  is  the  species  most  frequently 
found  in  man,  giving  rise  to  an  aspergillosis  of  various  organs.  The 
spores  are  very  resistant.  Perchloride  of  mercury  is  the  antiseptic 
which  has  the  greatest  destruct  ive  acl  ion  on  the  spores.  The  effects 
on  the  human  organism  are  due,  in  addition  to  mechanical  action, 
to  toxins  secreted  by  the  fungi.  Lucet  has  found  in  cultures  of 
A.  fumigatus  in  Raulin's  liquid  a  pyrogenic  substance;  Ceni  and 


1028  ASCOMYCETES  AND  BASIDIOMYCETES 

Besta  have  isolated  toxic  products  soluble  in  ether  and  alcohol, 
which  act  on  the  muscular  and  nervous  system  of  dogs  and  rabbits. 
(See  also  remarks  on  Aspergillomycoses,  p.  1031.) 

Aspergillus  flavus  De  Bary,  1870. 

Synonyms.- — Monilia  aurea  Gmelin,  1791 ;  Eurotium  flavum  De 
Bary,  1870;  Aspergillus  flavescens  Wreden,  1874. 

Mycelium  colourless;  conidiophore  hyphae  terminate  in  roundish 

formations  of  a  gold-yellow  colour.     The  conidia  are  dark  yellow, 

roundish,  5  to  7  /j,  in  diameter,  with  a  surface  showing  numerous 

minute    mammillar    prominences.     Found    by    several    observers 

(Wreden,   Siebenmann,  etc.)   in  the  ear.     Optimum  temperature, 

37°  C 

Aspergillus  bronchialis  Blumentritt,  1901. 

Mycelium  of  a  white  colour,  much  ramified;  conidiophore  hyphae 
are  6-2  to  12-6  [i  in  diameter,  280  to  300  (a,  in  length.  Conidia 
roundish,  3  to  4  /,i  in  diameter,  with  a  smooth  surface,  of  a  greyish- 
greenish  colour.  This  Aspergillus  was  found  by  Chiari  in  the 
bronchi  of  a  patient  who  had  died  from  diabetes;  it  was  investigated 
by  Blumentritt.     It  has  not  yet  been  found  as  a  saprophyte. 

Aspergillus  fontoynonti  Gueguen,  1909. 

Found  by  Fontoynont  and  Carougeau  in  a  European  living  in 
Madagascar,  who  was  suffering  from  multiple  abscesses  of  the  neck. 
In  the  pus  and  in  the  first  cultures  obtained  the  fungus  had  no  true 
aspergillar  appearance;  it  had  to  be  subcultured  several  times 
before  the  typical  aspergillar  fructifications  appeared.  Conidia 
4  to  5  fx  in  diameter,  with  surface  finely  verrucose.  Optimum 
temperature,  220  to  250  C. 

Aspergillus  malignus  Lindt,  1889. 

Synonym. — Eurotium  malignum  Lindt,  1889. 
Colourless  mycelium,  composed  of  short  articles.     Conidiophore 
hyphae  erected,  terminating  in  pyriform  formations,  22  to  24  jli  in 


Fig.  532. — Aspergillus  malignus  Fig.  533. — Aspergillus  repens 

Lindt.  De  Bary. 

(After  Lindt.)  (After  Siebenmann.) 

diameter,  on  which  are  situated  the  sterigmata,  which  are  10  [jl  long 
and  4  to  5  /j,  in  breadth.    Conidia  roundish,  of  a  greenish-bluish  colour. 


ASPERGILLUS  HE  NBA  RIO  RUM 


1029 


Pathogenicity. — This  Aspergillus  was  found  by  Lindt  in  a  case 
of  otomycosis;  according  to  this  author,  it  is  very  pathogenic  for 
rabbits. 

Aspergillus  herbariorum  Wiggers,  1780. 

Synonyms.  Mucor  herbariorum  Wiggers,  1780;  Aspergillus 
glaucus  L)e  Bary,  1870. 

Mycelium  at  first  colourless,  later  yellow  or  reddish-yellow.  This 
Aspergillus  is  characterized  by  the  large  size  of  the  conidia,  which 
are  9  to  15  u,  in  diameter.  It  is  in  nature  a  common  saprophytic 
fungus.  It  'has  been  found  by  Dunn  in  1896  in  the  nasal  cavities 
of  a  man,  and  by  Einhorn  in  1900  in  the  vomit  of  a  case  of  hyper- 
chloridia. 

Aspergillus  repens  De  Bary,  1870. 

Synonym. — Eurotium  repens  DeBary,  1870. 

This  fungus  is  very  similar  to  A.  herbariorum,  but  for  the  smalW 
size  of  the  conidia.  Mycelium  of  a  yellowish-green  colour.  Conidia 
large,  7  to  8-5  tu.  Found  by  Sieben- 
mann  in  the.  tar  three  times.  Its 
pathogenic  role  is  doubtful. 

Quevedo  has  described  an  aspergillus  very 
similar  to  A .  repens,  which  he  believes  to  be 
the  cause  of  a  type  of  encephalo-myelitis  in 
horses  in  South  America.  He  calls  the 
organism  A .  mayidis. 

Aspergillus  pictor  R.  Blanchard, 
1895. 

Synonym.  —  Trichophyton  pictor 
R.  Blanchard,  1895. 

The  term  Aspergillus  (Trichophyton) 
pictor,  introduced  by  Blanchard  in 
1895,  before  the  plurality  of  species  of 
the  fungi  found  in  pinta  was  demon- 
strated, is  now  used  to  denote  the 
species  of  Aspergillus  which  is  found  in 
the  pure  violet  variety  of  pinta.  This  fungus  shows  the  typical 
morphological  characters  of  the  genus  Aspergillus.  It  grows  easily 
on  various  sugar  media.  On  maltose  agar  the  growth  has  at 
first  a  whitish  colour,  which  afterwards  changes  into  greenish,  to 
become  violet  or  greenish  with  a  violet  tinge  at  a  later  period.  The 
colour  of  the  growth  may  vary  according  to  the  medium  on 
which  cultivation  takes  place.  The  conidiophores  are  comparatively 
thick;  the  conidia  are  globular,  with  a  smooth  surface. 

Several  other  species  of  aspergillar  and  aspergillar-like  fungi  are 
found  in  pinta,  but  their  botanical  position  has  not  yet  been  defined 
with  certainty. 


_*^ 


Fig.  534. — Aspergillus  pictor 

R.  Blanchard. 

(After  Montoya  y  Florez.) 


1030  ASCOMYCETES  AND  BASIDIOMYCETES 

Aspergillus  bouffardi  Brumpt,  1905. 

Found  by  Boufi'ard  in  a  case  of  black  mycetoma,  and  completely 
described  by  Brumpt.  Mycelium  whitish  in  some  zones,  dark 
brown  in  others.  Conidiophores  erect,  white,  each  terminating  in  a 
claviform  structure,  bearing  some  short  chains  of  roundish  conidia. 
Conidia  1-3  to  2  /j,  in  diameter,  roundish  with  a  smooth  surface,  white. 
Chlamydospores  present,  5  to  10  ^  in  diameter.  Attempts  at 
cultivation  did  not  succeed. 

Aspergillus  barbae  Castellani,  1907. 

Found  by  us  in  natives  of  Uganda,  and  in  natives  of  Ceylon.  Conidia 
spherical,  4  to  5  /*,  of  a  brownish  colour. 

Aspergillus  nigreseens  Robin,  1889. 
Doubtful  species,  which,  according  to  Wienfeld,  causes  a  faviform  eruption. 

Genus  Sterigmatocystis  Cramer,  1S59. 

Definition. — Aspergillales  with  conidiophores  terminating  in 
roundish  or  ovoid  formations,  on  which  are  situated  short  cylindrical 
structures — primary  sterigmata — surmounted  by  similar  elements — 
secondary  sterigmata.  Each  of  the  secondary  sterigmata  supports 
a  chain  of  roundish  conidia. 

Remarks. — The  genus  was  created  by  Cramer  for  a  fungus  found 
in  a  man's  ear. 

Type  Species. — Sterigmatocystis  antacustica  Cramer,  1859. 

Classification. — The  two  species  of  importance  to  us  can  be 
recognized  as  follows : — 

A.  Young  conidial  forms  green;  later  strongly  grey  to  brown.     Conidia 

small,  3  microns  in  diameter — Nidulans. 

B.  Conidial    forms    blackish    brown.      Conidia    small,    25    microns    in 

diameter- — Antacustica. 

Sterigmatocystis  antacustica  Cramer,  1859. 

Synonyms. — Sterigmatocystis  antacustica  Cramer,  1S59:  Eurotium 
nigrum  De  Bary.  1S70 :  Monilia  pull  a  Persoon;  Aspergillus  nigricans 
Wreden,  1874:  A.  niger  von  Tieghem,  1S67. 

Primary  and  secondary  sterigmata;  erected  conidiophores; 
hyphae  more  than  1  millimetre  in  length  (3-5  to  4-5).  Conidia 
globular,  2  5  /*  in  diameter,  provided  with  a  membrane  of  a  brownish 
colour.  Commonly  found  in  decaying  organic  substances.  It  was 
first  observed  in  man  by  Cramer,  who  observed  it  in  the  ear  of  a 
deaf  patient.  Later  it  was  observed  by  Fiirbringer  and  others  in 
mycotic  affections  of  the  lungs. 

Sterigmatocystis  nidulans  Eidam,  1883. 

Synonym. — Aspergillus  nidulans  Eidam,  1883. 
Mycelium  of  a  greenish  colour.     Conidiophores  are  erect,  0-5  to 
0-8  millimetre  in  length.     Presence  of  primary  sterigmata,   sup- 


STERIGMATOCYSTIS  NIDULANS  1031 

porting  secondary  sterigmata,  each  of  which  gives  rise  to  a  chain  of 
conidia.  Conidia  small  (2  to  3  /t  in  diameter),  globular,  of  a  greenish 
colour.  The  fungus  has  been  completely  investigated  by  Pinoy: 
grows  badly  in  Raulin's  liquid,  better  on  Sabouraud's;  is  non- 
pathogenic for  rabbits.     This  species  is  found  living  saprophytically 


FIG-  535. — Sterigmatocystis  Fig.   536. — Stevigmatocystis 

Fructification.  nidulans  Eidam. 

(After  Brumpt.)  (After  Eidam,  from  Brumpt.) 

in  certain  nests,  hence  the  name  5.  nidulans.  In  man  it  has  been 
found  in  several  cases  of  otomycosis.  Nicolle  and  Pinoy  have 
found  it,  or  a  very  similar  species,  in  a  case  of  mycetoma  with  white 
granules. 

General  Remarks  on  Mycoses  due  to  Species  of  the  Family 
Aspergillaceae. 

These  mycoses  are  generally  called  aspergillomycoses.  They 
have  been  recorded  several  times  in  man. 

i.  Aspergillosis  of  the  Lungs;  Aspergillar  Pseudo-tuber- 
culosis; Pneumomycosis  of  Aspergillar  Origin. — Aspergilli 
develop  sometimes  in  the  mucosa  of  the  trachea,  of  the  bronchi,  and 
even  in  the  pulmonary  alveoli,  without  giving  rise  to  any  pathogenic 
effect.  In  other  cases  the  fungi  induce  pseudo-membranous  and 
ulcerative  lesions.  A  very  serious  affection  is  a  form  of  pseudo- 
tuberculosis (pseudo-tuberculosis  aspergillina),  characterized  by  the 
presence  of  mycotic  nodules  in  the  lungs,  liver,  kidneys,  and  other 
organs.  This  affection,  due  to  A.  fumigatus,  is  very  common  in 
some  parts  of  France  among  pigeon-breeders  (gaveurs  de  pigeons). 
The  same  affection  attacks  the  pigeons.  The  infection  is  probably 
caused  by  spores  of  A.  fumigatus  being  present  in  the  grains  used 
for  feeding  the  pigeons. 

2.  Aspergillosis  of  the  Eye. — A.  fumigatus  has  been  found 
several  times  in  ulcers  of  the  cornea  (keratomycosis  aspergillina). 

3.  Aspergillosis  of  the  Ear  (Otomycosis  Aspergillina).— 
Various  species  of  Aspergillus  have  been  found  in  the  ear.  In  some 
cases  they  may  give  rise  to  a  serious  otitis,  deafness,  and  tinnitus. 
Aspergillosis  of  the  ear  is  not  rare  in  the  tropics.  Syringing  with 
hydrogen  peroxide  two  parts  and  alcohol  one  part  is  useful. 

4.  Aspergillosis  of  the  Nose. — A.  glaucus  and  A.  fumigatus 
have  been  found  in  the  nasal  cavities;  the  first  apparently  does  not 


1032  ASCOMYCETES  AND  BASIDIOMYCETES 

cause  any  disturbance.     The  second  causes  various  inflammatory 
symptoms. 

5.  Aspergillosis  of  Wounds  and  Ulcers.— In  wounds  not 
properly  treated,  and  in  old  ulcers,  Aspergilli  have  been  occa- 
sionally found. 

6.  Aspergillosis  of  the  Urethra . — In  several  cases  a  black 
urethral  discharge  has  been  observed,  due  to  Sterigmalocyslis  nigra. 

7.  Aspergillosis  of  the  Skin. — Montoya's  investigation  has 
shown  that  several  varieties  of  pinta  are  due  to  fungi  of  the  genus 
Aspergillus.  Another  important  tropical  skin  disease,  tinea  im- 
bricata,  was  believed  until  recently  to  be  due  to  an  Aspergillus — 
A.  tokelau  Wehmer,  1903.  In  our  experience  the  fungi  of  tinea 
imbricata  never  show  aspergillar  fructifications,  and  cannot  be 
considered  to  be  Aspergilli. 

Aspergilli  may  also  cause  some  varieties  of  mycetoma. 

PYRENOMYCETES. 

Ascomycetous  fungi  in  which  the  asci  are  contained  in  a  perithecium  pre- 
senting an  orifice  at  the  apex  for  the  escape  of  the  spores.  According  to  some 
authors,  species  of  this  family  have  been  found  parasitic  in  man.  This  is 
very  doubtful,  though  Schubert  states  that  he  found  in  the  nasal  mucus  of  a 
patient  an  organism  closely  allied  to  Botrytis  bassiana,  which  latter  species,  as 
is  well  known,  causes  the  disease  of  silkworms  called  muscardin. 

CLASS  BASIDIOMYCETES. 

Basidiomycetes  have  a  septate  mycelium,  and  are  devoid  of 
sexual  reproduction.  They  reproduce  by  formation  of  basidia. 
Other  accessory  fructifications  may  be  present — as,  for  example, 
chlamydospores.  The  basidia  are  of  two  principal  tj^pes:  (1)  auto- 
basidia;  (2)  protobasidia. 

The  autobasidia  are  large,  unseptated  cells,  giving  rise  at  their 
apices  to  four  delicate  sterigmata,  each  of  which  bears  a  spore. 

The  protobasidia  are  septated,  and  appear  in  two  chief  forms: — 

A.  Septated  into  four  cells,  each  giving  rise  to  a  spore  from,  a 
lateral  inserted  sterigma. 

B.  Septated  by  walls  intersecting  at  right  angles,  each  cell  ending 
in  an  elongated  tubular  sterigma. 

Of  the  Basidiomycetes,  one  species  (Ustilago  phyodytes)  of  the 
family  Ustilaginere  is  of  special  importance,  while  two  others 
(U.  carbo  and  Till  el  la  levis)  may  produce  otonvycosis. 

Ustilago  hypodytes  Schlecht. 

Synonyms. — Dendrodlchium  microsporus  Brigi;  Sporotvichuni  dennatodes 
Kane. 

The  mycelium  penetrates  the  stem  and  leaves  of  reeds  (Arundo  donax)  in 
some  parts  of  Provence,  Italy,  and  Greece.  After  a  time  the  mycelium  pro- 
duces innumerable  so-called  brand  spores  by  a  process  of  segmentation  of  its 
profusely  branched  hypha?.  In  this  way  the  mycelium  is  transformed  into  a 
brown  dark  mass  of  spores. 

These  brand  spores,  as  regards  the  mode  of  their  formation,  may  be  con- 
sidered chlamydospores.     The   brand   spores   are   resting  spores;  they   are 


REFERENCES  1033 

scattered  by  the  wind,  and  after  an  interval  of  rest  they  germinate,  producing 
conidiospores  of  a  basidium-like  type. 

The  spores  of  U.  hypodytes  are  the  cause,  according  to  most  authors,  of  a 
peculiar  affection  found  among  workers  who  have  to  do  with  the  cutting,  etc., 
of  reeds  (Arundo  donax).  This  affection  is  called  '  frienite,'  or  '  frien  disease.' 
The  patient  complains  of  symptoms  somewhat  resembling  hay-fever — sneezing, 
headache,  etc. — and,  in  addition,  shows  an  erythematous  erysipeloid  eruption 
on  the  uncovered  part  of  the  body,  and  often  also  on  the  genital  organs, 
which  may  become  greatly  oedematous.     Desquamation  follows. 

According  to  other  observers,  the  cause  of  this  peculiar  disease  is  to  be 
found,  not  in  the  spores  of  Ustilago,  but  in  an  insect — Aclerda  berletei,  dis- 
covered by  Berlese — which  often  swarms  on  various  reeds.  The  workers,  in 
manipulating  the  canes,  squash  some  of  these  insects,  and  the  irritating  juice 
exuding  therefrom  produces  a  dermatitis  of  an  erythematous  type. 


REFERENCES. 

A  very  valuable  work  on  the  Microsporums,  the  Trichophytons,  and  the 
Achorions  of  Temperate  Zones,  is  Sabouraud  (1910),  '  Les  Teignes,'  Paris. 
With  regard  to  Aspergillus,  the  most  important  is  Wehmer  (1910),  '  Die 
Pilzgattung  Aspergillus,'  Geneve. 

Brault  and  Viguier  (1914).     C.  R.  Soc.  Biol. 

Castellani  (1903-1919).     Numerous  papers  in  Journal  Ceylon  Branch  British 

.Medical    Association,    Reports    to     Advisory     Committee     on     Tropical 

Diseases,  Ceylon  Medical  Reports,  British  Journal  of  Dermatology,  British 

Medical    Journal,    Journal  of  Tropical  Medicine,    Annali    Med.   Navale, 

Archiv.  f .  Dermatologie  u.  Syphilis. 
Castellani  (1909).     Journ.  Ceylon  Branch  B.M.A.  (Epidermophyton  rubrum 

and  Other  Fungi). 
Castellani  (1910).     British  Journ. of  Dermatology  (Epidermophyton rubrum). 
Castellani  (1919).    Bull.  Soc.  Path.  Exot.  (Etiology  of  Tokelau). 
Castellani  and  Chalmers  (1913).     Manual  of  Trop.  Med.,  2nd  Ed. 
Chalmers   and   Marshall    (1914-15).     Journal   of   Tropical   Medicine   and 

Hygiene  (Trichophytons). 
Chalmers    and    Macdonald    (1915).     Journal    of 'Tropical    Medicine    and 

Hygiene  (Trichophytons) . 
Gedoelst  (191  i).     Synopsis  de  Parasitologic     Bruxelles. 
Pinoy  (1908-1918).     Numerous  papers  in  Bull.  Soc.  de  Path.  Exot. 
Thom    and    Currie    (1916.)     Journal    of    Agricultural    Research.    October 

(Aspergillus  niger  Group).     Washington. 


PLATE  VI 

NOCARDIAS  AND  ASSOCIATED  ORGANISMS 

i.  Hair,  natural  size:  Trichomycosis  flava. 

2.  Trichomycosis  flava. 

3.  Trichomycosis  flava. 

4.  Trichomycosis  nigra. 

5.  Trichomycosis  rubra. 

6.  Hair,  natural  size:  Trichomycosis  rubra. 

7.  RJiodococcus  castellanii  (Chalmers  and  O'Farrell,  1913). 
S.  Nocardia  indica  (Kanthack,  1893). 

9.  Nocardia  convoluta  Chalmers  and  Christopherson,  1916. 

10.  Hair,  natural  size:  Trichomycosis  nigra. 

11.  Cohnistreptothrix  tenuis  (Castellani,  191 1),  branching. 

12.  Cohnistreptothrix  tenuis  (Castellani,  191 1),  bacillary  forms. 

13.  Cohnistreptothrix  tenuis  (Castellani,  191 1),  long  form. 

14.  Cohnistreptothrix  tenuis  (Castellani,  191 1),  branching  forms  and  coccal 
forms  from  a  culture. 


LO^ 


PLATE    VI. 


11    f 


9  • 


Geo  Waterston  4  Sor»  Ltd  Edin 


12 

r              .     *•  ' 

-    ••    t* 

•' 

13 

[4 


To  face  page  1035 


CHAPTER  XXXIX 
FUNGI   IMPERFECTA 

Preliminary — Fungi  imperfecta — Hyphales — Vuillemin's  classification — Micro- 
siphonales  —  Thallosporales  —  Hemisporales  — ■  Conidiosporales —  Refer- 
ences. 

PRELIMINARY. 

We  now  come  to  the  last  class  of  Schroeter's  Eumycetes — viz.,  the 
Fungi  Imperfecti ;  that  is  to  say,  Eumycetes  with  a  septate  mycelium 
and  with  spores  which  are  not  contained  in  asci  or  basidia,  but  are 
carried  on  conidiospores,  which  may  or  may  not  be  enclosed  in 
pycnidia. 

This  class  contains  a  large  number  of  genera  of  importance  in 
tropical  medicine,  but  everyone  who  has  studied  these  fungi  must 
have  felt,  as  we  have,  the  great  difficulty  of  determining  to  what 
genus  the  organism  belonged  at  which  he  was  working. 

Various  systems  have  been  proposed,  such  as  the  mode  of  bearing 
spores  and  the  colour  of  the  fungus,  matters  which  change  with 
environment.  Further  septation  of  the  spores  often  depends  upon 
their  age  and  other  factors.  Similarly  new  species  have  been  made 
for  a  fungus,  very  like  another  fungus,  but  found  on  a  new  host. 
In  this  way  the  classification  has  become  almost  hopeless. 

Vuillemin  has,  however,  proposed  a  new  classification,  which 
prevents  the  same  fungus  being  variously  classified  in  different 
stages  of  its  life-history.     We  adopt  it  for  purposes  of  utility. 

CLASS:   FUNGI  IMPERFECTI  Fuckel,  1869. 

Synonym, — -Deuteromycetacece  Saccardo  ('  Sylloge,'  vol.  xvi., 
p.  825). 

Definition.-  -Fungi,  almost  invariably  minute,  in  which  asexual 
reproduction  takes  place  by  means  of  conidia  produced  on  conidio- 
phores,  which  are  either  enclosed  in  perithecia,  placed  on  discs,  or 
unprotected. 

Remarks.— Fuckel  gathered  together  under  the  above  name  all 
forms  of  fungi,  the  complete  life-history  of  which  was  unknown,  and 
made  this  class  in  contradistinction  to  his  other  class  of  Fungi 
Perfecti.  Vuillemin,  in  1910,  suggested  dividing  the  class  into  two 
subclasses,  Deuteromycetes  and  Hyphales. 

Classification.  The  Class  Fungi  Imperfecti  may  be  subdivided 
into  two  classes  as  follows: — 

1035 


1036  FUNGI  IMPERFECTI 

A.  Accessory  fructifications  present  in  the  form  of  closed  or  open  recep- 

tacles— Subclass  1,  Deuteromycetes  Saccardo,  1886,  emendavit  Vuille- 
min,  1910. 

B.  No  such  accessory  fructifications  present.     Reproduction  by  means 

of  spores,  isolated  or  in  groups,  situate  on  isolated  or  fasciculated 
hyphae — Subclass  2:  Hyphales  Vuillemin,  1910. 

SUBCLASS  1 :  DEUTEROMYCETES  Saccardo,  1886,  emendavit 
Vuillemin,  1910. 

Definition. — Fungi  Imperfecti  possessing  accessory  fructifications 
in  the  form  of  open  or  closed  receptacles. 

A.  Conidiophores    minute    and    enclosed    in    a    perithecium — Order    1, 

Sphceropsidales  Leveille,  emendavit  Saccardo,  1882. 

B.  Conidiophores  not  enclosed  in  a  perithecium,  but  crowded  on  a  disc 

arising  from  a  deeply  embedded  mycelium — Order  2,  Melan- 
coniales  Corda,  1842,  emendavit  Saccardo,  1882. 

SUBCLASS  2:  HYPHALES  Vuillemin,  1910. 

Synonyms. — Nematomyci  Nees,  1816;  Hyphomycetece  Martius, 
1817,  pro  parte;  Hyphomycetes  Fries,  1833;  Moniliales  Clements, 
1909. 

Definition. — Fungi  Imperfecti  with  hyphae  more  or  less  developed, 
lax,  or  more  or  less  compact,  superficial  or  subsuperficial,  or  more 
rarely,  as  in  man,  vertebrates,  and  insects,  endoparasitic.  Conidio- 
phores never  situate  in  closed  or  on  open  receptacles.  Reproduc- 
tion by  means  of  spores  isolated  or  in  groups,  situate  on  isolated  or 
fasciculated  hyphge. 

Remarks. — The  Hyphales  of  Vuillemin  correspond  to  the 
Hyphomycetes  of  Fries,  but  the  subdivision  into  families  is  so 
entirely  different  that  it  appears  better  to  adopt  a  change  of  name 
in  order  to  prevent  confusion. 

Vuillemin' s  classification  appears  to  us  to  be  more  suitable  from 
the  point  of  view  of  tropical  medicine,  and  therefore  we  adopt  it  in 
this  chapter;  but,  in  order  to  permit  comparison,  we  give  the  out- 
lines of  the  old  division  of  the  Hyphomycetes,  which  is  as  follows  :— 

ORDER  HYPHOMYCETES  Fries,  1833. 

A.  Hyphomycetes  with  hyaline  or  brightly  coloured  hyphae  which  do 

not  cohere  in  fascicles  and  with  concolorous  conidia — Family  1, 
MucidinacetB  Link,  1809. 

B.  Hyphomycetes  with  dark-coloured  or  black   hyphae  rarely  hyaline. 

and  then  with  dark-coloured  conidia.  The  hyphae  do  not  cohere 
into  fascicles — Family  2,  Dematiacece  Fries,  1832. 

C.  Hyphomycetes  with  hyaline  or  dark-coloured   hyphae  of  which  the 

sterile  are  scanty  and  creeping,  while  the  fertile  are  erect,  cohering 
into  elongated  fascicles  bearing  conidia  at  the  top  or  more  rarely 
along  the  side — Family  3,  Stilbellacece  Vuillemin,  1910. 

D.  Hyphomycetes  with  hyaline  or  dark-coloured  hyphae  compacted  into 

a  globose,  discoid,  or  verruciform  body  called  a  sporodochium — 
Family  4,  Tuberculariacece  Ehrenberg,  181 8. 


HYPHOMYCETES  1037 

With  reference  to  the  name  of  Family  3,  this  has  been  changed 
from  Stilbaccce  Fries,  1825,  to  its  present  name,  because  Juel  has 
demonstrated  that  some  of  the  species  of  the  genus  Stilbum  belong 
to  the  Basidiomycetes,  and  has  given  the  name  Stilbella  to  those 
left  in  Fungi  Imperfecti. 

The  basis  of  reference  with  regard  to  fungi  must  for  all  time  be 
Saccardo's  '  Sylloge  Fungorum,'  because  it  details  some  60,000 
species  of  fungi,  and  this  is  based  upon  the  colour  of  the  hypha.' 
and  conidia  and  the  number  of  septa  in  the  spore,  as  will  be  indi- 
cated when  detailing  the  hyphales.  Clements  has  published  a 
most  useful  key  in  English  to  Saccardo's  '  Sylloge.' 

Leaving  this  form  of  classification,  we  will  consider  Vuillemin's 
new  system. 

Vuillemin's  Classification. — -Vuillemin  has  pointed  out  a  diffi- 
culty which  we  have  also  experienced  in  classifying  the  fungi  of 
the  Hyphomycetes — viz.,  one  and  the  same  fungus  may,  under 
different  conditions,  show  a  mucedine  type,  a  stilbelline  type,  and 
a  tubercularine  type,  which  makes  its  recognition  most  difficult. 
To  obviate  this  difficulty  he  has  concentrated  his  attention  upon 
the  '  spore,'  in  order  to  form  the  orders  of  the  class  Hyphales,  and 
has  given  definitions  of  his  terms  so  as  to  prevent  confusion. 

Terminology. — The  following  terms  require  to  be  carefully 
studied:  Thallospore,  Blastospore,  Arthrospore,  Chlamydospore, 
Hemispore,  Protoconidium,  Deuteroconidium,  Conidium,  Aleurio- 
spore,  Sporophore,  Phialide,  and  Prophialide. 

I.  The  Thallospore  is  a  sporiform  element  which  is  really  only  a 
portion  of  the  thallus  secondarily  adapted  to  the  purposes  of  repro- 
duction. The  various  forms  of  the  Thallospore  are  named  Blasto- 
spores,  Arthrospores,  and  Chlamydospores. 

A  blastospore  (Tig.  537)  is  a  thallospore,  round  or  ovoidal  in 
shape,  developed  by  budding  from  the  summit  or  sides  of  a 
hypha  which  may  be  the  same  size  and  appearance  as  the 
blastospore,  as  in  Cryptococcus,  or  may  be  an  elongated 
filament. 

An  arthrospore  is  a  thallospore  developed  by  the  disarticula- 
tion of  hyphal  elements  at  first  with  square  cut  ends,  which 
subsequently  become  rounded  off,  and  with  thin  walls 
which  subsequently  become  thickened.  A  Chlamydospore 
(Fig.  538)  is  merely  a  variation  of  an  arthrospore,  and  may 
be  defined  as  an  intermediate  or  terminal  spore  larger  than 
the  ordinary  hypha,  which,  without  becoming  isolated, 
undergoes  a  kind  of  encystment,  with  the  formation  of  a 
thick  and  sometimes  coloured  wall  containing  cytoplasm 
loaded  with  food  material. 

II.  The  Hemispore  (Figs.  539  and  540)  starts  by  a  differentia- 
tion from  the  thallus,  the  '  Protoconidium,'  but  this  remains  where 
formed  while  the  hypha  continues  to  grow.     Eventually  the  proto- 


io38 


FUNGI  IMPERFECT  I 


conidium  forms  secondary  functional  spores  called  '  Deuteroconidia,' 
which  are  the  reproductive  spores. 

III.  The  Conidia  (sing.  Conidium)  are  spores  which  differ  from 
the  thallus  in  being  incapable  of  forming  new  spores  or  hyphae 
while  still  attached  to  the  parent  mycelium.     They  show  great 


Fig.  537. — A  Blastospore  from 
Cry ptococcus  myremecice  Chal- 
mers   AND  CHRISTOPHERSON. 


Fig.  538. — A  Chlamydospore  from 
Trichophyton  currii  Chalmers 
and  Marshall. 


variety  of  form,  being  rounded,  stellate  simple  or  septate  (stauro- 
spore) ;  needle-shaped,  simple  or  septate  (scolecospore) ;  or  spirally 
twisted,  simple  or  septate  (helicospore),  and  of  structure  being 
simple  (amerospore)  or  divided  by  septa  (didymospores  with  two 
cells  and  one  transverse  septum ;  phragmospores  with  two  or  more 


Fig.  539. — A  Hemi- 
spore:  Develop- 
ment from  Hemi- 
spora  stellata     Vuil- 

LEMIN. 

(a)  Protoconidia ; 

(b)  Deuteroconidia. 


Fig.  540. — A  Hemi- 
spore  from  Hemi- 
spora  stellata 
Vuillemin. 


(After  Vuillemin.) 


Fig.  541 .— Aleuriospores 
from  Alenrisma  flavis- 
simum      (Link,     1816), 

EMENDAVIT      CHEVA- 
LIER,  1836. 


transverse  septa  and  three  or  many  cells;  dictyospores  in  which 
there  are  longitudinal  septa  as  well  as  transverse  septa).  The 
variation  of  colour  is  also  of  importance  as  a  means  of  classification. 
The  colouring  matter  usually  occurs  in  the  membrane. 

Their  number  is  also  important,  as  they  may  be  single,  formed  in 


HYPHOMYCETES 


1039 


Fig.  542. — Sporophores 
and  conidia  from  a 
Cladosporium. 


Fig.  543 . — A  Phialide 

from  Spicaria  apho- 
dii  Vuillemin. 

(a)  Phialide. 

(After  Vuillemin.) 


basipctal  chains  which  are  more  or  less  persistent,  or  they  may  be 
glued  together  into  masses  by  agglutinating  material. 

The  Conidia  show  two  main  types — viz.,  the  Aleuriospore  and 
the  Conidium  Verum . 

An  Aleuriospore  (Fig.  541)  is  not  a  true  conidium.  It  may  be 
terminal,  lateral,  or  intercalary,  but  in  each  case  it  is  not 
originally  distinct  from  the  thallus,  and  is  only  set  free  by 
the  death  of  the  filament  to  which  it  is  attached.  It  has 
the  morphological  significance  of  a  chlamydospore. 


Fig.  544. — A  Prophi- 
alide  from  Urophial 
amycophiala  Vuil- 
lemin, 1910.  (a)  Pro- 
phialide. 

(After  Vuillemin.) 

A  Conidium  Verum  (Fig.  542)  is  quite  distinct  from  the  thallus, 
from  which  it  is  easily  detachable.  It  may  or  may  not  be  carried 
on  a  conidiophore,  the  varieties  of  which  are  as  follows : — - 

A  Sporophore  (Fig.  542)  is  another  name  for  a  conidiophore — ■ 
i.e.,  for  the  hypha  which  carries  the  conidia. 

A  Phialide  (Fig.  543)  is  a  flask-shaped  segment  on  the  sporo- 
phore comparable  to  the  sterigmata  of  the  Basidiomycetes 
and  interposed  between  the  sporophore  and  the  conidia. 

A  Prophialide  (Fig.  544)  is  a  special  article  on  the  sporophore 
from  which  phialides  arise. 

Having  thus  made  clear  Vuillemin's  differentiation  of  the  spores, 
it  is  possible  to  consider  his  classification  of  the  Hyphales. 

Classification.-  -Vuillemin  divides  the  Hyphales  as  follows  :— 

A.  Mycelium  composed  of  fine  bacilliform  hyphae  in  which  the 

nuclei  are  usually  indistinct — Order  1,  Microsiphonales 
Vuillemin,  1912. 

B.  Mycelium  not  so  composed: — 

1.  Reproduction  by  thallospores— Order  2,  Thallosporales 

Vuillemin,  1910. 

2.  Reproduction   by  hemispores — Order  3,   Hemisporales 

Vuillemin,  rgio. 

3.  Reproduction    by    conidia — Order    4,    Conidiosporales 

Vuillemin,  1910. 


1040  FUNGI  IMPERFECT  I 

ORDER  I.  MICROSIPHONALES  Vuillemin,  1912. 

Definition. — Hyphales  with  the  mycelium  composed  of  fine  bacilli- 
form  hyphge,  usually  1  micron  or  less  in  diameter.  Usually  Gram- 
positive,  when  young,  and  without  distinct  nuclei.  Parasitic  on 
man,  animals,  and  plants,  or  saprophytic. 

Remarks.— This  is  a  most  interesting  order,  as  its  members 
(Fig.  545)  are  nearly  always  mistaken  at  first  sight,  by  persons 
unaccustomed  to  them,  for  bacilli  (Fig.  548).  Hence  the  descrip- 
tions of  bacilli  as  the  cause  of  so  many  fungal  diseases  due  to 
these  organisms,  among  which  could  be  classified  the  diphtheria 
organisms,  the  tubercular  and  leprotic  bacilli. 

Thus  one  form  of  division  into  families  is  as  follows : — 

A.  Nocardiaceae  Castellani  and  Chalmers,  1918.     Synonyms. — 

Actinomycetes    Lachner- Sandoval,     1898;    Trichomycetes 

Petrusky,  1903. 
Definition.- — Microsiphonales  with  a  mycelium. 
Type  Genus.— Nocardia  Toni  and  Trevisan,  1889. 

B.  Mycobacteriaceae    Miehe,    1909.     Definition.— Microsiphon- 

ales without  a  mycelium. 
Genus  i. — Mycobacterium  Lehmann   and  Neumann, 

with  the  diphtheria  bacillus  as  a  type. 
Genus  2. — Cory  neb  acterium  Lehmann  and  Neumann, 

with  the  tubercle  bacillus  as  a  type. 

We  have,  however,  placed  the  Mycobacteriacece  under  the  Schizo- 
mycetes,  and  therefore  have  only  the  Nocardiacecc  to  consider. 

FAMILY  NOCARDIACEiE. 

Synonyms. — Actinomycetes  Lachner-Sandoval,  1898;  Trichomy- 
cetes Petrusky,  1903. 

Definition.— Microsiphonales  with  a  mycelium. 

Type  Genus. — Nocardia  Toni  and  Trevisan,  1889. 

Classification. — -Until  quite  recently  all  the  species  of  this  order 
were  considered  to  belong  to  one  genus — i.e.,  Nocardia  Toni  and 
Trevisan,  1889;  but  Pinoy  has  made  an  excellent  subdivision, 
separating  certain  species  into  another  genus,  which  he  calls  Cohni- 
streptothrix  Pinoy,  1911.  In  doing  this,  he  points  out  that  the 
original  discoverers  of  actinomycosis- — -viz.,  Harz  and  Bollinger  in 
1877  and  Rivolta  in  1878 — thought  that  they  were  dealing  with  one 
organism,  but  when  cultures  were  attempted  it  became  apparent 
that  more  than  one  organism  was  implicated.  Thus  Bostrom  iso- 
lated a  parasite  which  grew  well  aerobically,  producing  a  dry  mem- 
brane on  the  surface  of  broth  and  capable  of  growth  at  200  C.  on 
gelatine,  but  growing  better  on  potato  at  370  C.  and  forming  chains 
of  arthrospores.  Inoculation  into  animals  was,  however,  negative. 
This  form  is  commonly  called  Nocardia  bovis  (Harz,  1877). 

Wolf  and  Israel,  on  the  other  hand,  obtained  a  parasite  which  only 


NOCARDIACEM  1041 

grew  anaerobically  and  was  not  capable  of  growth  at  ordinary 
European  air  temperatures.  In  broth  it  formed  small  granules  or 
scales,  which  fell  to  the  bottom  of  the  tube.  These  cultures  often 
contained  club-like  forms,  and  the  branching  filaments  broke  up 
into  bacillary  or  coccal-like  forms.  Inoculations  of  gelatine  cultures 
into  the  peritoneal  cavities  of  guinea-pigs  produced  actinomycosis. 
This  form  is  commonly  called  Nocardia  Israeli  (Kruse,  1896). 
Wright  maintains  that  this  organism  is  the  true  cause  of  actino- 
mycosis and  that  N .  bovis  is  merely  a  contamination,  but  this  cannot 
be  accepted. 

There  are,  therefore,  two  distinct  organisms  which  can  cause 
actinomycosis  in  man  and  oxen— viz.,  N.  bovis  (Harz  1877)  and 
N.  israeli  (Kruse,  1896),  but  the  difference  between  them  is  consider- 
able; and  therefore  Pinoy  has  separated  off  the  latter  and  its  allies 
from  the  former  and  has  founded  the  new  genus  Cohnistreptothrix 
Pinoy,  1911.  The  name  is  derived  from  the  fact  that  in  1874  Cohn 
described  a  fungus  in  lachrymal  concretions  under  the  term  Strepto- 
thrix  foersteri,  which  was  considered  to  be  a  Nocardia  and  is  now  one 
of  the  species  of  Pinoy's  Cohnistreptothrix.  These  two  genera 
are  distinguished  as  follows : — ■ 

A.  Grows    aerobically,    easy   of    cultivation,    and    producing 

arthrospores   (Fig.  549) — Genus   1,    Nocardia  Toni   and 
Trevisan,  1889. 

B.  Grows  best  anaerobically,  but  can  often  grow  aerobically; 

difficult   of  culture,  and   not   producing   arthrospores— 
Genus  2,  Cohnistreptothrix  Pinoy,  1911. 

Genus  Nocardia  Toni  and  Trevisan,  1889. 

Synonyms. — A  ctinomyces¥i.a.rz,  1877,  w^cMeyen,  1829;  Discomyces 
Rivolta,  1878,  nee  DiscontycetaceczFries,  1836 ;  Bacterium  Affanasieff, 
1888,  nee  Ehrenberg,  1830,  emendavit  Cohn, 
Hiippe;  Streptothrix  Rossi-Doria,  1891,  nee  j 

Cohn,  1875;  Oospora  Sauvageau  and  Radais,  |  m 

1892,  nee  Wallroth,  1833;  CladothrixMa.ce,  /  ,♦* 

1897,  nee  Cohn,  1875.  \ 

Definition. — Nocardiaceae   growing   aero- 
bically, usually  easy  of  culture,  and  pro-  •  ■■-■■•»•" 
ducing  arthrospores. 

Type     Species. — Nocardia     bovis    (Harz, 
1877). 

Nomenclature.— Bollinger's    ray    fungus  ""  ***   * """ 

{Nocardia  bovis)  belongs  to  a  genus  of  ig.  545. — Microsipho- 
which  the  correct  name  is  Nocardia  Toni  NAL^S^FROM  ?  ~ 
and  Trevisan,  1889,  a  term  derived  from  Castellani  iqii. 
Nocard,  the  celebrated  French  parasito- 
logist, who  was  the  first  investigator  to  clearly  recognize  this 
fungus  in  France.  We  state  that  it  is  the  correct  name  for  the 
following  reasons : — 

66 


1042  FUNGI  IMPERFECTI 

i.  It  is  the  oldest  name,  against  which  no  objections  can  be 
raised. 

2.  It  has  been  formally  adopted  by  the  Botanical  Section  of  the 

First  International  Congress  of  Pathology. 

3.  The  objections  to  the  other  names  in  use  are  as  follows:- — 

{a)  Streptothrix,  as  proposed  by  Rossi-Doria,  cannot  be 
used,  as  it  was  originally  suggested  by  Corda  in 
1839  f°r  S-  fusca,  which  is  quite  a  different  fungus. 
It  was  also  used  in  1875  by  Cohn  for  another 
organism  closely  allied  to  a '  Nocardia,'  so  that  Cohn's 
and  Rossi-Doria' s  names  can  only  be  utilized  as 
synonjTris  of  the  organisms  to  which  they  were 
wrongly  applied  because  of  the  priority  of  Corda's 
name. 

(6)  Discomyces  was  used  by  Rivolta  in  1878  merely  as  a 
trivial  name,  and  though  it  has  not  been  applied  to 
any  other  genus,  still  the  word  Discomycetaue  was 
introduced  in  1836  by  Fries  for  a  large  fungal 
family,  and  has  come  into  general  use,  and  therefore 
has  the  double  claim  of  priority  and  general  use; 
and  as  its  type  genus  should  bear  the  name  Dis- 
comyces, confusion  is  bound  to  arise  if  the  same  term 
is  retained  as  the  generic  name  of  Bollinger's 
organism . 

(c)  Bacterium  was  suggested  by  Affanasieff  in  1888,  but 

Ehrenberg  had  used  this  name  in  1830  for  the 
organisms  popularly  known  as  bacteria,  and  there- 
fore Affanasieff  s  suggestion  falls  to  the  ground. 

(d)  Oospora,  as  utilized  by  Sauvageau  and  Radais  in  1892, 

is  not  available  because  it  is  younger  than  the  name 
'  Nocardia,'  and  because  it  was  previously  used  in 
1833  by  Wallroth  for  certain  fungi  previously  classi- 
fied as  Torula  Persoon,  1801. 

(e)  Cladothrix,  as  brought  forward  by  Mace  in  1897,  cannot 

be  used  because  the  name  '  Nocardia  '  has  priority, 
and  because  it  was  originally  used  by  Cohn  in  1S75 
for  the  organism  Cladothrix  dichotoma,  which  is 
septate  and  is  only  falsely  branched,  and  hence  is 
quite  different  from  Bollinger's  fungus. 

Remarks. — The  genus  Nocardia  contains  a  large  number  of  species 
which  live  saprophytically  in  soils,  from  whence  their  spores  can  be 
spread  by  the  agency  of  air  or  water  to  sewage,  sputum,  etc.  Some 
of  them  have  acquired  parasitic  habits,  living  in  plants^  in  which 
they  cause  root  tubercles,  or,  in  other  instances,  tumours  with  ray 
fungi,  thus  somewhat  resembling  the  actinomycosis  of  animals. 
They  have  also  been  found  living  in  molluscs  and  in  the  alimentary 
canals  of  larval  insects,  as  well  as  in  the  form  of  pathogenic  fungi  in 
reptilia,  aves,  and  mammalia,  in  which  they  mostly  occur  in  the 


NOCARDIA 


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Fig.  546. — Nocardia  convoluta 
Chalmers  and  Christopherson, 
1916.  Hypha  showing  Beading 
and  also  Commencing  Separa- 
tion into  Three  Portions. 
(x    1,500  Diameters.) 


Fig.  547. — Nocardia   convoluta 
to  show'' Branching. 


Fig.  548. — Nocardia  convoluta  in  situ  in  a  Grain  to  show  Bacilliform 

Appearance. 


1044 


FUNGI  IMPERFECT  I 


herbivora  or  in  omnivorous  man,  though  they  are  known  in  the 
grass-eating  dog,  but  are  rare  in  other  carnivora.  Their  geographical 

distribution  appears  to  be  world  wide. 

With  reference  to  their  method  of 
entry  into  the  human  body,  it  appears  to 
be  often  associated  with  some  slight 
traumatism  with  some  vegetal  substance, 
such  as  a  thorn,  while  the  best  treatment 
is  undoubtedly  complete  removal  wherever 
possible;  still,  partial  extirpation,  associ- 
ated with  treatment  by  iodide  of  potash, 
as  first  advocated  for  this  purpose  in  1885 
by  Tomassen,  but  in  large  doses  such  as 
90  grains  per  diem,  as  used  by  Carroll  with 
success  in  1905,  is  sometimes  also  capable 
of  effecting  a  cure. 

Morphology.  —  Mycelial  filaments  of 
various  sizes,  but  generally  very  thin 
(1  fz  or  less),  often  branching,  non-septate, 
and  without  differentiated  nuclei.  In 
certain  species  during  parasitic  life  some 
mycelial  threads  terminate  in  club-like 
formations  and  show  a  radial  arrange- 
ment. It  is  doubtful  whether  these  club- 
like formations  are  intrinsic  parts  of  the  fungus  or  partly  products  of 
reaction  of  the  invaded  tissues.     Masses  of  mycelia  may  form  in  the 


WJ'(i 

-    r 

'"'■ 

Fig.  549. — Nocardia  con- 
voluta  to  show  Arthro- 
spores. 


Fig. 550. 


Fig- 55°-  Fig. 551. 

-Nocardia  convoluta  to  show  Easy  Culture  and  Limited  Growth 
on  Sabouraud's  Preservative  Medium. 


Fig.  551. — Nocardia  convoluta  to  show  Easy  Culture  on  Inspissated 

Blood  Serum. 


SAPROPHYTICA  1045 

tissues  peculiar  grains  (sclerotia)  of  various  size,  shape,  colour,  and 
consistency.  Some  species  are  facultative  aerobes,  others  strictly 
anaerobic.  All  are  Gram-positive,  and  several  acid-fast.  In  cultures 
the  mycelium  very  often  undergoes  fragmentation,  and  only  bacil- 
lary  and  coccus-like  bodies  may  be  seen. 

Classification.— The  very  large  number  of  species  in  this  genus 
can  be  classified  as  follows  :— 

A.  Habitat,  soil;  can  be  found  in  air  or  water — Section  1, 

Saprophytica  Foulerton,  1910. 

B.  Habitat,  plants  or  animals— Section  2, Parasitica  Foulerton, 

1910. 

C.  Habitat,  soils,  plants,  or  animals,  but  imperfectly  described 

— Section  3,  IncertcB  sedis. 

Section  1:  Saprophytica  Foulerton,  1910. 
This  section  can  be  divided  into  subsections  as  follows: — 
Subsection  i:  Majora.  Subsection  2:  Minora. 

1 .  Grow  freely  under  artificial  condi-     i .  Grow   moderately   under   artificial 

tions  at  22°  C,  and  generally  at  conditions  at  220  C.  and  370  C. 

370  C,  with  a  few  exceptions. 

2.  Growth  usually  large  and  spread-     2.  Growth     usually     moderate     and 

ing.  circumscribed. 

3.  Development     of     aerial     hyphae     3.  Development     of     aerial     hyphae 

marked     by    a    bright    chalky  marked   by  a  dull  dry  powdery 

efflorescence.  appearance. 

4.  Earthy    or    mouldy    smell    often     4.  Earthy    or    mouldy    smell    either 

present  in  the  cultures.  faint  or  absent. 

5.  Generally  peptonize  gelatine   and     5.  Rarely     peptonize     gelatine     and 

blood  serum.  blood  serum. 

6.  Diastatic  action  often  present.  6.  Diastatic  action  usually  absent. 

7.  Hyphal  filaments  usually  coarser,     7.  Hyphal  filaments  usually  finer,  and 

and     branching    more     marked  branching    rarer    than    in    the 

than  in  next  series.  preceding  series. 

Saprophytica  Subsection  Majora. 
This  subsection  contains  the  following  species : — 

1.  Nocardia  saprophytica  (Foulerton,  1902):— 

Streptothrix  leucea  saprophytica  Foulerton,  1902. 

2.  Nocardia  dichotoma  (Mace,  1888): — 

C/ado/hrix  dichotoma  Mace,  1888,  nee  Cohn,  1875. 

Streptothrix  chromogena  Gasperini,  1890. 

Streptothrix  nigra  Rossi-Doria,  1890. 

( hispora  ntetschnikovi  Sauvageau  and  Kadais,  1892. 

Cladothrix  brauner  Hesse,  1892. 

Cladothrix  odorifer  Rullman,  1895,  nee  C.  odorifer  Rull- 

man,  1898,  parasitic  in  man. 
Streptothrix  mclanotica  Price-Jones,  1900. 
Streptothrix  humified  Beijernick,  1900. 
Streptothrix  nigrescens  Foulerton,  1902. 


1046  FUNGI  IMPERFECTI 

Actinomyces  erythrochromogenes  Krainsky,  1914. 
Actinomyces  diastaticochromogenes  Krainsky,  1914. 
Actinomyces  viridochromogenes  Krainsky,  1914. 
Actinomyces  flavochromogenes  Krainsky,  1914. 

3.  Nocardia  violacea  (Rossi-Doria,  1891): — 

Streptothrix  violacea  Rossi-Doria,  1891. 
Actinomyces  violaceus  Berestneff,  1897. 
?  Actinomyces  alni  Peklo,  1910. 
?  Actinomyces  myricce  Peklo,  1910. 

4.  Nocardia  beta  (Price-Jones,  1900): — 

Streptothrix  beta  Price- J  ones,  1900. 

5.  Nocardia  alba  (Rossi-Doria,  1891): — 

Streptothrix  alba  Rossi-Doria,  1891. 
Actinomyces  chromogenes  B  Gasperini,  1890. 
Streptothrix  I.,  II.,  and  III.  Almquist. 
Actinomyces  albus  Lehmann  and  Neumann. 
Oospora  guiguardi  Sauvageau  and  Radais,  1892. 
Actinomyces  albus  Gasperini,  1890. 
Oospora  dorice  Sauvageau  and  Radais,  1892. 
Streptothrix  foersteri  Gasperini,  1890,  nee  Cohn. 
Streptothrix  leucea  Foulerton,  1902. 
Streptothrix  alpha  Price- J  ones,  1900. 
Streptothrix  pyogenes  Caminiti,  1907. 
Actinomyces  grisea  Krainsky,  1914. 
Actinomyces  diastatica  Krainsky,  1914. 
Actinomyces  cellulosce  Krainsky,  1914. 
Actinomyces  nivea  Krainsky, .1914. 

6.  Nocardia  rosea  (Krainsky,  1914):— 

Actinomyces  roseus  Krainsky,  1914. 

7.  Nocardia  citrea  (Krainsky,  1914): — 

Actinomyces  griseoflavus  Krainsky,  1914 
Actinomyces  flavus  Krainsky,  1914. 
Streptothrix  flava  Sanfelice,  1904. 
Streptothrix  flava  Brins,  1899. 

8.  Nocardia  cinereonigra  (Berestneff,  1897): — 

Streptothrix  cinereonigra  aromatica  Berestneff,  1897. 

9.  Nocardia  orangica  (Berestneff,  1897): — 

Streptothrix  orangica  Berestneff,  1897. 

10.  Nocardia  albida  (Rossi-Doria,  1891): — ■ 

Streptothrix  albido- flava  Rossi-Doria,  1891. 
Actinomyces  farcinicus  Rossi-Doria,  1891. 
Nocardia  farcinica  Rossi-Doria,  1891. 

11.  Nocardia  invulnerabilis  (Acosta  and  Grande  Rossi,  1893): — 

Cladothrix  invulnerabilis  Acosta  and  Grande  Rossi,  1893. 

12.  Nocardia  rubea,  Chalmers  and  Christ opherson,  1916. 

Actinomyces  ruber  (no  name). 

Nee  Actinomyces  ruber  Krainsky,  1914. 


SAPROPHYTICA  1047 

Nec  Streptothrix  rubra  Casab6,  1894. 
Nec  Streptothrix  rubra  Kruse,  1896. 

13.  Nocardia  axlicolor  (R.  Miiller,  1904): — 

Streptothrix  ecelicolor  R.  Muller,  1904. 
Streptothrix  ecelicolor  Schurman,  1909. 

14.  Nocardia  glauca  (Lehmann  and  Schulze)  :— 

Actinomyces  glaucus  Lehmann  and  Schulze. 

15.  Nocardia  thermophila  (Gilbert,  1904):— 

Actinomyces  thermophilus  Gilbert,  1904. 
Cladothrix  thermophilis  Kedzior. 
Actinomyces  thermophilus  Berestneff,  1891. 

16.  Nocardia  monospora  (Schulze,  1908^: — 

Actinomyces  monosporus  Schulze  1908. 

These  species  may  be  recognized  as  given  on  p.  1048. 

Subsection  Minora. 
This  subsection  contains  the  following  species : — 

1 .  Nocardia  pluricolor  (Terni,  1894) : — 

Streptothrix  pluricolor  Terni,  1894. 
Actinomyces  gruberi  Terni,  1894. 

2.  Nocardia  carnea  (Rossi-Doria,  1891): — 

Streptothrix  carnea  Rossi-Doria,  1891. 

3.  Nocardia  aurantiaca  (Rossi-Doria,  1891):— 

Streptothrix  aurantiaca  Rossi-Doria,  1891. 

4.  Nocardia  melanosporea  (Krainsky,  1914): — 

Actinomyces  melanosporeus  Krainsky,  1914. 

5.  Nocardia  melanocy cla  (Krainsky,  1914):— 

Actinomyces  melanocyclus  Krainsky,  1914. 

6.  Nocardia  alb  osp  ore  a  (Krainsky,  1914):^ — ■ 

Actinomyces  albosporeus  Krainsky,  1914. 

7.  Nocardia  krainskii  Chalmers,  1916. 

Actinomyces  ruber  Krainsky,  1914,  nec  Carab6,  1894,  nec 
Kruse,  1896. 

8.  Nocardia  parva  (Krainsky.  1914):— 

Actinomyces  parvus  Krainsky,  1914. 

9.  Nocardia  microparva  (Krainsky,  1914):— 

Actinomyces  microparvus  Krainsky,  1914. 
10.  Nocardia  chalcea  (Foulerton,  1905):— 

Streptothrix  chalcea  Foulerton,  1905. 
ir.  Nocardia  erythrea  (Foulerton,  1910):— 

Streptothrix  erythrea  Foulerton,  1910. 
12.  Nocardia  hojfmanni  (Gruber,  1891): — 

Micromyces  hojfmanni  Gruber,  1891. 

These  species  may  be  recognized  as  given  on  p.  1049. 


1048 


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Section  2:  Parasitica  Foulerton,  1910. 

The  parasitic  section  can  be  classified  into  three  subsections,  as 
follows : — 


No. 

Test. 

Subsection  i : 
Major  a . 

Subsection  2 :           Subsection  3 : 
Minora.                    Brevis. 

1 

Cultivation     at 
220     C.      and 
37°  C. 

Easy 

Not  difficult            Difficult  at  37°C. 
Usually  nil   at 
22°  C. 

2 

Growth 

i 
Spreading                 Circumscribed 

Slight 

3 

Efflorescence 

Bright  chalky         Dull  powdery          Usually  absent 

4 

Hyphal  branch- 
ing 

Well  marked 

Poorly  marked 

Rare,  hypae  often 
bacilliform 

5 

Acid-fast  species 

Rare 

Common 

Rare 

6 

Odour    of     cul- 
tures 

Earthy       or 
mouldy 

Absent       or      Sometimes  fsecu- 
faintly  as  1                lent 

7 

Liquefaction   of      Often  present 
gelatine     and 
blood  serum 

Rare,  and  usual-  :  Often  very  slight 
ly    only    one          indications 
liquefied 

8 

Potato                        Growth 

Usually  growth       Often  no  growth 

9 

Diastatic  action      Often  present 

Usually  absent 

Not  known 

Subsection  i:  Majora. 
This  subsection  contains  the  following  species  :• — ■ 

1.  Nocardia  garteni  (Brumpt,  1910):— 

Cladothrix  liquefaciens  II.  Garten,  1895. 
Discomyces  garteni  Brumpt,  1910. 

2.  Nocardia  liquefaciens  (Hesse,  1892): — 

Cladothrix  liquefaciens  Hesse,  1892. 
Streptothrix  liquefaciens  (Hesse,  1892). 
Streptothrix  buccalis  Goadby,  1903,  nee  Roger,  Bory,  and 
Sartory,  1909. 

3.  Nocardia  modore  (Thiry,  1897) : — 

Cladothrix  modore  Thiry,  1897. 

Cladothrix  polychromes  Thiry,  1897. 

Actinomyces  rubidaureus  Lachner-Sandoval,  1898. 

4.  Nocardia  luteola  (Foulerton,  1910):- — 

Streptothrix  luteola  Foulerton,  1910. 

5.  Nocardia  appendicis  Chalmers  and  Christ opherson,  1916. 

Streptothrix  hominis  III.  Foulerton,  1910. 
Streptothrix  hominis  IV.  Foulerton,  1906. 


MAJORA  1051 

6.  Nocardia  Candida  (Petruschky,  1898): — 

Streptothrix  Candida  Petruschky,  1898. 
Streptothrix  gedanensis  II.  Petruschky,  1898. 
Streptothrix  lalhridii  Petruschky,  1898. 

7.  Nocardia  bovis  (Harz,  1877): — ■ 

Actinomyces  bovis  Harz,  1877.  • 

Bacterium  actino-cladothrix  Affanasieff,  1888. 

Actinomyces  hominis  (Affanasieff,  1888). 

Nocardia  actinomyces  de  Toni  and  Trevisan,  1889. 

Streptothrix  actinomyces  Rossi-Doria,  1891. 

Oospora  bovis  Sauvageau  and  Radais,  1892. 

Actinomyces  bovis  sulphur eus  Gasperini,  1894. 

Cladothrix  actinomyces  Mace,  1897. 

Discomyces  bovis  Blanchard,  1900. 

Streptothrix  hominis  III.  Foulerton,  1905,  nee  Foulerton, 

1910. 
Streptothrix  hominis  IV.  Foulerton,  1910,  nee  Foulerton, 

1906. 

8.  Nocardia  graminari urn  (Berestneff,  1891): — 

Streptothrix  graminarium  Berestneff,  1891. 

9.  Nocardia  rubra  (Carab6,  1894). 

Actinomyces  rubra  Carabo,  1894. 

Streptothrix  rubra  Kruse,  1896. 

Nee  Actinomyces  ruber  Krainsky,  1914. 

10.  Nocardia  lingualis  (Weibel,  1888) : — 

Vibrio  lingualis  Weibel,  1888. 
Spirosoma  lingualis  Migula,  1892. 
Streptothrix  lingualis  Bajardi,  1900. 

11.  Nocardia  odorifera  (Rullman,  1898): — 

Cladothrix  odorifera  Rullman,  1898,  in  sputum,  not  in  air. 

12.  Nocardia  enteritidis  (Pottien,  1902): — 

Streptothrix  enteritidis  Pottien,  1902. 

These  species  may  be  differentiated  as  given  on  p.  1052. 

Subsection  2:  Minora. 
The  species  belonging  to  this  section  are : — 

1 .  Nocardia  farcinica  Trevisan,  1889 : — 

Bacillus  du  Farcin  Nocard,  1888. 
Streptothrix  farcinica  Rossi-Doria,  1891. 

2.  Nocardia  somaliensis  (Brumpt,  1906):— 

Indiella  somaliensis  Brumpt,  1906. 
Indiellopsis  somaliensis  (Brumpt,  1913). 
Discomyces  somaliensis  Brumpt,  1913. 

3.  Nocardia  indica  (Kanthack,  1893):— 

Oospora  indica  Kanthack,  1893. 
Streptothrix  maduree  Vincent,  1894. 
Discomyces  maduree  Vincent,  1895. 


1052 


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MINORA  1053 

Nocardia  madurce  R.  Blanchard,  1895. 
Micrococcus  pelletieri  Laveran,  1906. 
Obspora  pelletieri  Thiroux  and  Pelletier,  1912. 
Nocardia  pelletieri  Pinoy,  1912. 
Nocardia  rivierei  Verdun,  1912  (?). 

4.  Nocardia  leislunani  Chalmers  and  Christopherson,  1916: — 

New    acid-fast    streptothrix    pathogenic    to    man    and 
animals  described  by  Birt  and  Leishman  in  1902. 

5.  Nocardia  gedanensis  (Scheele  and  Petruschky,  1897):— 

Streptothrix  gedanensis  I.  Scheele  and  Petruschky,  1897. 

6.  Nocardia  convoluta  Chalmers  and  Christopherson,  1916. 

7.  Nocardia  minutissima  (Burchardt,  1859): — ■ 

Microsporum  miniitissimum  Burchardt,  1859. 
Trichothecium  J.  Neumann,  1868. 
Microsporon  gracile  Balzer,  1883. 
Sporotrichum  miniitissimum  Saccardo,  1886. 
Microsp  oroides  minntissimtis  Neveu-Lemaire,  1908. 
Discomyces  minutissintus  Brumpt,  1910. 
Oospora  minutissima  Ridet,  1911. 
Nocardia  minutissima  Verdun,  1912. 

8.  Nocardia  rosenbachi  (Kruse,  1896): — 

Streptothrix  rosenbachi  Kruse,  1896. 

9.  Nocardia  cams  (Rabe,  1888): — 

Cladothrix  canis  Rabe,  1888. 
Streptothrix  caprce  Silberschmidt,  1899. 
10    Nocardia  asteroides  (Eppinger,  1890) : — 
Cladothrix  asteroides  Eppinger,  1890. 
Streptothrix  eppingeri  Rossi-Doria,  1891. 
0'6sj>ora  asteroides  Sauvageau  and  Radais,  1892. 
Nocardia  asteroides  R.  Blanchard,  1895. 
Streptothrix  hominis  Sabrazes  and  Riviere,  1895. 
Actinomyces  asteroides  MacCallum,  1902. 
Discomyces  asteroides  Brumpt,  1906. 
Streptothrix  freeri  Musgrave  and  Clegg,  1907. 
Discomyces  brasiliensis  Lindenberg,  1909. 
The    organisms    described    by   Ferre    and    Faguet,   by 

MacCallum,    by    Schabad,    probably   belong    to   this 

species, 
n.  Nocardia  hominis  (Berestneff,  1897): — 

Nee  Actinomyces  hominis  Bostroem,  synonym  of  N.  bovis. 
Nee  Actinomyces  hominis  Affanasieff=iV.  bovis. 
Nee  Actinomyces  hominis  Wolff  and  Israel=A7.  israeli. 
Nee    Streptothrix    hominis    Sabrazes    and    Riviere=iV. 

asteroides. 
Nee  Streptothrix  hominis  Hayo  Bruns,  1899. 
Nee  Streptothrix  hominis  Foulerton,  1902. 
Nee  Streptothrix  hominis  II.  Foulerton,  1910. 


1054  FUNGI  IMPERFECTI 

Nec  Streptothrix  horninis  III.  Foulerton,  1905=^/.  bovis. 
Nec  Streptothrix  horninis  IV.  Foulerton,  1910=^.  bovis. 
Nec  Streptothrix  horninis  III.  Foulerton,  1910. 

12.  Nocardia  nigra  (Castellani,  1913). 

Synonym,  Streptothrix  nigra  Castellani,  1913. 

13.  Nocardia  pijperi  Castellani  and  Chalmers,  1918. 

As  there  is  so  much  confusion  with  regard  to  the  specific  name 
horninis,  Chalmers  and  Christopherson  proposed  that— 

S.  horninis  Bruns  be  changed  to  Nocardia  bruni. 

S.  horninis  Foulerton  be  changed  to  Nocardia  foulertoni. 

S.  horninis  II.  Foulerton  be  changed  to  Nocardia  londinensis. 

S.  horninis  III.  Foulerton  be  changed  to  Nocardia  appendicis. 

These  species  may  be  separated  as  given  on  p.  1055. 

Subsection  3:  Brevis. 
This  subsection  contains  :• — ■ 

1.  Nocardia  valvules  (Luginger,  1904): — 

Streptothrix  valvulce  destruens  bovis  Luginger,  1904. 

2.  Nocardia  ponceti  Verdun,  1912. 

3.  Nocardia  buccalis  (Roger,  Bory,  and  Sartory,  1909): — 

Odspora  buccalis  Roger,  Bory,  and  Sartory,  1909. 
Nec  Streptothrix  buccalis  Goadby,  1903. 

4.  Nocardia  pulmonalis  (Roger,  Bory,  and  Sartory,  1909) : — 

Odspora  pulmonalis  Roger,  Bory,  and  Sartory,  1909. 

5.  Nocardia  dassonvillei  Brocq-Rousseu,  1907:— 

Gasperini's  Streptothrix,  1890. 

6.  Nocardi  krausei  (Chester,  1901): — 

Streptothrix  krausei  Chester,  1901. 

7.  Nocardia  foulertoni  Chalmers  and  Christopherson,  1916: — 

Streptothrix  horninis  Foulerton,  1902. 
Streptothrix  horninis  I.  Foulerton,  1906. 

8.  Nocardia  londinensis,  new  name:- — ■ 

Streptothrix  horninis  II.  Foulerton,  1906. 

9.  Nocardia  lignieresi  (Brumpt,  1910):— 

Actinobacillus  lignieresi  Brumpt,  1910. 
10.  Nocardia  bruni  Chalmers  and  Christopherson,  1916: — 

Streptothrix  horninis  Hayo  Bruns,  1899. 
it.  Nocardia  berestneffi.,  new  name: — 

Streptothrix  cases  1  and  2  Berestneff,  1897. 
12.  Nocardia  equi  (Dean,  1900):- — • 

Streptothrix  from  a  horse  of  Dean,  1900. 

Probably  the  organism  described  by  N orris  and  Larkin 
should  come  here,  but  we  have  been  unable  to  see  a 
description. 

These  species  may  be  differentiated  as  given  on  p.  1056. 


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INCERTM  SEDIS  1057 

Section  3:  Incertse  Sedis. 

In  this  list  we  have  included  the  forms  concerning  which  we  have 
been  unable  to  obtain  full  information,  and  have,  therefore,  been 
unable  to  classify  according  to  the  above  tables : — 

i.  Actinomyces  lacertcc  Terni,  1891. 

2.  Streptothrix  pseudotuberculosa  Flexner,  1898. 

3.  Streptothrix  of  Bonvicini,  1899. 

4.  Streptothrix  polychromogenes  Vallee,  1900. 

5.  Actinomyces  bicolor  Tvollender,  1903. 

6.  Nocardia  liguire  Urizer,  1904. 

7.  Actinomyces  verrucosus  Adler,  1904. 

8.  Nocardia  lasserei  Verdun,  1912. 

9.  Nocardia  decussata  Langeron  and  Chevalier,  1912. 
10.  Actinomyces  musculorum  suis  Duncker. 

ir.  Actinomyces  pseudotuberculosis  Hamm  and  Keller. 

12.  Discomyces  holmesi  mentioned  by  Goedelst. 

13.  Streptothrix  gelatinosa 

14.  Streptothrix  aquatilis 

15.  Streptothrix  lehmann 

16.  Streptothrix  chondri  Olsen,  1897^ 

17.  Nocardia  urinaria  Pijper,  1918. 


mentioned  by  Peklo. 


Nocardia  bovis  Harz,  1877. 

Synonyms. — Actinomyces  bovis  Harz,  1877;  Discomyces  bovis 
Rivolta,  1877;  Bacterium  actino-cladothrix  Affanasieff,  1888;  Nocar- 
dia Actinomyces  Toni  and  Trevisan,  1889;  Streptothrix  Actinomyces 
Rossi-Doria,  1891 ;  Oospora  bovis  Sauvageau  and  Radais,  1892 ; 
Actinomyces  bovis  sulphur eus  Gasperini,  1894;  Nocardia  bovis 
R.  Blanchard,  1895;  Actinomyces  bovis  sulphureus,  Gasperini,  1894; 
Cladothrix  Actinomyces  Mace\  1897;  Discomyces  bovis  R.  Blanchard, 
1900;  Streptothrix  spitzi  Lignieres  and  Spitz,  1903;  Nocardia  bovis 
Vuillemin,  1912. 

This  Nocardia  is  the  cause  of  some  cases  of  human  and  bovine 
actinomycosis,  and  of  the  actinomycotic  mycetoma.  The  fungus 
lives  parasitically  in  most  tissues,  in  which  it  gives  rise  to  degenera- 
tive and  purulent  changes.  In  the  pus  small,  soft  yellow  granules- 
so-called  '  sulphur  grains  ' — are  seen.  These  sulphur  grains  consist 
of  masses  of  mycelium.  At  the  periphery  of  the  granule  the  threads 
are  radially  arranged,  and  their  free  extremities  become  club-like, 
10  to  20  fj,  in  length  and  8  to  10  /li  in  breadth.  These  peculiar 
club-like  formations  have  been  considered  by  some  authorities  to  be 
degeneration  forms  of  the  fungus,  but  Brumpt  has  demonstrated 
that  they  are  young  active  forms,  and  disappear  in  old  granules. 
Other  writers  consider  that  these  club-like  formations  do  not  form 
an  intrinsic  part  of  the  fungus,  but  are  due  to  reactive  changes  in 
the  tissues. 

67 


io58  FUNGI  IMPERFECT  I 

Cultures. — The  fungus  grows  easily  on  agar,  glycerinated  agar, 
gelatine,  broth,  potato,  and  other  media.  Optimum  temperature, 
35°  to  370  C.  On  glycerinated  agar  the  fungus  grows  fairly  rapidly, 
giving  rise  to  small,  dry,  coarsely  granular,  brown-yellowish 
colonies,  which  latter  coalesce  together.  The  fungus  is  Gram- 
positive,  but  not  acid-fast. 

Saprophytic  Life.- — The  fungus  is  found  saprophytic  on  the 
spikelets  of  some  cereals  (Phleum  ftratense  Linnaeus,  Hordeum 
miurnum  Linnaeus,  etc.). 

Pathogenicity. — The  experimental  reproduction  of  the  disease  by 
inoculating  pure  cultures  has  not  so  far  succeeded.  Wright  there- 
fore goes  so  far  as  to  say  that  Actinomyces  bovis  is  a  contamination. 

Varieties.— Gasperini  describes  three  varieties :  N.  bovis  sulphured, 
N.  bovis  sulphur ea-alba,  N.  bovis  luteo-rosea.  Caminiti  has  described 
a  variety  which  he  thinks  may  be  a  new  species.  N,  lanfranchii 
Luigi  Sani  is  also  a  variety  of  this  Nocardia. 

Nocardia  rosenbachi  Kruse,  1896. 

Synonym. — Streptothrix  rosenbachi  Kruse,  1896. 

Isolated  by  Rosenbach  in  a  case  of  dermatitis,  called  by  him 
'  erysipeloid.'  Mycelial  threads  very  slender;  some  terminate  in 
club-like  swellings.  Can  be  cultivated  on  the  usual  laboratory 
media.     Does  not  liquefy  gelatine. 

Nocardia  asteroides  Eppinger,  1890. 

Synonyms. — -Cladothrix  asteroides  Eppinger,  1890;  Streptothrix 
eppingeri  Rossi-Doria;  1891;  Oospora  asteroides  Sauvageau  and 
Radais,  1892;  Nocardia  asteroides  R.  Blanchard,  1895;  Discomyces 
freeri  Musgrave  and  Clegg,  1907;  N.  brasiliensis  Lindenberg,  1909. 

Found  in  mycetoma  and  in  cases  of  abscess  of  the  brain.  Mycelial 
threads  very  slender  (0-2  /u,  wide);  the  mycelial  articles  become 
easily  dissociated,  when  they  look  bacillus-like.  This  fungus  is 
acid-fast  and  is  very  similar  to  Bacillus  tuberculosis,  but  grows 
much  more  quickly  on  ordinary  media :  obligative  aerobe.  Inocula- 
tions in  the  rabbit  and  guinea-pig  produce  a  form  of  pseudo- 
tuberculosis histologically  indistinguishable  from  true  tuberculosis. 

McCallum  has  found  a  Nocardia  very  similar  to  AT',  asteroides  in  a 
case  of  peritonitis. 

Nocardia  indica  Kanthack,  1893. 

Synonyms. — -Streptothrix  madurce  H.  Vincent,  1894;  Nocardia 
madune  R.  Blanchard,  1895:  Micrococcus  pellelieri  Laveran,  1906; 
Oospora  pelletieri  Thiroux  and  Pelletier,  1912;  Nocardia  pelletieri 
Pinoy,  1912. 

It  causes  Vincent's  white  mycetoma,  very  commonly  found  in 
Africa  and  Asia.  The  '  grains  '  which  are  found  in  the  pus  of  such 
cases  are  soft,  white,  or  slightly  yellowish,  and  have  a  mulberry-like 
surface.     At  the  periphery  of  the  grains  radiating  filaments  are 


NOCARDIA  INDICA  1059 

found,  but  claviform  swellings  are  usually  absent ;  mycelial  threads 
are  always  very  slender  (1  to  ih  /.<).  The  fungus  can  be  grown  on 
the  ordinary  media:  facultative  aerobe.  On  glycerinated  agar  it 
forms  discoid  colonies,  white  in  the  centre  and  reddish  at  the  peri- 
phery. In  the  cultures  the  mycelial  threads  are  as  slender  as  in  the 
grains.  Some  of  the  mycelial  threads  have  at  their  extremities 
short  chains  of  small  conidial  elements.  Gram-positive,  but  not 
acid-fast. 

It  is  to  be  noted  that  this  fungus  very  rarely  produces  bone 
lesions.     Most  strains  are  inoculable  into  monkeys. 

Nocardia  dassonvillei  Brocq-Rousseu,  1907. 

Synonym. — Streptothrix  foersteri  (Gasperini,  1890). 

Very  thin  ramified,  mycelial  threads,  which  easily  become 
fragmented  and  dissociated  into  bacillary-like  bodies.  Numerous 
spherical  coccus-like  bodies  (spores)  present.  Gram-positive.  The 
fungus  grows  fairly  well  on  gelatine,  giving  rise  to  small  white, 
roundish  colonies.  This  fungus  has  been  found  by  Landrieu  and 
Liegard  in  a  case  of  conjunctivitis  in  an  old  lady  who  powdered  her 
face  extensively  several  times  daily  with  rice-powder.  The  authors 
suggest  that  the  fungus  may  have  been  present  in  the  rice-powder, 
as  the  same  fungus  is  known  to  be  found  in  several  decaying  cereals. 

Gasperini  isolated  in  1890  from  the  air  a  Nocardia  which  he 
identified  as  N.  foersteri.  Further  researches  (Landrieu)  have 
shown  Gasperini' s  fungus  to  be  iV.  dassonvillei . 

Nocardia  decussata  Langeron  and  Chevalier,  1912. 

Synonym. — -Discomyces  decussatus  Langeron  and  Chevalier,  1912. 

Found  by  Langeron  and  Chevalier  in  a  patient  presenting 
peculiar  whitish,  dry,  squamous  patches.  The  fungus  grows  on 
ordinary  media  extremely  slowly.  Colonies  milk-white,  the  central 
portion  of  which  is  slightly  elevated  and  flattened,  but  has  a  minute 
nodule  in  the  middle ;  very  often  four  furrows,  forming  a  cross,  are 
seen.  The  mycelial  threads  are  thin,  non-septate,  and  are  easily 
dissociated  into  roundish  bodies,  1  to  1-5  ja  in  diameter. 

The  pathogenic  role  of  this  fungus  is  doubtful. 

Nocardia  pulmonalis  II.  Roger,  Bory,  and  Sartory,  1909. 

In  tlir  parasitic  stage  may  appear  in  the  shape  of  bacillary-like 
bodies,  about  0-5  /i  in  diameter.  In  cultures  (maltose  broth) 
thin  mycelial  filaments,  0-5  ft  in  diameter,  are  present,  some  branch- 
ing, some  terminating  in  club-like  formations.  Some  mycelial 
1  lin  ads  are  very  fragile,  and  become  fragmented  into  strings  of 
bacillary  or  coccus-like  bodies. 

Pathogenicity. — -Causes  a  type  of  pseudo-tuberculosis.  In  the 
expectoration  occasionally  small  white  granules,  composed  of 
masses  of  the  fungus,  are  present.  Sartory  has  found  the  fungus  in 
a  case  of  otitis 


'1060  FUNGI  IMPERFECTI 

Nocardia  pijperi  Castellani  and  Chalmers,  1919. 

Discovered  and  described  by  Pi j per  in  a  case  of  chronic  bronchitis 
in  South  Africa.  The  fungus  is  non-motile,  Gram-positive,  not 
acid-fast.  It  grows  on  agar,  giving  rise  to  small  whitish  colonies, 
becoming  visible  after  forty-eight  to  seventy-two  hours.  The 
colonies  increase  in  size,  slowly  becoming  hard  like  cartilage,  and 
very  adherent  to  the  medium.  The  surface  is  crinkled.  The  fungus 
does  not  grow  on  gelatine  nor  on  Sabouraud's  maltose  agar.  Broth 
remains  clear,  growth  taking  place  at  the  bottom. 

The  fungus  can  be  grown  also  anaerobically.  It  is  pathogenic  to 
guinea-pigs  by  intraperitoneal  injection.  Nodules  develop  on  the 
peritoneum,  consisting  of  an  outer  wall  of  epithelioid  cells  and  leuco- 
cytes surrounding  a  cavity  filled  with  fluid,  in  which  asteroid 
colonies  of  the  fungus  are  found. 

Nocardia  Candida  Petruscliky,   1901. 
Found  in  sputum. 

Nocardia  aurea  Du  Bois  St.-Severin,   1902. 
Found  in  a  case  of  ulcerative  conjunctivitis. 

Nocardia  odoriiera  Rullman  and  Perutz,   1898. 

Found  by  Rullmann  in  a  case  of  chronic  bronchitis.  Merely  a  synonym 
of  N.  chromogena  Gasperini. 

Nocardia  liquefaciens  Hesse,  1892. 

Synonym. — Cladothrix  liquefaciens  Hesse,  1892. 

Gives  rise  to  white  colonies  on  gelatine,  and  later  liquefies  the  medium. 
Was  isolated  from  a  case  of  actinomycosis.     Liquefies  serum. 

Nocardia  ponceti  Verdun,   1912. 

Not  cultivable  on  agar  or  gelatine.  Grows  well  on  serum,  where  it  takes  a 
bacillary-like  form.  Found  by  Moorhof,  Dor,  and  Poncet  in  a  case  of  myo- 
mycosis  resembling  actinomycosis. 

Nocardia  fusca  Karwacki,   191 1. 

Isolated  by  Karwacki  from  the  sputum  of  a  tubercular  patient.  Dark 
yellowish  colour. 

Nocardia  luteola  Foulerton  and  Jones. 

Found  in  a  case  of  purulent  conjunctivitis. 

Nocardia  carnea  Rossi-Doria,  1891. 
Isolated  by  Baldoni  from  a  case  of  chronic  bronchitis.     Red  colonies. 

Nocardia  garteni  Brumpt,  1910. 

Synonyms. — Cladothrix  liquefaciens  No.  2  Garten,  1895;  Discomyces  garteni 
Brumpt,  1 9 10. 

Liquefies  gelatine.  On  potatoes  gives  rise  to  white  colonies,  while  the 
medium  takes  a  greenish  colour.     Was  isolated  from  a  case  of  actinomycosis. 

Nocardia  enteritidis  Pottien,  1902. 
Found  in  cases  of  enteritis  by  Pottien. 


NOCARDIA  BUCCALIS  1061 

Nocardia  buccalis  H.  Roger,  Bory,  and  Sartory,  1909. 

Synonyms. — Oospora  buccalis  H.  Roger,  Bory,  and  Sartory,  1909; 
Discomyces  buccalis  Brumpt,  1910. 

Thin  mycelial  filaments  (0-7  to  o-8  ju,).  Some  ramified  mycelial 
threads  are  very  fragile,  becoming  fragmented  into  strings  of 
bacillary-like  or  coccus-like  bodies.     Can  be  cultivated. 


Fig.  552.  —  Nocardia  pulmonalis  Fig.  553.  —  Nocardia   buccalis 

H.  Roger,  Bory,  and  Sartory.  Roger,  Bory,  and  Sartory. 

(After  Roger  and  Sartory.) 

Pathogenicity.  -Mav  give  rise  to  a  form  of  stomatitis  somewhat 
resembling  thrush.     It  has  been  found  also  in  tonsillar  abscesses. 

Nocardia  lasserrei  Verdun,  1912. 

Synonym. — Nocardia  sp.  (?)  Lassere,  1904. 

Found  by  Lasserre  in  1904  in  an  ulcerative  lesion  situated  on 
the  pharynx  and  upper  lip.  Mycelial  filaments  very  thin  (0-5  to 
075  fj,);  fragile,  club-like  formations  present.  Can  be  cultivated. 
Pathogenic  to  rabbits  and  guinea-pigs,  but  only  by  intracerebral 

Nocardia  lingualis  Gueguen,  1908. 

Synonyms.— Oospora  lingualis  Gueguen,  1908 ;  Discomyces  lingualis 
(Brumpt,  1910). 

In  the  parasitic  stage  the  fungus  appears  in  the  shape  of  bacillary 
bodies,  less  than  0-3  /j,  in  diameter.  In  cultures  it  shows  a  mycelial 
type  with  very  thin  filaments.  It  is  probably  non-pathogenic;  it 
has  been  found  in  cases  of  lingua  nigra  in  association  with  Crypto- 
coccus  Ungues  piloses . 

Nocardia  rivierei  Verdun,  1912. 
Isolated  by  Riviere  (1895)  in  a  case  of  multiple  abscesses.     Is 
cultivable  on  ordinary  media. 

Nocardia  appendicis  Chalmers  and  Christopherson,  1916. 

Synonyms.  -Strcptotlirix  hominis  Foulerton,  1906;  Oospora 
hontinis  Ridet,  1911. 

Discovered  by  Foulerton  in  a  case  of  multiple  abscesses;  was 
present  also  in  the  expectoration  of  the  same  patient.  Foulerton 
has  found  similar  fungi  (V.  hominis  III.)  in  cases  of  appendicitis. 

Nocardia  minutissima  Burchardt,  1869. 
Synonyms.    -  Microsporum     minutissimum      Burchardt,     1869; 
M.   ^racile   Balzer,    1883;    Sporotrichum    minittissimiim    Saccardo, 


io62 


FUNGI  IMPERFECTI 


1896;  Discomyces  minutissimus  P.  Verdun,  1907;  Microsfi oroides 

minntissintus  Neveu-Lemaire,  1906;    Oospora  minutissima  Ridet, 

1911. 
Mycelial  threads  extremely  thin  (o-6/^);  seldom  ramified.    The 

mycelial  segments  get  easily  dissociated,  and  have  then  the  appear- 
ance of  bacilli.  Is  the  cause  of 
erythrasma.  Michele,  Ducrey, 
and  Reale  claim  to  have 
cultivated  it. 


)  IU 


Fig.  554. — Nocardia  minutissima 

BURCIIARDT. 


Fig.   555.  —  Cohnistveptohrix 
tenuis  Castellani. 


Nocardia  convoluta  Chalmers  and  Christopherson,  1916. 

Nocardia. — -Gram-positive,  but  not  acid-fast,  without  club 
formations;  found  parasitic  in  man;  easy  of  cultivation,  growing 
aerobically  and  anaerobically  at  22°  C.  and  370  C,  with  a  marked 
preference  for  alkaline  media,  and  with  the  production  of  good 
but  limited  growths  on  the  different  agars,  and  the  same  at  first  on 
blood  serum  and  potato,  on  which,  however,  it  becomes  more  pro- 
fuse later.  Not  liquefying  gelatine,  but  causing  liquefaction  of  in- 
spissated ox-blood  serum,  without  diastatic  action.  Colonies  usually 
somewhat  translucent  when  young,  of  a  light  to  warm  buff 
colour  (Ridgway's  Plate  XV.,  17,  O-Y,  f  or  d),  and  either  con- 
voluted or  having  the  appearance  of  a  jelly  turned  out  of  a  mould, 
later  developing  a  whitish  powdery  efflorescence,  without  distinct 
odour,  never  pigmenting  the  medium  on  which  it  is  grown;  not 
fermenting  or  peptonizing  milk.  Non-pathogenic  for  monkeys 
and  other  laboratory  animals. 

Remarks.- — -It  is  fairly  frequently  found  in  the  actinomycotic  type 
of  Madura  foot  in  Khartoum,  Anglo-Egyptian  Sudan. 

Nocardia  nigra  Castellani,  191 3. 
Nocardia,  Gram-positive,  some  strains  acid-fast,  no  definite  club  formations. 
Grows  aerobically  and  anaerobically  at  220  C.  and  350  C.     Colonies  on  maltose 
agar  and  ordinary  agar  are  black.     Most  strains  liquefy  gelatine. 

Nocardia  lutea  was  found  by  Christopherson  and  Archibald  in  191 8  in  the 
lachrymal  canal  of  a  case  in  Khartoum. 


COHNISTREPTOTHRIX  1063 

Genus  Cohnistreptothrix  Pinoy,  1911. 

Definition. — Nocardiaceae  growing  best  anaerobically,  but  can 
grow  aerobically;  usually  difficult  to  cultivate  and  do  not  produce 
arthrospores. 

Type  Species. — Cohnistreptothrix  israeli  (Kruse,  1896). 

Historical.— In  1891  Wolff  and  Israel  published  a  beautifully 
illustrated  account  of  a  streptothrix,  which  they  had  isolated  from 
two  cases  of  actinomycosis  in  man — viz.,  from  the  lungs  and  from 
a  retromaxillary  growth.  This  organism  was  considered  to  differ 
from  N.  bovis  in  that  it  grew  best  anaerobically,  that  branching  was 
absent,  and  that  its  injections  into  animals  were  regularly  positive 
in  their  result.  These  three  characteristics  induced  Kruse,  in  1896, 
to  make  a  new  species  for  it  under  the  name  Streptothrix  Israeli. 
In  191 1,  for  reasons  already  set  forth,  Pinoy  founded  a  new  genus, 
Cohnistreptothrix,  with  Israel's  organism  as  the  type  species,  and 
therefore  its  name  becomes  Cohnistreptothrix  israeli  (Kruse,  1896). 

It  appears  to  us  to  be  of  importance  to  give  a  brief  history  of  the 
species. 

Lachrymal  concretions  have  been  known  since  Cesoin  described 
them  in  1670.  In  1848,  Gruby,  examining  one  of  these  objects, 
found  it  to  be  composed  of  a  fungus,  which  he  believed  to  be  the 
same  as  that  causing  favus,  but  Cohn,  in  1875,  examining  another 
such  concretion,  also  saw  a  fungus,  for  which  he  created  a  new 
genus  streptothrix,  calling  the  fungus  in  question  Streptothrix 
foersteri  Cohn,  1875,  which  may  be  the  same  organism  as  S.  aureus 
Du  Bois  de  Saint  Severin,  1895,  and  must  be  closely  related  to 
Nocardia  tenuis  Castellani,  1911,  which  belongs  to  the  same  genus, 
and  as  its  colonies  on  agar  are  '  cerebriform  '  it  may  possibly  be  the 
same  as,  or  related  to,  Streptothrix  radiatus  and  S.  cerebriforiuis 
(both  described  from  cases  of  keratitis  by  Namyslowski  in  1909),  as 
well  as  the  more  aerobic  hyphal  form  of  Silberschmidt's  organism. 

Unfortunately,  a  mistake  was  made,  for  Cohn  was  not  aware 
that  the  name  Streptothrix  had  already  been  given  by  Corda,  in 
1839,  for  another  and  quite  different  fungus,  which  is  known  as 
Streptothrix  fusca  Corda,  1839,  and  is  to  be  found  in  all  works 
of  any  importance  on  systemic  mycology  Therefore,  as  strepto- 
thrix is  not  available,  after  many  changes,  the  generic  name  has 
become  Cohnistreptothrix  Pinoy,  1911,  and  to  this  genus  Israel's 
human  organism  belongs.  It  differs  from  Bollinger's  type  of  fungus 
in  growing  best  anaerobically,  in  being  difficult  to  cultivate,  and  in 
not  producing  arthrospores.  Other  allied  organisms  are  Cohni- 
streptothrix thibiergei  (Ravaut  and  Pinoy,  1909),  also  found  in  acti- 
nomycosis in  man ;  Streptothrix s-pitzi Lignieres,  1903,  found  in  cattle, 
is  probably  identical  with  C.  israeli,  as  may  be  Doyen's  streptothrix  ; 
while  Nocardia  carougeaui  ( rougerof,  1909,  in  juxta-articular  nodules, 
and  Streptothrix  cuuiculi  Schniorl,  1891,  probably  also  belong  to  this 
genus,  as  well  as  the  streptothrix  recently  discovered  in  a  liver 
abscess  in  America  by  Bloomlield  and  Baync-Jones  (1915)-     Perha]  s 


1064  FUNGI  IMPERFECT  I 

the  bacillus  described  by  Sawtschenko,  in  1896,  as  the  causal  agent 
of  a  pseudo-mycetomatous  condition  may  also  belong  to  this  genus, 
and  it  is  also  possible  that  the  Coccobacillus  pseudo-actinomycosis 
polvtnorphus  Berestneff,  1898,  may  be  the  same  as  the  chromogenic 
anaerobic  streptothrix  obtained  from  human  pus  by  Neschezadi- 
menko  in  1908. 

Classification. — The  species  included  in  this  genus  are : — 

1.  Cohni  streptothrix  silberschnidti  Chalmers  and  Christopherscn, 

1916:— 

This  name  is  given  to  distinguish  the  obligatory  anaerobic 
streptothrix  found  by  Silbersehmidt,  in  1900,  in  dacryo- 
cystitis, and  described  in  the  Centralblatt  fur  Bakterio- 
logie,  xxvii.,  and  further  cases  in  Zeitschrift  fur  Hygiene 
(1901),  xxxvii. 

2.  Cohni  streptothrix  cuniculi  (Schmorl,  1891): — 

Streptothrix  cuniculi  Schmorl,  1891. 

Actinomyces  cuniculi  Gasperini,  1894. 

Streptothrix  necrophora  Kitt,  1906. 

?  Bacillus  necroseos  Salmonsen . 

?  Necrosis  bacillus  of  Bang. 

?  Bacillus  diphtheria;  vilulorum  Fliigge. 

?  Bacillus  necrophorus  Fliigge. 

3.  C ohni streptothrix  neschezadimenki  Chalmers  and  Christopherson, 

1916 : — 

This  name  is  given  to  distinguish  the  obligatory  anaerobic 
streptothrix  found  by  Neschezadimenko,  in  1908,  in 
human  pus,  and  described  in  the  Centralblatt  fur  Bak- 
teriologie,  xlvi. 

?  Coccobacillus  pseudo-actinomycosis  polymorphic  Berest- 
neff, 1898. 

4.  Cohni streptothrix    americana    Chalmers    and    Christopherscn, 

1916 : — 
This  name  is  given  to  distinguish  the  streptothrix  which 
only  grows  under  partial  anaerobic  and  aerobic  con- 
ditions, obtained  from  a  liver  abscess  by  Bloomheld 
andi  Bayne-Jones  in  1915,  and  described  in  Johns 
Hopkins  Hospital  Bulletin,  xxvi.,  No.  292. 

5.  Cohni  streptothrix  israeli  (Kruse,  1896): — 

Streptothrix  israeli  Kruse,  1896. 

Streptothrix  spitzi  Lignieres,  1903. 

Possibly  the  streptothrices  described  by  Doyen  in  1891, 
by  Jurinka  in  1896,  and  some  of  those  by  Silbersehmidt 
in  1901,  by  Schukewitsch  in  1902,  by  Doepke  in  1903, 
and  by  Wright  in  1904. 

6.  Cohnistreptothrix  thibiergei  (Ravaut  and  Pinoy,  1909) : — 

Discomyces  thibiergei  Ravaut  and  Pinoy,  1909. 


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io66  FUNGI  IMPERFECTI 

7.  Cohnistreptothrix  foersteri  (Cohn,  1874): — 

Streptothrix  foersteri  Cohn,  1874. 

Leptolhrix  oculomm  Sorokin,  1881. 

Odspora  foersteri  Sauvageau  and  Radais,  1892. 

Streptothrix  aurea  Du  Bois  de  Saint  Severin,  1895. 

Streptothrix  foersteri  Kruse,  1896. 

The  aerobic  streptothrix  of  Silberschmidt  obtained  from 

a  case  of  dacryocystitis,  1901. 
?  Streptothrix  radiata  Namyslowski,  1909. 
?  Streptothrix  cerebriformis  Namyslowski,  1909. 

8.  Cohnistreptothrix  tenuis  (Castellani,  1911): — 

Nocardia  tenuis  Castellani,  1911. 

9.  Cohnistreptothrix  carougectui  (Gougerot,  1909): — 

Discomyces  carougeaui  Gougerot,  1909. 

Nocardia  carougeaui  Castellani  and  Chalmers,  1913. 

These  species  may  be  differentiated  as  given  on  p.  1065. 

Cohnistreptothrix  Israeli  Kruse,  1896. 

Synonyms.— Streptothrix  israeli  Kruse,  1896;  Cohnistreptothrix 
israeli  Pinoy,  191 1. 

Found  in  some  cases  of  human  and  bovine  actinomycosis.  It 
differs  from  N.  bovis  by  being  strictly  anaerobic.  Inoculations  of 
pure  cultures  have  reproduced  actinomycotic  lesions,  while  so  far 
such  experimental  lesions  have  not  been  obtained  by  using  cultures 
of  N.  bovis. 

Wright  states  that  N.  israeli  is  the  real  cause  of  actinomj^cosis, 
while  iV.  bovis  would  be  only  a  contamination  or  a  saprophytic 
agent.  We  agree,  however,  with  Pinoy' s  opinion  that  the  clinical 
features  of  actinomycosis  may  be  due  to  several  germs :  in  man  Pinoy 
has  found  N.  bovis  and  N.  israeli  ;  in  oxen  N .  israeli  in  most  cases, 
but  also  N.  bovis,  the  actinobacillus,  and  mixed  infections. 

The  actinobacillus  of  Lignieres  and  Spitz,  very  common  in  South  America, 
gives  rise  to  a  type  of  actinomycosis  of  cattle  affecting  generally  the  tongue 
and  neck,  in  which  no  grains  are  found.  The  germ  in  the  affected  tissues 
appears  in  the  shape  of  a  club-like  bacillus.  Cultivation  is  difficult,  the 
best  medium  being  glucose  serum  agar.  The  colonies  are  minute,  bluish, 
or  translucid,  with  irregular  edge.  The  germ  generally  dies  out  after  two 
or  three  subcultures.  Pinoy  and  Ravaut  have  described  a  case  of  menin- 
gitis in  man  due  to  this  bacillus. 

Cohnistreptothrix  thibiergei  Pinoy  and  Ravaut,  1909. 

Synonym. — Nocardia  thibiergei  Pinoy  and  Ravaut,  1909. 

Discovered  by  Pinoy  and  Ravaut  in  a  case  of  peculiar  nodular 
affection  of  the  subcutaneous  tissues  and  muscles.  In  the  lesions 
very  thin  (0-2  fi)  fragile  mycelial  threads  are  seen,  often  dissociated 
in  bacillary-like  bodies.  Masses  of  mycelia  embedded  in  amorphous 
cementing  substance  form  minute  grains  or  sclerotia,  with  a  maxi- 
mum diameter  of  about  80  fi.  Some  filaments  terminate  in  club- 
like  formations  about  3  ju,  in  breadth,  which  are  acid-fast. 


COHNISTREPTOTHRIX  FOERSTERI  1067 

The  fungus  is  easily  cultivated,  aerobically  and  anaerobically. 
On  maltose  agar  it  produces  small  white  colonies;  on  broth  it 
develops  only  at  the  bottom  of  the  tube. 

Cohnistreptothrix  foersteri  Cohn,  1874. 

Synonyms.  -Streptothrix  foersteri  Cohn,  1874;  Oospora  foersteri 
Radais  et  Sauvageau,  1892 ;  Discomyces  foersteri  Blanchard,  1895 ; 
Cohnistreptothrix  foersteri  Pinoy,  1911. 

Mycelial  threads  very  slender,  seldom  ramified,  often  terminating 
in  a  chain  of  rod-like  or  coccus-like  elements.  Masses  of  the  fungus 
form  some  peculiar  white  bodies  or  concretions  (Desmarres'  dacryo- 
lithes),  about  2  millimetres  in  diameter,  which  are  occasionally 
found  in  the  lachrymal  canals  of  man. 

The  fungus  has  been  cultivated  with  difficulty  aerobically  and 
anaerobically  by  several  authors,  among  whom  Kastalky,  Axenfeld, 
Morax,  and  Landrieu.  The  last  named  has  made  a  thorough  in- 
vestigation of  the  fungus,  which,  according  to  him,  shows  a  slow 
growth  and  gives  rise  on  maltose  agar  to  small  cerebriform  colonies 
of  a  grey-stone  colour. 

The  peculiar  concretions  found  in  the  lachrymal  canals  were  first  studied 
by  Cesoin  in  1670  and  Sandifors  in  1779.  Desmarres,  in  1842,  considered 
them  to  be  calculi  composed  of  lime  salts,  and  indicated  them  by  the  name 
of  dacryolithes.  Gruby  believed  they  were  induced  by  the  fungus  of  Favus, 
but  his  observations  remained  unpublished.  A.  de  Graefe,  in  1854,  first 
stated  in  a  published  work  that  these  concretions  were  of  mycotic  origin. 
He  thought  they  were  due  to  Achorion  schoenleinii,  while  Conheim  and  others 
believed  them  to  be  caused  by  Nocardia  (Streptothrix)  buccalis.  In  1875 
Cohn  described  the  fungus  under  the  name  of  Streptothrix  foersteri. 

Cohnistreptothrix  tenuis  (Castellani,  1911). 

Synonym. — Nocardia  tenuis  Castellani,  1910. 

Found  by  Castellani  in  a  nodular  affection  of  the  hair  of  the 
axillary  regions.  In  the  parasitic  stage,  the  germ  appears  in  the 
shape  of  bacillary-like  bodies,  varying  in  breadth  (0-2  to  o-6  jj,)  and 
in  length  (2  to  10  ju),  packed  together  and  embedded  into  an 
amorphous  cementing  substance.  The  bacillary  bodies  are  either 
straight  or  bent,  seldom  branching.  Gram-positive,  but  not  acid- 
fast.  Masses  of  this  fungus  embedded  in  amorphous  cementing 
substance  form  the  nodules  of  trichomycosis  flava  of  the  axillary 
regions.     (See  Plate  VI.,  p.  1034). 

In  the  black  variety  of  the  affection  Nocardia  tenuis  is  associated  with  a 

black  pigment-producing  coccus — -Xigrococcus  nigrescens  Castellani,  191 1.     In 

the  red  variety  the  same  Nocardia  is  associated  with  a  red  pigment-producing 

coccus  found  by  Castellani,  and  called  by  Chalmers  and  O'Farrell  Rhodococcus 

'laniii  halm ers and  O'Farrell,  [913. 

For  the  growth  of  the  black  pigment-producing  coccus,  sugar  media  are 
more  suitable  than  ordinary  agar.  On  Sabouraud's  agar  the  colonies  of  this 
coccus  appear  twenty-four  to  forty-eight  hours  after  inoculation.  They  are 
roundish,  at  first  white,  but  after  a  couple  of  days  the  centre  of  each  colony 
turns  black;  at  this  pigmentation  slowly  spreads  excentrically.  After  a 
time  the  colonies  coalesce  into  a  jet-black  mass.  On  glucose  agar  the  coccus 
presents  the  same  characters.  On  ordinary  agar  the  pigmentation  is  much  less 
marked  or  almost  absent. 


io68  FUNGI  IMPERFECTI 

The  red  pigment-producing  coccus,  on  the  other  hand,  grows  better  and 
shows  more  pigmentation  on  ordinary  agar  than  on  maltose  or  glucose  agar. 

ADDENDUM. 

A  few  words  may  be  inserted  on  certain  filamentous  vegetal  organisms,  on 
the  classification  of  which  there  is  much  discussion — viz.,  organisms  of  the 
genus  Leptothrix ,  of  the  genus  Cladothrix,  of  the  genus  Vibriothrix. 

Genus  Leptothrix  Kiitzing,  1S43. 

Definition. — Filamentous  fungi  with  long,  very  thin  mycelial  threads,  with 
no  capsule  or  only  a  very  delicate  one;  non-branching,  non-septate,  generally 
non-cultivable. 

Type  Species. — Leptothrix  maxima  Miller. 

The  following  species  concern  us : — 

Leptothrix  maxima  Miller,  1882. 

Synonym. — L.  buccalis  maxima  Miller. 

Long  thin  filaments,  unsegmented,  or  with  very  long  segments.  When 
treated  with  iodine  and  dilute  sulphuric  acid  gives  a  blue  granulose  reaction. 
Has  not  been  cultivated. 

Leptothrix  innominata  Miller,  1882. 

Morphologically  identical  with  L.  maxima,  but  when  treated  with  iodine  and 
dilute  sulphuric,  acid  does  not  give  a  blue  reaction.     Has  not  been  cultivated. 

Leptothrix  racemosa  Miller,  1882. 

Filaments  somewhat  thicker  than  those  found  in  the  two  preceding  species. 
On  staining  shows  a  peculiar  beaded  appearance.     Has  not  been  cultivated. 

Leptothrix  placoides  Dobrzyniecki. 
Very  long  thin  filaments,  Gram-positive,  non-motile.     Gelatine  liquefied. 
Growth  on  agar  very  slow;  produces  very  hard  granular  colonies.     Isolated 
from  human  mouth  by  Dobrzyniecki. 

Leptothrix  filiformis  Flexner,  1896. 

Synonym. — Bacillus  (Leptothrix  ?)  pyogenes  filiformis  Flexner,  1896. 
Isolated  by  Flexner  from  a  rabbit.  Is  non-motile,  of  difficult  cultivation, 
pathogenic. 

Leptothrix  vaginalis  Donne,  1885. 

Found  in  vagina  of  women  and  mammals. 

Genus  Cladothrix  Conn,  1875. 

Definition. — Filamentous  fungi  with  mycelial  threads  very  long,  thin,  show- 
ing pseudo-branching.  The  only  species  concerning  us  is  Cladothrix  dichotoma 
Cohn. 

Cladothrix  dichotoma  Cohn,  1875. 

Long  thick  mycelial  threads  straight  or  slightly  undulating.  They  are 
not  dichotomous,  as  the  name  would  suggest;  it  is  merely  a  case  of  pseudo- 
branching.  The  organism  can  be  cultivated  on  ordinary  laboratory  media, 
forming  on  agar  a  brownish,  wrinkled,  tough,  membranous  layer,  very 
adherent.  The  medium  may  become  stained,  slightly  brownish.  The  organ- 
ism is  found  often  in  waters.  We  have  found  it,  or  a  very  similar  species, 
in  an  ulcer  of  the  foot  in  association  with  many  other  organisms. 

Genus  Vibriothrix  Castellani,  191 7. 

The  mycelial  articles  are  motile,  of  very  different  shape:  bacillary,  vibrio- 
like, spirillum-like,  at  times   club-ended.     Globular   or  pear-shaped   bodies 


VIBRIOTHRIX  1069 

of  very  variable  size  may  be  present.  Gram-negative,  not  acid-fast.  Cultiv- 
able on  ordinary  media. 

Type  Species.—  Vibriothrix  zeylanica  Castellani,  1910. 

Synonyms.—  Spirillum  zeylanicum  Castellani,  1910;  Vibrio  zeylanicus 
Castellani,  1913;  Bacillus  zeylanicus  Castellani,  1913;  Vibriothrix  zeylanica 
Castellani,  1917;  Spirobacillus  zeylanicus  Castellani,  Spagnolo,  andRusso,  1918. 

Remarks. — Very  polymorphic  organism,  vibrio-like,  bacillus-like,  and 
undulating  forms  being  often  found  in  the  same  preparation.  Very  small, 
medium  size,  and  occasionally  large  roundish  bodies  are  at  times  observed, 
and  club-like  forms  may  also  be  present  {vide  Figs.  764,  765,  p.  1839). 

The  organism  is  motile,  Gram-negative,  not  acid -fast.  Easily  grown  on 
ordinary  media.  On  potato  the  growth  is  often  of  a  reddish  colour.  In 
broth  there  is  often  a  pellicle;  preparations  from  the  fluid  medium  generally 
show  a  predominance  of  vibrio-like  or  bacillary  forms,  while  in  the  pellicle 
long  undulating  forms  are  often  found.  On  MacConkey's  medium  the  colonies 
are  white,  and  somewhat  resemble  those  of  the  typhoid-dysentery  group. 
The  organism  does  not  ferment  any  of  the  usual  laboratory  carbohydrates  or 
alcohols:  glucose,  levulose,  galactose,  maltose,  lactose,  saccharose,  mannitol, 
dulcite,  raffinose.  There  is,  in  fact,  frequently  a  production  of  alkalinity. 
Milk  is  not  clotted  and  is  rendered  alkaline,  and  certain  strains  after  several 
weeks  may  induce  a  certain  degree  of  peptonization.  The  great  majority 
of  strains  are  non-pathogenic  to  rabbits  and  guinea-pigs. 

The  germ  was  first  isolated  by  Castellani  from  cases  of  dysenteric  enteritis 
in  Ceylon,  and  has  recently  been  observed  by  the  same  author  and  by  Spagnolo, 
Russo,  Taylor,  Douglas,  and  Ghiron,  in  Europe  (see  p.  1839). 

The  germ  is  found  in  great  abundance  in  a  number  of  cases  of  dysentery, 
while  it  seems  to  be  rare  in  other  conditions;  it  is  very  doubtful,  however, 
whether  it  can  really  become  pathogenic,  Castellani  having  found  it  also  in 
cases  in  which  the  typical  Shiga-Kruse  bacillus  was  present.  It  may,  perhaps, 
be  considered  to  be  a  so-called'  nosoparasite 'similarly  to  what  is  the  case  with 
certain  species  of  proteus  found  in  cholera,  in  typhus  fever,  and  other  conditions. 

ORDER  II.  THALLOSPORALES  Vuillemin,  1910. 

Definition. — -Hyphales  with  the  mycelium  composed  of  hyphas 
more  than  one  micron  in  diameter,  and  either  short  and  resembling 
the  conidia  or  longer  and  distinct  therefrom.  Reproduction  by 
means  of  thailospores.  Parasitic  on  man,  animals,  and  plants,  or 
saprophytic. 

Classification.— This  order  may  be  divided  as  follows  :— 

Reproduction  by  means  of  the  form  of  thallospore  called 
blastospore — -Suborder  1,  BlastosporinecB  Vuillemin,  1911. 

Reproduction  by  means  of  the  form  of  thallospore  called 
arthrospore — -Suborder  2,  Arthrosporinece  Vuillemin,  1911. 

SUBORDER  1.  BLASTOSPORINE^E  Vuillemin,  1911. 

Definition. — Thallosporales  with  hyphae  similar  to  or  dissimilar 
from  the  spores,  and  reproducing  by  means  of  blastospores,  which 
are  in  turn  capable  of  immediately  reproducing  themselves. 

Remarks. — -This  order  includes  Cryptococcus,  which,  in  its  old 
position  among  the  Ascomycetes,  was  certainly  an  anomaly,  being 
an  Ascomycete  without  an  ascus,  and  if  an  ascus  was  found  in  a 
species,  then  it  at  once  became  a  saccharomyces.  The  researches 
of  many  observers,  but  particularly  Busse,  tend  to  show  that  the 


1070  FUNGI  IMPERFECTI 

genus  Cryptococcus  Kutzing,  1833,  is  good,  and  therefore  should 
find  a  suitable  place  in  a  fungal  classification. 

Saccharomyces  and  its  allies  and  cryptococcus  and  its  allies  are, 
however,  so  closely  related  that  it  is  necessary  to  give  some  simple 
scheme  whereby  laboratory  workers  and  clinicians  may  easily 
differentiate  those  found  in  pathological  work;  and  such  a  scheme 
is  as  follows : — 

I.  In  cultures  budding  forms  present;  mycelium  absent,  or 
only  traces  thereof  present ;  asci  present — Saccharomyces. 
II.  As  I.,  but  no  asci  present — Cryptococcus. 

III.  Budding  forms  present;  mycelium  well  developed;  septate 

or  not,  branched  or  not;  asci  present — Endomyces. 

IV.  As  III.,  but  asci  not  present— Monili a. 

V.  Budding  forms  absent;  mycelium  well  developed,  septate; 
oval  or  rectangular  arthrospores  (thallospores)  present— 
Oidium. 

Classification. — -The  various  families  of  the  Blastosporineae  with 
which  we  are  concerned  may  be  recognized  as  follows : — 

A.  HyphcB  not  manifestly  different  from  the  spores  : — 

I.  Spores  not  in  chains.  Usually  do  not  ferment  carbo- 
hydrates with  the  production  of  gas — Family  I, 
Cryptococcacece  Kutzing,  1833. 
II.  Spores  in  chains.  Usually  ferment  carbohydrates 
with  the  production  of  gas — Family  2,  Oosporacece 
Saccardo,  1886. 

B.  Hyplice  manifestly  different  from  the  spores  :■ — ■ 

I.  Spores  not  in  chains,  but  arranged  verticillately — ■ 
Family  3,  Enanti  othamnacece  Chalmers  and  Archi- 
bald, 1915. 
II.  Spores  in  chains— Family  4,  Haplographiacece  Sac- 
cardo, 1886. 
III.  Spores  in  short  chains  or  solitary— Family  5,  Clado- 
sporiacecB  Saccardo,  1886. 

Family  i:  Cryptococcacece  Kutzing,  1833. 

Definition. — Blastosporineae  in  which  the  hyphse  are  little  different 
from  the  conidia,  both  being  yeast-like  in  form.  The  conidia  are  en- 
tirely formed  by  gemmation  from  the  hyphae  and  are  never  in  chains. 

Remarks.- — -This  family,  of  which  the  type  genus  is  Cryptococcus, 
is  very  commonly  classified  with  the  class  Ascomycetes,  which  in- 
cludes an  order  established  by  Brefeld  and  variously  named  hemi- 
ascomycetes,  hemi-asci,  proto-asci,  and  gymnascales.  This  order 
is  looked  upon  by  many  authorities  as  a  link  between  the  Phycomy- 
cetes  and  the  true  Ascomycetes,  and,  indeed,  its  founder,  Brefeld, 
believed  that,  in  process  of  evolution,  the  sporangium  of  the  Phy- 
comycetes  had  been  converted  into  the  ascus  of  the  Ascomycetes. 


CRYPTOCOCCACEAE  1071 

Classification. — The  family  contains  the  following  genera: — 
Tor ula  Persoon,  1801;  Cryptococciis  Kiitzing,  1833;  Pityrosfiorttvi 
Sabouraud,  1895;  and  Mycoderma  Persoon,  1822;  which  may  be 
differentiated  as  follows  :— 

A.  Vegetative  elements  not  elongate: — 

I.  Non-pathogenic  : — 

Vegetative  elements  roundish  or  oval,  containing  a  large  globule 
of  fat.  Budding  takes  place,  and  often  by  several  buds  at 
one  and  the  same  time.  Pigment  is  frequently  present. 
In  fluid  sugar  media  a  thick  pellicle,  without  bubbles  of  air, 
is  slowly  produced- — Tortila. 
II.  Pathogenic  : — ■ 

(a)  Vegetative  elements  with  well-developed  double  contour;  no 

large  globule  of  fat.  Budding  takes  place  with  a  single 
bud  at  a  time.  No  thick  pellicle  on  fluid  sugar  media. 
Cultivated — Cryptococciis. 

(b)  Vegetative  elements  often  without   double   contour.     Not 

cultivated — Pityrosporu  m. 

B.  Vegetative  elements  elongate: — 

In  fluid  sugar  media  a  thick  pellicle  containing  bubbles  of  gas  is 
quickly  produced — Mycoderma. 

The  genera  with  which  we  are  concerned  are  Cryptococcus  and 
Pityrosporum . 


Fig.  556.  —  Diagram  showing  Fig.  557. — Cryptococcus 

Budding  Characteristic  of  myrmecics. 

mycoderma  (a)  and  Torula  (b). 

(After  Hansen.) 

Genus  Cryptococcus  Kiitzing,  1833. 

Definition.— -Cryptococcaceae  with  vegetative  elements  not  elon- 
gate; pathogenic,  with  well-developed  double  contour,  but  no  globule 
of  fat  and  only  one  bud  at  a  time,  and  no  fonnation  of  thick  pellicle 
on  fluid  sugar  media.     Can  be  cultivated. 

Type  Species.    Cryptococcus  honrinis  Vuillemin,  1901. 

Remarks  and  Classification. — The  name  Cryptococcus  was  intro- 
duced by  Kiitzing  in  1833  as  the  generic  name  for  certain  forms  of 
his  algae,  which  he  classified  as  belonging  to  the  subclass  Malaco- 
phyceae,  tribe  (iymnospermeae,  order  Eremospermeae,  suborder 
Mycophyceae,  and  family  Cryptococcaceae.  This  family  he  defined 
as:  '  Globiili  gonintici  »ii nutissimi  mucosi  in  stratum  indefinitwn 
aggregati,'  and  in  this  family  he  placed  three  genera,  Cryptococcus, 
Ulvina,  and  Sphaerotilus.     The  genus  Cryptococcus  was  character- 


1072  FUNGI  IMPERFECT  I 

ized  as:  '  Globuli  gonimici  in  stratum  amorphum  diffusunt  aggregati.' 
In  this  genus  he  gathered  no  less  than  thirteen  species,  all  described 
by  himself  and  mostly  found  in  water  or  in  pharmaceutical  prepara- 
tions. 

His  twelfth  and  thirteenth  species  were,  however,  more  interest- 
ing, as  they  were  called  Cryptococcus  cerevisice  and  C.  vini . 

In  1837  Meyen  separated  C.  cerevisice  from  the  genus  Cryptococ- 
cus, because  it  reproduced  by  ascospores  as  well  as  by  budding, 
and  to  this  new  genus  he  gave  the  name  Saccharomyces,  so  that 
Cryptococcus  cerevisice  became  Saccharomyces  cerevisice. 

Cryptococcus  therefore  remained  for  those  yeast-like  fungi  which 
do  not  reproduce  by  ascospores,  but  only  by  budding. 

The  removal  of  the  species  cerevisice  from  Cryptococcus  was  not 
recognized  by  Charles  Robin,  and  with  it  he  grouped  the  fungus  found 
by  Remak  in  1845  in  the  biliary  passages  and  intestines  of  rabbits, 
to  which  in  1847  he  gave  the  name  Cryptococcus  guttulatus.  Later, 
however,  it  was  also  shown  to  belong  to  the  genus  Saccharomyces. 

In  1873  Rivolta  noticed  peculiar  bodies  in  a  form  of  lymphangitis 
in  horses,  and  in  1883  he  and  Micellone  named  this  organism  Crypto- 
coccus farciminosus . 

During  this  period  one  or  two  organisms  had  a  temporary  resting- 
place  in  this  genus — -e.g.,  Fresenius's  Cryptococcus  glutinus. 

The  first  case  in  which  a  cryptococcus  was  definitely  proved  to  be 
the  cause  of  disease  was  Busse's  case  of  cystic  swellings  of  the  tibia 
in  a  woman,  aged  thirty-one.  The  bodies  in  question  were  first  seen 
by  Buschke,  but  it  was  Busse  who  first  proved  that  they  were  the 
true  cause  of  the  disease,  and  showed  that  they  were  pathogenic  to 
animals.  These  yeast-like  organisms  were  found  at  the  autopsy 
some  thirteen  months  later  to  occur  in  sarcomatous-like  growths 
consisting  of  young  granulation  tissue  and  giant  cells,  not  merely 
in  the  cysts,  but  also  in  the  lungs,  kidneys,  spleen,  and  in  a  vesicle  on 
the  cornea.  The  organism  grew  well  on  potato  and  in  acid  media. 
It  fermented  glucose  and  was  specially  pathogenic  for  rats.  It 
only  reproduced  by  budding,  and  no  endospores  or  mycelium  were 
ever  seen.  It  was  this  that  induced  Vuillemin  to  give  it  the  name 
Cryptococcus  hominis,  1901. 

Including  C.  hominis,  and  after  excluding  several  wrongly  classi- 
fied forms,  there  are  about  fourteen  species  parasitic  in  man  which 
can  at  present  be  referred  to  the  genus  Cryptococcus,  e.g. : — 

Cryptococcus  breweri  Verdun,  1912,  described  in  an  abscess  of  the 
vertebral  column;  C.  tonkini  Legendre,  1911,  found  in  two  cases  of 
blastomycosis  in  Indo-China. 

In  addition  a  number  of  cryptococci  have  been  found  associated 
with  cancers,  sarcomata,  and  innocent  tumours— e.g.,  C.  plimmeri 
Constantin,  1901;  C.  degenerans  Vuillemin,  1896;  C.  corsellii  Neveu- 
Lemaire,  1908;  C.  hessleri  Rettger,  1904. 

The  following  have  been  found  in  the  mouth  or  throat: — C.  sul- 
fureus  Beauverie  and  Lesieur,  1912;  C.  lesieuri  Beauverie  and 
Lesieur,  1912;  C.salmoneus  Sartory,  1911;  C.  guillermondi  Beauverie 


CRYPTOCOCCUS  DERMATITIDIS  1073 

and  Lesieur,  1912;  C.  rogeri  Sartory,  1911;  and  C.  linguez-pilosce 
Lucet,  1901. 

According  to  most  authors,  Histoplasma  capsulatum  Darling, 
1906,  is  not  an  animal  but  a  vegetal  parasite,  and  should  be  classified 
as  a  cryptococcus. 

The  parasite  found  in  cases  of  chronic  ulcerative  dermatitis  in 
America,  and  named  Cryptococcus  dermatitis  Gilchrist  and  Stokes, 
according  to  some  authors,  does  not  belong  to  the  genus  Crypto- 
coccus of  Kutzing,  but  to  the  genus  Mycoderma  of  Persoon,  1822 ; 
but  we  have  retained  it  under  Cryptococcus. 

Recently  Chalmers  and  Christopherson  in  the  Anglo-Egyptian 
Sudan  have  found  a  cryptococcus  in  a  peculiar  disease  consisting  of 
spreading  warts,  to  which  they  have  given  the  name  Murmekias- 
mosis  amphilaphes.  As  the  cryptococcus  is  closely  associated  with 
the  condition,  they  have  named  it  C.  wtyrmecice  Chalmers  and 
Christopherson,  1914,  but  they  were  unable  to  prove  conclusively 
that  it  was  the  serological  factor,  though  they  brought  forward 
some  facts  to  support  such  a  contention. 

Cryptococcus  dermatitidis  Gilchrist  and  Stokes,  1898. 

Synonyms. — Blastomyces  dermatitis  Gilchrist  and  Stokes,  1898; 
Cryptococcus  gilchristi  Vuillemin;  Zymonema  gilchristi  de  Beurmann 
and  Gougerot. 

Found  by  Gilchrist  and  Stokes  in  a  case  of  chronic  ulcerative 
dermatitis,   and  later  in  a  case  which  had  been  diagnosed  as   a 
tuberculide  of  the  skin.     After  Gil- 
christ and  Stokes's  cases,  other  cases 
of  blastomycosis  due  to  an  identical  (vM^ 

or  similar  organism  have  been 
described  by  Hyde,  Oppenheim, 
Ricketts,  and  others.  Ricketts  con- 
sidered these  fungi  to  be  species  of 
Oidium,  and  proposed  the  name 
'  oidiomycosis  '  to  indicate  the 
disease  produced  by  them. 

C.  dermatitidis  in  the  affected  tis- 
sues has  the  appearance  of  a  typical    Fig.    558. — Cryptococcus    dermali- 
ye&st—i.e.,  large    globular  cells,    io        tidis  Gilchrist  and  Stokes. 
to   16   jj,  in   diameter,   reproducing  (After  Gilchrist.) 

by  budding.     In  cultures,  which  are 

white,  besides  these  globular  elements,  rudimentary  mycelial  tubes 
may  occasionally  be  found,  presenting  lateral  or  terminal  conidia; 
asci  arc  absent.  The  fungus  does  not  ferment  sugars,  and  there 
is  no  formation  of  a  pellicle.     Gelatine  not  liquefied. 

Cryptococcus  hominis  Vuillemin,  1901. 
Synonyms.— Saccharomyces   (sp.   ?)   Busse,    1894;   Atelosaccharo- 
myces  busse-buschki  de  Beurmann  and  Gougerot,  1909;  Atelosaccharo- 
myces  rudeli  de  Beurmann  and  Gougerot,  1911. 


io74  FUNGI  IMPERFECTI 

Found  in  abscesses  in  a  woman  by  Busse.  In  the  pus  the  fungus 
presented  itself  in  the  shape  of  oval  bodies,  with  a  membrane 
having  a  double  contour.  These  elements  were  arranged  in  groups, 
each  group  embedded  in  an  amorphous  substance  and  surrounded 
by  a  capsule.  Culturally  the  fungus  showed  only  roundish  budding 
forms,  no  mycelium,  no  asci.  Growth  on  solid  media  generally 
white.  Gelatine  not  liquefied.  Glucose  fermented.  Pathogenic 
to  rabbits,  white  mice,  and  dogs. 

Cryptococcus  linguae-pilos*  Lucet,  1901. 

Synonym. — Sacchayomyces  linguce-pilosce  Lucet,   1901. 

Found  by  Lucet  and  others  in  cases  of  so-called  '  black  tongue.'  It  appears 
on  the  surface  of  the  hypertrophied  ligual  papillae  in  the  shape  of  roundish 
bodies,  with  double  contour,  3  to  6  [A  in  diameter.     Grows  easily  on  sugar 

media.  Often  produces  pellicle  in  sugar 
media.  Glucose  and  levulose  fermented. 
Attempts  to  reproduce  the  disease  have 
failed.  Guegen  and  Thaon  believe  that 
this  fungus  becomes  pathogenic  only  when 
associated  with  Nocardia  lingualis. 

The  condition  known  under  the  name  of 
'  lingua  nigra  '  is  caused  in  addition  to  the 
above  fungus,  in  some  cases  by  Rhizopus 
niger,  in  other  cases  by  Nocardia  lingualis. 

Cryptococcus  plimmeri  Constantin,  1901. 

Fig.  559. — Cryptococcus  Ungues-       Found    by    Plimmer  in   many  cases   of 

piloses  Lucet  cancer;  is  probably  only  a  saprophyte.     In 

(After  Lucet,  from  Brumpt.)       th+e  tissues  r<™ndish  bodies  of  various  sizes, 

r    t       4  to  40  f.t  in  diameter,  are  seen,  occasionally 

budding,   and   either  free  or  intracellular. 

Cultivation  has  succeeded  only  on  one  occasion,  when  it  was  found  that  it 

produced  a  white  growth  on  agar  and  other  media.     Action  on  gelatine  and 

other  sugars  have  not  been  investigated.     Cryptococcus  plimmeri,  according  to 

some  authors,  has  been  applied  to  cellular  changes. 

Cryptococcus  degenerans  Vuillemin,   1896. 

Synonym. — Blastomyces  vitrosimile  degenerans  Roncali,   1896. 

Found  by  Roncali  and  others  in  malignant  tumours,  sarcomata,  and  car- 
cinomata.  Easily  grown;  on  potatoes  it  attains  a  much  larger  size  than  on 
any  other  medium;  on  gelatine  growth  greyish-yellow.  Sugar  reactions 
scarcely  known.  Dors  not  ferment  saccharose,  but  nothing  definite  known 
about  other  sugars.     Pathogenic  for  guinea-pigs. 

Cryptococcus  corsellii  Neveu-Lemaire,  1908. 

Found  by  Corselli  and  Frisco  in  a  sarcoma  of  the  mesenteric  glands.  The 
fungus  appeared  in  the  tumours  under  the  shape  of  black  masses.  It  was 
easily  cultivated,  and  found  pathogenic  to  guinea-pigs,  rabbits,  and  dogs. 
Sugar  reactions  unknown. 

Cryptococcus  hessleri  Rcttger,  1904. 

Synonym. — Blastomyces  hessleri  Rettger,   1904. 

Isolated  by  Hessler  from  a  small  tumour  which  developed  on  a  patient 
after  a  razor-cut.  Easily  cultivated,  especially  on  alkaline  media.  Patho- 
genic for  the  rabbit  and  guinea-pig.     Sugar  reactions  unknown. 


CRYPTOCOCCUS  BREWERI  1075 

Cryptococeus  breweri  Verdun,  1912. 

Synonym..    Atelosaccharomyces  breweri  Verdun,    1912. 

Found  by  Brewer  and  Wood  in  an  abscess  of  the  vertebral  column. 

Cryptococeus  tonkini  Legendre,   191 1. 

Synonym. — Blastomyces  tonkini  Legendre,   191 1. 

Found  by  Legendre  in  two  cases  of  blastomycosis  in  lndo-China.  Pinoy 
considers  that  the  characters  given  are  not  sufficient  to  create  a  new  species 
for  it. 

Cryptococeus  sulfureus  Beauverie  and  Lesieur,   1912. 

Found  by  Beauverie  and  Lesieur  in  certain  pharyngeal  lesions  of  a  case  of 
typhoid.     Ferments  slightly  dextrose,  saccharose,  and  lactose. 

Cryptococeus  lesieuri  Beauverie  and  Lesieur,   191 2. 
Found  in  a  case  of  stomatitis.     Ferments  dextrose  only. 

Cryptococeus  salmoneus  Sartory,  191 1. 

Described  by  Sartory.  Found  in  human  gastric  juice.  Growth  on  usual 
media  of  a  pinkish  or  reddish  colour.  Does  not  ferment  any  sugar.  Slowly 
coagulates  milk. 

Cryptococeus  guillermondi  Beauverie  and  Lesieur,   1912. 

Found  by  Guillermond  and  Lesieur  in  cases  of  stomatitis. 

Cellular  elements  in  situ  spherical,  10-25  microns;  surrounded  by  large 
mucilaginous  capsule.  Growth  on  agar  white  or  slightly  yellowish.  On 
potato  scanty  growth,  white.  Gelatine  not  liquefied.  Does  not  ferment  any 
sugar. 

Cryptococeus  harteri  de  Beurmann  and  Gougerot,  1913. 
Synonym. — Atelosaccharomyces  harteri  de  Beurmann  and  Gougerot, 

19*3- 

Cells  oval,  4-6  and  3-5  microns.  Growth  on  sugar  media  and 
gelatine,  which  is  not  liquefied,  white.  Does  not  ferment  any 
sugar.     Found  by  Harter  in  a  case  of  systemic  blastomycosis. 

Cryptococeus  hudelo  de  Beurmann  and  Gougerot,   1914. 

Cellular  elements  in  situ  mostly  spherical,  2-20  microns;  at  times  oval, 
easily  grown.  Colonies  white;  gelatine  not  liquefied.  Growth  on  potato  at 
first  white,  later  yellow,  and  finally  reddish  or  blackish.  Found  by  Hudelo, 
Duval,  and  Loederich  in  a  case  of  periostitis. 

Cryptococeus  membranogenes  Steinhouse,  19 16. 

Cellular  elements  roundish,  7-8  microns  in  diameter,  with  very  distinct 
double  contour.  Surrounded  by  a  thick  capsule.  Easily  grown  on  all  the 
usual  culture  media.  Colonies  white.  Gelatine  not  liquefied.  Ferments 
with  gas  production  glucose  but  not  maltose,  lactose,  or  saccharose.  Action 
on  other  sugars  not  known.     Very  pathogenic  for  rabbits. 

Found  by  Steinhouse  in  1916  in  a  case  of  scarlet  fever  showing  symptoms 
of  tracheal  obstruction. 

Cryptococeus  epidermidis  Castellani.  1914. 

Found  by  Castellani  in  saccharomycosis  epidermica.  Cells  of  very  variable 
size.     Has  not  yet  been  cultivated. 


io76  FUNGI  IMPERFECT  I 

Cryptoeoccus  niger  Vuillemin. 

Found  by  Maffucci  and  Sirleo,  in  1895,  in  a  pulmonary  myxoma  of  a 
guinea-pig.  Cells  in  situ  round  or  ovoid,  with  thick  mucilaginous  mem- 
brane. White  on  most  media;  on  potato  brown  or  black.  Gelatine  not 
liquefied.     Said  to  ferment  maltose.     Nothing  known  about  other  sugars. 

Cryptoeoccus  lithogenes  San  Felice. 

Synonym. — Saccharomyces  lithogenes  San  Felice. 

Found  by  San  Felice  in  the  lymphatic  glands  of  an  ox.  Roundish  cells 
with  a  membrane  which  is  at  times  calcified.  Growths  whitish  on  most 
media,  dark  brownish  after  a  time  on  potato.     Gelatine  not  liquefied. 

Cryptoeoccus  granulomatogenes  (San  Felice). 

Synonym,- — Saccharomyces  granulomatogenes  San  Felice. 

Isolated  from  the  lung  of  a  hog  by  San  Felice.  It  grows  easily  on  ordinary 
laboratory  media,  producing  white  colonies.  It  does  not  liquefy  gelatine,  but 
it  produces  slight  rose-red  pigment  on  slices  of  pear  and  on  honey. 

Cryptoeoccus  farciminosus  (Rivolta  and  Micellone,  1883). 

Synonyms.- — Cryptoeoccus  tokishigei  Vuillemin ;  Lymphosporidium 
equi  Gasperini,  1908;  Leucocytozoon  piroplasmoides  Ducloux,  1908. 

Definition. — Vegetative  cells  in  situ,  oval  or  roundish,  with  well- 
marked  double  contour. 

Remarks.— It  is  often  included  in  hypertrophied  endothelial  cells 
and  in  leucocytes  in  the  lesions  in  horses  suffering  from  lymphan- 
gitis epizootica  in  Europe,  Africa,  Asia,  and  America. 

Cultivation. — It  is  of  difficult  cultivation.  Negre  and  Boquet 
have  used  with  success  a  medium  made  of  agar  and  dried  horse-dung. 
Sugar  reactions  are  unknown. 

Cryptoeoccus  capsulatus  (Darling,  1906). 

Synonym. — Histoplasma  capsulatum  Darling,  1906. 

Definition.— In  the  affected  tissue  the  parasite  appears  in  round 
or  oval  form,  measuring  1-4  microns  in  diameter,  and  enclosed  in  an 
achromatic  retractile  capsule.     Cultivation  so  far  negative. 

Remarks. — -It  was  found  by  Darling  in  the  endothelial  cells  of 
capillaries  and  small  bloodvessels  in  the  lungs,  spleen,  liver,  intes- 
tines, and  lymph  glands,  as  well  as  in  the  leucocytes.  It  was  con- 
sidered by  Darling  and  others  to  be  a  protozoon,  and  for  it  the 
genus  Histoplasma  was  created.  At  present  there  is  a  consensus 
of  opinion  that  it  is  a  Cryptoeoccus. 

Pathogenicity. — It  is  pathogenic  for  man,  causing  disseminated, 
hyaline,  pseudogranulomata  in  the  lungs,  splenomegaly,  necrotic 
areas  in  the  liver,  and  ulceration  of  the  small  and  large  intestines. 

Cryptoeoccus  ruber  Demne,  1889. 

Synonym. — -Saccharomyces  ruber  Demne,  1889. 

This  organism  was  found  in  the  stools  of  children  suffering  from 
enteritis  and  also  in  certain  specimens  of  milk. 

It  grows  easily  on  ordinary  laboratory  media,  producing  red 
colonies.     According  to  Casagrandi,  it  does  not  ferment  any  sugar. 


PITYROSPORUM  1077 

Cryptococcus  myrmeciae  Chalmers  and  Christopherson,  1914. 

Cryptococcus  measuring  1-4-2-1  microns  in  diameter,  found  in  a 
case  of  murmekiasmosis  amphilaphes  in  the  Anglo-Egyptian  Sudan. 

All  attempts  at  cultivation  on  a  large  series  of  media  under  aerobic 
and  anaerobic  conditions  at  200,  37°,  and  400  C.  failed,  as  did  inocula- 
tions into  monkeys  and  dogs.  It  was  named  because  of  its  associa- 
tion with  the  peculiar  disease  called  munnekiasmosis,  but  evidence 
was  wanting  that  it  was  the  causal  organism,  although  its  associa- 
tion was  intimate. 

Genus  Pityrosporum  Sabouraud,  1895. 

Synonym. — Dermatophyton  Dodd,  1910. 

Definition. — -Cryptococcaceae  without  well-developed  double  con- 
tour. 

Type  Species.— Pityrosporum  ovale  (Bizzozzero,  1882). 

Remarks  and  Classification. — -This  genus,  which  is  difficult  to 
classify,  is  allied  in  appearance,  in  some  forms,  to  a  budding  yeast, 
and  as  such  comes  close  to  Cryptococcus.  No  species  has  so  far 
been  cultivated  (Dodd  claims  to  have  cultivated  P.  [malassezi), 
but  two  are  known — -viz. :  P.  ovale  Bizzozzero,  1882  (synonyms,  Sac- 
charomyces capillitii  Oudemans  and  Pekelharing,  1885 ;  5.  sphcericus 
Bizzozzero,  1884  ;  5.  ovalis  Bizzozzero,  1889  ;  Pityrosporum  malas- 
sezi  Sabouraud,  1895,  often  called  the  bottle  bacillus  of  Malassez,  in 
cases  of  pityriasis  simplex  capitis  and  pityriasis  alba  in  Europe) 
and  P.  cantliei  (Castellani,  1908)  in  cases  of  seborrhcea  capitis  in 
children  in  Ceylon. 

They  may  be  distinguished  as  follows  :— 

A.  Flask-shaped  or  oval,  3  to  15  microns,  but  usually  small — Ovale. 

B.  Generally  roundish,  5  to  16  microns,  but  usually  large — Cantliei. 

/.• 


Fig.  560.—  Pityrosporum  ovale  Fig.  561. — Pityrosporum  ovale 

Bizzozzero.  Bizzozzero. 

(After  Sabouraud.) 

Pityrosporum  ovale  (Bizzozzero,  1882). 

Synonyms.— Saccharomyces  ovalis  Bizzozzero,  1882 ;  Pityrosporum 
malassezi  Sabouraud,  1895.     Usual  term :  bottle  bacillus  of  Malassez. 

This  organism  was  first  described  by  Bizzozzero,  who  considered 
it  to  be  a  Saccharomyces.     Malassez  and  Sabouraud  associated  this 


1078  FUNGI  IMPERFECTI 

organism  with  the  aetiology  of  pityriasis  simplex  capitis  and  pityria- 
sis alba. 

Its  shape  somewhat  resembles  a  budding  yeast  or  a  flask.  The 
size  varies  greatly;  the  maximum  diameter  of  some  individuals 
may  be  as  much  as  10  to  15  /.t,  but  much  smaller  forms  (3  to  5  /j,) 
are  found. 

Pityrosporum  cantliei  (Castellani,  1908). 

Synonym. — Saccharomyces  cantliei  Castellani,  1908. 

Somewhat  similar  toPityrosporum  ovale,  but  the  cells  are  generally 
roundish  and  on  the  average  larger  (5  to  16  /j,).  Probably  the  cause 
of  a  variety  of  seborrhcea  of  the  scalp  occasionally  met  with  in 
children  in  the  tropics. 

"Family  2:  Oosporace^;  Saccardo,  1886. 

Definition.— Blastosporineae  in  which  the  hyphae  may  be  long  or 
little  different  from  the  spores,  which  are  typically  in  chains. 

Classification. — This  family  is  divided  into  several  genera— e.g. 
Oospora  Wallroth,  1833;  Monilia  Persoon,  1797;  andjDidium  Link, 
1809,  which  may  be  distinguished  as  follows:— 

A.  Hyphae  thin,  short,  simple,  or  nearly  simple,  terminating  in  chains 

of  spores — Oospora. 

B.  Hyphae  not  thin,  often  long  and  branched: — 

I.  Sporophores    simple    or    subsimple,    typically    with    disjunction 

apparatus.     Glucose    completely    fermented,    gas    being    pro- 
duced.    Numerous  budding  forms  in  cultures — Monilia. 

II.  Sporophores  simple,  septate  often  with  disjunction  apparatus. 

Glucose  not  completely  fermented,   gas  not  being  produced. 
Budding  forms  rare  in  cultures — Oidinm. 

These  genera  may  now  be  briefly  described. 

Genus  Oospora  Wallroth,  1833. 

Definition.- — Oosporaceae  with  a  lax  or  compact  mycelium  in 
which  the  hyphae  are  slender,  septate,  and  marked  by  differentiated 
nuclei.  The  fertile  hyphae  are  short,  slender,  and  nearly  simple. 
The  conidia,  which  are  globose  or  ovoidal,  hyaline  or  brightly 
coloured,  are  arranged  regularly  in  chains. 

Remarks. — Saccardo  in  his  '  Sylloge  Fungorum  '  recognizes  a 
large  number  of  species  as  belonging  to  this  genus,  and  these  are 
grouped  into  sections  by  the  varying  colour  of  the  conidia. 

The  only  species  known  to  cause  disease  in  animals  referable  to 
this  genus  is  Oospora  canina  Sabrazes,  1893,  which  causes  favus  in 
dogs,  and  which  can  produce  an  eruption  resembling  ringworm 
when  inoculated  into  man.  According  to  Sabouraud,  however,  it 
has  never  been  known  to  cause  disease  in  man  spontaneously  (i.e., 
without  experimental  inoculation),  and  is  therefore  of  little  import- 
ance at  present. 

Vuillemin  considers  that  Achorion  schoenleinii  Lebert,  1845,  the 
fungus  of  favus  of  human  origin,  belongs  to  this  genus. 


MONILIA 


1079 


Genus  Monilia  Persoon,  1797. 

Definition.  -Vague. 

Original  Definition. — -Slipitata  ant  effusa  byssoidea,  Fila  monili- 
formis articulate. 

Botanical  Definition. — Sporophorcs  simple  or  subsimplc,  producing 
by  constriction  at  their  extremities  a  chain  of  large  lemon-shaped 
conidia,  often  provided  with  a  disjunction  apparatus. 

Usual  Definition.- — 06sporace?e  possessing  in  situ  budding  forms 
and  mycelial  threads,  which  latter  are  often  long  and  branched ;  in 
cultures  mostly  budding  forms,  but  sometimes  filaments,  in  which 
thallospores  of  the  blastospore  type  are  formed.  Glucose  and  often 
other  carbohydrate  media  fermented  with  the  production  of  gas. 


R?o®° 


^O^S^OffoQ0Q 


Fig.  562. — Monilia  tropi- 
calis  Castellani.  Fresh 
Preparation  from  Sputum. 


Fig.  563. — Monilia  intestinalis  Castel- 
lani. Preparation  from  Glucose 
Agar   Culture. 


On  0 

0 


Nomenclature.— A  few  words  are  necessary  with  regard  to  the 
nomenclature  and  the  synonyms,  as  the  greatest  confusion  has 
existed  with  regard  to  this  genus.  The  first  description  of  the  genus 
Monilia,  as  we  understand  it,  was  given  by  Persoon  as  '  Stipitata,  ant 
effusa  byssoidea,  Fila  moniliformias  articulata,'  and  the  first  date 
given  by  Saccardo  1797,  though  the  earliest  we  have  found  is  in  his 
book  of  1801.  The  name  is  derived  from  monile,  a  necklace. 
Link's  description  in  Gmelin's  thirteenth  edition  (really  the  four- 
teenth edition)  of  Linn?eus's  '  Systema  Natura,'  1791,  refers,  it  is 
true,  to  Monilia  aurea  (Link,  1791),  but  it  was  described  as  Oidium 
aureum  Link,  1791.  The  other  synonyms  do  not  require  explana- 
tion. 

We  have  not  included  the  genus  Zymonema  de  Beurmann  and 
Gougerot,  1909,  in  the  synonyms  because  Z.  gilchristi,  the  cause  of 
American  blastomycosis,  more  usually  called  Cryfrtococcus  gilchristi, 


io8o 


FUNGI  IMPERFECT  I 


is  said  to  have  lateral  as  well  as  terminal  conidia,  and  is  classified 
here  as  a  cryptococcus. 

The  genus  ' Parasaccharomyccs '  de  Beurmann  and  Gougerot, 
1909,  with  its  species Parasaccharomyces  harteri  Verdun,  1912,  found 
in  a  case  of  enteritis  with  hepatic,  bronchial,  and  cutaneous  lesions, 
has  not  merely  yeast-like  forms,  but  septate  hyphse,  but  it  is  not 
known  whether  it  develops  terminal  conidia  in  chains,  and  there- 
fore it  may,  at  present,  correctly  be  placed  in  the  genus  Crypto- 
coccus until  more  is  known  about  it;  and  the  same  remarks  apply, 
we  think,  to  Parcndomyccs  Querat  and  Laroche,  1909. 


Fig.  564.  Fig.  565.  Fig.  566. 

Fig.  5O4. — Monilia  zeylanica  Castellani.     Glucose  Agar  Culture. 
Fig.  565. — -Monilia  bronchialis  Castellani.     Glucose  Agar  Culture. 
Fig.  566. — Monilia  nivea  Castellani.     Glucose  Agar  Culture. 


Remarks. — -A  number  of  species  belonging  to  this  genus  are 
known  to  exist  in  nature  growing  on  decomposing  wood,  dead  leaves, 
and  fruits. 

The  number  of  species  known  to  infect  man  has  been  considerably 
extended  during  recent  years  by  Castellani.  The  Monilias  are  of 
importance  in  that  they  are  considered  to  be  the  aetiological  agents 
of  thrush,  bronchomycosis  {pro  parte),  some  derm  atom  ycoses,  and, 
according  to  certain  authors,  of  sprue. 

Type  Species.— It  is  difficult  to  know  which  is  really  the  type 
species  of  this  genus,  but  probably  it  is  Monilia  aurea  (Link,  1791). 


MONILIA  1081 

Geographical  Distribution. — Possibly  world-wide. 

Biological  Characters.— Some  species  clot  milk,  others  have  no 
action  on  this  medium;  some  species  liquefy  gelatine  and  serum. 
Certain  fungi  of  this  genus,  when  growing  on  serum,  produce  a 
peculiar  zone  of  brownish  or  black  discoloration  of  the  medium  all 
round  the  growth  using  the  serum  of  Bos  indicus.  The  bio- 
chemical properties  and  sugar  reactions  vary  from  species  to 
species.  Rabbits  can  be  immunized  for  these  fungi,  and  attempts 
to  use  the  immunization  and  agglutination  reactions  in  the  differ- 
entiation of  the  various  species  have  been  made  with  only  partial 
success,  as  there  is  a  large  production  of  co-agglutinins  in  addition 
to  the  specific  ones  for  very  different  fungi — e.g.,  fungi  of  the  genus 
Sporotrichum. 

Pathogenicity. — -Fungi  of  this  genus  are  the  serological  agents  of 
thrush,  some  types  of  bronchomycoses,  and  some  dermatomycoses. 

Classification. — There  has  been  and  there  is  still  a  great  deal  of 
confusion  in  the  classification  of  such  fungi.  Many  of  the  species  of 
this  genus  can  hardly  be  distinguished  by  purely  morphological  and 
botanical  characters.  We  are  of  opinion  that  the  classification 
should  be  based,  not  only  on  morphological  data,  but  also  on  bio- 
chemical characters  and  immunization  phenomena.  Among  the 
biochemical  properties,  the  most  important  are  the  actions  on  milk, 
gelatine,  serum,  and  on  sugar  broths.  A  large  number  of  sugars 
should  be  used  in  the  same  manner  as  is  done  in  the  classification 
of  the  various  species  of  intestinal  bacteria.  It  is  to  be  noted  that 
the  reactions  with  certain  sugars  are  constant,  while  with  others 
(for  instance,  mannite)  these  may  vary;  and  the  fermentative  power 
on  certain  sugars — e.g.,  galactose — may  be  rapidly  lost.  Hence 
species  should  be  compared  only  in  strains  recently  isolated.  It  is 
to  be  noted  also  that  in  analogy  to  intestinal  bacteria,  a  species 
may  be  trained  to  ferment  certain  sugars  on  which  it  did  not  act 
when  recently  isolated. 

While  taking  all  this  into  account,  we  believe  the  investigation 
of  the  various  biochemical  reactions  to  be  of  great  value  for  classify- 
ing these  fungi,  and  for  this  purpose  give  the  table  on  pp.  1082,  10^3. 

Determination  of  Species. — By  means  of  the  sugar  reactions 
it  is  possible  to  divide  the  species  of  Monilia  into  groups  by  the  use 
of  the  following  carbohydrates  —  viz.,  glucose,  levulose,  maltose, 
galactose,  saccharose,  inulin,  and  dextrin.  When  the  Monilia  is 
classified  into  its  group  it  is  easy,  by  means  of  the  table  on 
pp.  1082,  1083,  to  make  the  specific  determination: — - 

A.  Gas  produced  in  glucose  only — Group  I.,  Balcanica  group: — M.  bal- 

canica,  M.  parabalcanica. 

B.  Gas    produced  in  glucose  and   levulose — Group  II.,  Krusei  group: —  , 

M.  krusei,  M.  parakrusei. 

C.  Gas  produced  in  glucose,  levulose,  and  maltose — Group  III.,  Pinoyi 

group: — M.  pinoyi,  M.  nabarroi. 

D.  Gas  produced  in  glucose,  levulose,  maltose,  and  galactose — Group  IV., 

Metalondinensis   group: — M.    metalondi:c;:sis,  M.    pseudometalon- 
dinensis. 


io82 


TABLE  SHOWING  PRINCIPAL  BIOCHEMICAL  AND  CULTURAL 
OF  THE  FUNGI   lis    ALPHABETICAL  ORDER  :   REACTIONS 


litmus 

Glu- 

Levu- 

Mal- 

Galac- Saccha- 

Lac- 

Man- 

Dul- 

Dex- 

Genus Monilia. 

Milk. 


AC 

cose. 
AG 

lose. 
AG 

tose. 

tose. 

rose. 

tose. 

nite. 

cite. 

trin. 

M.  alba  Castellani 

AG 

AC 

A 

O 

o 

o 

o 

M.  albicans  Robin,  emd.  Cast. 

AC 

AG 

AGs 

AGs 

AG 

Avs 

O 

o 

o 

o 

M.  balcanica  Cast. 

O 

AG 

As 

O 

O     ! 

O 

o 

o 

o 

o 

M.  blanchardi  Cast. 

Ays 

AGs 

A 

A 

A 

A 

o 

o 

o 

o 

M.  bronchialis  Cast. 

Alk 

o 

AG 

AG 

AG 

O 

AGs 

o 

o 

o 

A 

M.  burgessi  Cast. 

O 

AGs 

A     ; 

AGs 

A 

AGs 

o 

o 

o 

o 

M.  chalmersi  Cast.   . . 

Alk 
As 

AG 

AG 

As 

AGs 

AG 

o 

o 

o 

o 

M.  decolorans  Cast,  and  Low 

Alk 
DC 

AG 

AG1 

AG 

A 

A 

o 

o 

o 

A 

M.  enterica  Cast. 

O 
Alk 

A 
DPs 

0 
Alk 

AG 

AG 

AG 

AG 

AG 

o 

As 

o 

As 

M.  fsecalis  Cast. 

AG 

AG 

AG 

AGs 

AGs 

o 

O 

o 

o 

M.  guillermondi  Cast. 

AG 

AG 

As 

A 

AG 

o 

O 

o 

o 

M.  insolita  Cast 

As 
Alk" 

AG 

AG 

AG 

AG 

AG 

o 

As 

o 

o 

M.  intestinalis  Cast. 

ADs 

AG 

AG 

As 

A 

A 

o 

O 

o 

o 

M.  krusei  Cast. 

O 

AG 

AG 

O 

O 

O 

o 

O 

o 

o 

M.  londinensis  Cast. 

AC 

AG 

AG 

A 

A 

A 

A 

o 

o 

o 

M.  lustigi  Cast 

As 
D 
AC 

A 

AGs 

Avs 

A 

AGs 

o 

o 

o 

A 

M.  macedoniensis  Cast. 

AG 

AG 

AorO 

AG 

AG 

o 

o 

o 

o 

M.  metalondinensis  Cast.    .  . 

O 

AG 

AG 

AG 

AG 

O 

o 

o 

o 

o 

M.  metatropicalis  Cast. 

AC 

AG 

AG 

AG 

AG 

AG 

o 

o 

o 

o 

M.  nabarroi  Cast. 

AC 

AG 

AG 

AG 

O 

O 

o 

o 

o 

o 

M.  negrii  Cast. 

Avs 
Alk 

A 
DC 

O 
Alk 

AG 

AG 

As 

AGs 

AG 

o 

o 

o 

o 

M.  nitida  Cast. 

AG 

AG 

A 

A 

A 

A 

A 

o 

Avs 

M.  nivea  Cast. 

AG 

AG 

AG 

AG 

AGs 

o 

O 

o 

O 

M.  parabalcanica  Cast. 

AC 

AG 

As 

O 

O 

O 

o 

O 

o 

O 

M.  parachalmersi  Cast. 

AC 

AG 

AG 

O 

AG 

AG 

o 

o 

o 

o 

M.  parakrusei  Cast. 

AC 

AG 

AG 

° 

O 

O 

o 

o 

o 

o 

M.  paratropicalis  Cast. 

As 
Alk 

As 

AG 

AG 

AG 

AG 

AG 

o 

o 

o 

Avs 

M.  perryi  Cast. 

A 

;  AGs 

',     A 

A 

AGs 

o 

o 

o 

O 

D  Alk 

M.  pinoyi  Cast. 

o 

AG 

AG 

1  AG 

O 

O 

o 

o 

o 

O 

M.  pseudo-bronchialis  Cast. 

AC 

AG 

!  AG 

AG 

O 

AG 

o 

o 

o 

O 

M.  pseudo-guillermondi  Cast 

AC  or  I 

AG 

j  AG 

O 

O 

AG 

o 

o 

o 

O 

M.  pseudo-londinensis  Cast. 

o 

AG 

|  AG 

1  AG 

AG 

O 

o 

o 

o 

AG 

M.  pseudo-londinoides  Cast. 

AC 

AG 

AG 

AG 

AG 

O 

o 

o 

o 

AG 

M.  pseudo-metalondinensis 

AC 

AG 

;  AG 

AG 

AG 

O 

o 

o 

o 

O 

M.  pseudo-tropicalisCast.    .. 

ACs 

AG 

AG 

O 

AGs 

AG 

AG 

o 

o 

O 

M.  pulmonalis  Cast. 

<> 

Alk  1) 

AG 

AG 

AG 

AGs 

AG 

O 

Avs 

o 

O 

M.  rhoi  Cast. 

As 

Alk 

AG 

AG 

Avs 

AGs 

AG 

O 

O 

o 

O 

M.  rosea  Zenoni 

M.  tropicalis  Cast.    .  . 

A 

;  AG 

AG 

AG 

AGs 

ACs 

o 

O 

o 

o 

M.  zcylanica  Cast.    .  . 

ACs 

A 

1 

A 

A 

A     I     A 

j    As 

O 

o 

A 

IATIONS   used   in   the  Table.— A  =  acid  ;    G  =  gas;    C  =  clot  (milk),    clear  (broth   and   peptone   water) 
I    1  I'     clear  at  first,  then  thin  pellicle  present.       D  =  decolourized.       P  =  peptonized  (milk),   pellicle  (broth). 

Alk-alkaline.  ..,.  =  acid,  then  alkaline,        s  =  slight  ;  vs  =  very  slight. 


CHARACTERS  OF  CERTAIN  SPECIES  OF  MONILIA,  WITH  NAMES 
AFTER  FIFTEEN  DAYS'  INCUBATION  AT  350  C. 


1083 


Raf. 
finose. 

Ara- 
binose. 

Ado- 

nite. 

Inulin. 

1  Sor- 
bite. 

liroth. 

Pep- 
tone 
Water. 

Indol. 

Gram. 

Gela- 
tine. 

Serum. 

Neutral 
Red. 

Colour  of  Growth 
on  Glucose  Agar. 

0 

O 

O 

O 

O 

CTP 

C 

0  i 

+ 

0 

O 

0 

White 

0 

O 

O 

O 

O 

1    1  P 

c 

0 

+ 

+ 

+  s 

0 

White 

0 

OAs 

0 

O 

O 

GT 

c 

0 

+ 

0 

O 

0 

White 

As 

O 

0 

Avs 

O 

C 

c 

0 

+ 

0 

O 

0 

White 

O 

O 

0 

O 

O 

C 

c 

0 

+ 

0 

O 

0 

White 

O 

O 

0 

° 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

As 

O 

0 

AGs 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

O 

O 

0 

O 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

O 

O 

0 

O 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

0 

O 

0 

O 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

AGs 

O 

0 

O 

O 

CTP 

c 

0 

+ 

0 

O 

0 

Yellowish  or 
brownish 

O 

O 

0 

0 

O 

c 

c 

0 

+ 

0 

0 

0 

White 

O 

O 

0 

O 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

O 

O 

0 

O 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

O 

O 

0 

O 

O 

c 

c 

0 

+ 

0 

O 

— 

White 

AGs 

O 

0 

O 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

O 

O 

0 

AG 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

O 

O 

0 

O 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

0 

O 

0 

O 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

O 

O 

0 

O 

O 

c 

c 

0 

+ 

0 

O 

0 

White 

AGs 

O 

0 

O 

0 

c 

c 

0 

+ 

0 

O 

0 

White 

As 

O 

0 

O 

0 

CTP 

c 

0 

+ 

0 

O 

0 

White 

or  O 

AG 

O 

0 

O 

0 

c 

c 

0 

+ 

0 

O 

0 

White 

O 

O 

0 

O 

0 

c 

c 

0 

+ 

0 

O 

0 

White 

O 

O 

0 

AG 

0 

c 

c 

0 

+ 

+ 

O 

0 

White 

O 

O 

0 

O 

0 

CorP 

c 

0 

+ 

0 

0 

0 

White 

O 

O 

0 

O 

0 

CTP 

c 

0 

+ 

0 

0 

0 

White 

As 

O 

0 

Avs 

0 

C 

c 

0 

+ 

0 

0 

0 

White 

O 

O 

0 

O 

0 

C 

c 

0 

+ 

0 

0 

0 

White 

O 

O 

0 

O 

0 

C 

0 

0 

+ 

0 

0 

— 

White 

O 

O 

0 

O 

0 

C 

c 

0 

+ 

0 

0 

— 

White 

O 

O 

0 

O 

0 

C 

c 

0 

+ 

0 

0 

0 

White 

O 

O 

0 

O 

0 

C 

c 

0 

+ 

0 

0 

Q 

White 

0 

O 

0 

AG 

0 

C 

c 

0 

+ 

0 

0 

0 

White 

O 

O 

0 

O 

0 

C 

c 

0 

+ 

0 

0 

O 

White 

A 

AGs 

0 

O 

0 

CTP 

c 

0 

+ 

0 

0 

0 

White 

O 

O 

0 

O 

0 

c 

c 

0 

+ 

0 

0 

0 
0 

0 

White 
Pink 

0 

O 

0 

O 

0 

c 

c 

0 

+ 

0 

i  0 

0 

White 

Avs 

O 

0 

Avs 

0 

c 

c 

0 

+ 

0 

0 

0 

Yellowish 

Gvs 

1 

0  =  negative   result— viz.,  neither   acid    nor  clot   in   milk;    neither   acid    nor   gas  in  sugar   media;    non  production 

of  indol  ;    non-liquefaction  of  gelatine  or  serum,   as    the  case   may  be. 
+  =positive  result,  liquefaction  of  medium. 


1084  FUNGI  IMPERFECTI 

E.  Gas  produced  in  glucose,  levulose,  maltose,  galactose,  and  saccharose — 

Group    V.,    Tropicalis    group: — M.    tropicalis,    M.   paratropicalis, 
M.  pulmonalis,  M.  nivea,  M.  insolita,  M.  enterica. 

F.  Gas  produced  in  glucose,  levulose,  and  saccharose — Group  VI.,  Guiller- 

mondi group: — M .  guillermondi,  M .  pseudoguillermondi. 
H.  Gas  produced  in  glucose,  levulose,  galactose,  saccharose,  and  inulin— 

Group  VII.,   Chalmersi  group: — M.  chalmersi,   M.  parachalmersi. 

M.  macedoniensis. 
I.  Gas  produced  in  lactose  and  other  carbohydrates — Group  VIII.,  Pseudo- 

tropicalis  group  : — M.  pseudotropicalis. 
K.  Gas  produced  in  dextrin   in   addition  to  other   sugars — Group  IX., 

Pseudolondinensis  group: — M.  pseudolondinensis. 

A.  Species  believed  to  be  (etiological  factors  of  disease  in  man  : — 

I.  Species  found  in  thrush  and  allied  infections  : — 

1.  M.  albicans  (Robin,  1853). 

2.  M.  alba  (Castellani,  1911). 

3.  M.  londinensis  (Castellani,  19 16). 

4.  M.  metalondinensis  (Castellani,  1916). 

5.  M.  tropicalis  (Castellani,   1916),  and  most  of  those  found  in 

bronchomycosis. 
II.   Species  found  in  bronchomycosis  : — ■ 

6.  M.  tropicalis  (Castellani,  1909). 

III.  Species  found  in  otomycosis  : — 

7.  M.  rhoi  (Castellani,  1909). 

IV.  Species  found  in  pinta  : — ■ 

8.  M.  montoyai  Castellani,  1907. 

V.  Species  found  in  cases  of  generalized  moniliomycoses  : — 

9.  M.  rosea  (Zenoni,  1912). 

B.  Species  associated  with  a  disease  in  man  : — 

I.  Associated  with  bronchomycosis  : — ■  m 

(a)  By  their  presence  in  the  sputum  of  cases  of  bronchomycosis 

[in  alphabetical  order] : — 

1.  M.  guillermondi  (Castellani,  1910). 

2.  M.  krusei  (Castellani,  1909). 

3.  M.  negrii  (Castellani,  1910). 

4.  M.  nitida  (Castellani,  1910). 

5.  M.  parakrusei  (Castellani,  1916). 

6.  M.  paratropicalis  (Castellani,  1912). 

7.  M.  pinoyi  (Castellani,  1910). 

8.  M.  pseudo-tropicalis  (Castellani,  1910). 

(b)  By  their  presence  in  bronchitis  : — 

1.  M.  chalmersi  (Castellani,  191 2). 

2.  M.  parachalmersi  (Castellani,  1916). 

3.  M.  bethaliensis  (Pijper,   191 8). 

(c)  By  their  presence  in  human  sputum  : — 

1.  M.  balcanica  (Castellani,   1916). 

2.  M.  bronchialis  (Castellani,  1910). 

3.  M.  nabarroi  Castellani,  1917. 

4.  M.  nivea  (Castellani,  1910). 

5.  M.  parabalcanica  (Castellani,  1916). 

6.  M.  pseudo-guillermondi  (Castellani,  19 id). 

7.  M.  pseudo-londinensis  (Castellani,   19 16). 

8.  M.  pulmonalis  (Castellani,  1911). 

9.  M.  zeylanica  (Castellani,  1910). 

(d)  By  their  presence  in  tea-dust  : — - 

1.  M.  blanchardi  (Castellani,  1912). 

2.  M.  lustigi  (Castellani,  1912). 

3.  M.  perryi  (Castellani,  1912). 


MO  N I LI A  1085 

II.  Associated  with  sprue  : — 

1.  M.  decolorans  Castellani  and  Low,  191 3. 

2.  M.  enterica  Castellani,  191 1. 

3.  M.  faecalis  Castellani,  191 1. 

4.  M.  insolita  Castellani,  191 1. 

5.  M.  intestinalis  Castellani,  191 1. 

C.  Species  found  in  vaginal  discharge  in  the  tropics  and  in  Europe  : — 

1.  M.  balanica  (Castellani,  191 6). 

2.  M.  metalondinensis  (Castellani,  1916). 

3.  M.  naborroi  (Castellani,  19 17). 

4.  M.  parabalcanica  (Castellani,  1916). 

5.  M.  pinoyi  (Castellani,  19 10). 

6.  M.  tropicalis  (Castellani,  1909). 

D.  Species  found  in  man,  but  not  classified  : — 

1.  M.  lactea  Castellani,  1913. 

2.  M.  lacticolor  Castellani,  1913. 

A  brief  description  of  these  species  may  be  given. 

Monilia  albicans  Robin,  1853. 

Synonyms. — Oidium  albicans  Robin,  1853;  Syringosfiora  robini 
Ouinquaud,  1868;  Saccharomyces  albicans  Rees,  1877;  Monilia 
albicans  Zopf,  1890;  Endomyces  albicans  Vuillemin,  1898. 

One  of  the  fungi  giving  rise  to  thrush.  Widely  different  descrip- 
tions have  been  given  of  the  so-called  thrush-fungus.  Some  authori- 
ties (Hewett)  state  that  the  organism  liquefies  gelatine;  others  affirm 
the  reverse.  Several  writers  give  it  as  clotting  milk,  others  as 
having  no  action  on  this  medium.  Castellani  has  demonstrated 
that  man  can  be  affected  by  numerous  different  species  of  Monilia, 
and  that  the  term  thrush-fungus 
{Oidium  albicans,  Endomyces  albicans, 
Monilia  albicans)  has  been  in  the 
past  used  to  cover  a  number  of 
different  species,  in  the  same  manner 
that  the  term  B.  coli  was  for  years 
applied  to  a  multitude  of  different 
intestinal  bacteria,  when  a  few  fer- 
mentation tests  only  were  carried  FlG  567.— Monilia  albicans 
out.      As    the    species    M.   albicans  Robin. 

has  to  be  split  into  many  species, 

we  keep  the  term  M.  albicans  for  the  species  which  we  arc  now 
describing,  and  which  clots  milk  and  liquefies  gelatine. 

Parasitic  Life. — This  fungus  forms  white  patches  on  the  tongue  and 
oral  mucosa.  The  patches  are  easily  detached.  A  particle  of  the 
patch  examined  microscopically  shows  septate  mycelial  threads, 
occasionally  ramified,  with  segments  straight  or  somewhat  bent, 
and  easily  dissociated.  Each  segment  is  about  20  /.i  in  length 
and  3  to  5  ^  in  breadth.  At  the  terminal  end  of  each  mycelial  thread 
three  or  four  shorter  ovoid  elements  are  found,  which  reproduce  by 
budding.  Some  similar  ovoid  or  roundish  globular  refringent  cells 
may  be  observed  originating  laterally  at  the  septations  of  the  myce- 


io86 


FUNGI  IMPERFECTI 


Hum.     These  globular  elements   (conidia)   become  detached,    and 
reproduce  by  budding. 

Cultures. — The  fungus  grows  best  of  all  on  slightly  acid  Sabou- 
raud's  maltose  agar  or  on  glucose  agar,  but  grows  fairly  well  also 
on  all  alkaline  media.  In  cultures  the  fungus  appears  under  two 
forms — -a  globular  form  morphologically  similar  to  a  typical  yeast, 
and  reproducing  by  budding;  a  filamentous  form,  showing  mycelial 
threads,  simple  or  ramified.  Asci  and  internal  spores,  as  in  the 
genus  Endomyces,  are  absent.  On  Sabouraud's  and  glucose  agar 
the  growth  is  abundant,  smooth,  of  a 
creamy- white  colour;  on  ordinary  agar  the 
growth  is  less  abundant.  Gelatine  and 
serum  are  very  slowly  liquefied.  Milk  is 
rendered  acid,  and  after  a  time  it  clots. 
The  sugar  reactions  are  given  in  the  table. 

Pathogenicity.— M.  albicans  is  one  of  the 
fungi  which  gives  rise  to  thrush.  This 
condition  may  be  due  to  several  different 
fungi — M.  albicans,  Endomyces  vuilletnini, 
M.  tropicalis,  etc.  (p.  1741) .  Thrush  is  gene- 
rally restricted  to  the  oral  mucosa,  but  in  cer- 
tain cases  it  may  spread  to  the  oesophagus, 
stomach,  intestine.  M.  albicans  has  been 
found  also  in  a  few  cases  of  bronchomycosis. 

Monilia  tropicalis  (Castellani,  1909). 

Synonym. — Endomyces  tropicalis  Castel- 
lani, 1909. 

Found  by  Castellani  in  Ceylon  in  many 
cases  of  bronchomycosis.    In  the  expectora- 
tion  round   or   oval  shape   yeast-like  cells 
are  seen,  and  at  times  segments  of  myce- 
lium.     Cultures     are    easily    obtained    on 
Sabouraud's    or    glucose    agar,    and    even 
on  ordinary  agar.     It  grows  more  abund- 
antly on   slightly    acid    than    on    alkaline 
media.    On  Sabouraud's  and  glucose  agar 
the  growth  is  abundant,  creamy  white,  with 
a    smooth     surface    when    3^oung;    often 
slightty  crinkled    when  old.     The  growth  is  composed  practically 
of  only  globular  yeast-like  cells,  while  in  the  water  of  condensa- 
tion globular  cells  and  mycelium  may  be  found  together.     A  little 
mycelium  may  be  found,  however,  occasionally  in  the  growth  on 
the    slope.     Ascus   formations   are   absent.     Gelatine   and   serum 
are  not  liquefied;    there  is  no  brownish  discoloration  of  the  serum, 
as  is  the  case  with  some  other  species  of  Monilia  (M.  insolita,  etc.). 
Litmus  milk  is  generally  rendered  acid,  but  is  not  clotted.     The 
sugar  reactions  will  be  found  in  the  table  on  pp.  1082,  1683.     It 
produces  acid  and  gas  in  glucose,  levulose,  maltose,  and  also,  in  less 


Fig.  568. — Monilia  tropi- 
calis Castellani. 


MONILIA  1087 

amount,  in  galactose  and  saccharose.     After  some  transplantations 
it  often  loses  its  fermentative  power  on  galactose  and  saccharose. 

Pathogenicity.— Is  the  commonest  cause  of  a  type  of  bronchomy- 
cosis  (see  Bronchomoniliasis,  p.  1886).  In  Ceylon  it  has  been  found 
by  Castellani  also  in  a  few  cases  of  thrush,  and  in  a  case  of  pseudo- 
diphtheria  which  terminated  fatally.  This  case  was  a  little  native  girl, 
who  developed  white  patches  on  the  tonsils,  uvula,  and  soft  palate. 
The  microscopical  examination  revealed  absence  of  B.  diphtheria  and 
presence  of  M .  tropicalis.  Symptoms  of  broncho-pneumonia  soon 
developed,  and  the  child  died.  At  the  autopsy  the  fungus  was  found 
in  enormous  amount  in  the  bronchi;  it  was  pathogenic  for  guinea-pigs. 

Monilia  paratropicalis  (Castellani,  1909). 

Synonym. — Endomyces  paratropicalis  Castellani,  1910. 

Found  in  some  cases  of  bronchomycosis  by  Castellani.  Micro- 
scopically and  on  Sabouraud's  and  glucose  agars  identical  with  M. 
tropicalis.  Does  not  coagulate  milk.  Differs  from  the  typical 
M.  tropicalis  by  producing  acid  and  gas  in  very  large  amount  in 
saccharose  and  in  rendering  dextrin  acid  (see  table). 

The  same  fungus,  or  a  very  similar  one,  was  found  in  two  cases 
of  blastomycosis  of  the  skin  in  Ceylon. 

Monilia  pseudo-tropicalis  (Castellani,  1910). 

Synonym. — -Endomyces  pseudo-tropicalis  Castellani,  1910. 

Found  by  Castellani  in  a  few  cases  of  bronchomycosis.  Differs 
from  M .  tropicalis  and  M.  paratropicalis  by  clotting  milk  and  fer- 
menting lactose  with  the  production  of  gas.  For  the  sugar  re- 
actions see  table. 

Monilia  metatropicalis  Castellani,  1916. 
Differs  from  M.  tropicalis  in  clotting  milk 

Monilia  bronchialis  (Castellani,  1910). 

Synonym. — Endomyces  bronchialis  Castellani,  1910. 
Found  in  sputum.     Colonies  white.     Has   no   action   on   milk, 
gelatine,  serum.     Sugar  reactions  are  found  in  the  table. 

Monilia  chalmersi  Castellani,  1912. 

Found  by  Castellani  in  a  case  of  bronchitis.  Colonies  of  white 
colour.  Renders  the  milk  first  slightly  acid,  then  alkaline.  Does 
not  liquefy  either  gelatine  or  serum.  Sugar  reactions  are  collected 
in  the  table. 

Monilia  parachalmersi  (Castellani,  1917). 
Differs   from  M.  chalmersi  in  slowly  liquefying  gelatine  and  in 
other  minor  characters.    Found  in  sputum. 

Monilia  macedoniensis  Castellani,  1917. 
Found  in  sputum.     Clots  milk.    Belongs  to  the  Chalmersi  group. 


1088  FUNGI  IMPERFECTI 

Monilia  guillermondi  (Castellani,  1910). 

Synonym. — Endomyces  guillermondi  Castellani,  1910. 

Observed  in  sputum  once  by  Castellani.  Milk  is  rendered 
alkaline.  Serum  and  gelatine  are  not  liquefied.  For  sugar  re- 
actions see  table. 

Monilia  pseudo-guillermondi  Castellani,  1916. 

Clots  milk. 

Monilia  nivea  (Castellani,  1910). 

Synonym. — Endomyces  niveus  Castellani. 

Found  in  a  sample  of  sputum  which  had  not  been  collected  in  a 
sterile  vessel.  Of  doubtful  pathogenicity.  For  cultural  and  bio- 
chemical characters  see  table. 

Monilia  nitida  (Castellani,  1910). 

Synonym.— Endomyces  nitidus  Castellani,  1910. 

Observed  in  a  sample  of  sputum  by  Castellani.  Of  doubtful 
pathogenicity.  Milk  is  rendered  first  acid,  then  decolourized  and 
clotted.     Other  cultural  characters  are  found  in  the  table. 

Monilia  zeylanica  (Castellani,  1910). 

Synonym. — -Endomyces  zeylanicus  Castellani,  191 0. 

Found  in  sputum  by  Castellani.  Growth  on  glucose  agar  of  a 
yellowish  colour.  Milk  is  rendered  very  acid  and  is  slowly  clotted. 
Gelatine  and  serum  are  not  liquefied.  Does  not  produce  gas  in 
any  carbohydrate,  with  the  doubtful  exception  of  raffinose. 

Monilia  krusei  (Castellani,  1909). 

Synonyms. — Saccharomyces  krusei  Castellani,  Endomyces  krusei 
Castellani. 

Found  in  sputum  by  Castellani.  In  sputum  it  appeared  as  a 
saccharomyces,  and  in  cultures  had  all  the  characters  of  a  saccharo- 
myces at  first,  except  that  no  asci  were  observed;  after  several 
generations  a  little  mycelium  was  present  on  Sabouraud's  agar. 
The  sugar  reactions  are  found  in  the  table.  It  produces  acid  and 
gas  in  glucose  and  levulose.     Its  reactions  remain  constant  after 

Monilia  pinoyi  (Castellani,  1910). 

Synonym. — Endomyces  pinoyi  Castellani,  1910. 

Found  in  sputum.  Grows  well  on  Sabouraud's  and  glucose  agar, 
and  other  sugar  media;  also  on  ordinary  agar,  though  less  abun- 
dantly. Does  not  clot  milk;  does  not  liquefy  either  gelatine  or 
serum.     Produces  acid  and  gas  in  glucose,  levulose,  maltose. 

Monilia  enterica  (Castellani,  1911). 

Synonyms. — Endomyces  entericus  Castellani;  Monilia  psilosis 
Ashford ;  Parasaccharomyces  ashfordi  Anderson,  1916. 

Found  in  stools  by  Castellani.  Milk  is  rendered  alkaline. 
Gelatine  and  serum  are  not  liquefied.     For  sugar  reactions  see  table. 


MONILIA  1089 

Monilia  faeealis  (Castellani,  1911). 

Synonym.— Endomyces  fcecalis  Castellani,  1911. 

Found  in  intestinal  contents  by  Castellani.  Milk  is  rendered 
first  acid,  then  decolourized,  and,  later,  slightly  peptonized.  Gela- 
tine is  not  liquefied ;  serum  is  not  liquefied,  but  a  brownish  pigmenta- 
tion develops  on  the  medium  all  round  the  growth.  For  sugar  re- 
actions see  the  table  (p.  1082). 

Monilia  insolita  (Castellani,  1911). 

Synonym. — Endomyces  insolitus  Castellani,  1911. 

Found  in  stools  and  in  the  saliva.  The  milk  is  rendered  first 
slightly  acid,  then  alkaline.  On  serum  a  zone  of  dark  pigmentation 
develops  on  the  surface  of  the  medium  round  the  growth.  The 
medium  is  not  liquefied.  For  other  cultural  characters  see  the 
table. 

Monilia  intestinalis  (Castellani,  1911). 

Synonym.— Endomyces  intestinalis  Castellani,  1911. 

Found  in  stools  and  saliva  by  Castellani.  Colonies  on  solid 
media  white.  Milk  first  rendered  acid,  then  slowly  decolourized. 
The  growth  on  serum  is  not  surrounded  by  a  zone  of  dark  pigmenta- 
tion.    Further  cultural  characters  are  found  in  the  table  (p.  1082). 

Monilia  alba  (Castellani,  1911). 

Clots  milk.  Produces  acid  and  gas  in  glucose,  levulose,  maltose, 
galactose,  and  acid  only  in  saccharose.  Does  not  liquefy  gelatine 
or  serum. 

Monilia  rhoi  (Castellani,  1909). 

Synonym. — Endomyces  rhoi  Castellani,  1909. 
Found  by  Castellani  in  Ceylon  in  several  cases  of  otomycosis, 
and  once  in  a  sample  of  tea.     In  the  ear  the  fungus  forms  a  whitish 


Fig.  569. — Monilia  rhoi  Castellani. 
(From  a  fresh  preparation.     The  free  spores  are  not  shown.) 

69 


io9o  FUNGI  IMPERFECT  I 

mass  (generally  embedded  in  wax),  in  which  numerous  long,  septate 
mycelial  threads,  2  to  3-5  yt,  in  breadth,  and  numerous  roundish 
free  spores,  3-5  to  5  jj,  in  diameter,  are  seen.  On  laboratory  media 
it  generally  grows,  showing  a  yeast-like  type.  Does  not  clot  milk; 
does  not  liquefy  gelatine  and  serum.  The  sugar  reactions  are  quoted 
in  the  table  (p.  1082). 

In  the  cases  of  otomycosis  the  mycelium  was  abundant,  the 
mycelial  threads  being  very  long  and  septate,  3  to  4  ^  in  breadth; 
very  numerous  free,  round  spores,  4  to  5  p  in  diameter,  were  present. 
For  cultural  characters  see  table. 

Monilia  burgessi  (Castellani,  1912). 

Synonym.- — Endomyces  burgessi  Castellani,  191 1. 

Isolated  from  the  air.  Grows  abundantly  on  the  usual  sugar 
media,  the  growth  being  of  a  white  creamy  appearance.  Does  not 
render  acid  or  coagulate  milk.  Does  not  liquefy  serum  or  gelatine. 
On  serum  it  produces  a  zone  of  peculiar  brownish  or  black  dis- 
coloration in  the  medium  all  round  the  growth.  The  sugar  re- 
actions are  found  in  the  table. 

Monilia  pulmonalis  Castellani,  191 1. 

Found  by  Castellani  in  sputum  and  also  in  samples  of  tea.  For 
cultural  characters  see  table  (p.  k  82). 

Monilia  lustigi  Castellani,  1912. 

Found  in  samples  of  tea.  Grows  well  on  all  sugar  media  and 
also  on  ordinary  agar,  the  growth  being  of  a  snow-white  colour. 
Renders  litmus  milk  slightly  acid,  and  then  decolourizes  it  com- 
p'etely.  Does  not  liquefy  serum  or  gelatine.  On  serum  it  induces 
a  narrow  zone  of  black  discoloration  all  round  the  growth.  The 
sugar  reactions  are  found  in  the  table  (p.  1082) . 

Monilia  balcanica  Castellani,  1916. 

Found  in  sputum  and  also  in  a  case  of  dermatitis,  of  which  it  was 
not  the  cause.  Produces  gas  in  glucose  only.  Levulose  often 
rendered  acid  (see  table). 

Monilia  parabalcanica  Castellani,  1916. 
Differs  from  M.  balcanica  in  clotting  milk. 

Monilia  perryi  Castellani,  1912. 

Found  by  Castellani  in  samples  of  tea-dust.  The  cultural 
characters  and  chemical  properties  are  seen  in  the  table. 

Monilia  nabarroi  Castellani,  1917. 

Clots  milk  and  produces  gas  in  glucose,  levulose,  and  maltose. 
Found  in  sputum.  An  identical  or  very  similar  variety  has  been 
found  in  vaginal  mucus  by  Castellani  and  Taylor. 


MONILIA  1091 

Monilia  blanchardi  (Castellani,  1912). 

Synonym.— Endomyces  blanchardi  Castellani,  1912. 

Isolated  from  tea-dust  by  Castellani.  Grows  abundantly  on 
maltose,  glucose,  and  other  sugar  media;  also  on  ordinary  agar, 
though  less  vigorously.  The  growth  is  of  a  white  co  our  and 
smooth  surface.  Milk  rendered  at  first  very  slightly  acid,  and  then 
alkaline.  No  liquefaction  of  gelatine  or  serum.  Does  not  produce 
gas  in  any  sugar  except,  in  small  quantity,  in  glucose. 

Monilia  bethaliensis  Pijper,  1918. 

Found  by  Pijper  in  a  case  of  bronchitis.  Ferments  glucose  and 
maltose  with  production  of  gas.  Action  on  levulose  not  known. 
Gelatine  not  liquefied,  milk  not  clotted. 

Monilia  rosea  (Zenoni,  1912). 

Synonym. — Cidium  roseum  non  liquefaciens  Zenoni,  1912. 

The  cultures  on  Sabouraud's  and  other  sugar  media  are  of  a  pinkish  colour. 
Neither  serum  nor  gelatine  are  liquefied. 

Pathogenicity. — Was  isolated  by  Zenoni  in  a  peculiar  case  of  hepatitis  with 
fever  and  jaundice  which  ended  fatally.  Microscopically  conidia  and  myce- 
lial filaments  could  be  seen  very  abundant  in  and  about  the  smaller  hepatic 
bloodvessels  and  the  bile-ducts.  The  fungus  is  pathogenic  to  rabbits,  guinea- 
pigs,  and  white  rats. 

Monilia  subtilis  (Blanchard,  1895). 

Synonyms. — -'idium  subtile  cutis  Babes,  1895;  Mycoderma  subtile  Verdun, 
1912. 

Found  by  Babes  in  some  ulcers  on  which,  the  fungus  produced  white  mem- 
branes. The  mycelial  threads  were  thinner  than  in  most  species  of  Monilia. 
There  was  dichotomous  branching,  and  at  the  extremities  of  the  mycelial 
threads  ovoid  conidia  were  present.  Biochemical  properties  of  the  fungus 
not  known.     Pathogenic  for  the  rabbit. 

The  same,  or  a  very  similar,  fungus  was  later  found  by  Clozel,  de  Boyer, 
and  d'Antin  in  a  peculiar  pustular  affection  observed  in  cachectic  children. 

Monilia  pulmonea  (Bennett,  1842). 

Synonyms.— Cidium  pulmoneum  Bennett,  1842;  Obspora  pulmonea  Sac- 
cardo,  1886;  Mycoderma  pulmoneum  Vuillemin,  1891. 

The  organism  was  found  in  a  case  of  pneumothorax  by  Bennett  in  1842, 
it  was  observed  again  by  Vuillemin  in  the  sputum  of  a  tubercular  patient  in 
1891,  and  in  an  ulcerative  dermatitis  by  Balzer,  Burnier,  and  Gougerot  in 
1910.  It  grows  under  two  types — a  saccharomyces-like  and  a  filamentous 
type.     Colonies  on  glucose  agar  white.     Biochemical  reactions  not  given. 

Monilia  Candida  (Bonorden,   1851). 

Synonym. — M.  bonordeni  Vuillemin. 

Commonly  found  vegetating  in  decomposing  vegetable  matter;  occasionally 
seen  parasitic  in  Mammalia,  giving  rise  to  white  patches  on  the  tongue  and 
buccal  mucosa,  somewhat  similar  to  human  thrush.  Once  found  in  a  child  in 
some  white  patches  present  on  the  tongue.  Mycelium  elements  easily  disso- 
ciated. Yeast-like  conidial  elements.  Pellicles  in  fluid  sugar  media.  Ferments 
glucose  and  saccharose,  and,  according  to  Bau,  dextrin.  Its  action  on  other 
carbohydrates  and  gelatine  has  not  been  recorded.  Mycelial  tubes  thinner 
than  in  most  Monilias  (1  to  i£  /x  in  breadth) ;  conidia  roundish,  smooth,  7  to  8  fx 
in  diameter.  Biochemical  actions  of  the  fungus  have  not  yet  been  investigated 
completely.     Found  in  cow-dung,  on  which  it  forms  white  membranes. 


1092 


FUNGI  IMPERFECTI 


Monilia  kochi  (von  Wettstein,   1885). 

Synonym. —  Rhodomyces  erubescens  Aster,  1900. 

Morphologically  similar  to  M.  Candida  ;  grows  well  on  sugar  media,  where 
it  produces  pinkish  colonies;  was  observed  by  Wettstein  in  a  case  of  chronic 
acid  dyspepsia.     Biochemical  properties  not  studied. 

Monilia  montoyai  (Castellani,  1907). 

Synonym. — Monilia  pictor  Neveu-Lemaire,  1908. 

Discovered  by  Montoya  in  cases  of  white  pinta.  Some  fertile  hyphse  are 
much   thicker   than  others;  the  spores  are  large,   globular  (5  to  7  fj,),  and 

contain    a    large     nucleus.      Grows 
*jSr'  well  on  sugar  media,  giving  rise  to 

white  creamy  colonies  which  rapidly 
fuse  together.  Biochemical  proper- 
ties of  the  fungus  not  known. 

Monilia  cutanea  (de  Beurmann,  Gou- 
gerot,  and  Vaucher,  1909). 

Synonyms. — Oidium  cutaneum  de 
Beurmann,  Gougerot,  and  Vaucher, 
1909;  Mycoderma  cutaneum  Verdun, 
1912. 

Isolated  by  de  Beurmann,  Gou- 
gerot, and  Vaucher  from  a  case 
showing  a  peculiar  gummatous  con- 
dition clinically  resembling  sporotri- 
chosis or  syphilis.  The  fungus,  on 
certain  media  (glycerine  agar),  vege- 
tates as  a  saccharomyces  and  ferments  glucose ;  on  other  media  (agar)  myce- 
lium and  yeast-like  cells  are  present,  and  the  fungus  does  not  ferment  glucose 
any  longer.  On  glucose  agar  the  growth  is  white-yellowish,  mammillary, 
with  a  radiating  aureola.  The  fungus,  unless  injected  in  massive  doses,  is 
not  very  pathogenic  to  the  rabbit,  guinea-pig,  and  rat.  Intraperitoneal 
injections  of  rather  large  doses  induce  in  these  animals  a  nodular  peritonitis. 

Monilia  caoi  Verdun,   19 12. 
Found  by  Gao  in  the  sputum  of  a  tubercular  patient  in  association  with 
the  tubercular  bacillus.     Yellowish  colonies  on  ordinary  agar.     Pathogenic 
to  rabbits.     Biochemical  reactions  not  given. 

Monilia  harteri  Verdun,   1912. 

Synonym. — Parasaccharomyces  sp.  (?)  de  Beurmann  and  Gougerot. 

Found  by  Harter  in  a  case  of  enteritis  which  later  developed  hepatic, 
bronchial,  and  cutaneous  lesions,  due  to  the  same  fungus.  On  maltose  agar 
and  carrots  the  colonies  are  cream-white,  and  yeast-like  cells  only  are  generally 
found.  In  Raulin's  liquid  mycelial  threads  are  present,  septated,  2  /x  in 
breadth.  The  fungus  does  not  liquefy  gelatine,  does  not  coagulate  milk; 
produces  slight  acidity,  but  not  gas,  in  saccharose. 

Monilia  perieri  Matruchot  and  Antoine,  1917. 
Synonym. — Obspora  perieri  Matruchot  and  Antoine. 


Fig.  570. — Monilia  montoyai. 
(After  Montoya  y  Florez.) 


Found  in  a  case  of  thrush  of  a  wound, 
given. 


Biochemical  reactions  not 


Monilia  parakrusei  Castellani,  1912. 

Differs  from  M.  krusei  in  clotting  milk.     Found  by  Castellani  in 
sputum. 


OTDIUM 


1093 


Genus  Oidium  Link,  1809,  emendavit  Pinoy. 

Definition.— Oosporaceae  with  hyphge  terminating  in  chains  of 
spores.  Hyphse  long  and  branched.  Sporophores  simple,  septate, 
often  without  disjunction  apparatus.  Do  not  produce  gas  in  carbo- 
hydrates. 

Type  Species. — Oidium  lactis  Link,  1809. 

Remarks.— Pinoy  has  adjusted  this  genus,  so  that  now  it  contains 
human  parasites,  which  are: — - 

Oidium  lactis  Link,  1809. 
Oidium  rotundatum  Castellani,  1911. 
Oidium  asteroldes  Castellani,  1914. 
Oidium  matalense  Castellani,  1915. 

These  fungi  may  be  differentiated  as  follows  :— 

A.  Only  produces  slight  acidity,  and  only  at  times,  in  glucose;  cultures 

white — Lactis. 

B.  Produce  acidity  in  several  carbohydrates: — 

I.  No  acidity  in  glucose;  culture  white  and  hairy — Matalense. 
II.  Acidity  in  glucose: — ■ 

(a)  No  acidity  in  mannitol: — 

Mycelial  spores,  roundish  or  oval.     Typical  colonies  con- 
voluted— -Rotundatum. 

(b)  Acidity  in  mannitol : — 

Mycelial  spores,   quadrangular.     Typical  colonies  asteroid 
— Asteroides. 


Fig.  571. — Oidium  rotundatum 
Castellani.  Fresh  Pre- 
paration. 


Fig.  572.  —  Oidium  asteroides 
Castellani.  Fresh  Prepara- 
tion. 


Oidium  lactis  Link,  1809. 

Definition. — Oidium  found  in  milk,  in  which  it  produces  acid  and 
clot.  Grows  easily  on  ordinary  culture  media,  producing  white 
colonies.  It  does  not  form  gas  in  carbohydrate  media,  and  only 
slight  acidity  at  times  in  glucose. 


1094 


FUNGI  IMPERFECTI 


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OIDIUM 


1095 


Remarks.— It  was  found  by  Link  in  milk  and  recently  by 
Linossier  in  cases  of  bronchitis.  The  latter  was  considered  to  be 
slightly  different  and  to  form  a  pathogenic  race,  Oidiuni  lactis 
var.  A. 

Oidium  rotundatum  Castellani,  1911. 

Definition. — -Oidium  growing  on  glucose  agar  and  producing 
crinkled  or  vermiform  yellowish  growths.  It  gives  rise  to  acidity 
in  milk,  and  after  a  variable  time  may  form  a  clot.     Gelatine  is 


Fig.  573.  Fig.  574. 

Figs.  573  and   574. — Oidium  rotun- 
datum Castellani.     Culture. 


Fig.    575. — Oidium   asteroides 
Castella.ni.     Culture. 


liquefied,  but  liquefaction  may  be  extremely  slow  or  absent  with 
certain  strains.  For  the  sugar  reactions  see  the  table  (p.  1094).  It 
forms  acid  in  glucose,  levulose,  galactose,  maltose,  and  lactose. 

Remarks. — Found  in  cases  of  bronchitis  and  a  very  similar  or 
identical  form  in  the  faeces  of  cases  of  sprue  and  of  enteritis. 

Oidium  asteroides  Castellani,  1914. 
Definition.— Oidium  producing  colonies  with  a  characteristic 
radiating  appearance  on  glucose  agar,  from  which  it  derives  its 
name.  It  grows  badly  or  not  at  all  upon  inspissated  blood  serum, 
which  it  does  not  liquefy.  It  turns  milk  acid  and  clots  it  in  a 
variable  time.     No  gas  is  formed  in  any  carbohydrate  medium. 


1096 


FUNGI  IMPERFECT  I 


Remarks. — This  fungus  was  isolated  from  stools  in  cases  of  sprue 
and  from  the  sputum  in  cases  of  chronic  bronchitis. 

Oidium  matalense  Castellani,  1915. 

Definition.— Oidium  producing  a  white  growth 
on  glucose  agar.  It  turns  milk  sometimes  slightly 
acid,  without  the  formation  of  a  clot,  or  it  may 
have  no  effect.  Gelatine  is  not  liquefied,  nor  is 
any  gas  produced  in  carbohydrate  media. 

Family  3:  Enantiothamnace^e  Chalmers 
and  Archibald,  19 15. 

Definition. — -Blastosporinese  with  a  thallus 
composed  of  ramifying  hyphae,  with  regular  septa, 
which  easily  disappear,  thus  dissociating  the  seg- 
ments, which  are  2-2-5  microns  broad.  The 
conidia  are  arranged  verticillately  around  the 
septa. 

Remarks.— This  family  contains  only  one  genus, 
Enantiothamnus  Pinoy,  1911.  The  name  is  derived 
from  evavrios,  '  opposite/  and  ddfxvos,  '  a  shrub.' 

Genus  Enantiothamnus  Pinoy,  191 1. 

Definition. — Enantiothamnaceae  with  the  char- 
acters of  the  family. 

Remarks. — There  is  only  one  species  so  far 
known,  Enantiothamnus  braulti  Pinoy,  1911. 

Enantiothamnus  braulti  Pinoy, 
1911. 

Definition. — Enantiothamnus  with  oval 
conidia  2-2-5  by  1-1*5  microns. 

Habitat.— Parasitic  in  man. 

Remarks. — This  fungus  was  discovered 
by  Brault  in  umbilicated  tumours  con- 
taining pus,  in  the  gluteal  region  of  an 
Arab  in  Algiers. 

On  Sabouraud's  agar  the  colonies 
are  white,  with  a  yellowish  central 
portion. 

Pathogenicity. — Produces  tumours  and 
pus  in  man,  and  is  pathogenic  for 
guinea-pigs. 

Family  4:  HAPLOGRAPHiACEiE  Saccardo,  1896. 

Definition. — Blastosporineae  with  hypha?  manifest  and  distinct 
from  the  conidia,  which  are  usually  arranged  in  chains,  or,  in  para- 
sitic condition  in  man,  in  grape-like  masses. 


Fig.  576. — Oidium 
matalense  Cas- 
tellani. Cul- 
ture. 


Fig.   577. — Enantiothamnus 

braulti  Pinoy. 

(After  Brault  and  Pinoy.) 


HORMODENDRUM  1097 

Remarks.— This  family  contains  the  genera  Hormodendrum 
Bonorden,  1851,  and  Malassezia  Baillon,  1889,  which  are  recogniz- 
able as  follows  :— 

All  sterile  hyphae  creeping.     Conidia  all  alike  and  produced  on  the  hyphae. 
Conidiophores  not  spirally  twisted;  hyphae  dendroid: — 

A.  Conidia  in  cultures  in  chains,  in  parasitic  form  in  masses — Genus 

Hormodendrum  Bonorden,  1851. 

B.  Conidia  in  parasitic  form  in  masses.     Cultural  form  unknown — 

Genus  Malassezia  Baillon,  1889. 

Genus  Hormodendrum  Bonorden,  1851. 

Definition. — Haplographiaceae  with  creeping  dendroid  sterile 
hyphae  and  branched  conidiophores,  bearing  conidia  all  of  one  kind. 

Remarks. — The  genus  Hormodendrum  contains  about  ten 
species,  which  are  generally  parasitic  on  plants'or  saprophytic,  but 
one  is  known  to  occur  in  man- — viz.,  H.  fontoynonti. 

Type  Species. — Hormodendrum  olivaceum  (Corda,  1838).  The 
name  is  derived  from  <V>i"-os\  'a  chain,'  and  Serfyos  (or  SevSpov),  'a 
tree.' 

Hormodendrum  fontoynonti  Langeron,  1913. 

Definition. — Hormodendrum  in  cultures  with  sterile  hyphae  3  to 
8  microns  in  diameter,  greenish  brown  in  colour,  septate  with  thick 
walls.  Sporophores  well  defined,  not  swollen  at  the  extremity, 
carrying  chains  of  very  caducous  spores.  In  man  mycelium  broken 
in  segments,  long  and  undulating;  spores,  which  are  capable  of 
budding,  arranged  in  masses. 

Remarks.— Found  by  Fontoynont  and  Carougeau  in  the  scales  of 
a  dermatosis,  called '  hodi-potsy '  in  Madagascar,  which  is  comparable 
to  that  termed  'tinea  rtava'  in  other  tropical  countries.  It  is 
doubtful  whether  the  fungus  is  the  aetiological  agent  of  the 
condition. 

Genus  Malassezia  Baillon,  1889. 

Definition. — In  man  mycelium  broken  into  septate  segments, 
with  T-shaped  or  budding  extremities.  The  hyphae  carry  round  or 
oval  conidia,  which  may  be  solitary  or  in  grape-like  masses,  and 
may  be  smooth  or  with  longitudinal,  radial,  or  spiral  marks.  In 
culture  unknown. 

Remarks.— This  genus  is  only  known  to  contain  parasites  of  man. 
The  two  species  may  be  recognized  as  follows : — ■ 

I.  Causing  a  brown  eruption  on  the  white  skin— i.e.,  tinea 
versicolor.  Lesions  very  superficial  -Species  Malas- 
sezia furfur  Charles  Robin,  1853. 
1 1 .  Causing  a  red  eruption  on  the  white  skin  and  a  yellowerup- 
tion  on  the  dark  skin— i.e.,  tinea  flava.  Deeper  lesions — 
Species  Malassezia  tropica  (Castellani,  1905). 


iog8 


FUNGI  IMPERFECTI 


Fig.  578. — Malassezia  tropica  Castkllani. 
(From  a  fresh  preparation  in  liquor  potassa1.     Old  case. 


Fig.  579. — Cladosporium  mansoni  Castellani. 

(From  a  fresh  preparation  in  liquor  potassae.     The   mycelial   tubes    are   in 
reality  not  so  regular  in  outline  as  in  this  drawing.) 


MALASSEZIA   FURFUR 


Malassezia  furfur  Ch.  Robin,  1853. 

Synonyms. — -Microsporon  furfur  Ch.  Robin,  1853;  Sporotrichum 
furfur  Saccardo,  1S86;  Malassezia  furfur  Baillon,  1889;  Oidium 
furfur  Zopf,  1890;  0.  subtile  Kotliar,  1892. 

Mycelium  abundant,  septate,  non-ramified ;  some  mycelial  threads 
are  much  larger  than  others;  the  breadth  varies  between  3  and  4  jjl. 
The  spores  are  roundish  (3  to  5  pt  in  diameter),  and  run  into  clusters. 

Attempts  at  cultivation  have  failed.  It  is  the  cause  of  pityriasis 
versicolor. 

Malassezia  tropica  Castellani,   1905. 

Synonym. — Microsporon  tropicum  Castellani,  1905. 
Mycelial  threads  generally  thick  (3  to  5  pi  wide),  with  numerous 
swellings,  constrictions,  and  other  irregularities  of  shape;  spores 
's\<a  roundish  (4  to  5  pi),  with  a  double 

*^l  contour;    are    often    collected    in 

clusters.      The    fungus    does   not 
^>v  grow   on    artificial    media.     It   is 

b  ©  ^^  the  cause  of  tinea  flava  or  pity- 

riasis flava  of  tropical  climates. 


% 


Fig.   580. — Cladosporiwn  mansoni  Fig.    581. — -  Claiosporium    mansoni 

Castellani.  Castellani.    Hanging-drop  Cul- 

(From  a  preparation  stained  by  ture. 
fuchsin.) 

Family  5 :  CLADOSPORiACEiE  Saccardo,  1886. 

Definition. — Blastosporales  with  hypha?  manifest  and  distinct  from 
the  conidia,  which  are  either  solitary  or  arranged  in  short  chains. 

Remarks. — We  are  only  concerned  with  the  type  genus  Clado- 
sporium  Link,  which  may  be  recognized  as  follows: — 

Conidia  smooth,  not  capitate,  more  or  less  in  chains  at  first.  Hyphae 
and  conidia  uniform.  Hyphae  not  inflated,  but  decumbent;  conidia 
in  short  chains  and  finally  solitary — Genus  Cladosporium  Link.  1809 


FUNGI  IMPERFECT  I 


Genus  Cladosporium  Link,  1816. 

Definition. — Cladosporiaceae  with  decumbent  hyphse.  Conidio- 
phores  bearing  smooth,  uniform  conidia  arranged  in  short  chains  or 
solitary. 

Etymology. — -The  name  is  derived  from  k\o.8os,  '  a  young 
shoot.' 

Remarks.— The  type  species  is  Cladosporium  herbarium  Persoon, 
1801,  and  there  are  a  very  large  number  of  species  scattered  all  over 
the  world,  and  commonly  found  on  plants  in  tropical  gardens,  from 
whence  the  spores  can  easily  be  conveyed  to  the  human  skin,  and 
either  grow  there,  causing  a  lesion,  or  simply  remain  sheltered  among 
the  scales  of  other  lesions,  from  which  they  may  be  grown  in 
pure  culture,  thus  giving  rise  to  the  impression  that  they  may  be 
causal  organisms,  but  they  do  not  agglutinate  with  the  patient's 
serum. 

They  may  also  grow  as  contaminations  of  laboratory  media,  so 
commonly  may  their  spores  be  found  in  the  air.  The  two  species 
known  in  man  may  be  recognized  as  follows : — 

Habitat,  tinea  nigra — -Species  Cladosporium 
mansoni  (Castellani,  1908). 

Habitat,  ulcerating  nodules — -Species  Clado- 
sporium penicilloides  Gueguen,  1911. 

Cladosporium  mansoni  Castellani,  1905. 

Synonyms. — Microsporon  mansoni  Castellani, 
1905;  Foxia  mansoni  Castellani,  1908;  Clado- 
sporium mansoni  Pinoy,  1912. 

The  fungus  is  found  very  abundantly  in  the 
lesions  of  tinea  nigra;  the  mycelial  articles  are 
rather  short — 18  to  20  n  in  length  and  2.\  to 
3^  pi  in  breadth;  non-ramified.  Sometimes  they 
may  be  irregular  in  outline,  bent,  banana- 
shaped.  The  spores  are  globular,  and  most  of 
them  very  large — 5  to  10  pi.  They  are  fre- 
quently arranged  in  clusters. 

The    fungus    is    easily    cultivated    by  inoculating 

scrapings  of   the  affected   patches   on   maltose   agar. 

After  two  to  four  days  roundish  hemispheric  colonies 

appear,   which  are  black,  but  at  first   have  usually  a 

FlG.  582.     Clidospo-     greenish  tinge,  and  may  present  at  the  periphery  some 

r  turn  mar  so  fit  Cas-     radiating,     delicate,    pale    greenish    hyphae.      These 

tellani.      Young     colonies  may  remain  separate  or  more  often  gradually 

Agar  Culture.  coalesce  into  a  jet-black  knobby  mass,  deeply  rooted 

into  the  medium. 
The  fungus  grows  well,  though  less  abundantly,  on  the  other  sugar  agars, 
and  also  on  ordinary  agar.     In  broth  and  peptone-water  the  growth  is  very 
slow,  and  takes  place  at  the  botton  of  the  tubes,  with  formation  of  a  black 
or  greenish-black  sediment.     Gelatine  is  very  slowly  liquefied. 


CLADOSPORIUM  PENICILLOIDES  iioi 

The  optimum  temperature  for  the  growth  of  the  fungus  is  between  300  C.  and 
320  C. ;  above  350  C.  and  under  250  C.  the  growth  is  much  slower,  and  may  be 
nil  under  200  C. 

This  fungus  is  the  cause  of  tinea  nigra  (p.  2078). 

Cladosporium  penicilloides  Gueguen,  1911. 

Synonym.  — C.  Madagascariense  Verdun,  1913. 

Found  by  Fontoynont  in  a  patient  with  some  ulcerated  nodules 
of  the  leg  in  Madagascar.  The  fungus  grows  easily  on  Sabouraud's 
and  other  media,  giving  rise  to  black  cerebriform  colonies.  In 
hanging-drop  cultures  shows  the  typical  features  of  the  genus. 

Cladosporium  herbarium  Persoon  has  been  demonstrated  by  Nassee  to  be 
the  cause  of  the  black  spots  so  often  found  on  imported  frozen  meat. 

SUBORDER  2:  ARTHROSPORINE^E  Vuillemin,  1910. 

Definition. — -Thallosporales  with  yeast-like  forms,  associated  in 
cultures  with  hyphse  and  other  forms  with  longer  hyphge.  Repro- 
duction by  means  of  arthrospores  parasitic  on  man. 

Remarks. — Vuillemin  includes  in  this  suborder  the  genera  Tricho- 
phyton, Microsporu  n,  Achorion,  and  their  allies,  although  it  is  more 
usual  to  consider  these  to  be  allied  to  the  Gymnoascaceae,  because 
Ctenomyces  serrata  Eidam,  1880,  when  injected  into  animals,  develops 
a  trichophytonTike  mycelium  and  eruption,  which  classification  has 
recently  been  supported  by  the  work  of  Marshall  and  one  of  us  on 
T.  currii.  However,  for  the  present,  we  propose  to  leave  these 
genera  and  their  allies  out  of  consideration. 

Classification. — This  suborder  contains  the  following  genera : — 

A.  Producing  Piedra  on  hairs— Genus  Trichosporum  Behrend, 

1890. 

B.  Producing      Black      Maduromycosis  —-Genus      Madurella 

Brumpt,  1905. 

C.  Producing  White  Maduromycosis — Genus  Indiella  Brumpt, 

1906. 

Genus  Trichosporum  Behrend,  1890. 

Definition. — Arthrosporales  living  parasitically  on  the  hairs  of  man 
in  the  form  of  large,  oval,  or  roundish  bodies  embedded  in  a  ground 
substance.     In  cultures  elongated  hyph?e  and  spores  arc  formed. 

Remarks. — Care  must  be  taken  not  to  confuse  Trichosporum 
Behrend,  1890,  with  Trichosporium  Fries,  1849,  a  veiT  different 
genus  with  over  forty  species,  mostly  saprophytic. 

The  species  of  this  genus  give  rise  to  nodosities  on  hairs.  They 
are: — ■ 

T.  giganteum  Behrend,  1890,  the  cause  of  piedra  in  Columbia,  in 
hairs  of  the  head. 

T.  beigeli  (Rabenhorst.  1867),  the  cause  of  piedra  in  Europe,  in 
hairs  of  the  beard. 

T.  ovoides  (Behrend,  1890),  the  cause  of  piedra,  in  hairs  of  the 
moustache. 


FUNGI  IMPERFECT  I 


T.  ovale  Unna,  1896,  on  the  hairs  of  the  moustache  in  Europe. 
T.  glycophile  du  Bois,  1910,  on  the  pubic  hairs  of  a  diabetic. 
The  various  species  may  be  differentiated  as  follows  :— 

A.  Bodies  around  hair  polyhedral : — 

I.  Diameter  of  bodies  12-15  microns — Giganteum. 
II.  Diameter  of  bodies  3-4  microns — Beigeli. 

B.  Bodies  around  hair  oval  and  small,  3-4  microns  by  i'5-2'5  microns: — 

I.  In  cultures  hyphae  often  twisted  like  a  corkscrew — -Ovale. 
II.  In  cultures  hyphae  not  so  twisted — Ovoides. 

C.  Bodies  around  hair  roundish,  3-4  microns  in  diameter  : — 

Fung;  s  associated  with  a  coccus,  with  which  it  grows  well  on  sugar 
media — Glycophile. 

These  fungi  live  parasitic  on  the  surface  of  the  hairs,  but  do  not 
penetrate  into  their  interior;  during  their  parasitic  life  they  vege- 


6  >->- 


■  ,.> 


Fig.  583. — Trichosporum. 
(After  Vuillemin.) 


Fig.  584. — Transverse  Section 
through  a  pledra  nodule. 


tate  in  the  shape  of  large  oval  or  roundish  elements,  embedded 
in  an  amorphous  substance.  Saprophytically  (cultures)  they  vege- 
tate, forming  mycelial  threads  and  spores. 

Trichosporum  giganteum  Behrend,  1890. 

This  is  the  cause  of  piedra  of  Columbia;  develops  on  the  surface 
of  the  hair  in  the  shape  of  large  polyhedric  cells  12  to  15  fj,  in 
diameter.  Masses  of  the  fungus  form  hard  nodules  along  the  hair. 
The  fungus  is  easily  grown  on  various  media.  In  cultures  the 
mycelial  threads  are  septated,  cylindrical,  between  1  and  4  /lc  wide. 
The  spores  are  of  various  dimensions,  between  2  and  12  [m.  The 
colour  of  the  colonies  is  light  brownish.  Horta  describes  in  the 
nodules  of  a  variety  of  piedra  certain  large  cyst-like  bodies  con- 
taining generally  eight  fusiform  bodies.  When  the  membrane 
bursts,  these  bodies  escape,  being  provided  with  one  rlagellum  at 
each  end.  Pinoy  is  inclined  to  consider  these  formations  to  be 
asci  containing  ciliated  ascospores. 


TRICHOSPORUM  BEIGELI 


1 103 


Trichosporum  beigeli  Rabenhorst,  1867. 

Synonyms.  -Pleurococcus  beigeli  Rabenhorst,  1867;  Sclerotium 
beigelianum  Hallier,  1868;  Hyalococcus  beigeli  Schroeter,  1886; 
Chlctmydotomus  beigeli  Trevisan,  1889;  Micrococcus  beigeli  Migula, 
1900;  Trichosporum  beigeli  Vuillemin,  1901. 

This  fungus  has  been  found  in  Europe  several  times  in  nodosities 
of  the  hairs  of  the  moustache.  It  lives  parasitically  under  the  form 
of  ovoid  or  polyhedral  elements  massed  together  on  the  surface  of 
the  hair.  These  ovoid  or  polyhedral  elements  are  much  smaller 
than  those  of  the  preceding  species,  their  maximum  diameter 
varying  between  3  and  4  /j,.  It  is  easily  cultivated  on  ordinary 
media.  In  cultures  mycelial  threads  are  found,  septate,  slender 
(1-57  to  2  /j,).     In  old  cultures  chlamydospores  can  be  seen. 

Trichosporum  ovoides  Behrend,  1890. 

Found  by  Behrend  in  the  nodosities  present  on  the  moustache 
of  a  European  patient;  vegetates  parasitically  on  the  surface  of 

A 


Fig.  585. — Hair  affected  with  Trichosporosis.     (After  Vuillemin. 


the  hair  under  the  form  of  ovoid  elements;  3  to  4  /j.  long  and  i£  to 
2%  fi  wide.  Grows  easily  on  culture  media;  on  potatoes  the  colonies 
are  white,  while  the  medium  takes  a  brownish-black  colour. 

Trichosporum  ovale  Unna,  1896. 

Found  by  Unna  in  the  nodosities  present  on  the  moustache  of  a 
European  patient.  Very  similar  to  T.  ovoides  ;  in  cultures,  however, 
the  mycelial  threads  are  often  corkscrew-like,  and  the  spores  have 
thick  walls. 

On  potatoes  the  colonies  are  white-yellowish,  and  the  substratum 
takes  a  brownish-black  colour. 

Trichosporum  glycophile  du  Bois,  1910. 

Found  by  du  Bois  in  a  nodular  affection  of  the  pubic  hairs  in  a 
diabetic  patient.  In  the  nodules  roundish  elements,  3  to  4  u,  were 
present,  together  with  a  coccus.  The  fungus  was  easily  cultivated 
in  symbiosis  with  the  coccus  on  sugar  media. 


iio4  FUNGI  IMPERFECTI 

Genus  Madurella  Brumpt,  1905,  emendavit  Pinoy,  1912. 

Definition.— -Arthrosporineae  with  sterile  septate  hyphae,  repro- 
ducing the  thallus  by  fragmentation  and  secreting  a  black  pigment. 
The  spores  are  produced  secondarily  by  binary  division  of  the 
articles.     Found  in  black  maduromycosis  and  grow  well  at  370  C. 

Type  Species. — -Madurella  mycetomi  (Laveran,  1902). 

Historical.— In  1901,  Brumpt,  Bouffard,  and  Chabaneix  wrote  an 
account  of  a  case  of  black  mycetoma  which  they  observed  at 
Djibouti.  In  the  following  year  the  organism  found  in  this  case 
was  studied  by  Laveran,  who  gave  it  the  name  Sireptothrix  mycetomi 
Laveran,  1902 .  Brumpt  also  found  the  same  organism  in  a  maduro- 
mycosis in  the  centre  of  Somaliland,  and  also  in  an  amputated  foot 
sent  from  Madagascar. 


Fig.  586. — Madurella  mycetomi  Fig.  587. — Grains  of  Indiella 

Laveran.  reynieri  Brumpt 

(After  Brumpt.) 

Bouffard,  in  1905,  reported  the  presence  of  the  same  disease  in 
Senegal  and  in  the  French  Sudan. 

In  this  variety  the  grains  are  black  or  deep  brownish  red,  and 
always  hard  and  generally  small,  from  1-2  millimetres  in  diameter, 
when  single,  and  not  in  accumulated  masses.  The  surface  is 
irregular,  with  projecting  points.  On  clearing  with  Eau  de  Javelle, 
the  fungal  elements  can  be  clearly  seen. 

Brumpt  (1905)  formed  a  new  genus,  '  Madurella,'  for  this  fungus, 
defining  it  as  follows  :— 

'  Mucedine  with  white  thallus,  living  parasitically  in  various  animal  tissues 
(bone,  muscle,  connective  tissue),  possessing  during  its  vegetative  life  fila- 
ments with  a  diameter  greater  than  1  micron,  and  even  reaching  to  8-10 
microns.  These  filaments  are  septate  and  branch  from  time  to  time;  they 
secrete  a  brown  substance.  When  old,  these  filaments  form  a  sclerote,  and 
their  walls  sometimes  become  impregnated  with  a  brown  pigment.  In  this 
sclerote  there  are  a  number  of  rounded  corpuscles,  from  8-30  microns  in 
diameter  (chlamydospores).' 

The  type  species  is  the  organism  called  Sireptothrix  mycetomi 
by  Laveran,  in  1902,  which  therefore  becomes  Madurella  mycetomi 
(Laveran,  1902),  first  cultivated  by  Brault  (1911)  in  material  from 
Algerian  cases. 

This  form  of  mycetoma  was  reported  by  Balfour  (191 1)  to  be 
present  in  the  Anglo-Egyptian  Sudan. 


MADURELLA  1105 

It  is  generally  assumed  that  this  and  the  Asian,  together  with 
the  American  type,  are  one  and  the  same  disease,  but  this  still 
requires  proof. 

In  1908,  Nicolle  and  Pinoy  described  a  maduromycosis  which 
they  found  in  Southern  Tunisia,  near  the  Oasis  of  Tozeur,  with  hard 
dark  brown  grains  about  the  size  of  a  pin's  head,  in  which  segmented 
and  ramified  hyphae  about  1-4  microns  in  diameter  were  seen, 
as  were  rounded  bodies  arranged  in  chains  and  resembling  the 
mycelial  spores  of  a  trichophyton,  the  whole  being  embedded  in  a 
brownish  cement  substance.  Cultures  were  obtained  at  350  C,  and 
the  growths  were  identical  on  maltose  agar,  glycerine  agar,  potato, 
and  carrot,  and  all  the  media  became  pigmented  black,  due  to  a 
tyrosinase  produced  by  the  fungus,  while  the  colonies  which  devel- 
oped in  twenty-four  hours  at  370  C.  were  white.  Microscopically 
the  growths  showed  the  '  favic  nails  '  so  commonly  met  with  in 
cultures  of  A.  schoenleini.  The  authors  looked  upon  the  organism 
as  belonging  to  the  genus  O'dspora  Wallroth,  1833,  with  which 
Vuillemin  considers  A  chorion  schoenleini  Lebert,  1845,  should  be 
classified.  Its  name,  therefore,  became  O'dspora  tozeuri  (Nicolle 
and  Pinoy,  1908). 

Inoculation  experiments  were  unsuccessful  in  the  rabbit,  the 
guinea-pig,  and  the  monkey,  but  two  successful  infections  were 
obtained  in  pigeons. 

Brumpt,  however,  considers  the  fungus  to  be  a  Madurella,  and 
therefore  its  name  becomes  Madurella  tozeuri  (Nicolle  and  Pinoy, 
1908). 

Brault  (1911  and  1912)  cultivated  the  fungi  Madurella  mycetomi 
and  M.  tozeuri. 

The  former  grew  at  200  C.  and  370  C.  on  broth,  various  agars, 
potato,  carrot,  and  some  vegetal  liquid  media. 

In  the  liquid  media  the  growth  appeared  as  a  whitish  grey  puff- 
ball,  which  later  became  yellowish  or  brownish,  while  the  medium 
remained  clear  and  the  growth  fell  to  the  bottom  of  the  tube. 

On  solid  media  it  formed  a  greyish-white,  duvet-covered  growth, 
which  possessed  a  central  button,  surrounded  by  a  radiation,  and 
later,  when  the  culture  was  drier,  the  medium  became  coloured. 

Glycerine  agar  was  best,  as  the  growth  thereon  was  luxurious, 
and  when  old  became  yellowish  in  colour,  while  the  medium  showed 
a  caramel  tinge  in  its  entirety. 

Glucose  glycerine  agar  produced  a  growth  of  the  colour  of  touch- 
wood. This  culture  is  thrown  into  black  wrinkles,  producing  an 
appearance  seen  on  some  seashores. 

When  the  growths  of  M.  tozeuri  were  compared  with  those  of 
M .  mycetomi  a  number  of  differences  were  observed. 

The  cultures  of  M.  tozeuri  grew  more  quickly,  were  more  luxuriant, 
and  were  white,  resembling  powdered  flour.  Those  of  M .  mycetomi 
were  more  discrete,  grey,  duveteuse,  radiated,  and  sometimes  showed 
concentric  circles,  and  disassociated  more  easily  than  the 
preceding . 

70 


no6  FUNGI  IMPERFECTI 

Old  cultures  on  glucose  agar  or  on  glycerinated  glucose  agar 
were  quite  different  in  the  two  species. 

On  carrot  M.  tozeuri  attained  a  deeper  brownish -yellow  colour, 
while  in  old  cultures  on  this  medium  it  produced  spores  in  a  manner 
resembling  an  Oospora. 

Pinoy,  in  his  remarks  upon  the  mycology  of  these  two  species, 
says  that  Brault's  M.  mycetomi  very  closely  resembles  that  isolated 
by  Nicolle  under  the  name  of  Oospora  tozeuri.  Its  filaments  are 
2-8  microns  in  diameter,  and  do  not  possess  apparatus  for  fructifica- 
tion, reproducing  by  a  breaking  up  of  the  hyphse  of  the  thallus  into 
articles  5-10  microns  in  length,  which  divide  into  two  spores. 
These  spores  are  of  the  same  diameter  as  the  hyphse  from  which 
they  arise,  varying  from  2-5  microns,  while  the  membrane  becomes 
yellowish  with  age.  In  addition,  chlamydospores  can  be  observed 
forming  at  the  end  of  the  filaments,  more  or  less  like  favic  nails.  The 
spores  of  M.  tozeuri  are  smaller,  but  are  formed  in  the  same  manner. 

On  Sabouraud's  gelatine  M.  mycetomi  gives  rise  to  black  sclerotes 
in  the  depth  of  the  medium.  These  are  very  numerous,  measure 
A-i  millimetre  in  diameter,  and  are  composed  of  hyphal  segments, 
more  or  less  cylindrical.  Sometimes  the  sphere  attains  a  diameter 
of  10  microns,  and  usually  contains  only  one  nucleus;  but,  though 
studied  for  a  long  time,  these  sclerotes  were  never  observed  to  have 
any  higher  form  of  fructification.  In  M.  tozeuri  it  is  very  rare  to 
see  the  formation  of  sclerotes,  which  takes  place  on  the  surface  of 
the  medium. 

On  the  bases  of  the  researches  on  M.  mycetomi  and  M.  tozeuri, 
Pinoy  classifies  the  genus  Madurella  as  follows:- — • 

A.  Sclerotes   0-5-1    millimetre   in   diameter,    formed   in   the   depths   of 

medium  in  cultures — Mycetomi. 

B.  Sclerotes  rarely  produced,  and  then  on  the  surface  of  the  medium — 

Tozeuri. 

Madurella  mycetomi  (Laveran,  1902). 

Synonym. — Streptothrix  mycetomi  Laveran,  1902. 

Mycelium  greyish  white;  when  old,  yellowish  and  darkening  the 
media  in  sugar  cultures.  Spores  varying  in  dimension  from  2-5 
microns.  Sclerotes  black  and  sterile,  with  a  diameter  from  0*5-1 
millimetre,  formed  in  the  depths  of  the  medium  in  cultures.  Can 
invade  the  skin,  bone,  muscles,  and  connective  tissue  of  man, 
giving  rise  to  black  grains,  which  are  small,  hard,  round,  and  more 
or  less  warty,  and  which  morphologically  resemble  the  sclerotes 
formed  in  the  cultures.  Up  to  the  present  the  inoculation  into 
animals  is  negative.  Very  widely  spread  in  Africa.  Isolated  by 
Brault  from  a  mycetoma  with  black  grains  in  Algeria. 

Madurella  tozeuri  (Nicolle  and  Pinoy,  1908). 

Synonym.- — Oospora  tozeuri  Nicolle  and  Pinoy,  1908. 
Mycelium  white,  becoming  yellowish  with  age  and  darkening  the 
medium  in  sugar  cultures.     Spores  generally  small,  2  microns  or 


MADURELLA    TOZEURI  1107 

sometimes  even  5  microns  in  diameter.  Sclerotes  are  only  rarely 
produced,  and  then  they  appear  on  the  surface  of  the  medium. 
Occasionally  it  gives  rise  to  a  mycetoma  in  man,  in  which  it  forms 
black  amorphous  grains,  which  are  often  made  up  of  mycelial  rings, 
enclosing  some  degenerate  cellular  elements,  which  are  impregnated 
with  the  pigment  of  the  fungus,  and  also  of  small  diffuse  masses, 
formed  solely  by  the  filaments  of  the  fungus,  which  have  a  yellow 
membrane.  Inoculation  into  pigeons  positive.  Isolated  by  Nicolle 
from  a  mycetoma  at  Tozeur. 

Genus  Indiella  Brumpt,  1906. 

Definition. — Arthrosporineae  with  septate,  ramified  hyphae,  with- 
out black  pigment,  and  hence  sclerotia  white  or  yellowish. 

Type  Species. — Indiella  mansoni  Brumpt,  1906. 

Remarks.— White  thallus,  living  parasitic  in  various  animal 
tissues — -connective  tissue,  muscles,  and  bones.  Mycelial  threads 
1-8  or  10  ju.  septate,  ramified,  never  secreting — -in  contrast  to 
the  fungi  of  genus  Madurella — any  black  pigment.  Masses  of 
mycelial  threads  form  sclerotia-like  bodies  or  grains  of  various  shape 
containing  chlamydospores. 

Classification. — -The  species  may  be  recognized  as  follows : — 

A.  Sclerotia  hard  and  bean-shaped — Mansoni. 

B.  Sclerotia  soft  and  in  coiled  masses — Reynieri. 

Indiella  mansoni  Brumpt,  1906. 

Mycelial  threads  are  septated,  white,  thin,  1-5-2  jj,  when  young, 
larger  (3-5  fi)  and  of  irregular  shape  when  old.  Numerous  spherical 
chlamydospores,  generally  terminal,  5-12  jz  in  diameter.  Grains 
(sclerotia)  very  small,  of  |-J  millimetre,  white,  lenticular  or  reni- 
form,  very  hard,  do  not  soften  by  keeping  in  caustic  potash.  The 
fungus  has  not  been  grown. 

Pathogenicity.— It  is  the  cause  of  Manson's  white  mycetoma,  of 
which  only  one  case  is  known. 

Indiella  reynieri  Brumpt,  1906. 

White  thallus.  Most  mycelial  filaments  are  very  thin,  1-1A  p, 
septated;  some — those  at  the  periphery — are  of  irregular  shape, 
much  broader  (4-5  /j,),  moniliform.  Nearly  every  mycelial  thread 
has  at  the  peripheral  extremity  a  terminal  chlamydospore,  5-20  p,, 
often  septate  in  two  or  three  cells.  Grains  or  sclerotia  are  small, 
less  than  1  millimetre  in  diameter,  coiled  up  like  the  excrementa 
of  earth-worms. 

Pathogenicity. — This  fungus  causes  a  variety  of  mycetoma  with 
white  grains  (Reynier's  white  mycetoma),  of  which  there  is  only  one 
case  on  record — -a  European  patient  who  had  never  left  France. 
The  case  was  observed  and  reported  on  by  Reynier. 


no8  FUNGI  IMPERFECTI 

ORDER  III.  HEMISPORALES  Vuillemin,  1910 

Definition. — Hyphales  with  the  mycelium  composed  of  abundant 
hyph?e,  thin,  but  more  than  1  micron  in  diameter,  septate  and 
branched  conidiophores  ramified  basally,  each  branch  terminating 
in  a  protoconidium,  preceded  by  an  annular  construction  produced 
by  a  brown,  rigid  thickening  of  the  wall.  The  protoconidium  is 
transformed  completely  or  partially  into  deuteroconidia,  but  occa- 
sionally it  elongates,  forming  a  new  conidiophore,  or  puts  out 
branches  which  are  capable  of  becoming  conidiophores. 

Classification.— There  is  only  one  genus,  Hemispora  Vuillemin, 
1906. 

Genus  Hemispora  Vuillemin,  1906. 

Definition. — Mycelial  filaments,  thin,  hyaline,  septated,  ramified. 
Each  conidiophore  terminates  into  an  ampulliform  structure  (proto- 
conidium), which  later  divides  into  several  spore-like  segments 
(deuteroconidia). 

Hemispora  stellata  Vuillemin,  1906. 

Definition. — Hemispora  composed  of  white,  sessile  discs  covered 
with  conidiophores,  arranged  like  brown  stars  in  relief  on  the 
surface.  Deuteroconidia  subspherical,  measuring  2-6-3«5  microns, 
with  a  dark-coloured  granular  membrane  except  at  the  point  of 
attachment,  sometimes  elongated  and  barrel-shaped.  Habitat, 
parasitic  on  man  and  fungi. 

Remarks.— This  species  was  first  found  in  1904  by  Vuillemin, 
growing  on  Aspergillus  repens  (De  Bary,  1870).  In  1909  Gougerot 
and  Caraven  first  found  it  parasitic  in  man, 
and  this  has  since  been  confirmed  by  other 
cases  described  by  Auvray,  De  Beurmann, 
Clair  and  Gougerot,  and  by  Thiry.  So  far  it 
has  not  been  found  in  the  tropics. 

Pathogenicity.— It  is  the  cause  of  hemi- 
sporosis,  characterized  by  bon}'  lesions  and 
cold  abscesses  simulating  tertian  syphilis, 
tuberculosis,  or  sarcomata. 

Biology. — It  grows  well  on  sugar  media  at 

^ellS^SSr     the  temperature  of    the    room     and    when 

(After  Vuillemin )        separated  in  pure  culture  can  be  tested  by 

sero  agglutination  and  complement  fixation. 

Typical  colonies  asteroid. 

Treatment.— Iodide  of  potassium  gives  good  result. 

Hemispora  rugosa  Castellani,  1910. 

Synonym. — Monilia  rugosa  Castellani,  1910. 

Definition. — Hemispora  growing  on  all  ordinary  media,  with  a 
crinkled  surface  without  asteroid  colonies. 

Remarks.— Isolated  from  cases  of  bronchitis  and  a  case  of  tonsil- 
litis by  Castellani,  and  recently  from  a  case  of  thrush  by  Pijper. 


HEMISPORA   RUGOSA 


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i  no  FUNGI  IMPERFECTI 

The  growth  on  glucose  agar  is  abundant,  crinkled,  or  at  times  some- 
what cerebriform;  and  in  colour  is  amber,  yellow,  or  brownish. 
Grows  well  on  gelatine,  which  it  liquefies  very  slowly,  so  much  so 


Fig.  589. — Hmispora  rugosa 
Castellani,  1 910  :  Glu- 
cose Agar  Culture. 


Fig.  590. — Hemi-  Fig.  591.  —  Hemi- 

spora   rugosa:  spora  rugosa: 

Glucose    Agar  Glucose  Agar 

Culture.  Culture. 


that  at  first  it  was  believed  to  be  a  non-liquefier.  Gram-positive. 
Milk  is  not  changed  as  a  rule,  but  occasionally  it  undergoes  a  certain 
degree  of  peptonization,  with  a  very  small  coagulum  at  the  bottom 
of  the  tube.     For  sugar  reactions  see  the  table. 


ORDER  IV.  CONIDIOSPORALES  Vuillemin,  1910. 

Definition. — Hyphales  with  the  mycelium  composed  of  abundant 
hyphae,  more  than  I  micron  in  diameter,  septate  and  branched,  with 
or  without  true  conidiophores,  and  with  reproduction  by  means  of 
true  conidia. 

Remarks. — The  reasons  for  the  formation  of  this  order,  which 
contains  a  large  number  of  families,  have  already  been  given,  as 
well  as  its  advantage  over  the  more  fully  worked  out  system  of 
Saccardo  (p.  1037). 

Classification. — The  order  Conidiosporales  is  divided  into  five  sub- 
orders, which  may  be  recognized  as  follows : — 


CONIDIOSPORALES  nn 

A.  Conidiunt  imperfect :  Aleuriospore. 

Suborder  i:  Aleuriosporinece  Vuillemin,  1911. 

B.  Conidiunt  perfect :  Conidium  verum. 

I.  True  Conidiophores  absent:— 

Suborder  2 :  Sporotrichinect  Vuillemin,  1910. 
II.  True  Conidiophores  present: — 

(a)  Conidia  borne  on  sporophores. 
Suborder  3:  Sporophorctlinece  Vuillemin,  1910. 

(b)  Conidia  borne  on  phialides. 

1.  Prophialides  absent. 

Suborder  4:  Phialidinece  Vuillemin,  1910. 

2.  Prophialides  present. 

Suborder  5:  Prophialidinece  Vuillemin,  1910. 

The  fourth  suborder,  Phialidinese,  contains  species  of  the  genera 
Aspergillus  Micheli,  1729;  Penicillium  Link,  1809;  and  Sterigmato- 
cystis  Cramer,  1859,  in  which  asci  are  unknown;  but  though  logically 
correct  to  include  these  species  in  the  Fungi  Imperfecti,  it  is  more 
convenient  to  consider  them  under  the  heading  Ascomycetes,  though 
the  genus  Scopulariopsis  may  be  placed  here. 

The  last  suborder,  Prophialidales,  does  not  contain  any  genera 
with  species  parasitic  in  man. 

SUBORDER  1:  ALEURIOSPORINECE  Vuillemin,  191 1. 

Definition.— Conidiosporales  in  which  reproduction  takes  place 
by  aleuriospores. 

Classification. — The  suborder  contains  two  families,  which  can 
be  distinguished  as  follows: — 

A.  Conidiophores  absent — Aleurismacece . 

B.  Conidiophores  present — Monotosporacece. 

Family  Aleurismacece  Vuillemin,  1911. 
Definition. — Aleuriosporinece  without  conidiophores. 
Classification. — The  family  is  divided  into  two  tribes : — 

A.  Spores  simple  or  appendiculate — Aleurismece. 

B.  Spores  bi-  or  multi-cellular — Blastotrichecs. 

Only  the  first  tribe  is  of  interest  to  us. 

Tribe  Aleurismece. 
This  tribe  may  be  classified  as  follows : — 
A.  HyphcB  pale  : — 

I.  Hyphae  very  short;  sporogenous.     Apparatus  but  little  differ- 
entiated from  the  mycelium — Myceliophthora  Costantin,  1894. 
II.  Hyphae  elongate,  sporogenous  apparatus  but  little  differentiated 
from  the  mycelium — Acladium  link,  1809. 
III.  Hypha?    elongate,    sporogenous    apparatus    well    differentiated 
from  the  mycelium: — 


1 1 12  FUNGI  IMPERFECTI 

(a)  Aleuriospore,  smooth,  small,  acro-pleurogenous : — 

1.  Aleuriospores  coloured — Aleurisma  Link,  1809. 

2.  Aleuriospores  pale — Corethropsis  Corda,  1839. 

(b)  Aleuriospore,  large,  spiny,  acrogenous: — 

1 .  Aleuriospore  appendiculate — Mycogone  Link,  1 809. 

2.  Aleuriospore  non-appendiculate — Sepedonium  Link,  1809. 

B.  Hyph&  dark  : — 

I.  Hyphae  pale  and  dark.  Aleuriospores  become  dark  and  acro- 
pleurogenous  on  light  or  dark  hyphae,  small,  generally  6X  4. 
rarely  uX  5  microns — Glenospora  Berkeley  and  Curtis,  1876. 
II.  Hypha?  very  dark.  Aleuriospores  remain  hyaline,  situate  acro- 
genously  on  hyaline  hypha?  at  the  base  of  sterile  dark 
hyphae,  large  11-14  microns — Botryotrichum  Saccardo  and 
Marchal,  1885. 

Genus  Acladium  Link,  1809. 

Definition.— Aleurismeae  with  pale  elongate  hyphae  and  with 
sporogenous  apparatus,  but  little  differentiated  from  the  mycelium. 
vSporophores  unbranched.     Conidia  pleurogenous. 

Type  Species.— A cladium  consfierswn  Link,  1809. 

Remarks. — There  is  only  one  species  which  concerns  us — viz., 
A.  castellanii 

Acladium  castellanii  Pinoy,  1916. 

Definition.— Acladium  with  small  chains  of  acrogenously  placed 
chlamydospores.     The  aleuriospores  are  acropleurogenous. 

Remarks. — The  parasite  was  found  by  Castellani  in  cases  of  ulcera- 
tive dermatitis,  with  gumma-like  nodules,  in  Ceylon,  the  Federated 
Malay  States,  and  Macedonia;  and  fullytdescribed  by  Pinoy. 


Fig.  592.  Fig.  593-  Fig.  594. 

Figs.  592-594.' — Acladium  castellanii  Pinoy:  Cultures  on  Glucose  Agar 

Potato  and  Carrot. 

The  growth  on  artificial  media  (such  as  carrot,  potato,  glucose 
agar)  consists  of  many  small  roundish  masses,  which  later  on  may 
coalesce.    They  are  covered  byspiculated  formations,  giving  them  a 


ACLADIUM  CASTELLANII 


1113 


prickly  appearance,  and  consisting  of  erect,  straight  filaments, 
parallel  to  each  other,  or  at  times  interlacing.  These  filaments  are 
approximately  2  microns  in  diameter,  and  carry  laterally  pseudo- 
conidia  of  variable  shape,  cylindriform,  pyriform,  or  spherical, 
attenuated  in  size  at  their  points  of  insertion.  Most  of  these  pseudo- 
conidia  are  4  microns  in  length,  with  a  breadth  of  3  microns.  This 
type  of  fructification  recalls  the  type  Acladium  decribed  by  Bodin 
in  certain  species  of  the  genus  Trichophyton  (Malmsten,  1848). 


Fig.  596. — Microscopi-  Fig.  597. — Microscopi- 
cal Appearance  of  cal  Appearance  of 
the  Fungus  in  Hang-  .  the  Fungus  in  Hang- 
ing-Drop Culture,  ing-Drop  Culture, 
Twenty-Four  Hours  Three  Days  Old. 
Old. 

S,  pseudoconidia  ;  a,  b,  c,  development  of  mycelial  filaments  from 
pseudoconidia;  ch,  chlamydospores. 


Fig.  595. — Microscopi- 
cal Appearance  of 
Acladium  castellanii 
Pinoy  in  Hanging- 
Drop  Culture,  Five 
Days  Old. 


These  pseudoconidia  become  detached  and  then  develop  by 
sprouting,  and  mycelial  filaments  are  formed.  Certain  filaments 
produce  spherical  chlamydospores  arranged  in  small  strings,  as 
found  in  certain  fungi  of  the  genus  Fusarium.  These  small  chains 
of  chlamydospores  are  very  frequently  terminal,  the  dimensions 
being  variable — -8  to  10  microns  (Figs.  59V59?)- 

In  cultures  on  carrot  and  potato  the  colonies  are  white,  on 
glucose  agar  often  amber  colour.  Old  cultures  may  show  a  certain 
amount  of  pigmentation,  brown  or  black,  especially  on  potato. 

Genus  Glenospora  Berkeley  and  Curtis,  1876. 

Definition— Aleurismeae  with  pale  and  dark'hyphae.  Aleurio- 
spores  become  dark,  and  are  situate  acropleurogenous  on^  light  or 
dark  hyphae,  but  are  small  in  size,  being  generally  6x4  microns  in 
diameter  and  rarely  11  x  5  microns. 

Type  Species. — Glenospora  curtisii  Berkeley  and  Desmond. 

Classification.— Besides  the  type,  G.  ramorum  (Schweinitz,  1822) 
and  the  pathological  species  are  known.     The  latter  are : — 

G.  graphii  (Siebenmann,  1889),  found  in  cases  of  otomycosis  and 
keratomycosis. 


1 1 14  FUNGI  IMPERFECTI 

G.  sacchari  Spegazzini,  1896,  in  the  Argentine. 

G.  microspora  Spegazzini,  1891,  in  Brazil. 

G.  kkartoumensis  Chalmers  and  Archibald,  1916,  found  in  black 
maduromycosis. 

G.   semoni  Chalmers   and   Archibald, 
1917. 

The  various  species  may  be  recognized 
as  follows: — 


Fig.  598.  Fig.  599. 

Fig.  598  and  599. — Glenospora  kkartoumensis  Chalmers  and  Archibald  : 

Aleuriospores. 

A.  Aleuriospores  large,  usually  measuring  10  or  more  microns  in  dia- 

meter : — 
Parasitic  on  plants— (1)  Curtisii,  (2)  Ramorum. 

B.  Aleuriospores  medium,  measuring  6-8-9-1 1  microns — (3)  Sacchari. 

Parasitic  on  plants — (4)  Microspora. 

C.  Aleuriospores  small,  usually  measuring  5  or  less  microns  in  diameter : — 

I.  Parasitic    in    man,    causing    otomycosis    and    keratomycosis — 
(5)  Graphii. 

II.  Parasitic  in  man,  causing  black  maduromycosis: — 

(a)  Growth,  on  clear  maltose  agar  twelve  days,  uncapped  tube 

at  300  C.  Central  black  rounded  mass  surrounded  by  an 
abundant  white  fringe — (6)  Semoni  (in  India). 

(b)  Growth  in  exactly  same  conditions  as  in  (a).     Central  series 

of  small  elevations  from  which  radiate  furrows  cutting  in 
black  plateau.  Fringe  very  slightly  marked — (7)  Kkar- 
toumensis (in  Africa). 

Glenospora  graphii  Siebenmann,  1889. 

Synonyms.- — Graphiunt  penicillioides  Hallier,  1869;  Stemphylium 
polymorphum  Hallier,  1869;  Verticillium  graphii  Siebenmann,  1889; 
Glenospora  praphii  Vuillemin,  1912. 

Definition.— Glenospora  with  aleuriospores  large,  10  or  more 
microns  in  diameter. 

Mycelium  at  first  white,  later  dark  brownish.  The  filaments  are 
septated,  2  to  3  /j,  in  breadth,  ramified.  Fertile  hyphae  are  erected, 
often  dichotomous  or  trichotomous,  with  terminal  conidia,  which 
are  ovoid  with  a  smooth  surface,  and  of  a  greyish-brownish  colour. 
It  is  easily  grown  on  the  usual  laboratory  media;  gelatine  is  not 
liquefied.  This  fungus  has  been  found  in  cases  of  otomycosis  by 
Hassestein,  Bezold,  Siebenmann,  etc.,  and  in  a  case  of  keratomycosis 
by  Morax  and  Pinoy. 


GLEXOSPORA   KHARTOUMENSIS 


"15 


Fig.  600. — Glenospora  khartoumensis  Chalmers  and  Archibald:    In  Myce- 
toma Grain. 


Fig.  601  and  602. — Glenospora  khartoumensis  Chalmers   and   Archibald: 
Culture  on  Clear  Maltose  Agar. 

A,  Twelve  days;   B,  fourteen  days. 

Fig.  603  and  604. — Glenospora  semoni  Chalmers  and  Archibald:   Culture 
on  Clear  Maltose  Agar. 

A,  Twelve  days;  B,  fourteen  days. 


Glenospora  khartoumensis  Chalmers  and  Archibald,  1916. 

Definition. — Glenospora  with  aleuriospores  small,  5  or  less 
microns  in  diameter;  parasitic  in  man,  causing  black  maduromy- 
cosis,  and  differing  from  G.  semoni  in  cultural  characters. 


iii6  FUNGI  IMPERFECT  I 

History. — Found  by  Chalmers  and  Archibald  in  a  case  of  black 
maduromycosis  in  Khartoum,  Anglo-Egyptian  Sudan.  It  occurred 
in  the  sole  of  the  foot  of  a  native  hoy. 

Morphology. — All  cultures  show  septate  branched  hyphag,  varying 
in  diameter  from  2-8-1-4  microns,  and  increasing  in  very  old 
cultures,  when  all  the  hyphse  are  dark,  to  2-4  microns.  At  first  the 
hyphae  are  pale,  but  when  older  they  become  dark,  being  of  a 
greenish-black  tinge.  Thick  walled,  clear,  or  dark  coloured. 
Chlamydospores  (14x11-3  microns)  are  present,  and  are  especially 
marked  in  the  black  masses  on  the  surface  of  potato  infusions  and 
nutrient  gelatine.  Aleuriospores  are  to  be  found  acropleuro- 
genously  situated  in  the  surface  growth  of  old  potato  infusions. 

Cultures.— The  fungus  grows  well  aerobically  in  glucose  peptone 
at  300  C,  which  is  the  optimum  temperature.  It  also  grows  well 
on  maltose  agar,  on  glycerine  agar,  glucose  agar,  and  agar  agar.  It 
does  not  liquefy  inspissated  blood  serum  or  gelatine.  It  grows  on 
potato  and  carrot,  but  not  on  cheese  or  lard.  It  grew  well  on  litmus 
milk,  but  formed  neither  acid  nor  clot,  though  it  produced  a  flaky 
precipitate'.  On  maltose  agar  the  typical  growth  was  in  colour. 
Ridgway's  Standard  Colour  '  Dusky  Drab,'  and  had  a  central 
elevation  surrounded  by  a  depression,  which  separated  it  from  a 
grooved  raised  plateau  which  had  a  slight  fringe. 

Habitat. — So  far  it  is  only  known  in  man,  and  all  experiments  with 
grains  or  with  cultures  failed  to  infect  monkeys,  rabbits,  or  pigeons 
intraperitoneally,  subcutaneously,  intramuscularly  (with  or  without 
a  thorn),  or  into  the  anterior  chamber  of  the  eye.  Attempts  to  find 
a  similar  fungus  on  plants  have  so  far  failed. 

Pathogenicity. — It  causes  a  variety  of  African  black  maduro- 
mycosis. 

Glenospora  semoni  Chalmers  and  Archibald,  1917. 

Definition.— Glenospora  closely  resembling  G.  khartoumensis, 
but  differing  markedly  in  cultural  characters  on  maltose  agar  when 
grown  under  exactly  similar  conditions. 

Remarks. — -This  fungus  was  isolated  by  Semon  from  a  case  of 
black  maduromycosis  occurring  in  a  native  Indian  soldier  serving 
in  France. 

It  is  very  like  G.  khartoumensis,  but  differs  markedly  in  cultural 
appearances,  as  may  he  judged  by  a  comparison  of  Figs,  (x  1  and  602 
with  Figs.  603  and  604. 

Pathogenicity.' — It  causes  a  variety  of  Asian  black  maduromycosis. 

Genus  Trichothecium  Link,  1824. 

Fertile  hyphse  are  erect,  grouped  together,  each  terminating  in 
an  oval,  pear-shaped,  or  globular  conidium.  The  only  species  so 
far  observed  in  man  is  Trichothecium  roseum. 

Type. — Trichothecium  roseum  (Persoon,  1801),  emendaint  JLink, 
1824. 


SPOROTRICHIN&  ni7 

Triehothecium  roseum  Persoon,  1801. 

Synonyms. — Trichoderma  roseum  Persoon,  1801;  Sporocephalum 
roseum  Persoon,  1801;  Puccini  a  rosea  Corda,  1837. 

This  species  vegetates  on  decaying  vegetable^matter^the  colour 
is  at  first  white,  then  pinkish.  Each  fertile  hypha  terminates  in  a 
pear-shaped  conidium,  10  to  20  /j,  in  length  and  8  to  12  yt,  in  breadth. 

This  fungus  has  been  found  in  cases  of  otomycosis  by  Stendener, 
who  did  not  succeed  in  cultivating  it.  Some  authorities  believe 
it  to  be  identical  to  Glenospora  graphii. 

SUBORDER  2.  SPOROTRICHINE^  Vuillemin,  1910. 

Definition. — Conidiosporales  in  which  reproduction  takes  place 
by  means  of  true  conidia,  but  in  which  true  conidiophores  are  absent. 

Type  Genus.— Sporotrichum  Link,  1809,  which  has  a  very  large 
number  of  species  scattered  over  the  world,  of  which  100  are  de- 
scribed in  Saccardo's  '  Sylloge  Fungorum,'  vol.  iv. 

Genus  Sporotrichum  Link,  1809,  emendavit  Saccardo,  1882. 

Synonyms.— Miainomyces  Corda;  Chromelsporium  Corda. 

Definition.— Sporotrichales  with  the  characters  of  the  suborder. 

Type  Species. — Possibly  Sporotrichum  obducens  Link,  1809. 

Human  Species. — -There  has  been  considerable  discussion  as  to 
whether  the  human  species  belonged  to  this  or  another  genus — 
e.g.,  Oospora,  Botrytis,  Trichosporum,  Rhinocladium,  or  Torula — 
but  Smith,  de  Beurmann,  and  Gougerot's  belief  that  Sporotrichum 
is  the  correct  genus  has  been  supported  by  Matruchot,  Vuillemin. 
and  Pinoy,  and  may  be  considered  as  settled  as  far  as  our  present 
knowledge  goes. 

The  first  species  ever  associated  in  any  way  with  man  was : — 

Sporotrichum  inquinatum  (Link,  1809),  which  was  found  growing 
on  dry  human  faeces.  This  was  probably  a  saprophyte.  The  first 
ever  found  in  diseased  men  was  Sporotrichum  bronchiole  Montagne, 
1844.     It  was  discovered  by  Gubler  in  the  bronchi  of  sick  persons. 

Species  Parasitic  in  Man.— It  is  customary  at  the  present  time  to 
give  the  following  species  as  parasitic  in  man,  and  it  may  be  noted 
that  they  do  not  correspond  to  any  known  species  living  sapro- 
phytically  or  parasitically  on  plants  :— 

1.  5.  schenki  (Hektoen  and  Perkins,  1900). 

2.  S.  beurmanni  (Matruchot  and  Ramond,  1905). 

3.  5.  doride  Beurmann  and  Gougerot,  1906. 

4.  5.  indicum  Castellani,  1908. 

5.  S.  aster oides  Splendore,  1908. 

6.  5.  gougeroti  Matruchot,  1910. 

7.  S.  jeanselmi  Brumpt  and  Langeron,  1910. 

8.  S.  lesnei  (Vuillemin,  1910). 

9.  S.  councilmani  Wolbzch,  Sisson  and  Meier,  1917. 


iii8  FUNGI  IMPERFECT  I 

And  one  may  add : — 

10.  S.  bronchi 'ale  Montagne,  1844. 

There  is,  however,  some  difference  of  opinion  with  regard  to 
some  of  these  species;  thus  de  Beurmann  and  Gougerot  consider 
that  the  fourth  and  fifth  are  only  varieties  of  the  second. 

4.  5.  beurmanni  Matruchot  and  Ramond,  1905,  var.  indicant 
Castellani,  1908. 

5.  5.  beurmanni  Matruchot  and  Ramond,  1905,  var.  asteroides 
Splendore,  1908. 

Considering  them  all  provisionally  as  separate  species,  they  may  be 
recognized  as  follows : — 

A.  Conidia  large   (4-11   microns  in  greatest  diameter),   with  well-developed 

pedicle  and  presence  of  lateral  spore  clusters : — 
Mycetomas  in  Madagascar — Lesnei. 

Conidia  large  with  absence  of  lateral  spore  clusters : — 
Traumatic  arthritis  in  America — Councilmani. 

B.  Conidia  usually  small  with  very  short  pedicle,  which  may  be  absent: — 

I.  With  radiating  bodies.  Conidia  very  polymorphic,  round,  oval,  or 
bacilliform.  varying  from  4-8  microns  in  greatest  diameter — 
A  steroides 

II.  Without  radiating  bodies: — 

(a)  Conidia    not    numerous.     Ferments    lactose,    not    saccharose — 

Schenki. 

(b)  Conidia  numerous:— 

1 .  Hyphae  2  or  more  microns  in  diameter : — 

(a)  Cultivated: — 

(i.)  Colonies  dark  from  the  first — Gougeroti. 
(ii.)  Colonies  whitish  at  first: — 

(1)  Colonies  finally  black.     Ferments  saccharose, 

not  lactose — Beurmanni. 

(2)  Colonies  lightish  brown — Dori. 

(3)  Colonies  whitish  grey  to  black.     Hyphae  wide, 

3  to  4  microns — Indicum. 

(b)  Not  cultivated.     Hyphae  5  to  7  microns  in  diameter — 

Bronchiale. 

2.  Hyphae  less  than  2  microns  in  diameter.     Hyphae  0-5  to  1 

micron  in  diameter — Jeanselmi. 

Pathogenicity. — They  usually  give  rise  to  lesions  in  the  skin  and 
deeper  tissues,  resembling  those  of  tertiary  syphilis  (gummata,  etc.) 
or  tuberculosis,  but  S.  lesnei  produces  a  disease  like  mycetoma. 

Treatment. — As  a  rule  the  diseases  are  amenable  to  iodide  of 
potassium. 

Sporotrichum  schenki  Hektoen  and  Perkins,  1900. 

Synonyms. — Sporothrix  schenki  Hektoen  and  Perkins,  1900 ; 
Rhinocladium  beurmanni  Verdun,  1913. 

Discovered  by  Schenk  in  a  case  of  gummatous  lymphangitis  in 
1896  in  North  America.  Easily  grown  on  glucose,  maltose,  and 
other  sugar  media.  Optimum  temperature  300  to  380  C.  Growth 
with  an  irregular  surface,  generally  of  white  colour,  but  old  cultures 


SPOROTRICHUM  BEURMANNI  1119 

may  present  some  brownish  or  black  pigmentation.  Glucose 
gelatine  is  slowly  liquefied.  Mycelial  threads  as  a  rule  not  very 
straight,  rather  bent,  curved,  or  undulating;  they  are  about  2 //  in 
diameter.  Conidia  present  in  small  numbers,  oval,  supported  by 
a  short  sterigmata.  Ferments  lactose,  producing  acidity  but  no 
gas;  has  no  action  on  saccharose. 

Pathogenicity.— It  is  the  cause  of  Schenk's  sporotrichosis,  found  in 
North  America.  According  to  de  Beurmann,  this  fungus  is  very 
little  or  non-pathogenic  to  rats  and  mice. 

Sporotrichum  beurmanni  Matruchot  and  Ramond,  1905. 

Synonym. — Rhinocladium  beurmanni  Verdun,  1913. 

Discovered  by  de  Beurmann  in  France,  and  completely  investi- 
gated by  himself  and  Ramond,  Gougerot,  Dor,  Sicard,  Pinoy,  etc., 
in  that  country;  by  Adamson  in  England;  by  Lutz  and  Splendore 
in  South  America;  by  Carougeau  in  Madagascar,  etc. 

Parasitic  Life. — In  the  tissues  oval,  yeast-like  or  short  ba ciliary 
forms  are  seen,  3  to  5  fi  in  length  and  2  to  3  /u  in  breadth,  free  or 
engulfed  by  phagocytes.  Pinoy  has  described  some  minute  oval 
forms  the  shape  and  size  of  piroplasmata  inside  the  macrophages. 
In  a  case  of  general  infection  he  has  made  the  important  observa-. 
tion  that  typical  fructifications  may  be  seen  in  the  blood  capillaries. 

Cultures. — The  best  media  are  Sabouraud's  maltose  agar  and 
glucose  agar.  The  growth  begins  to  appear  between  the  fourth  and 
the  twelfth  day.  Optimum  tem- 
perature 220  C.  The  growth  may 
be  whitish  at  first,  but  soon 
becomes  completely  black  or  of  a 
brownish  chocolate-like  colour. 
The  surface  is  cerebriform. 
Glucose  gelatine  is  slowly 
liquefied .  Mycelial  threads 
about  2  (a  in  diameter,  rather  FlG  6o5  ^sporotrichum  beurmanni 
straight.     Conidia  oval,  5  to  6  fj,  Matruchot  and  Ramond. 

in  length  and  3  ^   in   breadth,  (After  Gougerot.) 

supported   by  short    sterigmata. 
In  contrast  to  Sp.  schenki,  the  conidia  are  extremely  numerous. 

Ferments  saccharose,  producing  acidity,  but  no  gas ;  has  no  action 
on  lactose. 

Pathogenicity. — Is  the  cause  of  by  far  the  greatest  number  of 
cases  of  sporotrichosis  in  Europe  (see  p.  2086).  Is  very  pathogenic 
to  rats  and  mice. 

Sporotrichum  dori  de  Beurmann  and  Gougerot,  1908. 
Found  by  Dor  in  a  case  of  gummatous  sporotrichosis.     In  con- 
trast to  the  typical  Sp.  beurmanni,  the  growth  on  maltose  and 
glucose  agars  is  slower;  the  colonies  do  not  coalesce  into  a  large 
mass,  but  remain  separate  and  small,  not  exceeding  l\  millimetres 


FUNGI  IMPERFECT  I 


in  diameter.     The  colour  is  light  brownish;  never  becomes  black. 

Does  not  grow  on  gelatine.     The  mycelial  filaments  are  very  thin 

(0-5  to  1  fjb),  with  short  mycelial  segments  occasionally  dichotomous. 

The  fungus  is  not  pathogenic,  or  very  slightly  so,  for  rats  and 

mice 

Sporotrichum  gougeroti  Matruchot,  1910. 

Synonym. — -Rhinocladiunt  gougeroti  Verdun,  1913. 

Differs  from  the  typical  Sp.  beurmanni  only  in  small  details,  the 
principal  ones  of  which  are  the  black  pigmentation  of  the  colonies 
from  the  very  beginning,  and  the  extremely  abundant  sporulation. 

Sporotrichum  indicum  Castellani,  1908. 

Found  by  Castellani  in  Ceylon.  It  is  doubtful  whether  it  is  a 
separate  species,  or  merely  a  variety  of  Sp.  beurmanni.  The 
mycelial  threads  are  often  somewhat  larger  (2  to  3  /n  wide) ;  conidia 
roundish  (3  to  5  /j)  or  oval  (4  to  5  /j  long  and  3  to  4  /li  in  breadth). 
The  colonies  on  maltose  and  glucose  agars  may  be  of  various  colour 
— white-greyish,  light  brownish,  dark  brownish,  black. 

Sporotrichum  jeanselmei  Brumpt  and  Langeron,  1910. 

Was  isolated  by  Jeanselme  and  P.  Chevalier  from  a  case  of 
gummatous  sporotrichosis,  and  was  studied  botanically  by  Brumpt 
and  Langeron.  It  differs  from  Sp.  beurmanni 
by  the  mycelial  filaments  being  thinner. 
These  are  septate,  ramified  with  short  lateral 
branches  supporting  clusters  of  spores.  The 
spores  are  oval  or  roundish,  2  5  to  3-5  ^it. 


Fig. 


607. — Sporotrichum  asie- 
roides  Splendore. 


Fig.  606. — Sporotrichum  asteroides 
Splendore  in  the  Tissues. 

Note  radiate  body.  Young  culture 

(From  photographs  by  Dr.  Splendore.) 


Sporotrichum  asteroides  Splendore,  190S. 
Synonym. — Rhinocladium  asteroides  Verdun,  1913. 
Discovered  by  Splendore  in  South  America.    Is  characterized  by 


SPOROTRICHUM  ASTEROIDES  1121 

the  presence  in  the  infected  tissues  of  spherical  bodies,  4  to  12  fj, 
in  diameter,  from  which  some  bacillary-like  formations  radiate. 
The  fungus  grows  well  on  maltose  and  glucose  agars,  the  colonies 
being  first  white  and  later  black.  Pathogenic  to  man,  rats,  and 
mice. 

Sporotrichum  lesnei  (Vuillemin,  1910). 

Synonym. — Rhinocladium  lesnei  Vuillemin,  1910. 

Differs  from  all  the  other  species  of  Sporotrichum  by  the  elongated 
shape  and  large  dimensions  of  the  conidia,  which  are  4  to  II  fi  in 
length  and  2-5  to  4  /j,  in  breadth.  Old  cultures  are  of  a  dark  sooty 
hue,  and  black  chlamydospores  may  be  present. 

Sporotrichum  councilmaniWolbach,  Sisson  and  Meier,  1917. 
Found  byWolbach,  Sisson  and  Meier  in  a  case  of  acute  arthritis 
of  the  knee  following  injury,  in  America.  This  species  is  character- 
ized by  the  large  size  of  the  spores  with  absence  of  lateral  spore 
clusters  and  by  the  occurrence  in  the  lesions  of  septate  branching 
filaments. 

SUBORDER  3.  SPOROPHORINEiE  Vuillemin,  1910. 

Definition. — Conidiosporales  reproducing  by  true  conidia  borne 
on  conidiophores. 

Remarks.— A  number  of  families  and  a  large  number  of  genera  are 
included  in  this  suborder,  but  we  are  only  concerned  with  four, 
which  may  be  separated  from  one  another  as  follows : — 

A.  Conidiophores  unbranched :— 

I.  Single  hyaline  or  lightly  coloured  terminal  spore — 
Acremonium  Link,  1809. 

B.  Conidiophores  branched : — 

I.  Conidiophores  erect — Monosporium  Bonorden,  1851. 
II.  Conidiophores     decumbent — Scedosporium     Saccardo, 
1911. 

Monosporium  is  only  mentioned  because  Scedosporium  apio- 
spermum  used  to  be  Monosporium  apiospermum. 

Genus  Acremonium  Link,  1809. 

Definition.— Sporophorineae  with  creeping  sterile  hyphae  but  little 
branched,  and  carrying  laterally  simple  unbranched  conidio- 
phores, broad  in  the  middle  and  gradually  reduced  towards  the 
distal  extremity,  terminating  in  a  single  hyaline  or  lightly  coloured 
spore. 

Type  Species. — Acremonium  allernatum  Link,  1809. 

Remarks. — A  small  number  of  species  are  known,  which  mostly 
live,  saprophytically,  on  decaying  wood,  leaves,  etc.  Two  species 
only  are  known  in  man. 

71 


FUNGI  IMPERFECT  I 


Acremonium  potroni  Vuillemin,  1911. 

Found  by  Potron  and  Noisette  in  a  case  of  subcutaneous  gum 
mata  with  fever,  somewhat  resembling  typhoid  before  the  gum- 
mata  appeared.  Easily  grown  on  Sabouraud's  agar;  colonies 
white,  then  pinkish,  and,  later,  orange-yellow.  Serum  is  liquefied. 
In  cultures  the  mycelial  filaments  are  septated;  numerous  conidio- 
phores  are  present  of  a 
peculiar  elongated  type, 
15  to  20  [x  in  length. 
Conidia  ovoid,  with  a 
smooth  surface,  4  to  5  /j, 
in  length  and  2  to  2-2  pi 
in  breadth;  of  pinkish 
colour.  This  fungus  is 
pathogenic  to  guinea- 
pigs. 


Fig.  608. — Acremonium 
potroni  Vuillemin. 

(After  Vuillemin.) 


Fig.  609. — Scedosporium  apiospermum 
Saccardo. 

(After  Radaeli.) 


Acremonium  niveum  Boucher,  19 18. 
Very  similar  to  A.  potroni,  but  colonies  are  generally  white. 

Genus  Scedosporium  Saccardo,  1911. 

Definition. — Sporophorineae  with  unbranched  decumbent  conidio- 
phores. 

Type  Species.— Scedosporium  apiospermum  (Saccardo,  1911). 

Remarks. — -The  other  known  species  are  Scedosporium  acremoni- 
oides  Harvey,  which  does  not  concern  us,  and  5.  sclerotiale. 

Scedosporium  apiospermum  (Saccardo,  1911). 

Definition. — -Scedosporium  with  mycelium  at  first  white  and  later 
slightly  brown;  bundles  3-5  mm.  broad  in  cultures.  Mycelial 
hypha;  creeping,  filiform.  Conidiophores  decumbent,  very  slightly 
branched,  hyaline,  2-5-3  microns,  with  one  spore  oblong,  14x5-6- 
11x5-7,  rarely  subround;  at  first  hyaline,  later  dilute,  dirty  rose 
yellow.     Scedosporium,  causing  white  maduromycosis. 

Remarks.— Easily  grown,  the  cultures  are  whitish  and  covered 
with  duvet;  may  become  brownish  when  old. 

Mycelial  tubes  septated  and  of  various  size;  may  reach  4  to  5  jli 


SCEDOSPORIUM  APIOSPERMUM  1123 

in  breadth.  Each  conidiophore  supports  a  terminal  spore,  which  is 
either  ovoid,  12  to  14  ft  in  length,  and  5  to  6  /j  in  breadth,  or 
roundish,  6  to  7  ^  in  diameter.  No  other  kind  of  fructification  is 
seen. 

Pathogenicity.— This  fungus  has  been  found  in  Italy,  in  cases  of 
mycosis  of  the  foot  resembling  madura  foot,  by  Tarozzi  and  Radaeli. 
Tarozzi  considered  the  fungus  to  be  a  Nocardia,  while  Saccardo  and 
Radaeli  described  it  as  a  new  species  of  the  genus  Monosporium. 
Saccardo  placed  it  later  in  the  genus  Scedosporium.  Radaeli  made 
a  complete  pathological  and  clinical  investigation  of  the  condition. 

Scedosporium  sclerotiale  (Pepere,  1914). 

Synonym. — Monosporium  sclerotiale  sen  nigricans  Pepere,  1914. 

Definition.— Scedosporium  causing  black  maduromycosis. 

Remarks.— This  fungus  resembles  5.  apiospermum,  with  the 
exception  that  it  produces  black  pigment.  It  was  ably  investi- 
gated by  Pepere,  who  grew  it  on  various  media,  studied  it  mycologi- 
cally,  studied  complement  fixation  with  it,  and  finally  obtained 
successful  inoculations  in  the  anterior  chamber  of  the  eye  in  guinea- 
pigs. 

Pathogenicity. — -It  was  found  in  a  case  of  black  maduromycosis 
in  a  peasant,  aged  thirty-three  years,  living  at  Domusnovas,  in  the 
province  of  Cagliari,  in  Sardinia. 

SUBORDER  4.    PHIALIDINE.E  Vuillemin,  1910. 

Definition.— Conidiosporales  with  conidia  borne  on  phialides. 

Remarks.— As  already  stated,  the  species  of  Aspergillus,  Sterig- 
matocystis,  and  Penicillium  in  which  asci  are  unknown  could  be 
classified,  here  but  we  will  only  consider  Scopulariopsis,  which  is 
closely  related  to  Penicillium . 

Genus  Scopulariopsis  Bainier,  1907. 

Synonym. — ■Penicillium  pro  parte. 

Definition.  —  Phialidalineae  resembling  Penicillium,  with  un- 
branched  erect  conidiophores,  bearing  phialides,  which  carry  a  chain 
of  large  ovoid  or  roundish  spores. 

Type  Species. — Scopulariopsis  brevicaulis  Saccardo,  emendavit 
Bainier,  1907. 

Remarks. — In  addition  to  those  found  in  man,  5.  rubellus  Bainier, 
1907,  S.  rufulus  Bainier,  1907,  S.  rcpens  Bainier,  and  S.  communis 
Bainier,  are  known. 

Species  found  in  Man. — -Two  species  are  found  in  man,  which  may 
be  differentiated  as  follows : — - 

A.  With  white  creamy  formation  in  old  cultures— Blochi. 

B.  Without  such  formations  in  old  cultures— Koningii. 


1124 


FUNGI  IMPERFECTI 


Scopulariopsis  blochi  Matruchot,  1911. 

Syncnyms. — Mastigocladium  blochi  Matruchot,  ign;  Scopula- 
riopsis blochi  Vuillemin,  1911. 

Found  by  Bruno  Bloch  in  a  case  of  gummatous  lymphangitis, 
clinically  very  similar  to  an  ordinary  case  of  sporotrichosis.     In 

cultures  the  mycelial  threads  are  slender 
(0-5  to  1-5  pi  in  breadth),  colourless,  sep- 
tated,  very  little  ramified.  Conidiophores, 
20  to  30  pi  in  length,  are  tapering,  and 
from  the  pointed  ends  chains  of  conidia 
take  origin.  Conidia  elongated,  ovoid, 
3  to  4  pi  in  length  and  1-5  to  2  pi  in 
breadth.  In  old  cultures  white-creamy 
formations  may  be  seen,  which  may 
possibly  be  undeveloped  perithecia. 

Scopulariopsis  koningii  Oudemans. 
Synonyms. — Monilia      koningii     Oudemans; 
Scopulariopsis    rufulus    Bainier;     S.     koningii 
Vuillemin,  191 2. 

A  scopulariopsis  isolated  by  Yanin  in  a  case  of  subcutaneous  gummata  has 
been  identified  by  Vuillemin  as  5.  koningii  Oudemans.  The  cultural  characters 
are  very  similar  to  those  of  the  previous  species,  but  the  peculiar  white-creamy 
formations  as  observed  in  old  cultures  of  S.  blochi  are  not  seen.  Boucher  in 
cases  of  gumma  -like  swellings  in  Madagascar  has  isolated  a  species  which  he 
calls  S.  ivorensis. 


Fig.  610. — Scopulariopsis 
blochi  Matruchot. 
(After  Vuillemin.) 


REFERENCES. 

In  Saccardo's  '  Sylloge  '  there  is  a  very  important  Bibliotheca  Mycologica 
attached  to  most  volumes. 

Brumpt  (1913).     Precis  de  Parasitologic,  2nd  ed.,  pp.  757-977.     Paris. 

Castellani  (191  i).  Br.  Jour,  of  Dermatology,  vol.  xxiii.,  p.  341  (Nocardia 
tenuis).  (1912).  Trans.  Royal  Soc.  of  Medicine,  p.  23.  (1917).  Pro- 
ceedings of  the  Royal  Society  of  Medicine  ( Acladiosis) .  (1914-1917). 
Journal  of  Tropical  Medicine  and  Hygiene  (several  papers  on  Monilia 
and  Oidium).  (191 7).  Presse  Medicale,  July  5  (Bronchomycosis) . 
(1909-1913).     Centralblatt  fur  Bakteriologie  (Monilia  and  Endomyces). 

Castellani  and  Pinoy  (1916).  Br.  Med.  Jour.  'A  New  Ulcerative 
Dermatomyco  is.' 

Castellani  (191 7).  Journ.  of  Trop.  Med.  October.  (Bronchial  Hemi- 
sporosis,  etc.). 

Chalmers  and  Christopherson  (1914).  Murmekiasmosis  Aniphiliphes. 
Journ.  Trop.  Med.  and  Hyg.  London.  (1916).  A  Sudanese  Actinomy- 
cosis (nocardial  classification).  Journal  of  Tropical  Medicine  and 
Parasitology.     Liverpool. 

Chalmers  and  Archibald  (1915).  Fungi  Imperfecti  in  Tropical  Medicine. 
London.  (1916).  Journal  of  Tropical  Medicine  and  Parasitology 
(Glenospora,  etc.).  Liverpool.  (1917).  New  Orleans  Medical  and 
Surgical  Journal  (Mycetoma  and  Pseudomycetomatous  Formations). 
New  Orleans. 

Chalmers  and  O'Farrell  (1913).  The  Trichonocardiases.  Ann.  Trop. 
Med.  and  Parasit.,  vii..  No.  4,  p.  527.     Liverpool. 

De  Beurmann  and  Gougerot  (1912).     Les  Sporotrichoses.     Paris. 


REFERENCES  1 1 :  ■ 

Engler  and  Prant,  L.  (1900).  Pflanzenfamilien,  vol.  i.,  pt.  i,  with  two 
stars  containing  Lindau's  '  Fungi  Imperfecti,'  pp.  347-517.     Leipzig. 

Jannin  (1913).  Les  Mycoderma,  leur  role  en  pathologic  These  de  Medecine 
de  Nancy.     Nancy. 

Magrou  (1916).    Montpellier  Medical,  vol.  xxxix.,  No.  8. 

Macfie  (1916).    Annals  of  Trop.  Med.  and  Paras.,  vol.  x.,  No.  3. 

Negre  and  Boquet  (1918).  Annales  Institut  Pasteur,  p.  215  (Cultivation  of 
(  ivptococcits  farciminosus). 

Pinoy  (1913).  Bull,  de  lTnstit.  Pasteur,  xi.,  pp.  929-938  (Actinomycoses  and 
Mycetomas).     Paris. 

Regies  Internationales  de  la  Nomenclature  Botanique  (1912).     Jena. 

Saccardo  (1886  and  1906).  Sylloge  Fungorum.  Published  in  eighteen 
volumes,  of  which  vol.  iv.,  1886,  and  vol.  xviii.,  1906,  are  the  most  useful, 
as  they  deal  with  the  Hyphomycetes.  In  the  complete  work  57,660 
species  of  fungi  are  described.     Padua. 

Vuillemin  (1906).  Hemispora  stellata.  Societe  Mycologique  de  France. 
(1910).  Les  Conidiospores.  (1911).  Les  Aleuriospores.  Society  des 
Sciences  de  Nancy.  (1912).  Glenospora  graphii  (Siebenmann).  Comptes 
Rend,  de  l'Acad.  des  Sci.     Paris. 

Winter,  Rehm,  Fischer,  and  Lindau  (1881  to  present  time).  Die  Pilze 
Deutschlands,  Oesterreichs  und  der  Schweiz.  This  is  from  Rabenhorst's 
'  Kryptogamen-Flora,'  Bd.  1,  Abteil.  viii.,  1907,  and  contains  the  Hypho- 
mycetes (erste  Halfte),  Mucedinacea?,  and  Dematiaceae  by  Lindau. 
Leipzig. 

Wolbach,  Sisson  and  Meier  (1917).     Jour.  Med.  Res. 


PART   III 
THE  DISEASES  OF  THE  TROPICS 

SECTION  A:  FEVERS 

SECTION  B:  GENERAL  DISEASES 

SECTION  C:  SYSTEMIC  DISEASES 


1127 


SECTION    A 
FEVERS 

DIVISION  I.   CAUSATION  PROTOZOAL  OR  PROBABLY  PROTOZOA  I .. 
Subdivision  A:  Carried  by  Mosquitoes. 

The  Malarial  Fevers. 

The  Tropical  Hemoglobinurias. 

Yellow  Fever. 

Dengue  and  Allied  Fevers. 

Subdivision  B:  Carried  by  Sand  Flies. 
Pappataci  Fever. 

Subdivision  C:  Carried  by  Tsetse  Flies,  Cone-nosed   Bugs,  and 
Unknown  Arthropoids. 

The  African  Trypanosomiases. 

The  South  American  Trypanosomiasis. 

The  Kala-Azars  and  Pseudo-Kala-Azars. 

Subdivision  D:   Carried  by  Lice,   Ticks,   and  Mites- 

The  Relapsing  Fevers. 

Typhus  Fever. 

The  Spotted  Fever  of  the  Rocky  Mountains. 

Tsutsugamushi  Fever. 

Subdivision  E:  Carried  by  Mammals. 
Rat-Bite  and  Cat- Bite  Fevers. 

DIVISION  II.    CAUSATION  BACTERIAL  OR  PROBABLY  BACTERIAL. 

The  '  Enteroidea  '  Group  of  Fevers. 

Plague. 

Undulant  Fever. 

DIVISION  III.    CAUSATION  PHYSICAL  OR  PROBABLY  PHYSICAL. 
Heat  Stroke  and  Heat  Syncope. 

DIVISION  IV.     UNCLASSIFIED,   COSMOPOLITAN,  AND  WAR  ZONE 

FEVERS. 

DIVISION  V.    DIFFERENTIAL  DIAGNOSIS. 


1128 


CHAPTER  XL 
THE    MALARIAL   FEVERS 

General  account — Quartan  fevers — Tertian  fevers — Subtertian  fevers — 
Pernicious  malaria — Chronic  malaria — Relapses — Reinfections — Compli- 
cations —  Sequelae  —  Diagnosis  —  Prognosis —  Treatment — Prophylaxis — 
References. 

I.  GENERAL  ACCOUNT. 

Definition. — The  malarial  fevers  are  a  group  of  specific  fevers  of 
protozoal  causation,  being  due  to  infections  with  the  parasites 
Plasmodium  malaria  (Laveran,  1881),  which  produces  the  quartan 
fevers,  Plasmodium  vivax  (Grassi  and  Feletti,  1890),  the  agent 
of  the  tertian  fevers,  and  Laverania  malarice  (Laveran,  1890),  the 
exciting  cause  of  the  subtertian  fevers,  which  are  carried  from 
man  to  man  by  the  agency  of  many  species  of  anopheline  mosquitoes. 

Nomenclature. — The  name  '  malaria  '  is  derived  from  two  Italian 
words,  mal  aria,  meaning  '  bad  air,'  and  was  intended  originally 
to  signify  that  the  bad  air  arising  from  marshes  was  the  cause  of  the 
fevers. 

Synonyms. — English  Names  :  Ague,  paludism,  marsh  fever, 
remittent  fever,  intermittent  fever,  climatic  fever,  jungle  fever, 
coast  fever. 

French  Names  :  Fievre  palustre,  paludisme,  fievres  paludiennes, 
fievres  des  marais,  impaludisme,  fievres  malariques,  fievres  tellu- 
riques. 

Italian  Names  :  Paludismo,  malaria,  febbre  intermittent e,  febbre 
palustre.  febbri  malariche,  febbri  di  stagione,  febbri  d'aria,  infezione 
malarica. 

Gmwflw  AT6TW<JS.-\Vechselfieber,KaltesFieber,  Intermittens;  Sumpf- 
fieber,  Klimafieber,  Marschfieber,  Kaltes  Fieber. 

Local  Names. — In  all  countries  local  names  have  been  applied 
to  the  malarial  fevers — for  example,  Roman  fever,  Sierra  fever, 
fever  of  Batavia,  Kurunegala  fever  (Ceylon),  Dambul  fever  (Ceylon), 
Kamerun  fever. 

Seasonal  Nam°s. — As  malarial  fevers  are  more  abundant  in  spring 
than  in  winter,  and  still  more  so  in  summer  and  autumn  than  in 
spring,  it  is  natural  that  seasonal  names  should  be  applied  to  them 
— e.g.,  spring  fevers,  summer  to  autumn  fevers,  autumn  fevers. 

Remarks. — The  malarial  fevers  cover  such  a  wide  field  of  clinical 
symptoms  and  pathological  phenomena  that  it  is  necessary  first 
of  all  to  give  a  general  account,  which  will  comprise  such  subjects 

II2Q 


H3o  THE  MALARIAL  FEVERS 

as  aetiology,  climatology,  pathology,  chemical  pathology,  andmorbid 
anatomy,  and  then  to  consider  the  type  of  fever  caused  by  each  of 
the  three  parasites  mentioned  above — viz.,  the  quartan  fevers,  the 
tertian  fevers,  and  the  subtertian  fevers — in  their  typical  and  atypical 
acute  phases.  Having  completed  this,  we  have  still  to  consider  the 
subject  of  chronic  malaria,  and  we  are  then  in  a  position  to  review 
the  complications,  sequelae,  diagnosis,  and  prognosis.  Finally,  the 
important  matters  of  treatment  and  prophylaxis  must  be  discussed. 

It  maybe  thought  that  it  would  be  better  to  write  three  separate 
chapters  detailing  what  is  known,  considering  the  three  types  of 
fever  separately;  and  though  scientifically  this  would  be  more 
accurate,  still,  clinically  it  would  not  benefit,  because  it  is  in  its 
atypical  forms  that  malaria  is  mostly  seen  by  the  physician  of  to- 
day, and  therefore  clinically  it  is  better  to  treat  the  malarial  fevers 
together  and  not  separately. 

It  is,  however,  necessary  to  preface  the  account  of  the  disease 
with  a  very  short  note  on  the  history,  in  order  that  the  reader  may 
understand  the  salient  features  of  the  evolution  of  knowledge  with 
regard  to  it. 

History. — It  is  suggested  that  the  references  in  the  '  Charaka-Samhita' 
to  fevers  spread  by  mosquitoes  refer  to  malaria,  and  that  this  fever  was 
recognized  at  the  time  of  Homer. 

In  any  case,  Hippocrates  clearly  distinguished  intermittent  from  continuous 
fevers,  while  among  the  former  he  noted  the  tertian  and  quartan  types,  and 
observed  their  frequency  in  summer  and  autumn  and  their  occurrence  near 
stagnant  water  and  after  rains.  In  11O  B.C.  Varro  drew  attention  to  the 
relationship  between  malaria  and  marshes,  a  fact  so  well  realized  in  the  Middle 
Ages  that  illustrations  are  given  of  mosquito-nets  as  the  only  way  to  live  near 
these  collections  of  water. 

We  thus  see  that  very  early  in  the  history  of  medicine  mosquitoes  were 
associated  with  fever,  which  was  also  associated  with  stagnant  water,  and 
that  fevers  were  divided  into  the  intermittent  and  the  continuous.  The  intro- 
duction of  cinchona  bark  into  medicine,  as  noted  in  Chapter  I.,  made  a  distinc- 
tion as  to  those  fevers  which  are  and  those  which  are  not  curable  by  that  drug, 
and  this  was  emphasized  by  thecure  of  '  Le  Grand  Dauphin  '  in  the  days  of 
Louis  XIV.  The  medicine  used  in  this  celebrated  case  appears  to  have  been 
cinchona  bark  soaked  in  Rhine  wine  and  presumably  strained,  and  having 
a  small  quantity  of  tincture  of  opium  added  thereto. 

The  pernicious  fevers  were  brought  into  special  prominence  by  Torti,  in 
1712,  in  his  celebrated  '  Theraputice  Specialis  Mutinae.' 

As  to  the  actual  cause  of  the  disease,  it  was  believed  to  be  minute  forms  of 
animal  life  arising  in  the  exhalations  from  decaying  vegetal  matters  in  marshes. 
This  is  the  miasm  theory  of  malaria,  which  was  fully  accepted  until  modern 
times,  but  in  1847  Meckel  noticed  black  pigment  (haemozoin)  in  the  organs  of 
people  dying  from  malaria.  There  was  much  discussion  as  to  the  origin  of 
this  pigment,  till,  in  1881,  Laveran  discovered  the  parasite  of  malarial  fever, 
and  thus  laid  one  of  the  principal  foundations  of  modern  tropical  medicine. 
Golgi  in  1886  demonstrated  its  life-cycle  in  man,  showing  the  relationship 
between  the  attacks  of  fever  and  the  sporulation  of  the  parasite,  as  well  as  the 
origin  of  the  haemozoin.  Golgi 's  researches  firmly  established  the  parasites 
of  quartan  and  tertian  malaria — i.e.,  Plasmodium  malaria  and  P.  vivax — 
while  Marchiafava  and  Bignami  in  1891  demonstrated  the  existence  of 
Laverania  malaria  and  its  relationship  to  subtertian  malaria. 

During  these  researches  the  presence  of  the  peculiar  crescent  bodies  in  cases 
of  subtertian  infection  became  known,  and  caused  much  speculation;  and  it 
was  now  that  King,  in  1883,  suggested  anew  that  mosquitoes  might  be  the 


HISTORY 


1131 


carrier  of  malaria,  a  suggestion  which  we  have  already  noted  to  be  present 
at  the  dawn  of  written  medicine.  In  1884  Laveran  pointed  out  that  Manson's 
researches  on  filariasis  opened  a  possibility  that  malaria  might  be  conveyed 
in  the  same  way,  but  these  suggestions  did  not  lead  to  anything,  and  it  was 
not  till  Manson,  in  1894,  emphasized  the  importance  of  this  possibility  that 
any  serious  notice  was  taken  of  the  problem  involved.  In  1898  Ross,  working 
on  Manson's  hypothesis,  discovered  the  important  fact  that  the  malarial 
parasite  could  grow  in  the  stomach  of  a  mosquito,  and  eventually  traced  out 
the  whole  cycle  of  the  parasite  of  bird  malaria  in  that  insect,  and  this  was 
subsequently  completed  as  regards  the  human  parasite  by  Grassi,  and  con- 
firmed by  Marchiafava  and  Bignami  with  regard  to  the  infection  in  man. 

Experimental  proof  of  the  truth  of  this  carriage  was  effected  by  Manson 
producing  typical  attacks  of  malaria,  in  persons  who  had  never  left  England, 
by  anopheline  mosquitoes  infected  with  the  parasites  in  Italy,  and  by  Low 
and  Sambon  living  during  the  malarial  seasonin  the  Roman  Campagna,  with 
no  other  protection  except  good  anti-mosquito  measures,  and  failing  to 
become  infected  with  the  disease. 

We  therefore  have  reached  this  stage  of  knowing  the  parasitic  cause  and  its 
life-cycle  in  man  and  the  mosquito,  but  there  are  some  things  which  we  do 
not  know,  and  these  are  the  reason  of  the  persistence  of  the  infection,  in  spite 
of  quinine  therapy,  in  some  people,  while  others  are  without  doubt  cured, 
and  the  reason  why  the  disease  appears  at  times  as  epidemics.  There  can  be 
no  doubt  that  the  realization  of  a  reservoir  for  the  disease  is  most  important, 
and  there  is  equally  no  doubt  that  this  reservoir  is  man,  especially  native  races, 
and  perhaps  more  especially  the  children  of  native  races. 

The  following  additional  points  appear  to  us  to  require  further  study: — ■ 

1 .  The  form  in  which  the  malarial  parasite  lies  dormant  in  the  human  body 
(with  special  reference  to  the  parthenogenesis  of  the  macrogametocyte) . 

The  question  of  parthenogenesis  is  still  much  debated.  Neeb  has  investi- 
gated it  in  L.  malaria,  and  has* contrasted  it  with  the  schizont  stage  of  the 
same  parasite  as  follows: —  j 


Character. 

Segmenting  Macrogametocyte. 

Schizont. 

Size 

Almost     fills     the     erythro- 

Fills   about    two-thirds    of 

cyte. 

the  erythrocyte. 

Shape 

Oval,    not    quite    centrally 

Circular,  and  centrally  situ- 

situated. 

ated. 

Chromosomes    .  . 

Large,      coarse,       purplish- 

Small,   fine,   separate,   pur- 

brown in  red-violet  basis, 

ple,  arranged  in  a  circle 

which  runs  in  a  band-like 

around  the  haemozoin. 

curve  along  periphery. 

Cytoplasm 

Resembles  that  of  a  typical 

Resembles  that  of  the  tro- 

macrogametocyte. 

phozoite. 

Haemozoin 

Coarse         yellowish  -  brown 

Fine,  dark  brown  or  black 

granules          excentrically 

granules,  usually  concen- 

placed. 

trated  into  one  centrally 
placed  clump.     |j 

Thompson  believes  that  Schaudinn  probably  mistook  for  parthenogenesis 
a  double  infection  of  a  corpuscle  with  a  gametocyte  and  a  schizont. 

Ross  believes  that  the  ordinary  asexual  forms  persist  in  the  blood  in  small 
numbers,  and,  undergoing  schizogony,  are  sufficient  to  account  for  the  in- 
definite persistence  of  the  infection.  Karrewij  has  found  parthenogenesis  to 
occur  in  P.  vivax  at  the  height  of  the  febrile  attack. 

2.  Whether  Schaudinn  is  correct  in  believing  that  the  eggs  of  the  mosquito 
can  become  infected,  and,  if  so,  whether  that  infection  is  capable  of  being 
spread  by  the  next  generation  of  mosquitoes. 


1 1 32  THE  MALARIAL  FEVERS 

With  regard  to  this  point  the  tendency  at  present  is  to  believe  that  Schau- 
dinn's  observations  will  not  be  confirmed. 

3.  Whether  any  mosquito  other  than  the  Anophelinae  carry  the  parasites. 
So  far,  no  evidence  in  favour  of  this  has  been  brought  forward. 

4.  Whether  there  is  any  animal  other  than  man  in  which  the  parasites  live 
in  nature. 

The  investigations  of  Fermi  and  Lumbau  in  191 2  are  steps  in  answering 
this  question  negatively,  but  many  more  observations  in  different  countries 
are  necessary  before  a  final  answer  can  be  given.  Mesnil  has  succeeded  in 
infecting  an  orang-utan  with  simple  tertian  malaria.  The  attacks  of  fever 
in  this  animal  were  mild,  but  for  several  weeks  typical  parasites  were  found. 

5.  Whether  there  are  any  malarial  parasites  of  man  which  have  so  far  not 
been  recognized. 

Thus  Stephens  has  insisted  upon  Plasmodium  tenue,  which  does  not  appear 
to  us  to  be  specifically  distinct,  and  Oswaldo  Cruz  has  invited  attention  to  a 
peculiar  quartan  type  of  parasite  found  in  the  valley  of  the  Amazon  and 
associated  with  cedema  of  the  legs  as  a  pronounced  symptom.  Laloir's  parasite 
is  mentioned  in  the  next  chapter,  and  several  other  observers  have  described 
new  varieties  of  the  malarial  parasites  which  require  confirmation. 

6.  Usually  it  is  believed  that  all  fevers  regularly  recurring  every  third  or 
fourth  day  are  malarial,  but  this,  while  correct  as  a  general  rule,  is  open  to 
doubt  in  certain  instances,  and  in  any  case  requires  careful  watch. 

etiology. — The  setiology  may  be  divided  into: — 

I.  The  Exciting  Causes. 
II.  The  Predisposing  Causes  (p.  1142). 

I.  Exciting  Causes. — Malarial  fevers  are  produced  by  the  para- 
sit  esPlasmodium  malaria  Laveran,  i88i,P.  vivax  Grassi  andFeletti, 
1890,  and  Laverania  malaria?  Grassi  and  Feletti,  1890,  because  they 
are  always  found  in  the  blood  or  organs  of  persons  suffering  from 
the  disease,  and  can  be  injected  into  healthy  persons,  producing 
in  them  typical  fevers,  the  different  stages  of  which  correspond  to 
the  stages  of  the  life-cycle  of  the  parasite.  These  parasites  can  be 
spread  from  human  being  to  human  being  by  mosquitoes,  in  whose 
bodies  they  undergo  development  as  ahead}'  described.  Infected 
mosquitoes  can  convey  the  parasites  to  healthy  persons,  living  in 
either  non-malarial  or  malarial  climates,  by  their  bites,  producing 
attacks  of  fever  typical  for  the  type  of  parasite  with  which  the 
mosquito  was  infected.  The  classical  experiment  is  the  infection 
of  Sir  Patrick  Manson's  son  with  tertian  malaria  by  means  of  infected 
anophelines  sent  from  Rome  to  London. 

There  are,  therefore,  three  factors  necessary  for  the  production 
of  malarial  fever:  (1)  the  blood  parasite;  (2)  the  mosquito;  (3)  man. 

1.  The  Blood  Parasite. — We  have  drawn  attention  to  three  para- 
sites in  connection  with  malaria,  and  we  believe  these  to  be  the  only 
three  at  present  known  to  cause  the  fevers,  but  it  is  necessary  to  say 
that  this  view  is  by  no  means  universal.  Some  authorities  believe 
in  a  quotidian  form  of  fever  due  to  a  species  of  Laverania,  or  to  two 
separate  species  of  the  same  genus.  These  parasites,  however,  if 
they  exist  as  distinct  species,  which  we  believe  to  be  very  doubtful, 
have  not  come  within  our  observation,  and  we  therefore  agree  with 
those  writ  erswho  only  acknowledgethethreetypesmentioned  above. 

The  descriptions  of  the  structure  and  life-histories  of  these  para- 


INFECTION  113  3 

sites  have  been  given  in  Chapter  XXI.  (p.  504),  and  need  not  be 
referred  to  here. 

Infection. — The  parasites  are  introduced  into  the  human  body 
as  sporozoites,  which  pass  from  the  salivary  glands  down  the  hypo- 
pharyngeal  canal  of  the  mosquito's  proboscis  into  the  blood  when 
a  human  being  is  bitten  by  an  infected  anopheline, 

Incubation. — Once  in  the  blood,  three  possibilities  confront  the 
parasites:  they  may  either  be  killed  and  no  infection  result,  or  they 
may  remain  dormant  in  some  form  in  the  spleen,  and  not  develop 
until  predisposing  causes,  by  lowering  the  vitality,  give  them  oppor- 
tunity, or  they  may  at  once  proceed  to  develop  and  give  rise  to  fever. 

In  this  latter  event,  there  is  usually  an  interval  between  the  period 
of  the  bite  and  the  attack  of  fever,  for  it  is  evident  that  in  order  to 
influence  the  metabolism  of  the  body  so  profoundly  as  to  produce 
a  rise  of  temperature  a  certain  amount  of  toxin  must  be  generated. 
This  requires  a  definite  number  of  parasites,  and  hence  the  incuba- 
tion period  may  be  short  if  many  parasites  are  simultaneously 
inoculated  by  the  mosquitoes,  or  long  if  but  few.  As  a  rule  it  may 
be  said  that  some  nine  to  twelve  days  are  required  for  the  develop- 
ment of  a  sufficient  number  of  parasites  to  produce  fever.  Acton 
gives  the  following  table  of  the  length  of  the  incubation  period: — 


n         ..  Maximum  in       Minimum  in         Average  in 

Parasite.  ^  t-s  ,-,  6 

Days.  Days.  Days. 


Quartan       ......  18  11  14 

Tertian         ......  21  6  11 

Subtertian  ......  14  2  6 


During  the  incubation  period,  however,  there  may  be  slight 
symptoms  of  lassitude,  or  pains  in  various  parts  of  the  body  coming 
on  at  regular  intervals,  and  often  not  much  regarded,  as  they  may 
pass  off  quickly.  We  are  inclined  to  consider  these  as  being  due  to 
parasites  as  yet  not  numerous  enough  to  produce  fever,  and  we 
think  these  symptoms  of  importance,  as  an  attack  of  fever  may  be 
prevented  by  the  prompt  administration  of  quinine.  This  subject 
will,  however,  be  further  discussed  under  the  Pathology  of  Latent 
Malaria. 

The  Fever. — The  life-history  of  the  parasite  has  a  definite  re- 
lationship to  the  disease,  as  can  be  noted  by  studying  the  diagrams. 
The  rise  of  body  temperature  is  always  associated  \vit h  the  sporu- 
lation  of  the  parasite  and  the  liberation  of  pyrogenetic  toxins,  the 
apyretic  interval  with  the  growth  and  maturation  of  the  parasites 
in  the  red  corpuscle.  This  point  has  been  recently  carefully  studied 
by  Ross  and  Thomson  by  their  enumerative  methods,  and  they 
find  that  there  is  a  distinct  correlation  between  the  number  of  the 
asexual  forms  found  in  the  peripheral  blood  and  the  fever,  and  that 


"34 


THE  MALARIAL  FEVERS 


no  fever  exists  unless  these  forms  exceed  some  hundreds  per  cubic 
centimetre  of  blood.  These  forms  persist  through  the  apyretic  in- 
terval before  a  relapse,  but  in  small  numbers,  which  increase  for 
some  days  before  the  relapse  takes  place.  The  pigmentation  of  the 
cells  and  organs  is  due  to  the  hsemozoin  liberated  by  the  disruption 
of  the  infected  red  cell.  The  liberated  spores  attack  new  erythro- 
cytes, and  so  the  numbers  of  the  parasites  may  increase,  until  in 
certain  pernicious  cases  it  appears  as  though  the  majority  of  the 
red  cells  were  infected  with  parasites,  and,  indeed,  two  or  more 
may  be  noted  in  one  cell.     Such  a  condition  must,  of  course,  lead 

to  death.  ..... 

But  this  does  not  by  any  means  always  happen;  for  it  is  well 
known  that  a  malarial,  especially  a  quartan  fever  may  wear  itself 

out,  the  attacks  becoming  less  and 
less  severe  until  they  cease. 

This  would  appear  to  be  due  to 
acquired  immunity,  which  no  doubt 
explains  the  known  fact  that  the 
European  in  West  Africa  on  first 
arrival  generally  suffers  from  repeated 
attacks  of  fever,  but  he  gradually 
becomes  partially  immune,  and  can 
then  live  there,  with  care,  for  years. 
Further,  it  would  certainly  explain, 
in  part,  the  relative  immunity  of  the 
native  races  in  that  region  who  are 
infected  from  earliest  childhood,  and 
no  doubt  this  is  the  true  cause  of  the 
racial  immunity  which  some  allege 
to  exist.  It  is  now  known  that 
the  merozoites  can,  although  very 
rarely,  penetrate  the  placenta,  and 
infect  the  foetus,  giving  rise  to  con- 
genital malaria. 

The  three  parasites  produce  very 
different  results,  apparently  due  to 
their  habitats.  Thus  Plasmodium  malaria  and  P.  vivax  as  a  rule 
live  mainly  in  the  circulating  blood,  in  which  the  former  sporulates, 
while  the  latter  develops  in  the  spleen;  their  toxins  will  therefore 
produce  general  symptoms.  Laverania  malaria,  on  the  other  hand, 
seems  to  affect  the  red  corpuscles  so  profoundly  that  they  are  liable 
to  adhere  to  the  walls  of  the  capillaries  of  the  organs  in  which  the 
parasite  sporulates.  Hence  this  parasite  may  produce  severe 
local  symptoms,  due  to  the  mechanical  blocking  of  capillaries  or  to 
the  more  intense  local  action  of  the  toxin,  or  to  both  of  these  causes, 
and  therefore  it  is  associated  with  what  are  called  the  pernicious 
fevers — that  is  to  say,  the  fevers  which  produce  severe  effects  on  one 
or  more  organs — e.g.,  on  the  brain,  causing  coma  or  paralysis;  or  on 
the  pancreas,  causing  haemorrhagic  pancreatitis. 


Fig.    6ii. — Plasmodium    vivax. 
(X  1,000  Diameters.) 

Schizont  or  sporulation  stage 
is  shown  enclosed  in  a  red  blood- 
corpuscle,  which  will  presently 
rupture  and  liberate  the  pyroge- 
netic  toxins,  which  will  cause  the 
fever.  At  the  same  time  the 
merozoites  and  ha^mozoin  will 
be  liberated. 

(From  a  photomicrograph 
by  Norman.) 


THE2FE  VER 


H35 


■?At  the  onset,  all  three  types  of  fever  are  apt  to  be  irregular, 
because  the  parasites  are  of  different  ages,  due  to  the  different 
times  of  inoculation,  but  they  settle  down  to  a  regular  type,  possibly 


Fig.  612. — Diagram  of  a  Temperature  Chart  in  Simple  Tertian 

Malarial  Fever. 
i,   Schizont,   with  commencing  sporulation;   2,   sporulating  schizont; 
3,  young  trophozoite;  4,  5,  trophozoites;  6,  schizont. 

because  the  amount  of  antitoxin  generated  is  able  to  kill  off  those 
parasites  which  do  not  conform  to  the  age-period^of  the  majority. 
Sometimes,  however,  two  distinct  broods  may  exist,  producing 
double  fevers,  or  three  distinct  broods,  causing  triple  fevers. 


Fig.   613. — Laverania   malaria.  Fig.   614.— Laverania   malaria. 

,       .                                 ,  (X  250  Diameters.) 

Diagram  showing  parasites  in  red  V'N    J                          ' 

corpuscles    blocking   a   brain   capil-  Photomicrograph    showing    para- 

lary  in  the  cerebral  type  of  pernici-  sites  in  situ  in  red  blood  cells  blocking 

ous  malaria.  capillaries  of  the  brain. 

(After  Norman.) 

The  malarial  parasite  acts  not  merely  by  destroying  the  cor- 
puscle in  which  it  lives  and  by  altering  the  metabolism  of  the 
body  by  the  pyretic  toxin  of  Rosenau  and  his  collaborators,  but  it 
also  has  a  hemolytic  toxin,  first  described  by  Casagrandi  and  Do 
Blasi,  which  destroys  the  red  corpuscles,  thus  throwing  more  work 
on  to  the  liver  and  leading  to  excessive  formation  of  bile,  with,  as 


1136 


THE  MALARIAL  FEVERS 


a  result,  diarrhoea  and  urobilin  in  the  urine.  If  the  blood-destruc- 
tion is  excessive,  the  liver  is  unable  to  convert  the  whole  of  the 
haemoglobin  liberated  into  bile,  with  the  result  that  some  may  be 
left  unaltered,  and  may  produce  haemoglobinuria. 

It  appears,  however,  that  an  antitoxin  is  quickly  formed,  of  the 
nature  of  an  anti-auto-complement,  which  neutralizes  this  haemo- 
lysin,  and  it  further  appears,  from  the  experiments  of  Casagrandi  on 
pigeons  infected  with  Hcemoproteus  (Halteridium),  that  the  anti- 
toxin may  be  a  cause  of  the  natural  disappearance  of  the  parasites 
and  the  cure  of  the  disease.  Of  course,  this  antitoxin  is  produced 
by  the  cells  of  the  body,  and  anything  which  lessens  its  formation, 
such  as  starvation,  gives  the  parasite  a  chance  to  grow  and  cause 


Fig.  615.- 


-Diagram  of  a  Temperature  Chart  in  Double  Tertian 
Malarial  Fever. 


The  fever  of  the  first  and  third  days  is  due  to  one  brood  of  parasites,  and 
that  of  the  second  day  to  another  brood. 

1,  Schizont  of  first  brood;  2,  sporulating  schizont  of  first  brood;  3-5,  tro- 
phozoites of  first  brood;  6,  schizont  of  first  brood;  A,  schizont  of  second 
brood;  B,  sporulating  schizont  of  second  brood;  C-E,  trophozoites  of  second 
brood;  F,  schizont  of  second  brood. 


disease.  Thus  Casagrandi  found  that  out  of  twenty-one  birds 
infected  in  1904,  ten  were  still  infected  in  1905.  On  semi-starving 
two  of  these,  he  produced  relapses,  while  two  others  treated  with 
antitoxin  obtained  from  guinea-pigs  inoculated  with  pigeon's  blood 
did  not  relapse. 

It  will  thus  be  seen  that  a  relapse  may  be  due  entirely  to  pre- 
disposing causes  which  lower  the  vitality  of  the  body  and  prevent 
the  production  of  sufficient  quantities  of  the  antitoxin. 

Besides  the  difference  pointed  out  above  as  to  the  place  of  sporula- 


LA  VERANIA   MALA  RUE  i  i  37 

tion,  there  is  also  a  great  difference  in  the  time  occupied  by  the  cycle 
of  schizogony.  Plasmodium  malaria  requires  seventy-two  hours 
to  complete  its  schizogony,  or,  in  other  words,  it  will  liberate  its 
toxins  and  cause  an  attack  of  fever  in  its  human  victim  every 
seventy-two  hours,  while  in  an  infection  with  only  one  brood  of 
parasites  the  intervening  period  will  be  without  fever.  This  inter- 
mission is  so  marked  that  it  was  noted  by  the  ancients,  and  formed 
one  of  their  types  of  intermittent  fever,  and  as  the  attack  of  fever 
occurred  on  the  fourth  day,  after  an  interval  of  seventy-two  hours, 
it  was  called  a  '  quartan,'  or  fourth-day  fever,  and  as  such  is  clearly 
described  by  Hippocrates.  Plasmodium  vivax  requires  forty-eight 
hours  to  complete  its  schizogony,  and  in  single  infections  pro- 
duces fever  every  forty-eight  hours — i.e.,  on  the  third  day — and 
therefore  this  type  of  fever  is  called  '  tertian.' 

Laverania  malaria,  on  the  other  hand,  does  not  appear  to  be  so 
regular  in  the  time  of  its  schizogony,  and  may  require  from  thirty- 
six  to  forty-eight  hours  for  the  purpose;  but  though  typically  pro- 
ducing a  tertian  fever,  the  effects  due  to  its  sporulation  in  the  organs 
are  much  more  severe  and  protracted  than  those  produced  by 
P.  vivax.  Clinically,  therefore,  there  are  two  types  of  tertian 
malarial  fever — a  benign  and  a  malignant.  The  former,  caused  by 
P.  vivax,  is  generally  called  '  tertian  malarial  fever,'  while  the  latter, 
caused  by  L.  malaria,  is  called  '  subtertian  malarial  fever,'  or 
malignant  tertian. 

In  addition  to  these  clearly  defined  parasites,  others  have  been  described 
by  various  authors,  and  have  been  named  Hcemamceba  pracox  and  H.  immacu- 
lata  by  Grassi  and  Feletti.  The  former  was  said  to  be  pigmented,  and  the 
latter  to  be  unpigmented.  These  parasites  require  only  twenty-four  hours 
for  the  completion  of  the  cycle  of  schizogony;  consequently  they  cause  fever 
every  twenty-four  hours,  which  is  therefore  of  the  nature  of  a  '  quotidian 
malarial  fever.'  Many  authorities,  with  whom  we  agree,  consider  these 
parasites  to  be  only  stages  in  the  development  of  Laverania  malaria.  Quoti- 
dian fever  can  be  produced  by  three  broods  of  P.  malaria,  or  two  of  P.  vivax 
or  L.  malaria,  and  does  not  require  a  special  quotidian  parasite.  Plasmodium 
tenue  Stephens,  191 3,  appears  in  part  to  be  related  to  P.  vivax  and  in  part  to 
L.  malaria,  while  P.  vivax  minutum  of  Emin,  P.  falciparum  quotidianum  of 
Craig  and  Oswaldo  Cruz's  parasite  require  confirmation. 

Therefore,  there  are  only  three  parasites  and  three  classes  of  fever 
to  be  considered — viz. :  (1)  Plasmodium  malaria,  causing  quartan 
malarial  fever;  (2)  P.  vivax,  causing  tertian  malarial  fever; 
(3)  Laverania  malaria,  causing  subtertian  malarial  fever. 

2.  The  Mosquito. — With  regard  to  the  Anophelinae,  we  know  posi- 
tively that  some  can  carry  the  germ,  while  others  cannot  (seep.  883). 
Further,  it  appears  quite  evident  that  Culex  and  Stegomyia  are 
not  carriers  of  malaria.  Daniels,  as  we  have  already  stated,  is 
inclined  to  suspect  the  ^Edinae  as  being  possible  disseminators  of 
malaria  in  jungles,  but  there  is  no  complete  proof  of  this.  Therefore 
we  have  at  present  only  the  Anophelinae  to  consider. 

For  the  various  species  of  the  Anophelinae  which  are  more  or  less  definitely 
known  to  carry  malaria  see  Chapter  XXXV.,  p.  883. 

72 


1 1 38  THE  MALARIAL  FEVERS 

The  presence  of  Anophelinae,  however,  does  not  indicate  that 
there  must  be  malaria  in  the  locality,  an  important  point  to  which 
Celli  was  the  first  to  call  attention. 

England,  for  example,  though  it  possesses  three  species  of  the 
Anophelinae — viz.,  Anopheles  maculipennis  Meigen,  1818;  A.  bifur- 
catus  Linnaeus,  1758;  and  A.  nigripes  St.,  of  which  the  two  former 
certainly  can  carry  malaria — is  practically  free  from  the  disease. 
Nuttall,  Cobbett,  and  Strangeways-Pigg  believe  that  this  condition 
has  been  arrived  at  by  the  reduction  of  the  numbers  of  the  mos- 
quitoes by  drainage. 

Since  the  war,  however,  a  certain  number  of  indigenous  cases  of  benign 
tertian  malaria  have  been  reported. 

On  the  other  hand,  there  is  no  evidence  of  the  existence  of  malaria 
without  some  of  the  Anophelinae.  On  the  contrary,  there  is  evi- 
dence that  where  there  are  no  Anophelinae  there  is  no  malaria 
(Barbados,  for  example,  as  first  noted  by  Low).  Further,  it  is 
highly  probable  that  the  endemic  malaria  of  Mauritius  and  Reunion 
is  due  to  the  introduction  of  Pyretophorus  costalis  Loew,  1866, 
as  has  been  pointed  out  by  Ross.  There  is  also  the  evidence  that 
in  places  where  successful  anti-anopheline  measures  have  been 
carried  out,  as  in  Ismailia,  malarial  fever  has  ceased  to  exist. 

In  order  that  there  may  be  plenty  of  these  insects,  there  must  be 
a  certain  degree  of  warmth;  for  as  a  rule  they  hibernate  in  the 
winter  of  the  temperate  zone,  coming  out  in  the  spring,  and  in- 
creasing in  numbers,  to  reach  a  maximum  in  the  warm  days  of 
autumn.  In  the  tropics,  of  course,  the  heat  is  present  all  the  year 
round.  Heat  alone,  however,  will  not  suffice  for  the  mosquito,  for 
there  must  be  water  for  the  development  of  the  larvae  and  pupae. 
Hence,  in  the  dry  season  in  the  tropics,  there  may  be  few  mosquitoes 
visible,  while  their  numbers  will  increase  remarkably  after  the  rains. 
In  the  dry  season  the  mosquitoes  and  their  larvae  aestivate,  and 
wait  for  more  suitable  conditions. 

There  is,  however,  a  third  factor  to  be  considered,  and  that  is  the 
effect  of  the  temperature  upon  the  parasite  in  the  mosquito.  For 
ages  it  has  been  noted  that  the  fevers  due  to  P.  malaria  and  P.  vivax 
occur  in  the  temperate  zone  in  the  earlier  period  of  the  year — i.e., 
in  the  spring — while  the  worst  fevers,  due  to  L.  malaria,  do  not 
occur  until  the  summer  or  autumn.  This  point  has  been  carefully 
studied  by  Grassi,  Jancs6,  Hollander,  and  others,  and  the  result  of 
their  experiments  tends  to  show  that  temperature  has  most  effect 
upon  the  ookinete  before  it  pierces  the  wall  of  the  stomach  of  the 
mosquito  and  becomes  encysted.  It  would  appear  that  if  the 
temperature  is  below  150  to  160  C,  no  further  development  of  the 
oocyst  will  take  place  in  any  form  of  parasite.  Further,  P.  malarice 
will  develop  at  a  lower  temperature  than  the  other  two,  while 
P.  vivax  will  also  develop  at  a  low  temperature,  but  L.  malarice 
requires  a  distinctly  higher  one. 

This  may  be  the  reason  of  the  scarcity  of  L.  malaria  in  the  tem- 
perate zone,  except  in  the  summer  and  autumn,  and  its  common 


THE   MOSQUITO  1139 

occurrence  in  the  tropics,  and,  possibly,  this  is  also  the  reason  of 
the  rarity  of  P.  malarice  in  the  low  country  of  the  tropics,  while  its 
presence  in  the  hills  is  common. 

Here  may  also  lie  the  explanation  of  the  universal  distribution 
of  P.  vivax  in  both  the  tropics  and  temperate  zone;  for  Jancso's 
researches  show  that  it  can  develop  through  a  wide  range  of  tem- 
peratures. 

But  these  are  not  the  only  factors  concerning  the  Anophelinae  and  malaria, 
for  Schaudinn  showed  that  the  mosquito  eggs  may  possibly  be  infected  by 
the  malarial  parasites,  and  this  at  once  raises  the  question  whether  they  cannot 
be  carried  via  eggs,  larvae,  and  pupae  into  a  second  generation  of  mosquitoes. 
If  so,  this  would  explain  some  outbreaks  of  malaria,  but  so  far  Schaudinn's 
work  has  not  been  confirmed. 

Another  point  of  importance  is  the  fact  that  when  new  lands  are 
opened,  it  is  asserted  that  people  suffer  more  severely  from  malaria 
than  can  be  explained  by  any  theory  brought  forward  at  present. 
For  example,  it  is  stated  that  if  a  zone  of  forest  on  a  steep  hillside 
be  burnt  in  the  dry  season,  and  then  cleared  by  coolies,  who  return 
every  night  to  the  quarters  where  the  other  estate  coolies  also  sleep, 
these  clearing  coolies  will  suffer  severely  from  malaria,  while  their 
fellows  working  on  other  portions  of  the  estate  will  be  but  little 
affected.  The  explanation  of  this  is  not  that  emanations  have 
arisen  from  the  soil  and  invaded  the  bodies  of  the  coolies — indeed, 
after  the  description  of  the  life-history  of  the  malarial  parasite 
already  given,  this  would  be  a  reductio  ad  absurdum — but  merely 
that  the  exposure  to  the  sun  or  the  harder  work  has  lowered  the 
vitality  of  these  coolies,  and  has  given  the  germs  already  in  their 
system  a  chance  to  develop. 

It  has  also  long  been  thought  that  the  mechanical  opening  of  new 
ground  by  digging  produced  the  disease,  but  Ross  has  pointed  out 
that  in  Mauritius  the  digging  of  earth  for  years  caused  no  malaria, 
until  some  new  factor  was  introduced  which  occurred  in  the  sixties 
of  last  century;  this  factor  we  now  know  to  have  been  the  introduc- 
tion oi  Pyrctophorus  costalis  into  the  island. 

When  an  attack  of  malarial  fever  occurs  in  a  person  living  in  a 
place  where  there  are  no  Anophelinae,  it  is  the  result  of  infection 
obtained  in  some  other  place  where  these  mosquitoes  are  to  be 
found. 

It  may  safely  be  concluded  that,  as  far  as  our  present  knowledge 
goes,  certain  of  the  Anophelinae  are  the  only  carriers  of  malaria,  and 
upon  this  public  prophylaxis  must  be  based. 

A  female  mosquito,  apparently,  can  live  for  at  least  a  month 
(Ross),  if  not  longer.  This  does  not  include  such  dormant  periods 
of  its  life  as  the  hibernation  in  the  cold  or  aestivation  in  dry  seasons, 
when  it  may  live  for  a  long  time  in  damp  places. 

The  eggs  of  the  Anophelinae  are  laid  only  in  natural  collections 
of  water  supplied  with  water-plants,  such  as  the  back  eddies  of 
streams,  close  under  the  banks,  which  are  especially  good  breeding- 
places.     The  young  imagines,  apparently,  do  not  usually  travel, 


1140  THE  MALARIAL  FEVERS 

but  remain  near  the  place  where  they  are  developed.  Occasionally 
they  can  be  carried  long  distances  by  ships,  trains,  coaches,  carts, 
etc. ,  but  this  is  the  exception,  and  not  the  rule.  Winds  do  not  appear 
to  carry  them  far,  as  they  generally  take  shelter  from  a  high  wind. 
The  natural  enemies  of  the  Anophelinae  are  numerous,  including  all 
insectivorous  animals,  such  as  bats  and  birds,  together  with  fish, 
which  eat  the  larvae. 

The  anopheline  not  merely  carries  the  germ,  but  because  of  its 
length  of  life,  a  single  individual  may  be  capable  of  infecting  several 
human  beings;  for  it  must  be  remembered  that  there  is  no  proof 
that  the  mosquito  is  in  any  way  deleteriously  affected  by  the 
malarial  parasite,  and  in  this  way  it  forms  a  reservoir  of  infection. 

3.  Man. — The  female  anopheline  requires  blood  for  the  purpose 
of  providing  its  eggs  with  sufficient  nourishment,  and  will,  therefore, 
bite  any  vertebrate  it  may  come  across  in  order  to  obtain  the  same. 
The  malarial  parasites  have,  so  far,  only  been  found  in  man,  and 
hence,  until  they  are  found  in  some  other  vertebrate,  we  are  not 
justified  in  assuming  that  the  anophelines  can  obtain  them  from 
any  other  source.  In  the  tropics  the  native  population  is  un- 
doubtedly the  great  source  of  the  gametocytes  by  which  the  infec- 
tion of  the  mosquito  is  brought  about,  because  the  majority  of 
them  do  not  protect  themselves  against  mosquito-bites.  Of  the 
native  population,  the  children  are  the  greatest  source  of  infection, 
because,  as  has  already  been  explained,  the  adults  obtain  a  partial 
immunity.  But  in  considering  the  native  as  a  source  of  infection, 
care  must  be  taken  not  to  forget  the  European,  whose  blood  is 
sometimes  swarming  with  gametocytes. 

Ross  has  pointed  out  that,  in  considering  the  amount  of  malaria  in  a  par- 
ticular locality,  imported  cases  must  be  distinguished  from  indigenous  cases, 
and  that  the  latter  should  be  further  classified  according  to  the  month  in  which 
they  are  infected.  He  has  also  attempted,  by  mathematical  formulae,  to 
investigate  the  infection-rate  of  the  disease,  which  method  he  terms  '  patho- 
metry ' ;  but  it  is  very  difficult  to  obtain  the  necessary  data  for  these  calcula- 
tions. He  points  out  that  the  number  of  infections  in  a  given  locality  during 
a  given  period  depend  upon — 

1.  The  number  of  persons  with  gametocytes  in  the  blood. 

2.  The  number  of  anophelines  which  have  bitten  these  people  and  become 
infected. 

3 .  The  number  of  infected  Anophelines  which  live  long  enough  to  transmit 
the  infection — i.e.,  at  least  a  week. 

4.  The  number  of  these  surviving  infected  Anophelines  which  get  the  chance 
of  biting  man  again. 

It  is  by  no  means  easy  to  determine,  even  approximately,  in  a  district  the 
number  of  Anophelines  capable  of  carrying  malaria;  but  an  attempt  might 
be  made  to  follow  Ross,  and  determine  the  output  from  one  or  two  of  the 
more  important  breeding-places  by  enclosing  a  given  area  with  mosquito- 
netting,  and  counting  daily  the  numbers  of  Anophelines  which  hatch  out.  A 
calculation  of  the  areas  of  the  breeding-places,  together  with  the  numbers 
hatching  per  diem,  will  give  a  rough  estimate  of  the  increase  during  that  time. 
Associated  with  this,  a  census  may  be  taken  of  the  Anophelines  found  inside 
damaged  mosquito-curtains  very  early  in  the  morning.  This  is  a  method  we 
have  used  in  Tropical  Africa  and  found  of  service,  for  it  supplies  not  merely 
the  number  of  the  Anophelines,  but  also  the  percentage  which  are  infected, 
though  of  course  the  error  is  likely  to  be  considerable.     Ross  proceeds  to  show 


MAN 


1141 


mathematically  that  the  increase  or  diminution  of  the  malaria  really  depends 
upon  the  ratio  to  the  population  of  Anophelines  capable  of  carrying  the  para- 
site; and  also  how  an  epidemic  gradually  increases,  and  how  it  diminishes 
when  the  Anophelines  are  reduced;  and  proves  that,  in  order  that  there  may- 
be a  reduction  of  the  malaria  in  man,  there  need  only  be  a  reduction  in  the 
numbers,  and  not  an  extermination  of  the  Anophelines,  which  is  what  would 
appear  to  have  happened  in  England,  and  to  be  the  cause  of  the  disappearance 
of  malaria  therein. 

Investigation  of  an  Endemic  Region. — In  investigating  malaria  in 
an  endemic  region,  it  is  necessary  to  find  out — 

1.  The  specific  diagnosis  of  the  parasite  or  parasites  causing  the 
malaria. 

2.  The  population  of  the  area. 

3.  The  average  number  of  infected  persons. 

4.  The  average  number  of  infected  persons  carrying  the  gameto- 
cytes  in  their  blood. 

5.  The  species  of  Anophelinae  in  the  district,  and  their  breeding- 
grounds. 

6.  The  species  which  carry  the  parasite. 

7.  The  species  in  which  the  parasite  is  found  in  nature. 

8.  The  number  of  Anophelines  in  the  affected  area. 

No  remarks  need  be  offered  with  regard  to  1,  2,  4,  5,  6,  and  7. 

With  regard  to  8,  the  method  suggested  by  Ross  should  be  adopted; 
and  as  regards  3,  the  quickest  and  the  best  method  is  to  estimate 
the  spleen-rate,  but  it  must  be  remembered  that  the  spleen  is  palpable 
in  1-07  to  2  per  cent,  of  non-malarial  children  living  in  London. 

Ross  suggests  that  the  term  '  endemic  index,'  which  was  intro- 
duced by  Stephens  and  Christophers  to  denote  the  percentage  of 
persons  carrying  parasites  in  their  blood,  should  be  extended  to 
include  not  merely  that  factor,  but  also  the  proportion  of  people 
with  spleens  enlarged  by  malaria. 

He  therefore  proposes  that  the  endemic  index  should  be  made  up 
of  a  parasite-rate  and  a  spleen-rate,  of  which  the  latter  is  the  more 
convenient,  and  if  applied  to  children  under  fifteen  years  of  age,  is 
useful,  provided  that  kala-azar  does  not  occur  in  the  locality  in- 
vestigated. Children  are  chosen  because  the  adults  have  acquired 
a  partial  immunity,  as  already  explained. 

But  the  endemic  index  as  defined  by  Ross  is  sure  to  be  higher 
than  the  mere  spleen-rate,  and  therefore  the  blood  must  be  ex- 
amined in  the  children  whose  spleens  are  not  enlarged,  and  the 
parasite-rate  must  be  added  to  the  spleen-rate  to  obtain  the  true 
endemic  index. 

In  all  calculations  such  as  the  above,  the  statistical  error  must  be  borne  in 
mind,  and  Poisson's  formula,  or  the  modification  by  Pearson  which  Ross 
recommends,  must  be  applied. 

Let  2V=total  number  of  children  under  fifteen  years  of  age  in  a  locality. 
tt=number  examined  for  spleen-rate. 
#=number  with  enlarged  spleen. 

ioo=spleen-rate. 

n  r 

e%=percentage  of  error. 


1 142  THE  MALARIAL  FEVERS 

Then  by  the  Poisson- Pearson  formula  the  percentage  error  will  be : — 
,0/  _  2°°      /2x(n-x)      /    _  n  -  i 

Latent  Malaria. — This  term  is  employed  to  denote  cases  in  which, 
without  any  sign  of  illness,  malarial  parasites  can  be  found  in  the 
blood  in  small  numbers.  These  cases  form  a  reservoir  of  transmis- 
sion to  the  anopheline.  Craig  states  that  out  of  1,267  cases  in 
which  malarial  parasites  were  demonstrated  in  the  blood,  21  per 
cent,  were  latent,  and  the  majority  of  these  were  found  to  be  caused 
by  the  subtertian  parasite. 

Congenital  Infection. — The  question  of  congenital  malaria  has 
been  much  debated,  but  Dumolard  and  Viallet  have  recorded  a 
case  in  which  a  woman  suffering  from  malaria  gave  birth  to  a  child, 
in  which  blood  from  the  umbilical  cord  during  life  and  from  the 
heart  after  death  contained  malarial  parasites  identical  with  those 
in  the  maternal  blood  and  placenta.  A  similar  case  has  been 
recently  reported  by  Leger. 

II.  Predisposing  Causes. — These  may  be  classified  into: — 

1.  Those  which  promote  infection  with  the  parasite. 

2.  Those  which  promote  the  increase  of  the  parasite  in  man  after 
its  inoculation. 

1.  Those  which  Promote  Infection  with  the  Parasite. — 
The  first  of  these  is  residence  in  an  area  which  contains  not  merely 
persons  with  gametocytes  in  their  blood,  but  also  mosquitoes 
capable  of  carrying  the  disease,  associated  with  an  atmospheric 
temperature  suitable  for  the  development  of  the  parasite  in  the 
mosquito. 

The  second  is  any  cause  which  produces  large  numbers  of  mos- 
quitoes capable  of  spreading  the  disease.  This  will  be  not  merely 
a  suitable  air-temperature,  but  also  moisture.  Hence  low-lying, 
marshy  places,  and  the  wet  season,  are  important  predisposing 
causes. 

The  third  is  occupation,  for  this  may  compel  people  to  live  in 
malarial  countries,  to  reside  in  the  low-tying  marshy  portions  of  the 
same,  to  work  in  rice-fields  covered  with  water,  etc.  Age  is  a  pre- 
disposing factor,  as  mosquitoes  have  more  opportunhy  of  biting  a 
young  child  than  an  adult.     Sex  has  no  influence. 

2.  Those  which  Promote  the  Increase  of  the  Parasite 
after  its  Inoculation.— These  predisposing  causes  are  subdi- 
visible into:  (a)  racial;  (b)  personal;  (c)  meteorological. 

(a)  Racial. — There  is  no  doubt  that  the  native  races  suffer  less 
than  an  immigrant  race  in  a  tropical  country,  where  there  is  always 
malaria  present,  and  this  we  believe  to  be  mainly  due  to  the  acquired 
partial  immunity  of  the  native  races,  as  already  explained. 

(b)  Personal. — It  will  be  obvious  from  the  above  remarks  that  the 
parasite  cannot  produce  the  markedly  deleterious  effects  which  we 
term  malarial  fever,  unless  there  be  a  sufficiently  large  number 
present.     Further,  there  appears  to  be  a  tendency  on  the  part  of 


CLIMATOLOGY  1143 

the  body  to  manufacture  protective  substances,  which  keep  the 
growth  of  the  parasite  in  check.  Anything,  therefore,  which  inter- 
feres with  the  production  of  these  checking  materials  will  enable 
the  parasite  to  grow  and  multiply,  and  will  thus  become  a  predis- 
posing cause  of  the  disease.  Such  conditions  are:  (1)  chills; 
(2)  starvation  or  overfeeding;  (3)  the  onset  of  another  acute  disease; 
(4)  the  presence  of  some  chronic  ailment,  which  may  often  be  but 
slight. 

(c)  Meteorological. — We  have  already  drawn  attention  to  the 
relationship  between  the  temperature  of  the  external  air  and  the 
development  of  the  parasites  in  the  mosquito.  It  now  remains  to 
point  out  that  a  similar  relationship  exists  between  that  condition 
and  the  development  of  the  parasite  in  the  human  being. 

Ross  is  of  the  opinion,  not  merely  from  observations  upon  man 
infected  with  malaria,  but  also  upon  birds  infected  with  Kalteridium, 
that  high  air-temperatures  are  favourable  to  the  increase  of  the 
malarial  parasites  in  man.  High  air-temperatures  are  therefore  a 
cause  of  the  relapses  met  with  so  frequently  in  the  hot  dry  season 
of  the  tropics. 

The  reverse  is  also  true;  hence  the  benefit  of  sanatoria  at  high 
altitudes  in  the  tropics,  and  also  of  sending  a  fever-stricken  patient 
to  cooler  climates,  provided  the  change  from  the  hot  to  the  cold 
climate  be  not  sudden,  but  gradual. 

Climatology. — The  geographical  distribution  of  malaria  is  deter- 
mined by  a  combination  of  the  conditions  suitable  for  the  production 
of  large  numbers  of  mosquitoes  capable  of  carrying  the  germ,  and  of 
those  suitable  for  the  development  of  the  parasites  in  the  mos- 
quitoes, together  with  the  presence  of  human  beings  with  numbers 
of  garnet ocytes  in  their  blood. 

The  virulence  in  one  region  more  than  in  another  may  depend 
upon  the  type  of  parasite.  Thus,  Laverania  malaria,  which  is  a 
more  virulent  parasite  than  Plasmodium  malaria  or  P.  vivax,  being 
very  common  on  the  West  Coast  of  Africa,  renders  that  area 
peculiarly  dangerous. 

Generally  speaking,  malaria  is  most  prevalent  in  the  region  of  the 
Equator,  and  diminishes  gradually  north  and  south  till  the  Arctic 
and  probably  Antarctic  Circles  are  reached.  The  malarial  area  lies 
between  630  north  latitude  (mean  summer  isotherm  of  150  to  160  C.) 
and  350  south  latitude.  Its  geography  may  alter  considerably  in 
the  course  of  years.  Thus  regions  in  England,  Holland,  France, 
Germany,  and  Austria-Hungary  are  much  less  malarial  than  they 
formerly  were.  On  the  other  hand,  it  has  been  known  to  affect 
countries  which  at  one  time  were  immune.  Thus  Ross  says  that 
he  believes  that  Mauritius  was  infected  in  the  early  sixties  of  last 
century  by  the  introduction  of  a  mosquito  capable  of  spreading  the 
disease,  and  hence  the  epidemic  which  occurred  in  that  island. 
Reunion  is  another  example.  Barbados  is  said  to  have  no  malaria 
and  no  anophelines.  Therefore  the  geography  to  be  described  is  that 
known  to  exist  at  present. 


1 1 44  THE  MALARIAL  FEVERS 

Africa. — The  worst  malarial  region  in  the  world  is  probably  the 
West  Coast  of  Africa,  from  Senegal  to  the  Congo,  but  the  whole  of 
Africa,  except  portions  of  Cape  Colony,  is  malarial. 

Asia. — Malaria  is  widespread  throughout  Asia,  being  very 
marked  in  certain  districts  of  India,  especially  the  swampy  land  at 
the  foot  of  the  Himalayas,  in  Ceylon,  and  Borneo;  while  Arabia, 
Syria,  the  Straits,  Siam,  and  China  are  also  malarial.  Little  is 
known  about  Siberia. 

Australasia  and  Polynesia.— Malaria  occurs  in  the  north  of 
Western  Australia,  the  Northern  Territory,  North  Queensland, 
Torres  Straits  Islands,  New  Guinea,  Finschaf  en,  the  Solomon  Islands, 
and  the  Bismarck  Archipelago. 

America. — Malaria  exists  in  Central  America,  the  West  Indies, 
with  the  exception  of  Barbados,  the  coast  of  the  Mexican  Gulf,  the 
north  of  South  America,  including  British  Guiana,  and  the  north 
of  Brazil  as  far  as  Rio  de  Janeiro.  Paraguay  and  Bolivia  are 
infected,  as  are  Peru  and  Chili,  but  the  south  part  of  South 
America  is  less  infected.  Many  places  in  the  United  States  are 
malarial,  but  Canada  is  not  markedly  infected,  except  about  the 
northern  shore  of  Lake  Ontario,  while  Greenland  is  supposed  to 
be  free. 

Europe. — Great  Britain  and  Norway  are  practically  free,  but 
most  of  the  other  countries  have  endemic  foci,  particularly  Russia, 
Italy,  Serbia,  Greece,  Turkey,  and  Austria-Hungary. 

In  France  malaria  exists  in  the  south  and  west :  in  Switzerland  in 
the  canton  of  Tessin;  in  Germany  along  the  course  of  the  Rhine, 
and  in  the  lowlands  watered  by  the  tributaries  of  the  Danube. 
Sweden  has  also  some  endemic  spots. 

Apart,  however,  from  mere  geographical  distribution,  it  will  be 
obvious  that  the  necessary  conditions  for  malarial  propagation  are 
best  supplied  in  the  tropics,  especially  near  the  Equator,  where 
there  is  generally  a  considerable  amount  of  atmospheric  moisture 
and  rain  as  well  as  heat. 

The  wet  season  has  also  a  great  influence,  supplying  the  necessary 
moisture  which  at  other  times  may  be  lacking.  The  effect  of  alti- 
tude has  already  been  mentioned. 

Pathology. — In  malaria  the  body  is  invaded  by  protozoal  para- 
sites, which  grow  and  increase  at  the  expense  of  the  red  cells  of  the 
blood,  and  in  doing  so  manufacture  toxins,  of  which  we  know  two 
— viz.,  a  pyrogenetic  toxin  and  a  hemolysin. 

Red  blood  cells  are  found  in  the  whole  of  the  circulatory  organs, 
but  are  generally  contained  in  arteries,  veins,  and  capillaries.  In 
two  places,  however — viz.,  the  spleen  and  bone-marrow — they  come 
intimately  into  relationship  with  the  parenchyma  cells.  Whatever 
function  the  spleen  may  in  future  be  found  to  possess  as  regards 
the  malarial  parasites,  it  probably  acts  as  a  purifier  to  the  blood 
which  passes  through  it.  Perhaps  the  bone-marrow  assists  in  such 
a  function. 

Parasites  contained  in  red  cells  should,  therefore,  be  able  to  pass 


PATHOLOGY  1145 

all  over  the  body,  and  should  be  found  equally  distributed,  no  matter 
what  organ  is  examined.  This  would  be  so  if  the  parasite  did  not 
seriously  damage  the  red -cell,  and,  by  its  toxins,  the  endothelium 
of  the  vessels,  especially  that  of  the  capillaries,  in  which  the  blood- 
flow  is  slowest.  It  would  appear  as  though  the  damage  done  to 
the  red  cell  by  the  quartan  parasites  is  not  severe  enough  to  cause 
them  to  be  caught  in  the  capillaries.  Therefore  the  whole  life- 
history  of  the  quartan  is  spent  in  the  circulation,  and  sporulating 
forms  can  be  readily  seen  in  finger-blood. 

Tertian  parasites,  on  the  other  hand,  seriously  affect  the  red  cells; 
causing  swelling,  degeneration,  and  decolorization.  The  tropho- 
zoite and  schizont  stages  are  easily  seen  in  the  peripheral  circulation. 
Still,  the  sporulating  forms  are  more  common  in  the  spleen,  which 
may  be  looked  upon  as  having  filtered  them  off  from  the  blood 
which  passes  through  it. 

The  subtertian  parasites  act  deleteriously  on  the  corpuscles, 
making  them  smaller  and  darker.  They  rarely  appear  in  the  peri 
pheral  circulation  in  the  sporulating  condition,  while  they  abound 
in  the  spleen  and  internal  organs.  On  examining  the  organs  post 
mortem,  it  will  be  found  that  the  schizont  and  sporulating  forms 
are  found  in  the  capillaries,  while  the  trophozoites  are  found  attached 
to  the  walls  of  the  arterioles  and  venules. 

The  sporulating  parasites  give  rise  to  haemozoin,  which  escapes 
from  the  corpuscle  along  with  the  merozoites,  and  will  therefore  be 
most  commonly  found  in  those  tissues  and  organs  in  which  sporula- 
tion  takes  place — e.g.,  spleen,  liver,  and  bone-marrow— and  will  give 
them  a  definite  coloration,  varying  from  a  reddish-brown  to  a 
black,  according  to  the  quantity  present. 

This  pigment  will,  of  course,  be  also  met  with  in  the  peripheral 
blood,  both  free  and  inside  mononuclear  leucocytes,  for,  on  escaping 
from  the  parasite,  the  haemozoin  is  seized  by  the  mononuclear 
leucocytes,  macrophages,  and  the  endothelial  cells  of  capillaries; 
therefore,  in  acute  malaria,  it  will  be  distributed  evenly  through  the 
organ  affected.  The  pigment  is  later  conveyed  from  the  blood- 
vessels into  the  tissues  by  the  phagocytes,  and  is  found  in  the  con- 
nective tissue  of  the  organ  close  to  the  bloodvessels.  Eventually  it 
disappears,  being  partially  digested  by  the  phagocytes  and  tissue 
cells  and  partially  removed  by  the  lymph.  This  process,  however, 
cannot  continue  without  causing  irritation  of  the  connective  tissue. 

Not  merely  does  pigment  escape  from  the  sporulating  parasite, 
but  also  haemolysin,  which  damages  the  red  cells,  and  causes  the 
appearance  of  another  pigment,  yellowish  in  colour,  called  '  haemo- 
siderin.'  This  is  deposited  in  the  parenchyma  cells  of  the  organs — 
e.g.,  the  liver — and  may  perhaps  damage  them.  The  presence  of 
this  haemolysin  has  been  confirmed  by  the  researches  of  Simpson. 

Another  toxin — this  time  pyrogenous — also  escapes  from  the 
sporulating  parasite,  and  may  be  the  cause  of  the  hyperaemia  found 
in  the  internal  organs — e.g.,  the  spleen  and  the  liver  in  acute  malaria 
— and  may  also  cause  the  destruction  of  the  parenchyma  cell?  of 


1 1 46  THE  MALARIAL  FEVERS 

those  organs.  After  a  series  of  attacks  the  blood  capillaries  and 
lymph  spaces  in  the  liver  and  spleen  remain  permanently  dilated, 
and  separated  by  only  a  slight  amount  of  damaged  parenchyma 
tissue.  Later,  regeneration  of  the  parenchyma  takes  place,  but 
the  organ  will  remain  permanently  altered,  even  though  all  pig- 
mentation may  have  disappeared. 

In  the  case  of  the  subtertian  parasite,  serious  local  damage  may 
be  caused  to  the  brain,  the  intestine,  the  pancreas,  or  other  organs, 
by  the  parasites  massing  in  the  capillaries  and  forming,  with  free 
pigment  and  swollen  endothelial  cells  laden  with  pigment  and 
parasites,  regular  thrombi,  sufficient  to  impede  the  circulation,  and 
thus  to  still  further  damage  the  toxin-poisoned  organ.  Finally,  the 
toxins  are  excreted  by  the  skin  and  by  the  kidney,  and  in  doing  so 
may  damage  the  latter  organ. 

There  are  two  main  conditions,  the  pathology  of  which  must  be 
explained — viz.,  acute  and  chronic  malaria.  In  acute  malaria  there 
are  the  effects  produced  by  each  of  the  three  parasites,  of  which  the 
subtertian  is  liable  to  seriously  damage  important  organs. 

Chronic  malaria  should  also  be  described  according  to  the  three 
types,  but  there  is  at  present  lack  of  material  to  evolve  such  a 
description.  Chronic  malaria  may,  however,  pass  to  an  advanced 
condition  called  '  malarial  cachexia,'  which  shows  itself  in  three 
ways — as  (i)  a  rare  acute  cachexia;  (2)  a  more  common  chronic 
cachexia;  (3)  cachexia  with  amyloidosis. 

In  addition,,  there  are  the  pathological  features  of  latent  malaria 
and  the  relapses. 

Before,  however,  proceeding  to  describe  the  actual  morbid 
anatomy  of  these  conditions,  a  few  words  must  be  said  upon  what 
we  know  of  the  chemical  pathology  of  the  disease  and  on  the  blood 
changes  which  take  place. 

Chemical  Pathology. — The  pyretogenous  toxin  has  already  been 
mentioned  among  the  poisons  of  animal  origin,  and,  though  long 
suspected  of  being  present,  its  actual  occurrence  was  first  proved 
by  Rosenau  and  his  collaborators.  Probably  it  is  the  poison  which 
acts  deleteriously  upon  the  tissues  of  the  organs  and  causes  meta- 
bolic changes,  but  this  is  only  a  matter  of  conjecture. 

We  know  that  the  heat  output  in  the  cold  stage  of  the  attack  is 
markedly  diminished — a  condition  met  with  in  many  fevers — but 
the  chemistry  of  the  metabolic  changes  is  but  little  known.  During 
the  attack  the  urine  is  at  first  increased  in  quantity,  which  is  thought 
to  be  due  to  the  rise  of  blood-pressure  internally,  owing  to  the 
contraction  of  the  cutaneous  vessels  during  the  cold  stage.  Not- 
withstanding this  increase  in  quantity,  the  specific  gravity  is  raised, 
because  of  the  increased  metabolism  caused  by  the  toxins,  as  is 
shown  by  the  large  increase  in  solids.  The  colour  is  dark,  and  the 
acidity  of  the  urine  is  increased,  as  in  most  fevers.  Nitrogen  is 
excreted  in  excess,  which  is  largely  due  to  the  increase  of  urea. 
Chlorides,  sulphates,  and  bases,  especially  potassium,  are  all  in- 
creased in  quantity.     Phosphates,  however,  are  diminished  during 


CHEMICAL  PATHOLOGY  1147 

the  actual  attack,  but  increased  as  it  is  passing  off,  and  are  con- 
siderably increased  in  the  intermission.  Phosphoric  acid  is  there- 
fore retained  in  the  body  during  the  attack. 

As  would  be  expected,  iron  is  excreted  in  increased  quantity, 
probably  due  to  hsemozoin  and  haemosiderin,  but  this  increase  does 
not  really  appear  until  after  the  actual  attack  is  over,  and  then 
continues  for  some  days. 

As  before  remarked,  the  urine  may  contain  a  considerable  quantity 
of  urobilin,  and  the  indigo-blue  may  be  also  increased. 

Schlesinger's  test  for  urobilin  in  the  urine  is  performed  by  adding  to  the 
unfiltered  urine  an  equal  quantity  of  a  solution  of  10  parts  of  zinc  acetate 
in  absolute  alcohol,  shaking  the  mixture,  and  adding  a  few  drops  of  a  solution 
of  lugol,  stirring  and  filtering,  when  a  fluorescence  will  appear,  varying  in 
intensity  according  to  the  quantity  of  urobilin  present. 

The  diazo-reaction  is  said  to  be  obtainable  in  about  5*5  per  cent, 
of  cases.  Serum-albumen  may  be  present  after  severe  attacks,  and 
proteose  has  been  reported,  as  well  as  nucleo-proteid. 

When  the  intermission  comes,  the  urine  diminishes  in  quantity, 
but  nitrogen  is  still  excreted  at  a  higher  rate  than  it  should  be, 
though  less  than  during  the  attack. 

Chlorides  are  diminished,  phosphates  increased;  sulphates, 
though  still  higher  than  normal,  are  less  than  during  the  attack, 
while  the  excretion  of  the  bases  is  diminished.  The  excretion  of 
iron  is  marked,  and  the  toxicity  of  the  urine  is  said  to  be  considerable. 

During  convalescence  the  most  marked  features  are  the  polyuria, 
with  low  specific  gravity,  which  in  subtertian  fevers  may  be  so 
marked  as  to  alarm  the  patient,  while  in  quartan  and  tertian  it 
may  be  so  slight  as  to  escape  attention.  There  is  also  increase  of 
chlorides  and  potassium  salts  excreted. 

Urriola  states  that  if  the  urine  in  malarial  cases  is  centrifuged,  four  types  of 
pigment  granules  may  be  found:  (1)  very  fine  granules;  (2)  larger  granules 
in  groups;  (3)  large  masses;  (4)  granules  in  leucocytes  and  hyaline  casts 
It  is,  however,  difficult  to  exclude  extraneous  matters. 

As  regards  the  faeces,  the  most  noticeable  feature  is  the  increase 
in  the  excretion  of  bile  and  iron,  both  of  which  are  related  to  the 
blood-destruction.  Ross  and  Thomson  have  shown  that  the  quan- 
tity of  faecal  urobilin  (stercobilin)  shows  a  marked  correlationship 
with  the  occurrence  of  the  fever,  being  increased  during  the  attack. 

The  sweat  of  a  malarial  patient  is  well  known  to  have  a  peculiar 
odour,  and  contains  substances  very  toxic  to  rabbits. 

The  above  chemical  features  point  to  the  fact  that  the  toxins  of 
malaria  are  excreted  from  the  body  by  the  sweat  and  the  urine,  and 
that  during  the  fever  there  is  very  active  nitrogenous,  potassic, 
chloride,  and  sulphate  metabolism. 

That  there  may  be  other  toxins  as  yet  unknown  is  obvious  from 
the  fact  that  the  Plasmodia  cause  marked  shivering  and  a  sensation 
of  coldness,  even  though  the  actual  blood  temperature  is  rising.  It 
would  appear  as-though  this  is  due  to  the  constriction  of  the  cuta- 
neous vessels  by  some  poison  which  acts  on  non-striped  muscle, 


n48  THE  MALARIAL  FEVERS 

for  the  arrectores  pilorum  are  also  affected,  producing  goose-skin. 
Laverania  malaria,  however,  because  it  sporulates  internally,  and 
not  in  the  peripheral  blood,  causes  chills  more  rarely  than  the  other 
two. 

De  Blasi  has  shown  that  an  antihasmolysin  is  formed  in  the  human 
body,  and  Casagrandi,  as  already  mentioned,  has  performed  experi- 
ments on  Halteridium  in  birds,  tending  to  show  that  this  substance 
has  a  restraining  power  against  increase  of  the  parasites. 

The  only  other  remarks  we  can  offer  on  the  chemical  pathology  are 
limited  to  the  nature  ot  the  pigments,  haemozoir  and  hsemosiderin. 

ILemozoin.— Hsemozoin  is  the  black  pigment  formed  from  haemo- 
globin by  the  malarial  parasites  while  living  in  the  erythrocytes, 
and  is  afterwards  distributed  over  the  body  on  the  disruption  of 
the  red  cells.  It  is  taken  up  by  phagocytes,  as  already  described, 
and  removed  from  the  bloodvessels  to  the  connective  tissue,  in  which 
it  can  be  seen  in  the  liver  and  spleen.  It  is  soluble  in  alkalis, 
but  not  in  water,  alcohol,  chloroform,  ether,  or  acids.  It  contains 
iron,  but  in  the  form  of  an  organic  compound,  which  will  not  give 
the  Berlin-blue  reaction.  Eventually  it  disappears  from  the  con- 
nective-tissue cells,  but  whether  it  is  eliminated  from  the  body  or 
used  in  some  altered  form  we  do  not  know.  As  it  is  formed  by 
malarial  parasites,  it  is  peculiar  to  the  diseases  caused  by  them. 
Brown  considers  that  it  is  formed  by  the  action  of  a  proteolytic 
enzyme  from  the  parasite  acting  upon  the  haemoglobin  of  the 
erythrocyte,  and  that  therefore  it  is  formed  from  haematin,  a 
conclusion  also  arrived  at  by  Carbone  and  V.  Ascoli. 

Hemosiderin. — This  is  the  yellow  pigment  found  in  the  form  of 
yellow  granules  in  the  parenchyma  cells  of  the  liver,  spleen,  kidney, 
bone-marrow,  endothelium  of  capillaries,  and  occasionally  in  leuco- 
cytes, after  any  great  destruction  of  blood  cells.  In  malaria  it  is 
undoubtedly  due  to  the  action  of  haemolysins  destroying  the  red 
cells.  It  contains  iron  in  the  form  of  an  inorganic  compound,  and 
gives  the  usual  Berlin-blue  reaction.  It  is  insoluble  in  alkalis  and 
acids,  but  is  soluble  in  alcohol. 

The  Blood. — The  parasites  live  in  the  blood,  in  which  they  produce 
changes  by  their  own  action  and  by  that  of  their  toxins. 

The  malarial  parasites,  being  true  blood  parasites  and  living  in 
the  red  cells,  form  the  most  important  feature  of  the  pathology  of 
the  blood,  but  their  structure  and  life-history  having  already  been 
described  in  Chapter  XVII.,  it  only  remains  to  estimate  their 
numbers. 

Ross  estimates  that  a  medium-sized  person  of  68  kilogrammes 
(150  pounds)  body  weight  possesses  25,000,000,000,000  erythrocytes. 
In  a  severe  infection  he  estimated  the  parasites  as  numbering  12  per 
cent,  of  the  corpuscles — i.e.,  3,000,000,000,000 — and,  further,  he 
considers  that  if  they  fall  below  1  to  100,000  corpuscles — i.e., 
250,000,000 — they  will  cause  but  little  disease.  Certainly,  large 
numbers  of  parasites  can  exist  in  the  body  and  go  through  their  life- 
cycle  in  the  spleen  without  causing  symptoms.     This  condition  is 


THE  BLOOD 


ii(9 


called  '  latent  malaria/  and  can  be  easily  converted  into  active 
malaria  by  any  cause  which  depresses  the  vitality  of  the  body. 

Erythrocytes. — In  quar- 
tan malaria  the  corpuscle  con- 
taining the  parasite  is  a  little 
smaller  than  a  normal  cor- 
puscle, and,  if  anything,  more 
darkly  coloured.  In  tertian 
malaria  it  is  swollen  and  more 
lightly  coloured,  and  on  treat- 
ment with  Leishman's  stain 
exhibits  fine  red  granules 
(Schiiffner's  dots),  which  are 
to  be  looked  upon  as  a  sign 
of  degeneration  of  the  cor- 
puscle. In  subtertian  malaria 
the  corpuscles  when  stained 
in  the  same  way  may  exhibit 
Maurer's  dots  or  clefts,  which 
appear  as  large,  irregular  red 
formations,  and  also  Marshall- 
Plehn's  bluish  dots,  the  signifi- 
cance of  which  is  uncertain.  The  red  cells  may  become  transformed 
into  brassy  bodies,  which  are  shrunken  red  corpuscles  which  have 

taken  on  the  colour  of 

:•■♦ 


Fig.      616. — Blood      Film      showing 
Schizont  of  Plasmodium  vivax. 

(From  a  micropb.otograph  by  J.  J.  Bell.) 


■-  .'■ 


. 


: 


brass.  These  are  cor- 
puscles which  have 
undergone  some  form 
of  necrosis,  probably 
due  to  the  haemolysin, 
though  it  has  been 
thought  that  they  were 
infected  corpuscles  in 
which  the  parasite  had 
died  as  a  result  of  the 
necrosis. 

Partial  decoloriza- 
tion  of  the  erythrocytes 
has  been  recorded  in 
subtertian  infections, 
and  is  especially  well 
marked  in  those  con- 
taining crescent  bodies. 
Bignami  thinks  that  in 
the  subtertian  fever  the 
red  corpuscles,  which 
are  infected  with  the 
parasite,  have  a  diminished  elasticity,  and  therefore  are  not  so 
capable  of  circulating,  and  cling  to  the  walls  of  small  capillaries. 


Fig.     617. — Blood     Film     showing     Heavy 
Infection  with  Laverania  malarice. 

(From  a  microphotograph  by  J.  J.  Bell.) 


1 1 50  THE  MALARIAL  FEVERS 

As  every  sporulation  causes  the  destruction  of  red  cells,  anaemia 
is  one  of  the  marked  features  of  malaria.  This  destruction  takes 
place  at  each  paroxysm,  and  though  in  quartan  and  tertian  fever  it 
may  be  slight,  in  subtertian  fever  it.  is  apt  to  be  considerable. 

After  a  certain  number  of  attacks  of  fever  the  loss  becomes  much 
less  than  in  the  earlier  seizures. 

When  the  fever  is  intermittent,  regeneration  takes  place  quickly, 
so  that  before  the  next  paroxysm  the  normal  number  of  erythrocytes 
may  be  nearly  reached;  but  even  in  quartan  and  tertian  fevers,  if 
long-continued,  anaemia  will  result. 

The  histological  changes  in  the  unaffected  corpuscles  are  pallor 

and  poikilocytosis,  with  demi-lune  and  crescentic  forms,  and  in 

severe   cases   megaloblasts,    with   polychromatophilia   and   basic 

granular  degeneration,  together  with  normoblasts,  may  be  noted. 

The  tonicity  of  the  corpuscles  is  increased  after  a  number  of  attacks, 

according  to  Viola.     In  the  blood  of  malarial 

cachectics  the  brothers  Sergent  have  described 

basophile  formations  having  the  shape  of  a 

figure  8,  with  a  double  contour,  and  Brumpt 

and  others  have  described  basophile  rings  with 

a  single  contour.      Laveran  considers    these 

appearances  to  be  due  to  artefacts. 

Leucocytes. — The  leucocytes  are  at  first 
increased  during  the  paroxysm,  and  then 
markedly  diminished,  so  that  a  leucopenia  is 

FlG    6lg  blood    ^^e  characteristic  of  the  simple  malarial  fevers. 

Film    showing    The  normal  ratio  of  white  to  red  corpuscles 

Partial  Decolor-     is   i   to   500   or  600.     From   observations   of 

ization     of     an    Stephens  and  Christophers  this  may  be  1  to  90, 

a^fTenVIod?     *  t0  2?°.  J  to  290  or  i  to  300  during  the  rigor 

of   Laverania   ma-      (*•«•»    leucocytosis),    becoming    I    to    764   (*.*., 

laricB.    (x  1,000.)      leucopenia)  when  the  rigor  is  completed,  and 

(After  Norman.)        when  the  temperature  falls  altering  to  1  to  968. 

Billet  has  shown  that  if  curves  are  made  of 

the  leucocytic  count  and  the  temperature  in  simple  tertian  and 

quartan  fevers,  the  two  curves  follow  one  another  in  their  rises 

and  falls.     In  pernicious  malaria  there  may  be  leucocytosis. 

Another  important  matter  is  the  relative  increase  of  the  large 
mononuclear  leucocytes,  and  this  is  better  marked  during  the 
leucopenia  of  apyrexia  than  during  the  leucocytosis  of  the  attack, 
for  Thompson  finds  that  it  is  usually  low  during  the  rigor  and  the 
febrile  stage,  but  with  the  decrease  of  the  fever  it  may  become  as 
high  as  90  per  cent,  of  the  total  leucocytes.  This  mononucleosis 
is  observed  for  a  long  time  after  an  attack  of  fever,  even  when 
quinine  therapy  is  persisted  in  continuously. 

The  following  are  some  examples  of  the  differential  count  accord- 
ing to  various  observers: — 


THE  BLOOD 

1151 

Kind  of  Corpuscles.              Da  Costa. 

Billings. 

Christo- 
phers and 
Stephens. 

Baslianelii. 

Polymorphonuclears    . .          . .        67*00 

Large  mononuclear  and  tran- 
sitional          . .          . .          .  .        15*94 

Lymphocytes    ..          ..          ..        15*33 

Eosinophiles      . .           . .           .  .          0*83 

65-04 

16-90 

16-90 

0-96 

50-2 

31*4 

iS-i 

o-4 

39-0 

41-0 

19-1 

o-6 

It  must  be  remembered  that  this  relative  increase  in  the  mono- 
nuclears has  been  noted  in  other  protozoan  infections. 

Phagocytosis  is  particularly  seen  in  the  large  mononuclear  and 
transitional  leucocytes,  and  to  a  less  degree  in  the  polymorpho- 
nuclear leucocytes  and  very  rarely  in  the  eosinophiles.  In  these 
cells  clumps  of  pigment  and  the  residue  left  after  segmentation  of 
a  schizont  are  not  uncommonly  seen.  If,  however,  something 
abnormal  takes  place  in  the  red  corpuscle,  a  phagocyte  may  engulf 
it  and  its  parasite,  or  only  the  parasites  if  they  have  escaped  from 
the  red  cell,  or  only  the  debris  of  the  red  cell. 

Vacuolization  and  diminution  of  the  staining  power  of  leucocytes 
are  to  be  seen.  Myelocytes  are  said  by  Da  Costa  to  be  found  in  sub- 
tertian  infection  up  to  0*51  per  cent.  Eosinophiles  diminish  during 
the  paroxysm,  and  increase  during  the  apyrexia. 

Hemoglobin. — 'This  is,  of  course,  reduced,  but  the  colour  index 
may  vary  sometimes,  being  less  than  normal.  Ross  and  Thomson 
find  that  it  falls  markedly  with  an  attack  of  fever,  but  rises  rapidly 
during  convalescence. 

The  Specific  Gravity  of  the  Blood. — Diminution  of  the  den- 
sity of  the  blood  begins  at  the  onset  of  the  attack,  and  becomes  more 
marked  as  it  proceeds,  and  may  amount  to  a  diminution  of  6-2 
degrees.  This  fall  is  probably  due  to  destruction  of  red  cells  and 
the  breaking  up  of  large  parasites,  which  more  than  balances  any 
loss  of  liquid  by  vomiting,  diarrhoea,  sweating,  and  polyuria. 

The  diminution  is  most  marked  in  full-blooded  persons,  in  primary 
affections,  and  first  attacks,  less  in  later  attacks,  and  least  in  chronic 
malaria.     The  density  recovers  after  treatment  by  quinine. 

Chronic  Malaria. — In  chronic  malaria  there  is  a  leucopenia  and 
a  marked  decrease  in  the  numbers  of  the  red  cells,  which  is  but  little 
affected  by  febrile  attacks. 

Post-malarial  An.emia. — Bignami  points  out  that  there  are  cases 
in  which,  in  spite  of  the  cessation  of  the  malarial  fever,  the  anaemia 
tends  to  progress,  and  these  he  calls  post -malarial  anaemias.  They 
are  generally  induced  by  age,  malnutrition,  overwork,  pregnancy, 
nursing,  etc.,  and  are  not  due  merely  to  the  malarial  infection. 
Bignami  divides  these  into  four  types,  according  to  the  characters 
of  the  blood. 


1 1 52  THE  MALARIAL  FEVERS 

First  Type. — This  form  of  anaemia  comes  on  after  attacks  of 
ordinary  acute  malaria,  and  is  characterized  by  well-marked 
diminution  in  the  erythrocytes,  the  presence  of  normoblasts,  diminu- 
tion of  the  colour-index,  and  leucopenia  associated  with  relative 
mononuclear  increase.     In  this  type  the  prognosis  is  good. 

Second  Type. — The  second  type  is  severe,  and  the  prognosis  is 
exceedingly  bad.  It  is  characterized  by  great  diminution  in  the 
red  cells,  presence  of  poikilocytes,  megalocytes,  normoblasts,  and 
megaloblasts,  with  leucopenia  and  relative  mononuclear  increase. 

Third  Type. — This  is  rapidly  fatal,  and  has  similar  characters  to 
the  second  type,  but  is  without  normoblasts. 

Fourth  Type. — This  type  is  really  grave  chronic  anaemia,  resem- 
bling the  first  type,  but  being  specially  characterized  by  the  paucity 
of  the  normoblasts  and  the  marked  leucopenia. 

Wassermann  reaction  is  in  our  experience  generally  negative. 

Morbid  Anatomy. — The  morbid  anatomy  of  malaria  has  been 
most  carefully  studied  in  recent  years  by  Bignami  in  Italy  and 
Ewing  in  America.  It  may  be  considered  under  the  following 
headings: — 

A.  Acute  Malaria. 

i.  Lesions  caused  by  Plasmodium  malaria. 

2.  Lesions  caused  by  Plasmodium  vivax. 

3.  Lesions  caused  by  Laverania  malaria. 

B.  Chronic  Malaria. 

1.  Lesions  caused  by  Plasmodium  vivax. 

2.  Lesions  caused  by  Laverania  malaria. 

3.  Malarial  cachexia. 

4.  Latent  malaria. 

A.  Morbid  Anatomy  of  Acute  Malaria — 1.  Lesions 
Produced  by  Plasmodium  malaria. — Plasmodium  malaria  goes 
through  the  entire  process  of  schizogony  in  the  circulating  blood, 
and  hence  is  evenly  distributed  all  over  the  body,  and  therefore 
does  not  especially  accumulate  in  any  one  organ.  Marchiafava  and 
Bignami  mention  that  they  have  made  two  autopsies,  one  on  a 
case  of  acute  quartan  malaria,  in  which  the  patient  died  of  nephritis, 
and  the  other  in  a  case  of  the  same  fever,  in  which  the  patient  died 
of  spinal  disease. 

The  visceral  lesions  are :  Spleen  enlarged,  not  softened  nor  very  melanotic ; 
liver  and  bone-marrow  not  markedly  melanotic;  parasites  in  the  spleen  and  in 
the  blood,  but  not  in  the  brain. 

Leishman  has  mentioned  that  he  has  received  films  from  the 
peripheral  blood  and  spleen  of  a  fatal  case,  in  both  of  which  the 
parasites  were  very  numerous,  but  he  was  not  in  a  position  to  state 
whether  the  patient  died  of  malaria  or  not.  If  P.  malaria  is  to 
produce  severe  symptoms,  it  would  appear  necessary  for  it  to  exist 
in  very  large  numbers. 


MORBID  ANATOMY  1153 

2.  Lesions  Produced  by  Plasmodium  vivax. — It  is  rare  for 
death  to  ensue  as  the  result  of  an  infection  with  P.  vivax.  Still,  this 
does  occur  at  times  when  there  is  a  heavy  infection.  Ewing  has 
described  a  case  of  tertian  infection  causing  coma,  haemoglobinuria, 
and  either  causing  or  associated  with  catarrhal  colitis. 

The  principal  features  are  the  pigmentation  of  the  bone-marrow,  liver,  and 
spleen,  which  last  is  also  enlarged.  The  blood  and  spleen  show  large  numbers 
of  P.  vivax.  The  kidneys  and  colon  are  inflamed,  and  the  endothelial  cells 
of  the  brain  are  swollen  and  contain  pigment. 

3.  Lesions  Produced  by  Laverania  malarice. — We  have  already 
insisted  several  times  upon  the  fact  that  L.  malaria  differs 
from  the  other  malarial  parasites  in  sporulating  in  the  organs, 
generally  in  the  spleen,  but  at  times  choosing  one  organ  and  at  other 
times  another.  The  organ  in  which  it  sporulates  in  large  numbers 
suffers  most,  and  produces  symptoms  which  give  the  characters  of 
that  particular  type  of  malarial  fever. 

Thus  the  parasite  may  attack  principally  the  brain,  the  intestine, 
the  heart ,  or  the  pancreas,  producing  marked  signs  of  disease  therein. 
Therefore  the  conditions  of  the  organs  vary  with  the  localization  of 
the  parasite. 

Macroscopical  Examination. — In  general  the  body  is  pale,  with  a  yellowish 
tinge,  which  may  be  noted  superficially  in  white  races,  but  which  may  only 
be  observed  in  the  subcutaneous  tissues  in  native  races.  The  heart  may  be 
small  or  dilated,  the  muscle  flabby  and  pale  or  brownish,  and  ecchymoses  may 
be  present  in  both  the  epicardium  and  endocardium.  The  lungs  may  be 
normal,  anaemic,  or  hyperaemic  and  congested.  Hasmozoin  is  not  easily 
detected  in  the  lungs,  because  of  the  usual  pigmentation.  As  first  described 
by  Laveran,  a  sclerosis  of  the  lungs  is  not  infrequently  met  with. 

The  liver  is  generally  enlarged,  and  varies  from  a  dark  brown  to  a  slate 
colour.  It  is  soft  and  congested,  and  the  outlines  of  the  lobules  are  usually 
indistinct.     The  gall-bladder  is  full  of  dark-coloured  bile. 

The  spleen  is  enlarged,  with  a  tense  capsule,  but  its  consistency  is  usually 
much  less  than  normal,  and  at  times  it  may  be  almost  diffluent  in  very 
acuie  cases.  We  have,  however,  seen  it  quite  firm  in  a  recent  infection. 
Its  colour  varies  from  a  deep  brown  to  black. 

The  stomach  and  intestines  may  show  but  little  change,  except  in  the  choleraic 
forms,  in  which  their  mucosa  may  be  intensely  congested  and  dark  red  in 
colour,  except  where  the  Peyer's  patches  and  the  solitary  glands  stand  out 
clearly.  The  intestine  is  darker  red  in  certain  places,  giving  it  a  mottled 
appearance,  and  the  contents  may  be  blood-stained  fluid  with  flakes  of  mucus. 
In  fact,  the  appearance  post  mortem  and  the  history,  if  death  takes  place 
rapidly,  so  much  resemble  those  of  cholera  that  in  regions  where  that  disease 
is  prevalent  mistakes  may  arise,  though,  indeed,  the  dark  pigmentation 
should  enable  errors  to  be  avoided.  We  have  not  infrequently  met  with 
dark  pigmentation  of  the  small  and  large  bowels  in  cases  of  pernicious  cerebral 
malaria,  and  in  general  infection  without  cerebral  symptoms.  This  pig- 
mentation is  due  to  ha?mozoin,  as  can  be  easily  proved  by  microscopical 
examination. 

The  lymphatic  glands  may  be  swollen,  while  the  pancreas  is  usually  normal, 
but  it  may  be  very  rarely  swollen  and  haemorrhagic — i.e.,  in  a  condition  of 
haemorrhagic  pancreatitis.  We  have  seen  it  quite  brown,  and  pigmented  with 
capillaries  choked  with  infected  corpuscle  debris,  pigment,  etc. 

The  suprarenal  capsules  may  be  congested.  The  kidneys  are  more  or  less 
normal,  but  sometimes  they  are  congested,  with  punctiform  haemorrhages  in 
the  pelvis  and  cloudy  swelling  in  the  parenchyma,  or  brownish.  The  serous 
membranes,   pleura,   and  peritoneum,   show  as  a  rule  nothing  remarkable, 

73 


1 1 54  THE  MALARIAL  FEVERS 

except,  perhaps,  a  little  pigmentation.  The  bone-marrow  is  generally  hyper- 
semic  and  chocolate-brown  in  colour.  The  brain  may  appear  normal,  but  in 
the  cerebral  type  of  pernicious  malarial  fevers  there  will  be  marked  changes. 
In  slight  cases  there  may  be  only  cedema  without  pigmentation  or  petechia?. 
Sometimes  there  is  brownish  pigmentation  without  petechiae,  and  with  or 
without  cedema.  Typically,  however,  there  are: — (i)  Hyperaemia  of  the 
leptomeninges,  which  may  be  cedematous  and  thickened;  (2)  brownish,  or 
even  blackish,  pigmentation  of  the  cortex;  and  (3)  punctiform  haemorrhages 
in  the  white  matter  under  the  cortex  or  elsewhere.  The  spinal  cord  exhibits 
changes  similar  to  those  in  the  brain,  while  the  retina  shows  numerous  haemor- 
rhages. 

Microscopical  Examination. — After  death,  parasites  may  be  found  in  the 
blood  of  the  heart,  spleen,  bone-marrow,  and  at  times  in  the  capillaries  of  the 
brain,  intestines,  pancreas,  etc. 

The  parasite,  however,  is  much  shrunken,  and  the  typical  forms  seen  during 
life  are  not  distinct  after  death.  Thus  the  ring  form  shrinks  and  becomes  a 
rounded  disc,  with  the  chromatin  particle  situated  at  the  periphery.  The 
fully  developed  schizont  is  more  typical,  the  merozoites  being  arranged  in  a 
ring  around  the  central  pigment  block.  If  the  post-mortem  is  made  quickly 
this  shrinking  is  not  noted.  The  mononuclear  leucocytes  will  be  noted  to 
have  pigment  granules,  while  the  polymorphonuclears  may  show  phagocytosis. 
In  films  from  the  internal  organs  macrophages  with  parasites  and  red  cells 
may  be  seen. 

In  the  heart  there  may  be  a  few  parasites,  but  very  rarely  the  capillaries 
will  be  found  filled  with  red  cells  containing  numerous  parasites,  and  the  heart 
muscle  laden  with  haemosiderin,  as  has  been  described  in  a  pernicious  cardiac 
form  of  malaria,  but  may  also  be  seen  in  cases  of  general  infection. 

The  lungs  may  contain  parasites  in  all  stages  of  their  existence,  as  well  as 
pigmented  macrophages  and  leucocytes.  It  is,  perhaps,  doubtful  whether 
there  is  a  true  form  of  malarial  pneumonia.  Bignami  has  stated  that  the 
pneumococcus  is  always  present,  and  that  a  pneumonia  in  a  malarial  patient 
is  a  double  infection. 

The  capillaries  of  the  liver  are  much  enlarged,  with  swollen  endothelial 
cells  often  laden  with  pigment.  These  capillaries  are  filled  with  blood  cells 
containing  parasites  and  leucocytes  with  pigment.  The  perivascular  lymph- 
spaces  are  swollen,  and  Kiipfer's  cells  contain  pigment.  The  liver  cells  are 
compressed  between  the  dilated  capillaries,  and  contain  haemosiderin  and  bile- 
pigment,  and,  in  addition,  isolated  cells  or  groups  of  cells  may  be  necrosed, 
but  this  is  rarely  extensive.  The  portal  canals  are  infiltrated  with  red  cells 
containing  parasites  in  all  stages  of  development. 

In  the  spleen  the  red  cells  of  the  pulp  are  seen  to  be  filled  with  schizonts 
and  crescents,  while  pigment  is  present  in  leucocytes  and  macrophages.  The 
kidneys  show  pigmentation  in  the  walls  of  the  capillaries  of  the  glomeruli,  as 
well  as  those  lying  between  the  tubules ;  but  parasites  are  rare  in  the  former, 
though  common  in  the  latter  situation.  Phagocytes  are  not  uncommon,  con- 
taining pigment,  red  cells,  and  parasites.  The  cells  of  the  glomeruli  degenerate, 
and  are  thrown  oft  into  the  capsule  along  with  exudation,  and  the  epithelial 
cells  of  the  convoluted  tubules  degenerate,  and  are  cast  off  into  the  lumen. 

The  suprarenal  capsule  shows  irregular  areas  of  vascular  dilatation  full  of 
erythrocytes,  many  of  which  contain  parasites,  while  macrophages  may  also 
be  present. 

The  capillaries  of  the  abdominal  fat  are  often  full  of  red  cells  containing 
parasites.  The  bone-marrow  is  chocolate-coloured  in  the  small  bones,  and 
brownish-red  in  the  long  bones.  Often  it  is  soft  and  diffluent,  and  contains 
sporulating  parasites  and,  in  particular,  crescents  (gametocytes),  which  are 
thought  to  start  their  life  here. 

When  the  intestine  shows  the  choleraic  appearances  described  above,  the 
capillaries  of  the  mucosa  and  villi  are  filled  -with  parasites  in  all  stages  of 
schizogony,  and  leucocytes  with  pigment  masses.  The  epithelial  cells  are 
necrotic,  but  the  submucosa  and  deeper  layers  escape  injury,  and  their  blood- 
vessels contain  nearly  normal  cells. 


MORBID  ANATOMY  1155 

The  brain  in  pernicious  cerebral  fevers  has  its  capillaries  filled  with  specu- 
lating parasites  and  mononuclear  macrophages  containing  degenerated  para- 
sites, while  the  arterioles  and  venules  are  freer,  and  only  contain  young  forms. 
Sometimes  no  parasites  are  to  be  seen,  and  only  pigment  in  the  endothelial 
cells,  which  may  be  swollen  and  fatty,  or  may  be  found  free  in  the  vessel, 
and  may  have  parasitic,  inclusions.  The  nerve  cells  may  be  affected,  showing 
damage  to  or  disappearance  of  Nissl's  bodies,  and  at  times  degeneration  of 
their  nuclei,  the  whole  cell  being  sometimes  filled  with  small  granules.  There 
may  be  fibrolysis — i.e.,  degeneration  of  the  neurofibrils — only  small  argento- 
phile  granules  remaining.  Rod-like  cells  attached  to  the  processes  of  the 
ganglion  cells  may  be  seen.  The  punctiform  haemorrhages  are  due  to  the 
diapedesis  of  apparently  normal  red  cells.  Occasionally  the  cerebro-spinal 
fluid  is  increased,  and  there  may  be  a  slight  lymphocytosis. 

B.  Morbid  Anatomy  of  Chronic  Malaria.— The  lesions  of 
chronic  malaria  fall  principally  upon  the  spleen,  the  liver,  and  the 
bone-marrow.  There  are  no  records  of  post-mortems  on  persons 
suffering  from  chronic  malaria  due  to  Plasmodium  malaria. 

1.  Lesions  due  to  Plasmodium  vivax. — 'The  best  recorded 
case  of  this  infection  is  that  given  by  Ewing  of  a  man  who  suffered 
from  the  disease  for  about  a  year,  and  died  from  endocarditis  about 
three  months  after  the  last  attack. 

The  spleen  was  enlarged,  firm,  and  dark,  and  contained  parasites  and  pig- 
ment in  endothelial  cells  about  the  Malpighian  bodies.  Some  hemosiderin 
could  also  be  seen.  The  liver  showed  no  gross  signs  indicating  malaria,  but 
microscopically,  pigment  was  collected  in  large  intracellular  masses  in  the 
portal  canals  and  slightly  in  a  few  endothelial  cells  throughout  the  lobule. 
Macrophages  also  contained  pigment.  The  marrow  was  but  slightly  pig- 
mented, snowing  a  few  endothelial  cells  with  black  pigment. 

2.  Chronic  Malaria  without  Definition  of  the  Parasite. — 
These  lesions  are  generally  due  to  Laverania  malarice,  and,  as  stated 
above,  affect  the  spleen,  liver,  and  bone-marrow. 

The  spleen  is  always  enlarged,  often  considerably,  and  is  firm  in  consistence, 
but  its  colour  varies  from  a  slate  to  a  dark  red,  which  depends  upon  the  amount 
of  pigment  deposited  therein.  Usually  there  are  some  adhesions,  indicating 
old  perisplenitis.  On  section  it  generally  appears  quite  black,  but  this  depends 
upon  the  amount  of  pigment;  the  capsule  is  thickened;  the  Malpighian  follicles 
stand  out  clearly,  as  they  are  enlarged  and  non-pigmented.  Microscopically 
the  capillary  vessels  are  seen  dilated  and  separated  by  splenic  pulp,  or  by 
connective  tissue  containing  giant  cells.  The  pigment  may  be  diffused 
through  the  organ,  but  is  generally  either  collected  around  the  follicles  or 
extracellular,  and  contained  in  the  lymphatics  of  the  arterioles  or  septa,  both 
of  which  are  thickened. 

The  liver  is  larger  and  harder  than  usual.  If  pigment  is  present,  it  will 
usually  be  gathered  around  the  periphery  of  the  lobules,  which  will,  therefore, 
stand  out  clearly.  Later  the  pigment  becomes  perivascular,  and  finally  dis- 
appears. The  capillaries  or  lymph-spaces  may  be  considerably  dilated,  and 
the  liver  cells  atrophied  by  pressure.  On  the  other  hand,  proliferation  of 
the  hepatic  cells  and  repair  of  the  damage  may  be  seen  taking  place.  Atrophy 
of  the  liver  is  not  usual,  but  may  occur  in  old  people  from  thrombosis  of  the 
portal  vein,  and  is  then  associated  with  necrosis. 

The  bone-marrow  is  usually  pigmented,  and  of  a  chocolate  hue  in  the  small 
bones,  while  in  the  long  bones  it  may  be  reddish,  except,  perhaps,  in  the  very 
centre.     This  colour  is  due  to  the  replacement  of  the  fat  by  vascular  tissue. 

3.  Malarial  Cachexia.— This  may  be  acute  when  it  develops 
after  a  tew  attacks  of  fever,  but  more  commonly  it  comes  on  as  a 
sequela  to  chronic  malaria. 


1 1 56  THE  MALARIAL  FEVERS 

The  anaemia  is  marked,  and  there  is  fluid  about  the  ankles  and  in  the 
abdominal  cavity.  The  spleen  is  enormously  enlarged,  as  is  also  the  liver, 
while  the  bone-marrow  is  yellow,  sclerotic,  or  gelatinous.  Parasites  may  be 
found,  or  they  may  be  absent. 

A  special  form  of  cachexia  is  that  in  which  amyloid  changes  are 
found  in  the  kidney  along  with  parenchymatous  nephritis,  associated 
more  rarely  with  amyloid  changes  in  the  intestine,  spleen,  and  liver, 
with  sometimes  simple  ulceration  of  the  intestine. 

4.  Latent  Malaria. — Plasmodium  vivax  and  Laverania  malarice 
can  exist  in  the  spleen  of  persons  who  show  no  sign  of  fever  or  malarial 
cachexia.  These  parasites  can  go  through  their  life-cycle  in  that 
organ,  and  in  the  case  of  L.  malaria  in  the  liver  also,  but  it  would 
appear  that  they  are  restrained  from  invading  the  circulation  by 
the  action  of  some  antitoxin,  and  therefore  do  not  increase  to  such 
numbers  as  to  cause  toxic  symptoms. 

It  is  obvious  from  the  above  that,  if  the  restraining  influences 
which  conduce  to  the  condition  of  latent  malaria  are  removed,  an 
attack  of  malaria  will  follow,  or  if  there  has  been  a  previous  attack,  a 
relapse  will  take  place. 

Observers  have  always  had  a  difficulty  in  admitting  that  the 
ordinary  form  of  the  parasite  could  be  latent  and  cause  a  relapse, 
though  there  appears  no  doubt  that  this  can  take  place.  Schaudinn, 
as  has  already  been  mentioned,  considers  that  the  macrogametocyte 
is  capable  of  undergoing  parthenogenesis  and  forming  merozoites, 
thus  starting  a  cycle  of  schizogony  anew  and  causing  fever.  Craig 
and  other  observers  insist  upon  conjugation,  causing  a  rejuvenes- 
cence of  the  parasite  and  a  relapse  of  the  fever. 

Classification. — As  there  are  three  parasites — Plasmodium  malarice, 
P.  vivax,  and  Laverania  malarice — there  are  therefore  three  clinical 
entities — quartan  malarial  fever,  tertian  malarial  fever,  and  sub- 
tertian  malarial  fever — due  to  these  parasites. 

Quartan  and  tertian  parasites  go  through  their  whole  life-bistor}' 
in  the  circulating  blood,  and  though  the  tertian  sporulating  forms 
are  found  in  internal  organs,  such  as  the  spleen,  yet  the}7  do  not  tend 
to  accumulate  in  those  organs  or  to  produce  special  effects.  On 
the  other  hand,  the  subtertian  parasite  sporulates  entirely,  or 
almost  entirely,  in  the  internal  organs;  and  if  one  particular  organ 
is  especially  attacked  bjr  the  parasites,  there  will  be  special  clinical 
features  to  that  phase  of  the  disease.  This  is  the  cause  of  the 
atypical  subtertian  fevers,  and  is  also  the  basis  of  those  serious 
symptoms  which  have  for  many  years  been  alluded  to  as  the  per- 
niciousness  of  this  type  of  fever.  The  nature  of  these  pernicious 
symptoms  will  depend  upon  whether  the  parasite  is  principally 
localized  in — (1)  the  cerebro-spinal  nervous  system;  (2)  the  gastro- 
intestinal mucosa;  (3)  the  pancreas;  (4)  the  heart;  (5)  the  lungs; 
(6)  the  liver,  etc. 

We  will  give  clinical  descriptions  of  the  different  quartan,  tertian, 
and  subtertian  fevers. 


QUARTAN  FEVERS  1157 


II.  THE  QUARTAN  FEVERS. 

Quartan  malarial  fever  depends  for  its  symptoms  and  course 
upon  the  life-history  of  Plasmodium  malarice,  introduced  into  the 
blood  of  man  by  an  anopheline  mosquito.  Its  clinical  course  will 
depend  entirely  upon  whether  the  parasites  are  of  approximately 
the  same  age,  or  whether  they  have  been  introduced  into  the  body 
on  different  days. 

If  only  parasites  of  approximately  one  age  exist  in  the  blood,  a 
typical  quartan  malarial  fever  ensues,  with  an  interval  of  seventy- 
two  hours  (the  length  of  time  which  a  merozoite  takes  to  become 
the  fully  developed  schizont).  Such  a  fever  is  called  'quartana 
simplex,'  or  simple  quartan  fever. 

If  the  parasites  have  been  introduced  on  two  different  days,  and 
are  therefore  of  different  ages,  the  patient  will  develop  fever  on  two 
successive  days,  and  be  free  from  it  on  the  third  day;  such  a  fever 
would  be  called  '  quartana  duplex,'  or  double  quartan  fever. 

If,  however,  the  parasites  were  introduced  on  three  successive 
days,  the  fever  may  be  daily — that  is  to  say,  may  be  a  quotidian 
fever — and  this  could  only  be  recognized  as  belonging  to  the  quartan 
fevers  by  its  parasite  being  discovered  microscopically;  such  a 
fever  would  be  called  a  '  quartana  triplex,'  or  triple  quartan  fever. 

If  the  parasites  exist  in  greater  numbers  and  groups  than  usual, 
the  fever  may  be  irregular  and  subcontinuous. 

There  are,  therefore,  several  types  of  quartan  fevers — viz. : — 

A.  Acute  quartan  malaria  :■ — 

1.  Simple  quartan  fever. 

2.  Double  quartan  fever. 

3.  Triple  or  quotidian  quartan  fever. 

4.  Irregular  subcontinuous  quartan  fevers. 

5.  Mixed  infections. 

B.  Chronic  quartan  malaria. 

Simple  Quartan  Fever. 

Definition. — Simple  quartan  malaria  is  characterized  by  attacks 
of  fever  recurring  every  seventy-two  hours  and  separated  by 
apyrexial  intervals  which  occupy  the  time  required  by  Plasmodium 
malaria  to  pass  from  the  merozoite  to  the  fully  developed  schizont. 

Incubation. — This  has  not  been  determined  with  any  degree  of 
certainty.  It  is  without  doubt  longer  than  either  tertian  or  sub- 
tertian.  Celli,  by  experiment,  came  to  the  conclusion  that  it  might 
be  very  long — two  months  or  more. 

By  the  experimental  inoculation  of  blood,  Marchiafava  and 
Bignami  calculated  the  maximum  incubation  at  18  days,  the  mini- 
mum at  11  days,  and  the  mean  at  14-3  days.  We  arc  not  aware  of 
any  accurate  experiment  to  determine  the  incubation  period  after 
the  bite  of  infected  mosquitoes.  The  only  observation  which  we 
know  is  the  very  doubtful  one  recorded  by  Buchanan  in  1901, 


1158 


THE  MALARIAL  FEVERS 


when  anopheline  mosquitoes  of  undetermined  species  were  allowed 
to  bite  men  in  India  from  the  gth  to  the  21st  of  January,  with  the 
result  that  one  developed  a  temperature  of  38-9°  C.  on  the  5th  of 
February,  but  parasites  were  not  found,  and  the  other  cases  were 
negative. 

Remarks. — The  clinical  description  may  be  divided  into  the 
febrile  attack  and  the  apyrexial  interval. 

The  Febrile  Attack. — Generally  there  are  prodromata  before  an 
attack  of  quartan  fever.  Some  few  hours  previously  the  patient 
may  complain  of  giddiness,  weakness,  malaise,  headache,  or  even 
nausea  and  vomiting.  If  the  blood  is  examined  during  the  occur- 
rence of  these  symptoms,  the  parasites  will  be  seen  to  be  schizonts, 
and  the  commencing  formation  of  merozoites  may  also  be  noted. 


ILLNESS 

1 

2 

3 

4 

5 

6 

7 

8 

TIME 

M 

E 

M 

£ 

M 

E 

M 

E 

M 

E 

M 

E 

M 

E 

M 

E 

104" 

toy 
-j-.      10a" 

g       101' 

t- 

>*-         100° 
5          99° 

ST 
9&° 

== 

EiE 

F/g.  619. — Temperature  Chart  of  a  Case  of  Simple  Quartan  Malarial 
Fever  in  the  .General  Hospital,  Colombo. 


In  a  short  time  the  definite  attack  begins.  It  may  roughly  be 
divided  into  three  stages:  (1)  The  cold  stage;  (2)  the  hot  stage; 
(3)  the  sweating  stage. 

1.  The  Cold  Stage. — The  patient  begins  to  feel  cold,  either  in  the 
legs,  arms,  or  back.  This  sensation  increases  until  actual  shivering 
sets  in.  In  quartan  fever  the  rigors  are  well  marked  and  charac- 
teristic, and  the  patient  may  shiver  until  he  shakes  the  bed;  the 
teeth  may  chatter,  the  lips  become  blue,  the  arms  and  legs  cold,  and 
goose-skin  may  be  present.  If  the  blood  is  examined  in  this  stage, 
some  of  the  parasites  may  be  seen  fully  sporulated,  or  only  young 
parasites  may  be  found. 

During  this  cold  stage,  which  is  the  most  uncomfortable  of  the 
three  stages,  the  internal  temperature  is  rising  rapidly,  and  the 
internal  organs  must  be  somewhat  congested  during  the  chill;  for 
there  are  symptoms  of  intense  headache,  visual  disturbance, 
vomiting,  and  at  times  diarrhoea.     The  temperature,  which  rises 


QUARTAN  FEVERS  1159 

before  the  chill  begins,  varies  at  first  from  100*4°  to  102*2°  F., 
but  generally  rises  rapidly  to  its  maximum — about  104°  or  105°  F. 
The  cold  stage  does  not  last  long,  fifteen  to  thirty  minutes  being 
the  average  time,  but  it  may  be  longer  or  shorter,  and  may  be 
irregular,  being  preceded  by  a  transient  sensation  of  heat. 

2.  The  Hot  Stage. — Gradually  the  shivering  ceases,  and  the  patient 
begins  to  feel  warmer  and  more  comfortable,  though  sensations  of 
cold  and  heat  may  succeed  one  another.  By  degrees  the  sensation 
of  heat  increases,  until  the  patient  becomes  burning  hot,  and  as  in 
the  cold  stage  he  desired  to  wrap  himself  up  with  coverings,  now 
he  desires  to  throw  these  off.  The  skin  feels  hot  and  dry,  the 
pulse  and  respirations  increase,  the  conjunctivae  become  injected. 
Vomiting  and  diarrhoea  may  take  place,  and  an  erythematous  rash 
sometimes  appears.  The  temperature  reaches  its  maximum,  and 
soon  declines. 

This  stage  may  last  about  three  to  four  or  more  hours. 

3.  The  Sweating  Stage. — Towards  the  end  of  the  hot  stage  the 
forehead  is  noticed  to  be  damp,  and  presently  the  sweat  begins 
to  appear  profusely,  and  great  relief  is  felt  by  the  patient.  As  the 
sweating  increases,  the  temperature  falls  rapidly  and  the  pulse-rate 
declines.  As  the  temperature  approaches  normal  the  patient  may 
fall  into  a  sleep,  from  which  he  will  wake  feeling  much  better,  and 
with  a  normal  or  subnormal  temperature.  The  total  duration  of 
the  attack  may  be  about  eight  to  ten  hours. 

The  Interval. — After  awaking  from  his  sleep  the  patient  feels 
quite  well,  though  weak,  and  generally  goes  about  his  ordinary  work 
during  the  two  days  of  this  interval.  But  signs  are  not  wanting 
that  everything  is  not  well;  for  the  temperature  is  often  subnormal 
and  the  pulse  slow,  while  in  the  blood  the  developing  parasites 
may  be  traced,  and  leukopenia  with  relative  mononuclear  increase 
noted.  At  the  end  of  seventy-two  hours  the  apyrexial  interval  will 
end  in  an  attack  of  fever,  as  described  above. 

The  Course  of  the  Fever. — Quartan,  rightly  or  wrongly,  is  believed 
to  have  a  great  tendency  to  relapse,  to  go  on  for  months,  and  even, 
it  is  said,  for  years,  if  not  treated.  The  parasites  rarely  appear 
to  multiply  to  any  great  extent  in  the  blood,  and  hence  pernicious 
symptoms  are  usually  absent.  If  left  to  itself,  the  fever  is  supposed 
to  gradually  die  out,  but  to  recur  at  times.  Spontaneous  cure  is, 
however,  rare. 

Irregularities. — Prolongation  of  the  attack  has  been  noticed. 
Marchiafava  and  Bignami  state  that  it  may  very  exceptionally  last 
for  more  than  twenty-four  hours,  in  which  case  the  temperature 
shows  two  chief  undulations — one  near  the  beginning  and  the  other 
near  the  end  of  the  attack — separated  by  a  marked  remission. 

Children. — Children  may  show  neither  cold  nor  sweating  stages. 
Very  often  convulsions  take  the  place  of  the  cold  stage,  but  these 
may  be  so  slight  as  not  to  be  noticed.  On  the  other  hand,  they 
may  be  very  severe. 


n6o  THE  MALARIAL  FEVERS 

Double  Quartan  Fever. 

In  this  form  there  is  an  attack  of  fever  on  two  successive  clays, 
and  an  apyrexial  interval  of  twenty-four  hours. 

Typically  the  two  attacks  should  be  equal  in  severity,  but  often 
that  is  not  so,  for  one  attack  is  less  severe  than  the  other.  As  already 
stated,  this  may  be  due  to  two  groups  of  parasites,  inoculated  on 
separate  days.  But  sometimes  quartana  simplex  may  become 
quartana  duplex,  and  this  is  explained  by  the  fact  that  there  may 
be  a  double  infection,  but  that  while  there  are  many  of  one  brood 
of  parasites,  and  hence  fever,  the  other  brood  may  be  so  few  at  first 
that  they  require  time  to  develop  to  such  numbers  as  are  necessary 
for  the  production  of  fever.  Consequently  quartana  duplex  may 
at  first  show  itself  by  a  very  slight  rise  in  the  temperature  on  the 
second  day,  which  increases  gradually  till  equal  to  that  produced 
by  the  stronger  infection. 

Triple  Quartan  Fever. 

This  is  a  quotidian  or  daily  fever  produced  by  three  broods  of 
quartan  parasites  coming  to  maturity  on  three  successive  days, 
and  can  only  be  diagnosed  by  an  examination  of  the  blood.  The 
three  attacks  may  be  similar,  and  may  begin  at  the  same  hour, 
or  they  may  vary  in  severity  and  begin  at  different  times.  In 
quartana  triplex  sometimes  an  attack  may  be  '  subintrant  ' — that 
is  to  say,  the  cold  stage  of  one  attack  may  begin  before  the  sweating 
stage  of  the  other  attack  is  finished;  but  this  is  not  common,  and 
usually  there  is  a  distinct  interval  of  normal  or  subnormal  tempera- 
ture. 

A  simple  or  a  double  quartan  may  become  a  triple  quartan  in 
the  manner  described  above  for  the  origin  of  a  double  from  a  simple 
fever.  On  the  other  hand,  it  may  start  as  quartana  triplex,  and 
become  a  duplex,  and  finally  a  simplex.  This  may  be  due  to  the 
weakening  of  certain  groups  of  parasites.  Sometimes  a  triplex  may 
directly  become  a  simplex  from  the  linking  together  of  two  other 
groups  of  parasites  at  the  same  time. 

Irregular  Subcontinuous.  Quartan  Fevers. 

Quartan  parasites  are  believed  not  to  cause  continuous  fever, 
but  very  rarely  they  may  cause  subcontinuous  or  remittent  fever. 
Such  a  condition  is  due  to  the  presence  in  the  blood  of  parasites  of 
all  ages,  which,  therefore,  are  continually  sporulating  and  dis- 
turbing the  metabolism,  thereby  producing  the  remittent  type  of 
fever. 

Mixed  Infections. 

Mixed  infections  may  occur  with  either  of  the  other  two  parasites 
— viz.,  P.  vivax  or  L.  malaria — and  an  intermittent  irregular  fever 
be  produced,  only  to  be  diagnosed  by  the  microscope. 

Chronic  Quartan  Malaria. 

See  Chronic  Malaria,  p.  1182. 


TERTIAN  FEVERS  1161 


III.  THE  TERTIAN  FEVERS. 


Tertian  malarial  fever  depends  for  its  symptoms  and  course  upon 
the  life-history  of  Plasmodium  vivax,  introduced  into  the  blood  of 
man  by  an  anopheline  mosquito.  Its  clinical  course  will  depend 
entirely  upon  whether  the  parasites  are  of  approximately  the  same 
age  or  whether  they  have  been  introduced  into  the  body  on  different 
days. 

If  only  parasites  of  approximately  one  age  exist  in  the  blood, 
a  typical  simple  tertian  malarial  fever  ensues,  with  an  interval  of 
forty-eight  hours  (the  length  of  time  which  a  merozoite  takes  to 
become  a  fully  developed  schizont).  Such  a  fever  is  called  '  tertiana 
simplex,'  or  simple  tertian  fever. 

If  the  parasites  belong  to  two  distinct  broods,  or  have  been  intro- 
duced on  two  different  days,  and  are  therefore  of  different  ages, 
the  patient  will  develop  fever  every  day.  Such  a  fever  would  be 
quotidian  in  type,  and  would  be  called  '  tertiana  duplex,'  or  double 
tertian  fever. 

If  many  broods  of  parasites  are  present,  the  fever  becomes  sub- 
continuous  and  irregular. 

There  are,  therefore,  several  types  of  tertian  fevers — viz. : — 

A.  Acute  tertian  malaria  : — 

1.  Simple  tertian  fever. 

2.  Double  or  quotidian  tertian  fever. 

3.  Irregular  subcontinuous  tertian  fevers. 

4.  Mixed  infections. 

B.  Chronic  tertian  malaria. 

Simple  Tertian  Fever. 

Definition. — Simple  tertian  malaria  is  characterized  by  attacks 
of  fever  recurring  every  forty-eight  hours,  and  separated  by  apy- 
rexial  intervals  which  occupy  the  time  required  by  Plasmodium 
vivax  to  pass  from  the  merozoite  to  the  fully  developed  schizont. 

Incubation. — -The  natural  incubation  period  is  believed  to  be 
from  eight  days  upwards.  The  period  of  incubation  in  experi- 
mental cases  in  which  quantities  of  infected  blood  were  inoculated 
varied  from  four  to  twenty-two  days.  The  period  of  incubation 
after  the  experimental  bites  of  infected  anophelines  varies  from 
seven  to  twenty-five  days. 

Remarks. — The  clinical  description  may  be  divided  into — (1)  the 
attack  of  fever;  (2)  the  apyrexial  interval. 

The  Attack  of  Fever. — There  may  be  no  prodromata,  or,  on  the 
other  hand,  these  may  be  most  characteristic.  When  present, 
they  take  the  form  of  pain  in  the  head  and  the  back,  and  especially 
in  the  bones  of  the  limbs — more  particularly  the  joints — which  lead 
to  their  being  considered  to  be  rheumatic,  together  with  a  feeling 
of  lassitude  and  illness.  On  the  day  succeeding  these  sensations 
the  patient  may  feel  quite  well,  but  on  the  next  day  they  may  recur. 


1 1 62 


THE  MALARIAL  FEVERS 


If  treated  in  this  stage,  the  fever  may  never  develop,  but  if  neglected, 
it  will  appear  in  the  course  of  a  few  days. 

After  a  feeling  of  illness,  giddiness,  nausea,  or  vomiting,  with 
perhaps  a  slight  rise  of  temperature,  the  patient  suddenly  becomes 
very  cold  and  shivers,  and  his  symptoms  resemble  in  detail  those 
already  described  for  quartan  malarial  fever,  except  that  they  may 
not  be  so  severe.  In  about  ten  to  thirty  minutes  the  warm  stage 
begins. 

As  the  chills  diminish,  sensations  of  warmth  appear;  at  first 
pleasurable,  they  soon  become  intense,  and  the  patient  feels  burning 
hot.  The  skin  is  hot,  flushed,  and  dry;  the  conjunctivae  injected; 
the  pulse  full,  quick,  and  often  dicrotic,  and  the  pains  in  the  head, 
back,  and  limbs  increase.  A  slight  cough  may  be  noted;  vomiting 
is  common,  and  sometimes  diarrhoea  occurs.     Very  often  the  white 


Fig.  620. — Temperature  Chart  of  a  Case  of  Simple  Tertian  Malarial 
Fever,  showing  the  Effect  of  Intramuscular  Injections  of 
1  Gramme  of  Quinine  Bihydrochloride. 


skin  shows  a  sallow  or  slightly  yellowish  tinge,  which  is  also  present 
in  native  races,  but  can  only  be  seen  in  the  conjunctivae.  The 
heart-sounds  are  usually  normal,  but  sometimes  a  soft  systolic 
murmur  can  be  heard.  In  the  lungs,  at  times,  sonorous  and  sibilant 
rales  occur.  The  spleen  is  enlarged  and  tender,  which  is  charac- 
teristic, and  a  soft  murmur  over  the  splenic  area,  like  a  uterine 
souffle,  is  said  to  be  sometimes  heard.  Skin  eruptions  have  been 
described;  the  commonest  in  our  experience  is  erythematous  or 
urticarial.     Herpes  may  occur  on  the  lips. 

The  temperature  begins  to  rise  before  the  chill,  and  continues  to 
ascend  during  the  cold  stage,  reaching  a  maximum  in  the  hot  stage, 
which  may  be  anything  from  1020  to  1080  F.,  but  is  generally 
about  1040  or  1050  F.  The  warm  stage  may  last  four  or  five  hours, 
when  it  passes  into  the" sweating  stage. 

The  mouth  becomes  moist,  and  sweat  gradually  comes  out  all 


DOUBLE  TERTIAN  FEVER 


116^ 


over  the  body,  and  soon  a  most  profuse  perspiration  may  take  place, 
and  the  pulse,  respirations,  and  temperature  may  fall  to  normal  in 
about  four  hours,  when  the  patient,  as  in  quartan  fever,  goes  off  into 
a  sleep.  The  attack  lasts  about  ten  to  twelve  hours,  and  generally 
begins  in  the  morning,  but  may  take  place  at  any  time  of  the  day. 

Apyrexial  Interval. — This  lasts  about  thirty-six  hours,  during 
which  the  temperature  is  often  subnormal.  In  the  interval  the 
patient  may  feel  well,  but  his  blood  will  show  developing  para- 
sites, reduced  erythrocytes,  and  a  leucopenia  with  a  mononuclear 
increase. 

Peculiarities. — As  in  quartan,  so  in  tertian  fever,  children  may 
have  neither  chill  nor  sweating  stage,  but  may,  on  the  other  hand, 
show  convulsions. 

Double  Tertian  Fever. 

When  parasites  mature  on  two  separate  days,  fever  is  produced 
every  day,  which  is  therefore  quotidian  in  type,  and  is  called  a  double 
tertian  (tertiana  duplex).  The  attacks  are  similar  to  those  described 
above,  but  usually  are  shorter,  and,  of  course,  the  apyrexial  in- 
terval is  shorter.  As  a  rule,  the  attacks  begin  at  the  same  hour 
each  day,  but  sometimes  one  attack  is  later  than  the  other.  Very 
often  one  attack  is  not  so  severe  as  the  other,  but  if  left  to  itself 
without  treatment,  it  may  become  similar  to  the  more  severe  attack. 


Fig.  621. — Chart  of  a  Case  of  Double  Tertian  Malarial  Fever 
General  Hospital,  Colombo. 

(Note  postponement  of  attack  in  third  and  fourth  days.) 


Double  tertians  may  arise  by  a  simple  tertian  anticipating.  If  this 
is  continued  after  the  double  tertian  is  developed,  or  if  one  of  the 
attacks  of  a  double  tertian  anticipates,  in  course  of  time  it  will  join 
in  with  the  originally  previous  attack,  so  that  a  person  who  is  in 
the  sweating  stage  of  one  attack  may  suddenly  start  the  cold  stage 
of  the  other. 

Clinical  Course. — Left  to  itself,  tertian  malaria  tends  to  a  spon- 
taneous cure  after  a  series  of  attacks,  but  relapses  may  occur. 
Groups  of  more  severe  attacks  alternate  irregularly  with  groups  of 


1 1 64  THE  MALARIAL  FEVERS 

milder  attacks.  Usually,  recurring  attacks  take  place  about  the 
same  time  on  the  succeeding  days. 

The  anaemia  of  tertian  fevers  is  more  easily  overcome  than  that 
of  quartan,  and  great  exhaustion  is  only  seen  in  old  debilitated 
subjects. 

Two  interesting  points  may  be  noticed — (i)  anticipation  of  the 
attacks;  (2)  retardation  of  the  attacks.  Anticipation  of  the  attacks 
means  shortening  of  the  apyrexial  interval,  so  that  they  begin  at 
short  intervals.  Retardation  means  prolongation  of  the  apyrexial 
interval,  and  is  generally  due  to  the  action  of  quinine,  but  may  be 
due  to  spontaneous  weakening  of  the  parasite. 

Irregular  Subcontinuous  Tertian  Fevers. 

Irregularity  may  be  brought  about  by  parasites  maturing  at 
different  times  on  the  same  day,  and  thus  producing  an  almost 
continuous  fever  with  exacerbations  and  remissions;  but  tertian 
fever  is  rarely  duplicated— that  is  to  say,  it  rarely  shows  two 
distinct  attacks  in  one  day.  Prolongation  of  the  attack  produces 
a  fever  resembling  the  subtertian,  while  in  very  chronic  tertians 
just  the  reverse  may  take  place — viz.,  prolongation  of  the  apyretic 
intervals — so  that  fever  appears  at  the  end  of  seven,  eight,  fourteen, 
or  sixteen  days. 

Mixed  Infections. 

Irregularity  may  also  be  produced  by  mixed  infections  of  Plas- 
modium vivax  with  Plasmodium  malarice,  or  with  Laverania  malaria. 
These  mixed  infections  can  only  be  recognized  by  the  microscopical 
examination  of  the  blood. 

Chronic  Tertian  Malaria. 

See  Chronic  Malaria,  p.  1182. 


IV.  THE  SUBTERTIAN  FEVERS. 

Synonyms. — Tropical  malaria,  Summer-autumnal  fever ,  Malignant 
tertian. 

Definition. — Subtertian  malarial  fevers  depend  for  their  symptoms 
and  course  upon  the  life-history  of  Laverania  malarice,  introduced 
into  the  blood  of  man  by  an  anopheline  mosquito. 

Remarks. — Their  clinical  symptoms  may  approximate  to  the 
type  described  for  the  other  two  malarial  fevers  when  Laverania 
malarice  lives  mainly  in  the  spleen  and  in  the  peripheral  blood,  but 
more  generally  the  symptoms  of  these  fevers  are  very  different  from 
those  produced  by  the  tertian  parasites.  The  essential  difference 
is  that  Laverania  malarice  can,  and  does,  live  largely  in  the  internal 
organs,  and  may  even  concentrate  its  forces  upon  one  organ.  As 
clinical  symptoms  are  produced  by  the  derangement  of  the  functions 
of  the  organs  and  systems  of  the  body,  so  the  symptoms  of  these 
types  of  subtertian  fever  may  point  to  a  given  organ  or  to  a  given 


SUBTERTIAN  FEVERS  1165 

system  of  the  body.  It  is  in  this  way  that  the  subtertian  fevers  can 
produce  signs  and  symptoms  which  medical  practitioners  are  more 
accustomed  to  associate  with  some  other  disease,  and  this  explains 
the  curious  phenomenon  of  malarial  mimicry.  As  the  parasite 
Laverania  malaria  can  live  in  any  organ,  it  can  therefore  produce  the 
signs  and  symptoms  of  any  disease,  and  we  know  practically  of  no 
clinical  picture  which  it  is  impossible  for  this  parasite  to  reproduce, 
be  it  an  acute  illness  or  a  chronic  ailment,  be  it  associated  with 
febrile  symptoms  or  free  from  fever.  Hence  the  great  necessity  for 
the  practitioner  to  be  careful  as  to  the  diagnosis  of  malaria,  and  to 
remember  that  in  atypical  cases  which  are  of  frequent  occurrence 
it  is  most  difficult,  and  that  the  microscope  is  not  infallible  in  its 
aid,  as  negative  microscopical  findings  do  not  exclude  a  diagnosis  of 
malaria,  as  will  be  emphasized  in  the  section  on  diagnosis. 

The  subtertian  fevers  are  therefore  capable  of  division  from  a 
practical  point  of  view  into  two  great  groups: — 

A.  Typical  Subtertian  Fevers. 

B.  Atypical  Subtertian  Fevers. 

In  the  first  group  comes  simple  subtertian  fever,  which  shows  an 
intermittency  of  the  symptoms,  which  is  due  to  the  fact  that  the 
time  required  by  a  merozoite  of  Laverania  malaria  to  attain  to  the 
stage  of  a  schizont  is  thirty-six  to  forty-eight  hours,  while  a  double 
infection  produces  a  quotidian  fever,  and  more  severe  infections, 
irregular,  remittent,  and  bilious  types  of  fever.  Mixed  and  chronic 
infections  may  also  ensue  as  in  the  other  types. 

The  fevers  of  the  second  group  may  be  subdivided  according  to 
the  syndrome  which  is  produced,  and  which  depends  upon  the  organ 
or  system  of  the  body  which  is  attacked. 

We  will  now  consider  these  various  clinical  conditions. 

A.  TYPICAL  SUBTERTIAN  FEVERS. 
The  typical  subtertian  fevers  may  be  divided  into: — 

1.  Simple  subtertian  fever. 

2.  Double  subtertian  fever. 

3.  Irregular  subtertian  fever. 

4.  Remittent  subtertian  fever. 

5.  Bilious  subtertian  fever. 

6.  Mixed  infections. 

1.  Simple  Subtertian  Fever. 

Definition. — This  form  of  subtertian  fever  usually  shows  inter- 
missions based  upon  a  tertian  type. 

Incubation. — The  incubation  period  has  been  studied  by  Marchia- 
fava  and  Bignami,  who  considered  it  to  be  of  nine  to  ten  days' 
duration  when  acquired  by  natural  mosquito  infection,  and  to  vary 
from  nineto  nineteen  days  when  acquired  by  experimental  mosquito 


n66 


THE  MALARIAL  FEVERS 


infection.     Prodromal  symptoms  resembling  those  of  tertian  fevers 
may  exist  before  an  attack. 

Febrile  Attack. — The  cold  stage  may  be  entirely  absent,  but  it 
often  occurs,  and  is  sometimes  severe.  Sometimes  the  attack  begins 
with  the  warm  stage,  in  which  the  symptoms  are  very  severe  pains 
in  the  limbs,  back,  and  head,  with  gastro-intestinal  disturbance  in 
the  form  of  vomiting,  diarrhoea,  and  coated  tongue.  The  skin  is 
often  flushed  and  dry  and  sometimes  icteric,  while  the  eyes  are 
injected.  The  sweating  stage  is  never  absent,  and  may  be  marked. 
The  spleen  is  usually  tender,  as  well  as  the  liver.  The  four-hourly 
temperature  chart  is  most  characteristic,  for  the  invasion  takes  place 
with  a  rapid  rise  to  1040  F.  to  1050  F.,  after  which  the  temperature 
remains  high,  oscillating  about  i°  F.  The  oscillation  which  imme- 
diately precedes  the  crisis  is  larger  than  the  others,  and  is  called 


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Fig.  622. — Chart  of  a  Case  of  Subtertian  Malarial  Fever. 
The  curve  is  most  typical  on  the  second  day,  before  quinine  was  administered. 

the  pseudo-crisis.  After  this  the  temperature  rises  to  its  highest 
point  (precritical  elevation),  and  then  suddenly  falls  (crisis)  below 
normal,  where  it  remains,  as  a  rule,  until  the  next  attack.  It  may, 
however,  rise  from  subnormal  to  normal,  and  just  prior  to  the  next 
attack  show  a  distinct  depression.  This  typical  temperature  may, 
however,  be  greatly  masked  by  an  absence  of  the  sudden  rise  at 
the  invasion,  or  of  the  precritical  elevation,  or  by  an  exaggeration 
of  the  pseudo-crisis,  making  the  single  attack  appear  double. 

Lastly,  the  whole  attack  may  be  shorter  than  usual,  and  resemble, 
as  regards  the  temperature,  a  simple  tertian  fever. 

The  duration  of  the  attack  in  subtertian  fever  is  about  twenty- 
four  hours  or  more. 

The  Interval. — The  interval  will  be  twenty-four,  ten,  or  even  eight 
hours  in  duration,  varying,  of  course,  with  the  length  of  the  attack. 


TYPICAL  SUBTERTIA\;   FEVERS  1167 

2.  Double  Subtertian  Fever. 

This  is  a  quotidian  fever,  caused  by  two  broods  of  Laverania 
malaria.  The  cold  stage  is  less  marked  than  in  a  quotidian  fever, 
due  to  quartan  or  tertian  parasites.  The  temperature  rises  rapidly, 
the  fastigium  is  very  short,  and  the  fall  is  to  below  normal.  There 
is  nothing  particular  to  remark  about  the  warm  or  sweating  stages, 
which  resemble  those  of  the  simple  subtertian  fever.  The  whole 
attack  only  lasts  six,  eight,  or  twelve  hours. 

3.  Irregular  Subtertian  Fevers. 

When  several  broods  of  Laverania  malaria  exist  together  in  the 
blood,  it  is  obvious  that,  instead  of  sporulation  taking  place  regu- 
larly every  day  or  every  other  day,  it  will  be  irregular,  and  hence 
the  attacks  will  run  into  one  another  and  produce  an  irregular 
type  of  fever,  which  is  commonly  met  with  on  the  West  Coast  of 
Africa. 

4.  Remittent  Subtertian  Fevers. 

Remittent  fevers  arise  by  prolongation  of  ordinary  attacks,  or  by 
anticipation  or  subintrance,  so  that  two  attacks  become  continuous, 
the  onset  of  the  second  attack  beginning  before  the  first  one  is  con- 
cluded.    Duplication  may  also  lead  to  a  remittent  fever. 

Febrile  Attack. — These  fevers  may  be  mild  or  grave,  and  may  be- 
come pernicious.  The  symptomatology  is  briefly  as  follows:  After  one 
or  two  days  of  prodromal  lassitude,  pains,  and  sensations  of  chilliness, 
etc.,  fever  comes  on  without  any  cold  stage.  The  skin  becomes  hot 
and  dry,  and  often  turns  yellowish,  and  headache,  with  pains  in  the 
different  parts  of  the  body,  is  a  source  of  trouble  to  the  patient. 

The  tongue  is  coated;  thirst  is  sometimes  intense,  and  may  be 
associated  with  vomiting  and  purging,  together  with  pains  in  the 
region  of  the  liver,  spleen,  and  stomach.  The  toxins  affect  the 
brain,  causing  sleeplessness,  restlessness,  and  delirium.  The  liver 
and  spleen  are  both  enlarged  and  tender,  and  at  times  there  is 
slight  cardiac  dilatation  on  the  right  side.  The  temperature  is 
characterized  by  high  fever  with  remissions. 

Interval. — The  time  of  the  remission  is  by  no  means  certain.  It 
may  take  place  in  the  morning  and  the  rise  in  the  evening.  Under 
treatment  the  parasites  rapidly  disappear  from  the  peripheral 
circulation,  but  last  longer  in  the  viscera,  so  keeping  up  the  fever. 

Course. — Mild  attacks  get  well  under  the  week,  but  without 
treatment  they  would  soon  become  the  more  serious  or  grave  type 
of  fever,  which  is  part  of  the  atypical  group  of  subtertian  fevers 
which  are  dealt  with  in  the  next  section.  Three  variations  may  be 
mentioned  here.  The  first  resembles  typhoid  in  its  clinical  features; 
the  second  is  distinguished  by  the  bilious  vomiting  and  diarrhoea, 
with  marked  enlargement  of  the  liver  and  jaundice,  which  is  often 
called  bilious  remittent  fever;  and  the  third  shows  a  tendency  to 
haemorrhages,  local  gangrene,  haemoglobinuria,  and  great  weakness, 
sometimes  called  '  adynamic  remittent  fever.' 


n6S  THE  MALARIAL  FEVERS 

Remarks. — Only  the  bilious  remittent  will  be  considered  here,  as 
malarial  hemoglobinuria  will  be  treated  in  the  next  chapter  on 
Tropical  Haemoglobinurias,  and  the  atypical  subtertian  fevers  will 
be  described  directly  after  bilious  remittent  fever. 

5.  Bilious  Remittent  Fever. 

This  is  a  type  of  subtertian  remittent  fever  in  which  there  is  great 
blood-destruction,  and  consequently  much  bile-production.  We 
have  seen  it  repeatedly  in  Africa,  and  mere  recently  in  theBalcanic 
Zone,  and  it  is  said  to  occur  in  all  highly  malarious  districts. 

The  attack  begins  as  an  ordinary  remittent  fever,  but  is  asso- 
ciated with  jaundice,  bilious  vomiting,  and  usually  bilious  diarrhoea, 
though  in  its  place  there  may  be  constipation.  The  patient  also 
complains  of  pain  and  tenderness  in  the  stomach  and  liver.  After 
a  few  days'  illness  the  symptoms  may  gradually  subside,  or,  with 
or  without  hiccough,  epistaxis,  or  haematemesis,  the  temperature 
may  rise  considerably,  and  the  patient,  becoming  comatose,  dies. 

We  have  noted  at  times  a  curious  intermission  in  the  symptoms, 
of  short  duration,  after  which  high  fever  ensues,  quickly  followed 
by  coma  and  death  (vide  Yellow  Fever-like  Type,  p.  1172). 

6.  Mixed  Infections. 

Mixed  infections  of  L.  malaria  with  the  other  malarial  parasites 
are  not  uncommon,  and  lead  to  a  type  of  quotidian  fever  which 
can  only  be  diagnosed  accurately  by  an  examination  of  the  blood 
and  a  differentiation  of  the  parasites  concerned. 

The  blood  may  show  only  forms  belonging  to  P.  vivax  at  times,  and  only 
forms  belonging  to  L.  malar  ice  at  other  times. 

B.  ATYPICAL  SUBTERTIAN  FEVERS. 

The  causation  of  this  group  of  subtertian  infections  is  due  to  the 
fact  that  Laverania  malaria  undergoes  schizogony  in  the  internal 
organs,  and  is  apt,  at  times,  to  specialize  upon  one  particular  organ, 
which  becomes  seriously  affected,  not  merely  because  it  has  to 
bear  the  full  brunt  of  the  liberated  toxins,  but  also  because  it  suffers 
from  malnutrition,  because  its  capillaries  become  blocked  by 
swollen  endothelial  cells  belonging  to  their  walls  and  by  red  blood- 
corpuscles  filled  with  malarial  parasites,  as  well  as  by  leucocytes 
laden  with  pigment,  and  by  the  pigment  and  merozoites  set  free 
during  schizogony. 

This  explains  not  merely  the  special  character  of  the  symptoms 
exhibited  in  any  case,  but  also  the  multiplicity  of  clinical  types  caused 
by  this  parasite,  and  the  peculiar  conditions  called  masked  malaria 
or  malarial  mimicry. 

These  various  syndromes  may  for  purposes  of  description  be 
arranged  as  follows: — 

I.  Subtertian  syndromes  without  localization. 
II.  Subtertian  syndromes  with  localization. 


ATYPICAL  SUBTERTTAN  FEVERS  1169 

1.  SUBTERTIAN  SYNDROMES  WITHOUT  LOCALIZATION. 

Though  it  is  true  that  one  and  the  same  case  may  show  fever  on 
one  day  and  not  on  another,  still,  for  practical  purposes,  it  is  con- 
venient to  subdivide  these  subtertian  syndromes  into  two  groups, 
according  as  to  whether  fever  at  the  time  of  first  examination  is  or 
is  not  a  marked  feature. 

A.  Non-Localized   Subtertian    Syndromes   without  Marked 
Fever  on  First  Examination. 

1.  Hemorrhagic  non-febrile  type. 

2.  Anemic  type. 

3.  Mental  types. 

4.  Algidetype. 

5.  Pseudo-alcoholic  type. 

Hemorrhagic  Non-Febrile  Type. — The  patients  are  pale,  very  weak, 
and  languid,  and  complain  of  pains  in  the  loins  and  limbs.  In 
most  cases  the  whole  body  is  covered  with  petechias,  and  tense 
indurated  swellings,  due  to  large  extravasations  of  blood,  may  be 
present.  The  gums  are  often  swollen,  spongy,  and  hemorrhagic. 
Epistaxis,  hematemesis,  and  passage  of  blood  per  rectum  may  take 
place,  as  well  as  hemoptysis  and  hematuria  from  kidney  or  bladder. 
Some  patients  have  large  indurated  spleens,  but  febrile  symptoms 
are  almost  constantly  absent.  Malarial  parasites  can  be  found  in 
the  peripheral  blood  in  some  cases.    Quinine  is  the  infallible  remedy. 

Ancemic  Type. — The  patient  shows  no  sign  of  typical  malaria; 
on  the  contrary,  he  is  pallid,  and  possesses  the  lemon-yellow  tinge 
of  pernicious  ancemia.  The  liver,  and  more  rarely  the  spleen,  is 
enlarged.  Usually  there  is  no  fever,  but  in  some  cases  the  tempera- 
ture may  rise  to  990  or  ioo°  F.,  which  is  common  in  pernicious 
ancemia.  Malarial  parasites  may  not  be  found  in  the  blood,  even 
after  repeated  examinations,  while  the  usual  signs  of  pernicious 
ancemia — e.g.,  poikilocytosis,  nucleated  red  blood-corpuscles,  high 
colour  index,  relative  increase  of  small  mononuclears  in  place  of  the 
increase  of  the  large  mononuclears  which  one  expects  to  see  in 
malaria,  may  be  present. 

This  type  of  anemia  may  lead  the  physician  to  suspect  malignant 
growth  in  elderly  patients,  especially  if  there  is  vomiting  and  pain 
after  taking  food. 

Qainine  acts  as  the  diagnostic  and  therapeutic  agent. 

Leukemia. — Certain  authors  believe  that  malaria  can  cause  leukaemia,  but 
this  appears  to  us  to  be  more  of  the  nature  of  a  complication. 

Mental  Types. — The  patient  is  melancholic  orapparently  demented, 
or  more  rarely  acutely  maniacal  and  violent,  with  usually  a  normal, 
subnormal,  or  but  slightly  raised  temperature.  The  spleen  may 
or  may  not  be  enlarged,  but  a  careful  examination  of  the  blood 
generally  reveals  a  mononucleosis  or  at  times  a  very  few  malarial 

71 


nyo  THE  MALARIAL  FEVERS 

parasites,  while  quinine  therapy  effects  a  disappearance  of  the 
symptoms. 

The  violent  cases  may  be  of  interest  from  a  medico-legal  point  of 
view,  because  the  patient  never  has  the  slightest  recollection  of  his 
acts,  and  cannot  be  held  responsible  for  them. 

Algide  Type.— The.  patient  is,  as  a  rule,  first  seen  in  a  condition 
of  such  extreme  collapse  as  to  make  the  practitioner  suspicious  of 
cholera.  The  nose  is  sharp,  the  cheeks  sunken,  the  lips  and  ex- 
tremities cyanotic,  the  nails  livid,  the  pulse  small,  soft,  and  frequent, 
becoming  thready  and  imperceptible,  the  skin  cold  and  clammy, 
and  the  respiration  laboured.  The  patient  may,  however,  be  con- 
scious, and  be  able  to  answer  questions  and  to  complain  in  a  weak 
voice  of  severe  thirst.  This  is  a  very  serious  and  fatal  form  of 
pernicious  malaria,  and  generally  kills  the  victim  in  a  few  hours. 

Pseudo-Alcoholic  Type. — The  patient  may  not  have  been  very 
well  for  a  few  days,  being  capable  of  doing  his  work,  but  irritable  and 
complaining  of  not  feeling  fit.  In  order  to  carry  on  his  duties  he 
may  or  may  not  take  a  certain  amount  of  alcohol.  Suddenly, 
during  or  after  a  dinner  or  at  a  public  performance,  he  tumbles  off 
his  chair,  and  the  impression  at  first  is  that  he  has  taken  too  much 
alcohol,  and  this  may  be  considered  to  be  confirmed  by  the  odour 
of  his  breath.  It  will,  however,  soon  be  evident  that  the  patient 
is  seriously  ill,  and  the  diagnosis  will  be  revised  and  apoplexy  prob- 
ably instituted.  Finally  a  blood  examination  will  generally  reveal 
a  number,  and  sometimes  a  large  number,  of  malarial  parasites  of 
the  subtertian  type.  At  a  post-mortem  these  parasites  will  be 
seen  to  be  blocking  the  capillaries  of  the  cerebral  cortex. 

The  poorer  type  of  native  patient  will  be  taken  as  a  '  drunk  '  to 
the  local  lock-up,  and  in  the  morning  the  so-called  drunken  man 
will  be  found  to  be  seriously  ill  and  may  even  be  dying.  Blood 
examination  generally,  but  not  always,  reveals  malarial  parasites. 
Generally  these  are  serious  infections,  and  the  prognosis  is  grave. 


B.  Non-Localized  Subtertian  Syndromes  with  Marked  Fever 
on  First  Examination. 

The  non-localized  subtertian  syndromes  with  marked  fever  on 
first  examination  may  be  divided  into: — 

1.  Subtertian  hyperpyrexial  fever. 

2.  Subtertian  syndromes  resembling  a  specific  fever. 

3.  Subtertian  syndromes  not  resembling  a  specific  fever. 

Subtertian  Hyperpyrexial  Fever. 

This  type  of  fever  is  characterized  by  very  high  temperatures, 
often  commencing  at  the  onset  of  the  illness.  It  may  be  continuous 
or  intermittent,  and  often  attains  temperatures  exceeding  1050  F. 
Sometimes  the  temperature  may  reach  heights  which  can  hardly 


ATYPICAL  SUBTERTIAN  FEVERS 


1171 


be  believed— £.g.,  in  two  of  our  cases  the  temperature  exceeded 
1080  F.  These  cases  have  a  very  serious  prognosis,  but  recoveries 
are  not  unknown. 


1. 
2. 
3- 
4- 
5- 
6. 


Fig.  62.}. — Temperature  Chart  of  a  Case  of  Hyperpyrexias  Subtertian 

Malaria. 

Syndromes  resembling  a  Specific  Fever. 

The  syndromes  resembling  a  specific  fever  may  be  divided  into 
types  as  follows: — 

Typhoid-like  type. 
Malt a-f ever-like  type. 
Typhus-like  type. 
Ccrebro-spinal-likc  type. 
Yellow-fever-like  type. 
Weil's-disease-like  type. 
7.  Scarlet-fever-like  type. 

Typhoid-like  Type. — This  fever  resembles  enteric  fever,  as  may 
be  judged  by  the  temperature  chart  (Fig.  624).  The  onset  is  slow, 
the  patient  apathetic,  the  tongue  coated,  and  headache  present, 
while  the  temperature  is  continuous  or  subcontinuous.  The 
abdomen  is  slightly  tumid,  the  spleen  usually  palpable,  but  not  large 
or  hard.  The  blood  usually  shows  subtertian  parasites,  and  the 
bacteriological  examination  for  'enterica'  is  negative,  but  quinine 
here  has  but  slight  action  on  the  course  of  the  fever  for  some  time. 
The  complication  of  typhoid  infections  in  the  course  of  malaria  is 
mentioned  on  p.  1184. 

MaUa-B 'ever-like  Type.— This  is  very  rare,  and  resembles  Malta 
fever,  but  malarial  parasites  can  be  easily  found  in  the  blood;  while 


1 1  72 


THE  MALARIAL  FEVERS 


bacteriological  tests  for  Micrococcus  melitensis  and  its  allies  are 
absent.     Finally  quinine  effects  a  cure. 

Typhus-like  Type. — The  cases  exactly  resemble  typhus  fever, 
but  malarial  parasites  are  often  present  in  the  blood,  and  the  disease 
yields  to  quinine  therapy. 

Cerebro -Spinal-like  Type. — The  symptoms  are  those  of  epidemic 
cerebro-spinal  meningitis,  but  the  cerebro-spinal  fluid  is  clear,  though 
its  pressure  may  be  increased;  its  cellular  contents  are  normal  in 
number  and  character,  while  meningococci  are  absent  and  the  blood 
shows  malarial  parasites.     The  spleen  may  or  may  not  be  enlarged. 


Fig.   624. — Atypical  Subtertian  Malaria   simulating   Typhoid   Fever. 

Haemocultures  and  serological  reactions  for  germs  of  the  Enteroidea 
group  of  fevers  were  negative. 


Sleeping-Sickness-like  Type. — This,  which  is  rare,  is  characterized 
by  low  fever,  slight  trembling  of  the  hands  and  tongue,  and  progres- 
sive general  weakness,  drowsiness,  and  occasional  convulsions. 
The  lymph  glands  in  the  neck  are  not  enlarged,  and  the  cases  may 
occur  in  regions  where  sleeping  sickness  is  unknown.  Malarial 
parasites  may  be  hard  to  find,  but  quinine  in  large  doses  cures  the 
affection. 

Yellow-Fever -like  Type. — This  is  characterized  by  fever,  without 
rigors,  severe  headache,  flushed  face,  pains  in  the  body,  pulse  quick, 
full,  and  bounding  at  first,  severe  vomiting,  tenderness  in  the 
epigastric  region,  and  slight  albuminuria.  On  the  third  day  the 
temperature  falls  from  1030  to  ioo°  F.,  and  the  symptoms  abate, 
while  the  patient  feels  better;  but  the  temperature  rises  again, 
jaundice  appears,  the  pulse  slows  to  about  60-70  per  minute,  dark 
brown  vomit  appears  containing  red  blood-corpuscles.  The 
symptoms  may  get  worse,  the  jaundice  may  deepen,  and  death 
ensue.  Subtertian  parasites  may  be  present  in  abundance  in  the 
blood,  and  quinine  may  be  ineffective  unless  given  in  massive 
doses. 

W eil' s-Disease-like  Type. — Cases  like  Weil's  disease,  with  cutane- 
ous haemorrhages,  are  occasionally  malarial,  and  may  end  fatally. 
The  mild  type  of  camp  jaundice  may  also  be  simulated  by  malaria, 
but  this  is  rare. 


ATYPICAL  SUDTERTIAN  FEVERS 


1173 


Fig.  625. — Atypical  Malaria  simulating  Malta  Fever. 

Hajmocultures  and  serological  reactions  for  Micrococcus  melitensis  and 
M.  paramelitensis  were  negative. 

Scarlet-Fever -like  Type.  —  Scarlatiniform  pernicious  fever  is 
characterized  by  a  diffuse  scarlatiniform  rash  all  over  the  body, 
with  desquamation  of  the  horny  layer  and  erythema  of  the  fauces, 
and  may  lead  to  a  typhoidal  state  in  which  the  patient  dies. 

Syndromes  not  resembling  Specific  Fevers. 
The  subtertian  syndromes  not  resembling  specific  fevers  are: — 

1 .  Hemorrhagic  febrile  type. 

2.  Hydrophobia-like  type. 

3.  Kussmaul  coma-like  type. 

4.  Diaphoretic-like  type. 

5.  Comatose  type. 

6.  Delirious  type. 

7.  Tetanus-like  type. 

8.  Convulsive  type. 

Hemorrhagic  Febrile  Type. — This  form  of  pernicious  fever  is 
apparently  rare.     It  is  characterized  by  haemorrhages  from  the 


1 1 74  THE  MALARIAL  FEVERS 

skin  and  mucosae  of  the  nose,  bronchi,  intestines,  stomach,  and 
generative  organs,  during  the  attack,  but  not  during  the  intermission. 

This  condition  rapidly  produces  acute  grave  anaemia,  with 
thready  pulse,  coma,  delirium,  convulsions,  and  death,  or  may 
become  the  milder  type,  in  which  fever  is  not  a  marked  symptom 
(vide  p.  1 169). 

Hydrophobia-like  Type. — Signs  of  hydrophobia  associated  with 
fever,  a  large  spleen,  and  malarial  parasites  in  the  blood,  call  for 
energetic  quinine  treatment,  when  the  symptoms  disappear,  unless 
it  is  true  hydrophobia  in  a  malarial  patient. 

Kussmaul  Coma-like  Type. — Signs  of  Kussmaul's  coma  coming 
and  going  every  alternate  day  and  associated  with  fever  in  a  diabetic 
patient  call  for  quinine  therapy,  even  if  the  spleen  is  not  enlarged, 
the  blood  free  from  malarial  parasites  and  mononucleosis.  Occa- 
sionally after  the  exhibtion  of  a  small  dose  of  quinine,  parasites  may 
be  found  in  the  blood. 

Diaphoretic  Type. — In  this  type  the  sweating  of  the  third  stage 
of  an  attack  is  so  exceedingly  copious  that  not  merely  is  the  bed 
saturated,  but  a  pool  may  even  form  on  the  floor.  Such  excessive  ex- 
cretion of  sweat  is  dangerous,  as  the  patient  becomes  more  and  more 
exhausted  as  it  goes  on,  and  a  most  dangerous  collapse  may  ensue. 

Comatose  Type. — This  may  begin  suddenly  or  slowly.  If  the 
latter,  there  may  be  weakness,  sleepiness,  headache,  disturbance  of 
vision,  stupor,  or  delirium,  which  ends  in  coma.  But  more  often 
the  patient  is  brought  to  the  hospital  quite  comatose.  He  lies  flat 
upon  his  back,  with  usually  no  paralysis  and  no  alteration  in  the 
reflexes.  The  pupils  may  be  contracted  and  give  the  idea  of  opium- 
poisoning,  while  the  patient  cannot  be  roused  to  answer  questions, 
but  will  only  frown  or  groan. 

Haemorrhages  may  be  found  on  the  skin  and  in  the  retina.  The 
urine,  which  may  have  casts  and  a  little  albumen,  is  usually  passed 
involuntarily,  as  are  the  motions.  The  heart  is  dilated,  and  the 
pulse,  at  first  slow,  soon  becomes  quick,  and  towards  the  fatal  ter- 
mination very  quick  and  thready.  Respiration  may  be  quiet  or 
noisy.  If  death  is  to  take  place,  the  patient  becomes  colder  and 
colder,.the  tongue  dry  and  thick,  and  respiration  ceases. 

If  he  is  about  to  recover,  the  coma  will  gradually  pass  away;  he 
will  be  able  to  answer  questions  when  roused,  and  after  a  time 
gradually  recovers  consciousness.  The  speech  is  at  times  most 
peculiar,  being  scanning  in  character. 

The  coma  may  be  present  one  day,  but  the  next  day  the  patient 
maybe  slightly  better,  with  a  subnormal  temperature  and  a  slower, 
fuller  pulse;  towards  evening,  however,  the  temperature  rises,  and 
the  coma  returns.  This  second  attack  is,  as  a  rule,  fatal.  The 
fever  may  be  remittent  or  intermittent.  In  the  latter  case  it 
returns  before  death.  Quinine  treatment  by  injection  and  other- 
wise appears  to  be  of  no  avail  at  times,  and  after  two  or  three  days 
of  coma,  even  when  the  parasites  have  disappeared  from  the  peri- 
pheral blood,  the  person  may  die. 


ATYPICAL  SUBTERTIAN  FEVERS  1175 

Delirious  Type. — In  this  form  delirium  is  the  most  marked 
feature,  and  in  a  short  time  is  followed  by  exhaustion,  coma,  and 
death.  Such  cases  are  apt  to  come  on  suddenly,  and  to  be  mistaken 
for  drunkenness,  sunstroke,  or  mania.  The  fever  is  usually  very 
high.  Recovery  is  supposed  to  occur,  but  we  have  never  seen  these 
cases  end  otherwise  than  fatally. 

Tetanic  Type. — Patients  delirious  from  malaria  may  show 
trismus,  contraction  of  the  limbs,  opisthotonos,  retraction  of  the 
abdomen,  and  conjugate  deviation  of  the  eyes.  The  contractions 
of  the  muscles  may  relax  and  increase  as  in  tetanus,  and  there 
may  be  priapism.  The  attack  may  resolve,  or  end  in  death  with 
high  temperature. 

Convulsive  Type. — Children  during  an  attack  of  fever  may  develop 
convulsions,  followed  by  stupor,  or  even  coma  and  death. 

II.  SUBTERTIAN   SYNDROMES   WITH   LOCALIZATION 

The  subtertian  syndromes  with  localization  may  be  classified 
into: — 

I.  Syndromes  with  '  nervous  system  '  localization. 
II.  Syndromes  with  '  digestive  system  -  localization. 

III.  Syndromes  with  '  respiratory  system  '  localization. 
IV.  Syndromes  with  '  circulatory  system  '  localization. 

V.  Syndromes  with  '  ductless  glands  '  localization. 
VI.  Syndromes  with  '  urogenital '  localization. 
VII.  Syndromes  with  '  cutaneous  '  localization. 
VIII.  Syndromes  with  '  special  sense  '  localization. 

I.  With  'Nervous  System'  Localization. 

The  atypical  subtertian  malarias  with  nervous  system  symptoms 
may  be  classified  as  follows: — 

1.  Meningitic  type. 

2.  Hemiplegic  type. 

3.  Monoplegic  type. 

4.  Myelitic  type. 

5.  Ataxic  type. 

6.  Disseminated  sclerotic  type. 

7.  Bulbar  type. 

8.  Cerebellar  type. 

9.  Cerebral  type. 

10.  Polyneuritic  type. 

11.  Korsakoff  type. 

12.  Aphasic  type. 

Meningitic  Type. — Fever  with  signs  of  meningitis  may  be  found 
in  young  persons  and  children.  The  symptoms  are  vomiting, 
headache,  retraction  of  the  head,  and  rigidity  of  the  neck,  convul- 
sions, hyperesthesia,  going  on  to  coma  and  death.  There  may  be 
hypertension  and  slight  lymphocytosis  of  the  cercbro-spinal  fluid. 


1 1 76  THE  MALARIAL  FEVERS 

Hemiplegic  Type. — The  patient  may  be  suddenly  taken  ill  with 
fever,  and  develop  a  typical  hemiplegic  attack. 

Monoplegia  Type. — This  simulates  a  cerebral  hemorrhage,  but 
is  associated  with  high  fever,  and  in  both  it  and  the  two  preceding 
subtertian  parasites  can  be  found  in  the  blood. 

Myelitic  Type. — This  simulates  a  transverse  myelitis. 

Ataxic  Type. — The  symptoms  are  slow  and  scanning  speech,  great 
muscular  weakness,  exaggeration  of  tendon  reflexes,  ataxia,  together 
with  vomiting.  Subtertian  parasites  are  found  in  the  blood.  At 
first  there  is  no  fever,  but  this  may  develop  later.  Such  patients 
generally  recover  on  quinine  treatment,  or,  indeed,  they  do  so 
spontaneously. 

Disseminated  Sclerotic  Type. — There  is  scanning  speech,  inten- 
tional tremor,  nystagmus,  spastic  gait,  and  increased  reflexes,  all  of 
which  yield  to  quinine  therapy. 

Bulbar  Type. — A  fever  with  bulbar  symptoms — that  is  to  say, 
difficulty  of  speech  and  deglutition,  with  facial  paralysis,  or  with 
a  weakening  of  the  muscles  of  the  face  and  also  frequently  of  the 
legs.  This  appears  to  be  by  no  means  rare,  and  yields  to  quinine 
therapy  if  taken  in  time.  Malarial  parasites  are  often  absent  from 
the  blood,  and  the  spleen  need  not  be  enlarged. 

Cerebellar  Type. — The  symptoms  of  this  type  are  ataxia,  the 
patient  walking  like  a  drunken  man  and  complaining  of  severe 
headache  and  almost  complete  loss  of  vision.  Vomiting  is  frequent ; 
often  there  is  no  fever,  and  the  spleen  and  liver  are  not  enlarged. 
The  blood  may  show  parasites,  and  quinine  therapy  cures  the  con- 
dition, which  may  be  suspected  to  be  cerebellar  tumour  or  abscess, 
according  to  the  absence  or  presence  of  fever. 

Cerebral  Type. — This  type  resembles  a  cerebral  abscess  to  such  a 
marked  degree  that  an  operation  may  be  considered  to  be  necessary, 
when  a  blood  examination  reveals  the  subtertian  parasites  and 
quinine  cures  the  condition. 

If  there  is  no  fever  cerebral  tumour  may  be  suspected,  but  the 
blood  examination  reveals  the  true  condition. 

Polyneuritic  Type. — This  type  closely  simulates  '  wet  beri-beri,' 
because  the  patient  is  cedematous,  with  the  characteristic  gait 
and  loss  of  knee-jerks.  There  is  neither  fever  nor  enlargement  of 
the  liver  or  spleen,  but  the  blood  contains  subtertian  parasites,  and 
the  condition  is  cured  by  quinine  therapy. 

Polyneuritis  without  cedema  is  also  known. 

Korsakoff -like  Type. — This  resembles  the  preceding  in  that  the 
patient  shows  polyneuritis,  but  in  addition  he  suffers  from  mental 
symptoms,  among  which  the  most  important  is  the  loss  of  memory 
for  recent  events,  all  of  which  disappear  under  the  influence  of 
treatment  by  quinine.  Subtertian  parasites  may  or  may  not  be 
present  in  the  blood,  and  the  liver  and  spleen  may  not  be  enlarged. 

Aphasic  Type. — In  this  type  motor  aphasia  develops  with  or 
without  other  paralyses. 


ATYPICAL    SUBTKRTIAN  FEVERS  n?7 

II.  With  'Digestive  System'  Localization. 

The  subtertian  malarias  with  digestive  system  symptoms  may  be 
classified  as  follows: — 

i.  Pseudo-cholera  type. 

2.  Pseudo-dysentery  type. 

3.  Pseudo-appendicitis  type. 

4.  Pseudo-peritonitictype. 

5.  Pseudo-liver  abscess  type. 

6.  Pseudo-cholecystitis  type. 

7.  Pseudo-cirrhosis  type. 

8.  Hemorrhagic  pancreatitis  type. 

9.  Gastritis  type. 

Pseudo-Cholera  Type. — This  is  merely  a  great  exacerbation  of 
the  ordinary  gastro-intestinal  symptoms  often  met  with  in  malarial 
fever.  There  is  vomiting,  abdominal  pain,  and  severe  diarrhoea,  with 
motions  typical  of  cholera — i.e.,  rice-water  motions.  A  micro- 
scopical examination  of  the  dejecta  may  show  a  few  leucocytes  in 
stages  of  degeneration.  The  spleen  may  be  palpable,  and  an 
examination  of  the  blood  will  show  subtertian  parasites,  while  a 
bacteriological  examination  shows  absence  of  cholera  and  of  para- 
cholera  vibros. 

During  the  attack  the  patient  is  pale  or  cyanotic,  the  eyes  sunken, 
the  skin  cold  and  clammy,  but  the  temperature  may  be  raised,  and 
hiccough,  severe  thirst,  and  painful  cramps  in  the  lower  limbs,  may 
also  be  present.  The  urine  is  scanty  or  suppressed.  Collapse, 
delirium,  or  coma,  may  precede  death,  or  the  patient  may  be 
sensible  to  the  end.  If  the  patient  is  to  recover,  the  algidity 
diminishes,  the  diarrhoea  ceases,  and  after  a  long  sleep  he  awakens 
refreshed  and  convalescence  sets  in. 

Pseudo- Dysentery  Type. — In  this  type  there  are  two  forms — viz., 
those  with  typical  dysenteric  motions  containing  blood  and  muco- 
pus,  and  the  other  with  haemorrhagic  motions  without  pus  and 
with  little  or  no  mucus.  Fever  may  be  high,  with  great  distress  and 
prostration  and  a  small  rapid  pulse,  but  at  times  the  temperature 
may  be  nearly  normal.  The  spleen  may  be  slightly  enlarged,  there 
may  be  history  of  previous  malaria,  and  there  may  or  may  not  be 
malarial  parasites  in  the  blood. 

Pseudo-Appendicitis  Type.— -The  attack  is  sudden,  with  marked 
pain  in  the  appendicular  region,  sometimes  vomiting,  and  usually 
fever,  but  no  rigors.  The  spleen  and  liver  may  not  be  enlarged, 
and  there  may  be  tenderness  and  rigidity  in  the  appendicular  region. 
There  may  or  may  not  be  subtertian  parasites  in  the  blood,  but  the 
condition  is  cured  by  large  doses  of  quinine. 

Pseudo-Liver  Abscess  Type. — This  type  is  associated  with  fever, 
often  of  an  intermittent  character,  profuse  sweating,  loss  of  flesh, 
spleen  often  not  palpable,  liver  enlarged,  with  pain  on  pressure  all 
over  the  hepatic  area.     Malarial  parasites  are  usually  present  in  the 


1178  THE  MALARIAL  FEVERS 

blood,  and  the  condition  yields  to  quinine  therapy  by  proper  means. 
The  condition  is  rare,  and  must  not  be  mistaken  for  true  liver  abscess, 
which  is  not  uncommon,  and  the  error  of  making  the  diagnosis  of 
malaria  in  abscess  of  the  liver  is  more  common  than  vice 
versa. 

Pseudo-Cholecystitis  Type. — There  is  severe  pain,  shooting  up  to 
the  right  shoulder,  tenderness  in  the  region  of  the  gall-bladder, 
severe  vomiting,  and  occasionally  slight  jaundice.  The  spleen  may 
or  may  not  be  enlarged,  and  the  same  is  true  for  the  liver.  The  blood 
usually  shows  subtertian  parasites,  and  the  condition,  which  re- 
sembles an  attack  of  cholecystitis  due  to  gall-stones,  is  cured  by 
quinine. 

Pseudo-Cirrhosis  Type. — This  is  rare,  and  is  characterized  by  the 
hepatic  f  acies  and  ascites.  After  tapping,  the  liver  and  spleen  may 
be  felt  to  be  enlarged  and  hard.  On  repeated  examination  sub- 
tertian  parasites  may  be  found  in  the  blood.  Quinine  very  slowly 
cures  the  condition. 

Hemorrhagic  Pancreatitis  Type. — The  attack  is  sudden,  with 
violent  pain  in  the  epigastrium,  followed  by  vomiting  and  collapse. 
Tenderness  and  tympanites  may  be  present  in  the  epigastrium. 
Blood  examination  reveals  subtertian  parasites,  and  quinine  effects 
a  cure. 

Pseudo-Peritonitic  Type. — This  is  characterized  by  fever,  pinched 
face,  vomiting,  pain  and  tenderness  all  over  the  abdomen.  Malarial 
parasites  are  found  in  the  blood,  and  quinine  cures  the  condition. 

Gastritis  Type. — This  is  characterized  by  acute  or  by  chronic 
indigestion,  yielding  to  quinine  treatment.  In  old  people,  especially 
when  anaemia  is  present,  cancer  may  be  suspected. 

III.  With  '  Respiratory  System  '  Localization. 

It  will  be  remembered  that  during  the  ordinary  attack  of  any 
malarial  fever  there  are  a  few  dry,  rather  coarse,  rales  to  be  heard 
when  the  temperature  begins  to  fall,  and  earlier,  at  the  beginning  of 
the  attack,  there  are  often — as  first  noted  by  Castellani — very 
minute  crepitations  at  the  base,  probably  of  pleural  origin,  which 
generally  disappear  when  the  temperature  has  reached  its  highest 
point.  They  both  speedily  disappear,  but  every  now  and  then, 
even  in  ordinary  attacks,  they  are  more  pronounced,  and  the 
patient  suffers  from  cough  or  pain  on  taking  a  deep  breath. 

Slight  as  these  usually  are,  they  nevertheless  are  the  basis  of  the 
respiratory  system  types  of  pernicious  malaria,  which  may  be 
classified  as  follows: — 

i.  Pseudo-bronchitic  type. 

2.  Pseudo-pneumonic  type. 

3.  Pseudo-pleuritic  type. 

Pseudo-Bronchitic  Type. — This  subacute  or  chronic  dry  bronchitis, 
with  little  or  no  fever,  is  cured  by  a  few  doses  of  quinine. 


ATYPICAL  SUBTERTIAN  FEVERS  1179 

Pseudo-Pneumonic  Type. — This  is  often  of  the  nature  of  a 
broncho-pneumonia,  and  is  accompanied  with  blood  expectoration, 
in  the  red  corpuscles  of  which  parasites  may  be  seen,  dyspnoea,  and 
cough.  The  symptoms  are  better  in  the  remission  of  the  fever,  and 
worse  during  the  attack.  The  blood  is  full  of  parasites.  In  many 
cases  broncho-pneumonia  in  malarial  patients  is  not  due  directly 
to  the  malarial  parasites,  but  is  a  complication  due  to  the  pneumo- 
coccus. 

Pseudo -Pleuritic  Type. — Intermittent  pleuritic  pernicious  fever 
has  been  described,  with  sharp  pricking  pain,  dry  cough,  and 
friction  sounds,  which  improve  in  the  remission,  and  become  worse 
again  in  the  attack. 

Pleurisy  of  malarial  origin  is  without  effusion. 

IV.  With  '  Circulatory  System  '  Localization. 

Uypical  subtertian  malaria  with  circulatory  system  symptoms 
may  be  classified  into: — 

1.  Pseudo-anginal  type. 

2.  Endarteritis  type. 

3.  Intermittent  claudication  type. 

4.  Erythromelalgia  type. 

Pseudo -Anginal  Type.— The  right  heart  has  been  noticed  to  be 
enlarged  in  attacks  of  malarial  fever,  and  sometimes  these  symptoms 
become  marked,  with  severe  pain  in  the  cardiac  region  of  an  anginal 
nature,  sometimes  accompanied  by  vomiting  of  blood,  a  development 
of  the  algide  condition  mentioned  above,  and  death. 

Sometimes  the  anginal  syndrome  is  very  marked,  but  the  con- 
dition is  amenable  to  treatment  by  quinine. 

Pseudo-Endarteritis  Type. — A  superficial  artery  may  swell,  become 
hard  and  knotty  to  the  touch,  and  extremely  painful.  There  is 
no  fever,  and  the  blood  examination  may  be  negative,  but  the 
condition  yields  to  quinine. 

At  other  times  dry  gangrene  may  be  the  only  sign  of  an  endar- 
teritis of  a  deeper  and  more  important  vessel.  Search  should  be 
made  for  malarial  parasites,  and  if  there  is  any  reason  to  suspect 
malaria  as  a  possibility,  quinine  should  be  administered. 

Intermittent  Claudication  Type. — From  time  to  time  the  patient 
is  unable  to  put  his  foot  to  the  ground,  because  he  feels  pain  in  the 
calf  of  the  leg  and  there  may  be  an  absence  of  pulse  in  the  dorsalis 
pedis  artery  or  in  the  posterior  tibial.    Quinine  cures  the  condition. 

Erythromelalgia  Type. — The  hands,  and  at  times  the  feet  as  well, 
become  flushed,  and  the  patient  complains  of  pain  and  tingling 
in  the  fingers  and  at  times  the  toes  also.  Quinine  is  the  correct 
treatment. 

Heart  Block. — This  may  be  due  to  malarial  parasites. 

Rarer  Forms. — Certain  authors  admit  endocarditis  as  being  of  malarial 
origin. 


n8o  THE  MALARIAL  FEVERS 

V.  With  '  Ductless  Glands  '  Localization. 

The  types  with  which  we  are  acquainted  are  those  concerning  the 
suprarenal  capsules — viz.,  suprarenal  haemorrhage  and  the  pseudo- 
Addison  type,  and  those  affecting  the  thyroid  gland. 

Suprarenal  Hemorrhage  Type. — The  sign  and  symptoms  are  those 
of  acute  peritonitis,  but  though  the  blood  shows  no  malaria  para- 
sites, it  equally  shows  no  signs  of  polymorphonuclear  leucocytosis. 
There  is  no  enlargement  of  the  spleen.  Quinine  should  be  adminis- 
tered, and  the  blood  again  and  again  examined  for  parasites.  So 
far  the  cases  have  ended  fatally  as  far  as  we  know. 

Pseudo-Addison  Type. — There  is  a  pigmentation  of  the  skin 
associated  with  great  loss  of  flesh  and  severe  asthenia,  with  or 
without  splenic  enlargement,  with  or  without  fever,  with  or  without 
parasites  in  the  blood,  but  benefited  by  quinine. 

Thyroid  Type. — Intermittent  and  slight  swelling  of  the  thyroid 
gland  has  been  observed  in  cases  of  malaria. 

VI.  With  'Urogenital'  Localization. 

Subtertian  malaria  with  genito-urinary  symptoms  may  be 
classified  into:— 

i.  Orchitic  type. 

2.  Ovaritis  type. 

3.  Priapism  type. 

4.  Functional  generative  changes. 

5.  Nephritic  type. 

6.  Polyuric  type. 

7.  Malarial  hemoglobinuria. 

Orchitic  Type. — Sudden  severe  pain  in  the  testicles  in  a  person 
who  may  never  previously  have  suffered  from  typical  malarial 
fever.  The  testicles  become  slightly  swollen  and  very  tender. 
There  is  no  effusion.  The  temperature  rises  and  the  patient  feels 
very  ill,  but  the  symptoms  may  be  intermittent.  A  blood  examina- 
tion reveals  malarial  parasites,  and  quinine  cures  the  condition. 

Ovaritis  Type. — Neuralgia  of  the  ovaries  is  met  with  at  times  as  a 
malarial  symptom. 

Priapism  Type. — This  is  rare  and  is  not  influenced  by  the  ordinary 
drugs,  but  is  cured  by  large  doses  of  quinine. 

Functional  Generative  Changes. — Impotence,  amenorrhcea,  and 
metrorrhagia  have  been  assigned  to  malaria. 

Nephritic  Type. — A  type  of  malarial  nephritis  has  been  described. 

Polyuric  Type. — After  one  or  two  days  of  malarial  fever,  due  to 
the  subtertian  parasites,  a  patient  may  begin  and  continue  to  pass 
enormous  quantities  of  urine,  which  may  cause  considerable  alarm. 
Energetic  quinine  therapy  will  stop  this  excessive  flow. 

Malarial  Hemoglobinuria. — This  will  be  considered  in  Chap- 
ter XLL,  p.  1213. 

Malarial  mastitis  has  been  recorded.  Quarelli  has  described  a  case  of 
malarial  chyluria. 


ATYPICAL  SUBTERTIAN  FEVERS  1181 

VII.  With  'Cutaneous'  Localization. 

Pseudo-Smallpox  Type. — This  is  characterized  by  high  fever, 
severe  pains  in  the  back,  associated  with  the  papular  eruption  which 
appears  on  the  second  or  third  day,  and  consists  of  small  shotty 
papules  which  never  become  vesicles  or  pustules,  which  are  especially 
abundant  on  the  face.  It  may  require  repeated  blood  examinations 
to  find  the  parasites,  and  the  spleen  may  not  be  enlarged,  but 
quinine  quickly  cures  the  condition. 

Herpes. — Herpes  is  not  rare  in  attacks  of  malarial  fever.  It 
recurs  with  each  attack,  and  usually  at  exactly  the  same  spot  on 
which  it  was  situate  during  a  previous  attack— e.g.,  on  the  lips,  the 
tongue,  the  face,  and  the  genital  organs,  etc. 

It  may  occur  without  febrile  symptoms,  at  a  time  when  an  attack 
of  fever  is  due.     Herpes  zoster  is  very  rarely  seen. 

Rarer  Eruptions.  —  Malarial  erythemata,  malarial  urticaria, 
malarial  purpura,  and  malarial  patchy  oedema,  resembling  Malabar 
swellings  or  Quincke's  cedema,  may  be  mentioned.  Ulcerative  and 
gangrenous  conditions  have  been  recorded. 

Pigmentation. — The  black  hyperpigmentation  of  malaria  is  quite 
common,  and  may  be  present  in  patches,  chloasma  malaricum,  or  it 
may  be  diffused,  and  in  the  latter  case  may  be  associated  with  the 
syndrome  of  Addison's  disease  (see  p.  11 80).  In  chronic  cases  the 
skin  takes  on  a  peculiar  pale  yellow  or  ashy  grey  tinge. 

VIII.  With  '  Special  Sense'  Localization. 

Subtertian  malaria  may  concentrate  its  attacks  upon  the  eye  or 
the  ear  (see  also  p.  2004). 

Amaurotic  Type. — During  an  attack  of  pernicious  fever  a  patient 
may  complain  that  he  is  unable  to  see.  When  treated  with  quinine, 
as  a  rule  sight  soon  returns,  but  more  rarely  blindness  may  result, 
due  to  thrombosis  of  the  retinal  vessels,  and  consequently  retinal 
haemorrhages  and  optic  neuritis.  One  eye  only  may  be  attacked. 
This  condition  must  be  differentiated  from  quinine  amaurosis. 
In  malarial  amaurosis  the  pupils  react  to  light,  and  vision  is,  as  a 
rule,  not  completely  lost.  In  quinine  amaurosis  the  pupils  are  widely 
dilated,  do  not  react  to  light  and  other  symptoms  of  cinchonism, 
such  as  deafness,  severe  tinnitus  aurium,  etc.,  will  be  present. 

Aural  Type. — In  this  there  is  a  deafness  which  is  not  due  to 
quinine,  but  to  the  lack  thereof  permitting  the  subtertian  parasites 
t<  1  <  latnage  the  organ  of  hearing.  It  is  rare  and  chronic.  Richardson 
records  cases  simulating  mastoid  disease. 

Meniere's  Type. — Buzzing  of  the  ears  with  giddiness,  and  at  times 
the  patient  falls  down.  These  attacks,  which  arc  very  severe,  are 
of  malarial  origin,  but  rare.  The  practitioner  must  differentiate 
this  disease  from  aural  symptoms  due  to  quinine,  which  may 
induce  buzzing,  but  seldom  severe  giddiness.  Moreover,  symptoms 
due  to  quinine  improve  or  disappear  on  the  drug  being  discontinued. 

Loss  of  taste  and  anosmia  may  be  noted.  Symptoms  simulating  a  frontal 
sinus  affection  may  occur. 


1 1 82  THE  MALARIAL  FEVERS 


PERNICIOUS  MALARIA. 


When  any  of  the  above-mentioned  syndromes  caused  by  the 
subtertian  parasite  becorne  serious,  and  threaten  to  endanger  the 
life  of  the  patient,  they  are  called  '  pernicious  malaria,'  which  is 
therefore  commonly  caused  by  Laverania  malaria. 

More  rarely  pernicious  malaria  may  be  due  to  the  quartan  or 
tertian  parasites  being  present  in  enormous  numbers  in  the  blood, 
when  the  syndrome  usually  produced  is  without  localization  and 
most  frequently  of  the  comatose  type. 

CHRONIC  MALARIA. 

Chronic  malaria  may  result  from  infection  by  any  of  the  three 
malarial  parasites,  but  is  usually  caused  by  Laverania  malarice,  the 
subtertian  parasite. 

The  symptoms  of  chronic  malaria  are  repeated  attacks  of  slight 
fever,  which  may  pass  unnoticed;  enlargement  of  spleen  and  liver; 
and  pigmentation  of  the  skin  and  mucosae.  This  pigmentation  is 
particularly  to  be  noted  in  the  tongue  in  dark  races,  while  in  white 
races  Gerhardt's  urobilin  icterus  may  be  seen  in  the  skin.  Other 
symptoms  are  oedema  about  the  feet,  associated  with  anaemia, 
which  may  be  marked;  the  presence  of  malarial  parasites  in  the 
peripheral  blood  during  an  attack  of  fever;  and  often  palpitation 
and  dizziness,  bronchitis  and  digestive  troubles,  and  a  general 
disinclination  for  exertion  and  work.  The  urine  shows  an  increase 
of  urea  and  urobilin.  If  this  state  of  affairs  is  allowed  to  continue, 
it  may  pass  into  malarial  cachexia  with  enormous  enlargement  of 
the  spleen,  which  is  firm  to  the  touch  and  not  tender  or  painful, 
associated  with  a  profound  secondary  anaemia,  and  great  reduction 
of  red  cells  and  haemoglobin,  with  increase  of  mononuclear  leuco- 
cytes. In  boys  and  girls  the  onset  of  puberty  may  be  arrested 
(malarial  infantilism) . 

In  malarial  cachexia  the  apyrexial  intervals  are  long,  during 
which  search  may  in  vain  be  made  for  the  parasite  in  the  peripheral 
blood,  but  it  is  usually  found  during  the  febrile  attacks,  which 
may  be  quite  mild.  This  is  a  condition,  however,  in  which  blood 
examination  does  not  help  the  diagnosis  as  it  does  in  other  forms 
of  malaria,  and  the  clinical  symptoms  require  to  be  studied,  for 
the  disease  resembles  kala-azar,  while  it  may  also  be  mistaken  for 
ankylostomiasis. 

Chronic  malaria,  of  course,  is  due  to  insufficient  treatment  of  the 
acute  disease  by  quinine. 

MALARIAL  RELAPSES. 

The  cure  of  an  attack  of  malaria,  unfortunately,  does  not  end 
the  disease,  for  relapses  are  the  rule  and  not  the  exception;  in  fact, 
using  an  expression  of  Mannaberg's,  '  Malaria  is  one  of  those  infec- 
tious diseases  in  which  a  relapse  may  be  considered  as  an  essential 


MALARIAL  RELAPSES  1183 

feature.'  The  reason  is  that  the  parasites  are  not  all  killed  off  by 
the  quinine.  There  are  two  different  types  of  relapses:  the  first, 
after  a  short  interval,  may  be  called  the  true  relapse;  the  second, 
after  a  longer  interval,  may  be  called  the  recurrence.  Relapses  and 
recurrences  are  probably  caused  by  parasites  belonging  to  the  cycle 
of  schizogony,  and  by  the  parthenogenesis  of  the  macrogametocyte, 
which  belongs  to  the  cycle  of  sporogony. 

Relapses  of  quartan  fevers  take  place  at  irregular  intervals,  and 
the  suggestion  that  they  are  most  usual  at  about  the  twentieth 
day  is  not  correct.  Tertian  fevers  relapse  most  commonly  from 
the  fifth  to  the  eighteenth  day,  and  subtertian  about  the  end  of  a 
week  after  the  original  attack,  but  these  times  are  extremely  vari- 
able. These  relapses  are  historically  interesting,  as  they  probably 
represent  the  quintans,  sextans,  septans,  octans,  nonans,  etc.,  of 
ancient  authors. 

Recurrences  take  place  after  long  intervals  without  fever  and 
without  reinfection.  Exactly  how  long  the  parasites  can  lie  dormant 
in  the  human  body  and  then  wake  to  activity  and  cause  fever  is 
not  known.  Intervals  of  two  and  three  years  are  readily  credited 
nowadays,  but  it  is  in  our  experience  certain  that  the  length  of 
time  may  be  much  longer. 

Parasites  can  certainly  be  found  in  the  blood  of  persons  long 
after  they  have  left  the  tropics;  thus,  Ross  mentions  that  they 
were  found  in  a  case  in  Liverpool  four  years  after  absence  from  any 
malarious  locality,  and  also  states  that  his  own  father  suffered  from 
attacks  once  or  twice  a  year,  even  after  nine  years'  residence  in 
England. 

It  is  probable,  then,  that  the  old  idea  that  the  malarial  parasite 
can  exist  or  lie  dormant  for  years  in  the  system,  and  awake  to  re- 
newed activity  when  given  a  suitable  opportunity,  is  true.  During 
the  apyrexial  intervals  it  must,  of  course,  be  going  through  a  cycle 
of  schizogony,  but  not  in  sufficient  numbers  to  cause  disease.  These 
parasites  will  increase  rapidly,  and  cause  fever  when  the  general 
vitality  of  the  body  is  lowered  by  any  of  the  predisposing  causes 
already  mentioned,  but  especially  by  a  chill,  coming  into  action. 

MALARIAL  REINFECTIONS. 

In  tropical  countries  where  there  are  plenty  of  anophelines  and 
many  inhabitants,  European  and  native,  adults  and  children,  with 
numerous  gametocytes  in  their  blood,  reinfections  are  found  to  be 
common.  Many  cases  of  apparent  recurrence  in  these  countries 
must  be  reinfections,  which,  of  course,  may  be  with  the  same  or  a 
different  species  of  parasite  from  that  causing  the  first  fever. 
Repeated  infections  are  the  great  cause  of  the  quotidian  and  irre- 
gular fevers  of  the  tropics. 


THE  MALARIAL  FEVERS 


COMPLICATIONS. 


Man}'  other  diseases  may  occur  in  the  human  body  at  the  same 
time  as  an  attack  of  malaria;  but  of  all,  the  most  important  are 
typhoid,  dysentery,  pneumonia,  and  nephritis. 

Typhoid  as  a  complication  is,  of  course,  due  to  the  Bacillus 
typhosus  occurring  in  a  person  who  is  also  infected  by  malarial 
parasites,  and  in  that  sense,  therefore,  the  old  term  '  typho-malaria  ' 
is  correct. 

Dysentery  may  be  a  complication  due  to  the  Loeschia  histolytica 
or  to  the  dysenteric  bacilli,  but  it  may  also  be  directly  caused  by 
the  malarial  parasite  alone  (p.  1177). 

As  to  whether  there  is  or  is  not  a  malarial  pneumonia  is  a  vexed 
question;  personally,  we  are  of  the  opinion  that  a  severe  subtertian 
fever  may  produce  symptoms  resembling  a  pneumonia,  but  that 
true  lobar  pneumonia,  when  present  in  a  malarial  subject,  is  due  to 
the  pneumococcus,  and  is  therefore  a  complication. 

Nephritis  may  be  found  in  tertian  and  subtertian  fevers,  being 
directly  due  to  the  irritation  of  the  kidney  by  the  malarial  toxins. 

SEQUELiE. 

Many  so-called  sequelae  have  already  been  described  under 
Atypical  Subtertian  Fevers  (see  p.  1168).  The  possible  sequelae  of 
malaria  are  very  numerous,  and  maybe  classified  into  those  belong- 
ing to  the  nervous  system  and  sense  organs,  the  blood,  the  liver, 
and  the  spleen. 

The  subtertian  parasite  may  leave  severe  traces  of  its  action  upon 
the  brain  after  pernicious  attacks,  and,  indeed,  the  mind  may  never 
regain  its  old  condition.  Apart  from  the  milder  alterations  of 
disposition  and  character,  actual  insanity  in  the  form  of  mania  or 
melancholia  may  result. 

Neuritis  in  some  form  is  sometimes  of  malarial  origin,  but  it  is 
quite  possible  that  alcoholic  and  arsenical  poisoning,  and,  indeed, 
beri-beri,  may  have  been  confused  with  it.  We  have  seen  cases  of 
polyneuritis  of  malarial  origin,  but  the  condition  is  rare.  Neuralgias 
have  already  been  mentioned,  and  are  probably  in  some  cases  due  to 
the  direct  influence  of  the  malarial  toxins.  Tinnitus  aurium,  vertigo, 
deafness,  anosmia,  and  loss  of  taste,  are  said  in  some  cases  to  be 
malarial  in  origin. 

Severe  and  long-continued  ancemia  may  result  as  a  consequence 
of  malaria  caused  by  the  subtertian,  and  much  more  rarely  by  the 
other  parasites.  The  classification  and  characters  of  these  anaemias 
have  already  been  given  in  the  section  on  Pathology,  to  which 
reference  should  be  made  (pp.  1144  and  1151). 

Cirrhosis  of  the  liver  of  malarial  origin  is,  in  our  experience,  much 
less  frequent  than  admitted  by  many  writers.  Cirrhosis  of  the  liver 
is  common  in  the  tropics,  and  in  certain  cases  is  due  to  alcohol;  but 
one  of  the  writers  has  pointed  out  that,  at  all  events  in  Ceylon,  a 


SEQUELM  1 1 85 

polyfibrosis  of  liver,  pancreas,  and  kidney  can  be  met  with  which 
has  no  malarial  origin. 

The  enlargement  of  the  spleen  has  already  been  described,  and 
rupture  as  the  result  of  blows  or  injuries  is  by  no  means  unknown, 
though  not  common,  and  requires  prompt  surgical  attention.  We 
have  only  come  across  one  case  in  our  experience. 

Tremors  are  not  infrequently  seen  in  chronic  malaria,  though 
more  rare  in  acute  malaria.  Fine  tremors,  consisting  of  bilateral 
fine  oscillations  of  small  amplitude,  caused  by  the  alternate  action 
of  antagonistic  muscles,  may  occur  in  the  limbs  and  more  rarely 
in  the  head.  They  are  most  common  in  the  upper  limbs,  and 
especially  in  the  hands.  In  the  head  there  may  be  nystagmus  or 
the  tongue  may  be  implicated.  These  tremors  are  increased  by 
effort,  fatigue,  or  emotion.  Coarse  tremors  are  usually  exaggerations 
of  fine  tremors,  and  are  often  due  to  emotion,  such  as  examination 
by  the  physician.  Intentional  tremors  are  produced  in  the  hands, 
and  sometimes  in  the  head  and  neck,  and  are  due  to  voluntary 
movement.     They  are  not  very  uncommon  in  malarial  infections. 

The  fine  tremors  must  be  distinguished  from  the  fine  tremors 
due  to  quinine,  which  are  not  very  rare  when  the  drug  has  been 
given  for  long  periods.  These  tremors  disappear  in  days,  weeks, 
or  months  after  the  drug  has  been  discontinued. 

In  malarial  patients  coming  from  war  zones  tremors  and  ataxic 
movements  are  not  rarely  seen,  but  these  tremors  are  neither 
due  to  malaria  nor  to  quinine,  being  of  hysterical  origin  (sensH 
lato),  and  disappear  often  after  treatment  by  suggestion. 

DIAGNOSIS. 

The  diagnosis  of  malaria  may  be  simplicity  itself,  or,  on  the  other 
hand,  it  may  be  most  difficult,  as  there  is  practically  no  sign  or 
symptom  of  disease  of  the  hitman  body  which  it  cannot  mimic.  We 
venture  to  impress  upon  the  reader  the  vital  necessity  of  making 
1  thorough  and  careful  clinical  examination,  as  in  many  cases  this 
alone  may  be  the  key  to  a  correct  diagnosis. 

The  positive  signs  of  malarial  infections  are: — 

r.  Tertian  or  quartan  periodicity,  no  matter  what  the  symptoms 
may  be. 

2.  Tertian,  quartan,  or  subtertian  parasites  present  in  the  peri- 
pheral blood. 

3.  Pigment  in  the  leucocytes. 

4.  Quinine,  properly  administered,  producing  beneficial  effect 
upon  the  symptoms. 

The  complementary  signs  suggesting  malarial  infections  are: — 

1.  Spleen  enlarged  and  hard,  no  matter  what  the  symptoms  may 
be. 

2.  Slightly  enlarged  and  tender  spleen  in  cases  exhibiting  syndromes 
usually  significant  of  another  disease,  if  the  usual  tests  for  the  causal 
agent  of  the  other  disease  are  negative. 

75 


1 1 86  THE  MALARIAL  FEVERS 

3.  Presence  of  mononucleosis  in  association  with  other  features  of 
malaria. 

4.  Pigmentation  of  the  skin. 

5.  History  of  old  malarial  infections. 
Malaria  should  not  be  excluded  by  :- 

1.  Absence  of  malarial  parasites  from  ihe  blood,  even  after  repeated 
examinations,  especially  in  people  who  have  taken  quinine,  and 
unless  the  examinations  have  been  repeated  many  times  and  at 
varying  intervals. 

2.  Absence  of  mononucleosis. 

3.  Absence  of  enlargement  of  the  spleen. 

4.  Absence  of '  prompt  reaction  '  to  quinine. 

The  question  of  driving  the  malarial  parasite  from  a  hiding-place  in  some 
organ  into  the  peripheral  blood  by  giving  a  small '  provocative  dose '  of  quinine, 
injections  of  vaccines,  of  sterile  milk,  of  strychnin,  of  adrenalin,  by  spleen 
douches,  violent  exercise,  by  ultraviolet  light,  etc.,  has  been  attempted,  but 
reliance  cannot  be  placed  upon  these  methods  as  a  practical  aid  to  diagnosis. 

Splenic  puncture,  and  the  subsequent  examination  of  the  blood 
obtained  in  this  way,  would  help  diagnosis  considerably,  but  is  not 
devoid  of  risk. 

It  is  generally  stated  that  a  fever  which  within  four  days  is  not  influenced 
by  quinine  in  full  doses  is  not  malaria.  This  is  correct  as  regards  malarial 
fevers  due  to  tertian  and  quartan  parasites,  but  not  always  as  regards  those 
caused  by  the  subtertian  parasite.  We  have  met  with  cases  in  which  the  fever 
has  remained  unaffected,  while  the  parasite  can  be  found  in  the  peripheral 
blood,  notwithstanding  several  weeks'  quinine  therapy  by  various  methods. 

In  malarial  cachexia  James  has  pointed  out  that  the  microscopical  is  inferior 
to  the  clinical  examination,  drawing  attention  to  the  fact  that  a  four-hourly 
temperature  chart  carefully  kept  during  one  of  the  febrile  attacks  will  often 
show  the  typical  curve  of  subtertian  fever.  In  such  difficult  cases  the  clinical 
signs,  together  with  the  reaction  of  the  disease  to  quinine,  must  be  utilized. 

In  latent  malaria  the  frequent  increase  of  the  urobilin  in  the  urine  may  be 
of  some  slight  help  in  the  diagnosis,  as  pointed  out  by  Plehn,  together  with 
indefinite  periodical  rheumatoid  pains.  Thomson  has  devised  a  diagnostic 
method  based  on  complement  deviation,  using  as  antigen  a  culture  of  malaria 
parasites  from  a  heavily  infected  case.  The  reaction,  however,  seems  to  be 
positive  also  in  cases  of  syphilis.  Details  may  be  found  in  Thomson's  paper, 
British  Medical  Journal,  December  7,  191 8. 

The  differential  diagnosis  of  the  various  forms  of  malarial  fever 
should  be  confirmed,  no  matter  how  evident  the  clinical  symptoms 
may  be,  by  microscopical  examination. 

The  most  important  diseases  to  differentiate  from  malaria  are 
typhoid,  insolation,  liver  abscess,  kala-azar,  Malta  fever,  influenza, 
yellow  fever,  dengue,  and  seven-days'  fever.  For  the  differential 
diagnosis  see  Chapter  LX.  (p.  1511),  which  deals  with  the  diagnosis 
of  a  tropical  fever. 

The  pernicious  forms  of  malaria,  in  whatever  way  they  attack  the 
patient,  will  in  most  cases  be  readily  diagnosed  by  blood  examina- 
tion, as  will  also  the  masked  form  of  the  disease. 

Fevers  due  to  septicaemia  caused  by  a  streptococcus,  the  pneumococcus, 
and  the  gonococcus,  may  resemble  malaria,  but  can  be  excluded  by  bacterio- 
logical examination,  as  can  influenza  when  it  gives  rise  to  an  intermittent 
type  of  fever. 


PROGNOSIS  ii  87 


PROGNOSIS. 


Quoad  vitam  the  prognosis  is  usually  good  if  an  appropriate 
quinine  therapy  is  carried  out,  but  it  must  be  remembered  that  per- 
nicious cases  tend  to  a  high  mortality,  notwithstanding  all  treat- 
ment, and  even  in  the  usual  benign  cases  the  cure  is  very  often 
merely  clinical  and  not  complete,  as  is  also  seen  in  other  protozoal 
diseases  such  as  syphilis,  yaws,  and  amoebiasis. 

There  are  two  further  points  to  be  considered  under  this  head- 
ing, and  they  are: — 

1.  The  probability  of  recovery. 

2.  The  probability  of  a  cure. 

1.  Probability  of  Recovery. — This  depends  upon: — 

(a)  The  type  of  fever. 

(b)  The  condition  of  the  patient  with  regard  to  race,  age,  sex, 
physical  fitness,  the  presence  or  absence  of  other  diseases,  idiosyn- 
crasy to  quinine,  and  the  duration  of  the  symptoms. 

(c)  The  nature  of  the  country  in  which  the  patient  is  living. 
The  Type  of  Fever. — Quartan  and  tertian  infections,  especially 

in  the  simple  type,  give  the  best  prognosis,  but  quotidian  infections 
and  fevers  due  to  the  subtertian  parasite  should  be  viewed  as  more 
dangerous,  while  pernicious  malaria  must  be  regarded  as  extremely 
dangerous. 

Race. — The  mortality  among  natives  of  bad  malarial  regions  is 
usually  low,  while  that  among  Europeans  is  high.  The  death-rate 
in  a  native  race  which  has  comparatively  recently  been  subjected 
to  increased  danger  of  malarial  infections  is  sometimes  truly 
appalling. 

Sex. — There  is  a  better  prognosis  for  males  than  for  females,  and 
there  is  a  distinctly  worse  prognosis  for  an  attack  taking  place  during 
pregnancy. 

Age. — Children  often  have  more  severe  attacks  than  adults,  but 
can  usually  stand  quinine  well,  which  rather  balances  this  disad- 
vantage. 

Physical  Fitness. — Persons  debilitated  by  long  residence  in 
tropical  countries  or  from  existence  upon  poor  food  are  not  in  a 
condition  to  resist  severe  malarial  infections,  and  therefore  the  prog- 
nosis is  rendered  more  serious. 

Complications. — The  presence  of  complications  in  any  form — ■ 
e.g.,  typhoid  fever,  etc. — naturally  makes  the  outlook  more  serious. 

Quinine. — Idiosyncrasy  to  quinine  of  an  anaphylactic  nature 
is  most  serious,  but  can  be  combated  by  commencing  with  very 
small  doses,  and  slowly  and  steadily  working  upwards. 

Duration  of  the  Symptoms. — If  the  symptoms  persist  in  the 
face  of  quinine  therapy  the  prognosis  is  serious. 

2.  Probability  of  a  Cure. — The  probability  of  a  cure — that  is  to 
say,  of  a  so-called  bacteriological  sterilization  of  a  patient  with 
regard  to  the  malarial  parasites — is  a  very  doubtful  matter,  as  the 


1 1 88  THE  MALARIAL  FEVERS 

affection  is  able  to  lie  dormant  for  months  and  years,  even  after 
the  tropics  and  any  source  of  infection  have  been  parted  with 
entirely.  At  times  one  may  be  lucky  enough  to  catch  all  the  para- 
sites sporulating,  and  to  kill  them  with  one  large  and  properly 
applied  dose  of  quinine.  This  has  certainly  happened  to  us  with 
regard  to  the  subtertian  parasite  in  certain  cases,  but  it  may  have 
been  accidental.  The  infection  may  remain  dormant  for  years,  and 
be  reawakened  by  any  cause  lowering  the  resisting  powers  of  the 
individual,  such  as  a  chill,  a  traumatism,  or  an  operation.  In 
temperate  climates  there  is  often  a  seasonal  dormancy  in  winter. 

TREATMENT. 

Essential  Treatment. — There  is  one  specific  remedy  for  malaria, 
and  this  is  Quinine,  which  should  be  given  immediately  upon  the 
diagnosis  of  malaria  being  made,  and  may  be  administered  as 
follows: — 

A.  When  the  Patient  is  First  seen  in  an  Acute   Attack. 

I.  In  Benign  Intermittent  Fevers  (Quartan  and  Simple  Tertian) 
give  quinine  in  solution  by  the  mouth,  if  the  patient  is  not  sick,  in 
10  grain  doses  three  times  a  day,  or  in  doses  of  15  grains  in  the 
morning  and  15  grains  in  the  evening. 

In  a  certain  number  of  cases  it  is  advisable  to  give  with  each  dose 
of  quinine  5  grains  of  sodium  bromide  in  solution,  in  order  to  combat 
any  nerve  effects  of  the  drug.  The  bowels  should  be  freely  opened 
with  calomel,  followed  by  salines. 

If  the  heart  is  not  working  properly,  caffeine  citrate  in  1  to  3  grain 
doses  may  also  be  administered,  either  by  the  mouth  or  hypo- 
dermic ally. 

If  this  dosage  of  quinine  is  found  to  be  insufficient,  as  judged  by 
the  persistence  of  the  symptoms,  increase  it  to  10  grains  every 
four  hours  instead  of  three  times  a  day. 

II.  In  Severe  Intermittent,  Remittent,  and  All  Subtertian  Fevers 
give  quinine  by  intramuscular  injection  in  a  dose  of  15  grains  as 
soon  as  the  diagnosis  is  made.  Repeat  the  injection  daily,  and  in 
addition  administer  the  drug  by  the  mouth  in  10  grain  doses  three 
times  a  day. 

In  these  fevers  as  much  as  45-60  grains  of  quinine  may  be  re- 
quired in  twenty-four  hours  to  combat  the  symptoms,  and  should 
be  given  by  a  combination  of  intramuscular  injections  with  oral 
administration. 

Sodium  bromide,  the  purgative  and  cardiac  drugs  mentioned 
in  the  preceding  section,  may  also  be  given. 

The  injection  is  to  be  made  in  a  thoroughly  antiseptic  manner.  Use  a  vial, 
containing  15  grains  of  quinine  bihydrochloride  ini  cubic  centimetre  of  fluid, 
manufactured  by  some  reputable  firm.  The  injection  may  be  made  deep 
into  the  muscles  of  the  gluteal  region,  care  being  taken  to  avoid  the  line  of  the 
sciatic  nerve,  or  deep  into  the  loose  tissue,  extending  from  the  lower  angle  of 
the  scapula  to  the  crest  of  the  ilium.     The  vials  made  by  different  firms  vary 


TREATMENT  1189 

very  much  in  the  degree  of  pain  or  discomfort  which  they  produce,  but  some 
(in  pre-war  preparations)  caused  very  little  pain  if  given,  as  should  always 
be  done,  with  the  strictest  antiseptic  precautions.  For  fuller  instructions 
see  Method  of  Administration,  p.  1193. 

Do  not  hesitate  to  give  intramuscular  injections  of  quinine.  They 
have  saved  many  lives,  but  the  strictest  antiseptic  methods  must 
be  used. 

III.  In  Pernicious  Malaria. — In  pernicious  fevers  give  quinine 
at  once  by  intravenous  injection. 

The  quinine  injection  should  be  made  into  the  median  basilic  or  median 
cephalic  veins,  and  not  less  than  1  gramme  (15  grains),  dissolved  in  sterile 
5  c.c.  of  physiological  salt  solution,  should  be  injected  at  a  time.  The 
skin  over  the  selected  vein  should  be  rendered  thoroughly  aseptic  by 
soap  and  water  and  carbolic  lotion,  or  by  painting  with  tincture  of  iodine, 
and  then  a  bandage  tied  round  the  arm,  so  as  to  retard  the  flow  of  venous 
blood  and  make  the  selected  vein  stand  out.  Then  the  needle  should  be 
inserted  into  the  vein  (care  being  taken  that  there  is  no  air  in  needle  or  syringe) 
in  a  sloping  direction,  with  the  point  towards  the  heart,  so  that  the  injection 
can  flow  with  the  circulation.  The  point  of  the  needle  should  be  felt  to  be 
loose  {i.e.,  in  the  vein).  The  bandage  must  now  be  loosened  and  the  injection 
made  slowly,  the  effect  on  the  pulse  being  noted.  The  needle  is  now  with- 
drawn, and  an  aseptic  pad  fixed  in  position  by  a  bandage. 

The  effect  of  quinine  on  the  circulation  must  be  remembered,  and  if  the 
pulse  is  bad,  it  is  advisable  to  give  an  injection  of  ether  as  a  preliminary. 

If  the  serious  symptoms  persist  the  intravenous  injection  may  be 
repeated  in  four  hours,  and  further  medication  may  then  be  carried 
on  by  intramuscular  injections.  Not  more  than  two  intravenous 
and  two  intramuscular  should  be  given,  under  any  circumstances, 
in  twenty-four  hours. 

When  the  serious  symptoms  abate  the  intramuscular  injections 
alone  should  be  used,  and  should  be  given  once  or  twice  a  day, 
and  supplemented  by  oral  administration,  as  indicated  above. 

B.  During  the  Course  of  the  Fever. 

I.  //  the  symptoms  are  abating  the  dosage  of  quinine  may  be 
reduced  slowly  to  about  30  grains  per  diem,  but  this  must  not  be 
done  too  quickly,  and  care  must  be  taken  to  increase  this  dosage 
at  once  if  there  are  any  signs  of  a  return  of  the  symptoms. 

During  the  course  of  the  fever  the  bowels  must  be  kept  regularly 
open,  the  urine  must  be  carefully  watched  as  to  quantity  and  colour, 
and  tested  chemically  from  time  to  time,  while  blood  examinations 
should  also  be  made  at  times  and  the  pulse  carefully  noted. 

II.  //  the  symptoms  are  not  abating  the  probability  is  that  in- 
sufficient quinine  is  being  administered,  and  in  such  cases  the  drug 
should  be  carefully  increased. 

If  only  oral  administration  has  been  used  it  should  be  at  once 
supplemented  by  intramuscular  injections. 

Care  should  also  be  taken  that  the  bowels  are  kept  well  opened, 
that  a  sufficiency  of  fluid  is  drunk  to  provide  a  good  flow  of  urine, 
and  that  the  heart's  action  is  well  supported  by  stimulants  and  by 
drugs  if  necessary. 


1 1 go  THE  MALARIAL  FEVERS 

In  order  to  combat  severe  symptoms,  it  may  be  necessary  to 
give  45-60  grains  of  quinine,  or  even  more,  per  diem,  but  this  must 
be  done  carefully,  and  the  dosage  must  at  once  be  reduced  when 
improvement  appears.  As  a  rule,  not  less  than  30  grains  in  the 
twenty-four  hours  should  be  given. 

Quinine  often  takes  effect  before  the  expiration  of  four  days  of 
thorough  treatment,  but  it  may  be  necessary  to  continue  the  ad- 
ministration of  large  daily  doses  longer  than  this  period.  If  quinine 
appears  to  be  ineffectual  in  checking  the  symptoms,  care  must  be 
taken  to  exclude  any  other  possible  cause  for  the  symptoms. 

C.  When  the  Acute  Attack  has  Subsided. 

Continue  to  administeF  quinine  orally  for  at  least  three  months. 

During  the  first  month  give  it  in  10  grain  doses  twice  or  thrice 
daily.  During  the  second  month  5  grain  doses  thrice  daily.  During 
the  third  month  5  grain  doses  twice  daily. 

The  quinine  may  be  administered,  as  the  bihydrochloride,  in  crushed  tabloids, 
but  if  it  is  desired  to  use  the  more  insoluble  salts  (see  the  paragraphs  on  the 
theoretical  considerations  lower  down  in  this  chapter)  a  mixture  such  as  the 
following  may  be  given: — 


Quinine  sulphate 
Dilute  sulphuric  acid 
Syrup  of  orange 
Distilled  water 


10  grains. 
10  minims. 
1  drachm. 
1  ounce. 


Euquinine  may  be  substituted  for  quinine  for  the  purposes  described  in  this 
paragraph,  but  must  be  given  in  slightly  larger  doses. 

With  the  commencement  of  convalescence  it  is  useful  to  give 
some  tonic  mixture  such  as: — 

Iron  and  quinine  citrate  .  .  10  grains. 

Liquor  strychninae  hydrochloratis  . .      3-5  minims. 

Syrup  of  orange         . .  . .  . .      1  drachm. 

Distilled  water  . .  . .  1  ounce. 

This  should  be  taken  three  times  a  day  half  an  hour  after  meals. 

See  that  the  patient's  bowels  are  kept  regularly  open  every  day. 

Notwithstanding  all  care  and  energetic  quinine  treatment, 
relapses  are  prone  to  occur  some  variable  time  after  medication 
has  ceased. 

D.  Relapses. 

When  relapses  occur  after  thorough  quinine  treatment  it  is 
advisable  to  combine  with  this  drug  arsenic  and  at  times  tartar 
emetic  and  phosphorus. 

The  following  mixture  introduced  byCastellani  indicates  the  line  of  medica- 
tion suggested: — Quinine  sulphate,  10  grains;  dilute  sulphuric  acid,  10  minims; 
tartar  emetic,  \-±  grain;  codein,  Jj-J  grain;  syrup,  1  drachm;  chloroform 
water,  to  t  ounce. 

Another  formula  used  by  Castellani  is:  Quin.  hydr.,  gr.  x.;  tartar  emetic, 
gr.  \;  liq.  Fowleri,  ll\i.;  syr.,  3"- ;  aq-  chlorof.  ad  §i. 

Two  tablespoonfuls  of  this  mixture  may  be  taken,  well  diluted  with  water, 
every  four  hours. 


QUININE 


1191 


In  addition  it  may  be  necessary  to  resort  to  intramuscular  injections  of 
15  grains  of  quinine  daily,  and  it  is  sometimes  advisable  to  alternate  this, 
every  other  day,  by  a  subcutaneous  injection  of  the  phosphorated  oil  of  the 
British  Pharmacopoeia  in  doses  of  from  1  to  4  minims. 

The  above  forms  the  quinine-phosphorus-tartar-emetic  treatment  for 
malarial  relapses  devised  by  Castellani,  and  found  useful  by  Quarelli  and  others . 

BacceUi's  mixture,  slightly  modified,  has  the  following  formula:  Quin. 
•  bisulph.,  gr.  8;  ferri  perchlor.  (Ital.  Pharm.),  gr.  3;  liq.  Fowled,  TI\.i;  aq.  to  §i. 
It  is  very  bitter. 

E.  Chronic  Malaria. 

Chronic  malaria  should  be  treated  by  the  methods  given  just 
above  for  relapses.  Intramuscular  injections  of  quinine  are  specially 
useful  in  this  condition,  and  should  be  given  in  courses  of  fifteen 
daily  injections.  The  courses  should  be  repeated  two  or  three 
times  after  varying  intervals. 

F.  Malaria  in  Pregnancy. 

Give  the  usual  twenty-four  hourly  dosage  of  quinine,  but  divide 
it  up  into  small  individual  doses  of  2  to  5  grains. 

G.  Malaria  in  Children. 
The  dosage  of  quinine  for  children  is  as  follows: — 


As,e  of  Child. 

Dose  of  Quinine. 

Number  of  Doses  in 
Twenty-four  Hours. 

Under  twelve  months 
1  to  3  years 
3  to  10  years 
10  to  16  years 

£  to  i£  grains. 

1  to  2  grains. 

2  to  3  grains. 

3  to  5  grains. 

Six. 
Six. 
Six. 
Six. 

H.  Remarks. 

It  may  be  thought  that  in  the  above  we  have  been  too  dogmatic, 
but  our  excuse  is  that  we  desire  to  lay  before  the  practitioner  our 
experience  of  many  years  of  tropical  practice. 


Fig.  626. — Temperature  Chart  to  illustrate  the  Benefit  of  Intra- 
muscular Injections  given  at  +  +  +  +  +  +,  as  compared  with 
the  Prolonged  Oral  Therapv  of  Days  Previously. 


1 1 92  THE  MALARIAL  FEVERS 

The  dosage  of  quinine  in  use  in  England  and  non-malarial  countries 
is  perfectly  useless  in  highly  malarial  tropical  districts. 

An  attempt  is  made  in  the  above  system  of  treatment  to  prevent 
relapses  and  recurrences  as  far  as  is  possible. 

Details  of  Treatment. — The  various  other  points  connected 
with  treatment  may  be  considered  as  follows: — 

A.  Quinine  therapy. 

B.  Symptomatic  treatment. 

Quinine  Therapy. — There  are  a  number  of  details  which  require 
elaboration  with  regard  to  quinine  therapy,  and  these  are: — (i)  The 
dose;  (2)  the  time  of  administration;  (3)  the  method  of  adminis- 
tration; (4)  the  duration  of  treatment. 

The  Dose. — To  adults  we  generally  give  three  times  a  day  by  the 
mouth  5  to  10  grains  of  the  ordinary  preparations  (sulphate,  hydro- 
chloride, etc.).  The  routine  mixture  is  composed  of  quinine  sul- 
phate, 5  to  10  grains;  dilute  sulphuric  acid,  5  to  10  minims;  syrup 
of  orange,  1  drachm ;  distilled  water,  1  ounce.  We  give  euquinine  in 
slightly  larger  doses. 

By  intramuscular  or  intravenous  injections  we  give  15  grains, 
by  the  rectum  30  grains;  but  when  given  by  the  last  method,  some 
tincture  of  opium  should  be  added,  to  prevent  irritation,  which 
otherwise  is  liable  to  occur.  Five  or  ten  grains  of  potassium  bromide 
added  to  each  dose  of  quinine  will,  to  a  certain  extent,  prevent 
tinnitus  aurium.  In  cases  in  which  the  heart  is  weak  a  few  minims 
of  tincture  of  digitalis  should  be  prescribed. 

Children  suffering  from  malaria  stand  quinine  well,  and  the 
minute  doses  advised  in  so  many  treatises  on  the  diseases  of  children 
are,  in  our  experience,  utterly  inadequate  in  the  tropics.  Infants 
under  one  year  of  age  may  receive  from  |  grain  to  1^  grains  six 
times  a  day;  children  between  one  and  three  years  of  age  from 
1  grain  to  2  grains  six  times  a  day,  and  those  between  three  and 
ten  years  2  to  3  grains  six  times  a  day. 

Nocht  has  advised  the  administration  in  adults  of  quinine  in  small  repeated 
doses  of  2  \  grains  five  times  a  day.  This  method  is  useful  when  there  is  a 
tendency  to  haemoglobinuria  and  in  pregnant  women  in  whom  the  administra- 
tion of  full  doses  may  induce  abortion;  but  this  action  has  been  greatly  exag- 
gerated, many  cases  ascribed  to  quinine  being  due  to  some  other  cause.  We 
have  often  given  15  grains  of  quinine  daily  to  pregnant  women,  but  divided 
into  small  doses  of  2  to  3  grains,  and  in  severe  cases  have  pushed  the  drug 
without  bad  effects.     The  addition  of  a  little  opium  may  prevent  bad  effects. 

In  patients  showing  anaphylactic  symptoms  such  as  dyspnoea,  dysphagia 
urticaria,  etc.,  Heran  and  Saint-Girons  give  quinine  as  follows:  the  first  day 
a  '  defensive  dose  '  of  gr.  ■£-  quinine  sulphate  mixed  with  gr.  8  sodium  bicar- 
bonate is  given,  and  two  hours  later,  gr.  i\.  The  second  day,  two  hours 
after  the  '  defensive  dose,'  gr.  3  is  administered.  The  third  day,  two  hours 
after  the  defensive  dose,  gr.  6  is  given,  and  so  on,  gradually  increasing  the 
amount  of  quinine. 

Time  of  Administration. — The  best  time  to  give  quinine  to  a 
healthy  person  for  purposes  of  prophylaxis,  or  to  a  convalescent  for 
purposes  of  effecting  a  cure,  will  be  at  meal-times,  and  preferably 


QUININE  1 1 93 

directly  at  the  end  of  the  meal,  so  that  it  can  enter  the  blood  with 
the  products  of  digestion,  and  so  obtain  its  fullest  action.  It  has 
been  our  rule  in  most  cases  to  advise  that  it  should  be  taken  directly 
after  the  early  morning  meal. 

The  haemolytic  action  of  quinine  must  be  remembered,  and  the 
fact  that  it  may  by  this  action  give  the  liver  more  work  by  extra 
bile  production.  Consequently,  it  is  most  necessary  to  remind  the 
above  class  of  patients  to  take  care  that  the  bowels  are  open  regu- 
larly, and  to  correct  by  suitable  aperients  any  irregularity  that  may 
exist. 

With  regard  to  mild  quartan  and  tertian  fevers,  there  is  not  the 
slightest  doubt  that  excellent  effects  are  obtained  by  giving  the 
drug  four  hours  before  the  attack — i.e.,  before  the  sporulation  of 
the  parasite  is  due.  In  this  way  the  merozoites  are  most  likely 
to  be  killed.  This  may  be  modified  by  giving  the  drug  twice  daily, 
one  dose  of  10  grains  by  the  mouth  in  the  morning,  and  the  other 
dose  of  10  grains  at  the  above-stated  time.  This  method  we  have 
found  most  useful,  as  it  allows  for  irregularity  in  sporulation. 

In  many  cases,  however,  we  give  the  drug  three  times  a  day, 
without  regard  to  the  conditions  of  parasitic  life,  and  this  method 
is  apparently  not  less  successful. 

In  more  severe  forms  of  quartan  and  tertian,  and  in  cases  of 
subtertian  fever  in  which  the  patient  is  seen  for  the  first  time  during 
the  attack,  the  drug  should  be  given  intramuscularly  or  by  the 
mouth,  when  it  may  be  administered  on  the  fall  of  the  tempera- 
ture, when  the  gastric  irritation  is  lessening,  and  then  continued  by 
one  of  the  above  methods. 

In  cases  of  serious  and  of  pernicious  attacks,  time  must  not  be 
wasted  in  waiting  for  temperatures  to  fall  or  for  symptoms  to  im- 
prove, otherwise  the  patient  will  die,  and  there  must  be  no  hesita- 
tion in  giving  either  an  intramuscular  or  an  intravenous  injection, 
according  to  the  severity  of  the  symptoms. 

Method  of  Administration. — For  practical  purposes  there  are 
only  four  methods  of  administration : — 
i.  By  the  mouth. 

2.  By  the  rectum. 

3.  By  intramuscular  injections. 

4.  By  intravenous  injections. 

By  the  Mouth. — If  expense  is  no  object,  take  the  most  soluble 
drug  that  can  be  got,  and  use  either  the  bihydrochloride  or  the 
bisulphate;  otherwise  the  sulphate  must  be  used.  In  cases  of 
women  and  children,  euquinine  may  be  used  with  advantage,  but  it 
should  be  remembered  that  it  is  very  insoluble  and  expensive. 

The  forms  in  which  the  chosen  drug  maybe  administered  are: — 

1.  Powder. 

2.  Solution. 

3.  Tabloid,  tablet,  or  pill. 

4.  Cachet  or  capsule. 


1 1 94  THE  MALARIAL  FEVERS 

It  is  presumed  that  no  doctor  would  allow  his  patient  to  take  quinine  in  a 
cigarette-paper,  though  non-medical  people  are  found  -who  have  got  into  the 
habit  of  using  this  method. 

As  regards  the  powder,  it  is  an  efficient  method  of  administering 
the  drug  to  the  healthy,  if  given  directly  after  a  meal,  but  the  taste 
is  most  unpleasant.     It  is  certainly  the  cheapest  method. 

The  acid  preparations — for  example,  the  hydrochloride  and 
bisulphate — may  be  dissolved  in  water,  but  should  have  some 
flavouring  added  to  disguise  the  taste,  while  the  sulphate  requires 
an  acid,  which  may  be  provided  by  suspending  some  of  the  powder 
in  natural  limejuice;  but  in  order  to  dissolve  the  sulphate  properly 
a  mineral  acid  should  be  used,  in  the  strength  of  i  minim  to  each 
grain,  but  more  than  this  will  be  required  if  the  unpleasant  after- 
taste is  to  be  avoided. 

In  hospitals  the  sulphate  must  be  used,  as  it  is  cheap  and  effective, 
but  it  is  as  well  to  have  it  periodically  reported  upon  by  an  analyst, 
in  order  to  see  what  is  really  being  given  to  the  patients.  For 
hospital  use  it  may  be  dissolved  in  dilute  sulphuric  acid,  and  have 
some  cheap  form  of  flavouring  added. 

We  have  used  Warburg's  tincture  on  the  West  Coast  of  Africa 
with  apparent  success  in  cases  of  chronic  subtertian  infection, 
which  resist  the  ordinary  methods  of  administering  quinine,  but 
care  is  required,  as  it  may  have  a  depressing  effect  upon  the  heart. 

Tabloids,  tablets,  and  pills  are  pleasant  methods  of  taking  quinine 
for  prophylaxis,  convalescence,  and  mild  attacks.  Moreover,  they 
are  extremely  useful  for  journeys,  being  readily  carried,  but  in  order 
to  be  successful  they  must  not  be  old  and  hard.  The  hydrochloride 
or  bisulphate  should  be  used  and  the  solubility  tested  from  time  to 
time  in  water,  otherwise  the  tabloid  must  be  reduced  to  powder 
and  taken  as  indicated  above. 

Pills  and  capsules  are  quite  good  when  fresh,  but  they  are  apt 
to  get  hard  when  old,  and  are  then  useless,  and  must  be  opened 
and  the  powder  used,  if  they  form  the  only  supply  available. 

The  quinine  tannate  chocolates  are,  of  course,  only  used  for 
prophylaxis  in  children. 

By  the  Rectum. — This  method  may  be  useful  in  gastric  disturbance, 
but  is  not  to  be  compared  with  the  intramuscular.  Twenty  grains 
of  the  bihydrochloride  are  made  into  a  solution  in  water,  and  then 
mixed  with  an  ounce  of  mucilage  of  starch  solution,  and  used  as  an 
injection.     It  is  advisable  to  add  a  few  drops  of  tincture  of  opium. 

Quinoform  suppositories  (gr.  iii.)  have  been  used  in  children  by  Pedro  and 
others. 

Intramuscular  Injections. — We  are  not  in  favour  of  hypodermic 
injections  of  quinine — i.e.,  of  injections  simply  under  the  skin — 
but  strongly  recommend  intramuscular  injections  in  all  cases  of 
malarial  fever  in  which  there  is  gastric  disturbance,  where,  for  any 
reason,  the  quinine  is  apparently  failing  to  act,  when  the  disease 
is  becoming  chronic,  or  in  serious  subtertian  infections.  For  this 
purpose  the  bihydrochloride  should  be  dissolved  in  normal  (075  per 


QUININE  1 1 95 

cent.)  saline  solution,  and  carefully  sterilized.  Baccelli's  formula 
is  10  grammes  of  quinine  and  0*075  gramme  (i|  grain)  of  salt 
dissolved  in  10  grammes  (2^  drachms)  of  water,  one-tenth  of  which 
is  used  for  an  injection;  but  the  greatest  care  must  be  taken  that 
this  solution  is  properly  sterile.  A  good  formula  for  a  solution 
which  does  not  cause  pain  is  Gaglio's  or  Giemsa's:  Quinine  hydro- 
chloride, 10  grammes;  aquae  destillatae,  18  grammes;  ethylurethane, 
5  grammes,  of  which  one-twenty-fifth  portion  is  used  for  an  injec- 
tion (1-5  c.c.  of  the  solution  contains  0-5  gramme  of  quinine). 

If,  however,  the  solution  is  to  be  prepared  and  sterilized  while 
the  patient  is  waiting  for  treatment,  much  time  is  lost.  We  there- 
fore recommend  the  tropical  practitioner  to  purchase  and  keep  by 
him  the  sterilettes,  which  are  little  hermetically  sealed  vials  con- 
taining a  gramme  (15  grains)  of  quinine  in  solution.  These  steri- 
lettes may  be  purchased  from  Squire  and  Sons,  or  Martindale,  of 
London;  Burroughs  Wellcome  and  Co.;  or  Molteni,  of  Florence. 
Giemsa's  solution  may  be  obtained  in  similar  sterile  vials. 

The  technique  is  simple:  First  cleanse  the  skin  of  the  patient 
carefully  with  1  in  40  carbolic  lotion;  then  break  off  the  glass  seal 
of  the  vial  at  the  nick  in  the  neck,  and  pass  the  open  mouth  of  the 
vial  through  a  flame;  then  draw  up  the  contained  fluid  into  a 
sterilized  all-glass  syringe  provided  with  a  platinum  iridium  needle. 
Plunge  the  hypodermic  needle  deeply  into  the  deltoid  or  gluteus 
maximus,  and  make  the  injection.  Withdraw  the  needle,  and  place 
a  little  pad  of  wool,  wrung  out  in  1  in  40  carbolic  lotion,  on  the  site 
of  the  injection.  Performed  carefully  in  the  above  manner,  there 
need  be  no  fear  of  tetanus  or  abscess  formation,  and  the  injection 
can  be  repeated  at  will.  If  necessary,  a  stimulant  or  an  injection 
of  ether  may  be  given  in  the  old  and  feeble  before  this  intramuscular 
injection.  After  repeated  injections  of  quinine,  even  if  adminis- 
tered antiseptically,  hard  swellings  may  appear  at  the  seat  of  the 
injections.  In  such  cases  the  hypodermics  should  be  stopped  for 
a  few  days,  and  an  ice-bag  may  be  applied  to  the  painful  part. 

Notwithstanding  the  objections  to  this  method  brought  forward  by 
some  authorities,  we  still  strongly  recommend  it,  as  we  have  found  it  to 
be  most  successful  in  intractable  cases,  and  have  never  so  far  seen  any  un- 
toward symptoms.  We  advise  that  the  hypodermic  syringe  and  needle 
should  be  sterilized  by  rinsing  with  1  in  20  carbolic  acid  after  boiling,  as  the 
carbolic  acid  does  not  interfere  with  the  action  of  the  quinine,  and  has  an 
unfavourable  influence  upon  any  tetanus  spores  which  may  by  any  chance 
be  present.  Care  should  be  taken  that  not  too  much  carbolic  lotion  is  left 
in  the  syringe  and  needle;  otherwise  a  precipitate  will  form. 

Intravenous  Injection. — In  cases  of  pernicious  infection  with  sub- 
tertian  parasites,  no  delay  should  be  made  in  giving  the  patient  an 
intravenous  injection,  but  the  effect  of  quinine  on  the  circulation 
must  be  remembered,  and  if  the  pulse  is  bad,  it  is  advisable  to  give 
an  intramuscular  inj  ection  of  ether  as  a  preliminary.  The  same  vials 
and  apparatus  should  be  used  in  the  intravenous  as  in  the  intra- 
muscular injection. 

The  injection  should  be  made,  using  a  5  "c.c.  or  10  c.c.  syringe, 


1 1 96  THE  MALARIAL  FEVERS 

into  the  median  basilic  or  median  cephalic  veins,  and  not  less  than 
i  gramme  (15  grains)  of  the  bihydrochloride  dissolved  in  five  or 
ten  cubic  centimetres  of  sterile  physiological  salt  solution  should  be 
injected  at  a  time.  The  skin  over  the  selected  vein  should  be  ren- 
dered thoroughly  aseptic  by  soap  and  water  and  carbolic  lotion, 
or  by  tr.  iodi,  and  then  a  bandage  tied  round  the  arm,  so  as  to 
retard  the  flow  of  venous  blood  and  make  the  selected  vein  stand 
out.  Then  the  needle  should  be  inserted  into  the  vein  (care  being 
taken  that  there  is  no  air  in  needle  or  syringe)  in  a  sloping  direc- 
tion, with  the  point  towards  the  heart,  so  that  the  injection  can 
flow  with  the  circulation.  The  point  of  the  needle  should  be  felt 
to  be  loose  (i.e.,  in  the  vein).  The  bandage  must  now  be  loosened 
and  the  injection  made  slowly,  the  effect  on  the  pulse  being  noted. 
The  needle  is  now  withdrawn,  and  an  aseptic  pad  fixed  in  position 
by  a  bandage. 

Duration  of  Treatment. — When  the  fever  has  subsided  and  the 
patient  is  feeling  better,  the  administration  of  quinine  must  not  be 
discontinued,  because  there  is  the  fear  of  a  relapse,  caused  by 
parasites  which  have  not  yet  been  destroyed,  and  which  may  be 
living  in  the  spleen ;  or,  again,  there  is  the  fear  of  the  parthenogenesis 
of  the  macrogametocyte.  In  order  that  the  treatment  may  be  suc- 
cessful, the  quinine  must  be  continued  for  a  long  time.  Our  routine 
practice  has  been  to  continue  with  10  grains  three  times  a  day 
for  a  month  after  the  cessation  of  the  fever,  5  grains  three  times  a 
day  during  the  second  month,  then  5  grains  twice  a  day  during  the 
third  month.  In  some  cases  when  the  fever  has  ceased  it  is  advis- 
able to  associate  some  iron  and  arsenic  with  the  quinine,  but  these 
drugs  should  not  be  administered  during  the  febrile  attack. 

Symptomatic  Treatment. — The  symptomatic  treatment  may  be 
considered  under  the  following  headings: —    ■ 

1.  Symptomatic  treatment  of  acute  malaria. 

2.  Diet  in  acute  malaria. 

3.  Treatment  of  symptoms  and  special  conditions. 

4.  Treatment  of  convalescence. 

5.  Treatment  of  chronic  malaria. 

6.  Treatment  of  malarial  cachexia. 

Symptomatic  Treatment  of  Acute  Malaria. — The  practitioner 
who  works  in  the  tropics  must  often  be  prepared  to  do  the  nursing  as 
well  as  the  medical  treatment.  When  the  attack  begins,  the  patient 
must  go  to  bed,  and  in  the  cold  stage  wrap  up  well  with  blankets. 
At  the  same  time  arrangements  must  be  made  in  case  of  sickness 
or  diarrhcea.  The  treatment  of  this  and  the  warm  stage  must  be 
to  encourage  perspiration,  by  warm  lime-drinks,  hot  tea,  etc.,  in 
order  that  the  toxins  may  be  passed  out  as  quickly  as  possible. 
Ziemann  recommends  hot-air  baths  to  bring  on  the  perspiration. 
We  have  tried  this  method  a  few  times,  but  have  not  been  greatly 
impressed  with  the  advantages. 

The  headache  may  be  relieved  by  cold  applications,  and  where 


SYMPTOMATIC  TREATMENT  1197 

there  is  no  ice,  dissolve  some  salt  and  juice  of  fresh  limes  or  lemons, 
together  with  some  vinegar  or  weak  acetic  acid  and  Florida  water 
or  eau-de-Cologne,  in  a  small  basin  of  water,  and,  after  soaking 
handkerchiefs  in  this  mixture,  apply  them  one  after  the  other, 
changing  as  they  get  warmed,  to  the  patient's  forehead. 

A  little  stimulation  of  the  auricular  branch  of  the  pneumogastric 
by  applying  some  of  this  cool  lotion  to  the  lobule  and  behind  the 
ear  is  most  refreshing  to  the  patient. 

Another  method  of  relieving  the  headache  and  pains  about  the 
body  is  to  give  phenacetin  and  caffein.  Phenacetin  or  antipyrin 
should  only  be  given  in  small  doses  (gr.  ii.-iii.),  and  not  to  debilitated 
patients. 

When  the  sweating  begins,  the  patient  usually  feels  much  better, 
but  care  must  be  taken  to  change  the  damp  clothing,  and  when  this 
stage  is  drawing  to  a  close  a  sponge  over  with  tepid  water  is  most 
refreshing,  after  which  he  will  probably  go  to  sleep  and  wake 
feeling  much  better. 

Diet  in  Acute  Malaria. — During  the  attack  the  strength  must 
be  maintained  by  light  food,  such  as  Brand's  essence  or  chicken- 
broth,  and  stimulants,  in  the  form  of  brandy  or  champagne,  may  be 
required.  Milk  or  whey  may  also  be  given,  and  in  cases  of  stomach 
irritation  albumen  water. 

During  remissions  broths  and  clear  soups  and  milk-puddings 
should  be  allowed.  In  the  intermission  of  a  quartan  or  tertian, 
and  during  convalescence,  regular  meals  of  good  plain  food  may 
be  given. 

Treatment  of  Symptoms  and  Special  Conditions. — Vomiting 
is  often  distressing,  and  can  be  relieved  by  sips  of  iced  soda-water 
or  champagne.  When  there  is  no  ice,  cover  the  bottle  with  a  thin 
layer  of  flannel  soaked  in  water,  and  hang  in  the  breeze.  If  these 
simple  remedies  fail,  and  the  symptom  is  really  urgent,  apply  a 
mustard-leaf  to  the  pit  of  the  stomach,  or  give  a  mixture  contain- 
ing chloroform  or  a  hypodermic  of  morphine.  If,  despite  all  this 
treatment,  the  vomiting  still  continues,  the  stomach  may  be  washed 
out  with  slightly  alkaline  water. 

Hiccough  is  not  often  present,  and  would  be  a  most  unpleasant 
sign.  It  can  be  checked  by  the  mustard-leaf,  by  codein,  or  by  a 
hypodermic  of  morphia  (gr.  £). 

Cough  not  infrequently  worries  the  patient.  It  may  be  sharp  and 
dry,  and  is  best  treated  by  codein  or  morphia  in  some  form,  e.g.: — 

Codeinae  . .  . .  . .  . .  .  .  gr.  £. 

Syrupi  tolutanae  . .  . .  . .  .  .  . .     3*- 

Aquae  chloroformi        .  .  . .  .  .  .  .  .  .     ad  §i. 

administered  every  four  hours. 

Constipation  must  not  be  allowed,  and  should  be  promptly 
relieved  by  a  dose  of  calomel  (1  to  3  grains),  if  necessary,  followed 
by  a  saline.  Ziemann  strongly  recommends  washing  out  the  rectum 
with  warm  normal  saline  solution  as  a  routine  practice,  but  though 


1198  THE  MALARIAL  FEVERS 

we  have  used  this  in  bad  cases,  we  have  no  experience  of  it  as  a 
routine  practice. 

Diarrhoea  is  at  first  useful  in  ridding  the  body  of  excess  of  bile 
and  other  waste  products.  Prolonged  diarrhoea  must  be  treated 
with  astringents  (bismuthi  subnitratis  or  salol  gr.  x.  every  four 
hours).  Meanwhile  it  should  be  borne  in  mind  that  though  quinine 
is  absorbed  by  the  stomach,  still,  with  much  diarrhoea  there  is  often 
gastric  disturbance,  and  therefore,  if  the  drug  is  given  by  the 
mouth  in  these  conditions,  its  utility  may  be  small. 

Splenic  pain  and  liver  pain  are  not,  as  a  rule,  severe  enough  to 
make  special  treatment  needful,  but  occasionally  the  splenic  pain 
may  be  severe  (due  to  perisplenitis),  when  hot  fomentations  will 
relieve  it,  if  it  is  thought  necessary  to  use  them. 

Hyperpyrexia  must  be  treated  by  cold  sponging — if  possible,  with 
ice;  if  not,  with  the  mixture  mentioned  above,  or  by  cold  packs, 
cold  baths,  and  cold  enemata. 

Cerebral  Malaria. — Give  large  hypodermic  saline  infusions  to 
wash  out  the  toxins  {vide  Algidity). 

Algidily  requires  special  treatment  with  hypodermic  saline  in- 
jections and  warm  applications  to  the  body,  and  especially  to 
the  region  of  the  heart.  The  saline  injections  consist  of  sterile 
normal  saline  solution,  and  are  injected  by  gravity  from  the  ordinary 
glass  reservoir  via  a  long  piece  of  indiarubber  tubing  and  a  stout 
hollow  needle,  such  as  those  in  the  Potain's  aspirator-case.  The 
usual  sites  for  the  injection  are  the  sides  of  the  chest,  just  below 
the  armpit,  and  the  outer  aspect  of  the  thighs.  At  least  a  pint 
should  be  injected  in  one  place.  Oxygen  inhalations,  if  available, 
may  also  be  used. 

Diaphoretic  pernicious  fever  requires  stimulants,  hypodermics  of 
atropine,  and  ether  or  strychnine,  and  treatment  as  for  algidity. 

Hemorrhagic  perniciosa  may  be  treated  with  calcium  chloride, 
and  with  local  applications  or  injections  of  adrenalin. 

Scarlatiniform  perniciosa  obviously  calls  for  dilution  of  the  toxins 
by  saline  injections. 

In  pernicious  cases,  when  the  patient  becomes  delirious  or  coma- 
tose, the  practitioner  must  be  careful  that  the  attendants  in  whose 
charge  he  is  left  are  really  trustworthy,  as  unfortunate  accidents 
have  been  known  to  happen.  Particularly  we  warn  the  practitioner 
to  make  sure  that  the  bladder  has  been  emptied,  especially  in 
delirious  patients,  not  by  mere  causal  inquiry,  but  by  percussion  of 
the  abdomen. 

In  choleraic  perniciosa  the  treatment  for  cholera  should  be  adopted 
in  addition  to  quinine.  In  dysenteric  perniciosa  the  treatment  must 
be  that  suggested  for  mild  dysentery,  and,  in  addition,  quinine, 
while  the  pseudo- Addison' s  disease  is  best  treated  in  our  experience 
by  io  minims  of  adrenalin,  given  twice  daily  in  addition  to  quinine. 
Treatment  of  Convalescence. — The  important  point  to  be 
remembered  in  convalescence  is  to  continue  the  quinine  in  smaller 
doses  for  at  least  three  months  after  the  attack.     The  patient 


TREATMENT  OF  CHRONIC  MALARIA  1199 

should  be  placed  on  a  tonic  with  iron  and  arsenic  in  some  form,  and 
if  he  has  been  seriously  ill  he  must  have  a  change  to  a  colder  climate. 
The  patient  must  be  impressed  with  the  fact  that  he  must  not  dis- 
continue the  quinine  on  arriving  in  a  cooler  climate,  as  an  attack 
of  fever  will  surely  take  place  if  he  does  so. 

Treatment  of  Chronic  Malaria. — -If  a  person  is  constantly 
suffering  from  attacks  of  malarial  fever,  he  should  be  sent,  whenever 
possible,  for  a  change  to  a  cooler  climate  in  the  hills  or  to  the  tem- 
perate zone,  but  should,  of  course,  continue  the  quinine  treatment. 
If  he  cannot  afford  a  change  of  climate,  he  must  be  placed  in  bed 
and  given  rest  from  work,  and  a  course  of  quinine  therapy  by  intra- 
muscular injections  carried  through.     Arsenic  is  useful. 

Treatment  of  Malarial  Cachexia. — The  most  important  fea- 
ture, in  addition  to  quinine  treatment,  is  to  send  the  malarial 
cachectic  for  a  change  of  climate,  as  mentioned  above,  and  treat 
the  anaemia  with  iron  and  arsenic.  A  course  of  injections  of 
cacodylate  of  quinine  is  often  useful. 

Theoretical  Considerations. — There  are  a  number  of  theoretical  consider- 
ations with  regard  to  the  treatment  which  may  perhaps  interest  the  reader, 
and  these  may  be  divided  into: — 

1.  Quinine. 

2.  Effects  on  man. 

3.  Effects  upon  malarial  parasites. 

4.  Immunity  of  parasite. 

5.  Prophylactic  use. 

6.  Other  drugs. 

Quinine. — The  aim  of  the  treatment  of  malaria  is  to  kill  the  parasites 
and  to  aid  the  excretion  of  the  toxins  and  relieve  the  symptoms  of  the  patient. 

Fortunately,  since  the  days  of  the  Countess  del  Chinchon,  the  world  has 
known  the  value  of  cinchona  bark  in  malaria,  and  later  it  learnt  that  this 
important  action  was  due  to  an  alkaloid,  quinine,  which  exists  in  the  bark  in 
the  form  of  a  hydrate.  In  1867  Binz  showed  that  quinine  killed  infusoria,  and 
he  believed  that  this  action  was  due  to  its  checking  oxidation. 

Quinine  is  usually  sold  in  the  form  of  the  sulphate,  [(C20H24N2O2)2. 
H2S04]2.i5H20,  which  is  only  soluble  1  in  800  of  cold  water,  but  is  readily 
soluble  in  water  acidulated  with  a  mineral  acid.  The  solution  gives  a  bluish 
fluorescence. 

It  must  be  remembered,  however,  that  it  may  not  be  pure,  and  may  contain 
lime,  chalk,  magnesia,  starch,  etc.  It  is  also  important  to  remember  that  it  is 
incompatible  with  alkali,  alkaline  carbonates,  and  astringent  infusions. 

Quinine  sulphate  is  by  no  means  the  best  preparation,  for  the  hydrochloride, 
(C20H24N2O2).HC1.2H2O,  is  soluble  1  in  40  of  water;  but  better  than  this  are 
the  acid  salts  of  the  sulphate,  called  the  '  bisulphate,'  (C20H24N2O2)H2SO4. 
7H20,  which  is  soluble  1  in  n  parts  of  water,  and  of  the  hydrochloride,  called 
the  '  bihydrochloride,'  (C20H24N2O2)2HCl,  which  is  soluble  1  in  1  of  water. 
Numerous  other  preparations  are  on  the  market,  of  which  quinine  bi hydro- 
bromide  is  recommended  in  persons  who  suffer  from  deafness,  and  quinine 
valerianate  in  those  who  are  very  nervous;  while  quinine  tannate,  which  is  not 
nearly  so  bitter  as  the  other  compounds,  especially  when  made  up  with  choco- 
late, has  been  used  by  Celli  in  quinine  prophylaxis  for  children  and  in  cases 
of  hemoglobinuria. 

Euquinine,  which  is  quinine  ethylcarbonate,  C2H50 — CO  -OC20H23N2O,  is 
also  not  so  bitter  as  the  ordinary  preparations,  and  is  therefore  suitable  for 
administration  to  women  and  children,  but  it  has  the  disadvantage  of  being 
expensive  and  very  insoluble  in  water,  and  must  be  given  in  cachets  or  dis- 


THE  MALARIAL  FEVERS 


solved  in  acidulated  water.     It  has  not  such  deleterious  effects  on  the  stomach 
and  nervous  system. 

Another  remedy  which  contains  quinine  sulphate,  and  which  was  much 
vaunted  in  days  gone  by,  is  Warburg's  tincture,  which  is  said  to  be  prepared 
by  macerating  for  seven  days  the  following  ingredients — 

Grains. 

Aloes  socotrinae        . .  .  .  . .  .  .  . .      240 


Rhei 

Fructi  archangelicae  officinalis 

Radicis  inula?  helenii 

Croci 

Fructi  foenicali 

Cretas  preparatae 

Radicis  gentianae 

Radicis  curcumae  zedoariae  . 

Cubebae 

Myrrhae 

Polypori  officinalis 

Opii 

Piperis  nigrae 

Cinnamonis 

Zingiberis 


80 
80 
40 
40 
40 
40 
20 
20 
20 
20 
20 

2* 

4 

3 
8 


in  a  pint  of  60  per  cent,  alcohol  for  a  week;  then  pressing,  filtering,  and  dis- 

«nlvincr  in  thf»  filtrate* 


Grains 

175 
20 


solving  in  the  nitrate : — 

Quininae  sulphatis 
Camphoris     . . 

and  after  three  days'  filtering,  making  up  to  the  pint  with  alcohol.  The  dose 
of  this  mixture  is  1  to  4  drachms. 

Other  preparations  can  hardly  be  said  to  have  any  particular  interest. 

In  order,  however,  to  bring  these  various  preparations  into  line  with  one 
another,  it  is  necessary  to  have  some  arbitrary  standard,  and  this  is  generally 
taken  as  quinine  sulphate,  which  is  reckoned  as  equal  to  1 .  The  hydrochloride 
will  then  be  0-9,  the  bisulphate  1*24,  the  bihydrochloride  1-02,  the  bihydro- 
bromide  1*23,  the  valerianate  i-oi,  the  tannate  3*67,  euquinine  i-o,  and 
Warburg's  tincture  1*09 

New  Salts  of  Quinine. — Dihydroquinine  hydrochloride  (o-6  gramme=i#o 
gramme  quinine  hydrochloride)  is  said  to  be  have  a  specific  antimalarial  action, 
but  aurochin,  chitenin,  and  tetrahydro-quinine  are  not  satisfactory. 

Cinchonin  Salts. — Various  cinchonin  salts  have  been  used  in  the  treatment 
of  malaria,  and  Sir  Leonard  Rogers  has  recently  recommended  intramuscular 
injections  of  cinchonin  bihydrochloride. 

Effects  on  Man. — When  taken  by  the  mouth,  quinine  should  be  dissolved 
in  the  acid  gastric  juice,  converted  into  the  bihydrochloride,  and  absorbed 
completely  into  the  blood  from  the  stomach,  especially  if  food  is  taken  at  the 
same  time.  If  this  does  not  happen,  then  such  a  salt  as  the  sulphate  may  not 
be  absorbed  at  all,  as  it  will  be  precipitated  in  the  alkaline  intestinal  contents. 
When  given  in  large  or  frequent  doses,  it  is  apt  to  irritate  the  stomach.  As 
to  what  happens  to  it  in  the  blood,  there  are  two  distinct  views — one  pointing 
to  rapid  elimination,  and  the  other  to  the  fact  that  it  undergoes  changes  in 
the  tissues.  It  would  appear  to  be  retained  longer  in  the  body  if  absorbed 
together  with  food. 

It  can  also  be  administered  by  intramuscular  injections,  when  it  is  said  to  be 
largely  precipitated  at  the  site  of  the  injection.  We  have  no  knowledge 
personally  of  this  precipitation,  and  our  experience  is  that  intramuscular 
injections  have  been  most  satisfactory,  though  it  must  be  admitted  that  there 
are  observers  who  think  that  administration  per  os  is  more  valuable  than  that 
by  intramuscular  injections.  It  may  also  be  given  intravenously,  as  will  be 
explained  later. 

Quinine  in  small  doses  is  a  vascular  tonic,  but  in  large  doses  it  is  a  cardiac 


EFFECT   UPON  MALARIAL  PAHA  SITES  i2oi 

depressant,  producing  a  fall  in  the  arterial  pressure,  with  decrease  in  the 
pulse-rate  and  strength.  This  is  an  important  matter,  to  be  remembered  in 
administering  the  drug  to  the  old  and  the  feeble,  especially  by  intravenous  or 
intramuscular  injections.  On  the  nervous  system  it  acts  as  a  stimulant,  and 
also  increases  the  flow  of  blood  to  the  brain.  In  the  tissues  it  is  partly 
destroyed  by  oxidation,  and  therefore  the  whole  quantity  administered  is 
hardly  likely  to  be  obtained  in  the  urine.  Excretion  takes  place  by  the 
kidney  almost  entirely  in  the  form  of  quinine  dihydroxyl.  It  can  be  recovered 
from  urine  by  acidulating  with  sulphuric  acid,  treating  with  solid  picric  acid, 
filtering  until  clear,  digesting  with  3  per  cent,  caustic  soda  solution,  and 
extracting  with  chloroform,  from  which  the  quinine  can  be  obtained  by 
evaporation.  Ramsden  and  Lipkin  have  described  a  new  process  for  isolating 
quinine  from  urine  (Annals  of  Tropical  Medicine  and  Parasitology,  May,  191 8). 

When  given  in  large  doses,  the  cerebral  congestion  which  it  produces  causes 
buzzing  in  the  ears,  deafness,  due  to  congestion  of  the  middle  ear,  and  head- 
ache, both  of  which  can  be  treated  by  bromides,  with  or  without  a  little  ergot. 
It  may  also  cause  erythematous,  erythemato-papular,  vesicular,  and  urti- 
carial eruptions. 

Quinine  Hcemoglobiniuia. — In  persons  who  have  suffered  from  malaria 
there  is  no  doubt  that  quinine  can  cause  haemoglobinuria,  but  the  way  in 
which  it  acts  is  doubtful.  Stephens  believes  that  the  haemoglobinuria  stands 
in  no  relationship  to  the  dose  of  quinine,  and,  further,  that  a  second  dose  may 
not  produce  the  result,  and  that  it  is  the  blood  condition  of  the  malarial  patient 
which  is  the  determining  factor.  Our  experience  has  tended  to  show  that 
there  is  a  direct  relationship  between  the  quinine  and  the  haemoglobinuria. 
Quinine  acts  in  this  way  by  causing  haemolysis  of  the  red  corpuscles.  Stephens 
and  Christophers  found  that  o*ooi  to  0-00082  gramme  of  quinine  haemolyzed 
1  c.c.  of  a  suspension  of  normal  human  red  cells  at  370  C.  The  hemolytic 
action  naturally  increases  the  quantity  of  bile  produced.  For  further  remarks 
on  this  subject,  see  the  next  chapter,  on  Tropical  Hemoglobinurias  (p.  1214). 

Quinine  Amblyopia. — Amblyopia  may  result  as  the  effect  of  large  doses  of 
quinine,  and  appears  to  be  due  to  constriction  of  the  retinal  arteries  in  tem- 
porary cases,  and  to  degeneration  of  the  retinal  ganglion  cells  and  their 
processes  in  permanent  cases  (see  also  p.  2007). 

Quinine  Fever. — In  latent  malaria  a  small  dose  of  quinine  may  occasionally 
provoke  a  febrile  paroxysm.  This  has  been  compared  to  the  action  of  a 
small  dose  of  salvarsan  in  provoking  an  exacerbation  of  symptoms  in 
latent  syphilis  (Herxheimer's  reaction). 

Action  on  the  Uterus. — Quinine  appears  to  act  upon  the  uterus,  and  may 
therefore  produce  an  unpleasant  effect  in  pregnancy,  though  whether  this  is 
really  due  to  the  quinine  or  to  the  malaria,  or  to  the  two  combined,  is  doubtful. 

Effect  upon  Malarial  Parasites. — Quinine  appears  to  particularly 
affect  the  merozoites,  trophozoites,  and  schizonts,  and  to  act  much  less  vigor- 
ously, if  at  all,  upon  the  gametocytes. 

It  appears  to  act  most  vigorously  upon  the  merozoites,  perhaps  because 
they  are  free  in  the  plasma ;  next  upon  the  young  trophozoites,  whose  cyto- 
plasm is  broken  up,  and  finally  it  and  the  nucleus  destroyed;  but  it  has  much 
less  effect  upon  the  fully  grown  schizont,  not  preventing  sporulation 

With  regard  to  the  gametocytes,  it  probably  has  a  deleterious  action  upon 
the  young  forms,  but  certainly  not  upon  the  fully  grown  micro-  and  macro- 
gametocytes.  It  is  thought  probable  that  it  may  act  upon  the  very  old  form 
of  microgametocyte,  but  this  cannot  take  place,  as  a  rule,  with  regard  to  the 
ordinary  fully  grown  microgametocyte,  for  anophelines  can  be  infected  by 
the  blood  of  persons  containing  the  two  kinds  of  gametocytes  even  when 
treated  vigorously  with  quinine.  On  the  macrogametocyte,  particularly  that 
of  Laverania  malaria,  it  appears  to  have  no  action.  Hence,  to  get  the  full 
effect  of  quinine  on  the  parasites  it  must  be  present  in  the  blood  at  the  time 
of  sporulation,  in  order  that  it  may  kill  the  merozoites,  young  sporonts,  and 
schizonts.  In  order  to  produce  this  effect,  it  is  judged  that  the  quinine  must 
be  present  in  the  blood  in  a  strength  of  at  least  1  in  20,000.  According  to 
Thomson,  though  quinine  has  no  direct  destructive  action  upon  the  crescents, 

76 


1202  THE  MALARIAL  FEVERS 

it  reduces  their  numbers  to  less  than  one  per  cubic  millimetre  of  blood  if  given 
daily  in  doses  of  20  to  30  grains  for  three  weeks;  this  action  is  believed  to  be 
due  to  cutting  off  the  source  of  supply  by  killing  the  asexual  forms.  Methy- 
lene blue  in  doses  of  12  grains  daily  is  said  by  Thomson  to  reduce  the  number 
of  crescents,  probably  by  some  direct  destructive  action.  Quinine-resisting 
forms  of  the  parasite  have  often  been  reported  from  South  America,  and  have 
also  been  studied  by  Ross  and  Thomson,  who  have  found  a  true  parasitic 
relapse  during  thorough  quinine  treatment.  In  these  cases  the  quinine  dosage 
must  be  increased.  We  have  administered  2  grammes  by  intramuscular 
injection  and  1  gramme  by  the  mouth  after  a  few  hours  as  a  single  dose 
in  such  a  case  with  very  beneficial  results. 

Immunity  of  the  Parasite.  —  The  immunity  of  the  malarial  parasite 
against  quinine  has  as  yet  been  but  little  studied,  but  this  is  a  subject  of  the 
greatest  importance  at  the  present  time,  when  quinine  prophylaxis  is  being 
extensively  employed.  It  has,  however,  been  commonly  noticed  that  the 
doses  of  quinine  have  often  to  be  increased  in  order  to  cure  an  attack  of  fever 
in  the  individuals  who  have  taken  quinine  more  or  less  irregularly,  and  that 
persons  who  have  taken  quinine  regularly  when  in  an  endemic  area  may  have 
an  attack  of  malarial  fever  after  leaving  this  area  and  ceasing  the  drug. 
Prophylactic  Use. — This  will  be  discussed  in  the  section  on  Prophylaxis. 
Other  Drugs. — It  is  almost  a  work  of  supererogation  to  mention  other 
drugs  in  the  treatment  of  malaria,  such  as  cuprein,  mercury,  atoxyl,  and 
treatment  by  the  serum  of  immune  animals,  and  by  violet  light  or  in  the  dark. 
Methylene  blue,  however,  has  been  used  by  several  authors  in  the  dose  of 
2  grains  every  four  hours.  In  our  experience  its  efficacy  cannot  be  compared 
to  that  of  quinine. 

Surveyor  has  recommended  the  administration  of  2  grains  of  picric  acid 
twice  or  three  times  a  day  by  the  mouth  as  a  method  of  destruction  for  the 
crescents  of  L.  malarics.  The  drug  can  also  be  administered  by  injections  of 
sodium  picrate.  Nicolle  and  Conseil  and  more  recently  Falconer,  Anderson, 
Micheli,  Quarelli  and  others  have  tried  salvarsan  in  malaria,  with  only 
moderate  results.  If  used,  it  must  be  combined  with  quinine.  Neosalvarsan 
has  been  found  to  be  useless  in  subtertian  fevers,  but  it  and  salvarsan  may 
act  upon  Plasmodium  vivax  intravenously  or  intramuscularly.  For  dosage 
see  p.  1313. 

Tartar  emetic  has  been  used  by  Rogers,  but  the  researches  by  Low  and 
others  have  shown  that  when  administered  alone  it  has  no  effect  upon  the 
malaria  parasites.  Rontgen  therapy  is  useless,  though  the  spleen  may  get 
smaller. 

PROPHYLAXIS. 

The  very  great  success  which  has  followed  every  serious  attempt 
at  prophylaxis  undertaken  during  the  last  few  years  has  made  it 
the  urgent  duty  of  each  community  to  scientifically  apply  a  well 
thought  out  scheme  of  a  not  too  expensive  nature  to  its  district 
with  the  view  of  reducing  the  malaria  endemic  therein. 

In  order  that  a  disease  may  be  scientifically  prevented,  a  thorough 
knowledge  of  its  aetiology  must  be  acquired  and  disseminated  not 
merely  among  medical  men,  but  also  among  the  public.  We  know 
that  malaria  depends  upon — 

1 .  The  presence  of  numerous  human  beings  infected  with  male 

and  female  gametocytes. 

2.  The  presence   of   numerous   anophelines    in  which    the 

gametocytes  are  capable  of  developing  into  sporozoites. 

3.  Free  access  of  these  anophelines  to  the  infected  human 

beings. 


PROPHYLAXIS  1203 

4.  Air-temperatures  suitable   for  the  development    of   the 

malarial  parasite  in  man  and  anophelines. 

5.  Free  access  of  infected  anophelines  to  non-immune  human 

beings. 

To  summarize,  there  are  three  factors:  (1)  Man;  (2)  the  anophe- 
line;  (3)  the  air-temperature. 

In  the  tropics  this  third  factor  is  in  favour  of  malaria,  and  it 
cannot  be  altered;  therefore  methods  of  prophylaxis  must  be 
devoted  to  the  human  being  and  the  anopheline. 

Man. — The  preliminary  step  with  regard  to  man  is  to  ask  his 
intelligent  assistance,  and  for  this  purpose  education  with  regard 
to  disease  in  general  and  malaria  in  particular  is  required.  First 
of  all  it  was  necessary  to  bring  the  medical  profession  into  touch 
with  the  discoveries  made  by  Laveran,  Manson,  Ross,  and  Grassi, 
and  this  has  been  done.  Secondly,  it  was  and  is  necessary,  by 
lantern  lectures,  illustrated  pamphlets,  etc.,  to  convince  the  edu- 
cated public  of  the  tropics  of  the  monetary  loss  caused  to  the 
Government,  the  planter,  the  merchant — i.e.,  to  the  employer  of 
labour — by  malaria.  Unless  this  can  be  done,  the  money  necessary 
for  the  effective  prophylaxis  will  not  be  forthcoming.  No  one  will 
deny  that  malaria  is  the  greatest  cause  of  sickness  in  the  tropics, 
though  there  may  be  places  where  its  mortality  is  low  and  places 
where  it  is  high,  but  that  which  people  fail  to  recognize  is  the 
financial  loss  caused  by  this  sickness. 

Therefore  we  quote  the  well-known  example  of  the  Adriatic 
Railway  Company,  which,  according  to  Ricchi,  used  to  spend  on 
account  of  malaria  among  6,416  workmen  living  in  malarious  areas 
no  less  than  1,050,000  francs  per  annum. 

But  a  serious  attempt  should  be  made  to  impress  the  uneducated 
masses  of  the  tropics  with  some  sort  of  knowledge  about  the  disease. 
This  can  best  be  done  by  simple  kindergarten-like  instruction,  with 
demonstration  of  actual  living  specimens  of  anopheles  and  their 
eggs,  larvae,  and  pupae,  together  with  the  presence  of  a  young  child 
with  a  huge  spleen  and  of  a  person  suffering  from  malarial  cachexia, 
and  then,  at  the  close  of  the  lecture,  to  distribute  illustrative 
pamphlets  in  the  vernacular,  written  in  simple  language,  reviewing 
the  subject  of  the  lecture,  together  with,  if  possible,  the  demonstra- 
tion of  the  larvae  in  a  neighbouring  stream  or  pool. 

This  attempt  to  instruct  the  poorer  classes  of  the  tropics  may  not 
be  productive  of  much  immediate  good,  but  it  may  bring  home  to 
them  that  malaria  is  a  potent  factor  in  causing  illness  and  death 
among  their  infants  and  young  children,  and  that  it  is  caused  by 
the  bite  of  a  particular  kind  of  insect,  and  can  be  to  a  great  extent 
prevented  by  proper  treatment  with  quinine. 

Another  method  employed  is  to  give  the  teachers  of  the  elemen- 
tary vernacular  schools  a  course  of  instruction  in  elementary  hygiene, 
including,  of  course,  malaria,  so  that  they  may  be  able  to  give  their 
pupils  elementary  instruction  in  these  matters. 


I204  THE  MALARIAL  FEVERS 

In  such  instruction  no  pamphlet  or  book  should  be  used,  other- 
wise there  is  a  danger  of  the  knowledge  being  acquired  by  rote. 
The  only  way,  however,  to  bring  about  any  result  by  this  method 
is  to  award  a  special  grant  to  the  school,  based  upon  the  knowledge 
of  the  scholars. 

All  these  methods  have  actually  been  and  are  being  carried  out, 
but  in  any  case  they  are  only  preliminaries,  and  any  good  which 
may  result  therefrom  will  not  be  immediate. 

Another  preliminary  matter  is  to  use  the  knowledge  acquired 
concerning  the  life-history  of  the  anophelines,  and  not  to  build 
houses,  coolie-lines,  etc.,  in  ravines  and  valleys,  or  on  the  margin 
of  water  likely  to  be  a  breeding-ground  for  these  insects.  Place  the 
buildings  on  high  ground,  and,  bearing  in  mind  the  fact  that  native 
children  harbour  gametocytes,  build  the  houses  for  Europeans 
away  from  the  native  town  or  village. 

Quinine. — Leaving  now  these  preliminaries,  we  come  to  the  actual 
question  of  prophylaxis  by  reducing  the  malaria  in  man  by  quinine 
administration,  as  recommended  by  Koch,  Celli,  Plehn,  Lustig, 
Negri,  and  others. 

Koch's  method  consists  in  taking  a  large  dose  (15  grains)  of 
quinine  on  two  consecutive  days  every  eight  or  ten  days  for  three 
months,  while  Celli's  method  consists  in  taking  about  6  grains  (0-40 
gramme)  of  quinine  daily;  Plehn's,  in  taking  8  grains  of  quinine 
every  fourth  day.  Our  own  method  is  to  give  5  grains  daily,  and, 
in  addition,  a  double  dose  (10  grains)  once  a  week;  and  in  order  to 
enable  the  patient  to  remember  the  routine,  we  advise  him  to  take 
the  double  dose  on  a  Sunday.  For  children  1  grain  of  quinine  may 
be  given  for  every  three  years  of  age,  or  euquinine  may  be  used  with 
advantage  in  doses  of  2  to  5  grains  daily.  It  is  not  very  bitter,  and 
may  be  given  with  a  little  sweetened  condensed  milk,  as  advised 
by  Watson,  or  chocolates  of  tannate  of  quinine  (2  to  5  grains),  as 
advised  by  Celli,  may  be  administered. 

In  very  malarious  zones  such  as  certain  tropical  countries  and  the 
Balkans,  the  doses  mentioned  are  not  sufficient  and  should  be 
increased. 

All  these  methods,  if  properly  carried  out,  give  fairly  good  results, 
but  it  must  be  remembered  that  unpleasant  symptoms  may  arise 
after  a  long  use  of  quinine,  of  which  the  most  frequent  in  our 
experience  is  a  tremor  of  the  hands;  but  various  other  nervous 
symptoms  may  appear — e.g.,  irritability. 

The  advantages  of  quinine  prophylaxis  are,  however,  in  excess  of 
its  disadvantages,  and  we  strongly  recommend  its  use.  In  Italy 
special  laws  have  been  passed,  due  to  the  efforts  of  Celli,  which 
render  quinine  prophylaxis  practicable  among  the  poorer  classes. 
The  quinine  is  manufactured  by  the  State  and  distributed  gratis 
to  the  poor,  while  employers  of  labour  are  compelled  to  supply 
it  to  their  work-people.  Governments,  municipalities,  etc.,  can 
also  help  in  this  way  by  giving  free  quinine  to  the  populace. 

The   systematic  free  distribution  of  quinine  powders,  tinted  if 


PROPHYLAXIS 


1205 


necessary,  and  enclosed  in  papers,  with  a  vernacular  label  informing 
the  recipient  that  there  is  no  charge,  is  also  useful  among  the  native 
population,  as  is  the  distribution  of  quinine  to  children  in  the 
schools  by  the  teachers.  The  distribution  must  be  carried  out  by 
itinerary  dispensers,  for  the  native  will  not  travel  far  to  obtain 
quinine.  It  is,  however,  necessary  to  see  that  the  quinine  is  actually 
taken,  and  the  use  of  Tanret's  reagent  will  be  found  useful  in  detect- 
ing individuals  who  do  not  take  quinine.  Tanret's  reagent  is  pre- 
pared by  dissolving  1-35  grammes  of  mercuric  perchloride  in  75  c.c. 
of  water,  and  5  grammes  of  potassium  iodide  in  20  c.c.  of  water  in  a 
100  c.c.  measuring  flask.  The  mercuric  solution  is  poured  into 
the  iodide  solution  under  agitation  and  water  added  to  the  mark. 
A  few  drops  of  this  reagent  are  added  to  about  5  c.c.  of  urine.  If  no 
distinct  turbidity  appears,  it  means,  as  a  rule,  that  quinine  has 
not  been  taken.  Turbidity  indicates  presence  of  quinine  in  the 
urine,  but  may  indi- 
cate also  presence  of 
various  other  sub- 
stances. 

By  this  method  Koch 
freed  Stephansort,  in 
New  Guinea,  from 
malaria,  but  there  is  a 
doubt  as  to  whether 
the  disease  will  not 
recur  if  this  method 
alone  is  used.  It  must 
be  remembered  that 
free  quinine  distribu- 
tion on  a  large  scale  is 
very  costly. 

Bite  Prevention.  — 
The  next  method  is  to 

prevent  man  from  being  bitten  by  anophelines.  This  may  be 
effected  by  the  constant  and  intelligent  use  of  the  mosquito-curtain; 
by  rendering  the  dwelling,  or  certain  portions  of  it,  gnat-proof;  or 
by  the  application  of  chemicals  which  will  keep  the  mosquitoes  away. 
It  is  also  advised  not  to  go  out  after  sunset,  and  to  protect  the 
whole  body  against  bites. 

Firstly,  with  regard  to  the  mosquito-curtain,  the  mesh  must  be 
suitable — i.e.,  twenty  to  twenty-four  meshes  to  the  square  inch. 
The  lower  part  of  the  net  should  be  tightly  tucked  in  under  the 
mattress:  on  no  consideration  whatever  must  it  be  allowed  to  hang 
loosely  or  to  fall  on  to  the  ground.  It  should  be  in  position  in  the 
early  afternoon,  and  must  be  in  good  repair,  for  if  it  is  torn  it  is 
worse  than  useless,  becoming  a  mosquito-trap.  It  must  be  kept 
clean,  especially  at  the  top,  which  is  apt  to  accumulate  all  sorts  of 
queer  things  from  the  roof.  Never  travel  into  a  malarious  region 
without  your  own  net,  as  the  condition  of  those  in  rest-houses  may 


Fig.  [627. — The     Simpsonette     designed    to 
protect  the  wearer  from  mosquito  bltes. 
(From   a   photograph   given    us    by   Mrs.  Mary- 
Simpson.) 


1206  THE  MALARIAL  FEVERS 

be  far  from  good.  The  Simpsonette  anti-mosquito  and  fly  protective, 
non-inflammable  headgear,  designed  by  Mrs.  Mary  Simpson  is  most 
useful,  as  it  can  be  worn  under  or  over  the  helmet  or  hat  as  well  as 
when  lying  down  or  sleeping. 

Secondly,  with  regard  to  gnat-proof  rooms  or  houses,  these  can 
be  easily  constructed  at  but  slight  cost  by  using  wire-netting  of 
twenty  to  twenty-four  meshes  to  the  inch,  preferably  the  latter. 
Rooms  and  verandas  enclosed  in  this  way  are  a  great  convenience, 
preventing  molestation  from  mosquitoes  and  other  insects. 

The  Irrigation  Department  of  Ceylon  possesses  movable  mos- 
quito-proof rooms,  which  its  engineers  can  take  with  them  as  their 
work  requires.  These  are  constructed  of  a  wooden  framework, 
supporting  the  gauze,  and  have  a  double  door.  They  are  only 
12  feet  by  12  feet  by  8  feet,  and  can  therefore  be  erected  inside  the 
room  of  a  native  house  if  desired,  or  on  a  veranda.  The  cost  is 
small. 

Hospital  wards  ought  certainly  to  be  rendered  gnat-proof  in 
malarious  districts,  as  persons  are  often  found  in  the  wards  with 
their  blood  teeming  with  gametocytes.  Hence,  if  there  are  any 
suitable  anophelines  in  the  hospital,  the  chance  of  future  patients 
suffering  from  other  diseases  becoming  infected  is  considerable. 

With  regard  to  coolies,  the  third  method  has  been  tried  to  a 
certain  extent  with  success — viz.,  that  of  rubbing  all  over  the  body 
an  oil  composed  of  i|  parts  of  citronella  oil,  1  part  of  kerosene, 
and  2  parts  of  cocoanut  oil,  to  which  1  per  cent,  of  carbolic  acid 
is  added.  Coolies  seem  to  like  this  mixture,  which  is  called  the 
'  bamber-green  oil.'  Menthol,  cinnamon  oil,  eucalyptol,  camphor 
ointments  or  powders,  may  be  used. 

Electric  fans  and  punkahs  are  secondary  methods  of  preventing 
anophelines  from  biting  human  beings. 

Sulphur. — According  to  some  authorities,  mosquitoes  and  flies  will  not 
bite  persons  who  take  small  doses  of  sulphur  regularly,  but  this  is  not  so  in 
our  experience. 

The  healthy  may  also  be  segregated  as  far  from  sources  of  infection 
as  possible.  This  may  be  temporary  or  permanent,  according  to 
local  conditions. 

The  Anophelines. — It  has  already  been  indicated  that  it  is  not 
necessary  to  exterminate  the  anophelines  in  order  to  prevent 
malaria,  but  that  all  that  is  needful  is  to  reduce  their  numbers. 
The  objection  has  been  raised  to  anopheline  destruction  that  as 
fast  as  they  are  destroyed  in  a  given  area  others  will  immigrate 
into  that  place  from  surrounding  areas. 

Ross  has  rather  aptly  answered  that  objection  by  pointing  out 
that  if  the  human  birth-rate  in  a  place  was  suppressed  without 
attracting  special  immigration,  the  population  would  soon  decrease, 
and  Professor  Pearson,  on  conjectural  bases,  has  shown  that  if  mos- 
quito propagation  is  suppressed  within  the  circular  area  of  a  mile, 
the  mosquito  density  at  the  centre  will  be  3  per  cent.,  a  quarter  of  a 
mile  from  the  centre  18  per  cent.,  and  at  the  periphery  75  per  cent. 


PROPHYLAXIS  1207 

of  the  density  surrounding  that  area.  A  square  one  mile  wide  will 
have  a  central  density  of  2  per  cent.,  at  a  quarter  of  a  mile  from 
the  boundary  11  per  cent.,  and  at  the  boundary  50  per  cent,  of  the 
surrounding  density.  No  experiments  have,  however,  been  carried 
out  to  determine  whether  these  assumptions  are  correct. 

There  is,  however,  no  doubt  that  anopheline  reduction  leads  to 
the  reduction  of  malaria.  The  work  done  under  Ross's  direction 
at  Ismailia  proves  this,  for  the  cases  of  malaria  were  reduced  from 
1,551  in  1902  to  37  in  1905,  and  these  latter  were  all  relapses.  The 
cost  of  this  is  given  as  50,000  francs  for  drainage  and  rilling  up  of 
pools,  with  a  yearly  expenditure  of  18,300  francs,  which  worked 
out  at  2-3  francs  per  head  of  population. 

Travers  and  Watson  at  Klang  and  Port  Swettenham,  in  the 
Malay  States,  by  similar  methods  reduced  the  cases  of  malaria 
admitted  into  the  hospitals  from  610  in  1901  to  23  in  1905,  while 
the  cases  from  the  surrounding  district  in  which  no  antimalarial 
methods  were  employed  were  197  in  1901  and  353  in  1905.  The 
children  found  infected  in  the  two  towns  in  1905  amounted  to 
0-5  per  cent,  of  those  examined,  while  in  the  surrounding  district 
they  were  more  than  23  per  cent.  The  financial  saving  is  also 
shown  by  the  fact  that  Government  employes  in  1901  obtained 
236  sick  certificates,  amounting  to  1,026  days'  leave,  and  in  1905 
only  4,  amounting  to  30  days'  leave.  The  cost  to  the  end  of  1905 
was  £10,100,  with  a  yearly  expenditure  of  £410.  The  cost  up 
to  the  end  of  1905  worked  out  at  £1  49.  per  head  of  the  popu- 
lation. 

Similar  work  has  been  done  in  Hong  Kong  by  Dr.  Thompson. 

In  Panama,  under  American  rule,  the  measures  taken  are  very 
elaborate  and  systematic,  because  the  sanitarian  is  given  a  free 
hand,  and  economy  is  not  considered  where  health  is  in  question, 
with  the  result  that  malaria  and  yellow  fever  have  disappeared. 
There  can  therefore  be  no  doubt  that  the  destruction  of  anophe- 
lines  will  lead  to  the  diminution  of  malaria. 

The  Insect.- — -The  measures  which  are  used  may  be  classified  into 
those  directed  against  the  insect  and  those  against  the  larvae.  With 
regard  to  the  insects,  fumigation  with  some  substance  such  as 
sulphur  (2  pounds  to  be  burnt  for  every  1,000  cubic  feet  of  space) 
or  pyrethrum  will  Stupefy  them  and  cause  them  to  fall  to  the  ground, 
when  they  can  be  swept  up  and  burnt.  This  is  useful  in  dealing  with 
individual  houses  prior  to  residing  therein.  The  insects  may  also 
be  destroyed  in  houses  by  the  use  of  the  hand-net  as  advocated 
by  Ross  and  Gorgas,  while  the  use  of  a  hand-fan  is  also  recom- 
mended. Mosquito  traps  have  also  been  used  and  Giemsa's 
pyrethrum  sprays. 

Spraying  is  specially  useful  for  outhouses,  stables,  etc.,  and  in 
addition  to  the  pyrethrum  spray  weak  formalin  may  be  used. 

The  Larva. — It  is,  however,  against  the  larvae  that  measures  are 
most  easily  taken,  and  these  include: — 


i2o8  THE  MALARIAL  FEVERS 

A.  Engineering  works  intended  to  eliminate  breeding  places: — 

i.  Draining  swamps. 

2.  Draining  roads. 

3.  Filling  in  hollows. 

4.  Training  streams. 

5.  Making  continuous  drains  along  ravines,  etc. 

6.  Planting  trees  at  intervals,  not  close  together  (this  is 

both  ornamental  and  useful),  or  the  thinning  down 
of  dense  plantations  until  the  trees  are  at  intervals, 
and  the  removal  of  trees  with  rot-holes',  which,  how- 
ever, may  be  filled. 

7.  Segregation  either  of  the  whole  community,  by  altering 

the  residences  from  some  very  infected  area  or  partial 
segregation  of  a  chosen  portion  of  the  community 
from  the  worse-infected  portion.  Simpson  recom- 
mends that  at  least  a  zone  of  300  yards  in  width, 
preferably  400  yards,  should  separate  the  residential 
European  quarters  from  the  Native  town.  Since 
segregation  has  been  introduced  in  West  Africa,  a 
considerable  improvement  in  the  health  of  the  Euro- 
pean community  has  taken  place. 

8.  Efficient  drainage  to  keep  down  subsoil  water-level. 

B.  Sanitary  works : — 

1.  Removal  of   small  collections  of  water.     Regular   in- 

spection of  compounds  and  careful  collection  and 
disposal  of  household  utensils  likely  to  harbour 
mosquito  larva.     Repair  of  house  gutters. 

2.  Oiling  collections  of  water  with  kerosene  (crude  petro- 

leum) by  means  of  sprays  every  ten  days,  1  gallon 
being  allowed  for  1,000  square  yards. 

3.  Larvicides. — Measure  the  length  and  breadth  of  the 

area  of  water  and  add  1  in  20,000  to  1  in  50,000 
sanitas  okol  or  1  in  40,000  izo-izal,  or  the  Panama 
disinfectant. 

Wise  and  Minnett  have  recommended  that  1  ounce  of  crude  carbolic  acid 
be  added  to  every  16  cubic  feet  of  water,  thus  giving  a  dilution  of  1  in  16,000, 
which  they  maintain  will  kill  the  larvae  without  injuring  any  animal  which 
might  happen  to  drink  the  water. 

4.  Screening  wells,  cisterns,  cesspits,  etc.,  with  wire  gauze. 

5.  Removal  of  plants  likely  to  contain  water  and  act  as 

breeding-places  (the  following  may  be  specially  noted 
bamboos,  pineapple  plants,  travellers'  palms,  fibre 
plants).  Water-weeds  in  streams  should  also  be 
removed,  as  the  larvae  are  often  found  to  be  protected 
by  these  against  their  natural  enemies.  Water- 
weeds  should  be  removed  before  oiling.  Brush  and 
grass  should  be  cut. 

6.  Introduction  offish,  especially  '  millions,'  into  collections 

of  water. 


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PROPHYLAXIS 


1209 


It  is  always  easy  to  find  some  local  fish  which  will  eat  larvae  readily.  Thus, 
in  Bengal  the  larvae-eating  fish  are:  Haplochilus  panchax,  H.  melastigma, 
Ambassis  nama,  A.  ranga,  Anabas  scandens,  Barbus  ticto,  and  several  species 
of  Trichogaster.     Tadpoles  and  water-boatmen  also  eat  mosquito  larva?. 

7.  Growth  of  weed  in  water,  especially  Lemna,  the  duckweed. 

8.  Attention  to  the  non-stagnation  of  water  in  gutters. 

Summary.— Every  district  must  be  considered  separately,  and  a 
systematic  malarial  survey  having  been  made,  those  methods  should 
be  applied  which  seem  most  adapted  for  success.  A  combination 
of  methods  must  be  better  than  any  one  individual  method.  In 
any  case,  a  definite  scheme  should  be  devised,  and  thoroughly 
and  continuously  carried  out.  But  a  word  of  caution  is  necessary. 
Having  made  the  survey  and  estimated  the  cost,  firstly,  leave  a 
good  margin  for  contingencies,  and,  secondly,  insist  upon  an 
adequate  supply  of  money  being  provided;  but  it  is  not  necessary 
to  embark  upon  an  expensive  scheme,  as  a  great  improvement  can 
be  effected  with  but  little  expenditure.  It  is,  however,  important 
to  make  a  beginning,  and  to  attempt  to  gain  the  confidence  of  the 
public,  as  to-day  there  is  no  difficulty  with  the  authorities,  who 
are  usually  very  willing  to  help. 

The  methods  mentioned  above  may  be  summarized  as  follows: — 

Reduction  of  Bites. — Mosquite-net,  screening  the  house,  use  of 
fans,  use  of  hand-net,  use  of  protective  oils. 

Mosquito  Reduction. — Insects  may  be  killed  by  hand-net,  by  culi- 
cides,  by  natural  enemies,  or  inconvenienced  by  diminution  of  dense 
vegetation. 

Larvae  may  be  attacked  by  removing,  oiling,  or  screening  col- 
lections of  water,  natural  or  in  plants,  by  introducing  fish  or  beetles 
into  water,  or  by  the  engineering  works  mentioned  above. 

The  smaller  methods  are  usually  carried  out  by  gangs  of  workmen 
— mosquito  brigades — under  trained  supervisors. 

Case  Reduction. — By  quinine  prophylaxis  and  by  segregation. 

Relative  Values. — The  relative  merits  of  protection  against  mos- 
quitoes and  quinine  prophylaxis  have  been  investigated  by  Celli, 
whose  results  are  embodied  in  the  following  table:  — 


Relative  Values  of  Quinine  Prophylaxis  and  Antimosquito 
Protection. 


Method  of  Prophylaxis. 


n    .    .  Anti-      I  Quinine  Pro- 

Qmmne       mosquito     phvlaxis  plus 
None.       Prophylaxis  Prot'ction    Antimosquito 
alone.      1  Protection. 


alone. 


Percentage  of  infections 


i'75% 


Results. — In  British  Guiana  the  cases  treated  in  hospitals  have 
been  reduced  from  33,748  in  1906-07  to  7,384  in  1912-13.     In  the 


1210  THE  MALARIAL  FEVERS 

Panama  Canal  Zone  the  death-rate  from  malaria  in  1881  was  20*5 
per  1,000 ;  in  1911  0-96  per  1,000.  The  malaria  cases  in  1906  were 
821  per  1,000,  and  in  1911  184  per  1,000.  In  Ismailia  in  1900  there 
were  2,284  cases  ;  in  1906-08  not  a  case.  In  Kuala  Lumpur  the 
death-rate  was  9*7  per  1,000  in  1907,  and  3-9  per  1,000  in  1914. 
These  figures  speak  for  themselves. 


REFERENCES. 

Only  a  few  references  are  given  here,  but  they  include  works  in  which  more 
detailed  lists  of  publications  are  published.  The  most  useful  general 
references  are  Atti  della  Society  per  gli  Studi  delta  Malaria,  and  the  Tropical 
Diseases  Bulletin.  ] 

General  Literature. 

Alport  (1919).     Malaria  and  its  Treatment.     London. 

Ascoli  (191 5).     La  Malaria.     Torino. 

Craig  (1907).     Osier  and  M'Crae's  System  of  Medicine. 

Craig  (1909).     The  Malarial  Fevers.     London.     (A  most  excellent  work.) 

Gray    and  Low  (1902).     Brit.  Med.    Journ.,   January  25.     Malaria  in    St. 

Lucia,  W.I. 
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references . 
Manson  (191 8).     Tropical  Diseases,  with  many  references. 
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with  references. 
Rogers  (1910).     Fevers  in  the  Tropics.     Second  edition.     London. 
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(A  standard  work  of  the  greatest  importance.) 
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Memoirs  of  the  Liverpool  School  of  Trop.  Med.,  Nos.  1.  2,  3,  6,  9,  10,  14,  20. 

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Chalmers  (1900).     Malaria  on  the  Gold  Coast.     Lancet. 

Chalmers  (1902).     Malaria  in  Ceylon.     London. 

Daniels  (1907).     Studies  in  Laboratory  Work.     London. 

James  (1905).     No.  2,  Scientific  Memoirs.     India. 

James  (1905).     No.  19,  Scientific  Memoirs.     India. 

James  (1919).     Trans.  Soc.  of  Trop.  Med.,  vol.  xii.,  No.  3.    (Malaria  contracted 

in  England.) 
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Paisseau  and  Hutinel  (1919).     Paris  Med.,  March  15. 
Quarelli  (191 7).     Pensiero  Medico. 
Ramsden  and  Lipkin   (1918).     Annals  of  Trop.  Med.  and  Paras.,  vol.  xi. 

No.  4. 
Rogers  (1918).     Brit.  Med.  Journ.,  October  26. 
Ross  (1918).     Transactions  Soc.  Trop.  Med.,  vol.  xi.,  Nos.  5  and  6. 
Stephens,  Yorke,  Blacklock,  Macfie,  Cooper  (1917-18).     Annals  of  Trop. 

Med.  and  Parasitology. 
Stephens,  Yorke,  Blacklock,  Macfie,  Cooper  and  Carter  (1918).      Annals 

Trop.  Med.  and  Paras.,  vol.  xi.,  Nos.  2,  3,  4. 
Stephens,  Yorke,   Blacklock,  Macfie,   Cooper  (1918)-     Annals  of  Trop. 

Med.  and  Paras.,  vol.  xi.,  No.  1. 
Stephens,    Yorke,    Blacklock,    Macfie,    Cooper    and    Carter    (1919)- 

Ann.  Trop.  Med.  and  Par.,  vol.  xii.,  Nos.  3  and  4. 


CHAPTER  XLI 
THE    TROPICAL    HEMOGLOBINURIAS 

General  remarks — Malarial  haemoglobinuria — Quinine  hemoglobinuria — 
Blackwater  fever — References. 

GENERAL  REMARKS. 

Hemoglobinuria  or  the  presence  of  more  or  less  altered  haemo- 
globin in  the  urine,  is  found  in  a  number  of  conditions  which  may- 
be approximately  classified  into: — 

i.  The  Symptomatic  Hemoglobinurias,  which  occasionally  occur 
in  the  course  of  such  diseases  as  malaria,  Raynaud's  disease,  the 
acute  specific  fevers,  and  after  severe  burns. 

2.  The  Toxic  Hemoglobinurias,  which  are  brought  about  by  the 
action  of  a  number  of  drugs,  as,  for  example,  quinine  and  its  salts, 
chlorate  of  potash,  antipyrin,  carbolic  acid,  and  naphthol,  and  by 
certain  vegetables  used  as  food,  as,  for  example,  certain  beans 
(Favism,  vide  p.  201). 

3.  The  Specific  Hemoglobinurias,  which  are  specific  diseases,  such 
as  blackwater  fever  and  paroxysmal  haemoglobinuria. 

In  the  tropics  we  are  concerned  with  one  entity  in  each  of  these 
groups — viz. : — 

1.  Malarial  haemoglobinuria. 

2.  Quinine  haemoglobinuria. 

3.  Specific  blackwater  fever. 

1.  MALARIAL  HEMOGLOBINURIA. 

Definition. — Malarial  haemoglobinuria  is  simply  a  haemoglobinuria 
caused  by  Laverania  malarice  Grassi  and  Feletti,  1890. 

History .-^-This  form  of  haemoglobinuria  has  been  much  confused 
with  quinine  haemoglobinuria  and  with  blackwater  fever.  It  is 
simply  a  haemoglobinuria  occurring  in  the  course  of  atypical  sub- 
tertian  malaria,  and  caused  by  the  malarial  parasites.  Stephens 
has  seen  it  associated  with  quartan  parasites. 

Etiology. — -The  aetiological  factor  is  L.  malarice  Grassi  and  Fel- 
letti  1890,  together  with  some  other  factor,  which  inhibits  the 
production  of  antihaemolysins. 

Climatology. — The  distribution  is  coextensive  with  the  distribu- 
tion of  the  more  severe  forms  of  malaria,  and  is  therefore  most 
evident  in  the  tropics  and  subtropics. 

1213 


i2i4  THE  TROPICAL  HEMOGLOBINURIAS 

Pathology. — As  has  been  shown  by  de  Blasi,  Brem,  and  Zeiler, 
the  malarial  parasites  give  rise  to  a  hemolysin  which  probably 
varies  in  quantity  and  quality  with  different  strains  of  parasites, 
but  is  kept  in  check  by  the  action  of  antihaemolysin,  which  is 
formed  in  the  body,  but  which  under  certain  circumstances — e.g., 
exposure  to  the  weather,  etc. — may  fail  to  be  produced  in  sufficient 
quantities,  and  haemoglobinaemia  with  hsemoglobinuria  may  occur. 
Brem  found  that  three  parts  of  a  haemolysin  extract  from  a  case  of 
pernicious  malaria  completely  destroyed  (haemolyzed)  one  part  of 
a  5  per  cent,  suspension  of  erythrocytes  in  twenty  minutes.  This 
haemolysin  is  thermolabile.  Zeiler  and  Brem  have  also  demon- 
strated the  presence  of  antihaemolysin  in  the  serum  of  normal  indi- 
viduals as  well  as  in  that  of  persons  suffering  from  pernicious 
malaria.  It  would  therefore  appear  as  though  the  presence  or 
absence  of  haemoglobin  in  an  attack  of  pernicious  malaria  depends 
upon  the  relationship  between  the  quantity  of  haemolysin  produced, 
and  the  amount  of  antihaemolysin  also  produced. 

Bijon  considers  that  the  resistance  of  the  red  corpuscles  to  lysin 
is  diminished,  and  Gasbarrini  believes  that  the  lysin  lies  inside  the 
red  cells. 

Symptomatology. — The  symptoms  are  those  of  an  attack  of  per- 
nicious malaria,  in  which  the  main  feature  is  the  presence  of  haemo- 
globinuria,  the  other  symptoms  being  high  fever,  shivering,  vomit- 
ing, great  prostration,  and  rapid  anaemia. 

Diagnosis. — The  diagnosis  is  to  be  made  by  first  demonstrating 
the  presence  of  L.  malarice  in  the  blood,  and  then  by  the  rarity  of 
severe  jaundice. 

Treatment. — This  is  the  same  as  for  other  forms  of  atypical  sub- 
tertian  malaria  (p.  1188) — viz.,  quinine  in  large  doses,  before  which 
calcium  lactate  in  5  to  10  grain  doses  may  be  given  with  advantage. 

Prophylaxis. — The  prophylaxis  is  the  same  as  for  malaria.  This 
has  been  exemplified  in  Robertville,  an  Algerian  village  which  was 
highly  malarious  and  where  the  malarial  fevers  were  associated  with 
pyrexial  haemoglobinuria.  After  1910,  when  preventive  measures 
were  instituted,  according  to  Ciavaldini,  the  malaria  decreased  and 
the  haemoglobinuria  disappeared. 

2.  QUININE  HEMOGLOBINURIA. 

Definition. — An  acute  non-contagious  fever  caused  by  the  ad- 
ministration of  any  of  the  ordinary  salts  of  quinine  in  certain  cases 
of  malarial  cachexia  and  chronic  malaria,  and  characterized  by 
haemoglobinaemia  and  haemoglobinuria. 

Remarks.— Sir  Patrick  Manson  has  pointed  out  that  an  attack 
of  haemoglobinuria  can  be  produced  in  certain  cases  by  the  ingestion 
of  a  single  small  dose  of  quinine.  Ross  and  Low  have  reported  such 
a  case,  under  the  care  of  Sir  Patrick  Manson,  where  the  administra- 
tion of  a  9-grain  dose  of  quinine  was  followed  by  haemoglobinuria 
in  a  few  hours.     Ketchen  has  recorded  a  case  of  seven  consecutive 


QUININE  HEMOGLOBINURIA  121 5 

hemoglobinurias  in  the  same  individual  in  whom  each  attack  was 
the  sequel  to  a  dose  of  quinine.  We  have  met  with  similar  cases, 
but  our  maximum  is  six  attacks  in  one  year. 

History. — Veratas  in  Greece,  in  1858,  was  the  first  to  draw  atten- 
tion to  this  form  of  fever,  and  to  definitely  ascribe  the  haemoglobin- 
uria  to  quinine,  and  he  was  followed  and  supported  by  Tomaselli, 
Grocco,  and  many  other  Italian  and  Grecian  observers.  Later 
Plehn,  Koch,  and  others,  have  strongly  advocated  this  theory,  but 
these  last  observers  have  applied  this  one  hypothesis  for  the  ex- 
planation of  all  the  conditions  included  under  the  term  '  blackwater 
fever.' 

Climatology.— The  attack  can  take  place  anywhere  for  the  first 
time,  provided  that  the  individual  is  suffering  from  chronic  malaria, 
etc.,  and  the  unknown  factor  or  factors  to  be  mentioned  below,  and 
has  taken  the  requisite  dose  of  quinine. 

etiology. — The  causation  of  this  condition  is  the  administration 
of  quinine  in  cases  of  malarial  cachexia  and  chronic  malaria,  but 
this  is  not  the  entire  aetiology,  otherwise  the  condition  would  be 
more  commonly  met  with  than  at  present,  and  also  it  is  quite  safe 
to  administer  quinine  to  the  majority  of  cases  of  chronic  malaria 
and  malarial  cachexia  without  causing  haemoglobinuria.  More- 
over, the  administration  of  a  dose  of  a  salt  of  calcium  prior  to  the 
quinine  will  prevent  the  haemoglobinuria,  which  in  the  same  indi- 
vidual has  occurred  after  such  administration. 

From  one  observation  which  we  have  made  we  would  throw  out  the  sugges- 
tion that  one  of  the  other  factors  in  quinine  haemoglobinuria  may  be  the 
condition  of  the  kidney,  and  that  the  site  of  the  haemolysis  may  be  in  that 
organ. 

Pathology. — The  pathology  of  quinine  haemoglobinuria  is  but 
little  understood,  but  it  has  been  very  ably  studied  by  Barratt  and 
Yorke,  who  demonstrated  the  action  of  quinine  in  alkaloidal  form, 
and  as  the  bihydrochloride  as  well  as  hydrochloric  acid  and  sodium 
hydrate  upon  healthy  red  blood  cells,  and  found  that : — ■ 

1.  All  the  above-mentioned  agents  produced  haemolysis. 

2.  In  equimolecular  concentration  the  haemolytic  power  is  nearly 
the  same. 

3.  The  haemolysis  produced  by  quinine  (alkaloid)  resembled  a 
catalytic  action,  and  took  place  at  a  monomolecular  rate. 

4.  During  life  it  is  not  possible  to  reach  a  percentage  of  quinine 
in  the  blood  sufficient  to  cause  haemolysis,  owing  to  the  toxicity  of 
the  drug. 

With  regard  to  the  action  of  the  quinine,  some  observers  believe 
that  it  produces  the  haemolysis  by  lowering  the  osmotic  pressure  of 
the  blood  plasma. 

Morbid  Anatomy. — We  are  not  acquainted  with  any  direct 
observations  on  this  subject,  but  the  appearance  of  the  kidney  in 
people  who  have  died  from  pernicious  malarial  fever  in  which  large 
doses  of  quinine  have  been  administered  without  success  resembles 


1 21 6  THE  TROPICAL  HEMOGLOBINURIAS 

both  macroscopically  and  to  some  extent  microscopically  the 
kidney  seen  in  blackwater  fever. 

Symptomatology.- — The  general  symptoms  resemble  those  of  an 
attack  of  blackwater  fever,  but  are  not  so  severe,  and  the  jaundice 
is  slight  or  absent. 

Diagnosis. — The  history  of  the  attack  following  the  administra- 
tion of  quinine  in  persons  suffering  from  malaria  cachexia  or  chronic 
malaria  may  give  a  clue. 

It  is  suggested  that  the  rate  of  haemolysis  of  the  erythrocytes,  when  treated 
with  quinine,  may  be  compared  with  that  for  normal  erythrocytes  similarly 
treated.  The  method  adopted  to  test  haemolysis  is  to  allow  i  c.c.  of  blood 
from  the  pricked  finger  to  fall  drop  by  drop  into  a  i  per  cent,  solution  of 
potassium  oxalate,  which  also  contains  0-45  per  cent,  of  sodium  chloride,  until 
a  proportion  of  four  parts  of  blood  to  one  part  of  the  oxalate  is  reached.  Then 
the  mixture  is  added  to  10  c.c.  of  a  0-9  per  cent,  solution  of  sodium  chloride, 
and  centrifugalized  until  the  red  cells  are  completely  precipitated,  when  the 
supernatant  fluid  is  pipetted  off,  and  then  sufficient  0-9  per  cent,  solution  of 
sodium  chloride  is  added  to  make  a  2*5  per  cent,  emulsion  of  red  cells.  This 
emulsion  is  then  placed  in  a  series  of  test-tubes  containing  various  strengths 
of  an  isotonic  solution  of  quinine  made  up  with  0-9  per  cent,  sodium  chloride 
when  necessary.  The  tubes  are  incubated  for  three  hours  at  370  G.,  and 
stirred  with  a  glass  rod  every  fifteen  minutes,  and  the  result  noted  at  the  end 
of  the  time. 

Prognosis. — This  is  usually  good. 

Treatment. — Quinine  administration  should  be  stopped,  and 
calcium  lactate  administered,  and  the  ordinary  treatment  for  black- 
water  fever  as  indicated  below  should  be  carried  out. 

Prophylaxis. — Europeans  about  to  visit  or  reside  in  the  tropics 
should  be  given  a  test  dose  of  10  or  15  grains  of  quinine  by  the  mouth, 
in  order  to  exclude  idiosyncrasy.  In  cases  of  chronic  malaria  or 
malarial  cachexia,  in  which  this  condition  may  appear,  calcium 
lactate  in  10  grain  doses  should  be  given  before  each  dose  of  quinine. 


3.  SPECIFIC  BLACKWATER  FEVER. 

Synonyms.  —  Malarial  Haemoglobinuric  fever,  Bilious  Haemoglobinuric 
fever,  Bilious  Remittent  fever.  Malignant  Bilious  fever,  Haemorrhagic  Malarial 
fever,  Melanuric  fever.  French  :  Fievre  Bilieuse  Hematurique,  Fievre  Bilieuse 
Hemoglobinurique,  Fievre  Bilieuse  Grave,  Fievre  Bilieuse  Melanurique,  Fievre 
Jaune  des  Creoles  ou  des  Acclimates.  Italian:  Febbre  emoglobinurica. 
German  :  Gallenfieber,  Schwarzwasserfieber. 

Definition. — Blackwater  fever  sensii  stricto  is  an  acute  specific 
fever  of  unknown  causation,  characterized  by  the  severity  of  the 
symptoms,  great  blood  destruction,  jaundice,  and  hemoglobinuria. 

History. — The  knowledge  of  this  fever  is  recent,  for  it  does  not 
appear  to  have  been  noted  by  Torti,  the  celebrated  writer  on  per- 
nicious fevers,  nor  by  his  predecessors,  and  the  first  information 
of  its  existence  appears  to  have  been  given  by  the  French  naval 
surgeons  Lebeau,  Daulle,  and  Le  Roy  de  Mericourt  in  1850-53, 
who  drew  attention  to  the  disease  in  Madagascar  and  Nossi-Be, 
after  which  it  is  mentioned  as  occurring  in  Senegal,  Cayenne,  and 


SPECIFIC  BLACKWATER  FEVER  121 7 

the  Antilles.  In  1858  Veratas  described  its  occurrence  in  Greece, 
and  in  1859  Cummings  met  with  it  in  America. 

The  clinical  signs  were  carefully  described  by  Dutroulau  in  1858; 
by  Corre  in  1861,  who  showed  that  the  colour  of  the  urine  was  due 
to  hemoglobin,  and  not  to  bile  or  blood,  as  had  been  thought; 
by  Barthelemy  and  Benoit  in  1865;  Berenger-Feraud  in  1874 
(in  which  year  Tomaselli  first  described  it  in  Italy) ;  Pellarin  in 
1876;  and  O'Neill  in  1882.  Kelsch  and  Kiener  in  1889  gave  an 
excellent  description,  together  with  a  history  of  the  disease  up  to 
that  date.  In  1890  Schilling  met  with  it  in  Kaiser  Wilhelm's  Land, 
and  Grocco  and  Cardarelli  in  Italy,  after  which  a  series  of  papers  by 
Mahly,  Easmon,  Eyles,  and  Papafio  appeared  on  the  disease  as 
seen  on  the  Gold  Coast,  where  it  is  called  '  attridi  assara,'  which 
means'  bilious  fever.'  The  name'  blackwater  fever,  'now  universally 
adopted,  was,  as  far  as  we  know,  first  used  by  Easmon. 

Researches  have  been  made  as  to  its  nature  and  treatment  by 
Koch,  Plelm,  Crosse,  Prout,  Stephens,  Christophers,  Bentley, 
Barratt,  Yorke,  Cardamatis,  Leishman,  Low  and  Wenyon,  Balfour, 
and  others. 

With  regard  to  the  parasitic  cetiology  Macfie  notes  that  in  these  cases  the 
cytoplasm  of  the  malarial  parasites  is  apt  to  stain  badly,  and  therefore,  as 
they  are  difficult  to  see,  they  may  often  be  missed. 

Laloir  thinks  that  the  peculiar  organism  which  he  has  described  as  a 
malarial  parasite  in  the  red  corpuscles  and  nuclei  of  the  mononuclears  and  in 
the  salivary  glands  of  Anopheles  listoni  var.  albo-apicalis  may  be  a  causal  agent. 

With  regard  to  chemical  (Etiology,  Lahille  has  shown  that  there  is  no  defici- 
ency of  salts  in  the  blood,  and  Burkitt  has  drawn  attention  to  the  high  acidity 
of  the  urine  and  the  diminished  alkalinity  of  the  blood. 

As  regards  records  Stephens  has  drawn  up  a  valuable  routine  form,  which, 
modified  in  some  particulars,  has  been  utilized  in  the  Sudan  for  some  time. 

In  regard  to  clinical  features,  under  the  term  Icteroideta  paludica  Salvin  has 
described  a  sort  of  bilious  remittent  fever  as  a  preha?moglobinuric  fever  in 
Venezuela,  and  Plehn  has  classified  blackwater  into: — 

1.  Simple  Attack. — Temperature  falls  to  normal  on  the  second  to  third 

day,  and  even  albumen  has  disappeared  from  the  urine  by  the  third, 
fourth  or  fifth  day.     The  only  danger  is  anuria  on  the  third  day. 

2.  Intermittent  Attacks. — The  haemoglobinuria  is  intermittent,  with  very 

slight  icterus,  progressive  anaemia,  and  death  on  fourth  to  fifth  day. 
Anuria  is  rare. 

3.  Fulminating  Type. — Very  slight  icterus,  anuria,  coma;  death  in  twenty- 

four  hours. 

4.  Hemorrhagic  Type. — This  appears  to  us  to  be  the  haemorrhagic  type 

of  atypical  subtertian  fever. 

5.  Abortive  Ambulant  Type. — This  appears  to  us  to  be  our  quinine  haemo- 

globinuria,   as  it   commences   after  a  small   prophylactic   dose   of 
quinine. 

It  seems  to  us  that  until  tropical  practitioners  accustom  themselves 
to  differentiate  from  specific  blackwater  fever  the  hemoglobinurias 
due  to  quinine  and  to  malaria  no  real  progress  will  be  made  with 
the  knowledge  of  this  serious  illness. 

Climatology. — The  disease  occurs  most  commonly  in  tropical 
Africa  and  in  certain  localities  in  India,  but  it  has  also  been  reported 
from  many  parts  of  the  tropics. 

77 


1 21 8  THE  TROPICAL  HEMOGLOBINURIAS 

In  Europe  it  is  found  in  South  Italy,  Sicily,  Sardinia,  Macedonia, 
Greece,  and  Southern  Russia.  In  Africa  it  occurs  in  Algeria,  and 
through  the  whole  of  the  tropical  area  of  West,  Central,  and  East 
Africa.  In  Asia  it  is  well  known  in  India,  especially  in  the  Duars,  the 
Terai,  Assam,  the  Jeypore  district  of  Madras',  and  the  Canara  district 
of  Bombay.  It  is  also  found  in  China,  Cochin  China,  and  Farther 
India.  In  America  cases  have  been  recorded  in  the  southern  regions 
of  the  United  States,  in  Central  and  South  America — especially 
Brazil — and  the  West  Indies.  It  occurs  in  the  Anglo-Egyptian 
Sudan,  but  there  are  many  other  parts  of  the  tropics  from  which 
it  has  not  been  reported.  Too  much  trust  must  not  be  placed  upon 
this  distribution,  as  confusion  exists  between  the  mild  attacks  of 
quinine  hemoglobinuria,  as  well  as  the  atypical  subtertian  malarial 
form.  True  blackwater  fever  can  exist  in  epidemic  form,  and  is  a 
very  fatal  infection. 

/Etiology. — The  causation  of  blackwater  fever  has  been  much 
complicated  by  the  confusion  arising  from  the  non-recognition  of 
quinine  and  malarial  hemoglobinurias,  but  when  these  conditions 
are  admitted  there  is  still  the  serious  disease,  '  blackwater  fever,'  to 
be  explained,  and  its  causation  appears  to  us  to  be  some  protozoal 
parasite  as  yet  unknown. 

The  various  theories  which  have  been  advanced  to  explain  the 
etiology  of  blackwater  fever  are: — 

i.  The  malarial  fever. 

2.  The  theory  of  malaria,  together  with  some  other  factor. 

3.  Malarial  anaphylaxis  theory. 

4.  An  unknown  agent  theory. 

5.  Bite  of  an  unknown  arthropod. 

1.  The  Malarial  Theory. — All  the  old  writers  on  the  aetiology  of  black- 
water  fever  attributed  its  cause  to  malaria,  in  much  the  same  way  as  they 
classed  most  tropical  fevers  under  the  same  term. 

When  these  fevers  came  to  be  differentiated,  blackwater  fever  was  assigned 
to  the  action  of  Laverania  malaria: ;  but  of  late  years  cases  have  occurred  in 
which  this  parasite  has  not  been  found,  but  only  Plasmodium  malaria  or 
P.  vivax,  because  these  parasites  are  very  commonly  met  with  in  the 
tropics. 

The  older  writers  maintained  that  blackwater  fever  existed  wherever  there 
was  severe  malaria,  and  that  it  was  not  found  where  this  was  absent,  and  they 
instanced  Southern  Italy,  where  malaria  causes  a  mortality  of  7  to  10  per  1,000, 
as  a  region  where  blackwater  fever  is  common,  and  compared  it  with  North 
Italy,  where  the  malarial  mortality  is  only  1  per  1,000,  and  where  blackwater 
fever  is  rare.  Further,  it  was  pointed  out  that  the  people  attacked  with 
blackwater  fever  had  always  previously  suffered  from  malarial  fever,  and 
had  generally  had  several  attacks.  This  view  may  be  said  to  have  been 
supported  by  Stephens,  who  states  that  the  blood  of  persons  examined  during 
the  day  preceding  the  hemoglobinuria  contained  parasites  in  95-6  per  cent, 
of  cases,  while  during  the  day  of  the  attack  these  parasites  were  found  in 
only  61*9  per  cent.,  and  during  the  day  after  the  attack  in  only  ifi  per  cent. 
Stephens  and  Christophers  point  out  that,  though  they  only  found  malarial 
parasites  in  1 2-5  per  cent,  of  all  their  cases,  still  they  found  evidence  of  malarial 
infection,  as  exemplified  by  the  presence  of  pigment  in  the  leucocytes  or  by 
an  increase  in  the  percentage  of  the  large  mononuclear  cells,  in  no  less  than 


MTIOLOGY  1 21 9 

93-8  per  cent.      Further,  the  presence  of  a  haemolysin  in  malaria  has  been 
demonstrated  by  de  Blasi  and  others. 

The  reply  to  these  points  is  that  the  geographical  distribution  of  blackwater 
fever  is  only  known  in  a  very  general  way,  and  even  this  superficial  know- 
ledge is  against  the  theory  that  it  is  due  to  malaria.  Incidentally,  we  may 
mention  that  no  one  has  attempted,  as  far  as  we  know,  to  make  a  spot-map 
of  a  district  where  there  is  much  blackwater  fever,  showing  as  far  as  possible 
where  the  disease  was  really  contracted,  and  to  compare  this  with  a  similar 
map  made  for  the  cases  of  malaria  in  that  district.  Nor,  as  far  as  we  know, 
has  anyone  attempted  to  show  whether  the  epidemiological  phenomena  of 
blackwater  fever  coincide  with  those  of  malaria.  The  West  Coast  of  Africa 
would  appear  to  be  a  suitable  place  for  these  inquiries. 

The  malarial  theory  is  disposed  of,  in  our  opinion,  in  that  it  has  many  times 
been  recorded  as  occurring  in  persons  who  have  never  suffered  from  malaria; 
indeed,  according  to  Craig,  it  has  occurred  in  people  who  have  not  only  never 
been  known  to  suffer  from  malaria,  but  in  whom  neither  before,  during,  nor 
after  an  attack  have  the  parasites  been  found,  and,  finally,  in  whom  a  post- 
mortem examination  failed  to  reveal  any  evidence  of  malaria.  Our  opinion 
is  more  or  less  confirmed  by  the  fact  that  an  attack  of  blackwater  fever  is 
uninfluenced  by  quinine.  However,  at  the  present  time,  there  are  few  advo- 
cates of  the  theory  that  it  is  simply  a  malarial  infection.  Here,  perhaps,  may 
be  mentioned  the  fact  that  Donovan  considers  that  it  is  malaria,  but  due  to  a 
species  of  Laverania  as  yet  unrecognized.  Laloir's  parasite  requires  confirma- 
tion, and  is  in  our  opinion  of  doubtful  value. 

2.  Malaria,  together  with  Some  Other  Factor. — As  malaria  by  itself  has  proved 
rather  Weak  aetiologically,  some  other  factor  has  been  brought  in  to  support  it. 
Thus  Corre  suggested  chills,  Berenger-Feraud  mercury,  and  others  acute  and 
chronic  alcoholism,  syphilis,  severe  muscular  exertion,  mental  excitement, 
and  change  of  climate;  but  of  all  theories,  that  connecting  malaria  with 
quinine  has  been  the  most  popular. 

Malaria  and  Quinine. — Stephens  has  supported  the  theory  that  the  disease 
is  partly  of  malarial  origin,  aided  by  a  second  factor— viz.,  quinine.  In  his 
article  in  Osier's  '  System  of  Medicine, '  Stephens  sums  up  his  view ;  '  Blackwater 
is  not  a  disease  per  se,  but  rather  a  condition  of  blood  in  which  quinine,  other 
drugs,  cold,  or  even  exertion,  may  produce  a  sudden  destruction  of  red  cells. 
The  condition  is  produced  only  by  malaria,  and  generally  by  repeated  slight 
attacks,  insufficiently  combated  by  quinine.  In  such  cases  of  chronic  malaria 
— i.e.,  in  those  suffering  from  anaemia,  with  repeated  attacks  of  fever  and 
repeated  doses  of  quinine— blackwater  fever  sooner  or  later  almost  certainly 
supervenes — at  least,  in  tropical  climates.' 

These  statements  are  too  sweeping  if  genuine  blackwater  fever  is  meant, 
otherwise  the  home  of  the  disease  would  be  Ceylon,  whereas  it  is  so  rare  that 
we  have  never  heard  of  a  genuine  non-imported  case ;  for  in  this  island  there 
are  Europeans  and  natives  with  just  the  conditions  required  by  Stephens, 
and  yet  they  do  not  develop  blackwater  fever,  because  the  only  two  cases 
which  we  have  met  with  or  heard  of  in  Ceylon  in  twelve  years  were  most  prob- 
ably cases  of  quinine  hemoglobinuria.  On  the  other  hand,  Stephens'? 
remarks  are  correct  if  applied  to  quinine  hemoglobinuria. 

Stephens  accounts  for  the  difference  between  India  and  Africa  as  regards 
the  prevalence  of  blackwater  fever  by  the  common  malarial  parasite  being  the 
tertian  in  India  and  the  subtertian  in  Africa.  Certainly  the  tertian  is  very 
common  in  Ceylon,  though  the  subtertian  is  also  frequently  found.  Another 
point  which  is  difficult  to  explain  is  the  frequency  of  the  disease  in  Assam, 
and  the  less  frequent  occurrence  in  other  parts  of  India  where  malaria  is 
common. 

According  to  McCay,  who  has  carefully  investigated  the  action  of  quinine 
in  causing  hemoglobinuria,  sulphuric  acid  and  the  sulphates  cause  a  decrease 
in  the  total  inorganic  salts  of  the  plasma,  which  he  thinks  implies  a 
decrease  in  its  osmotic  tension.  Water,  therefore,  passes  into  the  red  cells, 
causing  them  to  swell  up,  and,  if  the  decrease  in  osmotic  tension  of  the  plasma 
is  sufficient,  to  burst. 


1220  THE  TROPICAL  HEMOGLOBINURIAS 

He  considers  that  the  causation  of  blackwater  fever  is  threefold : — 

(i)  Injury  to  the  stroma  of  the  red  cell  by  the  malarial  parasite.  (2)  The 
action  of  the  malarial  haemolysin.     (3)  The  administration  of  sulphates. 

He  thinks  that,  though  the  first  and  second  causes  may  bring  about  the 
disease,  still  quinine  sulphate  or  any  other  sulphate,  by  its  action  on  the  plasma, 
is  the  exciting  cause  if  the  former  are  ineffectual.  On  the  other  hand,  he  finds 
that  chlorides  cause  an  increase  of  the  resisting  power  of  the  erythrocytes  to 
haemolysis.  Quinine  hydrochloride,  especially  when  combined  with  sodium 
chloride  and  dilute  hydrochloric  acid,  causes  usually  a  marked  rise  in  the 
resistance.  Therefore,  according  to  him ,  it  is  not  the  quinine,  but  the  sulphuric 
acid  in  the  form  of  quinine  sulphate,  which  produces  the  hemolytic  action. 
In  addition  to  sulphates,  McCay  found  that  alkaline  carbonates,  compounds 
of  alkalis  with  vegetal  acids  and  potassium  salts,  diminished  the  inorganic 
molecules  of  the  plasma,  thus  tending  to  help  haemolysis.  We  have,  however, 
seen  hsemoglobinuria  following  the  administration  of  euquinine,  the  hydro- 
chloride, and  even  the  tannate  of  quinine.  We  have  already  referred  to 
Barratt  and  Yorke's  experiments  on  this  subject  (see  p.  1215). 

Malaria,  Quinine,  or  Depressing  Influence. — Deeks  and  James  maintain, 
from  the  study  of  230  cases  of  blackwater  fever  in  Panama,  that  it  is  a  mani- 
festation of  malarial  toxicity  usually  induced  by  repeated  attacks,  but  also 
appearing  coinci dentally  with  an  acute  attack,  and  may  be  determined  by  any 
depressing  influence  or  quinine. 

This  is  really  a  malarial  toxicity  and  other  factor  theory.  In  order  to 
produce  the  requisite  conditions,  they  maintain  that  there  must  be  a  popula- 
tion non-immune  to  malaria,  of  which  infection  there  must  be  a  large  portion 
due  to  L.  malaricB,  and  malaria  must  be  in  such  quantity  as  to  produce  an 
almost  continuous  infection,  and  this  must  be  associated  with  a  neglect  of 
a  thorough  administration  of  quinine,  especially  in  primary  attacks. 

Against  the  view  that  it  is  caused  by  malaria  treated  with  insufficient  dosage 
of  quinine,  followed  by  a  large  dose  of  quinine,  we  may  quote  the  fact  that  we 
are  personally  acquainted  with  a  case  of  malaria  associated  with  depressing 
influences  in  which  the  infection  was  L.  malarice,  which  had  remained  latent 
for  a  considerable  period,  and  which  for  some  weeks  was  treated  by  quite 
inadequate  doses  taken  by  the  mouth,  and  after  severe  fever  varying  from 
1040  to  io5'8°  F.,  and  lasting  for  two  days,  1  gramme  of  the  bihydrochloride  of 
quinine  was  administered  by  the  mouth,  and  2  grammes  given  at  the  same  time 
by  intramuscular  injection,  with  the  result  of  a  quick  and  lasting  cure  of  the 
malaria  without  any  signs  of  blackwater  fever.  This  case  appears  to  us  to 
answer  every  point  required  by  the  supporters  of  the  malaria  quinine  theory  of 
blackwater  fever,  and  it  may  further  be  stated  that  the  original  infection  with 
L.  malarice  was  in  West  Africa  in  one  of  the  endemic  regions  of  blackwater  fever. 

Mutko  gives  great  importance  to  a  disturbance  in  the  phosphate  meta- 
bolism as  an  aetiological  factor.  According  to  his  researches  the  secondary 
and  tertiary  phosphates,  whether  of  sodium  or  potassium,  protect  against 
quinine  haemolysis,  while  the  primary  salts  do  not. 

3.  Anaphylaxis. — In  1909  Cleland  advanced  the  theory  that  the  disease 
might  be  an  expression  of  anaphylaxis  to  the  malarial  parasite  brought  about 
by  the  presence  in  the  serum  of  a  foreign  protein  in  the  shape  of  disintegrated 
merozoites.  But  this  is  open  to  serious  objections,  though  recently  supported 
by  Cardamatis,  who  considers  that  quinine  might  be  able,  when  converted  into 
the  albuminate,  in  certain  unknown  conditions  to  act  as  an  antigen,  which, 
when  combined  with  the  malarial  toxin,  might  produce  antibodies,  which 
might  provoke  a  sensitiveness  to  quinine  in  the  person  suffering  from  malaria, 
when  a  further  dose  of  the  drug  would  produce  anaphylaxis,  perhaps  because 
it  combines  with  the  antibodies,  or  perhaps  by  its  transformation  into  a 
hypertoxic  substance. 

4.  Unknown  Agent. — Sir  Patrick  Manson,  in  1893,  first  promul- 
gated the  theory  that  blackwater  fever  was  a  disease  distinct  from 
malaria,  and  supported  this  by  the  peculiar  distribution  of  the 
disease,  which  is  widespread  in  tropical  Africa,  and  very  local  in  India. 


PREDISPOSING  CAUSES  1221 

Sambon,  in  1898,  having  in  mind  the  haemoglobinuric  fevers  of  animals, 
brought  forward  the  theory  that  human  blackwater  fever  would  probably  be 
found  to  be  a  piroplasmosis,  and  has  informed  us  that  on  one  occasion  Sir  Patrick 
Manson  and  he  saw  one  body  in  a  red  blood-corpuscle  of  a  case  of  blackwater 
fever  which  very  closely  resembled  the  bacillary  form  of  Theileria,  but  it 
is  possible  that  this  was  merely  a  peculiar  form  of  Laverania  malarice. 

The  parasites  which  have  been  described  are  becoming  numerous.  There  is 
a  bacillus  by  Yersin  in  the  renal  epithelium,  which  has  since  been  shown  to  be 
a  strain  of  Bacillus  coli  communis  ;  while  the  other  parasites  suggested  as 
possible  ^etiological  factors  are  a  blood  parasite  by  F.  Plehn,  which  he  now 
identifies  with  the  subtertian  malarial  parasite;  and  a  double-contoured 
parasite  in  the  red  corpuscles  by  Fisch,  which  has  not  been  confirmed.  A 
body  resembling  a  Piroplasma  has  been  described  by  Forau,  but  has  been 
criticized  by  Stephens,  as  resembling  the  fragmentation  and  flagellation  of 
erythrocytes  commonly  seen  in  malarial  anaemia  in  the  tropics.  Leishman 
has  described  cell  inclusions  varying  from  1  to  5  ^  in  diameter,  and  usually 
found  in  large  mononuclear  cells  of  endothelial  origin.  These  inclusions 
are  either  structureless,  homogeneous,  circular  forms,  or  ring  forms.  They 
are  embedded  in  the  cytoplasm  of  the  cell,  and  usually  assume  a  chro- 
matin colour  with  Romanowsky's  stain.  As  a  rule,  several  inclusions  are 
found  together  in  the  same  cell;  more  rarely  they  are  solitary.  Leishman 
considers  that  possibly  they  are  Chlamydozoa.  These  bodies  have  bsen 
adversely  criticized  by  several  observers,  especially  by  von  Schilling-Torgau, 
who  considers  them  to  be  plasmosomata,  and  Low  has  found  similar  bodies 
in  other  diseases.  Balfour  has  seen  these  inclusions  in  a  case  of  blackwater 
fever  and  in  a  case  of  malaria.  Schiifner  has  tentatively  suggested  that  a 
form  of  the  disease  may  be  of  spirochaetic  origin. 

5.  Bite  of  an  unknown  Arthropod. — Balfour  suggests  that  the  disease  is  not 
of  parasitic  origin,  but  due  to  the  injection  of  some  powerful  haemolysin  intro- 
duced by  the  bite  of  some  unknown  insect  or  arachnid. 

In  our  opinion  blackwater  fever  is  a  disease  of  its  own,  though 
we  freely  admit  the  existence  of  hemoglobinuria  from  quinine  as 
well  as  from  other  drugs,  such  as  chlorate  of  potash,  of  which  we 
know  of  a  case  at  first  diagnosed  as  blackwater  fever. 

Predisposing  Causes.— The  predisposing  causes  of  blackwater  fever 
appear  to  be  first  racial,  second  bodily.  With  regard  to  the  first, 
the  immigrant  European  suffers  more  than  the  native,  though 
the  disease  also  attacks  natives  and  half-castes.  This  racial  dis- 
tinction is,  therefore,  probably  due  to  some  acquired  or  inherited 
immunity.  It  is  said  that  a  person  is  usually  not  attacked  until 
after  residence  for  at  least  a  year  in  the  endemic  area. 

The  second  series  of  predisposing  causes  appears  to  be  anything 
which  lowers  the  vitality  of  the  body — cold,  change  of  climate, 
another  disease — e.g.,  malaria,  syphilis — or  certain  drugs. 

Pathology.- — As  the  aetiology  of  the  disease  is  uncertain,  the 
pathogenesis  is  also  little  understood. 

Christophers  and  Bentley  have  brought  forward  an  explanation  of  the  patho- 
logy. Their  views  may  be  summarized  as  follows: — Laverania  malarice,  the 
subtertian  parasite,  acts  upon  the  endothelial  cells  of  the  blood  capillaries  of 
various  organs,  but  especially  upon  those  of  the  spleen  and  liver,  stimulating 
them  to  excessive  destruction  (erythrokatalysis)  of  red  blood  cells  by  phago- 
cytosis. This  phagocytosis  results  in  the  production  of  an  auto-haamolysin 
of  the  nature  of  a  haemolytic  amboceptor,  which  is  retained  in  the  endothelial 
cells  until  set  free  by  some  exciting  cause,  which  may  be  a  chill,  overexertion, 
etc.  The  result  of  this  excitation  is  to  suddenly  set  free  in  quantity  this 
haemolysin,  which  destroys  the  red  cells  by  solution  in  the  plasma  (lysaemia), 


1222  THE  TROPICAL  HEMOGLOBINURIAS 

principally  in  the  blood  of  the  liver  and  kidney,  and  to  a  less  extent  in  that  of 
the  spleen.  The  lysaemia  produces  haemoglobinaemia,  •which  is  best  demon- 
strated by  receiving  the  blood  into  hypertonic  citrate  solution  and  then  centri- 
fugalizing,  when  the  serum  is  observed  to  be  of  an  orange,  rarely  of  a  reddish, 
colour.  The  amount  of  haemoglobin  present  in  this  condition  was  estimated 
by  Christophers  and  Bentley  to  be  from  i  to  3*75  per  cent,  of  that  present  in 
normal  blood.  This  haemoglobin  quickly  appears  in  the  urine  as  oxyhemo- 
globin, which  may  become  methaemoglobin  on  standing.  All  the  haemo- 
globin probably  does  not  escape  by  the  kidney,  for  there  is  evidence  of  increased 
production  of  bile,  and  it  is  possible  that  only  such  quantity  as  the  liver  is 
incapable  of  converting  into  bile  appears  in  the  urine.  It  is,  however,  by  no 
means  certain  whether  the  pigment  escapes  only  by  the  glomeruli  or  through 
the  tubules,  or  by  both,  and  it  is  also  uncertain  whether  the  haemoglobin  can 
pass  through  the  cells  of  a  normal  kidney. 

Barratt  and  Yorke,  on  the  other  hand,  find  that  the  haemoglobinuria  is  not 
dependent  upon  haemolysinsemia,  but  that  it  is  due  to  a  haemoglobinaemia  the 
origin  of  which  they  were  unable  to  determine. 

They,  supported  by  de  Haan,  consider  that  the  suppression  of 
urine  is  due  to  a  mechanical  blocking  of  the  renal  tubes  by  the  forma- 
tion of  large,  firm,  coarsely  granular  casts  in  the  ducts  of  Bertini. 
Plehn,  however,  ascribes  this  suppression  to  a  nervous  inhibition  of 
the  glomerular  secretion.  Many  authors  ascribe  the  suppression  to 
nephritis  caused  by  the  disease.  Recently  the  subject  has  been 
reinvestigated  by  Yorke  and  Nauss,  who  support  the  mechanical 
theory,  and  find  that  it  is  considerably  facilitated  by  any  factor 
which  tends  to  lower  the  blood-pressure,  and  by  that  means  the 
secretion  of  water  by  the  glomeruli,  but  that  if  the  blood-pressure 
is  kept  up  by  the  injection  of  saline  solutions,  the  tendency  to 
suppression  is  decreased.  This  is  of  importance  in  guiding  the 
treatment  of  the  condition. 

Morbid  Anatomy. — There  are  three  cardinal  features  in  the 
morbid  anatomy  of  a  case  which  has  died  during  blackwater  fever, 
and  these  are:  (1)  Jaundice  of  the  tissues  ;  (2)  Non-coagulated  blood ; 
(3)  Swollen  congested  kidneys.  In  addition,  there  may  be  the  signs 
of  acute  or  chronic  malaria  in  the  liver,  spleen,  and  bone-marrow. 

On  making  the  post-mortem,  the  yellow  staining  of  the  skin  and 
organs  is  most  marked.  The  kidneys  are  enlarged,  dark  red  to  black 
in  colour,  while  microscopically  they  show  degeneration  of  the 
epithelium  of  the  convoluted  and  other  tubules,  the  lumen  of  which 
is  filled  with  granular  material,  while  the  glomeruli  may  contain 
granular  material,  and  show  desquamated  capsular  cells. 

The  liver  is  enlarged,  and  the  gall-bladder  full  of  inspissated  bile. 
Microscopically,  areas  of  necrosis,  with  thrombi  in  the  sublobular 
veins  and  quantities  of  hemosiderin  in  the  cells,  many  of  which  may 
be  in  a  state  of  fatty  degeneration,  are  to  be  seen. 

The  stomach  and  small  intestine  are  often  hyperaemic,  and  the 
bone-marrow  is  yellowish,  and  either  fluid  or  gelatinous. 

The  Blood. — The  blood  is  thin  and  watery,  and  there  may  be 
haemoglobinaemia  and  cholaemia,  with  lessened  tonicity.  The  red 
cells  and  haemoglobin  are  greatly  reduced,  and  the  former  may 
include  shadow  cells  and  small  fragments  of  cells,  and  deep  staining 
round  cells  (spherocytes)  in  the  early  stages,  and  later  may  show 


MORBID  ANATOMY  1223 

degenerative  changes  such  as  polychromatophilia  and  basophilia, 
while  megaloblasts  and  normoblasts  are  present.  Malarial  parasites 
or  pigment  may  be  seen.  During  the  fever  there  is  marked  leuco- 
cytosis,  with  polymorphonuclear  and  mononuclear  increase,  but 
when  the  fever  disappears  there  is  leucopenia,  with  a  mononuclear 
increase. 

The  Urine. — The  urine  is  dark  red  to  brownish-yellow  in  colour, 
becoming  sometimes  black,  like  stout,  the  reddish  tinge  not  being 
seen  until  it  is  diluted,  when  it  shows  with  the  spectroscope  the  ab- 
sorption bands  of  oxy-  or  methaemoglobin — the  latter  only  if  the 
urine  has  stood  some  time.  The  reaction  is  faintly  alkaline,  and 
the  specific  gravity  is  often  less  than  normal.  A  considerable 
amount  of  sediment  falls  when  the  urine  is  left  to  stand.  This 
sediment  is  composed  of  dark  brown  granular  material,  which  is 
the  debris  of  the  broken-down  red  cells,  very  few  of  which  remain 
intact.  Haematoidin  crystals  are  sometimes  met  with.  On  boiling 
the  urine,  and  then  allowing  it  to  stand  for  some  time,  a  bright 
purple  colour  develops  (Plehn's  reaction).  If  some  of  the  urine  is 
made  alkaline  with  potash  and  then  boiled,  a  purple  colour,  due  to 
luemochromogen,  is  produced  (Stephens  and  Christophers'  reaction). 
The  urine  resists  decomposition  for  some  time. 

The  presence  of  urobilin  can  be  detected  by  acidulating  with  a 
little  acetic  acid,  extracting  with  amyl  alcohol,  and  examining  with 
a  spectroscope,  when  a  broad  band  to  the  red  side  of  F  will  be 
seen.  Bile  pigments  are  seldom  present,  and  may  be  recognized 
by  Gmelin's  or  Marechal's  reactions.  There  is  a  considerable 
amount  of  albumen  present  in  the  form  of  serum  albumen,  serum 
globulin,  and  nucleo-albumen.  Phosphates  are  said  to  be  diminished. 
The  haemosozic  value  is  higher  than  that  of  the  red  corpuslces  of 
the  blood. 

Symptomatology. — Usually  the  patient  has  resided  six  months  or 
longer  in  one  of  the  regions  mentioned  above,  and  naturally  has  had 
attacks  of  malarial  fever,  and  has  taken  quinine. 

Prodromata. — Prodromata  may  be  almost  entirely  absent,  but 
usually  the  patient  complains  of  lassitude,  pains  all  over  the  body, 
loss  of  appetite,  restlessness  at  night,  and  an  entire  lack  of  energy 
during  the  day,  and  a  yellowish  tinge  may  be  noted  in  the  con- 
junctivae or  skin  for  a  day  or  so. 

Attack. — Suddenly  the  patient  feels  chilly,  and  shivering  fits  may 
occur,  accompanied  by  headache,  severe  pains  in  the  back  and 
legs,  and  an  intense  feeling  of  weakness  and  nausea,  which,  as  a 
rule,  quickly  ends  in  retching  and  then  vomiting,  first  of  food,  and 
then  of  green  bile.  The  tongue  is  coated  with  a  dirty-yellowish  fur, 
and  there  is  much  thirst  and  constipation,  the  faeces  at  first  being 
dark-coloured,  and  often  scybalous. 

The  liver  and  spleen  are  enlarged  and  tender;  the  skin  is  hot  and 
dry,  and  if  not  already  tinged  yellow,  rapidly  becomes  so,  deepening 
in  tint  as  time  goes  on.  It  is  said  that  itching  is  sometimes  felt, 
but  we  have  never  noted  this.     The  conjunctiva:  are  tinged  yellow, 


i224  THE  TROPICAL  HEMOGLOBINURIAS 

like  the  skin.  The  temperature  rises  quickly  to  1030  or  1040  F., 
and  the  pulse  is  regular,  rapid,  small,  and  compressible.  At  first 
the  urine  may  appear  normal,  but  sooner  or  later  the  characteristic 
stout-like  colour  appears,  with  pains  in  the  back  and  burning  sen- 
sations in  the  urethra.  On  the  other  hand,  this  may  be  the  first 
feature  of  the  attack,  and  causes  the  patient  to  send  at  once  for  the 
doctor,  though  he  may  not  at  the  time  feel  ill,  or  it  may  occur  at 
the  height  of  the  fever,  as  Kelsch  points  out. 

The  mind  may  be  clear  or  the  patient  may  be  brought  to  the 
hospital  quite  unconscious,  and  may  remain  so  for  days,  or  delirium 
may  set  in.  After  a  few  hours  perspiration  appears,  and  the 
temperature  remits  to  about  ioo°  F.,  the  urine  clears,  and  a  mild 
case  may  recover,  while  in  a  severe  case,  instead  of  the  remission, 
hyperpyrexia,  coma,  and  death  may  ensue. 

Usually,  however,  after  the  remission  the  temperature  again 
rises  (post-haemoglobinuric  fever),  and  the  shiverings,  vomitings, 
and  pains  return,  while  diarrhoea,  with  motions  full  of  bile,  and 
sometimes  also  with  blood  or  haemoglobin,  comes  on.  A  motion 
with  haemoglobin  may  present  a  most  striking  appearance,  being 
mainly  green  in  colour,  with  a  reddish  deposit  on  the  surface. 

This  second  paroxysm  may  be  the  last,  or  it  may  be  succeeded 
by  several  others,  after  which  the  patient  may  recover.  On  the 
other  hand,  he  may  die  during  these  attacks  from  exhaustion,  or 
from  hyperpyrexia  and  coma,  or  from  anuria  and  uraemia. 

Convalescence. — After  the  attacks  the  patient  is  exceedingly 
weak,  and  convalescence  is  protracted,  and  is  liable  to  be  compli- 
cated at  any  time  with  anuria,  leading  to  fatal  uraemia. 

Varieties. — Kelsch  and  Kiener  recognize  two  distinct  types — a 
mild  and  a  severe,  of  which  the  latter  is  subdivided  into  three — 
viz.,  the  ordinary  severe,  the  fulminating  with  a  rapidly  fatal 
issue,  and  the  uraemic  type. 

Complications. — The  most  usual  complication  is  the  passage  of 
haemoglobin  or  blood  per  anutn,  giving  rise  to  '  dysenteric  motions/ 
as  they  are  often  called.  Muco-pus  is,  however,  generally  absent. 
Inflammation  of  the  tonsils  and  salivary  glands  has  been  noted. 

Sequelae. — There  is  nearly  always  grave  anaemia  and  much  weak- 
ness as  the  result  of  an  attack,  with  often  stomach  and  intestinal 
derangements,  but  of  all,  the  most  serious  is  nephritis,  leading  to 
uraemia. 

Diagnosis. — Blackwater  fever  is  easily  recognized,  as  a  rule,  the 
diagnosis  being  based  on  the  hemoglobinuria  with  high  fever  and 
jaundice,  and  the  severity  of  the  symptoms. 

The  differential  diagnosis  has  to  be  made  from  yellow  fever,  in 
which,  however,  there  is  never  haemoglobinuria.  Acute  yellow 
atrophy  of  the  liver  and  Weil's  disease  are  easily  distinguished  by 
the  urine,  which  does  not  contain  haemoglobin,  and  by  the  presence 
of  the  peculiar  spirochaete  in  the  blood  and  urine  of  the  latter 
disease. 

Quinine  haemoglobinuria  is  not  a  serious  disease,  and  can  be  readily 


PROGNOSIS  1225 

prevented  and  cured,  and,  moreover,  is  directly  associated  with  a 
dose  of  quinine.  Malarial  haemoglobinuria  closely  resembles  black- 
water  fever,  but  is  definitely  associated  with  subtertian  parasites  as 
a  rule,  and  much  more  rarely  with  other  forms  of  malarial  parasites. 

Prognosis. — The  mortality  in  our  experience  varies 'greatly,  being 
very  high  in  some  epidemics  and  low  in  others.  The  mortalities 
given  by  Skelton  are  as  follows:  F.  Plehn,  4  per  cent.;  A.  Plehn, 
6-8  per  cent.;  Stendel,  16  to  17  per  cent.;  Koch,  21  per  cent.; 
Berenger-Feraud,  23  to  24  per  cent.;  Schellong,  42  per  cent.: 
Reynolds,  50  per  cent. 

Bad  signs  are: — ■ 

1.  Persistent  vomiting. 

2.  Hiccough. 

3.  Profuse  diarrhoea. 

4.  High  fever. 

5.  Sudden  decrease  in  the  tension  and  increase 

in  the  frequency  of  the  pulse. 

6.  Diminution  or  cessation  of  urine. 

7.  Coma. 

Good  signs  are:  — 

1.  Little  gastrointestinal  disturbance. 

2.  Low  temperature. 

3.  Good  pulse. 

4.  Clear  mind. 

It  is  usually  said  that  a  person  should  not  return  to  the  tropics 
after  suffering  from  blackwater  fever,  but  many  people  do  return, 
and  appear  to  remain  in  excellent  health.  Of  course,  there  is  the 
great  risk  of  further  attacks. 

Treatment. — This  may  be  considered  under  the  following: — 

1.  During  the  attack. 

2.  After  the  attack. 

3.  Remarks. 

1.  During  the  Attack. — The  treatment  during  the  attack 
may  be  considered  under  the  headings  (a)  Recommended  Therapy, 
(b)  General  Treatment,  (c)  Diet,  (d)  Symptomatic  Treatment. 

Therapy  Recommended. — We  recommend  the  Sternberg-Hearsey 
treatment  in  cases  of  true  blackwater  fever,  as  distinguished  from 
quinine  haemoglobinuria  and  malarial  haemoglobinuria. 

This  treatment  consists  in  administering 

Liquor  hyJr.irgyvi  perchloridi  ..  ..      30  minims. 

Sodium  bicarbonate  ..  ..  ..      10  grains. 

Water   ..  ..  ..  ..  to  1  ounce. 

every  two  to  four  hours  during  the  first  twenty-four  hours,  and  then 
every  three  hours  until  the  urine  clears.  (For  details  as  to  the 
Sternberg  method  see  Chapter  XLII.) 


1226  THE  TROPICAL  HEMOGLOBINURIAS 

General  Treatment. — In  treating  the  disease,  the  important 
features  to  be  remembered  are  that  the  patients  are  often  infected 
with  malaria;  that  they  suffer  from  a  great  blood  destruction,  and 
therefore  from  great  weakness;  that,  as  a  result  of  the  blood  destruc- 
tion, a  severe  Strain  is  thrown  on  the  liver  and  kidneys,  and  that  the 
latter  are  apt  to  be  damaged  by  the  haemoglobin.  In  fact,  some 
people  think  that  the  haemolysis  takes  place  in  the  kidney,  but  in 
any  case  there  is  danger  of  blocking  of  the  renal  tubules,  of  nephritis, 
anuria,  and  uraemia.     Lastly,  the  disease  is  apt  to  relapse. 

From  the  very  commencement,  the  patient  must  be  put  to  rest 
in  bed,  and  have  careful  nursing.  A  most  important  matter  is  to 
flush  out  the  kidneys,  and  this  should  be  done  by  introducing  water 
into  the  body  in  some  way.  If  the  patient  can  take  liquids  by  the 
mouth,  use  soda-water,  albumen-water,  whey,  cold  or  warm  tea, 
barley-water,  or  toast -water,  in  quantity.  If  vomiting  is  such  that 
liquids  cannot  be  retained  by  the  stomach,  use  rectal  enemata  of 
warm  physiological  saline  solution  (0*9  per  cent,  of  common  salt 
in  water)  or  sterile  subcutaneous  injections  (temperature  98-4°  F. 
or  370  C.)  of  a  mixture  such  as  the  following : — 

Calcium  chloride  . .  . .  . .      4-5  grammes. 

Sodium  chloride  . .  . .  10  grammes. 

Distilled  water    ..  ..  ..  ..      1,000  c.c. 

One  hundred  to  two  hundred  cubic  centimetres  of  this  mixture, 
properly  sterilized,  may  be  used  two  or  three  times  a  day  as  a  sub- 
cutaneous injection  in  bad  cases. 

Adam  Patrick  recommends  the  intravenous  injection  of  a  1  per  cent,  sterile 
sodium  chloride  solution.  He  has  injected  as  much  as  3  pints  at  one  time. 
Bayliss'  Solution,  containing  6  per  cent,  gum  acacia  and  0*9  per  cent,  sodium 
chloride,  may  also  be  used. 

Diet. — The  diet  must  be  fluid,  preferably  in  the  form  of  whey, 
milk,  chicken-broth,  albumen-water,  and  Benger's  food;  but  strong 
meat-extracts  should  be  avoided. 

If  the  vomiting  is  troublesome,  and  there  is  no  diarrhoea,  rectal 
feeding  might  be  tried.     Plenty  of  aerated  water  should  be  allowed. 

The  condition  of  the  stomach,  liver,  and  kidneys  may  counter- 
indicate  stimulants  at  times,  but  there  is  no  doubt  of  the  value  of 
champagne  and  brandy  when  they  can  be  administered. 

Symptomatic  Treatment. —  Vomiting  may  be  relieved  by  sips  of 
iced  or  cooled  soda-water  or  champagne.  If  these  simple  remedies 
fail,  apply  a  mustard-leaf  to  the  pit  of  the  stomach.  Tincture  of 
iodine  in  a  strength  of  1  to  2  drops  in  an  ounce  of  cinnamon  water, 
and  administered  orally  several  times  a  day,  may  be  useful.  If  this 
fails,  hypodermics  of  morphine  must  be  tried,  but  it  must  be  ad- 
mitted that  we  do  not  like  to  administer  this  drug  in  blackwater  fever 
unless  compelled,  and  prefer  to  combine  atropine  with  it,  and  even 
then  to  give  as  little  as  possible.  Constipation  may  be  combated  by 
means  of  calomel  in  repeated  small  doses,  helped  if  necessary  by 
enemata.     Diarrhoea  should  not  be  too  rapidly  stopped,  but  if  it  is 


SYMPTOMATIC  TREATMENT  1227 

a  pressing  symptom,  weakening  and  disturbing  the  patient,  then 
tannic  acid  in  15  grain  doses,  tannalbin  in  15  grain  doses,  or  bismuth 
subnitrate  in  10-20  grain  doses,  may  be  administered  by  the  mouth, 
or  enemata  of  tannic  acid  given  by  the  rectum  if  there  is  also  much 
vomiting. 

The  heart's  action  should  be  carefully  watched,  and  may  require 
support  by  hypodermic  injections  of  digitalin  or  caffeine.  Calcium 
lactate,  having  a  tonic  effect  upon  the  heart,  and  being  also  useful 
for  other  reasons  in  this  disease,  may  be  given  in  10  grain  doses 
twice  or  three  times  a  day,  or  in  the  form  of  the  injection  mentioned 
above.  Extract  of  the  pituitary  gland  has  been  recommended  in 
cases  of  cardiac  failure. 

Malarial  parasites ,  when  present  in  the  blood,  require  treatment  by 
intramuscular  injections  of  quinine  bihydro chloride  (p.  1 188)  .preceded 
by  a  dose  or  two  of  calcium  lactate,  but  the  sulphate  or  bisulphate 
of  quinine  are  contraindicated,  and  should  not  be  employed. 

Pain  in  the  back  should  be  treated  by  hot  fomentations,  and  if 
these  fail  and  the  symptoms  be  urgent,  by  morphine  given  sub- 
cutaneously. 

Anuria  must  be  met  by  vapour  baths,  before  which  a  hypodermic 
injection  of  pilocarpine  may  be  given.  If  this  fails,  dry  or  wet 
cupping  of  the  lumbar  renal  area  must  be  tried,  and  must  be  helped 
by  oxygen  inhalations  if  available  and  by  free  purgation. 

Headache  may  be  relieved  by  cool  applications  to  the  head,  but 
special  drugs  must  not  be  given. 

2.  After  the  Attack. — If  the  patient  survive  the  attack  of 
true  blackwater  fever,  which  is  often  fatal,  he  should  be  allowed 
a  long  convalescence,  with  a  change  to  a  temperate  climate  if 
possible.  During  this  time  he  will  require  good,  wholesome,  nourish- 
ing food  and  slowly  graduated  exercise. 

One  attack  of  '  blackwater  fever  '  per  se  should  not  necessarily 
lead  to  the  permanent  invaliding  of  the  patient  from  the  tropics, 
though  he  should  be  warned  that  he  returns  thereto  at  his  own  risk. 
If,  however,  permanent  damage  to  any  organ  is  also  present,  this 
should  be  the  deciding  factor  in  stating  that  a  return  will  be 
dangerous. 

3.  Remarks. — Such  is  the  outline  of  the  treatment  which  we 

advise,  but  other  authors  have  different  views,  and  one  or  two 

of  these  may  be  briefly  mentioned : — 

Dr.  O'Sullivan-Beare  strongly  recommends  the  decoction  or  the  fluid  extract 
of  the  root  of  Cassia  beareana  Holmes  ;  the  latter  can  be  obtained  from 
T.  Christy  and  Sons,  Old  Swan  Lane,  Upper  Thames  Street,  London,  and  should 
be  administered  in  1  fluid  drachm,  well  diluted  with  water,  every  two  hours  at 
first,  and  afterwards  at  longer  intervals.  We  have  no  experience  of  this  drug, 
but  its  introducer  praises  it  highly,  stating  that  it  relieves  all  the  symptoms 
quickly.  Skelton  says  he  has  never  seen  it  do  any  good,  but  that  it  does  no 
harm.  So  well  is  the  disease  known  in  West  Africa  that  several  native  remedies 
exist.  With  regard  to  other  drugs,  atoxyl  is  said  to  be  useless.  Canthe  has 
used  turpentine  in  mild  attacks.  Nightingale  recommends  sodium  dimethyl- 
arsenate  administered  in  1 -grain  doses  thrice  dailv  until  the  temperature  is 
below  normal  for  twenty-four  hours.     It  is  stated  to  soothe  the  gastric  lrnta- 


1228  THE  TROPICAL  HEMOGLOBINURIAS 

tion  and  to  clear  the  urine.  Cholesterin  in  doses  of  i  gramme  has  been  given 
at  intervals  of  four  hours  until  two  to  three  or  four  doses  have  been  admin- 
istered. It  is  given  in  suspension  in  thick  milk,  or  as  intramuscular  injections 
in  olive  oil,  and  has  been  advocated  on  account  of  its  antihsemolytic  action. 

Prophylaxis. — Very  little  can  be  said  with  regard  to  the  prophy- 
laxis, as  the  knowledge  of  the  aetiology  is  incomplete.  As  black- 
water  fever  generally  develops  in  persons  who  have  suffered  from 
malaria,  quinine  prophylaxis  should  be  carried  out  in  the  manner 
already  described  in  the  chapter  on  Malaria  (Chapter  XL.,  p.  1204), 
attacks  of  malaria  being  treated  by  quinine  tannate  in  small  repeated 
doses,  or  the  drug  should  be  preceded  by  a  dose  of  calcium  lactate. 


REFERENCES. 

Modern  literature  will  be  found  to  be  ably  reviewed  in  the  Tropical  Diseases 
Bulletin. 

Balfour  (1913).     Journal  of  Tropical  Medicine  and  Hygiene,  p.  35.     London. 
Barratt  and  Yorke  (1909).     Annals  of  Tropical  Medicine  and  Parasitology, 

p.  1.     Liverpool. 
Berenger-Feraud  (1874-78).     De  la  Fievre  Bilieuse  Melanurique  des  Pays 

Chauds.     Paris,  1874. 
Berenger-Feraud  (1878).     De  la  Fievre  Bilieuse  Inflammatoire  aux  Antilles 

et  dans  l'Amerique. 
Cardamatis  (191 2).     Bulletin  de  la  Societe  de  Pathologie  Exotique,  p.  521. 

Paris. 
Castellani  (191 7).     Tropical  Diseases  in  the  Balkans,  Journ.  of  Trop.  Med. 
Christophers  and  Bentley  (1908).     No.  35,  Scientific  Memoirs.     India. 
Eyles  (1893).     Malarial  Fever  as  met  with  on  the  Gold  Coast.     Lancet, 

February  4. 
Fink  (1912).     Journal  of  Tropical  Medicine  and  Hygiene  (several  papers). 

London. 
Kelsch  and  Kiener  (1889).     Traite  des  Maladies  des  Pays  Chauds. 
Leishman  (1912).    Journal  of  the  Royal  Army  Medical  Corps,  p.  151.    London. 
Low  (1912).     Journal  of  Tropical  Medicine  and  Hygiene.     London.      No.  11, 

vol.  xv. 
Low   and    Wenyon    (191 3).      Journ.   of    Tropical    Medicine   and   Hygiene, 

No.  li,  vol.  xvi. 
Manson  (1918).     Tropical  Diseases.     London. 
McCay  (1908).     Glasgow  Medical  Journal,  March. 
Matko  (1918).     Wien.  Klin.  Woch.,  June  6. 
Patrick  (1918).     Brit.  Med.  Journ.,  October  12. 

Plehn,  A.  (1903).     Archiv  fur  Schiffs-  und  Tropen-Hygiene,  Bd.  vii.,  p.  541. 
Ross,    W.    G.,  and   Low    (1903).      Journ.   Trop.   Med.   and   Hyg.,   May    1. 

Experimental  Haemoglobinuria.  . 

Skelton  (1908).     Journal  Royal  Army  Medical  Corps,  June. 
Stephens  (1903).     Thompson  and  Yates  and  Johnston,  Laboratory  Reports, 

vol.  v.,  part  i.,  217. 
Stephens    (1907).     Allbutt   and    Rolleston's    System   of   Medicine,    vol.   ii., 

part  ii.,  p.  289. 
Stephens  (1907).     Osier's  System  of  Medicine,  i.  448. 
Stephens  and  Christophers.     Reports  to  the  Royal  Society,  Series  I.,  V., 

and  VIII. 
Tomaselli  (1897).     La  intossicazione  chinica  e  l'infezione  malarica.     Catania, 

1897. 
Vincent  (1906).     Bull.  Societe  de  Biologie,  December,  1906. 
Yorke  and  Nauss  (191  i).     Annals  of  Trop.  Med.  and  Parasit.,  p.  2S7. 


CHAPTER  XLII 
YELLOW    FEVER 

Synonyms — History — Climatology — /Etiology — Pathology — Symptomatology 
— Diagnosis — Prognosis — Treatment — Prophylaxis — References. 

Synonyms.- — -Bilious  Remittent  fever,  Acclimatizing  fever,  Inflammatory 
fever,  Febris  Flava,  Pestis  Americana,  Typhus  Icteroides.  French  :  Fievre 
Jaune.  Italian  :  Febbre  Gialla,  Febbre  Amarilla.  German  :  Gelbfieber.  In 
addition,  there  are  a  large  number  of  local  names,  such  as  Bulam  fever 
(Grenada);  Kendal's  disease  (Barbados);  Pest  of  Havana  (Cuba);  Maladie  de 
Siam  (Martinique) ;  Febre  remittente  biliosa  dos  bezos  quentes  (Brazil) ;  Febre 
amarelle  dos  acclimatados  (Brazil);  Magdalena  fever  (Columbia). 

Definition. — An  acute  specific  non-contagious  fever  of  unknown 
causation  characterized  usually  by  two  paroxysms  of  fever,  separ- 
ated by  a  remission  or  intermission,  and  accompanied  with  albumin- 
uria, jaundice,  and  haemorrhages,  with  usually  a  normal  number 
of  leucocytes  and  polymorphonuclear  leucocytes.  It  is  spread  by 
the  agency  of  Stegomyia  calopus  Meigen,  1818  (synonym,  S.  fasciata 
Fabricius,  1805,  non  O.  F.  Miiller,  1764). 

History. — Yellow  fever  is  believed  to  have  originally  been  a 
disease  of  the  Antilles,  and  to  have  attacked  the  troops  of  Christopher 
Columbus  in  1495  in  the  Isle  of  Spain  (St.  Domingo),  from  which  it 
was  carried  by  the  Spaniards  to  the  mainland  of  America.  The 
endemic  home  of  the  disease  at  the  present  time  is  the  east  coast 
of  Mexico,  where  it  was  reported  in  1509  at  Vera  Cruz,  and  Central 
America  from  Cape  Tampies  to  Cape  Gracias  a  Dios,  and  the  Greater 
and  Lesser  Antilles.  From  this  area  it  can  spread  by  ships  to  various 
parts  of  the  world,  where  it  may  become  epidemic. 

The  first  clearly  written  description  of  yellow  fever  is  that  by 
P.  du  Tertre,  in  Guadeloupe,  in  1635,  but  it  soon  became  wett 
known  from  the  epidemic  in  Cuba  in  1648-49;  Jamaica,  1655; 
San  Domingo,  1656;  Martinique,  1688;  and  Vera  Cruz,  1690.  In 
1698  it  was  recognized  that  the  disease  was  being  carried  from  place 
to  place  by  ships,  and  a  quarantine  ordinance  was  brought  into 
force,  which  lasted  from  1709  till  1790,  when  the  extensive  wars 
of  the  period  caused  it  to  be  ineffective,  with  the  result  that  between 
1791  and  1815  most  extensive  epidemics  took  place,  and  gave 
ample  opportunity  for  the  study  of  the  disease.  In  1794  Drysdale, 
of  Baltimore,  in  1797  and  1805  Rush,  in  Philadelphia,  and  in  1802 
Vaughan,  in  Wilmington,  drew  attention  to  the  large  numbers  of 
mosquitoes  and  other  insects  which  abounded  in  their  respective 

1229 


1230  YELLOW  FEVER 

towns  during  yellow-fever  epidemics,  though  rare  in  preceding 
years.  With  regard  to  bilious  remittent  fever,  a  good  account 
of  this  disease  was  given  in  1842  by  Burton  in  the  first  volume  of  the 
British  Medical  Journal  (then  called  the  Provincial  Medical  Jour- 
nal). In  1848  Nott,  of  Mobile,  accused  some  insect  or  mosquito 
of  being  the  possible  carrier  of  yellow  fever.  In  1876  Dowell, 
of  Galveston,  showed  that  mosquitoes  and  yellow  fever  obeyed 
the  same  natural  laws,  and  in  1878  it  was  demonstrated  in  Mobile 
that  quarantine  of  the  patients,  together  with  sulphur  fumigation, 
could  control  the  epidemic.  But  it  was  not  till  1881  that  Charles 
Finlay,  of  Havana,  directly  attributed  the  spread  of  the  disease  to 
the  mosquito.  In  1882  Gererd,  having  caused  a  mosquito  to 
suck  the  blood  of  a  patient  on  the  fourth  day  of  the  fever,  then 
allowed  it  at  once  to  bite  his  hand,  with  the  result  that  he  developed 
in  due  course  a  mild  attack  of  yellow  fever.  The  credit  of  having 
supported  the  mosquito  theory  for  many  years  in  numerous  publica- 
tions belongs  to  Finlay. 

In  1883  Freire,  of  Rio  de  Janeiro,  thought  that  he  had  discovered 
the  cause  of  the  disease  in  the  shape  of  a  micrococcus,  and  later 
C.  Valle,  C.  Finlay,  and  Gibier  each  described  specific  bacteria. 
Sternberg  studied  the  disease  for  years,  but  could  find  no  definite 
bacterial  or  other  cause.  He,  however,  in  a  certain  number  of 
cases,  came  across  a  bacillus,  which  he  called  '  X. '  In  1897  Sanarelli 
announced  that  he  had  found  a  bacterium  (Bacillus  icteroides) 
which  he  believed  to  be  the  cause  of  the  disease,  and,  further,  he 
prepared  a  serum  for  its  treatment.  Sanarelli's  findings  were  at 
first  confirmed  by  a  large  number  of  observers. 

In  1900  Reed  and  Carroll  announced  that  Bacillus  X  belonged  to 
the  colon  group  of  bacteria,  andZ?.  icteroides  to  the  hog-cholera  group, 
and  was  probably  identical  with  B.  cholera  suis.  In  our  experience 
B.  icteroides  is  not  identical  with  B.  cholera  suis,  but  is  a  distinct 
species,  although  it  plays  no  part  in  the  aetiology  of  the  malady, 
and  is  merely  the  cause  of  a  secondary  infection.  In  the  same 
year  Reed,  Carroll,  Agramonte,  and  Lazear  proved  that  the  disease 
could  be  produced  by  the  subcutaneous  injection  of  infected  blood 
into  a  non-immune  person;  that  the  disease  was  not  contagious, 
and  was  only  spread  by  the  bites  of  Stegomyia  calopus.  The  agency 
of  the  mosquito  was  speedily  confirmed  by  Guiteras,  Ribas  and  Lutz, 
Marchoux,  Salimbeni  and  Simond,  Parker,  Beyer  and  Pothier,  and 
later  by  Rosenau,  Parker,  Francis  and  Beyer. 

In  1903  Parker,  Beyer,  and  Pothier  concluded  that  the  aetiological  cause 
was  Myxococcidium  stegomyice,  found  in  infected  mosquitoes,  which  they 
believed  to  be  an  animal  parasite  closely  resembling  a  Coccidium.  Carroll, 
however,  refuted  this,  as  did  Marchoux,  Salimbeni,  and  Simond,  and  finally 
Rosenau,  Parker,  Francis,  and  Beyer  clearly  proved  that  M.  stegomyice  was 
a  yeast  normally  found  in  mosquitoes. 

In  1905  Rosenau,  Francis  and  Beyer  showed  that  the  disease 
could  be  communicated  by  the  inoculation  of  infected  blood  filtered 
through  the  closest-grained  Pasteur-Chamberland  B  filter  which 


HISTORY 


1231 


they  could  obtain,  and  therefore  came  to  the  conclusion  that  the 
causal  agent  of  the  disease  must  be  of  ultramicroscopic  size. 

In  1909  Seidelin  described  the  presence  of  minute  bodies  (Paraplasma 
flavigenum)  in  the  red  cells  of  persons  suffering  from  yellow  fever,  but  these  are 
not  believed  to  have  anything  to  do  with  yellow  fever.  Low  and  Wenyon 
have  shown  that  Seidelin's  bodies  are  common  in  the  blood  of  young 
guinea-pigs. 


-  ^Kf  \  f  &     mm 


Fig.  628. — Map  of  the  Distribution  of  Yellow  Fever.  (After  Newstead.) 


/ 


1 1 1 i_ 


Fig.  629. — The  Distribution  of  Stegomyia  calopus.     (After  Newstead.) 

The  theory  of  the  propagation  of  the  disease  by  Stegomyia 
calopus  has  been  put  to  the  practical  test  of  prophylaxis  with  most 
excellent  results  in  Havana,  Texas,  Mexico,  and  New  Orleans,  and 
in  the  works  of  the  Panama  Canal.  The  late  Sir  Rubert  Boyce 
did  excellent  work  in  drawing  attention  to  the  yellow  fever  of 
West  Africa,  where  it  is  extremely  deadly  at  times,  and  which  is 
probably  a  secondary  endemic  centre. 


1 1 3 a  YELLO W  FEVER 

It  is  impossible  to  close  this  history  without  drawing  the  reader's 
at  t  cut  ion  t  o  t  he  groat  benefit  conferred  upon  mankind  by  the  labours 

of  Reed,  Carroll,  Agramonte,  and  La/ear.  the  last  named  dying 
from  yellow  fever  following  an  experimental  bite  of  an  infected 
mosquito, 

Climatology.— As  already  stated,  the  endemic  area  includes  a 
portion  of  the  Atlantic  coasts  of  Mexico  and  Central  and  South 
America,  as  well  as  the  Antilles.  Some  of  the  more  important 
endemic  centres  at  the  present  time  are  Guatemala,  Spanish  Hon- 
duras, Nicaragua,  Costa  Rica.  Salvador,  French  Guiana,  Dutch 
Guiana,  along  the  Rivers  Magdalena,  Orinoco,  and  Amazon,  and  in 
Ecuador.  There  is  evidence  that  the  Cape  Verde  Islands  were  in- 
fected in  1510-15,  and  that  the  Gulf  of  Benin  received  its  yellow 
fever  from  this  source  in  1520,  and  it  is  possible  that  it  has  been 
endemic  on  the  West  Coast  of  Africa  from  that  date.  Boyce  was  of 
the  opinion  that  it  has  been  a  disease  of  Africa  from  time  immemor- 
able,  but.  though  these  early  historical  points  cannot  satisfactorily 
be  settled,  there  is  more  evidence  that  the  true  home  is  Central 
America,  and  that  Africa  is  a  secondary  endemic  area,  in  which  very 
serious  outbreaks  have  been  recorded  in  the  past,  and  where  the 
disease  is  at  times  epidemic. 

From  the  endemic,  centre  the  disease  can  spread  by  the  agency 
of  ships  until  it  reaches  460  ^  N,  (Quebec)  and  340  54'  S.  (Monte 
Video);  which  correspond  to  the  isotherm  of  6oc  F.  (l6°  C.)  for  the 
mean  temperature  of  the  hottest  month  of  the  year.  At  its  northern 
limits  the  disease  is  generally  very  mild,  but  at  its  southern  limits 
it  may  be  very  severe. 

The  areas  most  usually  affected  arc  the  Atlantic  coasts  of  North 
America,  as  far  north  as  Charleston  (320  40'  N.\  and  of  South 
America  as  far  south  as  Rio  de  Janeiro  (22°  54'  S.).  Another  region 
commonly  affected  is  the  West  Coast  ^i  Africa  from  Senegambia  to 
Saint  Fan!  de  boa  do. 

Europe  has  frequently  been  attacked-  -e.g.,  England  ^Swansea1*  in 
r.865,  France  in  1861,  Spain  and  Portugal  in  the  eighteenth  and 
nineteenth  centuries,  the  last  infection  being  in  Madrid  in  1878, 
and  Italy  (Leghorn)  in  1804. 

The  disease  has  apparently  more  than  once  reached  the  Pacific, 
for  it  spread  in  1740  to  Guayaquil,  in  Ecuador,  and  in  1854  to  Fern. 

fhe  distribution  corresponds  with  that  of  Stegomyia  calopus,  and 
the  fact  that  the  disease  is  endemic  in  warm  climates  and  more 
marked  in  the  hot  season,  while  it  disappears  in  the  winter  of 
temperate  climates,  reappearing  in  the  summer,  coincides  with  the 
habits  of  the  mosquito.  Further,  the  facts  that  it  is  carried  by 
infected  ships  and  that  it  may  affect  low-lying  regions  near  the  coast , 
particularly  ports,  in  which  the  dwelling-houses  are  especially 
attacked,  are  explicable  by  its  mosquito  transmission. 

It  appears  to  us  that  the  fever  associated  with  black  vomit,  found  among 
children  in  '  Grande  terre.'  Guadeloupe,  must  either  be  a  form  of  yellow  fever 
or  closely  allied  to  it.  though  possibly  some  cases  may  be  confused  with  the 


ETIOLOGY  1233 

vomiting  sickness  of  Jamaica,  in  which  black  vomit  is  absent  (p.  1695).  At 
the  same  time  it  is  interesting  to  note  the  general  similarity  between  pappataci 
fever,  dengue,  and  yellow  fever,  which  appear  to  form  a  group  of  closely  allied 
diseases. 

Yellow  fever  has  been  recorded  by  Hudellet  at  Dinguira,  Mahina, 
Ouida,  between  Kayes  and  the  Niger  in  the  Sudan,  while  cases 
h  ive  been  recorded  in  Java. 

/Etiology. — -The  causal  agent  exists  in  the  blood  of  an  infected 
person,  as  can  be  proved  by  the  fact  that  the  subcutaneous  inocula- 
tion of  o-i  c.c.  of  the  infected  blood  into  non-immune  persons 
pro  luces  attacks  of  the  disease,  but  it  cannot  be  spread  to  man  by 
post-mortem  wounds.  This  causal  agent  appears  to  be,  at  least  in 
one  of  its  stages,  of  exceedingly  small  size,  for  diluted  blood  filtered 
through  a  Pasteur-Chamber  land  B  bougie  can  still  cause  the  disease 
if  inoculated  intravenously  into  a  non-immune. 

According  to  Seidelin,  it  is  a  small  protozoon  [Paraplasma  flavigenum 
Seidelin,  1909)  found  in  the  red  blood  cells,  but  the  parasitic  forms  described 
by  this  author  are  now  considered  to  be  artefacts. 

It  is  obviously  a  living  organism,  and  not  a  chemical  substance, 
because  of  the  time  it  takes  to  develop  in  man  and  the  mosquito, 
for  the  incubation  period  in  man  is  usually  three  days.  The  mos- 
quito, in  order  to  become  infected,  must  bite  a  patient  during  the 
first  three  days  of  his  illness,  and  then  fourteen  days  must  elapse 
before  the  infected  mosquito  can  transmit  the  disease. 

The  proof  of  the  transmission  of  the  disease  by  Stegomyia  calopus 
was  worked  out  by  Reed,  Carroll,  Agramonte,  and  Lazear,  by  con- 
structing a  gnat-proof  building  divided  into  two  gnat-proof  com- 
parl  ments,  into  the  first  of  which  infected  mosquitoes  were  liberated 
and  allowed  to  bite  a  non-immune,  while  other  non-immunes  slept 
in  the  second  compartment.  The  man  in  the  first  compartment 
developed  an  attack  of  yellow  fever,  while  the  others  did  not. 

Non-immunes  living  in  gnat-proof  houses,  with  articles  of  clothing 
and  bedding  soiled  with  urine,  faces,  black  vomit,  etc.,  from  cases 
of  yellow  fever,  did  not  contract  the  disease,  though  after  this 
experiment  was  finished  some  were  infected  by  means  of  the  bites 
of  infected  mosquitoes,  thus  proving  that  they  were  not  immune. 

Marchoux  and  Simond  extended  this  knowledge  by  showing  that 
a  Stegomyia  can  live  for  some  thirty  days,  and  lay  seven  batches  of 
eggs.  Those  laid  after  the  twelve  days'  incubation  by  an  infected 
mosquito  are  also  infected,  and  can  transmit  the  contagium  vivum 
to  a  second  generation  of  mosquitoes,  but  these  cannot  infect  non- 
immunes until  fourteen  days  after  hatching  as  imagines. 

Tiie  new  generation  of  Stegomyia  were  fed  upon  glucose,  and  were 
made  to  bite  a  recent  non-immune  arrival  in  Brazil,  but  no  infection 
followed.  A  week  later  the  same  mosquito  was  allowed  to  bite 
the  same  person,  who  then  developed  a  typical  attack  of  yellow  fever, 
from  which  he  subsequently  recovered  and  was  found  to  be  immune. 

This  is  believed  to  indicate  that  a  mosquito  requires  a  feed  of  blood 
before  it  can  produce  infection. 

78 


1234  YELLOW  FEVER 

It  is  also  stated  that  before  a  stegomyia  can  lay  eggs  she  must 
have  a  feed  of  blood,  the  eggs  being  laid  three  days  later,  after  which 
she  is  said  to  feed  only  at  night,  while  before  this  she  feeds  during 
the  day  and  during  the  night.  f- 

From  this  it  is  argued  that  any  stegomyia  which  bites  in  the  day- 
time can  have  only  immature  parasites,  and  therefore  cannot 
produce  an  infection. 

A  mosquito  can  produce  yellow  fever  some  fifty-seven  days  after 
infection,  which  appears  to  become  more  virulent  the  longer  it 
remains  in  the  insect,  especially  if  the  air  temperature  is  270  to  280  C. 

Further,  the  contagium  vivum  can  apparently  only  exist  in  man 
and  Stegomyia  calopus,  though  it  is  true  that  a  chimpanzee,  after 
an  incubation  of  three  days,  suffered  from  a  typical  attack  of  yellow 
fever,  induced  by  experimental  mosquito-bites,  as  was  shown  by 
Thomas  in  1907.  No  other  mosquito  so  far  has  been  proved  to 
carry  the  infection.  It  appears,  also,  that  the  development  in  the 
mosquito  depends  to  some  extent  upon  the  air  temperature,  as  in 
the  case  of  the  malarial  parasite. 

Thomas  has  succeeded  in  producing  a  reaction  in  a  chimpanzee  five  days 
after  infection  by  the  bite  of  an  infected  Stegomyia,  and  in  guinea-pigs  from 
four  and  a  half  to  thirteen  days  after  being  bitten  by  infected  Stegomyia. 
It  must  be  remembered  that  in  yellow  fever  epidemics  it  is  stated  that  dogs 
and  fowls  are  supposed  to  be  ill,  but  from  what  cause  is  unknown.  Manson 
has  suggested  that  the  disease  may  be  kept  up  by  animals. 

The  aetiology  may  therefore  be  summarized  by  saying  that  the 
causation  is  an  animal  parasite,  living  in  the  blood  stream  of  man 
and  in  the  body  of  Stegomyia  calopus  Meigen,  18 18  (S.  fasciata 
Fabricius,  1805,  non  O.  F.  Miiller,  1764),  by  the  bites  of  which  it  can 
be  transmitted  to  man  and  the  chimpanzee.  The  blood  of  the  in- 
fected man  is  transmissive  only  during  the  first  three  to  four  days. 
Stegomyia  calopus  begins  to  be  infective  fourteen  days  after  the 
transmissive  feed,  and  remains  infective  for  at  least  another  forty- 
three  days,  and  it  has  been  claimed  that  it  can  pass  on  the  infection 
to  its  young,  which  require  a  feed  of  blood  before  the  virus  bcccmes 
infective.  During  this  non-infective  period  they  bite  dirring  the 
daytime,  but  do  not  after  their  first  feed  and  the  deposition  of  their 
first  eggs.  It  is  possible  that  other  species  of  Stegomyia,  in  the 
future,  may  be  found  to  be  carriers  as  well  as  S.  calopus. 

Unfortunately,  according  to  Theobald,  it  is  necessary  to  change  the  old 
name  Stegomyia  fasciata  Fabricius,  1805,  to  S.  frater  Desvoidy,  1827,  or  to 
S.  calopus  Meigen,  1818,  though  there  is  some  doubt  as  to  whether  the  latter, 
which  is,  of  course,  the  older  term,  really  applies  to  the  insect  we  know  as 
S.  fasciata.  The  reason  for  this  change  is  because  the  term  fasciata  was  used 
by  O.  F.  Miiller  in  1764  (not  by  de  Villers,  often  wrongly  spelt  Villiers)  for  a 
Culex  distinct  from  S.  fasciata  Fabricius,  1805.  More  recently  there  seems 
to  be  some  doubt  as  to  the  correctness  of  the  new  term — that  is,  S.  calopus — 
and  a  return  to  the  old  term,  S.  fasciata,  may  be  necessary. 

Spirochete. — In  1909'  Stimson,  reported  the  presence  of  a  spiro- 
chete in  yellow  fever  [S.  interrogans  Stimson,  1909),  but  no  im- 
p  >rtance  was  given  to  thi?  observation.  Recently  Noguchi  has 
cultivated  from  the  blood  of  several  cases  a  spirochcete  somewhat 


PATHOLOGY  1235 

similar  to  5.  ictcroluemorrhagice,  and  has  named  it  Leptospira 
icteroides. 

Pathology. — In  yellow  fever  the  cells  of  the  liver  swell,  and, 
pressing  upon  the  bile  capillaries,  obstruct  the  flow  of  bile  and 
cause  a  hepatogenous  jaundice,  characterized  by  yellow  staining 
of  the  skin  and  tissues,  and  by  the  presence  of  bile  in  the  urine. 
Further,  the  swelling  blocks  the  intralobular  capillaries,  causing 
congestion  of  all  the  viscera  drained  by  the  portal  vein,  but  especially 
of  the  pyloric  end  of  the  stomach  and  the  duodenum,  because  of 
the  arrangement  of  the  veins  from  those  parts.  This  stagnation 
of  the  blood  may  allow  a  secondary  bacterial  infection  to  take 
place,  which  shows  its  effect  on  the  intestine  and  spleen. 

The  liver  cells  degenerate  so  extensively  in  bad  cases  as  to  cause 
the  urea  function  to  be  considerably  lessened  in  activity,  and  thereby 
a  condition  of  ammoniaemia  comes  about,  which  produces  most 
serious  toxic  effects  upon  the  brain  and  other  organs.  In  addition, 
the  disease  in  some  way  seriously  affects  the  endothelial  lining  of 
the  blood  capillaries,  producing  haemorrhages  in  various  parts  of 
the  body.  If  these  leading  features  of  the  pathology  are  borne  in 
mind,  the  post-mortem  appearances  and  the  symptomatology  will 
be  easily  understood. 

An  attack  generally  confers  a  lasting  immunity  upon  a  person, 
and  second  attacks  are  rare,  and  it  appears  that  the  so-called 
racial  immunity  of  people  living  in  endemic  regions  is  really  an 
acquired  immunity,  due  to  mild  attacks  in  childhood.  Relative 
immunity  can  be  acquired  by  inoculation  of  infected  blood  heated 
to  550  C.  for  five  minutes.  Further,  it  is  found  that  the  serum  of 
a  convalescent  has  some  protective  power. 

The  Blood. — There  is  no  marked  alteration  in  the  numbers  or 
appearance  of  the  erythrocytes,  even  in  fatal  cases.  A  few  normo- 
blasts are  said  to  be  present  at  times.  On  the  other  hand,  there  is  a 
decided  loss  of  haemoglobin,  though  this  is  rarely  much  reduced  in 
the  first  three  or  four  days;  and  haemoglobinaemia  is  said  to  occur 
in  fatal  cases  before  death.  But  this  does  not  appear  to  coincide 
with  the  fall  of  specific  gravity,  which  may  be  present  without  loss 
of  haemoglobin. 

The  leucocytes  do  not  appear  to  be  distinctly  increased  in  numbers, 
varying  from  3,200  to  20,000  per  cubic  millimetre,  the  increase, 
when  present,  being  largely  caused  by  polymorphonuclear  leuco- 
cytes. The  coagulation  of  the  blood  is  diminished,  and  ammoni- 
aemia  is  thought  to  be  present  in  bad  cases. 

The  Urine. — Albumen  appears  early — as  a  rule,  on  the  second 
day — and  increases  in  quantity  remarkably,  especially  in  severe 
cases.  During  convalescence  it  may  disappear,  or  may  last  for 
months.  Bile  is  present  about  the  fifth  or  sixth  day,  and  red  blood 
cells  may  also  occur,  though  leucocytes  are  rather  rare.  Casts  are 
present — first  hyaline,  then  granular,  and  finally  epithelial.  Urea 
is  diminished  in  bad  cases,  and  the  diazo-reaction  is  believed  to  be 
absent  in  uncomplicated  cases. 


1236  YELLOW  FEVER 

The  Vomit. — The  vomit  is  often  distinguished  as  white,  red,  and 
black.  The  white  is  acid,  colourless  or  bile-stained,  and  is  composed 
largely  of  mucus.  The  red  vomit  containsbright  blood,  while  theblack 
is  acid,  containing  hydrochloric  acid,  epithelial  cells,  red  corpuscles, 
fat,  debris,  and  micro-organisms,  its  colour  being  duetothe  presence 
of  haemoglobin,  turned  to  acid  haematin  by  the  hydrochloric  acid. 

Morbid  Anatomy. — The  skin  is  yellow  from  bile-pigment,  and 
blotched  with  post-mortem  lividity  and  haemorrhages.  The  mucosa 
of  the  tongue  is  fissured,  and  the  mouth  may  be  covered  with  blood. 
The  liver  is  yellowish  or  brownish  in  colour,  marked  by  haemorrhages. 
The  cells  are  swollen  and  in  a  state  of  advanced  fatty  degeneration. 
The  gall-bladder  contains  inspissated  bile,  sometimes  mixed  with 
blood.  The  spleen  is  normal  in  size,  but  may  be  congested  and  soft. 
The  stomach  and  intestines  may  be  full  of  blood,  usually  in  the  form 
of  a  black  homogeneous  tarry  fluid  containing  black  particles,  and  the 
mucosa  of  the  stomach,  especially  that  of  the  pylorus  and  duodenum, 
is  usually  much  swollen,  and  the  mesenteric  glands  may  sometimes 
be  enlarged.  The  kidneys  are,  as  a  rule,  normal  in  size,  and  show 
signs  of  some  congestion.  Bowman's  capsules  are  said  to  be  dilated, 
but  this  is  not  constant.  The  cells  of  the  tubules  show  fatty  de- 
generation, and  the  lumen  may  contain  granular  debris.  The  supra- 
renal capsules  may  be  hyperaemic  or  show  fatty  degeneration,  but 
neither  of  these  is  constant,  and  hyperaemia  or  fatty  degeneration 
of  the  pituitary  body  and  the  thyroid  gland  have  been  described, 
but  are  not  important.  The  bladder  is  usually  empty.  The  heart 
shows  ecchymoses,  and  effusions  may  be  found  in  the  pericardium. 
The  lungs  may  be  congested,  and  haemorrhages  may  be  found  beneath 
the  pleura.  The  uterine  mucosa  is  congested,  and  there  may  be 
blood  in  the  cavity.  The  meninges  of  the  brain  are  congested,  and 
haemorrhagic  spots  may  be  seen. 

Symptomatology — Incubation. — An  exact  knowledge  of  the  length 
of  the  incubation  period  is  of  the  utmost  importance  from  a  pro- 
phylactic point  of  view.  Calculated  from  experimental  mosquito 
bites,  it  varies  from  two  days  twenty-two  hours  to  seven  days  five 
hours,  but  the  latter  figure  was  in  a  man  who  had  had  a  mild  attack. 
With  regard  to  the  former  period,  it  is  the  shortest  actual  record, 
but  some  more  doubtful  figures,  as  low  as  two  days  one  hour,  are 
given.  Excluding  the  man  with  the  slight  attack,  the  incubation 
period,  as  generally  given  by  American  observers,  would  be  from 
two  days  twenty-two  hours  to  six  days  two  hours,  Marchoux. 
Salimbeni,  and  Simond  consider  that  the  incubation  may  be  as  long 
as  twelve  days,  and  draw  this  conclusion  from  inoculation  of  modified 
blood  serum,  and  also  from  natural  infection.  Carter's  careful 
clinical  records,  however,  give  the  incubation  period  as  varying  from 
three  to  five  and  three-quarter  days.  L 

UTlie  average  time  appears  to  be  about  five  days,  but  to  be  on  the 
safe  side  at  least  six  to  seven  days  must  be  allowed. 

The  Fever. — The  fever  is  divisible  into  two  paroxysms,  separated 
by  a  remission  or  intermission.     The  first  attack  is  characterized 


SYMPTOMATOLOGY  1237 

by  headache,  pale,  then  flushed,  face,  injected  eyes,  and  pains  in 
the  body,  and  after  the  second  day  albuminuria;  while  the  second 
attack  shows  the  jaundice  from  which  the  disease  obtains  its  name, 
and  the  haemorrhages,  of  which  black  vomit  and  black  motions  form 
such  ominous  signs. 

Onset. — Prodromata  are  usually  absent,  but  general  malaise  may 
be  felt  for  some  little  time  previously.  The  attack  begins  with  a 
sensation  of  coldness,  with  or  without  rigors,  and  with  severe  frontal 
headache,  pains  in  the  back  and  limbs,  while  the  face,  at  first  pale, 
becomes  flushed  and  painful,  the  skin  congested,  the  eyes  brilliant 
and  injected,  and  photophobia  is  often  present.  The  temperature 
rapidly  rises  to  1030  F.  or  more;  the  respiration  quickens  and  is 
laboured;  the  pulse  is  quick,  full,  and  bounding,  reaching  to  100  or 
120  per  minute.  The  appetite  is  lost,  and  there  is  usually  vomiting, 
associated  with  pain  and  tenderness  in  the  region  of  the  pylorus,  and 
usually  const ipat ion. __  The  urine  is  generally  diminished,  acid  in 
reaction,  with  a  high  specific  gravity,  and  albumen  is  present  from 
the  first  or  second  day.  Its  passage  may  cause  a  sensation  of  burn- 
ing.    During  this  stage  there  is  often  insomnia. 

Intermission. — On  the  second  to  fourth  day  the  remission  sets  in, 
the  temperature  either  dropping  with  a  crisis,  accompanied  by 
sweating,  to  normal,  or  remitting  to  about  100°  F.,  the  flush  and 
pains  disappearing.  In  the  former  case  the  disease  ends  and  con- 
valescence begins.  More  usually,  however,  after  a  few  hours'  re- 
mission, during  which  the  patient  feels  much  better  and  sleeps  well, 
the  temperature  again  rises  to  1040  or  1050  F. ;  but  a  most  char- 
acteristic feature,  called  '  Faget's  sign,'  now  shows  itself,  in  that  the 
pulse  does  not  increase  in  rapidity  as  the  temperature  rises.  On  the 
contrary,  as  days  go  on,  the  pulse-rate  tends  to  become  slower  and 
slower,  without  regard  to  the  temperature.  This  sign  depends  upon 
the  severity  of  the  case,  being  most  noticeable  in  severe  types,  in 
which  it  may  be  only  70  to  60  per  minute,  though  associated  with 
a  high  temperature. 

Second  Attack. — During  the  second  attack  all  the  symptoms  of 
the  first  paroxysm  return,  but  the  congestion  of  the  skin  is  not  so 
marked,  and  the  yellow  tint  of  jaundice  appears  for  the  first  time, 
and  deepens  as  the  illness  proceeds.  The  vomiting  and  tenderness 
in  the  stomach  return,  and  are  associated  now  with  much  thirst 
and  prostration.  The  tongue  is  dry  and  furred,  with  red  tip  and 
edges.  Haemorrhages  may  now  occur  from  the  nose,  mouth,  or 
uterus,  and  the  bad  signs  of  black  vomit  and  melaena  may  appear. 
The  urine  diminishes  in  quantity,  and  the  albumen  increases.  In 
bad  cases  its  excretion  may  totally  cease.  There  is  generally  much 
restlessness,  and  often  delirium. 

Terminations. — Two  courses  are  now  possible.  The  first  is  that 
after  three  to  four  days'  illness  the  temperature  may  decline,  the 
urine  increase  in  amount,  the  albumen  diminish,  and  the  vomiting 
gradually  cease;  while  sweating  may  occur,  and  the  patient,  passing 
into  a  deep  sleep,  awakens  on  the  road  to  convalescence.     The  second 


1238  YELLOW  FEVER 

is  that  the  temperature  does  not  decline,  the  jaundice  deepens, 
haemorrhages  appear  under  the  skin,  and  from  the  regions  indicated 
above,  hiccough,  subsultus  tendinum,  clammy  sweats,  anuria, 
coma,  and  convulsions  lead  to  death,  which  may,  however,  take 
place  before  the  full  development  of  these  symptoms  by  cardiac 
or  respiratory  failure. 

Varieties. — Three  varieties  may  be  recognized,  though  some 
authors  describe  more.  These  are  the  mild,  the  severe,  and  the 
malignant.  The  mild  type  consists  of  simply  the  first  paroxysm, 
in  which  the  temperature  does  not  rise  above  1020  F.,  the  urine 
contains  albumen,  and  the  fever  ceases  by  crisis  on  the  second  or 
third  day.  The  severe  type  shows  the  characters  given  above  as 
typical  for  the  disease.  The  malignant  tjTpe  begins  with  high  fever, 
1050  to  1070  F.,  with  violent  vomiting  and  the  early  appearance 
of  black  vomit  and  melaena,  when  the  patient  quickly  becomes 
delirious,  and  dies  in  the  initial  fever. 

Complications. — Any  pre-existing  pathological  condition  is  serious 
in  yellow  fever,  but  renal  and  cardiac  affections  are  perhaps  the  worst. 
Gangrene,  abscesses,  congestion  of  the  lungs,  and  intussusception 
are  possible  complications  arising  in  the  course  of  the  disease. 

SequelaB, — Boils  and  abscesses,  dysentery  and  hepatitis,  are  the 
common  sequels,  but  usually  convalescence  is  not  complicated  or 
protracted. 

Prognosis. — The  mortality  is  very  variously  given,  usually  10  to 
25  per  cent,  for  the  United  States  and  Europe,  and  45  to  80  per 
cent,  for  the  endemic  area  and  West  Africa.  The  extremes  are 
0-5  to  94*5  per  cent. 

All  cases  of  yellow  fever  must  be  considered  serious,  especially 
if  complicated  with  pre-existing  disease,  and  constant  care  must 
be  taken  to  measure  the  daily  quantity  of  urine  passed,  and  to 
estimate  the  amount  of  albumen;  for  marked  diminution  of  the 
urine,  especially  anuria,  is  a  grave  sign.  High  temperatures,  black 
vomit,  melaena  and  other  haemorrhages,  and  marked  disturbance 
of  the  nervous  system,  are  all  bad  omens. 

According  to  Sternberg,  if  the  temperature  does  not  rise  over 
1030  F.  the  prognosis  is  usually  good. 

Diagnosis. — The  typical  symptoms  in  an  epidemic  will  hardly  be 
mistaken  for  any  other  disease,  but  the  mild  early  case  is  very  diffi- 
cult to  recognize.  The  best  signs  for  a  positive  diagnosis  are  the 
early  albuminuria,  the  epigastric  tenderness,  and,  later,  the  jaun- 
dice, with  Faget's  sign,  and  the  black  vomit. 

Differential  Diagnosis.- — The  most  important  diseases  to  differen- 
tiate in  the  first  stage  are  dengue,  subtertian  malaria,  blackwatcr 
fever,  and  relapsing  fever.  Dengue  may  be  recognized  by  the 
absence  of  albuminuria,  the  preliminary  rash,  and  leucopenia; 
subtertian  malaria  by  the  parasites  in  the  blood,  and  in  some  cases 
the  typical  four-hourly  temperature  chart ;  blackwater  fever  by  the 
haemoglobin  in  the  urine  and  the  mononuclear  increase;  relapsing 
fever  by  the  parasites  in  the  blood  and  the  leucocytosis. 


TREATMENT  1239 

Treatment. — There  is  no  specific  remedy  known  for  yellow  fever. 
The  usual  treatment,  if  the  patient  is  seen  on  the  first  or  second 
day,  is  to  give  repeated  small  doses  of  calomel  until  3-5  grains 
have  been  administered,  and  then  a  draught  of  magnesium  sulphate 
and  sodium  sulphate.   Then  employ  Sternberg's  mixture,  which  is : — 

Sodium  bicarbonate  . .  . .  . .      150  grains. 

Perchloride  of  mercury      . .  .  •  . .  £  grain. 

Water    ..  ..  ..  ..  ..        60  ounces. 

This  is  given  in  three  tablespoonful  doses  every  hour. 
General  Treatment. — As  the  cause  of  the  disease  is  unknown,  the 
treatment  must  aim  at  the  prevention  of  the  spread  of  the  infection, 
the  rapid  elimination  of  the  toxins,  and  the  alleviation  of  the 
symptoms.  To  prevent  the  spread  of  the  disease,  the  patient's  bed- 
room must  be  rendered  gnat-proof.  The  excretion  of  the  toxins 
must  take  place  by  the  bowels,  skin,  and  kidneys,  and  therefore 
it  is  necessary  to  encourage  the  action  of  all  three.  The  action  of 
the  bowels  can  be  maintained  by  enemata  of  1  tablespoonful  of 
sodium  sulphate  dissolved  in  a  pint  of  warm  water,  and  given 
morning  and  night. 

When  there  is  severe  headache,  a  hot  mustard  foot-bath  may  be 
given,  which  should  relieve  the  head.  After  this  the  patient  is 
warmly  wrapped  up  in  blankets,  care  being  taken  that  he  is  not 
oppressed  by  the  clothing,  for  only  those  who  have  been  seriously 
ill  can  appreciate  how  embarrassing  the  weight  of  heavy  blankets 
is  to  the  heart.  It  is  hoped  that  by  these  means  the  action  of  the 
skin  will  be  stimulated. 

In  order  to  dilute  the  toxins,  and  at  the  same  time  to  stimulate 
the  action  of  the  kidneys,  an  alkaline  treatment,  with  plenty  of 
fluid,  is  required.  This  can  be  effected  by  administering  2  to 
4  quarts  of  iced  Celestin  variety  of  Vichy  water  in  the  twenty- 
four  hours,  or  the  same  quantity  of  any  alkaline  mineral  water, 
to  each  pint  of  which  30  grains  of  sodium  bicarbonate  have  been 
added;  or  by  Sternberg's  mixture  as  recommended  above;  or  an 
effervescing  drink  can  be  made  up  of  sodium  bicarbonate  and  fresh 
lime-juice,  but  care  should  be  taken  that  this  is  mixed  in  such 
quantities  as  to  be  neutral,  and  it  may,  if  necessary,  be  combined 
with  sodium  sulphate.  If  this  alkaline  treatment  cannot  be  given 
by  the  mouth,  then  the  bicarbonate  of  soda  must  be  administered 
as  warm  enemata. 

Symptomatic  Treatment. — As  regards  symptoms,  if  there  is  great 
pain,  this  can  be  relieved  by  a  small  dose  of  phenacetin,  while 
severe  lumbar  pain  may  be  relieved  by  hot  fomentations;  but  if  no 
urine  is  passing,  the  warm  mustard  bath  will  be  better. 

Vomiting  is  treated  by  sips  of  iced  Vichy,  iced  champagne,  a 
blister  to  the  pit  of  the  stomach,  a  dose  of  a  mixture  containing 
chloroform,  or  a  hypodermic  injection  of  morphia.  If  there  is 
much  fever,  this  must  be  treated  by  cool  sponging  and  cool  applica- 
tions to  the  head. 

Black  vomit  should  be  treated  by  the  application  of  the  ice-bag 


1 240  YELLOW  FEVER 

to  the  pit  of  the  stomach,  and  haemorrhages  in  general  should  be 
met  with  doses  of  calcium  chloride  or  hypodermic  injections  of 
adrenalin  or  ergotin. 

In  these  bad  cases  it  is  advised  by  some  authors  to  rub  olive  oil 
into  the  skin  in  quantity,  with  a  view  of  ladening  the  endothelial 
cells  of  the  blood  capillaries  with  fatty  particles,  and  so  protecting 
them  against  the  action  of  the  toxins. 

Anuria  requires  treatment  by  hot  fomentations  to  the  loins,  or 
cupping  and  hot-air  baths,  and  Carroll  recommends  the  injection  of 
15  grains  of  urea,  either  hypodermically  or  by  the  rectum,  with  a  view 
to  stimulating  renal  activity,  on  the  ground  that  in  these  bad  cases 
the  production  of  urea  by  the  liver  is  not  sufficient  for  that  purpose. 

Cardiac  failure  requires  hypodermic  injections  of  strychnine, 
camphor  dissolved  in  ether  or  oil,  or  simply  ether. 

Diet. — No  food  should  be  given  for  two  or  three  days,  but  only 
the  alkaline  drinks,  and  champagne  if  necessary,  the  idea  being  to 
relieve  the  stomach  and  prevent  the  accumulation  of  waste  products 
in  the  system,  and  so  to  save  the  kidney  from  too  much  work. 

After  this  time,  or  if  the  temperature  is  below  1020  F.,  milk  and 
lime-water,  toast -water,  and  barley-water  may  be  given.  With 
a  view  to  saving  tissue  waste  and  getting  fat  into  the  circulation, 
pure  frozen  cream,  cold  white  wine-jelly  or  lemon-jelly,  should 
be  given,  or  olive  oil  administered  by  the  mouth  or  rubbed  into  the 
skin,  as  indicated  above. 

After  the  temperature  has  been  normal  for  some  three  days, 
chicken-broth,  custard-pudding,  blanc-mange,  etc.,  can  be  tried, 
and  a  few  days  later  the  diet  can  be  gradually  increased. 

Strong  beef  extracts  and  strong  alcoholic  stimulants  should  be 
avoided,  the  best  stimulant  being  iced  champagne  in  tablespoonful 
doses. 

Prophylaxis.— Yellow  fever  is  generally  conveyed  from  one 
place  to  another  by  ships,  but  in  order  to  produce  an  epidemic 
several  factors  are  necessary — viz.,  cases  of  the  disease  from  which 
Stegomyia  calopus  may  become  infected,  together  with  conditions 
of  temperature,  moisture,  etc.,  suitable  for  the  development  of 
the  germ  in  the  mosquito,  and  also  for  the  propagation  of  the 
mosquito  itself,  together  with  the  presence  of  non-immune  people 
for  the  mosquito  to  infect.  It  is  also  necessary  to  bear  in  mind 
that  the  incubation  period  is  usually  from  three  to  six  days,  and 
therefore  quarantine  must  be  of  at  least  five  days,  or,  to  be  on  the 
safe  side,  of  six  or  seven  days'  duration.  In  order  thai  the  mos- 
quito mav Jbecom 0.  i n fort P(\  it  must  bite  a  patient  'during  the  first 
filree"  days  of  the  illnessL  and  another  fourteen  days  must  elapse"* 
bet  ore  it  is  able  to  infect  non-immunes.'  Therefore  an  infected 
ship  must  be  anchored  at  least  a  quarter  of  a  mile  from  the  shore 
and  from  other  ships.  The  sick  must  be  placed  in  mosquito-proof 
rooms,  the  crew  quarantined  for  at  least  six  to  seven  days,  and  the 
whole  ship  disinfected  by  a  Clayton's  disinfector,  preferably  be- 
tween  9  a.m.   and  3  p.m.,  while  the  mosquitoes  are  quiescent. 


PROPHYLAXIS  1 241 

Dock-labourers  working  on  suspected  or  disinfected  ships  should  live 
in  special  gnat-proof  buildings,  and  be  under  medical  supervision. 

With  regard  to  an  infected  area,  it  must  be  remembered  that 
Stegomyia  calopus  is  essentially  domestic  in  its  habits,  that  it  is 
active  from  2  p.m.  till  early  morning,  but  that  it  is  quiescent  between 
the  hours  of  9  a.m.  and  2  p.m.,  when,  therefore,  visits  can  be  made 
to  infected  areas  without  risk.  Further,  the  mosquito  is  known 
to  bite  dead  bodies  and  suck  the  blood,  but  this  will  seldom  infect 
it,  as  a  patient  generally  lives  longer  than  the  three  days  during 
which  the  disease  can  be  communicated  to  the  mosquito.  Lastly, 
it  can  pass  through  a  screen  with  fifteen  meshes,  but  not  through 
one  with  twenty  meshes  to  the  inch. 

The  mosquito  does  not  die  after  laying  its  eggs,  but  lives  until 
it  has  laid  seven  batches — i.e.,  some  thirty  days.  The  eggs  laid 
twelve  days  after  infection  are  capable  of  carrying  the  infection 
into  the  second  generation,  which  can  spread  the  disease  fourteen 
days  after  becoming  imagines.  As  the  mosquito  is  believed  to  be 
non-infective  when  it  bites  in  the  daytime,  non-immunes  may  visit 
an  endemic  area  in  the  day  with  impunity,  but  must  not  stay  late 
in  the  afternoon. 

When  a  person  is  moved  from  an  infected  room,  disinfection 
should  be  begun  at  once.  All  cracks,  openings,  etc.,  should  be 
closed  with  paper,  and  fumigation  carried  out,  preferably  by  means 
of  sulphur  dioxide  gas,  or  if  there  is  an  objection  to  this  because 
of  the  damage  it  causes,  pyrethrum  may  be  used,  but  must  be 
burned  in  the  proportion  of  1  pound  to  1,000  cubic  feet  of  air- 
space if  the  mosquitoes  are  to  be  merely  stupefied,  and  2  pounds 
if  they  are  to  be  killed;  or  tobacco,  1  pound  per  1,000  cubic  feet, 
may  be  used. 

In  addition,  if  an  epidemic  is  to  be  eradicated,  cases  must  be  at 
once  notified  to  the  central  authority,  and  patients  must  be  strictly 
treated  in  mosquito-proof  rooms,  and  every  person,  immune  or 
non-immune,  must  use  mosquito-curtains,  while  an  anti-mosquito 
scheme  on  the  lines  mentioned  under  Malaria  must  be  undertaken. 
Special  care  must,  however,  be  taken  to  eradicate,  after  a  careful 
survey,  all  the  breeding-places,  not  forgetting  those  in  old  tins, 
eocoanut-shells,  gutters,  small  pools,  etc.  In  endemic  areas,  houses 
and  public  buildings  should  be  rendered  gnat-proof.  Lastly,  when 
an  epidemic  breaks  out  in  any  place,  it  may  be  taken  for  granted 
that  the  importation  took  place  at  least  two  to  three  weeks  prior 
to  the  discovery,  for  this  is  the  time  required  for  the  incubation  of 
the  germ  in  the  mosquito  and  in  man;  and  it  may  also  be  assumed 
that  mild  cases  are  probably  being  treated  for  influenza  or  malaria. 
Therefore  a  house-to-house  visitation  is  almost  necessary,  in  order 
to  find  out  the  extent  of  the  outbreak. 

Given  a  free  hand  and  plenty  of  money,  there  should  bo  no 
difficulty  in  dealing  with  a  threatened  epidemic,  but  the  public 
must  be  won  over  to  assist,  and  offenders  must  be  fined  for  trans- 
gressions against  sanitation,  as  is  done  by  the  Americans  in  Panama, 


1242  YELLOW  FEVER 

the  offences  being  the  presence  of  mosquito  larvse,  imperfect  screen- 
ing of  the  house,  accumulation  of  water,  etc. 

The  prophylactic  measures  may  be  summarized  as  follows: — 

A.  Where  there  is  reason  to  believe  that  yellow  fever  is  endemic. 

(i)  Segregation  of  non-immunes,   partial  or  complete,  town  plan- 
ning. 

(2)  Screening: — 

(a)  The  bed. 

(b)  The  veranda. 

(c)  The  house. 

(3)  Systematic  mosquito  destruction  : — 

(a)  Removal  of  breeding-places. 

(b)  Screening  of  water  cisterns. 

(c)  Oiling. 

(d)  Drainage. 

(e)  Bush  clearing. 

(4)  Education.     Infliction  of  fines  for  transgressions. 

(5)  Quarantine  administration. 

(6)  Non-immunes  only  to  visit  endemic  area  in  the  daytime. 

B.  Where  yellow  fever  has  broken  out. 

(1)  Removal   of  all  non-immunes   outside  the  infected   area,   and 

deflection  of  the  traffic  outside  the  infected  area. 

(2)  Isolation  of  cases  and  suspected  cases. 

(3)  Provision  for  isolation  of  contacts. 

(4)  Early  notification. 

(5)  Fumigation. 

(6)  Emergency  mosquito  measures  : — 

(a)  Removal  of  receptacles. 

(b)  Oiling. 

(c)  Screening. 

(d)  Drainage. 

(7)  Education : — 

(a)  Lectures. 

(b)  Meetings. 

(c)  Pamphlets. 

(8)  General  organization  of  the  medical  forces. 

No  anxiety  need  now  be  felt  as  to  the  spread  of  yellow  fever 
to  Asia  though  the  Panama  Canal  has  been  opened,  for  it  appears 
as  though  not  merely  yellow  fever,  but  all  infectious  and  con- 
tagious fevers  are  bound  to  be  eradicated  from  the  Canal  zone 
under  the  able  American  rule. 


REFERENCES. 

The  Tropical  Diseases  Bulletin  and  the  Bulletins  of  the  Yellow  Fever 
Institute,  Treasury  Department,  United  States  iPublic  ^Health  and  Marine 
Hospital  Service,  and  of  the  old  Yellow  Fever  Bureau  in  Liverpool  (publica- 
tion ceased  after  1915).  are  most  important,  and  the  last  named  embraced 
dengue  and  pappataci  fever  also. 

A.  B.  (1804).  Prospetto  sulla  origine,  natura,  e  carattere  della  peste,  di 
contagi  della  febbre  gialla  di  America.     8vo.  br.     Lucca. 

Agramonte  (1912).     New  York  Medical  Journal. 

Augustin  (1909).     History  of  Yellow  Fever.     New  Orleans. 

Bally,  M.  (1823).  Histoire  M6dicale  de  la  Fievre  Jaune  observee  en  Espagne 
et  particuli^rement  en  Catalogne  dans  l'Annle  1821.  8vo.  m.p.  Paris. 
Imprim.  Royale. 


REFERENCES  1243 

Balme,  A.  (1822).     Observations  et  Reflexions  sur  les  causes,  les  symptomes, 

et  le  traitement  de  la  Contagion  dans  differentes  maladies  et  specialement 

dans  la  peste  d'Orient  et  la  Fievre  Jaune.     8vo.     Paris:  Lyon. 
Bancroft,  Ed.  Nat.  (1811).     An  Essay  on  the  Disease  called  Yellow  Fever, 

with  Observations  concerning  Febrile  Contagion,   Typhus,   Dysentery, 

and  the  Plague,  partly  delivered  as  the  Gulstonian  Lectures  before  the 

College  of  Physicians,  in  the  Years  1806  and  1807.    8vo.  cart.     London: 

T.  Cadel  and  W.  Davies. 
Berenger-Feraud  (1890).     La  Fievre  Jaune.     Paris. 
Blane,  Gilberto  (1820).    Elementi  di  Logica  Medica  illustrati  da  esempji  e 

prove  di  Fatto.     Contenenti  un  Esposizione  della  Febbre  Gialla.     Trad. 

dall'  Inglese.     8vo.  m.p.     Pisa. 
Bonneau,  J.  D.,  et  Sulpicv,  Eng.  (1823).     Recherches  sur  la  Contagion  de 

la  Fievre  Jaune  en  rapprochement  des  Faits  et  des  Raisonnements  les 

propres  a  l'eclairer  cette  Question.     8vo.     Paris. 
Boyce(iqii).     Yellow  Fever  and  its  Prevention.     London.     (1910).     Health 

Progress  and  Administration  in  the  West  Indies. 
Cailliot,    Louis    (1815).     Traite   de   la   Fievre    Jaune.     8vo.   m.p.     Paris: 

Megnignon. 
Carroll  (1902).     Journal  of  the  American  Medical  Association,  p.  117. 
Clarke  (1797).     Yellow  Fever.     London. 

Dariste  (1825).    Recherches  pratiques  sur  la  Fievre  Jaune.    8vo.  m.p.    Paris. 
Febbre  (1824).    Ricerche  Patologiche  sulla  Febbre  di  Livorno  del  1814.   Sulla 

Febbre  Gialla  Americana  e  sulle  Malattie  di  Genio  Analogo.     8vo  m.p. 
Fievre  Jaune  (1853).    Second  Rapport  sur  la  Quarantaine;  Conseil-General 

de  Santi.     8vo.  cart.     London:  Eyre  et  Spottiswoode. 
Low,   G.  C.   (1902).     Differential  diagnosis  oi  Yellow  Fever  and  Malignant 

Malaria.     Brit.  Med.  Journ.,  September  20. 
Manzini,  N.  B.  (1858).     Histoire  de  lTnoculation  preservative  de  la  Fievre 

Jaune    pratiquee   par   ordre   du   Gouvernement    Espagnole    a  l'Hopital 

Militaire  de  la  Havane.     8vo.     Paris  :  J.  B.  Bailliere  et  Fils. 
Marchoux,  Salimbeni,  and  Simond  (1903).     Ann.  d'Hyg.  et  de  Med.     Colon. 
Noc  (1912).     Rev.  Hyg.  Sanit. 

Noguchi  (1919).     Journ.  Exp.  Med.,  vol.  xxx.,  No.  1. 
O'Halloran,   Thomas   (1822).     A   Brief  View  of  the   Yellow   Fever   os   it 

appeared  in  Andalusia  during  the  Epidemic  of  1820,  together  with  the 

Mode  of  Treatment  adopted,  and  an  Account   of   the  Appearances  on 

Dissection.     8vo.  cart.     London:  Burgess  and  Hill. 
Pallani,  G.  (1804).     Parere  Medico  sulla  Malatia  febbrile  che  ha  dominato 

nella  citta  di  Livorno  l'Anno.     Firenze. 
Parker,  Beyer,  and  Pothier  (1903).     A  Study  of  Yellow  Fever.     Wash- 
ington. 
Reed,  Carroll,  and  Agramonte  (1901).     Journal  of  the  American  Medical 

Association. 
Rho  (1906).     Annali  Med.  Navale. 
Rochoux,  J.  A.  (1822).     Recherches  sur  la  Fievre  Jaune  et  Preuves  de  sa 

Non-contagion  dans  les  Antilles.     8vo.  br.     Paris:  Berchet  Jeune. 
Seidelin  (1912).     Yellow  Fever  Bureau  Bulletin. 
Stimson  (1909).     Transactions,  Society  Tropical  Medicine. 
Thomas  (1909).     Transactions,  Society  Tropical  Medicine. 
Tommasini,  G.  (1805).  Sulla  Febbre  Gialla  Americana,  sulla  Febbre  di  Livorno 

e  sulle  Malattie  di  Genio  Analogo.     8vo.  m.p.     Parma:  Luigi  Massi. 
Tommasini,   G.   (1834).     Ricerche  Patologiche   sulla   Febbre  di  Livorno  del 

1814.     Sulla  Febbre  Gialla  Americana  e  sulle  Malattie  di  Genio  Analogo. 

8vo.     Firenze:  A.  M.  Cardinali. 
Torrigiani.  F.  (1805).     Della  Febbre  Gialla.     Pisa. 
Towne  (1762).     Diseases  of  the  West  Indies.     London. 
Warren  (1740).     Malignant  Fever  in  Barbadoes. 
Wsnyon  and  Low  (1914).     Journ.  Trop.  Med.  and  Hyg.,  December  15 


CHAPTER  XLIII 
DENGUE  AND  ALLIED  FEVERS 

Dengue — Seven   days'   fever — Dengue-like   fevers — References. 

DENGUE. 

Synonyms. — Febris  Endemica  cum  Roseola,  Exanthesis  Athrosia,  Knok- 
kelkoorts,  Arthrodynie,  Fievre  Rouge,  and  probably  the  'seven  days'  fever.' 

There  are  upwards  of  one  hundred  known  synonyms  for  this  fever,  many 
of  which  refer  to  it  as  a  form  of  rheumatism,  or  give  it  fanciful  terms,  such  as 
'  breakbone  '  or  '  breakheart,'  '  broken  wing  '  or  '  giraffe  fever.'  It  is  some- 
times called  '  three  days'  fever,'  a  term  by  which  pappataci  fever  is  also 
known . 

The  word  '  dengue  '  is  said  by  Vambery  to  be  of  Arabic  origin,  and  to  mean 
weakness,  but  it  might  equally  be  of  East  African,  Indian,  or  Spanish  origin. 

Definition. — Dengue  is  a  term  covering  one  or  more  acute  specific 
non-contagious  fevers  of  unknown  origin,  but  caused  by  a  virus 
contained  in  the  blood.  It  is  characterized  by  two  febrile  paroxysms, 
separated  by  an  intermission  or  remission,  without  jaundice,  albu- 
minuria, or  haemorrhages,  and  with  a  marked  leucopenia,  and  a  pulse 
which  varies  directly  with  the  temperature.  It  is  spread  by  the 
agency  of  Stegomyia  calopas  Meigen,  1S18,  and  probably  by  Culex 
fatigans  Wiedemann,  1828. 

History. — It  appears  to  have  been  first  recognized  at  Batavia,  in 
Java,  in  the  year  1779,  by  Bylon,  though  it  may  have  been  noted 
by  Pazzio  previous  to  this  in  1764-68  in  an  epidemic  in  Seville. 
It  was  soon  discovered  in  other  places,  being  found  from  1779  to 
1780  in  Egypt,  Arabia,  Persia,  and  North  America,  and  in  1784  in 
Spain,  to  which  it  appears  to  have  come  from  the  West  Indies,  and 
in  1818  in  Peru.  In  1824-28  it  occurred  all  over  the  tropical  and 
subtropical  zones,  and  in  1830-70  it  formed  a  series  of  large  and 
small  epidemics  in  the  same  regions.  From  1871-73  there  was 
an  epidemic  implicating  East  Africa,  Egypt,  Arabia,  India,  Burma, 
Indo-China,  and  China,  and  spreading  later  to  America  and  North 
and  West  Africa — i.e.,  practically  to  all  the  tropical  regions.  In 
1876-88  it  was  epidemic  in  Hong  Kong,  Egypt,  Syria,  and  the 
Mediterranean,  and  in  the  Fiji  Islands  in  1885,  to  which  it  was 
conveyed  by  a  European  suffering  from  the  complaint.  In  1889 
it  was  especially  prevalent  in  Asia  Minor,  Turkey,  and  Greece. 
From  1890  to  1895  there  were  outbreaks  in  Senegambia  and  Hong 
Kong,  and  in  1894  it  was  introduced  into  North  Queensland.  From 
1895-96  there  were  epidemics  in  Bombay  and  in  Charleston.     In 

1244 


HISTORY  1245 

1897-98  it  was  epidemic  in  Georgia,  Florida,  and  Texas.  In  1901 
it  occurred  in  Penang  and  Asia  Minor;  in  1902  in  Hong  Kong, 
Singapore,  Madras,  Rangoon,  and  Upper  Burma.  In  1906  it 
occurred  in  Saigong  on  a  French  warship,  and  recently  it  has  been 
prevalent  in  Singapore,  West  Australia,  and  Ceylon.  Manson  says 
that  an  epidemic  or  pandemic  takes  place  about  once  in  twenty  years. 

The  discovery  of  the  disease,  therefore,  appears  to  have  been 
first  made  by  Pazzio  and  Bylon,  and  the  first  full  clinical  description 
given  by  Dickson  in  1828. 

The  first  attempt  to  find  a  causation  for  the  disease  was  by 
McLaughlin  in  1886,  who  found  micrococci  in  the  blood,  but  this 
was  disproved  by  Klein,  Wright,  Crookshank,  and  Macfadyen.  In 
1903  Graham  stated  that  he  had  observed  small  hyaline,  unstainable 
rods  or  dots  in  the  red  blood-corpuscles,  which  he  considered  to  be 
protozoal  parasites  of  the  nature  of  Plasmodia.  This  discovery 
has  been  refuted  by  Carpenter  and  Sutton,  Guiteras,  Agramonte, 
Kicwiet  de  Jonge  and  Hahn,  Still  and  Ashburn,  and  Craig.  Graham 
fed  Culex  fatigans  Wiedemann  on  patients  suffering  from  dengue, 
and  claimed  to  have  found  his  parasites  in  these  mosquitoes  up  to 
the  fifth  day  after  feeding.  He  did  not  find  any  ookinetes  or 
oocysts,  but  he  says  he  found  spores  in  the  cells  of  the  salivary 
glands  of  the  mosquitoes  from  forty-eight  hours  to  one  month 
after  they  had  fed  on  infected  blood.  Further,  he  states  that  he 
caused  a  typical  attack  of  dengue  by  injecting  subcutaneously  a 
solution,  in  normal  saline,  of  the  salivary  glands  of  a  mosquito 
which  had  bitten  a  dengue  fever  patient  twenty-four  hours  pre- 
viously. He  only  performed  one  experiment,  because  the  illness 
caused  was  very  severe,  but  he  succeeded,  after  an  incubation  of 
four  to  six  days,  in  infecting  healthy  people  by  the  bites  of  mos- 
quitoes [Culex  fatigans)  fed  on  dengue  fever  patients. 

Though  Ashburn  and  Craig  (in  1907)  have  not  supported  Graham 
by  finding  the  parasite,  they  have  supported  him  by  proving  that 
a  typical  attack  of  dengue  can  be  produced  by  the  intravenous 
inoculation  of  filtered  and  unfiltcred  blood  from  an  infected  patient, 
and  that  the  disease  can  be,  and  usually  is,  transmitted  by  the  bite 
of  Culex  fatigans  Wiedemann. 

In  1912  and  1913  Laloir  drew  attention  to  Stegomyia  calopus  as 
the  carrier  of  dengue.  Cleland,  Bradley,  and  McDonald  demon- 
strated that  the  virus  of  dengue  fever  was  carried  by  Stegomyia 
calopus,  in  which  it  underwent  development  Archibald  found  that 
the  same  insect  was  the  only  possible  carrier  in  certain  parts  of 
the  Sudan.  These  observations  support  Legendre's  earlier  views 
with  reference  to  Hanoi.  The  leucocytic  formula  has  been  carefully 
studied  by  Ashburn  and  Craig  and  by  Archibald. 

Climatology. — The  history  of  the  disease  indicates  roughly  its 
geography,  which  lies  mostly  in  the  tropics,  but  can  extend  to 
the  subtropcal  zones.  Cases  have  been  reported  from  Southern 
Europe.  Its  usual  boundaries  are  320  47'  N.  and  230  23'  S.,  but 
during  warm  weather  it  may  spread  to  360  io'  N.,  and  even  to 


1246  DENGUE  AND  ALLIED  FEVERS 

420  N.  and  280  S.  in  exceptional  cases.  It  is,  therefore,  a  disease 
of  tropical  climates,  and  of  warm  weather  in  other  climates.  It 
appears  to  be  favoured  by  low-lying  lands  near  the  sea,  well 
supplied  with  water,  and  not  to  be  found  at  high  altitudes  ;  but 
there  are  exceptions  to  this.  It  occurs  in  Australia,  where  it  has 
appeared  since  1885,  and  is  common  in  the  Anglo-Egyptian  Sudan 
and  along  the  Red  Sea. 

When  the  distribution  of  dengue  is  compared  with  that  known 
for  Culex  fatigans,  it  will  be  seen  that  the  two  coincide  most  re- 
markably. In  fact,  at  the  present  time  it  appears  as  though  the  geo- 
graphical distribution  depends  upon  the  distribution  of  that  insect, 
together  with  the  importation  or  presence  of  infected  persons. 

/Etiology. — We  are  indebted  to  Graham  and  Ashburn  and  Craig, 
and  to  Cleland,  Bradley,  and  McDonald,  for  our  knowledge  of  the 
aetiology  of  this  disease. 

There  appears  to  be  no  doubt  that  dengue  fever  is  caused  by  some 
unknown  living  organism  which  requires  over  two  days  to  increase 
so  as  to  produce  the  symptoms  of  the  disease  when  inoculated  into 
human  beings,  and  generally  five  to  nine  and  a  half  days  when 
produced  by  bites  of  an  infected  stegomyia. 

Both  Graham  and  Ardate  have  observed  small  bodies  in  the  red  blood- 
corpuscles,  which  are  described  as  small,  usually  round,  but  sometimes 
elongated,  bodies  about  one-fifth  to  one-third  of  the  size  of  a  red  corpuscle. 
They  divide  up  into  minute  granules,  which  become  extra-corpuscular. 

This  organism  exists  in  the  blood,  as  can  be  shown  by  the  intra- 
venous injection  of  20  c.c.  of  dengue  fever  blood  producing  typical 
attacks  of  the  disease,  the  incubation  usually  being  two  to  three 
days;  but  it  is  so  small  that  it  will  pass  through  the  pores  of  a  filter 
which  will  retain  Micrococcus  melitensis,  which  is  only  0-4  //.  in 
diameter,  as  is  demonstrated  by  the  production  of  the  disease  by 
intravenous  injections  of  filtered  dengue  fever  blood,  the  incubation 
being  two  or  three  days,  as  before.  It  may  also  be  present  in  the 
lymphatic  glands,  the  gland  juice  being  at  times  infective,  as  proved 
by  experiments. 

Blood  is  infective  from  two  to  eight  days,  but  not  after  the  four- 
teenth day,  and  the  virus  is  said  to  be  transmitted  by  the  bites  of 
Culex  fatigans,  which  is  thought  to  be  an  agent  in  the  spread  of  the 
disease,  but  Cleland,  Bradley,  and  McDonald's  experiments  have 
thrown  considerable  doubt  on  this.  There  may,  however,  be  two 
distinct  diseases,  one  caused  by  a  stegomyia  and  one  by  a  culex, 
the  incubation  period  being  about  three  days  sixteen  hours.  It  can 
also  be  transmitted  by  the  bites  of  Stegomyia  calopus,  when,  further, 
there  is  a  natural  immunity  against  the  disease  in  some  people,  and 
also  some  degree  of  acquired  immunity  of  unknown  duration  obtained 
by  an  attack. 

The  points  in  the  aetiology  which  require  further  research  are  the 
nature  of  the  organism  and  its  chemical  products;  the  changes,  if 
any,  which  the  parasite  undergoes  in  the  mosquito;  the  length  of 
time  during  which  the  mosquito  can  carry  the  infection;  whether  any 


SYMPTOM  A  TOLOG  Y  1247 

mosquito  other  than  Culex  fatigans  and  Stegomyia  calopus  can  spread 
the  disease  ;  and  how  long  the  acquired  immunity  lasts  in  man. 
In  conclusion,  it  may  be  said  that  there  is  no  evidence  of  infection 
other  than  by  the  bite  of  mosquitoes,  and  there  is  no  evidence  that 
a  monkey  can  be  infected  by  inoculation. 

Pathology. — There  is  but  little  that  can  be  written  on  this  subject, 
as  the  cause  of  the  disease  is  unknown,  and  therefore,  of  course,  its 
action  cannot  be  explained. 

Morbid  Anatomy. — This  appears  restricted  to  the  description  of  the 
complication  which  killed  the  person — viz.,  peritonitis  or  pleuritis. 

Symptomatology. — The  incubation  period,  judging  from  experi- 
mental infection  by  niosrpaiTo^^sT^axies  from  three  to  six  days 
in  the  case  of  cule^and  five  to  nfn^ancTa  nail  clays  m  tne  casejof 
stegomyja.  Proctromata  areusiiAHy  absent,  but  general  malaise 
maybe  f  elTctuTiiig  a  pci  iarTnoTexceeding  three  days  before  the  onset. 

The  attack  is  usually  sudden,  and  introduced  by  severe  pain  in 
some  part  of  the  body,  or  merely  by  the  sensation  of  extreme 
fatigue,  or  by  chilliness  and  shivering,  or  by  deep  flushing  of  the 
face.  In  children  convulsions  or  delirium  may  usher  in  the  illness. 
In  any  case  the  temperature  rapidly  rises,  the  pulse  quickens,  and 
the  skin  and  mucosae  become  markedly  congested,  especially  about 
the  face,  mouth,  and  throat.  The  conjunctivae  are  injected,  the 
eyes  watery,  and  sometimes  vomiting  and  purging  are  also  present. 
The  disease  now  progresses  for  one,  two,  or  three  days,  after  which 
there  is,  as  a  rule,  a  remission  or  an  intermission. 

Course. — During  this  period  the  temperature  rises  to  1030  to 
1060  F.,  and  the  pulse  increases  proportionately  with  the  tempera- 
ture to  go  to  120  per  minute.  Severe  pains  in  the  head,  and 
especially  in  the  eyeballs,  are  experienced,  and,  in  addition,  pains  in 
different  parts  of  the  body,  especially  in  the  lumbar  region  and  the 
legs.  Of  ten  the  joints  are  painful,  usually  without  any  sign  of  redness 
or  swelling.  This  pain  in  the  joints  appears  really  to  be  due  to  the 
muscles  in  the  neighbourhood,  as  the  joint  can  often  be  passively 
moved  without  pain,  while  active  movement  induces  almost  agony. 
There  are,  however,  rare  cases  in  which  the  joints  are  affected,  as 
is  shown  by  redness  and  swelling.  As  regards  the  alimentary  canal, 
the  tongue  is  moist,  but  becomes  covered  with  a  white-creamy  fur. 
There  is  no  appetite,  nausea  and  vomiting  are  not  uncommon,  and 
constipation  or  diarrhoea  may  be  present.  Enlargement  of  the 
cervical  and  axillary  glands  is  present  to  the  extent  of  30  per  cent. 
to  70  per  cent,  of  the  cases  of  some  epidemics.  The  glands  remain 
enlarged  for  some  time,  and  may  be  tender  on  pressure.  The  juice 
of  these  glands  has  reproduced  the  disease  in  two  out  of  three  cases. 
The  circulatory  system  is  not  affected,  except  that  fainting  occurs 
at  times,  while  a  sensation  of  praecordial  discomfort  or  of  suffocation 
may  be  complained  of.  Insomnia  and  delirium  are  not  infrequent, 
but  meningitis  and  neuritis  must  be  uncommon  if  they  occur  at  all, 
though  hyperesthesia  of  the  skin  may  be  observed.  The  skin  shows 
the  congestion  already  mentioned,  which  is  not  always  present, 


DENGUE  AND  ALLIED  FEVERS 


seen, 


Fig.  630. — Typical    Temperature     Chart 
of    Dengue    Fever. 


being  at  times  replaced  by  the  opposite  extreme  of  pallor.  Jaundice, 
it  it  occurs,  is  rare.  Haemorrhages  are  rare,  and  will  be  mentioned 
as  a  complication.  The  changes  in  the  blood  have  been  carefully 
worked  out  by  Ashburn  and  Craig.  The  erythrocytes  are  usually 
normal  in  appearance  and  number,  but  a  few  poikilocytes  may  be 
while   the   haemoglobin   and   colour-index   are  also   normal. 

Leucopenia  is  so  constant 
^|m7e'mT|m*t      as  to  be  of  diagnostic  im- 
portance,   varying    from 
4,860  to  1,200,  the  aver- 
age being  3,800  per  cubic 
millimetre.      The     leuco- 
cytes     are     normal      in 
appearance,  but  there  is 
an   increase  of  the  large 
mononuclears  and    eosin- 
ophiles,  and    a    decrease 
in  the  polymorphonuclear 
leucocytes.      The     urine 
appears    to    be     usually 
quite  normal,   except  that  it  is  high-coloured,  but  may  contain 
a  minute  trace  of  albumen,  and  in  severe  cases  Guiteras  says  the 
diazo-reaction  can  be  obtained. 

Intermission. — On  the  third  day  the  temperature  usually  falls, 
but  rarely  reaches  to  normal.  This  fall 'may  be  accompanied  by  the 
usual  signs  of  a  crisis — namely,  profuse  perspiration,  the  passage  of 
much  urine,  violent  diarrhoea,  and 
bleeding  from  the  nose — but  in  many 
cases  these  signs  may  be  absent.  The 
patient  now  feels  better,  except  for 
slight  pains,  and  a  genuine  intermis- 
sion in  the  disease  is  established.  In 
other  cases,  however,  this  inter- 
mission may  be  entirely  wanting, 
and  the  temperature  may  only  remit, 
remaining  at  ioo°  to  1020  F. 

Second  Attack. — The  intermission 
or — generally — remission  lasts  until 
the  fifth  day  of  the  illness,  when  the 
temperature  rises  to  some  point 
usually  below    1030   F.,  and  at  the 

same  time  a  rash  appears  on  the  palms  and  backs  of  the  hands, 
and  rapidly  spreads  to  the  arms,  the  trunk,  and  the  legs.  This 
rash  may  be  of  two  types— a  measly  eruption  of  small,  circular, 
dark  red  maculo-papules,  which  almost  entirely  disappear  on 
pressure,  or  a  scarlatiniform  eruption  of  close-set  bright  red  points, 
which  may  coalesce  and  form  large  red  patches.  Eruptions  inter- 
mediate in  appearance  between  these  two  types  may,  however,  be 
present,  and  occasionally  only  an  abortive  or  no  eruption  at  all  occurs. 


Dayetm 

Ml! 

lime 

M  E 

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M  E1M 

HIE 

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Fig.  631. — The  Atypical  Tem- 
perature Chart  of  Dengue 
Fever. 


VARIETIES  1249 

This  rise  of  temperature  may  last  from  a  few  hours  to  a  day,  and 
generally  declines  by  crisis,  with  or  without  perspiration,  on  the 
sixth  day.  The  skin  eruption  usually  lasts  from  two  to  eight  days, 
after  which  occasionally  there  is  a  desquamation,  which  may 
continue  for  two  to  three  weeks. 

The  typical  disease  shows  a  first  attack,  a  remission  or  inter- 
mission, and  a  second  attack,  though  the  two  attacks  may  become 
merged  together.  The  typical  rash  may  be  absent,  and  sometimes 
the  disease  is  so  mild  that  it  ends  on  the  third  day  with  the  first 
crisis. 

Convalescence  may  be  quick  and  permanent,  but,  on  the  other 
hand,  it  may  be  protracted  and  complicated  with  sequelae.  Im- 
munity is  said  to  be  complete  twenty-four  days  after  recovery 
from  a  typical  attack. 

Varieties. — It  is  now  generally  agreed  that  seven  days'  fever  is 
merely  a  variety  of  dengue  fever,  and  therefore  for  comparison  we 
attach  a  description  of  it  to  this  chapter. 

Megaw  distinguishes  the  following  varieties: — 

1.  The  Evanescent  Type,  with  only  a  short  slight  attack  of  fever, 
and  corresponds  with  one  variety  of  the  old  febricula,  and  cannot 
be  recognized  except  during  an  epidemic  of  dengue  fever. 

2.  The  Interrupted  Fever  Type. — This  is  the  three  days'  fever, 
followed  after  one  or  two  days  of  apyrexia  with  another  attack,  and 
is  typical  dengue  fever.  True  intermission  is,  however,  rare,  a  fever 
of  the  saddle-back  type  being  much  commoner. 

3.  The  Saddle-Back  Type. — This  is  the  so-called  seven  days'  fever. 

4.  The  Continued  Fever  Type. — This  is  rare,  and  is  characterized 
by  a  lack  of  the  usual  remission  or  intermission  of  the  fever. 

Complications. — The  rarity  of  the  symptoms  of  haemorrhage  may 
perhaps  justify  its  mention  as  a  complication.  It  takes  place  from 
the  mucosae,  as  already  mentioned,  of  the  nose,  stomach,  intestines, 
and  uterus.  Hyperpyrexia  may  occur  as  a  complication,  but  is 
rare,  and  pleurisy,  pericarditis,  orchitis,  endocarditis,  and  menin- 
gitis sometimes  complicate  the  disease  and  alter  its  characteristics. 
We  have  seen  enteric  develop  in  three  typical  cases  of  dengue,  and 
appendicitis  in  two  cases. 

Sequelae. — The  most  important  sequelae  are  the  pains  in  the  joints 
and  muscles,  which  worry  patients  considerably.  This  polyarthritis 
affects  joints  of  all  kinds,  both  small  and  large,  and  is  associated 
with  swellings,  so  that  the  condition  is  like  rheumatism,  but  sali- 
cylates are  useless.  The  severe  type  is  rare,  but  is  very  distressing, 
and  may  last  six  to  eight  weeks  or  longer.  It  is  not  uncommon  in  a 
milder  form,  with  pain  in  various  joints  and  slight  swelling,  and  in 
this  condition  may  last  for  months. 

Relapses  are  said  to  take  place,  but  Ashburn  and  Craig  doubt 
whether  any  occur  a  short  time  after  an  attack,  as  the  persons  who 
were  supposed  to  relapse,  in  their  experience,  really  suffered  from 
malarial  fever ;  for,  as  a  matter  of  fact,  there  is  an  acquired  immunity 
for  some  little  time  after  an  attack  which  prevents  such  relapses. 

79 


i25o  DENGUE  AND  ALLIED  FEVERS 

Reinfections. — These  are  not  uncommon,  and  each  attack  may  be 
quite  typical,  being  associated  with  the  rash. 

Diagnosis. — This  is  based  on  the  sudden  onset  with  extremely 
severe  muscular  pain,  the  remission  or  intermission  in  the  course 
of  the  fever  on  the  third  or  fourth  day,  the  rash  generally  appearing 
on  the  third  to  the  sixth  day.  The  diseases  most  likely  to  be  mistaken 
for  dengue  are  yellow  fever,  malaria,  influenza,  scarlet  fever,  measles, 
rheumatic  fever,  smallpox,  tonsillitis,  typhus,  and  pappataci  fever. 

Yellow  fever  is  recognized  by  its  slower  pulse,  jaundice,  albumen  in 
the  urine,  and  hasmatemesis;  malar  ia  by  its  blood  parasites;  influenza 
by  the  absence,  as  a  rule,  of  any  eruptions  and  the  presence  of  catar- 
rhal symptoms;  scarlet  fever  by  the  presence  of  the  sore  throat  with 
enlarged  cervical  glands;  measles  by  the  catarrhal  symptoms  and 
the  absence  of  the  severe  pains;  rheumatic  fever  by  the  swelling 
of  the  joints;  smallpox  may  be  with  difficulty  recognized  until  the 
eruption  comes  out ;  and  tonsillitis  may  be  recognized  by  examining 
the  throat.  In  the  tropics,  where  enteric  is  frequently  atypical  and 
often  begins  suddenly,  there  may  be  difficulty  during  the  first  few 
days  in  distinguishing  the  two  diseases.  The  very  severe  pains 
are,  however,  rare  in  enteric,  and  the  course  of  the  fever  will  clear 
the  diagnosis.  From  typhus  it  may  be  diagnosed  by  the  leucopenia. 
From  pappataci  fever  it  may  be  distinguished  by  the  presence  of  the 
rash  and  the  frequent  rise  of  the  temperature  on  the  fourth  to  fifth 
day. 

Prognosis. — This  is  quite  good,  as  the  mortality  is  usually  nil,  but 
in  Australia  it  caused  I  death  in  1,000  cases,  principally  in  those 
under  five  and  over  sixty  years  of  age. 

Treatment. — No  rational  treatment  can  be  given,  as  we  do  not 
know  what  the  nature  of  the  cause  will  prove  to  be.  Symptoms 
must,  however,  be  relieved.  The  fever  and  headache  may  be  com- 
bated with  cool  sponging  and  cool  applications;  the  pains  by 
hypodermic  injections  of  morphia  or  doses  of  Dover's  powder;  this 
will  also  relieve  the  nervous  symptoms,  which  otherwise  will  require 
bromides.  Antipyrin,  phenacetin,  and  aspirin,  may  be  administered 
with  care,  and  the  bowels  should  be  opened  by  calomel.  The  diet 
must  be  low,  and  stimulants  should  not  be  given. 

Prophylaxis. — Protection  against  mosquitoes,  as  described  under 
Malaria,  excluding,  of  course,  quinine  prophylaxis,  is  the  correct 
method  of  preventing  the  disease. 


SEVEN  DAYS'  FEVER. 

Remarks. — In  our  opinion  the  seven  days'  fever  is  dengue  or  a  variety  of 
it.  We  have  come  to  this  conclusion  after  having  had  the  opportunity  of 
studying  epidemics  of  dengue  and  of  the  so-called  seven  days'  fever  in  various 
countries. 

History. — This  disease  was  described  by  Rogers  in  1905-08  as  a  sporadic 
fever  of  Indian  seaport  towns.  It  is  probably  identical  with  Crombie's  simple 
continued  fever,  and,  according  to  many  observers,  including  ourselves,  is  a 
form  of  dengue. 


SEVEN  DAYS'  FEVER 


1251 


Climatology. — So  far,  in  India  and  Ceylon  it  has  been  found  in  towns  in 
low-lying  districts  near  the  sea,  and  is  believed  not  to  spread  inland.  In 
Calcutta  it  occurs  from  May  to  September,  and  is  very  common  in  Colombo 
during  the  same  months. 

etiology. — Rogers  found  a  motile  bacillus  related  to  the  coli  bacillus  in  the 
blood,  which  he  thinks  may  possibly  be  the  cause  of  the  disease.  It  resembles 
the  Bacillus  coli  communis  in  size  and  shape,  and  possesses  fiagella;  is  de- 
colourized by  Gram;  produces  a  diffuse  haziness  in  broth;  slowly  liquefies 
gelatine;  grows  on  agar  like  B.  coli  ;  does  not  produce  gas  in  glucose  agar;  nor 
gas,  nor  acid,  in  dextrose,  lsevulose,  and  maltose  broths;  nor  does  it  ferment 
arabinose,  galactose,  saccharose,  lactose,  inulin,  salicin,  erythrite,  mannite, 
or  dulcite.  It  is  agglutinated  in  1  in  20  and  1  in  40  dilutions  of  the  serum 
of  seven  days'  fever  patients.  These  observations  have  not  been  confirmed. 
Clayton  suggests  that  the 
disease  is  carried  by  mosqui- 
toes. The  fever  is  commonly 
found  among  Europeans,  and 
especially  among  people  having 
to  do  with  shipping,  and  also 
in  new-comers. 

Pathology. — The  morbid 
anatomy  is  unknown,  as  the 
mortality  is  nil. 

Symptomatology.  —  The  in- 
cubation period  is  unknown, 
and  no  prodromal  symptoms 
have  been  recorded.  The  in- 
vasion is  sudden,  with  a  rapid 
rise  of  temperature  to  1020  or 
1050  F.,  but  the  pulse  is  not  as 
quick  as  it  should  be,  compared 
with  the  temperature. 

The  face  is  flushed  and  the 
palpebral  conjunctivae  injected, 
and  some  rose-coloured  spots 
may  appear  on  the  skin.  Pain 
is  felt  in  the  back  and,  less 
commonly,  in  the  limbs.  After 
the  initial  rise  there  is  usually 
a  gradual  marked  remission 
of  the  temperature  for  two  to 
three  days,  when  the  fever 
again  rises,  producing  the 
typical  saddle- back  remission. 
After  the  second  rise  the  tem- 
perature gradually  or  quickly  falls  to  normal,  and  the  disease  ends  about 
the  seventh  to  eighth  day.  There  is  generally  frontal  headache,  and  the 
tongue  is  furred  on  the  dorsum,  while  the  edges  are  red.  Nausea  and  vomiting 
are  not  common  ;  the  bowels  are  usually  normal,  though  constipation  or 
diarrhoea  may  occur.  The  abdomen  is  often  distended,  and  may  be  painful. 
The  liver  is  usually  normal,  but  may  in  a  few  cases  be  slightly  enlarged,  and 
the  spleen  is  at  times  enlarged.  The  respiratory  and  circulatory  organs  are 
normal,  except  that  the  pulse  is  often  slow  as  compared  with  the  temperature. 

The  blood  shows  a  slight  reduction  of  the  erythrocytes  and  a  marked  leuco- 
penia — 2,000  to  4,000  per  c.c.  The  polymorphonuclear  leucocytes  are  re- 
duced, and  the  lymphocytes  and  mononuclears  are  increased.  Nothing 
abnormal  is  found  in  the  urine,  except  the  usual  appearance  of  febrile 
urine. 

Rashes  are  frequent.  The  most  common  is  a  mottling  or  a  diffuse  erythema 
of  the  extensor  surfaces  of  the  forearms  on  the  fourth  to  sixth  day,  which 
may  fade  before  the  temperature  falls. 


Fig.  632. — Temperature  Chart  of  a  Case 
of  Seven   Days'   Fever. 


1252 


DENGUE  AND  ALLIED  FEVERS 


There  are  no  complications  or  sequela?,  and  the  prognosis  is  excellent,  as 
the  mortality  is  nil.  Mild  recurrences  in  following  years  may  be  met  with, 
but  relapses  in  the  same  year,  though  rare,  do  occur,  as  we  have  met  with  such 
a  case.     Convalescence  is  rapid. 


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Fig.  633. — Temperature  Chart  of  a  Case  of  Seven  Days'  Fever. 

Diagnosis. — It  can  be  distinguished  from  malaria  by  the  absence  of  para- 
sites, and  the  slow  pulse  with  high  fever;  from  influenza  by  the  absence  of 
respiratory  symptoms. 

Treatment. — This  is  purely  symptomatic. 

DENGUE-LIKE  FEVERS. 

Synonym. — Climatic  fevers. 

Under  this  heading  come  the  fever  of  the  Antilles,  the  fever  of  the  Red  Sea, 
the  six  days'  fever  of  Asia,  the  fever  of  Massowah,  the  six  to  eight  days'  fever 
of  Aden  described  by  Smith  and  Loughman,  the  six  days'  fever  of  the  Canal 
zone  in  Panama  described  by  Deeks,  and  the  pseudo-dengue  fever  of  Cochin 
China,  winch  are  all  closely  allied  to  dengue  fever,  lasting  about  seven  days,  and 
being  associated  with  pains  in  different  parts  of  the  body,  and  having,  in  brief, 
the  symptoms  described  above  for  seven  days'  fever  or  for  dengue  fever. 

VAN  DER  SCHEER'S  FEVER. 

Synonym. — Five  days'  fever. 

Definition. — A  fever  usually  lasting  for  five  days,  and  associated  with  an 
eruption  of  red  macules  and  papules  about  the  size  of  a  pin's  head,  occurring 
on  the  trunk.     It  may  be  a  form  of  dengue. 

Remarks. — Tins  fever,  first  described  by  van  der  Scheer,  has  also  been 
investigated  by  Neeb,  but  its  nature  is  at  present  not  understood. 

Symptomatology. — The  illness  begins  suddenly  with  severe  headache  and 
backache,  the  temperature  rising  to  1040  to  1050  F.  in  the  evening,  but  re- 
mitting considerably  in  the  morning.  Sometimes  there  is  bilious  vomiting 
and  delirium.  On  the  third  day  the  eruption  appears  as  macules  or  papules 
about  the  size  of  a  pin's  head  on  the  chest,  which  spread  to  the  back  and 
abdomen.  After  five  days'  remittent  fever  the  crisis  comes  on  the  sixth  or 
seventh  day,  when  the  temperature  rapidly  falls  below  normal.  This  fall  is 
accompanied  by  moderate  sweating.  In  more  severe  cases  the  crisis  is  absent, 
and,  cardiac  failure  setting  in,  the  patient  dies  cyanosed. 


REFERENCES  1253 

Some  days  after  the  crisis  there  is  a  furfuraceous  desquamation  associated 
with  pruritus  on  the  palms  of  the  hands  and  soles  of  the  feet,  and  at  the  same 
time  there  is  a  considerable  loss  of  hair  and  a  bitter  taste  in  the  mouth. 

Diagnosis. — It  can  be  distinguished  from  malaria,  relapsing  fever,  etc.,  by 
the  absence  of  parasites  in  the  blood,  and  from  measles  by  the  absence  of  the 
catarrhal  symptoms,  from  scarlet  fever  by  the  absence  of  a  sore  throat,  and 
from  typical  dengue  fever  by  the  temperature  tracing. 

Treatment. — The  treatment  is  purely  symptomatic,  but  it  is  recommended 
that  injections  of  caffeine  be  administered  on  the  sixth  day  to  prevent  a 
possible  attack  of  cardiac  failure. 

IM-PYENG. 

According  to  Landis  and  Matignon,  there  exists  in  Corea  a  fever  called 
by  the  inhabitants  Im-Pyeng.  It  is  most  frequently  met  with  in  the  country 
districts  from  February  or  March  to  July,  when  it  is  most  common  among 
the  poor,  but  affects  all  classes  of  society.  It  would  appear  to  us  to  be  allied 
to  dengue  fever. 

/Etiology. — The  causation  is  unknown,  but  it  is  regarded  as  contagious  by 
the  inhabitants  of  Corea.  Matignon  considered  that  it  resembled  relapsing 
fever,  but  was  unable  to  find  a  Spiroschaudinnia  in  the  blood. 

Symptomatology. — The  disease  begins  with  headache,  backache,  or  vague 
pains,  which  may  become  violent,  while  the  temperature  may  rise  to  over 
1040  F.  in  the  evening,  but  remits  considerably  in  the  morning,  rising  again 
in  the  evening  to  about  1020  F.,  and  again  remitting  considerably  in  the  morn- 
ing, and  this  fever  may  be  accompanied  with  delirium.  The  fever  continues 
for  some  seven  to  ten  days,  but  usually  after  the  sixth  or  seventh  day  the 
fever  declines,  and  reaches  normal  in  twenty-four  to  thirty-six  hours,  this 
decline  being  associated  with  a  profuse  perspiration. 

Sequelae. — The  patient  is  left  with  both  general  and  cardiac  weakness  after 
an  attack. 

Treatment. — Quinine  sulphate  in  association  with  antipyrin  is  the  treatment 
usually  adopted. 

REFERENCES. 

Dengue  Fever. 

Ashburn  and  Craig  (1907).     The  Philippine  Journal  of  Science,  ii.  93. 
Castellani    (1917).     Journ.  of  Trop.  Med.,  August  15.      (191S)  Ann.  Med. 

Navale. 
Charles  (187.2).     Indian  Medical  Gazette,  p.  25. 
Clair  (191  i).     Traite  de  Grail  et  Clarac.     Paris. 
Cleland,    Bradley   and   McDonald    (1916).      Med.    Journ.    of    Australia. 

Nos.  10  and  1 1 . 
Coleman  (1907).     Osier  and  McCrae's  System  of  Medicine,  ii.  489. 
Dickson  (1828).     American  Journal  of, Medical  Sciences,  iii.  3. 
Graham  (1903).     Journal  of  Tropical  Medicine,  vi.  209. 
Manson  (1906).     Allbutt  and  Rolleston's  System  of  Medicine,  vol.  ii.,  part  ii., 

P-  345. 
Manson  (1918).      Tropical  Diseases. 
Rogers  (1908).     Fevers  in  the  Tropics,  p.  242. 
Ross,  P.  H.  (1908).     Annals  of  Tropical  Medicine  and  Parasitology,  ii.  193. 

(Prevention.) 
Van  de  Burg  (1905).     Mense's  Tropenkrankheiten,  ii.  95. 

Seven  Days'  Fever. 
Rogers  (1908).     Fevers  of  the  Tropics.     Oxford. 

Dengue-like  Fevers. 

Deeks,  W.  E.  (1912).     Journal  of  American  Medical  Association. 
Perry,  J.  C.  (1912).     United  States  Public  Health  Reports. 
Poleck  (1912).     Arch.  f.  Schiffs-  u.  Tropen-Hygiene. 


CHAPTER  XLIV 
PAPPATACI    FEVER 

Synonyms  —  Definition  ■ — ■  History  ■ —  Cli  matology — ■  /Etiology  —  Pathology  — 
Morbid  anatomy— Symptomatology— Diagnosis — Prognosis — Treatment 
- — -Prophylaxis- — -References . 

Synonyms. — -Three  days'  fever,  Phlebotomus  fever,  Sandfly  fever,  Summer 
fever.  French  :  Fievre  des  trois  jours,  Fievre  de  Pick,  Fievre  de  Pym. 
Italian  :  Febbre  gastrica,  Febbre  estiva,  Febbre  climatica,  Influenza  estiva, 
Influenza  malarica,  Mai  della  secca,  Febbre  dei  tre  giorni.  German:  Hunds- 
krankheit,  Sommerfieber,  Endemischer  Magenkatarrh.  Latin  :  Febricula  pro 
parte,  Gastro-enteritis  endemica,  Gastro-enteritis  climatica. 

Definition. — An  acute  specific  fever  of  unknown  causation,  lasting 
three  clays,  and  characterized  by  nervous  symptoms,  pains  in  various 
parts  of  the  body,  and  gastro-intestinal  disturbance,  and  spread  by 
the  agency  of  Phlebotomus  papatasii  Scopoli,  1786. 

History. — In  1804  Pym  described  a  fever  of  three  days'  duration 
as  occurring  in  the  Mediterranean  basin,  and  this  was  confirmed 
by  Burnett  in  1816.  From  that  time  constant  references  may  be 
found  to  this  complaint  in  the  English  Army  reports  concerning 
Malta,  where  it  was  sometimes  called  '  summer  fever.'  In  1855-56 
there  was  a  considerable  number  of  cases  in  that  island,  due  to  the 
passage  of  the  troops  en  route  to  the  Crimea.  The  fever  was  also 
described  by  Cicoli  in  1874-75  in  Pola,  by  Pick  in  1887,  by  Karlinski 
in  1889,  by  Taussig,  who  was  the  first  to  suspect  P.  papatasii,  in 
1905,  and  in  the  same  year  by  Panec.  In  1903  McCarrison  was 
the  first  observer  to  differentiate  the  disease,  which  he  did  in 
Chitral,  when  lie  suspected  the  sandfly  as  the  causal  agent.  In 
1907  it  was  noticed  that  although  undulant  fever  had  almost  dis- 
appeared from  Malta  there  were  no  less  than  340  admissions  for 
'  simple  continued  fever  '  into  the  Army  hospitals,  and  in  this  year 
Gerrard  and  Marratt  drew  attention  to  this  fever.  In  1909  Doerr, 
Franz,  and  Taussig  published  their  classical  account  of  the  aetiology 
and  symptomatology  of  the  disease,  thus  placing  it  upon  a  sound 
basis,  and  in  the  succeeding  year  Birt  confirmed  and  extended  these 
discoveries,  and  in  the  same  year  Tiraboschi  found  it  in  South 
America,  and  Phillips  in  Cairo.  In  1911-12  Miorcec  and  Laplanchi 
found  it  in  Crete,  Niclot  in  Oran,  Sergent  in  Biskra,  Leger  and 
Sequinaud  in  Corsica,  and  Wall  described  it  again  in  Chitral.  In 
1915  Castellani  found  it  in  Serbia  and  Macedonia  and  showed  that 
1  he  so-called  Skoplji  or  Uskub  fever  is  pappataci  fever.  It  occurs 
in  Khartum. 

1254 


CLIMATOLOGY 


1255 


Climatology. — It  is  found  in  all  the  countries  bordering  on  the 
Mediterranean  and  Adriatic  Seas,  and  it  is  known  in  India,  Egypt, 
South  America,  and  in  South  Africa  (Cairs).  It  is  possible  that  it 
may  be  found  to  be  cosmopolitan  in  its  distribution. 

In  temperate  climates  it  only  occurs  in  the  summer  months,  and, 
when  studied  epidemiologically,  it  is  found  to  be  correlated  with  the 
distribution  of Phlebotomus  papatasii.  How  the  infection  is  main- 
tained during  the  winter  months  is  not  understood,  as  the  imagines 
do  not  live  through  the  winter,  and  as  a  relapse  after  a  long  period  is 
unknown.  Doerr  believes  that  the  female  flies  transmit  the  infec- 
tion to  their  progeny,  which  in  turn  restart  the  disease  during  the 
succeeding  summer.  It  is,  however,  by  no  means  certain  that  the 
infective  agent  disappears  from  the  blood  when  it  ceases  to  be  infec- 
tive on  inoculation. 


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Figs.  634  and  635. — Temperature  Charts  of  Pappataci  Fever. 

/Etiology. — The  causation  of  the  fever  is  quite  unknown,  but  the 
researches  of  Doerr,  fully  confirmed  by  Birt  and  others,  have  proved 
that  a  virus  exists  in  the  blood  of  patients  suffering  from  the  disease; 
that  this  virus  is  infective  during  the  first  day,  and  up  to  the  end  of 
the  second  day  of  the  fever,  but  not  later;  that  it  is  filterable  through 
a  Pasteur-Chambcrland  candle  F;  that  Phlebotomus  papatasii 
Scopoli,  1786,  is  the  carrier  of  the  disease,  but  does  not  become 
infective  at  once  after  feeding,  but,  on  the  contrary,  is  not  infective 
under  a  week,  after  which  it  can  convey  the  infection.  This  proves 
that  the  organism  undergoes  development  in  the  fly.  How  long  the 
fly  remains  infective  is  not  known  with  certainty,  as  it  usually  dies 
after  ten  days'  captivity,  but  it  is  probable  that  the  disease  is  trans- 
missible to  young  broods  of  flies.  The  incubation  period  of  the 
experimental  cases  varied  from  three  days  sixteen  hours  to  seven 
days,  and  a  few  of  these  cases  showed  only  the  gastro-intestinal 
symptoms,  without  any  sign  of  fever.  Animals  have  so  far  not 
been  infected  with  fever  except  one  small  monkey  by  Tedeschi  and 
Napolitani.  Chalmers  and  O'Farrellhave  also  infected  a  monkey  by 
intravenous  inoculation  of  human  infected  blood.  It  may  be  noted 
that  phlebotomus  can  bite  in  the  daytime  and  not  merely  at  night. 

Pathology. — Antibodies  appear  to  be  generated  during  an  attack, 
as  Doerr  has  shown  that  the  serum  from  convalescents  may  neutral- 


1256  PAPPATACI  FEVER 

ize  infective  serum;  moreover,  this  action  may  be  demonstrated 
during  a  period  varying  from  one  week  to  two  years  after  an  attack. 
An  attack  of  fever  confers  a  relative  immunity,  as  relapses  are  seen, 
but  reinfections  are  believed  never  to  occur,  and  the  natives  of  an 
endemic  region  are  believed  to  be  immune,  possibly  because  there 
has  been  a  previous  attack  during  childhood. 

Morbid  Anatomy. — In  the  few  post-mortems  which  have  been 
performed,  the  signs  exhibited  have  been  those  of  the  complica- 
tion from  which  the  patient  died,  as  the  disease  per  se  is  not 
fatal. 

Symptomatology — Incubation. — The  incubation  varies  from  three 
to  seven  days.  Prodromal  symptoms  in  the  form  of  malaise,  vague 
pains,  discomfort,  and  weariness,  are  generally  present  in  India, 
but  rare  in*  Europe  and  Africa. 

Attack. — The  onset  is  sudden,  with  a  slight  rigor  or  a  feeling  of 
chilliness  and  severe  frontal  headache,  lumbar  and  body  pains. 
The  conjunctivae  are  injected  and  the  cheeks  slightly  flushed.     In  a 
fairly  large  number  of  cases  the  flushing  of  the  face  and  neck  is 
extremely  well  marked,  almost  amounting  to  an  erythematous  rash. 
A  peculiar  feature  of  this  symptom  has  been  described  by  Castellani 
— viz.,  the  flushing  is  persistent,  lasting  eight  to  fifteen  days  after 
the  fever  is  over,  and  fades  away  so  slowly  that  in  many  cases  it  is 
not  difficult  to  diagnose  the  disease  in  persons  convalescent  there- 
from.    The  skin  is  hot  and  dry,  and  the  temperature  rapidly  rises, 
reaching  1040  F.,  or  rarely  1050  F.,  in  twenty-four  hours.     The  pulse 
may  reach  100  to  116,  but  is  often  unduly  slow.     The  patient  is 
very  irritable,  and  intolerant  to  sounds.     Movements  of  the  eyes  are 
painful,  the  conjunctivas  are  injected,  and  often  show  a  red  band 
running  from  the  cornea  across  the  sclera.     Sleep  is  impossible  at 
times,  but  at  other  times  the  patient  may  be  very  drowsy.     The 
tongue  is  coated  on  the  dorsum  with  a  white  or  brown  fur,  and  the 
edges  may  be  red.     The  appetite  is  lost  and  the  sense  of  taste 
destroyed,  but  vomiting  is  uncommon,  though  there  is  pain  in  the 
epigastrium  and  sometimes  diarrhoea.     The  mouth  and  throat  are 
congested  and  irritable,  and  the  gums  may  show  a  tendency  to 
bleed,  and  there  may  be  a  little  bronchitis.     The  cough  is  generally 
dry,   with   thick,   tenacious,   muco-purulent    expectoration.     The 
tonsils  may  be  enlarged  and  the  uvula  congested,  but  this  is  not 
constant.     Not  only  is  there  the  congestion  of  the  tonsils  and 
pharynx,  but  the  mucosa  of  the  soft  palate  presents  a  peculiar 
appearance,  showing  small  hyperaemic  roundish  spots.     The  erup- 
tion is  sharply  limited  by  a  line  of  demarcation  between  the  soft 
and  hard  palates.     This  appearance  is  not  peculiar  to  the  disease, 
being  found  in  certain  cases  of  relapsing  fever,  typhus,  and  malaria. 
It  is  rare  in  typhoid.     The  liver  and  spleen  are  normal.     Vertigo 
and  faintness  may  be  present,  and  pains  in  the  joints,  especially  in 
the  elbow  and  knee,  as  well  as  in  the  bones  and  muscles,  and  burning 
sensations  in  the  palms  and  soles.     Cramps  arc  not  uncommon.     Ex- 
citation is  frequent,  and  delirium  occasionally  seen. 


SYMPTOM  A  TOLOG  Y 


1257 


The  blood  shows  a  leucopenia — 4,000  to  5,000  leucocytes  per 
cubic  millimetre — and  the  differential  count  is  as  follows: — 

Polymorphonuclears  . .  . .  . .  . .  . .  61*7 

Lymphocytes      . .  . .  . .  . .  . .  . .  21*3 

Mononuclears      . .  . .  . .  . .  . .  . .  14*0 

Eosinophils        . .  . .  . .  . .  . .  . .  2-7 

The  blood-pressure  is  normal  during  the  attack,  but  somewhat 
diminished  during  convalescence. 

The  urine  is  diminished  in  quant  ity ,  but  is  of  normal  colour,  specific 
gravity,  and  acid  reaction,  and  does  not  contain  albumen,  except 
rarely,  and  then  only  a  trace.     Ehrlich's  diazo-reaction  is  negative. 

The  skin  is  usually  dry  throughout,  but  profuse  sweating  may 
occur,  and  erythemata  of  a  morbilliform  or  a  multiform  character 
may  be  seen,  as  well  as  a  few  roseolse,  but  are  very  rare.  A  skin 
change,  which  starts  at  the  commencement,  is  a  delicate  subcuticular 
mottling  of  the  chest  and  abdomen,  '  Cutis  marmorata.' 

Course. — In  thirty-six  to  forty-eight  hours  the  temperature  falls 
to  normal,  but  may  show  a  terminal  rise.  This  fall  is  often  accom- 
panied with  epistaxis,  more  rarely  with  sweating,  vomiting,  or 
diarrhoea.  When  the  temperature  falls  the  symptoms  abate,  but 
much  weakness  is  felt,  the  convalescence  being  prolonged.  A  post- 
critical  rise  is  not  very  rare,  and  occasionally  there  may  be  a  low 
irregular  fever  lasting  for  about  a  week  and  even  longer. 


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Figs.  636  and  637. — Temperature  Charts  of  Pappataci  Fever. 


Diagnosis.- — In  a  country  where  sand-flies  exist  the  disease  may  be 
diagnosed  by  (1)  the  sudden  onset  of  the  fever,  ending  on  the  third 
day  without  any  roseolar-like  rash;  (2)  rheumatoid  pains  all  over 
the  body,  very  well  marked;  (3)  no  enlargement  of  the  spleen; 
(4)  persistent  erythematous  flushing  of  face  and  neck  after  defer- 
vescence in  40-50  per  cent,  of  cases— so-called  Ca  tellani's  sign. 
There  is,  however,  no  certain  sign  for  diagnosis  except  human  inocu- 
lation, and  as  the  incubation  is  so  long  the  fever  will  have  declared 
its  character  before  the  inoculated  person  develops  the  attack. 
Cuti-  and  ophthalmo-reactions  have  failed  to  be  demonstrated. 
The  differential  diagnosis  from  malaria  can  be  established  by  failing 
to  find  the  parasite  in  the  blood,  and  by  the  absence  of  enlargement  of 
the  spleen;  from  typhoid  fever  by  the  sudden  onset;  from  influenza 
by  the  absence  or  mildness  of  catarrhal  symptoms,  the  relative 


1258  PAPPATACI  FEVER 

slowness  of  the  pulse,  and  the  leucopenia,  but  both  diseases  may 
exist  together;  from  sunstroke  by  the  absence  of  the  severe  symp- 
toms, nervous  symptoms,  and  the  lower  temperature;  from  dengue 
fever  it  can  only  be  distinguished  by  the  fever  ending  the  third 
day,  and  by  the  absence  of  the  rash.  In  countries  where  pappataci 
fever  and  typhus  are  endemic  the  diagnosis  at  the  onset  between 
these  two  fevers  may  be  extremely  difficult.  Examine  the  blood: 
in  pappataci  there  is  generally  leucopenia;  in  typhus  no  leucopenia, 
frequently  leucocytosis. 

Varieties. — An  afebrile  variety,  with  only  headache  and  body 
pains,  is  described,  as  well  as  an  abortive  form  lasting  two  days. 
Relapses  and  true  reinfections  may  also  occur. 

Complications.- — The  complications  are  bronchitis  and  phlebitis. 

Sequelae. — Pains  in  the  bones,  neuritis,  and  a  peculiar  loss  of 
memory  may  be  sequelae. 

Prognosis. — This  is  good,  as  no  one  has  been  known  to  die  of  the 
uncomplicated  complaint. 

Treatment. — The  treatment  is  purely  symptomatic,  and  consists 
in  sending  the  patient  to  bed,  in  administering  a  saline  purga- 
tive, and  following  this  by  aspirin  in  5  to  15  grain  doses  given  three 
times  a  day.  This  treatment  is  said  not  merely  to  relieve  the  pains, 
but  to  render  the  attack  milder.  Pyramidon  also  promptly  relieves 
the  pains,  while  it  has  been  recommended  that  the  phlebotomus  bite 
should  be  painted  with  tincture  of  iodine. 

Franz  and  Kolar  recommend  the  subcutaneous  or  intravenous  injections 
of  colloidal  silver,  but  this  hardly  appears  necessary  in  such  a  mild  fever. 
Atoxyl  has  been  found  to  be  useless,  and  quinine  to  be  harmful. 

During  convalescence  a  change  of  air  and  an  iron  tonic  may  be 
recommended. 

Prophylaxis. — The  only  obvious  means  of  prophylaxis  consists  in 
isolating  the  sick  and  protecting  them  against  the  phlebotomus  by 
means  of  mosquito  curtains  of  a  sufficiently  fine  mesh.  It  must  be 
remembered  that  the  little  fly  bites  mostly  in  darkness,  and  chiefly 
in  houses. 

As  regards  ordinary  prophylaxis,  a  fine  mosquito  curtain,  together 
with  the  use  of  camphor,  is  to  be  tried.  Fumigation  by  burning 
pyrethrum  may  also  be  tried. 

REFERENCES. 

Castellani  (1917).     Journ.  of  Trop.  Med.,  August  15.     (Tropical  Diseases  in 

the  Balkans.) 
Castellani  (1918).     Ann.  Med.  Nav.,  vol.  i.,  Nos.  3  and  4. 
Delmege  and  Staddon  (1918).     Brit.  Med.  Journ.,  April  6. 
Doerr,  Franz,  and  Taussig  (1909).     Das  Pappataci -fieber.     Leipzig. 
Du  Birt  (1910).     Journal  Royal  Army  Medical  Corps.     London. 
Gabbi  (1918).     Malaria,  vol.  ix.,  Nos.  3  and  4. 
Higgins  (1916).     British  Medical  Journal,  i.  166-167. 
Howlett  (191 5).     Bulletin  of  Entomological  Research,  December. 
Lambert  (1918).     Journ.  Roy.  Nav.  Med.  Serv.,  vol.  iv.,  No.  2. 
McCarrison  (1906).     Indian  Medical  Gazette.     Calcutta. 
Seidei.in  (1912).     Yellow  Fever  Bulletin.     Liverpool. 


CHAPTER  XLV 
THE    AFRICAN    TRYPANOSOMIASES 

General  remarks — The  sleeping  sicknesses — The  trypanosome  fevers — 

References. 

GENERAL  REMARKS. 

The  human  African  trypanosomiases  include  two  different  clinical 
conditions — viz. — 

A.  The  sleeping  sicknesses  characterized  by  the  fact  that  we 
definitely  know  that  the  preliminary  fever  leads  to  meningo-en- 
cephalitis  and  meningo-myelitis. 

B.  The  trypanosome  fevers  characterized  by  the  fact  that  we  do 
not  know  that  in  these  cases  the  disease  will  end  in  meningo- 
encephalitis and  meningo-myelitis. 

Before  Castellani  discovered  a  trypanosome  in  sleeping  sickness, 
Ford  and  Dutton  had  demonstrated  that  '  Gambia  fever  '  was  due 
to  a  trypanosome.  After  this  discovery  this  disease  was  named 
'  trypanosome  fever,'  and  was  considered  to  be  quite  distinct 
from  sleeping  sickness.  After  Castellani  had  found  a  trypanosome 
in  sleeping  sickness  the  two  diseases,  trypanosome  fever  and 
sleeping  sickness,  were  at  the  time  judged  to  be  covered  by  the 
one  name  '  sleeping  sickness.'  Recently,  however,  Lanfranchi' s 
laboratory  infection  with  a  trypanosome  has  lasted  for  more  than 
seven  years,  and  there  is  no  sign  of  meningo-encephalitis,  as  may 
be  judged  inter  alia  by  the  excellent  papers  which  the  distin- 
guished professor  produces.  In  fact,  judging  by  the  symptoms 
exhibited  by  Lanfranchi,  which  resemble  those  found  in  the  trypano- 
somiases of  animals,  it  seems  very  doubtful  whether  he  will  ever 
show  signs  of  what  we  clinically  call  '  sleeping  sickness.'  Further, 
the  organism  with  which  he  is  affected  appears  to  be  of  the  Evansi 
type,  a  form  known  to  be  in  his  laboratory  when  infection  took 
place. 

Under  these  circumstances,  it  appears  to  us  to  be  useful  to  return 
to  the  old  name  trypanosome  fever  for  infections  of  man  and  animals 
with  those  pathogenic  trypanosomes  which  produce  fever  and 
do  not  end  in  meningo-myelitis.  At  present  those  known  in  man 
are  the  case  of  Professor  Lanfranchi  and  the  infection  with  a  variety 
of  the  Vivax  type  described  by  Macfie,  both  of  which,  in  our 
opinion,  should  remain  under  this  denomination  until  it  is  proved 
that  they  belong  to  the  sleeping  sickness  group. 

1259 


1260  THE  AFRICAN  TRYPANOSOMIASES 

THE  SLEEPING  SICKNESSES. 

Synonyms.  —  Sleeping  dropsy,  Negro  lethargy,  Morbus  dormitivus. 
French  :  Maladie  du  Sommeil.  Portuguese  :  Doen9a  de  Sonno.  Italian  : 
Malattia  del  Sonno,  Letargia  dei  Negri.  German  :  Afrikanische  Schlaf- 
krankheit,  Trypanosomen  Fieber.  Native  names  are  very  numerous — 
Lalangola,  Laa  La-negulo,  N'tansi,  Mongota,  Konje  Marree,  Kaodzera,  N'dulu, 
Tula  Manugina,  Nelavare,  Dadane,  Toruahebue,  etc. 

Definition. — The  sleeping  sicknesses  are  chronic  specific  fevers 
caused  by  the  trypanosomes  Castellanella  gambiensis  Dutton,  1902; 
Castellanella  castellanii  Kruse,  1903,  spread  by  Glossina  palpalis  ; 
and  Castellanella  rhodesiensis  Stephens  and  Fantham,  1910,  spread 
by  Glossina  morsitans,  characterized  by  an  inflammatory  condition  of 
the  lymphatic  system  leading  to  a  meningo-encephalitis  which  shows 
itself  as  dulness  of  the  intellect,  apathy,  and  lethargy,  associated 
with  tremors  and  a  peculiar  gait,  and  unless  treated  ending  fatally. 

Remarks. — This  chapter  should  be  read  in  conjunction  with 
Chapter  XIX.  (p.  380),  in  which  we  have  outlined  anew  classification 
of  the  trypanosomes  with  the  view  of  crystallizing  the  knowledge 
obtained  up  to  date  with  regard  to  these  parasites.  In  so  doing  we 
have  been  compelled  to  introduce  new  terms,  which  we  have  made 
as  few  as  possible  by  utilizing  those  found  in  the  literature  with 
which  we  are  acquainted.  Two  of  these  new  terms  occur  in  this 
chapter,  because  we  have  gone  more  fully  into  the  trypanosomes  of 
man  than  into  those  of  animals,  because  this  is  a  work  on  tropical 
medicine  and  not  upon  trypanosomes,  and  because  those  of  man 
are  the  forms  which  have  been  most  satisfactorily  studied. 

Chalmers  has  introduced  the  name  Castellanella  as  the  generic 
name  for  the  group_of  trypanosomes  which  includes  the  organisms 
of  sleeping  sickness,  because  Castellanella  castellanii  (Kruse,  1903) — 
synonym,  Trypanosoma  castellanii  Kruse,  1903 — is  the  organism 
upon  which  practically  all  the  work  in  connection  with  sleeping 
sickness  was  done  prior  to  the  discovery  of  C.  rhodesiensis ,  which  is 
quite  distinct  from  the  other  two  forms. 

This  is  a  point  not  generally  recognized,  nor  is  it  realized  that 
though  C.  castellanii  and  C.  gambiensis  are  morphologically  alike, 
they  may  be  very  different  if  studied  carefully  from  a  pathological 
and  serological  point  of  view,  as  there  is  a  suspicion  that  the  well- 
known  difference  in  type  between  the  milder  form  of  the  disease  as 
seen  in  portions  of  the  West  Coast  of  Africa  and  the  severer  as  seen 
in  Uganda  may  not  be  due  to  acquired  partial  immunity,  but  to  a 
difference  in  the  two  organisms. 

In  order  to  emphasize  the  necessity  for  further  work  with  regard 
to  C.  gambiensis,  we  have  isolated  it  from  C.  castellanii. 

We  would  also  point  out  that  in  the  few  papers  in  which  compari- 
sons have  been  made  with  regard  to  the  pathological  effects  of 
C.  castellanii  as  found  in  sleeping  sickness  and  C.  gambiensis  as 
found  in  trypanosome  fever,  they  both  refer  to  C.  castellanii 
obtained  from  cases  in  Uganda  showing  at  the  time  signs  of  sleeping 
sickness  or  simply  symptoms  of  trypanosome  fever. 


THE  SLEEPING  SICKNESSES  1261 

It  appears  to  us  that  Castellanella  gambiensis  as  seen  on  the  West 
Coast  of  Africa,  and  as  originally  described  by  Dutton  and  Todd, 
requires  more  study,  and  we  are  supported  in  this  by  Macfie's  work 
with  regard  to  C.  nigeriensis,  which  we  believe  to  be  the  same  organ- 
ism, and  by  the  observations  of  Yorke  and  Blacklock  at  Sierra  Leone. 

To  summarize,  we  believe  that  though  C.  gambiensis  and  C. 
castellanii  are  morphologically  similar,  the  clinical  difference  be- 
tween the  milder  form  of  the  disease  as  seen  on  the  West  Coast  of 
Africa  and  the  terribly  severe  form  found  in  Uganda  is  such  as  to 
demand  the  separation  of  these  two  forms  until  it  is  proved  that  they 
are  really  identical  from  a  pathogenicity  and  serologicalpoint  of  view. 

History. — The  earliest  mention  of  sleeping  sickness  so  far  dis- 
covered is  by  John  Atkins,  in  his  little  book  entitled  '  The  Navy 
Surgeon,'  published  in  1734,  in  the  appendix  to  which  he  describes 
'  the  sleeping  distemper,'  common  among  the  negroes  on  the 
Guinea  Coast  among  whom  he  had  travelled  in  172 1.  In  1803 
Winterbottom  gave  an  interesting  account  of  the  disease  as  he  met 
with  it  on  the  West  Coast  of  Africa  near  Sierra  Leone.  His  descrip- 
tion is  quite  understandable,  and  he  draws  attention  to  the  presence 
of  the  enlarged  glands  of  the  neck,  the  association  of  which  with 
the  disease  was  so  well  understood  that  slave-traders  would  not  buy 
slaves  who  had  enlarged  glands. 

In  1808  Moreau  de  Jonnes  described  the  disease  in  negro  slaves 
in  the  Antilles.  In  1849  Clarke  on  the  Gold  Coast,  Davis  and  Daniell 
on  the  Guinea  Coast,  and  Ferreira,  came  across  it  at  St.  Thomas. 
During  the  next  twenty  years  a  number  of  observers  described 
sleeping  sickness,  among  whom  it  is  important  to  note  that  Guerin 
met  with  it  in  1869  in  Martinique  in  negro  slaves  who  had  been 
imported  from  Africa.  In  1876  Corre  gave  a  good  description  of 
the  disease  as  he  knew  it  in  Senegal. 

In  1891  the  first  case  was  brought  to  London,  and  was  studied  by 
Sir  Stephen  Mackenzie;  and  in  1900  two  more  cases  were  brought 
to  London,  this  time  under  the  care  of  Sir  Patrick  Manson.  The 
morbid  anatomy  of  these  cases  was  carefully  studied  by  Dr.  Mott, 
who  has  done  so  much  to  clear  up  the  pathology  of  this  disorder. 

In  1901  Forde  and  Dutton  found  a  trypanosome  T.  gambicnse 
(C.  gambiensis)  Dutton,  1902,  in  the  blood  of  a  patient  suffering  from 
a  peculiar  type  of  fever  on  the  Gambia  (Gambia  fever,  Dutton's 
disease) ,  which  was  never  thought  by  them  to  be  connected  with  sleep- 
ing sickness.  In  1902-03  Castellani  in  Uganda  found  a  trypanosome 
in  the  cerebro-spinal  fluid  of  persons  suffering  from  sleeping  sickness, 
and  in  1903  reported  that  it  was  the  ^etiological  basis  of  the  disease. 
It  was  named  Trypanosoma  castellanii  by  Kruse  in  1903,  and  on  it 
most  of  the  work  with  regard  to  sleeping  sickness  has  been  done  prior 
to  the  discovery  of  Stephens  and  Fantham's  organism.  Low  and 
Castellani  gave  a  clinical  account  of  the  disorder  which  is  largely 
followed  in  this  chapter,  which,  therefore,  contains  a  clinical  account 
of  the  illness  produced  by  C.  castellanii.  Low  and  Castellani  called 
attention  to  two  constant  symptoms  which  had  not  been  remarked 


1262  THE  AFRICAN  TRYPANOSOMIASES 

by  previous  observers,  the  fever  and  the  peculiar  tremors;  and 
Christy  published  many  interesting  epidemiological  features  con- 
cerning the  disease.  In  1903  Sir  David  Bruce  and  Nabarro  showed 
that  the  trypanosome  was  spread  by  Glossina  palpalis  Robineau- 
Desvoidy,  a  conclusion  already  reached  by  Sambon  and  Brumpt 
on  epidemiological  grounds.  From  1903-05  much  clinical,  experi- 
mental, and  epidemiological  work  was  done  by  Dutton,  Todd,  and 
Christy,  the  Commissions  of  the  Royal  Society  and  various  Govern- 
ments, and  by  the  members  of  the  Liverpool  School  of  Tropical 
Medicine.  Kleine,  in  a  series  of  important  researches,  has  experi- 
mentally shown  that  C.  castellanii  undergoes  a  cycle  of  development 
in  G.  palpalis — a  fact  which  has  been  fully  confirmed  and  extended 
by  Sir  David  and  Lady  Bruce,  Hamerton  and  Mackie,  and  Miss 
Robertson,  as  well  as  Fraser  and  Duke. 

Koch,  Laveran,  Mesnil,  Minchin,  Blanchard,  Greig,  Gray,  Tulloch, 
Kinghorn,  Montgomery,  Martin,  Pittaluga,  Lebceuf,  and  Roubaud, 
have  all  studied  the  disease  and  its  epidemiology,  and  an  Inter- 
national Conference  was  held  in  1907  in  London,  and  a  Bureau  for 
the  study  of  the  disease  founded.  This  bureau  for  some  time 
issued  monthly  bulletins,  which  are  most  valuable  to  the  student  of 
the  disease ;  but  recently  it  has  become  converted  into  the  Bureau  of 
Tropical  Diseases. 

In  1910  Stephens  and  Fantham  created  a  new  species  of  trypano- 
some (C.rhodesiensis  Stephens  and  Fantham,  1910)  for  the  parasites 
found  in  cases  of  sleeping  sickness  in  the  Luangeva  Valley  in 
Rhodesia,  because  the  trophonucleus  of  a  certain  percentage  of 
short  forms  was  situate  either  close  to,  or  even  on  the  aflagellar 
side  of,  the  kinetonucleus.  In  1912  Kinghorn  and  Yorke  showed 
that  this  trypanosome  was  transmissible  by  G.  morsitans  West- 
wood,  1850;  and  in  the  same  year  these  observers  pointed  out  the 
importance  of  the  meteorological  conditions  on  the  development 
of  the  trypanosome  in  the  fly.  Further  work  has  been  done  by 
Sanderson,  Murray,  Shircore,  and  others.  As  regards  the  history  of 
the  treatment,  arsenic  was  long  ago  considered  beneficial  for  the 
trypanosomiases  of  animals,  Livingstone  being  the  first  to  apply 
the  drug  to  a  horse  for  the  purpose  of  treating  nagana.  Since  then 
it  has  been  used  for  the  same  purpose  by  several  persons,  notably 
by  Lingard  (1893)  for  surra  and  by  Bruce  (1896)  for  nagana, 
while  Laveran  and  Mesnil  introduced  sodium  arseniate  in  1902  for 
the  same  disease,  E.  J.  Moore  and  Chichester  advocated  the  use 
of  hypodermic  injections  of  arsenic,  and  Thomas  and  Breinl  of 
the  same  of  sodium  arseniate.  In  the  meanwhile  Manson  had 
treated  several  cases  of  sleeping  sickness  with  arsenic  (liquor 
arsenicalis) ;  and  Ehrlich  and  Shiga  had  treated  various  experi- 
mental trypanosomiases  with  colouring  compounds  belonging  to 
the  benzo-purpurin  group,  of  which  trypan-red  is  the  best  known. 
Laveran  and  Mesnil  also  did  some  valuable  researches  on  the 
subject.  Thomas,  in  1905,  first  brought  the  drug  '  atoxyl '  to  the 
notice  of  the  profession  as  a  means  of  treatment  of  experimental 


THE  SLEEPING  SICKNESSES  1263 

trypanosome  affections;  and  Kopke,  in  1906,  tried  it  in  human 
beings  affected  with  sleeping  sickness. 

The  beneficial  action  of  atoxyl  in  sleeping  sickness  was  further  con- 
firmed by  Broden,  van  Campenhout,  Manson,  Koch,  and  many 
others.  In  1907  Ehrlich  and  his  pupils,  Franke  and  Roehl,  dis- 
covered the  very  important  fact  that  trypanosomes  may,  after  a 
time,  become  atoxyl-resistant.  Ehrlich  therefore  suggested  mixed 
or  alternating  treatment  with  various  preparations,  and  the  same 
suggestion,  though  based  on  different  grounds,  was  made  by  Moore, 
Nierenstein,  and  Todd.  Plimmer  and  Thomas  introduced  tartar 
emetic,  which  has  been  found  to  be  very  beneficial,  especially  if 
associated  with  the  atoxyl  treatment. 

Geography  and  Epidemiology. — The  disease  was  first  noticed  on 
the  West  Coast  of  Africa  at  Sierra  Leone,  but  was  soon  found  to 
extend  far  southwards,  and  was  also  noted  to  be  imported  from  this 
endemic  area  at  times  to  the  West  Indies,  where,  however,  it  soon 
died  out,  becoming  neither  epidemic  nor  endemic.  This  fact  clearly 
proved  that,  though  the  disease  may  be  introduced  by  man  along 
channels  of  intercommunication  into  a  strange  country,  some  other 
factor  is  necessary  before  it  can  spread  from  the  infected  new-comer 
to  the  inhabitants.     This  factor  we  now  know  to  be  a  tsetse-fly. 

In  1882  the  disease  had  a  geographical  distribution  from  Senegal 
to  Loando,  and  also  to  the  islands  of  the  Gulf  of  Guinea.  Gradu- 
ally, as  civilization  spread,  it  became  known  that  the  disease  was  not 
confined  to  the  coast,  but  extended  far  inland.  Thus,  in  1898  it 
was  known  to  be  at  Jebba,  on  the  Upper  Niger,  and  at  the  Stanley 
Falls,  on  the  Upper  Congo.  In  the  meanwhile  Stanley  had  travelled 
across  Africa  with  a  large  number  of  Congolese  followers,  and  had 
relieved  Emin  Pasha  and  his  people  at  Wadelai,  on  the  Victoria 
Nile.  These  followers  of  Emin  Pasha,  together  with  some  of  Stanley's 
expedition,  who  had  settled  in  the  country  about  Kavali,  to  the 
west  of  the  Albert  Nyanza,  were  brought  by  Sir  F.  Lugard,  for 
political  reasons,  to  Busoga  and  Uganda.  Christy  and  Hodges 
believe  that  the  disease  was  carried  from  the  Congo  by  Stanley's 
men,  and  that  they  and  Emin  Pasha's  people  brought  the  disease 
with  them  into  Busoga  and  Uganda  when  they  were  moved  from 
Kavali.  But  the  fact  is  clear  that  when,  in  1900,  the  Cooks  first 
noticed  the  disease  in  Uganda,  it  was  widespread,  and  had  been 
there  for  some  time,  and  it  seems  probable  that  Busoga  was  infected 
in  1896.  Certainly,  in  1901,  Mengo,  the  Sese  Islands,  and  the 
western  shores  of  the  Victoria  Nyanza,  were  infected,  and  the  disease 
spread  in  1902  to  the  eastern  shores  and  to  late  German  East  Africa. 

In  1904-05  Dutton  and  Todd  found  that  it  had  become  widely 
disseminated  throughout  the  Congo  Free  State,  spreading  by  human 
agency  along  trade  routes,  and  expressed  the  opinion  that  before 
long  it  would  pass  from  the  Congo  into  Eastern  Rhodesia.  Since 
then  sleeping  sickness  has  been  found  in  that  country,  though, 
the  trypanosome  found  in  Rhodesia  being  a  different  species,  it  is 
more  probable  that  the  disease  has  been  endemic  there,  and  not 


1264 


THE  AFRICAN  TRYPANOSOMIASES 


recognized  for  a  long  time.  It  appears  also  to  be  spreading  north- 
wards from  Uganda,  for  Greig,  in  1904,  found  it  at  Wadelai,  on  the 
Victoria  Nile,  but  not  as  high  as  Nimuli.  It  invaded  the  Lado 
earlier  than  1908,  and  in  1909  the  disease  was  recognized  definitely 
in  the  Bahr-el-Ghazal  Province  of  the  Sudan. 

Therefore  the  distribution  of  the  disease  at  the  present  time  may 
be  said  to  extend  along  the  West  Coast  of  Africa,  from  St.  Louis,  in 
Senegal,  to  Mossamedes,  in  Angola;  from  the  coast  to  Timbuktu 
on  the  Niger;  through  the  whole  of  the  Congo  into  Uganda  and 
Rhodesia ;  from  Uganda  and  Busoga  southwards  to  late  German  East 
Africa;  and  northwards  into  the  Bahr-el-Ghazal  Province.  The 
discovery  of  the  tsetse-fly  in  Arabia  makes  it  possible  that  the 
disease  may  some  day  still  farther 
extend  its  area. 

There  does  not  appear  to  be 
any  seasonal  influence. 

etiology. — From  the  present 
state  of  our  knowledge  it  would 


Fig.  638. — Trypanosoma  in 

Cerebrospinal  Fluid.  Fig_  638A.— Lymphocytic    Accumu- 

Preparation  from  the  cerebro-spinal  lation  around  a  Vessel  in  the 

fluid  of  a  case  of  sleeping  sickness.  Brain. 

appear  that  from  a  clinical  and  etiological  point  of  view  there  are 
three  types  of  sleeping  sickness,  which  may  be  differentiated  as 
follows: — 

I.  The  Equatorial  type,  caused  by  Castellanella  castellanii  and 

spread  by  Glossina  palpalis. 
II.    The  Southern  type,  caused  by  Castellanella  rhodesiensis 

and  spread  by  Glossina  morsitans. 
III.  The  North-Western  type,  caused  by  Castellanella  gambiensis 
(synonym,  C.  nigeriensis)  and  spread  by  some  as  yet 
not  clearly  differentiated  tsetse-fly,  which  may  or  may 
not  be  Glossina  palpalis,  and  which  Dutton  suggested 
might  possibly  be  G.  tachinoides. 

For  description  of  the  parasites,  see  p.  417. 

Duke's  researches  made  it  possible  that  there  is  a  vertebrate 
reservoir  for  C.  castellanii  in  the  antelope,  because  he  found  a 
trypanosome  very  like  this  organism  in  these  animals,  and  because 


THE  SLEEPING  SICKNESSES  1265 

Sortie  boys  working  on  an  uninhabited  island  in  Lake  Victoria 
became  infected  with  sleeping  sickness.  We  feel,  however,  that  the 
proof  is  not  quite  absolute  with  regard  to  this  point. 

Yorke  and  Blacklock  with  regard  to  C.  gambiensis  find  that  man 
is  the  principal  vertebrate  reservoir,  with  a  possible  secondary 
reservoir  in  domestic  cattle. 

With  regard  to  C.  rhodesiensis,  as  long  as  the  view  held  that  this 
was  identical  with  C.  brucei  there  was  no  difficulty  in  believing  that 
the  vertebrate  reservoir  was  in  such  animals  as  the  hartcbecst, 
water-hogs,  and  domestic  dogs;  but  with  the  human,  crossed 
immunity,  and  serological  experiments  detailed  on  page  426,  it 
again  becomes  evident  that  these  two  trypanosomes  are  distinct, 
and  therefore  the  question  as  to  the  existence  of  C.  rhodesiensis  in 
game  animals  must  again  be  considered  as  sub  judice.  The  con- 
tusion has  arisen  by  trusting  too  implicitly  to  only  morphological 
characters,  and  ignoring  serological  tests. 

In  Chapters  XIX.,  p.  j88,  and  XXXV.,  p.  878,  we  have  con- 
sidered tlie  tsetse  in  relationship  to  its  carriage  of  these  organisms, 
and  in  Chapter  XXXIII.,  p.  837,  we  have  described  these  flies. 
C.  caslellanii  is  spread  by  the  agency  of  Glossina  palpalis  and 
C.  rhodesiensis  by  Glossina  morsitans,  but  it  is  not  proved  by  actual 
experiment  what  fly  carries  C.  gambiensis.  It  is  assumed  that  it  is 
Glossina  palpalis,  but  the  subject  obviously  requires  careful  study. 

The  tsetse  flies  obtain  the  trypanosomes  by  sucking  infective 
human  blood  containing  the  organisms,  which  undergo  development 
in  the  bodies  of  the  flies.  In  due  time  (vide  Chapter  XIX.)  the 
young  trypanosomes  in  short  form  appear  in  the  salivary  glands 
of  the  tsetse-fly,  and  from  these  organs  they  pass  into  man  when 
the  fly  next  feeds  upon  him. 

The  fly  appears  to  be  the  definitive  host  of  the  trypanosome, 
but  there  is  no  evidence  that  the  infection  is  passed  on  to  the  suc- 
ceeding generation. 

From  a  practical  point  of  view  the  bite  of  the  infected  tsetse  is 
the  most  important  method  of  infection,  but  less  important  methods, 
such  as  sexual  intercourse,  are  possible  and  must  be  remembered. 

With  regard  to  predisposing  causes,  race,  sex,  and  age  have  not 
been  proved  to  have  any  influence,  though  the  last  two  have  been 
thought  to  be  predisposing  cause's. 

Occupation,  however,  has  a  considerable  influence,  for  persons 
who  live  near  the  shores  or  work  along  the  shores  of  lakes  and 
streams,  such  as  fishermen,  arc  more  liable  than  others  to  contract 
the  disease,  because  of  the  habits  of  the  fly,  while  porters  marching 
through  fly-zones  are  also  liable  to  be  attacked. 

Pathology. — The  trypanosome  either  enters  the  lymph-stream 
directly  alter  the  bite  of  the  fly,  and  is  blocked  in  the  lymphatic 
glands,  which  it  inflames,  and  through  which  it  passes  to  the 
Blood-stream  and  cerebro-spinal  fluid,  or,  less  probably,  it  enters 
the  blood-stream  first,  and  escapes  by  rupture  of  a  capillary  into  a 
lymph-gland.     But  the  polyadenitis  is  not  the  only  change  induced, 

80 


1266  THE  AFRICAN  TRYPANOSOMIASES 

for  the  lymphatic  tissues  of  the  intestine  (solitary  or  agminated 
glands)  are  also  inflamed,  and  the  heart  and  other  organs  infiltrated 
with  lymphocytes.  This  stage  is  marked  by  fever,  but  sooner  or 
later,  as  a  result  of  this  lymphatic  disease,  changes  are  induced  in 
the  membranes  and  substances  of  the  brain  and  spinal  cord  (chronic 
meningo-encephalitis  and  meningo-myelitis),  especially  along  the 
course  of  the  vessels,  which  result  in  the  proliferation  of  the  neuroglia 
and  in  a  lymphocytic  accumulation  around  the  vessels.  These  two 
processes  compress  the  vessels,  and  lessen  the  supply  of  blood  to 
the  cells  of  the  brain  and  spinal  cord,  in  which,  as  the  result  of 
malnutrition,  changes  ensue,  which  produce  the  typical  symptoms 
of  the  cerebral  stage  of  the  disease,  which  is  often  called  '  sleeping 
sickness.'  The  trypanosome  apparently  cannot  pass  through  the 
placenta,  as  infected  women  give  birth  to  healthy  babies. 

Towards  the  end  secondary  infections  with  bacteria  may  take 
place,  the  most  constant  of  these  being  due  to  streptococci  and  the 
pneumococcus,  which  probably  shorten  the  life  of  the  patient. 

Cerebrospinal  Fluid. — The  cerebro-spinal  fluid  was  first  studied 
by  Castellani,  and  it  may  be  noted  here  that  it  was  during  his 
researches  on  the  leucocytic  formula  that  he  discovered  trypano- 
somes  for  the  first  time  in  sleeping  sickness.  More  recent  researches 
are  those  by  Broden  and  Rodhain  and  others.  During  the  first 
stage  of  the  disease  it  is  usually  of  normal  appearance  and  clear, 
while  on  centrifugalization  there  is  practically  no  sediment,  though 
occasionally  a  few  small  mononuclear  cells  may  be  present,  and 
trypanosomes  are,  as  a  rule,  absent. 

In  the  sleeping  sickness  stage  it  is  often  slightly  turbid,  and  con- 
tains an  amount  of  serum  albumen  and  serum  globulin;  and  on 
centrifugalization  some  sediment  is  obtained,  consisting  of  a  few 
cells,  which  are  mostly  mononuclear  leucocytes,  endothelial-like  and 
vacuolated  cells,  while  trypanosomes  are  almost  constantly  present, 
and  also  often  aflagellate,  roundish,  or  oval  forms,  with  one  or  two 
chromatin  masses,  as  described  by  one  of  us  in  1903.  These  may 
probably  be  compared  to  the  so-called  latent  forms  described  in 
the  spleen  by  Brcinl  and  others,  though  Laveran  and  other  authori- 
ties consider  them  to  be  degenerated  or  fragmented  forms. 

MorbM  Anatomy  an1  Histopathology. — The  macroscopical  changes 
found  post  mortem  are  principally  in  the  central  nervous  system 
and  in  the  lymphatic  glands,  but  pathological  changes  brought 
about  by  complications  may  also  be  noted. 

The  body  is  usually  emaciated  and  anremic,  rigor  mortis  is  well 
marked,  and  the  skin  may  be  normal,  or  dry  and  desquamating, 
or  may  show  pustular  eruptions  on  the  hands  and  forearms,  or  ulcers 
on  the  feet  which  arc  generally  due  to  jiggers  (Dermatophilits  pene- 
trans,). Enlargement  of  the  lymphatic  glands  of  the  neck  and  groins 
is  generally  easily  seen.  On  opening  the  brain-case,  it  will  be  noted 
that  the  under  surface  of  the  scalp  is  pale,  that  the  dura  mater 
may  or  may  not  be.  adherent  to  the  bone,  that  the  cerebro-spinal 
fluid  is  increased  in  quantity,  and  the  gyri  of  the  brain  are  often 


THE  SLEEPING   SICKNESSES  1267 

flattened.  On  careful  examination,  the  pia  arachnoid  will  be  found 
to  be  thickened  in  places,  and  may  or  may  not  be  adherent  to  the 
grey  matter.  The  brain  substance,  which  is  generally  firmer  than 
normal,  but  may  be  soft  and  oedematous,  is  usually  congested,  and 
the  fluid  in  the  ventricles  is  increased. 

With  regard  to  the  spinal  cord,  it  will  be  seen  that  there  is  an 
increase  of  fluid,  which,  if  examined  with  the  microscope  after 
centrifugalization,  generally  shows  leucocytes  and  trypanosomes. 
The  cauda  equina  may  be  found  at  times  surrounded  by  gelatinous 
tissue.  The  cord  itself  is  often  congested,  and  haemorrhages  have 
been  described. 

The  lymphatic  glands  of  the  submaxillary  region,  anterior  and 
posterior  triangles,  around  the  bronchi,  of  the  mesentery,  behind 
the  peritoneum,  as  well  as  those  of  the  inguinal  and  femoral  regions, 
may  one  or  all  be  enlarged,  congested,  and  even  hemorrhagic.  At 
times  abscesses  are  found  in  these  glands,  but  they  are  due  to 
secondary  infection.  The  abdominal  cavity  often  contains  some 
straw-coloured  fluid,  and  the  pericardial  fluid  may  also  be  ex- 
cessive. There  may  be  some  increase  in  size  of  the  lymph-follicles 
and  Peyer's  patches  of  the  small  intestine.  The  lungs  may  show 
signs  of  pneumonia  and  other  complications.  The  other  organs  are 
usually  not  markedly  affected. 

The  microscopical  examination  of  the  organs  has  been  performed 
with  the  greatest  care  by  Mott  and  Breinl  and  the  members  of  the 
Portuguese  Commission  (Bettencourt,  Kopke,  Rezeide,  and  Maude). 

The  utmost  care  must  be  taken  to  distinguish  between  the  lesions 
due  to  the  trypanosomes  and  those  caused  by  terminal  infections 
such  as  the  diplococci,  streptococci,  and  colon  bacilli;  for  these  infec- 
tions may  give  rise  to  chromatolysis  in  the  nerve  cells  and  degenera- 
tion in  the  nerve  fibres  of  the  brain  (pons  and  medulla)  and  spinal 
cord  (especially  in  the  posterior  and  lateral  columns),  and  perhaps 
in  the  peripheral  nerves,  which  have  nothing  to  do  with  the  disease 
in  question.  With  this  proviso  the  microscopical  examination  is 
characterized  by  a  round-celled  infiltration  surrounding  the  vessels 
of  the  pia  arachnoid  of  the  brain  and  spinal  cord.  This  infiltration, 
first  described  by  Mott,  is  best  seen  in  the  membranes,  where  there  is 
an  accumulation  of  cerebro-spinal  fluid,  and  in  the  brain,  around 
the  vessels  of  the  medulla,  pons,  cerebellum,  and  those  entering  the 
base.  The  process  appears  to  begin  with  a  growth  in  size,  and  then 
a  proliferation  of  the  neuroglia  elements,  which  has  been  minutely 
described  by  Eisath,  and  is  found,  not  merely  around  vessels,  which 
show  a  small  celled  infiltration,  but  around  those  which  do  not. 
Round  cells  are  found  later  in  the  meshes  of  this  proliferated  glia. 

These  cells  arc  (a)  lymphocytes;  (b)  peculiar  cells  called  the 
'  plasma  cells  of  Marschalko,'  characterized  by  the  nucleus  becoming 
situated  at  one  end  of  the  cell,  and  staining  blue  with  methylene 
blue  and  eosine,  while  a  clear  halo  separates  it  from  the  cytoplasm, 
which  stains  pink;  (c)  '  morula  cells  of  Mott,'  which  are  large  round 
or  oval  cells  with  an  cxcentric  blue  nucleus  and  a  cytoplasm  contain- 


1268  THE  AFRICAN  TRYPANOSOMIASES 

ing  a  clear  eosinophile  area;  (d)  a  few  mononuclear  leucocytes; 
(e)  a  few  polymorphonuclear  leucocytes.  The  cells  of  Marschalko 
are  considered  by  Mott  to  be  derived  from  lymphocytes,  and  the 
morula  cells  to  be  degenerated  cells  of  Marschalko.  Mott  considers 
that  the  lymphocytes  are  probably  formed  by  proliferation  of  the 
endothelial  cells  of  the  perivascular  lymphatic  space.  According 
to  Breinl,  a  layer  of  blood  cells  may  be  found  external  to  the  round 
cells,  and  haemorrhages  may  be  found  in  the  cord.  The  ependyma  of 
the  lateral  ventricle  also  shows  a  proliferation  and  dense  fibrous 
formation  at  times.  With  regard  to  the  parenchymatous  elements, 
Mott  considers  that  there  may  be  increase  in  neuroglial  nuclei  and 
lymphocytes  in  the  perineural  spaces,  while  there  is  atrophy  of  the 
dendrons  and  diminution  of  the  Nissl  bodies,  and  alteration  in  the 
nucleus,  which  becomes  large,  clear,  and  excentric.  These  changes 
are  most  marked  in  the  cerebral  cortex  and  medulla,  and  less  so  in  the 
spinal  cord.  The  cells  of  the  posterior  spinal  ganglion,  however,  show 
chromatolysis.  The  central  canal  of  the  spinal  cord  may  be  dilated, 
but  is  more  generally  occluded  by  proliferation  of  the  cells  of  the 
ependyma.  It  is  interesting  to  note  that  Mott  did  not  find  any  of 
these  changes  in  the  brain  and  spinal  cord  of  a  cured  case  of  try- 
panosomiasis, who  died  several  years  later  of  cystic  disease. 

The  histological  lesions  of  the  encephalitis  found  in  sleeping  sickness  closely 
resemble  those  of  general  paralysis  and  encephalitis  lethargica  (nona). 

The  next  series  of  characteristic  changes  are  in  the  lymphatic 
glands,  in  which  trypanosomes  are  often  found.  These  changes 
begin  with  a  conversion  of  the  lymphocytes  into  cells  of  Marschalko, 
and  these,  again,  into  morula  cells.  The  endothelial  cells  of  the 
lymph  sinus  proliferate  and  take  on  a  phagocytic  action,  containing 
lymphocytes,  red  blood  cells,  and  chromatin  particles.  At  the  same 
time  the  gland  becomes  intensely  congested,  and  the  fibrous  tissue 
of  the  capsule  and  septa  proliferates,  so  that  they  and  the  walls  of 
the  lymph  sinuses  and  of  the  vessels  become  thickened. 

A  lymph  nodule  therefore  appears  to  be  surrounded  by  a  fine 
connective  meshwork,  containing  few  lymphocytes,  but  many  red 
corpuscles  and  phagocytes.  As  time  goes  on,  the  inflammation  in 
the  gland  subsides,  and  it  becomes  less  vascular,  firm,  and  hard,  and 
full  of  dense  fibrous  tissue.  Secondary  infection,  however,  may 
occur  with  the  formation  of  abscesses. 

Microscopically,  the  lungs  may  be  found  to  be  hyperaemic,  even 
when  normal,  to  the  naked  eye,  while  the  complication  of  pneu- 
monia will  give  rise  to  the  usual  appearances.  The  heart  shows 
small-celled  infiltration  in  all  its  layers,  with  sometimes  haemor- 
rhages. Vianna  has  noted  in  animals  infected  with  C.  castellanii 
cysts  in  the  muscles  similar  to  those  of  S.  cruzi,  and  appears  to  have 
found  them  also  in  the  muscular  and  nervous  tissues  from  a  case  of 
sleeping  sickness.  The  liver  and  spleen  may  show  thickening  of  the 
capsule,  while  the  latter  is  very  congested,  and  its  trabecula;  are  in- 
creased in  thickness.     In  natives  signs  of  chronic  malaria  are  almost 


the  slei:ping  sicknesses 


1269 


constantly  present  in  the  spleen  and  liver.  The  bone-marrow  may 
be  very  cellular,  with  congested  vessels  and  haemorrhages. 

Stevenson  and  others  have  found  trypanosomes  scattered  through  the  brain 
substance  in  no  special  relation  to  the  capillaries  and  smaller  bloodvessels 
in  animals  inoculated  with  CastellaneUa  gambiensis  (nigeriensis)  and  other 
trypanosomes. 

Symptomatology. — The  course  of  the  disease  may  be  roughly 
divided  into  three  stages — the  incubation,  the  febrile,  called  also 
glandular  stage,  and  the  cerebral  stage. 

Incubation. — The  duration  of  the  incubation  period  is  not  cer- 
tainly known  in  man,  but  may  be  considerably  shorter  than  was 
believed  by  the  old  authors:  probably  in  most,  cases  it  does  not 
exceed  two  or  three  weeks,  and,  according  to  Martin  and  Lebceuf's 
observations  in  Europeans,  it  may  be  even  less  than  ten  days. 
On  the  other  hand,  some 
infected  individuals  may 
not  show  any  sign  of 
disease  for  months,  and. 
it  is  said,  even  five  or  six 
years.  The  bite  of  the 
infected  Glossina  gives 
rise,  as  a  rule,  only  to 
very  slight  local  irritation, 
which  quickly  subsides, 
and  is  often  overlooked 
by  the  patient. 

Febrile  or  Glandular 
Stage. — The  onset  of  the 
disease  is  characterized  by 
attacks  of  fever  almost 
constantly  associated  in 
Europeans  with  an  ery- 
thematous eruption.  This 
fever  lasts  about  a  week, 
and  disappears,  to  recur 
again  later  for  the  same 
or  much  longer  periods. 
It  is  generally  of  an  inter- 
mittent or  remittent  type. 
During  an  attack  the 
pulse-rate  and  the  res- 
pirations   are    increased, 

and  there  is  often  enlargement  of  the  liver  and  spleen,  though 
how  much  of  this  may  be  due  to  recurrent  malaria  is  not  known; 
the  pulse  often  remain  rapid  during  the  apyrexial periods.  Neuralgic 
pains  and  headache  may  also  be  complained  of. 

An  erythematous  eruption  is  often  found  on  Europeans.  It 
begins,  as  a  rule,  with  badly  defined,  pinkish  patches,  which  clear 
in  the  centre  until  a  ring  is  produced;  if  a  portion  of  the  ring  fades 


Fig.  639. — Negro  Patient  in  the  Late 
Stage  of  Sleeping  Sickness. 


1270 


THE  AFRICAN  TRYPANOSOMIASES 


a  crescent  may  be  produced.  This  circinate  eruption  may  appear 
on  any  part  of  the  body,  but  is  especially  frequent  on  the  trunk; 
in  some  cases,  instead  of  rings,  solid  infiltrated  patches,  the  size  of 
a  half-crown  or  larger,  are  present.  Rubeloid  spots  and  a  mottled 
appearance  of  the  skin  are  not  rare.  A  vesiculo-papular  eruption  has 
also  been  described,  but  is  rare  in  our  experience.  Dermatographia 
is  common  in  Europeans.  In  full-blooded  negroes  the  erythematous 
eruption  may  not  be  noticeable;  in  them  very  often  a  dry,  scaly 
condition  of  the  skin  is  found.  These  various  eruptions  are  called 
Trvpanides.  Patches  of  localized  oedema  maybe  seen  in  some  cases. 
The  most  typical  sign  of  the  disease  in  this  stage  is  enlargement 
of  one  or  more  lymphatic  glands,  especially  those  of  the  neck,  in 
the  posterior  triangle  (Winterbottom's  sign.)  The  enlarged  glands 
are  in  this  period  generally  fusiform,  and  of  rather  soft  consistency. 
Another  early  symptom,  noted  by  Kerandel,  is  a  general,  intense, 
deep  hyperesthesia.  As  repeated  attacks  of  fever  increase,  the 
patient  may  become  ansemic  and  asthenic,  but  the  febrile  condition 
may  last  for  years,  and,  indeed,  in  this  stage  the  disease  may  be  cured. 


Fig.  640. — Sleeping  Sickness,   Late  Stage,  in  Anglo-Egyptian  Sudan. 
(Photograph  kindly  lent  by  Colonel  A.  Balfour.) 

The  Cerebral  Stage  (the  So-called  Sleeping  Sickness). — After  the 
febrile  stage  has  lasted  some  time  (weeks  or  months),  and  even  years, 
a  change  begins  to  appear  in  the  habits  and  disposition  of  the 
patient.  Previously  bright,  intelligent,  and  hard-working,  he  be- 
comes apathetic,  dull,  with  a  disinclination  for  exertion,  preferring 
to  sit  quietly  or  to  lie  down.  He  also  becomes  careless  in  his  work 
and  dirty  in  his  habits,  and  at  the  same  time  a  difficulty  in  walking 
begins  to  be  noticed.  Tn  this  condition  the  sleeping  sickness  stage 
of  the  disease  may  be  said  to  have  been  properly  entered.  Typi- 
cally, the  patient  is  dull  and  apathetic,  but  can  be  easily  roused,  and 
answers  questions  rationally,  without  difficulty  in  speech.  Sleep 
may  be  excessive,  but  is  not  the  prominent  symptom  so  often  de- 
scribed, the  condition  being  more  one  of  lethargy,  from  which  the 
patient  can  be  easily  roused.  Fine  tremors  are  noticed  in  the 
tongue  at  first,  later  in  the  hands  and  arms,  and  sometimes  also  in 


SYMPTOMATOLOGY  1271 

the  legs,  and  even  in  the  abdominal  muscles.  The  tremor  of  the 
tongue  and  hands  may  be  a  very  early  symptom  and  may  be  present 
in  the  febrile  stage.  These  tremors  may  occasionally  be  so  severe 
that  they  cause  the  whole  body  to  shake,  and  at  times  epileptiform 
fits,  general  or  localized,  may  be  seen.  The  gait  is  peculiar,  there 
being  apparently  a  difficulty  in  raising  the  feet,  so  that  the  patient 
shuffles  along;  but  there  is  no  paralysis  as  a  rule,  and  the  superficial 
reflexes  are  normal;  the  deep  reflexes  may  be  exaggerated  and  then 
lost;  there  is  no  clonus.  There  is  inco-ordination  in  some  cases, 
and  Romberg's  sign  may  be  present.  As  the  disease  advances, 
rigidity  appears,  especially  in  the  muscles  of  the  neck  and  legs, 
which  latter  may  assume  the  position  of  flexion  of  the  thighs  on  the 
abdomen  and  the  legs  on  the  thighs.  Babinski's  sign  is  generally 
absent.  Sensation  is  at  first  normal,  but  there  may  be  hyperesthesia 
in  the  region  of  the  fifth  nerve  and  other  nerves,  and  at  times  the 
patient  complains  of  headache.  The  pupils  are  equal,  moderately 
contracted,  and  react  to  light  and  accommodation.  There  is  nothing 
abnormal  in  the  organs  of  special  sense  as  a  rule.  There  is  usually 
fever,  the  temperature  rising  in  the  evening  from  ioo°  to  1040  F., 
and  falling  to  subnormal  in  the  morning;  but  this  may  be  varied 
in  many  ways:  thus  for  a  period  the  temperature  may  be  almost 
normal  or  subnormal,  while  for  some  days  before  death  it  becomes, 
as  a  rule,  permanently  subnormal. 

There  are  no  special  symptoms,  such  as  rigors  or  sweating,  asso- 
ciated with  the  rise  of  temperature.  The  pulse  is  quick  (90  to  140), 
but  it  is  independent  of  the  temperature,  being  quick  with  a  low 
temperature.  It  is  regular,  but  small  and  very  low  in  tension,  and 
generally  is  imperceptible  at  the  wrist  for  some  time  before  death. 
The  heart  as  a  rule  shows  no  abnormal  symptoms,  though  systolic 
inorganic  murmurs  may  be  present.  The  respirations  are  regular 
and  equal,  but  are  increased  in  number,  especially  towards  evening, 
varying  from  20  to  30;  before  death  they  not  uncommonly  take  on 
the  Cheyne-Stokes  type.  Congestion  and  oedema,  with  patches  of 
pneumonia,  are  not  infrequently  met  with  before  death.  The 
appetite  is  good,  and  may  even  be  increased;  digestion  is  usually 
satisfactory,  but  constipation  may  be  marked,  or  there  may  be  occa- 
sionally diarrhoea.  The  tongue  is  frequently  flabby  and  covered  with 
white  fur;  the  faeces  of  native  patients  are  typical  of  a  vegetable  diet, 
and  show  the  usual  parasites  of  a  tropical  country.  The  spleen  and 
liver  may  be  enlarged,  which  perhaps  may  partly  be  due  to  malaria. 

The  Blood. — The  examination  of  the  blood  is  complicated,  because 
its  condition  is  bound  to  be  influenced  by  the  secondary  infections 
with  other  parasites,  animal  and  vegetal. 

With  this  understanding  trypanosomiasis  causes  in  a  certain 
number  of  cases  a  gradual  diminution  of  the  red  cells  to  2,000,000 
or  less,  with  a  corresponding  decrease  in  the  haemoglobin;  but  it  is 
to  be  noted  that,  as  first  observed  by  Low  and  Nabarro  in  several 
cases,  the  actual  number  of  erythrocytes  may  be  above  normal. 
The  red  cells  are  usually  normal  in  appearance,  but  normoblasts 


1272 


THE  AFRICAN  TRYPANOSOMIASES 


may  be  seen.  The  leucocytes  are  normal  in  number,  as  a  rule,  with 
an  increase  of  mononuclear  cells,  while  there  may  be  a  terminal 
polymorphonuclear  increase  before  death. 

In  fresh  preparations  the  red  cells  are  not  evenly  distributed,  nor 
do  they  form  rouleaux,  being  generally  clumped  into  masses.  This 
phenomenon  of  auto-agglutination  was  first  noticed  by  Kanthack, 
Durham,  and  Blandford  in  the  lower  animals  inoculated  with 
nagana;  and  in  man,  in  cases  of  sleeping  sickness,  by  Dutton,  Todd, 
and  Christy,  and  may  be  of  diagnostic  value.  The  phenomenon  of 
auto-erythrophagocytosis  has  occasionally  been  noted. 

The  chemical  examination  of  the  blood  in  trypanosome  infections 
of  animals  has  been  performed  by  Takinioff  and  by  Nierenstein, 
the  latter  of  whom  found,  by  Moore  and  Wilson's  method  of  testing 
the  alkalinity  of  the  ash,  that  the  acidity  of  the  blood  was  increased, 


Fig.  641. — Temperature  Chart  of  a  Case   of  Sleeping  Sickness. 
(From  Low  and  Castellani  Reports  of  the  Royal  Society  on  Sleeping  Sickness.) 

probably  due  to  the  formation  of  amido-acids,  either  secreted  by 
the  parasites  or  produced  by  their  action  upon  the  proteids  of  the 
serum.  The  acidity  was  tested  by  phenolphthalein  and  Congo  red, 
and  the  alkalinity,  which  remained  fairly  constant,  was  tested  by 
d  i  met  1  lyl-amido-azo-benzol. 

The  animals  were  infected  with  C.  brucei  and  C.  equip erdutn,  but 
so  far  no  observations  have  been  made  on  human  blood. 

Urine. — No  abnormality  is  found  in  the  urine,  but  the  reaction, 
amount  of  phosphates,  etc.,  of  course,  varies  with  the  food  taken. 
In  native  patients  it  is  very  often  alkaline. 

Sexual  desire  and  menstruation  are  normal  at  first,  but  later  arc 
lost.  The  lymphatic  glands  throughout  the  body,  but  especially 
those  of  the  neck,  and  more  especially  those  of  the  posterior  triangle, 
are  enlarged.  It  is  to  be  noted,  however,  that  in  the  last  stages 
the  lymph  glands  often  undergo  a  process  of  fibrosis,  becoming 


COMPLICA  T10XS— DIAGNOSIS  1273 

smaller  and  harder.  The  skin  becomes  dry  and  rough,  but  may  be 
perfectly  normal,  though  a  papulo-pustular  eruption  may  at  times 
be  noted  on  the  backs  of  the  hands  and  forearms.  Nutrition  suffers, 
and  the  patient  generally  becomes  much  emaciated. 

As  the  disease  progresses  the  muscular  weakness  and  emaciation 
becomes  worse  and  worse,  the  tremors  more  pronounced,  the  saliva 
dribbles  from  the  mouth,  the  urine  and  faeces  are  passed  involun- 
tarily, and  bedsores  form,  while  the  intelligence  becomes  more  and 
more  affected,  and  the  patient  passes  into  a  state  of  coma,  with  a 
permanently  subnormal  temperature  and  an  absence  of  pulse  at  the 
wrist,  and  in  a  short  time  is  liberated  from  his  sufferings  by  death. 
The  duration  of  the  cerebral  or  sleeping  sickness  stage  varies  from 
a  few  weeks  to  several  months.  Since  the  atoxyl  treatment  has 
become  of  general  use,  Hodges  has  noted  that  convulsive  and  mental 
symptoms  are  more  prominent,  and  that  death  is  often  sudden, 
without  being  preceded  by  a  period  of  coma. 

Varieties. — When  the  disease  is  due  to  C.  rhodesiensis,  it  generally 
runs  a  more  rapid  course,  seldom  exceeding  four  or  five  months. 
Lethargic  symptoms  may  not  appear,  and  the  enlarged  glands  in 
the  posterior  triangle  of  the  neck  may  be  absent,  while  enlargement 
of  the  epitrochlear  glands  seems  to  be  frequent.  The  disease  caused 
by  C.  gambiensis  appears  to  be  of  a  milder  type  than  that  due  to 
C.  castellanii. 

Complications. — The  patient  is  often  infected  by  parasites  other 
than  trypanosomes;  thus,  Plasmodium  and  Laverania,  Filaria, 
Schistosoma  mansoni,  Ancylostoma  ditodenale,  Ascaris  lumbricoides, 
Trichurus  trichiura,  Strongvloides  stercoralis,  Trichomonas  intesti- 
nalis,  T.  vaginalis,  Dermatophilus  penetrans,  and  Loeschia  may  all 
be  found.  The  commonest  complication  during  the  last  stage  is  a 
cerebro-spinal  meningitis,  due  to  streptococci,  the  pneumococcus, 
or  the  meningococcus. 

Pneumonia,  laryngitis,  and  oedema  of  the  glottis  are  not  rare, 
while  iritis  is  seen  at  times,  and  symptoms  of  mania,  delirium,  and 
epilepsy  may  be  observed. 

Diagnosis".— In  the  first  stage  (febrile  or  glandular  stage)  the 
disease  may  be  readily  confused  with  malaria  and  other  fevers, 
but  in  endemic  areas  the  true  nature  of  the  malady  may  be  often 
suspected  on  certain  clinical  data,  the  principal  of  which  are  the 
attacks  of  fever  not  influenced  by  quinine,  the  erythematous  erup- 
tion in  Europeans,  the  rapid  pulse  frequently  present  also  during  the 
apyrcxial  periods,  the  asthenia,  the  deep  hyperesthesia  (Kerandel's 
symptom),  the  fine  tremor  of  the  tongue  (Low-Cast ellani's  symp- 
tom), the  cervical  polyadenitis  (Winterbottom's  symptom).  Dur- 
ing the  sleeping  sickness  stage  the  clinical  diagnosis  is  based,  in 
addition  to  the  above  symptoms,  on  the  drowsiness  and  apathetic 
appearance  of  the  patient,  on  the  remarkable  wasting  and  debility, 
and  the  more  marked,  and  occasionally  generalized,  tremors. 
The  long  course  and,  usually,  absence  of  facial  paralysis  differen- 
tiates  clinically   sleeping    sickness   from    encephalitis    lethargica 


1274  THE  AFRICAN  TRYPANOSOMIASES 

(nona).  To  make  a  definite  diagnosis,  the  demonstration  of 
C.  castellanii,  C.  gambiensis,  or  C.  rhodesiensis  in  the  body  of  the 
patient  is  necessary.     The  following  methods  should  be  used:  — 

i.  Microscopical  Examination  of  the  Peripheral  Blood  from  the 
Finger  or  Ear. — This  procedure  is  often  a  failure,  even  using  thick 
films. 

2.  Scarification  of  the  Erythematous  Eruption  and  Examination  of 
Blood  Films. — This  method  is  more  useful  than  the  first,  but  may  fail. 

3.  Nabarro's  Method. — Repeated  centrifugalization  of  10  cc.  of 
citrated  blood,  and  examination  of  the  third  sediment.  The  results 
are  good. 

4.  Dutton-Todd's  Method.- — Some  citrated  blood  is  centrifugalized 
in  small  tubes  and  the  leucocytic  layer  examined  for  trypanosomes. 

5.  Greig-Grey's  Method. — Aseptic  puncture  of  the  enlarged  cervical 
glands  with  a  sterile  syringe.  The  gland-juice  is  examined  for 
trypanosomes.  This,  from  a  practical  point  of  view,  is  the  most 
valuable  method.  To  Mott  belongs  the  credit  of  having  first  sug- 
gested the  search  for  trypanosomes  in  the  lymph  glands  as  a  diag- 
nostic method.  Balfour  has  devised  a  '  gland-holder,'  which  is 
useful  in  some  cases. 

6.  Castellani's  Method. — Centrifugalization  for  fifteen  minutes  of 
10  cc.  of  cerebro-spinal  fluid,  aseptically  removed  by  means  of 
Lumbar  puncture.  The  sediment  is  examined  for  trypanosomes 
by  making  fresh  and  stained  preparations.  The  result  is  almost 
constantly  positive  in  the  sleeping-sickness  stage,  but  negative,  as 
a  rule,  in  the  first  stage  of  the  malady. 

The  technique  to  perform  lumbar  puncture  is  as  follows:  The  patient  may 
be  given  chloroform,  but  usually  a  local  anaesthetic  spray  is  sufficient.  Lay 
the  patient  on  the  right  or  left  side;  flex  the  thighs  on  the  abdomen.  Then 
make  the  skin  of  the  lumbar  region  aseptic,  and,  feeling  with  the  tip  of  the 
finger  the  position  of  the  laminae,  thrust  the  sterile  needle  between  the  laminae 
of  the  third  and  fourth  lumbar  vertebrae,  £  inch  from  the  median  line,  obliquely 
outwards  and  forwards  into  the  canal.  The  fluid  will  escape,  and  can  be 
collected  in  a  sterile  tube.  After  withdrawing  the  needle,  the  area  should 
be  covered  with  an  aseptic  pad  and  bandage. 

7.  Inoculation  of  Susceptible  Animals. — Ten  cc.  or  20  cc  of  blood 
arc  aseptically  removed  from  a  vein  and  inoculated  into  sus- 
ceptible animals,  or  10  cc  of  cerebro-spinal  fluid  may  be  inocu- 
lated. The  animals  most  suitable  are  monkeys,  guinea-pigs,  and 
dogs.  The  most  suitable  monkeys,  according  to  Thironx  and 
d'Anfreville,  are  those  of  the  species  Cercopithccus  ruber,  while 
some  other  species — e.g.,  C .  fuliginosus — are  almost  refractory. 

The  following  biological  phenomena  and  reactions  may  sometimes  be  of 
diagnostic  value: — • 

1  [uto- Agglutination. — In  many  cases  of  sleeping  sickness,  in  wet  pre- 
parations of  blood  examined  microscopically  with  a  low  power,  the  red 
corpuscles  are  not  evenly  distributed,  nor  are  they  arranged  in  rouleaux, 
but  are  clumped  together--' agglutinated  ' — in  irregular  masses.  This 
appearance  is  noi  specific  of  trypanosomiasis,  having  been  found  in  cases 
oi  filariasis,  malaria,  syphilis,  and  yaws. 


PROGNOSIS  1275 

2.  Complement  Fixation.  —  Levaditi  and  Muttermilch  have  applied  the 
Bordet-Gengou  reaction  to  trypanosome  infections.  According  to  them, 
the  complement  can  be  fixed  by  using  as  antigen  an  extract  of  trypanosomes 
separated  from  red  cells. 

3.  Levaditi  and  Muttermilch' s  Leucocytic  Attachment  Reaction. — Levaditi  and 
Muttermilch  have  shown  that  trypanosomes  treated  with  the  specific  serum 
(heated  at  550  C.)  develop  a  property  of  becoming  attached  to  leucocytes, 
and  that  this  phenomenon  is  specific.  The  test  may  be  used  for  identifying 
a  trypanosome  or  for  diagnosis,  but,  according  to  Laveran  and  Mesnil,  is 
not  very  reliable  in  the  case  of  C.  castellanii  infections. 

Attempts  have  been  made  to  evolve  agglutination  reactions,  trypanolytic 
precipitin,  and  other  biological  tests  tor  purposes  of  the  diagnosis  of  sleeping 
sickness,  but  so  far  with  little  success. 

Prognosis. — The  prognosis  is  serious,  but  not  quite  so  serious  as 
it  Wets  before  the  introduction  of  atoxyl  and  the  mixed  atoxyl 
tartar  emetic  treatment.  If  the  patient  is  in  the  early  stage,  and 
can  be  removed  from  the  endemic  area  and  put  under  good  hygienic 
conditions  and  atoxyl  treatment,  the  disease  may  be  cured,  or 
at  least  a  marked  improvement  may  be  obtained.  Great  care, 
however,  is  necessary  before  saying  that  a  patient  is  really  cured, 
and  at  least  two  blood  injections  into  susceptible  animals  should 
be  performed  before  giving  a  decided  opinion.  If,  however,  the 
patient  is  compelled  to  live  in  the  endemic  area,  and  cannot  be 
treated  with  atoxyl,  the  outlook  is  most  hopeless.  It  is  to  be  noted 
that  there  are  several  strains  or  varieties  of  different  virulence.  The 
Uganda  and  French  Congo  strains  caused  by  C.  castellanii,  as  noted 
by  Laveran  and  Mesnil,  cause  a  more  acute  type  of  the  disease  than 
the  (iambia  strain  due  to  C.  gambiensis,  and  C.  rhodesiensis  is  in 
laboratory  animals  more  virulent  than  C.  castellanii,  and  the  disease 
caused  by  it  in  man  runs  a  more  rapid  course. 

Treatment. — The  only  medicaments  which  have  been  so  far  found 
to  be  of  any  real  value  are,  first,  arsenic  in  the  form  of  atoxyl,  and,  in 
a  less  degree,  antimonium  in  the  form  of  tartar  emetic,  the  best 
method  of  treatment  being  a  combined  treatment  wit  h  1  he  two  drugs. 

Atoxyl. — We  recommend  2  to  3  grains  of  atoxyl  by  intramuscular 
injection  every  third  day  for  at  least  two  years,  or  0-3  gramme  every 
fourth  day  for  the  same  period,  with  o-i  gramme  for  a  childten  years 
old. 

Borden  and  Rodhain's  method  is  7J  grains  of  atoxyl  by  intramuscular 
injection  every  fifth  day.  Koch  recommended  the  subcutaneous  injection  of 
jh  grains  (£  gramme)  on  two  successive  days  every  ten  days  for  two  months, 
when  the  treatment  is  to  Ik-  stopped  until  further  symptoms  develop,  and 
when  this  occurs  the  treatment  should  lie  repeated.  The  drug  can  be  obtained 
or  imported  from  any  chemist  in  sterile  vials  ready  for  hypodermic  medication. 
Tlie  injection  of  atoxyl  is  occasionally  followed  by  a  febrile  reaction,  due, 
according  to  some  observers,  to  the  absorption  of  products  of  trypanolysis. 

/ONa 
Atoxvl    is    sodium-£-aminophenyl    arseniate — NH2CfiH4AsO(  and 

oil 
contains  from  i^OS  to  20-78  per  cent,  of  arsenic,  according  to  the  amount  of 

/ONa 
water  of  crystallization.  Mono-acetylatcd  atoxyl  is  CH.jCONHCfiH5AsO\ 

\OH 
According  to  Mesnil  and  Nicolle's  observations,  and  the  more  recent  observa- 


1276  THE  AFRICAN  TRYPANOSOMIASES 

tions  of  Nierenstein,  it  is  not  the  arsenic  in  these  sompounds  which  is  to  be 
looked  upon  as  the  effective  agent,  but  the  amido-group,  which  may  possibly 
be  the  effective  agent  in  trypan  red,  afridol  blue,  afridol  violet,  and  para- 
fuchsin,  which  do  not  contain  arsenic,  but  possess  amido-groups,  and  affect 
trypanosomes  in  a  similar  manner  to  atoxyl.  According  to  Ehrlich,  Leva- 
diti,  and  Yamanouchi,  atoxyl  undergoes  a  reduction  in  the  animal  tissues. 
Ehrlich  has  prepared  two  derivatives  of  atoxyl,  one  of  which,  already  men- 
tioned (arseno-phenylglycin),  is  very  effective  in  mice  on  atoxyl-resistant 
trypanosomes.  Levaditi  and  Yamanouchi  have  also  prepared  an  active 
derivative  of  atoxyl,  which  they  call  trypanotoxyl.  Nierenstein  thinks  that 
atoxyl  is  oxydized  in  the  tissues,  and  it  is  only  in  the  nascent  state  that  it 
becomes  efficacious. 

Soamin. — Owing  to  the  fact  that  large  doses  of  atoxyl  lead  to  such  un- 
pleasant results  as  optic  atrophy,  gastro-intestinal  inflammation,  and  peri- 
pheral neuritis,  other  arsenical  preparations  have  been  recommended;  and 
the  firm  Burroughs  and  Wellcome  has  introduced,  under  the  trade  name  of 
soamin,  a  preparation  somewhat  similar  to  atoxyl,  but  said  to  be  less  poisonous. 
It  is  given  in  the  same  doses  as  atoxyl,  but  the  therapeutic  results  do  not 
appear  to  have  been  very  successful.  Soamin,  according  to  the  published 
formula,  is  C2H4NH2AsO(OH)(ONa)5H20. 

Arseno-phenylglycin. — Ehrlich  has  prepared  a  derivative  of  atoxyl,  called 
arseno-phenylglycin,  whichis  from  two  to  four  times  less  toxic  than  atoxyl  itself. 

This  preparation  has  been  tried  by  Ehrlich,  Mesnil,  Kerandel,  and  others 
upon  lower  animals  experimentally  infected  with  C.  castellanii,  and  has 
been  found  to  be  very  effective,  being  also  a  prophylactic.  It  has  been  used 
in  man  by  Kleine  in  the  same  doses  as  atoxyl,  but  has  now  been  abandoned. 

Liquor  Arseuicalis. — When  for  special  reasons  it  is  impossible  to  carry  out 
the  treatment  by  injections,  arsenic  may  be  given  by  the  mouth  in  the  form 
of  Fowler's  solution,  which  must  be  given,  well  diluted  in  water  or  milk,  in 
5-minim  doses,  and  gradually  increased  to  15-minim  doses. 

Loffler  and  Ruh's  neutral  solution  of  arsenious  acid  (1  c.c.  of  which  contains 
1  centigramme  of  arsenious  acid)  may  be  given  in  doses  of  2  c.c.  daily  for  three 
days,  and  then  continued  in  doses  of  1  c.c.  per  diem  for  several  weeks,  after 
which  it  must  be  temporarily  discontinued,  but  must  after  a  time  be  restarted, 
and  in  this  manner  continued  for  months,  provided  no  ill-effects  are  produced. 

Salvarsan  and  Neosalvarsan. — Their  action  is  less  efficacious  than  atoxyl. 

Atoxylale  of  Mercury. — This  preparation,  introduced  by  Uhlenhuth,  has 
given  less  satisfactory  results  than  atoxyl. 

Quinine  Derivates.- — Morgenroth  and  Halberstaedter  have  shown  that 
some  quinine  derivatives,  such  as  hydroquinin,  have  a  preventive  and  curative 
effect  in  certain  experimental  trypanosomiases. 

Ipecacuanha  Derivates. — The  emetine  salts  might  be  studied  in  regard  to 
their  possible  action  on  trypanosomes. 

Anarcotine. — The  use  of  this  opium  alkaloid  has  been  suggested  by  Johnson. 

Combined  Therapy. — As  the  result  cf  the  important  observations 
of  Ehrlich  on  the  phenomenon  of  chemio-resistancy,  which  may 
be  acquired  by  trypanosomes  after  a  long  use  of  the  same  dFug, 
numerous  combined  treatments  have  been  Suggested.  Of  these, 
the  most  important  are: — (1)  antimony  and  atoxyl;  (2)  mercury 
;md  atoxyl;  (3)  orpiment  and  atoxyl;  (4)  various  dyes  and  atoxyl. 

Antimony  and  Atoxyl  Treatment. — Antimony  salts,  as  well  as  phosphorus, 
wen-  tirst  suggested  by  Mesnil  as  likely  to  be  of  use  in  trypanosomiasis.  To 
Plimmer  ami  Thomas  belongs  the  credit  of  having  experimentally  shown  the 
powerful  trypanocide  action  of  antimony.  In  man  the  subcutaneous  or  intra- 
muscular injections  of  solutions  of  the  various  salts  of  antimony  (sodo-tartrate 
of  antimony,  sulphide  of  antimony  and  soda,  etc.)  are  very  painful.  Plimmer 
therefore  suggests  oil  emulsions,  Manson  gives  the  drug  by  the  mouth 
or  by  the  rectum,  and  other  authors  by  intravenous  injection.     Daniels  and 


TREATMENT  1277 

Newham  recommend  the  painless  Martindale's  injectio  antimonii  oxidi, 
30  minims  (  =  gr.  ^  antim.  ox.)  to  be  given  subcutaneously  once  or  twice 
daily.  Apparently  the  trypanocide  action  of  antimony  is  more  powerful 
in  the  lower  animals  than  in  man,  in  whom  the  results  are  inferior 
to  those  given  by  atoxyl.  A  mixed  antimony  and  atoxyl  treatment  is, 
however,  of  advantage  in  most  cases,  an  atoxyl  injection  (3  grains)  being 
given  every  third  day,  or  7^  grains  every  fifth  day,  and  sodio-tartrate  of 
antimony  (Plimmer's  salt)  administered  daily — 2  grains  dissolved  in  a  large 
quantity  of  water  (2  pints)  by  the  mouth  or  by  the  rectum.  Tartar  emetic, 
however,  is  best  given  by  intravenous  injections,  using  solutions  of  1  in  100 
or  1  in  1,000.  The  dose  of  the  drug  to  be  given  is  5  to  10  centigrammes  per 
injection.  It  is  important  that  none  of  the  fluid  of  the  injection  should  escape 
into  the  surrounding  tissues,  as  a  violent  inflammation  may  result.  These 
injections  should  be  administered  monthly  on  ten  consecutive  days  for  a  long 
period.  The  injection  of  salts  of  antimony  may  produce  a  marked  fall  in  the 
blood-pressure)  dyspnoea,  and  signs  of  collapse,  and  therefore  Thiroux  sug- 
gested that  subcutaneous  injections  of  caffein  should  precede  ten  or  fifteen 
minutes  their  administration. 

Basing  his  opinions  upon  th~  very  successful  treatment  carried  out  by 
Captain  Sims'  n,  R.A.M.C.,  at  the  Yei  Sleeping  Sickness  Camp  in  the  Mongalla 
Province  of  the  Sudan,  Captain  Spence,  R.A.M.C.,  is  treating  cases  in  the 
Bahr  el-Ghazal  Province  as  follows  : — 

A.  Cases  in  the  early  stage  :■ — ■ 

1.  Six  intravenous  injections  each  of  6  centigrammes  of  antimony  at 

three-day  intervals. 

2.  Interval  one  month. 

3.  Twelve  intramuscular  injections  each  of  30  centrigrammes  of  atoxyl 

at  three-day  intervals. 

4.  Interval  one  month. 
5  and  6.   Repeat  1-4. 

7.  Three  months  after  last  t  eatment  the  blood  of  the  patient  is 
inoculated  int  >  an  animal.  If  the  animal  remains  uninfected  the 
patient  is  given  a  numbered  disc  and  told  to  report  every  three 
months. 

Total  dosage:  Atoxyl,  io-8  grammes  in  about  one  year;  antimony, 
1  08  grammes. 

B.  Relapses  and  cases  first  seen  in  a  late  stage  of  the  disease  : — 

1.  Nine  intramuscular  injections  each  of  1  gramme  of  atoxyl  at  ten- 

day  intervals. 

2.  Interval  one  month. 

3.  Nine   intramuscular    injections   each    of    1    gramme    of   atoxyl  at 

twenty-day  intervals. 

4.  Interval  one  month. 

5.  Nine  intramuscular  injections  of  atoxyl  at  thirty-day  intervals. 

6.  Interval  of  three  months. 

7.  Animal  is  inoculated  as  above. 

Total  dosage:  27  grammes  of  atoxyl  in  two  years. 

Cases  in  which  no  symptoms  are  noted  and  in  which  animal  inoculations 
are  negative  are  kept  under  close  control  for  twj  years,  alter  which  they 
report  every  six  months  for  two  years  and  the  result  judged. 

Mercury  and  Atoxyl. — Mercury  was  first  introduced  in  1902  for  the  treat- 
ment of  sleeping  sickness  by  Low  and  Castellani,  using  intravenous  injection 
of  Baccelli's  sublimate  solution  (hydrargyri  perchloridi,  o*io  gramme;  sodii 
chloridi,  0-50  gramme;  aquae  destillatai,  ioo*oo  c.c;  1  to  4  c.c.  per  intra- 
venous injection),  in  association  with  arsenic  and  quinine  by  the  mouth.  A 
fall  of  the  temperature  was  observed  in  some  cases,  but  the  fatal  course  of  the 
disease  was  not  influenced.  Moore,  Nicrenstein,  and  Todd  have  used  mercury 
and  atoxyl  in  combination  or  alternation,  with  the  idea  that  mercury  might 


I278  THE  AFRICAN  TRYPANOSOMIASES 

act  upon  the  latent  form  of  the  trypanosome,  while  atoxyl  would  influence 
the  active  form.  In  man  this  combined  treatment  has  apparently  not  given 
any  better  results  than  atoxyl  alone. 

Orpiment  and  Atoxyl.- — This  combined  treatment,  consisting  of  atoxyl  and 
an  inorganic  salt  of  arsenic  such  as  orpiment,  has  been  recommended  by 
Laveran  and  Thiroux,  and  has  been  used  in  man  with  good  results. 
The  orpiment  should  be  given  in  pills,  in  the  dose  of  2  grains  of  orpiment  two 
or  three  times  daily.  The  administration  of  orpiment  frequently  causes 
diarrhoea.  Thiroux  therefore  incorporates  in  the  orpiment  pills  some  opium. 
Thiroux's  formula  is: — 

Orpiment     . .  . .  .  .  .  .  .  .  . .      20  grammes. 

lixtr.  opii    .  .  . .  .  .  .  .  .  .  .  .      0-40  gramme. 

Gumm.         .  .    \ 

Pulv.  glyceriz./      ""  . .      q.  . 

To  be  divided  into  200  pills. 

Various  Dyes  and  Atoxyl. — Combined  treatments  of  Mesnil's  afridol  and 
atoxyl,  Ehrlich's  parafuchsin  and  atoxyl,  picric  acid,  safranin,  tryparlavin 
and  other  dyes  and  atoxyl,  have  been  suggested,  but  in  man  the  results  have 
not  been  so  successful  as  in  the  lower  animals. 

Treatment  ot  Natives. — In  the  case  of  native^  it  is  necess  ryto  gather  them 
into  special  sleeping  sickness  camps  in  order  that  treatment  n>ay  be  efficiently 
carried  out.  These  camps  should  be  in  some  fl.  -free  area,  and  should  be 
provided  with  a  rained  medical  staff.  Patients  able  to  work  should  be 
employed  to  raise  crops  for  their  own  consumption,  to  supplement  the  diet 
provided  by  the  Government. 

Symptomatic  Treatment. — In  addition  to  the  atoxyl  treatment  or 
combined  treatments,  malaria  and  the  intestinal  parasites  must  be 
treated  if  present.  The  patient  should,  if  possible,  be  removed  from 
the  area  of  infection  and  placed  under  good  hygienic  conditions  and 
on  good  food,  and  no  case  should  be  considered  to  be  cured  until  the 
injection  of  the  blood,  on  more  than  one  occasion,  into  susceptible 
animals  fails  to  infect  them. 

Prophylaxis. — At  the  present  time  prophylaxis  must  be  under- 
taken on  the  assumption  that  the  disease  is  spread  from  place  to 
place  by  man  along  channels  of  human  intercommunication,  and 
from  man  to  man  by  Glossina  palpalis  and  G.  morsitans,  and  that 
at  least  in  the  case  of  C.  rhodesiensis  there  are  animals  which  act  as 
reservoirs  of  the  virus.  With  regard  to  these  flies,  further  infor- 
mation is  required  as  to  their  bionomics,  though  Bagshawe's  and 
Hodges'  researches,  as  well  as  those  of  Zupitza,  Sander,  Minchin, 
Kinghorn  and  Yorke,  Carpenter,  and  others  have  thrown  some  light 
on  the  subject. 

Before  enumerating  the  principal  prophylactic  measures  to  be 
recommended,  we  wish  to  draw  attention  to  the  fact  that  these, 
as  pointed  out  by  Bagshawe,  will  be  useless  without  the  co-opera- 
tion of  the  natives.  This  co-operation  may  be  obtained  by  ex- 
plaining to  them  at  every  possible  opportunity  the  reason  for  the 
measure  taken.  In  this  missionaries  and  native  chiefs  may  be  of 
i  he  greatest  help.  With  this  proviso  we  consider  the  following  to 
be  tlif  principal  prophylactic  measures: — 

Public  Prophylaxis. — We  advocate: — 

1.  The  formation  of  a  Central  Executive  International  Board, 
with  headquarters  in  either  Paris  or  London. 


PROPHYLAXIS  1279 

2.  The  formation  of  an  Executive  Sleeping  Sickness  Commission 
in  each  political  division  of  Africa  in  which  the  disease  exists. 

The  different  Governments  should  be  invited  to  co-operate  to 
prevent  persons  travelling  from  districts  where  the  disease  exists 
into  non-infected  regions,  and  medical  posts  of  inspection  should 
be  established  for  the  examination  of  natives.  According  to 
some  authorities  (Dutton,  Todd),  all  natives  presenting  enlarged 
glands  should  be  considered,  from  a  practical  point  of  view,  as 
trypanosome  carriers,  and  prevented  from  emigrating.  This  is, 
perliaps,  going  a  little  too  far,  inasmuch  as,  in  our  experience,  and 
in  that  of  Low,  Bagshawe,  Koch,  Hodges,  etc.,  numbers  of  natives 
have  enlarged  glands,  though  not  suffering  from  trypanosomiasis; 
and,  on  the  other  hand,  cases  of  trypanosomiasis  occur  in  which 
there  is  no  enlargement  of  the  lymphatic  glands.  We  admit,  how- 
ever, that  gland  palpation  may  be  of  some  use  in  formulating  an 
approximate  idea  of  the  extent  of  the  dissemination  of  the  disease. 

The  sick  should  be  removed  from  the  fly  regions  and  segregated 
in  places  where  the  Glossina  palpalis  and  G.  morsitans  are  not  found, 
or  where  the  temperature  and  climatic  conditions  are  unfavourable 
to  the  development  of  trypanosomes  in  the  flies.  They  should  be 
treated  with  atoxyl  before  being  moved. 

In  the  regions  where  the  disease  is  due  to  Castellanclla  castcllanii, 
which  is  mostly  carried  by  Glossina  palpalis,  villages  should  be 
removed,  if  possible,  from  the  fly  zones;  and  the  occupations  carried 
on  in  fly  zones,  such  as  fishing,  should  be  discouraged.  This  has 
been  done  in  certain  regions  round  the  Victoria  Nyanza  Lake,  but 
the  result  has  not  been  completely  successful,  as  infected  flies  were 
found  to  be  plentiful  three  years  after  the  measures  had  been  carried 
out.  The  waste  land  became  full  of  game  and  wild  animals,  some  of 
which  are  probable  reservoirs  of  the  infection.  Duke,  in  fact,  has 
found  C.  castcllanii  in  two  marsh  antelopes  or  situtunga  (Tragela- 
phus  spekei),  and  believes  this  observation  to  be  confirmed  by  the 
infection  of  two  boys  working  on  an  uninhabited  island  in  Lake 
Victoria. 

Clearing  of  the  bush  along  the  water's  edge  for  100  yards,  and 
round  a  village  for  300  yards,  at  least,  is  to  be  advised. 

European  bungalows  should  be  segregated  from  native  quarters. 
Houses  should  be  rendered  gnat-proof,  and  natives  bringing  water 
from  streams  should  not  be  allowed  to  enter  the  house,  as  they 
are  liable  to  be  surrounded  by  tsetse-flies  which  have  followed  them. 
Indeed,  some  authorities  look  upon  the  bath-room  as  a  source  »>i 
European  infection. 

Destruction  of  the  Animals  on  which  the  Fly  feeds. — Koch  recom- 
mended the  destruction  of  the  crocodiles  by  poison,  and  by  collecting 
and  destroying  their  eggs.  Unfortunately,  the  crocodile  is  not  the 
only  animal  on  which  the  fly  feeds.  The  blood  of  many  other  verte- 
brate animals  is  palatable  to  the  fly,  and  therefore  thks  method  of 
prophylaxis  is  without  much  practical  importance. 

Destruction  0/  the   Vertebrate  Reservoir.— Many  authorities  have 


1280  THE  AFRICAN  TRYPANOSOMIASES 

supported  the  idea  of  exterminating  the  big  game,  because  they 
may  be  the  vertebrate  reservoir,  but  this  requires  further  proof, 
and  is  therefore  at  present  too  radical  a  measure. 

Destruction  of  the  Pupa.— Minchin  has  suggested  the  breeding  of- 
the  jungle-fowl  to  destroy  the  pupae,  which,  as  discovered  by  Bag- 
shawe,  are  found  in  the  turf  among  the  roots  of  banana  and  other 
trees.  Balfour  and  others  have  suggested  trapping  the  adult  flies 
in  various  ways.  Further  information,  however,  is  necessary  on 
the  enemies  of  the  pupae  and  adult  tsetse-flies. 

Personal  Prophylaxis. — Natives  in  the  fly  zones  should  be  en- 
couraged to  wear  suitable  clothing,  and  the  reason  explained  to  them. 
Europeans  should  be  careful  not  to  expose  their  legs  and  hands 
to  be  bitten.  High  boots,  puttees,  or  leggings  should  be  worn,  and 
where  the  flies  abound  gloves  and  veils,  though  very  uncomfortable, 
are  of  service.  White  clothes  are  better  than  dark  ones,  as  it  has 
been  long  observed  that  the  tsetse-fly,  as  well  as  many  other  insects, 
have  a  preference  for  black  or  dark  colours.  The  use  of  volatile 
substances  such  as  citronella  oil  has  been  advised  by  some.  Unfor- 
tunately, the  odour  of  such  substances  is  repellent  to  many  persons. 

Morgenroth  and  H  alb  erst aedter  have  shown  that  certain  derivates 
of  quinine,  in  the  lower  animals,  prevent  an  experimental  trypano- 
some  infection,  and  Bagshawe  suggests  that  a  daily  dose  of  quinine 
may  be  useful  in  man. 

Vaccination. — Attempts  at  vaccination  have  not  yet  entered  a 
practical  stage,  as  inoculation  with  dead  or  attenuated  viruses  have 
so  far  failed  in  the  lower  animals. 

Summary  of  Prophylactic  Measures. 

I.  General  measures: — 

i.  Co-operation  of  various  Governments,   especially  in  controlling 
the  movements  of  non-infected  natives. 

2.  Formation  of  medical  posts  of  inspection  at  suitable  places  to 

prevent  infected  natives  entering  non-infected  areas  and  vice 
versa. 

3.  Segregation  of  the  sick,  if  possible,  in  districts  free  from  Glossinca, 

or   where   the   climatic   conditions   are   unfavo  irabic   for   the 
development  of  the  trypanosome  in  the  fly. 

4.  Clearing  of  the  bush  near  villages  and  along  the  water's  edge, 

especially  at  landing-places,  fords,  and  ferries. 

5.  In  certain  cases — especially  with  regard  to  C.  rhodesiensis — the 

destruction  of  large  game,  especially  antelopes.     (This  is  still 
sub  judice.) 
II.   Personal  measures:- — - 

1 .  Avoidance  of  bites  by  wearing  white  clothing,  high  boots,  puttees, 

and  the  putty  pattern  of  leggings. 

2.  Immediate  disinfection  of  a  bite  by  painting  it  with  tincture  of 

iodine  or  by  applying  a  solution  of  formalin  (1  in  40). 

TRYPANOSOME  FEVERS. 

Definition.— The  trypanosome  fevers  of  man  are  caused  by  a 
monomorphic  trypanosome  allied  to  Duttonella  vivax  Ziemann, 
1905,  and  to  an  unspecified  germ  allied  to  Castellanella  evansi,  and 


REFERENCES  128 1 

are  characterized  by  milder  symptoms  and  the  absence  of  meningo- 
encephalitis as  far  as  is  known. 

Remarks. — In  Macfie's  case  of  infection  with  a  trypanosome 
allied  to  D.  vivax,  apart  from  slight  fever  there  were  no  symptoms, 
and  after  a  single  injection  of  atoxyl  the  trypanosomes  disappeared 
from  the  blood. 

In  Lanfranchi's  case  of  accidental  laboratory  infection  there  have 
been  irregular  attacks  of  fever  lasting  seven  years,  and  general 
debility  associated  with  large  patches  of  cutaneous  oedema.  But 
there  has  been  neither  mental  symptoms  nor  tremor.  He  has 
been  treated  by  atoxyl  and  tartar  emetic. 

It  will  thus  be  seen  that  the  trypanosome  fevers  resemble  mild 
infections  in  animals  rather  than  human  sleeping  sickness. 

Diagnosis. — This  can  only  be  made  by  finding  the  trypanosomes 
in  the  blood. 

Prognosis. — This  appears  to  be  good  quoad  vitam. 

Treatment. — -The  treatment  is  atoxyl  administered  as  in  sleeping 
sickness. 

Prophylaxis. — Nothing  can  be  said  at  the  present  time  with  regard 
to  this. 


REFERENCES. 

The  most  useful  references  are  the  Reports  of  the  various  Sleeping  Sickness 
Commissions,   Laveran    and    Mesnil's    '  Trypanosomes   et    Trypanosomiases 
(English  translation,  by  Nabarro),  and  the  Bulletins  of  the  Sleeping  Sickness 
Bureau,  which   has    now    become  the   Tropical  Diseases    Bull. tin.     A   good 
general  account  maybe  found  in  W.  H.  Hoffmann's  monograph  (vide  infra). 

Archibald  (1909).     Third  Report  Wellcome  Laboratory,  p.  98. 

Bagshawe  (191 3).     Proc.  Soc.  Trop.  Med. 

Bassett-Smith   (1918).     Journ.   Royal  Nav.  Med.  Serv. 

Boyce  and  Breinl  (1908).  Annals  of  Tropical  Medicine  and  Parasitology,  ii.  i . 

Broden  and  Rodhain  (1909).     Rapport  sur  les  travaux  du  Laboratoire  de 

Leopoldville. 
Bruce,  Minchin,  and  Sambon  (1907).     Proceedings  of  the  First  International 

Conference  on  Sleeping  Sickness.     London. 
Bruce,   Nabarro,  and  Grkig   (1903  and  190S).     Reports  of  the    Sleeping 

Sickness  Commission  of  the  Royal  Society. 
Castellani  (1903).     Journal  of  Tropical  Medicine. 
Castellani   (1903).     Reports   of  the  Sleeping  Sickness  Commission  of  the 

Royal  Society. 
Chalmers  (1918).     Journ.  of  Trop.  Medicine. 

Dutton  and  Todd  (1903).     Memoir  XL,  Liverpool  School  of  Tropical  Medi- 
cine. 
Dutton  and  Todd  (1905-06).     Transactions  of  the  Epidemiological  Society, 

xxv.  1. 
Dutton,  Todd,   and  Christy  (1904).     Memoir  XIII,,   Liverpool  School  of 

Tropical  Medicine. 
Dutton,  Todd,  and  Hannington  (1907).     Annals  of  Tropical  Medicine  and 

Parasitology,  i.  161,  201. 
Heckenroth  (1916).      BjII.  Soc.  Path.  Exot.,  November  8.      (Senegal  virus.) 
Hodges,  Minchin,  Tulloch,  etc.  (1902  and  1908).     Reports  of  the  Sleeping 

Sickness  Commission  of  the  Royal  Society. 

81 


1282  THE  AFRICAN  TRYPANOSOMIASES 

Hoffmann  (191 2).     Erg.  d.  All.  Pathol.     (Good  general  account.) 

Kerandel  (1908).     Bull.  Soc.  Path.  Exot.,  i.  261,  515. 

Kerandel  and  Morax  (1908).     Ibid.,  i.  398. 

Kermorgant  (1908).     Ibid.,  i.  247. 

Kinghorn   and   Montgomery    (1908).     Annals   of   Tropical   Medicine   and 

Parasitology,  ii.  53. 
Lanfranchi    (1913-1919).     Several   important   papers   in   the     Bull.    Path. 

Exot.,  Rendicouti  R.  Accademia  Lincei,  etc. 
Laveran  (1908).  Bull.  Soc.  Path.  Exot.,  i.  503. 
Laveran    and    Thiroux    (1908).       Annales    de    l'lnstitut    Pasteur,     xxii., 

February;  Bull.  Soc.  Path.  Exot.,  i.  28,  617. 
Levi  (1907).     Policlinico. 

Low  (1903).     Reports  of  the  Sleeping  Sickness  Commission. 
Low  and  Castellani  (1903).     Reports  of  the  Sleeping  Sickness  Commission. 
Macfie  (1916).     British  Medical  Journal,  January  6,  12-13.     London. 
Manson  (1908).     Annals  of  Tropical  Medicine  and  Parasitology,  ii.  33. 
Marinesco  (1918).     Reports  to  the  Local  Government  Board.      New  Series, 

No.    121.     (Histopathology   of   Encephalitis    Lethargica   and    Sleeping. 

Sickness.) 
Martin  and  Darre  (1908).     Bull.  Soc.  Path.  Exot.,  i.  15,  569. 
Martin,  Lebceuf,  and  Roubaud  (1908).     Ibid.,i.  144,  258,  351,  355.     (1909). 

La  Maladie  du  Sommeil.     Paris. 
Masters  (1918).     Journ.  of  Trop.  Med. 

Mesnil  (1908).     Documents  Francais  sur  la  Maladie  du  Sommeil. 
Moore,  Xierenstein,  and  Todd  (1907).     Annals  of  Tropical  Medicine  and 

Parasitology,  i.  275. 
Mott  (1907).     Histological  Observations  on  Sleeping  Sickness.     New  York. 
Nabarro  (1908).     Journal  of  Tropical  Medicine. 
Nierenstein    (190S).     Annals   of   Tropical   Medicine   and   Parasitology,    ii. 

227,  249.     (1911).   Ber.  Deut.  Chem.  Gesellschaft. 
Ottolenghi  (1908).     Atti  Accademia  Fisiocritici. 
Russo  (1914).     Annali  d'  Igiene. 
Sambon  (1933).     Journ.  of  Trop.  Med.,  July  i. 
Shircore  (1913).     Trans.  Society  of  Trop.  Med. 
Teague  and  Clark  (1918).     Journ.  of  Infectious  Diseases.      (A  Method  for 

Concentrating  Trypanosomes  in  the  Peripheral  Blood.) 
Thomas  and  Breinl  (1905).     Memoir  XVI.,  Liverpool  School  of  Tropical 

Medicine. 
Von  Economo  (1917).     Wien.  Klin.  Woch.     (Encephalitis  Lethargica.) 
Winterbottom  (1803).     An  Account  of  the  Native  Africans  in  the  Neigh- 
bourhood of  Sierra  Leone.     London. 


CHAPTER  XLV1 
SOUTH    AMERICAN    TRYPANOSOMIASIS 

Synonyms — Definition — History — -.Etiology- — Pathology — Symptomatology — 
Diagnosis — Treatment — -Prophylaxis — References. 

Synonyms. — Oppilacao;  Canguary  (both  indicate  ankylostomiasis);  Schizso 
trypanose  or  Douenga  de  Carlos  Chagas,  Coreotry panosis  (eom=bug);  Molestia 
de  Carlos  Chagas,  Tripanozomiase  braziliera,  Tireoidite  parasitaria,  Molestia 
do  barbeiro  (popular  name),  Molestia  de  Cruz  e  Chagas. 

Definition. — South  American  trypanosomiasis  is  an  acute  or 
chronic  specific  disease  caused  by  Schizotrypanum  cruzi  Chagas, 
1909,  and  spread  by  the  bug  Lamus  megistus  (Triatoma  megista) 
Burmeister,  and  perhaps  other  allied  bugs. 

History. — In  February,  1909,  Chagas  reported  that  he  had  fre- 
quently found  a  new  trypanosome,  which  he  named  T.  cruzi,  in  the 
intestine  of  a  species  of  Lamus,  which  occurred  in  the  State  of 
Minas  in  Brazil.  He  also  reported  that  he  was  able  to  infect 
marmosets,  dogs,  cats,  guinea-pigs,  and  rabbits  by  the  bites  of  the 
infected  insects,  and  also  to  grow  the  parasite  on  blood  agar. 

In  May,  1909,  he  announced  that  he  had  made  an  investigation 
of  the  mines  of  the  State  of  Minas,  and  found  the  Lamus  in  large 
numbers  in  the  houses  of  the  poorer  inhabitants.  He  noticed  that 
the  bite  was  painful,  and  that  the  insect  was  very  voracious,  and 
also  that  it  generally  attacked  people,  especially  children,  at  night, 
luting  the  face,  from  which  fact  the  inhabitants  called  it  '  barbeiro  ' 
or  '  barber.' 

He  suspected  this  Lamus  of  causing  a  disease  marked  by  extreme 
amemia,  which  occurred  especially  among  the  children,  and  he 
was  able  to  find  in  the  blood  of  a  two-year-old  child  during  an 
attack  of  fever  a  trypanosome  identical  with  S.  cruzi,  morpho- 
logically and  biologically.  Since  then  Chagas  has  not  merely 
worked  out  the  life-history  of  the  trypanosome  in  man  and  in 
the  Lamus,  but  he  has  also  studied  carefully  the  clinical  and 
pathological  aspects  of  the  disease,  while  Vianna  has  reported 
upon  the  histopathology,  Dias  on  the  blood,  and  Guerreiro  on  the 
urine. 

Chagas  has  also  shown  that  in  all  probability  the  armadillo 
commonly  called  '  tatu,'  and  scientifically  Dasypus  novemcinctus , 
or  loss  correctly  Tatusia  novemcincta,  may  be  the  reservoir  for 
Trypanosoma  cruzi,  and  that  Triatoma  genicul  at  a  (synonym,  Conor- 

1283 


1284  SOUTH  AMERICAN  TRYPANOSOMIASIS 

hinus  geniculatus)  of  the  family  Reduviidae  is  one  of  the  carriers  of 
the  same  trypanosome.  He  also  believes  that  Triatoma  infestans 
and  T.  sordida  may  be  carriers.  It  may  be  stated  that  T.  geniculate!, 
lives  in  the  burrows  of  the  armadillo,  the  flesh  of  which  is  rather  a 
delicacy. 

With  regard  to  the  history  of  the  discovery  of  a  trypanosome  in  man  in 
South  America,  Sambon  informs  us  that  in  1904  de  Lacerda  published  a 
paper  entitled  '  Etiologia  de  Beri-Beri  '  in  the  Brazil  Medico,  in  which  he 
stated  that  he  had  found  trypanosomes  in  films  taken  from  the  spinal  cord  of 
a  case  of  beri-beri.  We  have  been  unable  to  obtain  this  paper,  and  therefore 
cannot  verify  the  statement,  nor  can  we  say  whether  the  disease,  which  de 
Lacerda  was  considering,  was  beri-beri  or  some  other  complaint.  It  would, 
however,  be  interesting  to  have  this  historical  problem  elucidated. 

Climatology. — The  disease  is  known  among  the  poorer  inhabitants 
of  the  State  of  Minas  in  Brazil,  where  it  appears  to  attack  the  whole 
population,  so  that  the  children  all  become  affected  and  either 
recover,  die,  or  pass  into  the  chronic  stage. 

./Etiology. — The  disease  is  caused  by  S chizotryp anum  cruzi  Chagas, 
1909.  This  trypanosome,  which  is  remarkable  because  of  the  large 
size  of  its  kinetonucleus,  is  capable  of  being  transmitted  by  Lamits 
megistus,  and  perhaps  by  species  belonging  to  other  genera  of  the 
Reduviidae — e.g.,  Triatoma — to  domestic  animals  and  to  man. 
The  reservoir  of  the  trypanosome  appears  to  be  an  armadillo — 
Dasypits  novemcinctus. 

In  the  blood  three  forms  are  seen:  the  first  with  a  large  nucleus 
and  loose  chromatin  and  a  terminal  kinetonucleus;  the  second 
narrower,  with  an  oval  nucleus  and  dense  chromatin;  the  third 
with  a  long  nucleus.  The  parasite  undergoes  schizogony  in  the 
lungs,  after  which  the  merozoites  enter  the  red  blood  cells  and 
become  trypanosomes  again.  Sporogony  takes  place  in  the  bug 
Lamus  megistus,  the  final  forms  being  found  in  the  salivary  glands, 
from  which  they  pass  during  the  act  of  biting  into  the  verte- 
brate. (For  a  description  of  the  parasite  and  its  life-history,  see 
Chapter  XIX.,  p.  427.) 

Pathology. — The  trypanosomes  enter  the  cells  of  the  various 
tissues  and  organs  of  the  body,  but  especially  those  of  the  muscular 
system,  and  more  particularly  those  of  the  muscles  of  the  extremities 
and  back.  Inside  these  cells  they  assume  Leishmania-like  forms 
without  flagella,  but  provided  with  trophonucleus  and  kinetonucleus. 
These  forms  divide  by  binary  division,  and  so  increasing  in  numbers, 
dilate  the  cell  considerably.  During  this  process  there  is  no  reaction 
upon  the  part  of  the  surrounding  tissue,  but  after  a  time  the  cell 
membrane  ruptures,  and  the  parasites  which  have  already  become 
flagellate  inside  the  dilated  remains  of  the  cell,  which  is  virtually 
a  cyst,  escape.  With  this  escape  of  the  parasites  into  the  tissues 
tlic  local  inflammatory  reaction  appears,  and  with  the  appearance 
of  the  trypanosomes  in  the  blood  the  general  symptoms  make 
themselves  evident.  Whether  the  parasites  produce  any  toxins 
or  not  is  unknown,  but  it  is  probable  that  they  do  so,  because  of  the 


MORBID  ANATOMY  1285 

fatty  degeneration  described  in  the  liver,  as  well  as  because  of 
the  other  pathological  features. 

As  a  result  of  this  activity  on  the  part  of  the  parasites  and  of  the 
reaction  on  the  part  of  the  body,  local  pathological  changes  take 
place  in  different  organs,  and  these  are  in  general  agreement  with 
the  symptoms  exhibited  by  the  particular  case. 

At  present  there  is  no  evidence  of  any  secondary  infection  being 
responsible  for  any  of  the  essential  pathological  features  of  the 
disease. 

Morbid  Anatomy. — In  an  autopsy  upon  the  body  of  a  person 
dying  from  the  acute  phase  of  the  infection,  a  certain  amount  of 
serous  effusion  is  remarked  upon  opening  the  abdomen.  The  liver 
is  seen  to  be  enlarged,  and  to  be  in  a  state  of  fatty  degeneration. 
The  spleen  is  also  enlarged,  hyperaemic,  and  very  soft,  as  are  the 
mesenteric  glands.  On  opening  the  chest  serous  effusion  is  seen 
in  both  pleural  cavities,  as  well  as  in  the  pericardial  sac.  The 
pericardium  shows  signs  of  hemorrhagic  pericarditis,  while  the 
enlarged  heart  is  in  a  condition  of  intense  myocarditis.  The 
lymphatic  glands  of  the  mediastinum  are  also  swollen  and  hyper- 
aemic. In  the  neck  the  thyroid  gland  is  seen  to  be  enlarged,  as  are 
the  lymphatic  glands.  The  dura  mater  is  congested,  and  there  is 
leptomeningitis  and  encephalomeningitis,  and  firm  adhesions  be- 
tween the  leptomeninges  and  the  cerebral  cortex.  The  liquor 
cerebro-spinalis  is  increased  in  amount.  There  is  a  generalized 
myxedematous  condition  under  the  skin. 

Histopathology. — As  already  stated,  the  most  likely  place  to  find 
the  parasites  is  in  the  muscular  system.  In  the  heart  they  occupy 
the  central  undifferentiated  protoplasmatic  portion  of  the  muscle 
cell,  and  growing  therein,  destroy  the  sarcoplasm,  and  convert 
the  body  of  the  cell  into  a  parasitic  cyst  without  affecting  the  pro- 
cesses. When  this  cyst  ruptures,  the  now  flagellate  parasites 
escape  into  the  intermuscular  tissue,  and  give  rise  to  patches  of 
interstitial  myocarditis.  No  changes  are  to  be  seen  in  the  larger 
bloodvessels  of  the  heart,  nor  can  parasites  be  found  associated 
with  patches  of  pericarditis  or  endocarditis  which  may  be  present. 
In  the  skeletal  muscles  the  parasites  are  mostly  found  in  those  of 
the  extremities  and  the  back.  Here,  again,  the  parasites  grow 
in  the  centre  of  the  muscle  fibre  (Fig.  114,  p.  428). 

In  the  central  nervous  system  a  similar  process  appears  to  take 
place.  The  parasites  invade  a  neuroglia  cell,  which  becomes  con- 
verted into  a  parasitic  cyst,  on  the  rupture  of  which  a  patch  of 
inflammatory  reaction  is  produced.  Parasites  have  never  been 
seen  to  invade  the  nerve  cells  or  the  leucocytes  of  the  central 
nervous  system  (vide  Figs.  642  and  643). 

A  similar  invasion  of  the  medulla  or  cortex  of  the  suprarenal 
capsule  and  inflammatory  reaction  can  also  be  seen  in  the  kidneys, 
the  hypophysis,  and  the  thyroid  gland.  In  animals  the  parasites 
have  been  seen  in  the  testicular  tubules,  but  they  have  not  been 
noted  in  the  human  ovary. 


1280 


SOUTH  AMERICAN  TRYPANOSOMIASIS 


Symptomatology. — There  are  two  principal  varieties  of  the  disease 
— the  acute  and  the  chronic. 

In  the  acute  stage  the  disease  begins  with  a  violent  attack  of  fever 
in  a  young  child  or  a  new-comer  into  the  district.  This  fever  shows 
a  morning  remission  and  an  evening  rise,  and  is  associated  with  a 
palpable  increase  in  the  thyroid  gland,  oedema  of  the  face,  in  which 
characteristic  crepitation  can  be  felt  by  palpation,  enlargement  of 
the  lymphatic  glands  in  various  regions  of  the  body,  but  especially 
of  the  neck;  and  fugitive  cedemas  in  different  parts  of  the  body— as, 
for  example,  the  forehead  and  extremities.  The  spleen  enlarges 
and  becomes  painful,   and  the  liver  also  becomes  enlarged,   and 


Fig.  642. — Neuroglia  Cell  of 
Brain  distended  to  a  Cyst  and 
filled  with  Trypanosoma  cruzi. 
(X  2,000.)     (After  Vianna.) 


Fig.  643. — Trypanosoma 
in  a  Neuroglia  Cell 
Brain.     (X  2,000.) 

(After  Vianna.) 


crust 

OF    THE 


there  may  be  signs  of  meningitis,  and  also  of  albumen  in  the  urine. 
After  a  time  the  attack  of  fever  passes  off,  only  to  return  after 
periodical  intervals.  During  an  attack  the  typical  trypanosomes 
can  be  found  in  the  blood,  but  during  the  apyrexial  interval  they 
are  absent.  After  these  attacks  have  lasted  some  time  the  child 
either  dies,  recovers,  or  passes  into  the  chronic  stage. 

In  this  chronic  stage  the  children  show  signs  of  marked  thyroiditis 
anel  loss  of  hair,  with  hypertrophy  of  the  lymphatic  glands,  a  dull 
expression,  a  peculiar  bluish-bronze  pallor,  tachycardia,  and  in- 
testinal and  nervous  disorders,  especially  convulsions. 

Chagas  has  classifieel  the  various  symptoms  of  the  chronic  stage 
of  the  disease  into  five  subvarieties:  — 


SYMPTOMATOLOGY  1287 

i.  The  pseudo-myxcedematous  form. 

2.  The  myxedematous  form. 

3.  The  cardiac  form. 

4.  The  nervous  form. 

5.  The  chronic  form  with  acute  or  subacute  exacerbations. 

r.  The  Pseudo-Myxcedematous  Form. — In  this  subvariety  of  the 
chronic  stage  there  is  usually  hypertrophy  of  the  lateral  lobes  of 
the  thyroid  gland,  more  rarely  a  globular  enlargement  of  the  central 
lobe.  This  hypertrophy  is  usually  well  marked  in  quite  young 
children,  but  is  by  no  means  evident  in  older  children.  In  young 
children  the  face  is  thin  and  the  skin  of  a  peculiar  light  bronze  colour, 
said  to  be  quite  different  from  the  pallor  of  an  anaemia.  In  older 
children  the  skin  colour  is  violet-bronze.  These  colourations  are 
believed  to  be  associated  with  a  parasitic  invasion  of  the  suprarenal 
capsule. 

There  is  enlargement  of  the  lymphatic  glands  in  the  neck,  axilla, 
and  groins,  while  the  parotid  gland  is  also  often  hypertrophied. 

In  young  children  the  liver  and  spleen  may  be  found  to  be 
enlarged,  but  in  older  cases  the  abdominal  signs  are  not  well  marked. 

With  regard  to  the  circulatory  system,  there  may  be  tachy- 
cardia, sinus  irregularities,  and  an  extra  systole,  and  the  blood- 
pressure  may  be  lower.  Convulsions  have  been  noted,  and  at  times 
slight  fever,  while  the  occurrence  of  conjunctivitis  is  also  recorded. 

2.  The  Myxedematous  Form. — In  this  form  the  thyroid  gland  is 
atrophied,  and  associated  with  the  usual  symptoms  of  myxcedema, 
such  as  the  rough  skin,  loss  of  hair,  and  the  presence  of  a  firm 
oedema  not  pitting  on  pressure,  together  with  an  arrest  of  mental 
development  in  young  children,  or  a  mental  degeneration  in  older 
persons.  The  lymphatic  glands  of  various  regions  are  enlarged, 
and  there  may  be  inflammatory  eye  affections. 

3.  The  Cardiac  Form. — In  the  cardiac  form  there  is  disturbance 
of  the  heart's  action  associated  with  arrhythmia,  allarrhythmia,  extra 
systole,  or  sinus  irregularities.  The  greater  number  of  the  cases 
would  be  classed  under  Mackenzie's  '  Rhythmus  nodalis.' 

4.  The  Nervous  Form. — Various  brain  and  spinal  cord  symptoms 
are  seen  in  this  disease — e.g.,  spastic  paralysis  in  the  legs,  athetosis  in 
the  arms,  aphasia,  pseudo-bulbar  paralysis,  or  suprabulbar  paralysis. 
They  are  associated  with  the  other  symptoms  oi  the  disease. 

5.  Acute  or  Subacute  Exacerbations. — The  principal  feature  of 
this  form  is  the  preponderance  of  fever,  and  this  may  be  due  to 
exacerbations  of  an  old  infection  or  to  new  infections.  This  form 
is  the  cause  of  much  mortality,  and  is  separated  from  the  acute 
form  by  the  rarity  of  the  parasites  in  the  blood,  and  by  the  history 
of  the  long  duration  of  the  illness.  As  a  rule  it  occurs  in  patients 
who  show  marked  hypertrophy  of  the  thyroid  gland,  and  there  may 
also  be  signs  of  suprarenal  insufficiency. 

Blood.— The  hematology  has  been  investigated  by  Uias,  who  finds  that 
the  haemoleucocytic  formula  has  a  great  similarity  to  that  found  in  African 


1288  SOUTH  AMERICAN  TRYPANOSOMIASIS 

trypanosomiasis.  As  a  rule,  there  is  no  globular  anaemia,  but  there  is  a 
definite  diminution  in  the  haemoglobin  and  in  the  specific  gravity.  The 
leucocytosis  is  slight  in  the  acute  and  exceptional  in  the  chronic  cases.  In 
acute  cases  there  is  a  macrolymphocytosis. 

Metabolism. — Guerreiro,  from  careful  experiments  associated  with  urine 
analysis,  concludes  that  there  is  a  true  liver  insufficiency  in  most  forms  of  the 
disease,  but  not  in  the  cardiac  form  unless  associated  with  other  symptoms. 

Sequelae. — Chagas  considers  that  infantilism  may  be  a  sequel  of 
the  disease,  especially  as  it  is  associated  with  hypothyroidism. 

Diagnosis. — The  diagnosis  must  be  effected  by  finding  the  para- 
site in  the  blood  during  a  febrile  attack.  The  disease  is  most  likely 
to  be  confounded  with  ankylostomiasis,  from  which  it  can  be 
recognized  by  the  absence  of  the  typical  ova  in  the  faeces  and  the 
presence  of  S.  cruzi  in  the  blood,  though,  of  course,  both  infections 
may  occur  together. 

It  might  also  be  mistaken  for  malaria  during  the  febrile  attack, 
especially  as  there  is  splenic  enlargement,  but  the  absence  of  the 
malarial  parasite  and  the  presence  of  S.  cruzi  in  the  peripheral 
blood  will  enable  a  diagnosis  to  be  made. 

In  the  chronic  stage  it  may  be  mistaken  for  goitre,  especially 
when  the  myxcedematous  or  pseudo-myxcedematous  symptoms  are 
present,  and  the  diagnosis  will  depend  upon  the  discovery  of  the 
parasite  or  the  history. 

Prognosis, — The  prognosis  is  most  serious  in  the  acute  attacks 
and  the  acute  or  subacute  exacerbations.  The  severer  cardiac 
forms  are  also  of  grave  import. 

Treatment. — The  indications  for  treatment  are  the  same  as  those 
for  African  trypanosomiasis,  associated  with  treatment  for  hypo- 
thyroidism. 

Prophylaxis. — The  prophylaxis  must  aim  at  the  prevention  of  the 
Lamus  biting  man. 

REFERENCES. 

All  the  more  important  papers  are  to  be  found  in  the  Memorias  do  Instituto 
Oswaldo  Cruzi,  Rio  di  Janeiro,  for  the  years  1909  to  1916  inclusive. 

Brumpt  (1919).     Bull.  Acad,  de  Medecine,  March  4. 

Chagas  (1909).     Archiv  f.  Schiffs-  u.  Tropen-Hygiene,  120,  351.     Leipzig. 

Chagas  (1909).     Brazil  Medico,  April  22.     Rio  di  Janeiro. 

Chagas  (1909).     Bulletin  de  la  Societe  de  Pathologie  Exotiquc,  304.     Paris. 

Chagas  (1910).     Revista  Medica  de  Sao  Paulo,  Nos.  22  and  23. 

Chagas    (1911).     Memorias    do    Instituto   Oswaldo   Cruzi.     Rio    di    Janeiro 

(Clinical). 
Chagas  (191 2).     Brazil  Medico,  August.     Rio  di  Janeiro. 
Chagas  (1916).     Memorias  do  Instituto  Oswaldo  Cruzi.  viii.,  II.,  5  and  37. 

Rio  di  Janeiro. 
CHAGAS  (1918).      Rev.  Med.  Cirurf,'.  do  Brazil,  vol.  xxvi..  No.  5. 
Dias  (1912).     Memorias  do  Instituto  Oswaldo  Cruzi.     Rio  di  Janeiro  (Blood). 
GriiKKRiRO  (1912).     Memorias  do  Instituto  Oswaldo  Cruzi.     Rio  di  Janeiro 

(Urine). 
NrcivA  and  Penna  (1910).     Mem.  Inst.  O.  Cruz.,  vol.  viii..  No.  3. 
Vianna    (1911).     Memorias   do   Instituto   Oswaldo   Cruzi.     Rio   di    Janeiro 

(Pathology). 


CHAPTER  XLVII 

THE    KALA-AZARS   AND    PSEUDO-KALA- 

AZARS 

General — Tropical  kala-azar— Mediterranean  Kala-azar — The  pseudo-kala- 
azars— Tropical  febrile  splenomegaly — Toxoplasmosis— Krempf's  spleno- 
megaly— -Tropical  afebrile  splenomegaly — References. 

GENERAL. 

The  present  chapter  is  devoted  to  those  fevers  which  are  known 
as  the  kala-azars  and  those  allied  conditions,  tropical  febrile  spleno- 
megaly and  tropical  afebrile  splenomegaly,  which  clinically  resemble 
kala-azar,  in  one  variety  of  which  Castellani  has  obtained  protozoal 
bodies  from  spleen  which  are  classified,  at  present,  in  the  genus 
Toxoplasma. 

With  regard  to  the  kala-azars,  of  which  Ross  has  pointed  out  that 
the  correct  name  is  '  kala-jwar  ' — i.e.,  black  or  mortal  sickness — we 
have  already  in  Chapter  XIX.,  p.  369,  pointed  out  that  we  consider 
that  tropical  kala-azar  should  be  treated,  at  all  events  at  present, 
separately  from  Mediterranean  kala-azar,  and  this  we  shall  do  in 
the  present  chapter,  although  the  general  tendency  of  modern 
thought  is  to  consider  the  two  diseases  to  be  identical.  We  invite 
the  reader's  attention  especially  to  the  first  half  of  Chapter  XIX., 
in  so  far  as  it  deals  with  the  Herpetomonince,  and  especially  to  the 
experimental  work  of  Fantham  and  Porter  (p.  363),  as  having 
a  direct  bearing  upon  the  unknown  method  of  infection  of  man 
with  the  germs  of  kala-azar. 

TROPICAL  KALA-AZAR. 

Synonyms.— Indian  Kala-Azar,  Kala-jwar,  Kala-Dukh,  Sirkari  disease, 
Sahib's  disease,  Dum-Dum  fever,  Non-malarial  remittent  fever,  Cachectic 
fever,  Tropical  splenomegaly,  Tropical  Leishmaniasis,  Internal  Leishmaniasis. 

Definition. — Tropical  kala-azar  is  a  subacute  or  chronic  febrile 
disorder  characterized  by  splenic  and  often  hepatic  enlargement, 
progressive  wasting  and  anaemia,  and  caused  by  Leishmania  donovam 
R.  Ross,  1903.     The  method  of  infection  is  unknown. 

History. — In  1869,  when  the  district  of  the  Garo  hills  was  first 
occupied  by  the  British,  a  disease  believed  to  be  a  very  severe  form 
of  malarial  cachexia  was  found  to  be  endemic.  This  disease  the 
Garos  called  'kala-azar,'  which  means  the  black  fever,  so  named 

1289 


i2go  THE  KALA-AZARS  AND  PSEUDO-KALA-AZARS 

from  the  appearance  of  the  victims.  In  1875  it  began  to  spread, 
and  became  epidemic,  and  by  its  high  death-rate  attracted  atten- 
tion. In  1882  the  first  account  of  the  disease  was  published  by 
Clarke  from  notes  of  120  cases  compiled  by  McNaught,  the  Civil 
Medical  Officer  of  the  district.  In  1889,  when  it  had  spread  into 
Assam,  following  the  lines  of  human  intercommunication,  Giles 
investigated  the  epidemic,  and  concluded  that  it  was  ankylosto- 
miasis. In  1894  Stephens,  in  his  yearly  report,  stated  that  the 
disease,  though  allied  to,  was  distinct  from  malaria.  In  1897 
Rogers  reported  that  it  was  malarial,  and  this  was  further  supported 
by  Ross  in  1899.  In  1902  Bentley  ascribed  the  disease  to  Micro- 
coccus melitensis,  on  the  basis  of  serum  reactions. 

Up  to  this  point  the  history  of  the  disease  remarkably  resembles 
the  present  history  of  blackwater  fever.  A  change  now  comes 
over  the  aetiology,  for,  in  1900,  Sir  William  Leishman  found  the  para- 
sites already  described  under  the  heading  Leishmania  donovani  in 
films  taken  post  mortem  from  the  spleen  of  a  soldier  who  died  in 
Netley  from  fever  contracted  at  Dum-Dum,  but  he  did  not  publish 
this  discovery  till  1903.  In  July,  1903,  Donovan  observed  the  same 
parasite  in  blood  obtained  by  splenic  puncture  performed  during 
life.  In  1904  Christophers  published  a  valuable  report  on  the 
parasite  and  the  disease,  and  in  the  same  year  Rogers  observed 
the  development  of  the  parasite  into  a  flagellate  organism  when 
splenic  blood  was  incubated  at  220  C.  in  citrate  of  soda  solution. 
In  1907  Patton  showed  that  the  parasite  could  be  found  in  numbers 
lying  in  leucocytes  in  the  peripheral  blood,  and,  further,  that  it 
became  flagellated  in  the  alimentary  canal  of  bugs. 

In  1904  Neave  in  Omdurman  discovered  the  existence  of  this 
disease  in  a  child  coming  from  the  Bahr-el-Ghazal  province  of  the 
Anglo-Egyptian  Sudan,  and  in  the  same  year  Philips  in  Cairo  dis- 
covered it  in  two  adults  coming  from  the  Yemen  district  of  Arabia. 
In  1907  Pirrie,  who  had  been  working  in  the  Sudan,  died  in  England 
from  kala-azar.  In  1908  Cummins  discovered  a  case  contracted 
at  Singa  on  the  Blue  Nile;  Carroll  recorded  a  second  case  from 
the  same  district,  while  Black  met  with  two  other  cases;  Bousfield 
recorded  seven  cases  from  the  province  of  Kassala  and  one  from 
Mafaza,  and  Thomson  and  Marshall  found  forty-one  new  cases  in 
children  and  adults  along  the  Blue  Nile  towards  Abyssinia,  which 
forms  an  endemic  zone,  which  has  been  carefully  studied  by 
Archibald.  It  corresponds  to  the  Blue  Nile,  Sennar,  and  Kassala 
districts,  while  the  infection  in  one  case  of  a  woman  is  regarded  as 
coming  from  quite  a  different  part  of  the  Sudan- — i.e.,  from  Urn 
Ruaba  near  Talodi.  Archibald  has  studieel  a  small  epidemic  at 
Kurmok  on  the  Abyssinian  frontier.  This  Sudan  kala-azar  is 
peculiarly  interesting  because  of  its  limited  endemicity  (as  far  as  is 
known)  and  by  the  peculiar  features  shown  by  Archibald  to  be 
associated  with  its  parasite. 

In  19T.3  Gaspar  Vianna  introduced  the  intravenous  injections 
of  tartar  emetic  for  the  treatment  of  the  American  mucocutaneous 


TROPICAL  KALA-AZAR  1291 

Leishmaniasis.  According  to  Christopherson  the  drug  was  dis- 
covered by  Basil  Valentine  in  the  sixteenth  century,  and  accident- 
ally caused  the  death  of  several  monks,  and  thus  acquired  its 
name  'antimony' — i.e.,  anti-moine,  against  the  monk.  In  1914 
Castellani  in  Ceylon  used  this  method  combined  with  oral  therapy 
for  the  treatment  of  tropical  kala-azar.  In  1915  Rogers  treated 
cases  in  India  in  the  same  manner,  and  later  in  the  same  year  Rogers 
and  Hume  administered  this  treatment  to  six  cases  of  kala-azar  in 
Europeans.  Christopherson  has  successfully  employed  the  same 
method  in  the  Sudan;  and  this  has  now  become  the  recognized 
method  of  treatment. 

In  addition  to  the  above,  much  work  has  been  done  by  the  Indian 
investigators,  such  as  Mackie,  Cornwall,  and  others,  as  well  as  by 
Hanson,  Low,  Statham,  and  others. 

Climatology. — The  disease  is  especially  spread  through  the  tropics, 
but  is  unknown  in  Tropical  America  an:l  Oceania.  It  is  found  in 
the  Sudan,  Arabia,  India  and  Ceylon,  Burma,  Indo-China,  and 
China. 

/Etiology. — Kala-azar  is  caused  by  a  herpetomonad  parasite 
called  Leishmania  donovani  R.  Ross,  1903,  described  on  pp.  369-37°. 
which  lives  especially  in  the  endothelial  cells  of  bloodvessels  and 
lymphatics,  and  is  especially  numerous  in  the  spleen,  the  liver,  and 
the  bone-marrow,  but  is  also  found  in  other  organs,  such  as  the 
lungs  and  the  kidney.  Especially  must  be  mentioned  its  presence 
in  the  mesenteric  lymphatic  glands,  and  in  ulcers  of  the  intestinal 
mucosa. 

It  can  also  be  found  in  mononuclear  and  polymorphonuclear 
leucocytes  in  the  peripheral  blood,  but  only  occasionally,  as  at  other 
times  it  is  most  difficult  to  find  it  in  this  situation.  It  also  at  times, 
but  very  rarely,  lies  in  the  hollow  of  the  biconcave  disc  of  a  red 
blooi  cell,  thus  looking  as  though  it  was  contained  therein.  The 
pirasites  hive  been  cultured  from  the  blood  by  using  the  N.N.N. 
medium. 

They  are  most  abundant  in  the  blood  towards  the  fatal  end  of  the 
illness,  and  during  fever  or  the  presence  of  intestinal  symptoms. 
They  are  said  to  have  been  found  in  the  motions  during  an  attack 
of  kala-azar  dysentery,  and  also  in  the  scrapings  from  intestinal 
ulcers.  They  have  also  been  found  in  papules  and  ulcers  in  the 
skin. 

As  they  occur  in  the  peripheral  blood  and  in  the  skin,  it  is  possible 
tint  they  may  pass  into  the  alimentary  canal  of  some  blood-sucking 
arthropod,  but  these  animals  are  often  naturally  infected  with 
11  igellate  parasites  of  the  leptomonad,  crithidial,  and  Lrypanosomal 
types,  and  therefore  the  mere  finding  of  a  flagellate  in  the  interior 
of  a  blood-sucking  arthropod  which  has  been  fed  upon  a  man  or 
animal  infected  with  L.  donovani  is  worthless  from  an  etiological 
point  of  view. 

As  they  occur  in  the  peripheral  blood  and  in  the  intestinal  mucosa, 
they  can  equally  escape  in  the  faeces  in  the  form  of  cysts,  and  thus 


1292  THE  KALA-AZARS  AND  PSEUDO-KALA-AZARS 

get  into  water,  from  which  they  can  be  ingested  by  some  aquatic 
arthropods,  many  of  which  naturally  contain  flagellates. 

The  work  of  Laveran  and  Franchini,  of  Fantham  and  Porter,  has 
demonstrated  that  these  natural  arthropodal  parasites  can  by  in- 
gestion or  by  inoculation  produce  a  fatal  illness  resembling  kala- 
azar  in  mammals.  Archibald,  experimenting  with  human  kala-azar 
parasites  in  the  Sudan,  has  shown  that  monkeys  can  be  similarly 
infected  by  feeding  with  kala-azar  material,  and  this,  together  with 
the  curious  endemicity  of  the  disease  in  the  Sudan,  and  with  Laveran, 
Franchini,  Fantham,  and  Porter's  researches,  make  the  possibility 
of  water  carriage  of  cysts  from  infected  arthropods  to  man  worthy 
of  consideration. 

From  the  above  it  will  be  clear  that,  though  the  parasite  is  known, 
the  method  of  infection  is  still  unknown,  and  the  cultivation  of  the 
parasite  into  flagellate  form  clearly  indicates  that  this  is  part  of  the 
life  cycle. 

The  predisposing  causes  appear  to  depend  upon,  and  be  capable 
of  explanation  by,  the  habits  of  man.  Thus  the  disease,  when 
epidemic,  always  spreads  relatively  slowly  along  channels  of  human 
intercommunication,  and  apparently  is  directly  due  to  the  intro- 
duction of  an  infected  human  being  into  the  district.  It  runs  in 
families,  in  which  children  particularly  suffer,  while  the  class  of 
people  who  are  mainly  affected  are  the  poorer  sections  of  the 
European  and  native  communities.  Season  and  sex  appear  to 
have  no  influence,  but  there  is  no  doubt  about  the  infection  of  the 
dwelling  or  perhaps  its  water-supply,  nor  of  the  capability  of  the 
disease  spreading  from  one  dwelling  to  another,  or  from  one  water- 
supply  to  another. 

Pathology. — Introduced  into  the  body,  the  parasite  appears  to 
enter  the  endothelial  cells  of  a  capillary  bloodvessel  or  lymphatic, 
and  to  grow  therein,  and  to  increase  in  numbers  by  simple  fission 
until  a  very  large  number — Leishman  says  upwards  of  220 — may 
be  counted  in  one  cell.  The  organs  principally  affected  in  this 
manner  are  the  liver,  spleen,  bone-marrow,  and  lymphatic  glands, 
and,  to  a  less  extent,  the  pancreas,  kidneys,  suprarenals,  testicles, 
and  lungs. 

The  parasites  may  now  escape  from  the  enclosing  cell  by  rupture, 
and  are  then  taken  up  by  the  leucocytes,  particularly  by  the  poly- 
morphonuclears, but  also  by  the  mononuclears  and  rarely  by  the 
eosinophils,  by  means  of  which  they  appear  in  the  peripheral 
blood  even  in  early  cases,  but  are  much  more  common  late  in  the 
disease,  especially  if  there  is  diarrhoea  due  to  ulceration  of  the 
intestine,  in  which  condition  the  polymorphonuclear  leucocytes 
are  increased  in  numbers  in  the  peripheral  blood,  and  many  of 
them  contain  parasites.  The  further  development  has  still  to  be 
worked  out,  as  all  that  is  definitely  known  is  that  in  cultures  the 
parasite  becomes  flagellate. 

It  would  appear  as  though  the  parasite  could  produce  some  sort 
of  toxin  which  causes  the  marked  changes  in  the  spleen,  liver,  and 


TROPICAL  KALA-AZAR 


1293 


bone-marrow,  as  well  as  the  ulceration  of  the  skin  and  intestinal 
mucosa,  because  sometimes,  and  in  an  inconstant  manner,  it  can 
produce  a  reaction  on  the  part  of  the  body,  as  is  seen  in  the  format  ion 
at  times  of  agglutinins,  specific  precipitins,  inconstant  in  presence 
and  feeble  in  action,  and  useless  from  a  diagnostic  point  of  view, 
as  is  complement  deviation.  At  the  commencement  of  the  infection 
there  appears  to  be  generally  an  attempt  to  produce  an  immunity, 
and  it  is  this  which  produces  the  rare  natural  cure  in  man.  It  may 
be  the  cause  of  the  refrac- 
tory nature  of  certain 
animals  to  the  disease  and 
the  limitation  of  infection 
in  endemic  communities. 
After  the  infection  has 
obtained  its  hold  on  the 
body  as  a  rule  the  struggle 
for  immunity  becomes  less 
and  less,  and  disappears 
eventually. 

By  some  means  or  other 
the  parasite  irritates  the 
organ  it  infects,  causing 
marked  changes  in  the 
spleen,  liver,  and  bone- 
marrow,  and  also  causing 
ulceration  of  the  intestine 
and  skin. 

The  Blood. — The  exam- 
ination of  the  blood  is 
most  important  because, 
firstly,  the  parasite  may  be 
found  in  a  leucocyte  if 
carefully  looked  for,  even 
in  the  early  stages  of  the 
disease;  secondly,  the  leu- 
cocytic  changes  are  of  the 
utmost  importance.  There 
is  marked  anaemia — 54*2 
per  cent,  of  Rogers'  cases 
giving  from  4,000,000  to 
2,500,000  corpuscles  per 
cubic  millimetre — and  the  haemoglobin  is  reduced  in  propor- 
tion to  the  erythrocytes,  the  colour-index  being  normal.  There 
is  a  most  marked  leucopenia,  and  Rogers  reports  that  in  42-1  per 
cent,  of  his  cases  the  leucocytes  were  1,000  or  less,  in  30-3  per 
cent.  1,000  to  2,000,  and  in  22*6  per  cent.  2,000  to  3,000.  The 
proportion  of  white  to  red,  according  to  the  same  author,  is 
less  than  1  :  1,500  in  67*9  per  cent.,  or,  if  inflammatory  cases  are 
excluded,  in  nearly  90  per  cent,  of  the  cases  he  examined.     There 


Fig.  644. — Indian  Kala-Azar. 

The  distension  of  the  abdomen  by  the 
greatly  enlarged  spleen  should  be  noted. 
(Photograph  of  a  case  in  the  Tropical 
Clinic,  Colombo.) 


1294 


THE  KALA-AZARS  AND  PSEUDO-KALA-AZARS 


is  a  reduction  in  the  polymorphonuclear  leucocytes  and  in  the 
eosinophils,  and  an  increase  in  the  mononuclear  leucocytes  and 
lymphocytes.  The  diminution  of  the  polymorphonuclear  leucocytes 
is  thought  to  explain  the  tendency  to  bacterial  infections.  The 
coagulability  of  the  blood  is  decreased,  which  explains  the  tendency 
to  hemorrhage,  and  renders  occasionally  splenic  puncture  dangerous. 
The  alkalinity  of  the  blood  has  been  shown  by  Archibald  to  be 
diminished — a  fact  which  may  be  of  some  secondary  diagnostic 
importance. 

The  Urine. — The  urine  in  our  cases  did  not  show  anything  ab- 
normal. 

Morbid  Anatomy. — The  body  is  much  emaciated,  and  there  is 
marked  muscular  atrophy,  together  with  oedema,  enlargement  of 
the  spleen,  and  often  of  the  liver,  ulceration  of  the  skin  and  intestine, 
sometimes  haemorrhage  in  various  places,  and  generally  the  presence 
of  some  complication.  The  spleen  is  greatly  enlarged,  firm,  and 
deep  red  in  colour,  though  it  may  at  times  show  malarial  pigment. 


Fig.  645. — Temperature    Chart    of    Kala-Azar    from    a    Sudan    Case. 

(After  Christopherson.) 

+  ,  Leishman  bodies  found;   XXXX,  injection  of  tartar  emetic. 


The  capsule  and  septa  are  thickened,  and  the  whole  organ  is  con- 
gested with  blood,  and  contains  numerous  mononuclear  cells  and 
macrophages  full  of  parasites. 

In  the  liver,  which  may  or  may  not  be  enlarged,  the  most  marked 
changes  are  in  the  intralobular  capillaries,  which  are  dilated  and 
contain  macrophages,  derived  from  their  endothelial  wall,  full  of 
parasites,  while  the  liver  cells  are  atrophied  and  degenerated. 
Cirrhosis  has  been  noted  in  some  cases. 

The  bone-marrow  contains  numerous  parasites  in  the  usual  cells, 
and,  as  in  malaria,  the  yellow  marrow  is  converted  into  red,  and  is 
soft  and  diffluent.  The  skin  may  show  papules  and  ulcers,  in  which 
the  parasites  can  be  found,  while  the  colon  is  often  ulcerated,  or 
shows  the  cicatrices  of  old  ulcers. 

Symptomatology — Incubation. — The  incubation  period  appears 
to  be  very  variable,  and,  indeed,  it  is  difficult,  in  a  chronic  disease 
1  if  this  nature,  to  decide  when  it  first  begins.  It  is  said  to  range  from 
ten  days  to  three  weeks  or  several  months. 


TROPICAL  KALA-AZAR  1295 

Onset. — The  onset  may  be  heralded  by  a  rigor,  which  may  be 
repeated  daily,  and  by  an  attack  of  irregular,  high,  remittent  fever, 
which  may  early  show  two  remissions  per  diem  in  a  four-hourly 
temperature  chart.  This  double  remission  is  considered  by  Rogers 
to  be  almost  diagnostic  of  the  disease.  Towards  the  end  of  the  third 
to  sixth  week  of  the  fever  the  temperature  declines,  and  the  initial 
stage  of  the  disease  may  be  said  to  have  terminated.  During  this 
period,  however,  the  spleen  and  liver  will  have  enlarged,  and  may 
be  both  painful  and  tender.  Headache  is  present  at  times,  but  is 
not  severe.  Nausea  and  vomiting  are  unusual,  while  the  bowels  are 
-regular,  and  there  is  no  abdominal  distension.  The  pulse  may  be 
slow  or  quick. 

The  attack,  however,  may  begin  with  a  continuous  fever,  which 
shows  two  fluctuations  in  the  twenty-four  hours,  which  Rogers 
considers  as  almost  diagnostic  of  the  disease.  In  other  cases  the 
disease  may  begin  with  gastro-intestinal  disturbances  or  with 
dysenteric  symptoms,  or  quietly,  without  any  marked  initial  stage, 
the  patient  gradually  developing  an  enlarged  liver  and  spleen,  anaemia 
and  weakness.  \ 

Course. — The  course  of  the  disease,  after  the  decline  of  the  tem- 
perature, is  marked  by  what  is  called  an  apyrexial  interval;  but  it 
appears  that — in  some  cases,  at  all  events — there  is  a  slight  daily 
rise  of  temperature,  not  exceeding  ioo°  F.  After  some  weeks  this 
apyrexial  interval  ends  in  an  attack  of  fever  resembling  the  onset. 
Periods  of  apyrexia  and  pyrexia  now  alternate  with  one  another, 
while  the  spleen,  and  sometimes  the  liver,  enlarge.  Anaemia  com- 
mences and  increases,  while  asthenia  not  merely  appears,but  deepens, 
until  the  wretched  patient  presents  the  typical  appearance,  which 
may  be  described  as  follows: — He  is  thin  and  wasted,  with  the  abdo- 
men much  swollen  and  protuberant,  the  chest  so  thin  that  the  ribs 
show  clearly,  the  arms  and  legs  wasted,  the  cheeks  sunken,  the  nose 
sharp,  and  the  ankles  puffy,  while  the  skin  and  tongue  are  often 
distinctly  darker  than  they  should  be,  the  former  being  fur- 
furaceous. 

On  examining  the  swollen  abdomen,  the  enlarged  spleen  may  be 
felt  reaching  almost  to  the  pelvis,  while  the  enlargement  of  the 
liver  may  be  marked  or  may  be  absent.  In  this  condition  intestinal 
disturbances  in  the  form  of  diarrhoea  or  dysenteric  attacks  are 
common,  and  may  be  due  to  the  actual  disease  or  to  complication 
with  true  dysentery.     Dyspeptic  symptoms  may  also  be  present. 

Haemorrhages  may  occur  from  the  nose,  the  gums,  the  stomach, 
the  bowels,  or  under  the  skin.  Papular  eruptions  are  to  be  seen, 
especially  on  the  thighs,  and  ulcers  may  be  present.  The  weakened, 
emaciated  patient  may  now  die  of  asthenia,  but  more  usually  the 
long-drawn-out  illness  is  brought  to  a  close  by  some  complication. 
The  total  duration  varies  from  about  seven  months  to  two  years, 
and  generally  ends  fatally. 

Complications. — It  appears  as  though  the  reduction  in  the  number 
of  the  polymorphonuclear  leucocytes  laid  the  patient  open  to  in- 


1296  THE  KALA-AZARS  AND  PSEUDO-KALA-AZARS 

vasion  by  pathogenic  bacteria,  for  septic  infections,  such  as  cancrum 
oris,  or  lung  infections — for  example,  pneumonia,  phthisis,  and 
pleurisy — or  abdominal  troubles  of  the  nature  of  diarrhoea,  dysen- 
tery, and  cystitis,  are  not  uncommonly  met  with,  and  may  cause 
the  death  of  the  patient.  Sometimes,  after  a  severe  attack  of 
septicaemia  or  some  other  complication,  the  disease  is  found  to  be 
cured,  but  this  is  rare. 

Diagnosis. — The  only  certain  method  of  diagnosis  is  to  find  the 
parasite,  and  as  Donovan  and  Patton  have  reported  its  frequent 
occurrence,  even  in  early  stages,  in  the  peripheral  blood,  this  should 
be  possible,  especially  if  aided  by  dilution  with  normal  saline 
solution,  and  centrifugalization  and  examination  of  the  leucocytes. 
In  our  experience,  the  search  for  the  parasite  in  the  leucocytes  of 
the  peripheral  blood  requires  an  extremely  long  time,  and  is  often 
negative.  If  the  parasites  cannot  be  found  in  the  blood,  an  attempt 
may  be  made  to  find  them  by  the  examination  of  the  exudate 
obtained  by  exciting  artificial  pustulation  of  the  skin  by  some 
irritant,  as  suggested  by  Cummins.  Failing  this,  there  is  puncture 
of  the  spleen  or  of  the  liver,  and  withdrawal  of  blood,  which 
can  be  examined  by  the  microscope.  The  diagnostic  puncture 
of  the  spleen  in  the  tropics  is,  however,  not  to  be  undertaken 
lightly,  because  splenic  enlargement  due  to  leukaemia  is  by  no  means 
unknown,  and  puncture  of  the  spleen  in  this  disease,  or,  indeed, 
in  that  of  chronic  malaria,  may  lead  to  most  unfortunate  results. 
The  blood  of  the  peripheral  circulation  should  therefore  be  examined 
to  exclude  leukaemia. 

Certainly,  the  first  thing  to  do  is  to  examine  the  peripheral  blood 
and  exclude  leukaemia.  Secondly,  the  coagulability  of  the  blood 
should  be  tested  by  Wright's  method,  and  if  found  to  be  decreased, 
the  puncture  should  not  be  performed.  Thirdly,  if  the  puncture 
is  to  be  carried  out,  the  liver  should  be  chosen  for  exploration,  not 
the  spleen,  particularly  in  the  later  stages,  in  which  haemorrhages 
are  to  be  feared.  In  the  early  stages  there  may  not  be  so  much 
risk,  but  it  must  be  done  with  the  greatest  care,  aseptically,  and  the 
patient  must  be  kept  at  rest  for  some  time  afterwards,  the  site  of 
puncture  being  covered  with  an  aseptic  pad  and  a  firm  bandage. 
The  syringe  should  be  sterile,  and  perfectly  dry.  Rogers  recom- 
mends that  a  dose  of  30  grains  of  calcium  chloride  in  a  couple  of 
ounces  of  water  be  administered  directly  after  a  puncture,  in  order 
to  promote  coagulability  of  the  blood.  Attempts  at  cultivation 
from  the  blood  and  inoculations  into  susceptible  animals  may  also 
help,  rats  and  monkeys  being  used  by  preference. 

Differential  Diagnosis. — In  the  early  stages  the  diagnosis  has  to  be 
principally  made  from  acute  malaria  and  typhoid,  when  the  positive 
signs  in  favour  of  kala-azar  are: — (1)  Presence  of  the  characteristic 
daily  double  remission  of  the  fever;  (2)  absence  of  constitutional 
symptoms,  proportional  to  the  severity  of  the  fever;  (3)  absence  of 
malarial  parasites  and  Widal's  reaction,  though,  of  course,  the  latter 
reaction  is  negative  in  true  typhoid  during  the  first  week;  (4)  marked 


TREATMENT  1:297 

enlargement  of  the  spleen;  (5)  great  leucopenia,  especially  in  rela- 
tion to  the  erythrocytes,  which,  however,  may  also  be  found  in 
typhoid  and  malaria;  (6)  increase  in  mononuclear  leucocytes; 
(7)  presence  of  Leishmania  donovani  in  the  leucocytes. 

In  advanced  cases  the  diagnosis  has  to  be  made  from  malarial 
cachexia  and  ankylostomiasis  by  (1)  the  presence  of  Leishmania 
donovani  in  the  leucocytes  of  the  peripheral  blood,  or  in  the  juice 
from  the  liver  and  spleen;  (2)  by  the  absence  of  the  typical  febrile 
attacks  of  subtertian  or  tertian  fever;  (3)  by  the  absence  during 
the  febrile  attack  of  malarial  parasites;  (4)  by  the  absence  of 
ancylostomes,  or,  if  they  are  present,  by  the  continuation  of  the 
symptoms  after  their  expulsion.  Mixed  infections  of  kala-azar 
and  malaria  may  occur. 

Prognosis. — The  prognosis^is  much  less  serious  than  before  the 
introduction  of  the  tartar  emetic  treatment.  Formerly  the  mor- 
tality was  about  98  percent.  It  istruethat  some  people  recover  after 
having  nearly  died  from  a  complication,  or,  more  rarely,  without 
this  episode,  but  why  they  recover  is  not  known. 

Leucocytosis  and  increase  of  the  polymorphonuclears  are  con- 
sidered to  be  good  signs,  while  leucopenia  and  polymorphonuclear 
decrease  are  bad  signs.  Complications,  of  course,  increase  as  a 
rule  the  gravity  of  the  prognosis. 

Treatment — Essential  Treatment. — As  soon  as  a  diagnosis  is 
made  give  tartar  emetic  either — 

(a)  Intravenously  (this  is  the  method  to  be  preferred) ; 

(b)  Intramuscularly; 

(c)  Orally  combined  with  (a)  or  (b). 

Intravenously. — Give  2-10  cubic  centimetres  of  a  sterile  1  per  cent, 
solution  in  warm  normal  saline  solution  daily  for  five  to  ten  days, 
and  then  every  other  day,  and  finally  twice  a  week.  This  is  the  best 
method  of  treatment. 

Dose  for  Children. — This  is  as  follows: — 

Intravenous  Dosage  of  i  per  Cent.  Tartar  Emetic. 


Dose. 


Number. 


Under  one  year  .  . 
One  to  five  years 
Five  to  ten  years 
Ten  to  sixteen  years 


£-1  c.c. 

One  daily  for  seven  days 

1-3  c.c. 

Ditto. 

1-5  c.c. 

Ditto. 

1  £-8  c.c. 

Ditto. 

Important. — The  sterilization  of  the  tartar  emetic  solution  must 
be  made  in  flowing  steam  on  two  or  three  consecutive  days,  and  must 
not  be  performed  in  an  autoclave,  in  which  the  drug  is  liable  to 
decomposition  and  may  then  cause  serious  symptoms.  Some 
authorities  advise  using  a  solution  merely  filtered  through  a 
Chamberland  filter.    One  of  us  has  used  a  solution  containing  \  per 

82  " 


1298 


THE  KALA-AZARS  AND  PSEUDO-KALA-AZARS 


cent,  carbolic,  which  in  practice  renders  unnecessary  a  sterilization 
by  heating. 

Intramuscularly . — Intramuscular  injections  are  painful  and  often  become 
inflamed.     The  following  solution  may  be  used: — 

Tartrate  of  antimony        ..  ..  ..      8  grains. 

Carbolic  acid 


Glycerine 

Bicarbonate  of  sodium 
Distilled  water 


10  minims. 
3  drachms. 
I  grain. 
1  ounce. 


The  dose  is  £-1  cubic  centimetre  every  other  day  injected  intramuscularly 
into  the  gluteal  region. 

Martindale's  formula  may  also  be  used: — 

Antimonii  oxidi  . .  . .  . .  . .     gr.  3V 

Glycerin.  \ 

Aq.  dest.j aa  "lxv- 

One  ampoule. 

Combined. — Oral  administration   may  be   combined   with  intravenous  or 
intramuscular  injections.     The  following  mixture  may  be  given: — 
Tartrate  of  antimony        .  .  . .  5  grains. 


Bicarbonate  of  sodium 
Glycerine 

Chloroform  water  . . 
Water 


30  grains. 
1  ounce. 
1  ounce, 
to  3  ounces. 


The  dose  is  one  to  two  teaspoonfuls  in  water  three  times  a  day. 

Rogers  regards  sodium  antimonyl  tartrate,  given  intravenously,  as  being 
more  efficacious  than  tartar  emetic.  Colloidal  antimonial  preparations  have 
been  recommended. 

Symptomatic  Treatment.- — Hemorrhagic  symptoms  may  be  treated 
by  calcium  lactate  in  10-grain  doses  twice  or  three  times  a  day. 
Diarrhoea  may  be  combated  by  bismuth  subnitrate  in  10-12  grain 
doses,  with  or  without  5-10  grains  of  salol,  every  four  to  six  hours, 
as  may  be  required.  Intestinal  parasites  should  be  looked  for  and 
treated  as  prescribed  in  the  chapters  pertaining  to  the  different 
forms.  The  heart  must  be  watched  and  cardiac  tonics  or  saline 
injections  given  if  required  [vide  Treatment  of  Malaria,  p.  1188). 

General  Treatment. — The  patient  should  be  kept  in  bed  and  well 
nursed  during  this  treatment. 

Diet. — The  diet  should  be  good  and  nourishing,  but  if  there  is  much 
diarrhoea  it  is  necessary  to  restrict  it  to  milk,  Benger's  food  and  the 
like,  soups,  etc. 

Prophylaxis. — As  the  method  of  infection  is  unknown,  all  that 
can  be  done  is  firstly  to  segregate  the  sick  and  carefully  disinfect 
his  motions,  as  well  as  protect  him  against  blood-sucking  arthropods. 
Secondly,  to  remove  the  healthy  from  the  infected  area,  and  to 
disinfect  or  destroy  the  clothing,  furniture,  and  houses,  while  a 
complete  change  of  the  drinking-water  supply  is  essential.  If  this 
latter  cannot  be  done  and  the  water-supply  is  a  well,  it  may  be 
sterilized  by  blowing  in  steam,  as  in  the  case  of  prophylaxis  against 
the  guinea-worm  (p.  1971) ;  or  if  this  cannot  be  done,  the  simple  boil- 
ing of  all  drinking-water  should  be  carried  out.  It  does  not  appear 
probable  that  infection  comes  about  via  unbroken  skin. 


MEDITERRANEAN  KALA-AZAR  1299 

MEDITERRANEAN  KALA-AZAR. 

Synonyms. — Infantile  kala-azar,  Infantile  leishmaniasis,  Mediterranean 
leishmaniasis.  Febrile  splenic  anaemia  (Fede),  AncBmia  infantum  a  Leish- 
mania  (Pianese),  Leishmania  ancemia  (Jemma  and  di  Cristina),  Mar  da  tal  biccia 
(Malta),  Ponos  (Greece),  Malattia  da  mensa  (Sicily). 

Definition. — Mediterranean  kala-azar  is  a  subacute  or  chronic 
specific  disease  due  to  Leishmania  infantum  Nicolle,  and  clinically 
closely  resembling  tropical  kala-azar,  but  occurring  in  temperate  or 
subtropical  climates. 

Historical. — Fede  several  years  ago  described  in  Italy  a  form  of 
splenic  anaemia  among  young  children  characterized  by  irregular 
fever,  progressive  anaemia,  and  a  fatal  ending.  He  considered  it  a 
disease  by  itself,  separating  it  from  the  non-febrile  type  of  splenic 
anaemia.  In  1904  Laveran  and  Cathoire  found  a  Leishmania  in 
films  from  the  spleen  of  a  child  who  had  died  of  an  ill-defined  disease 
in  Tunisia.  Pianese  in  1905  called  attention  to  the  similarity  of  the 
symptoms  of  Fede's  splenic  anaemia  with  kala-azar,  and  described 
parasitic  bodies  in  the  spleen  of  the  affected  children  morphologi- 
cally identical  with  Leishmania  donovani.  Later  Nicolle  suggested 
for  the  disease  the  name  of  '  infantile  kala-azar,'  and  completed 
the  study  of  the  parasite,  which  he  called  Leishmania  infantum. 
Gabbi  considers  the  disease  to  be  identical  with  tropical  kala-azar, 
having  found  it  also  among  adults.  A  fuller  account  of  the  history 
will  be  found  on  p.  373. 

Cristina  and  Caronia  in  1915  applied  to  this  complaint  Vianna's 
tartar  emetic  treatment  for  American  muco-cutaneous  leishmaniasis. 

Climatology. — The  malady  is  met  with  in  Southern  Europe,  in 
the  northern  regions  of  Africa,  and  perhaps  Egypt.  Future  in- 
vestigations will  probably  show  that  it  is  endemic  in  many  countries. 

/Etiology. — The  malady  is  due  to  Leishmania  infantum  Nicolle- 
The  description  of  this  parasite  will  be  found  on  p.  373.  Nicolle 
has  succeeded  in  reproducing  the  disease  in  monkeys,  and  less 
typically  in  dogs.  He  has  also  found  that  dogs  may  be  spon- 
taneously affected  with  a  leishmania;  in  fact,  in  his  opinion,  the 
dog  acts  as  a  reservoir  of  L.  infantum,  and  its  ectoparasites,  such  as 
fleas,  may  possibly  serve  as  the  transmitting  agents  to  human  beings. 
These  views  have  been  tested  experimentally  by  Basile,  but  to-day 
doubt  is  cast  upon  canine  leishmaniasis  being  the  same  disease  as 
that  in  man,  and  the  flea  infection  of  man  is  also  considered  to  be 
doubtful. 

The  majority  of  the  cases  occur  in  young  children  of  two  to  three 
years  of  age,  among  whom  there  is  a  slight  preponderance  of  males. 
The  disease  sometimes  occurs  in  more  than  one  member  of  a  family, 
and  more  often  begins  in  the  spring  or  early  summer. 

Pathology. — The  pathology  has  been  carefully  studied  by  Pianese, 
who  finds  that  the  post-mortem  lesions  arc  similar  to  those  observed 
in  Indian  kala-azar,  the  spleen  and  liver  being  greatly  enlarged. 
Microscopically,  there  is  great  increase  of  the  lymphoid  tissue  in 


1300  THE  KALA-AZARS  AND  PSEUDO-KALA-AZARS 

the  spleen  and  hypertrophy  of  the  islands  of  Langerhans  in  the 
pancreas.  In  the  bone-marrow  there  is  hyperproduction  of  the 
myeloid  and  lymphoid  tissues. 

Symptomatology — Onset. — The  disease  begins  in  a  very  insidious 
manner,  and  is  usually  first  noticed  when  the  child  has  some  dis- 
turbance of  the  alimentary  canal,  such  as  an  attack  of  vomiting 
and  diarrhoea,  when  the  spleen  may  or  may  not  be  found  to  be 
enlarged;  and  as  the  child  is  anaemic  and  has  a  very  irregular  fever, 
the  complaint  is  wont  to  be  diagnosed  as  malaria,  especially  as 
some  seizures  are  apt  to  come  on  suddenly,  and  to  be  associated  with 
rigors. 

The  child  becomes  pale,  ceases  to  be  interested  in  its  games,  and 
suffers  from  attacks  of  diarrhoea  [alternating  with  periods  of  con- 
stipation, from  attacks  of  irregular  fever  separated  by  apyrexial 
intervals,  and  from  epistaxis. 


-f  taU 


K3.9 


Fig.  646. — Leishmania  infantum        'Fig.  647. — Child    suffering    from 
Nicolle.  Infantile  Kala-Azar. 

(After  Marzinowsky.)  (After  Marzinowsky.) 

Course. — After  the  above  symptoms  have  lasted  some  time,  the 
spleen  begins  to  enlarge,  and  presently  protrudes  from  under  cover 
of  the  ribs;  the  attacks  of  fever  become  more  marked;  haemorrhages 
from  the  nose  and  gums  and  into  the  skin  are  seen,  and  the  diarrhceic 
or  dysenteric  attacks  become  pronounced.  The  child  now  wastes 
and  becomes  progressively  anaemic;  the  face,  conjunctiva,  and  whole 
body  taking  a  peculiar  white  tinge,  and  the  disease  may  be  said  to 
be  fully  established. 

With  regard  to  the  special  symptoms,  the  fever  is  very  irregular, 
with  exacerbations  sometimes  twice  a  day — in  the  morning  and  in 
the  evening — and  sometimes  several  times  a  day.  High  tempera- 
tures at  times  appear  in  cycles,  or  there  may  be  sudden  falls  to 
subnormal  temperatures. 

The  alimentary  canal  is  always  disturbed,  but  the  appetite  is 
preserved,  and  may  even  be  increased,  although  the  little  patient 


SYMPTOMATOLOGY  1301 

is  suffering  from  alternate  attacks  of  diarrhoea  and  constipation;  but 
this  is  not  always  so,  and  some  observers  have  recorded  anorexia. 
The  motions  may  be  very  foul,  containing  undigested  food,  and  at 
times  blood  and  mucus.  Ulcerative  stomatitis,  and  even  noma, 
may  occur,  and  the  last  may  appear  on  the  face  or  on  the  genitalia. 
Noma  appears  to  be  not  uncommon  in  Greece. 

The  spleen,  as  stated  above,  is  always  enlarged  from  the  time 
of  the  full  establishment  of  the  symptoms,  but  this  enlargement  is 
not  stationary.  On  the  contrary,  it  steadily  increases  until  an  enor- 
mous size  is  sometimes  reached,  so  that  it  fills  the  left  side  of  the 
abdomen  and  projects  across  the  median  line  into  the  right  half, 
causing  the  abdomen  to  bulge  and  become  prominent.  On  palpa- 
tion it  is  found  to  move,  and  notches  may  be  felt  through  the 
attenuated  abdominal  wall.  It  moves  with  the  respiratory  move- 
ments, and  may  be  altered  in  position  from  side  to  side,  and  up  and 
down  by  manipulation.  There  is  not,  however,  any  constant  rela- 
tionship between  the  progress  of  the  disease  and  the  size  of  the  spleen. 
Jemma,  Di  Cristina,  and  Critien  state  that  it  diminishes  with  a 
persistent  and  profuse  diarrhoea,  especially  during  the  last  few  days 
of  life. 

There  is  not  always  a  concord  between  the  temperature  and  the 
pulse-rate;  on  the  contrary,  the  latter  is  almost  constantly  rapid, 
even  during  the  apyrexial  intervals,  but  may  rise  to  150  to  160  beats 
per  minute  during  attacks  of  fever.  Haemic  murmurs  may  occur 
over  the  heart,  but  are  rare.  The  blood  is  pale,  and  shows  a  decrease 
in  the  number  of  erythrocytes  (1,500,000  to  3,000,000),  and  in 
the  haemoglobin  (below  50  per  cent.),  which,  however,  is  reduced 
in  proportion  to  the  red  corpuscles;  and  also  in  the  leucocytes 
(1,500  to  3,000),  though  the  leucocytic  formula  is  mononuclear  (70 
to  80  per  cent.),  being  especially  composed  of  medium-sized  cells. 
The  mononuclears  are  increased  at  the  expense  of  the  polymorpho- 
nuclear cells,  which  make  up  the  remaining  20  to  30  per  cent. 
There  is  usually  some  poikilocytosis  and  anisocytosis,  but  nucleated 
cells  are  rare  or  absent.  The  opsonic  index  is  diminished  below 
that  which  is  normal  for  a  healthy  child,  and  is  especially  low  for 
Bacillus  coli  communis,  which  is  held  to  be  responsible  for  the 
frequency  of  the  intestinal  symptoms.  (Edemas  of  the  face,  hands, 
genitalia,  and  feet,  coming  on  suddenly  and  disappearing  suddenly, 
are  not  unusual:  they  have  a  tendency  to  bilateral  symmetry,  but 
are  influenced  by  the  position  of  the  patient,  and  may  occur  at  any 
stage  of  the  disease.  At  times  they  are  painful  and  may  show  signs 
of  inflammation. 

The  liver  is  very  generally  enlarged,  but  to  a  much  less  extent  than 
the  spleen.  On  palpation,  its  edge  is  felt  to  be  smooth  and  hard, 
and  is  not  tender. 

As  the  spleen  and  liver  enlarge,  the  abdomen  also  enlarges  and 
becomes  prominent,  while  the  superficial  veins  may  stand  out 
distinctly,  and  there  may  be  a  slight  degree  of  ascites  at  times. 
The  urine  is  usually  normal,  but  there  may  be  slight  signs  of  albu- 


1302  THE  KALA-AZARS  AND  PSEUDO-KALA-AZARS 

minuria,  or  a  decrease  in  the  output  of  urea.  The  lymphatic  glands 
are  as  a  rule  not  enlarged. 

The  mental  and  physical  activity  of  the  child  decreases  as  the 
disease  progresses;  it  emaciates,  and  becomes  extremely  pallid, 
thereby  assuming  a  prematurely  aged  appearance.  The  bones 
become  evident,  especially  the  ribs  and  shoulder-blades,  and  the 
child  dies  from  exhaustion,  often  due  to  an  attack  of  dysentery  or 
diarrhoea.     Spontaneous  recovery  may  take  place,  but  this  is  rare. 

Complications.- — Respiratory  complications  are  not  unusual. 
Bronchitis  is  common,  while  broncho-pneumonia  and  pleurisy  may 
occur,  as  may  a  rapidly  developing  fatal  dyspnoea,  which  is  prob- 
ably due  to  oedema  of  the  glottis.  Perhaps  noma,  as  already  men- 
tioned, is  a  fairly  common  complication  in  Italy  and  Greece,  and 
should  come  in  this  place  as  a  complication  rather  than  a  symptom 
of  the  disease.  Otitis  media  has  been  recorded  not  merely  as  a 
complication,  but  also  as  a  cause  of  death.  Ankylostomiasis  asso- 
ciated with  lipuria  has  been  recorded  as  a  complication. 

Diagnosis. — The  symptoms  more  or  less  closely  resemble  those  of 
kala-azar,  but  differ  in  that  this  disease  occurs  in  children  and  is  in- 
oculable  into  dogs,  while  kala-azar  occurs  mostly  in  young  adults  and 
is  with  difficulty  inoculable  into  dogs.  The  temperature  chart  may 
resemble  that  of  kala-azar,  but  is  generally  more  irregular.  The 
characteristic  clinical  symptoms  of  the  disease  are  the  enlarged 
spleen,  the  irregular  fever,  and  the  pallor  occurring  in  a  child.  The 
essential  feature  in  the  diagnosis  is  the  parasite,  which  may  be 
obtained  by  splenic  puncture,  by  liver  puncture,  by  examination 
of  the  bone-marrow  obtained  by  a  modified  trocar  and  cannula, 
as  designed  by  Caccioppoli,  to  which  a  Potain's  aspirator  with  a 
strong  pump  is  attached;  rarely  by  blood  examination.  Other 
methods  are  by  vesication  and  examination  of  the  fluid;  and  by 
lumbar  puncture,  if  there  are  cerebral  symptoms. 

Having  obtained  the  splenic  or  hepatic  pulp,  etc.,  the  diagnosis 
may  be  made  by  microscopical  examinations  and  by  cultivation 
on  the  medium  devised  by  Novy  and  McNeil,  and  modified  by 
Nicolle,  usually  known  as  the  N.N.N,  medium  (p.  377)- 

It  has  been  suggested  by  Cochrane  that  removal  of  one  of  the  post-cervical 
lymphatic  glands  might  be  adopted  as  a  diagnostic  method.  The  removed 
gland  is  cut,  and  a  smear  made,  when  numerous  parasites  may  be  seen.  This 
method  is  said  to  be  the  most  certain  means  of  diagnosis.  It  is  recommended 
that  the  glands  be  removed  under  the  influence  of  a  local  anaesthetic. 

Differential  Diagnosis. — The  differential  diagnosis  has  to  be  made 
from  kala-azar,  undulant  fever,  enteric  fever,  malaria,  other  forms 
of  splenic  anaemia,  and  syphilis. 

Kala-Azar. — This  fever  occurs  in  adults,  and  is  characterized  by 
the  double  daily  rise  of  the  temperature,  and  by  the  difficulty  of 
successful  inoculation  into  dogs.  In  this  disease  the  spleen  is  not 
so  markedly  enlarged. 

Undulant  Fever. — In  contrast  to  undulant  fever,  in  infantile  kala- 
azar  the  temperature  is  much  less  regular,  never  showing  a  typical 


THE  PSEUDO-KALA-AZARS  1303 

undulating  type;  the  enlargement  of  the  spleen  is  much  greater;  the 
articular  symptoms  are  lacking,  and  Wright's  agglutination  test  is 
negative. 

Enteric  Fever. — -From  enteric,  infantile  kala-azar  differs  by  the 
splenomegaly,  by  the  irregular  fever,  by  the  absence  of  Widal's 
reaction. 

Malaria. — The  absence  of  the  typical  blood  parasites,  and  the 
fact  that  quinine  has  no  influence  on  the  irregular  fever,  are  points 
of  diagnostic  value. 

Other  Forms  of  Splenic  Ancetnia. — From  the  splenomedullary 
leukaemia,  infantile  kala-azar  is  distinguished  by  the  leucopenia; 
from  syphilitic  splenomegaly,  by  the  history  and  inutility  of  mercury 
and  salvarsan;  from  the  various  types  of  infantile  afebrile  spleno- 
megaly, by  the  fever  and  the  presence  of  the  parasite;  from  the 
splenomegaly  found  in  rickety  children,  by  the  absence  of  deformity 
of  the  bones  and  by  microscopical  examination. 

Prognosis. — The  prognosis  is  much  more  favourable  since  the 
introduction  of  the  tartar  emetic  treatment,  the  mortality  having 
been  reduced  from  90  per  cent,  to  less  than  20  per  cent. 

Treatment. — This  is  the  same  as  for  tropical  kala-azar  (p.  1297). 

Prophylaxis. — -As  canine  leishmaniasis  (p.  377)  is  now  considered 
to  be  a  separate  disease,  and  as  the  flea  is  doubtful  as  an  infective 
agent,  prophylaxis  cannot  be  advised  until  more  is  known  as  to  the 
method  of  infection,  but  the  suggestions  made  under  the  heading  of 
Tropical  Kala-Azar  may  perhaps  be  applicable,  and  in  any  case 
it  is  unnecessary  to  keep  dogs  and  fleas  in  a  house. 

Basile  has  sufficiently  indicated  the  possibilities  of  this  method 
of  infection  being  correct  to  make  the  simple  methods  of  prophy- 
laxis of  such  a  fatal  disease  imperative  even  before  the  full  proof 
of  the  researches  has  been  obtained. 

THE  PSEUDO-KALA-AZARS. 

These  are  febrile  and  afebrile  diseases  which  resemble  kala-azar  in 
that  they  are  associated  with  splenomegaly,  anaemia,  and  often 
emaciation.     They  can  be  divided  into:  — 

Tropical  febrile  splenomegaly. 

Toxoplasmosis. 

Krempf 's  splenomegaly. 

Tropical  afebrile  splenomegaly. 

TROPICAL  FEBRILE  SPLENOMEGALY. 

Synonyms.  —  Tropical  splenomegaly,  Pseudo-kala-azar,  Esplenomegalia 
tropical  (Columbia),  Wenku  (Karonga),  Gobora  or  Tebi  (New  Guinea). 

Definition. — A  chronic  irregular  febrile  disorder  of  unknown 
causation,  characterized  by  splenic  hypertrophy  and  gastrointes- 
tinal disturbance,  followed  by  emaciation. 

History  .—A  form  of  febrile  splenomegaly  resembling  kala-azar 
has  been  long  known  in  the  tropics;  but  the  typical  parasites  of 


1304  THE  KALA-AZARS  AND  PSEUDO-KALA-AZARS 

that  infection  cannot  be  found  either  during  life  or  after  death. 
Though  well  known,  there  is  but  little  literature  upon  the  subject. 
Woolley  first  gave  an  excellent  account  of  the  disease  as  seen  in 
the  Philippine  Islands,  and  Day  and  Ferguson  as  seen  in  Egypt.  We 
have  repeatedly  in  local  publications  called  attention  to  the  disease 
in  Ceylon.  Gabbi  has  ably  described  the  disease  in  Italy,  and  so  has 
Leys,  in  1917,  from  Karongo,  and  it  is  probably  the  same  disease 
as  that  described  by  Breinl,  in  1915,  in  New  Guinea.  In  1916 
Spagnolio  recorded  cases  from  Calabria  and  Sicily. 

In  one  form  of  this  complaint  (p.  1305)  Castellani  has  found 
protozoal  bodies,  Toxoplasma  fiyrogenes,  which  may  be  causal 
(vide  p.  490),  but  there  may  be  many  varieties  of  the  disease. 

Climatology. — The  disease  has  been  reported  from  India,  Ceylon, 
China,  the  Philippines,  Egypt,  Arabia,  Tunis,  Algiers,  the  Belgian 
Congo,  Italy,  and  South  America. 

^Etiology. — The  causation  of  the  disease  is  quite  unknown. 
Gabbi  suggests  that  it  maj^  be  a  filterable  virus. 

Pathology. — It  is  thought  probable  that  the  disease  may  be  a 
primary  infection  of  the  alimentary  canal,  and  that  the  fibrosis  is 
secondary,  but  we  would  rather  distinguish  this  from  the  ordinary 
forms  of  polyfibrosis,  and  would  consider  that  the  seat  of  the  dis- 
order was  in  the  spleen  and  liver,  and  that  the  alimentary  canal 
signs  were  secondary. 

Morbid  Anatomy. — On  post-mortem  examination,  the  body  is 
seen  to  be  emaciated  as  a  rule,  but  there  may  be  oedema  of  the  feet 
and  legs,  and  there  may  be  ascites  if  the  liver  is  seriously  affected. 
Upon  opening  the  abdomen,  the  principal  object  of  interest  is  the 
extremely  enlarged  firm  spleen.  The  liver  may  be  enlarged  and 
smooth,  and  does  not  show  the  hobnailed  appearance  of  alcoholic 
cirrhosis,  while  the  lymphatic  glands  in  various  regions  of  the  body 
may  be  slightly  enlarged.  The  intestines  show  signs  of  catarrhal  or 
ulcerative  enteritis.  The  bone-marrow  is  diffluent  and  pale  in  colour. 
Haemorrhages  may  at  times  be  found  in  different  parts  of  the  body. 
Microscopical  examination  reveals  hyperplasia  of  the  lymphoid 
elements  of  the  spleen,  associated  with  hyperplasia  of  the  fibrous 
tissue,  dilatation  of  the  vascular  sinuses,  and  sometimes  haemor- 
rhages. The  microscopic  examination  of  the  liver  shows  the  usual 
appearances  of  monolobular  and  polylobular  cirrhosis.  The  bone- 
marrow  is  seen  to  be  congested  and  hemorrhagic,  and  the  lryaline 
cells  are  increased,  while  the  granular  cells  are  reduced. 

Symptomatology. — The  onset  of  the  disease  is  quite  gradual  and 
unnoticed  by  the  patient,  although  at  times  a  history  of  diarrhoea, 
dysentery,  or  of  attacks  of  fever  may  be  obtained.  Usually  the 
patient  comes  to  the  hospital  complaining  of  weakness  and  vague 
rheumatic  pains,  although  he  may  come  in  the  later  stages  because 
of  the  ascites.  On  examination,  the  patient  is  found  to  be  more  or 
less  emaciated,  and  to  have  a  large  firm  spleen  projecting  from 
under  the  ribs,  and  sometimes  making  a  considerable  protuberance 
of  the  thin  abdominal  wall.     Thcamount  of  anaemia  is  usually  not  ex- 


COMPLICA  TIONS  1 3°5 

treme,  the  average  number  of  red  corpuscles  being  between  2,500,000 
and  3,500,000,  while  microcytes,  megalocytes,  and  polychromato- 
philia  are  not  unusual.  The  leucocytes  are  more  or  less  normal. 
Frequently  there  is  some  fever  of  an  irregular  type,  and  there  ma}^  be 
exacerbations,  and  at  times  there  may  be  a  double  remission  similar 
to  that  found  in  kala-azar ;  but  there  may  be  long  periods  of  apyrexia. 
In  addition,  in  a  few  cases  there  may  be  all  the  signs  and  symptoms 
of  cirrhosis  of  the  liver,  with  the  abdomen  distended  from  ascites. 

By  some  authorities  the  disease  has  been  subdivided  into  two 
stages — the  first  or  splenic  stage  before,  and  the  second  or  hepatic 
stage  after,  the  hepatic  cirrhosis.  The  first  may  last  for  many  years, 
but  the  latter  is  much  shorter,  lasting  a  variable  number  of  months, 
and  ending  fatally  by  the  patient  passing  into  a  condition  of  coma, 
sometimes  accompanied  by  jaundice.  Death  in  the  first  stage  is, 
in  our  experience,  not  rare,  and  may  be  due  to  haemorrhages  or 
exhaustion. 

Complications. — Pregnancy  is  a  serious  complication,  and  may 
hasten  the  end,  even  after  the  child  has  been  born.  Ankylosto- 
miasis and  other  parasitic  diseases  may  occur  along  with  tropical 
febrile  splenomegaly. 

Diagnosis. — The  leading  features  of  the  disease  are  the  great 
enlargement  of  the  spleen,  associated  with  wasting  and  irregular 
fever,  in  people  in  whom  examination  fails  to  reveal  any  obvious 
parasitic  cause.  Tropical  febrile  splenomegaly  must  be  differ- 
entiated from  kala-azar  by  the  absence  of  Leishmania  donovani  in 
the  spleen  pulp  as  obtained  by  puncture.  It  can  also  be  distin- 
guished from  chronic  malaria  by  the  absence  of  the  typical  parasites 
or  pigment  from  the  splenic  juice,  and  from  cirrhosis  of  the  liver 
by  the  presence  of  the  enlarged  spleen.  From  leukaemia  it  is  easily 
distinguished  by  the  absence  of  a  lencocytosis.  From  infantile 
kala-azar  it  may  be  distinguished  by  the  absence  of  Leishmania 
infantum,  as  seen  in  the  splenic  juice.  The  disease  can  be  dis- 
tinguished from  Banti's  disease  by  the  febrile  attacks,  and  appar- 
ent ly  splenic  removal  does  not  effect  a  cure. 

Prognosis. — The  illness  is  very  chronic,  but  the  prognosis  is  bad, 
as  no  cure  is  at  present  possible,  and  the  patient  tends  to  go  from 
bad  to  worse. 

Treatment. — Arsenical  injections  are  the  most  valuable,  and  sal- 
varsan  may  be  tried.    Removal  from  the  endemic  area  is  advisable. 

Prophylaxis. — As  the  aetiology  is  unknown,  nothing  can  be  said 
under  this  heading. 

TOXOPLASMOSIS. 

In  1913  Castellani  recorded  a  case  of  splenomegaly  associated 
with  fever  of  long  standing  and  terminating  fatally,  in  which  he  had 
found  protozoal  bodies  which  eventually  received  the  name  Toxo- 
plasma pyrogenes  Castellani,  1913  (vide  p.  490). 

Morbid  Anatomy. — -The  body  was  much  emaciated,  and  the 
principal  feature  was  the  greatly  enlarged,  smooth,  not  very  hard 


1306  THE  KALA-AZARS  AND  PSEUDO-KALA-AZARS 

spleen,  which  was  reddish  in  colour.  No  malarial  parasites  could 
be  found,  but  there  were  some  light  yellowish  pigment  granules, 
quite  different  from  malarial  pigment. 

Toxoplasma  Pyrogenes. — This  was  rarely  found  in  the  blood, 
but  was  abundant  in  the  spleen.     (For  a  description,  see  p.  490.) 

Symptomatology. — The  fever  starts  in  youth  and  lasts  many  years, 
defying  all  treatment.  In  character  it  is  intermittent,  reaching 
1030  to  1050  F.  at  times.  The  attacks  of  fever  do  not  start  with 
shivering,  and  the  fall  is  not  associated  with  sweating.  The  spleen 
is  much  enlarged  and  hard,  while  the  liver  is  also  enlarged,  but 
neither  organ  is  tender  on  pressure.  All  the  other  organs  are 
normal,  and  there  is  no  enlargement  of  the  lymphatic  glands. 

Blood  Counts. — The  red  blood-corpuscles  in  an  advanced  case 
number  2,000,000,  the  leucocytes  5,200  per  c.mm.  A  few  nucleated 
red  cells  are  present,  and  basophilia  and  chromatophilia  are  marked. 
The  leucocytic  count  is  as  follows: — Polymorphonuclear  leucocytes, 
50  per  cent.;  lymphocytes,  40  per  cent.;  large  mononucleurs,  7  per 
cent. ;  eosinophiles,  3  per  cent. ;  haemoglobin,  30  per  cent. 

No  malarial  parasites  could  be  found,  and  the  serum  reactions 
for  typhoid,  the  paratyphoids,  and  Malta  fever,  were  absent. 

The  urine  sometimes  contained  a  trace  of  albumen. 

Course. — The  case  grew  gradually  worse,  emaciation  set  in,  and 
the  patient  died. 

Treatment.— Quinine  was  given  by  the  mouth  and  intramuscularly 
in  doses  of  30-60  grains  a  day  without  effect. 

KREMPF'S  SPLENOMEGALY. 

In  1917  Krempf  described  a  case  of  splenomegaly  in  a  young 
Chinaman.  He  suffered  from  a  malarial  infection,  and  stated  that 
in  his  village  near  Tientsin  splenomegaly  was  frequently  observed 
in  both  sexes  and  at  all  ages. 

On  making  a  splenic  puncture,  Krempf  found  bodies  either  en- 
closed in  red  cells  or  free  in  the  plasma.  They  were  only  found  in 
the  spleen. 

The  red  cells  were  deformed  and  contained  a  capsule  10x5  microns 
in  size,  inside  which  lay  a  vermicular  sporont  often  curved  like 
the  letter  U.  Extracted  from  a  red  corpuscle,  these  bodies  measured 
20x1*5  microns. 

These  bodies  were  believed  to  be  the  sporonts  of  a  haemogregarine, 
and  were  named  Hczmogregarina  hominis  Krempf,  1917.  No 
further  history  of  the  case  is  given. 

Recently  Raubaud,  examining  the  blood  of  a  lady  who  had  resided  for 
two  years  in  the  Congo,  observed  that  some  red  cells  contained  a  haemo- 
grcgarina  9-11  fi  by  2-8-3-5  fi,  which  differed  from  Krempf's  parasite  by 
having  a  crescenting,  not  vermicular  shape.  Raubaud  has  named  it  Hcemo- 
gregarina  inexpectata.  There  was  no  fever,  and  no  enlargement  of  the  liver 
or  spleen.     The  blood,  however    showed  a  marked  mononucleosis. 

AFEBRILE  SPLENOMEGALY. 

Synonym.— Pseudo-Banti's  disease. 

Delinition. — A  chronic  afebrile  disorder  characterized  by  splenomegaly 
and  severe  anaemia. 


REFERENCES  1307 

History. — There  is  no  literature  on  the  subject  as  far  as  we  know. 

Climatology. — We  have  observed  it  in  tropical  Africa,  Ceylon,  and  India, 
and  probably  it  will  be  found  in  many  other  places. 

Symptomatology.  —  The  disease  begins  insidiously  in  either  children  or 
adults,  but  usually  the  case  is  not  observed  until  either  the  anaemia  becomes 
well  marked  or  the  splenomegaly  attracts  attention.  The  symptoms  are 
more  or  less  severe  anaemia  and  a  painless  firm  enlargement  of  the  spleen,  with- 
out increase  in  size  of  the  liver  or  other  important  signs.  The  blood  shows  the 
ordinary  signs  of  a  severe  anaemia,  but  no  parasites  can  be  observed.  There 
is  no  diarrhoea,  and  the  mucosa  of  the  mouth  is  not  inflamed  or  ulcerated. 

Diagnosis. — The  disease  can  be  differentiated  from  malaria  by  the  absence 
of  fever  and  of  the  absence  of  the  parasites  in  the  blood  and  spleen;  from 
kala-azar  by  the  absence  of  the  parasites  in  the  spleen;  from  forms  of  febrile 
splenomegaly  by  the  absence  of  fever;  from  leucocythemia  by  the  absence 
of  the  great  increase  of  the  white  blood  cells.  From  other  forms  of  splenic 
anasmia  it  may  be  differentiated  by  the  absence  of  any  history  or  signs  of 
rickets,  syphilis,  etc. 

Prognosis. — Patients  appear  to  live  for  years. 

Treatment. — This  is  purely  symptomatic,  but  arsenic  may  be  administered. 

Leger's  Disease. 

Leger  has  recorded  a  case,  from  Guiana,  of  prolonged  fever  with  great 
enlargement  of  the  liver,  in  which  he  found  organisms  of  two  types.  Some 
were  3-5  y,  in  length  by  1  /u  in  breadth,  with  a  flagellum  3-5  [A,  long.  Others 
were  of  oval  shape,  without  any  flagellum.  Leger  considers  his  parasite  to 
differ  from  Hesmocystozoon  brasiliense  Franchini  (p.  1468),  as  it  never  con- 
tained any  pigment,  and  encysted  forms  were  absent. 

REFERENCES. 

The  most  complete  and  valuable  references  may  be  found  in  the  Kala-Azar 
Bulletin  (1911-1912),  which  was  published  separately  by  the  Bureau  of  Sleeping 
Sickness,  but  is  now  merged  in  the  Tropical  Diseases  Bulletin,  in  which  many 
references  will  be  found.  The  most  valuable  single  work  is  the  excellent 
monograph  of  Laveran  (1917),  'Leishmaniases,'  Paris. 

Indian  Kala-Azar. 

Leishman  (1906).     Allbutt  and  Rolleston's  System  of  Medicine,  vol.  ii.,  part  ii. 

Low  (1919).     Br.  Med.  Journ.,  June  7. 

Manson  (1908).     Annals  of  Tropical  Medicine  and  Parasitology,  II.,  iii.  147. 

Manson  and  Low  (1909).     British  Medical  Journal,  i.  843. 

Patton  (1907).     Nos.  27  and  31,  Scientific  Memoirs  of  India. 

Rogers  (1908).     Fevers  in  the  Tropics. 

Mediterranean  Kala-Azar. 

Bandi  (191 3).     Journal  of  Tropical  Medicine. 

Gabbi  (1908).     Policlinico. 

Marcel,  Targhetta  and  Ameuille  (1918).     Bull.  Ac.  de  Med.,  April  25. 

Nicolle  and  Cassuto  (1907).     Academie  de  Medecine. 

Pianese,  G.  (1905).     Gazz.  Internaz.  Medicina. 

Visentini  (191 3).     Quart.  Journal  Micro.  Science. 

Pseudo-Kala-Azars. 
Castellani  and  Chalmers  (1910-11).     Ceylon  Medical  Reports,  etc. 
Day  and  Ferguson  (1909).     Annals  of  Tropical  Medicine  and  Parasitology, 

iii-  3.  379-     Liverpool. 
Gabbi  (1912).     Malaria.     Roma. 
Leger  (191 9).     Bull.  Soc.  Path.  Ex.,  February. 
Raubaud  (1919).     Bull.  Soc.  Path.  Ex.,  February. 
Woolley  (1906).     Philippine  Journal  of  Science.     Manila. 

Toxoplasmosis. 

Castellani  (191 3).     Journal  of  Tropical  Medicine,  April  15. 


CHAPTER  XLVIII 
THE   RELAPSING  FEVERS 

General — Louse  group  :   European — North    African — Indian — Manchurian — 
Tick  group  :  Tropical   African — Persian — American — References. 

GENERAL. 

The  relapsing  fevers  are  caused  by  various  species  of  spirochetes, 
and  may  for  purposes  of  description  be  arranged  partly  by  their 
carrier  and  partly  b}'  their  geography  as  follows: — 

A.  Louse  group: — 

i.  European  relapsing  fever. 

2.  North  African  relapsing  fever. 

3.  Indian  relapsing  fever. 

4.  Manchurian  relapsing  fever. 

B.  Tick  group  : — 

1.  Tropical  African  relapsing  fever. 

2.  The  tick  fever  of  Miana,  Persia. 

3.  American  relapsing  fevers. 

THE  RELAPSING  FEVER  OF  EUROPE. 

Synonyms. — English :  Recurrent  fever,  Five  Days'  fever,  Spirillum 
fever,  Five  Days'  fever  with  relapses,  Typhus  Recurrens,  Seven  Days'  fever 
(not  Rogers'),  Icteric  typhus,  Remittent  fever,  Bilious  typhoid,  Epidemic 
remittent  fever,  Miliary  fever,  Relapsing  fever.  French  :  Fievre  a  Rechute. 
Italian  :  Febbre  Ricorrente.     German  :  Riickfallfieber,  Die  Hungerpeste. 

Definition. — An  acute  specific  relapsing  fever,  caused  by  Spiro- 
schaudinnia  recurrentis  Lebert,  1874,  and  spread  from  man  to  man 
by   lice,  Pediculus    corporis  de  Geer,    1778,   and  by  P.   humanus/J>i^ 
Linnaeus,  1758.  ' 

History. — Hippocrates  was  the  first  writer  to  describe  an  epidemic 
of  relapsing  fever  in  Thasos,  but  this  knowledge  was  entirely  lost, 
and  the  reference  was  not  understood  until  after  relapsing  fever 
was  properly  defined.  Strother  and  other  observers  refer  to  fevers 
with  relapses  in  London  and  in  Ireland  in  the  eighteenth  century. 
In  1826-27  there  was  an  epidemic  of  fever  in  the  United  Kingdom, 
during  which  it  was  recognized  that  there  were  two  distinct  types 
of  typhus — viz.,  a  mild  and  a  severe.  In  1842  this  mild  type  again 
appeared  in  Scotland,  and,  to  a  lesser  extent,  in  England,  and 
continued  in  the  years  1843,  1846,  and  1847.     In  1843  Henderson 

1308 


CUM  A  TO  LOG  Y—MTIOLOG  Y 


1309 


of  Edinburgh  defined  this  mild  type  as  a  fever  distinct  from  typhus, 
and  about  the  same  time  it  was  recognized  in  Germany,  and  some- 
what later  in  Russia. 

In  1868  there  was  an  epidemic  in  Berlin,  when  Obermeyer,  one 
of  Virchow's  assistants,  first  saw  a  spirochsete  in  the  blood  of  a 
patient;  but  he  does  not  appear  to  have  been  very  certain  about 
this  at  the  time,  for  he  waited  till  the  next  epidemic  in  1872,  and 
even  then  did  not  publish  his  account  till  1873.  This  spirochete 
was  named  S.  recurrentis  by  Lebert  in  1874,  and  S.  obermeyeri  by 
Colin  in  1875,  and  was  proved  by  Munch,  of  Moscow,  to  be  the 
cause  of  the  disease  by  the  successful  inoculation  of  blood  containing 
the  spirochetes  into  healthy  human  beings — an  experiment  which 
has  since  often  been  repeated  accidentally  at  post-mortems.  It  has 
been  inoculated  with  success  by  Metchnikoff  and  others  into 
monkeys  and  mice.  In  1888  Sakharoff  suggested  that  this  organism 
was  a  protozoon — -a  view  which  later  met  with  great  support. 

In  Russia,  where  the  disease  has  been  well  known  since  1863,  there  is  a 
popular  belief  that  it  is  spread  by  the  bed-bug  Clinocoris  lectularius  L.,  which 
belief  was  supported  by  Fliigge  in  1891.  In  1897  Tictin  found  that  he  could 
infect  monkeys  by  inoculation  of  the  blood  obtained  by  crushing  bugs  which 
had  very  recently  been  fed  on  a  patient — i.e.,  within  forty-eight  hours. 

Spirochetes  have  been  found  in  bugs  during  relapsing  fever  epidemics  by 
Karlinski  in  1902,  and  later  by  Schaudinn.  Nuttall  has  successfully  trans- 
mitted 5.  recurrentis  from  mouse  to  mouse  by  the  bites  of  bugs.  Donitz's 
hypothesis,  that  S.  recurrentis  is  conveyed  by  ticks,  has  not  been  supported 
by  experiments. 

The  role  of  the  louse  in  this  disease  has  been  studied  by  Koch 
and  by  Werner  and  Wiese  in  1917,  but  requires  the  accurate  study 
given  to  the  North  African  type  by  Nicolle,  Blaizot,  and  Conseil. 
It  has  also  been  studied  by  Toyoda,  who  has  shown  it  to  be  closely 
related  to  the  North  African  type  by  means  of  immunity  experiments. 

Climatology. — The  disease  is  endemic  in  Russia,  Ireland,  Turkey, 
the  Balkans,  Denmark,  Norway,  Bohemia,  and  in  some  parts  of 
Poland  and  Germany,  while  the  same  or  a  similar  type  is  found  in 
Lower  Egypt,  in  Southern  China,  and  perhaps  in  the  Philippines. 
There,  however,  appears  to  be  some  doubt  about  the  presence  of 
the  disease  in  these  islands;  the  authority  for  the  statement  is 
McCrae,  in  Osier's  '  System  of  Medicine.' 

iEtiology. — This  type  of  relapsing  fever  is  caused  by  5.  recurrentis 
Lebert,  1874,  which  is  generally  to  be  found  in  the  peripheral  blood 
during  the  attacks,  but  is  usually  absent  in  the  apyrexial  interval, 
though  individuals  may  occasionally  be  found  after  prolonged 
search.     (For  description  of  the  organism,  see  p.  443.) 

This  spirochete  is  carried  from  the  sick  to  the  healthy  by  the 
agency  of  lice,  P.  humanus  and  P.  corporis  (se^-^^oi^  The 
subject,  however,  requires  further  study  on  the  llne"s~l)ftne  North 
African  type  (vide  infra).  It  is  known  that  the  human  blood  is 
infective  during  the  pyrexial  and  apyrexial  stages,  and  that  the 
spirochetes  reach  the  ccelom  of  the  louse  between  the  second  and 


1 3 1  o  THE  RELA  PSING  FE  VERS 

eighth  day  after  the  transmissive  feed.  It  can  also  be  spread  by 
direct  inoculations  such  as  may  take  place  accidentally  in  labor- 
atories or  at  post-mortems. 

The  blood  is  not  merely  transmissive  to  the  louse  during  the  time 
when  the  spirochaete  can  be  found  therein,  but  also  during  the 
apyrexial  interval.  The  louse  may  be  infective  for  a  few  hours 
after  a  transmissive  feed,  and  perhaps  a  few  cases  of  human  infection 
may  be  accounted  for  in  this  way,  but  this  is  not  the  usual  method. 

After  a  transmissive  feed  the  spirochaetes  quickly  disappear  from 
the  alimentary  canal  of  the  louse,  and  do  not  reappear  in  the  ccelomic 
fluid  until  the  eighth  to  ninth  day  after  the  feed ;  but  before  this  the 
louse  becomes  infective  from  the  third  to  fifteenth  day,  and  usually 
on  the  sixth  day  the  louse  is  most  infective. 

Infection  is  not  conveyed  by  the  louse  bite,  but  by  the  parasite 
escaping  from  the  body  of  the  crushed  louse  and  entering  man 
through  excoriations  in  the  skin,  generally  made  by  scratching. 
One  crushed  louse  is  sufficient  to  produce  the  disease. 

The  incubation  period  under  experimental  conditions  appears  to 
be  six  to  eight  days. 

The  louse  is  not  pathologically  affected  by  the  germ,  of  which  it  is 
the  natural  reservoir,  the  spirochaete  being  passed  from  one  genera- 
tion to  the  next  succeeding  generation,  as  has  been  shown  by  the 
discovery  that  the  young  of  infected  lice  are  themselves  infective. 

Pathology. — The  presence  of  the  spirochaetes  in  the  blood  is 
associated  with  fever,  which  must  be  due  to  toxins  produced  by 
these  organisms,  though  the  severity  of  the  symptoms  bears  no 
relationship  to  the  number  of  the  organisms  found  in  the  peri- 
pheral blood.  The  spirochaetes  disappear  from  the  circulation 
when  the  temperature  falls  to  normal.  The  disappearance  of  the 
parasites  from  the  blood  is  brought  about  by  the  presence  of  anti- 
bodies (agglutinins  and  parasiticidal  substances).  In  those  cases, 
however,  in  which  relapses  occur,  the  blood  remains  infectious 
during  the  intervals.  This  is  due  to  some  parasites  resisting  the 
action  of  the  antibodies.  These  resistant  spirochaetes  after  a  time 
multiply  again  in  large  numbers,  giving  rise  to  the  relapse.  Leva- 
diti  and  Roche  have  demonstrated  that  serum  collected  after  a 
first  attack  destroyed  the  spirochaetes  which  caused  the  attack,  but 
had  no  effect  whatever  on  the  spirochaetes  which  caused  the  second 
attack.  The  relapses,  therefore,  are  caused  by  the  survival  of 
resistant  types  of  spirochaetes,  and  recovery  depends  upon  the 
existence  of  protective  substances  in  the  blood.  The  immunity 
acquired  after  one  or  several  attacks  may  last  for  some  weeks  or 
months.  Animals  can  be  hyperimmunized  by  repeated  inocula- 
tions after  recovery  from  the  first  attack.  The  serum  of  such 
hyperimmunized  animals  shows  definite  protective  and  curative 
properties. 

Morbid  Anatomy. — The  principal  pathological  feature  of  the  post- 
mortem is  the  enlargement  of  the  liver  and  spleen,  the  latter  organ 
reaching  a  weight  of  I  to  2  kilogrammes  at  times.     On  section, 


S  YMPTOMA  TOLOG  Y 


1311 


the  spleen  is  dark-coloured  and  soft,  with  enlarged  follicles,  and  on 
microscopical  examination  shows  congestion  and  a  cellular  in- 
crease. The  liver  is  enlarged,  and  its  lobules  are  poorly  defined, 
while  microscopically  cloudy  swelling  and  fatty  infiltration  may  be 
seen,  as  well  as  leucocytic  infiltration  into  the  portal  system.  The 
kidneys  are  enlarged  and  congested,  and  microscopically  show 
cloudy  swelling  and  fatty  degeneration  of  the  cells,  while  the 
stomach  shows  signs  of  inflammation,  and  the  heart  is  soft  and 
flabby.  The  bronchi  are  generally  congested,  and  contain  frothy 
mucus,  and  the  lungs  show  hypostasis.  The  brain  may  be  con- 
gested, and  all  the  organs  may  be  stained  yellow  with  bile. 

Symptomatology. — The  incubation  period  is  said  to  vary  between 
two  and  twelve  days,  but  in  accidental  inoculations  it  is  aboutjseven 
days'    During  this~period  prodromal  symptoms,   in  the"  form   o 
slight  malaise,  may  be  felt. 


Fig.  648. — Temperature  Chart  of  the  Relapsing  Fever  of  Europe. 


The  onset  is  usually  sudden,  but  it  may  be  gradual,  the  patient 
suffering  from  rheumatic-like  pains,  headache,  and  constipation. 
When  it  begins  suddenly,  there  are  rigors,  with  severe  frontal  head- 
ache, pains  in  the  back  and  limbs,  epigastric  pain  and  tenderness, 
associated  with  a  sense  of  weakness.  The  face  becomes  flushed,  the 
conjunctivae  injected,  and  the  temperature  rises  to  1030  to  1040  F., 
with  a  pulse^rate  of  no  to  120,  quickened  respirations,  and  some- 
times nausea  and  vomiting. 

The  Course. — The  temperature  continues  high  until  the  sixth  or 
seventh  day,  during  which  period  the  skin  may  be  yellowish  in  colour, 
hot  and  damp  from  perspiration,  with  at  times  a  rose-coloured 
macular  eruption,  disappearing  on  pressure,  on  the  thorax,  abdomen, 
and  legs,  which  lasts  for  a  day  or  so.  Thetongueismoist,redat  the 
tip,  and  covered  with  a  white  fur.  Vomiting  of  greenish-yellow 
matter  may  occur,  but  nausea  is  always  present,  and  thirst  is  com- 
mon; the  bowels  are  usually  constipated,  and  diarrhoea  is  more  a 


13 12  THE  RELAPSING  FEVERS 

complication  than  a  feature  of  the  disease.  The  liver  is  enlarged 
and  tender,  and  so  is  the  spleen,  which  may  reach  a  considerable 
size.  The  heart  sounds  are  normal,  but  the  pulse-rate  is  quick, 
reaching  120  to  140,  or  even  more,  per  minute;  but  it  is  not  dicrotic. 
The  erythrocytes  and  the  haemoglobin  are  reduced  in  amount,  while 
a  polymorphonuclear  leucocytosis  may  be  present.  Spirochaetes  can 
be  found  in  the  blood,  and  occasionally  can  be  seen  engulfed  by 
leucocytes.  There  is  generally  a  troublesome  cough,  with  scanty 
bronchitic  expectoration,  and  rales,  which  can  be  heard  over  the 
chest  and  trachea.  The  respirations  follow  the  pulse-rate,  being 
increased  to  48  to  50  per  minute  if  the  temperature  is  high.  The 
pains  in  the  muscles  and  joints  continue,  and  sleeplessness  may 
result,  while  a  noisy  delirium  is  not  rare,  but  stupor  is  uncommon. 
The  urine  is  febrile,  and  may  contain  a  little  albumen.  About  the 
sixth  or  seventh  day  the  crisis,  sometimes  ushered  in  by  a  rigor, 
intervenes,  with  violent  perspiration,  or  diarrhoea,  with  or  without 
epistaxis,  and  with  a  sudden  rapid  fall  of  temperature,  while  the 
pulse  and  respirations  also  return  to  normal,  and  the  patient  falls 
into  a  deep  sleep,  and  awakens  much  better. 

The  Intermission. — The  intermission  now  begins,  during  which  the 
temperature  returns  to  normal.  The  spleen  often  remains  enlarged, 
the  temperature  chart  may  show  small  rises,  and  the  patient's 
strength  slowly  improves. 

The  Relapse. — The  disease  may  now  end;  but  this  is  exceptional, 
and  more  usually,  about  the  fourteenth  day  from  the  first  commence- 
ment of  the  illness,  the  relapse  occurs,  beginning  with  a  rigor  and 
symptoms  resembling  the  attack,  but  often  more  severe,  and,  after 
lasting  three  or  four  days,  terminating  in  a^nsisTwliicli  generally 
ends  the  illness.  Very  rarely  is  there  zsecondjelafese,  in  which  case 
the  same  symptoms"occur,  but  much  less  severely,  and  a  third  relapse 
is  most  uncommon-     Convalescence  is  sometimes  slow. 

Complications. — The  complications  are  numerous,  affecting  the 
lungs  in  the  form  of  bronchitis  and  pneumonia,  or  the  alimentary 
canal  as  dysentery,  diarrhoea,  and  haematemesis;  while  cerebral 
haemorrhage,  conjunctival  haemorrhage,  iritis,  and  corneal  ulcers, 
have  all  been  recorded. 

Abortion  often  complicates  the  first  relapse  in  pregnant 
women. 

Diagnosis. — In  the  first  instance,  before  the  relapsing  character  Afy- 
has  appeared,  the  disease  requires  to  be  diagnosed  from  mjj^rj^/p^i 


■  typhi??,  typhoid  fever,  yellow^fever,  and  seven  days^fever^ — The  Jiy' 
principal  positive  signs  indicating  relapsing  fe>eTlffe>^(Tp?resence 
of  the  spirochaetes  in  the  blood;  (2)  agglutination  or  Lowenthal's 
reaction,  which  consists  of  taking  a  drop  of  blood  from  the  suspected 
case  and  adding  it  to  another  drop  of  blood  containing  spirochaetes 
taken  from  a  patient,  mixing  the  two  drops  together,  and  covering 
with  a  cover-glass,  which  is  then  sealed  and  placed  in  an  incubator 
at  370  C.  for  half  an  hour.  A  positive  reaction  is  indicated  by  the 
clumping  of  the  spirochaetes  into  non-motile  masses. 


DIAGNOSIS— TREATMENT  1313 

Differential  Diagnosis. — -Malaria  can  be  diagnosed  by  the  discovery 
of  the  malarial  parasite  in  the  blood. 

Typhoid  is  indicated  by  the  positive  results  of  haemo-cultures  and 
by  tiie  fever  having  started  gradually.  Widal's  reaction  is  not  of 
much  help  during  the  first  week.  Typhus  can  be  separated  by  the 
absence  of  spirophaetes.  by  a  negative  Lowenthal's  reaction,  and 
by  the  presence  of  its  characteristic  rash.  Yellow  fever  can  be 
diagnosed  by  its  black  vomit,  though  at  first  the  differentiation 
may  be  impossible  without  a  microscopical  examination  of  the 
blood.      Dengue  fever  is  characterized  by  its  slow  pulse  and,   of    >o  •*■ 

course,  by  the  absence  of  spirochetes.     Weil's  disease  may  be  dis-  <rloOv 
tinguished  by  the  more  marked  jaundice  and  by  the  different 
nature  of  the  spirochaetes,  which  are  seldom  found  by  the  simple 
microscopical  examination  of  the  blood. 

Prognosis.— The  prognosis  is  usually  favourable.  Marked  jaun- 
dice is  a  bad  sign,  while  pregnant  women  generally  abort.  The 
mortality  appears  to  vary  considerably,  being,  according  to  Mur- 
chison,  only  4  per  cent,  in  the  United  Kingdom;  while,  according 
to  Sandwith,  it  is  14*4  per  cent,  in  Egypt,  which  is  nearly  the  same 
percentage  as  that  reached  in  Russia.  The  causes  of  death  are 
toxaemia  in  the  first  attack,  and  collapse  in  the  first  intermission, 
but  it  may  be  caused  by  one  of  the  above-mentioned  compli- 
cations. 

Treatment.  —  This  may  be  discussed  under  the  following 
headings: — 

1.  Specific  Treatment. 

2.  Symptomatic  Treatment. 

Specific  Treatment. — Salvarsan  or  neosalvarsan  or  their  sub- 
stitutes may  be  administered  either  by  intramuscular  injection  or, 
better,  intravenously.  This  is  a  specific  treatment,  most  effica- 
cious, but  care  should  be  taken  not  to  inject  a  large  dose,  as 
certain  patients,  especially,  it  seems,  those  suffering  from  Asiatic 
relapsing  fever,  stand  the  drug  badly,  cases  of  death  having  been 
recorded,  even  aft  era  medium  dose,  such  as  7^  grains  (0*5  gramme). 
According  to  Mouzels,  an  intravenous  injection  of  4  or  5  grains 
(o -3  gramme)  does  not  give  rise  to  any  unpleasant  symptom,  and 
is  generally  sufficient  to  make  the  spirochetes  disappear  from  the 
blood  and  cure  the  attack.  If,  however,  another  attack  of  fever 
develops,  a  second  injection  of  the  same  dose  may  be  given. 

Symptomatic  Treatment. — Pains  in  the  head  and  muscles  may  be 
relieved  by  small  doses  (2  to  3  grains)  of  salicylates,  aspirin,  antipyrin, 
or  by  quinine.  If  these  pains  are  very  severe,  opium  or  a  hypo- 
dermic injection  of  morphia  may  be  necessary.  Epigastric  pain 
may  be  relieved  by  fomentations  sprinkled  with  tincture  of  opium, 
while  vomiting  should  be  treated  with  ice,  champagne,  and  bismuth 
mixtures,  though  occasionally  morphia  or  codeine  may  be  required. 
Effervescing  ammonium  carbonate  mixtures  are  often  grateful. 

A  dry,  troublesome  cough  may  be  relieved  by  codeine  or  small 

83 


I3i4  THE  RELAPSING  FEVERS 

doses  of  heroin;  in  other  cases  an  expectorant  mixture  will  be 
found  useful.  Constipation  must  be  treated  by  laxatives  or  enemata, 
and  high  temperatures  by  cool  sponging,  which,  however,  will  but 
seldom  be  required.  The  complications  must  be  met  by  the  treat- 
ment laid  down  in  textbooks  on  general  medicine. 

Prophylaxis. — Prophylaxis  consists  in  the  destruction  of  lice  by 
steaming  clothes,  as  can  be  done  in  railway  TruckTTy  IeaHmg  in 
steam  from  the  engine  or  by  boiling  clothes,  while  the  patient  is 
thoroughly  bathed.  For  further  particulars  see  the  prophylaxis 
of  typhus  (p.  1338}. 

THE   RELAPSING  FEVER   OF  NORTH  AFRICA. 

Synonyms. — Algerian  relapsing  fever;  Egyptian  relapsing  fever;  Arabic: 
Homa  el  Hugga,  Homa  en  Naxy,  Naushah. 

Definition.- — An  acute  specific  fever  caused  by  Spiroschaiidinuia 

a  |J<V1  ^  berbera  Sergent  and  Foley,   1910,  and  spread  by  the  agency  of 

j  Pediculus  corporis  de  Geer,  1778. 

A    cffl       History. — It  was  noticed  by  the  surgeons  of  Napoleon's  army  in 

ff  1  Egypt,  and  later  by  Griesinger  in  1851,  when  it  was  called  '  bilious 

typhoid ' ;    while    more    recently    Sandwith,  Cummins,   Bousfield, 

Balfour,  and  Graham-Smith,  have  published  excellent  accounts  of 

the  disease.     In  1910  Sergent  and  Foley  differentiated  S.  berbera 

Sergent  and  Foley,  in  a  case  in  South  Oran.     The  transmission  of 

the  disease  by  lice  has  been  worked  out  by  Nicolle,  Blaizot,  and 

Conseil.        Toyoda's   immunological   experiments   show   that   this 

fever  is  closely  related  to  the  European  type. 

Climatology. — It  is  known  to  exist  in  Algeria,  Tunis,  Tripoli, 
Egypt,  and  the  Anglo-Egyptian  Sudan. 

/Etiology. — It  is  caused  by  S.  berbera  Sergent  and  Foley,  1910, 
spread  by  the  agency  of  lice,  as  shown  by  Nicolle,  Blaizot,  and 
Conseil  (see  p.  447). 

Symptomatology. — The  length  of  the  incubation  period  is  not 
known,  but  is  believed  to  be  more  than  twelve  days.  The  fever, 
which  may  be  associated  with  rigors,  reaches  its  height  during  the 
first  twenty-four  hours,  and  afterwards  shows  morning  remissions. 
The  spleen  enlarges,  and  the  liver  becomes  tender  and  painful  in 
some  cases;  but  jaundice  is  generally  absent.  Vomiting  is  present, 
but  diarrhoea  is  absent.  The  attack  is  apparently  not  very  severe. 
Apyrexia  lasts  from  two  to  nine  days,  and  is  followed  by  one, 
two,  or,  more  rarely,  three  relapses. 

Diagnosis. — The  spirochetes  must  be  found  in  the  blood,  as  the 
cases  may  occasionally  resemble  cerebro-spinal  meningitis  and  acute 
rheumatism. 

Prognosis. — This  is  usually  good,  the  mortality  being  nil  in 
fifty  cases. 

Treatment. — This  is  the  same  as  for  the  other  relapsing  fevers. 


THE  RELAPSING  FEVERS  OF  ASIA  1315 

THE  RELAPSING  FEVERS  OF  ASIA. 

There  are  probably  a  number  of  relapsing  fevers  in  Asia,  but  we 
only  know  two  which  have  lice  as  carriers,  and  these  are: — 

1.  The  Indian  relapsing  fever. 

2.  The  Manchurian  relapsing  fever. 

The  Relapsing  Fever  of  India. 

Definition. — An  acute  specific  relapsing  fever  caused  by  Spiro- 
schaudinnia  carteri  Manson,  1907,  and  spread  by  the  louse  in  all 
probability. 

History. — Relapsing  fever  is  one  of  the  endemic  diseases  of  India, 
being  traceable  back  into  the  eighteenth  century.  The  credit  of 
first  clearly  defining  the  disease,  however,  rests  with  Lyall  in  the 
epidemic  fever  in  the  Punjaub  in  1852-53;  but  Vandyke  Carter, 
in  1876-77,  in  the  Bombay  Presidency  found  spirochetes  in  the 
blood  of  patients  suffering  from  fever,  and  his  work  on  the  subject, 
published  in  1882,  is  to  be  regarded  as  the  Indian  classic  on  this 
fever.  Schellach,  in  1907,  separated  this  spirochaete  from  S.  re- 
currentis  and  S.  novyi  by  finding  that  it  is  not  agglutinated  by  the 
serum  of  animals  infected  with  these  parasites.  Rogers  points  out 
that  the  disease  has  often  been  confounded  with  typhus  fever  in 
India.  In  1911  Stott  suggested  that  two  varieties  of  fever  may 
be  included  under  this  term,  and  recent  research  shows  that 
several  varieties  of  relapsing  fever  probably  exist  in  India. 
Types  of  relapsing  fever,  which  may  possibly  be  different  from 
the  Indian  ones,  occur  in  China  and  French  Indo-China,  while 
the  Arabian  type  may  be  identical  with  the  West  African  relapsing 
fever. 

Climatology. — The  real  home  of  the  disease  appears  to  be  the 
Bombay  Presidency,  but  it  is  also  known  in  the  Punjaub  and  in  the 
Kumaon  Hills  of  the  North-Western  Provinces. 

/Etiology. — The  cause  of  the  disease  is  the  spirochaete  found  by 
Vandyke  Carter  in  1877.  It  is  inoculable  into  man,  as  was  proved 
by  Carter  inoculating  himself  twice,  with  an  interval  of  two  and  a 
quarter  years.  It  can  also  be  inoculated  into  monkeys,  but  not  into 
rats  and  mice.  Bugs  are  capable  of  retaining  it  alive  in  their 
alimentary  canals  for  from  four  to  seven  days  when  obtained  from 
monkeys,  but  do  not  appear  to  be  so  effective  in  obtaining  it  from 
man,  as  only  one  in  fifty-three  were  found  infected  after  feeding  on 
human  beings.  Infected  bugs  are  capable  of  transmitting  the 
disease  to  monkeys.  Rogers,  however,  thinks  that  mosquitoes_ 
may  be  found  to  be  more  effective  than  bugs.  Mackic  haTbroughT 
foTward  evidence  m  favour  of  Pedicuhis  corporis  being  a  carrier. 
(For  description  of  the  spirochaete,  see  p.  446.) 

S.  carteri  is  separated  from  S.  duttoni  by  the  latter  being  far  more 
easily  inoculable  into  animals  and  producing  numerous  relapses 


1316 


THE  RELAPSING  FEVERS 


*S 


/ 


when  injected  into  monkeys,  while,  according  to  Lamb,  the  former 
only  causes  one  relapse.  Moreover,  the  two  spirochsetes  may  be 
differentiated  by  immunization  and  agglutination  tests.  S.  macaci, 
observed  by  us  in  monkeys  in  Ceylon,  appears  to  be  closely  related 
to  S.  carteri,  and  may  be  identical  with  it. 

'  Strong,  experimenting  with  whit  e  mice,  has  come  to  the  conclusion 
that  the  Indian  Spiroschaudinnia  is  closely  allied  to  the  European 
and  North-American  types. 

Pathology. — The  morbid  anatomv  resembles  that  of  the  European 
type. 

Symptomatology. — In  accidental  inoculations  in  the  post-mortem 
pj-"'  i room  the  incubation  period  varies  from  three  and  a  half  to  seven 

^~    -wjfdays,  during  which  prodromata  resembling  those  of  the  European 
^aaP^    v)  type  may  occur. 

Theronset  is  generally  sudden,  but  in  most  cases  without  the 
rigors  defined  in  Europe,  though  chilliness  occurs,  and  the  disease 
progresses  as  in  the  Obermeyer  fever.     On  the  fall  of  temperature 

to  submormal,  however,  on  the 
sixth  or  seventh  day,  which  is 
associated  with  profuse  perspi- 
ration and  polyuria,  instead  of 
the   patient    feeling   better,   he 
often  becomes   collapsed,    with 
a  small  weak  pulse  and  a  cold 
clammy  skin,  in  which  condition 
he  may  resemble  at  first  sight  a 
cholera   patient.      In    the    first 
intermission,   which   lasts  from 
three  to  twelve  days — generally 
aT5buf""eig"ht  days — the   patient 
improves  "slowly,    there    being 
much  debility,  and  in  one  case 
in  six  there  is   a   sudden  tem- 
porary rise  of  temperature  after 
the  crisis.     Spirochsetes  are  not 
to  be  seen  in-  the  blood,   but  Carter  and  Pisani  have  described 
peculiar  structures.     The  first  relapse  occurs  about  the  fourteenth 
day  of  the   disease,  and  the    seventh    of   the  Jn^rrrmsidh,  "and" 
resembles  the  first  attack,  but  tEe  temperature  may  reach  a  higher 
level,  and  the  illness  is  shorter,  ending  in  a  crisis. 

The  second  int  ermission  may  last_abput_ten  days,  being  longer 
than  the  first,  and  a  second  relapse  takes  place,  often  commencing 
with  chills.  The  liver  does  not  markedly  enlarge,  but  the  spleen 
increases  in  size.  The  fever  is  remittent' or  intermittent,  and  the 
crisis  is  not  marked.  It  is  now  rare  for  the  disease  not  to  end,  but 
after  an  interval  of  fourteen  to_sevcntccn  days  a  third  relapse  may 
take  place,  with  a  sudden  rise  of  temperature,  which  lasts  one  to 
jour  days.  Very  rarely  a  fourth  intermission  of  about  eleven  days 
ends  in  a  fourth  relapse,  lasting  only  two  days. 


Fig.  649. — Spiroschaudinnia  from 
a  Case  of  Asiatic  Relapsing 
Fever. 

(From  a  microphotograph  by 
J.  J-  Bell.) 


VARIETIES— TREA  TMENT 


With  regard  to  the  frequency  of  the  relapses,  Rogers  gives  the 
following  percentages:  — 

Without  relapse  ..  ..  ..  ..      23*8  per  cent. 

With  one  relapse        ..  ..  ..  ..      49'2 

With  two  relapses      ..  ..  ..  ..      20-0 

With  three  relapses  ..  ..  ..  ..        5*0 


With  four  relapses 

Varieties. — The  typical  course. 


may  be  varied  in  about  25  per 


cent,  of  cases,  and  present  (a)  a  short,  irregular,  remittent  fever  ; 
(b)  a  so-called  bilious  remittent  fever,  called  by  Carter  '  icteric  fever.' 

(a)  Short,  Irregular,  Remittent  Fever. — This  is  very  like  malaria, 
from  which  it  is  only  to  be  diagnosed  by  blood  examination. 

(b)  So-called  Bilious  Remittent  Fever  (Icteric  Fever). — So-called 
bilious  remittent  fever  very  closely  resembles  typhus  fever,  and  to 
some  extent  yellow  fever,  showing  deep  jaundice,  with  an  eruption 
of  red  spots.  The  temperature  is  irregular,  and  the  pyrexia  pro- 
longed; prostration  comes  on  early,  and  may  develop  into  a  '  status 
typhosus.'     The  death-rate  of  these  cases  is  high,  being  70  per 


|M  e  |m  e]m  e  1  m ,  eTm"  e  .V  e|m  e  IM  KiM 


/  a.  5 

IART    OF    T 


:he  Relatsing  Fever! 


)f  India. 


Fig.    65o.-4-Tempera^ure  Cp_ ___ 

J  (Chart  maVie  by  Major  Archibald.) 

cent.     They  are  to  be  diagnosed  from  typhus  by  the  blood  examina- 
tion, and  from  yellow  fever  by  the  absence  of  black  vomit. 

Complications. — These  are  the  same  as  in  the  European  type. 

Diagnosis. — This  is  based  on  the  microscopical  examination  of 
the  blood.  ^P^b 

Prognosis. — A  prolonged,  irregular  first  attack,  ending  by  lysis, 
and  attacks  showing  marked  jaundice  are  bad  omens. 

The  mortality  is  higher  than  in  Obermeyer's  type,  being  18-02 
per  cent.,  of  which  about  one-half  take  place  in  the  attack",  and> 
one-quarter   in  the  first   interval,   and   one-fifteenth   in.  the  first 
relapse,  and  the  remainder  from  complications. 

Treatment. — The  treatment  and  diet  differ  in  no  respect  from 
that  already  laid  down,  except  that  these  patients  often  stand 
large  doses  of  salyarsan  badly,  and  therefore  one  should  not  give 
more  than  5  grains  of  the  drug  by  intravenous  injection;  more- 
over, the  disease  being  of  a  severer  type  than  the  European  form, 


1318  THE  RELAPSING  FEVERS 

and  sudden  heart  failure  being  common,  cardiac  stimulants  should 
be  given  during  the  attack,  and  preparation  made  for  preventing 
the  collapse  by  means  of  hypodermics  of  strychnine  and  ether,  or 
camphor  in  ether,  as  well  as  by  hot  bottles,  blankets,  etc. 

Prophylaxis. — See  remarks  with  reference  to  the  European  type. 

Manchurian  Relapsing  Fever. 

This  type  of  relapsing  fever  is  due  to  a  spirochete  which  Toyoda 
in  1916  demonstrated  by  immunity  experiments  to  be  distinct 
from  the  African  and  the  European  types.  The  organism  is  short, 
7-20  microns  by  0-4  micron,  and  its  spirals  number  4-8;  it  is  spread 
by  lice. 

Liver  enlargement  and  albuminuria  are  physical  signs  of  import- 
ance. The  first  paroxysm  lasts  five  to  thirteen  days,  the  first 
interval  two  to  fourteen  days;  the  second  attack  one  to  nine  days, 
interval  two  to  thirteen  days;  the  third  paroxysm  lasts  one  to  six 
days,  the  third  interval  two  to  ten  days;  the  fourth  paroxysm  lasts 
two  to  six  days. 

The  mortality  rate  is  5*3  per  cent.     Two  paroxysms  are  common. 


THE   TICK    GROUP. 
THE  RELAPSING  FEVERS  OF  AFRICA. 

The  tick  relapsing  fevers  of  Africa  may  be  classified  as  follows:' — 

1.  West  African  relapsing  fever. 

2.  East  African  relapsing  fever. 

1.  The  Relapsing  Fever  of  West  Africa. 

Synonyms. — Tick  fever  (Livingstone),  African  tick  fever. 

Definition. — An  acute  specific  relapsing  fever  caused  by  Spiro- 
y  schaudinnia  duttoni  Novy  and  Knapp,  1906,  and  spread  by  Ornitho- 
doros  moubata  Murray. 

'  History. — The  peoples  of  Africa  from  time  immemorial  have  had 
a  dread  of  tick-bites,  which  they  thought  caused  fever,  and  this 
appears  to  have  been  noted  by  Livingstone,  Kirk,  Hinde,  and 
many  other  people,  with  the  result  that  a  tick  fever  of  an  unknown 
nature  was  spoken  of  as -occurring  in  Africa.  Xabarro,  in  August, 
1903,  was  the  first  to  observe  a  spirochaete  in  human  beings  in 
Uganda,  but  as  his  publication,  through  no  fault  of  his  own 'did 
not  appear  till  much  later,  his  discovery  was  forestalled  by  those 
of  Ross  and  Milne  in  1904,  and  Dutton  and  Todd,  also  in  1904,  who 
found  the  cause  of  the  tick  fever  to  be  a  spirochaete,  the  latter 
observers  also  proving  that  it  was  introduced  into  the  blood  by 
the  bite  of  a  tick — Ornithodoros  moubata.  Since  that  date  Koch, 
Todd,  Novy  and  Knapp,  Breinl  and  JKinghorn,  and  others,  have 
studied  the  disease  carefully.  Frankcl  has  proved  by  biological 
tests  that  the  spirochsete  of  East  African  relapsing  fever  differs 
from  S.  duttoni,  as  observed  in  West  Africa,  and  Nuttall  proposed 


THE  TICK  GROUP  13  ig 

the  name  S.  rossi  Nuttall,  1908,  for  this  new  species;  but  recent 
researches  seem  to  have  proved  the  identity  of  the  two  conditions. 

Climatology. — The  disease  is  found  in  Angola,  the  Congo  Free 

State,   Uganda,  late  German  East  Africa  and  Portuguese  East 

Africa,  and  in  the  Valley  of  the  Zambesi.     Franco,  Robledo,  and 

others  have  described  a  spirochaetiasis  in  Colombia,  which  is  caused 

by  a  spirochaete  morphologically  resembling  S.  duttoni,  and  said 

A        to  be  spread  by  Qrnitiiodoros_tiiricatus.,  with  reference  to  which  it 

0  Q    ^  may  be  noted  that  BukTow  observed  relapsing  fever  in  the  Andes 

s^    in  1865.     Robledo  asserts  that  it  is  spread  by  the  bite  of   Orni- 

tliodoros  megiiini. 

"The  climatic  conditions  required  appear  to  be  heat  and  moisture, 
but  according  to  Franco's  observations,  the  disease  can  occur  at  an 
altitude  of  7,000  feet.  No  observations  appear  to  be  recorded  as 
to  variations  due  to  season.  Carter's  investigations  would  tend 
to  show  that  Arabian  relapsing  fever  is  either  a  separate  form  of 
fever,  or  is  allied  to  this  West  African  form,  as  it  may  be  spread  by 
an  Omithodoros. 

Etiology. — The  cause  of  the  fever  is  S.  duttoni  Novy  and  Knapp, 
1906,  which  is  proved  to  be  distinct  from  the  other  spirochaetes, 
because  an  animal  immunized  against  one  of  these  is  capable  of 
being  successfully  inoculated  by  it.  S.  duttoni  can  be  inoculated 
into  a  number  of  animals — namely,  dogs,  goats,  sheep,  rabbits, 
guinea-pigs,  rats,  and  mice — but  not  into  cats,  chickens,  pigeons, 
or  goldfish.  The  spirochaetes  can  pass  through  the  placenta  into 
the  circulation  of  the  foetus,  which  they  infect.  These  organisms 
are  easily  seen  jn  tjie  blood  during  an  attack,  but  disappear  during 
an  apyrexial  interval.     The  spirochaete  is  describecTon  p.  444. 

The  life^history  in  the  vertebrate  has  been  worked  out  by  Breinl, 
who,  as  already  described,  showed  that  just  before  the  crisis  the 
spirochaetes  become  encysted  and  undergo  schizogony  into  small 
bodies,  from  which  the  new  generation  develop.  Leishman  has 
demonstrated  that  when  the  spirochaetes  pass  into  the  intestinal 
sac  of  the  tick  they  lose  their  motility  and  their  characteristic 
appearance,  while  the  central  core  of  chromatin  segments  into 
small  masses,  which  are  set  free  into  the  lumen  of  the  gut.  These 
small  bodies,  which  resemble  small  rods,  or  are  rounded,  like 
micrococci,  appear  to  multiply  in  the  body  of  the  tick,  and  to  pass 
into  the  cells  of  the  Malpighian  tubules  and  into  the  tissue  of  the 
ovary.  In  the  latter  position  they  enter  the  immature  eggs,  and 
can  be  traced  through  all  stages  of  development  into  the  adult 
ticks.  In  the  embryo,  and  in  all  the  later  stages  of  development  up 
to  and  including  the  adults,  they  are  found  as  small  chromatin 
bodies  lying  in  the  cells  of  the  Malpighian  tubules.  Inoculation  of 
crushed  tissue  containing  these  bodies  produces  a  typical  infection. 
From  his  experiments,  Leishman  concludes  that  it  is  by  these 
chromatin  bodies  that  the  disease  is  carried  from  the  egg  to  the 
new  generation  of  ticks,  and  that  infection  of  man  does  not  take 
place  via  the  salivary  glands,  but  by  the  small  bodies  gaining  access 


1320  THE  RELAPSING  FEVERS 

to  the  wound  produced  by  the  tick's  bite,  by  being  voided  in  the 
Malpighian  secretion  passed  by  the  tick  during  feeding,  or  perhaps 
by  regurgitation  of  the  intestinal  contents.  More  recently  Leish- 
man  and  Hindle  have  shown  that  the  tick  produces  infection  only 
as  the  result  of  its  infected  faeces  contaminating  the  tick-bite.  This 
is  a  typical  example  of  the  contaminative  mode  of  infection. 

The  principal  predisposing  causes  are  anything  which  facilitates 
the  life  of  the  tick,  such  as  bad  hygienic  conditions,  which  are  well 
exemplified  by  the  native  huts  of  Africa.  These  huts  contain  many 
cracks  in  the  walls  and  floor,  which  afford  shelter  to  the  tick,  and 
hence  predispose  to  the  disease. 

Pathology. — Very  little  can  at  present  be  said  as  to  the  pathology. 
The  post-mortem  reveals  only  an  enlarged  firm  spleen,  while  smears 
taken  from  the  liver  and  lungs  show  large  numbers  of  spirochetes. 

Symptomatology.— The  symptomatology  still  requires  careful 
investigation  on  the  lines  carried  out  by  Carter  in  India,  but  much 
good  work  has  been  done  on  the  subject  by  Dutton,  Todd,  Ross, 
and  others. 

Incubation. — The  period  of  incubation  is  usually  about  seven 
days,  but  it  may  extend  to  eleven  or  twelve  days. 

The  tick-bite  may  be  accompanied  by  local  inflammatory  symp- 
toms, but  in  some  cases  the  bite  is  not  even  noticed.  According  to 
Wellman,  natives  believe  that  when  the  tick-bite  is  accompanied  by 
a  severe  local  reaction,  the  individual  probably  escapes  fever,  and 
Nuttall  calls  attention  to  the  possible  protective  effect  of  a  local 
reaction. 

Usually  mental  heaviness,  lack  of  activity,  profuse  sweating,  and 
constipation,  are  mentioned  as  prodromal  symptoms. 

Onset. — The  attack  may  c^mec^graduaJlly,  with  a  feeling  of 
malaise,  faintness,  and  a  disrnclinatlonTor  fooa,  or  even  vomiting, 
and  a  slight  rise  of  temperature.  In  a  few  hoursthe  temperature  will 
have  risen  to  1030  to  1050  F.,  associated  with  Ijeadache,  pains  in 
the  back  and  limbs,  and  intense  pain  in  the  regipnOTThe^leen,  and 
chilliness]  TTienTTs*'  vomiting,  first  of  food,  and  TTTeh  of  lS3p,  with 
often  diarrhoea,  and  everi"aT"Hmes  streaks  of  blood  in  the  motions. 
The  spleen  is  generally  found  to  be  enlarged,  and  spirochetes  in 
scanty  numbers  occur  in  the  peripheral  blood,  but  may  be  hard  to 
find.  — 

bourse. — The  next  day  the  symptoms  are  worse,  and  the  patient  is 
hot  and  restless,  complaining  of  thirst  and  splenic  pain,  and  often 
troubled  by  a  cough.  The  temperature  shows  a  morning  fall,  without 
improvement  in  the  symptoms,  and  an  evening  rise,  during  which 
the  pains  increase,  and  the  patient  may  become  delirious.  The 
liver  does  not  enlarge,  but  the  spleen  projects  below  the  costal 
margin.  Spirochetes  are  now  found  in  greater  numbers,  but 
diminish  remarkably  before  the  crisis.  There  is  a  slight  dccnv.se 
in  the  red  cells  and  haemoglobin,  and  a  marked  leucocytosis  before 
the  crisis,  while  polychromatophile  degeneration  is  noted  in  the 
red  cells,  and  a  very  marked  increase  in  blood  platelets.     The 


CLINICAL   VARIETIES  1321 

symptoms  last  three  to  four  days,  and  end  by  a  crisis  marked  by 
profuse  sweats  and  a  fall  of  temperature  below  normal.  On  the 
day  before  f he  crisis  there  is  a  pseudo-crisis,  with  a  fall  of  tempera- 
ture, but  no  improvement  in  the  symptoms. 

Intermission. — •The  patient  feels  weak  and  tired,  but  slowly  re- 
gains his  appetite  and  strength,  and  no  parasites  are  found  in  the 
blood.     The  disease  may  now  terminate,  or  the  intermission  may 
last  from  one  to  twenty-one  days,  according  to  Ross;  but  five  to_ 
eight  days  is  more  usual. 

i&fiipse. — The  first  relapse  begins  with  a  rise  of  temperature 
and  a  return  of  the  ojiginal-symptoms,  and  also  of  the  parasites 
into  the  peripheral  blood.  After  lasting  three  to  four  days,-it 
ends  in  a  crisis  marked  bysweating,  and  showing  a  pseudo-crisis 
on  the  preceding  day. 

Intermissions    and    relapses   follow    one    another    regularly    or 
irregularly,  the  intervals  being  from  one  day  to  two  months,  and 
the  relapses  usually  lasting  three  days,  and  showing  a  pseudo- 
crisis  on  the~second  day  and  a  crisis  on  the  third  day.     As  many  as 
five_to_  eleven  .relapses  may  take  place,  and  end  by  reducing  the 
patient  both  in  weight  and  strength.     (Edema  of  the  eyelids  has 
been  notecTm  trie  relapses! 
Complications  and  Sequela. — Iritis  is  frequently  observed. 
Clinical  Varieties.— According  to  Ross,  there  appears  to  be  a 
marked  difference  in  the  severity  of  the  attack  in  new-comers,  such 
as  Europeans,  and  natives.     Though  the  attack  shows  much  the 
same  symptoms  in  natives  as  in  Europeans,  it  is  often  far  less 
severe,  and  the  spleen  may  not  enlarge.     The  attack  frequently 
lasts  twenty-four  to  forty-eight  hours,  and  ends  by  crisis,  after 
which  the  patient  rapidly  recovers,  as  a  rule  without  a  relapse. 
Should  this,  however,  take  place,  it  is  found  to  be  less  severe  than 
the  attack.     Koch  believes  that  these  mild  attacks  and  the  native 
immunity  are  due  to  infection  in  early  childhood.     Dutton  and 
Todd,  on  the  other  hand,  describe  cases  very  much  resembling 
that  in  the  European,  with  enlargement  of  the  spleen,  and  with  more 
than  one  relapse,  leaving  the  patient  anaemic,  thin,  and  weak. 
Hence  it  may  be  concluded  that  the  disease  shows  two  types  in 
natives — a  mild  type  and  a  severe  type — and  that  the  latter  may 
end  in  death. 

Diagnosis. — This  can  only  be  made  by  finding  the  spirochetes. 

Lowenthal's  method  of  agglutination  can  be  applied  in  doubtful  cases. 

Prognosis. — This   is   usually   good    for   both   the   natives    and 

Europeans,  but  death  may  occur  in  both  races,  and  is  signalled  by  a 

rapid  fall  of  temperature  without  improvement  of  the  symptoms. 

No  figures  have  so  far  been  recorded  with  regard  to  the  mor- 
tality, but  it  may  be  taken  that  it,  as  a  rule,  is  low,  though  under 
adverse  circumstances  it  may  be  high.  Dutton  and  Todd  record  that 
of  twenty  men  who  contracted  the  disease  in  one  caravan,  ten  died. 
Treatment.— This  is  the  same  as  for  the  European  form  (see 
P  I3I3)- 


1322  THE  RELAPSING  FEVERS 

Prophylaxis. — The  prophylaxis  is  based  on  the  avoidance  of 
localities  where  tick^.abound  and  the  destruction  of  these  parasites. 
Koch  rightly  advised  that  Europeans  should  camp  at  least  20  to 
30  yards  away  from  infected  native  huts  and  rest-houses. 

2.  The  Relapsing  Fever  of  East  Africa. 

The  relapsing  fever  found  in  Uganda  and  East  Africa  is  clinically 
indistinguishable  from  the  West  African  type,  and  is  carried  by 
the  same  tick,  but  the  Spiroschaudinnia,  according  to  Frankel,  is 
a  different  species  (S.  rossi  Nuttall,  1908).  Recent  researches  seem, 
however,  to  identify  it  with  the  West  African  type. 

THE  TICK  FEVER  OF  MIANA,  PERSIA. 

Definition. — A  specific  fever  of  unknown  cause,  brought  about  by  the  bite 
of  a  tick  (Argas  persicus  Oken,  181 8). 

Historical. — Dupre,  in  1809,  first  described  this  disease,  stating  that  the 
bite  of  A.  persicus,  locally  known  as  '  Guerib-guez,'  '  Garib-guez,'  '  Miane- 
bug,'  or  '  punaise  de  Miana  '  (Maflet  de  Mianeh),  was  at  times  dangerous, 
producing  prolonged  illness.  Kotzebue,  in  181 9,  stated  that  the  natives 
were  immune,  and  only  foreigners  suffered.  Fischer  de  Waldheim,  in  1823, 
said  that  the  bite  was  fatal,  and  Heller,  in  1858,  described  the  effects  as  being 
caused  by  the  mechanical  injury  of  the  bite  of  the  tick.  Taschenburg,  in 
1873,  considered  the  symptoms  to  point  to  a  disease,  and  not  merely  to  the 
effects  of  the  bite  of  the  tick;  and  Schlimmer,  in  1874,  considered  the  im- 
munity of  the  natives  to  be  due  to  the  fact  that  they  had  been  bitten,  and 
so  become  vaccinated.  Megnin,  in  1882,  showed  that  the  bite  per  se  was  not 
dangerous,  and  later  was  supported  by  Fumouze  and  Loundsbury. 

^Etiology. — The  causation  of  the  disease  is  quite  unknown,  but  some  virus 
must  be  inoculated  when  the  tick  bites,  for  the  disease  is  apparently  confined 
to  Persia ;  and  the  experiments  of  Megnin,  Loundsbury,  and  others  show  that 
in  certain  regions  the  effects  of  the  bite  are  insignificant. 

Manson  thinks  that  this  virus  will  some  day  be  found  to  be  a  spirochaete, 
which,  indeed,  is  not  unlikely,  as  A.  persicus  is  well  known  to  be  the  carrier 
of  Spiroschaudinnia  marchouxi  Nuttall,  1904,  which  causes  a  very  fatal  disease 
in  fowls.  Native  Persians  probably  develop  a  relative  immunity  due  to 
previous  slight  infections,  but  new-comers  suffer  severely. 

Symptomatology. — The  knowledge  of  the  symptoms  of  the  disease  is  very 
meagre.  Severe  pain  is  felt  at  the  site  of  the  bite  of  the  tick,  and  this  is 
followed  by  remittent  fever  lasting  from  a  few  days  to  several  weeks,  delirium, 
convulsions,  and  even  at  times  by  death. 

Treatment. — The  treatment  is  entirely  symptomatic,  but  salvarsan  might 
be  tried. 

Prophylaxis. — According  to  Nuttall,  the  Persians  burn  their  villages  when 
they  suffer  severely  from  the  attentions  of  the  tick.  In  order,  however,  to 
devise  a  rational  method  of  prophylaxis,  it  must  be  remembered  that  A .  per- 
sicus is  essentially  a  parasite  of  the  domestic  fowl  and  other  birds,  and  that 
its  eggs  are  laid  in  batches  of  20  to  100  in  cracks  in  the  walls,  and  take  three 
weeks  to  develop  into  the  larva,  which,  after  sucking  blood,  in  eight  days 
becomes  the  nymph.  This  may  require  several  weeks  before  it  becomes  the 
adult,  which  is  said  to  feed  only  once  a  month.  After  considering  this  life- 
history,  it  will  be  obvious  that  fowls  should  be  disinfected  with  a  kerosene 
emulsion,  creozozone,  or  oil  of  sassafras  in  the  case  of  old  birds,  while  young 
birds  may  be  isolated  in  cages  until  the  ticks  drop  off.  Houses  and  fowl- 
houses  should  be  cleansed  and  treated  by  lime  and  corrosive  sublimate,  and 
old  nests  and  roosts  should  be  burnt,  and  after  that  the  new  fowl-houses  may 
be  sprayed  with  kerosene  emulsion. 


THE  RELAPSING  FEVERS  OF  AMERICA  1323 

THE  RELAPSING  FEVERS  OF  AMERICA. 

The  relapsing  fevers  of  America  comprise: — 

1.  North  American  relapsing  fever. 

2.  Central  American  relapsing  fever. 

3.  South  American  relapsing  fever. 

1.  Relapsing  Fever  of  North  America. 

Definition. — An  acute  specific  fever  caused  by  Spiroschaudinnia  ^p^ 
novyi  Schellach,  1907.     Mode  of  infection  not  known. 

History. — Relapsing  feveFTias  been  known  in  America  for  many 
years,  being  recognized  as  far  back  as  1844;  but  it  was  considered 
to  be  identical  with  the  European  type  until,  in  1906,  an  Englishman 
who  repeatedly  travelled  between  New  York  and  the  West  Indies 
was  treated  by  Carlisle  in  New  York  for  fever  which  relapsed,  and 
in  which  spirochetes  were  found.  Novy  and  Knapp  studied  these 
spirochaetes,  and  showed  that  they  were  distinct  from  5.  duttoni. 
Later,  Mackie  also  studied  them  by  the  agglutination  method,  and 
agreed  with  Novy,  who  had  concluded,  from  morphological  reasons, 
that  they  were  distinct  from  5.  carteri.  Finally,  in  1907,  Manteufel 
compared  them  with  true  S.  recurrentis,  and  found  that  the  serum 
of  a  person  suffering  from  their  type  of  fever  did  not  agglutinate 
true  S.  recurrentis.  Subsequently  Schellach,  after  studying  and 
comparing  the  different  spirochaetes,  named  this  particular  species 
S.  novyi  Schellach,  1907. 

Climatology. — The  disease  is  known  in  North__ America  and  in 
Europe.  In  America  the  disease  is  acquired  naturally?  Tn  Europe 
the  cases  recorded  are  due  to  laboratory  infection. 

/Etiology. — The  cause  of  the  disease  is  S.  novyi  Schellach,  1907. 

Symptomatology. — The  symptoms  appear  to  be  much  the  same 
as  in  the  European  type  of  fever.  The  incubation  period  seems  to 
be  at  least  five  to  seven  days  in  durationTThough  cases  have  been 
recorded  in  which  symptoms  developed  almost  immediately  after 
exposure  to  infection.  In  experimental  cases  it  varied  between 
six  and  eight  days.  The  duration  of  the  first  attack  is  about  five_ 
tojsix  days,  and  it  often  begins  with  rigors;  theTongue  is  moist, 
except  in  grave  cases,  and  the  jaundice  is  mild,  except  in  severe 
cases;  but  the  vomiting  of  bile  is  not  uncommon,  while  diarrhoea  is 
only  moderate  in  amount.  Tympanites,  hiccough,  and  haemor- 
rhages from  the  nose,  stomach,  and  bowels,  as  well  as  the  kidney, 
may  be  present  in  severe  cases.  The  apyrexial  interval  is  usually 
seven  to  ten  days,  and  is  followed  by  the  relapse,  which  is  not 
uncommonly  absent.  Usually  there  is  only  one  relapse,  and  more 
rarely  two  to  five  relapses. 

"Mortality.— The  mortality  is  not  high,  varying  between  2  and 
6  per  cent. 

Treatment. — The  treatment  is  the  same  as  in  the  European  type. 


1324  THE  RELAPSING  FEVERS 

2.  Relapsing  Fever  of  Central  America. 

Darling  has  described  cases  of  relapsing  fever  in  Panama, 
clinically  similar  to  the  North  American  type,  bivt  the  organism 
has  not  been  definitely  classified. 

3.  Relapsing  Fever  of  South  America. 

In  South  America  (Colombia)  a  relapsing  fever  occurs  in  which 
the  spiroschaudinnia  resembles  more  closely  S.  dittloni  than  S.  novyi. 
According  to  Robledo,  this  parasite  is  carried  by  Omithodoros 
turicatus. 

REFERENCES. 
European  Relapsing  Fever. 

Birt  (1913).     Journal  of  the  Royal  Army  Medical  Corps,  London. 

Castellani  (1912).     Archiv  fur  Schiffs-  und  Tropen-Hygiene.     Leipzic. 

Castellani  (191 7).  Journal  of  Tropical  Medicine  (Tropical  Diseases  in  the 
Balcanic  War  Zone).     (191 8)   Ann.  Med.  Nav. 

Fehrmann,  E.  (1910).     Archiv  f.  Sch.  u.  Trop. -Hygiene. 

Jancso  (1918).     Centr.  f.  Bakt.,  July. 

Karlinski  (1902).     Centralb.  f.  Bakt.,  xxxi.  566. 

Martini  (1917).      Arch.  f.  Schiffs.  u.  Trop.-Hyg.,  vol.  xxi.,  Nos.  23  and  24. 

Nuttall  (1908).     J.  Parasit.,  i.  2,  143. 

Obermeyer  (1873).     Centralb.  fur  die  Med.  Wissenschaft,  1873,  xi.  145. 

Rabagliati  and  Bulloch  (1905).  Allbutt  and  Rolleston,  System  of  Medi- 
cine, i.  1 167. 

Sandwith  (1905).     Medical  Diseases  of  Egypt,  i.  33. 

Sandwith  (1906).     Journal  of  Infectious  Diseases,  iii.  3. 

Tictin  (1894).     Centralb.  f.  Bakt.,  xv.  840.     Ibid.,  1897,  xxi.  179. 

Wells  and  Perkins  (191 8).     Journ.  Am.  Med.  Assoc,  March  16. 

American  Relapsing  Fevers. 

Carlisle  (1906).     Journal  of  Infectious  Diseases,  iii. 

Darling  (1909).     Archives  of  Internal  Medicine. 

Now  and  Knapp  (1906).     Journal  of  Infectious  Diseases,  iii.  291. 

Robledo  (1909).     Bulletin  de  la  Soci6te  Exotique,  iii.  117. 

Waring  (1918).     Am.  Journ.  Med.  Sci.,  June. 

Asiatic  Relapsing  Fevers. 

Carter  (1882).     Spirillum  Fever.     London. 

Choksy  (1909).     Transactions  Bombay  Medical  Congress. 

Hermant  (1912).     Bulletin  de  la  Societ6  de  Path.  Exotique.     Paris. 

M\ckie  (1907).     Preliminary  Note  on  Bombay  Spirilla  Fever. 

Mouzels  and  Nguykn-Xuan-Mai  (1912).     Bulletin  de  la  Society  de  Path 

Exotique.     Paris. 
Pisani  (1897).     Pathology  of  Relapsing  Fever.     Calcutta. 
Rogers  (1908).     Fevers  of  the  Tropics,  p.  149.     Oxford. 

African  Relapsing  Fevers. 

Breinl  and  Kinghorn  (1906).     An  Experimental  Study  of  the  Parasite  of 

the  African  Tick  Fever.     Memoir  XXL,  Liverpool   School  of  Tropical 

Medicine. 
Button  and  Todd  (1905).     The  Nature  of  Human  Tick  Fever  in  the  Eastern 

Part  of  the   Congo   Free  State.     Memoir   XVII. ,    Liverpool    School   of 

Tropical  Medicine. 


REFERENCES  1325 

Hodges  and  Ross  (1905).     British  Medical  Journal,  vol.  i.     London. 

Koch  (1906).  Iber  Afrikanischen  Rekurrens.  Berlin.  Klin.  Wochen- 
schrift,  7. 

Nabarro  (1904).  Reports  of  the  Royal  Society's  Sleeping  Sickness  Com- 
mission.    No.  6. 

Nuttall  (1909).     Journal  of  the  Royal  Army  Medical  Corps,  xii.  2,  123. 

Ross  and  Milne  (1904).     British  Medical  Journal,  ii.  1453. 

Ross  (1907).  Allbutt  and  Rolleston,  System  of  Medicine,  vol  ii.,  part  i., 
p. 301. 

Werner  (1906).  Zur  Epidemiologic  des  Afrikanischen  Rekurrens.  Arch, 
fur  Schiffs-  u.  Tropen-Hygiene,  xxiv.  776. 

North  African  Relapsing  Fever. 

Balfour  (191 1).     The  Spirochete  of  Egyptian  Relapsing  Fever.     Khartoum 

Reports. 
Bousfield  (1911).     Notes  on  Human  Spirochetosis.     Khartoum  Reports. 
Cummins  (1910).     Journal  of  the  Royal  Army  Medical  Corps,  199.     London. 
Nicolle,  Blaizot  and  Conseil  (1912).     Arch.  Inst.  Pasteur.     Tunis. 
Sergent  and  Foley   (1908-16).     Several  papers   in   Bulletin  de  la    Societe 

Pathologie  Exotique. 
Smith,  G.  A.  (1909).     On  some  Cases  of  Relapsing  Fever  in  Egypt,  and  the 

Question  of  Carriage  by  Domestic  Vermin.     London. 

The  Tick  Fever  of  Miana. 

Duprb  (1809).     Voyage  en  Perse  fait  dans  les  Annees,  1807,  1808,  and  1809. 

Paris. 
Fischer  de  Waldheim  (1823).  Notice  sur  l'Argas  de  Perse  (Mallet  de  Miandh). 

Mem.  Soc.  Imp.  de  Nat.  de  Moscow,  vi.  269. 
Kotzebue   (1819).     Voyage  en  Perse  a  la  Suite  de  l'Ambassade  Russe  en 

1817.     Paris. 
Loundsbury  (1903).     Agricultural  Journal  of  Cape  Town,  ix. 
Nuttall   (1899).     On   the   Role  of   Insects,    Arachnids,   and   Myriapods  as 

Carriers  in  the  Spread  of  Bacterial  and  Parasitic  Diseases  of  Man  and 

Animals.     Johns  Hopkins  Hosp.  Reports,  vol.  viii.,  p.  46. 
Nuttall  (1908).     Ticks.     Cambridge. 
Schlimmer     (1874).     Terminologie    Medico-Pharmaceutique    et     Anthropos 

logique  Francaise-Persane  sur  les  Maladies  Endemiques  et  Particuliere- 

les  plus  interessants  des  Habitants  de  la  Perse.     Teheran. 


CHAPTER  XLIX 
TYPHUS 

Synonyms. — Typhus  exanthematicus,  Synochus  putrida,  Spotted  fever, 
Gaol  fever,  Prison  fever.  Brill's  disease;  French,  Typhus  exanthematique; 
Italian,  Tifo  esantematico,  Tifo  petecchiale;  Spanish,  El  Tarbardillo;  German, 
Exanthematischer  typhus,  Fleckfieber;  Dutch,  Vlekkoorts;  Arabic,  Homma 
typhuisa,  Tkout  fever;  South  Africa,  M'betalala^  black  fever. 

Definition. — Typhus  is  an  acute  specific  fever  of  unknown  but 
probably  protozoal  cause,  spread  by  the  agency  oiPediculus  corporis 
de  Geer,  1778,  and  characterized  by  a  sudden  onset,  a  maculo- 
petechial  eruption,  and  severe  toxaemia,  lasting  some  twelve  to 
fifteen  days,  and  ending  in  a  more  or  less  abrupt  lysis. 

History. — The  early  history  of  typhus  is  wrapped  in  obscurity  by 
reason  of  its  confusion  with  plague;  for  though  Hippocrates  mentions 
the  word  'typhus,'  he  applied  it  to  stuporous  and  delirious  conditions, 
and  does  not  appear  to  have  been  acquainted  with  the  fever  in 
question.  This  confusion  with  plague  continued  until  Fracastorius, 
in  the  sixteenth  century,  called  it  '  petechie,'  and  gave  such  an 
account  as  enabled  them  to  be  separated  from  one  another,  though 
the  nomenclature  at  first  indicated  that  they  were  related,  and  it 
was  not  until  1760  that  the  term  '  typhus  '  was  first  applied  to  the 
disease  by  Boissier  de  Sauvages.  In  an  interesting  historical  paper 
Crawford  has  shown  that  the  only  possible  explanation  of  some  of 
the  old  outbreaks  is  by  means  of  the  louse. 

During  the  eighteenth  and  nineteenth  centuries  typhus  was  well 
known  in  Europe,  but  included  typhoid  and  relapsing  fevers,  from 
the  former  of  which  it  was  distinguished  by  a  long  series  of  researches, 
beginning  with  those  of  Strother,  Gilchrist,  and  Huxham,  in  the 
early  eighteenth  century,  and  ending  with  Still's  classical  work  in 
1837.  while  the  history  of  the  differentiation  from  the  latter  has 
already  been  described  in  the  chapter  on  the  Relapsing  Fevers. 

For  a  long  time  the  disease  passed  unrecognized  in  the  tropics, 
and,  indeed,  in  the,  Lancet  of  1871  it  is  even  debated  as  to  whether  it 
could  exist  in  those  regions;  but  though  it  is  impossible  to  deny 
that  Lyell,  in  his  observations  in  1852,  mistook  relapsing  fever  for  it, 
and  that  Fairweatber  in  1869  was  confusing  it  with  typhoid,  it 
would  appear  as  though  Lyons,  in  1869,  clearly  recognized  the 
disease  as  occurring  in  North-West  India,  where  it  is  now  well  known 
to  be  endemic,  and  it  has  since  been  reported  from  many  parts  of 
the  tropics. 

Brill's  disease  appears  to  be  a  mild  form  of  typhus  fever,  attenu- 

1326 


HISTORY  1327 

ated,  perhaps,  by  environment,  and  improved  sanitation.  He  has 
failed  to  produce  the  disease  in  monkeys. 

It  is  curious  the  way  in  which  different  epidemics  have  been 
reported  as  being  characterized  by  special  features;  thus  the  Serbian 
epidemic  of  1914-15  showed  a  great  tendency  to  gangrene  of  the 
feet,  while  those  in  Silesia  and  Ireland  have  been  associated  with 
bronchial  and  pneumonic  complications. 

Causal  Agent. — The  next  point  in  the  history  is  the  search  for  the 
causal  agent.  In  1908  Yersin  and  Vassal  succeeded  in  communicat- 
ing the  disease  from  man  to  man  by  the  inoculation  of  blood,  but 
failed  to  infect  rats,  guinea-pigs,  or  rabbits. 

In  1909  Nicolle  first  produced  typhus  in  a  monkey  by  injecting 
the  blood  from  a  patient,  thus  showing  that  the  virus  was  present 
in  the  peripheral  blood.  Later  it  was  discovered  that  guinea-pigs 
also  could  be  infected. 

In  19 10  Ricketts  and  Wilder,  in  Mexico,  showed  that  the  virus 
was  contained  in  the  blood  serum,  from  which  it  could  be  removed 
by  filtration  through  a  Berkefeld  candle. 

In  191  r  Wilder  repeated  the  filtration  experiments  with  confirma- 
tory results,  but  subsequent  experiments  showed  that  the  control 
monkey  may  have  been  immune,  a  point  subsequently  confirmed 
by  Nicolle,  Conor,  and  Conseil. 

In  19 1 1  Nicolle,  Conor,  and  Conseil  considered  that  the  virus  was 
mainly  associated  with  the  leucocytes,  and  that  the  plasma  was 
merely  virulent  from  the  debris  of  these  cells.  Red  blood-corpuscles 
and  cerebro-spinal  fluid  were  proved  not  to  contain  the  virus. 

In  1912  Anderson  and  Goldberger  showed  that  the  evidence  was 
in  favour  of  a  parasite  living  freely  in  blood  plasma,  and  not  of  an 
intraleucocytic  localization;  and,  further,  they  confirmed  the  work 
of  Ricketts  and  Wilder. 

In  1917  Miss  Robertson  summarized  these  investigations  b}f  stat- 
ing that  there  is  no  recorded  experiment  which  demonstrates  that 
an  injection  of  the  filtered  serum  from  a  typhus  patient  can  produce 
an  infection.  The  conclusion  is  that  the  virus  is  too  large  to  pass 
through  the  pores  of  a  Berkefeld  candle  in  good  condition.  Further, 
this  virus  is  capable  of  producing  a  reaction  on  the  part  of  the 
patient,  because  after  an  attack  there  is  a  solid  immunity  against 
subsequent  attacks,  both  in  men  and  animals. 

The  causation  of  typhus  remains  undiscovered,  though  many  re- 
searches have  been  made,  first  by  Hallier,  who  in  1868  described  a 
fungus  as  the  causal  agent;  and  then  by  Klebs,  who  found  bacilli 
in  1881;  and  by  Mott  and  Blore,  who  in  the  same  year  described 
minute,  screw-like,  motile  organisms  as  present  in  the  blood  during 
life,  and  micrococcal-like  bodies  found  in  cells  between  the  muscular 
fibres  of  the  heart  after  death. 

In  1891  Hlava  described  ovoid  bodies  which  he  believed  to  be 
part  of  a  streptobacillus;  in  1892  Thoinot  and  Calmette  saw  flagellate 
bodies;  and  in  1892  Lewaschew  found  a  motile  organism,  sometimes 
like  a  thread,  sometimes  oval  and  flagellate;  in  1893  Dubieff  and 


1328  TYPHUS 

Briihl  described  a  diplococcus;  in  1899  Balfour  and  Porter  found 
another  diplococcus.  In  1903  Gottschlich  described  a  Piroplasma 
existing  in  non-motile  endocorpuscular  and  flagellate  free  forms 
in  cases  in  Egypt,  but  these  parasites  may  have  only  been  cellular 
degenerations;  and  Horiachi  described  a  bacillus  which  he  isolated 
from  the  faeces  and  urine  of  Japanese  troops  which  in  the  war  in 
Manchuria  suffered  from  a  disease  which  was  probably  typhus. 
Krompecher,  Goldzieher,  and  Augyan  have  described  intracorpus- 
cular  bodies  somewhat  resembling  a  Piroplasma.  In  1909  Rabino- 
witsch  grew  an  aerobic  coccobacillus;  in  1914  Hort  and  Ingram 
described  a  pleomorphic  bacillus,  and  in  1915  Plotz  a  pleomorphic 
bacillus,  the  so-called  B.  typhi-exanthematici.  In  1916  Penfold, 
and  later  Miss  Robertson,  found  a  blood  diphlococcus.  In  1919 
Borrel,  Cantacuzene,  Jonesco  and  Nasha  have  isolated  a  capsulated 
cocco-bacillus  somewhat  similar  to  one  previously  found  by  Pret- 
jetschsky. 

In  1910  Ricketts  and  Wilder  saw  some  curious  double  bodies  in 
the  blood  of  a  number  of  cases.  In  1913  Hegler  and  Prowazek  saw 
numerous  long,  round,  and  diplococcal  bodies  in  the  leucocytes 
some  time  after  infection  began,  but  not  at  the  commencement 
thereof.  These  bodies  are  believed  to  be  the  same  as  those  described 
in  1905  by  Rabinowitsch  as  '  Turkischen  Reizformen.'  In  addition, 
they  observed  the  forms  described  by  Ricketts  and  Wilder,  not 
merely  in  the  blood,  but  also  in  polymorphonuclear  leucocytes  in 
the  exudate  of  a  blister.  During  convalescence  the  bodies  agglome- 
rate in  the  cells,  and  finally  tend  to  disappear.  Post-mortem 
trachoma-like  bodies  were  found  in  the  endothelial  cells  of  the  heart , 
the  lung,  the  liver,  and  the  kidney.  They  are  found  in  infected 
monkeys,  but  not  in  guinea-pigs.  Infected  lice  were  seen  to  contain 
small  coccoid  and  diplococcal  bodies.  These  bodies  are  believed  to  be 
Chlamydozoa,  and  to  be  allied  to  Lipschutz's  genus  Strongoplasma. 

Prowazek  distinguishes  them  from  Doehle's  bodies.  To  sum- 
marize, these  bodies  appear  in  the  leucocytes  on  the  third  day  of  the 
illness,  and  persist  until  convalescence,  in  one  case  as  late  as  the 
nineteenth  day  of  the  illness.  These  bodies  are  called  Rickettsia 
prowa'ieki  Da  Rocha-Lima,  1916,  and  according  to  this  author  are 
never  found  in  typhus-free  lice,  but  can  be  found  in  lice  infected 
bv  sucking  infected  blood;  then  they  penetrate  into  the  cells  of  the 
alimentary  canal  of  the  louse  on  the  fourth  to  fifth  day  after  an 
infective  feed,  and  multiply  therein,  and  do  not  reach  full  develop- 
ment until  the  eighth  to  ninth  day.  In  this  situation  they  are  very 
small,  shortly  elliptical,  or  oval,  and  often  lie  in  pairs.  Noller  in 
1916  considers  that  the  ^etiological  role  of  this  organism  is  no  longer 
doubtful,  and  in  1917  Foulerton  considered  that  it  was  probably  a 
phase  in  the  evolution  of  the  ^etiological  agent.  In  1919  Arkwright, 
Bacot  and  Duncan  confirm  Da  Rocha-Lima  observations.  Bradford, 
Bashford,  and  Wilson  state  that  they  have  succeeded  in  cultivating 
the  virus,  using  Noguchi's  method,  from  the  blood  of  two  cases. 
The  virus,  according  to  these  authors,  consists  of  minute  coccus-like 


THE  CARRIER  1329 

bodies,  Gram-positive,  grouped  in  pairs,  varying  in  size  from  03  /* 
to  0-5  /x,  capable  of  passing  through  Berkefeld  N  and  V  filters. 

The  Carrier. — With  regard  to  the  spread  of  the  disease,  there  was 
a  great  conflict  of  opinion  as  to  whether  it  was  infectious;  most 
certainly  it  does  not  cross  air-spaces,  though  it  seems  to  be  associated 
with  bedding,  fomites,  furniture,  and  dirt,  which  causes  the 
suspicion  that  the  agent  may  be  an  animal  parasite.  Moreover, 
the  fact  that  it  only  appears  in  the  cool  season  of  the  tropics, 
and  its  rapid  disappearance  in  the  warm  season,  is  also  in  favour 
of  its  transmission  by  some  animal.  Its  non-infectious  nature 
has  been  proved  by  Jiirgens  keeping  twenty  healthy  men  confined 
with  twenty  typhus  patients  freed  from  lice,  with  negative  results ; 
therefore  suspicion  is  aroused  that  it  may  be  spread  by  a  blood- 
sucking parasite,  perhaps  an  insect. 

Patton  has  shown  that  Clinocoris  lectularius  Linnaeus,  1758,  is 
found  along  the  north-west  frontier  of  India;  and  Husband  and 
MacWalters  draw  attention  to  the  fact  that  the  distribution  of  this 
bug  curiously  coincides  with  the  distribution  of  typhus  in  India. 

These  latter  observers  point  out  that  in  an  epidemic  occurring 
in  a  gaol,  the  hospital  was  found  infected  with  bugs,  which  occurred 
nowhere  else.  On  the  destruction  of  these  pests  the  epidemic 
ceased.  Moreover,  they  draw  attention  to  the  fact  that  predisposing 
causes  of  typhus,  such  as  dirt,  overcrowding,  and  the  way  in  which 
the  infection  hangs  about  bedding,  buildings,  and  furniture,  are 
easily  explicable  on  the  bug  hypothesis.  Sambon,  in  his  article  on 
Rocky  Mountain  fever  in  Allbutt  and  Rolleston's  'System,'  advances 
arguments  in  favour  of  the  identity  of  Rocky  Mountain  and  typhus 
fevers;  but  Husband  and  MacWalters'  researches  are  not  in  favour 
of  a  tick  being  the  carrier  of  the  disease.  It  may  be  that  typhus 
and  Rocky  Mountain  fevers  are  caused  by  allied  protozoan  parasites 
spread  by  different  blood-suckers.  In  Glasgow  the  flea  was  sus- 
pected to  be  the  cause  of  the  dissemination  of  the  disease.  Nicolle 
suspected  Pediculus  corporis,  and  this  was  soon  confirmed  on 
epidemiological  grounds,  which  Crawford  supported  by  a  study  of  the 
history  of  the  epidemics. 

In  1909  Nicolle,  Comte,  and  Conseil  transmitted  the  virus  from 
infected  monkeys  to  non-infected  monkeys  by  means  of  the  bites 
of  lice,  Pediculus  corporis  de  Geer,  1778.  In  1910  Ricketts  and 
Wilder  found  that  they  could  immunize  monkeys  against  infection 
with  virulent  blood  by  the  bites  of  infected  lice.  In  1911  Wilder 
showed  that  lice  became  infective  between  the  second  and  fifth  day 
after  feeding,  thus  proving  that  the  causal  agent  had  undergone  some 
sort  of  development  in  the  louse.  In  1912  Anderson  and  Goldberger 
supported  Wilder,  and  concluded  that  P.  humanus  Linnams,  1775, 
andP.  corporis  de  Geer,  1778,  could  both  become  infected,  and  that 
this  infection  could  be  transmitted  by  the  crushed  insects  or  by  their 
bites.  In  19 14  Sergent,  Foley,  and  Vialatte  found  cocco-bacilli  in 
lice,  and  in  the  same  year  Prowazek  and  Rocha-Lima  found  short 
elliptical  coccal  bodies  and  rods.     In  handling  the  infected  lice  both 

84 


1330  TYPHUS 

these  observers  contracted  the  disease,  and  Prowazek  died.  The 
further  investigations  of  Rocha-Lima  have  already  been  noted,  and 
it  only  remains  to  say  that  he  found  that  lice  kept  at  230  C.  did  not 
become  infective,  and  the  organism  did  not  develop,  but  at  320  C. 
the  organism  did  develop,  and  the  lice  became  infective.  These 
results  are  in  direct  contradiction,  as  regards  temperature,  to  those 
of  Nicolle,  Comte,  and  Conseil,  of  Ricketts  and  Wilder,  and  of 
Anderson  and  Goldberger,  and  directly  opposed  to  the  distribution 
of  the  disease.  Da  Rocha-Lima  believes  the  virus  is  passed  on  to 
a  second  generation  of  lice,  of  which  larvse  produced  from  eggs  laid 
by  a  louse  six  days  after  an  infective  feed  are  themselves  infected. 
The  organism  will  develop  in  the  human  and  not  in  the  pig 
louse. 

In  1917  Da  Rocha-Lima  pointed  out  that  Ricketts  and  Wilder, 
Gavino  and  Girard,  and  McCampbell,  have  found  the  parasite  in 
human  blood;  Von  Prowazek  in  leucocytes;  and  himself  in  blood, 
in  smears,  and  in  sections. 

Also  in  1917  Otto  and  Dietrich  obtained  infections  best  by 
allowing  lice  to  feed  on  the  fifth  to  seventh  day  of  the  illness,  as 
only  4-5  per  cent,  became  infected  on  the  twelfth  day,  and  all  are 
negative  after  the  fall  of  the  temperature.  They  infected  lice  from 
a  patient  sine  exanthem,  and  they  confirm  Rickettsia.  On  the 
other  hand,  Brumpt  is  of  opinion  that  this  organism  in  the  louse  has 
nothing  to  do  with  typhus.  Arkwright,  Bacon,  and  Duncan's  recent 
observations  are  in  favour  of  Rickettsia  prowazeki  playing  an  etio- 
logical role.  Futaki's  Spirochceta  exanthematotyphi,  found  in  April, 
1917,  has  been  proved  to  have  nothing  to  do  with  the  disease. 

Serological  Investigations. — In  1916  Nicolle  and  Blaizot  prepared 
an  immune  serum  in  horses  and  asses  by  the  inoculation  of  emulsions 
of  spleen  and  suprarenal  capsules  of  infected  guinea-pigs,  and  tested 
its  curative  power  on  non-immune  guinea-pigs,  in  which  it  prevents 
the  disease  if  inoculated  in  the  stage  of  incubation,  and  stops  the 
fever  at  the  onset  and  during  the  first  and  second  day,  but  later 
its  action  is  doubtful.  They  then  tested  it  upon  nineteen  human 
patients,  when  all  cases  treated  in  the  early  stage  recovered  quickly, 
the  temperature  fell,  the  pulse  and  urine  quickly  improved,  but  the 
nervous  symptoms  required  repeated  inoculation.  It  was  used 
in  maximum  doses  of  10  c.c.  per  diem.  In  cases  in  which  the 
disease  had  been  progressive  for  some  time  the  serum  acted  slowly. 
In  1918  Netley  and  Blaizot  showed  that  the  so-called  Brill's  disease 
in  Paris  is  typhus,  and  that  guinea-pigs  rendered  immune  to  the 
Parisian  typhus  are  immune  to  the  Tunisian  strain. 

Prophylaxis. — Many  observers  (Maitland,  Strong,  Hunter, 
Jackson,  Castellani,  etc.)  have  demonstrated  in  practice  the  vital 
importance  of  louse  destruction  in  the  prophylaxis  of  the  disease. 

Relapsing  Fever. — Since  1739  it  has  been  noticed  that  typhus 
and  relapsing  fever  go  side  by  side  in  an  epidemic.  We  now  know 
that  the  reason  is  because  they  are  both  spread  by  lice. 

Climatology. — Typhus  is  essentially  a  disease  of  temperate  and 


CLIMATOLOGY  1331 

cold  climates,  and  therefore  is  well  known  to  occur  in  Europe  and 
America. 

In  the  tropics  it  principally  appears  in  places  situated  at  high 
altitudes,  or  where  there  are  cool  seasons,  in  which  case  it  disappears 
in  a  most  remarkable  manner  as  soon  as  the  warm  season  sets  in. 

In  Africa  it  is  said  by  Hirsch  to  be  endemic  in  Nubia,  and  has  been 
carefully  studied  in  Egypt  by  Sandwith,  where  he  says  that  it  has 
been  definitely  recognized  since  1836,  and  where  a  few  cases  are 
reported  every  year  in  the  spring  months.  It  is  also  reported 
from  Tripoli,  Tunis,  Algeria,  and  Morocco.  In  Asia  it  appears  to 
occur  only  in  epidemic  form  in  Asia  Minor  and  Syria,  but  is  believed 
to  be  endemic  in  Persia,  and  possibly  also  in  Afghanistan,  because 
it  is  said  to  be  regularly  imported  into  India  by  caravans  from  this 
country.  In  India  an  endemic  area  exists  on  the  west  of  the  Indus, 
stretching  from  Beloochistan  in  the  south  to  Yusufzai,  Hazara,  and 
Kashmir  in  the  north,  and  then  passing  eastwards  along  the  ranges 
of  the  Himalayas,  where  it  is  especially  prevalent  at  Kulu,  and  also 
passing  southwards  into  the  district  of  Rawal  Pindi.  In  Ceylon 
we  have  met  with  a  few  cases  in  European  sailors,  who  have,  however, 
acquired  the  disease  elsewhere.  It  occurs  in  Indo-China ;  in  Northern 
China,  where  it  is  endemic,  becoming  epidemic  every  spring;  and  in 
Japan,  where  it  occurs  yearly  in  the  province  of  Hiogo.  It  does 
not  occur  in  Australasia  or  Oceania.  In  tropical  America  it  is 
endemic  in  Mexico,  rare  in  Central  America,  absent  in  the  West 
Indies,  the  Guianas,  Colombia,  and  Venezuela,  and  is  rare  in  Brazil, 
though  it  is  common  in  Peru  and  Northern  Chili. 

This  climatology  depends  upon  the  louse  and  the  air  temperature 
which  is  best  for  the  parasite  to  develop  therein. 

The  Louse. — As  Pediculus  corporis  belongs  to  man,  it  can  go 
wherever  man  goes,  but  typhus  fever  does  not,  being  absent  in  the 
tropics  during  the  hot  seasons. 

The  Parasite. — The  fact  that  most  observers  believe  that  a  low 
temperature  is  necessary  for  the  development  of  the  virus  in  the 
louse  is  borne  out  by  the  climatology,  being  limited  to  the  cold  and 
temperate  climates,  and  only  appearing  in  tropical  or  subtropical 
climates  during  the  cold  weather  or  in  the  hills. 

In  Mexico  it  is  found  on  the  lofty  plateau,  in  India  in  the  hills,  in 
Egypt  and  Northern  Africa  in  the  cool  season,  and  it  will  be  remem- 
bered that  the  clothes  louse  is  exposed  to  the  effects  of  air  tempera- 
tures. 

Epidemiology. — Epidemics  are  caused  by  anything  which  favours 
the  propagation  of  and  dissemination  of  lice.  The  principal  factors 
which  do  so  are  (1)  massing  together  of  people  of  all  classes; 
(2)  retaining  these  masses  under  conditions  which  render  personal 
cleanliness  and  clean  clothing  difficult  or  impossible.  Such  con- 
ditions are  typically  produced  in  times  of  war  and  famine,  and  exist 
endemically  among  the  poor.  To  these  we  must  add  a  third 
condition,  (3)  an  atmospheric  temperature  not  too  high — i.e.,  a 
Temperate  Zone  temperature.     All  this  has  been  well  exemplified 


1332  TYPHUS 

in  the  Serbian  epidemic  of  1914-15,  when  nearly  one-tenth  of  the 
population  died  from  the  disease. 

^Etiology. — The  causal  agent,  which  is  unknown,  is  spread  by 
means  of  the  louse,  Pediculus  corporis  de  Geer,  1778.  This  insect 
obtains  the  virus  from  the  blood  of  a  case  in  which  it  is  present 
from  the  fifth  to  twelfth  day,  but  in  greatest  abundance  from  the 
fifth  to  seventh  day,  and  from  which  it  is  absent  after  the  fall  of  the 
temperature.  The  louse  requires  some  eight  to  nine  days'  interval 
before  it  becomes  infective.  It  probably  remains  infective  for  the 
rest  of  its  life,  but  it  is  not  certain  whether  it  passes  the  virus  on 
to  the  next  generation  or  not.  When  an  infected  louse  bites  a  non- 
immune human  being,  some  six  to  ten  to  twelve  days  elapse  before 
symptoms  appear.  An  attack  of  typhus  confers  an  immunity 
upon  man  and  susceptible  animals.  Natural  immunity  exists  in 
many  animals. 

With  regard  to  Rickettsia  prowazeki  Da  Rocha-Lima,  1916, 
Brumpt,  in  19 18,  found  that  it  was  present  in  seventy-two  P.  corporis 
removed  from  healthy  persons  who  never  had  had  or  subsequently 
did  have  typhus  fever.  The  bites  of  these  lice  did  not  cause  the 
disease  in  susceptible  animals,  nor  did  they  infect  the  persons  who 
handled  them.  Pediculus  kumanus  has  no  Rickettsia  prowazeki. 
Brumpt's  researches  tend  to  show  that  R.  prowazeki  is  not  the 
causal  agent  of  typhus  fever,  while  the  observations  of  Arkwright, 
Bacot,  and  Duncan  are  favourable  to  Da  Rocha-Lima's  theory. 

Futaki  in  April,  1917,  reported  the  presence  of  a  spirochete 
which  he  named  S.  exanthematotyphi  Futaki,  1917,  in  sections  of 
typhus  kidneys  and  in  the  urine  of  patients,  but  in  1918  Mijashima, 
Kusama,  Takano,  Yabe,  and  Kanai  proved  that  it  was  non-patho- 
genic to  guinea-pigs  and  monkeys  which  are  susceptible  to  the 
typhus  virus.  It  therefore  has  nothing  to  do  with  typhus.  Doehle's 
scarlet  fever  bodies  have  been  found  by  Lopez  Vallejo  in  typhus, 
but  have  nothing  to  do  with  either  disease.  Hort  has  described 
peculiar  coccoid  bodies  in  filtered  blood.  Bradford,  Bashford,  and 
Wilson  state  that  they  have  grown  minute  bodies,  similar  to  those 
they  have  found  in  trench  fever. 

Pathology. — According  to  Zuelzer,  the  liver  and  spleen  begin  to 
increase  in  size  during  the  incubation  period,  and  reach  their  maxi- 
mum size  at  the  commencement  of  the  illness,  while  von  Chiari 
looks  upon  the  congestion  of  the  conjunctiva  as  due  to  the  action 
of  the  virus  on  the  walls  of  the  small  vessels,  causing  perivascular 
infiltration,  which  he  looks  upon  as  a  sign  of  the  roseolar  rash  in 
this  situation. 

The  virus  can  produce  immune  bodies  in  infected  animals.  In 
man  a  second  attack  is  rare,  but  has  been  recorded,  and  relapses  have 
been  known  to  occur. 

The  virus  lives  in  the  blood  from  the  fifth  to  the  twelfth  day,  but 
is  scarce  after  the  seventh  day  and  absent  after  the  fall  of  the 
temperature,  when  it  is  evidently  killed  by  the  immune  substances 
produced  by  the  reaction  of  the  body. 


SYMPTOMATOLOGY 


1333 


Morbid  Anatomy. — Death  is  most  common  about  the  tenth  day, 
being  due  either  to  the  action  of  the  virus  of  the  disease  or  to  com- 
plications such  as  pneumonia  and  septic  infections.  The  spleen 
is  enlarged  and  engorged  if  the  post-mortem  takes  place  up  to  the 
middle  of  the  second  week,  but  not  later.  There  is  oedema  of  the 
lungs  and  hypostatic  pneumonia,  cloudy  swelling  and  fatty  degenera- 
tion of  the  heart,  cloudy  swelling  of  the  liver  and  kidneys,  and 
hyperemia  of  all  the  organs.  The  cerebro-spinal  fluid  may  show 
a  slight  lymphocytosis. 

The  muscles  are  dry  and  the  rectus  abdominalis  may  show 
Zenker's  degeneration.  The  spleen  is  enlarged,  dark  red  in  colour, 
with  juicy  dark  red  pulp,  while  the  kidneys  may  show  punctate 
haemorrhages. 

Symptomatology — Incubation. — This  varies  from  four  to  five 
to  twenty-one  days,  according  to  the  older  views,  but  the  more 
correct  opinion  is  some  four  to  ten  to  twelve  days. 


Fig.  651. — Temperature  Chart  of  Typhus  Fever. 

Prodromal  symptoms  are  often  entirely  absent,  or  consist  of  vague 
feelings  of  fatigue,  giddiness,  and  headache. 

Attack. — The  onset  is  usually  sudden,  being  characterized  by 
frontal  headache;  pains  in  various  parts  of  the  body,  of  which  pain 
in  the  chest,  giving  rise  to  the  suspicion  of  pneumonia,  is  important ; 
rigors;  marked  rise  of  temperature  from  1010  to  1040  F. ;  quick  pulse 
(100  to  120) ;  flushed  face  and  suffused  eyes;  quickened  respirations; 
and  a  sensation  of  great  weakness.  Rarely,  however,  the  onset  is 
slow  and  typhoid-like. 

Course. — The  duration  of  the  symptoms  is  from  fourteen  to 
eighteen  days.  During  the  first  two  or  three  days  the  temperature 
continues  to  rise  at  night,  with  remissions  in  the  morning,  to  a 
maximum  of  about  1040  to  1050  F.  on  the  second  to  fourth  days, 
during  which  time  the  tongue  becomes  dry,  swollen,  and  cracked, 
with  a  thick  brown  deposit  on  the  dorsum,  while  the  tip  and  sides 


i334  TYPHUS 

are  red;  nausea  may  be  experienced,  but  vomiting  is  rare,  and  the 
bowels  are  either  constipated  or  normal. 

The  nervous  system  is  early  affected,  the  patient  being  apathetic, 
drowsy,  with  a  dull  expression.  The  changes  in  the  blood  are  of  the 
utmost  importance,  and  should  be  carefully  studied.  There  is 
sometimes  an  increase  in  the  red  cells,  with  a  corresponding  increase 
in  the  haemoglobin,  and  a  leucocytosis,  which  is  usually  well  marked, 
being  on  an  average  about  24,000  per  cubic  millimetre,  but  varying 
between  the  extremes  of  8,000  and  54,000.  The  differential  leuco- 
cyte count  is  also  of  importance,  for  in  cases  uncomplicated  with 
malaria  or  other  protozoal  infections  the  polymorphonuclear  increase 
is  a  characteristic  feature,  and  may  exceed  90  per  cent.,  while  the 
mononuclears  and  lymphocytes  may  be  reduced,  especially  if  the 
case  is  to  end  fatally,  while  eosinophiles  are  often  entirely  absent — 
a  most  characteristic  feature  in  a  case  in  the  tropics,  where  worm 
infection  is  common.  The  mononuclear  decrease  is,  however,  not  so 
evident  in  cases  about  to  recover,  nor  is  it  present  in  natives  in  the 
tropics,  who,  of  course,  are  liable  to  previous  protozoal  infections, 
and  this  may  lower  the  relative  polynuclear  count  in  these  regions 
to  60  per  cent,  or  less. 

Though  there  is  sometimes  an  increase  in  the  red  and  almost 
always  in  the  white  corpuscles,  the  specific  gravity  is  said  to  be 
lower  than  normal,  which  is  rather  extraordinary,  and  must  indicate, 
if  true,  considerable  alterations  in  the  plasma.  As  the  disease 
progresses  the  rapidity  of  the  pulse  increases,  and  may  reach  140  per 
minute,  and  is  usually  small  and  of  low  tension.  The  blood  pressure, 
according  to  Rizzuti  and  Scordo,  shows  nothing  characteristic. 
The  respirations  are  always  quickened,  and  there  are  generally  signs 
of  pharyngitis,  bronchitis,  or  broncho-pneumonia,  while  delirium  is 
not  uncommon,  especially  at  night. 

The  Rash. — Definite  preliminary  rashes  are  rare,  but  there  is 
often  very  marked  flushing  of  the  face,  neck,  and  upper  part  of  the 
chest,  with  a  cutis  marmorata  or  subcuticular  mottling  of  the  skin 
of  the  lower  part  of  the  chest  and  abdomen.  The  true  rash  appears 
on  fourth  to  fifth  day,  in  the  form  of  roseolar  macules,  like  those 
seen  in  typhoid  fever,  but  often  more  abundant.  They  are  first, 
seen  upon  the  abdomen,  and  later  spread  to  the  chest,  arms,  and  legs 
on  the  two  latter  of  which,  at  all  events  in  recent  epidemics,  they 
are  rare,  although,  according  to  the  older  authors,  they  first  appear 
and  are  most  abundant  in  this  position.  The  roseolar  spots  at  first 
disappear  on  pressure,  and  later  some  of  them  may  slowly  fade 
away,  while  others,  ceasing  to  disappear  on  pressure,  become 
petechiae,  though  it  is  rare  for  them  to  develop  the  dark  blue  appear- 
ance of  the  petechiae  of  such  eruptions  as  those  of  purpura.  This 
petechial  eruption  must  not  be  confused  with  flea-bites,  which  are 
characterized  at  first  by  a  central  haemorrhagic  spot,  which  is 
surrounded  by  a  circular  hyperaemic  zone,  disappearing  on  pressure 
and  fading  in  a  day  or  so  and  leaving  a  perfectly  circular,  dark  red, 
not  raised  petechial  spot  which  does  not  disappear  on  pressure. 


TERMINA  TION—  VA  RIETIES 


1335 


A  petechial  eruption  may  also  appear  somewhat  later,  but  is  often 
wanting,  and  when  widespread  is  an  indication  of  a  bad  prognosis. 
A  miliary  eruption  may  appear  later  in  the  attack,  and  be  followed 
by  a  desquamation.  After  the  appearance  of  the  eruption  the  leuco- 
cytosis  becomes  more  marked,  as  do  the  nervous  symptoms,  the 
patient  suffering  from  severe  delirium,  which  may  become  quite 
violent;  or  he  may  show  a  stuporous  condition,  which  becomes 
a  semi-coma,  and  in  fatal  cases  deepens  into  a  profound  comatose 
condition. 

Termination. — As  a  rule  the  duration  of  the  fever  is  from  fourteen 
to  eighteen  days.  On  or  about  the  fifteenth  day  the  temperature 
generally  falls  by  crisis  or  by  rapid  lysis,  which  may  extend  through 
three  to  five  days,  the  rash  fades,  the  spleen  becomes  normal,  the 
leucocytosis  increases,  and  convalescence  begins. 

In  more  serious  cases  the  toxaemia  may  become  severe  during  the 


Fig.  652. — Temperature  Chart  of  Typhus  Fever. 
(Chart  made  by  Dr.  G.  C.  Shattock.) 

first  week,  and  the  patient  may  die  from  the  seventh  to  tenth  dav 
or  even  earlier. 

Convalescence. — This  may  be  slow,  and  not  rarely  there  is  danger 
during  this  stage,  as  the  general  condition[may  not  improve  with  the 
cessation  of  the  fever,  and  death  may  ensue  some  two  to  three 
weeks  after  defervescence.  In  such  cases  the  pulse  does  not 
improve,  and  the  patient  becomes  weaker  and  weaker  until  he  dies. 
These  are  very  trying  cases  for  the  medical  practitioner.  Myocarditis 
may  develop  during  this  stage,  and  shows  a  weak  irregular  pulse. 

Varieties. — The  varieties  which  may  be  mentioned  are: 
(1)  Mild  or  ambulatory  cases.  (2)  Abortive  attacks.  (3)  Malignant 
attacks,  causing  death  on  the  second  or  third  day.  (4)  Typhus  sine 
exanthem — i.e.,  typhus  without  the  rash.  (5)  Typhus  in  children. 
This  is  usually  mild,  and  it  is  said  that  death  in  uncomplicated 
cases  properly  looked  after  is  rare.     Moreover,  these  cases  are  im- 


1336  TYPHUS 

portant  because  they  are  apt  to  be  missed.  Rigors  are  rare,  and 
often  the  temperature  rises  by  steps,  while  the  fever  lasts  only  some 
nine  to  thirteen  days.  Bronchitis  is  frequent.  The  spleen  is 
constantly  enlarged,  but  the  rash  is  generally  scanty.  Insomnia 
is  not  frequent,  but  high  temperatures  often  occur.  Children  remain 
throughout  the  illness  in  a  condition  of  semi-stupor,  and  waste  in  a 
remarkable  manner.  (6)  Typhus  with  an  extensive  exanthem  all  over 
the  body  and  into  the  mouth,  with  or  without  patches  of  gangrene. 

Complications  and  Sequelae. — Mixed  infections  with  relapsing  fever, 
malaria,  pneumonia,  typhoid,  and  acute  miliary  tuberculosis  occur. 
Complications  are: — Parotitis,  ending  often  in  suppuration,  gangrene 
of  the  feet,  and  polyarthritis,  neuritis,  hemiplegia,  severe  mental 
depression,  amounting  almost  to  melancholia  (seen  during  convales- 
cence) may  be  mentioned.  Also  bubonic  swellings,  venous  throm- 
bosis, diarrhoea,  otitis  media,  abscesses,  and  boils  occur,  while 
jaundice,  endocarditis,  and  meningitis  are  rare,  but  myocarditis 
is  fairly  common. 

Diagnosis. — This  may  be  most  difficult,  especially  in  children. 
The  cardinal  points  in  the  diagnosis  are: — 

(a)  Incipient  Typhus. — (i)  The  sudden  onset,  with  sometimes 
headache,  rigors,  and  vomiting.  (2)  The  congested  eyes  and  face, 
and  the  subcuticular  mottling  of  the  skin  over  the  chest.  (3)  The 
mental  confusion  and  stupor,  associated  with  the  log-like  attitude 
of  the  whole  body.     (4)  The  leucocytosis. 

(b)  Fully  Developed  Typhus. — (1)  The  typical  rash.  (2)  The 
leucocytosis.     (3)  The  history  of  the  sudden  onset,  etc. 

Remarks  on  the  Diagnosis. — Leucocytosis  averages  24,000  per 
c.mm.,  and  is  present  in  proportion  to  the  gravity  of  the  illness; 
it  is  therefore  of  double  value,  diagnostic  and  prognostic.  It 
persists  through  the  fever^and  declines  after  the  return  of  the  tem- 
perature to  normal,  and  reaches  the  usual  count  on  or  about  the 
twelfth  day  after  defervescence. 

The  differential  count  shows  polymorphonuclear  leucocytes 
65-78  per  cent. ,  lymphocytes  23-34  per  cent.,  mononuclear  leucocytes 
7-14  per  cent.  Eosinophile  leucocytes  are  rarely  met  with,  but  in 
rare  cases  may  reach  to  2-6  per  cent. 

Weil-Felix  Reaction. — From  the  blood  of  patients  suffering  from 
typhus  Weil  and  -Felix  isolated  a  bacillus,  which  they  grew  on 
agar  and  called  X10,  0.  This  was  completely  agglutinated  by  the 
serum  of  typhus  parents. 

For  the  reaction  the  organisms  must  be  grown  on  neutral  agar 
slants,  and  must  be  alive.  Cultures  of  two  to  three  days'  growth 
are  best.  The  reaction  is  said  to  be  positive  on  the  sixth  day  of  the 
illness,  and  to  be  useful  in  retrospective  diagnosis.  Some  observers 
believe  that  the  reaction  is  due  to  a  mixture  of  the  true  virus  with 
B.  proteus,  but  others  consider  it  to  be  of  the  nature  of  a  par  agglu- 
tination. The  organism  X:9  belongs  to  the  Bacillus  proteus  group 
of  organisms.  It  is  not  suggested  that  the  organism  has  any  causal 
effect  in  the  production  of  typhus  fever.  It  may  give  complement 
deviation  when  used  as  an  antigen  with  typhus  serum,  whichTis 


DIAGNOSIS  1337 

negative  to  Wassermann's  reaction.  A  modification  of  the  Weil- 
Felix  reaction  with  killed  X,9  is  called  '  Neuber's  diagnosticum.' 
It  is  praised  by  some  and  condemned  by  others. 

The  differential  diagnosis  has  to  be  made  from  pappataci  fever, 
dengue  fever,  relapsing  fever,  malaria,  '  enteroidea '  fevers,  rat- 
bite  fever,  cerebro-spinal  meningitis,  pneumonia,  septicaemias  or 
pyaemias,  and  uraemia. 

From  pappataci  fever  it  can  only  be  recognized  at  its  commence- 
ment by  the  presence  of  leucocytosis  and  the  absence  of  leucopenia, 
and  the  same  holds  good  for  dengue  fever. 

From  relapsing  fever  it  may  be  diagnosed  by  a  blood  examination 
showing  the  absence  of  spirochaetes  and  the  presence  of  leuco- 
cytosis, as  well  as  by  the  clinical  symptoms,  but  especially  the 
mental  disturbance. 

From  malaria  it  can  only  be  separated  by  the  absence  of  the 
malarial  parasites,  which  may  be  present  in  double  infections,  and 
by  the  leucocytosis. 

From  '  enteroidea  '  fevers  it  may  be  distinguished  by  the  often 
abrupt  onset,  by  the  leucocytosis,  and  by  the  absence  of  the 
specific  '  enteroidea  '  organisms  in  the  blood  and  faeces. 

From  rat-bite  fever  it  may  be  known  by  the  absence  of  the  mark 
of  a  rat -bite,  absence  of  the  enlarged  lymphatic  glands,  and  of  the 
spirochaetes  in  the  blood. 

From  cerebrospinal  meningitis  it  may  be  told  by  the  clear  cerebro- 
spinal fluid  containing  no  meningococci,  and  by  the  absence  of  stiff- 
ness of  the  neck,  Kernig's  sign,  and  the  presence  of  the  typical  rash. 

From  pneumonia  it  may  be  parted  by  the  absence  of  definite 
apical  or  basal  dulness,  of  the  bronchial  respiration,  as  well  as  by 
the  character  of  the  sputum,  with  absence  of  blood. 

From  septicemias  and  pycemias  by  blood  cultures  showing  an 
absence  of  pyogenic  organisms,  by  the  absence  of  blood  destruction, 
and  by  the  presence  of  cerebral  symptoms.  From  septicemic 
plague  it  can  be  distinguished  by  the  course  and  blood  cultures. 

From  uremia  it  is  known  by  the  presence  of  fever  and  by  the 
analysis  of  urine. 

From  'flea-bites  '  the  diagnosis,  of  course,  has  only  to  be  made 
in  cases  of  fever,  and  can  be  done  by  the  history,  the  patient  often 
stating  that  the  rash  was  in  existence  a  long  time  before  the  fever. 
The  distribution  is  on  the  limbs  equally  to  the  body.  The  rash  is 
composed  of  a  number  of  petechial  spots  of  a  dark  red  colour  and 
perfectly  circular  in  outline  (see  p.  1334). 

From  smallpox,  by  absence  of  the  fall  in  the  temperature  on  the 
fourth  day,  absence  of  shotty  papules  appearing  on  the  face  on 
the  fourth  day;  but  the  diagnosis  in  times  of  contemporaneous 
epidemics  may  be  almost  impossible.  When  in  doubt  and  before 
the  specific  rash  appears  the  presence  of  well-marked  vaccination 
marks  are  in  favour  of  typhus. 

From  influenza,  by  the  absence  of  the  catarrhal  symptoms. 

From  plague,  by  the  absence  of  the  buboes  and  the  plague  bacilli 
therein. 


1338  TYPHUS 

To  facilitate  the  diagnosis  in  cases  of  typhus  with  a  faint  rash  Dietsch 
recommends  applying  a  rubber  band  round  the  arm.  This  procedure  makes 
the  rash  below  the  point  of  application  more  visible,  and  may  cause  forma- 
tion of  petechise. 

Prognosis. — The  case-mortality  is  variously  stated  as  being  from 
10  to  50  per  cent.  The  signs  indicative  of  serious  trouble  and  grave 
prognosis  are  the  absence  of  eosinophiles  in  the  blood,  decrease  in 
the  number  of  the  mononuclears,  slow  pulse,  severe  petechial  erup- 
tion or  nervous  symptoms,  alcoholism,  pulmonary  complaints, 
meteorism,  gangrene,  and  cyanosis  of  the  face. 

The  signs  indicative  of  a  hopeful  prognosis  are  an  increase  in  the 
eosinophiles  and  mononuclears,  the  absence  of  the  petechial  erup- 
tion and  slight  nerve  symptoms. 

Mortality  is  low  in  the  young  and  extremely  fatal  in  the  old; 
it  is  slightly  more  fatal  in  males  than  in  females,  while  alcoholism, 
kidney  disease,  are  bad  prognostic  elements,  as  is  a  fat  or  very- 
muscular  subject.  Pregnant  women  generally  abort,  and  this 
complicates  the  chance  of  recovery.  Complications  are  generally 
serious  in  regard  to  prognosis. 

Treatment. — The  patient  should  be  placed  in  an  airy,  well-lighted 
room,  sparsely  furnished,  and  placed  upon  a  diet  of  milk,  broths, 
jellies,  etc.,  while  plenty  of  water  is  allowed  to  be  drunk.  Careful 
attention  and  nursing  are  required,  especially  when  delirious 
The  temperature  should  be  controlled  by  cool  sponging,  and  the 
nervous  symptoms  by  ice  to  the  head,  hyoscin,  bromides,  or  mor- 
phine, while  the  heart  is  supported  by  hypodermic  injections  of 
strychnine,  digitalin,  etc.  Nicolle  finds  that  the  serum  of  convales- 
cent cases  for  ten  to  twelve  days  after  the  temperature  has  fallen 
to  normal  has  prophylactic  and  curative  properties  when  given  in 
doses  of  20  c.c,  repeated  if  necessary,  and  has  manufactured  a 
special  horse  serum  for  this  purpose.  He  suggests  that  in  grave 
cases  it  should  be  given  intravenously.  Salvarsan  and  neosalvarsan 
have  been  tried  without  any  great  success. 

Prophylaxis. — This  is  summarized  in  one  word,  '  lousing,'  in  which 
we  include  the  destruction  of  lice  on  the  person  and  on  the  clothes. 

The  procedure  is  sufficiently  simple:  the  person  goes  into  a  room, 
takes  off  the  clothes,  which  are  steamed  or  boiled,  passes  into 
another  room,  and  is  sprayed  with  kerosene  oil  or  petrol,  passes 
into  a  third  room,  and  receives  clean  or  sterilized  clothes. 

The  sterilization  of  the  clothes  may  be  conducted  by  boiling, 
but  better  still  by  making  them  into  lightly  packed  bundles  and 
placing  them  into  a  truck  or  room  into  which  steam  is  blown.  This 
is  easiest  done  in  a  truck,  the  steam  being  brought  from  the  engine. 

A  campaign  against  lice  may  be  conducted  on  the  following  lines : — 
A.  Methods  applied  to  Man: — 

I.  Give  illustrated  lectures,  so  that  people  may  understand  about 
the  louse,  its  habits,  its  association  with  disease,   and  its 
prevention. 
II.  Advocate  the  use  of  soap  and  water  and  of  the  frequent  bath, 
as  well  as  of  clean  linen  frequently  changed. 


PROPHYLAXIS  1339 

B.  Methods  applied  to  the  louse  : — 

I.  Pedulicides  : — 

(a)  Dry  Heat. — Lice  and  nits  can  be  killed  by  exposing  them  for 

fifteen  minutes  at  6o°  to  650  C. 
{b)  Moist  Heat. — Lice  and    nits  are   killed   instantaneously  by 
moist  heat  at  or  over  8o°  C. 
This  is  the  method  most  used  for  clothing,  which  may  be 
boiled  or  exposed  to  steam,  but  must  not  be  in  tightly 
rolled  bundles. 

C.  Chemicals  : — 

For  Use  on  the  Person. — Kerosene  oil  or  petrol  spray  or  vaseline,  or 

cresol  soap. 
For  Use  on  Stored  Clothing. — Naphthalene. 
II.  Lice  Repellents: — 

Better-class    patients:' — Dusting   powder    of    menthol    3-5 

grains,  zinc  oxide  1  ounce. 
Poorer-class  patients : — Naphthalene  as  a  dusting  powder. 

III.  Special  Points  : — 

Head  Lice. — Shave  the  head  or  cut  the  hair  very  short,  or 
wash  the  hair  thoroughly  with  1  in  40  carbolic  acid  lotion, 
which  is  left  to  act  for  an  hour,  the  head  being  wrapped 
up  in  a  towel  in  the  form  of  a  turban.  Then  wash  the 
head  with  soap  and  water  and  apply  a  dressing  to  any 
raw  areas,  carbolic  vaseline  (2  per  cent.)  or  white  precipi- 
tate ointment  may  also  be  used  to  destroy  head  lice. 
Body  Lice. — The  following  drugs  arranged  in  order  of  effici- 
ency (according to  Castellani  and  Jackson)  may  be  used: — 

1.  Petrol  and  kerosene  oil. 

2.  Plain  vaseline. 

3.  Guaiacol. 

4.  Anise  preparations. 

5.  Iodoform. 

6.  Lysol,  cyllin,  etc. 

7.  Carbolic  acid,  5  per  cent. 

8.  Naphthalene. 

9.  Camphor. 
IV.  General  Insecticides  : — 

The  experiments  of  Castellani  and  Jackson  in  Serbia  have 
demonstrated  that  pyrethrum  is  a  very  feeble  pediculi- 
cide,  while  sulphur,  boric  acid,  perchloride  of  mercury, 
when  used  in  powder,  have  no  action  whatever. 

Substances  which  may  be  efficient  pediculicides  may,  how- 
ever, have  little  or  no  action  upon  other  insect  parasites 
of  man,  such  as  bugs  and  fleas.  For  example,  iodoform 
will  kill  lice  in  ten  to  fifteen  minutes,  but  has  no  action 
on  bugs  and  little  on  fleas.  Pyrethrum  acts  more  power- 
fully upon  bugs  than  upon  lice.  In  order  to  formulate 
a  general  insecticide  several  chemical  substances  must 
be  combined.  As  an  example  of  a  general  insecticide 
for  use  against  lice,  bed  bugs,  and  fleas,  the  following  is 
given: — 

Equal  proportions  of  naphthalene,  previously  soaked  in 
guaiacol  or  creosote,  pyrethrum,  zinc  oxide. 

The  wearing  of  undergarments  made  liceproof  by  soaking  in 
various  disinfectants  (crude  carbolic  acid  and  soft  soap 
emulsion),  as  recommended  especially  by  Bacot,  is  useful. 
Legroux's '  sachets  '  or  small  bags  containing  naphthalene 
treated  with  citronella'oil  may  be  used. 


1340  TYPHUS 


REFERENCES. 

The  literature  of  modern  date  is  very  large.     The  reader  should  consult 
Tropical  Diseases  Bulletin,  vols,  x.,  xi.,  and  xii. 

Arkwright,  Bacot,  and  Duncan  (1919).     Trans.  Soc.  Trop.  Med. 

Birt  (1912).     Journ.  Royal  Army  Medical  Corps. 

Borrel,  Cantactjzene,  Jonesco  and  Nasha  (1919).     C.  R.  Soc.  Biol. 

Bradford,  Bashford  and  Wilson  (191 9).     Brit.  Med.  Journ.,  February  1. 

Castellani   (1917).     Journal  of  Tropical  Medicine  and  Hygiene,   July  16, 

August   1   and    15,   September  1    and  15,   October  1      (Diseases  in  the 

Balcanic  and  Adriatic  Zones).     With  Jackson  (1916).     Ibid. 
Craig  and  Fairley  (1918).     Lancet,  September  21. 
Futaki  (1917).     British  Medical  Journal,  October  13. 
Jaff£  (1918).     Med.  Klinik,  vol.  xiv.,  No.  9. 
Jorge  (1918).     Med.  Contemporanea,  No.  9. 

Krompecher,  Goldzieher,  and  Augvan  (1909).     Centralblatt  f.  Bak. 
Maitland  (1915).     Brit.  Med.  Journ. 
Martini    (1918).     Deutsche  Medicinische  Wochenschrift,    February    7  (Das 

Fleckneber  der  Kinder) . 
Nicolle  (1912).   Bull.  Path.  Exot.    Paris.    With  Comte  and  Conseil  (1909 

and   1910).     Comptes  Rendus  de   l'Acad6mie  des    Sciences,  cxlix.  486. 

Conseil.    Ibid. ,cli.  454  and  598.     Consor  and  Conseil  (191 1).     Annales 

de  lTnstitut  Pasteur,  xxv.  13. 
Nuttall    (1919).      Parasitology,  February.     (1918)  Parasitology,  x.  4,  413. 

(1917)  Ibid.,  x.  1,  43.     (Important  papers.) 
Plotz  (19 1 9).     Journ.  Am.  Med.  Ass.,  February  1. 
Rizzuti  and  Scordo  (1912).    Malaria. 
Robertson  (191 7).     Proceedings  of  the  Royal  Society  of  Medicine,  x.     Section 

Epidemiology,  95-110  (iEtiology  of  Typhus). 
Sandwith  (1907).     Medical  Diseases  of  Egypt,  i.  15. 
Sergent,  Foley,  and  Vialatte  (1914).    Comptes  Rendus  Societe  de  Biologie, 

Ixxvii.  101. 
Simpson  (1918).     Trans.  Soc.  Trop.  Med. 

Soubbotitch  (1918).     Proceedings  of  the  Royal  Society  Medicine,  xl.  (Epi- 
demiology), 31-37  (Serbian  Epidemic). 
Strong  (1915).     Am.  Red  Cross  Scientific  Reports. 
Yersin  and  Vassal  (1908).     Bulletin  de  la  Society  de  Path.  Exot.,  i.  156. 


CHAPTER  L 

THE  SPOTTED  FEVER  OF  THE  ROCKY 
MOUNTAINS 

Synonyms — Definition — History — Climatology — /Etiology — Morbid  anatomy 
— Symptomatology — Diagnosis — Prognosis — Treatment — Prophylaxis — 
The  intermittent  tick  fever  of  Wyoming — References. 

SPOTTED  FEVER  OF  THE  ROCKY  MOUNTAINS. 

Synonyms. — Black  fever.  Blue  disease.  Rocky  Mountain  spotted  fever. 
Spotted  fever  of  Montana,  Rocky  Mountain  fever,  Piroplasmosis  hominis. 
Spotted  fever  of  Idaho,  Tick  fever  of  the  Rocky  Mountains. 

Definition.— An  acute  endemic  febrile  disorder,  associated  with 
a  petechial  or  purpuric  eruption  of  the  skin,  which  occurs  after  the 
bites  of  infected  ticks,  Dermacentor  andersoni  Stiles,  1905  (which 
is  the  same  as  D.  venustus  Banks,  1908),  and  probably  other  ticks — 
e.g.,  D.molestus  and  D.  maturatus — in  certain  regions  of  the  Rocky 
Mountains. 

History. — The  first  case  of  the  disease  is  believed  to  have 
occurred  in  Bitter  Root  Valley,  in  1873,  and  from  that  date  until 
1902  it  is  said  that  about  200  cases  were  observed,  with  a  mor- 
tality of  70  to  80  per  cent.  During  this  period  it  was  generally 
known  as  the  '  black  fever,'  the  '  blue  disease,'  or  the  '  spotted 
fever.' 

In  1898,  according  to  Anderson,  Major  M.  W.  Wood  made  an 
unpublished  report  on  the  disease  to  the  Surgeon-General  of  the 
United  States  Army.  In  1899  Maxy  wrote  a  paper  on  '  The  So- 
called  Spotted  Fever  of  Idaho,'  which  he  described  as  an  acute, 
endemic,  non-contagious,  but  probably  infectious  febrile  disorder, 
characterized  clinically  by  a  continuous,  moderately  high  fever, 
severe  arthritic  and  muscular  pains,  and  a  profuse  petechial  or 
purpuric  eruption  of  the  skin,  appearing  first  on  the  ankles,  wrists, 
and  forehead,  but  rapidly  spreading  to  all  parts  of  the  body.  In 
1902  Gwim  and  McCullough  read  separate  papers  on  the  disease 
at  a  meeting  of  the  Montana  State  Medical  Association,  and  in  the 
same  year  Wilson  and  Chowning  were  deputed  to  investigate  it  in 
the  Bitter  Root  Valley.  As  a  result  of  their  investigation,  they 
concluded  that  it  was  caused  by  a  Piroplasma.  They  believed  this 
Piroplasma  to  be  parasitic  in  a  squirrel  (Spermophilis  columbianus) , 
and  to  be  spread  to  human  beings  by  a  tick,  Dermacentor  reticulatus 

1341 


1342  SPOTTED  FEVER  OF  THE  ROCKY  MOUNTAINS 

(  =  D.  andersoni  =  D.  venustus  Banks  nee  Marx).  In  1903  Anderson 
was  instructed  to  investigate  the  disease,  and  as  a  result  of  his 
inquiries  he  supported  Wilson  and  Chowning  as  regards  both  the 
parasite  and  the  tick.  In  1905  Stiles  published  his  zoological 
investigation  into  the  cause,  transmission,  and  source  of  Rocky 
Mountain  spotted  fever,  in  which  he  failed  to  find  evidence  of  the 
existence  of  the  parasite  in  man  or  squirrel,  and  of  the  transmission 
by  the  tick.  His  researches  were  supported  in  the  same  year  by 
Ashburn.  In  1906  King  found  distinct  experimental  evidence  of 
the  transmission  of  the  disease  by  the  tick.  From  1906  until  his 
recent  death  Ricketts  has  been  working  at  the  aetiology  of  the 
malady,  and  has  proved  that  the  tick  D.  andersoni  spreads  the 
disease — a  conclusion  which  he  has  supported  by  experiments  on 
guinea-pigs  and  monkeys;  but  he  says  that  the  credit  for  proving 
the  transmission  of  the  disease  from  man  to  man  by  the  tick  must 
be  given  to  McCalla  and  Brereton.  In  1908  Ashburn  and  Craig 
published  an  excellent  paper  on  this  and  the  tsutsugamushi  disease, 
which  they  indicate  to  be  distinct  from  one  another,  and  in  this 
paper  Ashburn  accepts  the  transmission  by  the  tick.  Ricketts 
in  1909  found  that  there  were  really  two  different  ticks  implicated 
in  the  spread  of  the  disease,  and  these  were  recognized  as  D. 
venustus  Banks,  1908  =D.  andersoni  Stiles  =  Z).  venustus  Marx,  1897, 
pro  parte,  and  D.  modest  us  Banks,  of  which  we  have  been  unable 
to  find  a  description.  It  is  obvious  that  there  is  great  confusion 
as  to  the  correct  nomenclature  of  the  ticks  causing  this  fever.  We 
follow  Stiles,  and  call  the  best-known  tick  D.  andersoni. 

Climatology. — The  disease  is  only  known  in  the  United  States, 
in  Washington  State,  Oregon,  Montana,  Idaho,  Nevada,  Wyoming, 
Utah,  and  Colorado.  It  has  not  been  reported  from  New  Mexico, 
as  far  as  we  know,  but  the  causal  tick  is  found  there  and  the  fever 
probably  exists  therein.  In  Montana  it  is  found  in  the  Bitter  Root 
Valley,  on  the  eastern  slopes  of  the  Bitter  Root  Mountains,  and 
from  there  to  the  western  bank  of  the  Bitter  Root  River,  by  which 
it  is  apparently  bounded,  the  worst  area  being  from  Lo-lo  to  Como, 
a  distance  of  about  fifty  miles  in  length,  but  only  about  four  to  five 
miles  in  breadth.  This  country  has  a  considerable  snowfall,  which, 
though  it  begins  to  melt  in  March,  lies  on  the  mountains  until  mid- 
June.  The  melted  snow  drains  into  the  river,  which  does  not  reach 
low-water  until  July.  It  is  only  during  this  period  that  the  ticks 
(D.  andersoni)  appear  in  large  numbers,  and  infest  men  and  animals 
who  pass  through  the  forests,  thickets,  and  uncultivated  regions. 
The  disease  is  also  known  at  Rock  Creek,  20  miles,  and  at  Bridger, 
200  miles,  east  of  the  Bitter  Root  River.  In  Idaho  it  occurs  through- 
out the  entire  valley  of  the  Snake  River,  including  its  tributaries, 
and  the  foot-hills  in  the  neighbourhood.  In  Wyoming  it  is  found  at 
Cody  and  Meeteeste.  In  Nevada  it  is  only  known  in  the  north, 
in  the  valley  of  the  Quinn  River,  where  it  was  recognized  as  far 
back  as  1887.  In  Oregon  it  is  said  to  be  mild,  and  to  be  found 
only  in  the  eastern  portion,  towards  Idaho. 


CLIMATOLOGY— ETIOLOGY  1343 

In  1915  it  was  noticed  at  Ismay  and  Fallow  in  Montana,  which 
was  an  extension  of  its  distribution.     Possibly  it  occurs  in  Alaska. 

It  will  be  noted  that  these  districts  extend  from  400  to  470  N. 
latitude,  and  that  the  elevation  is  about  3,000  to  4,000  feet  above 
sea-level,  and  are  sharply  defined  regions  in  valleys  or  at  the  foot 
of  hills. 

Wilson  and  Chowning  noted  that  the  cases  occur  from  March  to 
July,  as  is  shown  by  the  following  list,  taken  from  their  report : — 


March 

April 

May.. 

June 

July 

Spring  (exact  month  not  known) 


6 

24 
46 

35 

5 

10 


Total  .  .  .  .    126  cases. 

This  seasonal  occurrence  is  associated,  as  stated  above,  with  the 
prevalence  of  D.  andersoni  during  the  same  months.  There  is  a 
growing  suspicion  that  there  is  a  difference  between  the  Montana 
and  the  Idaho  strains  of  infection. 

/Etiology. — According  to  Wilson,  Chowning,  and  Anderson,  the 
cause  of  the  disease  is  a  Piro plasma,  but  Stiles,  Ashburn;  and 
Ricketts  have  failed  to  find  this  parasite.  Stiles,  Ashburn,  and 
Craig  seem  to  have  thought  that  the  disease  was  due  to  a 
trypanosome.  If  so,  this  has  not  been  confirmed.  The  bacterial 
growths  so  far  obtained  from  cultures  of  internal  organs  or  of  the 
blood  can  be  considered  as  merely  accidental  contaminations. 

Ricketts  has  shown  that  blood  taken  from  a  human  being  suffer- 
ing from  the  disease  can  be  inoculated  successfully  into  guinea-pigs 
and  monkeys  (Macacus  rhesus),  and  that  the  transmission  from 
animal  to  animal  can  go  on  apparently  indefinitely  (100  generations) . 
These  inoculations  produce  a  disease  characterized  by  an  incubation, 
a  fever,  an  eruption,  and  post-mortem  appearances  similar  to  those 
found  in  human  cases.  No  bacteria  can  be  cultivated  from  the 
internal  organs  or  blood  of  the  infected  animals,  but  the  virus  exists 
not  merely  in  the  serum,  but  so  closely  attached  to  the  corpuscles 
(white  and  red)  that  it  cannot  be  separated  from  them  by  washing; 
moreover,  it  will  not  pass  through  the  pores  of  a  Berkefeld  filter. 
Immunity  follows  an  attack,  and  hyperimmunity  can  be  induced 
in  guinea-pigs. 

Fricks  by  centrifuging  infected  serum  for  four  to  six  hours  at 
2,000  revolutions  per  minute  separated  a  virulent  deposit,  in  which 
he  found  in  the  serum  bright  red  granular  and  light  blue  bodies 
when  stained  by  Giemsa  and  in  the  corpuscles  elongated  chromatinic 
bodies.  He  hesitates  to  draw  any  conclusion  concerning  these 
bodies,  but  thinks  that  the  virus  multiplies  in  his  cultures.  Wolbach 
finds  diplo-bacillary-like  bodies,  resembling  those  found  by  Ricketts, 
in  large  numbers  in  endothelial  cells  in  and  around  vessels  and 
lymphatics,  and  in  the  muscle  cells  of  vessels.    He  thinks  that  these 


i344  SPOTTED  FEVER  OF  THE  ROCKY -MOUNTAINS 

organisms  may  possibly  be  allied  to  spirochetes.     He  has  been 
unable  to  cultivate  them. 


Fig.  654:  Female. 
Figs.  653  and  654. — Dermacentor  andersoni  Stiles,  1905. 

The  virus  can  be  acquired  and  transmitted  by  the  larva,  the 
nvmph,  and  the  male  or  female  adults  of  Dennatocentor  andersoni, 


&TIOLOGY  i345 

and  in  a  few  instances  can  pass  through  the  eggs  into  a  second 
generation  of  ticks.  According  to  Ricketts,  the  Idaho  disease  is 
spread  by  Dermatocentor  modesties,  and  the  Montana  by  D.  venustus 
Banks,  1908,  nee  Marx,  1897  (  =  £>.  andersoni  Stiles,  1905).  He  is 
inclined  to  think  that  there  is  a  difference  between  the  two  forms 
of  fever,  especially  as  the  former  has  a  death-rate  of  some  5  per 
cent,  and  the  latter  of  about  90  per  cent. 

Infected  ticks  are  found  but  sparingly  in  Nature.  Thus,  of 
513  ticks  found  on  animals,  296  or  more  were  allowed  to  attack 
guinea-pigs,  with  the  result  that  only  one  of  the  animals  took  the 
disease  after  an  incubation  of  seven  days.  The  infected  guinea- 
pig  was  found  to  have  thirty-six  male  ticks  upon  it,  all  of  which 
had  come  from  a  horse. 

A  tick  fed  on  a  human  being  suffering  from  the  disease  com- 
municated it  first  to  a  man  and  afterwards  to  a  woman  by  its 
bites.  Ricketts,  examining  the  blood  of  patients  and  the  eggs  of 
infected  ticks,  has  observed  peculiar  bacillary-like  structures, 
which  show  bi-polar  staining.  He  has  not  succeeded  in  cultivating 
the  germ.  Wolbach  in  1916  and  1918  has  confirmed  Ricketts' 
observations.  Arkwright,  Bacot  and  Duncan  consider  the  Rickett- 
sia bodies  found  in  Rocky  Mountain  Fever  to  be  slightly  larger  and 
usually  longer  and  more  lancet-shaped  than  those  observed  in  typhus 
and  trench  fever.  Michie  and  Parsons  have  no  doubt  that  the 
infective  agent  is  in  the  salivary  glands  of  the  tick.  Transmission  to 
a  tick  requires  twenty-four  hours,  and  infection  of  a  guinea-pig  one 
hour  and  forty-five  minutes  at  least.  The  tick  is  the  natural 
reservoir  of  the  parasite  of  the  disease,  and  lives  upon  domestic 
animals,  horses,  and  cattle,  as  well  as  upon  six  varieties  of  wild 
rodents,  including  Citellus  Columbian  us  and  Marmot  a  flaviventes,  and 
the  jack-rabbit ;  but  according  to  Fricks  sheep  are  unsuitable  as  hosts, 
but  this  has  failed  to  be  confirmed.  There  is  no  doubt  that  the 
parasite  of  the  fever  multiplies  in  the  tick,  and  there  seems  to  be  an 
opinion  that  Dermatocentor  andersoni  (=D.  venustus)  in  Montana 
produces  a  fever  with  a  90  per  cent,  mortality,  while  D.  maturatus 
in  Idaho  one  with  a  5  per  cent,  mortality.     See  also  Chapter  XXXV. 

With  regard  to  predisposing  causes,  there  are  sex  and  age  in- 
fluences to  be  noted.  Men  are  more  frequently  attacked  than 
women,  and  the  most  common  age  is  from  fifteen  to  fifty 
years,  both  of  which  merely  signify  that  persons  performing  out- 
door work  run  a  greater  risk  of  infection  than  those  otherwise 
employed. 

Pathology. — During  the  fever  the  virus  can  be  found  in  the  red 
and  white  cells  as  well  as  in  the  serum.  It  also  exists  in  the  liver  and 
spleen. 

Morbid  Anatomy. — Rigor  mortis  is  well  marked,  and  the  skin  shows 
lividity  in  dependent  and  petechia?  in  non-dependent  parts,  and  at 
times  the  marks  of  the  tick-bites  may  still  be  visible. 

The  pleura,  lungs,  and  pericardium,  and  most  of  the  organs,  are 
normal,  but  petechia  may  be  seen  on  the  epicardium;  while  the 

&5 


1346  SPOTTED  FEVER  OF  THE  ROCKY  MOUNTAINS 

liver  and  spleen  are  enlarged,  congested,  and  soft,  and  the  kidneys 
are  congested,  and  may  show  subcapsular  haemorrhages. 

Histo-pathology. — The  microscope  shows  capillary  congestion  of 
the  organs,  with  an  excess  of  leucocytes,  and  an  extravasation  into 
and  pigmentation  of  the  skin.  Acute  parenchymatous  degenera- 
tions of  the  heart  muscle,  the  sp^en,  liver,  and  kidneys,  are  also  to 
be  noted. 

Symptomatology — -Incubation. — The  incubation  period  varies  from 
two  to  seven  days,  during  which  prodromata,  in  the  form  of  irritation 
in  the  tick-bites,  from  which  pains  may  radiate,  and  chilliness  with 
malaise  and  nausea,  may  be  experienced. 

Onset. — The  illness  often  begins  with  a  distinct  chill,  accompanied 
by  severe  headache,  pains  in  the  back  and  other  parts  of  the  body, 
and  a  rapid  rise  of  temperature  to  1030  to  1040  F.,  associated  with 
a  furred  tongue,  a  dry  skin,  yellow  and  congested  conjunctivae,  an 
irritating  cough,  at  times  epistaxis,  and  the  passage  of  febrile 
urine. 

The  fever  continues  to  rise,  with  slight  morning  remissions, 
until  a  maximum  of  1050  to  1070  F.  is  reached  about  the  fifth  to 
the  twelfth  day.  About  the  third  day  (second  to  seventh)  a 
macular  eruption  appears  on  the  wrists  and  ankles  which  quickly 
spreads  up  the  arms  and  legs  on  to  the  back,  forehead,  chest,  and 
abdomen,  so  that  the  whole  body  is  included  in  about  one  to  two 
days.  The  macules  vary  in  size  from  1  to  5  millimetres  in  diameter. 
They  are  not  elevated,  and  at  first  disappear  on  pressure,  but 
later  become  permanent,  and  finally  turn  petechial  about  the  sixth 
to  the  tenth  day.  Associated  with  the  eruption  is  a  dusky-red 
mottling  of  the  skin,  and  often  a  subicteric  tinge  of  both  the  skin 
and  the  conjunctivas.  The  eruption  is,  however,  by  no  means 
always  well  marked,  and,  in  fact,  mild  cases  have  been  reported 
in  which  it  was  absent. 

The  pulse  is  from  the  first  very  rapid,  reaching  from  no  to  150 
per  minute,  and  not  as  a  rule  in  proportion  to  the  temperature. 
At  first  full  and  strong,  it  becomes  gradually  feebler  and  smaller, 
and  is  often  dicrotic,  and  in  severe  cases  may  be  intermittent  and 
irregular.  The  blood  shows  a  diminution  of  the  erythrocytes  and 
hemoglobin,  with  a  slight  increase  in  the  total  number  of  leuco- 
cytes and  a  relative  increase  of  the  mononuclear  leucocytes;  but 
in  considering  these  blood-counts,  allowance  must  be  made  for  the 
all  itude  at  which  the  disease  occurs.  (Edema  of  the  face  and 
limbs  may  be  present  in  severe  cases. 

Course. — At  first  the  tongue  is  covered  by  a  thick  white  fur,  but 
later  it  becomes  dry,  cracked,  and  brownish,  and  sordes  collect  on  the 
teeth.  Nausea  may  be  present  during  the  first  week,  but  is  more 
common  in  the  second,  and  generally  lasts  till  the  end  of  the  illness. 
Constipation  is  usually  present  throughout  the  attack,  and  the 
liver  is  often  slightly  enlarged,  while  the  spleen  extends  beyond  the 
costal  margin,  and  is  tender.  There  is  usually  a  slight  sore  throat, 
and  there  may  be  signs  of  a  mild  bronchitis,   associated  with   an 


S  YMPTOMA  TO  LOG  Y—DIA  GNOSIS  1347 

increase  in  the  number  of  respirations,  which  may  reach  from 
twenty-six  to  sixty  per  minute. 

The  urine  presents  the  usual  febrile  character,  and  often  contains 
a  trace  of  albumen,  which  occasionally  may  reach  considerable  pro- 
portions, and  be  accompanied  by  a  few  granular  casts.  More 
rarely  the  urine  may  be  scanty  or  even  suppressed.  The  mind  is 
usually  clear,  but  in  severe  cases  a  low  muttering  delirium  may 
occur. 

Terminations. — After  the  fever  has  reached  its  height  on  the  fifth 
to  the  twelfth  day,  the  temperature  either  declines  by  lysis,  and 
recovery  takes  place,  or  it  remains  high,  and,  a  typhoid  state  de- 
veloping, death  ensues.  If  the  former  event  is  to  take  place,  the 
temperature,  falling  by  lysis,  reaches  normal  about  the  fourteenth 
to  the  eighteenth  day,  the  eruption  commences  to  fade,  and 
desquamation  begins,  which  extends  all  over  the  body,  while  the 
other  symptoms  gradually  abate  and  the  patient  becomes  convales- 
cent. If,  however,  death  is  to  ensue,  the  temperature  remains  about 
104°  to  1060  F.,  but  sometimes  shows  a  sudden  final  fall  just  before 
the  fatal  event. 

Convalescence. — Convalescence  may  take  some  time,  and  it  is  said 
that  the  sites  of  the  eruption  are  clearly  visible  even  twenty-four 
days  after  recovery  if  a  warm  bath  is  taken. 

Complications. — Pneumonia  is  a  comparatively  frequent  com- 
plication, but  gangrene  of  the  fingers,  toes,  and  skin  of  the  scrotum 
and  penis  may  occur.  Nephritis,  cardiac  weakness,  and  meningitis 
are  possible  complications. 

Diagnosis. — The  malady  may  be  difficult  to  differentiate  from 
typhoid  fever,  typhus,  and  the  Japanese  river  fever.  From  typhoid 
fever  it  can  be  distinguished  by  the  more  acute  onset,  the  petechial 
eruption,  commencing  on  the  hands  and  wrists,  the  absence  of 
marked  intestinal  symptoms,  and  the  presence  of  leucocytosis. 
In  doubtful  cases  all  the  modern  bacteriological  methods — scrum 
reaction,  search  for  the  Bacillus  typhosus  in  the  blood,  stools,  and 
urine— will  have  to  be  used  to  exclude  typhoid. 

The  distinction  between  spotted  fever  and  typhus  on  clinical 
grounds  seems  to  us  impossible.  Though  in  typhus  the  disease 
may  end  more  often  by  crisis  than  by  lysis,  all  the  other  clinical 
symptoms,  and  the  appearance  of  the  eruption,  are  practically 
identical;  in  fact,  Sambon  and  others  believe  that  the  Rocky 
Mountain  spotted  fever  and  typhus  are  the  same  entity.  Possibly 
typhus  and  Rocky  Mountain  spotted  fever  are  due  to  two  varieties 
of  the  same  organism,  or  two  very  closely  allied  species,  in  the  same 
way  as  African,  European,  American,  and  Asian  relapsing  fevers 
are  due  to  very  closely  allied  organisms.  It  has  been  noted  that 
guinea-pigs  are  susceptible  to  inoculation  of  Rocky  Mountain  fever 
virus.  Inoculation  of  blood,  especially  if  taken  at  the  end  of  the 
febrile  stage,  produces  pronounced  swelling  of  the  scrotum  in 
guinea-pigs,  and  this  ha-  been  suggested  as  a  test  to  differentiate 
Rocky  Mountain  fever  from  typhus.    Recent  immunological  studies 


1348  SPOTTED  FEVER  OF  THE  ROCKY  MOUNTAINS 

have  thoroughly  established  the  difference  between  Rocky  Mountain 
fever  and  typhus. 

The  ts  it  tsugamushi  fever  may  present  a  course  very  similar  to  the 
Rocky  Mountain  spotted  fever,  but  the  presence  of  one  or  more 
eschars  near  the  genitals  or  the  axilla,  and  the  eruption  begin- 
ning on  the  face,  and  not  becoming  petechial,  are  characteristic. 

Prognosis. — It  appears  that  the  prognosis  is  much  more  serious 
in  some  localities  than  in  others.  In  Montana  the  mortality  has 
been  as  high  as  90  per  cent.,  while  in  Idaho  it  has  always  been 
very  low  (5  per  cent.).  The  reason  for  this  difference  may  be  that 
there  are  two  distinct  varieties,  one  spread  by  D.  andersoni  (D. 
venustus)  and  the  other  by  D.  maturatus.  When  the  eruption  is 
not  much  marked  and  not  generalized,  the  prognosis  is  favourable. 

Treatment. — Quinine  has  been  advised  and  given  in  large  doses, 
but  it  does  not  show  any  specific  effect.  Atoxyl  and  salvarsan  have 
no  effect.  Adrenalin  has  also  been  advised.  The  treatment  can 
be  only  symptomatic.  To  relieve  the  severe  headache  cold  appli- 
cations may  be  used,  or,  with  prudence,  small  doses  of  antipyrin,  or 
pyramidon,  or  Dover's  powders.  Large  quantities  of  water  should 
be  drunk,  so  as  to  flush  out  the  kidneys.  The  water  maybe  slightly 
acidulated.  Tepid  sponging  is  useful  and  refreshing.  When  the 
temperature  rises  above  1030  F.,  cold  sponging  should  be  used,  and, 
if  necessary,  the  cold  bath  or  cold  pack.  Should  the  pulse  become 
small  and  irregular,  cardiac  stimulants  must  be  administered. 
The  room  should  be  darkened,  and  the  patient  kept  undisturbed. 

The  diet  should  be  liquid,  chiefly  milk  and  broths.  Alcoholic 
stimulants  may  be  indicated  in  some  cases. 

Prophylaxis. — This  may  be  considered  under  two  headings: — 

{a)  Man. 

{b)   The  Tick. 

(a)  Man. — This  consists  in  avoiding  as  much  as  possible  localities 
where  the  ticks  are  abundant,  and  destroying  these  arachnids.  A 
tick  should  be  removed  by  applying  ammonia,  turpentine,  kerosene, 
or  carbolized  vaseline,  and  then  the  bite  may  be  cauterized  with 
pure  carbolic  acid.  Some  authorities  advise  the  internal  adminis- 
tration of  quinine,  but  this  does  not  prevent  the  development  of 
the  fever. 

(b)  The  Tick. — The  prophylaxis  campaign  against  the  tick  is 
divided  into:  — 

1.  Destruction  of  ticks. 

2.  Removal  of  natural  tick  hosts. 

3.  Protection  of  domestic  animals  against  the  tick. 

These  ends  are  accomplished  by  periodic  dipping  of  cattle  and 
horses  in  the  usual  arsenic  solution  to  destroy  the  ticks,  by  poisoning 
and  shooting  rodents,  by  restricting  the  movements  of  domestic 
animals  from  infected  areas,  and  prohibiting  the  entrance  of  animals 
into  these  areas  during  the  period  from  February  to  July. 


REFERENCES  1349 

The  arsenical  solution  used  as  a  dip  is  composed  of  the  following 
ingredients: — 

Sodium  carbonate  . .  . .  .  .  .  .  24  pounds. 

Trioxide  of  arsenic  ..  ..  ..  ..  8 

Pine  tar  . .          . .  . .  . .  . .  . .  2  gallons. 

Water      ..          ..  ..  ..  ..  to  500 

A  galvanized  tank  is  used  containing  30  to  40  gallons  of  water,  which  is 
brought  to  the  boil.  The  sodium  carbonate  is  now  added  and  dissolved  by 
stirring,  and  then  the  arsenic  is  dissolved  in  the  same  way.  The  fire  is  now 
stopped  and  the  pine  tar  added  in  a  thin  stream  and  thoroughly  mixed  by 
stirring.  The  solution  so  formed  is  the  stock,  and  can  be  diluted  to  500  gallons 
as  required. 

THE  INTERMITTENT  TICK  FEVER  OF  WYOMING. 

Definition. — An  intermittent  fever  due  to  the  bite  of  Dermacentor  ander- 
soni. 

History  and  Geography. — This  fever  was  described  by  Kieffer  in  1907  as 
being  found  at  Fort  D.  A.  Russell,  in  Wyoming,  United  States  of  America, 
but  his  account  so  far  has  not  been  confirmed. 

/Etiology. — The  fever  comes  on  after  the  bite  of  D.  andersoni — i.e.,  the  same 
tick  which  causes  the  spotted  fever  of  the  Rocky  Mountains — but  no  specific 
organism  has  so  far  been  described. 

Symptomatology. — The  incubation  period  varies  from  three  to  seven  days, 
after  winch  the  disease  begins  suddenly  with  a  rigor,  nausea,  vomiting,  and 
pains  in  the  joints  and  muscles.  The  temperature  rises  between  1030  and 
1040  F.,  and  continues  high  for  twenty-four  to  forty-eight  hours,  after  which 
a  remission  of  forty-eight  hours  occurs,  and  then  another  attack,  and  so  on 
for  three  to  seven  attacks.  Less  frequently  the  attack  resembles  typhoid, 
with  a  ladder-like  rising  temperature  and  abdominal  symptoms,  but  Widal's 
reaction  is  absent.  There  is  marked  decrease  of  the  erythrocytes  and  haemo- 
globin, and  a  slight  lymphocytosis,  due  to  increase  in  the  number  of  the  large 
mononuclear  leucocytes. 

Treatment. — Hypodermic  injections  of  arsenic  in  some  form  are  recom- 
mended as  the  best  treatment  for  the  disease.     Salvarsan  should  be  tried. 


REFERENCES. 

Anderson    (1903).      Spotted  Fever  (Tick  Fever)  of  the  Rocky  Mountains. 

Hyg.  Lab.,  U.S.  Pub.  Health  and  Mar.  Hosp.  Service,  Wash.,  Bulletin  14. 
Arkwright,  Bacot  and  Duncan  (1919).    Transactions  Soc.  of  Trop.  Medicine. 
Fricks  (1916).     United  States  Health  Report,  31,  9,  516-521. 
Hunter  and  Bishop  (191 1).     Bulletin  105  U.S.A.  Department  of  Agriculture, 

Washington. 
Megaw  (1917).    Indian  Medical  Gazette.     (A  Case  like  Brill's  Disease  or  Idaho 

Spotted  Fever.) 
Michie  and  Parsons  (1916).     Medical  Record,  265-277. 
Ricketts  (1907).     Transactions  of  the  Chicago  Pathological  Society. 
Ricketts  (1909).     Bulletin  Johns  Hopkins  Hospital. 
Ricketts  (1909).     Journal  American  Medical  Association. 
Ricketts  (1909).     Journal  of  Tropical  Medicine. 
Ricketts  (1910).     Journal  of  Tropical  Medicine. 
Wilson  and  Chowning  (1904).     Studies  in  Piroplasmosis  Hominis.     Journal 

of  Infectious  Diseases,  i.  31. 
Wolbach  (1916).     Journal  of  Medical  Research,  121-126  and  147-150. 

The  Intermittent  Tick  Fever  of  Wyoming. 
Kieffer  (1907).     Journal  of  American  Medical  Association,  April  6. 


CHAPTER  LI 

TSUTSUGAMUSHI   FEVER  AND  ALLIED 

FEVERS 

Synonyms  —  Definition — -History  —  Climatology —  .Etiology  —  Pathology — 
Symptomatology — Diagnosis  —  Prognosis — Treatment  —  Prophylaxis — 
Allied  fevers — References. 

TSUTSUGAMUSHI  FEVER. 

Synonyms.  —  Japanese  River  fever,  Flood  fever,  Island  disease  (Shima 
disease),  Kedani  disease  ('  kedani  '  is  the  hair-louse),  Akamushi  disease 
('  mushi  '  is  the  Japanese  for  a  bug  or  insect ; '  akamushi  '  means  '  red  insect  '), 
Shima  mushi  disease  (Island  bug  disease),  Tochu-bio,  Shashitsu,  Pseudo- 
typhus. 

Definition. — Tsutsugamushi  disease  is  an  acute  endemic  febrile 
disorder  caused  by  the  bite  of  a  mite,  Microtrombidium  akamushi 
Brumpt,  1910,  producing  a  small  local  necrotic  area,  painful  en- 
largement of  the  proximal  lymphatic  glands,  and  an  exanthematous 
eruption. 

History. — Tsutsugamushi  disease  is  said  by  Ashburn  and  Craig 
to  have  been  mentioned  under  the  term  '  shashitsu  '  in  Chinese 
writings  more  than  one  thousand  years  ago,  when  it  was  described 
as  a  fever  due  to  the  bite  of  a  mite,  which  produced  a  pustule  in 
summer-time  in  people  who  entered  those  parts  of  the  country 
which  had  been  flooded  by  the  spring  rains.  The  Japanese  litera- 
ture on  the  subject  is  considerable,  but  the  descriptions  written  in 
European  languages  are  not  extensive,  the  earliest  contributions 
being  by  Palm  in  1878  and  Baelz  in  1879,  while  Ashburn  and  Craig, 
in  1908,  give  an  excellent  account  of  the  disease  and  its  causation, 
together  with  a  comparison  with  the  spotted  fever  of  the  Rocky 
Mountains. 

Climatology. — The  geographical  distribution  is  limited  to  the 
island  Nippon,  of  Japan,  where  it  is  confined  to  the  districts  Akita- 
ken  and  Nugata-ken  ('  ken  '  means  a  '  district  '),  in  which  certain 
lands  are  flooded  in  June,  in  the  former  district  by  the  Rivers 
Omonogawa  and  Minascgawa,  and  in  the  latter  by  the  Rivers 
Shinanogawa,  Akagawa,  Uwonumagawa,  and  Hajadegawa.  Further, 
it  is  limited  to  certain  parts  of  the  regions  flooded  by  these  rivers. 
The  floods  only  last  a  few  days,  and  the  regions  do  not  become 
dangerous  till  after  a  few  weeks,  when  a  red  mite  appears,  which 
may  attack  any  person  entering  these  places.     In  fact,  so  great 

1350 


CLIMATOLOGY— /ETIOLOGY 


1 35i 


is  this  danger  that  the  lands  have  been  abandoned,  except  by  the 
very  poor,  who  enter  them  in  order  to  cultivate  hemp  or  corn, 
or  to  gather  mulberry-leaves  to  feed  silkworms.  The  disease  is  to 
a  limited  extent  transportable  with  corn,  hemp,  and  other  articles. 
It  occurs  most  frequently  from  the  middle  of  July  to  October. 

According  to  Weir,  a  similar  disease  exists  in  Korea;  to  Dowden, 
in  the  Malay  States;  to  Schoffner,  in  Deli;  and  to  Noc  and  others, 
at  Saigon. 

/Etiology  (vide  also  pp.  726  and  920). — The  causation  of  the 
disease  is  not  known,  but  there  are  three  theories  which  have  been 
supported  by  various  investigators. 

These  theories  are: — 

1.  The  Bacterial  Theory. — Many  bacteria  have  been  described  as  the  cause 
of  the  disease,  the  first  being  a  Proteus,  found  by  Balz  and  Takana,  associated 
with  staphylococci  and  streptococci  in  the  lungs,  sputum,  and  urinary  sedi- 
ment. 

1.  The  Protozoan  Theory. — -Ogata  considers  that  the  cause  of  the  disease 
is  a  Plasmodium,  which  he  states  he  has  found  in  the  blood  of  numerous 
patients.  Ogata's  observations  have  not  been  confirmed.  In  191 7  Hayashi 
claimed  that  the  parasite  was  a  Piroplasma  which  existed  in  monkeys,  guinea- 
pigs,  and  calves,  inoculated  with  blood  from  a  patient,  in  the  form  of  granules 
and  rod-shaped,  globular,  and  annular  masses  in  giant  cells  found  in  the 
lymphoid  tissue,  especially  of  the  guinea-pigs. 

Myashima  has  found  rodlets  in  the  akamushi  and  in  inoculated  animals. 

Nagayo,  Miyagawa,  Mitamura  and  Imamura  state  that  they  have  culti- 
vated an  oval,  non-capsulated,  non-motile  organism  from  patients  suffering 
from  the  disease. 

3.  The  Chemical  Theory. — Tanaka  believes  that  the  true  cause  is  a  toxin 
contained  in  the  body  of  the  mite,  and  introduced  by  its  bite. 


Fig.  655. —  Microtrombidium  akamushi  Brumpt. 
(After  Hirst,  from  the  Journal  of  Economic  Biology.) 

The  only  certain  facts  which  we  know  concerning  the  etiology 
of  this  disease  is  that  the  symptoms  follow  the  bite  of  the  larva  of 
•  Microtrombidium  akamushi  Brumpt.  and  that  immunity  is  not  con- 
ferred by  an  attack.     This  larva  (akamushi),  which,  though  bright 


1352  TSUTSUGAMUSHI  FEVER  AND  ALLIED  FEVERS 

red  or  orange  in  colour,  is  so  small  that  it  is  almost  invisible  to  the 
naked  eye,  is  found  in  large  numbers  on  the  inner  surfaces  of  the 
ears  of  field-mice  (Arvicola  natanedzumi  Sasaki)  caught  in  July 
and  August  in  the  infected  regions.  The  akamushi  of  other  regions 
do  not  cause  the  disease,  which,  of  course,  is  against  the  chemical 
theory  as  to  the  aetiology.  Miyajima  claims  to  have  infected 
monkeys  by  inoculating  blood  derived  from  a  person  suffering 
from  the  disease,  and  also  by  the  bites  of  the  mites.  Mice  and 
guinea-pigs  are  said  to  be  immune— a  statement  which,  however, 
is  opposed  by  Ogata.  The  larva  has  been  reared  and  adult  mites 
obtained  by  Nagayo,  Miyagawa,  Mitamuar,  and  Imamura,  as  well 
as  by  Miyajima  and  Okumura.  The  last-named  suggest  that  the 
correct  name  for  the  mite  is  Leplits  akamushi  (Brumpt). 

Only  poor  people  enter  the  infected  lands  during  the  months  of 
July  to  October,  and  as  any  person  who  does  so  is  liable  to  infection, 
the  disease  is  mostly  found  among  the  poor. 

Pathology. — The  post-mortem  reveals  a  small  ulcer,  sometimes 
still  covered  by  an  eschar  at  the  site  of  the  bite,  and  enlargement 
of  the  proximal  lymphatic  glands.  The  spleen  is  enlarged  and 
softened,  the  lungs  are  cedematous  and  congested,  and  the  bronchial 
mucosa  is  often  slighthy  swollen  and  reddened,  and  the  kidneys  are 
inflamed.  We  are  not  acquainted  with  any  description  of  the 
histology  of  the  organs. 

Symptomatology. — The  incubation  period  varies  from  four  to 
ten  days  (4-7  Scheube),  during  which  there  may  be  a  feeling  of 
prostration,  giddiness,  and  general  malaise,  but  definite  prodromata 
are  wanting. 

The  disease  begins  with  a  chill  and  rigors,  accompanied  by 
severe  pain  in  the  forehead  and  temples,  and  a  sensation  of  weak- 
ness, while  the  temperature  quickly  rises  to  1010  to  103°  F.  The 
patient  usually  complains  of  pain  in  certain  enlarged  lymphatic 
glands,  which,  on  inspection,  are  found  to  be  tender,  quite  distinct 
from  one  another,  and  freely  movable  under  the  skin.  A  search 
in  the  region  drained  by  these  glands  may  reveal  a  circular  vesicle 
measuring  2  to  4  millimetres  in  diameter,  but  more  usually  one  or 
more  black  or  brownish  necrotic  areas  of  skin,  surrounded  by  a 
dullish  red  areola,  are  found.  These  areas  indicate  the  sites  of  the 
bites  of  the  mite. 

The  temperature  continues  to  rise  during  the  next  few  days, 
reaching  a  maximum  in  the  second  week,  when  it  may  be  as  high 
at  1050  F.  During  this  time  the  eschar  has  been  thrown  off  the 
necrotic  area,  and  reveals  a  circular  punched-out  ulcer,  the  peri- 
phery of  which  is  red  and  infiltrated,  but  not  painful  nor  tender. 
About  the  fifth  to  the  seventh  day  an  eruption  appears  on  the 
face  in  the  form  of  large  red  papules,  which  may  become  confluent 
on  the  cheeks,  giving  the  face  a  swollen  appearance.  From  this 
situation  the  eruption  spreads  all  over  the  body,  but  more  in  the 
form  of  macules  than  papules.  These  maculae,  which  are  2  to 
5  millimetres  in  diameter,  fade  on  pressure,  but  quickly  return 


SYMPTOMA  TOLOGY—VARIETIES— COMPLICATIONS      1353 

when  the  pressure  is  removed,  and  do  not  itch.  Between  the  spots 
on  the  trunk  and  forearms  follicular  papules  may  be  noted,  but 
the  eruption  is  not  so  well  marked  on  the  arms  and  thighs. 

At  first  the  pulse  is  full,  and  not  very  rapid,  varying  from  80  to 
100  per  minute;  later  it  may  become  small  and  quick,  and  at  times 
dicrotic.  The  first  cardiac  sound  is  often  impure,  and  the  trans- 
verse diameter  of  the  cardiac  dulness  may  be  increased. 

In  the  blood  the  red  cells  are  found  to  be  diminished,  and  the 
haemoglobin  proportionately  reduced.  In  mild  cases  there  is  often 
an  increase  in  the  large  mononuclear  leucocytes  and  lymphocytes, 
but  in  severe  cases  the  total  number  of  leucocytes  is  often  diminished, 
though  there  may  be  a  relative  polymorphonuclear  increase. 

The  tongue  is  at  first  moist  and  slightly  coated,  but  later  it 
becomes  dry,  brown  in  the  centre,  and  glazed  at  the  tip  and  edges. 
The  gums  in  some  cases  are  spongy,  and  bleed,  while  sordes  may 
collect  on  the  teeth,  and  a  few  punctiform  spots  be  noted  on  the 
palate.  The  epigastrium  and  left  hypochondrium  are  tender; 
the  liver,  however,  is  not  as  a  rule  palpable,  though  the  spleen  is 
usually  slightly  enlarged. 

The  nose  and  throat  are  normal,  but  the  rate  of  the  respirations 
is  increased,  and  the  breath-sounds  are  harsh  and  accompanied  by 
rhonchi,  which  can  be  heard  all  over  the  chest.  Usually  there  is  a 
certain  amount  of  coughing,  but  the  expectoration  is  scanty. 

The  urine  is  diminished  in  quantity,  high-coloured,  and  may 
contain  albumen,  and  often  gives  the  diazo-reaction.  Strangury 
may  occur. 

The  conjunctivae  are  early  injected,  a  feature  which  becomes 
more  marked  as  the  disease  progresses,  and  is  associated  with 
lachrymation. 

From  the  very  first  there  is  a  great  hyperaesthesia  all  over  the 
body,  and  there  may  be  delirium  at  night,  and  difficulty  in 
hearing. 

About  the  fourteenth  day  of  the  illness  the  eruption  begins  to 
fade  and  the  fever  to  remit,  and  in  the  next  five  or  six  days  the 
temperature  falls  by  lysis  to  normal,  and,  the  general  condition 
rapidly  improving,  convalescence  begins.  Recovery  is  usually 
quick,  and  by  the  twenty-first  day  from  the  commencement  of 
the  attack  the  patient  is  well. 

In  bad  cases,  however,  coma  and  hyperpyrexia  may  develop  in 
the  second  week,  and  cause  the  death  of  the  patient.  In  other 
cases  death  may  be  caused  by  complications,  which  may  arise 
either  in  the  second  week  or  during  convalescence. 

Varieties. — Severe  types  of  the  disease  end  in  death  about  the 
ninth  to  the  fifteenth  day  from  hyperpyrexia,  cardiac  failure, 
pulmonary  oedema,  or  from  complications.  Mild  types,  showing 
only  the  bite  and  the  enlargement  of  the  lymphatic  glands,  and 
associated  with  but  little  fever  or  eruption,  quickly  end  in  recovery. 

Complications. — The  commonest  complications  are  parotitis, 
melaena,  mania,  and  cardiac  failure  with  pulmonary  oedema. 


1354  TSUTSUGAMUSHI  FEVER  AND  ALLIED  FEVERS 

Diagnosis. — The  differential  diagnosis  from  Rocky  Mountain 
spotted  fever  and  typhus  has  already  been  discussed  (p.  1347).  At 
the  onset — when  the  inguinal  or  other  lymphatic  glands  are  enlarged 
and  painful — plague  might  be  suspected.  The  presence  of  the 
necrotic  area,  and,  in  any  doubtful  case,  the  microscopical  examina- 
tion of  the  gland  juice,  which  in  plague  contains  numerous  bi-polar 
staining  bacilli,  will  enable  a  diagnosis  to  be  made. 

Prognosis.— The  prognosis  is  good  in  the  young,  and  in  second 
and  third  attacks,  which  are  always  milder  than  the  first.  It, 
however,  gets  worse  as  age  progresses,  and  especially  in  first  attacks. 
The  mortality  is  about  30  per  cent.,  but  increases  markedly  with 
age,  being  only  12-5  per  cent,  in  the  first,  and  57  per  cent,  in  the 
seventh  decade  of  life. 

Treatment.- — Quinine  is  generally  administered,  but  it  does  not 
influence  the  fever  to  any  marked  extent.  Salvarsan  might  be 
tried.  Narcotics  may  be  required  to  combat  the  sleeplessness,  and 
constipation  must  be  relieved  by  purgatives  and  enemata.  Phen- 
acetin,  antipyrin,  and  salicylates  are  generally  badly  borne  by  the 
patient. 

Prophylaxis.— The  prophylaxis  consists  in  the  avoidance  of  the 
infective  regions  during  the  months  of  July  to  October  inclusive, 
while  the  cultivation  of  the  infected  regions,  and  especially  the 
planting  of  Eucalyptus  globulus  and  Paulonnia  impen'alis,  are 
advised,  as  well  as  the  smearing  of  the  exposed  parts  of  the  body 
with  eucalyptus  oil  and  balsam  of  Peru,  which  are  said  to  keep 
away  the  mites. 

The  natives  believe  that  the  manuring  of  the  infected  lands  with  human 
faeces  for  three  consecutive  years  will  make  them  free  from  the  mites,  provided 
there  is  no  flooding  during  that  period. 


ALLIED  FEVERS. 

PSEUDO-TYPHUS  OF  DELI,  SUMATRA. 

In  1902  Schuffner  observed  a  peculiar  fever  in  Deli,  Sumatra, 
which  he  described  in  1913,  and  which  he  thinks  may  possibly  be 
due  to  a  tick. 

In  occurs  from  June  to  August  and  from  November  to  January. 

The  site  of  the  inoculation  is  marked  by  a  small  red  spot,  followed 
by  necrosis  of  skin  and  inflammation  of  the  local  lymphatic  glands. 
The  necrotic  ulcer  may  measure  2-7  mm.  in  diameter,  and  shows 
little  tendency  to  heal,  while  other  lymph  glands  enlarge. 

On  or  about  the  second  to  third  day  a  roseolar  eruption  appears 
all  over  the  body,  being  most  marked  upon  the  trunk  and  flanks,  and 
less  so  on  the  face  and  limbs.  This  eruption  slowly  fades  during 
eight  to  ten  days.  Sometimes  it  is  but  slightly  marked;  sometimes 
it  is  hemorrhagic  and  followed  by  desquamation. 

The  fever  is  like  that  in  enteric  fever,  and  is  associated  with  severe 
nervous  symptoms. 


REFERENCES  1355 

Diarrhoea  is  rare,  but  pulmonary  complications  are  not  unusual, 
and  albuminuria  is  generally  present.  The  blood  shows  an  increase 
in  the  white  cells,  particularly  the  lymphocytes,  while  the  eosino- 
phils are  diminished. 

No  organisms  could  be  found  in  the  blood,  and  there  were  no 
reactions  to  serum  tests  for  the  enteric  fevers,  nor  could  monkeys  be 
infected  by  inoculation. 

KOREAN  CONTINUED  FEVER. 

A  somewhat  similar  fever  to  the  Sumatra  fever  is  described  by 
Weir.  It  occurs  in  spring  and  early  summer.  No  bite  is  mentioned, 
but  there  is  the  rash;  no  diarrhoea,  but  frequent  pulmonary  com- 
plications and  the  nervous  symptoms.  The  course  of  the  fever  is 
often  short  and  terminates  by  lysis. 

MALAY  STATES  FEVER. 

Dowden  in  1915  described  a  somewhat  similar  fever  in  the 
Federated  Malay  States,  but  gave  no  aetiological  information. 


REFERENCES. 

Tsutsugamushi  Disease. 

Ashburn  and  Craig  (1908).  A  Comparative  Study  of  Tsutsugamushi 
Disease  and  Spotted  or  Tick  Fever  of  Montana.  Philippine  Journal  of 
Science,  B,  vol.iii.,  p.  i. 

Baelz  and  Mawakami  (1878).  Die  Japanische  Fluss  oder  Ueberschwem- 
mungsfieber.     Archiv  far  Path.  Anat.     Berlin.     Virch.  Archiv,  lxxviii. 

373- 
Katishima    and    Miyajima    (1918).       Kitasato   Archives    of    Experimental 

Medicine,  vol.  ii.,  No.  2. 
Miyajima  and  Okumura  (191 7).     Kitasato  Archives  of  Experimental  Medi- 
cine, vol.  i.,  No.  1. 
Ogata  (1906).     Vorlaufige  Mitteilung  liber  die  Mt\o\og\e  der  Tsutsugamushi 

(Kedani)  Krankheit.     Deutsche  Med.  Wochensch.,  xlvi.  1868. 
Palm   (1878).     Some  Account  of  a  Disease  called  Shima   Mushi  or  Island 

Insect  Disease  by  Natives  of  Japan.     Edinburgh  Medical  Journal,  p.  128. 
Scheube  (1885).      Klinische   Beobachtungen  iiber  die   Krankheiten   Japan. 

Virch.  Archiv,  xcix.  368. 
Scheube  (1910).     Die  Krankheiten  der  Warmen  Lander,  p.  488.     Jena. 
Tanaka  (1899).     Ueber  .-Etiologie  und   Pathogenie    der   Kedani  Krankheit. 

Centralb.  f.  Bakteriol.,  p.  432. 

Allied  Fevers. 

SchSffner  (1914).     Proceedings  of  the  Far  Eastern  Association  of  Tropical 

Medicine  for  1913,  309-315. 
Weir  (1915).     China  Medical  Missionary  Association. 


CHAPTER  LII 
RAT-BITE  AND  CAT-BITE  FEVERS 

Rat-bite  fever — Cat-bite  fever — Squirrel-bite  disease — Addendum— References. 

RAT-BITE  FEVER. 

Synonyms. — Sodoku    (So=rat,   doku=bite);    Fievre    par  Morsure   de    rat 
Morso-di-Topo ;  Rattenbisskrankheit.;  Rattenbeetziekte. 

Definition. — A  relapsing  fever  of  long  duration  characterized  by 
redness  and  swelling  at  the  site  of  a  rat -bite,  often  by  a  generalized 
papular  eruption,  and  caused  by  Spiroschaudinnia  morsusmurii, 
Futaki,  Takaki,  Taniguchi,  and  Osumi,  1916,  living  in  the  mouth 
of  Epimys  norvegicus  Erxleben,  1777,  in  many  parts  of  the  world, 
and  inoculated  by  means  of  their  bite. 

History. — Rat -bite  fever  is  mentioned  in  Japanese  medical  books 
from  the  most  ancient  times,  and  Scotch,  French,  and  Spanish 
literature  have  references  to  the  disease,  but  it  was  not  until 
Katsura  in  1890  and  Miyake  in  1899  reported  cases  that  any  interest 
was  taken  in  the  malady.  In  1908  some  twenty-one  Japanese 
investigators,  according  to  Hora,  had  reported  some  thirty  cases, 
which  have  recently  been  increased  very  considerably.  It  has  also 
been  recorded  by  Horder  in  England;  by  Proescher  in  the  United 
States,  in  which  the  literature  of  the  nineteenth  century  shows 
occasional  cases  among  settlers;  by  Frugoni  in  Italy,  who  has 
given  a  very  good  general  account  of  the  malady,  and  by  Lou  and 
Cockin  from  East  Africa.  As  we  stated  under  this  heading  in  the 
first  edition  of  this  book,  there  is  a  curious  belief  in  Ceylon  that  a 
rat's  bite  is  a  serious  injury,  and  is  apt  to  be  followed  by  a  chronic 
disorder  which  is  popularly  called  leprosy,  but  which  we  have  never 
been  able  to  see.  In  Ceylon  the  belief  is  that  the  rat's  bite  is  only 
pernicious  in  the  breeding  season.  And  in  Japan  Hora's  case  is 
stated  to  have  been  due  to  a  bite  of  a  female  rat  which  was  suckling 
its  young.  It  is  said  that  the  same  disease  may  follow  the  bite  of 
a  weasel,  and  it  is  known  that  weasels  kill  rats,  and  therefore  it  is 
possible  that  infection  may  come  in  this  manner  to  the  weasel. 

In  189S  Millot  and  Carpentier,  and  in  1907  Roger,  drew  attention 
to  the  existence  of  the  disease  in  France. 

In  1908  Ogata  considered  that  the  causal  organism  was  a  sporo- 
zoon  (Rattengift  sporozoon).  In  1914  Schottmuller  obtained  a 
nocardia,  which  he  called  Streptothrix  murisratti,  from  the  blood  of 
cases  of  the  disease.  This  organism  has  been  supported  by  the 
observations  and  experiments  of  Blake  and  others,  but  is  now 
merely  of  historical  interest.     Douglas,  Colebrook,  and  Fleming, 

1356 


CLIMATOLOGY— ETIOLOGY  1357 

in  1918,  found  a  streptococcus,  while  Coles  has  suggested  that  more 
than  one  germ  may  be  the  causal  agent. 

In  19 16  Futaki,  Takaki,  Taniguchi,  and  Osumi  discovered  a 
spii  ochete  in  the  lymph  glands  and  pathological  products  of  patients 
suffering  from  the  disease.  In  the  same  year  Costa  and  Troisier 
reported  cases  in  France. 

Climatology. — As  the  rat  is  widespread,  so  the  disease  is  found  in 
many  parts  of  the  world,  being  recorded  in  Japan,  China,  Ceylon, 
India,  Dutch  Indies,  East  Africa,  England,  France,  Italy,  Balkans, 
Holland,  Germany,  and  North  and  South  America. 

^Etiology. — Futaki  and  his  collaborators,  in  1916,  reported  the 
presence  of  a  spirochete  9-10  microns  in  length  in  the  lymph  glands 
and  in  the  tissue  fluid  from  the  bitten  area.  Later  they  found  in 
man  and  inoculated  animals  shorter  and  thicker  spirochetes 
2-6  microns  long,  with  regular  close  steep  waves  and  a  filament  at 
each  end.  Ishiwara,  Ohtawara,  and  Tamura,  in  1916  and  1917, 
in  investigations  with  regard  to  experimental  rat -bite,  found  spiro- 
chetes morphologically  identical  with  the  short  forms  described 
above,  and  Kitagawa  and  Mukoyama,  in  1917,  found  forms  measur- 
ing 6-10  microns  in  length,  with  a  smaller  one  measuring  some 
4  microns  and  a  larger  measuring  12  microns,  in  their  inoculated 
guinea-pigs. 

In  1917  Kaneko  and  Okuda,  in  performing  a  post-mortem  on  a 
case,  found:  — 

1.  Long  spirochetes,  6-10  microns  in  length,  with  numerous  small, 
steep,  irregular  waves,  identical  with  Futaki's  long  spirochete. 

2.  Short  spirochetes,  17-5  microns  in  length,  with  two  to  six 
steep,  close,  regular  waves,  identical  with  the  short  spirochete  of 
Ishiwara  and  Futaki,  and  also  to  the  spirochetes  found  by  Ido  and 
his  collaborators  in  guinea-pigs  bitten  by  rats  and  so  infected. 

These  short  parasites  have  been  found  by  Ido  and  others  in  human 
blood  films  taken  at  the  height  of  the  disease.  Kaneko  and  Okuda 
found  the  spirochetes  in  the  kidney  in  casts  in  the  straight  tubules, 
the  canals  of  Henle,  and  the  intercalary  portion  of  the  boundary 
layer.  They  have  also  been  found  in  the  cortical  cells  of  the  supra- 
renal capsules  and  in  an  interstitial  space  in  the  testicles,  but  not 
in  other  organs. 

The  long  and  the  short  spirochetes  belong  to  the  same  species,  as 
is  proved  by  pure  cultures.  The  long  spirochetes  are  considered  to 
be  old  forms,  and  are  exclusively  found  in  human  tissues.  The  short 
spirochetes  are  the  typical  young  forms,  and  can  be  found  in  the 
blood  of  patients  suffering  from  rat -bite  fever,  as  well  as  in  experi- 
mental animals.  In  no  instances  have  they  been  found  in  healthy 
guinea-pigs,  white'rats,  or  mice.  They  are  absent  from  the  blood 
and  tissues  of  infected  animals  receiving  salvarsan  treatment. 

Ido,  Ito,  Wani,  and  Okuda  have  demonstrated  that  the  serum  of 
persons  who  have  recovered  from  the  disease  containsan  immune  body 
which  destroys  S.  morsusmuris,  as  demonstrated  by  Pfeiffer'stest  and 
by  the  fact  that  the  guinea-pigs  employed  for  this  test  remain  well. 


1358  RAT-BITE  AND  CAT-BITE  FEVERS 

Human  serum  shows  definite  spirochgetolytic  and  spirochaeticidal 
properties  eleven  months  after  the  onset  of  the  disease. 

These  researches  make  it  probable  that  S.  morsusmuris  is  the 
serological  agent  of  the  disease. 

Naturally  infected  guinea-pigs  have  been  seen  by  Niowaka, 
Yoshizawa,  and  Mumento,  who  have  shown  that  the  disease  can 
be  spread  from  guinea-pig  to  guinea-pig  by  subcutaneous  injections 
of  the  saliva  or  by  bites  of  infected  guinea-pigs.  The  organisms 
may  possibly  live  in  the  salivary  glands  of  rats.  The  men  mostly 
infected  are  agriculturists  and  sailors,  but  it  has  been  seen  in  soldiers 
in  the  trenches  and  persons  living  in  ordinary  houses. 

Row  regards  the  strain  found  by  him  in  Bombay  as  being  different  from 
the  Japanese  strain. 

Pathology . — At  first  the  reaction  against  the  organism  is  weak, 
but  later  immune  bodies  specific  against  the  spirochetes  are  found. 

Morbid  Anatomy. — Only  four  post-mortem  examinations  are 
on  record — viz.,  those  by  Miura  and  Toriyama  in  1897,  by  Blake  in 
1916,  and  two  by  Kaneko  and  Okuda  in  1917. 

In  the  first  the  conditions  were  increase  of  the  cerebro-spinal  fluid, 
hyperemia  of  the  meninges,  inflammatory  oedema  of  the  lungs,  and 
cloudy  swelling  of  the  liver. 

In  the  second  there  were  acute  ulcerative  endocarditis,  subacute 
myocarditis,  interstitial  hepatitis,  glomerular  and  interstitial 
nephritis,  infarcts  in  the  spleen  and  kidney,  haemorrhages  and 
oedema  of  the  lungs.  Microscopically,  degeneration  and  necrosis 
of  the  cardiac  muscles;  polymorphonuclear  infiltration  into  the  liver 
and  into  the  shrunken  kidney,  but  many  of  the  changes  may  have 
been  due  to  the  nocardia  found  by  Blake. 

In  the  third  case  there  were  no  marked  pathological  changes, 
except  parenchymatous  changes  in  the  organs,  such  as  hyperaemia, 
swelling,  and  degeneration  of  the  tubular  epithelium  of  the  kidney. 
There  is  degeneration,  necrosis,  and  destruction  of  the  liver  cells, 
particularly  in  the  centre  of  the  lobule,  with  hyperaemia  and  fatty 
degeneration  of  the  periphery  of  the  lobule,  with  also  haemor- 
rhages. No  abnormalities  in  the  spleen,  lymphatic  glands,  or 
bone-marrow,  except  that  the  local  lymph  glands  show  a  hyperplasia 
of  the  parenchymatous  cells.  Catarrhal  changes  are  seen  in  the 
mucosa  of  the  stomach,  as  well  as  catarrhal  cystitis,  congestion  of 
the  lungs  and  meninges,  and  degeneration  of  the  muscles  of  the  leg 
and  nerve  cells  of  the  brain  cortex  and  spinal  cord. 

The  skin  near  the  bite  shows  hyperaemia,  oedema,  and  polymorpho- 
nuclear infiltration  into  the  corium  and  subcutaneous  tissue,  but  no 
changes  in  the  epidermis. 

The  changes  found  in  experimental  animals  agree  with  those  seen 
in  man. 

Symptomatology — Incubation. — The  incubation  period  varies 
from  seven  to  twenty-two  days,  but  the  average  is  twelve  days. 
During  this  period  the  wound  caused  by  the  bite  heals. 

The  Attack. — The  onset  is  sudden.     The  site  of  the  bite,  which,  in 


SYMPTOM  A  TOLOGY— VARIETIES— COMPLICA  TIONS      1 359 

the  large  proportion  of  cases,  is  on  the  head  or  upper  extremity, 
becomes  red  and  swollen,  and  an  ulcer  forms,  while  the  regional 
lymph  glands  become  enlarged.  The  temperature  now  rises  (1030 
to  1050  F.),  the  pulse  becomes  small  and  rapid,  and  there  may  be 
sensations  of  chilliness,  while  an  eruption  of  purple  spots,  which 
often  resembles  erythema  polymorphum,  appears  on  the  body,  and 
the  patient  feels  very  ill,  with  pains  in  the  muscles  and  joints,  and 
perhaps  delirium.  In  a  few  days  the  temperature  declines  and  the 
patient  feels  well. 


Fig.  656. — Rat-Bite  Fever. 




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Fig.  657. — Rat-Bite  Fever. 

Relapse. — After  a  few  days  or  a  couple  of  weeks  of  apyrexia,  how- 
ever, the  attack  is  repeated,  and  these  intervals  of  apyrexia  and 
attacks  of  fever  may  be  repeated  for  months  or  years.  The  relapses 
may  be  fairly  regular,  at  five  days'  intervals,  for  months,  and  may  be 
preceded  by  premonitory  symptoms.  Thus  Hora's  case  had  about 
ten  relapses  a  year  for  a  period  of  seventeen  years.  The  blood  may 
show  eosinophilia.  During  the  fever  red  cells  are  about  four  millions 
and  the  leucocytes  about  six  to  twelve  thousand.  In  the  interval 
there  may  be  only  four  thousand  leucocytes.  Death  may  occur  in 
old  people  from  exhaustion,  or  in  others  from  complications. 

Varieties. — Three  different  types  of  the  disease  are  described :  a 
febrile  type  with  a  marked  eruption,  a  febrile  type  with  nervous 
symptoms,  and  an  abortive  type;  but  the  first  is  most  common. 

Complications. — Sloughing  and  gangrene  at  the  site  of  the  bite 
and  nephritis  may  occur. 

Diagnosis. — The  presence  of  a  relapsing  fever  associated  with  a 


1360  RAT-BITE  AND  CAT-BITE  FEVERS 

purple-coloured  eruption  and  a  non-suppurative  adenitis  following 
a  rat-bite  should  make  the  diagnosis  easy.  The  discovery  of  the 
spirochete  in  the  blood  confirms  the  diagnosis. 

Prognosis. — This  is  good,  as  the  mortality  is  only  about  io«5  per 
cent.,  and  death  is  most  usually  due  to  collapse  or  septicemic 
symptoms  during  the  first  attack,  or  to  nephritis  or  to  complications. 

Treatment. — Treatment  by  salvarsan  is  quite  successful.  For 
details  of  the  treatment  see  pp.  1313  and  1560.  Mercury  has  been 
recommended  by  Borelli. 

Prophylaxis. — The  rat -bite  should  be  thoroughly  disinfected. 

CAT-BITE  DISEASE. 

Definition. — A  relapsing  fever  caused  by  a  spirochete,  probably 
identical  with  Spiroschaudinnia  morsustnuris,  introduced  b}^  a  cat's 
bite  or  scratch. 

History. — Cat -bite  disease  was  first  described  in  Japan  by  Fujida 
and  Sato  in  1902,  while  Izumi  and  Kato,  in  1917,  brought  forward 
evidence  to  show  that  the  causal  organism  was  a  spirochete,  probably 
identical  with  S.  morsustnuris.  In  1917  Sano  described  a  case  due 
to  scratches  caused  by  a  cat. 

^Etiology. — Futaki  and  Ishihara,  Tdo,  Ito,  Wani  and  Okuda, 
Izumi  and  Kato,  have  all  found  spirochetes  in  the  blood  of  patients. 
They  were  discovered  by  the  first  named  and  confirmed  by  the 
others.  The  last  named  believe  this  spirochete  to  be  the  same 
as  that  causing  rat -bite,  because — 

I.  The  serum  of  a  patient  suffering  from  cat -bite,  when  mixed 
with  an  equal  quantity  of  guinea-pig  blood  containing  rat -bite 
spirochetes,  immobilizes  them.  When  repeated  with  normal  and 
svphilitic  serum  the  spirochetes  are  not  affected. 

II.  When  1  cubic  centimetre  of  guinea-pig  blood  containing  rat- 
bite  spirochetes  is  mixed  with  2  cubic  centimetres  of  the  blood  of 
a  patient  suffering  from  cat -bite,  and  then  the  mixture  injected  into 
the  peritoneal  cavity  of  a  guinea-pig  and  removed  in  an  hour,  no 
spirochetes  are  found.  In  a  control  guinea-pig  the  spirochetes  were 
abundant  and  active. 

III.  In  II.  the  first  guinea-pig  remained  healthy  and  the  control 
died. 

Symptomatology — Incubation. — This  varies  from  ten  to  twenty- 
one  days. 

Attack. — The  onset  begins  with  some  premonitory  symptoms, 
followed  by  fever,  pains  in  the  muscles  and  joints,  enlargement  of 
the  spleen  and  the  lymphatic  glands.  Infiltration  of  the  skin  takes 
place  near  the  site  of  the  bite,  and  macular  or  urticarial  eruptions 
which  spread  all  over  the  body. 

The  bite  may  heal  readily  or  may  ulcerate  deeply. 

Course. — The  fever  is  of  the  relapsing  type,  the  intervals  being 
some  three  to  nine  days,  and  without  treatment  the  disease  will 
last  for  months. 

Diagnosis. — -This  is  the  same  as  for  rat-bite  fever. 


REFERENCES  1361 

Prognosis.—  This  is  good  quoad  vitam,  except  in  old  age  or 
debilitated  persons. 

Treatment. — One  injection  of  salvarsan  will  cure  some  cases, 
while  others  require  several  injections. 

SQUIRREL-BITE  DISEASE. 

Synonym. — Eichhdrnchen-Bisskrankheit, 

Schott  in  tiller  described  a  case  of  this  infection  in  1914  in  a  woman 
bitten  by  an  African  squirrel,  Taraxenis  cepapi.  The  disease  was 
characterized  by  fever  and  also  by  nodules,  which  destroyed  the 
sight  of  one  eye.  Another  case  was  a  man  bitten  by  the  same 
squirrel,  and  from  the  pus  of  this  case  Schottmuller  obtained  a 
nocardia  which  he  called  Streptothrix  taraxcri  cepapi.  The  nocardia 
infection  is  probably  a  complication,  possibly  also  introduced  at 
the  time  of  the  bite,  as  its  presence  has  been  confirmed  by  numerous 
observers,  and  species  of  nocardia  are  well  known  to  live  in  the 
human  tonsil,  and  may  well  exist  in  the  mouth  of  rats,  squirrels,  and 
other  animals. 

ADDENDUM. 

Weasels  are  also  said  to  cause  similar  symptoms  by  their  bites, 
and  it  is  likely  that  many  other  animals  do  the  same,  and  it  is 
possible  that  they  inoculate  the  bitten  person  or  animal  with  various 
types  of  organisms,  of  which  spirochetes  appear  to  be  more  impor- 
tant as  regards  the  causation  of  fever. 

REFERENCES. 
Rat-Bite  Fever. 

Borelli  (1918).     Policlinico,  January  13. 

Cavina  (1917).     Morgagni,  August  31. 

Chagas  (1Q15).     Brazil  .Medico,  July  22. 

Coles  (1918).     Lancet,  March  2,  p.  350. 

Crohn  (1915).     Archives  of  Internal  Medicine,  June  15. 

Cruickshank  (191 1).     British  Medical  Journal. 

D'HALLUIN  and  Fievez  (1918).     Paris  Medicale,  March  23. 

Douglas,  Colerrook,  and  Fleming  (1918).     Lancet,  February  16. 

Frugoni  (191  i).     Kiv.  Crit.  Clinica  Medica. 

Kara  (1906).     Sei-J.-Kwai  Medical  Journal,  xxv.,  vii.  75. 

Hata  (1912).     Munch.  Med.Woch. 

Hi  J  MANS  VAN  DEN  BERGH  (hum).  Xeder.  Tijdschr.  voor  Geneeskundc, 
February  22. 

Horder  (1910).     Quarterly  Journal  of  Medicine,  iii.  121. 

Ido,  Ito,  Vv'ani,  and  Okuda  (1917).     Journ.  of  Exp.  Med.,  Sept.  1. 

Kaneko  and  Okuda  (1917).     Journal  of  Experimental  Medicine,  September  1. 

Kitagawa  and  Mukoyama  (1917).     Arch,  of  Int.  Med.,  Sept.  15. 

Low  and  COCKIN  (1018).      British  Medical  Journal,  February  16. 

NIOWAKA,  Voshizawa,  and  MuMEMOTO  (1017).  Tokyo  Iji  Shinshi  (Spiro- 
chetosis in  the  Guinea-pig),  January  20. 

Row  (1918).      Bull.  Soc.  Path.  Exot.,March. 

Solly  (191S).     Lancet,  March  2S. 

Cat-Bite  Fever. 
Izumi  and  Kato  (191-7).     Tokyo  Iji  Shinshi,  April  28. 
Kitagawa  (1917).     Saikingaku  Za'sshi,  May  15. 
Sano  (1917).     Iji  Shimbun,  September  10. 

86 


CHAPTER  LIII 

THE    ENTEROIDEA   GROUP   OF    TROPICAL 

FEVERS 


General   remarks- 


-Enteroidea    or    intestinal   fevers- 
References. 


-Enteric — Parenteric- 


CxENERAL  REMARKS. 

We  use  the  word  enteroidea,  or  intestinal  fevers,  for  all  those 
fevers  which  are  caused  by  any  of  the  intestinal  bacteria,  while  the 
term  enteric  fever  denotes  those  which  are  called  typhoid  and  para- 
typhoid A  and  B  fevers.  By  par enteric  fever  we  mean  those  febrile 
conditions  which,  though  clinically  resembling  '  enteric  fever,'  are 
caused  by  intestinal  bacilli  specifically  different  from  B.  typhosus 
and  B  paratyphosus  A  and  B.  These  parenteric  germs  may  be 
closely  related  to  the  enteric  germs  or  may  be  widely  separated 
therefrom  {vide  Chapter  XXXVI. ,  p.  934). 

ENTEROIDEA  OR  INTESTINAL  FEVERS. 

The  term  enteroidea  covers  both  the  enteric  and  the  parenteric 
groups,  and  applies  to  any  fever  caused  by  intestinal  germs  in  the 
widest  sense  of  the  word  (p.  934).  These  fevers  may  be  classified 
as  follows: — 

(Enteric  Fevers  : —  I  Typhoid. 

Synonym:   Enterica-    Paratyphoid  A. 
sensu  siricto  I  Paratyphoid  B. 

A,  due  to  germs  of  genus  Eber- 
thus  and  Alcaligenes. 

B,  due  to  germs  of  genus  Sal- 
monella. 

C,  due  to  germs  of  genus  En- 
teroides. 

D,  due  to  germs  of  genus  Lan- 
koides. 

E,  due  to  germs  of  genus  Bal- 
kanella  and  Wesenbergus. 

E,  due    to     germs     of    genus 
Escherichia. 

ENTERIC. 

Synonyms. — Typhoid  Ecver,  Abdominal  Typhus,  Gastric  Fever,  Pytho- 
genic  Fever,  Endemic  Fever,  Autumnal  or  Fall  Fever,  Remittent  Fever  of 
many  writers,  Common  Continued  Fever,  Slow  or  Lent  Fever,  Nervous  Fever, 

1362 


Enteroide 

Fevers  : — 

Synonyms : — Enter- 
oidea, Intestinal 
fevers,  Enterica 
sensfi  Into 


Parenteric  Fevers  : — 
ISynonym  :  Parenterica  -l 


ENTERIC  1363 

Little  Fever,  Irregular  Low  Fever,  Low  Fever,  Bilious  Fever,  Bilio-gastric 
Fever,  Bilious  Continued  Fever,  Night-soil  Fever,  Cesspool  Fever. 

French  Synonyms. — Fievre  Typhoide,  Dothienentcrite,  Fievre  Continue, 
Fidvre  gastrique,  Fievre  nerveuse,  Entente  septicemique,  Adeno-meningee, 
Fievre  meningogastrique. 

Italian  Synonyms. — Febbre  tifoide,  Tifo  addominale. 

German  Synonyms.  —  Abdominaltyphus,  Nervenneber,  Darmtyphus, 
Gastricb.es  Fieber. 

The  Latin  synonyms  are  very  numerous,  and  have  been  classified  by 
Murchison  into: — 

(a)  From  supposed  resemblance  to  typhus:  Typhus  nervosus,  T.  mitior; 
T.  gangliaris  vel  entericus,  lleo-typhus;  Typhios,  Typhus  (of  many  old 
writers). 

(b)  From  mode  of  prevalence:  Febris  non-pestilens. 

(c)  From  its  remittent  character:  Febris  semitertianae  seu  composita; 
Tritseophya  typhodes. 

(d)  From  its  length:  Febris  lenta. 

(e)  From  septic  symptoms:  Febris  putrida,  Febris  putrida  quae  vulgo  lenta 
appelatur;  Febris  putrida  aut  biliosa;  Febris  a  putredine  orta. 

(/)  Resemblance  to  hectic  fever:  Febris  hetica. 

(g)  Occurrence  of  gastric  symptoms:  Febris  gastrica,  Febris  acuta  stoma- 
chica  aut  intestinalis;  Synochus  biliosis. 

(h)  From  intestinal  symptoms:  Febris  mucosa,  Febris  pituitosa,  Febris 
mesenterica  maligna,  Febris  intestinalis. 

(i)  From  supposed  origin  from  worms  :  Febris  verminosa,  Typhus 
verminosus. 

With  regard  to  the  nomenclature,  we  have  adopted  the  term  Enteric  Fever, 
used  by  Ritchie  in  1846,  because  we  describe  under  the  term  three  distinct 
diseases  caused  by  distinct  micro-organisms,  all  of  which  produce  symptoms 
either  identical  with  or  so  closely  resembling  one  another  as  to  be  nearly 
impossible  of  clinical  separation  at  the  present  time. 

Definition. — The  term  '  enteric  fever  '  is  used  at  the  present  time 
to  indicate  three  clinically  similar  fevers:  typhoid  fever  due  to 
Bacillus  typhosus  Eberth,  1880,  the  paratyphoid  fevers  due  to 
B.  paratyphosus  A  Schottmiiller,  1901,  and  B.  paratyphosusB  Schott- 
miiller,  1901,  and  varieties  of  these  bacilli. 

History. — The  history  of  enteric  fever  may  be  considered  under 
t  \v(  1  headings — viz. ,  the  general  history  of  the  disease,  and  the  special 
history  of  its  occurrence  in  the  tropics. 

It  is  quite  impossible  to  recognize  it  with  any  degree  of  certainty 
in  the  meagre  descriptions  written  by  Hippocrates  and  the  ancient 
physicians,  which  may  or  may  not  have  referred  to  this  disease. 
In  the  Middle  Ages  enteric  fever,  typhus  fever,  and  relapsing  fever 
were  always  confused  with  plague  until  Fracastorius,  in  the  six- 
teenth century,  distinguished  typhus  (which  included  enteric  fever 
and  relapsing  fever),  or  febris  pestilens,  from  plague,  or  febris  vere 
pestilens.  Spigelius,  in  1624,  is  probably  the  first  writer  to  clearly 
recognize  the  symptoms  of  enteric  fever,  because  he  described  in 
Padua  a  disease  characterized  by  fever,  abdominal  pain  and  tender- 
ness, diarrhoea  and  delirium,  having  remissions  and  relapses,  and 
associated  with  the  post-mortem  appearances  of  inflammation  in 
the  ileo-caecal  region.  Similar  descriptions  can  be  found  in  the 
writings  of  Willis  in  1659,  who  drew  a  distinction  between  febris 
pestilens  and  a  febris  lenta,  the  latter  being  associated  with  the  en- 


1364        THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

largement  of  the  mesenteric  glands.  Sydenham,  in  1685,  described 
a  fever  lasting  fourteen  to  thirty  days,  and  associated  with  diarrhoea, 
vomiting,  epistaxis,  etc.,  as  distinct  from  febris  pestilens.  In  1715 
Baglivi  of  Rome  described  the  hemitritaeus  of  older  writers  under 
the  term  '  febris  mesenterica.'  This  fever  was  characterized  by 
being  irregularly  remittent,  lasting  from  fourteen  to  twenty-one 
days,  and  associated  with  inflammation  of  the  intestines  and 
mesenteric  glands.  Lancisi  thought  that  the  enteric  ulcers  were 
caused  by  round  worms.  Hoffman's  febris  petechizans  vel  spuria, 
Strother's  lent  fever,  Gilchrist's  nervous  fever,  Huxham's  slow 
nervous  fever,  Riedel's  febris  intestinalis,  and  Manningham's 
febricula,  are  all  synonyms  of  enteric  fever.  In  1810  Hildenbrand 
distinguished  between  contagious  typhus  and  a  non-contagious 
nervous  fever,  which  were  respectively  named  typhus  exanthemati- 
cus  and  typhus  abdominalis  by  German  authors. 

In  1813  Bretonneau  of  Tours  associated  this  fever  with  hyperplasia 
of  the  solitary  and  agminated  glands  of  the  ileum,  and  gave  it  the  name 
'  dot hienent eric  '  (from  Sodtijv,  a  tumour,  and  evrepov,  the  intestine). 

In  1829  Louis  gave  the  fever  the  name  '  fievre  typhoide,'  and  the 
work  of  Gerhard  of  Philadelphia  in  1837,  Shattuck  of  Boston  in 
1839,  Barlow  in  1840,  Bartlett  in  1842,  Ritchie  in  1846  (who  intro- 
duced the  term  '  enteric  fever  '),  Jenner  in  1849-51,  completed  the 
clinical  differentiation  of  enteric  fever  from  typhus,  from  which 
relapsing  fever  was  also  being  separated.  Thus  arose  the  clinical 
conception  of  enteric  fever,  but  in  the  meanwhile  many  theories 
had  been  promulgated  as  to  its  causation;  thus  Bretonneau  held  the 
view  that  it  was  spread  by  means  of  contagion,  but  this  opinion 
was  slow  in  gaining  definite  support.  In  1847  Canstatt  pointed  out 
'  that  truly  the  exhalations  of  the  sick  man,  his  excrements,  and  possibly 
the  typhus  eruption  in  the  skin,  arc  the  carriers  of  the  contagion.' 

In  1850  Riecke  recorded  outbreaks  due  to  drinking-water  be- 
coming contaminated  with  sewage;  Murchison  implicated  milk. 

In  1880  Eberth  discovered  the  B.  typhosus  in  the  mesenteric 
glands  and  spleens  of  persons  dying  from  enteric  fever,  and  in  1884 
Gaffkey  cultivated  the  bacillus  so  discovered. 

In  1885  Fraenkel  and  Simmonds  obtained  definite  animal  reac- 
tions in  guinea-pigs,  mice,  and  rabbits;  and  more  recently  Griin- 
baum,  Metchnikoff,  and  Besredka  reproduced  the  typical  characters 
of  the  disease  in  chimpanzees;  and  Bland-Sutton  described  death? 
of  lemurs  and  monkeys  in  London  which  were  associated  with  post 
mortem  appearances  resembling  enteric  fever. 

The  diagnosis  of  the  disease  was  greatly  facilitated  by  Griiber 
and  Durham's,  Widal  and  Griinbaum's,  works  on  agglutinins  and 
specific  agglutination  reactions.  Later,  the  cultivation  of  the 
bacilli  from  blood  obtained  by  splenic  puncture,  and  by  the 
dilution  method  as  devised  by  Castellani  from  the  circulating  blood, 
assisted  the  diagnosis:  while  the  bile  enrichment  method  and  the 
Conradi-Drigalski's,  MacConkey's,  and  other  media  generally  aided 
the  investigation  of   the  disease.      Chantemesse   has  devised  an 


HISTORY  1365 

ophthalmo-diagnostic  method.  The  diagnosis  of  a  mixed  infection 
has  been  rendered  easier  by  the  absorption  test  as  introduced 
by  Castellani  in  1902,  which  is  of  use  also  in  the  determination  of 
closely  allied  bacteria.  The  B.  typhosus  has  been  found  to  be 
capable  of  living  for  weeks  in  the  spleen,  and  for  years  in  the  gall- 
bladder, of  people  who  are  designated  'typhoid-carriers,'  as  the 
bacilli  escape  in  the  faeces  in  the  latter  case.  The  bacilli  have  been 
shown  to  occur  naturally  in  water-supplies,  earth,  dust,  fomites, 
flies,  shellfish,  and  milk,  etc.  The  subject  of  relapses  has  been 
studied  by  Chantemesse  and  Widal  in  1892,  Wright  and  Lamb  in 
1899,  and  Durham  in  190 1. 

Attempts  to  obtain  an  antityphoid  serum  by  Macfadyen,  Hewlett, 
and  Chantemesse,  have  not  been  successful,  but  Wright  and  Semple 
devised  a  vaccine  in  1897  which  was  perfected  by  Leishman,  and 
has  been  much  used  and  has  rendered  great  service;  later  Castellani 
brought  forward  vaccination  with  a  mixed  typhoid  +  paratyphoid 
A  +  paratyphoid  B  vaccine  dead  or  living  (attenuated)  as  a  method 
of  prophylaxis,  while  more  recently  Besredka  and  Metchnikoff  have 
advised  a  living,  not  attenuated,  sensitized  vaccine. 

The  subject  of  variation  of  the  B  typhosus  has  been  studied  by 
Twort,  Horrocks,  and  Penfold. 

In  1895  Gilbert  gave  the  name  '  para-colon  '  to  bacilli  occupying 
an  intermediate  position  between  B.  coli  and  B.  typhosus.  In  1896 
Archard  and  Bensaude  used  the  term  '  paratyphoid  '  as  a  name  for 
such  organisms  when  capable  of  producing  the  symptoms  of  enteric 
fever,  but  this  name  dropped  into  oblivion,  only  to  be  revived 
by  Schottmiiller  in  1901,  when  he  clearly  demonstrated  his  B. 
paratyphosus  A  and  B.  paratyphosus  B  as  the  cause  of  two  forms 
of  enteric  fever,  the  diagnosis  of  such  cases  being  obtained  by  the 
specific  agglutinative  reactions,  or,  better,  by  cultivation  from  the 
circulating  blood.  This  is  the  reason  why  the  symptoms  charac- 
teristic of  enteric  fever  are  ascribed  to  three  allied  organisms — viz. ,5. 
typhosus  Eberth,  B.  paratyphosus  A  Schottmiiller,  and  B.  para- 
typhosus B  Schottmiiller. 

The  presence  of  typhoid  fever  in  the  tropics  has,  even  in  recent 
times,  been  much  debated,  and  apparently  the  view  has  been  held 
that  it  was  overlooked  by  the  older  tropical  physicians.  This, 
however,  is  quite  erroneous,  for  typhoid  fever  was  early  recognized 
in  the  tropics  after  its  separation  as  a  clinical  entity  by  the  workers 
in  the  Temperate  Zone.  Thus  Scott  and  Milley,  in  1830,  showed 
that  it  existed  in  Tasmania;  Levacher,  in  1840,  in  St.  Lucia;  while 
it  was  recognized  in  1841  on  the  Niger  River,  in  West  Africa,  and 
in  Martinique,  and  somewhat  later  in  Sierra  Leone  and  Gaboon. 
In  1842  an  epidemic  is  mentioned  as  occurring  in  Rio  di  Janeiro 
in  Brazil,  and  others  in  Tahiti  in  1847,  1849,  1853-54,  and  also  in 
Damascus  in  1852,  and  in  Cayenne  in  1852-53.  Other  epidemics 
were  recorded  in  Cuba  in  1853-54,  while  in  the  latter  year  Scriven 
definitely  proved  its  existence  in  India  by  demonstrating  the 
typhoid  ulcers  found  by  post-mortem  examination.     In  the  same 


1366        THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

year  Thomson  described  enteric  fever  in  New  Zealand,  and  Ripley 
about  the  same  time  in  Fiji.  In  1865  Massey  recognized  it  in 
Newera  Eliya,  in  Ceylon,  while  its  occurrence  in  Trinidad  and  the 
Bermudas  was  known  in  1866,  and  Davidson,  in  1868,  described  it  in 
Madagascar.     In  1877  Defant  said  it  was  common  in  Senegambia. 

Notwithstanding  all  this  early  work,  the  fact  of  its  prevalence  in 
the  tropics  was  not  generally  recognized,  the  disease  being  concealed 
under  the  terms  '  remittent  fever  '  and  '  malarial  fever  '  with  ulcers, 
which  latter  became  the  so-called  '  typho-malarial  fever,'  which  we 
now  know  to  be  a  mixed  infection — enteric  fever  complicated  by 
malaria.  The  cause  of  this  long  delay  in  the  general  diagnosis 
appears  to  have  been  the  slow  recognition  of  the  disease  by  the  pro- 
fession as  a  whole  in  England,  which  reflected  itself  upon  India  and 
the  British  Colonies;  while  the  authority  of  Morehead,  who  in  the 
first  edition  of  his  book,  '  Researches  on  Disease  in  India,'  stated 
that  typhoid  fever  was  unknown  in  that  country,  is  also  believed 
to  have  had  a  deterrent  effect  upon  the  diagnosis  of  enteric  fever 
therein.  He,  however,  soon  doubted  the  correctness  of  his  original 
statement,  for  in  i860  he  writes  that  in  1856  he  recognized  the 
disease  in  Bombay,  and  he  quotes  a  lecture  given  by  Goodeve  on 
seven  cases  of  undoubted  typhoid  fever;  still,  he  is  of  the  opinion 
that  typhoid  fever  will  be  found  in  extra-tropical  India  or  in  inter- 
tropical provinces  in  the  near  proximity  of  the  tropics. 

Another  point  which  prevented  the  general  recognition  of  enteric 
fever  was  the  supposed  antagonism  of  malaria  to  it,  and  the 
immunity  of  malarial  districts  from  its  attacks.  These  views  were 
simply  based  upon  the  opinion  that  all  remittent  fevers  were 
malarial,  and  that  swelling  and  ulcerations  of  Peyer's  patches  could 
take  place  in  these  fevers;  and  the  practitioner  in  the  tropics  was 
carefully  warned  that  he  was  not  justified  in  asserting  the  existence 
of  typhoid  fever  from  the  mere  character  of  the  post-mortem 
appearances,  and  that  the  so-called  '  typhoid  symptoms  '  were  not 
peculiar  to  one  form  of  fever,  but  might  occur  in  all. 

Such  teaching  probably  had  a  marked  effect  upon  the  diagnosis 
of  enteric  fever  in  the  tropics  until  the  recent  establishment  of 
bacteriological  institutions,  wherein  a  bacteriological  diagnosis 
could  be  made. 

Still  more  recent  is  the  general  recognition  of  the  fact  that  the 
disease  may  be  prevalent  among  the  natives;  in  Ceylon,  however, 
the  fact  that  the  malady  is  common  among  natives  has  been  recog- 
nized for  several  years,  and  typhoid  wards  for  natives  have  been 
established,  as  well  as  a  special  typhoid  hospital. 

It  may  now  be  said  that  it  is  well  known  that  enteric  fever  is 
prevalent  in  many,  if  not  most,  tropical  countries,  and  that  it 
occurs,  not  merely  in  Europeans,  but  in  natives  also. 

Etiology. — Enteric  fever  is  caused  by  the  B.  typhosus  Eberth, 
B.  paratyphosus  A  Schottmiiller,  B.  paratyphosus' B  Schottmuller. 
The  description  of  these  germs  may  be  found  in  any  manual  of 
bacteriology.     It   is  probable  that  there  are   several  varieties  of 


/ETIOLOGY  1367 

each  of  these  germs,  and  certain  characters  have  been  given  in 
Chapter  XXXVI.,  p.  934.  Of  the  B.  typhosus,  for  instance,  two 
varieties  can  be  easily  differentiated — one  rendering  milk  alkaline 
after  an  initial  acidity;  the  other  making  milk  permanently  acid. 

Of  B.  paratyph'osus  B  several  varieties  have  been  described  by 
Castellani,  Alcock,  and  others.  As  regards  the  so-called  B.  para- 
typhosus  C,  this  term,  used  by  several  observers,  among  whom 
recently  Hirschfeld,  covers  different  germs,  one  ot  which  is  sero- 
logically identical  with  B.  aertrykc. 

With  regard  to  the  B.  typhosus  of  Eberth,  it  is  found  in  the  intes- 
tine, not  merely  during  the  attack  of  fever,  but  during  the  incuba- 
tion, and  for  a  period  extending  perhaps  as  long  as  thirty  years 
alter  an  attack — that  is  to  say,  the  bacillus  has  been  grown  from  the 
faeces  of  a  person  thirty  years  after  an  attack  of  enteric  fever;  but 
whether  it  had  existed  in  the  bowels  for  the  whole  period  is  naturally 
not  known,  but  it  is  possible.  In  other  words,  the  bacillus  can  live 
in  the  bodies  of  people  for  years  after  an  attack.  These  people 
are  reservoirs  or  carriers  of  the  bacillus,  and  may  be  called  intes- 
tinal carriers.  People  who  pass  the  bacilli  in  their  faeces  during 
the  period  of  incubation  are  called  precocious  intestinal  carriers  ; 
the  patients  passing  the  bacilli  during  the  attack  and  convalescence 
are  called  acute  intestinal  carriers  ;  while  people  who  continue  to 
pass  the  bacilli  in  their  fasces  for  a  year  or  less  than  a  year  after 
an  attack  of  enteric  fever  are  called  temporary  or  transitory  intes- 
tinal carriers  ;  and  those  in  whose  faeces  the  bacilli  are  found  after 
an  interval  of  longer  than  a  year  are  called  chronic  intestinal  carriers. 

In  addition,  there  are  carriers  who  are  not  known  to  have  had 
an  attack  of  typhoid;  that  is  to  say,  there  may  be  people  in  whom 
the  B.  typhosus  Eberth  may  live  for  an  unknown  period  without 
showing  any  pathological  signs  at  any  time.  These  are  known  as 
paradoxical  intestinal  carriers.  This  is  possible,  but  it  is  also  prob- 
able that  some  of  the  carriers  in  question  may  have  been  cases  of 
ambulatory  typhoid,  and  therefore  really  belonged  to  the  class  of 
chronic  intestinal  carriers.  As  to  the  habitat  of  the  bacilli  while 
in  the  carrier,  it  seems  that  the  gall-bladder  is  of  the  greatest 
importance,  while  during  the  actual  attack  of  fever  the  bacilli  are 
to  be  found  not  merely  in  the  intestinal  contents,  but  also  in  the 
mesenteric  glands,  the  spleen,  and  the  circulating  blood.  Now, 
the  proportion  of  female  carriers  to  male  carriers  is  as  five  is  to  one. 
This  is  a  curious  fact,  and,  moreover,  the  bacillus  is  often  found  in 
the  gall-bladder.  Now,  the  frequency  of  gall-stones  in  women  as 
compared  with  men  is  as  three  is  to  one;  further,  it  is  a  well-known 
fact  that  gall-stones  are  often  discovered  for  the  first  time  at  an 
autopsy;  in  fact,  it  is  believed  that  only  10  per  cent,  of  the  persons 
suffering  from  gall-stones  show  any  sign  of  the  disease  during  life, 
and  it  is  a  curious  fact  that  the  percentage  of  persons  showing  signs 
of  gall-stones  after  an  attack  of  enteric  fever  is  14  per  cent. 

All  these  factors  considered  together,  along  with  the  known  fact 
that  B.  typhosus  has  been  isolated  on  several  occasions  from  the 


136S        THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

centre  of  gall-stones  removed  by  surgical  operations,  tend  to 
support  the  view  that  the  gall-bladder  is,  at  all  events  in  some 
cases,  the  home  of  the  B.  typhosus  in  a  chronic  carrier.  Fornet, 
in  1909,  has,  however,  stated  that  he  believes  the  bacilli  found 
in  the  faeces  of  a  carrier  are  not  descended  from  those  which  caused 
the  attack  of  fever,  but  are  derived  from  a  reinfection  which  does 
not  produce  any  clinical  symptoms,  because  the  human  host  has 
attained  a  tolerance  to  the  parasite,  which  therefore  leads  a  sapro- 
phytic existence,  presumably  in  the  lumen  of  the  intestines. 

The  discharge  of  bacilli  by  means  of  the  faeces  appears  to  be  inter- 
mittent, and  not  continuous,  which  is  a  most  important  fact,  as 


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CUDINS I  JUNE 

Fig.  658 


Curves  illustrating  Number  of  Flies  and  Cases  of  Enteric 
Fever.     (After  C.  J.  Martin.) 


the  duration  of  the  possible  intermission  is  not  positively  known, 
and  therefore  it  is  difficult  to  say  definitely  when  the  carrier  is  really 
clear  of  the  parasite. 

The  reason  why  women  are  more  commonly  carriers  than  men  is 
said  to  be  due  to  the  loss  of  resisting  power  brought  about  by  the 
decrease  in  the  alexins  of  the  blood  during  the  menstrual  and 
puerperal  periods,  and  this  is  supported  by  the  fact  that,  while  the 
incidence  of  enteric  fever  is  greater  in  females  from  fifteen  to  twenty 
years  of  age,  the  possibility  of  becoming  a  chronic  intestinal  carrier 
increases  steadily  from  the  fifteenth  to  the  forty-fifth  year.  A 
more  probable  reason  seems  to  us  to  be  that  women  arc  more  liable 
than  men  to  affections  of  the  gall-bladder. 


/ETIOLOGY  1369 

With  regard  to  age,  it  appears  that  the  transitory  carriers  arc 
generally  young — five  to  twenty  years  of  age — while  the  chronic 
carriers  are  usually  old — thirty  to  forty-five  years  of  age. 

The  greatest  inf  ectivity  of  a  carrier  is  during  the  incubation  period, 
and  the  first  weeks  of  the  attack  of  fever;  but  chronic  carriers  are 
important  in  producing  the  endemicity  of  enteric  fever  in  houses, 
groups  of  houses,  and  streets,  as  well  as  in  institutions,  etc. 

As  to  the  method  of  infection  of  the  healthy  by  the  carrier, 
evidence  is  being  produced  in  favour  of  food  contamination.  So 
far,  the  evidence  produced  in  favour  of  milk  contamination  by 
carriers  is  very  strong,  and  it  is  quite  possible  that  water,  dust, 
fomites,  etc.,  will  all  in  course  of  time  be  shown  to  often  obtain 
their  inf  ectivity  from  carriers. 

The  question  of  the  infection  of  the  house-fly  {M  it  sea  domestica) 
by  means  of  the  bacilli  in  the  faeces  of  carriers  is  most  important, 
because  the  fly  may  take  the  bacilli  into  its  crop  or  alimentary  canal, 
where  they  not  merely  increase  in  amount,  but  also  increase  in 
virulence.  Moreover,  according  to  Nicoll's  work,  it  is  probable  that 
larvae  may  become  infected,  and  this  infection  pass  to  the  adult 
insect.  The  mouth-part  of  the  fly  consists  of  a  proboscis  (vide 
Fig.  469)  with  oral  lobes  provided  with  tubules,  so  that  solid 
particles  and  liquids  pass  up  readily.  It  is  a  matter  of  everyday 
observation  that  the  house-fly  apparently  tastes  everything  on 
which  it  settles— that  is  to  say,  it  extends  its  proboscis  and 
presses  on  the  substance  on  which  it  is  standing  by  means  of 
its  oral  lobes.  When  this  proceeding  is  carefully  examined,  it  is 
seen  that  the  fly  is  regurgitating  a  little  fluid  from  its  crop  via  the 
pseudo-tracheae  of  the  oral  lobes  on  to  the  solid  substance,  with  the 
view  of  attempting  to  dissolve  some  of  the  solid  substance  so  that 
it  may  be  able  to  pass  readily  along  the  minute  pseudo-tracheae. 
This  simple  act  is  of  the  gieatest  importance  pathologically,  because 
the  house-fly  is  an  exceedingly  foul  feeder,  and  may  absorb  the  liquid 
from  the  faeces  of  a  case  of  enteric  fever  or  from  those  of  a  carrier. 

In  this  way  the  bacilli  enter  its  crop,  only  to  be  extruded  on  to 
sugar,  bread,  milk,  meat,  the  rim  of  a  cup,  etc.,  and  in  this  way  to 
gain  entrance  to  the  human  victim.  Naturally,  the  presence  of 
carriers  increases  greatly  the  opportunity  for  the-infection  of  flies. 
But  it  is  not  merely  by  the  mouth  that  the  fly  can  infect  food 
materials  and  utensils,  but  also  by  means  of  its  faeces;  for  the  fly 
defaecates  very  frequently,  and  the  typhoid  bacilli  can  pass  from 
its  alimentarv  canal  in  an  enhanced  condition  of  virulence — accord- 
ing to  some  authors — on  to  food,  drink,  or  utensils,  and  so  reach  the 
human  host. 

Intestinal  carriers  are  not  the  sole  carriers  of  the  enteric  germs, 
for,  though  more  rarely,  the  bacilli  can  escape  in  the  urine  of  people 
who  have  recovered  from  enteric:  these  people  are  called  urinary 
carriers.  It  is  not  uncommon  to  find  bacilli  in  both  the  faeces  and 
the  urine  in  the  case  of  transitory  carriers,  but  it  is  much  more 
uncommon  to  find  them  in  the  fasces  and  the  urine  in  the  case  of 


137°       THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

chronic  carriers  if  precautions  are  taken  to  prevent  the  contamina- 
tion of  the  urine  during  or  after  micturition. 

In  urinary  carriers  the  B.  typhosus  has  its  habitat  generally  in 
the  renal  pelvis,  which  is  usually  chronically  inflamed  or  cystic,  and 
it  has  also  a  secondary  habitat  in  the  chronically  inflamed  bladder; 
but  it  appears  possible  that  it  may  also  live  in  recesses  in  the  pelvis 
of  the  kidney,  the  bladder,  the  urethra,  the  prostate,  and  the 
vesiculae  seminales,  from  which  bacilli  pass  into  the  urine.  The 
methods  of  urine  infectivity  are  the  same  as  faecal  infectivity. 

To  summarize,  the  reservoir  or  carrier  of  theB.  typhosus  Eberth  is  a 
human  host  who  has  suffered  from  enteric  fever,  and  who  affords  food 
and  protection  for  the  bacilli  in  the  gall-bladder  in  ihe  case  of  intes- 
tinal carriers,  or  in  some  recess  or  recesses  in  the  urinary  tract  from 
the  pelvis  of  the  kidney  downwards,  and  in  the  male  in  the  prostate 
and  vesiculae  seminales  in  the  case  of  urinary  carriers.  This  carrier 
passes  the  bacilli  into  the  exterior  in  the  faeces  and  urine,  and  these 
may,  in  cases  of  defective  hygienic  surroundings,  directly  infect  air, 
food,  or  drinking-water,  or  may  be  conveyed  by  fomites  or  by  flies 
to  the  victim's  hands,  or  food,  or  food  utensils. 

The  problem  of  the  carriers  of  the  paratyphoid  bacilli  is  a  similar 
one.  B.  paratyphosus  B  is  commonly  met  with  in  Europe,  where 
it  is  disseminated  by  means  of  intestinal  carriers  when  it  lives 
in  the  gall-bladder;  but  its  urinary  carriers  have  so  far  not  been 
recognized.  It  has,  however,  been  found  in  the  common  house-fly 
in  191 1  by  Nicoll.  Its  infectivity  and  its  auto-infectivity  are  well 
known.  B.  paratyphosus  A  is  prevalent  in  India  and  Ceylon, 
where  precocious  and  acute  carriers  are  frequently  met  with.  The 
germ,  however,  during  the  war  has  now  become  common  also  in 
Europe.  It  is  known  that  it  can  live  in  the  gall-bladder  for  a  con- 
siderable time  and  pass  out  in  the  faeces,  and  several  outbreaks  of 
enteric  fever  have  been  traced  to  this  source. 

With  regard  to  the  general  question  of  carriers,  the  persons  most 
liable  to  be  carriers  are  first  of  all  those  who  have  had  attacks  of 
enteric  fever,  and,  secondly,  nurses  and  other  attendants  upon 
these  patients;  while  the  carrier  who  is  likely  to  prove  most  dan- 
gerous in  spreading  the  infection  is  a  person  who  is  in  any  way 
engaged  in  the  preparation  or  the  handling  of  food  intended  for 
other  people  to  consume,  because  the  infection  of  the  hands  is  a 
prolific  source  of  infection  for  healthy  people. 

So  far  we  have  merely  referred  to  Musca  domestica  Linnaeus  as 
an  important  intermediary  host  for  these  bacilli,  but  the  fruit -fly, 
Drosophila  ampelopJiila  Loew,  has  been  definitely  implicated  by 
Dutton  in  1909.  With  regard  to  the  accusations  against  the  bug, 
Clinocoris  lectularius  Linnaeus,  and  the  flea,  it  can  only  be  said  that 
there  is  as  yet  no  definite  proof  that  they  play  an  active  part  in  the 
spread  of  enteric  fever. 

To  summarize,  it  may  be  stated  that  B.  typhosus,  B.  paratyphosus 
A,  and  B.  paratyphosus B  can  escape  from  the  bodies  of  precocious, 
acute,  temporary,  chronic,  or  paradoxical  carriers  by  means  of  the 


ETIOLOGY  1 371 

feces  or  the  urine,  and  can  infect  food  and  drink  directly  or  in- 
directly through  the  agency  of  flies,  and  by  means  of  this  infected 
food  or  infected  hands  the  bacilli  can  gain  entrance  into  another 
human  host,  and  set  up  the  infection  anew.  Of  the  foods  and  drinks 
which  are  of  importance,  the  first  and  most  important  is  milk,  while 
water,  shellfish,  fish,  and  dried  fish,  may  also  be  mentioned  as  of 
great  importance.  Attacks  have  also  been  traced  to  ice,  and, 
indeed,  no  food  or  cooking  utensil  can  be  considered  free  from 
possible  infection.  Of  great  importance  in  the  tropics  are  un- 
cooked green  vegetables,  which  are  grown  in  gardens  often  manured 
by  means  of  human  excrement.  FaecaUy  polluted  dust  and  faecally 
polluted  clothes  must  also  be  assigned  a  prominent  place  in  connec- 
tion with  the  spread  of  the  disease. 

With  regard  to  the  epidemicity  of  enteric  fever,  it  will  be  clearly 
understood  that  the  basis  of  the  epidemic  as  the  basis  of  the  endemic 
is  the  carrier,  but  the  characters  of  the  epidemic  will  largely  depend 
upon  the  means  by  which  the  bacilli  are  introduced  into  the  new 
non-immune  hosts.  Often  this  is  by  flies;  hence  the  name  '  autum- 
nal fever  '  sometimes  applied  to  the  disease,  because  the  local  epi- 
demic takes  place  after  the  time  of  their  greatest  prevalence. 
Epidemics  due  to  milk  will  be  found  to  agree  with  the  distribution 
of  this  food  by,  generally,  one  dairy.  The  present  writers  once, 
during  an  outbreak  of  enteric  fever  and  dysentery  in  a  tropical 
town,  bought  by  chance  a  sample  of  milk  which,  on  investigation, 
was  found  to  contain  the  B.  coli — a  sure  proof  of  human  faecal 
contamination,  which  might  have  arisen  from  watering  the  milk, 
because  water  is  often  added  by  the  seller  to  the  milk  of  Bos  indicus, 
and  this  escapes  the  notice  of  the  buyer,  because  the  milk  is  much 
richer  than  that  of  Bos  taurus,  and  therefore  does  not  appear  to  be 
diluted.  As  the  water  may  have  come  from  some  polluted  source — 
e.g.,  a  well  or  a  roadside  drain — this  is  very  dangerous.  Epidemics 
due  to  oysters  and  other  shellfish  will  agree  with  the  seasonal  use 
of  these  shellfish,  and  may  even  be  traced  to  certain  breeding- 
grounds  which  may  be  situate  near  the  mouth  of  a  sewer,  or  in 
which  the  oyster-bed  itself  has  become  infected  with  bacilli. 
Another  good  instance  of  the  cause  of  small  epidemics  is  the  tracing 
of  the  infection  by  Hamer  to  the  fried-fish  shops  so  common  in 
London.  But  the  infection  of  food  materials  will  not  give  rise  to 
the  sudden  widespread  epidemic  which  will  arise  if  the  water-supply 
is  contaminated.  Maidstone,  in  1896,  had  35,000  inhabitants,  of 
whom  1,900  persons  suffered  from  enteric  fever  during  the  months 
of  September,  October,  and  November,  due  to  contamination  of  the 
town's  water-supply.  In  the  tropics  polluted  wells  are  a  prevalent 
cause  of  endemic  and  epidemic  enteric  fever.  The  present  writers 
were  acquainted  with  a  town  in  which  so-called  '  remittent,'  really 
typhoid,  fever  was  very  prevalent,  and  where  in  a  certain  area  the 
wells  and  the  cesspits,  which  always  contained  water,  were  only 
separated  by  a  wall  one  brick  thick. 

The  bacilli  do  not  live  when  dried;  still,  it  is  probable  that  they 


1372        THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

can  live,  attached  to  particles  of  dust,  long  enough  to  contaminate 
food,  which  in  certain  tropical  regions  may  become  covered  with 
dust. 

Predisposing  Causes. — With  regard  to  predisposing  causes,  it  was 
long  considered  that  the  native  of  the  tropics  enjoyed  a  partial  or, 
as  some  said,  an  absolute  immunity  against  enteric  fever.  This 
cannot  be  maintained,  as  we  know  definitely  that  enteric  fever 
is  quite  common  in  all  races.  The  position  at  the  present  time  is 
that,  while  certain  authorities  consider  that  a  considerable  number 
of  cases  of  enteric  fever  still  lie  hidden  under  the  terms  '  remittent 
fever  '  and  '  simple  continued  fever,'  and  perhaps  '  febricula,'  as 
applied  to  natives,  and  especially  to  native  children,  who  are  not 
often  treated  by  physicians  trained  in  modern  methods,  still,  there 
are  others  who  maintain  that  there  is  a  partial  immunity  in  some 
races — e.g.,  such  an  immunity  is  said  to  exist  among  the  native 
Egyptians,  Sudanese,  and  Japanese,  which  is  believed  to  be  due  to 
racial  inheritance.  This  question  has  been  investigated  by  the 
Board  for  the  Study  of  Tropical  Diseases  in  the  Philippine  Islands, 
and  ably  reported  by  Chamberlain,  who  finds  that  epidemics  of 
great  severity  among  Filippinos  are  rare  or  unnoticed;  that  Widal 
reactions  performed  on  the  blood  of  591  healthy  Filippinos  suggest 
a  comparatively  recent  attack  of  enteric  fever  in  about  6  per  cent, 
of  adults,  but  do  not  indicate  that  the  disease  is  prevalent  in  child- 
hood; that  the  native  Filippino  scouts  show  a  lower  typhoid  rale 
than  the  white  troops,  possibly  due  to  failure  to  diagnose  the 
atypical  cases;  that  more  than  one-third  of  the  cases  of  enteric 
fever,  whether  among  Americans  or  Filippinos,  are  entirely  atypical, 
and  cannot  be  diagnosed  without  laboratory  methods.  One-half 
of  the  total  number  of  cases  can,  however,  be  diagnosed  clinically, 
and  do  not  differ  from  enteric  fever  as  seen  in  the  Temperate  Zone. 
He  concludes  that  much  work  still  needs  to  be  done  among  the 
natives  to  estimate  the  actual  amount  of  mild  and  atypical  enteric 
fever  which  is  occurring,  and  to  determine  why  extensive  and 
destructive  epidemics  are  not  more  often  seen. 

Our  own  experience  in  Ceylon  causes  us  to  believe  that  the  disease 
is  very  prevalent  among  the  natives  of  that  island,  and  as 
dangerous  among  them  as  in  Europeans.  When  the  causes  of 
death  in  the  races  of  Ceylon  were  considered  by  us  some  years 
ago,  it  was  noted  that  the  total  deaths  contained  the  following 
percentages: 


Race.  Enteric  Fever.  Simple  Fever.        Remittent  Fever. 


Per  Cent.  Per  Cent.  Per  Cent. 
European  . .          . .                  io-i                             1-7  1*5 

Sinhalese    ..  ..  7-6  12-0  0-3 

Tamils        ..  ..  0-7  17*3  3-8 


PREDISPOSING  CAUSES  1373 

Added  together,  these  give — Europeans,  13-3  per  cent.;  Sin- 
halese, ig»9  per  cent.;  Tamils,  218  per  cent.  The  incidence  of 
enteric  fever  among  these  peoples  is  probably  more  nearly  approxi- 
mating the  conjoint  figures  than  those  given  solely  under  Enteric 
Fever.  Tamils  are  labourers  on  estates,  and  cases  of  fever  among 
them  are  generally  lumped  together  under  the  heading  of  Malaria. 

Age  is  another  predisposing  cause,  for  there  appears  to  be  a 
general  consensus  of  opinion  that  twenty  to  twenty-five  years  of 
age  is  a  period  more  susceptible  to  the  disease  than  the  other 
periods  of  life,  but  no  age  period  is  free  from  attacks. 

During  the  first  journey  from  the  Temperate  Zone  to  the  tropics 
the  metabolism  of  the  young  resident  in  the  Temperate  Zone  is 
possibly  somewhat  disturbed,  leading  to  a  weakening  in  the  anti- 
bacterial and  phagocytic  reactions,  as  some  authorities  maintain; 
and  hence,  perhaps,  his  great  liability  to  attacks  of  enteric  fever 
and  other  complaints.  It  must  not  be  forgotten  that  the  young 
new  arrival  is  apt  to  eat  too  much,  to  drink  too  much,  and,  being 
stimulated  by  the  heat — the  bad  effects  of  which  at  first  he  does 
not  notice — is  apt  to  work  too  hard  and  play  too  hard,  or,  in  other 
words,  to  attempt  to  exhaust  his  system  in  every  possible  way, 
and  to  thoroughly  disregard  the  evil  effects  of  the  sun ;  and  we  con- 
sider these  indiscretions  play  a  certain  role  in  the  relative  frequency 
with  which  these  young  new  arrivals  become  infected. 

Young  people  often  live  together  in  what  are  called  '  chummeries  ' 
— i.e.,  several  of  them  live  together  in  a  house,  while  one  of  them 
runs  the  messing.  These  houses,  having  no  proper  supervision,  are 
allowed  to  become  most  insanitary,  especially  with  regard  to  the 
servants'  quarters,  which  are  naturally  the  nearest  to  the  kitchen 
and  the  places  in  which  food  is  stored.  The  pollution  of  food  in 
these  places  is  often  self-evident  to  the  naked  eye,  while  the  whole 
place  teems  with  flies.  Moreover,  the  weakening  of  the  system  by 
venereal  disease  may  play  a  part  in  producing  the  heavy  incidence 
of  enteric  fever  in  new  arrivals.  In  Bengal  50  per  cent,  of  the  cases 
in  Europeans  occurred  within  one  year  of  arrival  from  Europe. 

In  India  the  disease  is  believed  to  be  common  among  native 
children  and  among  Europeans  born  in  India;  thus  it  was  noticed 
by  Rogers  that  41-67  per  cent,  of  the  cases  were  under  fifteen  years 
of  age,  whereas  in  Europe,  and  America  only  945  of  cases  are  under 
fifteen  years  of  age. 

As  regards  sex,  we  have  already  drawn  attention  to  the  apparently 
special  incidence  upon  women  between  fifteen  to  forty-five  years 
of  age. 

With  regard  to  the  conditions  of  life,  the  poor  whites  living  in 
insanitary  conditions  are  very  liable  to  be  attacked,  and  this  may 
account  for  the  prevalence  of  the  disease  among  Europeans  born 
and  living  in  India,  as  may  the  natural  habits  of  children  playing 
among  earth  and  rubbish,  which  are  often  more  or  less  foecally 
polluted.  But  of  all  predisposing  causes,  that  of  bad  sanitation 
stands  out  pre-eminently  fust;  thus  Europeans  are  apt  to  get  the 


1374       THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

disease  most  commonly  in  the  dry  season,  when  it  is  spread  by  dust 
and  flies,  and  the  natives  in  the  wet  season,  when  it  may  be  due  to 
water  contamination. 

With  regard  to  meteorological  conditions,  we  have  observed  that 
anything  which  prevents  the  heavy  rainfall  at  the  proper  season 
tends  to  an  increase  in  the  enteric,  dysentery,  etc.,  rates;  and, 
absurd  though  it  may  read,  certain  observations  which  we  made 
some  years  ago  led  us  to  believe  that  the  eruption  of  Mount  Pelee 
may  have  had  a  disturbing  effect,  upon  the  meteorological  con- 
ditions, producing  less  rainfall,  and  preventing  the  filthy  drains  and 
other  places  being  properly  flushed,  and  thus  indirectly  causing 
an  increased  incidence  of  epidemic  intestinal  diseases. 

Pathology. — Enteric  fever  is  a  septicemia  which  is  produced  by 
the  bacilli  already  mentioned  entering  the  body  by  the  mouth,  and 
passing  into  the  small  intestine  and  colon,  the  lymphoid  tissue  of 
which  they  invade.  In  this  tissue  they  increase  in  number,  and 
pass  via  the  lymphatics  to  the  abdominal  lymphatic  glands  and 
spleen,  in  all  of  which  they  multiply.  No  doubt  they  very  soon 
reach  the  blood,  but  are  probably  quickly  destroyed  and  their  toxins 
neutralized,  and  so  long  as  this  continues  the  patient  is  without 
definite  signs  of  the  disease.  This  constitutes  '  the  period  of  in- 
cubation '  or  latency,  and  may  possibly  be  the  explanation  of  those 
persons  who,  though  chronic  carriers  of  virulent  typhoidal  germs, 
maintain  that  they  themselves  have  never  had  any  illness. 

If  the  quantity  of  antitoxin  substances  produced  are  only  suffi- 
cient barely  to  neutralize  the  toxins,  then  an  ambulatory  or  an 
abortive  attack  may  ensue. 

When,  however,  the  bacilli  multiply  in  such  numbers  that, 
though  still  largely  destroyed  by  the  bacteriolysins  of  the  blood, 
there  is  insufficient  antitoxin  to  neutralize  their  liberated  toxins, 
then  the  fever  begins.  The  possible  explanation  of  the  intermittent 
type  of  the  fastigium  of  the  tropics  is  that  the  supply  of  antitoxic 
substances  in  the  blood  waxes  and  wanes.  The  evidence  in  favour 
of  the  above  theory  is  the  presence  of  the  bacilli  in  the  faeces  in  the 
incubation  period,  the  presence  of  enlarged  Peyer's  patches, 
mesenteric  glands  and  spleen  found  accidentally  in  post-mortem 
examinations  of  people  who  have  died  from  other  causes,  and  in 
whom  enteric  fever  was  not  suspected;  the  possibility  of  cultivating 
the  bacilli  from  specimens  of  the  circulating  blood  obtained  during 
the  first  week  of  the  fever;  and  the  constant  necessity  for  immediate 
dilution  of  this  blood  if  a  successful  culture  is  to  be  obtained. 

Relapses  can  be  explained  as  being  due  to  any  cause  which  so 
disturbs  the  metabolism  of  the  body  that  the  antitoxin  production 
decreases,  and  the  germs  again  gain  entrance  to  the  blood  in  such 
quantity  as  to  produce  fever. 

The  endotoxin  contained  in  the  bacilli  has  a  markedly  stimulant 
effect  upon  endothelial  cells,  causing  them  to  swell  and  to  block 
small  lymph  capillaries,  thus  causing  patches  of  focal  necrosis  in  the 
liver. 


PATHOLOGY— MORBID  ANATOMY  1375 

The  bacilli  can  occur  in  any  part  of  the  body,  but  they  have  a 
predilection  for  the  lymphatic  system.  When  arrested  in  the  lym- 
phatics of  the  skin,  they  give  rise  to  the  rose-coloured  maculo- 
papules  so  characteristic  of  the  disease.  The  appearance  and  dis- 
tribution of  these  red  maculo-papules  in  the  skin  of  the  anterior 
abdominal  wall,  chest,  and  back  is  believed  by  Greenhalgh  to  agree 
with  the  cutaneous  distribution  of  the  nerves  which  supply  the 
small  intestine,  the  mesenteric  lymph  nodules,  and  the  spleen.  But 
this  seems  hardly  possible,  as  papules  can  appear  on  the  arms,  legs, 
and  other  regions.  It  would  appear  as  though  local  heat  was  a 
more  important  factor  in  their  production  than  nerve-supply.  The 
bacilli  may  attack  the  respiratory  system,  giving  rise  to  bronchitis, 
pneumonia,  etc.,  and  they  are  commonly  found  in  the  gall-bladder, 
in  which  they  cause  cholecystitis,  and  may  give  rise  to  gall-stones. 
They  also  pass  through  the  kidney  into  the  urinary  passages,  and 
at  times  appear  in  large  quantities  in  the  urine  (bacilluria). 

They  are  also  capable  of  living  locally  in  the  tissues,  giving  rise  to 
inflammation,  abscess  formation,  and  local  death  of  the  tissue. 

It  has  already  been  noted  that  they  can  live  for  years  in  the 
gall-bladder  and  the  pelvis  of  the  kidney,  producing  the  chronic 
intestinal  and  urinary  carriers,  who  are  liable  to  infect,  not  merely 
themselves,  but  others  also. 

Auto-infection  may  possibly  be  the  explanation  of  such  cases  as 
have  second  or  even  third  attacks,  within  a  short  period  after  the 
first  attack. 

The  typical  gradual  onset  of  the  disease  may  be  explained  by  the 
struggle  between  the  antitoxins  of  the  body  and  the  bacterial  toxins. 

The  occasional  sudden  onset  seen  especially  in  the  tropics  may  be 
due  to  lowered  resistance,  owing  to  many  causes — e.g.,  climatic  in- 
fluences, other  infections,  etc. 

Immunity  is  generally  acquired  after  an  attack,  but  second 
attacks  are  by  no  means  rare;  moreover,  the  immunity  is  homo- 
logous— viz.,  an  attack  of  typhoid  fever  will  protect  against  B. 
typhosus,  but  not  against  the  paratyphoid  bacilli. 

The  fever  is  due  to  a  lessened  loss  of  heat  rather  than  to  an  in- 
creased production  of  heat,  and  this  is  the  reason  why,  in  ordinary 
cases,  there  may  not  be  marked  emaciation. 

Morbid  Anatomy. — On  opening  the  abdomen  in  a  typical  post- 
mortem, the  bowels  will  usually  be  seen  to  be  distended  with  gas, 
and  the  small  intestine  will  be  noticed  to  present  marked  areas  of 
congestion,  especially  near  the  ileo-caecal  junction. 

The  mesenteric  glands  will  be  observed  to  be  enlarged  and  con- 
gested, as  will  the  spleen  and  at  times  the  liver.  If  there  has 
been  a  perforation,  a  faecal  odour  will  be  perceived  on  opening  the 
abdomen,  and  there  may  be  gas,  faecal  matter,  round  worms,  or  pus 
in  the  peritoneal  cavity,  while  careful  search  will  reveal  the  perfora- 
tion; but  care  must  be  taken  not  to  artificially  perforate  the  gan- 
grenous, or  almost  gangrenous,  intestinal  wall  by  manipulation. 

On  opening  the  intestines,  it  will  be  noted  that  the  most  important 


1376        THE  ENTEROIDEA  GROUP  OF  TROPICAL  FEVERS 

site  of  disease  is,  as  already  stated,  in  the  ileum  near  the  ileo-caecal 
valve;  while  the  contents  of  the  bowel  will  be  noted  to  be  of  a 
yellowish  colour,  unless  there  has  been  a  haemorrhage,  when  blood 
will  be  seen,  or  unless  medicines  have  been  administered  which 
alter  the  colour  of  the  motions.  The  Peyer's  patches  in  the  lower 
few  feet  of  the  ileum  will  be  enlarged,  prominent,  and  whitish  in 
colour,  and  covered,  perhaps,  with  yellowish  sloughs,  or  perhaps 
containing  ulcers,  which  may  be  in  the  form  of  one  large  central  or 
several  small  ulcers. 

On  inspection,  a  typical  ulcer  will  be  noted  to  have  its  long  axis 
in  the  same  direction  as  the  long  axis  of  the  bowel,  to  be  of  ovai 
form,  with  thin  and  undermined  edges,  and  a  base  formed  from  the 
muscularis  mucosae,  the  infiltrated  submucosa,  or  from  the  muscular 
or  even  the  peritoneal  coats  of  the  bowel;  while  in  cases  of  perfora- 
tion a  rent  may  be  noticed  through  this  last  coat,  permitting  com- 
munication between  the  lumen  of  the  bowel  and  the  cavity  of  the 
peritoneum.  In  cases  of  extensive  haemorrhage  injection  of  water 
into  the  carefully  dissected  out  mesenteric  artery  may  demonstrate 
more  or  less  correctly  the  source  of  the  bleeding.  The  solitary  glands 
will  also  be  seen  to  be  enlarged  and  congested  with  sloughs  or 
roundish  ulcers,  while  the  mucosa  around  these  and  the  Peyer's 
patches  will  be  seen  to  be  intensely  congested  and  red  in  colour. 
This  congestion  may  be  traced  for  a  considerable  distance  along  the 
ileum  and  into  the  jejunum,  but  it  is  rare  to  find  the  duodenum  or 
the  gastric  mucosa  in  a  state  of  acute  congestion. 

Tracing  the  bowel  downwards  into  the  ascending  colon,  it  will  be 
noticed  that  the  mucosa  of  the  caecum  and  ascending  colon  is  often 
congested,  and  at  times  the  solitary  glands  will  be  seen  to  be  swollen; 
but  as  a  rule  they  are  not  ulcerated. 

These  typical  appearances  may  be  varied  by  finding  only  one  or 
two  Peyer's  patches  enlarged,  and  perhaps  only  one  or  two  small 
ulcers,  and  very  rarely  there  may  be  no  signs  beyond  a  catarrhal 
inflammation  of  the  mucosa  of  the  bowel.  On  the  other  hand,  the 
ulceration  in  the  region  of  the  ileo-caecal  junction  may  be  so  exten- 
sive that  there  are  only  ridges  and  islands  of  intensely  congested 
mucosa  left,  while  at  other  times  pieces  of  the  bowel  may  be  black 
and  almost  or  quite  gangrenous. 

The  mesenteric  glands  will  be  seen  to  be  swollen  and  congested, 
and  on  section  they  will  show  marked  congestion  and  perhaps  pus. 

The  spleen  is  enlarged  and  swollen,  dark  red  in  colour,  friable, 
with  a  tense  capsule,  while  the  liver  may  also  be  enlarged  and  con- 
gested, and  may  even  on  rare  occasions  show  multiple  abscesses 
brought  about  by  a  septic  pylephlebitis.  The  gall-bladder  and 
biU '-ducts  may  be  congested,  or  more  rarely  may  contain  pus,  while 
the  bile  is  usually  light-coloured  and  watery,  but  may  be  inspissated. 
The  pancreas  is  usually  normal,  but  we  have  seen  it  congested  and 
even  hemorrhagic.  The  suprarenal  capsules  are  generally  normal 
in  uncomplicated  cases.  The  kidneys  are  usually  enlarged  and 
congested,  with  a  capsule  which  strips  off  readily.     On  section,  both 


morbid  anatomy  1377 

cortex  and  medulla  are  seen  to  be  congested,  with  often  fatty 
degeneration,  and  more  rarely  small  abscesses  or  infarcts.  The 
pelvis  is  congested,  but  the  ureter  and  bladder  are  usually  normal, 
though  signs  of  cystitis  may  be  found  at  times. 

With  regard  to  the  thorax,  if  there  is  much  meteorism,  the  dia- 
phragm may  be  noted  to  be  pushed  up  considerably  higher  than 
usual.  The  trachea  and  bronchi  may  show  signs  of  inflammation, 
and  in  the  lung  pneumonia,  hemorrhagic  infarcts,  pyemic  abscesses, 
and  purulent  infarcts  may  be  seen.  The  heart  is  usually  flabby  and 
without  any  sign  of  rigor  mortis,  and  is  often  pale,  soft,  and  friable, 
from  fatty  degeneration.  Rarely  will  vegetative  or  ulcerative  endo- 
carditis or  aortitis  be  found. 

In  the  neck  the  thyroid  gland  may  in  cases  of  great  rarity  be 
seen  to  be  enlarged,  and  even  to  have  abscesses.  There  may  be 
congestion  and  dlceration  of  the  larynx  and  tonsils,  but  they  are  not 
common  in  our  experience.  The  tongue  will  be  seen  to  be  covered 
with  sordes,  and  may,  perhaps,  show  fissures. 

The  brain  is  often  congested,  as  are  the  meninges,  but  meningitis 
and  other  naked-eye  signs  are  rarely  met  with.  Venous  and,  much 
more  rarely,  arterial  thrombosis  may  be  seen,  while  Zenker's 
vitreous  degeneration  may  be  found,  especially  in  the  adductors 
of  the  thigh,  the  rectus  muscles  of  the  abdomen,  the  pectoralis, 
and  the  diaphragm,  and  very  rarely  one  of  these  degenerated 
muscles  may  be  found  ruptured  and  surrounded  by  haemorrhages. 
The  bone-marrow  may  also  be  congested  and  show  signs  of  focal 
necrosis. 

Finally,  there  may  be  the  signs  of  the  complications  or  sequelae — 
as,  for  example,  the  arthritis  of  the  joints,  the  abscesses  in  various 
parts  of  the  body.  etc. 

The  pathological  history  of  these  post-mortem  appearances  may 
now  be  briefly  related,  beginning  with  the  history  of  the  lesions  of 
the  Peyer's  patches. 

At  first  a  Peyer's  patch  or  lymphoid  follicle  is  hyperaemic,  but 
this  is  followed  by  a  proliferation  of  the  lymphoid  and  epithelioid 
cells  of  the  follicles,  together  with  a  swelling  of  the  endothelial  cells 
of  the  capillary  vessels,  and  these  together  produce  a  more  or  less 
definite  blocking  of  the  capillary  vessels,  which  causes  an  anaemia, 
and  produces  the  whitish  colour  of  the  hyperplastic  Peyer's  patches, 
to  which  attention  has  already  been  drawn.  The  typical  bacilli 
can  be  found  lying  in  the  centre  of  the  follicle,  and  also  in  the  lym- 
phatic vessels,  not  merely  of  the  follicle,  but  also  of  the  submucosa. 
Such  is  the  condition  of  the  follicle  about  the  eighth  to  the  tenth 
day,  and  now  one  of  two  things  may  happen:  either  the  excess  of 
lymphoid  cells  undergo  fatty  degeneration  and  absorption,  with 
the  result  that  the  blood-flow  returns,  and  the  follicle  becomes 
normal;  or  the  blockage  of  the  bloodvessels  is  increased  by  fibrinous 
thrombosis,  with  the  result  that  the  superficial  portion  of  the 
swollen  follicle  dies  and  forms  a  slough,  which,  separating  from  the 
edges  towards  the  centre,  becomes  an  ulcer  some  time  during  the 

87 


1378        THE  ENTEROIDEA  GROUP  OF  TROPICAL  FEVERS 

second  week.  These  ulcers  may  increase  in  depth  by  an  extension 
of  the  necrosis,  and  may  lead  to  perforation;  on  the  other  hand, 
there  may  be  a  formation  of  granulation  tissue  over  the  base,  which 
subsequently  leads  to  fibrous  tissue  formation,  and  thus  eventually 
to  the  healing  of  the  ulcer,  which  process  is  completed  by  the  growth 
of  the  mucosa  over  the  young  fibrous  tissue.  The  site  of  a  previous 
typhoid  ulcer  is  often  clearly  visible  as  a  depressed  pigmented  area, 
which,  on  microscopical  examination,  is  seen  to  consist  of  atrophic 
mucosa  covering  a  fibrous  submucosa,  which  is  also  often  atrophic. 

The  mesenteric  glands  show  at  first  hyperaemia  and  cell  prolifera- 
tion, among  which  the  typical  bacilli  can  be  found.  Pus  formation 
may  also  be  found  at  times. 

The  spleen  early  becomes  hyperaemic,  and  swells  considerably, 
remaining  enlarged  until  the  third  or  fourth  week.  The  capsule 
becomes  tense,  and  the  pulp  assumes  a  dark  red  colour.  The 
swelling  is  due  to  the  hyperemia  and  cellular  infiltration  with  leuco- 
cytes, endothelial  cells,  and  macrophages,  among  which  the  typhoid 
bacilli  may  be  found.  During  the  third  week  the  pulp  becomes 
softer,  and  the  Malpighian  bodies  become  prominent,  and  absorption 
begins  to  take  place,  which  produces  a  paler  colour  in  the  pulp,  and 
eventually  leads  to  an  increase  in  the  amount  of  fibrous  tissue. 

The  liver  shows  cloudy  swelling  and  fatty  degeneration  of  the 
cells  and  spots  of  focal  necrosis,  which  may  be  produced  by  accumu- 
lations of  epithelioid  cells  in  the  lymphatic  spaces  of  the  portal 
system,  or  to  small  areas  of  necrosis  of  liver  cells  owing  to  occlusion 
of  adjacent  capillaries.  These  foci  are  associated  with  clumps  of 
the  specific  bacilli. 

The  kidneys  show  cloudy  swelling  of  the  cells  of  the  convoluted 
tubules,  but  in  the  cases  when  the  kidney  is  specially  involved  there 
may  be  considerable  hyperaemia,  together  with  perivascular  cellular 
exudation  and  granular  degeneration  of  the  cells  of  the  convoluted 
tubules. 

The  heart  muscle  may  show  fatty  or,  rarely,  waxy  degeneration, 
while  endarteritis  obliterans  in  the  small  arteries  is  said  to  be  seen 
in  cases  of  sudden  death  without  obvious  cause. 

In  the  nervous  system  there  are  no  very  marked  changes,  but 
pigmentation  of  the  ganglion  cells  and  leucocytic  infiltration  of  the 
perivascular  spaces  may  be  seen,  as  well  as  fatty  degeneration  of 
the  nerve  fibres. 

The  bone-marrow  is  generally  congested,  and  may  show  signs  of 
focal  necrosis,  with  hyperplasia  of  lymphoid  cells  and  clumps  of 
typhoid  bacilli. 

Symptomatology. — Enteric  fever  is  a  very  protean  disease,  the 
description  of  which  is  usually  divided  into  incubation  period, 
onset,  course,  subdivided  into  weeks,  relapses,  and  terminations  in 
death  or  convalescence.  In  general  terms,  it  may  be  stated  that 
the  fever  presents  physical  signs  and  symptoms  not  unlike  those 
seen  in  the  Temperate  Zone,  but  a  number  of  cases  are  atypical. 

These  atypical  cases  may  have  a  slight  and  short  attack  of  fever 


S  YMPTO  MA  TOLOG  Y  137^ 

presenting  but  few  symptoms,  and  very  liable  to  be  overlooked,  or 
the  attack  may  be  ushered  in  by  some  other  fever — as,  for  example, 
malaria  or  dengue.  We  will  first  describe  a  typical  attack  with 
mild  or  severe  symptoms. 

Incubation. — The  incubation  period  of  enteric  fever  ranges  in  its 
known  extremes  from  three  days  to  twenty-three  days,  or  much 
longer.  The  shortest  known  period — that  is  to  say,  the  one  with 
three  days'  incubation — was  exceptional,  the  infection  being  due  to 
swallowing  a  culture  of  virulent  bacilli,  and  therefore  it  may  be 
excluded  for  ordinary  purposes.  It  is  by  no  means  easy  as  a  rule 
to  define  the  incubation  period,  and  it  is  usual  to  agree  with  Murchi- 
son,  and  to  state  that  it  is  most  commonly  about  two  weeks  (ten  to 
fourteen  days),  but  that  it  is  often  less  than  this,  and  may  possibly 
be  as  short  as  four  or  five  days;  while,  on  the  other  hand,  it  is  often 
longer,  and  no  definite  maximal  limit  can  be  mentioned,  because 
the  study  of  typhoid  carriers  has  demonstrated  that  persons,  appar- 
ently in  good  health,  may  be  infected  with  the  bacillus,  and  it  has 
further  been  shown  that  these  people  may  suffer  from  auto-infection, 
all  of  which  naturally  complicate  the  question  of  the  duration  of 
the  period  of  incubation. 

We  therefore  conclude  that  the  usual  incubation  period  for  enteric 
fever  is  about  two  weeks. 

During  this  period  the  patient  may  apparently  show  no  signs  or 
symptoms  of  the  disease,  though  at  times  headache  and  general 
malaise  may  be  felt. 

Onset. — Typically  the  onset  is  gradual,  the  patient  attending  to 
his  ordinary  duties,  though  suffering  more  markedly  from  the 
feeling  of  malaise  and  lassitude  and  from  headache  than  during  the 
period  of  incubation,  and  associated  with  these  symptoms  there 
may  be  constipation,  or  there  may  be  diarrhoea  with  pains  in  various 
parts  of  the  body,  but  especially  in  the  back,  the  iliac  regions,  or 
the  legs.  At  times  there  is  a  troublesome  cough.  The  disinclina- 
tion for  exertion,  mental  or  bodily,  increases,  as  does  the  headache 
and  the  pains,  until  the  patient  feels  so  ill  that  he  consults  his 
medical  attendant,  when  it  is  found  that  the  temperature  is  raised 
above  normal  (ioo°  to  1010  F.  in  the  morning) ;  that  it  is  higher  in 
the  evening  (1030  to  1040  F.)  than  in  the  morning;  that  the  pulse, 
though  accelerated  (80  to  go  per  minute),  is  relatively  slow  as  com- 
pared with  the  temperature,  and  may  be  dicrotic ;  while  the  tongue 
is  coated  on  the  dorsum,  though  red  at  the  tip  and  along  the  margins; 
the  headache  is  generally  frontal,  and  there  may  be  thirst,  vomiting, 
or  epistaxis,  as  well  as  abdominal  tenderness  and  slight  distension, 
especially  in  the  right  iliac  region.  If  the  case  is  observed  early, 
a  step-like  rise  of  the  temperature  may  be  noted — that  is  to  say,  the 
evening  temperature  is  always  slightly  higher  than  that  of  the  pre- 
ceding evening — while  the  morning  remission  is  less,  until  about  the 
third  or  fourth  day,  when  the  temperature  reaches  1030  to  1050  F. 
at  night. 

The  onset,  however,  is  often  atypical  in  the  tropics,  the  symptoms 


1380       THE  ENTEROIDEA  GROUP  OF  TROPICAL  FEVERS 

being  but  little  marked,  and  the  patient,  though  feeling  wretched 
and  ill,  perseveres  with  his  work,  and  may  never  consult  a  doctor 
until  well  into  the  second  week  of  the  fever,  and  in  some  cases  may 
even  advance  farther  in  the  illness  than  this  before  the  complaint  is 
diagnosed. 

With  regard  to  the  other  atypical  onsets,  it  is  well  to  remember 
that  the  disease  is  a  septicaemia,  and  that,  following  the  account  of 
the  pathology  given  above,  any  organ  or  system  of  the  body  may 
be  specially  attacked.  Thus,  for  example,  the  nervous  system  may 
be  specially  attacked,  with  theresult  that  the  most  urgent  symptom 
is  a  neuralgia,  an  earache,  a  backache,  or  pains  resembling  those  of 
pleurisy;  or,  again,  there  may  be  signs  as  though  cerebro-spinal 
meningitis  were  coming  on,  or  there  may  be  early  delirium.  If  the 
respiratory  system  is  specially  attacked,  the  signs  will  be  those  of 
bronchitis,  pneumonia,  or  suggestive  of  acute  tuberculosis.  If  the 
alimentary  canal  is  selected,  there  will  be  symptoms  indicating 
irritant  poisoning  or  appendicitis;  if  the  renal  system  is  marked  out 
for  attack,  they  will  resemble  the  signs  of  acute  nephritis.  The 
above  remarks  do  not  by  any  means  cover  all  the  possibilities  of 
the  onset,  but  enough  has  been  said  to  indicate  the  remarkably 
protean  nature  of  the  signs  and  symptoms  of  enteric  fever,  and  of 
the  way  in  which  it  imitates  other  diseases. 

The  First  Week. — The  early  days  of  this  week  are  as  a  rule  occu- 
pied by  the  onset  of  the  fever,  as  described  above,  and  often  the 
medical  attendant  does  not  see  the  patient  until  about  the  end  of 
the  third  or  fourth  day  of  the  illness.  In  the  tropics,  however,  the 
attack  is  at  times  ushered  in  by  some  other  fever — as,  for  example, 
malaria,  by  which  its  symptoms  are  more  or  less  masked.  It  is, 
however,  possible,  even  at  this  early  stage,  to  observe,  associated 
with  the  symptoms  of  the  predominant  disease,  signs  and  symptoms 
which  arouse  suspicion  of  enteric  fever.  This  suspicion  is  presently 
converted  into  certainty  as  these  signs  increase  in  evidence,  while 
the  symptoms  of  the  original  ailment  decrease  and  finally  dis- 
appear. The  signs  and  symptoms  to  which  we  specially  refer  are 
the  alteration  of  the  temperature  chart  from  one  of  remittent  or 
intermittent  fever  in  malaria  to  one  of  more  continued  fever,  with 
more  marked  headache,  slowing  the  pulse,  the  appearance  of 
dicrotism,  the  signs  of  abdominal  distension,  the  local  pains,  the 
tenderness,  and  perhaps  the  gurgling  in  the  right  iliac  region,  and 
the  altered  condition  of  the  tongue. 

During  this  first  week  the  facies  of  the  patient  becomes  at  times 
typical— i.e.,  the  cheeks  are  flushed  and  the  eyes  bright,  and  there 
may  be  some  photophobia.  The  decubitus  is  almost  always  dorsal. 
As  the  week  proceeds,  the  patient  becomes  more  or  less  apathetic, 
listless,  and  drowsy.  Headache,  noises  in  the  ears,  and  pains  in 
various  parts  of  the  body  arc  the  marked  symptoms  of  this  weds:, 
while  sleeplessness  is  often  another  marked  symptom.  Delirium 
is,  however,  rare.  The  temperature  continues  high,  being  usually 
from  1030  to  1040  F.  in  the  evening,  with  a  remission  of  a  degree 


SYMPTOMATOLOGY  1381 

or  so  in  the  morning ;  but  in  our  experience  a  much  greater  remission 
than  a  degree  or  so  is  by  no  means  unusual,  and  the  temperature, 
as  already  mentioned,  may  assume  an  intermittent  character. 
The  pulse  is  about  80  to  100  beats  per  minute,  often  with  more 
or  less  dicrotism,  while  the  blood-pressure  varies,  the  systolic  being 
about  120  millimetres,  and  the  diastolic  about  90  millimetres  of 
mercury.  At  this  stage  of  the  disease  there  is  usually  little  or  no 
change  in  the  blood,  though  slight  leucopenia  may  be  present. 
The  specific  agglutinin  reaction  is  not  available,  but  the  bacilli 
can  be  cultivated  from  the  blood.  In  uncomplicated  cases  the 
spleen  is  more  or  less  normal  at  the  commencement,  but  enlarges 
distinctly  towards  the  end  of  the  week.  The  respiratory  symptoms 
may  cause  the  patient  much  annoyance,  especially  the  dry,  hacking 
cough,  and  there  may  be  signs  of  mild  tonsillitis,  pharyngitis, 
laryngitis,  or  bronchitis.  Pneumonia  must  be  looked  upon  rather 
as  a  complication  than  as  a  symptom  of  the  disease.  The  gastro- 
intestinal symptoms  present  much  variability.  The  mouth  is 
often  dry,  and  the  patient  may  be  worried  by  thirst.  The  lips  and 
teeth  are  normal,  but  the  tongue,  which  is  moist,  is  generally  coated 
by  a  white  fur  on  the  dorsum,  while  the  tip  and  edges  are  red.  There 
is  little  or  no  desire  for  food;  the  stomach  is  irritable,  and  vomiting 
may  occur,  especially  if  indiscretions  in  feeding  are  allowed.  The 
abdomen  is  more  or  less  distended,  especially  in  the  region  of  the 
right  iliac  fossa,  where  it  is  often  painful  and  tender,  as,  indeed,  it 
may  be  in  other  places.  There  may  be  constipation  or  there  may  be 
diarrhoea;  the  motions  may  be  of  an  ordinary  colour,  but  more 
typically  they  are  ochre-yellow.  It  is  not  often  that  haemorrhage 
is  seen  during  this  week,  and  is  then  generally  small  in  amount ; 
but  its  presence  is,  in  our  opinion,  a  relatively  serious  symptom. 
The  urine  is  generally  diminished  in  quantity,  high  in  specific 
gravity,  dark  in  colour,  with  a  markedly  acid  reaction,  but  there  is 
usually  no  albumen,  no  casts,  and  the  diazo-reaction  cannot  be 
obtained. 

The  skin  is  hot  and  dry,  with,  however,  paroxysms  of  greater  or 
lesser  amount  of  perspiration,  followed  by  the  presence  of  more  or 
less  sudamina.  The  typical  rose  spots  do  not  as  a  rule  appear 
before  the  seventh  day,  and  therefore  will  not  be  described  under 
this  week.  At  times  a  bluish  subcuticular  mottling  is  to  be  observed, 
especially  on  the  abdominal  wall,  towards  the  end  of  this  week  of 
quite  a  different  nature  to  the  bluish  spots  (taches  bleudtres),  which 
are  generally  assigned  to  the  action  of  lice.  There  is  often  a  yel- 
lowish coloration  of  the  palms  of  the  hands,  the  lateral  aspects  of 
the  fingers,  and  the  soles  of  the  feet,  sometimes  called  '  Philipo- 
wicz's  sign,'  which,  however,  is  by  no  means  characteristic  of 
enteric  fever. 

The  most  marked  feature  of  the  week  is  the  gradual  increase  in 
severity  of  the  disease  as  marked  by  the  growing  apathy  and 
dulness  of  the  patient;  the  aggravation  of  the  symptoms,  with  the 
exception  of  the  pains,  which  tend  rather  to  abate  towards  the  end 


1382        THE  ENTEROIDEA  GROUP  OF  TROPICAL  FEVERS 

of  the  week;  the  enlargement  of  the  spleen;  the  possible  occurrence 
of  the  typical  spots ;  and  the  continued  fever. 

The  Second  Week. — The  signs  and  symptoms  described  in  the 
first  week  continue  to  increase,  with  the  exception  of  the  headache 
and  local  pains,  which  usually  diminish  and  disappear  by  about  the 
middle  of  the  week.  The  tendency  to  haemorrhage  is,  however, 
more  marked,  and  the  danger  of  perforation  of  the  bowels  has  now 
to  be  considered,  while  the  typical  rose-coloured  rash  should  appear 
to  a  greater  or  lesser  extent ;  the  specific  agglutinin  reaction  should 
be  obtainable,  as  well  as  the  diazo-reaction  in  the  urine,  while  the 
specific  bacilli  are  much  more  difficult  to  obtain  from  the  circulating 
blood,  but  can  still  be  recovered  from  the  spleen,  the  fasces,  the  rose 
spots,  and  often  from  the  urine.  Liver  or  gall-bladder  symptoms 
and  other  complications  may  appear.  With  this  introduction  the 
signs  and  symptoms  of  the  second  week  may  be  considered  in 
slightly  more  detail. 

During  this  week  the  patient,  who  may  have  been  up  and  about, 
is  generally  confined  to  bed,  and  may  be  seen  for  the  first  time  by 
the  physician.  The  facies  is  dull,  apathetic,  and  listless;  the 
reaction  time  is  prolonged  for  answering  questions;  the  hearing 
may  be  diminished;  and  the  patient  is  drowsy.  At  night  there 
may  be  sleeplessness  and  mild  delirium.  There  may  be  slight  sub- 
sultus  tendinum.  The  decubitus  is  dorsal.  The  temperature  con- 
tinues high,  varying  from  about  1020  to  1050  F.,  while  the  pulse  is 
generally  relatively  slow  (90  to  100  beats  per  minute),  although  it 
may  reach  to  120.  The  dicrotism  may  have  disappeared,  but  the 
blood-pressure  has  generally  diminished  somewhat,  and  the  first 
sound  of  the  heart  is  not  as  appreciable  as  normal.  The  circulation 
is  as  a  rule  not  good;  the  extremities  are  apt  to  be  cool,  or  even 
cold;  and  the  hands  and  feet,  or  more  usually  the  tips  of  the  fingers 
and  toes,  may  be  of  a  bluish  colour.  The  nails  often  show  signs  of 
lack  of  vitality,  and  transverse  ridges  may  be  observed.  Philipo- 
wicz's  sign  may  disappear,  or  may  persist  through  the  week,  and 
even  later.  The  typical  rose-red  or  pink  maculo-papules  appear  in 
successive  crops  on  the  front  of  the  abdomen  or  chest,  beginning 
about  the  seventh  to  twelfth  days,  though  in  exceptional  cases  they 
may  occur  as  early  as  the  fifth  day,  or  they  may  be  delayed  as  late 
as  the  twentieth  day,  while  they  may  be  entirely  absent.  Their 
number  and  presence  depends  upon  some  unknown  secondary  cause 
and  not  upon  the  severity  of  the  attack,  to  which  they  bear  no  refer- 
ence. They  are  pinkish  or  rose-red,  circular,  slightly  elevated, 
isolated  maculo-papules  about  4  millimetres  in  diameter,  usually  few 
in  number,  which  disappear  temporarily  on  pressure,  but  reappear 
as  soon  as  the  pressure  is  removed.  They  usually  last  three  to  five 
days,  more  rarely  as  long  as  ten  days,  and  as  a  rule  undergo  no  change 
until  they  fade  and  disappear,  leaving  occasionally  a  brownish  stain. 
They  are  not  associated  with  any  subcuticular  mottling,  and  are 
but  rarely  met  with  on  the  face,  though  they  may  at  times  be  found 
on  the  arms  and  legs.     They  continue  to  appear  until  the  end 


SYMPTOM  A  TOLOGY 


I3§3 


1384       THE  ENTEROIDEA  GROUP  OF  TROPICAL  FEVERS 

of  the   second  week,    during   the   third   week,    or    even   during 
convalescence. 

The  lips  and  tongue  at  the  commencement  of  the  second  week 
are  in  much  the  same  condition  as  at  the  end  of  the  first  week,  and 
if  the  attack  is  of  mild  or  medium  virulence,  they  may  remain  in 
this  condition  during  the  whole  week;  but  if  the  attack  is  severe, 
and  if  the  patient  passes  into  the  typhoid  state,  they  alter  in  appear- 
ance; for  in  this  condition  the  patient  lies  on  his  back,  breathing 
through  the  partially  open  mouth,  with  the  lips  and  teeth  covered 
with  the  dark  brown  scabs,  formed  from  epithelial  debris,  micro- 
organisms, and  food,  which  are  called  '  sordes.'  The  tongue 
becomes  dry,  and  is  covered  with  a  brown  or  brownish-black  fur 
or  crust,  and  may  have  painful  cracks;  but  this  condition  is  largely 
due  to  oral  sepsis,  and  is  not  part  of  the  disease,  and  may  be  more 
or  less  avoided  by  careful  nursing  and  oral  antisepsis.  The  pharynx 
is  generally  more  or  less  inflamed,  and  may  be  ulcerated,  as  may 
the  tonsils.     Gastric  disturbance,  if  present  in  the  first  week,  is  not 


Fig.  659B. — Temperature  Chart  of  a  Case  of  Paratyphoid  A  Fever. 
(Chart  made  by  Major  Archibald.) 


continued  into  the  second  week  as  a  rule,  and  it  is  rare  to  observe 
vomiting  in  this  week  unless  there  is  some  complication.  There 
may  be  constipation  or  there  may  be  diarrhoea,  and  the  motions  are 
often  of  a  yellowish  colour,  with  alkaline  reaction  and  somewhat 
offensive  odour,  and  ma}7  contain  sloughs,  which  will  be  recognized 
as  greyish-yellow  fragments  of  tissue  about  an  inch  in  length. 

Haemorrhage  is  said  to  occur  in  about  10  per  cent,  of  cases,  but 
our  experience  would  indicate  that  it  is  more  frequent  than  this. 
It  varies  from  a  mere  trace  to  a  serious  haemorrhage,  and  most 
usually  occurs  from  the  end  of  the  second  to  the  end  of  the  third 
week — that  is  to  say,  during  the  period  of  separation  of  the  sloughs. 

Often  there  are  little  or  no  signs  or  symptoms  to  mark  a  slight 
haemorrhage,  but  a  profuse  haemorrhage  produces  serious  symptoms. 
Often  a  haemorrhage  takes  place  without  warning,  but  as  it  is  known 
to  be  possible,  the  attendants  will  be  on  the  outlook  for  signs;  and 
our  experience  is  that  there  often  is  warning  given  by  the  presence 
of  a  trace  of  blood  in  the  motions,  by  the  slight  increase  of  the  pulse- 


SYMPTOM  A  TOLOG  Y 


1385 


rate,  or  by  a  slight  drop  in  the  temperature.  In  sudden  severe  cases 
of  haemorrhage  the  facies  alters,  becoming  pinched  and  pallid; 
the  pulse  increases  in  frequency,  and  the  temperature  drops  perhaps 
quite  suddenly.  In  very  severe  cases  a  sudden  fatal  collapse  may 
take  place  before  any  sign  of  blood  has  been  visible  in  the  motions. 

More  or  less  meteorism  is  always  present  during  this  week,  and 
at  times  this  becomes  a  great  trouble  to  the  patient,  and  very 
rarely  may  reach  to  such  a  degree  that  it  embarrasses  the  heart's 
action.  It  is  dangerous  in  that  it  favours  perforation,  which  may 
occur  in  this  week,  but  is  more  commonly  met  with  in  the  third  week, 
under  which  heading  it  will  be  described. 

Usually  the  spleen  is  distinctly  enlarged  during  this  week,  and 
the  blood  shows  an  anaemia  due  to  the  reduction  of  red  blood  cells, 
while  the  haemoglobin  and  the  leucocytes  are  also  reduced.  The 
leucopenia  is  due  to  a  reduction  of  the  polymorphonuclear  leuco- 
cytes and  eosinophiles,  while  the  mononuclear  leucocytes  are  usually 
increased   in  numbers.     The   presence   of    a   marked  leucocytosis 


Fig.  659c. — Temperature  Chart  of  a  Case  of  Paratyphoid  B  Fever. 
(Chart  made  by  Major  Archibald.) 

would  indicate  the  occurrence  of  some  complication.  The  coagula- 
bility of  the  blood  is  reduced. 

Pain  and  tenderness  may  occur  in  the  right  hypochondrium  over 
the  area  of  the  gall-bladder,  and  is  often  due  to  a  slight  attack  of 
cholecystitis,  which  may  also  be  indicated  by  slight  enlargement  of 
the  liver,  slight  jaundice,  and  rigidity  of  the  abdominal  muscles. 

The  lungs  should  be  carefully  watched  during  this  period,  as  lobar 
pneumonia  may  occur,  and  as  the  symptoms  are  not  marked,  and 
rusty  sputum  is  rare,  it  may  be  overlooked. 

Rarer  symptoms  during  this  week  are  local  neuritis,  tetany,  eye 
troubles,  and  ear  complications;  but  muscular  cramp  is  by  no 
means  rare,  and  may  cause  great  inconvenience  to  the  patient. 

The  urine  is  febrile,  and  may  contain  albumen.  The  diazo- 
reaction  may  appear  before  the  rash,  or  may  be  deferred  as  late  as 
the  end  of  the  third  week.  Bacilluria  is  found  in  about  one-third 
of  the  cases,  while  urobilin  and  indicanuria  are  also  fairly  frequently 
met  with.     Acetone  and  diacetic  acid  occur,  but  may  be  due  to  the 


13S6        THE  ENTEROIDEA  GROUP  OF  TROPICAL  FEVERS 

starvation.  In  mild  cases  the  patient  may  show  marked  improve- 
ment during  this  week,  and  the  temperature  may  decline  gradually, 
and  reach  normal  about  the  fourteenth  day.  This,  however,  is 
rare,  and  usually  the  temperature  keeps  high  during  the  whole 
week,  and  the  patient  enters  the  third  week  with  all  the  signs  and 
symptoms  of  the  fully  developed  attack. 

The  Third  Week. — During  the  third  week  the  temperature  may 
gradually  fall  to  normal  about  the  twenty-first  day  in  typical  cases, 
and  with  this  the  various  symptoms  may  subside  and  convalescence 
begin.  In  moderately  severe  cases  all  the  symptoms  described  in 
the  second  week  may  continue,  but  the  fever  may  be  less,  and  may 
gradually  remit  towards  the  end  of  the  week.  In  the  severer  cases 
the  fever  continues,  and  the  patient  passes  into  a  condition  com- 
monly called  the  '  status  typhosus.'  This  is  the  week  in  which 
there  is  a  great  danger  of  haemorrhage  and  perforation  of  the  intes- 
tine. 


Fig.  660. — Temperature  Chart  of  a  Double  Infection  of  Typhoid  and 
Paratyphoid  B  Fevers. 


In  the  severe  cases  the  temperature  remains  high;  the  pulse 
becomes  quick;  the  tongue,  teeth,  and  lips  become  covered  with 
sordes;  the  diarrhoea  and  abdominal  distension  become  worse; 
and  the  toxaemia  produces  delirium,  at  first  mainly  at  night,  but 
later  more  or  less  continuously;  or  the  patient  may  develop  a  quiet 
state  of  delirium,  lying  quietly  in  the  bed  with  the  eyes  open  and 
staring,  and  quite  unconscious  of  the  surroundings.  The  muscles 
are  markedly  irritable,  and  show  fibrillar  contractions,  tremblings, 
and  twitchings,  with  or  without  subsultus  tendinum.  Emaciation 
now  progresses,  and  the  anaemia  is  more  marked.  This  is  the  time 
for  the  pharyngo-typhoid  ulcer  to  appear,  and  tympanites  develops. 

The  great  danger  of  the  third  week  is  perforation,  which  is  said 
to  occur  in  about  3  per  cent,  of  cases.  It  may  take  place  in  the 
mildest  of  cases,  and  we  have  seen  it  in  one  in  which  only  two 
small  ulcers  could  be  found  at  the  post-mortem  examination,  so 
that  no  case  can  be  said  to  be  free  from  this  danger. 

The  symptoms  are  often  sudden,  severe,  stabbing  pain  in  some 
part  of  the  abdomen,  and  often  referred  to  the  region  of  the  right 
iliac  fossa,  but  may  also  be  referred  to  the  left  iliac  fossa.     This 


VARIETIES  1387 

sharp  pain  disappears,  but  is  replaced  by  a  more  general  pain  all 
over  the  abdomen,  which  may  be  persistent  or  intermittent.  At 
times  this  general  pain  may  be  absent.  Sometimes,  but  by  no 
means  always,  there  is  vomiting.  Usually  there  is  more  or  less 
collapse,  as  indicated  by  the  pinched  features  and  the  quick,  small, 
thready  pulse.  The  temperature  generally  falls,  but  quickly  rises 
again;  the  abdomen  becomes  distended;  the  liver  dulness  is  en- 
croached upon  by  the  tympanites,  and  the  breathing  becomes 
thoracic;  while  the  urine  may  be  suppressed.  The  prostration 
increases,  and  the  patient  may  gradually  sink  and  die.  In  other  cases 
peritonitis  may  intervene  before  death.  A  small  perforation  may 
not  present  the  above  typical  symptoms,  and  may  be  only  suspected 
at  first  by  the  fall  of  temperature  and  the  rise  of  the  pulse-rate. 

The  Fourth  Week. — In  typical  cases  the  temperature  has  fallen 
to  normal  by  the  commencement  of  this  week,  and  the  tongue  has 
begun  to  clean  and  all  the  symptoms  abate  and  gradually  disappear, 
and  convalescence  begins.  Now  comes  the  danger  of  a  relapse,  as 
towards  the  end  of  this  week  the  patient  begins  to  get  hungry. 

In  severe  cases  the  symptoms  may  continue  unabated,  and  com- 
plications may  occur. 

In  protracted  cases  the  patient  lies  in  the  status  typhosus  with  a 
high  temperature,  passing  urine  and  faeces  involuntarily,  and  may 
die  from  cardiac  failure,  from  perforation,  or  some  other  complica- 
tion. 

The  Fifth  and  Sixth  Weeks.- — These  should  be  weeks  of  convales- 
cence, but  at  any  time  a  relapse  may  take  place,  while  complications 
and  sequelae  may  occur. 

Varieties. — The  various  types  of  typhoid  fever  may  be  classified 
in  the  following  sequence:  Ambulatory,  abortive,  mild,  typical, 
severe,  and  the  masked. 

The  ambulatory  is  typically  presented  by  a  person  who  feels  ill 
for  some  days  or  weeks,  but  goes  about  his  usual  work,  feeling 
exceedingly  wretched,  until,  perhaps,  someone,  noticing  how  ill 
he  looks,  may  take  his  temperature,  and  perhaps  find  it  over 
1040  F. ;  thereupon  the  patient  seeks  advice  for  the  first  time, 
and  may  be  well  into  the  second  or  even  third  week  of  the  disease. 
More  rarely  a  patient  may  go  through  the  whole  attack  without 
medical  assistance.  Often,  however,  the  illness  may  begin  with 
the  ambulatory  variety  and  end  with  an  exceedingly  severe  attack. 

The  mild,  the  typical,  and  the  severe,  have  been  included  in  our 
general  or  typical  account  given  above,  and  these  are  estimated 
to  be  about  two-thirds  of  all  cases  of  enteric  fever. 

The  masked  type  of  fever  is  that  in  which  one  special  group  of 
symptoms  is  pronounced,  as,  for  example,  the  nervous,  with  the 
severe  headaches,  neuralgias,  early  delirium,  and  other  marked 
mental  symptoms — e.g.,  mania  or  the  signs  of  meningitis.  Another 
example  is  that  in  which  the  pulmonary  symptoms  are  speci- 
ally marked — e.g.,  the  early  bronchitis  or  the  pneumonia.  Other 
examples   are   the   severe   gastro-intestinal   symptoms,    imitating 


138S       THE  EXTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

poisoning,  or  the  signs  of  an  acute  nephritis.  Lastly,  the  type  in 
which  haemorrhages  begin  early  and  are  persistent  is  often  spoken 
of  as  the  hemorrhagic  type. 

One  curious  form  may  be  just  mentioned,  as,  for  example,  the 
spleno-typhoid,  in  which  the  spleen  is  very  markedly  enlarged, 
without  signs  of  malaria  or  relapsing  fever. 

Complications  and  Sequela?. — The  most  important  complication 
is  malaria,  but  dengue  and  certain  unclassified  fevers  of  intestinal 
origin  are  occasionally  met  with  during  the  first  week,  and  com- 
plicate the  diagnosis.  Bedsores  and  boils  are  not  infrequent 
complications,  and  loss  of  hair  is  a  frequent  sequel.  Venous  throm- 
bosis in  the  femoral  vein  is  a  frequent  complication,  and  infarction 
may  occur  in  various  organs.  Arterial  thrombosis  is  much  rarer. 
Acute  ascending  myelitis  is  noted,  while  joints  may  be  attacked, 
giving  rise  to  a  typhoidal  arthritis,  and  the  spine  to  a  typhoidal 
spondylitis.  Periostitis  of  various  bones  is  not  rare.  Inflamma- 
tion of  the  thyroid  gland  may  also  occur.  Haemorrhage  and  per- 
foration have  been  noted.  Iritis,  orbital  cellulitis,  and  purulent 
choroiditis  have  been  recorded  as  due  to  typhoid  fever,  but  purulent 
otitis  media  and  mastoiditis,  described  as  associated  with  typhoid 
fever,  are  generally  due  to  other  causes  than  the  typhoid  bacilli. 
Appendicitis  and  meningitis  may  also  occur. 

Relapse. — One  of  the  most  important  sequels  to  an  attack  of 
enteric  fever  is  the  relapse  which  may  occur  at  any  time  during 
the  three  or  four  weeks  following  the  fall  of  temperature  to  normal. 
It  usually  resembles  an  ordinary  attack  of  typhoid  fever. 

Diagnosis. — The  diagnosis  of  enteric  in  typical  cases  is  not 
difficult,  being  based  principally  on  the  slow  onset  of  the  feyer,  the 
enlargement  of  the  spleen,  the  presence  of  roseola  at  the  beginning 
of  the  second  week,  the  apathetic  appearance  of  the  patient,  the 
leucopenia.  Every  medical  man,  however,  practising  in  the  tropics 
has  noticed  that  enteric  fever  there,  much  more  frequently  than  in 
temperate  climates,  presents  an  atypical  course.  The  temperature 
chart  may  be  very  irregular,  sometimes  of  a  well-marked  remittent 
or  intermittent  type  (Fig.  659) ;  the  enlargement  of  the  spleen  may 
be  absent  during  the  whole  course  of  the  disease,  or  in  other  cases 
it  may  be  much  more  enlarged  and  harder  than  is  usually  the 
case;  roseola,  invisible,  of  course,  in  natives,  may  be  absent  in 
Europeans,  while  at  times  these  may  present  a  profuse  rash.  In 
a  few  cases  some  of  the  peculiarities  met  with,  especially  the  very 
irregular  type  of  temperature,  are  explained  by  the  presence  of 
two  infections — typhoid  and  malaria.  Individuals  who  have  had 
an  attack  of  malaria  may  harbour  in  their  spleen  Laveran's 
parasites  for  a  long  time  without  any  symptoms,  but  as  soon  as 
the  resistance  of  the  organism  is  diminished  by  any  cause  like  a 
chill,  a  disorder  in  dietetics,  or  the  onset  of  some  disease,  an  attack 
of  malarial  fever  ensues.  When  these  malarial  carriers  develop 
enteric,  the  malarial  infection  breaks  out  again,  and  probably 
modifies  the  course  of  the  temperature.     It  must.be  admitted,  how- 


DIAGNOSIS 


1389 


ever,  that  in  the  largest  number  of  cases  no  such  explanation  can 
be  found.  As  regards  a  clinical  differentiation  of  the  three  varieties 
of  enteric — typhoid,  para  B,  para  A — this  is  impossible,  at  least  in 


*,..„.. 

v 

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v 

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g 

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., 

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sj 

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A 

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l  A  /I       '    • 

y  yy  y  x ;  v  |  }  ,y 

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t 

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Fig.  661. — Temperature    Chart    of   a    Triple    Infection    of    Typhoid, 
Paratyphoid  A  and  B  Fevers. 


the  tropics.  With  these  clinical  difficulties  the  bacteriological 
diagnosis  of  enteric  fever  acquires  in  the  tropics  even  more  import- 
ance than  in  temperate  climates. 

The  bacteriological  diagnosis  of  enteric  is  based  on  the  following 
methods: — 

1.  Agglutination  test. 

2.  Hsemocultures. 

3.  Search  for  the  enteric  bacilli  (B.  typhosus,  B.  paratyphosus  A, 
B.  paratvphosus  B)  in  stools  and  urine. 

4.  Splenic  puncture. 

5.  Ophthalmoreaction  and  cuti-reaction. 

6.  Subcutaneous  inoculations  of  dead  cultures  and  Vincent's 
splenic  diagnosis. 

7.  Complement  fixation,  etc. 

The  first  two  processes  are  really  the  only  ones  of  practical  im- 
portance, but  a  few  words  may  be  said  also  on  some  of  the  others. 

Agglutination  Test  (Widal  Reaction). — This  test  is  based  on 
the  work  of  Griiber,  Durham,  Widal,  and  Griinbaum.  Either  the 
microscopical  or  the  macroscopic  method  may  be  used.  The  simplest 
way  to  perform  the  microscopical  test  is  to  place  on  a  slide  19  loop- 
fuls  of  broth  and  1  of  blood,  and  mix  the  whole  gently  together. 
A  loopful  of  this  dilution  is  then  mixed  with  a  loopful  of  a  young 
typhoid  broth  culture,  a  hanging-drop  made,  and  the  preparation 
examined  microscopically  for  agglutination  after  one  hour.  The 
technical  details  may  be  found  in  any  textbook  on  bacteriology. 
It  suffices  here  to  say  that  the  blood  should  be  sufficiently  diluted — 
at  least  1  in  40— and  the  agglutination  should  be  first  tried,  using 
the  typhoid  bacillus,  and  if  this  is  negative,  the  paratyphoid  A  and 
the  paratyphoid  B  bacilli.  If  the  medical  man  in  attendance 
cannot  perform  the  test  himself,  he  should  send  the  blood  to  a 
bacteriological  institute.  The  sample  of  blood  is  obtained  by  pi  Pek- 
ing the  finger  and  collecting  a  few  drops  of  blood  in  a  capillary  tube. 
After  closing  both  ends  in  the  flame,  the  tube  is  parked  in  cotton- 
wool, and  despatched  to  the  bacteriological  institute. 


1390       THE  ENTEROlDEA  GROUP  OF  TROPICAL  FEVERS 

Macroscopic  tests  (sedimentation  test)  are  also  in  use,  and  various 
forms  of  apparatus  (agglutinometers)  can  be  obtained,  which  enable 
the  general  practitioner  to  carry  out  the  test  himself  without  using 
a  microscope.  A  convenient  rapid  method  is  Alcock's,  the  blood 
being  diluted  very  little  and  examined  after  only  a  few  minutes. 
Dreyer's  method,  using  specially  standardized  emulsions,  is  useful, 
as  this  method  renders  much  easier  the  making  of  agglutination 
curves,  which  are  of  great  practical  importance  in  the  diagnosis 
of  enteric  in  inoculated  individuals.  Technical  details  may  be 
found  in  any  modern  textbook  on  bacteriology. 

In  the  tropics,  even  at  the  present  time,  one  is  apt  to  be  asked  what  value 
is  to  be  placed  on  the  result  of  the  agglutination  reaction.  Some  medical 
practitioners  are  inclined  to  be  sceptical,  while  others  tend  to  base  their 
diagnosis  solely  on  the  result  of  the  test.  We  would  emphasize  the  fact  that 
in  enteric  fever,  as  in  any  other  bacterial  disease,  in  order  to  come  to  a  definite 
diagnosis  the  results  of  the  clinical  examination  and  those  of  the  laboratory 
must  not  be  dissociated. 

The  practitioner  should  give  his  attention  to  the  following  points: — 
Reaction  Negative.- — -(i)  The  reaction  is  generally  absent  during  the  first 
week  of  the  disease. 

(2)  In  some  very  rare  cases- — in  our  experience  generally  of  very  malignant 
type — the  test  may  remain  negative  during  the  whole  course  of  the  malady. 

(3)  The  reaction  with  the  B.  typhosus- — which  in  certain  tropical  labora- 
tories is  still  the  only  bacillus  of  the  typhoid  group  used  for  the  test — is 
negative  in  two  varieties  of  enteric  fever — paratyphoid  A  and  paratyphoid  13. 

Reaction  Positive. — (1)  When  the  reaction  is  positive,  it  should  be  remem- 
bered that  the  blood  may  contain  specific  agglutinins  many  years  after  an 
attack  of  typhoid  is  over.  In  the  event  of  fever  in  such  a  case  the  medical 
man  who  would  solely  rely  on  the  Widal  test  would  easily  fall  into  error. 

(2)  The  reaction  is  not  rarely  positive  in  cases  of  jaundice,  but  recent 
researches  have  demonstrated  the  fact  that  these  cases  are  in  reality  often 
due  to  the  colecystitis  caused  by  B.  typhosus. 

(3)  The  reaction  is  positive  in  vaccinated  persons  for  a  variable  period  of 
time  after  inoculation. 

(4)  One  must  be  sure  that  the  test  has  been  carried  out  with  sufficiently 
diluted  blood.     A  dilution  of  1  in  40  is  sufficient  for  ordinary  purposes. 

H.emocultures.— Two  methods  may  be  used— the  so-called 
'  dilution  method,'  introduced  by  Castellani  in  1898,  and  the  '  bile- 
enrichment  method,'  introduced  by  Drigalski  and  Conradi,  and 
modified  by  many  authors.  The  latter  is  at  the  present  time  to  be 
preferred,  being  simpler.  The  former  is  still  of  use  when  a  mixed 
infection  is  suspected,  as,  for  instance,  a  typhoid-pneumococcus 
infection.  The  pneumococcus  and  many  other  germs  would  grow 
very  badly,  or  not  at  all,  in  bile  media. 

Castellani 's  Dilution  Method. — The  region  of  the  bend  of  the  elbow 
is  cleaned  with  spirit  or  ether,  then  disinfected  with  perchloridc 
lotion  (1  in  1,000),  then  a  little  spirit  or  ether  is  poured  again  on 
the  skin,  or  the  region  may  be  simply  painted  with  tincture  of  iodine. 
When  this  has  become  dry,  a  few  c.c.  (2  to  5)  of  blood,  by  means  of 
a  sterile  all-glass  syringe,  are  taken  aseptically  from  a  vein  of  the 
region,  generally  the  median  basilic.  The  blood  is  immediately 
added  to  several  large  sterile  flasks  (at  least  three),  each  containing 


H^EMOCULTURES  1391 

200  of  300  c.c.  of  faintly  alkaline  broth.  A  dilution  of  about  1  in 
100  to  1  in  200  is  generally  sufficient.  The  flasks  are  incubated 
at  370  C.  Generally,  after  twelve  to  twenty-four  hours  in  positive 
cases,  the  broth  becomes  cloudy,  and  shows  a  growth  of  the  germ. 
The  germ,  of  course,  must  be  further  identified  in  the  usual 
way  by  cultivation  in  milk,  various  sugar  broths,  and  by  the  agglu- 
tination test.  The  method  gives  satisfactory  results,  theS.  typhosus 
having  been  found  by  Schottmuller,  Auerbach,  Widal,  Pinot, 
Vegres,  and  others,  in  a  percentage  varying  from  70  to  100  per  cent. 
The  novelty  of  the  method  is  the  dilution  of  the  blood  in  a  very  large 
amount  of  broth  instead  of  employing  the  usual  small  quantities 
of  the  medium.  This  simple  innovation  makes  all  the  difference 
in  the  result.  With  the  old  methods  the  majority  of  observers 
failed  to  detect  the  germ.  These  satisfactory  results  are  probably 
due  to  the  fact  that  the  blood  being  greatly  diluted,  the  agglu- 
tinins are  also  diluted,  and  any  bactericidal  properties  of  the  blood 
serum  greatly  weakened. 

Gildemcister  recommends  dilution  in  sterile  water,  while  Cummins  and 
dimming  consider  a  solution  of  0-5  per  cent,  taurocholate  of  soda  to  be  a 
very  efficient  medium. 

Drigalski  and  Conradi's  Bile- Enrichment  Method. — We  use  the 
following  modification:  2  to  5  c.c.  of  blood  are  withdrawn  from 
a  vein  by  means  of  a  sterile  syringe  (see  above),  or  if  a  vein 
puncture  is  objected  to,  a  deep  prick  is  made  in  a  finger,  and  the 
blood  collected  and  dropped  in  Coleman  and  Buxton's  glycerine- 
ox-bile  medium,  which  consists  of  ox-bile  qo  c.c,  glycerine  10  c-c, 
peptone  2  grammes,  distributed  in  small  flasks,  each  containing 
20  c.c.  of  the  medium.  If  the  blood  is  taken  in  the  evening  the 
percentage  of  positive  results  seems  to  be  larger. 

Ophthalmo-Diagnosis. — Chantemesse  has  introduced  a  method  of  diag- 
nosis similar  to  the  ophthalmo-diagnosis  of  tuberculosis.  An  extract  of 
typhoid  bacilli,  specially  prepared,  is  used.  A  drop  is  instilled  into  the  con- 
junctival sac;  after  two  to  three  hours,  if  the  case  is  typhoid,  the  conjunctiva 
becomes  very  red,  and  the  inflammation  persists  for  two  or  three  days. 

Cuti-Reaction. — Attempts  have  been  made  by  several  authors  to  evolve 
a  method  of  cuti-reaction  for  enteric  in  analogy  to  that  which  has  been  done  in 
tuberculosis.     The  results  have  not  been  very  satisfactory. 

Silvestrini's  Test. — A  small  amount  of  broth  typhoid  culture  killed  by 
heat  is  injected  subcutaneously.  If  the  case  is  typhoid,  this  procedure  induces 
a  sharp  rise  of  the  temperature  lor  a  day  or  two. 

Complement  Fixation.- — A  complement  fixation  test  has  been  worked  out 
for  typhoid,  para  A  and  para  B,  by  several  authors,  but  its  use  has  not 
become  general. 

Vincent's  Spleno-Keaction. — -Vincent  has  noticed  that  in  many  cases 
after  the  subcutaneous  injection  of  dead  vaccine  the  spleen  becomes  tem- 
porarily distinctly  larger.  The  reaction  is  specific — viz.,  a  patient  suffering 
from  typhoid  shows  an  enlargement  of  the  spleen  if  he  is  injected  with  typhoid 
vaccine,  but  not  if  injected  with  paratyphoid  A  or  paratyphoid  B  vaccines. 

Spleen  Puncture. — The  point  of  maximum  spleen  dulness  is  found,  the 
skin  is  disinfected  by  painting  with  tincture  of  iodine,  and  the  puncture  made 
by  using  a  sterile  syringe  supplied  with  a  long,  strong  needle.  A  lew  drops 
of  splenic  blood  and  juice  are  obtained  with  facility,  and  should  be  immediately 


1392        THE  ENTEROIDEA  GROUP  OF  TROPICAL  FEVERS 

sown  in  bile-glycerine  medium.     The  method  gives  good  results,  but  is  not 
advised  as  a  routine  procedure. 

Bacteriological  Examination  of  Stools  for  B.  typhosus  and  Para- 
typhosus  A  and  B. — A  small  portion  of  the  stool  recently  passed  and  collected 
into  a  sterile  vessel  is  smeared  on  several  large  MacConkey's  agar  plates.  These 
are  incubated  for  twenty-four  to  forty-eight  hours  at  350  to  370  C,  and  then 
any  suspicious  white  colonies  further  investigated.  As  is  well  known,  on 
MacConkey's  medium  the  colonies  of  coli-like  bacteria  are  red,  while  those  of 
the  typhoid  and  dysentery  group  appear  whitish.  Instead  of  MacConkey's 
agar,  the  Drigalski  medium  may  be  used,  or  Holt-Harris  and  Teague's  methy- 
lene blue-eosin  medium,  the  inoculation  of  which  may  be  done  from  a  growth 
of  the  faeces  in  Douglas'  peptone-free  broth. 

Castellani's  Contemporaneous  Gas-Agglutination  Test. — Twenty 
tubes  of  salicin  (or  rafnnose)  peptone  water,  each  containing  a  small  fermenta- 
tion tube,  are  used,  and  to  each  tube  1-2  drops  of  trivalent  typhoid  and  para 
A  and  para  B  agglutinating  serum  are  added,  or  1  drop  of  each  mono- 
serum  may  be  added  instead  of  the  trivalent  one.  Each  tube  is  inoculated 
from  one  of  the  lactose  non-fermenting  white  colonies  present  on  the  MacConkey 
plates  made  from  the  suspected  faecal  matter.  The  tubes  are  placed  in  the 
incubator  at  35°-37°  C.  for  twelve  to  twenty-four  hours  and  then  examined. 
All  tubes  showing  diffuse  turbidity  or  gas,  or  both,  are  discarded.  If  one  (or 
several)  of  the  tubes  shows  agglutinated  growth  as  well  as  absence  of  gas  a 
diagnosis  of  enteric  may  be  made,  at  once,  for  practical  purposes. 

If  the  search  is  limited  only  to  typhoid  and  not  para  A  or  para  B,  it  is  better 
to  use  glucose-peptone-water  tubes  slightly  tinged  with  litmus,  to  which  1-2 
drops  of  typhoid  agglutinating  monoserum  have  been  added.  If  one  of  the 
tubes  (or  several)  shows  agglutination  and  absence  of  gas  while  the  medium 
has  taken  a  reddish  colour  (acidity),  the  diagnosis  of  typhoid  may  be  made. 

Castellani's  Poliserum  Method. — This  is  an  application  of  Castellani's 
general  method  to  isolate  a  bacterium  from  a  mixture  of  other  bacteria  by 
using  a  multivalent  serum  which  will  agglutinate  and  delay  the  growth  of  all 
or  most  of  the  bacteria  present,  while  it  does  not  influence  the  growth  of  the 
germ  or  group  of  germs  one  desires  to  isolate.  Great  difficulty,  however,  is 
found  in  practice  in  preparing  such  a  serum,  the  best  method  of  preparation 
being  that  of  mixing  several  plurivalent  sera.  The  poliserum  method  may 
be  carried  out  in  various  ways.     Two  may  be  mentioned: — 

1.  {a)  Inoculate  with  the  faecal  matter  to  be  investigated  several  tubes  of 
taurocholate  of  soda  peptone  water,  or  Browning,  Gilmore,  and  Mackie's 
telluric  acid  peptone  water  may  be  used. 

(b)  Immediately  after,  or  better  immediately  before,  the  inoculation,  add 
3  drops  polyvalent  lactose-fermenting-intestinal-bacteria  serum,  3  drops  poly- 
valent non-lactose  fermenting  faecal  bacteria  serum  (B.  proteus  group,  etc.), 
taking  care  to  use  serums  containing  only  a  very  small  amount  of  typhoid 
coagglutinin;  or  serums  can  be  used  from  which  the  typhoid  coagglutinin  has 
been  removed  by  absorption. 

(c)  Incubate  for  twelve  or  twenty-four  hours,  then  make  plates  on  Mac- 
Conkey, Conradi-Drigalski,  or  similar  media,  from  the  most  superficial  portion 
of  the  liquid  medium,  and  investigate  further  any  suspicious  colonies  which 
may  develop,  testing  them  with  typhoid,  paratyphoid  A,  and  paratyphoid  B 
serums,  etc.  When  there  are  many  flocculi  of  agglutinated  bacilli  also  in  the 
upper  portion  of  the  tube,  these  may  be  got  rid  of  by  a  short  centrif ligation. 
A  short  centrifugation  with  an  ordinary  electric  centrifuge  will  cause  the  agglu- 
tinated bacilli  to  fall  to  the  bottom,  while  it  has  practically  no  effect  on  the 
non-agglutinated  germs  in  young  cultures. 

2.  Instead  of  inoculating  the  suspected  fascal  matter  direct  in  taurocholate 
peptone  water  and  poliserum,  the  stool  is  plated  on  MacConkey's  medium. 
After  fifteen  to  twenty-four  hours'  incubation  at  35°-37°C.  all  the  white 
colonies  (lactose  non-ferment ers)  are  inoculated  in  a  tube  of  peptone  water, 
to  which  has  been  added  2-3  drops  of  the  poliserum  for  lactose  non-fermenters 
apart  from  enteric  group.  After  fifteen  to  twenty-four  hours'  incubation 
the  growth  from  the  top  of  the  tube  is  further  investigated. 


DIAGNOSIS  OF  ENTERIC  IN  INOCULATED  PERSONS    1393 

Bacteriological  Examination  of  Urine. — The  urine  should  be  collected 
aseptically.  In  women  a  catheter  should  be  used.  In  males  this  is  not  neces- 
sary. It  is  sufficient,  after  purifying  the  glans  and  meatus  first  with  a  dis- 
infecting lotion,  and  then  with  boiled  water,  to  make  the  patient  pass  his  urine. 
Any  germs  of  the  anterior  portion  of  the  urethra  will  probably  pass  with  the 
first  portion  of  urine,  which  is  thrown  away,  while  the  last  portion  is  collected 
into  a  sterile  vessel,  and  immediately  sown  in  tubes  containing  Coleman  and 
Buxton's  bile-glycerine  medium.  These  are  incubated  at  350  to  370  C.  for 
twenty-four  to  thirty-six  hours,  and  then  the  further  bacteriological  investiga- 
tion is  carried  out  in  the  usual  manner  by  making  plates,  etc. 

Diazo-Reaction. — A  chemical  laboratory  test  often  used  is  Ehrlich's  diazo- 
reaction,  which,  however,  is  positive  in  several  other  febrile  conditions. 

Marris's  Atropine  Test. — Marris  found  out  that  the  injection  of  ^  grain 
of  atropine  sulphate  in  fevers  of  the  enteric  group  hardly  accelerated  the  pulse- 
rate,  while  in  patients  suffering  from  other  diseases  such  an  injection  will 
increase  the  rate  of  the  heart  by  some  twenty  to  forty  beats  per  minute  in 
the  same  manner  as  in  normal  individuals. 

Marris's  technique  is  as  follows:  —  The  patient  should  lie  horizontally, 
perfectly  quiet,  and  the  test  should  be  carried  out  at  least  one  hour  after  meals. 
The  pulse-rate  is  taken  and  recorded  minute  by  minute  until  found  to  be 
steady.  This  usually  takes  ten  minutes.  An  injection  of  -fa  grain  of  atropine 
sulphate  is  then  given  in  the  deltoid  region.  The  patient  remains  absolutely 
quiet,  and  after  twenty-five  minutes  the  pulse-rate  is  taken  and  recorded 
minute  by  minute.  An  increase  of  the  pulse-rate  by  about  twenty  or  more 
per  minute  indicates  that  the  patient  is  not  suffering  from  enteric.  If  the 
increase  in  the  pulse-rate  is  only  ten  beats  or  less,  the  reaction  is  suggestive 
of  enteric. 

Diagnosis  of  Enteric  in  Inoculated  Persons. — The  diag- 
nosis of  enteric  in  inoculated  persons  may  be  very  difficult,  the 
symptoms  being  often  most  atypical.  Moreover,  the  commonest 
laboratory  test — agglutination — is  of  little  use  unless  carried  out 
according  to  certain  methods. 

It  is  well  known  that  in  individuals  inoculated  with  the  triple 
vaccine  typhoid  and  para  A  and  para  B,  specific  agglutinins  develop 
for  the  three  germs,  as  was  shown  by  one  of  us  long  ago.  The  maxi- 
mum agglutination  titre  is  reached  two  to  three  weeks  after  the 
first  inoculation,  then  the  titre  falls  at  first — for  a  few  weeks — 
rapidly,  but  later  on  in  an  extremely  slow,  gradual  manner,  so  slow 
as  to  remain  practically  constant  for  months  and  years.  After  two 
months  from  inoculation  only  very  exceptionally  one  finds  an  agglu- 
tination limit  greater  than  1  in  320  for  B.  typhosus  and  B.  para- 
typhosus B,  and  fori?,  paratyphosus  A  greater  than  1  in  180.  There- 
fore, in  a  person  inoculated  longer  than  two  months,  if  the  agglu- 
tination limit  is  higher  than  1  in  300  fori?,  typhosus  or  paraB,  or 
more  than  1  in  180  for  B.  para  A,  and  there  is  fever,  a  provisional 
diagnosis  of  enteric  may  be  made.  It  is  always  advisable,  however, 
as  emphasized  especially  by  Dreyer,  Walker,  and  Gibbon,  to  take 
the  agglutination  titre  at  intervals  of  three  to  five  days  several  times 
during  the  course  of  the  suspected  fever  and  make  an  agglutination 
curve  forS.  typhosus,  B.  paratyphosus B,  and Z?.  paratyphosus  A. 

If  the  agglutination  for  B.  typhosus  exhibits  a  regular  rise,  with 
a  maximum  of  even  roo  per  cent,  in  the  third  or  fourth  week  from 
onset  of  fever,  and  then  a  subsequent  regular  fall,  as  seen  in  non- 
inoculated  subjects,  but  starting  from  and  returning  towards  the 

88 


1394        THE  ENTEROIDEA  GROUP  OF  TROPICAL  FEVERS 

higher  base  line  of  inoculated  persons,  while  there  is  little  or  no 
rise  in  the  agglutination  titre  iorB.  paratyphosusB  or  A,  a  diagnosis 
of  typhoid  fever  may  be  suggested  with  great  probability. 

If  there  is  a  regular  rise  and  subsequent  fall  in  the  agglutination 
for  B.  paratyphosus  B,  while  the  agglutination  titres  for  B.  typhosus 
andS.  paratyphosus  A  show  only  a  slight  or  no  increase,  the  diagnosis 
of  paratyphoid  B  may  be  suggested. 

If  there  is  a  regular  rise  and  later  fall  in  the  agglutination  titre 
for  B.  paratyphosus  A,  while  the  titre  for  B.  typhosus  and  B.  para- 
typhosus B  is  only  slightly  raised  or  not  at  all,  a  diagnosis  of  para- 
typhoid A  fever  may  be  made  with  a  certain  degree  of  probability. 

If  there  is  a  very  distinct  rise  in  the  agglutination  for  all  three 
germs  or  any  one  of  them,  there  is  the  possibility  of  the  patient 
suffering  from  one  of  the  three  fevers  with  non-specific  agglutinins 
for  one  or  both  the  germs  producing  the  other  two,  or  there  is  the 


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ME  'Iff  ME  ■!>[>[  MEM  EME  M  E  M  E .  M_  EM  E  ME  BY  MEM  E  M~E M  E  ME  M  E  «.E  ■>■  M  EM  E  ri  ■/  •  E  I  C  ■!■  I 

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Fig.   662. — Temperature  Chart  of  a  Triple  Infection:  Typhoid  and 
Paratyphoid  A  and  B  Fever. 


possibility  of  the  patient  suffering  from  a  mixed  infection.  In  the 
first  case  the  agglutination  curves  are  generally  synchronous, 
and  the  germ  for  which  the  agglutination  is  highest  is  often  the 
infective  germ. 

In  mixed  infections,  whether  in  inoculated  or  non-inoculated 
subjects,  the  agglutination  curves  for  the  various  infecting  germs 
are  as  a  rule  not  synchronous,  and  follow  their  ordinary  course 
independently  of  each  other. 

To  carry  out  the  above  tests  it  is  necessary  to  have  recourse  to 
an  accurate  quantitative  method,  and  we  recommend  for  the 
purpose  Dreyer's  standard  agglutination  method,  using  standard 
agglutinable  emulsions.  Details  will  be  found  in  any  modern 
manual  of  bacteriology,  such  as  Hewlett's  seventh  edition. 

Of  course,  in  inoculated  persons  the  search  for  the  infecting  organ- 
isms in  the  blood,  stools,  and  urine,  as  already  described,  is  even  of 


DIFFERENTIAL  DIAGNOSIS  1395 

greater  importance  than  in  non-inoculated  individuals.  Marris's 
atropine  test  may  also  at  times  help  the  diagnosis  of  enteric  in 
inoculated  people,  the  test  apparently  not  being  affected  by  previous 
vaccination. 

Differential  Diagnosis. — The  term  '  enteric  fever,'  as  already 
stated,  is  used  to  cover  three  infections — typhoid  fever,  para- 
typhoid fever  A,  and  paratyphoid  fever  B,  which  clinically,  at  least 
in  the  tropics,  cannot  be  distinguished  from  one  another,  except  by 
bacteriological  methods.  Enteric  fever  imitates  many  diseases,  and 
many  diseases  resemble  enteric  fever,  and  this  renders  the  differential 
diagnosis  complicated  and  difficult.  Of  the  many  fevers  which  may 
possibly  be  mistaken  for  some  usual  or  unusual  attack  of  enteric 
fever,  we  have  chosen  the  following  for  differential  diagnosis — viz., 
malaria,  the  relapsing  fevers,  dengue,  undulant  fever,  plague,  yellow 
fever,  typhus,  influenza,  trichuriasis,  acute  miliary  tuberculosis, 
appendicitis,  pneumonia,  rat-bite  disease,  psittacosis,  parenteric 
fevers,  ulcerative  endocarditis,  and  pyaemia. 

Malaria. — Intermittent  fevers  are  hardly  likely  to  be  confused 
with  enteric  fever,  but  remittent  fevers  are  liable  to  cause  difficulty, 
and  may  be  recognized  by  the  presence  of  the  parasites  in  the  peri- 
pheral blood,  by  the  presence  of  pigment  in  the  leucocytes,  by  the 
enlargement  of  the  spleen,  and  the  reaction  to  quinine.  Moreover, 
the  attack  of  fever  is  usually  sudden,  the  temperature  quickly 
rising  to  1050  F.,  while  the  pulse  is,  as  a  rule,  not  dicrotic,  and  if 
the  fever  has  lasted  a  few  days,  there  is  generally  some  sign  of 
anaemia.  It  must,  however,  be  remembered  that  malaria  is  a  not 
infrequent  complication  of  the  first  week  of  an  attack  of  enteric 
fever  in  the  tropics,  as  malarial  carriers  are  very  apt  to  develop 
this  fever  when  commencing  an  attack  of  enteric  fever. 

Relapsing  Fevers. — In  these  fevers  the  onset  is  sudden,  and  char- 
acterized by  chills  and  severe  pains  in  some  region  of  the  body, 
while  a  careful  examination  of  the  blood  in  a  first  attack  should 
reveal  the  spirochetes. 

Dengue. — Dengue  begins  suddenly  with  often  severe  pain  in 
some  part  of  the  body,  and  often  congestion  of  the  conjunctiva, 
and  perhaps  a  sensation  of  chilliness.  It  must  not  be  forgotten 
that  typical  cases  of  dengue  fever  sometimes  develop  enteric 
fever. 

Undulant  Fever. — This  disease  may  very  closely  resemble  enteric 
fever,  and  during  the  first  week  can  only  be  definitely  recognized 
in  a  locality  in  which  both  diseases  occur  by  cultivation  of  the 
specific  germ  from  the  blood,  while  later  sweating  and  the  undulating 
type  of  fever,  together  with  the  articular  symptoms,  are  charac- 
teristic. 

Plague. — The  ordinary  severe  type  of  plague  may  be  recognized 
by  the  sudden  onset,  the  severity  of  the  symptoms,  the  mental 
dulness,  and  the  full  development  of  the  typical  symptoms  and 
bubo  in  a  few  hours. 

The  milder  forms  of  plague  are  more  difficult  to  recognize,  because 


1396        THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

there  is  little  fever;  but  the  enlargement  ot  a  group  of  lymphatic 
glands  will  arouse  suspicion  as  to  the  true  nature  of  the  disease. 

Plague  pneumonia  may  be  distinguished  from  the  pneumonic 
form  of  enteric  fever  by  an  examination  of  the  sputum. 

Yellow  Fever. — Mistakes  are  most  apt  to  occur  at  the  commence- 
ment of  a  yellow-fever  outbreak  before  the  disease  is  recognized. 
The  diagnosis  may  be  effected  by  the  rapid  onset  of  the  fever,  the 
tenderness  in  the  region  of  the  pylorus,  and  by  the  albuminuria 
which  is  often  present  on  the  first  day,  and  later  by  the  vomit.  But 
in  such  an  important  point  as  the  diagnosis  between  yellow  fever 
and  typhoid  fever,  bacteriological  examination  of  the  blood  and 
motions  should  not  be  neglected. 

Typhus. — This  fever  may  be  distinguished  by  its  sudden  onset, 
and  by  the  early  appearance  of  mental  symptoms,  and  especially 
by  the  early  appearance  of  delirium  and  coma,  while  the  macular 
petechial  eruption  appearing  on  the  fourth  day  materially  assists 
the  diagnosis.  Brill's  disease  is  merely  a  mild  form  of  typhus, 
and  may  be  differentiated  by  the  appearance  on  the  fifth  or  sixth 
day  of  a  maculo-papular  eruption,  which  does  not  disappear  on 
pressure,  and  does  not  appear  in  crops. 

Influenza. — The  diagnosis  between  influenza  and  enteric  fever 
can  be  made  by  the  presence  of  catarrhal  symptoms  in  the 
former. 

Trichiniasis. — The  presence  of  oedema  of  the  eyelids,  together 
with  swelling  and  painful  tension  of  the  muscles,  associated  with 
dyspnoea,  are  in  favour  of  trichiniasis.  The  blood  should  be 
examined  for  any  signs  of  eosinophilia,  while  the  worms  may  be 
discovered  in  the  motions. 

Acute  Miliary  Tuberculosis. — The  differential  diagnosis  here  is 
very  difficult,  and  is  complicated  by  the  fact  that  the  two  diseases 
may  occur  together.  The  fever  in  acute  miliary  tuberculosis  is 
irregular,  and  the  pulse  and  respiration  are  rapid,  and  there  is 
embarrassment  of  the  breathing,  often  leading  to  cyanosis;  but 
the  diagnosis  is  very  difficult,  and  may  have  to  depend  entirely 
upon  bacteriological  research. 

Appendicitis. — In  appendicitis  the  onset  is  usually  abrupt,  and 
the  pain  in  the  right  iliac  fossa  is  distinctive,  but  there  are  cases 
which  closely  resemble  enteric ;  and  it  must  be  remembered  that 
the  typhoid  bacillus  can  cause  appendicitis. 

Pneumonia. — Enteric  fever  may,  though  very  rarely,  begin  with 
a  typical  attack  of  pneumonia,  when  the  specific  organisms  may  be 
found  in  the  sputum;  otherwise,  a  diagnosis  must  be  made  by  the 
examination  of  the  blood,  or  later  clinically,  when  the  more  typical 
symptoms  of  enteric  arise  in  the  second  week. 

Rat-Bite  Disease. — This  may  be  recognized  by  the  history,  by 
the  blotchy,  measly  eruption,  and  by  the  fact  that  the  fever  ends 
for  the  first  time  after  a  few  days,  only  to  reappear  again  later. 

Psittacosis. — This  enteric-like  fever  may  be  suspected  by  the 
history  of  there  having  been  sick  parrots  in  the  house  in  which  the 


DIAGNOSIS  OF  MIXED  INFECTION  >  1397 

patient  has  been  residing,  and  this  can  be  confirmed  by  the  isola- 
tion of  the  specific  bacilli  from  the  blood. 

Parcnteric  Fevers. — These  can  only  be  diagnosed  by  the  bacterio- 
logical examination  of  the  blood  and  fasces. 

Ulcerative  Endocarditis. — Usually  in  this  complaint  there  are 
recurring  chills,  irregular  fever,  substernal  pains,  and  endocardial 
murmurs,  while  bacteriological  examination  of  the  blood  may  not 
merely  differentiate  it  from  enteric  fever,  but  may  indicate  the 
germ  which  is  causing  the  endocarditis. 

Pycemia. — In  the  first  week  this  may  be  difficult,  and  depend 
upon  the  bacteriological  examination,  but  the  usually  intermittent 
fever,  the  prostration,  and  the  sweats,  may  give  rise  to  suspicion. 
The  marked  leucocytosis  may  also  arouse  suspicion. 

Weil's  Disease. — This  may  be  recognized  by  the  early  onset  of 
jaundice. 

Diagnosis  of  Mixed  Infections. — As  already  stated,  mixed  infec- 
tions, especially  typhoid  and  malaria,  typhoid  and  paratyphoid, 
typhoid  or  paratyphoid  and  coli-like  germs,  are  not  rare.  In  the 
typho-malarial-infection  cases  the  microscopical  examination  of 
the  blood  will  reveal  Laveran's  parasites.  As  regards  the  diagnosis 
of  the  second  group  of  mixed  infections — viz.,  typhoid  +  para- 
typhoid, or  typhoid +coli  infections — the  diagnosis  is  based  on: — 

1.  Hasmocultures. 

2.  Castellani's  absorption  test. 

The  technique  for  haemocultures  has  already  been  given.  We  may 
here  remind  our  readers  that  the  finding  in  the  blood  of  some  other 
organism  besides  the  B.  typhosus  does  not  mean  always  that  the  case 
is  a  real  mixed  infection.  The  organism  found  may  play  only  a 
Saprophytic  role,  especially  if  the  blood  does  not  contain  specific 
agglutinins  for  the  germ. 

Castellani's  A  bsorption  Test. — The  usual  agglutination  tests  are  not , 
as  a  rule,  sufficient  to  make  a  diagnosis  of  mixed  infection,  because 
coagglutination  does  not  always  mean  multiple  infection.  If  the 
blood  of  a  typhoid  patient  agglutinates  the  B.  paratyphosus,  besides 
the  B.  typhosus,  one  is  not  justified  in  coming  to  the  diagnosis  of 
a  mixed  infection  brought  about  by  the  B.  typhosus  and  the 
B.  paratyphosus  B,  because  it  is  well  known  that  the  blood  of  a 
typhoid  patient  may  contain,  besides  the  specific,  primary  or  homo- 
logous agglutinins  for  the  typhoid  bacillus,  secondary  or  non- 
specific or  heterologous  agglutinins  for  B.  paratyphosus  B  and  many 
other  bacilli,  such  as  many  strains  of  coli.  This  has  been  demon- 
strated by  many  authors.  Griiber  and  Durham,  as  long  ago  as 
1896,  demonstrated  that  the  typhoid  sera  may  agglutinate  Gaertner 
bacilli.  Zupnik  and  Poser  later  found  out  that  89  per  cent,  of 
typhoid  sera  reacted  with  paratyphoid  B,  and  40  per  cent,  with 
paratyphoid  A. 

Boycott,  who  has  made  a  very  complete  investigation  of  the 
subject,  has  noted  that  59  per  cent,  of  typhoid  sera  present  co- 


1398       THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

agglutinations;  55  per  cent,  reacted  with  Gaertner,  or  Brion  and 
Kayser;  41  per  cent,  with  Schottmuller  B;  33  per  cent,  with  Aer- 
trycke;  and  12  per  cent,  with  Schottmiiller  A. 

The  greater  the  quantity  of  typhoid  agglutinin,  the  greater,  as  a 
rule,  the  subsidiary  agglutination. 

To  distinguish  between  primary  and  secondary  agglutinins,  and 
to  facilitate  the  diagnosis  of  closely  allied  organisms  and  mixed 
infections,  the  absorption  test,  discovered  by  Castellani  in  1902,  is 
useful.  This  test  has  been  further  studied,  and  the  technique 
improved,  by  Boycott,  Bainbridge,  O'Brien,  Cummins  and  Cumming, 
Alcock,  and  others.  An  excellent  monograph  on  the  absorption 
test  is  the  very  recent  one  by  Frank  E.  Taylor. 

Castellani  found  out  that  in  rabbits  immunized  for  typhoid 
only,  whose  serum  agglutinated  besides  the  typhoid  bacillus,  also 
certain  '  coli '  germs,  the  saturation  with  an  excess  of  typhoid 
bacilli  would  remove  not  only  the  primary  (specific,  homologous) 
typhoid  agglutinin,  but  also  the  secondary  (heterologous,  non- 
specific) coli  agglutinin;  while  in  a  serum  derived  from  rabbits 
immunized  both  for  typhoid  and  coli  bacilli,  neither  saturation 
with  typhoid  alone  nor  coli  alone,  but  only  both  together,  simul- 
taneously or  successively,  would  remove  the  whole  of  the  agglu- 
tinins present  in  the  serum. 

He  experimented  with  various  other  germs,  and  applied  the 
method  to  the  differentiation  of  closely  allied  bacilli  and  mixed  in- 
fections in  man.  For  practical  clinical  purposes  it  may  be  said 
that  if  the  blood  of  a  typhoid  patient  presents,  besides  agglutination 
for  the  B.  typhosus,  also  agglutination  for,  say,  B.  paratyphosus  B 
or  A,  or  a  coli-like  germ,  and  if  this  agglutination  for  the  B.  para- 
typhosus B  or  A,  or  coli-like,  persists  to  a  great  extent  after  satura- 
tion with  B.  typhosus,  the  case  is  very  probably  one  of  true  mixed 
infection:  typhoid  +  paratyphoid  B,  or  paratyphoid  A,  or  coli- 
like,  as  the  case  may  be. 

Of  course,  as  with  every  other  biological  test,  the  results  obtained 
cannot  be  accepted  as  absolute,  but  are  only  of  relative  value. 

To  remove  the  typhoid  agglutinin  from  the  typhoid  serum,  this  is  diluted, 
and  an  excess  of  typhoid  bacilli  from  young  agar  cultures  added  and  kept  in 
contact  for  two  hours.  The  serum  is  then  tested  for  agglutination  for  the 
various  germs.  A  similar  technique  is  used  for  removing  the  specific  para- 
typhoid B,  paratyphoid  A  agglutinins,  etc.;  by  adding  to  the  serum  an  excess 
of  paratyphoid  B  or  paratyphoid  A,  etc.,  bacilli.  For  technical  details  one 
should  consult  books  on  advanced  bacteriology,  or  Taylor's  excellent  mono- 
graph on  the  absorption  test. 

Prognosis. — The  typhoid  mortality  is,  in  the  tropics,  about  20  to 
25  per  cent,  for  ordinary  hospital  practice,  and  rather  lower  for 
private  practice.  The  mortality  from  paratyphoid  A  and  para- 
typhoid B  is  lower.  Unfavourable  symptoms  are  the  early  appear- 
ance of  haemorrhage,  severe  nervous  symptoms,  considerable 
meteorism,  and  severe  diarrhoea.  A  bad  sign,  pointing  to  a  probable 
relapse,  is  the  temperature  falling  while  the  pulse  remains  rapid. 


THE  TREATMENT  DURING  THE  ATTACK  1399 

Severe  haemorrhages  are  of  grave  import,  as  is  perforation.     Sudden 
death  may  occur  at  any  stage  of  illness  and  during  the  convalescence, 
but  is,  fortunately,  very  rare. 
Treatment. — Thetreatment  of  enteric  fever  may  be  divided  into : — 

A.  The  treatment  during  the  attack. 

B.  The  treatment  during  the  convalescence. 

A.  The  Treatment  during  the  Attack. — This  may  be  subdivided 
into: — 

I.  Treatment  of  a  simple  uncomplicated  case. 
II.  Treatment  of  special  symptoms. 

I.  The  treatment  of  a  Simple  Uncomplicated  Case  may  be 
considered  under  the  following  headings:  (1)  General  hygiene; 
(2)  nursing;  (3)  diet;  (4)  medicines. 

1.  General  Hygiene. — A  well-ventilated,  airy,  and  well-lighted 
room  should  be  chosen,  and  all  superfluous  furniture,  hangings, 
belongings,  etc.,  removed,  except  such  few  things  as  may  be  de- 
sirable to  render  the  general  appearance  cheerful.  Special  atten- 
tion should  be  paid  to  the  bed,  because  the  patient  is  to  remain 
in  bed  for  about  one  month  after  reaching  a  permanently  normal 
temperature.  The  bed  should  not  be  too  broad  or  too  narrow, 
and  should  have  a  wire-woven  mattress,  which  is  part  of  the  bed. 
Over  this  a  soft  horsehair  mattress  should  be  placed,  and  a  reserve 
mattress  should  be  kept  handy.  Over  the  horsehair  mattress 
two  folds  of  blankets  should  be  placed,  and  then  the  sheet,  and  in 
the  middle  third  there  should  be  the  draw-sheet,  with  its  water- 
proof sheeting.  The  bed  should  be  provided  with  an  easily  movable 
mosquito-net .  The  whole  room  should  be  thoroughly  cleansed  once 
a  day  by  means  of  damp  cloths  dipped  in  Jeyes'  fluid.  All  motions 
and  urine  should  be  protected  against  flies,  and,  after  being  in- 
spected by  the  physician,  should  be  disinfected  with  Jeyes'  fluid 
or  crude  carbolic  acid,  which  is  allowed  time  to  act  before  the  con- 
tents are  thrown  away.  A  separate  set  of  feeding  appliances  should 
be  reserved  for  the  patient,  and  these  should  be  sterilized  after 
use.  All  fomites  should  be  soaked  in  Jeyes'  fluid  or  carbolic 
lotion  for  some  hours  immediately  after  use  and  before  being  washed. 
A  large  piece  of  ice  is  very  useful  to  keep  down  the  temperature 
of  the  room  in  the  tropics. 

2.  Nursing. — The  most  important  feature  of  the  treatment  of 
a  case  of  enteric  fever  is  the  nursing.  Two  nurses,  one  for  the  day 
and  one  for  the  night,  are  absolutely  necessary,  and  their  work 
may  be  rendered  easier,  and  the  patient  considerably  benefited, 
especially  if  he  is  over  the  average  weight,  by  the  use  of  a  Sherrington 
lifter,  or,  failing  this,  by  some  simple  apparatus  based  upon  the 
plan  of  this  ingenious  lifter.  The  temperature  should  be  recorded 
every  four  hours,  and  as  haemorrhage  is  so  common  in  the  tropics, 
both  nurses  should  be  warned,  and  should  be  instructed  to  be  on 
the  watch  for  the  slightest  suspicion  of  this  symptom.     Moreover, 


1400        THE  ENTEROIDEA  GROUP  OF  TROPICAL  FEVERS 

they  should  be  instructed  how  to  act  when  it  occurs,  in  order  that 
there  may  be  no  delay.  The  nurse  should  also  be  warned  to  be 
careful  as  to  the  disinfection  of  her  own  hands.  Nurses  who  are 
to  attend  enteric  fever  cases  should  be  selected  from  among  those 
who  have  been  vaccinated,  in  order  to  prevent  the  possibility  of 
infection;  failing  this,  a  course  of  intestinal  disinfection  at  the  end 
of  nursing  a  case  of  enteric  fever  is  not  without  its  benefits,  as 
many  nurses  contract  the  disease. 

The  patient  should  be  sponged  all  over  with  tepid  water  twice  a 
day,  in  the  morning  and  in  the  evening,  and  this  may  be  repeated 
if  the  temperature  rises  above  1030  F.  An  excellent  plan  is  to  add 
to  the  water  a  little  of  a  lotion  of  thymol  40  grains,  spirits  of 
lavender  2  ounces,  rectified  spirits  of  wine  3  ounces,  dilute  acetic 
acid  3  ounces,  in  16  ounces  of  rose-water.  The  patient  generally 
finds  this  admixture  to  be  most  refreshing. 

From  the  first  the  back  should  be  carefully  inspected  and  dried, 
and  dusted  with  a  powder  composed  of  boric  acid,  zinc  oxide,  and 
starch,  or  some  similar  powder.  Any  irritated  region  should  be 
bathed  with  rectified  spirits. 

The  mouth  must  be  carefully  attended  to,  and  a  mouth-wash  of 
glycothymoline,  listerine,  or  other  antiseptic  mouth-wash,  must  be 
used,  while  the  teeth  should  be  carefully  cleaned  by  the  nurse  by 
means  of  a  small  stick  carrying  a  little  cotton-wool. 

The  bed-pan  or  slipper  and  the  urine-bottle  must  be  used  through- 
out the  illness  and  the  early  part  of  the  convalescence. 

When  the  temperature  is  high,  a  light  ice-bag  to  the  head  is  useful. 

3.  Diet. — With  regard  to  the  diet,  the  patient  should  not  be  un- 
duly starved,  but  should  be  given  liquid  food  in  small  quantities 
at  stated  intervals.  The  best  basis  for  the  dietary  is  good  chicken- 
broth  and  milk,  and  special  attention  should  be  paid  to  the  fact 
that  the  liquid  actually  given  to  the  patient  is  chicken-broth,  and 
not  some  greyish  warm  water,  with  yellow  fat  floating  on  the  sur- 
face. To  this  broth  some  Plasmon  may  be  added,  if  desired.  With 
regard  to  the  milk,  it  should  be  boiled  and  diluted  in  the  proportion 
of  1  to  2  with  either  soda-water,  Perrier-water,  lime-water,  or  barley- 
water,  and  attention  should  be  paid  as  to  whether  it  is  properly 
digested  or  not  by  examining  the  faeces.  If  it  is  not  digested,  it 
must  be  replaced  by  malted  milk,  zymonized  or  peptonized  milk, 
or  by  whey.  Junket  and  weak  tea  may  also  be  used.  The  patient 
should  be  given  plenty  of  water  to  drink,  either  plain  or  as  albumen- 
water,  and  it  is  very  soothing  to  occasionally  rinse  out  the  mouth 
with  soda-water.  But  no  very  warm  or  very  cold  foods  or  drinks 
should  be  given. 

4.  Medical  Treatment.— The  less  medicine  given  to  a  person 
suffering  from  uncomplicated  and  mild  enteric  fever  the  better  for 
the  patient. 

Some  mild  medicine — e.g.,  an  intestinal  antiseptic,  or  quinine  in  some 
form— is  often  given — e.g.,  the  quinine  and  chlorine  made  by  pouring  about 
30  minims  of  strong  hydrochloric  acid  upon  30  grains  of  chlorate  of  potash. 


THE  TREATMENT  DURING  THE  ATTACK  1401 

and  dissolving  the  chlorine  gas  so  evolved  in  12  ounces  of  water,  which  con- 
stitutes the  first  bottle,  and  should  be  dispensed  in  a  non-actinic  bottle  with 
a  glass  stopper.  The  second  bottle  contains  quinine  bihydrochloride  36  grains, 
syrup  of  lemons  1  ounce,  also  dissolved  into  12  ounces  of  water.  One  table- 
spoonful  from  each  bottle  is  mixed  and  taken  three  times  a  day.  A  thin  slice 
of  orange  is  sucked  after  each  dose  to  remove  the  unpleasant  taste.  Some 
authorities  prefer  giving  tincture  of  iodine  2  to  3  minims  in  an  ounce  of  water 
every  three  to  four  hours ;  others  prefer  /3-naphthol  2  to  3  grains  mixed  with 
bicarbonate  of  soda  2  to  3  grains,  or  eucalyptus  oil  or  cinnamon  oil  2  to  3 
minims  in  a  suspension. 

Constipation  must  be  counteracted  by  a  simple  enema  or  an 
enema  with  a  little  turpentine  if  there  is  some  tympanites  every 
other  day. 

After  the  second  week  urotropine  may  be  given  in  10-grain  doses 
three  times  daily  in  order  to  disinfect  the  urine  and  gall-bladder. 

Serums  and  Vaccines. — Serums  have  not  been  successful ;  some- 
what better  results  have  been  recorded  by  a  number  of  authorities 
by  the  use  of  vaccines.  We  do  not  use  the  vaccine  treatment 
except  in  some  protracted  cases  with  low  fever  and  fairly  good 
general  condition. 

Tchikana,  Fagiuoli,  Micheli,  Quarelli,  and  others,  give  the  enteric  vaccines 
by  intravenous  injection.  Kraus,  De  Castello,  and  Lucksh,  claim  to  have  had 
good  results  in  enteric  by  the  intravenous  injection  of  heterologous  vaccines, 
as,  for  example,  a  B.  coli  vaccine.  Intravenous  injections  of  a  peptone  solu- 
tion have  also  been  used. 

II.  The  Treatment  of  Special  Symptoms.' — The  special  symp- 
toms which  require  treatment  may  be  considered  under  the  follow- 
ing headings: — 

1.  Tympanites.  7.  Delirium. 

2.  Haemorrhages.  8.  Cardiac  failure. 

3.  Perforation.  9.  Phlebitis. 

4.  Diarrhoea.  10.  Bedsores. 

5.  Cholecystitis.  n.  Abscesses. 

6.  Hyperpyrexia.  12.  Bone  lesions. 

1.  Tympanites. — Tympanites  is  to  be  treated  by  fomentations, 
turpentine  stupes,  by  the  administration  of  15  minims  of  turpentine 
every  three  hours,  or  3  to  5  minims  of  cinnamon  oil  at  the  same 
intervals,  or  by  a  hypodermic  injection  of  ■£$  grain  of  eserine. 

2.  Intestinal  Hemorrhage. — The  nurse  should  be  prepared  on  the 
onset  of  this  complication  to  stop  all  food  and  drink  except  a  few 
sips  of  cold  water,  to  apply  an  ice-bag  to  the  abdomen,  and  to  raise 
the  bedclothes  on  a  cradle  and  to  administer  either  the  enema 
mentioned  above  or  to  give  a  capsule  of  3  minims  of  turpentine,  or 
both.  This  is  of  the  utmost  importance,  as  then  time  is  not  wasted 
in  getting  the  treatment  under  way.  When  the  physician  is  certain 
that  a  perforation  has  not  occurred,  a  hypodermic  injection  of 
morphia  is  very  useful,  but  this  should  not  be  given  so  as  to  hide 
the  signs  of  a  perforation.  The  turpentine  capsules  may  be  con- 
tinued three  or  more  times  a  day,  and  calcium  lactate  in  10-grain 
doses  may  also  be  given. 


i4Q2        THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

3.  Perforation. — The  only  chance  is  to  perform  a  laparotomy, 
and  deal  with  the  perforation  surgically;  but  this  must  be  done  as 
soon  as  possible.  After  the  operation  the  Fowler-Murphy  after- 
treatment  should  be  carried  out,  and  the  patient  placed  as  nearly 
in  an  upright  sitting  position  as  compatible  with  comfort.  This 
position  is  maintained  for  four  days.  At  the  same  time  a  con- 
tinuous administration  of  salt  solution  per  rectum  is  carried  out, 
and  so  arranged  that  the  patient  obtains  2  to  6  litres  per  diem  for 
a  week,  and  Wainwright's  special  apparatus  for  this  purpose  may 
be  employed. 

4.  Diarrhoea. — This  may  be  checked  by  tannalbin,  10  to  20  grains, 
three  times  a  day,  or  tannigen  in  the  same  dose.  A  very  useful 
adjunct  is  an  enema  containing  Dover's  powder,  5  grains;  tannin, 
10  grains;  mucilage  of  gum,  1  ounce;  and  thin  starch  solution, 
1  ounce.  Bismuth  preparations  should,  if  possible,  be  avoided,  as 
they  are  apt  to  obscure  traces  of  blood,  which  may  be  valuable 
hints  of  a  possible  haemorrhage. 

5.  Cholecystitis. — This  should  be  treated  by  urotropine,  and  when 
chronic  by  antityphoidal  vaccination,  or  a  surgical  treatment  may 
be  advisable. 

6.  Hyperpyrexia  must  be  combated  by  tepid,  cool,  or  even  iced 
sponging,  by  immersion  in  baths  of  a  temperature  between  750  to 
850  F.     Antipyretic  drugs  should  not  be  given. 

7.  Delirium. — Acute  mental  symptoms  require  sedatives  or  relief 
of  intracranial  pressure  by  lumbar  puncture. 

8.  Cardiac  Failure. — This  may  require  to  be  combated  by  hypo- 
dermic injections  of  digitalin  or  camphor  in  ether,  or  by  strychnine 
and  by  saline  injections. 

9.  Phlebitis. — This  usually  occurs  in  one  of  the  legs,  which  must 
be  wrapped  in  cotton-wool  after  applying  ichthyol  in  lanoline 
(2  per  cent.). 

10.  Bedsores. — These  are  usually  quite  preventable,  but  great 
care  is  necessary  to  dry  and  to  disinfect  the  back  and  to  harden  the 
skin  with  spirit  lotion.  When  the  sores  have  developed  they  should 
be  disinfected  twice  daily  with  hydrogen  peroxide,  and  a  xeroform 
or  zinc  oxide  powder  applied.  In  some  cases  a  protargol  ointment 
(5  per  cent.)  or  a  balsam  of  Peru  ointment  (1  to  2  per  cent.)  are 
useful. 

11.  Abscesses. — Local  inflammations  should  be  treated  with  ice- 
bags,  and  when  pus  has  formed  incisions  must  be  made. 

12.  Bone  Lesions. — A  stiff  jacket  may  be  necessary  to  relieve  the 
pain  of  a  typhoid  spine,  and  the  osteitis  or  periostitis  may  require 
surgical  treatment. 

B.  The  Treatment  of  Convalescence. — This  may  be  subdivided 
into — (I.)  The  treatment  of  a  simple  case;  (II.)  the  treatment  of 
sequela?:  (III.)  the  treatment  of  the  acute  carrier. 

I.  The  Simple  Case.— The  most  important  factor  is  to  keep  the 
patient  in  bed  without  any  change  of  diet  until  twenty-one  days 
after  the  temperature  has  permanently  reached  normal,  and  then 


THE  TREATMENT  OF  CONVALESCENCE  1403 

to  gradually  increase  and  modify  the  dietary.  The  patient  should 
not  be  allowed  to  sit  up  or  to  get  out  of  bed  until  the  temperature  has 
remained  normal  for  about  four  weeks.  In  the  meanwhile  the 
urotropine  treatment  should  be  carried  out,  and,  if  possible,  a 
bacteriological  examination  of  the  urine  and  feces  should  be  made 
six  weeks  after  the  permanent  return  to  a  normal  temperature. 

II.  The  Treatment  of  the  Sequelae. — The  phlebitis  has  been 
mentioned,  and  as  it  is  followed  by  oedema  will  require  a  bandage 
or  elastic  stocking.  Post-typhoidal  neuritis  requires  massage  and 
electricity.  Nervous  sequelae  are  not  very  uncommon,  giving  rise 
to  a  temporary  form  of  mental  weakness,  or  to  types  resembling 
disseminated  sclerosis,  myelitis,  etc. 

III.  The  Treatment  of  the  Acute  Carrier. — If  a  patient  has 
become  an  acute  carrier,  he  should  be  treated  by  antityphoid  vac- 
cination, as  already  described,  and  urotropine  should  also  be  ad- 
ministered, for  this  drug,  in  addition  to  its  action  on  the  kidney, 
is  excreted  during  twenty-four  hours  by  the  liver  cells  and  by  those 
of  the  gall-bladder.  A  dose  of  15  grains  per  diem  is  said  to  be 
sufficient  to  destroy  the  B.  typhosus  in  a  gall-bladder  in  ten  days, 
but  the  complete  cure  of  carriers  is  very  difficult,  even  having 
recourse  to  surgical  measures. 

Prophylaxis. — The  essential  features  in  the  prophylaxis  of  enteric 
fever  are  a  pure  water-supply,  a  good  system  of  drainage,  and 
sewage  and  dust  disposal,  a  pure  food  and  milk  supply,  the  destruc- 
tion  and  prevention  of  fly-breeding  grounds. 

Another  essential  feature  is  the  watering  of  the  streets  with  anti- 
septic solutions  when  there  is  much  dust,  and  lastly,  and  by  no 
means  least,  the  search  for,  discovery,  isolation  when  possible,  and 
treatment  of  the  typhoid  carriers. 

Vaccination. — At  the  present  time  Castellani's  triple  vaccination 
(typhoid,  para  A  and  para  B)  has  come  into  general  use.  The  triple 
vaccine  can  be  prepared  according  to  various  methods:  broth  cul- 
tures killed  by  heat,  carbolic  salt  solution  emulsions,  oily  emulsions, 
sensitized  vaccines,  etc.  In  a  general  way,  it  may  be  stated  that, 
whatever  the  method  of  preparation,  the  results  are  satisfactory. 
We  generally  use  a  vaccine  consisting  of  an  emulsion  of  typhoid, 
para  A  and  para  B  bacilli  in  normal  salt  solution,  to  which  |  per 
cent,  carbolic  acid  has  been  added.  The  details  of  preparation  may 
be  found  in  various  papers  by  one  of  us.  Each  cubic  centimetre  con- 
tains typhoid  500  millions,  para  A  250  millions,  para  B  250  millions. 
Half  a  cubic  centimetre  is  inoculated  the  first  time  and  1  cubic  cent  i- 
metre  a  week  later.  Certain  authorities  recommend  a  double  dose, 
1  c.c.  the  first  time  and  2  c.c.  the  second.  Thetriple  vaccine  gives  a 
certain  amount  of  immunity  for  the  three  varieties  of  enteric — viz., 
typhoid,  para  B,  and  para  A ;  the  immunity  for  typhoid  and  para  B 
seems  to  be  more  marked  than  that  for  para  A. 

The  inoculation  of  the  triple  vaccine  gives  rise  to  a  local  and 
general  reaction,  which  is  not  more  marked  than  after  the  old 
typhoid  monovaccine:  some  infiltration  and  pain  at  the  point  of 


1404        THE  ENTEROIDEA  GROUP  OF  TROPICAL  FEVERS 

inoculation;  fever  with  headache  and  rheumatoid  pains.  The 
inoculated  persons  are  generally  fit  to  resume  their  duties  twenty- 
four  to  forty-eight  hours  after  inoculation. 

In  countries  where  cholera  is  endemic  in  addition  to  enteric, 
the  tetravaccine,  typhoid,  para  A,  para  B,  cholera,  should  be 
used.  Certain  observers  describe  a  '  vaccine  disease  '  in  analogy 
to  a  '  serum  disease,'  and  state  that  the  human  organism  becomes 
sensitized  by  a  previous  injection  of  vaccine.  This  phenomenon, 
however — at  least  with  marked  features — is,  in  our  experience, 
extremely  rare. 

Until  1916,  in  the  British  Army  and  practically  in  every  other 
army — with  exception  of  the  Serbian  Army,  which  adopted  Castel- 
lani's  tetravaccine  (TABC)  in  1915 — the  vaccine  used  was  the 
Wright -Leishman  typhoid  monovaccine,  which,  as  regards  preven- 
tion of  typhoid,  gave  good  results,  but  naturally  was  of  no  efficacy 
in  the  prevention  of  the  paratyphoid  fevers. 

Vaccination  by  a  Single  Inoculation. — This  has  been  attempted 
with  a  certain  degree  of  success  by  using  oil  emulsions  of  the  various 
bacteria  (lipovaccines) ,  as  done  by  Le  Moignic  and  Pinoy,  or  by  using 
2  per  cent,  glycerin  emulsions,  as  done  by  Castellani. 

As  regards  the  results  of  simple  typhoid  vaccination,  Firth's  figures  worked 
out  by  Pearson's  methods  showed  that  out  of  55, 368  inoculated  persons  in  the 
army  in  India,  61  were  attacked  by  typhoid,  and  out  of  12,074  non-inoculated 
45  were  attacked ;  while  another  series  of  figures  showed  58,481  inoculated  and 
34  attacked,  as  against  10,927  non-inoculated  and  22  attacks. 

The  vaccine  used  in  the  army  was  the  Wright-Leishman,  made  from  cultures 
not  more  than  forty-eight  hours  old,  which  were  sterilized  at  530  C,  and  to 
which,  when  cold,  0-4  per  cent,  of  lysol  was  added.  This  vaccine  was  to  be 
used  during  the  period  extending  from  three  weeks  to  three  months  after  its 
preparation,  and  was  to  be  injected  under  the  skin  opposite  the  insertion  of 
the  left  deltoid. 

The  first  dose  was  500  million  bacilli,  and  the  second,  given  ten  days  after, 
was  1,000  million  bacilli,  and  sometimes  a  third  dose  of  1,000  million  was 
also  given.  Inoculation  takes  place  at  4  p.m.,  and  the  soldier  goes  to  bed  at 
8  p.m.,  when  the  reaction  begins,  and  is  on  light  duty  for  two  days.  There 
is  practically  no  negative  phase,  and  the  reaction  consists  of  a  localized 
hypersemia  with  oedema  and  some  slight  fever,  malaise,  and  chilliness.  Occa- 
sionally the  symptoms  are  more  severe,  but  usually  disappear  in  forty-eight 
hours.  The  typhoid  monovaccine  was  prepared  according  to  many  other 
methods:  the  Pfeiffer-Kolle  vaccine,  the  Vincent  vaccine,  the  nucleo-proteid 
vaccine  of  Lustig  and  Galeotti,  etc.  An  attenuated  live  vaccine  was  prepared 
by  one  of  us,  and  a  non-attenuated  sensitized  live  vaccine  was  prepared  by 
^letchnikoff  and  Besredka,  and  extensively  used  by  Alcock. 

PARENTERIC. 

Synonyms. — Typhoid-like  and  paratyphoid-like  fevers;  Enteric-like  fevers; 
Fevers  due  to  intermediate  germs. 

Definition. — The  term  '  parenteric  '  indicates  a  group  of  fevers 
clinically  hardly  distinguishable  from  one  another,  and  from 
enteric,  but  due  to  intestinal  bacteria  specifically  different  from 
B.  typhosus  Eberth,  B.  paratyphosus  B  Schottmiiller,  and  B.  para- 
typhosus  A  Schottmuiler. 


PARENTERIC 


I4°5 


Historical.— Since  the  discovery  of  the  paratyphoid  bacilli 
cases  of  clinical  enteric,  but  apparently  due  to  germs  different  from 
those  of  the  enteric  group  (typhoid,  para  A,  para  B),  were  placed  on 
record  by  a  few  observers.  These  cases  were  generally  viewed 
with  much  scepticism,  which  was  to  a  certain  extent  justified, 
as  in  a  number  of  cases  the  germ  believed  to  be  the  cause  of  the  fever 
represented  in  reality  merely  a  secondary  infection.  After  our 
work,  that  of  Balfour,  and  of  Archibald,  the  fact  that  there  is  a 
group  of  fevers  due  to  so-called  intermediate  intestinal  germs  began 
to  attract  more  general  attention,  and  is  now  accepted  by  most 
authorities. 

Geographical  Distribution. — Parenteric  occurs  apparently  in  every 
climate,  but  is  of  much  more  frequent  occurrence  in  tropical  and 
subtropical  countries.  Cases  have  been  reported  from  Ceylon, 
India,  Egypt,  the  Sudan,  the  Balkans,  Southern  and  Central 
Europe. 

/Etiology  and  Classification. — Parenteric  is  caused  by  a  large  num- 
ber of  intestinal  bacteria,  excluding  B.  typhosus,  B.  paralyphosus  A, 
and  B.  paratyphosus  B.  ^Etiologically  one  might  differentiate  a 
variety  of  parenteric  for  each  species  of  intestinal  germ  capable  of 
becoming  the  aetiological  agent  of  a  fever,  but  such  a  procedure 
would  differentiate  several  scores  of  parenteric  fevers,  and  we 
therefore  consider  it  simpler,  for  the  time  being,  to  classify  par- 
enteric according  to  six  types,  corresponding  to  the  six  principal 
groups  in  our  classification  of  intestinal  bacteria  (Chapter  XXXVI., 
p.  932),  as  follows: — 

A.  Parenteric  due  to  bacteria  of  genus  Eberthus  Castellani  and 
Chalmers,  excluding  B.  typhosus,  and  of  genus  Alkali  genes  Castellani 
and  Chalmers. 

These  cases  do  not  seem  to  be  very  rare.  Among  the  germs  found 
we  may  mention  B.  fcBcalis  alkaligenes  Petrewsky,  B.  fcscaloides 
Castellani,  B.  meta-alkaligenes  Castellani,  B.  para-alkaligenes  Castel- 
lani, B.  vivax  Archibald,  B.  pritnitzi  Castellani,  B.  kandiensis 
Castellani,  etc.  It  would  appear  that  these  germs  are  usually  non- 
pathogenic, but  under  certain  circumstances,  of  which  very  little 
is  known,  may  become  so. 

B.  Parenteric  due  to  intestinal  bacteria  of  genus  Salmonella  Lig- 
nieres  emend.  Castellani  and  Chalmers,  apart  from  B.  paralypliosiis 
A  and  B.  These  cases  seem  to  be  the  most  frequently  met  with. 
Among  the  bacteria  found  we  may  mention  B.  psittacosis  Nocard, 
B.  columbensis  Castellani,  B.  archibaldi  Castellani  and  Chalmers. 
These  three  germs  seem  to  be  constantly  pathogenic,  while  many 
other  members  of  the  group  are  often  non-pathogenic,  representing 
when  found  only  secondary  infections,  although  it  is  not  excluded 
that  at  times  they  may  become  pathogenic. 

Two  very  important  germs  of  the  genus  Salmonella  are  B.  acrtrykc 
.  De  Nobele  ( =B.  suipestifcr)  and  B.  entcritidis  Gaertner,  but  these  two 
germs  very  seldom  give  rise  to  an  enteric-like  fever;  usually  they 
give  rise  to  acute  enteritis. 


1406        THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

C.  Parenteric  due  to  germs  of  genus  Enter oides  Castellani  and 
Chalmers.  Cases  of  parenteric  seem  occasionally  to  be  caused  under 
certain  circumstances  by  such  germs,  which  as  a  rule  are  not  patho- 
genic faecal  bacteria.  The  following  germs  have  been  found  capable 
at  times  of  becoming  pathogenic:  B.  entericus  Castellani:  B.  khartou- 
mensis  Chalmers  and  MacDonald ;  B.  parentericus  Castellani. 

D.  Parenteric  due  to  germs  of  genus  Lankoides  Castellani  and 
Chalmers.  These  seem  to  be  rare,  though  a  few  cases  have  been 
recorded  due  to  B.  ceylonensis  A  Castellani  and  B.  ceylonensis  B 
Castellani. 

E.  Parenteric  due  to  germs  of  genus  Balkanella  Castellani  and 
Chalmers  and  genus  Wesenbergus  Castellani  and  Chalmers.  These 
cases  appear  to  be  very  rare,  the  germs  of  this  group  apparently 
seldom  becoming  pathogenic. 

F.  Parenteric  due  to  bacteria  of  genus  Escherichia  Castellani  and 
Chalmers.  Cases  of  parenteric  due  to  bacteria  of  this  group  (so- 
called  coli  group)  are  in  our  experience  very  rare.  True,  germs  of 
this  group  are  comparatively  often  found  in  the  blood  of  cases  of 
fever,  and,  moreover,  are  often  agglutinated  by  the  blood  of  the 
patient,  but  repeated  bacteriological  examinations  very  frequently 
show  that  these  germs  play  only  the  role  of  secondary  or  associated 
infections,  and  that  the  cases  are  often  true  cases  of  enteric  (typhoid, 
para  A,  or  para  B),  the  coliform  germs  having  entered  the  general 
circulation  through  the  intestinal  ulcers.  One  should  also  keep  in 
mind  the  frequent  invasion  of  germs  of  this  group  in  the  pre- agonic 
period. 

Parenteric  due  to  germs  of  the  tribe  Protecs,  such  as  B.  cloacce,  B.pyocyaneus, 
B.  proteus  vulgaris,  etc.,  is  rare,  these  germs  generally  acting  as  secondary 
infective  agents. 

Morbid  Anatomy.— Very  little  is  known.  Intestinal  ulcers  do 
not  seem  to  be  present.  The  mesenteric  lymph  glands  may  be 
larger  than  normal,  and  the  spleen  and  liver  may  be  enlarged,  and 
the  latter  organ  may  show  cloudy  swelling  and  fatty  degeneration. 
The  heart  is  flabby,  and  may  be  in  a  condition  of  fatty  degeneration. 

Pathology. — This  seems  to  be  somewhat  similar  to  the  pathology 
of  enteric. 

Symptomatology. — Parenteric  is  clinically  very  similar  to  enteric, 
the  onset  being  at  times  slow,  the  fever  subcontinuous  or  con- 
tinuous, ending  by  lysis. 

At  times,  however,  the  onset  is  sudden,  and  the  fever  may  have 
a  most  irregular  course.  The  duration  varies  between  ten  days  and 
several  weeks,  or  occasionally  months.  The  patient  in  some  cases 
takes  the  'typhoid  look, 'being  apathetic  and  expressionless;  at  other 
times  he  does  not  appear  to  be  very  ill.  Intestinal  symptoms  may 
be  present  or  totally  absent,  but  a  certain  amount  of  meteorism  is 
often  noticeable.  The  spleen  may  be  palpable,  but  this  is  of  much 
less  frequent  occurrence  than  in  enteric.  Roseola  is  extremely 
rare  and  intestinal  haemorrhages  practically  unknown,  the  germs  of 
the  parenteric  group  giving  rise  very  seldom  to  intestinal  ulcers. 


FREQUENCY  OF  PARENTERIC—PROPHYLAXIS  1407 

Frequency  of  Parenteric. — It  is  well  to  keep  in  mind  that  par- 
enteric  is  on  the  whole  much  less  frequent  than  true  enteric  (typhoid, 
para  A,  para  B).  The  observation  has  been  made  that  persons 
inoculated  against  enteric  (typhoid,  para  A,  para  B)  seem  occasion- 
ally to  become  more  proneto  contract  parenteric,  in  the  same  manner 
that  persons  inoculated  against  typhoid  only,  seem  at  times  to  de- 
velop a  tendency  to  contract  paratyphoid  A  and  paratyphoid  B 
more  frequently  than  non-vaccinated  individuals.  This,  however, 
cannot  be  used  as  an  argument  against  vaccination  by  the  enteric 
or  triple  vaccine  (typhoid,  para  A,  para  B),  because,  although 
individuals  vaccinated  therewith  may  develop  a  slight  tendency 
to  contract  parenteric,  still  the  total  number  of  enteroidea  fevers 
(enterica  and  parenterica)  observed  in  such  individuals  is  greatly 
less  than  in  non-vaccinated  people  or  in  people  vaccinated  only 
with  typhoid  monovaccine. 

Diagnosis. — When  a  patient  is  suffering  from  enteric-like  symp- 
toms, while  all  serological  and  bacteriological  investigations  for 
enteric  remain  constantly  negative,  the  practitioner  is  justified  in 
suggesting  the  possibility  of  parenteric.  The  diagnosis,  however, 
should  always  be  confirmed  by  a  complete  and  repeated  bacterio- 
logical examination  of  the  blood,  stools,  and  urine,  with  the  object 
of  isolating  the  causative  organism  and  of  determining  from  what 
variety  of  parenteric  the  patient  is  affected.  We  should  like  to 
emphasize  here  that  the  mere  presence  of  an  intestinal  germ  in  the 
blood  is  not  sufficient  to  come  to  the  conclusion  that  this  fever  is 
due  to  that  germ.  Repeated  examinations  may  show  that  it  is 
present  in  association  with  true  B.  typhosus,  B.  paratyphosus  A, 
or  B.  paratyphosus  B,  and  may  have  little  or  no  part  in  the  causation 
of  the  symptoms,  quite  a  number  of  faecal  bacteria  being  capable  of 
entering  the  general  circulation  through  intestinal  ulcers.  If, 
however,  the  germ  not  only  is  found  in  the  blood,  but  the  blood 
contains  specific  agglutinins  for  it,  while  hsemocultures  and  serum 
reactions  are  constantly  negative  for  enteric,  the  probabilities 
are  that  the  germ  isolated  is  the  real  astiological  agent  of  the 
fever. 

Prognosis. — This  is,  on  the  whole,  much  more  favourable  than  in 
enteric  (typhoid,  paratyphoid  A,  paratyphoid  B). 

Treatment. — This  should  be  on  the  same  lines  as  for  enteric. 
Complete  rest  in  bed  and  fluid  diet  are  necessary.  Drugs  are  of 
little  or  no  use  except  occasionally.  Urotropine  may  be  given  in 
doses  of  10  grains  three  or  four  times  a  day.  The  vaccine  treatment 
with  autogenous  vaccines  seems  to  give  better  results  than  in  enteric. 

Prophylaxis. — As  regards  general  prophylactic  measures  (sanitary 
improvements,  destruction  of  flies),  these  are  the  same  as  for 
enteric.  The  usual  enteric  vaccination  (TAB)  does  not,  of  course, 
protect  against  parenteric,  and  when  certain  forms  of  parenteric 
become  frequent  the  bacteria  causing  them  may  be  added  to  the 
enteric  bacilli  in  the  preparation  of  a  prophylactic  vaccine. 


1408        THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

VARIETIES  OF  PARENTERIC. 

In  the  general  account  we  have  given  of  parent  eric  we  have  stated 
(see  .Etiology)  that  aetiologically  very  numerous  varieties  might  be 
differentiated,  but  we  have  limited  ourselves  to  distinguish  six  chief 
types  in  relation  to  the  six  principal  groups  of  intestinal  bacilli 
which  may  cause  the  condition.  We  consider,  however,  it  advisable 
to  give  a  brief  separate  description  of  certain  varieties  of  parenteric 
which  have  been  more  completely  worked  out.     These  are : — 

Psittacosis  parenteric. 
Alkaligenes  parenteric. 
Columbensis  parenteric. 
Archibaldi  parenteric. 
Asiaticus  parenteric. 
Khartoumensis  parenteric. 

Psittacosis  Parenteric. 

Definition. — A  very  fatal  specific  epizootic  among  parrots,  which  is  capable 
of  spreading  to  man  and  causing  a  febrile  condition  resembling  typhoid  fever 
in  its  characters,  and  which  is  very  liable  to  be  complicated  with  severe 
pneumonia. 

History. — Ritter,  in  1 879,  was  the  first  to  suspect  that  there  was  a  connection 
between  small  epidemics  of  pneumonia  limited  to  certain  houses  and  an  illness 
among  parrots  in  the  same  houses.  In  1880  Eberth  obtained  large  numbers 
of  micrococci  from  the  bodies  of  grey  parrots.  Ritter 's  observations  were 
confirmed  by  Ost  of  Berne,  in  1882,  and  by  Wagner  of  Leipsic,  in  1885.  In 
1S92,  500  parrots  were  shipped  from  South  America  for  Paris,  but  no  less 
than  300  died  en  route  from  enteritis.  On  arrival  in  Paris  the  surviving  birds 
were  divided  into  two  lots,  and  sold  to  various  people,  with  a  result  that 
within  twenty-six  days  of  their  arrival  an  epidemic  of  psittacosis  broke  out, 
which  resulted  in  forty-nine  cases,  with  sixteen  deaths.  The  epidemic  was 
characterized  by  being  of  the  house  type,  by  which  is  meant  that  several  persons 
in  the  same  house  were  attacked  by  the  complaint. 

Smaller  epidemics  occurred  in  1893  and  1894,  and  in  the  same  year  Banti, 
Malenchini,  and  Palamidessi  reported  an  epidemic  in  Florence.  In  1895 
there  were  outbreaks  at  Prato,  Cologne,  and  Paris;  in  1897  at  Genoa;  in  1898 
at  Cologne;  in  1901  at  South  Elpidio,  Ancona,  and  Hull;  in  1904  at  New 
Hampshire,  one  of  the  Eastern  United  States  of  America.  Beddoes  in  1914 
reported  several  cases  in  England.  We  have  seen  epidemic  enteritis  of  this 
nature  develop  in  parrots  in  the  Sudan,  but  prophylactic  measures  being 
immediately  instituted  it  did  not  spread  to  man. 

/Etiology. — The  disease  is  apparently  due  to  a  bacillus  belonging  to  the 
genus  Salmonella  Lignieres  of  our  classification,  first  isolated  from  the  wings  of 
parrots  which  had  died  from  the  disease  by  Nocard  in  1893,  and  subsequently 
found  by  Gilbert  and  Fournierin  1897  in  the  intestine  of  the  sick  birds,  and  also 
i  n  the  heart-blood  of  a  man  who  died  from  the  disease.  The  bacillus  in  question 
is  pathogenic  for  parrots  and  other  birds.  It  is  possible  that  this  bacillus 
exists  normally  in  parrots,  and  only  becomes  pathogenic  under  circumstances 
of  bad  hygiene,  when  it  causes  an  enteritis.  The  feathers,  becoming  contamin- 
ated with  faecal  matter,  are  cleaned  by  the  parrot  with  its  tongue  in  the  usual 
way,  so  that  its  mouth  and  bill  become  infected,  and  by  this  means  the  disease 
is  spread  to  persons  who  feed  or  caress  the  bird.  Very  rarely  the  disease 
spreads  from  man  to  man.  According  to  Bainbridge,  Bacillus  psittacosis  is 
identical  with  B.  aertryhe  (p.  954). 

Pathology. — In  parrots  the  disease  causes  a  very  fatal  form  of  enteritis. 
In  man  it  produces  a  septicaemia,  often  complicated  by  a  pneumonia,  brought 
about  as  a  rule  by  the  pneumococcus. 


VARIETIES  OF  PARENTERIC  1409 

The  post-mortem  reveals  lobular  pneumonia  in  the  lungs,  fatty  degeneration 
of  the  heart-muscle  and  liver,  enlargement  and  softening  of  the  spleen,  and 
congestion  of  the  kidneys,  with  swelling  of  the  tubular  epithelium. 

Symptomatology. — The  incubation  period  varies  from  seven  to  twelve  days, 
after  which  the  disease  may  begin  suddenly  with  a  chill,  but  more  usually 
commences  insidiously,  like  typhoid  fever,  with  headache,  malaise,  etc.,  and 
a  rise  of  temperature  from  1020  to  1040  F.,  with  a  pulse-rate  of  100  to  120  per 
minute,  quickened  respirations,  cough,  and  muco-purulent  expectoration. 
Rales  may  be  heard  over  the  lungs,  while  the  spleen  is  enlarged,  the  tongue 
dry  and  furred,  and  diarrhoea  or  constipation  may  be  present.  Rose-coloured 
spots  appear  on  the  skin,  and  the  patient  becomes  dull  and  stupid,  in  which 
condition  he  may  remain  for  several  days,  and  as  a  rule  will  recover  in  about 
fifteen  to  twenty  days  if  no  pneumonic  complication  intervenes.  If,  how- 
ever, pneumonia  sets  in,  the  patient  becomes  much  worse,  and  as  a  rule  dies. 

Diagnosis. — The  diagnosis  is  to  be  made  by  the  discovery  of  sick  parrots  in 
houses  in  which  people  are  suffering  from  typhoid-like  fevers  and  pneumonia. 
Bacteriologically,  attempts  may  be  made  to  obtain  cultures  of  the  bacilli 
from  the  blood. 

Prognosis. — The  prognosis  is  grave  in  old  people  and  when  pneumonia  sets 
in,  the  mortality  being  stated  to  be  about  35  to  40  per  cent. 

Treatment. — The  treatment  must  be  conducted  on  the  lines  usually  laid 
down  for  typhoid  fever  and  pneumonia. 

Prophylaxis. — The  infected  parrots  appear  always  to  come  from  South 
America;  therefore  care  should  be  taken  that  only  healthy  birds  are  allowed 
to  be  shipped,  and  that  these  are  kept  in  good  hygienic  conditions  during  the 
voyage.  On  arrival  at  their  destination,  they  should  be  quarantined  for 
about  a  couple  of  weeks,  and,  if  found  to  be  infected,  should  be  destroyed, 
and  their  dead  bodies  and  cages  burnt.  The  places  in  which  they  were  kept 
should  also  be  thoroughly  disinfected.  Parrots  should  not  be  allowed  to  take 
food  out  of_people's  mouths,  and  should  always'be^kept  in  good  hygienic 
conditions.  " 

Alkaligenes  Parenteric. 

Remarks. — B.jcecalis  alkaligenes  Petruschky — which  belongsto  the 
genus  Alkaligenes  of  our  classification — is  generally  a  harmless  faecal 
germ,  but  researches  by  various  observers  have  demonstrated  that  it 
may  occasionally  become  pathogenic  for  man,  and  produce  fever. 
Cases  have  been  recorded  by  Straub  and  Krais  (1914),  by  Rochaix 
and  Marode  (1916) ,  by  Shearman  (1916) ,  by  Hirst  (1917) ,  and  others. 

Symptomatology. — The  fever  often  resembles  a  mild  type  of 
enteric,  and  is  generally  of  short  duration,  twelve  to  fifteen  days, 
though  protracted  cases  are  occasionally  met  with.  At  times  the 
temperature  is  very  irregular,  subcontinuous  or  intermittent,  and 
even  a  tertian  periodicity  is  said  to  be  occasionally  present,  though 
possibly  some  of  these  cases  may  have  been  associated  with  malaria. 
The  spleen  is  seldom  enlarged,  roseola  is  not  present,  and  intestinal 
haemorrhages  have  never  been  recorded. 

Diagnosis. — This  is  based  on  the  isolation  of  B.  facalis  alkaligenes 
from  the  blood,  and  the  presence  of  specific  agglutinins  for  this  germ, 
while  all  bacteriological  tests  for  enteric  and  other  intestinal  germs 
are  negative.  The  bacteriological  examination  of  the  blood  is 
carried  out  as  in  enteric,  either  using  Castellani's  dilution  method, 
details  of  which  have  been  given  when  discussing  the  bactericlcgical 
diagnosis  of  enteric,  or  one  of  the  modifications  of  Drigalski-Cc  uracil  s 
bile  method.    The  technique  which,  in  the  hands  of  Sheaiman,  has 


i4io        THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

given  good  results  is  the  following: — 5  c.c.  of  blood  drawn  aseptically 
from  a  vein  is  placed  in  50  c.c.  of  a  2  per  cent,  solution  of  tauro- 
cholate  of  soda  in  distilled  water,  incubated  at  350  C.  for  twenty-four 
hours,  and  then  plated  out  on  MacConkey's  plates.  These  are  incu- 
bated for  twenty-four  hours,  and  any  white  colony  present  is  further 
investigated. 

Prognosis. — This  is  favourable. 

Treatment. — The  treatment  is  symptomatic.  Vaccines  have  been 
tried  in  a  few  cases,  but  no  definite  results  have  been  so  far  obtained. 

COLUMBENSIS   PARENTERIC. 

Synonym. — Febris  columbensis. 

Historical  and  Geographical  Distribution. — The  disease  and  its 
causative  germ  were  described  by  Castellani  in  Ceylon  in  1905. 
Spaar  published  a  case  in  1914.  Recently  cases  have  been  recorded 
in  India  by  De  Mello,  in  Europe,  in  the  Balcanic  Zone  by  Lurie,  and 
in  the  South  of  Europe  by  Conte.  It  also  occurs  in  the  Anglo- 
Egyptian  Sudan. 


Fig.  663. — Temperature  Chart  of  Columbensis  Parenteric. 

/Etiology. — The  causative  germ  is  B.  columbensis  Castellani,  1905. 
This  germ  is  somewhat  peculiar  in  that  occasionally  when  recently 
isolated  its  action  on  lactose  may  not  be  constant,  the  same  strain 
having  at  times  no  action  whatever  on  lactose,  at  other  times  slightly 


Fig.  664. — Temperature  Chart  of  Columbensis  Parenteric  Fever. 


fermenting  it.  After  several  subcultures  all  the  strains  become 
non-lactose  fermenters.  It  is  not  agglutinated  by  typhoid,  para- 
typhoid A  and  paratyphoid  B  sera.  Its  biochemical  characters  can 
be  found  in  the  table  of  intestinal  bacteria  on  p.  946.  It  differs  from 
B.  par  city phosus  A  and  B  in  producing  gas  in  glycerine  and  other 


COLUMBENSIS  PARENTERIC  Mn 

minor  characters.  It  is  not  agglutinated  by  either  paratyphoid  B 
or  paratyphoid  A  serum. 

Symptomatology. — Two  types  of  the  fever  may  be  differentiated, 
one  closely  resembling  typhoid,  the  other  characterized  by  numerous 
relapses.  Enlargement  of  the  spleen  and  meteorism  may  be 
present,  but  are  not  constant  symptoms.  Roseola  has  not  been 
recorded,  nor  intestinal  haemorrhages.  Urinary  complications 
(cystitis,  etc.)  are  not  rarely  met  with.  All  the  cases  recorded  have 
ended  in  recovery. 

Prognosis. — Appears  to  be  favourable  quoad  vitam,  but  in  the 
relapsing  type  the  disease  may  last  for  four  to  six  months,  the  patient 
having  several  attacks  of  fever,  each  lasting  a  couple  of  weeks. 

Treatment.- — This  is  on  the  same  lines  as  for  enteric,  including 
complete  rest  in  bed  and  fluid  diet.  Urotr opine  is  useful,  especially 
when  there  arc  urinary  complications. 

Prophylaxis.— Castellani  has  used  in  Ceylon  a  B.  cohtmbensis 
vaccine  in  the  form  of  a  combined  B.  columbensis,  B.  typhosus, 
B.  paratyphosus  A  and  B,  paratyphosus  B  vaccine. 

Archibaldi  Parenteric. 

This  fever  and  its  etiological  agent  were  described  by  Archibald 
in  the  Sudan  in  1912.  The  bacillus  was  believed  by  Archibald 
at  one  time  to  belong  to  theB.  cloacce  group.  It  seems  to  us  prob- 
able that  the  germ  belongs  to  the  genus  Salmonella  of  our  classifica- 
tion, and  that  it  is  related  to  5.  columbensis  Castellani. 

Symptomatology. — As  a  rule  the  symptoms  presented  by  the 
patient  are  not  unlike  those  of  the  second  week  of  enteric  fever. 
There  is  high  fever,  ranging  from  1010  to  1030  F.,  associated  with 
drowsiness  and  perhaps  delirium,  but  this  is  often  absent,  with 
furred  dry  tongue,  but  without  diarrhcea  or  tympanites,  and  with 
or  without  some  very  slight  enlargement  of  the  spleen.  Sometimes 
the  temperature  falls  to  normal  after  a  week,  but  this  intermission 
is  followed  by  a  prolonged  fever  of  a  remittent  type,  or,  instead, 
the  fever  may  be  more  or  less  remittent  from  the  commencement. 

Complications.- — Complications  in  the  form  of  pneumonia,  ab- 
scesses, femoral  thrombosis,  etc.,  may  occur. 

Asiaticus  Parenteric. 
This  fever  was  differentiated  by  Castellani  in  Ceylon  by  obtaining 
the  specific  bacillus  from  the  blood  and  motions.  There  are  two 
varieties  of  the  bacillus,  which  may  be  called  B.  asiaticus  Nos.  1 
and  2.  (For  the  specific  characters  see  table  in  Chapter  XXXVI., 
p.  944.)  Culturally  these  bacilli  are  identical,  but  the  biological 
reactions  are  slightly  different.  The  possibility  of  a  double  infection 
of  one  of  these  bacilli  or  other  parenteric  germs  with  those  of  enteric 
fever  must  not  be  forgotten.  The  diagnosis  will  then  depend  upon 
the  absorption  test. 


1 41 2        THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

Symptomatology. — B.  asiaticus  No.  I  is  associated  with  a  long, 
protracted,  rather  low  fever  of  medium  severity,  which  shows 
usually  a  remittent  or  an  intermittent  character  {vide  Fig.  665). 
B.  asiaticus  No.  2  produced  a  fever  resembling  certain  types  of 
protracted  enteric  fever,  but  without  any  enlargement  of  the  spleen, 
without  roseobe,  but  associated  with  rather  severe  abdominal  pains 
of  long  duration,  though  as  a  rule  there  is  no  diarrhoea  and  the 
stools  never  contain  blood  or  mucus. 


Fig.  665. — Portion  of  Temperature  Chart  of  a  Case  of  Asiaticus 
Parenteric  Fever. 

One  case  due  to  B.  asiaticus  No.  1  was  associated  with  a  severe 
ancylostome  infection,  while  one  due  to  B.  asiaticus  No.  2  was 
associated  with  a  heavy  ascaris  infection.  The  fever  did  not  stop 
when  the  patients  got  rid  of  the  parasites. 

Diagnosis. — The  only  possible  method  of  diagnosis  is  the  early 
bacteriological  examination  of  5  to  10  c.c.  of  the  blood  taken  asepti- 
cally  from  the  median  basilic  vein,  and  examined  as  already  de- 
scribed for  enteric  fever,  while  an  attempt  may  also  be  made  to 


103- 
100* 

nt 

;  I  3  I  1 

a   |   •  I   7  I   a  |   3  I   't  |  i'  I  i: 

^, 

1 1 1  j  m  g 

j 

Fig.    666. — Temperature  Chart  of  Khartoumensis  Parenteric. 


isolate  the  bacillus  from  the  faeces.     The  specific  bacillus  will  be 
agglutinated  by  the  patient's  serum  in  high  degrees  of  dilution. 

Treatment. — The  cases  must  be  treated  on  the  lines  already  laid 
down  for  enteric  fever,  but  the  most  suitable  special  treatment  is  the 
injection  of  autogenous  vaccines  prepared  like  the  typhoid  vaccines, 
provided  the  acute  symptoms  are  over  and  the  fever  is  of  very  low 
type. 

Khartoumensis  Parenteric. 

This  fever  and  its  etiological  agent  have  been  described  by 
Chalmers  and  MacDonakl  in  the  Sudan.  The  germ  B.  khartou- 
mensis Chalmers  and  MacDonald,  1915,  belongs  to  our  genus  Enter- 


KHARTOUMENSIS  PARENTERIC 


Mi3 


oides  of  intestinal  bacteria,  and  is  closely  related  to  B.  entericus 
Castellani,  1911,  and  B.  parentericus  CastelJani,  1914. 

Symptomatology. — After  a  preliminary  period  of  one  to  three 
days,  during  which  the  patient  suffers  from  headache,  constipation, 
and  malaise,  with  marked  or  slight  fever,  the  febrile  attack  sets  in 
with  constipation,  headache,  and  a  disinclination  for  mental  or 
bodily  work.  The  heart,  lungs,  liver,  and  spleen  remained  normal, 
and,  except  for  the  usual  febrile  changes,  the  urine  was  also  normal. 
Except  for  headache,  the  nervous  system  was  normal,  and  no  skin 
eruptions  were  noticed.  The  cardinal  features  of  the  illness  were 
constipation,  fever,  relatively  slow  pulse,  headache,  malaise,  and  a 
general  feeling  of  illness. 

After  about  seven  days  from  the  commencement  of  the  true  rise 
of  temperature  the  fever,  which  had  gradually  risen  to  a  maximum 


Fig.  667. — Temperature  Chart  of  Khartoumensis  Parenteric. 

lying  between  1010  and  1030  F.,  subsided  quickly,  and  in  about  an- 
other three  days  fell  to  normal,  when  the  disease  ended,  or  to  nearly 
normal,  and  was  followed  by  a  relapse  of  a  more  irregular  and  pro- 
longed nature.  When  the  temperature  subsided  all  symptoms 
gradually  disappeared  and  the  patient  felt  quite  well,  but  if  the 
relapse  occurred  the  headache,  lassitude,  constipation,  etc.,  re- 
turned. At  no  time  was  any  patient  seriously  ill,  and  at  no  time 
did  a  purgative  produce  other  than  good  effects. 

The  condition  somewhat  resembles  a  case  of  enteric,  but  the 
spleen  is  not  enlarged  and  roseola  is  not  present. 

The  diagnosis  is  made  on  finding  B.  khartoumensis  in  the  faeces 
and  by  the  serological  reactions,  while  all  the  tests  for  enteric  are 
negative. 

The  prognosis  is  favourable. 

The  treatment  is  symptomatic,  but  vaccines  might  be  tried. 


REFERENCES. 
Enteric. 

The  literature  on  Enteric  Fever  is  very  large,  and  for  the  more  important 
references  the  reader  is  advised  to  consult  the  '  Index  Medicus.' 

Bainbridge  and  O'Brien  (1912).     Journal  of  Hygiene.     Cambridge. 
Birt  (1907).     Journal  Royal  Army  Medical  Corps.     London.     (Typhoid  and 
Paratyphoid  Fevers.) 


1 4i 4        THE  ENTEROIDEA   GROUP  OF  TROPICAL  FEVERS 

Bahr  and  Garrow  (1919).     Journ.  Roy.  Army  Med.  Corps,  March. 
Broughton-Alcock  (1919).     Lancet,  June  14. 
Calabresi  and  Gaetano  (1919).     Pathologica,  March  i 
Castellani  (1899).     Riforma  Medica.     (Dilution  Method.) 
Castellani  ( 1 901-1902).     Zeitschrift  fur  Hygiene.     (Absorption  Test.) 
Castellani   (191 3).     Proceedings  of  the  Society  of  Tropical  Medicine  and 

Hygiene. 
Castellani  (1904-12).     Ceylon  Medical  Reports. 

Chalmers  (1907).     Report  on  the  Sanitation  of  Colombo.     Colombo. 
Cummins  and  Cumming  (1910-12).     Journal  of  Royal  Army  Medical  Corps. 

London. 
Escallier  (1912).     These  de  Paris.     Paris.     Rechute  de  Fievre  Typhoide. 
Gautier  and  Weissenbach  (1916).     Presse  Med.,  September  21. 
Ledingham   and    Arkwright    (1912).     The  Carrier  Problem   in   Infectious 

Diseases.     London.     (Most  excellent  articles,  with  references  on  Typhoid 

and  the  Paratyphoid  Fevers.) 
Leishman  (1910).     Journal  of  Royal  Institute  of  Public  Health.     London. 

(Antityphoid  Inoculation.) 
LtJDKE      (1912).       Miinchener      medizinische     Wochenschrift.       September. 

Munich. 
Martin  and  Upjohn  (1916).     Brit.  Med.  Journal. 
Nicolle,  Raphael,  Debains  (1918).     Ann.  Inst.  Pasteur. 
Perguis  (1904).     Presence  du  Bacille  d'Eberth  dans  le  Sang.     Recherches 

par  le  Procede  de  Castellani  Modifie.     Paris. 
Roberts  (1906).     Enteric  Fever  in  India  and  Other  Tropical  and  Subtropical 

Regions.     Calcutta. 
Rogers     (1910).     Fevers    in     the     Tropics.     2nd     edition.     London.     (An 

excellent  account  of  Typhoid  Fever  in  India.) 
Stolkind  (1909)  (1915).     Arch.  f.  Kinderheilk.      Proc.  Royal  Soc.  Med. 
Stolkind  and  Lorey  (1918).     Brit.  Journ.  of  Children's  Diseases. 
Taylor  (1918).     Journal  of   Hygiene.     The   Absorption   Test   of   Castellani 

(very  complete  monograph.) 
Wolf  (191 2).     These  de  Lyon  28.     Fievre  Typhoide  a  Lyon. 
Wright  (1904).     A  Short  Treatise  on  Antityphoid  Inoculation. 

Parenteric. 

Archibald  (1912).     Journal  of  Tropical  Medicine. 

Castellani  (1905).  Ceylon  Branch  B.M.A.  (1905-1914).  Ceylon  Medical 
Reports.  (1907).  Journ.  of  Hyg.,  vol.  vii.,  No.  1.  (1912).  Centr.  f. 
Bakter.,  Orig.,  Bd.  39,  p.  14.  (1915).  Journ.  of  Trop.  Med.  (A  Case  of 
Triple  Infection.)  (1916).  Annali  Med.  Navale.  (1917).  Journal  of 
Tropical  Medicine.     (Tropical  Diseases  in  the  Balcanic  Zone.) 

Castellani  and  Chalmers  (1919).  Annales  Institut  Pasteur  and  Journ.  of 
Trop.  Med.     (Classification  of  Intestinal  Bacteria.) 

Chalmers  and  Macdonald  (1917).     Lancet. 

Hikschfeld  (1919).     Lancet. 

Klimenko,  W.  N.  (1907).     Cent.  f.  Bakt.,  Orig.,  Bd.  43,  p.  755. 

Krencker,  E.  (1905).     Cent.  f.  Bakt.,  Orig.,  Bd.  39,  p.  14. 

Lurie  (1916).     Lancet.     (Febris  columbensis.) 

Petruschky,  J.  (1889).     Cent.  f.  Bakt.,  Bd.  6,  p.  657. 

Petruschky  J.  (1896).     Cent.  f.  Bakt.,  Bd.  19,  p.  187. 

Rochaix,  A.,  et  Marotte,  H.  (1916).     Compt.  rend.  Soc.  Biol.,  t.  79   p.  316. 

Shearman  (1916).     British  Medical  Journal. 

Spaar  (1915).  Journ.  Trop.  Med.,  November  15.  (Case  of  Fever  due  to 
B.  columbensis  Castellani.) 

Straub,  H.,  and  Krais,  W.  (1914).     Deutsch.  med.  Woch.,  1914   p.  380. 

Thomson  and  Hirst  (1918).     Lancet,  April  20. 


REFERENCES  1415 

Typhoid  Monovaccine. 

Besredka  and  Metchnikoff  (1910).     Annales  Institut  Pasteur. 
Chantemesse  (1904-1914).     Papers  in  Presse  Medicale,  etc. 
Leishman  (1910).     Journal  Royal  Institute  of  Public  Health. 
Li:  MoiGNIC  and  Pinoy  (1916).     C.  R.  Soc.  Biologic      (Lipovaccine.) 
Vincent  (1904-1914).     Papers  in  Presse  Medicale  etc. 

Wright  (1900-1903).  Numerous  important  papers  in  the  Lancet.  (1904). 
'  A  Short  Treatise  on  Antityphoid  Inoculation.' 

Combined  Enteric  Vaccines. 

Castellani  (1904-1909).  Ceylon  Medical  Reports.  (1909).  Centr.  f.  Bakt., 
Bd.  32,  Heft  1  (Triple  Enteric  Vaccines;  Quadruple  Vaccines).  (1910). 
Transactions  Bombay  Med.  Congress.  (1912).  Transactions  Society  of 
Tropical  Medicine,  December.  (1913).  Lancet.  British  Medical  Journal, 
vol.  ii.,  p.  1577:  Typhoid  — Paratyphoid  Vaccination  with  Mixed 
Vaccines.  Journal  Ceylon  Branch  B.M.A.,  October  18.  (1914). 
Brit.  Med.  Journ.,  November  7,  p.  814  (Enteric-Cholera  Mixed  Vaccines) ; 
Centr.  f.  Bakt.,  Bd.  72;  Journal  Ceylon  Branch  B.M.A.,  June:  Triple, 
Quadruple,  Quintuple,  Sextuple  Vaccines.  (1915).  Sperimentale,  No.  3 
(Combined  Vaccines);  Brit.  Med.  Journ.,  May  1  (Further  Remarks  on 
Triple  Vaccination);  Brit.  Med.  Journ.  (Correspondence),  p.  758: 
A  Further  Plea  for  Enteric  Mixed  Vaccines;  Indian  Medical  Gazette, 
November  (Multiple  Vaccines) ;  Transactions  Soc.  of  Trop.  Med.,  vol.  ix., 
No.  2  (Combined  Vaccines).     (1916).  Policlinico,  October. 

Castellani  and  Mendelson  (1915).  Brit.  Med.  Journ.,  November  13: 
Tetra  vaccine. 

Castellani  and  Taylor  (191 7).  Brit.  Med.  Journ.,  September  5:  Quad- 
ruple, Quintuple,  and  Sextuple  Vaccines. 

Chantemesse  (1915).     Paris  Medical. 

Conte  (1915).     Annali  Medicina  Navale,  August. 

Cummins  and  Cumming  (1913).     Journ.  R.A.M.C. 

Dreyer  Walker,  and  Gibson  (1915).     LAncet. 

Dreyer,  Gardner,  Gibson,  Walker,  (191 8).     Lancet. 

Kabeshima  (1914).     Centr.  f.  Bakt. 

Lurie  (1916).  Brit.  Med.  Journ.,  January  8:  Notes  on  Castellani's  Tetra- 
vaccine  and  Pentavaccine. 

Micheli  and  Quarelli  (1916).     Archivio  Scienze  Mediche,  vol.  xii. 

Porcelli  (1915).     Riforma  Medica.     II  Tetravaccino  Castellani. 

Quarelli  (1917).     Riforma  Medica,  September  22. 

Vincent  (1914).     Presse  M6dicale. 

Visentini  (1917).     Riforma  Medica,  September  22. 

Widal  (191 5).     Presse  Medicale. 


CHAPTER  LIV 
PLAGUE 

Synonyms  —  Definition  — ■  History  —  Climatology  —  yEtiology — Pathology  — 
Symptomatology — Liagnosis —  Prognosis  — Treatment  —  Prophylaxis  — 
References. 

Synonyms. — Black  Death,  Pestis,  Lues.  French,  La  Peste; 
Italian,  Peste  Bubbonica;  German,  Die  Peste;  India,  Mahamari; 
Japan,  Yeki;  China,  Kota-wen;  Uganda,  Kaumpuli. 

Definition. — Plague  is  a  septicaemia  caused  by  Pasteur ell a  pestis 
Kitasato  and  Yersin  1894  (usual  name  Bacillus  pestis) ,  which  pro- 
duces an  epizootic  in  rats,  from  which  it  spreads  to  man  and  other 
animals  by  the  agency  of  fleas. 

In  man  it  causes  an  acute  specific  fever,  characterized  by  an 
inflammation  of  the  lymphatic  glands;  a  secondary  septicaemia,  with 
haemorrhages,  skin  necrosis,  and  often  a  secondary  pneumonia;  or 
it  may  give  rise  to  a  primary  pneumonia  or  a  primary  septicaemia. 
The  pneumonic  forms  are  highly  infectious,  spreading  from  man  to 
man  by  aerial  convection. 

History  and  Epidemiology. — Plague,  because  of  its  epidemicity  and  its  high 
mortality,  is  much  feared,  and  has  been  noticed  from  early  times  to  be  associ- 
ated with  a  mortality  among  rats.  Thus,  the  Bible  contains  an  account  of 
an  epidemic  disease  in  the  Philistine  country  winch  produced  buboes  in  human 
beings  and  killed  rats  ('  mice  of  the  field  '),  and  there  is  also  reference  in 
Simpson's  work  on  plague  to  the  fact  that  Sennacherib's  army  was  attacked 
by  a  pestilence  in  which  field-mice  were  in  some  way  concerned. 

But  it  was  not  until  the  outbreak  in  Pelusium,  a  great  Egyptian  market, 
in  a.d.  542,  that  the  disease  was  seriously  considered,  for  it  spread  to  Byzan- 
tium, at  that  time  the  city  of  the  world,  and  then  passed  into  Asia,  and  through 
North  Africa  into  Western  Europe  as  far  as  Ireland,  lasting  in  epidemic  form 
for  about  200  years. 

The  next  outbreak  is  in  the  eleventh  century,  when  it  spread  as  a  pandemic, 
reaching  a  maximum  in  the  fourteenth  century,  and  gradually  declining,  until 
suddenly,  in  the  seventeenth  century,  it  left  Western  Europe,  and  in  1844  it 
vanished  from  Eastern  Europe,  and  practically  from  Asia  Minor,  remaining, 
however,  in  the  district  of  Assyr,  in  West  Arabia. 

This  great  pandemic  stirred  Governments  to  take  prophylactic  measures, 
and  Count  Bernabo,  of  Reggio,  is  found  impressing  stern  quarantine  laws 
in  1374,  while  the  Venetians,  in  1403  and  subsequent  years,  laid  the  founda- 
tions of  modern  prophylaxis  by  erecting  the  first  lazaretto,  or  depot  for  the 
isolation  of  the  sick,  by  instituting  the  quarantine  for  forty  days  (hence  the 
term),  and  by  the  disinfection  of  clothing  and  merchandise.  Further,  they 
compelled  the  ship  coming  from  an  infected  port  to  hoist  a  yellow  flag,  and 
to  allow  an  inspection  of  the  crew  and  passengers  before  it  was  given  pratique 

In  the  meanwhile  plague  occurred  in  India,  where  the  first  records  are  t 

1416 


HISTORY  AND  EPIDEMIOLOGY  141 7 

be  found  in  a  sacred  Hindu  book,  the  '  Bhagavat  Purana,'  believed  to  be 
800  years  old,  which  describes  a  disease  in  man  associated  with  death  among 
rats,  and  advises  the  vacation  of  a  house  in  which  dead  rats  are  found.  Plague 
is  known  to  have  formed  epidemics  in  the  eleventh,  twelfth,  fourteenth, 
fifteenth,  sixteenth,  and  seventeenth  centuries,  after  which,  apparently,  it 
disappeared,  only  to  reappear  in  Gujurat  and  Sindh  in  1S12.  In  1823  it  was 
discovered  that  plague  existed  in  the  districts  of  Garhwal  and  Kumaon,  but  no 
one  has  been  able  to  determine  from  whence  it  came,  or  how  long  it  had  existed 
in  those  places.  It  is  now  said  to  be  endemic  there,  and  to  form  the  focus  for 
the  epidemic  of  Delhi  in  1825,  and  Rohilcund  in  1836.  In  1836  plague  broke 
out  in  Rajputana — the  so-called  Pali  Plague,  from  the  place  first  infected — 
and  lasted  two  years.  Since  then  plague  has  been  introduced  into  India  from 
China,  and  has  spread  therein,  as  will  be  explained  later.  With  regard  to 
China,  it  is  difficult  to  obtain  any  exact  information,  but  it  is  possible  that 
plague  may  have  been  introduced  at  some  time  by  Mohammedans  returning 
from  Mecca  via  Burma  to  the  province  of  Yunnan,  where,  according  to  Mina- 
kata,  it  was  known  some  time  between  1736  and  1809,  for  a  Chinese  author 
who  lived  during  this  period  gives  an  account  of  a  disease  which  caused  death 
in  men  and  rats.  From  that  time  plague  has  been  endemic  in  Yunnan,  from 
which  it  appears  to  have  spread  southwards,  reaching  Pakhoi,  on  the  southern 
coast,  about  1867,  where  it  disappears  and  reappears  at  intervals  without 
apparently  affecting  otrur  regions,  until  1894,  when,  after  an  absence  of  ten 
years,  it  again  reappears,  and,  infecting  the  district  of  Kaochao,  spreads  via 
Canton  to  Hong-Kong.  In  June,  1894,  the  causative  bacillus  was  discovered 
by  Kitasato  in  cases  in  Hong-Kong,  and  a  little  later  by  Yersin  in  the  same 
town.  In  1896  plague  spread  from  China  to  Bombay,  from  which  it  has 
gradually  extended  over  the  larger  portion  of  India,  causing  an  enormous 
number  of  deaths. 

In  1897  a  most  important  international  conference  was  held  at  Venice, 
when  protective  measures  were  agreed  to,  and  regulations  framed  to  combat 
the  disease,  based  upon  the  view  that  the  sick  person  and  his  personal  effects 
were  the  chief  source  of  danger,  and  a  quarantine  of  ten  days  from  the  last 
infected  port  was  placed  upon  healthy  ships.  In  1898  the  pandemic  spread 
from  India  to  Madagascar,  and  from  there  to  Lorenzo  Marquez  and  Mauritius. 
In  1899  it  affected  the  Malay  States,  the  Philippine  Islands,  New  Caledonia, 
the  Sandwich  Islands,  Australia,  San  Francisco,  New  York,  Asuncion,  Rosario, 
Buenos  Ayres,  Rio  de  Janeiro,  Oporto,  Lisbon,  and  Alexandria.  In  1900 
it  passed  from  Rosario  to  Cape  Town,  and  also  appeared  in  Glasgow. 

In  1900  Clemow  pointed  out  that  the  disease  had  existed  endemically  in 
Mongolia,  Southern  China,  the  Himalayas,  Mesopotamia,  Persia,  Arabia, 
Uganda,  Transbaikalia,  Russian  Central  Asia,  and  Tripoli,  between  1850  and 
1894. 

In  1903  a  Second  International  Conference  was  held  in  Paris,  which  issued 
a  series  of  regulations  confirming  those  of  the  Venetian  Conference,  except 
that  the  quarantine  of  ships  was  reduced  to  five  days,  and  that  the  agency  of 
the  rat  in  the  disease  was  clearly  recognized,  and  regulations  for  its  destruction 
framed.  Further,  this  Conference  established  an  International  Sanitary 
Office  in  Paris  for  the  purpose  of  collecting  and  transmitting  sanitary  informa- 
tion to  the  different  countries.  In  1904  Johannesburg  was  attacked,  in  1905 
Persia  and  Russia,  in  1906  Leigh,  and  in  1907  Accra,  on  the  Gold  Coast,  in 
which  year  the  disease  was  widespread  throughout  the  world,  occurring  in 
India,  Persia,  Arabia,  Egypt,  Tunisia,  Algeria,  West  Africa,  South  Africa, 
East  Africa,  Russia,  Glasgow,  Argentina,  Brazil,  Chili,  Paraguay,  Peru,  Uru- 
guay, United  States,  Australia,  New  Zealand,  Japan,  China,  and  Indo-China. 

Turning  to  Africa,  winch  has  already  been  mentioned  to  have  been  often 
infected,  it  is  now  known  to  possess  two  infected  endemic  areas — -viz.,  Ben- 
ghazi, in  Tripoli,  and  Buddu,  Koki,  and  Nkole,  in  Uganda,  from  the  latter  of 
which  an  epidemic  is  supposed  to  have  spread  into  the  Kissiba  district  of 
East  Africa. 

Such  a  pandemic  as  the  one  just  described  could  hardly  exist  without 
numerous  careful  inquiries  into  its  causation  and  spread,  for  Governments 


1418 


PLAGUE 


were  interested  in  its  prevention.  Therefore  Austrian,  German,  and  Russian 
Commissions  were  appointed,  and  did  excellent  work.  In  1898  the  first 
Plague  Commission  of  India  was  appointed,  and  was  followed  by  an  Advisory 
Committee  of  the  India  Office,  Royal  Society,  and  Lister  Institute,  appointed 
in  1904,  and,  finally,  in  conjunction  with  this  committee,  the  Second  Indian 
Commission  was  appointed  in  1907,  and  has  done  excellent  work  in  tracing 
the  aetiology  to  the  rat-flea. 

In  the  meanwhile  individual  observers  had  also  studied  the  disease — e.g., 
Haffkine  of  India,  and  Lustig  of  Florence,  had  brought  forward  protective 
vaccines,  while  Verjbitski,  of  St.  Petersburg,  showed,  in  1908,  the  importance 
of  the  bug  as  a  carrier  of  the  disease. 

Of  great  value  have  been  the  researches  carried  out  in  various  colonies  by 
Professor  Simpson. 

According  to  Nicolas,  plague  is  almost  constantly  present  in  New  Caledonia, 
where  the  bacillus  is  believed  to  exist  in  a  latent  form. 

During  1909-ro  in  Manchuria  there  was  a  very  severe  epidemic  of  pneumonic 
plague  with  a  few  cases  of  the  bubonic  type.  It  was  studied  by  Strong, 
Kitasato,  Teague,  Galeotti,  and  others. 


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AM 

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Fig.  668. — Distribution  of  Plague  in  1914. 


In  1 91 4  plague  appeared  in  Colombo,  Ceylon,  where  the  epidemic  was 
studied  by  Castellani,  who  isolated  the  bacillus,  Philip,  and  Hirst.  Several 
features  of  the  onset  were  of  interest: — 

1.  The  human  epidemic  was  certainly  not  preceded  by  a  diffuse  rat  epi- 
zootic, as  for  years  the  bacteriological  examination  of  rats  had  been  carried 
out  by  the  Municipal  Health  Office  with  negative  results,  and  it  was  several 
weeks  after  the  onset  of  the  human  epidemic  that  the  first  infected  rats  were 
discovered. 

2.  Practically  all  the  cases  were  of  the  acute  septicaemic  type,  and  were 
associated  with  an  extremely  high  mortality  without  distinctive  features,  either 
clinically  or  post-mortem;  and  it  is  interesting  to  note  that  when  infection 
was  found  in  the  rats  it  was  also  of  the  septicaemic  type,  and  in  them  also  the 
post-mortem  findings  were  non-characteristic  of  plague,  there  being  no 
buboes,  no  mottled  appearance  of  the  liver,  no  pleural  effusion. 

3.  The  strain  of  plague  bacillus  isolated  (B.  pestis  Yersin-Kitasato  var. 
metapestis  Castellani)  differed  in  some  minor  points  from  the  typical  one. 

4.  The  commonest  rat  flea,  as  noted  by  Hirst,  was  different  from  that  found 
on  rats  in  the  majority  of  plague-infested  areas,  such  as  Bombay,  but  it  is  the 
same  as  that  found  in  Madras  and  Rangoon. 


CLIMATOLOGY  1419 

Climatology. — At  the  present  moment  the  so-called  endemic  regions 
are  an  area  in  the  Kurdistan  Hills,  with  a  secondary  area  in  Irak, 
in  Mesopotamia:  another  area  about  the  Himalayas — i.e.,  Kumaon 
and  Garhwal,  in  India,  Thibet  and  Yunnan,  in  China — and  four 
lesser  areas — viz.,  Benghazi,  in  Tripoli,  Uganda,  in  Central  Africa, 
Azeer,  in  Arabia,  and  the  trans-Baikal  Province  of  Siberia— but  only 
the  first  two  are  of  real  importance  as  far  as  we  know.  On  the 
strength  of  these  two  different  regions  an  attempt  has  been  made 
to  differentiate  two  distinct  types  of  the  disease:  the  first,  the 
Western  Asiatic,  being  mild,  and  pneumonic  cases  rare,  while  it  is 
often  self-limited,  not  capable  of  wide  distribution,  and  not  asso- 
ciated with  an  epizootic  in  rats;  the  second  is  the  Indo-Chinese 
plague,  or  the  disease  as  it  is  known  to-day.  It  seems,  however, 
hardly  likely  that  such  a  distinction  will  be  supported  when  the 

disease    in    the    first     area    is . 

carefully  studied.  Climate 
appears  to  have  but  little 
influence  on  the  distribution 
of  the  disease,  and  soil  appar- 
ently none.  In  India  an  ex- 
cessive rainfall  seems  to  favour 
the  spread  and  virulence  of 
the  malady.  The  hot  season 
of   the  tropics  and  the  winter  ^ 

season  of  the  Temperate  Zone 
are  deleterious  to  the  spread 
of  the  disease.  The  reason  for 
this  appears  to  be  the  effect  of 
temperature  on  the  bacilli  in 
the     41ea,     which     disappear 


rapidly  from  its  stomach  above        Fig.  669. — Plague  Bacilli  in  the 

850  F.,  and  are  very  ineffectual  Blood,     (x  i.ooo.) 

at  that  temperature,  while  at  (From  a  photograph  by  J.  J.  Bell.) 

700    F.     they     are     virulent. 

Moreover,  as  has  already  been  stated  in  the  chapter  on  Fleas,  high 

temperatures  restrain  the  adults  from  laying  eggs  and  the  larvae  from 

developing.    When  temperatures  below  50°  F.  are  reached,  it  is  found 

that  rats  die  before  the  bacilli  pass  into  the  blood,  and  therefore  the 

fleas  do  not  become  infected  when  sucking  the  blood.    A  temperature 

of  about  700  F.  is  therefore  best  for  the  propagation  of  an  epidemic. 

/Etiology  (vide  also  pp.  909  and  943).— The  aetiology  of  plague 
has  been  placed  on  a  sure  footing  by  the  labours  of  Kitasato, 
Yersin,  Cantlic,  Simpson,  Thompson,  Ogata,  Kolle,  Martini,  and 
the  Special  Committee  already  mentioned,  together  with  the  Second 
Indian  Commission. 

It  is  caused  by  the  Pasteur ella  peslis  (usual  name:  Bacillus  pestis) 
of  Kitasato  and  Yersin,  which  is  found  in  the  fluid  of  the  initial 
cutaneous  vesicle,  the  buboes,  the  spleen,  the  blood,  and  the  sputum 
in  cases  of  pneumonia.     When  inoculated  into  monkeys,  cats,  rats, 


i420  PLAGUE 

guinea-pigs,  squirrels,  mongooses,  bats,  jerboas,  etc.,  it  causes  the 
typical  disease,  while  in  bovines  and  equines  it  only  causes  local 
reactions,  while  camels  are  insusceptible.  Canines,  birds,  and 
reptiles  appear  to  be  immune.  It  causes  a  natural  epizootic  in  rats, 
which  apparently  is  the  true  disease,  from  which  that  of  man  must 
be  looked  upon  as  an  offshoot.  In  typical  outbreaks  there  should 
be,  firstly,  the  enzootic;  secondly,  the  epizootic;  then  the  endemic,  fol- 
lowed by  the  epidemic  in  the  affected  country;  and  finally  pandemic. 
In  rats  it  produces  either  an  acute  or  a  chronic  attack,  the  post- 
mortem appearances  of  which  are  different  {vide  Chapter  XXXV.). 

In  the  acute  type  a  bubo  is  found  in  85  per  cent,  of  infected  rats, 
being  present  usually  in  the  neck  or  axilla.  If  the  bubo  is  absent, 
a  plague  rat  can  often  be  recognized  by  the  subcutaneous  congestion, 
the  purplish-red  appearance  of  the  muscles,  the  waxy,  mottled,  or 
finely  granular  appearance  of  the  liver,  the  haemorrhages,  and  the 
pleural  effusions.  The  diagnosis  can  be  confirmed  by  finding  the 
bacilli  in  the  bubo,  the  spleen,  or  the  blood. 

The  chronic  type  of  the  disease  consists  of  encapsuled  caseous 
foci,  or  abscesses  containing  bacilli,  and  found  in  the  spleen  and 
other  organs.     This  form  plays  no  part  in  the  spread  of  the  disease. 

The  epizootic  does  not  continue  with  equal  virulence  all  the  year 
round,  for  it  appears  to  be  profoundly  altered  by  the  temperature, 
being  diminished  in  the  hot  weather  of  the  tropics  and  the  cold 
weather  of  the  Temperate  Zone.  Thus  in  Bombay  the  Plague 
Commission  found  1,766  plague-infected  rats  in  one  week  in  the 
season  December  to  May,  and  only  20  to  30  in  the  season  June  to 
November.     The  cause  of  this  variation  has  already  been  given. 

But  all  rats  are  not  equally  infected,  for  it  was  found  in  Bombay 
that  there  were  two  -pvincipalspecies, Epimys  norvegicus  and  E. rattus, 
and  that  during  the  epizootic  period  no  less  than  1,334  °f  t he  1,766 
belonged  to  the  former  species,  while  in  the  non-epizootic  period 
it  alone  carried  on  the  disease.  The  reason  assigned  for  this  differ- 
ence was  that  the  numbers  of  the  flea  population  of  the  two  rats 
were  very  different,  E.  norvegicus  possessing  about  double  the 
number  of  E.  rattus.  Further,  it  was  noticed  that  the  curve  of 
E.  norvegicus  infection  began  to  rise  about  ten  days  before  that 
of  E.  rattus,  which  points  to  the  origin  of  the  infection  of  the  latter 
from  the  former  in  the  first  instance. 

In  Ceylon  also  the  percentage  of  infected  rats  was  higher  in 
E.  norvegicus  than  in  E.  rufescens,  the  local  representative  of 
E.  rattus,  but  the  septicemic  type  was  more  frequent  in  the  latter. 

E.  norvegicus,  which  is  not  nearly  so  numerous  in  Bombay  as 
E.  rattus,  lives  outside  houses,  for  the  most  part  in  sewers,  drains, 
and  stables,  and  has  a  great  facility  for  burrowing,  and  is  a  good 
climber.  It,  however,  has  never  been  found  above  the  third  floor 
of  a  house.  It  forms  its  nest  in  one  of  its  burrows,  and  breeds  all 
the  year  round,  but  has  two  special  seasons,  one  in  March  and  one 
from  June  to  October,  the  average  family  being  eight. 

E.   rattus   is   more    common    in    Bombay   than   E.    norvegicus, 


CLIMATOLOGY  1421 

especially  in  houses,  where  it  increases,  relatively  to  the  other,  up 
to  the  third  floor,  but  above  that  level  it  alone  infects  the  house.  It 
is  not  so  common  in  gullies,  compounds,  stables,  go-downs,  and  food 
and  tea  shops  as  E.  norvegicus.  The  common  meeting-ground  of 
the  two  species  appears  to  be  the  lower  floors  of  houses,  gullies,  and 
go-downs.  Though  a  domesticated  rat,  it  can  climb  and  burrow. 
It  forms  its  nest  in  cupboards,  heaps  of  firewood,  etc.,  and  breeds 
all  the  year  round,  but  especially  from  June  to  October,  the  average 
family  being  five. 

The  spread  of  the  plague  from  E.  norvegicus  to  E.  rattus,  accord- 
ing to  the  experiments  of  the  Commission,  is  neither  by  direct  con- 
tact nor  by  air,  soil,  or  food,  but  solely  by  the  flea.  Contact  was 
excluded  by  placing  healthy  rats  in  the  same  room  with  plague- 
infected  animals  from  which  the  fleas  had  been  removed,  when  it 
was  found  that  none  of  them  developed  plague.  The  experiment 
was  kept  up  for  a  long  time,  replacing  dead  infected  rats  with 
freshly  infected  rats,  and,  further,  the  room  was  never  cleaned  out,  so 
that  the  healthy  animals  lived  in  contact  with  the  infected  urine  and 
faeces,  and  even  ate  food  polluted  therewith,  and  yet  not  one  con- 
tracted plague,  thus  excluding  transmission  by  contact,  soil,  and  food. 

Again,  when  healthy  animals  were  suspended  in  cages  2  feet 
from  the  ground,  so  that  the  fleas  could  not  get  to  them,  or  placed 
on  the  ground,  and  surrounded  by  6  inches  of  tangle-foot,  over 
which  a  flea  cannot  pass,  as  it  is  said  to  be  incapable  of  jumping 
more  than  4  inches,  or  surrounded  by  a  curtain  of  wire  gauze  so 
fine  that  a  flea  could  not  penetrate  it,  and  exposed  to  infection, 
they  escaped,  though  others  not  so  protected  became  infected,  thus 
disproving  aerial  infection.  Further,  the  transmission  by  the  rat- 
flea  was  proved  by  constructing  a  glass  box,  inside  which  two  wire 
cages  were  placed  at  a  little  distance,  but  side  by  side,  each  standing 
in  a  tray  filled  with  sand.  Each  cage  had  a  lid,  through  which  rats, 
food,  water,  etc.,  could  be  introduced,  and  the  whole  apparatus 
was  covered  in  with  fine  muslin  to  prevent  the  escape  of  the  fleas. 
A  plague-infected  rat  and  a  number  of  rat -fleas  were  placed  in  one 
cage.  When  this  rat  died,  a  healthy  rat  was  placed  in  the  other 
cage,  and  after  some  time  the  dead  body  of  the  infected  rat  was 
removed,  when  it  was  found  that  the  new  rat  became  infected  with 
plague,  and  fleas  containing  bacilli  were  found  upon  it.  This 
experiment  was  repeated  many  times,  45  per  cent,  of  the  exposed 
rats  taking  the  disease.  Further,  fleas  infected  by  biting  plague 
rats,  when  placed  upon  healthy  rats,  produced  the  disease  in  55  per 
cent,  of  the  experiments. 

The  Commission  calculated  that  the  blood  of  an  ordinary  plague 
rat  in  two-thirds  of  the  cases  contains  more  than  100,000,000  bacilli 
per  cubic  centimetre,  and  that  a  flea's  stomach  could  hold  0-5  cubic 
millimetre  of  blood.  Therefore,  when  the  flea  gorged  itself  on  the 
average  plague-stricken  rat  it  received  at  least  5,000  bacilli.  These 
bacilli  are  found  only  in  the  stomach  and  in  the  alimentary  canal 
posterior  to  that  viscus,  especially  the  rectum,  and  escape  from  the 


i422  PLAGUE 

flea  solely  with  the  faeces.  It  was  proved,  however,  that  the  bacilli 
multiplied  in  the  body  of  the  flea  by  allowing  infected  fleas  to  feed 
solely  on  uninfected  rats,  a  fresh  one  being  supplied  each  day,  when 
abundant  bacilli  were  found  up  to  the  twelfth,  and  once  to  the 
twentieth  day,  thus  proving  that  multiplication  must  have  taken 
place,  otherwise  the  original  number  of  bacilli  would  have  become 
much  diluted  by  the  feeds  with  fresh  blood.  Further,  it  was  dis- 
covered that  the  proportion  of  fleas  in  whose  stomach  multiplication 
took  place  was  six  times  greater  in  the  epidemic  than  in  the  non- 
epidemic  season.  In  the  former  season  the  bacilli  could  be  found 
easily  up  to  the  fourth  and  even  to  the  twelfth  day,  while  in  the 
latter  never  after  the  seventh  day.  Infected  fleas  were  found  to 
transmit  the  disease  for  seven  to  fifteen  days. 

The  method  of  infection  probably  is  in  one  of  two  ways — either 
faecal  pollution  of  the  proboscis,  or  else  faecal  pollution  of  the  wound 
made  by  the  proboscis,  which  was  found  quite  large  enough  for  the 
purpose  of  introducing  the  bacilli  into  the  skin.  Martin's  experi- 
ments tend  to  show  that  regurgitation  often  takes  place,  due  to 
plugs  of  bacilli  in  the  oesophagus  (see  Chapter  XXXV. ) .  Both  males 
and  females  can  transmit  the  disease,  but  it  was  found  that  one  in- 
fected flea  alone  was  unlikely  to  do  so.  The  flea  most  commonly 
found  on  rats,  and  the  one  by  which  the  infection  in  these  experi- 
ments was  usually  spread,  was  Xenopsylla  cheofiis  Rothschild,  but 
others — e.g.,  Ceratophyllus  fasciatus  and  Pulex  irritans — were  found 
also  capable  of  causing  the  disease. 

With  regard  to  the  spread  of  the  disease  to  man,  the  Commission 
believes  that  the  infection  generally  comes  from  Epimys  rattits, 
because  the  habits  of  that  rodent  bring  it  into  close  relationship 
with  man,  and  because  the  curve  of  its  epizootic  begins  to  rise  ten 
to  fourteen  days  before  that  of  the  epidemic.  This  period  is  calcu- 
lated to  be  made  up  of  three  days,  during  which  the  flea  leaves 
the  dead  rat,  to  which  is  added  another  three  days,  which  is  the 
incubation  period  of  plague  in  man,  and  five  and  a  half  days,  which 
is  the  average  duration  of  the  fatal  illness  in  man. 

Xenopsylla  cheopis  appears  to  be  the  flea  by  which  plague  is 
spread  from  Epimys  rattus  to  man.  This  rat-flea  will  not  merely  bite 
man  when  it  cannot  get  rat's  blood,  but  is  capable  of  living  for 
three  to  four  weeks  on  man's  blood,  and  is  often  found  on  human 
beings  after  inspection  of  plague-stricken  houses. 

Further,  it  is  believed  that  the  spread  of  plague  is  due,  not  to 
migration  of  rats,  but  to  the  carriage  of  infected  rats  on  ships,  and 
of  fleas  in  merchandise  or  on  human  beings.  The  Commission 
apparently  consider  the  last  to  be  the  most  important  method. 

In  Ceylon,  as  observed  by  Hirst,  the  commonest  rat-flea  is  Xeno- 
psylla astia  Rothschild,  which  seems  to  bite  man  with  great  reluct- 
ance at  temperatures  over  80 °  F. 

Pneumonic  plague,  which  occurs  only  in  2*5  per  cent,  of  cases 
during  bubonic  epidemics,  spreads  from  man  to  man  by  bacilli 
carried  by  the  air,  for  Strong  and  Teague  demonstrated  that  the 


CLIMATOLOGY  1423 

sputum  in  invisible  droplets  containing  viable  plague  bacilli  was 
frequently  to  be  found  in  the  air  near  a  patient.  Teague  and  Barber 
have  shown  that  the  fine  droplets  of  sputum  disappear  very  quickly 
unless  there  is  a  considerable  amount  of  aqueous  vapour  in  the 
atmosphere,  as  is  found  in  very  cold  climates,  and  hence  the  ten- 
dency for  pneumonic  plague  to  spread  in  those  rather  than  in  warm 
climates.  On  the  other  hand,  the  bubonic  or  septicemic  is  not 
spread  from  man  to  man,  but  from  rats  to  man.  The  epizootic 
is  the  real  disease,  and  the  epidemic  is  only  an  offshoot. 

The  above  aetiology  explains  fully  the  predisposing  causes  of  sex, 
women  staying  more  in  the  house  than  men;  of  house,  of  season,  of 
climate,  and  also  the  carriage  of  the  disease  from  one  place  to 
another  by  people,  fodder,  grain,  bales  of  cotton,  and  clothing, 
rags,  etc. 

Verjbitski  in  1908  showed  that  bugs  could  act  as  carriers  of  the 
bacilli,  and  this  has  been  confirmed  by  Jordansky  and  Kladnitsky, 
while  Walker  considers  Clinocoris  rotundatus  to  be  one  of  the 
carriers  of  plague  in  India,  having  found  22  per  cent,  infected  with 
B.  pestis  when  collected  from  infected  native  huts.  Moreover,  he 
successfully  transmitted  the  disease  from  man  to  the  rat  by  means 
of  Clinocorus  rotundatus. 

The  possibility  of  lice  acting  as  occasional  carriers  should  not  be 
forgotten.  Lice  caught  on  patients  suffering  from  plague  have  at 
times  been  found  infected  with  B.  pestis. 

In  California,  Wherry,  McCay,  and  others  have  shown  that  the 
ground-squirrel  (Citellus  beecheyi)  is  subject  to  plague,  and  that  its 
commonest  flea,  Ceratophyllus  acatus  Baker,  is  the  vector  from 
squirrel  to  squirrel,  and,  further,  that  this  flea  will  bite  man. 
Further,  they  record  a  subacute  case  of  plague  in  a  boy  where  the 
infection  was  believed  to  be  acquired  by  contact  with  ground 
squirrels.  With  regard  to  the  outbreak  in  Manchuria  and  North 
China,  Gray  has  shown  that  it  started  among  men  who  handled  the 
tarbagan  (Arctomys  bobak  Miiller),  which  is  susceptible  to  epizootic 
plague,  and  that  these  men  on  returning  to  their  homes  introduced 
the  disease  into  three  provinces,  as  pneumonic  and  septicemic 
plague,  while  it  was  spread  by  the  agency  of  the  breath  and  personal 
contact  of  clothes  and  belongings  by  coolies  travelling  in  parties 
and  sleeping  together  in  overcrowded  insanitarjr  inns,  especially 
as  the  cold  of  the  winter  induced  an  indoor  existence.  These 
travelling  parties  infected  adult  males  who  stayed  at  the  inns  or  were 
travelling,  and  so  it  spread  to  the  ordinary  population.  No  infected 
rats  could  be  found,  in  20,000  examined,  while  isolation  of  the 
patients  and  their  contacts,  together  with  efficient  disinfection,  were 
sufficient  to  diminish  the  death-rate.  This  shows  how  important 
the  pneumonic  form  of  plague  may  be  in  epidemics,  especially  in 
cold  weather,  but  it  is  also  to  be  noted  that,  although  it  starts  from 
association  with  an  epizootic,  it  tends  to  die  out  without  being  suc- 
ceeded by  a  bubonic  outbreak,  but  it  may  infect  rats  and  so  cause 
a  bubonic  epidemic.     There  has  been  an  epizootic  in  Suffolk,  in 


1424  PLAGUE 

England,  but  only  a  few  cases  of  bubonic  plague  in  man.  The 
tarbagan  suffers  at  times  from  plague,  but  the  epizootic  is  not 
extensive,  and  its  direct  relationship  to  human  plague  is  negligible. 
Spermophilus  citellus,  the  marmot,  is  susceptible  to  plague. 

Attention  may  be  called  to  epidemic  diseases  in  the  lower  animals  due  to 
bipolar  staining  bacilli,  somewhat  resembling  the  plague  germ.  We  have 
observed  one  such  epidemic  in  cats  in  Ceylon  in  1904.  A  bipolar  staining 
bacillus  was  found  to  be  the  cause  {Bacillus  felisepticus  Castellani),  but  the 
cultural  characters  were  somewhat  different  from  those  of  the  true  plague 
bacillus. 

Pathology. — Plague  is  a  hemorrhagic  septicaemia  in  the  rat,  which 
is  communicated  to  the  human  being  by  flea-bites.  The  site  of 
inoculation  is  sometimes  marked  by  a  vesicle,  the  contents  of  which 
contain  the  Bacillus  pesfis  in  considerable  numbers.  The  bacilli 
then  travel  via  the  lymphatics  to  the  nearest  lymphatic  glands, 
which  they  may  traverse,  and,  passing  through  the  thoracic  duct, 
enter  the  blood  stream,  and  cause  a  septicaemia.  More  usually  they 
remain  and  grow  in  the  peripheral  lymph  sinuses  of  those  glands  in 
which  they  or  their  toxins  cause  degenerations  of  the  cells,  peri- 
glandular serous  infiltration,  and,  later,  degeneration  of  the  walls 
of  the  bloodvessels  and  haemorrhage.  The  lymphatic  glands  are 
matted  together  by  the  exudation  from  the  primary  bubo.  The 
glands  usually  affecled  are  the  femoral,  inguinal,  axillary,  iliac,  or 
cervical,  which  may  briefly  be  classified  into  the  groin,  the  axillary, 
and  cervical  glands. 

The  Indian  Commission  points  out  that  the  reason  why  the 
groin  glands  are  so  frequently  attacked  is  simply  because  they 
drain  the  largest  skin  area,  for  they  say  that  the  areas  drained  by 
the  glands  of  the  neck,  axilla,  and  groin  are  in  the  proportions  of 
1 :  1-8:5,  while  the  number  of  cervical,  axillary,  and  inguinal  buboes 
are  in  the  proportions  of  1 :  1-3 :  5-8,  and  that  therefore  there  is  no 
seat  of  election  as  to  where  the  plague  bacillus  enters. 

From  the  primary  bubo  the  bacilli  may  travel  along  the  lymphat  ics 
to  the  next  chain  of  glands,  in  which  they  produce  the  secondary 
bubo,  and  from  this  they  may  enter  the  blood  stream  via  the 
lymphatics.  The  bacilli,  however,  may  gain  direct  access  to  the 
blood  stream  through  the  injuries  to  the  walls  of  the  veins  in  the 
primary  bubo.  Once  the  blood  stream  is  reached  the  disease 
becomes  a  septicaemia,  and  affects  the  lymphatic  glands,  forming 
tertiary  buboes;  the  lungs,  causing  bronchitis  and  secondary 
pneumonia;  the  spleen,  liver,  kidneys,  skin,  and  other  organs;  and, 
finally,  leaves  the  body  through  the  kidneys,  skin,  and  mucosae, 
escaping  in  the  urine,  faeces,  and  sputum  (if  there  is  pneumonia),  as 
well  as  by  any  discharges  or  haemorrhages  from  the  skin.  The 
excretion,  via  the  sputum  and  saliva,  can  proceed  for  a  period  of  at 
least  forty-eight  days  after  the  temperature  is  normal.  Further, 
as  in  chronic  plague  in  rats,  the  bacilli  may  be  found  in  abscesses 
some  two  and  a  half  months  after  an  attack.  The  chemical  patho- 
logy of  the  disease  is  not  well  known. 


PATHOLOGY— MORBID  ANATOMY  1425 

Strong,  Crowell,  and  Tea.gue,  from  a  study  of  the  pathology  of 
Mukden  plague,  have  concluded  that  epidemic  pneumonic  plague 
results  from  inhalation  of  the  bacilli.  The  primary  infection  appears 
to  be  the  bronchi,  while  it  extends  along  the  bronchioles  by  con- 
tinuity into  the  infundibula  and  air-cells,  or  through  the  walls  of 
bronchioles  into  the  lung  tissue,  causing  a  peribronchial  inflamma- 
tion. From  these  centres  the  infection  spreads  to  the  adjacent 
pulmonary  tissue  and  to  the  visceral  pleura,  the  bacilli  growing 
rapidly,  and  causing  first  a  lobular  pneumonia  and  later  a  lobar 
pneumonia,  while  the  blood  becomes  quickly  infected,  causing  a 
septicaemia.  Secondary  pathological  changes  take  place  in  the 
spleen,  bronchial  glands,  heart,  bloodvessels,  kidneys,  liver,  and 
tonsils,  which  may  at  times  become  primarily  affected.  No  sign 
of  any  intestinal  plague  was  found,  although  plague  bacilli  must 
have  been  repeatedly  swallowed  in  the  bronchial  secretions  and 
saliva  by  the  patients. 

Morbid  Anatomy. — The  characteristic  features  of  a  plague  post- 
mortem are  the  haemorrhages  and  the  buboes,  which  have  been 
studied  in  detail  by  Diirck.  The  skin  in  the  region  of  buboes 
and  on  the  head,  arms,  neck,  and  shoulders  may  show  haemorrhages, 
which  arise  from  the  action  of  the  toxins  upon  the  endothelial  cells 
of  the  vessels.  These  cells  increase  in  size,  and  perhaps  in  number, 
and  some  macrophages  arise,  after  which  they  degenerate,  and  allow 
haemorrhages  by  rhexis  to  take  place.  These  haemorrhages,  there- 
fore, may  be  petechial  or  diffuse,  and  will  contain  bacilli.  Besides 
these,  however,  vesicles,  pustules,  or  carbuncles,  may  be  seen. 

The  vesicle  arises  from  the  irritation  caused  by  the  bacilli  in  the 
skin,  producing  inflammation  with  exudation,  which  may  go  on  to 
pustulation,  or,  the  vesicle  drying  up,  the  cutis  may  become  much 
inflamed  and  degenerated,  forming  the  so-called  carbuncle,  which 
in  no  respect  resembles  a  true  carbuncle. 

The  primary  bubo  shows  a  periglandular  infiltration,  which  may 
spread  from  the  site  of  the  enlarged  glands  in  all  directions.  When 
this  gelatinous  exudate  is  cut  into,  the  enlarged  glands  can  be  seen 
matted  together,  grey  or  yellowish-grey  in  colour,  with  a  soft  centre 
and  numerous  haemorrhagic  spots,  or  perhaps  large  haemorrhages. 
The  secondary  buboes  are  seen  to  consist  of  degenerated  glands 
without  the  oedema,  but  with  endo-  and  peri-glandular  haemorrhages. 
The  tertiary  buboes  contain  hard  hyperaemic  glands  marked  by 
haemorrhages. 

The  muscles  of  the  body,  but  especially  those  of  the  abdominal 
wall,  will  be  seen  to  be  haemorrhagic.  The  spleen  is  enlarged  and 
congested,  and  shows  hemorrhages  and  contains  bacilli.  The  liver 
may  be  slightly  enlarged  and  haemorrhagic,  with  cloudy  swelling  and 
fatty  degeneration  of  the  cells.  The  lungs  usually  show  some 
bronchitis,  and  often  patches  of  secondary  broncho-pneumonia. 
The  right  heart  is  usually  dilated,  and  the  musculature  shows  fatty 
degeneration,  cloudy  swelling,  and  haemorrhage.  Primary  broncho- 
pneumonia may,  however,  exist,  and  be  followed  by  a  septicaemia 

90 


1426 


PLAGUE 


and  bubo  formation.  The  stomach  is  hyperaemic  and  hemorrhagic, 
while  the  solitary  glands  and  Peyer's  patches  of  the  intestine  are 
swollen  and  the  mesenteric  glands  enlarged.  The  kidney  may  be 
normal,  or  show  haemorrhages.  The  nervous  system  seldom  shows 
any  changes,  but  haemorrhages  and  meningitis  may  occur. 

The  post-mortem  appearances  of  plague  in  rats  are: — 

Bubonic  Type. — Lymphatic  glands  enlarged  and  haemorrhagic.  liver  and 
spleen  enlarged  and  congested ;  the  former  shows  granular  degeneration  of  a 
peculiar  nature,  and  the  latter  is  speckled  with  whitish  spots  as  seen  on  section. 
There  is  often  fluid  in  the  pleural  sacs.  These  features  have  been  found  useful  in 
diagnosis  of  plague  rats  when  microscopical  examinations  cannot  be  carried  out. 

Septicemic  Type. — There  are  no  characteristic  macroscopic  features,  and 
the  diagnosis  is  solely  based  upon  microscopic  findings  of  the  splenic  juice 
and  heart  blood. 

Doell  and  Warner  have  applied  to  the  diagnosis  of  plague  infection  in  rats 
Ascoli's  thermoprecipitation  method. 

In  cases  of  acute  septicemic  type  there  is  no  post-mortem  charac- 
teristic feature  on  which  the  diagnosis  of  plague  may  be  made  or 

even  suspected.  The  lym- 
phatic glands  are  not 
enlarged,  though  the  spleen 
may  be  of  larger  size  than 
normal. 

Symptomatology  — Incuba- 
tion.— The  incubation  period 
varies  from  two  to  ten  days,, 
the  averag"e  being  three 
days.  During  this  period 
there  may  be  prodromal 
symptoms  in  the  form  of 
general  malaise,  headache, 
gastro-intestinal  disturbance, 
pain ,  or  feeling  of  discomfort 
in  the  site  of  the  future  bubo,  chilliness,  giddiness,  and  mental  dulness. 
Onset.- — The  onset  is  usually  sudden,  with  rise  of  the  temperature 
to  1030  to  1040  F.,  pulse  of  120,  and  respirations  30  to  40,  and  marked 
prostration,  with  an  aggravation  of  the  prodromal  symptoms- — i.e.. 
severe  headache,  furred  tongue,  vomiting,  at  times  diarrhoea,  pains 
in  the  back  and  limbs,  and  at  the  site  of  the  future  bubo,  marked 
chilliness  or  a  rigor,  staggering  gait,  and  marked  mental  dulness. 

Course. — In  a  few  hours  the  disease  becomes  properly  established, 
when  the  patient  presents  a  typical  facial  expression  of  fear  or 
anxiety,  the  eyes  being  bloodshot,  bright,  and  staring,  the  face  drawn 
and  the  nostrils  dilated.  The  temperature  rises  during  the  first  day, 
but  may  remit  a  degree  or  so  on  the  second  day,  but  if  so,  it  rises 
quickly  again  to  the  same  or  a  higher  degree  than  at  first.  As  a 
rule,  however,  the  temperature  is  most  irregular.  Towards  the  end 
it  may  fall  by  lysis,  if  recovery  is  to  take  place,  or  fall  rapidly  to 
normal  or  subnormal,  and  then  as  rapidly  to  rise  about  1070  F.,  or 
may  simply  rise  directly  to  about  1070  F.,  and  death  ensue.     There 


Fig. 


670. — Temperature  Chart 
of  Plague. 


SYMPTOMATOLOGY  1427 

is  much  thirst,  and  the  tongue  is  coated  at  first  with  a  whitish  fur, 
but  later  it  becomes  covered  with  sordes,  as  do  the  teeth  and  lips. 
Vomiting  is  frequently  met  with,  as  well  as  diarrhoea;  but  the 
abdomen  is  not  tender,  unless  there  are  enlarged  abdominal  glands. 
The  spleen  is  always,  and  the  liver  often,  enlarged.  Cardiac  dilata- 
tion is  an  important  feature  of  the  disease,  and  systolic  murmurs 
may  be  heard.  The  pulse  is  rapid,  reaching  120  to  180  early  in  the 
disease,  and  later  becoming,  in  bad  cases,  not  countable.  At  first 
it  is  full  and  of  moderate  tension,  but  later  it  becomes  small,  weak, 
and  intermittent. 

The  coagulation  of  the  blood  is  diminished.  Plague  bacilli  can 
be  found  culturally  in  about  a  third  of  the  cases  examined.  The 
number  of  erythrocytes  and  the  amount  of  haemoglobin  are  distinctly 
increased  above  the  normal,  and  there  is  a  great  leucocytosis — i.e., 
90,000  to  100,000  and  more — but  in  the  septicemic  form  there  may 
be  a  leucopenia.  The  leucocytosis  is  almost  entirely  due  to  an 
increase  in  the  polymorphonuclear  leucocytes. 

The  breathing  is  rapid,  and  the  breath  sounds  harsh,  with  moist 
rales,  but  signs  of  lobular  pneumonia  and  pleuritis  may  also  occur. 
The  sputum  in  this  type  of  pneumonia  is  very  hemorrhagic  and  full 
of  bacilli. 

Buboes  of  varying  sizes  may  be  noted  in  the  groin,  the  axilla,  or 
the  neck,  and  are  very  painful,  respectively  causing  the  patient  to 
lie  with  the  leg  drawn  up  close  to  the  chest  wall,  or  the  head  bent 
towards  the  affected  side.  They  usually  appear  during  the  first 
twenty-four  hours,  and  they  may  decline  or  suppurate. 

The  skin  is  hot  and  dry,  and  may  show  vesicles,  pustules,  or  areas 
of  necrosis,  often  called  '  carbuncles  '  (they  are,  of  course,  not  true 
carbuncles).  Hemorrhages,  in  the  form  of  petechia:  or  ecchymoses, 
may  be  seen  under  the  skin,  and  epistaxis,  hematemesis,  melena, 
and.  hematuria  may  occur. 

The  quantity  of  urine  is  usually  diminished,  the  specific  gravity 
is  high,  and  plague  bacilli  may  be  found.  If  hemorrhages  have 
occurred  in  the  urinary  tract,  there  will  be  erythrocytes  and 
leucocytes,  with  albumen  and  globulin,  though,  apart  from  this, 
there  is  often  a  trace  of  albumin  present,  while  anuria  is  generally 
present  before  death.     Pregnant  women  always  abort. 

Termination.— As  the  disease  progresses  the  patient  becomes 
weaker  and  weaker,  the  mind  wanders,  and  a  wild  delirium  may 
occur;  but  later  a  low  muttering  delirium  passes  into  coma,  and 
death  ensues  from  the  third  to  the  fifth  day.  In  favourable  cases  the 
tongue  becomes  moist  and  clean,  the  temperature  declines  by  lysis, 
the  pulse-rate  diminishes,  and  convalescence  begins,  but  may  be 
much  prolonged  by  suppuration  of  the  buboes  or  by  a  secondary 
septicemia.  Even  now  death  may  occur  from  cardiac  failure, 
suppuration,  septic  infection,  or  secondary  hemorrhage. 

Varieties. — Four  variations  of  the  disease  are  recognized:  (1)  The 
ambulatory  type;  (2)  the  bubonic  type;  (3)  the  acute  septicemic 
type;  and  (4)  the  pneumonic  type. 


i428  PLAGUE 

The  Ambulatory  Type. — This  is  the  mildest  form  of  the  disease, 
and  is  characterized  by  but  little  fever,  with  slight  enlargement  and 
tenderness  of  a  group  of  lymphatic  glands.  If  the  area  of  skin 
drained  by  these  glands  is  carefully  investigated,  a  primary  vesicle 
will  often  be  seen  at  the  site  of  the  inoculation,  and  considerably 
helps  in  the  diagnosis,  for  its  fluid  contains  typical  bacilli.  The 
symptoms  of  this  type  resemble  those  already  described  as 
prodromata. 

TheBubonic  Type. — This  type  agrees  with  the  general  description, 
the  bubo  being  usually  in  the  groin,  less  commonly  in  the  axilla,  and 
least  commonly  in  the  neck.  The  fever  reaches  its  maximum  on 
the  fourth  to  fifth  day,  and  lasts  till  the  seventh  to  tenth  day,  when 
it  falls  by  lysis,  though  it  may  rise  again  if  suppuration  is  taking 
place  in  the  buboes.  The  attitude  of  the  patient  depends  upon  the 
position  of  the  bubo,  as  described  above. 

The  Acute  Septicemic  Type. — Here  the  onset  is  sudden,  and  the 
temperature  very  high,  with  very  rapid  pulse,  marked  prostration, 
and  delirium.  There  may  be  severe  vomiting,  and  occasionally 
diarrhcea.  No  enlarged  lymphatic  glands  are  found,  and  the 
diagnosis  on  clinical  grounds  may  be  impossible.  Haemorrhages 
may  at  times  occur  in  the  skin  and  from  the  regions  indicated  above, 
and  death  rapidly  takes  place  in  from  eighteen  hours  to  three  days. 
This  type  of  the  disease  is  often  common  at  the  onset  of  an  epidemic. 

ThePneumonic  Type. — There  are  two  distinct  types  of  pneumonia 
in  plague — a  pneumonia  secondary  to  bubonic  plague  and  a  primary 
pneumonia.  This  latter  begins  suddenly  without  prodromata,  after 
an  incubation  of  two  to  five  days,  with  chilliness,  high  fever,  head- 
ache, anorexia,  and  rapid  pulse.  Within  twenty-four  to  thirty-six 
hours  the  temperature  is  1030  to  1040  F.,  and  the  pulse  no  to  130 
beats  per  minute.  Cough  and  dyspnoea  appear  within  twenty-four 
hours,  when  the  expectoration  is  at  first  scant}7,  but  soon  becomes 
abundant.  At  first  it  is  only  composed  of  mucus,  but  it  soon 
becomes  tinged  with  blood  and  later  very  hemorrhagic,  and  is  full 
of  bacilli.  The  conjunctivae  become  injected,  and  the  tongue 
coated  with  a  white  or  brownish  fur.  The  breathing  is  very  rapid, 
and  dulness  may  or  may  not  be  present  over  the  bases;  the  breath 
sounds  are  usually  tubular  and  crepitant,  and  sibilant  rales  are 
heard,  while  the  vocal  fremitus  may  be  increased.  Dyspnoea  and 
cyanosis  are  early  marked  features,  as  is  the  fluid  bloody  sputum 
which  is  found  by  the  second  or  third  day,  and  is  full  of  bacilli. 
Pleuritis,  with  its  usual  symptoms,  may  also  occur.  Prostration  is 
extreme;  the  heart  becomes  very  weak  and  the  pulse  rapid,  while 
the  spleen  is  usually  not  palpable.  A  marked  leucocytosis  may 
occur.  This  is  a  very  fatal  type  of  the  disease;  delirium  and  coma 
appear,  and  cases  die  at  the  end  of  sixteen  hours,  two  or  three  or, 
much  more  rarely,  four  days. 

Sequela. — Cardiac  weakness,  with  proneness  to  syncopal  attacks, 
paralyses,  septic  infections  of  the  buboes,  or  a  general  septic  infec- 
tion, or  gangrene  of  the  lung,  may  occur. 


DIAGNOSIS  1429 

Diagnosis. — This,  in  the  bubonic  type,  which  is  commonest,  is 
based  on  the  acute  onset  with  high  fever,  great  prostration,  and 
the  presence  of  a  bubo.  Difficulty  may  arise  in  the  diagnosis 
between  the  bubonic  type  of  plague  and  climatic,  venereal,  and 
symptomatic  buboes;  between  pneumonic  plague  and  ordinary 
pneumonia;  and  between  septicemic  plague  and  various  fevers. 

In  venereal  bubo  there  will  be  found  ulcers  on  the  genital  organs, 
or,  at  least,  the  patient  will  give  a  history  of  such.  In  climatic 
buboes  and  various  symptomatic  buboes  due  to  small  ulcerative 
lesions  on  the  legs,  etc.,  the  general  condition  of  the  patient  is  usually 
far  from  being  so  grave  as  in  plague.  In  any  doubtful  case  bacterio- 
logical methods  should  be  employed.  A  little  of  the  fluid  from  the 
suspected  bubo  is  withdrawn,  under  aseptic  precautions,  by  means  of 
a  sierile  syringe,  and  films  are  made  and  stained  with  methylene 
blue,  diluted  carbol-fuchsin,  or  Leishman's  stain.  The  presence  of 
bipolar  staining  bacilli  is  sufficient,  for  all  practical  purposes,  to 
diagnose  the  case  as  one  of  plague,  though  it  is  desirable,  whenever 
possible,  to  complete  the  investigation  by  cultural  methods  followed 
by  inoculations  into  animals. 

In  pneumonic  plague  the  expectoration  is  generally  fluid  and 
greatly  hemorrhagic,  and  is  not  purulent,  as  it  frequently  is  in 
catarrhal  bronchitis  or  in  bronchial  pneumonia,nor  is  it  tenacious,  as 
in  croupous  pneumonia;  the  examination  of  the  sputum — instead 
of  the  sputum,  the  lung  juice,  obtained  by  puncture  with  a  sterile 
syringe,  may  be  examined — will  reveal  the  presence  of  numerous 
plague  bacilli,  easily  distinguishable  from  the  pneumococcus  by 
their  being  Gram-negative. 

Acute  Septicemic  Plague. —The  diagnosis  is  most  difficult,  as  there 
are  no  characteristic  symptoms  and  no  glandular  enlargements.  In  a 
country  where  plague  is  endemic  any  case  of  sudden  high  fever,  with 
extreme  prostration  and  blood  examinations  negative  as  regards 
malaria  and  relapsing  fever,  should  be  viewed  with  suspicion.  The 
fever  is  generally  higher  than  in  dengue  or  pappataci  fevers,  often 
reaching  1050  F.,  while  the  prostration  is  much  more  marked.  The 
microscopical  examination  of  the  blood  for.B.  pestis  is  unfortunately 
often  negative,  and  the  cultural  examination  requires  time,  and 
hence  the  diagnosis  may  be  made  too  late,  as  by  that  time  the  patient 
may  be  dead.  It  may  be  dist  inguished  from  malaria  by  the  absence 
of  Lavenm's  parasites,  from  relapsing  fever  by  the  absence  of  spiro- 
chetes, but  it  is  to  be  noted  that  cases  of  mixed  infection  occur.  In 
India,  as  observed  by  Polverini  and  others,  cases  of  mixed  infection 
of  plague  and  relapsing  fever  are  not  rare.  The  diagnosis  between 
septicemic  plague  and  cryptogenic  septicemias  due  to  the  pneumo- 
coccus and  other  germs,  as  well  as  occasionally  the  differential  diag- 
nosis from  pernicious  malaria,  typhus  and  typhoid,  may  be  impossible 
without  a  complete  bacteriological  examination  of  the  blood. 

The  simple  microscopical  examination  of  thick  films  of  blood  (Manson-Ross 
method)  for  the  presence  of  bipolar  staining  bacilli  is  often  a  failure.  The 
so-called  dilution  method  introduced  by  Castellani  for  the  search  of  the  Bacillus 


i43o  PLAGUE 

typhosus  in  the  blood  of  typhoid  patients  is  useful  also  for  the  search  of  the 
plague  bacillus,  as  proved  by  Kolle  and  others:  10  c.c.  of  blood  are  collected, 
under  aseptic  precautions,  with  a  sterile  syringe  from  a  vein,  and  immediately 
distributed  into  several  flasks  of  slightly  alkaline  broth,  each  containing 
300  cubic  centimetres  of  the  medium.  In  this  way  the  bactericidal  substances 
of  the  blood  are  greatly  diluted,  and  the  growth  of  the  plague  bacillus  facilitated. 
Agglutination  tests  are  not  of  much  use  in  the  diagnosis  of  plague. 

In  places  far  from  bacteriological  laboratories  Broquet  recommends  that  a 
gland  or  a  portion  of  a  gland  obtained  as  soon  after  death  as  possible  should 
be  placed  in  a  vial  containing  125  to  175  c.c.  of  a  mixture  of  neutral  glycerine 
(300  B.)  20  c.c,  distilled  water  80  c.c,  and  carbonate  of  lime  2  grammes. 
The  mouth  of  the  vial  or  flask  is  flamed  and  sealed  with  paraffin.  On  arrival 
at  the  laboratory  the  glycerine  is  wiped  off  the  gland,  which  is  made  into  an 
emulsion  with  normal  saline,  and  injected,  half  into  a  guinea-pig  and  half 
into  a  rat.  It  is  stated  that  by  this  method  virulence  is  maintained  for 
thirteen  days,  which  is  of  great  importance  in  the  tropics.  A  dead  animal 
should  be  immersed  in  a  solution  of  strong  disinfectant,  such  as  carbolic  5  per 
cent.,  in  order  to  kill  the  fleas,  and  should  then  be  placed  in  sawdust  or  other 
packing  in  a  hermetically  sealed  air-tight  metal  case,  and  forwarded  for 
examination,  if  the  distance  is  not  too  far,  to  the  laboratory. 

Prognosis. — Simpson  quotes  Procopius  of  Caesarea  as  saying, 
with  regard  to  the  plague  in  Byzantium,  that  many  whose  death 
the  physicians  predicted  recovered,  while  those  who  were  supposed 
to  be  about  to  recover  often  quickly  died,  from  which  it  may  be 
inferred  that  the  prognosis  in  cases  of  plague  has  to  be  most  guarded, 
for  dangers  are  numerous  even  in  convalescence — e.g.,  cardiac 
failure. 

The  prognosis  varies  with  the  character  of  the  epidemic,  some 
being  milder  than  others,  and  is  better  when  the  number  of  cases 
is  declining.  It  also  varies  for  the  type  of  the  disease,  being  best 
for  the  ambulatory  and  worst  for  the  pneumonic.  As  75  per  cent, 
of  the  deaths  occur  before  the  sixth  day,  after  that  time  the  prognosis 
improves. 

A  good  pulse,  a  clear  mind,  a  normal  quantity  of  chlorides  and 
no  albumen  in  the  urine,  are  good  signs.  High  fever,  rapid,  thready 
pulse,  violent  delirium,  sudden  fall  in  the  temperature,  disappear- 
ance of  the  buboes  on  the  fourth  or  fifth  day,  and  anuria,  are  bad 
signs.  But  in  all  cases  be  cautious  about  the  prognosis,  and  re- 
member the  physicians  of  Byzantium.  In  pneumonic  plague  the 
prognosis  is  most  unfavourable — e.g.,  in  the  Manchurian  epidemic 
of  pneumonic  plague  no  case  in  which  the  bacteriological  diagnosis 
was  positive  was  known  to  recover. 

Treatment. — The  treatment  should  aim  at  killing  the  bacillus 
and  neutralizing  its  toxins,  and  naturally  one  hopes  to  find  those 
requirements  supplied  by  sera.  Unfortunately  no  such  serum  has 
as  yet  been  found,  though  encouraging  reports  have  been  recorded 
by  Choksy  and  Polverini  concerning  Yersin's  and  Lustig's  sera,  and 
by  others  concerning  Cruz's  serum.  Whatever  the  serum,  it  should 
be  given  in  large  doses  (30  to  50  c.c,  and  even  more)  by  subcu- 
taneous injection.  A  second  and  a  third  injection  can  be  given 
during  the  course  of  the  disease,  but  one  should  keep  in  mind  the 
possibility   of    anaphylactic   symptoms   in   people   previously    in- 


TREATMENT—PROPHYLAXIS  I43X 

oculated  with  serum.     Several  such  cases  have  been  recorded  by 
Darling.     The  serum  may  be  given  also  by  intravenous  injection. 

Yersin's  serum  is  prepared  by  the  inoculation  of  horses  with 
fresh  agar  cultures,  and  is  such  that  o«i  c.c.  should  protect  a  mouse 
from  a  dose  of  bacilli,  which  otherwise  would  kill  it  in  two  to  three 
days.  The  dose  for  man  is  60  to  300  c.c,  given  intravenously  and 
also  subcutaneously  near  the  buboes.  Lustig  and  Galeotti's  serum 
is  prepared  by  injecting  a  horse  with  a  vaccine  which  contains 
nucleo-proteid  from  cultures.  The  mode  of  action  of  these  sera  is 
said  by  so*me  not  to  be  bactericidal,  but  to  encourage  phagocytosis. 

Though  admitting  that  the  serum  treatment  is  far  from  being 
perfect,  we  advise  its  use  at  the  very  beginning,  as  it  gives  somewhat 
better  results  than  the  ordinary  symptomatic  treatment  or  the 
so-called  antiseptic  treatment,  such  as  the  internal  administration 
of  carbolic  acid. 

As  regards  the  symptomatic  treatment,  the  first  indication  is  to 
keep  the  patient  in  bed,  because  of  the  danger  of  syncope,  and  to  give 
him  good  nursing  and  fresh  air.  Fever  must  be  treated  by  sponging 
and  cool  or  cold  applications;  buboes  by  cold  applications  and 
ichthyol,  and  when  they  suppurate  an  incision  must  be  made  and 
the  wound  treated  aseptically.  Not  much  good  is  to  be  obtained 
by  excising  the  glands  even  in  an  early  stage,  though  several 
authors — e.g.,  Terni — have  recommended  it.  The  heart's  action 
must  be  maintained  by  digitalis,  strophanthus,  and  strychnine. 
Restlessness  may  require  a  hypodermic  of  hyoscin;  haemorrhage 
will  require  treatment  by  calcium  chloride;  the  so-called  car- 
buncles must  be  treated  antiseptically;  pneumonia  and  bron- 
chitis require  the  ordinary  treatment;  and  if  there  is  constipation, 
calomel  and  a  saline  purge  may  be  given;  while  vomiting  is  to 
be  treated  as  described  under  Malaria.  A  sufficiency  of  fluid  should 
be  given,  so  as  to  keep  up  the  action  of  the  kidneys. 

The  diet  should  consist  of  broths  and  milk,  while  stimulants  are 
usually  required. 

Tincture  of  iodine  has  been  recommended,  and  is  given  by  oral  administra- 
tion, a  few  drops  at  a  time,  diluted  with  cinnamon  water,  and  may  be  given 
also  by  intravenous  injection,  5  to  7  minims  once  or  twice  daily.  Eusol  has 
been  recommended  by  Brayne. 

Prophylaxis. — Bacillus  pestis  being  conveyed  by  the  rat -bite  from 
rats  to  man  as  a  rule,  and  more  rarely  from  man  to  man,  it  is 
obvious  that  prophylaxis  must  include  methods  directed  against 
rats  and  fleas,  and  methods  for  the  protection  of  human  beings. 

The  spread  of  the  disease-  from  place  to  place  is  thought  to  be 
mainly  by  the  flea  being  carried  by  human  beings  on  their  person, 
or  in  their  clothing,  or  by  means  of  the  merchandise,  or  by  rats. 

The  prophylaxis  will  be  considered  under  two  headings — Public 
Prophylaxis  and  Personal  Prophylaxis. 

Public  Prophylaxis. — It  is  necessary,  in  order  to  prevent  a 
country  from  being  infected  with  plague,  to  institute  a  Sanitary 
Service,  which  should  consist  of  a  central  authority  for  collecting 


1432  PLAGUE 

and  dealing  with  information  on  a  large  scale,  and  to  which  will 
be  attached  bacteriologists,  who  will  carry  out  the  necessary 
bacteriological  examinations  and  prepare  prophylactics;  and  a 
Port  Sanitary  Branch,  for  investigating  and  disinfecting  ships. 

It  is  as  well,  if  possible,  to  limit  the  communication  with  infected 
areas  to  as  few  ports  as  possible,  and  to  provide  isolation  hospitals 
for  the  sick  and  for  the  healthy  coming  from  infected  areas.  The 
length  of  quarantine  is  fixed  at  present  at  five  days,  but  this  appears 
to  be  too  short,  if  the  findings  of  the  Indian  Commission  with  regard 
to  fleas  are  considered. 

Attempts  can  be  made  to  prevent  the  disease  crossing  land 
frontiers  by  the  medical  inspection  of  persons  coming  by  rail,  road, 
or  river,  but  this  method  of  prophylaxis  is  liable  at  any  time  to 
break  down. 

It  would  appear  most  necessary  to  disinfect  the  clothing  and 
persons  of  all  people  coming  from  infected  areas,  as  they  may  carry 
fleas,  and  this  is  most  difficult  to  effect;  but  it  is  not  so  difficult  to 
disinfect  merchandise  by  the  Clayton  apparatus. 

In  addition,  rats  must  be  caught  regularly  in  places  situated  in 
danger  zones,  and  inspected  to  see  if  any  are  becoming  diseased, 
for  the  epizootic  begins  before  the  epidemic  as  a  rule. 

But  of  all  things  the  most  difficult,  as  well  as  the  most  important, 
appears  to  be  the  recognition  of  early  cases,  and  pneumonia,  buboes, 
and  sudden  deaths  must  be  regarded  with  the  greatest  suspicion. 

When  an  epidemic  begins  there  are  two  periods,  as  Simpson  points 
out,  at  which  the  populace  takes  fright,  and  has  to  be  firmly  handled : 
one  at  the  beginning,  and  the  second  when  the  deaths  begin  to 
increase  rapidly  in  number.  Riots  and  assassinations  of  magistrates, 
medical  officers,  and  inspectors  may  occur,  and  must  be  foreseen. 

As  diagnosis  is  so  difficult  at  first,  a  house-to-house  inspection 
by  competent  medical  officers  will  be  necessary  to  find  out  the 
number  of  cases,  and  in  no  instance  must  a  body  be  allowed  to  be 
buried  without  being  viewed  by  a  medical  officer.  If  this  is  not 
done,  it  will  be  impossible  to  gauge  the  extent  of  the  disease. 

Rats  must,  of  course,  be  regularly  and  systematically  examined, 
and  their  mortality  curves  constructed.  The  sick  must  be  isolated, 
and  the  persons  and  clothing  of  contacts  disinfected  to  kill  the  fleas. 
Every  infected  house  must  be  disinfected  by  filling  the  adjoining 
houses  with  the  gas  from  a  Clayton  apparatus,  and  after  this  the 
house  itself.  If  this  method  is  not  carried  out,  the  rats  will  simply 
pass  from  the  infected  to  the  non-infected  houses,  and  spread  the 
plague.  Village  houses  might  be  burnt,  which  is  cheaper  and  a 
fairly  effective  method,  though,  of  course,  measures  should  be  taken 
to  prevent  the  rats  escaping.  The  gas  in  question  is  generated  by 
burning  sulphur  at  a  very  high  temperature  in  a  special  apparatus, 
when  S02  and  S03  and  some  unknown  gases  are  evolved,  which  are 
passed  into  the  ship,  house,  warehouse,  etc.,  and  drawn  through  by 
an  exhaust-pipe  until  a  3  per  cent,  mixture  of  gas  and  air  comes  out, 
when  the  exhaust  is  stopped,  and  gas  passed  in  until  10  to  12  per  cent. 


PROPHYLAXIS  1433 

is  reached,  at  which  it  is  allowed  to  remain  for  four  hours.  For  the 
fumigation  of  ships  it  is  found  to  be  much  more  satisfactory  if  the  gas 
is  made  to  circulate  and  to  penetrate  better  by  means  of  electric  fans 
and  similar  devices.  This  gas  kills  rats,  rat-fleas,  and  other  insects, 
and  plague  bacilli,  and,  if  dry,  will  not  injure  food-stuffs,  except  fruit 
and  some  vegetables,  nor  will  it  harm  merchandise  or  machinery. 
A  mixture  of  equal  parts  of  cyllin  and  petrol  constitutes  a  reliable 
pulicide  and  bactericide. 

Rats  may  also  be  killed  by  means  of  Danysz's  virus,  which  is  a 
bacillus  easily  recognized  from  Bacillus  pestis,  and  kills  the  rat  by  a 
septicaemia,  causing  oedema  of  the  intestinal  walls,  infiltration  of 
Peyer's  patches,  and  enlargement  of  the  spleen,  with  sometimes 
peritonitis,  and  only  then  enlargement  of  the  lymphatic  glands. 
Danysz's  virus  is  administered,  by  Simpson's  method,  on  bread,  and 
is  said  not  to  affect  human  beings,  though  recently  complaints  of 
illness  of  persons  living  in  places  where  some  sort  of  virus  was  being 
used  has  been  recorded.  Danysz's  and  similar  viruses  are  very 
often  inert  and  inefficacious  in  the  tropics  and  require  to  be  exalted 
by  passage  through  animals  before  being  used. 

Bannerman  has  strongly  advised  cats  as  a  method  of  rat 
exterminatiqn,  but  it  must  be  noted  that  cats  are  not  refractory  to 
plague. 

It  appears  to  us  that  Black's  methods  of  dealing  with  an  outbreak 
of  plague  are  the  best.  First  of  all,  he  localizes  the  outbreak,  and 
begins  his  prophylactic  measures  in  a  circle  well  outside  this  area, 
and  works  towards  the  centre.  This  is  of  great  importance,  because 
beginning  in  the  centre  and  working  towards  the  periphery  merely 
disseminates  the  disease.  Secondly,  he  has  recognized  the  fact 
that  rats  will  not  eat  food  handled  by  human  beings,  and  therefore 
the  people  who  handle  and  cut  the  bread  into  cubes  prior  to  dipping 
it  into  poison  have  their  hands  smeared  with  oil  of  aniseed,  as  is  also 
the  board  on  which  the  bread  is  cut.  The  poison  which  he  has  used 
with  great  success  is  phosphorus  paste.  The  phosphorus  is  mixed 
with  glucose  to  prevent  spontaneous  combustion,  and  then  a  paste 
is  made  with  a  fatty  base  such  as  lard,  but  it  is  advisable  to  vary 
from  time  to  time  the  fatty  base.  To  our  minds  these  little  points 
make  all  the  difference  between  failure  and  success.  Liston  advises 
the  centralization  and  isolation  of  the  stock  of  grain  in  villages, 
and  an  organization  of  the  system  of  the  refuse  disposal,  while 
the  stabling  of  cattle  in  houses  should  be  prohibited.  He  lays 
stress  on  the  disinfection  of  the  clothes  of  travellers  coming  from 
infected  areas.  Traps  equivalent  in  number  to  2  per  cent,  of  the 
population  should  be  used  to  catch  rats. 

With  regard  to  the  destruction  of  fleas  in  human  habitations, 
washing  the  floors  and  walls  with  crude  oil  emulsion  such  as  the  one 
recommended  by  Burke  will  be  found  useful,  as  demonstrated  by 
Jackson  and  others.  Burke's  formula  is  crude  oil  80  parts,  whale- 
oil  soap  20  parts.  The  preparation  is  a  jelly  mixing  freely  with 
water,  and  a  10  per  cent,  solution  of  it  will  destroy  fleas  with 


1434  PLAGUE 

certainty,  as  well  as  other  insects.  One  gallon  of  the  10  per  cent, 
solution  is  sufficient  to  disinfect  a  room  12  by  12  in  a  few  minutes; 
the  solution  may  be  washed  out  afterwards  with  water.  Tobacco 
and  infusions  of  tobacco  will  also  be  found  useful,  as  first  demon- 
strated by  Castellani  and  Low  when  studying  the  prophylactic 
measures  to  be  taken  against  Pulex  penetrans  infections  in  Africa. 

Personal  Prophylaxis. — Ever  since  the  middle  of  the  eighteenth 
century  there  has  been  an  idea  that  a  vaccine  should  be  obtained 
for  the  purpose  of  protecting  the  individual.  Weszpremi  and, 
later,  Samoilowitz  and  Cerutti  tried  artificial  inoculation,  but  the 
results  were  by  no  means  satisfactory,  persons  dying  from  plague 
as  the  result  of  the  inoculation.  Recently  a  number  of  vaccines 
have  been  prepared  for  the  purpose  of  personal  prophylaxis,  which 
may  be  classified  into:  (1)  Vaccines  composed  solely  of  the  chemical 
products  of  the  bacilli;  (2)  vaccines  composed  of  chemical  products 
and  dead  bacilli;  (3)  vaccines  composed  of  living  attenuated  bacilli; 
(4)  polivaccines. 

Chemical  Vaccines. — In  1897  Lustig  and  Galeotti  prepared  a 
plague  vaccine,  composed  of  the  nucleo-proteids  of  the  bacilli 
obtained  by  shaking  agar  cultures  with  1  per  cent,  caustic  potash 
solution,  and  after  two  hours  adding  0-5  per  cent,  acetic  acid, 
and  thus  obtaining  a  precipitate  of  nucleo-proteids.  It  is  adminis- 
tered by  subcutaneous  or  intramuscular  injections  in  doses  of  from 
2  to  3  milligrammes.  This  method  has  been  adopted  in  La  Plata 
with  success,  and  has  been  experimentally  supported  by  Rowland. 

Vaccines  composed  of  Chemical  Products  and  Dead  Bacilli. — The 
most  important  is  Haffkine's  plague  prophylactic,  prepared  by 
growing  the  bacillus  for  four  to  six  weeks  in  broth,  and  then 
sterilizing  at  650  to  700  C.  for  one  hour,  and  then  decanting  into 
bottles,  with  or  without  the  addition  of  a  little  carbolic  acid.  The 
dose  for  an  adult  man  is  3  c.c,  for  an  adult  woman  2  to  2 J  c.c,  and 
children  in  proportion  to  their  age  (or  size).  The  injection  is  made 
subcutaneously  into  the  arm  or  loin  under  strict  antiseptic  pre- 
cautions. Three  or  four  hours  after  inoculation  the  temperature 
rises,  and  in  twelve  hours  reaches  1020  to  1030  F.,  while  tenderness 
and  swelling  may  occur  at  the  site  of  the  inoculation,  and  malaise 
and  general  discomfort  be  felt,  which  disappear  in  one  to  two  days, 
and  the  swelling  in  about  a  week  or  so.  There  is  no  doubt  of  the 
benefit  of  this  prophylactic,  which  gives  protection  for  a  considerable 
number  of  weeks,  and  perhaps  months,  as  shown  by  Haffkine  and 
Simpson.  Haffkine  considers  that  the  active  principle  lies  in  the 
liquid,  but  it  appears  more  likely  that  it  is  in  the  dead  bacilli. 
Haffkine's  vaccine  has  been  very  extensively  used  in  India  and  other 
countries  since  several  years,  and  on  the  whole  has  given  extremely 
good  results. 

The  German  Plague  Commission  used  a  growth  of  the  bacilli  on 
agar  killed  by  heating  to  650  C,  and  then  suspended  in  normal 
saline,  to  which  0.5  per  cent,  carbolic  acid  was  added. 

Terni  and  Bandi  used  the  sterilized  exudate  from  the  peritoneum 


PROPHYLAXIS  1435 

of  guinea-pigs  inoculated  intraperitoneally  with  plague  bacilli,  and 
killed  some  little  time  before  they  would  have  died  naturally.  The 
exudate  is  diluted  with  a  solution  of  carbolic  acid  and  sodium 
carbonate  and  chloride,  and  given  in  a  dose  of  1-5  to  2-5  c.c.  By 
this  method  plague  aggressins  are  produced  and  used. 

Klein  lias  advocated  an  '  organ  prophylactic,'  obtained  by  drying 
and  powdering  buboes,  spleens,  lungs,  and  livers  of  infected  animals. 
The  dose  for  an  individual  is  from  5  to  7  milligrammes,  made  into 
an  emulsion  with  warm,  sterile,  distilled  water,  and  injected  sub- 
cutaneously,  but  it  has  not  yet  been  tried  on  man  as  far  as  we  know. 

Vaccines  composed  of  Living  Attenuated  Bacilli. — Strong  and  Kolle 
have  recommended  the  use  of  living  virulent  cultures,  and  Strong 
has  practically  shown  that  this  method  of  vaccination  can  be 
carried  out  without  danger.  This  vaccination  consists  of  the  intra- 
muscular injection  of  one  whole  twenty-four  hour  agar  slant  of  the 
living  virulent  culture  in  the  adult,  and  one-quarter  to  one-half  of 
such  a  culture  in  a  child.  The  reaction  is  not  excessive.  About 
ten  days  after  the  inoculation  Strong  has  observed  a  marked  rise 
in  the  opsonic  index,  and  that  the  phenomenon  of  complement 
fixation  is  given  by  the  blood  serum,  thus  proving  the  presence  of 
specific  antibodies. 

Simpson,  Strong,  and  Kitasato  are  of  the  opinion  that  Governments 
should  unite  to  deal  with  plague  by  attacking  it  in  the  endemic 
centres  by  general  vaccination  of  the  population. 

Poly  vaccines. — During  the  contemporaneous  epidemics  of  plague 
and  cholera  in  Ceylon,  in  1914,  Castellani  used  with  satisfactory 
results  a  mixed  bivaccine  plague  +  cholera,  using  the  local  Strain  of 
B.  pestis.  He  also  prepared  and  used  a  pentavaccine  plague  + 
cholera  +  typhoid  +para  A  +para  B,  and  an  hexavaccine  containing 
in  addition  Malta  fever. 

The  double  vaccine  plague-cholera  consisted  of  a  carbolized 
emulsion  of  B.  pestis  and  V.  cholera,  containing  per  c.c.  1,000  million 
plague  and  2,000  million  cholera  organisms.  One  c.c.  was  given  by 
subcutaneous  injection  the  first  time,  and  2  c.c.  a  week  later.  The 
pentavaccine  consisted  of  a  carbolized  saline  emulsions  of  B.  pestis, 
B.  typhosus,  B.  paratyphosus  A,  B.  paratyphosus  B,  V.  cholera  con- 
taining per  c.c.  500  million  plague,  2,000  million  cholera,  500  million 
typhoid,  250  million  para  A,  and  250  million  para  B ;  \  c.c.  was  given 
the  first  time  and  double  the  dose  a  week  later.  The  reaction  was 
severe,  but  not  more  than  after  Haffkine's  monovaccine.  The  inocu- 
lated persons  developed  immune  bodies  for  the  five  diseases.  The 
penta-  and  hexavaccines  have  recently  been  further  investigated  by 
Castellani  and  Taylor,  Journal  oJTropicalMedicine,  November  1, 1917. 

Masks. — These  used  to  be  worn  in  the  Middle  Ages  as  a  prophy- 
lactic measure,  the  use  of  which  has  been  demonstrated  by  Strong  and 
Teague,  and  by  Barber  and  Teague,  in  epidemics  of  plague  pneu- 
monia. The  best  mask  is  a  hood  of  heavy  Canton  flannel-clot  li 
covering  the  entire  head  and  tied  round  the  neck,  and  provided  with 
a  window  in  front  composed  of  sheet  celloidin. 


1436  PLAGUE 

REFERENCES. 

Advisory  Committee  of  the  India  Office,  Royal  Society,  and  Lister  Institute, 
Journal  of  Hygiene,  vi.  (1906),  vii.  (1907),  and  viii.  (1908).  The  Transactions 
of  the  Bombay  Medical  Congress,  held  in  1909,  and  of  the  Hong  Kong 
Congress  in  191 1,  contain  several  very  valuable  papers  on  Plague,  and  the 
current  literature  is  found  in  the  Tropical  Diseases  Bulletin. 

Bannerman  (1900).     Statistics  of  Haffkine's  Anti-Plague  Vaccine.     Bombay. 

Barber  (1912).     The  Philippine  Journal  of  Science. 

Barreto  (1914).     The  Plague  in  Portuguese  India.     Nova-G6a. 

Brayne  (1917).     Indian  Med.  Gaz. 

Castellani  (1914).     Journ.  Ceylon  Branch  B.M.A. 

Castellani    (191 5).     Indian   Medical   Gazette;    Sperimentale;    Transactions 

Society  of  Trop.  Med. 
Castellani    and  Philip  (1914).     Brit.  Med.   Journ.,   April  4.      (Plague  in 

CeyPon.) 
Castellani  and  Taylor  (191 7).     Journ.  of  Trop.  Med.,  November  1. 
Choksy  (1903).     Treatment  by  Lustig's  Serum.     Bombay. 
Choksy  (1909).     Bombay  Medical  Congress. 
Clemow  (1900).     Journal  of  Tropical  Medicine  and  Hygiene,  ii.  200,  223,  241. 

(Most  interesting  account  of  endemic  centres.) 
D'Ormea  (1919).     La  Peste.     Rome. 

Doell  and  Warner  (191 7).     Zeit.  f.  Hyg.,  vol.  lxxxiv.,  No.  1. 
Eager  (1908).     The  Present  Pandemic  of  Plague.     Washington. 
Grubbs   (191 8).     Public  Health   Reports,  October   19,  p.   1759  (Fumigation 

of  Ships). 
Indian  Plague  Commission  (1908).     iEtiology  and  Epidemiology  of  Plague. 

Calcutta. 
Jackson   (1916).     Plague.     Press  of  Lippincott  Company.     (A  very  useful 

manual.) 
Klein  (1906).     Bacteriology  of  Oriental  Plague.     London. 
Kitano  and  Sukegawa  (1918).      Kitasato  Archives. 
Lustig  and  Galeotti  (1897- 191 2).     Numerous  valuable  articles  in  Deutsche 

Med.  Wochenschrift,  etc. 
Martin  (1910-14).     Journal  of  Hygiene.     (Several  valuable  papers.) 
Philip  and  Hirst  (1917)-     Journ.  of  Hygiene. 
Polverini  (1901).     La  Peste.     Firenze. 
Rowland  (1910-14).     Journal  of  Hygiene. 
Shiva yama  (1912).     Transactions  of  the  Hong  Kong  Congress. 
Simpson  (1901-1914).     Reports  to  the  Colonial  Office  on  Plague  in  Capetown, 

1901 ;  Hong-Kong,  1903;  Gold  Coast,  1909;  British  East  Africa,  Uganda, 

and  German  East  Africa,  1914.     (Most  valuable.) 
Strong  (1907).     The  Philippine  Journal  of  Science,  B,  vol.  ii.     Manila. 
Strong  (1912).     The  Philippine  Journal  of  Science,  B,  No.  3.     Manila. 
Simpson  (1905).     Treatise  on  Plague.     Cambridge. 
Teacue  (1912).     The  Philippine  Journal  of  Science. 
White  (1918).     Ind.  Journ.  Med.  Res.,  October. 


CHAPTER  LV 
UNDULANT    FEVER 

Synonyms  —  Definition  —  History  —  Climatology  ■ —  .-Etiology  —  Pathology  — 
Symptomatology —  Diagnosis —  Prognosis — Treatment — Prophylaxis — 
Para-undulant  fever — References. 

Synonyms. —  Mediterranean  fever,  Malta  fever,  Melitensis  septicaemia, 
Melitococcaemia,  Brucc's  septicaemia,  Goat  fever,  Mountain  fever,  Slow  fever 
(Texas),  Gibraltar  fever,  Neapolitan  fever,  Cyprus  fever,  Munhinyo  (Uganda). 
Latin  :  Febris  Undulans,  Febris  Sudoralis,  Septicaemia  Melitensis.  French  : 
Melitoccie,  Fievre  Caprine,  Fievre  Capriense.  Italian:  Febbre  Mediterranea, 
Febbre  Maltese.     German  :  Malta  Fieber. 

Definition. — Undulant  fever  is  a  chronic,  rarely  an  acute,  febrile 
disorder,  with  many  undulatory  relapses,  caused  by  Micrococcus 
melitensis  Bruce,  1893,  and  probably  other  closely  allied  germs,  and 
usually  spread  by  the  agency  of  goat's  milk. 

Remarks. — It  seems  certain  that,  like  enteric,  the  term  '  undulant 
fever  '  may  cover  in  reality  a  group  of  infections  due  to  very 
closely  allied  germs.  Negre  and  Raynaud  have  described  a  Micro- 
coccus paramelitensis,  and  previously  to  them  Sergent  and  Zammit  a 
M.  pseudomelitensis.  These  germs  have  been  proved  to  differ 
biologically  from  the  common  type  of  M.  melitensis  by  means  of 
agglutination  and  absorption  tests. 

History. — Undulant  fever  has  probably  existed  in  the  neighbour- 
hood of  the  Mediterranean  for  centuries,  and  passages  are  cited 
from  Hippocrates  recounting  cases  of  long-drawn-out  fevers,  with 
short  apyrexial  intervals  lasting  as  long  as  120  days,  which  may 
perhaps  refer  to  the  disease. 

In  the  eighteenth  and  the  early  part  of  the  nineteenth  centuries 
references  were  made  to  protracted  fevers  occurring  in  Malta  by 
various  observers — e.g.,  Howard  in  1786,  Hennen  in  1816-25, 
Davy  in  1842-62 — but  it  is  difficult  to  be  certain  what  disease  is 
referred  to.  During  the  Crimean  War  there  appears  to  have  been 
a  very  large  temporary  increase  of  the  fever  incidence  in  Malta, 
much  of  which  was  undoubtedly  enteric,  but  some  of  it  was  not. 
The  change  in  the  type  of  fever  appears  to  have  been  so  marked 
that  some  people  thought  that  a  new  disease  had  been  imported 
from  the  Crimea  by  the  returning  troops. 

In  1859  Marston,  who  personally  suffered  from  the  fever,  first 
gave  an  accurate  account  of  its  clinical  history  and  post-mortem 
appearances  under  the  term  '  Mediterranean  remittent  '  or  '  gastric 

1437 


U3* 


UNDULANT  FEVER 


remittent  fever,'  distinguishing  it  clearly  from  enteric  and  what  he 
called  '  Maltese  fever.' 

From  this  date  there  seems  to  have  been  much  confusion,  for  it 
was  often  diagnosed  as  some  form  of  rheumatism,  but  the  disease 
appears  to  have  been  clearly  recognized  by  Boileau,  Chartres, 
Thomas,  and  others.  In  1879  Veale  gave  an  account  of  it  as 
seen  in  invalids  at  Netley,  as  did  Fazio  in  Naples,  who  not  merely 
described  the  disease,  but  suggested  that  it  might  be  found  to  be 
of  bacterial  origin. 

In  1886  it  was  proved  to  be  a  separate  pathological  entity  by 
Bruce,  who  discovered  a  micrococcus  in  the  spleen.  In  1887  he 
found  the  organism  several  times,  and  was  able  to  cultivate  it  on 
agar-agar,  and  to  reproduce  the  disease  by  inoculation  in  monkeys, 
from  which  he  again  obtained  the  organism  in  pure  culture.  In 
1889  he  published  the  first  full  account  of  the  clinical  symptoms, 


Fig.  671. — Distribution  of  Undulant  Fever. 
(After  Bassett-Smith.) 


and  in  1891  he  grew  the  micrococcus  from  blood  aspirated  from  the 
spleen  during  life.  Thus,  Bruce  proved  that  this  organism,  which 
he  called  Micrococcus  melitensis,  was  the  true  cause  of  the  fever. 

In  1897  Wright  and  Semple  showed  that  the  disease  could  be 
diagnosed  by  the  agglutination  of  the  micro-organism  by  the  serum 
of  patients,  and  in  the  same  year  Hughes  published  a  full  historical 
and  clinical  account. 

In  1904  a  Commission  was  appointed  by  the  Admiralty,  the  War 
Office,  and  the  Civil  Government  of  Malta  to  investigate  the  disease. 
This  Commission  (J.  C.  Kennedy,  Zammit,  Horrocks)  demon- 
strated that  the  micrococcus  leaves  the  body  mainly  in  the  urine, 
and  is  then  capable  of  existing  for  a  long  period  outside  the  body. 
Zammit  discovered  that  the  milk  of  many  goats  agglutinated 
M.  melitensis,  and  Horrocks  isolated  the  germ  from  such  goats. 
It  does  not  appear  to  affect  injuriously  such  animals  living  in  the 


HISTORY— ETIOLOGY  1439 

blood-stream,  and  also  occurring  in  the  milk,  by  means  of  which  the 
disease  is  conveyed  to  man. 

Eyre  has  made  the  suggestion  that  undulant  fever  was  primarily 
a  disease  of  the  goat,  which  had  its  origin  in  the  Persian  hills,  and 
has  been  carried  by  these  animals  all  over  the  world. 

Prophylaxis  on  the  lines  indicated  by  the  aetiology  has  resulted 
in  the  reduction  of  the  disease  in  British  troops  in  Malta  from 
643  cases  in  1905  to  7  cases  in  1907,  and  1  case  in  1910.  In  1906 
Lamb  and  Pai  proved  that  the  organism  existed  in  India  in  men, 
while  Foster  did  the  same  for  goats. 

In  1912  Bassett-Smith  drew  attention  to  the  fact  that,  though 
the  disease  has  been  reduced  by  prophylactic  measures  in  some 
places,  it  had  spread  to  (or  been  diagnosed  in)  Spain,  Portugal,  and 
France.  In  the  same  year  Negre  and  Raynaud  described  M.  paya- 
melitcnsis,  and  their  findings  have  been  confirmed  by  Bassett-Smith, 
who  has  fully  described  a  case  of  para-undulant  fever  contracted  in 
the  South  of  France. 

Climatology.— The  endemic  areas  of  the  disease  are,  undoubtedly, 
firstly,  the  coasts  and  islands  of  the  Mediterranean,  Italy,  France, 
Greece,  Spain,  Northern  Africa,  the  Levant,  etc.;  and,  secondly, 
India,  especially  the  Punjab,  where  the  causative  organism  has  been 
obtained  in  human  beings  and  goats.  We  have  met  with  cases  in 
Ceylon.  Recently  it  has  been  reported  from  many  other  parts  of 
the  world — in  fact,  it  may  be  said  to  be  cosmopolitan,  and  to  extend 
into  the  interior  of  the  continents.  A  case  contracted  in  Northern 
Nigeria  has  been  reported  by  Low. 

It  is  certainly  a  disease  of  tropical,  subtropical,  and  temperate 
climates,  and  exists,  in  addition  to  the  localities  mentioned,  in 
Russia,  East  and  South  Africa,  Uganda,  where  it  is  called  '  mun- 
hinyo,'  the  Sudan,  Mauritania,  China,  the  Philippine  and  Fiji 
Islands,  North  and  South  America,  and  the  West  Indies.  It  occurs 
all  through  the  year,  but  is  more  common  in  the  warm  weather  in 
Malta. 

/Etiology. — The  cause,  as  has  been  indicated  in  the  history,  is 
M.  melitensis,  and  some  extremely  closely  allied  bacteria,  M.  para- 
melitensis  Negre  and  Raynaud,  1912,  and  M.  pseudomelitensis 
Sergent  and  Zammit,  1908,  which  can  be  differentiated  by  aggluti- 
nation and  absorption  tests.  M.  melitensis  is  found  in  the  spleen, 
liver,  kidney,  lymphatic  and  salivary  glands,  the  blood,  bile,  faeces 
(rarely),  and  probably  in  the  alimentary  canal  (as  Eyre's  researches 
on  rabbits  indicate),  the  urine,  and  the  milk.  It  does  not  occur 
in  the  expired  air,  the  sweat,  the  saliva,  or  in  scrapings  from 
the  skin.  I 

It  can  be  inoculated,  and  it  may  be  found  in  the  stomach  of 
mosquitoes  which  have  fed  upon  patients,  but  neither  they  nor  any 
Other  biting  fly,  such  as  a  Stomoxys,  or  a  flea,  have  been  proved 
capable  of  spreading  the  disease.  It  is,  however,  very  resistant, 
and  can  live  for  eighty  days  in  dust,  or  in  water,  fresh  or  salt,  for  a 
month,  but  has  never  yet  been  found  naturally  in  air,  dust,  soil,  or 


1440  VNDVLANT  FEVER 

water,  neither  have  any  of  these  in  a  natural  way  been  proved 
capable  of  spreading  the  disease.  It  is,  however,  true  that  dust, 
infected  with  damp  organisms  from  a  culture,  has  infected  monkeys, 
as  have  suspensions  of  the  organism  when  applied  to  mucosae  of  the 
nose  or  throat.  It  appears,  however,  to  be  best  conveyed  to 
animals  in  food,  especially  milk. 

The  organism  has  also  been  found  by  the  serum  reaction  to  be 
present  in  50  per  cent,  of  the  goats  examined  in  Malta,  and  has  also 
been  obtained  from  the  milk  of  10  per  cent,  of  the  goats  investi- 
gated, and,  when  looked  for,  it  has  been  found  in  the  blood  of  goats 
and  other  animals.  The  milk  of  such  animals  contains  agglutinins 
for  the  germ  (Zammit's  lacto-reaction).  Notwithstanding  this 
infection,  the  animals  are  quite  healthy,  though  a  chronic  mastitis, 
as  observed  by  Neri,  may  occasionally  be  noted.  It  appears  to  be 
conveyed  to  man  by  infected  milk,  the  best  evidence  in  favour  of 
which  is  the  infection  of  a  ship's  crew  by  the  milk  of  goats,  which 
were  being  conveyed  from  Malta  to  America,  53  per  cent,  of  which 
were  found  to  be  infected. 

The  distribution  of  the  disease,  therefore,  depends  upon  the  con- 
sumption of  infected  goat's  milk,  for  people  who  use  this  milk  will 
be  more  liable  to  infection  than  others — hence  its  occurrence  in 
Malta  and  the  Mediterranean  districts,  in  South  Africa  and  India. 
This  is  also  the  reason  why  the  richer  classes  are  more  affected  than 
the  poorer,  and  why  individual  institutions  are  picked  out.  It  also 
explains  why  there  is  no  age  or  sex  incidence,  why  infants  rarely 
suffer,  and  why  occupation  and  surroundings  have  but  little  in- 
fluence. 

How  the  disease  spreads  from  goat  to  goat  is  not  known.  Brumpt 
states  that  they  drink  human  and  animal  urine  if  deprived  of  salt, 
and  in  this  way  the  infection  may  be  kept  up.  The  percentage 
of  infected  goats  has  been  found  to  be  3*4  per  cent,  in  Algeria, 
29  per  cent,  in  St.  Marthal,  30-7  per  cent,  in  Tunis,  34*2  per  cent. 
in  Marseilles,  and  50  per  cent,  in  Malta. 

Mules,  asses,  horses,  oxen,  cows,  dogs,  rabbits,  and  fowls,  are  all 
apparently  capable  of  spreading  the  infection,  while  often  they  do 
not  show  any  sign  of  disease. 

The  question  of  the  human  carrier  is  only  just  coming  forward 
with  any  degree  of  prominence  as  a  factor  to  be  considered  in  the 
spread  of  the  disease,  but  Shaw  has  drawn  attention  to  this  possi- 
bility in  Malta,  where  many  of  the  dock  labourers  showed  agglu- 
tinins in  their  blood  for  M.  melitensis,  and  Missiroli  has  obtained  the 
micrococcus  from  the  blood  of  an  apparently  healthy  man  who 
subsequently  developed  the  fever  typically  in  fifteen  days. 

The  carriers  and  ambulant  human  cases  may  pass  the  Micrococcus 
melitensis  in  the  urine,  infecting  the  soil,  and  in  this  way  may  convey 
indirectly  the  malady  to  other  persons. 

Four  modes  of  infection  are  described:  (1)  By  the  alimentary 
canal,  which  is  the  usual  method;  (2)  by  the  respiratory  system, 
inhaling  dust  contaminated  by  goat's  urine,  which  is  rare;  (3)  by 


PA  THOLOG  Y-  S  YMPTOMA  TOLOG  Y  1 441 

the  cutaneous  system,  which  is  very  rare;  (4)  by  sexual  intercourse, 
which  is  possible. 

A  variety  of  M.  tnelitensis,  called  M.  paramelitensis,  is  described 
by  Negre  and  Raynaud  as  the  cause  of  a  variety  of  fever  termed 
'  para-undulant  fever  '  (see  p.  1447). 

Pathology. — The  micrococcus  enters  the  blood-stream  via  the 
mucosae  of  the  alimentary  canal,  and  causes  a  genuine  septicaemia, 
with  enlargement  and  congestion  of  the  spleen  as  the  most  marked 
feature;  so  that  the  disease  somewhat  resembles  typhoid  fever  in 
many  of  its  characters,  without,  however,  producing  such  typical 
intestinal  lesions  as  that  disease.  According  to  some  authors 
(Ross,  etc.),  the  germ  can  be  conveyed  by  mosquitoes,  but  this  has 
not  been  proved.  For  clinical  and  experimental  reasons  Bruce 
believes  that  one  attack  produces  an  immunity,  but  Manson  and 
Bassett-Smith  doubt  this.  The  organism  produces  haemolysins, 
while  the  reaction  on  the  part  of  the  body  is  shown  by  the  formation 
of  agglutinins,  which  may  last  from  four  to  ten  years,  and  a  specific 
serum,  which  may  be  useful  for  immunization.  There  is  also  an 
immune  body  in  the  blood  suitable  for  complement  deviation,  and 
this  corresponds  generally  with  the  quantity  of  the  agglutinins. 

Morbid  Anatomy. — The  morbid  anatomy  shows  an  enlarged  and 
congested  spleen,  some  congestion  of  the  liver,  kidney,  and  mesen- 
teric glands,  duodenum,  jejunum,  large  intestine,  and  lungs.  The 
spleen  is  usually  much  enlarged,  weighing  from  10  to  44  ounces. 
It  is  dark  red  in  colour,  and  may  be  soft  and  friable,  and  is  very 
congested,  with  enlarged  Malpighian  bodies.  The  liver  is  con- 
gested and  enlarged,  and  shows  cloudy  swelling,  with  a  round- 
celled  infiltration  between  the  lobules.  The  kidney  is  congested, 
and  may  show  a  glomerular  nephritis.  The  alimentary  canal  may 
not  merely  be  congested,  but  the  colon  may  also  be  ulcerated, 
particularly  in  cases  of  haemorrhage.  The  lungs  are  congested, 
especially  at  the  bases,  and  may  show  patches  of  consolidation. 

Symptomatology — Incubation. — Monkeys  fed  with  infected  milk 
require  an  incubation  of  fifteen  days,  while  in  human  beings  the 
period,  according  to  Johnstone,  is  fourteen  days.  The  prodromata 
are  usually  malaise,  chilliness,  headache,  muscular  pains,  and 
dyspepsia. 

Onset. — -The  onset  comes  on  gradually,  and  the  patient  con- 
tinues his  work  though  feeling  ill,  while  the  temperature  rises 
in  a  ladder,  being  higher  each  evening,  and  remitting  somewhat 
in  the  morning.  About  the  fourth  or  fifth  day  of  the  illness 
a  doctor  is  consulted  for  the  headache,  and  pains  in  the  body 
and  limbs,  which  may  have  been  thought  to  be  rheumatic.  The 
patient  looks  ill,  and  his  temperature  is  found  to  be  about  103  1., 
his  pulse  80  to  90,  and  his  tongue  coated  dorsally  with  a  white  fur, 
while  the  edges  arc  red,  and  may  be  indented  by  the  teeth.  There 
is  usually  a  slight  sore  throat  and  a  tender  epigastrium,  with  some 
bronchial  catarrh  or  congestion  of  the  lungs,  and  enlargement  and 
tenderness  of  the  spleen,  which  develop  in  the  course  of  a  wick  or  so. 

yi 


1442 


UNDULANT  FEVER 


Course. — All  these  symptoms  continue  for  about  a  couple  of  weeks, 
the  temperature  remaining  high — 1030  to  1050  F. — but  at  the  end 
of  this  period  the  fever  declines,  and  the  temperature  may  become 
normal,  while  the  patient  feels  much  better.  In  a  day  or  so, 
however,  a  relapse  occurs  with  much  the  same  symptoms  as  the 
attack.  This  relapse  subsides,  and  another  follows,  relapses  and 
intermissions  recurring  for  months. 

The  temperature  now  becomes  undulating,  with  a  marked  rise 
at  night  and  fall  in  the  morning,  while  the  patient  becomes  more 
and  more  anaemic,  weak,  and  wasted.  The  alimentary  canal  is 
irritated,  as  is  shown  by  the  dyspepsia  and  the  constipation  or 
diarrhoea.  The  throat  may  be  sore,  the  gums  spongy,  and  bleed 
on  pressure;  the  spleen  is  often  enlarged  and  painful,   and  the 


Fig.  672. — Temperature  Chart  of  Undulant  Fever. 

lungs  may  show  signs  of  bronchitis,  and  occasionally  lobular 
pneumonia,  while  the  heart  is  easily  excited,  and  hsemic  murmurs 
are  heard.  The  patient  shows  signs  of  prostration  and  head- 
ache, and  pains  all  over  the  body  are  felt.  Insomnia  and  hysterical 
emotions  are  not  uncommon,  but  actual  delirium  is  not  usual,  and 
the  memory  may  be  impaired,  while  neuritis — e.g.,  sciatica — may 
occur.  The  skin  is  pale  but  damp,  due  to  local  or  general  perspira- 
tion, which  is  very  common,  and  occurs  with  each  remission  of  the 
temperature,  the  sweat  being  of  a  peculiar  disagreeable  odour. 
Sudamina  is  not  uncommon  after  the  third  week.  Desquamation 
may  occur,  as  well  as  prickly  heat,  boils,  bedsores,  subcutaneous 
abscesses,  or  haemorrhages. 

The  joints  may  become  swollen  and  very  painful,  but  the  skin  over 


SYMPTOMATOLOGY— VARIETIES  1443 

them  is  seldom  reddened.  Of  all  the  joints  the  hip,  shoulder,  ankle, 
and  knee  appear  most  commonly  affected.  Inflammation  or 
neuralgia  of  the  testes  may  occur,  and  at  times  the  parotid  also 
becomes  inflamed. 

The  blood  has  been  more  particularly  studied  by  Bassett-Smith 
and  Gabbi,  who  find  a  secondary  anaemia  with  a  loss  of  20  to  40  per 
cent,  of  the  corpuscles,  with  some  poikilocytosis  and  an  even 
greater  reduction  of  the  haemoglobin.  The  leucocytic  count  is 
normal,  but  there  is  a  decrease  in  the  polymorphonuclears,  and  an 
increase  in  the  mononuclears  up  to  as  much  as  80  per  cent,  in  some 
cases.  Phagocytosis  is  said  to  be  diminished,  as  is  also  the  bac- 
tericidal power  of  the  blood. 

The  urine  is  passed  in  fair  quantity,  and  has  a  slightly  acid 
reaction,  with  a  deposit  of  urates  and  phosphates,  but  there  is  very 
seldom  any  albumen,  though  bile  may  be  present  in  severe  cases,  and 
the  specific  germ  can  be  found  in  the  urine  even  two  years  after  an 
attack.  Albuminuria  and  nephritis  may  occur,  and  very  rarely 
hematuria. 

The  patient  is  now  anaemic,  and  prostrated  by  the  repeated 
attacks  of  fever,  when  gradually  the  symptoms  begin  to  improve, 
the  intermissions  lengthen,  the  attacks  lessen  in  length  and  severity, 
the  temperature  becomes  normal  or  subnormal  in  the  morning, 
rising  a  little  at  night.  Gradually  the  evening  rise  diminishes  until 
it  stops,  the  tongue  clears,  the  symptoms  abate,  and  convalescence 
begins  after  an  illness  of  from  20  to  300  days,  with  an  average  of 
90  days. 

Varieties. — Two  varieties  distinct  from  the  typical  description 
given  above  are  recognized  by  Hughes — viz.,  a  malignant  and  an 
intermittent — to  which  a  third  or  ambulatory  variety  may  be  added. 

The  Malignant  Variety. — Suddenly,  without  warning,  the  patient 
is  attacked  with  high  fever,  the  temperature  rising  to  1040  or 
1050  F.,  with  severe  pains  all  over  the  body,  flushed  face,  and  all 
the  other  symptoms  already  mentioned,  but  in  an  aggravated  form, 
and  often  associated  with  basal  pneumonia,  and  diarrhoea  with 
offensive  stools. 

After  a  little  the  symptoms  abate  somewhat,  but  instead  of 
improving,  the  pulse  becomes  intermittent, the  breathing  is  laboured, 
and  vomiting  becomes  serious,  and  the  patient  gradually  passes  into 
the  typhoid  state,  when  hyperpyrexia  sets  in,  and  death  takes  place 
from  the  fifth  to  the  twenty-first  day  of  the  illness. 

The  Intermittent  Variety. — The  onset  in  this  variety  is  very 
gradual.  When  the  attack  is  fully  developed,  the  temperatun  is 
about  normal  in  the  morning,  but  rises  in  the  afternoon  to  99°  or 
much  higher,  up  to  1050  F.,  this  rise  being  accompanied  by  malaise, 
irritability,  and  chilliness.  During  the  night  sweating  occurs,  and 
the  temperature  falls  to  nearly  normal.  This  fever  continues  usually 
for  about  six  weeks,  but  may  be  prolonged  for  about  six  months,  and 
is  usually  unassociated  with  any  serious  symptoms — in  fact,  so 
mild  may  the  attack  be  that  it  is  not  discovered  until  the  patient's 


i444  UNDULANT  FEVER 

general  health  begins  to  be  unsatisfactory,  and  he  seeks  medical 
advice. 

The  Ambulatory  Variety. — Apparently  at  times  the  organism  may 
produce  such  little  effect  that  the  infected  person  may  be  unaware 
that  he  is  suffering  from  any  complaint,  and  may  pursue  his  daily 
vocation.  Thus,  out  of  525  dock-hands  examined  by  Shaw  at  Malta 
for  the  serum  reaction,  79  gave  positive  results;  and  of  22  tested, 
9  contained  the  organism  either  in  the  blood  or  urine,  or  both. 

Complications. — Ulcers  may,  though  rarely,  occur  in  the  small  and 
large  intestine,  and  give  rise  to  haemorrhage,  while  persistent  vomit- 
ing, diarrhoea,  hyperpyrexia,  pneumonia,  pleuritis,  effusion,  and 
cardiac  failure  all  form  serious  complications.  Orchitis  is  common. 
As  shown  by  Trotta,  the  micrococcus  may  occasionally  acquire  a 
pyogenic  action,  and  cases  of  suppurative  localized  periostitis  have 
been  recorded  similar  to  those  seen  in  enteric  infections. 

Sequelae. — Paralysis,  neuritis,  common  in  Cairo,  wasting  of 
muscles,  loss  of  memory,  tremulousness,  and  neurasthenia  are 
possible  sequelae. 

Diagnosis. — The  principal  clinical  signs  on  which  to  base  a 
diagnosis  are  the  prolonged  undulant  character  of  the  fever,  the 
profuse  sweatings,  and  the  articular  symptoms. 

Bacteriological  methods  of  diagnosis  should  be  always  resorted 
to  whenever  possible.  The  agglutination  reaction,  if  the  blood  is 
sufficiently  diluted  (at  least  1  in  80),  the  test  properly  performed 
and  carried  out,  using  a  known  and  reliable  strain  of  the  germ,  is,  in 
our  experience,  sufficiently  certain.  The  agglutination  test  must 
be  performed  in  a  dilution  of  at  least  1  in  80,  otherwise  errors 
in  diagnosis  will  result.  Bassett-Smith  recommends  a  high  dilution 
(1  in  1,000),  but  in  our  experience  1  in  80  is  generally  sufficient, 
with  a  time-limit  of  thirty  minutes.  This  reaction  is  said  to  last 
for  a  very  long  time — i.e.,  two  to  seven  years.  Birt  and  Lamb 
have  made  this  serum  reaction  the  basis  of  prognosis,  which  is 
considered  to  be  unfavourable  if  continuously  low,  or  rapidly  alter- 
ing from  a  high  to  a  low  figure.  Agglutinins  are  present  also  in  the 
saliva  (saliva-reaction  of  Polacci  and  others).  Whenever  possible 
the  agglutination  test  should  be  carried  out  in  various  dilutions, 
to  avoid  results  caused  by  a  paradoxical  reaction — viz.,  the  possi- 
bility of  the  serum  agglutinating  in  high  dilutions  and  not  in  low  or 
medium  dilutions.  In  any  doubtful  case  the  blood  should  be  inves- 
tigated for  the  presence  of  M.  melitensis,  using  nutrose  media  or 
Castellani's  dilution  method,  as  in  enteric  infections  (see  p.  1390). 
In  case  of  a  negative  result,  the  examination  should  be  repeated 
at  least  three  times  at  different  periods  of  the  disease. 

Nicolle  and  Conor  consider  that  many  of  the  errors  are  due,  firstly,  to 
leaving  the  serum  in  contact  with  the  clot,  and  state  that  either  the  blood 
should  be  used  at  once  or  the  serum  separated  from  the  clot;  and,  secondly, 
in  order  to  prevent  obtaining  positive  reactions  with  non-undulant  fever 
serum,  that  sera,  to  be  tested,  should  be  heated  to  56°  C.  for  half  an  hour  in 
order  to  destroy  the  non-specific  agglutinins,  as  first  recommended  by  Negre 
and  Raynaud. 


PROGNOSIS— TREATMENT  1445 

Saisawa  and  later  Missiroli  and  others  have  apphed  to  Malta  fever  the 
Bordet-Gengou  complement-deviation  reaction,  but  the  technique  is  rather 
complicated  for  routine  work. 

The  presence  of  a  high  opsonic  index  for  M.  melitensis  may  help  the  diag- 
nosis.    A  precipitin  test  has  been  worked  out  by  Vigano. 

The  diseases  from  which  Malta  fever  must  be  distinguished  are 
typhoid,  recognized  by  a  positive  Widal  reaction;  malaria,  recog- 
nized by  the  presence  of  the  blood  parasites;  and  kala-azar,  by  its 
parasite  in  the  spleen  juice. 

Prognosis.—  The  prognosis  in  the  usual  form  and  the  mild  type  is 
good  quoad  vitam,  the  dangers  being  syncope  and  complications. 
The  sudden  malignant  type  is  rare,  but  very  fatal.  The  mortality 
is  placed  as  low  as  2  per  cent,  by  Bruce,  but  others  have  reckoned 
it  as  high  as  13  per  cent,  for  the  army  in  Malta,  and  9  per  cent,  for 
the  civilian  population. 

Treatment. — The  treatment  is  symptomatic,  as  no  drug  is  known 
which  will  kill  the  parasite,  and  vaccine  and  serum  treatments 
have  not  been  very  successful.  The  principal  symptoms  which 
require  treatment  are  fever,  pain,  gastric  and  intestinal  disturbances, 
congestion  of  the  mouth  and  throat,  nervous  symptoms,  and  haemor- 
rhages.    Attention  must  be  paid  to  the  skin,  lungs,  and  heart. 

The  patient  also  requires  the  utmost  care  as  regards  nursing, 
and  in  the  acute  stages  the  bed-pan  should  be  used.  Chills  must 
be  avoided  by  the  use  of  warm  clothing,  and  the  room  should  be 
rendered  gnat -proof  to  keep  off  flies.  Care  must  be  taken  that  the 
bladder  is  emptied  regularly. 

The  fever  is  best  treated  by  tepid  sponging  when  moderate,  and 
cold  sponging  and  ice-packs  when  severe.  As  regards  pains, 
headache  is  treated  by  bromides,  with  or  without  morphia,  or  small 
doses  of  phenazone  or  phenacetin  with  caffeine  may  be  used;  pains 
in  the  joints  by  hot  fomentations  with  belladonna  or  opium ;  general 
pains  by  a  hypodermic  injection  of  morphia.  Scott's  dressing  may 
be  applied  to  a  swollen  and  painful  joint,  and  pain  in  the  soles  of  the 
feet  may  be  treated  by  cold-water  applications.  Vomiting  is  to 
be  treated  as  described  under  Malaria.  Constipation  is  met  by  a 
dose  of  calomel  and  a  saline,  and  the  bowels  kept  open  by  compound 
liquorice  powder  or  enemata.  Diarrhoea  is  controlled  by  some 
ordinary  astringent  mixture,  or  bismuth,  or  tannalbin  powders  in 
some  form,  while  Dover's  powder  is  very  useful,  as  it  also  relieves 
pain. 

If  the  colon  is  affected,  the  treatment  may  be  on  the  same  lines 
as  for  a  mild  attack  of  dysentery,  boracic  enemata  being  used. 
Small  doses  of  calomel — \  grain — three  or  four  times  a  day  as 
an  intestinal  disinfectant,  are  useful.  The  dyspepsia  may  require 
treatment  on  the  ordinary  lines.  A  mouth-wash  of  glycothymoline 
or  glycerine,  borax,  and  myrrh,  or  listerine,  should  be  used,  and  the 
throat  cleaned  by  an  alkaline  spray,  and  then  astringed  by  a  gargle. 
The  nervous  symptoms  are  soothed  by  cool  sponging,  or  by  the 
bromide  and  morphia  ment  ioned  above.     Insomnia  is  a  common  and 


1446  UNDULANT  FEVER 

distressing  symptom,  and  trional  and  other  hypnotics,  and  occa- 
sionally opium  preparations,  may  have  to  be  administered.  Haemor- 
rhages must  be  controlled  by  rest,  applications  of  ice,  careful 
regulation  of  food,  and  administration  of  adrenalin  and  calcium 
chloride.  The  skin  must  be  carefully  watched,  and  prickly  heat, 
boils,  or  threatening  bedsores  promptly  treated,  and  special  care 
must  be  taken  that  after  sweating,  which  often  occurs  at  night,  the 
clothes  are  changed.  The  lungs  should  be  watched  for  signs  of 
congestion  and  pneumonia  or  pleurisy,  which  must  receive  the  usual 
treatment.  The  heart  must  be  carefully  studied,  and  digitalis, 
strychnine,  iron,  or  some  other  cardiac  tonic  administered  as 
required. 

Low  diet  is  necessary  during  the  attack;  but  if  milk  is  used,  care 
must  be  taken  that  it  is  not  goat's  milk,  or  derived  from  an  infected 
source,  otherwise,  while  treating  the  patient,  a  process  of  reinfection 
may  also  be  carried  out.  During  the  intermission  the  patient 
should  be  given  light  nutritious  food,  care  being  taken  to  see  that 
it  is  really  digested. 

Stimulants,  in  the  form  of  champagne  or  brandy,  are  often 
necessary  in  severe  cases,  because  of  the  cardiac  and  general 
depression. 

De  Brum  claims  to  have  had  good  results  in  the  treatment  of  Malta  fever 
by  giving  massive  doses  of  quinine  (1  drachm  daily).  Gabbi  uses  thymol 
enemata 

Scordo  recommends  intravenous  injections  of  perchloride  of  mercury,  while 
Bassett-Smith  and  others  suggest  preparations  of  yeasts  (2  drachms  twice 
daily),  with  the  object  of  increasing  the  polymorphonuclear  leucocytes,  and 
so  of  facilitating  the  destruction  of  the  infecting  organisms  and  also  of  reducing 
the  tendency  to  neuritis,  which  is  a  common  feature  of  certain  types  of  the 
disease,  and  especially  of  those  seen  in  Egypt.  Summa  and  others  have  used 
intravenous  injections  of  protargol,  and  Marshall  has  obtained  satisfactory 
results  in  animals  with  salvarsan. 

Treatment  by  Serums  and  Vaccines.- — Serums  have  been  prepared  and  used 
by  various  authors,  but  the  results  have  been  disappointing.  Vaccines  at 
times  give  better  results,  especially  in  protracted  cases  with  low  fever,  and 
Bassett-Smith  has  recommended  that  autogenous  vaccines  in  doses  of  100- 
500  millions  should  be  given  According  to  some  workers,  these  vaccines  give 
better  results  when  administered  intravenously  in  doses  of  25-80  millions. 
Various  types  of  sensitized  vaccines  have  been  used  and  have  given,  at  times, 
fairly  satisfactory  results. 

Prophylaxis. — The  prophylaxis  appears  to  be  simple  and  to  consist 
in  the  avoidance  of  goat's  milk.  The  Gibraltar  authorities  have 
completely  stamped  out  Malta  fever  by  prohibiting  the  importation 
of  goats  from  Malta,  which,  together  with  the  diminution  of  the 
disease  in  Malta,  clearly  demonstrates  the  great  practical  value  of 
the  work  performed  by  the  late  Commission.  The  average  number 
of  cases  in  the  British  troops  stationed  at  Malta  before  1906  used 
to  be  240  per  annum;  since  1906  condensed  milk  only  is  supplied, 
and  the  number  of  cases  has  steadily  decreased,  until  in  1910  one 
case  only  was  recorded.  It  should  be  kept  in  mind,  however,  that 
the  source  of  infection  is  not  limited  only  to  the  ingestion  of  con- 
taminated milk,   and  importance  should  be  given  also  to  direct 


PARA-UNDULANT  FEVER  1447 

infection  caused  by  human  carriers  and  ambulant  cases,  and  disin- 
fection of  excreta,  etc.,  should  be  carefully  carried  out. 

Vaccination. — The  use  of  a  preventive  vaccine  prepared  with  M.  melitensis 
has  not  >et  become  general.  It  should  contain  both  M.  melitensis  and 
M.  paramelitensis.  For  a  number  of  years  Castellani  has  prepared  and  used 
polyvaccines  containing  .1/.  melitensis- — e.g.,  a  double  vaccine,  Malta  fever  and 
typhoid ;  a  quadruple  vaccine,  Malta  fever,  typhoid,  para  A  and  B  ;  a  quintuple 
vaccine,  Malta  fever,  typhoid,  para  A  and  B,  and  cholera;  a  sextuple  vaccine, 
Malta  fever,  typhoid,  para  A  and  B,  cholera,  and  plague.  Recently  Lurie  and 
others  have  used  the  quadruple  and  quintuple  vaccines  with  good  results. 
The  former  contains  in  1  cubic  centimetre,  M.  melitensis  4,000  millions  (or 
M.  melitensis  2,000  millions,  and  M .  paramelitensis  2.000  millions),  B.  typhosus 
500  millions,  B.  paratyphosus  A  250  millions,  B.paratyphosus  B  250  millions; 
but  care  should  be  taken,  in  preparing  this  vaccine,  to  select  strains  of 
M.  melitensis  rich  in  antigen.  The  dose  is  £  cubic  centimetre  for  the  first  and 
1  cubic  centimetre  for  the  second  injection,  which  is  given  one  week  later. 

A  general  vaccination  of  goats  has  been  suggested  by  Vincent  and  other 
authorities. 

The  prophylactic  measures  may  be  summarized  as  follows: — 

A.  General  Measures. 

(1)  Notification. 

(2)  Isolation. 

(3)  Disinfection. 

(4)  Sterilization  of  milk  and  water. 

(5)  Good  hygiene. 

B.  Personal  Measures. 

(1)  Personal  cleanliness. 

(2)  Prevention  of  infection  from  mother  to  child. 

(3)  Vaccination. 

C.  Veterinary  Measures. 

(1)  Investigation  of  goats  by  serum  and  Zammit's  lacto-reaction. 

(2)  Slaughter  of  infected  goats. 

(3)  General  immunization  of  the  goats  by  vaccines. 

(4)  Prevention  of  importation  of  infected  animals. 

(5)  Inspection  of  stables,  etc. 

PARA-UNDULANT  FEVER. 

Definition. — Para-undulant  fever  is  clinically  similar  to  or  iden- 
tical with  undulant  fever,  but  is  caused  by  organisms  which  differ 
biologically  from  the  typical  Micrococcus  melitensis. 

Historical. — In  1912  Negre  and  Raynaud  described  an  organism 
which  they  called  Micrococcus  paramelitensis,  but  previously  Sergent 
and  Zammit  had  found  a  M.  pseudomelitensis.  Later  Bassett-Smith 
fully  confirmed  these  findings,  and  described  a  case  of  para-undulant 
fever  contracted  in  the  South  of  France.  M.  paramelitensis  has  been 
found  in  man  and  goat  s. 

Geography. — Cases  have  been  described  from  Africa  and  Europe. 

/Etiology. — The  germs  mentioned  above  are  the  causal  agent  of  the 
disease,  and  differ  from  M.  melitensis  both  in  agglutinative  and 
absorptive  tests. 

Symptomatology. — From  the  cases  so  Ear  reported  it  is  not  possible 
to  distinguish  clinically  between  the  typical  undulant  fever  and  its 
para  variety. 

Diagnosis. — This  is  based  upon  serological  tests. 

Prognosis  and  Treatment. — As  for  undulant  fever. 


1448  UNDULANT  FEVER 


REFERENCES. 

The  most  important  references  are  found  in  Reports  of  the  Commission 
for  the  fnvestigation  of  Mediterranean  Fever  (1905-07,  Reports  I.  to  VII., 
London),  the  Tropical  Diseases  Bulletin,  London,  and  in  Bulletin  de  I' Office 
International  d'Hygi&ne  Publique. 

Axisa  (1906).     British  Medical  Journal,  September. 

Bassett-Smith  (1904).     British  Medical  Journal,  ii.  325. 

Bassett-Smith  (191 4).     Transactions  Society  of  Tropical  Medicine,  February. 

Birt  and  Lamb  (1899).     Lancet,  vol.  ii. 

Bousfield  (1907).     Journal  of  the  Royal  Army  Medical  Corps. 

Bruce   (1887-1908).     Practitioner,   xxxix.;   ibid.,   1887,   p.   161;  ibid.,   1888, 

p.  241 ;  British  Medical  Journal,  1889,  i.  1101 ;  Osier's  System  of  Medicine, 

1908,  iii.  17. 
Castellani    (1914).     Journal    Ceylon    Branch    British    Med.    Ass.     (1915). 

Sperimentale  and  Transactions  Soc.  Tr.  Med.,  December  (Vaccines). 
Castellani  and  Taylor  (191 7).     British  Med.  Jour.  (Combined  Vaccines). 
Eyre  (1909).     Proceedings  of  the  Royal  Society  of  Edinburgh,  vol.  xxix., 

No.  34. 
Gabbi  (1909).     Policlinico  and  Malaria,  1-12. 
Hughes  (1897).     Mediterranean  Fever.     London. 
Kennedy  (1914).     Journal  of  the  R.A.M.C.,  No.  1,  pp.  9-14. 
Lamb  and  Pain  (1906).     No.  22,  Scientific  Memoirs.     India. 
Levi  Della  Vida  (1913).     Annali  Igiene  Sper.,  No.  3. 
Lew,  G.  C.  (1911).     Soc.  Tr.  Tropical  Medicine,  vol.  ii. 
Lurie    (191 6).     British    Medical    Journal   (Combined    Vaccines    containing 

M.  melitensis). 
Marston  (1863).     Army  Medical  Report,  iii.  4 So. 
Missiroli  (1912).     Riforma  Med.,  No.  32. 
Negre  and  Raynaud  (1912).     Comptes  Rendus  de  la  Societe  de  Biologie, 

vol.  lxxii.,  Nos.  15,  18,  and  24.     Paris. 
Xicolle  (1917).     Arch.  Inst.  Pasteur  de  Tunis,  October. 
Nicolle  and  Conor  (1912).     Archives  de  lTnstitut  Pasteur,  Tunis,  No.  3. 
Sergent  Negre  and  Bories  (1916).     Bull.  Pathol.  Exotique. 
Strachan  (1906).     South  African  Medical  Review. 
Summa  (1913).     Arch.  f.  Sp.  Trop.  Hyg..  vol.  xvii.,  No.  35. 
Vallardi  (191 7).     Riforma  Med.,  February  24. 
Veale  (1879).     Arm}''  Medical  Report,  xxi.  260. 

Vincent  (1918).     Comptes  rendus  Acad,  des  Sciences,  February  25. 
Wimberley  (1907).     Indian  Medical  Gazette. 
Wright  (1897).     Lancet,  i.  656. 


CHAPTER  LVI 
HEAT  STROKE  AND  HEAT  SYNCOPE 

Diseases    due  to  physical    causes — Heat   stroke — Heat    syncope — Heat   low 
f  e  ver—  -References . 

DISEASES  DUE  TO  PHYSICAL  CAUSES. 

In  Chapters  VII.  (p.  137),  VIII.  (p.  142),  and  IX.  (p.  147)  of  this 
book  we  have  discussed  the  physical  causes  of  disease  as  we  under- 
stand them.  Chapter  IX.  deals  with  traumatism,  and  includes  such 
clinical  facts  as  we  thought  necessary  in  a  work  on  tropical  medicine; 
it  therefore  does  not  require  amplification  in  the  clinical  portion 
of  this  work.  The  same  remarks  apply  to  the  symptoms  produced 
by  increased  or  diminished  atmospheric  pressure,  and  by  electricity. 

Excluding  these  physical  causes  of  disease,  we  are  left  with  the 
pathological  effects  of  high  atmospheric  temperatures  in  association 
with  high  relative  humidity  and  with  those  due  to  the  rays  of  the 
sun,  both  of  which  conditions  may,  in  our  opinion,  cause  the  same 
clinical  phenomena  which  we  term  heat  stroke  and  heat  syncope, 
and  we  base  our  opinion  upon  the  simple  experiments  which  we 
have  given  at  the  commencement  of  Chapter  VII.  (p.  137)  and  under 
the  section  Radiation  in  Chapter  VIII.  (p.  144). 

In  these  chapters  we  did  not  discuss  the  illnesses  produced  in  man 
by  these  causes,  because  it  appeared  to  us  that  the  clinical  portion 
of  the  book  was  the  more  suitable  place  for  this  purpose,  and  there- 
fore the  present  chapter  is  devoted  to  their  consideration. 

HEAT  STROKE. 

Synonyms. — Sunstroke,  sun-traumatism,  insolation,  siriasis  (not 
Sambon's  siriasis),  thermic  fever.  French,  '  coup  de  chaleur,'  '  coup 
de  soleil ' ;  Italian,  '  colpo  di  sole,'  '  colpo  di  calorc ' ;  German,  '  Hitz- 
schlag,'  '  Sonnenstich.' 

Definition. — Heat  stroke  is  caused  by  a  high  air  temperature, 
especially  when  associated  with  marked  humidity,  and  is  charac- 
terized by  high  fever  and  often  extreme  pulmonary  congestion, 
convulsions,  coma,  and  death. 

Remarks. — Heat  stroke  is  the  form  of  sunstroke  and  thermic 
fever  which  we  have  commonly  met  with  in  our  experience  in  the 
tropics. 

1449 


1450  HEAT  STROKE  AND  HEAT  SYNCOPE 

History. — In  the  section  entitled  High  Atmospheric  Temperatures 
contained  in  Chapter  VII.  we  have  set  forth  the  views  of  a  number 
of  authors  with  regard  to  heat  stroke,  sunstroke,  and  heat  syncope 
from  early  times  down  to  1908,  and  it  seems  to  us  to  be  inexpedient 
to  repeat  that  which  we  have  already  written.  We  will,  therefore, 
merely  continue  that  history  in  the  following  paragraphs.  In 
1912  and  1913  Hiller  made  a  number  of  investigations  on  this  subject 
in  the  German  Army,  and  Fiske  in  that  of  the  United  States,  while 
Segale  published  remarks  upon  thermo-calorimetry. 

In  1913  and  1914  Pembrey,  and  separately  Simpson  and  Woolley, 
wrote  an  important  series  of  papers  dealing  with  heat  strokes. 

It  is  to  be  noted  that,  like  ourselves,  Simpson  and  Ogilvie  hold 
that  there  is  no  difference  between  heat  stroke  and  sunstroke  from 
a  clinical  point  of  view,  while  Rogers,  and  later  Bram,  consider 
that  there  is  a  difference. 

Thus  Rogers  says  that  the  syncopal  form  is  due  to  the  sun  and  the 
Iryperpyrexial  to  the  heat,  whereas  Bram  maintains  inter  alia  that 
sunstroke  is  associated  with  a  very  high  temperature  and  heat  stroke 
with  either  a  normal  temperature  or  a  low  fever  running  from 
ioo°  to  102°  F. 

Simpson's  experiments,  as  well  as  our  own  described  in  Chap- 
ter VII.  (p.  137),  show  that  Haldane's  researches  detailed  in 
Chapter  III.  (p.  62)  apply  to  tropical  climates. 

In  1915  Puntoni,  in  studying  sunstroke,  made  a  number  of 
experiments,  by  means  of  a  photographic  camera,  with  regard  to 
the  penetrating  powers  of  various  kinds  of  rays,  in  which  the  place 
of  the  camera  was  taken  by  a  piece  of  the  cranium  obtained  from  a 
post-mortem  and  containing  blood.  He  concluded  that  the  human 
cranium  was  diathermal  for  violet  ultra-violet  rays,  which  he  con- 
sidered to  be  the  causal  agents  of  sunstroke,  and  to  avoid  which  he 
advised  the  use  of  clothing  composed  of  white  externally  and  green 
internally,  and  also  of  green  glasses  for  the  eyes.  With  reference  to 
this,  we  may  perhaps  draw  attention  to  Sir  William  Crookes'  non- 
actinic  glasses,  with  which  we  have  performed  some  few  experiments 
in  the  Sudan,  and  which,  tested  therein,  are  capable  of  protecting 
photographic  plates. 

In  1916  Koizumi,  as  the  result  of  experiments  upon  animals, 
bTieved  that  during  severe  manual  labour  in  high  atmospheric 
temperatures  the  products  of  metabolism  are  produced  in  such 
abnormal  amount  that  they  cannot  be  removed,  properly  and  effi- 
ciently, from  the  blood,  and  so  act  as  causal  agents  in  the  production 
of  heat  stroke.  This  may  perhaps  help  to  explain  the  importance 
of  diet  in  the  prevention  of  heat  stroke. 

In  1917  Gauss  and  Meyer  gave  an  excellent  clinical  account  of  an 
outbreak  of  heat  stroke  in  Chicago,  and  Amur  investigated  the  effects 
of  muscular  exertion  in  high  atmospheric  temperatures  and  drew 
attention  to  the  use  of  deep  breathing  in  these  conditions. 

In  1918  McKenzie  and  Le  Count  concluded  that  the  chief  cause 
of  heat  stroke  was  the  inability  of  hot  air  in  the  vicinity  of  the  body 


HISTORY— CUM  ATOLOGY  14  51 

to  receive  moisture  therefrom,  because  of  its  being  already  suffi- 
ciently laden  with  moisture.  They  also  held  that  tight  and  heavy 
clothing,  the  ingestion  of  too  little  water,  were  minor  causes,  but 
they  were  not  sure  as  to  the  evil  effects  of  alcohol,  and  saw  no  evi- 
dence in  favour  of  any  causal  effect  due  to  the  actinic  rays  from  the 
sun;  but  they  discuss  the  possible  action  of  a  poison  produced  by 
heat  affecting  metabolism. 

In  191S  Shakles  made  an  important  series  of  experiments  upon 
Cercopil/iecus  monkeys  exposed  to  the  sun  at  Manila.  He  found  that 
though  the  sun's  rays  per  se  were  not  harmful,  still  unacclimatized 
monkeys  invariably  die  of  heat  stroke  after  an  exposure  for  some 
time.  This  helps  to  prove  that  the  clinical  effects  of  heat  stroke 
can  be  produced  by  exposure  to  the  sun  as  well  as  by  heat  in  the 
shade. 

He  noted  that  anything  which  disturbed  heat  regulation  produced 
fatal  results — for  example,  a  small  dose  of  atropine  did  so  by  dis- 
turbing the  loss  of  heat  due  to  perspiration  (vide  Chapter  III.). 

He  also  observed  that  intestinal  toxins  lowered  the  resistance 
of  the  experimental  monkeys,  which  is  most  interesting  in  view 
of  the  prodromal  symptoms  sometimes  experienced  by  man  and 
referable  to  the  alimentary  canal.  With  reference  to  man,  this 
observer  considers  that  the  regulation  of  diet  in  great  heat  is  most 
important.  He  further  notes  that  the  effects  of  the  tropical  sun  are 
exactly  the  same  as  that  of  the  Northern  United  States  during 
certain  seasons  of  the  year. 

Climatology. — The  tropics  are  the  principal  seat  of  the  complaint. 
Of  these  India  appears  to  be  the  most  important,  and  in  it  the  Punjab, 
Sind,  and  the  North-West  Provinces  are  the  worst,  as  can  be  judged 
by  a  reference  to  their  climatology. 

In  Ceylon  sunstroke  is  said  to  be  much  less  common  than  in  India. 
Thus,  in  1903,  according  to  Sir  Joseph  Fayrer,  in  statistics  given 
to  him  by  Surgeon-General  Sir  A.  Keogh,  there  were  303  cases  in 
India  among  the  European  troops,  with  53  deaths;  and  in  Ceylon  11, 
with  2  deaths,  the  total  for  the  British  Army  for  that  year  being 
385  cases  and  61  deaths. 

In  Asia  it  is  well  known  in  the  Red  Sea,  the  Persian  Gulf,  Burma, 
the  Straits  Settlements,  South  China,  and  Cochin  China.  In  Africa 
it  is  met  with  in  all  parts  of  the  tropical  region.  It  is  common  in 
Mauritius,  and  is  also  well  known  in  the  United  States,  Canada, 
Nova  Scotia,  New  Brunswick,  and  the  West  Indies.  In  South 
America  it  is  met  with  in  Guiana,  Brazil,  Peru,  and  the  Argentine. 
In  Australia  it  has  also  been  recognized,  and  in  Europe  in  summer. 
It  is,  of  course,  associated  with  the  warm  seasons  in  all  countries, 
and  with  eit  her  very  high  air  temperatures  in  relat  ively  dry  climates, 
or  with  not  so  high  temperatures  if  there  is  much  atmospheric 
humidity. 

The  disease  stands  in  direct  relationship  to  heat-waves,  as  has 
been  pointed  out  by  Rogers  in  India  and  well  known  in  temperate 
climates.     Thus,  according  to  Gauss  and  Meyer,  in  July,  1916,  the 


1452  HEAT  STROKE  AND  HEAT  SYNCOPE 

monthly  mean  temperature  in  Chicago  was  78*4°  F.,  the  highest  on 
record,  and  152  men  and  6  women  were  admitted  to  the  hospital  for 
heat  stroke  or  heat  syncope. 

/Etiology  {vide  also  Chapters  VI.  and  VII.). — The  causation  of 
the  disease  is  the  action  of  high  air  temperatures  associated  with  a 
high  relative  humidity  on  man,  which  generally  act  during  the  day- 
time, but  may  also  have  an  effect  at  night. 

It  has  already  been  pointed  out  that  a  human  being  can — for  a 
short  time  at  all  events— stand  a  very  considerable  amount  of  dry, 
but  not  moist,  heat.  The  heat  regulation  of  the  body  is  disturbed 
and  the  loss  of  heat  prevented  by  the  humidity;  consequently  the 
body  temperature  rises. 

Haldane's  experiments  have  shown  that  if  the  wet  bulb  thermo- 
meter rises  to  88°  F.  (310  C.)  in  still  air,  or  to  930  F.  (34*4°  C.)  in 
air  moving  at  the  rate  of  170  feet  (51  metres)  per  minute,  or  to  780  F. 
(25-5°  C.)  with  leisurely  work,  some  pathological  effects  appear 
and  the  temperature  of  the  body  begins  to  rise.  It  is  of  interest  to 
note  that  the  temperature  of  the  body,  instead  of  rising  to  a  certain 
height  with  a  given  atmospheric  temperature  and  then  remaining 
stationary,  in  Haldane's  experiments  went  on  rising;  and  in  some 
measure  this  corresponded  with  the  temperature  of  the  air. 

Thus,  with  reference  to  the  rectal  temperature,  which  is  the  best 
indication  of  the  true  bodily  temperature,  Haldane  found  that  with 
a  wet  bulb  at  890  to  900  F.  the  rise  was  i°  to  1-4°  F.  (0-5°  to  0750  C.) 
per  hour;  at  about  940  F.  (34-4°  C.)  it  was  20  F.  (i-i°  C.)  per  hour;  at 
980  F.  (36-4°  C.)  it  was  about  40  F.  (2-2°  C.)  per  hour. 

If  this  condition  can  be  induced  in  healthy  persons  at  rest  in 
England,  it  does  not  seem  impossible  or  improbable  that  lower  tem- 
peratures may  act  as  vigorously  or  more  vigorously  upon  Europeans 
in  the  tropics  or  elsewhere,  especially  if  living  under  conditions  of 
poor  bodily  health  and  bad  sanitation,  or  if  they  are  improperly  clad 
or  exhausted  mentally  or  physically.  Simpson,  in  1914,  showed 
that  Haldane's  results  were  applicable  to  ordinary  climatic  condi- 
tions in  hot  countries. 

The  fact  that  new-comers  are  more  apt  to  suffer  than  old  residents 
has  been  put  on  an  experimental  basis  by  Rosenthal,  who  has  shown 
that  a  kind  of  active  immunity  to  heat  can  be  established  by  repeated 
exposure  of  an  animal  to  a  temperature  lower  than  that  which 
would  have  been  fatal.  These  animals,  when  subsequently  exposed 
to  a  very  high  temperature,  do  show  symptoms,  but  they  are  less 
marked;  the  rise  in  temperature  is  not  so  high,  the  respirations 
and  the  pulse  not  so  accelerated,  and  the  general  distress  less. 

The  effect  of  clothing,  load,  and  work  has  been  calculated  by 
Zuntz  and  Schumburg,  who  estimate  that  a  resting  soldier  weighing 
70  kilogrammes  produces  from  1-2  to  1-3  calories  per  minute,  and 
when  marching,  with  a  load  of  31  kilogrammes,  produces  773 
calories  per  minute,  which  Mali  raise  the  temperature  of  the  body 
i°  C.  in  87  minutes.  Under  ordinary  circumstances  the  soldier 
is  not  affected,  but  if  he  is  wearing  thick,  tight-fitting  uniform 


ETIOLOGY— PATHOLOGY  1453 

(especially  in  the  old  days  of  stocks),  with  a  tight  belt  and  knapsack 
with  cross-belts,  and  is  at  the  same  time  marching  in  close  formation 
(when  the  air  must  certainly  be  impure  from  carbon  dioxide  and 
dust)  under  a  tropical  sun,  it  is  obvious  that,  especially  if  there  is 
a  fairly  high  relative  humidity  in  the  atmosphere,  he  cannot  get 
rid  of  this  heat,  and  there  is  bound  to  be  either  thermic  fever  or 
heat  syncope  in  a  certain  number  of  cases. 

Predisposing  Causes. — Heat  stroke  is,  if  anything,  more  common 
among  children  than  adults,  but  it  is  very  liable  to  be  mistaken  for 
other  diseases.  It  is  more  common  among  men  than  women,  owing 
to  the  greater  exposure  of  the  former.  Among  men  it  is  principally 
found  in  stokers  and  in  soldiers  during  exhausting  marches.  Among 
soldiers  the  classical  instance  often  quoted  is  the  account  of  the 
march  of  the  43rd  Regiment  in  the  Indian  Mutiny  for  over  1,100 
miles,  mostly  across  the  plains  of  India,  in  the  hottest  weather. 

The  men  "remained  quite  well  for  969  miles,  when  they  became 
exhausted,  and  even  emaciated;  but  in  the  narrow  Kowri  of  the 
Bisramgunge  Ghat,  when  the  temperature  in  the  tents  ranged 
from  1150  to  1270  F.  in  the  day,  and  on  one  occasion  was  1050  F. 
at  midnight,  they  suffered  severely,  and  two  officers  and  eleven  men 
died  in  four  days,  and  later  on  seven  more  died  in  three  days. 

There  is  no  doubt  that  exhaustion  and  unsuitable  clothing  were 
formerly  the  great  causes  of  the  frequency  of  attacks  of  heat  stroke 
in  the  army.  In  Chicago,  in  1916,  labourers  formed  64-9  per  cent, 
of  the  cases,  but  the  majority  of  them  were  also  complicated  with 
alcoholism. 

Race  appears  to  have  a  certain  amount  of  effect,  for  it  is  more 
common  in  Europeans  than  in  negroes  or  East  Indians,  though 
it  is  met  with  in  all.  In  Chicago,  in  1916,  79-8  per  cent,  of  the 
cases  were  in  the  third,  fourth,  and  fifth  decades,  so  that  age  may 
also  be  a  predisposing  cause.  Previous  illness  is  a  great  predisposing 
cause.  Hot  winds  help  to  induce  this  condition  ;  in  India  the 
hot  wind  '  loo  mama '  is  much  dreaded  by  the  natives.  Of  all 
predisposing  causes,  alcohol  is  probably  the  most  important. 

Pathology.-- Marincsco  has  shown  that  a  temperature  of  470  C.  is 
immediately  fatal  to  animals,  while  a  temperature  of  450  C.  kills  in 
one  hour,  and  one  of  43°C.  after  a  longer  lapse  of  time,  the  essential 
pathological  change  being  chromatolysis  in  the  nerve  cells;  therefore 
high  bodily  temperature  may  cause  acute  serious  nerve-cell  changes. 

But  the  effect  of  high  internal  temperature  has  been  further  in- 
vestigated by  Halliburton  and  Mott,  who  have  shown  that  a  tem- 
perature of  470  C.  (1170  F.)  is  the  coagulation  temperature  of  neuro- 
globulin ;  while  Hewlett  had  previously  shown  that  egg-white  would 
coagulate  at  a  much  lower  temperature  than  usual  if  this  is 
maintained  for  some  time.  His  experiments  were  repeated  by 
Halliburton  and  Mott  on  cat's  brains,  and  they  found  that  at 
420  C.  (1080  F.)  the  neuroglobulin  separated  out,  but  not  at  lower 
temperatures.  Cat's  brains  kept  at  420  to  430  C.  for  three  and  a 
half  hours  showed  chromatolysis  in  the  nerve  cells.     They,  there- 


M54 


HEAT  STROKE  AND  HEAT  SYNCOPE 


fore,  came  to  the  conclusion  that  a  coagulation  necrosis  takes  place 
in  the  nerve  cells,  due  to  the  coagulation  of  the  cell  globulin,  and 
that  when  this  occurs  the  protoplasm  is  destroyed. 

Our  own  observations  entirely  agree  with  those  of  Marinesco, 
Mott,  and  Halliburton.  Fig.  673  shows  a  nerve  cell  in  a  condition 
of  coagulation  necrosis,  with  disappearance  of  the  Nissl  bodies, 
from  a  case  of  sunstroke  in  which  no  pathogenic  micro-organisms 
could  be  found  post-mortem.     It  appears  probable,  then,  that  the 


W 
3. 


Fig.  673. 


-Nerve  Cells  from  the  Medulla  of  a  Case  of  Heat  Stkoke, 
showing  chromatolysis. 


seat  of  the  lesion  of  thermic  fever  is  in  the  cells  of  the  cerebro- 
spinal nervous  system,  and  particularly  those  of  the  medulla. 

Koizumi  considers  acidosis  to  be  the  most  important  pathological  finding  in 
thermic  fever.  He  has  noted  that  animals  raised  on  a  diet  richin  albumin  show 
a  higher  degree  of  blood  alkalinity,  and  are  more  resistant  to  heat-stroke. 

Morbid  Anatomy. — The  body  retains  a  high  temperature  for 
some  hours  after  death;  rigor  mortis  comes  on  quickly,  and  passes 
off  quickly,  and  decomposition,  on  account  of  the  high  atmospheric 
and  body  temperatures,  sets  in.  Lividity  is  well  marked.  The 
blood  is  dark,  fluid,  and  acid.  The  brain  and  membranes  are  con- 
gested, and  there  may  be  minute  haemorrhages  in  the  white  matter, 
and  marked  increase  of  fluid  under  the  membranes  and  in  the  ven- 
tricles.  Microscopically,  the  minute  vessels,  especially  of  the  medulla, 


MORBID  ANA  TOMY— SYMPTOM  A  TOLOGY 


1455 


are  very  congested,  and  the  nerve  cells  show  coagulativc  necrosis 
and  disappearance  of  the  Nissl  bodies,  together  with  a  swollen  and 
chromatolytic  condition  of  the  nucleus,  though  the  nucleolus  may 
remain  apparently  intact. 

The  cerebro-spinal  fluid  is  clear  and  colourless,  and  usually  in- 
creased in  amount.  McKenzie  and  Le  Count  have  shown  a  higher 
water  content  for  the  brain. 

The  organs  of  the  body  are  in  general  congested,  but  especially 
the  lungs,  which  appear  almost  black.  Some  observers  have  re- 
corded enlargement  of  the  spleen.  In  our  experience  there  may 
be  enlargement  of  the  spleen,  but  it  has  nothing  to  do  with  heat 


XJ 


Fig.  674. — -Temperature  Chart  of  a  Case  of  Heat  Stroke  in  a  Stoker 
while  working  in  the  engine  room  of  a  steamer  in  colombo 
Harbour. 

Temperature  1030  F.  three  hours  after  the  onset. 


stroke.  The  heart  is  often  in  a  state  of  marked  rigor  mortis,  and 
there  may  be  cloudy  swelling  of  the  myocardium,  as  well  as  in  the 
kidneys  and  liver.  Petechial  haemorrhages  may  be  found  in  the 
organs  and  the  skin. 

Symptomatology — Prodromata. — Sometimes  the  symptoms  come 
on  suddenly,  but  mure  frequently  there  are  prodromata.  The 
patient  often  complains  of  feeling  out  of  sorts  and  weak,  especially 
in  the  legs,  together  with  headache  and  drowsiness,  and  sometimes 
of  nausea.  Longmore  lays  stress  on  a  frequent  desire  to  micturate  as 
a  prodromal  sign  of  importance,  because,  as  mentioned  by  Simpson, 


1456  HEAT  STROKE  AND  HEAT  SYNCOPE 

perspiration  is  diminished  or  stopped,  and  the  bowels  are  constipated, 
while  the  urine  is  copious  and  limpid. 

Intolerance  of  light  and  chromatopsia — red,  yellow,  or  green 
spots,  wth  suffusion  of  the  eyes — have  been  noted,  as  well  as  other 
nerve  symptoms  such  as  restlessness  and  insomnia.  Sometimes 
these  symptoms  point  to  disturbance  of  the  digestive  system,  in 
that  the  patients  complain  of  anorexia,  polydypsia,  nausea,  epi- 
gastric distress,  or  diarrhoea.  All  these  prodromal  symptoms  simply 
indicate  that  the  patient  is  not  in  a  normal  condition  of  health. 
Onset. — The  attack  begins  with  a  sudden  sharp  rise  of  temperature 
to  I040-i07°-iio0-ii4°  F.,  and  a  pulse-rate  in  proportion  to  the  fever, 
while  the  skin  becomes  dry,  burning,  and  flushed,  with  occasionally 
a  macular  eruption.  The  patient  becomes  unconscious,  delirious, 
or  comatose,  usually  the  latter.  The  pupils  are  often  very  con- 
tracted. The  respirations  are  noisy  and  quick,  and  rales  and 
rhonchi  are  heard  on  auscultation.  The  pulse  is  rapid,  and  though 
at  first  of  good  volume,  soon  becomes  irregular,  intermittent,  and 
thready.  The  urine  is  scanty,  and  may  contain  albumen  and  casts. 
The  motions  are  passed  involuntarily. 

Course  and  Termination. — If  the  patient  is  going  to  die,  convulsions 
appear,  and  the  skin  becomes  cyanosed  and  clammy;  the  respirations 
become  slower  and  slower,  and  more  and  more  stertorous;  the  pulse 
weaker  and  weaker,  until  the  patient  dies  of  asphyxia  after  an  illness 
varying  from  a  few  hours  to  a  day  or  so.  If  recovery  is  to  take 
place,  the  temperature  often  falls  rapidly  by  crisis,  the  respirations 
become  quieter,  the  pulse  slows,  there  is  a  critical  discharge  of 
urine,  and  the  patient  falls  asleep,  to  awaken  much  better. 

Secondary  Fever. — In  some  cases  the  course  of  the  fever  is  much 
longer  (see  Fig.  674),  lasting  eight  to  ten  days.  Possibly  this  is  due 
to  secondary  infection  with  intestinal  bacteria,  and  blood  cultures 
should  be  made. 

Convalescence. — The  patient  remains  very  susceptible  to  high 
atmospheric  temperatures  for  a  long  time  after  recovery.  There  may 
be  persistent  headache,  photophobia  and  giddiness,  and  definite 
cerebral  and  cerebellar  syndromes  have  been  noted  as  sequelae. 

Diagnosis.— The  cardinal  signs  of  heat  stroke  are  the  association 
of  a  high  bodily  temperature,  and  often  coma,  with  a  high  atmo- 
spheric temperature  and  a  high  relative  humidity.  The  differential 
diagnosis  is  most  important,  and  has  to  be  made  from  malaria, 
epidemic  cerebro-spinal  meningitis,  alcoholism,  opium  poisoning, 
renal  coma,  apoplexy,  and  epilepsy.  Heat  stroke  must  be  diag- 
nosed from  pernicious  malaria  by  the  absence  of  parasites  in  the 
blood;  from  cerebro-spinal  fever  by  the  absence  of  Kernig's  sign,  and 
absence  of  contracture  of  the  muscles  of  the  neck.  The  high 
temperature  should  enable  it  to  be  differentiated  from  alcoholic  cr 
renal  coma,  as  well  as  from  apoplexy  and  epilepsy  (in  both  of  which 
the  temperature  may  be  slightly  raised)  and  opium  poisoning. 

Prognosis. — The  death-rate  varies,  as  a  rule,  between  15  per  cent, 
and  25  per  cent.,  but  it  may  be  as  high  as  51  per  cent,  at  times.     The 


PROGNOSIS—TREATMENT  1457 

prognosis  is,  therefore,  always  serious,  and  becomes  worse  if  cyanosis 
or  convulsions  appear.  In  the  Chicago  outbreak  68  out  of  158  died, 
and  58  of  these  never  recovered  consciousness. 

It  is  too  early  at  present  to  say  how  far  lumbar  puncture  will  aid 
tbe  prognosis. 

Treatment. — Loosen  the  clothing  at  once,  and  remove  the  patient 
to  as  cool  a  place  as  can  be  found  and  take  off  his  clothes,  and,  if 
possible,  lay  him  on  a  bed  covered  with  a  large  indiarubber  sheet, 
or  put  him  in  a  bath  (care  being  taken  to  keep  the  head  supported 
by  some  mechanical  means,  so  that  it  cannot  slip  down  into  the 
water) ,  and  apply  an  ice-bag  to  the  head,  while  pieces  of  ice  arerubbed 
over  the  body,  and  at  the  same  time  cold  sponging  is  carried  on. 
The  cold  douche  may  also  be  applied  with  markedly  beneficial 
effect.     Also  large  enemata  of  iced  water  may  be  given. 

While  this  is  being  done,  vigorous  friction  should  be  applied  to 
the  parts  which  have  been  rubbed  with  ice,  in  order  to  promote 
circulation  in  the  cooled  skin. 

If  there  is  no  ice,  wring  out  a  sheet  in  as  cold  water  as  can  be 
found,  and  allow  water  to  drip  on  the  patient  all  over. 

In  places  where  no  cold  water  is  available,  the  ordinary  water 
can  be  chilled  by  dissolving  a  fair  quantity  of  salt  in  a  bath  of  water, 
squeezing  the  juice  of  some  limes  into  this,  and  then  adding  a  quantity 
of  vinegar  and  a  little  eau-de-Cologne,  and  sponging  the  patient 
with  this  mixture. 

The  danger  in  cold  sponging  is  collapse;  consequently  the  rectal 
temperature  must  be  carefully  taken  every  few  minutes,  and  when  it 
falls  in  the  rectum  to  about  ioi-6°  F.  sponging  must  be  stopped,  the 
patient  covered  up  with  blankets,  put  to  bed,  and  must  be  most 
carefully  watched. 

If  the  temperature  comes  down  with  a  run  and  collapse  sets  in,  the 
cold  applications  should  be  stopped,  and  treatment  must  be  applied 
as  described  under  heat  syncope  (p.  1459).  The  patient  must  in 
any  case  be  carefully  watched,  and  ice,  cold  sponging,  or  both,  must 
be  resorted  to  again  and  again  till  the  temperature  remains  down. 

While  these  immediate  remedies  are  being  applied  preparations 
may  be  made  for  lumbar  puncture  and  the  removal  of  a  quantity 
of  cerebro-spinal  fluid.  If  the  fever  is  not  reduced  by  this  treatment , 
and  the  pulse  is  bounding,  the  body  cyanosed,  and  the  heart's 
action  embarrassed,  the  median  basilic  vein  may  be  opened  and 
the  patient  freely  bled;  but  if  little  or  no  blood  comes,  then  an 
intravenous  injection  of  a  pint  of  normal  saline  at  98-6°  F.  (370  C.) 
may  be  run  in.  Cardiac  stimulants  such  as  caffein,  digitalis,  and 
strophanthus  must  be  employed  to  keep  up  the  heart's  action. 

Antipyretics  are  useless,  as  is  also  quinine,  for  this  fever. 

If  the  breathing  stops,  it  is  advisable  to  try  artificial  respiration 
for  half  an  hour,  or,  according  to  some  observers,  for  several  hours, 
as  sometimes  good  results  have  ensued.  If  the  heart  begins  to  fail, 
hypodermics  of  strychnine,  provided  there  are  no  convulsive 
symptoms,  digitalin,  or  adrenalin,  may  be  given.     If  convulsions 

.92 


1458  HEAT  STROKE  AND  HEAT  SYNCOPE 

are  severe,  inhalations  of  chloroform  and  oxygen  mixed  may  be 
administered. 

When  the  temperature  is  reduced,  and  the  patient  is  conscious 
and  can  swallow,  a  dose  of  calomel  (gr.  iii.  to  v.),  followed  by  saline 
purgatives,  is  advantageous.  As  soon  as  urine  can  be  collected, 
it  must  be  carefully  examined  for  signs  of  renal  trouble,  which, 
if  present,  must  be  treated.  Recurrent  temperatures  may  be 
bacterial  in  origin  and  will  not  be  easily  reduced,  but  blood  cultures 
should  be  made  and  the  causal  organism  determined  with  a  view 
to  vaccine  therapy  if  prolonged. 

Bromides  may  be  required  to  soothe  the  irritated  nervous  system, 
and  do  more  good  than  hypnotics  or  morphine. 

Food  must  at  first  consist  of  only  milk  with  barley-water  or 
toast -water,  and  be  given  in  small  quantities  and  often;  but  as  con- 
valescence proceeds,  broths,  soups,  eggs,  milk-puddings,  etc.,  can 
be  added.  No  alcohol  on  any  account  must  be  given,  except  on  the 
advent  of  collapse. 

The  room  in  which  the  patient  is  lying  must  be  kept  as  cool 
as  possible  by  punkahs  and  large  blocks  of  ice  placed  in  baths,  and 
it  must  also  be  kept  daxk—i.e.,  well  protected  from  the  sun's  rays, 
and  also  from  the  glare  of  electric  light.  There  is  apt  to  be  great 
intolerance  of  light  and  heat,  and  therefore,  after  thermic  fever,  the 
patient  should,  if  possible,  go  on  leave  to  a  cool  climate. 

An  alkaline  treatment  (ammonium  carbonate,  sodium  bicarbonate)  has  been 
recommended  with  the  object  of  combating  acidosis. 

Prophylaxis. — Prophylaxis  consists  in  protecting  the  head  and 
eyes  from  the  sun,  in  wearing  proper  clothing,  in  living  in  dwellings 
and  offices  protected  against  the  sun  and  kept  as  cool  as  possible, 
as  described  in  the  preceding  chapter. 

Muscular  exertion  should  not  be  taken  in  the  heat  of  a  tropical 
day  if  it  can  be  avoided,  and  during  these  hours  alcohol  should  not 
be  touched. 

If  any  of  the  prodromata  are  noticed,  the  person  should  be  put 
on  the  sick-list,  and  treated  as  though  he  were  ill.  He  should  be 
kept  in  a  cool  shaded  room ;  the  bowels  should  be  freely  opened,  and 
cool  applications  applied  to  the  head.  The  diet  should  be  light 
without  alcohol,  and,  when  better,  the  patient  should  be  extremely 
careful  not  to  expose  himself  m  any  way. 

In  regard  to  railway  travelling,  Nicholson  advises  the  avoidance 
of  coupe  and  corridor  compartments  and  the  use  of  carriages  running 
the  length  and  breadth  of  the  coach.  This  probably  refers  to  second 
and  third  class  carriages,  as  the  small  compartment  for  one  person 
in  the  first-class  carriages  of  Sudan  trains  is  most  excellent.  He 
advises  the  use  of  fans,  which  are  constantly  employed  on  Sudan 
trains,  and  the  running  at  the  highest  speeds  possible.  Double 
roofs  and  windows  well  protected  by  coloured  glass  and  jalousies 
should  also  be  noted,  as  they  have  been  used  for  years  in  the  Sudan. 


HEAT  SYNCOPE  i459 

HEAT    SYNCOPE. 

Synonyms. — Heat  exhaustion,  prostratio  thermica. 

Definition. — Heat  exhaustion  is  a  condition  of  syncope  brought 
about  by  action  of  high  air  temperatures,  especially  if  associated 
with  a  considerable  atmospheric  humidity,  upon  persons  whose 
bodily  health  or  conditions  are  abnormal. 

Climatology. — The  climatology  is  the  same  as  for  thermic  fever. 

iEtiology . — Two  distinct  factors  are  necessary  for  the  development 
of  this  condition: — 

1.  High  wet -bulb  temperatures. 

2.  Abnormal  bodily  health  or  conditions. 

The  first  factor  has  been  sufficiently  explained,  but  a  word  or  two 
about  the  second  is  necessary.  The  second  factor  consists  of  any 
organic  disease  or  chronic  alcoholism,  especially  the  latter,  which 
is  apt  to  cause  fatty  infiltration  and  degeneration  of  the  heart  wall, 
thus  allowing  dilatation  of  the  organ  under  the  stress  of  high  air 
temperature. 

This  second  factor  also  includes  unsuitable  clothing  and  too 
violent  exercise,  which  under  high  wet-bulb  temperatures  are 
especially  liable  to  induce  syncope. 

But  alcohol  is  by  far  the  most  important  predisposing  cause,  and 
accounts  for  the  difference  in  mortality  of  expeditions  in  which 
soldiers  are  allowed  to  drink  it  and  those  in  which  they  are  not. 

Morbid  Anatomy. — As  was  shown  by  Pfeiffer  in  1851,  the  heart 
may  be  flaccid  and  very  much  softened,  and  full  of  blood,  especially 
on  the  right  side,  but  apart  from  this  there  is  little  morbid  change. 
There  may  be  congestion  of  the  brain,  lungs,  and  other  viscera,  but 
generally  there  is  little  to  note. 

Symptomatology. — The  symptoms  begin  suddenly  by  the  person 
feeling  very  giddy,  and  sometimes  sick  and  weak.  If  he  attempts 
to  walk,  he  staggers,  and  may  fall.  He  is  pale,  his  pulse  small  and 
soft,  his  pupils  dilate,  and  his  skin  is  cold.  The  temperature' is 
subnormal,  or  there  may  be  a  transient  initial  rise,  ioo°  to  1020  F., 
and  there  may  be  loss  of  consciousness,  but  this  does  not  always 
take  place.     There  is  often  considerable  pain  in  the  head. 

Generally  the  condition  is  quickly  recovered  from,  sometimes 
after  a  little  sickness  or  fever,  but  at  times  it  deepens  into  uncon- 
sciousness, and  ends  in  coma  and  death. 

Treatment. — When  a  person  complains  of  feeling  faint,  lay  him 
flat  on  his  back  in  as  cool  a  place  as  can  be  found,  and  loosen  his 
clothing.  Dash  a  little  water  on  his  head,  face,  and  chest,  and 
give  him  a  little  brandy-and-water  or  sal  volatile,  if  he  can  swallow ; 
but  if  he  cannot,  give  a  hypodermic  injection  of  strychnine  or  of 
ether  and  camphor.  As  soon  as  possible  wrap  the  patient  in 
blankets,  and  apply  hot  bottles  to  various  parts  of  the  body. 

Prophylaxis. — The  prophylaxis  is  the  same  as  for  thermic  fever. 
Giles  advises  nux  vomica  to  be  administered  before  hard  work  in 
the  sun. 


i4bo  HEAT  STROKE  AND  HEAT  SYNCOPE 

HEAT  LOW  FEVER. 

Definition.— A  low  intermittent  fever  of  long  duration,  occurring 
in  persons  in  poor  health  conditions,  under  the  influence  of  continued 
high  air  temperatures  and  a  degree  of  atmospheric  humidity. 

Remarks. — The  temperature  generally  rises  to  about  ioo°  F.  or 
less  every  day  for  months,  but  the  patient  may  experience  little 
discomfort,  except  that  he  does  not  feel  very  fit  or  is  in  a  vague  way 
slightly  indisposed. 

Diagnosis. — It  must  be  diagnosed  from  low  intermittent  fever 
by  the  fact  that  in  this  complaint  the  patient  feels  ill. 

Treatment. — Rest  and  change  of  climate  effects  a  cure,  for  the 
time  being  at  all  events. 

REFERENCES. 

Brown,   Carnegie   (1906).     British  Medical   Journal   (Degeneration   of  the 

Myocardium  in  Hot  Climates),  i.  1462,  1463. 
Cleaves  (1904).     Light  Energy,  pp.  253,  254,  and  798-801. 
Duncan  (1904).  Journal  of  Tropical  Medicine. 
Duncan  (1908).     Journal  Royal  Army  Medical  Corps,  xi.  71. 
Fayrer  (1893).     Davidson's  Hygiene  and  Diseases  of  Warm  Climates,  p.  691. 
Fayrer  (1907).     Allbutt  and  Rolleston's  System  of  Medicine,  II.,  ii.  771-7S2. 
Freund  (1904).     Radiotherapy.     London. 
Gauss   and   Meyer    (1917).     American   Journal   of  the    Medical   Sciences, 

October,  pp.  554"564- 
Gihon    (1893).     Twentieth-Century  Practice  of  Medicine,   iii.   253-285.     (A 

good  description  of  typical  cases  and  a  considerable  literature.) 
Giles  (1906).     British  Medical  Journal,  ii.  596. 
Haldane  (1905).     Journal  of  Hygiene,  v.  494-513. 

Halliburton  (1904).     Bio-chemistry  of  Muscle  and  Nerve,  pp.  107-115. 
Hill  (1906).     Recent  Advances  in  Physiology  and  Bio-chemistry,  pp.  271-274. 
Hirsch.     Handbook  of  Geographical  and  Historical  Pathology,  iii.  626-651. 

(A  very  full  literature  till  about  1883.) 
Koizumi  (1918).     Mitteil.  Med.  Gesellsch.  z.  Tokio,  vol.  xxxii.,  No."  11. 
Manson  (1918).     Tropical  Diseases. 
McKenzie  and  Le  Count  (1918).     Journal  American  Medical  Association, 

July  27. 
Pembry  (1914).     Journal  of  the  Royal  Army  Medical  Corps,  xxii.  629-63S. 
Rawling  (1918).    British  Medical  Journal,  May  4. 
Rho  (1907).     Mense's  Tropenkrankheiten  (Italian  translation). 
Rogers  (1908).     Journal  Royal  Army  Medical  Corps,  x.  25. 
Sambon  (1898).     British  Medical  Journal,  i.  744-748. 
Sellards,    Bovie,    and    Brooks    (191 8).      Journal    of    Medical    Research, 

New  Ser.,  vol.  xxxiii.,  No.  3. 
Shakles  (1917).     Philippine  Journal  of  Science.     Section  B.  Tropical  Medi- 
cine, 1-22. 
Simpson  (1908).     Journal  Royal  Army  Medical  Corps,  xi.  441;  1914,  xxiii., 

1-11. 
Wood  (1887).     Pepper's  System  of  Medicine,  v.  387-400.     (A  most  excellent 

account,  with  many  quotations.) 


CHAPTER  LVII 

THE    UNCLASSIFIED   FEVERS   OF   THE 
TROPICS 

General  remarks — Cobb's  pigmentary  fever — Robles'  fever — Forrest's  fever 
— Naegele's  urticarial  fever — Hyperpyrexial  fever — Double  continued 
fever — Low  intermittent  non-malarial  fever — -High  intermittent  non- 
malarial  fever — Mossman  fever — Nasha  fever — Tientsin  fever — Whit- 
more's  fever — YVoolley's  fever  with  jaundice — The  macular  fever  of 
Tunisia — Tacamocho  fever — Kyoto  fever— Ban  bach — Febris  palustris 
remittens — Reiter's  disease — Ovoplasmosis — Haemocystozoon  fever — 
Septic  bilious  fevers — Bungpagga — Robb's  heat  fever — Non-malarial 
quartan  fever — Anaemic  low  fever — Vesicular  fever — Papular  fever — 
Haemorrhagic  febrile  gastro-enteritis  of  children — References. 

GENERAL    REMARKS. 

Since  Crombie  in  1898  attempted  to  arrange  tropical  fevers  much 
has  been  done  to  define  these  maladies,  as  may  be  judged  by  the 
preceding  chapters.  Nevertheless,  it  is  curious  to  note  that  the 
more  these  fevers  are  defined  and  sorted  out  the  greater  the  number 
of  forms  which  cannot  be  classified,  notwithstanding  a  clear  definition 
of  enteroidea. 

Hume  attempted  to  arrange  these  fevers  into  a  typhoid  colon 
group,  a  dengue  group,  and  an  influenza  group,  but  we  have  placed 
all  that  we  could  recognize  as  belonging  to  the  first  group  under 
enteroidea  (Chapter  Lilt.,  p.  1362),  and  to  the  second  under  dengue 
fever  (Chapter  XHIL,  p.  1244).  We  have  failed  to  meet  with  any 
which  could  be  classified  as  influenza-similar,  though  epidemics 
of  true  influenza  do  occur  in  the  tropics  (Chapter  LVIIL,  p.  1497). 
Under  these  circumstances  we  simply  describe  the  various  forms 
known  to  us  without  any  system  or  order. 

COBB'S  PIGMENTARY  FEVER. 

This  latter  is  peculiar,  and  reads  like  a  mild  attack  of  insolation. 
It  occurs  in  the  hottest  months  of  the  year.  The  onset  is  sudden, 
the  temperature  rising  to  io3°to  1040  F.,  with  headache,  nausea,  and 
vomiting,  associated  with  a  peculiar  pigmentation  of  the  nose  and 
cheeks.  The  fever  is  continued,  and  lasts  eight  to  ten  days.  The 
pigmentation  slowly  fades  some  months  after  the  fever  is  over. 
It  requires  further  investigation. 

1 461 


1462  THE  UNCLASSIFIED  FEVERS  OF  THE  TROPICS 

ROBLES'  FEVER. 

A  peculiar  form  of  continued  fever,  which  is  said  not  to  be  typhoid 
and  not  to  be  malaria,  is  described  by  Robles,  of  Quezaltenango,  and 
Gann,  of  British  Honduras. 

Robles  has  separated  from  the  blood  of  the  patients  a  micro- 
coccus resembling  Micrococcus  melitensis,  but  liquefying  gelatine. 
The  patients,  who  are  usually  derived  from  the  younger  members 
of  the  poorer  classes,  are  anaemic  and  debilitated,  and  live  under 
insanitary  conditions.  The  fever  is  very  irregular,  being  at  first 
remittent,  but  becoming  intermittent,  while  the  periods  of  apyrexia 
increase  in  length  and  frequency  as  the  disease  progresses.  The 
symptoms  are  but  slight,  consisting  of  headache,  malaise,  furred 
tongue,  thirst,  and  anaemia,  with  slight  constipation.  The  spleen 
is  either  not  enlarged  or  but  slightly  so,  while  the  liver  is  a  little 
tender  on  firm  pressure.  The  duration  of  the  disease  is  from  two 
to  three  weeks  to  several  months.  Convalescence  is  long  drawn 
out,  there  being  much  debility  and  disinclination  for  mental  or 
physical  exertion.  The  prognosis  is  good,  as  recovery  is  the  rule. 
The  best  treatment  is  change  to  a  cooler  climate,  good  sanitation, 
a  light,  nourishing  diet,  and  a  tonic  of  iron  and  strychnine. 

FORREST'S  FEVER. 

Forrest  has  described  a  fever  in  Rangoon  which  he  called '  Rangoon 
local  fever,'  which  lasts  three  to  fifteen  days,  and  shows  a  tem- 
perature curve  resembling  a  parabola,  ascending  and  descending 
gradually.  The  maximum  temperature  is  1040  F.,  and  the  blood 
shows  a  polymorphonuclear  leucocytosis. 

NAEGELE'S  URTICARIAL  FEVER. 

Naegele  described  this  in  1912  as  occurring  in  South-West  Africa. 
It  consists  of  fever  associated  with  an  urticarial  eruption,  affecting 
the  skin  and  mucosae,  and  associated  with  marked  nervous  symptoms, 
loss  of  muscular  power,  neuritis,  pains  in  the  joints,  affections  of 
the  glands.  When  the  wheals  disappear  the  skin  exfoliates. 
Relapses  are  frequent.  Bassett-Smith  has  suggested  that  it  may  be 
due  to  some  food  toxin. 

HYPERPYREXIA!  FEVER. 

Remarks. — There  is  a  peculiar  form  of  fever  which  we  met  with 
on  the  Gold  Coast  and  in  Ceylon,  and  which  was  first  described 
by  Thompstone  and  Bennett  in  Southern  Nigeria. 

Climatology. — It  is  known  to  occur  on  the  West  Coast  of  Africa 
and  in  Ceylon. 

/Etiology. — The  causation  is  entirely  unknown,  but  peculiar 
bodies  (Fig.  675)  have  been  seen  in  smears  from  the  spleen.  We 
are  inclined  to  consider  them  contaminations. 


PATHOLOGY— DOUBLE  CONTINUED  FEVER 


M63 


Pathology. — Nothing  is  known  as  to  the  pathology  of  the  disease. 

Morbid  Anatomy. — There  is  nothing  characteristic  to  be  seen  in 
an  autopsy. 

Symptomatology. — The  illness  begins  with  a  mild  fever  which 
looks  like  a  typical  malarial  attack,  the  temperature  falling  after 
the  ordinary  sweating  stage,  though  no  malarial  parasites  appear 
in  the  blood.  The  next  day  the  temperature  is  almost  normal,  and 
no  anxiety  is  felt  about  the  patient.  But  on  the  third  day  the 
temperature  begins  to  rise,  and 
reaches  1040  to  1070  F.,  at  which 
it  will  remain  if  only  drugs  are 
used;  but  if  cool  bathing  is 
resorted  to,  the  temperature  will 
fall  temporarily,  rising  in  due 
course  until  cool  bathing  is  again 
performed.  This  struggle  con- 
tinues, despite  any  medical  treat- 
ment that  may  be  employed, 
until,  at  the  end  of  six  to  seven 
days,  the  cool  bathing  ceases  to 
have  its  effect,  and  the  tempera- 
ture goes  on  until  no°  F.  is 
reached  about  the  eighth  day, 
and  the  patient,  after  having 
been  delirious,  becomes  comatose 
and  dies;   or,    in  about   50   per 

cent,  of  Thompstone  and  Bennett's  cases,  the  temperature  remains 
at  about  1050  F.  for  three  weeks,  and  then  gradually  falls  to  normal 
about  the  sixth  week. 

The  spleen,  liver,  abdominal  organs,  urine,  and  blood,  appear 
quite  normal,  except  that  coagulation  is  said  to  be  quick.  The 
conjunctivae  are  injected,  and  the  mind  is  clear  until  the  terminal 
delirium  sets  in.     The  aetiology  is  quite  unknown. 

Treatment.— Cool  sponging,  cool  baths,  and  cool  packs,  are  the 
only  useful  treatment. 


Fig.  675. — Bodies  found  in  a  Case 
of  Hyperpyrexia!,  Fever. 


DOUBLE  CONTINUED  FEVER. 

This  disease,  which  closely  resembles  enteric  fever,  was  first  met  with  by 
Manson,  and  subsequently  by  Thorpe  and  Rousseau  in  China. 

The  disease  begins  insidiously,  the  temperature  rising  to  1040  F.,  and 
remitting  about  30  F.  per  diem,  with  slow  pulse,  a  moist  red  tongue,  and 
constipation.  The  spleen  is  slightly  enlarged,  and  all  the  other  organs  are 
normal.  After  ten  to  fifteen  days  the  temperature  falls  gradually  by  lysis  to 
normal,  at  which  it  remains  for  two  to  seven  days,  when  a  second  paroxysm 
of  fever  sets  in  of  the  same  type  as  the  first,  only  lasting  some  ten  days,  after 
which  the  patient  becomes  convalescent.  There  is,  however,  a  considerable 
amount  of  anaemia,  and  it  is  a  long  time  before  the  strength  is  regained.  There 
are  no  complications  or  sequelae. 

Treatment  must  be  symptomatic;  quinine  is  useless. 


1464 


THE  UNCLASSIFIED  FEVERS  OF  THE  TROPICS 


LOW  INTERMITTENT  NON-MALARIAL  FEVER. 

Remarks.- — This  fever  has  been  described  by  Crombie  and  Castel- 
lani.  Cases  have  been  reported  from  India,  Ceylon,  China,  and 
Siam,  where  it  was  observed  by  Murray.  Recently  cases  have  been 
observed  in  the  south  of  Italy  and  the  Balcanic  zone  by  Rho  and 
Piebroforte,  and  others. 


■38 


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Fig.   676. 


-Temperature  Chart   of  a  Case   of  Low   Intermittent 
Non-Malarial  Fever. 


Symptomatology. — The  onset  of  the  disease  is  insidious,  or  it  may 
follow  what  to  all  purposes  appears  to  be  a  mild  attack  of  influenza, 
the  patient  feeling  out  of  sorts,  feverish,  and  complaining  of  muscular 
rheumatoid  pains  all  over  the  body.  The  type  of  the  fever  is  inter- 
mittent. Every  day,  generally  between  the  hours  of  ten  and  twelve, 
the  patient  feels  somewhat  chilly,  but  there  is  no  shivering  fit.  The 
temperature  rises,  the  maximum  varying  between  990  and  1020  F. 
The  temperature  never  rises,  in  our  experience,  above  1020  F.  In 
the  evening,  between  eight  and  midnight,  the  temperature  slowly 
decreases  and  becomes  normal.  Occasionally  the  patient  may 
perspire  when  the  temperature  falls,  but  this  is  not  a  constant 


SYMPTOMATOLOGY— MOSSM AN   FEVER  1465 

symptom.  The  physical  examination  of  the  patient  will  reveal 
nothing  abnormal,  apart  from,  occasionally,  signs  of  slight  anaemia. 
The  liver  and  spleen  are  not  enlarged.  In  a  few  cases  some  super- 
ficial lymphatic  glands  may  be  slightly  enlarged.  In  some  cases 
the  red  blood  cells  are  decreased.  An  interesting  feature  in  most 
cases  is  the  distinct  increase  in  the  number  of  eosinophile  leucocytes, 
even  when  no  evidence  of  intestinal  worms  can  be  found  in  the 
motions.  The  course  of  the  fever  is  very  long.  We  have  seen  cases 
lasting  six  months. 

Diagnosis. — This  fever  may  be  diagnosed  from  Malaria  by  the 
absence  of  Laveran's  parasites,  and  by  the  fact  that  the  spleen  is 
not  enlarged;  from  Malta  fever,  a  type  of  which  it  closely  resembles 
clinically,  by  the  absence  of  the  Micrococcus  melitensis  in  the  blood, 
and  the  constant  negative  result  of  Wright's  reaction :  from  trypano- 
somiasis by  the  absence  of  trypanosomes;  from  low  fever  of  tuber- 
cular origin  by  the  negative  cutireaction. 

Prognosis.- — This  is  good- — quoad  vitam — but  the  patient  feels 
weak,  tired,  nervous,  and  unfit  to  do  his  work  properly  for  months. 

Treatment. — A  change  of  climate  is  always  beneficial,  and  often 
quickly  stops  the  fever.  A  long  course  of  injections  of  quinine 
cacodylate  is  useful  in  many  cases.  The  ordinary  preparations  of 
quinine  by  the  mouth  or  by  injection  do  not  influence  the  fever 
in  the  least. 

HIGH  INTERMITTENT  NON-MALARIAL  FEVER. 

Remarks. — This  fever  has  been  described  by  Castellani  in  1909 
in  children  in  Ceylon. 

Symptomatology. — Apart,  perhaps,  from  slight  anaemia,  the  child 
does  not  show  any  symptoms  except  the  fever.  He  takes  his  food 
well,  runs  about  and  plays,  and  seems  apparently  in  his  usual 
health.  The  fever  begins  in  the  late  morning,  and  lasts  several 
hours  every  day,  reaching  1030  to  1040  F.  and  more.  There  is  no 
shivering  fit  at  the  onset,  nor  perspiration  when  the  temperature 
falls  to  normal.  The  blood  does  not  show  anything  abnormal, 
except,  occasionally,  a  slight  degree  of  anaemia.  The  course  of  the 
fever  is  very  long,  lasting  at  times  several  months. 

Treatment. — Quinine  does  not  influence  it  in  the  least.  As  a 
rule,  a  change  of  climate  stops  the  fever  almost  immediately. 

MOSSMAN  FEVER. 

Synonym. — Endemic  glandular  fever. 

In  1 910  Smithson  described  a  fever,  which  he  called  Mossman  fever,  and 
which  was  characterized  by  an  irregular  remittent  fever  of  three  to  twenty- 
one  days'  duration,  accompanied  by  painless  enlargement  of  the  posterior  or 
subscapular  group  of  axillary  glands,  which  were  tender.  The  symptoms  were 
mdd,  accompanied  by  a  macular  or  vesicular  rash.  It  almost  exclusively  affects 
sugar-cane  cutters.  The  blood  is  normal  and  the  death-rate  is  low,  but  it 
may  end  fatallv,  apparently  from  a  form  of  septicaemia.  It  affects  white  and 
black  people  in  the  endemic  area.  The  incubation  period  is  six  to  ten  days, 
and  the  onset  is  sudden  or  gradual. 


1466  THE  UNCLASSIFIED  FEVERS  OF  THE  TROPICS 

The  mortality  is  less  than  1  percent.,  and  an  attack  confers  a  slight  immunity. 
It  is  thought  that  it  may  be  due  to  some  insect  on  the  cane.  The  dermatitis 
often  found  in  cane  cutters  is  described  in  Chapter  XCIV.  on  p.  2163. 

In  191 3  Clarke  described  this  disease  more  fully,  and  in  1914  Breinl,  Priestley, 
and  Fielding  gave  a  longer  account. 

NASHA  FEVER. 

Synonyms. — Nakra  fever,  Nakhra  Jawhur. 

Remarks. — Under  the  above  terms  Fernandez,  in  1894,  described  a  fever 
characterized  by  swelling  of  the  nasal  mucosa  as  occurring  in  Bengal. 

Climatology.- — It  is  found  mostly  in  the  months  of  April  to  August,  and  is 
rare  in  the  cold  weather. 

/Etiology. — The  causation  is  unknown. 

Symptomatology. — The  illness  is  ushered  in  by  a  chill  associated  with  high 
fever  and  hyperemia,  with  swelling  of  the  mucosa  of  the  nose,  and  pains  in  the 
head,  neck,  shoulders,  and  small  of  the  back.  The  face  is  flushed,  the  pupils 
contracted,  and  there  is  an  eruption  of  small  papules,  often  accompanied  by 
bronchial  symptoms. 

The  fever,  which  is  usually  remittent  in  character,  disappears  in  three  to 
five  days,  when  the  nasal  swelling  also  subsides. 

Relapses  may  occur  in  one  to  four  weeks,  and  sometimes  a  severe  relapse 
may  end  in  delirium,  coma,  and  death. 

Treatment.— A  saline  purgative  and  a  mild  diaphoretic  are  first  adminis- 
tered, and  then  the  nose  is  sprayed  with  iced  water  two  to  three  times  a  day, 
or  the  congestion  is  relieved  by  pricking  the  mucous  membrane.  Tannin  and 
10  per  cent,  cocaine  solution  may  also  be  applied  to  the  nasal  mucosa. 

TIENTSIN  FEVER. 

A  somewhat  similar  fever  has  been  reported  by  A.  C.  Fox  from 
Tientsin,  but  in  his  cases  the  fever  lasted  from  ten  to  fourteen  days. 
He  thinks  it  may  have  been  a  paratyphoid  infection. 

It  is  characterized  by  sudden  onset,  remittent  fever  for  ten  to 
fourteen  days,  frontal  headache,  constipation,  slow  pulse.  The 
constitutional  symptoms  are  slight,  relapses  are  rare,  and  the 
mortality  is  nil,  while  convalescence  is  rapid.  It  occurs  in  persons 
inoculated  against  typhoid  and  having  no  malaria.  It  may  be 
enteroidea. 

WHITMORE'S  FEVER. 

Synonym. — Morphine  injector's  septicaemia. 

YVhitmore,  in  1915,  has  described  several  cases  of  a  glanders-like 
disease  in  Rangoon,  characterized  by  intermittent  fever,  broncho- 
pneumonic  symptoms,  and  often  multiple  abscesses  in  various  parts 
of  the  body.  The  bacillus  isolated  seems  to  be  very  similar  to 
B.  mallei. 

In  1915  Knapp  came  to  the  conclusion  that  this  fevei  might  exist 
in  other  parts  of  India,  and  showed  that  the  disease  is  due  to  the 
contamination  of  the  hypodermic  syringe. 


THE  MACULAR  FEVER  OF  TUNISIA  1467 

WOOLLEY'S  FEVER  WITH  JAUNDICE. 

This  fever  was  described  by  Woolley  as  occurring  in  the  Andaman 
Islands.     He  thinks  that  it  is  separate  from  malaria. 

Jaundice  appears  on  the  third  to  fourth  day,  and  in  bad  cases 
there  are  haemorrhages,  delirium,  and  a  rapid  pulse,  while  40  per 
cent,  of  the  cases  die. 

It  seems  to  us  that  it  must  be  Febris  caslrensis  gravis — i.e.,  Weil's 
disease. 

THE  MACULAR  FEVER  OF  TUNISIA. 

Synonym. — La  fievre  boutonneuse  de  Tunisie. 

Definition. — -An  acute  febrile  disorder  of  unknown  causation,  characterized 
by  a  peculiar  macular  eruption  on  the  abdomen,  palms  of  the  hands,  and 
soles  of  the  feet,  winch  often  persists  for  several  days  after  the  temperature 
has  fallen  to  normal. 

Remarks. — This  lever  was  described  by  Conor,  Bruch,  and  Hayat  in  1910 
in  Tunisia,  and  by  other  persons  more  recently. 

/Etiology. — The  causation  is  unknown,  and  inoculations  into  monkeys 
were  negative. 

Symptomatology. — The  onset  is  sudden  and  accompanied  by  rigors,  fever, 
pains  in  the  joints,  injection  of  the  conjunctiva,  nausea,  vomiting,  constipa- 
tion, and  insomnia.  The  rash  appears  on  the  second  to  fourth  day  in  the 
form  of  rose-red  or  dark  red  spots  about  the  size  of  a  lentil,  which  disappear 
on  pressure.  The  blood  shows  a  lymphocytosis  of  about  35  per  cent.  These 
spots  appear  upon  the  abdomen  and  the  palms  of  the  hands  and  feet.  After 
lasting  about  two  weeks  the  temperature  falls  to  normal,  and  after  a  few  days 
the  rash  dies  away  without  any  desquamation. 

Diagnosis. — The  characteristic  feature  of  this  fever  is  the  distribution  of  the 
eruption  and  the  fact  that  it  frequently  persists  for  several  days  after  a  normal 
temperature  has  been  reached.  It  most  nearly  resembles  Brill's  disease — 
that  is  to  say,  a  mild  form  of  typhus  fever — which,  indeed,  it  may  well  be. 

Prognosis. — This  is  good. 

Treatment. — The  treatment  is  purely  symptomatic. 

TACAMOCHO  FEVER. 

In  1918  Henao  gave  an  account  of  five  cases  of  a  fever  at  Taca- 
mocho,  on  the  Antioquia  Railway,  Colombia.  It  was  characterized 
by  high  fever,  vomiting,  intense  headache,  and  diarrhoea.  The 
vomit  might  have  blood  in  it  or  might  be  bilious.  The  liver  was  not 
enlarged.  There  was  temporary  suppression  of  urine,  followed  by 
albuminuria  in  the  cases  which  recovered.  Two  cases  died. 
Microscopical  findings  did  not  confirm  the  idea  that  it  was  a  form 
of  yellow  fever. 

KYOTO  FEVER. 

A  fever  lasting  for  seven  days  in  Kyoto,  Japan,  and  described  by 
Masuda  in  1918.  Ineda  found  a  spirochete  in  the  blood.  The 
peculiar  feature  was  that  adult  males  of  the  farmer  class  were  the 
principal  sufferers,  and  that  it  produced  a  cloudiness  in  the  vitreous 
humour  of  the  eye. 


1468  THE   UNCLASSIFIED  FEVERS  OF  THE  TROPICS 

BAN  BACH. 

Synonym. — La  miliaire  cristalline  febrile. 

This  fever  was  first  described  by  Montel  in  1912,  and  in  1916 
by  Sarailhe  in  Cochin  China.  It  is  characterized  by  an  insidious 
onset,  followed  by  six  to  eight  weeks'  fever,  terminating  by  lysis, 
and  attended  by  pulmonary  catarrh  and  a  very  abundant  vesicular 
eruption,  which  is  difficult  to  see  unless  looked  for,  and  which  comes 
out  in  crops.  The  skin  is  dry,  conjunctiva  yellow,  and  there  is  con- 
stipation, lassitude,  and  enlargement  of  the  spleen  and  liver,  with 
rapid  compressible  pulse  and  sometimes  delirium.  Convalescence  is 
prolonged,  and  there  is  a  complete  loss  of  hair.  Blood  tests  show  no 
parasites,  and  are  negative  for  the  enteric  fevers.  It  is  thought  io 
be  infectious.  This  resembles  in  many  particulars  the  cases  de- 
scribed by  Smith  and  Loughman  at  Aden  in  1914,  but  they  do  not 
mention  the  vesicular  rash  or  the  loss  of  hair.  Both  fevers  probably 
belong  to  the  enteroidea,  and  should  be  examined  bacteriologically 
as  to  the  blood  and  the  fseces. 

FEBRIS  PALUSTRIS  REMITTENS. 

Described  by  Ludwig  in  1917  as  being  characterized  by  an  in- 
cubation of  twenty-one  days  and  a  fever  of  seven  to  ten  days, 
of  a  remittent  type,  with  headache,  pains  in  the  muscles,  weakness, 
jaundice,  and  nephritis.     It  sounds  like  enteroidea. 

REITER'S  DISEASE. 

This  was  also  described  in  1917,  and  resembles  the  above,  but 
there  were  pains  in  the  joints,  conjunctivitis,  iritis,  and  cystitis, 
with  enlargement  of  the  spleen  and  fever  lasting  about  seventeen 
days. 

OVOPLASMOSIS. 

A  fatal  fever  described  by  de  Raadt  in  an  Annamese  aged  forty- 
four  years,  with  enlargement  of  the  spleen,  but  not  of  the  liver, 
and  with  a  temperature  somewhat  resembling  subtertian  malaria, 
without  malarial  parasites  in  the  blood,  but  with  pigment  in  the 
mononuclear  leucocytes  and  resisting  quinine  therapy.  The  tem- 
perature rose  very  high,  and  the  patient  died.  Small  intraglobular 
rings  were  seen  staining  blue  with  Giemsa's  mixture,  and  without 
any  trace  of  chromatin.  These  were  also  seen  in  the  mononuclear 
leucocytes,  and  were  called  Ovo plasma  anucleahtm  de  Raadt,  1913. 
This  sounds  like  subtertian  malaria. 

H^EMOCYSTOZOON  FEVER. 

Hcemocystozoon  brasilicnse  Franchini,  1913,  is  a  flagellate  which 
encysts  in  the  peripheral  blood,  and  was  judged  to  be  the  fatal  cause 
of  a  quotidian  fever  in  an  Italian  physician  coming  from  Brazil. 


HJEMOCYSTOZOON  FEVER  1469 

The  fever  came  on  after  the  removal  of  a  tumefaction  in  the  neck. 
Spleen  and  liver  were  enlarged,  and  there  was  great  anaemia  and 
emaciation.  Brumpt  considers  that  the  organism  is  a  herpetomonas, 
and  compares  the  non-flagellate  forms  to  Schizotrypanum  cruzi, 
while  the  flagellate,  he  thinks,  are  contaminations,  but  Franchini 
does  not  agree. 

He  reports  that  he  has  found  in  smears  from  the  liver — 

(i)  Oval  and  lanceolate  forms  3-6  and  1-2-5  microns,  without 
blepharoplast  or  flagella.  (2)  Oval  or  lanceolate  forms,  sometimes 
dividing,  16x3  microns.  (3)  Flagellate  forms,  with  a  flagelluni 
arising  near  the  blepharoplast.  (4)  Non-flagellate  forms  with  a 
large  nucleus.     (5)  Encysted  forms  with  chromatinic  masses. 

The  patient  had  enjoyed  good  health  until  three  years  previously, 
when  he  began  to  feel  ill  and  lost  his  appetite,  while  his  weight 
declined.  One  year  later  a  hard  indolent  tumefaction  appeared 
on  the  right  side  of  the  neck.  This  was  removed,  but  the  wound 
did  not  heal  and  discharged  a  white  non-purulent  secretion.  He 
now  began  to  suffer  from  irregular  quotidian  fever,  preceded  by 
shivering  and  followed  by  sweating.  The  spleen  became  somewhat 
enlarged,  but  the  liver  gradually  extended  to  the  umbilicus,  and  a 
cyst  formed  in  the  right  lobe,  puncture  of  which  gave  a  reddish 
fluid.  The  patient  now  became  very  anaemic  and  emaciated.  The 
lymphatic  glands  were  normal,  the  urine  showed  traces  of  albumen, 
the  blood  showed  signs  of  acute  anaemia,  with  leucopenia,  no  eosino- 
philia,  and  a  few  parasites.  Puncture  of  the  liver  showed  more 
parasites. 

No  malarial  parasites,  leishman  bodies,  spores,  or  fungi  could 
be  found  by  examination  or  by  cultures.  Wassermann's  reaction 
was  negative.  Sections  of  the  tumefaction  showed  granulomatous 
tissue  and  some  parasites. 

SEPTIC  BILIOUS  FEVERS. 

A  febrile  complaint  described  by  Gartan,  in  1918,  as  occurring 
mostly  in  women,  associated  with  enlargement  and  tenderness 
of  the  liver,  and  lasting  five  to  thirty  days.     One  death  is  recorded. 

BUNGPAGGA. 

This  appears  to  us  to  be  myositis  purulenta  tropica  {vide  p.  1975) 

ROBB'S  HEAT  FEVER. 

This  is  described  as  non-infective  cercbro-spinal  fever,  occurring 
in  East  Africa. 


147° 


THE  UNCLASSIFIED  FEVERS  OF  THE  TROPICS 


NON-MALARIAL  QUARTAN  FEVER. 

This  fever,  described  by  Castellani,  is  characterized  by  having  a 
quartan  periodicity  and  no  malarial  parasites  in  the  blood,  and 
quinine  given  in  massive  doses  does  not  influence  the  course,  which 
is  prolonged,  lasting  several  months. 


Fig.  677. — Temperature  Chart  of  Non-Malarial  Quartan  Fever. 


ANAEMIC  LOW  FEVER. 

In  young  European  and  native  women  aged  sixteen  to  twenty- 
two  years  there  is  a  persistent  low  fever  lasting  for  several  months, 
reaching  above  99*4°  F.  in  the  afternoon  and  associated  with  a  certain 
degree  of  anaemia,  which  is  met  with  at  times.  The  patient  may 
become  extremely  nervous  and  hysterical.  This  temperature  may 
be  due  to  the  degree  of  chloranaemia,  and  has  nothing  to  do  with 
hysterical  fever  of  certain  authors,  as  it  disappears  on  the  anaemia 
being  treated. 

VESICULAR  FEVER. 

Definition. — A  febrile  disorder  associated  with  acute  pain  in 
some  region  of  the  body,  followed  by  the  appearance  of  a  vesicular 
eruption  which  becomes  general. 

Remarks. — This  is  a  fever  which  at  its  commencement  resembles 
an  attack  of  chicken-pox,  and  when  it  is  fully  developed  closely 
resembles  modified  smallpox.  We  have  seen  several  such  cases  in 
Ceylon  during  the  last  ten  years. 

/Etiology. — The  causation  is  unknown. 

Symptomatology.- — At  no  stage  of  the  illness  is  the  patient  severely 
ill,  but  the  commencement  is  ushered  in  with  sometimes  pain  in 
some  part  of  the  body,  followed  in  a  day  by  a  rise  of  temperature 
to  about  ioi°  F.  and  a  quick  pulse.  The  eruption  may  appear  at 
first  in  the  region  of  the  pain,  or  may  be  general  from  the  com- 
mencement, which,  however,  is  not  relieved,  and  may,  on  the  con- 
trary, have  extended  to  other  regions  of  the  body.  The  pain 
gradually  disappears,  a  scattered  general  eruption  of  vesicles  appears, 
and  the  temperature  becomes  normal,  while  the  patient  feels  better. 
The  vesicles  are  discrete,  dome-like,  or  flattened;  later,  a  few  may 


VESICULAR  FEVER— PAPULAR  FEVER  1471 

become  umbilicated.  The  size  is  generally  much  less  than  those 
of  chicken-pox,  and  a  few  may  become  umbilicated.  There  is  little 
or  no  inflammation  of  the  base.  The  contents  are  at  first  clear  and 
then  purulent.  Superficial  scabbing  may  occur,  and,  as  a  rule,  no 
scars  are  left,  though  rarely  some  scars  may  be  found. 

Diagnosis, — The  diagnosis  is  based  upon  the  characters  of  the 
eruption,  there  being  no  true  pustulation,  with  scabbing  and  scars, 
as  in  smallpox,  and  by  the  fact  that  during  convalescence  Jenner's 
vaccination  is  generally  successful. 

In  chicken-pox  the  vesicles  are  generally  larger,  and  often  leave 
thick  crusts. 

In  alastrim  the  eruption  is  often  confluent,  pustular,  and  clinically 
almost  identical  with  smallpox. 

Prognosis. — This  is  good. 

Treatment. — The  treatment  is  purely  symptomatic. 

PAPULAR  FEVER. 

Definition. — A  slight  febrile  disorder,  described  by  Castellani,  of 
unknown  causation,  characterized  by  a  maculo-papular  eruption 
and  rheumatoid  pains. 

Remarks.— We  have  seen  an  epidemic  of  this  peculiar  fever  in 
Ceylon;  it  resembled  measles  in  the  appearance  of  the  rash,  but 
was  without  any  catarrhal  symptoms. 

/Etiology. — This  is  quite  unknown. 

Symptomatology. — The  disease  begins  with  a  prodromal  period, 
during  which  the  patient  suffers  from  malaise,  depression,  and 
rheumatoid  pains,  especially  in  the  back,  which  are  associated  with 
chilliness.  After  three  or  four  days  the  rash  comes  out  suddenly  all 
over  the  body,  but  most  marked  on  the  arms,  trunk,  and  legs,  the 
face  being  least  affected.  The  eruption  is  morbilliform,  being  com- 
posed of  bright  red  pin-head  papules  and  red  maculae.  It  is,  as 
already  stated,  visible  on  the  arms,  legs,  and  chest ;  while  there  may 
be  a  few  maculae  on  the  palms  of  the  hands  and  soles  of  the  feet. 
The  face  is  not  much  affected,  and  there  the  eruption  is  rather  more 
macular  than  papular.  Filatow's  papules  in  the  mouth  are  absent. 
There  is  generally  slight  fever  lasting  for  a  day  or  two.  There  are 
no  catarrhal  symptoms  of  the  eyes,  nose,  or  throat,  no  enlargement 
of  the  lymphatic  glands.  The  eruption  generally  lasts  between  two 
to  five  days,  and  then  fades  without  any  desquamation  and  without 
leaving  any  marks.  In  most  cases  the  eruption  is  associated  with 
itching,  especially  on  the  arms,  and  in  a  few  cases  there  is  no 
fever. 

Diagnosis. — -It  is  to  be  distinguished  from  measles  by  the  absence 
of  the  catarrhal  symptoms,  absence  of  Filatow's  and  Koplik's  signs, 
from  German  measles  by  its  longer  duration  and  the  diffuse  type 
of  the  eruption,  from  toxic  rashes  of  intestinal  origin  by  the  absence 
of  any  intestinal  symptoms,  and  from  dengue  by  the  rash  being 
frankly  papular. 


1472  THE   UNCLASSIFIED  FEVERS  OF  THE  TROPICS 

Prognosis. — This  is  good. 

Treatment. — The  treatment  is  symptomatic,  small  doses  of  aspirin 
or  pyramidon  being  given  to  relieve  the  pains,  and  calamine  lotion  to 
alleviate  the  rash. 

HEMORRHAGIC  FEBRILE  GASTRO-ENTERITIS  OF 
CHILDREN. 

Synonym. — Fievre  a  Vomissements  noirs  des  Enfants. 

Definition. — An  endemic  fever  limited  to  '  Grande  terre  '  in 
Guadeloupe,  and  characterized  by  black  vomit  and  by  occurring 
only  in  children. 

Remarks. — This  disease,  which  closely  resembles  yellow  fever, 
was  first  described  by  Dr.  Guesde  in  1891. 

Climatology. — It  is  only  known  in  '  Grande  terre  '  in  Guadeloupe. 

Symptomatology. — The  disease  begins  suddenly  with  an  attack 
of  vomiting,  and  is  followed  by  an  attack  of  febrile  bilious  vomiting. 
The  child  then  becomes  very  ill,  with  remittent  fever,  slight  icterus, 
obstinate  constipation,  and  later  black  vomit.  After  lasting  from 
two  to  five  days  the  symptoms  may  improve,  sleep  returns,  the 
fever  disappears,  and  the  child  gradually  recovers;  on  the  other 
hand,  the  symptoms  may  become  worse,  and  the  child  die.  Conva- 
lescence is  prolonged. 

Diagnosis. — The  disease  seems  to  us  to  be  indistinguishable  from 
yellow  fever. 

Prognosis. — The  prognosis  is  always  grave. 

Treatment. — This  is  symptomatic. 


REFERENCES. 

Unclassified  Fevers. 

Birt  (1908).     Journal  Royal  Army  Medical  Corps. 

Castellani  (1904-12)  Ceylon  Medical  Reports;   (1907)   Journal  of  Hygiene. 

vol.  vii.;  and  Lancet;   (191 7)   Journal  of  Tropical  Medicine.     (Tropical 

Diseases  in  the  Balkans.) 
Cobb  (1906).     Indian  Medical  Gazette,  p.  135. 
Crombie  (1898).     Unclassified  Fevers  of  Hot  Climates.     Journal  of  Tropical 

Medicine,  p.  128. 
Fox,  A.  C.  (191 2).     Journal  Royal  Army  Medical  Corps. 
Grall  and  Clarac  (191  i).     Traite  Pratique  de  Pathologie  Exotique  Pox, 

vol.  ii.     Fievres  Climatiques.     Paris. 
Le  Dantec  (1911).     Pathologie  Exotique,  third  edition.     Paris. 
Manson  (1918).     Tropical  Diseases. 
McCarrison  (1906).     Indian  Medical  Gazette,  p.  7. 
Montel  (1918).     Bull.  Soc.  Path.  Exot. 

Nagele  (1912).     Archiv  f.  Schiffs-  u.  Tropen-Krankhygiene. 
Rogers  (1908).     Fevers  of  the  Tropics.     Oxford. 
Rousseau  (1902).     Archiv.  de  Med.  Navale,  lxxvii.  129. 
Thorpe  (1903).     Journal  of  Tropical  Medicine,  p.  25. 


REFERENCES  1473 

Hyperpyrexial  Fever. 

Thompstone  and  Bennett.     Referred  to  in  Hanson's  Tropical  Diseases. 

Double  Continued  Fever. 
Manson  (1918).     Tropical  Diseases. 

Urticarial  Fever. 

Houghton.    Quoted  by  Logan  (vide  infra). 

Lambert   (191 1).     Transactions  of  the   Society  of  Tropical   Medicine  and 

Hygiene.     London. 
Logan,  O.  T.  (1912).     China  Medical  Journal. 


93 


CHAPTER  LVIII 
COSMOPOLITAN  FEVERS 

General — Epidemic  cerebrospinal  meningitis — -The  exanthemata — Vaccina- 
tion—  Alastrim  —  Vaccinia  in  natives  —  Vaccine  rashes  —  Influenza — 
References. 

GENERAL. 

At  the  present  time  many  so-called  tropical  diseases  have  become  cosmopolitan 
— e.g.,  amoebic  dysentery — while  others,  such  as  malaria,  probably  have 
always  been  world-wide  in  their  distribution.  There  are,  however,  some  few 
fevers  which,  though  they  really  belong  to  cool  climates,  nowadays  are  of 
importance  in  the  tropics  —  for  example,  the  exanthemata  and  influenza. 
We  think  it  advisable  to  give  a  brief  account  of  these. 

EPIDEMIC  CEREBRO-SPINAL  MENINGITIS. 

Synonyms. — Spotted  fever.  French,  Meningite  cerebro-spinale  epidemique; 
Italian,  Meningite  cerebro-spinale;  German,  Epidemische  Genickstarre. 

Definition. — -An  acute  specific  fever  caused  by  Neisseria  intracellularis 
Weichselbaum,  1887  (Diplococcus  intracellularis), and  allied  organisms,  spread 
from  man  to  man  by  aerial  carriage,  and  characterized  by  a  brief  septicaemia, 
leading  to  a  cerebro-spinal  meningitis,  and  occasionally  by  a  more  prolonged 
and  dangerous  septicaemia  associated  with  a  petechial  eruption. 

History. — -The  disease  may  have  been  known  to  the  ancients,  but  to  our 
minds  the  phrenitis  of  Hippocrates  and  of  Celsus  has  nothing  in  common  with 
cerebro-spinal  meningitis.  We  have  been  unable  to  refer  to  the  works  of 
Aretaeus  or  of  Paul  of  .ZEgina,  and,  therefore,  are  unable  to  state  whether  the 
disease  which  they  are  said  by  Kutscher  to  have  described  in  Italy  resembled 
cerebro-spinal  meningitis  or  not,  and  the  same  remarks  hold  good  with  regard 
to  the  epidemic  described  by  Abdere  de  Lucien. 

On  the  other  hand,  we  have  carefully  read  Sydenham's  'Rise  of  a  New 
Fever,'  which  Arnell  considers  to  be  identical  with  the  disease  which  he  saw 
in  Connecticut  in  1 807,  and  which,  he  also  says,  is  the  same  as  Cullen's  '  Typhus 
Petechialis  '  and  the  disease  described  in  Medicus  Novissimus,  published  at 
the  beginning  of  the  eighteenth  century.  When  superficially  considered. 
Sydenham's  new  fever  docs,  at  the  first  glance,  read  like  cerebro-spinal 
meningitis,  but  when  the  symptoms  are  carefully  analyzed  they  will  be 
observed  to  resemble  those  of  the  enteroidea  group  of  fevers,  and  therefore  we 
are  convinced  that  Sydenham's  new  fever  is  not  cerebro-spinal  meningitis. 

We  have  been  unable  to  peruse  Vieusseux's  original  account  of  the  outbreak 
in  1805  at  and  around  Geneva,  but  North's  translation  in  181 1  of  the  article 
in  the  Journal  de  Midecine  de  Paris  makes  it  quite  clear  that  this  was  un- 
doubtedly the  disease  in  question,  and  the  sameauthor's  verbatim  account  of 
Danielson  and  Mann's  article  published  in  the  Medical  and  Agricultural 
Register  of  Boston,  with  its  careful  clinic  and  post-mortem  histories,  leaves  no 
doubt  that  these  two  authors  were  dealing  with  an  epidemic  of  cerebro-spinal 
meningitis  at  Medfield  in  March,  1 806.  North's  valuable  little  book  containing 
all  the  early  histories  of  the  disease  appeared  in  New  York. 

1474 


EPIDEMIC  CEREBROSPINAL  MENINGITIS  1475 

From  this  date  onwards  till  about  1884  the  whole  ground  of  the  history  has 
been  reviewed  by  Hirsch  in  the  third  volume  of  his  classical  '  Handbook  of 
Geographical  and  Historical  Pathology,'  in  which  he  divides  the  epidemics  of 
cerebro-spinal  meningitis  in  Europe  and  America  into  four  cycles,  viz. : — 

(1)  1 805- 1 830,  Europe  and  North  America. 

(2)  1837-1850,  Europe,  North  America,  and  Algiers. 

(3)  1 854- 1 875,  Europe,  North  America,  Africa  (parts),  Western  Asia,  and 
South  America. 

(4)  1 876- 1 884,  small  epidemics  in  former  areas,  to  which  may  be  added  : — 

(5)  1885  to  present  time.  Recognition  of  the  disease  in  the  tropics,  West 
Indus,  Fiji,  Anglo-Egyptian  Sudan,  West  Africa,  Western  Australia,  Mexico. 
Severe  epidemics  in  America  and  Europe — i.e.,  this  is  the  period  of  the  first 
pandemic. 

It  will  thus  be  seen  that  the  area  in  which  the  disease  is  recognized  has 
gradually  extended,  and  that  this  has  been  quicker  of  late  years,  probably 
due  to  increased  facilities  for  travel  which  has  introduced  it  by  the  agency 
of  carriers  into  lands  in  which  it  probably  did  not  previously  exist,  as,  for 
example,  Fiji,  the  result  being  that  at  the  present  time  it  appears  to  be  diffused 
all  over  the  world  and  to  occur  as  localized  epidemics  in  different  places  in 
different  years. 

In  the  study  of  these  epidemics  certain  important  features  were  brought 
out — viz.,  the  influences  of  over-exertion,  starvation,  overcrowding,  and  bad 
ventilation,  which  account  for  the  prevalence  of  the  disease  among  soldiers 
and  poor  people  and  for  its  increase  in  different  countries  in  periods  of  bad 
weather — e.g.,  during  the  winter  and  spring  in  cold  climates  and  during  the 
Haboub  seasons  of  the  hot  Anglo-Egyptian  Sudan,  or  to  a  less  extent  the  cold 
weather  of  the  Sudan,  when  the  people  huddle  together  into  crowded,  ill- 
ventilated  huts  and  houses. 

The  historical  portions  with  which  we  are  mainly  interested  are  those 
concerned  first  withits  occurrence  in  the  tropics,  and  secondly  with  its  aetiology. 

Occurrence  in  the  Tropics. — The  first  record  we  have  been  able  to  find  of 
the  disease  in  a  subtropical  land  is  the  occurrence  of  an  epidemic  in  1 840-1847 
in  Algiers,  in  which  country  it  has,  from  time  to  time,  been  reported.  It  is 
also  said  to  have  occurred  in  1840  in  Brazil  and  in  Monte  Video  in  South 
America . 

In  1 872  it  was  reported  in  Asia  from  Smyrna  and  in  1 874-75  in  Persia,  accord- 
ing to  Bruce  Low  in  Ms  paper  on  epidemic  cerebro-spinal  meningitis  published 
in  1899. 

It  is  believed  to  have  been  present  in  Central  America  and  in  the  West 
Indies  prior  to  1S84,  but  without  trustworthy  information. 

Corney  has  given  an  excellent  account  of  the  invasion  of  Fiji  by  the  disease. 
It  would  appear  that  the  first  cases  were  noted  in  1876  in  an  immigrant 
labourer's  depot  at  Levuka,  and  from  that  time  onwards  it  was  probably 
diagnosed  as  tetanus,  sunstroke,  or  meningitis,  until  it  assumed  epidemic  form 
in  1  885,  which  he  believed  was  due  to  the  contagion  being  spread  from  man  to 
man — a  very  advanced  idea  at  that  time. 

Cerebro-spinal  meningitis  was  reported  from  the  West  Coast  of  Africa  by 
the  Williams  in  1900,  and  from  then  onwards  from  time  to  time.  In  1905 
there  was  a  severe  epidemic  in  Northern  Nigeria,  which  was  reported  upon  by 
Twomey  and  Davidson,  and  in  [906  08  in  the  northern  territories  of  the  Gold 
Coast,  where  it  was  ably  investigated  by  Horn.  In  Northern  Nigeria  it  was 
said  that  cattle  were  attacked,  and  in  the  Lorha  district  of  the  northern 
territories  of  the  Gold  Coast  the  natives  are  said  to  have  noted  a  great  mor- 
tality among  fowls  prior  to  the  epidemic  of  the  disease.  According  to  Bargy 
and  Horn,  the  disease  was  marked  at  this  time  in  French  West  Africa  to  the 
west  of  the  Black  Volta. 

In  1909  it  was  reported  as  being  present  in  1907  in  the  northern  districts  of 
Togoland  by  Jaffe,  when  it  was  known  to  cause  300  deaths.  Jaffe  obtained 
the  true  diplococcus  of  Weichsclbaum  from  his  cases. 

Epidemic  cerebro-spinal  meningitis  has  been  recorded  in  British  East  Africa 


1476  COSMOPOLITAN  FEVERS 

since  1906,  when  Haran  noted  five  cases,  and  has  been  ably  described  by 
Shircore  and  Ross  in  1913. 

In  1915  Butler  drew  attention  to  a  curious  feature  of  the  disease,  in  that 
there  are  places  in  East  and  Central  Africa  where  it  has  always  been  endemic 
and  seldom  epidemic,  and  he  quotes  Uganda  in  general,  whilst  in  the  high- 
lands of  British  East  Africa  the  endemic  form  is  seldom  seen,  but  epidemics  of 
greater  or-less  virulence  are  known.  He  says  that  in  one  tribe  alone  between 
20,000  and  40,000  deaths  are  attributed  to  this  disease,  a  mortality  which 
sleeping  sickness  can  hardly  be  said  to  rival. 

In  India  it  appears  to  have  been  first  reported  by  Vandyke  Carter  as  occur- 
ring in  July,  1878,  in  Bombay,  where  he  says  that  he  is  not  aware  that  it  had 
been  previously  recognized.  He  does  not  appear  to  have  published  this 
observation  until  1882,  and  then  only  in  his  work  '  Spirillum  Fever,'  p.  436, 
when  he  gives  not  merely  a  clinical  but  a  post-mortem  account  of  one  case  and 
clinical  histories  of  three  others.  As  he  has  been  said  not  to  have  recognized 
the  disease,  it  may  be  well  to  note  that  he  heads  the  paragraphs  in  question 
cerebrospinal  meningitis. 

In  1884  Dimmock  gave  a  full  account  of  an  outbreak  in  the  preceding  year 
in  the  Shikarpur  Jail.  Since  then  some  cases  have  generally  been  reported 
year  by  year,  and  the  whole  subject  of  epidemic  cerebro-spinal  meningitis  in 
India  was  ably  reviewed  by  Robertson-Milne  in  1906. 

In  1905  Castellani  described  two  cases  which  occurred  in  Singhalese  natives 
in  Ceylon. 

In  19 1 6  Chalmers  and  O'Farrell  published  a  series  of  investigations  upon 
the  disease  as  seen  in  the  Anglo-Egyptian  Sudan. 

History  of  the  Organism. — In  1875  Klebs  was  the  first  to  see  cocci  in  the 
cerebro-spinal  fluid  of  cases  of  meningitis,  and  to  assign  to  them  a  causal 
function.  He  was  followed  by  Eberth  in  1 881,  in  which  year  Gaucher  was  the 
first  to  see  micrococci  in  the  blood  and  urine  in  a  patient  during  life  and  in  the 
exudate  from  the  spinal  canal  after  death;  and  in  connection  with  these 
findings  in  the  blood  one  may  invite  attention  to  the  observation  of  Cole  in 
1915,  who  obtained  films  of  the  peripheral  blood  in  which  ten  out  of  2,000 
leucocytes  showed  the  organism,  and  also  to  Osier's  statement  that  Gwyn  in 
1899  was  the  first  to  isolate  the  organism  from  the  blood  in  pure  culture. 
In  1883  Ughetti  also  found  micrococci  in  the  exudate  and  in  the  blood,  and  in 
1884  Marchiafava  and  Celli  wrote  a  short  work  on  the  occurrence  of  micro- 
organisms, and  especially  diplococci,  in  cerebro-spinal  meningitis.  They  were 
also  seen  in  meningeal  exudates  by  von  Leyden  in  1883,  and  byLeichstenstern 
in  1885,  and  the  last-mentioned  observer  noted  that  they  resembled  the  gono- 
coccus  by  being  found  in  the  leucocyte. 

In  1886  Senger  also  noted  them  in  the  cerebro-spinal  exudate,  while  Frankel 
with  Weichselbaum,  Foa  with  Bordoni,  Uffreduzzi,  and  Lemoine  described  the 
pneumococcus  as  the  causal  organism  of  a  series  of  cases  of  cerebro-spinal 
meningitis  unassociated  with  pneumonia. 

In  1887  Weichselbaum  published  his  paper  '  Ueber  die  ^Etiologie  der  akuten 
Meningitis  Cerebro-spinalis,'  in  winch  he  described  eight  cases  of  meningitis 
without  pneumonia,  two  of  which  were  due  to  the  pneumococcus  and  six  were 
caused  by  an  organism  which  differed  therefrom  by  being  generally  a  diplo- 
coccus,  more  rarely  arranged  as  tetrads,  and  resembling  the  gonococcus,  being 
often  contained  in  leucocytes  and  being  Gram-negative.  He,  however, 
distinguished  this  organism  from  the  gonococcus  by  the  fact  that  it  produces 
in  subcultures  on  agar-agar  slopes  a  flat  viscous  growth  which  is  greyish  when 
seen  by  reflected  and  greyish-white  when  examined  by  transmitted  light.  It 
only  grew  at  incubator  temperatures,  and  had  but  a  slight  vitality.  This 
organism  he  called  Diplococcus  intracellularis  meningitidis,  and  looked  upon 
its  action  as  being  toxic  in  nature,  while  he  hesitated  to  regard  it  as  the  causal 
agent  of  the  disease. 

Although  Weichselbaum's  observations  were  confirmed  by  Goldschmidt  in 
1887,  and  by  Edler  and  himself  in  1888,  they  produced  comparatively  little 
influence,  and  were  almost  unnoticed  until  a  polemic  was  started  in  1890,  which 
raged  till  1893,  as  to  the  identity  of  Bonome's  streptococcus  of  epidemic  cere- 


HISTORY  OF  THE  ORGANISM  1477 

bro-spinal  meningitis  first  reported  in  1890,  and  x-oa's  meningococcus  and  the 
Diplococcus  pneumonia,  in  which  it  was  decided  that  Bonome-'s  organism  was 
the  pneumococcus,  but  the  confusion  was  increased  by  Bordoni,  Ulfreduzzi 
regarding  D.  intracellular i±  as  a  variety  of  D.  pneumonia. 

This  unhappy  condition  was  accentuated  in  1895,  when  Jaeger,  while  study- 
ing a  regimental  epidemic  of  fourteen  cases  occurring  in  Stuttgart,  found  the 
pneumococcus  in  two  cases,  a  streptococcus  in  one  case,  and  in  eleven  cases 
an  intracellular  Gram  positive  diplococcus  morphologically  resembling  the 
gonococcus,  producing  turbidity  in  broth,  and  forming  short  or  even  at  times 
long  chains,  while  it  retained  its  Gram-positive  character  in  cultures.  It  grew 
well  on  gelatine  at  the  temperature  of  the  laboratory,  and  preserved  its  vitality 
during  fourteen  days  or  more  on  artificial  media.  He  concluded  that  this 
organism  was  Weichselbaum's  D.  intracellulars,  and  in  this  unfortunate  con- 
clusion he  remained  unopposed  for  years,  and  was  supported  by  Heubner 
in  Berlin  in  1896,  who  not  merely  was  tne  first  to  obtain  a  coccus  from  the 
cerebro-spinal  fluid  during  life,  but  who  produced  a  fata!  meningitis  in  goats 
with  this  germ,  which  at  the  time  was  considered  to  be  an  important  experiment, 
as  an  epizootic  meningitis  was  present  in  horses  and  horned  cattle  in  Germany; 
further,  he  proposed  the  name  meningococcus  for  this  organism,  notwith- 
standing the  fact  that  Bonome  had  already  used  it  for  the  pneumococcus 
mentioned  above. 

This  meningitis  cerebro-spinalis  enzootica,  or  epizootic  cerebro-spinal 
meningitis,  is  often  called  the  Bor-na  disease,  because  of  the  attention  paid  to 
a  malignant  outbreak  in  horses  at  Borna  in  1894. 

It  is  obvious  that  it  must  be  of  the  greatest  importance  to  definitely  settle 
the  question  as  to  whether  (as  is  generally  believed)  the  two  diseases  are  quite 
separate,  or  whether  there  is  some  relationship  between  the  human  and  some 
undefined  fraction  of  the  animal  complaint. 

Thus  we  see  that  confusion  has  arisen  not  only  between  a  disease  seen  in 
animals,  but  also  between  two  human  organisms. 

Jaeger  and  Heubner's  results  were  more  or  less  confirmed  by  Holdheim, 
Petersen,  Urban  (1897),  Rameny  (1898),  Vanzetti  (1901),  and  many  others, 
while  Kiefer,  Kister,  Kischensky,  and  Berdach  and  Froz  supported  Weichsel- 
baum,  and  so  great  a  confusion  arose  between  the  Gram-negative  Diplococcus 
intracellularis  Weichselbaum,  1887,  and  the  Gram-positive  coccus  of  Jaeger 
and  Heubner,  which  is  also  known  as  D.  crassus  von  Lingelsheim,  1906,  that 
every  coccus  found  in  connection  with  the  meninges  was  considered  to  be  a 
true  meningococcus. 

In  1898  Still  showed  that  posterior  basic  meningitis  was  associated  with  an 
organism  like  D.  intracellularis,  and  Councilman,  Mallory,  and  Wright  obtained 
Weichselbaum's  coccus  from  thirty-one  cases  of  the  disease,  while  Faber  in 
1900  found  the  same  organism  in  an  epidemic  in  Copenhagen,  and  Canuet  in 
the  same  year  showed  that  it  was  an  obligatory  aerobe. 

Pfaundler  in  1899  recognized  both  the  Weichselbaum  type  and  the  Jaeger- 
Heubner  type,  and  in  this  he  was  supported  by  Hunter  and  Nuttall  and  by 
Lazarus-Barlow  in  1901,  in  which  year  Albrecht  and  Ghon,  reporting  upon 
the  1898  epidemic  at  Trefail  in  Steiermark,  not  merely  confirmed  Weichsel- 
baum's researches,but  were  the  first  toobtain  the  organism  by  cultural  methods 
from  the  naso-pharynx  of  cases  of  the  disease,  an  observation  which  is  now 
of  almost  daily  occurrence,  although  we  are  still  uncertain  as  to  the  proportion 
of  cases  which  become  permanent  carriers.  They  also  obtained  Gram-negative 
cocci  in  the  throats  of  fifteen  healthy  persons  who  were  contacts  with  cases, 
and  in  one  such  person  the  meningococcus  was  identified  by  cultural  tests. 

In  1902-03  Bettencourt  and  Franca,  in  Portugal,  found  the  meningococcus 
to  be  present  271  times  in  274  cases  of  cerebro-spinal  meningitis,  and  Lepierre 
in  1903  described  a  meningococcus  which,  although  originally  Gram-negative, 
became  Gram-positive,  and  the  same  year  saw  the  Meningococcal  polemic 
between  Jaeger,  as  representing  the  German  school,  and  Weichselbaum, 
Albrecht,  and  Ghon  on  behalf  of  the  Austrian  schools,  as  a  result  of  which 
Weichselbaum's  organism  became  firmly  established. 

In  1905  Kob  and  Weyl  wrote  on  the  subject  of  Gram-negative  and  Gram- 


1478  COSMOPOLITAN  FEVERS 

positive  diplococci,  and  in  the  same  year  Castellani  described  Weichselbaum's 
organism  in  cases  in  Ceylon,  and  Dunn  and  Gordon  reported  upon  an  epidemic 
simulating  influenza  in  Hertford  in  which  they  obtained  Micrococcus  catar- 
rhalis  and  forms  resembling  the  meningococcus.  It  was  during  this  investi- 
gation that  Gordon  brought  forward  the  carbohydrate  tests  as  differential 
agents  for  the  meningococcus,  a  point  which  he  further  elaborated  in  1907, 
in  which  year  Buchanan  introduced  a  modification  of  Loefner's  blood  serum 
by  adding  neutral  red  in  a  proportion  of  1  in  10,000. 

The  outbreaks  of  cerebro-spinal  meningitis  in  1905  in  Prussia  and  New 
York  produced  excellent  work,  in  the  former  by  von  Lingelsheim  and  by 
Kolle  and  Wassermann  with  reference  to  the  organism,  which,  together  with 
the  labours  of  other  collaborators,  was  published  in  one  volume  in  1906.  In 
this  epidemic  von  Lingelsheim  found  the  meningococci  to  be  present  in  23*12 
per  cent,  of  the  cases,  but,  as  many  of  the  samples  came  from  a  long  distance, 
it  is  interesting  to  note  that  he  obtained  70-6  per  cent,  positive  results  from 
examinations  in  the  hospital  near  the  laboratory  and  taken  during  the  first 
day  of  illness,  and  66-6  per  cent,  in  those  taken  from  first  to  fifth  day  of  the 
illness,  while  he  obtained  24-5  per  cent,  from  sixth  to  tenth  day,  ii'29  per 
cent,  from  eleventh  to  twentieth  day,  and  only  4*39  per  cent,  after  the  twenty- 
first  day.  Thus  in  three  weeks  90  per  cent,  of  the  cases  were  free  from  meningo- 
cocci, but  he  found  that  15  per  cent,  of  the  contacts  became  carriers.  He 
also  gave  an  account  of  D.  crassus  and,  with  Leuchs,  of  experiments  on  animals 
with  the  meningococcus. 

The  American  epidemic  was  investigated  by  Elser,  Durham,  Goodwin,  and 
Sholly,  and  produced  results  similar  to  those  of  von  Lingelsheim,  and  in  the 
same  year  Robertson-Milne  reported  upon  cerebro-spinal  meningitis  as  seen 
in  India. 

In  this  year  Kutscher  described  a  coccus  in  the  naso-pharynx  of  carriers 
which  agreed  morphologically  and  culturally  with  the  meningococcus,  but 
which  could  be  differentiated  by  Castellani's  absorption  test,  and  Westen- 
hoeffer  stated  that  the  primary  focus  of  the  disease  was  in  the  pharyngeal 
tonsils,  post-nasal  region,  and  the  nasal  sinuses,  in  which  in  the  early  days  of 
the  disease  he  reported  that  it  caused  an  inflammation.  In  1907  Taylor 
investigated  the  opsonic  index  with  a  view  to  diagnosis.  In  1909  Elser  and 
Huntoon  named  Kutscher's  organism  the  Pseudo-meningococcus.  At  first  it 
was  thought  that  organism  was  rare  and  had  nothing  to  do  with  the  disease, 
but,  when  Gordon  and  Murray's  researches  mentioned  below  are  considered, 
it  is  obvious  that  it  would  agree  with  such  of  their  groups  as  do  not  agglutinate 
with  and  absorb  intracellularis  serum ;  at  the  present  it  is  only  differentiated 
from  the  strains  with  which  Kutscher  and  Elser  and  Huntoon  were  working, 
and  may  or  may  not  be  the  same  as  Dopter's  parameningococcus,  which  is 
mentioned  below. 

In  1908  von  Lingelsheim  gave  the  following  differentiation  of  the  organisms 
found  by  him  in  the  naso-pharynx  of  the  contacts: — 

(1)  Micrococcus  catarrhalis. — Frequent;  colonies,  dry  crumbling;  when  seen 
under  microscope  granulated,  generally  with  irregular  borders.  Attacks 
neither  grape-sugar,  nor  maltose,  nor  levulose. 

(2)  Diplococcus  flavus  I . — Colonies  on  ascitic  agar  very  similar  to  those  of 
meningococcus.  Twenty-four  hours'  culture  exhibits  clear  yellow  pigment  in 
thick  layer. 

(3)  Diplococcus  flavus  II. — Colonies  polymorphic,  sometimes  moist  and 
glistening,  sometimes  dry  and  wrinkled.  Twenty-foxir  hours'  culture  exhibits 
yellow  pigment  in  thick  layer. 

(4)  Diplococcus  flavus  III. — -At  commencement  difficult  to  cultivate,  and 
therefore  rarely  coming  under  observation.  All  three  species  of  flavus  form 
acids  in  the  presence  of  grape-sugar,  maltose,  and  levulose;  whilst  the  meningo- 
coccus ferments  only  grape-sugar  and  maltose,  the  latter  regularly. 

(5)  Diplococcus  tnucosus. — Colonies  more  prolific  and  juicy  than  those  of 
meningococcus.  Grows  also  on  gelatine  at  room  temperature.  According  to 
many  authors,  markedly  pathogenic  for  mice. 

(6)  Micrococcus  cinereus. — Coarse,  uneven  granular.     Colonies  and  cultures 


HISTORY  OF  THE  ORGANISM  1479 

delicate,  reminding  one  of  D.  crassus.  Does  not  attack  grape-sugar,  levulose, 
and  maltose. 

He  also  considered  the  possibility  of  the  spread  of  the  disease  by  insects. 
by  dwellings,  and  by  clothing,  food,  and  water,  and  concluded  that  none  of 
these  were  effective  agents  in  the  propagation  of  the  disease. 

In  1909  there  appeared  a  most  important  work  by  Elser  and  Huntoon  in 
which  they  described  most  carefully  the  cultural,  biochemical,  and  serum 
reactions  of  the  meningococcus  and  its  allies,  as  well  as  its  viability,  and 
especially  its  selective  affinity  for  the  cerebro-spinal  fluid,  a  point  little  con- 
sidered by  the  majority  of  investigators.  They  also  considered  the  subject 
of  mixed  infections,  which  was  dealt  with  by  Spccht  in  the  following  year. 

In  the  same  year  Dopter  described  his  Parameningococcus,  which  was  not 
agglutinated  by  meningococcus  serum  (a  fact  confirmed  by  Gordon  and  Murray 
in  19 1 5),  but  showed  complement-fixation.  Two  years  later  he  described 
seven  cases  of  cerebro-spinal  meningitis  as  being  due  to  this  organism,  and 
in  191  [  used  Castellani's  saturation  test  to  differentiate  it  from  the  meningo- 
coccus. 

The  agglutination  reactions  of  the  meningococcus  are  unsatisfactory,  as 
may  be  gathered  by  a  study  of  Elser  and  Huntoon's  careful  work,  as  well  as 
by  the  discordant  results  obtained  by  numerous  observers.  In  19 15  Hime 
instituted  a  rapid  method  of  preparation  of  a  high-titre  agglutinating  serum 
in  rabbits,  and  Gordon  and  .Murray  investigated  genuine  strains  of  meningo- 
cocci obtained  from  the  cerebro-spinal  fluid  of  cases,  and  found  that  by  agglu- 
tination tests  and  by  Castellani's  absorption  method  they  could  split  up 
thirty-two  strains  into  the  following  groups: — 

(I.)  With  serum  from  No.  1,  19  strains. 

(II.)  With  serum  from  No.  20,  8  strains. 

(III.)  With  serum  from  No.  28,  4  strains. 

(IV.)  With  serum  from  No.  32,  1  strain. 

They  also  distinguished  by  these  sera  Dopter's  parameningococcus  from  all 
the  other  groups,  and  they  noted  that  one  strain  absorbed  the  specific  agglu- 
tinins from  two  groups;  while  out  of  ten  carriers  one  belonged  to  Group  (I.) 
and  five  to  Group  (II.),  while  the  others  were  not  classified. 

In  the  same  year  Crowe  attempted  to  meet  the  difficulties  met  with  in  the 
agglutination  tests  by  devising  a  simpler  method. 

We  have  now  given  a  rough  sketch  of  the  history  of  Weichselbaum's 
organism,  and  we  might  well  pause,  as  Crowe  has  done,  and  ask  where  do  we 
stand  as  regards  its  recognition. 

It  is  admitted  on  all  sides  that  there  is  a  close  resemblance  between  the 
gonococcus  and  the  meningococcus,  except  as  regards  the  human  diseases 
which  they  produce, and,  indeed,  many  years  ago  it  was  suggested  that  the  latter 
might  be  the  former  adapted  to  the  cerebro-spinal  nervous  system  and  the 
na-M)-j)harynx,  but  to-day  it  is  admitted  on  all  sides  that  they  are  separate, 
mainly  because  of  an  experiment  in  which  the  meningococcus  was  found  not 
to  cause  gonorrhoea  when  injected  into  the  human  urethra. 

As  regards  the  meningococcus,  we  can  aptly  quote  Crowe,  who,  writing  in 
19 1 5,  says:— 

'  The  present  state  of  our  knowledge  so  far  as  it  bears  on  the  carrier  may 
be  summed  up : — 

'  No  Gram-negative  organism  isolated  from  the  naso-pharynx  can  be  proved 
to  be  a  meningococcus. 

'  No  Gram-negative  organism  which  resembles  even  faintly  a  meningo- 
coccus can  be  regarded  with  certainty  as  incapable  of  producing  meningitis.' 

Hem  e  we  have  not  improved  our  position  since  the  days  of  the  meningo- 
coccal controversy,  but  are  actually  in  a  position  of  greater  uncertainty  as  to 
the  differentiation  ol  \Wii  hselbaum's  Diplococcus  intracellularis,  and,  this 
being  so,  we  will  now  brieily  review  our  position  as  to  the  causal  relationship 
between  this  organism  and  epidemic  cerebro-spinal  meningitis. 

Indeed,  this  is  exceedingly  necessary  at  the  present  time,  because,  firstly,  a 


1480  COSMOPOLITAN  FEVERS 

certain  amount  has  been  written  with  regard  to  the  so-called  pleomorphism 
of  the  meningococcus — e.g.,  the  papers  in  191 5  by  Lundie,  Thomas,  and 
Fleming,  and  by  Donaldson  in  the  same  year,  while  in  191 5  and  1916  Hort, 
Lakin,  and  Benians  have  doubted  the  causal  action  of  the  meningococcus, 
and  in  the  last  publication  Hort  has  stated : — 

4  In  order  to  discover  the  true  infective  agent,  whether  biologically  related 
to  the  meningococcus  or  not,  further  research  is  imperative,  attention  being 
particularly  directed  to  filtrable  organisms  in  the  naso-pharnyx  and  cerebro- 
spinal fluid  of  acute  cases.' 

With  regard  to  the  question  of  filtrable  organisms,  Chalmers  and  O'Farrell 
have  performed  an  experiment  of  this  nature  with  a  fresh  cerebro-spinal  fluid, 
but  the  result  was  negative. 

With  regard  to  the  meningococcus  being  the  causative  factor  in  epidemic 
cerebro-spinal  meningitis,  the  above  observations  make  it  sufficiently  clear 
that  it  has  been  regularly  found  in  the  cerebro-spinal  fluid  of  persons  suffering 
from  the  disease,  and  that  it  has  been  found  in  the  blood  and  also  in  the  urine 
when  looked  for  at  the  correct  time  or  in  suitable  infections.  It  is  also  generally 
present  in  the  naso-pharynx  of  the  cases,  and  was  found  by  Sophian,  Westen- 
hoffer,  and  others  in  such  complications  as  arthritis,  pyelitis,  pneumonia,  endo- 
carditis, and  in  purulent  conjunctivitis  from  a  virulent  case  of  the  disease. 

Epidemiological  studies  easily  convince  anyone  associated  with  the  disease 
that  some  contagion  can  at  times  pass  from  the  sick  to  the  healthy,  causing 
an  attack  of  the  disease,  and,  moreover,  as  we  have  pointed  out  above,  many 
of  the  contacts  show  the  meningococcus.  It  is  true  that,  as  a  rule,  but  few 
attendants  on  cases  acquire  the  disease,  though  there  are  marked  exceptions. 

It  is  also  true  that  the  accidental  infection  by  Kief er  of  his  own  nose  with  a 
culture  from  the  laboratory  produced  a  severe  rhinitis,  but  he  did  not  develop 
meningitis,  and  one  of  us  accidentally  infected  his  thumb  from  some  cultures, 
with  the  result  that  hemorrhagic  granulation  tissue  formed  from  which  the 
germ  was  recovered,  cultivated,  and  tested  biochemically,  and  agreed  with  the 
meningococcus  in  these  details.  Although  the  lymphatic  glands  enlarged 
and  a  mild  chronic  fever  lasting  for  months  ensued,  with  almost  constant 
and  sometimes  very  severe  headache,  no  meningitic  symptoms  developed, 
although  the  opsonic  index  varied  from  o-8  to  1*3,  until  meningococcal  vaccine 
therapy  cured  the  condition. 

In  the  first  case  it  is  possible  that  the  coccus  never  got  into  the  system,  and 
in  the  second  that  it  never  entered  the  blood-stream,  and  hence  the  lack  of 
meningeal  infection. 

Turning  now  from  man  to  experiments  upon  animals,  von  Lingelsheim  and 
Leuchs,  followed  by  Flexner  in  1906,  reported  successful  inoculations  of 
monkeys  subdurally.  They  were  followed  in  1908  by  M'Donald,  but  neither 
he  nor  Davis  in  1905,  nor  any  of  the  above  experimenters,  were  able  to  infect 
animals  by  injections  into  the  blood-stream,  although  M'Donald  produced 
an  acute  toxaemia  by  this  method,  nor  were  Kolle  and  Wassermann  or  Davis 
able  to  reproduce  the  disease  in  the  same  animals  via  the  nose.  Elser  and 
Huntoon  consider  that  the  value  of  these  experiments  is  questionable  when  the 
peculiar  affinity  of  the  meningococcus  for  the  leptomeninges  is  taken  into 
account.  They  point  out  that  other  organisms  injected  subdurally  will  cause 
a  meningitis,  but  no  other  common  pathogenic  organism  shows  a  similar 
selective  action  for  the  meninges  of  man. 

Further,  it  is  to  be  remarked  that  Bettencourt  and  Franca  and  Kolle  and 
Wassermann  were  unable  to  infect  monkeys  even  by  means  of  subdural 
injections,  and  this  has  happened  to  us  both  with  fresh  cerebro-spinal  fluid 
from  which  growths  were  subsequently  obtained  and  with  cultures,  although 
we  have  also  had  successes. 

Only  Councilman,  Mallory,  and  Wright  have  succeeded  in  infecting  a  goat 
when  dealing  with  the  true  meningococcus,  and  Vansteenberghc  and  Grysez 
produced  meningitis  in  rabbits  and  guinea-pigs,  but  it  seems  to  us  to  be  doubt- 
ful whether  they  worked  with  a  true  meningococcus. 

We  have  been  unable  to  peruse  Flexner's  original  papers,  but  according  to 
Batten  the  general  circulation  became  infected  in  his  monkeys. 


HISTORY  OF  THE  ORGANISM  1481 

We  shall  give  below  reasons  why  carriers  do  not  become  infected,  and  it 
is  possible  that  monkeys  may  be  resistant  except  when  damaged  by  an  opera- 
tion like  trephining  or  otherwise  below  par ;  moreover,  the  meningococcus  is 
often  damaged  in  the  drawn  fluid  and  degenerated  on  cultivation,  for  we  have 
seen  it  fail  to  infect  a  monkey  after  five  generations  of  growth  of  the  same 
organism  which  was  infective  during  the  second  generation. 

We  now  turn  to  inquire  in  what  way  the  human  body  reacts  to  the  organism. 
Davis  showed  in  1907  that  at  the  end  of  the  first  week  agglutination  up  to 
1  in  50  could  be  obtained,  and  in  the  eighth  week  up  to  1  in  200,  and  pointed 
out  that  the  agglutinins  were  thermostable,  resisting  a  temperature  of  650  C. 
for  an  hour,  while  they  appear  to  be  practically  absent  from  the  cerebro- 
spinal fluid,  but  many  observers,  including  ourselves,  have  found  this  test 
uncertain. 

Davis  in  1905  showed  that  the  coccus  multiplied  in  two  normal  defibrinated 
bloods,  but  in  four  other  bloods  it  was  killed,  as  it  was  by  the  blood  from 
patients  after  the  tenth  day.  He  noted  that  the  meningococcidal  power  of 
the  blood  serum  of  patients  which  seemed  to  be  greater  than  that  of  normal 
blood  serum  was  diminished  by  heating  to  60°  C.  for  thirty  minutes.  He 
found  that  the  phagocytic  index  was  13  for  normal  human  serum,  o  for  serum 
heated  to  6o°  C.  for  thirty  minutes,  while  in  meningitic  serum  from  cases 
between  the  second  and  seventh  week  of  convalescence  it  was  1  i-i  .  Normal 
cerebro-spinal  fluid  did  not  contain  opsonins. 

Houston  and  Rankin  in  1907  found  that  opsonins  were  exceedingly  low  in 
normal  serum,  and  lower  still  in  cerebro-spinal  fluid,  while  in  cases  from  the 
sixth  day  onwards  they  rose  remarkably,  except  in  two  fatal  cases,  while  in 
one  relapse  the  rise  was  postponed  till  the  eleventh  day. 

MacGregor  observed  that  the  highest  indices  occur  in  the  second  and  third 
week  of  the  disease,  but  that  the  degree  of  immunity  after  recovery,  as 
measured  by  the  opsonic  index,  was  variable,  and  concluded  that  a  high 
opsonic  index  was  a  sign  of  forcible  reaction  to  a  fairly  severe  infection. 

Meakers  and  Dopter  have  shown  the  presence  of  immune  bodies  in  the  blood 
of  meningitic  patients  by  means  of  complement-fixation,  and  McKenzie  and 
Martin  have  also  demonstrated  the  presence  of  these  bodies  by  injecting  the 
serum  of  recovered  cases  intraspinally  into  other  acute  cases  with  fair  results. 
It  would  therefore  appear  that  immune  bodies  are  formed  in  patients'  systems, 
which  is  in  support  of  the  causal  action  of  the  meningococcus. 

We  now  turn  to  see  whether  specific  serum  treatment  and  vaccine  therapy 
will  help  the  problem. 

With  regard  to  the  serum  treatment,  Jochmann  in  1905  experimented  with 
a  specific  immune  serum  which  was  afterwards  manufactured  by  Merck.  He 
tested  his  scrum  by  the  opsonic  test,  the  bactericidal  test,  and  by  agglutina- 
tion. 

Kolle  and  Wassermann  also  made  an  immune  serum  upon  which  they 
reported  in  1907. 

In  1906  Flexner  wrote  upon  a  specific  serum  which  protected  monkeys  and 
small  animals.  Later  this  serum  was  made  from  immunized  horses,  and  has 
been  extensively  used. 

With  regard  to  vaccine  treatment,  Davis  in  1907  was  the  first  to  inject  killed 
meningococci  into  normal  persons  and  into  patients  suffering  from  the  disease, 
and  Collis  in  1 9 1 3  tried  specific  serum  treatment  together  with  vaccine  therapy. 
In  the  same  year  Sophian  reported  on  his  experimental  inoculation  ol  eleven 
medical  students,  and  eleven  months  after  these  inoculations  Merck  re-tested 
eight  of  them,  comparing  the  results  with  those  of  a  normal  person  and  a 
recently  recovered  case,  and  concluded  that  a  person  so  vaccinated  may  consider 
himself  to  be  immune  for  at  least  one  year. 

In  October,  19 15,  Surgeon-General  Rolleston  reported  upon  sixteen  cases  of 
vaccine  treatment  with  four  deaths  and  twelve  recoveries ;  the  vaccine,  how- 
ever, was  never  used  alone,  but  combined  with  serum  treatment  in  some  form 
or  with  soamin.  In  his  report  lumbar  puncture  alone  in  thirteen  cases  re- 
sulted in  four  deaths  and  nine  recoveries,  serum  intrathecally  alone  forty- 
three  deaths  and  nineteen  recoveries,  or  alone  and  combined  with  vaccine, 


1482  COSMOPOLITAN  FEVERS 

soamin,  or  hexamine,  sixty-four  deaths  and  forty-one  recoveries,  while  symp- 
tomatic treatment  gave  ten  deaths  and  four  recoveries. 

In  19 16  Chalmers  and  O'Farrell,  studying  an  outbreak  of  cerebro-spinal 
meningitis  in  the  Anglo-Egyptian  Sudan,  came  to  the  following  con- 
clusions:— 

1.  The  important  causal  agent  is  Neisseria  intracellularis  (Weichselbaum, 
1887),  and  only  once  has  Diplococcus  crassus  von  Lingelsheim,  1906,  been 
found  acting  in  this  capacity,  and  so  far  no  other  organism. 

2.  Only  man  has  been  found  to  be  the  host  of  Neisseria  intracellularis,  and 
he  acts  in  this  capacity  as  the  true  carrier  of  the  germ,  and  as  such  does  not 
acquire  the  disease  because  of  an  immunity  conferred  by  auto  vaccination. 

3.  In  order  to  acquire  the  disease,  two  factors  at  least  are  required,  viz.: — - 

(a)  Infection  with  Neisseria  intracellularis. 

(b)  Lack  of  capability  on  the  part  of  the  body  to  produce  the  necessary 
immunity. 

The  infection  takes  place  from  the  nose  of  a  carrier  or  a  case  to  the  nose  of 
an  uninfected  person,  and  is  favoured  by  overcrowding  and  bad  ventilation. 
The  lack  of  power  to  produce  the  necessary  immunity  is  favoured  by  poor  and 
insufficient  food,  bad  hygienic  conditions,  and  over-exertion. 

4.  In  susceptible  persons  the  germ  passes  into  the  mucous  membrane  of 
the  nose  and  of  its  connected  cells,  and  multiplies  therein,  and  then  entering 
the  blood-stream  forms  in  the  early  days  of  the  disease  a  bacteriaemia. 
Normally,  however,  it  does  not  long  remain  in  the  blood-stream,  and  therefore 
normally  does  not  produce  a  prolonged  septicaemia,  which,  when  present,  should 
be  considered  as  a  complication.  Apparently  the  organism  is  strongly 
attracted  to  the  cerebro-spinal  fluid,  into  which  it  quickly  passes  via  the 
choroid  plexus  of  the  lateral  ventricle,  and  perhaps  other  vascular  structures 
of  the  brain  and  spinal  cord,  and  so  causes  the  disease. 

The  reason  why  the  cocci  as  a  rule  do  not  pass  in  relays  day  after  day  from 
the  mucous  membrane  of  the  nose  into  the  blood  is  because  the  patient  is 
either  dead  or  the  resistance  is  raised  in  a  short  time,  but  if  this  resistance 
again  becomes  lowered  it  is  possible  that  relays  may  again  pass  from  the  nose, 
and  in  this  way  a  relapse  or  recurrent  attack  ensues. 

5.  There  are  various  strains  of  Neisseria  intracellularis ,  and  to  be  successful 
in  treatment  a  polyvalent  serum  and  a  polyvalent  vaccine  made  from  local  strains 
are  necessary.  Vaccine  alone  will  cure  many  cases,  but  requires  time  to  act, 
which  may  not  be  available,  and  hence  the  value  of  the  serum  in  such  cases, 
especially  when  followed  by  subsequent  vaccine  therapy. 

6.  Prophylaxis  depends  upon: — ■ 

(a)  The  search  for,  isolation  of,  and  treatment  of  cases  and  carriers,  and  here 
vaccine  therapy  is  of  use  in  helping  to  cleanse  cases  and  carriers. 

(b)  The  increase  of  the  immunity  of  the  general  population,  which  can  prob- 
ably be  done  by  prophylactic  vaccination  in  doses  of  5,  50,  and  100  millions, 
but  further  experience  is  required  of  this  when  given  on  a  large  scale.  There 
is  little  doubt  that  a  negative  phase  is  produced,  at  all  events  at  times,  in  the 
first  stages  of  this  vaccination,  and  this  may  possibly  be  aggravated  by  fear, 
poor  or  insufficient  food,  and  bad  hygiene.  It  also  appeared  to  them  that  vaccine 
prophylaxis  ought  to  be  tried  on  a  large  scale,  as  it  causes  no  general  or  local 
symptoms  if  the  germs  are  killed  at  500  C,  and  the  vaccine  is  aseptic  and 
isotonic  with  the  fluids  of  the  body,  and  if  the  site  of  injection  is  the  subcutane- 
ous tissue  just  below  the  angle  of  the  scapula,  which  in  their  opinion  is  the  best 
place  for  prophylactic  and  other  subcutaneous  injections. 

7.  There  are  a  great  many  questions  with  regard  to  epidemic  cerebro-spinal 
meningitis  which  are  at  present  unsolved,  and  one  of  the  most  important 
appears  to  be  the  question  as  to  whether  any  animal  or  animals  act  as  hosts 
of  the  germ. 

In  1917  the  Medical  Research  Committee  of  the  National  Health  Insurance 
issued  a  report  on  bacteriological  studies,  and  in  191 8  upon  serum  treatment 
in  connection  with  the  disease. 

^Etiology. — The  causal  agent  in  the  large  proportion  of  cases  is  Neisseria 
in  true  el  I  atari.--  (common  name:  meningococcus)  or  one  of  its  immediate  allies. 


ETIOLOGY— SYMPTOMATOLOGY  1483 

It  lives  in  the  naso-pharynx  of  healthy  people  whose  opsonic  index  for  the 
germ  is  abnormally  high,  and  it  passes  from  these  carriers  to  healthy  people, 
who  may,  according  to  their  resistance,  become  carriers,  temporary  or  per- 
manent, of  the  germ,  or  victims  to  the  disease. 
Its  aetiological  relationship  depends  upon: — 

1 .  Its  presence  in  all  cases  of  the  true  epidemic  disease. 

2.  Its  pure  culture  from  these  cases,  and  the  reproduction  of  the  disease  in 
monkeys  by  inoculation  of  cultures. 

3.  The  sera  of  persons  suffering  from  the  disease  can  agglutinate  and  give 
positive  complement-fixation  with  meningococci  obtained  from  other  patients. 

4.  It  produces  a  protective  mechanism  in  carriers  which  is  lacking  in  sus- 
ceptible persons. 

Pathology. — The  meningococcus  appears  to  enter  the  blood  via  the  mucosa 
of  the  nose  and  air  sinuses,  but  it  quickly  leaves  this  fluid  and  enters  the 
cerebro-spinal  fluid  via  the  choroid  plexuses,  and  perhaps  by  other  routes. 
Arrived  in  the  cerebro-spinal  fluid,  it  causes  a  cerebro-spinal  meningitis. 

Morbid  Anatomy. — In  fulminating  infections  meningitis  is  absent,  ard  little 
is  to  be  seen  beyond  haemorrhages  in  various  parts;  while  the  cerebral  vessels 
are  intensely  congested  and  the  perivascular  subarachnoid  spaces  show 
scattered  patches  of  pus. 

In  ordinary  fatal  cases  there  is  considerable  amount  of  purulent  exudate 
in  the  subarachnoid,  the  most  intense  being  over  the  uppermost  part  of  the 
vertex. 

In  chronic  cases  there  may  be  but  little  sign  of  pus  and  no  vascular  conges- 
tion, but  the  ventricles  are  distended  by  a  quantity  of  fluid,  the  pressure  of 
which  causes  flattening  of  the  convolutions. 

Symptomatology — General  Remarks. — As  seen  in  the  tropics  the  disease  is 
of  sudden  onset,  with  or  without  a  rigor,  but  with  marked  headache, 
vomiting,  and  fever.  The  next  day  there  is  often  some  remission  in  the 
symptoms,  but  with  stiffness  in  the  muscles  of  the  neck  and  sometimes 
Kernig's  sign.  On  the  third  daj'  vomiting  returns,  with  headache  and  a 
condition  of  resistant  stupor,  retraction  of  the  head  and  Kernig's  sign,  and 
from  this  time  onwards  the  symptoms  in  fatal  cases  go  from  bad  to  worse,  and 
the  patient  dies  within  four  to  six  days  of  the  commencement  of  the  attack. 
If  the  case  is  to  recover,  the  symptoms  begin  to  abate  about  the  seventh  to 
eighth  day,  the  temperature  falls  to  normal,  and  convalescence  begins. 

Slightly  fuller  details  of  this  usual  type  may  be  given. 

Incubation  Period. — Judging  by  persons  who  have  left  an  uninfected  area, 
visited  an  infected  anel  returned  to  the  uninfected  area,  the  incubation  period 
is  short,  varying  from  two  to  five  clays,  and  more  usually  about  four  days; 
but  there  are  obvious  fallacies  in  this  calculation,  and  it  may  perhaps  be  better 
to  admit  that  the  length  of  time  of  the  incubation  period  is  only  approximately 
known. 

Attack. — -The  onset  is  sudden  and  may  begin  with  a  rigor  in  an  adult  or 
convulsions  in  a  child,  but  these  may  be  absent.  The  patient  feels  very  ill 
and  exhibits  three  so-called  cardinal  symptoms — viz.,  fever  rising  to  1020  to 
1040  F.,  vomiting,  marked  headache,  which  may  be  associated  with  severe 
giddiness.  As  the  first  day  progresses  there  may  be  pain  anel  stiffness  in  the 
neck  and  some  retraction  of  the  head.  If  the  blood  be  examined  at  this  early 
stage  of  the  disease,  only  a  moderate  amount  of  leucocytosis,  amounting  to 
about  [0,000  cells  per  cubic  millimetre,  will  be  found,  while  the  differentia] 
count  will  show  an  enormous  preponderance  of  polymorphonuclear  leucoi  vies, 
amounting  to  over  90  per  cent,  in  some  cases. 

Blood  cultures  are  usually  very  successful  at  this  early  stage  of  the  disease, 
but  not  later  in  uncomplicated  cases.  By  direct  examination  of  blood  films 
Gram-negative  diplococci  can  be'  seen  in  about  1  per  cent,  of  the  polymorpho- 
nuclear leucocytes  examined,  while  a  very  few  similar  organisms  may  be 
found  outside  the  cells.  Even  at  this  early  stage  of  the  disease  the  cerebro- 
spinal fluid  is  usually  more  or  less  turbid,  and  shows  a  variable  number  of 
white  cells,  which  may  amount  to  20,000-30,000  per  cubic  millimetre,  and  of 
which  some  98  per  cent,  are  polymorphonuclear  leucocytes,  while  the  remain- 


1484  COSMOPOLITAN  FEVERS 

ing  2  per  cent,  are  generally  mononuclears.  As  the  day  goes  on  there  may  be 
pains  in  the  limbs  and  some  slight  catarrhal  symptoms  in  the  nose  and  throat. 
Slight  Remission. — On  the  second  day  there  is  often,  but  not  always,  a 
slight  remission  of  the  symptoms,  which  may  be  assigned  to  the  treatment, 
but  which  is  really  part  of  the  disease. 

k>  Course. — On  the  third  day,  if  there  has  been  some  slight  remission  the 
symptoms  all  return,  as  violent  as  before,  the  temperature  continues  to  be 
high,  but  the  pulse  varies — it  may  be  quick  or  it  may  be  slow — the  respirations 
are  irregular,  vomiting  returns,  and  there  is  an  intolerance  of  light  and  noise, 
while  the  stiffness  of  the  neck,  the  retraction  of  the  head,  and  Kernig's  sign, 
become  well  marked,  and  headache,  insomnia,  restlessness,  and  delirium 
may  be  present,  or  the  patient  may  be  huddled  up  in  a  state  of  resistant  stupor, 
from  which  he  can  be  temporarily  roused. 

This  is  about  the  time  at  which  a  rash  should  appear,  but  this  must  be 
extremely  rare  in  the  tropics,  as  we  have  never  yet  met  with  it  in  this  ordinary 
acute  type  of  the  illness.  Flushing  may  be  present  and  herpes  of  the  lips 
may  develop,  but  the  petechial  rash  is  extremely  rare.  The  leucocytosis  is 
now  more  marked. 

Terminattions. — During  the  fourth  and  fifth  days  death  is  not  uncommon, 
but  the  symptoms  may  persist  and  death  occur  later  on,  somewhere  ahout 
the  sixth  to  eighth  day  or  later;  the  temperature  may  decline,  the  symptoms 
abate,  and  the  patient  become  convalescent. 

Varieties. — Such  is  the  common  course  of  the  disease,  but  there  are  other 
types — e.g.,  the  fulminating  type,  spotted  fever  type,  chronic  type,  abortive 
type,  infantile  type. 

The  Fulminating  or  Septicemic  Type  is  associated  with  a  sudden  attack, 
rapid  development  of  coma,  and  death  in  a  few  hours.  It  is  often  associated 
with  a  purpuric  rash,  with  petechial  or  large  haemorrhages.  The  cerebro- 
spinal fluid  may  be  quite  clear  when  first  examined,  but  it  contains  a  number 
of  meningococci,  and  in  a  few  hours  has  a  typical  appearance  and  shows  poly- 
morphonuclear leucocytes. 

Usually  by  the  time  death  has  taken  place  there  is  sufficient  evidence  of  pus 
at  the  vertex  of  the  brain  to  support  the  diagnosis,  even  without  microscopical 
examination.  There  are,  however,  cases  which  die  before  this  pus  is  formed, 
and  then  the  brain  and  meninges  are  congested,  but  the  pia  mater  at  the  base 
shows  patches  of  cloudiness  due  to  pus  cells. 

Spitted  Fever  Type. — Somewhere  between  the  first  and  the  fifth  day 
generalized  petechial  eruption  may  appear,  which  is  most  marked  on  the  inner 
side  of  the  knee,  but  it  may  also  be  found  wherever  there  is  pressure — e.g., 
the  great  trochanter,  the  points  of  the  shoulder,  etc.  It  is  a  sign  of  severe 
toxaemia,  and  when  exaggerated  becomes  the  purpuric  rash.  Other  rashes 
are: — A  macular  rash  appears  at  times  after  the  second  day.  It  comes  oiit 
in  one  crop,  and  is  seen  on  the  lower  part  of  the  abdomen  and  the  thighs,  but 
may  occur  on  the  forearms,  legs,  hands,  or  feet. 

A  fugitive  erythema  or  blush  has  already  been  mentioned. 
Chronic  Type. — The  acute  symptoms  of  an  attack  pass  away,  the  tempera- 
ture may  become  normal,  but  the  patient  does  not  improve,  and  fever  of  an 
irregular  type  may  or  may  not  return,  while  opisthotonus  may  occur,  wasting 
set  in,  and  the  patient  slowly  die  of  exhaustion,  the  amount  of  cerebro-spinal 
fluid  obtained  by  puncture  becoming  less  and  less  and  thicker  and  thicker 
as  time  passes  on. 

Abortive  Type. — These  are  cases  which,  though  beginning  with  the  ordinary 
symptoms,  undergo  the  remission  on  the  second  day,  are  much  better  on  the 
third  day,  and  convalescent  on  the  fourth  day  or  thereabouts. 

Infantile  Type. — This  is  the  so-called  cervical  opisthotonus  of  infants,  a 
symptom  which  is  en  evidence  by  the  fourth  day,  while  as  a  rule  there  is  little 
or  no  fever,  but  considerable  and  progressive  wasting  and  marked  vomiting. 
It  is  chronic  and  has  a  high  mortality,  death  commonly  ensuing  in  four  to 
six  weeks  after  the  onset. 

Mimicry. — At  times  the  disease  imitates  enteric  fever,  broncho-pneumonia, 
gastro-enteritis,  or  rheumatic  fever. 


DIAGNOSIS— PROPHYLAXIS  1485 

Relapses. — These  are  not  uncommon,  and  are  usually  mild  in  type. 

Sequels. — There  is  usually  some  permanent  damage  to  the  nervous  system 
in  cases  which  recover. 

Diagnosis. — The  cardinal  early  signs  are: — (1)  The  sudden  onset;  (2)  the 
headache  and  sense  of  general  illness;  (3)  the  vomiting;  (4)  the  fever;  (5)  stiff- 
ness in  the  neck  muscles;  (6)  the  presence  of  the  meningococcus  in  the  cerebro- 
spinal fluid  as  obtained  by  lumbar  puncture. 

The  Differential  Diagnosis  has  to  be  made  from  malaria,  relapsing  fever, 
typhus,  enteric,  influenza,  and  pneumonia. 

From  malaria  it  can  be  recognized  by  the  absence  of  the  leucopenia,  the 
presence  of  the  leucocytosis,  and  the  absence  of  malarial  parasites  from  the 
blood,  as  well  as  the  absence  of  a  large  spleen.  It  may,  however,  occur  in  a 
malarial  subject,  but  the  leucocytosis  will  be  present. 

From  relapsing  fever  it  can  be  separated  in  the  early  stages  by  a  blood  ex- 
amination revealing  the  absence  of  spirochetes. 

From  typhus  it  can  be  distinguished  by  the  vomiting,  by  the  stiffness  in 
the  neck,  and  Kernig's  sign. 

From  enteric  it  may  be  diagnosed  by  the  headache  and  delirium  occurring 
together,  by  the  rigidity  of  the  neck,  Kernig's  sign,  and  lumbar  puncture. 

From  influenza  it  may  be  differentiated  by  Kernig's  sign  and  by  lumbar 
puncture,  which  may  relieve  some  of  the  symptoms  of  a  cerebral  influenza. 

From  pneumonia  by  the  irregular  pulse-rate,  the  presence  of  Kernig's  sigr, 
and  the  absence  of  those  of  consolidation  of  the  lungs. 

Prognosis. — This  is  always  serious — firstly,  quoad  vilam ;  secondly,  with 
regard  to  after-effects. 

Treatment. — Systematic  daily  lumbar  puncture,  with  the  withdrawal  of  a 
few  cubic  centimetres  of  cerebro-spinal  fluid  and  the  intrathecal  injection  of 
anti-meningococcal  serum,  in  quantity  to  be  judged  by  the  amount  of  cerebro- 
spinal fluid  withdrawn  at  the  time  and  by  the  blood -pressure  and  pulst-ratc. 

In  cases  where  the  pus  is  very  thick  an  attempt  to  wa^h  the  spinal  canal  by 
intrathecal  injections  of  warm  sterile  saline,  followed  by  serum  injections,  may 
be  tried. 

In  chronic  cases  or  relapses  vaccine  therapy  may  be  attempted. 

Symptomatic  treatment  and  careful  nursing  are  also  required. 

Prophylaxis. — The  proper  method  in  prophylaxis  is  to  avoid  overcrowdir  g, 
bad  hygiene,  and  to  provide  ample  space,  good  ventilation,  and  ample  and 
good  food  for  a  community.  When  an  attack  has  begun  the  sick  and  their 
attendants  should  be  isolated,  or  the  attendants  should  be  constantly  examined 
bacteriologically  and  have  systematic  nasc-pharyngeal  disinfection. 

Contacts  should  beisolated  and  examined  bacteriologically  on  three  separate 
occasions,  and  have  the  naso-pharynx  disinfected. 

A  search  for  carriers  should  be  made  in  the  immediate  neighbourhood  of  the 
patient,  and  these  carriers  should  be  isolated  and  treated. 

The  nose  and  fauces  should  be  sprayed  with  a  solution  of  1  per  cent,  iodine, 
2  per  cent,  menthol  in  parolin,  or  if  this  is  too  expensive  with  £  per  cent. 
watery  solution  of  formalin,  which  may  be  sniffed  into  the  nose  if  an  instru- 
ment is  too  expensive.  This  solution  of  formalin  is  especially  useful  for 
natives;  it  is  rather  too  strong  for  Europeans. 

If  this  fails  and  the  carriers  be  isolated  and  placed  under  improved  sanitary 
and  dietetic  conditions,  vaccine  treatment  is  beneficial,  and  may  succeed  when 
under  other  conditions  the  natural  vaccination  of  contained  organisms  will 
fail.  General  vaccination  of  the  population  may  be  tried,  but  it  is  r.ot  certain 
as  yet  whether  it  will  be  successful  or  not,  as  the  application  so  far  has  been 
limited. 

THE  EXANTHEMATA. 

Scarlet  fever  has  often  been  introduced  into  the  tropics.  but  it  docs  11  t 
spread.  Thus  we  have  seen  cases  introduced  into  Colombo  from  the  steamers, 
bat  there  has  never  been  an  epidemic  of  scarlet  fever  in  that  town  to  our 


i486  COSMOPOLITAN  FEVERS 

knowledge,  nor  have  we  seen  an  indigenous  case.  The  tropical  practitioner 
should  be  careful  not  to  mistake  for  true  scarlet  fever,  cases  of  scarlet  fever- 
like eruptions  such  as  erythema  scar latini forme. 

Measles  is  endemic  in  most  tropical  countries,  but  differs  in  no  important 
details  as  a  rule  from  the  same  disease  in  the  Temperate  Zone,  except  that 
when  first  introduced  into  Fiji  it  gave  rise  to  a  severe  epidemic,  and  is  still 
severe  in  Oceania. 


Fig.  678.- — Chicken-Pox:  Fifth  Day  of  the  Eruption. 

Chicken-pox  in  the  tropics  is  very  often  a  disease  of  the  adult,  btirg  nxst 
common  in  India  in  February  to  March.  The  majority  of  the  cases  are  mild, 
but  some  are  severe,  and  there  may  be  great  difficulty  in  diagnosing  chicken- 
pox  from  smallpox.  Varicella  cannot  be  transmitted  to  man  very  readily  by 
inoculation.  Rabbits'  cornea  can  be  inoculated,  and  fine  granulations  nave 
been  described  by  several  observers  in  the  epithelial  cells,  which  may  be  early 
stages  of  a  cytoryctes  arrested  in  its  development,  which  would  support  the 
people  who  believe  the  two  diseases  to  be  closely  allied. 


VARIOLA. 

Synonyms. — Smallpox.  French,  La  petite  verole;  Italian,  Vajuolo;  German, 
Blattcrn;  Spanish,  Viruelas;  Arabic,  Jadari. 

Definition. — Variola  is  an  acute  specific  fever  of  unknown  causation  spread 
by  various  agencies,  but  especially  by  air,  and  characterized  by  a  more  or 
less  general  eruption  passing  through  the  stages  of  papule,  vesicle,  pustule, 
crust,  and  often  scar. 

History. — There  can  be  no  doubt  of  the  great  antiquity  of  the  occurrence 
of  smallpox  in  Inelia  and  Africa,  but  whether  it  arose  de  novo  in  these  two 
centres  we  cannot  say,  but  there  is  a  suspicion  that  there  are  two  varieties  of 
the  disease — viz.,  the  ordinary  smallpox,  which  may  have  had  its  origin  in 
India  and  spread  to  Europe,  and  so  to  America,  and  later  to  the  islands  of 
Oceania;  and  an  African  variety  variously  known  as  South  African  Amaas, 
or  milk-pox,  which  may  have  been  imported  by  the  negro  slaves  into  the  West 
Indus,  where  it  is  called  West  Indian  modified  smallpox.  Apart,  however, 
from  conjectures  of  this  nature,  there  are  the  facts  that  in  India  there  was  a 
special  worship  defined  in  the  Atharvaveda,  and  there  were  special  prayers 
to  be  said  by  the  Brahmins  when  performing  the  operation  of  inoculation 
of  smallpox  virus.  References  in  the  Charaka-Sarhhita.  and  the  Susruta- 
Sa-hhita  make  it  almost  certain  that  the  disease  was  well  known  when  they 


CLIMATOLOGY— SYMPTOMATOLOGY  1487 

were  written.     It  would  appear  that  the  disease  was  introduced  into  China 
perhaps  from  India,  in  the  course  of  the  third  century  B.C. 

Equally  ancient  is  the  evidence  of  the  existence  of  smallpox  in  Africa,  for 
Riitfer  and  Ferguson  have  found  an  eruption  on  the  skin  of  a  mummy  belong- 
ing to  the  period  of  the  twenty-eighth  dynasty  (1200-1100  B.C.),  which  they 
believe  to  be  suggestive  of  smallpox,  and  it  is  quite  possible  that  there  has 
existed  from  time  immemorable  an  endemic  focus  in  Africa,  perhaps  in  Central 
Africa. 

From  these  two  foci  in  Asia  and  Africa  it  would  appear  probable  that  the 
disease  has  spread  all  over  the  woild.  With  its  introduction  and  spread  in 
Europe  we  are  not  concerned,  but  with  that  into  America  a  few  remarks  must 
be  made,  as  it  is  very  interesting.  It  would  appear  not  to  have  been  known  in 
America  until  after  the  advent  of  the  Spaniards ;  it  is  first  recorded  as  occurring 
in  the  West  Indies  in  the  year  1507,  when  it  was  introduced  from  Europe, 
as  has  happened  on  many  occasions  since — e.g.,  into  Chili  in  1554 — also  by 
the  agency  of  the  Spaniards. 

More  interesting  than  this  is  the  fact  that  it  is  recorded  that  importations 
of  slaves  from  Africa  were  often  followed  by  the  appearance  of  the  disease — 1 
as,  for  example,  in  Brazil,  where,  according  to  Piso.it  appeared  in  156c,  being 
introduced  in  this  manner. 

With  regard  to  Oceania,  it  has  been  introduced  from  Asia  or  America  at 
various  times- — as,  for  example,  Australia  in  1838,  from  China  to  Sydney;  the 
Hawaiian  Islands  in  1853,  from  San  Francisco  to  Honolulu;  while  New  Cala- 
donia  became  infected  in  1859,  and  Marquesas  in  1863. 

To-day  the  disease  is  widespread  all  over  the  world,  but  is  especially  common 
in  the  tropics,  where  institutes  for  the  preparation  of  calf-lymph  are  urgently 
required  in  order  that  efficient  vaccination,  the  only  method  of  keeping  the 
disease  in  check,  may  be  successfully  carried  out. 

Climatology. — It  is  believed  that  smallpox  is  perhaps  most  active  at  the 
present  time  in  Central  Africa,  but  if  this  is  true  certainly  some  portiors  of 
tropical  Asia  must  come  very  nearly  equal  in  endemicity ,  and  briefly  the  disease, 
though  world-wide  in  its  distribution,  is  of  the  utmost  importance  in  the 
tropics.  When  first  introduced  among  peoples  previously  unaffected  with 
the  disease,  it  was  most  virulent — as,  for  example,  its  incidence  on  the  Mexi- 
cans and  the  North  American  Indians. 

/Etiology. — The  causation  is  unknown,  but  various  protozoal  bodies  have 
been  described,  of  which  the  most  important  is  Cytoryctes  variola  Guarnieri, 
[892,  minute  spherical  homogeneous  bodies  3  to  4  fi  in  diameter,  and  staining 
well  with  Romano wsky,  when  it  takes  on  a  chromatin  coloration,  while 
Councilman   and    his   colleagues   have  described   a   complicated   life-history 

(P-535)- 

Whatever  the  virus  may  be,  it  is  usually  spread  by  the  air,  and  enters  the 
body  by  mcansof  the  respiratory  passages.  Cases  areon  record  of  the  infection 
being  probably  carried  by  cotton  from  Egypt  to  England,  and  there  starting 
sporadic  outbreaks,  and  this  is  possible  if  the  cotton  was  handled  by  an  in- 
fected-person. Hence  the  request  lor  the  vaccination  and  revaccination  of 
cot  ton -workers. 

Symptomatology. — This  is  described  in  all  books  on  general  medicine,  and 
need  he  onlv  very  briefly  repeated  here. 

Briefly,  a  typical  attack  of  discrete  smallpox,  after  an  incubation  of  nine 
to  fifteen  days,  begins  with  a  chill  in  an  adult  and  a  convulsion  in  a  child, 
and  continues  with  high  fever,  severe  headache,  lumbar  pains,  and  vomiting, 
with  or  without  a  scarlatiniform  or  morbilliform  rash  on  the  second  day,  which 
may  be  general  or  local;  or  hemorrhagic  rashes,  which  are  cither  petechial  or 
petechio-erythematous,  which  appear  from  the  fust  to  the  third  day.  If  tin  se 
latter  rashes  are  associated  with  haemorrhages  from  the  internal  organs,  they 
indicate  the  onset  of  hemorrhagic  smallpox.  Generally  the  initial  st;  ge  of 
the  disease  lasts  two  clays,  but  it  may  be  shorter  and  milder  than  that  recorded 
above,  or  more  severe.  The  peculiar  odour  of  a  smallpox  case  may  be  noted 
in  these  early  stages. 

The  typical  rash  appears  on  the  second,  third,  or  fourth  day  as  papules  on 


1488 


COSMOPOLITAN  FEVERS 


the  face,  arms,  back  of  the  wrists  and  hands,  and,  later,  on  the  trunk  and 
limbs ;  and  at  the  same  time  on  the  mucosa  of  the  mouth,  nose,  and  throat,  and 
more  rarely  on  the  vulva,  vagina,  and  rectum.  Generally  it  is  more  marked  on 
the  extensor  surfaces  of  the  limbs  than  on  the  flexor  surfaces,  and  is  often  most 
marked  in  areas  where  there  has  been  pressure.  The  papules  are  bright  red 
in  colour,  but  this  may  not  be  very  evident  in  the  dark  skin,  2  to  3  millimetres 
in  diameter,  and  have  a  hard,  shotty  feeling.  As  the  rash  comes  out  the 
temperature  falls,  and  the  initial  symptoms  improve.  "  On  the  fifth  to  sixth 
day  the  papules  become  umbilicated  vesicles,  which  turn  into  pustules  when 
the  umbilication  disappears,  and  a  surrounding  areola  of  injection  appears. 
During  the  maturation  of  the  pustules  the  secondary  fever  appears,  and  the 
eyelids  become  swollen  and  closed.  In  the  discrete  form  the  fever  disappears 
by  the  tenth  to  eleventh  day,  and  convalescence  sets  in. 

The  confluent  type  of  smallpox  is  more  severe  than  in  the  above,  and  presents 
much  less  difficulty  in  its  recognition,  and  need  not  be  described. 

Varieties. — There  are,  however,  two  varieties  which  are  of  importance  in 
the  tropics — viz.,  variola  haemorrhagica  and  varioloid — and  these  must  be 
mentioned  at  greater  length. 


Fig.  679. — SMALLrox. 
(From  a  photograph  by  Balfour.) 


Variola  Hemorrhagica. — Hemorrhagic  smallpox  is,  or  was,  by  no  means 
rare  in  Africa,  and  is  met  with  in  Asia,  though  by  no  means  so  frequently. 

There  are  two  varieties:  Purpura  variolosa  and  Variola  hcevorrhagica 
pustulosa. 

Purpura  Variolosa. — This  variety  commences  with  the  same  symptoms  as 
ordinary  smallpox,  but  they  are  much  more  severe.  The  fever  is  not  con- 
siderable, and  may  be  below  ioo°  F.,  but  the  pains  in  the  body,  especially  the 
backache,  is  very  severe,  and  the  vomiting  may  be  very  persistent  and  asso- 
ciated with  severe  epigastric  pain.  The  pulse  and  the  respirations  are  both 
much  increased  in  frequency.  At  the  end  of  the  second  or  the  beginning  of 
the  third  day  an  erythematous  rash  appears  in  some  part  of  the  body,  very 
often  in  the  groins  and  flexure  of  the  joints,  but  it  may  be  absent,  or  it  may 
extend  and  become  general.  At  the  same  time  and  in  the  same  places  appear 
red  and  purple  petechiae,  and  about  the  same  time  subconjunctival  ha morrhages 
in  one  or  both  eyes,  while  purple  spots  appear  on  the  forehead,  eyelids,  and 
face,  and  ecchymotic  areas  in  various  parts  of  the  skin,  and  also  on  the  tongue 
and  pharynx.     The  patient  now  becomes  pale  and  anaemic,  except  where  the 


VARIETIES  1489 

blotches  are  situate,  and  bleeding  occurs  from  the  mucous  membranes  and 
internal  organs,  of  which  the  most  common  are  oozing  from  the  gums  and 
hematuria,  but  epistaxis,  haematemesis,  haemoptysis,  melaena,  and  metror- 
rhagia, may  one  or  all  be  present.     Even  retinal  haemorrhages  may  occur. 

The  temperature  is  now  below  normal,  the  patient  is  restless,  with  often 
a  sensation  of  weight  in  the  praccordiurn.  The  pulse  is  now  soft  and  com- 
pressible. Sordes  iorm  on  the  gums,  and  the  patient  dies  on  the  third  to 
sixth  day,  with  a  clear  mind  and  often  without  any  sign  of  the  typical  smallpox 
eruption. 

Purpura  variolosa  fulminans. — Very  rarely  the  disease  is  more  severe,  with 
a  temperature  ol  105  F.  or  more,  associated  with  delirium,  coma,  and  collapse, 
and  followed  by  death  in  a  few  hours  without  any  signs  of  external  haemorrhage. 
Variola  hemorrhagica  pustulosa. — In  this  variety  the  initial  symptoms  are 
severe,  and  delirium  sets  in  early.  Haemorrhages  appear  from  and  under 
the  mucous  membranes  and  under  the  skin,  and  at  the  same  time  the  typical 
smallpox  eruption  appears,  into  which  blood  also  passes.  The  symptoms 
resemble  those  of  confluent  smallpox,  with  the  addition  of  haemorrhages. 

A  milder  form  is  when  the  haemorrhage  occurs  only  into  the  eruption,  and 
may  or  may  not  be  associated  with  haematuria  and  some  bleeding  from  the 
mouth. 

Varioloid. — -Repeated  vaccination  is  an  excellent  protective  against  small- 
pox, but  il  the  disease  does  appear  in  a  person  who  has  been  several  times 
vaccinated,  it  is  remarkably  modified  and  is  most  difficult  to  recognize. 
Epidemics  have  been  known  to  show  such  a  mild  type  that  the  disease  was 
mistaken  for  a  length  of  time  for  chicken-pox,  and  have  also  been  considered 
to  be  due  to  a  new  form  of  disease,  to  which  such  names  as  '  Cuban  itch  '  and 
'  Philippine  itch  '  have  been  given.  Indeed,  such  epidemics  have  in  some 
cases  not  been  recognized  until  a  fatal  case  has  occurred  ;  and  Osier  and  McCrae 
have  recorded  a  small  outbreak  in  one  of  their  wards  for  coloured  patients  in 
which  the  disease  was  at  first  mistaken  for  chicken-pox. 

The  varieties  of '  Varioloid  '  are  numerous.  In  the  first  place,  there  may  be 
no  eruption,  and  the  usual  initial  symptoms  may  be  slight,  or  they  may  be 
severe  and  accompanied  by  an  erythema,  but  all  symptoms  disappear  by 
the  third  or  fourth  day. 

In  other  cases  the  disease  begins  with  the  usual  symptoms,  but  at  the  end 
of  the  first  day  a  few  maculae  appear,  which  become  vesicles  in  another  twenty- 
four  hours,  when  the  constitutional  symptoms  begin  to  abate,  and  are  full 
grown  in  about  three  to  four  days,  when  they  are  seen  to  be  conical  vesicles, 
often  without  any  depression,  surrounded  by  a  very  faint  red  line.  On  the 
third  to  fourth  day  they  become  somewhat  opaque,  and  then  shrink  and 
desiccate,  forming  small  dry  prominences  on  the  skin,  which  finally  desqua- 
mate, and  the  patient  is  convalescent.  Inother  cases  a  few  vesicles  may  become 
pustules  by  the  sixth  day  of  the  eruption,  which  dry  up  and  cast  off  their 
crusts  in  about  a  week. 

Diagnosis. — -The  headache,  the  severe  backache,  the  epigastric  pain,  the 
vomiting,  the  high  temperature,  and  the  rapid  pulse,  associated  with  an 
erythematous  or  petechial  eruption  on  the  abdomino-crural  region,  are 
important  factors.  The  erythema,  however,  is  apt  to  be  irregularly  dis- 
tributed in  blotches,  but  it  does  not  affect  the  face.  The  petechial  eruption  is 
usually  found  about  the  flexures  of  the  joints  as  small  bright  red  petechias. 
Any  acute  iebrile  disorder  associated  with  purpura  should  be  suspected  as 
being  probably  variola. 

flu  typi<  al  eruption  comes  out  on  the  second  or  third  day  of  the  illness  as 
hard  snotty  papules  on  the  forehead,  face,  arms,  and  legs,  which  have  become 
papulo-vesicles  and  pustular,  presenting  umbilication,  and  not  flattening  on 
pricking. 

From  Varicella. — The  first  point  in  the  differential  diagnosis  between 
smallpox  ami  chicken-pox  is  to  remember  that  it  is  very  difficult,  and  that  the 
most  distinguished  physicians  have  owned  to  not  one  mistake,  but  a  series. 
No  one  point  of  absolute  diagnostic  value  can  be  given,  but  the  following 
table  will  indicate  some  of  the  points: — 

94 


i4go 


COSMOPOLITA  N  FE VERS 


Sigyi  or  Symptom. 


Chicken-pox. 


Smallpox. 


Initial  symptoms 
Temperature 
Situation  of  rash 
Vesicles 


Absent  as  a  rule,  but  may 
resemble  smallpox. 

Does  not  fall  with  the 
appearance  of  the  rash. 

Most  marked  on  the 
trunk. 

Develop  in  twelve  to 
twenty-four  hours;  are 
rarely  umbilicated ;  col- 
lapse on  pricking;  all 
stages,papules, vesicles, 
and  flattened  scabbing, 
puckered  pocks,  appear 
together. 


Usually  well  marked,  but 

may  be  absent. 
Falls  with  the  appearance 

of  the  rash. 
Most  marked  on  the  face 

and  limbs. 
Papules  hard  and  shotty; 

are  slow  in  developing; 

vesico-pustules  are  more 

commonly  umbilicated ; 

eruption  more  uniform, 

and  the  scabbing  margin 

is  not  puckered. 


From  Measles. — 'The  diagnosis  from  measles  may  be  made  as  follows: — 


Sign  or  Symptom. 


Measles. 


Smallpox. 


Catarrhal  symptoms 


Filatow  or   Koplik's 

spots 
Eruption 


Temperature 


Lachrymation,  coryza, 
cough  present  from  the 
beginning  and  marked . 

Usually  present. 

Appears  on  the  third  to 
fourth  day  as  minute 
pink  papules  behind 
the  ears,  on  the  fore- 
head, chin,  cheeks, 
neck,  limbs,  and  chest. 
Papules  not  hard  or 
shotty. 

Reaches  its  height  with 
the  appearance  of  the 
rash. 


Usually  absent,  but  there 
may  be  some  conjunc- 
tival effusion. 

Absent. 

Initial  measly  eruption  on 
the  first  or  second  day 
on  face,  trunk,  and 
limbs  simultaneously. 
If  partial,  appears  in 
the  abdomino  -  crural 
area.  Papules  hard  and 
shotty. 

Falls  with  the  appearance 
of  the  rash. 


From  Influenza,  etc. — In  German  measles  the  initial  severe  symptoms  are 
absent,  and  in  the  fourth  disease  the  face  is  free,  while  in  influenza  the  typical 
eruption  fails  to  appear. 

From  Typhus. — The  diagnostic  features  are: — 


Sign  or  Symptom. 

Typhus. 

Smallpox. 

Erythema 

Typical  eruption     .  . 

Appears  on  the  third  to 
fourth  day  of  the  illness. 

Petechial.  Appears  on  the 
fourth  or  fifth  day,  and 
is  rarely  seen  on  the 
face. 

Appears  on  the  first  or 
second  day  of  the  illness. 

Papulo-pustular.  Appears 
on  the  third  or  fourth 
day,  and  is  common  on 
the  face. 

ALASTRIM  1491 

From  Hemorrhagic  Diseases. — Any  case  of  high  fever  of  an  acute  nature 
associated  with  purpura  may  be  smallpox.  It  is  extremely  difficult  to  separate 
hemorrhagic  measles  and  scarlet  fever  from  hemorrhagic  smallpox,  but  in 
the  former  diseases  there  is  not  so  much  bleeding  from  the  mucous  membranes. 
The  isolation  for  sixteen  days  and  vaccination  of  all  contacts,  and  the  isolation 
of  the  sick  are  the  most  important. 

Prophylaxis. — As  smallpox  is  endemic  in  nearly  all  tropical  countries,  it  is 
important  that  the  natives  should  be  taught  concerning  it,  and  the  fact  that 
vaccination  is  an  excellent  prophylactic  measure,  and  this  should  be  done  by 
verbal  instruction  and  by  vernacular  pamphlets,  if  possible  illustrated;  in 
this  way  the  native  prejudices,  which  are  usually  not  strong,  must  be  overcome. 
Secondly,  vaccination  should  be  made  compulsory  by  law;  and,  thirdly,  a 
vaccine  service  should  be  established.  This  vaccine  service  should  consist 
of  an  institute  for  the  preparation  of  lymph,  with  a  reliable  man  to  make  the 
lymph,  an  inspector  of  vaccination,  or  more,  according  to  the  needs  of  the 
country,  and  a  series  of  native  vaccinators. 

ALASTRIM. 

Synonyms. — African,  Varioloid  varicella,  Amaas,  Kaffir  milk-pox ;  A  merican , 
West  Indian  modified  smallpox,  Epidemic  varioloid  varicella ;  perhaps  Pseudo- 
smallpox  (Kersten),  Sanaga  smallpox  (Plehn). 

Definition. — An  acute  specific  fever  resembling  in  all  its  symptoms  and 
pathological  appearances  a  mild  form  of  variola. 

History. — As  already  stated  in  the  history  of  smallpox,  there  is  a  possibility 
that  there  were  originally  two  distinct  endemic  foci  of  variola- — viz.,  Asia  and 
Africa — and  therelore,  bearing  in  mind  the  different  varieties  of  relapsing 
fever,  it  is  hardly  surprising  that  there  should  be  at  least  two  varieties  of 
smallpox,  even  though  the  clinical  symptoms  are  similar,  and  Guarnieri's 
bodies  are  found  in  both.  Moreover,  the  disease  is  known  in  Africa  and 
America,  and  there  is  no  reason  why  it  should  not  occur  also  in  Asia  when  the 
considerable  intercommunication  between  India,  Ceylon,  and  China,  with 
Africa,  is  considered.  One  of  the  earliest  descriptions  is  by  Anderson,  in 
1866,  of  an  epidemic  in  1865  in  Jamaica,  and  there  was  another  epidemic 
described  by  Dickson  and  Lasselle  in  1903,  while  Korte  gave  an  account  of 
amaas,  or  Kaffir  milk-pox,  in  1904.  In  1905  Welch  and  Schamberg  gave  an 
account  of  it  in  their  work  on  'Acute  Contagious  Diseases'  in  1908;  Scheult 
described  it  as  seen  in  Trinidad  from  1902  to  1904;  while  Grant,  in  1910, 
described  '  amaas'  as  seen  in  South  Africa;  and  in  the  same  year  Ribas 
describes  it  as  seen  in  Brazil  in  1909,  and  Carini  as  seen  in  the  States  of  St. 
Paul,  Minas,  and  Parana. 

Etiology.— The  causation  would  appear  to  be  the  same  as  that  of  ordinary 
smallpox,  as  it  is  generally  agreed  that  Jenner's  vaccination  is  protective,  and 
Guarnieri  bodies  have  been  found,  and  the  classical  reaction  in  the  inoculated 
cornea  of  the  rabbit  has  been  produced  ;  after  sixty  hours  the  Guarnieri  bodies 
have  been  recovered  from  the  cornea,  but  it  would  appear  to  be  due  to  an 
attenuated  virus. 

The  question  which  has  been  much  debated  is  whether  it  is  smallpox, 
chicken-pox,  or  a  new  disease  halfway  between  the  two.  In  the  first  place, 
there  are  still  some  persons  who  disbelieve  in  the  difference  between  variola 
and  varicella,  but  their  objection  is  usually  disregarded.  In  the  second  place, 
alastrim  differs  from  varicella  because  of — 

1 .  Confluence  of  the  vesicles  in  certain  cases, 

2.  Its  frequency  among  adults. 

3.  The  partial  protection  by  Jenner's  vaccine. 

It  differs  from  variola  vera  by — 

1.  Its  low  mortality  (1  to  2  per  cent.). 

2.  Because  it  is  less  severe  in  children  than  in  adults,  and  is  often  found 
among  babies,  in  whom  the  vesicles  are  often  small. 


1492 


COSMOPOLITAN  FEVERS 


3.  There  is  no  secondary  fever  in  children. 

4.  Though  Jenner's  vaccine  is  in  some  degree  protective,  the  disease  can 
occur  after  recent  successful  vaccination. 

5.  Jenner's  vaccination  can  be  successfully  carried  out  shortly  after  an 
attack  of  alastrim. 

6.  According  to  some  authorities,  an  attack  of  smallpox  does  give  a  lasting 
immunity  to  alastrim. 

Provisionally  we  may  conclude  that  it  is  probably  a  slightly  different  form 
of  disease  from  true  variola. 

Symptomatology. — It  begins  with  high  fever,  severe  pains,  and  vomiting, 
with  very  often  delirium.     The  rash  comes  out  on  the  third  day,  when  the 


Fig.  6 


Alastrim.     (After  Ribas. 


temperature  descends,  the  symptoms  disappear,  and  the  patient  feels  so  well 
that  he  may  resume  his  ordinary  avocations.  Secondary  fever  is  usually 
absent,  especially  in  children,  but  may  occur  about  the  eighth  day.  Papules 
become  pustules  and  scabs,  and  these  drop  off,  leaving  little  scarring,  but 
only  pigmentation. 

Complications. — Hemorrhagic  cases  are  unknown. 

Mortality. — The  death-rate  is  remarkably  low,  about  1  to  2  per  cent. 

Prophylaxis. — The  usual  isolation,  quarantine,  and  vaccination  of  contacts 
and  cases  must  be  adopted. 


VACCINATION  1493 


VACCINATION. 


Vaccination  from  arm  to  arm  is  very  dangerous  in  the  tropics,  as  syphilis, 
yaws,  relapsing  fever,  sleeping  sickness,  etc.,  may  be  inoculated.  It  should 
therefore  only  be  performed  when  calf-lymph  is  not  available,  and  only  by 
means  of  children  under  eight  years  of  age  who  are  found  to  be  healthy. 
These  vaccinifers  can  be  sent  to  suitable  districts  if  necessary;  and  if  the 
amount  of  lymph  required  is  considerable,  two  or  three  drops  of  glycerine  may 
be  placed  on  the  vesicles,  which  are  then  punctured  in  several  places,  and  the 
mixture  used  for  immediate  vaccination.  With  regard  to  the  systematic  work, 
lanolated  seed-lymph  can  be  obtained  from  many  institutes  at  present;  for 
example,  from  the  Lister  Institute  in  London. 

Preparation  of  Lymph. — The  vaccine  institute  requires  an  inoculating-room, 
a  preparation-room  for  the  lymph,  an  office,  a  store-room,  a  good  stable  for 
the  calves — all  of  which  should  be  rendered  flyproof ,  and  should  have  cement 
floors  and  be  as  cool  as  possible,  and  have  a  good  supply  of  water.  The  special 
apparatus  required  are  means  for  sterilization,  Dornig's  hand  roller  machine 
for  trituration,  and  Entrican's  machine,  fitted  with  a  small  Geryk  pump,  for 
filling  the  tubes,  as  well  as  the  ordinary  glass  and  other  materials  of  a  laboratory. 

The  lymph  should  be  obtained  as  lanolated  seed-lymph  from  a  reliable 
institute,  and  should  be  inoculated  into  fair-skinned  heifers,  not  into  black- 
skinned  heifers,  which  should  be  specially  fed  during  and  after  inoculation. 

When  tubes  of  calf-lymph  cannot  be  obtained,  monkeys  may  be  directly 
inoculated  from  cases  of  variola,  and  the  calves  may  then  be  subinoculated 
from  the  monkeys,  and  if  calves  cannot  be  obtained  rabbits  may  be  used. 

All  animals  should  be  carefully  isolated  anel  watched  for  a  week  before  being 
used  for  inoculation.  During  this  period  the  temperature  should  be  taken 
and  a  tuberculin  test  applied. 

When  lymph  first  arrives  in  a  tropical  country  from  the  temperate  zone  it 
requires  to  be  acclimatized — that  is  to  say,  its  virulence  should  be  increased 
by  passing  it  through  about  three  calves  before  use,  otherwise  failures  may 
occur. 

The  calves  are  vaccinated  on  the  shaved  abdomen,  which  has  been  washed 
with  soap  anel  sterile  water,  by  linear  incisions,  about  1  inch  apart,  into  which 
the  lymph  is  gently  and  immediately  rubbed,  and  a  sterile  cloth  tied  over 
the  vaccinaterl  area.  No  straw  should  be  given  for  bedding,  but  a  wooden 
grating  should  be  used,  and  the  calf's  head  should  be  secured  by  two  tie-ropes 
to  prevent  it  kicking  the  inoculateel  area. 

The  lymph  may  be  collected  after  96  to  120  hours  by  first  washing  the  area 
with  soap  and  water,  then  with  sterile  water  and  a  sterile  gauze  mop,  and  then 
removing  the  contents  of  the  liver  vesicles  by  means  of  a  Volkmann's  spoon. 

The  lymph  is  now  weighed  and  mixed  with  an  equal  weight  of  sterile 
distilled  water  or  glycerine,  and  after  being  worked  into  a  paste  is  triturated 
until  it  is  in  an  extremely  fine  condition,  and  if  urgently  required  is  treated 
with  a  stream  of  chloroform  vapour  for  fifteen  to  thirty  minutes,  after  which 
sterile  air  is  bubbled  through  until  no  chloroform  remains,  and  another  part 
of  sterile  water  and  2  parts  of  sterile  glycerine,  or  3  to  5  parts  of  anhydrous 
lanoline  are  added.  The  lymph  is  now  filtered  through  a  special  fine  sieve  into 
test-tubes  till  nearly  filled,  and  stored  in  cold  climates  for  four  to  five  weeks 
at  a  temperature  of  150  to  200  C,  when  the  number  of  micro-organisms  is 
found  to  have  decreased  considerably.  The  chloroform  method  of  purifying 
the  lymph  is  to  be  preferred  in  the  tropics,  as  it  is  much  quicker.  The  tech- 
nique is  found  in  any  modern  work  on  the  preparation  of  lymph. 

A  bacteriological  examination  is  always  necessary,  especially  to  discover 
whether  tetanus  bacilli  are  present,  and  if  these  are  found  the  lymph  must 
be  rejecteel.  The  lymph  must  be  stored  at  temperatures  at  50  to  io°  C;  if 
this  precaution  is  not  used  the  lymph  becomes  inert  very  quickly  in  tropical 
countries. 

The  capillary  tubes  are  filled  in  a  vacuum  in  the  Entrican  filling- machine, 
and  should  lie  tested  for  vaccine  activity  before  being  issued. 


1 494 


COSMOPOLITAN  FEVERS 


Lanolated  lymph,  not  being  sterile,  is  more  apt  to  contain  a  large  number 
of  micro-organisms.  Dried  lymph  has  been  placed  upon  the  market,  and 
is  now  on  trial  on  a  large  scale. 

In  vaccinating  natives  the  left  arm  should  be  used  about  the  middle,  and 
not  near  the  shoulder.  % 

Vaccinia. — The  only  modifications  in  vaccinia  between  the  Native  and  the 
European  is  the  difference  produced  by  the  colour  of  the  skin,  and  the  greater 
risk  of  septic  sequela?;  therefore  the  area  of  skin  should  be  carefullj-  cleared 
before  being  utilized  for  vaccination. 

The  slight  redness  and  swelling  due  to  the  scratches  disappear  in  twenty- 
four  hours,  while  the  papules  appear  on  the  third  to  fourth  day,  and  are 
succeeded  by  the  vesicles,  which  become  umbilicated  pustules  atout  the 
eighth  to  ninth  day.  These  quickly  begin  to  dry  in  the  centre  and  form 
a  scab,  which  falls  off  about  the  fourteenth  to  twenty-first  day  and  leaves 
a  scar. 

VACCINATION  RASHES. 

Generalized  Vaccinia. — This  eruption  is  rare,  but  has  been  reported  upon 
in  natives  by  Hill  and  Ross  in  Natal,  and  by  Chalmers  and  Archibald  in  the 
Anglo -Egyptian  Sudan.  It  appears  some  twelve  to  twenty-two  days  after 
vaccination,  associated  with  fever,  in  the  form  of  a  generalized  papular  rash, 
which  as  a  rule  comes  out  during  several  days.  The  papules  form  vesicles 
which  become  umbilicated,  and  then  the  case  resembles  closely  a  very  mild 
attack  of  varioloid.  The  vesicles  pass  on  to  pustules,  and  these  to  scabs, 
which  eventually  leave  small  depressed  scars. 


Fig.  68i. — Generalized  Vaccinia. 


In  a  typical  case  the  rash  appears  twelve  to  twenty-two  days  after  vaccina- 
tion, requires  some  six  days  to  reach  its  full  development,  and  another  eight 
days  to  decline  to  the  stage  when  the  scabs  are  thrown  off  and  the  patient 
is  convalescent. 

Localized  Gangrenous  Vaccinia. — Fortunately  this  is  a  very  rare  disease, 
but  has  been  met  in  the  tropics  by  Chalmers  and  Archibald.  It  occurs  in 
cases  in  which  no  reasonable  precaution  has  been  omitted  to  guard  against 
septicity  in  the  performance  of  the  vaccination,  and,  indeed,  there  may  be 


VACCINATION  RASHES  M95 

no  sign  of  septic  infection  in  the  disease,  of  which  the  following  is  a  typical 
case : — 

During  the  first  three  days  after  vaccination  there  was  nothing  to  report, 
but  on  the  third  day  the  area  became  red  and  swollen,  and  on  the  fourth  there 
was  a  number  of  small  vesicles. 

On  the  fifth,  although  there  was  only  slight  fever,  the  patient  felt  ill,  while 
some  of  the  vesicles  ruptured  and  discharged  their  contents. 

On  the  sixth  day  the  vaccination  area  was  covered  by  a  yellow  crust,  and 
surrounded  by  a  ring  of  vesicles  and  by  a  congested  dark  red  area  measuring 
about  i  inch  in  diameter.     The  temperature  on  this  day  did  not  exceed  102°  F. 

On  the  seventh  day  the  crusted  area  became  quite  black,  and  extended  until  it 
measured  some  2  inches  in  diameter.  It  was  surrounded  by  a  ring  of  umbilicated 
vesicles  and  by  a  dark  red  border  measuring  1  inch  in  width,  outside  of  which 
was  a  light  red  area  of  about  the  same  depth.  The  whole  region  felt  somewhat 
brawny  to  the  touch,  and  the  temperature  rose  to  between  104°  and  1050  F. 

On  the  eighth  day  the  condition  of  the  leg  may  be  described  as  follows: — 

In  the  centre  there  lay  a  black  slough  some  2  inches  in  diameter,  surrounded  by 
a  ring  of  collapsed  vesicles  and  by  a  raised  dark  red  border,  which,  in  its  turn, 
was  surrounded  by  a  purplish  area  of  skin  some  3  inches  in  width,  while,  finally, 
the  whole  area  was  defined  by  a  red  zone  of  about  an  inch  in  diameter.  On 
this  day  the  temperature  did  not  exceed  1030  F.,  and  the  patient  felt  better, 
though  the  leg  looked  worse. 

On  the  ninth  day  there  was  a  decided  improvement,  the  ring  of  vesicles  had 
dried  and  formed  a  circular  scab,  the  brawny  resistance  was  softer  and  was 
beginning  to  disappear  at  the  edges.  The  purple  hue  was  lighter  and  showed 
signs  of  becoming  reddish  in  places.  The  surrounding  red  area  had,  however, 
extended  down  to  the  ankle  and  up  to  the  knee.  The  temperature  did  not 
exceed  1020  F. 

From  this  date  onwards  the  signs  and  symptoms  began  to  steadily  improve. 
The  temperature  fell  slowly,  remaining  about  1010  F.  for  two  days,  about 
ioo°  F.  for  another  day,  and  then  reached  990  F.  The  purple  area  became 
reddish  and  the  reddish  area  white. 

At  this  stage  an  attack  of  acute  gout  set  in,  beginning  on  the  thirteenth  day, 
when  the  temperature,  which  had  never  reached  normal,  rose  to  ioo°  F.  The 
gouty  symptoms  were  marked  in  the  left  hip,  left  arm,  left  side  of  the  jaw, 
left  wrist,  the  back,  and  the  right  ribs.  These  symptoms  lasted  some  seven 
days,  but  gradually  gave  way  to  the  usual  remedies,  and  the  temperature 
slowly  sank  to  normal. 

During  this  time  the  slough,  mentioned  above,  came  away,  and  a  clean, 
healthy-looking,  healing  surface  was  left  at  the  bottom  of  a  depressed  ulcer 
with  raised,  but  not  undermined,  red  edges,  while  the  surrounding  skin  had 
returned  to  its  normal  colour. 

There  were  no  enlarged  lymphatic  glands,  and  no  signs  of  sepsis.  The  urine 
was  febrile,  but  did  not  contain  albumen  or  sugar. 

The  patient  made  a  good  and  rapid  recovery. 

^Etiology. — In  attempting  to  define  the  causation  of  the  above  condition 
it  is  important  to  clearly  distinguish  between  localized  gangrenous  vaccinia 
and  the  condition  called  dermatitis  gangrenosa  infantum,  as  the  latter  is  a 
generalized  eruption  probably  of  septic  origin,  following  Varicella  and  other 
pustular  eruptions  in  children,  and  often  assumed  to  have  something  to  do 
with  vaccination. 

Localized  gangrenous  vaccinia,  on  the  other  hand,  is  quite  different.  It 
is  not  septic,  but  vaccinal  in  origin  and  it  is  not  generalized,  but  localized  to 
the  vaccination  area. 

Acland,  Crocker,  Balzer,  and  Hutchinson  have  met  with  similar  cases, 
some  of  which  are  stated  to  have  ended  fatally. 

In  such  cases  as  Chalmers  and  Archibald  have  been  able  to  find  any  account 
of,  there  has  been  some  latent  infection  or  disease  in  the  patient.  Thus,  for 
example,  in  Crocker's  case  there  was  latent  scarlet  fever,  and  in  Chalmers  and 
Archibald's  case  there  was  latent  gout. 

It  therefore  seems  probable  that  localized  gangrenous  vaccinia  can  be  pro- 


1496  COSMOPOLITAN  FEVERS 

duced  by  perfectly  pure  calf -lymph  and  by  a  satisfactory  technique  in  persons 
suffering  from  any  form  of  latent  constitutional  disturbance  of  severe  nature,  and 
that  the  severity  of  the  local  signs  is  caused  by  the  lowered  resistance  of  the 
tissues  due  to  this  latent  infection,  which,  judging  from  this  and  other  cases, 
makes  itself  sufficiently  evident  in  the  course  of  the  illness  which  follows 
the  vaccination. 

Treatment. — At  first  the  area  should  be  merely  protected  from  septic  infec- 
tion by  pieces  of  sterilized  lint  lightly  held  in  position  by  pieces  of  bandage. 
When  the  inflammatory  symptoms  appear,  antiseptic  dressings  in  the  form  of 
i  in  80  carbolic  lotion  may  be  applied  on  lint,  while  the  whole  area  is  covered 
with  cotton-wool,  loosely  held  in  position  by  first  a  bandage  and  then  a  hand- 
kerchief. 

Closed  dressings  are  not  indicated,  and  the  affected  area  should  be  simply 
exposed  to  the  air  in  an  elevated  position,  and  treated  at  first  by  dry  powders, 
later  by  lead  and  opium  lotion,  and  finallv  by  calamine  lotion. 

Papulo-Vesicular  Vaccinia  (Synonym,  Vaccine  Lichen). — This  rash,  which 
was  first  described  by  Crocker  as  vaccine  lichen,  has  been  observed  in  a  number 
of  cases  by  Chalmers  and  Byam  in  the  Anglo-Egyptian  Sudan.  Some  seven 
or  eight  days  after  vaccination  the  patient  suffers  from  a  mild  attack  of  fever, 
which  may  reach  1020  F.,  and  may  be  attended  with  a  slight  sensation  of  itching 
in  various  parts  of  the  body.  The  febrile  symptoms  subside  as  the  rash  appears , 
and  do  not  return ;  but  during  the  fever  some  of  the  patients  suffer  from  a  dry 
cough,  which  becomes  worse  as  the  eruption  develops,  and  then  slowly  dis- 
appears. There  is  no  vomiting  or  diarrhoea  or  other  symptom  worthy  of 
record,  while  the  vaccination  pursues  a  normal  course. 

With  regard  to  the  rash,  it  appears,  as  already  stated,  some  seven  to  nine 
days  after  vaccination  in  the  form  of  dark-coloured  macula?,  which  quickly 
become  papules  or  papulo-vesicles,  because,  although  no  actual  vesicles  can 
be  seen  by  the  naked  eye,  still  they  produce  a  hard  shotty  sensation  on  palpa- 
tion, and  on  microscopical  examination  show  minute  vesicles  in  the  epidermis. 
A  fully  developed  papule  is  about  the  size  of  a  large  pin's  head,  dome-shaped, 
and  projects  above  the  surrounding  skin,  which,  as  a  rule,  is  quite  normal, 
though  in  some  cases  it  maybe  distinctly  congested  and  may  even  be  swollen. 
They  appeared  firstly  upon  the  back  of  the  hands  and  forearms,  then  on  the 
back  of  the  neck,  then  on  the  face,  chiefly  on  the  forehead,  and  then  on  the 
chest  and  back,  and  varied  considerably  in  number  from  a  few  dozen  to 
several  hundreds. 

The  blood  showed  no  parasites,  but  there  was  a  leucocytosis  and  a  marked 
relative  increase  of  mononuclear  and  eosinophile  leucocytes. 

After  lasting  some  four  or  five  days,  the  rash  slowly  disappears,  and  is 
followed  by  a  well-marked  desquamation. 

With  regard  to  its  aetiology,  it  was  associated  with  vaccination  because  it 
occurred  in  two  quite  distinct  detachments  of  Nuers  and  Nubas.  The  first 
detachment  of  twenty-four  were  vaccinated  on  February  10,  1914,  and  the 
eruption  developed  in  eight,  while  the  second  detachment  of  thirty-six  was 
vaccinated  on  February  23,  1914,  and  three  developed  the  rash.  It  is  to  be 
noted  that  the  vaccination  in  all  was  performed  with  lymph  from  one  and  the 
same  calf.  In  every  case  the  vaccination  took  well  and  developed  normally, 
and  in  no  case  was  there  any  sign  of  scpiicitv  or  infection .  No  fungi  or  bacteria 
could  be  found  in  or  cultivated  from  the  papules;  on  the  other  hand,  bodies 
which  bore  a  resemblance  to  Guarnieri  bodies  were  found  in  the  vesicles. 

The  chief  diagnostic  points  are: — 

A  papular  or  papulo-vesicular  eruption  beginning  about  eight  days  after 
vaccination  and  heralded  by  slight  or  no  constitutional  disturbance,  but  with 
moderate  itching,  and  usually  commencing  on  the  arms,  is  most  probably 
this  eruption,  which  maybe  called  a  vaccine  lichen,  but  which  would  be  better 
termed  a  papulo-vesicular  vaccinia. 

The  diagnosis  should  be  confirmed  by  attempts  at  vaccination  of  a  monkey 
from  a  papule  or  a  vesicle. 

The  differential  diagnosis  may  be  made  from: — 

Lichen  acuminatus  by  the  fact  that  the  hair  follicles  are  not  attacked. 


INFLUENZA 


1497 


From  craw-craiv  (in  the  restricted  sense  of  the  word)  by  the  absence  of  the 
horny  consistency,  and  by  the  smaller  size  of  the  vaccinal  papules. 

From  lichen  convex  by  being  non-follicular  and  by  being  an  acute  and  not  a 
chronic  eruption. 

From  an  ordinary  generalized  vaccinia  by  the  main  lesion  being  a  papule 
and  by  the  usually  small  size  of  the  vesicles. 

Prognosis. — This  is  invariably  good,  as  all  our  cases  and  apparently  most 
of  Crocker's  cases  recovered  very  quickly  without  any  scarring  or  pigmentation . 
Crocker  has  pointed  out  that  it  may  go  on  to  vesiculo-pustular  formation,  and 
in  some  of  these  cases  fresh  crops  may  continue  to  appear  for  months,  or  the 
vesicles  may  enlarge  and  become  herpctiform  or  bullous;  but  it  is  possible 
that  these  exceptional  forms  are  due  to  secondary  infections  and  not  solely 
to  the  lymph. 

Treatment. — The  essential  treatment  is  rest  and  quiet.  On  quinine  by 
the  mouth  and  an  antiseptic  ointment — i.e.,  carbolic  ointment — for  the  skin, 
rapid  recovery  takes  place. 

Prophylaxis. — There  is  no  explanation  why  eleven  out  of  sixty  persons  vac- 
cinated by  the  same  lymph  and  be  lunging  to  the  same  African  tribes,  living  under 
similar  conditions,  and  about  the  same  age  and  of  the  same  sex,  should  develop 
an  eruption  while  others  did  not.  Therefore  it  is  not  possible  to  suggest  any 
prophylactic  measures. 

INFLUENZA. 

Remarks. — An  acute  specific  fever,  until  recently  believed  to  be  caused  by 
Hcs  nophilia  influenza  (Pfeiffer,  1892)  (usual  term:  Bacillus  influenza),  spread 
from  man  to  man  aerially,  and  typically  characterized  by  a  sudden  and 
severe  onset,  pains  in  various  parts  of  the  body,  some  catarrh  of  the  respira- 
tory passages,  which  typically  subside  in  some  two  or  three  days  and  are 
apt  to  be  followed  by  a  prolonged  convalescence.  Recent  researches  by 
Charles  Nicolle  and  Charles  Lebailly  tend  to  show  that  the  malady  may 
be  due  to  a  filter-passing  virus.  Bradford,  Bashford,  and  Wilson  state 
that  the  virus  isolated  in  cases  of  influenza  consists  of  minute  Gram-positive, 
roundish,  coccus-like  bodies,  varying  from  0-15  /u  to  05  /li,  capable  of  passing 


Pi   ,.    i), 2.     -TEMPERATURE    CHART    OF    INFLUENVA. 


through  Berkcfeld  N  and  V  filters.  It  is  an  anaerobe,  and  is  not  destroyed 
by  heating  to  56°  C.  for  thirty  minutes.  They  have  isolated  this  organism 
from  the  blood  and  sputum  of  a  number  of  cases. 

It  is  notour  intent  to  discuss  the  aetiology  or  to  enter  upon  a  full  description 
of  inlluenza.  which  can  be  found  in  any  textbook  on  medicine,  but  rather  to 
attempt  to  impress  upon  the  tropical  practitioner  the  necessity  of  recognizing 
this  complaint,  which  is  very  apt  to  be  mistaken  for  pappataci  and  dengue 
fever,  and  vice  versa. 

Typical  Attack. — -Suddenly,  without  warning,  the  victim  feels  very  ill;  he 
may  shiver,  feel  sick,  or  be  giddy,  but  in  any  case  he  feels  acute  pains  in  various 
parts  of  the  body,  but  especially  in  the  lumbar  region,  behind  the  eyeballs,  and 


1498 


COSMOPOLITAN  FEVERS 


in  the  muscles  and  bones,  as  well  as  a  dry  burning  sensation  in  the  eyes,  rose, 
and  throat,  and  sometimes  also  behind  the  sternum.  His  temperature  rises 
quickly  to  io3°to  i05°F.,  his  pvdse  and  respirations  are  increased,  and  hesuffers 
from  a  troublesome  cough,  and  herpes  may  occasionally  appear  onthe  lips. 

After  two  or  three  days  :  f  these  symptoms  the  temperature  falls,  slight 
catarrhal  symptoms  appear,  the  patient  becomes  convalescent,  and  may 
recover  completely  or  may  feel  out  of  sorts  for  weeks  or  months. 

In  the  catarrhal  type  there  are  the  ordinary  signs  of  a  bronchitis,  to  which 
may  be  added  those  of  a  lobular  pneumonia,  and  such  cases  are  very  dangerous. 
In  the  gastro-intestinal  type  there  are  the  signs  of  gastro-intestinal  catarrh, 
which  is  rare,  but  more  frequently  there  is  a  pseudo-enteric  condition,  with 
fever,  lasting,  however,  about  a  week. 

In  the  cerebral  type  the  onset  may  be  sudden  or  gradual,  be  with  or  without 
catarrhal  symptoms,  and  is  associated  with  pains  in  various  parts,  delirium, 
aphasia,  hemiplegic  or  monoplegic  symptoms,  and,  indeed,  may  at  times 
simulate  a  cerebral  haemorrhage,  especially  in  afebrile  cases.  These  are  very 
fatal  cases,  but  at  times  recovery  takes  place,  often  with  permanent  mental 
disturbance. 

Blood. — The  blood  practically  shows  no  change.  The  total  leucocytes  vary 
from  8,000-12,000,  while  the  differential  count  is  within  normal  limits. 


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Fig.  6S4. 
-Tempfrature  Charts  of  Influenza. 


Complications  and  Sequelae. — These  are  numerous  and  frequent,  but  for 
them  an  ordinary  textbook  of  medicine  must  be  consulted. 

Diagnosis. — The  cardinal  features  of  a  typical  attack  of  influenza  are: — 
(1)  The  sudden  and  violent  onset;  (2)  the  high  fever  and  quick  pulse;  (3)  the 
violent  pains  in  the  muscles  and  bones;  (4)  the  catarrhal  symptoms;  (5)  the 
absence  of  any  typical  rash;  (6)  the  presence  of  Pfeiffer's  organism,  whether 
it  is  the  true  specific  agent  or  a  nosoparasite ;  (7)  the  absence  of  a  marked 
leucocytosis. 

In  the  tropics  the  most  important  points  in  the  differential  diagnosis  are  the 
separation  of  the  malady  from  malaria,  dengue  and  pappataci  fevers,  and 
from  plague.  From  malaria  it  can  be  recognized  by  the  absence  of  the 
parasites  in  the  blood,  the  absence  of  the  mononucleosis  and  of  the  enlarged 
and  tender  spleen,  and  by  the  presence  of  catarrhal  symptoms. 

From  dengue  it  can  be  separated  by  the  absence  of  the  leucopenia  and  of  the 
rash,  and  by  the  presence  of  catarrhal  symptoms. 

From  pappataci  fever  it  can  be  diagnosed  by  the  absence  of  the  leucopenia, 
the  quickness  of  the  pulse,  and  as  a  rule  the  presence  of  the  catarrhal  symptoms, 
which  in  pappataci  fever  are  absent  or  slight. 

From  plague  by  the  absence  of  plague  bacilli  in  the  sputum  in  the  pneumonic 
type,  or  in  blood  as  demonstrated  by  haemo-cultures  in  the  septicaemic  variety. 

Prognosis. — This  is  good  quoad  vitam  in  typical  uncomplicated  cases,  and 
bad  in  the  varieties  mentioned  above. 


REFERENCES  1499 

Treatment. — It  is  important  that  the  patient  should  remain  in  bed  and  be 
carefully  nursed. 

Liquor  ammoniae  acetatis  in  \  drachm  doses  in  a  mixture  combined  with 
3  to  5  grains  of  sodium  salicylate,  alternated  with  1  drachm  doses  of  the 
ammoniated  tincture  of  quinine,  well  diluted,  should  be  given  every  two 
hours  until  the  symptoms  are  relieved. 

Pyramidon  may  be  administered  with  benefit,  if  desired. 

The  diet  should  be  light  and  nutritious,  and  the  heart  and  respiratory  organs 
should  be  carefully  watched. 

Prophylaxis. — The  patient  should  be  isolated  as  far  as  possible,  and  on 
recovery  his  room,  beddjng,  clothing,  etc.,  should  be  disinfected.  Vaccines 
have  not  been  very  successful. 

REFERENCES. 

Epidemic  Cerebro-Spinal  Meningitis. 

Altmann   and  Others   (1906).     Genickstarre  in   Preusscn  im   Jahre   1905. 

Abdruck  aus  dem  Klinischen  Jahrbuch.      (Tins  is  a  collection  of  valuable 

papers.)     Jena. 
Archibald  (1915).     Report  on  the  Epidemic  of  Cerebro-spinal  Meningitis  at 

Maiaza.    Khartoum. 
Arkwright  (1909).   Journ.  of  Hyg.,  ix.  104.    Cambridge.    (1915).    Brit.  Med. 

Journ.,  i.  494.     London. 
Balfour  (1904-1911).     Reports  of  the  Wellcome  Tropical  Research  Labora- 
tories, 1st,  2nd,  3rd,  and  4th.     London. 
Buchanan,  R.  E.  (1915).     Journ.  Infect.  Dis.,  xviii.,  No.  3,  p.  528.     Chicago. 
Buchanan,  R.  M.  (1907).     Lancet,  i.  1590-     London. 

Busse  (1910).     Klin.  Jahr.,  xxiii.     Abdruck.     (A  very  full  literature.)     Jena. 
Castellani  (1905).     Lancet,  ii.  353.     (Cases  in  Ceylon.)     London. 
Chalmers    and    Innes    (191 7).      The    Journal    of    Tropical   Medicine    and 

Hygiene.     London. 
Chalmers  and  O'Farrell  (1916).     The  Journal  of  Tropical  Medicine  and 

Hygiene.     London. 
Christiani  (1909).     Die  Aetiologie  der  sporadischen  und  epidemischen  Cere- 

brospinalmeningitis  des  Pferdes.     Berlin. 
Cole  (1915).     Lancet,  i.  750.     London. 
Colebrook   and  Tanner   (1916).     Journ.   R.A.M.C,   xxvi.,   No.    1,    p.    76. 

London. 
Corney    (1889).     Epidemic   Cerebro-spinal   Meningitis  in   the   Fiji    Islands. 

Trans.  Epidem.  Soc,  N.S.,  vii.  no.     London. 
Davis  (1905).     Journ.  Infect.  Dis.,  ii.  602;  (1907),  ibid.,  iv.  558.     Chicago. 
Dopter  (1909).     Compt.  Rend.  Soc.  Biol.    (1913).    Presse  M6dicale,  Ko.  25. 

p.  1025  (Parameningococcus).     Paris. 
Dopter  and  Koch  (1908).     Compt.  Rend.  Soc.  Biol.,  ii.  74.     Paris. 
Dopter  and  Pauron  (1914).     Compt.  Rend.  Soc.  Biol.,  lxxii.,  p.  231. 
Dunn  and  Gordon  (1905).     Brit.  Med.  Journ.,  ii.  421.     London. 
Ellis  (1916).     Journ.  R.A.M.C,  xxvi.,  No.  1,  p.  64.     London. 
Elser   and   Huntoon  (1909).     Journ.  Med.  Res.,  xx.,  No.  4,  pp.  377"536- 

(Very  complete  research  on  meningococci.)     Boston. 
Embleton   and   Peters    (1915).     Journ.    R.A.M.C,   xxiv.,   No.   5,    p.   468. 

London. 
Foster  and  Gaskell  (1916).     Cerebro-spinal  Fever.     Cambridge. 
Gordon  (1907).     Reports  of  the  Local  Government  Board,  1905-06,  p.  435. 

(1915).     Journ.  R.A.M.C,  xxiv.,  No.  5,  p.  455. 
Gordon   and    Murray    (1915).     Journ.     R.A.M.C,    xxv.,    No.    4,    p.    411. 

London. 
Hachtel  and  Hayward  (1911).     Journ.  Infect.  Dis.,  viii.  444.     Chicago. 
Hirsch  (1886).     Geographical  and  Historical  Pathology,  iii.   174-186.     (All 

the  older  literature.)     London. 
Horder  (191 5).     Cerebro-spinal  Fever.     (A  small  and  most  useful  work  for 
medical  officers.)     Oxford. 


1500  COSMOPOLITAN  FEVERS 

Horn  (1908).     Trans.  Soc.  Trop.  Med.  and  Hyg.,  ii.,  No.  1,  p.  2.     (Northern 

Territories  of  the  Gold  Coast.)     London. 
Hort  (1916).     Brit.  Med.  Journ.,  i.  156.     London. 

Hort,  Lakin,  and  Benians  (1915).     Brit.  Med.  Journ.,  i.  541,  715.     London. 
Houston  and  Rankin  (1907).     Brit.  Med.  Journ.,  ii.  1416.     London. 
Jaeger    (1901).      Die    Cerebrospinalmeningitis    als    Heeresseuche.    Eerlin. 

(1903).     Centralbl.  f.  Bakt.,  Orig.,  xxxiii.  23.     Jena. 
Jaff£  (1909).     Klin.  Jahr.,  xx.  4.     (Togoland.)     Jena. 
Kutscher   (1912).     Uebertragbare   Genickstarre,    Kolle  and   Wassermann's 

Pathogenen  Mikroorganismen.     2nd  edition,  iv.  589.     Jena. 
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(An  account  of  the  diseases  of  Darfour.)     Paris.' 
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Diseases.     (Most  valuable.)     London. 
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New  York. 
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Cerebrospinalfliissigkeit.     Jena. 
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by  Swan,  pp.  495-522.     London. 
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p.  708.     London. 
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May  16.     London. 
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CHAPTER   L1X 
WAR   ZONE    FEVERS 

General  remarks — Trench  fever- — Icterus  castrensis  gravis — Icterus  castrentis 

levis — References. 

GENERAL  REMARKS. 

It  may  be  thought  that  it  is  unnecessary  to  introduce  the  subject 
of  the  diseases  of  the  different  zones  of  the  war  into  a  work  on 
tropical  diseases,  but  many  of  the  maladies  which  have  affected 
the  troops  during  the  war  in  the  Salonica  area,  in  Egypt  and 
Palestine,  in  Mesopotamia  and  East  Africa,  are  essentially  tropical 
diseases,  as  were  those  of  Gallipoli.  Most  of  the  fevers  from  which 
the  troops  suffered  have  been  described  in  the  preceding  chapters, 
and  many  of  the  other  diseases,  such  as  the  dysenteries  and  skin 
diseases,  will  be  dealt  with  in  the  chapters  which  follow;  but, 
excluding  these,  there  are  three  conditions  which  merit  a  little 
consideration — viz.,  trench  fever  and  the  severe  and  mild  forms 
of  infective  jaundice,  often  called  icterus  castrensis  gravis  (or  Weil's 
disease),  and  camp  jaundice — because,  in  making  a  diagnosis  of  a 
fever,  these  conditions  must  be  considered,  and  we  are  now  pre- 
paring the  way  for  the  chapter  on  diagnosis. 

We  therefore  consider  that  a  very  brief  account  of  these  three 
conditions  is  necessary  for  our  present  purpose. 

TRENCH  FEVER. 

Synonyms. — Periodic  one-day  fever,  Salonica  fever,  Pyrexia  of  unknown 
origin,  Five  days'  lever,  Volhynia  fever,  Russian  remittent  lever,  Meuse 
fever,  Trench  skin,  Gaiter  fever,  Shin  fever,  Trench  shin,  Shank  fever,  Polish 
fever.  Quintan  Eever.  French,  La  Fi&vredcstrenchees;  German,  His-Wernersche 
Krankheit,  Futtftagefieber,  Periodische  Fieber;  Latin,  Febris  quintana, 
Febris  volhynica. 

Definition.— A  relapsing  fever  of  as  yet  unknown  origin,  and  spread 
by  Pediculus  corporis  de  Geer,  1778,  commonly  by  the  infected  taxes 
being  rubbed  into  the  excoriated  skin.  It  is  characterized  by  a  sudden 
onset  of  fever  associated  with  pains  in  muscles  and  bones,  particu- 
larly in  the  legs,  with  especial  tenderness  of  the  shins,  and  lasting 
twenty-four  to  forty-eight  hours  or  longer,  followed  by  other  attacks 
of  fever  of  less  and  less  severity,  separated  by  apyrexial  intervals 
of  five  days'  duration  (more  or  less),  and  ending  in  complete  recovery. 

1 501 


1502  WAR  ZONE  FEVERS 

History. — As  Strong  has  pointed  out,  there  is  insufficient  data 
to  permit  any  of  the  diseases  described  by  the  ancients,  or  in 
mediaeval  or  modern  times,  being  connected  with  the  disease; 
while  McNee  believes  that  it  is  unlike  any  disease  reported  in  other 
wars,  and  that  it  may  have  been  introduced  into  the  British  Army 
by  Colonials.  Early  in  1915  Graham  drew  attention  to  the  disease 
as  seen  in  the  British  Army,  in  which  thousands  of  cases  occurred 
between  April  and  October.  In  January,  1916,  it  was  observed  in 
Salonica  by  McGavin,  Wylie,  and  Acland,  of  No.  1  New  Zealand 
Stationary  Hospital.  In  May,  1916,  it  was  observed  in  Mesopotamia, 
and  in  the  same  month  was  reported  by  Beauchant  and  Boidin  as 
being  present  in  the  French  Army  in  France,  and  about  this  time 
Werner  in  Warsaw  drew  attention  to  its  existence  in  the  German 
armies,  and  Hurst  gave  a  good  general  account  of  the  disease.  In 
the  same  year  McNee,  Renshaw,  and  Brunt  showed  that  the  disease 
could  be  transmitted  to  healthy  men  by  intramuscular  and  intra- 
venous injections  of  the  blood  of  patients,  and  the  Germans  also  were 
similarly  successful.  In  the  same  year  it  was  observed  at  Salonica 
that  the  clothes  or  body  louse,  Pediculus  corporis,  was  the  only 
possible  source  of  infection  in  a  certain  hospital  orderly  who  had 
never  been  in  contact  with  patients,  and  in  whom  the  incubation 
was  eighteen  days  from  the  first  time  he  became  infected  with  lice 
from  some  clothing.  In  1918,  Strong,  Swift,  Opie,  McNeal,  Baelzer, 
Pappenheimer,  and  Peacock,  in  France,  showed  that  the  virus  was 
present  in  the  blood  plasma  and  would  not  pass  through  a  filter. 
They  also  proved  that  the  louse  was  the  infective  agent,  and  that 
the  virus  was  naturally  conveyed  by  its  bite.  This  virus  is  present 
in  the  plasma,  sometimes  in  the  urine,  and  occasionally  in  the 
sputum.  Artificially  the  disease  may  be  transmitted  by  rubbing 
lice  fasces,  human  infected  urine  or  sputum,  into  excoriated  skin,  but 
the  incubation  resembles  that  of  the  inoculation  of  infected  plasma. 

A  little  later,  in  the  same  year,  the  British  Committee  in  London 
showed  that  lice  bites  did  not  produce  the  disease,  which,  however, 
could  be  produced  in  healthy  men  by  rubbing  infected  louse  fasces 
into  excoriated  cutaneous  areas.  Further,  they  demonstrated 
that  the  incubation  period  was  six  to  eight  days,  and  that  blood 
taken  from  the  infected  men  and  injected  into  healthy  men  could 
reproduce  the  disease  after  an  incubation  of  five  days.  Also,  in 
1918,  Couvy  and  Dujarric  de  la  Riviere  claimed  that  a  spiro- 
chaete,  S.  gallica  Couvy  and  de  la  Riviere,  1918,  could  be  found  in 
the  blood  of  man  and  infected  guinea-pigs,  and  in  the  liver  and 
kidneys  of  these  guinea-pigs.  The  infected  guinea-pigs  were  shown 
to  suffer  from  a  fever  resembling  that  in  man.  They,  however, 
did  not  retransfer  the  disease  from  the  guinea-pig  to  man,  and 
the  general  opinion  at  present  is  that  the  organism  is  not  the  cause 
of  the  disease.  Other  organisms  such  as  a  piroplasma  and  a 
haemogregarina  have  been  described  as  causal. 

In  1916  Toepfer  found  Rickettsia  bodies  similar  to  those  described 
in  1909  by  Ricketts  in  Rocky  Mountain  spotted  fever,  and  by 


HISTOR  Y—S  YMPTOMA  TOLOG  Y 


1503 


Ricketts  and  Wilder,  in  1910,  in  typhus.  In  1917  Da  Rocha  Lima 
called  the  bodies  found  in  trench  fever  Rickettsia  quintana,  to  dis- 
tinguish them  from  those  found  in  typhus  (R.  prowazecki)  and 
those  occasionally  seen  in  normal  lice  (R.  pediculi).  These  findings 
were  supported  in  1918  by  Arkwright,  Bacot,  and  Duncan. 

In  1919  Bradford,  Bashford,  and  Wilson  described  minute  bodies 
which  they  had  succeeded  in  cultivating  from  the  blood  of  patients, 
using  Noguchi's  method  of  anaerobic  cultures.  These  bodies  are 
morphologically  identical  with  Rickettsia  bodies,  but  they  are 
Gram-positive. 

Climatology. — The  disease  is  known  to  exist  in  England,  Flanders, 
France,  Salonica,  Greece,  Macedonia,  Tyrol,  Galicia,  Poland,  Russia, 
and  Mesopotamia. 

/Etiology. — The  aetiology  has  not  been  completely  elucidated. 
Toepfer  first  found  minute  bodies  in  the  intestinal  contents  of  lice 
fed  on  trench  fever  patients,  which  he  considered  to  be  Rickettsia 
bodies;  these  bodies  were  somewhat  similar  to  those  found  in 
Rocky  Mountain  fever  and  typhus.  Toepfer's  work  was  confirmed 
and  enlarged  by  Da  Rocha  Lima,  who  called  the  parasite  Rickettsia 
quintana,  and  more  recently  by  Arkwright,  Bacot,  and  Duncan. 
These  latter  authors  describe  the  bodies  as  being  minute  Gram- 
negative  organisms,  round,  oval,  or  lancet-shaped  diplococci, 
0-3  microns  in  their  shorter  diameter  by  0-3  to  0-4  in  length;  the 
first  appearance  in  the  excreta  of  lice  being  as  a  rule  eight  to  ten 
days  after  the  first  infecting  feed.  They  seem  to  be  slightly  smaller 
and  less  frequently  lancet-shaped  than  those  found  in  typhus.  The 
size  of  these  bodies  is  such  that  they  should  not  pass  as  a  rule  a 
bacterial  filter,  but  may  occasionally  pass  a  filter  which  retains 
such  bacteria  as  B.  typhosus. 

Bradford,  Bashford,  and  Wilson  report  that  they  have  cultivated 
from  the  blood  of  patients,  by  using  Noguchi's  method,  minute 
bodies  which  seem  to  be  very  similar  to  Rickettsia  bodies,  but  are 
Gram-positive. 

The  trench  fever  virus  is  considered  to  be  a  resistant  filterative 
virus  by  the  American  Commission.  This  Commission  (composed 
of  Strong,  Swift,  Opie,  Macneal,  Baetjer,  Pappenheimer,  Peacock, 
and  Rapport)  carried  out  a  very  thorough  investigation  in  191S,  and 
came  to  the  conclusion  that  the  virus  was  carried  from  the  sick  to 
the  healthy  by  the  agency  of  the  clothes  louse,  Pedicuhts  corporis 
de  Geer,  1778,  and  that  it  was  usually  conveyed  by  the  bites. 

The  War  Office  Commission  !(composed  of  Byam,  Carroll, 
Churchill,  Dimond,  Lloyd,  Sorapure,  and  Wilson)  came  to  the 
conclusion,  after  a  series  of  important  experiments,  that  the  infec- 
tion was  contaminative  by  means  of  the  louse  faeces  infecting 
scratches  on  the  skin. 

Pathology  and  Morbid  Anatomy. — Unknown. 

Symptomatology — Incubation. — Clinically  the  incubation  period 
is  believed  to  vary  from  fourteen  to  thirty  days,  because  this  is 


i5o4  WAR  ZONE  FEVERS 

the  time  required  to  induce  the  disease  experimentally  by  infected 
lice  when  permitted  to  bite  healthy  persons.  Experimentally  it  is 
six  to  eight  days  from  the  time  that  infected  lice  faeces  are  rubbed 
into  scratches,  and  five  days  after  the  inoculation  of  infected  blood. 
During  this  stage  there  may  be  slight  prodromata  in  the  form  of 
headache  and  pains  in  the  limbs,  but  these  may  be  absent. 

Attack. — -The  onset  is  sudden,  the  patient  feeling  giddy,  weak, 
and  shivering.  He  feels  so  ill  that  he  has  at  once  to  stop  his  work, 
and  complains  of  shortness  of  breath,  pain  in  the  left  side,  in  the  back, 
legs,  and  behind  the  eyeballs,  as  well  as  of  headache.  The  tempera- 
ture quickly  rises  to  ioi°  to  1040  F.  The  conjunctivae  are  injected, 
and  nystagmus  may  be  present  if  the  eyes  are  turned  completely 
sideways. 

There  are  two  curious  types  of  this  stage  of  the  illness — viz.,  the  appendi- 
cular and  the  cerebrospinal.  In  the  former,  the  patient  suffers  from  abdominal 
pain,  constipation,  slight  abdominal  distension,  tenderness,  and  vomiting, 
and  in  Allied  and  German  armies  the  diagnosis  of  appendicitis  has  been  made. 

At  other  times  there  may  be  pains  and  stiffness  of  the  neck,  and  the  case 
may  be  mistaken  for  cerebro-spinal  meningitis. 

The  Course  of  the  disease  is  that  the  next  morning  the  temperature 
has  fallen  to  normal  or  nearly  normal,  but  it  may  remain  high,  the 
appetite  is  lost,  the  tongue  is  furred,  and  there  may  be  pharyngitis 
and  constipation.  Now  the  patient  complains  of  pains  in  the 
muscles  and  bones  of  the  legs,  and  has  tenderness  in  the  shins,  over 
which  there  is  cutaneous  hyperesthesia,  and  there  may  be  pain  and 
tenderness  inthe  fibula,  humerus,  ulna,  or  along  the  vertebral  column. 

Herpes  labialis  may  appear,  and  fairly  often  a  discrete  roseolar 
rash,  and  very  rarely  a  scarlatiniform  or  small  papular  rash,  may  be 
seen  on  the  chest,  back,  or  abdomen.  The  spleen  and  more  rarely 
the  liver  may  now  enlarge.  The  blood  shows  a  leucocytosis,  with 
a  relative  mononuclear  increase.  The  red  corpuscles  are  not 
reduced  in  amount,  but  the  haemoglobin  is  usually  reduced,  and 
there  is  polychromatophilia. 

First  Intermission. — After  twenty-four  to  forty-eight  hours,  or 
longer,  the  temperature  falls  to  normal,  the  symptoms  disappear, 
and  the  patient  feels  well,  though  sometimes  he  feels  slight  discom- 
fort in  the  muscles  and  bones. 

Second  Attack. — Some  two  to  ten,  but  more  usually  five,  days  after 
the  cessation  of  the  first  attack  the  patient  begins  to  feel  ill,  with 
headache,  pains  in  the  legs,  and  fever,  the  temperature  rising  to 
about  1010  F.  Next  day  the  temperature  is  normal,  and  this  attack 
may  cease,  or  the  fever  may  recur  in  the  evening,  but  usually  ceases 
next  day. 

Intermissions  and  Attacks. — These  now  succeed  one  another  at 
regular  intervals  of  about  five  days'  duration,  but  the  attacks  of 
fever  become  shorter  and  shorter  and  the  temperature  lower  and 
lower,  so  that  unless  care  is  taken  to  register  the  temperature  every 
two  hours  about  the  time  of  an  expected  attack,  the  fever  may 
be  missed  by  the  day  and  night   temperature  chart.     Although 


SYMPTOMATOLOGY— ICTERUS  CASTRENSIS  GRAVIS    1505 

the  patient  does  not  feel  or  look  ill,  the  pains  and  tenderness  in  the 
shins  may  become  worse  during  each  attack  and  may  keep  him  from 
sleeping.  The  number  of  relapses  is  variable,  and  may  reach  six 
or  seven. 

Rash. — In  a  fairly  large  number  of  patients  a  delicate  macular 
rash  appears  with  each  recurrence  of  the  fever.  It  is  generally 
seen  on  the  chest  and  abdomen,  and  consists  of  small  red  macules 
which  disappear  on  pressure. 

Termination.  — After  lasting  a  variable  time  (five  to  six  weeks) ,  the 
disease  gradually  dies  out  and  the  recovery  is  complete. 

Complications  and  Sequelae. — Tachycardia  and  so-called  soldier's 
heart  may  occur. 

Varieties. — English  observers  recognize  a  short  and  a  long  type. 
In  the  former  the  fever  lasts  for  three  to  four  days,  falls  to  normal, 
and  after  a  few  hours  rises  again  for  two  to  five  days,  when  it  falls 
to  normal  and  the  fever  stops.  This  variety  resembles  dengue  fever. 
The  long  type  is  the  typical  fever. 

The  Germans  also  recognized  a  simple  paroxysmal  form,  but  they 
also  mention  a  typhoidal  and  a  rudimentary  form. 

Diagnosis. — This  has  to  be  made  from  influenza,  dengue,  pappa- 
taci  fever,  relapsing  fever,  malaria,  smallpox,  typhus, and  enteroidea. 

From  influenza  it  may  be  distinguished  by  the  absence  of  catarrhal 
symptoms  and  the  mononucleosis. 

From  dengue  and  pappataci  by  the  absence  of  leucopenia. 

From  relapsing  fever  by  the  absence  of  marked  enlargement  of 
the  spleen  and  of  the  spirochetes  in  abundance  in  the  blood. 

From  smallpox  and  typhus  by  the  absence  of  the  severe  consti- 
tutional symptoms. 

From  malaria  by  the  absence  of  the  leucopenia  and  of  the  typical 
parasites  from  the  blood. 

From  enteroidea  by  the  sudden  onset  and  the  pains  in  the  muscles 
and  bones,  and  by  negative  hsemoculture  and  serological  reactions. 

Prognosis. — This  is  good,  as  the  mortality  is  nil  and  the  recovery 
complete. 

Treatment. — Pyramidon  is  strongly  recommended,  but  constipa- 
tion must  be  relieved,  and  the  patient  should  be  disinfected  at  once. 
His  clothing  and  bedding  should  be  disinfected  in  moist  heat  at 
700  C.  for  half  an  hour. 

Prophylaxis.— This  is  mainly  louse  destruction  {vide  the  chapter 
on  Typhus,  p.  1338),  but  the  urine  and  sputum  of  patients  should 
also  be  disinfected.     Cups  should  be  provided  for  the  sputum. 

ICTERUS  CASTRENSIS  GRAVIS. 

Synonyms.— Weil's  disease,  Epidemic  jaundice,  Infective  jaundice,  Spiro- 
chaetal  jaundice,  Spirochaetosis  ictcrhaemorrhagica,  Larrey-Weil  disease. 
French,  Maladie  de  Weil,  Typhus  hepatique;  German,  Infektioser  Fieberhafter 
Ikterus,  Infektionikterus,  Wcilschen  Krankheit;  Japanese,  Odan-eki;  Latin, 
Icterus  f ebrilis  seu  infectiosus,  Typhus  biliosus  nostras,  Morbus  weili. 

95 


I*o6  WAR  ZONE  FEVERS 

Definition. — An  acute  specific  fever  caused  by  Spiroschaudinnia 
icterohmnorrhagice  (Inada,  Ido,  Hold,  and  Keneko,  1915),  and 
characterized  by  jaundice,  albuminuria,  enlargement  of  the  spleen, 
pains  in  the  muscles,  with  sometimes  haemorrhages  and  a  high 
mortality. 

History. — The  disease  was  first  mentioned  in  Minorca  in  1745, 
and  then  along  the  coast  of  Italy.  Larrey,  in  1800,  seems  to  have 
described  this  disease  as  seen  in  Napoleon's  army  in  Egypt.  It 
was  also  noted  by  Carville  in  1859,  and  by  Worms  in  1865,  while  a 
number  of  cases  occurred  during  the  American  Civil  War.  As  the 
mortality  from  jaundice  was  low  in  the  South  African  War,  it  is 
probable  that  it  was  absent.  In  the  present  war  it  has  occurred 
in  the  British,  French,  Italian,  Serbian,  and  German  armies,  though 
it  has  been  confused  with  the  milder  type.  In  1886  Hirsch  popu- 
larized the  complaint  and  Weil  again  drew  attention  to  the  disease, 
and  in  1911  Hecker  and  Otto  wrote  a  monograph  on  it.  As  regards 
the  tropics,  it  was  noted  in  India  in  1849,  and  in  subtropical  countries 
it  was  seen  in  Smyrna  and  Egypt.  In  this  history  authors  noted  two 
types,  a  mild,  resembling  simple  catarrhal  jaundice,  and  a  severe, 
which  some  of  them  called  a  type  of  bilious  remittent  fever,  and  said 
that  some  of  the  cases  had  haemorrhages  and  nervous  symptoms. 
During  the  last  few  years  it  has  received  much  attention,  because 
cases  of  jaundice  have  been  frequently  noted  in  the  armies.  In 
1915  the  Japanese  investigators  mentioned  above  discovered  the 
causal  agent,  and  this  has  been  confirmed  by  French,  English, 
Italian,  and  German  workers.  Noguchi  has  found  that  strains  of 
S.  icterohcemorrhague  isolated  from  patients  in  Japan  and  Belgium, 
and  from  rats  in  America,  are  identical  morphologically  and  sero- 
logically. He  has  created  for  the  organism  a  new  genus,  Lepto- 
spira, which  will  probably  be  generally  accepted  in  the  near  future. 

/Etiology. — -The  causal  agent  is  Spiroscliaudinnia  icterohcemorrhagice 
(p.  447),  which  is  considered  to  be  the  same  as  the  spirochete  found 
in  the  kidneys  and  urine  of  wild  rats,  in  which  it  lives.  It  is 
believed  that  the  organism  escaping  in  the  rats'  urine,  and  to  a 
less  extent  in  human  urine,  is  the  source  of  infection,  which  takes 
place  through  the  skin  when  walking  barefoot  on  sodden  ground 
or  by  entering  the  alimentary  canal  in  water. 

Pathology. — The  jaundice  is  probably  caused  by  obstruction  to 
the  smallest  bile  ducts,  brought  about  by  a  polymorphonuclear 
exudate  into  the  tissues  surrounding  them. 

Symptomatology. — The  incubation  period  varies  from  five  to  seven 
days,  the  average  being  six  days,  which  agrees  with  an  accidental 
infection. 

The  onset  is  usually  abrupt,  with  occasional  shivering  and  high 
fever,  faintness,  giddiness,  and  prostration.  The  patient  is  flushed 
and  looks  and  feels  very  ill.  The  spleen  and  liver  enlarge,  and  the 
superficial  lymph  glands  may  become  palpable. 

Course. — Jaundice  appears  two  or  three  days  after  the  onset. 
The  tongue  is  coated  with  a  brown  fur,  and  sordes  form  on  the  lips 


S  YMPTOMA  TOLOG  Y—DIA  GNOSIS  1 507 

and  teeth.  Vomiting  may  be  present  from  the  first,  and  hiccough 
may  also  be  troublesome.  There  may  be  pain  and  tenderness  in 
almost  every  part  of  the  body.  The  neck  may  be  stiff,  and  in  these 
cases  the  cerebro-spinal  fluid  maybe  under  pressure  and  contain  an 
excess  of  polymorphonuclear  cells  and  lymphocytes,  as  well  as 
albumen  and  bile. 

The  conjunctivae  may  be  injected,  and  herpes  may  be  present 
on  the  lips. 

Jaundice  usually  appears  two  or  three  days  after  the  onset  of  the 
symptoms,  but  may  be  later,  though  it  is  almost  always  present 
before  the  temperature  drops.     Pruritus  is  slight  or  absent. 

The  blood  shows  a  diminution  of  red  corpuscles  and  haemoglobin, 
and  an  increase  of  leucocytes,  while  a  very  few  spirochaetes  are 
present  between  the  fourth  and  ninth  day.  The  pulse  is  slow  in 
proportion  to  the  temperature.  The  urine  usually  contains  bile, 
albumen,  granular  and  hyaline  casts,  and  sometimes  a  few  red  cor- 
puscles, and  the  spirochaete  can  be  found  after  the  first  week. 

Haemorrhages  from  the  lungs,  the  stomach,  or  more  rarely  the 
bowels,  may  occur,  while  epistaxis  and  purpura  may  be  seen  in 
severe  cases. 

Termination.— The  temperature  drops  by  crisis  or  rapid  lysis  from 
the  eighth  to  tenth  day. 

Relapse. — There  is  often  a  return  of  the  fever  some  few  days  after 
it  falls  to  normal,  and  the  relapse  may  last  from  a  few  days  to  ten  or 
even  fifteen  days,  but  there  is  no  increase  in  the  symptoms. 

Convalescence. — This  is  often  prolonged. 

Diagnosis. — -The  cardinal  diagnostic  points  are: — 

1.  The  presence  of  the  spirochete  in  the  blood  between  the  fourth 
and  ninth  day  (it  is  difficult  to  see),  and  in  the  urine.  Blood  may 
be  inoculated  into  the  peritoneal  cavity  of  guinea-pigs,  in  which 
illness  supervenes  after  inoculation  of  not  less  than  six  days. 

In  order  to  discover  the  spirochaete  in  the  urine,  it  is  necessary 
to  adopt  Castellani's  method  of  centrifuging  20  c.c.  and  pouring 
off  the  supernatant  fluid,  then  adding  another  20  c.c.  and  again 
centrifuging,  and  so  on  until  about  200  c.c.  of  urine  has  been  centri- 
fuged,  after  which  the  deposit  may  be  examined. 

2.  The  severity  of  the  symptoms  and  the  sudden  onset,  the 
severe  pains,  the  jaundice,  the  enlargement  of  the  liver  and  spleen, 
the  albumen  in  the  urine,  with  casts  and  a  few  red  blood  corpuscles. 

3.  The  pulse  is  slow  in  proportion  to  the  temperature. 

The  differential  diagnosis  has  to  be  made  from  camp  jaundice, 
enteric  jaundice,  septic  jaundice,  malarial  jaundice,  acute  yellow 
atrophy  of  the  liver,  typhus,  blackwater  fever,  pneumonia  with 
jaundice,  yellow  fever,  and  relapsing  fever. 

From  camp  jaundice  {icterus  castrensis  levis)  it  can  be  diagnosed 
by  the  sudden  onset,  the  severity  of  the  symptoms,  and  the  short- 
ness of  the  illness. 

From  enteric  jaundice,  which  is  rare,  it  may  be  recognized  by  the 
presence  of  the  polymorphonuclear  leucocytosis  and  the  absence 


1508  WAR  ZONE  FEVERS 

of  leucopenia,  and  the  usual  signs  of  enteric  fever,  while  blood  cul- 
tures fail  to  demonstrate  the  typhoid  bacillus  and  its  allies. 

From  septic  jaundice  it  can  be  separated  because  the  jaundice 
appears  at  an  early  and  not  at  a  late  stage  in  the  disease,  and  by 
the  absence  of  septic  infections  clinically  and  by  hsemoculture. 

From  malarial  jaundice,  and  especially  the  Weil's  disease-like 
type,  by  the  absence  of  the  malarial  parasites  in  numbers  and  by 
the  presence  of  the  slight  leucocytosis. 

From  acute  yellow  atrophy  by  the  absence  of  the  diminution 
of  urea  and  uric  acid,  by  the  absence  of  leucine  and  tyrosin  in  the 
urine,  and  by  the  increase  in  size  of  the  liver. 

From  typhus  by  the  absence  of  the  peculiar  facies,  of  the  sub- 
cuticular mottling  and  the  typical  rash,  and  by  the  presence  of 
jaundice,  which  is  only  occasionally  seen  in  that  disease. 

From  blackwater  fever  by  the  absence  of  haemoglobin  from  the 
urine. 

From  pneumonia  with  jaundice  by  the  absence  of  right-sided  lobar 
pneumonia. 

From  yellow  fever  by  the  pulse  being  rapid  from  the  first  and  falling 
as  the  temperature  falls. 

From  rMapjmgJ&u&r  by  the  absence  of  abundant  ordinary  spiro- 
chetes from  the  blood,  and  by  the  peculiar  characters  of  the  typical 
spirochetes  of  Weil's  disease  when  present  in  blood,  in  which  it  is 
found  only  in  small  numbers. 

Prognosis.- — This  is  serious,  the  death-rate  being  some  30  per  cent., 
and  convalescence  being  prolonged. 

Treatment. — The  repeated  subcutaneous  or  intravenous  injection 
of  20  to  60  c.c.  of  the  serum  prepared  by  Inada,  Ido,  Hoki,  Ito 
and  Wani  or  of  Martin  and  Pettit's  immunized  horse  serum  is 
recommended.  Salvarsan  and  its  allies  are  useless.  Symptomatic 
treatment  for  constipation  by  salines  and  aperients  is  also  to  be 
remembered. 

Prophylaxis. — Disinfect  the  urine  of  patients  for  some  nine  weeks 
from  the  onset  of  the  attack.  Catch  and  kill  rats.  Disinfect  the 
ground  of  the  endemic  area  or  remove  the  persons  from  this  area. 

ICTERUS  CASTRENSIS  LEVIS. 

Synonym. — Camp  jaundice. 

Definition. — A  slightly  febrile  disorder,  characterized  by  mild 
febrile  symptoms,  followed  by  a  mild  attack  of  jaundice  lasting 
some  two  to  eight  weeks,  after  which  there  is  a  very  prolonged 
convalescence. 

Remarks. — We  have  already  noticed  that  older  writers  have 
divided  Weil's  disease  into  two  types,  one  mild  and  the  other  severe. 
Camp  jaundice  represents  the  mild  form,  and  clinically  is  practically 
indistinguishable  from  catarrhal  jaundice.  It  was  very  common 
in  Eastern  war  zones,  and  its  symptomatology  may  be  divided  into 
the  pre-jaundice  period  and  the  jaundice  period. 


CLIMATOLOGY— DIAGNOSIS  1509 

Climatology. — It  was  common  in  Gallipoli,  the  Balkans,  Italy,  and 
France. 

etiology. — This  is  at  present  unknown.  Certain  authors  con- 
sider  it  to  be  of  paratyphoid  origin,  but  this  is  not  so.  Spirochetes 
have  been  described  in  the  urine  by  several  observers,  including 
one  of  us.  These  organisms  are  often  not  pathogenic  to  guinea-pigs, 
and  have  not  yet  been  demonstrated  to  be  the  cause  of  the  disease. 

Pathology. — It  would  appear  as  though  the  jaundice  was  due  to 
obstruction  to  the  common  bile  duct,  either  by  swelling  of  the 
duodenal  mucosa  or  to  mucus  in  the  duct. 

Symptomatology. — The  onset  is  gradual.  The  patient  feels  tired, 
complains  of  aches  in  various  joint  sand  muscles  for  weeks,  the  skin 
may  appear  to  be  normal,  and  the  temperature  is  either  normal  or 
not  very  high  (990  to  ioo°  F.).  The  patient  has  often  the  sensation 
of  suffering  from  very  high  fever,  while  on  taking  his  temperature 
he  may  find  it  normal  or  subnormal.  During  this  stage  very  often 
the  urine  is  darker  than  usual  and  contains  biliary  pigments.  We 
have  come  across  patients  feeling  fairly  well,  but  complaining  of 
what  they  called  rheumatism  for  months  before  the  jaundice 
appeared;  others  had  remarked  the  staining  of  their  shirts  by 
the  urine.  This  stage  may  last  for  several  weeks;  in  one  of  our 
cases  it  lasted  three  months  before  the  jaundice  appeared. 

The  Jaundice  Stage. — First  the  sclerotics,  then  the  skin,  slowly 
become  icteric.  The  degree  of  jaundice  is  seldom  so  marked  as  in 
cases  of  true  obstructive  j  aundice.  The  patient  generally  feels  abso- 
lutely done  up,  often  with  pains  and  aches  all  over  the  body;  as 
a  rule  there  is  very  little  or  no  pruritus,  in  contrast  to  so. many  other 
types  of  jaundice.  He  has  no  appetite,  and  may  feel  inclined  to 
vomit.  The  temperature  is  normal  or  subnormal,  pulse  usually 
slow,  but  may  be  of  normal  frequency;  the  spleen  generally  is  not 
palpable,  nor  is  the  liver  in  most  cases ;  there  may  be  pain  on  pressure 
in  the  region  of  the  gall-bladder,  but  this  is  not  a  constant  symptom. 
There  is  often  constipation,  and  the  stools  may  be  whitish  or  of  the 
usual  brownish  colour;  at  times  there  are  periods  of  diarrhoea, 
alternating  with  periods  of  constipation.  The  urine  is  scarce  and 
very  dark-coloured;  it  may  contain  a  trace  of  albumen  and  casts. 
The  jaundice  stage  lasts  between  two  and  eight  weeks.  Recovery  is 
slow,  and  for  weeks  and  months  after  the  jaundice  is  over  the  patient 
may  feel  very  weak. 

Diagnosis. — The  characteristic  features  of  the  disease  are: — 
(1)  Its  cpidemicity;  (2)  its  slow  onset;  (3)  its  long  course  divided 
into  a  pre-icteric  and  an  icteric  period. 

With  regard  to  the  differential  diagnosis,  it  can  be  separated  from 
catarrhal  jaundice  only  by  its  epidemicity. 

From  icterus  castrensis  gravis  (Weil's  disease)  it  can  be  differen- 
tiated by  the  mildness  of  the  symptoms,  by  the  slowness  of  the 
onset,  and  by  the  slight ness  or  absence  of  the  febrile  symptoms 
and  the  absence  of  haemorrhages. 

From  enteric  jaundice  it  can  be  separated  by  the  absence  of  enteric 


i5io  WAR  ZONE  FEVERS 

organisms,  as  shown  by  haemocultures,  and  by  the  absence  of  the 
enteric  serum  reactions  in  the  later  stages. 

From  malarial  jaundice  it  can  be  diagnosed  by  the  absence  of 
malarial  parasites  in  the  blood  and  also  by  the  absence  of  serious 
symptoms. 

Prognosis. — This  is  favourable  quoad  vitam,  but  the  course  of 
the  disease  may  be  prolonged,  and  for  weeks  and  months  the  patient 
may  be  very  depressed  and  weak. 

Treatment. — There  is  no  specific  therapy,  and  hence  treatment 
must  be  symptomatic,  with  rest  in  bed,  milk  diet,  and  urotropin 
in  io-grain  doses  three  times  a  day. 

Prophylaxis. — The  urine  and  faeces  should  be  disinfected. 

Nanukayami. 

A  seven-day  fever  resembling  a  typical  Weil's  disease  has  been 
reported  from  several  Japanese  observers  from  the  province  of 
Fukuoka.  Ido,  Ito  and  Wani  have  found  that  the  causative  agent 
is  a  spirochaete — S.  hebdomadis — which  is  serologically  distinct 
from  S.  icterohcemorrhagice.  The  normal  host  of  the  spirochaete 
seems  to  be  the  field-mouse,  Microtus  montebelli. 

REFERENCES. 

The  Tropical  Diseases  Bulletin  is  most  useful  for  the  diseases  of  the  war 
zones,  as  it  contains  not  merely  epitomes  of  English,  French,  Italian,  and 
Greek  papers,  but  also  those  written  by  Germans. 

Archibald,   Hadfield,  Lodgan,  and   Campbell   (1916).     Journal    of   the 

R.A.M.C.,  June. 
Arkwright,  Bacot,  and  Duncan  (1919).     Trans.  Soc.  Trop.  Med.  (Rickettsia 

in  Trench  Fever). 
Balfour  (1915).     Diseases  of  the  Mediterranean  War  Zone. 
Bradford,  Bashford,  and  Wilson  (1919).     Brit.  Med.  Journ.,  February  1. 
Buchanan  (1917).    Proceedings  Royal  Society  of  Medicine  (Certain  Epidemics 

of  the  Eastern  Campaigns),  vol.  ii.,  No.  2,  1-30. 
Byam,  Carroll,  Churchill,  Dimond,  Lloyd,  Sorapure,  and  Wilson  (1918). 

Trans.  Soc.  Trop.  Med. 
Carnot  and  Turquety  (191 7).     Les  maladies  d'importation  exotique  depuis 

la  guerre.     Paris. 
Castellani   (1917).     Journal  of  Tropical   Medicine  and  Hygiene,   July  16; 

August  1,   15;    September  1,   15;  October  1    (Diseases  of  the  Balcanic 

War  Zone). 
Castellani  (191 8).     Annali  Medicina  Navale. 
Dawson,  Hume  and  Bedson  (1917).     Brit.  Med.  Jour. 
Hurst  (1918).     Medical  Diseases  of  the  War.     Second  edition.     London. 
Ido,  Ito  and  Wani  (1918).     Jour.  Exper.  Med.  (Nanukayami). 
Inada,  Ido,  Hoki,  Kaneko,  Ito  (1916).     Jour.  Exper.  Med. 
Legroux  (1916).     C.  R.  Soc.  Biologie. 

Martin  and  Pettit  (1919).     Spirochetose  Icterohemorragique.     Paris. 
McNee,  Renshaw  and  Brunt  (1916).     Brit.  Med.  Jour.,  February  12. 
Noguchi  (1917).     Jour.  Exper.  Med. 
Rivas  (1917).     New  Orleans  Medical  and  Surgical  Journal  (Consequences  of 

the  European  War  from  a  Medical  Point  of  View).     London. 
Stokes  and  Ryle  (1916).    Jour.  Royal  Army  Med.  Corps,  vol.  xxvii.,  No.  3. 
Strong,  Swift,  Opie,  McNeal,  Baelzer,  Pappenheimer,  Peacock,  Rapport 

(1918).     Trench  Fever.     Oxford. 


CHAPTER  LX 
THE   DIAGNOSIS  OF  A  TROPICAL  FEVER 

Preliminary — Thermometric  pseudo-fever— Acute  fevers — Fevers  of  less  than 
eight  days'  duration — Fevers  of  more  than  eight  days'  duration — Chronic 
fevers — Summary . 

PRELIMINARY. 

The  method  of  diagnosis  contained  in  the  present  chapter  is  not 
intended  to  be  comprehensive,  and  the  reader  who  expects  to  find 
every  possible  situation  dealt  with  will  be  disappointed,  because 
this  is  not  our  intent,  and,  indeed,  would  be  a  practical  impossibility. 

We  are  endeavouring  to  place  before  him  such  information  as 
we  have  found  necessary  to  use  in  some  twenty-odd  years  of  tropical 
life,  and  we  may  perhaps  be  pardoned  if  we  mention  some  plain 
facts  before  starting  on  our  subject. 

Firstly,  we  trust  that  our  reader  will  realize  that  it  is  one  thing 
to  draw  up  a  nice-looking  scheme  of  diagnosis  upon  paper,  and  it  is 
quite  a  different  thing  to  give  a  system  which  will  be  applicable 
at  the  bedside;  but  no  one  knows  better  than  we  do  how  difficult  it 
is  to  write  a  system  so  applicable. 

Secondly,  we  trust  that  our  reader  has  not  forgotten  that  there 
is  such  a  thing  as  clinical  medicine — that  is  to  say,  a  system  of 
diagnosis  based  upon  the  bedside  examination  of  the  patient. 
In  our  opinion,  every  patient  should  be  most  carefully  examined, 
from  the  crown  of  his  head  to  the  soles  of  his  feet,  by  ordinary 
clinical  methods  before  any  attempt  is  made  to  utilize  the  resources 
of  the  laboratory. 

A  systematic  clinical  examination  of  every  patient  is  most 
essential.  It  is  the  sum  total  of  the  various  symptoms,  none 
alone  pathognomonic,  which  establishes  the  diagnosis  in  conjunc- 
tion with  which  the  results  from  the  laboratory  must  be  considered. 
A  practitioner  who  is  unable  to  come  to  some  sort  of  a  diagnosis 
without  the  aid  of  a  laboratory  should,  in  our  opinion,  utilize  his 
earliest  spare  moments  in  a  course  of  post-graduate  instruction 
with  regard  to  clinical  methods. 

Thirdly,  we  are  of  the  opinion  that  the  laboratory  work  should 
never  be  omitted  as  a  check  to  confirm  or  to  adjust  this  clinical 
diagnosis.  Specimens  sent  for  diagnosis  to  a  laboratory  should 
always  be  carefully  collected.  This  collection  should  at  least  be 
supervised  by  the  practitioner,  and  not  left  to  subordinates  entirely, 

*5" 


I5i 2  THE  DIAGNOSIS  OF  A   TROPICAL  FEVER 

otherwise  mistakes  will  be  possible.  The  specimens  should  always 
be  collected  and  forwarded  in  the  most  aseptic  method  possible, 
and  should  be  accompanied  by  a  statement  recording  the  nature 
of  the  specimen,  the  date  and  time  of  its  collection,  the  nature  of 
the  examination  desired  (which  should  not  be  vague — e.g.,  not 
'  urine  for  examination,'  but  clearly  stated,  '  urine  to  be  examined 
quantitatively  for  sugar  '),  and  a  brief  statement  of  the  salient 
features  of  the  case  and  the  suspected  clinical  diagnosis,  because 
it  is  the  duty  of  the  practitioner  to  help  the  laboratory  in  its  work. 
Finally,  we  desire  most  earnestly  to  impress  upon  the  reader 
that  the  essential  feature  in  the  diagnosis  of  a  tropical  fever  is  a 
combination  of  clinical  examination  with  laboratory  work. 

THERMOMETRICAL  PSEUDO-FEVER. 

The  practitioner  working  in  high  air  temperatures  should  re- 
member that  the  clinical  thermometer,  being  of  the  maximum 
type,  will  rise  quickly  to  some  temperature  corresponding  to  that 
of  the  air,  and  will  remain  thereat.  Mistakes  have  been  made,  such 
as  recording  a  number  of  cases  of  fever  in  an  institution.  In  high 
air  temperatures  the  thermometer  should  be  taken  out  of  cool 
water,  placed  in  the  patient's  rnouth,  left  there  long  enough  to 
record  the  actual  temperature,  and  then  quickly  replaced  into  cool 
water,  in  which  it  is  examined. 

The  practitioner  knows  well  the  precautions  re  hot  liquids  or 
solids  having  been  placed  in  the  mouth  before  the  thermometer, 
thus  giving  high  readings,  and  the  effect  of  draughts  falling  on 
the  cheeks  preventing  the  rise  of  the  mercury;  or,  in  other  words, 
of  the  possible  thermometrical  fallacies  of  which  these  are  examples. 

ACUTE  FEVERS. 

The  acute  fevers  may,  for  purposes  of  diagnosis,  be  divided  into 
those  which  have  lasted  less  than  eight  days,  and  those  which  have 
been  in  progress  eight  or  more  days  when  seen  by  the  practitioner. 

FEVERS  OF  LESS  THAN  EIGHT  DAYS'  DURATION. 

These  fevers  may  be  divided  into : — 

I.  Those  exhibiting  some  striking  physical  sign. 
II.  Those  not  exhibiting  any  striking  physical  sign. 

I.  WITH  SOME  STRIKING  PHYSICAL  SIGN. 

The  physical  signs  to  which  we  refer  may  be  classified  into: — 

A.  Traumatisms. 

B.  Skin  eruptions. 

C.  Derangement  of  some  bodily  system. 

D.  Localized  derangement  of  some  organ. 


TRAUMATISM— SKIN  ERUPTIONS  151 3 

A.  TRAUMATISM. 

The  presence  of  a  traumatism  suggests  that  an  acute  fever  may 
be  septic  in  nature,  but  in  the  tropics  no  one  should  forget  the 
possibility  of  the  fever  being  caused  by  the  reawakening  of  old 
malarial  infections,  or  even  being  associated  with  a  new  malarial 
infection,  acquired,  perhaps,  at  the  same  time  as  the  traumatism. 

If  the  fever  is  intermittent,  recurring  every  third  or  fourth  day, 
it  is  malaria.  If  it  is  quotidian,  pay  attention  to  the  following 
points:  If  the  spleen  is  hard  it  is  probably  malaria — make  a  blood 
film;  if  Laveran's  parasites  are  present  or  marked  mononucleosis, 
it  is  probably  malaria;  if  polymorphonuclear  leucocytosis  is 
present,  it  is  probably  septic  fever. 

If  the  evidence  is  in  favour  of  sepsis,  or  if  malaria  has  been  ex- 
cluded, bacteriological  examination  of  the  blood  and  of  the  local 
discharge  should  be  made,  and  should  include  search  for  aerobic 
and,  if  necessary,  anaerobic  organisms. 

B.  SKIN  ERUPTIONS. 
These  may  be  considered  under  the  following  headings: — 
r.  Erythematous  eruptions. 

2.  Papular  eruptions. 

3.  Urticarial  eruptions. 

4.  Purpuric  eruptions. 

5.  Vesicular  eruptions. 

6.  Bullous  eruptions. 

7.  Pustular  eruptions. 

8.  Pigmentation. 

1.  ERYTHEMATOUS  ERUPTIONS. 

(A)  Erythematous  Rash  Generalized. 
I.  The  rash  is  more  or  less  typical  of  scarlet  fever  : — 

(a)  Onset  of    eruption  less  than  forty-eight  hours  after  the 

appearance  of  the  sore  throat — Scarlet  fever. 

(b)  Onset  of  eruption  more  than  forty-eight  hours  after  the 

appearance  of  the  sore  throat — Erythema  or  dermatitis 
scarlatiniformis. 

(c)  Throat  symptoms  mild  or  absent : — 

(a)  Examine  blood  for  malarial  parasites: — 

1.  If  present — Malaria. 

2.  If  absent  inquire  into  drugs,  especially  quinine — 

Anaphylactic  drug  eruptions. 

II.  The  rash  has  some  maculo-papidar  elements  : — 

(a)  Coryza  and  Koplik's  spots  have  been  or  are  still  present — 

Measles. 

(b)  Coryza  and  Koplik's  spots  absent : — 

With  enlargement  of  the  occipital,  cervical,   and  other 
lymphatic  glands — German  measles. 


i5i 4  THE  DIAGNOSIS  OF  A   TROPICAL  FEVER 

III.  The  rash  has  the  characters  of  a  blush,  with  or  without  oedema  : — 

(a)  The  rash,  though  general,  is  more  marked  in  one  area : — 

i.  Evidence  of  a  bite  or  sting — Bite  or  sting  of  a  venomous 
animal. 

2.  No  such  evidence,  special  region  pits  on  pressure: — 
Examine    night     and    day   blood    for    microfilariae — 

Filar  iasis. 

3.  Macules  on  wrist  and  ankles  only  becoming  general 

on  third  day;  severe  symptoms;  yellow  tinge  in  con- 
junctivae. Occurs  in  Rocky  Mountains — Spotted 
fever  of  the  Rocky  Mountains. 

(b)  The  rash  is  not  specially  marked  in  one  area: — 
Examine  blood  for  eosinophilia  and  the  faeces,  after  a  purge, 

for  the  eggs  of  intestinal  worms — Helminth  infections. 

IV.  Erythema  fugitive,  faint,  annular,  most  marked  on  trunk  : — 
History  of  residence  in  Tropical  Africa.     Glands  in  posterior 

triangle  of  neck  enlarged.     Examine  gland  juice  and  blood 
for  trypanosomes — Sleeping  sickness. 

V.  Erythema  with  marked  cerebral  symptoms,  vomiting,  retraction  of 
head — Kernig's  sign. 

1.  Examine  the  blood  for  malarial  parasites,  if  present — 

Malaria. 

2.  If  absent,  perform  lumbar  puncture  and  examine  for 

meningococci — Epidemic  cerebrospinal  meningitis. 

VI.  Erythema  mild,  amounting  to  very  severe  blushing,  and  most 
marked  on  the  face : — 
Eyes  injected,  severe  pain  at  back  of  eyes,  high  fever.     Occurs 
in  locality  where  phlebotomus  is  endemic — Pappataci  fever. 

VII.  Erythema  with  little  or  no  fever ,  but  with  marked  gastro-intestinal 
symptoms  : — 
With  or  without  signs  of  collapse — Ptomaine  poisoning. 

(B)  Erythematous  Rash  Localized. 

I.   Rash  distributed  on  parts  exposed  to  light : — 

On  face,  neck,  and  hands,  often  feet;  associated  with  gastro- 
intestinal and  nervous  symptoms.  Fever  is  not  a  marked 
feature  of  simple  pellagra,  and  when  this  occurs  it  is  due  to  a 
complication,  generally  with  one  of  the  ent erica  group  of 
fevers — So-called  typho-pellagra. 

II.   Rash  not  specially  confined  to  parts  normally  exposed  to  light : — 
(a)  Associated  with  oedema  in  some  part : — 

1.  (Edematous  and  erythematous  areas  coincide,  (a)  Area 
defined  by  sharp  edges.  Sometimes  vesicles  present 
and  leucocytosis — Erysipelas.  (b)  Lymphatics  in- 
flamed, microfilariae  in  blood. — Filarial  lymphangitis. 


ERYTHEMATOUS  RASH  LOCALIZED  151 5 

2.  (Edema  of  face  and  eyelids  and  gastrointestinal  dis- 

turbance, eosinophilia,  and  leucocyiosis — Trichinosis. 

3.  No  oedema  of  the  face  and  eyelids.     Very  rare — Polymyo- 

sitis. 

4.  Swollen  area  affected  with  leprotic  eruption.     Signs  of 

leprosy  in  various  parts  of  the  body — Leprotic  fever. 

(b)  Not  associated  with  oedema : — 

1.  Severe  constitutional  symptoms  and  marked  backache; 

signs  of  vaccination  absent,  poor,  or  old.  Case  of 
smallpox  known  to  exist  in  neighbourhood — Suspect 
smallpox. 

2.  There  is  a  recent  wound  due  to  a  rat -bite,  or  a  history 

of  a  rat-bite  seven  to  twenty-one  days  previously, 
of  which  the  wound  may  have  healed.  Site  of  bite 
red  and  swollen,  becomes  ulcerated.  Enlarged 
lymphatic  glands.  Erythematous  eruption  with 
purple  spots — Rat-bite  fever. 

3.  History  of  a  cat-bite  some  ten  to  twenty-one  days 

before  illness;  maculae  around  site  of  bite  and  then 
on  limbs;  infiltration  of  skin,  enlarged  lymphatic 
glands.  Pains  in  muscles  and  joints.  Splenic  en- 
largement.    Fever  relapsing  in  type — Cat-bite  fever. 

4.  Pains  and  aches  all  over  the  body,  but  constitutional 

symptoms  not  very  severe.  Rash  appears  with  the 
fall  of  the  temperature  on  the  third  day.  No  malarial 
parasites  in  the  blood.  Stegomyia  (or  Culex)  mos- 
quitoes abundant.  Endemicity  of  dengue-like  fevers 
known — Dengue. 

2.  PAPULAR  ERUPTIONS. 

These  eruptions  often  form  part  of  the  evanescent  early  "symptoms 
ot  some  fever,  and  are  therefore  difficult  to  arrange  in  a  satisfactory 
manner.  The  practitioner  will  remember  that  drugs  like  iodides 
and  the  bromides  may  give  rise  to  papular  eruptions. 

I.  Catarrhal  symptoms  present : — 

Maculo-papular  eruption  tending  to  form  blotches.     Koplik's 
spots  present — Measles. 

II.  Catarrhal  symptoms  slight  or  absent : — 
(a)  Constitutional  symptoms  severe  : — 

1.  Markedly    severe    headache    and    backache.     Papules 

bright  red  and  shotty,  appearing  between  the  third 
and  fourth  day,  first  on  the  forehead — Smallpox. 

2.  In  a  child  which  has  been  ill  for  three  days  with  pain  all 

over  the  body  and  often  delirium  or  convulsions. 
Papules  about  the  size  of  a  pin's  head  on  chest,  back, 
and  abdomen—  Dengue  (Van  der  Scheer's  fever). 


1 5i 6  THE  DIAGNOSIS  OF  A    TROPICAL  FEVER 

3.  Pale  dusky  red  papules  or  macules,  fading  into  the 

normal  skin,  but  slightly  elevated,  disappearing  on 
pressure,  at  the  margins  of  the  axillae,  wrists,  flanks, 
chest,  back,  shoulders,  arms,  and  legs,  with  sub- 
cuticular mottling.  Exclude  malaria  by  blood 
examination — Typhus  fever. 

4.  Large  red  papules  on  face  on  the  fifth  to  seventh  day 

of  illness,  spreading  over  body  as  macules,  after  a 
visit  to  Akitaken  and  Nugataken,  of  the  Island  of 
Nippon,  Japan.  Enlarged  lymphatic  glands  in  some 
area  of  the  body,  and  a  few  vesicles  on  area  drained 
by  lymphatics  going  to  these  glands,  are  indicative 
of  bites  by  Microtrombidium  akamushi — Tsutsuga- 
mushi  fever. 

(b)  Constitutional  symptoms  not  severe  and  not  following  recent 

vaccination  : — 

1.  Rash    of    maculo-papules,    circular,    discrete;    not    as 

bright  or  as  elevated  as  measles.  No  Koplik  spots. 
Occipital  and  other  lymphatic  glands  enlarged. 
Pink  eye  present — German  measles. 

2.  Fever  slight  or,  at  times  of  epidemic,  absent  in  some 

cases.  Rash  general,  composed  of  bright  pinhead 
papules  or  red  macules  (i.e.,  morbilliform),  associated 
with  itching  and  with  a  few  macules  on  the  palms 
and  soles — Papular  fever  (Castellani  and  Chalmers). 

(c)  Constitutional  symptoms   not  severe,  following  recent  vac- 

cination y — 
Rash  composed  of  papules  and  papulo-vesicles,  of  large 
pinhead  size,  appearing  some  seven  to  nine  days  after 
vaccination — Vaccine  lichen. 

3.  URTICARIAL  ERUPTIONS. 

(a)  Fever    slight,    after    ingestion    of    certain    foods — Febrile 

urticaria. 

(b)  Worms  present — Helminthic  febrile  urticaria. 

4.  PURPURIC  ERUPTIONS. 
Purpuric  puncta  may  be  caused  by  flea-bites  and  pediculi,  and 
have  nothing  to  do  with  the  fever.  Many  drugs,  ptomaine  poison- 
ing, and  snake-bite  produce  purpuric  spots  or  patches.  Very  rarely 
serum  injections  produce  purpuric  eruptions  about  seven  to  nine 
days  after  the  injection.  The  leukaemias,  chronic  alcoholism, 
Bright 's  disease,  and  jaundice,  may  be  associated  with  purpuric 
rashes.  In  fevers  as  a  rule  it  points  to  septicaemia,  and  is  more  of  a 
prognostic  than  of  a  diagnostic  value,  even  in  epidemic  cerebro- 
spinal meningitis,  in  which,  in  our  tropical  experience,  it  is  rare. 
Peliosis  rheumatica,  with  its  associated  tonsillitis  and  pains  in  the 
joints,  is  very  rare.  It  will  be  remembered  that  in  scurvy  there  is 
no  fever.     With  these  provisos  we  make  the  following  suggestions: — 


PURPURIC  ERUPTIONS  151 7 

Clear  signs  of  the  disease  causing  the  purpuric  eruption: — 

(a)  Yellow  tinge  in  skin  or  eyes: — 

1.  Urine  black  from  haemoglobin — Blackwater  fever. 

2.  Urine  without  haemoglobin: — 

(a)  Bile  in  the  urine : — 

fi.)  Examine  blood  and  urine  for  the  peculiar 
spirochete  with  its  central  minute 
waves — Icterus  casirensis  gravis  (Weil's 
disease) . 

(ii.)  Spirochetes  of  doubtful  pathogenicity  may 
be  present  or  they  may  be  absent;  little 
or  no  fever — Non-febrile  jaundice  (camp 
jaundice) . 

(b)  Bile  not  in  urine : — 

Severe  fever;  examine  blood  for  malarial  para- 
sites— Malarial  fever. 
(C)   Albumen  in  urine  .' — 

Epigastric    tenderness.       Faget's    sign — Yellow 
fever. 

[b)  Without  yellow  tinge  in  the  skin  or  eyes:- — 

1.  Retraction  of  head.     Kernig's  sign  present.     Lumbar 

puncture  reveals  meningococci — Epidemic  cerebro- 
spinal meningitis. 

2.  With    developed    disease — e.g.,    typhoid,    diphtheria, 

scarlet  fever,  smallpox,  measles  (hemorrhagic 
conditions  known  in  the  tropics)- — Septicemic 
condition. 

3.  With  buboes  or  marked  pneumonic  symptoms.     Ex- 

amine blood  culturally,  sputum  and  fluid  from  en- 
larged lymphatic  glands  microscopically,  for  plague 
bacilli — Plague . 

4.  Without  marked  signs  of  any  disease.     Blood  culture 

— Septicemia. 

5.  VESICULAR  ERUPTIONS. 

The  practitioner  will  be  on  his  guard  to  exclude  vesicles  which 
are  the  result  of  bites  of  insects,  such  as  sand-flies  and  mosquitoes, 
as  well  as  those  due  to  the  ingestion  of  drugs,  such  as  bromides 
and  iodides.  Also  the  pyoses,  which  are  without  fever.  Among 
these,  pyosis  corletti  causes  bullae. 

I.  Onset  with  severe  constitutional  disturbance: — 

Rash  on  third  to  fourth  day;  shotty  papules  becoming  vesicles 
fifth  to  sixth  day.  Vesicles  circular,  tense,  umbilicated, 
and  multilocular — Smallpox. 

II.  Onset  with  mild  constitutional  symptoms,  but  with  severe  local  pain, 
generally  along  a  nerve,  but  in  any  case  confined  to  one  region : — 


1518  THE  DIAGNOSIS  OF  A   TROPICAL  FEVER 

Rash  a  couple  of  days  or  more  after  commencement  of  the  pain. 
Usually  confined  at  first  to  painful  region,  and  then  becomes 
general,  but  may  be  general  from  first.  Vesicles  dome- 
like or  flattened,  become  umbilicated;  no  inflammatory 
areola;  leave  scars —  Vesicular  fever  (Castellani  and 
Chalmers). 

III.  Onset  mild  and  without  severe  local  pain,  without    history  of 

recent  vaccination  : — 

Rash  on  first  to  third  day.  Often  first  sign  of  illness.  Appears 
on  back,  chest,  and  abdomen.  First  in  form  of  pale  red 
macules,  often  with  raised  centre,  quickly  developing  into 
superficial  unilocular  vesicles,  some  of  which  may  become 
umbilicated — Chicken-pox. 

IV.  Onset  mild,  history  of  vaccination  twelve  to  twenty-two  days  or 

more  before  eruption  : — 

Generalized  vesicular  eruption,  not  umbilicated  at  first,  and 
preceded  by  a  papular  rash.     Vesicles  become  umbilicated 

— Generalized  vaccinia. 

6.  BULLOUS  ERUPTIONS. 

Bullous  eruptions  ma}'  be  caused  by  plants  and  drugs.  In  newly- 
born  children  bullae  on  the  hands  and  feet  suggest  congenital 
syphilis. 

I.  There  is  a  well-defined  raised  erythematous  area  upon 
which  the  bullae  are  present.  Bullae  to  be  examined 
for  streptococci- — Erysipelas. 
II.  No  such  area  present,  but  wounds,  enlarged  lymphatic 
glands,  with  severe  constitutional  symptoms,  common 
in  the  tropics.  Examine  blood  and  bullae  for  organisms 
— Septic  pemphigus. 
III.  In  recently-born  children  examine  bullae  for  strepto- 
cocci and  other  pyogenic  organisms  —  Pemphigus 
neonatorum. 

7.  PUSTULAR  ERUPTIONS. 

It  will  be  remembered  that  there  are  pustular  syphilides  un- 
attended by  fever,  and  pustular  tuberculides  of  which  fever  is  not 
a  marked  sign. 

I.  Clear  history  of  recent  vaccination  with  Jennerian  vaccine :  — 

Small  dark-coloured  or  black  centre  in  the  vaccine  area, 
surrounded  by  dark  reddish  swollen  area,  on  which  are  the 
vaccinial  vesicles  and  pustules.  Around  this  a  bluish  area, 
the  whole  surrounded  by  a  wide  erythematous  blush — 
Gangrenous  vaccinia. 


PIGMENTATION— BODY  SYSTEMS  1519 

II.  No  history  of  recent  vaccination: — 

{a)  Localized  red  swelling,  with  several  points  of  suppuration. 
Examine  bacteriologically  for  cocci — Carbuncle. 
Localized  red  solid  swelling,  with  black  centre,  and  round 
it  pustules  often  mixed  with  vesicles  and  bullae.     Ex- 
amine bacteriologically  for  Bacillus  anthracis — Malignant 
pustule, 
(b)   Generalized  pustular  eruption  in  a  patient  who  has  been 
seriously  ill  for  six  days  or  more,  with  at  times  swelling 
of  eyelids,  lips,  or  eyes — Smallpox. 

8.  PIGMENTATION. 

In  acute  fevers  the  important  cutaneous  pigmentation  is  the 
yellow  tinge  due  to  jaundice.  This  is  rare  in  malaria  and  in  the 
early  stages  of  the  enteric  fevers,  and  hence  need  only  be  mentioned. 
For  blood  pigments  in  the  skin  see  the  purpuric  eruptions,  and  for 
black  pigmentation  see  the  chronic  fevers. 
I.  Liver  and  spleen  one  or  both  enlarged : — 

(a)  Abdominal  tenderness.     Typical   spirochetes  in   blood — 

Relapsing  fevers. 

(b)  Abdominal  tenderness  not  marked  :• — 

1.  Peculiar  spirochetes  in  blood  and  urine — Weil's  disease. 

2.  No  spirochetes  in  the  blood: — 

(A)  Hemoglobinuria — Blackwater  fever  and  its  allies. 
(b)  No  hemoglobinuria,  severe  symptoms,  albumin- 
uria, black  vomit,  etc— Yellow  fever. 

II.  Liver  and  spleen  not  enlarged : — ■ 

(a)  Symptoms  mild.     Fever   slight   or   absent.     No   signs  or 

symptoms  of  pneumonia — Icterus  castrensis  levis  (camp 
jaundice). 

(b)  Physical  signs  and  symptoms  of  pneumonia.     Pneumo- 

coccus  in  sputum — Pneumonia. 

C.  BODY  SYSTEMS. 

Fevers  associated  with  some  marked  sign  or  symptom  directing 
attention  to  a  given  system  of  the  body  may  be  arranged  according 
to  the  system  deranged  as  follows: — 

A.  Derangements  of  the  Alimentary  Canal. 

B.  Derangements  of  the  Respiratory  System. 

C.  Derangements  of  the  Circulatory  System. 

D.  Derangements  of  the  Urinary  System. 

E.  Derangements  of  the  Generative  System. 

F.  Derangements  of  the  Lymphatic  System. 

G.  Derangements  of  the  Muscular  System. 
H.  Derangements  of  the  Osseous  System. 

I.    Derangements  of  the  Connective  Tissue. 
J.    Derangements  of  the  Nervous  System. 


1520  THE  DIAGNOSIS  OF  A   TROPICAL  FEVER 

A.  Symptoms  pointing  to  the  alimentary  canal : — 
I.  Mouth  and  Throat ; — 

(a)  Pyorrhoea,  marked  gingivitis,  or  even  the  presence  of 

bridges,  crowned  or  stopped  teeth,  with  pain, 
shrinking  of  the  gums,  etc.- — Septic  fever. 

(b)  Angina  with  whitish   or   greyish   membrane   on  the 

fauces  or  tonsils: — 

Examine  bacteriologically : — 

1.  Streptococci  present — Streptococcal  angina. 

2.  Klebs-Loeffler  bacilli  present — Diphtheria. 

3.  Fusiform  bacilli  present — Vincent's  angina. 

II.  Stomach : — ■ 

(a)  Black  vomit : — 

Associated  with  jaundice,    Faget's  sign,  and   severe 
constitutional  disturbance — Yellow  fever. 

(b)  Vomiting,  pain  and  tenderness  in  diaphragmatic  region. 

Severe  constitutional  symptoms,  with  or  without 
hiccough;  passage  of  blood  per  anum — Poisoning 
with  viperine  venom  or  phlegmonous  inflammation  of 
the  stomach. 

III.  Intestines  c — 

(a)  Choleraic  diarrhoea,  or  profuse  diarrhoea,  or  dysenteric 
diarrhoea  with  fever. 

Examine  blood : — 

1.  Malarial  parasites — Pernicious  malaria. 

2.  Marked    mononucleosis    with    enlargement    of    the 

spleen  :■ — 
Splenic  or  hepatic  puncture  : — 

(A)  Malarial  parasites — Pernicious  malaria. 

(B)  Kala-azar  bodies — Kala-azar. 

3.  Eosinophilia    without    enlargement    of    the    spleen. 

Blood  cultures — Intestinal  septicemias  or  toxcemias 
due  to  worms. 

{b)  Vague  bowel  symptoms  or  signs  of  intestinal  schisto- 
somiasis. Examine  faeces  for  eggs  and  blood  for 
eosinophilia — Fevers  due  to  intestinal  worms. 

(c)  Pain  in  the  appendicular  region — Appendicitis. 

(d)  Slight  diarrhoea  or  constipation.     General  disturbance 

of  health  slight  or  moderately  severe. 

Examine  motions  for : — 

1.  Amoebae— Amebiasis. 

2.  Enteric    bacilli.     Confirm    by    blood    cultures — 

Enter  0  idea. 


BODY  SYSTEMS  1521 

B.  Symptoms  pointing  to  the  respiratory  system  : — 
I.  Nose: — 

(a)  Acute  rhino-pharyngitis  : — 

Examine  secretion  microscopically  and  culturally: — 

1.  Spirochetes— Spirochetal  rhino-pharyngitis. 

2.  Micrococcus  catarrhalis  and  similar  organisms 

— Common  cold. 

3.  Influenza  bacillus  or  filterable  virus  present — 

Influenza. 

4.  Influenza  baccillus,   or  filterable  virus  with 

Streptococci— Streptococcal  complications  of 
influenza. 

(b)  Nose  partially  blocked : — 

Examine  swabs  microscopically  and  cultural^  for  the 
Klebs-Loefflcr  bacillus — Diphtheria. 

(c)  Larynx  : — 

More  or  less  stridor.     Examine  swabs  of  throat  for 
Klebs-Loeffler  bacillus — Diphtheria. 

(d)  Bronchi : — 

Signsof  bronchitis,  withorwithout  blood  inthe  sputum. 
Examine    fresh    sputum   microscopically,    and    if 
necessary  by  the  dark  ground  illumination: — 

1.  Eggs — Paragonimiasis. 

2.  Spirochetes — Bronchospirochcetosis. 

3.  Fungi — Bronchomycosis. 

4.  Acid-fast  organisms: — 

(A)  Tubercle  bacilli — Tuberculosis. 
(b)  Nocardia — Pulmonary  Nocardiasis. 

(e)  Lungs  and  pleura  : — 

Physical  signs  of  inflammation  of  the  lungs  or  pleura, 
or  both : — 

1.  Expectoration       chocolate  -  coloured  —  Liver 

abscess. 

2.  Expectoration    bloody    or    rusty.     Examine 

microscopically  for  the  same  points  as  under 
bronchi  and  for  the  pneumococcus — Pneu- 
monia. 

3.  Expectoration    not     chocolate-coloured     nor 

bloody — Diseases  of  lungs  and  pleura  other 
than  above. 
C.  Symptoms  pointing  to  the  circulatory  system  ' — 

1.  Marked  collapse  after  exposure  to  great  heat  (especially 

associated  with  high  atmospheric  humidity)  or  to  the 
sun's  rays.  There  may  or  may  not  have  been  ini.  ial 
fever — Heat  syncope. 

2.  Disturbed  action  of  the  heart,  with  severe  constitu- 

tional symptoms  and  petechial  eruption — Infective 

endocarditis. 

96 


1522  THE  DIAGNOSIS  OF  A   TROPICAL  FEVER 

D.  Symptoms  pointing  to  the  urinary  system  : — 

(a)  Urine  black,  due  to  haemoglobin: — 

i.  Following  on  a  dose  of  quinine — Quinine  hemo- 
globinuria. 

2.  With  malarial  parasites  in  numbers  in  blood — 

Malarial  hemoglobinuria. 

3.  Not  associated  with  quinine  or  malarial  parasites 

in  numbers  in  the  blood — Blackwater  fever. 

4.  Associated  with  the  administration  of  some  drug 

such  as  chlorate  of  potash  for  a  sore  throat — 
Toxic  hemoglobinuria. 

(b)  Suppression  or  marked  diminution  of  the  urine: — 

Differentiate  by  the  history  of  the  case,  the  region  of 
infection,  the  presence  or  absence  of  Faget's  sign, 
black  vomit,  etc. — Blackwater  fever  or  Yellow  fever. 

(c)  Passage  of  large  quantities  of  urine: — 

Examine  for  malarial  parasites  or  other  signs  of 
malaria- — e.g.,  enlarged  and  tender  spleen- — 
Pernicious  malaria. 

(d)  Bile  in  the  urine: — 

1.  Associated  with  haemoglobin — Blackwater  fever. 

2.  Not  associated  with  haemoglobin: — 

(a)  In  epidemic  form: — 

Examine  blood  and  urine  for  spirochaetes. 
(i.)  Mild  cases — Icterus  castrensis  levis. 
(ii.)  Severe   case   with   haemorrhages- — 
Icterus   castrensis  gravis   {Weil's 
disease). 

(b)  Not  in  epidemic  form: — 

No  spirochaetes.  During  or  after  an  attack 
of  typhoid  or  paratyphoid  fever — Bacillary 
jaundice  [Enteric  jaundice) . 

E.  Symptoms  pointing  to  the  reproductive  system  : — 

(a)  Chill,  sudden  pain  and  swelling  along  the  spermatic 
cord,  with  often  severe  fever,  but  no  erysipelatous 
appearance  of  the  skin — Endemic  funic ulitis. 

{b)  Fever  after  childbirth.  Examine  the  aseptically 
collected  uterine  dis  harge  for  streptococci  and 
other  organisms — Puerperal  fever. 

F.  Symptoms  pointing  to  the  lymphatic  system  : — 

(a)  Cervical  glands  enlarged : — 

1.  Most  marked  on  the  left  side,  associated  with 
obstinate  constipation  and  mild  symptoms. 
Puncture  of  glands  reveals  no  organisms — 
Pfeiffer's  glandular  fever. 


BODY  SYSTEMS  1523 

2.  Most  marked  in  the  posterior  triangles  of  both 

sides  of  the  neck.  History  of  residence  in  sleep- 
ing sickness  areas.  Glandular  fluid  obtained  by 
puncture  shows  trypanosomes  —  Trypanosomi- 
asis. 

3.  Enlarged  glands  in  neck  and  other  parts.     (Edema 

of  face  with  characteristic  crepitation.  Fugitive 
cedemas  in  various  parts.  Enlarged  and  tender 
spleen.  Enlarged  liver.  Increase  in  size  of  the 
thyroid  gland.  Residence  in  Tropical  South 
America— Chagas'  disease. 

(b)  Lymph  glands  anywhere  enlarged : — 

4.  Pain    in  some  lymph  glands ;    tender,    enlarged, 

freely  movable  under  skin.  Search  area  drained 
by  lymphatics  going  to  gland  for  circular  vesicle 
or  small  black  or  brownish  necrotic  area  indica- 
tive of  a  bite.  Puncture  of  glands  shows  no 
bipolar  plague  bacilli.  History  of  residence  in 
the  Akitaken  and  Nugataken  of  the  Island  of 
Nippon,  Japan — Tsutsugamushi  disease. 

(c)  Inguinal  or  axillary  glands  enlarged: — 

5.  Acute  onset,  high  fever,  great  prostration.     Punc- 

ture of  glands  reveals  plague  bacilli — Plague. 

6.  Gradual  onset,  slight  fever.     Very  mild  symptoms, 

malaise,  pain  on  walking.  Inguinal  or  crural 
glands  enlarged,  hard,  very  painful  on  pressure. 
Puncture  shows  sterile  fluid — Climatic  bubo. 

7.  Glands  enlarged,  inflamed,   or  suppurating,  with 

chancre  on  penis,  septic  wound,  or  ulcer  or 
gonorrheal  infection — Septic  infections. 

8.  Occurring  in  the  course  of  one  of  the  enteroidea 

fevers — Intestinal  infections. 

9.  High    fever,    lymphangitis,    associaced    with    an 
j  erysipelatous    condition    of    the    skin.     Blood 

examination  during  night  (or  during  the  day  in 
•  ertain  cases)  reveals  microfilaria  —  Filarial 
lymphadenitis. 

G.  Symptoms  pointing  to  the  muscular  system  : — 

(a)  Remittent    or    intermittent    fever,   with   rheumatoid 

pains  and  abscesses  in  various  parts  of  the  body — 
Myositis  purulenta  tropica. 

(b)  Remittent    fever,    with    rheumatoid    pains,    but    no 

abscess     formation.     (Edematous     patches     often 
present,  marked  eosinophilia — Trichinosis. 
H.  Symptoms  pointing  to  the  osseous  system  :■ — 

(a)  Pain  and  tenderness,  especially  near  a  joint — Osteo-. 

myelitis. 


1524  THE  DIAGNOSIS  OF  A   TROPICAL  FEVER 

(b)  Sudden  attack  of  fever,  with  great  tenderness  over, 
and  pain  in,  the  os  calcis  or  other  tarsal  bone,  which 
begins  to  increase  in  size — Endemic  enlargement  of 
the  os  calcis. 

I.  Symptoms  pointing  to  the  connective  tissue: — 

Rigors  with  fever  and  aching  or  dragging  sensation,  and 

outline  of  a  worm  under  the  skin  of  affected  area — 

Dracontiasis. 
J.  Symptoms  pointing  to  the  nervous  system : — 

(a)  Almost  any  acute  sign  or  symptom  pointing  to  the 

nervous  system,  including  signs  of  mania,  melan- 
cholia, or  dementia,  and  associated  with  fever,  with 
or  without  enlargement  of  the  spleen.  Examine 
blood  for  malarial  parasites  or  mononucleosis — 
Malaria. 

(b)  Signs  of  meningitis  present — e.g.,  Kernig's  sign,  re- 

traction of  the  head,  etc.  Examine  cerebro-spinal 
fluid:— 

i.  Polymorphonuclear  leucocytes  and  cocci  present — 
Epidemic  cerebro-spinal  meningitis. 

2.  Trypanosomes  present;  also  in  juice  from  enlarged 
neck  glands.  Residence  in  Tropical  Africa — 
Sleeping  sickness. 

(c)  Signs  of  acute  alcoholism: — 

If  picked  up  by  the  police,  even  if  there  is  a  smell  of 
alcohol,  examine  spleen  and  take  blood  films  if 
necessary.  Drunk  or  dying  in  the  tropics  is  often  a 
question  of  alcoholism  or  malaria.  Fever  may  be 
absent  in  both  instances — Acute  alcoholism  or 
malaria. 

D.  DERANGEMENT  OF  SOME  ORGAN. 

The  signs  and  symptoms  associated  with  some  organ  of  the  body 
may  be  considered  under  the  following  headings: — 

i.  The  Spleen. 

2.  The  Liver. 

3.  The  Pancreas. 

4.  The  Suprarenal  Capsules. 

5.  The  Parotid. 

A.  The  spleen  : — 

I.  Enlargement  slight : — 
Rose-coloured    spots    on    the    abdomen.     Symptoms    of 
typhoid  fever.     Make  blood  cultures  and  faecal  cultures 
— Enter  oidea  fevers. 


DERANGEMENT  OF  SOME  ORGAN  1525 

II.  Enlarged  and  tender  : — • 

(a)  Examine  blood  films  for  malarial  parasites  and  for 

spirochsetes— Malaria  or  Relapsing  fevers. 

(b)  With   oedema   of  the   face   and   enlargement    of   the 

thyroid  and  lymphacic  glands  and  liver.  Residence 
in  South  America — Chagas'  American  trypano- 
somiasis. 

III.  Enlargement  considerable  : — 

(a)  Generally  a  history  of  illness  lasting  some  time,   of 

which  present  fever  is  only  a  recurrence.  Firm 
enlargement.  Malarial  parasites  in  blood — Exacer- 
bation oj  chronic  malaria. 

(b)  No  malarial  parasites  in  the  blood: — 

Great  increase  in  white  blood  cells  with  myelocytes — 
Leukcemia. 

(c)  No  malarial  parasites  and  no  great  increase  of  leuco- 

cytes in  the  blood: — 

1.  Splenic    or    hepatic     puncture     shows    Leishman- 

Donovan  bodies — Kala-azar. 

2.  Shows     no     Leishman-Donovan     bodies  —  Febrile 

splenomegaly. 

3.  Toxoplasma  bodies  present — Toxoplasmosis. 

B.  The  liver : — 

Enlarged  and  tender: — 

1.  Pain  in  the  right   shoulder,  rigidity  of  right  rectus, 

diminution  of  movement  of  right  side  of  the  dia- 
phragm. Examine  motions  for  amoebic  cysts  and 
the  blood  for  mononucleosis  (present)  and  malarial 
parasites  (absent) — Amoebic  liver  abscess. 

2.  Signs   of    severe    septic    infection,    jaundice,    etc.     If 

origin  of  sepsis  not  evident,  examine  faeces  for  intes- 
tinal worms  and  for  cnteroidea  micro-organisms — 
Multiple  septic  liver  abscesses. 

3.  Slight  yellowish  tinge  in  the  sclerotic,  seldom  signs  of 

general  jaundice.  Patient  not  seriously  ill.  No 
amcebiasis — Tropical  liver. 

C.  The  pancreas  : — 

I.  With  intense  pain  in  the  upper  and  left  part  of  the  abdomen, 
which  is  distended  with  gas;  vomiting  and  constipation — 
Acute  pancreatitis. 

II.  Signs  and  symptoms  of  diabetes;  threatened  Kussmaul's 
coma.  Recurrent  attacks  of  fever  every  other  day. 
Examine  for  malarial  parasites;  if  absent  and  if  only 
polymorphonucleosis  give  a  few  doses  of  quinine  and 
note  action  on  fever — Malaria  and  diabetes. 


1526  THE  DIAGNOSIS  OF  A   TROPICAL  FEVER 

D.  Suprarenal  capsules  .* — 

Signs  suggestive  of  acute  peritonitis —  i.e.,  high  fever,  distended 
tympanitic  abdomen,  quick  pulse.  No  effusion  into  abdo- 
minal cavity.  Examine  blood  for  malarial  parasites  and  for 
mononucleosis.  If  absent,  give  quinine  and  again  test  blood 
— Acute  malaria  attacking  suprarenals. 

E.  Parotid  glands  : — 

Painful   tender    swelling    of   parotid,  especially   if   bilateral — 

Mumps. 

II.  ACUTE  FEVERS  WITHOUT  STRIKING  PHYSICAL  SIGN. 

A   Patient  is  carrying  on  his  ordinary  work : — 

I.  Fever  is  intermittent,  every  third  or  fourth  day.  Examine 
spleen  for  enlargement  and  tenderness,  and  examine  blood 
for  malarial  parasites  and  mononucleosis,  which  may  be 
absent.  Clinical  symptoms  alone  may  be  positive — 
Malarial  fevers. 

II.  Fever  is  quotidian.  Examine  spleen  for  tenderness  and 
enlargement.  Examine  blood  for  malarial  parasites 
and  mononucleosis.  If  none,  give  quinine  and  note 
action  on  fever — Malaria. 

III.  No  malarial  parasites,  and  quinine  therapy  without  effect : — 

(a)  Pulse  dicrotic;  slow  in  proportion  to  the  temperature. 

History  of  several  days'  indisposition.  Tongue 
furred,  constipation,  or  diarrhoea.  Gurgling  on 
pressure  in  right  iliac  region.  Make  blood  and 
fffical  cultures,  and  examine  for  enteroidea  organisms 
— Enter oidea group  of 'fevers. 

(b)  Pulse  not  dicrotic;  slow  in  proportion  to  the  tempera- 

ture. Attack  sudden,  with  at  first  pain  and  tender- 
ness, which  later  disappear  in  the  region  of  the 
appendix.  No  malarial  parasites  in  blood — Gan- 
grenous appendicitis. 

(c)  Abrupt  onset,  catarrhal  symptoms,  with  sensation  of 

considerable  illness  and  with  generalized  pains,  often 
in  epidemic  form — -Influenza. 

(d)  With  or  without  signs  of  bronchitis,  enlargement  of 

liver  and  spleen,  or  with  signs  of  broncho-pneumonia. 
Examine  sputum  for  tubercle  bacilli,  or  if  lung 
symptoms  absent  test  cuti-reaction — Acute  phthisis 
or  tuberculosis. 

(e)  Gradual  onset,   temperature  increasing   every  night. 

Headache  and  rheumatoid  pains  in  body  and  limbs. 
Tongue  furred.  Blood  cultures  for  M.  melitensis 
and  M .  paramelitensis — Undid ant  fever. 


ACUTE  FEVERS  WITHOUT  STRIKING  PHYSICAL  SIGN     1527 

B.  Patient  unable  to  carry  on  his  usual  duties  : — 

(a)  Liver  and  lymphatic  glands  enlarged.      Spleen   not    en- 

larged. Examine  blood.  Signs  of  great  destruction  of 
red  blood-corpuscles  (presence  of  Bartonella  bacilliformis) . 
Residence  in  Peru — Oroya  fever. 

(b)  Sudden  onset,  with  injected  conjunctivae  (pink  eye),  high 

fever,  comparatively  slow  pulse.  Severe  rheumatoid 
pains.  Liver  and  spleen  normal.  Patient  irritable, 
with  pain  in  head  and  eyes,  and  may  be  delirious. 
Endemic  area  iorPhlebotomus  flies — Pappataci  fever. 

(c)  Sudden  onset,  with  severe  pain  in  some  part  of  the  body 

or  all  over  the  body.  With  or  without  enlargement  of 
the  lymph  glands,  with  generally  a  maculo-papular  erup- 
tion on  the  third  or  fourth  day.  Conjunctivae  injected. 
Fauces  congested.  Pulse  increases  proportionately  with 
the  fever.  Endemic  area  for  stegomyia  (perhaps  also 
for  Culex  fatigans) — Dengue  fever. 

(d)  Sudden  onset.     Hyperesthesia  over  shins.     Pains  in  the 

legs.  Often  slight  splenic  enlargement.  Mononucleosis 
in  blood.  May  or  may  not  be  history  of  association  with 
lice.  Blood  examination  excludes  malaria,  relapsing 
fever,  etc. — Trench  fever. 

(e)  Sudden  onset,  with  or  without  rigors  and  pains.     Examine 

blood  for  malarial  parasites— Malaria. 

(f)  Gradual  onset.     Signs  of  enteric  fever.     Make  blood  and 

faecal  cultures — Enteroidea  group  of  fevers. 

(g)  Blood  examination  reveals  marked  polymorphonuclear  in- 

crease. Examine  gums,  teeth,  ear,  nose,  throat,  fingers, 
toes,  bones,  and  every  orifice  of  the  body,  for  possible 
source  of  infection;  make  blood  cultures — Septicemia. 

(h)  Blood  examination.  Examine  night  and  day  blood  for 
microfilariae — Filar  iasis. 

(i)  Examine  faeces  for  intestinal  eggs,  especially  after  a  purga- 
tive— Toxcemias  due  to  intestinal  worms. 

(j)  Gradual  onset,  with  marked  pains  in  the  joints,  profuse 
sweating,  high  fever,  and  relatively  slow  pulse.  Furred 
tongue — Undul ant  fever. 

(k)  Sudden  onset,  with  hyperpyrexia,  delirium,  or  coma  asso- 
ciated with  high  atmospheric  temperatures — Thermic 
fever  (heat-stroke). 

(I)  Sudden  onset,  with  or  without  history  of  fever.  Syncope 
associated  with  high  atmospheric  temperatures — Heat 
syncope. 


1528  THE  DIAGNOSIS  OF  A   TROPICAL  FEVER 

FEVERS  OF   MORE  THAN    EIGHT  DAYS' 
DURATION. 

Fevers  of  more  than  eight  days'  and  less  than  six  weeks'  duration 
may  be  classified  as  follows: — 

A.  Fever  of  intermittent  type  : — 

With  malarial  parasites  or  pigment  in  blood  or  with  enlarged 
spleen : — 

I.  Fever  every  day — Quotidian  malaria. 

II.  Intermittent  fever  every  third  day — Tertian  malaria. 

III.  Intermittent  fever  every  fourth  day — Quartan  malaria. 

B.  Fever  of  the  relapsing  type  : — 

I.  Without  malarial  parasites  or  pigment,  and  not  reacting 
to  quinine  therapy.  Intervals  between  attacks  several 
days.  During  attack  spirochetes  in  blood — Relapsing 
fevers. 

II.  With  malarial  parasites  and  no  signs  of  spirochetes,  and 
reacting  to  quinine  therapy — Malaria. 

III.  Without  parasites,  and  only  one  or  two  relapses;  not 
reacting  to  quinine  therapy.  After  a  long  fever  pre- 
sumed or  proved  to  be  enteroidea  in  type.  Examine 
faeces  and  urine  for  enteroidea  organisms — Enteroidea 
type  of  fever. 

C.  Fever  remittent  or  continuous  : — 

I.  Reacting  to  quinine  therapy — Malaria. 
II.  Not  reacting  to  quinine  therapy. 

A.  WITH  MARKED  PHYSICAL  SIGNS. 

i.  Well-defined  local  pain  and  tenderness  : — 

Examine  blood  films.  Leucocytosis,  blood  cultures,  urine 
cultures.  Lastly,  examine  cerebro-spinal  fluid  (earlier 
if  head  or  spine  symptoms) — Septicemias  or  toxemias 
due  to  foci  of  deep  suppuration. 

2.  Signs  of  lung  disease  : — ■ 

Examine  sputum: — 

(a)   Tubercle  bacilli — Tuberculosis, 
{b)    Other    organisms    and    signs    of    pneumonia — 
Broncho-pneumonia. 

3.  Organic  cardiac  murmurs  : — 

With  or  without  petechial  eruptions.  Signs  of  gonorrhoea 
or  rheumatism — Infective  endocarditis. 

4.  Nervous  symptoms  : — 

Pain  in  the  head,  retraction  of  the  head.  Kernig's  sign. 
Examine  cerebro-spinal  fluid — Meningitis. 


WITH  MARKED  PHYSICAL  SIGNS  1529 

5.  Skin  eruptions  : — 

(a)  Rose-red  spots — Enteric  fevers. 

(b)  Flushing  of  the  face,  with  subcuticular  mottling  and 

severe  symptoms.     Typical  eruption  on  fourth  day — 
Typhus  fever. 

(c)  Purulent  discharge  from  nose.      Bulls,  nodules,  and 

ulcers    in     skin,    with    papulo-pustular     eruption. 
Work  with  horses — Glanders. 

(d)  Pustular  eruption — Glanders. 

(e)  Dark  or  black  pigmentation — Addison's  disease. 

6.  Enlarged  lymphatic  glands— Hodgkin's  disease. 

7.  Tenderness   in    a   bone,    especially   near    a   joint.     Blood 

cultures — Osteomyelitis. 

8.  Nodules  and  tenderness  in  muscles.     Puncture  the  nodules 

and  examine: — 

(a)  Pus — Purulent  myositis. 

(b)  Filaria — Filariasis. 

9.  Splenic  enlargement : — 

Examine  blood: — 

(a)  Marked  increase  of  lymphocytes  or  leucocytes  with 

myelocyt  es—Leukcemia . 

(b)  Malarial    parasites    or    pigment    in  leucocytes — 

Malaria. 
Splenic  or  hepatic  puncture  : — 

(a)  Malarial  parasites  or  pigment — Malaria. 

(b)  Leishmania  parasites— Kala-azar. 

(c)  Absence  of  Leishmania  parasites — Splenomegaly, 

febrile  form. 

(d)  Toxoplasma  bodies  present — Toxoplasmosis. 

B.  WITHOUT  MARKED  PHYSICAL  SIGNS. 

A.  Intermittent  fevers  : — 

I.  Fever  every  third  or  fourth  day — Malaria. 
II.  Fever  every  day.     Examine  blood : — 

1.  Malarial  parasites  or  distinct  mononucleosis — Malaria. 

2.  Malarial  parasites  absent;    distinct  pohymorpholeuco- 

cytosis — Septic  fevers. 

B.  Relapsing  fevers  : — 

Fever  for  several  days  after  period  of  apyrexia — Relapsing 
fevers. 

C.  Remittent  and  continuous  fevers  : — 

I.  Benefited  by  quinine,  with  or  without  parasites  in  blood — 
Malaria. 


1530  THE  DIAGNOSIS  OF  A   TROPICAL  FEVER 

II.  Not  benefited  by  quinine: — 

(a)  Test  the  serum  reactions  for  typhoid  and  the  para- 

typhoids, and  the  other  common  enteroide  organ- 
isms of  the  period  and  locality.  Confirm  by  blood 
cultures — large  quantities,  10  ex.,  of  blood  taken 
at  night — or  by  faecal  cultures — Enteroidea  group. 

(b)  Test  for  Mediterranean  fever  by  serum  reactions  and 

blood  cultures — Undulant  fever. 

(c)  Culture  of  aseptically  collected  urine — Pyelitis. 

(d)  Examine  motions  for  eggs  of  intestinal  worms — In- 

testinal toxesmias  due  to  worms. 

(e)  Wassermann  reaction — Syphilis. 

(/)  Cuti  reaction  for  tuberculosis — Tuberculosis. 

(g)  Other  causes  having  been  excluded.  Bodily  tempera- 
ture 99°-ioi°  F. ;  shows  only  slight  rise  once  a  day- 
Patient  indisposed  during  the  attack — Low  inter- 
mittent fever. 

(h)  Patient  residing  in  locality  with  high  atmospheric 
temperatures.  Patient  not  indisposed  during  the 
attack — Low  heat  fever. 

(i)  Same  as  in  (g),  but  in  children  with  higher  tempera- 
tures, i03°-i04°  F.,  or  more — High  intermittent 
fevers. 

CHRONIC   FEVERS. 

By  the  term  '  chronic  fevers  'we  mean  those  which  continue  longer 
than  six  weeks. 

A.  Intermittent  in  type  : — 

I.  Occurring  every  third  day,  with  enlargement  of  the  spleen 
and  malarial  parasites,  or  yielding  to  quinine  therapy — 
Tertian  malaria. 

II.  Occurring  every  fourth  day,  with  enlargement  of  the 
spleen,  and  malarial  parasites  or  pigment  in  the  blood, 
or  yielding  to  quinine  therapy — Quartan  malaria. 

III.  Occurring  every  day,  with  enlargement  of  the  spleen  and 
malarial  parasites,  yielding  to  quinine  therapy — 
Quotidian  malaria. 

B.  Relapsing  in  type  : — 

Attacks  of  fever  lasting  a  few  days,  separated  by  intervals  of 
several  days,  with  severe  symptoms.  Examine  blood  for 
spirochetes.  If  necessary,  inject  monkeys  and  examine 
blood  during  an  attack  of  fever  for  spirochetes — Relapsing 
fevers. 


CHRONIC  FEVERS  1531 

Remittent  or  continuous  in  type  : — 

I.  Benefited  by  quinine  therapy — Malaria. 
II.  Apparently  not  benefited  by  quinine  therapy: — 

(a)  Ulcers  or  tumours  present  in  some  part  of  the  body. 

Examine  thoroughly,  including  nose,  naso-pharynx, 
and  all  apertures  of  body.  Especially  examine  the 
teeth,  particularly  crowned  teeth  or  bridges.  Ex- 
amine fingers  and  toes  carefully — Septic  infection  or 
absorption. 

(b)  Cutaneous  dark  pigmentation  a  marked  feature  : — 

1.  Examine  spleen  for  enlargement   and  blood  for 

malarial   parasites    or    mononucleosis.     Insuffi- 
cient quinine  administered — Malaria. 

2.  Fever    generally    absent.     No    signs    of    malaria. 

Vomiting  at  times.     Weakness,  etc. — Addison's 
disease. 

(c)  Splenic  enlargement  a  marked  feature  :— 

I.  Examine  blood  films: — 
No  malarial  parasites  seen. 

(a)  Marked  increase  in  white  cells,  lymphocytes, 

or  with  myelocytes — Leukcemia. 

(b)  Having   excluded  leukaemia,   but  not  before, 

examine  blood  obtained  by  splenic  punc- 
ture:— 

1.  Malarial  pigment  or  parasites  present — 

Malaria. 

2.  Leishman-Donovan  bodies  present — Kala- 

azar. 

3.  Leishman  -  Donovan     bodies     absent  — 

Febrile  splenomegaly. 

4.  Toxoplasma-like    bodies    present — Toxo- 

plasmatic febrile  splenomegaly. 

5.  All  parasites  absent — Pseudo-kala-azar. 

(d)  (Edema  a  marked  feature  :—- 

I.  Examine  blood  for  malarial  pigment,  parasites, 
or  mononucleosis,  and  the  spleen  for  enlarge- 
ment— Chronic  malaria. 

II.  No  signs  of  malaria: — 

(A)  Examine  motions  for  eggs  of  intestinal 
worms,  especially  ancylostoma  ova  — 
Ankylostomiasis. 

(b)  No  eggs  or  signs  of  worms.  In  South 
America.  Examine  blood  during  an  attack 
of  fever  for  trypanosomes — Chagas' 
disease. 


1532  THE  DIAGNOSIS  OF  A    TROPICAL  FEVER 

(e)  Intestinal  indigestion  a  marked  feature  : — 

I.  Examine  motions  after  test-meal  for  muscle 
fibres,  fat  globules;  extract  fat.  Examine  urine 
for  Cammidge's  reaction.  Fever  not  a  marked 
symptom — Chronic  pancreatitis. 
II.  Attacks  of  fever  a  marked  symptom.  No  muscle 
fibres,  etc.,  in  motions.  No  Cammidge's  urin- 
ary reaction.  Examine  fseces  after  a  purge  for 
eggs  of  intestinal  worms,  and  if  absent,  for 
micro-organisms  of  proteus  and  allied  groups — 
Intestinal  infections  and  loxcemias  in  helmin- 
thiasis. 

(/)  Enlarged  lymphatic  glands  a  marked  feature  : — 

I.  Fever  not  a  marked  feature:  glands  very  much 

enlarged  in  many  parts  of  the  body.  No  very 
great  increase  in  the  number  of  leucocytes — 
Hodgkin's  disease. 

II.  Attacks  of  fever  a  marked  feature.     Glands  only 

moderately  enlarged,  especially  in  the  posterior 
triangles  of  the  neck.  Residence  in  Tropical 
Africa.  Examine  gland  juice  for  trypanosomes 
— Sleeping  sickness. 

Summary. 

This  small  sketch  of  the  diagnosis  of  certain  tropical  fevers  may 
be  found  useful  when  read  in  conjunction  with  the  preceding 
chapters.  We  would,  however,  again  emphasize  the  point  that 
the  only  method  of  diagnosing  fevers  is  by  long  bedside  experience, 
associated  with  careful  laboratory  work. 


SECTION    B 
GENERAL   DISEASES 

DIVISION.  I:  CAUSATION,  ANIMAL  PARASITES. 
Subdivision  A:  Due  to  Parasitic  Protozoa. 

Framboesia  Tropica. 
Verruga  Peruviana. 
Rhinosporidiosis  and  Sarcosporidiosis. 

Subdivision  B:  Due  to  Parasitic  Worms. 

Paragonimiasis. 
Katayama  Disease. 
Filariasis. 

Subdivision  C:  Due  to  Parasitic  Arthropods. 

Myiasis. 
Porocephalosis. 

DIVISION  II.:  CAUSATION,  VEGETAL  PARASITES. 

Leprosy. 
Histoplasmosis. 

DIVISION  III.:  CAUSATION,  CHEMICAL. 
Subdivision  A:  Due  to  Chemical  Deficiency. 
Beri-Beri  and  Epidemic  Dropsy. 

Subdivision  B:  Due  to  Poisons. 
Tropical  Poisonings. 

DIVISION  IV.:  CAUSATION,  UNKNOWN. 
Pellagra. 


1533 


CHAPTER  LXI 
FRAMBCESIA   TROPICA 

Synonyms  —  Definition  —  History  —  Geographical  distribution  —  ^Etiology— 
Histopathology — -Symptomatology  —  Diagnosis —  Prognosis — Treatment 
— Prophylaxis — References. 

Synonyms. — In  the  British  Colonies  the  disease  is  usually  called 
'  yaws  ';  in  the  French  colonies  '  pian.'  In  Venezuela  and  other 
South  American  countries  the  name '  bubas  '  is  much  used.  German 
and  Italian  authors  generally  use  the  term  '  Frambcesia,'  which  was 
first  used  by  Sauvage  in  1750  on  account  of  the  raspberry-like 
appearance  of  the  eruptive  elements.  Charlouis  in  1882  suggested 
the  term  'Polypapilloma  tropicum';  Noc,  Stevenel,  and  Iman 
introduced  the  term  '  Castellani's  spirochetosis,'  Da  Matta  'Cas- 
tellani's  treponemosis/  and  Violle  the  term  'cutaneous  spirochae- 
tosis.'  Other  local  names  are  '  gattoo  '  (West  Coast  of  Africa), 
'  dubi '  (Gold  Coast),  '  framosi '  (Calabar),  '  ab  oukine  '  (Gaboon), 
'  nkoulou,'  'tetia'  (Congo  Coast),  '  momba  '  (Angola),  '  parangi ' 
(Ceylon),  '  buena  '  (Burma),  '  puru  '  (Borneo,  Federated  Malay 
States),  '  patek  '  (Dutch  Indies),  'tonga'  (New  Caledonia  and 
Loyalty  Islands),  'coco'  (Fiji),  '  tona  '  (Tonga  Island),  '  lupani 
tono '  (Samoa),  '  galis  pateros '  (some  parts  of  the  Philippine 
Islands),  '  ki-mo  '  (French  Indo-China). 

Definition.— A  tropical  specific  infectious  and  contagious  disease 
caused  by  Treponema  pertenue  Castellani,  and  characterized  by 
framboesiform  granulomatous  eruption. 

History. — It  has  been  suggested  by  Hume,  Adams,  and  others  tha 
frambcesia  was  the  disease  which  afflicted  the  Israelites  during  then 
emigration  from  Egypt,  and  that  therefore  the  term  '  saraat  ' 
in  the  thirteenth  chapter  of  Leviticus  does  not  mean  leprosy,  as 
usually  translated.  Ali  Abbas  and  Avicenna,  who  wrote  at  the 
end  of  the  tenth  century,  mention  a  disease  called  '  safat,'  or 
'  sahafati,'  with  symptoms  not  unlike  those  of  frambcesia;  but  most 
authors  are  of  the  opinion  that  the  disease  referred  to  by  the  two 
Arabian  physicians  was  syphilis.  The  study  of  the  disease  first 
began  to  engage  the  attention  of  European  physicians  after  the 
discovery  of  America.  Oviedo  y  Valdez  (1478-1557)  describes  it  in 
his  work,  '  Historia  General  e  Natural  de  las  Indias.'  Piso  (1648) 
refers  to  the  malady  in  his  work,  '  De  Medicina  Brasiliensis.'  Roche- 
fort  (1656),  Raymond  Breton  (1665),  and  Labat  (1694),  report  it 
from  the  West  Indies,  stating  that  it  occurs  frequently  among  the 

1535 


1536  FRAMBCESIA   TROPICA 

natives  (Caribs),  who  called  it '  pyans,'  or  '  yaya.'  Bontius,  in  1718, 
reported  that  frambcesia  was  endemic  not  only  in  the  West  Indies, 
but  also  in  Java,  Sumatra,  and  other  Dutch  colonies  of  the  East, 
where  it  was  known  by  the  name  of  '  anboyna  pox,'  or  '  pimple.' 
In  the  days  of  the  slave-trade,  outbreaks  of  frambcesia  frequently 
occurred  in  the  crowded  ships  carrying  African  slaves  to  America. 
Special  hospitals  for  the  isolation  and  treatment  of  slaves  suffering 
from  the  disease  were  built  on  all  the  important  estates  in  the  West 
Indies.  Occasionally  in  the  countries  in  which  it  is  endemic  the 
disease  may  increase  to  such  an  extent  as  to  cause  veritable  epi- 
demics. An  example  of  such  an  epidemic  occurred  in  Dominica  in 
1871,  when  two  special  segregation  hospitals  had  to  be  built  for 
frambcesia  patients. 

In  1769  an  outbreak  of  a  peculiar  disease  occurred  in  Scotland. 
It  was  called  '  sibbens,'  or  '  sivvens  '  (sivvi,  Celtic  for  raspberry), 
and  was  apparently  imported  by  sailors  belonging  to  a  vessel  coming 
from  the  West  Indies,  which  was  wrecked  off  Wigton  in  Cumberland. 
The  so-called  '  button  scurvy  '  of  Ireland,  endemic  there  in  the 
eighteenth  and  the  beginning  of  the  nineteenth  centuries;  the 
'  radesyge,'  which  broke  out  in  Sweden  and  Norway  in  1710;  and 
the  '  mal  de  chicot  '  in  Canada,  have  likewise  been  considered  by 
some  writers  to  be  forms  of  frambcesia. 

Several  authors  have  endeavoured  to  distinguish  between  '  yaws,' 
'  pian,' '  boubas,'  and  '  parangi ' ;  but  those  who  have  had  the  oppor- 
tunity to  study  the  disease  in  different  countries  have  all  come  to 
the  conclusion  that  '  yaws,'  '  pian,'  '  boubas,'  and  '  parangi,'  are 
simply  different  names  for  the  same  disease,  though  of  course  each 
of  these  terms  is  often  used  by  natives  to  cover  several  closely 
allied  conditions.  The  term  '  boubas,'  for  instance,  is  used  by  the 
inhabitants  of  Brazil  for  various  ulcerative  conditions,  such  as 
frambcesia,  leishmaniasis,  and  blastomycosis,  but  most  of  the 
medical  South  American  authorities  use  it  as  a  synonym  for  fram- 
bcesia. Unfortunately,  Breda  used  it  to  denote  a  form  of  leish- 
maniasis, and  caused  much  confusion.  The  experimental  researches 
of  one  of  us  in  cases  of  frambcesia  contracted  in  different  parts  of 
the  world  (tropical  America,  East  and  West  Africa,  etc.)  show  that 
'  yaws,'  '  pian,'  '  boubas,'  and  '  parangi,'  are  merely  synonyms, 
but  it  is  possible  that  there  may  be  several  varieties  of  the  spiro- 
chete which  is  the  cause  of  the  disease. 

Since  the  time  of  Labat  several  authors  have  upheld  the  syphilitic 
nature  of  frambcesia.  This  theory  was  supported  at  one  time  by 
Sir  J.  Hutchinson.  In  recent  times  the  disease  has  been  investi- 
gated, both  clinically  and  experimentally,  by  a  large  number  of 
observers. 

In  1882  Charlouis  proved  by  actual  experiment  that  syphilis  and 
frambcesia  are  two  different  maladies.  The  clinical  investigation  of 
the  disease  by  Numa  Rat  was  also  of  great  value.  His  report, 
published  in  1891,  has  become  classical. 

Among  the  more  recent  observers  who  have  investigated  the 


GEOGRAPHICAL  DISTRIBUTION 


1537 


disease  in  various  parts  of  the  tropics  arc  Ncisscr,  Daniels,  Wellman, 
Jeanselme,  Powell,  Braush,  Martin,  Halberstadter,  von  Prowazek, 
Ashburn,  J.  Craig,  Nichols,  Strong,  Flu,  Noc,  Stevenel,  Iman, 
Da  Matta,  Spronk,  Shennan,  Schiiffner,  Maul,  and  many  others. 

Geographical  Distribution. — Frambcesia  is  essentially  a  tropical 
disease,  as  few,  if  any,  genuine  cases  have  been  reported  from 
places  outside  the  tropical  and  subtropical  zone,  and  in  the  tropics 
it  is  never  found  on  the  mountains  and  cold  districts,  as  we  remarked 
in  the  previous  editions  of  this  manual.  Bahr  states  that  cases 
who  have  contracted  the  disease  at  a  higher  elevation  than  800  feet 
are  very  rare.  At  the  present  time  a  skin  disease  not  unlike 
frambcesia  has  been  reported  from  Greece  by  several  writers. 


Fig.  085.- — -Distribution  of  Frambcesia  Tropica. 

Africa. — The  disease  till  recently  was  said  to  be  very  rare  in 
the  northern  regions  of  the  continent,  though  some  cases  were 
reported  from  Algeria;  the  researches  of  Gabbi  and  Sabella  have 
demonstrated,  however,  that  it  is  common  in  Tripoli.  It  is  appar- 
ently rare  in  Egypt,  though,  according  to  some  writers,  it  is 
observed  fairly  frequently  in  the  Sudan.  It  is  very  common  on 
the  West  Coast,  especially  on  the  Gaboon  River,  in  the  Congo  Free 
State,  and  in  Angola.  The  disease  is  quite  common  in  Nigeria. 
It  is  also  found  in  Mozambique,  in  Madagascar,  and  the  Comoro 
Islands.  In  Uganda  and  the  region  of  the  Great  Lakes  it  is  occa- 
sionally met  with.  It  has  been  noted  among  the  Kaffirs  in  South 
Africa,  near  Kimberley,  by  Griffith,  and  by  many  other  observers 
in  several  other  districts  of  South  Africa,  Rhodesia,  and  Nyasaland. 

Asia. — The  disease  is  very  common  in  the  Malay  Peninsula, 
Assam,  Upper  Burma,  Siam,  Java,  Batavia,  and  is  extremely 
frequent  in  Ceylon,  where  the  number  of  cases  treated  in  the 
Government  Hospitals  during  the  last  ten  years  has  been  on  the 
average  3,500  per  year,  and  it  must  be  noted  that  the  patients 
treated  in  hospitals  represent  only  a  small  portion  of  all  the  cases. 

97 


I538  FRAMBCESIA   TROPICA 

In  India  it  is  very  rare,  though  small  outbreaks  of  the  disease 
have  been  described  by  various  observers.  It  occurs  in  certain 
parts  of  China,  but  is  unknown  in  Japan  and  the  central  and  western 
regions  of  the  Asiatic  continent.  It  is  present  in  the  Philippine 
Islands. 

America. — It  is  very  common  in  the  West  Indies,  and  occurs  in 
British  Guiana,  Venezuela,  Colombia,  and  Brazil.  Cases  have  been 
reported  from  the  southern  United  States,  but  never  from  the 
northern  States  nor  from  Canada.  Recently  Wood  has  recorded 
a  case  in  a  white  child  in  North  Carolina. 

Australasia. — The  disease  is  present  in  Northern  Australia,  and 
occurs  frequently  in  many  of  the  Pacific  Ocean  islands — Samoa, 
New  Hebrides,  New  Caledonia,  and  Fiji.  It  is  absent  in  New 
Zealand  and  Tasmania. 

etiology. — Different  kinds  of  bacteria  have  been  described  as 
causative  agents  of  framboesia.  Eijkman  found  some  .peculiar 
bacilli:  Pariez  observed  numerous  micrococci;  Powell,  in  1896,  culti- 
vated from  two  cases  a  yeast;  Nicholls  and  Watts,  in  1899,  isolated 
a  coccus  which,  inoculated  into  animals,  failed  to  reproduce  the 
disease.  In  February,  1905,  Castellani  observed  a  Treponema,  or 
spirillum,  as  he  thought  it  at  the  time.  This  organism,  which  he 
called  T.  pertenue,  is  now  generally  admitted  to  be  the  cause  of  the 
disease.     For  the  description  of  the  organism,  see  p.  457. 

Incidence  of  the  T.  pertenue  in  Framboesia  Lesions. — The  presence 
of  the  Treponema  is  constant  in  the  primary  lesion  and  in  the  un- 
broken papules  of  the  general  eruption.  It  may  be  found  in  the 
spleen,  lymphatic  glands,  and  bone-marrow.  In  the  blood  it  has 
not  yet  been  demonstrated  microscopically,  though  there  is  no 
doubt  that  the  blood  of  the  general  circulation  is  infectious,  inas- 
much as  monkeys  inoculated  with  it  develop  typical  yaws  lesions 
in  which  the  Treponema  is  abundantly  present.  The  Treponema  is 
absent  in  the  cerebro-spinal  fluid,  and  generally  in  the  tertiary 
lesions. 

Bacteriological  Flora  found  in  Open  Sores  of  Framboesia. — While 
T.  pertenue  is  the  only  germ  found  in  the  non-ulcerated  lesions,  the 
ulcerated  lesions  of  framboesia  are  soon  invaded  by  all  kinds  of  germs. 
Apart  from  innumerable  bacteria,  various  kinds  of  spirochetes  are 
present.  One  form  is  rather  thick,  and  takes  up  the  stain  easity. 
It  is  morphologically  very  similar  to  the  Spirochata  refringens  of 
Schaudinn.  Another  form  is  thin,  delicate,  with  coils  varying  in 
size  and  number,  and  with  blunt  extremities— S.  obtusa  Castellani. 
A  third  form  is  likewise  thin  and  delicate,  but  tapers  at  both  ends 
— S.  acuminata  Castellani;  T.  pertenue  is  also  present  in  many 
cases. 

Inoculation  Experiments  of  Framboesia  in  Man.- — Paulet,  in 
1848,  inoculated  fourteen  negroes  with  the  secretion  taken  from 
frambcetic  granulomata.  All  of  them  developed  frambcesia,  the 
inoculation  period  varying  from  twelve  to  twenty  days,  when  at 
the  seat  of  inoculation  in  ten  cases  the  first  nodule  appeared,  soon 


MTIOLOGY 


1539 


followed  by  a  typical  general  eruption.     In  two  cases  apparently 
the  eruption  did  not  start  from  the  seat  of  inoculation. 

Charlouis,  in  1881,  inoculated  thirty-two  Chinese  prisoners,  who 
had  never  suffered  from  the  disease,  with  crusts  and  scrapings  from 
a  case  of  yaws.  The  disease  developed  in  twenty-eight  of  them, 
beginning  invariably  at  the  seat  of  inoculation.  Moreover,  he 
inoculated  a  native  suffering  from  typical  yaws  with  syphilis.  The 
inoculation  was  quite  successful,  a  primary  syphilitic  sore  develop- 
ing, followed  by  all  the  usual  types  of  secondary  eruption.  That 
yaws  patients  are  not  immune  against  syphilis  is  proved  also  by 
Powell  and  Nichols  and  others,  who  have  described  several  cases 
of  syphilis  supervening  on  yaws.  Syphilitic  patients  may  contract 
frambcesia  naturally  and  experimentally. 

Inoculation  Experi- 
ments in  Monkeys  and 
Other  Animals. — Neis- 
ser,  Prowazek,  Halber- 
stadter  in  Java,  and 
shortly  afterwards  Cas- 
tellani  in  Ceylon,  have 
shown  that  monkeys 
are  susceptible  to  fram- 
boesia. According  to 
their  experiments,  the 
inoculation  period  varies 
from  a  minimum  of  six- 
teen days  to  a  maxi- 
mum of  ninety-two. 
The  appearance  of  the 
lesions  developing  at  the 
seat  of  inoculation  is 
practically  the  same  in 
all  cases — viz.,  an  infil- 
trated spot  slowly  in- 
creasing   in     size,    and 

soon    becoming    moist,    the   secretion  drying  into  a  thick  crust. 
Removal  of  the  crust  exposes  a  raw,  granulating,  red  surface. 

In  the  monkeys  of  a  low  class  (genus  Macacus,  genus  Semnopi- 
thecus)  the  eruption  is,  as  a  rule,  localized  to  the  seat  of  inoculation. 
The  infection,  however,  is  general,  as  is  proved  by  the  presence  of 
T.  pertenue  in  the  spleen  and  lymphatic  glands  besides  the  local 
lesions.  Halberstadter  has  obtained  a  general  eruption  in  ourang- 
outangs.  According  to  Castellani's  experiments,  splenic  blood,  ob- 
tained by  puncturing  the  spleen  of  a  patient  affected  with  fram- 
bcesia,  can  reproduce  the  disease  in  monkeys.  The  inoculation  of 
the  blood  of  the  general  circulation  also  may  occasionally  produce 
the  disease.  The  inoculation  of  cerebro-spinal  fluid  into  normal 
monkeys  has  always  proved  negative. 

Neisser,  Halberstadter,  von  Prowazek  in  Java,  and  later  Castellani 


Fig.  686.- 


-MONKEY    INOC 

Frambcesia. 


1540  FRAMBCESIA    TROPICA 

in  Ceylon,  have  proved  that  monkeys  successfully  inoculated  with 
framboesia  do  not  thereby  become  immune  to  syphilis,  and,  vice 
versa,  monkeys  successfully  inoculated  with  syphilis  do  not  thereby 
become  immune  to  framboesia.  According  to  Levaditi,  monkeys 
immunized  for  yaws  do  not  acquire  any  immunity  for  syphilis,  but 
monkeys  immunized  for  syphilis  ma}'  acquire  a  partial  immunity 
for  framboesia.  According  to  Ashburn  and  Craig,  monkeys  of  the 
species  Cynomolzus  philippinensis  are  susceptible  to  frambcesia, 
but  not  to  syphilis. 

The  following  facts  are  in  favour  of  the  T.  pertenue  being  the 
specific  cause  of  framboesia: — 

i.  In  the  non-ulcerated  papules,  in  the  spleen,  in  the  lymphatic 
glands  of  framboesia  patients,  as  well  as  in  inoculated  monkeys, 
the  T.  pertenue  is  the  only  organism  present.  No  other  germ 
can  be  demonstrated  either  microscopically  or  by  cultural 
methods. 

2.  The  extract  of  framboesia  material  containing  the  T.  pertenue, 
but,  so  far  as  our  present  methods  of  investigation  permit  us  to  say, 
no  o+her  germs,  is  effective  when  inoculated  into  monkeys. 

3.  The  extract  of  frambcesia  material  from  which  the  T.  pertenue, 
has  been  removed  by  filtration  becomes  inert,  and  monkeys  inocu- 
lated with  it  do  not  contract  the  disease. 

Predisposing  Causes. — As  is  the  case  in  other  infectious  diseases, 
dirt  and  other  insanitary  conditions  favour  to  a  certain  extent 
the  development  and  dissemination  of  the  disease.  The  malady 
is  rare  among  Europeans,  and  also  among  the  better-class  natives, 
who  live  amidst  good  sanitary  surroundings,  while  it  is  very 
common  among  the  villagers  and  low-caste  natives,  who  live  in 
uncleanly  overcrowded  huts.  Sex  does  not  exercise  any  influence, 
nor  does  age  to  any  great  extent,  though  the  disease  is  more  fre- 
quently met  with  in  children  and  young  people.  The  native  prac- 
titioners of  Ceylon  are  inclined  to  ascribe  an  important  predis- 
posing influence  to  certain  foods.  Some  incriminate  a  kind  of 
fish  called  '  balla  mal,'  others  a  cereal  known  as  '  kurrakan.' 
Daprey  inculpates  in  the  West  Indies  the  abuse  of  mango  fruit. 

Histopathology. — The  histopathology  of  frambcesia  has  been  in- 
vest igaied  by  Unna,  Macleod,  Jeanselme,  PI  elm,  and  more  recently 
by  Schuffner,  Marshall,  Shennan,  Siebert,  Ashburn,  Craig,  and  Lohe. 
In  the  frambcetic  papidcs  the  surface  epithelium  is  greatly  increased 
in  thickness,  and  numerous  elongated  down-growths  arc  seen.  The 
epithelial  layers  show  many  patches,  in  which  the  epithelial  cells  are 
swollen,  vacuolated,  and  degenerating.  Small,  sharply  circum- 
scribed areas  are  also  seen  containing  polymorphonuclear  leucocytes 
and  detritus.  The  layers  near  the  corium  and  its  processes  are, 
however,  almost  normal  in  appearance.  The  connective-tissue 
corium  forms  a  thin  layer,  from  which  narrow,  elongated,  papillary 
processes  pass  into  the  epithelium,  some  of  them  nearly  reaching 
the  surface.  Tiie  corium  is  the  seat  of  marked  oedema.  There  is  a 
diffuse  cellular  infiltration  made  up  of  polymorphonuclear  leuco- 


HI  STOP  A  THOLOG  Y—S  YMPTOMA  TOLOGY 


i54i 


cytes,  large  and  small  mononuclear  leucocytes,  eosinophils,  plasma 

cells,  mast  cells,  connective-tissue  cells,  and  some  extravasated 

erythrocytes.     In  the  older  nodules  the  plasma  cells  are  present 

in  such  enormous  numbers  as  to  dominate  all  the  others.     Macleod 

has  shown  that  there  is  no  perivascular  mononuclear  infiltration 

so  characteristic  of   syphilis,  nor 

any    endothelial    proliferation    in 

the  vessel  walls.     The  frambcetic 

lesion  also   differs   from   that    of 

syphilis  in  affecting  the  epithelium 

rather  than  the  cutis,  in  the  more 

considerable   oedema,  and   in  the 

absence,    as  a  rule,    of   the  giant 

cells. 

When  the  frambcetic  granulo- 
mata  have  reached  a  certain  stage, 
a  very  well-marked  hyperkera- 
tosis is  noticeable.  One  of  us  has 
called  attention  to  the  appearance 
of  the  films  taken  in  the  usual 
way  from  the  granulomata,  and 
stained  according  to  Leishman's 
method.  In  such  films  it  is  inter- 
esting to  note  the  presence  of  a 
large  number  of  polychromatic 
red  blood  cells  of  very  different 
sizes,  some  much  larger  than  the 
normal  erythrocytes,  some  much 
smaller.  They  are  stained  deep 
or  light  blue  instead  of  pink,  and 
sometimes  have  a  granular  appear- 
ance. The  leucocytes  present  in 
the  films  frequently  contain  in 
their  protoplasm,  and  sometimes 
in  their  nuclei,  roundish  or  oval, 
more  or  less  deeply  blue  stained 
bodies,  which  are  probably  poly- 
chromatic micro- erythrocytes  en- 
gulfed by  phagocytes.  Some  of 
these  bodies  present  peculiar 
chromatin  dots.  In  such  films 
the  Treponemata  are  almost  con- 
stantly found.     The  Treponemata 

may  be  put  in  evidence  also  in  sections  by  using  the  Volpino- 
Bertarelli  or  Levaditi's  silver  staining,  as  used  by  Spronk,  Shennan, 
and  Schuffner.  The  examination  of  sections  so  stained  shows  that 
the  parasite  is  mostly  found  in  the  epithelial  layers. 

Symptomatology. — The  course  of  frambcesia  may  be  divided  into 
three  periods — a  primary  stage,  comprising  the  development  of  the 


Fig.  687. — Frambcesia  :    Primary 

Stage,  showing  the  Primary 
Lesion  or  Frambcesoma  below 
mi    Right  Knee. 


1542  FRAMBCESIA    TROPICA 

primary  lesion  or  framboesoma;  a  secondary  or  granulomatous  stage, 
during  which  the  characteristic  framboetic  granulomatous  eruption 
appears;  a  tertiary  or  late  stage,  in  which  the  late  manifestations 
of  the  disease  develop — deep  ulcerations  and  gummatous-like 
nodules.  A  fourth  period  may  perhaps  be  added  (paraframbcesial 
affections).  This  division  into  three  or  four  periods  is,  of  course, 
somewhat  arbitrary,  as  symptoms  considered  to  be  characteristic 
of  one  period  may  make  their  appearance  in  another:  tertiary 
symptoms,  for  instance,  may  appear  during  the  secondary  stage. 

It  has  been  stated  again  and  again  that  the  whole  course  of  the 
disease  lasts  from  three  to  six  months  in  children,  and  six  to  twelve 
in  adults,  but  according  to  our  experience  it  has  a  much  longer 
duration,  and  unless  it  becomes  extinct  after  the  secondary  stage 
it  may  extend  to  many  years.  Indeed,  we  believe  that  in  a  certain 
number  of  cases,  although  there  are  periods  during  which  the  patient 
is  apparently  free  from  symptoms,  the  infection  is  merely  latent, 
and  sooner  or  later  gives  rise  to  renewed  manifestations. 

The  Primary  Stage :  Framboesoma. — After  a  period  of  incu- 
bation, varying  in  time  between  two  to  four  weeks,  characterized 
often  by  signs  of  malaise,  rheumatoid  pains,  headache,  irregular 
rise  of  temperature,  the  primary  lesion  or  framboesoma  appears  at 
the  seat  of  inoculation,  which  is  always  extragenital.  The  primary 
lesion  is  a  papule,  which  after  about  a  week  becomes  moist,  develop- 
ing a  yellowish  secretion,  which  dries  into  a  crust.  Often  at  the 
place  of  inoculation  several  papules  appear,  become  moist,  and 
coalesce  into  a  single  element,  covered  by  a  thick  crust.  If  after 
some  days  the  crust  is  removed,  the  primary  sore  will  appear  as  an 
ulcer,  not  rarely  of  large  dimensions,  with  clean-cut  edges  and  a 
granulating  fundus.  This  ulcer  may  heal,  leaving  a  whitish  scar, 
which  may  later  become  pigmented;  or  in  other  cases  it  may 
develop  into  a  granulomatous  mass,  not  dissimilar  to  the  granulo- 
mata  of  the  secondary  eruption,  which  appear  later  on,  but  fre- 
quently much  larger.  This  large  single  projecting  nodule  is  called 
'  mother  yaw,'  or  '  maman  pian '  in  French  patois,  '  buba  madre  ' 
in  Columbia  of  South  America.  Occasionally  round  it,  before  the 
general  eruption  begins,  several  smaller  granulomata  develop  like 
satellites.  The  primary  sore  never  feels  indurated,  and  is  often 
painful  during  the  first  stage  of  development.  Later  it  may  be  quite 
painless.  Occasionally  there  may  be  pruritus.  The  proximal 
lymphatic  glands  may  become  hard  and  enlarged,  but  they  do  not 
suppurate. 

The  seat  of  the  primary  sore  is  usually  extragenital.  The  lesion 
may  develop  on  an  old  ulceration,  an  itch  pustule,  an  insect  bite,  a 
wound,  or  a  vaccination  mark.  The  smallest  abrasion  is  sufficient 
for  the  entrance  of  the  virus.  Most  of  our  female  patients  pre- 
sented the  primary  sore  on  one  of  the  mammae,  developing  on  some 
crack  or  abrasion  of  the  nipple  and  areola.  In  several  other  women 
the  primary  lesion  was  found  on  the  skin  of  the  trunk,  just  above 
the  hip,  this  being  due  to  the  custom  of  the  Ceylon  woman  carrying 


THE  PRIMARY  STAGE—FRAMBOLSOMA 


1543 


her  child  astride  of  the  hip.  Any  frambcetic  element  present  on 
the  scrotum  or  nates  of  the  child,  being  continually  rubbed  against 
the  skin  of  the  mother,  is  likely  to  cause  infection  in  the  latter 
through  any  slight  abrasion  already  present,  or  brought  about  by 
the  friction.  In  men  and  children  the  primary  lesion  is  frequently 
found  on  the  hands,  arms,  and  legs,  but  it  may  develop  on  any 
part  of  the  body. 


Fig.  688. — Child  with  General  Granulomatous  Eruptions,  and 
Mother  with  the  Primary  Lesion  (Frambcesoma)  on  the  Left  Mamma. 

The  primary  lesion  or  frambcesoma  may  heal  before  the  general 
eruption  begins,  but,  as  a  rule,  is  still  present  when  the  secondary 
eruption  appears.  We  observed  a  case  in  which  the  primary  lesion 
was  still  present  six  months  after  its  first  appearance,  and  when 
the  secondary  granulomatous  eruption  had  nearly  undergone  com- 
plete involution.  The  duration  of  the  primary  lesion,  therefore, 
may  vary  between  a  few  weeks  and  several  months.  The  primary 
lesion  leaves  a  whitish  scar,  which  later  on  may  become  pigmented. 


1544 


FRAMBCESIA    TROPICA 


In  some  cases  the  scar  is  small  and  smooth,  in  others  it  is  large  and 
very  thick.  It  is  to  be  noted,  however,  that  in  Ceylon  the  dis- 
figuring scar  so  frequently  seen  is  partly  due  to  thejcustom  the 
natives  have  of  cauterizing  the  sore  deeply  by  very  primitive 
methods.  In  other  cases  the  large  disfiguring  cicatrix  is  due  to 
the  frambcesoma  having  developed  on  an  old  ulcer,  which  on  healing 
leaves  a  coarse  scar. 


Fig.  689. — -Frambcesia:  General  Granulomatous  Eruption. 

The  Secondary  or  Granulomatous  Stage.— The  general  eruption 
usually  begins  between  one  and  three  months  after  the  first  appear- 
ance of  the  primary  lesion.  It  is  preceded  by  malaise,  headache, 
severe  pains  in  the  muscles,  joints,  and  bones.  In  some  cases  there 
may  be  fever  of  an  intermittent  type.  The  patient,  however,  is 
ordinarily  able  to  attend  to  his  work.  The  general  eruption  develops 
as  follows:  minute  roundish  papules,  the  size  of  pin-heads,  appear 
on  various  parts  of  the  body;  some  papules  soon  show  a  yellow 
point  or  minute  yellow  crust  at  their  apex.     Most  of  the  papules 


PLATE    VII. 


Geo  Wiforaton  *  Sons,  Ltd  Edlnl 


FRAMBOESIA  TROPICA. 
General  Eruttion. 


To  /ace  page  15*4 


THE  SECONDARY  OR  GRANULOMATOUS  STAGE  1545 

remain  of  practically  the  same  size  for  many  weeks,  and  disappear, 
leading  occasionally  some  furfuraceous  patches  :  others  become 
larger,  several  often  coalescing,  and  frequently  acquiring  a  dark 
areola  in  natives,  a  reddish  one  in  Europeans.  Some  of  the  larger 
papules  increase  in  size,  and  develop  into  the  characteristic  large 
granulomatous  nodules  covered  with  a  crust,  honey-yellow  or 
brownish,  formed  of  desiccated  secretion.  If  the  crust  covering 
the  granulomata  be  removed,  there  will  be  seen  a  raw  surface 
throwing  up  red  or  yellowish  fungoid  granulations  secreting  a  thin, 


Fig.  690. — Frambcesia  (Secondary  Stagi):  General  Eruption. 

slightly  purulent  secretion,  which  soon  dries  into  a  crust.  These 
frambcetic  granulomata  are  of  various  size,  from  a  large  pea  to  a 
nut,  and  may  be  found  on  practically  any  part  of  the  body.  They 
are  extremely  common  on  the  upper  and  lower  limbs,  and  on  the 
face.  On  the  scalp  they  are  very  rare.  They  may  form  rings  round 
the  mouth  and  anus,  and  may  enclose  sound  skin  (so-called  yaws 
ringworm).  They  may  remain  of  the  same  size  and  appearance  for 
months.  Often,  after  a  few  weeks,  the  secretion  diminishes,  and 
a  process  of  hyperkeratosis  sets  in.  They  then  become  of  much 
harder  consistency,  and  some  of  them,  especially  those  on  the 
dorsum  of  the  feet  and  toes,  may  be  covered  with  numerous  small, 


1546 


FRAMBQ2SIA   TROPICA 


hard,  verrucose-like  protuberances.  In  the  majority  of  cases — 
within  three  to  six  months  in  children,  and  six  to  twelve  months 
in  adults — the  granulomata  dry  up,  shrink,  and  disappear,  leaving 
dark  hyperpigmented  spots,  or  occasionally  apigmented  areas,  on 
their  site,  which  are  most  persistent.  In  some  cases  the  granulo- 
matous eruption  may  continue  for  several  years,  new  crops  of 
nodules  appearing  from  time  to  time  in  succession.  Each  fram- 
boetic  granuloma  generally  undergoes  involution  within  two  to  four 
months,  leaving  behind,  as  a  rule,  a  dark  area  or,  more  rarely,  a 
depigmented  spot.  Occasionally,  however,  the  granuloma  does  not 
regress  so  soon.  In  one  of  our  patients  a  single  granuloma  persisted 
for  two  years  after  all  the  others  had 'disappeared. 


Fig.  6qi. — Frambcesia:  General  Eruption  of  the  Secondary  Stage. 


The  granulomata  are  seldom  painful,  unless  they  develop  between 
the  toes,  on  the  soles  of  the  feet,  or  round  the  nails.  They  very 
often  cause  itching.  The  patient  often  exhales  a  peculiar  offensive 
odour,  which  has  been  variously  described  as  sour  or  musty.  This 
is  probably  due  to  the  growth  of  various  bacteria,  representing 
secondary  infections  beneath  the  crusts  of  the  granulomata.  This 
offensive  odour  is  especially  noticeable  when  the  secondary  infec- 
tion is  due  to  bacilli  of  Vincent's  fusiform  type  and  coarse  spiro- 
chetes. In  such  cases,  if  the  sores  are  well  washed  with  perchloride 
solution  for  two  or  three  days,  these  organisms  disappear,  and  the 
smell  is  no  longer  noticeable,  though  the  granulomata  do  not  under- 
go any  change.     Though  the  framboetic  granuloma  is  the  charac- 


THE  SECONDARY  OR  GRANULOMATOUS  STAGE  1547 


Fig.  692. — Frambcesia  (Secondary  Stage):  General  Eruption. 


Fig.  693. — Frambcesia:  Eruption  on  the  Hands. 


1548 


FRAMBCESIA   TROPICA 


teristic  eruption  of  the  secondary  stage,  there  are  during  this  stage 
other  types  of  eruption  or  frambcesides — papular,  scaly,  and  occa- 
sionally ulcerative.     An  average  ordinary  case  will  present  at  the 


I 

1 

M             ! 

um£* 

B  ■     i 

m  ■:  ***5^M 

2E2tI 

i 

Fie.  694. — Frambcesia:  Circinate  Eruitiox. 


Fig.  695. — Frambcesia:  Granulomata  on  the  Heels  of  the  Feet. 

same  time  several  typical  frambcesiform  granulomata,  numerous 
small  reddish  papules  with  the  epidermis  intact,  other  papules 
which  have  become  moist  and  are  covered  by  a  tiny  yellow  crust, 


ERUPTIONS  ON  THE  PALMS  AND  SOLES 


1549 


several  furfuraceous  patches  here  and  there,  and  spots  of  increased 
pigmentation  at  the  place  of  previous  granulomal a.     Occasionally 


Fig.  696. — Frambcesia:   Lesions  on  Sole  of  Foot. 


Fig.  697. — Frambcesia:  Lesions  on  Sole  of  Foot. 


some  granulomata  break  down,  and  large  irregular  ulcers  form, 
presenting  in  their  centre  reddish  papillomatous  masses,  which  in 
our  experience  do  not  usually  heal  spontaneously.     At  times  in 


1550 


FRAMBCESIA   TROPICA 


the  latter  period  of  the  secondary  stage  peculiar  roundish  or  irregu- 
larly outlined  whitish  patches  are  present,  especially  on  the  back 
and  arms,  with  a  nutmeg-grater-like  surface.  On  closer  observa- 
tion these  patches  are  seen  to  consist  of  numerous  hard,  conical 
papules,  containing  in  their  centre  an  epidermic  plug,  which  is 
easily  removed,  leaving  a  depression  in  the  papules.  Sometimes 
the  plugs  are  spiny,  and  in  this  case  the  eruption  closely  resembles 
lichen  spinulosus. 

Eruptions  on  the  Palms  and  Soles. — The  granulcmatous 
eruption  very  frequently  attacks  the  soles  of  the  feet.  At  first 
dark  brownish  or  intensely  livid  spots  appear;  the  thick  epidermis 
is  gradually  pierced  by  framboesial  nodules  similar  to  those  found 
in  other  regions  of  the  body.  This  affection  of  the  soles  is  very 
painful;  the  natives  of  Ceylon  call  it  '  dumas.'     Similar  lesions  may 


Fig.  698. — Frambcesia:  Pitted  Appearance  of  the  Hands. 


occur  on  the  hands.  The  granulomatous  infiltration  may  attack 
the  matrix  and  margins  of  the  nails  (framboetic  onychia  and  par- 
onychia). The  nails  become  thickened,  dry,  brittle,  and  may  be 
cast  off  entirely,  though  later  they  grow  again. 

After  the  granulomata  have  disappeared,  occasionally  at  the 
same  time  peeling,  whitish  patches  may  be  seen  on  the  palms  of 
the  hands  and  soles  of  the  feet  closely  resembling  the  syphilitic 
psoriasis  palmar  is  and  plantar  is. 

Peculiar  Pitted  Frambceside  of  the  Palms  of  the  Hands. — 
In  several  cases  in  the  latter  part  of  the  secondary  stage  hard,  round, 
flattened  papules  or  small  nodules,  having  a  thick,  hard,  epidermic 
plug  in  their  centre,  may  be  observed  on  the  palms  and  wrists.  This 
plug  falls  off  spontaneously  or  is  easily  pulled  out,  when  a  deep 
depression  remains.    The  papules  gradually  disappear,  but  the  de- 


THE  SECONDARY  OR  GRANULOMATOUS  STAGE 


i55i 


pressions  remain,  and  the  palms  acquire  a  peculiar  pitted  appear- 
ance. This  condition  of  the  palms  may  remain  unchanged  for 
several  years  after  all  symptoms  of  frambcesia  have  disappeared. 
A  somewhat  similar  appearance  of  the  soles  of  the  feet  is  occasionally 
met  with. 

P*  Lesions  of  the  Hair  and  Nails. — We  have  never  noticed  any 
change  in  the  appearance  of  the  hair,  or  alopecia.  A  few  hair- 
follicles  may  be  destroyed  when  the  granulomata  develop  on  the 
scalp,  which,  however,  seldom  occurs. 

Lesions  of  Mucosae. — These  are  not  very  common.    During  the 
secondary  stage  small  granulomatous  nodules  may  develop  at  the 


Fig.  699. — Frambcesia:  Dactylitis. 


base  of  the  tongue,  also  whitish  patches  closely  resembling  syphilitic 
leukoplakia.  Small  granulomata  may  develop  on  the  nasal 
mucosa. 

Constitutional  Symptoms— Fever.— As  already  stated,  fever  is 
frequently  present,  of  intermittent  or  remittent  type,  before  the 
general  secondary  eruption  begins.  During  the  secondary  stage  it 
is  usually  absent,  unless  complications  supervene. 

Lymphatic  Glands. — In  a  number  of  cases  in  our  experience 
various  groups  of  lymphatic  glands  are  found  to  be  enlarged.  The 
enlarged  glands  are  roundish  or  spindle-shaped,  hard,  painless,  and 
never  come  to  suppuration,  unless  a  secondary  pyogenic  infection 


1552  FRAMBCESIA   TROPICA 

is  present.     The  cervical  and  inguinal  glands  are  most  frequently 
enlarged. 

Alimentary  System. — As  a  rule  the  digestive  functions  are  not 
disturbed.  In  children  slight  diarrhoea  may  be  occasionally  noticed 
preceding  the  general  eruption.  The  spleen  and  liver  are  fre- 
quently found  enlarged  in  children,  but  this  is  probably  due  to 
preceding  or  concomitant  malaria  infection.  The  microscopical 
examination  of  the  fseces  of  frambcesia  patients  will  frequently  reveal 
ova  of  various  worms — Ascaris  lumbricoides,  Trichuris  trichiura, 
and  occasionally  Ancylosioma  duodenale — but  this  is  of  frequent 
occurrence  also  in  normal  natives. 

Respiratory  System.— As  a  rule  the  respiratory,  as  well  as  the 
circulatory,  system  is  not  affected.  Occasionally  small  granulo- 
matous ulcers  are  to  be  found  in  the  nasal  mucosa  and  more  rarely 
in  the  larynx. 

Locomotory  System — Joints. — In  some  patients  several  of  the 
large  articulations  may  become  swollen  and  very  painful.  The  con- 
dition is  often  of  an  acute  character,  and  may  be  accompanied  by 
fever,  so  that  an  attack  of  articular  rheumatism  complicating  the 
frambcetic  infection  might  be  suspected.  Sodium  salicylate,  how- 
ever, is  not  beneficial,  while  the  administration  of  large  doses  of 
potassium  iodide  speedily  reduces  the  temperature  to  normal  and 
cause  the  swelling  of  the  articulation  to  subside.  At  other  times 
one  articulation  only  is  involved,  and  the  symptoms  may  become 
so  serious  as  to  suggest  purulent  arthritis.  In  many  cases  the 
smaller  articulations  become  involved.  The  symptoms  in  such 
cases  are  not  acute,  and  there  is  usually  no  fever. 

Bones.—  Inflammation  of  the  periosteum  of  various  bones  is  of 
common  occurrence.  Very  frequent  is  a  form  of  multiple  periostitis 
of  the  digital  phalanges,  the  cause  of  the  multiple  dactylitis  so  often 
seen  in  frambcesia  patients. 

Maul  has  investigated  the  bone  and  joint  lesions  of  Frambcesia,  and  has 
noted  that,  in  the  Philippine  Islands,  20  per  cent,  of  the  cases  are  suffering 
from  such  lesions,  winch  may  simulate  tubercular  or  central  septic  abscesses, 
gummata,  hydatid  cyst,  benign  cyst,  fibrous  osteitis,  enchondroma,  endo- 
thelioma, secondary  carcinoma,  myeloma,  and  sarcoma.  The  same  author 
has  made  a  careful  roentgenological  survey,  and  has  found  that  in  the  majority 
of  cases  thp  bone  lesions  appear  as  rarefied  areas,  irregularly  oval,  with  the 
long  axis  parallel  to  that  of  the  bone,  from  a  few  millimetres  to  2  or  3  centi- 
metres in  length.  Most  of  the  lesions  seem  to  originate  in  the  interior  of 
the  bone,  but  some  appear  as  small  excavations  on  its  outer  surface. 

Muscles. — Contractures  of  various  groups  of  muscles  may  be 
observed.  Fairly  common  is  a  contracture  of  the  flexor  muscles 
of  the  forearms.  This  contracture  is  often  permanent,  and  in  our 
opinion  is  probably  due  to  pathological  alteration  of  the  peripheral 
nerves,  rather  than  being  of  direct  muscular  origin. 

Nervous  System — Neuritis. — Neuralgic  pains  are  often  observed, 
but  also  a  true  form  of  neuritis  must  be  admitted.  We  have  seen 
in  several  cases  clear  symptoms  of  neuritis  of  the  sciatic  nerve,  with 


THE  SECONDARY  OR  GRANULOMATOUS  STAGE         1553 

severe  pain  along  the  course  of  the  nerve,  and  signs  of  motor  and 
trophic  disturbances. 

Hyperidrosis. — In  several  of  our  patients  we  have  noticed 
hyperidrosis.  The  phenomenon  was  limited  to  the  face  in  some 
cases,  to  the  hands  and  soles  of  the  feet  in  others.  It  never  ex- 
tended to  the  whole  body,  and  generally  affected  symmetrical  regions. 
Hyperidrosis  is  more  frequently  observed  in  children  than  in  adults. 
In  a  case  at  the  Colombo  Clinic  a  boy  of  fourteen,  presenting  a 
general  eruption  of  framboesia,  the  hyperidrosis  of  the  face  was  so 
marked  that  large  drops  of  perspiration  were  constantly  dropping 
down.  He  was  treated  with  potassium  iodide.  After  a  month  the 
granulomata  had  disappeared,  and  the  hyperidrosis  was  no  longer 
noticeable.  In  some  cases  the  hyperidrosis  ceases  suddenly  with- 
out any  treatment.  The  condition,  however,  may  last  for  some 
weeks  or  months. 

The  Eyes. — Granulomatous  and  papular  eruptions  may  develop 
on  the  eyelids.  A  slight  periostitis  of  the  orbital  margin  is  not  rare, 
the  margin  becoming  thickened  and  very  painful  on  pressure.  The 
occurrence  of  iritis  is  denied  by  most  authors.  In  the  Colombo 
Clinic  two  typical  cases  were  observed  during  the  general  granulo- 
matous eruption.  In  both  cases  the  affection. was  of  moderate 
severity.  There  was  photophobia,  ciliary  congestion,  discolora- 
tion of  the  iris.  Pupillary  reaction  was  almost  absent.  Both  cases 
recovered  on  large  doses  of  iodides  without  any  local  treatment. 

The  Genito-urinary  System. — The  primary  lesion  is  rarely,  if 
ever,  found  on  the  genital  organs.  In  fact,  in  all  the  cases  we  have 
seen  the  primary  lesion  was  always  extragenital.  Eruptions  of  the 
secondary  stage,  papular  and  granulomatous,  frequently  involve 
the  skin  of  the  penis  and  of  the  labia.  Granulomatous  ulceration 
may  be  found  on  the  vaginal  mucosa.  The  urine,  as  a  rule,  does 
not  contain  anything  abnormal;  only  when  there  is  fever — as,  for 
instance,  when  the  articulations  are  acutely  involved — then  a  slight 
amount  of  albumen  may  be  present. 

The  Blood. — -There  is  often  a  certain  degree  of  anaemia,  never 
very  severe.  The  number  of  red  blood-corpuscles  varied  in  our 
cases  from  3,000,000  to  4,000,000,  the  haemoglobin  index  (Fleischl) 
from  50  to  75.  The  red  blood-corpuscles  did  not  show  anything 
abnormal  in  their  shape.  On  several  occasions  a  comparatively 
large  number  of  polychromatic  erythrocytes  were  noticed,  staining 
blue  instead  of  pink  with  Leishman's  method.  Many  of  these 
basophile  red  cells  are  micro-erythrocytes.  The  leucocytes  varied 
from  7,000  to  11,000  per  cubic  millimetre.  In  the  majority  of  cases 
an  increase  was  noticeable  in  the  number  of  the  large  mononuclears, 
even  when  there  was  no  sign  and  no  history  of  malaria.  The  number 
of  lymphocytes  is  generally  normal.  Clapier  and  Violle  have  re- 
cently emphasized  this,  and  note  that  it  is  in  contrast  to  what  one 
sees  in  syphilis,  in  which  the  lymphocytes  are  increased  in  number, 
while  the  large  mononuclears  are  in  normal  amount.  In  many 
cases  the  eosinophiles  are  increased,  this  being  probably  due — in 

98 


1554  FRAMBCES1A    TROPICA 

part,  at  least — to  the  presence  of  intestinal  worms,  as  revealed  by 
the  microscopic  examination  of  the  stools,  which  shows  frequently 
ova  of  Ascaris  ktmbricoides,  Trichuris  Irichiwa,  and  in  a  few 
instances  of  Ancylostoma  duodenale.  Density  and  viscosity  of 
blood  seem  to  be  normal  according  to  Violle,  and  the  coagulability 
is  not  impaired.  Auto-agglutination  is  generally  absent,  but  has 
been  recorded  in  certain  cases. 

Complement-Fixation  Reactions. — Wassermann  reaction  is  posi- 
tive in  the  great  majority  of  recent  cases,  but  is  fairly  often  negative 
in  old  cases.  According  to  Schiiffner  and  Violle,  in  frambcesia  there 
is  often  fixation  if  an  alcoholic  extract  of  syphilitic  liver  is  used  as 
antigen,  while  there  is  no  fixation  if  an  aqueous  extract  is  used. 
In  syphilis  there  is  generally  complete  fixation. 

Cuti-Reactions. — The  cuti-reaction  with  '  frambcesin,'  prepared  with  cultures 
of  T.  pertenue  according  to  the  technique  used  by  Noguchi  in  the  preparation 
of  luetin,  is  often  positive.  Luetin  also  may  at  times  give  a  positive  reaction, 
though  less  marked. 


Fig.  700. — Frambcesia:  Pseudo-Mycetoma. 

Cerebrospinal  Fluid.— The  liquid  is  in  all  cases  perfectly  clear, 
like  distilled  water.  No  cellular  sediment  on  centrifugalization  is 
found  in  most  cases.  In  a  few  some  rare  mononuclear  cells  are 
found.  The  pressure  is  not  increased.  The  physical  and  chemical 
characters  do  not  show  much  variation  from  what  is  found  in  normal 
conditions.  The  density  varied  in  our  cases  between  1003  to  1005. 
A  certain  amount  of  globulin  was  present,  and  a  substance  (dex- 
trose ?)  reducing  Fehling's  solution.  This  reducing  substance  was 
in  several  cases  distinctly  in  excess  of  what  is  observed  in  the  normal 
fluid.  No  cholin  is  found.  The  reaction  of  the  fluid  is  alkaline. 
The  liquid  is  sterile;  no  treponemata  can  be  detected. 

Tertiary  or  Late  Stage. — The  disease  often  terminates  with  the 
secondary  stage.  In  some  cases,  however,  the  infection  does  not 
become  extinct,  and  tertiary  lesions  appear.     These  have  been 


TERTIARY  OR  LATE  STAGE 


15-55 


denied  by  many  observers,  but  having  been  able  to  watch  cases  for 
several  years  through  the  whole  course  of  the  disease,  we  have  no 
doubt  as  to  their  existence.  Sometimes  the  secondary  and  tertiary 
stages  merge  into  each  other,  but 
frequently  the  tertiary  symptoms 
appear  after  the  lesions  of  the 
secondary  stage  have  undergone 
complete  involution.  The  interval 
of  time  varies  considerably  in  length, 
and  may  extend  to  many  years.  The 
characteristic  lesions  of  the  tertiary 
period  are  gummatous-like  nodules 
and  deep  ulcerative  processes.  These 
gummatous  nodules  may  develop  in 
any  tissues.  When  developed  in  the 
skin  and  subcutaneous  tissues,  they 
are  indolent,  and  by  their  softening 
and  breaking  down  ulcers  are  pro- 
duced which  may  occasionally  present 
clear-cut  margins  and  a  granulating 
fundus,  and  when  several  contiguous 
nodules  break  down,  serpiginous  ulcers 
are  left.  In  other  cases  deep,  irregu- 
larly shaped  ulcerations  with  very 
thick  and  undermined  edges  are  seen; 
in  others — and  these  are  the  more 
numerous — large  fungating  ulcers  are 
present.  On  healing,  these  various 
ulcers  leave  whitish  scars,  which  are 
often  thick  and  disfiguring.  Fre- 
quently the  scar-tissue  undergoes  re- 
traction, and  thereby  causes  per- 
manent contractures  and  disfigure- 
ment. Lesions  of  the  osseous  type 
are  very  frequent,  painful  nodes 
developing  under  the  periosteum  of 
several  bones,  ribs,  sternum,  etc., 
and  we  arc  inclined  to  believe  thai 
Gangosa  (p.  1876),  an  ulcerative 
condition  of  the  palate,  nose,  and 
pharynx,  is  in  reality  a  tertiary  mani- 
festation of  yaws.  In  other  cases  a 
diffuse  chronic  periostitis  is  present, 
altering  the  normal  shape  of  the 
bones.  Contractures  of  various  groups 
of  muscles  are  frequently  seen. 
Tertiary    affections   of    the    internal 

organs  and  of  the  central  nervous  system  seem  to  be  rare.     Cases 
of  aneurysm  considered  to  be   of    frambcesial   origin   have   been 


Fig.  701. — Framboesia: 
Tertiary  Stage. 


1556  FRAMBCESIA   TROPICA 

observed.  The  malady  does  not  appear  to  be  hereditary;  in  fact,  it 
is  worth  noting  that,  in  contrast  to  syphilis,  parents  generally 
contract  the  malady  from  their  children. 

Fourth  Stage :  Paraframbcesial  Affections. — Cases  of  tabetic 
symptoms  and  symptoms  pointing  to  paralysis  progressiva  believed 
to  be  due  to  an  old  frambcesial  infection  have  been  placed  on  record 
by  Harper  and  others. 

Communicability. — Frambcesia  is  usually  conveyed  by  direct 
contact  from  person  to  person.  It  appears,  however,  that  the 
germ  is  unable  to  enter  through  the  normal  skin,  and  that  there  must 
be  some  pre-existing  abraded  surface,  small  wound,  or  ulcera- 
tion. Women  are  frequently  infected  by  their  children,  the 
primary  lesion  appearing  often  on  the  mammse.  In  the  native 
women  of  Ceylon  the  primary  lesion  frequently  develops  on  the  skin 


Fig.  702. — Frambcesia:  Tertiary  Stage. 

of  the  trunk  just  above  the  hip,  slight  abrasions  caused  by  friction 
being  usually  present  on  this  part,  owing  to  the  habit  they  have  of 
carrying  their  children  astride  of  the  hip.  Among  certain  Congo 
tribes  it  is  a  common  dictum  that  a  woman  affected  with  theNkoulou 
(yaws)  should  not  sleep  with  her  child,  or  he  will  certainly  contract 
the  malady.  The  natives,  however,  believe  that  the  infection  may 
be  contracted  also  by  partaking  of  contaminated  food.  In  our 
opinion  there  can  be  little  doubt  that  in  certain  cases  insects  may 
carry  the  disease.  It  is  very  noticeable  that  flies  eagerly  crowd 
on  the  open  sores  of  framboesia  patients.  In  the  hospitals,  as  soon 
as  the  dressings  are  removed,  the  framboetic  ulcerations  become 
covered  with  flies,  sucking  with  avidity  the  secretion,  which  they 
may  afterwards  deposit  in  the  same  way  on  ordinary  ulcers  of  other 
patients.     Ants  also  are  occasionally  seen  to  go  on  to  the  framboetic 


COMMUNICABILITY— DIAGNOSIS  1557 

ulcerations,  as  well  as  on  to  ordinary  ulcers.  In  Nuttall's  classical 
work  on  the  role  of  insects  as  carriers  of  parasitic  diseases  several 
authors  are  quoted  (Alibert,  Hoish,  Cadet,  Wilson)  who  believe  that 
the  infection  may  be  conveyed  from  one  individual  to  another  by 
flies.  Wilson  states  that  this  belief  prevails  among  the  natives  of 
the  West  Indies. 

One  of  us  made  some  experiments  to  prove  that  flies  are  instru- 
mental in  the  dissemination  of  the  disease.  A  number  of  flies  were 
fed  on  scrapings  from  slightly  ulcerated  frambcetic  papules.  The 
flies  (Musca  dumestica  and  allied  species),  before  feeding  on  the 
framboetic  material,  wore  examined.  The  examination  showed 
that  they  did  not  harbour  any  treponemata,  either  on  their  mouth 
organs  or  on  their  legs.  On  examination  after  feeding,  the  majority 
presented  coarse  spirochetes,  and  a  few  of  them  also  T.  pertenue. 
In  another  experiment  flies  fed  on  yaws  material  were  placed  on 
scarified  spots  over  the  eyebrows  of  several  monkeys,  and  kept 
there  for  two  hours  by  means  of  strips  of  gauze  smeared  with 
collodion  at  their  margins.  One  of  the  monkeys  became  infected. 
Sambon  considers  that  a  fly  of  the  genus  Hippelates  plays  a  very 
important  role  in  the  dissemination  of  the  disease  in  the  West  Indies. 

Modder  some  years  ago  suggested  that  Ixodes  bovis — i.e.,  Mar  gar  opus 
annulatus  var.  australis — or  some  of  the  Argasidae  might  be  the  transmitting 
agent.  Bahr  has  suggested  that  the  causative  treponema  may  be  transmitted 
by  some  blood-sucking  insect  whose  range  is  definitely  limited  by  the  character 
of  the  vegetation  or  by  climatic  factors.  According  to  certain  authorities 
yaws  may  be  communicated  by  means  of  food.  R.  P.  Greggio  states  that 
natives  of  some  Congo  tribes  suffering  from  yaws  place  inside  the  manioc 
they  are  selling  portions  of  crusts  removed  from  their  own  yaws  lesions,  in 
the  belief  that  in  this  way  the  disease  will  leave  them,  will  '  emigrate  '  to 
the  buyers,  who  will  become  infected  by  eating  the  manioc. 

Diagnosis. — In  countries  where  the  disease  is  endemic  the  diag- 
nosis is  generally  easy,  the  large  frambcesiform  nodules,  capped  with 
thick  yellow  crusts,  being  typical.  By  some  observers  the  disease 
has  been  confused  with  verruga  peruviana  and  with  syphilis. 

Verruga  Peruviana. — This  disease  is  strictly  limited  to  certain 
valleys  of  the  Andes  at  an  elevation  of  from  3,000  to  10,000  feet. 
Its  eruptive  elements,  unlike  those  of  frambcesia,  frequently  attack 
the  various  mucosae,  and  bleed  with  great  facility.  The  micro- 
scopical examination  for  spirochetes  is  negative. 

Syphilis. — By  some  authors  frambcesia  has  been  looked  upon  as 
a  form  of  syphilis.  The  results  of  experimental  investigations  of 
yaws  and  syphilis  prove  conclusively  that  the  two  diseases  are 
distinct,  inasmuch  as  (1)  patients  suffering  from  syphilis  may 
contract  yaws,  and  patients  suffering  from  yaws  may  contract 
syphilis;  (2)  monkeys  successfully  inoculated  with  yaws  do  not 
acquire  any  immunity  against  syphilis;  (3)  mercury  has  practically 
no  action  on  frambcesia. 

Syphilis  has  a  world-wide  distribution;  frambcesia,  on  the  other 
hand,  is  restricted  to  certain  parts  of  the  tropics.  Frambcesia  is 
extremely  common  in  Ceylon,  extremely  rare  in  India.     Syphilis  is 


1558 


FRAMBCESIA   TROPICA 


common  to  both  countries.  In  Samoa,  according  to  Turner,  syphilis 
was  unknown  up  to  at  least  1880,  while  framboesia  has  been  endemic 
there  ever  since  the  group  was  discovered.  In  Fiji,  too,  up  to  a  few 
years  ago  syphilis  was  not  present,  while  framboesia  was  almost 
universal.  Daniels  has  made  the  interesting  observation  that  in 
British  Guiana  framboesia  of  late  has  disappeared,  while  syphilis 
is  still  rampant.  As  regards  clinical  features,  framboesia  differs 
from  syphilis  by  the  following  characters:  the  primary  lesion  is, 
as  a  rule,  extragenital;  the  principal  type  of  eruption  is  a  papule, 
which  proliferates  into  a  characteristic  frambcesiform  granulo- 
matous growth;  there  is  an  extremely  well-marked  pruritus.  The 
disease  is  apparently  not  hereditary;  in  fact,  in  contrast  to  syphilis, 
parents  generally  contract  the  malady  from  their  children.  The 
histopathology  differs  also  in  the  two  diseases.  In  framboesia  the 
proliferative  changes  of  the  epidermis  are  much  more  marked,  the 
granulomata  present  a  more  diffuse  plasma  cell  infiltration,  and 
their  bloodvessels  have  no  tendencv  to  the  thickening  of  their  walls, 


Fig.  703. — Frambcesia:  Tertiary  Stage. 

which  is  so  characteristic  of  syphilis.  Giant  cells  are  generally 
absent.  Naturally  these  differential  histological  details  must  be 
considered  collectively,  as  there  is  no  individual  histological  char- 
acter which  exceptionally  might  not  be  present  in  both  syphilis 
and  framboesia. 

Boubas  and  Plan. — Some  of  the  older  authors  believed  that  under 
the  names  of  yaws,  boubas,  and  pian  three  different  diseases  were 
indicated.  All  those,  however,  who  have  had  opportunity  to  in- 
vestigate framboesia  in  different  parts  of  the  tropics  have  come 
to  the  conclusion  that  these  various  denominations  are  simply  local 
synonyms  indicating  the  same  pathological  entity,  though,  of  course, 
each  of  these  terms  is  sometimes  used  by  natives  to  indicate, 
besides  frambcesia,  other  clinically  similar  conditions.  Comparative 
experimental  investigations  made  by  one  of  us  have  led  to  the  same 
result,  inasmuch  as  he  has  been  able  to  demonstrate  that  monkeys 
successfully  inoculated  with  Ceylon  frambcesia  become  immune  to 
boubas  and  pian,  and  vice  versa. 

Breda  and  De  Amicis,  in  Italv,  have  not  found  T.  pertenue  in 


PROGNOSIS 


1559 


Italian  emigrants  returning  from  Brazil,  and  suffering  from  what 
they  considered  to  be  boubas;  but  Splendore  has  shown  their  cases 
to  have  been  cases  of  leishmaniasis  and  blastomycosis.  The  fact 
is,  that  in  South  America  the  term  boubas  is  used  by  the  natives  to 
cover  several  clinically  similar  diseases,  while  most  medical  writers 
use  the  term  as  a  synonym  for  frambcesia.  Rivas,  Linderman,  and 
Robledo  have  found  the  T.  pertenue  in  their  cases  of  boubas  in 
Venezuela,  Brazil,  and  Colombia.  It  is  not  to  be  excluded,  how- 
ever— in  fact,  it  is  probable — that  future  investigation  will  show 
that  there  are  several  varieties  of  T.  pertenue. 


^FlGS.    704   AND    705. FRAMBCESIA    BEFORE    AND    AlTER  TEN   DAYS'  TREAT- 
MENT   WITH    CASTELLANl'S    MIXTURE. 


Cutaneous  Leishmaniasis. — A  type  of  cutaneous  leishmaniasis 
(Bush-Yaws),  fairly  common  in  the  West  Indies,  may  simulate 
yaws,  !but  the  presence  of  leishmania  bodies  and  absence  of  the 
Treponema  pertenue  will  clear  the  diagnosis. 

Prognosis. — The  prognosis  is  not  serious  so  far  as  life  is  con- 
cerned. In  1908,  in  the  Ceylon  hospitals,  3,246  cases  were  treated, 
wiih  twenty-three  deaths;  in  1904,  out  of  3,591  cases,  sixteen  died; 
in  C903,  out  of  3,254  cases,  ten  only  died.  The  prognosis  is  far  more 
serious  in  children  than  in  adults.  When  the  disease  ends  fatally  the 
termination  is  gradually  due  to  secondary  infection,  the  frnmbcetic 


1560  FRAMBCESIA   TROPICA 

ulcerated  lesions  becoming  phagedenic,  and  giving  opportunity 
to  septicaemia  and  pyogenic  processes  to  develop.  Though  fram- 
bcesia  rarely  terminates  in  death,  its  long  duration  and  great  con- 
tagiousness render  it  a  serious  malady.  The  patients  suffering 
from  it  are  unable  to  attend  to  their  work.  Epidemics  of  fram- 
bcesia,  therefore,  are  of  the  greatest  consequence  on  tea,  sugar,  and 
other  plantations,  as  they  reduce  the  supply  of  labour. 

Treatment. — The  most  efficacious  and  quickest  treatment  is  by 
Ehrlich-Hata  salvarsan  or  neo-salvarsan,  while  potassium  iodide 
and  tartar  emetic  are  fairly  efficacious,  and  mercury  practically 
useless.  Salvarsan  and  neo-salvarsan  and  their  substitutes  seem 
to  act  in  frambcesia  more  quickly  and  more  powerfully  than  in 
any  other  spirochaetal  and  treponemal  condition;  in  fact,  in  fram- 
boesia  the  therapia  sterilans  magna  in  Ehrlich's  meaning,  by  a 
single  dose,  can  at  times  be  obtained.  Salvarsan  was  first  tried 
with  good  results  in  experimental  yaws  by  Nichols,  and  in 
patients  suffering  from  the  disease  by  Strong  in  the  Philippine 
Islands,  and  Castellani  in  Ceylon,  while  Alston  in  the  West  Indies 
made  the  interesting  observation  that  the  serum  of  patients  treated 
with  salvarsan  showed  remarkable  curative  powers  when  injected 
in  framboesia  patients.  Recently  the  salvarsan  treatment  of  fram- 
bcesia has  become  general,  having  been  used  with  very  good  results 
by  De  Gorge  and  Mouzels,  Sabella,  Born,  and  many  others.  The  sal- 
varsan treatment  is  especially  efficacious  in  recent'  cases.  Relapses, 
however,  occasionally  occur.  In  very  old  cases  with  tertiary 
lesions  the  treatment  may  fail.  At  the  present  time  neo-salvarsan, 
instead  of  salvarsan,  is  generally  used. 

Mode  of  Administration  and  Dosage. — Neo-salvarsan  and  its 
substitutes  novarsenobenzol,  neokharsivan,  novoarsenobillon,  and 
to  a  certain  extent  galyl,  are  much  more  soluble  than  salvarsan 
and  its  substitutes  arsenobenzol,  kharsivan,  etc.,  and  are  therefore 
used  in  practice  in  preference  to  salvarsan.  Moreover,  Castelli  has 
shown  that  the  dosis  tolerata  of  neo-salvarsan  in  infected  rabbits  is 
nearly  three  times  larger  than  for  salvarsan,  and  that  the  dosis 
sterilans  is  one-tenth  of  the  dosis  tolerata. 

The  dosage  of  neo-salvarsan  and  most  of  its  substitutes  is,  in 
adults,  0*4  to  o-6  gramme,  though  larger  doses  up  to  1  gramme  have 
been  given  with  impunity.  The  dosage  is  therefore  approximately 
col  gramme  per  kilogramme  of  weight ;  in  children  half  or  one-third 
doses  should  be  given.  The  best  method  of  administration  is  by 
intravenous  injection,  and  we  have  found  Ravaut's  method  of 
concentrated  solutions  very  convenient,  although  we  do  not  use 
such  highly  concentrated  solutions  as  does  Ravaut,  who  recommends 
dissolving  neo-salvarsan  in  only  1  or  2  c.c.  of  water.  We  generally 
dissolve  0*3  or  0*4  gramme  of  neo-salvarsan  in  10  c.c.  of  sterile 
distilled  water  or  sterile  physiological  salt  solution,  and  make  the 
intravenous  injection,  using  a  10  c.c.  syringe. 

The  patient  is  made  to  lie  down  quietly  on  a  couch  or  in  bed. 
The  ^kin  is  pain+ed  with  tr.  iodi  and  the  veins  of  the  bend  of  the 


TREATMENT  1561 

elbow  made  turgid  by  applying  an  elastic  band  round  the  arm. 
The  needle,  already  attached  to  the  syringe  containing  the  solution, 
is  inserted  in  one  of  the  veins;  if  blood  appears  in  the  liquid,  it 
means  that  the  needle  is  in  the  vein,  and  the  piston  of  the  syringe 
is  then  very  slowly  and  gradually  pressed  down  until  all  the  liquid 
has  been  injected. 

Three  to  six  injections  of  neo-salvarsan  at  three  to  six  days' 
interval  are  generally  sufficient  to  obtain  a  cure,  though  in  a  number 
of  cases  one  injection  is  sufficient  to  make  all  the  symptoms  dis- 
appear. If  one  injection  only  is  given,  0*4  to  o-6  gramme  should 
be  injected;  when  a  course  of  three  or  more  injections  is  carried  out 
we  often  give  0-3  gramme  the  first  time,  0-4  gramme  the  second 
time,  and  o-6  gramme  the  third  time  and  afterwards. 

The  patient  should  keep,  if  possible,  at  complete  rest  in  bed  for 
several  hours  after  the  injection,  and  in  individuals  with  weak 
heart. the  injection  of  neo-salvarsan  maybe  preceded  by  a  hypo- 
dermic injection  of  caffein.  The  patient  may  complain  at  times 
of  headache,  and  there  may  be  a  rise  of  temperature,  but  very 
seldom  are  serious  symptoms  caused  by  the  drug,  though  cases 
of  transient  coma,  delirium,  epileptiform  crisis,  nephritis,  and 
jaundice  have  been  recorded. 

Salvarsan. — Salvarsan  may  be  given  by  intramuscular,  subcutaneous,  or 
intravenous  injection;  by  the  mouth  in  alkaline  solution;  and  also  by  the 
rectum  in  the  form  of  enemas  or  suppositories.  We  recommend  the  intra- 
muscular and  intravenous  injections.  The  administration  by  the  rectum  in 
our  experience  does  not  give  any  good  result,  and  of  the  oral  administration 
we  have  no  personal  experience. 

Intramuscular  Injections. — The  injection  is  generally  given  in  the  buttocks, 
with  the  usual  precautions  as  regards  the  disinfection  of  the  skin,  and  the  use 
of  a  sterile  all-glass  syringe.  The  quickest  method  of  disinfecting  the  skin 
is  to  paint  it  with  tincture  of  iodine.  The  dose  to  be  given  in  adult  males  is 
0*40  to  0*50  gramme;  in  adult  females  and  thin  individuals  0-30  and  0-40 
gramme.  A  dose  exceeding  o*6o  gramme  should  never  be  given  either  in 
males  or  females.  In  children  the  dose  is  0-03  to  0*04  gramme  for  each  year 
of  age,  or  0*008  gramme  for  each  kilogramme  of  weight. 

The  injection  of  salvarsan  in  the  same  dose  can  be  repeated  after  two  or 
three  weeks,  if  the  first  one  has  not  been  completely  successful.  The  drug  is 
not  easily  soluble,  and  various  methods  of  preparing  the  liquid  to  be  injected 
have  been  described.  The  simplest  method  is  Ehrlich's.  The  salvarsan 
powder  (0-30  to  o-6o  gramme)  is  rubbed  with  a  little  methyl  alcohol  (pure)  in  a 
sterile  vessel,  and  then  mixed  with  10  to  20  c.c.  of  normal  salt  solution. 

An  alkaline  or  neutral  solution  is  preferable,  and  is  prepared  by  rubbing  the 
drug  in  a  sterile  mortar  with  10  to  20  drops  of  a  15  per  cent,  solution  of  sodium 
hydrate,  and  adding  8  to  10  c.c.  of  sterile  distilled  water,  stirring  continuously. 
In  order  to  prepare  a  clear  solution,  it  generally  requires  1  c.c.  to  1*2  c.c.  of  the 
sodium  hydrate  solution  for  o-6  gramme  of  salvarsan ;  a  suspension  of  the  drug 
in  olive-oil  or  some  other  fatty  material  may  also  be  used.  A  good  prepara- 
tion of  this  type,  which  we  have  often  used,  is  by  Pasini. 

The  suspensions  in  oil  may  often  be  given  with  advantage  subcutaneously 
in  the  interscapular  region.     The  intramuscular  or  subcutaneous  injection 
of  salvarsan,  especially  the  acid  solution,  is  generally  painful,  and  is  followed  ■ 
by  a  hard  infiltration,  which  lasts  for  some  weeks.     Occasionally  a  slough 
forms,  which  has  to  be  removed  surgically. 

Intravenous  Injections. — The  dose  is  smaller  than  for  the  intramuscular 
injection,  0-4  gramme  for  men  and  0-3  gramme  for  women  being  sufficient. 


1562  FRAMBCESIA   TROPICA 

The  preparation  of  the  solution  to  be  injected  is  as  follows:  One  of  the  glass 
phials  in  which  salvarsan  is  put  up  in  the  dose  of  o-6  gramme  is  broken,  and 
the  contents  (o-6  gramme  of  salvarsan)  is  carefully  added  to  30  or  40  c.c. 
of  physiological  salt  solution  made  with  distilled  water  in  a  sterile  stoppered 
vessel.  It  is  dissolved  by  shaking  thoroughly,  and  by  adding  1-2  c.c.  (about 
23  drops)  of  15  per  cent,  sodium  hydrate  solution.  A  precipitate  is  formed 
which  redissolves.  The  solution  should  then  be  diluted  to  300  c.c.  with 
normal  saline;  1  or  2  more  drops  of  sodium  hydrate  may  be  required  if  the 
liquid  is  not  clear.  Each  50  c.c.  of  this  solution  contains  o-i  gramme  of  salvar- 
san. In  man,  200  c.c.  should  be  injected,  in  women  150,  in  children  less, 
according  to  the  rules  given  supra. 

For  the  intravenous  injections  special  apparatus  have  been  devised,  based 
on  the  principle  of  the  Grantly  douche.  A  convenient  one,  which  may  serve 
for  all  these  forms  of  injection,  has  been  placed  on  the  market  by  W.  H. 
Martindale. 

Precautions  to  be  Observed  . — The  solution  should  be  prepared  with  sterile 
salt  solution  made  with  freshly  prepared  distilled  water  and  chemically  pure 
sodium  chloride.  It  should  be  perfectly  clear  ;  it  should  be  slowly  infused  into 
the  vein  (200  c.c.  in  about  eight  minutes) ;  it  should  not  be  cold  (about  the 
temperature  of  the  body  if  possible) ;  the  patient  should  be  in  bed,  and  should 
be  kept  there  for  a  couple  of  days.  If  signs  of  collapse  occur  during  the 
infusion,  it  should  be  stopped  at  once,  and  an  injection  of  caffein  given. 

Tartar  Emetic. — Broden,  in  1910,  and  later  on  other  observers, 
tried  antimonial  preparations  by  intravenous  injection  as  in  sleeping 
sickness.  The  results  are  much  less  satisfactory  than  with  salvarsan 
or  neo-salvarsan. 

Intravenous  Injections  of  Tartar  Emetic  associated  with  Other  Drugs.— 
Potass,  iodide  and  mercury  were  associated  by  one  of  us  with  tartar  emetic, 
but  the  mercury  elid  not  seem  to  increase  the  action  of  tartar  emetic.  Here- 
with two  formula?: — 

1.  Tartar  emetic 
Potass,  iodid. 
Aq.  dest. 

2.'  Tartar  emetic 
Potass,  iodid. 
Hydrarg.  perchlor. 
Aq.  dest. 

One  to  3  c.c.  may  be  given  diluted  in  8  or  10  c.c.  of  sterile  water  by 
intravenous  injection  every  other  day. 

Treatment  by  Oral  Administration  of  Drugs. — When  neo-salvarsan, 
salvarsan,  or  their  substitutes,  are  unobtainable,  or  in  districts 
where  lack  of  medical  men  and  skilled  nurses  makes  any  method 
of  treatment  by  injections  difficult  or  impossible,  treatment  by  oral 
administration  is  very  convenient,  and  the  mixture  known  in  the  ■ 
tropics  as  '  Castellani's  yaws  mixture  '  will  be  found  effective  in 
many  cases. 

This  mixture  contains  tartar  emetic,  gr.  i. ;  potass,  iodid.,  5i. ; 
sodium  salicylate,  gr.  x. ;  bicarbonate  of  soda,  gr.  xv. ;  water  or 
chloroform  water,  to  1  oz.  One  ounce  is  given  three  times  daily 
diluted  in  three  or  four  times  the  amount  of  water,  to  adults  and 
youngsters  of  over  fourteen  years;  half  doses  to  children  of  eight 
to  fourteen  years  of  age,  and  one-third  or  less  to  younger  children. 


gr- 

111. 

gr- 

XXX 

ad 

§'• 

gr- 

iii. 

gr- 

XXX 

gr 
ad 

\ 

TREATMENT  1563 

To  Europeans  it  is  advisable  to  give  half  doses,  as  they  do  not  stand 
full  doses  so  well  as  do  natives. 

The  active  drugs  in  the  mixture  are  the  potassium  iodide  and  the 
tartar  emetic;  the  salicylate  of  soda  does  not  influence  the  yaws 
lesions,  but  seems  to  hasten  the  disappearance  of  the  thick  crusts, 
while  the  bicarbonate  of  soda,  though  rendering  the  mixture  cloudy 
and  inelegant,  prevents  to  a  great  extent  the  symptoms  of  iodism 
and  decreases  the  emetic  properties  of  the  mixture,  in  this  way 
rendering  possible  the  administration  of  massive  doses  of  potas- 
sium iodide,  and  large  doses  of  tartar  emetic.  In  the  few  cases  in 
which  emesis  is  produced,  the  bicarbonate  may  be  increased,  or 
a  small  amount  of  liq.  morphias  or  codein  given  before  each  dose; 
and  in  the  comparatively  rare  cases  in  which  severe  iodism  appears, 
epinephrine,  as  suggested  by  Milian,  in  grm.  0-002  doses,  may  be 
given  by  the  mouth  or  by  subcutaneous  injection,  twice  daily. 

The  mixture  as  set  down  is  cloudy,  although  it  becomes  clear 
when  diluted  with  water  at  the  time  of  administering  it.  At  the 
suggestion  of  Dr.  Dawson  Williams  some  experiments  were  carried 
out  to  obtain  a  clear  mixture,  and  it  was  found  that  the  addition 
of  sodium  tartar,  gr.  x.,  or  of  glycerine  3ii.  or  of  syrup  3i-  per  dose, 
was  sufficient  to  keep  the  mixture  clear  for  weeks.  The  modified 
formula  of  the  mixture  is  therefore  as  follows: — Tartar  emetic, 
gr.  i. ;  potass,  iodid.,  3i-;  sodii  salicyl.,  gr.  x.;  sodii  bicarb.,  gr.  xv. ; 
sodiitartarat.,  gr.  x.,  or  glycerine,  3ii.,  or  syrup,  3i-,  Aq.  ad  §i.  It  is 
given  in  the  same  doses  as  the  original  mixture,  and  well  diluted  in 
water  to  prevent  a  severe  sensation  of  burning  in  the  stomach. 

Either  the  original  or  the  modified  mixture  is  given  in  the  doses 
mentioned  for  ten  to  fifteen  days,  then  it  is  discontinued  for  about 
a  week,  and  then  given  again  for  another  ten  to  fifteen  days.  The 
results,  as  shown  by  Castellani,  Spaar,  Thomson,  and  more  recently 
by  Guerrero,  Domingo,  and  Arguelles,  who  have  carefully  investi- 
gated this  method  of  treatment  in  the  Philippines,  are  usually  very 
satisfactory  in  recent  and  fairly  recent  cases  when  they  may  be  com- 
pared with  those  obtained  by  the  salvarsan  treatment.  In  chronic 
cases  the  results  are  not  so  striking,  but  as  a  rule  much  better  than 
with  any  other  known  treatment,  except  salvarsan  or  neo-salvarsan. 

The  natives  treat  the  disease  in  various  ways.  In  Samoa  the  patient  is 
rubbed  down  with  sand  and  washed  in  the  sea,  after  which  the  yaws  are 
scraped  with  a  shell.  In  the  West  Indies  boiled  and  beaten-up  leaves  of 
the'  physic-nut'  are  applied  ,or  powdered  alum  and  sulphur  used.  In  the 
Congo  pieces  of  forge  scoriae  are  made  incandescent  and  the  yaws  lesions 
touched  with  them.  In  Ceylon  the  vedaralas  (native  doctors)  apply  concoctions 
of  various  herbs,  and  give  decoctions  of  sarsaparilla  and  other  roots.  They 
also  use  mercury  disguised  in  various  ways.  The  majority  of  European 
practitioners  use  potassium  iodide.  Others  affirm  this  drug  to  be  quite  useless, 
and  believe  that  cleanliness  and  good  and  abundant  food  are  quite  sufficient 
to  bring  about  a  cure. 

In  the  Colombo  Clinic  for  Tropical  Diseases  some  experiments  have  been 
made  on  the  various  treatments,  and  the  conclusion  arrived  at  has  been  that 
the  salvarsan  and  neo-salvarsan  treatment  is  the  most  effective  of  all,  while 
the  mixture  tartar  emetic,  potass,  iodide,  bicarb,  of  soda,  and  sod.  salyr.  is 


1564  FRAMBCESIA   TROPICA 

also  very  successful.  Some  cases  may  recover  spontaneously,  but  this  is 
certainly  the  exception,  not  the  rule.  Occasionally  cases  are  met  with  re- 
fractory to  any  treatment,  and  tertiary  lesions  are  often  intractable.  An 
important  point  often  overlooked  by  the  practitioner  is  that  the  oral  treatment 
should  be  prolonged  for  a  time  after  the  complete  disappearance  of  the  erup- 
tion, inasmuch  as  clinical  experience,  as  well  as  experiments  on  inoculated 
monkeys,  prove  that  the  specific  treponemata  may,  and  do,  persist  in  the 
lymphatic  glands  and  internal  organs  long  after  the  cutaneous  manifestations 
have  disappeared.  Atoxyl  has  been  tried  by  Neisser  in  monkeys  experi- 
mentally inoculated  with  the  disease,  and  by  one  of  us  in  human  patients. 
The  results  are  occasionally  fairly  good.  Spittel  has  used,  by  intravenous 
injection,  a  solution  of  arsenious  and  mercuric  iodide. 

Local  Treatment. — This  consists  chiefly  in  keeping  the  skin 
scrupulously  clean,  washing  the  eruption  twice  daily  with  a  per- 
chloride  of  mercury  solution  (1  to  1,000),  which  greatly  allays  the 
itching.  The  ulcerated  lesions  may  be  dusted  with  iodoform, 
europhen,  xeroform,  or  boracic  acid.  Mercury  ointments  may  be 
beneficial,  but  in  our  experience  are  not  sufficient  to  hinder  secon- 
dary pyogenic  infections.  Caustics  are  not  called  for  unless  the 
ulcers  become  phagedenic.  In  such  cases  pure  carbolic  acid  is  best. 
Though  the  external  treatment  may  be  useful,  one  must  bear  in 
mind  that  it  is  not,  as  a  rule,  sufficient  alone  to  cure  the  disease. 

Prophylaxis. — In  countries  where  frambcesia  is  endemic  the 
slightest  abrasions  of  the  skin  should  be  taken  care  of  and  properly 
treated  with  antiseptics.  Frambcesia  patients  should  be  prevented 
from  mixing  with  the  rest  of  the  population,  and  should  be  isolated 
in  special  hospitals  till  the  disease  is  cured.  Their  skin  lesions  should 
be  properly  dressed,  and  thus  prevented  from  becoming  a  source 
of  infection  through  the  agency  of  flies  and  other  insects.  Their 
huts  and  belongings  should  be  thoroughly  disinfected. 


REFERENCES. 

Alston  (1911).     British  Medical  Journal.     London. 

Ashburne  and  Craig  (1907).     Philippine  Journal  of  Science,  B.     Manila. 

Bahr  (1915).     Ann.  Trop.  Med.  and  Parasit. 

Barret  (1905).     Pathological  Society  of  London,  November. 

Blanchard  (1906).     Arch,  de  Parasitologic     Paris. 

Borne  (1906).     Geneeskundig  Tijdschrift. 

Branch  (1906).     Journal  of  Tropical  Medicine.     London. 

Breda  (1906).     Giornale  d.  mal.  ven.  e  d.  Pelle. 

Brochard  (1913).     Bull.  Path.  Exot. 

Brozrtjes  (1917).  Salvarsan  bij  frambcesia  tropica.  Geneesk.  Tijdschr. 
v.  Nederl. -Indie. 

Casoni  (1915).     Malaria  c  Mal.  Paesi  Caldi. 

Castellani  (1905-17).  Ceylon  Medical  Reports;  Journal  of  the  Ceylon 
Branch  of  the  British  Medical  Association,  June  17,  1905;  Lancet, 
August,  1905;  British  Medical  Journal,  November,  1905;  Journal  of 
Tropical  Medicine,  August,  1905,  and  January  1,  1906;  Deutsch.  med. 
Woch.,  January  1,  1906;  Journal  of  Cutaneous  Diseases,  1908;  Avchiv 
liir  Schiffs-  und  Tropen-Hy«iene,  Bd.  XL,  1907  and  191 1. 

Castellani  (1917).  Transactions  Society  of  Tropical  Medicine,  1917.  vol«  x«» 
No.  8,  July. 

Castelli  (191-2).     Zeitschrift  liir  Chemoterapie. 

Clemow  (mnO.     Geoeraphv  of  Disease.     London. 


REFERENCES  1565 

Cockin  (1912).     Journal  of  Tropical  Medicine. 

Crocker  (1905).     Diseases  of  the  Skin.     London. 

Da    Matta    (1917).     Treponemose   de  Castellani.     Bull.    Soc.    Path.    Exot., 

vol.  x.,  No.  10. 
De  Gorge  and  Mouzels  (1912).     Bull.  Soc.  Med.  Indo-Chine. 
Gabbi  and  Sabella  (191 2).     Malaria. 
Greggio   (1917).     Transactions  Soc.  of  Trop.  Med. 
Guerrero,  Domingo,  and   Arguelles   (1918).     Treatment  of  Yaws   with 

Castellani's     Mixture.      Philippine     Journal     of     Science.     Section     B, 

vol.  xiii.,  No.  4. 
Harper  (191 6).     Lancet,  October  14,  p.  67b  (Late  Sequelae  of  Framboesia). 
Jeanselme  (1903).     Dermatologie  Exotique. 

Leger,  Mouzels,  Ryckev^rt  (1917).     Bull.  Path.  Ex.,  vol.  x.,  No.  7. 
Linderman  (1909).     Bulletin  de  Path.  Exotique. 
Lohe  (1909).     Dermat.  Zeitschrift. 
MacLeod  (1902).     British  Medical  Journal.     London. 
Manson  (1918).     Tropical  Diseases.     London. 
Marshall  (1908).     Philippine  Journal  of  Science,  B.     Manila. 
Martinez  Santamaria  (191 3).     Journal  of  Tropical  Medicine. 
Maul    (191 7).     Bone    Lesions    in    Yaws.     Philippine    Journal    of    Science, 

Section  B,  vol.  xii..  No.  5. 
Modder  (190S).     Journal  of  Tropical  Medicine.     London. 
Neisser,  Baermann,  Halberstaedter  (1906) .     Munch,  med.  Woch. ;  quoted 

in  Archiv  fur  Schiffs-  und  Tropen-Hygiene,  Bd.  X.,  Heft  1. 
Neisser  (190S).     Archiv  fur  Schiffs-  und  Tropen-Hygiene. 
Noguchi  (191 2).     Journal  of  Experimental  Medicine. 
Nuttall,  G.  F.  H.  (1899).     On  the  Role  of  Insects  as  Carriers  of  Bacteria 

and  Parasitic  Diseases.     Johns  Hopkins  Hospital  Reports,  vol.  viii. 
Nichols  (1909).      Philippine  Journal  of  Science;  (191 1)  Journal  of  Experi- 
mental Medicine. 
Perry  (1904-14).     Medical  Reports  Ceylon. 
Plehn  (1906).     Mense's  Handbuch  der  Tropenkrankheiten. 
Powell    (1898-1905).     Pathological    Society,     London,     November,     1905: 

British  Medical  Journal  of  Dermatology,  1898. 
Pupo  (1917).     Bouba.  Ann.  Paul.  Med.  e  Cirurg.,  vol.  viii.,  No.  1. 
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Caracas. 
Robledo  (1909).     Bulletin  de  Pathologie  Exotique.     Paris. 
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January.     (Full  bibliography.) 


CHAPTER  LXII 
VERRUGA   PERUVIANA 

Synonyms  —  Definition  —  History  —  Climatology  —  etiology — Pathology — 
Histopathology — Symptomatology —  Diagnosis  — Prognosis  —  Treatment 
— Prophylaxis — References. 

Synonyms. — Peruvian  wart,  Verruga  Blanda,  Carrion's  Fever,  Verruga  de 
Castilla,  Verruga  of  the  Andes,  Verruga  de  Zapo  6  de  Quinua,  Verruga  Andi- 
cola,  Verruga  Mular,  Verruga  de  Sangre,  Fiebre  de  la  Oroya,  Verruga  de 
Crapaud,  Bouton  des  Andes.     The  word '  verruga'  signifies  in  Spanish  a  wart. 

Definition. — Verruga  peruviana  is  a  chronic  endemic  specific 
general  disorder  of  unknown  origin,  not  contagious,  but  apparently 
inoculable,  and  characterized  by  an  irregular  fever  associated  with 
rheumatoid  pains  and  anaemia,  followed  by  granulomatous  swellings 
in  the  skin,  mucous  membranes,  and  organs  of  the  body. 

History. — It  is  probable  that  the  disease  existed  in  South  America 
before  the  advent  of  the  Spaniards,  for  the  earliest  references  to  it 
are  found  in  Spanish  works  on  Peru  in  the  sixteenth  century.  The 
first  record  is  by  Agustin  de  Zarate,  Treasurer  of  Lima,  in  his 
'  History  of  the  Conquest  of  Peru,'  written  in  1543,  in  which  he 
relates  that  warts  or  small  tumours  appeared  on  the  face  and  other 
parts  of  the  body,  which  were  more  deadly  than  smallpox,  and 
almost  as  fatal  as  plague. 

Garcilas  de  la  Vega  records  that  a  quarter  of  the  small  army  of 
Francois  Pizarre  perished  from  this  cause,  while  Gomara,  Garcilazo 
(1617),  and  other  early  writers,  also  drew  attention  to  the  disease. 
After  this  period  writers  on  Peru  either  fail  to  mention  the  disease 
at  all,  or  only  write  short  paragraphs  such  as  that  in  Cosme  Bueno's 
geographical  description  of  the  province  of  Canta,  published  in 
1764,  in  which  it  is  mentioned  under  its  ancient  name  of  '  berrugas.' 

The  modern  descriptions  of  the  disease  begin  with  the  works  of 
Tschudi  in  1843,  Malo  in  1852,  Smith  in  1858,  Salazar  and  Manuel 
Odriozola  in  1858,  Velez  in  1861,  and  Dounon  in  1871,  the  last  named 
giving  a  very  clear  account  of  the  complaint. 

But  little  interest  was,  however,  taken  in  it  until  1870,  when  a 
severe  outbreak  of  fever  took  place  among  the  workpeople  laying 
the  railway-line  between  Lima  and  Oroya.  This  complaint  for 
some  reason  was  called  '  Oroya  fever,'  although  it  did  not  affect 
Oroya.  About  the  same  time  Dounon's  excellent  paper  appears  to 
have  interested  French  naval  surgeons,  so  that  numerous  investiga- 
tions as  to  verruga  and  Oroya  fever  were  made  both  by  Peruvian 

1566 


HISTORY  1567 

doctors,  such  as  Pancorvo  and  others  in  1875,  and  French  surgeons, 
such  as  Fournier  in  1874,  Bourse  in  1876,  and  Tupper  in  1877. 
During  this  period  there  was  much  disputation  as  to  whether  Oroya 
fever  was  related  to  verruga,  or  was  a  distinct  clinical  entity.  In 
1885  Daniel  A.  Carrion,  a  student  of  the  Faculty  of  Medicine  of 
Lima,  who  had  for  some  time  been  studying  the  disease,  attempted 
to  settle  this  question  by  vaccinating  both  his  arms  with  the  blood 
from  a  verruga  tumour  on  August  27,  1885,  and  on  September  17 
he  began  to  suffer  from  the  symptoms  of  Oroya  fever,  from  which  he 
died  on  October  5.  In  honour  of  his  noble  attempt  to  elucidate 
the  aetiology  of  the  fever,  his  compatriots  have  since  referred  to 
Oroya  fever  as  Carrion's  disease. 

The  unfortunate  death  of  this  brave  young  man  stimulated 
inquiry,  and  a  very  large  number  of  investigations  were  published, 
of  which  it  is  only  possible  to  mention  a  few. 

In  1885  Izquierdo  announced  the  discovery  of  a  bacillus  in  some 
specimens  sent  to  him  in  spirit,  which,  of  course,  prevented  anything 
of  the  nature  of  a  thorough  bacteriological  investigation. 

In  1887  Florez  grew  a  coccus  on  agar-agar  inoculated  with  the 
blood  from  persons  suffering  from  verruga.  In  1898  a  most  elabor- 
ate monograph  by  E.  Odriozola  appeared,  which  the  reader  inter- 
ested in  the  subject  is  strongly  advised  to  peruse. 

In  the  same  year  Nicolle  and  Letulle  independently  described 
bacilli  resembling  those  of  tuberculosis  in  the  skin  lesions.  Barton, 
in  1902,  published  the  first  careful  bacteriological  examinations  of 
Carrion's  fever,  and  from  1903  to  the  present  time  Biffi  has  written 
a  series  of  able  papers  on  the  disease. 

We  are  therefore  confronted  with  two  conditions  described  by 
authors — viz. ,  a  disease  which  may  or  may  not  begin  with  fever,  and 
which  ultimately  ends  with  a  most  peculiar  and  typical  eruption, 
verruga  peruviana,  and  another  disease  characterized  by  an  incuba- 
tion period  of  twenty-one  days,  as  proved  by  Carrion's  inoculation, 
and  of  a  severe  type  often  ending  in  death,  without  the  appearance  of 
any  eruption.  Are  these  two  conditions  one  and  the  same  disease — 
that  is  to  say,  is  Carrion's  fever  Peruvian  wart  without  an  eruption, 
or  are  the  two  separate  pathological  entities?  Tasset,  in  1872, 
held  that  they  were  separate  entities,  and  that  Carrion's  fever  was 
a  tvpho-malarial  fever,  but  since  the  inoculation  of  Carrion  most 
authors  have  considered  the  two  diseases  to  be  one  and  the  same, 
though  every  now  and  again  some  author  has  objected,  and  has 
held  that  Carrion's  fever  was  typhoid.  In  1901-02,  Barton,  as 
the  result  of  careful  bacteriological  researches,  concluded  that  in 
the  blood  and  organs  of  persons  dying  from  Carrion's  fever  a  micro- 
organism could  be  found  which,  though  similar  to  Bacillus  coli 
communis  in  many  respects,  was  easily  separable  therefrom.  This 
organism  was  fatal  to  inoculated  animals,  causing  a  septicaemia 
and,  it  is  said,  a  verruga-like  eruption  in  the  skin.  Biffi  has  carefully 
investigated  this  bacillus,  and  finds  that  it  is  present  constantly  and 
in  abundance  in  persons  suffering  from  Carrion's  fever,  but   is 


1568  VERRUGA  PERUVIANA 

absent  in  patients  suffering  from  verruga  peruviana  without  fever. 
It  is  agglutinated  by  the  serum  of  persons  suffering  from  Carrion's 
fever,  but  not  by  that  of  patients  suffering  from  verruga  who  have 
not  had  fever.  The  micro-organisms  are,  however,  not  always  of 
the  same  strain.  Thus,  Biffi  has  separated  two  different  strains, 
one  of  which  resembles  Schottmiiller's  B.  paraiyphosus  B,  and  the 
other  Gartner's  bacillus.  Biffi  and  Carbajal  were  unable  to  confirm 
Barton's  results  as  to  the  presence  of  a  skin  eruption  in  animals 
inoculated  by  these  strains.  They  therefore  conclude  that  Carrion's 
fever  is  a  separate  pathological  entity  distinct  from  verruga,  and 
that  it  is  a  fever  belonging  to  the  paratyphoid  group,  but  differs 
from  the  usual  types  by  being  due  to  a  different  organism,  and  by 
occurring  in  patients  suffering  from  verruga.  In  this  finding  they 
are  supported  by  the  clinical  observations  of  several  observers, 
among  whom  may  be  mentioned  Eder. 

The  next  question  which  must  be  considered  is  the  nature  of 
verruga  peruviana,  for  it  has  been  suggested  that  it  is  fram- 
bcesia,  and  this  has  been  specially  emphasized,  since  it  has  been 
realized  that  it  may  run  its  course  without  any  fever.  Biffi,  how- 
ever, has  clearly  shown  that  they  are  separate,  frambcesia  being 
contagious,  verruga  not;  frambcesia  beginning  with  an  initial 
lesion,  verruga  not;  frambcesia  being  due  to  Treponema  pertenue 
Castellani,  verruga  not.  We  may  therefore  conclude  that  verruga 
peruviana  is  a  definite  pathological  entity.  Further  researches  in 
the  disease  have  been  made  by  Bassett-Smith,  Mayer,  and  others. 

In  1915  Strong,  Tyzzer,  Brues,  Sellards,  and  Gastiaburu  published 
a  valuable  report,  pointing  out  that  Oroya  fever  was  distinct  from 
verruga  peruviana. 

The  former,  according  to  these  investigators,  is  due  to  Bartonella 
bacilliformis  {vide  p.  502),  which  in  many  ways  resembles  Theileria 
parva,  while  the  latter  is  probably  caused  by  a  filterable  virus,  and 
can  be  inoculated  into  monkeys;  it  resembles  closely  Bassewitz's 
angiofibroma  cutis  contagiosum  tropicum  (p.  2253).  Verruga  may  be 
spread  by  a  blood-sucking  arthropod.  Townsend,  in  1914  and  1915, 
declared  his  belief  that  this  arthropod  \va.sPhlebotomus  verrucanim. 

Climatology. — Verruga  peruviana  is  confined  to  South  America, 
and  to  the  western  slopes  of  the  Andes  in  Ecuador,  Peru,  Bolivia,  and 
the  northern  parts  of  Chili,  the  most  important  endemic  area  being 
Peru,  where  it  is  almost  limited  to  the  departments  of  Ancachs  and 
Lima,  lying  north  and  south  of  the  tenth  parallel,  and  on  the  western 
side  of  the  Andes.  The  department  of  Ancachs  comprises  seven 
provinces,  of  which  the  provinces  of  Pallusca,  Huaylas,  Huaraz, 
and  Cajatambo,  which  are  on  the  western  slopes  of  the  Andes,  are 
most  affected,  while  that  of  Santa,  which  runs  along  the  littoral,  is 
almost  free.  The  disease  is,  however,  peculiarly  limited  to  certain 
places  in  these  provinces.  The  heights  of  these  places  vary  from 
Cochas,  in  the  province  of  Cajatambo,  which  is  only  at  an  elevation 
of  406  metres,  to  Cajatambo,  in  the  same  province,  which  is  at  an 
altitude  of  3,350  metres,  but  according  to  Monge  it  is  never  naturally 


CLIMA  TOLOG  Y—MTIOLOG  Y  1569 

acquired  at  an  elevation  below  2,800  feet  or  above  9,000  feet,  nor 
does  it  originate  in  the  main  valleys. 

One  striking  peculiarity  common  to  all  the  places  is  that  they  are 
in  narrow  valleys  along  tributaries  of  rivers.  The  principal  infected 
areas  are  Tablachaca,  Pallusca,  Corongo,  Pacatqui,  and  Ninabamba, 
in  Pallusca;  Huaylas  and  Caraz,  in  Huaylas;  Yautan,  Pariacoto, 
Rurasca,  Nanca,  Jangas,  Pongor,  Anta,  and  another  district  on  a 
branch  of  the  River  Huarmey,  in  Huaraz;  Cochas,  Huaylillas,  and 
Cajatambo,  in  Cajatambo. 

In  the  department  of  Lima  there  are  six  provinces,  of  which 
Chancay,  Canta,  Huarochiri,  and  Yauyos  possess  endemic  areas, 
which  vary  in  height  from  900  to  2,030  metres.  In  Chancay 
there  is  Huaycho;  in  Canta,  Acos,  Viscas,  Yasu,  Magdalena,  and 
Yangas;  in  Huarochiri,  Santa  Eulalia,  Palle,  San  Geronimo,  San 
Pedro  de  Casta,  Surco,  Cocachacra,  Santa  Ana,  and  Sisicaya;  and 
in  Yauyos,  Omas. 

The  best -known  area  is  that  which  lies  along  the  railway  from 
Lima  to  Oroya,  which  begins  a  little  below  the  division  of  the  River 
Rimac  into  the  rivers  Santa  Eulalia  and  Cocachacra,  along  both  of 
which  the  disease  is  endemic  for  some  distance,  including  Santa 
Eulalia,  San  Geronimo,  Cupichi,  San  Pedro  de  Casta,  San  Pedro 
de  Mama,  Santa  Ana,  Corcona  Cocachacra,  San  Bartolome  (where 
the  stream  which  runs  into  the  Cocachacra  River  is  called  the 
Aqua  de  Verrugas,  because  the  people  believed  the  disease  came 
from  drinking  the  water),  Cuesta  Blanca,  and  Surco. 

Here  again,  as  in  the  department  of  Ancachs,  the  disease  is 
restricted  to  certain  deep,  narrow  valleys,  locally  known  as 
'  quebradas,'  along  which  streams  flow,  and  which  are  some  28  to 
60  kilometres  distant  from  the  littoral,  where  the  disease  never 
occurs.  A  very  important  epidemiological  point  is  that  the  disease 
only  occurs  in  the  summer  when  the  rivers  are  in  flood,  and  when  all 
sorts  of  insects  abound.  Monge  points  out  that  earthquakes  are 
correlat  ed  with  small  epidemics,  probably  because  the  disturbed  popu- 
lation becomes  more  exposed  to  the  infection,  whatever  that  may  be. 

Etiology. — The  causation  of  verruga  peruviana  is  unknown. 
Popularly  the  disease  is  believed  to  be  conveyed  by  the  drinking- 
water,  which,  however,  has  long  been  discredited.  In  1875  Pan- 
corvo,  taking  into  consideration  the  well-known  fact  that  the  persons 
who  mostly  suffer  are  people  who  work  in  the  fields  or  disturb  earth, 
suggested  that  it  was  an  intoxication  due  to  sulphuretted  hydrogen 
liberated  from  the  earth,  a  view  which  never  received  any  marked 
support.  Odriozola  and  Tamayo  have  failed  to  find  any  bacteria 
in  people  suffering  from  the  eruption  of  Peruvian  wart.  It  is  said 
to  occur  in  animals,  especially  quadrupeds,  and  not  to  be  con- 
tagious. Chastang  believes  that  some  germ  is  inoculated  by  the 
thorns  of  Cactus  opunlia.  Long  ago  Raymondi  suggested  that 
verruga  would,  like  rabies  and  syphilis,  be  found  some  day  to  be 
due  to  a  definite  virus.  Translating  Raymondi's  views  into  modern 
thought,  it  would  mean  that  the  three  diseases  would  be  found  to  be 

99 


157°  VERRUGA   PERUVIANA 

due  to  a  parasitic  protozoon,  and,  indeed,  there  is  no  doubt  about 
the  truth  of  this  with  regard  to  syphilis  and  with  regard  to  rabies, 
and  it  is  quite  possible  that  verruga  peruviana  will  some  day  be 
found  to  be  of  protozoan  origin,  thus  confirming  Raymondi's  striking 
conjecture. 

The  study  of  the  distribution  of  the  disease  in  the  various  pro- 
vinces of  Peru,  as  detailed  above,  with  the  aid  of  a  large-scale  map, 
will  impress  the  reader  with  the  similarity  to  the  distribution  of 
Rocky  Mountain  fever,  and  will  lead  him  to  the  conclusion  that  the 
^etiological  cause  must  in  some  way  be  associated  with  some  blood- 
sucking animal,  perhaps  an  arachnid;  and,  indeed,  this  is  supported 
by  a  fact  well  known — that  the  persons  most  prone  to  the  infection 
are  those  who  work  in  the  fields.  Such  ideas  must,  however,  be 
taken  as  mere  suggestions,  as  at  present  there  is  no  direct  evidence 
in  favour  of  them.  Very  minute  bacillary-like  rods,  thicker  in  the 
middle  than  at  the  ends  and  variable  in  number,  have  been  described 
in  the  red  cells  by  Barton,  Gastiaburu,  Rabagliati,  and  Biffi.  They 
become  scanty  after  the  eruption,  and  disappear  during  convales- 
cence. Similar  bodies  have  been  seen  by  De  Vecchi,  Bassett-Smith, 
and  Martin  Mayer.  De  Vecchi  considers  them  to  be  products  of 
degeneration. 

Strong,  Tyzzer,  Brues,  Sellards,  and  Gastiaburu 's  experiments 
would  point  to  the  virus  being  a  filterable  one,  and  inoculable  in 
monkeys.  Inoculated  in  the  testes  of  the  dog  and  rabbit  it  induces 
characteristic  changes.  As  already  stated,  these  authors  believe 
that  the  disease  is  not  connected  with  Oroya  fever,  which,  according 
to  them,  is  due  to  Bartonella  bacilliformis  (p.  502),  and  is  not  inocul- 
able inhmonkeys. 

Age,  sex,  and  race  appear  to  have  no  influence,  though  it  has  been 
asserted  that  the  coloured  races  have  a  partial  immunity,  which 
is  due  to  mild  attacks  at  a  very  early  age,  as  nearly  every  inhabitant 
in  the  towns  of  the  endemic  areas  acquires  verruga,  and  if  reinfected 
has  only  a  very  mild  attack,  for,  as  a  rule,  an  attack  confers  a 
lasting  immunity.  Strangers  visiting  an  endemic  area  are  attacked 
almost  at  once  with  the  disease  in  its  gravest  form.  The  disease 
may  be  acquired  by  travelling  through  an  endemic  area,  but  there 
is  much  more  risk  of  infection  if  a  night  is  spent  therein,  and  if  the 
endemic  zone  is  quitted  before  sunset  the  risk  of  infection  is  greatly 
diminished.  Another  important  point  is  that  newly-born  infants 
may  acquire  the  disease.  Cole  has  made  some  inoculation  experi- 
ments in  monkeys  with  a  certain  degree  of  success. 

Pathology. — As  the  causation  is  unknown,  the  account  of  the 
pathology  must  be  limited  to  very  few  remarks.  There  has  been 
great  doubt  as  to  whether  verruga  can  be  transmitted  to  animals  by 
inoculation,  though  Odriozola  related  that  he  inoculated  a  bitch  with 
the  blood  from  verruga  lesions  obtained  from  a  post-mortem,  with 
the  result  that  the  animal  developed  a  typical  skin  eruption,  and 
eventually  died.  The  disease  is  said  to  occur  naturally  among 
animals — e.g.,  horses,  mules,  asses,  dogs,  and  fowls — but  especially 
among  quadrupeds,  although  Monge  states  that  no  one  has  definitely 


PATHOLOGY— HI  STOP  ATHOLOGY  1571 

proved  that  this  is  the  verruga  of  man,  and  the  ordinary  laboratory 
animals  cannot  be  infected  with  the  disease.  According  to  some 
observers,  the  infection  in  man  begins  with  a  general  illness, 
which  would  appear  from  the  fever,  the  anaemia,  and  the  pains 
in  different  parts  of  the  body,  to  be  of  the  character  of  a 
septicaemia,  after  which  the  typical  eruption  appears  on  the 
skin,  mucous  membranes,  and  internal  organs,  when  as  a  rule 
the  general  symptoms  of  fever,  etc.,  abate,  from  which  one 
would  infer  that  the  organism  had  left  the  blood  stream,  and  become 
located  in  the  skin  and  other  organs.  It  is  possible  that  it  leaves  the 
body  by  way  of  the  skin.  If,  however,  the  local  lesion  develops  in 
such  places  as  the  meninges,  the  choroid  plexus,  the  choroid  coat 
of  the  eye,  the  intestines,  the  oesophagus,  or  larynx,  severe  symptoms 
are  apt  to  appear,  and  complicate  the  illness.  If  at  the  same  time 
a  paratyphoid-like  infection  takes  place  during  the  febrile  stage,  the 
true  symptoms  are  masked,  and  a  peculiar  and  very  deadly  type 
of  fever,  called  '  Carrion's  disease,'  is  produced. 

The  morbid  anatomy  is  characterized  by  marked  pallor  of  the 
body,  oedema  and  dropsy,  hypostasis  of  the  lungs,  enlargement  of 
the  liver  and  spleen,  and  hyperemia  of  the  bone-marrow;  but 
apart  from  these  general  signs,  the  characteristic  features  are  the 
appearance  of  the  verrugas  in  the  skin  and  subcutaneous  tissues,  in 
the  ocular  and  palpebral  conjunctivae,  the  mucosa  of  the  nose,  the 
lips,  gums,  palate,  tongue,  pharynx,  larynx,  trachea,  oesophagus, 
stomach,  small  and  large  intestine,  in  the  substance  of  the  liver, 
spleen,  lungs,  thymus,  thyroid,  testicles,  kidneys,  and  lymphatic 
glands,  and  at  times  in  the  leptomeninges,  the  choroid  plexuses,  the 
choroid  coat  of  the  eye,  in  the  substance  of  the  muscles,  on  the 
periosteum  of  bones,  on  the  peritoneal  coverings  of  organs,  and  on 
the  pleura  and  pericardium. 

Histopathology. — The  histopathology  of  the  disease  has  been 
carefully  studied  by  Letulle,  Jamayo,  Escomel,  Jeanselme,  Her- 
cules, Biffi,  De  Vecchi,  and  very  completely  by  Strong  and 
his  co-workers.  The  miliary  and  nodular  forms  take  origin  around 
the  capillary  bloodvessels  in  the  form  of  a  neoplasm  which 
is  the  reaction  of  the  areolar  tissue  to  some  perivascular 
irritant.  The  connective-tissue  fibres  become  swollen,  and 
between  them  lie  embryonic  connective-tissue  cells,  while  the 
inter  areolar  spaces  contain  polymorphonuclear  cells  and  macro- 
phages. Microscopically  a  non-ulcerated  skin  lesion  shows  the  cells 
of  the  surface  epithelium  swollen  and  distended  with  glycogen.  The 
papillary  layer  of  the  cutis  has  disappeared,  and  the  dermis  proper 
is  infiltrated  with  round  cells,  which  are  mostly  mononuclear  or 
polymorphonuclear  leucocytes,  separated  by  a  slight  amount  of 
fibrillar  connective  tissue,  which  may  in  places  be  entirely  absent. 
There  is  some  doubt  as  to  whether  the  connective-tissue  corpuscles 
contribute  to  the  round-celled  infiltration,  as  has  been  asserted  by 
Izquierdo;  in  any  case,  the  recognizable  connective-tissue  cells  are 
always  swollen,  and  their  nuclei  are  altered  in  various  ways.  The 
cellular  infiltration  is  very  vascular,  and  in  the  case  of  the  older 


1572  VERRUGA  PERUVIANA 

tumours  almost  cavernous  in  structure;  hence  the  liability  to 
haemorrhage,  which  is  such  a  marked  feature  of  the  disease. 

The  subcutaneous  fatty  tissue  is  always  inflamed.  In  addition 
to  these  features,  Letulle  describes  and  figures  some  most  peculiar 
structures  seen,  under  a  magnification  of  400  diameters,  between 
the  cells  of  the  epidermis,  which  he  considers  to  be  clasmatocytes. 

The  growths  appear  to  be  often  invaded  secondarily  with  micro- 
organisms, especially  if  ulcerated,  while  the  eosinophiles  disappear 
and  the  mononuclears  diminish.  Myelocytes  may  be  present,  and 
may  number  0-5  per  cent.,  and  there  maybe  some  large  mononuclear 
cells  like  macrophages.  The  nuclei  of  the  polymorphonuclears  are 
simply  bilobed. 

Symptomatology.— The  incubation  period  is  not  definitely  known, 
and  is  stated  to  vary  from  eight  to  forty  days,  but  to  be  most  usually 
from  twenty  to  thirty  days,  during  which  time  prodromata,  in  the 
form  of  malaise,  lassitude,  and  depression,  may  be  experienced. 

Febrile  Stage  (Oroya  Fever). — The  invasion  is  gradual,  the 
prodromal  symptoms  increasing  in  virulence,  while  anaemia 
becomes  apparent,  and  peculiar  rheumatoid  pains  appear  in 
different  parts  of  the  body.  These  pains  are  very  striking 
and  very  misleading,  for  they  may  in  some  cases  be  limited 
to  a  single  region,  or  even  to  a  single  joint  or  muscle;  on  the 
other  hand,  they  may  be  more  extensive,  and  lead  to  a  diagnosis 
of  some  nerve  disorder.  As  a  rule,  but  not  invariably,  fever 
appears,  and  varies  in  intensity  with  the  severity  of  the  attack. 
There  is  usually  insomnia  and  often  delirium.  Usually  it  is  inter- 
mittent in  character,  the  paroxysm  beginning  about  noon  with 
chills,  severe  pains,  much  thirst,  and  a  rise  of  temperature  to  about 
1040  F.,  with  a  quick,  soft,  compressible  pulse,  and  ending  in  about 
twelve  hours  by  crisis,  associated  with  sweating  and  an  amelioration 
of  the  pains.  The  liver  and  lymphatic  glands  enlarge,  but  accord- 
ing to  some  authorities  the  spleen  is  not  palpable.  The  patient 
rapidly  becomes  very  anaemic  and  feeble,  and  usually  constipated, 
but  may  at  times  suffer  from  severe  diarrhoea.  The  destruction  of 
red  cells,  according  to  Monge,  is  enormous,  the  number  falling  to 
()oo, 000  per  cubic  millimetre,  with  microcytes  in  large  numbers, 
macrocytes,  normoblasts  (2,000  per  cubic  millimetre),  megaloblasts 
(200  per  cubic  millimetre),  polychromatophilia,  and  poikilocytosis, 
while  the  haemoglobin  value  is  always  increased.  There  is  the  pic- 
ture of  the  blood  in  a  pernicious  anaemia.  There  is  always  a  marked 
leucocytosis,  the  count  rising  to  20,000  per  cubic  millimetre  after 
the  first  few  days,  and  increasing  later.  The  polymorphonuclear 
leucocytes  number  about  75  per  cent.  The  condition  of  the  bone- 
marrow  has  been  studied  by  Corvallo,  who  finds  excess  of  normo- 
blasts and  neutrophile  myelocytes. 

Eruptive  Stage  [Verruga,  senst'i  stricto). — In  many  cases,  after  the 
febrile  stage  has  lasted  from  twenty  days  to  eight  months,  the 
skin  begins  to  itch,  and  an  eruption  appears  on  the  face,  neck,  the 
extensor  surfaces  of  the  arms  and  legs,  and  at  times  on  the 
conjunctivae,  the  lips,  tongue,  gums,  palate,  and  pharynx.     This 


ERUPTIVE  OR  MILD  FORM  1573 

eruption  shows  itself  at  first  as  small,  pinkish-red,  erythematous 
spots,  sometimes  associated  with  small  vesicles,  or  more  rarely 
with  bullae  or  pustules.  The  erythematous  areas  speedily  become 
papules,  and  finally  nodules,  which  may  vary  in  size  and  in  number. 
The  usual  size  is  about  that  of  a  pea. 

When  fully  developed,  they  appear  as  elevated,  cylindrical,  fungi- 
form, or  irregular  wart-like  bodies,  usually  discrete,  red  in  colour, 
generally  firm  to  the  touch  (though  they  may  be  soft),  and  very 
liable  to  bleed.  This  type  of  eruption  is  the  forme  miliare  (miliary 
type)  of  the  Odriozolas  and  Salazar.  In  addition  to  these  super- 
ficial tubercles  there  are  deep  subcutaneous  nodules  (nodular  type), 
which  lie  under  the  unaltered  skin,  and  from  which  at  first  they  are 
quite  free.  These  nodules  may  reach  a  large  size,  and  become 
adherent  to  the  skin,  ulcerate,  and  reach  the  surface  as  large  red 
f ungating  masses,  which  readily  bleed.  This  is  the  forme  midair e 
of  the  above-mentioned  authors.  Both  types  appear  on  the  skin, 
but  the  miliary  type  may  also  appear  on  the  mucous  membranes 
and  internal  organs,  while  the  nodular  type  is  confined  to  the  skin, 
especially  at  the  flexures  of  the  elbows  and  knees.  The  first  crop 
usually  appears  on  the  face,  and  the  extremities  may  be  discrete  or 
confluent ;  in  the  latter  case  no  healthy  area  of  skin  may  be  visible. 
The  miliary  eruption  may  appear  when  the  general  symptoms  have 
abated,  but  the  nodular  is  accompanied  by  fever. 

The  area  of  the  skin  on  which  the  spots  appear  is  usually 
eedematous,  a  feature  most  commonly  observed  on  the  legs.  With 
the  appearance  of  the  eruption  the  fever  declines,  the  general 
symptoms  abate,  and  the  patient  feels  better,  but  the  blood  shows 
a  marked  diminution  in  the  red  cells,  some  of  which  are  nucleated, 
and  a  corresponding  reduction  in  the  haemoglobin,  and  this  anaemia 
may  be  aggravated  by  haemorrhages  from  the  nodules,  which  may 
be  so  severe  as  to  cause  the  death  of  the  patient.  This  blood 
condition  has  been  carefully  investigated  by  Monge,  who  finds  that 
at  the  commencement  of  the  illness  there  is  oligocythemia,  micro- 
cyces,  macrocytes,  normoblasts,  and  megaloblasts  (under  1,000  per 
cubic  millimetre),  with  poikilocytosis,  polychromatophilia,  and 
granular  red  cells.  The  haemoglobin  value  is  raised.  The  white 
cells  are  increased,  and  there  is  slight  polymorphonucleosis.  The 
mononuclears  have  well-marked  basophilic  protoplasm.  At  this 
stage  the  verrugas  may  develop  in  the  internal  organs,  and  cause 
serious  symptoms;  thus  in  the  larynx  they  will  cause  dyspnoea;  in 
the  bronchi,  bronchitis;  in  the  lungs,  pneumonia;  in  the  pleura, 
pleurisy;  in  the  nose,  epistaxis  and  difficulty  in  nasal  breathing; 
in  the  oesophagus,  dysphagia;  in  the  intestine,  bloody  diarrhoea;  in 
the  meninges,  brain  symptoms;  in  the  eye,  amblyopia;  and  in  the 
uterus,  metrorrhagia. 

After  Lasting  from  four  to  six  months,  during  which  several  crops 
appear  and  disappear,  cacli  preceded  by  an  attack  of  fever,  the 
eruption  finally  disappears,  and  the  nodules,  becoming  pale  and 
drying  up,  disappear  without  producing  a  scar,  while  the  ulcerated 
nodules  dry  up  and  heal  hv  cicatrization,  and  the  patient  is  left 


1574 


VERRUGA  PERUVIANA 


\g...-j* 


Fig.  706. — Verruga  Peruviana:  Eruption  on  Extremities. 
(After  Biffi,  from  the  Archiv  fi'tr  Schiffs-  it.  Tropen-Hygiene.) 


ACUTE  OR  SEVERE  FORM— DIAGNOSIS  1575 

convalescent,  but  anaemic  and  feeble.  According  to  Monge,  syste- 
matic examination  of  the  blood  reveals  the  fact  that  a  time  arrives, 
which  he  calls  the  critical  period,  when  the  leucocytes  are  reduced; 
the  polymorphonuclear  leucocytes  also  diminish  in  numbers,  and 
the  eosinophiles,  which  have  been  practically  absent,  reappear,  and 
a  definite  mononuclear  increase  supervenes.  This  critical  period 
lasts  four  to  five  days,  and  changes  completely  the  blood  picture. 

During  the  decline  of  the  disease  there  is  slight  oligocythemia  and 
granular  red  cells,  while  the  mononuclear  cells  are  increased  to 
50  to  60  per  cent.;  there  is  slight  eosinophilia,  and  the  haemoglobin 
value  is  normal. 

The  course  of  the  disease,  however,  is  by  no  means  as  straight- 
forward as  depicted,  for  at  times  the  eruption  comes  out  poorly, 
and  is  limited  in  its  distribution,  or,  having  developed,  may  dis- 
appear, in  which  cases  the  general  symptoms,  which  may  have 
improved,  are  apt  to  return  and  cause  a  serious  illness. 

Acute  or  Severe  Form. — This  form — Carrion's  disease,  sensu 
stricfo — is  considered  by  many  authorities  to  be  a  condition  separate 
from  verruga,  and  when  present  in  verruga  to  be  merely  a  compli- 
cation. It  seems  to  be  a  fever  of  the  enteroidea  group.  The 
temperature  becomes  almost  continuous,  the  pains  and  the  diar- 
rhoea severe,  the  urine  dark  and  scanty,  acid  in  reaction,  with  high 
specific  gravity,  increased  indican  and  urobilin,  but  rarely  albumen, 
and  never  blood.  It  contains  something  which  reduces  Fehling's 
solution.  According  to  some  observers  the  anaemia  becomes  pro- 
found, the  red  cells  being  reduced  to  500,000,  according  to  Monge, 
nucleated  red  cells  appearing,  while  death  results  in  about  two  or 
three  weeks. 

Varieties. — Slight  cases  may  pass  through  the  whole  illness 
without  fever,  while  more  severe  cases  show  intermittent  or  even 
remittent  fever. 

Complications. — The  complications  are  numerous,  and  include 
septic  poisoning,  malaria,  tuberculosis,  and  syphilis. 

The  observers  who  consider  Oroya  fever  a  separate  entity  from  ver- 
ruga, admit  that  it  is  not  rarely  complicated  with  the  latter. 

Sequelae. — The  usual  sequelae  are  anaemia,  dropsy,  and  affections 
of  the  nervous  system. 

Diagnosis. — The  most  important  feature  in  the  diagnosis  is  resi- 
dence in  one  of  the  endemic  areas,  when  a  person  complaining  of 
vague  pains  and  illness,  with  distinct  anaemia,  with  or  without 
febrile  symptoms,  should  be  regarded  as  most  likely  to  be  suffering 
from  the  febrile  or  anaemic  stage  of  verruga.  The  rapidity  with 
which  the  anaemia  is  developed  is  an  important  point  in  the 
diagnosis,  for  in  the  severe  forms  of  the  disease  the  number  of 
the  red  cells  will  fall  in  three  to  four  days  to  less  than 
1,000,000  per  cubic  millimetre,  and  even  in  slight  cases  there  will 
be  a  marked  diminution.  Concurrently  in  the  severe  forms  all 
the  signs  of  the  blood  picture  of  pernicious  anaemia  will  develop. 
This  anaemia  imprints  a  typical  facies  upon  the  patient.  The 
febrile  stage  must  be  differentiated  from  malaria  by  the  absence 


I57& 


VERRUGA   PERUVIANA 


of  the  parasites  in  the  blood,  from  typhoid  by  the  serum  reactions, 
from  tuberculosis  by  skin  and  ophthalmic  reaction,  from  rheumatism 
by  the  absence  of  the  swelling  of  the  joints,  and  from  histoplasmosis 
by  the  absence  of  the  parasite.  The  stage  of  eruption  must  be  dis- 
tinguished from  framboesia  by  the  absence  of  the  eruption  on  the 
trunk,  by  the  tendency  to  haemorrhage,  and  the  absence  of  Trepo- 
nema pertcnue. 

It  should  be  remembered  that  according  to  Strong,  Tyzzer,  Brues,  Sellards, 
and  Gastiaburu's  valuable  researches,  Oroya  fever  and  verruga  are  two 
separate  diseases,  Oroya  fever  being  characterized  by  the  profound  anaemia, 
the  fever,  the  presence  of  Bartonella  bacilliformis  in  the  blood,  its  non-inocu- 
lability  in  monkeys,  while  uncomplicated  verruga  is  clinically  identical  with 
angiofibroma  contagiosum ;  there  is  no  fever,  no  severe  ansemia,  there  is 
absence  of  B.  bacilliformis  and  the  condition  is  inoculable  in  monkeys  and 
human  beings. 


Fig.  707. — Verruga  Peruviana  :  Eruption  on  the  Face,  Lips,  and  Tongue. 
(Alter  Biffi,  from  the  Archiv  fi'tr  Schiffs-  u.  Tropen-Hygicne.) 

Prognosis. — With  the  possibility  of  such  a  serious  complication 
as  Carrion's  fever  arising,  or  in  later  stages  of  internal  verrugas 
forming,  the  prognosis  must  be  very  guarded.  A  good  sign  is  an 
early  appearance  of  a  widely-spread  eruption,  while  a  poorly- 
developed  eruption  associated  with  anaemia  and  marked  weakness 
is  of  grave  import.  Monge  stales  that  the  difference  between  two 
consecutive  blood  counts  is  of  importance  in  deciding  the  prognosis, 
as  an  increase  in  the  mononuclears  and  of  the  erythrocytes  and  the 
appearance  of  eosinophile  cells  marks  an  improvement. 

The  appearance  of  the  eruption  per  se  should  not  be  considered  a 
good  sign  if  there  is  still  marked  oligocythemia  and  polymorpho- 
nucleosis. 

Especially  serious  is  the  disappearance  of  a  poorly-marked  crup- 


REFERENCES  1577 

tion,  and  the  reappearance  of  fever  pains,  etc.  Cold  weather  and 
high  altitudes  are  unfavourable,  and  complications  increase  the 
gravity  of  the  case  considerably,  the  former  because  it  delays  the 
development  of  the  eruption  and  may  cause  it  to  abort,  and  the 
latter  because  it  increases  the  tendency  to  haemorrhage.  The 
mortality  varies  from  10  to  40  per  cent. 

Treatment. — No  specific  treatment  is  known,  but  Odriozola 
recommends  hypodermic  injections  of  arsenic,  and  removal  from 
the  endemic  region  to  the  warm  countries  along  the  littoral  will  also 
be  of  benefit.  Atoxyl,  salvarsan,  and  neo-salvarsan  may  be  tried. 
Chills  and  cold  baths  must  be  specially  avoided  as  being  apt  to  stop 
the  development  of  the  eruption,  and  hence  to  endanger  the  life  of 
the  patient.  Drugs  appear  to  be  useless  in  the  febrile  stage,  and 
though  decoctions  of  maize,  of  Butlneria  cor  data  (Buttneriacese), 
Buddleiaincana  (Scrofulariacese),  orSs/w-m/s  wo//6'(Terebinthinaceae), 
have  been  popular,  they  are  now  believed  to  be  useless. 

Tonics  of  iron  and  arsenic  are  useful  during  convalescence,  but 
the  iron  is  best  administered  by  hypodermic  injections.  Carrion's 
fever  must  be  treated  in  the  same  manner  as  typhoid  fever. 

Prophylaxis. — In  the  present  state  of  our  knowledge  the  only 
possible  prophylaxis  is  to  avoid  the  endemic  regions,  and  to  protect 
the  body  against  biting  arthropods,  especially  at  night. 

REFERENCES. 

There  are  numerous  references  in  the  '  Cronica  Medica,'  published  in  Lima, 
but  the  most  important  monograph  is  that  by  E.  Odriozola.  which  is  excellently 
illustrated  with  maps  and  coloured  plates,  and  in  which  the  subject  is  treated 
in  the  fullest  manner.  See  also  the  valuable  pubheations  by  Strong  and  his 
collaborators. 

Arce  (1918).     An.  Facult.  Med.  de  Lima,  vol.  i.,  Nos.  1,  2,  and  4. 

Bassett-Smith  (1901-12).     British  Medical  Journal. 

Biffi  (1908).     Archiv  f.  Schiffs-  u.  Tropcn-Hygiene,  xii.  1. 

Bourse  (1876).     Archiv.  de  Med.  Nav.,  p.  353. 

Chastaxg  (1879).     Ibid.,  p.  417. 

Cole  (191 2).     Arch,  of  Inter.  Med. 

Dounon  (1871).     Ibid.,  p.  255.     (A  very  excellent  paper.) 

Fournier  (1874).     Ibid.,  p.  15G. 

Hall  (1883).     Lancet,  ii.  S45.      (Verruga  in  Ecuador.) 

Hercelles  (1918).     An.  Facult.  Med.  de  Lima,  vol.  i.,  No.  4. 

Hirsch  (1883).     Handbook  of  Histology  and  Geographical  Pathology,  ii.  114. 

(A  most  useful  account.) 
Letulle  (1898).     Comptes  Rendus  de  !a  Societe  de  Biologie.  p.  704. 
Mayer  (1910).     Cent,  fur  Baktci . 
Monc'.e,  C.  (1911).     Carrion's  Disease,  or  Verruga  Peruviana.     These  de  Lima. 

Lima.     (Translation  in  the   Journal  of  the  London   School  of  Tropical 

Medicine,  1912.) 
Odriozola,  E.  (1898).     La  Maladie  de  Carrion.     Paris. 
Odriozola,  M.  (1858).     Medical  Times  and  Gazette,  p.  280. 
Smith  (1858).     Edinburgh  Medical  and  Surgical  Journal,  p.  67. 
Strong,   Tyzzer,   Brues,   Sf.llards,   and  Gastiaburu   (191 5).      Report  of 

the  First  Expedition  to  South  America  of  the  Harvard  School  of  Tropical 

Medicine.     Cambridge,  U.S.A. 
Townsend    (1913).     Journal    of    Economical    Entomology,    vh.   5,    357-367. 

(191 5.)     American  Journal  of  Tropical  Diseases,  iii.  16-32. 
Tschudi  (1S43).     Viagesal  Peru. 
Vecchi  (1909).     Beihefte  Archiv  f.  Schiffs-  u.  Tropcn-Ilygicne,  No.  4. 


CHAPTER  LXIII 

RHINOSPORIDIOSIS   AND    SARCO- 
SPORIDIOSIS 

Rhinosporidiosis — The  Sarcosporidioscs — Sergentelliasis— References. 

RHINOSPORIDIOSIS. 

Definition. — -Rhinosporidiosis  is  a  chronic  infection  caused  by 
Khinosporidimn  seebcri  Wernicke,  1900,  and  characterized  by  the 
production  of  polypi  on  mucous  membranes  and  papillomata  on 
cutaneous  surfaces. 

History. — The  disease  was  first  recognized  by  Malbran  in  South 
America  in  1892,  then  by  Seeber  in  1896  in  Buenos  Aires,  in  a  nasal 
polypus  occurring  in  a  young  man  aged  nineteen  years.  In  1900 
he  gave  a  description  of  the  parasite  and  its  development,  which 
we  have  been  unable  to  obtain,  but  which  is  said  to  be  a  most 
excellent  account.  Later  he  found  two  other  cases  in  the  same 
town,  and  in  1900  the  parasite  was  named  Coccidium  seeberi  by 
Wernicke. 

In  1903  Kinealy  reported  to  the  Laryngological  Society  a  peculiar 
case  of  a  polypus  which  he  had  found  in  1S04  growing  from  the 
septum  of  the  nose  of  an  Indian  in  Calcutta  in  the  form  of  a  pedun- 
culated, raspberry-like  body,  with  whitish  spots  on  the  generally  red 
surface.  On  section  this  tumour  was  found  to  have  peculiar  bodies 
embedded  in  it.  It  was  then  carefully  examined  and  described 
by  Minchin  and  Fantham,  who  came  to  the  conclusion  that  the 
peculiar  bodies  were  Haplosporidians,  and  named  them  Rhinospori- 
dium  kinealyi.  In  1905,  Nair  of  Madras  found  similar  nasal  polypi 
in  several  people,  who  all  came  from  the  small  native  State  of  Cochin, 
on  the  west  coast  of  India.  These  polypi  were  carefully  described 
by  Beattie  in  1906. 

In  1910  we  observed  the  same  parasite  in  a  nasal  polypus  in 
Ceylon,  and  in  the  same  year  Ingram  published  an  account  of  its 
occurrence  in  a  conjunctival  polypus  and  in  a  papilloma  on  the  penis. 

In  19 14  Tirumurti  gave  a  most  excellent  account  of  the  disease. 

In  19 18  Chelliah,  in  Ceylon,  not  merely  confirmed  our  original 
discovery  of  the  disease  in  that  island,  but  reported  several  more 
cases  in  Singhalese  and  moormen. 

Climatology. — Rhinosporidiosis  occurs  in  South  America,  in 
India,  and  in  Ceylon,  and  quite  possibly  in  other  regions. 

157S 


.ETIOLOGY—MORBID  ANATOMY 


1579 


/Etiology. — The  cause  of  the  disease  is  Rhinosporidiiim  seeberi 
Wernicke,  1900  (p.  533),  which  is  present  in  the  growths  in  the 
form  of  clear  hyaline  roundish  cysts  of  varying  diameter. 
The  life-history  in  man  appears  to  be  as  follows:  — 
The  free  spores,  which  are  small  spherical  ovoid  bodies  with  single 
chromatinic  masses,  grow  into  sporocysts  which  have  a  few  chroma- 
tinic  granules.  These  sporocysts  grow  into  larger  bodies  containing 
a  few  centrally  placed  pansporoblasts.  When  these  cysts  are 
mature  they  are  filled  with  pansporoblasts  which  have  formed  spore 
moruke  containing  some  fourteen  to  sixteen  clear  shining  spores. 


Fig.  708. — Section  of  Nasal  Polypus  showing  Rhinospovidium  seeberi 
at  1  and  2.     (X  30.)     Ceylon  Case.     (Photomicrograph.) 

1  is  reproduced  much  more  highly  magnified  in  Fig.  yog. 


The  cyst  ruptures,  the  pansporoblasts  escape  and  rupture,  and  so 
allow  the  spores  to  be  liberated.  Spores  probably  escape  from  the 
nose  and  other  parts,  and  possibly  infect  man  in  this  way,  because 
there  is  some  slight  evidence  of  transference  direct  from  man  to 
man,  though  we  were  unable  to  trace  any  such  cause  in  our  Ceylon 
case.  Probably  the  reservoir  for  the  parasite  is  in  some  unknown 
animal.  Spores  which  do  not  escape  from  the  body  propagate 
the  parasite  in  the  patient. 

Morbid  Anatomy. — When  a  polypus  is  teased  out  in  the  normal 
saline  it  will  be  observed  that  it  is  stalked,  and  that  from  this  central 
peduncle  strands  of  fibrous  tissue  branch  out  into  processes.     The 


r53o 


RHINOSPORIDIOSIS  AND  SARC0SP0RID10SIS 


tissue  is  studded  with  pin-head  sized  whito  dots  which  represent  the 
cysts. 

As  can  be  judged  from  Fig.  708,  the  mucous  membrane  is  thrown 
into  folds  which  form  papillomatous-like  processes,  in  which,  here 
and  there,  the  epithelium  is  thin  or  wanting.  The  subepithelial 
tissue  is  very  vascular,  and  is  infiltrated  with  polymorphonuclear 
leucocytes,  and  shows  small  haemorrhages  at  times,  and  in  the  nose 
may  also  be  myxomatous  in  places.  The  cysts  may  be  seen  lying 
in  this  tissue  or  bulging  through  the  epithelium  (vide  2  in  Fig.  708 
and  also  in  Fig.  709,  which  shows  a  cyst  full  of  pansporoblasts,  which 
appear  under  higher  magnification  in  Fig.  710). 


Fig.  709. — ■Rhinospovidium  seebevi  Wernicke  as  seen  at  2  in  Fig.  70S. 
(X  300.)     Ceylon  Case.     (Photomicrograph.) 


Pathology. — The  parasite  spreads  in  the  body  by  the  rupture  of 
the  cyst  and  the  liberation  of  the  spores.  We  suspect  that  it  may, 
at  times,  give  rise  to  a  condition  resembling  a  septicemia. 

Symptomatology. — The  patient  has  his  attention  drawn  to  his 
nose  by  profuse  bleedings,  and  in  a  little  time  notices  a  growth. 
On  examination  this  is  found  to  be  a  small  vascular  pedunculated 
tumour,  about  the  size  and  shape  of  a  pea,  freely  movable  and 
painless,  attached  to  the  anterior  and  upper  part  of  the  cartilaginous 
septum.     In  appearance  it  resembles  a  strawberry  or  a  raspberry. 

It  may,  however,  form  polypi  in  other  regions,  as,  for  example, 
on  the  conjunctiva,  or  papillomata  on  cutaneous  surfaces,  as,  for 
example,  on  the  penis. 


DIAGNOSIS— THE   S. I RCUSPORIDIOSES 


1 581 


Diagnosis.— The  diagnosis  can  only  be  made  by  removal  of  the 
whole  or  a  portion  of  the  growth,  which  in  most  cases  has  the  ap- 
pearance of  a  nasal  polypus,  followed  by  a  microscopical  examina- 
tion, when  the  parasite  will  be  easily  seen  as  a  roundish  cyst  filled 
with  granules  which,  when  examined  under  a  higher  power,  are 
seen  to  be  the  pansporoblasts. 


Fig.  710. — ■Rhinosporidiuiii  sebeeri  Wernicke  as  seen  at  2  in  Fig.  708. 
(X  1,000.)   Ceylon  Case.     (Photomicrograph.) 

Prognosis.— This  is  usually  said  to  be  good,  but  if  it  can  cause, 
as  we  suspect,  a  general  infection,  it  may  be  dangerous  to  life. 

Treatment. — The  treatment  is  to  remove  the  growth  and  cauterize 
its  base. 

Prophylaxis. — As  we  are  entirely  ignorant  of  the  life-cycle  of  the 
parasite  or  where  it  exists  outside  the  human  body,  no  remarks 
can  be. made  as  to  the  prophylaxis. 


THE  SARCOSPORIDIOSES. 

Definition. — Sarcosporidiosis  is  a  chronic  infection  caused  by  the 
invasion  of  the  body  by  Sarcocystis  linJananni  Rivolta,  1878, 
Sarcocvstis  muris  R.  Blanchard,  1885,  and  perhaps  other  allied 
organisms. 

History. — In  icS()8  Lindemann  found  some  indefinite  bodies  in 
the  myocardium  and  on  the  valves  of  the  heart  of  a  person  who 
had  died  ot  dropsy.  It  is  thought  that  these  bodies  may  possibly 
have  belonged  to  the  genus  Sarcocystis,  but  it  is  very  doubtful 
what  they  really  represented.     In  1887  Koch  described  the  first 


1582  RHINOSPORIDIOSIS  AND  SARCOSPORIDIOSIS 

genuine  case  in  Egypt.  In  1894  Baraban  and  St.  Remy  found 
these  parasites  in  the  laryngeal  muscles  of  a  man  who  had  been 
executed.  In  1902  Rosenberg  reported  a  doubtful  case,  and 
Kartulis  another  doubtful  case.  In  1903  Et.  and  Ed.  Sergent 
described  a  parasite  which  later  was  called  Sergent  ell  a  hominis 
Brumpt,  1910,  in  the  blood  {vide  p.  537),  and  in  1905  Castellani  and 
Willey  described  rather  different  bodies  also  in  the  blood  (vide 
PP-  537  and  538),  which  they  were  inclined  to  consider  of  protozoal 
origin,  and  later  similar,  but  somewhat  larger,  forms  were  found 
by  Castellani  and  Sturgess  in  the  blood  of  Bos  indicus  (Fig.  189, 
p.  531)-  In  1909  Darling  described  a  case  of  sarcosporidiosis  in  a 
Barbadian  negro  in  which  the  parasite  appeared  to  be  Sarcocystis 
maris  Blan chard. 

Climatology. — Sarcosporidiosis  being  only  a  chance  infection  in 
man,  and  the  parasite  normally  occurring  in  monkeys,  buffaloes, 
cattle,  sheep,  pigs,  rats,  and  other  animals,  it  is  obvious  that  not 
merely  will  the  disease  be  very  widespread,  but  that  different 
varieties  will  occur  in  the  different  zoological  regions.  The  cases 
so  far  described  are  in  Central  America,  Europe,  and  Egypt,  and 
doubtful  cases  in  Algeria  and  Ceylon.  We  are  suspicious  that 
the  Ceylon  case  may  have  some  connection  with  S.  tenellce,  var. 
bubalis  Willey,  Chalmers,  and  Philip,  1904,  which  is  very  com- 
monly found  in  buffalo  meat  in  Ceylon. 

/Etiology.— The  causation  of  sarcosporidiosis  is  the  presence  of 
some  species  of  sarcocystis  in  man,  but  the  method  of  entry  is  not 
obvious.  It  would  seem  possible  that  eating  undercooked  meat 
infected  with  Sarcocystis  might  produce  the  infection,  as  Darling 
has  shown  that  guinea-pigs  can  be  infected  by  feeding  them  with 
rat's  muscle  containing  S.  muris,  and  by  feeding  them  with  the 
ripe  sporozoites  of  the  same  species.  In  our  opinion  this  is  a  very 
probable  method  of  chance  infection,  because  the  buffalo  meat  in 
Ceylon  is  heavily  infected  (vide  p.  531). 

Morbid  Anatomy. — The  spores  can  be  found  in  the  blood  and  the 
parasites  in  the  muscle  fibres. 

Symptomatology. — The  incubation  period  in  animals  appears  to 
be  very  long,  some  152  to  164  days.  During  the  invasion  the 
patient  suffers  from  an  irregular  fever,  which  may  resemble  enteric 
fever,  and  in  severe  cases  this  fever  may  be  complicated  with 
myositis  and  even  necrosis  of  the  muscles. 

Diagnosis. — The  symptoms  are  those  of  an  irregular  fever,  which 
in  some  cases  may  be  typhoidal-like,  and  in  others  of  a  very  low 
type  without  much  general  disturbance,  while  some  cases  may 
never  show  pyrexia.  The  nature  of  these  fevers  may  be  suspected 
by  finding  bodies  resembling  the  spores  of  Sarcocystis  (vide  Fig.  189, 
p.  531)  in  the  blood.  Failing  this,  and  especially  if  there  are  any 
si(^ns  of  myositis,  the  diagnosis  can  be  cleared  by  excision  and 
examination  of  a  piece  of  diseased  muscle. 

Prognosis. — This  is  good  after  the  parasites  have  become  quies- 
cent, for  no  one  has  so  far  been  known  to  die  of  the  disease. 


REFERENCES  1583 

Treatment.— The  treatment  is  entirely  symptomatic. 

Prophylaxis. — Meat  should  be  carefully  inspected,  and  any  found 
heavily  infected  with  Sarcocystis  should  be  condemned,  while  all 
meat  should  be  well  cooked. 

SERGENTELLIASIS. 

The  brothers  Sergent,  in  1903,  described  a  peculiar  parasite 
(the  description  of  which  is  found  on  p.  537)  in  a  person  suffering 
from  night  sweats  and  attacks  of  nausea.  There  was  apparently 
no  fever,  and  the  general  condition  was  good.  This  parasite,  to 
which  Brumpt  has  given  the  name  of  SergenteUa  hominis,  might  be 
the  free  spores  of  a  species  of  Sarcocystis. 


REFERENCES. 

Rhinosporidiosis. 

Beattie  (1906).     British  Medical  Journal,  vol.ii. 

Chelliah  (1918).     Ind.  Med.  Gaz.,  November. 

Minchin  and  Fantham  (1905).     Quart.  Journ.  of  Micr.  Science,  vol.  xlix. 

O'Kinealy  (1903).     Proceedings  Laryngol.  Soc,  vol.  x. 

Tirumurti  (1914).     Practitioner,  xciii.  704. 

Sarcosporidiosis. 

Castellani  and  Willey  (1904).     Spolia  Zeylanica,  ii.,  vi.  78-92.     Colombo. 
Darling '(1909).     Archives  of  Internal  Medicine. 
Darling  (1910).      Journal  of  Expe.ri mental  Medicine.     April. 
Sergent,  Ed.  and  Ex.  (1903).     Comptes  Rendus  de  la  Societe  de  Biologie, 
October.     Paris. 


CHAPTER  LXIV 
PARAGONIMIASIS 

Svnonyms  —  Definition  — -History  —  Climatology  ■ —  ^Etiology  —  Pathology  — 
Morbid  anatomy — Symptomatology — Complications — Diagnosis — Treat- 
ment— Prophylaxis — References. 

Synonyms.  —  Parasitic     haemoptysis,     Pulmonary     distomatosis,     Endemic 
haemoptysis. 

Definition. — Paragonimiasis  is  a  chronic  or  subacute  general  or 
local  infection  of  man  by  means  of  Paragonimus  ringeri  Cobbold, 
1880,  which  produces  cystic  lesions,  containing  a  thick,  opaque, 
reddish  fluid,  in  which  are  found  at  times  the  parasite  or  its  eggs. 

History. — In  1879  Ringer  discovered  the  parasite  of  this  disease 
in  a  patient  at  Tamsui  in  Formosa,  and  it  was  named  Distomum 
ringeri  by  Cobbold  in  1880.  In  1878  Kerbert  had  discovered  similar 
parasites  in  the  lungs  of  two  Bengal  tigers  which  died  in  the  Zoo- 
logical Gardens  of  Amsterdam  and  Hamburg.  Subsequently  it 
was  considered  that  the  two  parasites  were  one  and  the  same  species, 
and  as  Kerbert  had  named  his  species  Paragonimus  westermani 
in  1878,  this  name  was  applied  to  the  human  parasite  until  Ward  and 
Hirsch  stated  that  the  spines  which  cover  the  cuticle  and  which 
are  arranged  in  groups  are  different  in  the  two  species.  Thus 
Paragonimus  ringeri  has  chisel-shaped  moderately  heavy  spines, 
while  P.  westermani  has  lancet-shaped  and  very  slender  spines.  The 
human  species  is,  therefore,  known  by  Cobbold's  name  of  P.  ringeri. 

In  1880  Baelz  found  bodies  in  cases  of  haemoptysis  which  he 
thought  were  psorosperms,  and,  therefore,  he  called  the  disease 
'  gregarinosis  pulmonum,'  but  when  the  bodies  were  shown  to 
Leuckart  he  said  that  they  were  ova  of  a  distomum. 

In  the  same  year  (1880)  Manson  found  the  eggs  in  a  case  of  haemo- 
ptysis in  a  Chinaman  from  Northern  Formosa,  and  later  in  a  Portu- 
guese with  similar  symptoms  from  Tamsui  in  Northern  Formosa. 
This  Portuguese  died  in  Formosa,  and  Ringer  discovered  in  the 
lungs  during  the  post-mortem  examination  a  minute  fleshy  oval 
body,  grey  in  colour.  This  specimen  was  forwarded  to  Manson, 
who  sent  it  to  Cobbold,  who  named  it  Distomum  ringeri. 

In  1883  Baelz  also  found  adult  specimens  in  the  lungs,  and  gave 
them  the  name  Distomum  pulmonale.  In  1890  Otani  and  Yamagiwa 
showed  that  it  could  give  rise  to  a  general  infection  and  could  be 
found  in  the  brain.    In  1902  Musgrave  gave  a  very  complete  account 

1584 


HISTORY— ETIOLOGY  1585 

of  the  disease  as  seen  in  the  Philippine  Islands.  In  1910  Nagano 
reported  upon  the  prevalence  of  the  disease  in  Northern  Formosa, 
around  the  prefecture  of  Shinchika;  and  Nakagawa  in  1913  and 
10,14  found  1,249  cases,  of  which  922  occurred  in  that  prefecture, 
and  believes  that  there  are  not  less  than  13,000  cases  therein.  In 
i<)i2  Masuo  and  Yokokawa  found  the  disease  in  Sansaka,  Koryo, 
Jukirin,  and  Nansho.  In  1914  Nakagawa  investigated  the  inhabi- 
tants of  the  lowlands  occupied  by  savage  tribes,  and  found  that 
about  50  per  cent,  of  the  population  were  infected;  but  in  the  high- 
lands the  cases  were  less  in  number. 

In  the  meanwhile  observations  had  been  made  as  to  the  develop- 
ment of  the  worm  in  the  egg  by  Nakahama  in  Japan,  by  Manson  in 
China,  and  by  Garrison  and  Leynes  in  the  Philippines.  In  1914 
Nakagawa  found  that  the  cercariae  developed  in  the  mollusc  Melania 
libertina  Gould,  which  lives  in  pools  and  sluggish  streams;  in 
Melania  obliquegranosa  Smith,  which  inhabits  slowly  moving 
streams;  and  in  Melania  tuberculata  Mueller. 

The  life-history  would  be  as  follows : — -The  miracidia  attach  them- 
selves by  means  of  suckers  to  the  head,  jaws,  and  feet  of  these 
molluscs, and  then  bore  their  way  by  means  of  their  proboscis  into  the 
liver,  the  heart,  and  the  kidneys,  where  they  become  sporocysts 
and  cercariae.  These  latter  possess  an  unforked  tail  and  measure 
0'i2Xo«09  mm.,  and  a  tail  of  0-054  mm-  They  also  show  a  spine, 
two  suckers,  three  pairs  of  poison  glands,  and  a  heart-shaped  excre- 
tory vesicle.  They  encyst  on  the  gills  of  certain  crabs — viz. , Potamon 
(geotheiphusa)  obtitsipes  Stimpson,  the  red  crab;  Potamon  (geothel- 
phusa)  dehaanii  White,  the  dung  crab;  Eriocheir  japonicns  de  Haan, 
the  hairy  crab;  and  perhaps  on  those  of  Sesarma  dehaanii  Milne 
Edwards,  and  Potamon  (par  athel pint  sa)  sinensis  Milne  Edwards. 

Dogs  fed  upon  these  crabs  showed  eggs  in  ninety  days  after 
infection.  The  young  distome  escapes  from  the  cyst  in  the  intestine 
of  the  dog,  pierces  the  wall  of  the  jejunum  and  passes  into  the  peri- 
toneal cavity,  pierces  the  diaphragm  and  pleura  and  entersthe  lungs, 
where  it  encysts  and  becomes  adult. 

More  recently  other  observers  have  doubted  the  necessity  of  the 
crab  in  the  case  of  the  infection  of  man,  which  apparently  can  take 
place  via  the  skin. 

Kobayashi  believes  that  the  cercariae  observed  by  Nakagawa  in 
molluscs  of  the  genus  Melania  are  not  those  of  P.  ringeri. 

Climatology. — Paragonimiasis  is  found  in  China,  Corea,  Japan, 
Formosa,  the  Philippine  Islands,  and  Sumatra.  The  infection 
is  more  prevalent  among  people  living  along  large  rivers,  according 
t<>  Nakagawa,  and  less  so  among  people  who  use  well  water. 

/Etiology.— The  causal  agent  is  Paragonimus  ringeri  Cobbold 
(p-  573)-  which  lives  not  merely  in  man,  but  also  in  the  cat,  the  dog, 
and  the  pig.  The  intermediate  hosts  are  molluscs  of  the  genus 
Melania,  in  which  the  cercariae  are  developed,  and  these  pass  to 
man  either  directly  or  through  the  agency  of  certain  crabs,  in  which 
they  become  encysted.     Infection  may  be  by  the  alimentary  canal, 


1586  '   PARAGONIMIASIS 

and  also  perhaps  by  the  skin.  The  worms  become  adult  in  the 
lungs  and  other  organs. 

The  disease  appears  to  be  very  widespread  in  certain  districts, 
and  the  old  idea  that  it  is  more  common  in  males  than  in  females 
requires  reinvestigation. 

Pathology. — The  pathology  of  the  disease  is  by  no  means  clear, 
and  how  the  various  pathological  changes  are  evolved  is  unknown. 

Musgrave  has  classified  the  lesions  into: — 

1.  The  non-suppurating  lesion. 

2.  The  tubercle-like  lesion. 

3.  The  suppurating  lesion. 

4.  The  ulcerative  lesion — 

(a)  in  the  skin; 

(b)  in  the  bronchial  mucosa ; 

(c)  in  the  intestinal  mucosa; 

(d)  in  the  bile-duct. 

The  simplest  lesion  appears  to  be  an  infiltration  of  the  connective 
tissue  of  an  organ  with  eggs,  without  any  histological  changes  at 
first,  but  later  with  a  proliferation  of  the  connective  tissue  and  the 
formation  of  a  cirrhosis  or  a  round-celled  infiltration,  with  some- 
times many  eosinophiles,  which  may  lead  to  abscess-formation,  and 
finally  to  ulceration.  The  abscess-formation  may  at  times  produce 
caseous  material,  giving  a  tubercular  appearance. 

The  non-suppurating  lesion  may  therefore  be  simple  infiltration 
of  the  tissue  by  eggs,  with  or  without  inflammation.  On  the  other 
hand,  cirrhotic  changes  may  be  seen,  especially  in  the  liver.  In  serous 
membranes  an  adhesive  inflammation  is  often  produced,  associated 
with  the  presence  of  eggs  in  brown  patches  at  the  points  of  contact. 

The  inflammation  of  the  organ  may,  however,  proceed  to  pus- 
formation,  resulting  in  a  typical  abscess.  On  the  other  hand,  the 
tissues  generally  attempt  to  circumscribe  this  abscess  by  a  fibrous 
wall,  and  thus  produce  what  is  called  the  typical  lesion  of  the 
disease.  In  the  centre  of  the  abscess  will  be  seen  degenerated  cells, 
blood,  eggs,  and  perhaps  a  parasite.  Then  comes  a  capsular  wall 
of  fibrous  connective  tissue,  smooth  towards  the  centre,  and  join- 
ing the  rest  of  the  organ  externally.  Around  this  wall  the  connec- 
tive tissue  of  the  organ  is  proliferating  and  congested.  In  this  way 
the  typical  little  cysts,  with  dull  blue-grey  walls,  smooth  internally, 
and  containing  a  thick,  reddish  fluid,  with  or  without  eggs  or  a 
parasite,  are  formed.  These  lesions  may  work  their  way  to  a 
cutaneous  or  mucous  surface,  and  so  open  into  a  bronchus,  or  into 
the  intestine,  Or  the  bile-duct,  or  on  to  the  skin,  thus  giving  rise 
to  ulcers  in  those  regions.  The  intestinal  ulcers  closely  resemble 
dysenteric  ulcers,  and,  indeed,  may  become  secondarily  infected 
with  amoeba?  or  bacteria. 

In  course  of  time  these  lesions  may  show  some  attempt  at  healing 
and  scar-formation,  but  generally  this  is  not  very  successful. 

The  blood  may  show  a  deviation  of  complement  with  worm-body  used  as 
antigen. 


SYMPTOM  A  TOLOG  Y—PROPH  YlA  X.IS  i 58  7 

Morbid  Anatomy.— The  body  may  be  well  nourished,  but  more 
usually  is  emaciated  and  anaemic.  Ulcers  can  be  seen  at  times  in 
the  axillae  and  groin,  leading  into  diseased  glands.  The  muscles 
may  contain  abscesses.  The  pleura,  pericardium,  peritoneum,  and, 
more  rarely,  the  meninges,  show  the  chronic  inflammations  and  the 
non-suppurative  lesions  mentioned  above.  The  lesions  found  in 
the  lungs  arc  diffuse  cirrhosis,  bronchiectatic  cavities,  pneumonia, 
and  caseous  abscesses,  while  those  of  the  liver  are  cirrhosis,  peri- 
hepatitis, and  abscess-formation.  The  typical  lesions  mentioned 
above  may  be  found  in  the  spleen,  pancreas,  small  and  large  intes- 
tines, kidneys,  bladder,  epididymis,  prostate,  and  in  the  choroid 
plexus  of  the  brain. 

Symptomatology. — As  the  invasion  of  the  body  is  so  generalized, 
the  symptoms  are  very  varied.  Musgrave  differentiates  four 
varieties — the  generalized,  the  thoracic,  abdominal,  and  cerebral; 
but  there  is  nothing  very  characteristic  about  any  of  these  types. 

In  the  generalized  type  there  may  be  fever,  enlarged  lymphatic 
glands,  general  muscular  pains,  and  ulceration  of  the  skin. 

In  the  thoracic  type  there  will  be  cough,  with  the  expectoration 
of  purulent  or,  more  generally,  blood-stained  sputum,  in  which  the 
eggs  may  be'best  seen  by  the  addition  of  a  little  o-i  per  cent,  solu- 
tion of  sulphuric  acid.  More  rarely  an  adult  parasite  appears  in 
the  sputum,  which  also  may  contain  Charcot-Leyden  and  creatinin 
crystals.  The  patient  generally  complains  of  pain  in  some  part  of 
the  chest.  The  physical  signs  may  indicate  broncho-pneumonia  or 
pleural  effusion,  which  may  be  serous  or  purulent. 

In  the  abdominal  form  of  the  disease  there  are  only  the  vaguest 
symptoms  of  dull,  aching  pains  and  tenderness,  while  diarrhoea, 
appendicitis,  epididymitis,  or  cirrhosis  of  the  liver,  may  be  demon- 
strat  ed  by  the  usual  physical  signs  and  symptoms.  When  diarrhoea 
occurs,  the  eggs  may  be  found  in  the  faeces. 

The  cerebral  type  is  associated  with  epilepsy,  which  may  be 
Jacksonian  in  character,  while  neuritis  or  paralysis  may  also  be 
present. 

The.  blood  and  urine  have  not  yet  been  fully  examined.     Though 
generally  chronic,  the  course  may  be  acute  if  complicated  by  septic" 
or  other  diseases. 

Complications.— The  most  usual  complications  are  tuberculosis 
and  entamoebic  dysentery. 

Diagnosis.— With  the  above  symptomatology,  it  will  be  obvious 
that  the  diagnosis  depends  entirely  upon  finding  the  eggs  of  the 
parasite  in  the  sputum,  the  faeces,  the  scrapings  from  the  ulcers, 
or  the  fluids  obtained  by  puncture  of  a  hydro-  or  pyothorax. 
Suspicions  as  to  the  presence  of  the  disease  will  be  strongesl  when 
cases  showing  any  of  the  above  signs  occur  in  the  endemic  area. 

Treatment.  -Tlu-  treatment  must  be  devoted  to  relieving  indi- 
vidual symptoms,  but  Musgrave  recommends  treatment  by  iodide 
of  potash.  Removal  from  the  endemic  area  is,  of  course,  indicated. 
Perhaps  tartar  emetic  injected  intravenously  might  do  good. 


1 5  88  PARAGONIMIASIS 

Prophylaxis.— In  the  endemic  region  drinking  and  bathing  water 
should  be  boiled  or  filtered,  and  crabs  should  not  be  eaten. 


REFERENCES. 

Ando     (191 7).     Verhand.     Japan.     Path.     Gesellsch.,     April.     (Complement 

Deviation.) 
Garrison  and   Leynes    (1909).     Philippine    Journal   of   Science,   iv.      177. 

Manila. 
Kobayashi  (191 8).     Mitt.  Med.  Fachschule  zu  Keijo. 

Manson  (1 881 -1 882).     Medical  Times  and  Gazette,  ii.  8  and  42.     London. 
Musgrave  (1902).     Philippine  Journal  of  Science,  ii.  15.     Manila. 
Nakagawa  (1915).     Taiwan  Igakkwai  Zasshi.     (1915).     Tokyo  Iji  Shenshi. 

(1915).     Chyugwai  Iji  Shempo.     (1916).     Journal  of  Infectious  Diseases, 

xviii.    131.     (1917).     Journal  of  Experimental  Medicine,   xxvi.,  No.   3, 

297-323.     (A  very  important  publication.) 


CHAPTER  LXV 
KATAYAMA    DISEASE 

Synonyms  —  Definition  —  History  —  Climatology —  /Etiology  —  Pathology  — 
Morbid  anatomy — -Symptomatology — Varieties — Complications — Diag- 
nosis—Prognosis— Treatment — Prophylaxis— References. 

Synonyms.— Urticarial  fever,  Asiatic  schistosomiasis,  Schistosomiasis  japonica, 
Kabure  (cutaneous  symptoms). 

Definition. — Katayama  disease  is  caused  by  Schistosoma  japonicum 
Katsurada,  1904,  and  is  characterized  by  urticarial  and  dysenteric 
symptoms,  painful  enlargement  of  the  liver  and  spleen,  with  or 
without  fever,  dropsy,  progressive  anaemia,  and  sometimes  pulmo- 
nary and  brain  symptoms. 

History. — -In  1887  Mazimi  drew  attention  to  a  peculiar  form  of 
cirrhosis  of  the  liver  which  was  found  in  certain  districts  in  Japan, 
and  was  caused  by  the  ova  of  some  unknown  parasite.  His  dis- 
covery was  confirmed,  and  the  ova  were  found  in  other  organs 
besides  the  liver;  and  the  disease,  which  became  well  known  among 
Japanese  medical  men,  was  named  '  Katayama  disease,'  from  a 
town  in  Bingo,  one  of  the  districts  in  which  it  is  common.  In  1904 
Katsurada,  who  was  resident  in  the  infected  area,  discovered  that 
the  ova  were  those  of  a  Schistosoma,  and,  further,  found  the 
adults  in  the  portal  vein  of  a  cat.  He  named  the  parasite 
Schistosoma  japonicum.  In  the  same  year  Fujinami  discovered  a 
female  worm  in  a  human  being.  Meanwhile  Catto  found  the  same 
parasite  in  a  Chinaman  from  Fukien,  and  described  it  in  1905,  and 
in  the  same  year  Stiles  and  Looss  gave  accounts  of  the  disease.  In 
1906  Woolley,  in  a  most  excellent  paper,  described  its  occurrence 
in  the  Philippine  Islands.  Logan  has  found  it  in  a  Chinaman  from 
Hunan,  and  in  1909  Peake  recorded  three  cases  from  a  small  town 
on  the  Siang  River,  in  the  Hunan  province  of  Central  China.  In 
1911  Houghton,  Logan,  and  Lambert,  drew  attention  to  cases  of 
fever  with  urticaria,  and  eosinophilia  connected  with  infections  with 
S.  japonicum. 

In  the  same  year  Edgar  drew  attention  to  this  fever  in  the  Yangtze 
Valley,  near  Hankow,  and  noted  that  nearly  every  patient  had 
bathed  or  waded  in  marshy  ground  near  the  river. 

In  1912  Miyagawa  did  not  believe  that  the  worm  was  the  cause  of 
the  dermatil  is. 

In  1913  Miyairi  and  Suzuki  noticed  that  the  eggs  of  the  worm, 
when  kept  for  one  to  two  hours  in  faeces  and  water  at  a  suitable 

1589 


1590  KATAYAMA  DISEASE 

temperature,  hatched  out,  the  shell  being  broken.  The  newly-born 
miracidia  swim  about  vigorously  and  enter  a  snail,  said  at  the  time 
to  be  a  species  of  Limncsus,  in  which  after  twelve  days  rediae  appear 
in  the  liver.  They  further  found  that  mice  placed  in  the  same  vessel 
with  these  snails  for  three  hours  a  day  develop  5.  japonicum  in 
their  livers. 

Also  in  1913  Katsurada  found  that  the  worms  reached  maturity 
in  two  weeks  and  produced  eggs  in  three  weeks,  and  that  the  method 
of  infection  of  the  vertebrate  was  by  the  skin,  as  could  be  demon- 
strated by  producing  the  disease  in  cats  and  dogs  (Katsurada), 
in  cattle  (Fujinami),  in  man  (Matsura  in  himself). 

In  1914  White  gave  an  account  of  a  case  of  the  disease,  as  seen 
on  H.M.S.  Cadmus,  under  the  term  urticarial  fever.  The  patient 
suffered  from  fever  about  1020  to  1030  F.  in  the  evening  and  normal 
in  the  morning,  pains  in  the  lumbar  and  epigastric  regions,  pulse- 
rate  90,  with  a  temperature  of  1030  F.,  slight  reduction  of  the  red 
corpuscles,  4,800,000  per  c.mm.,  and  50  per  cent,  to  70  per  cent, 
of  eosinophiles,  and  loss  of  weight  associated  with  the  appearance 
of  urticarial  eruptions  in  various  parts  of  the  body. 

In  the  same  year  Lanning  noted  that  it  was  not  uncommon  for  a 
fair  proportion  of  the  crews  of  gunboats  patrolling  the  Yangtze 
River  to  become  infected  after  wading  through  the  water-covered 
paddy  fields  in  search  of  snipe. 

Miyairi's  work  induced  Leiper  and  Atkinson,  in  1914,  to  proceed 
to  Shanghai  and  later  to  Katayama  in  Japan  to  investigate  the 
parasite.  Their  results  were  published  in  1915.  At  Katayama 
they  found  a  small  brown  snail,  with  eight  spirals  and  an  operculum, 
known  at  that  time  as  Katayama  nosophora,  which  had  an  extra- 
ordinary attraction  for  the  miracidia,  its  small  head  and  foot 
becoming  festooned  with  white  specks  (the  miracidia),  which 
appeared  to  irritate  the  snail.  Later  the  liver  was  found  to  be  full 
of  cercariae  with  bifid  tails,  which  infected  laboratory-bred  mice  by 
passing  through  the  skin,  male  and  female  adult  worms  being  found 
in  the  portal  vessels  one  month  after  infection. 

In  1916  Koiki  drew  attention  to  the  fact  that  in  forty-two  cases 
found  near  Shushin,  in  Japan,  all  but  three  were  farmers,  and  most 
had  had  an  itchy  eruption  on  the  legs  about  a  year  before.  In  the 
same  year  Mann  reported  upon  the  disease,  and  said  that  salvarsan 
was  beneficial  in  the  second  stage;  and  Narabayashi  studied  the 
life-history  of  the  parasite  (vide  p.  592)  and  pointed  out  the  re- 
lationship between  it  and  the  skin  disease  called  kabure. 

Climatology. — It  occurs  in  Japan,  China,  and  the  Philippine 
Islands:  in  the  first  in  the  provinces  of  Bingo,  Yamanashi,  Hiro- 
shima, and  Saga;  in  the  second  it  is  reported  up  to  date  from  Hunan, 
Honan,  Hupeh,  Kiangsi,  and  Anhwci  provinces,  and  from  Fukien. 
In  Wuhu  8  per  cent,  of  all  male  cases  entering  the  General  Hospital 
show  either  latent,  active,  or  overwhelming  infection.  In  China 
only  the  low-lying  lands  appear  to  be  infected;  no  cases  from  the 
hills  or  mountains  are  known, 


.ETIOLOGY— S  YMPTOMA  TOLOGY 


i59i 


In  the  Philippine  Islands  one  case  has  been  reported  by  Woolley 
as  occurring  in  a  Filippino  who  had  never  left  the  islands. 

etiology. — The  cause  of  the  disease  is  Schistosoma  japonicum 
Katsurada,  1904,  which  is  spread  by  Blandfordia  japonica,  in  which 
the  worm  develops  into  cercarise  which  penetrate  the  skin.  The 
vertebrate  reservoirs  are  cats,  dogs,  and  pigs.  For  description  of 
the  worm  see  p.  590. 

Pathology. — After  penetrating  into  the  skin  the  parasites  enter 
either  veins  or  arteries.  In  the  former  case  they  pass  to  the  right 
heart  and  hence  to  the  lungs,  at  the  bases  of  which  they  collect, 
and  then,  passing  through  the  mediastinum,  diaphragm,  and  liver, 
reach  the  portal  system.  Sueyasu,  in  1916,  obtained  complement 
fixation  with  the  blood  of  immune  animals. 

Morbid  Anatomy. — On  opening  the 
abdomen,  signs  of  old  peritonitis  may  be 
seen,  the  appendices  epiploic^  being 
matted  together,  and  at  times  there  are 
also  signs  of  old  pelvic  peritonitis.  The 
liver  is  cirrhotic  and  less  than  its  normal 
size,  and  its  surface  is  studded  by 
nodules,  usually  larger  than  those  of 
alcoholic  atrophic  cirrhosis.  Glisson's 
capsule  is  thickened,  and  shows  much 
connective  tissue  with  round-celled  in- 
filtration, in  which  lie  the  ova  of  the 
worm. 

The  small  and  large  intestines  and 
appendix  may  be  thickened,  and  their 
mucosa  is  swollen  and  hypenemic,  and 
shows  patches  of  ulceration  and  necrosis, 
and,  in  addition,  papillomata,  resembling 
those  of  bilharziosis.  The  eggs  may  also 
be  found  in  the  mesentery  and  in  the 
mesenteric  glands,  the  wall  of  the  gall- 
bladder, the  pancreas,  the  walls  of  the  mesenteric  vessels,  and  the 
pylorus.  The  adult  worms  may  be  found  in  some  of  the  veins  of  the 
porl  al  system,  especially  at  the  bifurcations  of  the  smaller  mesenteric 
vessels. 

In  addition,  the  eggs  may  be  found  in  fibrous  and  round-celled 
infiltrations  in  the  lungs  and  in  the  brain.  This  infiltration  often 
takes  the  form  of  nodules. 

Symptomatology.  The  early  symptoms  of  the  disease  may  be 
slight,  or  perhaps  it  may  begin  with  attacks  of  fever,  with  urticarial 
rashes,  in  which  there  is  marked  eosinophilia,  and  this  may  be 
associated  with  cough,  scanty  expectoration,  some  impairment  of 
resonance  over  the  bases  or  other  parts  of  the  lungs,  with  fine 
crepitant  rales  on  dee])  inspiration,  and  a  diminution  of  the  breath- 
sounds. 

About  two  years  later  there  arc  diarrhceic  or  dysenteric  symp- 


Fig  .  711.  —  Schistosoma 
japonicum  Katsurada. 
(After  Manson.) 


i592  K  AT  AY  AM  A  DISEASE 

toms,  with  or  without  fever,  and  the  presence  of  the  ova  in  the 
faeces.  Associated  with  these  symptoms  are  abdominal  pains,  en- 
largement and  tenderness  of  the  liver,  the  hypogastrium  shrinking, 
and  the  epigastrium  enlarging  and  giving  rise  to  a  characteristic 
abdominal  appearance.  At  the  same  time  the  dysenteric  symp- 
toms cease,  and  an  irregular  chronic  diarrhoea  sets  in,  with  motions 
containing  much  undigested  food,  and  associated  with  dyspepsia. 

In  course  of  time  the  preliminary  enlargement  of  the  liver  may 
cease,  and  the  organ  may  begin  to  shrink,  but  in  any  case  the  spleen 
becomes  tender  and  enlarges,  ascites  appears,  and  the  patient 
becomes  steadily  weaker,  more  and  more  anaemic,  emaciated,  and 
incapable  of  mental  or  physical  work.  The  average  of  three  differ- 
ential blood-counts  by  Peake  is  as  follows:  Polymorphonuclears, 
56-6  per  cent.;  mononuclears,  13-2  per  cent.;  lymphocytes,  15-6  per 
cent.;  eosinophiles,  14-1  per  cent.,  but  the  eosinophilia  may  reach 
50  per  cent.  Attacks  of  fever  may  occur  nightly,  otherwise  the 
temperature  may  be  subnormal.  The  vascular,  respiratory,  nervous, 
and  urinary  systems  are  usually  normal.  If,  however,  the  ova  affect 
the  lungs,  there  may  be  signs  of  bronchitis,  broncho-pneumonia, 
and  fibrosis;  and  if  the  brain,  those  of  Jacksonian  epilepsy.  In 
children  the  development  is  stunted.  Death  may  result  directly 
from  the  action  of  the  parasite,  or  be  due  to  some  intercurrent  disease. 

Lanning  distinguishes  three  stages  in  the  disease,  viz. : — 

Initial  Stage. — This  lasts  three  to  six  weeks,  and  is  characterized  by  high 
afternoon  temperatures,  with  slow  pulse-rate,  evanescent  cedemas  and  urti- 
carias, pains  in  the  abdomen,  especially  in  the  upper  part,  diarrhoea  or  con- 
stipation, marked  eosinophilia,  and  often  mental  depression. 

Second  Stage. — During  this  stage  the  liver  and  spleen  are  enlarged  with 
anaemia ;  there  is  loss  of  weight,  slight  fever  at  times,  and  the  passage  of  blood- 
stained mucus,  associated  with  more  or  less  tenesmus  and  straining,  and 
either  diarrhoea  or  constipation.  The  characteristic  ova  can  be  found  in  the 
motions. 

Third  Stage. — This  may  or  may  not  be  present,  and  then  only  after  three 
to  five  years,  and  especially  if  frequent  reinfection  takes  place.  It  is  charac- 
terized by  cirrhosis  of  the  liver,  which  may  be  enlarged  or  shrunken,  ascites, 
oedema  of  the  extremities,  emaciation,  anaemia,  weakness,  passage  of  blood 
and  mucus  in  the  motions,  and  a  little  fever. 

Termination. — Death  may  occur  from  exhaustion  or  some  terminal  infection. 

Varieties. — Houghton  recognizes  the  following  types  of  the 
disease:  (a)  Typical  cases,  with  enlarged  liver  and  spleen,  ascites, 
and  blood  in  the  motions;  (6)  cases  with  only  splenic  enlargement, 
and  with  or  without  blood  in  the  motions;  (c)  cases  with  cerebral 
symptoms  and  marked  eosinophilia,  to  which  may  be  added — 
(d)  urticarial  fever,  with  marked  eosinophilia  in  the  early  stages; 
(c)  cases  only  showing  eosinophilia,  often  associated  with  some  other 
concurrent  disorder;  (/)  latent  cases  showing  ova  in  the  motions, 
but  no  bodily  disturbance. 

The  splenic  type,  when  present  without  blood  in  the  motions, 
may  give  rise  to  difficulties  of  diagnosis,  which  may  be  cleared  up  by 
an  examination  of  the  blood  and  faeces.  The  eosinophilia  in  these 
cases  is  from  25  to  51  per  cent. 


VARIETIES—PROGNOSIS  1593 

The  cerebral  type  is  exemplified  by  partial  hemiplegia  and  slight 
disturbance  of  speech  after  high  fever,  and  associated  with  an 
eosinophilia  of  about  50  per  cent.  Jacksonian  epilepsy  has  also 
been  reported  as  due  to  this  parasite. 

The  urticarial  fever  is  characterized  by  a  remittent  type  of  fever, 
usually  ranging  at  first  from  990  to  ioo°  F.  in  the  morning  to  1020 
to  1030  F.  in  the  evening,  and  after  a  time  from  normal  to  about 
ioo°  F.,  associated  with  marked  urticaria,  followed  by  pale  raised 
blotches  on  the  arms,  trunk,  and  legs,  and  associated  with  a  marked 
urticarial  rash.  The  fever  lasts  some  weeks,  and  very  closely 
resembles  malaria  at  first,  because  the  daily  fall  of  temperature  is 
associated  with  sweating. 

Complications. — The  infection  is  generally  complicated  by  the 
presence  of  Trichuris  trichiura,  Ancylostoma  duodenalc  or  Necator 
atnericanus,  and  Ascaris  lum- 

bricoides.    Dysentery  is  a  com-  ->«,;.  >'    -. 

plication  which  may  occur  and  -  x 

prove  fatal  to  the  patient. 


Diagnosis. —  The    character- 


m 


istic  signs  are  chronic  painful  JK 
enlargement  of  the  liver  and  flg 
spleen,  associated  with  ascites 
and  chronic  irregular  diarrhoea, 
and  marked  eosinophilia  (10  to 
50  percent.).     A  definite  diag-       ^ 

nosis  is  tobe  effected  by  finding  ^ 

the  ova  in  the  fseces.  These  ova  ^ 

are  large  (o-i   by   0-07   milli- 
metre), oval,  non-operculated, 

laterally  spined  (75  per  cent.), 

smooth,  and  transparent,  with  Fig.  712.— Egg  of  Schistosoma 

a  double   contour    sometimes  japonicum. 

showing    a    Miracidium,     and      (From  a  photomicrograph  by  J.  J.Bell.) 

when  kept  in  water  for  a  short 

time  give  rise  to  a  free-swimming  ciliated  Miracidium.     These  ova 

are  apt  to  be  mistaken   for   Ascaris   lumbricoides,   or   less   likely 

for    an   Ancylostoma   ovum.     The   ova   require   to   be  looked  for 

carefully. 

Other  points  which  assist  in  the  diagnosis  are  the  greatly  exag- 
gerated knee-jerks,  the  peculiar  muddy  complexion  suggestive  of 
anaemia,  the  lack  of  leucocytosis  (the  counts  in  uncomplicated  cases 
being  about  2,000  to  8,500  per  cubic  millimetre),  and  the  emaciation 
without  obvious  cause. 

Prognosis. — The  prognosis  is  very  bad,  as  the  parasite  directly 
or  indirectly  leads  to  the  death  of  the  patient.  The  mortality  is 
not  known,  but  Katsurada  met  with  between  thirty  to  fifty-four 
cases  every  year  for  five  years  in  the  infected  area  in  Japan,  and 
saw  three  to  five  deaths  per  annum,  which  he  considered  directly 
due  to  the  parasite — i.e.,  a  mortality  of  about  10  per  cent. — but 


1594  KATAYAMA  DISEASE 

he  thinks  that  the  indirect  mortality  would  raise  the  percentage 
considerably. 

Treatment. — The  only  treatment  that  can  be  suggested  is  to 
administer  salvarsan  or  tartar  emetic. 

Prophylaxis. — Avoid  contaminated  water  in  drinking  and  bathing 
— i.e.,  use  boiled  water  in  infected  areas  for  both  purposes. 
Wading  in  swamps,  lakes,  and  paddy  fields,  is  very  dangerous,  and 
is  the  method  of  infection  of  man. 


REFERENCES. 

Bayer  (1905).     American  Medicine,  x.  57S. 

Catto  (1905).     Journal  of  Tropical  Medicine,  vii.  78. 

Catto  (1905).     British  Medical  Journal,  i.  11. 

Cort  (1919).     Univ.  California  Publicat.  in  Zoology,  vol.  xviii.,  No.  18. 

Houghton   (1910).     Transactions  of  the  Society  of  Tropical  Medicine  and 

Hygiene,  vol.iii.,  No.  7,  342.     London. 
Katsurada.     Journal   of   American   Medical   Association,    xlv.    So    (review 

only).     1905. 
Lambert   (1911).     Transactions   of   the    Society   of   Tropical   Medicine   and 

Hygiene,  vol.  v..  No.  1,  38.     London. 
Laning  (1914).     United  States  Naval  Bulletin,  viii.  16-36. 

Leiper  and  Atkinson  (1915).  British  Medical  Journal,  January  30,  201-203. 
Mann  (1916).  Journal  American  Medical  Association,  vol.  lxvii.,  1366-1368. 
Miyairi   and    Suzuki    (1914).     Mittelungen   aus  der  Medicinische    Fakuitat 

Kyashu  Fukuoka,  i.  187-197,  also  Tokyo  Medical  Journal  for  September, 

IQI3- 
Narabayashi  (1916).     Kyoto  Igaku  Zassi,  vol.  xxii.,  1-63. 
Peake  (1909).     Journal  of  Tropical  Medicine,  xii.  64. 
Reed  (1915).     American  Journal  of  Tropical  Diseases,  iii.  250-273. 
Skinner  (1911).     Journal  of  Tropical  Medicine  and  Hygiene,  129.     London. 
Stiles  (1905).     American  Medicine,  ix.  821. 
Woolley  (1906).     Philippine  Journal  of  Science,  B.,  i.  83. 


CHAPTER  LXVI 
THE    FILARIASES 

Synonyms — Definition — Filariasis  caused  by  Filaria  bancrofti Cobbold,  1877 — 
History  —Climatology — ^Etiology —  Pathology — Clinical  description  — 
Filarial  lymphangitis — Filarial  orchitis  and  hydrocele — Lymphatic 
varix — Varicose  lymphatic  glands — Chylous  effusions — Elephantiasis — 
Rarer  affections- — Filariasis  caused  by  other  Filaridae — References. 

Synonyms. — -Filarial     disease.       French,     Filariose,      Maladies      filariennes  ; 
Italian,  Filar  iasi;    German,  Filaria  Krankheit. 

Definition. — -Filariasis  is  a  term  denoting  the  infection  of  man 
or  animals  by  any  species  of  Filaria — e.g.,  Filaria  bancrofti  Cobbold, 
1877,  and  some  others. 

FILARIASIS  CAUSED  BY  FILARIA  BANCROFTI  Cobbold,  1877. 

The  diseases  produced  in  man  by  Filaria  bancrojli  Cobbold,  1S77, 
include  lymphangitis,  orchitis,  varix  in  lymphatics  and  lymphatic 
glands,  chylous  and  lymphatic  extravasations,  and  elephantiasis. 

History. — The  appearance  of  the  huge  leg  of  elephantiasis  is  so  striking 
that  it  was  early  noticed  by  ancient  Indian  writers,  who  give  descriptions  of 
diseases  which  clearly  refer  to  elephantiasis  of  the  leg  and  of  the  scrotum, 
and  also  less  clearly  to  lymph  scrotum.  Further,  they  appear  to  have  known 
that  elephantiasis  could  affect  the  hands  and  other  parts  of  the  body. 

The  word  '  elephantiasis  '  was  first  used  by  Celsus  to  indicate  leprosy, 
and  in  this  he  was  followed  by  most  writers  until  Galen,  who  included  true 
elephantiasis  under  the  same  term,  an  error  which  became  firmly  established 
as  time  passed.  In  the  ninth  and  tenth  centuries  Rhazes  and  Avicenna, 
and  other  Arabian  physicians,  described  true  elephantiasis  of  the  leg  under 
the  term  '  da-Id  '  or  '  dau-ool-fil,'  or  elephantine  disease,  which,  however, 
only  served  to  make  the  confusion  between  the  two  diseases  more  com- 
plete. In  the  seventeenth  century  Leonicenus  and  Varandanis  pointed  out 
that  they  were  two  distinct  clinical  entities,  and  in  1709  Clarke  described 
elephantiasis  on  the  Malabar  coast  of  India  under  the  term  '  Cochin  leg.' 
In  1712  Kaempfer  described  endemic  hydrocele,  under  the  term  '  anilrum,' 
as  occurring  in  India,  and  being  associated  with  erysipelatous  eruptions 
on  the  scrotum,  which  recurred  at  the  time  of  the  new  moon.  He  also  de- 
scribed a  large  foot  under  tin-  term'  pcrical,'  but  his  description  agrees  more 
with  Madura-foot  than  with  elephantiasis,  though  it  is  probable  that  he  was 
confusing  both  diseases  under  the  same  term.  In  1750  Hillary,  a  most 
careful  and  skilled  observer,  gave  the  first  full  and  accurate  account  of  the 
evolution  of  the  large  let;  of  elephantiasis,  which  he  clearly  differentiates 
from  true  leprosy,  dt-si  ribing  the  successive  attacks  of  fever,  the  lymphangitis 
and  lymphadenitis,  and  the  swelling  of  the  limb,  which,  gradually  becoming 
permanent  and  slowly  increasing,  produces  the  well-known  condition. 

He  was  ably  supported  in   1  7S.J  by  llendv,  who,  in  a  subsequent  treatise 

1595 


1596  THE  FILARIASES 

in  1789,  gave  the  first  full  account  we  have  been  able  to  trace  of  the  develop- 
ment of  elephantiasis  of  the  scrotum,  which  he  clearly  recognized  to  be  the 
same  disease  as  that  affecting  the  legs.  He  describes  and  figures  an  elephan- 
tiasis of  the  scrotum  24  inches  in  height  and  6  feet  in  circumference  at  its 
base,  and  he  further  notes  cases  of  spontaneous  cure  by  sloughing.  In  1809, 
and  again  in  1824,  Alard  wrote  most  excellent  treatises  on  the  elephantiasis 
of  the  Arabs. 

In  1 8 12  Chapotin  was  the  first  to  describe  haematochyluria  in  Mauritius,  and 
he  was  followed  by  Salese  in  1832,  whose  paper  aroused  so  much  interest 
in  Brazil,  where  the  disease  had  for  long  been  well  known,  that  in  1835  a 
conference  on  the  subject  was  held  in  Rio  de  Janeiro,  after  which  there  were 
many  investigations,  among  which  may  be  mentioned  those  of  Rayer  in  1838, 
Quevenne  in  1839,  Siguad  in  1844,  and  Mozae-Azema  in  1858,  the  last-named 
observer  reporting  it  in  Reunion.  In  1854  Jamsetjee  described  lymph 
scrotum.  The  result  of  all  this  work  was  to  produce  a  consensus  of  opinion 
among  Brazilian,  French,  and  Indian  physicians  that  haematochyluria  and 
elephantiasis  were  merely  different  aspects  of  the  same  disease,  and  at  the 
same  time  the  classical  researches  of  Danielssen  and  Boeck  in  1 848  on  leprosy, 
and  of  V.  Carter  in  i860  on  mycetoma,  ended  the  confusion  of  these  two 
diseases  with  elephantiasis. 

In  1863  Demarquay,  in  Paris,  discovered  a  Microfilaria  in  the  fluid  from  a 
hydrocele  in  a  person  who  had  come  from  Havana,  but  this  discovery  passed 
unnoticed  at  the  time.  In  1866  Wucherer,  stimulated  by  the  discovery  of 
Schistosoma  hcematobium  in  haematuria  in  Egypt,  found  a  Microfilaria  in 
the  urine  of  a  case  of  haematuria  in  Brazil,  but  at  first  thought  it  to  be  of  no 
importance;  but  when,  after  two  years  of  careful  work,  he  regularly  found  the 
same  small  worm  in  the  urine  of  persons  suffering  from  haematochyluria,  he 
published  his  discovery  in  1868,  in  the  same  year  in  which  Lewis  independently 
found  the  same  parasite  in  the  urine  of  a  case  of  chyluria  in  India.  Lewis 
also  found  the  same  small  worm  in  the  blood  and  lymph  of  persons  suffering 
from  elephantiasis  of  the  leg,  and  concluded  that  it  was  the  cause  of  the 
chyluria  and  the  elephantiasis.  In  1 876  Winckel  found  the  same  small  parasite 
in  the  fluid  from  a  case  of  chylous  ascites. 

In  1876-77  Bancroft  discovered  adult  female  worms  in  a  lymphatic  abscess 
in  the  arm,  and  in  a  hydrocele  of  the  cord,  and  these  worms  were  later  de- 
scribed by  Cobbold,  who  gave  them  the  name  Filaria  bancrofti.  About  the 
same  time  Manson  found  the  Microfilarice  in  the  lymph  from  the  enlarged 
lymphatics  of  a  lymph  scrotum  and  from  varicose  lymphatic  glands,  and 
suspected  that  the  so-called  malarial  orchitis  must  be  of  filarial  origin.  He 
also  obtained  a  female  worm  from  a  case  of  elephantiasis  of  the  scrotum, 
and  in  1879  Lewis  found  pieces  of  male  anel  female  worms;  while  in  1888 
Sibthorpe  obtained  perfect  specimens  of  a  male  and  female  from  a  lymph 
scrotum,  the  former  being  described  by  Bourne.  Lastly,  in  1898,  Maitlar.d 
drew  attention  to  the  occurrence  of  synovitis  in  cases  of  filariasis,  which  he 
considered  could  not  be  looked  upon  as  accidental,  and  must  be  held  to  be 
of  filarial  origin,  but  this  view  cannot  be  regarded  as  proved. 

In  this  way  arose  the  knowledge  that  the  causation  of  a  form  of  lym- 
phangitis, of  lymphatic  abscesses,  of  varices  of  lymphatics,  and  of  lymph 
glands,  of  haematochyluria,  of  chylous  extravasations,  and  of  elephantiasis, 
was  the  invasion  of  the  body  by  Filaria  bancrofti  Cobbold,  1877. 

In  the  meanwhile  the  epoch-making  discovery  of  the  agency  of  the  mos- 
quito in  the  dissemination  of  Filaria  bancrofti  was  made  by  Manson  in  1878, 
as  well  as  the  periodicity  of  the  Microfilarice,  which  only  appear  in  the  blood 
in  large  numbers  at  night,  anel  in  1899  he  discovered  that  they  retire  to  the 
vessels  of  the  lungs  (luring  the  day.  With  regard  to  this  periodicity,  Bahr  has 
shown  that  it  does  not  depend  upon  the  human  host,  but  upon  the  habits  of  the 
insect  host  being  nocturnal  when  the  host  is  Culex  fatigans,  anel  nocturnal  anel 
diurnal  when  the  host  is  Stcgomyia  pscudo-scntellaris,  which  is  a  day-feeding 
mosejuito.  Thorpe's  view  with  regard  to  the  diurnal  and  nocturnal  periodicity 
is  that  it  is  caused  by  the  irregular  habits  of  the  human  hosts,  but  this  latter 


CLIMATOLOGY  i597 

theory  has  not  been  supported  by  Fulleborn's  observations  on  Samoan 
natives.  Low,  Grassi,  Noe,  and  Fiilleborn,  have  supplied  the  information  as  to 
the  method  by  which  the  Filaria  escapes  from  the  mosquito  and  enters  man 
during  the  act  of  biting.  While,  therefore,  much  has  been  done  to  elucidate 
the  nature  of  the  lesions  due  to  the  worm,  researches  are  still  required  with 
regard  to  the  method  by  which  the  worms  produce  the  various  pathological 
phenomena  attributed  to  them,  especially  elephantiasis,  and  the  role  of  a 
secondary  bacterial  infection  in  the  production  of  the  lymphangitis,  abscesses, 
and  elephantiasis. 

The  morbid  anatomy  has  been  investigated  by  but  few  observers,  notably 
by  Mackenzie,  Manson,  Low,  Young,  and  Bahr. 

Climatology. — The  fact  that  ancient  Indian  writers  were  ac- 
quainted with  elephantiasis  of  the  leg  and  scrotum,  while  Celsus 
docs  not  appear  to  have  known  the  disease,  and  the  further  fact, 
mentioned  by  both  Hillary  and  Hendy,  that  elephantiasis  was  rare 
in  Barbados  at  the  beginning  of  the  eighteenth  century,  together 
with  Hillary's  views  that  the  disease  was  introduced  into  that 
island  by  negro  slaves  from  Africa,  awaken  suspicions  that  the 
endemic  home  of  filariasis  is  Asia,  and  that  it  has  spread  from  thence 
to  Africa,  and  from  Africa  to  America.  If  this  gradual  dissemina- 
tion of  filariasis  is  correct,  it  may  explain  many  features  of  the 
epidemiology  which  are  difficult  at  the  present  time  to  comprehend. 

Be  this  as  it  may,  filariasis  is  now  widely  distributed  throughout 
the  tropics  and  the  subtropics,  extending  from  about  410  N.  to 
about  280  S.  in  the  Eastern  Hemisphere,  and  from  about  310  N.  to 
about  230  S.  in  the  Western  Hemisphere. 

In  Asia  it  is  known  in  Arabia,  India,  Ceylon,  Burma,  Indo-China, 
the  Philippine  Islands,  Guam,  China,  and  Japan. 

It  is  known  in  Australasia,  especially  in  Queensland,  and  in 
Oceania,  especially  in  Fiji,  in  Samoa  and  the  Friendly  Islands, 
but  is  absent  in  the  Sandwich  Islands.  It  is  also  known  in  New 
Guinea. 

In  America  it  occurs  in  the  Southern  United  States,  in  Central 
America,  the  West  Indies,  in  Guiana,  Venezuela,  Brazil,  Peru,  and 
Columbia. 

In  Africa  it  is  common  on  the  West  Coast,  in  South  Africa,  East 
Africa,  Madagascar,  Reunion,  Mauritius,  Morocco,  and  Egypt  and 
Northern  Africa. 

In  Europe  it  is  said  to  exist  near  Barcelona  and  in  Turkey. 

In  these  countries  its  distribution  is  unequal,  being  in  general 
more  common  along  sea-coasts  and  the  banks  of  large  rivers,  but 
presenting  peculiar  circumscribed  endemic  areas.  Thus,  Daniels 
points  out  that  in  the  Shire  Highlands  filariasis  and  elephantiasis 
are  only  found  in  immigrants,  while  along  the  lower  Shire"  River 
both  are  common. 

Still  more  interesting  is  his  observation  that  at  the  southern  end 
of  Lake  Nyassa  there  was  only  one  case  of  filariasis  met  with,  and 
none  of  elephantiasis,  while  at  the  northern  extremity  both  were 
frequently  seen. 

Low  has  also  studied  the  distribution  in  the  West  Indies.     Here, 


1598  THE  FILARIASES 

again,  this  is  very  unequal,  some  of  the  islands — Barbados,  for 
example — being  heavily  infected,  while  in  others,  Grenada,  the 
infection  does  not  appear  to  exist. 

The  distribution  must  depend  upon  the  presence  or  absence  of 
mosquitoes  capable  of  disseminating  the  worm,  but  this  aspect  of 
the  epidemiology  still  requires  a  considerable  amount  of  research; 
further,  the  distribution  of  the  suitable  mosquitoes  must  depend 
upon  many  factors  concerning  which  we  are  quite  ignorant.  When 
these  conditions  are  better  understood,  the  climatology  will  be 
rendered  more  explicable. 

Two  atmospheric  conditions — viz.,  high  air-temperature  and  con- 
siderable atmospheric  humidity — have  long  been  known  to  be 
associated  with  the  prevalence  of  filariasis  and  elephantiasis,  and 
the  reason  of  this  has  recently  been  explained  by  Fulleborn's  ex- 
periments on  Dirofilaria  immitis.  This  observer  found,  as  the  result 
of  most  careful  experiments,  that  the  Dirofilaria  developed  better  in 
mosquitoes  if  the  air-temperature  was  high,  and  in  that  respect 
resembled  the  malarial  parasite;  and,  further,  that  at  high  tempera- 
tures the  Dirofilaria  are  able  to  leave  the  proboscis  more  easily,  and 
to  penetrate  the  skin  more  quickly  than  at  a  low  temperature. 

Further,  the  moisture  in  the  air  is  of  importance,  as  the  Dirofilaria 
passes  from  the  proboscis  on  to  the  skin,  and  either  makes  its 
own  way  through  this  into  the  tissues,  or  enters  the  aperture  of 
the  mosquito's  bite  after  it  has  withdrawn  its  stilettes,  and,  there- 
fore, has  to  be  for  some  time  in  contact  with  the  skin,  which,  if  dry, 
will  have  a  harmful  effect  upon  it,  but  if  moist,  will  not  be  injurious 
to  it. 

With  reference  to  Fiji,  Bahr  concludes  that  it  is  possible  that  at 
one  time  or  another  nearly  every  Fijian  is  the  subject  of  filariasis, 
because  27*1  per  cent,  were  found  to  harbour  Microfilaria?  in  their 
blood,  and  adult  worms  could  be  found  in  the  lymphatics  and  other 
tissues,  and  others  (25-4  per  cent.)  were  found  to  suffer  from  filarial 
disease  when  no  Microfilaria  could  be  found  in  the  blood;  and, 
lastly,  in  patients  while  still  under  observation  the  Microfilaria? 
have  disappeared  from  the  blood. 

Etiology. — The  causation  of  the  various  pathological  phenomena 
mentioned  above  is  F.  bancrofli  Cobbold,  1877  (p.  633),  introduced 
into  the  body  by  the  bite  of  a  mosquito. 

The  known  carriers  of  the  worm,  as  given  by  Theobald,  are  Culex 
fatigans  Wiedemann,  1828;  Mansonia  itniformis  Theobald,  iqoi; 
M.  pseudotitillans  Theobald;  Pyrciophorus  costalis  Loew,  1866; 
Myzomia  rossti  Giles,  189c):  Myzorhynchus  nigerrimus  Giles;  M. 
minuius  Theobald,  1903;  Cellia  albimana  Wiedemann,  1821;  Stego- 
myia  pseudo-scutellaris  Theobald,  1910;  while  the  worm  is  known  to 
be  capable  of  undergoing  a  part  of  its  development  in  certain  other 
mosquitoes  already  mentioned  in  Chapter  XXIV. 

The  reason  of  the  non-completion  of  full  development  in  any  and 
every  mosquito  is  not  known. 

After  development  in  the  thoracic  muscles  of  the  mosquito  the 


ETIOLOGY  1599 

embryo  passes  into  the  labium,  and  when  the  mosquito  bites,  it 
works  its  way  through  Dutton's  membrane  on  to  the  skin,  its  passage 
being  favoured,  according  to  Fiilleborn,  by  high  air-temperatures 
and  moist  conditions  of  the  skin.  Arrived  on  the  skin,  it  may  work 
its  own  way  into  the  body  through  the  skin  like  an  Ancylostoma 
embryo;  or  it  may  enter  through  the  aperture  of  the  mosquito-bite 
when  the  stilettes  have  been  removed,  for  before  this  takes  place 
it  is  impossible  for  it  to  pass  through  this  aperture,  which  is  com- 
pletely filled  by  these  appendages. 

Its  further  history  and  wanderings  in  the  body  are  quite  unknown 
until  the  adult  condition  is  reached.  The  adults  (males  and 
females)  are  generally  found  lying  together,  though  the  females 
appear  to  be  in  preponderant  numbers  in  lymphatic  vessels,  but 
they  can  also  be  found  in  the  lymphatic  glands;  while  dead  and 
calcified  worms  have  been  found  not  merely  in  lymphatic  glands, 
but  also  in  the  testes,  epididymis,  spermatic  cord,  and  tunica 
vaginalis.  Here  the  female  produces  the  thin  Microfilarice,  which 
pass  through  the  lymphatic  glands  and  thoracic  duct  into  the  blood 
stream,  in  which  they  are  found  in  large  numbers  at  night,  retiring 
in  the  day-time  mostly  into  the  bloodvessels  of  the  lungs. 

When  taken  into  the  mosquito's  stomach  they  escape  from  their 
enclosing  egg-shell,  and,  entering  the  thoracic  muscles,  complete  the 
cycle  of  development. 

It  is  interesting  to  note  that  in  various  parts  of  the  tropics  natives  believe 
that  elephantiasis  and  other  filarial  diseases  may  be  transmitted  through 
sexual  intercourse. 

The  adults  lying  in  the  lymphatic  vessels  may  mechanically  cause 
obstruction  to  the  flow  of  lymph,  and  thus  produce  varices,  inflam- 
mation of  vessels  and  glands,  and  if  the  varicose  vessels  rupture, 
extravasation  of  lymph  or  chyle. 

While  this  ^etiological  relationship  of  the  worm  to  the  lymphan- 
gitis and  lymphatic  abscesses,  to  the  varices  in  lymphatics  and 
lymphatic  glands,  to  ruemato-chyluria  and  chylous  extravasations, 
is  admitted  by  all  observers,  there  are  those  who  doubt  this  relation- 
ship with  regard  to  elephantiasis.  These  authors  base  their  objec- 
tions upon  the  facts  that  the  worm  and  its  larvae  may  be  absent  in 
well-developed  cases,  and  that  the  disease  can  occur  in  countries 
in  which  filariasis  is  believed  not  to  be  present,  both  of  which  are 
quite  true,  but  are  capable  of  explanation.  There  is  an  undoubted 
general  ivlat  ionship  between  the  number  of  cases  of  filariasis  and  of 
eh  pliant  iasis  in  a  district.  Where  there  is  no  filariasis,  elephantiasis 
i>  either  extremely  rare  or  unknown;  where  there  is  abundant 
filariasis,  there  are  also  many  cases  of  elephantiasis. 

[n  investigating  this  point  in  a  locality  care  must  be  taken  to 
exclude  immigrant  cases  of  both  filariasis  and  elephantiasis.  Thus, 
Low  failed  to  find  either  condition  in  the  inhabitants  of  the  forests 
of  British  Guiana  and  in  the  Wagandas,  natives  of  Uganda,  though 
immigrant  cases  were  met  with. 


i6oo  THE  FILARIASES 

The  adult  Filaria  has  been  found  in  the  tissues  removed  by 
operation  from  a  case  of  elephantiasis  of  the  scrotum;  and,  further, 
the  condition  of  elephantiasis  is  produced  as  a  rule  by  a  series  of 
attacks  of  lymphangitis,  which  in  every  particular  resemble  un- 
doubted filarial  lymphangitis. 

It  is  true  that  a  secondary  bacterial  infection  may  possibly  assist 
the  development  of  the  disease,  for  a  diplococcus  has  been  found  by 
Dufogere,  which  he  calls  the  '  lymphococcus,'  and  his  findings  have 
been  confirmed  by  Foulerton.  Le  Dantec  describes  a  similar 
organism,  which  he  calls  the  '  dermatococcus  ';  but  the  main  cause 
of  elephantiasis  in  the  tropics  is  Filaria  bancrojti,  though  it  is  quite 
possible  that,  exceptionally,  other  causes  may  lead  to  occlusion  of 
lymphatics  and  the  formation  of  elephantiasis. 

Pathology. — -If  the  parent -worms  live  in  positions  in  which  they 
do  not  obstruct  the  flow  of  the  lymph,  and  if  they  are  not  acci- 
dentally injured,  no  pathological  effects  will  be  produced  on  the 
host;  and  our  observations  support  Hanson's  theory  that  the 
presence  of  the  worms  may  produce  no  ill-effect  upon  the  host, 
for  we  know  of  a  case  where  for  years  they  have  produced  no 
symptoms. 

But  if  the  parent-worms  obstruct  the  circulation  of  the  lymph 
mechanically — for  example,  when  three  or  four  come  together  in 
an  important  main  lymphatic  trunk — then  the  retained  lymph  is 
certain  by  mechanical  pressure  to  damage  the  tributary  channels. 
Further,  if  any  accidental  injury  is  inflicted  upon  the  female  parent- 
worm,  this  may  cause  abortion,  and  as  a  result  the  production  of 
oval  eggs  instead  of  elongated  embryos  (Fig.  268),  and  these,  as 
will  be  explained  below,  are  liable  to  block  up  the  small  lymph 
channels  of  the  skin  or  of  a  lymphatic  gland.  Therefore  Low  is 
quite  correct  in  his  statement  that  '  the  Filaria  is  not  entirely 
compatible  with  health,'  for  very  slight  causes  will  produce  disease. 
In  certain  districts  from  5  to  27  per  cent,  of  the  population  is 
infected  with  filariasis,  and  therefore  if  there  are  many  mosquitoes 
capable  of  carrying  the  worm,  there  ought  to  be  multiple  infection 
of  the  individual  host;  and  one  would  also  assume  that  the  heavier 
the  infection,  the  greater  the  liability  to  obvious  disease.  Multiple 
infection  would  be  more  liable  to  occur  in  natives  than  in  Europeans. 
As  a  matter  of  fact,  heavy  infections  with  the  parent-worms  have 
not  yet  been  described,  though  it  must  be  admitted  that  but  few 
post-mortem  examinations  are  on  record;  and,  moreover,  as  Ftille- 
born  has  shown,  it  is  at  times  by  no  means  easy,  even  with  the 
utmost  care,  to  find  the  adult  worms,  though  they  may  be  found 
even  in  fair  numbers  after  considerable  search  in  those  parts  of  the 
lymphatic  system  which  appear  to  be  least  affected.  When  the 
case  is  one  of  varicose  lymphatics,  or  lymphatic  glands  with  clear 
lymph,  the  obstruction  must  be  looked  for  below  the  junction  of 
the  lacteals  with  the  receptaculum  chyli,  but  when  the  fluid  is 
milky,  it  is  obvious  that  the  obstruction  must  be  beyond  this  point. 
The  cause  of  the  obstruction  may  be  a  coilcd-up  mass  of  worms — 


PATHOLOGY  1601 

e.g.,  Young  found  six  females  and  one  male  in  such  a  bundle — and 
they  may  be  discovered  behind  a  valve  or  in  a  dilated  sinus.  A 
single  female  worm  may,  however,  be  found  lying  in  a  dilated 
lymphatic,  the  draining  gland  being  probably  blocked  by  the 
aborted  ova.  The  irritation  caused  by  the  worms  may  lead  to  a 
permanent  blocking  of  a  main  lymph  channel,  which  will  persist 
even  after  the  irritating  worms  have  died  and  disappeared,  as  has 
been  observed  by  Mackenzie;  or,  again,  the  thoracic  duct  may  be 
found  dilated  in  part  of  its  course,  but  quite  patent  throughout, 
though  associated  with  enormous  varicose  glands  and  vessels  and  a 
complete  absence  of  worms,  which  simply  means  that  the  parasites 
having  caused  the  lesions  have  died  and  disappeared. 

Low  and  Bahr  have  shown  that  the  worms  lead  to  great  fibrosis 
in  the  glands,  and  that  lymphocytes  are  collected  in  clusters  between 
the  strands  of  this  tissue.  This  fibrosis  is  associated  with  an 
excessive  number  of  eosinophile  cells  in  the  glandular  substance. 

In  chylous  extravasations  the  blocking  of  the  thoracic  duct  leads 
to  engorgement  of  the  renal,  the  lumbar,  and  the  pelvic  lymphatic 
channels  with  lymph,  as  well  as  that  of  engorgement  and  dilatation 
of  the  lacteal  vessels  themselves. 

If  the  lymphatic  vessels  of  the  bladder  or  other  parts  of  the 
urinary  tract  rupture  as  a  consequence  of  this  pressure,  the  result 
will  be  chyluria,  and  if,  as  often  happens,  some  bloodvessels  also 
rupture,  there  will  be  haemato-chyluria.  Wise  states  that  in  chyluria 
the  milky  opacity  is  due  to  a  large  amount  of  proteid,  and  not  to 
fat,  and  this  observation  has  been  confirmed  by  Low,  who  in  one 
case  found  the  lacteals  normal,  and  showed  that  the  milky  fluid 
was  lymph  proceeding  from  dilated  lymphatics  in  the  kidneys, 
ureter,  and  bladder.  If  the  abdominal  lymphatics  rupture,  there 
will  be  chylous  ascites;  if  those  of  the  tunica  vaginalis,  there  will 
be  chylocele. 

If,  on  the  other  hand,  the  obstruction  is  posterior  to  the  junction 
of  the  lacteals  with  the  receptaculum  chyli,  then  ordinary  ascites, 
hydrocele,  and  varicose  lymphatics  of  the  scrotum  (lymph  scrotum), 
of  the  leg,  and  varicose  groin  glands,  will  result.  More  rarely  the 
lymphatics  of  the  arm  may  be  affected  in  the  same  manner. 

The  lowered  resistance  of  the  tissues  engorged  with  lymph 
renders  them  specially  liable  to  inflammation,  which  may  at  times 
go  on  to  abscess-formation,  and  which,  if  often  repeated,  will  end 
in  elephantiasis. 

Manson  believes  that  elephantiasis  arises  by  a  damage  to  the 
female  worm,  causing  her  to  produce  immature  embryos,  which  lie 
coiled  up  in  the  egg-shell,  instead  of  stretching  it  considerably. 
The  immature  egg  is  50  /*  in  length  by  34 p  in  breadth,  while  the 
fully-developed  Microfilaria  is  250  to  300 /x  in  length  by  5  to  8 /a 
in  breadth:  therefore  it  is  not  difficult  to  imagine  that  a  lymphatic, 
along  which  the  slim  Microfilaria  passes  with  ease,  might  be  quite 
blocked  by  the  immature  egg,  and  that  if  sufficient  channels  in  the 
skin  or  in  the  lymphatic  glands  were  blocked,  lymph  stasis  would 


x6o2  THE  FILARIASES 

occur,  and,  as  a  result,  the  connective  tissue  would  become  inflamed 
and  hypertrophied,  which,  together  with  the  excess  of  lymph, 
would  increase  the  size  of  the  part.  Manson  bases  this  theory  on 
his  observation  of  eggs  escaping  from  the  ruptured  vesicles  of  a 
lymph  scrotum.  Bahr  is  of  the  opinion  that  tropical  elephantiasis 
can  best  be  explained  by  the  blockage  of  the  lymphatic  channels 
of  the  diseased  area  by  the  frequent  and  long-continued  invasion  of 
the  adult  Filarial.  He  finds  that  the  Microfilaria  may  not  reach 
the  blood,  but  die  in  the  gland  or  organ  in  which  they  are  lying. 
He  also  finds  that  the  periodical  discharge  of  these  Microfilaria 
may  be  a  factor  in  the  production  of  lymphangitis,  orchitis,  and 
funiculitis,  and  that  the  parent-worm  may  die  after  these  inflam- 
matory attacks. 

It  is  believed  that  the  smooth  elephantiasis  (elephantiasis  glabra), 
in  which  the  skin  is  smooth,  is  due  to  blocking  of  the  channels  in 
the  groin  glands,  and  rough  elephantiasis  (elephantiasis  verrucosa^, 
in  which  the  skin  is  very  nodular,  is  due  to  blocking  of  the  small 
skin  capillaries,  but  we  are  not  acquainted  with  definite  proofs  of 
this  theory. 

The  Blood. — The  blood  in  filariasis  does  not  exhibit  anaemia  unless 
there  is  haemato-chyluria  or  diarrhoea;  the  number  of  leucocytes  is 
normal,  but  there  may  be  leucocytosis  during  the  attacks  of  fever. 
The  eosinophiles  are  at  times  increased. 

Morbid  Anatomy. — The  morbid  anatomy  naturally  varies  with  the 
variety  of  the  pathological  lesion  produced. 

In  lymphangitis  the  lymphatic  vessels  will  be  found  enlarged  and 
inflamed,  and  abscesses  of  varying  size  may  at  times  be  found  con- 
taining the  dead  worms,  which  are  apt  to  become  calcified  by  the 
deposition  of  lamellar  plates  of  calcium  carbonate  in  the  interior 
of  the  worm.  The  calcified  worms  were  first  described  by  Wise  as 
small  yellow  bodies,  with  the  shape  and  structure  of  Filarice,  which 
he  found  in  the  pelvis  of  the  kidney.  Bahr  states  that  at  a  later 
stage  the  calcareous  deposit  may  be  gradually  absorbed  until  only 
minute  yellow  spicules  are  left.  The  calcified  (and  also  the  living) 
worms  are  surrounded  by  eosinophile  cells  in  large  numbers.  Bahr 
has  found  filarial  abscesses  to  be  of  common  occurrence  amongst 
the  Fijians  in  the  substance  of  the  gastrocnemius,  the  popliteal  space, 
the  groin,  and  in  the  quadriceps  extensor  in  the  leg,  and  over  the 
internal  condyle,  in  the  axilla,  in  the  latissimus  dorsi  and  serratus 
magnus  muscles  in  the  arm  In  these  abscesses  the  dead  worm  was 
found  associated  witli  Staphylococcus  pyogenes  aureus  and  Strepto- 
coccus pyogenes. 

With  regard  to  the  lymphatic  vessel,  Bahr  is  of  the  opinion  that 
the  worm,  both  during  its  lifetime  as  well  as  after  its  death,  exerts 
an  influence  on  the  vessel  wall,  leading  to  proliferation  of  the  endo- 
thelium and  to  an  invasion  of  the  vessel  wall  with  fibrous  tissue. 
In  this  manner  the  lymphatic  becomes  thickened,  but  shows  also 
numerouscvst-like  dilatations  in  which  the  dead  worms  may  be  found. 

The  fugitive  swellings  found  in  filariasis  have  been  proved  by 


MORBID  ANATOMY  1603 

Young  to  be  composed  of  dilated  lymphatic  tissue.  Inflammatory 
masses  adherent  to  the  skin  in  various  parts  of  the  body  have  been 
found  to  contain  the  adult  worm. 

In  lymphatic  varix  or  varicose  lymphatic  glands  the  obvious 
lesions  may,  and  generally  do,  form  part  of  a  much  larger  dilatation 
of  the  pelvic  and  lumbar  lymph  vessels  and  glands.  The  vessels 
are  found  enormously  dilated  with  thickened  walls,  while  the 
glands  are  riddled  with  dilated  channels.  At  first  the  appearance 
of  the  gland  may  not  be  much  altered,  and  on  section  it  may  show 
the  appearance  of  a  sieve  riddled  with  holes,  but  in  more  advanced 
cases  all  appearance  of  a  lymphatic  gland  disappears,  and  it  is 
transformed  into  a  large  sac  divided  by  fibrous  tissue,  septated  into 
numerous  compartments. 

In  chylous  extravasations  the  thoracic  duct  may  or  may  not  be 
found  impervious,  but  in  any  case  the  lacteals,  the  lumbar,  pelvic, 
pudendal,  and  crural  lymph  vessels  will  be  found  enormously 
dilated,  and  the  lumbar  lymph  glands  converted  into  septated  sacs. 
The  site  of  the  ruptured  lymphatics  is,  however,  by  no  means  easy 
to  find. 

*-  In  elephantiasis  the  lymphatic  vessels  will  be  found  dilated  and 
thickened,  and  in  early  cases  a  round-celled  infiltration  may  be 
seen  in  the  connective  tissue  of  the  part ;  but  in  later  cases  this  has 
led  to  a  hypertrophy  of  the  connective  tissues  of  the  skin  and  the 
fasciae,  including  those  around  the  muscles,  the  vessels,  and  nerves, 
while  all  the  tissues  are  sodden  with  retained  lymph.  The  muscles 
of  the  affected  regions  arc  found  to  be  in  a  state  of  fatty  degeneration ; 
the  bones  may  be  thickened  and  covered  with  osteophytes,  or  more 
rarely  atrophied,  and  still  more  rarely  invaded  by  caseous  abscesses. 

Microscopically  the  epidermis  may  be  normal,  or  thickened  with 
atrophied  or  elongated  papillae;  the  sweat  glands  and  hair  follicles 
may  or  may  not  be  degenerate. 

In  cutting  into  the  tissue  of  a  region  affected  with  elephantiasis 
the  skin  may  be  noted  to  be  thickened,  and  below  it  there  will  be 
found  dense  fibrous  trabecular,  with  the  spaces  filled  with  yellow, 
oily,  fatty  substance,  which  exudes  lymph,  while  the  vessels  and 
nerves  will  be  found  much  increased  in  size. 


THE  CLINICAL  DESCRIPTION. 

General  Remarks. — The  clinical  description  of  the  various 
lesions  will  be  arranged  under  the  headings  Filarial  Fever,  Filarial 
Lymphangitis,  Orchitis,  Lymphangiectasis,  Phlebectasis,  Varicose 
Lymphatic  Glands,  Chylous  Effusions,  and  Elephantiasis  of  various 
parts  ;»f  the  body — e.g.,  scrotum,  leg,  etc. — and,  finally,  a  few 
remarks  will  be  made  with  regard  to  rarer  lesions.  As  regard 
general  treatment,  salvarsan,  neosalvarsan  and  galyl  have  been  recom- 
mended and  tartar  emetic  might  be  tried,  but  no  good  results  have  so 
far  been  obtained  in  our  experience.  Prevention  is  to  be  based  on 
antimosquito  measures  as  described  in  the  chapter  on  malaria,  p.  1202. 


1604 


THE  FILARIASES 


FILARIAL  LYMPHANGITIS. 


Synonyms, — Elephantoid  fever,  Liliwa  (Fijian  term  for  a  rigor), 
fever  and  ague  (Barbados). 

Definition. — Filarial  lymphangitis  is  an  inflammation  of  lymphatic 
vessels  in  any  part  of  the  body  caused  by  Filaria  bancrofti. 

Remarks. — Attacks  of  lymphangitis,  associated  with  an  erysipe- 
latous eruption  of  the  skin,  are  extremely  common  in  the  tropics, 
and  are  often  of  a  filarial  nature,  and  by  their  repeated  recurrences 
produce  elephantiasis. 

Symptomatology. — The  attack  often  begins  with  a  shivering  fit, 
and  a  rise  of  temperature  to  any  degree  from  ioi°  to  104°  F.,  with 
vomiting  and  headache.     In  some  cases  there  is  no  pain  in  the 


■      TIME 

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t       '01° 

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Fig.  713. 


-Temperature  Chart  of  a  Case  of  Elephantiasis  of  the  Leg 
during  an  Attack  of  Filarial  Fever. 


affected  area,  but  a  careful  examination,  or  the  sensation  of  pain  on 
the  part  of  the  patient,  will  lead  to  the  discovery  of  a  red  cedema- 
tous  area  of  skin,  from  which  the  inflamed  lymphatic  may  be  noted 
extending  towards  the  nearest  lymphatic  glands,  which  may  or  may 
not  be  inflamed  and  painful.  Usually  the  temperature  falls  quickly 
in  a  couple  of  days  to  normal,  and  does  not  rise  again,  though  it 
may  be  several  days  before  the  erysipelatous  rash  disappears  and 
the  lymphatics  return  to  normal. 

Complications. — Rarely  does  this  condition  go  on  to  abscess, 
which  may  be  caused  by  a  dead  filarial  worm  or  a  secondary  infection. 

Sequelae. — Sometimes,  after  the  acute  inflammation  has  subsided, 
a  lymphatic  can  be  felt  as  a  hardened  cord,  which,  if  excised,  will 
be  found  to  contain  adult  Filaria. 

Diagnosis. — The  only  condition  which  could  reasonably  be  mis- 
taken for  this  affection  is  a  caterpillar  sting,  which  closely  resembles 
it  in  all  details.  The  history  of  the  case  will  indicate  the  correct 
diagnosis. 

Treatment. — The  treatment  consists  of  rest  in  bed,  a  mild  purga- 
tive, and  a  little  phenacetin  and  caffeine  to  relieve  the  headache, 
while  some  of  the  old  authors  advise  arsenic  or  tinctura  ferri  per- 


FILARIAL  LYMPHANGIECTASIS  1605; 

chloridi,  lllx.-xx.,  given  three  times  a  day,  well  diluted.  Locally, 
at  first  lead  and  opium  lotion,  and  later  an  ointment,  composed  of 
ichthyol  and  lanoline,  gives  relief.  If  an  abscess  forms,  it  must 
be  evacuated  and  treated  on  ordinary  principles. 

FILARIAL  ORCHITIS  AND  HYDROCELE. 

Symptomatology. — This  complaint  begins  with  pains  in  the 
testicle,  fever;  and  at  times  rigor,  pains  in  the  back  and  lower  part 
of  the  abdomen  and  groins,  and  bilious  vomiting.  The  testicle  en- 
larges, and  is  tender  arid  painful, While  an  effusion  forms  in  the  t  unie.a 
vaginalis  of  either  lymph  or  chyle.  The  lymph  thrown  out  is  at 
first  inflammatory,  and  may  coagulate,  and  is  usually  absorbed 
alter  the  fever  subsides,  but  may  persist  and  form  a  filarial  hydro- 
cele. The  effusion  of  chyle  is,  however,  more  usually  permanent, 
and  forms  one  of  the  varieties  of  chylocele  to  be  mentioned  later. 

Treatment. — -The  treatment  consists  of  rest  in  bed  and  the  applica- 
tion of  lead  and  opium  lotion,  and  cool  applications,  together  with 
fairly  vigorous  purgation  of  the  bowels. 

FILARIAL  LYMPHANGIECTASIS. 

Synonyms. — Lymphatic  varix,  Lymph  scrotum. 

Definition. — Filarial  lymphangiectasis  is  the  dilatation  of  lymph 
vessels  brought  about  by  obstruction  to  the  flow  of  lymph,  due  to 
the  presence  of  Filavia  bancrofti. 

Remarks. — Filarial  lymphangiectasis  can,  of  course,  take  place 
in  any  part  of  the  body,  but  the  most  common  situations  are  in  the 
scrotum,  where  it  is  called  '  lymph  scrotum,''  in  the  spermatic  cord, 
in  the  leg,  and  in  the  arm. 


Fig.  714. — Filarial  Lymphangiectasis. 

Symptomatology.— In  the  scrotum  the  affection  begins  with  an 
attack  of  fever,  associated  with  redness,  swelling,  and  pain  in  that 
region.  When  the  fever  has  subsided,  the  whole  scrotum  is  found 
swollen  and  elastic.  It  may  be  smooth  or  rugose,  and  on  inspection 
the  skin  shows  a  number  of  small  clear  vesicles,  which,  if  ruptured, 


l6o6 


THE  FILARIASES 


discharge  either  lymph  or  chyle  containing  filarial  embryos,  or,  much 
more  rarely,  eggs. 

If  the  vesicles  are  ruptured,  the  discharge  of  lymph  may  be  quite 
considerable  in  the  Lwenty-four  hours,  and  may  produce  such 
marked  exhaustion  in  the  patient  as  to  necessitate  an  operation. 

In  the  spermatic  cord  the  disease  begins  with  pain  and  swelling 
in  the  testicle,  cord,  and  lower  part  of  the  abdomen,  associated  at 
times  with  fever.  When  the  acute  symptoms  have  subsided,  a 
swelling  like  a  varicocele,  which  disappears  in  the  prone  position 
and  reappears  when  standing  erect,  will  be  noticed  along  the  cord, 
but  the  vessels  constituting  the  swelling  will  be  noted  to  be  softer, 
less  tortuous,  and  more  like  a  series  of  pouches  than  a  true  varicocele. 


Fig.  715. — Filarial  Lymihangiectasis. 

In  lymphangitis  of  the  leg  there  is  the  same  fever,  with  swelling 
of  the  glands,  leaving  a  soft  swelling  in  the  groin,  which  disappears 
on  lying  down  and  reappears  on  standing  up,  and  which  has  no 
impulse  on  coughing. 

Treatment. — As  the  local  condition  is  simply  part  of  a  much  more 
generalized  varicosity  of  the  lymphatic  vessels,  it  is  best  to  treat  it 
symptomatically  with  antiseptic  dusting-powders,  such  as  boracic 
acid,  zinc  oxide,  and  dermatol,  etc. 

If,  however,  lymphorrhagia  is  taking  place  and  the  patient  is 
becoming  exhausted,  it  is  necessary  to  remove  some  of  the  diseased 
tissue  and  to  ligate  the  dilated  vessels,  but  in  so  doing  it  is  as  well 
to  warn  the  patient  that  this  will  not  cure  the  disease,  and,  indeed, 
may  be  followed  by  elephantiasis  or  even  chyluria. 

FILARIAL  ABSCESSES. 

Manson,  Low,  Wise,  Bahr,  and  others,  have  called  attention  to 
the  frequency  of  filarial  abscesses  in  various  parts  of  the  body. 
The  most  important  are  those  found  in  the  thorax  and  in  the  retro- 
peritoneal tissues.  In  the  latter  situation  the  symptoms  may  be 
those  of  peritonitis. 


FILARIAL  PHLEBECTASIS 


1607 


Fig.  716. — -Filarial  Phlebectasis  simulating  Varicose  Lymphatic 
Glands,  and  Varicocele:  Patient  in  the  Upright  Position. 


Fig.  717. — Filarial  Phlebectasis:  Same  Patient  Lying  Down. 
(Photograph  taken  from  above.     Note  the  disappearance  of  the  swellings.) 


FILARIAL  PHLEBECTASIS  (Filarial  Varix). 

At  times  persons  suffering  from  filariasis  exhibit,  as  observed  by 
us,  marked  varicose  conditions  of  various  veins.  Occasionally  in 
association  with  enlarged  superficial  veins  large  masses  are  to  be 


i6o8  THE  FILARIASES 

seen  in  the  axilla,  groins,  and  other  regions,  which  on  superficial 
examination  might  be  taken  for  enlarged  glands,  but  on  palpation 
it  can  be  ascertained  that  they  are  composed  of  veins,  the  same 
sensation  being  obtained  as  that  experienced  when  palpating  a 
varicocele.  When  these  masses  occur  in  the  groins  they  disappear 
when  the  patient  lies  down. 

VARICOSE  LYMPHATIC  GLANDS. 

Synonyms. — Helminthoma  elastica,  Adenolymphoceles. 

Definition. — Varicose  lymphatic  glands  are  glands  enlarged,  some- 
times to  an  enormous  extent,  by  dilatation  of  their  lymph  paths, 
brought  about  by  obstruction  to  the  flow  of  lymph. 

Remarks. — The  glands  most  commonly  found  enlarged  in  patients 
are  the  groin  glands,  less  frequently  those  of  the  axillae,  while  even 
the  parotid  lymphatic  gland  has  been  recorded  to  have  been 
affected.  In  post-mortems,  as  already  noted,  the  lumbar  glands 
may  be  found  converted  into  septated  sacs. 

Symptomatology. — The  glands  enlarge  after  attacks  of  fever,  and 
are  usually  found  as  soft,  elastic  swellings,  which  are  easily  movable 
when  small,  and  are  covered  with  normal  skin.  They  are  found 
in  the  groin,  inguinal  or  femoral  regions,  and  in  the  axilla.  If 
punctured  with  a  hypodermic  needle,  lymph  or  chyle  can  be 
obtained  at  times  containing  Microfilaria.  Usually  small,  they 
may  assume  enormous  proportions,  reaching  below  the  knee,  and 
seriously  impeding  locomotion. 

Treatment. — They  may  be  removed  if  necessary,  but  this  should 
not  be  done  without  due  cause,  as  they  are  only  part  of  a  more 
widespread  disorder.  Radium  treatment  has  been  advised  by 
Sir  Havelock  Charles. 

FILARIAL  LYMPH  AND  CHYLOUS  EXTRAVASATIONS. 

Lymph  and  chylous  extravasations  are  due  to  the  rupture  of 
dilated  lymph  or  lacteal  vessels  into  the  urinary  passages,  the  bowel, 
the  tunica  vaginalis,  or  peritoneum. 

They  may,  therefore,  be  considered  under  the  headings  of 
Chyluria  and  Lymphuria,  Chylous  and  Lymphatic  Diarrhoea, 
Chylocele,  and  Chylous  Ascites.  Perhaps  further  investigations 
will  show  that  Wise  and  Low  are  correct,  and  that  in  addition  to 
hgemato-chyluria  and  other  chylous  conditions  there  may  also  be  a 
pure  haemato-lymphuria,  lymphatic  diarrhoea,  lymphocele,  and 
lymphatic  ascites. 

Chyluria  and  Lymphuria. 

Definition. — Chyluria  is  the  passage  of  chyle  with  the  urine,  and 
is  due  to  the  rupture  of  dilated  chyle-containing  lymphatic  vessels; 
when  mixed  with  blood  it  is  known  as  hremato-chyluria.  When 
lymph  only  is  passed  the  term  lymphuria,  suggested  by  Low,  should 
be  adopted,  and  if  mixed  witli  blood,  luemato-lymphuria. 


CHYLURIA  AND  LYMPHURIA  1609 

Pathology. — This  has  been  worked  out  principally  by  Mackenzie 

and  Manson,  and  more  recently  by  Low  and  Wise.  The  presence 
of  chyle  in  the  urine  is  due  to  the  rupture  of  dilated  chyle-containing 
lymphatic  vessels.  Owing  to  some  obstruction  in  the  thoracic  duct 
with  varicosity  of  lymphatics  below  the  scat  of  obstruction,  the 
lymphatics  in  the  bladder  walls  become  dilated  and  rupture,  and  so 
the  chyle  passes  into  the  bladder. 

Low  has  demonstrated  that  lymphyuria  takes  place  when  the  blockage 
of  the  lymphatics  is  below  the  thoracic  duct  and  reccptaculum  chyli.  Chemi- 
cally the  only  difference  between  lymph  and  mesenteric  lymph  or  chyle  is 
that  the  latter  contains  a  much  larger  amount  of  fat,  which  is  derived  from 
the  lacteals  of  the  intestine.  According  to  Delamere,  the  fat  conlair.cd  in 
lymph  does  not  exceed  3-0  per  mille.,  while  in  chyle  it  may  be  as  much  as 
0-5  per  mille. 

Symptomatology. — The  onset  of  the  attack  is  usually  abrupt, 
without  marked  symptoms,  though  vague  pains  may  be  felt,  and 
at  times  there  may  be  fever,  pains  in  back,  perina?um,  and  thighs. 
Usually,  however,  the  patient  simply  asks  advice  because  he  is 
passing  milky  or  bloody  urine. 

As  a  rule  the  urine  clears  in  the  course  of  time,  but  it  is  merely  an 
intermission,  and  the  symptoms  will  in  due  course  recur,  and  inter- 
missions and  attacks  will  follow  each  other  for  years;  on  the  other 
hand,  however,  it  may  be  continuous,  and  not  intermittent.  The 
duration  of  the  intermissions  may  be  days,  months,  or  years,  while 
the  attacks  may  be  attributed  to  exertion  or  emotion.  After  con- 
tinuing for  some  time  it  may  lead  to  exhaustion,  neuralgic  pains  in 
different  parts  of  the  body,  disordered  bowels,  coated  tongue,  dry, 
harsh  skin,  and  a  state  of  cachexia. 

If  the  urine  cloLs  in  the  bladder,  there  may  be  severe  pain  and 
strangury.  The  urine  generally  presents  the  appearance  of  milk, 
but  mav  be  pinkish  in  colour  from  admixture  with  blood,  and  a 
large  portion  may  clot  into  a  semitransparent  gelatinous  mass.  It 
is  usually  passed  in  fair  quantity,  and  it  will  be  noticed  that  the 
morning  urine  is  usually  very  clear,  while  that  at  night  is  much 
more  milky  or  red.  On  standing,  in  true  chyluria,  the  fat  accumu- 
lates on  the  surface,  giving  rise  to  a  cream-like  appearance.  Under 
the  microscope,  as  a  rule,  no  fatty  globules,  however  minute,  are 
observed,  but  white  corpuscles,  especially  lymphocytes,  and  red 
corpuscles,  and  at  times MicrofilaricB  and  crystals  of  calcium  oxalate, 
may  be  seen.  The  specific  gravity  is  low,  varying  from  1015  to  1020. 
The  reaction  is  usually  acid.  On  shaking  the  urine  with  ether,  the 
fat  can  be  removed  and  estimated,  when  it  will  be  found  to  vary 
from  o-8  to  1-8  per  cent.  After  the  removal  of  the  fat,  the  urine 
can  be  tested  for  albumen,  which  is  always  present,  and  which 
usually  persists  for  some  time  after  the  fat  has  disappeared.  The 
quantity  of  albumen  varies  from  o-6  to  0-9  per  cent.  Albumoses  and 
sugars  are  absent. 

When  the  urine  does  not  contain  any  distinct  amount  of  fab  one 
speaks  of  lymphuria,  and  if  blood  is  present  haemato-lymphuria.   The 


i6io  THE  FILARIASES 

same  patient  may  have  at  times  attacks  of  chyluria  and  hsemato- 
chyluria,  and  at  other  times  attacks  of  lymphuria  and  haemato- 
lymphnria. 

Treatment.— The  treatment  is  purely  symptomatic,  and  consists 
of  rest  in  bed,  lying  as  much  as  possible  in  the  prone  position,  while 
in  some  cases  methylene  blue  may  be  given  in  2-grain  doses,  together 
with  salol,  5  grains,  or  urotropine  in  5-grain  cachets.  The  diet  must 
be  bland,  non-irritating.  Astringent  injections  into  the  bladder  have 
been  used,  and  gallic  acid,  nitrate  of  silver,  acetate  of  lead,  iodide 
of  potassium,  and  thymol  have  been  administered  internally,  but 
have  not  been  found  to  be  efficacious.  Indeed,  there  is  no  justifica- 
tion for  their  use.  Administration  of  quinine,  combined  with 
exposure  to  X  rays,  has  been  recommended  by  Musgrave  and 
McDill. 

If  the  urine  clots  in  the  bladder,  it  must  be  washed  out  under 
chloroform  by  means  of  an  aspirator,  and  if  this  is  not  successful, 
the  bladder  may  have  to  be  opened  and  drained. 

Chylous  and  Lymph  Diarrhoea. 

Diarrhoea  with  chyle  or  lymph  and  blood  in  the  motions  has  been 
recorded,  but  is  rare. 

Chylocele  or  Lymphocele. 

This  may  develop  gradually,  the  tunica  vaginalis  filling  up  with 
an  opaque  fluid,  which  on  tapping  is  found  to  be  chylous,  and  may 
contain  Microfilaria.  It  may,  however,  be  preceded  by  an  attack 
of  fever  and  orchitis.  It  is  said  that  the  sac  is  less  tense  in  the 
morning,  and  more  so  at  night. 

Treatment. — A  chylocele  does  not  grow  to  any  large  size,  and 
only  requires  occasional  tapping. 

Chylous  Ascites. 

Chylous  ascites  is  rarely  met  with  in  human  beings,  though  we 
have  seen  two  cases.  It  is  common  in  animals  as  the  result  of 
filarial  infection. 

ELEPHANTIASIS. 

Synonyms.— Elephant  Leg,  Cochin  Leg,  Barbados  Leg,  Galle 
Leg,  Glandular  Disease  of  Barbados,  Elephantiasis  Arabum, 
Da-Fil,  Dau-ool-Fil,  Pes  Fcbricitans,  Perical,  Phlegmasia  Mala- 
barica,  Elephantiasis  Indica,  Bucnemia  Tropica,  Morbus  Elephas, 
Spargosis  Fibroareolaris,  Pachydermia,  Hernia  Carnosa,  Elephan- 
tiasis Tuberosa  et  Scrotalis,  Hypersarcosis,  Mai  de  Cayenne,  Sarco- 
cele  d'Egypte,  Roosbecn  von  Surinam,  Shlipada,  Kosharriddki, 
Barawa  (Sinhalese) . 

Definition. — Elephantiasis  is  a  chronic  inflammatory  hypertrophy 
of  the  fibrous  connective  tissue  of  a  region  of  the  body  induced  by 
lymph  stasis,  and  resulting  in  a  considerable  hypertrophy  of  the 
skin  and  subcutaneous  tissues. 


ELEPHANTIASIS 


1611 


Varieties. — The  most  common  varieties  of  elephantiasis  are  the 
affection  of  the  leg,  scrotum,  vulva,  arm,  and  breast,  while  other 
regions  are  much  more  rarely  affected.  The  different  varieties 
must  now  be  briefly  described. 

Elephantiasis  of  the  Leg. 

Symptomatology.— During  attacks  of  filarial  lymphangitis  of  the 
leg  it  is  noticed  that  the  limb  becomes  swollen,  and  though  after  the 
first  attack  it  may  resume  its  normal  size,  this  does  not  happen 
after  repeated  successive  attacks,  and  gradualby  the  limb  becomes 


Fig.  718.- — Elephantiasis  of  the  Legs. 


more  and  more  swollen,  while  the  natural  folds,  especially  the  ankle 
fold,  become  much  exaggerated  by  the  swelling  on  either  side,  so 
that  deep  sulci  are  formed.  The  dorsum  of  the  foot  becomes 
swollen  and  puffy,  and  is  separated  by  the  deep  ankle  sulcus  from 


1612  THE  FILARIASES 

the  swollen  lower  part  of  the  leg.  In  these  sulci  the  debris  of  the 
cast-off  epithelium,  together  with  the  excretions  of  the  skin,  accu- 
mulate and  give  rise  to  a  foul-smelling  discharge,  and  ulcers  may 
form.  At  first  the  skin  is  smooth  and  soft,  forming  the  smooth 
variety  of  the  complaint,  which  may  persist,  or  it  may  become  dark, 
hard,  thick,  and  rough,  being  elevated  into  bosses  or  warty  eleva- 
tions, forming  the  verrucose  variety.     The  appendages  now  atrophy 


Fig.  719. — Elephantiasis  of  the  Legs. 

from  malnutrition,  the  hairs  may  dr;op  off,  and  the  nails  become 
rough  and  thickened,  while  the  skin  perspires  less  and  the  sen- 
sibility is  diminished.  Ulcers  may  now  form  on  almost  any  part  of 
the  foot.  The  swelling  is  more  commonly  met  with  below  the  knee, 
but  the  whole  thigh  may  become  implicated. 

If  left  untreated,   the  size  of  the  leg  gradually  increases  with 
repeated  attacks  of  fever,  and  may  reach  considerable  dimensions. 


ELEPHANTIASIS 


1613 


After  some  years  the  attacks  of  fever  may  cease  altogether,  though 
the  condition  of  the  leg  usually  remains  unchanged.  In  some 
rare  cases  elephantiasis  may  develop  without  the  patient  ever  having 
an  attack  of  fever. 

Treatment. — A  radical  method  of  treatment  has  yet  to  be  found. 
Of  the  various  palliative  ones  the  most  satisfactory  is  perhaps  that 
introduced  by  Castellani,  which  consists  in  keeping  the  patient  at 
complete  rest  in  bed,  with  thiosinamin  or  fibrolysin  injections  and 
methodical  bahdaging.  The  details  of  the  treatment  are  as  follows: 
The  patient  is  kept  in  bed  and  an  injection  of  2  to  4  c.c.  of  fibrolysin 
Merk  (which  consists  of  thiosinamin  and  salicvlic  acid  dissolved 


Fig.  720. — Elephantiasis  of  the  Leg:  Before  Treatment. 

in  water)  is  given  daily  for  three  to  six  months,  the  injections  being 
interrupted  for  a  few  days  from  time  to  time.  The  injections  may 
be  made  in  the  affected  parts,  or  deeply  into  the  gluteal  region, 
where  they  cause  much  less  pain.  After  each  injection  the  whole 
limb  is  tightly  bandaged  with  flannel  bandages,  which  are  kept  in 
place  day  and  night.  In  some  cases  rubber  bandages  may  be  used 
with  great  advantage,  especially  in  cases  of  verrucose  elephantiasis, 
because  they  render  the  skin  much  smoother.  Unfortunately, 
many  patients  cannot  stand  rubber  bandaging.  To  increase  the 
pressure  on  the  hardest  parts  pads  of  inelastic  material  may  be 
applied  before  bandaging,  and  for  this  purpose  small  cylindrical 


1614 


THE  FILARIASES 


gauze  bags  filled  with  ordinary  small  lead  shot  are  found  especially 
useful.  In  some  cases  massage  of  the  whole  limb  before  bandaging 
is  useful.  It  is  of  the  utmost  importance  that  the  pressure  on  the 
whole  limb  should  be  well  distributed,  otherwise  the  parts  on 
which  insufficient  pressure  has  been  made  will  be  found  to  become 
swollen.  It  is  also  useful  to  keep  the  affected  limb  continually 
elevated  by  means  of  pillows,  etc.  In  cases  of  verrucose  elephan- 
tiasis in  which  the  skin  is  covered  with  numerous  horny  masses,  a 
spirit  lotion  of  resorcin  and  salicylic  acid  (ac.  salicylici,  resorcin, 
aa  gr.  xxx. ;  sp.  rect.,  §iv.)  is  useful  in  removing  these  horny  masses. 


Fig..  721. — The  Same  Case  as  in  Fig.  720:  After  Treatment  by  Fibfo- 
lysin  and  Bandaging,  and  without  any  Operative  Measures. 


In  successful  cases  after  three  to  six  months  of  this  treatment  the 
affected  parts  are  of  much  smaller  size,  the  skin  is  smoother,  more 
elastic,  and  can  be  pinched  into  folds.  Long  elliptical  strips  of  the 
redundant  skin  and  subcutaneous  tissue  may  then  be  removed,  the 
margins  of  the  wound  being  stitched  together.  This  would  not  be 
practicable  before  the  medical  treatment,  as  the  skin  being  enor- 
mously thickened  and  inelastic,  the  coaptation  of  the  opposed  sur- 
faces could  not  be  obtained. 

In  our  experience  this  treatment  has  generally  only  a  slight  and 
temporary  effect  in  recent  cases  when  the  disease  is  in  the  acute 
stage  with  frequent  attacks  of  filarial  fever.     On  the  other  hand, 


ELEPHANTIASIS 


1615 


the  treatment  gives  much  better  and  more  lasting  results  in  old- 
standing  cases,  especially  in  those  of  the  verrucose  type,  charac- 
terized by  the  enormous  new  formation  of  fibrous  tissue  and  absence 
of  fever.  After  treatment  the  patient  should  wear  puttees  or  elastic 
stockings,  and  the  rubber  bandage  should  be  applied  from  time  to 
time. 

Handley  has  treated  cases  by  first  preparing  a  vaccine  from  the  diplococcus 
which  he  found  in  the  blood,  and  administering  this  until  the  blood  and 
lymph  become  sterile,  and  then  performing  his  operation  of  '  lymphangio- 
plasty,'  by  silk  introduced  by  means  of  long 
probes,  which  are  pushed  along  the  subcu- 
taneous tissues,  through  small  incisions, 
until  a  path  is  made  from  the  affected  region 
to  one  with  a  normal  lymph  circulation. 
In  the  cases  so  far  reported  there  was 
marked  improvement  at  first  after  opera- 
tion, but  this  did  not  last  long.  Madden 
and  Ferguson  report  unfavourably  on  lym- 
phangioplasty  as  a  treatment  for  elephan- 
tiasis of  the  legs,  as  they  find  the  temporary 
improvement  not  maintained,  because  the 
reactive  changes  in  the  tissues  immediately 
around  the  thread  eventually  obliterate  the 
new  vessels.  Sistrunk  reports  favourably  on 
the  Kondoleon  Operation,  the  aim  of  which 
is  to  establish  by  a  wide  excision  of  the 
aponeurosis,  a  communication  between  the 
superficial  and  deep  lymphatic  channels. 

Other  methods  of  treatment  consist 
in  bandaging,  massage,  tapping  with 
Southey  tubes,  and  even  amputation, 
but  none  of  these  are  satisfactory. 

Elephantiasis  of  the  Scrotum. 

The  disease  may  begin  as  a  lymph 
scrotum,  or  with  recurring  erysipela- 
tous attacks,  with  a  red  inflammatory 
blush  on  the  skin,  and  fever.  After 
each  attack  the  scrotum  is  larger  than 
it  was  before,  and  it  goes  on  growing, 
if  left  alone,  until  it  may  reach  the 
weight  of  224  pounds,  as  mentioned 
by  Chevers,  which  is  probably  the 
largest  ever  described.  When  well  developed  it  forms  a  triangular- 
shaped  mass  hanging  down  between  the  legs,  with  the  base  down- 
wards, and  the  apex  upwards  towards  the  pubes.  On  its  anterior 
and  upper  aspect  there  is  an  aperture  which  leads  into  a  canal, 
formed  by  the  inverted  prepuce,  at  the  bottom  of  which  is  the  glans 
penis.  The  penis  itself  is  buried  in  the  tumour.  The  testicles 
are  situated  at  the  upper  and  back  part  of  the  tumour,  and  are  usually 
surrounded  by  hydroceles. 

If  large,  the  base  of  the  tumour  is  frequently  ulcerated. 


Fig.  722. — Elephantiasis   of 
the  Scrotum. 


1616  THE  FILARIASES 

Treatment.— The  treatment  is  removal,  which  is  a  very  easy 
operation,  and  very  successful,  following  either  Manson's  or 
Charles's  method.  "Manson  says  that  the  mortality  need  not 
exceed  5  per  cent. 

The  most  important  feature  of  the  whole  operation  is  to  have 
the  skin  perfectly  clean  and  aseptic,  and  to  carefully  choose  the 
parts  of  the  skin  which  are  to  be  used  as  flaps. 

An  elastic  tourniquet  in  a  figure  of  eight  is  applied  round  the 
pelvis  and  the  neck  of  the  tumour.  The  skin  flaps  are  now  marked 
out  and  deepened,  the  vessels  being  carefully  ligatured  as  they  are 
exposed. 

The  testicles  are  then  dissected  by  perpendicular  cuts,  and  the 
penis  is  set  free  by  dissection,  after  cutting  down  the  canal  already 
mentioned  as  formed  by  the  prepuce.  This  is  best  done  with  a  pair 
of  scissors. 

The  general  mass  of  elephantoid  tissue  is  now  cut  away,  gradually 
ligaturing  the  vessels  as  the  cutting  process  goes  on,  this  preventing 
any  of  the  vessels  being  passed  over.  The  tourniquet  is  now 
loosened,  and  any  bleeding  spot  secured. 

If  there  are  hydroceles  present,  these  are  opened,  and  the  sac 
turned  inside  out,  and  after  any  redundancy  has  been  removed,  it 
is  stitched  around  the  testicle  in  the  inverted  condition.  The  flaps 
are  now  brought  together  and  stitched  over  the  testes,  a  drain  of  some 
description  being  introduced  at  the  lower  portion  of  the  wound  if 
this  is  considered  to  be  necessary.  Skin  flaps  should,  if  possible, 
be  made  for  the  penis;  failing  this,  the  raw  area  must  be  covered 
with  protective,  and  allowed  to  granulate.  The  whole  wound  must 
now  be  antiseptically  dressed,  and  usually  heals  without  difficulty. 

Sir  Havelock  Charles'  Operative  Method. — After  the  usual  prep- 
aration an  incision  is  made  in  the  median  line  from  near  the  pubis 
to  the  preputial  mouth  deepening  it  to  the  dorsum  of  the  penis. 
Enucleation  of  the  organ  is  performed  from  the  suspensory  ligament 
to  its  free  extremity.  There  the  glans  is  still  separated  from  the 
finger  by  the  lining  membrane  of  the  prepuce.  The  head  of  the  penis 
is  pulled  up  and  this  cap  of  mucous  membrane  is  cut  through  in  front 
of  the  glans,  which  is  easily  palpable  through  it.  The  organ  is  now 
free,  with  its  head,  covered  with  a  sort  of  cap,  which  is  next  slit 
up,  and  the  parts  thoroughly  cleaned.  Now  the  mass  is  pulled  to 
the  patient's  right,  exposing  the  left  side  of  the  neck  of  the  tumour. 
Cut  from  above,  near  external  abdominal  ring,  curving  towards  the 
median  line  in  front  of  the  anus.  Deepen  this  incision  gradually 
with  finger  and  scalpel  to  near  the  bulb,  avoiding  hurting  it.  The 
trunks  of  the  vessels  can  be  seized  with  pressure-forceps  before 
section  or  after  cutting.  The  same  procedure  is  repeated  on  the 
right  side  of  the  neck  of  the  tumour.  The  two  incisions  will  meet 
in  front  of  the  anus,  all  the  main  vessels  will  be  seized  and  divided, 
and  the  bulb  almost  cleared  on  both  sides. 

Then  the  testicles  arc  enucleated,  and  after  wrapping  them,  as 
well  as  the  cords,  in  gauze,  they  are  placed  on  the  pubis.     The 


ELEPHANTIASIS  1617 

flaps  are  now  made,  practice  determining  the  amount  of  covering 
necessary.  Place  the  right  testicle  under  the  skin  flap  on  the  thigh. 
Repeat  the  same  with  the  left  testicle  and  draw  the  flaps  to  the 
median  line.  A  few  temporary  stitches  to  keep  them  in  position, 
whilst  a  continuous  suture  run  quickly  up  holds  them  firmly. 
Lastly  flaps  are  stitched  to  the  body  of  the  penis. 

After  the  operation  careful  dressing,  well  and  equally  applied,  is 
of  great  practical  importance. 

Elephantiasis  of  the  Vulva. 

This  arises  in  the  same  manner  as  elephantiasis  of  the  scrotum, 
and  may  affect  the  labia  majora  or  the  clitoris.  It  is,  however, 
very  rare.  The  tumour,  according  to  Manson,  may  weigh  8  to 
10  pounds,  or  more.     The  treatment  is  removal. 

Elephantiasis  of  the  Breast. 

Elephantiasis  of  the  breast  is  very  rare,  but  does  occur,  and  the 
enlarged  breast  may  reach  to  the  pubes  or  the  knee.  It  may  affect 
one  or  both  breasts.     The  treatment  is  removal. 

Elephantiasis  of  the  Arm. 

This  is  rare,  but  may  arise  in  the  same  manner  as  in  the  leg. 
One  arm  or  both  arms  may  be  affected.  Bahr  reports  that  the 
natives  of  Fiji  and  probably  of  other  South  Pacific  Islands  are,  in 
comparison  with  natives  of  other  regions,  peculiarly  liable  to  this 
form  of  elephantiasis. 

Elephantiasis  of  the  Scalp. 

Rarely  the  whole  scalp  is  enormously  thickened,  and  presents 
deep  furrows. 

Circumscribed  Elephantiasis. 

Large  pendulous  tumours  of  filarial  origin,  one  to  several,  may 
be  found.  These  are  commonest  in  the  upper  part  of  the  thigh, 
just  below  the  groin. 


RARER  AFFECTIONS. 

Lewis  has  recorded  a  case  of  filariasis  in  which  chyle  containing 
Microfilaria  was  discharged  from  both  conjunctiva?,  while  Maitland 
has  described  cases  of  acute  synovitis  of  the  knee  associated  with 
filariasis  as  being  of  too  frequent  occurrence  to  be  looked  upon  as 
merely  coincidences. 


i6i8  THE  FILARIASES 


FILARIASIS  CAUSED  BY  OTHER  FILARIID^. 

The  lesions  produced  by  Dracunculus  tnedinensis  (Linnaeus,  1758), 
Loa  loa  (Guyot,  1778),  Onchocerca  volvulus  (Leuckart,  1893),  and 
other  filarial  worms,  are  described  in  Chapters  LXXXVIL,  p.  1964, 
and  LXXXVIII.,  p.  1968,  while  the  zoological  account  of  these 
worms  can  be  found  in  Chapter  XXVI. ,  p.  621.  It  will  be  remem- 
bered that  Filaria  immitis  Leidy,  1856,  found  in  the  dog,  does  not 
occur  in  man,  the  supposed  case  being  wrongly  quoted. 

REFERENCES. 

Alard  (1809-24).     Histoire  de  1' Elephantiasis  des  Arabes.     Paris. 

Bahr,  P.  H.  (1912).     Filariasis  and  Elephantiasis  in  Fiji.     London. 

Bancroft  (1877).     Lancet,  70  and  495. 

Bremont  and  Leger  (1917).     Bull.  Path.  Exot.,  vol.  x.,  No.  10. 

Chapotin  (1812).     Topographie  Medicale  de  l'lle  de  France. 

Castellani  (1907).     Journal  of  Tropical  Medicine,  x.  250,  297. 

Castellani  (1908).     Journal  of  Cutaneous  Diseases,  May. 

Castellani  (1908).     British  Medical  Journal. 

Charles  (1880).     Indian  Med.  Gazette. 

Clair  (1908).  Traitement  palliatif  du  Dr.  Castellani  dans  1' Elephantiasis. 
Bull.  Soc.  Path.  Exot.,  vol.  i.,  No.  5. 

Daniels  (1908).     Journal  of  Tropical  Medicine,  xi.  280. 

Dubruel  (1909).     Bulletin  Path.  Exotique. 

Esmarch  and  Kulenkampff  (1885) .  Die  elephantiastichen  Formen.  Ham- 
burg. 

Fulleborn  (1912).     Archiv  fur  Schiffs-  u.  Tropen-Hygiene. 

Goebel  (1911).     Chirurgie  des  Heissen  Lander  Erg.  d.  Chirurgie,  Bd.  iii. 

Handley  (1909).     Lancet,  January  2. 

Hebra  (1885).     Elephantiasis  Arabum.     Wien. 

Hendy  (1784).     Glandular  Disease  in  Barbadoes.     London. 

Hillary  (1750).  Diseases,  Acute  and  Chronic,  Peculiar  to  the  Island  of 
Barbadoes.     London. 

Hirsch  (1885).     Historical  and  Geographical  Pathology,  ii.  226;  iii.  491. 

Jamsetjee  (1854).  Transactions  of  the  Medical  and  Physical  Society, 
Bombay,  ii.  341. 

Kampfer  (1712).     Amoenitates  Exoticae.    Lemgovia. 

Lewis  (1872).     Haematozoa in  Human  Blood.     Calcutta. 

Low  (1912).     Journal  of  the  London  School  of  Tropical  Medicine.     Vol.  i., 
part  3,  Journal  of  Tropical  Medicine,  March  15,  191 1. 

McNaughton  (1919).     Jour.  Trop.  Med.,  No.  1  (Galyl  in  Filariasis). 

Maitland  (1898).     Indian  Medical  Gazette,  32,  81,  361.     Calcutta. 

Manson  (1876-1918).  Numerous  publications  in  China  Maritime  Customs, 
British  Medical  Journal,  Lancet,  Journal  of  Tropical  Medicine,  and 
Text-Book  of  Tropical  Diseases,  Davidson's  Hygiene  and  Diseases  of 
Warm  Climates.  Allbutt  and  Rolleston's  System. 

Nisbet  and  Lilley  (1918).     Brit.  Med.  Jour.,  November  23. 

Raymond  (1767).     Histoire  de  l'Elephantiasis.     Lausanne. 

Rimmer  (1918).     Brit.  Med.  Jour.,  October  12. 

Sistrunk  (1918).  Journ.  Amer.  Med.  Ass.,  September  (Technic  of  the 
Kondoleon  Operation) . 

White  (1909).     Journal  of  Tropical  Medicine.     London. 

Wise  (1909).     Journal  of  Tropical  Medicine,  227.     London. 

Young  (1879).     British  Medical  Journal,  i.  1037.     London. 


CHAPTER  LXVII 
THE  MYIASES  AND  ALLIED  CONDITIONS 

The  Myiases:  Rhinal;  Aural;  Ocular;  Urinary;  Vaginal;  Gro-gaslro-intestinal ; 
Dermal — Allied  conditions — References. 

THE  MYIASES. 

Definition. — The  myiases  are  the  invasions   of  any  part  of  the 
body  of  man  or  animals  by  dipterous  larvae. 

Nomenclature. — In  1815  Kirby  and  Spence  suggested  the  name  '  schole- 
chiasis  '  for  the  infestations  of  man  and  animals  by  insects  and  their  larvae. 
In  1840  Hope  proposed  a  series  of  terms  applying  to  various  groups  of  insects, 
some  of  which  have  come  into  general  use,  and  all  of  which  are  employed  in 
this  chapter.  Thus  he  names  the  invasion  of  dipterous  larva?  '  myiasis,' 
while  that  due  to  the  larvae  of  lepidoptera  he  calls  'scolechiasis,'  and  that 
brought  about  by  beetles  '  canthariasis.'  In  the  present  chapter  we  utilize  all 
these  old  terms  and  keep  the  names 'diplopodiasis  '  and  'chilopodiasis,'  which 
we  have  already  used  in  previous  editions,  while  we  increase  the  number 
by  turning  one  of  Hope's  terms  into  '  dermapteriasis.'  Some  of  these  old 
terms  may  not  appear  very  suitable,  but  they  are  the  first  to  be  suggested. 

Historical. — The  history  of  the  myiases  may  be  divided  into 
'  ancient  knowledge  '  and  '  modern  knowledge.' 

Ancient  Knowledge. — As  the  disease  is  much  more  frequently 
found  in  animals  than  in  man,  it  is  not  surprising  to  find  that  it  was 
first  recorded  in  them.  According  to  Sambon,  it  was  well  known  in 
animals  to  the  Babylonians,  and  to  the  Ancient  Egyptians,  Greeks, 
and  Romans.  According  to  the  same  authority,  it  was  recognized 
in  man  even  in  the  Middle  Ages.  In  the  tenth  century  there  appeared 
a  book  entitled  '  The  Leech  Book  '  of  Bald,  or  Medicinale  Anglicum, 
which  described  the  '  ana-worm  '  as  growing  in  man  and  eating 
through  to  the  outside  and  shedding  itself  out  of  the  hole  so  made. 
Sambon  says  this  may  well  have  been  the  larva  of  Hypoderma  bovis. 
In  the  eleventh  and  twelfth  centuriesthe  Arabian  physicians  mention 
a  malady  called '  bovine  disease,'  which  may  have  been  an  infestation 
with  the  larva  of  the  same  fly.  In  the  sixteenth  century  Ambrose 
Pare  gave  an  account  of  several  infestations  by  larvae,  and  illus- 
trated the  paragraphs  with  fanciful  drawings  of  maggots. 

In  1589  Father  Pedro  Simon  wrote  an  account  of  the  occurrence 
of  the  fly  which  we  now  call  Dcrmatobia  hominis,  as  seen  along  the 
banks  of  the  Rio  Magdalena  and  in  the  low  plains  to  the  east  of  the 
Andes.  This  appears  to  be  the  first  reference  to  the  subject  as  seen 
in  the  tropics. 

These  observations  were  extended  in  1653  by  Father  Bernabe 

1619 


1620  THE  MYIASES  AND  ALLIED  CONDITIONS 

Cobo,  who  states  that  in  each  wound  caused  by  the  common  mosquito 
there  grows  a  spine-covered  worm  the  size  of  a  haricot  bean  or  larger. 

About  this  time  Fernelius  described  some  form  of  nasal  infesta- 
tion— perhaps  a  myiasis — as  occurring  in  soldiers. 

In  16S7  Leuwenhoek,  in  Europe,  mentions  two  cases,  one  of 
dermal  myiasis  in  the  leg  of  a  woman  who  made  a  good  recovery, 
and  another  in  the  mouth  of  a  second  woman,  who  died.  The  larva? 
are  thought  by  Hope  to  belong  to  the  Muscidae. 

Modern  Knowledge. — With  the  appearance  of  the  work  of  Antonio 
Vallisneri  in  the  early  years  of  the  eighteenth  century,  a  much 
better  conception  of  these  infestations  of  animals  and  man  became 
possible,  and  from  this  time  onwards  the  knowledge  of  the  subject 
increased  and  improved.  In  1745  there  appeared  a  work  entitled 
'  Relation  abregee  d'un  voyage  fait  dans  1'interieur  de  l'Amerique 
Meridionale,'  by  De  la  Condamint,  where,  on  p.  170,  he  mentions 
the  '  ver  macaque  ' — i.e.,  the  larva  of  Dermatobia  hominis  (Linnaeus 
junior),  and  says  that  it  takes  its  birth  in  the  wounds  made  by  a 
kind  of  mosquito,  but  from  whence  its  egg  comes  is  unknown.  This 
observation  has  since  been  fully  confirmed  by  recent  research.  In 
1757  Arture  drew  attention  to  the  occurrence  of  Dermatobia 
hominis  in  Cayenne,  and  in  17S1  Linnaeus  junior*did  the  same  as 
regards  Peru  in  a  letter  addressed  to  Pallas,  in  which  he  gave  the 
fly  its  present  name.     Gmelin  subsequently  published  this  letter. 

Somewhere  about  this  time  Turner  described  two  cases  of  urinary 
myiasis  in  England. 

In  1770  Wohlfart  published  an  account  of  rhinal  myiasis  in  his 
work  entitled  '  De  Vermibus  per  nares  excretis.' 

In  1809  Azara  gave  a  history  of  his  journey  in  1781-1801  into 
Paraguay,  and  wrote  an  account  of  a  rhinal  myiasis,  most  probably 
due  to  the  larvae  of  the  fly  we  now  call  Chrysomyia  macellaria. 

About  the  same  time  Lempriere  described  the  same  condition 
in  Jamaica,  where  it  caused  the  death  of  a  woman,  and  Sells  gave 
an  account  of  probably  the  same  larva  causing  infestations  of  the 
eyes,  ears,  nose,  and  mouth  in  the  same  islands.  Some  of  Sells's 
cases  ended  in  recovery  and  others  in  death.  Also  about  the  same 
time  (1S06)  comes  the  case  of  the  soldier  believed  to  be  infested  with 
CEstrus  hominis  Curtis  in  the  skin  near  the  scapula  in  Surinam. 

In  1817  Schock  studied  gastro-intestinal  myiasis. 

In  1830  a  sailor  in  Demerara  is  noted  to  be  suffering  from  myiasis 
in  the  arm.  This  was  thought  to  be  caused  by  a  species  of  CEstrus. 
In  1832  Howship  recorded  CEstrus  hominis  in  the  scrotum  of  a 
carpenter  in  Colombia;  in  1S35  Guyon  mentioned  a  dermal  myiasis 
in  a  negro  in  Martinique;  in  1837  Hope  described  Dermatobia 
hominis  in  the  head  of  a  man,  and  called  it  CEstrus  guildingii,  after 
L.  Guilding  of  Trinidad,  who  found  the  case. 

In  1840  there  appeared  the  classical  and  much  neglected  work 
on  the  whole  subject  by  Hope,  in  which  not  merely  are  the  older 
accounts  gathered  together,  but  also  clear  definitions  of  the  various 
conditions  are  provided. 


MTIOLOGY  1 62 1 

From  this  time  onwards  the  observations  on  myiasis  increase  in 
number— e.g.,  Duncan  in  1854,  while  in  1856  Lahory  described 
'  peenash,'  an  East  Indian  name  for  an  infection  due  to  the  larvae  of 
sarcophaga,  while  in  1879  Portschinsky  again  drew  attention  to 
gastro-intestinal  myiasis.  From  1890  to  1896  there  appeared  a 
series  of  classical  works  by  R.  Blanchard  on  myiasis  in  general. 
From  1895  to  the  present  time  Austen  has  contributed  many 
valuable  articles  dealing  with  these  infestations.  In  1903  Ward  gave 
an  excellent  and  well-illustrated  account  of  the  larva  of  Dermatobia 
hominis,  Kayser  in  1905  of  ocular  myiasis,  Henneberg  in  1903  and 
Vesescu  in  1906  of  aural  myiasis,  the  Sergents  in  1907  of  thim'ni,  and 
in  1908  Austen  and  Smith  gave  accounts  of  infestation  with  Cordy- 
lobia  anthropophaga.  In  1913  Rodhain,  Pons,  and  others,  studied 
the  method  of  infection  by  this  maggot.  Finally,  in  1915,  Sambon 
gave  an  interesting  account  of  Dermatobia  hominis  and  its  larva. 

The  above  history  is  sufficient  to  indicate  the  large  amount  of 
scattered  literature  in  existence  dealing  with  the  subject  of  myiasis 
in  one  or  more  of  its  phases,  and  of  which  Peiper's  book,  published 
in  1900,  gives  a  summary. 

/Etiology. — At  the  present  moment  too  little  is  known  as  to  the 
characters  of  the  larvse  of  the  diptera  to  permit  their  recogni- 
tion, unless  belonging  to  a  well-known  species,  and  it  is  obviously 
incorrect  to  assume  that  larvse  are  those  of  a  given  fly.  It  is  there- 
fore necessary  for  the  medical  observer  to: — 

1.  Preserve   specimens   of  the  larvse,    as  little  damaged   as 

possible,  in  4  per  cent,  formalin,  and  held  in  position  in 
the  tube  by  means  of  fine  tissue-paper. 

2.  Rear  the  larvse  or  pupse  and  so  obtain  the  imago,  which 

should  be  fed  for  a  day  or  so  before  being  killed,  and 
should  then  be  carefully  mounted  and  preserved.  Mr. 
Austen  has  asked  that  some  of  the  larvse  should  be  placed 
at  once  on  the  top  of  a  pot  of  fairly  dry  earth,  which  is 
then  covered  with  muslin.  After  the  flies  have  appeared 
they  should  be  allowed  to  remain  undisturbed  for  about 
twenty-four  hours  in  order  that  they  may  dry  themselves, 
and  in  order  that  they  may  develop  their  specific  colours, 
after  which  they  may  be  killed  with  chloroform,  screwed 
up  in  cigarette-paper,  packed  in  small  metal  boxes,  and 
forwarded  to  England  for  identification. 

3.  Label  all  the  specimens,  especially  noting  the  part  of  the  body 

infected,  the  locality  of  infection,  and  the  time  of  the  year. 

4.  Send  the  complete  collection  to  the  British  Museum,  Natural 

History  Section,  Cromwell  Road,  London,  S.W. 

If  this  is  done  systematically  it  will  be  possible  to  obtain  a  correct 
diagnosis  as  to  the  fly  causing  the  myiasis. 

The  lists  of  flies  known  to  cause  the  various  forms  of  myiasis  will 
be  given  under  the  different  diseases,  but  it  may  be  noted  that  the 
principal  families  concerned  are: — 


1 622  THE  MYIASES  AND  ALLIED  CONDITIONS 

i.  Muscidte  (Subfamily:  Muscinae). — Genera:  Musca,  Calliphora, 
Chrysomvia,  Cordylobia,  and  Lucilia. 

2.  Sarcophagida. — Genera :Sarcophaga,Sarcophila,andCynomyia. 

3.  AnthomyidcB. — Genus:  Fannia. 

4.  (EstridcB. — Genera:  Hypoderma.Gastrophilus,  (Estrus(Cephalo- 
myia),  (Estromvia,  Spilogaster.  For  zoological  details  on  flies  see 
Chapter  XXXIII.,  p.  814. 

Less  important  families  a.re:—TacMnidce,  Micropezida,  Syrphidce, 
PhoridcB,  Therevidce,  Sepsidce,  and  Drosophilidce. 

The  larvae  appear  to  be  attracted  by  faecal  or  urinary  substances, 
and  also  by  any  purulent  or  putrefactive  discharges. 

Pathology.— The  changes  produced  in  the  body  by  these  larvae 
appear  to  depend  upon  the  question  of  food.  In  such  positions  as 
the  alimentary  tract  they  appear  to  do  little  harm,  probably  because 
there  is  plenty  of  food  available  without  hurting  the  tissues  of  the 
host;  on  the  other  hand,  in  the  nose,  ear,  and  eye  they  may  cause 
much  destruction  of  tissue,  firstly  by  eating  into  the  tissues,  secondly 
by  the  microbic  infections  which  follow  in  their  track,  and  in  this 
way  they  may  cause  the  death  of  the  host. 

Symptomatology. — As  may  be  expected  from  the  last  paragraph, 
the  symptoms  of  the  victim  may  vary  from  nil,  local  signs  of  destruc- 
tion of  tissue,  with  inflammation  and  pus  formation,  to  signs  of 
general  septicaemia. 

Diagnosis.— This  is  usually  easy,  and  depends  upon  the  discovery 
of  the  larvae,  which,  indeed,  are  usually  sufficiently  obvious  to  the 
patient  and  practitioner  alike. 

Treatment. — When  the  larvae  live  in  passages  such  as  the  nose  or 
ear  it  is  usual  to  expel  them  by  douches  of  chloroform  water;  when 
in  the  alimentary  canal,  by  anthelmintic  treatment :  when  in  the 
skin,  by  the  knife  and  forceps,  or  simply  by  the  latter.  The  asso- 
ciated inflammation  as  well  as  the  conditions  causing  the  original 
stinking  discharge  which  attracted  the  flies  require  treatment,  other- 
wise the  patient  will  again  be  in  danger  of  infection. 

Prophylaxis. — Any  person  suffering  from  a  purulent  or  odoriferous 
discharge  in  any  part  of  the  body  should  be  especially  careful  to 
avoid  myiasis  by  sleeping  under  mosquito  curtains  until  this  disease  is 
cured.  Other  people  should  be  careful  not  to  sleep  in  the  open  with- 
out some  protection,  especially  in  the  daytime,  and  in  certain  cases — 
as,  for  example,  Dermatobia  cyaniventris— -to  use  mosquito  curtains. 

Varieties.— The  various  forms  of  myiasis  may  be  classified  as 
follows: — 

A.  Internal  or  Cavity  Myiases  •■ — 
T.  Rhinal  myiasis. 
II.  Aural  myiasis. 

III.  Ocular  myiasis. 

IV.  Urinary  myiasis. 
V.  Vaginal  myiasis. 

VI.  Gastro-intestinal  myiasis. 


THE  INTERNAL  OR  CAVITY  MYIASES  1623 

B.  External  or  Dermal  Myiases  : — 

VII.  Traumatic  dermal  myiasis. 
VIII.  Subcutaneous  myiasis. 

With  regard  to  the  ocular  myiases,  they  may  be  a  true  cavity 
myiases  if  the  larva  lives  in  the  lachrymal  sac,  but  they  may  resemble 
a  cutaneous  myiasis  if  the  larva  penetrates  into  the  tissues  under  the 
conjunctiva,  when,  indeed,  it  may  destroy  the  eye. 


THE  INTERNAL  OR  CAVITY  MYIASES. 
RHINAL  MYIASIS. 

For  purposes  of  description  this  may  be  divided  into  the  American 
rhinal  myiasis,  the  African  rhinal  myiases,  the  Asian  rhinal 
myiases,  and  the  European  nasal  myiases. 

American  Rhinal  Myiasis. 

BlCHEIRO. 

Definition. — Bicheiro  is  a  rhinal  myiasis  found  in  Tropical 
America,  and  caused  by  the  larvae  of  Chrysomyia  macellaria  (Fabri- 
cius,  1794)  and  allied  species. 

Climatology. — The  causal  fly  extends  really  from  Canada  to  Pata- 
gonia, but  is  so  much  more  common  in  the  tropical  regions  as  to 
justify  the  definition.  In  Canada  it  is  diminished  in  numbers  by 
the  cold  of  the  winters.  In  the  Southern  United  States  it  is  met  with 
principally  in  the  months  of  July  to  October. 

/Etiology. — Chrysomyia  macellaria  (p.  847)  usually  deposits  its 
eggs  in  some  wound  in  cattle — e.g.,  in  the  wounds  after  castration, 
spaying,  branding,  dehorning,  in  barbed-wire  wounds,  and  where 
ticks  have  been  burst  or  in  the  vulva,  especially  if  there  is  a  retained 
placenta,  or  in  the  navel  or  mouth  of  young  calves.  More  rarely 
they  lay  eggs  in  the  wounds  of  horses  and  mules  produced  by 
barbed  wire,  in  the  sheaths  of  horses,  the  vaginae  of  mares,  and 
the  navels  of  colts.  Hogs  are  also  liable  to  be  infested,  but  sheep 
are  rarely  attacked  unless  they  have  been  worried  by  dogs. 

In  place  of  these  more  natural  hosts  the  fly  may  at  times  attack 
man,  probably  being  attracted  by  the  odour  of  what  to  the  human 
being  is  an  offensive  breath,  or  by  an  ozaena,  or  even  a  chronic 
catarrh.  The  fly  then  passes  into  one  nostril,  and  if  it  is  expelled 
dashes  into  the  other  nostril,  and  quickly  deposits  its  eggs,  sometimes 
in  large  numbers. 

In  Trinidad,  Lawrence  reports  that  the  disease  may  be  caused 
by  Chrysomyia  viridula  Robineau-Desvoidy. 

Pathology. — The  eggs  deposited  in  the  manner  just  described 
become  larvae  in  the  course  of  a  couple  of  days.  The  larvae  proceed 
to  feed  upon  the  tissues  of  the  nose  and  to  burrow  deeply  into  this 
mucous  membrane,  down  to  and  even  through  the  bone.        The 


1624  THE  MYIASES  AND  ALLIED  CONDITIONS 

feeding  excites  a  violent  reaction  on  the  part  of  the  body,  which  can 
be  exemplified  by  the  fever,  the  discharge,  the  pains,  etc. 

Morbid  Anatomy. — The  morbid  anatomy  includes  the  destruction 
of  the  nose,  pharynx,  hard  and  soft  palates,  larynx,  etc.  Fistulous 
channels  may  be  seen  packed  with  larvae  and  extending  in  all 
directions. 

Symptomatology. — Some  couple  of  days  after  a  person  suffering 
from  a  chronic  catarrh,  foul  breath,  or  ozaena,  has  slept  in  the  open, 
or  has  been  attacked  by  a  fly  when  riding  or  driving — i.e.,  when  the 
hands  are  engaged — signs  of  a  severe  catarrh  appear,  accompanied 
with  inordinate  sneezing  and  severe  pain  over  the  root  of  the  nose 
or  the  frontal  bone.  Quickly  the  nose  becomes  swollen,  and  later 
the  face  also  may  swell,  while  examination  of  the  nose  may  show  the 
presence  of  the  larva?.  Left  untreated,  the  patient  rapidly  becomes 
worse,  and  pus  and  blood  are  discharged  from  the  nose,  from 
which  an  offensive  odour  issues.  Cough  appears  as  well  as  fever, 
and  often  some  delirium.  If  the  patient  lives  long  enough,  the 
septum  of  the  nose  may  fall  in,  the  soft  and  hard  palates  may  be 


Fig.  723. — Chrysomyiamacellaria:  Larva.     (X4.)     (After Blanchard .) 

pierced,  the  wall  of  the  pharynx  may  be  eaten  away,  exposing  the 
vertebrae,  and  even  the  hyoid  bone  may  be  destroyed.  By  this 
time,  however,  the  course  of  the  disease  will  have  become  quite 
evident  by  the  larvae  dropping  out  of  the  nose,  and  if  the  patient 
continues  to  live  all  the  larvae  may  come  away  naturally. 

Diagnosis. — Any  case  with  the  history  of  a  fly  having  darted 
into  the  nose  should  be  assumed  to  be  a  case  of  nasal  myiasis  until 
proved  by  careful  nasal  examination  not  to  be  so.  The  onset  of 
peculiar  sensations  at  the  root  of  the  nose  and  along  the  orbital 
processes,  together  with  the  signs  of  an  aggravated  nasal  catarrh 
occurring  in  the  endemic  region  especially  in  the  months  of  July  to 
October,  when  the  fly  abounds  in  the  Southern  United  States, 
makes  the  diagnosis  probable,  and  this  becomes  a  certainty  on  finding 
a  larva  by  examination  or  douching.  The  onset  of  the  severe 
symptoms  will  clear  the  diagnosis  if  not  evident  at  an  earlier  stage. 

Prognosis. — The  prognosis  is  always  serious,  as  it  is  difficult  to 
be  sure  that  all  the  larvae  have  been  removed. 

Treatment. — The  best  treatment  is  to  douche  out  the  nose  with 
chloroform  water  or  a  solution  of  chloroform  in  sweet  milk  (10  to 
20  per  cent.),  and  to  follow  this  with  douches  of  mild  antiseptics. 


THE  AFRICAN  RHINAL  MYIASIS  1625 

Calomel  may  be  insufflated  after  douching.     It  may  be  necessary  to 
open  the  frontal  or  other  sinuses,  and  to  irrigate  the  passages. 

Prophylaxis. — The  prophylaxis  consists  in  the  avoidance  of 
sleeping  in  the  open  air  except  under  a  mosquito  curtain,  and  in  the 
prompt  treatment  of  anj^  case  in  which  a  fly  has  been  known  to  enter 
the  nose. 

The  African  Rhinal  Myiasis. 
Thim'ni. 

Synonym. — Tamne  (Ahaggar  Mountains). 

Definition. — Thim'ni  is  a  facial  myiasis — that  is  to  say,  an  ocular, 
rhinal,  and  oral  myiasis — found  in  certain  parts  of  Algeria  and  the 
Ahaggar  Mountains  of  Central  Sahara,  where  the  human  population 
is  relatively  great  and  the  numbers  of  sheep  relatively  small.  It  is 
caused  by  the  larvae  of  CEstrns  (Cephalomyia)  ovis  Linnaeus,  1761. 

Historical. — In  1881  Kirschmann  in  Russia  reported  a  case  of 
myiasis  due  to  (Estrus  ovis,  but  was  disbelieved.  In  1907  the 
Sergentsdrew  attention  to  the  disease  thim'ni,  and  inio,i3totamne. 

Climatology. — It  occurs  in  Algeria,  but  not  everywhere,  being 
confined  to  certain  mountainous  regions  where  the  ovine  population 
is  relatively  little  numerous  as  compared  with  the  human  population, 
and  the  fly  is  compelled  to  find  new  abodes  for  its  larvae.  These 
regions  are,  La  Grande  Kabylie,  La  Petite  Kabylie,  and  Le  Dahra 
Oriental.  It  also  occurs  in  the  Ahaggar  Mountains  of  the  Central 
Sahara. 

JEtiology. — Oestrus  ovis  (pp.  826,  827)  should  lay  its  eggs  in  the 
nasal  cavities  of  sheep,  and  is  only  driven  by  force  of  circumstances 
to  occasionally  attack  man.  It  only  infests  the  shepherds  and  their 
dogs,  being,  it  is  thought,  attracted  by  the  cheese  which  both  eat. 
It  appears  in  the  hottest  part  of  the  day  in  the  warm  weather,  and, 
flying  swiftly,  deposits  its  egg,  while  still  on  the  wing,  into  the 
nose,  on  to  the  conjunctiva  or  lips.  The  larva  enters  these  cavities 
and  causes  much  pain  and  inflammation. 

Symptomatology. — In  the  nose  it  causes  severe  pain  and  inflam- 
matory swelling  of  the  whole  organ.  Frontal  headache  is  intense, 
sleep  is  impossible,  while  a  serous  discharge  runs  away  from  the 
nose.  In  the  eye  vision  is  impossible,  the  eyelids  and  conjunctivae 
swell,  and  little  worms  are  seen  on  their  surface.  In  the  mouth 
there  is  much  inflammation  of  the  throat,  which  renders  swallowing 
a  difficult  proceeding. 

The  duration  is  from  three  to  ten  days,  being  longest  in  the  nose. 

Prognosis. — This  is  quite  good,  as  all  cases  recover. 

Treatment. — The  essential  treatment  is  tobacco,  as  smoke  or  as 
injections  or  washes,  but  in  the  eye  gentle  removal  is  all  that  is 
required. 

Other  African  Rhinal  Myiases. 

In  addition  to  thim'ni,  rhinal  myiasis  in  Africa  is  known  to  be 
due  to: — Lucilia  hominivorax  {vide  Bouchet  at  Barika  in  1895); 


1626  THE  MYIASES  AND  ALLIED  CONDITIONS 

Sarcophaga  nura  Rudolphi,  by  Mouchet  at  Katanga;  Pycnosoma 
putorutn  Wiedemann,  1830,  in  Abyssinia,  Belgian  Congo,  and 
Lorenzo  Marques.  The  condition  has  been  reproduced  experi- 
mentally in  animals  by  Wellman,  in  1906,  with  S.  regularis  Wiede- 
mann in  a  goat. 

Asian  Rhinal  Myiases. 

Peenash. 

Definition. — Peenash  is  a  word  which  may  be  used  for  the  Indian 
rhinal  myiases  caused  by  the  larvae  of  species  of  Pycnosoma  Brauer 
and  von  Bergenstamm,  and  by  larvae  of  species  of  Sarcophaga 
Meigen,    especially   by  those   of    Sarcophaga   camaria    Linnaeus, 

1758. 

Climatology. — The  disease  is  spread  throughout  India  and  Assam. 

Symptomatology. — As  far  as  is  known,  the  symptoms  resemble 
those  produced  by  other  forms  of  rhinal  myiasis. 

Treatment.— This  is  the  same  as  for  other  forms  {vide  supra) . 

European  Rhinal  Myiases. 

These  are  known  to  be  caused  by  Piophila  casei  and  by  species  of 
Sarcophaga  Meigen,  1826,  while  Calliphora  limea  is  also  said  to  be 
causal. 

AURAL  MYIASIS. 

Definition. — Aural  myiasis  is  the  invasion  of  the  external  auditory 
meatus,  the  middle  ear,  and  associated  cavities,  by  the  larvae  of 
certain  dipterous  flies,  especially  those  of  the  Muscidae  and  Sarco- 
phagidae. 

Historical. — Aural  myiases  have  been  recorded  by  Taschenberg 
in  1870,  Blake  in  1872,  Johnson  in  1892,  and  Austen  in  1912,  but 
the  most  complete  study  is  that  by  Francaviglia  in  1914. 

^Etiology. — The  following  larvae  have  been  noted  as  causal 
agents: — 

Muscidce  (Subfamily:  Muscinae) : — 
Musca  domestica  Linnaeus. 
Musca  vomitoria  Linnaeus,  1758. 
Calliphora  erythrocephala  Meigen. 
Chrysomyia  macellaria  Fabricius,  1794. 
Lu cilia  catsar  Linnaeus. 
Lucilia  nobilis  Meigen. 

Sarcophagidce : — 

Sarcophaga  camaria  Linnaeus,  1758 ;  synonym,  5.  cnmosa 

L.,  1758. 
Sarcophaga  magnifica  Schiner,  1862 ;  synonyms,  5.  wohlfarti 

Portschinsky,    1875,    S.    ruralis    Meigen,    S.    meigeni 

Portschinskv. 


OCULAR  MYIASIS  1627 

Anthomyidcs  : — 

Fannia  scalaris  Meigen. 
Fannia  canicitlaris  Linnaeus. 
Fannia  incisurata  Zett. 
Hydrotcea  meteorica  Linnaeus. 

Syrphidce  : — 

Syrphus,  sp.r? 

(Estridce  : — 

Gistrus  oris  Linnaeus,  1761. 

Symptomatology. — If  lodged  in  the  external  auditory  meatus, 
they  may  simply  cause  deafness  and  ringing  in  the  ears,  but  if 
eating  into  the  middle  ear  they  may  give  rise  to  a  discharge  of  blood 
and  pus. 

Treatment.- — It  is  usual  to  drop  into  the  ear  warm  olive  or  carbolic 
oil,  and  then  to  syringe  out  the  larvae  by  means  of  boric  lotion.  If 
the  larvae  are  outside  the  tympanum,  inject  a  few  drops  of  chloroform 
dissolved  in  water. 

Prophylaxis. — Some  protection  such  as  wool  is  necessary  when 
suffering  from  an  aural  discharge. 

OCULAR  MYIASIS. 

Definition. — Ocular  myiasis  is  the  invasion  of  the  spaces  under 
the  eyelids,  the  lachrymal  sac,  the  subconjunctival  tissue,  or  the 
eyeball  itself,  by  dipterous  larvae  usually  belonging  to  the  families 
Sarcophagidae  or  (Estridae. 

Historical. — In  1905  Kayser  studied  this  form  of  myiasis  and 
Portschinsky  in  1913  reported  some  cases.  Malgahaes  has  investi- 
gated this  disease  in  Brazil.  In  1913  Griinberg  found  a  larva 
of  a  species  of  hypoderma  in  the  anterior  chamber  of  the  eye 
of  a  girl. 

/Etiology. — The  larvae  so  far  recognized  as  causing  this  form  of 
myiasis  are: — 

Sarcophagida  : — 

W ohlfarlia  magnifica  (Schiner,  1862). 
Necrobia,  sp.  ? 

Glstridte  : — 

(Estrns  ovis  Linnaeus,  1761. 

Dcrmatobia  cyaniventris  Macquart,  1843. 

Hypoderma,  sp.  ? 

Symptomatology. — -This  varies  from  the  discovery  of  a  larva  lying 
like  a  foreign  body  under  the  eyelid,  to  infection  of  the  lachrymal 
sacs  or  the  tissue  under  the  palpebral  or  ocular  conjunctiva,  to  the 
total  destruction  of  the  eyeball. 

Treatment. — This  consists  of  the  prompt  removal  of  the  larva  by 
surgical  means. 


1628  THE  MYIASES  AND  ALLIED  CONDITIONS 

Prophylaxis.— The  prophylaxis  consists  of  prompt  treatment  of 
conjunctivitis  and  the  protection  of  the  head  when  sleeping  out 
of  doors.  Natives  wrap  themselves  up  completely  when  sleeping 
out  of  doors. 

URINARY  MYIASIS. 

Definition. — Urinary  myiasis  is  the  invasion  of  theurinarypassages, 
particularly  the  urethra  and  bladder,  by  dipterous  larvae,  especially 
those  of  the  Anthomyidae. 

Historical. — This  form  of  myiasis  is  rare,  but  has  been  recorded 
by  Ambrose  Pare  in  1582  and  by  Turner  in  the  seventeenth  century, 
when  he  recorded  two  cases,  while  in  1909  Rene  Chervel  analyzed 
all  cases  reported  up  to  that  date,  and  concluded  that,  of  twenty 
reported  cases,  six  were  genuine,  ten  were  probable,  and  four  were 
doubtful.  He  also  added  one  of  his  own  observation.  King,  in 
1914,  reported  an  American  case.  Palmer  and  Austen  have  recorded 
a  case  in  England.  Hagen  has  also  drawn  attention  to  a  case  in 
Boston. 

etiology. — It  is  thought  that  the  flies  deposit  the  eggs  near  the 
meatus  urinarius,  and  that  the  newly-born  larvae  pass  up  into  the 
urethra.  Sleeping  in  the  open  is  generally  accused  as  the  method 
of  infection,  but  paralyzed  persons  become  infected,  especially 
those  with  urinary  troubles.  The  larvae  which  so  far  have  been 
recognized  are  those  of  Fannia  canicularis  Linnaeus,  1761,  and 
Fannia  scalaris  Fabricius  (p.  852). 

Symptomatology. — Generally  the  larvae  are  discovered  accidentally 
when  passing  urine,  when  they  may  cause  some  slight  obstruction. 

Treatment. — This  apparently  is  unnecessary,  as  the  larvae  come 
away  without  causing  harm. 

VAGINAL  MYIASIS. 

Definition. — Vaginal  myiasis  is  the  invasion  of  the  vagina  by  the 
larvae  of  dipterous  insects,  especially  those  of  the  Muscidae. 

Historical. — This  form  of  myiasis  appears  to  be  rare,  but  Cipriani, 
in  1902,  came  across  a  case  which  had  a  recto-vaginal  fistula,  and 
Castellani  saw  two  cases  in  Ceylon,  but  the  larvae  were  not  identified, 
except  Sarcophaga  carnaria  Linnaeus,  1758.  In  1912  Pieter  re- 
ported the  presence  of  Chrysomyia  macellaria  Fabricius,  1794,  in 
the  vagina  of  a  beggar-woman,  and  Low  has  seen  a  similar  case  in 
the  West  Indies. 

Symptomatology. — There  is  a  thick  purulent  discharge  containing 
the  larvae,  and  some  ulcerations  deep  in  the  walls  of  the  vagina. 

Treatment. — Vaginal  douches  with  an  antiseptic  are  recommended. 

Prophylaxis. — Recto-vaginal  fistulae  should  be  operated  upon. 

ORO-GASTRO-INTESTINAL  MYIASIS. 

Definition. — Intestinal  myiasis  is  the  invasion  of  the  intestine  by 
the  larvae  of  certain  species  of  flies,  but  especially  by  those  belonging 


ORO-GASTRO-INTESTINAL  MYIASIS  1629 

to  the  genera  Sarcophaga  (p.  830),  Fannia  (p.  852),  and  Aphiocluzta 
(p.  824). 

History. — Many  stray  cases  of  myiasis — e.g. ,  Jenyns  (1839) — -have 
been  reported  from  time  to  time,  but  these  have  been  gathered 
together  by  Portschinsky  in  1879  in  the  twelfth  volume  of  the  Horce 
Societis  EntomologiccB  Russicce,  by  Huber  in  1899  in  Bibliographic 
dcr  Klinischen  Entomologie,  Heft  3  (Dipt era),  and  by  Calandruccio 
in  the  same  year  in  the  Archives  de Parasitologic  ;  by  Pfeiffer  in  1900 
in  his  work  FliegcnlarvcB  als  gelcgentliche  Parasiten  des  Menschen  ;  in 
190 1  by  Thebault  in  the  Archives  deParasitologie  ;  also  by  Wellman, 
and  by  Austen  in  an  excellent  paper  read  before  the  Society  of 
Tropical  Medicine  and  Hygiene  of  London  in  March,  1910.  Cases  are 
also  referred  to  by  Splendore  [Arch,  de  Parasitologic,  19 10),  by 
Garrod,  and  by  Soltau  in  the  Journal  of  Parasitology,  1910.  We 
have  seen  several  cases  in  Ceylon  and  in  the  Balkans.  Cases  have 
been  reported  in  England  by  Stephens  (1905),  Hewitt  (1909), 
Cattle  (1906),  Garrod  (1909),  Soltau  (1910),  and  Austen  (1912). 

./Etiology. — Intestinal  myiasis  may  be  produced  by  the  larvae  of 
the  following  species: — 

Sarcophagid^e  : — 

Sarcophaga  camaria  Linnaeus,  1758. 

,,  havnorrhoidalis  Fallen,  18 10. 

,,  tusmatodes  Joseph. 

,,  affinis. 

magnifica  Schiner,  1862. 
wohlfarti  Portschinky,  1875. 
latifrons  Meigen. 
,,  ruralis  Fallen. 

,,  meigeni  Schiner. 

Cynomyia  mortuorum  Linnaeus,  1761. 
Anthomyid^e  : — 

Fannia  canicularis  Linnaeus,  1761. 
,,      incisurata  Lett. 
,,       manicuta  Meigen. 
,,      saltatrix. 
,,      desjardensii. 
Hydrotcea  meteorica  Linnaeus. 
Muscid^e: — 

Musca  domestica  Linnaeus. 
„     corvina  Fabricius. 
,,     nigra. 
Cyrtoneura  stabulans  Macquart. 
Pollenia  rudis  Fabricius. 
Calliphora  vomitoria  Linnaeus,  1758. 
,,  erythrocephala  Meigen. 

,,  azurea. 

Lucilia  ccesar  Linnaeus. 

,,       regina  Macy. 
Chrysomyia  polita  Linnaeus. 
Teichomyza  fusca  Macquart  (?). 

Tachinidjb: — 

Tachina  larvarum  Meigen. 

Micropezid^: — 

Calobata  cibaria  Meigen. 


1630  THE  MYIASES  AND  ALLIED  CONDITIONS 

Sykphid^:  : — 

Eristalis  tenax  Fabricius. 

,,        arbustonim  Fabricius. 
„        dimidiatus. 

Helophilus  pendulinus  Meigen. 
Phorid^e: — 

Aphioch&ta  ferrnginea  Brunner. 

Phora  rufipes  Meigen;  synonym,  P.  palhpes  Latreille. 
Therevid;e: — 

Thereva  nobilitata. 
Sepsid^e: — 

Piophila  casei  Linnagus. 
Drosophilid^  : — 

Drosophila  funebris  Meigen. 

,,  melanogastra  Brunner. 

CEsTRIDiE: — 

Spilogaster  divisa  Meigen. 
Gastrophilus  pecorum. 

Sometimes  more  than  one  species  may  be  found  in  the  same  case. 

Rarer  forms  of  myiasis  are  those  by  larvae  of  the  Tipulidae,  by 
eggs  and  larva  of  the  Culicidae,  and  by  the  bots  of  Gastrophilus  equi. 

The  eggs  or  larvae  of  the  above-mentioned  flies  enter  the  ali- 
mentary canal  with  the  food,  especially  with  vegetable  food  in  an 
uncooked  or  partially  cooked  condition.  Another  method  is  for 
the  fly  to  deposit  its  eggs  on  the  nostrils  and  lips  of  children,  from 
which  they  pass  into  the  stomach  and  intestines,  and  a  third  method 
is  entry  of  the  larvae  into  the  rectum  while  using  a  privy.  Intes- 
tinal myiasis  is  not  uncommon  in  cattle,  both  in  the  Temperate 
Zone  and  in  the  tropics.  There  seems  to  be  no  doubt  that  the 
larvae  can  live  for  a  considerable  time  in  the  intestine,  but  the  most 
marked  example  of  this  is  Aphiochczta  ferruginea  Brun,  which  is 
believed  to  be  capable  of  passing  through  its  entire  life-cycle  in 
the  human  colon,  because  both  newly  hatched  and  fully  grown 
larvae  were  passed  by  a  patient  every  two  months  for  nearly  a  year, 
notwithstanding  the  fact  that  nothing  was  said  to  be  eaten  which 
could  have  contained  either  eggs  or  larvae.  It  is  stated  that  species 
of  the  Phoridae  have  been  found  in  corpses,  and  it  has  been  stated 
that  the  living  larvae,  pupae,  and  imagines  of  species  of  Conicera 
were  found  in  numbers  in  a  corpse  exhumed  at  La  Fayette,  Indiana, 
U.S.A.,  two  years  after  burial. 

If  there  is  any  truth  in  this  statement,  it  proves  that  the  life-cycle 
of  these  flies  can  be  completed  in  a  parasitic  state,  and  would 
explain  the  possibility  of  a  patient  suffering  from  myiasis  for 
twelve  years,  and  during  treatment  passing  1,000  to  1,500  larvae. 
Fenwick  also  reports  cases  in  which  it  seemed  probable  that  the 
whole  life-cycle  was  completed  in  man.  It  is  obvious  that  these 
statements  require  careful  confirmation  by  other  similar  cases 
before  they  can  be  accepted  without  reservation. 

Pathology. — The  larvae  usually  cause  gastro-intestinal  symptoms. 
Those  of  the  Muscidae  may  cause  little  or  no  disturbance,  but  those 
of  the  (Estridae  and  Tipulidae  cause  much  disturbance. 


ORO-GASTKO-INTESTINAL  MYIASIS  1631 

Morbid  Anatomy. — We  are  not  acquainted  with  the  details  of 
any  post-mortem  examination  in  man,  but  in  dogs  the  mucosa  of 
the  intestine  is  congested  and  marked  by  numerous  small  haemor- 
rhages, and  it  is  thought  that  bacteria  may  enter  the  blood  through 
these  wounds. 

Symptomatology. — After  an  incubation  period  varying  from  four 
to  twelve  days  after  the  ingestion  of  the  eggs,  the  patient,  who  has 
either  felt  quite  well  or  has  suffered  from  vague  abdominal  pains 
and  anorexia,  begins  to  feel  ill  with  general  malaise,  headache,  thirst, 
and  faintness,  and  in  children  with  rigors,  convulsions,  and  even 
delirium.  Vertigo  may  be  felt,  and  generally  there  is  some  fever, 
which  may  last  two  to  ten  days  or  longer.  Sometimes  the  continued 
fever  and  the  diarrhoea  renders  the  diagnosis  of  enteric  fever  prob- 
able. Pains  vary  from  vague  sensations  to  violent  colic.  Retch- 
ing and  vomiting  may  occur,  and  sometimes  hsematemesis,  while 
dysenteric-like  symptoms  may  also  occur.  When  the  larvae  attain 
maturity,  they  are  sometimes  violently  evacuated. 

Diagnosis. — The  diagnosis  can  only  be  made  by  repeated  examina- 
tion of  the  motions  and  the  discovery  of  the  larva,  the  nature  of 
which  may  be  determined  in  the  same  way  as  in  nasal  myiasis 
(p.  1621).  Care  must  be  taken  that  the  larvae  really  come  from  the 
bowels,  and  are  not  contaminations  of  the  faeces. 

Prognosis. — This  is  good. 

Treatment.— The  bowels  should  be  cleared  with  a  dose  of  castor 
oil  and  then  an  anthelmintic — e.g.,  Filix  mas — should  be  adminis- 
tered.    Thymol  or  santonin  may  also  be  used. 

Prophylaxis. — All  vegetables  should  be  carefully  washed  and  by 
preference  cooked  before  being  eaten,  and  fresh  salads  should  be 
avoided. 

Ovaenya. 

This  word  means  maggots,  and  is  applied,  according  to  Wellman, 
by  the  natives  in  Angola  to  an  alimentary  canal  myiasis  associated 
with  dysenteric  symptoms  and  caused  by  Fannia  desjardensii 
Macquail.     It  is  easily  treated  by  castor  oil. 

Muculo. 

This  is  the  African  myiasis,  concerning  which  the  editors  of  the 
Journal  of  Tropical  Medicine  and  Hygiene  asked  for  information 
in  1907,  but  which  so  far  has  not  been  traced. 

THE  EXTERNAL  OR  DERMAL  MYIASES. 

These  are  the  infections  of  the  skin,  whether  wounded  or  not  by 
dipterous  larvae.  There  are  two  varieties  of  this  type — viz.,  trau- 
matic dermal  myiasis  and  subcutaneous  myiasis. 


1632  THE  MYIASES  AND  ALLIED  CONDITIONS 

Traumatic  Dermal  Myiasis. 

Definition.— Traumatic  dermal  myiasis  is  the  invasion  of  wounds 
or  ulcers  of  the  skin  by  the  larvae  of  dipterous  insects,  principally 
belonging  to  the  Muscidae  and  Sarcophagidae. 

Historical. — One  of  the  earliest  publications  with  references  to 
this  is  Joseph  in  his  '  Myiasis  Externa  Dermatosa,'  published  in 
Hamburg  in  1800,  but  a  large  number  of  observations  have  been 
published  since  then. 

./Etiology. — The  larvae  which  have  been  recognized  so  far  are : — 

Muscicke  (Subfamily:  Muscinse) : — 
Chrysomyia  macellaria  Fabricius. 
Chrysomyia  viridida  Robineau-Desvoidy. 
Calliphora,  sp.  ? 

Lucilia  argyrocephala  Macquart. 
Lucilia,  sp.  ? 

Cordylobia  anthropophaga. 
Musca  putrida. 
Sarcophagidce  : — 

Sarcophaga  camaria  Linnaeus,  1758. 
,,  magnified  Schiner,  1862. 

ruficomis. 
,,  chrysostoma  Wiedemann. 

„         plinthopegga  Wiedemann.     (The  adult  is  one 
of  the  '  yaws  flies  '  of  Dominica.) 
sp.  ? 

Symptomatology. — The  larvae  accentuate  the  putrid  condition  of 
the  sores  and  the  sufferings  of  the  patient. 

Treatment. — Antiseptic  douches,  syringing,  with  removal  of  the 
larvae,  and  subsequent  antiseptic  dressing. 

Prophylaxis. — The  myiasis  can,  of  course,  be  prevented  by  simply 
applying  aseptic  dressings  to  wounds. 

Subcutaneous  Myiasis. 

Synonyms. — Cutaneous  myiasis.  French,  Myase  cutanee,  Myase  furon- 
culeuse,  Myase  rampante  sous-cutanee;  Italian,  Myasis  cutanea;  German, 
Myasis. 

Definition.— Dermal  myiasis  is  the  invasion  of  the  skin  by  the 
larvae  of  species  of  the  (Estridae,  especially  by  Dermatobia  cyani- 
ventris  Macquart,  1843,  and  by  those  of  the  Muscidae,  especially 
Cordylobia  anthropophaga  Blanchard. 

Remarks. — It  is  necessary  to  be  careful  to  consider  the  zoological 
region  when  determining  the  species  of  the  fly  to  which  a  maggot 
found  in  a  case  of  dermal  myiasis  belongs,  as  it  is  unlikely  that  a 
species  known  to  occur  in  Africa  will  be  found  in  America,  and  vice 
versa.  Further,  it  is  desirable  to  determine  definitely  the  nature 
of  the  fly  causing  the  myiasis,  and  therefore  this  should  be  bred  out 
as  described  in  the  opening  sections  of  this  chapter. 


AMERICAN  DERMAL  MYIASIS  1633 

/Etiology. — The  following  larvae  are  known  to  cause  subcutaneous 
myiasis  in  man : — 

(Estridce  : — 

Hypoderma  bovis  de  Geer. 

Hypoderma  lineata  de  Villiers. 

Hypoderma  diana  Brauer. 

Dermatobia  cyaniventris   Macquart,    1843;    synonym,    D, 

hominis  (Linnaeus  junior,  1781). 
Dermatobia  (?)  kenice  Kolb. 
CEstrus  (C ephalomyia)  ovis  Linnaeus. 

Muscidce  (Subfamily  Calliphorinae) : — 

Cordylobia  anthropophaga  E.  Blanchard. 
Cordylobia  rodhaini. 

The  life-history  of  the  oestridae  is  curious,  as  will  be  discussed 
below.  With  reference  to  Cordylobia  anthropophaga,  by  a  mistake 
the  cutaneous  myiasis  of  Natal,  Rhodesia,  British  Central  Africa, 
Uganda,  and  the  Sudan,  was  assigned  to  Bengalia  depressa,  while  it 
should  have  been  placed  under  this  heading. 

Varieties. — As  geographical  distribution  is  important  from  the 
point  of  view  of  the  causal  parasite,  it  appears  to  us  to  be  convenient 
to  utilize  this  and  to  divide  the  subcutaneous  myiases  into  the 
American,  the  African,  the  Asian,  and  the  European,  while  the  last 
variety  is  not  geographical,  but  pathological— viz.,  creeping 
eruption. 

American  Dermal  Myiasis. 

Synonym. — Neotropical  dermal  myiasis,  Dermatobiasis. 

Definition. — Dermal  myiasis  as  seen  in  Tropical  America  is 
caused  by  the  larva  of  Dermatobia  hominis  (Linnaeus  junior,  178 1), 
better  known  as  Dermatobia  cyaniventris  Macquart,  1843,  and 
perhaps  by  other  allied,  but  as  yet  unknown,  forms. 

Nomenclature. — The  fly  which  causes  this  myiasis  has  a  large 
number  of  scientific  and  popular  names: — 

Scientific  Names.— Dermatobia  hominis  (Linnaeus  junior,  1781) ; 
CEstrus  hominis  Linnaeus  junior,  1781;  (E.  humanus  Humboldt  and 
Boupland,  1805;  Cuterebra  hominis  (Linnaeus  junior)  Say,  1822; 
CEstrus  guildingii  Hope,  1837;  Dermatobia  cyaniventris  Macquart, 
1843;  Cuterebra  noxialis  Gondot,  1845;  Dermatobia  mexicana  Serna, 
1896. 

Popular  Names. — Brazil,  hiira  (boil),  verme,  berne  or  berme; 
British  Honduras,  beef  worm,  cormollote;  Colombia  and  Venezuela, 
gusano,  husano  (worm),  gusano  de  monte  (forest  worm),  gusano 
peludo  (hirsute  worm),  gusano  macaco  (macaw  worm,  because  it 
attacks  the  macaw-headed  Capuchin  monkeys);  Costa  Rica, 
torcel;  Guatemala,  colmoyote;  Pungoa,  mirunta;  Mayan  name, 
suglacura. 

Names    Suggestive    of    Mosquito    Carriage. — Mexico,    moyocuil 

103 


1634  THE  MYIASES  AND  ALLIED  CONDITIONS 

(flyworm),  gusano  moyocuil  (maggot  flyworm) ;  Colombia,  Venezuela, 
and  Guatemala,  gusano  de  zancudo  (maggot  of  mosquito) ;  Dutch 
Guiana,  Trinidad,  mosquito  worm. 

History. — In  1569  Friar  Pedro  Simon  appears  to  have  been  the 
first  to  have  drawn  attention  to  this  myiasis  as  seen  along  the  banks 
of  the  Rio  Magdalena  and  the  low  plains  to  the  east  of  the  Andes. 
He  was  followed  in  1653  by  Father  Bernabe  Cobo,  who  reported  its 
occurrence  in  the  Mexican  lowlands  in  the  coast  district  of  Alvarado, 
in  the  state  of  Vera  Cruz.  In  1745  De  la  Condamine  reported  it 
from  French  Guiana,  as  did  Arture  in  1757.  In  1781  Linnaeus 
junior  reported  it  from  Peru  and  gave  a  brief  mention  of  the  fly, 
while  in  1822  Say  gave  a  description  of  the  larva  as  received  from 
South  America.  In  1835  Hope  gave  an  account  of  the  larva  from 
under  the  skin  of  the  head  of  a  man  from  Trinidad.  The  specimen 
was  deposited  in  the  museum  of  the  Royal  College  of  Surgeons  of 
England. 

From  that  date  scattered,  but  fairly  numerous,  references  can 
be  found — e.g.,  Hill  (1830),  Guyon  (1835),  Gondot  (1845),  Coquerel 
(1859),  Laboulbene  and  Davaine  (i860),  Bonnet  (1870),  Der  Verteuil 
(1884),  Ormerod  (1886),  etc. — until  between  1890  and  1896  Blan- 
chard  published  a  resume  of  known  facts,  then  a  series  of  admirable 
investigations  upon  the  subject;  and  in  1915  Sambon  again  gathered 
together  known  facts,  together  with  the  history  of  the  mosquito 
carriage  of  the  eggs,  and  extended  this  with  his  own  personal 
observations. 

With  reference  to  the  mosquito  carriage,  it  is  remarkable  to  note 
that  Father  Cobo,  in  1653,  says  that  each  wound  produced  by  the 
common  mosquito  produces  within  the  flesh  a  spine-covered  worm  the 
size  of  a  haricot  bean  or  even  larger. 

In  191 1  Morales  of  Guatemala  first  described  the  transmission 
of  the  eggs  as  being  due  to  a  mosquito,  and  performed  an  experiment 
on  a  man,  first  noting  the  escape  of  the  larva  from  the  egg  carried 
by  a  living  mosquito  when  placed  on  the  palm  of  the  hand,  then 
allowing  this  larva  to  wander  about  the  forearm,  and  then  scratching 
the  skin  and  watching  the  larva  burrow  in,  then  noting  the  gradual 
development  of  the  furuncle,  and  finally,  when  threatened  with  sup- 
puration, removing  the  larva,  transplanting  it  into  the  back  of  a 
rabbit,  and  watching  its  escape  as  a  nymph.  Also  in  1911  Tovar  of 
Maturin,  in  Venezuela,  had  noted  this  mosquito  carriage,  which 
was  also  studied  by  Blanchard  in  191 2,  Rincones,  Zepeda,  and  Sur- 
couf  in  1913,  and  Sambon  in  1915. 

Climatology. — The  causal  agent  being  a  neotropical  insect,  the 
distribution  of  the  disease  is  confined  to  Tropical  America,  in  which 
it  occurs  in  the  lowlands  along  the  coast  and  also  in  the  valleys  of 
the  river,  but  it  is  absent  in  the  hills  and  mountains.  It  begins 
near  the  southern  borders  of  the  United  States,  being  found  in 
Mexico,  in  Central  America — i.e.,  British  and  Spanish  Honduras, 
Guatemala,  Nicaragua,  Costa  Rica,  and  Panama;  in  South  America 
— i.e.,  Colombia,  Venezuela,  the  Guianas,  Brazil,  and  Peru;  while 


AETIOLOGY 


1635 


it  is  known  to  occur  among  the  West  Indian  Islands  near  South 
America — e.g.,  Trinidad. 

It  requires  a  warm,  moist  climate,  with  surface  water  and  forest 
vegetation. 

/Etiology . — The  cause  of  the  disease  is  the  invasion  of  the  body 
by  means  of  the  larva  of  Dermatobia  hominis  (Linnaeus  junior,  1781). 


Fig.  724. — J anthinsoma  lutzi  Theobald,  carrying  the  Eggs  of  Dermatobia 
hominis  Linnaeus  junior. 

(After  Sambon.) 

On  the  evidence  at  present  available  it  would  seem  that  the  fly 
seizes  the  female  mosquito  of  the  species  j anthinsoma  lutzi  Theobald 
and  attaches  her  eggs  to  the  ventral  aspect  of  the  abdomen,  but  it 
has  been  suggested  that  it  deposits  the  eggs  upon  foliage,  and  these 
accidentally  reach  the  mosquito,  which  appears  hardly  probable. 

When  the  mosquito  feeds  upon  man  or  animals  the  little  larva 
which  has  been  held  in  position  in  the  egg  by  its  spines  slips  out 


i636 


THE  MYIASES  AND  ALLIED  CONDITIONS 


and  pierces  the  skin  by  means  of  the  aperture  made  by  the  mos- 
quito bite. 

Pathology. — As  it  escapes  from  the  egg,  the  larva  possesses,  in 
addition  to  the  numerous  spines  on  its  first  seven  segments,  a  crown 
of  large  black  rose  thorn-shaped  spines  along  the  anterior  border  of 
the  fifth,  sixth,  and  seventh  segments,  while  the  last  shows  two 
posterior  stigmata.  When  it  has  pierced  the  skin  the  spines  on  the 
fifth  to  seventh  segment  are  shed  (they  are  no  longer  required,  as 
their  function  is  to  keep  the  larva  in  the  egg-case),  and  the  stigmata 
become  three  in  number.  "What  happens  to  the  larva  in  the  body 
is  not  known,  but  that  it  can  wander  under  the  skin  is  known,  and  its 
production  of  the  warble  and  escape  therefrom  is  also  known. 

Symptomatology.- — The  incubation  period  or  time  between  the 
infection  and  the  first  appearance  of  the  warble  is  unknown. 

Appearance  of  the  Warble. — Suddenly  the  patient  feels  a  sharp  pain 
in  some  region  of  the  skin.  It  may  last  two  to  three  minutes,  and 
then  pass  away,  but  after  a  time  it  will  return  either  in  the  morning 

or  in  the  evening.  These  inter- 
mittent seizures  will  continue, 
and  the  pain  will  increase  as  the 
little  rounded  swelling  which 
appears  in  the  affected  region 
increases  in  size.  This  swelling 
is  the  warble. 

The  Warble  Stage.  ■ —  When 
fully  developed  the  warble 
resembles  a  boil,  being  some 
2-3  centimetres  in  diameter 
and  of  a  dark  red  or  bluish-red 
colour.  At  the  apex  there  is  a 
more  or  less  centrically  placed 
small  circular  aperture  which 
increases  till  it  reaches  a  size  of  3-6  millimetres.  It  is  usually 
covered  by  a  scab,  which,  if  removed,  shows  amoving  body  with 
two  small  brownish-yellow  spots.  This  is  the  posterior  end  of  the 
larva.  These  warbles  may  be  single  or  multiple,  placed  in  close 
proximity  or  scattered,  with  usually  only  one  larva  to  a  warble, 
but  sometimes  with  more  and  rarely  as  many  as  five  larvae  to  one 
warble.  Warbles  may  exist  in  any  part  of  the  body,  but  are 
more  painful  in  regions  like  the  nose.  Usually  there  are  no  con- 
stitutional symptoms,  but  there  may  be  slight  fever,  and  there 
may  be  swelling  of  the  surrounding  subcutaneous  tissue,  especially 
in  the  head,  where  the  cedematous  swelling  may  be  limited  by 
the  adhesions  of  the  fascine.  When  the  warble  is  mature  the  larva 
may  be  seen  actively  moving  up  and  down  like  a  jack-in-the-box, 
appearing  and  disappearing  from  the  aperture.  In  due  course 
it  gradually  dilates  the  opening  in  the  warble  by  means  of  its 
posterior  end,  and  eventually  escapes  and,  falling  to  the  ground, 
crawls  away  and  becomes  a  pupa. 


Fig.  725. — Warble  caused  by  Der- 

matobia  hominis  (LiNNiEus  junior). 

(After  Sambon.) 


AFRICAN  DERMAL  MYIASIS  1637 

Post-Warble  Stage. — After  a  period  varying  from  six  weeks  to 
six  months  the  larva  escapes  and  leaves  behind  an  empty  cavity, 
which  is  closed  by  granulation  tissue  and  heals,  leaving  a  hardly 
visible  scar. 

Complications. — Secondary  bacterial  infections  may  take  place, 
giving  rise  to  erysipelas,  tetanus,  lymphangitis,  and  enlargement 
of  the  lymphatic  glands.     If  the  larva  dies  an  abscess  is  formed. 

Diagnosis. — The  cardinal  points  in  the  diagnosis  are: — 

r.  The  formation  of  boil-like  swellings  on  the  skin. 

2.  The  presence  of  an  aperture  at  the  apex  of  these  swellings. 

3.  The  presence  of  the  posterior  end  of  a  larva,  with  its  stigmata 
in  the  opening. 

4.  The  boils  forming  in  the  neotropical  zoological  region. 
Treatments — The  native  places  a  tobacco-leaf  over  the  aperture  in 

the  warble,  or  squirts  tobacco-juice  therein,  and  after  twenty-four 
hours  squeezes  the  larva  out. 

Tincture  of  iodine  may  be  used  in  a  similar  manner  or  1  in  20 
carbolic  lotion.  When  the  larva  has  departed,  wash  the  empty 
warble  out  with  antiseptic  lotion  and  dress  aseptically. 

African  Dermal  Myiasis. 

The  known  form  of  African  dermal  myiasis  is  tumbu  disease, 
caused  by  members  of  the  Calliphorinas  subfamily  of  the  Muscidae. 

Tumbu  Disease. 

Definition.— Tumbu  disease  is  an  African  dermal  myiasis  caused 
by  the  larva;  of  Cordyiobia  anthropophaga  E.  Blanchard  and  allied 
species  living  under  the  skin. 

Historical. — It  was  reported  from  Senegal,  where  the  larva  is 
called  '  ver  de  cayor  '  by  Berenger  Feraud,  and  later  by  E.  Blanchard 
from  Natal,  when  it  was  called  the  Natal  worm,  while  the  fly  was 
named  Ochromyia  anthropophaga.  A  similar  larva  was  found  in  the 
arm  of  Commander  Lund  in  the  Congo,  and  was  long  known  as 
Lund's  larva  until  it  received  the  name  Cordyiobia  rodhaini  Gedoelst, 
1905. 

In  1901  it  was  reported  that  there  was  a  maggot  fly  in  Natal, 
limited  to  the  coast,  not  extending  inland,  and  not  rising  higher 
t  han  r,ooo  feet.  It  was  also  found  about  Delagoa  Bay,  in  Rhodesia, 
British  Central  Africa,  Uganda,  and  the  Anglo-Egyptian  Sudan. 
Unfortunately  this  fly  was  recognized  as  Walker's Bengalia  depressa, 
when  it  was  really  the  well-known  Cordyiobia  anthropophaga,  and  the 
true  Bengalia  is  altogether  a  different  genus,  probably  an  Auchmero- 
myia  with  an  unknown  life-history.  It  also  occurs  in  late 
German  East  Africa,  where  it  was  called  Ochromyia  anthropophaga 
by  Griinberg  and  Cordyiobia  griinbergi  by  Doenitz. 

Austen  has  described  a  third  species,  Cordyiobia  prcegrandis,  in 
Nyasaland,  Cape  Colony,  Transvaal,  Natal,  North-West  Rhodesia, 
and  late  German  East  Africa,  and  contributed  a  valuable  paper  on 


1638  THE  MYIASES  AND  ALLIED  CONDITIONS 

the  whole  subject  in  1908  to  the  Journal  of  the  Royal  Army 
Medical  Corps  ;  while  Smith  described  the  symptoms  of  the  disease 
in  the  same  journal. 

In  1913  Rodhain,  Pons,  Vandenbranden,  and  Bequaert,  demon- 
strated by  experiment  the  method  of  infection;  and  Heckenroth  and 
Blanchard  recorded  four  cases  due  to  Cordylobia  rodhaini  in  French 
Equatorial  Africa. 

Climatology. — Tumbu  seems  to  be  widespread  throughout  tropical 
Africa,  extending  from  Senegal  in  the  north  to  Natal  in  the  south, 
and  from  the  west  to  the  east  coasts. 

etiology. — The  cause  of  the  disease  is  the  invasion  of  the  sub- 
cutaneous tissues  by  the  larva  of  Cordylobia  anthropophaga  and  allied 
species.  The  method  of  infection,  thanks  to  the  labours  of  Smith 
in  1908,  and  Rodhain,  Pons,  Vandenbranden,  and  Bequaert  in  1913, 
is  fairly  well  known. 

The  eggs  are  apparently  sometimes  laid  on  the  clothing,  the  fly, 
perhaps,  being  attracted  by  the  odour,  or  perhaps  at  other  times  the 
egg  is  laid  in  dirt  or  facal  matter  on  the  floor,  from  which  the  larva 
wanders  on  to  the  human  being,  especially  when  using  the  latrine. 

Having  arrived  on  the  skin  of  man  or  animals,  it  penetrates  this 
by  means  of  its  buccal  hooks,  but  seems  to  require  a  long  time  to  do 
so,  as  one  experiment  took  six  hours.  If  this  is  really  so,  then  there 
must  be  some  ancillary  process,  as  this  is  not  natural. 

Monkeys,  goats,  rabbits,  dogs,  and  cats  are  also  attacked. 
Symptomatology. — During  the  attack  slight  pricking  sensations 
may  be  noted.  The  parts  most  affected  are  the  scrotum,  thigh, 
and  buttocks  in  Europeans,  but  the  forearm,  axilla  (especially 
in  natives),  and  the  head  also  may  be  invaded.  The  infected  area 
presents  the  appearance  of  a  boil,  in  the  central  portion  of  which 
there  is  an  opening,  more  or  less  clearly  defined,  which  is  marked 
by  black  matter  (the  excrement  of  the  larva).  In  this  hole  the 
posterior  end  of  the  larva  may  be  noted,  and  on  pressing  on  it  con- 
siderable pain  is  produced,  probably  due  to  the  movements  of  the 
larva.  Surrounding  the  central  opening  is  an  inflamed  area  about 
I  inch  in  diameter.  The  opening  may,  however,  be  obscured  by 
dried-up  discharge.  Strong  pressure  easily  expels  the  maggot, 
so  that  it  is  seldom  allowed  to  grow  old.  In  children  and  helpless 
persons  it  may  attain  its  full  size,  and  is  then  usually  associated 
with  suppuration,  and  when  full  grown  is  about  12  millimetres  in 
length,  of  a  yellowish-white  colour,  and  bluntly  pointed  anteriorly, 
while  it  possesses  twelve  segments,  on  the  posterior  aspect  of  the 
last  of  which  are  the  two  posterior  stigmatic  plates,  which  are  visible 
in  the  orifice  of  the  swelling,  appearing  and  disappearing  after  the 
manner  of  a  jack-in-the-box. 

Treatment. — The  larva  is  easily  expressed  by  strong  pressure, 
and  then  the  resulting  hole  can  be  cleansed  with  antiseptic  solutions 
and  the  wound  dressed  aseptically. 


CREEPING  ERUPTION  1639 

Asian  Dermal  Myiasis. 

Myiasis  has  not  been  sufficiently  studied  in  Asia,  though  it  is 
fairly  common  there.  Sarcophaga  ruficornis  is  reported  as  causing 
occasionally  a  very  severe  form  of  cutaneous  myiasis,  but  beyond 
this  much  cannot  be  said. 

European  Dermal  Myiasis. 

The  myiasis  of  Europe  scarcely  comes  under  the  scope  of  tropical 
medicine,  but  it  may  be  mentioned  that  dermal  myiases  are  known 
to  be  caused  by  Hypoderma  boi>is  de  Geer,  1776  (p.  826) ;  H .  diana 
Brauer;  H.  lineata  de  Villers,  1789:  Gastrophilis  nasalis  Linnaeus, 
1758;  G.  hamorrlioidalis  Leach,  1761;  G.  veterinits;  and  Lucilia 
sericaia. 

Creeping  Eruption. 

Synonyms. — Creeping  disease,  Larva  migrans.  Bulgarian,  Nova  Bolest, 
Pnlziasta  Bolest;  German,  Hautmauhvarf,  Kreechkrankheit,  Hautkratzschorf. 

History. — This  disease  was  first  described  by  A.  Lee  in  1875. 
Later  on,  Procke,  Blanchard,  Topsent,  Fiilleborn,  and  others  have 
recorded  several  cases.  It  is  not  rare  in  some  parts  of  Europe, 
Africa,  and  Asia,  and  in  South  America.  We  have  seen  numerous 
cases  in  Ceylon.     It  is  extremely  rare  in  North  America. 

etiology  and  Pathology. — Larvae  of  the  genera  Gastrophilus, 
G.  luemorrhoidalis  and  G.  nasalis,  CEstromyia  satyrus,  Hypoderma 
bovis,  and  H.  lineata  have  been  found  in  several  cases.  In  others 
no  larva  whatever  was  found.  Looss  states  that  the  same  clinical 
picture  may  be  caused  occasionally  by  Ancylostoma  and  Strongy- 
loi  les  (Anguillula)  larvae,  or  even  by  an  inanimate  object  like  a 
piece  of  horsehair.  A  larva  has  been  found  2  millimetres  from  in- 
flamed end,  under  a  small  dark  spot. 

Symptomatology. — The  eruption  is  characterized  by  the  presence 
of  a  narrow  raised  red  lino,  |to  1  inch  broad.  This  line  extends 
daily  one  or  several  inches,  and  is  generally  sinuous,  but  may  be 
straight.  While  the  advancing  end  progresses,  the  opposite  end 
slowly  fades  away.  The  duration  of  the  malady  is  long,  generally 
several  months,  but  occasionally  two  or  three  years.  There  is  much 
pruritus. 

Treatment. — Hypodermic  injections  of  various  disinfectants 
have  been  tried,  with  little  success.  Hutchins  recommends  a 
cocaine  injection,  followed  by  the  injection  of  1  or  2  drops  of  chloro- 
form. 

ALLIED  CONDITIONS. 

Allied  to  the  myiases  are  infestations  by  the  larva-  or  imagines 
of  the  Lepidoptera,  Coleoptera,  Diplopoda.  Chilopoda,  and 
Dermoptera. 


1640  THE  MYIASES  AND  ALLIED  CONDITIONS 

Scolechiasis. 

Synonym. — Scholechiasis. 

Definition. — Scolechiasis  is  the  invasion  of  the  body  by  the  larvae 
of  the  Lepidoptera. 

History. — Originally  the  term  '  scolechiasis  '  was  used  by  Kirby 
and  Spence  for  the  invasion  of  the  body  by  the  larvae  of  any  insects, 
but  Hope  suggested  that  the  term  should  be  restricted  as  indicated, 
and  invented  new  terms  for  other  infestations. 

Varieties. — Hope  gives  a  list  of  seven  cases,  of  which  five  were 
gastro-intestinal,  one  was  rhinal,  and  one  was  not  classified. 

Gastro-intestinal  Scolechiasis. — This  is  due  to  Poniia  brassicce 
Linnaeus,  belonging  to  the  Papilionidae,  and  observed  by  Calderwood 
in  Scotland.  Two  were  duetoCrambas  pinguinalis,  of  theNoctuidae, 
one  being  observed  by  Linnaeus  in  Sweden  and  one  by  Church  in 
England,  and  one  was  due  toPhryganea  grandis,  observed  by  Church 
in  England.  The  one  without  determination  was  found  by  Lister 
in  England. 

Rhinal  Scolechiasis. — There  is  only  one  case  caused  by  Cr ambus 
pinguinalis,  and  recorded  by  Kirby  and  Spence,  on  the  authority 
of  Fulvius  Angelinus,  as  occurring  in  Ravenna. 

Canthariasis. 

Synonym. — Scolechiasis  as  used  by  us  in  the  second  edition. 

Definition. — Canthariasis  is  the  invasion  of  the  body  by  the  larvae 
of  the  Coleoptera. 

Remarks. — The  term  used  above  was  introduced  by  Hope  in  1840, 
when  he  recorded  a  number  of  cases  of  rhinal,  gastro-intestinal,  and 
urinary  infestations. 

Rhinal  Canthariasis. — This  was  due  to  Tenebrio  moletor 
Linnaeus,  and  was  recorded  by  Tulpius  and  by  Oswald  Allen. 

Gastro-Intestinal  Canthariasis. — The  genera  recorded  are 
numerous. 

Carabida. — Sphodrus  leucoplithalanus  by  Paykull  in  Sweden,  in 
1797;  Dermestcs  lardarius  by  Otto  and  Chichester,  in  1807,  in 
England ;  and  D.  murmus  by  Otto,  also  in  England. 

Staphylinidce. — Pcederus  elongatus  Fabricius;  Oxvporus  subicr- 
raneus  Fabricius;  Staphylinus  splendens  Fabricius;  S.  politus 
Fabricius;  S.  fuscipes  Fabricius;  and  S.  punctulaius  Fabricius  by 
Paykull  in  Sweden,  in  1796-1798. 

Scarabceidce. — Gcotrupcs  vemalis  bv  Van  Brommell  in  Sweden, 
in  1729;  Melolontha,  sp.  ?,  by  Lcmaout,  Depalsc  (1817  ?),  and 
Desvoidy  in  France. 

TenebrionideB. — Tenebrio  moletor  Linnaeus  by  Forestus,  in  1568, 
at  Brielle;  by  Kellie  in  Scotland;  by  Pickells  and  bv  Thomson  in 
Ireland;  by  Traill  and  others  in  England;  by  Acrel  in  Sweden,  in 

Blapidce. — Blaps  mortisaga  Fabricius  by  Pickells,  Thomson,  and 
O'Brien  in  Ireland,  in  1827:  bv  Ba.teman"and  others  in  England. 


REFERENCES  164 1 

Mordellida. — M  or  dell  a ,  sp.  ?,  by  Rosen,  in  1752,  in  Sweden. 

Cantharidee. — Melee  proscarabesits  Fabricius  by  Germar  in  Silesia, 
in  1816. 

Circulionidce. — Balaninus  nucutn  Fabricius  by  Henry,  Astley 
Cooper,  and  others  in  England,  in  1805-1809. 

Urinary  Canthariasis. — Tenebrio  moletor  Linnaeus  is  recorded 
by  Tulpius  as  occurring  in  the  bladder  of  a  female  aged  fifty  years: 
Balaninus,  sp.  ?,  by  Henry  and  Phillips  in  the  urinary  passages  of  a 
man  aged  sixty-two  years,  in  Lancashire,  in  1809.  King  in  the 
Anglo-Egyptian  Sudan  has  recorded  a  case  where  the  larva  depicted 
in  Fig.  460,  p.  870  was  passed  per  urethram. 

Dermal  Canthariasis. — Dyticus  marginalis  Linnaeus  is  recorded 
by  Hope,  in  1831,  in  England. 

Diplopodiasis  and  Chilopodiasis. 

Diplopodiasis  occurs  in  the  alimentary  canal,  and  is  caused  by 
Julus  terrestris  Linnaeus,  /.  londinenensis ,  and  Polydesmus  com- 
planatus. 

Chilopodiasis  occurs  in  the  rhinal  passages,  where  Geophilits 
carpophagus  Leach,  G.  electricus  Linnaeus,  G.  cephalicits  Wood, 
G.  similis  Leach,  Lithobius fortificaius  Linnaeus,  andL.  melanops  have 
been  found,  while  G.  electricus  and  5.  coleoptrata,  Chcetechelyne 
vesuviana,  Himantarium  gervaisi,  and  Stigmatogaster  subterrancus 
occur  in  the  alimentary  canal. 

Dermapteriasis. 

Dermapteriasis  of  the  alimentary  canal  caused  by  Forficula 
auricularia  has  been  reported  by  Griffin  in  1836. 


REFERENCES. 

The  most  useful  account  of  the  old  cases  is  Hope  (1840),  Transactions  oj  the 
Entomological  Society  of  London,  ii.  256-271.  See  also  Austen  and  Smith 
(separately),  in  190S,  in  the  Journal  oj  the  Royal  Army  Medical  Corps,  and  also 
Sambon  (191 6),  Report  of  the  Advisory  Committee  of  the  Tropical  Diseases 
Research  Fund,  London;  also  the  works  of  Ambrose  Pare. 

Adams    (1904).     Journal   American   Medical   Association,    April  9    (Tropical 

Cutaneous  Myiasis). 
Blanchard  (1892).    Annales  de  la  Societe  Entomologique  de  France  (CEstrides 

Americains  dans  la  peau  de  l'homme). 

\  kici.  (1909).     Archives  de  Parasitologic,  xii.  369-450.     Paris. 
Dyer  (1918).     New  Orleans  Med.  and  Surg.  Jour.,  August. 
Graham-Smith  (1914).    flies  in  Relation  to  Disease.    (Good  general  account.) 

Cambridge. 
Monchet  (191 7).     Bulletin  de  la  Societe  de  Pathologie  Exotique. 
Petrovskala  (1910).     Myiases  Produite  chez  l'homme.     These  de  Paris. 
RlELEY  and  IIowi.ETT  (1914).     Indian  Medical  Gazette,  xlix.  S-io. 
SERGENT,  Ed.  and  Et.  (1913).     Annales  de  l'lnstitut  Pasteur,  xxi.  392. 
Ward  (1903).     Mark  Anniversary  Volume,  Article  25. 
Wohl  (1913).     New  York  Medical   Journal,   xcviii.    1018-1020.     (Collection 

of  known  cases.) 


CHAPTER  LXVIII 
POROCEPHALOSIS 

Synonym  —  1  'efinition  —  History  —  Climatology  —  .^Etiology  —  Pathology  — 
Morbid  anatomy  —  Symptomatology  —  Diagnosis  —  Prognosis  - —  Treat- 
ment— Prophylaxis — References. 

Synonym. — Porocephaliasis. 

Definition. — Porocephalosis  is  the  invasion  of  the  body  by  the 
larvae  of  Poroccphalus  armillatus  Wyman,  1848,  and  P.  moniliformis 
Diesing,  1836,  and  possibly  other  forms,  which  become  encysted  in 
the  liver  and  lungs,  and  ultimately  develop  into  nymphae,  which 
may,  by  their  wanderings,  cause  inflammation  of  organs  and  serous 
membranes. 

History. — P.  armillatus  was  first  found  in  man  by  Pruner  in  1846, 
and  has  since  been  studied  by  Bilharz,  Fenger,  Aitken,  Giard, 
Broden  and  Rodhain,  Dutton  and  Todd,  and  one  of  us.  P.  monili- 
formis has  been  met  with  in  Asia,  and  by  Salm  in  Java.     Sambon 

thinks  that  Welch's  Indian  para- 
site    may    have    been    P.    najce 
■^-■^  Leuckart,  i860,  or  P.  crocidurce 

,i  Parona,    1890,  found  in  Blyth's 

/  musk  shrew  Crocidura  fuliginosa; 

/  and  that  Flint's  case  in  America 

s; '■■'>'''  may  have  been  an  infection  with 

P.   crotali  Humboldt,   1808,  but 
r"z'"  for  details  with  regard  to  these 

Fig.  j26.—Porocepkalus  armillatus     parasites,  see  pp.  734  and  736. 
encysted  in  Liver.  Climatology.    —    Porocephalus 

(After  Sambon,  from  our  West        armillatus  is  confined  to  Africa, 
African  case.)  being  met  with  in  negroes  resi- 

dent, or  who  have  resided, 
therein.  It  has  been  reported  from  Egypt  and  various  parts  of 
the  West  Coast  of  Africa,  but  especially  from  the  Congo. 

With  regard  to  P.  moniliformis,  it  occurs  in  Java  and  the  Philip- 
pine Islands.  Welch  described  a  peculiar  parasite  as  occurring  in 
the  mucosa  of  the  intestine  of  a  man  in  India  which  he  considered 
to  be  an  Echinorhynchus.  but  which,  judging  from  the  drawing, 
might  well  be  a.  Porocephalus. 

/Etiology. — The  adults  of  both  P.  armillatus  and  P.  moniliformis 
live  in  the  nasal  cavities  and  lungs  of  pythons  and  snakes,  and 
though  the  life-history  is  as  yet  unknown,  it  is  quite  possible  that 

1642 


REFERENCES  1643 

Sambon's  suggestion  that  the  ova  pass  into  the  drinking-water,  and 
so  to  man,  may  be  correct.  It  is  possible  that  the  eggs  hatch  in  the 
alimentary  canal,  and  that  the  larvae  then  pass  into  the  organs. 

Pathology. — The  larvae  are  found  lying  coiled  in  cysts  in  the  liver 
and  lungs.  In  due  course  these  larva;  become  nymphae,  which  leave 
the  cysts  and  wander  through  the  body,  appearing  in  the  lungs  and 
bronchi,  causing  bronchitis  and  broncho-pneumonia;  in  the  peri- 
toneal cavity,  causing  peritonitis;  in  the  bowels,  causing  irritation. 
Perhaps  they  leave  the  body  by  the  faeces;  perhaps,  also,  by  the 
sputum;  but  in  any  case  they  cause  serious  illness  in,  and  death  of, 
the  victim. 

Morbid  Anatomy. — In  opening  the  abdomen,  the  nymphae  may 
be  found  quite  free  in  the  peritoneal  cavity,  and  may  crawl  up  the 
hands  and  arms  of  the  pathologist.  They  may  also  be  found  in 
the  lumen  of  the  alimentary  canal,  in  the  mucosae,  and  thickness  of 
the  wall  of  the  bowel.  The  larvae  may  be  seen  encysted  in  the  liver 
and  lungs. 

In  the  cysts  they  lie  in  a  curved  position,  with  the  ventral  surface 
on  the  outer  aspect  of  the  curve.  The  lungs  show  signs  of  bron- 
chitis and  pneumonia,  and  the  peritoneum  is  usually  chronically 
inflamed,  but  not  always. 

Symptomatology. — The  symptoms  of  the  early  stages  of  the 
disease  are  at  present  quite  unknown,  but  the  terminal  symptoms 
are  emaciation  and  weakness,  associated  with  attacks  of  bronchitis, 
pleurisy,  or  other  respiratory  symptoms.  There  may  be  cavities 
in  the  lungs,  and  the  sputum  may  be  offensive  and  may  contain 
the  parasites,  of  which  as  many  as  75  to  100  have  been  recorded 
as  being  expectorated  by  a  single  patient.  The  liver  is  usually 
considerably  enlarged. 

Diagnosis. — The  disease  has  often  been  mistaken  for  phthisis; 
therefore  any  patient  in  the  tropics  suffering  from  the  usual  symp- 
toms of  phthisis  associated  with  enlargement  of  the  liver  may  be 
suspected,  and  the  sputum  and  faeces  carefully  watched  for  the 
possible  appearance  of  the  parasites.  When  a  parasite  is  found,  it 
may  not  necessarily  be  either  P.  armillatus  or  P.  moniliformis,  but 
is  more  likely  to  be  some  form  found  in  some  animal  which  lives  in 
the  region  where  the  patient  resides  or  works. 

Prognosis. — The  disease  is  generally  chronic.  The  prognosis  is 
serious. 

Treatment. — There  is  no  known  treatment. 

Prophylaxis. — If  the  drinking-water  is  boiled  or  filtered,  there 
ought  to  be  no  danger  of  infection. 

REFERENCES. 

Broden  and  Rodhain  (1907).     Annals  of  Tropical  Medicine  and  Parasitology, 

p.  493.     Liverpool. 
Chalmers  (1899).     Lancet,  i.  (January  10).     London. 
Sambon    (1910-12).     Journal    of    Tropical    Medicine,     London.     (Series    of 

valuable  articles,  not  yet  completed.) 
Welch  (1872).     Lancet,  ii.  703.     London. 


CHAPTER  LXIX 
LEPROSY 

Synonyms — Definition — History — Climatology — yEtiology — Symptomatology 
— Diagnosis — Prognosis — Treatment — Prophylaxis — References. 

Synonyms. — Elephantiasis  Graecorum.    French  :  La  Ldpre.    Italian  :  Lebbra. 
German:  Aussatz.     Norwegian  :   Spedalskhed.     Arabic:  Djudsam. 

Definition. — Leprosy  is  a  chronic  general  disease,  caused  by  "the 
Mycobacterium  lepra  Hansen,  1874,  (usual  term  Bacillus  lepra), 
which  produces  characteristic  lesions  in  the  skin,  mucosa?,  and 
nerves.     The  method  of  infection  is  unknown. 

History. — Even  at  the  present  time  there  is  occasionally  much 
difficulty  with  regard  to  the  diagnosis  of  leprosy  from  allied  diseases, 
and  therefore  in  ancient  times  and  in  the  Middle  Ages  syphilis 
and  skin  diseases  without  doubt  were  confused  with  it.  Hence 
the  history  is  not  easy  to  write.  Nevertheless,  such  a  repulsive 
and  striking  disease  must  have  been  noticed  by  the  ancients,  and 
therefore  it  is  possible  that  the  references  in  the  Ebers  Papyrus, 
and  in  the  English  Bible,  the  Rig  Veda,  and  ancient  Japanese 
books,  actually  refer  to  what  we  call  leprosy,  together  with  other 
diseases.  If  this  is  so,  leprosy  is  indeed  ancient  and  widespread. 
Certain  authorities,  however,  are  of  opinion  that  the  Hebrew  word 
Tsaraath,  which  the  translators  of  the  Bible  have  rendered  as 
leprosy,  does  not  refer  to  such  disease.  It  is  probable  that 
the  malady  passed  from  Egypt  to  Greece,  and  later  to  Italy, 
by  means  of  Pompey's  troops,  and  that  it  was  disseminated 
throughout  Europe  by  the  Roman  legions,  by  traders,  and  later, 
perhaps,  by  the  Crusaders  returning  from  the  East.  In  any  case, 
leprosy  gradually  increased  in  Europe  from  the  days  of  Pompey  till, 
in  the  thirteenth  century,  it  existed  to  such  an  extent  as  to  move 
Church  and  State  alike  to  combat  its  ravages.  Stern  measures  were 
enforced,  and  the  lepers  were  isolated  in  lazarettos.  They  were  com- 
pelled to  wear  a  special  dress,  to  use  a  clapper  when  passing  along 
the  roads,  to  only  indicate  with  a  stick  the  articles  they  desired  to 
buy  in  a  market ;  while  they  were  forbidden  to  drink  from  public 
fountains,  to  touch  children,  to  speak  to  a  healthy  person  in  a  loud 
voice,  or  to  eat  with  any  person  other  than  a  leper.  Further,  the 
Church  performed  the  Burial  Service  over  a  person  who  was  diag- 
nosed to  be  a  leper,  and  therefore  officially  he  was  dead.  The  resull 
of  this  appears  to  have  been  beneficial,  as  the  number  of  lepers 

1644 


HISTORY  iG45 

diminished  rapidly  in  the  fourteenth  and  fifteenth  centuries,  since 
when  the  disease  has  almost  disappeared  from  many  parts  of  Europe. 
But  while  abating  in  Europe,  it  appears  to  have  been  introduced 
into  Madeira  and  the  Canary  Islands  about  the  end  of  the  fifteenth 
century,  and  perhaps  also  into  America  by  the  Spaniards.  The 
infection  of  the  West  Indies  would  appear,  however,  to  have  been 
mainly  due  to  the  negro  slaves  brought  from  Africa  about  the  middle 
of  the  sixteenth  century,  after  which  the  disease  became  common. 
There  is  great  doubt  as  to  whether  it  did  not  exist  in  South  America 
in  ancient  times,  but  no  clear  evidence  is  forthcoming  at  present. 

In  India,  Japan,  and  probably  China,  leprosy  is  most  ancient, 
while  it  is  very  common  in  South  China.  During  recent  years  the 
Chinese  have  been  moving  about  the  world,  and  are  accredited 
with  introducing  the  disease  into  Kamschatka,  the  Sandwich 
Islands,  Polynesia,  Columbia.  California,  Australia,  New  Zealand, 
and  also  into  Indo-China. 

Though  very  common  in  North  and  Tropical  Africa,  it  appears 
to  have  been  unknown  in  South  Africa  until  introduced  in  1756 
by  the  Dutch  from  Java,  who  carried  it  through  Cape  Colony  and 
the  Orange  Free  State  into  the  Transvaal.  It  must,  however,  be 
stated  that  some  people  think  it  has  existed  for  a  long  time  in 
South  Africa. 

It  is  said  that  the  numbers  of  lepers  have  markedly  increased  in 
South  Africa  since  the  advent  of  the  East  Indian  troops  in  the 
middle  of  last  century. 

As  regards  medical  literature.  Hippocrates  says  but  little  about  the 
disease,  and  perhaps  really  refers  to  psoriasis,  while  Aristotle  defines 
it  better.  It  is  not,  however,  until  the  first  century  that  Aretaaus 
of  Cappadocia  gives  a  clear  description  of  the  disease,  and  not  till 
1847  that  the  first  modern  clinical  account  by  Danielssen  and 
Boeck  appeared.  The  pathology  of  the  disease  has  been  carefully 
studied  by  Virchow,  Vandyke  Carter,  Leloir,  Babes,  Unna,  Zam- 
baco,  Innes,  Campana,  De  Amicis,  Philipson,  Mantegazza,  and 
Bergmann.  In  1871  Hansen  discovered  the  bacillus,  and  in  1877 
definitely  associated  it  with  the  causation  of  leprous  lesions,  and  it 
has  subsequently  been  studied  by  Neisser  in  1879,  and  many  others. 
Many  attempts  have  been  made  to  cultivate  this  bacillus,  notably 
by  the  Indian  Commission,  van  Houten  and  Rost,  and  more  recently 
by  Keebrowsky,  Clegg,  Bayon,  and  Duval.  In  1903  Stephansky 
and  Dean,  and  later  Rabinowitsch  and  Tidswell,  discovered  a 
peculiar  leprosy-like  disease  in  rats,  the  lesions  of  which  contain 
bacilli  closely  resembling  Hansen's  bacillus  in  appearance,  and 
not  capable  of  cultivation.  A  diphtheroid  bacillus  has,  however, 
been  cultivated  by  Dean  from  two  cases,  and  is  said  by  him  to  be 
capable  of  being  agglutinated  by  human  leprous  serum.  There  is 
probably  no  connection  between  the  human  and  the  rat  disease, 
though  some  authorities  admit  it.  The  condition  has  been  recently 
investigated  by  Marchoux  and  Sorel,  Bayon,  and  others. 

The  method  of  infection  is  at  present  unknown,  though  there  are 


1646  LEPROSY 

various  theories,  more  or  less  ably  defended,  which  will  be  men- 
tioned later.  Marchoux  and  Bourret  consider  that  they  have 
successfully  inoculated  a  chimpanzee,  and  Nicolle  and  Blaizot  have 
produced  lesions  resembling  leprosy  in  lower  monkeys.  The  con- 
dition of  the  eye  has  been  much  neglected  until  recent  years,  when 
the  researches  begun  by  Ball  and  Hansen  as  far  back  as  1873  have 
been  extended  by  Grossman  in  1906,  de  Silva  in  1907,  but  most 
importantly  by  Borthen  in  1899. 

Deycke  and  Reschad  inoculated  the  surface  cream  of  sterilized 
unskimmed  milk  with  material  obtained  from  the  under  aspect 
of  leprotic  tubercles  by  throwing  back  a  flap  of  skin.  Incubated 
at  300  C,  a  growth  forms  in  fourteen  days,  which  is  characterized 
by  its  bright  orange  tint.  This  organism  they  called  Streptothrix 
leproides,  and  from  this  they  obtain  a  neutral  fat,  '  nastin,'  which 
is  similar  to  a  fat  found  in  Hansen's  bacillus,  and  this  Deycke 
considered  to  be  the  agent  which  produced  favourable  symptoms 
when  cultures  of  Streptothrix  leproides  were  injected  into  patients. 
Later  he  noticed  that  these  favourable  conditions  were  associated 
with  a  leucocytosis,  and  therefore  used  nastin  mixed  with  cinnamic 
acid,  which  is  excreted  as  hippuric  acid,  the  two  acids  being  connected 
by  benzoic  acid  as  an  intermediate  product.  He  therefore  used 
benzoyl  chloride  to  extract  the  '  nastin,'  and  injected  the  '  benzoyl 
nastin  '  into  patients,  producing  a  reaction.  Deycke  believes  that 
the  nastin  is  only  a  carrier  of  the  benzoyl  chloride  to  the  bacilli, 
which  it  deprives  of  their  fat,  and  so  allows  the  phagocytes  to  attack 
them.  Four  solutions  were  prepared:  Nastin  B  o,  Nastin  B  1, 
Nastin  B  2,  and  K.,  this  last  being  only  benzoyl  chloride,  and  being 
used  to  shorten  and  reduce  the  severity  of  the  reaction  if  required. 
The  others  represent  nastin  in  varying  degrees  of  strength, 
Nastin  B  2  containing  an  excess  of  nastin,  while  Nastin  B  1  is  that 
usually  employed.  Unfortunately  no  general  success  has  followed 
this  line  of  treatment. 

Climatology. — At  the  present  time  there  is  but  little  leprosy 
in  many  parts  of  Europe,  but  it  is  still  common  in  Iceland,  while 
it  is  found  in  Spain,  Italy,  the  Balkans,  Turkey,  Crete,  and  Cyprus. 
It  is  less  frequent  than  formerly  in  Norway,  Sweden,  Greece,  and 
some  of  the  Mediterranean  islands,  rare  in  France  and  Germany, 
and  almost  extinct  in  Denmark,  Belgium,  Holland,  Austria- 
Hungary,  and  England. 

It  is  very  common  throughout  the  whole  of  Asia.  In  Ceylon 
there  are  numerous  lepers,  many  of  whom  are  treated  in  a  leper 
asylum  at  Hendela,  near  Colombo,  which  is  believed  to  be  one  of 
the  best  in  the  world. 

In  Australia  the  disease  is  known  principally  in  Queensland  and 
New  South  Wales,  and  also  in  Victoria;  while  in  New  Zealand  it  is 
known  among  the  Maoris.  It  occurs  in  New  Caledonia,  Tahiti, 
and  the  Sandwich  Islands. 

It  is  spread  sporadically  over  the  United  States,  but  is  rare  in 
Canada,  while  it  is  well  known  in  Mexico  and  Central  America, 


ETIOLOGY  1647 

and  common  in  the  West  Indies.  In  South  America  it  appears  to 
be  common  in  Colombia,  Venezuela,  the  Guianas,  and  Brazil,  but 
whether  it  is  rare  or  simply  not  recognized  in  other  countries  is 
unknown. 

It  appears  to  be  spread  all  through  Africa,  but  is  certainly  rare 
in  West  Africa,  more  common  in  Central  and  East  Africa,  and 
decidedly  more  common  in  North  and  in  South  Africa,  where  there 
is  the  celebrated  Robbin  Island  Leper  Asylum.  There  are  people 
who  believe  Egypt  to  be  the  original  home  of  the  disease,  from 
whence  it  spread  to  Asia  and  Europe. 

/Etiology. — The  disease  is  caused  by  Hansen's  bacillus,  which 
morphologically  has  the  greatest  resemblance  to  the  tubercular 
bacillus,  and  is  stained  by  the  same  methods. 

With  regard  to  the  cultivation  of  the  bacillus  there  are  three 
views : — 

1.  That  it  has  never  been  cultivated. 

2.  That  it  can  be  cultivated  as  a  streptothrix  or  nocardia. 

3.  That  it  can  be  cultivated  as  a  bacillus. 

1.  That  it  has  never  been  cultivated. — This  is  still  the  most 
generally  accepted  view. 

2.  That  it  can  be  cultivated  as  a  Streptothrix.- — This  is  the  view 
held  by  Bordoni-Uffreduzzi,  Babes,  Rost,  Kedrowsky,  Shiga,  Hew- 
lett, Bayon,  Johnston,  and  others.  They  maintain  that  Hansen's 
bacillus  in  cultures  becomes  a  filamentary  branching  non-acid- 
resisting  organism,  which,  when  injected  persistently  into  animals, 
produces  the  signs  of  leprosy.  From  these  animals,  they  say,  it  can 
be  recovered  as  an  acid-resisting  bacillus.  The  strain  separated  by 
Kedrowsky,  and  further  investigated  by  Bayon,  is  the  one  which  in 
our  opinion  is  the  most  important  with  a  view  to  further  researches. 
The  growth  of  the  germ  is  slow,  and  the  colonies  coalesce  into  a 
whitish  mass.  The  inoculation  of  cultures  into  monkeys,  rats,  and 
guinea-pigs,  gives  rise,  according  to  Bayon,  to  leprosy-like  lesions, 
with  very  little  tissue  proliferation,  no  caseation  necrosis,  no 
vascular  sclerosis,  and  with  presence  of  numerous  acid-fast  bacilli. 
Serological  reactions,  such  as  agglutination  and  complement  fixa- 
tion, are  rather  in  favour  of  Bayon's  theory.  Moreover,  the 
inoculation  of  an  extract  of  the  cultures  induces  in  leprotic  patients 
a  reaction  with  fever,  comparable  to  that  induced  in  tubercular 
patients  by  tuberculin. 

In  1915  Fraser  and  Fletcher  were  unable  to  confirm  Kedrowsky 
and  Bayon's  results,  and  came  to  the  conclusion  that  Kedrowsky's 
bacillus  is  not  the  leprosy  bacillus. 

3.  That  it  can  be  cultivated  as  a  Bacillus. — This  is  the  view  held 
by  Clegg,  Duval,  and  others.  Clegg  succeeded  in  cultivating  his 
bacillus  in  symbiosis  with  an  amoeba.  The  cultures  are  chromo- 
genic.  The  inoculation  of  this  germ  apparently  does  not  produce 
leprotic  lesions.  Duval  gives  importance  to  a  non-chromogenic 
always  acid-fast  bacillus  he  has  isolated,  which  grows  very  slowly, 


1648  LEPROSY 

and  only  on  special  media.  He  states  that  in  addition  to  this 
bacillus  he  has  at  times  grown  a  polymorphic  organism,  sometimes 
diphtheroid,  sometimes  streptothrical,  and  of  varying  degrees  of  acid- 
fastness.  He  compares  this  type  of  germ  to  those  isolated  by  Ked- 
rowsky  and  Bayon,  and  is  not  inclined  to  give  it  any  importance. 

The  bacilli,  which,  as  will  be  shown  later,  exist  practically  all 
over  the  body  wherever  diseased  tissue  is  found,  leave  it  by  the 
nasal  secretion,  the  tears,  the  salivary  secretion,  the  sputum,  the 
milk,  the  semen,  urethral  and  vaginal  secretions,  and  by  the  faeces, 
and  are  cast  off  with  the  scales  of  skin  or  the  discharge  of  disin- 
tegrating tubercles.  Of  all  these,  the  secretion  of  the  nose  appears 
to  be  of  great  importance,  for,  as  Sticker  and  van  Houten  showed, 
the  bacilli  are  very  commonly  met  with  in  that  situation.  The 
bacilli  are  reported  to  have  been  found  in  Culex  pungens  and 
Clinocoris  lectularius  by  Goodhue,  of  the  Molokai  Leper  Settlement. 
Finally,  notwithstanding  one  or  two  observations,  the  bacillus  has 
never  been  found  in  earth,  dust,  air,  water,  or  food. 

With  regard  to  inoculations  of  leprotic  tissues  and  nodules  into 
animals,  experiments  have  been  negative  in  rabbits,  guinea-pigs, 
dogs,  cats,  bats,  pigs,  and  birds,  even  though  some  experiments 
were  thought  at  the  time  to  be  successful.  Nicolle  produced  a 
hard  indolent  swelling  with  a  few  lepra  bacilli  by  injection  of  leprous 
tissue  in  a  Macacus  monkey.  Marchoux  and  Bourret  have  made 
inoculation  experiments  in  a  chimpanzee  with  partial  success. 
Stanziale  has  inoculated  leprotic  material  in  the  cornea  of 
rabbits,  inducing  certain  lesions  which  he  has  been  able  to 
transmit,  to  a  certain  point,  from  animal  to  animal.  In  rats  a 
peculiar  skin  disease,  somewhat  resembling  leprosy,  occurs  spon- 
taneously, as  observed  by  Stephansky,  Dean,  and  Rabinowitsch. 
This  has  been  investigated  by  Marchoux  and  Sorel,  who  have 
come  to  the  conclusion  that  it  is  generally  transmitted  by 
contact,  and  not  by  parasitic  agencies.  They  have  not  succeeded 
in  cultivating  the  bacillus,  while  Bayon  has  cultivated  a  strepto- 
thrix  very  similar  to  the  Kedrowsky  strain  isolated  from  human 
lesions. 

With  regard  to  the  experimental  inoculation  of  human  beings, 
the  only  case  cited  as  successful  is  Arning's  inoculation  of  a  Sand- 
wich Island  criminal  in  the  arm  with  a  leprous  tubercle.  This 
man  developed  a  neuritis  of  the  ulnar  and  median  nerves  four 
weeks  after  the  inoculation,  a  tubercle  five  months  later,  the  full 
signs  of  leprosy  two  and  a  half  years  later,  and  died  a  leper  six 
years  after  the  inoculation.  It  is,  however,  to  be  noted  that  he 
lived  in  a  leprous  country,  and  that  there  was  leprosy  in  his  family — 
facts  which  decrease  the  importance  of  the  experiment. 

There  can,  however,  be  no  real  doubt  that  the  disease  is  in  some 
way  spread  from  human  being  to  human  being.  In  support  of  this 
there  are  many  well-known  facts—  e.g.,  the  case  reported  by  Benson, 
where  an  Irishman,  having  acquired  leprosy  in  the  West  Indies, 
returned  to  Ireland,  and  died  from  the  effects  of  the  disease  in 


MTIOLOGY  1649 

about  eleven  months.  During  this  period  his  brother  not  merety 
lived  with  him,  but  slept  in  the  same  bed,  and,  after  his  death,  wore 
his  clothes.  In  about  four  to  five  years  this  brother  showed  all 
the  typical  signs  of  tubercular  leprosy,  though  he  had  onty  once 
been  out  of  Ireland,  and  then  only  to  visit  England.  Another 
similar  case  may  be  quoted  of  a  person  who,  acquiring  leprosy  in 
Tonkin,  returned  to  Strasburg  and  lived  with  a  nephew,  who 
subsequently  developed  the  disease.  Turning  to  the  evidence  of 
history,  there  is  the  spread  of  leprosy  throughout  Europe,  and, 
later,  the  rapid  spread  of  the  disease  in  the  Sandwich  Islands, 
where,  though  existing  probably  for  many  years,  it  increased  from 
1859,  when  it  was  hardly  known,  till  in  1S81  no  less  than  800  lepers 
were  isolated,  and  it  is  said  that  no  less  than  one-tenth  of  the 
population  were  affected.  Another  instance  is  the  case  of  New 
Caledonia,  in  which  the  disease,  though  now  common,  is  believed 
to  have  been  introduced  for  the  first  time  in  i860,  and  Pine  Island, 
which  is  said  to  have  been  infected  from  New  Caledonia;  or 
Mauritius,  which  was  infected  by  a  single  leper,  and  from  which, 
later,  the  island  of  Rodriguez  was  infected,  also  by  a  single  leper. 

As  to  individual  cases  of  infection  by  residence  among  lepers, 
the  most  noted  is  that  of  Father  Damien  de  Venster,  who  went 
from  Belgium  as  a  missionary  to  the  Molokai  Leper  Asylum  of  the 
Sandwich  Islands  in  1873,  and  who  was  first  recognized  to  be  suffer- 
ing from  the  disease  in  1882,  from  which  he  died  in  1889. 

Again,  the  prophylactic  success  of  even  partial  isolation  of  lepers, 
as  evinced  in  Europe  in  the  thirteenth  and  fourteenth  centuries, 
and  to-day  in  Norway,  Sweden,  and  Iceland,  is  in  favour  of  the 
view  that  the  disease  passes  from  man  to  man.  But  it  is  not  wise 
to  hastily  conclude  that  this  transference  is  direct,  for  any  of  the 
above  cases  are  easily  explicable  by  the  disease  being  conveyed 
by  food  or  biting  animals.  The  success  of  partial  isolation  might 
be  simply  to  diminish  the  chance  of  infection  by  these  means. 
Moreover,  the  fact  that  the  attendants  of  the  Hendela  Leper 
Asylum  of  Ceylon  have  so  far  not  been  known  to  contract  the 
disease  is  against  the  theory  of  direct  contagion.  Further,  though 
there  is  evidence  that  married  people  may  both  suffer  from  the 
disease,  there  is  no  proof  that  sexual  intercourse  is  a  means  of 
infection.  Nor  is  there  any  evidence  of  heredity  being  a  source 
of  infection,  for  never  has  a  child  been  born  in  a  leprous  condition, 
though  it  is  said  that  10  per  cent,  of  the  children  of  leprous  mothers 
become  sooner  or  later  lepers  themselves. 

If  the  germs  are  not  carried  from  one  person  to  another  by  con- 
tact, sexual  or  germinal  transmission,  they  might  still  be  con- 
veyed by  air,  dust,  water,  or  food,  and,  indeed,  all  these  theories 
have  their  supporters. 

It  does  not  appear  likely  that  it  is  conveyed  by  air,  otherwise  it 
would  surely  be  spread  more  commonly  from  patients  to  attendants 
in  leper  asylums.  With  regard  to  dust,  it  is  quite  true  that,  though 
some  persons  report  the  presence  of  a  very  few  bacilli  in  earth 

104 


1650  LEPROSY 

taken  from  places  frequented  by  lepers,  the  majority  have  failed 
to  find  them;  and,  again,  what  has  been  remarked  with  regard  to 
air  also  applies  to  dust.  The  germs  have  never  been  found  in  the 
water  of  the  most  highly  infected  places. 

Many  articles  of  food  have  been  suspected,  especially  fish,  and 
more  particularly  salted  fish — a  view  which  Sir  Jonathan  Hutchin- 
son has  strongly  advocated;  but  even  he  admits  that  it  will  not 
explain  all  cases,  particularly  its  presence  in  people  who  have  no 
chance  of  eating  cured  fish. 

After  excluding  all  these,  there  is  still  the  possibility  of  the  in- 
fection being  carried  by  some  blood-sucking  insect.  This  subject  has 
been  most  ably  discussed  by  Nuttall,  who  points  out  that  Linnaeus 
and  Rolander  considered  Chlorops  (Musca)  lepra  to  be  the  active 
a^ent;  while  Corredor  suspected  flies  in  general;  Sabrazes,  insects; 
Joly,  Sarcoptes  scabiei  and  Pediculi  ;  and  Sommer,  mosquitoes. 
Nuttall  himself  says  that  the  possibility  of  such  transmission 
cannot  be  denied.  Goodhue  has  demonstrated  the  bacilli  in  Culex 
pungens  and  in  Clinocoris  lectularius  ;  and  Marchoux  and  Bourret 
have  suggested  that  some  Simuliidas  might  be  the  carriers  of  the 
disease.  Flies,  lice,  bugs,  fleas,  ticks,  etc.,  have  all  been  studied 
recently  without  any  great  success. 

It  might  be  thought  that,  direct  inoculation  having  failed,  the 
infection  by  means  of  insects  would  be  unlikely.  But  that  is  not 
so,  because  it  is  well  known  that  the  passage  of  bacilli  through 
another  animal  may  markedly  modify  the  virulence  of  the  germ. 
On  the  other  hand,  a  great  many  facts  are  in  favour  of  the  insect 
spread  of  the  disease — e.g.,  the  infection  in  a  family.  The  cases 
cited  above  as  examples  of  contagion  would  be  easily  explicable 
by  the  action  of  an  insect,  as  would  the  effect  of  isolation  in  pre- 
venting the  disease.  Moreover,  the  predisposing  causes  of  dirt, 
poverty,  etc.,  are  also  explicable  on  the  same  reasoning,  especially 
the  curious  disappearance  of  the  disease  in  the  families  of  Nor- 
wegian peasants  emigrating  to  America,  where  they  became  much 
cleaner  in  their  habits.  The  difficulty  of  cultivating  the  germ  on 
ordinary  media  is  very  suggestive  of  its  being  accustomed  to  live 
solely  in  animal  tissues;  while  the  abundance  of  the  bacilli  in  the 
skin  is  also  sugges+ive  of  that  being  the  natural  method  of  leaving 
the  body.  Everything  in  the  history  of  the  disease  appears  to  us  to 
favour  its  spread  by  animal  agency. 

Cases  of  infection  by  vaccination  and  variolization  are  on  record.  Natives 
of  Ceylon  generally  state  that  the  disease  begins  after  a  bite  by  a  rat. 

Pathology. — According  to  different  theories,  the  bacillus  enters 
the  body  via  the  skin,  the  nasal  or  respiratory  mucosae,  the  ali- 
mentary canal,  or  the  generative  organs. 

The  list  is  so  comprehensive  that  it  will  be  obvious  that  the  real 
method  of  entry  is  entirely  unknown.  On  arrival  inside  the  body, 
the  baoillus  is  supposed  to  come  to  rest  inside  a  lymph  space  some- 
where, and  there  to  grow  and  form  colonies,  from  whence  it  can  be 


PATHOLOGY  1651 

disseminated  through  the  body,  perhaps  by  the  blood  and  the 
lymph  streams.  It  must  be  remembered,  however,  that  the 
nature  of  the  initial  lesions  is  quite  unknown.  So  enormously  do 
the  bacilli  multiply  in  the  body  that  there  are  few  diseases  which 
show  an  equal  infection. 

The  pathogenesis  of  the  lesions  is  not  very  well  known,  and  there  are  many 
points  of  dispute  which  so  far  have  not  been  settled.  The  early  stages  have 
been  most  carefully  studied  by  Unna  in  the  neurolepride,  in  which  there  is 
at  first  a  dilatation  of  the  capillary  vessels  of  the  skin,  on  the  walls  of  which 
the  typical  bacilli  can  be  found.  The  organisms  now  pass  into  the  wall  of 
the  vessel,  and  appear  to  irritate  the  connective- tissue  cells  of  the  vicinity, 
which,  becoming  plasma  cells,  surround  the  periphery  of  the  vessel. 

There  is  a  dispute  as  to  whether  any  diapedesis  of  the  white  cells  takes 
place.  Thus  Thin  and  Neisser  support  the  view  of  a  diapedesis,  to  which, 
however,  Unna  is  opposed.  According  to  the  former  observers,  the  cells  of 
the  leproma  contain  not  merely  plasma  cells,  but  also  leucocytes  and  lym- 
phocytes, while  according  to  the  latter  they  are  entirely  plasma  cells  and  their 
derivatives,  for  Unna  holds  the  view  that  the  bacillus  has  but  little  attraction 
for  the  white  cell.  The  organisms  pass  from  the  vessel  wall  into  the  lymph 
capillaries,  in  which  they  grow.  These  early  stages  have  not  been  seen  in  the 
typical  leproma,  in  which  the  bacilli  from  the  first  are  met  with  in  the  lym- 
phatics, in  which  they  grow  luxuriantly,  causing  the  considerable  dilatation 
which  is  a  marked  feature  of  the  lesion. 

Now  occurs  a  phenomenon  concerning  which  there  is  much  difference  of 
opinion,  for  either  the  plasma  cells  increase  in  size,  and,  becoming  multi- 
nucleated, engulf  the  bacilli,  forming  in  this  way  the  typical  '  lepra  cells  ' 
of  Virchow — a  view  supported  also  by  Neisser  and  others — or  the  bacilli 
attack  the  plasma  cells,  destroy  their  cytoplasm,  and  so  damage  the  nucleus 
that  it  becomes  achromatic  and  breaks  into  several  pieces,  which  remain  sur- 
rounded by,  or  on  the  side  of,  a  mass  of  bacilli  embedded  in  mucus,  thus  giving 
rise  to  a  false  appearance  of  a  giant  cell  or  chorio-plaque  enclosing  baciFi, 
as  asserted  by  Unna  and  others.  Unua's  staining  method  with  Victoria  blue 
and  saffranin  colours  normal  bacilli  blue,  and  dead  bacilli  yellow. 

The  lesions  show  large  cells — the  '  lepra  cells,'  containing  large  masses  of 
bacilli — but  in  addition  to  these  cells  there  are  also  masses  of  bacilli  embedded 
in  mucus,  and  not  enclosed  in  cells,  which  are  the  '  globi  '  of  older  writers, 
and  which  in  fresh  preparations  appear  as  large,  rounded,  brownish  masses. 
Bayon  believes  that  the  bunches  of  bacilli  arise  partially  by  the  choking  of 
the  lymphatics  by  phagocytes  swollen  by  the  numbers  of  the  bacilli  which 
they  have  engulfed,  and  partially  by  the  endothelium  of  the  vessel  wall  also 
becoming  distended  with  bacilli.  The  nuclei  of  these  cells  degenerate  and  are 
eliminated,  while  the  remnants  of  the  cells,  together  with  the  bacilli,  form 
'  the  globi,'  and  when  these  remnants  disappear  the  bacilli  are  left  free  in 
the  tissues.  The  hyaline  coating  of  many  bacilli  may  be  a  product  of  the 
protoplasm  of  these  cells  or  may  be  secreted  by  the  bacilli  themselves.  Some- 
times typical  giant  cells,  called  '  Langhans'  cells,'  are  seen.  Marchoux  and 
Eourret  consider  the  so-called  lepra  cells  to  be  undistinguishable  from  the 
large  mononuclear  leucocytes. 

The  bacilli  do  not  invade  the  surface  epithelium,  nor  the  layer  of  the  cutis 
directly  below  this;  nor  do  they  affect  the  sweat  glands,  nor  the  hair  sheaths 
superficial  to  the  opening  of  the  sebaceous  glands. 

The  typical  leproma,  therefore,  shows  superficially  epithelium,  normal  in 
every  respect,  except  that  there  are  no  interpapillary  processes.  Below  the 
epithelium  there  is  a  layer  of  connective  tissue,  free  from  bacilli,  under 
which  lies  the  typical  lesion,  composed  of  lepra  cells,  plasma  cells,  and  con- 
nective-tissue cells,  separated  by  a  very  slight  amount  of  fibrillar  connective 
tissue,  and  containing  vessels,  whose  walls  are  thickened  by  an  infiltration  of 
the  adventitia,  media,  and  intima  to  such  an  extent  that  at  times  the  lumen 
may  be  obliterated,  while  the  lymphatic  spaces  are  dilated  and  filled  with 


1652  LEPROSY 

bacilli  surrounded  by  mucus,  forming  the  '  globi.'  Beneath  the  lesion  the 
connective  tissue  may  be  more  or  less  normal. 

The  attacks  of  fever  and  the  erysipelatous  eruptions,  which  will  be  described 
under  the  Symptomatology,  are  explicable  by  the  dissemination  of  the  bacilli 
throughout  the  body  by  the  blood  stream,  the  bacilli  being  contained  in  the 
large  mononuclear  leucocytes,  according  to  Marchoux  and  Bourret,  and  by  the 
embolism  of  the  capillaries  of  the  skin  by  bacilli  and  white  cells,  which,  how- 
ever, are  soon  recovered  from. 

Lesions  may  remain  stationary  for  years,  and  retrogression  may  take  place 
as  the  result  of  treatment,  or  spontaneously,  in  which  case  the  dead  bacilli 
are  absorbed,  and  sac-like  spaces  left,  which  rarely  become  sclerosed  by 
connective  tissue.  If  on  a  surface,  the  leproma  may  soften,  break  down,  and 
ulcerate,  thus  disseminating  the  bacilli  in  the  discharge. 

The  bacilli  may  also  enter  into  the  nerves  and  cause  a  hyperplasia  of  the 
connective-tissue  cells  of  the  coats  and  the  formation  of  typical  leproma 
cells  at  first  around  the  vasa  nervorum,  and  later  in  the  perineurium  and 
endoneurium. 

These  cells  press  on  the  nerve  fibres,  causing  a  degeneration  of  the  neuri- 
lemma, and  later  a  disintegration  of  the  arteries  and  a  destruction  of  the 
nerve  fibres,  which  finally  results  in  the  nerve  being  largely  converted  into 
connective  tissue.  In  places  where  the  nerve  is  apt  to  suffer  from  compres- 
sion or  other  slight  injuries,  it  becomes  so  thickened  as  to  be  easily  palpable— 
a  fact  which  Lie  explains  by  saying  that  the  bacilli  which  he  found  in  the 
cutaneous  nerves  pass  up  the  nerves  and  become  located  at  spots  liable  to 
injury. 

It  is  usually  believed  that  the  nerves  only  are  affected,  and  that  the  paralyses, 
etc.,  are  the  results  of  disease  of  the  peripheral  nerves,  but  it  has  been  shown 
that  the  bacilli  attack  the  anterior  cornua  of  the  spinal  cord,  and  therefore 
this  may  play  a  part  in  the  production  of  the  symptoms. 

The  bacilli  may  be  carried  by  the  blood  stream  all  over  the  body,  but  show 
a  selective  affinity  for  certain  organs,  in  which  the}'  develop  the  typical 
leprotic  lesions.  A  certain  number  of  leprotic  subjects  react  to  tuberculin 
injections,  and  give  a  positive  Wassermann  reaction. 

Morbid  Anatomy. — The  skin  lesions  which  may  be  found  are  the 
tubercles,  which  may  or  may  not  be  ulcerated,  and  the  pigmented 
and  apigmented  areas.  On  cutting  into  the  leproma,  it  is  seen  to  be 
situated  usually  in  the  cutis,  and  covered  by  the  epidermis;  but  it 
may  lie  in  the  subcutaneous  tissue,  in  which  case  it  does  not  form 
a  tubercle.  It  is  yellowish-white  in  colour,  firm  in  consistency, 
and  if  squeezed,  usually  a  little  clear  fluid  can  be  obtained.  It 
will  be  noted  that  the  sweat  and  sebaceous  glands  and  the  hair 
follicles  are  compressed  and  as  a  rule  atrophied,  while  vesicles 
and  pustules  may  occur  on  the  surface,  which  may  be  ulcerated 
and  covered  with  crusts.  The  macules  consist  of  round-celled 
infiltration,  with  but  few  large  cells,  which  are  generally  free  from 
bacilli.  In  the  spots  which  during  life  were  anaesthetic,  which  are 
derived  from  the  macules,  the  corium  is  largely  converted  into 
fibrous  connective  tissue,  which  has  caused  glands  and  hairs  to 
atrophy  and  disappear. 

The  typical  lepromatous  infiltration  may  occur,  not  merely  in 
the  skin,  but  in  the  mucosas  of  the  tongue,  pharynx,  larynx,  epi- 
glottis, and  in  the  submucosal  of  the  intestine. 

The  liver,  which  is  usually  enlarged,  shows  a  leprous  infiltration 
of  the  portal  systems,  while  the  spleen,  which  also  may  be  enlarged, 
shows  the  same  along  the  course  of  its  vessels,  particularly  while 


MORBID  ANATOMY  1653 

they  are  in  the  septa,  and  a  similar  infiltration  may  be  seen  at  times 
around  the  bronchi. 

The  ovaries  and  testes  may  show  infiltrations  and  fibrosis  of  the 
interstitial  tissue,  which  destroys  the  secretory  elements,  and 
causes  the  sterility  which  is  usually  so  marked  among  lepers.  The 
lymphatic  glands  are  often  enlarged,  infiltrated,  and  full  of  bacilli, 
especially  the  femoral.  Nephritis  and  leprous  infiltration  of  the 
kidneys  may  be  seen.  The  nerves  most  commonly  affected  are  the 
palmar  branch  of  the  ulnar,  the  ulnar,  the  median,  the  peroneal, 
posterior  tibial,  and  the  great  auricular.  When  exposed,  the  nerve 
is  seen  to  show  a  fusiform,  reddish-grey  swelling,  which,  when 
examined,  is  found  to  consist  of  lepromatous  tissue  lying  among  the 
nerve  fibres. 

In  the  spinal  cord  there  may  be  posterior  sclerosis  and  meningitis, 
though  it  is  doubtful  whether  these  are  really  due  to  the  disease 
or  to  some  complication.  The  cells  of  the  posterior  cornu  have 
been  said  to  be  atrophied,  as  well  as  those  of  the  anterior  cornu, 
in  which  Lie  has  found  bacilli. 

In  the  circulatory  organs  periarteritis  and  endarteritis  are 
met  with,  while  osteomyelitis,  necrosis,  caries,  and  absorption  of 
the  bones  may  be  seen,  and  will  be  mentioned  again  later.  Trophic 
changes  in  the  joints  and  perforating  ulcers  are  met  with  in  the 
nerve  form  of  the  disease. 

For  a  long  time  the  presence  of  lepromata  in  the  lung  was  dis- 
puted, but  recently  it  has  been  proved  that  the  lungs  can  become 
infected  with  leprotic  lesions.  The  lesions  of  leprotic  lungs  are 
very  similar  to  those  of  tubercular  lungs,  but  are  more  solid,  caseate 
less  frequently,  and  are  less  prone  to  be  destroyed.  Some  of  the 
earliest  signs  are  petechial  haemorrhages,  which  upon  microscopical 
examination  show  a  diffuse,  small,  round-celled  infiltration,  with 
occasionally  a  giant  cell,  but  without  fibrosis,  but  with  a  slight 
cellular  exfoliation  in  the  surrounding  alveoli  and  congestion  of  the 
bloodvessels  and  capillaries.  In  these  areas  there  are  numerous 
intracellular  leprosy  bacilli  (Wise).  In  addition  there  may  be  an 
acute  and  at  times  caseating  parenchymatous  inflammation  or 
chronic  diffuse  interstitial  inflammation.  These  are  distinguished 
from  similar  tubercular  affections  by  inoculation  into  guinea-pig? 
with  negative  results. 

Symptomatology. — The  incubation  period  is  entirely  unknown, 
and  must  necessarily  remain  so  until  the  method  of  infection  and 
the  date  of  the  onset  of  the  disease  is  discovered;  hence  the  state- 
ments made  by  the  different  observers  that  it  may  last  for  a  few 
weeks  or  months  up  to  many  years.  The  method  of  invasion  is 
also  quite  unknown.  Sticker  suggests  that  it  begins  with  nasal 
symptoms — blocking  of  the  nose,  epistaxis,  and  frontal  headache; 
other  observers  with  skin  eruptions.  The  truth  appears  to  be 
that,  so  far,  the  initial  lesions  and  their  symptoms,  if  any,  have 
escaped  notice. 

Before  the  eruption  appears  there  are,  in  many  cases,  attacks  of 


1654  LEPROSY 

fever  of  an  intermittent  or  irregular  character,  with  a  marked 
feeling  of  general  illness,  associated  with  headache  and  pains  in 
different  parts  of  the  body,  peculiar  sensations  of  cold,  formication 
or  numbness  in  various  places,  and,  above  all,  of  abnormal  local  or 
general  perspirations.  These  attacks  of  leprotic  fever,  without  any 
definite  clinical  signs  of  leprosy,  may  occur  at  intervals  for  years. 
This  fever  is  probably  due  to  the  dissemination  of  the  bacilli  through 
the  body,  and  may  represent  a  septicemic  process  due  to  the 
Bacillus  lepra. 

After  the  general  dissemination  through  the  body,  the  bacilli 
appear  to  settle  mainly  in  the  skin  or  in  the  nerves,  though,  of 
course,  there  are  many  cases  in  which  they  settle  in  both.  It  is 
therefore  convenient  to  distinguish  the  two  varieties  of  the  disease, 
first  differentiated  by  Danielssen  and  Boeck — viz.,  'lepra  tuber- 
culosa,' or  '  nodular  leprosy,'  and  '  lepra  maculo-ansesthetica,'  or 
'  smooth  leprosy  ' — remembering  that  the  division  is  artificial,  and 
that  numerous  cases  exist  which  show  both  forms. 

TUBERCULAR  LEPROSY. 

After  repeated  attacks  of  fever  the  patient  has  a  more  severe  one, 
during  which  an  erythematous,  diffuse,  or  macular  eruption  appears 
on  the  face  and  limbs.  The  fever  subsides,  and  the  maculae  may 
disappear  or  thicken  and  become  tubercles,  which  are  dermal  lesions 
projecting  from  the  skin  or  mucosas,  in  addition  to  which  there  are 
subdermal  infiltrations,  which  can  be  more  easily  felt  than  seen. 
If  they  disappear,  it  is  only  for  the  time,  as  new  maculae  will  appear 
with  a  new  attack,  and  sooner  or  later  the  thickening  will  take 
place,  and  the  nodules  or  tubercles,  typical  of  the  disease,  will 
appear.  Each  outbreak  of  nodules  is  in  some  cases  preceded  by 
an  attack  of  fever,  with  or  without  an  erysipelatous-like  eruption 
in  the  area  to  be  affected,  associated  with  enlargement  of  the 
lymphatic  glands.  In  our  experience,  however,  the  fever  may  be 
absent  in  many  cases. 

The  nodules  may  form  all  over  the  skin,  but  are  most  common 
on  the  face  and  limbs.  In  the  former  situation  they  appear  on  the 
forehead,  cheeks,  alae  of  the  nose,  lobules  of  the  ears,  lips,  and  chin, 
and  as  they  increase  in  size,  totally  alter  the  appearance  of  the 
patient,  defacing  the  natural  facial  lines,  and  forming  new  furrows 
between  adjacent  nodules;  while  at  the  same  time,  in  many  cases,  the 
hair  of  the  beard,  moustache,  and  eyebrows  drops  out .  These  changes 
result  in  the  countenance  becoming  like  that  of  a  satyr  or,  when 
the  furrows  are  more  marked,  like  that  of  a  lion;  hence  the  terms 
'  satyriasis '  and '  leontiasis,'  which  the  ancients  applied  to  the  disease. 

Eye  lesions  are  more  commonly  met  with  in  this  form  of  the 
disease,  for  Borthen,  as  the  result  of  his  investigations,  concludes 
that  only  8-o8  per  cent,  of  women  and  1-67  per  cent,  of  men  suffer- 
ing from  tubercular  leprosy  escape  without  some  form  of  disease  of 
the  eyes  or  their  adnexa.     Women  are,  however,  less  affected  than 


TUBERCULAR  LEPROSY 


i655 


men,  but  age  shows  no  influence  on  the  production  of  eye  affections. 
In  tubercular  leprosy  the  eye  is  attacked  by  genuine  leprotic  lesions, 
and  secondary  infections  are  rare. 

The  supraciliary  region,  as  has  already  been  mentioned,  is  early 
attacked,  and  complete  madarosis  is  not  uncommon,  and,  later, 
paralysis  of  the  frontalis  muscle  sets  in.  The  eyelids  are  often 
attacked  by  diffuse  or  nodular  lepromata,  which  may  be  ..merely 


Fig.  727. — Leprosy,  showing  the^Erysipelatous-like  Eruption 
on  the  Arms  and  Face. 


extensions  from  the  disease  already  in  the  supraciliary  region, 
or  may  be  quite  distinct  lesions.  As  a  result  of  ulceration  of  these 
nodules,  the  eyelids  may  be  destroyed. 

The  conjunctiva  may  be  infiltrated,  leading  to  hyperemia,  or, 
more  rarely,  anaemia,  and  producing  lagophthalmos,  ectropion,  and, 
if  cicatrization  takes  place,  xerophthalmia. 

The  episclera  is  apt  to  become  infiltrated  along  the  external 


1656  LEPROSY 

aspect  of  the  corneo-selerotic  junction,  resulting  in  white,  grey,  or 
yellow  flattish  masses,  which  spread  round  the  cornea  dorsally  and 
ventrally,  and  are  prone  to  invade  its  tissue  in  the  form  of  a  diffuse 
infiltration,  which  spreads  from  the  outer  side  towards  the  pupil. 

More  rarely  small  spots  form  on  the  cornea,  giving  rise  to  the 
'  keratitis  punctata  leprosa  '  of  authors. 

The  disease  may  also  spread  to  the  uveal  region,  in  the  form  of 
an  infiltration,  which  causes  an  anterior  or  posterior  iritis;  or,  more 


Fig.  728. — Typical  Tubercular  Leprosy,  showing  the  Leonine  Expres- 
sion, the  Thickened  Superciliary  Ridges,  and  the  Madarosis. 

rarely,  nodules  may  form  in  the  ciliary  body  or  near  the  canal  of 
Fontana,  giving  rise  to  an  irido-cyclitis  or  irido-choroiditis. 

Lie  has  studied  the  pathology  of  these  lesions,  and  has  shown 
that  it  is  rare  for  the  optic  nerve,  the  retina,  the  lens,  and  the 
vitreous  humour  to  be  affected. 

The  mucosae  of- the  nose  may  be  attacked,  with,  first,  blocking  of 
the  passage,  and  then,  when  the  leproma  extends  down  to  the 
cartilage  and  ulcerates,  falling-in  or  destruction  of  the  nose,  with 
much  disfiguration  of  the  countenance,  resulting  from  the  cica- 
trization which  follows  the  ulceration.     The  tongue  may  also  be 


TUBERCULAR  LEPROSY 


1657 


affected,  and  show  numerous  tubercles,  separated  by  furrows,  or 
it  may  be  simply  infiltrated.  The  walls  of  the  mouth  and  pharynx 
may  become  lepromatous,  which  causes  mastication  and  deglutition 
to  be  rendered  difficult,  while  the  same  condition  in  the  larynx 
makes  the  voice  raucous,  and  may  impede  respiration,  especially 
if  there  is  ulceration  and  cicatrization. 
The  skin  of  the  hands,  arms,  and  legs  also  shows  numerous  raised 


Fig.  729. — Diffuse  Infiltration  of  Both  Corneas  and  Deformities 
in  the  Fingers  of  the  Right  Hand. 


tub'crcles.  which  may  ulcerate.  The  nipple  is  often  infiltrated. 
The  submaxillary,  cervical,  and  femoral  glands  may  be  enlarged, 
and  may  suppurate.  The  testes  often  become  fibrous,  and 
menstruation  becomes  irregular  and  stops. 

Blood. — In  the  early  stages  the  blood  shows  no  changes,  but  later 

it  shows  a  diminution  in  the  erythrocytes  and  a  lowering  in  the 

.colour  index.     The  red  cells  may  show  abnormalities  in  the  form  of 

poikilocytes,  polychromatophilia,  and  basophilia.     The  number  of 


i658 


LEPROSY 


leucocytes  is  generally  normal,  or,  according  1  o  Bourret,  diminished; 
while  this  observer  records  an  eosinophilia  in  all  stages  of  the 
disease,  which  he  says  may  at  times  be  quite  considerable.  There 
may  be  leucocytosis  during  the  febrile  attack.  Neutrophile  myelo- 
cytes may  also  be  observed.  According  to  our  researches  the 
leucocytic  formula  is  extremely  variable,  and  is  of  no  help  in  the 


Fig.  730. — Leproma  of  the  Tongue. 


diagnosis  of  the  malady.  In  an  early  case  the  differential  count 
of  i.ooo  leucocytes  showed  polymorphonuclears  52  per  cent.,  large 
mononuclears  38  per  cent.,  small  lymphocytes  3-3  per  cent.,  eosino- 
phil es  6  per  cent.,  basophile  cells  07  per  cent.  This  agrees  with 
Sadi  de  Buen's  observations, who  also  finds  that  Arneth's  index  is 
generally  shifted  to  the  left,  but  who  also  finds  that  there  is  no 


MACULO-AN ESTHETIC  LEPROSY  1659 

special  leucocytic  index.  Some  authors  state  that  they  have  found 
the  specific  bacillus  in  leucocytes,  or,  more  rarely,  free  in  the  peri- 
pheral blood.  Wassermann's reaction  is,  in  our  experience,  at  times 
present  even  in  cases  where  there  is  no  history  of  syphilis  or  yaws. 

Urine. — There  are  not  "many  observations  upon  the  urine.  The 
most  marked  feature  is  a  great  increase  in  the  ethereal  sulphates. 
Brinton,  of  Rio  de  Janeiro,  has  isolated  two  ptomaines  from  the 
urine,  one  allied  to  choline  and  the  other  to  muscarine. 

The  nerves  may  become  attacked,  and  the  signs  and  symptoms 
of  nerve  leprosy  be  added  to  those  of  the  tubercular,  forming  a 
variety  of  mixed  leprosy. 

The  ulcerations  generally  become  marked  towards  the  end  of 
the  disease.  If  treated,  they  cicatrize  and  produce  deformities; 
if  left  to  themselves,  they  suppurate  and  produce  amyloidosis,  or, 
becoming  phagedaenic,  cause  gangrene  of  the  fingers  or  toes,  and 
septic  poisoning. 

Complications,  in  the  form  of  phthisis  and  amyloidosis,  appear, 
causing  fever,  cough,  and  expectoration,  diarrhoea,  and  enlargement 
of  liver  and  spleen. 

Unfortunately,  in  the  midst  of  disease  of  almost  every  organ 
of  the  body,  the  mind  is  quite  clear;  but  the  patients  are  most 
irritahle,  and  it  is  not  surprising  that,  under  these  circumstances, 
the  patients  of  a  leper  asylum  require  considerable  tact  in  manage- 
ment, and  are  often  peevish  and  discontented,  and  that  small 
rebellions  occur. 

MACULO-AN^STHETIC  LEPROSY. 

In  this  form  of  leprosy  the  infiltration  takes  place  principally 
into  the  nerves,  with  the  result  that  first  the  fibres  are  irritated, 
and  later  they  become  destroyed.  The  first  stage  is  therefore  one 
of  irritation  of  the  nerves,  with  such  symptoms  as  shooting-pains 
down  certain  nerves,  especially  the  ulnar  and  the  peroneal,  accom- 
panied with  sensory  disturbances,  such  as  burning,  numbness, 
formication,  along  with  vasomotor  disturbance — e.g.,  flushings  of 
the  face,  glossy  skin — and  motor  disturbance,  such  as  twitching 
of  the  muscles,  particularly  of  the  face. 

Sooner  or  later  a  macular  eruption  appears,  which  is  looked  upon 
by  some  as  due  to  a  lepromatous  infiltration  of  the  skin,  and  by 
others  as  nervous  in  origin.  This  macular  eruption  may  appear 
as  flat  red  spots  of  various  shapes  and  sizes,  neither  hyperaesthetic 
nor  anaesthetic  at  first,  which  appear  without  fever  or  any  general 
disturbance  of  the  health.  Other  maculae  may  appear  which, 
instead  of  being  red,  are  simply  pigmented,  while  still  others  may 
be  seen  in  which  the  pigmentation  is  les?  than  usual.  In  any  case 
the  spots  grow  larger,  the  centres  becoming  pale,  while  the  peri- 
pheries, which  are  usually  raised,  and  occasionally  marked  with 
papules  or  vesicles,  or  covered  with  dry  whitish  scales,  may  coalesce 
with  other  spots,  forming  large  areas. 


i66o 


LEPROSY 


The  skin  in  the  affected  area  becomes  anaesthetic;  the  hairs  fall 
out,  and  wrinkles  and  scales  appear.  After  a  time  the  areas  cease 
to  spread,  the  raised  margin  disappears,  and  the  disease  becomes 
quiescent. 

Meanwhile  the  infiltration  into  the  nerve  trunks  has  proceeded 
to  such  an  extent  that  a  swelling  can  be  easily  felt  in  certain  regions 
— as,  for  example,  in  the  ulnar  behind  the  internal  condyle,  in  the 
great  auricular  over  the  sterno-mastoid,  in  the  peroneal  just  below 
the  head  of  the  fibula,  and  in  other  nerves  in  suitable  places  if 
affected.  With  the  destruction  of  the  nerve  fibres,  the  hyper- 
aesthetic  stage  ceases  and  the  anaesthetic  stage  of  the  disease  begins. 


Fig.  731. — Maculo- Anesthetic  Leprosy:  Circinate  Type. 


This  is  to  be  noticed  along  the  ulnar  side  of  the  hand,  forearm,  and 
arm,  or  on  the  inner  side  of  the  foot,  first  of  all,  and  afterwards  in 
other  places.  It  may  be  segmental  in  arrangement,  restricted  to  the 
distribution  of  a  nerve,  or  in  patches.  At  the  same  time  the  muscles 
may  be  found  to  be  paralyzed,  notably  the  interossei  of  the  hands, 
but  also  those  of  the  foot,  if  carefully  looked  for.  The  lower  efferent 
neurones  being  affected,  the  symptoms  resemble  those  of  muscular 
atrophy  of  the  Aran-Duchcnne  type,  with  the  production  of  the 
main-en-griffe  and  the  extension  of  the  paralysis  to  the  muscles  of 
the  forearm,  and  even  at  times,  according  to  Jeanselme,  to  the 
deltoid.  As  a  result  of  the  paralysis  of  the  muscles  of  the  fore- 
arm the  occurrence  of  dropped  wrist  is  not  uncommon. 


MACULO- AN /ESTHETIC  LEPROSY 


1661 


In  the  lower  limb  the  plantar  muscles  of  the  toes  maybe  affected, 
while  the  spread  of  the  paralysis  to  the  peronei  and  extensors  may 
result  in  a  dropped  foot  with  an  internal  twist.  The  reflexes  are 
exaggerated  at  first,  but  when  paralysis  sets  in  they  diminish,  and 
when  the  muscles  waste,  the  reaction  of  degeneration  may  be 
obtained  electrically. 


Fig.  732. — Maculo-An^esthetic  Leprosy. 


Trophic  lesions  may  also  appear  in  the  form  of  whitlows  in  t lie 
fingers  and  necrosis  of  the  phalanges,  or,  instead  of  this,  a  simple 
absorption  of  the  bone  of  the  phalanx  or  metacarpal,  so  that  the 
nail  may  ultimately  appear  to  spring  from  the  metacarpal,  the 
wris^,  or  even,  it  has  been  said,  from  the  elbow.  Similar  trophic 
lesions  may  appear  in  the  foot.     Bullae  may  appear  on  the  hands 


1662 


LEPROSY 


or  feet,  and  when  broken  may  form  ulcers.  Injuries  to  anaesthetic 
areas  may  also  result  in  ulcers,  which  may  be  of  the  perforating 
type.  Fissures  may  form  in  the  digits,  hands,  or  feet,  and,  more 
rarely,  dry  gangrene  may  cause  loss  of  the  fingers  or  toes,  or  greater 
portions  of  the  limbs,  and,  still  more  rarely,  the  bones  of  the 
fingers  will  soften  and  become  osteomalacic.  Trophic  lesions  of 
the  elbow  or  knee,  like  Charcot's  joints,  have  been  recorded. * 

Jeanselme,  Bourret,  and  one  of  us  have  studied  the  cerebro- 
spinal fluid,  and  have  found  in  a  few  cases  a  lymphocytosis,  but 
more  usually  no  cells  or  bacilli. 

The  eye  is  far  less  commonlyaff  ected  than  in  the  tubercular  variety, 
Borthen's  figures  showing  that  in  anaesthetic  leprosy  no  less  than 
36*83  per  cent,  of  the  female  cases  and  26-80  per  cent,  of  the  male 
cases  escape  without  eye  complications.     True  leprotic  lesions  are 


Fi".  733. — Leprosy:  Ulcer  of  the  Foot. 


much  rarer,  the  eye  beinsr  damaged  by  secondary  infections  brought 
about  by  the  absence  of  the  lachrymal  secretion  and  the  lagoph- 
thalmos.  The  forehead  and  supraciliary  regions  are  often  red- 
dened and  cedematous,  but  complete  madarosis  is  rare;  while 
paralysis  of  the  frontalis,  corrugator  supercilii,  and  orbicularis 
palpebrarum  cause  lagophthalmos  and  ectropion;  and  as  there  is 
a  diminution  in  the  secretion  of  tears,  xerophthalmia  with  posterior 
or  total  symblepharon,  while  desiccation  and  destruction  of  the 
cornea  may  result. 

Secondary  infections  may  lead  to  keratitis,  onyx,  hypopyon, 
iritis,  irido-cyclitis,  and  destruction  of  the  eye. 

Sterility  is  not  so  frequent  in  nerve  as  in  tubercular  lepros}'. 
The  skin  may  become  infected  at  an  early  or  late  stage  of  nerve 
leprosy,  thus  forming  one  of  the  types  of  mixed  leprosy. 


MACULO-ANMSTHETIC  LEPROSY  1663 

Mixed  Leprosy. 

This  term  has  been  used  to  comprise  those  cases  of  tubercular 
leprosy  which  develop  nerve  symptoms,  and  those  of  maculo- 
amesthetic  leprosy  which  develop  nodules,  as  well  as  those  general 
cases  in  which  both  nerve  and  skin  lesions  advance  hand  in  hand. 

Paraleprosis. 

Zambaco,  Von  Duhring,  Gliick,  Lebceuf,  and  others  have  drawn 
attention  to  various  phenomena  indicating  an  attenuated  in- 
fection in  regions  in  which  leprosy  has  long  existed.  These 
conditions  are  mostly  nerve  or  trophic  changes — e.g.,  thickening  of 
the  ulnar  nerve,  the  curving  of  the  fingers,  the  loss  of  phalanges,  the 
atrophy  of  the  muscles  of  the  hand  or  face,  which  are  present  in  the 
children  or  grandchildren  of  lepers.  Further,  it  is  believed  by  some 
authors  that  syringomyelia  and  Morvan's  disease  may  be  modified 
forms  of  leprosy.  Paraleprosis,  however,  requires  further  investiga- 
tion. 

Complications. — The  important  complications  of  leprosy  are 
nephritis,  phthisis,  chronic  enteritis,  and  dysentery.  Amyloidosis 
occurs  in  the  internal  organs  if  there  is  much  discharge  from 
ulcerated  surfaces.  An  interesting  case  of  mixed  infection — 
leprosy  and  syphilis — has  been  described  by  Frugoni. 

Diagnosis. — The  diagnosis  of  ca?es  of  the  nodular  type  is  generally 
easy,  and  may  be  readily  confirmed  bacteriologically  by  excision  of 
a  nodule  and  microscopical  examination  of  a  portion  for  Hansen's 
bacillus.  The  diagnosis  of  the  maculo- anaesthetic  cases  presents 
greater  difficulties,  especially  as  in  most  cases  the  bacteriological 
examination  of  excised  portions  of  the  patches  will  give  a  negative 
result,  though  occasionally  the  examination  of  the  blood  taken  from 
the  patches  or  the  surrounding  zone  may  show  a  few  mononuclear 
leucocytes  containing  bacilli.  In  these  cases  the  diagnosis  must 
be  based  on  the  presence  of  anaesthesia  in  the  erythematous,  non- 
pigmented,  or  hyperpigmented  patches.  Another  valuable  sign 
will  be,  in  many  cases,  the  palpable  enlargement  of  the  ulnar, 
peroneal,  and  other  nerves.  The  search  for  the  lepra  bacillus  in 
the  nasal  mucus  is  sometimes  useful  to  clear  the  diagnosis.  This 
method  of  diagnosis  may  be  facilitated  by  administering  a  full  dose 
(30  grains)  of  iodide  of  potassium,  which  oft  en  produces  nasal  catarrh. 
Sometimes  this  drug  produces  a  general  reaction  accompanied  by 
fever,  and  the  appearance  of  fresh  nodules.  Lebceuf,  acting  on 
Marchoux's  suggestion,  has  found  Hansen's  bacillus  in  the  enlarged 
superficial  lymphatic  glands,  and  recommends  the  examination  of 
the  gland  juice  as  a  method  of  diagnosis.  It  is  to  be  noted,  how- 
ever, that  this  examination  will  give  a  positive  result  much  more 
frequently  in  nodular  cases  than  in  the  macular  type  of  the  disease. 

Chujo  recommends  drawing  5  c.c.  of  blood  from  the  arm, ^diluting  it  with 
200  c.c.  of  a  3  p^r  cent,  solution  of  acetic  acid,  avoiding  contact  with  the  air. 


1664  LEPROSY 

The  microscopical  examination  would  give  more  than  50  per  cent,  of  positive 
results. 

Some  authors  recommend  the  blistering  of  the  skin,  and  examination  of 
the  liquid  of  the  blebs  for  the  presence  of  Hansen's  bacillus.  Thompson 
recommends  for  diagnostic  purposes  the  injection  of  pilocarpine,  with  the 
view  of  discovering  dry  areas  in  the  sweating  skin. 

Differential  Diagnosis. — In  countries  where  leprosy  is  endemic, 
other  diseases  are  liable  to  be  mistaken  for  it.  One  of  the  diseases 
most  frequently  mistaken,  as  has  been  pointed  out  by  Powell  and 
others,  is  frambcesia,  which  may  be  recognized  by  the  presence  of 
the  Treponema  pertenue  and  the  frambcesiform  appearance  of  the 
nodules.  Leucodermic  patches  and  morphcea  are  also  occasionally 
mistaken  for  leprosy,  but  in  such  conditions  there  is  no  anaesthesia. 

Prognosis. — The  prognosis  is  not  good.  The  probability  of  a 
permanent  cure  is  slight,  but  the  disease  may  last  a  long  time. 
Four  to  twelve  years  is  laid  down  for  the  mixed  or  tubercular 
leprosy,  and  longer  for  the  maculo-anaesthetic,  and  during  that 
time  a  great  deal  can  be  done  by  appropriate  treatment;  and, 
indeed,  the  disease  may  be  stopped  for  the  time  being,  only, 
usually,  to  recur  again.  It  has  been  shown  by  Lie  that,  even  when 
all  the  skin  eruptions  have  disappeared,  and  the  patient  is  only 
troubled  by  anaesthesia,  and  the  atrophy  of  the  muscles,  and  may 
be  thought  to  be  cured,  still  the  bacilli  are  present  in  the  nerves 
and  spinal  cord. 

Lebceuf  from  his  recent  investigations  in  New  Caledonia  has  come  to  the 
conclusion  that  in  a  certain  number  of  cases  showing  slight  symptoms,  an 
actual  cure  takes  place. 

Treatment. — So  far  no  specific  treatment  has  been  found,  though 
Carrasquilla  attempted  to  prepare  a  serum  by  the  injection  of  the 
blood  of  lepers  into  equines,  and  Abrahams  and  Hermann  by 
inoculating  the  juice  from  lepromata  into  an  animal.  These  sera 
have  been  found  useless.  Rost  prepared  a  substance,  which  he 
called  '  leprolin,'  on  the  lines  of  tuberculin,  but,  unfortunately, 
the  bacillus  he  was  using  was  not  the  leprosy  organism.  Clegg's 
vaccine  and  Bayon's  extract  of  Kedrowsky's  strain  have  not  been 
very  successful.  Tuberculin  has  been  tried  without  success,  and, 
in  fact,  very  serious  symptoms  may  follow  its  injection. 

Chanhnoogra  Oil. — As  regards  symptomatic  treatment,  there  is 
no  doubt  as  to  the  great  value  of  Chaulmoogra  oil,  which  is  said  to 
be  obtained  by  cold  expression  from  the  seeds  of  some  species  of 
Gynocardia  [vide  infra),  but  may  be  adulterated  with  other  oils, 
especially  that  of  Hydnocarpns  wightiana,  or  may  be  altered  by  being 
expressed  when  heated.  It  should  be  rubbed  into  the  diseased 
patches,  and  also  given  internally  in  doses  of  5  to  10  minims, 
working  up  gradually  to  30  to  60  minims,  in  capsules,  or  in  a  pill 
with  tragacanth  and  soap,  or  in  an  emulsion,  or  as  Engel-antileprol 
capsules.  To  remove  the  after-taste  a  lime  can  be  sucked.  This 
treatment  must  be  persisted  in  for  a  very  long  time,  and  should  be 


TREATMENT  1665 

combined  with  hot  baths,  and,  in  nerve  cases,  with  doses  of  strych- 
nine, ^V  grain  three  times  a  day,  which  may  gradually  be  increased. 
After  a  length  of  time  it  is  as  well  to  make  a  slight  break  in  the 
treatment,  to  prevent  toleration,  and  therefore  Unna's  ointment  of 
ichthyol,  5  per  cent.;  salicylic  acid,  2  per  cent.;  and  pyrogallol, 
5  per  cent. ,  or  some  other  ointment,  may  be  temporarily  substituted. 
But  the  Chaulmoogra  oil  must  not  be  long  discontinued,  and  must 
be  persisted  in  for  two  years  or  longer  if  any  good  is  to  be  obtained. 
The  oil  may  be  given  hypodermically,  but  is  badly  absorbed. 
To  facilitate  its  absorption  Heiser  has  successfully  combined  it  with 
camphorated  oil,  and  Mercado  has  combined  the  mixture  with  the 
resorcin  formula  of  Unna.     Heiser's  present  formula  is — 

Chaulmoogra  oil         . .  . .     60  c.c. 

Camphorated  oil         . .  .  .     60    , , 

Resorcin  . .  . .  . .     grms.  4 

Mix  and  dissolve  with  the  aid  of  heat  on  a  water  bath  and  then  filter. 

The  injections  are  made  in  the  gluteal  region,  at  weekly  intervals, 
in  ascending  doses,  one  to  five  or  ten  cubic  centimetres.  During 
the  treatment  the  patient  takes  a  hot  sodium  bicarbonate  bath 
(2  per  cent.)  every  other  day.  The  results  are  fairly  satisfactory. 
Sodium  Gynocardate. — Rogers  recommends  the  intravenous  in- 
jections of  sodium  gynocardate,  which  is  supplied  in  sterile  vials  by 
Smith,  Stanistreet  and  Co.  in  doses  of  TV  grain  and  upwards.  There 
is  a  definite  reaction,  local  and  general,  after  the  injection.  He  also 
gives  gynocardic  acid  and  sodium  gynocardate  orally  in  2  grain 
pills  after  meals,  or  by  subcutaneous  injection. 

Neumann  has  advised  the  combination  of  salve  and  theonin  with  Chaul- 
moogra, given  either  by  the  mouth  or  hypodermically,  but  the  advantages 
are  doubtful,  and  Hollmann  has  recommended  the  use  of  eucalyptus  oil  in 
conjunction  with  opia  leaves  (Jambos  malaccenois)  or  with  Chaulmoogra  oil. 

Sources  of  Chaulmoogra  Oil. — According  to  Ghosh,  true  Chaulmoogra  is 
Taractogenes  kurzii  from  Burma  and  Assam ;  false  Chaulmoogra  is  Gynocardia 
odorata  from  Sikkim,  Assam,  and  Chittagong;  other  Chaulmoogras  are  Asteri- 
astigma  macrocarpa,  Hydnocarpus  venenatus,  H.  wightianus,  H.anthclminticus. 
The  oil  known  in  Europe  as  Chaulmoogra  is  said  never  to  come  from  G.  odorata. 

Cod-liver  Oil  and  Sodium  Morrhuate. — Cod-liver  oil  is  occasionally 
beneficial.  Rogers  recommends  an  intramuscular  injection  (1  to  3  c.c.) 
every  other  day  of  a  3  per  cent,  solution  of  sodium  morrhuate. 

Other  remedies  are  legion — e.g.,  X  rays  have  been  well  spoken 
of,  but  must  be  pushed  to  the  extent  of  almost  burning  the  patient. 
A  10-inch  spark-coil  with  a  bifocal  tube,  situate  7  to  10  inches 
from  the  lesion,  has  been  used.  Hypodermic  injections  of  per- 
chloride  of  mercury,  as  advocated  by  Crocker  (o-oi  gramme  every 
other  day),  have  been  found  satisfactory  at  times — a  treatment 
which  we  recommend  in  cases  at  the  very  beginning  of  the  disease. 

Cashew  nuts  (Beauperthuy  treatment)  have  been  applied  to  the  lepromata 
with  the  idea  of  local  caustic  action.  Thyroid  gland,  salol,  salicylates,  arsenic, 
Gurjun  oil,  chlorate  of  potash,  iodine,  hypodermic  injections  of  iodoform, 
have  all  been  tried  and  found  wanting. 

i°5 


1 666  LEPROSY 

Hypodermic  injections  of  '  nastin  '  have  been  tried.  This  is 
a  fatty  principle  extracted  by  Deycke  from  cultures  of  a  strep- 
tot  hrix  (Streptothrix  leproides),  which  he  found  in  the  nodules 
of  leprotic  patients.  The  nastin  is  combined  with  benzoyl  chloride, 
and  made  into  ampoules  with  sterilized  olive  oil  by  Kolle  and 
Company,  of  Biebrich,  on  the  Rhine.  Each  ampoule  contains  from 
0*0005  to  0-0002  gramme  of  nastin,  which  is  to  be  injected  once  a 
week,  and  in  the  small  doses  produces  no  local  reaction,  but  in  the 
larger  dose  causes  considerable  local  inflammation.  Deycke's 
views  as  to  the  method  of  action  are  that  the  nastin  attaches  itself 
to  the  lepra  bacillus,  and  then  the  benzoyl  acts  on  the  bacillus, 
damaging  it  by  removal  of  its  fat,  when  the  normal  fluids  of  the 
body  complete  its  destruction. 

Wise  and  Minett  and  others  have  reported  unfavourably  on  this 
treatment,  but  recommend  benzoyl  chloride  in  petroleum  oil  as  a 
valuable  nasal  spray  or  paint,  as  it  renders  the  discharge  from  the 
nose  free  from  bacilli. 

Castellani  and  Woolley,  and  more  recently  Nicholls,  have  tried 
a  vaccine  prepared  by  triturating  nodules  rich  in  bacilli  in  salt 
solution  or  broth,  then  filtering  through  gauze,  and  finally  heating 
to  6o°  C.  for  an  hour. 

Pasini  has  tried  Finsen  light,  and  Beurmann  radium,  with  good  results,  and 
Duque,  Moreno,  and  Padilla  have  obtained  considerable  improvement,  and  it  is 
said  cures,  by  treatment  with  decoctions  of  20  to  60  grammes  or  2  to  5  grammes 
of  the  powdered  mangrove  Rhizophora  mangle,  which,  given  in  small  doses 
at  first,  and  gradually  increased,  are  well  stood,  and  produce  a  gradual 
improvement  in  the  symptoms;  and  in  the  course  of  a  year,  it  is  said,  cases 
may  be  cured.  A.  Bertarelli  has  obtained  temporary  good  results  by  treating 
a  patient  with  hypodermic  injections  of  a  solution  of  carbolic  acid.  Wellman 
and  Rocamara  have  tried  salvarsan,  and  claim  good  results.  Maxwell  has  tried 
Williams'  leprolin  and  Malegin  Sprengler's  I.K.  Lepra  with  good  results. 
Sugai  recommends  intravenous  injections  of  a  solution  of  potassium  cupro- 
cyanide. 

Surgical  treatment  on  the  ordinary  lines  is  required  for  ulcers, 
whitlows,  etc.  Eye  lesions  should  be  treated  as  though  the  disease 
was  non-leprous,  and  should  not  be  neglected.  Grossmann  thinks 
that  leprous  infiltration  might  be  arrested  by  the  production  of 
cicatricial  tissue,  by  a  corneal  or  pericorneal  incision. 

With  regard  to  other  measures,  lepers  should  be  provided  with 
plenty  of  fresh  air  and  good  food,  and  their  quarters  should  be 
kept  strictly  clean.  Care  should  also  be  taken  that  they  are 
supplied  with  some  form  of  light  work  and  amusement,  and  the 
institution  of  rural  colonies,  provided  they  are  well  supervised,  is 
to  be  recommended. 

Prophylaxis. — Beyond  isolation  and  antiseptic  precautions  after 
handling  leprous  people,  nothing  more  can  be  done,  as  so  little  is 
known  about  the  causation  of  the  disease.  The  financial  burden  of 
isolating  large  numbers  of  lepers  is  very  heavy.  Hence  the  diffi- 
culty of  carrying  out  this  very  necessary  method  of  protection 
completely  and  efficiently. 


REFERENCES  1667 


REFERENCES. 

The  current  literature  may  be  found  in  the  periodical  Lepra,  which  started 
in  1897, and  inthe  Tropical  Diseases  Bulletin.  In  1915  McCoy  gave  a  summary 
up  to  date  of  our  knowledge  of  leprosy  in  the  American  Journal  of  Tropical 
Diseases  and  Preventive  Medicine  for  August,  vol.  hi.,  No.  2,  pp.  83-91. 

Abraham    (1890-1918).      Several   important   papers   in   the    Brit.    Jour,    of 

Dermatology. 
Balzer  (1918.)     Bull.  Soc.  Med.  Hop.  de  Paris,  May  (Cod-liver  Oil  in  Leprosy). 
Barl£zieux  (1914).     Janus,  132-149  (History). 
Bayon    (191 2).     South    African    Medical    Record.     Cape    Town.     (Present 

Position  of  Leprosy  Research.)     (1913).     Ibid.,  June  14. 
Bensen  (1877).     Dublin  Journal  of  Medical  Science. 
Black  (1906).     Lancet,  i.  1167 ;  ii.  1064. 
Borthen   (1899).     Klinische   Studien,  iv.     Leipzig.     (This  is  the  standard 

work  on  leprosy  of  the  eye.) 
Bourret  (1908).     Bull,  de  la   Societe  de  Path.  Exot.,  56  (Blood  Examina- 
tion). 
Bull  and  Hansen  (1873).     Leprous  Diseases  of  the  Eye.     Christiania. 
Campana  (1907).     La  Lebbra.    Roma. 

Castellani  (1906).     Journal  Ceylon  British  Medical  Association. 
Coghill   (191 7).     Annals   of  Tropical   Medicine   and   Parasitology   (Heiser's 

Treatment). 
Danielssen  and  BoecK  (1848).     Traite  de  la  Spedalskhed.     Paris. 
Dean  (1905).     Journal  of  Hygiene,  v. 
De  Silva  (1907).     British  Medical  Journal,  ii.  1235. 
Deycke    (1905).      Deutsche    Medicinische    Woch.,    1314    (1907);    ibid.,    3; 

1907,  Lepra,  vii.  3,  174  (Nastin). 
Diaz  (1918).     Bol.  Asoc.  Med.  de  Puerto  Rico,  March. 
Dubreuilh  and  Bargues  (1914).     La  Lepre  de  la  Bible.     Lepra,  vol.  xv., 

No.  1,  p.  5. 
Duval  (191 2).     British  Medical  Journal. 
Fijik  (1918).     Treatment  of  Leprosy.     Suva. 
Frugoni  (1909).     Arch.  f.  Dermat.  u.  Syph. 
Frugoni  and  Pisani  (1909).     Arch.  Scienze  Mediche. 
Grossman  (1906).     British  Medical  Journal,  i.  11  (Eye  Lesions). 
Heiser  (1916).     New  York  Med.  Journal,  February  12  (Chaulmoogra  Oil  by 

Hypodermic  Injection). 
Hill  (1916).     New  York  Med.  Journal  (The  Non-Identity  of  Modern  Leprosy 

and  Biblical  Leprosy). 
Honeij    (1916).     New   Orleans   Medical   and   Surgical   Journal,    September, 

219-222  (Bone  Changes). 
Hutchinson  (1907).     Leprosy  and  Fish-eating.     London. 
Jamamento  (1908).     Centralblatt  fur  Bakteriologie. 

Kedrowsky  (1914).     Archiv  f iir  Dermatologie,  vol.  120,  267-284  (Histology). 
Leboeuf,  A.  (1912).     Bull.  Path.  Exot. 

Leloir  (1886).     Trait6  Pratique  et  Theoretique  de  la  Lepre.     Paris. 
Macleod    (1909).     British    Medical    Journal.     (1912).     British    Journal    of 

Dermatology. 
Mantegazza,  U.  (1903).     La  Lepra.     Florence. 
Marchoux   and   Bourret  (1908).     Bull,  de  la  Soc.   de  Path.   Exot.,  416 

(Inoculation  of  a  Chimpanzee) . 
Marchoux  and  Sorel  (1912).     Ann.  Inst.  Past. 
Minnet  (1912).     Journal  of  the  London  School  of  Tropical  Medicine.     London. 

(Nastin  Treatment.) 
Montgomery  (191 5).     Journal  American  Medical  Association,  September  11 

(History  of  Leprosy) . 
Muir  (1919).     Indian  Med.  Gazette. 
Neve  (1900).     British  Medical  Journal,  i.  1153  (Eye  Lesions). 


1 658  LEPROSY 

Nicholson  (1905).     Journal  of  Tropical  Medicine,  viii.  293   (Treatment  by 

Mangrove) . 
Nicolle  (1905).     Compt.  rendus  de  l'Acad.  de  Science.     Paris. 
Peacock  (1918).     Indian  Med.  Gazette,  March. 
Rogers  (1916).     British  Medical  Journal,  ii.  550-552  (Intravenous  Injections 

of  Sodium  Gynocardate) .     Also  Lancet,  February  5. 
Rogers  (1919).      Brit.  Med.  Jour.,  February  8  (Sodium  morrhuate). 
Spittel  (1918).     Indian  Med.  Gazette. 
Stanziale  (1915).     Centr.  f.  Bakt.,  March. 
Suldey  (1918).     Bull.  Soc.  Path.  Exot.,  vol.  xi.,  No.  2. 
Terra  and  Moreira  (191 8).     Brazil  Medico,  August  24. 
Terra  (1919).     Brazil  Medico,  February  1. 
Thompson  (1907).     Lancet,  ii.  1514. 
Tonkin  (1903).     Lancet,  i.  1077. 

Unna  (1896).     Histopathology  of  the  Skin,  118  (Neurolepride),6o6  (Leproma). 
Van  Houten  (1902).     Journal  of  Pathology  and  Bacteriology,  viii.  260. 
Wise  (1912).     Journal  of  the  London  School  of  Tropical  Medicine.     London, 

(Pulmonary  Lesions.) 
Woit  (1900).     Lepra,  i.  50,  103,  179  (Spinal  Cord). 
Wood  (191 3).     South  African  Medical  Record  (Eye  Complications). 
Woolley  (1907).     Proceedings  of  the  Society  of  Experimental  Biology  and 

Medicine. 


CHAPTER  LXX 
HISTOPLASMOSIS 

Definition — History — ^Etiology — Pathclcgy — Morbid    anatomy — Symptoma- 
tology— Treatment — References. 

Definition. —  Histoplasmosis  is  an  acute  specific  infection  caused 
by  Histoplasma  capsulatum  Darling  (Cryptococcus  capsulatus 
Darling). 

History. — This  disease  has  been  described  by  Darling,  who  also 
found  the  parasite,  but  being  first  discovered  post  mortem,  the 
clinical  signs  are  rather  deficient.  The  first  case  was  in  a  negro 
who,  three  months  previously,  had  come  from  Martinique  to  the 
Canal  zone  of  Panama. 

/Etiology. — The  disease  is  caused  by  the  parasite  Histoplasma 
capsulation  Darling,  which  was  at  first  considered  to  be  a  proto- 
zoon,  but  is  now  believed  to  be  a  fungus  (Cryptococcus  capsulatus 
Darling,  p.  1076). 

Pathology. — -The  parasite  infects  epithelial  and  endothelial  cells 
of  the  lungs,  liver,  and  spleen.  It  also  exists  free  in  these  organs. 
In  the  lungs  it  gives  rise  to  pseudo-tubercles  resembling  miliar}- 
tubercles. 

Morbid  Anatomy. — In  the  first  case  there  were  ecchymoses  and 
small  nodules  beneath  the  visceral  pleura  of  both  lungs,  which  was 
studded  throughout  with  pale  grey  hyaline  and  miliary  tubercles, 
2  to  3  millimetres  in  diameter,  while  the  remainder  of  the  organs  were 
of  a  bright  red  colour.  The  peribronchial  glands  were  full  of  soft 
caseated  tubercles.  The  heart  was  small,  but  normal.  The  liver 
was  enlarged,  pale,  and  in  a  condition  of  slight  atrophic  cirrhosis. 
The  spleen  was  enlarged  to  about  three  times  its  usual  size,  very 
firm,  with  distinct  Malpighian  bodies.  The  kidneys  were  slightly 
cirrhotic;  the  pancreas,  bladder,  bone-marrow,  and  brain  were 
normal,  and  no  tubercle  bacilli  could  be  found. 

Microscopically  the  lung  tubercles  were  found  to  consist  of 
alveoli,  the  walls  of  which  were  broken  and  collapsed,  and  were 
filled  with  alveolar  epithelial  cells  distended  with  parasites.  In  the 
liver  the  hepatic  cells  and  the  vascular  endothelial  cells  were  much 
infected  with  parasites.  Some  areas  which  stained  badly  were 
found  to  consist  simply  of  the  debris  of  cells  with  numerous  para- 
sites.    The  spleen  showed  intracellular  and  free  parasites. 

1669 


1670  HISTOPLASMOSIS 

Symptomatology. — The  symptoms  closely  resemble  those  of 
Indian  kala-azar,  there  being  irregular  fever  with  enlargement 
of  the  spleen  and  liver,  and  severe  anaemia  with  marked  leuco- 
penia. 

Treatment. — Nothing  is  known  as  to  the  treatment  or  prophylaxis. 


REFERENCES. 

Darling  (1907).     Journal  of  American  Medical  Association. 
Darling  (1909).     Journal  of  Experimental  Medicine. 


CHAPTER  LXXI 
BERI-BERI    AND    EPIDEMIC    DROPSY 

Beri-beri — Infantile  beri-beri — Epidemic   dropsy — Potter's  disease — 
References. 

BERI-BERI. 

Synonyms. — Polyneuritis  Endemica,  Neuritis  Multiplex  Endemica,  Hydrops 
Asthmaticus,  Synclonus  Beriberia,  Myelopathia  Tropica  Scorbutica,  Para- 
plegia Mephitica,  Sero-phthisis  Perniciosa  Endemica,  Panneuritis  Endemica, 
Berbiers,  Kakke  (signifying  a  disease  of  the  legs  in  Japan  and  China),  Loempoe 
(Java),  Kaki-lem-but,  Hinchazon  de  los  Negros  y  Chinos,  Maladie  des  Sucreries 
(French  Antilles),  Hinchazon  (Cuba),  Inchacao,  or  Perneiras  (Brazil). 

Etymology. — The  word  '  beri-beri  '  is  said  to  be  derived  from  the 
Sinhalese  term,  meaning  '  cannot,'  which  is  used  as  a  phrase, 
which  means  '  I  cannot,'  employed  in  the  sense  that  the  person  is  too 
ill  to  do  anything.  There  is  another  Sinhalese  word  which  may 
equally  be  translated  as  '  cannot,'  but  this  means  that  the  person 
is  unwilling  to  do  something,  not  that  he  is  too  ill  to  do  it.  It  is 
possible  that  the  above  interpretation  of  the  word  is  correct,  for 
Ceylon  has  long  been  in  the  hands  of  Europeans — e.g.,  Portuguese, 
Dutch,  and  English — and  therefore  a  term  used  therein  would  be 
widespread.  There  is  no  doubt  that  the  word  covered  a  large 
number  of  diseases,  from  which  a  definite  pathological  entity  has 
gradually  been  separated  out.  It  is  to  be  noted,  however,  that— 
at  all  events,  at  the  present  time — the  disease  does  not  exist  en- 
demically  in  Ceylon,  where  there  are  only  imported  cases. 

Definition.— Beri-beri  is  an  acute  or  chronic,  endemic  or  epidemic, 
disease,  of  unknown  causation,  which  is  characterized  by  degenera- 
tion of  many  peripheral  nerves,  especially  the  vagi,  the  phrenics,  and 
those  of  the  limbs,  associated  with  gastro-intestinal  disturbance, 
cardiac  disturbance,  and  oedema. 

History. — According  to  Scheube,  it  is  possible  that  the  first  men- 
tion of  beri-beri  is  to  be  found  in  the  accounts  given  by  Strabo  and 
Pio  Cassius  of  a  disease  which  attacked  a  Roman  army  in  24  B.C.  in 
Arabia.  Kakke  is  also  mentioned  in  a  Chinese  pamphlet  belonging 
to  the  second  century  of  the  present  era,  and  is  minutely  described 
in  another  belonging  to  the  seventh  century,  while  it  is  recorded  as 
occurring  in  Japan  in  the  ninth  century.  In  the  tenth  century  a 
distinction  was  made  between  the  atrophic,  dry,  or  paralytic,  and 
the  hypertrophic,  wet,  or  dropsical  forms  of  the  complaint. 

In  1758-59  Bontius  was  the  first  European  doctor  to  give  an 
account  of  the  disease,  which  he  described  under  the  term  '  beri-beri.' 

1671 


1672  BERI-BERI  AND  EPIDEMIC  DROPSY 

Later,  Tulpius,  a  Dutch  physician,  also  described  the  symptoms  of 
the  disease  as  seen  in  a  person  who  had  returned  to  Holland  from 
the  Indies.  From  that  time  the  literature  on  beri-beri  has  grown 
until  it  has  reached  enormous  proportions,  but  unfortunately  there 
is  no  doubt  that  until  recently  several  diseases,  especially  ankylo- 
stomiasis and  epidemic  dropsy,  were  confounded  with  it.  Rogers 
in  1808,  and  later  Davy,  described  the  disease  as  '  beri-beria,'  while 
the  latter  says  that  it  is  almost  peculiar  to  Ceylon.  There  is  little 
doubt  that  the  condition  described  by  Davy  was  in  reality  ankylo- 
stomiasis. 

In  1847  Carter  gave  a  description  of  the  disease,  indicating  asthma 
as  the  principal  feature,  probably  because  of  the  cardiac  dyspnoea. 
In  1873  Fayrer  laid  great  stress  on  oedema  as  the  important  clinical 
feature.  In  1877  Wernich  defined  the  disease  kakke  in  Japan, 
while  van  Meedervoort  showed  that  it  was  the  same  disease  as 
beri-beri.  In  1886  Kynsey  published  an  account  of  the  anaemia  or 
beri-beri  of  Ceylon,  by  which  he  really  meant  ankylostomiasis; 
hence  the  idea  that  beri-beri  was  due  to  Ancylostoma  duodenale, 
and  hence  the  large  number  of  cases  of  so-called  beri-beri  in  Ceylon 
years  ago. 

The  scientific  and  clinical  study  of  the  disease  has  been  largely 
due  to  the  work  of  Oudenhoven,  Da  Sylva  Lima,  Overbeck  de 
Rieyer,  Baelz,  Scheube,  Pekelharing  and  Winckler,  Hamilton  Wright, 
Jataki,  Braddon,  Fraser  and  Stanton.  The  workers  on  the  aetiology 
of  the  disease  are  so  numerous  that  this  part  of  the  history  is  best 
treated  in  the  section  on  the  causation. 

Beri-beri  is  in  certain  regions  a  most  serious  disease.  Thus 
Braddon  says  that  in  the  Straits  Settlements  and  Malaya,  where 
the  population  is  only  1,250,000,  no  less  than  150,000  cases  of  the 
disease,  with  30,000  deaths,  have  occurred  in  Government  hospitals 
and  infirmaries  in  the  last  twenty  years;  but  he  says  that  only 
one-third  of  the  deaths  of  Chinese  took  place  in  those  hospitals,  and 
therefore  the  total  deaths  in  that  period  would  be  about  100,000. 
It  is  also  a  great  element  in  inefficiency,  for  it  is  reckoned  that 
33  per  cent,  of  the  sailors  of  the  Japanese  Navy  prior  to  1884  were 
continuously  disabled  by  it.  In  1904-05  it  is  said  that  24  per 
cent,  of  the  entire  sick  and  wounded  in  the  Japanese  armies — 
i.e.,  about  85,000  men — were  also  disabled  by  it.  It  is  obvious, 
therefore,  that  the  disease  is  of  great  medical  and  economic  interest, 
for  its  incidence  particularly  falls  upon  the  labourer,  the  sailor,  the 
soldier,  and  the  prisoners  in  the  gaols,  and  hence  hampers  both  the 
employer  of  labour  and  the  Government.  Braddon  estimates  the 
cost  of  the  disease  to  the  Government  of  Malaya  as  £10,000  per 
annum  in  direct  hospital  charges  only. 

Much  work  has  been  done  by  Eijkman,  Vordeman,  Fraser,  Stanton, 
Funk,  and  many  other  observers,  with  the  result  that  the  consensu? 
of  opinion  at  the  present  time  is  that  beri-beri  is  ^.deficiency  disease 
— i.e. ,  is  caused  by  the  deficiency  of  some  essential  substance  in 
the  dietary  (vide Chapter  IV.,  p.  109). 


CLIMATOLOGY— ETIOLOGY  1673 

In  1913  Cooper,  and  in  1917  Chick  and  Hume,  studied  the  subject 
of  vitamines,  the  two  latter  especially  dealing  with  beri-beri 
vitamine. 

Climatology. — The  endemic  centre  of  beri-beri  appears  to  be 
Eastern  Asia,  Japan,  China,  the  Philippine  Islands,  Indo-China, 
Java,  and  Malaya.  It  is  also  said  to  occur  in  Brazil  and,  according 
to  Plehn,  in  Reunion,  Mauritius,  Nossi-be,  Zanzibar,  Cape  Colony, 
Senegal,  Angola,  the  Congo  Free  State,  and  the  Cameroons.  We 
have  met  with  the  disease  on  the  Gold  Coast  in  Chinese  miners,  but 
have  not  noted  it  in  the  native  population,  though  it  may  possibly 
exist.  Isolated  epidemics,  sporadic  or  imported  cases,  occur  in 
England,  Ireland,  and  other  parts  of  Europe,  the  United  States, 
Canada,  and  in  Ceylon.  In  the  last-named  place  it  is  now  almost 
entirely  absent,  and,  indeed,  it  is  possible  that  many  of  the  cases 
reported  years  ago  may  have  been  ankylostomiasis  or  some  other 
disease.  Imported  cases  from  India  and  China  are  frequently  met 
with  in  Colombo,  owing  to  its  possessing  a  large  harbour  where 
numerous  vessels,  with  Chinese  and  Indian  crews,  call. 

It  is  believed  that  the  Bihimbo  disease  of  the  Chaka  district  of 
Uganda  is  beri-beri.  The  disease  known  in  that  country  as  mun- 
hiyo,  and  believed  at  one  time  to  be  beri-beri,  has  been  demon- 
strated to  be  Malta  fever.  In  the  tropics  it  is  said  to  occur  more 
often  in  the  cool  wet  months. 

etiology. — The  causation  of  beri-beri  is  at  the  present  time 
believed  to  be  due  to  the  deficiency  of  some  essential  substance  in 
the  food,  but  as  may  be  imagined  in  such  a  widespread  and  fatal 
disorder,  the  investigators  have  been  many,  and  hence  the  theories 
are  legion.  In  order  to  comprehend  the  present  state  of  the  ques- 
tion, it  is  necessary  very  briefly  to  review  a  few  of  these  theories, 
which  will  be  best  done  by  following  a  method  of  classification. 

A.  Physical  Cause. — The  older  writers,  like  Davy,  considered  that  it  was 
brought  about  by  some  unusual  state  of  the  atmosphere,  but  they  said, 
honestly,  that  this  was  merely  a  cloak  for  their  ignorance  of  the  true  cause. 

B.  Chemical  Causes. — The  chemical  causes  which  have  been  advanced  are:  — 

1.  Arsenical  poisoning  (Ross) . 

2.  Oxalate  poisoning  (1'reu  tlein) . 

3.  Carbon  dioxide  poisoning  (Ashmead). 

4.  Food  poisoning: — 

(a)  Ichthyotoxismus  (Grimm  and  Miura) . 

(b)  Sitotoxismus    (Eijkman,    Vorderman,    Yamagiwa,    Van 

Dieren) ;  rice  (Gelpke,  Braddon) ;  lathyrism  (I,e  Roy  de 
Mericourt). 

5.  Some  deficiency  in  the  food : — 

(a)  Deficient    nitrogenous     complex     (vitamine)     (Eijkman. 

Fraser,  and  Stanton), 
(fc)  Deficient  nitrogen  (Takaki). 

(c)  Deficient  fat  (Br6maud  and  Laurent) . 

(d)  Deficient  vegetables,  together  with  an  infection  (Fales). 

(e)  Deficient  phosphorus. 

(f)  Deficient  choleslerin  (Chrisostem). 

6.  An  intoxication  from  a  germ  living  outside  the  body  (Manson). 

7.  An  intoxication  or  an  auto-Intoxication  (Duerck). 


1 674  BERI-BERI  AND  EPIDEMIC  DROPSY 

i.  Arsenical  Poisoning. — R.  Ross,  in  1900  and  subsequent  years,  drew 
attention  to  the  similarity  between  beri-beri  and  the  arsenical  poisoning  which 
at  that  time  was  prevalent  throughout  Lancashire,  being  brought  about 
through  the  agency  of  arsenical  beer.  He  further  supported  this  by  finding 
arsenic  in  the  hair  in  recent,  but  not  in  old,  cases  of  the  disease  in  Penang,  and 
woke  up  a  controversy  as  to  whether  arsenic  existed  in  normal  hair  or  not.  But 
apart  from  the  obvious  reasons  against  this  theory  as  an  explanation  for  such 
a  widespread  disease,  Herzog  has  definitely  shown  that  no  arsenic  could  be 
found  in  the  hair  of  ten  cases  of  different  types  of  the  disease.  There  is  no 
doubt  that  cases  of  chronic  arsenical  poisoning  do  occur  in  the  tropics,  as  we 
have  seen,  particularly  in  Europeans  who  have  had  to  live  for  a  long  time  on 
tinned  food,  but  these  cases  are  not  beri-beri. 

2.  Oxalate  Poisoning.- — The  oxalate  theory  is  based  upon  the  fact  that 
Maurer  and  Treutlein  were  able  to  produce  a  condition  resembling  beri-beri 
in  fowls  by  giving  them  oxalic  acid  in  their  food.  The  latter  observer  con- 
sidered that  the  acid  removed  the  calcium  salts  from  the  body  of  these  animals, 
and  caused  thereby  a  degeneration  of  the  peripheral  nerves  and  heart  muscle, 
and  considered  that  this  was  proved  by  curing  them  by  the  administration 
of  calcium  salts.  Further,  he  showed  that  there  was  an  excessive  excretion 
of  calcium  in  the  urine  of  beri-beri  patients.  But  polyneuritis  has  been 
produced  in  fowls  by  Eijkman  by  feeding  them  with  cooked  rice,  and  it  is 
possible  that  neither  oxalic  acid  nor  rice,  but  an  infection,  was  the  cause  of 
the  disease,  which  may,  of  course,  be  quite  different  from  true  beri-beri. 

3.  Carbon  Dioxide  Poisoning. — Ashmead  believes  that  the  disease  is 
caused  by  the  excessive  inhalation  of  carbon  dioxide,  but  outbreaks  occur 
without  any  overcrowding,  as  we  have  seen  ourselves. 

4.  Food  Poisoning — (a)  Ichthyotoxismus.- — Grimm  considers  the  ingestion 
of  raw  fish  to  be  the  cause  of  the  disease,  and  Miura  the  consumption  of 
species  of  the  Scombridae;  but  Wright  has  shown  that  in  the  gaol  at  Kwala 
Lumpur,  the  disease  infected  forty-nine  prisoners  when  no  fish  had  been 
given  for  eight  months. 

(b)  Sitotoxismus. — Rice  poisoning  at  present  is  the  favourite  theory,  and  has 
had  many  supporters.  Thus  Eijkman  and  Vorderman  consider  that  it  is 
due  to  eating  rice  without  husk,  which  is  the  natural  protection.  Gelpke 
considers  that  it  is  due  to  stale  or  badly-kept  rice.  Yamagiwa  considers  it 
due  to  rice  improperly  stored  and  preserved,  as  it  occurs  even  when  this  rice 
is  well  boiled.  Braddon,  who  is  often  wrongly  quoted,  ascribes  the  disease 
to  the  ingestion  of  a  poison  found  in  the  rice,  which  is  the  result  of  the  specific 
product  of  some  organism — epiphyte  or  parasite — but  he  does  not  believe 
that  the  disease  is  due  to  the  ingestion  of  the  organism.  Contrary  to  Eijkman 
and  Vorderman,  Braddon  looks  upon  the  husk  as  the  dangerous  element,  as 
it  is  in  this  that  the  germ  grows. 

But  the  disease  has  been  observed,  according  to  Scheube,  who  quotes 
Fiebig  and  Voorthuis,  in  Brazil,  the  Moluccas  and  Liugga,  where  the  people 
live  on  sago,  fish,  and  game,  and  where  the  attacked  Europeans  had  never 
eaten  rice. 

Travers  details  an  interesting  observation  on  this  point  concerning  an 
epidemic  of  beri-beri  in  the  Pudoh  Gaol  of  Kwala  Lumpur,  in  August,  1895, 
when  some  of  the  cases  were  transferred  to  the  Old  Gaol,  one  and  a  half 
miles  distant,  on  October  1,  1895,  because  the  mortality  in  the  Pudoh  Gaol 
was  extremely  high;  and  on  October  25,  1895,  sixty  prisoners,  showing  no 
signs  of  the  disease,  and  apparently  in  good  health,  were  similarly  transferred. 
From  October  1  to  December  14,  1895,  all  food  supplied  to  the  healthy 
prisoners  in  the  Old  Gaol,  as  well  as  to  the  beri-beri  patients  transferred  from 
the  Pudoh  Gaol,  was  cooked  in  the  Pudoh  Gaol  with  the  food  for  the  other 
prisoners  who  were  suffering  from  the  disease. 

This  food  was  carried  to  the  Old  Gaol  twice  daily,  and  the  diet  was  exactly 
the  same  in  both  gaols,  the  rice  being  taken  out  of  the  same  bag  and  cooked 
in  the  same  steamer.  Further,  it  appears  from  Braddon's  remarks  that  in 
1895  a  new  scale  of  ordinary  diets,  with  an  increased  amount  of  rice,  was 
allowed,  fresh  fish  was  replaced  by  salted,  and  beans  were  omitted,  and 


MTIOLOGY  1675 

Braddon  considers  that  it  was  this  increase  of  the  rice  that  increased  the 
poison  and  made  people  ill;  but  this  ought  to  apply  to  both  places. 

Moreover,  Braddon  considers  deductions  adverse  to  rice  in  the  above 
experiment  to  be  fallacious,  for  he  holds  that  the  length  of  period  of  incar- 
ceration of  the  above  prisoners  is  an  important  factor;  for  the  liability  to 
acquire  the  disease,  he  says,  increases  with  and  varies  directly  according 
to  the  length  of  the  time  served  in  prison,  which  must  be  more  than  six  months. 
He  points  out  that  it  is  not  stated  how  many  long-sentence  prisoners  were 
sent  to  the  Old  Gaol,  which  he  thinks  may  not  have  been  more  than  two  or 
three;  and  concerning  these,  he  says,  there  is  no  proof  that  any  of  them 
were  kept  for  the  period  necessary  to  acquire  the  disease  by  rice  intoxica- 
tion. He  therefore  concludes  that  Travers'  experience  affords  no  ground 
for  opposing  the  theory  that  beri-beri  is  incurred  through  the  consumption 
of  certain  sorts  of  rice. 

5.  Some  Deficiency  in  the  Food — (a)  Deficiency  of  Certain 
Nitrogenous  Complexes. — There  is  a  growing  tendency  to  consider 
that  certain  diseases — e.g.,  beri-beri,  polyneuritis  of  birds,  epidemic 
dropsy,  scurvy,  experimental  scurvy,  infantile  scurvy,  and  ship 
beri-beri — are  diseases  due  to  the  deficiency  in  some  essential  sub- 
stance in  the  food.  These  diseases  Funk  classifies  together  as 
'  deficiency  disease,'  and  characterizes  them  by  certain  genera 
symptoms — e.g.,  (1)  Cachexia,  with  great  loss  of  weight;  (2)  marked 
nervous  symptoms,  generally  of  the  nature  of  peripheral  neuritis. 
He  divides  these  diseases  into  two  groups — the  beri-beri  group 
comprising  beri-beri,  polyneuritis  in  birds,  and  epidemic  dropsy; 
and  the  scurvy  group. 

With  regard  to  beri-beri,  as  already  pointed  out,  Braddon  drew 
attention  to  the  importance  of  rice  as  an  etiological  factor.  Eijk- 
man  in  1897  had  shown  that  it  could  be  prevented  and  cured  by 
the  use  of  hand-milled  rice.  Prisoners  fed  upon  red  rice  escaped, 
and  those  on  white  rice  were  very  prone  to  take  the  disease.  Fraser 
and  Stanton  showed  that  members  of  gangs  of  coolies,  who  had 
previously  remained  quite  healthy,  developed  beri-beri  when  fed 
on  white  rice,  while  other  members  fed  on  brown  rice  remained 
healthy.  Strong  and  Crower  observed  that  in  eight  out  of  seven- 
teen prisoners  fed  on  white  rice,  symptoms  of  beri-beri  appeared 
in  from  61  to  75  days.  The  difference  between  these  two  forms  of 
rice  is  that  the  white  rice  is  deprived  of  its  subpericarpal  layers 
(vide  pp.  104  and  105)  by  the  process  of  milling. 

These  layers  contain  a  substance  called  by  Funk  beri-beri  vita- 
mine,  which  is  probably  a  base  belonging  to  the  pyramidine  group, 

and  lias  the  formula —  -TTT 

NH\ 

CO  ->C16H1806 

NH/ 

and  not  C17H1804N(HN03),  as  previously  stated.  This  substance 
is  soluble  in  water,  alcohol,  and  acidulated  alcohol,  is  dialyzable, 
and  can  be  destroyed  by  heating  to  1300  C.  It  is  present  in  the 
proportion  of  o-i  gramme  to  the  kilogramme  of  rice.  According  to 
Funk,  this  substance  is  essential  for  the  metabolism  of  nervous 
tissue;  and  if  it  is  not  present  in  the  dietary,  must,  be  supplied  by  the 


1676  BERI-BERI  AND  EPIDEMIC  DROPSY 

animal  body,  and  if  this  fails,  the  nervous  tissues  begin  to  break 
down,  and  as  a  result  the  signs  and  symptoms  of  beri-beri  appear. 

Fraser  and  Stanton  believe  that  the  phosphorus  content  of  the 
rice  is  a  good  index  as  to  whether  it  is  harmless  or  harmful.  A  safe 
rice  yields  more  than  0-4  per  cent,  of  phosphorus  pentoxide,  v/hile 
a  dangerous  rice  yields  less  than  this  figure.  Chamberlain  and 
Vedder  have  sviggested  that  potassium  should  be  used  instead  of 
phosphorus  for  standardization  purposes. 

With  regard  to  these  findings  there  is  an  almost  unanimous 
support  from  all  sides,  but  the  Philippine  investigators,  while 
believing  that  their  studies  support  the  polished  rice  theory,  bring 
forward  the  Curious  fact  that  beri-beri  began  to  diminish  among 
their  Native  Scouts  during  the  last  half  year  of  1910  without  any 
decrease  in  the  general  incidence  of  the  disease  in  the  islands,  and 
four  months  before  the  use  of  under-milled  rice  ivas  introduced  into  the 
dietary.  They  consider  that  the  reduction  was  either  due  to 
unknown  causes  acting  coincidentally  with  a  reduction  in  the 
amount  of  rice  in  the  dietary,  together  with  the  addition  of  a 
legume,  or  was  due  directly  to  these  dietetic  changes. 

Eijkman,  Braddon,  Fraser,  Stanton,  Vedder,  and  Chamberlain 
have  done  sufficient  work  to  make  imperative  the  use  of  brown  rice 
cooked  in  ordinary  vessels,  and  the  exclusion  of  the  white  rice  as 
a  staple  article  of  food. 

Edie,  Evans,  Moore,  Simpson,  and  Webster  have  separated  an 
antineuritic  base  called  '  torulin  ' — N(CH3)3C4H702(HN03)-rfrom 
yeast,  and  Thomson  and  Simpson  have  noted  rapid  recovery  of 
patients  placed  on  a  full  diet,  and  given  1  ounce  of  yeast  and 
200  grammes  of  katjangido-beans  daily. 

Heiser  reports  that  after  being  present  for  five  years  in  the 
Culion  Leper  Colony  in  the  Philippines,  beri-beri  disappeared  in 
nine  months  on  a  dietary  of  unpolished  rice. 

In  1917  Chick  and  Hume  showed  that  in  order  to  keep  a  man  in 
health  there  must  be  (a)  a  suitably  proportioned  supply  of  protein, 
fat,  carbohydrate,  salts,  and  water:  (b)  an  adequate  amount  of  vita- 
mines;  and  that  these  two  factors  could  not  replace  one  another. 
The  vitamines  of  importance  in  beri-beri  they  call '  antineuritic  or 
anti-beri-beri,'  as  the  first  term  covers  the  polyneuritis  in  fowls. 
Neither  vitamine  has  yet  been  isolated  in  a  pure  condition.  Pigeons 
deprived  of  anti-beri-beri  vitamine  develop  acute  polyneuritis  in 
fifteen  to  twenty-five  days.  The  principal  source  of  this  vitamine 
is  the  seeds  of  cereals  and  pulses.  In  the  former  it  is  mainly  de- 
posited in  the  germ  or  embryo  of  the  grain  and  to  a  less  extent  in  the 
grain.  It  is  also  found  in  eggs  and  yeast.  It  can  withstand  drying 
and  also  temperatures  of  ioo°  C,  but  is  destroyed  at  1200  C.  The 
deduction  is  that,  in  order  to  prevent  beri-beri,  bread  and  biscuit 
should  be  made  from  the  germ-containing  or  wholemeal  flour. 
Antineuritic  vitamines  cannot  be  expected  to  survive  in  tinned 
or  sterilized  foods-;  hence  the  necessity  in  armies  to  supply  vitamine 
from  other  sources. 


ETIOLOGY  1677 

The  deficiency  theor}'  in  some  form  is  at  the  present  time  accepted 
all  over  the  world,  but  there  are  still  some  observers  who  think 
that  there  may  be  more  than  one  form  of  disease  concealed  under  the 
name  beri-beri. 

The  following  objections  have  been  raised  against  the  food  theory: — 

(1)  Beri-beri  may  occur  in  people  who  do  not  feed  on  rice.     We  have 

seen  an  epidemic  among  oiheers  on  a  man-of-war. 

(2)  The  geographical  distribution.     In  populations  eating  the  same  kind 

of  rice  some  suffer  from  beri-beri  and  others  do  not. 

(3)  Tamil  coolies  in   Ceylon  do  not  get  beri-beri,   though  they  suffer 

from  this  disease  in  the  Straits  Settlements.     In  both  countries 
they  are  mostly  supplied  with  the  same  kind  of  rice  (Rangoon  rice). 

(4)  People  recovei  ed  from  beri-beri  go  back  to  their  usual  rice  diet  without 

again  suffering  from  the  disease.     Thus  in  the  Malay  States  the 
mortality  is  only  20  per  cent.;  therefore  80  per  cent,  of  sufferers 
recover.     Do  these  people  change  their  diet  ? 
Fraga,  having  failed  to  produce  beri-beri  in  prisoners  fed  on  polished  rice, 
believes  that  dietary  deficiency  acts  merely  as  a  predisposing  cause. 

(b)  Deficient  Nitrogen. — Previous  to  1884,  33  per  cent,  of  the  sailors  in  the 
Japanese  Navy  were  disabled  owing  to  beri-beri. 

In  1883  the  Ryujo,  a  Japanese  warship,  went  on  a  voyage  of  271  days  to 
New  Zealand  and  South  America,  and  developed  160  cases  of  the  disease 
out  of  a  crew  of  350  men.  Takaki  investigated  this  outbreak,  and  came 
to  the  conclusion  that  there  was  too  little  nitrogen  in  the  diet,  the  nutritive 
value  of  which  was:  Proteids,  109-29  grammes;  fats,  15*8  grammes;  carbo- 
hydrates, 622-32  grammes.  He  therefore  changed  the  diet  to:  proteids, 
196  grammes;  fats,  43  grammes;  and  carbohydrates,  775  grammes;  and  on 
this  dietary  the  warship  Taukuba  was  sent  the  same  cruise,  taking  287  days, 
and  only  suffered  from  sixteen  cases  of  the  disease.  Takaki  attributed 
the  success  to  the  increased  nitrogen,  a  portion  of  the  rice  being  replaced 
by  corn  or  bread;  but  Tales  has  pointed  out  that  fresh  vegetables  were  in- 
creased from  215  grammes  to  450  grammes,  and  that  therefore  nitrogen 
alone  may  not  have  been  the  cause  of  the  decrease  of  the  disease.  This 
dietary  was  applied  to  the  Japanese  Army  and  Navy,  and  beri-beri  decreased 
enormously.  But  Baelz  has  pointed  out  that  this  decrease  was  associated 
with  a  great  improvement  in  general  hygiene,  and  that  it  also  took  place 
in  barracks  in  which  the  food  had  not  been  changed.  A  similar  decrease  in 
the  Dutch-Indian  Navy,  associated  with  a  better  diet,  was  attributed  by  some 
to  the  improved  hygiene  rather  than  to  the  diet. 

(c)  Deficient  Fat. — Bremaud  and  Laurent  believe  that  the  disease  is  due  to 
too  little  fat  in  the  food,  and  consider  that  an  epidemic  at  Chaudabum,  in 
Siam,  was  stopped  by  causing  fat  to  be  more  freely  consumed  by  the  healthy. 
This  theory,  however,  has  found  but  little  support. 

(d)  Deficient  Vegetables,  together  with  an  Infection. — Fales,  from  a  study  of 
an  outbreak  of  an  epidemic  of  beri-beri  in  the  Bilibid  Prison,  in  Manila,  came 
to  the  conclusion  that  the  lack  of  fresh  vegetables  conduced  powerfully  to 
both  beri-beri  and  scurvy. 

In  November,  1901,  there  were  two  cases  of  the  disease,  and  no  deaths, 
in  that  gaol.  The  food  was  then  changed  to  a  ration  consisting  of  97-17 
grammes  of  proteids,  17-24  grammes  of  fats,  491-04  grammes  of  carbo- 
hydrates, and  26-52  grammes  of  salts.  In  this  diet  there  were  85-05  grammes 
of  potatoes,  and  453-60  grammes  of  rice.  Put  into  other  figures,  this  diet 
consisted  of:  Nitrogen,  172-1  grammes;  carbon,  4,166-5  grammes;  hydrogen, 
61-9  grammes;  sulphur,  13-2  grammes;  salts,  140-2  grammes — the  propor- 
tion of  nitrogen  to  carbon  being  as  1  to  24-2.  Whereas,  calculating  the 
weight  of  Filipinos  at  125  pounds,  it  was  estimated  that  proteids  ought, 
according  to  Voigt's  diet,  to  have  been  at  least  94  grammes,  fats  45  grammes, 
and  carbohydrates  400  grammes;  or,  according  to  Moleschott's  diet,  nitrogen 
256  grammes;  carbon,  3,789  grammes;  hydrogen,  143  grammes;  sulphur, 
23  grammes;  salts,  172  grammes — i.e.,  N:  C  ::  1 :  0-15. 


1678  BERI-BERI  AND  EPIDEMIC  DROPSY 

The  epidemic  of  beri-beri  now  began:  December,  1901,  52  cases  and  2 
deaths;  January,  1902,  169  and  12;  February,  1,087  and  16;  March,  576 
and  15;  April,  327  and  15;  May,  310  and  19;  June,  451  and  17;  July,  233 
and  33;  August,  571  and  24;  September,  522  and  31. 

On  October  20  the  diet  was  again  changed,  and  this  time  proteids  were 
101*71  grammes;  fats,  19*37  grammes;  carbohydrates,  395*73  grammes; 
salts,  29*13  grammes;  including  119*07  grammes  of  potatoes  and  255*15 
grammes  of  rice.  Nitrogen  was  209*8  grammes;  carbon,  3,816*2  grammes; 
hydrogen,  70*4  grammes;  sulphur,  17*2  grammes;  and  salts,  185  grammes — 
N:  C::  1 :  13*4. 

In  October  there  were  579  cases  and  34  deaths;  November,  476  and  8; 
December,  89  and  3;  half  January,  1903,  4  cases  and  no  deaths. 

Along  with  the  beri-beri  there  was  an  epidemic  of  scurvy,  and  Fales  was  of 
the  opinion  that  both  diseases  were  led  up  to  by  a  deficiency  of  vegetables, 
the  essential  principle  of  which  he  believes  to  be  potassium  carbonate,  of  which 
rice  contains  only  o*oi  grain  per  ounce,  while  potatoes  contain  1*875  grains. 
Hence,  according  to  Fales,  the  disappearance  of  the  disease  when  a  suffi- 
ciency of  vegetables,  especially  potatoes,  was  given.  But  he  says  this 
deficiency  was  only  a  predisposing  cause,  which  enables  the  micro-organism, 
whatever  it  is,  which  is  the  true  cause  of  the  disease,  to  flourish  and  produce 
the  symptoms.  In  other  words,  the  people  get  run  down  by  a  bad  diet,  and 
are  ready  for  any  disease,  so  that  this  does  not  clear  up  the  aetiology. 

Recently  Ingram  has  drawn  attention  to  an  outbreak  in  the  81st  Pioneers 
and  the  2nd  Battalion  of  the  King's  Own  Scottish  Borderers,  at  Aden,  in 
which  he  could  find  no  clear  evidence  that  beri-beri  was  due  to  diet  alone, 
whether  insufficient  proteids  or  excessive  rice,  or  bad  rice,  but  he  considered 
a  diet  rich  in  proteids  good  as  a  preventative.  He  could  only  find  one  thing 
in  common  in  the  two  regiments — viz.,  both  brought  the  disease  with 
them — but  was  unable  to  find  any  source  of  infection,  parasitic  or 
otherwise. 

{e)  Deficient  Phosphorus. — Schaumann  and  others  have  maintained  that 
deficient  organically  combined  phosphorus  in  the  uncured  rice  is  the  setio- 
logical  factor. 

(/)  Deficient  Cholesterin. — Chrisostem  has  treated  cases  with  injections  of 
cerebrin  with  good  results,  and  with  5  per  cent,  cholesterin  in  olive  oil  with 
better  results. 

6.  An  Intoxication  from  a  Germ  living  Outside  the  Body. — Manson 
brought  forward  the  hypothesis  that  a  germ  may  live  in  the  soil,  the  house, 
or  the  ship  occupied  by  the  human  being,  under  certain  conditions  of  tem- 
perature and  moisture,  and  may  grow  and  produce  some  kind  of  toxin  which, 
being  inhaled  or  swallowed,  or  otherwise  introduced,  causes  the  disease.  More- 
over, this  germ  may  be  carried  by  men  from  place  to  place. 

He  supports  this  theory  by  pointing  out — (1)  that  when  patients  are 
removed  from  an  endemic  spot  they  at  once  begin  to  recover ;  (2)  he  quotes 
Hirota's  observation  that  fifty-two  infants  nursed  by  beri-beric  mothers 
showed  signs  of  the  disease,  and  did  not  improve  when  treated  medicinally, 
but  rapidly  improved,  if  the  disease  had  not  advanced  too  far,  when  taken 
from  these  mothers  and  placed  on  artificial  food  or  given  to  a  healthy  wet- 
nurse.  Further,  Herzog  says  that,  according  to  Dr.  Albert,  similar  cases 
are  not  very  infrequent  in  the  Philippine  Islands,  but  the  removal  of  the 
child  from  the  mother  is  most  difficult,  as  the  people  do  not  understand  the 
necessity. 

Manson  rightly  points  out  that  these  children  must  have  been  poisoned 
with  some  chemical  substance,  and  not  infected  with  a  germ.  But,  of  course, 
the  germ  causing  the  toxin  might  be  in  the  mother's  body. 

Again,  Manson  points  out  that  the  disease  clings  to  ships,  in  which  it 
appears  year  after  year  when  the  tropics  are  reached.  There  is  also  evidence 
that  the  cause,  whatever  it  is,  clings  to  rooms  for  a  short  time. 

7.  An  Intoxication  or  an  Auto-Intoxication. — Duerck  is  convinced 
from  the  study  of  the  pathology  that  the  cause  of  the  disease  is  a  toxaemia, 
and   points  out  that  substances  formed   in   the  body  by  process  of  auto- 


MT 10  LOGY  1679 

intoxication  may  produce  peripheral  neuritis,  but  the  epidemics  of  the 
disease  are  quite  against  a  theory  of  auto-intoxication. 

C.  Parasitic  Causes. — A  great  many  observers  are  in  favour  of  a  parasitic 
cause  for  the  disease,  without  committing  themselves  as  to  whether  it  is 
animal  or  vegetal.  Among  these  may  be  mentioned  Sambon,  who  con- 
siders that  the  specific  agent  lives  in  the  patient's  body.  Scheube  considers 
that  it  is  an  infectious,  but  not  a  contagious,  disease,  and  says  that  the 
analogy  with  malaria  is  in  some  respects  striking,  and  that  it  is  spread  by 
mechanical  transmission  of  the  disease  by  human  intercourse  in  some  way 
or  another.  This  is  quite  true,  because  there  are  numerous  instances  of 
disease  being  imported  by  human  beings  into  a  fresh  place  and  spreading, 
but  the  curious  point  is  that  it  generally  sticks  to  one  race. 

Thus,  in  Malaya  it  is  a  common  disease  among  imported  Chinese,  and 
hardly  known  among  the  natives.  In  the  Bilibid  Prison,  mentioned  above, 
the  prisoners  included  Filipinos,  Spaniards,  Chinese,  Japanese,  Indians, 
American  negroes,  Americans,  and  Europeans,  but  the  disease  fell  most 
severely  on  the  Filipinos,  the  Chinese  being  almost  exempt,  only  one  or  two 
contracting  the  disease,  while  the  Americans  were  immune.  Van  der  Scheer 
suggested  that  perhaps  insects,  such  as  cockroaches,  might  be  the  spreaders  of 
the  disease,  but  Durham's  investigations  are  contrary  to  this.  It  would  seem 
as  though  the  causal  agent  was  spread  by  some  parasite,  for  Daniels  has 
carefully  considered  the  question  of  infection,  and  does  not  find  any  evidence 
in  favour  of  it  being  conveyed  by  the  excreta  of  persons  suffering  from  the 
disease,  especially  the  faeces. 

Further,  he  points  out  that  infection  by  air  and  water  can  be  excluded,  as  in 
Kwala  Lumpur  all  races  drink  the  same  water,  but  only  Chinese  are  attacked, 
even  though  they  drink  little  unboiled  water;  and  the  immunity  of  prison 
officials  from  the  disease  while  an  epilemic  rages  among  the  prisoners 
excludes  air.  Disinfection  appears,  from  Durham's  results  on  Christmas 
Island,  to  be  useless.  As  regards  parasites,  Durham  and  Daniels  are  both 
against  mosquitoes  as  being  the  cause — and,  indeed,  this  is  hardly  likely — and 
also  against  bugs. 

On  the  other  hand,  there  appears  to  be  some  evidence  in  favour  of  Pediculus 
capitis,  which  is  apt  to  cling  to  one  race,  and  this  is,  according  to  Daniels,  a 
plausible  theory  in  explaining  the  racial  selection  of  the  disease.  Experi- 
ments on  an  orang-outang  with  pediculi  from  a  beri-beri  case  were  negative, 
the  lice  rapidly  disappearing.  Daniels  could  not  exclude  fomites  as  a  carrier 
of  the  disease  in  his  observations.  Only  one  observer,  Taylor,  is  said  to  have 
produced  the  disease  in  animals  by  the  inoculation  of  the  blood  from  patients. 

Having  thus  briefly  considered  the  general  question  of  contagium  vivum,  and 
its  method  of  entry  into  the  body,  it  is  necessary  to  review  the  various 
organisms  which  have  been  held  to  be  the  cause  of  the  disease. 

They  may  be  classified  into : — 

Animal  Parasites: — 

(a)  Protozoa. 

1.  Plasmodium  in  the  blood  (Glogner). 

2.  Protozoon  in  the  urine  (Hewlett  and  Korte). 

3.  Haematozoa  in  the  blood  (Fajardo  and  Voorthuis). 

(b)  Nemathelminthes. 

1.  Some  form  of  Tvichinella  (Gelpke). 

2.  Trichnris  trichiura  (Erni  and  Kynsey). 

3.  Ancylostoma  duodenale  (Erni  and  Kynsey). 

Vegetal  Parasites — Fungi  : — 
(a)  Coccacea. 

1.  Cocci  in  the  alimentary  canal,  etc.  (Dangerfield). 

2.  Diplococcus  in  the  urine  (Tsuzuki). 

3.  Diplococcus  from  the  blood  and  urine  or  organs  post  mortem 

(Okata  and  Kokubo). 

4.  Four  kinds  of  cocci  (Musso  and  Morelli). 


t68o  BERT-BERT  AND  EPIDEMIC  DROPSY 

(b)  Coccus  and  Bacillus. 

Pleomorphic  organism   obtained   by   Pekelharing  and   Winckler 

from  the  blood. 
Bacilli  and  cocci  by  Lacerda. 

(c)  Bacilli. 

i.  Bacillus  by  Taylor. 

2.  Bacillus  by  Rost. 

3.  Bacillus  by  Ogata. 

4.  Three  kinds  of  bacilli  by  Nepveu. 

5.  Bacillus  by  Ecckf. 

Toxins  from  a  bacillus  in  the  alimentary  canal  (Hamilton  Wright). 

(d)  Fungi  higher  than  Bacteria. 

Mouldy  rice  (Hose). 

Protozoa. — Glogner's  parasites  were  similar  to  malarial  parasites,  but  were 
distinguished  therefrom  by  being  found  only  in  splenic  blood,  by  being 
always  extracorpuscular,  and  by  increasing  by  gemmation.  They  were  more 
pigmented  than  malarial  parasites.  Scheube  thinks  that  Glogner's  cases 
were  complications  of  beri-beri  with  malaria. 

Hewlett  and  Korte  centrifugalized  the  urine  of  beri-beri  cases,  and  found 
small  retractile  spherical  bodies,  2  to  3  fz  in  diameter,  with  a  thick  capsule 
and  hyaline  contents;  others  20  [i  in  diameter,  with  a  cytoplasm  studded 
with  retractile  granules,  and  containing  a  single  nucleus;  and  others  30  /a, 
with  a  thick  capsule,  an  oval  nucleus,  and  a  rounded  nucleolus.  They  further 
described  the  congestion  of  the  glomerular  vessels  and  haemorrhages  into  the 
tubules  of  the  kidney.  Further,  they  saw  a  somewhat  similar  disease  in 
monkeys,  the  urine  of  which  contained  highly  refracted  cells.  The}'  conclude 
that  the  above  are  either  peculiar  degenerate  cells  or  protozoa,  and  suggest 
that  the  disease  is  a  protozoan  infection,  and  that  the  causal  agent  is  elimi- 
nated by  the  urine.  Fijordo  and  Voorthuis  separately  describe  haematozoa, 
partly  free  and  partly  in  the  red  cells,  which  are  similar  to,  but  not  identical 
with,  the  malarial  parasites.  Their  organisms  do  not  agree  with  one  another, 
nor  do  they  correspond  to  Glogner's. 

Nemathelminthes . — Gelpke  suggested  that  the  disease  might  be  due  to  a 
Trichmella  in  fish,  but  he  has  withdrawn  this.  Trichiuris  and  Ancylostoma 
need  not  seriously  be  considered,  as  this  idea  arose  from  a  misunderstanding. 

Fungi. —  Pekelharing  and  Winckler's  bacillus  has  also  been  found  by  Hunter, 
and  experimental  inoculations  by  both  sets  of  observers  produced  degenera- 
tions of  the  nerves.  But  it  must  be  admitted  with  regard  to  bacteria  that 
competent  observers  have  found  the  blood  sterile  time  after  time. 

Hamilton  Wright's  bacillus,  which  occurs  in  the  alimentary  canal,  has  been 
found  by  Dudgeon  to  be  non-pathogenic  for  monkeys,  and  not  to  be  aggluti- 
nated by  the  blood  of  beri-beri  patients.  Stanley's  experiments  on  animals 
with  mouldy  rice  have  been  negative.  Finally,  attention  may  be  drawn  to 
the  researches  of  Hoist,  Nocht,  and  the  Norwegian  Ship  Beri-Beri  Committee, 
which  indicate  that  the  so-called  ship  beri-beri  is  not  beri-beri,  as  the  symp- 
toms are  shortness  of  breath  and  weak  heart,  with  weakness  and  dropsy  of 
the  lower  limbs,  but  not  paralysis  of  the  limbs — i.e.,  the  degeneration  of 
the  nerves  is  not  an  essential  phenomenon. 

Chalmers  and  Archibald  separately  have  found  fungi  in  the  organs 
of  cases  of  beri-beri  occurring  at  different  times  in  British  troops  in 
Khartoum.  We  feel  that  more  than  one  disease  is  included  under 
the  term  beri-beri.  One  of  these  diseases  is  a  deficiency  disease, 
but  the  others  await  discovery. 

Predisposing  Causes. — The  disease  can  occur  in  all  races,  and  at 
all  ages,  and  in  both  sexes,  but  it  is  apt  to  cling  particularly  to  one 
race  in  a  country — e.g.,  the  Chinese  in  Malaya,  the  Filipinos  in  the 


PREDISPOSING  CAUSES  1681 

Philippine  gaol  outbreak.  This  racial  incidence  is  most  marked. 
Thus,  Braddon  says  that  of  the  Chinese  immigrants  into  the  Straits 
and  Malaya,  it  may  be  reckoned  that  of  every  1,000  living,  120  suffer 
and  16  die  of  the  disease.  The  Malayas  are  said  to  suffer  but  little, 
if  at  all.  In  the  Bilibid  Prison  in  Manila,  on  the  other  hand,  ac- 
cording to  Fales,  the  Filipinos  suffered  most  severely,  the  Chinese 
were  almost  exempt,  only  one  or  two  contracting  the  disease,  while 
the  Americans  were  entirely  free. 

With  regard  to  age,  it  is  most  commonly  met  with  in  young  adults 
between  fifteen  and  thirty  years,  but  it  has  also  been  noted  in  babies 
at  the  breast  and  in  old  men.  It  is  more  commonly  met  with  in 
men  than  in  women. 

Occupation  has  been  carefully  investigated  by  Hunter  and  Koch 
in  Hong-Kong,  and  they  con  hide  that  the  disease  is  universally 
present  throughout  the  community,  but  especially  affects  the 
working  classes,  while  the  professions,  the  merchants,  and  the 
leisured  classes  are  practically,  but  not  entirely,  exempt.  Other 
predisposing  causes  are  disturbance  of  the  soil  and  a  high  atmos- 
pheric temperature. 

ImpDrtant  Features. — The  peculiar  features  of  the  disease  are 
that,  though  it  generally  occurs  among  rice-eating  peoples,  yet  at 
times  it  occurs  in  other  communities,  as  in  the  British  regiment,  in 
whose  ration  there  was  but  a  small  quantity  of  rice,  which  was  cured 
Rangoon  rice.  Finally,  if  observers  are  to  be  trusted,  there  are 
places  where  beri-beri  occurs  and  rice  is  not  eaten. 

Pathology.— As  the  cause  of  the  disease  is  unknown,  but  little 
can  be  said  as  to  the  pathology,  but  Mott  and  Halliburton  have 
performed  an  experiment  which  throws  much  light  on  the  disease. 
They  injected  blood  taken  from  an  acute  case  of  beri-beri  into  a 
cat,  and  found  a  fall  of  blood-pressure,  with  dilatation  of  the  vessels 
of  the  stomach,  intestines,  and  liver,  as  well  as  general  venous 
engorgement,  and  they  also  noted  dilatation  of  the  right  side  of  the 
heart,  and  microscopical  haemorrhages  into  the  liver.  This  would 
clearly  indicate  that  a  poison  capable  of  producing  great  vaso- 
motor changes  was  circulating  in  the  blood  of  beri-beri  patients. 
In  addition  to  the  engorgements  found  in  the  cat,  the  human  being 
suffers  from  congestion  of  the  pharynx,  and  degeneration  of  the 
cardiac,  muscular,  and  sensory  nerves.  The  oedema  is  probably 
due  to  the  vasomotor  disturbance. 

Durham  considers  that  the  urine  indicates  a  serious  diminution 
of  the  metabolism. 

Morbid  Anatomy. — The  morbid  anatomy  and  histopathology 
have  been  studied  by  numerous  observers,  among  whom  the  in- 
vestigations of  Wright,  Duerck,  and  Scheube  must  be  especially 
mentioned.  In  acute  cases  there  is  always  some  oedema,  but  at 
times  this  may  be  excessive,  and  the  veins  of  the  neck  are  swollen. 
Hypostasis  is  always  well  marked,  but  may  be  excessive,  especially 
about  the  face.  There  is  often  froth  at  the  mouth.  In  chronic 
cases  the  body  is  pale,  and  may  be  swollen  with  dropsy  or  emaciated. 

106 


1 682  BERI-BERI  AND  EPIDEMIC  DROPSY 

In  the  former  the  post-mortem  rigidity  develops  quickly,  and  is 
well  marked.  In  the  latter,  however,  it  is  not  so  marked.  On 
cutting  into  the  body  the  subcutaneous  tissues  are  usually  oedema- 
tous,  and  the  veins  are  filled  with  dark  fluid  blood.  There  is  a 
varying  quantity  of  serous  fluid  in  the  abdomen,  the  chest,  and  the 
pericardium,  and  there  may  be  petechial  haemorrhages  under  the 
visceral  pleura  and  pericardium  in  acute,  but  not  in  chronic,  cases. 
The  throat  and  tonsils  are  generally  congested  in  acute  cases, 
but  they  may  be  normal;  the  larynx  may  be  congested  or  normal. 
The  mucosa  of  the  trachea  and  bron<.  hi  may  be  ©edematous,  with 
the  lumen  full  of  fluid.  The  lungs  may  be  congested  and  oedema- 
tous,  and  may  contain  little  air. 

The  right  side  of  the  heart  is  always  greatly  dilated  in  acute 
cases,  and  is  also  hypertrophied  in  older  cases,  but  it  is  rare  for  the 
left  ventricle  to  be  hypertrophied,  though  it  may  be  dilated  to  a 
moderate  extent.  The  myocardium  generally  shows  fatty  degenera- 
tion, the  striation  is  often  absent,  and  segmentation  and  vacuolation 
of  the  fibres,  with  an  increase  of  the  interstitial  tissue,  can  also 
be  seen,  and  there  is  a  round-celled  infiltration  beneath  both  endo- 
and  epi-cardium  in  acute  cases.  (These  changes  are  said  by  Scheube 
to  be  like  those  found  in  rabbits  after  section  of  both  vagi.) 

According  to  Wright,  the  entire  nervous  system  of  the  heart  is 
damaged  in  acute  cases,  the  cells  of  the  bulbar  nuclei  and  the 
nucleus  ambiguus  on  both  sides  being  swollen,  with  excentrically 
placed  nuclei  and  a  disappearance  of  Nissl's  bodies  in  the  processes, 
and  to  a  less  extent  at  the  periphery.  These  changes  may  also 
be  seen  in  the  first  and  second  pair  of  the  thoracic  ganglia,  and 
in  the  intrinsic  ganglionic  cells  of  the  heart,  while  the  vagal  nerve- 
endings  show  rounded  droplets  of  altered  myelin  (neurokeratin?), 
especially  near  the  nodes.  In  chronic  cases  only  the  vagi  may  show 
degeneration,  the  ganglia  in  the  heart  being  normal. 

In  acute  cases  the  stomach  and  duodenum  are  markedly  affected, 
the  mucosa  being  hyperaemic,  with  more  or  less  marked  hemorrhagic 
extravasations,  and  even  at  times  effusion  of  blood  into  the  lumen  of 
the  viscus.  This  inflammation  may  extend  to  the  ileum,  or  very 
rarely  even  to  the  caecum,  but  usually  the  small  and  large  intestines 
show  nothing  abnormal,  for  the  acute  irritation  is  located  to  the 
pylorus  and  the  duodenum. 

Microscopically  there  is  an  acute  congestion  with  round-celled 
infiltration,  with,  according  to  Herzog,  a  very  large  number  of 
eosinophile  cells  and  necrosis  of  the  glandular  epithelium.  The 
cells  of  Auerbach  and  Meissner's  plexuses  are  degenerate,  and  the 
nerve  fibres  in  the  stomach  and  duodenum  also  show  signs  of 
degeneration.  In  chronic  beri-beri  these  gastro-duodenal  signs  are 
absent. 

In  an  acute  case  the  lymphatic  glands  near  the  stomach  and 
duodenum  are  enlarged  and  congested.  The  liver  is  generally  en- 
larged and  congested,  and  at  times  in  a  nutmeg-like  condition,  and, 
according  to  Hewlett  and  Korte,  there  may  be  extensive  haemor- 


MORBID  ANATOMY 


1683 


rhagic  patches.  Scheube  and  Plehn  draw  attention  to  a  round- 
celled  infiltration  of  the  interlobular  connective  tissue,  which  the 
latter  calls  a  beri-beric  interstitial  hepatitis.  The  cells  show  fatty 
degeneration,  cloudy  swelling,  and  at  times  necrosis.  The  spleen 
may  show  some  cyanosis,  and  be  slightly  enlarged  and  indurated, 
but  usually  it  is  normal.  The  wall  of  the  gall-bladder  may  be 
oedematous  at  times;  the  pancreas  is  normal.     The  suprarenals 


Fig.  734. — Beri-Beri:  Dropsical 
or  Hypertrophic  Form. 


Fig.  735. — Beri-Beri:  Dry  or 
Atrophic  Form. 


may  be  pigmented  and  congested  with  vacuolated  cells.  The 
kidneys  are  usually  swollen  and  hyperaemic,  and  there  may  be 
hemorrhages  into  the  glomeruli,  tubules,  and  pelvis,  together  with 
cloudy  swelling  and  cellular  infiltration.  The  ureters  and  bladder 
are  usually  normal. 

The  nervous  system  is  markedly  affected.  The  meninges  of  the 
brain  m  ly  be  hyperaemic,  and  there  may  be  some  hyperemia  of  the 
brain  substance  itself,  and  increase  of  fluid  in  the  ventricles,  but 


i684  BERI-BERI  AND  EPIDEMIC  DROPSY 

the  microscope  shows  nothing  abnormal  except  in  the  bulb,  where, 
according  to  Wright,  there  are  the  changes  already  mentioned  in 
the  vagal  nucleus.  Kustermann  also  describes  acute  degeneration 
of  the  vagal  ganglia  at  the  base  of  the  fourth  ventricle. 

The  spinal  cord  is  usually  normal.  Hamilton  Wright  and  others 
have  described  degeneration  of  the  cells  of  the  posterior  spinal 
ganglia  and  anterior  cornua  of  the  lumbar  cord,  together  with 
atrophy  of  Goll's  column,  in  which  histological^  there  is  a  thicken- 
ing of  the  glia  tissue  and  a  complete  disappearance  of  the  nerve 
fibres,  with  the  presence  of  many  granular  cells. 

The  peripheral  nerves  are  usually  normal  to  the  naked  eye,  but 
may  be  injected  and  hemorrhagic.  Scheube  and  Baelz  first  showed 
that  these  nerves  were  degenerated,  the  muscular  branches  of  the 
nerves  of  the  limbs  being  most  affected,  but  even  the  fine  sensory 
cutaneous  branches  were  also  attacked.  The  changes  in  the  auto- 
nomic nervous  system  do  not  appear  to  have  been  closely  studied, 
though  several  observers  have  recorded  changes  in  the  ganglia,  and 
in  the  cardiac  and  other  plexuses. 

The  degeneration  of  the  nerve  fibres  has  been  carefully  studied 
by  Scheube,  Baelz,  Hamilton  Wright,  and  Duerck.  The  neuro- 
keratin network  becomes  irregular,  and  its  meshes  wider,  while  its 
rods  disappear.  The  medullary  sheath  becomes  vacuolated,  and 
its  inner  boundary  ill-defined.  In  other  places  the  neurokeratin 
network  condenses  into  small  rosary-like  masses  or  larger  lumps, 
somewhat  regularly  arranged.  Later  the  medullar}''  sheath  breaks 
up  into  spherical  or  elongated  masses  separated  by  clear  intervals. 
The  axone  undergoes  first  chemical  changes,  and  then  appears  like 
a  wavy  cord,  or  as  a  series  of  comma-like  segments,  or  twisted  up 
into  a  coil.  Finally,  both  axone  and  medullary  sheath  disappear, 
while  Schwann's  sheath  collapses,  and  so  the  nerve  fibres  become 
lost  in  the  connective  tissue  of  the  endoneurium.  Along  with  these 
changes  there  is  a  cellular  infiltration  of  the  perineurium,  especially 
of  the  perivascular  spaces,  and  also  of  the  endoneurium.  These 
cells  are  said  to  be  like  a  similar  infiltration  met  with  in  traumatic 
lesions  of  nerves,  and  to  resemble  the  granule  cells  of  the  central 
nervous  system.  When  fully  degenerated,  the  nerve  may  consist 
simply  of  connective  tissue.  Regeneration  has  not  been  observed, 
but  must  occur — at  all  events,  to  some  extent — in  cases  which 
recover. 

The  muscles  show  atrophied  and  normal  fibres  side  by  side.  The 
diseased  fibre  first  loses  its  striation,  and  becomes  oval  or  round  in 
transverse  section.  A  colloid  degeneration  occurs,  with  prolifera- 
tion of  the  nuclei  of  the  sarcolemma.  The  fibre  now  appears  of  a 
homogeneous  grey  colour,  and  is  very  brittle.  As  it  atrophies  the 
connective  tissue  of  the  muscle  increases  in  amount.  The  bone- 
marrow  is  said  to  be  normal. 

Symptomatology. — As  the  cause  of  the  disease  is  unknown,  and 
the  invasion  is  insidious,  the  incubation  period  is  also  unknown. 
H  mrlton  Wright  places  it  at  some  ten  to' fifteen  days. 


SYMPTOMATOLOGY  1685 

The  disease  is  insidious  in  its  onset,  and  is  characterized  by 
gastro-intestinal,  cardiac,  and  nervous  symptoms.  For  purposes 
of  description  three  types  may  be  recognized — viz.,  (1)  the  acute 
pernicious  form;  (2)  the  typical  form;  (3)  the  rudimentary  form. 

1.  Acute  Pernicious  Form. — -The  acute  pernicious  form  may 
exhibit  itself  in  several  ways.  The  most  acute  is  when  the  person, 
without  previous  illness,  suddenly  dies,  and  the  autopsy  reveals 
that  he  has  died  of  beri-beri. 

The  more  usual  history  is  that  the  patient  feels  a  disinclination 
for  food,  followed  in  a  short  time  by  a  sensation  of  depression  or 
pain  in  the  epigastrium,  and  nausea.  Tenderness  is  evinced  if 
pressure  is  made  over  the  pylorus  or  duodenum,  while  the  throat  is 
seen  to  be  congested.  The  temperature  is  usually  normal,  though 
slight  febrile  rises  have  been  recorded.  Soon  the  heart  symptoms, 
characteristic  of  the  attack,  appear  in  the  form  of  a  sensation  of 
oppression  over  the  heart,  throbbing  vessels  in  the  neck,  epigastric 
pulsation,  cardiac  palpitation,  and  dyspnoea,  while  the  slightest 
exertion  increases  the  pulse-rate  markedly.  The  right  side  of  the 
heart  dilates,  and  haemic  murmurs  are  heard.  As  a  result  of  this 
cardiac  disturbance  the  urine  diminishes  and  dropsy  appears,  but 
this  varies  from  being  trivial  to  fairly  considerable,  with  effusion 
into  the  pericardium,  pleura,  and  peritoneum. 

There  may  early  be  found  patches  of  anaesthesia  or  hyperesthesia, 
particularly  in  the  course  of  the  anterior  tibial  and  musculo- 
cutaneous nerves.  Paralysis  now  appears,  and  may  be  slight,  or 
may  be  so  extensive  as  to  prevent  all  voluntary  movements,  and 
at  the  same  time  the  anaesthesia  may  increase  considerably. 

Sooner  or  later  the  cardiac  symptoms  become  worse;  the  peri 
cardial  distress  becomes  agony,  the  lungs  become  engorged,  and 
the  unhappy  individual,  unable  to  obtain  proper  aeration  of  his 
blood,  gasps  for  breath  with  open  mouth  and  expanded  nostrils, 
while  the  pupils  dilate.  His  face  becomes  cyanosed,  his  extremities 
cold,  and  he  becomes  unconscious,  and  shortly  dies  of  cardiac 
failure.  During  this  dying  agony  the  mind  is  clear  almost  to  the 
last.  The  duration  of  such  an  attack  is  from  twelve  hours  to  a 
few  days. 

2.  The  Typical  Form. — The  typical  form  of  the  disease  begins 
insidiously  with  malaise,  lassitude,  loss  of  appetite,  dull  pain  in  the 
stomach,  tenderness  on  pressure  over  the  pylorus  and  duodenum, 
headache,  difficulty  of  breathing  and  palpitation,  often  some 
cedema  along  the  shin,  exaggerated  knee-jerks,  and  a  sensation  of 
heaviness  in  the  limbs,  especially  in  the  legs.  Sooner  or  later  a 
difficulty  in  walking  sets  in,  and  the  knee-jerk  diminishes  and  dis- 
appears, or  the  patient  may  suddenly  find  himself  on  wakening  in 
the  morning  unable  to  raise  himself.  If  he  is  capable  of  walking, 
the  gait  is  peculiar,  somewhat  resembling  that  of  locomotor  ataxia, 
but  generally  being  more  of  the  '  high-stepping  '  type,  the  foot 
being  raised  with  difficulty  from  the  ground,  brought  forward 
with  a  jerk,  and  lowered  abruptly.     He  walks  with  a  support,  and 


i636  BERI-BERI  AND  EPIDEMIC  DROPSY 

often  with  the  legs  wide  apart,  in  order  to  give  stability  to  his 
locomotion.  He  cannot  stand  long  with  closed  eyes,  and  complains 
that  he  feels  as  though  he  were  walking  on  something  soft.  In 
addition  he  suffers  from  cramp,  and  his  calves  are.  very  tender,  and 
sensations  of  pins  and  needles,  burning,  etc.,  may  be  felt.  It  will 
be  noticed  that  the  anterior  tibial  and  the  peroneal  muscles  are 
mostly  affected,  and  that  often  there  is  a  tendency  for  the  foot  to 
assume  the  equino-varus  position,  and  that  ankle-drop  is  often 
seen. 

The  forearms  may  also  be  paralyzed,  and  wrist-drop,  with  great 
loss  of  power  in  the  grip,  may  be  noted.  As  the  paralysis  proceeds 
the  muscles  waste,  and  electrical  excitation  is  much  altered.  Miura's 
rule  is  that  if  the  foot  can  be  flexed  on  the  ankle,  the  excitation 
is  only  diminished;  if  only  the  toes  can  be  dorsally  flexed,  there 
is  a  partial  reaction  of  degeneration;  but  if  no  dorsal  movement  is 
capable  of  being  made,  then  the  reaction  of  degeneration  will  be 
fully  developed.  The  paralysis  spreads  to  the  muscles  of  the  calf, 
the  muscles  of  the  thigh,  and  the  gluteal  region,  and  to  those  of  the 
hand  and  arm;  then  to  the  abdomen,  the  diaphragm,  the  inter- 
costals,  and  the  larynx,  and,  in  rare  cases,  to  the  intra-  and  extra- 
ocular muscles. 

Fletcher  has  drawn  attention  to  jongkok,  or  squatting  test  The 
person  places  both  hands  on  the  top  of  the  head,  and  slowly  squats 
down  on  his  heels,  and  then  rises  up  again.  In  beri-beri  this  cannot 
be  performed. 

Associated  with  the  paralysis  there  is  at  first  hyperesthesia 
especially  in  the  calf  muscles;  paresthesia,  as  alreads'  mentioned; 
and  partial  anaesthesia,  which  may  be  characterized  by  saying  that 
the  patient  feels  as  though  he  were  touched  through  some  protecting 
cloth.  There  is  also  loss  of  sense  of  heat,  and  cold,  and  pain.  This 
anesthesia  varies  much  in  site  and  extent.  Usually  it  begins  about 
the  feet  and  wrist,  and  moves  upwards  over  the  legs,  thighs,  fore- 
arms, and  arms,  and  down  into  the  fingers.  It  is  this  numbness  of 
the  fingers  which  incapacitates  the  patient  from  doing  many  simple 
actions.  There  is  said  to  be  a  peculiar  ring  of  anaesthesia  around 
the  mouth.  The  areas  of  loss  of  sensation  do  not  correspond  with 
segmental  or  nerve  areas,  but  are  remarkably  patch}'.  The  nerves 
of  the  affected  regions  may  be  tender. 

The  heart  is  also  markedly  affected,  being  dilated,  especially  the 
right  side,  with  a  diffuse  apex-beat,  a  spacing  of  the  sounds,  so  that 
the  intervals  may  be  nearly  equal;  while  systolic  murmurs  may  be 
heard,  and  reduplication  of  the  second  sound  is  common,  particu- 
larly over  the  pulmonary  area.  Palpitation  and  epigastric  pulsation 
are  common,  as  is  pulsation  of  the  carotids  and  veins  of  the  neck. 
The  pulse  is  usually  much  increased  in  frequency  and  low  in  tension. 
The  great  danger  of  the  disease  is  death  from  sudden  cardiac 
failure. 

The  blood  does  not  show  much  abnormality  beyond  a  certain 
amount  of  anaemia.     The  differential  leucocyte  count  contains  about 


THE  TYPICAL  FORM  1687 

58  per  cent,  of  polymorphonuclears,  36  per  cent,  of  lymphocytes, 
4  per  cent,  of  mononuclear  leucocytes,  and  2  per  cent,  of  eosino- 
philes. 

The  cerebrospinal  fluid  is  generally  normal.  Lumbar  puncture 
rarely  shows,  in  our  experience,  any  alteration  of  pressure,  although 
a  few  authors  have  noted  an  increase. 

The  urine  may  be  much  diminished  when  there  is  cedema,  but 
when  this  is  passing  off  there  is  a  large  increase  in  the  quantity. 
The  total  solids  are  said  to  be  below  normal,  urea  and  chlorides 
being  diminished,  phosphates  and  indican  being  increased,  and 
albuminuria  being  rare. 

Dropsy  may  or  may  not  be  present,  but  some  cedema,  most 
marked  anteriorly  in  the  legs,  is  a  practically  constant  symptom. 
It  usually  begins  along  the  shin  in  the  form  of  a  rather  solid  oedema. 
It  may  spread  over  the  legs  into  the  scrotum,  on  to  the  abdominal 
wall,  and  into  the  face  and  arms,  and  is  characterized  by  being  at 
times  in  peculiar  localized  patches,  and  if  it  takes  place  in  the 
muscles,  gives  rise  to  an  appearance  like  pseudo-hypertrophic 
paralysis.  Along  with  the  cutaneous  cedema  there  is  often  exuda- 
tion into  the  peritoneal,  pleural,  and  pericardial  cavities. 

When  the  dropsy  is  marked  there  may  be  a  great  diminution  of 
the  urine.  This  dropsical  condition  is  often  improperly  considered 
to  form  a  separate  variety  of  the  disease,  and  is  called  the 
'  wet,'  '  hypertrophic,'  or  '  dropsical  '  form,  while  another  variety, 
called  '  dry '  or  '  atrophic  '  beriberi,  is  mentioned  by  many 
authors,  the  two  forms  being  merely  the  early  and  late  stages  of  the 
disease. 

The  tongue  is  usually  clean;  the  throat  may  be  slightly  con- 
gested; digestion  is  fair,  but  a  large  meal  will  increase  the  precordial 
or  epigastric  distress.  Vomiting  is  a  bad  sign.  The  bowels  are 
often  constipated,  the  temperature  normal  or  subnormal.  The 
urine  may  be  diminished,  increased,  or  normal  in  quantity,  accord- 
ing to  the  presence,  the  passing  off,  or  the  absence  of  oedema. 

The  larynx  may  be  paralyzed  partially  or  completely,  and  the 
voice  rendered  raucous  or  lost.     The  lungs  may  be  ©edematous. 

In  this  condition  the  patient  may  remain,  at  times  better,  at 
times  worse,  for  weeks  and  months,  and  may  proceed  slowly  to 
recovery,  with,  of  course,  deformities  if  paralysis  remains,  or  may 
die  suddenly  of  cardiac  failure  when  sitting  up  or  getting  out  of 
bed,  or  from  some  complication. 

3.  Rudimentary  Form. — There  is  a  rudimentary,  abortive,  or 
ambulatory  form  in  which  the  symptoms  are  so  slight  that  perhaps 
the  sufferer  does  not  seek  medical  advice,  but  in  whom  there  may 
be  first  increase  and  then  diminution  of  the  knee-jerks,  patches  of 
anaesthesia,  some  muscular  weakness,  some  gastric  catarrh,  and 
general  malaise.     Repeated  attacks  may  occur. 

Complications.  —Whenever  fever  develops  in  a  beri-beri  patient 
there  is  sure  to  be  a  complication.  The  most  common  are  tuber- 
culosis, dysentery,  and  malaria. 


1688  BERI-BERI  AND  EPIDEMIC  DROPSY 

Sequelae. — Many  authors  do  not  believe  in  sequelae  to  beri-beri, 
but  certainly  there  may  be  the  contraction  left  after  the  paralysis 
and  anaemia,  and  attacks  of  palpitation  may  occur. 

Diagnosis. — The  principal  positive  signs  on  which  to  base  the 
diagnosis  are:  (i)  Loss  of  knee-jerks;  (2)  patches  of  anaesthesia, 
and  occasionally  hyperesthesia,  on  the  legs;  (3)  pain  on  pressing 
the  calf  muscles;  (4)  oedema  along  the  shin;  (5)  absence  of  marked 
albuminuria;  and  (6)  the  absence  of  fever. 

Suspicious  early  signs  in  endemic  areas  are  loss  of  appetite  and  a 
desire  for  lighter  food,  together  with  tenderness  over  the  pylorus 
and  duodenum,  with  exaggerated  knee-jerks. 

Several  diseases  have  to  be  distinguished  from  beri-beri;  first  of 
all  the  different  kinds  of  peripheral  neuritis — e.g.,  alcoholic  neuritis, 
by  the  history  and  the  general  tremulousness;  arsenical  neuritis, 
by  the  abdominal  pains  and  the  diarrhoea;  lead  paralysis,  by  the 
colic  and  the  blue  line  of  the  gums. 

Secondly,  dropsies  due  to  heart  disease  are  recognized  by  the 
murmurs  and  the  history  of  rheumatic  fever,  or  other  infectious 
disease;  kidney  disease,  by  an  examination  of  the  urine;  ankylo- 
stomiasis, by  the  ova  being  found  in  the  faeces;  epidemic  dropsy, 
by  the  fever  and  the  absence  of  anaesthesia  and  paralysis;  malarial 
cachexia,  by  the  enlargement  of  the  spleen,  and  perhaps  the  para- 
sites in  the  blood;  and  kala-azar,  by  the  enlarged  spleen  and  liver. 

Thirdly,  certain  diseases  of  the  spinal  cord  ;  myelitis,  by  the  loss 
of  control  over  the  bladder  and  rectum;  locomotor  ataxy,  by  the 
Argyll-Robertson  pupil;  pellagra,  by  the  skin  eruptions. 

Fourthly,  certain  intoxications,  such  as  ergotism  by  the  gan- 
grene and  the  history,  and  lathyrism  by  the  absence  of  tender 
muscles. 

Prognosis. — The  acute  pernicious  form  is  always  fatal,  the  rudi- 
mentary never.  The  general  mortality  varies  in  different  countries, 
as  follows: — 

Per  Cent. 


Sumatra 

60  to  70 

Hong-Kong 

48-6 

Malaya 

19-7 

Java 

2  to  6 

Japan 

2-5  to  3-5 

But  it  apparently  depends  upon  many  things,  of  which  the  most 
important  is  the  avoidance  of  sudden  cardiac  failure.  If  the  patient 
is  treated  carefully  in  bed  the  danger  is  much  diminished,  but  if  he 
is  allowed  to  sit  up  and  move  about  the  danger  is  great.  Complica- 
tions are  most  unfavourable. 

An  attack  does  not  confer  an  immunity.  On  the  contrary,  it 
rather  predisposes  to  another  attack. 

Observers  who  believe  in  the  infectious  nature  of  the  malady  are 
generally  of  opinion  that  there  are  no  relapses,  but  that  reinfections, 
even  shortly  after  an  attack,  are  common. 

Treatment.— The    treatment    is    essentially    symptomatic,    the 


TREATMENT  1689 

patient  being  placed  in  bed,  and  care  being  taken  to  avoid  anything 
which  is  likely  to  bring  on  cardiac  failure.  Especial  care  is  re- 
quired if  the  patient  gets  up  or  moves  about.  A  cardiac  tonic,  in 
the  form  of  strophanthus  or  digitalis,  is  advisable,  and  amyl  nitrite, 
nitroglycerine,  or  trinitrin  should  be  placed  at  hand,  in  order  that 
they  may  be  used  at  once  if  a  sudden  cardiac  attack  takes  place. 
If  the  attack  is  severe,  with  great  embarrassment  of  the  right  heart, 
it  has  been  advised  to  perform  venesection,  and  remove  some 
eight  ounces  of  blood.  Oxygen  is  useful  during  the  attacks  of 
dyspnoea.  For  the  paralysis  strychnine  should  be  administered,  and 
the  muscles  massaged  to  prevent  atrophy  and  cramps.  Electrical 
excitation  is  also  good. 

If  possible,  the  patient  should  at  once  be  removed  from  the  place 
in  which  he  is  supposed  to  have  acquired  the  disease. 

Braddon  strongly  recommends  atropine  either  as  the  alkaloid  in 
hypodermic  injections  of  y^  to  -^  grain,  according  to  the  urgency 
of  the  symptoms,  or  in  the  form  of  the  tincture  of  belladonna.  He 
considers  that  the  atropine  is  specially  useful  in  cases  of  dyspnoea 
due  to  cardiac  failure  and  pulmonary  embarrassment,  while  he 
gives  a  mixture  of  tincture  of  belladonna  ^  drachm,  tincture  of 
scilla  I  drachm,  and  citrate  of  potash  h  drachm,  in  4  ounces  of 
water  three  times  a  day  for  three  or  more  days. 

With  regard  to  after-treatment,  any  deformity,  such  as  club- 
foot, must  be  rectified,  as  described  in  works  on  orthopaedic  surgery. 
Fraser  and  Stanton  have  prepared  a  remedial  agent  on  the 
lines  indicated  by  their  researches,  and  this  should  be  tried 
when  available.  Only  harmless  rice; — i.e.,  brown  rice  with  more 
than  0.4  per  cent,  of  phosphorus  pentoxide — should  be  given 
to  the  patients,  and  care  should  be  taken  that  it  is  cooked  in 
ordinary  pots,  and  not  under  pressure.  Thomson  and  Simpson 
recommend  a  full  diet  with  1  ounce  of  yeast  and  200  grammes  of 
katjangido-beans  daily.  Chamberlain  and  Vedder  recommend 
that  5  c.c.  of  an  extract  of  rice  polishings  be  given  daily  to  infants 
suffering  from  beri-beri,  and  this  is  administered  in  20-drop  doses 
every  two  hours.  The  patient  must  be  placed  upon  a  good  nourish- 
ing diet,  with  plenty  of  proteid  and  good  vegetables,  and  rice 
should  be  eliminated  from  this  diet.  Careful  nursing  is  necessary 
because  of  the  danger  of  cardiac  failure,  and  good  hygiene  is  also 
necessary. 

Prophylaxis.— Rice  should  be  avoided  as  a  staple  article  of  diet, 
but  if  it  has  to  be  used  it  should  be  in  the  form  of  the  Indian,  country 
rice,  or  paddy,  variously  described  as  the  cured,  stale,  unpolished, 
or  parboiled  rice.  Great  care  should  be  taken  with  the  cooking, 
for  a  good  rice  can  be  converted  into  a  harmful  rice  by  cooking, 
which  should  always  be  performed  in  ordinary  pots,  and  never 
under  pressure  by  steam.  With  regard  to  the  different  kinds  of 
rice,  Schuffner  and  Kuenen  find  that  Rangoon  rice  contains  0-42  to 
0.46  per  cent,  of  P205,  while  Siam  and  Java  rice  is  much  lower. 
They  maintain  that  there  should  be  a  rice  reform,  and  that   a 


1690  BERI-BERI  AND  EPIDEMIC  DROPSY 

minimum  legal  limit  of  0-5  per  cent.  P205  for  dry  rice  should  be 
imposed,  or,  failing  this,  the  substitution  of  other  foods,  to  make 
up  the  deficient  ingredient,  and  a  strict  control  of  cured  rice — i.e., 
white  rice.  Pregnant  and  nursing  women  especially  should  have  a 
liberal  diet  and  harmless  rice. 

A  good  nourishing  diet  is  most  important. 

Good  hygienic  surroundings — i.e.,  good  ventilation,  the  avoid- 
ance of  overcrowding,  plenty  of  sunshine,  and  exercise  in  the  open 
air — may  be  mentioned. 

It  is  as  well  to  thoroughly  disinfect  with  Clayton  gas  or  sulphur 
and  formalin  any  room  in  which  beri-beri  patients  have  been 
living,  or  any  infected  house  or  ship. 

SHIP  BERI-BERI. 

Synonym. — Norwegian  Beri-beri.  Some  authorities  consider  ship  or 
Norwegian  beri-beri  to  be  a  separate  entity  from  tropical  beri-beri,  and  believe 
it  to  be  a  deficiency  disease  taking  an  intermediate  position  between  true 
beri-beri  and  scurvy.  Clinically,  however,  the  condition  is  identical  with 
tropical  beri-beri,  and  runs  the  same  course. 

INFANTILE  BERI-BERI. 

Synonyms. — Philippines  :  Taon,  taol  suba. 

Infants  nursed  by  mothers  suffering  from  beri-beri,  and  living  on 
a  defective  dietary  in  the  Philippine  Islands,  suffer  from  oedema, 
dyspepsia,  and  cyanosis,  and  often  die  suddenly.  Post-mortem 
investigations  show  degenerations  in  the  vagi,  phrenics,  intercostals, 
and  anterior  tibial  nerves,  but  not  so  extensive  as  in  adults. 
Chamberlain,  Vedder,  Andrews,  and  others  conclude  that  this  is  an 
infantile  beri-beri  due  to  some  deficiency  in  the  mother's  milk,  and 
find  that  it  causes  56  per  cent,  of  the  infantile  mortality  in  the 
Philippines. 

EPIDEMIC  DROPSY. 

Synonym. — Acute  anaemic  dropsy. 

Definition. — Epidemic  dropsy  is  an  acute  infectious  disease  of 
unknown  cause,  characterized  by  fever,  drops}',  an  erythematous 
eruption,  and  sometimes  cardiac  symptoms,  but  without  paralysis 
or  anaesthesia. 

History. — In  1876-77  there  was  a  great  famine  in  Southern 
India,  during  which  a  dropsical  disease,  at  the  time  called  '  beri- 
beri,' was  noted.  It  is  possible  that  this  dropsical  disease  was  con- 
veyed in  some  way  from  Madras  to  Calcutta,  for  in  1877  there  was 
an  outbreak  of  epidemic  dropsy  for  the  first  recorded  time  in  that 
city.  It  appeared  when  the  rains  were  over,  and  extended  through 
the  cold  season  into  1878,  disappearing  when  the  warm  weather 
commenced  in  April.  It  recurred  again,  and  followed  the  same 
course  in  the  cold  season  of  1878  and  1879,  and  it  disappeared  in  the 
warm  weather  of  1880,  reappearing  this  time  in  the  warm  weather 
of  1881.     It  only  attacked  natives  of  India,  but  it  spread  from 


EPIDEMIC  DROPSY  1691 

Calcutta  to  Shillong,  Dacca,  and  South  Sylhet,  and  to  Mauritius, 
by  means  of  labourers  passing  through  that  town.  Mauritius 
became  infected  in  1878,  and  was  clear  of  the  disease  in  1879. 

No  further  accounts  of  the  complaint  appeared  until  1901,  when 
it  was  again  recognized  in  Calcutta  and  Madras.  In  1902  it  occurred 
in  the  Barisal  Gaol  in  Bengal,  and  in  1907  it  occurred  in  Assam  and 
the  two  Bengals.  It  is  probable  that  during  the  intervening  years 
it  has  really  been  present  in  some  part  of  India,  but  has  been  called 
'  beri-beri.'  Greig  has  come  to  the  conclusion  that  it  is  a 
deficiency  disease. 

Climatology. —  The  disease  is  met  with  in  India  and  Mauritius, 
and  generally  in  the  cold  season.  Recently  cases  of  this  condition 
have  been  reported  by  Leporini  from  Cirenaica. 

etiology. — The  causation  of  the  disease  is  unknown,  but  there 
are  various  theories — e.g.,  (1)  that  it  is  beri-beri;  (2)  that  it  is  a 
post-dysenteric  anaemia  or  hydremia;  (3)  that  it  is  due  to  nitrogen 
starvation;  (4)  that  it  is  due  to  eating  Burma  rice,  the  action  of 
which  is  explained  in  various  ways;  (5)  that  it  is  dal  poisoning; 
(6)  that  it  is  a  special  bacterial  disease  conveyed  from  person  to 
person  by  the  bed-bug. 

This  latter  is  Delany's  theory,  and  is  supported  by  the  fact  that 
the  disease  is  epidemic,  and  spreads  apparently  by  the  agency  of 
human  beings,  but  not  from  man  to  man;  that  it  begins  with  an 
initial  fever,  and  has  a  rash,  and  that  there  is  a  local  house  infection; 
and,  finally,  by  its  sudden  disappearance  and  reappearance.  Other 
theories  are  that  it  is  a  ptomaine  poisoning,  or  a  bacillus  in  fish,  or 
a  rust  or  fungus  on  rice. 

Pathology. — No  remarks  can  be  made  on  this  part  of  the  subject. 

Morbid  Anatomy. — There  is  subcutaneous  oedema  and  fluid  in 
the  peiitoneal  and  pleural  cavities.  The  mouth  and  pharynx  are 
cedematous,  and  the  oesophagus  may  be  ulcerated.  The  stomach 
is  very  congested,  and  may  show  hemorrhagic  patches,  and  the 
jejunum  is  congested,  as  are  the  mesenteric  glands  and  the  liver. 
The  pancreas  is  normal.  The  aryepiglottidean  folds  and  the  lungs 
are  cedematous  and  congested.  The  kidney  is  congested,  and  may 
show  cloudy  swelling,  but  the  bladder  is  normal.  The  spleen  is 
shrunken;  the  pericardium  may  be  normal,  but  the  heart  is  dilated. 

Symptomatology. — Generally  there  are  no  distinct  prodromata; 
occasionally  the  onset  of  the  disease  is  preceded  by  diarrhoea. 

Epidemic  dropsy  begins  with  anattack  of  fever  without  any  initial 
rigor,  the  temperature  rising  to  990  to  104°  F.,  and  continuing  of  low 
type  with  remissions  and,  later,  intermissions  for  a  variable  period  of 
time,  sometimes  as  long  as  a  month.  Associated  with  the  fever, 
and,  indeed,  the  most  constant  and  characteristic  symptom,  is  the 
dropsy,  which,  beginning  in  the  feet  and  legs,  may  spread  up  the 
thighs  to  the  abdomen,  and  even  to  the  hands,  arms,  and  face. 

There  is  distinct  anaemia  after  the  disease  has  lasted  a  little  time. 
Rogers  records  a  count  of  3,090,000  erythrocytes  per  cubic 
centimetre,  and  a  haemoglobin  count  of  54  to  65  per  cent.     The 


1 692  BERI-BERI  AND  EPIDEMIC  DROPSY 

colour  index  is  said  by  other  observers  to  be  about  normal,  and 
the  proportion  of  white  to  red  cells  to  vary  from  i  to  430  at  the 
invasion,  to  1  to  384  in  the  course,  to  1  to  615  at  the  end. 
Leucocytes  are  apparently  always  increased  in  number,  but  only 
slightly.     The  differential  count  is: — 

Per  Cent. 

Polymorphonuclears  .  .  .  .  . .     60-2 

Lymphocytes              . .  . .  .  .  ..21-4 

Mononuclears             ..  ..  ...  ..      11-7 

Eosinophiles   . .          . .  . .  . .  . .        6*7 

No  animal  01  vegetal  parasites  have  been  discovered  in  blood 
which  is  sterile. 

The  condition  of  the  urine  is  described  as  very  variable,  but  there 
is  no  albumen  and  no  casts  are  to  be  found. 

Effusions  into  the  peritoneal  and  pleural  cavities  may  take  place. 
The  alimentary  canal  is  early  irritated,  and  vomiting  and  diarrhoea 
are  common  occurrences.  A  rash  appears  early  on  the  extremities 
in  the  dropsical  areas;  it  is  usually  erythematous  or  '  measly,'  but 
vesicles  and  haemorrhages  may  be  seen.  Anaemia,  as  remarked,  is 
progressive  during  the  disease,  and  there  may  be  cardiac  dilatation 
with  haemic  murmurs.  In  severe  cases  there  may  be  cough  and 
dyspnoea,  due  to  cedema  into  the  lungs.  Recovery  is  the  rule,  but 
death  may  occur  from  cardiac  or  pulmonary  complications. 

Sequelae. — The  only  sequela  so  far  observed  is  cardiac  weakness. 

Diagnosis. — Epidemic  dropsy  shows  the  following  characteristic 
signs:  dropsy,  slight  fever,  diarrhoea,  rash,  anaemia,  and  no  albu- 
minuria. 

Its  diagnosis  from  beri-beri  is  based  upon  the  presence  of  fever, 
the  persistence  in  some  cases  of  the  knee-jerk,  the  lack  of  paralysis, 
of  painful  muscles,  and  of  anaesthesia.  Some  authorities  maintain, 
however,  that  in  epidemic  dropsy  there  is  no  fever  and  no  rash,  and 
is  indistinguishable  from  beri-beri. 

Prognosis. — The  prognosis  is  favourable  except  in  the  aged,  the 
case  mortality  being  only  2  to  8  per  cent. 

Treatment. — Rest  in  bed  and  the  administration  of  calcium 
chloride,  or  iron  and  strophanthus,  are  the  onby  remedies  usually 
required.  High  temperatures  should  be  treated  by  diaphoretics, 
quinine,  and  sponging. 

Prophylaxis, — Segregation  and  disinfection  are  recommended,  but 
no  rational  prophylaxis  can  be  advised  so  long  as  the  cause  remains 
unknown. 

POTTER'S  DISEASE. 

In  1913  Potter  in  Jamaica  described  a  disease  which  began  with 
numbness,  tingling  cramps,  loss  of  power,  loss  of  hearing,  and  defec- 
tive vision,  without  skin  or  mental  symptoms,  cedema  or  cardiac 
symptoms.  Both  sexes  are  attacked," generally  after  puberty  and 
in  rural  districts.     Whole  families  may  be  attacked. 


REFERENCES  1693 

WAR  ZONE  CEDEMA. 

In  soldiers,  prisoners  of  war,  and  refugees,  having  a  very  scanty  and  un- 
suitable diet  an  cedematous  condition  of  the  legs  and  feet  is  far  from  rare. 
It  is  a  deficiency  condition  more  closely  related  to  scurvy  than  true  beri-beri. 
It  should  be  differentiated  by  blood  examinations  from  a  clinically  similar 
condition  due  to  malaria. 

TROPICAL  CEDEMA. 

Some  years  ago  we  called  attention  in  Ceylon  to  an  cedematous  condition 
of  the  legs,  seen  especialyin  new-comers  and  tourists  in  the  hot  season.  The 
whole  leg  from  below  the  knee  is  affected,  but  if  the  person  wears  boots 
tightly  laced,  the  foot  and  ankle  do  not  show  any  oedema.  There  is  no 
anaesthesia,  the  knee-jerks  are  normal,  and  the  general  condition  is  good. 
The  condition  is  not  related  in  any  way  to  beri-beri  or  scurvy,  and  is  not 
influenced  by  a  change  of  diet.  It  disappears  rapidly  on  going  to  the  hills. 
The  same  condition  has  been  recently  recorded  by  Marshall  from  the  Red  Sea 
and  Bagdad. 

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Bontius    (1645).     De   Medicina   Indorum,   lib.  iii.,   cap.    1.     De   paralyseos 

quandam  Specie  quam  Indigenae  beri-beri  vocant. 
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1694  BERI-BERI  AND  EPIDEMIC  DROPSY 

Stanley  (1902).     Journal  of  Hygiene,  p.  369. 

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Epidemic  Dropsy. 

Anderson  (1908).     Indian  Medical  Gazette,  xliii.  85. 

Campbell  (1908).     Ibid.,  327. 

Delany  (1908).     Ibid.,  167. 

Greig  (1911).     Indian  Med.  Gazette. 

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Pearse  (1908).     Indian  Medical  Gazette,  lxiii.  128. 
Rogers  (1908).     Fevers  of  the  Tropics,  p.  186. 
Rutherford  (1809).     Indian  Medical  Gazette,  xliii.  174. 
Sarkar  (1915).     Ind.  Med.  Gaz.,  October. 

Potter's  Disease. 

Potter  (191 3).     Reports  on  Peripheral  Neuritis  in  Jamaica. 


CHAPTER  LXX1I 
TROPICAL    POISONINGS 

General    Remarks — Ackee   poisoning — Onyalai — References. 

GENERAL  REMARKS. 

We  have  already  defined  a  poison  and  discussed  criminal  poisoning, 
accidental  poisoning,  stimulant  and  sedative  poisoning,  and  the 
poisons  used  in  trial  by  ordeal  in  Chapter  X.  (p  161),  in  which  we 
gave  a  brief  outline  of  the  symptoms  produced  by  a  number  of  these 
poisons,  as  well  as  some  few  remarks  with  regard  to  treatment. 

There,  however,  remains  one  form  of  accidental  poisoning,  to 
which  we  have  already  referred  on  p.  173,  to  which  special  reference 
may  be  made  here,  and  that  is  ackee  poisoning,  which  was  long  known 
as  the  vomiting  sickness  of  Jamaica,  and  was  included  in  the  clinical 
part  of  the  last  edition. 

This  particular  variety  of  poisoning  might  also  be  looked  upon  as 
a  form  of  vegetal  food  poisoning,  a  subject  which  is  considered  in 
Chapter  XIII.,  p.  193. 

Other  forms  of  poisoning,  such  as  arrow  poisons,  animal  poisons, 
trade  poisons,  can  be  found  in  Chapters  XI.  (p.  180),  and  XII. 
(p.  187). 

ACKEE  POISONING. 

Synonym. — The  vomiting  sickness  of  Jamaica. 

Dsflnition. — An  acute  and  often  fatal  illness,  occurring  mostly 
in  children  and  to  a  less  extent  in  adults  in  Jamaica,  characterized 
by  sudden  onset,  persistent  vomiting,  causing  in  fatal  cases  collapse, 
and  bi ought  about  by  eating  the  unsound  fruit  of  the  ackee  tree, 
Blighia  sapida  Koenig,  or  drinking  the  water  in  which  such  fruit 
has  been  cooked. 

History. — For  many  years  the  term  '  vomiting  sickness  '  was 
applied  to  any  disease  associated  with  this  symptom,  but  as  various 
diseases  became  differentiated  and  better  diagnoses  were  made,  it 
became  evident  to  Turton  in  1904  and  to  Kerr  in  1905  that  there  was 
a  definite  disease  in  Jamaica  to  which  the  term  could  be  applied. 

This  disease  only  appeared  in  the  cooler  months,  and  was  asso- 
ciated with  vomiting  and  convulsions,,  and  a  death-rate  of  80  per 
cent,  to  90  per  cent.,  the  end  coming  in  a  few  hours. 

In    1906   Branch  considered   it   to   be   a  syndrome,   and  inen- 

1695 


1696  TROPICAL  POISONINGS 

tioned  the  ackee,  without,  however,  being  definite  as  to  its  causal 
effect. 

In  1912  Potter,  after  considering  cerebro-spinal  meningitis, 
ptomaine  poisoning,  ackee  poisoning,  and  cassava  poisoning,  came 
to  the  conclusion  that  it  was  a  phase  of  yellow  fever. 

In  1913  Scott  suggested  that  it  might  be  fulminating  cerebro- 
spinal meningitis,  and  in  the  same  year  Seidelin  opposed  the  yellow 
fever  and  the  meningitis  views  and  believed  it  to  be  a  local 
disease. 

In  1915  Scott,  as  a  result  of  an  investigation  into  an  outbreak  at 
Montego  Bay,  found  that  in  the  majority  of  cases  ackees  formed  part 
of  the  last  meal  taken  in  health,  and  that  they  could  not  be  excluded 
in  a  single  case.  Persons  taking  soup  or  pot-water  made  with 
ackees  developed  symptoms  in  two  hours,  and  death  nearly  always 
resulted. 

The  ackee  is  the  fruit  or  aril  of  Blighia  sapida  Koenig,  belonging 
to  the  natural  order  Sapindaceae,  and,  being  a  native  of  West  Africa, 
is  merely  an  introduced  plant  in  Jamaica. 

Only  unsound  ackees  cause  the  symptoms,  and  an  ackee  is  un- 
sound (1)  when  it  is  unopened;  (2)  when  it  is  picked  from  a  decayed, 
bruised,  or  broken  branch;  (3)  when  it  has  been  forced  open; 
(4)  when  it  has  a  soft  spot. 

In  19 17  Scott  confirmed  this  view  as  to  the  causal  effect  of  the 
ackee,  and  by  his  experiments  upon  animals  demonstrated  the  nature 
of  vomiting  sickness. 

Climatology. — So  far  the  disease  is  only  known  in  Jamaica,  but 
it  must  be  remembered  that  the  tree  is  a  native  of  West  Africa. 
We,  however,  do  not  know  whether  the  fruit  is  used  as  a  food  in 
this  country,  and,  at  all  events,  up  to  the  present  no  one  has  reported 
the  poisoning  from  that  part  of  the  world. 

^Etiology. — Vomiting  sickness  is  caused  by  eating  the  unsound 
fruit  of  Blighia  sapida  Koenig,  the  ackee  plant,  or  taking  the  soup 
or  '  pot-water  '  made  with  this  fruit.  These  latter  are  the  more 
severe  cases,  because  the  poison  appears  to  be  extracted  by  boiling 
with  water.  Alcoholic  extract  of  unsound  ackees  is  not  poisonous. 
The  watery  extract,  on  the  other  hand,  when  administered  to  cats 
and  dogs,produced  the  same  symptoms  and  mortality  rate  as  in  man, 
and  after  death  the  same  post-mortem  signs  were  found.  Herbi- 
vorous animals  are  unaffected.  The  poisoning  takes  place  in  the 
months  from  November  to  April,  which  corresponds  with  the 
ackee  season.  Several  members  of  a  family  are  taken  ill  at  one  and 
the  same  time,  as  would  be  expected  from  a  food  poisoning.  It  also 
occurs  among  near  neighbours  in  the  settlement,  and  is  rare  in  white 
children  and  East  Indians,  being  confined  to  the  children  of  the 
indigenous  population.  There  is  no  indication  that  sex  plays  any 
part  in  the  aetiology,  which  must  be  looked  upon  as  an  acute  poison- 
ing. A  case  of  known  ackee  poisoning  occurring  in  man  showed  the 
same  symptoms,  cause,  and  post-mortem  changes  as  cases  of 
vonrting  sickness,  and  as  the  experimental  animals. 


MORBID  ANATOMY  1697 

Morbid  Anatomy.— There  is  a  general  hyperemia,  with  a  tendency 
to  haemorrhages  in  various  organs.  The  mucous  membrane  of  the 
stomach  and  the  bowels  is  congested,  while  the  lumen  of  these 
organs  may  contain  a  dark  slimy  substance.  There  is  fatty 
degeneration  in  the  liver  and  kidneys,  and  in  the  former  case  this 
change  is  said  to  be  more  acute  than  in  phosphorus  poisoning. 
Microscopically  necrobiotic  changes  are  found  in  the  cells  of  the 
liver,  kidneys,  and  pancreas. 

Pathology. — -The  illness  comes  on  suddenly  in  a  person  who  has 
previously  been  in  perfect  health,  and  is  characterized  by  primary 
or  gastric  vomiting,  followed  by  a  few  hours  of  temporary  cerebral 
vomiting,  which  is  rapidly  followed  by  convulsions,  coma,  and 
death,  the  average  duration  of  the  illness  being  twelve  and  a  half 
hours. 

The  poison  appears  to  be  an  irritant  to  the  stomach,  and  to  cause 
vomiting,  which  may  rid  the  body  of  it,  when  the  patient  rapidly 
recovers;  but  if  it  remains  in  the  system  it  acts  upon  the  nervous 
system,  causing  the  cerebral  vomiting,  convulsions,  and  coma, 
which,  apparently,  always  end  in  death. 

Symptomatology. — Somewhere  about  midnight  a  child  wakes  up 
and  complains  of  pain  in  its  stomach,  in  a  little  time  vomits  its 
last  meal,  and  after  this  feels  better.  In  certain  cases  no  further 
symptoms  occur,  and  there  is  a  rapid  recovery. 

.More  usually,  however,  after  a  period  of  temporary  relief  the 
vomiting  commences  again,  and  may  be  accompanied  by  fever,  while 
the  vomit  consists  of  frothy  mucus.  These  symptoms  continue 
until  the  child  passes  into  a  state  of  collapse,  with  cold  sweats,  a 
weak  and  rapid  pulse,  and  irregular  respirations. 

These  symptoms  invariably  lead  to  death,  which  is  preceded  by 
convulsions. 

Variety. — In  rare  cases  there  is  no  vomiting,  and  only  the  cerebral 
symptoms,  drowsiness,  convulsions,  and  coma,  leading  to  death. 
This  is  the  so-called  '  vomiting  sickness  without  vomiting.' 

Diagnosis. — -The  cardinal  points  in  the  diagnosis  are: — Its 
endemicity;  its  seasonal  prevalence;  its  sudden  onset  in  mem- 
bers of  one  family  or  in  neighbours;  in  native  children  without 
regard  to  sex;  the  quick  complete  recovery  of  some  cases,  while 
others,  after  showing  cerebral  symptoms,  end  fatally;  and  finally 
the  evidence  of  having  partaken  of  a  meal  containing  ackees  or  their 
extracts.  It  can  be  diagnosed  from  yellow  fever  by  the  absence  of 
the  black  vomit,  and  from  cerebrospinal  meningitis  by  an  absence 
of  Koenig's  sign  and  of  the  meningococcus. 

Prognosis. — This  is  very  bad,  as  some  80  to  go  per  cent,  of  the 
patients  die.     If  recovery  is  to  take  place,  it  is  rapid  and  complete. 

Treatment. — No  specific  treatment  is  known. 

Prophylaxis. — Instruct  the  people  not  to  use  unsound  ackees. 
This  has  been  done,  with  the  resuL  that  in  1916  there  were  only  three 
deaths  from  vomiting  sickness  in  Jamaica. 

107 


1698  TROPICAL  POISONINGS 


ONYALAI. 


Synonyms. — Edyuo  (Bukoba);  Kafindo  (Congo). 

Definition. — An  acute  disease  of  unknown  causation,  characterized 
by  the  appearance  of  bullae  containing  blood  on  the  surface  of  the 
body,  the  tongue,  soft  palate,  or  buccal  mucous  membrane. 

History. — The  disease  was  discovered  by  Yale  Massey  in  Angola 
in  1904,  and  fully  described  by  Wellman  later  in  the  same  year  in 
Portuguese  West  Africa,  and  by  Feldman,  in  1905,  in  East  Africa, 
where  it  is  called  '  ed3aio  '  by  the  natives  of  Bukoba.  Mense  (1906) 
thinks  that  the  '  kafindo  '  disease  of  the  Unyamwezi  people  of  the 
Congo  is  the  same  disease.  Hasmorrhagic  bullae  in  the  mouth,  but 
without  general  symptoms,  have  been  described  by  Maxwell  in 
Changpo,  South  China,  as  being  due  to  the  accidental  introduction 
into  the  mouth  of  a  kind  of  spider's  web. 

]/Etiology. — This  is  unknown,  but  Mense  thinks  it  may  be  some 
kind  of  poisoning,  perhaps  with  some  species  of  the  Euphorbiacese. 
Wellman  considers  that  it  is  not  a  manifestation  of  malaria;  nor 
is  it  a  vegetal  poisoning,  nor  a  snake-poisoning,  though  the  bite 
of  Bitis  arietans,  the  puff-adder,  simulates  some  cases  closely. 
Neither  trypanosomes  nor  bacteria  were  found.  It  is  not  a  pur- 
pura haemorrhagica,  nor  Henoch's  purpura,  nor  Schonlein's  disease. 

Symptoms. — The  onset  is  sudden,  and  is  accompanied  by  lassitude 
and  a  dazed  appearance.  Sometimes  the  parotids  are  tender,  and 
the  eyes  may  be  somewhat  reddened,  and  in  about  66  per  cent,  of 
cases  there  is  a  slight  rise  of  temperature.  Numbness  and  pain  in 
various  parts  of  the  body  may  be  noted. 

The  appetite  is  poor;  bullae  may  be  seen  on  the  tongue  and  in 
the  mouth  and  pharynx,  while  they  also  occur  in  the  oesophagus, 
stomach,  and  bowels.  The  tongue  is  swollen  and  painful.  Vomit- 
ing of  blood  is  not  rare,  and  bloody  diarrhoea  may  take  place. 
Hematuria  has  been  noted,  and  cerebral  haemorrhage,  with  the 
usual  signs,  has  been  seen.  It  is  believed  that  haemorrhage  into 
the  pancreas,  liver,  and  spleen,  may  take  place  in  some  cases. 
Bullae  may  also  appear  in  the  skin,  ranging  from  the  size  of  a  split 
pea  to  several  inches  in  diameter.  The  typical  bullae,  whether  on 
a  mucosa  or  in  th;;  skin,  extend  deeply,  involving  the  submucosa 
or  the  corium,  and  are  crossed  by  fibrous  trabecule,  in  the  meshes 
of  which  lies  partially  coagulated  blood,  which  appears  dark 
through  the  skin  or  mucosa.  The  red  corpuscles  are  not  disin- 
tegrated, and  can  be  seen  by  the  microscope. 

The  disease  is  said  to  have  a  tendency  to  recur  two  or  three 
times. 

Diagnosis. — The  diagnosis  from  snake-bite  maybe  effected  only  by 
the  history,  as  the  bullae  may  not  be  visible  on  the  skin  or  mucosa. 
Miliaria  can  be  excluded  by  the  blood  examination.  Schonlein's 
disease,  or  peliosis,  is  diagnosed  by  the  rash,  painful  swelling  of 
the  joints,  and  the  purpuric  eruption.  Henoch's  purpura  is  met 
with  generally  in  children,  and  has  joint  symptoms  as  well  as  a  rash. 


REFERENCES  1699 

Prognosis. — Wellman  reports  three  deaths  in  fourteen  cases,  and 
says  that  the  malignancy  varies  in  different  seasons  and  districts. 

Treatment. — Wellman  thinks  that  arsenic  in  full  doses  is  the  best 
treatment.  He  says  the  natives  use  empirically  Geigera  wdlmani 
Hatch  and  Albizzia  anthelmintic  a  A.  Broga.  Massey  recommends 
large  doses  of  bicarbonate  of  soda  and  cod-liver  oil. 


REFERENCES. 

Ackee  Poisoning. 

The  most  valuable  account  is  Scott  (1915),  Ninth  Six-Monthly  Report  of 
the  Government  Bacteriologist,  March  to  September,  Kingston,  Jamaica. 

Scott  (191 7).     Transactions  of  the  Society  of  Tropical  Medicine  and  Hygiene, 
x.  3,  47-62.     London. 

Onyalai. 

Feldman  (1905).     Medizinalberichte  iiber  die  deutschen  Schutzgebiete,  S.  45. 
Massey  (1904).     Journal  of  Tropical  Medicine,  September  1,  p.  269. 
Mense  (1906).     Tropenkrankheiten,  iii.  789. 
Wellman  (1904).     Journal  of  Tropical  Medicine,  February  15,  p.  55;  April  15, 

1908,  p.  119. 
Wellman  (1905).     New  York  Medical  Journal,  September  2,  p.  495. 
Wellman  (1907).     Atti  della  Societa  per  gli  Studi  della  Malaria,  vii.  29. 


CHAPTER  LXXIII 
PELLAGRA 

Synonyms  —  Etymology  —  Definition  —  History  —  Climatology — JEtiology — 
Pathology  —  Morbid  anatomy  —  Histopathology  — •  Symptomatology — 
Diagnosis — Prognosis — Treatment — Prophylaxis — References. 

Synonyms. — Italian  :  Umor  Salso,  Scottatura  di  Sole,  Malattia  della  Miseria, 
Mai  del  Sole,  Malattia  della  In^olazione  di  Primavera,  Risipola  Lombarda,  Mai 
della  Spienza,  Mai  del  Padrone,  Jettatura  di  Sole,  Cattivo  Male,  Mai  della 
Vipera,  Calore  del  Fegato,  Salso,  Pelandria,  Pellarella,  Pellarina,  Psychoneuro- 
sis  Maidica,  Mai  Rosso,  Maidismus,  Lepra  Italica  Maiidica,  Scorbuto  Montano, 
Scorbuto  Alpino,  Elephantiasis  Italica.  Spanish :  Mai  de  la  Rosa,  Mai 
d'Asturias,  Mai  del  Higado,  Calor  del  Higado,  Escamadura  del  Higado,  Flema 
Salada.  French  •'  Maladie  de  la  Teste,  La  Gale  de  Sainte  Ignace,  Mai  de  Saint 
Amans,  Mai  des  Saintes  Mains,  Mai  de  Sainte  Rose,  Mauvais  Dartre.  German  : 
Der  Lombardische  Aussatz.  Roumanian  :  Buba  Tranjilor,  Rana  Tranjilor, 
Parleala,  Jupuiala.  Greek :  Grasci  Elephantiasim.  Egyptian  :  Inshup, 
Qushuf,  Gofar,  Lahooh.     South  America  :  Chichismo. 

Etymology. — The  name  '  pellagra '  is  an  Italian  word,  possibly- 
coined  by  the  peasants  from  two  word? — pelle,  meaning  '  skin,' 
and  agra,  meaning  '  rough  ' — though  other  possible  origins  are  also 
given.  It  was  introduced  into  medical  literature  by  Frapolli  in 
177 1  in  his  work,  '  Animadversiones  in  Morbum  Vulgo  Pelagram/ 
when  he  spelt  it  with  only  one  I  instead  of  with  two. 

Definition. — Pellagra  is  an  endemic  disease,  usually  of  long 
duration  and  of  unknown  causation,  which  is  characterized  by 
cutaneous,  gastro-intestinal,  and  nervous  symptoms,  which  under- 
go exacerbations  at  recurrent  intervals,  usually  in  the  spring  or 
autumn. 

History. — When  it  is  considered  that  pellagra  has  been  over- 
looked in  quite  recent  years  in  America,  Scotland,  and  England, 
and  probably  in  many  other  parts  of  the  world,  it  will  not  be  thought 
to  be  astonishing  that  ancient  literature  is  silent  as  to  its  existence 
in  Europe,  but  the  absence  of  these  references  by  no  means  proves 
that  the  disease  itself  was  not  present.  Strambio  finds  that  some 
of  the  symptoms  mentioned  in  Hippocrates  may  be  those  of  pellagra, 
and  says  that  his  description  of  '  Sollicitudo  '  indicates  a  disease 
resembling  the  mental  condition  found  in  pellagra  during  an  acute 
exacerbation.  We  have  searched  through  Hippocrates,  and  have 
been  unable  to  find  anything  which  to  our  mind  bears  any  resem- 
blance to  pellagra.  Trie  peculiar  symptoms  from  which  St.  Francis 
of  Assisi,  who  lived  in  a  district  which  to  this  day  is  pellagrous, 

1700 


HISTORY 


1701 


suffered,  markedly  resemble  pellagra,  as  he  had  an  eruption  upon 
his  hands  and  feet,  associated  with  an  extraordinary  mental  condi- 
tion; but  though  these  speculations  are  interesting,  they  are  far  too 
uncertain  to  be  of  any  use  in  determining  the  interesting  point  as  to 
whether  pellagra  existed  in  Europe  before  the  introduction  of  maize 
by  Columbus.  In  1578  the  disease  seems  to  have  been  known  in 
Milan  as  '  pellarella,'  but  was  confounded  with  eczema,  leprosy, 
erysipelas,  and  scurvy,  and 
no  real  importance  can  be 
attached  to  a  simple  name 
unaccompanied  by  any  de- 
scription of  the  disease  to 
which  it  was  applied.  A 
slightly  more  definite  refer- 
ence is  found  in  17 13  in 
Ramazzini's  work,  '  De 
Morbis  Artificium  Diatriba,' 
under  the  heading  '  Agri- 
colae,'  where  he  says:  '  Eas- 
dem  ob  causas,  iis  pers^epe 
contingunt  dolores  colici  et 
affecto  Hippocondriaca 
quam  ipsi  appellant,  il  mal 
del  Padrone.' 

The  recognition  that  the 
cutaneous,  gastro-intestinal, 
and  mental  symptoms  ex- 
hibited by  the  sufferers 
constituted  a  clinical  entity 
was  first  made  by  Gaspar 
Casal  on  March  26,  1735, 
but,  unfortunately,  was  not 
published  until  1762,  when 
his  work,  '  Historia  Natural 
y  Medica  del  Principado  de 
Asturias  Sequida  de  la 
Descripcion  de  la  Enfer- 
medad  conocida  per  el  Vulgo 
con  il  Nombrc  de  Mal  de  la 
Rosa,' appeared.  Casal  gave 
arepresentation of  the  disease 

(Fig.  736),  showing  the  eruption  around  the  neck  and  down  the  front 
of  the  chest  (called  Casal's  necklace),  and  on  the  dorsa  of  the  hands 
and  feet.  With  Sambon  one  of  us  has  visited  the  Oviedo  district 
of  the  Asturias  in  North  Spain,  where  Casal  first  recognized  pellagra, 
and  find  that,  as  regards  the  cases  along  the  River  Nero  the  disease 
exists  as  it  did  in  his  days.  On  December  2,  1740,  a  leai  ned  monk 
named  Feijoo  wrote  to  Casal  stating  that  '  Mal  de  la  Rosa  '  existed 
in  his  native  country,  Galicia.    Before  Casal's  publication  appeared 


Fig.  736. — Mal  de  la  Rosa. 
(After  Casal.) 


1702  PELLAGRA 

the  celebrated  Thiery  visited  Madrid,  where  he  met  Casal,  and  was 
shown  cases  of  pellagra,  and  afterwards  he  observed  one  case  him- 
self. On  his  return  to  Paris  he  wrote  a  paper  entitled,  '  Description 
d'une  Maladie  appellee  Mai  de  la  Rose  aux  Asturies,'  which  was 
published  in  the  second  volume  of  Vandermonde's  journal  called 
'  Recueil  Periodique  d'Observations  de  Medecine,  de  Chirurgie,  et 
de  Pharmacie,'  in  May,  1755.  It  is  pleasing  to  record  that  not 
merely  did  Thiery  give  a  most  excellent  description  of  the  clinical 
signs  of  pellagra,  but  he  also  gave  full  credit  to  Casal  for  his,  as  yet 
unpublished,  great  discovery. 

These  publications  of  Casal  and  Thiery  laid  the  foundations  of 
the  modern  knowledge  of  pellagra.  We  will  now  turn  to  the  various 
countries,  and  study,  very  briefly,  the  history  of  the  disease  therein. 

Italy. — Early  in  the  eighteenth  century  the  disease  appears  to  be 
well  known  to  the  medical  men  of  Cremona  and  Cremasco,  as  well 
as  to  Antonio  Terzaghi  at  Sesto  Calende  on  Lago  Maggiore,  and  to 
Francesco  Zanetti,  who  recognized  it  in  1769  at  Canobis,  also  on 
Lago  Maggiore.  It  will  thus  be  seen  that  pellagra,  hinted  at 
in  1578  in  Milan,  written  about  by  Ramazzini  in  1713,  had  become 
a  disease  well  known  to  the  general  practitioner  and  peasantry,  and 
only  required  an  historian  to  become  recognized  by  the  medical 
profession.  This  historian  was  found  in  Francesco  Frapolli,  one  of 
the  physicians  in  the  large  hospital  in  Milan,  who  in  1771  published 
his  work,  'Animadversiones  in  Morbum  Vulgo  Pelagram,'  in  which 
for  the  first  time  the  word  '  pellagra  '  (spelt  with  a  single  I)  was  used. 
This  work,  followed  by  those  of  a  number  of  authors,  drew  more 
attention  to  the  disease,  with  the  result  that  the  Patriotic  Society 
of  Milan  offered  a  prize  for  the  best  essay  on  the  subject,  while  the 
Kaiser  Joseph  founded  a  special  hospital  for  pellagrins,  and  placed 
it  under  the  charge  of  Gaetano  Strambio,  whose  justly  celebrated 
work,  '  De  Pellagra/  appeared  in  three  volumes  during  the  years 
1 786-1789.  In  1787  two  young  Dutch  doctors,  Jensen  and  Hollen- 
hagen,  and  a  young  Frenchman,  Levacher  de  la  Feutrie,  visited 
Italy  to  study  pellagra,  concerning  which  they  published  reports 
on  their  return  to  Holland  and  France.  In  1799  Chevalier  gave 
an  account  of  Jensen's  work  in  the  London  Medical  Review  and 
Magazine.  In  this  way  the  knowledge  of  the  disease  called  pellagra 
started  and  spread. 

In  the  meanwhile  a  disease  called  '  Scorbuto  Alpino  '  had  been 
definitely  recognized  by  Giuseppe  Antonio  Pujati  in  1740  in  Feltre, 
to  the  north  of  Venice,  and  the  same  disease  was  found  later  by 
Antonio  Gaetano  Pujati,  the  son  of  Giuseppe  Antonio  Pujati,  and 
Nascimbeni  in  the  Venetian  Friuli,  and  this  disease  found  its  his- 
torian in  Odoardi,  a  pupil  of  the  older  Pujati,  who  in  1776  published 
his  work,  '  Di  Una  Specie  Particolare  di  Scorbuto,'  in  which  an 
account  of  Professor  Pujati's  discoveries  was  given.  In  this  way 
the  knowledge  of  the  disease  '  Scorbuto  Alpino  '  was  started,  so 
that  in  Italy  at  this  time  there  were  described  two  separate  diseases 
under  different  names,  and  found  in  different  regions;  and  it  was 


HISTORY  1703 

not  till  Fanzago  in  1789  published  his  work,  '  Memoria  sopra  la 
Pellagra  del  Territorio  Padovano,'  that  these  two  diseases  were 
recognized  to  be  one  and  the  same.  After  this  date  the  literature 
concerning  pellagra  increased'considerably,  but  no  work  of  great 
importance  appeared  until  1810,  when  Marzari  published  his  book, 
'  Saggio  Medico-Politico  sulla  Pellagra  e  Scorbuto,'  in  which  he 
laid  stress  upon  '  maize '  as  the  principal  etiological  factor  in  the 
disease — a  view  which  had  previously  been  mentioned,  but  not 
so  forcibly,  by  Casal  and  others.  The  importance  of  this  work  is 
that,  ever  since  its  publication,  the  maize  theory  in  some  form  has 
been  generally  adopted  in  Italy.  Marzari  was  of  the  opinion  that 
it  was  the  deficiency  of  the  gluten  in  the  maize  which  was  the  main 
agent  of  the  disease,  but  he  also  suspected  toxicity.  From  Marzari 's 
time  there  are  very  numerous  publications,  among  which  may  be 
mentioned  those  by  Henry  Holland  in  1817  on  the  pellagra  of 
Lombardy,  published  in  the  Medico-Chirurgical  Transactions,  and 
by  Zecchinelli  in  1818. 

Balardini  in  1845,  in  his  work  entitled  '  Delia  Pellagra,  del  Grano 
turco  quale  Causa  Precipua  di  quella  Malattia  e  dei  Mezzi  per 
Arrestarla,'  promulgated  the  view  that  the  causation  was  a  fungus 
growing  in  the  maize,  which  fungoid  growth  was  called  'Verderame,' 
and  was  thought  to  be  due  to  Sporisorium  maidis.  This  publication 
was  of  the  greatest  importance,  as  it  afforded  an  explanation  as  to 
why  the  disease  should  attack  some  people  and  not  others,  and  thus 
gave  the  maize  theory  greater  importance.  This  subject  was 
further  studied  by  Costallat  and  others,  who  produced  symptoms 
in  chickens  by  feeding  them  on  maize  containing  verderame,  which 
were  said  to  resemble  those  of  pellagra. 

In  1872  Lombroso  began  to  study  pellagra,  and  continued  to  do 
so  till  he  died  in  1909.  He  believed  that  the  disease  was  an  intoxi- 
cation produced  by  the  toxins  manufactured  by  organisms,  harm- 
less in  themselves,  and  growing  on  maize.  More  recently  a  view 
has  been  promulgated  that  the  disease  is  due  to  good  maize,  which 
in  certain  people  produces  the  symptoms  of  the  disease,  and  in 
others  does  not.  Such,  briefly,  was  the  condition  when  Sambon  in 
1905  began  his  work,  which  he  has  continued  up  to  the  present 
time.  This  work,  which  is  mainly  epidemiological,  has  thoroughly 
shaken,  if  not  completely  destroyed,  the  maize  theory,  and  has 
brought  forward  many  facts  which  support  strongty  a  parasitic 
theory  of  the  causation  of  the  disease  as  well  as  a  probability  of  the 
infection  being  spread  by  one  of  the  biting  flies. 

Spain.— -The  discovery  of  the  disease  by  Casal  in  1735  in  the 
Oviedo  district  of  the  Asturias  has  already  been  mentioned,  as  well 
as  the  fact  that  Feij6o  had  recognized  it  in  Galicia.  The  next 
publication  is  by  an  Englishman,  called  Townsend,  entitled  '  A 
Journey  through  Spain,'  and  published  in  three  volumes  in  London 
in  1791.  In  the  second  volume,  on  p.  10,  there  is  a  short  clear 
account  of  '  Mai  de  Rosa.'  This  is  the  earliest  known  account  of 
pellagra  in  English.     In  1820  Eximeno  made  an  inquiry  into  the 


1704  PELLAGRA 

disease,  and  came  to  the  conclusion  that  '  Mai  del  Higado,'  '  Mai  de 
la  Rosa,'  and  pellagra  were  one  and  the  same  disease.  In  1835 
Mendez  Alvaro  recognized  pellagra  in  the  malady  called  '  Flema 
Salada,'  and  in  1847  Henriquez  showed  that '  Mai  de  Monte  '  was  the 
same  disease.  In  1849  Roussel  visited  Spain,  and  recognized  that  the 
disease  in  France  and  that  in  Spain  were  the  same  clinical  entity. 
Since  that  date  many  excellent  works  have  been  published  in  Spain 
on  pellagra,  notably  by  Calmarza  and  Roel,  while  of  late  the  disease 
has  been  carefully  studied  by  Huiteras,  Pittaluga,  and  the  physicians 
of  Oviedo. 

The  maize  theory  of  the  aetiology  of  pellagra  has  never  gained 
credence  in  Spain,  and  hence  the  term  '  Spanish  pellagra,'  or  a 
pellagra  not  due  to  maize,  has  been  used  by  some  Zeists  as  a  medical 
synonym  for  a  hoax. 

Portugal. — Pellagra  is  known  to  exist  in  Portugal,  but  we  are  in 
the  same  condition  as  older  writers,  in  that  we  can  give  no  history 
of  its  recognition  or  spread. 

France. — We  have  already  noted  Thiery's  publication  in  1755, 
and  the  fact  that  in  1787  a  young  Frenchman,  Levacher  de  la 
Feutrie,  proceeded  to  Italy  to  study  the  disease,  concerning  which 
he  subsequently  published  accounts  in  1802  and  i8c,6;  but  it  was 
Hameau  in  1818  who  first  recognized  the  disease  in  France  as 
occurring  around  Teste-de-Buch,  in  the  Plain  of  Arcachon.  Hameau 
was  not  acquainted  with  the  literature  which  had  sprung  up  con- 
cerning pellagra,  and  his  observations  were  in  reality  a  rediscovery 
of  the  disease.  In  1829  he  read  an  excellent  dissertation  on  the 
subject  before  the  Society  of  Medicine  of  Bordeaux,  under  the  title 
'  Description  d'une  Maladie  Nouvelle.'  It  would  appear  that  he 
considered  it  to  be  an  infection  in  some  way  acquired  from  sheep. 
In  all  he  observed  no  less  than  seventy-six  cases. 

There  is,  however,  evidence  in  favour  of  the  suggestion  that 
pellagra  had  long  existed  in  France,  and  this  is  to  be  found  in  the 
fact  that  the  peasants  used  to  call  the  disease  '  Mai  de  Saint  Amans/ 
because  there  was  a  statue  to  St.  Amans  in  Bascons  which  was 
always  moist,  and  this  moisture  was  used  by  the  pellagrins  as  an 
application  to  their  eruption.  According  to  Roussel,  there  was 
another  curious  custom  followed  by  the  peasants  of  the  Landes, 
which  was  to  visit  a  certain  statue  in  which  the  Christus  was  repre- 
sented with  red  hands.  The  priest  was  wont  to  apply  an  ointment 
to  these  hands,  from  which  the  sufferers  removed  a  little  of  the 
ointment  and  applied  it  to  their  own  inflamed  hands,  feet,  face,  etc. 
From  this  interesting  ceremony  the  disease  was  called  the  '  Mai  des 
Saintes-Mains.'  Other  popular  names,  such  as  '  Mai  d' Arouse  ' 
and  '  Mai  de  Saint e-Rosa,'  tend  to  show  that  the  common  people 
were  well  acquainted  with  the  disorder.  Sambon  has  also  informed 
us  that  some  of  Napoleon's  soldiers  became  affected  by  pellagra 
during  the  campaigns  in  Italy,  and  certainly  cases  are  recorded  in 
the  Hotel  Dieu  and  in  the  Hopital  Saint-Louis,  while  Jourdan 
published  a  paper  on  the  disease  in  1819. 


HISTORY  1705 

Briere  de  Boismont  in  1830  drew  attention  to  the  fact  that 
pellagra  occurred  around  Paris,  and  in  1847  Ardusset  showed  that 
the  '  Maladie  de  la  Teste '  of  Hameau  was  pellagra.  In  1843 
Marchand,  after  investigations  extending  from  1836  to  1842,  em- 
phasized the  fact  that  pellagra  was  essentially  a  disease  of  the 
country,  and  not  of  the  town.  In  1845  appeared  Roussel's  account 
of  his  researches  in  France  and  Spain,  to  which  reference  has  already 
been  made.  In  1865  Billod  published  his  account  of  asylum  pel- 
lagra as  a  pseudo-pellagra — that  is  to  say,  a  pellagra  not  due  to 
maize.  Sambon  and  one  of  us  have  investigated  the  pellagra  of 
the  Landes,  where  the  disease  has  greatly  diminished,  and  this 
appears  to  be  associated  with  a  diminution  in  the  malaria  of  the 
same  region,  which  appears  to  be  due  in  part,  at  least,  to  the  im- 
proved cultivation  of  the  soil,  the  drainage  of  swamps,  etc.,  and 
the  stocking  of  the  waters  with  fish. 

Austria. — -The  disease  was  first  noticed  in  the  Tyrol,  where  it 
is  still  very  prevalent,  and  where  it  is  being  ably  studied  by 
Merk,  Weiss,  and  others.  In  1794  Nicolas  and  Jambon  reported 
its  presence  near  Vienna. 

Hungary  and  Roumania. — In  1846  Lachaise  drew  attention  to  an 
epidemic  of  pellagra  in  Roumania,  in  1856  Julius  Theodori  reported 
its  presence  in  the  Danube  provinces,  while  in  1862  Bouchard 
pointed  out  that  Sigmund  said  that  the  Hungarian  pellagra  existed 
solely  in  the  vast  plains  bordering  the  Rivers  Danube  and  Theiss 
— i.e.,  in  the  Alfold — Which  were  often  covered  by  inundations.  It 
is  interesting  to  note  that  these  rivers  have  been  regulated,  and 
that  the  disease  is  said  to  have  considerably  abated  there.  Be  that, 
as  it  may,  there  is  to  our  personal  knowiedge  a  considerable  amount 
of  pellagra  in  Transylvania,  where  it  has  been  studied  by  Hollander, 
Kaiser,  and  others,  and  in  Roumania,  where  Babes  says  there  are 
more  than  200,000  cases. 

Macedonia. — Cases  of  pellagra  have  been  observed  by  us  in 
Macedonia. 

The  British  Islands. — Though  reported  as  long  ago  as  i860  by 
Brown,  and  again  in  1909  by  Cranston  Low  in  Scotland,  no  attention 
has  been  seriously  paid  to  the  disease  until  recently,  when  Sambon 
and  one  of  us,  searching  through  the  British  Islands,  came  across 
cases  in  both  Scotland  and  England,  and  it  appears  probable  that 
more  definite  information  with  regard  to  the  spread  of  pellagra  in 
these  islands  will  soon  be  forthcoming.  The  interest  with  regard  to 
these  cases  is  that  while  it  is  impossible  to  mathematically  exclude 
all  possibility  that  a  patient  had  never  tasted  a  grain  of  maize,  still 
it  would  be  straining  the  maize  hypothesis  to  an  unjustifiable  extent 
to  try  to  make  it  apply  to  all  of  these  oases.  It  is  interesting  to 
note  that  pellagra  has  been  found  as  far  north  as  the  Shetland 
Islands.  Of  late  years  quite  a  number  of  cases  of  pellagra  have 
been  reported  in  the  British  Isles. 

Iceland. — We  have  no  information  as  to  the  presence  of  pellagia 
in  Iceland,  with  the  sole  exception  of  a  statement  by  Holland  that 


i7o6  PELLAGRA 

he  had  seen  cases  in  Iceland  resembling  the  pellagra  which  he  had 
observed  in  Italy. 

Africa. — Though  first  noticed  in  Egypt  by  Pruner  in  1847  under 
the  term  '  leproses,'  its  recognition  therein  is  principally  due  to  Sand- 
with,  who  found  it  in  1893,  and  to  Keatinge  and  Warnock,  who  have 
not  merely  kept  that  knowledge  alive,  but  have  added  considerably 
to  the  study  of  the  disease.  There  is,  however,  still  a  tendency  to 
consider  pellagra  a  part  of  the  syndrome  of  ankylostomiasis. 
More  recently  pellagra  has  been  recognized  in  other  parts  of  Africa, 
and  it  is  possible  that  it  will  eventually  be  found  to  be  widespread 
in  that  continent. 

America. — Notwithstanding  careful  inquiries,  Wood  has  failed  to 
discover  any  evidence  of  the  existence  of  pellagra  among  the  North 
American  Indians  during  the  eighteenth  century,  but  he  has  found 
some  evidence  of  cases  in  the  early  years  of  the  nineteenth  century. 
In  1864  Gray  and  Tyler  first  definitely  reported  cases  in  them,  but 
though  at  times  recognized,  the  disease  was  not  generally  admitted 
to  be  present  until  1907,  when  Searcy  reported  eighty-eight  cases, 
of  which  fifty-seven  were  fatal.  From  that  date  the  works  of  Bab- 
cock,  Lavinder,  Siler,  Roberts,  Niles,  Wood,  and  many  others,  have 
made  the  disease  well  known.  In  the  meanwhile,  pellagra  has  been 
recognized  in  the  West  Indies,  Mexico,  and  other  parts  of  America. 

Asia  and  Oceania. — During  recent  years  pellagra  has  been  recog- 
nized in  India,  the  Straits  Settlements,  the  Philippine  Islands,  and 
the  Sandwich  Islands. 

Summary. — The  above  history  of  pellagra  demonstrates  the  ease 
with  which  the  disease  may  be  overlooked,  even  when  abundantly 
present,  by  well-trained  and  most  competent  observers.  It  also 
impresses  us  with  the  fact  that  pellagra  should  be  looked  for  in 
every  country,  without  any  preconceived  idea  as  to  its  aetiology. 

Climatology. — It  appears  probable  that  before  many  years  have 
passed,  pellagra  will  be  found  to  be  prevalent  all  over  the  world. 
At  present  it  is  known  to  exist  in : — 

Europe. — Scotland,  England,  France,  Spain,  Portugal,  Italy, 
Austria  (including  the  Tyrol,  Bosnia,  and  Herzegovina),  Hungary, 
Roumania,  Russia,  Serbia,  Macedonia,  Bulgaria,  Greece,  and  Turkey. 
Cases  have  been  reported  as  far  north  as  the  Shetland  Islands. 

Africa. — Algeria,  Tunisia,  Egypt,  Central  Africa,  Rhodesia,  and 
South  Africa. 

Asia. — Asia  Minor,  Persia,  India,  and  the  Straits  Settlements. 

Oceania. — Sandwich  Islands. 

America. — United  States,  Mexico,  West  Indies,  Brazil,  Columbia, 
and  the  Argentine. 

The  feature  of  the  last  few  years  with  regard  to  the  climatology 
has  been  the  recognition  of  pellagra  as  an  endemic  disease  in  Scot- 
land, England,  and  the  United  States.  Mere  geographical  distri- 
bution per  se  is  not  so  important  as  an  epidemiological  inquiry 
into  the  actual  localities  in  which  the  disease  occurs.  Pellagra 
is  essentially  a  disease  of  long  duration,  and  patients  are  capable 


CLIMATOLOGY 


1707 


of  moving  far  from  the  place  in  which  the  first  symptoms  appeared, 
and,  again,  the  first  symptoms  often  appear  in  early  childhood  and 
reappear  after  some  years'  interval,  when  the  patient  may  be 
living  in  quite  a  different  district  from  that  in  which  he  resided 
during  his  younger  years.  It  is  therefore  necessary  to  prepare 
and  study  spot  maps  showing  where  the  patients  were  first  attacked 
by  the  signs  and  symptoms  of  the  disease,  and  this  is  being  done 
at  the  present  time  by  Sambon,  whose  results  will  be  awaited  with 
interest.  In  general  it  may  be  stated  that  inquiries  of  this  nature 
show  that  by  far  the  larger  number  of  cases  occur  in  country  dis- 
tricts, and  not  in  towns,  and  that  the  densest  localization  is  in 
houses  near  or  alongside  certain  streams.     In  fact,  study  the  locali- 


JAN    FEB      MAP  APRIL    MAY  JUNE    JULY    AUG   SEPT    OCT      NOV    DEC. 


70 


60 


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40 


30 
20 
10 


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37- 

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1 

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2 

5 

26 

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I 

9 

*y. 

Fig.  737. — Seasonal   Variation    in  the  Admissions    for   Six  Years  of 
Pellagra  Cases  into  the  Kasr-el-Ainy  Hospital,  Cairo. 

(Specially  prepared  by  Keatinge  and  Stiven.) 


zation  in  what  country  you  will,  as  we  have  done  in  France,  Spain, 
Italy,  Austria,  Hungary,  Roumania,  and  Egypt,  it  is  impossible 
not  to  be  impressed  with  the  relationship  between  pellagra  and 
water.  Generally  the  water  is  moving,  and  often  it  is  moving 
rapidly,  but  this  last  does  not  appear  to  be  absolutely  necessary. 
As  a  rule,  the  nearer  the  dwellings  are  to  such  water,  the  greater 
the  number  of  cases.  Cases  do,  however,  occur  at  a  distance 
from  water,  but  inquiry  will  often  demonstrate  that  the  affected 
people  work  near  or  have  been  in  some  way  connected  with  a 
stream.  Cases  do  occur  in  towns,  but  they  are  relatively  few, 
and  careful  inquiry  will  usually  elicit  a  perhaps  almost  forgotten 
fact  that  the  disease  really  began  after  some  visit  to  the  country. 
Inquiries,  however,  must  be  made  with  care,  otherwise  wrong  im- 
pressions may  be   obtained.     One  of  the  most  interesting  cases 


1708  PELLAGRA 

which  we  have  met  with  was  that  of  a  young  boy  who  was  sup- 
posed never  to  have  left  a  large  town,  and  yet  was  suffering  from 
pellagra.  Careful  inquiry  elicited  the  fact  that  he  was  in  the  habit 
of  going  for  a  day  or  so  every  year  to  stay  with  some  relatives 
who  lived  in  a  pellagrous  area,  and  the  time  of  the.  year  chosen  for 
this  visit  was  one  in  which  acute  cases  occurred.  In  a  locality 
pellagra  usually  occurs  among  the  poor,  especially  among  fiefd 
labourers;  but  it  may  also  occur  among  the  rich  and  among 
persons  who  habitually  work  indoors;  it  is,  however,  usually  not 
difficult  to  trace  a  relationship  between  the  commencement  of  the 
disease  and  a  visit  or  residence  in  some  pellagrous  area,  and  very 
often,  again,  a  relationship  to  water. 

With  regard  to  seasons,  there  is  a  universal  consensus  of  opinion 
that  most  attacks  appear  in  the  spring  or  early  summer  (in  Egypt 
with  the  Khamseen),  after  which  there  is  a  diminution  in  the  cases, 
and  although  attacks  may  begin  in  the  summer,  they  are  not 
common.  In  the  autumn,  however,  there  is  a  definite,  though 
secondary  increase  in  the  number  of  cases,  which  decrease  almost 
to  nil  in  the  winter.  These  statements  are  well  borne  out  by  the 
curve  of  pellagra  admissions  into  the  Kasr-el-Ainy  Hospital, 
Cairo,  for  the  years  1906-1911  inclusive.  This  curve,  for  which  we 
are  indebted  to  the  kindness  of  Dr.  Keatinge,  was  most  carefully 
prepared  by  Dr.  Stiven,  and  demonstrates  the  incidence  of  pellagra 
as  seen  in  that  hospital. 

Pellagra  may  occur  in  hilly  or  even  mountainous  regions,  where 
it  is  often  very  common — as,  for  example,  the  Tyrol — but  can 
equally  occur  on  the  flat  alluvial  deposit  of  rivers— as,  for  example, 
the  delta  of  the  Nile.  It  would  appear  that  pellagra  extends  from 
near  the  Equator  to  the  Shetland  Islands  in  the  north,  and  to  South 
Africa  in  the  south,  and  that  it  encircles  the  world  in  an  easterly 
or  westerly  direction.  In  our  experience  the  one  important  factor 
to  be  certain  that  pellagra  is  endemic  in  a  region  is  to  find  it  in 
very  young  children  born  in  the  region  from  which  they  have  never 
stirred. 

To  summarize,  pellagra  has  a  world-wide  distribution.  It 
occurs  in  hills  and  plains.  The  cases  are  densest  near  moving 
freshwater,  and  usually  begin  in  spring  or  autumn. 

/Etiology. — The  causation  of  pellagra  is  at  the  present  time 
unknown,  so  that  we  are  compelled  to  consider  possibilities 
instead  of  facts — a  point  which  we  desire  the  reader  to  bear  in  mind 
while  perusing  the  remarks  we  are  about  to  offer  for  his  con- 
sideration. 

The  extraordinary  theories  which  we  have  found  still  in  existence  among 
medical  men  in  the  various  pellagrous  regions  which  we  have  visited  are: — 

1  That  it  is  not  a  disease,  but  merely  dirt,  and  can  be  cured  by  turpentine, 
soap,  and  water.  This  theory  of  course  applies  only  to  the  quiescent  stage 
of  a  very  chronic  case,  and  is  easily  excluded  by  a  little  knowledge  of  the 
disease. 

2.  That  it  is  not  a  disease  per  se,  but  merely  a  series  of  stray  symptoms, 
and  that  no  one  has  studied  the  cases  from  the  commencement  of  the  disease 


MTIOLOGY  i7o9 

to  its  fatal  termination.  A  study  of  merely  Hameau's  writings,  excluding  all 
the  modern  Italian,  Roumanian,  and  American  literature  on  the  subject, 
would,  we  think,  satisfy  any  unbiassed  person  that  this  view  is  untenable. 

3.  That  it  is  not  a  disease  per  se,  but  merely  symptoms  of  some  other 
well-known  disorder.  The  disease  which  it  is  most  commonly  said  to  belong 
to  is  ankylostomiasis,  but  most  of  our  readers  will  themselves  have  treated 
many  cases  of  ankylostomiasis  without  meeting  with  the  symptoms  of 
pellagra,  and  many  will  be  acquainted  with  pellagrins  who  show  no  signs  of 
ankylostomiasis. 

The  above  can  be  easily  dismissed,  and  would  not  have  been  men- 
tioned if  we  had  not  personally  met  with  believers  in  all  of  them. 
With  regard  to  the  more  likely  theories,  we  must  discuss  the 
following: — 

I.  The  deficiency  theory. 
II.  The  maize  theory. 
III.  The  parasite  theory. 

I.  The  Deficiency  Theory. — In  Chapter  IV.,  p.  94,  we  have 
briefly  traced  the  evolution  of  foods  and  the  effects  of  a  low  protein 
dietary,  as  well  as  the  effects  of  certain  nitrogenous  complexes  on 
man,  and  therefore  need  not  recapitulate  what  we  have  written  on 
those  pages.  Arguing  upon  the  theory  of  the  causation  of  beri-beri 
by  the  absence  of  a  nitrogenous  complex,  some  people  have  asked 
whether  pellagra  may  not  be  due  to  the  lack  of  some  nitrogenous 
complex  in  the  food;  and,  further,  it  has  been  suggested,  or  rather 
hinted,  that  this  might  explain,  not  merely  the  maize  theory  of 
pellagra,  but  those  cases  in  which  no  maize  has  been  eaten,  but  in 
which  the  diet  has  been  largely  oatmeal  or  rice.  Thus,  Nightingale 
in  his  paper  on  Zeism,  which  appears  to  us  to  be  pellagra,  finds  that 
when  steam-milled  mealie  bread  alone  was  supplied  to  the  prisoners 
in  the  Victoria  Gaol  in  Rhodesia  the  disease  broke  out,  and  when  this 
was  stopped,  and  meat,  vegetables,  and  rice  were  substituted,  the 
epidemic  ceased ;  and  when  hand-milled  rapoko  (maize)  was  obtained, 
the  effect,  in  Nightingale's  words,  was  '  immediate  and  almost 
magical,'  as  the  patients  began  quickly  to  recover.  In  this  rapoko 
the  husk  was  not  eliminated  by  the  hand-milling.  The  parallel 
between  this  and  beri-beri  is  obvious.  In  our  opinion  there  is  one 
great  flaw  in  this  theory,  and  this  is  that  pellagra  may  occur  in 
people  provided  with  an  excellent  dietary.  To  this  it  might  be 
replied  that  some  peculiarity  of  the  individual's  body  destroyed 
the  necessary  vitamine,  but  this  argument  is,  to  our  minds,  rather 
strained.  Modern  work  tends  at  the  moment  to  support  this  theory 
as  being  the  true  course  of  the  disease,  but  there  are  man}'  difficulties, 
and  it  cannot  be  said  to  be  proven. 

II.  The  Maize  Theory. — Much  of  a  most  convincing  nature,  if  left 
unanalyzed,  can  be  written  in  support  of  the  maize  theory  in  general. 
It  can  be  pointed  out  that  maize  [Zea  mais  Linnaeus)  was  original^  a 
native  of  America,  where  it  has  been  found  in  its  ancient  form  of 
small  grains  in  the  graves  of  the  Incas,  and  that  it  was  introduced 
by  Columbus  or  his  followers  into  Europe,  where  it  did  not  grow 


1710  PELLAGRA 

well  in  certain  countries,  like  the  British  Islands,  which,  therefore, 
remained  free  from  the  disease  until  the  nineteenth  century,  when 
importation  of  maize  took  place  in  greater  quantities  than  hereto- 
fore, but  where  now  there  is  plenty  of  maize  sold  as  pop-corn  for 
children,  and  it  may  possibly  be  made  into  bread,  cakes,  scones, 
porridge,  etc.,  while  whisky  is  often  partially  made  from  the  same 
grain.  On  the  other  hand,  it  grew  well  in  Spain,  Italy,  and  France, 
and  that  its  introduction  into  a  country  has  always  been  followed 
by  the  appearance  of  pellagra  in  that  country,  and  quotations 
supporting  maize  can  be  drawn  even  from  the  writings  of  its  most 
vigorous  opponent,  Sambon,  who  states: — '  From  authentic  docu- 
ments of  the  time  we  learn  that  "  melica,"  or  "  fromentone  "  ' 
— i.e.,  maize— 'was  grown  in  Cremona  in  the  sixteenth  century, 
and  ...  in  1556  a  Cremona  nobleman  offered  the  Duke  of 
Florence  ten  staia  of  the  new  cereal.'  When  this  statement  that 
there  is  plenty  of  maize  in  Cremona  in  1556  is  compared  with  the 
statement  that  pellagra  was  well  known  in  Cremona  about  1700  to 
peasants  and  medical  men  alike,  a  Zeist  would  maintain  that, 
allowing  for  the  disease  being  so  liable  to  be  overlooked,  this  was 
a  remarkable  coincidence.  Another  epidemiological  fact  which, 
taken  by  itself,  would  strongly  support  the  maize  theory  is  the  well- 
known  fact  that  in  the  delta  of  the  Nile  there  is  plenty  of  pellagra 
and  plenty  of  maize,  but  as  the  Nile  is  ascended  the  maize  diminishes, 
millet  being  used  instead,  and  the  incidence  of  pellagra  also  di- 
minishes, and  at  present  it  is  said  to  be  unknown  south  of  Assouan, 
which  statement  must  be  received  with  caution,  as  pellagra  has  so 
often  been  reported  absent  from  places  where  it  is  now  known;  and, 
moreover,  pellagra  is  known  to  exist  in  Central  Africa.  In  Columbia 
pellagra  is  said  to  be  found  only  in  people  who  regularly  take  a 
drink  made  from  fermented  maize.  This  drink  is  called  '  chicha  ' 
and  the  malady  'chichismo.'  The  Zeist  states  that  pellagra  is 
found  wherever  maize  is  used,  at  all  events,  as  an  important  article 
of  food.  As  a  matter  of  fact,  maize,  either  growing  or  imported, 
is  found  all  over  the  world,  and  pellagra  would  appear  also  to  be 
found  all  over  the  world. 

Against  the  maize  theory  there  are  the  facts  that  tend  to  demon- 
strate that  persons  who  are  alleged  never  to  have  tasted  maize  have 
suffered  from  pellagra ;  moreover,  relapses  have  occurred  after  three, 
five,  and  even  fifteen  years'  residence  in  gaols  or  asylums  in  which 
maize  is  not  merely  not  allowed  to  be  used  as  an  article  of  diet,  but 
care  is  taken,  by  inspection  and  by  (periodical  chemical  and  micro- 
scopical examination,  to  exclude  it.  A  Zeist  would  answer  to  these 
objections  that  there  was  some  fallacy,  and  that  nothing  short  of 
being  the  victim  yourself  would  make  it  reasonably  certain  that 
maize  was  not  consumed,  and  even  then  it  might  have  been  eaten 
unwittingly;  and,  further,  that  all  safeguards  designed  1o  prevent 
food  sophistications  in  institutions  break  down. 

Notwithstanding  this,  some  of  the  Scotch  cases  appear  to  exclude 
the  possibility  of  maize  being  an  aetiological  factor,  and  prophylactic 


ETIOLOGY  1 711 

work  on  this  basis  has  been  so  far  a  failure,  for,  although  the  disease 
has  diminished  in  certain  regions  for  a  time,  it  has  later  returned 
with  considerable  vigour.  With  regard  to  the  presence  of  pellagra 
in  Europe  before  the  introduction  of  maize  there  is  no  trustworthy 
evidence,  and  the  possible  occurrence  of  the  disease  in  the  celebrated 
St.  Francis  of  Assisi  is  only  an  interesting  speculation. 

After  carefully  considering  all  the  facts  in  support  of  the  maize 
theory,  and  comparing  them  with  those  against,  we  have  come  to 
the  opinion  that  the  maize  theory,  in  general,  is  so  far  based  upon 
insufficient  foundations.  It  is,  however,  necessary  to  lay  before 
the  reader  the  various  phases  of  this  theory,  which  may  be  classified 
as  follows: — 

1.  Photodynamic  theory. 

2.  Deficiency. 

3.  Toxicity. 

4.  Infectivity. 

1.  Photodynamic  Theory. — The  special  promoter  of  this  theory  is 
Raubitschek,  whose  work  has  tended  to  show  that  an  exclusive 
maize  diet,  good  or  bad,  proves  deleterious  to  white  mice  and  guinea- 
pigs  if  these  animals  are  exposed  to  sunlight.  He  also  suggests  that 
an  exclusive  diet  of  other  cereals,  such  as  rice,  millet,  or  wheat, 
might,  under  similar  circumstances,  produce  the  same  phenomena. 
This  theory  maintains  that  photodynamic  substances  are  introduced 
by  the  cereals  into  the  blood,  and  these,  under  the  influence  of  sun- 
light, become  toxins,  and  thus  cause  inflammation  of  the  skin 
and  other  symptoms  resembling  to  some  extent  pellagra.  More- 
over, Raubitschek  maintains  that  he  has  cured  mice  suffering  from 
fagopyrism  by  keeping  them  in  darkness,  even  though  the  diet  was 
unaltered,  and,  further,  that  he  has  obtained  favourable  results 
by  excluding  light  from  the  skin  of  pellagrins  by  means  of  darkened 
rooms,  red  windows,  ointments,  bandages,  etc.  Hirschfelder  has 
searched  for  this  fluorescent  (photodynamic)  substance  in  the 
blood  serum  of  five  patients  suffering  from  severe  pellagra,  and 
found  that  there  was  no  difference  in  the  fluorescence  between 
their  serum  and  that  of  healthy  persons.  Moreover,  fagopyrism 
only  occurs  in  white  animals,  and  not  in  black;  whereas  pellagra 
can  occur  in  the  jet  black  negro,  which  appears  to  us  to  be  a  strong 
objection. 

2.  Deficiency. — This  theory  has  been  mentioned  above  with  regard 
to  the  absence  of  nitrogenous  complexes,  and  it  only  remains  to 
add  that  protein  deficiency  has  also  been  brought  forward  as  a 
possible  explanation  of  the  action  of  maize  in  producing  pellagra, 
but  has  no  sound  foundation.  Moreover,  many  people  live  on  rice 
and  potato,  which  have  lower  nitrogen  ratios  than  maize. 

3.  Toxicity. — Volpino,  Mariani,  Bordoni,  and  Alpago-Novcllo, 
have  made  investigations  with  regard  to  inoculating  maize  ex- 
tracts into  patients,  obtaining  several  general  reactions.  These 
experiments  support  the  latest  view,  which  is  really  only  the  revival 


1712 


PELLAGRA 


of  an  older  view,  that  normal  maize  in  certain  individuals  may 
produce  pellagra,  or,  in  other  words,  that  there  is  an  individual 
susceptibility  to  maize.  This  subject  has  been  recently  carefully 
investigated  by  Rondoni  in  human  beings.  He  procured  his  maize 
from  the  domestic  store  of  certain  pellagrins,  and  having  tested 
his  cases  for  tuberculosis  by  von  Pirquet's  test,  administered  ex- 
tracts of  the  maize  by  intramuscular  injections  to  thirty-three 
pellagrins  and  thirty  non-pellagrins.  He  did  not  find  any  violent 
reaction,  as  described  by  other  writers,  but  he  found  that  recent 
cases  of  pellagra  and  convalescents  reacted  more  definitely  than 
non-pellagrins,  showing  slight  fever,  headache,  malaise,  excitability, 
and  sleeplessness,  and  considered  that  this  increased  sensibility 
might  be  regarded  as  an  anaphylactic  reaction  to  some  undefined 
factor  in  the  maize  extract.  If  this  anaphylactic  theory  held,  then 
any  person  who  for  a  few  weeks  ate  a  quantity  of  maize  at  any  time 
of  the  year  should  develop  acute  pellagra.  The  Illinois  Commission 
attempted  anaphylactic  tests  by  von  Pirquet's  method,  substituting 
maize  extracts  for  tuberculin,  and  the  result  was  negative. 

A  second  theory  states  that  pellagra  is  due  to  toxins  produced 
during  the  spring  by  the  germination  of  the  maize.  The  objection 
to  this  is  that  some  cases  start  in  the  autumn. 

The  third  theory  asserts  that  poisons  are  generated  in  the  bowel 
from  the  grain  (Neusser)  by  the  aid  of  the  Bacillus  coli  communis 
(De  Giaxa).  This  latter  theory  of  De  Giaxa  is  supported  by  experi- 
ments, for  he  produced  the  symptoms  in  animals  inoculated  by  the 
toxin  produced  by  growing  theB.  coli  communis  in  maize  media. 

Numerous  observers  have  reported  poisons  in  fermenting  maize. 
Thus,  Lombroso  in  1871  obtained  two  alkaloids,  one  like  conium 
and  the  other  like  strychnine,  but  the  symptoms  produced  b}^  these 
on  men  and  animals  were  not  like  those  of  pellagra.  Others  have 
reported  tetanic  or  narcotic  poisons,  etc.,  but,  on  the  other  hand, 
Monselice  failed  to  obtain  any  such  poisons  in  damaged  grain  from 
pellagrous  districts. 

4.  Injectivity. — At  the  present  time  the  popular  belief  is  that  the 
disease  is  caused  by  maize  damaged  by  being  cultivated  and  har- 
vested under  unfavourable  circumstances,  and  stored  in  such  a  damp 
condition  that  it  becomes  mouldy.  This  has  been  supported  by 
Hirsch,  who  points  out  that  a  bad  maize  harvest  is  followed  by  an 
increase  in  the  cases  of  the  disease.  The  theories  as  to  the  sub- 
stance in  the  damaged  maize  which  causes  the  disease  are  manifold, 
and  may  be  classed  into  (a)  fungi,  (b)  bacteria,  (c)  chemical  sub- 
stances. 

(a)  Fungi. — Monti  and  Tirelli  showed  that  fungi  were  commonly 
found  in  maize,  those  most  usually  met  wilh  being  Pcnicillium 
glaucum,  Rhyzopus  nigricans,  Mucor  racemosus,  and  species  of 
Aspergillus  and  SaccJiaromyces.  The  special  fungus,  Sporisorinm 
maidis,  described  by  Ballardini  in  1845  as  the  cause  of  the  disease, 
is  probably  only Penici 'Ilium  glaucum  or  Mucor  racemosus,  the  former 
being  held  by  some  writers  to  be  the  causative  agent,  but  its  effects 


PARASITIC  THEORY  171 3 

on  men  and  animals  are  quite  different  from  pellagra.  Aspergillus 
fumigatus  and  Aspergillus  flavescens  (or  A.  varians)  have  been 
obtained  by  Ceni  in  pure  cultures  from  the  lungs,  pleura,  and 
pericardium  of  pellagra  cadavers,  but  the  symptoms  of  the  disease 
are  quite  different  from  aspergillosis.  Later,  Ceni  and  Fossati  have 
stated  that  the  real  cause  of  the  disease  is  the  toxin  from  the  fungi. 

(b)  Bacteria. — Monti  and  Tirelli  showed  that  many  bacilli  grow  in 
maize — e.g.,  Bacillus  solanacearum,  and  another  like  B.  subtilis — 
and  it  has  been  shown  by  Paltauf  that  the  so-called  B.  maidis  of 
Majocchi  and  Cuboni  is  only  the  common  potato  bacillus.  Another 
bacillus,  called  B.  pellagra,  is  stated  by  Carrarioli  to  produce  toxins, 
which,  when  injected  into  animals,  produce  the  typical  symptoms 
of  the  disease. 

Tizzoni  has  described  a  bacillus  found  in  the  cerebro-spinal  fluid 
of  pellagra  patients  and  on  maize,  but  this  bacillus  will  be  con- 
sidered at  greater  length  below. 

The  maize  theory  is  therefore  by  no  means  proved,  and  in  fact 
is,  in  our  opinion,  very  doubtful. 

Parasitic  Theory. — The  parasitic  theory  of  the  origin  of  pellagra, 
which  is  supported,  to  a  certain  extent,  by  our  own  observations 
and  by  the  Illinois  Commission,  who  conclude  that  it  is  a  disease 
due  to  infect  ion  with  some  living  organism,  may  be  classified  into: — 

A.  Vegetal  parasite. 

Tizzoni's  streptobacillus. 

B.  Animal  parasites. 

Alessandrini's  theory,  1910. 
Long's  theory,  1910. 
Perroncito's  theory,  1910. 
Babes'  theory,  1911. 
Sambon's  theory,  1905. 

Tizzoni's  Streptobacillus.— This  is  really  a  part  of  the  maize 
theory,  as  Tizzoni  has  found  the  bacillus  on  maize;  but  it  is  also 
a  genuine  parasitic  theory,  because  he  has  also  found  it  in  the  blood, 
cerebro-spinal  fluid,  and  organs  of  pellagrins  after  death.  He  has 
found  it  in  both  acute  and  chronic  pellagra;  it  is  a  non-spore- 
bearer,  and  resists  temperatures  of  8o°  and  900  C.  for  one  hour. 
It  is  easily  cultivated,  and  is  believed  to  be  taken  into  the  body  with 
the  food,  so  causing  the  infection.  Tizzoni  claims  that,  this  organism 
is  the  cause  of  the  disease,  but  this  claim  has  been  refuted  by  Wood, 
Raubitschek,  the  Illinois  Pellagra  Commission,  and  others,  and 
therefore  cannot  be  accepted  as  proven. 

Alessandrini's  Theory.  —  From  epidemiological  researches 
mainly  undertaken  in  Umbria,  Alessandrini  has  come  to  the  con- 
clusion that  there  is  some  relationship  between  pellagra  and  drinking- 
water,  and  he  has  found  a  slender  nematode  worm  in  the  drinking- 
water  of  pellagrous  places.     This  worm,  which  he  places  in  the 

108 


1714 


PELLAGRA 


family  Filariidse,  he  considers  to  be  the  cause  of  the  disease.     He 
also  states  that  he  has  found  a  filarial  egg  in  the  skin  of  pellagrins. 

According  to  Sambon,  who  has  seen  Alessandrini's  specimens, 
the  thick-shelled  egg  belongs  to  one  of  the  nematode  worms  infect- 
ing pigs.  Alessandrini's  theory  has  not  received  much  support  up 
to  date. 

Long's  Theory.— This  theory  suggests  that  pellagra  is  merely  a 
phase  of  amoebic  dysentery,  but  the  Illinois  Commission,  as  well  as 
the  observations  of  Sambon  and  one  of  us,  do  not  support  this 
theory.  Dysenteric-like  ulcers  can  be  found  in  the  intestine,  but 
they  often  do  not  contain  amoebae. 

Perroncito's  Theory . — Perroncito  has  found  peculiar  parasitic 
bodies  in  the  skin  of  pellagrins.  This  is  an  important  statement, 
and  further  investigation  of  these  forms  is  awaited  with  interest. 

Babes'  Theory. — 'Babes  states  that  he  has  found  bodies  re- 
sembling a  Chlamydozoon,  in  the  skin. 

Sambon's  Theory.— This  theory  is  double-barrelled— i.e.,  it 
brings  forward  the  proposition  that  pellagra  is  a  protozoan  infec- 
tion, and  that  it  is  spread  by  the  agency  of  a  biting  fly. 

Parasite. — His  reasons  for  believing  that  it  is  a  parasitic  disease 
are  almost  entirely  epidemiological.    They  are: — 

i.  The  Mononucleosis  present  in  the  blood. 

2.  The  Presence  of  Long  Intervals  of  Quiescence,  followed  by  a 
Relapse. — Thus,  a  young  pellagrin  with  marked  symptoms  who 
comes  to  London,  and  receives  most  excellent  food,  without  any 
admixture  of  maize,  suffers  from  a  mild  relapse  every  year  in  the 
month  of  April.  In  this  case  there  can  be  no  question  of  maize 
causing  these  relapses.  Further,  we  may  state  that  the  young 
person  appears  to  be  in  the  very  best  of  health  at  the  time  of  writing 
(January).  Similar,  but  not  such  convincing,  cases  have  often  been 
reported  in  gaols  and  asylums,  as  mentioned  above. 

Siler  and  Nichols  in  Peoria  Asylum  filled  two  cottages  with 
about  sixty  insane  persons  in  each.  One  cottage  was  placed  on 
a  generous  maize  diet  and  the  other  on  a  maize-free  diet.  At  the 
end  of  twelve  months  the  maize-eaters  had  four  certain  cases  and 
one  doubtful  case  of  pellagra,  while  the  maize-free  group  included 
five  certain  and  five  doubtful  cases  of  pellagra.  Probably  these 
were  merely  relapses  of  the  disease  which  had  occurred  long  before, 
but  as  we  have  only  seen  a  summary  of  the  Illinois  Pellagra  Com- 
mission Report,  we  cannot  give  details. 

A  point  has  been  made  that,  while  patients  in  asylums  develop 
acute  symptoms,  the  attendants  do  not,  and  this  is  held  to  be  an 
argument  against  the  parasitic  cause  of  the  disease.  But  this 
is  just  where  the  experience  of  Sambon  and  one  of  us  differs  from 
those  of  many  authorities,  because  we  have  seen  the  disease  begin 
so  often  in  early  childhood.  The  youngest  case  seen  was  three 
months  of  age,  and  we  have  obtained  excellent  histories  of  long 
intervals  occurring  between  one  series  of  acute  attacks  and  the  next. 
We  look  upon  these  asylum  cases  as  probably  relapses  of  earlier 


PARASITIC  THEORY  171 5 

attacks,  and  are  therefore  not  surprised  that  attendants  are  not 
attacked,  because  probably  the  agent  of  the  conveyance  of  the 
disease  is  not  present  in  the  vicinity  of  the  asylum. 

In  other  asylums,  however,  it  is  possible  that,  if  suitable  con- 
ditions were  present,  the  disease  might  spread  among  the  inmates 
and  attendants. 

3.  The  Constant  and  Characteristic  Topographical  Distribution. — 
We  have  already  drawn  attention  to  the  topographical  distribution, 
and  to  the  fact  that  pellagra  remains  endemic  in  the  same  localities 
for  very  long  periods,  and  we  have  also  referred  to  the  case  of  a 
young  boy  developing  pellagra,  though  constantly  residing  in  a 
town,  after  a  brief  visit  to  a  pellagrous  region.  The  case  of  the 
fishermen  of  Burano  (vide  infra)  may  also  be  quoted;  and,  finally, 
attention  may  be  invited  to  many  similar  instances  quoted  by 
Sambon  in  his  able  '  Progress  Report  on  the  Investigation  of 
Pellagra,'  published  in  London  in  1910.  Associated  with  this,  it 
may  be  mentioned  that  of  two  places  almost  contiguous  one  may  be 
affected  and  the  other  not. 

4.  Its  symptoms,  course,  duration,  morbid  anatomy,  as  well  as 
therapy,  are  similar  to  those  found  in  parasitic  diseases. 

5.  Spirochete. — Sambon  found  a  spirochete  in  the  liquor  from 
a  bulla  on  the  hand  of  a  case  of  acute  pellagrous  dermatitis  in 
Roumania. 

These  points  will  be  dealt  with  under  Pathology,  and  need  not 
be  discussed  here. 

Objections. — The  principal  objection  to  Sambon's  theory  is  that 
up  to  the  present  no  parasite  has  been  definitely  associated  with 
the  disease,  but  this  may  be  at  any  time  rectified  in  the  near 
future. 

The  very  few  experiments  performed  on  white  rabbits,  by  inject- 
ing liquor  cerebro-spinalis,  blood  from  the  erythema,  or  lymph 
from  bullae,  subdermally  or  into  the  spinal  canal,  have  produced 
no  definite  results,  nor  have  attempts  at  intradermal  inoculation 
of  these  animals  with  the  same  fluids  been  more  successful.  Neither 
have  the  attempts  made  by  the  Illinois  Commission  to  transmit 
the  disease  to  monkeys  and  guinea-pigs  met  with  more  success. 
Recently,  however,  Siler  in  a  communication  to  Sambon  has  stated 
that  injections  of  defibrinated  blood  taken  from  pellagrins  have 
produced  pellagra-like  symptoms  in  monkeys. 

In  our  opinion  there  is  need  for  much  more  extended  experiment  s, 
and  we  are  supported  in  our  belief  by  the  finding  of  the  Illinois 
Commission  that  'Pellagra  is  a  disease  due  to  infection  with  some 
living  organism.' 

Carrier. — Sambon,  however,  has  not  been  content  to  remain 
with  an  incomplete  theory,  but  has  advanced  the  view  that  the 
disease  is  conveyed  by  some  biting  fly. 

His  reasons  for  this  theory  are: — 

t.  Pellagra  is  essentially  a  disease  of  rural  districts. 

2.  It  is  in  some  way  related  to  moving  water. 


1716  PELLAGRA 

(3.  It  has  a  definite  seasonal  incidence — spring  and  autumn— 
which  coincides  with  the  appearance  of  certain  flies. 

4.  It  largely  affects  field  labourers  and  new  residents  in  endemic 
areas. 

5.  It  is  not  contagious,  and  neither  food  nor  water  can  account 
for  its  peculiar  epidemiology. 

6.  In  the  endemic  centres  it  affects  all  ages,  both  sexes  (as  a 
rule,  females  are  more  frequently  attacked  than  males). 

7.  An  endemic  centre  is  one  in  which  it  is  usually  easy  to  find 
young  children  with  the  symptoms  of  the  disease. 

8.  In  endemic  centres  whole  families  may  show  signs  of  the 
disease,  but  outside  these  only  one  or  two  individuals  may  be 
affected. 

Researches  on  the  Island  ofBurano  in  the  Venetian  Lagoon. — With 
regard  to  the  theory  of  a  biting  fly,  Sambon  is  supported  by  the 
inquiry  into  the  pellagra  of  the  Island  of  Burano  made  by  himself, 
Colonel  Belli,  and  one  of  us,  in  which  it  was  found  that  the  fisher- 
men and  the  boys  who  went  fishing  with  them,  were  attacked  by 
the  disease,  while  the  men  who  worked  in  the  Venice  Arsenal  were 
said  by  the  medical  authorities  to  be  free  from  the  disease.  The 
women,  the  girls,  and  the  young  children  showed  no  signs  of  pellagra, 
with  the  exception  of  two  or  three  women,  who  gave  a  history  of 
working  on  the  mainland  or  on  other  islands  adjoining.  Many 
of  these  young  children,  girls,  and  even  women,  were  alleged 
never  to  have  moved  from  Burano,  with  the  exception  in  some 
instances  of  an  occasional  visit  to  Venice.  These  points  are  con- 
trary to  the  maize  theory,  as  all  the  inhabitants  in  Burano  eat  maize. 
They  are  also  against  a  hereditary  transmission  of  the  disease,  for 
with  pellagrous  fathers  it  would  be  imagined  that  the  young  children 
should  show  signs  of  pellagra,  especially  as  the  male  influence  is 
said  to  be  preponderant  by  those  who  believe  in  the  heredity  of 
pellagra.  They  are  against  sexual  infection,  as  the  women  would 
acquire  the  disease;  they  are  against  infection  by  contact,  by 
kissing,  etc.,  because  certain  men  and  boys  have  the  disease,  but 
the  women  and  girls  are  remarkably  free;  they  are  against  a  para- 
site being  carried  from  the  sick  to  the  healthy  by  house  parasites, 
such  as  bugs  or  fleas,  or  personal  parasites,  such  as  lice.  The 
difference  between  the  persons  who  suffered  from  pellagra  in  Burano 
and  those  who  did  not  appeared  to  be  the  fact  that  the  former 
either  worked  upon  other  islands  or  fished  on  the  lagoon  and  up 
the  streams  leading  into  the  lagoon.  On  the  other  islands  and  on 
terra-firma  there  are  plenty  of  pellagrins,  and  everywhere  there  is 
a  history  of  small  black  biting  flies  occurring  on  quiet  days  in  the 
early  morning  or  late  evening. 

Sambon  considers  that  the  peculiar  feature  of  the  erythema 
coming  in  the  spring  and  the  autumn  must  be  a  correlation  with 
some  insect,  and  considers  that  the  Simuliidae  or  some  allied  family 
would  be  the  most  likely  to  supply  the  requisite  fly.  He  chose  first 
the  Simuliidae  because  its  larvae  lived  in  running  water,  and  because 


PREDISPOSING  CAUSES  171 7 

it  had  two  seasons,  during  which  it  appeared  in  swarms  and  at- 
tacked man  and  animals — viz.,  spring  and  autumn,  and  not  in 
summer — a  fact  which  we  have  been  able  to  confirm  for  one  of  the 
regions  which  we  visited. 

The  Illinois  Commission  and  many  others  have  been  unable  to 
support  the  relationship  of  pellagra  to  Simulhim. 

The  epidemiological  evidence  in  favour  of  the  spread  by  a  biting 
fly  is,  however,  very  strong. 

Summary. — It  appears  to  us  that  while  at  present  the  causa- 
tion of  pellagra  is  unknown,  and  while  the  modern  tendency 
is  to  claim  it  as  a  deficiency  disease,  still  the  investigations 
of  a  possible  protozoan  parasite  and  its  carrier  should  not  be 
given  up. 

Predisposing  Causes. — Sex  would  appear  to  be  a  predisposing 
cause,  because  the  disease  is  often  more  prevalent  in  women  than 
in  men,  and  this  would  not  appear  to  be  so  mysterious  as  it  seems 
at  first  sight,  for  if  there  is  anything  in  Sambon's  fly  theory,  the 
women  ought  to  be  more  exposed  to  the  flies  than  the  men,  because 
they  wash  the  clothes  in  the  neighbouring  streams.  In  one  place 
where  this  incidence  was  most  marked  the  men  worked  all  day 
underground  in  mines,  and  the  women  presumably  in  and  about  the 
houses,  which  were  on  the  banks  of  a  fly-infested  stream.  Here 
the  children  also  were  much  affected.  In  interesting  contra- 
distinction is  the  incidence  in  the  women  of  Burano,  who  mostly 
work  indoors  and  among  whom  pellagra  was  very  rare ;  but  it  was 
common  among  the  fishermen  and  boys  who  fish  in  the  rivers,  etc., 
where  biting  flies  are  common. 

Age  would  not  appear  to  have  any  marked  influence,  but  it 
would  seem  as  though  the  disease  was  very  prevalent — in  a  mild 
form,  at  all  events — in  the  early  years  of  life,  as  the  children  of 
a  pellagrous  district  are  often  early  affected,  and  some  of  these 
attacks  are  by  no  means  mild,  but  very  severe. 

With  regard  to  social  position,  poverty,  lack  of  sufficient  food, 
and  bad  hygienic  surroundings,  it  was  long  considered  that  these 
had  a  marked  influence  in  producing  the  disease,  but  though  they 
may  help,  as  they  would,  with  almost  any  form  of  disease,  still, 
the  American  and  our  own  experience  show  that  they  have  no  real 
connection  with  pellagra,  which  can  equally  well  occur  among  the 
well-to-do,  the  well-fed,and  those  living  in  circumstances  of  good 
hygiene,  though  more  commonly  met  with  among  the  poor  and  those 
ill-fed  and  living  in  circumstances  of  bad  hygiene. 

There  is  a  definite  correlation  between  the  lowering  of  the  general 
resistance  of  the  body  against  disease  and  an  acute  exacerbation 
of  pellagra.  Thus  pregnancy,  an  attack  of  any  illness,  but  especially 
enteric  fever,  may  induce  either  an  exacerbation  or  the  first  re- 
membered attack  of  the  disease. 

Sunlight  per  se  is  not  a  causal  factor,  as  far  as  we  know,  in  the 
disease,  but  it  is  a  powerful  predisposing  cause  in  helping  to  develop 
the  dermatitis. 


I7i8  PELLAGRA 

Pathology. — As  the  causation  of  pellagra  is  entirely  unknown, 
the  pathology  must  be  purely  speculative. 

The  Zeists  see  in  the  phenomena  exhibited  by  the  morbid  anatomy 
and  histopathology  changes  which  appear  to  them  allied  to  those 
found  in  scurvy,  beri-beri,  or  ergotism,  and  believe  that  these 
changes  support  the  maize  theory. 

The  Fagopyrists  see  in  the  phenomena  found  in  the  skin  lesions 
as  well  as  in  those  of  the  rest  of  the  body  the  signs  and  symptoms 
which  can  be  produced  in  white  animals  fed  on  maize  and  exposed 
to  sunlight,  and  believe  that  these  changes  support  the  photo- 
dynamic  theory. 

Those  who  support  the  Parasitic  Theory  quote  the  mononucleosis 
of  the  blood,  the  leptomeningitis,  the  perivascular  infiltration, 
and  the  primary  degeneration  of  the  nerve  cells,  as  well  as  the 
long  intervals  of  apparent  quiescence,  as  phenomena  similar  to 
those  seen  in  syphilis  and  sleeping  sickness,  and  therefore  believe 
that  these  changes  support  the  parasitic  theory. 

Sambon,  however,  has  extended  the  parasitic  theory  by  arguing 
that  the  erythemata  appearing  on  the  hands,  feet,  face,  and  neck, 
and  more  rarely  on  the  genital  organs,  in  the  spring  and  autumn, 
are  brought  about  by  the  combined  action  of  the  parasite,  whatever 
it  may  be,  and  sunlight  in  correlation  with  the  habits  of  some 
biting  fly.  From  epidemiological  studies  he  suggested  that  some 
member  or  members  of  the  family  Simuliidae  might  be  the  insect 
in  question.  He  came  to  this  conclusion  because  of  the  known 
habits,  life-history,  etc.,  of  the  Simuliidse,  which  were -in  general 
agreement  with  the  epidemiology  of  pellagra. 

The  reason  why  there  is  such  a  confusion  of  ideas  with  regard 
to  the  pathology  is  not  difficult  to  understand,  as  a  post-mortem 
made  on  a  case  of  acute  pellagra  within  an  hour  or  so  of  death 
is  of  great  rarity,  and  has  often  been  performed  under  conditions 
of  difficulty  as  regards  cleanliness  or  preparation.  Post-mortems 
on  cases  of  recurrences  or  of  chronic  pellagra  have  been  abun- 
dantly performed  under  the  best  auspices,  but  the  main  features 
of  the  disease  are  often  obscured  by  secondary  changes;  while 
even  in  the  acute  cases  the  phenomena  are  complicated  by  the 
presence  of  malaria,  typhoid,  tuberculosis,  syphilis,  etc. 

Notwithstanding  all  these  objections,  there  is  some  evidence  in 
favour  of  an  early  lesion  of  the  central  nervous  system,  especially 
the  posterior  portion  of  the  spinal  cord  in  the  lower  cervical  and 
dorsal  regions,  as  congestion  and  haemorrhages  have  been  found 
there,  while  in  the  more  chronic  condition  degeneration  of  the 
cells  in  the  posterior  cornu,  in  Clarke's  column,  and  in  the  spinal 
ganglia  have  been  seen,  as  well  as  the  later  degeneration  of  some 
of  their  axones.  Further,  according  to  Brugia,  acute  degenerative 
changes  can  be  seen  in  the  cells  of  the  sympathetic  ganglia  of  the 
cervical  and  abdominal  regions  associated  with  a  diffuse,  round- 
celled  infiltration  of  the  interstitial  tissue,  which  eventually  leads 
to  sclerosis.     Degenerative  changes  have  also  been  recorded  in 


MORBID  ANATOMY  1719 

Parkinje's  cells,  in  the  cerebellum,  and  in  the  cortical  cerebral 
cells. 

If  these  accounts  are  confirmed,  they  might  be  found  to  stand 
in  relationship  to  the  angio-neurotic  process  in  the  skin,  the  con- 
gestion of  the  alimentary  canal,  the  vertigo,  and  the  mental 
condition. 

However,  all  these  points  are  at  present  extremely  obscure,  and 
are  only  brought  forward  here  because  they  appear  to  require 
investigation. 

The  lesions  found  in  post-mortems  in  cases  of  acute  pellagra,  in 
o.ir  opinion,  apparently  support  the  theory  of  some  protozoan 
parasite,  as  suggested  above,  acting  upon  the  central  nervous 
system  and  the  autonomic  nervous  system. 

Morbid  Anatomy.— The  principal  point  in  studying  the  morbid 
anatomy  of  pellagra  is  to  attempt  to  distinguish  between  the  ap- 
pearances truly  produced  by  the  disease  and  the  signs  caused  by 
complications.  As  we  are  unacquainted  with  either  the  aetiology 
or  the  pathology  of  pellagra,  this  is  most  difficult,  and  only  an 
attempt,  which  may  possibly  be  fallacious,  can  be  made. 

The  Essential  Lesions. — Our  experience  would  indicate  that  in  acute  cases 
the  body  need  not  be  emaciated,  and  that  no  trace  of  the  erythema  may  be 
visible,  but  that  the  lines  of  demarcation  can,  as  a  rule,  be  easily  seen  on  the 
arms,  legs,  and  neck,  as  well  as  thickened  or  pigmented  areas  of  the  epidermis, 
bulla?,  etc. 

In  these  cases  there  may  be  fluid,  and  at  times  haemorrhages  under  the 
cerebral  dura  mater,  oedema  and  thickening  of  the  pia-arachnoid,  which, 
however,  is  not  adherent  to  the  cortex.  The  cerebro-spinal  fluid  is  usually, 
but  not  always,  increased  in  amount.  In  the  cord  there  may  be  subdural 
haemorrhages,  sometimes  extensive,  especially  in  the  region  of  the  lower 
cervical  and  upper  dorsal  cords,  and  there  may  be  congestion  of  that  area 
of  the  cord;  otherwise  the  naked-eye  appearances  of  brain,  spinal  cord,  and 
nerves,  may  be  normal. 

Sometimes  the  alimentary  canal  is  almost  normal,  but  this  is  rare,  and 
usually  there  is  more  or  less  congestion  and  at  times  even  ulceration  of  the 
mucosa  of  the  small  intestine,  and  the  valves  of  Kekring  may  show  small 
haemorrhages.  The  ileum  may  be  thinned,  and  Peyer's  patches  may  be 
diminished  in  number  and  atrophied  (these  lesions  are,  of  course,  found  in 
many  diseases).  The  large  bowel  may  be  thickened,  congested,  and  ulcer- 
ated, but  the  ulcers  need  not  contain  amoebae.  Pancreas,  liver,  and  kidneys 
may  show  signs  of  cirrhosis  (the  above  intestinal  lesions  are  often  associated 
with  polyfibrosis).  The  mesenteric  glands  may  be  enlarged  and  congested. 
The  spleen  may  or  may  not  be  slightly  enlarged,  and  the  suprarenal  capsules 
may  be  larger  than  normal,  and  the  cortex  may  be  black,  while  the  medulla 
is  whitish  in  colour;  but,  on  the  other  hand,  the  capsules  may  appear  to 
be  perfectly  normal.  In  chronic  cases  the  body  is  often  emaciated  and  anaemic, 
the  skin  rough,  hypertrophied  in  places  and  atrophied  in  others,  the  changes 
being  marked  on  the  face,  neck,  arms,  hands,  legs,  and  feet.  The  subcutaneous 
fat  is  diminished.  The  muscles,  heart,  liver,  spleen,  and  kidne}^,  are  all 
atrophied  ;  the  stomach  is  usually  normal,  but  the  intestines  may  be  atrophied, 
as  described  above,  and  the  rectum  may  be  ulcerated.  The  nervous  system 
shows  a  diffuse  leptomeningitis,  with  marked  thickening  in  places;  the  frontal 
convolutions  may  be  atrophied  in  some  cases  and  the  motor  convolutions  in 
others.  The  bloodvessels  may  show  calcareous  degeneration,  and  there  may 
be  sclerosis  of  the  postero-lateral  and  postero-median  columns  of  the  cord, 
and  in  the  dorsal  region  there  may  be  also  lateral  sclerosis.     The  posterior 


1720  PELLAGRA 

nerve  roots  may  be  implicated,  and  the  intervertebral  foramina  may  be 
narrowed  by  a  firm  cartilaginous-like  deposit. 

The  Complicatorv  Lesions. — Very  often  in  pellagra  post-mortems  the  signs 
of  secondary  septicaemia  (bacillary  or  streptococcal),  of  ankylostomiasis,  of 
malaria,  of  enteric  fever,  of  bacillary  dysentery,  of  amoebic  dysentery,  and 
of  tuberculosis,  may  be  seen,  and  complicate  the  pathological  picture.  In 
performing  post-mortems,  it  is  necessary  to  attempt  to  unravel  the  true 
lesions  from,  those  caused  by  complications.  The  so-called  characteristic 
intestinal  lesions  described  above  are  met  with  in  many  post-mortems  in 
which  there  is  no  sign  of  pellagra. 

Histopathology. — With  regard  to  the  autonomic  nervous  system,  the  nerve 
cells  of  the  sympathetic  ganglia  of  the  neck  and  abdomen  are  described  by 
Brugia  as  becoming  swollen,  and  showing  chroma  to  lysis,  with  changes  in  the 
nucleus  and  nucleolus  in  acute  cases.  Associated  with  this  there  is  infiltration 
of  the  interstitial  tissue  and  proliferation  of  the  endothelial  cells  of  the 
capillaries  and  circumscribed  haemorrhages. 


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Fig.  738. — Cells  of  Clarke's  Column  in  a  Case^of  Acute  Pellagra. 
(X  -250.)      (After  Sambon  and  Chalmers.) 

With  regard  to  the  chronic  cases,  there  is  atrophy  and  reduction  in  number 
of  the  nerve  cells  and  sclerosis  of  the  ganglion.  The  atrophied  cells  may  be 
pigmented,  but  this  is  by  no  means  constant. 

In  the  spinal  cord  our  own  observations,  as  well  as  those  of  others,  show 
that  the  posterior  area  is  congested,  and  haemorrhages  are  often  present. 
Degeneration  has  been  met  with  in  the  cells  of  the  spinal  ganglia,  in  those  of  the 
posterior  cornu,  and  in  those  of  Clarke's  column.  In  these  cells  the  Nissl 
bodies  and  the  fibrils  disappear,  while  the  nucleus  is  placed  excentrically,  and 
often  peripherally.  Degenerated  nerve  fibres  have  been  found  in  the  posterior 
roots,  in  Lissauer's  tract,  in  Burdach's  column,  and  in  Goll's  column,  and  less 
commonly  in  the  lateral  columns.  Some  of  the  cells  of  the  anterior  cornu  also 
degenerate.  Degenerated  nerve  fibres  may  also  be  seen  in  the  peripheral 
nerves. 

In  the  brain  the  cortical  cells  have  been  found  to  be  degenerated,  swollen, 
and  even  disintegrated;  while  Purkinje's  cells  in  the  cerebellum  are  also  said 
to  degenerate.     Mott  has  shown  that  while  the  fibrils  surrounding  these  cells 


SYMPTOMATOLOGY  i72i 

may  be  intact,  those  passing  through  the  cells  disappear.  A  perivascular 
infiltration  around  the  vessels  of  the  brain  has  been  described  by  some  authors, 
but  was  not  present  in  our  specimens  nor  in  those  described  by  Mott.  There 
is  also  an  increase  in  the  neuroglia  tissue  in  our  specimens,  but  there  is 
no  cellular  infiltration  into  grey  or  white  matter,  or  any  sign  of  acute 
inflammation. 

The  cerebro-spinal  fluid  is  usually  present  in  considerable  quantity,  and 
exhibits  a  medium  amount  of  tension.  It  is  alkaline,  specific  gravity  varying 
from  about  1004  to  1007;  it  generally  gives  reactions  indicating  the  presence 
of  some  protein  and  butyric  acid,  and  it  generally  reduces  copper  sulphate. 
The  number  of  cells  per  cubic  millimetre  varies,  but  is  about  thirty-five, 
according  to  Hindman,  whose  differential  count  is:  Small  lymphocytes, 
36-3  per  cent.;  polymorphonuclears,  18-6  per  cent.;  large  mononuclears, 
19-2  per  cent.;  plasma  cells,  7  per  cent.;  lymphocytes,  5-1  per  cent.  The 
liquor  is  sterile,  and  injections  into  rabbits  have  been  negative. 

The  skin  has  been  reinvestigated  by  the  Illinois  Commission,  who  find 
that  the  changes  can  be  described  as  due  to  an  angio-neurotic  process. 
There  is  infiltration  of  the  true  skin,  and  especially  the  pars  papillaris,  and 
oedema  of  the  connective  tissue.  The  rete  Malpighii  is  infiltrated  with  cells, 
but  otherwise  normal.  The  stratum  granulosum  is  normal,  but  the  stratum 
corneum  is  thickened,  and  shows  parakeratosis. 

In  the  blood  there  is  a  reduction  in  the  numbers  of  the  red  cells,  which 
usually  appear  quite  normal.  There  is  mononucleosis,  and  Low  has  described 
granules  in  the  mononuclear  leucocytes,  which,  however,  he  has  also  found  in 
other  diseases.  Fatty  degeneration  and  cloudy  swelling  have  been  recorded 
in  the  liver,  but  no  constant  changes  have  so  far  been  found  in  the  spleen. 

Symptomatology. — The  incubation  period  of  pellagra  is  unknown, 
but  it  cannot  be  of  long  duration,  as  we  have  known  it  to  occur  in 
a  child  three  months  of  age,  and,  as  we  have  already  advanced 
arguments  against  heredity,  this  case  is  in  favour  of  a  short  incubation 
period.  We  have  also  met  with  a  case  in  which  the  skin  symptoms 
are  said  to  have  appeared  about  two  weeks  after  return  from  a 
visit  to  a  pellagrous  area  in  a  person  who  was  said  to  have  always 
lived  in  a  non-pellagrous  area.  We  are  always  very  sceptical  of 
these  histories,  and  should  not  have  mentioned  it  if  it  had  not 
curiously  coincided  with  the  case  recorded  by  Sambon,  where  he 
states  that  a  child  born  in  an  Italian  gaol  was  nursed  by  its  own 
mother  in  gaol  until  five  months  old,  and  then  sent  to  some  peasants 
living  in  a  pellagrous  area,  when  it  developed  pellagra  in  two 
weeks. 

The  description  of  a  typical  case  is  something  of  this  nature: — 
A  person,  male  or  female,  young  or  old,  in  apparently  excellent 
health  or  in  bad  health,  living  or  working  in  the  sunshine  of  a 
spring  day,  notices  that  a  sunburn  appears  on  the  backs  of  his 
hands,  and  perhaps  the  dorsa  of  his  feet,  if  bare,  and  more  rarely, 
also,  on  his  face  or  neck.  He  thinks  little  of  it,  though  the  in- 
flamed area  burns,  and  may  even  blister.  Perhaps  he  has  a  sore 
mouth,  and  perhaps  he  has  a  little  diarrhoea  or  constipation. 
Perhaps  he  feels  a  little  giddy  in  the  morning,  and  perhaps  he  is 
easily  tired.  In  a  week  or  so  the  redness  dies  down,  and  the 
affected  area  is  seen  to  be  pigmented,  and  perhaps  to  have  the  skin 
thickened  in  places.  In  the  course  of  a  few  days,  or  a  week  or 
so,  these  thickened  areas  desquamate,  and  the  skin  underneath 


1722 


PELLAGRA 


Fig.   739. — Acute   Exacerbation    of 
Pellagra. 

Note  the  marked  erythema  on  the  hands 
and  feet,  and  the  less  evident   ery- 
thema on  the  neck  and  face. 
(From  a  photograph  by  Terni.) 


may  be  found  to  be  normal,  or 
may  be  found  to  be  slightly 
atrophic,  and  to  appear  whiter 
than  the  surrounding  pig- 
mented area. 

The  patient  thinks  no  more 
of  his  troubles,  the  autumn 
comes,  and  he  feels  well,  and 
during  the  winter  there  is  no 
alteration  in  his  good  health. 
Perhaps  the  next  spring  may 
pass  without  a  recurrence, 
and  perhaps  even  several 
springs  may  elapse  before  the 
patient,  who  all  this  time  may 
consider  himself  to  be  in  ex- 
cellent health,  has  a  return 
of  his  symptoms.  But  though 
the  interval  may  be  long  or 
short,  this  relapse  will  surely 
occur,  and  often  it  will  be  in 
a  severer  form  than  it  was  at 
first.  It  will  usually  recur  in 
the  spring,  but  it  may  take 
place  in  the  autumn,  or,  much 
more  rarely  in  our  experience, 
in  the  summer. 

This  time  the  symptoms 
may  be  mild,  as  before,  but, 
on  the  other  hand,  they  may 
be  severe  ;  the  erythema 
appears  with  severe  burning 
sensations,  and  a  real  derma- 
titis, with  bulla  formation, 
may  develop. 

The  tongue,  lips,  mucosa  of 
the  mouth  and  palate,  may 
become  inflamed,  and  show 
the  presence  of  vesicles  and 
ulcers.  The  parotid  gland 
may  enlarge  (this  is  common 
in  Egypt,  but  rare  in  other 
countries),  the  saliva  may  be 
so  increased  in  amount  that 
it  pours  from  the  mouth. 
There  may  be  signs  of  dys- 
pepsia, pains  in  the  abdomen, 
and  diarrhoea,  or  even  dys- 
entery may  develop.  The 
vertigo     already     mentioned 


SYMPTOMATOLOGY  1723 

may  become  quite  distressing  to  the  patient,  who,  upon  quickly 
rising  from  a  sitting  or  a  lying  posture,  may  even  fall  to  the 
ground.  The  muscular  power  may  now  be  diminished,  and  the 
patient  may  no  longer  be  able  to  do  his  work;  tremblings  in  various 
parts  of  the  body,  but  more  especially  in  the  head  and  arms, 
may  be  noticed,  and  the  legs  seem  scarcely  able  to  support  the 
victim,  who  now  shows  decided  melancholic  symptoms,  avoiding 
his  fellows,  becoming  highly  emotional,  and  perhaps  threatening, 
or  actually  committing,  suicide,  often  by  drowning  in  water. 

Pains  are  felt  in  various  parts  of  the  body,  but  especially  in  the 
head,  the  stomach,  and  the  feet.  A  most  unpleasant  symptom 
is  the  burning  sensation  complained  of  by  the  patient  after  retiring 
to  bed  at  night.  So  severe  is  this  that  patients  have  been  known 
to  strip  off  all  their  clothes  and  lie  naked  on  their  beds.  By  this 
time  the  unfortunate  victim  will  have  learnt  by  bitter  experience 
that  sunlight  is  deleterious  to  his  condition,  and  will  try  to  avoid 
it  as  much  as  possible. 

Again,  as  winter  approaches,  the  symptoms  will  diminish  and  die 
away,  and  the  patient  will  feel  better;  but  this  time  the  skin  does 
not  recover  itself,  but  remains  thickened  and  pigmented  in  places, 
and  thinned,  whitened,  and  atrophic  in  other  places. 

Again,  there  may  be  only  an  interval  till  the  next  spring  or 
autumn,  or  the  succeeding  spring,  or  there  may  be  a  longer  interval, 
and  again  mild  or  severe  symptoms  may  appear. 

With  repeated  attacks  the  skin  changes  become  marked,  the 
mind  becomes  often  permanently  affected,  and  melancholic  or 
maniacal  symptoms  are  often  observed. 

Pain  is  often  complained  of  in  the  back,  and  tenderness  is  found 
on  pressure  over  the  spinal  nerves  on  either  side  of  the  dorsal  or 
lumbar  portions  of  the  vertebral  column.  Muscular  weakness  is 
noted,  especially  in  the  legs.  The  knee-jerk  is  at  first  exaggerated, 
but  later  is  diminished,  and  finally  lost.  Ankle  clonus  and  wrist 
clonus  are  rare,  and  only  occur  when  the  knee-jerk  is  exaggerated, 
when  there  is  tenderness  on  both  sides  of  the  dorsal  and  lumbar 
cord,  and  when  abdominal  and  epigastric  reflexes  are  also  increased. 

There  is  no  special  gait,  but  there  is  a  tendency  to  fall  backwards 
or  forwards,  and  hence,  though  the  patient  walks  with  the  legs  well 
apart,  in  a  very  bad  case  he  can  only  take  a  few  steps  without 
falling  down.  There  may  be  tremors  in  the  legs  and  tongue.  The 
bladder  and  rectum  are  not  as  a  rule  affected  until  the  end,  but 
there  are  exceptions  to  this,  and  contraction  of  the  limbs  does  not 
take  place  till  bedridden;  but  moderate  rigidity  of  the  muscles  of 
the  arms  and  legs,  associated  with  stiff  and  at  times  irregular  spas- 
modic movements,  has  been  recorded  as  occurring  early  in  rare 
acute  cases.  A  sudden  rigidity  of  the  body  associated  with  re- 
traction of  the  head  has  also  been  observed.  These  attacks  last  only 
a  short  time,  but  are  recurrent.  Trophic  lesions,  such  as  bedsores, 
are  of  rare  occurrence.  Hyperesthesia  may  occur  in  different  parts 
of  the  body,  and  pains  (even  of  a  lightning  nature)  may  exist  in  the 
head  and  back,  and  be  associated  with  cramps. 


I724 


PELLAGRA 


The  facies  of  the  pellagra  patient  is  one  of  anxiety  and  mental 
worry.  He  cannot  sleep,  and  there  is  often  great  mental  depression 
and  discontent ;  but  some  [are  excitable  and  irritable,  while  others 
are  stupid  and  morose.  He  loses  his  memory,  and  has  vague 
feelings  of  pressure,  weight,  or  pulsation  about  his  head.  From 
this  he  proceeds  to  refusal  of  food  and  suicidal  tendencies,  with 
delusions  of  sorcery  and  persecution,  and  has  a  tendency  to  suicide 
by  drowning.  Melancholia  may  now  become  confirmed,  and  may 
eventually  pass  into  dementia. 


Fig.  740. — Hand  in  Chronic  Pellagra, 
(From  a  photograph  by  Sambon  and  Chalmers.) 


Various  paralyses  develop,  such  as  spastic  paralysis,  ptosis, 
hemianopsia,  diplopia,  amblyopia,  and  mydriasis.  The  extremities 
and  bladder  now  become  paralyzed,  and  the  demented,  paralyzed, 
rapidly  emaciating  patient,  suffering  from  bad  sweats,  profuse 
diarrhoea,  and  sometimes  dropsy,  obtains  a  relief  from  his  sufferings 
in  death,  the  disease  hav      ;  usually  lasted  from  ten  to  fifteen  years. 

Such  is  a  general  account  of  this  rather  protean  disease,  and  we 
note  that  there  is  an  onset  in  the  spring,  or  more  rarely  in  the 
autumn  or  summer,  an  intermission  in  the  winter,  and  a  relapse 
in  the  next  or  some  following  spring  or  autumn. 

Very  rarely  a  case  of  pellagra  may  be  acute,  lasting  only  a  few 
months. 

Children. — The  disease  is  so  common  among  young  children  in 
bad  pellagrous  districts,  and  so  often  can  one,  by  careful  inquiry, 


SYMPTOM  A  TOLOG  Y 


1725 


elicit  curious  facts  that  tend  to  show  that  pellagra,  though  occurring 
in  the  person  in  question  in  adult  life,  probably  really  began  in 
infancy,  that  we  are  inclined  to  believe  that  the  cases  in  young 
children  are  often  overlooked,  and  we  are  supported  in  this  belief 
by  the  mildness  of  the  symptoms  which  we  have  observed  in  some 
children,  which  indicate  merely  a  sunburn  on  the  face,  hands, 
arms,  feet,  legs,  and  perhaps  the  neck,  associated  with  a  little 
diarrhoea  or  constipation.  The  child  recovers,  the  skin  becomes 
normal,  the  attack  is  forgotten,  and  does  not  return  until  adult 


Fig. 


741. 


-Hand  in  Chronic  Pellagra. 


Note  the  thickening  of  the  epidermis  and  the  line  of  demarcation.  The 
hands  in  both  figures  had  been  vigorously  scrubbed  by  the  patient  to  try 
to  remove  the  scabs. 

(From  a  photograph  by  Sambon  and  Chalmers.) 

life,  when  the  patient  may  have  grown  up  and  been  living  for  years 
in  a  town,  when  a  typical  relapse  appears — a  new  case  (a  town  case 
it  would  be  classified  by  many  authors),  but  a  careful  inquiry  into 
the  history  of  the  case  may  elicit  the  fact  from  intelligent  people  that 
the  first  attack  began  in  childhood,  when  it  may  be  explained  by 
the  friends  as  being  in  reality  a  sequela  of  Jenner's  vaccination. 

Inquiry  may  often  elicit  the  fact  that  when  this  occurred  the 
patient,  at  that  time  a  child,  was  living  in  the  country,  and  often 
in  close  proximity  to  a  stream — a  fact  which  may  be  confirmed  by 
a  visit  to  the  locality. 

Another  curious  point  with  regard  to  some  of  these  early  cases 


1 726  PELLAGRA 

is  the  history  given  by  the  friends  of  the  development  of  some 
extraordinary  habit  of  dietary,  to  the  influence  of  which  the  disease 
is  often  assigned.  These  extraordinary  cravings  appear  to  us  to 
be  due  to  the  dyspepsia  (hypochlorhydria)  so  commonly  met  with 
in  pellagrins. 

We  have  rather  insisted  upon  the  occurrence  of  pellagra  in  young 
children  because  we  are  of  the  opinion  that  it  is  often  overlooked. 

Skin  Eruption. — The  skin  eruption  is  usually  limited  to  the 
regions  exposed,  being  at  first  delineated  in  a  most  exact  manner 
by  the  clothing;  but  in  very  rare  cases  it  may  be  universal,  and  it 
is  said  sometimes  to  appear  limited,  as  though  by  clothing,  in  naked 
gipsy  children.  It  appears  on  the  dorsum  of  the  foreaims,  and  on 
the  hands  and  feet,  only  reaching  the  flexor  aspect  after  several 
attacks.  The  most  common  sites  are  the  hands  and  forearms, 
elbows,  feet,  legs  and  knees,  the  upper  part  of  the  chest,  the 
shoulders,  neck,  and  face.  More  rarely  it  appears  on  the  genital 
organs  and  around  the  anus  in  both  sexes.  Sandwith  points  out 
that  in  Egyptian  peasants  the  unguinal  phalanx  of  the  hand  is 
seldom  affected,  due  to  the  fact  that  when  the  hoe  is  grasped  it 
is  protected  against  the  sun's  rays.  The  nails  and  hair  are  not 
affected,  but  rarely  there  is  a  dry,  scaly  condition  of  the  palms 
of  the  hands. 

The  skin  eruption  may  show  the  following  conditions: — (i)  Con- 
gestion; (2)  inflammation;  (3)  thickening  and  pigmentation; 
(4)  atrophic  thinning. 

The  affected  part  turns  a  bright,  dark,  or  livid  red  colour,  which 
at  first  disappears  on  pressure,  and  is  generally  delineated  by  a  very 
clearly  raised  limiting  line.  Associated  with  this  erythema  there 
is  a  burning  sensation,  but  usually  no  pain.  In  course  of  time  the 
part  becomes  swollen  and  tense,  and  bullae  may  form.  After 
lasting  a  variable  period  of  days  or  weeks,  the  eruption  gradually 
subsides,  leaving  the  skin  rough,  pigmented,  and  thickened,  and 
thus  earning  the  names  of  '  pell'agra '  and  '  qushuf.' 

This  erythema  disappears  in  the  winter,  but  reappears  the  next 
spring  with  increased  virulence,  and  in  due  course  develops  into  a 
dermatitis,  which  produces  an  exfoliation  of  the  epidermis  in  grey 
or  brown  flakes.  Every  attack  leaves  the  affected  area  a  little 
more  pigmented,  a  little  more  thickened,  and  a  little  less  elastic. 

After  lasting  about  four  or  five  years  the  skin  begins  to  atrophy, 
and  becomes  wrinkled  and  inelastic.  This  atrophy  is  most  marked 
on  the  back,  hands,  and  feet.  Special  terms  have  been  given  to 
the  eruption  when  in  certain  areas — e.g.,  the  'glove,'  the  'boot/ 
Casall's  '  necklace,'  or  '  cravat,'  and  the  '  mask.' 

Roberts  has  introduced  the  rather  useful  term  '  dermotagra  '  for 
the  dry,  scaly,  thickened  skin  seen  over  the  olecranon  process, 
over  the  knees,  and  more  rarely  on  the  palms  of  the  hands.  Over 
the  elbow  and  knee  the  skin  is  rough,  thickened,  and  wrinkled; 
on  the  palms  of  the  hands  it  is  merely  rough  and  thickened. 

Another  interesting  dermatological  feature  of  pellagra  is  the 


SYMPTOMATOLOGY  1727 

frequency  of  nasal  or  facial  seborrhcea,  which  is  to  be  especially 
noted  in  the  nose  where  the  sebaceous  follicles  are  very  prominent 
and  filled  with  plugs  of  sebaceous  material. 

The  Mouth. — The  tongue  is  generally  coated  with  a  whitish  fur 
during  the  onset  of  an  attack,  but  later  it  becomes  abnormally 
clean — •'  Sandicith's  bald  tongue  '—red,  swollen,  and  sometimes 
ulcerated  near  the  tip.  It  may  also  become  fissured,  but  in  mild 
cases  it  recovers  as  soon  as  the  attack  is  over. 

During  attacks  the  gums  may  become  spongy,  and  may  bleed, 
and  ulceration  may  appear,  both  here  and  on  the  palate,  as  well 
as  on  the  pillars  of  the  fauces.  There  may  be  pharyngitis,  and  more 
rarely  oesophagitis. 

The  Blood. — The  red  cells  are  usually  reduced  in  number,  and  the 
haemoglobin  proportionally  reduced.  Usually  the  form  of  the  red 
cells  is  normal,  but  microcytes,  and  more  rarely  megalccytes,  may 
be  found.  There  is  usually  only  a  slight  leucocytosis  in  uncompli- 
cated cases,  but  there  is  in  our  experience  generally  a  distinct 
mononucleosis.  When  the  polymorphonuclear  cells  are  increased, 
it  would  appear  to  always  indicate  a  complication. 

Circulatory  Organs.- — The  blood-pressure  is  usually  low,  and  the 
heart-rate  may  be  markedly  increased.  Vasomotor  changes  can 
be  observed  in  the  coldness  of  the  extremities,  the  bluish  conges- 
tion of  the  feet  and  hands,  the  goose  skin,  and  the  neuroparalytic 
dilatation  of  the  vessels  of  the  face  often  giving  rise  to  an  appear- 
ance seen  in  alcoholics. 

Respiratory  Organs,  etc. — The  respiratory  organs  are  not  affected 
in  pellagra  unless  there  is  some  complication,  but  there  may  be  an 
exudation  of  fluid  into  the  pleural  cavities  in  the  late  stages  of 
the  disease,  as  well  as  cedema  of  the  bases  of  the  lungs. 

Urinary  Organs. — Usually  the  urine  is  normal,  or  nearly  so, 
and  any  great  change  must  be  considered  to  be  a  complication. 

Sexual  Organs. — -Sexual  power  is  usually  diminished,  especially 
in  the  later  stages.  Amenorrhcea,  metrorrhagia,  and  inflammatory 
conditions  of  the  vagina,  uterus,  ovaries,  etc.,  are  described,  but 
must  be  considered  as  complications. 

Special  Senses. — The  eyes  suffer  most  in  pellagra,  but  the  changes 
— -e.g.,  weakness  of  vision,  photophobia,  etc. — are  not  dependent 
upon  the  disease  per  se,  but  upon  the  weakness  which  it  produces. 
The  patients  often  complain  of  a  saltish  taste  in  the  mouth. 

Fever. — As  a  rule  the  temperature  is  but  little  altered  from  normal 
in  pellagra,  but  it  may  be  raised  at  intervals  as  high  as  1010  to 
1020  F.  (Wood)  for  two  to  three  days  at  a  time,  but  it  may  also 
be  subnormal  in  other  cases. 

Complications. — As  may  be  imagined,  in  a  disease  of  such  long 
Juration  as  pellagra,  the  complications  are  numerous,  and  induce 
malaria,  tuberculosis,  ankylostomiasis,  bilharziosis,  eye  affections, 
and  many  skin  diseases,  including  itch. 

The  most  interesting  complication  is  enteric  fever ,  which  may  gh  e 
rise  to  the  form  often  called  '  typho-pellagra,'  which  is  apparently 


1728  PELLAGRA 

simply  a  pellagrin  with  an  infection  with   one   or  more   of   the 
organisms  causing  enteric  fever. 

Terminal  infections  with  various  micro-organisms  have  been  noted, 
and  complicate  the  post-mortem  findings.  Thus,  Bon  records  the 
occurrence  of  Streptococcus  pyogenes  in  the  blood  as  found  by 
examination  immediately  after  death. 

Diagnosis. — Everywhere  since  pellagra  was  first  recognized  there 
has  been  great  difficulty  in  its  diagnosis,  and  it  would  appear 
necessary  to  consider  not  merely  the  signs  exhibited  by  the  patient, 
but  the  frame  of  mind  in  the  observer  in  attempting  to  write  upon 
this  subject. 

For  the  diagnosis  of  pellagra  two  conditions  are  necessary  in  the 
observer.  The  first  is  that  he  must  suspect  its  presence,  and  be 
on  the  outlook  for  it  in  any  and  every  country;  and  the  second 
is  that  he  must  not  be  unduly  swayed  by  any  ^etiological  theory, 
and  must  be  prepared  to  make  a  diagnosis  of  pellagra  in  a  person 
of  any  age,  any  race,  any  social  condition,  living  in  any  place, 
whether  tropical,  temperate,  or  frigid;  resident  in  a  town  or  in 
the  country;  and  he  must  do  this  without  consideration  of  the 
dietary  or  the  surroundings,  with  perhaps  the  sole  exception  of 
being^more  intently  awake  to  the  possible  occurrence  of  the  disease 
in  lunatic  asylums. 

As  there  are  at  present  no  microscopical,  bacteriological,  para- 
sitological,  hematological,  or  chemical  reactions  which  can  be  said 
to  be  diagnostic  of  the  disease,  with,  perhaps,  the  sole  exception 
of  the  pellagra-like  symptoms  produced  by  one  of  the  American 
Commissions,  by  injecting  defibrinated  blood  into  monkeys,  and  as 
these  animal jinjections  are  not  within  the  range  of  practical  politics 
for  purposes  'of  diagnosis,  we  must  trust  entirely  to  clinical  mani- 
festations. 

The  cardinal  signs  of  the  disease  may  be  summarized  into- — 
(1)  the  cutaneous  signs,  (2)  the  gastro-intestinal  signs,  and  (3)  the 
nervous  signs. 

In  order  to  make  a  definite  diagnosis,  there  must  be  either  the 
presence  or  a  definite  history  of  the  cutaneous  signs  of  pellagra 
associated  with  symptoms  belonging  to  one  of  the  other  groups. 

1.  Cutaneous  Signs. — When  a  person  shows  more  or  less  sym- 
metrical erythema,  dermatitis,  pigmentation,  or  a  condition  more 
or  less  resembling  chronic  dry  eczema  on  either  the  backs  of  the 
hands,  the  dorsa  of  the  feet,  the  face,  the  back  and  sides  of  the 
neck,  or  the  front  of  the  chest,  especially  if  these  eruptions  are 
limited  by  a  more  or  less  definite  elevated  margin  to  the  areas 
habitually  exposed  to  light,  suspicion  should  at  once  be  aroused 
that  the  disease  is  pellagra.  If  a  history  can  be  obtained  that  this 
eruption  appeared  for  the  first  time  in  spring  or  aul  umn,  and  more 
especially  if  a  history  of  recurring  attacks  can  be  obtained,  the 
suspicion  becomes  almost  a  certainty.  If  to  these  signs  there  are 
added  the  fact  that  the  skin  symptoms  become  worse  on  exposure 
to  the  sun,  or  that  there  are  at  the  same  time  disturbances  of  the 


DIAGNOSIS  1729 

alimentary  canal  or  of  the  nervous  system,  and  especially  if  there 
is  the  presence  or  the  history  of  vertigo,  then  the  diagnosis  is  certain. 

2.  Gastro -Intestinal  Signs.  —  Gastro- intestinal  symptoms  are 
usually  present,  but  they  may  be  extremely  mild,  and  they  may  be 
absent.  Those  most  commonly  met  with  during  exacerbations  are  — 
Salivation,  stomatitis,  dyspepsia  due  to  hypochlorhydria,  diarrhoea, 
dysenteric  symptoms,  alternating  with  constipation,  or  simply 
constipation  appearing  or  recurring  in  the  spring  or  autumn. 
A  diagnosis  cannot  be  made  by  these  symptoms  alone,  which  must 
be  considered  in  conjunction  with  the  cutaneous  in  order  to  arrive 
at  a  conclusion.  If  no  cutaneous  symptoms  are  visible,  it  is  justi- 
fiable to  place  the  patient  in  strong  sunlight  in  order  to  see  whether 
the  dermatitis  will  appear. 

3.  Nervous  Symptoms.- — Of  all  the  nervous  symptoms  early  ex- 
hibited, the  vertigo  is  the  most  common,  and  should  be  carefully 
inquired  for,  as  the  patient  often  does  not  associate  slight  morning 
vertigo  with  the  disease,  and  will  therefore  omit  to  mention  the  feet. 

Other  important  symptoms  are  the  melancholia,  the  myas- 
thenia, the  tremblings,  and  often  curious  delusions,  and  the  irritable 
condition  of  the  temper,  recurring  in  the  spring  or  autumn;  but 
these  must  be  associated  with  evidence  of  skin  lesions  before  a 
diagnosis  can  be  made. 

It  will  thus  be  observed  that,  while  the  diagnosis  may  be  a  matter 
of  extreme  simplicity  in  a  typical  case,  it  may  also  be  one  of  great 
difficulty  in  atypical  cases.  Perhaps  [the  greatest  difficulty  is 
met  with  in  lunatics  and  young  'children. 

1.  Lunatics. — In  these  cases  the  patient  has  been  admitted  into 
the  asylum  suffering  from  one  of  the  well-known  forms  of  mental 
disease,  but  most  probably  from  melancholia  or  dementia,  more 
rarely  from  attacks  of  mania.  It  may  be  noted  that  at  times  he 
suffers  from  diarrhoea  or  dysentery,  which  is  often  assigned  to  what 
used  to  be  called  '  lunatic  asylum  diarrhoea '  or  '  dysentery.'  It 
may  also  be  noted  that  at  ^times  he  spits  considerably,  which  s'mply 
means  that  he  has  an  excess  of  saliva;  but,  much  more  importantly, 
it  is  noticed  that  he  suffers  from  chronic  eczema  on  the  back  of  his 
hands,  from  angioneurotic  oedema  so  called,  both  of  which  are  often 
common  in  lunatics.  Such  cases  require  careful  investigation, 
not  with  a  view  of  making  a  diagnosis  of  pellagra,  but  with  a  view 
of  excluding,  if  possible,  the  diagnosis  that  the  case  is  really 
pellagra. 

2.  Young  Children. — In  young  children  the  disease  is  very  apt 
to  be  overlooked,  and  the  red  eruption  on  the  face  and  hands,  etc., 
followed  by  pigmentation,  is  generally  attributed  to  sunburn  or 
to  eczema,  while  the  alimentary  disturbance  is  assigned  to  infantile 
gastro-intestinal  derangements,  and  not  connected  with  the  skin 
lesions.  A  careful  inquiry  will  show  whether  these  symptoms 
have  or  have  not  a  seasonal  incidence,  and  in  any  case  they  should 
arouse  suspicion  "of  pellagra,  which  should  only  be  eliminated  after 
careful  inquiry. 

109 


1730  PELLAGRA 

Differential  Diagnosis.- — As  the  symptoms  are  divisible  into 
three  groups,  so  the  discussion  of  the  differential  diagnosis  is  equally 
capable  of  arrangement  under  the  same  three  headings. 

Skin  Diseases. — The  skin  diseases  which  are  to  be  differentiated 
from  pellagra  are  classifiable  into  those  rescmblirg  the  acute 
cutaneous  symptoms  and  those  resembling  the  chronic  cutaneous 
appearances. 

i.  Resembling  the  Acute  Dermatitis. — Under  this  heading  comes, 
first  of  all,  erythema  solar e,  from  which  pellagra  may  be  distinguished 
by  the  inflammation  of  the  mouth,  by  the  presence  of  the  alimentary 
canal  symptoms,  and  by  the  vertigo,  as  well  as  by  the  fact  that  the 
pellagrous  eruption  at  times  appears  on  parts  not  usually  exposed 
to  the  sun,  and  by  the  fact  that  the  lesions  in  sunburn  are  usually 
very  superficial. 

The  same  diagnostic  points  will  help  to  differentiate  pellagrous 
dermatitis  from  erythema  or  eczema  due  to  winds,  salt  air,  eic. 

The  erythema  on  the  face,  hands,  arms,  etc.,  in  cases  of  dermatitis 
venenata  may  simulate  pellagra  closely.  The  pellagrous  condition 
may  be  differentiated  by  the  presence  of  gastro-intestinal  nervous 
symptoms,  by  the  less  general  extension  of  the  eruption,  by  the  less 
involvement  of  the  eyelids,  and  by  the  more  acute  course. 

From  acarine  dermatitis  pellagra  may  be  distinguished  by  the 
localization  of  the  eruption,  which  does  not  appear  on  the  trunk, 
by  the  absence  of  the  vesiculo- papules  and  pustules,  and  by  the 
absence  of  itching. 

From  alcoholic  erythemata  it  may  be  recognized  by  the  history 
of  the  attack  and  by  the  presence  of  the  typical  eruption  on  the 
hands  and  feet. 

Some  authorities  have,  however,  described,  under  the  teim 
pseudo-pellagra,  of  alcoholic  origin,  an  erythematous  eruption  on 
the  hands  associated  with  nervous  symptoms  which  is  indistinguish- 
able from  true  pellagra,  being,  in  fact,  the  same  disease. 

From  angioneurotic  oedema  it  may  be  differentiated  by  the  absence 
of  marked  oedema  and  the  presence  of  more  inflammation  in  the 
skin,  as  well  as  by  the  more  regular  distribution  of  the  eruption, 
and  by  the  limiting  line. 

2.  Resembling  the  Chronic  Dermatitis.- — From  chronic  eczema 
occurring  in  mentally  sound  persons  or  in  lunatics  pellagra  is 
recognized  by  the  typical  distribution  of  the  eruption,  b}^  the  line 
of  demarcation,  and  by  the  marked  pigmentation,  when  present, 
and  absence  of  pruritus.  From  chronic  syphilides  by  the  distribu- 
tion of  the  eruption,  and  by  the  absence  of  any  reaction  to  mer- 
cury. Here  mention  may. again  be  made  of  the  damotagra  on  the 
palms  of  the  hands,  over  the  olecranon,  and  about  the  knee,  in 
chronic  cases  of  pellagra,  which  is  apt  to  he  overlooked,  or  to  be 
considered  as  points  in  favour  of  a  diagnosis  of  eczema  rather  11. an 
of  pellagra. 

From  biotripsis  (vide  p.  2282),  which  it  closely  resembles,  pellagra 
is  differentiated  by  the  limitation  of  the  eruption  to  the  areas  so  often 


DIFFERENTIAL  DIAGNOSIS— PROGNOSIS  1731 

mentioned  above,  by  the  presence  of  the  line  of  demarcation.  In 
biotripsis  the  skin  is  dry  and  wrinkled,  and  may  be  thickened 
in  places  with  dark-coloured  patches,  alternating  with  shinirg, 
smooth,  inelastic,  atrophic  areas;  but  this  condition  is  by  no  means 
limited  to  the  hands  or  feet,  but  spreads  up  the  arms  and  legs,  and 
is  not  visible  on  the  face. 

It  is  hardly  possible  that  Kaposi's  disease  (xerodermia  pigment  osa) 
could  be  mistaken  for  pellagra,  nor  is  ichthyosis  likely  to  be  con 
founded  with  it. 

The  wrinkled  skin  of  the  washerwoman's  fingers  is  hardly  likely 
to  be  confused  with  the  chronic  thickening  found  in  pellagra, 
though  this  disease  is  often  found  in  women  who  wash  clothes,  and 
who  explain  their  own  dermal  condition  in  this  way. 

Gastro-Intestinal  Diseases. — Of  all  the  gastro-intestir.al 
diseases,  sprue  is  the  only  one  which  in  any  way  resembles  pellagra, 
which  can  be  readily  distinguished  therefrcm  by  1he  presence  of 
the  skin  eruption.  It  must,  however,  be  remembered  that  the 
psilosis  linguae  pigmentosa?  of  West  Indian  writers  is  really  pellagra. 

Attacks  of  diarrhoea  or  dysenteric-like  attacks  can  only  be  recog- 
nized as  belonging  to  the  syndrome  of  pellagra  if  the  dermal  signs 
are  present  at  the  same  time,  or  if  they  can  be  produced  by  exposure 
to  the  sun,  or  if  there  is  a  very  definite  history  of  their  previous 
occurrence;  unless,  indeed,  they  are  associated  with  marked 
ptyalism  or  bilateral  swelling  of  the  parotid  glands,  or  some  other 
symptom  tending  to  indicate  that  pellagra  was  the  cause.  The 
special  cases  in  which  diarrhoea  and  dysentery  require  careful 
diagnosis  are  those  in  which  they  occur  in  lunatics. 

Typho-Pellagra. — 'In  this  disease  the  dermal  signs  of  pellagra 
are  sufficiently  evident  to  enable  its  diagnosis  to  be  made,  as  a  rule, 
without  difficulty,  while  the  diagnosis  of  typhoid  fever  can  be  made 
by  the  methods  already  described  on  pp.  1389-1394. 

Nervous  Diseases. — Melancholia,  dementia,  mania,  etc.,  can 
only  be  diagnosed  as  pellagrous  when  associated  with  its  skin 
lesions;  but  here  care  must  be  taken  not  to  mistake  the  dermal 
signs  of  pellagra  for  chronic  eczema,  etc.;  but  this  point,  having 
been  already  discussed  above,  need  not  again  be  argued. 

Prognosis. — This  would  appear  to  be  good  in  early  cases,  in  mild 
cases,  and  even  in  moderately  severe  cases,  if  the  patient  can  be 
removed  from  the  pellagrous  area  and  placed  in  good  condition  of 
food  and  hygiene  in  a  non-pellagrous  area. 

But  predictions  as  to  a  cure  must  be  guarded,  and  it  must  be 
remembered  that  cases  have  relapsed  after  two,  five,  and  even 
fifteen,  years'  intervals. 

In  severe  cases  the  prognosis  must  be  guarded,  and  the  low  blood- 
pressure  remembered,  as  well  as  the  possibility  of  sudden  death 
from  exertion  after  lying  down. 

Cases  of  typho-pellagra  have  a  high  mortality,  and  here  the 
prognosis  is  obviously  bad. 

Complication    with    ankylostomiasis,     tuberculosis,     etc.,    also 


1732  PELLAGRA 

render  the  prognosis  more  unfavourable,  as  does  continued  residence 
in  a  pellagrous  area. 

Treatment. — There  can  be  no  doubt  that  the  essential  basis  of 
the  treatment  of  pellagra  is  to  remove  the  patient  from  the  pel- 
lagrous area  in  which  he  has  been  living  to  a  non-pellagrous  area; 
and,  secondly,  to  give  a  good  and  liberal  diet,  preferably  without 
any  admixture  of  maize,  although  Devoto  has  shown  that  good 
maize  not  merely  does  no  harm  to  pellagrins,  but  is  very  suitable 
for  some  of  them,  as  it  is  their  usual  diet.  If  this  is  done,  most  early 
cases  quickly  improve,  and  apparently  are  cured,  but,  unfortunately, 
this  is  not  so,  because,  even  if  they  remain  under  these  excellent 
conditions,  sooner  or  later  a  recrudescence  occurs.  These  recru- 
descences may  be  mild,  but  at  any  time  they  may  become  severe, 
even  when  maize  is  excluded  from  the  dietary. 

Arsenic. — This  being  so,  it  is  obvious  that  some  medicinal  treat- 
ment is  necessary,  in  addition  to  change  of  locality  and  diet,  and 
apparently  the  best  xemedy  is  arsenic  in  some  foim.  Of  all  forms 
of  the  drug,  that  most  commonly  in  uie,  and  also  much  vaunted, 
is  '  atoxyl,'  which  is  administered  by  intramuscular  injection  of 
3  grains  per  diem. 

Other  methods  of  giving  arsenic  are  salvarsan,  neosalvarsan,  and 
soamin. 

Other  methods  are  the  cacodylate  of  sodium,  administered  in  3-grain 
doses  by  intramuscular  injection  every  third  day  until  three  doses  have  been 
given,  and  then  every  second  day  until  three  more  doses  have  been  adminis- 
tered, and  then  increasing  to  5-grain  doses  every  second  day  until  the  symp- 
toms have  improved. 

Associated  with  these  injections,  it  is  as  well  to  give  liquor 
arsenicalis  in  small  doses  internally,  and  to  continue  this  inter- 
ruptedly for  some  three  months  after  the  symptoms  have  dis- 
appeared. In  addition,  it  is  as  well  to  repeat  the  liquor  arsenicalis 
some  weeks  before  the  advent  of  spring,  and  to  continue  it  inter- 
mittently into  the  summer  for  a  few  years  after  an  attack,  in  order 
to  attempt  to  guard  against  the  almost  inevitable  relapse. 

Radio- Active  Serum.—  Nicolaidi  has  devised  an  artificial  organo -mineralized 
radio-active  serum  from  horse  serum,  together  with  all  the  organic  and 
mineral  salts  of  the  blood,  in  a  solution  saturated  with  carbon  dioxide  gas, 
which  was  then  rendered  radio-active.  This  serum  is  administered  by  injec- 
tions until  twenty  to  twenty-five  are  given,  when,  according  to  the  author, 
supported  by  several  eminent  authorities,  most  remarkable  improvement 
in  the  cases  resulted. 

Symptomatic  Treatment. — The  patients  must  be  protected  frem 
the  sunlight  by  clothing,  veils,  hats,  gloves,  etc.,  and  the  deima- 
titismust  be  treated  by  emollient  lotions,  such  ascakmir.e,  scoihirg 
and  dark  ointments,  such  as  ichthj'ol  in  lanoline. 

The  indigestion  should  be  treated  by  a  mixture  containing  dilute 
hydrochloric  acid  and  infusion  of  gentian. 

The  diarrhoea  and  dysentery  should  be  treated  as  indicated  on 
p.  1854  for  bacillary,  or  on  p.  1834  for  amoebic,  dysentery. 


SYSTEMATIC  TREATMENT— PROPHYLAXIS  1733 

With  regard  to  the  nervous  symptoms,  the  irritation  on  retiring 
to  bed  and  the  sleeplessness  should  be  remembered,  and  combated 
with  cool  bathing,  and,  when  necessary,  by  doses  of  bromides, 
which,  however,  are  apt  to  increase  the  depression. 

The  vertigo  should  be  borne  in  mind,  and  precautions  taken  to 
prevent  accidents  being  caused  by  it. 

The  mental  condition  should  be  cheered  by  pleasant  surroundings, 
and  in  severe  cases  a  watch  taken  to  prevent  the  suicidal  tendencies 
taking  action. 

Diet. — The  diet  must  vary  with  the  condition  of  the  digestion 
and  the  bowels,  and  during  attacks  of  dysentery  or  diarrhoea  that 
laid  down  on  p.  1858  should  be  adopted. 

Complications. — Search  should  be  made  for  signs  of  ankylosto- 
miasis, ascariasis,  etc.,  tuberculosis,  malaria,  etc.,  and  these  should 
receive  their  appropriate  treatment. 

Typho  Pellagra. — This  serious  complication,  which  is  really  only 
an  attack  of  enteric  fever  in  a  pellagrin, in  whom  the  acute  symptoms 
at  once  become  aggravated,  must  be  treated  by  a  combination  of 
the  treatments  laid  down  for  enteric  fever  on  p.  1399,  and  pellagra, 
as  above. 

Prophylaxis— As  the  setiology  of  pellagra  is  unknown,  it  is 
obvious  that  remarks  as  to  prophylaxis  must  be  more  or  less  specu- 
lative. It  does  not  appear  to  be  directly  contagious,  and  therefore 
isolation,  quarantine,  etc.,  appear  to  be  useless.  In  accordance  with 
certain  aetiological  views,  it  is  advisable  to  attempt  to  avoid  being 
bitten  by  flies  in  the  early  morning  or  late  evening  in  the  endemic 
areas  by  the  use  of  protective  veils,  fly-brushes,  etc.  Protection 
against  the  sun,  as  described  above,  is  also  of  great  importance. 

It  is  obvious  that  the  consumption  of  diseased  or  damaged  maize 
must  be  injurious,  and  the  action  taken  by  the  Italian  Government 
to  prevent  the  sale  of  bad  maize  is  not  merely  highly  commendable, 
but  must  be  most  beneficial  to  the  community  at  large. 

Further,  the  excellent  attempt  to  find  out  every  pellagrin  by 
means  of  local  lists  is  good,  as  it  enables  the  Government  to  know 
exactly  the  condition  of  this  dreadful  malady,  provided  the  lists 
are  carefully  compiled;  on  the  other  hand,  if  these  lists  are  in- 
accurate, they  may  result  in  much  misconception  of  the  incidence 
of  the  disease.  The  provision  of  one  good  meal  a  day  to  poor 
pellagrins  during  the  spring  and  autumn  is,  in  our  opinion,  highly 
to  be  praised.  That  these  meals  are  good,  we  can  certify  from 
personal  experience.  We  fail,  however,  to  see  the  utility  of  the 
free  distribution  of  salt,  but  it  does  no  harm. 

The  methods  adopted  by  the  Italian  and  other  Governments  may  be 
summarized  as  follows: — 

1.  Laws  and  Regulations. 

(a)  Prohibiting  the  importation  and  sale  of  spoiled  corn. 

(b)  Government  inspection  of  all  corn  dried,  stored,  or  consumed.  This 
includes  the  erection  of  public  storehouses. 

(c)  Provision  of  desiccating  plants  to  dry  corn. 


1734 


PELLAGRA 


(d)  Cases  of  pellagra  to  be  reported,  and  lists  to  be  kept  and  emended 
every  year.     Unfortunately,  they  are  not  always  very  accurate. 

(e)  Formation  of  locande  sanitarie — i.e.,  kitchens  where  excellent  free 
meals  are  given  to  pellagrins,  and,  it  is  to  be  hoped,  to  other  deserving  poor 
people  also. 

(/)  Free  distribution  of  17J  pounds  of  salt  to  every  adult  pellagrin  and 
1 1  pounds  of  salt  to  every  child  pellagrin  per  annum.  This  distribution  is 
arranged  by  a  ticket  system. 

(g)  Establishment  and  upkeep  of  pellagrosaria — i.e.,  special  hospitals  for 
the  treatment  of  pellagrins. 

(h)  Establishment  of  pellagrological  commissions  in  every  province  affected 
with  pellagra,  with  powers  to  work  the  laws  and  to  investigate  the  disease. 

(i)  Financial  supply. 

2.  Formation  of  Rural  Bakeries. 

Model  central  bakehouse,  controlled  by  Government,  in  which  the  only 
bread  allowed  to  be  used  is  baked  from  good,  wholesome  wheat-flour.  The 
best  model  we  have  seen  was  in  the  Tyrol. 

3.  Improvement  of  Agriculture. 

(a)  By  cattedre  ambulanti,  or  farmers'  institutes,  designed  to  teach  locally 
modern  methods  of  agriculture,  with  the  result  that  the  farmers  become  less 
poverty-stricken. 

(b)  Advising  the  farmers  no  longer  to  plant  second  crops  of  inferior  qualities 
of  maize,  called  quarantino  {Zea  mats  v.  pracox)  and  cinquantino  (Z.  mais 
v.  subprcECOx),  which,  being  gathered  in  the  wet  month  of  October,  were 
often  only  half-ripe,  and  soon  decayed. 

(c)  By  organizing  agricultural  shows,  which  include  the  exhibition  of  maize. 


REFERENCES. 

The  most  useful  reference  is  Salveraglio  (1887),  Giornale  delta  Socitta  Italiar.a 
d'Igiene,  Milano,  whose  paper  of  156  pages,  entitled  '  Bibliographia  della 
Pellagra,'  contains  a  list  of  the  articles  published  up  to  1887.  Lavinder  and 
Babcock's  translation  of  Marie's  '  La  Pellagra  '  brings  the  literature  in  English 
up  to  1910.  The  most  useful  journals  are  the  Rivista  Pellagrologica,  published 
in  Udine;  the  Tropical  Diseases  Bulletin,  published  in  London;  while  the  Atti 
dei  Congressi  Pellagrologici  and  the  Reports  of  the  Triennial  Meetings  of  the 
American  Society  for  the  Study  of  Pellagra  also  contain  valuable  information. 
A  very  valuable  series  of  papers  is  to  be  found  in  the  publications  of  the  United 
States  Senate,  and  also  in  the  United  States  Public  Health  Reports,  and 
in  the  Transactions  of  the  Society  of  Tropical  Medicine,  London. 

Antonini  (1902).     La  Pellagra.     Milano. 

Babcock  (1910).  Journal  of  South  Caroline  Medical  Association,  Charles- 
town.     (Psychology  of  Pellagra.) 

Babes  and  Sion  (1901).  Nothnagel's  Special  Pathol,  u.  Therap.  Die 
Pellagra,  xxiv.  ii.;  in  addition,  many  publications  in  Romanisch  by 
Babes  up  to  191 2. 

Billod,  E.  (1865).     Traite  de  la  Pellagre.     Paris.     (A  most  useful  work.) 

Box  (1913).  Transactions  Society  of  Tropical  Medicine.  London.  (Pellagra 
in  England.) 

Butler  and  Hakansson  (191 7).     U.S.  Naval  Medical  Bulletin,  vol.  ii.,  No.  4. 

Chevalier  (1799).  London  Medical  Review  and  Magazine,  May.  London. 
(The  first  paper  on  pellagra  in  English.) 

Chittenden  and  Underhill  (1917).     Amer.  Jour.  Phys. 

Cutting  (191 1).  Senatorial  Paper  706.  Washington.  (Often  called  the 
Dunning  Report.) 

Davenport  (1916).     Archives  of  Internal  Medicine,  July  15. 


REFERENCES  i735 

Goodhue    (191 2).     Orleans    Medical    and    Surgical    Journal.     (Pellagra   in 

Hawaii.) 
Huertas,  F.  (1903).     Archivos  Latinos  de  Medicine  y  de  Biologia.     Madrid. 
Lombroso  (1898).     Die  Lehre  von  der  Pellagra.     Berlin. 
Long  (1910).     Journal  American  Medical  Association.     Chicago. 
Low    (1909).     Edinburgh    Medical    Journal.     (Case    of    Pellagra    from    the 

Shetland  Islands.) 
Merk   (1909).     Die   Hauterscheinungen   der  Pellagra.     Innsbruck.     (A   fine 

atlas.) 
Mott     (191 3).      Transactions     Society     of     Tropical     Medicine.     London. 

(Nervous  System  in  Pellagra.) 
Nicholls,  L.  (1912).     Journal  of  Tropical  Medicine  and  Hygiene.     London. 
Niles,  G.  M.  (1912).     Pellagra.     Philadelphia  and  London. 
Procopiu  (1903).     Li  Pellagre.     Paris. 
Raubitschek      (1912).     Deutsche      Medici  nischc     Wochenschrift.        Berlin. 

(Fagopyrism.) 
Roberts,  S.  R.  (191 2).     Pellagra.     London. 
Roel,    F.    (1880).     Etiologia   de   la    Pellagra.     Oviedo.      (Many    references, 

plates,  etc.) 
Rondoni  (1915).     Sperimentale. 
Rondoni  (1919).      Brit.  Med.  Jour. 
Roussel  (1845).     Trait6  de  la  Pellagra  et  des  Pseudopellagrcs.     Paris.      (This 

and  all  Roussel's  publications  are  to  be  recommended  for  perusal.) 
Sambon  (1910).     Progress  Report  on  the  Investigation  of  Pellagra.     London. 

(The  exposition  of  the  parasite  fly  theory  of  the  aetiology.)        (1917). 

Report  on  Pellagra  in  the  West  Indies.     London. 
Sambon  and  Chalmers  (191 2).     British  Medical  Journal.     (Pellagra  in  the 

British    Islands.)     For   work   done   in    Roumania   vide   leading   article 

Journal  Tropical  Medicine  and  Hygiene,   December  15,   191 1;  and  for 

the  work  done  at  Burano,  the  same  journal  and  article  for  October, 

1912. 
Sambon  (1916).     Presse  Medicale,  December  18. 

Sandwith  (1905).     Medical  Diseases  of  Egypt,  i.     London.     (A  most  excel- 
lent account ;  should   be  studied.)      (1913)  Society  of  Tropical  Medicine. 

London.     (Insufficiency  theory.) 
Strambio,  Junior  (1890).     La  Pellagra.     Milano. 
Warnock  (Yearly).     Reports  of  the  Lunatic  Asylum  at  Abbassia,   Cairo, 

Egypt;  also  (1902)  Journal  of  Mental  Science.     London. 
Wood,  T.  F.  (1912).     Pellagra.     New  York  and  London. 


SECTION  C 
SYSTEMIC   DISEASES 

DISEASES  OF  THE  ALIMENTARY  CANAL. 
DISEASES  OF  THE  SYSTEMS. 
SKIN  DISEASES. 


1737 


DIVISION  I. :  DISEASES  OF  THE  ALIMENTARY  CANAL. 

Diseases  of  the  Mouth  and  Stomach. 

Helminth  Infections. 

Sprue  and  the  Diarrhoeas. 

The  Choleras. 

The  Dysenteries. 

Intestinal  Schistosomiasis. 

Epidemic  Gangrenous  Rectitis. 


1738 


CHAPTER  LXXIV 

DISEASES    OF    THE    MOUTH,    THROAT, 
AND  STOMACH 

General  remarks — Oral  infections — Thrush — Gingivitis — Lingual  affections — 
Halzoun  —  Tonsillar  affections  —  Gastric  diseases  —  Earth-eating  —  Be.l- 
yando  spew — Entalacilo — References. 

GENERAL  REMARKS. 

In  this  chapter  we  make  some  remarks  concerning  the  diseases  of 
the  mouth  and  the  stomach,  which  we  will  preface  with  a  few  general 
statements  concerning  the  intestines,  as  this  is  the  most  convenient 
place  for  so  doing,  though  we  describe  the  more  important  diseases  of 
these  parts  of  the  alimentary  canal  in  separate  chapters. 

External  hernia  is  common,  but  internal  hernia  is  rare;  we  have 
only  met  with  one  example,  and  then  of  a  most  unusual  form,  the 
displacement  being  through  a  rupture  in  the  transverse  mesocolon, 
forming  a  hernia  into  the  lesser  sac.  This  hernia  probably  took 
place  through  the  recessus  intermesocolicus  transversus  (Broscke). 
Intussusception  and  volvulus  are  known,  as  well  as  intestinal 
obstruction  due  to  bands,  and  we  have  met  with  one  unique  case 
of  fatal  intestinal  obstruction  in  a  native  found  dead,  caused  by  the 
compression  of  the  rectum  against  the  pelvic  wall  by  an  enormously 
distended  bladder,  which  we  had  not  thought  to  be  possible. 

Cancer  oj  the  bowels  is  by  no  means  uncommon.  Tuberculosis  of 
the  bowel  is  generally  secondary  to  tuberculosis  in  some  other 
regions,  but  we  have  seen  primary  tuberculosis.  Appendicitis  is 
quite  common  in  both  Europeans  and  natives,  and  is  caused  by 
bacteria  acting  either  directly,  or  introduced  by  the  action  of 
Trichuris  and  Ascaris.  Appendicitis  of  schistosomic  origin  has  been 
recorded  by  Mursell. 

In  previous  editions  we  called  attention  to  the  frequency  of 
intestinal  sand.  The  true  intestinal  sand  of  animal  origin  composed 
of  dark  grey  or  colourless  gritty  particles,  and  largely  composed  of 
lime  salts,  is  occasionally  met  with,  but  far  more  common  is  the 
so-called  pseudo-intestinal  sand  composed  of  undigested  remains  of 
vegetable  food  (bananas,  etc.),  which  may  become  encrusted  with 
earthy  salts.  Delgado  Palacios  has  called  the  condition  '  faecal 
sarcoma.'  In  these  cases  there  may  be  diarrhoea  and  colicky 
pains. 

1739 


1740  DISEASES  OF  THE  MOUTH,   THROAT,  AND  STOMACH 

Uronema  caudatum  has  been  recorded  by  Fischer,  in  1914,  in  the 
diarrhceic  stool  of  a  European  in  Shanghai.  Two  days  later  only 
cysts  were  present. 

ORAL  INFECTIONS. 

The  protozoal  parasites  reported  as  being  found  in  the  mouth 
are: — 

Loeschia  gingivalis  Gros. 

Leishmania   tropica   Wright,    var.    americana   Laveran   and 

Nattan-Larrier. 
Spiroschaudinniadentium  Miller,  and  many  other  spirochetes. 
Spiroschaudinnia  buccalis  Steinberg. 
Treponema  mucosum  Noguchi. 
Treponema  macrodentium  Noguchi. 
Treponema  micro  dentium  Noguchi. 

Flagellates  have  also  been  recorded. 

Gongylonema  pulchrum. — This  filarial  worm  is  a  parasite  of  the  pig 
in  Europe  and  America,  but  was  described,  in  1916,  by  Ward  as 
occurring  in  the  lower  lip  of  a  girl,  aged  sixteen  years,  at  Jefferson  in 
Arkansas.  The  worm  was  42*1  millimetres  in  length,  and  tapered 
slightly  at  each  extremity,  of  which  the  anterior  was  ornamental, 
by  a  system  of  cuticular  tubercles,  while  a  cuticular  ridge  ran  along 
the  lateral  line. 

The  most  common  and  perhaps  most  serious  affection  is  Pyorrhoea 
alveolaris,  in  which  condition  pus  wells  up  from  alongside  the  roots 
of  the  teeth,  while  the  gums  become  swollen,  reddish,  and  inflamed, 
the  teeth  loose,  and  general  septic  absorption  or  infection  may  result. 

The  organisms  associated  with  this  lesion  are  innumerable — 
amoebae,  spirochetes,  bacteria,  etc. — and,  therefore,  the  causal  germ 
is  unknown,  but  the  treatment  is  quite  clear — viz.,  to  remove  all 
teeth  which  are  too  far  decayed  to  allow  any  hope  of  improvement, 
or  which  are  viewed  as  dangerous  from  a  general  health  point  of  view. 
Having  done  this,  the  next  and  most  important  point  is  ionization 
with  zinc  sulphate. 

Apart  from  this,  all  bridges,  crowns,  and  fillings  have  to  be  viewed 
with  suspicion  in  the  tropics,  and  vague  septic  conditions,  diarrhoea] 
or  even  dysenteric-like  symptoms,  and  more  especially  inflammatory 
changes  about  the  jaw,  should  lead  to  careful  examination  of  teeth 
treated  in  this  manner. 

It  will  be  remembered  that  streptococci  are  apt  to  enter  the  system 
alongside  the  teeth  and  via  the  tonsils,  and,  therefore,  the  strepto- 
coccal infection  should  be  thoroughly  and  carefully  treated. 

The  inflammations  oj  the  tonsils,  diphtheritic,  pseudodiphthcritic, 
and  streptococcal,  are  common  in  the  tropics,  though  diphtheria  is 
somewhat  rarer  than  in  temperate  climates,  and  require  careful 
treatment  with  local  antiseptics  and  either  serums  or  vaccines. 

Salivary  calculi  have  been  reported  by  Christ opherson,  and  are 
certainly  not  uncommon  in  Europeans  and  natives,  and  are  apt  to 


THRUSH 


1741 


recur  after  removal.  A  favourite  seat  appears  to  be  the  sublingual 
duct,  where  the  calculus  is  apt,  on  superficial  examination,  to  be 
mistaken  for  an  enlarged  lymph  gland. 

Espundia  or  oro-nasal  leishmaniasis  is  fairly  frequently  met  with, 
and  is  described  on  p.  2175;  while  gangosa  or  its  syphilitic  counter- 
part is  frequently  seen,  and  is  described  on  pp.  1876-1879. 


Fig.  742. — Leucoplakia. 

Leucoplakia  and  cancers  of  the  lips,  cheeks,  and  tongue  are  fre- 
quently met  with  in  the  tropics,  and  appear  in  a  curious  way  to  be 
related  to  mycetoma,  via  the  condition  called  paramycetoma  (vide 
Chapter  XCIII.,  p.  2145). 

THRUSH. 

Synonyms.  —  Saccharomycetic  stomatitis,  Oral  oidiomycosis.  French, 
Muguet,  Millet  blanchet;  Italian,  Mughetto;  German,  Schwamchen. 

Definition. — A  stomatitis,  or,  more  correctly,  a  group  of  stomatites, 
characterized  by  the  presence  of  creamy  white  patches,  believed  in 
the  past  to  be  produced  by  Oidium  albicans  Robin,  while  at  the 
present  time  it  is  recognized  that  they  may  be  produced  by  a  multi- 
plicity of  fungi. 

Historical. — The  affection  was  clinically  known  to  Hippocrates, 
forming  part  of  the  a-i-o/xaTa  d</>0ojSea  described  by  him.  It  was  also 
certainly  known  to  Galen  under  the  term  of  aphthce  albce  injanhttn. 

Sauvage called  the  affection  aphtluzlactamen,  and  Ba.tema.ri  apht/ue 
lactantium. 

In  1839  Langenbeck  first  discovered  that  the  condition  was  due 
to  a  fungus.  It  is  interesting  to  note  that  the  thrush  case,  micro- 
s'; vvc  illy  investigated  by  Langenbeck,  was  a  patient  suffering 
from  typhoid,  and  that  Langenbeck  suggested  that  the  fungus 
might  be  the  cause  of  this  malady. 


1742  DISEASES  OF  THE  MOUTH,   THROAT,  AND  STOMACH 

Berg  in  Stockholm,  in  1842,  studied  the  condition  very  carefully 
and  gave  some  details  on  the  morphology  of  the  fungus,  while  Vogel 
demonstrated  the  contagiousness  of  the  malady.  Gruby,  in  1842, 
considered  the  fungus  to  belong  to  the  genus  Sporotrichum,  and 
called  the  affection  aphthaphyte. 

Robin  gave  a  full  description  of  the  fungus  in  1847,  and  considered 
it  to  be  closely  related  to  Oidium  tuckeri,  which  attacks  the  leaves 
of  vine-trees,  and  to  Oidium  lactis.  In  1853  he  called  it  Oidium 
albicans. 

In  1866  Hallier  considered  the  fungus  to  be  a  Stemphylium,  and 
called  it  Stemphylium  polymorphum.  In  1868  Quinquaud  created  a 
new  genus,  Syringospora,  and  named  the  fungus  Syringospora  robini. 
In  1877  Grawitz  considered  the  organism  to  be  identical  with 
Mycodcrma  vini. 

In  1878  Rees  placed  the  fungus  in  the  genus  Saccharomyces 
(S.  albicans).  In  1885  Plaut  grew  it  in  pure  culture  and  considered 
it  to  be  identical  with  Monilia  Candida  Bonorden,  which  is  often 
found  in  cow-dung. 

In  more  recent  times  the  condition  has  been  studied  by  Klemperer, 
Roux,  Linossier,  Vuillemin,  and  others,  while  Castellani  has  shown 
that  the  affection  may  be  caused  by  a  multiplicity  of  fungi.  Pi j per 
has  recently  described  a  case  of  thrush  in  South  Africa  due  to 
Hemispora  rugosa  Castellani. 

Climatology. — Thrush  is  very  common  throughout  the  tropics, 
but  it  is  found  also  very  frequently  in  temperate  and  cold  climates. 

Etiology. — It  is  generally  stated  that  thrush  is  due  to  Oidium 
albicans  Robin  (synonyms:  Monilia,  Saccharomyces,  Parasaccharo- 
myces,  Endomyces,  Syringospora  albicans,  Syringospora  robini, 
Stemphylium  polymorphum) ,  but  the  researches  of  Castellani  carried 
out  both  in  the  tropics  and  in  temperate  zones  have  shown  that  the 
term  Oidium  albicans  has  been  used  to  cover  a  multiplicity  of  fungi, 
and  that  the  affection  may  be  caused  by  hyphomycetes  belonging 
to  different  species,  genera,  and  families.  The  fungi  capable  of 
producing  thrush  may  be  classified  as  follows: — 

Fungi  Imperjecti : — 

Genus  Monilia  Persoon. 

Genus  Oidium  Link. 

Genus  Hemispora  Vuillemin. 
Ascomycetacece  : — 

Genus  Endomyces  Link. 

Fungi  of  Genus  Monilia  Persoon. — Fungi  of  the  genus  Monilia 
Persoon  are  by  far  the  most  frequently  met  with,  and  there  is  little 
doubt  that  the  fungus  described  by  Robin  under  the  name  Oidium 
albicans  belongs  to  this  genus.  For  details  on  fungi  of  this  genus  the 
reader  is  referred  to  Chapter  XXXIX.,  p.  1079.  The  species  most 
commonly  found  in  the  tropics  are  of  the  types  Monilia  tropicalis 
Castellani,  Monilia  pinoyi  Castellani,  Monilia  parapinoyi  Castellani, 


ETIOLOGY— CLINICAL   VARIETIES  1743 

less  frequently  of  the  Monilia  bronchialis  Castellani  type  and  other 
types,  while  Monilia  albicans  Robin  scnsu  stricto  is  seldom  found 

In  cases  of  thrush  in  London  Castellani  isolated  in  191 3  fungi  of  the  types 
Monilia  pinoyi  Castellani,  M.parapinoyi  Castellani,  M. landinensis Castellani, 
M.  nietalondinensis  Castellani,  M.  bronchialis  Castellani,  occasionally  M.  fropi- 
calis  Castellani,  and  rarely  other  types. 

Fungi  of  Genus  Oidium  Link. — The  following  fungi  of  the  genus 
Odium  have  been  found  in  a  few  cases  of  thrush : — Oidium  matalense 
Castellani,  Oidium  rotundatum  Castellani,  Oidium  aster oides  Castel- 
lani. The  same  species  have  been  found  in  the  expectoration  of 
certain  cases  of  bronchitis,  and  Oidium  rotundatum  and  Oidium 
asteroides  also  in  the  faeces  of  certain  cases  of  enteritis. 

Fungi  of  the  Genus  Hemispora  Vuillemin. — The  fungus  Hemispora 
rugosa  Castellani,  found  by  Castellani  in  certain  cases  of  subacute 
tonsillitis  and  cases  of  bronchomycosis,  has  been  recently  observed 
by  Pijper  in  a  peculiar  case  of  thrush  in  South  Africa. 

Fungi  of  Genus  Endomyces  Link. — Vuillemin  in  old  cultures  of 
so-called  Oidium  albicans  Robin  found  asci,  and,  therefore,  con- 
sidered the  thrush  fungus  to  be  an  endomyces.  Vuillemin's  findings 
were  not  confirmed,  and  Landrieux  created  a  new  species  for  the 
fungus  in  which  Vuillemin  found  asci :  Endomyces  ruillcmini  Land- 
rieux. 

Predisposing  Causes. — General  weakness,  marasma,  and  the  late- 
stages  of  tuberculosis  and  diabetes,  favour  the  development  of 
thrush,  though  at  times  perfectly  sound  individuals  may  suffer 
from  it. 

Symptomatology. — On  the  mucous  membrane  of  the  cheeks,  soft 
palate,  and  tongue,  white  small  spots  appear,  which  gradually 
spread.  There  is  often  a  certain  degree  of  inflammation,  and  the 
oral  mucosa  may  be  red  and  swollen  and  the  saliva  very  acid. 
Nursing  and  chewing  are  painful,  and  infants  and  children  with 
thrush  have  often  diarrhoea.  Certain  authors,  however,  maintain 
that  the  severe  signs  of  stomatitis  are  not  due  to  the  thrush 
fungi;  bacteria  and  other  organisms  would  be  the  real  cause  of  the 
oral  inflammation,  which  would  prepare  the  ground  for  the  fungus 
to  thrive,  and  by  abundantly  growing  produce  the  white  patches. 
Thrush  not  rarely  spreads  to  the  pharynx  and  the  upper  portion  of 
the  oesophagus.  It  is  interesting  to  note  that  the  fungus  grows  from 
the  surface  downward  fairly  deep  into  the  mucous  membrane. 
It  was  believed  at  one  time  that  thrush  never  affected  cylindrical 
epithelium.  Thrush  runs  a  variable  course,  and  in  many  cases  shows 
little  tendency  to  spontaneous  cure. 

Clinical  Varieties. — In  cases  of  thrush  due  to  Oidium  rotundatum, 
Oidium  asteroides,  and  Monilia  zeylanica,  the  colour  of  the  patches 
may  be  yellowish  instead  of  creamy  white.  The  same  appearance 
has  been  recently  noted  by  Pijper  in  an  interesting  case  of  thrush 
he  has  carefully  described  in  South  Africa,  due  to  Hemispora  rugosa 
Castellani. 


1744  DISEASES  OF  THE  MOUTH,   THROAT,  AND  STOMACH 

Diagnosis. — The  diagnosis  can  often  be  made  clinically,  the 
creamy  white  patches  being  characteristic,  but  it  should  always 
be  confirmed  by  the  microscopical  examination,  which  will  reveal 
a  large  amount  of  mycelial  threads  and  conidial  forms.  If  it  is 
desired  to  know  the  ^etiological  variety  of  thrush  the  patient  is 
suffering  from,  cultural  methods  are  necessary.  These  are  described 
in  the  chapter  on  Bronchomycosis  (see  p.  1888). 

Prognosis. — Thrush  per  se  is  not  a  serious  affection,  but  its  occur- 
rence in  cachectic  patients  is  a  bad  omen. 

Treatment. — Glycerine  of  borax  applied  to  the  patches  several 
times  a  day  is  efficacious  in  many  cases,  or  an  aqueous  solution  of 
borax  (1  in  30)  may  be  used.  The  addition  of  honey  to  the  latter  is 
to  be  deprecated.  In  resistant  cases  the  addition  of  carbolic  acid 
to  the  glycerine  of  borax,  10  minims  to  the  ounce,  will  be  found 
useful.  In  marasmic  children  or  adults  suffering  from  some  incur- 
able disease  any  treatment  may  fail  to  bring  about  a  complete 
disappearance  of  the  thrush. 

Prophylaxis. — In  the  case  of  infants  there  is  no  doubt  that  in 
many  cases  the  infection  is  carried  by  contaminated  nursing  bottles 
and  their  rubber  nipples.  These  should,  therefore,  be  kept  scrupu- 
lously clean.  As  regards  children,  and  more  especially  adults,  quite 
a  number  of  them,  although  in  apparent  perfect  health,  harbour 
thrush  fungi  in  the  mouth,  and  are,  therefore,  carriers.  In  them 
the  use  of  alkaline  tooth-pastes  and  mouth-washes  is  to  be  re- 
commended. 

GINGIVITIS. 

During  the  last  few  years  much  attention  has  been  paid  to 
gingivitis,  or  inflammation  of  the  gums,  which  may  be  divided  into 
simple  gingivitis,  pyorrhoea  alveolaris,  and  ulcerative  gingivitis. 
They  are  all  of  tropical  importance. 

Simple  Gingivitis. 

In  this  disease  the  gums  are  bright  red  in  colour,  especially  near 
the  margin,  becoming  normal  when  traced  towards  the  buccal 
mucosa.  The  interdental  papillse  are  swollen,  but  are  neither  pain- 
ful nor  ulcerated.  There  is  no  odour,  no  pain  at  night,  and  no 
enlargement  of  lymph  glands,  but  the  teeth  may  be  covered  with 
tartar  and  show  food  debris.  A  carbolic  rose-water  mouth-wash 
(|  per  cent.)  will  be  found  useful. 

Pyorrhoea  Alveolaris. 

This  is  a  chronic  condition,  in  which  there  is  little  sign  of  inflam- 
mation of  the  gums,  but  in  which  pus  can  by  pressure  be  made  to 
exude  from  the  peridental  pockets.  If  it  is  allowed  to  proceed 
unchecked  it  will  produce  ulceration  of  the  bottom  of  the  peridental 
sulcus  and  destruction  of  the  periodontal  membrane,  and  will  set 
up  a  rarefying  osteitis,  which  will  injure  the  bony  socket  and  loosen 
the  teeth. 


ULCERATIVE  GINGIVITIS  1745 

Ulcerative  Gingivitis. 

Synonym.-  Mai  de  Bocha. 

This  was  studied  by  Miller,  an  American  dental  surgeon,  in  1882, 
who  first  saw  the  spirochetes  and  the  fusiform  organisms  which 
were  subsequently  described  by  Vincent,  in  1898,  as  the  causal  agent 
of  a  membrano-ulcerative  pharyngitis  and  tonsillitis,  a  membrano- 
ulcerative  stomatitis,  and  a  membrano-ulcerative  gingivitis,  two  of 
which  are  commonly  present  when  a  case  comes  to  be  noted, 
although  the  gingivitis  is  nearly  always  the  primal  disease. 

All  forms  are  common  in  the  tropics,  and  their  relative  frequency 
has  been  investigated  in  Palestine  by  Schimeoni-Meckler,  in  1917, 
who  found  that  78  cases  of  mouth  disease  could  be  resolved  into 
28  cases  of  ulcerative  gingivitis,  17  of  ulcerative  stomatitis,  6  cf 
Vincent's  angina,  and  27  of  mixed  types.  The  whole  subject  has  been 
ably  studied  by  Barlow  in  1914,  Bowman  in  1916,  by  Taylor  and 
Mo  Kinsty  in  1917,  and  by  Colyer  in  1918.  There  are  three  varieties 
of  the  complaint — viz.,  the  acute,  the  subacute,  and  the  chronic. 

Acute  Variety. — This  is  an  acute  inflammation  of  the  margins 
of  the  gums,  of  gradual  onset,  but  which  spreads  rapidly  and  causes 
ulceration  of'  the  interdental  papillae  and  sloughing  of  the  gums 
around  the  necks  of  the  teeth,  and  in  severe  cases  ulceration  of  the 
oral  mucosa,  associated  with  malaise,  fever,  and  enlargement  of  the 
lymph  glands,  haemorrhage  from  the  gums,  and  pain  therein, 
especially  at  night,  bad  taste  in  the  mouth,  offensive  breath,  difficult 
and  painful  mastication,  and  loose  and  tender  teeth.  There  is 
oedema  of  the  interdental  papillae,  which  are  bluish-red  in  colour  or 
covered  with  a  brownish  friable  slough.  It  usually  attacks  the 
gums  around  the  upper  incisor  teeth,  but  may  begin  anywhere  where 
food  tends  to  accumulate.  It  spreads  from  person  to  person,  but  is 
commonly  met  with  in  persons  living  under  bad  conditions. 

Subacute  Variety. — The  gums  are  spongy  and  tender,  and  a  whitish 
pellicle  often  forms  which  on  superficial  examination  may  give  the 
appearance  of  a  purulent  exudate.  The  condition  often  spreads 
to  the  cheeks  and  lips,  and  may  involve  the  soft  and  hard  palate 
and  even  the  tonsils.  The  pellicle  after  a  time  separates,  leaving 
an  eroded  surface  which  gradually  deepens. 

Chronic  Variety. — If  untreated  the  acute  and  subacute  varieties 
pass  into  the  chronic,  and  lead  in  a  year  or  so  to  destruction  of  the 
bony  sockets. 

Treatment. — -The  best  treatment  for  these  infections  is  to  remove 
the  tartar,  disinfect  the  mouth  with  a  spray  of  peroxide  of  hydrogen 
or  of  glycothymoline,  and  then  to  treat  by  ionization  witli  zinc 
sulphate  and  afterwards  to  use  antiseptic  washes  of  smiths  or 
similar  preparations.  Roberts  recommends  the  local  application  of 
the  following:  Hydrogen  peroxide, ~>v.,vinum  ipecac.  3m\>  glycerin  3  v., 
aq.  ad  Jviii. 


1746   DISEASES  OF  THE  MOUTH,   THROAT,  AND  STOMACH 


LINGUAL  AFFECTIONS. 

Patches  of  Leucoplakia  of  the  tongue  are  common  in  natives,  and 
may  be  of  various  origin — syphilitic,  frambcetic,  or  due  to  irritation 
caused  by  smoking  or  chewing  various  substances.  Case  of  the 
so-called  Circinate  pityriasis  linguae  or  Annulus  migrans  are  not 
rare.  Lingua  nigra  is  occasionally  seen.  We  have  already  called 
attention  to  the  dark  patches  found  on  the  tongue  in  natives,  and 
which  by  some  writers  have  been  described  as  a  sign  of  ankylo- 
stomiasis. These  pigmented  patches  are  roundish  or  oval,  and 
may  be  found  also  on  the  gums,  the  mucosa  of  the  lips,  on  the  soft 
and  hard  palate,  and  are  apparently  congenital.  A  condition 
which  might  be  called  Red  or  Purple  tongue,  and  which  often 
puzzles  the  newly  arrived  medical  man,  who  does  not  know  its 
origin,  is  extremely  common  in  Ceylon  among  the  coolies  and 
lower-class  natives,  and  is  simply  due  to  chewing  betel.  The  pig- 
mentation slowly  disappears  on  the  native  discontinuing  the  use  of 
betel.  Cases  of  Furrowed  tongue  (scrotal  tongue)  are  not  rare. 
We  have  seen  a  case  of  Fordyce's  disease  (pseudo-colloid  of  the 
lips)  in  a  half-caste.  A  case  of  Chelitis  exfoliativa  in  a  European 
lady  and  cases  of  Perleche  have  been  observed  by  us  among 
European  children.  Under  the  term  seasonal  recurrent  ulceration 
of  the  lips,  Gros  has  described  a  very  superficial  ulceration  on  the 
lower  lips  in  Algerian  natives  which  is  very  common  in  the  hot 
season,  and  is  due,  according  to  him,  to  a  diplobacillus. 

Pityriasis  Linguae  Spirochaetica  —  This  condition  has  been  described 
by  Castellani.  There  is  as  a  rule  no  sign  of  acute  inflammation 
and  no  ulcers,  but  the  dorsum  of  the  tongue  is  covered  by  a  thick, 
persistent,  whitish-yellowish  or  greyish-brownish  fur,  which  on 
microscopical  examination  seems  to  consist  solely  of  innumerable 
spirochetes,  with  some  epithelial  cells.  Of  course,  a  few  spirochaetes 
are  always  found  in  scrapings  from  the  tongue,  but  never  in  such 
enormous  amounts. 

HALZOUN. 

Definition. — Halzoun  is  the  invasion  of  the  pharynx  by  the 
adults  of  Fasciola  hepatica  (Linnseus,  1758),  which  cause  dyspnoea, 
dysphagia,  and  sometimes  more  severe  symptoms,  and  even  death. 

Historical.- — In  1904  Khouri  described  this  disease  as  occurring 
in  Northern  Lebanon. 

/Etiology. — The  disease  is  caused  by  eating  raw  livers,  especially 
raw  goat  (Capra  hircus  Linnaeus)  livers,  which  are  infected  with 
Fasciola  hepatica  (Linnaeus,  1758),  when  the  worm  (p.  565)  fastens 
itself  on  to  the  mucosa  of  the  pharynx  and  sucks  blood. 

Symptomatology.  --The  patients  suffer  from  dyspnoea,  dysphagia, 
dysphonia,  and  congestion  of  the  head,  and  occasionally  die,  but 
more  usually,  after  lasting  from  a  few  hours  to  a  few  days,  the  victim 
vomits  and  the  parasites  are  expelled,  and  recovery  results. 

Treatment. — An  emetic  will  cause  the  parasites  to  come  away. 


TONSILLAR  AFFECTIONS 


1747 


TONSILLAR  AFFECTIONS. 

Every  type  of  tonsillitis  met  with  in  temperate  climates  is  observed 
also  in  the  tropics,  although  there  is  no  doubt  that  tonsillar  andjthroat 
affections  are  less  frequent  in  warm  climates  than  in  cold.  Diph- 
theria is  on  the  whole  less  frequent  than  in  temperate  zones,  |but  a 
fairly  large  number  of  cases  occur  in  every  tropical  country.  We 
have  seen  a  number  of  cases  of  follicular  tonsillitis  and  other  strepto- 
coccal affections ;  quinsy  or  tonsillar  abscess  is  not  rare,  and  cases 
of  Vincent's  angina  occur,  due  to  Vincent's  Bacillus  fusiformis  in 
association  very  often  with 
spirochetes.  We  do  not 
propose  giving  a  description 
of  Vincent's  angina,  which 
may  be  found  in  any  text- 
book on  general  medicine, 
but  we  would  call  attention 
to  the  possibility  of  mis- 
taking it  for  a  syphilitic 
condition.  Certain  authori- 
ties state  that  Wassermann 
reaction  is  positive  in  Vin- 
cent's angina,  but  in  our 
experience  this  is  not  so, 
and  we  can  confirm  the 
researches  of  Taylor  and 
others,  according  to  which 
Wassermann  reaction  is 
negative  in  Vincent's  angina, 
except,  of  course,  when  it 
develops  in  a  syphilitic 
person.  Cases  of  tonsillitis 
possibly  due  to  amoebae  and 
flagellates  have  also  been 
recorded.  We  propose  say- 
ing a  few  words  on  certain 
affections  of  the  tonsils  to 
which  little  attention  has  so  far  been  paid — viz.,  mycotic  infections. 

Tonsillar  nocardiomycosis  and  lesions  of  the  tonsils  due  to 
Nocardia  bovis  and  other  species  of  the  genus  Nocardia  and 
Cohnistreptothrix  have  been  placed  on  record,  but  we  desire  to  call 
attention  to  the  comparative  frequency  of  a  granular  Nocardiasis 
of  the  crypts  which  may  lead  to  the  formation  of  tonsillar  calculi. 
The  affection,  which  is  not  new,  but  is  little  known,  runs  a  chronic 
course  and  is  not  painful.  The  patient  often  does  not  come  to 
consult  the  doctor  because  of  sore  throat,  but  because  of  the  un- 
pleasant odour  of  the  breath.  On  examination  the  teeth  and  gums 
may  be  quite  healthy,  but  on  examining  the  throat  small  whitish- 


Fig.  743. — Tonsillar  Affection  caused 
by  Hemispora  vugosa  Castellani. 


1748  DISEASES  OF  THE  MOUTH,   THROAT,  AND  STOMACH 

yellowish  spots  will  be  seen  on  the  tonsils;  these  spots  are  in  reality 
the  surface  portion  of  granules  contained  in  the  crypts,  and  may  be 
extracted  with  more  or  less  ease.  These  bodies  when  squashed 
have  a  very  offensive  odour ;  under  the  microscope  they  consist  of 
masses  of  Nocardia-like  organisms  at  times,  at  other  times  masses 
of  leptothrix;  in  certain  cases  both  Nocardial  fungi  and  Leptothrix 
are  seen  and  various  bacteria,  and  even  protozoa  such  as  amoebae 
and  flagellates  The  nocardia  fungi  are  very  difficult  to  grow. 
After  several  years  the  masses  in  the  crypts  may  become  calcified, 
and  real  calculi  may  be  formed,  which  at  times  are  the  starting- 
point  of  some  very  severe  inflammation. 

Varieties  of  Tonsillonocardiasis. — Clinically  the  usual  form  is  the 
yellow  or  whitish  type.  A  case  observed  by  one  of  us  was  charac- 
terized, however,  by  the  presence  of  black  granules,  from  which  a 
nocardia  similar  or  identical  to  Nocardia  nigra  Castellani,  1912,  was 
grown. 

Tonsillar  moniliomycosis.— Moniliasis  of  the  tonsils  has  been 
described  by  Castellani.  Three  types  may  be  distinguished:  the 
acute,  the  subacute,  the  chronic.  The  acute  type  is  important,  as 
such  cases  have  often  been  taken  for  diphtheria.  The  tonsils  are 
covered  by  creamy  white  patches,  which  at  times  extend  to  the 
soft  palate,  the  pharynx,  and  larynx.  There  is  difficulty  in  swallow- 
ing, and  the  patient  may  have  some  fever.  Diphtheria  is  often 
suspected,  but  the  microscopical  and  cultural  examination  clears 
the  diagnosis  at  once.  The  fungus  most  commonly  found  in 
Ceylon  is  Monilia  tropicalis  Castellani.  Cases  of  mixed  infections 
of  diphtheria  and  moniliasis  have  occasionally  been  seen  by  us. 

In  the  subacute  and  chronic  types  of  moniliasis  the  subjective 
symptoms  are  often  nil.  The  diagnosis  is  based  on  the  microscopical 
examination.  The  treatment  consists  in  applications  of  glycerine 
of  borax  and  of  carbolic  acid. 

Tonsillar  Oidiomycosis. — The  condition  is  due  to  fungi  of  the 
genus  Oidium  Link.  Clinically  the  affection  is  very  similar  to 
moniliasis,  but  in  the  case  in  which  Oidium  rotundatum  Castellani 
was  found  the  patches  were  yellowish  and  not  white. 

Tonsillar  Hemisporomycosis. — In  certain  cases  of  tonsillitis  in 
Ceylon  Castellani  found  a  fungus  which  he  had  previously  observed 
in  cases  of  bronchomycosis.  He  was  doubtful  about  the  classifica- 
tion of  the  fungus,  and  at  first  placed  it  temporarily  in  the  genus 
Monilia,  naming  it  Monilia  rugosa  Castellani,  1909.  Recently  Pinoy 
has  placed  it  in  the  genus  Hemispora,  the  name  of  the  fungus  be- 
coming Hemispora  rugosa. 

The  case  in  which  the  fungus  was  first  observed  had  been  suspected 
by  the  house  physician  to  be  a  case  of  diphtheria,  as  the  patient 
complained  of  great  pain  in  swallowing.  There  was  fever,  the 
submaxillary  lymphatic  glands  were  enlarged,  and  on  examination 
of  the  throat  several  greyish  patches  were  seen  on  the  left  tonsil 
and  on  the  soft  palate.  At  times,  however,  the  patches  are  yellowish. 
Under  appropriate  treatment  they  become  smaller  and  smaller, 


GASTRIC  DISEASES— BELYANDO  SPEW  1749 

but  one  or  two  small  spots  remain  often  for  weeks  and  even  months. 
As  regards  treatment,  painting  with  a  5  or  10  per  cent,  solution  of 
carbolic  acid  is  found  useful. 


GASTRIC  DISEASES. 

All  forms  of  Dyspepsia  are  common,  but  hyperchlorhydria  and 
fermentation  are  especially  common  in  our  experience. 

Ulcers  and  Cancers  of  the  stomach  are  met  with  at  times,  as 
well  as  dilatation  of  the  veins  at  the  lower  end  of  the  cesophagus, 
leading  to  severe  haematemesis.  In  children  Pyloric  stenosis  has 
been  seen  several  times  by  us.  We  have  met  with  one  case  of  diffuse 
inflammation  which  resembled  '  phlegmon  of  the  stomach  '  in  its 
gastric  symptoms,  but  which  was  associated  with  other  signs  point- 
ing to  a  more  general  poisoning  of  the  system. 

EARTH-EATING. 

Synonyms. — Geophagy.     French  :  Mai  d'estomac. 

Remarks. — -Earth-eating  is  common  in  many  parts  of  the  tropics,  especially 
in  certain  parts  of  Africa  (e.<f.,  the  Sudan  and  Southern  Tunisia)  and  Asia 
(Malasia,  Java,  Borneo),  but  is  observed  also  in  Temperate  Zones,  in  Europe, 
Northern  China,  and  Japan.  It  is  common  in  children  and  pregnant  women, 
It  is  believed  to  be  acquired  by  the  children  being  left  to  crawl  about  and  eat 
anything  which  comes  to  hand.  It  is  also  acquired  by  being  taken  as  a 
remedy  for  syphilis  and  other  diseases. 

Christopherson  says  that  it  is  common  in  the  Sudan,  where  two  forms  of 
earth  are  eaten:  (1)  Karkooti  (Nile  mud);  (2)  taffel  (some  form  of  calcium 
carbonate).  In  Giava  the  earth  eaten  consists  of  bituminous  clay,  called 
ampor,'  which  is  taken  especially  by  pregnant  women,  who  believe  it  will 
benefit  their  unborn  babies.  In  Guatemala  and  other  Central  American 
countries  natives  occasionally  eat  a  yellowish  eaith  containing  sulphur  as 
a  prophylactic  against  disease.  In  Japan  it  is  said  that  the  Ainus  used  to 
cat  a  paste  made  of  starch  and  of  diatomaceous  earths  in  famine  years. 

Symptomatology. — The  symptoms  are  usually  emaciation  and  anaemia, 
with  pain  in  the  epigastrium  ami  a  sensation  of  hunger,  while  constipation 
is  common.  Earth-eaters  frequently  suffer  from  ankylostomiasis,  and  often 
have  a  yellowish  muddy  or  earthy  colour. 

BELYANDO  SPEW. 

Synonyms. — Grass  sickness  (Western  Australia),  Gastric  spirochetosis 
(Ernest  Black). 

Definition. — A  gastric  disturbance  characterized  by  vomiting:  occurring 
suddenly  after  meals,  and  unaccompanied  by  nausea  in  certain  tropical  regions 
without  any  immediate  cause. 

History. --Under  the  above  terminology  Dr.  Ernest  Black  has  described  to 
us  a  disease  which  he  has  met  with  in  Western  Australia. 

Geographical  Distribution. — It  has  long  been  known  as  a  distinct  disease 
in  Queensland  under  the  name  derived  from  the  Belyando  district,  250  miles 
inland,  and  in  Western  Australia  in  certain  tropical  districts,  chiefly  coastal, 
where  it  is  called  '  grass  sickness.'  It  also  exists  in  some  tropical  districts 
in  Brazil. 

/Etiology. — -The  cause  of  the  disease  is  unknown.  Black  has  found  a 
spirochaete  in  the  mucous  membrane  of  the  stomach.  Phis  spirochaete  is  of 
variable  size,  small  and  slender. 


1 75°  DISEASES  OF  THE  MOUTH,   THROAT,  AND  STOMACH 

Black  thinks  that,  like  other  members  of  that  class,  it  generates  no  free 
toxins,  but  its  pathological  effect  is  produced,  on  its  death  and  disintegration, 
by  the  liberation  and  absorption  of  toxins. 

The  mode  of  conveyance  is  not  conclusively  determined,  but  it  seems  to  be 
by  means  of  contaminated  food  or  water.  In  one  district  in  Western  Aus- 
tralia all  the  evidence  pointed  to  milk  as  the  medium.  In  Queensland,  on  the 
other  hand,  many  years  ago  there  was  no  fresh  milk  used  in  a  district  where 
the  disease  was  common. 

Climatology  and  Incidence. — In  Queensland  it  persisted  in  the  past  in  an 
endemic  area  in  spite  of  a  drought  lasting  several  years.  In  Western  Australia 
the  outbreaks  are  strictly  limited  to  the  wet  season,  and  start  with  the  rapid 
growth  of  grass  after  the  first  rains.     Hence  its  local  name  in  that  district. 

Persons  of  both  sexes,  any  age,  and  all  races  may  be  affected,  those  in  robust 
health  equally  with  those  in  ill-health. 

Symptomatology. — The  solitary  symptom  is  vomiting,  which  occurs  only 
after  taking  food.  This  may  be  within  a  few  minutes,  or  may  be  delayed  for 
some  time  after  a  meal.  The  character  of  the  vomiting  is  quite  distinctive, 
and  reminds  one  of  the  action  of  apomorphia.  It  is  very  sudden,  and  rarely 
preceded,  accompanied,  or  followed  by  any  nausea,  straining,  or  pain.  There 
is  seldom  any  premonitory  sensation;  consequently  it  is  so  sudden  as  often  to 
be  extremely  embarrassing.  It  may  occur  after  every  meal  or  only  after  one 
or  two  meals  in  a  day.  It  may  be  every  day,  or  there  may  be  intervals  of  one 
or  several  days  between  the  attacks,  which  also  vary  in  their  duration.  From 
the  results  of  experiments,  Black  has  come  to  the  conclusion  that  the  attacks 
are  concurrent  with  and  due  to  the  death  of  some  of  the  organisms,  and  that 
the  intermissions  are  periods  during  which  none  or  too  few  die.  In  the  inter- 
mittent form  there  is  little  if  any  interference  with  the  general  health,  but  in 
the  more  or  less  continuous  cases  there  is  sometimes  considerable  loss  of 
weight,  the  malnutrition  then  resulting  in  ill-health.  There  is  no  loss  of  appe- 
tite; but  rather  the  reverse.  If  the  attacks  are  short  and  the  intermissions 
long,  patients,  especially  children,  sometimes  increase  in  weight. 

Treatment. — According  to  Black,  the  aim  of  the  treatment  is  to  destroy 
the  causal  organism  in  the  mucous  membrane  of  the  stomach.  Cyllin  in  pala- 
tinoids  of  3  minims  each  with  a  wine-glassful  of  water  three  times  a  day  is  gener- 
ally effectual  and  convenient.  Thymol  may  be  given  in  1 -grain  doses  three 
times  a  day,  the  patient  being  warned  not  to  take  anv  alcohol  or  oil.  Chlorine 
solution,  freshly  prepared,  has  been  strongly  recommended.  Other  drugs 
suggested  are  carbolic  acid,  creosote,  and  /3-naphthol.  Whatever  drug  is 
used,  it  should  be  given  at  least  half  an  hour  before  meals. 

Prophylaxis. — Nothing  is  known  about  this. 

ENTALACAO. 

* 

Synonyms.— Mai  d'engasgo,   Dysphagie   Tropicale,  Tropical   Cardiospasm. 

Remarks. — -This  disease  has  been  known  for  a  long  time  in  certain  parts 
of  Brazil,  having  been  described  by  Botelo,  Langard,  and  by  Paranhos. 
Bouchard  has  noticed  a  somewhat  similar  disease  in  pheasants  which  is  due 
to  a  worm. 

Climatology. — It  appears  to  be  localized  to  some  districts  in  the  interior 
of  Brazil. 

etiology. — The  causation  is  unknown,  but  it  has  been  suggested  that  it 
is  a  parasitic  disease,  that  it  is  a  neurosis,  or  that  it  is  connected  with  eating 
diseased  manioc.     The  last  theory  has  been  brought  forward  by  Paranhos. 

Morbid  Anatomy. — No  macroscopical  lesions  have  so  far  been  discovered. 

Symptomatology. — -The  patient  complains  of  severe  difficulty  in  swallowing 
even  liquids,  and  feels  as  though  the  food  had  stopped  in  the  oesophagus 
aiul  had  not  reached  the  stomach;  hence  the  name  '  d'engasgo,'  meaning 
choked.  During  the  attack  the  patient  becomes  anxious-looking,  throws 
the  arms  about,  and  becomes  dyspneeic.  The  face  is  congested  and  the  eyes 
protrude.     The  swallowed  food  is  brought  up  by  a  process  of  regurgitation 


REFERENCES  1751 

rather  than  of  true  vomiting.  The  attacks  are  recurrent,  with  intervals  of 
freedom.  After  a  time  the  patient  may  become  cachectic  from  lack  of  nutri- 
tion, and  die. 

Treatment. — This  is  very  unsatisfactory,  and  merely  symptomatic.     Bro- 
mides and  chloral  have  been  given,  but  a  change  of  climate  is  essential. 


REFERENCES. 

General. 

Anxaratone  (191 2).     Condizioni  Igieniche  Colonia  Eretrea.     Roma. 

Branch  (1906).     Journal  of  Tropical  Medicine,  ix.  374. 

Chalmers  (1903).     Spolia  Zeylanica. 

Gabbi  (1908).     Riv.  Critica  Clinica  Medica. 

Garrison  (190S).     Philippine  Journal  of  Science,  Book  III.,  No.  3,  p.  191. 

Jansen  (191S).     Faecal  Sarcoma.     Geneesk.  Tijdschr.  v.  Nederl.  Indie. 

Splendore  (1908).     Arch,  de  Paras. 

Stiles    and   Garrison   (1906).     Bull.    Hyg.    Lab.   U.S.    Public   Health  and 

Marine  Hospital  Service,  Washington,  28,  p.  74. 
Stiles  (1907).     Osier  and  McCrae's  System  of  Medicine,  i.  525-637. 

Thrush. 

Castellani  (1908-1917).  Numerous  papers  in  the  Centralblatt  fur  Bakterio- 
logie,  Archives  de  Parasitologic  (1 91 3 ,  tome  xvi .,  p.  1 84) ,  Journal  of  Tropical 
Medicine,  etc.,  among  which  may  be  mentioned  '  Plurality  of  Species  of 
the  so-called  Thrush  Fungus  '  in  the  Journal  of  the  Ceylon  Branch  of 
the  British  Medical  Association,  June,  1914. 

Langenbeck  (1839).     Frorieps  Notizen,  No.  252. 

Pijper  (191 7).  Thrush  due  to  Hemispora  rugosa  Castellani.  Journ.  of 
Tropical  Medicine. 

Roux  and  Linossier  (1890).     Archives  de  Medecine  Experimental. 

Gingivitis. 

Barlow    (1914).     Am.    Journ.    Trop.    Diseases    Prevent.    Med.,   No.  4.   (Mai 

de  Boca). 
Colyer  (1918).     British  Medical  Journal,  ii.  396-39S.     London. 
Roberts  (1917).     British  Medical  Journal,  September  15. 
Taylor    and    McKinsty    (191 7).       British     Medical    Journal,    March    31. 

London. 

Halzoun. 

Kfouri  (1904).     Archives  de  Parasitologic,  ix.  78.     Paris. 

Tonsillar  Affections. 

Castellani  (1904).  Journ.  Trop.  Med.,  May  2.  (1904-14)  Ceylon  Med. 
Reports.  (1909)  Journ.  Ceylon  Branch  Brit.  Med.  Assoc.  (1915)  Ton- 
silliti  acute  e  subacute  di  origine  ifomicetia.  Ricerche}[di  Biologia 
dedicate  al  Prof.  Lustig.     Florence. 

Entalacao. 

Paranhos  (191 3).     Bulletin  de  la  Societe  de  Pathologie  Exotique.     Paris. 

Earth-Eating. 

Christopherson  (1910).  Journal  of  Tropical  Medicine  and  Hygiene- 
London. 


CHAPTER  LXXV 
HELMINTH    INFECTIONS 

General  remarks— The  intestinal  tiemato  liases — -The  intestinal  cestodiases — 
The  intestinal  nematodiases — -Trichuriasis — -Ankylostomiasis  — ■  Ascariasis 
— Oxyuriasis — Intestinal  polyparasitism — Rare  infections — References. 

General  Remarks. 

In  the  present  chapter  we  propose  to  consider  the  helminth 
infections  of  the  intestines,  and  in  so  doing  exclude  those  found  in 
the  liver  or  the  bloodvessels  of  the  intestines,  though  it  is  true  that 
the  eggs  in  both  cases  may  be  found  in  the  fasces. 

The  Intestinal  Trematodiases. 
Definition. — An  intestinal  trematodiasis  is  an  infection  of  the 
alimentary  canal  with  adult  trematode  worms. 

Remarks. — The  intestinal  trematode  worms  of  man  are: — 

i.  Watsonius  watsoni  (Conyngham,  1904). 

2.  Gastrodiscns  hominis  (Lewis  and  McConnell,  1876). 

3.  Fasciolopsis  fiillebomi  Rodenwalt,  1909. 

( Fasciolopsis  rathouisi  Poirier,  1887. 
4'    \  Fasciolopsis  buski  Lankester,  1857. 

5.  Hctcrophyes  heterophyes  (von  Siebold,  1852). 

6.  Metagonimus  yokogawai  (Katsurada,  1913). 

7.  Echinostoma  ilocanum  Garrison,  1908. 

o  >?\  (Echinostoma  (Euparyphium)  malayanum  Leiper,  1911. 
' '  *' '  \Artvfechinostomum  sufrartyfex  Clayton  Lane,  1915. 

Eurytrema  pancreaticum  (Janson),  fully  described  by  Loos  (Annals  of  Trop. 
Medicine,  1907,  vol.  i.,  p.  128),  has  occasionally  been  found  in  man  in  Chin;  . 

In  addition  to  adult  worms,  the  ova  of  the  Schistosomidre  (Chapters 
XXIV.,  LXIV.,  LXXVIL,  and  LXXXIII.)  and  those  of  the  liver 
flukes  (Chapter  LXXXI.)  pass  down  the  alimentary  canal  and 
escape  in  the  faeces. 

Fasciola  hepatica  is  the  cause  of  halzoun,  described  in  Chapter 
LXXIV.,  p.  1746. 

Symptomatology. — Diarrhoea  has  been  described  as  being  caused 

by  Watsonius  watsoni  (p.  562),  while  Fasciolopsis  buski  (p.   508) 

es  dysenteric  diarrhoea,  F.  rathouisi  (p.  568)  colic,  F.  fiillebomi 

(p.  569)  fever,  and  Kwan's  fluke  (p.  569)  gastric  disturbance,  but 

1752 


INTESTINA I    T.EXUA SES 


1753 


the  recorded  cases  are  few,  the  method  of  infection  is  unknown, 
and  the  symptomatology  has  still  to  be  carefully  studied. 
Diagnosis. — The  presence  of  trematode  worms  can  only  be  diag- 
nosed by  the  discovery  of  the 
eggs  or  the  adult  in  the  faeces. 
Treatment. — The  treatment 
must  be  on  the  same  lines  as 
that  described  for  ankylosto- 
miasis. 


Fig.  744. — -Eggs  of Eurytretna  pancreaticum  Fig.  745. — Gastrodiscus 

IN    THE    FAECES    OF   A    CHINESE    COOLIE.  IlODlinis. 

(X  250.)       (From     a     photograph    by  (After  Leuckart.) 

J.J.Bell.) 

Intestinal  Taeniiases. 

Definition. — An  intestinal  tamiiasis  is  an  infection  of  the  alimen- 
tary canal  by  adult  cestode  worms. 

Symptomatology. — Cestode  parasites  cause  gastric  and  reflex  symp- 
toms, mostly  of  a  vague  nature.  The  former  comprise  salivation, 
diarrhoea,  or  constipation,  with  colicky  pains,  nausea,  vomiting,  or 
dyspepsia,  while  the  latter  include  faintness,  unequal  pupils,  dis- 
orders of  vision  and  hearing,  headache,  itching  of  the  nose  or  anus, 
vertigo,  epilepsy,  etc.  Anaemia  and  skin  eruptions  have  also  been 
recorded.  Christopher  son  and  Izzedin  have  recorded  a  case  of  acute 
intestinal  obstruction  due  to  T.snia  saginata. 

Treatment. — The  treatment  is  the  usual  anthelmintic  remedy 
of  Filix  mas,  in  capsules  (six  10-minim  capsules)  or  emulsion 
such  as  olei  filicis  3i.  to  oi.ss.,  gummae  acaciae  q.s.,  syrupi 
zingiberis  3i.,  aquae  ad  §ii.  Fiat  haust.  To  a  child  six  to  eight 
years  of  age  olei  filicis  *";SS.  may  be  administered,  followed  by 
a  saline  purg  itive  six  hours  later.  Filmaro.i,  which  contains  the 
active  principle  of  filix,  may  be  given  in  capsules  (two  or  three). 
Turpentine  may  be  given  in  doses  of  20  minims  three  times  a 
day,  or  kousso  2  drachms,  or  kamala  1  drachm.  Thymol  has 
also  been  recommended.  Naphthalene  in  2-grain  doses  has  been 
used  in  children. 

Taniiasisis  extremely  common  in  certain  parts  of  the  tropics — 
as,  for  instance,  Abyssinia — where  some  natives  take  every  two 
months  kousso  flowers  {Brayera  anthelmintica  Kunth).  Several 
other  native  drugs  have  been  used,  among  which,  according  to 
Annaratone,  the  following  are  the  principal  ones:  Bulbs  of  cossala 
(Mollugoliro),  habbeciacco  (seeds  of  Oxalis  anthelmintica) ,  the  bark  of 


OVA  OF  INTESTINAL  WORMS  AS  SEEN  IN  THE 
FAECES. 

Trematoda. 

F,  Schistosoma  japonicum  (after  Leiper). 
P,    Schistosoma  mansoni  (after  Holcomb). 

G,  Fasciolopsis  buski  (after  Looss). 

H,  Heterophyes heterophyes  (after Looss) . 
Q,   Dicroccelium  lanceatum  (after  Looss). 

Cestoda. 
J,    Dibothriocephalus   cordatus.     (Outline  only   to   show   relative  size. 

Figure  K  is  placed  inside  it  in  order  to  economize  space.) 
L,    Taenia  solium  (after  Leuckart). 
Mj  Taenia  confusa  (modified  after  Guyer). 
N,  Dibothriocephalus  latus  (modified  after  Schauinsland). 

0,  Taenia  saginata  (after  Leuckart). 
R,  Hymenolepis  nana  (after  Stiles). 

T,    Hymenolepis  lanceolata  (after  Railliet). 
W,  Hymenolepis  diminuta  (after  Blanchard). 
S,    Dipylidium  caninum  (after  Diamare). 
V,   Diplogonoporus  grand  is  (after  Brumpt). 

Nematoda. 

A,  Ancylostoma  duodenale. 

B,  Strongyloides  stercoralis  (after  Thayer). 

C,  Oxyuris  vermicularis  (after  Leuckart). 

D,  Necator  amcricanus. 

E,  Trichostrongylus  instabilis  (after  Ward). 

1,  Gigantorhynchus  gigas  (after  Ward). 

K,   Trichuris    trichiura.     (Placed     inside     the     outhne     of     Dibothrio 

cephalus  cordatus  for  the  sake  of  economy  in  space.) 
U,   Ascaris  lumbricoides. 
X,   Ascaris,  sp.  ?      (We  have  seen  large  eggs  of  this  nature  in  Ceylon.) 


1754 


Fig.  746. — Ova  of  Intestinal  Worms  as  seen  in  the  Faeces. 

1755 


1756 


HELMINTH  INFECTIONS 


Albizzia  anthelmintica  (Bessina),  flowers  and  leaves  of  buddleia, 
polistachya  (mattari),  the  bacchae  of  Mcesa  lanceolata  (Saoria),  and 
of  Nijrsine  africana  (ssa'htso),  leaves,  flowers,  and  fruits  of  Celosia 
erygina  (bcllilda),  efficacious  also  for  ascarides.  Large  doses 
of  melon  seeds  are  also  used. 


Fig.  747. — Kecal  Eggs  of  Tcenia 

solium. 

(Fromamicrophotograph  by  J.  J.Bell.) 


Fig. 


748. — Tcenia  saginata. 
(After  Braun.) 


Rare  Taeniiases. 

Some  of  the  Treniiases — e.g.,   those  due  to   Tcenia  philippina, 
T.  confusa,  T.  bremneri,  T.  hominis,  and  T.  africana — are  so  rare 


Fig.  749. — Tcenia 

africana. 

(Alter  von  Linstow. 


Fig.  750. — Tcenia  africana. 
(After  von  Linstow.) 


that  no  further  mention  is  necessary  beyond  the  descriptions  which 
have  been  given  in  Chapter  XXV.,  p.  614. 


The  Dibothriocephaliases. 

The  Dibothriocephaliases  are  produced  by  Dibothriocephaluslatus, 
D.  cordatus,  and  I),  parvus.    D.  latus  (p.  604)  causes  severe  anaemia, 


THE  DIPL0G0N0P0R0SES—DIPYL1DIA  SIS 


1757 


and  at  times  fever  associated  with  serious  symptoms,  but  this 
infectibn  is  not  common  in  the  tropics.  The  treatment  is  the 
same  as  for  Tamiiasis. 

The  Diplogonoporoses. 

Diplogonoporosis  is  found  in  Japan,  where  it  is  due  to  Diplo- 
gonoporus  grandis  (p.  605),  and  in  Roumania,  where  it  is  caused 
by  D.  braitni  (p.  605).  The  recorded 
symptoms  somewhat  resemblethose  ^^ 

produced  by Dibothriocephalus  lotus. 

Hymenolepsiasis. 

Hymenolepsis  nana  (p.  610)  may 
give  rise  to  severe  reflex  nervous 
symptoms,  but  only  when  present 


'!  ,'.<'i'  ^sdR^?^  ''"'•'  «*  •  •  *"»%".' 


■"•'agg  SP 


Fig.  751. — Dibothriocephalus  laius 
(Proglottis). 
(After    Braun.) 


V 


*C>. 


Fig.   752A. — Egg  of  Hymenolepsis 
nana  in  Human  F^ces.     (x  300.) 


Fig.  7 52. — Dipylidium  caninum. 

(After  Diamare.) 

in  considerable  numbers.  It  has 
been  found  in  Egypt,  Siam,  Japan, 
North  and  South  America,  and 
Europe,  and  is  by  no  means  a  rare 
parasite  in  man.  H.  diminula 
(p.  609)  is  a  common  parasite  in 
rats,  but  does  not  occur  so  fre- 
quently in  man,  though  a  number 
of  eases  have  been  recorded  in 
America  and  Europe.  It  doesnot 
cause  any  appreciable  symptoms. 

Dipylidiasis. 

Dipylidium  caninum  (p.  608) 
has  often  been  found  in  man,  but 
is  harmless. 


1758  HELMINTH  INFECTIONS 

Davaineiasis. 

Davainea  madagascariensis  (p.  611)  is  normally  found  in  birds, 
but  about  nine  cases  have  been  recorded  in  children  in  Madagascar, 
Mauritius,  Siam,  and  New  Guinea. 

Intestinal  Nematodiases. 

Definition. — Intestinal  nematodiasis  is  the  invasion  of  the  alimen- 
tary canal  by  adult  nematode  worms. 

Strongyloidosis. 

Synonym. — Intestinal  anguillulosis. 

Strongyloidosis,  usually  called  intestinal  anguillulosis,  is  the 
infection  of  man  with  Strongyloides  stercoralis  Bavay,  1876  (vide 
p.  628),  which  produces  no  symptoms  if  present  in  small  numbers, 
but  induces  an  intestinal  catarrh  leading  to  anaemia  and  an  inter- 
mittent diarrhoea  when  in  large  numbers.  The  disease  is  met  with 
all  over  the  tropical  world,  and  even  in  the  temperate  zone.  Diag- 
nosis can  only  be  effected  by  finding  the  rhabdite  embryo  (the  so- 
called  Angnilhda  stercoralis)  or  the  eggs  in  the  faeces,  in  which  the 
latter  will  only  be  found  when  violent  diarrhoea  is  present.  The 
treatment  is  the  same  as  for  ankylostomiasis. 

Trichuriasis. 

Synonyms. — Whip-worm  infection,  Trichocephaliasis. 

Nomenclature. — Biittner  in  1761  first  named  the  worm  Trichuris, 
or  thread-tail,  for  he  mistook  the  posterior  end  for  the  anterior. 
Linnaeus  in  177 1  called  the  worm  Ascaris  trichiura,  but  Goeze  in 
1782  changed  the  name  to  Trichocephalus  trichiura,  because  he  recog- 
nized the  error  made  by  Biittner.  The  term  Trichuris  trichiura 
Linnaeus  must,  however,  stand,  and  the  term  for  any  disease 
associated  with  this  worm  must  be  '  trichuriasis.' 

Definition. — Trichuriasis  is  an  infection  of  the  large  intestine 
appendix,  or  ileum  by  Trichuris  trichiura  Linnaeus,  1771  (vide  p.  677), 
which  produces  no  symptoms  unless  it  is  present  in  large  numbers, 
when  anaemia,  nervous  and  gastro-intestinal  symptoms  may  appear. 

History. — From  the  time  of  Barth,  who,  in  1845,  was  the  first  to 
ascribe  a  pathogenic  role  to  the  worm,  there  have  been  a  large 
number  of  observers  who  have  considered  it  to  be  the  cause  of 
gastro-intestinal  and  nervous  symptoms,  while  Metchnikoff  and 
Guiart  in  1901  considered  it  to  be  a  cause  of  appendicitis.  In  the 
same  year  Girard  drew  attention  to  the  possible  transmission  of 
pathogenic  bacteria  into  the  tissues  via  the  wounds  produced  by 
the  worm.  In  1902  Schiller  ascribed  a  case  of  high  fever  to  the 
action  of  a  heavy  infection  with  the  parasite.  In  1908  Musgrave, 
Clcgg,  and  Polk  contributed  an  excellent  monograph  on  the  whole 
subject  of  trichuriasis,  together  with  full  accounts  of  four  cases. 
Our  own  experience  is  in  favour  of  the  worm  being  occasionally 


TRICHURIASIS  i759 

directly  the  cause  of  appendicitis,  for  several  times  we  have  found  it 
in  the  inflamed  appendix  removed  by  operation. 

Geographical  Distribution. — Trichitris  trichiura  is  cosmopolitan 
in  its  distribution. 

etiology. — Trichuriasis  is  caused  by  Trichuris  trichiura  Linmeus, 
1771,  which,  as  far  as  is  known,  is  really  a  parasite  of  man  and 
monkeys,  while  allied  forms  exist  in  other  animals.  The  eggs 
escape  with  the  faeces,  and  require  tliree  to  six  months  for  the 
development  of  the  embryo,  which  can  then  remain  alive  for  years 
inside  the  shell  if  kept  on  moist  earth.  Usually  the  eggs  gain  access 
to  man  by  means  of  contaminated  food,  especially  uncooked  vege- 
tables, and  to  a  less  extent  fruits.     This  is  especially  likely  to  occur 


Fig.   75$.—Trichi<>'is  trichiura. 
(Micro photograph  by  J.  J.  Bell.) 

in  the  tropics,  where  human  faecal  matter  is  often  allowed  to  be 
deposited  in  vegetable  gardens.  Musgrave,  Clegg,  and  Polk 
report  finding  the  ova  in  washings  from  fresh  vegetables.  Domestic 
animals,  insects,  flies,  dust,  etc.,  are  also  considered  to  be  possible 
means  of  infection.  When  taken  into  the  alimentary  canal,  it 
hatches  and  reaches  sexual  maturity  in  sixteen  days. 

It  occurs  more  commonly  among  children  than  adults,  women 
than  men,  and  native  races  than  European.  Biit  all  these  factors 
appear  simply  to  depend  upon  good  or  bad  sanitation,  for  the  latter 
is  the  principal  factor  in  producing  infection. 

Pathology. — -It  is  believed  that  the  worms  attached  themselves 
to  the  mucosa  of  the  bowel  by  the  head  penetrating  deeply  into  its 
tissue  either  via  a  gland  or  directly.  In  this  position  the  worm  is 
firmly  fixed,  and  is  more  or  less  protected  against  the  action  of 


1760  HELMINTH  INFECTIONS 

anthelmintics.  They  do  not  appear  to  be  blood-suckers,  nor  is 
there  any  evidence  that  they  produce  toxins — at  all  events,  in 
sufficient  quantity  to  affect  man.  On  the  other  hand,  it  is  believed 
that  micro-organisms  can  gain  entrance  to  the  blood  through  the 
wounds  produced  by  the  head,  and  this  secondary  infection  may  be 
the  cause  of  the  appendicitis  and  other  pathological  phenomena. 

Morbid  Anatomy. — A  post-mortem  simply  reveals  anaemia  and 
dropsy,  with  at  times  appendicitis.  The  most  marked  feature  is 
the  presence  of  large  numbers  of  Trichuris  trichiic  a. 

Symptomatology. — The  symptomatology  may  be  subdivided  into 
the  intestinal  and  appendicular  varieties. 

Intestinal  Variety. — The  illness  begins  with  dizziness,  tinnitus 
aurium,  and  a  sensation  of  weakness,  which  may  be  followed  by 
slight  daily  fever  and  later  by  oedema  of  the  face  and  extremities, 
while  anaemia  appears  and  gradually  progresses.  Seen  at  this  stage 
of  the  illness,  the  mucosa  of  the  lips  and  tongue  appear  pale,  the 
appetite  is  poor,  and  dyspepsia,  followed  later  by  nausea  and 
vomiting,  with  or  without  slight  diarrhoea,  occurs. 

The  liver  and  spleen  are  normal,  but  a  haemic  murmur  may  be 
heard  at  the  apex  of  the  heart,  while  the  blood  examination  reveals 
a  great  decrease  in  the  number  of  red  cells  and  the  presence  of 
poikilocytes,  but  as  a  rule  no  nucleated  elements.  The  haemoglobin 
is  also  reduced,  while  the  leucocytes  are  increased,  and  also  in  most 
cases  there  is  an  absence  of  an  eosinophilia.  The  urine  is  normal. 
There  is  mental  depression,  restlessness,  headache,  and  at  times 
insomnia.  As  the  disease  progresses  the  anaemia  becomes  more 
and  more  marked,  and  death  may  eventually  ensue. 

Appendicular  Variety. — The  ^mptoms  of  this  variety  are  the 
same  as  those  for  appendicitis  arising  from  other  causes.  Operative 
treatment  reveals  the  nature  of  the  malady.  The  symptoms  are 
the  same  as  those  for  appendicitis  due  to  other  causes — viz.,  severe 
pain  in  the  region  of  the  appendix,  tenderness  on  pressure,  with 
often  vomiting  and  fever. 

Diagnosis. — The  disease  closely  resembles  ankylostomiasis,  from 
which  it  may  be  differentiated  by  finding  trichuris  ova  and  no 
ancylostome  ova  in  the  faeces,  and  also  by  the  absence  of  marked 
eosinophilia. 

Prognosis.— The  ordinary  slight  infection  which  is  frequently  met 
with  may  be  considered  to  be  harmless,  but  the  prognosis  is  grave 
in  those  rare  cases  of  very  heavy  infection  presenting  the  symptoms 
described  above. 

Treatment. — -The  treatment  at  present  advised  is  the  administra- 
tion of  thymol  by  the  mouth  in  the  manner  presently  to  be  de- 
scribed fur  ankylostomiasis,  and  enemata  of  solutions   of   benzine. 

Prophylaxis. —Good  sanitation  and  proper  disposal  of  sewage, 
associated  with  cleanliness  in  the  preparation  of  food,  as  well  as 
with  personal  cleanliness,  constitute  important  prophylactic 
measures.  Uncooked  vegetables  and  skins  of  fruits  should  not  be 
eaten. 


ANKYLOSTOMIASIS  1761 

Ankylostomiasis. 

Synonyms. — Ancylostomiasis  (this  is  the  latinized  Agthylostomiasis,  and 
is  a  term  much  recommended  by  many  authorities),  Agchylostomiasis,  Anchy- 
lostomiasis,  Uncinariasis,  Dochmiosis,  Dochmiasis.  Latin  :  Anemia  inter- 
tropicalis,  Hypoxemia  intertropicalis,  Geophagia  {pro  parte).  English  :  Ceylon 
anasmia,  Negro  consumption,  Tropical  chlorosis,  Egyptian  chlorosis,  Miners' 
anaemia,  The  Great-lazies  (Florida),  Tunnel- workers'  anaemia,  Hook-worm 
disease,  Porto  Rican  anaemia.  French  :  Anemic  des  Pays  Chauds,  Cachexie 
Atncaine,  Mai  de  Cceur,  Mai  d'estomac,  Ankylostomasie.  Italian :  Anchilosto- 
manemia,  Anchylostomiasi.  German  :  Ankylostomen-Krankheit,  Tunnel- 
krankheit,  Wurmkrankheit.  Spanish  •'  Aquilostomiasis.  Portuguese  : 
Oppilaciio,  Amerellao,  Cancacuo.      Arabic  :  Rihagan,  Sufura,  Tun-tun. 

Definition.— Ankylostomiasis  is  a  toxaemia  resulting  in  a  pro- 
gressive anaemia,  caused  by  Ancylostoma  duodcnale  Dubini,  1843, 
and  Necator  americanus  Stiles,  1902. 

History. — The  history  of  the  discovery,  together  with  the 
structure,  life-history,  and  geographical  distribution  of  the  two 
parasites,  has  been  described  on  pp.  666-673,  and  it  now  remains 
to  give  an  account  of  the  history  of  the  disease  produced  by  them 
in  man. 

If  the  references  contained  in  the  Ebers  papyrus,  as  well  as  those 
in  the  '  Harita  Sarhhita,'  really  refer  to  ankylostomiasis,  they 
would  make  the  history  of  the  knowledge  of  the  disease  very  ancient. 
It  was,  however,  early  recognized  that  there  was  a  fatal  disease  of 
unknown  causation  in  the  New  World.  Thus  in  1648  Piso,  in  his 
work  '  Historia  Medica  Brasilia;, '  gives  an  account  of  a  fatal  disease, 
Oppilatio  (or  Oppilacao),  present  in  Brazil,  by  which  he  probably 
meant  ankylostomiasis.  After  him  it  was  described  by  Pere 
Labat  in  Guadeloupe  in  1742,  by  Chevalier  in  St.  Dominique  in 
1752,  by  Desportes  in  the  same  place  in  1770,  by  Bayon  in  Cayenne 
in  1780,  by  Hunter  in  Jamaica  and  Rodschield  in  British  Guiana 
in  1796,  by  Bryon  Edwards  in  Jamaica  in  1799,  by  P^t  m  x8o8  m 
the  United  States,  and  by  Moreau  de  Jonnes  in  1816  in  Guadeloupe, 
while  Chabert's  celebrated  account  appeared  in  1821.  In  Peru 
Castelnau  found  it  in  1820,  Jobim  in  Brazil  in  1835,  and  Clarke 
in  West  Africa  in  i860.  In  the  meanwhile  a  peculiar  anasmia  had 
been  found  among  miners,  first  of  all  in  Hungary  in  17S6,  and  later 
in  France,  Belgium,  Germany,  and  Cornwall,  which  for  a  long  time 
was  misunderstood,  until  Dubini's  worms  were  found  in  the  victims. 
In  fact,  nothing  certain  could  be  said  about  this  peculiar  form  of 
'  tropical  anasmia '  or  '  miners'  anaemia '  until  Dubini  found 
Ancylostoma  dnodenale  as  the  cause  of  the  disease,  thus  definitely 
separating  ankylostomiasis  from  '  malarial  cachexia,'  and  also 
clearing  the  diagnosis  of  miners'  anasmia  and  tunnel  disease.  He 
proposed  the  name  Agchylostoma  for  his  new  worm,  deriving  it 
from  uiKi'Aos,  meaning  'bent,'  and  o-rofia,  meaning  'mouth,' 
which  he  latinized  Into  Agchylostoma,  which  therefore  ought  to  have 
remained  as  the  name  of  the  worm,  though  Ancylostoma  is  doubtless 
a  better  rendering.  Still,  whether  he  misspelt  the  word  or  not,  his 
name,  according  to  the  old  rules  of  nomenclature,  ought  to  have 

in 


1762 


HELMINTH  INFECTIONS 


stood,  but  the  Zoological  Committee  decided  otherwise,  and  we  have 
no  choice  in  the  matter,  and  simply  carry  out  the  rules  for  the  time 
being  in  force.  After  his  discovery  the  recognition  of  the  disease 
spread,  at  first  slowly,  but  later  rapidly.  Thus  Bilharz  in  1853 
and  Griesinger  in  1854  recognized  it  in  Egypt,  and  Wucherer  in 
1872  in  Brazil,  while  Grassi  and  Parona,  in  1877,  drew  attention  to 
the  importance  of  finding  the  ova  in  the  faeces  as  a  method  of  diag- 
nosis, and  in  1899  Ashford  drew  attention  to  the  importance  of  the 
high  eosinophilia.  In  1898  Looss  traced  the  method  of  infection 
by  the  skin,  the  lungs,  trachea,  etc.,  while  more  recently  Sambon, 
Fulleborn,  and  v.  Schilling-Torgau  have  traced  a  subsidiary  route 
from  the  lungs  via  the  blood-stream  to  the  alimentary  canal.  In 
1902  Stiles  described  Necator  americanus,  and  in  the  same  year 
Boycott  and  Haldane  found  the  disease  in  the  mines  of  Cornwall. 
Climatology. — The  disease  will  be  found  wherever  there  is  a 

suitable  temperature  and  mois- 
ture for  the  development  of 
the  parasites.  It  is  therefore 
spread  throughout  the  tropics 
of  America,  Africa,  and  Asia, 
and  is  also  found  in  Queensland, 
New  Guinea,  and  Fiji,  and  also 
in  mines  or  tunnels  in  Europe, 
where  the  conditions  of  tem- 
perature and  moisture  resemble 
the  tropics. 

/Etiology. — The  disease  is 
due  to  the  presence  of  Ancy- 
lostoma  duodenale  and  Necator 
americanus  in  the  body.  These 
parasites,  as  far  as  is  known, 
live  entirely  in  human  beings, 
and  are  therefore  kept  alive  by 
'  patients  '  suffering  from  the 
disease  and  by  '  carriers  '  or 
persons  infected  with  so  few  worms  that  little  or  no  symptoms 
are  produced.  As  already  noted,  the  larvae  live  in  earth,  and 
infection  takes  place  by  two  routes — either  through  the  skin  or 
by  the  mouth.  In  the  latter  instance,  it  is  generally  acquired  by 
eating  contaminated  vegetables,  or  through  the  habit  of  geophagy 
met  with  in  some  natives.  It  is  probable,  in  our  opinion,  that  the 
pathological  phenomena  may,  partly  or  principally,  be  due  to  toxins, 
either  set  free  by  the  embryo  in  its  travels  from  the  skin  to  the 
alimentary  canal,  or  inoculated  into  the  blood-stream  from  the 
cephalic  glands  of  the  adult  worm  as  it  grips  the  villi  of  the  intestine. 
But  absolute  proof  is  still  required  of  the  presence  of  these  toxins, 
notwithstanding  the  work  of  De  Giovanni,  Loeb,  Gabbi,  Noc,  Ales- 
sandrini,  and  many  others.  Weinberg's  researches  on  various 
helmintotoxins  must   be   specially   mentioned.    The   Porto   Rico 


Fig.  754. — Necator  americanus. 
(Natural  size.) 


PATHOLOGY 


1763 


Commission  confirms  the  suspicion  which  had  long  existed  as  to 
a  relative  racial  immunity,  finding  71  per  cent,  of  the  cases  in 
Europeans,  54  per  cent,  of  the  cases  in  mulattoes,  and  41  per  cent, 
of  the  cases  in  negroes,  to  vary  from  medium  to  very  severe,  though 
the  degree  of  infection  of  the  three  races  was  in  the  proportions 
of  jS  per  cent.,  72  per  cent.,  and  76  per  cent. 

With  regard  to  the  two  worms  it  is  useful  to  note  that  Ancylostoma  dtiodenale 
is  larger  and  coarser  looking,  with  thicker  and  coarser  head,  armed  with  four 
hooks  on  the  buccal  rim,  and  with  the  dorsal  conical  tooth  not  markedly  pro- 
jecting into  the  mouth.  Female  with  sexual  opening  in  the  posterior  third. 
Male  with  larger  caudal  bursa,  with  dorsal  lobe.  Ova  slightly  smaller. 
Necator  americantts  is  smaller,  with  small  and  finely  tapering  head,  simple 
chitinous  lips  on  the  buccal  rim,  dorsal  conical  tooth  projecting  well  into  the 
mouth.  Female  with  sexual  opening  in  the  anterior  half  of  the  body.  Male 
with  smaller  bursa  and  subdivided  dorsal  lobe.     Ova  slightly  larger. 


Fig.  755. — Case  of  Ankylostomiasis. 
(Note  the  swollen  face.) 

Pathology. — When  the  embryos  enter  the  skin  in  sufficient 
numbers  they  cause  an  eruption  of  papules  or  vesicles,  but  some  of 
these  are  more  probably  due  to  the  pyococci  and  bacteria  introduced 
along  with  the  larvae,  which  are  the  true  cause  of  the  dermatitis,  as 
alcoholic  extracts  of  the  larvae  are  said  to  produce  similar  lesions. 
These  skin  lesions  are  called  '  bunches  '  in  Cornwall,  '  mazamorra ' 
in  Porto  Rico,  and  '  ground-itch  '  in  Assam.  Smith  has  shown  that 
experimental  dermal  infection  with  Ar.  americanus  causes  local 
itching  and  a  macular  eruption,  followed  next  day  by  a  vesicular 
rash  and  swelling  of  the  part,  and  on  the  fifth  day  marked  swelling 
and  enlargement  of  the  lymph  glands.  This  dermatitis  disappears 
by  the  twelfth  day.  There  may  be  sore  throat  and  uneasy  sensa- 
tions in  the  stomach  for  a  few  weeks,  and  the  ova  appear  in  the 
faeces  about  the  middle  of  the  seventh  week. 


1764  HELMINTH  INFECTIONS 

It  is  not  known  what  effect  the  journey  from  the  skin  to  the 
alimentary  canal  has  upon  the  host,  but  it  is  certain  that  in  course 
of  time  a  marked  effect  upon  the  blood  and  the  organs  of  the 
bodv  is  produced,  which  often  appears  out  of  proportion  to  the 
number  of  worms  which  can  be  found  in  the  intestine.  Loeb  and 
Smith  find  that  the  worm  produces  a  substance  which  hinders  the 
coagulation  of  the  blood.  Some  observers — e.g.,  Gabbi — have 
found  that  the  blood  of  ancylostome  patients  is  more  toxic  than 
the  blood  of  healthy  people,  and  contains  more  hemolytic  sub- 
stances, but  this  has  been  denied  by  Marini.  Padoa  and  others 
have  observed  that  the  processes  of  intestinal  putrefaction  are  very 
marked  in  ankylostomiasis.  In  our  opinion  the  anaemia  is  due  to 
a  complex  of  causes — viz.,  the  hemolytic  toxins  secreted  by  the 
worm,  actual  loss  of  blood  from  the  bites  of  the  worms,  and  microbic 
secondary  infections. 

Morbid  Anatomy. — An  eruption  about  the  feet,  oedema  about  the 
ankles,  with  a  peculiar  dead-white  appearance  of  the  conjunctiva, 
are  often  seen  on  the  post-mortem  table.  On  opening  the  abdomen, 
it  will  be  noted  that  the  tissues  are  damp,  the  peritoneum  sodden, 
the  intestines  very  pale,  and  some  straw-coloured  fluid  will  generally 
be  seen  in  the  peritoneal  cavity.  All  the  organs  appear  damp  and 
pale.  The  lungs  are  oedematous,  the  heart  pale  and  fatty,  with 
sometimes  hypertrophy  of  the  left  ventricle.  The  liver  is  fatty; 
the  spleen  presents  various  appearances,  but  generally  is  shrunken; 
the  pancreas  is  normal,  as  are  the  suprarenals;  the  stomach  shows 
chronic  gastritis;  the  jejunum  and  ileum  are  usually  contracted; 
and  the  mucosa  is  often  dark  red  in  colour,  and  marked  by  small 
hemorrhagic  points,  which  indicate  the  position  of  the  bites.  The 
ancylostomes  may  be  found  in  large  numbers,  or  may  require 
considerable  looking  for.  Sometimes  they  are  firmly  attached  to 
the  mucosae.     The  kidneys  are  usually  enlarged,  pale,  and  fatty. 

Symptomatology. — The  first  stage  or  invasion  of  the  body  by  the 
embryos  may  be  marked  by  dermatitis  of  various  types,  papulo- 
vesicular or  pustulo-ulcerative.  The  dermatitis  is  generally 
situated  on  the  soles  of  the  feet,  and  called  by  the  natives  of  the 
West  Indies  '  mazamorra '  (ground-itch),  and  is  also  known  as 
'  pani-ghao  '  and  the  sore  feet  of  coolies.  It  is  probable,  as  remarked 
by  Balfour,  that  the  symptoms  of  the  initial  dermatitis,  urticarial 
wheals,  redness,  and  itching,  are  due  directly  to  the  larvae,  while  the 
pustular  stage  is  caused  by  secondary  pyogenic  infection.  The 
second  stage  is  the  development  of  a  leucocytosis  and  an  eosinophilia 
before  the  definite  disease  begins.  The  third  stage  is  when  the 
anaemia  begins  to  be  appreciable. 

The  patient  becomes  pale,  weak,  and  dropsical,  the  pallor  being 
most  marked  in  the  conjunctiva  of  the  lower  eyelid,  which  becomes 
of  a  peculiar  dead-white  appearance.  The  emaciation  may  be 
marked,  but,  on  the  other  hand,  it  may  be  concealed  by  the  dropsy. 
In  many  cases  there  is  oedema  round  the  ankles,  and  in  others  there 
may  be  general  oedema,  with  often  ascites,  oedema  of  the  legs, 


SYMPTOMATOLOGY  1765 

scrotum,  or  face.  When  the  ascites  is  marked,  the  patient  has  a 
protuberant  abdomen,  and  looks  at  first  sight  not  unlike  a  person 
suffering  from  malarial  cachexia  or  kala-azar.  The  tongue  is  said 
by  some  observers  to  have  two  purplish  smears,  one  on  each  side 
of  the  median  line,  and  to  be  pigmented,  but  this  in  our  experi- 
ence can  be  seen  in  normal  natives.  The  appetite  may  be  per- 
verted and  geophagy  result,  and  in  addition  there  are  signs  of 
dyspepsia  due  to  the  chronic  gastritis,  and  there  may  be  nausea, 
vomiting,  heartburn,  and  pain  over  the  pit  of  the  stomach.  The 
bowels  may  be  constipated,  or  there  may  be  diarrhoea.  Ova  of 
Ascaris  and  Trichnris,  together  with  those  of  Ancylostoma,  are  often 
seen  in  the  faeces.  Occasionally  a  little  blood  and  mucus  are 
present,  and  Charcot-Leyden  crystals  may  also  occur. 

Blood. — There  is  marked  anaemia,  which  has  been  shown  by 
Boycott  and  Haldanc,  by  using  Haldane  and  Lorrain-Smith's 
method  of  estimating  the  total  volume  of  the  blood,  to  be  due  to  a 
hydraemia;  that  is  to  say,  the  total  volume  of  the  blood  is  increased 
without  a  corresponding  increase  in  the  cellular  elements  and  haemo- 
globin. This  is  analogous  to  the  blood  condition  found  in  chlorosis, 
and  is  the  reverse  of  that  found  in  pernicious  anaemia,  the  features 
of  which  are  very  rarely  met  with  in  ankylostomiasis. 

The  counts  given  by  different  observers  vary.  Thus,  Ashford  gives  as  the 
average  of  nineteen  cases  the  following  figures:  Erythrocytes,  1,776,000; 
haemoglobin,  21  per  cent.;  colour-index,  0-6;  leucocytes,  7,000;  eosinophiles, 
10-3  per  cent.  Boycott  and  Haldane  in  seventeen  cases  found  erythrocytes 
from  4,072,000  to  1,533,000;  haemoglobin  from  58  to  17  per  cent.;  colour- 
index  from  0-71  to  0-56;  leucocytes  from  44,800  to  3,800;  polymorphonuclears, 
48-7  per  cent.;  lymphocytes,  14-4  per  cent.;  mononuclears,  5-9  per  cent.; 
transitionals,  7-4  per  cent.;  eosinophiles,  23  per  cent.;  mast  cells,  o«6  per 
cent.  Ashford,  King,  and  Gutierrez  found  erythrocytes  from  normal  1»> 
754,000;  haemoglobin  from  8  to  10 1  per  cent.;  leucocytes  from  5,000  to 
10,000;  polymorphonuclears,  54-5  per  cent.;  lymphocytes,  i6'3  per  cent.; 
mononuclears,  8-6  per  cent.;  eosinophiles,  17-1  per  cent.;  other  forms,  3*5  per 
cent. 

The  red  cells  may  show  pathological  changes  and  poikilocytes; 
megalocytes  and  polychromasia  may  be  seen,  as  well  as  normoblasts 
and  megaloblasts.  The  diminution  of  the  colour-index  is  said  to  be 
the  first  pathological  sign  in  the  blood.  In  some  very  rare  cases  a 
condition  of  hyperglobulia  has  been  observed  instead  of  the  usual 
oligocythaemia. 

Boycott  has  shown  that  the  principal  leucocytic  changes  are  to 
be  seen  in  the  blood  before  a  condition  of  marked  anaemia  has  set  in, 
when  it  is  found  that  there  may  be  high  leucocytosis — 20,600  to 
56,000 — with  a  very  high  eosinophile  figure  of  56-2  to  66*2  per  cent., 
while  the  hamoglobin  was  from  98  to  80  per  cent.  When  anaemia 
sets  in,  a  leucocytosis  is  much  less  frequent,  being  met  with  in  cases 
in  which  anaemia  develops  quickly.  On  the  other  hand,  a  leuco- 
penia  may  be  seen  if  the  case  is  very  anaemic,  ["he  reason  for  this 
alteration  from  a  high  state  of  leucocytosis  wit hout  anaemia  to  that 
of  leucopenia  with  severe  anaemia  might  at  first  sight  be  thought 


1766  HELMINTH  INFECTIONS 

to  be  explicable  by  the  hydremia  producing  the  anaemia.  Boycott, 
however,  considers  that  this  is  not  so,  for  he  points  out  that  leuco- 
cytosis  can  occur  with  marked  anaemia,  and  that  there  is  always  a 
tendency  on  the  part  of  the  blood  to  restore  its  average  volume  and 
composition  when  altered  from  the  normal,  and  comparing  the 
normal  leucocytic  count  of  the  hydremia  of  chlorosis,  says  that, 
if  there  was  no  other  factor,  the  leucocytic  count  of  ankylostomiasis 
would  not  be  affected  by  the  hydremia. 

He  thinks  that  the  true  explanation  is  probably  exhaustion  of 
the  bone-marrow  produced  by  the  anaemia,  and  that  it  is  partially 
due  to  a  failure  on  the  part  of  the  individual  to  react  to  the  stimulus 
to  produce  the  eosinophile  leucocytes.  In  any  case,  the  leucocytic 
reaction  does  not  bear  any  relationship  to  the  anaemia.  According 
to  Boycott  and  Haldane,  if  the  eosinophiles  are  deducted  from  the 
total  number  of  the  leucocytes,  and  the  percentage  of  the  remainder 
then  calculated,  it  will  be  found  to  be  nearly  normal.  The  eosino- 
philia  has  been  found  to  remain  after  the  ova  have  quite  disappeared 
from  the  faeces.  Any  inflammatory  complication  which  leads  to  a 
polymorphonuclear  increase  may  hide  the  true  eosinophilia.  The 
leucocytes  are  normal  in  structure,  a  few  neutrophils  but  no 
eosinophile  myelocytes  are  to  be  seen.  Weinberg  and  Mello  have 
shown  that  the  injection  into  guinea-pigs  of  extracts  of  various  worms 
induces  a  certain  degree  of  eosinophilia. 

Reviewing  this  description  of  the  blood,  we  would  point  out  that 
it  looks  as  though  toxins  were  stimulating  the  production  of  the 
eosinophiles,  and  at  the  same  time  preventing  a  proper  formation 
of  haemoglobin,  and  finally  producing  the  hydraemia.  We  must 
state,  however,  that  occasionally  we  have  come  across  severe  cases 
showing  no  eosinophilia.  Low  has  demonstrated  that  eosinophilia 
is  generally  well  marked  in  children,  while  it  may  be  absent  in 
adults,  and  suggests  that  the  eosinophiles,  which  are  tissue  cells  at 
first,  come  into  the  blood  in  response  to  some  stimulus  set  up  by 
the  infection,  but  gradually  disappear  as  this  stimulus  weakens 
with  the  prolongation  of  the  infection.  As  a  result  of  the  diminution 
of  the  production  of  haemoglobin,  the  iron  in  the  liver  is 
diminished. 

Patients  often  complain  of  palpitation  or  difficulty  in  breathing. 
The  lungs  will  be  found  normal,  but  the  heart  may  be  displaced 
downwards  and  to  the  left,  and  be  feeble,  with  a  haemic  bruit  at  the 
base.  The  vessels  of  the  neck  may  be  seen  to  pulsae  markedly. 
The  pulse  is  quick,  and  may  be  weak,  thready,  dicrotic,  and  in- 
termittent.    The  liver  is  very  often  enlarged,  especially  in  children. 

Fever. — Fever  in  ankylostomiasis  was  described  years  ago  by 
Manson,  Fernando,  and  others,  and  more  recently  attention  has  been 
called  to  it  by  Gabbi  and  one  of  us.  In  some  cases  there  is  no 
fever,  while  in  others  this  feature  is  present.  In  our  experience 
three  types  of  ankylostomiasis  fever  may  be  met  with: — 

i.  The  low  intermittent  type,  which  is  the  commonest,  and  in 
which  the  temperature  seldom  rises  above  ioo°  F. 


SYMPTOMA  TOLOGY 


1767 


2,  An  irregular  type,  at  times  intermittent,  and  at  times  sub- 
continuous. 

3.  An  undulating  type.     This  is  very  rarely  observed. 

Great  care  should  be  taken  in  making  the  diagnosis  of  ankylo- 
stomiasis fever  to  exclude  other  conditions — e.g.,  malaria,  Malta 
fever,  kala-azar,  trypanosomiasis,  etc.  There  is  much  diversity 
of  opinion  on  the  origin  of  this  fever.  In  our  experience  the  fever 
is  not  due  to  the  worm  itself.  It  is  of  bacterial  origin,  being  probably 
due  to  infections  by  intestinal  bacteria  entering  the  general  circula- 
tion through  the  small  wounds  produced  in  the  intestinal  mucosa 
by  the  worm.  The  term  '  ancylostoma  fever  '  is,  therefore,  not 
quite  appropriate.  In  several  cases  the  fever  continues  long  after 
the  patient  has  got  rid  of  the  ancylostomes  by  adequate  treatment. 


Tim  e      ° 
-v.      I0> 

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1    99 

Normal  ] 

Temp.  1 

of  Body  l 

98 

97 

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___ . 

Fig.  756.— Temperature  Chart  of  a  Case  of  Ankylostomiasis  Fever. 
(From  a  case  in  the  Clinic  for  Tropical  Diseases,  Colombo.) 


Urine.—  The  urine  is  copious,  pale,  and  often  alkaline,  with  a 
specific  gravity  varying  from  1010  to  1015.  Albumen  is  rarely  seen, 
but  there  is  an  increase  of  indigo-blue  and  urobilin,  and  there  is 
albumosuria  at  times.  The  excretion  of  nitrogen  is  said  to  be 
much  increased.  Lussana  believes  that  there  are  toxins  in  the 
urine  which  can  be  separated  by  the  following  method:  The  urine 
is  condensed  in  a  water-bath  at  60 °  to  700  C.  to  a  syrup,  and  then 
extracted  with  absolute  alcohol,  which  is  driven  off,  and  tlie  residue 
dissolved  in  sterilized  water,  and  injected  subcutaneously  into 
rabbits.  This  is  believed  to  produce  diminution  of  the  red  corpuscles, 
loss  of  haemoglobin,  and  poikilocytosis,  which  speedily  disappear  on 
stopping  the  injections.  These  findings  of  Lussana  have  been 
confirmed  by  some  and  refuted  by  other  observers. 


1768  HELMINTH  INFECTIONS 

Mental  and  physical  hebetude  are  marked,  and  other  nervous 
symptoms  may  be  observed.  Children  do  not  develop  properly, 
and  sterility,  with  delayed  menstruation,  has  been  noted. 

When  the  anaemia  becomes  profound  death  may  ensue  from 
cardiac  failure,  but  any  intercurrent  affection  hastens  the  end  in  a 
case  of  ankylostomiasis. 

Complications. — Any  intercurrent  disease  is  a  serious  complica- 
tion, as  also  is  pregnancy. 

Diagnosis.- — The  definite  diagnosis  depends  upon  finding  the  ova 
in  the  faeces. 

Anaemia  in  tropical  countries,  especially  if  associated  with 
dropsy,  should  at  once  lead  the  practitioner  to  suspect  ankylosto- 
miasis. It  must  be  remembered,  however,  that  it  is  by  no  means 
easy  to  find  the  ova  in  the  faeces  at  the  first  examination,'  and  that 
sometimes,  even  in  the  worst  cases,  they  require  to  be  looked  for 
on  several  days.  Occasionally  it  is  useful  to  give  an  aperient  to 
make  the  eggs  appear  in  the  stools. 

To  facilitate  the  search  for  the  eggs  in  the  stools  several  methods  have  been 
elaborated  by  Fulleborn,  Pepper,  and  others.  Pepper's  method  is  based  on 
the  stickiness  of  the  ova;  a  portion  ©f  the  sedimented  faeces  is  placed  on  a 
slide  for  a  few  minutes,  and  then  gently  immersed  in  water;  after  this, 
although  all  other  materials  are  washed  away,  the  ova  still  adhere  to  the  slide. 
If  this  process  is  repeated  several  times,  numerous  eggs  may  accumulate  on 
the  slide.  It  is  to  be  noted  that  eggs  of  Ascaris,  Trichuris,  etc.,  do  not  possess 
this  physical  property,  and  therefore  do  not  remain  on  the  slide. 

Telemann's  method  is  to  shake  up  a  small  portion  of  faeces  with  equal  parts 
of  ether  and  Ivy dro chloric  acid,  filter,  centrifuge,  and  examine  the  bottom 
deposit. 

Bass's  method  is  to  dilute  the  faeces  with  ten  or  more  times  their  bulk  of 
water,  strain  through  two  or  three  layers  of  gauze  in  a  funnel,  centrifuge, 
pour  off  fluid,  fill  up  with  diluted  faeces,  shake,  centrifuge,  repeat  a  third 
time,  then  examine  deposit  removed  by  a  clean  pipette. 

It  must  be  admitted,  as  noted  by  Miss  Porter  and  other  observers,  that 
concentration  methods  for  the  detection  of  ova  are  of  relatively  little  use,  as  in 
practice  they  take  too  long. 

Prognosis. — -There  is  no  doubt  that  ankylostomiasis  is  one  of 
the  great  factors  in  producing  the  death-rate  of  a  tropical  native 
community,  very  often  because  it  is  not  diagnosed.  Ashford,  King, 
and  Gutierrez  placed  the  deaths  of  Porto  Rico  caused  by  ankylosto- 
miasis at  30  per  cent,  of  the  total  death-rate,  and  we  are  not  at  all 
surprised  at  this,  for  our  experience  indicates  that  the  disease  is 
frequently  entered  in  death  certificates  as  anaemia,  general  dropsy, 
and  malarial  cachexia. 

Treatment.- — The  aim  of  the  treatment  is  to  kill  and  remove  the 
parasites,  and  this  can  be  effected  by  thymol,  eucalyptus  oil, 
eucalyptol,  bcta-naphthol,  or  male-fern.  A  case  must  not  be  con- 
sidered cured  until  the  faeces  show  no  ova  on  repeated  examina- 
tion after  two  or  three  weeks. 

In  all  cases  the  patient  should  be  carefully  examined  as  to  the 
condition  of  all  his  organs  before  treatment  is  begun,  and  should 
be  placed  on  low  or  liquid  diet  for  a  day  or  so,  and  while  being 


TREATMENT  1769 

treated  should  be  kept  in  bed,  and  care  taken  that  the  bowels  have 
been  well  opened. 

Thymol,  introduced  by  Bozzolo,  should  be  given  in  cachets,  or  as 
an  emulsion.  Generally  15  to  30  grains  are  given,  and  two  hours 
later  another  15  to  30  grains,  followed  in  some  cases  by  a  third 
dose  of  15  to  30  grains  after  another  two  hours.  If  the  bowels 
do  not  act  within  four  hours  of  the  last  dose,  a  saline  aperient 
should  be  given.  The  treatment  may  be  repeated  on  the  following 
day.  Another  method  is  to  give  10  grains  in  cachets  at  night  until 
the  desired  result  is  attained.  Yet  another  method,  recommended 
by  the  International  Health  Board,  is  to  mix  it  with  an  equal  quan- 
tity of  bicarbonate  of  soda,  as  this  addition  is  believed  to  aid  the 
cure  and  prevent  unpleasant  symptoms. 

Thymol  is  a  very  poisonous  drug  in  large  doses,  causing  first 
irritation  of  the  cerebral  centres,  with  excitement  and  vertigo, 
while  a  dark  colour  may  appear  in  the  urine,  or,  according  to  Blum, 
may  be  produced  by  the  addition  of  hydrochloric  acid  to  the  urine. 
According  to  the  same  authority,  this  colour  exists  in  the  form 
of  a  chromogen  in  the  urine,  the  chemical  nature  of  which  is 
threefold:  thymolsulphuric  acid,  thymolhydrochinon  sulphuric 
acid,  and  thymolglycuric  acid.  In  larger  doses  the  nerve  centres 
are  paralyzed,  the  blood-pressure  falls,  and  the  patient  dies  of 
collapse. 

Thymol,  however,  is  very  insoluble  in  water — -only  1  in  1,500  of 
cold  water — but  it  is  easily  soluble  in  alcohol,  ether,  chloroform, 
glycerine,  and  turpentine;  hence  no  alcoholic  stimulant  whatever 
must  be  given  to  a  patient  who  is  to  take  or  has  taken  thymol, 
and  not  merely  must  care  be  taken  not  to  order  stimulants,  but  the 
nurses  must  be  warned  of  the  danger  of  giving  them.  Thymol  is  also 
soluble  in  oil.  Hence  no  purgative  of  castor  oil  should  be  ordered 
after  its  administration.  Thymol  certainly  should  never  be  given 
if  there  is  marked  visceral  disease,  nor  do  we  think  that  it  should 
be  given  in  very  profound  anaemia — i.e.,  when  the  number  of  red 
cells  is  below  1,500,000  per  cubic  millimetre.  It  is,  however,  very 
satisfactory  in  its  lethal  action  on  the  worms,  but  the  treatment 
must  be  repeated  in  many  cases  in  a  week,  and  again  repeated  if 
ova  are  seen  in  the  faeces.  Sandwith  recommends  a  hypodermic 
injection  of  strychnine  before  thymol  is  administered. 

Eucalyptus  Oil  and  Chloroform. — A  much  less  dangerous  treat- 
ment is  by  oil  of  eucalyptus  and  chloroform,  which  may  be 
preceded  by  a  saline  purgative  given  a  few  hours  earlier. 

The  usual  formula  is: — 

Olci  eucalypti     ..  ..  ..  ..  ..     Il\xxx. 

Chlorotormis       ..  ..  ..  ..  ..     IT\xlv. 

Olci  ricini  ..  ..  ..  ..  . .     5>c. 

One  half  to  be  given  first  thing  in  the  morning,  and  the  other  half 
in  half  an  hour.  The  chloroform  is  probably  the  active  principle 
of  this  mixture.     It  does  not  work  as  satisfactorily  as  thymol,  but 


I77Q  HELMINTH  INFECTIONS 

it  is  safer,  and  can  be  used  several  days  in  succession.  We  use  it 
often  in  children  and  debilitated  adults.  We  have  not  seen  the 
alarming  symptoms  described  by  some  authorities  as  occurring  in 
children  and  debilitated  subjects.  Some  physicians  prefer  euca- 
lyptol  instead  of  the  oil  of  eucalyptus.  The  difference  is  that 
eucalyptol  is  that  portion  which  passes  over  between  3470  to 
35 1  °  F.  when  the  oil  is  being  distilled  from  the  leaves. 

Chenopodium  Oil. — The  International  Health  Board  of  the  Rockfeller 
Foundation  in  191 7  stated  that  this  oil  was  the  most  effective  remedy  for  the 
treatment  of  ascaris,  oxyuris,  and  trichiuris,  but  that  its  utility  for  the  treat- 
ment of  ankylostomiasis  was  conflicting,  and,  further,  that  it  produced  at 
times  alarming  symptoms  and  even  death. 

It  is  either  used  alone  or  with  oil  of  eucalyptus  in  the  proportion  of  three 
parts  of  chenopodium  to  one  part  of  eucalyptus.  The  method  of  administra- 
tion is  to  forbid  all  solid  food  after  midday,  to  give  a  purge  of  Epsom  salts  at 
4  p.m.,  and  then  at  6  p.m.  the  first  dose  of  sugar  containing  chenopodium; 
this  is  continued  at  hourly  or  two-hourly  intervals  until  the  full  dose  has  been 
taken,  and  finally,  two  hours  after  the  last  dose,  more  than  1  ounce  of  Epsom 
salts  is  taken  by  an  adult  and  repeated  if  necessary  in  another  two  hours. 

The  dosage  of  oil  of  chenopodium  is  as  follows : — 

1-2  years  of  age  .  .  .  .  . .     2  minims  for  three  doses. 

3-5         ....  3-5 

6-10       ,,       ,,  ..  ..  ..     6-9 

1 1-16       ,,       ,,  .  .  .  .  .  .    10-13 

17-50        ,,       „  14-16 

Over  50  ,,       ,,  .  .  . .  ..    12-14 

It  can  be  given  on  sugar  or  in  gelatine  capsules.  The  Epsom  salts  administere  1 1 
are  in  a  solution  of  5  pounds  in  5  gallons  of  water,  4  drachms  being  given  to  a 
child  one  to  five  years  of  age,  8  drachms  to  one  of  six  to  ten  years,  12  drachms 
to  one  of  eleven  to  fifteen  years,  16  drachms  to  one  of  sixteen  to  twenty  years, 
and  24  drachms  above  that  age.  Castor  oil  may  be  given  instead  of  salts, 
2  drachms  for  a  child  of  one  to  three  years,  3-5  drachms  for  a  child  of  four 
to  eight  years,  6-10  drachms  for  nine  to  sixteen  years,  and  above  sixteen 
years  8-16  drachms,  while  1 J  ounces  is  considered  to  be  the  maximum  for  a 
female. 

No  alcohol  or  acids  are  to  be  ingested  for  a  period  of  twelve  hours  antecedent 
to  and  after  the  treatment.     Pregnant  women  should  not  be  treated  in  this  way. 

Treatment  should  be  repeated  after  ten  days,  and  one  week  after  the  second 
course  the  faeces  should  be  examined  microscopically  to  see  whether  further 
medication  is  necessary,  and  if  so  it  shoidd  be  repeated  at  ten  days'  intervals 
according  to  the  microscopical  findings. 

Beta-naphthol,  finely  powdered,  can  be  given  in  cachets  in  15  to  20  grain 
doses,  administered  in  the  same  manner  as  thymol — viz.,  one  cachet  every 
two  hours  for  two  or  three  times,  with  the  same  precautions  as  with  thymol. 
The  patientsof  ten  complain  of  severe  burning  of  the  stomach  after  taking  them. 
The  drug  should  never  be  given  to  individuals  suffering  from  diseases  of  the 
kidneys,  as  it  may  cause  fatal  haemorrhagic  nephritis. 

In  debilitated  patients  beta-naphthol  may  be  given  in  5-grain  pills  made 
up  with  pulvis  tragacanthaecomposita  and  syrup.  One  to  three  pills,  according 
to  age,  should  be  administered  early  in  the  morning  on  six  successive  days. 
No  preliminary  preparation  is  necessary.  The  results,  however,  as  regards 
the  destruction  of  the  parasites,  are  not  brilliant. 

Nicol  recommends : — 

Beta-naphthol  (finely  powdered)         .  .  .  .      Jiv. 

Mucilaginis  tragacanthae  .  .  . .  .  .      §i. 

Aquae  menthae  piperilac  ..  ..  ..ad  gvi. 


ANKYLOSTOMIASIS  1771 

of  which  6  drachms  (gr.  ixx.  of  beta-naphthol)  is  given  to  an  adult  male. 
5  drachms  to  an  adult  female,  and  1  to  2  drachms  to  children,  for  a  dose. 
Three  doses  are  given  at  intervals  of  two  hours.  Two  hours  after  the  last 
dose  a  saline  aperient  is  given.  Beta-naphthol  does  not  keep  well,  and  should 
be  stored  in  J-pound  bottles,  and  kept  in  a  cool  place. 

Male  fern,  followed  by  castor  oil,  or  calomel,  or  infusion  of  senna,  has  also 
been  strongly  recommended,  and  was  generally  used  before  Bozzolo  introduced 
thymol  in  1880.  The  Porto  Rico  Commission  found  it  useless  even  in  doses 
which  produced  toxic  symptoms. 

Nattan-Larrier  recommends  the  following  method  of  administering  Filix 
mas : — 

First  day:  Milk  diet  and  saline  purge.  Second  day:  Milk  diet;  a  capsule 
containing  0-30  centigramme  of  oil  of  Filix  mas  every  ten  minutes  until  twenty 
have  been  taken,  followed  in  one-quarter  of  an  hour  by  a  capsule  of  ether 
every  three  minutes  until  eight  have  been  taken.  After  the  last  capsule, 
['5  grams  of  castor  oil  arc  administered,  and,  after  half  an  hour,  25  grammes 
ol  castor  oil.  Third  day:  A  saline  purge.  Fourth  day:  Examination  of  the 
faeces  and  repetition  of  the  treatment.  Brimont  recommends  the  essence  of 
Melaleuca  viridiflora. 

Worms  in  the  Faces. — Whatever  treatment  be  adopted  its  effect 
must  be  judged  by  the  worms  found  on  examining  all  the  faeces 
passed  during  the  first  twelve  to  twenty-four  hours  after  dosage. 
These  faeces  are  stirred  up  with  water,  allowed  to  settle,  and  the 
water  decanted,  and  this  process  repeated  several  times,  after  which 
the  deposit  is  placed  on  a  flat  dish  with  a  black  background,  and 
the  whitish  or  greyish  little  worms  looked  for. 

Treatment  of  the  Skin  Eruption. — The  area  showing  the  eruption 
should  be  painted  with  a  solution  of  salicylic  acid  in  collodion  (1  in  6) 
in  the  early  stages,  or  later  it  should  be  soaked  in  a  weak  solution  of 
carbolic  lotion  (1  in  100),  and  the  vesicles,  pustules,  etc.,  should  be 
opened  and  cleaned  with  1  in  40  carbolic  lotion,  and  the  whole  area 
dressed  with  a  carbolic  lotion  or  carbolic  ointment  dressing.  The 
itching  may  be  relieved  by  an  ointment  of  salicylic  acid  gr.  v. 
in  5ii.  of  zinc  oxide  ointment  and  vaseline.  The  dressing  should 
be  performed  twice  daily,  and  the  internal  treatment,  as  de- 
scribed above,  begun  at  once,  and  repeated  every  week  for  some  time. 
Treatment  of  the  Mouth. — For  about  two  weeks  after  infection 
the  patient  should  use  a  mild  antiseptic  gargle  several  times  a  day, 
and  should  be  instructed  to  spit  out  his  saliva,  sputum,  etc.,  and 
not  to  swallow  it.  The  gargling  should  be  performed  before  drinking 
or  eating  anything.  The  sputum  should  be  collected  and  examined 
for  larvae. 

Prophylaxis. — Prophylaxis  must  be  based  upon  an  attempt  to  kill 
the  parasites  in  the  human  being,  and  to  prevent  the  infection  of 
the  human  being  by  the  parasite,  but  in  order  to  be  successful  in 
these  methods  it  is  absolutely  necessary  to  educate  both  the  rich 
and  the  poor  of  a  district  in  the  essentials  of  the  disease.  This  must 
be  done  by  illustrated  lectures  and  pamphlets  in  the  vernacular. 
An  appeal  must  also  be  made  to  the  people  to  come  at  once  for 
treatment  when  suffering  from  skin  eruptions  or  anaemia. 

The  first  method  is  the  most  feasible,  and  has  been  tried  on  a  large 
scale  at  Porto  Rico,  and  on  many  estates  and  in  mines.     The 


1772 


HELMINTH  INFECTIONS 


quickest  way  is  to  examine  the  people  for  anaemia,  and  treat  the 
anasmics  with  thymol,  the  eucalyptus-oil  mixture,  or  /3-naphthol, 
after  the  examination  of  the  faces.  On  estates  the  method  of 
examining  the  blood  of  non-anaemic  persons  for  an  eosinophilia 
might  be  adopted,  as  the  worms  may  be  present  before  the  anaemia 
shows  itself.  The  faeces  of  persons  showing  eosinophilia  should 
then  be  examined  for  ova,  and  treatment  instituted  on  the  findings. 
Of  course  a  certain  degree  of  eosinophilia  is  also  present  in  cases  of 
ascariasis  and  other  kinds  of  helminthiasis. 

With  regard  to  the  second  method,  the  formation  and  use  of 
proper  latrines  may  do  much.     With  regard  to  estates,  tea-bushes, 


Fig.  757. — A  Cheap  and  Easily  Constructed  Incinerator. 

etc.,  should  not  be  allowed  to  grow  right  up  to  the  coolies'  lines, 
but  a  clear  area  should  be  left,  and  this  should  be  treated  from  time 
to  time  with  quicklime.  Further,  every  alternate  row  of  bushes 
might  be  left  out  in  the  half-acre  adjoining  the  lines,  and  in  the 
vacant  spaces  latrine-holes  lined  with  lime  might  be  dug.  The  use 
of  bucket-latrines  and  the  destruction  of  the  faeces  in  a  small  crude 
incinerator  would  be  better,  and  could  be  easily  managed  on  estates. 
The  best  cheap  latrine  is  'Bailey's  patent,'  manufactured  by  the 
Empire  Engineering  Company  of  Cawnpore,  at  a  cost  of  118  rupees 
for  a  two-seat,  and  360  rupees  for  an  eight-seat  latrine. 

Leiper  has  suggested  that  fruitful  results  would  be  obtained  from  a  more 
detailed  study  of  the  larvicidal  effects  of  chemical  manures  such  as  '  nitro- 
line,'  etc.  According  to  certain  experiments  made  by  this  author,  it  would 
seem  that  after  treatment  with  such  chemicals  human  ordure  could  perhaps 
be  used  on  the  land  with  safety. 


ANKYLOSTOMIASIS 


1773 


The  figures  show  small  incinerators  in  use  in  a  mill  and  in  a 
gaol  in  Colombo,  but  it  must  be  remembered  that  faeces  require 
a  considerable  amount  of  fuel  and  a  considerable  draught  before 
they  are  properly  burnt.  There  is,  however,  no  need  to  go  to  great 
expense,  and  a  simply  constructed  incinerator  will  often  work  well, 
if  a  little  smell  is  not  objected  to.  In  order  to  calculate  the  size  of 
latrine  required,  it  must  be  remembered  that  an  Indian  community 


Fig.  758. — Another  Cheap  and  Easily  Constructed  Incinerator. 

is  estimated  to  pass  8  ounces  of  faecal  matter  per  diem  in  a  mixed 
population  of  races,  sexes,  and.  ages,  and  40  ounces  of  urine.  The 
usual  size  of  a  galvanized  iron  latrine-bucket  is  14  inches  high  by 
12  inches  broad  at  the  mouth  and  9  inches  at  the  base,  and  it  has  a 
cubic  capacity  of  0.9  cubic  foot,  and  is  said  to  weigh  10  pounds 
when  full.  Coir  fibre  is  often  mixed  with  the  faecal  matter  in  the 
proportion  of  2\  pounds  of  coir  to  1  pound  of  faecal  matter  or  1  gallon 
of  urine. 


1774  HELMINTH  INFECTIONS 

Messrs.  Freudenberg  and  Company,  of  Colombo,  use  a  simple  incinerator, 
and  they  have  kindly  supplied  us  with  the  following  details  of  their  process, 
which  is  carried  out  at  night : — 

Average  number  of  buckets  of  faecal  matter  burnt  per  night,  20. 

Average  weight  contents  of  a  bucket,  26  pounds. 

Average  quantity  of  ash  left  after  burning  the  above,  5  buckets. 

Average  amount  of  coir  dust  used  per  bucket,  2  pounds. 

Average  amount  of  firewood  used  per  burning,  2  hundredweight. 

Average  amount  of  rubbish  burnt  at  the  same  time,  together  with  a 
few  old  gunny  bags,  i£  hundredweight. 

Average  number  of  coolies  whose  faecal  matter  is  dealt  with,  400. 

Latrine  coolies  at  6ii  cents  per  diem  to  do  the  work,  2. 

Firing  starts  at  7  p.m.,  and  is  finished  by  8  a.m.;  the  highest  tempera- 
ture recorded  was  1,050°  C. 

The  urine  can,  of  course,  be  separated  from  the  faeces  by  using  a  Donaldson's 
separator  latrine.  The  urine  can  then  be  disposed  of  by  burial,  and  the  faeces 
burnt. 

There  is  no  doubt  that  some  such  method  would  have  excellent  results  in 
dealing  with  the  problem  in  small  communities  and  estates  if  carried  out 
properly. 

Badly  infected  lands  might  be  treated  with  lime.  It  has  been  recommended 
that  coolies  should  protect  their  feet  by  first  dipping  them  in  a  bucket  of 
tar,  and  then  in  one  with  sand. 

The  method  of  dealing  with  a  large  community  is  best  exemplified 
by  quoting  the  excellent  work  of  the  two  Porto  Rico  Commissions, 
temporary  and  permanent,  the  former  consisting  of  Ashford,  King, 
and  Igaravdez,  and  the  latter  of  Igaravdez,  Martinez,  and  Sein  y  Sein. 

Patients  attend  at  a  central,  or  one  of  the  outlying  depots  or  dispensaries, 
where  their  stools  are  examined,  and  they  are  given  medicines,  and  a  card 
with  the  following  instructions : — 

1.  Take  one  of  the  two  purgatives  given  to  you  to-night  (sodium  sulphate). 

2.  Take  at  6  a.m.  to-morrow  half  the  capsules  [all  the  capsules  equal  45  to 
60  grains  (3  to  4  grammee)  of  thymol,  or  23  to  45  grains  (1-5  to  3  grammes)  of 
/3-naphthol] . 

3.  Take  the  other  half  at  8  a.m.  the  same  morning. 

4.  Take  the  other  purgative  at  10  a.m. 

5.  You  should  neither  drink  wine  nor  any  alcoholic  liquor  during  the  time 
you  are  taking  these  medicines. 

6.  Come  for  more  medicines  until  the  physician  says  you  are  cured. 

7.  Have  a  privy  in  your  house.  Do  not  defaecate  on  the  surface  of  the 
ground,  but  in  the  privy. 

8.  Do  not  walk  barefooted,  so  that  you  may  avoid  catching  mazamorra  in 
your  feet.     Wear  shoes,  and  you  will  never  surfer  from  anaemia. 

In  addition,  farmers  were  requested  to  stop  the  pollution  of  the  ground,  and 
to  introduce  the  use  of  shoes. 

The  result  was  that  1 1  per  cent,  of  the  population  were  treated  in  the  year 
1906-07  (89,233),  and  of  these,  25-7  per  cent,  were  cured,  17-4  per  cent,  practi- 
cally cured,  40-5  per  cent,  were  under  treatment,  16-2  per  cent,  ceased  to 
return,  and  0-2  per  cent,  died,  at  a  total  cost  of  ^9,600,  of  which  ^7,200  went 
in  salaries  and  £1,100  in  drugs. 

Again,  the  highest  credit  must  be  given  to  the  Americans  for  the  fearless  way 
in  which  they  spend  money  on  the  prevention  of  disease  and  the  free  hand 
which  they  give  to  the  sanatarian  in  the  tropics. 

In  mines  Oliver  recommends  that  a  solution  of  iron  sulphate  be  used  as  a 
wash  for  the  floors. 

Salt  has  also  been  recommended  by  Perroncito,  and  later  by  other  observers, 
but  as  a  solution  of  at  least  2  per  cent,  is  necessary  to  kill  the  larvae,  this 
method  is  too  expensive. 


A  SC  ARIA  SIS  1775 

f      Summary  of  Preventive  Measures. 
Educational : — ■ 

Instruction  of  rich  and  poor  with  regard  to  the  methods  of  infection, 
symptoms,  treatment,  ami  prophylaxis. 
Personal  1  'roph  yla  vis  : — 

1 .  Protection  ol  the  Eeet. 

2.  Protection  ol  the  hands. 

3.  Immediate  treatment  of  the  eruption  on  feet  or  hands. 

4.  Necessity  of  early  treatment. 
Public  Prophylaxis  : — 

1 .  Search  for  and  treatment  of  carriers. 

2.  Search  for  cases  of  the  skin  eruption  and  treatment  of  the  same. 
}.   Search  for  cases  of  anaemia  and  treatment  of  same. 

4.,  Provision   of   sanitary  conveniences    kept  in    good    condition,  and 
associated  with  a  good  system  of  conservancy. 

Ascariasis. 

•  Definition. — -Ascariasis  is  infection  with  Ascaris  lumbricoides 
Linnaeus,  1758;  Toxascaris  canis  Werner,  1782;  or  Bel 'ascaris  mystax 
Zeder,  1800,  the  first  named  being  much  the  most  common. 

Symptomatology. — The  symptoms  may  be  nil,  or  may  resemble 
those  of  cestode  infections,  being  partly  gastro-intestinal,  partly 
reflex,  while  skin  irritation  and  eruptions  may  also  be  present.  If, 
however,  the  number  of  parasites  be  very  considerable,  signs  of 
toxic  poisoning,  or  even  of  intestinal  obstruction  from  interlacing 
of  the  worms,  may  develop,  but  the  great  danger  is  from  the 
wandering  of  the  parasites.  If  they  wander  up  the  bile-duct  and 
inn  the  liver,  they  may  cause  abscesses  in  the  liver.  We  have 
found  as  many  as  eleven  worms  in  the  bile-duct,  with  a  large 
number  in  the  liver,  three  of  which  lay  in  abscess  cavities.  They 
may  also  enter  the  duct  of  Wirsung,  and  cause  slight  inflammation 
of  the  pancreas,  or  go  into  the  appendix,  and  cause  appendicitis. 
Further,  they  may  pierce  the  bowel  in  cases  of  ulcerative  conditions 
of  the  bowels,  and  enter  the  peritoneum  or  the  bladder,  or  enter  the 
lung,  the  nose,  or  the  ear  by  the  Eustachian  tube— in  fact,  they  may 
wander  all  over  the  body.  The  observer  must,  however,  be  careful 
to  distinguish  between  the  post-mortem  and  ante-mortem  wander- 
ings of  these  worms;  in  the  former  case  the  worms  are  generally 
found  alive.  The  most  important  reflex  symptoms  are  the  con- 
vulsions so  commonly  met  with  in  children,  and  attacks  of  so-called 
'  wormy  '  cough  are  not  rare.  We  have  seen  cases  of  fever  re- 
sembling typhoid  (typho-lumbricosis)  which  on  post-mortem  ex- 
amination have  shown  no  lesions  of  typhoid,  but  enormous  numbers 
of  ascaris. 

Diagnosis. — The  diagnosis  will  depend  upon  the  discovery  of  the 
eggs  in  the  faeces. 

Treatment. — The  best  treatment  is  santonin,  with  some  form  of 
purgative.  Usually  santonin  is  mixed  with  an  equal  quantity  of 
calomel,  and  given  in  doses  of  1  to  3  grains  for  an  adult,  and  ,1  grain 
for  every  year  of  life  for  a  child.  The  dose  is  given  every  morning 
for  two  or  three  days,  and  repeated  again  in  a  week  if  eggs  still 


1776  HELMINTH  INFECTIONS 

appear  in  the  faeces.     It  is  as  well  to  remember  that  santonin  may 
cause  blue  or  yellow  vision. 

Oil  of  chenopodium  may  be  given  in  gelatine  capsules  or  in  castor  oil.  (Fcr 
dosage  see  p.  1770.)  In  China  Quisqitalis  indicais  at  times  used:  2  drachms  of 
the  powder. 

Oxyuriasis. 

Definition. — Oxyuriasis  is  infection  with  Oxyaris  vermicular  is 
Linnaeus,  1767  (see  p.  857),  and  is  common  all  over  the  world. 

Symptomatology.- — The  symptoms  are  irritation  in  the  region  of 
the  anus,  with  sometimes  a  distinct  entero-colitis,  and  sometimes 
slight  fever.  It  is  usually  stated  that  there  is  a  sense  of  irritation 
in  the  nose.  The  diagnosis  is  to  be  made  by  finding  the  worms  in 
the  motions  after  a  purgative.  In  girls  the  worms  may  enter  the 
vagina  and  cause  vaginitis. 

Treatment.- — The  gravid  females  can  be  killed  by  rectal  injections 
of  quassia,  alum  (5i-  to  a  pint),  salt  (5ii.  to  a  pint),  but  the  young 
forms  require  internal  treatment  with  santonin  and  calomel,  as 
described  under  Ascariasis.  Flynn  recommends  sulphur  (gr.  iii.) 
three  times  a  day  in  adults.and  gr.  i.ss.  in  children,  given  as  a  cachet 
or  lozenge.  A  10  to  20  per  cent,  calomel  ointment,  diluted  unguen- 
tum  hydrargyri  (1  in  4),  may  be  applied  to  the  anus,  or  iodoform 
and  naphthalan  suppositories  may  be  used. 

Intestinal  Polyparasitism. 

Definition. — Intestinal  polyparasitism  is  the  invasion  of  the 
alimentary  canal  by  more  than  one  species  of  parasite. 

Remarks. — We  have,  since  1903,  investigated  the  question  as  to 
which  parasites  are  commonly  present  in  natives  of  tropical  Africa 
and  Ceylon,  and  find  that  it  is  the  rule  rather  than  the  exception 
for  their  intestines  to  harbour  more  than  one  species  of  parasite. 

Statistical  information  with  regard  to  the  prevalence  of  the 
various  forms  in  different  tropical  regions  is  still  wanting,  but  some 
valuable  observations  have  been  made,  especially  in  the  Philippine 
Islands  by  Garrison,  and  in  South  Africa  by  Miss  Porter.  The  rela- 
tive prevalence  of  the  various  intestinal  parasites  in  the  Philippines 
has  been  carefully  studied  by  Garrison,  who  finds  that  84  per  cent, 
of  the  investigated  persons  were  infected  with  fifteen  genera  and 
about  twenty  species,  multiple  infections  being  the  rule,  the  average 
number  of  infections  being  2-25  per  head. 

The  prevalence  of  the  various  parasites  were  as  follows: — ■ 

Per  Cent. 

Trichuris      . .           . .           . .  . .  . .  . .      59*o 

Ancylostoma  and  Necator  . .  . .  . .      52-0 

Ascaris        . .          .  .          .  .  . .  . .  .  .      26*0 

Amoebae       . .          .  .          .  .  . .  .  .  .  .      23*0 

Flagellates  and  Ciliates     ..  ..  ..  ..21-0 

Strongyloides          . .          . .  .  .  .  .  . .        3*0 

Oxyuris       . .          . .          .  .  . .  . .  . .       o«8 

Taenia           . .          .  .          . .  .  .  . .  . .       0-7 

Schistosoma  japonicum    ..  ..  ..  ..       o-6 

Paragonimus           . .          .  .  .  .  .  .  . .       0-4 

Opisthorchis           . .         . .  . .  . .  . .       0-3 

Hymenolepsis        ..          ..  ..  ..  ..       o«i 


INTESTINAL  POLY  PARASITISM  1777 

Besides  these,  however,  there  were  a  number  of  undetermined 
forms.  The  infection  with  Trichuris  is  variously  given  in  different 
countries— e.g.,  Porto  Rico  (Commission),  7-27  per  cent.;  India 
(Fearnside),  6-95  per  cent.;  India  (Dobson),  4*4  per  cent.;  Central 
Africa  (Daniels),  279  per  cent.  The  infection  with  Ancylostoma 
and  Necator  is  given  in  India  (Calvert),  83  per  cent.;  (Dobson), 
57-58  per  cent.;  (Fearnside),  65-83  per  cent.  Ascaris  infection  in 
West  Africa  (Wellman)  is  50^97  per  cent.  Garrison  considers  his 
figure  of  26  per  cent.,  which  is  based  upon  adults  only,  as  much  too 
low.  Strongyloides  is  placed  in  Central  Africa  at  (Daniels)  1.5  per 
cent.;  West  Africa  (Wellman),  0-65  per  cent.;  Porto  Rico  (Com- 
mission), o-8  per  cent.  Oxyuris  is  given  in  India  (Dobson)  at 
15-37  per  cent. 

/Etiology. — Ascaris  Utmbricoides  is,  in  our  experience,  by  far  the 
most  common  parasite,  and  it  is  often  associated  with  either  Trichuris 
trichiura  or  Necator  americanus  (or  Ancylostoma  duodenale)  in 
double  infections,  but  triple  infections  with  these  three  parasites  are 
not  uncommon,  and  quadruple  infections  of  the  three  associated 
with  Strongyloides  intestinalis  are  also  common. 

Associated  with  one  or  more  of  these  worms  it  is  by  no  means 
unusual  to  find  Loeschice  and  flagellates,  especially  Trichomonas 
hominis,  and  more  rarely  ciliates — e.g.,  Balantidium  coli.  Oxyuris 
vermicular  is  is  fairly  common  in  children,  but  tapeworms  are  not 
so  frequently  met  with  in  Ceylon,  India,  and  Equatorial  Africa, 
while  they  are  extremely  common  in  Abyssinia. 

In  China  and  other  countries  Trematode  infections  must  also  be 
considered,  and  in  the  West  Indies  and  Africa  infection  with 
Schistosoma  mansou i. 

Symptomatology. — The  symptoms  presented  by  the  patients  may 
be  nil  if  the  parasites  are  few  in  number,  and  will  in  any  case  depend 
mostly  upon  the  action  of  that  species  which  is  known  to  be  the  more 
pathogenic  or  which  is  most  abundant,  but  it  may  be  very  difficult 
or  impossible  to  separate  the  symptoms  caused  by  one  parasite  from 
those  due  to  another.  Cases  may  show  signs  of  fever,  anaemia, 
diarrhoea,  and  even  dysenteric  symptoms  may  appear  if  the  infection 
is  heavy. 

Treatment. — The  treatment  must  commence  with  that  laid  down 
for  the  parasite  which  is  the  more  important  from  a  pathogenic  point 
of  view — e.g.,  in  the  case  of  a  double  infection  with  Ancylostoma 
and  Ascaris,  the  ankylostomiasis  must  be  treated  first  and  then 
the  ascariasis. 

Rare  Infections. 
Gordiaceiasis  and  Acanthocephaliasis  (see  pp.  67S  and  679). 

Infections  with  species  of  the  Gordiacea  and  Acanthocephala  are  rare. 
Treatment  would  be  on  the  same  lines  as  for  'ascariasis.' 


1778  HELMINTH  INFECTIONS 


Intestinal  Diplopodiasis  and  Chilopodiasis  (see  pp.  689  and  739). 

Diplopodiasis  and  chilopodiasis  are  rare  and  unimportant,  giving  rise  to 
intestinal  pains  and  diarrhoea.  The  diagnosis  is  only  possible  on  discovery 
of  the  parasites  in  the  faeces.  The  treatment  is  the  chloroform  mixture,  as 
for  ankylostomiasis. 

These  infestations  are  placed  here  only  for  convenience. 


REFERENCES. 

Trichuriasis. 

Garin  (191 1).     Entente  Trichocephalienne.     Paris. 

Musgrave,  Clegg,  and  Polk  (1908).     Philippine  Journal  of  Science,  B.  III.  6, 
p.  545  (full  literature). 

Ankylostomiasis. 

Abstracts  of  Reports  of  Campaign  against  Ankylostomiasis  (1906) .  Journal 
of  Hygiene,  vi.  656  (1908),  viii.  553;  see  also  the  Annual  Report  of  the  Inter- 
national Health  Board  of  the  Rockefeller  Foundation  published  in  1917. 

Alessandrini  (1904).     Policlinico. 

Allan,  W.  (1912).     Journal  of  American  Medical  Association. 

Allaria  (1904).     Scritti  medici  in  onore  di  Bozzolo.     Torino. 

Baermann  (1918).     Geneesk.  Tijdschr.  v.  Nederl. -Indie. 

Boycott  (1904).     Journal  of  Hygiene,  vol.  iv. 

Boycott  and  Haldane  (1903).     Journal  of  Hygiene,  iii.  95;  (1904),  vol.  iv. 

Cafiero  (1899).     X.  Congr.  di  med.  interna. 

Calamida  (1901).     Giorn.  R.  Ace.  di  med.  di  Torino. 

Calamida  And  Messineo  (1901).     Giorn.  R.  Ace.  di  Torino. 

Castellani  (1906).     British  Medical  Journal. 

Castellani  (1903-12).     Ceylon  Medical  Reports. 

Cattaneo  (1903).     Assoc,  med.  di  Parma. 

Chanson  (1896).     Comp.  Rend.  Soc.  de  Biologic 

Cosentino  (1904).     Lo  Sperimentale. 

De  Figueiredo  (1918).     Brazil  Medico. 

De  Lanney  (191 9).     Military  Surgeon. 

De  Matteis  (1900).     Gazz.  degli  Ospedali. 

Gabbi  (1908).     Rivista  Critica  di  Clinica  Medica. 

Gabbi  e  Nadala  (iqoi).     Gazz.  degli  Osped. 

Gagnoni  (1903).     Riv.  di  clin.  pediatr. 

Girotti  (1902).     Gazz.  degli  Ospedali. 

Low,  G.  C.  (191 2).     Journal  of  State  Medicine. 

Luna,  Marchese  de'  (1902).     Gazz.  degli  Ospedali. 

Mandoul,  James  e  (1904).     C.  R.  Acad,  des  Sciences. 

Makagliano  (1902).     Gazz.  degli  Ospedali. 

Marini  (1904).     Rivista  Critica  di  Chnica  Medica. 

Messineo  (1905).     Giornale  medico  del  R.  esercito. 

Mingazzini  (1900-01).     Rass.  intern,  di  medicina  mod. 

Mursell  (1912).     Lancet. 

Naab  (1902).     Munch,  med.  Woch. 

Padoa  (1909).     Rivista  Critica  Clinica  Medica. 

Prentiss  (1902).     British  Medical  Journal. 

Sandwith  (1894).     Observations  on  400  Cases  of  Ankylostomiasis.     London. 

Siccardi  (190S).     Riv.  Critica  di  Clinica  Medica. 

Stiles    (1903).     Bulletin    10,    Hyg.   Lab.    U.S.    Public    Health   and   Marine 

Hospital  Service. 
Turton  (1904).     Journal  of  Tropical  Medicine. 


REFERENCES  1779 

Vannini  (1900).     II  Policlinico. 

Warner  (1919).     Brit.  Med.  Journ.,  July  26.     (A  Case  of   Ankylostomiasis 

in  London.) 
Weinberg  (191 2).     Bull.  Inst.  Pasteur. 
Wintrehert  (1881.)     Rev.  de  med.  franc,  et  etrang. 

Ascariasis. 

Annaratone  (191 2).     Condizioni  Igieniche  Colonia  Eritrea.     Roma. 

Branch  (1906).     Journal  of  Tropical  Medicine,  ix.  374. 

Castellani  (1906).     Brit.  Med.  Journ.  (Appendicitis   with   Presence  of  an 

Ascaris  in  the  Organ.) 
Chalmers  (1903).     Spolia  Zeylanica. 
Christopherson  and  Izzedin   (1918).     British  Medical  Journal,   June   22. 

London. 
Gabbi  (1908).     Riv.  Critica  Clinica  Medica. 

Garrison  (1908).     Philippine  Journal  of  Science,  Book  III.,  No.  3,  p.  191. 
Heiser  (191S).     Med.  Record. 

Pantin  (1918).     Brit.  Med.  Journ.,  September  14. 
Splendore  (190S).     Arch,  de  Paras. 
Stiles  and  Garrison   (1906).     Bull.   Hyg.   Lab.   U.S.   Public  Health  and 

Marine  Hospital  Service,  Washington,  28,  p.  74. 
Stiles  (1907).     Osier  and  McCrae's  System  of  Medicine,  i.  525-637. 


Intestinal  Polyparasitism. 

Castellani  and  Low  (1904).     Arch.  f.  Sch.  u.  Trop. -Hygiene,  Bd.  viii. 

Castellani  and  Chalmers  (191 3).     Manual  of  Trop.  Med.,  2nd  Edit. 

Garrison  (190S).     Philippine  Journal  of  Science,  Book  III.,  No.  3. 

Porter  (1918).  Intestinal  Entozoa  observed  among  Natives  in  Johannes- 
burg. Publications  of  the  South  African  Institute  of  Medical  Research 
(No.  11). 


CHAPTER  LXXVI 
SPRUE  AND  OTHER  DIARRHOEAS 

Sprue — Pseudo-Sprue- — -Hill  diarrhoea — Low-country  morning  diarrhoea — 
Flagellate  diarrhoea — Famine  diarrhoea — Coeliac  disease — References. 

SPRUE. 

Synonyms. — Ceylon  sore  mouth,  Aphthoides  Chronica,  Tropical  aphtha?, 
Impetigo  Primarum  Viarum,  Diarrhoea  Alba,  Psilosis  Linguae  et  Mucosae 
Intestini,  Phthisis  Abdominalis,  Blastomycosis  Intestinalis,  Endemic  diarrhoea, 
Cochin  China  diarrhoea. 

The  term  '  sprue  '  (sprew,  sprau,  sprulf,  spru,  spre,  spree,  spro)  is  a  phrase 
used  in  Holland  and  Scotland  for  aphthous  stomatitis  in  children,  Aphtha? 
fropicalis  der  deutschen,  and  was  applied  to  this  disease  by  Manson  and  Van 
der  Burg,  the  latter  calling  the  disease  in  Batavia  '  Indische  spruw.' 

Definition. — Sprue  is  a  chronic  catarrhal  inflammation  of  the 
alimentary  canal,  of  unknown  cause,  characterized  by  a  peculiar 
ulcerative  condition  of  the  tongue  and  mouth,  and  by  the  passage 
of  large,  pale,  frothy  motions,  the  symptoms  waxing  and  waning 
periodically. 

History. — According  to  Hiatt,  sprue  was  first  mentioned  in  the 
writings  of  John  Bicknell,  in  America,  in  1737.  Hillary,  of  Barba- 
dos, in  1766,  in  a  most  remarkably  able  manner,  describes  the 
disease  for  the  first  time  under  the  name  '  aphthoides  chronica.' 
His  account  is  well  worth  reading,  and  there  can  be  no  possible  doubt 
that  his  description  refers  to  the  disease  we  now  call  sprue.  The 
Indian  physicians  Twining  (1835),  Grant  (1854),  Cunningham  (1877), 
mention  symptoms  indicating  that  they  were  acquainted  with  a 
disease  of  this  nature,  while  Elliott  of  Ceylon  gave  a  very  good 
account  of  the  malady,  which  he  called  '  phthisis  abdominalis.' 

At  the  same  time — i.e.,  1864  to  1883 — French  physicians  noted 
a  peculiar  form  of  diarrhoea,  commonly  met  with  in  Cochin  China, 
which  perplexed  them  considerably,  a  large  number  believing  that 
it  was  dysenteric  in  nature,  while  others  considered  that  it  was 
probably  a  new  disease. 

In  1880  Manson  was  the  first  after  Hillary  to  clearly  define  the 
disease,  which  he  called  '  sprue  ' ;  and  in  the  same  year,  and  inde- 
pendently, Van  der  Burg  described  it  under  the  term  '  Indische 
spruw  '  in  Batavia.  In  the  next  year  (188 1)  Sir  Joseph  Fayrer 
delivered  the  Lettsomian  Lectures  on  chronic  white  tropical  diar- 
rhoea. These  three  authors  permanently  established  the  disease  as 
a  clinical  entity.     Since  then  many  important  papers  and  articles 

1780 


CLIMATOLOGY— JETIOLOGY  i78i 

have  appeared,  notably  Roux's  '  Traite  '  in  1888,  Thin's  '  Psilosis  ' 
in  1897,  and  Cantlie's  papers,  and  the  publications  by  Brown,  Begg, 
Castellani,  Low,  Bahr,  Ashford,  Rogers,  Nicholls  and  many  others. 

Climatology. — The  endemic  home  of  sprue  appears  to  be  Asia, 
especially  Malaya,  Sumatra,  Java,  Siam,  and  Annam;  but  it  also 
extends  into  Burma,  India  and  Ceylon,  China,  Australia  (East  and 
South),  New  Caledonia,  the  Fiji  Islands,  and  Japan.  Possibly  it 
exists  in  the  West  Indies,  where  Hillary  originally  described  it,  and 
it  may  occur  all  through  the  tropics;  but  if  so,  it  must  be  rare  in 
certain  regions — as,  for  example,  West  Africa.  Rare  cases  of  sprue 
occur  in  Europe. 

/Etiology. — The  etiology  of  sprue  has  not  yet  been  elucidated, 
but  of  the  many  etiological  theories  brought  forward,  the  one 
which  at  the  present  time  receives  more  acceptance  is  the  monilia 
or  oidium  theory,  also  known  as  Kohlbrugge's  theory.  Kohl- 
brugge,  in  190 1,  found  in  cases  of  sprue  in  Java  a  fungus  which  he 
identified  with  Monilia  albicans  Robin,  at  that  time  better  known 
under  the  name  of  Oidium  albicans.  He  made  a  very  complete 
histological  study  of  one  of  his  cases  which  ended  fatally,  and 
emphasized  the  fact  that  the  fungus  in  sections  of  the  tongue,  etc., 
had  invaded  the  deep  strata  of  the  mucosa,  the  glands,  and  portions 
of  the  submucosa.  He  concluded  that  the  fungus  was  the  cause 
of  the  disease.  Kohlbrugge's  findings  were  speedily  confirmed  by 
many  observers,  especially  French  and  Dutch,  and  Le  Dantec  gave 
to  the  malady  the  name  of  blastomycosis  intestinalis. 

In  1905  and  1912  cases  of  sprue  with  presence  of  monilia  fungi 
were  placed  on  record  by  Castellani,  who,  in  1912,  described  several 
species,  Monilia  intestinalis,  M.  enterica,  etc.  This  author's  opinion 
was  that  such  fungi  were  the  cause  of  some  of  the  symptoms  of 
sprue,  as,  for  instance,  the  frothy  appearance  of  the  stools,  but 
doubted  their  being  the  primary  cause  of  the  malady.  He  believed 
them  to  be  the  cause  of  the  frothy  diarrhoea,  because  he  had  noted 
that  this  symptom  generally  improved  after  large  doses  of  bicar- 
bonate of  soda.  He  thought  that  sodium  bicarbonate  given  in 
large  doses  might  decrease  the  acidity  of  the  intestinal  contents, 
and  in  this  way  check  the  growth  of  fungi,  which,  as  is  well  known, 
grow  better  on  acid  than  on  alkaline  media.  In  1913  Castellani 
and  Low  described  a  new  monilia  found  in  a  case  of  sprue,  M.  deco- 
lorans  Castellani  and  Low,  1913.  They  came  to  the  conclusion  that 
this  and  other  monilias  (M.  intestinalis,  etc.)  were  the  cause  of  certain 
important  symptoms  of  the  disease  such  as  frothiness  of  the  stools, 
etc.,  but  they  were  not  inclined  to  consider  them  to  be  the  primary 
cause  of  the  malady:  they  quoted  in  analogy  the  example  of  scabies, 
in  which  the  main  part  of  the  symptoms  is  due  to  the  secondary  in- 
vasion by  staphylococci,  and  not  to  the  primary  cause,  the  acarus. 

In  1914, Bahr,  in  a  series  of  interesting  publications,  supported 
Kohlbrugge's  theory,  believing  that  the  cause  of  the  malady  was 
probably  Monilia  albicans  Robin. 

From  1915,  Ashford,  in  several  able  papers,  has  supported  the 


I782  SPRUE  AND  OTHER  DIARRHCEAS 

same  theory,  though  he  does  not  consider  that  M.  albicans  is  the 
cause  of  the  malady.  He  calls  the  monilia  observed  in  his  cases 
M.  psilosis,  but,  according  to  the  laws  of  nomenclature,  the  correct 
term  would  seem  to  be  Monilia  ent erica. 

Monilias  found  in  Sprue. — The  principal  species  of  monilia  so  far 
found  in  sprue  are  the  following: — 

i.  Monilia  albicans  Robin. 

2.  Monilia  decolorans  Castellani  and  Low. 

3.  Monilia  intestinalis  Castellani. 

4.  Monilia  fcBcalis  Castellani. 

5.  Monilia  insolita  Castellani. 

6.  Monilia  tropicalis  Castellani. 

7.  Monilia  enterica   Castellani   (probable  synonyms: 

Monilia  psilosis  Ashford,  Parasaccharomyces  ash- 
fordi  Anderson). 

For  description  of  .these  fungi  see  p.  1079. 

Species  of  the  Genus  Oidium  found  in  Sprue. — The  principal 
species  of  the  genus  Oidium  scnsu  stricto  so  far  found  in  sprue  are : — 

Oidium  rotundatum  Castellani. 
Oidium  asteroides  Castellani. 

For  description  of  these  fungi  see  p.  1093. 

Remarks. — Kohlbrugge's  theory  is  the  one  finding  most  support 
at  the  present  time,  and,  according  to  various  authors,  agglutination 
and  complement  fixation  tests  are  supporting  it,  and  certain  ob- 
servers have  claimed  to  have  succeeded  in  reproducing  the  malady 
in  the  lower  animals  by  injection  of  intestinal  monilias.  We  be- 
lieve that  if  the  malady  is  eventually  demonstrat  ed  to  be  a  moniliasis, 
then  a  group  of  monilias,  and  not  one  only,  will  be  found  to  be 
capable  of  producing  the  affection;  this  in  analogy  to  what  one  sees 
in  bacillary  dysentery,  and  in  affections  due  to  the  higher  fungi, 
such  as  ringworm. 

It  must  be  noted  that  fungi,  especially  in  tropical  countries,  may  be  found 
also  in  stools  of  normal  individuals,  and  persons  suffering  with  affections 
which  are  not  connected  with  sprue.  Such  fungi  mostly  belong  to  the  genera 
Monilia,  Saccharomyces,  Cryptococcus,  YYillia,  Mycoderma,  Oidium. 

The  Helminthic  Theory. — Some  authorities  consider  Strongyloides 
stercoralis  to  be  the  cause  of  the  disease,  but  in  our  experience  the 
worm  has  nothing  to  do  with  the  malady,  being  found  in  all  sorts 
of  pathological  conditions. 

The  Bacterial  Theory. — Numerous  different  cocci,  bacilli,  etc., 
have  been  described  as  the  causative  agents  of  sprue,  but  so  far 
none  has  been  demonstrated  t<>  be  the  primary  cause  of  the  malady. 
Rogers  and  Nicholls  have  suggested  that  the  disease  may  be  a 
streptococcal  infection,  both  authors  having  obtained  good  results 
by  using  streptococcal  vaccines.    The  streptococci  found  by  Nicholls 


THE  BACTERIAL  THEORY— PATHOLOGY  1783 

were  of  the  viridans  type,  as  found  also  in  normal  mouths. 
Complement  fixation  tests  carried  out  by  Nicholls  would  seem  to 
support  the  streptococcal  theory.  Nicholls  believes  the  etiology 
to  be  in  reality  twofold,  there  being  an  infection  factor  and  a 
dietary  factor. 

Attention  must  be  called  to  certain  cases  of  pseudo-sprue, 
described  by  one  of  us,  and  due  to  a  bacillus  of  the  Flexner  group. 
These  cases  are  not  true  sprue,  as  they  get  well  either  spontaneously 
without  leaving  the  tropics  or  by  a  course  of  vaccine  treatment 
prepared  with  the  Flexner-like  bacilli  isolated  from  the  stools. 

The  Protozoan  Theory. — Various  protozoan  organisms  have  been 
found  in  cases  of  sprue,  amoebae,  spirochetes,  flagellates,  etc.,  but 
none  have  been  demonstrated  to  be  the  cause  of  the  malady. 

The  Climatic  Theory. — This  does  not  need  to  be  discussed,  though 
a  hot  damp  climate  is  an  important  predisposing  cause. 

The  Food  Theory.— This  also  does  not  need  to  be  discussed, 
though  spicy  foods  and  alcohol  may  be  predisposing  causes,  and 
dietary  errors,  as  emphasized  by  Nicholls,  may  lower  the  resistance 
of  the  alimentary  mucosa  to  germ  infection. 

The  Deficiency  Theory. — This  theory  has  been  ably  brought 
forward  by  Cantlie,  who  noticed  in  certain  cases  signs  of  scurvy. 

Syndrome  Theory. — Finally,  the  theory  must  be  mentioned 
according  to  which  sprue  is  not  a  separate  disease,  but  is  a  syndrome 
met  with  in  various  pathological  conditions,  such  as  chronic  dysen- 
tery and  pernicious  anaemia.  This  theory  is  not  supported  by  any 
medical  man  of  long  tropical  experience.  The  disease  presents 
typical  symptoms  and  a  typical  course,  but,  as  in  dysentery,  so  in 
sprue,  it" is  in  our  opinion  probable  that  the  clinical  term  covers 
several  closely  allied  conditions — e.g.,  it  is  possible  that  there  may 
be  a  sprue  of  hyphomycetic  origin,  a  sprue  of  bacterial  origin,  and 
a  sprue  of  protozoan  origin. 

Pathology. — With  an  unknown  causation,  it  is  not  easy  to  write 
an  account  of  the  pathology.  It  would  appear  as  though  the 
primary  lesions  are  beneath  the  epithelium  in  both  the  tongue  and 
the  intestine,  and  cause  the  superficial  desquamation  and  catarrh. 
In  the  intestine  the  disease  begins  with  submucous  congestion,  after 
which  follows  thrombosis  of  the  vessels,  and  exudation  of  haemo- 
globin, and  a  round-celled  infiltration.  The  mucosa  suffers  because 
its  blood  supply  is  damaged,  and  therefore  necrosis  takes  place, 
the  glands  and  villi  being  affected.  The  oesophagus  and  stomach 
also  suffer.  The  liver  is  at  first  enlarged  and  congested,  but  later 
becomes  atrophied  and  small.  The  fact  that  the  tongue,  oesophagus, 
stomach,  and  intestines  are  affected  would  indicate  that  something 
deleterious  is  being  carried  by  the  blood  stream  to  these  organs, 
rather  than  that  something  is  acting  from  the  surface.  The  irrita- 
tion of  the  liver  may  be  due  to  the  same  cause. 

When  once  the  mucosae  are  damaged,  the  chemical  processes  of 
digestion  and  the  absorption  of  their  products  must  be  interfered 
with;  while  at  the  same  time  the  absorption  of  poisons  from  the 


1784  SPRUE  AND  OTHER  DIARRHCEAS 

alimentary  canal  must  be  easier.     Indeed,  there  is  evidence  of  this 
in  the  increase  of  indigo  blue  in  the  urine,  which  is  at  times  marked. 

These  two  conditions  would  lead  to  an  atrophy  of  the  liver,  which 
organ  is  one  of  the  great  safeguards  against  a  toxaemia  of  intestinal 
origin.  When  the  liver  is  sufficiently  damaged,  a  toxsemia  is  pos- 
sible, and  occurs;  hence,  possibly,  the  advantage  of  the  treatment 
by  liver-soup  or  other  preparations  of  liver. 

The  damaged  condition  of  the  mucosa  of  the  mouth  and  tongue 
makes  mastication  difficult.  The  denuded  condition  of  the 
oesophagus  causes  the  burning  pain  during  swallowing;  the  con- 
dition of  gastric  and  intestinal  mucosae  causes  the  dyspepsia  and 
diarrhoea  of  the  disease.  The  diarrhoea  is  characterized  by  pale, 
frothy  motions,  the  explanation  of  which  is  as  follows: — 

On  opening  the  bowels  post  mortem,  the  observer  is  struck  by 
the  fact  that,  though  there  may  be  plenty  of  bile  in  the  duodenum 
and  in  the  higher  portions  of  the  bowel,  this  gradually  disappears 
until,  in  the  lower  parts  of  the  small  intestine,  the  contents  appear 
white.  In  normal  faeces  bilirubin  should  be  changed  into  sterco- 
bilin  (hydrobilirubinb  which  is  urobilin,  and  is  identical  with  that 
found  in  the  urine.  The  white  appearance  of  the  intestinal  contents 
is  probably  partly  due  to  certain  bacteria,  especially  B.  albofaciens. 

Vaughan  Harley  has  shown  that  in  the  upper  third  of  the  small 
intestine  the  normal  faeces  are  of  a  yellowish  colour,  due  to  bili- 
rubin. In  the  middle  third  they  are  of  a  whitish  or  greyish  colour, 
probably  owing  to  the  bile-pigments  being  converted  into  chromo- 
gens,  which  become  green  in  the  lower  third.  After  passing  the 
ileo-caecal  valve,  the  bile-pigments  are  converted  into  urobilin  by 
the  action  of  putrefactive  bacteria,  but  a  considerable  quantity  of 
this  is  in  the  form  of  a  chromogen.  If  the  pancreatic  juice  is  absent 
a  colourless  form  of  urobilin  is  found,  called  leuco-urobilin;  the 
blood  pictures1  in  the  last  stage  closely  resemble  that  of  pernicious 
anaemia.  A  very  common  feature  is  the  presence  of  true  chromatin 
granules  in  certain  red  cells. 

Histopathology. — The  histopathology  of  the  disease  requires  much 
further  study.  The  principal  histopathological  feature  of  the 
malady  is  a  severe  process  of  desquamation  of  the  mucosae  of  the 
digestivetract,  togethcrwith  atrophic  changes  of  the  mucosae,  glands, 
pancreas,  and  liver.  One  of  us,  in  association  with  E.  H.  Ross, 
Low,  and  Cropper,  has  studied  certain  histological  features  of  the 
cpit  helial  cells  of  the  tongue  and  the  condition  of  the  blood. 

Changes  in  the  Epithelial  Cells  of  the  Tongue. — These  cells  present 
often  a  fatty  degeneration,  but  an  interesting  feature  is  the  great 
increase  in  the  presence  of  certain  inclusions,  which,  as  demon- 
strated by  one  of  us,  maybe  found  also  in  various  kinds  of  stomatitis, 
including  the  usual  tobacco  variety,  and  even  in  normal  people. 
These  peculiar  inclusions  arc  of  two  types. 

Type  I. — This  is  by  far  the  commoner.  The  cell  presents  a 
various  number — one  to  twelve  or  fifteen — of  roundish  or  oval  form- 
ations of  variable  size,  2  or  8  fi  in  diameter,  which  in  preparations 


HI  STOP  A  THOLOGY—  SYMPTOM A  TOLOGY  1785 

coloured  by  Leishman's  stain  take  up  a  reddish  or  purplish  colour. 
They  are  apparently  structureless,  but  they  may  present  one  or 
two  small  vacuoles.  These  inclusions  stain  beautifully  by  using 
H.  C.  Ross's  jelly  method,  but  even  with  this  method  do  not  show 
any  structure.  They  are  not  fat  drops,  as  they  colour  deeply  with 
Leishman's  stain  instead  of  becoming  dissolved  in  the  alcohol. 
They  do  not  appear  to  be  of  nuclear  substance,  as  the  masses  are 
structureless.  They  do  not  seem  to  be  parasitic,  as  they  are 
structureless  and  homogeneous.  The  severer  the  inflammation  of 
the  tongue,  whatever  the  cause,  the  more  numerous  are  these 
bodies.  The  greatest  probability  is  that  they  are  merely  masses 
of  keratohyalin. 

Type  II. — Occasionally  instead  of  structureless  homogeneous 
masses,  granular  agglomerations  somewhat  resembling  chlamydozoa 
are  seen.  Whether  these  are  a  stage  of  the  former  inclusions  is 
not  known,  but  they  appear  to  be  merely  cell  degenerations. 

Changes  in  the  Cells  of  the  Blood. — These  have  already  been  men- 
tioned  under  the  heading  Pathology. 

Morbid  Anatomy. — The  body  is  emaciated,  and  the  skin  often 
hangs  loosely,  and  there  may  be  oedema  about  the  ankles.  The 
tongue  shows  small  areas  of  infiltration  into  the  connective  tissue, 
vesicles,  and  small  ulcers.  The  filiform  papilla;  atrophy,  and  the 
fungiform  papillae  become  swollen  and  prominent.  The  pillars 
of  the  fauces  and  the  tonsils  may  show  subepithelial  inflammation, 
and  even  suppuration  and  ulceration.  The  oesophagus  is  inflamed, 
and  its  mucosa  is  attenuated  in  places.  The  mucosa  of  the  stomach 
may  be  pale  and  atrophied,  or  rough  and  cirrhotic.  The  mucosa 
of  the  small  intestine  may  be  slightly  eroded,  or  may  be  so  de- 
stroyed that  the  whole  bowel  is  diaphanous  with  vascular  arboriza- 
tions; or  there  may  be  effusion  into  the  solitary  and  agminated 
glands.  The  contents  are  bile-stained  in  the  upper  parts,  and 
whitish  lower  down.  The  large  bowel  may  be  ulcerated.  The 
liver  is  atrophied,  but  otherwise  normal.  The  pancreas  may  be 
normal,  inflamed,  or  cirrhotic.  The  peritoneum  may  be  thickened 
and  chronically  inflamed,  and  in  some  cases  show  adhesions.  The 
other  organs  are  normal  as  a  rule,  but  sometimes  they  are  atrophied. 

Symptomatology. — The  incubation  period  of  sprue  is  quite  un- 
known, and  the  onset  is  insidious,  without  marked  symptoms, 
which  are  usually  merely  failing  strength  and  an  undefined  sense 
of  illness.  The  disease  may  begin  with  diarrhoea  and  intestinal 
symptoms,  or  with  mouth  symptoms  only. 

Usually  it  begins  with  slight  attacks  of  sore  mouth,  indigestion, 
and  morning  diarrhoea,  often  of  a  bilious  nature;  but  as  none  of 
these  are  severe,  and  all  are  evanescent,  the  patient  thinks  little  or 
nothing  about  them,  and  does  not  consult  a  medical  man  until 
the  disease  is  well  established.  Three  symptoms  now  worry  the 
patient — viz.,  sore  mouth,  indigestion,  and  morning  diarrhoea. 

On  examining  the  mouth,  the  dorsum  of  the  tongue  will  be  seen 
to  have  a  whitish  fur,  through  which  the  swollen  fungiform  papillae 


I7§6  SPRUE  AND  OTHER  DIARRHCEAS 

are  projecting.  The  sides  and  tip  of  the  tongue  are  red  and  in- 
flamed, with  often  small  vesicles,  small  ulcers,  and  bare  patches, 
which  are  very  tender.  Similar  patches  may  be  noted  under  the 
tongue  near  the  frenum,  on  the  inside  of  the  cheeks,  on  the  palate, 
and  on  the  pillars  of  the  fauces.  A  little  ulcer,  called  Crombie's 
molar  ulcer,  may  be  seen  near  the  two  last  upper  or  lower  molar 
teeth.  So  tender  is  the  mouth  at  times  that  deglutition,  mastica- 
tion, warm  or  spiced  foods,  acid  or  alcoholic  liquors,  cause  much 
pain.  In  addition,  mucus  may  be  noticed  clinging  to  the  pillars 
of  the  fauces  and  to  the  back  of  the  pharynx.  This  mucus  is  a 
source  of  great  distress  to  the  patient,  as  it  accumulates  in  con- 
siderable quantities,  especially  if  some  warm  fluid  has  been  taken, 
and  the  effort  to  get  rid  of  it  makes  him  almost  sick.  On  swallowing 
food,  a  burning  pain  is  felt  along  the  course  of  the  cesophagus  and 
over  the  sternum,  as  though  there  was  something  raw  inside  (as, 
indeed,  there  is).  The  voice  is  said  by  Thin  to  be  altered  at  times, 
but  we  have  not  specially  noted  this. 

The  neck,  thorax,  and  arms  may  show  signs  of  emaciation.  The 
abdomen  is  swollen,  sometimes  markedly  so,  especially  in  the 
epigastric  region,  and  the  wall  is  soft  and  relaxed.  The  patient 
complains  of  dyspeptic  symptoms— viz.,  a  sensation  of  discomfort 
and  distension  after  meals,  with  acid  eructations  and  sometimes 
vomiting.  Early  in  the  morning  he  feels  symptoms  of  intestinal 
discomfort,  and  passes  a  few  copious,  greyish,  offensive,  frothy 
motions,  and  no  more  for  the  rest  of  the  day.  After  these  motions 
he  may  feel  much  better,  and  have  a  good  appetite. 

Examination  of  the  faeces  shows  mucus,  epithelial  debris,  and 
many  bacteria,  and  often  yeast-like  fungi,  and  in  some  cases  eggs  of 
various  worms  may  be  present.  The  quantity  of  faeces  passed  varies 
with  each  motion,  but  is  in  excess  of  the  normal,  this  being  due  to 
solids  rather  than  liquids.  The  excretion  of  nitrogen  and  fat  is 
increased.  Fat  constitutes  over  20  per  cent.,  often  40  to  50 
per  cent,  of  the  stools,  while  in  normal  individuals  on  a  mixed  diet 
it  averages  6  to  8  per  cent.  Some  observers  believe  that  this  is 
not  due  to  the  fat-splitting  enzymes  non-acting,  but  to  the  absorp- 
tive power  of  the  upper  parts  of  the  intestine  being  interfered  with. 

The  analysis  of  gastric  contents  may  show  a  decrease  in  hydro- 
chloric acid  and  pepsin.  The  pancreatic  juice  may  show  absence 
of  diastase,  trypsin,  and  lipase. 

The  most  complete  analysis  of  urine  and  faeces  has  been  carried  out  by  V. 
Harley  and  Goodbody.  The  patient,  weighing  36-87  kilogrammes,  was  on  a 
milk  diet,  containing  12-99  grammes  of  nitrogen,  76-44  grammes  of  fat,  82-32 
grammes  of  carbohydrates,  and  1,960  c.c.  of  fluid.  The  urine  passed  measured 
1,050  c.c;  specific  gravity,  1012;  urea,  16-8  grammes;  uric  acid,  o-8  gramme; 
ammonia,  0-44  gramme;  phosphates,  1-27  grammes;  chlorides,  3-89  grammes. 
Total  sulphates,  1-47  grammes,  of  which  1-35  grammes  were  alkaline  and  0-12 
aromatic.  The  average  daily  quantity  of  the  motions  was  255  grammes,  of 
which  79-46  were  water,  1-47  nitrogen,  35-92  fat.  The  nitrogen  given  in  the 
food  was  12-99  grammes,  and  that  in  the  faeces  1-47  grammes;  therefore  88-86 
per  cent,  had  been  absorbed.  The  fat  in  the  food  was  76-44  grammes,  and 
that  in  the  faeces  35-92  grammes;  therefore  53-01  per  cent,  had  been  absorbed. 


SYMPTOMATOLOGY— DIAGNOSIS  1787 

The  colour  of  the  faeces  was  greyish-green  to  greyish-white,  but  gave  a  distinct 
urobilin  reaction,  due  to  the  leuco-urobilin.  Schmidt's  test  for  urobilin  is 
performed  by  adding  a  concentrated  solution  of  perchloride  of  mercury  to  the 
faeces,  when  a  bright  red  colour  is  developed  if  urobilin  is  present.  If  there 
is  much  urobilin,  the  colour  appears  within  five  minutes;  if  little,  in  five  to 
fifteen  minutes ;  if  very  little,  in  half  an  hour.  The  colour  deepens  for  twenty- 
four  hours.  More  analyses  on  the  above  lines  are  required.  Halberkann 
in  a  case  he  studied  found  a  large  amount  of  indican  in  the  urine  and  a  reducing 
Fehling  substance,  which  was  not  glucose,  undetermined.  In  the  stools  he 
found  presence  of  urobilinogen,  and  they  contained  a  large  amount  of  fat. 

The  blood  coagulates  slowly,  and  there  is  always  some  reduction 
of  the  red  cells,  which  may  fall  as  low  as  3,000,000  to  1,000,000  per 
cubic  millimetre.  The  colour-index  is  low,  and  the  structure  of  the 
cells  is  normal.  The  white  cells  are  also  reduced  to  about  6,000  to 
2,800  per  cubic  millimetre.  The  ratio  of  white  to  red  is  about  1  to 
400  in  bad  cases.  A  differential  count  shows  an  increase  in  the  mono- 
nuclears and  eosinophiles. 

The  urine  requires  more  investigation,  but  as  far  as  evidence  goes 
at  present  it  is  not  abnormal,  showing  only  an  increase  in  indigo 
blue  and  urobilin,  and  at  times  Cammidge's  reaction  for  pancreatitis. 

Schmitter  has  often  noted  loss  of  sexual  power. 

The  buccal,  intestinal,  and  other  symptoms  may  markedly  im- 
prove, even  without  treatment,  but  only  to  get  worse  again;  and 
this  is  repeated  time  after  time. 

In  due  course  the  patient  becomes  very  emaciated,  weak 
physically,  and  depressed  and  irritable  mentally.  The  skin  becomes 
harsh;  the  mucosae  anaemic;  the  tongue  becomes  smooth,  glazed, 
reddish-yellow,  and  small,  and  is  often  furrowed  by  cracks;  indiges- 
tion is  marked;  and  the  diarrhoea  is  worse.  The  patient  continues 
to  lose  weight,  and  emaciates  rapidly,  the  skin  hanging  in  loose 
folds,  the  abdomen  blown  out  with  gas,  the  liver  small  and  atrophied, 
the  ankles  cedematous,  while  the  pulse  becomes  slow  and  feeble. 

After  this  has  gone  on  for  a  long  time,  the  emaciated,  worn-out, 
irritable  person  dies  of  an  acute  attack  of  diarrhoea  or  cardiac 
failure.  Sprue  is  essentially  a  chronic  disease,  with  remissions, 
intermissions,  and  recurrences,  but,  unless  taken  seriously  in  hand, 
goes  steadily  from  bad  to  worse. 

Some  writers  distinguish  three  stages- — a  first  stage,  with  oral 
and  dyspeptic  symptoms;  a  second  stage,  with  marked  intestinal 
symptoms;  and  a  third  stage,  with  toxaemia,  emaciation,  and 
anaemia;  while  cases  are  sometimes  seen  which  are  atypical — that 
is  to  say,  where  there  are  the  mouth  symptoms  without  the  intes- 
tinal symptoms,  and  vice  versa. 

Complications. — The  complications  met  with  in  the  course  of  the 
disease  are: — Acute  diarrhoea;  dysenteric  diarrhoea;  haemorrhage; 
meteorism;  pancreatitis;  myalgia;  insomnia;  helminthiasis, 
especially  ankylostomiasis;  impacted  faeces;  chronic  appendicitis; 
jaundice;  diabetes;  and  pernicious  anaemia. 

Diagnosis. — The  diagnosis  of  the  disease  is  to  be  based  upon  the 
irregular  chronic  diarrhoea  occurring  especially  in  the  morning,  and 
associated   with   flatulent    dyspepsia,    causing   distension    of   the 


ZjSS  SPRUE  AND  OTHER  DIARRHOEAS 

abdomen,  and  the  passage  of  fermenting,  abundant,  clay-coloured 
motions.  With  these  symptoms  there  will  be  progressive  emacia- 
tion and  anaemia,  and  when  to  these  the  characteristic  mouth- 
lesions  occurring  in  a  person  living  in  the  tropics  are  added,  it 
is  indeed  difficult  to  imagine  any  disease  with  which  it  could  be 
confounded.  Van  der  Scheer  considers  that  the  discovery  of  fat 
in  the  motions  is  a  diagnostic  sign  before  the  disease  begins;  but 
this  condition  may  also  be  found  in  pancreatitis.  Low  says  that 
the  so-called  psilosis  pigmentosa  of  Barbados  is  pellagra.  The 
diseases  from  which  sprue  should  be  distinguished  are  stomatitis, 
hill  diarrhoea,  chronic  dysentery,  and  chronic  pancreatitis. 

Stomatitis. — All  forms  of  stomatitis  are  very  common  in  the 
tropics,  and  may  be  accompanied  by  intestinal  symptoms  such  as 
diarrhoea.  The  stools,  however,  do  not  show  the  peculiar  char- 
acteristics of  sprue — viz.,  the  white  colour,  the  frothy  appearance, 
and  the  copious  amount  passed  in  the  twenty-four  hours. 

Thrush, — This  is  easily  diagnosed  by  examination  of  the  white 
patches,  in  which  fungi  of  the  genus  Monilia  will  be  found.  It  is, 
however,  to  be  noted  that  in  long-standing  cases  of  sprue,  as  in  all 
chronic  complaints,  thrush  may  develop. 

H ill  Diarrhoea. — The  patient  generally  gives  a  history  of  residence 
at  a  high  elevation,  and  the  diarrhoea  is  as  a  rule  present  only  in 
the  morning,  while  mouth  symptoms  are  absent.  We  have,  how- 
ever, seen  several  patients  in  whom  sprue  has  developed  after 
repeated  attacks  of  what  to  all  appearance  was  simply  hill  diarrhoea. 

Chronic  Dvsentery. — In  chronic  dysentery  there  is  an  absence  of 
the  mouth  symptoms,  while  the  motions  are  not  whitish  in  colour, 
and  may  contain  blood  and  mucus  during  the  exacerbations.  The 
diarrhoea  of  dysentery  is  generally  accompanied  by  griping,  while 
that  of  sprue  is  not.  In  chronic  dysentery  pain  is  often  felt  on 
pressure  over  the  sigmoid  and  descending  colons.  In  some  cases 
microscopical  and  bacteriological  examination  of  the  stools  for 
entamoeba?  and  the  Shiga-Kruse  bacillus  may  be  necessary  to  clear 
the  diagnosis. 

Though  personally  we  consider  sprue  and  chronic  dysentery  to 
be  different  diseases,  still  we  have  seen  several  cases  of  sprue  develop- 
ing in  old-standing  cases  of  chronic  dysentery. 

Chronic  Pancreatitis. — Absence  of  the  mouth  symptoms  of  sprue 
and  presence  of  tenderness  in  the  region  of  the  epigastrium  cmd 
the  passage  of  large  quantities  of  fat  in  the  motions,  together  with 
Cammidge's  crystals  in  the  urine,  will  enable  the  diagnosis  of 
chronic  pancreatitis  to  be  made. 

Prognosis. — The  prognosis  in  any  case  of  sprue  is  serious,  because, 
unless  the  patient  will  honestly  co-operate  with  the  doctor,  he  will 
go  from  bad  to  worse.  We  are  of  the  opinion  that,  no  mailer 
how  mild  the  case  may  be,  the  patient  should  be  warned  of  the 
danger. 

If  treatment  is  properly  carried  out,  the  prognosis  improves  con- 
siderably, but  even  then  relapses  are  apt  to  occur. 


TREATMENT  1789 

Treatment. — The  treatment  is  symptomatic. 

An  attempt  must  be  made  to  soothe  the  alimentary  canal,  and 
to  give  it  as  little  work  to  do  as  possible,  so  that  it  may  repair  itself. 
This  line  of  treatment  will  necessitate  rest  in  bed  and  a  careful  diet, 
after  the  bowels  have  been  swept  as  clear  as  possible  of  decom- 
posing material. 

While  this  is  proceeding,  care  must  be  taken  to  avoid  chills,  as 
they  aggravate  the  disease.  Lastly,  an  attempt  should  be  made 
to  heat  those  symptoms  which  worry  and  annoy  the  patient. 

The  treatment,  therefore,  may  be  classified  into: — 

1.  The  co-operation  of  the  patient. 

2.  Rest  in  bed. 

3.  Suitable  clothing. 

4.  Removal  of  fermenting  bowel  contents. 

5.  Diet. 

6.  Medical  treatment. 

7.  Change  of  climate. 

1.  The  Co-operation  of  the  Patient. — The  nature  of  the  com- 
plaint and  the  dangers  which  the  patient  runs  must  be  carefully 
explained  to  him,  and  the  line  of  treatment  sketched  out.  Further, 
he  must  be  told  that  its  success  or  failure  largely  lies  in  his  own 
hands.  If  he  has  not  the  strength  of  will  to  persevere,  even  when 
at  first  success  seems  far  from  certain,  he  might  as  well  not  begin. 

If  he  agrees  to  co-operate,  then  he  must  be  carefully  weighed,  and 
a  chart  kept  of  his  weights. 

2.  Rest  in  Bed. — The'second  point  is  that  the  patient  must 
remain  in  bed  for  a  little  time,  and  use  the  bed-pan  and  the  urine- 
bottle,  in  order  to  give  the  bowels  as  much  rest  as  possible,  and 
warm  water  must  be  used  in  sponging. 

3.  Suitable  Clothing. — -The  underclothes  and  pyjamas  should 
be  of  wool  or  flannel,  in  order  to  avoid  chills. 

4.  Removal  of  Fermenting  Bowel  Contents.' — The  treatment 
should  begin  with  a  dose  of  castor  oil,  to  remove  the  fermenting 
contents  of  the  bowel. 

5 .  Diet. — -The  various  diets  advised  may  be  arranged  as  follows : — 

(a)  The  milk  diet. 

(b)  The  milk  and  fruit  diet. 

(c)  The  fruit  diet. 

(d)  The  meat  diet. 

(e)  The  meat  and  milk  diet. 

(a)  Milk  Diet. — The  real  basis  of  the  treatment  of  sprue  at 
present  is  the  milk  diet. 

In  the  tropics,  this  milk  should  be  obtained  from  a  cow  kept  for  the  purpose 
or  from  some  really  reliable  dairy,  as  the  danger  of  contamination  is  great. 
Even  when  the  cow  belongs  to  the  patient,  great  care  has  to  be  taken  that  the 
milk  is  not  adulterated  by  the  household  servants.  We  can  never  forget 
that  once  the  milk  of  a  peculiarly  careful  household,  collected,  apparently, 
under  strict  precautions,  was  found  on  analysis  to  be  grossly  adulterated. 


1790  SPRUE  AND  OTHER  DIARRHCEAS 

The  lesson  we  have  drawn  from  the  above  is  to  get  a  sample  analyzed  from 
time  to  time.  This  analysis  costs  but  little,  and  the  possibility  of  its  being 
carried  out  at  any  time  puts  a  certain  amount  of  restraint  upon  would-be 
adulterators. 

There  is  a  considerable  difference  between  the  average  composition  of  the 
milk  supplied  by  Bos  taurus,  the  straight-backed  cow,  and  B.  indicus,  the 
hump-backed  cow,  which,  in  general  terms,  may  be  summarized  by  saying 
that  the  milk  of  the  latter  is  much  richer  than  that  of  the  former.  We  have 
investigated  this  point,  and  are  of  the  opinion  that  if  3  per  cent,  of  fat  is  con- 
sidered to  be  an  average  for  B.  taurus,  then  5  per  cent,  should  be  reckoned 
fir  B.  indicus. 

In  placing  a  patient  upon  a  milk  diet,  the  composition  of  the  milk 
should  be  carefully  considered,  especially  as  regards  the  fat,  for, 
as  Harley  and  Goodbody  have  shown,  no  less  than  47  per  cent, 
of  the  milk-fat  is  passed  out  in  the  faeces. 

Milk  with  high  percentages  of  fat  should,  therefore,  be  diluted 
with  whey,  when  the  amount  of  nitrogen  will  be  kept  up,  while 
the  percentage  of  fat  is  diminished.  Whey  is  easily  made  in  the 
tropics  by  means  of  the  juice  of  limes. 

Preferably  the  milk  should  not  be  boiled  or  sterilized,  but  boiling, 
apparently,  does  not  interfere  with  its  beneficial  properties,  and, 
therefore,  if  desired  or  thought  necessary — i.e.,  owing  to  the  risk 
of  typhoid — there  is  no  harm  in  so  doing.  In  cold  weather  it 
should  be  warmed  before  being  taken.  It  can  be  aerated  in  a 
seltzogene  if  desired,  and  can  be  mixed  with  Vichy  water.  Finally, 
it  must  be  remembered  that  milk  is  not  a  perfect  food  for  an  adult, 
however  suitable  it  may  be  for  a  child. 

It  is  as  well  to  begin  with  a  small  quantity,  and  gradually  to 
increase  the  amount.  Every  medical  man  sooner  or  later  adopts 
his  own  method  of  carrying  this  out,  and  we  will,  therefore,  only 
give  general  directions.  If  the  case  is  very  severe,  with  vomiting 
and  much  diarrhoea,  it  is  as  well  to  begin  with  whey  only,  which  the 
patient  should  sip  slowly,  and  practically  ad  libitum — i.e.,  about 
7  to  8  pints  per  diem.  As  soon  as  the  urgent  symptoms  are  relieved, 
milk  must  be  added  to  the  diet,  as  whey  alone  is  starvation. 

If  the  case  is  of  moderate  severity,  milk  can  be  begun  at  once, 
3  pints  per  diem  being  given  in  the  more  severe,  and  4  pints  in  the 
less  severe  cases — i.e.,  60  to  80  ounces — which  should  be  divided 
into  not  less  than  ten  meals  at  regular  intervals  during  the  day. 
The  milk  must  be  slowly  sipped  or  taken  through  a  glass  tube,  which, 
of  course,  should  be  carefully  boiled  after  each  meal.  On  no 
account  must  the  patient  be  allowed  to  drink  the  milk  in  gulps. 
It  is,  perhaps,  as  well  to  define  a  limit  of  time — say  about  twenty 
minutes — as  the  minimum  time  for  a  meal. 

If  the  symptoms  improve,  it  is  necessary  to  increase  the  milk 
gradually  every  few  days  until  6  to  7  pints — i.e.,  120  to  140  ounces- — 
are  given;  but  in  doing  this,  it  is  better  to  increase  the  number  of 
meals  rather  than  the  quantity  at  a  given  meal.  Twelve  meals  in 
the  twenty-four  hours  are  not  difficult  to  arrange. 

If  the  symptoms  do  not  improve,  the  milk  must  be  reduced  gradu- 
ally, or  whey  must  be  tried:  but  as  soon  as  the  urgent  symptoms  of 


TREATMENT  1791 

diarrhoea  and  vomiting  abate,  the  milk  must  be  gradually  increased, 
and,  indeed,  the  starvation  must  not  be  long  continued  in  any 
case.  Starvation  diets  are  dangerous  in  severe  cases,  when  the 
patients  are  emaciated  and  weak;  and  hence,  while  they  are  being 
employed,  great  care  is  required  in  nursing. 

If  the  milk  is  succeeding,  the  diarrhoea  ceases,  the  mouth  troubles 
diminish,  and  the  patient  feels  better.  The  faeces  will  at  first  be 
pale  and  grey,  but,  as  improvement  continues,  stercobilin  will 
appear,  as  evinced  by  the  brown  colour.  This  change  in  the  colour 
of  the  faeces  is  a  most  important  sign. 

But  even  if  milk  is  agreeing  with  the  patient,  there  will  be  much 
trouble,  as  there  is  often  strong  objection  to  milk  only.  Another 
difficulty  is  constipation,  and  this  must  be  relieved  by  enemata. 
Sometimes  the  milk  does  not  agree,  causing  vomiting  and  pain. 
Usually  this  can  be  relieved  by  alkalinizing  the  milk  with  bi- 
carbonate, i  grain  to  the  ounce,  or  the  citrate  of  soda,  2  grains  to 
the  ounce  of  milk  (convenient  tabloids  of  this  salt  are  prepared  by 
Burroughs  Wellcome  and  Co.),  or  by  adding  Apollinaris  or  Ems 
water  in  the  proportion  of  equal  parts,  or  lime-water,  1  to  6  of 
milk.  As  soon  as  a  definite  improvement  appears,  and  the  weight 
begins  to  increase,  the  patient  should  be  allowed  to  sit  up,  but  great 
care  must  be  taken  to  avoid  chills.  Milk  diet  should  be  persisted  in 
for  a  month  or  six  weeks,  but  may  be  modified  by  the  addition  of  fruit 
— e.g.,  strawberries,  bananas,  or  apples — as  will  be  described  later. 

Then  eggs  may  be  beaten  up  in  the  milk;  chicken-broth  can  be 
tried;  then  Benger's  food,  or  some  other  simple  food — Allen  and 
Hanbury's,  Mellin's,  Albany  food,  Carnrick's  soluble  food,  Sana- 
togen,  or  Plasmon.  Then  fish,  chicken,  or  sweetbreads,  with  a 
biscuit,  and,  later,  potatoes;  and  finally,  the  patient  is  put  on  to 
a  diet  of  eggs,  toast,  dilute  China  tea,  soups,  white  meats,  custard- 
puddings,  milk.  But  he  must  avoid  dark  meats,  most  vegetables, 
spiced  foods,  iced  drinks,  and  all  indigestible  substances.  Alcoholic 
drinks  in  every  form  are  bad,  both  during  the  illness  and  afterwards. 
Nor  is  smoking  to  be  encouraged;  we,  personally,  are  much  against  it. 

But,  unfortunately,  a  case  of  sprue  is  not  so  easy  to  treat  as  indi- 
cated above,  for,  while  the  food  is  being  gradually  and  carefully 
increased,  relapses  are  not  infrequent,  and  a  return  to  milk  may  be 
necessitated.  The  patient  gets  weary,  and  at  times  exceedingly 
angry  about  this  dieting,  and,  indeed,  is  apt  surreptitiously  to  kick 
over  the  traces,  with  disastrous  results.  The  prohibition  of  alcohol 
also  leads  to  trouble,  but  our  experience  about  this  is  quite  clear: 
if  alcohol  is  taken,  the  progress  of  the  patient  is  seriously  hindered. 

Before  leaving  the  milk  diet,  two  points  ought  to  be  mentioned, 
concerning  one  of  which  we  have  had  considerable  experience; 
concerning  the  other,  none  at  all.  First  of  all,  there  can  be  no 
reasonable  doubt  as  to  the  advantages  of  liver-soup — i.e.,  soup 
prepared  from  calves'  or  sheep's  livers — in  the  milder  cases  of  sprue, 
or  in  the  return  to  ordinary  food  of  a  severe  case.  The  liver  treat- 
ment is  really  an  old  native  remedy  in  Ceylon.     We  do  not  profess 


1792  SPRUE  AND  OTHER  DIARRHEAS 

to  advance  views  as  to  its  action,  but  in  a  certain  class  of  cases  it 
is  of  benefit.  Secondly,  gall-pills  or  inspissated  bile,  as  suggested 
by  C.  J.  Martin,  and  pancreatic  preparations  have  been  advocated 
by  some;  but  of  these  we  have  no  experience. 

(b)  Milk  and  Fruit  Diet. — A  milk  and  fruit  diet  has  been  found 
to  be  even  better  than  a  pure  milk  diet  in  many  cases.  The  milk 
is  administered  as  already  described,  but,  in  addition,  fruit  is  given. 
Strawberries  are  most  highly  recommended,  beginning  with  |  pound 
and  gradually  increasing  to  2\  pounds  per  diem.  They  should  be 
crushed,  and  eaten  with  sugar  and  cream.  In  lieu  of  strawberries, 
bananas  (not  plantains,  though  people  often  call  bananas  plantains, 
the  difference  being  that  a  banana  shows  three  cells  on  transverse 
section  and  a  plantain  five),  pears,  grapes,  in  the  same  weight  as 
the  strawberries  or  apples,  from  \  pound  to  \\  pounds  per  diem. 
If  these  cannot  be  obtained,  the  juice  of  oranges,  papaya  (i£  pounds 
per  diem),  avocado  pears,  mangosteens,  and  sapodilla,  may  be  used. 

Fresh  Bael  fruit  is  excellent,  but  must  be  carefully  prepared.  It 
may  be  boiled  in  water  and  then  cut  open  and  shredded  by  means 
of  a  fork  into  warm  milk,  in  which  it  is  pounded  with  castor-sugar, 
and  finally  strained  through  a  fine  strainer  to  remove  all  debris. 
This  should  be  used  three  times  a  day.  Preserved  fruit  is  said 
to  be  useful,  if  fresh  fruit  cannot  be  obtained.  Acid  fruits,  such  as 
pineapples  and  sour-sops,  should  be  avoided,  and,  personally,  we 
do  not  advise  the  use  of  mangoes. 

(c)  Fruit  Diet.— This  was  first  advocated  by  Van  der  Burg,  and  usually 
consists  of  grapes  and  pears;  but  it  appears  as  though  almost  any  fruit  which 
is  not  acid  might  be  used. 

(d)  Meat  Diet.- — If  the  milk  or  fruit  diets  fail,  it  is  advisable  to  try  a  meat 
diet,  or  this  may  be  made  the  basis  of  treatment  from  the  beginning.  Cantlie 
is  the  great  supporter  of  this  dietary. 

If  the  patient  is  very  ill,  it  may  be  necessary  to  begin  with  raw-meat  juice 
prepared  by  pounding  sufficient  good  raw  flesh  in  a  mortar,  so  that,  with  the 
addition  of  2  ounces  of  water  and  20  minims  of  dilute  hydrochloric  acid, 
6  ounces  of  meat-juice  is  obtained  on  straining.  The  quantity  of  meat  re- 
quired to  obtain  these  6  ounces  will  sometimes  be  quite  considerable,  and,  as 
it  varies  in  different  regions,  must  be  obtained  by  preliminary  experiment.  A 
little  salt  should  be  added  to  this  juice,  and  1  teaspoonful  should  be  given 
every  quarter  of  an  hour  in  very  bad  cases,  and  rapidly  increased  in  amount 
if  successful. 

As  soon  as  the  very  serious  symptoms  subside,  the  meat  diet  should  be 
started.  Brown  gives  the  following  directions  for  preparing  a  meat  diet: 
Take  2  pounds  of  good  raw  meat,  free  from  fibrous  matter,  fat,  and  gristle, 
and  2  ounces  of  fresh  suet,  and  mince  and  pound  them  up  thoroughly. 
Sprinkle  the  pounded  mass  with  a  little  salt,  and  divide  into  six  portions.  One 
portion,  cooked  in  a  small,  well-buttered  saucepan  until  the  red  colour  has 
just  disappeared,  is  given  six  times  a  day,  as  convenient.  This  portion,  when 
cooked,  is  estimated  as  weighing  4  ounces.  In  addition,  £  pint  of  plain  warm 
water,  rice  or  toast  water,  is  sipped  half  an  hour  before  a  meat  meal,  and  a 
little  tea,  with  lemon-juice  instead  of  milk,  taken  twice  daily.  It  may,  perhaps, 
be  as  well  to  remind  the  reader  that  rice-water  is  an  infusion  of  roasted  rice. 

In  about  a  week  this  meat  diet  should  be  changed  to  a  modified  meat  diet, 
which  is  first  produced  by  the  addition  of  fruit,  followed  in  a  little  time  by 
chicken,  then  and  gradually  by  eggs,  biscuits,  and  fish,  until  the  dietary 
already  mentioned  under  Milk  is  reached. 

With  a  modified  meat  diet  some  people  combine  curdled  milk.     This  is 


TREATMENT  1793 

based  upon  Metchnikolt's  researches,  which  showed  that  if  the  Bacillus  acidi 
lactici  is  taken  with  milk,  it  generates  large  quantities  of  lactic  acid  in  the 
intestines,  particularly  in  the  large  bowel,  and  that  this  acid  interferes  with 
intestinal  toxins.  Various  preparations  of  the  germ  have  been  placed  on 
the  market,  including  '  Sauerin  '  made  by  Messrs.  Allen  and  Hanbury,  and 
said  to  be  a  pure  culture  of  the  germ.  Brown  gives  the  following  directions 
for  its  use:  2  pints  of  milk  are  heated  to  1600  F.,  to  kill  off  any  bacteria  which 
might  happen  to  be  present,  and  then  are  allowed  to  cool  in  a  jug  which  has 
been  boiled.  When  ioo°  F.  is  reached,  6  tablets  of  Sauerin  are  added,  and 
2  tablespoonfuft  of  sugar,  when  the  milk  is  curdled  in  about  three  hours. 
This  curdled  milk  is  taken  four  times  a  day,  between  the  meals  of  a  modified 
meat  diet,  and  is  said  to  be  efficacious. 

ft  may  be  mentioned  that  curdled  buffalo-milk  is  commonly  used  by  the 
natives  of  Ceylon  as  a  part  of  their  food,  and  curdled  milk  is  also  used  in 
fndia,  and,  indeed,  in  many  other  places  by  natives. 

Under  the  heading  of  Meat  Diets  must  be  placed  Cantlie's  treatment,  which 
consists  of  putting  the  patient  to  bed,  applying  a  hot  wet  pack  from  the  nipples 
to  the  groin  for  two  hours,  morning  and  evening,  and  giving  three  meals  of 
5  ounces  of  meat  per  diem,  and,  in  addition,  either  beef-tea,  beef-jelly, 
calves'-foot  jelly,  or  a  plain  jelly  every  two  hours.  Castor  oil  is  administered 
in  i^-drachm  doses  every  morning  for  the  lirst  three  days,  and  santonin  in 
3-grain  doses  morning  and  evening  for  three  days.  Strawberries,  to  the 
quantity  of  3  to  4  pounds  per  diem,  are  also  allowed  between  meals.  When 
the  stools  become  solid,  and  show  brown  colouring  matter,  a  poached  egg  and 
pounded  chicken  are  added,  and,  later,  minced  chicken,  and,  still  later,  the 
undercut  of  meat,  with  stewed  celery,  seakale,  vegetable-marrow,  pulled  bread, 
and  thin  slices  of  bread,  baked  in  an  oven  for  twenty  minutes. 

(e)  Meat  and  Milk  Diet.— Cantlie  now  advocates  that  when  a  patient  is 
on  a  meat  diet,  this  should  be  stopped  every  third  or  fourth  day  for  twenty- 
four  hours,  and  that  milk  only  be  given  during  this  period. 

6.  Medical  Treatment.— It  may  be  said  at  once  that  astrin- 
gents as  a  rule  are  dangerous,  and  that  antiseptics  are  not  useful. 

Santonin,  which  must  be  yellow,  has  been  strongly  recommended  by  Begg, 
who  gives  5  grains  night  and  morning  in  salad  oil;  but  we  have  seen  no  benefit 
by  this  treatment.     Mixtures  containing  bicarbonate  of  soda  are  often  useful. 

People  complain  that  yellow  santonin  cannot  be  obtained,  but  it  can  be 
easily  prepared  from  white  santonin  by  exposure  to  the  sun  for  a  few  days. 
The  crystals  are  turned  from  time  to  time  until  yellow  throughout,  as  demon- 
strated by  crushing.  The  chromosantonin  of  Monte-Martini  is  not  santonin, 
which,  according  to  Lestini,  is  changed  into  formic  acid  and  photosantonin 
acid  and  a  red  resinous  substance.  Peter  Sys's  remedy,  which  is  much  used 
in  China,  is  simply  powdered  cuttle-fish  bone. 

Cantlie  has  had  good  results  by  the  administration  of  20  grains  of  ipeca- 
cuanha daily  for  two  or  three  days  in  advanced  cases,  and  emetin  has  been 
administered  by  several  authors.  Schmidt  has  used  oxygen  introduced  per 
rectum,  |to  1  litre  weekly. 

Castellani  has  obtained  in  some  cases  a  remarkable  improvement  by  giving 
massive  doses  of  bicarbonate  of  soda. 

The  mouth  may  be  treated  with  any  appropriate  mouth-wash — 
e-S->  glyco-thymoline,  glycerine  and  borax,  diluted  liquor  aluminis, 
etc.  The  teeth  require  attention,  and,  if  there  is  any  pyorrhoea, 
this  should  at  once  be  treated  by  syringing  or  spraying  between 
the  teeth  with  peroxide  of  hydrogen  solution.  Pain  may  be  re- 
lieved by  painting  the  raw  surfaces  with  1  to  5  per  cent,  solution  of 
cocaine,  novocain,  alypin,  or  stovain.  The  pain  along  the  oesopha- 
gus requires  morphia.  Janowski  recommends  5  to  10  drops  of  a  solu- 
tion of  1  in  1,000  adrenalin,  which,  he  says,  gives  prompt  and 

113 


J794 


SPRUE  AND  OTHER  DIARRHOEAS 


permanent  relief  for  oesophagitis.  The  muscular  pains  may  be 
relieved  by  massage,  or  by  pilocarpine  nitrate,  given  in  TVto  i  grain 
doses  three  times  a  day.  Intestinal  pain  may  be  relieved  by  hot 
packs,  as  recommended  by  Cantlie.  Acute  diarrhoea  must  be 
checked  by  a  dose  of  liquor  opii  sedativus  or  lead  and  opium  pills. 
Dysenteric  symptoms  must  be  treated  as  described  under  Dysentery. 

7.  Change  of  Climate. — It  is  obvious  that,  if  possible,  the  patient 
should  be  transferred  from  the  tropics  to  the  temperate  zone, 
but  only  if  he  is  strong  enough  to  travel.  There  is  no  advantage 
in  putting  him  on  board  a  ship  in  such  a  condition  that  he  will 
probably  die  when  changing  from  the  warm  to  cooler  weather. 
Personally,  we  are  not  in  favour  of  a  patient  being  sent  from  the 
low  country  to  the  hills.  If  he  is  able  to  travel,  let  him  go  to  the 
temperate  zone. 

Vaccine  Treatment. — Vaccines  have  been  prepared  with  various 
bacteria  from  the  mouth,  and  Rogers  and  Nicholls  report  very 
encouraging  results  by  the  use  of  streptococcal  vaccines  prepared 
with  streptococci  isolated  from  the  mouth  lesions.  Monilia  vaccines 
have  been  used  by  Ashford,  Michel,  Taylor,  and  others,  who  claim 
satisfactory  results. 

Prophylaxis. — -Nothing  ot  any  practical  value  can  be  said  under 
this  heading. 

PSEUDO-SPRUE. 

One  of  us  has  called  attention  to  some  cases  presenting  clinical  symptoms 
closely  allied  to  sprue  and  due  to  bacilli  of  the  Flexner  group.  Such  cases 
have  no  dysenteric  symptoms,  but  present  the  white  frothy  motions,  the  sore 
tongue,  and  the  anaemia  as  found  in  typical  sprue,  but  in  contrast  to  this 
disease  they  may  recover  without  any  change  from  the  tropics,  and  a  vaccine 
treatment  is  very  useful. 


.§> 

« 

£ 

d 

•3 

<a 

5a 

g 

«i 

0 

si 

s 

<u 

0 

0 

IS 

<a 
e 

<a 

0 
<a 

3 

"3 

■a 

s 

ft* 

S 

0 

"3 

-0 
0 
E/3 

0 

A 

0 

O 

0 

A 

A 

A 

A 

A 

A 

0 

O 

O 

A 

A 

Inosite. 
Salicin. 

.8 

Isodulcite. 
Erythrite. 

s 

0 

1 

Gram. 
Gelatine. 

Serum. 
Broth. 

0        0        0    ,    A       0      As* 

+  s 

0        0 

O 

0        00     G.T. 

G.T. 

Abbreviations. — A,  acid;  G.T.,  general  turbidity;  s,  slight;  o,  negative 
result-  -viz.,  neither  acid  nor  gas  in  sugar  media,  non-motile,  non-liquefaction 
of  gelatine  or  serum,  as  the  case  may  be. 

*  Certain  strains  are  distinctly  acid  on  ninth  day. 


PSEUDO-SPRUE— HILL  DIARRHCEA  I?95 

The  Flexner-like  bacillus  found  in  these  cases  is  identical  with  the  typical 
Flexner,  but  for  the  fact  that  litmus  milk  was  rendered  permanently  acid 
instead  of  the  medium  becoming  first  acid  and  then  alkaline.  Minor  differ- 
ences with  regard  to  some  sugar  broths  may  occasionally  also  be  noted. 

HILL  DIARRHCEA. 

Definition. — Hill  diarrhoea  is  a  gastro-intestinal  catarrh  of  un- 
known cause,  occurring  mostly  at  high  altitudes  in  tropical  regions, 
and  characterized  by  the  passage  of  several  liquid,  frothy,  light- 
coloured  motions  in  the  early  morning. 

History. — -Hill  diarrhoea  was  first  described  by  Grant  in  1854,  in 
the  same  paper  as  that  in  which  he  dealt  with  sprue  and  dysentery, 
and  later  as  a  disease  quite  distinct  from  sprue  by  Crombie  in  1892. 
The  latter  writer  held  that  it  was  liable  to  occur  at  an  elevation  of 
6,000  or  more  feet  in  India,  Europe,  and  elsewhere.  In  India  he 
believed  the  monsoon  to  be  a  potent  factor,  associated,  probably, 
with  a  diminished  barometric  pressure.  We  have  seen  cases  in 
Ceylon  occurring  at  a  much  less  elevation — for  example,  at  about 
3,000  to  4,000  feet. 

More  recently  Duncan  has  put  forward  the  view  that  mica  in 
the  water  is  the  causative  agent.  This  mica  is  found  in  the  laterite 
— i.e.,  weathered  gneiss — -which  is  a  common  geological  formation 
in  the  tropics.  Singer  considers  that  he  has  met  this  disease  in 
four  out  of  six  Europeans  on  an  expedition  to  Abyssinia,  when  they 
reached  a  height  of  about  5,000  feet. 

/Etiology. — The  causation  of  the  disease  is  quite  unknown.  The 
theories  are: — -Diminished  atmospheric  pressure,  the  irritation  of 
mica,  fyecal  contamination  of  the  water,  and  exposure  to  cold. 

Pathology. — Very  little  can  be  said  under  this  heading,  except 
to  invite  attention  to  what  has  already  been  written  under  the 
heading  of  Sprue  with  regard  to  the  formation  of  leuco-urobilin, 
and  to  point  out  that  it  is  obviously  to  the  formation  of  this  body, 
and  not  to  anything  wrong  with  the  liver,  that  the  colour  of  the 
motion  is  due.  The  morbid  anatomy  would  appear  to  be  totally 
different  from  that  of  sprue,  and  to  be  a  congestion  of  the  mucosa? 
of  the  stomach  and  bowels,  with  a  proliferation  of  the  mucosal 
lymph  and  fibrous  tissue  in  chronic  cases.  On  the  surface  of  the 
mucous  membrane  of  the  small  and  large  bowels  there  is  a  thick 
layer  of  mucus,  but  no  ulceration. 

Symptomatology. — The  disease  generally  begins  soon  after  the 
patient  has  arrived  in  the  hills  from  the  plains. 

The  onset  is  sudden,  beginning  with  abdominal  pain  in  the  early 
hours  of  the  morning,  with  the  passage  of  large,  frothy,  greyish 
or  whitish  motions,  which  produce  a  sense  of  relief.  The  patient 
goes  about  his  work,  but  in  the  early  hours  of  the  next  morning 
the  symptoms  are  repeated,  and  he  will  complain  that  his  stomach 
feels  blown  out,  and  that  he  can  hear  gurgles,  and  this  goes  on 
morning  after  morning. 

If  now  the  patient  leaves  the  hills  and  comes  down  to  the  plains 


1796  SPRUE  AND  OTHER  DIARRHCEAS 

to  consult  a  doctor,  he  is  astonished  to  find  that  he  is  quite  well, 
and  perhaps  goes  back  to  the  hills  without  having  obtained  the 
medical  advice  which  he  desired.  A  relapse  takes  place,  for  which 
he  does  not  as  a  rule  seek  advice,  as  he  considers  it  a  trivial  com- 
plaint, until  later  he  begins  to  feel  dyspeptic,  disinclined  for  his 
food  or  work,  and  now  he  will  seek  treatment,  notwithstanding  the 
fact  that  he  feels  better  on  returning  to  the  plains.  The  disease 
may  become  chronic,  and  rarely  may  lead  to  a  fatal  result. 

Sequela. — It  is  said  that  neglected  hill  diarrhoea  may  develop 
into  sprue. 

Diagnosis. — The  history  of  the  case  and  the  absence  of  mouth 
symptoms  are  sufficient  to  enable  the  diagnosis  as  a  rule  to  be 
made  from  sprue. 

Prognosis. — The  prognosis  is  good,  as  recovery  is  generally  quick 
under  suitable  treatment,  but  in  certain  cases  it  is  found  necessary 
to  abandon  residence  at  high  elevations. 

Treatment. — The  treatment  is  simple  and  effective.  It.  consists 
in  rest  in  bed,  warm  clothing,  and  h  to  i  drachm  of  liquor  hydrargyri 
perchloridi,  given  fifteen  minuces  before  each  meal,  and  12  to  15 
grains  of  pepsin,  ingluvin,  or  lactopeptin  two  hours  after  the  meal. 
The  diet  is  to  be  milk,  which  may  be  diluted  as  advised  in  the  treat- 
ment of  sprue. 

Prophylaxis. — Persons  liable  to  the  disease  should  avoid  the  hills, 
especially  in  the  monsoon  season,  and  if  compelled  to  go  to  high 
altitudes  should  do  so  by  easy  stages. 

LOW-COUNTRY  MORNING  DIARRH02A. 

This  affection,  described  by  Castellani,  is  common  in  Ceylon,  and 
somewhat  resembles  hill  diarrhoea,  but  is  found  in  the  plains. 

Symptomatology. — The  patient  wakes  up  about  3  to  4  a.m.  with 
an  urgent  call  to  evacuate  the  bowels,  but  there  is  no  abdominal 
pain  or  straining.  After  an  interval  of  one  to  two  hours  the  bowels 
are  again  evacuated,  and  perhaps  again  two  or  three  more  times  in 
the  course  of  the  morning.  The  motions  are  liquid,  generally 
yellowish  or  brownish,  and  do  not  contain  blood  or  mucus.  The 
condition  lasts  as  a  rule  for  months,  but  usually  ceases  on  a  change 
of  climate. 

Treatment. — A  dose  of  tannalbin  (gr.  xv.-xxx.)  or  bismuth  sub- 
nitrate  (gr.  xv.-xxx.)  may  be  given  at  bedtime  as  a  palliative. 

FLAGELLATE  DIARRHOZA. 

Definition. — Flagellate  diarrhoea  is  an  acute  or  chronic  diarrhoea  due  to 
infections  of  the  intestine  with  Oicomovas  hominis  (Davaine,  1854),  Chilo- 
mastix  mesnili  (Wenyon,  1910),  Giardia  intestinalis  (Lambl,  1859),  and  Entcr>- 
monas  hominis  da  Fonseca,  1915.  and  other  flagellates. 

History. — From  the  days  of  Davaine,  observers  have  from  time  to  time  drawn 
attention  to  cases  of  diarrhoea  or  enteritis  thought  to  be  caused  by  these 
parasites — e.g.,  Roos,  Epstein,  Castellani,  Nattan-Larrier,  Brumpt,  da  Fonseca, 
Chalmers  and  Pekkola,  Escomel,  Paranhos,  etc. 


FLAGELLATE  DIARRHCEA 


1797 


On  the  other  hand,  of  late  years  a  number  of  observers — e.g.,  Wenyon  and 
O'Connor — do  not  believe  in  the  pathogenic  action  of  these  germs.  It  is 
quite  true  that  flagellates  may  be  aerial  contaminations  of  faxes,  and  that 
others  may  perhaps  be  non-pathogenic.  Still,  in  our  opinion,  when  these 
parasites  are  very  numerous  there  can  be  no  doubt  that  they  can  and  do 
cause  irritation  of  the  bowel  and  diarrhoea.  It  is  equally  true  that  they  can 
live  in  considerable  numbers  in  man's  intestine  without  causing  diarrhoea, 
but  such  a  person,  in  our  belief,  is  a  carrier. 


Fig.  759. — Cercomonas  longicauda  Davaine. 

(Alter  Wenyon  and  O'Connor,  from  the  publications  of  the  Wellcome  Bureau 
of  Scientific  Research.) 


Climatology. — The  flagellates  and  their  associated  diarrhoeas  are  to  be  found 
in  temperate  and.  tropical  climes.  They  are  common  in  Ceylon,  the  Anglo- 
Egyptian  Sudan,  the  Balkans,  and  Brazil,  but  have  been  reported  from  many 
parts  of  Africa,  Asia,  and  America. 

etiology. — It  is  difficult  to  prove  that  the  flagellate  is  the  cause  of  the 
diarrhoea,  but  if  one  of  these  organisms  is  present  in  very  large  numbers  in 
a  case,  if  bacteriological  research  fails  to  demonstrate  any  pathogenic  bacteria, 
and  no  other  cause  can  be  found,  it  may  be  provisionally  admitted  that  they 
are  causal.  If  the  causal  organism 
is  killed  off  and  the  diarrhoea  ceases 
pari  passu  with  this  process,  and 
docs  not  return,  and  the  flagellate 
is  cither  absent  or  only  present  in 
small  numbers,  the  first  assumption 
receives  support,  but  beyond  this  we 
cannot  at  present  go. 

The  difficulty  is  that  the  numbers 
of  the  parasites  wax  and  wane  in 
the  carrier  without  producing  sym- 
ptoms, but  when  present  in  large 
numbers  they  are  generally  associ- 
ated with  diarrhoea.  Infection  may 
be  by  t'.e  cysts  passing  into  the 
alimentary  canal  of  flies,  and  so  to 
human  food,  but  perhaps  it  may  take 
place  more  directly  at  times.  We 
have  never  seen  them  cause  true 
dysenteric  symptoms. 

From  certain  experiments  carried 
out  by  Miss  Porter,  it  would  seem 
that  cockroaches  may  play  a  role  as 
transmitters  of  flagellate  diarrhoeas 
of  man.  This  observer  succeeded 
in  transmitting  Giardia,  Tricho- 
monas and  Chilomastix  of  human 
origin  to  clean  white  rats  by  allow- 
ing their  food  to  be  contaminated  with  the  excrement  of  cockroaches  (Peri- 
planeta  americana  and  P.  orientalis)  which  had  fed  on  infected  stools. 


Litardia    inles- 

CONDITION       IN 


Fig.    759A. — Cyst    01 
tinalis    in     Fresh 
Human  Faeces. 
(Photomicrograph,  X  70  diameters.) 


1798 


SPRUE  AND  OTHER  DIARRHOEAS 


Symptomatology. — When  in  small  numbers  there  may  be  no  symptoms,  or 
the  only  symptoms  are  those  of  diarrhoea,  with  liquid  brown  motions,  con- 
taining yellow  flakes,  which  are  composed  of  epithelial  cells  and  leucocytes, 
around  which  the  parasites  are  formed  in  large  numbers. 

Treatment. — This  is  not  very  satisfactory.  It  is  easy  in  most  cases  to  stop 
the  diarrhoea  by  giving  a  small  dose  of  castor  oil  followed  after  some  hours  by 
the  administration  of  astringents  such  as  tannalbin  and  salol  in  large  doses, 
but  it  is  most  difficult  to  obtain  a  complete  disappearance  of  the  parasites. 
Methylene  blue  acts  fairly  well  on  flagellates  of  the  genera  Cercomonas,  Oico- 
monas,  Trichomonas  and  Chilomastix,  but  has  practically  no  action  on 
Giardia  (Lamblia).  It  is  given  in  i  or  2  grain  doses  twice  daily  in  cachets 
or  gelatine  capsules,  and  in  addition  enemata  of  3  pints  of  1  in  3,000  solution 
of  methylene  blue  may  be  given  twice  daily.  The  patient  should  be  told  that 
the  urine  will  become  blue,  otherwise  he  will  be  much  alarmed. 

Another  method  of  treatment  is  to  administer  calomel  at  night,  a  saline 
purgative  in  the  morning,  and  during  the  day  powders  or  cachets  of  salol 
combined  with  bicarbonate  of  soda.  This  is  done  for  several  days,  while 
the  patients  are  kept  on  a  restricted  diet  and  the  motions  carefully  examined 
daily  for  the  flagellate.  Iodine  solution  (1 :  1,000)  by  rectal  injection  has  been 
recommended  by  Escomel,  but  is  painful. 

Thymol,  turpentine,  etc.,  have  also  been  recommended,  but  these  various 
methods  of  treatment  do  not  induce  a  complete  disappearance  of  Lamblia 
infections. 

Prophylaxis.— This  consists  in  preventing  flies  and  cockroaches  from  access 
to  food  by  keeping  kitchens  and  outhouses,  and  all  the  immediate  surroundings 

of  a  house,  in  a  good  sanitary  condition. 
Kitchens  may  be  wire-netted  and  fly-traps 
may  be  provided  both  inside  the  kitchen 
and  outside.  Balfour  says  that  '  chicken 
entrails  '  are  the  best  baits  for  large  fly- 
traps situate  in  the  open  air.  The  flies 
may  be  killed  after  being  caught  by  means 
of  a  daisy  killer  or  any  other  smoke 
apparatus. 

All  fly-breeding  places  should  be  de- 
stroyed by  the  removal  of  the  dirt  and 
the  digging  up  and  disinfection  of  the 
ground. 

FAMINE  DIARRHCE^. 

Historical  and  Geographical. — This  con- 
dition has  been  observed  in  India  during 
periods  of  famine,  and  recently  by  us  in 
the  Balkans,  in  Serbian  and  Montenegrin 
troops  after  the  retreat  through  Albania. 

^Etiology. — Bad,  insufficient  food  and 
extreme  fatigue  play  a  very  important 
role  in  the  causation.  No  specific  germ 
has  been  found. 

Symptomatology. — The  patient  is  ex-" 
tremely  weak  and  terribly  wasted,  though 
the  abdomen  may  at  times  be  prominent 
and  distended.  He  may  feel  famished, 
but  when  given  food  can  take  very  little  of 
it,  and  cannot  digest  it.  He  complains  of 
slight  abdominal  pains  and  has  diarrhoea ; 
the  motions  may  not  be  very  numerous; 
they  are  liquid,  of  fsecaloid  or  at  times 
greenish  colour,  with  some  mucus,  but 
no  blood.  The  condition  lasts  usually  between  a  couple  of  weeks  and  one  to 
two  months,  and  often  terminates  fatally. 


Fig.  760. — Serbian  Soldier 
suffering  from  the  effect 
of  Famine  Diarrhcea  after 
the  Albanian  Retreat. 


FAMINE  DIARRHCEA—CCELIAC  DISEASE  1799 

Diagnosis. — This  is  based  on  the  history  of  starvation  and  extreme  fatigue, 
with  diarrhoea  without  blood,  while  the  patient  wastes  horribly  in  a  short 
time,  and  there  are  no  signs  of  tuberculosis.  It  may  be  differentiated  from 
dysentery  by  the  stools  not  containing  blood,  and  by  the  absence  of  dysenteric 
germs;  from  cholera  by  the  longer  course  and  absence  of  cholera  and  para- 
cholera  germs. 

Prognosis. — This  is  serious,  many  cases  terminating  fatally. 

Treatment. — This  is  very  unsatisfactory.  Astringents  such  as  bismuth 
subnitrate,  etc.,  even  when  given  in  massive  doses,  may  not  stop  the 
diarrhoea;  at  times  they  may  check  it,  but  the  patient  continues  to  become 
weaker  and  weaker,  and  often  dies. 

CCELIAC  DISEASE. 

Gee  described  in  England,  in  1888,  an  infantile  affection  characterized  by  its 
long  course,  anaemia,  great  wasting,  and  pale  greyish  abundant  stools.  Cases 
are  not  very  rare  in  Great  Britain,  and  have  been  reported  also  from  other 
countries.  The  aetiology  is  unknown,  though  various  germs  have  been  found. 
In  three  cases  Nabarro  has  carried  out  a  very  complete  investigation,  and 
has  isolated  from  the  faeces  a  dysenteric  bacillus  of  the  Flexner  type.  This 
result  would  suggest  that  the  condition  might  perhaps  be  astiologically  related 
to  the  so-called  pseudo-sprue  of  the  tropics,  described  by  one  of  us. 

In  cceliac  disease  the  tongue  apparently  does  not  become  affected,  and  this 
and  also  the  fact  that  it  is  found  in  children  rather  than  in  adults  differentiates 
the  malady  from  tropical  sprue. 

The  treatment  consists  in  very  careful  dieting.  Fresh  cow  milk  should  be 
prohibited,  and  dried  milk  given  instead,  using  one  of  the  preparations  on  the 
market  which  contain  only  a  very  low  proportion  of  fat.  Condensed  milk 
may  also  be  used,  but  is  generally  less  successful  than  dried  milk.  A  fruit 
diet,  in  contrast  to  what  one  sees  in  true  sprue,  is  badly  tolerated,  and  should 
never  be  ordered.     As  regards  drugs,  Still's  mixture  is  often  found  useful: 


Ol.  ricini  .  . 
Salol 

Spir.  chlorof. 
Muc.  acaciae 
Aq.  anethi 


Ter  die. 


TT|v. 

nu. 

TT|xv. 
ad  3i. 


Occasionally  silver  nitrate  is  valuable  when  the  diarrhoea  is  very  marked, 
and  Still  recommends  it  to  be  given  thus: — 

Arg.  nitratis        . .  . .  . .  .  .  •  •  gr-  !-,- 

Glycerini  fi\v. 

Aq.  dest.  ad  3i. 

Ter  die. 

Bismuth  preparations  are  practically  useless,  but  tannalbin  has  at  tunes  a 
favourable  action. 


REFERENCES. 

Sprue. 

The  current  literature  may  be  found  in  the  Bulletin  for  Tropical  Diseases. 

Ashford  (191 7).     American  Journal  of  Medical  Science. 

Bahr  (191 4).     Transactions  Society  of  Tropical  Medicine. 

Begg  (1907).     Journal  of  Tropical  Medicine,  p.  293. 

Bertrand  et  Fontan  (1887).     De  l'Entero-colite  chronique  Endemique  des 

Pays  chauds.     Paris. 
Brown  (1916).     Bull.  Johns  Hopkins  Hospital. 


1800  SPRUE  AND   OTHER  DIARRHCEAS 

Cammidge  (1907).     Journal  of  Tropical  Medicine,  x.  293. 

Cantlie   (1905-07).     British  Medical  Journal,  ii.   1287.     (1907).  Journal  of 

Tropical  Medicine,  x.  293. 
Castellani    (1905-12).     Ceylon   Medical    Reports.     (1912).  British   Medical 

Journal.      (1914).   Journal    of    Tropical    Medicine.      (Hyphomycetes    in 

Sprue.) 
Castellani  and  Low  (191 3).     Journal  of  Tropical  Medicine. 
Dold  (191 7).     China  Medical  Journal. 

Fayrer  (1885).     Tropical  Dysentery  and  Chronic  Diarrhoea.     London. 
Galloway  (1905).     Journal  of  Tropical  Medicine,  vol.  viii.,  October  2  and  16. 
Harley  and  Goodbody   (1906).     Chemical   Investigations  of  Gastric  and 

Intestinal  Diseases.     London. 
Hartigan  (1905).     Journal  of  Tropical  Medicine,  vol.  viii.,  March  1. 
Hiatt  (191 8).     Ref.  Handbook  of  the  Medical  Sciences,  pp.  917-919. 
Hillary  (1772).     Observations  on  the  Changes  of  the  Air,  etc..  in  the  Island 

of  Barbadoes.     London. 
Kelsch  and  Kiener  (1889).     Traite  des  Maladies  des  Pays  chauds. 
Kohlbrugge  (1901).     Archiv  fur  Schiffs-  und  Tropen-Hygiene,  No.  12. 
Low  (191 2).     Journal  of  Tropical  Medicine. 
Manson  (1880).     China  Imperial  Maritime  Customs. 
Martinez  (1916).     American  Journal  of  Tropical  Diseases. 
Mayo  Robson  (1907).     British  Medical  Journal,  vol.  ii. 

Michel  (1917).     American  Journal  Medical  Sciences.    (1918).    Journal  Infec- 
tious Diseases. 
Nicholls     (1918).      Indian    Medical    Gazette,    November     (Streptococci    in 

(Sprue).     (1919).  Journ.  Trop.  Med.,  February  1. 
Rogers  (1918).     Indian  Medical  Gazette,  April. 
Schmidt  (1916).     Zeitschrift  fiir  Inner  Medicin,  vol.  37,  No.  4. 
Schmitter  (1919).     Oral  communication. 
Thin  (1897).     Psilosi:;.    Second  Edition.     London. 
Van  der  Burg  (1880).     Indische  Spruw.    Batavia. 
Waterfield  (191 7).     Transactions  Society  of  Tropical  Medicine. 

Hill  Diarrhoea. 

Crombie  (1880).     Indian  Medical  Gazette,  vol.  xv.;  ibid.  (1892),  p.  129. 
Duncan  (1905).     British  Medical  Journal,  p.  1283. 
Grant  (1854).     Indian  Annals  of  Medical  Science,  i.  342. 
Younge  (1905).     British  Medical  Journal,  vol.  ii. 

Pseudo-Sprue. 
Castellani  (191 2).     Journal  of  Tropical  Medicine. 

Flagellate  Diarrhoea. 

Castellani  (1905).  British  Medical  Journal,  November  11.  (1915).  British 
Medical  Journal,  November  16.  (Treatment  by  Methylene  Blue.)  (1917). 
Journal  of  Tropical  Medicine. 

Castellani  and  Willey  (1905).     Spolia  Zeylanica. 

Chalmers  and  Pekkola  (1908).  Annals  of  Tropical  Medicine  and  Parasito- 
logy, vol.  xi.,  No.  3  (ChilomasHx  mesnili).  Liverpool.  (1917).  Pro- 
it  '-dings  of  the  Society  of  Tropical  Medicine  and  Hygiene,  December 
(Enteromonas  hominis  in  the  Sudan).  London.  (1917).  Bulletin  de  la 
Societe  de  Pathologie  Exotique,  vol.  x.,  No.  8  (Enteromonas  hominis  in  a 
British  Officer).  Paris.  (191 8).  Journal  of  Tropical  Medicine  and 
Hygiene,  July  1.     (Enteromonas  Diarrhoea.) 

Escomel  (1918).  An.  Fai  Mid.  Montevideo,  September  -  October. 
(Trichomonosis.) 

Lab  be  (1919)-     Presse  M6dicale,  March  24.     (Lambliosis.) 

Low  (1916).     British  Medical  Journal. 

Paranhos  (1918).  B'azil  Medico.  (Trichomoniasis  successfully  treated  with 
Methylene  Blue.) 


CHAPTER  LXXVI1 
THE    CHOLERAS 

Cholera — Synonyms — Definition — -History,  Geography,  and  Epidemiology — 
.Etiology  —  Pathology  —  Symptomatology —  Diagnosis  —  Prognosis — 
Treatment — Prophylaxis — Paracholcra — Pseudocholera — References. 

CHOLERA. 

Synonyms. — Cholera  Asiatica.     Hindustani:  Haiza.     Tamil:  Enerum  Vandee. 
Chinese  :  Hodouan.     Arabic:  Duba. 

Definition. — Cholera  is  an  acute  specific  endemic  or  epidemic 
disease  caused  by  Vibrio  cholercz  Koch,  1883,  and  characterized  by 
violent  purging,  vomiting,  muscular  cramps,  suppression  of  urine, 
and  collapse. 

Remarks. — There  is  little  doubt  that  in  the  past  the  term  '  cholera  ' 
— in  analogy  to  other  diseases — has  been  used  to  cover  a  group  of 
clinically  similar  affections  caused  by  closely  allied  germs.  See 
remarks  on  paracholera,  p.  18 19. 

History,  Geography,  and  Epidemiology.— Cholera  appears  to  have 
been  known  in  India  from  the  most  ancient  times,  for  Charaka 
and  Susruta  describe  symptoms  which  most  probably  refer  to  this 
disease.  The  name  is  of  Greek  origin,  being  perhaps  derived  from 
X'lXepa,  a  spout,  which  may  have  been  applied  with  the  idea  that 
the  violent  purging  resembled  the  water  rushing  out  of  a  spout. 
Apart  from  the  two  authors  mentioned  above,  the  earliest  record  of 
the  disease  is  found  in  1438,  when  Ahmed  Shah's  army  is  said  to 
have  been  decimated  by  it.  After  this  date  there  are  several  refer- 
ences, for  it  is  mentioned  by  Vasco  da  Gama  in  1490;  an  account 
is  given  of  an  outbreak  in  Goa  in  1543,  another  in  Pondicherry  in 
1768,  and  another  in  Calcutta  in  1781-82,  the  last  of  which  appears 
to  have  spread  to  Madras,  Ceylon,  and  Burma  in  1782-83.  Out- 
breaks occurred  in  Travancorc  in  1792,  and  in  the  Mahratta  country 
in  1794.  But  these  are  only  a  few  of  the  recorded  outbreaks,  for, 
according  to  Macnamara,  no  less  than  sixty-six  separate  observers 
mention  the  disease  between  the  years  1438  and  1817. 

With  regard  to  Europe,  cholera  was  recorded  at  Nismes  in  1564,  but  it  and 
the  sporadic  outbursts  in  the  seventeenth  century  may  not  have  been  true 
cholera.  It  also  appears  to  have  been  endemic  in  Java  as  far  back  as  1629, 
and  occurs  yearly  in  Southern  China  and  the  Philippine  Islands. 

In  1817  began  an  epidemic  which  may  have  originated  in  Cal- 
cutta or  in  Jessore,  and  which  lasted  till  1823.    During  this  time 

1801 


1802  THE  CHOLERAS 

it  spread  to  the  west  coast  of  India,  Arabia,  Ceylon,  Burma,  Malacca, 
Penang,  Singapore,  and  Manilla,  reaching  Mauritius  in  1819  and 
China  in  1820.  This  is  certainly  the  first  extensive  epidemic  ever 
recorded  outside  India.  In  1826  the  first  pandemic,  which  lasted 
till  1837,  and  spread  into  Europe,  Africa,  and  America,  began  in 
India,  through  which  it  spread  slowly,  and  then  passed  to  Europe 
and  Africa  by  three  rout es,the  first  and  earliest  via  Kabul,  Bokhara, 
and  Khiva  to  the  Russian  province  of  Orenburg,  which  was  reached 
in  1829.  The  second  route  was  through  Persia,  Tabriz,  and  Tiflis, 
to  Astrakhan  in  1830.  In  this  year  the  two  routes  met  at  Nijni- 
Novgorod,  where  there  is  an  annual  peasant  gathering.  These 
peasants,  on  returning  home,  infected  Moscow,  and  as  there  were 
military  operations  proceeding  in  Poland,  the  disease  rapidly  spread 
through  Western  Russia  into  Poland,  and  on  to  Germany,  Austria, 
Sweden,  and  England.      In  1831  France  became  infected,  and  from 


Fig.  761. — Distribution  of  Cholera  in  1915. 

1832-33  the  whole  of  Europe  was  ravaged,  and  the  disease  spread 
to  the  United  States,  Mexico,  Cuba,  and  Guiana,  and  even  to 
Australia.  In  the  meanwhile  the  epidemic  had  spread  by  the  third 
route  from  Bombay  to  Arabia  in  1826,  and  then  to  Syria,  Turkey, 
Egypt,  and  finally  to  North  Africa  in  1834,  after  which  it  died  down. 
In  1840  troops  were  collected  together  in  India  for  service  in 
China,  and  as  they  travelled  eastwards  they  carried  the  cholera, 
which  was  present  in  Bengal  and  Madras,  to  Malacca  and  China, 
in  which  country  it  was  very  prevalent  in  1841,  and  through  which 
it  spread,  reaching  Northern  Burma  in  1842.  It  now  proceeded 
north  of  the  Himalayas,  reaching  Yarkand,  from  whence  it  passed 
to  Bokhara  and  Afghanistan,  and  spread  into  the  Punjaub  and  the 
North-West  Provinces  in  1844,  and  into  Persia  in  1845,  when  it 
again  travelled  via  Tabriz  and  Derbend  to  Orenburg  in  1847,  and 
so  to  Europe  and  America  in  1848.     In  this  year  it  was  very  pre- 


HISTORY,  GEOGRAPHY,  AND  EPIDEMIOLOGY  1803 

valent  in  India,  spreading  again  from  Bombay  to  Arabia  in  1851, 
and  to  Turkey  in  1853;  while  it  also  again  travelled  via  Persia  to 
Russia  in  1852,  and  so  over  Europe.  This  epidemic  lasted  till  1857, 
and  affected  the  troops  engaged  in  the  Crimean  War. 

The  fourth  extensive  epidemic  began  in  1863,  and  spread  to 
Europe  by  the  two  usual  routes — viz.,  via  Persia  and  Arabia— and 
lasted  till  1875,  extending  as  usual  to  America. 

The  fifth  epidemic  began  in  1879,  when  the  disease  passed  from 
Mecca  to  Egypt,  and  so  to  Europe.  It  was  during  this  epidemic 
that  Koch  discovered  the  Vibrio  cholera  in  Egypt  in  1883. 

The  sixth  epidemic  (1891-96)  appears  to  owe  its  origin  in  India 
to  the  great  bathing  festival  at  Karagola,  on  the  Ganges,  which, 
being  only  held  once  in  thirty  years,  came  as  a  surprise  to  the 
officials,  who  were  not  prepared  for  it.  Cholera  broke  out  among 
the  pilgrims  on  February  8,  189 1,  and  spread  rapidly,  reaching 
Europe  in  1892. 

The  seventh  epidemic  began  in  1900,  and  may  be  said  to  be  con- 
tinuing at  the  present  time.  It  started  in  1900  in  India  after  a 
severe  famine,  and  spread  extensively  through  that  country,  and 
then  began  to  travel,  reaching  Japan  in  1901;  Arabia,  Mecca  and 
Jeddah,  Egypt  and  Erythrsea,  Syria,  Persia,  and  the  Philippines 
in  1902;  Palestine,  Asia  Minor,  and  Mesopotamia  in  1903;  Persia, 
Russia,  and  Turkey  in  Asia  in  1904;  Russia,  Germany,  and  the 
Philippine  Islands  in  1905;  Russia  (few  cases),  Burma,  Siam, 
Singapore,  Japan,  China,  and  the  Philippine  Islands  in  1906;  Ceylon, 
Peshawar,  Singapore,  Philippines,  Japan,  Korea,  Manchuria,  China, 
Russia,  Turkey,  and  Persia  in  1907;  China,  Russia,  Mecca,  and 
Medina  in  1908;  and  Russia  in  the  beginning  of  1909.  In  1910  it 
was  present  in  Russia  and  Italy.  In  1911  it  was  recognized  in 
Turkey,  Roumania,  Hungary,  Austria,  Italy,  and  Russia,  and  in 
1912  in  Turkey,  Italy,  and  Russia. 

In  1914  the  Dutch  East  Indies  were  attacked,  and  during  the 
war  the  Austrian  Army  and  civil  population  were  attacked, 
especially  in  Galicia,  as  well  as  Bulgaria  and  Greece,  while  Turkey 
has  also  suffered.     In  1915  Brcka,  in  Northern  Bosnia,  was  infected. 

Some  places  have  always  so  far  escaped  the  visitation  of  cholera. 
These  are  either  situated  in  the  colder  regions,  of  which  the  climatic 
conditions  are  unsuitable  for  the  propagation  of  the  disease,  or  are 
islands  to  which  the  disease  is  less  likely  to  be  brought,  or  where 
precautions  are  taken.  As  examples  of  these  islands  may  be  men- 
tioned the  Andaman  and  Pacific  Islands,  Reunion,  the  Azores,  etc. 
Tropical  and  Southern  Africa  have  not  yet  been  infected. 

The  climatic  influences  which  appear  to  favour  the  development 
of  the  disease  are  low-lying  areas,  and  soils  easily  permeable  to 
water,  especially  if  they  are  polluted  with  decomposing  matter. 
It  would,  however,  appear  that  the  most  inimical  climatic  condi- 
tions can  be  overcome  if  there  is  lack  of  cleanliness,  especially  with 
regard  to  drinking-water  and  food,  together  with  bad  sanitation, 
and  the   disease   may  spread  where  every  climatic   influence  is 


i8o4  THE  CHOLERAS 

opposed  to  it.  With  regard  to  the  use  of  permanganate  of  potash  in 
cholera,  it  was  recommended  in  1866  by  Everest,  who  treated  seven- 
teen cases  with  Condy's  fluid,  with  only  one  death.  Dr.  Mackie  in 
the  same  year  treated  six  cases  similarly  without  a  death.  In  1884 
J.  W.  Fry  stated  that  the  only  thing  he  found  of  remedial  use  was 
an  enema  of  diluted  Condy's  fluid.  In  1910  Rogers  reported 
favourably  of  the  use  of  the  permanganates  given  liberally  in 
cholera.  In  1913  Castellani  definitely  separated  the  condition 
which  he  called  paracholera,  from  cholera. 

/Etiology — The  Vibrio. — The  cause  of  the  disease  is  undoubtedly 
Koch's  vibrio  (p.  962) ;  still,  this  alone  may  not  produce  illness, 
for,  as  Dunbar  showed  in  1892  in  Hamburg,  people  who  had  never 
suffered  from  the  disease,  and  who  were  in  good  health,  might  still  be 
passing  quantities  of  the  virulent  micro-organisms  in  their  faeces.  It 
is  evident,  therefore,  that  these  persons  lacked  some  predisposing 
condition,  and,  further,  that  they  must  have  been  a  fruitful  source 
of  infection.  What  this  condition  may  be  we  do  not  definitely 
know,  but  it  would  appear  that  such  factors  as  mental  worry, 
underfeeding,  and  any  slight  disorder,  but  specially  any  derange- 
ment of  the  alimentary  canal  producing  diarrhoea,  are  predisposing 
causes.  With  regard  to  these  causes,  it  may  be  mentioned  that 
unripe  fruit,  and  especially  melons,  are  regarded  with  suspicion 
in  times  of  epidemics,  probably  because  they  cause  diarrhoea,  and 
thus  predispose  to  the  disease. 

It  may  be  that  the  vibrio  merely  lives  in  the  lumen  of  the  bowel 
in  the  cases  in  which  it  causes  no  symptoms,  and  only  gains  access 
to  the  epithelial  cells  and  mucosa  in  cases  of  lowered  vitality,  and 
perhaps  is  only  toxic  in  this  situation ;  but  if  this  is  so  it  still  remains 
to  be  proved. 

This  lowered  vitality  would  explain  the  apparently  extraordinary 
cases  which  at  times  appear  in  gaols  when  the  town  is  apparently 
free.  The  reason  may  be  that  short-sentence  prisoners  are  generally 
on  a  very  low  diet,  while  long-sentence  prisoners  often  have  such 
hard  manual  labour  to  perform  that  they  are  exhausted  at  night. 
Therefore,  if  a  carrier  is  introduced  into  a  gaol,  the  disease  may 
easily  start  apparently  de  novo  among  incarcerated  inmates. 

The  disease  is  communicable  directly  from  man  to  man  by  con- 
tamination. As  an  example  from  our  own  experience,  a  medical 
man  examines  a  patient  suffering  from  cholera,  and  then  proceeds  to 
have  his  lunch,  with  the  result  that  both  patient  and  doctor  were 
dead  within  twenty-four  hours  of  cholera.  Again,  there  is  the 
chance  of  infection  from  dead  bodies  in  performing  autopsies,  but 
graveyards  are  not  important  means  of  dissemination  of  the  disease, 
because  the  germ  rapidly  disappears  from  the  dead  body.  Fomites 
may  also  spread  the  contamination,  but  these  are  not  the  usual 
method  of  infection,  which  is  generally  by  water.  The  vibrios 
pass  out  with  the  faeces,  in  which  they  are  capable  of  living  a  long 
time  (163  days) ;  hence  the  great  danger  of  faecally  contaminated 
fields,  rubbish-heaps,  gardens,  etc. ;  for  if  there  is  a  poor  sanitary 


SETIOLOGY  1805 

system  in  the  place,  and  if  faecal  pollution  of  the  drinking-water  is 
possible,  the  disease  may  easily  become  epidemic,  for  it  has  been 
shown  that  the  vibrios  can  not  merely  live,  but  multiply,  in  water, 
though  the  conditions  under  which  they  do  this  are  not  perfectly 
understood. 

Two  classical  instances  are  usually  quoted  as  evidence  of  the 
spread  of  the  disease  by  water.  The  first  of  these  is  the  infection 
in  1854  of  a  lady  and  her  servant  in  Hampstead,  where  there  was 
no  cholera,  by  drinking  the  water  of  the  Broad  Street  well,  which 
was  infected,  the  water  being  carried  all  the  way  from  Broad  Street 
to  Hampstead  because  the  lady  in  question  had  a  special  liking 
for  it.  The  second  is  the  infection  of  Hamburg  in  1892  from  the 
waters  of  the  Elbe,  in  which  cholera  vibrios  were  found  in  the  river- 
water  and  that  of  the  hydrants. 

As  water  is  a  method  of  infection,  it  is  quite  easy  to  understand 
that  milk  is  specially  dangerous,  for  it  is  often  diluted  with  water, 
and,  moreover,  forms  an  excellent  medium  in  which  the  germs  can 
grow.  Thus  Haffkine  and  Simpson  found  that  an  outbreak  of 
cholera  in  the  Gaya  Gaol  was  due  to  the  contamination  of  the  milk, 
from  which  they  obtained  the  vibrio. 

The  Carrier. — Of  great  importance  in  the  dissemination  of  the 
malady  are  the  so-called  vibrio-carriers — viz.,  persons  who,  though 
themselves  in  good  health,  still  harbour  the  germ  in  their  intestines, 
or  individuals  who  continue  to  harbour  the  germ  for  months  and 
years  after  an  attack  is  over. 

Greig  has  demonstrated  that  carriers  can  show  an  increased  tit  re 
for  the  agglutination  of  the  vibrio.  His  researches  also  show  that 
the  vibrio  can  live  for  long  in  the  gall-bladder  of  animals,  and  he 
has  also  demonstrated  it  in  the  human  gall-bladder. 

The  fact  that  the  germs  can  live  for  a  long  time  in  faecal  matter 
enables  them  to  infect  insects  such  as  flies,  and  perhaps  ants.  With 
regard  to  flies,  the  germs  have  been  found  not  merely  on  the  ex- 
terior of  the  body,  but  also  in  the  alimentary  canal,  in  which  they 
are  believed  to  multiply.  The  habits  of  flies  make  them,  therefore, 
an  important  possible  means  of  dissemination  of  the  disease. 

Barber,  in  1914,  brought  forward  experimental  evidence  showing 
that  the  germ  could  live  for  a  time  in  the  alimentary  canals  of 
Periplaneta  americana  (the  cockroach)  and  Monomorium  latinode 
Mayr  (the  red  ant). 

Faecal  matter  may  also  pollute  green  vegetables,  for  in  the  East 
vegetable-gardens  are  often  contaminated  with  human  faecal  matter. 
The  most  dangerous  vegetables  are  those  which  are  eaten  raw,  such 
as  lettuces,  watercress,  and  tomatoes.  While,  however,  the  above 
methods  explain  many  points  in  the  epidemiology  of  cholera,  they 
do  not  afford  a  full  explanation  of  the  spread  of  the  disease.  As  we 
have  already  said,  the  principal  endemic  centre  is  Lower  Bengal, 
whence  it  can  spread  through  India,  and,  indeed,  over  the  greater 
part  of  the  world,  by  human  agency  and  along  lines  of  human  inter- 
communication, but  in  so  doing  it  may  miss  places  on  the  direct 


i8o6  THE  CHOLERAS 

route  of  its  march.  The  reason  of  this  is  not  clear.  Certainly 
climatic  conditions  may  be  of  importance,  and  perhaps  a  low  level 
of  the  subsoil  water  and  a  high  earth  temperature,  together  with  an 
imperfect  sewage  disposal  and  contaminated  source  of  the  drinking- 
water  of  the  place,  may  have  something  to  do  with  this  anomaly. 

Another  point  which  is  by  no  means  understood  is  the  fact  that 
the  disease  remains  for  years  in  the  endemic  region,  and  then 
suddenly  spreads  in  epidemic  and  pandemic  form,  extending  at 
times  over  the  whole  world. 

The  aetiology  may,  therefore,  be  summarized  by  saying  that  the 
disease  is  caused  by  Koch's  Vibrio  cholera  acting  in  the  presence 
of  some  unknown  bodily  condition  or  conditions,  and  spread  directly 
from  man  to  man  by  fomites,  water,  insects,  and  food,  but  the 
reasons  for  its  endemicity  and  epidemicity  are  unknown. 

When  travelling  from  one  place  to  another,  it  always  adopts 
channels  of  human  intercommunication,  which  may  be  ships,  rivers, 
roads,  or  railways.  When  introduced  into  a  locality,  it  will  give 
rise  to  a  widespread  epidemic  if  the  sanitation  is  so  defective  that 
the  germs  gain  access  to  the  drinking-water,  but  will  be  far  less 
extensively  spread  if  due  to  food  or  insects,  and  will  be  merely 
sporadic  if  spread  from  man  to  man. 

Pathology.— The  vibrio  grows  in  the  lumen,  the  glands,  the 
epithelial  cells,  and  the  mucosa  of  the  small  lnt|estiTier~prob"abrv 
producing  an  endocelfular  toxin,  which  is  set  free  and  causes  the 
symptoms. 

The  question  of  toxin  formation  has,  however,  been  much  debated. 
Thus,  in  1905,  Brau  and  Denier  considered  that  they  had  obtained 
a  soluble  toxin.  In  1906  Kraus  said  that  he  had  obtained  a  soluble 
toxin  which  caused  the  disease,  and  in  the  same  year  MacFadyen 
obtained  a  virulent  endotoxin.  In  1907  Strong  carefully  investi- 
gated the  subject,  and  concluded  that  he  was  unable  to  find  a 
soluble  toxin  as  described  above,  but  that  MacFadyen's  endotoxin 
was  the  true  toxin  which  caused  the  symptoms  in  man.  This  endo- 
toxin causes  great  gastro-intestinal  disturbance,  leading  to  the 
passage  of  fluid  from  the  blood  to  the  bowel  in  the  following  order: 
First  water,  and  then  inorganic  salts,  especially  sodium  chloride; 
later,  phosphates  and  potassium  salts;  and  still  later  organic  sub- 
stances. This  endosmosis  causes  a  great  concentration  of  the  blood, 
producing  a  high  specific  gravity,  which  may  reach  1073  to  1078, 
which  is  associated  with  a  great  increase  in  the  erythrocytes — 
8,000,000  per  cubic  millimetre,  according  to  Rogers  and  Megaw — 
with  a  corresponding  increase  of  the  haemoglobin  and  of  the  leuco- 
cytes, which  may  number  from  14,000  to  60,000  per  cubic  millimetre. 
At  the  same  time  the  alkalinity  of  the  blood  is  decreased  and  its 
coagulative  power  altered,  while  the  oxygen  contained  therein  is 
decreased. 

The  decrease  of  the  alkalinity  of  the  blood  may  be  very  marked 
in  severe  cases,  and  Rogers,  Sellards  and  Shaklu  give  great  import- 
ance to  this  so-called  cholera  acidosis. 


PATHOLOGY  1807 

The  concentration  of  the  blood  causes  a  fall  in  the  blood-pressure, 
which  is  indicated  by  the  feeble  compressible  pulse,  but  which,  to 
be  studied  properly,  requires  investigation  by  means  of  a  Riva- 
Rocci's  instrument,  as  has  been  done  by  Rogers  and  Megaw,  who 
found  that  in  typical  collapse  the  blood-pressure  might  be  only 
60  to  50  millimetres  of  mercury,  when  the  patient  is  markedly 
cyanosed  and  restless.  If  the  case  is  not  so  serious,  the  pressure 
may  be  higher — 70  to  80  millimetres  of  mercury — and  if  the  patient 
is  on  the  road  to  recovery  it  may  reach  to  90  millimetres.  As  a 
result  of  this  low  blood-pressure,  the  urine  may  be  suppressed  or 
scanty,  with  a  high  specific  gravity,  albumen,  casts,  and  a  large 
quantity  of  indican. 

The  body  appears  to  react  to  the  disease  by  the  pouring  out  of 
substances  from  the  blood  which  are  probably  bactericidal,  though 
Edwards's  attempt  to  prove  this  failed  because  of  decomposition 
and  the  admixture  of  other  micro-organisms.  Agglutinins  are 
absent  in  fatal  cases,  but,  according  to  Greig,  in  non-fatal  cases  they 
begin  to  rise  after  the  sixth  day,  but  drop  after  the  twentieth  day. 

When  recovery  is  about  to  take  place,  the  specific  gravity  of  the 
blood  decreases,  the  blood-pressure  rises,  and  the  urine  becomes 
abundant.  As  convalescence  continues,  the  great  danger  is 
secondary  infection  of  the  body  by  other  micro-organisms,  which 
may  cause  serious  illness  and  even  death. 

It  is  important  to  note  that  Greig  has  found  the  germ  in  the  gall- 
bladder (40-70  per  cent,  of  cases) — where  it  causes  cholecystitis, 
and  in  animals  may  give  rise  to  gall-stones- — in  the  lung,  kidney,  and 
urine.  According  to  Violle's  researches,  bile  in  vivo  tends,  however, 
to  hinder  the  development  of  the  cholera  vibrio.  According  to  the 
same  author  a  small  dose  of  cholera  toxin  excites  the  secretion  of 
bile  while  a  large  dose  stops  it.  It  is  suggested  that  a  septicaemia 
takes  place,  but  this  has  not  been  demonstrated.  Manson  suggests 
that  it  may  pass  by  the  lymph  channels. 

Danysz  regards  the  disease  as  of  anaphylactic  origin. 

Morbid  Anatomy. — Usually  post-mortem  rigidity  is  very  well 
marked,  and  the  body  keeps  warm  for  some  time  after  death. 
On  cutting  into  the  tissues,  it  is  noticed  that  they  are  very  dry, 
and  that  the  blood  is  often  thick  and  tarry.  On  opening  the  peri- 
toneal cavity,  the  hand  experiences  a  peculiar  sticky  sensation  not 
felt  in  any  other  disease  with  which  we  are  acquainted. 

The  stomach  is  usually  empty,  and  the  bowels  are  reddish  in 
appearance,  with  injected  vessels.  When  a  piece  of  small  bowel  is 
opened,  the  contents  are  usually  found  to  be  whitish  or  greyish 
grumous  material;  more  rarely  will  the  contents  be  blood-stained. 
These  contents  consist  of  food  particles,  epithelial  cells,  red  and 
while  corpuscles,  and  micro-organisms.  When  allowed  to  stand, 
they  separate  into  liquid  and  solid  portions,  the  former  containing 
albumen,  and  having  a  specific  gravity  varying  from  1005  to  1015. 
The  mucosa  of  the  stomach  and  bowels  is  hyper aemic  and  swollen, 
and  may  be  marked  by  ecchymoses.    There  is  usually  some  enlarge- 


i8o8  THE  CHOLERAS 

ment  of  the  solitary  and  agminated  glands,  as  well  as  of  the  mesen- 
teric glands. 

The  liver  is  generally  congested,  and  the  ducts  full  of  bile;  the 
spleen  is  shrunken;  the  kidneys  are  swollen,  and  often  ecchymotic, 
with  tubules  blocked  with  granular  debris  and  cells  in  a  state  of 
cloudy  swelling.  The  right  heart  is  often  dilated,  and  the  whole 
venous  system  full  of  blood,  while  the  arterial  system  and  the  left 
heart  is  empty.  The  lungs  are  collapsed,  dry,  and  anaemic,  and 
the  brain  may  be  congested. 

Microscopically,  the  vibrios  may  be  seen  in  Lieberkiihn's  follicles 
in  the  epithelial  cells,  and  in  the  mucosa  of  the  intestine  and  the 
stomach.  The  kidney  shows  vascular  congestion  and  destruction 
of  the  epithelium.  Usually  the  vibrios  do  not  penetrate  into  the 
blood-stream,  and  therefore  the  disease  is  mainly  a  general  intoxica- 
tion; but  Rebowski  records  cases  in  which^they  have  been  found 
in  the  liver,  the  kidney,  and  the  heart,  thus  producing  a  general 
infection. 

If  the  post-mortem  is  held  on  a  case  which  has  died  during  the 
state  of  reaction,  pneumonia  and  the  signs  of  other  secondary 
infections  may  be  found. 

Symptomatology. — A  typical  case  of  cholera  has  an  incubation 
period  which  varies  from  a  few  hours  to  a  few  days  (three  to  six). 
The  onset  is  usually  sudden,  but  there  may  be  prodromata  in  the 
form  of  diarrhoea,  or  merely  a  feeling  of  illness  and  malaise.  The 
attack  begins  with  diarrhoea,  with  or  without  colicky  pains  in  the 
abdomen.  The  motions  are  at  first  faeculent,  and  contain  bile,  but 
soon  assume  the  typical  rice-water  appearance,  in  which  they  are 
fluid  and  acholic,  containing  numerous  white  flakes,  which,  when 
examined,  are  found  to  be  composed  of  mucus  containing  vibrios 
and  epithelial  cells,  while  exceptionally  the  motions  contain  blood. 
Vomiting  generally  appears  early,  food  being  first  expelled,  followed 
later  by  a  watery  fluid,  with  which  bile  and  occasionally  blood  may 
be  mixed.  The  patient  complains  of  thirst,  and  at  times  of  hiccough. 
As  the  purging  and  vomiting  proceed  the  urine  diminishes,  and  may 
stop,  and  fluid  departs  from  the  subcutaneous  tissues,  which  there- 
fore contract,  so  that  thefacies  alters,  the  nose  becoming  sharp,  the 
cheek-bones  prominent,  the  eyes  sunken,  and  the  skin  of  the  fingers 
becomes  wrinkled  like  that  of  a  washerwoman.  Whilst  this  is 
taking  place,  the  circulation  becomes  profoundly  affected,  the  blood- 
pressure  falls,  the  pulse  becomes  weak  and  rapid,  the  heart-sounds 
diminish,  and  the  lips,  face,  and  nails  become  bluish.  The  patient 
now  ha?  difficulty  with  his  breathing,  and  his  voice  becomes  weak 
and  husky.  Painful  cramps  appear  in  various  muscles,  but  espe- 
cially in  the  calf,  arm,  and  abdominal  muscles,  while  the  reflexes 
are  diminished.  The  mind  is  quite  clear,  but  the  patient  is  apathetic, 
except  when  agonized  by  the  cramps.  The  skin  feels  cold,  and  the 
axillary  temperature  falls  below  normal,  but  that  of  the  rectum 
may  be  considerably  raised.  If  no  change  for  the  better  takes 
place,  the  patient  passes  into  the  algide  stage,  in  which  the  failure 


SYMPTOMATOLOGY— VARIETIES  1809 

of  the  circulation  becomes  more  marked,  the  pulse  almost  disap- 
pearing at  the  wrist,  the  heart  becoming  weak  and  irregular,  the 
respirations  laboured,  the  skin  cold  and  deeply  cyanosed,  the  urine 
suppressed,  while  the  diarrhoea  may  or  may  not  cease,  and  the 
temperature  falls  far  below  normal.  The  first  heart-sound  becomes 
impure,  or  a  hsemic  systolic  murmur  may  be  present,  and  the  second 
may  be  faint,  and  friction-sounds  maybe  heard  over  both  the  peri- 
cardium and  pleura.  The  patient  may  now  become  comatose,  and 
death  supervenes  in  from  twelve  to  thirty-six  hours  after  the  onset 
of  the  attack.  If  recovery  is  to  take  place,  the  diarrhoea  diminishes, 
the  skin  becomes  warmer,  the  pulse  and  blood-pressure  improve, 
and  after  a  time  bile  appears  in  the  motions,  and  the  skin  fills  out 
with  fluid  again. 

Sometimes  convalescence  is  rapid.  In  some  a  secondary  febrile 
condition  ensues,  which  may  last  for  several  days,  or  even  for  a 
couple  of  weeks. 

The  patient  may  at  times  pass  into  a  status  typhosus,  with 
flushed  face,  raised  temperature,  dry  brown  tongue,  low  muttering 
delirium,  with  subsultus  and  toxic  tremblings  and  toxic  rashes, 
which  may  be  erythematous,  papular,  or  haemorrhagic.  The  urine 
is  diminished  in  quantity,  has  a  high  specific  gravity,  and  contains 
albumen  and  casts.  The  motions  are  somewhat  like  those  of 
typhoid,  or  may  be  bloody. 

Death  may  take  place  during  this  stage  from  complications,  or 
recovery  may  ensue  after  a  long  convalescence.  The  infection  of 
the  convalescent  may  be  said  to  have  ceased  when  on  three 
separate  days  the  bacteriological  examination  of  the  motions  is 
negative. 

The  typical  course  of  the  disease,  as  described  above,  is  often 
arbitrarily  subdivided  into  three  stages:  (1)  The  stage  of  evacua- 
tion; (2)  the  algide  stage;  and  (3)  the  stage  of  reaction,  when  the 
patient  is  about  to  recover. 

Varieties. — Cholera  cases  at  times  present  many  varied  features, 
which  are  usually  classified  into: — 

1.  Ambulatory  Cases. — There  are  cases  in  which,  without  any 
signs  of  disease,  the  vibrio  may  be  obtained  from  the  faeces.  These 
people  are  genuine  carriers  of  the  disease. 

2.  Choleraic  Diarrhcea. — Choleraic  diarrhoea  is  characterized  by 
severe  purgation,  associated  with  the  passage  of  yellowish  motions, 
which  contain  the  specific  vibrio.  This  condition  may  be  recovered 
from,  or  may  pass  into  a  typical  attack  of  the  disease. 

3.  Cholerine. — The  patient  is  suddenly  seized  with  abdominal 
pains,  and  passes  numerous  faeculent  motions,  followed  by  typical 
rice-water  motions,  which  speedily  cease,  and  the  patient  quickly 
recovers  without  further  symptoms. 

4.  Cholera  Gravis. — This  is  the  typical  form  already  described. 

5.  Cholera  Sicca. — In  this  type  the  patient  becomes  rapidly  col- 
lapsed, and  dies  before  the  typical  symptoms  of  diarrhcea  and 
vomiting  can  appear.    The  post-mortem  and  the  bacteriological 

"4 


i8io  THE  CHOLERAS 

examination  of , the  bowel  contents  reveal  the  true  nature  of  the 

disorder.  • 

Complications.—In  rare  cases  hyperpyrexia  has  been  noted  during 
the  attack,  but  usually  all  the  complications  occur  during  the  stage 
of  reaction,  and  are  due  to  secondary  infections.  The  most  common 
are  pneumonia,  enteritis,  and  inflammation  of  the  kidney.  Preg- 
nant women  always  abort,  and  the  foetus  may  show  signs  of  the 
disease.  The  reason  of  this  abortive  tendency  is,  according  to 
Schutz,  because  cholera  has  a  powerful  effect  upon  even  the  non- 
pregnant uterus,  causing  haemorrhage  during  the  stage  characterized 
by  muscular  cramps. 

i.  Sequelae. — After  such  a  severe  illness,  it  is  usual  to  find  more  or 
less  permanent  damage  to  the  health  of  the  victim.  Thus  anaemia, 
inflammation  of  the  parotid,  gangrene,  ulceration  of  the  cornea, 
astigmatism,  or  other  errors  of  refraction,  a  tendency  to  diarrhoea, 
and  digestive  disturbances,  may  persist  for  a  long  time. 

Diagnosis. — The  diagnosis  is  easy  during  an  epidemic,  but  it  may 
be  very  difficult  in  the  period  when  there  are  only  a  few  sporadic 
cases  preceding  the  outbreak. 

So  closely  may  cholera  be  simulated  by  ptomaine  poisoning  as 
regards  the  collapse,  and  by  infections  with  germs  of  the  Aertrycke- 
Gartner  group,  which  we  have  seen  produce  typical  rice-water 
motions,  that  it  is  perfectly  useless  in  a  sporadic  case  to  attempt 
to  make  an  accurate  diagnosis  without  a  bacteriological  examination, 
and  even  this  has  to  be  performed  with  the  greatest  care,  as  there  are 
many  vibrios  which  are  undistinguishable  without  special  tests  from 
the  Vibrio  cholerce  Koch.    We  recommend  the  following  method:- — 

i.  Make  films  from  the  rice-like  flakes,  and  stain  with  diluted 
Ziehl  carbolic  fuchsin  (i  in  50)  for  ten  minutes,  or  with  Lofner's 
blue,  five  minutes.  If  a  large  number  of  curved  rods  be  present, 
cholera  may  be  suspected;  but  a  definite  diagnosis  should  never  be 
based  on  the  simple  microscopical  examination,  as  comma-like 
germs  are  found  in  many  cases  of  ordinary  diarrhoea,  and  even  in 
normal  stools. 

2.  Inoculate  four  tubes  of  peptone  water  with  the  suspected 
stools,  the  first  with  J  c.c,  the  second  with  |cc,  the  third  with 
1  c.c,  and  the  fourth  with  2  c.c;  or  inoculate  each  of  two  Erlen- 
meyer  flasks,  capped  with  sterile  filter-paper  without  wool-plugs, 
with  1  c.c.  of  the  stools.  The  formation  of  a  scum  on  the  surface 
of  the  medium  within  eight  to  ten  hours  is  suspicious  of  cholera. 
The  pellicle  and  the  upper  portions  of  the  medium  should  be  ex- 
amined microscopically  for  the  presence  of  vibrios,  and  a  micro- 
scopical agglutination  test  carried  out,  mixing  one  loopful  of  the 
culture  with  one  loopful  of  diluted  cholera  serum  (1  in  1,000).  The 
peptone  water  should  be  tested  for  the  presence  of  indol,  adding  a 
few  drops  of  pure  sulphuric  acid.  In  true  cholera  the  indol  reaction 
is  generally  present  eight  to  ten  hours  after  inoculation.  From  the 
pellicle  and  upper  portion  of  the  peptone-water  tubes  ordinary  agar 
and  MacConkey  agar  plates  should  be  made,  and  any  suspicious 


DIAGNOSIS  1811 

colony   developing    should    be    further  examined    and    the  germ 
investigated  as  regards  the  following  characters : — 

(a)  Motility. — The  cholera  vibrio  is  very  actively  motile. 

(b)  Morphology.— The  cholera  organism  is  often  bent,  comma-like, 
but  may  be  straight,  bacillus-like. 

(c)  Agglutination. — A  strong  anticholera  serum  obtained  from 
some  well-known  laboratory  should  be  used.  Any  vibrio  found 
in  stools  which  is  agglutinated  by  this  serum  in  a  dilution  not  less 
than  1  in  2,000  can  safely  be  considered,  as  a  rule,  to  be  the  true 
germ  of  cholera.  In  doubtful  cases,  all  the  cultural  characters 
should  be  studied,  and  Pfeiffer's  test  and  Castellani's  absorption 
test  should  be  carried  out. 

Dunbar  has  recommended  a  special  agglutinative  test,  which  consists  in 
mixing  directly  a  drop  of  the  stools  with  diluted  immune  serum.  The  cholera 
vibrios  become  agglutinated.  This  process  is  practicable  only  when  the  stools 
contain  many  vibrios. 

3.  Take  a  rice-like  flake,  and  smear  it  direct  on  to  the  surface  of 
MacConkey's  lactose-agar  plate,  using  a  sterile  bent  glass  rod  or 
Kruse's  platinum  pencil.  Inoculate  with  the  same  rod  or  pencil 
without  recharging  the  surface  of  two  more  plates,  and  incubate  at 
350  C.  The  colonies  of  the  cholera  and  cholera-like  vibrios  develop 
on  MacConkey's  medium  as  delicate,  small,  yellowish,  roundish  dots 
within  twelve  to  eighteen  hours.  Any  suspicious  yellowish  colony 
should  be  examined,  and  the  germ  investigated  as  regards 
motility,  morphology,  and  agglutination,  as  already  mentioned. 

4.  Inoculate  the  surface  of  three  ordinary  serum-tubes  with  the 
suspected  stools,  and  incubate  at  350  C.  If  within  sixteen  hours 
there  is  no  zone  of  liquefaction  in  the  medium,  cholera  may  be  practi- 
cally excluded.  If  there  is  liquefaction,  this  may  be  due  to  the 
presence  of  the  cholera  or  other  serum-liquefying  germs,  or  to  the 
stools  containing  an  amount  of  proteolytic  substances.  The  liquefied 
serum  may  be  plated  on  MacConkey  or  ordinary  agar  plates,  and 
any  suspicious  colony  further  investigated. 

5.  Dieudonne's  special  strongly  alkaline  blood  agar  may  be  used 
for  the  isolation  of  the  cholera  vibrio  in  faeces.  On  this  medium 
the  cholera  germ  grows  well,  forming  pearl-like  colonies,  while  the 
coli  and  coli-like  organisms  scarcely  vegetate.  Of  course,  the  colonies 
which  grow  must  be  carefully  investigated,  as  already  described. 

6.  Bandi's  Method. — The  suspected  faecal  matter  is  inoculated  into  a 
sedimentative  tube  containing  peptone  water  and  a  certain  amount  of  immune 
serum.  After  incubation  at  370  C.  for  three  to  seven  hours  this  tube  shows, 
if  the  case  is  one  of  cholera,  numerous  small  flocculi,  which  at  first  are  in 
suspension,  and  later  sink  to  the  bottom.  These  flocculi  consist  of  agglutinated 
vibrios. 

7.  Ottolenghi's  Method. — The  suspected  stools  are  inoculated  in  a  medium 
consisting  of  pure  bile  mixed  with  3  per  cent,  of  a  10  per  cent,  solution  of 
sodium  carbonate,  which  after  incubation  at  370  C.  for  some  hours  is  plated 
and  further  investigated. 

8.  Ardnson's  Method. — This  is  an  alkaline  agar  medium  containing  cane 
sugar  and  dextrin,  with  fuchsin  and  sodium  sulphite  as  indicator.  Good 
results  have  been  recorded  by  several  observers. 


1812  THE  CHOLERAS 

g.  Castellani's  Method. — Inoculate  peptone  water  tubes  (it  is  of  advantage 
to  use  centrifuge  tubes)  with  the  faecal  matter  in  the  usual  way,  but  before  or 
immediately  after  making  the  inoculation  add  to  each  tube  3  to  5  drops  poly- 
valent lactose  fermenting  faecal  bacteria  serum  (B.  coli,  B.  pseudo-coli,  B.  colt 
tropicalis,  etc.),  or  the  respective  mono-serums  may  be  used;  3  to  5  drops 
polyvalent  non-lactose  fermenting  faecal  bacteria  serum  {B.  proteus  group,  etc.) ; 
3  to  5  drops  paratyphoid  B  serum.  The  addition  of  the  last-named  serum  is 
made  with  the  object  of  agglutinating  and  delaying  the  growth  of  the  bacilli 
of  the  paratyphoid  B  and  aertrycke  type,  which,  in  the  tropics  at  least,  are 
not  very  rarely  found  in  the  intestinal  fluid.  Care  should  be  taken,  of  course, 
to  use  serums  containing  no  coagglutinin  for  the  cholera  vibrio,  or  only  in 
very  small  amount.  Or  serums  can  be  used  from  which  the  cholera  coagglu- 
tinin-— which  is  always  in  very  much  smaller  amount  than  the  other  coagglu- 
tinins — has  been  removed  by  absorption.  The  tubes  are  placed  in  the  incu- 
bator, and  the  further  steps  in  the  investigation  are  carried  out  in  exactly  the 
same  manner  as  with  the  ordinary  methods.  For  details  see  British  Medical 
Journal,  October  13,  191 7. 

A  modification  of  the  method  consists  in  inoculating  ordinary  peptone-water 
tubes  with  the  faecal  matter,  and,  after  four  to  six  hours,  from  the  upper 
portions  of  these  tubes  inoculations  are  made  in  peptone- water  tubes  containing 
a  few  drops  of  intestinal  bacteria  polyserums. 

If  material  has  to  be  sent  to  a  central  depot  for  bacteriological 
examination,  certain  precautions  must  be  carried  out.  The  faeces 
must  be  carefully  collected,  if  possible  into  a  bed-pan  which  has  been 
scalded  or  boiled,  or  a  loop  of  small  intestine  carefully  removed  post 
mortem.  These  specimens  must  be  forwarded  in  a  glass  bottle,  which, 
as  well  as  the  cork,  has  been  boiled.  It  is,  perhaps,  hardly  necessary 
to  state  that  no  antiseptic  must  be  mixed  with  the  specimens. 

Prognosis. — The  prognosis  is  usually  bad  at  the  beginning  of  the 
epidemic,  but  improves  as  the  epidemic  continues.  The  case- 
mortality  may  be  stated  to  be  on  the  average  about  50  per  cent. 

Treatment. — The  treatment  of  cholera  must  aim  at  the  destruc- 
tion and  removal  of  the  vibrios,  the  neutralization  of  the  toxins, 
the  prevention  of  secondary  infection  through  the  damaged  intes- 
tinal mucosa,  the  healing  of  which  must  be  assisted,  and  the  relief 
of  symptoms. 

To  promote  these  objects,  the  patient  must  at  once  be  sent  to 
bed,  no  matter  how  slight  the  attack  may  seem  to  be.  His  room 
should  be  airy,  and  he  should  not  be  allowed  to  leave  the  horizontal 
position.  The  bed-pan  and  urine  bottle  must  be  used,  and  the 
former  should  be  slightly  warmed. 

The  best  treatment  is  that  devised  by  Rogers,  which  is  as  follows  :— 

The  patient  is  given  as  much  calcium  permanganate  water  (1  to  6 
grains  to  the  pint)  as  he  can  drink,  and  permanganate  pills  every 
quarter  of  an  hour  for  two  hours,  and  then  one  pill  every  half  hour 
(any  pill  rejected  by  vomiting  being  immediately  replaced).  These 
pills  are  continued  until  the  stools  become  green  and  less  copious, 
which  may  occur  in  twelve  to  twenty-four  hours.  At  the  beginning 
of  the  second  twenty-four  hours  eight  pills  are  administered  within 
four  hours,  and  in  severe  cases  this  is  repeated  at  the  beginning  of 
the  third  twenty-four  hours.  In  mild  cases  after  the  first  twenty- 
four  hours  the  pills  are  only  administered  every  four  hours. 


TREATMENT  1813 

The  composition  of  the  pills  is: — 

Potassium  permanganate       .  .  . .  .  .      2  grains. 

Kaolin  and  vaseline  as  may  be  required  to  make  a  pill. 

This  pill  is  coated  with  a  varnish  composed  of  1  part  of  salol  and 
5  parts  of  sandarach  varnish,  or  with  keratin.  Pills  kept  for  any 
length  of  time  are  apt  to  become  hard  and  useless. 

The  patient  must  be  kept  warm,  and  supplied  with  plenty  of 
water  to  drink,  which  preferably  should  be  taken  in  sips,  and 
sinapisms  or  turpentine  stupes  should  be  applied  to  the  abdomen. 

When  collapse  has  set  in,  hot  bottles  must  be  applied  to  the 
extremities  and  round  the  body,  and  when  the  pulse  fails,  the 
median  cephalic  vein  should  be  opened  at  the  elbow,  and  Rogers's 
special  silver  cannula,  made  by  Messrs.  Down  and  Company,  in- 
serted, and  through  this  injections  of  hypertonic  saline  solution 
should  be  injected  until  the  blood-pressure  returns  as  tested  by  the 
pulse,  or  more  preferably  by  a  Riva-Rocci's  instrument.  If  the 
blood-pressure  sinks  below  70  millimetres,  Rogers  considers  this  to 
indicate  the  presence  of  a  dangerous  degree  of  collapse  and  an 
indication  for  an  immediate. intravenous  injection.  He  takes  the 
specific  gravity  of  the  blood  by  the  simple  method  of  placing  a  drop 
of  blood  in  the  centre  of  a  small  vial  containing  a  mixture  of  glycerine 
and  water  of  known  specific  gravity  (at  the  mean  temperature  of 
the  air),  and  if  the  droplet  rises  or-  falls,  trying  another  vial  of  lesser 
or  greater  density  until  the  right  specific  gravity  is  reached. 

He  concludes  that,  if  the  specific  gravity  is  over  1060,  while  the 
blood-pressure  is  low,  a  copious  intravenous  injection  may  be  safely 
administered.  If  the  specific  gravity  is  over  1065,  even  if  the  blood- 
pressure  is  over  70  millimetres,  it  is  advisable  to  give  an  intravenous 
injection,  as  the  blood  is  dangerously  concentrated,  and  a  single 
evacuation  may  lead  to  a  rapidly  fatal  collapse. 

Restlessness,  cyanosis,  and  cramps  are  also  taken  as  indications  for 
intravenous  injection,  especially  if  the  blood  from  the  pricked  finger 
is  black,  and  may  be  obviously  thicker  in  consistency  than  normal. 

The  hypertonic  saline  solution  recommended  by  Rogers  is: — 

Sodium  chloride     ..  ..  ..      120  grains  (8  grammes). 

Calcium  chloride    ..  ..  ..  4       ,,      (0*25  gramme). 

Potassium  chloride  ..  ..  6       ,,       (0*4  ,,  ). 

Water  ..  ..  ..  ..To  1  pint  (568  c.c). 

The  temperature  of  the  sterilized  solution  (in  an  emergency  pure 
water  filtered  through  cotton-wool,  and  boiled  for  fifteen  minutes 
will  suffice)  has  to  be  judged  by  the  rectal  temperature.  If  this  is 
990  F.  or  over,  Rogers  injects  the  fluid  at  about  the  normal  tempera- 
ture of  the  body  (98-4°  F.) — i.e.,  the  flask  temperature  is  about 
ioo°  F.  If  the  rectal  temperature  is  a  degree  or  so  below  990  F.,  the 
temperature  of  the  solution  in  the  flask  should  vary  from  1020  to 
1040  F.  If  the  rectal  temperature  is  high — i.e.,  over  ioo°  F. — the 
•  solution  should  be  run  in  below  98-4°  F. ;  if  the'temperature  is  over 
1020  F.  the  solution  should  not  be  warmed.     About  4  pints  of  fluid 


1814  THE  CHOLERAS 

are  required  for  an  adult  male,  but  the  case  must  be  carefully 
watched,  and  the  injection  stopped  if  any  distress  of  increased 
frequency  of  respiration  is  noted.  These  injections  may  have  to  be 
repeated  several  times,  and  therefore  the  cannula  must  be  left  in  situ. 
At  the  same  time,  hypodermic  injections  of  strychnine,  provided 
there  are  no  severe  cramps,  with  or  without  atropine,  should  also  be 
given,  and  warm  rectal  injections. 

During  this  treatment  the  bladder  must  be  carefully  watched  to 
see  whether  urine  is  being  passed  or  not,  and  if  suppression  occurs, 
dry-cupping  should  be  performed  over  each  loin. 

In  some  cases,  especially  when  anuria  has  developed,  an  alkaline 
solution  acts  better,  and  Rogers  recommends  the  following:  Sodium 
chloride,  4  grammes;  sodium  bicarbonate,  10  grammes;  water, 
500  c.c.  Bayliss'  solution  (6  per  cent,  gum  acacia  in  0-9  per  cent, 
sodium  chloride  solution)  may  be  used. 

When  the  stage  of  reaction  sets  in,  a  mixture  containing  salicylate 
of  bismuth  gr.  xv.,  bicarbonate  of  soda  gr.  v.,  liquor  opii  sedativus 
min.  v.,  mucilage  q.s.,  and  chloroform  water  1  ounce,  should  be 
given,  and  later  one  containing  alkalis  and  digitalis  is  useful. 

With  regard  to  symptoms,  the  persistent  vomiting  may  be 
relieved  by  small  pieces  of  ice  or  by  -J  grain  of  cocaine  dissolved  in 
a  teaspoonful  of  water,  or  by  a  dose  of  10  minims  of  mistura  pepsini 
composita  et  bismutho  every  half -hour  until  four  doses  have  been 
given,  or  by  one  or  two  drops  of  tincture  of  iodine  in  water.  Cramps 
are  treated  by  massage,  assisted  by  rubbing  with  dry  powdered 
ginger,  by  hypodermic  injections  of  morphia,  or  by  inhalations  of 
a  mixture  of  chloroform  and  oxygen.  Prostration  must  be  com- 
bated by  hypodermic  injections  of  strychnine  or  of  camphor  in 
ether.  Delirium  must  be  relieved  by  bromides  with  tincture  of 
hyoscyamus. 

The  treatment  of  complications,  such  as  pneumonia,  etc.,  must  be 
conducted  on  the  lines  laid  down  in  textbooks  on  general  medicine. 

Other  methods  of  treatment  may  be  briefly  mentioned.  Many  disinfectants 
are  recommended  by  different  authors — e.g.,  a  mixture  of  sulphocarbolates 
of  zinc,  2  grains;  soda,  2  grains;  calcium,  3  grains,  dissolved  in  peppermint. 
Acetozone,  alphazone,  and  medical  cyllin  are  recommended  by  O'Gorman, 
and  both  he  and  Waters  advise  the  administration  of  15  minims  of  medical 
izal  dissolved  in  1  ounce  of  water  every  two  hours.  Salol  has  been  strongly 
recommended  by  some  writers,  and  Brown  and  Banerji  praise  an  emulsion 
of  eucalyptus  oil  with  mucilage  and  syrup  of  lemons,  of  which  5  minims  are 
given  for  a  dose.  O'Gorman  advises  copper  arsenite  for  infants,  while  Duke 
recommends  red  iodide  of  mercury  in  the  algide  stage,  and  Choksy  cyanide 
of  mercury  in  ^-grain  doses  in  syrup  and  water  every  two  or  three  hours,  but 
says  this  is  apt  to  cause  stomatitis  during  convalescence,  which  can  be  avoided 
by  regulating  the  doses.  Cantani  long  ago  advised  slow  intestinal  injections 
of  3  to  4  pints  of  a  1  per  cent,  solution  of  tannin,  with  or  without  20  to  40 
drops  of  tincture  of  opium,  and  warmed  to  ioo°  F.  and  given  every  three  to 
four  hours.  Denier's  serum  treatment  has  been  found  useless  by  Strong, 
but  Kolle's  serum  promises  to  be  more  useful.  Berdnikoff  gave  30  to  50  c.c. 
of  Schurupon's  serum  intravenously  and  subcutaneously  with  success.  Salim- 
boni''  used  100  to  350  c.c.  Pasteur  Institute  serum  together  with  saline 
injected  subcutaneously  and  intravenously.     Macfadyen  and  Hewlett  have 


PROPHYLAXIS  1815 

prepared  an  endotoxic  serum,  and  Violle  has  prepared  a  serum  by  inoculating 
the  cholera  vibrio  in  the  gall-bladder  of  rabbits.  Several  authors  recommend 
treatment  by  repeated  hypodermic  injections  of  morphia,  and  others  adrenalin 
and  pituitary  extract.  Kuhne  recommends  massive  doses  of  bolus  alba  (kaolin) . 

With  regard  to  diet,  no  food  should  be  given  during  the  acute 
attack,  but  merely  liquids,  which  should  consist  of  water,  iced 
water,  iced  soda-water.  Stimulants  should  only  be  given  with 
great  moderation,  and  carefully  by  the  mouth,  as  at  times  they  are 
apt  to  do  more  harm  than  good.  In  the  algide  state  the  liquids 
given  should  be  warmed,  and  hot  black  coffee  may  be  used  as  a 
cardiac  stimulant. 

When  reaction  sets  in,  only  the  mildest  foods  must  be  allowed, 
and  then  only  with  care.  Begin  with  thin  arrowroot,  and  continue 
with  milk  mixed  with  soda-water,  and  then  with  milk,  barley- 
water,  rice-water,  etc.  Sanatogen,  plasmon,  and  somatose  are  also 
recommended.  Meat-extracts  should  be  avoided.  As  improve' 
ment  continues,  the  diet  may  be  slowly  and  carefully  increased,  but 
the  greatest  care  must  be  taken  for  a  long  time. 

Prophylaxis. — The  prophylaxis  must  be  based  upon  the  know- 
ledge that  the  disease  is  carried  by  man,  and  is  spread  from  one 
man  to  another  by  water,  milk,  contaminated  food,  especially  green 
vegetables,  and  insects,  especially  flies  and  perhaps  ants. 

The  methods  which  may  be  adopted  are  classifiable  into  private 
and  public. 

Private  Methods. — At  the  beginning  of  an  epidemic  it  is  as  well 
to  circulate  a  printed  notice  in  English  and  in  the  vernacular  telling 
the  householder  what  he  should  do  to  prevent  the  disease  attacking 
his  household.  It  is  the  duty  of  the  head  of  every  household  to 
personally  inspect  twice  a  week  at  least  his  kitchen  and  go-downs, 
and  especially  his  servants'  latrines,  and  to  see  that  the  house  and 
compound  are  kept  in  a  clean,  sanitary  condition.  He  must  also 
see  that  the  filters  are  properly  cleaned,  and  should  flies  abound 
in  the  house,  their  source  should  be  diligently  sought  for,  or,  if  it 
cannot  be  found  and  dealt  with,  the  Sanitary  Authority  should  be 
informed.  He  should  also  see  that  the  whole  household  keep  them- 
selves strictly  clean,  especially  the  cooks. 

With  regard  to  food  and  drink,  care  should  be  taken  that  all 
cooking  and  serving  vessels  are  thoroughly  cleansed  with  boiling 
water,  and  that  kitchen  cloths  are  washed  in  a  solution  of  cyllin 
or  carbolic  acid.  Especial  care  should  be  taken  with  regard  to  the 
ice-safe,  which  is  apt  to  become  coated  internally  with  green  slime, 
which  may  cause  diarrhoea.  This  ice-safe  must  be  thoroughly 
cleaned  with  hot  soda  and  water,  and  exposed  to  the  sun  at  least 
once  a  week.  Food  must  not  be  stored  near  latrines,  and  must  be 
protected  from  flies  and  ants,  and  the  rooms  and  cupboards  in 
which  it  is  placed  must  be  thoroughly  cleansed  with  soda  and  hot 
water  at  least  once  a  week. 

All  water  must  be  boiled  and  filtered,  and  stored  in  covered 
vessels,  and  all  milk  must  be  boiled  and  carefully  protected  horn 


1816  THE  CHOLERAS 

flies  and  other  insects.  Care  should  be  taken  that  good  milk  is 
procured.  No  uncooked  vegetables  or  salads  should  be  used ;  fruit 
must  be  sparingly  indulged  in,  and  unripe  fruit,  especially  melons, 
must  be  avoided.  Balfour  advises  that  jellies  in  particular  should 
not  be  used  during  a  dangerous  season.  Weak  tea  and  lime  drinks 
made  with  boiling  water  should  be  used  as  beverages. 

All  cases  of  illness,  but  especially  diarrhoea,  must  be  promptly 
treated  by  a  medical  man. 

With  regard  to  prophylactics,  eucalyptus  oil  in  io-minim  doses 
twice  daily  has  been  strongly  recommended  by  some  authors,  but 
the  most  usual  prophylactic  is  a  protective  inoculation,  which  was 
first  introduced  by  Ferran  in  Spain,  and  has  been  studied  and 
improved  by  Haffkine  and  Gamaleia;  by  Tamancheff,  who  added 
0-5  per  cent,  carbolic  acid  to  the  sterilized  prophylactic;  and  by 
Strong  and  others. 

Vaccines. — Haffkine  originally  used  two  prophylactics — a  weak 
and  a  strong — with  the  idea  that  the  strong  would  produce  too 
violent  a  local  reaction ;  but  this  proving  to  be  wrong,  only  the  strong 
is  now  used.  This  prophylactic  is  prepared  by  intensifying  the 
virulence  of  the  vibrios  by  passing  them  through  a  series  of  rabbits, 
and  then  growing  on  agar,  from  which  the  growth  is  washed  off  by 
sterile  broth  which  is  made  up  to  8  c.c,  of  which  one  is  injected 
hypodermically  into  the  flank  as  a  dose.  There  is  some  local  reac- 
tion in  the  form  of  redness,  swelling,  and  pain,  and  some  general 
febrile  reaction.  The  result  is  that  after  an  initial  diminution  of 
the  resistance  against  the  disease  this  becomes  considerably  increased 
after  the  fifth  day.  Haffkine's  statistics  show  that  it  diminishes  by 
one-tenth  the  liability  to  the  disease,  and  increases  the  chance  of 
surviving  if  attacked.  Thus,  according  to  Powell,  in  6,549  non- 
vaccinated  there  were  198  cases  and  124  deaths,  and  in  5,778 
vaccinated  there  were  27  cases  and  14  deaths.  Vaccination 
confers  a  partial  immunity,  which  is  said  to  last  about  fourteen 
months,  after  which  it  diminishes,  and  finally  disappears.  Re- 
vaccination  is,  therefore,  necessary  after  this  period. 

Strong's  method  is  to  spray  agar  which  is  contained  in  large  flat- 
sided  flaskswith  a  twenty-four-hour-old  culture  of  thevibrioinbroth, 
and  then  to  incubate  the  flasks  at  370  C.  for  twenty  hours,  and  to 
suspend  the  subsequent  growth  in  sterile  water,  which  is  first  heated 
to  6o°  C.  for  one  to  twenty-four  hours,  then  incubated  at  370  C.  for 
two  to  five  days,  and  then  filtered  through  a  Reichel  candle.  Two 
c.c.  (the  equivalent  of  10,000  units  of  immunity  in  a  rabbit)  of  the 
filtrate,  which  must  be  sterile,  are  inoculated.  This  prophylactic, 
which  is  said  to  be  capable  of  being  kept  for  a  year,  produces  no 
local  reaction,  and  but  slight  general  reaction,  and  increases  the 
bactericidal  and  agglutinative  powers  of  the  serum  considerably. 
Strong  considers  that  it  contains  receptors  separated  from  the 
vibrios,  and  that  it  probably  acts  by  increasing  the  bactericidal 
and  antitoxic  powers  of  the  epithelial  cells  of  the  mucosa  of  the 
alimentary  canal. 


PROPHYLAXIS  1 817 

One  of  us  has  prepared  an  attenuated  live  vaccine  by  heating 
emulsions  of  agar  cultures  to  450  C.  or  480  C.  for  one  hour. 

A   nucleo-proteid  vaccine,   according  to   Lustig  and  Galeotti's 
method,  can  also  be  prepared. 

Tetravaccine  (T.A.B.C.) — This  is  a  vaccine  prepared  and  used  by 
Castellani  since   1909,   and  now  frequently  employed  in  various 
countries  as  a  prophylactic  measure  against  cholera  as  well  as 
typhoid  and  the  paratyphoid  fevers.     It  has  been  adopted  in  the 
Serbian  Army  since  1915.     It  is  prepared  as  follows: — 

The  growth  of  typhoid  cultures  is  washed  off  with  sterile  0*85  per 
cent,  salt  solution,  to  which  0*5  per  cent,  carbolic  acid  has  been 
added;  the  emulsion  so  obtained  is  stored  at  room  temperature 
(180  to  200  C.)  for  twenty-four  hours,  and  then  standardized.     To 
standardize  it  the  germs  are  counted  by  using  a  Thoma-Zeiss 
apparatus,  and  sufficient  carbolic  salt  solution  is  added  to  bring  the 
number  of  germs  down  to  2,000  millions  per  cubic  centimetre.    The 
standardized  emulsion  is  tested  for  sterility.     The  same  procedure  is 
carried  out  with  paratyphoid  A  and  paratyphoid  B  cultures,  these 
two  emulsions  being  also  standardized    to   contain  1,000  million 
germs  per  cubic  centimetre.     The  above  procedure  is  also  carried 
out  with  cholera,  the  emulsion  of  which,  however,  is  standardized 
to  contain  4,000  million  germs  per  cubic  centimetre.     The  four 
standardized  emulsions  when  found  sterile  are  mixed  together  in 
equal  proportions,  and  the  vaccine  will  therefore  contain  per  cubic 
centimetre: — 

Typhoid  .  .  . .  .  .  .  .  500  millions. 

Paratyphoid  A  .  .  .  .  . .  250        ,, 

Paratyphoid  B  .  .  .  .  . .  250        ,, 

Cholera  . .  .  .  . .  .  .      2,000        ,, 

Of  this  mixture,  0-5  to  o»6  c.cm.  are  given  under  the  skin  of  the 
arm,  or  better  into  the  loose  tissue  below  the  angle  of  the  scapula, 
the  first  time,  and  double  the  amount  a  week  later.  A  third  dose, 
also  \  c.cm.,  given  two  weeks  after  the  first,  is  of  advantage,  but  not 
essential  for  practical  purposes.  The  amount  of  agglutinins  for 
each  germ  is  about  the  same  as  if  monovalent  vaccine  had  been 
injected.  The  protection  for  cholera  seems  to  last  for  about  six 
months. 

Castellani  has  prepared  also  a  glycero-tetra vaccine  containing  2  per  cent, 
pure  glycerine  and  standardized  as  to  contain  per  c.c.  typhoid  2,000  millions, 
paratyphoid  A  100  millions,  paratyphoid  B  1 ,000  millions,  cholera  4,000  millions. 
Of  this  vaccine  only  one  inoculation  of  1  c.c.  is  given. 

A  pentavaccine  having  in  addition  300  millions  of  B.  pestis  may  also 
be  prepared.  The  effect  of  the  vaccine  in  man  lasts  for  several 
months  (six  to  seven). 

Public  Prophylaxis. — It  is  the  duty  of  the  State  to  attempt  to 
ward  off  cholera  by  preventing  human  beings  introducing  the  germ. 
This  involves  the  careful  watching  of  the  frontiers,  especially  along 
the  lines  of  intercommunication,  whether  roads,  railways,  or  water- 
ways.    Under  the  last  heading  must  be  included  ships,  boats,  and 


1818  THE  CHOLERAS 

rafts,  for  it  must  be  remembered  that  chc-Jera  is  very  apt  to  be 
introduced  by  persons  travelling  along  rivers. 

Any  suspicious  case  must  be  detained  for  five  days  in  quarantine 
in  suitable  isolation  hospitals  erected  near  the  frontiers,  while  the 
sick  must  be  tended  in  special  hospitals  with  all  the  precautions  to 
be  mentioned  later. 

Merchandise  does  not,  as  a  rule,  require  any  disinfection,  unless 
there  is  reason  to  suspect  that  some  of  it  has  been  fsecally  con- 
taminated from  a  case. 

When  an  epidemic  begins,  the  first  duty  is  to  form  a  special 
Cholera  Board  to  deal  with  the  outbreak,  and  this  Board  should  be 
composed  of  financial  and  legal  authorities,  as  well  as  of  doctors 
and  bacteriologists.  This  Board  will  form  the  central  authority  for 
the  control  of  the  epidemic.  All  suspicious  cases  must  be  reported 
to  this  central  authority  at  once. 

Then  central  and  outlying  bacteriological  stations  must  be  pro- 
vided, and  special  hospitals  and  isolation  hospitals  built,  and,  if 
possible,  nurses  and  medical  men  obtained  who  have  some  practical 
knowledge  of  the  disease.  If  time  permits,  it  is  as  well  to  have 
these  vaccinated  against  the  disease,  but  it  should  be  remembered 
that  five  days  must  elapse  before  the  immunity  is  effective. 

Arrangements  must  then  be  made  for  the  prompt  bacteriological 
diagnosis  of  cases,  for  the  prompt  treatment  of  all  disorders,  espe- 
cially intestinal,  and  extra  dispensaries  must  be  opened,  and  the 
public  informed  of  the  necessity  of  availing  themselves  of  these 
medical  arrangements.  If  necessary,  a  house-to-house  inspection 
should  be  made,  in  order  to  find  out  if  there  are  mild  concealed 
cases,  and  nobody  should  be  buried  without  a  proper  medical 
certificate. 

All  patients  must  be  removed  to  the  hospitals,  and  the  houses 
disinfected  with  the  Clayton  gas  apparatus,  in  order  to  kill  not 
merely  the  germs,  but  also  the  flies  and  ants.  If  this  is  not  avail- 
able, formalin  sprays,  together  with  burning  sulphur,  may  be  used. 
Fomites  should  be  carefully  disinfected,  and  persons  attending  the 
sick  must  avoid  infection  by  careful  disinfection  of  the  hands  and 
by  wearing  overalls. 

The  dejecta  of  patients  should  be  carefully  disinfected  with  cyllin 
or  carbolic  acid,  and  no  patient  should  be  liberated  from  the  hospital 
until  bacteriological  examinations  of  his  faeces  on  three  successive 
days  are  negative.  This  is  a  most  necessary  precaution,  because 
otherwise  he  may  spread  the  germs  broadcast  for  a  period  of  about 
six  weeks  at  least. 

Care  must  be  taken  to  disinfect  and  bury  the  dead  with  least 
chance  of  the  infection  spreading.  Cremation  should  be  encouraged 
in  preference  to  burial. 

A  systematic  search  must  be  made  for  the  origin  of  the  infection, 
and  drinking-water,  well-water,  etc.,  must  be  regularly  examined 
bacteriologically.  Dangerous  wells  must  be  closed,  and  all  wells 
may  be  Hankenized — i.e.,  disinfected  with  permanganate  of  potash. 


SUMMARY  OF  PROPHYLACTIC  MEASURES  1819 

The  milk,  ice,  and  aerated  waters  should  be  taken  under  the 
municipal  control,  and  not  merely  must  care  be  taken  that  they 
are  pure,  but  they  must  be  tested  bacteriologically  from  time  to 
time. 

Vegetables  must  be  inspected,  and  the  place  where  they  are  grown 
ascertained  and  inspected,  in  order  to  find  whether  there  is  faecal 
pollution.  A  crusade  must  be  made  against  flies  and  dirt  in  general. 
The  disposal  of  sewage  should,  of  course,  have  been  dealt  with 
before  the  epidemic  has  occurred;  but  if  it  is  defective,  attempts 
should  be  made  to  remedy  this  as  far  as  possible,  and  a  scheme  at 
once  started  for  proper  collection  and  disposal. 

Bathing-places  must  be  carefully  inspected,  and  bad  places  closed, 
and  only  pure  water  allowed  to  be  used.  No  washing  must  be 
allowed  near  wells.  Drugs  must  be  given  free,  and  means  for 
inoculation  of  the  prophylactic  provided  on  a  large  scale. 

When  the  epidemic  is  past,  the  sanitary  defects  found  out  during 
its  course  should  be  remedied,  and  not  forgotten  until  another 
outbreak  occurs. 

Summary  of  Prophylactic  Measures. 

Public  Prophylaxis : — 

1.  Protection    of    the   frontiers    by    regular    inspection    posts    and 

quarantine  stations. 

2.  A  central  Cholera  Board,  with  full  staff  and  apparatus  for  bac- 

teriological disinfection  and  hospital  work. 

3.  Instruction  of  the  populace  by  means  of  pamphlets. 

4.  House-to-house  search  for  cases. 

5.  Search  for  carriers  and  sources  of  infection. 

6.  Distribution  of  medicines  and  disinfectants. 

7.  Provision  of  medical  aid  which  can  be  readily  obtained  by  anyone. 

8.  Crusade  against  house-flies. 

Private  Prophylaxis  : — 

1 .  Personal  cleanliness. 

2.  Avoidance  of  foods  liable  to  be  contaminated  or  to  cause  diarrhoea. 

3.  Avoidance  of  pollution  of  foods,  especially  by  flies. 

4.  Filtration  and  boiling  of  all  water  used  for  cooking,  drinking,  etc. 

Filters  to  be  kept  strictly  clean. 

5.  Boiling  of  milk  and  protection  against  flies. 

6.  Clean,  sanitary  dwelling  free  from  flies. 

7.  Anti-cholera  vaccination,  repeated  yearly  in  endemic  centres. 

8.  Immediate  application    for    medical  aid   in   case   of    diarrhceal 

illness  of  any  description. 

PARACHOLERA. 

Synonym.— N'diank  (Senegal). 

Definition.— Parachnlera,  a  term  first  introduced  by  Castellani, 
indicates  an  acute  attack  of  colic  and  diarrhoea,  with  or  without 
rice-water  motions,  which  resembles  cholera  in  the  severity  of  the 
symptoms,  but  differs  therefrom  in  that  its  causal  organism  is  a 
vibrio  different  from  Vibrio  cholerce  Koch. 

Remarks. — The  work  of  Castellani,  Thiroux,  Lamas,  Greig,  Orti- 
coni,  Chalmers  and  Water  field,  and  many  others,  has  demonstrated 


1820  THE  CHOLERAS 

the  existence  of  a  clinical  entity  differing  from  true  cholera  mainly  in 
the  fact  that  the  causal  organism  is  not  the  cholera  vibrio. 

/Etiology. — The  organisms  which  have  been  isolated  from  cases 
of  paracholera  are : — 

Vibrio  kegallensis  vel  paracholera  Castellani  in  Ceylon. 

Vibrio  Jreseris  Lamas  in  Spain. 

Vibrio  gindha  Pfeiffer,  by  Chalmers  and  Waterfield,  in  1916, 
in  the  Anglo-Egyptian  Sudan. 

Orticoni's  vibrio  in  Marseilles  in  1911. 

Symptomatology. — Clinically  the  symptoms  resemble  those  of 
Asiatic  cholera,  and  as  such  the  cases  are  generally  diagnosed.  The 
motions  are  generally  of  the  rice-water  type,  but  are  sometimes 
slightly  greenish,  therein  differing  from  true  cholera. 

Treatment. — This  is  the  same  as  for  cholera. 


PSEUDOCHOLERA. 

Synonyms. — Choleraic  diarrhoea,  so-called  ptomaine  poisoning,  Serous 
diarrhoea,  Trench  diarrhoea. 

Definition.— Pseudocholera  is  an  acute  attack  of  serous  diarrhoea 
which  resembles  cholera  and  paracholera  in  its  symptoms,  but  diffeis 
therefrom  in  being  due  to  various  causes,  none  of  which  is  a  vibrio. 

Remarks.- — Cases  of  profuse  serous  diarrhoea  associated  with 
algidity,  muscular  cramps,  and  in  general  showing  symptoms 
resembling  cholera  or  paracholera,  are  not  rare,  in  our  experience, 
in  tropical  and  subtropical  lands  and  war  zones. 

etiology. — The  causal  agents  are  very  various — e.g.,  food  poison- 
ing, generally  caused  by  bacilli  of  the  aertrycke  type;  serous 
diarrhoea,  caused  by  bacilli  of  the  dysentery  group;  atypical  subter- 
tian  malaria  ;  certain  poisons.  We  will  now  consider  the  symp- 
tomatology of  these  varieties. 

Food-Poisoning  Pseudocholera. 

This  form  of  pseudocholera  is  generally  due  to  B.  aertrycke.  The 
cases  are  of  mild  or  moderate  severity,  and  are  often  termed 
'  ptomaine  poisoning.'  The  onset  is  acute,  with  severe  abdominal 
pain,  furred  tongue,  and  diarrhoea.  The  motions  do  not  contain 
blood  or  mucus,  nor  are  they  usually  of  the  nature  of  rice-water,  but 
in  the  more  severe  cases  the  stools  are  choleraic  and  there  may  be 
algidity  and  cramp. 

Bacillus  aertrycke  can  be  differentiated  from  B.  paratyph.osas  B  by  means 
of  Castellani's  absorption  test.  Broughton  Alcock  has  described  several 
varieties  of  B.  aertrycke  which  can  be  distinguished  by  this  method.  For  its 
biochemical  characters  see  table  of  intestinal  bacteria,  p.  944. 

Dysenteric  Pseudocholera. 

Castellani  some  years  ago  showed  that  the  type  of  choleraic 
diarrhoea,  called  serous  diarrhoea,  was  often  due  to  bacilli  of  the 


PSEUDOCHOLERA— REFERENCES  1821 

dysentery  group,  and  therefore  of  dysenteric  origin.  Recently 
Besredka  in  cases  of  so-called  trench  choleraic  diarrhoea  has  also  found 
bacilli  of  the  dysentery  group.  The  onset  is  sudden,  and  at  times 
the  symptoms  may  be  mild,  but  more  commonly  they  are  severe. 
The  patient  passes  a  number  of  serous  motions  resembling  those  of 
cholera.  There  may  be  algidity,  cramps,  and  the  illness  may 
terminate  in  death.  In  most  cases,  however,  the  motions  are  now 
and  then  tinged  with  blood,  which  arouses  suspicion  as  to  its 
dysenteric  nature.  Microscopical  examination  of  a  fresh  prepara- 
tion of  the  faeces  may  show  a  few  red  cells  and  leucocytes,  instead 
of  the  epithelial  desquamation  found  in  true  cholera.  Bacterio- 
logical examination  demonstrates  the  presence  of  dysentery  bacilli 
and  the  absence  of  cholera  and  paracholera  vibrios. 

Malarial  Pseudocholera. 

This  type  is  not  rare  in  the  tropics.  The  onset  is  sudden,  with 
profuse  serous  diarrhoea,  algidity,  and  other  symptoms  closely 
resembling  true  cholera  (see  p.  njj).. 

If  the  spleen  is  enlarged  the  diagnosis  is  facilitated,  though  true 
cholera  may  develop  in  cases  of  malarial  infection.  Microscopical 
examination  of  the  blood  and  bacteriological  investigation  of  the 
fasces  are  also  useful  in  demonstrating  the  presence  of  malarial 
parasites  and  the  absence  of  cholera  and  paracholera  vibrios. 
Intramuscular  injections  of  quinine  quickly  cures  this  type  of 
choleraic  diarrhoea. 

Pseudocholera  caused  by  Poisons. 

This  is  most  usually  caused  by  arsenic,  which  is  commonly  in  use 
in  the  tropics,  especially  in  Ceylon,  where  it  can  be  bought  in  the 
local  markets.  The  diagnosis  may  be  established  by  the  history 
and  by  chemical  analysis  of  the  vomit  and  faeces  and  negative 
bacteriological  examination. 


REFERENCES. 

Cholera. 

The  most  useful  general  reference  is  Rogers's  excellent  work  (1911),  'Cholera 
and  its  Treatment,'  London.  A  valuable  recent  work  is  Violle's  monograph 
(1919),   '  Le  Cholera,'  Paris. 

Bayliss   (1919).     British  Medical   Journal,  June  7. 

Blell    (1906-07).     Zeitschrift   fur   Hygiene,    lv.    187.     (Immunization   with 

Nucleo-Proteid.) 
Castellani  (191 7).    A  Method  to  Facilitate  the  Isolation  of  the  Cholera  Vibrio 

and  Other  Organisms.   British  Medical  Journal,  October  13,  and  Journal 

of  Tropical  Medicine,  December  1. 
Craster  (191 3).     Journal  of  Infectious  Diseases,  xii.  3,  pp.  472-480,    Chicago. 
Crendiropoulo   (191 3).     Recherches  sur  les  Vibrions  au  Lazaret  de  Tor. 

Alexandria. 
Danysz  (1918).     Presse  Med.,  January  17 
De  Bonis  (1912).     Pathologica. 


1822  THE  CHOLERAS 

Defressine  and  Cazeneau   (1914).     Archives  de  Medecine  et   Pharmacie 

navales,  ci.,  pp.  46-55;  ciii.-cxix.     Paris. 
Drennan  (1914).     Journal  of  Infectious  Diseases,  xiv.  2,  pp.  251-254.    Chicago. 
Dieudonne  (1909).     Centr.  f.  Bakter. 

Duke  (1905).     Prevention  of  Cholera,  and  its  Treatment.     Calcutta. 
Dunbar  (1907).     Osier  and  McCrae's  System  of  Medicine,  ii.  714. 
Flu    (1914).     Geneeskundigen   Tijdschrift   voor  Nederlandsch-Indie,   liv.   5, 

pp.  524-539.     Batavia. 
Gauducheau  (1915).     Bull.  Soc  Med.-Chir.  Indochine,  vol.  vii.,Nos.  6,  10. 
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Gloster  (191 3).     Proceedings  of  the  Second  All-India  Sanitary  Conference, 

hi.,  pp.  252-264.     Simla. 
Gordon  (1906).     Centralblatt  fur  Bakteriologie,  i.  Orig.,  xlii.  5.     Jena. 
Greig  (1914).     Indian    Journal  of  Medical  Research,  vi.  2,  pp.  1-27,  28-45, 

604-622,  623-647,  733-762.     (1917).  Indian  Journal  of  Medical  Research, 

vol.  v.,  No.  2.     Calcutta. 
Haffkine  (1895).     British  Medical  Journal, ii.  1541.      (Cholera Prophylactic.) 
Hirsch  (1883).     Handbook  of  Geographical  and  Historical  Pathology.     (New 

Sydenham  Society.) 
Horowitz    (191 1).     Archives    des    Sciences    biologiques    (Russes),    xvi.     5. 

Petrograd. 
Klimenko  (1914).     Centralblatt  fur  Backteriologie,  i.  Orig.,  lxxiii. 
Kolle  (1909).     Deutsche  Medizinische  Wochenschrift. 

Kolle  and  Gotschlich  (1903).     Zeitschrift  fur  Hygiene,  xliv.  1.     Leipzig. 
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men,  ii.  4,  p.  1. 
Lamas  (191 3).     Boletin  Instituto  Nacional  de  Higiene  Alfonso  XIIL,  xix., 

pp.  173-210.     Madrid. 
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Paris. 
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No.  4,  pp.  403-432.     Manila. 
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Diseases  Bulletin,  vi.,  No.  1.     London. 
Migula  (1900).     System  der  Bakterien,  ii.  960-1003.     Jena. 
Neufeld  and  Haendel  (1907).     Arbeiten  aus  dem  kaiserlichen  Gesundheit- 

samte,  xxvi.  3.     Berlin. 
O'Gorman  (1905).     Indian  Medical  Gazette,  xl.  414.     (Treatment.) 
O'Meara  (1908).     Indian  Medical  Gazette,  xliii.  375. 
Pane  (1912).     Riforma  Medica. 
Pasquale  (1891).    Ricerche  batteriologiche sul  cholera  a  Massahua.    Giornale 

Medico  Regio  Esercito.     Roma. 
Prausnitz  (1903).     Zeitschrift  fiir  Hygiene  und  Infektionskrankheiten,  xliii., 

p.  239.     Leipzig. 
Rogers  (1909).     Proceedings  of  the  Royal  Society.     (Salines.) 
Rogers  and  Mackelvie  (1908).     Indian  Medical  Gazette,  xliii.  165.     (Saline 

Injections.) 
Rogers  and  Megaw  (1908).     Indian  Medical  Gazette,  xliii.  80.     (Salines.) 
Rogers  (1911).     Cholera  and  its  Treatment,  pp.  53-70.     London. 
Ruffer  (1907).     British  Medical  Journal,  i.,  p.  735.     London. 
Ruffer,  Calmette,  Gaffky,  Geddings,  Murillo,  Praun,  and  Pottevin 

(191 1).     Le  Diagnostic  bacteriologique  du  Cholera.     Paris. 
Schmitz  (1906).     Zeitschrift  fur  Hygiene,  lii.  1.     (Cholera  Vaccines.) 
Schutz  (1894).     Centralblatt  fiir  Gynakologie,  p.  45.     (Influence  of  Cholera 

on  Female  Genital  Organs.) 
Schutze    (1907).     Berliner   klinische   Wochenschrift,    July    1,    pp.    800-809. 

Berlin. 


REFERENCES  1823 

Simpson  (1894).     Cholera  in  Calcutta. 

Snow   (1855).     Report  of  the  Committee   for  Scientific   Inquiries  into  the 

Cholera  of  1S54.      (Broad  Street  Pump  Case.) 
Telle  and   Huber    (191 1).     Centralblatt   fur   Bakteriologie,  i.  Orig.,   lviii. 

Jena. 
Violle  (1919).     Le  Cholera.     Masson.     Paris.     (A  valuable  monograph). 
Wall  (1893).     Asiatic  Cholera.     London. 
Wankel  (191 2).     Zeitschrift  fur  Hygiene   und    Infektionskrankheiten,  lxxi., 

March  1,  p.  172.     Leipzig. 
Wherry  (1904).     Bureau  of  Government  Laboratory,  No.  19.     Manila. 
Wherry  (1905).     Some  Observations  on  the  Biology  of  the  Cholera  Spirillum. 

Cholera  Vaccination 

Castellani  (1908).  Bombay  Medical  Congress.  (1909)  Centralblatt  fur 
Bakteriologie.  (1912).^  Lancet.  (1913).  British  Medical  Journal. 
(1915).  Indian  Medical  Gazette  and  Transactions  of  Society  of  Tropical 
Medicine. 

Castellani  and  Mendelson  (1915).  The  Tetra vaccine :  Typhoid4- Para- 
typhoid A  +  Paratyphoid  B  +  Cholera.  British  Medical  Journal, 
November  13.     (Full  references.) 

Castellani  and  Taylor  (1917).  Combined  Vaccination  with  Multiple 
Vaccines  {Quadruple,  Quintuple  and  Sextuple).  Journal  of  Tropical 
Medicine,  November  1. 

Choksy  (1907).     Lancet,  i.  1077. 

Galeotti  (1912).     Centr.  f.  Bakt. 

Quarelli  (1917).      Riforma  Medica,  September  22. 

Strong  (1907).     Philippine  Journal  of  Science,  ii.  413. 

Paracholera. 

Castellani  (1914).     Vibrio    Isolated    from    Cases  of  Paracholera.    Journal 

Ceylon  Branch  B.M.A. 
Castellani  (1915).     Note  on  a  Vibrio  Isolated  from  Cases  of   Paracholera 

(V.  kegallensis  Castellani,  1913).     The  Journal  of  Tropical  Medicine  and 

Hygiene,  xviii.,  No.  8,  p.  85.     London. 
Castellani  (1916).     Paracholera.     British  Medical  Journal,  March  25. 
Chalmers   and   Waterfield    (191 6).     Journal   of   Tropical    Medicine   and 

Hygiene,  July  15.     London. 


CHAPTER  LXXVIII 
THE  DYSENTERIES 

The  term  '  dysentery  ' — Dysentery  and  dysenteric  diarrhoea — Dysenteries 
caused  by  animal  parasites — Protozoal  dysenteries — Amoebic  dysen- 
tery— Laveranic  dysentery — Leishmanic  dysentery — Ciliar  dysenteries — 
Balantidic  dysentery — Spirochaetic  dysentery — Entoplasmic  dysentery — 
Platyhelminthic  dysenteries — Nemathelminthic  dysenteries — Arthropodic 
dysenteries — Dysenteries  caused  by  bacteria- — Pseudo-dysenteries — 
References. 

The  Term  *  Dysentery.' — The  term  '  dysentery  '  is  derived  from 
ovo-ei/repla,  signifying  a  bowel  trouble,  and  was  first  employed  by 
Hippocrates.  As  used  at  present,  it  covers  a  large  number  of  dis- 
tinct affections,  induced  by  various  species  of  animal  and  vegetal 
parasites.  In  England  it  used  to  be  called  theBloodyflttx,  in  France 
Tenesme,  and  in  Italy  Flusso  sangtiigno.  The  Latin  equivalent  is 
Tormina,  the  German  Ruhr  ;  while  the  native  terms  applied  to  it 
are  too  numerous  to  be  considered  here,  but  we  may  mention 
the  Sinhalese  term  Lehedanpachanai  (L^=  blood,  hedan=ra\xc\xs, 
pachanai  =  diarrhoea) ,  and  the  Indian  term,  Rattam-seedam-banthala- 
porado  or  Wayatholechell. 

Dysentery  and  Dysenteric  Diarrhoea. — The  occurrence  of  a  bowel 
disease  in  which  blood  appeared  in  the  motions  was  well  known  to 
the  ancients,  for  descriptions  of  such  a  condition  can  be  found  in 
the  works  of  the  old  authors  Charaka  and  Susruta,  in  which  dysen- 
tery was  called'  Atisar,' and  acute  dysentery '  Ama-apaka,'  while  the 
chronic  variety  was  called  '  Pakitsar.' 

Hippocrates  recognized  two  distinct  types  of  disease  of  the  bowels 
— one  characterized  by  the  number  and  fluidity  of  the  motions, 
which  he  called  Biappoea,  and  the  other,  by  the  presence  of  blood  in 
the  motions,  which  he  termed  Svo-evrepia. 

At  first  the  term  '  dysentery  '  included  any  disease  in  which  there 
was  a  discharge  of  blood  per  anitm,  but  Aretaeus,  Celsus,  Archigenes, 
Galen,  and  other  ancient  physicians,  soon  differentiated  the 
disease  more  clearly  by  emphasizing  the  fact  that  there  should  be 
mucus  as  well  as  blood  in  the  motions,  and  that  the  symptoms  of 
tormina  and  tenesmus  must  be  present.  They  further  stated  that 
the  disease  was  due  to  an  ulcerated  condition  of  the  bowels,  and  the 
contagious  nature  of  the  malady  was  early  recognized  and  it  was 
thought  that  its  epidemics  were  due  to  miasmata.  According  to 
these  ancient  writers,  in  order  to  make  the  diagnosis  of  dysentery, 

1824' 


DYSENTERY  AND  DYSENTERIC  DTARRHCEAS  1825 

it  was  necessary  to  have  blood  and  mucus  in  the  motions.  Recent 
investigations  have,  however,  shown  that  certain  cases  of  diarrhoea 
and  dysentery  are  brought  about  by  the  same  organism,  and 
that  a  form  of  diarrhoea  which  may  be  called  dysenteric  diarrhoea 
is  only  one  phase  of  the  clinical  appearances  of  a  dysentery,  and 
is  aetiologically  in  no  way  different  from  what  might  be  termed 
a  true  dysentery,  except  in  the  severity  of  the  symptoms  and  the 
post-mortem  appearances.  Briefly,  dysenteric  diarrhoeas  are 
dysentery  under  a  somewhat  different  clinical  aspect — -viz.,  the 
stools  do  not  contain  blood  and  mucus,  although  the  complaint 
is  due  to  the  same  organisms  as  true  dysentery.  Hence  it  is  not 
expedient  to  attempt  to  classify  dysenteries  by  their  clinical  symp- 
toms or  by  their  post-mortem  appearances,  and  any  rational  classi- 
fication and  description  of  the  complaint  must  be  based  on  the 
causation. 
We  therefore  classify  dysenteries  and  dysenteric  diarrhoeas  into : — 

A.  Dysenteries  caused  by  Animal  Parasites: — 

I.  The  Protozoal  Dysenteries. 
II.  The  Plat yhelmint hie  Dysenteries. 
III.  The  Nemathelminthic  Dysenteries. 
IV.  The  Arthropodic  Dysenteries. 

B.  Dysenteries  caused  by  Bacteria. 

C.  Pseudo-dysenteries. 

By  the  last  expression  we  mean  such  forms  of  the  complaint  as 
may  be  due  to  the  irritation  of  fish-bones,  glass,  cancer,  or  inflam- 
mations of  organs  adjoining  the  alimentary  canal. 

A.  DYSENTERIES  CAUSED  BY  ANIMAL  PARASITES. 

I.  THE  PROTOZOAL  DYSENTERIES. 

The  protozoal  dysenteries  are  classified  into: — 

(a)  Amoebic  Dysentery. 

(b)  Laveranic  Dysentery. 

(c)  Leishmanic  Dysentery. 

(d)  Ciliar  Dysenteries. 

(e)  Balantidic  Dysentery. 

(/)    Spirochaetic  Dysentery. 
(g)    Entoplasmic  Dysentery. 

With  regard  to  the  term  '  amoebic  dysentery,'  we  prefer  this  term 
as  less  likely  to  be  altered  rather  than  the  more  correct  nomen- 
clature Loeschial  dysentery  or  Loeschiasis. 

(a)  Amcebic  Dysentery. 

Synonyms. — Loeschiasis,  Loeschial  dysentery,  Entamcebiasis,  Amce- 
biasis,  Entamcebic  dysentery,  Amcebic  enteritis,  Amoebic  colitis. 
French:  Dysenterie  Amibienne,  Dysenterie  a  Amibes.  Italian  :  Dis- 
senteria  Amebica.     German  :  Amobenruhr. 

"5 


1 826  THE  DYSENTERIES 

Definition. — Amoebic  dysentery  is  an  acute  or  chronic  specific 
disease  of  the  intestine,  caused  most  commonly  by  Loeschia 
histolytica  Schaudinn,  1903,  and  possibly  by  other  species.  These 
amoebae  enter  the  body  with  food  or  water,  and  produce  colitis, 
rectitis,  and  enteritis,  characterized  by  the  passage  of  frequent 
motions,  which  generally  contain  blood  and  mucus,  and  are  asso- 
ciated with  abdominal  pain  and  tenesmus.  At  times  they  also 
produce  abscesses  in  the  liver  and  other  parts  of  the  body. 

History. — In  i860  Lambl  noticed  amoebae  in  the  motions  of  a 
child  suffering  from  diarrhoea,  and  in  1870  Lewis  found  the  same 
organisms  in  the  motions  of  cholera  patients;  while  Loesch,  in  1875, 
gave  a  careful  description  of  certain  amoebae  which  he  found  in  the 
motions  of  a  man  suffering  from  chronic  diarrhoea.  Loesch's 
drawing  signifies  that  he  saw  the  organism  which  we  call  now 
Loeschia  histolytica.  Further,  he  found  that  solutions  of  quinine 
of  a  strength  of  1  in  5,000,  when  injected  per  rectum,  temporarily 
benefited  his  patient,  who,  however,  subsequently  died  of  pneu- 
monia, when  a  post-mortem  revealed  that  the  bowels  were  ulcer- 
ated. Loesch  was  able  to  infect  dogs;  but,  on  the  other  hand, 
Grassi,  and  later  Cunningham  and  Lewis,  showed  that  the  motions 
of  healthy  people  also  contained  amoebae.  Koch,  in  1883,  found 
amoebae  in  the  ulcers  in  cases  of  dysentery  in  Egypt,  and  Kartulis 
began  a  series  of  investigations,  which  finally  ended  by  his  defining 
the  types  of  dysentery  as  '  endemic,'  due  to  amoebae,  and 
'  epidemic,'  due  to  bacteria.  In  1891  Councilman  and  Lafleur 
introduced  the  term  '  amoebic  dysentery,'  and  Quincke,  Roos, 
Vivaldi,  and  many  others  published  experimental  researches  on  the 
infection  of  animals  by  amoebae  and  the  production  of  dysentery. 

In  the  meanwhile  a  prolonged  discussion  took  place,  some 
observers  denying,  and  others  asserting,  the  pathogenicity  of  the 
amoebae.  Kruse  and  Pasquale  were  the  first  to  throw  light  upon 
this  difference  of  opinion  by  suggesting  that  both  theories  might  be 
correct,  and  that  there  might  be  two  species  of  amoebae,  one  patho- 
genic and  the  other  harmless;  but  this  was  not  finally  settled  until 
the  researches  of  Casagrandi  and  Barbagallo,  together  with  those 
of  Jiirgens,  were  confirmed  and  greatly  extended  by  Schaudinn, 
who  showed  that  there  were  two  forms  of  amoebae  quite  distinct 
from  one  another — viz.,  a  Loeschia  coli  Loesch,  which  was  harm- 
less, and  another,  L.  histolytica  Schaudinn,  which  was  the  true 
cause  of  entamoebic  dysentery. 

During  recent  years  the  labours  of  Hartmann,  Whitmore,  Wenyon, 
Fantham  and  Porter,  Dobell  and  others,  have  proved  that  the 
amoeba  which  most  commonly  causes  dysentery  is  L.  histolytica, 
and  that  the  other  forms  of  amoebae  described  in  dysentery  by 
Viereck  (L.  tetragena)  and  other  observers  are  different  stages  of 
this  amoeba,  the  cysts  of  which  can  be  carried  by  domestic  flies. 

Climatology. — Amoebic  dysentery  is  found  throughout  the 
tropical  world,  and  also  occurs  in  the  Temperate  Zone.  In  general 
terms  it  may  be  stated  that  amoebic    dysentery    is    common    in 


CLIMATOLOGY— AETIOLOGY  1827 

tropical  and  subtropical  Africa,  especially  in  Senegambia,  Algeria, 
and  Egypt.  It  is  common  in  Mauritius  and  Ceylon,  and  is  possibly* 
not  as  rare  in  India  as  it  is  alleged  to  be.  It  is  common  in  China, 
Indo-China,  and  the  Philippines,  and  not  infrequent  in  North 
America,  but  is  said  to  be  rare  in  Central  America,  in  the  West 
Indies,  and  the  Guianas,  while  common  in  Brazil  and  Chili.  In 
Europe  it  is  endemic  in  Russia  and  Germany,  and  fairly  frequently 
met  with  in  the  south,  especially  in  Italy  and  in  the  Balkans. 
Sporadic  indigenous  cases  have  been  reported  also  from  Great 
Britain,  where  carriers  of  Loes-chia  histolytica  cysts  are  not  very 
rare  especially  among  miners. 

Our  observations  do  not  lend  support  to  the  theory  that  amoebic 
dysentery  is  more  common  in  the  hills  than  in  the  plains  of  the 
tropics,  as  we  have  frequently  met  with  it  in  persons  residing  in 
the  low  country.  We  have  noted  the  disease  all  the  year  round, 
but  it  would  appear  to  be  more  prevalent  towards  the  end  of  the 
dry  and  the  beginning  of  the  wet  seasons,  which  probably  merely 
means  that  the  chance  of  drinking  polluted  water  is  greater  at  that 
time,  for  though  the  climatological  characters  are  not  well  under- 
stood, the  disease  appears  to  bear  a  relationship  to  contaminated 
water,  though  flies  are  also  very  important. 

Amoebic  dysentery  is  generally  endemic,  and  does  not  spread 
m  epidemic,  still  less  in  pandemic,  form.  Probably,  as  medical 
science  advances,  it  will  be  found  to  be  of  more  frequent  occurrence 
and  of  wide  distribution. 

/Etiology. — -The  prevalent  opinion  at  the  present  time  is  that 
amoebic  dysentery  is  generally  caused  by  Loeschia  histolytica  Schau- 
dinn,  1903,  but  the  possibility  is  not  excluded  of  there  being  other 
pathogenic  Loeschia.  The  life-histories  of  the  various  species,  as 
far  as  they  are  known,  have  already  been  described  in  Chapter  XVII., 
p.  285.  The  most  common  source  of  infection  is  the  drinking- 
water,  which  has  been  contaminated  by  fasces,  and  contaminated 
food,  and  especially  green  vegetables,  which  may  be  infected  prin- 
cipally by  the  agency  of  flies  carrying  the  cysts  in  their  intestine 
and  depositing  them  upon  the  food,  and  less  frequently  by  actual 
human  faecal  contamination. 

Woodcock  has  called  attention  to  the  importance  of  a  hot,  damp 
climate  as  a  factor  in  the  spread  of  amoebic  dysentery,  as  cysts 
survive  much  longer  in  a  hot,  damp  climate  than  in  a  dry  climate. 
Cysts  cannot  withstand  drying;  while  the  experiments  of  Penfold, 
Woodcock  and  Drew  have  shown  that  cysts  of  Loeschia  histolytica 
can  retain  their  vitality  for  more  than  a  fortnight  in  water. 

There  does  not  appear  to  be  any  well-established  racial  or  age 
predisposition,  but  the  disease  is  less  common  in  women  than  in 
men,  perhaps  because  they  are  in  some  way  less  exposed  to  infection. 

Pathology. — The  spores  of  the  amoebae  enter  the  body  by  the 
drinking-water,  and  by  food  contaminated  with  cysts,  often 
deposited  by  flies,  and  produce  the  young  amoebae  on  arrival 
in    the    large    bowel.     These    young    forms    enter    the    mucosa, 


1828  THE  DYSENTERIES 

probably  by  passing  between  the  cells  lining  Lieberkiihn's  follicles, 
and  then,  entering  the  lymphatics,  make  their  way  through  the 
muscularis  mucosae  into  the  submucosa,  where  they  live  and  feed 
upon  the  tissue  cells,  red  cells,  and  perhaps  leucocytes.  They, 
however,  invade  not  merely  the  tissue  of  the  submucosa,  but  also 
the  radicles  of  the  portal  vein,  and  at  times  the  branches  of  the 
mesenteric  arteries,  in  which  they  may  cause  thrombosis.  From 
the  radicles  of  the  portal  vein  they  may  be  carried  to  the  liver,  and 
cause  hepatitis  and  hepatic  abscess. 

In  the  submucosa  they  induce  cellular  and  cedematous  infiltra- 
tions, which  cause  the  mucosa  to  project  in  the  form  of  small 
elevations,  which  generally  show  a  minute  blackish  point  or  slough 
at  the  summit.  This  slough  is  cast  off,  and  a  small  ulcer  is  formed, 
which  rapidly  deepens  until  it  extends  into  the  submucosa.  These 
ulcers  become  infected  with  bacteria,  and  quickly  extend  by  the  j  oint 
action  of  the  bacteria  and  the  amoeba,  forming  roundish  or  oval 
ulcers  with  undermined  edges;  in  the  latter  case  the  long  axis  of 
the  ulcer  lies  transverse  to  the  direction  of  the  bowel.  These  ulcers 
may  deepen  until  the  muscular  and  the  peritoneal  coats  are  exposed, 
and  even  perforated,  which,  of  course,  leads  to  peritonitis  or  abscess 
formation,  according  to  the  position  of  the  perforation. 

Amoebic  dysentery  would  appear  to  undergo  in  many  cases  no 
spontaneous  cure,  but  may  at  times  remain  quiescent,  forming  a 
type  of  latent  amoebic  dysentery,  which  may  be  found  accidentally 
while  performing  an  autopsy.  When  the  ulcers  heal,  which  they 
do  by  the  formation  of  connective  tissue,  a  distinct  scar  is  formed, 
which  is  often  black  in  colour  from  the  action  of  the  sulphuretted 
hydrogen  of  the  bowel  upon  the  iron  of  the  blood.  When  cica- 
trization takes  place,  the  lumen  of  the  bowel  may  be  constricted, 
causing  stenosis  and  obstinate  constipation.  Peritonitic  adhesions 
are  also  very  common,  binding  the  large  bowel  to  the  viscera  or 
walls  of  the  abdomen  and  pelvis. 

Sometimes,  when  the  infection  is  severe,  the  bowel  becomes 
gangrenous;  at  other  times  the  amoebae  may  be  carried  to  the  liver 
or  other  parts  of  the  body,  and  form  abscesses,  which,  though  most 
commonly  met  with  in  the  liver,  may  still  occur  in  the  spleen,  the 
salivary  glands,  and  elsewhere. 

Morbid  Anatomy.— Usually  the  body  of  a  person  dying  from 
amoebic  dysentery  is  emaciated,  and  the  abdomen  is  sunken. 
Rigor  mortis  begins,  and  passes  off  early,  and  decomposition  sets 
in  quickly.  On  opening  the  abdomen,  it  is  noticed  that  the  tissues 
are  dry,  and  that  a  peculiar  odour  is  perceived;  the  omentum  may 
be  normal  or  congested,  and  may  or  may  not  be  adherent.  The  coils 
of  the  small  intestines  are  usually  normal,  but  may  be  congested. 
The  large  intestine  is  generally  contracted  and  thickened,  but  may 
be  gangrenous  in  places  or  along  its  entire  length.  There  may  be 
perforation  and  purulent  peritonitis.  The  mesocolon  may  be 
congested  and  cedematous,  or  thin  and  fibrous,  and  adhesions  to 
various  organs  may  be  noted.     The  mesocolic  glands  are  usually 


MORBID  ANATOMY 


1829 


enlarged  and  hyperaemic.  The  colon  may  be  found  adherent  to 
the  liver,  the  spleen,  or  the  wall  of  the  pelvis,  while  internally  the 
mucosa  will  be  found  to  be  reddened  and  inflamed,  and  to  show 
more  or  less  numerous  areas  of  ulceration  and  infiltration.  These 
areas  are  most  commonly  found  in  the  caecum,  the  hepatic  flexure, 
and  the  sigmoid  colon,  but  may  occur  anywhere  along  the  course 
of  the  large  intestine.  In  places  small  nodules  surrounded  by  a  ring 
of  dilated  vessels  may  be  observed,  between  which  the  mucosa  may 
or  may  not  be  normal,  while  the  nodules  may  show  superficial  or 
deep  ulceration.  Deeper  circular  or  oval  ulcers  may  be  noted  with 
their  surface  covered  with  a  dark  reddish  slough,  their  edges  under- 


Fig.  762. — The  Colon  in  a  Case  of  Amoebic  Dysentery. 

mined,  and  their  base  formed  by  the  muscular  coats.  In  the  case 
of  the  oval  ulcers,  the  longer  diameter  lies  transverse  to  the  long 
diameter  of  the  bowel,  as  a  rule.  The  peritoneal  coat  may  be 
normal,  inflamed,  or  softened  and  gangrenous.  Usually  the  mus- 
cular coat  is  thickened,  as  are  the  remains  of  the  submucosa. 
Scrapings  from  these  ulcers  reveal  blood  cells,  leucocytes,  bacteria, 
and  amoebae.  The  small  intestine  may  show  small  bright  red 
nodules,  and  the  Peyer's  patches  may  be  enlarged.  The  vermiform 
appendix  is  usually  normal,  but  occasionally  may  be  ulcerated. 

The  liver  is  often  fatty,  but  may  be  congested  and  inflamed,  or 
may  show  one  or  more  abscesses.     The  pancreas  is  generally  normal, 


1830  THE  DYSENTERIES 

but  may  be  cirrhotic  in  chronic  cases.  The  spleen  is  also  usually 
normal,  but  may  contain  an  abscess;  the  kidneys  often  show 
signs  of  parenchymatous  inflammation.  The  heart  and  lungs  are 
generally  normal,  but  the  former  may  be  fatty  or  show  brown 
atrophy,  and  the  latter,  especially  the  right  lung,  may  show  a 
hepato-pulmonary  abscess. 

Symptomatology. — The  symptomatology  of  amoebic  dysentery 
may  be  classified  into: — 

1.  Acute  Type. 

2.  Chronic  Type. 

3.  Latent  Type. 

4.  Mixed  Type. 

1.  Acute  "Type. — The  onset  is  abrupt,  but  may  occasionally  be 
preceded  for  a  few  days  by  slight  diarrhoea,  alternating  with  con- 
stipation. Pain  is  felt  in  the  lower  part  of  the  abdomen,  which 
may  become  very  severe,  while  the  motions  are  attended  with  much 
griping  and  straining.  These  motions,  which  rarely  exceed  thirty 
per  diem,  contain  blood  and  mucus,  and  occasionally  greenish 
material,  and  when  examined  by  the  microscope  reveal  leucocytes, 
mucus,  Charcot-Leyden  crystals,  amoebae,  bacteria,  and  at  times 
shreds  of  tissue. 

The  tongue  is  moist,  and  often  coated  with  a  white  fur,  and  there 
is  usually  anorexia,  and  there  may  be  nausea  and  vomiting,  while 
digestion  is  usually  much  impaired.  The  abdomen  is  sunken,  the 
liver  and  spleen  normal,  but  tenderness  is  felt  on  pressure  along  the 
whole  or  a  part  of  the  large  bowel. 

The  examination  of  the  heart  and  lungs  reveals,  as  a  rule,  no 
abnormality,  but  the  pulse  and  respirations  are  quickened.  The 
microscopical  examination  of  the  blood  usually  shows  that  the  red 
cells  are  diminished,  and  sometimes  that  there  is  leucocytosis 
(upwards  of  20,000  per  cubic  millimetre),  and  at  times,  as  first 
pointed  out  by  Billet,  the  number  of  eosinophils  is  distinctly 
increased,  even  when  there  is  no  concomitant  helminthiasis. 

The  urine  is  diminished  in  quantity,  and  sometimes  contains 
albumen  and  casts;  but  the  skin  is  generally  normal,  though  there 
is  often  some  fever  of  a  remittent  type,  which,  however,  may  be 
entirely  absent. 

When  thetemperature  fallsto  normal,  and  the  pain  and  tenderness 
abate,  these  may  be  favourable  signs,  or  may  be  merely  a  prelude 
to  a  gangrenous  complication  or  a  haemorrhage.  If  recover}*  is  to 
take  place,  the  motions  become  less  frequent  and  more  faeculent ,  and 
contain  less  blood  and  mucus,  and  gradually  improve  until  normal 
motions  are  passed.  If  death  takes  place,  which  usually  happens 
about  the  end  of  the  first  week,  and  ten  days  from  the  commence- 
ment, it  is  generally  caused  by  exhaustion,  or  much  more  rarely  by 
perforation  and  peritonitis  or  haemorrhage. 

2.  Chronic  Type. — This  may  follow  an  acute  attack,  or,  in  many 
cases,  may  begin  .quite  insidiously,  the  symptoms  being  merely 


SYMPTOM  A  TO  LOGY 


1831 


those  of  diarrhoea,  associated  at  times  with  abdominal  pain  and  the 
passage  of  faeculent  motions  mixed  with  mucus  and  sometimes 
streaked  with  blood,  while  in  the  intervals  between  these  exacerba- 
tions there  may  be  constipation.  An  exacerbation  is  usually 
ushered  in  by  pain  in  the  abdomen,  slight  fever,  griping,  and 
tenesmus,  and  passage  of  blood  and  mucus  in  the  motions,  while 
the  faeces  contain  small  greyish  masses,  in  which  the  amoebae  may 
be  found.  The  number  of  motions  per  diem  is  not  excessive,  and 
may  be  only  twelve  to  fourteen.  Usually  they  are  passed  somewhat 
more  frequently  at  night  than  in  the  day.  Gangrenous  complica- 
tions may,  however,  occur  at  any  time  in  the  course  of  an  exacerba- 
tion, or,  indeed,  during  any  stage  of  this  type,  when  large  sloughs, 
smelling  offensively,  may  be  passed  with  the  motions.  Chronic 
dysentery  may  persist  for  years,  and  cause  the  patient  to  slowly 
emaciate.  The  blood,  as  shown  by  Chalmers  and  Archibald,  often 
shows  an  increase  in  the  large  mononuclears. 


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#  Ipecacuanha  Treaimenl  begun.         +  Rise  due  to  Vaccination.           £  Patient  Convalescent. 

Fig.  763. — Temperature  Chart  of  a  Case  of  Amcebic  Dysentery 
complicated  by  hepatitis. 


3.  Latent  Type. — We  have  several  times  met  with  cases  in  which, 
though  dysenteric  symptoms  were  absent,  still,  amoebae  were  present 
in  the  motions,  and  others  in  which  dysenteric  ulcers  were  only  dis- 
covered accidentally  on  post-mortem  examination,  the  death  being 
due  to  other  causes.  This  latent  condition  is  important,  as  it  can 
easily  lead  to  an  acute  attack  or  to  liver  abscess,  and  no  doubt  these 
"  entamoebic  carriers,'  as  has  been  noted  by  Martini,  Vincent,  and 
others,  are  a  source  of  the  dissemination  of  the  infection. 

4.  Mixed  Type.- — These  are  cases  in  which  there  is  a  mixed  in- 
fection of  Loeschia  histolytica  and  the  Shiga-Kruse  bacillus. 
Usually  in  these  cases  the  motions  are  numerous  from  the  first,  and 
there  is  considerable  fever,  nausea,  vomiting,  and  great  constitu- 
tional disturbance.  The  motions  are  apt  to  be  very  offensive,  and 
to  contain  sloughs,  indicating  a  gangrenous  condition  of  the  bowel. 
Exhaustion  may  come  on  early,  and  the  patient  may  die  delirious 
or  comatose,  or,  more  rarely,  from  peritonitis,  with  or  without  per- 
foration. More  rarely  improvement  sets  in,  and  the  disease  becomes 
chronic. 


1832  THE  DYSENTERIES 

Amoebic  Fever  or  General  Amcebiasis. — This  term  has  been  applied 
to  certain  cases  of  L.  histolytica  infections  in  which  there  is  fever,  but 
no  dysenteric  symptoms  and  no  sign  of  hepatitis.  A  few  cysts  are 
generally  found  in  the  stools,  and  emetine  induces  a  prompt  dis- 
appearance of  the  fever. 

Complications. — The  most  usual  complication  is  hepatitis  and 
hepatic  abscess;  more  rarely  gangrene  of  the  bowel  and  peritonitis 
may  supervene  during  an  attack;  while  haemorrhage  is  a  most 
unusual  complication.  The  hepatitis  is  recognized  by  the  tender- 
ness in  the  right  hypochondrium  and  by  the  rise  in  the  temperature, 
but  it  and  the  hepatic  abscess  will  be  discussed  in  a  subsequent 
chapter.  In  Ceylon  we  have  observed  cases  of  mixed  infection, 
dysentery  and  enteric,  the  two  infections  developing  apparently 
contemporaneously. 

Sequelae. — The  important  sequel  to  an  attack  of  amoebic  dysen- 
tery is  liver  abscess,  but  abscesses  in  other  parts  of  the  body  such 
as  the  spleen  may  be  met  with.  Stenosis  of  the  sigmoid  colon,  due 
to  cicatrization  of  the  healing  ulcers,  is  well  known,  and  will  be 
dealt  with  under  the  heading  of  Bacterial  Dysentery.  Sprue  is 
often  said  to  be  a  sequel  of  dysentery,  but  this  must  be  considered 
to  be  doubtful.  Certain  authors  have  described  a  persistent 
bradycardia. 

Diagnosis. — The  diagnosis  between  bacterial  and  amoebic  dysen- 
tery by  clinical  phenomena  only  is,  in  our  opinion,  impossible  in 
most  cases,  though  several  observers  have  attempted  to  define 
some  differential  points.  These  authors  state  that  amoebic 
dysentery  is  to  be  distinguished  from  bacillary  dysentery  by  its 
chronic  course,  its  rare  pyrexia,  and  the  absence  of  toxic 
symptoms,  while  it  is  often  followed  by  liver  abscess.  Apart  from 
the  last  feature,  the  other  so-called  differential  signs  have,  in 
our  experience,  no  importance,  as  we  have  come  across  ex- 
tremely acute  cases  of  amoebic  dysentery  with  fever  and  toxic 
symptoms. 

The  only  certain  method  of  diagnosis  is  by  the  discovery  of 
Loeschia  histolytica  in  the  stools,  and  this  should  be  done  by  picking 
out  and  examining  any  mucus  which  may  be  seen.  It  is  of  practical 
importance  to  distinguish  between  L.  histolytica  and  the  harmless 
L.  coli,  and  this  differentiation  may  at  times  be  difficult.  The  former 
is  often  larger,  and  possesses  an  ectoplasm,  which  is  easily  differ- 
entiated from  the  endoplasm;  it  is  more  actively  motile  than 
L.  coli,  and  often  contains  erythrocytes,  which  is  the  most  important 
character.  The  nucleus  of  L.  histolytica  is  eccentric,  small,  and 
generally  indistinct,  does  not  stain"  deeply,  and  has  very  little 
chromatin  (see  p.  313). 

In  order  to  expedite  the  diagnosis  the  French  method  is  to  add 
a  drop  of  a  1  per  cent,  solution  of  methylene  blue  to  the  mucus 
before  placing  on  the  coverslip,  when  the  pus  and  epithelial  cells 
will  be  stained,  and  the  amoebae  more  easily  recognized  as  unstained, 
clear  objects. 


DIAGNOSIS  1833 

The  diagnosis  of  latent  cases  and  of  carriers  is  based  on  the  finding 
of  the  characteristic  histolytica  cysts  containing  four  nuclei.  It  is 
important  to  note  that  cysts  are  not  often  seen  during  the  acute 
attacks  with  blood  and  muco-pus. 

In  the  search  for  cysts,  only  a  small  quantity  of  material  should  be  used 
well  diluted  with  saline.  The  addition  of  a  little  iodine  solution  is  useful,  as 
it  makes  the  nuclei  more  visible.  Dead  cysts  are  easily  stained  by  eosin, 
while  live  ones  are  not. 

Cysts  of  Loeschia  histolytica  have  to  be  differentiated  principally  from  cysts 
of  L.  coli,  Vahlkamfia  nana,  amoebae  of  Limax  type,  Chilomastix,  Lamblia,  and 
from  the  structures  known  as  Blastocystis  hominis.  The  characters  of  all 
these  cysts  have  been  given  in  detail  in  Chapters  XVII.  and  XVIII.  For 
diagnostic  purposes  it  is  sufficient  to  remember  the  following: — 

I.  Cysts  of  L.  histolytica  in  fresh  preparations  from  stools  mixed  with  salt 
solution  appear  as  spherical,  greenish,  very  refractile  bodies  10-14  microns 
in  diameter,  containing  four  nuclei  (at  times  two)  and  one  or  two  highly 
refractile  homogeneous  rods  known  as  chromidial  bodies.  Several  vacuoles 
may  be  present.  Dobell  and  others  have  called  attention  to  the  fact  that  the 
size  may  vary  a  great  deal,  there  being  races  of  histolytica  (minuta  type) 
giving  rise  to  much  smaller  cysts,  7  to  9  microns,  and  others  to  much  larger 
ones,  12  to  20  microns. 

II.  Cysts  of  L.  coli  vary  between  15  and  20  microns,  are  rarely  larger,  occasion- 
ally smaller.  They  are  clear  spherical  bodies  of  sharp  outline,  less  refractile 
than  those  of  L.  histolytica.  They  contain  8  nuclei,  which  appear  as  faint 
granular  rings  with  a  central  dot  (karyosome).      Often  only  one  vacuole. 

III.  Cysts  of  Vahlkamfia  nana  are  oval  or  spherical  structures  7  to  9  microns 
in  diameter,  with  one,  two,  or  four  nuclei,  very  rarely  eight;  in  addition,  a 
variable  number  of  highly  refringent  granules  and  sometimes  a  large  dull 
inclusion  (glycogen).  There  is  absence  of  chromidial  bodies,  and  this  dis- 
tinguishes the  cyst  at  once  from  the  small  ones  of  L.  histolytica. 

IV.  Cysts  of  amoebae  of  Limax  type  are  found  in  stale  stools,  are  always 
small,  uninucleated,  and  often  have  a  thick  wall  of  brownish  colour. 

V.  Cysts  of  Chilomastix  mesnili  are  often  lemon-shaped,  and  are  charac- 
terized by  the  presence  of  the  chromatic  rod  (parabasal). 

VI.  Cysts  of  Giardia  intestinalis  are  easily  recognized  by  their  egg-shaped 
appearance;  they  are  about  14  microns  in  length  and  very  transparent,  so 
that  the  lamblia  can  be  seen  within  it  with  the  characteristic  central  paired 
rod-like  structure  in  which  originate  the  four  pairs  of  flagelli. 

VII.  Cysts  of  Oicomonas,  Bodo,  Prowazekia  are  very  small,  spherical, 
6-8  microns  in  diameter,  uninucleated,  very  similar  to  those  of  Amoeba  limax, 
but  the  wall  is  not  so  thick  nor  of  brownish  colour,  and  the  outline  is  more 
regular.  Sometimes,  however,  it  is  impossible  to  distinguish  these  cysts  from 
those  of  Amoeba  limax.  They  can  always  be  differentiated,  however,  from 
those  of  L.  histolytica,  as  they  are  very  small  and  uninucleated. 

VIII.  The  structures  known  as  Blastocystis  hominis — considered  by  some 
authors  to  be  vegetal  organisms — -are  more  or  less  spherical,  5  to  15  microns 
in  diameter,  with  a  more  delicate  capsule  than  the  cysts  of  Loeschiae,  and 
contain  a  very  large  vacuole,  which  reduces  the  cytoplasm  to  a  narrow  rim 
at  one  pole  or  both  poles  of  the  cyst. 

IX.  Iodine  cysts  (I-cysts).  These  structures,  described  by  Wenyon  and 
O'Connor,  are  generally  roundish  or  oval,  varying  between  6  and  16  microns 
in  diameter,  and  show  frequently  a  iodophilic  body,  which  tends  to  be 
rounded  or lobed. 

To  facilitate  the  detection  of  cysts  when  these  are  in  very  small 
numbers  various  methods  have  been  suggested,  though  in  practice, 
as  shown  by  Miss  Porter,  such  methods  take  a  great  deal  of  time,  and 
the  results  are  not  much  better  than  those  obtained  by  the  simple 
immediate  microscopical  examination  of  several  preparations.     It 


1834  THE  DYSENTERIES 

is  of  advantage  to  give  the  patient  a  saline  purge,  and  then  one  of 
the  so-called  enrichment  methods  of  Cropper  and  others  may  be 
used :  about  I  gramme  of  faecal  matter  is  mixed  with  30  c.c.  of  salt 
solution  in  a  conical  glass,  and  ether  added  in  the  amount  of  about 
10  to  20  per  cent.  The  cysts  are  generally  found  in  the  supernatant 
fluid,  and  may  be  collected  by  centrifuging  it. 

Cysts  maintain  all  their  morphological  characters  for  a  very  long 
period  in  faecal  matter  mixed  with  a  formalin  solution  (2  per  cent.). 

The  presence  in  dysenteric  stools  of  Charcot-Leyden  crystals,  as  emphasized 
by  Acton,  points  to  the  condition  being  of  amoebic  origin  rather  than  bacterial, 
especially  if  there  is  scanty  cellular  exudate  with  preponderance  of  mono- 
nuclears. 

Prognosis. — The  prognosis  in  a  case  of  amoebic  dysentery  must 
always  be  guarded,  as  there  is  the  possibility  of  hepatic  abscess 
as  sequela  of  the  mildest  case,  and  the  cure  induced  by  emetine  and 
ipecacuanha,  though  striking,  is  often  merely  clinical,  complete 
sterilization  not  being  attained.  The  prognosis  is  worst  in  the 
gangrenous  cases,  better  in  the  acute,  and  still  better  in  the  mild 
chronic  cases,  but  the  danger  of  latency  after  an  apparent  cure 
must  be  remembered.  In  the  acute  type  hiccough  is  an  un- 
favourable sign,  often  indicating  the  approach  of  exhaustion  and 
death. 

Treatment. — It  is  of  the  utmost  importance  that  the  patient 
should  be  placed  at  rest  in  bed.  For  the  same  purpose  the  urine 
bottle  and  the  bed-pan  must  be  used.  It  is  advisable  to  relieve  the 
severe  griping  and  straining  by  either  a  hypodermic  injection,  of 
morphia  or  by  small  enemata  of  40  minims  of  laudanum  in  1  ounce 
of  mucilage  of  starch,  or  by  using  a  morphia  (gr.  £),  or  codeine 
(gr.  I)  suppository. 

At  first  the  bowels  should  be  swept  clean  by  a  dose  of  castor  oil 
(3iv.  to  5vi.),  with  or  without  a  few  minims  of  liquor  opii  sedativus, 
or  a  few  doses  of  saline  may  be  given  during  the  first  twenty-four 
hours  (see  Bacillary  Dysentery).  After  the  castor  oil  has  acted,  or 
simultaneously,  the  emetine  treatment  should  be  begun.  One-third 
to  half  a  grain  of  emetine  hydrochloride,  dissolved  in  sterile  normal 
saline  solution,  should  be  administered  as  a  hypodermic  injection 
two  or  three  times  a  day  for  several  days.  Emetine  hydrobromide 
may  also  be  used  in  the  same  dosage,  but  it  is  not  quite  so  soluble. 
These  drugs  may  be  obtained  in  sterile  tubes  ready  for  injection. 
We  have  never  seen  any  bad  effects  on  the  heart  from  the  adminis- 
tration of  emetine,  but  we  have  met  with  cases  of  dermatitis  prob- 
ably due  thereto,  while  Dale  and  Low  have  noted  diarrhoea  after 
prolonged  administration. 

A  combined  subcutaneous  and  oral  administration  of  emetine  as  recom- 
mended by  Wenyon  and  O'Connor  (one  grain  emetin  by  injection  in  the 
morning  and  a  \  grain  emetine  tablet  at  night)  answers  well,  especially  in 
subacute  an    chronic  cases,  and  in  carriers. 

If  emetine  cannot  be  obtained,  then  ipecacuanha  should  be  administered 
in  5-grain  doses  every  three  or  six  hours,  or  in  larger  doses  (gr.  x.  to  xx.)  twice 


TREATMENT  1835 

daily,  given  either  in  the  form  of  '  membroids  '  or  as  pills  coated  with  salol 
varnish  or  keratin.  Our  experiments  in  vitro  tend  to  show  that  membroids 
and  salol  varnish  do  not  dissolve  freely  in  peptic  juice,  while  they  do  so  in 
pancreatic  juice.  The  salol  varnish  was  very  efficient,  but  care  must  be  taken 
that  too  thick  a  coating  is  not  used,  as  it  may  not  dissolve  in  pancreatic  juice. 
Martindale's  method  of  stearin-coated  pills  is  good.  In  this  way  the 
nauseating  effects  of  the  ipecacuanha  are  often  avoided  without  diminishing 
its  efficiency,  which  is  the  result  of  using  the  de-emetized  drug.  Rarely  the 
membroids  and  salol  varnished  pills  may  be  passed  unaltered  in  the  motions, 
and  in  such  cases  ipecacuanha  may  be  given  in  suspension  in  mucilage  and 
chloroform  water  or  in  cachets  or  pills  (gr.  x.  to  xx.  twice  a  day),. and  should 
be  preceded  a  quarter  of  an  hour  by  a  dose  of  15  minims  of  tincture  of  opium, 
in  order  to  prevent  the  possible  vomiting. 

With  regard  to  ipecacuanha,  it  is  of  great  importance  to  use  the  best  Brazilian, 
which  should  contain  72  per  cent,  of  emetine  (methyl-cephaeline)  in  its  total 
alkaloids,  the  other  alkaloids  being  cephaeline  26  per  cent.,  and  psychotrine 
2  per  cent.;  on  the  other  hand,  Carthagena  ipecacuanha  contains  cephaeline 
57  per  cent,  and  emetine  only  40  per  cent.  The  powdered  ipecacuanha  should 
have  an  alkaloidal  strength  of  2  per  cent. 

Emetine  and  bismuth  iodide  has  been  introduced  by  Dale,  and  its 
efficacy  has  been  confirmed  by  Low  and  Dobell  and  numerous 
other  observers,  including  ourselves.  It  is  especially  useful  in  the 
treatment  of  carriers,  inducing  at  times  a  complete  disappearance  of 
the  cysts.  It  is  useful  also  in  amoebic  hepatitis  and  general  amcebia- 
sis.  It  is  given  in  gelatine  capsules,  one  capsule  containing  gr.  iii., 
at  night  for  two  or  three  weeks,  or  salol-coated  tablets  may  be 
used.  A  shorter  course  seldom  induces  a  cure.  Not  rarely  the 
drug  produces  nausea  and  at  times  actual  vomiting;  in  such  cases 
the  same  precautions  may  be  taken  as  when  giving  ipecacuanha. 

When  the  acute  symptoms  have  passed  away,  intestinal  irriga- 
tions are  useful,  and  should  be  administered  every  other  day,  or 
once  or  twice  daily.  We  generally  use  a  solution  of  tannic  acid 
(3  to  5  in  1,000),  or  a  solution  of  the  bihydrochloride  of  quinine  in 
varying  strength  from  1  in  5,000  to  1  in  750.  About  \  to  3  pints 
should  be  very  slowly  injected  by  gravity  from  a  glass  douche 
vessel  by  means  of  a  long  soft  rectal  tube  well  greased  with  boric 
vaseline.  This  injection  may  be  preceded  by  a  cocaine  or  morphine 
(gr.  \)  suppository  introduced  half  an  hour  previously. 

Other  substances  used  for  rectal  irrigations  are: — Acetozone  (1  in  2,000); 
alphozone  (1  in  2,000);  argentum  nitras  (1  in  2,000  or  1  in  1,000),  useful  in 
some  very  chronic  cases;  protargol  (1  in  500).  Creosote  is  recommended  by 
Zanardini,  and  may  be  used  by  injecting  2  pints  of  1  in  300  or  1  pint  of  1  in 
100.  The  injection,  however,  may  be  followed  by  symptoms  of  absorption — - 
e.g.,  dyspnoea  and  faintness.  A  solution  of  sodium  hypochlorite  may  be 
used,  2  pints  of  8  to  12  in  1,000  being  recommended  by  Vincent  once  or 
twice  a  day,  which  is  also  useful  for  amoebic  carriers. 

In  gangrenous  dysentery  the  only  chance  of  saving  the  life  of  the  patient 
is  to  perform  the  operation  of  appendicostomy,  and  irrigate  the  whole  lower 
bowel  with  quinine  lotion  (1  in  1,000)  or  collargol  (1  in  500).  The  details  of 
this  operation  are  given  under  the  heading  Bacterial  Dysenteries. 

With  regard  to  the  treatment  of  symptoms,  the  most  important 
is  the  relief  of  pain  by  hypodermic  injections  of  morphia  or  by 
fomentations  sprinkled  with  opium  and  applied  to  the  abdomen. 
As  the  case  progresses  favourably,  a  bismuth  mixture  or  tannalbin 


1836  THE  DYSENTERIES 

in  cachets  (gr.  xx.  every  two  to  four  hours)  may  be  given,  while  the 
irrigation  may  be  diminished  and  stopped,  and  finally  a  tonic  may 
be  prescribed. 

"\Ye  are  strongly  of  opinion  that  the  ipecacuanha  or  the  emetine  should 
continue  to  be  given  in  smaller  doses  long  after  the  dysenteric  symptoms  have 
disappeared,  in  order  to  prevent  relapses,  and  possibly  also  the  development 
of  a  liver  abscess,  which  is  the  most  dangerous  sequel.  Among  the  other 
drugs  which  have  been  recommended  in  the  treatment  of  amoebic  dysentery 
are  Simaruba  officinalis  and  the  so-called  Kho-sam  powder. 

The  former  is  recommended  by  Manson  to  be  used  as  a  decoction  which  is 
prepared  by  taking  simaruba  bark,  pomegranate  fruit-rind,  and  gum  arabic, 
15  grammes  of  each,  and  placing  in  a  litre  of  warm  water,  which  is  boiled  till 
reduced  to  half  its  bulk,  and  of  this  decoction  1  ounce  is  taken  three  or  four 
times  a  day.  Shepherd  and  Lillie  have  cured,  using  preparations  of  chaparro 
or  simaruba,  34  cases  out  of  80  cases  of  Loeschial  carriers,  refractory  to  emetine. 

Nixon  and  Sellards  and  Mclver  have  had  good  results  by  using  preparations 
of  Castela,  a  genus  of  the  Simarubaceae. 

The  Kho-sam  powder  is  derived  from  the  berries  of  Brucia  antidys- 
enterica  and  B.  sumatrana,  which  grow  in  Indo-China.  It  is  administered 
in  pill  form,  1  grain  being  given  two  to  four  times  a  day.  Cinnamon  has  been 
often  used  in  the  past,  and  the  compound  extract  of  garcinia  known  also  by  the 
trade  name  of  amibiasine  is  praised  by  several  authors. 

If  cicatrization  of  the  colon  results  with  stenosis,  then  sigmoid- 
oscopy must  be  performed,  and  the  condition  treated  as  described 
under  Bacterial  Dysentery.  Liver  abscess  is  considered  separately. 
Abscesses  in  other  parts  of  the  body — e.g.,  the  spleen — are  rarely 
met  with,  though  it  is  possible  that  some  of  the  inexplicable  deep- 
seated  abscesses  may  have  their  causation  in  amoebae. 

The  diet  should  be  the  same  as  that  to  be  described  presently 
under  the  heading  Bacterial  Dysentery.  During  convalescence  the 
food  must  be  slowly  and  carefully  increased,  no  acid  or  very  warm 
substances  being  allowed. 

Prophylaxis.- — The  prophylaxis  consists  in  the  drinking  of  only 
boiled  and  filtered  water,  and  the  avoidance  of  salads  and  uncooked 
vegetables  and  the  prevention  of  fly  infestation  of  food. 

Stools  of  dysentery  patients  and  carriers  should  be  disinfected 
with  cresol,  1  in  10. 

Amoebae,  probably  non-parasitic,  were  shown  to  exist  in  the 
drinking-water  in  Manila,  and  it  was  found  that  copper  sulphate 
and  filter-beds  were  useless.  The  only  safeguard  was  to  sterilize 
the  water  by  boiling. 

(b)  Laveranic  Dysentery. 

Definition. — An  acute  enteritis  and  colitis  caused  by  Laverania  malaria 
Laveran,  and  characterized  by  high  fever,  associated  with  the  passage  of 
frequent  motions  containing  blood  and  mucus. 

Symptomatology. — The  attack  usually  begins  suddenly,  with  high  fever, 
great  distress,  and  prostration.  The  tongue  is  coated,  the  abdomen  tender, 
and  many  motions  are  passed  containing  blood  and  mucus.  The  spleen  may 
or  may  not  be  palpable.  Unless  correctly  treated,  the  condition  becomes 
serious,  and  rapidly  leads  to  the  death  of  the  patient. 

Diagnosis. — The  routine  examination  of  the  blood  in  all  cases  of  tropical 
disease  will  prevent  mistakes  being  made,  as  the  presence  of  numerous  sub- 
tertian  parasites  in  the  blood,  with  absence  of  amoebae  and  dysenteric  bacilli 
in  the  stools,  will  reveal  the  nature  of  the  complaint.      It  should  be  kept  in 


BALANTIDTC  DYSENTERY  1837 

mind,  however,  that  most  cases  of  dysenteric  colitis  in  malarial  patients  are, 
in  reality,  of  amoebic  and  bacillary  origin,  and  not  of  Laveranic  origin. 

Treatment. — Quinine  should  be  given  in  large  doses,  best  by  intramuscular 
injection,  and  the  intestinal  symptoms  first  treated  with  castor  oil  or  salines, 
and  then  with  astringents,  such  as  bismuth  subnitrate,  tannalbin,  and  salol. 

(c)  Leishmanic  Dysentery. 

Definition. — An  acute  enteritis  and  colitis  caused  by  Leishmania  donovani 
Laveran  and  Mesnil,  and  characterized  by  the  passage  of  blood  and  mucus  in 
the  motions. 

Symptomatology  and  Treatment.— As  already  mentioned  in  the  chapter 
on  Kala-Azar,  dysenteric  symptoms  closely  allied  to  true  dysentery  may 
appear  during  the  course  of  that  disease,  and  must  be  treated  on  the  same 
lines  as  those  laid  down  lor  the  treatment  of  kala-azar,  together  with  sympto- 
matic treatment  as  indicated  above.  The  diagnosis  is  based  on  the  presence 
of  Leishmanic  bodies  in  the  spleen  or  liver  and  absence  of  amoebae  and  dysentery 
bacilli  in  the  stools.  True  bacterial  or  amoebic  dysentery  is  far  from  rare  in 
cases  of  kala-azar. 

(d)  Ciliar  Dysenteries. 

One  variety  of  the  ciliar  dysenteries  may  be  briefly  described — 
viz.,  that  caused  by Balantidium  coli  Malmsten.  Other  less  known 
causes  axeColpoda  cucullus  Schutz, Balantidium minutum  Schaudinn, 
Nyctotherus  faba  Schaudinn,  Nyctotherus  giganteus  P.  Krause. 
Other  possible  causes  are  Uronema  caudatum  Dujardin,  Balantidium 
italicum  Sangiorgi  and  Ugdulena,  and  Nyctotherus  africanus 
Castellani.     For  description  of  these  parasites  see  p.  544. 

(e)  Balantidic  Dysentery. 

Definition. — An  acute  or  chronic  ulceration  of  the  large  intestine 
caused  by  Balantidium  coli  Malmsten,  1857. 

History. — Leeuwenhoek  originally  discovered  the  parasite  Balan- 
tidium coli,  but  Malmsten  described  and  named  it.  The  latter 
observer  found  it  in  the  motions 
of  a  man  suffering  alternately 
from  diarrhoea  and  constipation. 
Other  cases  have  been  recorded 
by  Stieda,  Henschen,  Treille, 
Graziadei,  Railliet,  Blanchard, 
Collmann,  Strong,  Bowman, 
Manlove,  Mason,  and  others. 

Climatology. — The  disease  is 
known  to  occur  in  man  in  the 

Philippine  Islands,  Japan,  and 

t-  v.-i      ±1.      ~„\-„„;+„    ir     Fig.    76^a. — Balantidium     Coli     in 

Europe,    while  the  parasite   is      HuM7AN3FvECES  (x  520  diameters). 

said  to  be  constantly  found  in 

pigs.     We  have  seen  a  case  in  (Photomicrograph.) 

Ceylon. 

^Etiology  —  The  cause  of  the  disease  is  Balantidium  coli  Malmsten, 
which  may  be  different  from  the  parasite  found  in  pigs  (for  descrip- 
tion of  the  parasite  see  Chapter  XVIII.,  p.  547). 

Pathology.— The  method  of  infection  is  unknown.     The  parasite 


1838  THE  DYSENTERIES 

appears  to  enter  the  mucosa,  in  which  it  wanders,  causing  an  in- 
flammatory reaction  and  ulceration. 

Morbid  Anatomy. — This  has  been  investigated  principally  by 
Strong.  The  intestine  may  show  a  diphtheritic  false  membrane, 
with  often  deep  burrowing  ulcers  in  the  rectum  and  colon  indis- 
tinguishable from  those  of  amoebic  dysentery.  On  microscopical 
examination  the  parasites  can  be  found  in  the  mucosa  surrounded 
by  a  round-celled  infiltration,  and  several  observers  have  noted  a 
marked  eosinophilia  of  the  intestinal  wall. 

Symptomatology. — The  disease  is  insidious  in  its  onset,  being 
marked  by  attacks  of  diarrhoea,  alternating  with  constipation  and 
vomiting,  with  anorexia  and  at  times  the  passage  of  blood  and 
muco-pus  in  the  motions.  (Edema  of  the  face  and  limbs  may  set 
in,  and  death  result  from  exhaustion. 

In  our  patient,  a  little  native  girl,  there  was  rather  high  fever, 
with  persistent  diarrhoea,  great  wasting,  and  severe  anaemia.  No 
blood  in  the  motions.  The  Balantidia,  which  were  abundant,  were 
associated  with  numerous  Trichomonata  and  Oicomonas ;  moreover, 
the  patient  harboured  various  worms,  ova  of  Ancylostoma  duodenale, 
Ascaris  lumbricoides ,  and  Trichuris  trichiura  being  present.  Some 
of  the  symptoms  may  have  been  caused  by  these  parasites. 

Complications. — The  parasite  may  enter  the  liver  and  form  cysts. 
It  may  be  associated  with  other  parasites — Amcebce,  Trichomonata, 
Oicomonata,  etc. 

Treatment. — The  symptomatic  treatment  laid  down  for  amoebic 
dysentery  may  be  tried,  beginning  with  castor  oil  or  salines,  and 
followed  by  intestinal  irrigations  of  tannic  and  boric  acids  or 
quinine.  Ipecacuanha  and  emetine  may  be  administered  as  de- 
scribed for  amoebic  dysentery.  Large  rectal  injections  of  a  solution 
of  methylene  blue  (1  in  3,000),  combined  with  the  internal  adminis- 
tration of  the  same  drug  in  1  or  2  grain  doses  in  cachets  or  pills,  may 
also  be  tried.     Oil  of  chenopodium  has  been  recommended. 

Some  authorities  give  Salvarsan,  by  intravenous  injection. 

Prophylaxis. — It  is  not  certain  that  the  parasite  found  in  the  pig 
is  the  same  as  the  human  parasite,  and,  further,  the  method  of  in- 
fection being  quite  unknown,  no  useful  remarks  can  be  made  with 
regard  to  prophylaxis. 

{/)  Spirochaetic  Dysentery. 

This  type  of  dysentery  was  first  described  by  Le  Dantec.  It  has  not  been 
generally  accepted,  as  spirochaetes  may  be  found  in  cases  of  typical  bacterial 
and  amoebic  dysentery  and  even  in  normal  stools  in  which  Spiroschaudinnia 
eugyrata  Werner,  emendavit  Fantham,  is  commonly  met  with.  It  is  very 
probable,  however,  in  our  opinion,  that  there  may  be  pathogenic  intestinal 
spirochaetes  capable  of  giving  rise  to  dysenteric  symptoms.  In  a  case  observed 
by  one  of  us  preparations  from  the  muco-pus  were  teeming  with  spirochetes, 
while  amoebae  and  ciliates  were  absent,  and  the  further  bacteriological  ex- 
amination showed  absence  of  dysentery  bacilli.  Emetine  and  serum  treat- 
ment had  no  effect,  and  the  patient  made  a  very  slow  recovery. 

Remarks. — A  mistake  not  rarely  made  is  to  recognize  as  spirochaetes  the  un- 
dulating forms  of  a  germ  found  by  Castellani  in  Ceylon,  and  described  by  him 
in    1910,    under   the   term   of    Spirillum  {Vibrio,    Vibrioihrix,    Spirobacillus) 


SPIROCHMTIC  DYSENTERY  1839 

zeylanicum,  in  the  Philippine  Journal  of  Science,  vol.  v.,  No.  2,  Section  B, 
'  Medical  Sciences,'  July,  1910. 

The  generic  classification  of  this  germ  is  most  difficult,  as  it  is  extremely 
polymorphic,  the  same  preparation  showing  bacillary,  vibrionic,  undulating 
forms. 

At  times  coccus-like  and  also  fairly  large  spherical  bodies  are  seen  and 
claviform  swellings,  and  Castellani  has  recently  created  a  new  genus  for  it, 
vibriothvix,  the  name  of  the  organism  becoming,  therefore,  Vibriothrix  zeylanica 
Castellani,  1910.  This  germ  is  found  also  in  Europe,  as  recently  shown  by 
Castellani,  Spagnuolo  and  Russo,  by  Taylor,  Ghiron,  and  by  Douglas. 

Morphology. — The  best  way  to  see  the  characteristics  of  the  germ  is  to 
make  a  preparation  from  the  water  of  condensation  of  a  glucose  agar  tube 
inoculated  with  it.  In  the  same  preparation  forms  so  different  in  shape 
may  be  met  with,  that  one  might  think  one  had  to  deal  with  two  or  more 
organisms  living  in  symbiosis,  but  by  plating  and  replating  one  never  succeeds 
in  separating  the  various  forms.  Long  undulating  forms  may  be  present  20 
to  40  microns  in  length,  and  also  numerous  short  vibrio-like  and  bacillary 


+  h 


1     tr„*\ 

Fig.  764.—  Vibriothrix  zeylanica  Fig.  765. —  Vibriothrix  zeylanica 

(Castellani,  1910).  (Castellani,  1910). 

(Vibrio-like  forms  from  a  culture.)      (Forms  from  the  pellicle  in  a  culture.) 

forms,  and  in  preparations  from  the  pellicle  which  forms  in  certain  media, 
curved  filaments  may  be  found  with  claviform  swellings,  and  also  globular 
small  bodies. 

The  germ  is  easily  stained  by  the  usual  aniline  dyes.     It  is  Gram-negative. 

Motility. — The  germ  is  motile. 

Cultural  and  Biochemical  Characters.- — On  MacConkey,  Endo,  and  Drigalski- 
Conradi  plates  the  colonies  are  similar  to  those  of  the  germs  of  the  typhoid 
dysentery  group,  the  organism  being  a  non-lactose  fermenter.  The  micro- 
organism grows  well  on  all  the  usual  laboratory  media,  in  the  water  of  condensa- 
tion of  glucose  agar  tubes  producing  a  rather  characteristic  pellicle.  It  often 
produces  a  pellicle  also  in  broth  and  several  sugar  media.  It  produces  neither 
acidity  nor  gas  in  any  of  the  usual  carbohydrates — lactose,  glucose,  levulose, 
galactose,  saccharose,  dulcite,  mannite,  maltose,  dextrin,  rafhnose,  arabinose, 
adonite,  inulin;  on  the  contrary,  there  is  often  production  of  alkalinity. 

Most  strains  are  non-pathogenic  to  rabbits  and  guinea-pigs  when  inoculated 
subcutaneously,  but  there  are  exceptions. 


1840 


THE  DYSENTERIES 


{g)  Entoplasmic  Dysentery. 
In  two  cases  of  dysentery  contracted  apparently  in  Burma,  Castellani 
observed  peculiar  protozoal  bodies,  while  amoebae  and  dysentery  bacilli  were 
absent.  In  fresh  preparations  one  sees  large  rather  elongated  or  oval  bodies 
with  one  extremity,  the  one  which  in  stained  preparations  appears  mammillary, 
shaken,  so  to  speak,  by  an  extremely  frequent  vibrating  movement,  which 
makes  one  suspect  the  presence  of  flagella  or  cilia,  or  an  undulating  membrane. 
No  such  structures,  however,  can  be  detected  either  in  fresh  preparations  or  in 
slides  stained  with  the  usual  methods,  such  as  Giemsa,  iron — hematoxylin,  etc. 
The  protoplasm  presents  numerous  roundish  vacuoles,  none  of  which  is 
contractile.  No  distinct  nucleus  is  evident  in  fresh  preparations.  The  parasite 
does  not  emit  true  pseudopodia,  but  changes  in  the  shape  of  the  body  take  place. 
Stained  Preparations. — The  typical  forms  have  a  peculiar  flask-like  appear- 
ance, but  round  forms  are  also  found,  the  maximum  diameter  varying  between 
45  and  80  microns.  In  preparations  stained  with  Leishman  the  protoplasm 
is  stained  blue  and  presents  numerous  non-stained  roundish  vacuoles  regularly 
distributed  all  over.  In  certain  individuals  a  large  mass  of  chromatoid 
roundish  coccoid  granules  are  present,  which  represent,  according  to  Mesnil,  a 
diffuse  nucleus.  In  one  specimen  the  granules  were  bacillary  in  shape.  In 
none  of  the  bodies  were  flagella,  cilia,  or  evidence  of  any  undulating 
membrane  seen   by  Castellani,  Mesnil  or  any  protozoologist  to  whom  the 

specimens  were  submitted.  It  may 
be,  of  course,  that  such  organs  were 
of  such  extremely  delicate  nature  that 
they  required  the  use  of  special  methods 
to  put  them  in  evidence. 

Zoological  Position  of  the  Parasite.— 
It  is  impossible  to  classify  this  parasite, 
which,  for  convenience'  sake,  might 
be  maintained  in  the  temporary  genus 
Entoplasma,  until  further  researches 
render  possible  its  proper  classifica- 
tion. The  suggestion  has  been  made 
that  these  bodies  are  probably  forms 
of  Chilomastix  mesnili  Wenyon,  but 
the  size  of  the  bodies  apart  from  other 
characters  is  evidently  against  this 
hypothesis. 

Symptomatology^ — This  was  identical 
to  what  one  sees  in  a  case  of  amoebic 
or  bacterial  dysentery  of  medium 
gravity,  the  stools  containing  blood 
and  mucus. 

Treatment.-- Salines  were  administered  with  good  effects.  Emetine  was 
also  given,  but  it  is  difficult  to  say  whether  it  had  any  part  in  inducing  the 
cure  of  the  condition. 

II.  THE  PLATYHELMINTHIC  DYSENTERIES. 

Fasciolopsis  buski,  Schistosoma  japonicum,  and  S.  mansoni  cause  dysen- 
teric symptoms,  which  can  only  be  diagnosed  by  the  discovery  of  the  eggs  in 
the  motions.  The  symptoms  produced  by  the  latter  worms  are  described  in 
detail  in  Chapter  LXXiX.  (p.  1864),  while  those  of  the  former  still  require 
detailed  investigation. 

III.  THE  NEMATHELMINTHIC  DYSENTERIES. 

Nemathclminthic  dysentery  is  due  to  the  sclerostome  (CEsophagostomum 
brumpti  Railliet  and  Henry,  1905),  immature  females  of  which  were  found  by 
Brumpt  in  cyst-like  nodules  in  the  caecum  and  colon  of  a  negro  in  West  Africa. 
Similar  symptoms  are  caused  by  CEs.  stephanostomum  var.  thomasi  Railliet 
and  Henry,  1909,  discovered  in  South  America  by  Thomas  (see  p.  661). 


Fig.  766. — Entoplasma  castellanii 
Paul,  1914. 


DYSENTERIES  CAUSED  BY  BACTERIA  1841 

IV.  THE  ARTHROPODIC  DYSENTERIES. 

We  have  already  drawn  attention  to  the  fact  that  diarrhoeas  and  dysenteries 
may  be  caused  by  the  presence  of  species  of  the  Chilopoda  and  Diplopoda, 
and  by  the  larvae  of  flies  in  the  intestine,  but  these  are  rare,  and  are  sufficiently 
described  in  Chapters  XXVIII.  and  LXVII. 


B.  DYSENTERIES  CAUSED  BY  BACTERIA. 

The  Bacillary  Dysenteries. 

Synonyms. — French  :  Dysenterie  Bacillaire.  Italian  :  Dissenteria 
Bact erica.     German  :  Bacillenruhr. 

Definition. — The  bacillary  dysenteries  are  acute  or  chronic, 
endemic  or  epidemic,  specific  intestinal  disorders  caused  by  several 
varieties  of  bacteria,  which  are  disseminated  largely  by  means  of 
the  faecal  matter  of  dysentery  carriers,  as  well  as  by  that  of  persons 
suffering  from  these  disorders.  From  the  sources  of  infection  the 
germs  are  conveyed  to  food  or  drink  by  the  agency  of  flies,  dust,  sur- 
face water,  and  by  direct  contact  with  any  contaminated  substance. 
Infection  usually  takes  place  by  the  consumption  of  contaminated 
food  or  drink,  more  rarely  by  direct  contact  with  contaminated 
substances.  In  the  body  the  micro-organisms  cause  a  specific 
inflammation  of  the  large,  and  occasionally  also  of  the  small,  intes- 
tine, which  is  characterized  by  diarrhoea,  usually  accompanied  by 
pain,  tenesmus,  and  the  passage  of  blood  and  mucus  in  the  motions. 
More  rarely  the  bacilli  cause  a  general  septicaemia. 

History. — For  years  the  theory  of  a  bacterial  causation  for 
dysentery  found  many  supporters,  among  whom  may  be  mentioned 
Klebs,  Prior,  Ziegler,  Hlava,  Chantemesse,  Widal,  and  Grigoriew, 
all  of  whom  attempted  to  isolate  a  specific  organism. 

Maggiora,  Laveran,  Arnaud,  and  Escherich  believed  that  the 
Bacillus  coli  communis  was  the  true  cause,  while  Celli  described  as 
the  cause  of  the  disease  a  bacillus  fermenting  glucose  and  clotting 
milk,  which  he  called  the  Bacillus  coli  dyscntericus  ;  but  according 
to  his  more  recent  description  some  strains  produce  very  little  or 
no  gas  in  glucose  media,  and  may  not  clot  milk,  and  closely  resemble 
Flexner's  bacillus. 

During  an  epidemic  in  the  province  of  Oita,  in  Japan,  Ogata 
isolated  a  bacillus  which  liquefied  gelatine,  stained  by  Gram's 
method,  and  produced  intestinal  ulcers  in  guinea-pigs  and  cats,  a 
discovery  which  was  confirmed  by  Vivaldi  of  Padua,  but  not  by 
other  observers. 

In  the  same  year  Calmette  announced  that  the  Bacillus  pyo- 
cyaneus  was  a  cause  of  dysentery  in  Cochin  China,  an  observation 
since  confirmed  by  Lartigan  in  the  United  States,  Adami  in  Canada, 
and  others,  but  not  generally  accepted. 

The  elucidation  of  the  aetiology  of  bacillary  dysentery  is  due  to 
the  investigations  of  Shiga  in  Japan  and  Kruse  in  Germany  during 
the  years  1898-1900.     They  described  as  the  cause  of  the  malady 

116 


1.842  THE  DYSENTERIES 

a  short  bacillus,  not  decolourized  by  Gram,  not  clotting  milk,  not 
producing  gas  in  any  sugar  media.  There  was  at  first  some  differ- 
ence of  opinion  as  regards  motility,  but  Kruse's  statement  that  the 
bacillus  was  always  non-motile  has  been  proved  to  be  correct. 
Kruse  was  also  the  first  observer  to  state  that  there  was  more 
than  one  variety  of  dysenteric  bacilli. 

In  1900  Flexner  reported  that  he  had  isolated  a  moderately 
motile  bacillus  from  cases  of  dysentery  in  Manila  identical  with 
Shiga's  bacillus,  and  producing  a  severe  muco-hsemorrhagic  diarrhoea 
in  a  human  being  who  was  the  victim  of  an  accidental  laboratory 
infection.  This  bacillus  was  later  demonstrated  to  be  non-motile, 
and  to  differ  in  several  respects  from  Shiga's  bacillus,  notably  in 
fermenting  certain  sugar  media,  and  could  be  distinguished  there- 
from by  the  different  biological  tests.  These  results  have  been 
frequently  confirmed  by  observers  in  different  parts  of  the  world. 
Strong  isolated  a  bacillus  slightly  different  from  that  of  Flexner, 
also  from  cases  in  Manila. 

In  1903  Hiss  and  Russell  separated  a  bacillus  which  closely 
resembles  Flexner's  bacillus,  but  fails  to  ferment  maltose.  This 
bacillus  is  often  called  the  Y  bacillus.  In  1904  Castellani  isolated 
a  bacillus  from  cases  in  Ceylon  which  he  named  the  '  paradysentery; 
bacillus,'  and  later  he  described  the  group  of  metadysentery  bacilli. 
Several  other  germs  have  been  described  by  various  authorities, 
while  Kruse,  Flexner,  Strong,  Lucet,  Conradi,  and  others  have 
made  a  detailed  study  of  the  pathogenesis  of  the  disease. 

Climatology. — Bacillary  dysentery  is  found  all  over  the  world, 
in  cold,  temperate,  and  warm  climates,  but  especially  in  the  latter. 
In  temperate  climates  the  germs  probably  cause  a  type  of  the  in- 
fantile diarrhoeas  which  are  such  potent  factors  in  the  infantile 
mortality  of  those  regions,  while  they  are  also  responsible  for  the 
endemic  and  epidemic  cases  so  frequently  met  with  in  Europe  and 
America. 

In  the  tropics  they  are  also  extremely  common,  occurring  more 
frequently  at  the  end  of  the  dry  and  the  beginning  of  the  wet  seasons. 
In  certain  regions  and  at  certain  times  the  virulence  of  the  com- 
plaint appears  to  be  increased,  the  reason  of  which  is  not  at  present 
apparent.  Probably  it  depends  upon  the  greater  possibility  of 
infection,  owing  to  the  drinking-water  being  highly  contaminated 
in  warm  weather,  or  perhaps  to  the  presence  of  multitudes  of  flies. 
The  agency  of  these  or  other  factors  has  not  been  completely 
inquired  into.  Whatever  the  cause  may  be,  it  is  well  known  that 
at  times  the  disease  may  spread  in  epidemic  form  over  larger  or 
smaller  areas.  These  epidemics  may  be  institutional,  urban,  or 
rural,  or  they  may  attack  a  district,  a  country,  or  a  continent. 
Thus,  celebrated  epidemics  are  known  to  have  occurred  in  Europe 
in  1538,  1717-19,  I779"83>  and  1834-36. 

Dysentery  is  particularly  prone  to  occur  whenever  sanitation 
is  defective,  and  hence  is  found  prevalent  in  lunatic  asylums  and 
in  armies  in  times  of  active  service,  asis  clearly  shown  by  the  present 


JETIOLOGY  1843 

war;  and  this  factor  appears  to  be  more  potent  than  any  climato- 
logical  cause,  and,  indeed,  may  be  the  principal  reason  why  the 
disease  is  so  prevalent  in  the  tropics,  though  the  high  atmospheric 
temperature  of  these  regions  must  assist  the  growth  of  the  organisms. 
^Etiology. — Bacillary  dysentery  is  brought  about  by  a  group  of 
closely  allied  bacilli  which  may  be  separated  into  several  principal 
types  according  to  their  fermentative  action  on  glucose,  mannite, 
maltose,  saccharose,  lactose. 

I.  Shiga-Kruse  Type. — Glucose  fermented  (acid  only);  mannite, 
maltose,  saccharose,  lactose  not  fermented.  Agglutinated  only  by 
homologous  serum.  Not  agglutinated  by  normal  horse  serum. 
Very  toxic  to  rabbits. 

II.  Flexner  Type. — Glucose,  mannite,  maltose  fermented  (acid 
only);  saccharose  not  fermented,  but  there  are  exceptions;  lactose 
not  fermented.  Agglutinated  by  homologous  serum  and  Y  serum, 
and  not  unfrequently  by  Shiga  serum  and,  as  shown  by  M. 
Nicolle,  normal  horse  serum.    Non-toxic  to  the  rabbits. 

III.  Strong  Type. — Glucose,  mannite,  and  saccharose  fermented 
(acid  only) ;  maltose  not  fermented.  Agglutinated  by  homologous 
serum  only.  Most  authorities  consider  it  non-toxic,  but  the 
original  Strong  strain  was  very  toxic  to  rabbits. 

IV.  Hiss  and  Russell  Type.—  Glucose  and  mannite  fermented 
(acid  only) ;  maltose,  saccharose,  lactose  not  fermented.  Agglu- 
tinated by  homologous  and  Flexner  serums,  at  times  by  Shiga 
serum  and  normal  horse  serum. 

V.  Metadysentery  (Castellani)  Type. — Differs  from  all  above 
groups  in  fermenting  (slowly  and  acidity  only)  lactose  in  addition 
to  glucose.  Well  agglutinated  by  homologous  serum  ;  not  aggluti- 
nated by  Flexner  and  Shiga  serum.     Non-toxic  to  rabbits. 

For  more  details  on  bacteria  of  the  dysentery  group  the  reader  is 
referred  to  Chapter  XXXVI.,  p.  936.  Less  important  types  are  Riiffer 
and  Willmore's  Bacillus  ElTorNo.  1,  Baerthlein's  Bacillus  dysenteric, 
Shiga's  B.  dysenterice  Tokio,  Castellani's  Bacillus  paradysentericus,  etc. 

Hiss  divides  the  dysentery  bacilli  into  four  principal  groups: — ■ 

Group  1 :  Ferments  glucose  only  (Shiga-Kruse  bacillus). 

Group  2:  Ferments  glucose  and  mannite  (Bacillus  Y). 

Group  3 :  Ferments  glucose,  mannite,  and  saccharose  (Flexner  -  Manila 
bacillus) . 

Group  4:  Ferments  glucose,  mannite,  saccharose,  maltose,  and  dextrine 
(Harris's  bacillus,  Wollstcin's  bacillus). 

Leitz,  Kruse,  and  Shiga  have  called  attention  to  the  fact  that  while  the 
fermentation  of  mannite  is  a  reliable  means  of  differentiation,  not  so  much 
importance  can  be  given  to  the  fermentation  of  maltose,  saccharose,  and 
dextrine. 

Lehman  and  Neumann  give  the  following  classification:— 

1.  Shiga-Kruse:  No  fermentation  of  mannite,  maltose,  saccharose. 

2.  Flexner:  Ferments  mannite  and  maltose. 

3.  Strong:  Ferments  mannite  and  saccharose. 

4.  B.Y.:  Ferments  mannite;  has  no  action  on  maltose  and  saccharose. 

Bahr  has  noted  that  the  various  strains  may  vary  their  fermentative 
character  when  passing  through  flies. 


1844  THE  DYSENTERIES 

Under  the  term  B.  pseudo-dysentericus ,  Kruse  described  a  non- 
lactose  fermenting  bacillus  which  is  the  cause  of  many  outbreaks  of 
asylum-dysentery  in  Germany.  Later  he  used  the  term  '  pseudo- 
dysentery  '  to  denote  every  variety  of  dysentery  caused  by  bacilli 
other  than  those  of  the  Shiga-Kruse  type. 

Celli's  B.  coli  dysentericus,  according  to  the  original  description, 
is  motile,  clots  milk,  and  produces  gas  in  some  sugar  media,  and 
therefore  cannot  be  considered  to  belong  to  the  dysentery  group. 
According,  however,  to  more  recent  descriptions  by  De  Blasi  and 
others,  some  strains  of  the  B.  coli  dysentericus  may  not  produce  gas, 
and  may  not  clot  milk,  and  closely  resemble  Flexner's  bacillus. 

The  true  dysenteric  bacilli  may  be  differentiated  from  one  another 
by  their  varying  fermentative  actions  upon  carbohydrates,  by 
agglutination,  Pfeiffer's  reaction,  and  Castellani's  absorption 
method.  A  table  showing  the  characters  of  the  more  important 
dysentery  germs  as  well  as  other  intestinal  bacteria  will  be  found 
in  Chapter  XXXVI.,  p.  944.  We  wish  to  emphasise,  however, 
the  fact  that  the  biological  reactions  of  the  bacilli  are  much  more 
reliable  than  the  fermentative  changes. 

The  dysenteric  bacilli  are  distributed  mainly  by  the  faeces  of 
persons  suffering  from  the  disease,  but  there  are  also  '  dysentery 
carriers  '  in  the  true  sense  of  the  word,  who  are  perhaps  not  merely 
an  important  source  of  infection,  but  possibly  the  important  factor 
in  the  dissemination  of  dysentery. 

Strong  and  Musgrave  have  proved  that  infection  takes  place  by 
the  mouth  by  feeding  a  man  with  pure  cultures  of  the  dysentery 
bacillus,  which  quickly  produced  an  attack  of  dysentery,  charac- 
terized by  motions  containing  blood  and  mucus,  from  which  the 
typical  bacilli  were  grown. 

The  most  prevalent  method  of  infection  is  direct  contact  with  a 
patient  or  a  carrier,  or  with  articles  or  more  especially  food  con- 
taminated by  them.  The  bacilli  are  conveyed  from  faecal  matter 
to  the  mouth  by  the  contamination  of  food  or  drink,  or  the  utensils 
for  preparing  or  serving  the  same.  This  method  of  infection  is  prob- 
ably common  in  hospitals  and  asylums,  cooks  and  all  persons  engaged 
in  handling  food  being  possible  disseminators.  Another  method  of 
dissemination  would  appear  to  be  the  dust,  especially  in  places  with 
badly  polluted  soils.  Flies,  as  has  been  experimentally  demon- 
strated by  one  of  us,  are  capable  of  carrying  the  bacilli,  and  are 
therefore  probably  a  prolific  source  of  infection  in  tropical  countries. 
Luckily  the  water-supply  is  very  rarely  infected.  With  regard  to 
lower  animals,  Kruse  and  Bowman  have  recorded  spontaneous 
bacillary  dysentery  in  monkeys,  due  to  bacilli  of  the  Flexner 
group,  and  Messerschmidt  has  found  a  bacillus  of  Type  Y  in  the 
faeces  of  apparently  healthy  rabbits,  so  that  there  may  be  a  possi- 
bility that  lower  animals  are  of  importance  in  the  spread  of  the 
disease. 

It  would,  however,  appear  that  the  bacilli  are  capable  of  living 
in  the  alimentary  canal  without  causing  the  symptoms  of  the 


/ETIOLOGY  1845 

disease  until  the  vitality  of  the  host  is  lowered  by  some  agency, 
such  as  a  chill,  an  attack  of  diarrhoea,  or  some  intercurrent  disorder, 
when  they  are  capable  of  producing  their  ill-effects. 

This  carrier  problem  in  the  aetiology  of  dysentery  is  of  great 
importance,  and  though  as  yet  it  has  never  been  conclusively  proved 
that  an  outbreak  has  been  due  to  a  carrier,  still  it  is  known  that  the 
bacilli  can  be  excreted  in  an  intermittent  manner  by  people  suffering 
from  mild  relapses.  The  dysentery  carriers  are  classified  into — ■ 
(1)  healthy,  (2)  precocious,  (3)  convalescent,  (4)  relapsing,  and 
(5)  chronic  carriers.  The  healthy  carrier  is  rare,  but  May  has 
found  22  out  of  573  persons  examined  during  an  epidemic.  The 
precocious  are  believed  to  be  very  rare.  The  convalescent  and  re- 
lapsing carriers  are  well  known,  of  which  the  latter  are  of  the  greatest 
importance  in  spreading  the  disease.  The  chronic  carrier  excretes 
but  few  bacilli,  but  may  be  of  importance  in  the  spread  of  the  disease. 
With  regard  to  the  geographical  distribution  of  the  principal  forms 
of  bacilli,  it  maybe  stated  that  practically  all  of  them  seem  to  have 
a  cosmopolitan  distribution. 

^Etiological  Classification  of  Bacterial  Dysenteries. — An  serological 
classification  of  bacterial  dysenteries  has  been  suggested  as  follows : — 

I.  Due   to  B.    dysenteries   Shiga-Kruse — Bacterial   dysentery 

sensii  stricto. 
II.  Due  to  mannite  fermenting  dysentery  bacilli   (Flexner, 

Hiss  and  Russell,  Strong) — Paradysentery. 
III.  Due  to  germs  having  the  general  character  of  the  dysentery 
bacilli ;  but  slowly  fermenting  (acidity  only)  lactose  and 
not    agglutinated  by  Shiga-Kruse,  and  paradysenteric 
serums — Metadysentery. 

Pathology. — The  bacilli  taken  into  the  body  with  food  and  drink 
pass  to  the  intestine,  in  which  they  grow  and  multiply,  and  along 
the  whole  length  of  which  they  can  be  found.  The  researches  of 
Flexner  and  Sweet  have  proved  that  the  bacilli  can  abound  in  the 
small  intestine,  where  no  pathological  lesion  may  be  found.  In 
the  bowel  they  give  rise  to  the  toxins,  of  which  two  are  known — 
one  which  acts  upon  the  lower  bowel,  and  the  other  on  the  nervous 
system.  Both  these  toxins  are  absorbed  into  the  blood,  but  the 
first,  being  excreted  by  the  large  bowel,  causes  the  lesions  well 
known  to  be  associated  with  dysentery,  and  explains  the  localiza- 
tion of  these  lesions.  In  the  process  of  excretion  this  toxin  first 
causes  an  exudation  of  lymph  into  the  submucosa,  and  later  into 
the  mucosa.  This  lymph  coagulates,  and  is  invaded  by  a  cellular 
exudate,  and  in  due  course  the  glands  and  the  tissue  of  the  mucosa 
and  the  muscularis  mucosae  are  destroyed  by  coagulative  necrosis, 
with  thrombosis  of  the  vessels.  This  fibrinous  or  diphtheroid 
membrane  is  at  first  most  marked  on  the  summits  of  the  ridges, 
and  may  not  be  found  at  the  bottom  between  the  ridges.  It  con- 
tains large  numbers  of  micro-organisms  of  varying  characters, 
while  the  depths  of  the  submucosa  may  reveal  accumulations  of 


1846  THE  DYSENTERIES 

leucocytes,  and  the  peritoneal  coat  may  be  cedematous.  The 
micro-organisms  destroy  the  fibrinous  false  membrane,  which  may 
separate  off  in  flakes,  thus  causing  ulcers,  which  are  at  first  super- 
ficial, but  later  become  deep  and  extensive.  After  treatment  these 
ulcers  heal  with  the  formation  of  connective  tissue,  thus  producing 
a  scar  in  the  mucous  membrane,  which  in  due  course  becomes 
pigmented  from  the  sulphuretted  hydrogen  of  the  bowel  acting  on 
the  iron  of  the  blood.  The  other  toxin  may  attack  the  nervous 
system,  causing  peripheral  neuritis. 

Very  rarely  do  the  bacilli  enter  the  blood  stream,  and  cause 
true  septicaemia,  though  such  cases  have  been  recorded  by  Rosen- 
thal and  Markwald,  the  latter  observer  stating  that  he  found  the 
bacilli  in  the  blood  and  intestinal  contents  of  a  foetus  which  had 
been  prematurely  expelled  from  the  uterus  of  a  mother  who  was 
suffering  from  bacillary  dysentery.  Darling  has  actually  grown  the 
bacillus  from  the  blood  of  cases  of  bacterial  dysentery.  Occasionally 
the  bacilli  affect  the  joints  and  very  rarely  the  conjunctiva. 

Morbid  Anatomy. — On  opening  the  abdomen,  the  peritoneum  is 
found  in  general  to  be  normal,  but  the  bloodvessels  of  the  large 
bowel  are  seen  to  be  injected,  and  the  mesocolons  may  be  infil- 
trated with  lymph,  or  firm  and  fibrinous.  There  may  be  adhesions 
of  the  sigmoid  colon  to  the  omentum,  pelvis,  bladder,  or  small 
intestines,  while  the  splenic  flexure  may  be  adherent  to  the  spleen 
and  surrounding  parts,  and  the  hepatic  flexure  to  the  liver.  The 
caecum  may  show  adhesions  to  the  omentum,  and  more  rarely  there 
may  be  pericaecal  abscess.  Signs  of  a  general  peritonitis  may  be 
met  with,  and  will  generally  be  associated  with  a  gangrenous  or 
perforated  condition  of  the  intestine. 

The  small  bowel  is  usually  normal,  but  may  be  hyperaemic  or, 
much  more  rarely,  ecchymotic.  The  walls  of  the  large  intestine 
are  usually  considerably  thickened  and  hyperaemic,  and  may  at 
times  be  found  to  be  gangrenous  along  a  great  or  lesser  extent  of 
their  course.  On  opening  the  large  bowel,  the  mucosa  will  be  seen 
to  be  covered  with  a  coagulated  exudate  in  the  form  of  a  false 
membrane,  which  is  more  evident  on  the  summits  of  the  folds, 
and  is  especially  well  marked  in  the  sigmoid  colon,  the  caecum,  and 
the  ampulla  of  the  rectum.  Around  the  areas  covered  by  the  false 
membrane  the  mucosa  is  seen  to  be  hyperaemic  and  cedematous. 
As  a  rule,  numerous  ulcers  are  also  to  be  seen,  with  clean  surfaces, 
elevated  edges,  and  a  base  formed  by  the  submucosa.  These 
ulcers  may  be  very  extensive,  leading  to  the  separation  of  large 
sloughs,  or  may  extend  deeply  into  the  coats  of  the  bowel,  causing 
perforation  and  peritonitis,  or  in  less  serious  cases  induce  the 
exudation  of  much  lymph  into  the  peritoneum  coat,  which  subse- 
quently causes  adhesions. 

In  post-mortem  examinations  of  cases  which  have  died  from 
some  other  complaint  it  is  not  unusual  to  find  the  intestines  matted 
together  in  the  pelvis,  the  omentum  adherent  to  the  colon,  and  the 
colon  to  the  bladder,  etc.     On  opening  such  a  colon  it  will  be  found 


MORBID  ANATOMY 


1847 


scarred  by  old  dark-coloured  cicatrices,  indicating  the  position  of 
the  healed  ulcers  of  a  previous  dysentery.  More  rarely  the  cica- 
trization may  have  proceeded  to  such  an  extent  as  to  cause  narrow- 
ing of  the  lumen  of  the  gut,  and  still  more  rarely  may  the  process 
lead  to  abscess  formation  in  the  adherent  omentum,  the  pus  of  this 
abscess  slowly  working  its  way  into  the  anterior  abdominal  wall, 
and  so  to  the  exterior.  The  caecum  and  other  parts  of  the  bowel 
may  show  polypi  protruding  from  the  mucous  membrane,  a  con- 
dition  often  called  '  colitis  polyposa.' 

In  the  epidemic  diarrhoea  of  infants,  the  lesions  which  may  be 
found  are  classifiable  into  hyperplasia  of  the  agminated  and  solitary 
glands,  superficial  ulcers,  lesions  resembling  those  described  above, 
or  invisible  lesions. 


Fig.  767. — The  Colon  in  a  Case  of  Bacillary  Dysentery 


Microscopically,  there  is  at  first  an  exudation  of  fluid  containing 
but  few  cells  into  the  submucosa,  while  the  mucosa  is  congested, 
but  the  glands  are  seen  to  be  quite  normal.  A  little  later  the 
exudate  into  the  submucosa  is  seen  to  have  formed  fibrin,  and  the 
vessels  of  this  coat  are  noted  to  be  dilated,  to  contain  numerous 
polymorphonuclear  leucocytes,  which  may  be  seen  undergoing 
diapedesis  into  the  surrounding  tissue.  In  this  stage  the  exudate 
has  also  affected  the  mucosa,  the  glands  and  tissue  of  which  may  be 
seen  to  be  undergoing  coagulative  necrosis.  In  a  still  later  stage 
nothing  is  to  be  seen  of  the  mucosa,  and  in  bad  cases  of  the  sub- 
mucosa, except  fibrinous  exudate,  mixed  with  cells  and  blood- 
vessels.    Often,  however,  the  submucosa  shows  dense  collections 


1848  THE  DYSENTERIES 

of  leucocytes.  Where  ulcers  occur,  the  amount  of  exudate  covering 
the  muscular  coat  may  be  thin,  while  in  other  places  it  may  be 
thick.  The  peritoneum  is  also  generally  infiltrated  by  a  coagulated 
exudate. 

Symptomatology. — The  different  appearances  presented  by  the 
bacillary  dysenteries  may  be  grouped  into: — 

i.  The  acute  type. 

2.  The  gangrenous  type. 

3.  The  entero-dysenteric  type. 

4.  Choleraic  dysentery. 

5.  Chronic  dysentery. 

6.  Dysenteric  diarrhoea. 

7.  Dysenteric  infantile  diarrhoea. 

1.  AcuteBacterial  Dysentery. — The  incubation  varies  from  twenty- 
four  hours  to  three  or  four  days,  and  is  not  well  known  in  natural 
infections.  Usually  after  an  incubation  of  a  few  days,  during  which 
the  patient  may  not  feel  quite  well,  and  may  complain  of  constipa- 
tion or  diarrhoea,  with  loss  of  appetite  and  malaise,  the  disease 
begins  with  an  attack  of  pain  in  the  lower  part  of  the  abdomen, 
and  an  urgent  desire  to  defaecate,  which  results  in  the  passage  of 
perhaps  an  ordinary  formed  faeculent  motion,  which  temporarily 
relieves  the  pain.  Soon,  however,  another  attack  of  pain  is  felt, 
generally  in  the  region  of  the  umbilicus,  from  which  it  radiates  to 
any  part  of  the  large  intestine,  and  this  is  again  associated  with  a 
desire  to  defaecate  and  the  passage  of  a  motion  which  is  composed 
of  faecal  matter,  but  may  now  be  soft.  The  pain  increases,  and  the 
desire  to  defecate  becomes  more  and  more  frequent,  until  almost 
constantly  present,  while  any  nourishment,  however  bland  and  uii- 
irritating,  at  once  produces  a  desire  to  defaecate.  After  a  time 
the  patient  sits  almost  continuously  upon  the  commode,  straining 
violently,  and  passing  at  first  motions  of  faeculent  matter  mixed  with 
blood  and  mucus,  and  then  blood  and  mucus  mixed  with  a  little 
faeculent  matter,  and  finally  nothing  but  a  little  blood  and  mucus. 
As  a  result  of  the  straining  and  the  passage  of  numerous  motions, 
the  anus  becomes  inflamed  and  very  painful,  and  prolapse  of  the 
bowel  is  not  uncommon,  and  adds  greatly  to  the  distress  of  the 
patient.  The  urine  diminishes  in  quantity,  and  therefore  may  show 
an  increased  quantity  of  urea,  and  at  times  may  contain  a  trace 
of  albumen.  Pain  is  often  complained  of  in  the  region  of  the  bladder 
during  and  after  straining  at  the  commode.  In  slight  cases  the 
number  of  motions  may  be  only  about  one  every  hour,  but  in  more 
severe  cases  they  number  from  fifty  upwards,  until  they  are  passed 
almost  continuously.  This  constant  pain  and  desire  to  defaecale 
naturally  weakens  and  exhausts  the  patient  very  quickly,  for  it 
prevents  sleep  and  rest. 

In  ordinary  cases  the  tongue  is  moist  and  coated  with  a  white 
fur,  and  usually  the  patient  is  thirsty,  but  not  markedly  so,  except 
in  bad  cases.     Nausea  is  often  present,  and  there  is  no  desire  for 


SYMPTOMATOLOGY  1849 

food,  which  is  badly  digested.  There  is  often  epigastric  pain. 
Vomiting  occurs,  but  is  relatively  unusual  in  cases  which  are 
taken  in  hand  early  and  properly  treated.  The  abdomen  soon 
becomes  sunken  and  tender,  especially  along  the  course  of  the  large 
bowel,  but  this  tenderness  may  be  restricted  to  certain  areas  only 
of  that  bowel.  On  careful  palpation  the  thickened  bowel  may  at 
times  be  felt,  but  usually  it  is  too  tender  to  allow  such  manipula- 
tion. With  the  numerous  motions,  it  may  be  imagined  that  con- 
stipation would  not  occur;  but  this  is  not  so,  for  the  disease  may  be 
limited  to  the  lower  bowel,  and  as  it  is  the  involvement  of  the 
rectum  which  causes  the  tenesmus  and  constant  desire  to  defalcate, 
faeces  may  be  accumulating  in  the  higher  region  of  the  large  bowel 
— a  condition  which  may  be  recognized  by  the  distension.  Shiga, 
indeed,  describes  an  ascending  variety  of  acute  dysentery,  which, 
beginning  in  the  rectum,  spreads  upwards  along  the  large  bowel, 
as  well  as  a  descending  variety,  which  usually  starts  in  the  small 
intestine.  The  typical  motions  are  composed  of  blood  and  mucus 
only,  but  in  bad  cases  they  may  consist  of  a  reddish  albuminous 
fluid  containing  white  shreds.  The  typical  dysenteric  motions  have 
no  faecal  smell,  and  microscopically  show  numerous  micro-organisms, 
leucocytes,  and  red  cells,  and  epithelial  debris  and  cells.  Usually 
there  is  some  fever,  ranging  from  990  to  1030  F.  The  pulse  is  quick- 
ened, and  in  bad  cases  may  be  not  merely  rapid,  but  irregular,  when 
the  heart  will  be  found  to  be  dilated,  and  perhaps  haemic  murmurs 
may  be  heard;  but  these  symptoms  are  unusual,  except  in  grave 
cases.  The  blood  usually  shows  a  diminution  in  the  red  cells, 
and  a  slight  polymorphonuclear  leucocytosis.  The  lungs  are  usually 
normal.     Delirium  is  unusual. 

If  the  patient  is  to  die,  the  motions  assume  the  serous  character 
mentioned  above,  the  pulse  becomes  rapid  and  irregular,  the  tem- 
perature drops  to  subnormal,  the  motions  diminish  in  number, 
hiccough  appears,  and  exhaustion  ushers  in  death  generally  during 
the  second  or  third  week. 

If  the  patient  is  to  recover,  the  motions  become  more  faeculcnt, 
and  the  blood  and  mucus  generally  disappear,  while  the  pain  and 
tenesmus  subside,  the  pulse  returns  to  normal,  the  tongue  cleans, 
and  convalescence  begins  about  the  end  of  one  week  in  mild,  or  of 
one  month  in  more  severe  cases. 

2.  Gangrenous  Dysentery. — This  most  severe  type  of  the  disease 
may  begin  insidiously  with  some  slight  faeculent  diarrhoea,  which  may 
not  attract  attention  until  suddenly  the  patient  becomes  collapsed 
and  dies  within  a  few  hours  without  the  passage  of  the  typical 
motions.  Thus  a  prisoner  may  stand  in  the  dock  throughout  the 
whole  day,  and  then  die  in  the  night  from  gangrenous  dysentery, 
while  his  sudden  death  may  awake  suspicions  of  suicide. 

The  more  usual  history  is  that,  during  an  attack  of  acute  dysen- 
tery, the  abdominal  pain  and  tenesmus  become  very  severe,  while 
the  motions  alter  their  characters,  becoming  exceedingly  offensive, 
and  containing  gangrenous  sloughs  composed  of  the  mucosa  and  the 


i85o 


THE  DYSENTERIES 


submucosa.  These  sloughs  may  be  small  or  large,  and  even  at 
times  may  be  tubular.  The  mot  ions  are  now  exceedingly  numerous, 
and  sometimes  haemorrhage  per  anum  may  take  place.  The  patient 
becomes  extremely  exhausted,  the  pulse  small  and  frequent,  the 
temperature  falls  to  subnormal,  and  the  extremities  become  cold 
up  to  the  knees  and  elbows,  while  the  motions  are  passed  in- 
voluntarily, and  death  takes  place  in  some  two  or  three  days  from 
exhaustion.  Recovery  from  an  attack  of  gangrenous  dysentery  is 
extremely  unusual,  but  when  it  does  occur  the  pulse  slows,  the 
temperature  rises,  the  motions  become  faeculent  again,  and  the 
urine,  which  has  been  suppressed,  reappears. 

3.  Enter 0- Dysentery. — This  variety  begins  with  one  or  more  rigors, 
and  a  rise  of  temperature  to  1030  F.  or  more.  The  temperature 
keeps  high,  assuming  either  a  continuous  or  a  high  remittent  type, 
and  is  associated  with  a  dry  tongue,  and  a  mouth  covered  with 
sordes,  foetid  breath,  headache,  malaise,  pains  in  various  parts  of 
the  body,  marked  epigastric  disturbance,  and  occasionally  with 
ecchymoses  under  the  skin  in  various  parts  of  the  body.  The  char- 
acteristic signs  of  abdominal  pain  and  tenesmus  are  absent,  and  the 


Fig.    768. — Temperature  Chart  of  a  Case  of   Bacillary  Dysentery, 
showing  the  effect  of  serum  treatment. 

Chart  by  Archibald. 

motions,  though  containing  blood  and  mucus,  are  mixed  with 
considerable  quantities  of  faeculent  matter.  The  mind  is  clouded, 
the  patient  becoming  very  stupid,  sleepless,  and  at  times  delirious. 
Abscesses  may  now  appear  in  varying  parts  of  the  body,  but 
especially  in  the  parotid  or  theischio-rectal  fossae,  while  carbuncles, 
bedsores,  and  peritcnitis  may  also  occur.  Death  usually  ensues 
after  ai  few  days'  illness  from  exhaustion,  toxaemia,  or  hyperpyrexia. 

4.  Choleraic  Dysentery.  -Castellani  called  attention  some  years 
ago  in  the  tropics,  and  again  recently  in  various  war  zones,  to  a 
type  of  dysen-ery  or  serous  diarrhoea  which  is  often  mistaken  for 
cholera.  The  onset  is  sudden,  with  rice-water-like  or  serous  motions; 
there  may  be  vomiting,  and  the  condition  of  the  patient  becomes 
rapidly  very  grave.  In  most  cases,  however,  a  motion  is  passed 
now  and  then  tinged  with  blood,  and  this  clears  the  diagnosis. 

5.  Chronic  Bacterial  Dysentery. — Chronic  dysentery  appears  ah  er 
an  attack  of  acute  dysentery  which  has  apparently  been  cured, 
but  in  which,  after  a  period  of  quiescence,  diarrhoea  appears. 
About  five  or  six  motions,  composed  of  watery,  evil-smelling,  faecu- 


SYMPTOM  A  TOLOG  Y— COM  PLICA  TIOSS  1851 

lent  matter,  are  passed  per  diem,  and  may  at  times  contain  blood 
and  mucus,  or  simply  mucus.  After  a  time  these  symptoms  dis- 
appear, and  the  motions  become  normal,  or  there  may  be  slight 
constipation.  In  due  course,  however,  the  diarrhoea  returns,  and 
these  exacerbations  recur  for  months  and  years,  and  seriously  affect 
the  patient's  general  health.  The  appetite  becomes  bad;  the 
tongue  red  and  smooth,  or  flabby  and  coated;  digestion  is  impaired, 
and  fermentative  changes  cause  the  bowels  to  be  distended  with 
gas;  while  haemorrhage,  slight  or  severe,  may  take  place  from  the 
nose  or  under  the  skin.  Profuse  sweats  may  occur  at  night,  and 
tend  to  exhaust  the  patient.  Recovery  may  take  place  spon- 
taneously, or  after  treatment,  or  the  diarrhoea,  continuing  fitfully, 
may  gradually  wear  out  the  patient,  who  may  die  of  exhaustion 
or  some  intercurrent  disease.  Some  authorities  believe  that  chronic 
dysentery  may  become  sprue.  We  do  not  agree  with  them,  although, 
of  course,  sprue  may  develop  in  a  case  of  chronic  dysentery. 

6.  Dysenteric  Diarrhoea. — The  term  '  dysenteric  diarrhoea  '  may 
be  applied  to  the  non-bloody  diarrhoea  of  chronic  dysentery,  and  to 
those  cases  of  diarrhoea  which  occur  during  an  epidemic  of  dysentery, 
and  in  which  the  bacillus  is  either  proved  to  be  present  in  the 
motions,  or  the  patient's  blood  agglutinates  in  high  dilution  one  of 
the  dysenteric  bacilli.  The  attack  may  in  no  way  differ  from  an 
ordinary  attack  of  diarrhoea  due  to  other  causes,  but  is  apt  to  recur 
and  to  turn  into  chronic  dysentery. 

7.  Dysenteric  Infantile  Diarrhoea. — Diarrhoea  is  an  extremely  com- 
mon disease  among  infants  in  the  tropics,  but  has  not  yet  received  the 
attention  which  it  has  in  the  United  States,  in  Europe,  and  in  Japan, 
where  it  is  called  '  ekiri.'  It  is  believed  to  be  due  to  Flexner's 
bacillus,  or  more  rarely  to  Shiga-Kruse's  bacillus;  while  the 
symptoms  resemble  entero-dysentery,  being  characterized  by  be- 
ginning with  vomiting,  and  a  rise  of  temperature  from  1030  to 
1040  F.,  a  dry  mouth,  coated  tongue,  distended  and  tender  abdomen, 
and  the  passage  of  motions  containing  fseculent  matter,  often  green 
in  colour,  generally  mixed  with  blood  and  mucus.  The  fever  is  of 
the  remittent  type,  and  as  the  disease  progresses  the  child  wastes, 
and  may  become  convulsed  or  comatose  and  die,  or  may  live  for 
weeks,  suffering  from  repeated  attacks  of  diarrhoea,  and  finally  die 
from  exhaustion.  If  recovery  is  to  take  place,  the  temperature 
declines  and  the  diarrhoea  ceases,  but  the  child  is  left  in  a  pale  and 
emaciated  condition,  from  which  it  takes  months  to  recover. 

Complications. — Peripheral  neuritis  is  not  uncommonly  met  with, 
generally  in  a  mild  form,  and  often  confined  to  one  nerve.  Arthritis 
and  polyarthritis  are  also  not  uncommon,  while  inflammation  of 
the  tendon-sheaths  may  also  take  place.  In  entero-dysentery 
parotid  buboes  are  not  uncommon,  while  abscesses  in  other  parts  of 
the  body  and  peritonitis  may  develop.  In  gangrenous  dysentery 
haemorrhage  may  be  a  serious  complication.  Typhoid  fever  may 
occur  at  the  same  time  as  a  dysenteric  attack,  and  is  a  serious 
complication.     We  have   met  with  several  cases  of  appenditicis 


l852  THE  DYSENTERIES 

developing  in  people  convalescent  from  dysentery.     Conjunctivitis 
and  iritis  have  been  recorded. 

Sequelae. — One  of  the  most  important  sequels  of  dysentery,  to 
which  Cantlie  has  drawn  attention,  is  stenosis  of  the  large  bowel, 
and  more  particularly  of  the  sigmoid  flexure,  due  to  cicatricial 
contraction  of  the  healing  ulcers.  The  symptoms  are  the  onset 
of  an  insidious  constipation,  associated  in  due  course  with  a  sensa- 
tion of  distension  in  the  abdomen,  loss  of  appetite,  and  nausea. 
The  constipation  is  apt  to  alternate  with  attacks  of  diarrhoea. 
In  due  course  the  constipation  becomes  severe,  and  is  accompanied 
with  recurrent  attacks  of  colic,  in  which  the  pain  may  be  localized 
or  radiating,  and  sooner  or  later  vomiting  occurs.  On  inspecting 
the  abdomen  a  swollen  region  may  be  observed,  and  the  attacks  of 
colic  may  be  seen  to  be  associated  with  visible  peristaltic  move- 
ments, while  more  or  less  meteorism  occurs.  Succussion  sounds 
may  be  heard  over  the  dilated  bowel.  This  condition  is  serious, 
and  must  be  energetically  treated. 

According  to  some  authors,  '  sprue  '  is  a  sequel  to  dysentery,  and 
we  have,  in  fact,  seen  several  cases  of  sprue  developing  in  patients 
who  have  been  suffering  from  chronic  dysentery.  We  believe, 
however,  the  two  diseases  to  be  of  different  aetiology. 

Diagnosis. — It  may  be  of  advantage  to  say  a  few  words,  first, 
on  the  diagnosis  of  dysentery  in  general.  In  presence  of  a  patient 
suffering  from  abdominal  pains,  with  frequent  stools  containing 
blood  and  mucus,  the  practitioner  is,  as  a  rule,  justified  in  making  the 
generic  diagnosis  '  dysentery.' 

Next  the  specific  diagnosis  must  be  made — viz.,  what  type  of 
dysentery  is  the  patient  suffering  from.  For  practical  purposes'  it 
is  sufficient  in  the  enormous  majority  of  cases  to  keep  in  mind  the 
following  types :  amoebic  dysentery,  ciliar  dysentery,  bacterial 
dysentery.  A  particle  of  the  muco-pus,  immediately  after  evacua- 
tion, should  be  examined  microscopically,  and  this  examination  can 
be  carried  out  with  great  advantage  at  the  bedside  by  means  of 
a  portable  microscope.  If  the  microscopical  examination  shows 
presence  of  amoebae  of  the  histolytica  type,  especially  if  containing 
red  blood  cells,  the  diagnosis  will  be  amoebic  dysentery.  If  amoebae 
of  the  histolytica  type  are  absent,  and  ciliates  of  the  balantidium 
type  are  present,  the  diagnosis  will  be  ciliar  dysentery.  If  on  pro- 
longed and  repeated  examination,  amoebae  and  ciliates  are  absent,  the 
diagnosis  of  probability  will  be  bacterial  dysentery.  A  probable  diag- 
nosis of  bacterial  dysentery  can  be  made  also  by  the  practitioner  who 
is  not  in  position  to  carry  out  microscopical  examinations,  if  emetine 
does  not  make  the  dysenteric  symptoms  disappear  within  three  days 

The  diagnosis  of  bacillary  dysentery  has  to  be  made  with  special  reference 
to  pseudo-dysentery  and  amoebic  dysentery,  especially  when  there  is  blood 
and  mucus  in  the  motions,  and  from  the  various  forms  of  diarrhoea  when  these 
signs  are  absent. 

With  regard  to  pseudo-dysentery,  cancer  and  syphilis  of  the  rectum  and 
inflamed  haemorrhoids  may  give  rise  to  tenesmus  and  the  passage  of  blood 
and  mucus,  but  can  be  differentiated  by  the  history  and  by  an  examination 


DIAGNOSIS  1853 

of  the  rectum.  Cancer  of  the  colon  and  intussusception  may  also  cause  the 
passage  of  blood,  with  or  without  mucus  and  with  or  without  tenesmus,  but 
the  history  and  a  careful  abdominal  examination,  together  with  the  discovery 
of  a  localized  swelling,  should  serve  to  distinguish  these  affections.  Para- 
metritis on  the  left  side  may  cause  diarrhoea,  and  more  rarely  the  passage  of 
blood  and  mucus,  but  the  absence  of  tenesmus,  the  presence  of  pain  more  at 
the  side  of  the  uterus  than  in  the  sigmoid  colon,  should  indicate  the  necessity 
of  an  examination  per  vaginani  or  per  rectum,  when  the  nature  of  the  case  will 
be  cleared  up.  A  careful  examination  of  the  faeces  should  exclude  such  causes 
as  fish-bones  injuring  the  rectum.  Mercurial  poisoning  can  be  distinguished 
by  the  history,  the  presence  of  salivation,  etc.  The  diagnosis  from  amoebic, 
balantidic,  and  the  other  dysenteries  of  animal  origin  can  only  be  made  by 
the  careful  microscopical  examination  of  the  faeces,  when  the  absence  of  these 
parasites  will  be  made  certain.  The  absence  in  dysenteric  stools  of  Charcot- 
Leyden  crystals  and  presence  of  very  abundant  cellular  exudate  with 
macrophages  and  preponderance  of  polymorphonuclears  points  to  the  con- 
dition being  bacterial  rather  than  amoebic. 

Positive  diagnosis  can,  however,  only  be  made  by  a  bacterio- 
logical examination  of  the  faeces  and  the  determination  of  the 
specific  bacillus.  Agglutination  tests  with  the  patient's  blood  are 
not  of  much  use  in  acute  cases,  as  agglutinins  are  not  present  in  the 
blood  the  first  few  days  of  the  disease. 

For  the  bacteriological  diagnosis  a  shred  of  mucus  or  pus  is  smeared  over 
a  plate  of  MacConkie's  bile — salt-lactose-neutral-red  agar,  by  means  of  a  bent 
glass  rod  or  Kruse's  platinum  pencil. 

Two  more  plates  of  the  same  medium  are  prepared  in  a  similar  manner 
without  recharging  the  rod  or  pencil. 

Any  white  colonies  which  develop  are  further  investigated  as  to  their  sugar 
reactions,  and  by  using  the  agglutination  and  absorption  methods. 

The  following  method  will  be  found  useful :— Twenty  white  colonies  are 
selected;  in  this  way  we  discard  all  lactose  rapid  fermenters.  From  each 
colony  one  glucose  peptone  water  (or  glucose  agar)  and  a  litmus  milk  are 
inoculated.  After  sixteen  to  twenty-four  hours  at  35°  C.  to  370  C.  the  glucose  and 
milk  tubes  so  inoculated  are  examined:  all  the  strains  which  have  produced 
gas  or  clotted  milk  are  discarded.  In  this  way  we  discard  all  germs  of  the 
genus  Salmonella,  Lankoides  (p.  938),  etc.,  and  we  retain  only  the  strains 
which  do  not  produce  gas  in  glucose  and  do  not  clot  milk.  If  a  germ  does 
not  produce  gas  in  glucose,  as  a  rule  it  does  not  produce  it  in  any  other  carbo- 
hydrate, and  therefore  we  may  say  that  we  are  left  with  strains  which  do  not 
produce  gas  in  any  sugar  and  do  not  rapidly  clot  milk,  and  which,  therefore, 
if  they  are  bacilli,  must  belong  to  one  of  the  following  groups: — {a)  Eberthus 
(P-  93°).  (b)  Alcaligenes  (p.  930),  (c)  Vibriothrix  (p.  1068),  (d)  dysentery- 
metalkali genes  group  sensii  lato.  From  the  glucose  tubes  hanging-drops  are 
made;  all  germs  which  are  not  bacilli  are  discarded,  and  similarly  all  motile 
germs.  In  this  way  we  shall  retain  only  germs  which  are  non-motile  bacilli, 
which  do  not  produce  gas  in  any  sugar,  and  do  not  clot  milk — bacilli, 
therefore,  which  belong  to  the  dysentery  (glucose  acid)  and  metalkaligenes 
group  (glucose  not  acid).  Those  which  ferment  glucose  (acidity  only)  are 
further  investigated,  and  agglutination  reactions  are  carried  out,  using 
Shiga,    Flexner,  and  other  dysenteric  sera. 

At  times  it  will  be  found  of  advantage  to  use  the  so-called  Castellani's 
contemporary  gas-agglutination  test.  Tubes  of  glucose  peptone  water  with 
Durham's  fermentation  small  tubes  are  prepared,  and  two  or  three  drops  of  a 
mixed  serum,  Shiga-Flexner,  Hiss,  etc.,  added.  Twenty  white  colonies  are 
inoculated  in  twenty  such  tubes.  If  any  of  these  tubes,  after  twelve  hours 
in  the  incubator,  shows  absence  of  gas  and  presence  of  agglutination,  a  diagnosis 
of  bacterial  dysentery  can  be  made,  though  not  of  what  variety  of  bacterial 
dysentery.  It  must  be  remembered  also  that  there  are  rare  strains  of  dysen- 
teric bacilli  which  are  not  agglutinated  by  any  of  the  usual  antidysenterysera. 


1 854  THE  DYSENTERIES 

We  wish  to  emphasize  the  fact  that  simple  agglutination  is  not  sufficient 
to  diagnose  that  a  certain  bacillus  is  a  dysentery  bacillus.  As  shown  by  Levi 
della  Vida,  by  one  of  us,  and  other  observers,  it  is  not  at  all  rare  to  isolate 
from  dysentery  patients  bacilli  which  are  extremely  well  agglutinated,  say, 
by  Shiga  serum,  but  which  produce  gas  in  glucose.  Notwithstanding  the 
opinion  of  a  few  authorities,  such  germs  cannot  be  considered  to  be  true 
dysentery  bacilli,  they  are  noso parasites  or  secondary  invaders.  Hence  the 
importance  of  carrying  out  fermentation  tests  in  addition  to  serological  tests. 

To  the  bacteriological  diagnosis  of  bacterial  dysentery  may  be  applied  also 
Castellani's  polyserum  method  as  used  for  the  diagnosis  of  cholera.  A  large 
number  of  the  white  colonies  from  MacConkey  plates  are  inoculated  in  a  tube 
of  peptone  water  containing  a  few  drops  of  lactose  non-fermenters  agglutinating 
polyserum  (excepting  the  dysentery  group).  In  theory  all  non-lactose  fer- 
menters,  apart  from  the  dysentery  bacilli,  will  be  agglutinated,  while  the 
dysentery  bacilli  will  grow  diffusely;  in  practice,  however,  many  difficulties 
are  met  with,  owing  to  the  great  difficulty  in  producing  an  efficient 
polyserum. 

Finally,  we  wish  to  call  attention  to  the  necessity  of  carrying  out 
the  bacteriological  examination  for  dysentery  on  stools  absolutely 
fresh,  as  soon  as  evacuated,  plates  being  made  at  the  bedside  and 
then  sent  to  the  laboratory.  If  this  precaution  is  not  carried  out, 
a  very  large  number  of  cases  will  give  negative  results. 

Prognosis. — In  the  milder  forms  of  acute  dysentery,  the  prognosis 
is  good,  recovery  being  the  rule,  but  the  death-rate  of  severe  acute 
dysentery  is  high,  while  the  prognosis  in  gangrenous  dysentery  is 
very  bad.  As  an  average,  the  mortality  of  the  various  forms 
may  perhaps  range  from  12  to  25  per  cent.,  for  there  is  no  doubt 
that  in  Ceylon  and  other  tropical  countries  dysentery  is  a  more 
potent  factor  in  the  death-rate  than  malaria,  though  the  latter 
may  cause  more  illness. 

The  site  of  the  disease  is  also  a  factor  in  determining  the  prognosis, 
being  as  a  rule  better  if  it  is  situate  low  down,  and  worse  if  high  up 
in  the  bowel.  According  to  Kruse,  Shiga,  Duval,  Dopter,  and  our 
own  experience,  early  serum  treatment  lessens  the  mortality 
and  therefore  improves  the  prognosis. 

As  regards  age  and  sex,  the  prognosis  is  better  for  adults  than 
for  children,  and  for  men  than  for  women.  The  European  or 
new-comer  into  the  tropics  suffers  more  severely  than  the 
native  resident  race,  but  this  racial  difference  is  merely  relative. 

Treatment. — In  all  cases,  however  mild,  the  patient  should  be 
kept  at  rest  in  bed,  and  the  urine-bottle  and  bed-pan  must  be  used. 
The  latter  should  preferably  be  slightly  warmed  before  being  used, 
especially  in  cool  climates.  Damp  cotton-wool  should  be  sub- 
stituted for  sanitary  paper,  in  order  to  prevent  irritation  of  the 
region  of  the  anus. 

All  motions  should  be  disinfected,  after  having  been  seen  by  the 
physician,  with  Jeyes'  fluid  or  carbolic  acid,  and  they  should  also 
be  protected  from  flies.  It  is,  however,  most  necessary  that  the 
motions  should  be  saved  for  the  physician  to  see,  because  they  are 
extremely  important  in  judging  the  progress  of  the  case. 

In  very  mild  cases  the  bowels  should  be  cleansed  by  an  initial 
dose  of  one  tablespoonful  of  castor  oil,  which  may  be  administered 


TREATMENT  1855 

in  neat  brandy,  with  or  without  a  few  drops  of  liquor  opii  sedativus 
or  tincture  of  opium,  and  this  should  be  followed  a  few  hours  later 
by  the  administration  of  astringents,  such  as  bismuth  salicylate 
5  grains,  and  salol  5  grains,  made  into  cachets,  and  taken  every  two 
or  four  hours  at  first,  and  less  frequently  when  the  character  of  the 
motions  improves.  In  these  mild  cases  tenesmus  rarely  requires 
any  special  treatment,  and  rectal  injections  are  well  borne,  and  may 
be  administered  twice  daily,  though  in  most  cases  they  are  un- 
necessary. These  injections  should  consist  of  either  boric  acid 
(1  in  100),  which  is  probably  the  best,  salicylic  acid  (1  in  500),  tannic 
acid  (1  in  500),  normal  saline  solution,  or  borax  and  bicarbonate 
of  soda  (5  grains  of  each  to  the  ounce).  In  administering  these 
enemata,  the  patient  should  lie  on  the  left  side,  with  the  buttocks 
elevated  on  a  pillow  and  the  head  placed  low.  A  soft  rectal  tube 
should  be  smeared  with  vaseline  and  passed  as  high  up  the  bowel 
as  possible.  Two  pints  of  the  enema  are  now  run  in  by  gravity 
from  a  glass  irrigation  vessel,  and  should  be  warmed  to  a  tempera- 
ture of  about  990  to  ioo°  F.  The  enema  should  be  retained  as  long 
as  possible.  This  treatment,  with  an  appropriate  diet,  soon  gives 
relief,  the  pain  disappearing,  the  motions  becoming  faeculent. 
During  convalescence  a  tonic  of  hydrochloric  acid,  cinchona  bark, 
and  gentian  is  found  to  be  very  serviceable. 

In  severe  cases  the  serum  treatment  should  be  used  as  soon  as 
possible,  though  at  times  it  is  useful  to  precede  it  with  a  dose  of 
castor  oil  and  associate  to  it  the  saline  treatment.  Kruse's  serum, 
Shiga's  serum,  the  Lister  Institute  serum  (Todd),  and  that  of  the 
Pasteur  Institute  (Vaillard  and  Dopter),  are  all  good.  A  polyvalent 
serum,  such  as  that  of  Shiga,  is  preferable  in  those  cases  in  which 
a  complete  etiological  diagnosis  of  the  malady  cannot  be  made. 

The  serum,  in  our  experience,  should  be  given  in  large  doses;  thus 
that  from  the  Pasteur  Institute  and  the  Lister  Institute  should  be 
given  in  20  c.c.  to  40  c.c.  doses  twice  daily,  and  in  very  severe  cases 
four  times  daily.  The  injection  should  be  made  under  the  skin  of  the 
abdomen  or  flank,  using  the  ordinary  aseptic  precautions.  These 
injections,  as  a  rule,  need  not  be  continued  after  the  second  or  third 
day.  They  may  be  followed  by  urticarial-like  eruptions  and  pains 
in  the  joints.  Calcium  chloride  or,  better,  calcium  lactate  in  doses 
of  gr.  x.  may  be  administered  if  these  symptoms  are  severe  three  or 
four  times  daily.  When  the  blood  and  mucus  have  disappeared 
from  the  stools,  salol  (gr.  x.  every  four  hours)  or  the  ordinary  astrin- 
gents, such  as  bismuth  subnitrate,  or  tannalbin  (gr.  x.  to  xv.  every 
two  hours),  should  be  prescribed. 

Our  rules  for  the  administration  of  the  polyvalent  serum  are: — 

I.  In  mild  cases  inject  one  dose  of  20  c.c. 
II.  In  cases  of  medium  severity  inject  two  doses  daily  of  20  c.c. 

for  two  days. 
III.  In  severe  cases  inject  40  c.c.  twice  or  thrice  a  day  for  two 
or  three  or  four  consecutive  days. 


1856  THE  DYSENTERIES 

As  a  rule  the  serum  treatment  should  not  be  continued  for  more  than  four 
or  five  days,  and  it  should  not  be  repeated  later  on,  or  symptoms  of 
anaphylaxis  may  develop. 

The  serum  has  often  a  marked  effect  upon  the  disease,  hastening 
the  cure,  ameliorating  the  symptoms,  and  reducing  the  mortality, 
but  it  must  be  admitted  that  in  certain  cases  it  has  practically  no 
action  whatever. 

When  the  serum  treatment  cannot  be  carried  out,  the  saline 
treatment  is,  in  our  experience,  the  most  useful.  Two  drachms 
of  magnesium  sulphate  and  2  drachms  of  sodium  sulphate,  dis- 
solved in  an  ounce  of  water,  chloroform  water,  or  peppermint  water, 
should  be  administered,  and  then  1  drachm  of  each  should  be  given 
every  two  hours,  or  half  doses  every  hour,  until  the  motions  become 
faeculent. 

There  is  generally  considerable  pain  in  these  more  acute  cases, 
and  therefore  a  fomentation  sprinkled  with  laudanum  should  be 
applied  to  the  abdomen,  and  the  tenesmus  should  be  relieved  by 
suppositories  of  morphia  or  of  cocaine.  If  these  remedies  fail, 
then  hypodermic  injections  of  morphia  or  opium  (gr.  ^)  by  the 
mouth  must  be  given,  for  it  is  a  most  important  factor  in  the  treat- 
ment that  the  patient  should  not  suffer  more  than  can  possibly  be 
avoided  from  this  distressing  symptom.  If  prolapse  of  the  anus 
or  rectum  occurs,  it  is  important  that  this  should  be  reduced  and  re- 
lieved by  an  astringent  ointment,  such  as  hazeline  or  gall  and  opium. 

Rectal  injections  may  be  given,  as  described  above,  but  in  sensi- 
tive cases  it  is  as  well  to  pass  in  a  second  tube  alongside  the  enema- 
tube,  so  that,  instead  of  the  inflamed  bowel  being  distended  by  the 
injection,  it  may  be  simply  washed  by  the  irrigation  of  the  boric 
lotion. 

During  the  treatment  of  the  severe  acute  forms  a  great  danger 
is  to  stop  the  saline  treatment  too  quickly,  and  to  allow  constipa- 
tion to  occur,  by  which  is  meant  that,  though  the  patient  may 
be  having  fifty  to  a  hundred  motions  per  diem,  still,  faeculent  matter 
is  being  retained.  On  the  other  hand,  there  is  danger  in  continuing 
the  saline  treatment  too  long,  for  in  our  experience  this  should  be 
stopped  on  the  third  day  if  there  is  no  improvement,  and  also  when 
the  motions  become  serous. 

After  the  acute  stage  is  over  it  may  be  found  useful  to  employ 
some  astringent  drugs,  such  as  tannalbin,  15  grains  every  two  hours, 
or  large  doses  of  bismuth  subnitrate  (gr.  xv.  to  xxx.,  with  or  without 
salol  (gr.  v.  to  x.),  every  two  hours,  in  cachets  or  emulsion,  and  an 
enema  of  boracic  or  tannic  acid  (-£-  to  1  per  cent.)  per  rectum  may  be 
administered. 

If  there  is  a  tendency  to  chronicity,  fresh  Bael  fruit  may  be 
given.  It  must,  however,  be  both  fresh  and  ripe,  and  should  be 
prepared  by  being  boiled,  and  then  shredded  with  a  fork  into 
warm  milk,  pressed  and  strained,  and  then  a  little  sugar  added. 
A  tumblerful  of  the  milk  extract  of  Bael  fruit  may  be  taken 
twice  daily. 


TREATMENT  1S57 

Tincture  of  Mansonia  ovata  in  i-drachm  closes  is  also  recom- 
mended. Other  remedies  resembling  the  above  are  the  roots  of 
Pelargonium  tuberosum  and  P.fldbelUfolium. 

With  regard  to  individual  symptoms,  collapse  should  be  treated 
by  the  hypodermic  injection  of  saline,  hemorrhage  by  calcium 
lactate. 

Very  severe  cases,  involving  the  whole  of  the  large  bowel,  and  gangrenous 
cases  may  be  treated  by  appendicostomy  and  washing  out  of  the  bowel  with 
a  weak  permanganate  or  boric  acid  solution. 

The  simple  operation  is  performed  as  follows:— The  patient  is  placed  under 
chloroform,  after  the  usual  antiseptic  preparation  of  the  area  of  the  opera- 
tion. An  incision  of  about  3  inches  in  length  is  made  in  the  usual  site  for 
the  operation  of  appendectomy,  and,  the  layers  of  the  abdominal  wall  having 
been  incised,  the  peritoneum  is  carefully  opened,  and  the  appendix  is  searched 
for  and  brought  forward  into  the  wound,  so  that  about  1  inch  protrudes. 
Here  it  is  stitched  by  four  stitches  to  the  muscles.  The  wound  is  now  closed, 
the  appendix  being  fixed  to  the  skin  by  a  couple  of  stitches.  The  wound  is 
now  dressed  aseptically  with  a  thin  layer  of  wool  and  covered  with  collodion. 
The  tip  of  the  appendix  is  now  removed,  and  a  No.  8  or  No.  6  catheter  inserted. 
The  wound  is  now  dressed  antiseptically  and  left  for  twenty-four  hours,  at 
the  end  of  which  time  a  large  tube  is  placed  in  the  rectum,  and  the  whole 
bowel  is  irrigated  with  1  percent,  solution  of  bicarbonate  of  soda  to  remove 
the  mucus,  and  then  with  a  boracic  acid  lotion,  1  drachm  to  the  pint.  This 
is  repeated  daily,  but  if  the  case  tends  to  become  chronic  a  solution  of  silver 
nitrate  (5  to  20  grains  to  the  pint)  is  used. 

When  the  cure  is  effected,  the  small  wound  is  easily  closed. 

Other  methods  of  treatment  include  the  calomel  treatment  much  praised  by 
Scheube  and  Kartulis,  and  begun  long  ago  by  the  Indian  physicians,  and 
among  the  various  forms  in  which  it  has  been  applied,  Twining's  pill  of  calomel, 
blue  pill,  and  ipecacuanha  used  to  be  very  celebrated.  Plehn  recommends 
that,  after  a  preliminary  dose  of  castor  oil,  £  grain  of  calomel  be  administered 
hourly  until  twelve  doses  have  been  taken  during  the  day.  The  treatment  is 
discontinued  during  the  night,  and  repeated  in  the  same  manner  during  the 
second  and  third  days,  after  which  bismuth  subnitrate  is  given  in  6-grain 
doses  hourly  during  the  day  for  a  long  period  of  time. 

Yellow  santonin,  0-3  gramme  in  8  grammes  of  olive  oil,  administered  three 
times  a  day,  has  been  recommended  by  Drake.  Musgrave  recommends  that 
acetozone  (strength  1  in  5,000;  aerated  if  necessary)  should  be  freely  drunk, 
so  as  to  prevent  fermentation  in  the  stomach  and  bowels.  In  all  cases  a  mouth- 
wash— -e.g.,  glyco-thymoline — should  be  ordered.  During  convalescence  the 
great  point  is  to  prevent  chills  and  indiscretions  in  diet,  which  may  induce 
attacks  of  diarrhoea.  Turpentine  duotal  and  styracol,  especially  in  com- 
bination with  castor  oil,  have  been  recommended  by  some. 

Cyllin  and  other  similar  disinfectants  have  been  advised,  but  have  not  given 
any  very  good  results  in  our  experience.     Bolus  alba  has  been  advocated. 

Various  colloidal  silver  preparations  have  been  recommended. 

The  sour-milk  treatment  may  be  tried  in  subacute  or  chronic  cases,  with 
sauerin,  lacto-bacillin,  fermenlactyn,  or  any  other  preparation  on  the  market, 
or  by  using  the  ferment  as  prepared  by  the  natives  of  the  country.  Consti- 
pation is  counteracted  by  small  doses  of  castor  oil,  liquid  paraffin,  Carlsbad 
salts,  Hunyadi  Janos,  Apcnta  water,  or  enemata,  but  if  of  a  marked  nature 
should  arouse  suspicions  of  stenosis,  especially  if  the  ordinary  laxative  remedies 
do  not  ameliorate  the  condition.  Under  these  circumstances  sigmoidoscopy 
should  be  performed,  and  the  stricture  dilated  by  bougies  or  catheters. 

Treatment  of  Dysenteric  Infantile  Diarrhoea. — The  treatment  of 
infantile  diarrhoea  and  of  dysentery  in  children  is  best  conducted 
by  administering  a  small  dose  of  castor  oil  (3i.  to  3ii.),  followed  by 

117 


1858  THE  DYSENTERIES 

calomel  (gr.  })  or  grey  powder  (gr.  £),  every  hour  until  six  doses 
are  given  in  a  child  of  two  years  of  age.  The  dosage  may  be 
decreased  or  increased  according  to  age.  Afterwards  astringents 
such  as  tannigen  (gr.  iii.)  or  tannalbin  (gr.  v.)  may  be  given  every 
two  to  four  hours. 

In  severe  cases,  due  to  the  Shiga-Kruse  or  the  Flexner  bacillus, 
serum  treatment  is  the  best,  5  to  10  c.c.  being  injected  twice  daily. 
The  diet  should  be  altered  from  milk  to  albumen  water,  whey, 
diluted  meat -juice,  or  clear  soup. 

Pain  must  be  combated  by  hot  fomentations,  and  convulsions 
by  bromides  given  in  gr.  xv.  as  enemata,  or  in  small  doses  by  the 
mouth  in  albumen  water.  Chloroform  may  require  to  be  adminis- 
tered, while  some  authors  recommend  minute  doses  of  morphia. 

Treatment  of  Chronic  Dysentery. — The  treatment  of  chronic 
dysentery  varies,  for  sometimes  the  malady  is  easily  amenable 
to  the  treatment  laid  down  for  mild  cases  of  acute  dysentery, 
while  at  other  times  many  remedies  may  be  tried  without  success. 
After  an  initial  dose  of  castor  oil,  tannigen,  in  3  to  8  grain,  or 
tannalbin  in  10  to  20  grain  doses,  in  cachets,  may  be  tried  three 
to  six  times  a  day.  In  old-standing  cases  pilula  plumbi  cum 
opio  should  be  given  twice  a  day.  Serum  treatment  should  also 
be  tried  during  the  exacerbations,  as  indicated  above.  Bael  fruit, 
the  rind  of  the  mangosteen,  simaruba  bark,  etc.,  are  all  useful  in 
this  condition,  and  the  lavage  treatment  is  more  useful  than  in  acute 
cases.  Rectal  irrigations  should  always  begin  with  2  pints  of 
1  per  cent,  solution  of  bicarbonate  of  soda  to  remove  the  adherent 
mucus,  and  then  the  medicated  enema  may  be  administered,  and 
may  consist  of  boracic  acid  (1  per  cent.),  followed  by  an  enema 
containing  bismuth  subnitrate  and  sodium  salicylate  suspended  in 
a  pint  or  less  of  mucilage,  silver  nitrate  (|  to  1  grain  to  the  ounce), 
copper  sulphate  (2  grains,  with  5  minims  of  tincture  of  opium  to  the 
ounce  of  water),  tannin  (0*2  to  0-5  per  cent.),  resorcin  (1  to  2  per 
cent.),  creolin  (1  drachm  to  the  pint),  lysol  (1  per  cent.),  or  formalin 
(1  in  5,000),  may  all  be  used.  Silver  nitrate)  however,  gives  the 
best  results,  gr.  x.  to  the  pint.  Albargin  (1  in  500,  1  in  1,000)  has 
also  been  recommended.  Perchloride  of  mercury  (1  in  20,000) 
should  not  be  used  as  a  rectal  enema,  as  it  is  dangerous,  and  may 
increase  the  symptoms  instead  of  diminishing  them.  In  chronic 
or  subacute  obstinate  cases  the  vaccine  treatment  first  introduced 
for  dysentery  by  Castellani  and  Greig  may  be  tried,  using  vaccines 
prepared  from  the  dysenteric  bacilli  isolated  from  the  stools  of  the 
patient.  Forster  has  tried  this  treatment  also  in  acute  cases.  In 
our  experience  it  gives  good  results  in  several  cases  of  the  chronic 
type,  but  in  acute  dysentery  is  much  inferior  to  the  serum  and  saline 
treatment.  If  all  these  methods  of  treatment  fail,  appendicostomy 
should  be  tried. 

Diet. — There  is  no  point  in  the  treatment  of  dysentery  of  greater 
importance  than  the  diet.  The  bowel  requires  physiological  rest, 
and  therefore,  in  very  severe  cases,  the  diet  must  be  restricted 


PROPHYLAXIS  1859 

to  albumen  water  and  whey,  and  brandy  given  only  if  absolutely 
necessary. 

In  milder  cases  the  diet  should  consist  of  milk,  which  must  be 
diluted  with  Perrier,  soda,  Vichy,  or  barley  water,  or  may  be  mixed 
with  powders  of  sodium  bicarbonate  (gr.  vi.),  potassium  bicarbonate 
(gr.  vi.),  sodium  chloride  (gr.  iii.),  or  sodium  citrate  (gr.  xl.),  to  the 
pint  of  milk,  and  less  in  proportion.  Arrowroot  made  with  water 
or  milk,  at  first  thin  and  later  thick  and  flavoured  with  a  little 
brandy,  is  most  useful.  Benger's  food  and  Horlick's  malted  milk  are 
also  useful.     Strong  meat-essences  and  alcohol  should  be  avoided. 

In  all  severe  cases  the  food  must  be  given  in  small  quantities 
every  two  hours,  about  4  ounces  at  a  time,  and  must  be  taken  very 
slowly,  and  should  be  neither  very  warm  nor  cold.  In  chronic 
dysentery  this  milk  diet  is  of  the  greatest  importance,  and  may, 
as  already  stated,  be  supplemented  by  the  sour-milk  treatment. 

When  convalescence  begins,  chicken-broth  and  milk-puddings 
may  be  added  to  the  diet,  and  then  lightly-boiled  eggs  and  toast; 
then  chicken,  cream,  and  fish;  but  for  a  long  time  only  white  flesh 
should  be  allowed,  and  not  much  of  this,  for  the  diet  should  for 
several  weeks  consist  largely  of  milk  foods.  Of  especial  importance 
in  convalescence  is  the  chewing  of  the  food,  and  care  must  be  taken 
not  merely  that  the  teeth  are  in  good  order,  but  that  the  patient 
is  directed  not  to  swallow  any  tough  or  very  fibrous  piece  of  food. 
Fruit  must  be  avoided  for  a  long  time. 

Prophylaxis. — One  of  the  important  prophylactic  measures  which 
is  at  present  but  little  used,  owing  to  practical  difficulties,  is  the 
isolation  of  the  convalescent  until  three  bacteriological  examinations 
of  the  faeces  give  a  negative  result.  Another  is  the  search  for  dysen- 
tery carriers  in  a  locality  in  which  the  disease  is  endemic  or  occa- 
sionally epidemic.  The  treatment  of  a  carrier  must  be  the  same 
as  for  a  case  of  chronic  dysentery,  but  here  vaccination  will  be 
distinctly  useful.  The  persons  to  be  suspected  are  those  with  a 
history  of  dysentery,  or  with  a  history  of  having  nursed  a  case  of 
dysentery,  and  people  occupied  in  the  cooking  or  handling  of  food 
materials. 

Another  very  important  measure  is  the  destruction  by  burning  or 
the  disinfection  of  the  dysenteric  motion  by  either  crude  carbolic 
acid  or  by  Jeyes'  fluid,  together  with  its  careful  protection  against 
flies  before  its  final  disposal. 

The  personal  prophylaxis  consists  in  drinking  only  filtered  and 
boiled  water,  and  using  the  same  for  cleaning  the  teeth,  in  avoiding 
salads  and  fresh  vegetables  and  unripe  fruit,  and  in  carefully 
washing  the  exterior  of  any  fruit. 

With  regard  to  public  prophylaxis,  a  modern  method  of  collecting 
and  disposing  of  the  sewage  of  towns  is  necessary  everywhere  in 
order  to  prevent  the  disease  from  spreading,  and  there  is  no  doubt 
that  for  this  purpose  the  best  method  for  tropical  towns  is  the 
Shone  or  pneumatic  system,  as  introduced  into  Rangoon,  Bombay, 
and  Karachi. 


i860  THE  DYSENTERIES 

Good  scavenging  and  strict  hygienic  laws  are  necessary  to  prevent 
the  breeding  of  flies,  and  if  an  epidemic  of  dysentery  occurs,  a 
special  crusade  against  the  common  house-fly,  if  not  begun  before, 
should  at  once  be  undertaken,  as  has  been  done  for  other  reasons 
in  Liverpool  and  elsewhere,  especially  in  America. 

Dust  should  be  diminished  in  the  warm  dry  weather  by  the 
efficient  watering  and  brushing  of  the  roads  of  towns,  and  in  this 
water  some  cheap  disinfectant  such  as  permanganate  of  potash 
should  be  used,  especially  for  the  more  important  streets. 

The  drinking-water  of  all  large  towns  should  be  filtered,  though 
it  must  be  admitted  that  this  alone  is  not  a  sufficient  safeguard 
against  a  water-borne  epidemic. 

Vaccination. — Owing  to  bacterial  dysentery  being  due  to  several  different 
bacilli,  and  owing  to  the  fact  that  the  Shiga- Kruse  bacillus  is  very  toxic  the 
preparation  of  an  efficient  vaccine  giving  a  not  too  severe  reaction  is  difficult. 

Broth  Cultures  Vaccine.— Antidysentery  vaccines  prepared  with  broth 
cultures  should  never  be  used,  as  they  give  rise  to  an  extremely  severe  local 
reaction,  with  at  times  abscess  formation. 

Peptone  Water  Vaccine. — Castellani,  in  1904,  prepared  a  mixed  peptone 
water  vaccine  which  gave  fairly  satisfactory  results.  The  preparation  was 
as  follows : — The  Shiga-Kruse  bacillus  and  three  other  species  of  dysentery 
bacilli  were  grown  in  peptone  water  tubes  for  three  days  at  350  C.  They 
were  kept  for  an  hour  at  the  temperature  of  55°-6o°  C,  and  then  mixed,  three 
parts  Shiga-Kruse  and  one  part  of  each  of  the  others.  Of  the  resulting  mixed 
vaccine  1  c.c.  (sometimes  J  c.c.)  was  injected,  the  inoculation  being  repeated 
after  a  week  or  two.  The  reaction  was  not  severe.  Later  Castellani  prepared 
the  same  vaccine  without  heating,  adding  simply  \  per  cent,  carbolic.  Accord- 
ing to  Castellani,  the  very  much  less  marked  reaction  noted  than  when  using 
broth  vaccines,  is  not  merely  due  to  the  fact  that  peptone  water  cultures 
contain  fewer  bacilli  than  broth  cultures. 

Carbolized  Emulsion  Mixed  Vaccine. — Since  191 2  Castellani  has  used  in 
Ceylon  a  carbolized  mixed  vaccine  containing  B.  dysenteries  Shiga-Kruse, 
Hiss-Russell  Y,  original  Flexner,  Ceylon  Flexner-like  No.  1,  Ceylon  Flexner- 
like  No.  2.  The  preparation  of  this  mixed  vaccine  is  as  follows:- — The  indi- 
vidual vaccines  are  prepared  by  making  emulsions  from  twenty-four  hours' 
old  agar  cultures  in  normal  salt  solution  (0-75  per  cent.),  to  which  0-5  per 
cent,  of  carbolic  acid  has  been  added, and  the  individual  vaccines  are  standard- 
ized in  such  a  way  as  to  contain  per  c.c.  1,000  million  germs.  These 
monovaccines  so  standardized  are  mixed  in  equal  parts,  so  that  1  c.c.  of  the 
mixed  vaccine  will  contain  125  millions  of  each  of  the  organisms  used.  Of  this 
mixed  vaccine  0-5  to  o*6  c.c.  is  given  hypodermically  the  first  time,  and  the 
same  or  double  the  amount  after  a  week.  Agglutinins  generally  develop  for 
all  the  inoculated  germs,  but  their  amount  is  not  high,  and  may  be  inconstant 
and  irregular,  but  the  same  may  be  said  of  simple  monovaccines,  Shiga, 
Flexner,  etc. 

It  is  essential  to  prepare  the  vaccine  with  strains  which,  though  rich  in 
antigen,  are  only  slightly  virulent.  It  is  extremely  rare  to  come  across  such 
a  strain  of  Shiga-Kruse.  A  large  series  of  strains  of  this  species  are  inoculated 
into  rabbits,  and  the  least  virulent,  provided  it  is  rich  in  antigen,  is  kept 
permanently  as  a  stock  culture  to  prepare  the  vaccine. 

Combined  Carbolized  Dysentery  and  Typhoid  and  Para  A  and  Para  B  Vaccine. 
— -This  vaccine  has  been  prepared  by  Castellani,  in  191 3,  following  this 
technique: — The  individual  vaccines  are  prepared  by  making  emulsions  from 
twenty-four  hours'  old  agar  cultures  in  normal  salt  solution  (0-75  per  cent.),  to 
which  £  per  cent,  carbolic  has  been  added.  The  monovaccines  are  then 
standardized  as  follows:' — Typhoid  vaccine  4,000  millions  per  c.c,  para  A 
1,000,  para  B  1,000,  Shiga  1,000,  Flexner  1,000,  Hiss-Russell  Y  1,000,  Flexner 
Ceylon  (No.  1)  1,000,  Flexner  Ceylon  (No.  2)  1,000.     The  monovaccines  are 


PSEUDO-DYSENTERIES  1861 

mixed  in  equal  parts.  The  mixed  vaccine  will  therefore  contain  200  millions 
typhoid  and  125  millions  each  of  the  other  Oganisms  used.  Of  this  vaccine 
0-5  to  o-6  c.c.  is  given  hypodermieally  the  first  time,  and  the  same  or  double 
the  amount  after  a  week.  The  reaction  is  somewhat  more  severe  than  after 
inoculation  with  the  triple  typhoid  para  A  and  para  B  vaccine. 

In  the  preparation  of  the  vaccine  it  is  necessary  to  use  a  selected  strain 
of  Shiga-Kruse,  as  little  virulent  as  possible. 

Sensitized  Vaccine. — An  emulsion  in  normal  saline  is  made  from  twenty- 
four  hours'  old  agar  cultures.  To  the  suspension  is  added  some  undiluted 
dysentery  serum,  and  after  twenty-four  hours  it  is  centrifuged  and  the  serum 
and  saline  pipetted  off.  The  sediment  is  washed  in  normal  saline,  and  then 
a  suspension  is  made  in  fresh  saline  containing  1  per  cent,  carbolic,  and 
standardized  to  contain  100  million  bacilli  or  more;  J-  c.c.  is  injected  the  first 
time,  and  the  same  or  double  the  dose  a  week  later. 

A  sensitized  dysentery  vaccine  was  first  prepared  and  used  by  Broughton 
Alcock  in  1914.  It  has  been  used  later  by  other  observers,  and  experiments 
on  it  have  been  carried  out  recently  by  Gibson.  The  reaction  is  much  less 
severe  than  using  broth  vaccines. 

Serum-Vaccine. — In  Japan  a  vaccine  has  been  given  mixed  with  anti- 
dy.senteric  serum,  with  the  object  of  neutralizing  the  bacillary  endotoxin 
■with  the  anti-endotoxin  present  in  the  serum.  The  injection  of  such  serum- 
vaccine  docs  not  give  rise  to  any  production  of  agglutinins,  and  the  doubt 
has  arisen,  to  which  Gibson  has  called  attention,  that  the  antiserum  might 
neutralize  all  the  antigenic  properties  of  the  vaccine,  besides  neutralizing 
the  toxin. 

Gibson's  '  Absorbed-Serum  Vaccine.' — Gibson  mixes  the  dysentery  vaccine 
with  antidysentery  serum  from  which  the  agglutinins  and  other  antibacterial 
substances  have  been  removed  by  means  of  Castellani's  absorption  method. 
Suspensions  in  normal  saline  are  made  from  agar  cultures  of  Shiga-Kruse, 
Flexner,  and  Y;  they  are  standardized,  and  then  mixed  in  such  proportion 
that  1  c.c.  of  the  mixture  will  contain  2,000  millions  Shiga-Kruse,  2,000  millions 
Flexner,  2,000  millions  Y. 

Trivalent  antidysentery  serum  (Shiga-Flexner-Y)  is  absorbed  with  Flexner, 
then  with  Y,  then  with  Shiga.  It  is  centrifuged  and  filtered  through  a 
Chamberland.  The  filtered  serum  is  then  so  diluted  that  1  c.c.  of  the  resulting 
dilution  will  contain  0-4  of  serum.  The  diluted  serum  and  the  vaccine  are 
fdled  into  twin  non-communicating  phials,  which  are  joined  together. 
The  inoculation  is  carried  out  as  follows: — 0-25  c.c.  is  aspirated  in  the  syringe 
from  each  phial  and  injected  subcutaneously  in  the  usual  way.  The  first 
dose  contains  Shiga  500  millions,  Flexner  500  millions,  Hiss  and  Russell  500 
millions,  and  o-io  absorbed  serum.  A  week  later  double  the  amount  is 
given.  This  absorbed  serum-vaccine  gives  only  a  very  moderate  reaction, 
and  seems  to  induce  in  the  blood  of  the  inoculated  persons  a  satisfactory 
amount  of  antibacterial  substances  as  well  as  antitoxin. 

Dysbackta. — This  is  a  vaccine  prepared  according  to  a  special  method  by 
Boehncke. 

Lipovaccine. — A  vaccine  consisting  of  an  oil  emulsion  of  dysentery  bacilli 
h  v\  been  prepared  according  to  Le  Moignic's  method.  The  reaction  is  said 
to  be  mild. 

C.  PSEUDO-DYSENTERIES. 

Definition. — Pseudo-dysenteries  are  diseases  other  than  those 
defined  above,  which  ;;ive  rise  to  diarrhoea,  with  the  passage  of  blood 
and  mucus  in  the  motions,  and  are  sometimes  associated  with 
abdominal  pain  and  tenesmus,  and  may  readily,  on  superficial 
examination,  be  mistaken  for  true  dysentery. 

Remarks. — It  should,  however,  be  noted  that  the  term  '  pseudo- 
dysentery  '  has  been  used  by  Kruse  to  signify  a  form  of  bacteria  1 
dysentery  commonly  found  among  inmates  of  lunatic  asylums,  and 


1 862  THE  DYSENTERIES 

later  to  denote  every  variety  of  the  disease  not  caused  by  the  Shiga- 
Kruse  bacillus. 

/Etiology. — -The  most  common  causes  of  the  pseudo-dysenteries 
are  cancer  of  the  intestine,  especially  of  the  rectum,  inflamed 
piles,  gummata  in  the  rectum,  cancers  of  the  large  bowel  other  than 
the  rectum,  and  intussusception.  The  native  habit  of  eating 
the  small  bones  of  fish  along  with  the  flesh  is  apt  to  cause  irritation 
of  the  rectum  and  a  pseudo-dysenteric  attack.  Inflammations  of 
the  broad  ligament,  especially  on  the  left  side,  are  apt  to  be  con- 
fused with  a  mild  attack  of  dysentery.  Poisons,  such  as  mercury, 
ptomaines,  ricin,  abrin,  etc.,  may  also  produce  symptoms  resembling 
dysenteric  attacks.  Prout  has  described  a  form  of  dysentery  in  the 
Gambia  due  to  drinking-water  containing  the  excreta  of  locusts. 

Diagnosis. — The  diagnosis  of  these  various  conditions  has  already 
been  discussed  in  the  Diagnosis  of  Bacillary  Dysentery,  and  need 
not  be  repeated. 

Treatment. — The  treatment  must  be  adapted  to  the  specific  com- 
plaint, while  the  bowel  symptoms  may  be  relieved  as  indicated 
under  the  treatment  of  Bacillary  Dysentery. 

REFERENCES. 

Protozoal  Dysenteries. 

Amoebic  Dysentery. 

The  current  literature  is  found  in  the  Bulletin  of  the  Tropical  Diseases 
Burea.u. 

Barbagallo  and  Casagrandi  (1897).    Annali  d' Igiene  Sperimentale.    Roma. 

Bayliss  (1919).     Lancet,  January  n. 

Buchanan  (191 7).     Proc.  Roy.  Soc.  Med.,  vol.  xi.,  No.  2. 

Castellani  (1901).     RivistaCriticaClinica  Medica.     (1902-03).  Zeitschrift  fur 

Hygiene,  Bd.  xxxvii.,  xi.    (1905).  Archiv  fiirSchiffs-und  Tropen- Hygiene. 

(i9io).Philipp.  Journ.of  Science,  vol.  v.,  No.  2,  Section  B.    (1914).  Journ. 

i>t   Trop.  Med.,  March  2  and   16  (Entoplasma).     (1917).  Journ.  of  Trop. 

Med.,  August  15.      (igt.S).  Annali  Med.  Navale,  vol.  i.,  fasc.  i.-ii. 
Chalmers  and  Archibald  (1915).    Journal  of  Tropical  Medicine  and  Hygiene. 

181-183. 
Craig  (1912).     New  Orleans  Medical  and  Surgical  Journal,  lxv.,  i.  1-17. 
Darling  (191 2).     Journal  of  Tropical  Medicine  and  Hygiene,  September  2. 

London. 
Dale  and  Dobell  (1917-18).     Journal  of  Pharmacology  and  Experimental 

Therapy. 
Franchini  (191 2).     Malaria. 
Gabbi   (1918).     Publicazioni   Monografiche   delle    Malattie   degli  Eserciti  in 

Guerra.     Roma. 
Kruse  (1900).     Deutsche  Medizinische  Wochenschrift,  No.  41;  (1901)  Nos. 

23  and  24;  (1903)  Nos.  1,  3,  12. 
Laidlau  (1919).     Guy's  Hospital  Reports. 
Rho  (1903).     La  Dissentera  e  le  sue  forme.     Roma. 
Rogers    (1912).     British   Medical    Journal,    June    22,    August    24;    Lancet 

October  19. 
Sellards  and  McIver  (1918).     Journal  of  Pharmacology,  vol.  xi.,  No.  4. 
Simon  (1918).     Journ.  Am.  Med.  Ass. 
Vaccarezza  (1918).     Semana  Med.,  No.  36. 
Vedder  (1912).     Transactions  Hong  Kong  Congress. 

Wenyon  and  O'Connor  (191 7).     Journal  Royal  Army  Medical  Corps,  May. 
Woodcock  (1918).     British  Medical  Journal,  December  28. 
Yorke  (19x8).     Transactions  Society  Tropical  Medicine,  vol.  xi. 


REFERENCES  1863 

Laveranic  and  Leishmanic  Dysenteric?. 
The  literature   on    these  subjects    may   be   found   under   Malaria    (Chap- 
ter XL.)  and  Kala-Azar  (Chapter  XLVIL). 

Ciliar  Dysenteries. 
Bowman  (1909).     Philippine  Journal  of  Science,  December.     Manila. 
Manlove  (191 7).     Phil.  Journ.  Science.    Manila. 
Mason  (1919).     Journ.  of  Parasitology  of  Urbana,  111.,  March. 
Strong  (1904).     Philippine  Journal  of  Science.     Manila. 

Platyhelminthic  Dysenteries. 
The  literature  on  these  subjects  may  be  found  under  Katayama  Disease 
(Chapter  LXV.)  and  Intestinal  Schistosomiasis  (Chapter  LXXIX.). 

Arthropodic  Dysenteries. 

See  the  literature  on  Intestinal  Myiasis  (Chapter  LXVII.). 

Bacillary  Dysenteries. 

The  current  literature  is  found  in  the   Bulletin  of  the  Tropical  Diseases 

Bureau. 

Alcock  (1919).     Brit.  Med.  Journ. 

Bahr  (1912).     Report  on  Dysentery  in  Fiji. 

Castellani  (1904).  Journal  Ceylon  Branch  of  the  British  Medical  Associa- 
tion. Colombo.  (1910).  Philipp.  Journ.  of  Science,  vol.  v.,  No.  2, 
Section  B.  (1917).  Journ.  of  Trop.  Med.  August  15.  (1918).  Annali 
Med.  Nav.,  vol.  1.,  fasc.  ii. 

Castellani,  Spagnuolo  and  Russo  (1918).  Bull.  Soc.  Pathol.  Exotique, 
April  10  (Spirobacillus  zeylanicus). 

Fletcher  and  Mackinnon  (1919).     Lancet,  June  14. 

Flexner  (1901).     British  Medical  Journal,  ii.  786.     London. 

Gibson  (1917.)     Journ.  R.A.M.C.,  June. 

Hunt  (1912).     Journal  American  Medical  Association,  September. 

Kruse  (1900-1907).  Deutsche  Med.  Wochenschrift ;  (1900)  40;  (1901)  23,  24; 
(1903)  12 ;  (1907)  8  and  9. 

Ledingham  and  Arkwright  (191 2).  The  Carrier  Problem  in  Infectious 
Disease.     London. 

Levi  della  Vida  (1918).     Gior.  Med.  Militare. 

Ludke  (191  i).  Die  Bazillenruhr.  Jena.  (Important  monograph  with 
full  bibliography.) 

Martin  and  Williams  (1917).     Brit.  Med.  Journ.,  April  14. 

Martin  and  Williams  (1918).     Journ.  Hyg.,  vol.  xvi.,  No.  3. 

Meserschmidt  (1912).     Deutsch  Med.  Wochenschrift,  September. 

Muller  (191 2).     Munch.  Med.  Wochenschrift,  October. 

Nicolle,  Debains,  Loiseau  (1916).  Annales  Inst.  Pasteur.  (A  valuable 
paper.) 

Nuttall  and  Jephson  (1909).  Reports  Local  Government  Board  (New 
Series),  No.  16,  4,  p.  20. 

Scheube  (1910).     Krankheiten  der  Warmen  Lander. 

Shiga  (1898).     Centralblatt  fur  Bakteriologie,  xxiii.  599;  xxiv.  817,  870,  913. 

Taylor  (1919).     Journ.  of  Pathology  {Spirobacillus  zeylanicus). 

Violle  (1912).     Archiv.  Medic,  et  Pharm.  Nav.,  July. 

Watt  (1919).     Journ.  of  Trop.  Med.,  March  15. 

Dysentery  Vaccines. 

Alcock  (1914).     Brit.  Med.  Journ.,  August. 

Castellani  (1904).  Ceylon  Med.  Reports.  (1909).  Centr.  f.  Bakter.  (1914). 
Journal  Ceylon  Branch  Brit.  Med.  Ass.  (1915).  Sperimentale;  Trans- 
actions Soc.  Trop.  Med.,  December.  (1916).  British  Med.  Journal, 
February  26.     (1917).   Journ.  Trop.  Med.,  August. 

Gibson  (191 7).     Journal  R.A.M.C.,  June. 


CHAPTER  LXXIX 
INTESTINAL   SCHISTOSOMIASIS 

Synonyms  —  Definition  —  History  —  Climatology  —  ^Etiology  —  Pathology 
— Sy  mp  to  ma  to  logy — Diagno  sis — Progno  sis — Treatment — Prop  hyla  xis — 
References. 

Synonyms.— Intestinal  bilharziosis,  Rectal  bilharziosis,  Hepatic  bilharziosis, 
American  bilharziosis,  Manson's  bilharziosis,  Manson's  disease. 

Definition. — Intestinal  bilharziosis  is  infection  with  Schistosoma 
mansoni  Sambon,  1907,  the  eggs  of  which  invade  and  irritate  the 
intestines  and  the  liver,  and  cause  inflammation. 

History. — It  has  long  been  known  that  the  eggs  found  in  cases  of 
intestinal,  rectal,  and  hepatic  bilharziosis  are  laterally  spined,  as 
Bilharz  pointed  out  in  1851;  and  Sonsino  once  stated  that  the  two 
worms  must  belong  to  different  species,  but  this  statement  did  not 
attract  attention.  In  1903  Manson  first  suggested,  on  grounds  of 
dissimilar  geographical  distribution,  that  these  eggs  might  belong 
to  a  new  species  of  Schistosoma,  and  in  1907  Sambon  showed  that  a 
separate  species  really  did  exist,  calling  this  S.  mansoni,  in  which 
he  has  been  supported  by  Holcomb,  Firket,  Broden,  Grun,  and 
others,  though  opposed  by  the  great  authority,  Looss. 

A  description  of  the  adult  worms  has  been  given  by  Da  Silva 
and  by  Flu,  confirming  the  differentiation  of  the  two  species. 

The  fact  of  the  existence  of  a  separate  disease  caused  by  the 
lateral-spined  eggs  of  S.  mansoni  is  supported  by  all  authors  who 
have  studied  the  disease  in  America,  where  the  patienl  s  are  said 
never  to  have  eggs  in  the  urine,  and  never  to  suffer  from  urinary 
schistosomiasis.  It  is  further  supported  by  the  work  of  Mathis  and 
Baujeau  on  a  case  from  Gaudeloupe,  and  by  that  of  Turner  in  South 
Africa.  Flu,  after  examining  1,000  eggs  from  fifteen  cases  of 
intestinal  schistosomiasis  in  Paramaribo,  never  found  one  with  a 
terminal  spine.  Reference  may  also  be  made  to  Letulle's  paper  on 
'  Bilharziose  Intestinale,'  published  in  1905,  to  Madden's  work  in 
1907,  and  to  Symmer's  work  in  1902  and  1906,  from  the  latter  of 
which  we  have  taken  our  two  illustrations.  Reference  must  also 
be  made  to  the  admirable  exposition  of  the  disease  by  Mathis,  Noc, 
and  Leger  in  1913.  In  1914  and  1915  Leiper  thoroughly  established 
the  species  S.  mansoni,  and  worked  out  its  life-history.  He  has 
traced  the  life-cycle  of  the  parasite  through  the  snails  to  its  adult 
condition  in  rabbits,  guinea-pigs,  and  man.  Lutz  has  published 
his  extended  researches  into  the  disease  and  its  parasite  as  seen 

1864 


CLIMATOLOGY 


1865 


in  Bahia  and  Northern  Brazil.  It  will  thus  be  seen  that  the 
recognition  of  the  disease  is  becoming  generally  accepted,  although 
this  was  by  no  means  the  case  when  this  chapter  was  first  written. 

Climatology. — As  far  as  is  known  at  present,  the  disease  exists  in 
Egypt,  Central  Africa,  Uganda,  South  Africa,  the  Belgian  Congo, 
Central,  South,  and  North  America,  and  the  West  Indies.  In 
Brazil  it  is  confined  to  the  northern  districts,  being  unknown  in  the 
South.  In  Venezuela  it  is  common  around  Caracas,  where  its 
intermediate  host  is  believed  to  be  Planorbis  guadehipensis  Sowerby 
by  Iturbe  and  Gonzalez. 

/Etiology. — The  cause  of  the  disease  is  Schistosoma  mansoni.  The 
description  and  life-historv  of  the  parasite  is  given  in  Chapter  XXIV., 
P-  587- 

Wr 


*M* 


Fig.  768B. — Cercaria  of  Schistosoma  mansoni 
from  Planorbis  boissyi. 


Fig.    jG^a.  —  Miracidium 

of       Schi  sto  so  mum 
mansoni. 

(Photomicrograph.) 


Fig.  768c. — Planorbis  boissyi. 


Pathology.- — The  worms  live  in  the  portal  vein,  but  are  especially 
attracted  to  the  bowels,  in  the  capillaries  of  which  they  lay  their 
eggs,  which  burst  those  vessels,  and  escape  into  the  mucosa,  causing 
therein  a  dense  cellular  infiltration  which  leads  to  a  thickening  of 
the  coats  of  the  bowel,  and  to  the  formation  of  papillomata,  which 
may  become  detached  and  form  ulcers.  Dense  fibrous  infiltration 
of  the  peritoneum  may  also  occur,  and  contain  both  eggs  and 
worms.  The  mucosa  of  the  bowel  is  protected  by  a  quantity  of 
mucus.  In  the  rectum  the  mucus  membrane  is  apt  to  become 
hypertrophied,  and  to  grow,  forming  large  polypoid  masses,  or 
adenomata,  which  may  protrude  through  the  anus.  The  ova  may 
affect  the  subcutaneous  tissue  of  the  sacral  and  coccygeal  regions, 


1 866 


INTESTINAL  SCHISTOSOMIASIS 


Fig.  769. — Intestinal  Schistosomiasis. 

(After  Symmers.) 
Polypoid  growths  in  descending  colon. 


Fig.  769A. — Bowel  in  a  Case  of  Intestinal  Schistosomiasis. 


S  YMPTOMA  TOLOG  Y  1 867 

and  cause  dense  cellular  infiltrations,  giving  rise  to  fistulae,  which 
may  spread  and  infect  a  large  cutaneous  area. 

When  the  ova  reach  the  liver  by  the  blood-stream,  they  give  rise 
to  fibrous-tissue  formation  or  an  abscess.  The  surface  of  the  liver 
shows  in  places  a  whitish  network  and  also  flat,  china-white  plaques. 
On  section  a  marked  increase  in  Glisson's  capsule  may  be  seen,  the 
portal  vessels  lying  in  circular  or  slightly  oval  areas  of  connective 
tissue.  Gall-stones  may  also  form  round  the  ova  in  the  gall-bladder. 
The  pancreas  and  spleen  may  also  be  infected,  and  the  vulva  and 
vagina. 

The  ova  may  also  reach  the  lungs,  causing  a  chronic  interstitial 
pneumonia,  and,  passing  through  these  organs,  may  enler  the  heart 
and  the  general  circulation. 


Fig.  770. — Liver  in  Intestinal  Schistosomiasis. 

(After  Symmers.) 

Shows  the  increase  of  fibrous  tissue  in  the  portal  canals. 

Symptomatology. — The  incubation  period  seems  to  be  one  to  three 
months.  The  clinical  appearances  of  the  disease  may  be  classified 
into  four  varieties: — 

1.  Slight  infections. 

2.  Schistosomic  dysentery. 

3.  Schistosomic  tumours. 

4.  Schistosomic  fever. 

Slight  Injections. — In  these  cases  there  are  no  symptoms,  and  the 
disease  is  discovered  by  the  examination  of  the  faeces  by  a  microscope. 

Schistosomic  Dysentery. — The  symptoms  resemble  those  of  chronic 
dysentery,  consisting  of  pains  in  the  abdomen  and  the  passage  of 
blood  and  mucus.  The  faeces  contain  the  characteristic  ova. 
The  attack  begins  with  a  hypersecretion  of  mucus,  followed  by 
frequent  small  motions  containing  but  little  faecal  matter  and  much 
mucus.     The  result  of  these  frequent  motions  is  to  cause  prolapse 


1 868 


INTESTINAL  SCHISTOSOMIASIS 


of  the  rectum.  Papillomatous  growths  may  form  in  the  rectum, 
and  can  be  distinguished  from  piles  by  their  large  number.  They 
may  protrude  from  the  anus,  when  the  removal  and  microscopical 
examination  of  a  small  portion  will  clear  up  the  diagnosis.  When 
the  lower  part  of  the  rectum  is  involved,  much  agony  from  tenesmus 
and  constant  desire  to  defalcate  is  experienced.  The  rectal  prolapse 
becomes  very  distressing,  as  it  has  to  be  constantly  replaced  by  the 
patient  himself,  and  as  both  the  mucous  membrane  of  the  bowel 
and  that  of  the  anus  become  much  inflamed  and  irritated. 

Incases  in  which  there  is  much  sclerosis,  with  a  scarcity  or  absence 
of  polypi,  the  dysenteric  symptoms  are  not  so  marked.  On  the 
contrary,  the  patient  complains  of  constipation,  not  relievable  by 
ordinary  methods,  alternating  with  bouts  of  diarrhoea. 


Fig.  771. — Prolapse  of  the  Rectum  in  Intestinal  Schistosomiasis. 
(From  a  photograph  by  Christopherson.) 

Schistosomic  Tumours. — When  an  emaciated  patient  in  one  of 
the  endemic  regions  is  examined,  one  or  more  abdominal  tumours 
may  be  found  in  the  region  of  the  caecum  or  colon.  These  tumours, 
which  are  fairly  hard,  are  somewhat  movable,  and  are  usually 
elongated,  with  the  long  axis  corresponding  to  the  direction  of  the 
long  axis  of  the  bowel  in  the  region  in  which  the  tumour  is  lying. 
The  tumour,  accidentally  discovered,  continues  to  increase  in  size 
for  months  and  years,  while  the  patient  becomes  very  emaciated, 
and  suffers  from  attacks  of  colic  at  times. 

Liver  and  Pancreas. — The  liver  may  be  found  to  be  enlarged  and 
cirrhotic,  the  spleen  also  be  enlarged,  and  there  may  be  signs  of 
cirrhosis  of  the  pancreas. 

If  the  patient  removes  from  the  endemic  area,  improvement  will 
take  place;  but  if  he  remains,  then  no  cure  appears  to  be  possible, 
and  he  dies  sooner  or  later  from  exhaustion. 

Blood. — The  blood  in  intestinal  schistosomiasis  requires  further 
study,  but  it  would  appear  that  usually  there  is  a  marked  anaemia, 
with  oligochromasia,  slight  leucocytosis,  and  very  slight  eosino- 
philia. 


COM  PLICA  TIONS—TREA  TMENT  1 869 

Urine. — In  cases  uncomplicated  with  the  presence  of  S.  hcema- 
tobinm  there  is  no  albumer,  no  sugar,  and  no  ova  in  the  urine. 

Schist osomic  Fever. — Flu  in  191 1  reported  that  Schistosoma 
mansoni  could  give  rise  to  an  illness  resembling  katayama  disease. 
Archibald  has  also  called  attention  to  the  fact  that  intestinal 
schistosomiasis  caused  by  S.  mansoni  is  capable  of  producing  a 
fever  associated  with  splenomegaly,  enlargement  of  liver,  a  poly- 
morphonuclear leucocytosis  and  lymphocytosis,  together  with  a 
diminution  or  absence  of  eosinophiles.  The  absence  of  eosinophilia 
was  constantly  noted  in  intestinal  schistosomiasis  in  contrast  to 
urinary  schistosomiasis  when  the  reverse  holds  good.  Two  cases 
treated  with  an  autogenous  vaccine  of  the  predominant  coli  organisms 
present  in  the  stools  derived  benefit  and  lessened  the  symptoms 
of  intestinal  toxaemia. 

Urticaria  has  been  noted  by  Lawton,  who  reports  also  presence  of  eosinophilia. 

Complications.- — A  case  may  be  complicated  with  urinary  bil- 
harziosis,  ankylostomiasis,  and  other  intestinal  parasitic  diseases. 

Diagnosis. — The  diagnosis  must  be  made  by  finding  the  charac- 
teristic lateral-spined  eggs  in  the  fasces. 

Prognosis. — The  prognosis  is  unfavourable.  It  must  be  noted, 
however,  that  in  some  cases  the  parasite  does  not  give  rise  to  any 
distinct  pathological  symptoms  for  a  long  time.  One  of  us  has 
observed  in  Uganda  several  natives  with  eggs  of  S.  mansoni  in  their 
fasces,  although  they  were  apparently  in  good  health.  The  stools, 
apart  from  the  eggs  of  the  worm,  were  normal. 

Treatment. — Christ  opherson  has  recommended  the  intravenous 
injection  of  tartar  emetic  (antimonium  tartaratum).  He  gives 
\  grain  dissolved  in  20  minims  of  distilled  water,  and  diluted  with 
two  volumes  of  normal  saline  at  the  time  of  use.  The  dose  is  in- 
creased by  £  grain  every  other  day  until  2  grains  are  reached,  and 
this  dose  is  continued  until  30  grains  in  all  have  been  injected. 
In  children  he  began  with  \  grain  for  a  boy  of  ten  years.  Care  has 
to  be  taken  to  avoid  acute  or  chronic  antimony  poisoning,  and  the 
maximum  dose  for  a  boy  of  ten  is  given  as  1  grain,  for  an  adult 
2  to  3  grains.     The  drug  appears  to  have  a  cumulative  action. 

Christopherson's  results  have  been  confirmed  by  Low,  Taylor  and 
others. 

Filix  mas  may  be  administered  with  the  purpose  of  eradicating  the  worms, 
and  symptomatic  treatment  may  be  carried  out  as  mentioned  under  Urinary 
Bilharziosis.  Madden  advises  an  enterotomy  and  a  cleaning  out  of  the  bowei, 
when  a  tumour  can  be  felt,  and  a  Whitehead's  operation  may  be  done  to  relieve 
the  rectal  symptoms.  Vincent  has  suggested  that  large  intestinal  irrigations  of 
a  solution  of  sodium  hypochlorite  (8  to  10  per  1,000)  should  be  given,  and 
other  authorities  tannic  acid  enemata  (3  per  1,000).  Some  authorities  recom- 
mend the  intravenous  or  intramuscular  injections  of  salvarsan,  and  others  the 
use  of  emetine. 

Prophylaxis. — This  is  based  principally  on  Leiper's  work.  Filtered 
water  should  be  used  for  all  personal  purposes.  If  this  is  not  possible, 
tap-water  should  be  stored  for  forty-eight  hours  before  use,  as 


1870  INTESTINAL  SCHISTOSOMIASIS 

freshly  discharged  cercariae  do  not  usually  live  in  it  for  more  than 
twenty-four  hours.  Chemical  sterilization  may  be  carried  out  by 
using  sodium  bisulphate  tablets,  each  containing  1  grm.  of  the 
chemical.  Two  tablets  are  dissolved  in  a  quart  water  bottle. 
Leiper  has  shown  that  sodium  bisulphate  in  a  dilution  of  1  in  1,000 
is  lethal  to  the  cercariye.  For  small  detachments  of  troops  in  outside 
districts  Leiper  recommends  that  the  drinking-water  should  be 
separated  from  ablution  water,  the  former  being  sterilized  by  boiling 
or  by  tablets  of  acid  sulphate  of  soda,  while  the  ablution  water 
should  be  rendered  safe  for  immediate  use  by  adding  ordinary  Cresol 
in  the  dilution  1  in  10,000. 


REFERENCES. 

Archibald  (1917).  British  Medical  Journal,  February  7.  (1919).  Journal  of 
Tropical  Medicine,  April  1. 

Bandi  (191 3).     Journal  of  Tropical  Medicine. 

Boune  (1919).     Transactions  of  the  Society  of  Tropical  Medicine. 

Castellani  (1903).  Annali  Medecina  Navale,  October.  (Intestinal  Bil- 
harziosis  in  Equatorial  Africa.) 

Christopherson  (1918).     Lancet,  ii.     London. 

Christopherson  (1919).     Lancet,  June  14. 

Flu  (1908).     Centralblatt  fur  Bakteriologie,  Parasit.  u.  Infekti. 

Grall  and  Clarac  (191 3).  Traite  Pratique  de  Pathologie  Exotique,  vi.  166. 
Paris. 

Holcomb  (1907).     United  States  Naval  Bulletin,  vol.  i.,  No.  2,  pp.  55-80. 

Lawton  (1918).     Journ.  Royal  Army  Med.  Corps. 

Leiper  (1915).  Journal  of  the  Royal  Army  Medical  Corps,  vol.  xxv.  (1916). 
Journal  of  the  Royal  Army  Medical  Corps,  vol.  xxv.  (1916).  Proceedings 
of  the  Royal  Society  of  Medicine,  vol.  ix.,  pp.  145-172;  Bulletin  de 
l'lnstitute  Egyptien,  serie  v.,  t.  x.  (1918).  Journal  of  the  Royal  Army 
Medical  Corps,  vol.  xxx. 

Madden  (1907).     Bilharziosis.     London. 

Manson  (1907).     Tropical  Diseases.     London. 

Mathis  and  Baujeau  (1910).  Bulletin  de  la  Societe  Medico-Chirurgicale  de 
l'lndochine.     March. 

Sambon  (1907).     Journal  of  Tropical  Medicine,  x.  117  and  303. 

Symmers  (1902).  Journal  of  Pathology  and  Bacteriology;  (1906)  Patho- 
logical Studies,  Aberdeen  University. 

Taylor  (1919)-     Lancet. 


CHAPTER  LXXX 
EPIDEMIC   GANGRENOUS    RECTITIS 

Synonyms. — Caribi  (British  Guiana),  El  bicho  (Venezuela). 

Definition. — An  endemic  very  contagious  disease  of  South 
America,  and  perhaps  Fiji  and  other  South  Pacific  Islands,  of 
unknown  causation,  and  characterized  by  dysenteric  symptoms 
leading  to  prolapse  and  gangrene  of  the  rectum,  or  at  times  to 
disease  of  the  colon. 

History. — Chalmers  and  Archibald,  in  1914,  drew  attention  to  the 
fact  that  an  eighteenth-century  writer,  D.  L.  F.,  in  his  work 
entitled  '  Traite  des  maladies  particulieres  aux  pays  orientaux,' 
had  described  this  disease  in  Brazil  under  the  name  of '  bicho.'  His 
report  is  similar  to  the  latest  information  on  the  subject,  which  is 
curious.     He  wrote  as  follows: — 

'  Du  Mal  que  les  Portugais  appellent  Bicho.' 
'  Les  Portugais  habituez  au  Bresil  appellent  encore  Bicho,  une  inflamma- 
tion du  fondement,  qui  est  egalement  frequente  et  dangereuse  dans  ce  pays, 
elle  est  toujours  suivie  du  mal  de  tete,  d'epreintes,  grande  chaleur  en  la  partie 
malade,  et  quelquefois  de  la  nevre.  Si  Ton  la  neglig6  il  s'y  fait  en  peu  de 
jours  des  ulceres  venimeux,  qui  ont  donnelieu  au  nom  de  Bicho. 

'  Ceux  qui  se  la  vent  souvent  ces  parties,  sont  moins  sujets  a  cette  incom- 
modite  que  ceux  qui  ne  le  font  pas.  D'abord  qu'on  s'en  croit  attaque,  il  faut 
etuver  plusieurs  fois  le  jour,  la  partie  avec  une  decoction  de  limons,  a  laquelle 
on  ajoutera  quelques  grains  de  sel.  L'on  introduit  aussi  heureusement  dans 
l'intestin,  des  petits  quartiers  de  limon,  etcela  arrete  quelques-fois  le  mal  tout 
court  dans  son  commencement;  s'il  y  a  deja  une  corruption  notable,  Ton  a  de 
coutume  de  detremper  de  la  poudre  a  canon  dans  de  l'eau  de  rose,  ou  de  l'eau 
de  plantain,  et  de  ce  liniment  Ton  en  imbibe  de  petits  linges,  que  Ton  met  dans 
le  fondement.  Apres  l'avoir  bien  etuve  avec  la  decoction  de  limons,  quoy  qu'il 
y  ait  de  la  fievre,  il  faut  bien  se  donner  garde  de  saigner  dans  cette  occasion, 
l'exp6rience  ayant  fait  connoitre  que  ce  remede  est  fort  prejudiciable:  Ton  peut 
seulement  donner  frequemment  les  lavement  anodins  ou  detersifs,  suivant  que 
la  corruption  ou  rinflammation,  sont  plus  ou  moins  grandes,  et  purger  douce- 
ment  sur  la  fin.' 

More  than  one  hundred  and  fifty  years  later  Ackers  of  Curacoa 
gave  Manson  an  account  of  the  disease  as  seen  in  Venezuela.  It 
appears  to  us  that  some  endeavour  should  be  made  to  discover  the 
aetiology  of  this  disease  and  to  study  it  by  modern  methods,  which 
ought  to  be  easy  in  an  endemic  area  where  animals  are  attacked. 

Climatology. — The  disease  is  apparently  known  in  Brazil,  British 
Guiana,  and  Venezuela,  and  with  perhaps  the  addition  of  Fiji  and 
other  islands  in  the  South  Pacific. 

1871 


r872  EPIDEMIC  GANGRENOUS  RECTITIS 

/Etiology. — This  is  entirely  unknown.  The  disease  occurs  in 
man  and  animals,  fowls,  dogs  and  calves,  and  is  said  to  be  very 
contagious.  The  Venezuelan  natives  say  that  it  arises  from  children 
chewing  the  green  tender  stalks  of  unripe  maize. 

Pathology. — -The  disease  presents  two  pathological  pictures — 
viz.,  a  high  injection  in  the  colon,  which  is  rare,  and  a  low  infection 
in  the  rectum. 

Symptomatology. — The  disease  begins  as  an  itching  about  the  anus, 
followed  by  symptoms  of  acute  dysentery,  which  increase  in  severity 
until  there  is  a  constant  discharge  of  blood-stained  or  greenish  feel  id 
fluid.  Prolapse  and  gangrene  of  the  rectum  may  now  occur,  or 
convulsions  may  supervene,  but  in  either  case  the  patient  dies. 

Diagnosis. — In  an  endemic  area  severe  dysenteric  symptoms  in 
a  native  child  would  lead  one  to  suspect  the  disease. 

Prognosis. — This  is  extremely  bad,  as  the  disease  appears  to  be 
always  fatal. 

Treatment.- — Natives  treat  the  disease  by  enemata  of  strong 
lemon-juice  mixed  with  dilute  rum,  a  dose  of  castor  oil  being  given 
at  the  same  time.  Enemata  and  decoctions  of  Spigelia  anthelmia 
are  also  prescribed.  In  children  a  portion  of  a  lemon  is  roasted  and 
inserted  per  anum.  According  to  local  medical  men,  this  native 
treatment  is  more  efficacious  than  boric  acid  and  similar  enemata. 

Prophylaxis. — Nothing  can  be  said  with  regard  to  this  until  the 
disease  is  scientifically  investigated  and  its  aetiology  discovered. 


REFERENCES. 

Ackers  (1900).     Quoted  by  Manson. 

Chalmers  and    Archibald  (191 4).     Proceedings  of   the    Royal    Society  of 

Medicine,  vii.  (Section  of  the  History  of  Medicine),  98-106.     London. 
Manson  (1900).     Tropical  Diseases  (Ackers'  account).     London. 


DIVISION  II.:  DISEASES  OF  THE  SYSTEMS. 

Respiratory  System. 

Circulatory  System. 

Liver  and  Pancreas. 

Ductless  Glands  and  Metabolism. 

Urinary  System. 

Generative  System. 

Lymphatic  System. 

Connective  Tissues,  Muscles,  Bones,  and  Joints. 

Nervous  System. 

Organs  of  Special  Sense. 


1873  118 


CHAPTER  LXXXI 
DISEASES  OF  THE  RESPIRATORY  ORGANS 

General  remarks — Rhinitis  spastica  vasomotoria — Gangosa — Hirudiniasis — 
Rhinal  chilopodiasis — Linguatuliasis — Rhino-pharyngitis  spirochaetica — 
Bronchial  spirochetosis —  Tropical  bronchomycoses — Pulmonary 
no  cardiasis — References . 

GENERAL  REMARKS. 

Diseases  of  the  respiratory  organs  are  of  common  occurrence 
in  the  tropics,  in  the  form  of  acute  or  chronic  inflammation  of  the 
nose,  throat,  larynx,  bronchi,  or  lungs.  Pneumonia  is  less  common 
than  in  Europe,  and  must  be  carefully  diagnosed  from  pneumonic 
plague,  liver  abscess,  and  malaria,  by  careful  physical  examination, 
as  well  as  by  microscopical  examination  of  the  sputum  and  blood. 
Liver  abscess  may  burst  into  the  lung  or  pleural  cavity,  and  may 
cause  the  expectoration  of  a  peculiarly  brown  and  viscid  sputum. 
Emphysema  and  asthma  axe  fairly  common,  and  all  types  of  bronchitis 
are  met  with,  though  more  rarely  than  in  temperate  zones. 

Phthisis  is  common,  and  appears  to  be  increasing  in  the  East, 
but  it  must  be  remembered  that  the  pulmonary  lesions  of  paragoni- 
miasis, histoplasmosis,  bronchospirochxtosis,  and  certain  broncho- 
mycoses, closely  simulate  this  disease,  and  the  examination  of  the 
sputum  is  imperative.  The  occurrence  of  Porocephalus  in  the  lungs 
must  also  be  remembered,  and  the  intense  congestion  in  heat-stroke. 
There  are  several  conditions  which  deserve  special  mention  with 
regard  to  tropical  disease. 

RHINITIS  SPASTICA  VASOMOTORIA. 

Synonyms.— Rhinitis  nervosa,  Coryza  spasmodica,  Dispnee  tropi- 
cale,  Tropical  hay  fever. 

Definition. — A  rhinitis  characterized  by  fits  of  sneezing,  with 
the  production  of  much  nasal  mucus,  and  obstruction  of  the  nose 
from  swelling  of  the  mucous  membrane  over  the  turbinated  bones. 
The  affection  has  the  greatest  resemblance  to  hay  fever. 

History. — This  disease  appears  to  have  been  first  described  by 
Zegers  in  1901,  in  Batavia,  while  Brero  gives  a  full  description  in 
Mense's  '  Tropenkrankheiten,'  and  we  have  seen  several  cases  in 
Ceylon.  O'Zoux  has  recorded  numerous  cases  in  the  island  of 
Reunion. 

1875 


1876  DISEASES  OF  THE  RESPIRATORY  ORGANS 

Symptomatology. — The  affection  is  characterized  by  attacking 
adults,  in  whom  it  causes  violent  fits  of  sneezing,  lasting  from  a  few 
minutes  to  two  hours,  during  which  time  the  victim  sneezes  ten  to 
seventy  times,  while  fluid  pours  from  the  nose,  tears  roll  down 
from  the  eyes,  the  conjunctivae  are  injected,  the  eyelids  swollen, 
the  head  aches,  and  the  patient  is  unable  to  do  his  work.  The 
attacks  are  repeated  constantly,  and  may  take  place  several 
times  during  the  day,  or  may  not  recur  for  weeks.  They  may 
be  associated  with  or  followed  by  dyspnceic  conditions  resembling 
to  some  extent  asthma.  At  the  beginning  the  mucosa  of  the 
inferior  turbinated  bone  may  appear  hyperaemic,  but  later  it 
becomes  swollen,  and  has  a  macerated  appearance.  The  disease 
therefore  closely  resembles  hay  fever,  but  is  supposed  to  be  caused 
by  dust  acting  upon  the  nasal  mucosa  of  persons,  the  resistance  of 
whose  nervous  system  has  been  lowered  by  long  residence  in  the 
tropics.  We  have  frequently  met  with  the  disease  in  people 
exposed  to  the  dust  of  tea  and  copra. 

Treatment. — The  only  successful  treatment  in  many  cases  is  a 
change  of  climate,  when  the  symptoms  stop  at  once.  When  the 
patient  cannot  have  a  change  of  climate,  atropine  and  strychnine 
pills,  or  small  doses  of  quinine,  may  be  recommended,  and  locally  a 
spray  of  a  solution  of  cocaine  (J  or  1  per  cent.)  and  adrenalin 
(1-2  per  cent.). 

GANGOSA. 

Synonyms. — Rhinopharyngitis  mutilans  (Leys) ;  Granuloma 
gangrenosum;  Kaninloma  (Fiji). 

Definition.— Gangosa  is  an  ulcerative  condition  of  the  palate,  nose, 
pharynx,  and  skin  surfaces  of  the  body,  of  unknown  cause,  though 
possibly  a  late  sequela  of  yaws,  which  slowly  spreads  to  the  nose 
and  larynx,  destroying  cartilage  and  bone,  and  causing  much 
deformity. 

History. — The  disease  appears  to  have  been  first  described  in 
1828  by  a  Spanish  Royal  Commission  to  the  Marianne  or  Ladrone 
Islands  under  the  name  '  gangosa,'  which  means  '  nasal  voice,'  and 
is  derived  from  gangoser,  '  to  snuffle.'  It  was  carefully  studied  by 
Seligmann  in  British  New  Guinea  in  1898  and  1904,  who  describes 
the  implication  of  the  skin  of  the  face,  and  draws  attention  to  the 
fact  that  it  is  the  disease  described  by  Sir  William  MacGregor  as 
lupus  and  by  the  white  residents  as  cancer.  In  1906  the  disease 
in  the  endemic  area  was  studied  by  Fordyce  and  Arnold,  by  Leys 
in  Guam,  an  island  to  the  south  of  the  Ladrone  Islands,  and  by 
Mink  and  McLean  in  the  Ladrone  and  Caroline  Islands.  In  1907 
a  paper  appeared  by  Musgrave  and  Marshall  on  a  case  from  the 
Batanes  Islands,  120  miles  north  of  Luzon,  and  by  Stitt  on  a  case 
in  a  European  in  Guam.  It  has  been  studied  by  Angeny  and  Kerr. 
Breinl  has  found  it  on  Murray  Island,  and  thinks  that  it  closely 
resembles  the  condition  known  in  Fiji  as  Kaninloma. 

Climatology.— There   appears  to  be   an   endemic   area  for   the 


CLIMA  TOLOG  Y —HI  STOP  A  THOLOG  Y  1 877 

disease,  it  being  common  in  the  Batanes  Islands  (where  the  cases 
are  mistaken  for  leprosy),  in  the  Ladrone  Islands,  Guam,  and  the 
Caroline  Islands.  Cases  occur  also  in  Fiji,  Murray  Island,  Panama, 
British  Guiana,  Ceylon,  Nevis,  Dominica,  and  Equatorial  Africa. 
In  the  Anglo-Egyptian  Sudan  there  is  a  disease  closely  resembling 
gangosa,  though  probably  syphilitic. 

/Etiology. — Daniels  and  several  other  authors  believe  it  to  be  a 
sequel  to  yaws,  but  Rat  is  opposed  to  this,  as  are  Mink,  McLean, 
Musgrave,  and  Marshall  and  Angeny,  who  point  out  that  the  disease 
is  absent  or  very  rare  in  many  countries  where  yaws  is  common. 
Kerr,  however,  has  noted  that  yaws  is  an  almost  constant  antece- 
dent of  gangosa.  Alverez  suggested  that  it  was  syphilis,  but 
Musgrave,  Marshall,  and  Leys  are  opposed  to  this,  because  no 
syphilis  exists  in  Guam,  where  gangosa  is  common.  There  are  no 
signs  or  symptoms  of  syphilis  in  this  disease.  Treponemata  cannot 
be  found,  and  mercury  is  without  effect.  It  is  not  leprosy,  because 
of  the  absence  of  nodules,  infiltration,  anaesthesia,  and  Hansen's 
bacillus.  It  is  distinguished  from  epithelioma  by  the  absence  of  the 
histological  characters  and  metastases,  as  well  as  by  the  rapid  onset 
and  protracted  course.  It  is  excluded  from  tuberculosis  by  the 
absence  of  Koch's  bacillus  and  other  symptoms  of  the  disease,  and 
the  failure  to  inoculate  guinea-pigs  successfully.  It  may  therefore 
be  a  separate  disease  of  unknown  causation,  though  we  believe  that 
it  is  probably  a  late  manifestation  of  yaws.  Schmitter  regards  it  as 
a  sequela  of  a  special  variety  of  yaws.  It  appears  to  be  equally 
common  in  males  and  females. 

Pathology. — It  appears  to  begin  sometimes  as  a  sore  throat  or 
coryza,  or  as  a  tubercle  on  the  palate.  In  any  case,  an  ulcer  soon 
forms,  which,  though  superficial  at  first,  eats  through  cartilage  and 
bone,  with  periods  of  quiescence  and  of  activity.  This  ulceration 
is  due  to  a  necrosis  of  the  tissue  elements,  with  very  little  reaction 
on  the  part  of  the  body.  This  reaction  is  apparently  limited 
to  a  small-celled  infiltration,  some  giant-celled  formation,  and 
proliferation  of  bloodvessels  with  formation  of  granulation  tissue. 

Morbid  Anatomy. — The  post-mortem  may  reveal  signs  of  some 
concomitant  affection — for  example,  tuberculosis,  pleurisy,  or 
cardiac  hypertrophy — which  have  nothing  to  do  with  the  disease, 
the  important  features  of  which  are  ulceration  and  destruction, 
together  with  scar  formation  in  the  larynx,  pharynx,  palate,  nose, 
and  perhaps  the  antrum  of  Highmore. 

Histopathology. — Microscopically,  the  following  changes  are  ob- 
served as  the  diseased  area  is  approached  from  healthy  tissue:  First 
there  is  an  ©edematous  infiltration,  then  an  infiltration  with  round 
cells,  which  are  principally  lymphocytes,  associated  with  another 
variety  possessing  more  protoplasm,  and  a  small  dark  nucleus. 
Sometimes  there  are  giant  cells  and  proliferating  vessels,  and  there 
are  always  haemorrhages.  Then  comes  a  layer  of  necrosis,  forming 
the  surface  of  the  ulcer,  at  the  edges  of  which  the  epithelium  can  be 
seen  sending  processes  into  the  subcutaneous  tissue,  which  consist 


i878 


DISEASES  OF  THE  RESPIRATORY  ORGANS 


of  large  vacuolated  cells  with  pale  vesicular  nuclei.  Some  diplo- 
cocci,  micrococci,  and  bacilli  have  been  noted,  but  no  acid-fast 
bacilli  or  Treponemata  have  been  seen. 

Symptomatology.— The  disease  begins  sometimes  as  a  sore  throat, 
and  on  examination  a  nodule  maybe  seen  on  the  back  of  the  pharynx, 
the  posterior  pillars  of  the  fauces,  or  the  edge  of  the  soft  palate.  This 
becomes  a  superficial  ulcer  covered  with  a  brownish-grey  slough. 
This  ulcer  spreads  rapidly  at  first,  but  more  slowly  later,  and  eats 
away  first  the  soft  jparts,  and  then  the  bone  of  the  palate,  the  nasal 


Fig.  772. — Gangosa. 
(From  a  photograph  by  Arnold.) 

septum,  and  the  cartilages  of  the  nose,  so  that  the  skin  falls  in,  and 
the  nose  and  mouth  are  converted  into  one  cavity.  It  may  then 
extend  on  to  the  face  or  lip,  or  affect  the  larynx.  When  it  spreads 
over  the  face  it  may  involve  the  eyelids,  erode  the  cornea,  and  even 
destroy  the  vision.  In  some  advanced  cases  the  entire  front  of  the 
face  is  replaced  by  a  large  opening  ringed  about  by  foul  ulcers. 
Sensation  is  diminished  over  the  ulcer,  and  a  most  objectionable 
odour  is  exhaled,  while  a  slight  discharge  of  granular  and  necrotic 
debris  is  generally  present.  The  ulcers  may  also  appear  on  the 
skin  of  the  extremities  or  on  parts  of  the  body  not  usually  covered 


S  YMPTOMA  TOLOG  Y—PROPH  YLA  XI S  1 879 

with  the  clothing.  At  times  the  ulcers  may  remain  quite  super- 
ficial, spreading  at  one  edge  while  healing  at  another.  Scarring 
similar  to  that  seen  after  burns  may  result,  which  by  contraction 
may  lead  to  obliteration  of  the  palpebral  fissures,  the  nasal  orifices, 
and  to  reduce  the  size  of  the  mouth,  as  well  as  to  produce  great 
deformities  in  the  hands  and  feet.  It  may  cause  a  chronic  osteitis 
resembling  that  seen  in  syphilis.  It  appears  to  be  in  some  way 
self-limited,  as  it  does  not  attack  the  trachea  or  genital  organs. 
The  ulceration  may  progress  continuously  for  a  period  of  ten  to 
thirty-five  years,  or  it  may  advance  at  certain  times  and  be  quiescent 
at  others,  or  it  may  cease  at  any  time,  leaving  a  chronic  ulcer.  Its 
duration  varies,  therefore,  from  a  few  months  to  many  years. 

With  regard  to  the  blood,  Musgrave  and  Marshall  report  that 
their  case  showed  no  marked  leucocytosis  and  no  abnormal  elements. 
The  haemoglobin  was  80  per  cent.,  the  leucocytes  11,600  per  cubic 
millimetre,  the  small  lymphocytes  10  per  cent.,  large  lymphocytes 
4-6  per  cent.,  polymorphonuclears  82  per  cent.,  eosinophils  2-6  per 
cent.,  basophiles  0-4  per  cent.  Wassermann's  reaction  is  often 
positive.  Kerr  believes  this  to  be  due  to  pregressed  yaws.  Noguchi's 
cuti-reaction  may  be  positive. 

The  disease  is  not  limited  to  the  throat  and  nose,  but,  as  already 
stated,  may  spread  to  the  face  or  appear  on  the  extremities,  but  as 
a  rule  the  general  health  is  but  little  affected. 

Variety. — A  fulminating  variety  has  been  described  by  Mink  and 
McLean  in  children,  which  is  fatal  in  forty-eight  hours,  and  closely 
resembles  diphtheria,  without,  however,  the  presence  of  the  specific 
bacilli. 

Diagnosis. — The  diagnosis  has  been  practically  discussed  in  the 
/Etiology,  and  need  not  be  repeated,  except  to  say  that  it  must  be 
made  by  a  process  of  exclusion. 

Prognosis. — The  disease  is  rarely  fatal,  and  all  cases  tend  to  ulti- 
mate recovery,  but  the  course  is  very  long  and  the  disfigurement 
great.  The  general  health  is  also  good  as  a  rule,  although  death 
may  take  place  from  intercurrent  disorders,  such  as  tuberculosis, 
dysentery,  and  other  internal  causes. 

Treatment. — Mercury  is  useless  and  potassium  iodide  has  little 
action  on  the  condition.  Salvarsan  and  neosalvarsan,  or  their 
substitutes,  seem  to  give  much  better  results.  An  application  of  a 
strong  solution  (1  per  cent.)  of  permanganate  of  potash  is  recom- 
mended as  a  deodorant,  and  local  application  of  tincture  of  iodine  or 
the  actual  cautery. 

Prophylaxis. — Nothing  definite  can  be  said  under  this  heading, 
as  the  aetiology  is  not  known  with  certainty,  but  segregation  of  the 
patients  in  a  colony  or  special  hospital  until  they  are  cured  is  advis- 
able. In  Guam,  according  to  Angeny,  the  disease  is  steadily 
decreasing,  thanks  to  the  measures  taken  of  segregating  the  patients, 
and  possibly  to  the  thorough  treatment  of  yaws  patients,  and  also 
probably  to  the  improvement  in  general  sanitation  since  the 
American  occupation. 


i88o  DISEASES  OF  THE  RESPIRATORY  ORGANS 

HIRUDINIASIS. 

Definition. — Hirudiniasis  is  the  invasion  of  the  nose,  mouth, 
pharynx,  or  larynx  by  leeches. 

Remarks. — Leeches  have  already  been  described  in  Chapter 
XXVII.  (p.  683) ,  when  it  was  mentioned  that  they  were  apt  to  invade 
the  nose,  mouth,  pharynx,  or  larynx.  Master  man  has  given  a  very 
excellent  account  of  hirudiniasis  as  seen  in  Palestine. 

Climatology. — Leeches  are  most  troublesome  in  Algeria,  Palestine, 
and  Ceylon,  less  so  in  the  Philippine  Islands,  Java,  Sumatra, 
Australia,  and  Japan. 

/Etiology. — It  is  the  water-leech,  which  lives  in  springs,  which  is 
the  cause  of  the  trouble  to  man,  as  it  is  apt  to  be  swallowed  with 
drinking-water.  This  is  particularly  liable  to  take  place  when  the 
traveller  drinks  the  water  hastily  at  dusk. 

Pathology. — The  leech,  when  in  the  mouth,  nose,  pharynx,  or 
larynx,  does  not  suck  blood  until  gorged,  and  then  detaches  itself 
from  the  affected  part,  as  is  the  rule  when  it  attacks  the  skin,  but 
apparently  bites  and  sucks  a  little  in  one  place,  and  then  passes  to 
another,  and  bites  and  sucks  again,  and  so  on.  Of  course  the  sites 
of  the  bites  bleed,  and  hence  the  patient  may  in  course  of  time 
become  very  anaemic,  and  even  die.  It  is  hardly  likely  that  a  leech 
could  live  in  the  stomach  if  swallowed,  though  such  an  occurrence 
has  been  described. 

Symptomatology. — The  patient  usually  knows  that  he  has 
swallowed  a  leech,  and  has  felt  the  animal  catch  hold  of  the  mucosa 
of  the  pharynx  during  the  swallowing  of  the  water.  But  children, 
and  even  adults,  may  be  quite  unaware  of  the  accident  having 
happened.  The  most  important  sign  is  the  bleeding  from  the  nose 
or  mouth,  or  the  hawking  up  of  blood  from  the  pharynx,  or 
haemoptysis  from  the  larynx,  accompanied  by  a  short  irritating 
cough,  dyspnoea,  and  sometimes  cyanosis  from  the  impediment  to 
the  respiration.  Rhinoscopic  or  laryngoscopic  examination  may 
be  necessary  in  order  to  see  the  parasite,  and  will  require  to  be  done 
with  cocaine.  In  the  larynx  the  head  of  the  leech  is  usually  fixed 
just  inside  or  outside  of  the  vocal  cords,  and  the  body  may  flop 
backwards  and  forwards  with  respiration. 

Diagnosis. — The  bleeding  and  the  examination  with  a  nasal 
speculum  or  a  laryngoscope  make  the  diagnosis  easy. 

Prognosis. — This  is  usually  good  if  the  parasite  is  removed  in 
time,  but  if  left  for  long,  removal  may  be  too  late,  and  the  patient 
succumb. 

Treatment. — -Apply  a  pledget  of  cotton-wool  soaked  in  30  per 
cent,  solution  of  cocaine  to  the  parasite.  This  produces  a  paralyzing 
effect  on  the  animal,  and  it  can  then  be  removed;  As,  however,  the 
drug  requires  some  time  to  act,  and  the  leech  might  fall  from  the 
larynx  into  the  trachea,  it  is  advisable  to  make  the  patient  lie 
prone  on  a  couch,  with  the  head  hanging  over,  when  the  paralyzed 
parasite  will  be  coughed  up. 


RHINOPHARYNGITIS  SPIROCHMTICA  1881 

Prophylaxis. — Filtration  of  the  water  will  prevent  the  parasite 
entering  the  body.  Masterman  says  that  a  kind  of  carp,  Capocta 
jratercula,  will  keep  the  water  free  from  leeches. 

RHINAL  CHILOPODIASIS. 

Definition. — Rhinal  chilopodiasis  is  the  invasion  of  the  nose  by  a  species  of 
the  Chilopoda  (see  p.  739). 

^Etiology  and  Symptomatology  .—The  Chilopoda  have  already  been  described 
in  Chapter  XXVIII.,  and  it  has  been  pointed  out  that  Geophilus  carpophagus 
Leach,  G.  similis  Leach,  G.  electricus  Leach,  G.  cephalicus  Wood,  Lithobius 
fovficatus  Leach,  and  L.  melanops  have  been  found  in  the  nasal  cavities, 
causing  inflammation,  with  at  times  a  great  flow  of  mucus,  while  at  others 
there  is  a  stoppage  of  the  discharge.  Associated  with  this  flow  there  is  head- 
ache, with  more  or  less  marked  remissions  at  times,  and  also  general  symptoms, 
such  as  convulsions,  angina,  dyspnoea,  etc.,  which  are  thought  to  be  produced 
reflexly  by  stimulation  of  the  fifth  nerve.  The  symptoms  are  thought  to  be 
produced  mechanically,  and  not  to  be  due  to  an)'  action  of  venom  secreted  by 
the  parasite. 

Diagnosis  is  to  be  made  by  examination  of  the  nose  by  a  speculum. 

Treatment. — -The  affection  is  not  serious,  and  often  the  parasite  is  expelled 
by  merely  sneezing.  More  rarely  chloroform-water  injections,  snuff,  eau-de- 
Cologne,  or  turpentine  injections  are  needed.  Still  more  rarely  will  a  sinus, 
such  as  the  frontal  sinus,  require  to  be  opened. 

LINGUATULIASIS. 

Linguatula  serrata  FrSlich,  1789,  has  been  found  occasionally  in  the  nose  of 
man  in  Europe  and  in  the  tropics  [vide  p.  732). 

RHINO-PHARYNGITIS  SPIROCHMTICA. 

Definition. — A  rhino-pharyngitis  characterized  by  the  presence 
of  numerous  spirochetes  in  the  nasal  and  pharyngeal  secretion. 

Historical  and  Geographical. — This  affection  has  been  described 
by  Castellani,  who  has  found  cases  of  it  in  the  tropics,  in 
the  Balcanic-Adriatic  zone,  and  one  in  England. 

/Etiology.- — In  the  nasal  and  pharyngeal  secretion  large  numbers 
of  spirochaetes  are  present  at  the  beginning  of  the  attack,  while  other 
organisms  are  practically  absent ;  in  a  later  stage,  however,  bacteria 
are  present  in  great  abundance.  The  spirochaete  found — Spiro- 
schaudinnia  minuta  Castellani — is  very  delicate,  more  delicate  than 
S.  bronchialis.  It  can  be  put  in  evidence  by  the  ultra-microscope, 
or  by  staining  with  various  modifications  of  Romanowsky,  the  best 
for  this  particular  spirochete  being  apparently  Jenner's  modification. 
Silver  methods  of  staining  (especially  using  Fontana-Tribondeau's 
technique)  give  good  results.  In  preparations  stained  with 
Romanowsky,  or  other  modifications  of  this  method,  the  organism 
takes  often  a  pinkish-red  or  purplish  tinge.  The  length  of  the  organ- 
ism varies  from  3  to  10  or  12  or  more  microns.  The  beginner  should 
be  careful  not  to  mistake  for  spirochaetes  undulating  fibrin  threads, 
particles  of  detached  ciliated  epithelium,  and  detached  cilia. 

Symptomatology. — The  affection  does  not  clinically  differ  from 
an  ordinary  attack  of  coryza.     There  is  sneezing,  sero-mucous  nasal 


1 882  DISEASES  OF  THE  RESPIRATORY  ORGANS 

discharge,  occasionally  a  slight  cough.  The  patient  may  complain 
of  headache,  and  there  may  be  some  slight  fever. 

In  a  few  days,  as  a  rule,  all  the  symptoms  disappear,  but  occasion- 
ally the  affection  may  run  a  much  longer  course,  and  may  spread 
to  the  larynx,  trachea,  and  bronchi.  In  two  cases  of  bronchitis 
following  an  attack  of  spirochetic  coryza  above  described  Castellani 
observed  in  the  expectoration  the  same  type  of  spirochete,  and 
it  would  appear,  therefore,  that  there  may  be  several  types  of 
bronchial  spirochetosis. 

Diagnosis. — This  is  based  on  the  microscopical  examination 
of  the  nasal  and  pharyngeal  secretion.  The  beginner  should  be 
careful  not  to  recognize  as  spirochetes  detached  cilia  and  segments 
of  undulating  fibrin  threads. 

Prognosis. — This  appears  to  be  favourable. 

Treatment. — A  carbolic  cocaine  spray  (carbolic  acid  3  minims, 
cocaine  hydrochloride  1  grain,  water  1  ounce)  will  be  found  useful. 
Aspirin,  pyramidon,  and  quinine  may  be  administered  internally  in 
5  grain  doses  three  or  four  times  daily.  In  cases  running  a  pro- 
tracted course  arsenic  may  be  tried. 

In  a  few  cases  of  nasopharyngitis  preceding,  at  times,  typical  cases  of 
bronchospirochaetosis  the  nasal  and  pharyngeal  secretion  may  contain  S. 
bronchialis,  though  this  is  rare.  Several  aetio logical  types  of  nasal  spirochetosis 
might  therefore  be,  perhaps,  distinguished.  In  the  tropics  one  comes  across 
occasionally  ulcerative  affections  of  the  nose,  with  presence  of  numerous  coarse 
spirochetes  and  Bacillus  fusiformis,  but  these  conditions  have  nothing  to  do 
with  true  rhino-pharyngitis  spirochaetica. 

BRONCHIAL  SPIROCHETOSIS. 

Synonyms. — Castellani's  bronchitis  (Galli  Valerio),  Spirochetose 
bronchopulmonaire  de  Castellani  (Violle),  Bronchite  sanglante 
(Violle). 

Definition. — A  type  of  bronchitis  and  broncho-alveolitis  charac- 
terized by  the  presence  of  enormous  numbers  of  spirochetes  in  the 
expectoration. 

History.- — The  affection  was  described  by  Castellani  in  1905 
and  1906.  He  named  the  causative  spirochete  S.  bronchialis  in  1907. 
Castellani's  findings  were  speedily  confirmed  by  Branch,  in  1906 
and  1907,  in  Kingstown,  St.  Vincent,  and  by  Jackson,  in  1908,  in 
the  Philippine  Islands.  In  1909  Waters  described  numerous  cases 
of  the  disease  occurring  in  India,  and  Phalen  and  Kilbourne  a  case 
in  the  Philippine  Islands,  where,  in  1911,  Chamberlain  recorded  two 
further  cases. 

In  1913  Chalmers  and  O'Farrell  carried  out  an  investigation 
on  the  malady  in  the  Sudan,  and  succeeded  in  reproducing  it  in 
a  monkey.  In  1914  Taylor  investigated  the  condition  in  Uganda. 
In  191 5  Fantham  published  a  classical  paper  on  Spirocheta  bronchialis, 
studying  it  completely  from  a  morphological  point  of  view,  and  de- 
scribed its  granular  stage  and  the  intracellular  forms  of  the  parasite. 

In  the  same  year  Macfie  reported  cases  from  West  Africa,  and 


BRONCHIAL  SPIROCHETOSIS  1883 

Galli  Valerio  recorded  several  interesting  cases  of  the  malady  in 
Switzerland,  and  Lurie  one  in  Serbia.  In  1917  Galli  Valerio  recorded 
further  cases  in  Switzerland.  In  1917  Violle  first  discovered  the 
affection  in  France,  making  a  very  complete  investigation  and 
publishing  numerous  papers  on  it.  Violle's  observations  stimulated 
further  research  in  France,  and  a  number  of  cases  of  the  malady 
were  reported  by  Bine,  Dide,  and  Ribereau,  by  Netter,  by  Dalimier, 
by  Barbary,  and  others.  Alcock  has  described  a  case  in  an  English 
soldier  in  the  North  of  Italy.  Villa  and,  later,  Corvetto  have 
recorded  cases  in  South  America. 

Geographical. — The  disease  has  probably  a  cosmopolitan  dis- 
tribution. It  has  been  found  in  Ceylon,  India,  Philippine  Islands, 
China  and  Indo-China,  North  and  Equatorial  Africa,  being 
especially  common  in  the  Sudan,  West  Indies,  America,  and 
recently  in  Europe  in  the  Balkans,  Italy,  Switzerland,  France,  and 
England. 

/Etiology. — -The  disease  is  due  to  S.  bronchialis  Castellani, 
1907.  The  parasite  has  been  further  investigated  by  several 
observers,  and  in  a  masterly  manner,  in  1914,  by  Fantham,  who 
described  its  coccoid  and  intracellular  stages.  The  organism  is 
extremely  polymorphic,  being  very  variable  in  length,  thickness, 
and  the  number  of  waves.  One  may  distinguish  thick  and  thin 
forms,  long,  short,  and  intermediate  types.  The  length  may  vary 
between  5  and  30  microns,  its  breadth  between  0-2  and  o-6  micron. 
A  number  of  the  parasites  are  between  14  and  16  microns,  or  7  and  10 
microns,  the  latter  resulting,  as  shown  by  Fantham,  from  transverse 
division  of  the  former. 

The  ends  are  of  variable  shape,  but  mostly  somewhat  acuminate. 

The  number  of  spirals  varies  between  two  and  eight.  Flagella 
seem  to  be  absent,  but  Fantham  has  noticed  the  presence  of  a 
delicate  membrane  or  '  crista  '  in  certain  specimens. 

In  fresh  preparations  S.  bronchialis  is  actively  motile  for  only  a 
short  time;  the  motile  phase,  as  demonstrated  by  Fantham,  is  suc- 
ceeded by  one  of  granule  formation  the  granules  or  coccoid  bodies 
representing  a  resting  stage  from  which  new  spirochaetes  develop. 
Fantham  has  carefully  compared  5.  bronchialis  with  the  common 
mouth  spirochaetes,  and  has  come  to  the  conclusion  that  they  differ 
in  several  features.  S.  bronchialis  is  more  actively  motile  than  the 
oral  spirochaetes;  it  dies,  as  observed  first  by  Chalmers  andO'Farrell, 
and  later  by  Taylor,  very  quickly  in  fresh  preparations,  while  the 
oral  spirochaetes  may  live  for  hours  outside  the  human  mouth. 
Coccoid  bodies  are  much  more  frequently  produced  by  5.  bronchialis 
than  by  the  spirochaetes  of  the  mouth.  Intracellular  stages  are 
occasionally  seen  in  the  case  of  S.  bronchialis,  but  not  in  the  case  of 
spirochaetes  from  the  mouth.  S.  bronchialis  stains  with  more 
difficulty  than  the  oral  spirochaetes,  is  slenderer  than  one  of  them, 
S.  buccalis,  and  does  not  appear  to  produce  pseudo-membranes. 

Predisposing  Causes. — A  chill  acts,  in  our  experience,  as  a  very 
important  predisposing  or  secondary  cause. 


i884  DISEASES  OF  THE  RESPIRATORY  ORGANS 

Experimental  Reproduction. — Chalmers  and  O'Farrell  have  suc- 
ceeded in  reproducing  the  disease  in  monkeys.  Cases  of  human 
laboratory  infections  have  been  recorded  by  some  authorities. 
Attempts  to  infect  guinea-pigs  and  rabbits  have  failed. 

Method  of  Infection. — Infection  takes  place  from  infected  to  healthy 
persons,  the  spray  exhaled  in  coughing,  etc.,  being  contaminated 
with  the  spirochetes  or,  more  probably,  according  to  Fantham, 
with  the  resistant  coccoid  bodies  produced  by  S.  bronchialis.  It 
is  also  probable  that  a  certain  number  of  persons  may  harbour 
S.  bronchialis,  and  that  a  chill  or  any  cause  decreasing  their  organic 
resistance  may  induce  an  increase  in  its  virulence  in  the  same  way 
that  a  chill  may  act  on  the  pneumococcus.  To  this  latter  possi- 
bility Violle  and  others  have  called  attention. 

Symptomatology. — Three  types  of  the  disease  may  be  distinguished 
— the  acute  type,  the  subacute  type,  the  chronic  type. 

Acute  Bronchospirochcetosis.  —  In  the  acute  type  the  patient 
■feels  chilly  and  develops  fever,  which  generally  is  not  very  high, 
rarely  exceeding  1030  F.  The  fever  may  last  between  two  and  eight 
days.  The  patient  coughs  a  great  deal,  and  may  have  rheumatoid 
pains  all  over  the  body.  The  expectoration  is  scanty,  muco- 
purulent, very  seldom  containing  traces  of  blood.  In  most  cases 
the  general  condition  of  the  patient  is  not  much  affected;  in  others 
the  patient  feels  very  tired  and  ill. 

Subacute  Bronchospirochcetosis . — The  attack  begins  suddenly  or 
gradually,  and  lasts  between  two  and  several  weeks;  in  many  cases 
there  is  very  little  or  no  fever,  and  the  general  condition  of  the  patient 
may  be  fairly  satisfactory.  The  cough  is  frequent  and  there  is  often 
expectoration  of  pink  jelly-like  mucus,  and  true  hasmoptysis  may 
take  place.  The  physical  examination  of  the  chest  may  reveal 
nothing  at  all,  or  only  signs  of  simple  bronchitis ;  but  at  times  patches 
of  slight  dulness  with  crepitations  may  be  observed.  The  blood  may 
show  a  slight  degree  of  anaemia,  but  the  number  of  leucocytes  is 
normal,  and  so  is  the  differential  leucocytic  count. 

Chronic  Bronchospirochalosis. — Chronic  bronchial  spirochetosis 
may  follow  on  an  acute  or  subacute  attack  or  several  such  attacks, 
but  frequently  the  onset  is  quite  insidious  and  slow.  The  patient  has 
a  chronic  cough,  which  is  in  certain  cases  more  severe  in  the  morning. 
The  expectoration  is  not  very  abundant,  and  may  be  muco-purulent 
in  character,  but  in  many  cases  for  periods  of  two  or  three  days,  and 
even  much  longer,  the  expectoration  contains  blood.  Sometimes 
attacks  of  genuine  haemoptysis  occur,  one  or  two  teaspoonfuls  or 
much  more  of  blood  being  expectorated.  In  some  cases  there  is  no 
fever;  in  others  a  true  hectic-like  fever  may  be  present.  In  some 
cases,  however,  the  rise  of  temperature  takes  place  in  the  morning, 
and  not  in  the  afternoon;  in  others  the  fever  is  present  only  occa- 
sionally, and  is  very  irregular.  The  physical  examination  of  the 
chest,  reveals  in  many  cases  very  little  except  a  few  dry  or  coarse 
moist  rales.  In  others  there  may  be  signs  of  consolidation.  The 
general  condition  may  remain  fairly  good  for  a  long  time,  though  a 


COMPLICATIONS— TREATMENT  1885 

certain  degree  of  anaemia  is  often  present.     A  few  cases  waste 
rapidly. 

The  course  of  the  disease  may  be  prolonged,  with  periods  of  great 
improvement  and  even  apparent  cure. 

BronchospiiochcBtosis  in  the  Lower  Animals. — Mendelson  in  Siam  has 
recently  made  the  interesting  observation  of  the  occurrence  of  a  form  of 
bronchopulmonary  spirochetosis  in  cats. 

Complications. — Pneumonia  and  bronchopneumonia  have  been 
observed.  Rhinitis  has  been  noted.  The  disease  may  be  com- 
plicated with  tuberculosis  and  bronchomycosis. 

Diagnosis. — This  is  based  on  the  microscopic  examination  of  the 
expectoration  collected  after  rinsing  the  mouth  and  gargling  with 
sterile  water.  The  sputum  may  be  examined  fresh,  using  the  dark 
ground  illumination,  or  may  be  stained,  using  one  of  the 
many  modifications  of  the  Romanowsky  stain,  or  nitrate  of  silver 
staining  methods,  such  as  the  Fontana-Tribondeau,  may  be  em- 
ployed. The  Spirochceta  bronchialis  is  generally  present  in  large 
numbers,  while  bacteria  are  very  few. 

Differential  Diagnosis. — The  acute  type  is  often  mistaken  for 
influenza  or  malaria.  The  examination  of  the  sputum,  in  which  no 
Pfeiffer's  bacilli  are  found,  will  distinguish  the  affection  from 
influenza,  and  the  examination  of  the  blood  will  exclude  malaria. 

Cases  of  the  subacute  and  chronic  type  presenting  blood  in  the 
expectoration  are  generally  diagnosed  as  phthisis.  The  examination 
of  the  sputum  for  tubercular  bacilli  will  be  always  negative,  and  the 
animal  inoculations  will  remain  without  effect.  The  ophthalmo- 
and  cuti-reactions  are  negative  in  the  great  majority  of  cases. 
Occasionally,  however,  cases  of  mixed  infections  of  tuberculosis  and 
spirochaetosis  occur.  From  bronchomycosis  the  affection  is  dis- 
tinguished by  the  absence  of  fungi;  cases  of  double  infection,  how- 
ever, bronchospirochaetosis,  and  bronchomycosis,  may  at  times  be 
observed,  though  very  rarely. 

Spirochaetosis  is  easily  distinguished  from  endemic  haemoptysis 
by  the  examination  of  the  sputum,  which  will  show  absence  of  the 
ova  of  Paragoninuts  ringeri  Cobbold,  and  from  bronchomycosis  by 
the  absence  of  fungi. 

Prognosis. — The  prognosis  is  favourable  quoad  vitam,  but  the 
disease  may  take  a  chronic  course  with  anaemia  and  wasting. 

Treatment. — In  the  acute  cases  all  the  symptoms  as  a  rule 
disappear  after  a  few  days'  rest  in  bed.  Codeine  (J  grain)  and 
aspirin  (5  grains)  may  be  administered  when  the  cough  is  painful 
and  the  patient  complains  of  rheumatoid  pains.  In  the  subacute 
and  chronic  types  of  the  disease,  arsenic,  introduced  by  Castellaniin 
the  treatment  of  the  malady  since  1906,  gives  good  results.  It  may 
be  administered  by  the  mouth  in  the  form  of  liquor  arsenicalis  or 
arsenious  acid  pills,  or  may  be  given  subcutaneously  in  the  form  of 
cacodylates.  Plaut  and  Galli  Valerio  recommend  salvarsan. 
When  the  expectoration  is  profuse,  glycerophosphates  and  balsamics 
are  useful. 


iSS6  DISEASES  OF  THE  RESPIRATORY  ORGANS 

*j§In  certain  cases  tartar  emetic,  especially  if  combined  with  arsenic,  is 
efficacious.  The  following  formula  may  be  used :— Tartar  emetic,  £-|  grain; 
liquor  arsenicalis,  2-3  minims;  codein,  £  grain;  glycerine,  1  drachm;  syrup  of 
tolu,  1  drachm;  aquae  chloroformi,  1  drachm.  One  ounce  to  be  taken  three 
times  a  day  well  diluted. 

Occasionally  in  cases  with  very  dry  cough,  potassium  iodide  may  be  found 
useful;  for  instance: — Tartar  emetic,  £-£  grain;  potassium  iodide,  5  grains; 
bicarbonate  of  soda,  10  grains;  glycerine,  1  drachm;  syrup  of  tolu,  1  drachm; 
chloroform  water,  1  ounce.  One  ounce  to  be  taken  three  times  a  day  well 
diluted  with  water. 

Dalimier  recommends  injections  of  camphorated  oil  with  gomenol  in  acute 
cases,  and  Liquor  Fowleri  in  cinchona  wine  in  chronic  cases. 


TROPICAL  BRONCHOMYCOSES. 

General  Remarks.— Affections  of  the  bronchi  and  lungs  due  to 
fungi  are  common  in  the  tropics,  though  very  little  attention  has 
been  paid]to  them  till  recently.  These  conditions  may  be  due  to  a 
variety  of, fungi,  and  may  be  classified  in  several  groups: — 

1.  Due  to  fungi  of  the  genus  Monilia  Persoon,  1797;  Oidium  Link, 
1809;  Saccharomyces  Meyen,  1833;  Willia  Hansen,  1904;  Cryptococcus 
Gilchrist  and  Stoker,  1896;  Coccidiodes  Rixford  and  Gilchrist,  1898. 

2.  Due  to  fungi  of  the  genus  Hemispora  Vuillemin,  1906. 

3.  Due  to  fungi  of  the  genus  Nocardia  Toni  and  Trevisan,  1899: 
Cohnistreptothrix  Pinoy,  191 1. 

4.  Due  to  fungi  of  the  genus  Aspergillus,  1729;  Sterigmatocystis 
Cramer,  1869  ;  Penicillium  Link,  1908;  Mucor  Micheli,  1729; 
Rhizomucor  Lucct  et  Costantin,  1900 ;  Lichtheimia  Vuillemin,  1904. 

5.  Due  to  fungi  of  the  genus  Sporolrichum  Link,  1809. 

For  description  of  above  fungi  the  reader  is  referred  to'Chapters 
XXXVIL,  p.  967,  XXXVIIL,  p.  978,  and  XXXIX.,  p.  1035. 

The  symptoms  are  somewhat  similar,  whichever  fungus  is  the 
aetiological  factor.  In  mild  cases  there  are  signs  of  slight  bronchitis 
with  muco-purulent  expectoration  in  which  the  fungi  are  found. 
In  severe  cases  the  patient  presents  all  the  symptoms  of  phthisis, 
with  hectic  fever  and  haemorrhagic  expectoration. 

Mild  cases  may  get  cured  spontaneously;  but  they  are  often 
benefited  by  potassium  iodide.  We  will  describe  in  detail  the  forms 
of  bronchomycosis  which  has  been  more  completely  investigated. 

Bronchomoniliasis. 

Synonyms. — Broncho-alveolar  moniliasis  (Castellani),  Broncho- 
blastomycosis  pro  parte. 

Definition. — An  infection  of  the  bronchial  mucosa  due  to  fungi  of 
the  genus  Monilia  Persoon,  1797. 

Historical. — Since  1905  Castellani  has  published  many  cases, 
divisible  into  a  mild  type  and  a  severe;  type  of  the  disease,  and  has 
described  several  new  species  of  Monilia.  Castellani's  work  has 
recently  been  confirmed  by  Pijper,^  Pantin,  and  other  observers. 
Magrou  has  recorded  a  case  in  France  in  1916. 


BRONCHOMONILIASIS  1887 

Geographical  Distribution. — The  disease  is  found  all  over  the 
tropics,  especially  in  places  with  a  damp  climate,  such  as  Ceylon 
and  the  Malay  Peninsula.  The  affection  may  be  met  with  also  in 
Europe  and  America,  cases  having  been  recently  recorded  by  Pinoy, 
Iacono,  and  others. 

^Etiology. — In  Ceylon  the  malady  is  generally  due  to  Manilla 
tropicalis  Castellani,  1910.  The  same  fungus  may  be  found  in 
cases  coming  from  South  India  and  the  Malay  States.  It  would 
appear  that  the  fungus  is  the  real  cause  of  the  disease,  as  'no  other 
etiological  agents,  such  as  the  tubercle  bacillus,  etc.,  are  found. 
Moreover,  when  the  patient  gets  better,  the  fungus  becomes  very 
scanty,  or  disappears  completely.  In  some  cases  other  species  of 
the  fungus  may  be  observed,  but  it  is  doubtful  whether  all  of  these. 


Fig.  773. — Fungus  from  a  Case  of  Bronchomycosis  (Undetermined) . 

are  really  pathogenic.  These  species  are  Monilla  paratro  pic  alls 
Castellani,  M.  plnoyi  Castellani,  M.  giillllermondl  Castellani,  M. 
negrli  Castellani,  M.  Candida  Castellani,  M.  nlvea  Castellani,  M. 
Insolita  Castellani,  M.  pseudotroplcalls  Castellani,  M.  lactlcolor 
Castellani,  M.  nltlda  Castellani.  M.  lactea  Castellani,  M.  krusei 
Castellani,  and  other  monilias,  among  which  M.  bethalicnsis  Pijper. 
For  the  cultural  characters  of  these  species  see  p.  1079. 

The  infection  may  take  place  from  man  to  man,  and  also  probably 
by  the  fungi  living  saprophytically  in  nature.  Monilia-like  fungi 
are  extremely  common  in  Ceylon  in  tea-dust,  and  it  is  very  probable 
that  the  so-called  '  tea-factory  cough  '  is  a  type  of  moniliasis. 

Symptomatology. — A  mild  and  a  severe  type  of  the  malady  may 
be  distinguished.  In  the  mild  type  the  general  condition  of  the 
patient  is  fairly  good,  there  is  no  fever,  and  he  simply  complains  of 


1 888  DISEASES  OF  THE  RESPIRATORY  ORGANS 

cough.  The  expectoration  is  muco-purulent  and  very  often  scanty, 
and  no  blood  can  be  seen.  The  physical  examination  of  the  chest 
will  reveal  only  a  few  coarse  rales  or  absolutely  nothing.  The 
condition  may  last  several  weeks  or  months,  and  may  get  cured 
spontaneously,  or,  continuing,  may  turn  into  the  severe  type.  The 
severe  type  closely  resembles  phthisis;  the  patient  becomes  ema- 
ciated, there  is  hectic  fever,  muco-purulent  and  bloody  expectora- 
tion. Occasionally  true  haemoptysis  occurs,  a  teaspoonful  or  more 
of  bright  blood  being  spat  up  at  a  time.  The  physical  examination 
of  the  chest  may  show  patches  of  dulness,  fine  crepitations,  and 
pleural  rubbing.  This  type  is  often  fatal.  Between  these  two 
extreme  types  there  are  of  course  cases  of  intermediate  severity, 
apjTetic  or  with  subcontinuous  and  continuous  fever,  and  more  or 
less  marked  bronchial  and  broncho-alveolar  symptoms. 


Fig.  774. — Sputum  in  Bronchomoniliasis  (Severe  Case). 
(From  a  preparation  stained  with  methylene  blue.) 

Diagnosis. — The  diagnosis  of  moniliasis  is  based  on  finding  the 
fungus  in  the  sputum.  It  is  absolutely  necessary  that  this  should 
be  collected  in  sterile  petri  dishes  and  examined  as  soon  as  possible, 
as  sputum  exposed  to  the  air  becomes  contaminated  with  all  sorts 
of  fungi  in  the  tropics.  In  fresh  preparations  of  the  expectoration 
spore-like,  roundish,  or  oval  cells  4  to  6  /a  are  seen,  often  presenting 
a  double  contour,  alone  or  more  rarely  with  some  mycelial  articles. 
The  fungus  is  Gram-positive. 

To  identify  the  fungus  cultural  researches  are  necessary.  A  particle  of  the 
sputum  is  smeared  on  maltose  or  glucose  agar  plates;  after  two  or  three  days 
white,  rather  large,  roundish  colonies  appear,  easily  distinguishable,  even 
macroscopically,  with  a  little  practice,  from  the  colonies  of  cocci  and  other 
bacteria.  The  fungus  colonies  are  further  investigated  by  inoculating  maltose 
agar,  ordinary  agar,  gelatine,  serum,  and  a  set  of  sugar  broths.  All  the 
species  of  Monilia  found  in  our  cases  grow  well  on  ordinary  agar,  but  much 
more  abundantly  on  maltose  and  glucose  agar,  especially  if  slightly  acid. 


DIFFERENTIAL  DIAGNOSIS  1889 

On  these  media  the  growth,  which  is  generally  white  with  a  smooth  surface 
when  young,  slightly  crinkled  when  old,  is  composed  practically  of  globular, 
yeast-like  cells,  while  in  the  water  of  condensation  globular  cells  and  mycelial 
elements  arc  found  together.  A  little  mycelium  may,  however,  be  found  also 
occasionally  in  the  growth  on  the  slope.  On  serum  all  the  strains  produce  at 
first  a  white  growth,  but  some,  later  on,  induce  a  peculiar  brownish-black 
discoloration  of  the  medium  round  the  growth.  Most  species  do  not  liquefy 
the  medium. 

On  gelatine  all  the  species  grow  fairly  well;  a  few,  including  Monilia 
albicans,  produce  liquefaction  of  this  medium.  In  milk  some  do  not  produce 
either  acid  or  clot,  others  produce  a  temporary  or  permanent  acidity,  others 
clot  the  milk  or  peptonize  it.  The  reactions  in  the  various  sugar  broths  are 
important,  and  in  association  with  the  behaviour  of  the  fungi  on  serum, 
gelatine,  and  milk,  give  the  data  on  which  to  differentiate  the  various  species 
{vide  p.  10S1). 

Differential  Diagnosis. — Primary  bronchomoniliasis,  as  described 
in  this  chapter,  should  be  distinguished  from  the  secondary  broncho- 
moniliasis occasionally  met  with  in  cachectic  patients  suffering 
from  cancer,  diabetes,  tuberculosis,  etc.  In  such  cases  there  is 
generally  thrush  of  the  oral  mucosa,  and  the  thrush  Monilias  spread 
to  the  pharynx,  larynx,  and  bronchial  mucosa,  while  in  primary 
bronchomoniliasis  the  oral  mucosa  is  not,  as  a  rule,  affected. 

From  pulmonary  tuberculosis  the  condition  is  distinguished  by 
the  absence  of  the  tubercle  bacillus  in  the  sputum  and  the  negative 
animal  inoculations.  Cases  of  mixed  infection,  however — tubercu- 
losis and  moniliasis — are  occasionally  met  with,  the  sputum  con- 
taining both  the  tubercle  bacillus  and  the  Monilia  fungi. 

From  bronchospirochsetosis  it  is  recognized  by  the  absence  of 
spirochetes,  though  occasionally  cases  of  mixed  infection  occur;  from 
endemic  haemoptysis  by  the  absence  of  the  ova  of  Paragonimus 
ringeri  Cobbold. 

Prognosis. — The  cases  of  a  mild  type  may  recover  spontaneously 
or  under  appropriate  treatment.  Those  of  the  severe  type  usually 
end  fatally. 

Treatment. — Mild  cases  and  those  of  medium  gravity  respond 
often  to  potassium  iodide  (gr.  x.  to  xx.)  given  well  diluted  in  water 
or  milk  three  times  daily.  When  potassium  iodide  causes  severe 
symptoms  of  iodism,  saiodin  in  the  same  doses  (in  cachets)  may  be 
administered.  In  the  cases  of  the  severe  type  we  have  seen  no 
improvement  from  the  many  different  treatments  administered. 
Potassium  iodide,  however,  should  always  be  tried  also  in  these 
cases,  as  well  as  balsamics.  The  diet  should  be  nourishing;  hypo- 
phosphites  and  glycerophosphates  may  be  tried  to  keep  up  the 
strength  of  the  patient,  as  in  phthisis. 

Broncho-Oidiosis. 

Synonyms. — Bronchial  oidiomycosis,  Broncho-endomycosis. 
Historical. — Cases  have  been  described  by  Blanchard,  Chantcmesse 
and  Vidal,  Linossier,  Pinoy,  Castellani,  and  others. 

Geographical  Distribution. — The  same  as  bronchomoniliasis. 

no 


1890  DISEASES  OF  THE  RESPIRATORY  ORGANS 

^Etiology. — The  following  species  of  the  genus  Oidium  Link  have 
been  found  in  cases  of  bronchitis,  although  it  is  doubtful  whether 
they  are  all  pathogenic : — 

Oidium  lactis  Link,  including  0.  lactis  A,  a  variety  described 

by  Linossier. 
Oidium  matalense  Castellani. 
Oidium  rotundatttm  Castellani. 
Oidium  aster oides  Castellani. 

For  description  of  these  fungi  the  reader  is  referred  to 
Chapter  XXXIX.,  p.  1093. 

Symptomatology.— This  is  identical  with  that  of  bronchomoniliasis, 
and  two  types  may  be  distinguished:  the  mild  type  and  the  severe 
one. 

Prognosis.— Favourable  in  a  certain  number  of  cases,  but  cases 
are  met  with  which  do  not  respond  to  any  treatment  and  terminate 
fatally. 

Diagnosis. — This  can  be  made  only  by  cultural  methods. 

Treatment. — Potassium  iodide  should  be  tried  in  all  cases,  but 
its  action  in  a  large  number  of  them  is  very  uncertain  or  completely 
negative.  It  may  be  given  in  combination  with  glycerophosphates. 
A  change  of  climate  is  often  useful.  \ 

I  jBronchohemisporosis. 

General  Remarks. — This  bronchomycosis  has  been  described  by 
Castellani.  The  fungus  found  so  far  is  Hcmispora  rugosa  Castellani, 
a  description  of  which  will  be  found  in  Chapter  XXXIX.,  p.  1108. 

Symptomatology. — The  symptoms  are  very  similar  to  those  seen 
in  bronchomoniliasis,  and  a  mild  and  a  severe  type  of  the  affection 
may  be  distinguished.  In  the  mild  type  the  general  condition  of 
the  patient  is  good,  there  is  no  fever,  and  he  simply  complains  of 
cough.  The  expectoration  is  muco-purulent  and  does  not  contain 
blood.  The  physical  examination  of  the  chest  is  negative  or  reveals 
only  a  few  rales.  The  severe  type  closely  resembles  phthisis.  The 
patient  becomes  emaciated,  there  is  hectic  fever,  and  the  expec- 
toration may  be  bloody.  The  physical  examination  may  reveal 
patches  of  dulness,  fine  crepitations,  pleural  rubbing. 

Complications. —  The  affection  may  be  complicated  with  a 
tonsillitis,  caused  by  the  same  fungus  and  characterized  by  the 
presence  of  yellowish  or  greyish  patches;  at  other  times  the 
tonsillitis  is  the  primary  lesion. 

Treatment. — Potassium  iodide  seems  to  be  more  efficacious  in  this 
condition  than  in  bronchomoniliasis.  It  should  be  given  in  10-grain 
doses,  well  diluted  in  water  or  milk,  twice  or  four  times  daily. 
Glycerophosphates  and  balsamics  are  useful. 

Tea-Factory  Cough. 

This  affection  described  by  Castellani  in  1910,  is  common  in 
Ceylon.     It    is    probably    a    form    of    broncho-mycosis.     Coolies 


TEA-FACTORY  COUGH  j8gi 

working  in  tea- factories  are  occasionally  observed  to  deteriorate 
in  their  general  health,  losing  flesh  and  becoming  easily  tired ;  at  the 
same  time  they  develop  a  cough  with  muco-purulent  expectoration. 
The  physical  examination  of  the  chest  reveals  nothing  except 
occasionally  a  few  coarse  rales.  If  these  coolies  are  taken  away 
from  the  factory  and  sent  to  work  in  the  fields,  all  the  symptoms 
slowly  disappear. 

A  similar  affection  may  be  observed  in  tea-tasters.  Tea-tasters, 
m  order  to  juelge  of  the  quality  of  teas,  not  only  taste  infusions,  but 
frequently  fill  their  hands  with  the  leaves  and  bury  their  noses  in 
them,  snuffing  them  up:  in  this  way  a  certain  amount  of  tea-dust 
enters  their  nasal  cavities,  and  with  the  tea-dust  the-  micro- 
organisms which  are  found  in  it.  According  to  the  researches  of 
one  of  us,  tea  and  tea-dust  in  Ceylon  contain: — 

i.  Fungi  of  the  genus  Monilia  constantly. 

2.  Fungi  of  the  genus  Oidium  occasionally. 

3.  Fungi  of  the  genus  Aspergillus,  Sterigmatocystis,  and  Peni- 
cillntm  frequently. 

4.  A  peculiar  streptococcus,  somewhat  different  from  S.  pyogenes , 
frequently. 

It  is  interesting  to  note  that  such  germs  are  verv  rare  or  absent 
m  samples  of  tea  examined  in  England.  The  same  organisms  may 
be  found,  in  Ceylon,  in  nasal  cavities  of  tea-tasters:  in  their  ex- 
pectoration the  Manilla-like  fungi  are  practically  constant,  the 
streptococci  very  frequent,  while  Aspergillus  and  Penicillimn  fungi 
are  rare.  Guinea-pigs  in  whose  nostrils  tea-dust  is  daily  insufflated 
for  months  develop  a  broncho-alveolar  moniliasis. 

Bronchial  Aspergillosis. 

Synonyms. — Broncho-alveolar  aspergillosis,  Aspergillar  pseudo-tuberculosis, 
Pneumomycosis  of  aspergillar  origin. 

Definition. — A  form  of  bronchitis  and  broncho-alveolitis  clue  to  fungi  of 
the  genus  Aspergillus  Micheli,  1729,  and  Sterigmatocystis  Cramer,  1869  (p.  1026). 

Historical. — The  condition  has  been  studied  by  Virchow,  Lichtheim,  Dieula- 
foy,  Chantemesse,  Widal,  one  of  us,  Wise,  and  others. 

Climatology. — -The  geographical  distribution  of  the  disease  seems  to  be 
cosmopolitan.  It  is  very  common  in  certain  parts  of  France,  and  one  of  us  has 
seen  two  cases  in  the  Balkans.  In  the  tropics  we  have  seen  some  cases  in 
Ceylon  and  Tropical  Africa,  and  Wise  has  reported  a  case  from  British  Guiana. 

/Etiology. — The  condition  is  due  to  fungi  of  the  genus  Aspergillus  Micheli 
and  Sterigmatocystis  Cramer.  It  is  common  especially  in  people  who  have 
to  handle  various  grains  on  which  spores  of  those  fungi  are  often  found.  In 
France  it  is  extremely  frequent  among  pigeon-breeders  (gaveurs  de  pigeons), 
who  fill  their  mouths  with  grain  and  blow  it  into  the  mouths  of  the  pigeons. 
Of  the  two  cases  observed  by  us  in  the  Balkans,  one  was  apparently  due  to 
Aspergillus  fumigatus  Fresenius,  the  other  to  Sterigmatocystis  nigra  Cramer. 

It  is  probable  that  the  deleterious  effects  caused  by  the  fungi  are  due  not 
only  to  a  mechanical  irritative  action,  but  also  to  toxins  secreted  by  the  fungi. 

Morbid  Anatomy. — The  lungs,  and  occasionally  the  liver,  kidneys,  and  other 
organs,  may  show  a  type  of  pseudo-tuberculosis  characterized  by  the  presence 
of  numerous  mycotic  tubercular-like  nodules. 

Symptomatology. — The  presence  of  the  fungi  in  the  bronchi,  when  in  smal 
amount,  may  not  give  rise  to  any  symptom.     When  the  infection  is  heavy, 


1892  DISEASES  OF  THE  RESPIRATORY  ORGANS 

symptoms  of  bronchitis  with  muco-purulent,  and  occasionally  bloody,  expec- 
toration are  present,  and  in  severe  cases  the  patient  may  have  hectic 
temperature,  with  sweatings  and  great  wasting. 

Diagnosis.— This  is  based  on  finding  the  fungus.  It  is  to  be  noted  that  in 
the  sputum  as  a  rule  only  mycelial  threads  are  found,  and  cultivations  are 
therefore  necessary. 

Prognosis.— Mild  cases  often  recover,  but  in  severe  cases  with  bloody  ex- 
pectoration the  prognosis  is  bad.  x ■■ 

Treatment.— A  change  of  climate  and,  when  the  condition  is  brought  about 
by  certain  occupations,  a  change  of  occupation  is  very  beneficial.  Potassium 
iodide  (gr.  xv.  to  xx.)  may  be  administered. 

Bronchial  Penicilliosis. 

One  of  us  has  observed  cases  of  bronchitis  and  broncho-alveolitis  due  to 
fungi  of  the  genus  Penicillium  in  the  tropics  and  one  in  the  Balcanic  zone.  The 
fungus  isolated  from  the  last  case  was  P.  crustaceum  Linnaeus. 

The  symptomatology,  diagnosis,  and  treatment  are  the  same  as  in  Bronchial 
Aspergillosis. 

Bronchial  Mucormycosis. 

Cases  of  bronchitis  caused  by  fungi  of  the  genus  Mucor  Mich  eli,  1729, 
Lichtheimia  Vuillemin,  1904,  Rhizomucor  Lucet  and  Costantm,  1900,  Rhizopus 
Ehrenberg  1820,  may  be  met  with,  but  are  of  rare  occurrence.  The  sympto- 
matology is  the  same  as  that  of  Bronchial  Aspergillosis.  V  e  have  seen  a  case 
in  the  Balcanic  zone  due  to  Mucor  mucedo  Linnaeus.  For  description  of  the 
fungi  see  p.  972. 

Bronchial  Sporotrichosis. 

A  few  cases  have  been  described  of  a  bronchitis  due  to  fungi  of  the  genus 
Sporotrichum  Link,  1809. 

Undetermined  Bronchomycosis. 

One  of  us  has  described  cases  of  bronchomycosis  due  to  fungi  which  have  no  t 
yet  been  classed . 

PULMONARY  NOCARDIASIS. 

Synonyms. — Pulmonary  streptothromycosis,  Pseudo-tuberculosis. 

Definition. — Pulmonary  nocardiasis  is  an  infection  of  the  lung,  and  usually 
other  organs,  with  ;i  species  of  the  fungal  genus  Nocardia  Toni  and  Trevisan, 
in  which  the  signs  and  symptoms  more  or  less  resemble  those  of  phthisis. 

Historical. — In  1897  Flexner  described  this  disease,  isolating  the  causal 
organism,  which  he  named  Streptothrix  pseudotuberculosa  Flexner,  1897.  In 
the  same  year  Buchholz  found  a  similar  case  in  Berlin,  and  Scheele  and 
Petruschky  described  a  third  at  the  Wiesbaden  Congress.  In  1902  Birtand 
Leishman  met  with  a  case  in  a  soldier,  and  since  then  similar  cases  have  been 
recorded  by  Foulerton,  by  Roger,  Bory,  and  Sartory  in  1909,  and  have  been 
seen  by  ourselves  in  Ceylon,  the  Balcanic  zone,  and  the  Anglo-Egyptian  Sudan, 
.'.nd  by  Pijpei   in  South  Africa. 

Climatology. — The  disease  occurs  in  the  Temperate  and  Tropical  Zones,  in 
the  New  and  the  Old  World,  and  may  therefore  be  widespread. 

/Etiology. — The  causal  agents  appear  to  be  varying  species  of  nocardia — 
thus,  lor  example,  Flexner's  case  was  caused  by  Nocardia  pseudotuberculosa 
( Flexner,  1 897) ;  Birt  and  Leishman's  case  by  Nocardia  leishmani  Chalmers  and 
Christophcrson,  1916;  Scheele  and  Petruschky's  case  by  N.  gedanensis  (Scheele 
and  Petruschky,  1897);  and  Foulerton's  organism  by  N.  foulertoni  Chalmers 
and  Christopherson,  191 6;  while  Roger,  Bory,  and  Sartory's  organism  is 
called  N.  pulmonalis  (Roger,  Bory,  and  Sartory,  1909).  Very  commonly  these 
fungi  are  present  in  the  sputum  as  acid-fast  rods  which  may  or  may  not  appear 
in  branched  form.     When  present  in  rod-like  forms  they  give  rise  to  an  appear- 


REFERENCES  1893 

ance  somewhat  resembling  the  tubercle  bacillus.  Other  species  of  nocardia, 
also  found  in  sputum,  may  not  be  acid-fast,  and  these  are  more  easily  recognized. 

Morbid  Anatomy. — As  a  rule  the  appearances  found  post-mortem  are  not 
unlike  that  of  tuberculosis.  There  is  consolidation,  necrosis,  and  cavity 
formation  in  the  lung,  with  or  without  the  signs  of  caseous  pneumonia  or  of 
calcareous  deposition,  or  there  may  be  small  cirrhotic  nodules  scattered 
through  the  lung.  There  may  also  be  nodules  in  the  liver,  spleen,  peritoneum, 
and  lymph  glands,  and  there  may  be  chocolate-coloured  exudate  into  the 
pleural  or  peritoneal  cavities.  This  exudate  may  be  odourless  or  foetid  in 
odour.     The  fungus  can  be  easily  found  in  these  pseudo-tubercles. 

Symptomatology. — In  general  it  may  be  stated  that  the  symptoms  resemble 
those  of  phthisis,  and  as  such  the  disease  is  usually  recognized.  Usually  there 
is  fever,  cough,  a  muco-purulent  sputum  containing  blood  at  times  and  showing 
acid-fast  rods  resembling  the  Bacillus  tuberculosis,  but  careful  search  may  reveal 
a  few  elongate  or  branching  forms.  The  physical  signs  are  those  of  chronic 
broncho-pneumonia,  with  or  without  cavity  formation,  and  with  or  without 
those  of  pleural  effusion.  The  liver  and  spleen  are  often  enlarged.  The  cases 
usually  go  from  bad  to  worse,  and  end  in  death. 

Diagnosis. — Many  of  these  cases  are  diagnosed  as  pulmonary  tuberculosis 
at  the  present  time.  The  correct  diagnosis  can  only  be  established  by  a 
careful  examination  of  the  sputum,  by  microscopical  and  bacteriological 
methods,  including  the  culture  of  the  organism. 

The  differential  diagnosis  has  to  be  made  from  phthisis  and  liver  abscess. 

It  may  be  distinguished  from  phthisis  by  the  recognition  of  the  beaded 
branched  organism  in  the  sputum  and  the  culture  of  it  therefrom. 

In  cases  giving  a  history  of  dysentery  and  exhibiting  enlargement  of  the 
liver,  fever,  and  a  purulent  chocolate-coloured  effusion  into  the  pleural  cavity, 
the  diagnosis  can  only  be  effected  by  finding  the  fungus  and  by  the  absence  of 
any  pus  in  the  liver.  In  such  cases  the  dysenteric  amoeba  may  be  present  in 
the  fasces. 

For  the  morphological  and  cultural  characters  of  the  species  of  nocardia 
see  Chapter  XXXIX.,  p.  1040. 

Prognosis. — So  far  the  prognosis  is  very  bad,  as  all  known  cases  have  died. 

Treatment. — Iodide  of  potash  in  large  doses  may  be  tried  or  a  vaccine  made 
from  the  patient's  causal  organism. 

Prophylaxis. — Nothing  whatever  can  be  said  on  this  part  of  the  subject. 

REFERENCES. 

Bronchial  Spirochetoses. 

Alcock  (1918).     Communication  by  letter. 
Barbary  (191S).     Bull.  Ac.  de  Med. 

Beat,  Dide,  and  Ribereau  (1918).     Society  Med.  des  Hopiteaux. 
Branch  (1907).     British  Medical  Journal. 

British    Medical    Journal.     Broncbospirochastosis.     Leader,    p.    727,    De- 
cember 28,  1918. 
Castellani  (1906).     Lancet,  May  19.     (1906-13).     Ceylon  Medical   Reports. 
(1909).    British.  Medical  Journal,  September  is  (Tropical  Diseases  Section). 
(1917).     Presse  Me-dicale,  No.  37,  and  also  Journal  of  Tropical  Medicine, 
August  and  September. 
Chalmers  and  O'Farrell  (1913).     Journ.  of  Trop.  Med. 
CORVETTO     (1918).     Espiroquetosis     bronco-pulmonar     dc     Castellani.      An. 

Facult.  Med.  de  Lima.,  vol.  v.,  No.  5. 
Dalimier  (1919).     A  propos  de  la  broncho-spirochetose  de  Castellani.    Presse 

Medicale,  No.  14,  p.  124. 
Delamare  (1919).     Soc.  de  Biologic. 

Derrien  (191 8).     Reunion  Medico-Chirurgicale  de  la  15'^"^  Region. 
I^antham  (1915).     Annals  Trop.  Med.  and  Paras. 
Galli-Valerio     (1915).     Centr.    f.     Bakt.     (1917).     Correspondenzblatt    f. 

Schweizer-Aerzte. 
Hallenberger  (1916).     Arch.  f.  Schirfs-u.  Tropen-Hygiene. 


1 894  DISEASES  OF  THE  RESPIRATORY  ORGANS 

Harper  (1914).     Journ.  of  Trop.  Med.,  July. 

Jackson  (1908).     Philippine  Journal  of  Science. 

Macfie  (1915).     Journ.  of  Trop.  Med.  and  Hyg.,  May. 

Xetter  (191S).     Bull.  Acad,  de  Med.,  September  17." 

Nolf  and  Spehl  (1918).     Arch.  Med.  Beiges,  July. 

Ragazzi  (1916).  Un  caso  di  Spirochetosi  Bronchiale  (Castellani) .  Patho- 
logica,  January'  i. 

Rothwell  (1910).     Journ.  Amer.  Med.  Ass. 

Sabrazes  (1918).     Gaz.  hebd.  des  Sciences  medicates  de  Bordeaux,  June  30. 

Taylor  (1914)-     Annals  Trop.  Med.  and  Paras. 

Thomson  (1918).     Brit.  Med.  Journal. 

Verliac  and  Turlais  (191 8).     Quoted  by  Netter. 

Villa  (1916).  Espiroquetosis  Pulmonar.  Repert.  de  Med.  y  Cirugia.  vol.  vii., 
No.  6. 

Vioi.le  (1918).  Bull.  Path.  Exot.,  No.  1,  tome  xi.  (1918).  Bull.  Acad,  de 
Medecine.  (191 8).  Presse  Medicale,  La  Bronchite  Sanglante  (Spiro- 
chetose  Bronchopulmonaire  de  Castellani),  No.  39,  p.  359.  (1918.) 
Haemorrhagic  Bronchitis  (Castellani's  Broncho-pulmonary  Spirochartosis). 
Lancet,  December  7. 

Waters  (1909).     Transactions  Society  of  Tropical  Medicine. 

Rhinitis  Spastica  Vasomotoria. 

Brero  (1905).     Mense's  Tropenkrankheiten,  i.  218. 
O'Zoux  (1909).     Bull.  Path.  Exot. 

Gangosa. 

Angeny  (191 2).     New  Orleans  Medical  and  Surgical  Journal. 

Branch  (1906).     Journal  of  Tropical  Medicine,  ix.  156. 

Brennan  and  Pirie  (1918).     Jour.  South  Africa,  June. 

Fordyce  and  Arnold  (1906).     Journal  of  Cutaneous  Diseases,  xxiv.  1. 

Jagatpati  (1918).     Ind.  Med.  Gaz.,  May. 

Leys  (1906).     Journal  of  Tropical  Medicine,  ix.  47. 

Mink  and  McLean  (1906).     Journal  of  the  American  Medical  Association, 

xlvii.  1166. 
Musgrave  and  Marshall  (1907).     Philippine  Journal  of  Science,  ii.  387. 
Stitt  (1907).     U.S.  Naval  Medical  Bulletin,  i.  96. 

Hirudiniasis. 

Masterman  (1908).     Journal  of  Parasitology,  i.  182. 

Rhinal  Chilopodiasis. 

Blanchard  (1898).     Archives  de  Parasitologic. 
Laveran  and  Roubaud  (1916).     Bull.  Path.  Exotique. 

Tropical  Bronchomycoses. 

Castellani  (1904-14).  Ceylon  Medical  Reports.  (1910).  Philippine  Journal 
of  Science  and  British  Medical  Journal.  (1911).  Lancet.  (1913).  Journal 
of  Clinical  Research  and  Journal  of  Tropical  Medicine.  (1917).  Journal  of 
Trop.  Medicine  (Diseases  of  the  Balkans) ;  Presse  Medicale,  No.  14,  p.  124. 

Magrou  (1916).     Montpellier  Medical,  vol.  xxxix.,  Xo.  8. 

Pijper  (1918).     South  African  Med.  Record. 

Pantin  (1918).     China  Med.  Jour..  July. 

Pulmonary  Nocardiasis. 

Birt  and  Leishman  (1902).     Journal  of  Hygiene,  ii.  120. 

Buchholz  (1897).     Zeitschrift  fiir  Hygiene,  xxiv.  470. 

Flexner    (1897).     Johns    Hopkins    Hospital    Bulletin,    viii.    128.     (1898). 

Journal  of  Experimental  Medicine,  iii.  435. 
Pijper  (191 7).     Folia  Microbiologica,  vol.  v.,  No.  1. 


CHAPTER  LXXXII 
DISEASES  OF  THE  CIRCULATORY  SYSTEM 

General  remarks — The  blood — Blood  puzzles — Anaemia  and  allied  conditions — 
Leukaemia — General  dropsy — The  heart — The  vessels — The  spleen — 
The  bone-marrow — References. 

GENERAL  REMARKS. 

In  this  chapter  we  merely  make  a  Jew  allusions  to  some  points  of 
tropical  importance  with  regard  to  the  blood  and  the  organs  which 
produce  and  circulate  it.  The  subject  is  not  merely  a  large  one,  but 
is  of  great  importance  in  the  tropics,  and  our  few  remarks  are  merely 
of  an  introductory  nature. 

THE  BLOOD. 

We  in  no  way  intend  to  enter  at  all  fully  into  an  important  study 
of  the  blood,  which  is  to  be  found  in  detail  in  the  special  books 
devoted  to  its  elucidation;  but  we  desire,  in  the  briefest  manner 
possible,  to  present  to  the  reader  a  few  remarks  which  have  a  direct 
bearing  upon  the  various  references  which  we  have  made  from 
time  to  time  in  the  preceding  chapters  with  regard  to  it. 

The  Erythrocyte. 

In  embryonic  life  the  first  sign  of  the  blood  cell  is  to  be  found  in 
those  mesoblast  cells  of  the  vascular  area  which  contain  haemoglobin 
and  are  called  megaloblasts,  and  to  these  are  added  later  similar 
cells  without  haemoglobin  and  found  in  the  liver.  In  post-embryonic 
life  these  cells  are  found  in  the  red  marrow  lying  at  the  ends  of  long 
bones  and  in  flat  bones,  and  normally  do  not  appear  in  the  circulating 
blood,  but  are  the  parents  of  the  normoblasts,  which  are  commonly 
found  in  the  blood  after  mid-term  of  fcetal  life  and  in  the  red  bone- 
marrow  of  post-embryonic  existence. 

These  normoblasts,  multiplying  by  mitosis,  are  the  source  of  the 
erythrocyte,  which  alone  is  the  proper  denizen  of  the  circulating 
blood. 

An  erythrocyte,  according  to  von  Schilling-Torgau,  is  saucer- 
shaped,  with  a  thickeneel  edge,  and  consists  of: — 

i.  An  ectoplasmic  cell  membrane,  inside  which  lies  the  cndoplasm, 
of  which  the  peripheral  portion  is  condensed  to  form  the  endoplasmic 
capsule,  which  isWeidenreich'scholestcrin-lccithin  membrane,  inside 

1895 


1896  DISEASES  OF  THE  CIRCULATORY  SYSTEM 

which  lies  the  stroma,  in  the  form  of  a  network  of  protoplasmic 
threads  and  nodes,  which  contains  the  haemoglobin,  and  in  the 
saucer-shaped  corpuscle  forms  a  cap  over  the  archoplasm,  which  lies 
just  over  the  concavity  of  the  saucer. 

2.  The  archoplasm  is  composed  of  a  central  clear  haemoglobin-free 
area,  and  is  composed  of  a  glassy  body,  which  is  rest  material,  and 
which  in  ordinary  cells  forms  the  achromatic  spindle  in  mitosis. 
Excentrically  placed  and  surrounded  by  the  glassy  body  lies  the 
capsule  corpuscle,  near  which  lie  two  sharply  defined  bodies  embedded 
in  a  substance  which  may  contain  a  vacuole.  These  are  the 
centrioles. 

3.  The  blood  plate  is  the  metamorphosed  nucleus  of  the  normo- 
blast, which  lies  excentrically  on  one  side  of  the  archoplasm.  It  is 
easily  extruded  in  making  the  blood  film,  and  gives  rise  to  the  blood 
platelets  which  are  so  well  known.  Its  peculiar  appearance  is 
possibly  due  to  physiological  modification  during  mitosis  of  the 
normoblast. 

4.  Aleve's  plastokonten  are  granular  bodies  of  unknown  nature 
scattered  through  the  erythrocyte,  but  mostly  seen  near  the 
archoplasm. 

As  we  shall  see  later,  these  various  parts  of  the  erythrocyte  are  the 
explanation  of  the  intracorpuscular  blood  puzzles  and  the  origin  of 
the  numerous  intracorpuscular  pseudo-parasites  of  many  observers. 

The  red  corpuscles  number  some  five  millions  in  a  healthy  male, 
and  some  four  and  a  half  millions  in  a  healthy  adult  female  under 
the  climacteric  age,  but  there  are  physiological  increases  of  these 
numbers  in  infancy,  by  cold  and  at  high  altitudes,  while  race  has 
but  little  influence. 

Pathologically  they  can  be  increased  by  mechanical  means — 
e.g.,  the  concentration  of  the  blood  caused  by  diarrhoea,  sweating, 
vomiting,  and  polyuria,  or  by  heart  disease.  They  can  also  be  in- 
creased in  toxic  conditions  and  in  polycj'themic  splenomegaly. 
They  may  be  decreased  by  any  mechanical,  toxic,  or  parasitic  cause 
which  induces  blood  destruction. 

The  normoblasts  of  the  bone-marrow  may  accidentally  occur  in 
the  normal  circulating  blood  as  an  isolated  form,  but  in  numbers 
they  indicate  that  there  is  an  abnormal  demand  for  erythrocytes — 
as,  for  example,  after  a  haemorrhage.  A  normoblast  is  about  the 
same  size  as  an  erythrocyte  (7-5  microns),  but  contains  a  rounded 
nucleus  composed  of  a  nuclear  membrane  containing  dense  chro- 
matin and  measuring  about  4  microns. 

The  megaloblasts  may  be  found  in  the  circulating  blood  if  some 
toxin  is  attacking  the  bone-marrow.  They  are  usually  of  large  size 
(20  microns),  but  this  is  not  their  characteristic,  which  is  the  large 
nucleus  measuring  some  10  microns  and  containing  loosely  arranged 
chromatin.  The  nucleus  may  undergo  the  usual  changes,  and  the 
megaloblast  become  a  megalocyte. 

Microblasts  are  small  cells  or  abnormal  normoblasts  or  megalo- 
blasts. 


THE  LEUCOCYTE  1897 

The  Leucocyte. 

In  post-embryonic  life  the  home  of  the  leucocyte  or  colourless 
blood  cell  is  the  bone-marrow.  They  may  be  divided  into  the 
hyaline  cells  or  lymphocytes,  which  are  the  least  differentiated 
cells,  both  ontogenetically  and  phylogenetically,  being  the  first 
to  appear  in  the  embryo  and  in  the  lower  animals,  and  the  granular 
cells  or  leucocyte  sensu  stricto,  which  are  more  highly  evolved  cells. 

It  is  usual  to  consider  the  large  lymphocytes,  the  small  lympho- 
cytes, the  large  mononuclears,  and  the  transitional  cells,  as  all 
belonging  to  the  same  denomination.  According  to  Heidenhain, 
there  is  a  tendency  on  the  part  of  the  centrosome  to  reach  the  centre 
of  the  lymphocyte,  being  pulled  thereto  by  cytoplasmic  radii. 
It  is,  however,  prevented  from  assuming  this  position  by  the  nucleus, 
which  succeeds  in  this  obstruction  in  the  case  of  the  small  and 
large  lymphocyte,  because  there  is  insufficient  cytoplasm;  but  in  the 
case  of  the  large  mononuclear  it  pushes  the  nucleus  to  one  side,  and 
in  the  case  of  the  transitional  it  so  indents  the  nucleus  that  it  attains 
in  both  cases  the  central  position.  Thus  the  small  lymphocyte  by 
growth  can  become  the  large  lymphocyte,  from  which  are  descended 
the  large  mononuclear  and  the  transitional,  which  may,  therefore, 
be  reckoned  as  a  single  type  in  making  a  differential  count. 

The  small  lymphocyte  is  about  the  size  of  an  erythrocyte,  but 
somewhat  smaller;  it  possesses  a  rounded  or  slightly  indented 
nucleus,  colouring  deeply  with  basic  stains,  and  surrounded  by  a 
very  slight  amount  of  cytoplasm,  which  shows  a  reticulum  with 
basophile  granules  as  the  nodal  points.  There  are  also  some 
azurophile  granules. 

The  large  lymphocyte  is  larger,  reaching  to  20  microns,  and  is 
characterized  by  a  central  roundish  or  slightly  indented  nucleus, 
which  contains  less  chromatin  than  in  the  small  variety.  There  is 
more  abundant  cytoplasm,  which  does  not  stain  so  deeply,  but 
contains  the  same  reticulum  and  Wolff's  azurophile  granules. 

The  large  mononuclear  leucocyte  possesses  an  excentric  nucleus 
relatively  poor  in  chromatin,  surrounded  by  a  larger  amount  of 
cytoplasm,  with  the  usual  reticulum  and  azurophile  granules. 

The  transitional  cell  has  its  nucleus  indented  into  a  horseshoe 
or  sometimes  twisted.  Lymphocytes  and  myeloblasts  may  contain 
fuchsinophile  granules  called  Schridde's  granules.  The  true  leuco- 
cytes or  granular  white  cells  are  classified  according  to  their 
granules  into  neutrophile,  eosinophile,  and  basophile.  Their  parent  s 
are  the  myelocytes  of  the  bone-marrow,  which  are  cells  of  large  size 
possessing  rounded  pale-staining  nuclei  and  the  granules  typical  of 
the  particular  leucocyte  to  which  they  are  to  give  rise. 

The  most  primitive  form  is  the  eosinophile  leucocyte  which  is  so 
common  in  lower  animals.  It  probably  has  a  secondary  home  in 
connective  and  lymphoid  tissue.  They  are  characterized  by  their 
large  retractile  granules,  which  have  an  affinity  for  acid  stains  and  a 
twisted,  trilobed,  or  dumb-bell-shaped  nucleus. 


1898  DISEASES  OF  THE  CIRCULATORY  SYSTEM 

The  polymorphonuclear  neutrophile  leucocyte  is  generally 
called  by  the  first  portion  of  its  name.  It  varies  considerably  in 
size,  and  is  characterized  by  alobulated  nucleus  in  which  the  lobules 
vary  in  number,  but  however  separate  they  may  appear,  are  always 
connected  by  fine  threads.  It  is  upon  this  lobulation  that  the  Arneth 
count  is  based,  and  the  form  of  the  nucleus  can  be  explained  in  the 
same  way  as  in  the  transitional  (vide  supra). 

The  basophile  leucocyte  or  mast  cell  has  a  trilobed  nucleus  poor 
in  chromatin  and  a  cytoplasm  containing  basophile  granules.  The 
corresponding  myelocytes  may  under  abnormal  circumstances 
be  found  in  the  circulating  blood,  and  even  at  times  the  pro-myelo-. 
cytes,  which  resemble  myelocytes,  but  possess  a  basophile  cytoplasm 
with  a  few  neutrophile  granules.  More  rarely  cells  with  a  large 
rounded  nucleus  containing  a  fine  chromatinic  network  and  three 
t  o  four  nucleoli,  and  surrounded  by  an  intensely  basophile  cyt  oplasm , 
may  be  seen.     These  are  Naegeli's  myeloblasts. 

Under  pathological  conditions  such  as  anaemia,  with  jaundice 
and  leucocythemia,  a  few  plasma  cells  may  be  seen  in  the  blood. 
They  are  triangular,  with  an  excentric  nucleus  and  a  markedly 
basophile  granular  cytoplasm. 

The  number  of  white  cells  varies  from  time  to  time  from  about 
5,000  to  g,ooo  per  cubic  millimetre,  but  the  average  is  about  7,000, 
or  one  to  every  700  erythrocytes. 

Following  Gulland  and  Goodall,  the  average  differential  count  is 
as  follows: — 

Per  Cent. 


Polymorphonuclear  neutrophile  leucocytes  .  .      70] 

Small   hfmnlin.-vtoc  ->/-,  '. 


Small  lymphocytes 
Large  lymphocytes  . . 
Eosinophile  leucocytes 
Basophile  leucocytes 


20  -Average. 
5) 
4  \ Maximum. 


The  Arneth  count  formulated  in  1904  is  based  upon  the  number 
of  lobules  in  the  nucleus  of  100  polymorphonuclear  or  100  eosinophile 
leucocytes.  Class  I.  contains  those  with  a  single  rounded  or  in- 
dented nucleus,  and  would  include  any  neutrophile  myelocyte  which 
happened  to  be  present.  Class  II.  has  two,  Class  III.  three,  Class  IV. 
four,  and  Class  V.  five  lobules.  The  numbers  in  Classes  I.  and  II. 
added  together  give  the  Arneth  index,  and  in  Classes  I.,  II.,  and 
half  III.  give  the  Bushnell-Trenholtz  index.  Arneth  subdivided 
each  class  into  smaller  groups  by  the  indentations  and  the  character 
of  the  loops  and  lobes,  but  these  are  not  now  considered.  He 
restricted  his  counts  to  polymorphonuclears,  but  to-day  eosinophile 
leucocytes  are  also  considered.  In  counting  it  is  wise  to  follow 
Chamberlain  and  Vedder,  and  to  consider  as  one,  lobules  with  a 
distinct  isthmus,  and  in  cases  of  doubt  to  place  the  number  in  the 
higher  class.  Arneth  considered  that  the  youngest  cells  were  those 
in  Classes  I.  and  II.,  and  that  those  in  Class  V.  were  the  oldest,  while 
Classes  III.  and  IV.  are  believed  to  be  adult.  These  views  have  been 
contested,  as  has  Pottenger's  opinion  that  the  phagocytic   power 


THE  LEUCOCYTE 


1899 


increases  from  Class  I.  to  Class  IV.,  and  falls  in  Class  V.  When  the 
numbers  in  Classes  I.  and  II.  are  increased  above  normal  it  is  called 
'  a  shift  to  the  left,'  and  the  reverse'  a  shift  to  the  right,' terms  which 
have  been  used  in  Chapter  IV.  According  to  Arneth,  a  shift  to  the 
left  is  evidence  of  lower  resistance  on  the  part  of  the  patient  to  a 
disease.  This  count  has  been  tested  in  the  tropics  by  Chamberlain 
and  Vedder,  Macfie,  Breinl,  and   others,  as  has  been  set  forth  on 

P-  75- 

A  few  examples  may  be  given  as  follows: — 

Arneth  Count. 


Kind  of        Nature  of 
Leucocyte.     Observation. 

Observer. 

Class 
I. 

Class 
II. 

Class 
III. 

Class 
IV. 

Class 
V. 

Arneth 
Index. 

Polymorphs 

Normal  in 
Europe 

Arneth 

5 

35 

41 

17         2'0 

40*0 

Polymorphs 

Normal  in 
America 

Kagan 

5 

19 

46 

25       5-o 

24*0 

Polymorphs 

Normal 
Americans 
in  Philip- 
pines 

Chamber- 
lain and 
Vedder 

13*3 

32-9 

37'2 

14-6 

2-0 

46*2 

Polymorphs 

Normal 
Philippinos 

Chamber- 
lain and 
Vedder 

2  7*5 

38-3 

25-8 

7'5 

0-9 

65-8 

Polymorphs ,     Normal 
limits 

Simon 

4-9 

21-47 

33-48 

9-23 

2-4 

25-56 

Eosinophiles 

Normal  in 
Europe 

Arneth 

1 1 

69 

19 

1 

— 

80 

Von  Schilling-Torgau  suggests  a  modification,  which  is  to  classify 
the  neutrophils  as  myelocytes,  myelocytes  with  indented  nucleus, 
polymorphs  with  rod-shaped  nuclei,  polymorphs  with  segmented 
nuclei.  It  is  said  that  this  simple  method  gives  the  same  results  as 
the  Arneth  count. 

The  Arneth  count  is  being  used  at  present  in  tropical  work,  but  its 
value  is  still  sub  judice. 

The  leucocytes  vary  in  number  under  physiological  and  patho- 
logical conditions: — 

Leucopenia,  or  diminution  in  their  numbers,  may  occur  in  physio- 
logical conditions  such  as  hot  or  cold  baths,  or  in  pathological  condi- 
tions such  as  certainprotozoal  infections,  malaria,  trypanosomiases, 
and  kala-azar;  in  bacterial  infections  such  as  enteroidea,  undulant 
fever,  tuberculosis,  and  influenza,  or  in  severe  toxaemias  of  any  kind. 
The  leucopenia  is  usually  polymorphonuclear,  but  in  fevers  there  is 
a  diminution  of  eosinophiles. 


igoo  DISEASES  OF  THE  CIRCULATORY  SYSTEM 

Leucocytosis,  or  increase  in  their  numbers,  may  occur  in  physio- 
logical conditions  such  as  infancy,  pregnancy,  digestion,  and 
exercise,  and  there  is  a  terminal  or  agonal  leucocytosis  before  death. 
In  pathological  conditions  a  leucocytosis  due  to  polymorphonuclear 
leucocytes  may  occur  in  septic  or  inflammatory  conditions,  many 
fevers  and  toxaemias,  after  haemorrhage,  and  with  malignant  disease. 

Lymphocytosis  may  be  relative  when  there  is  a  relatively  high 
percentage  of  lymphocytes  and  low  of  polymorphs,  with  no  increase 
in  the  total  number  of  white  cells,  or  absolute  when  the  total  number 
of  white  cells  as  well  as  of  lymphocytes  is  increased.  The  former 
occurs  in  protozoal  infections  such  as  malaria,  amoebic  dysentery, 
etc.,  and  the  latter  in  leukaemia,  etc. 

Eosinophilia,  or  increase  in  the  eosinophile  leucocytes,  occurs 
in  helminth  infections,  in  skin  diseases,  in  asthma,  in  toxic  states, 
and  in  myelocythaemia. 

Basophilia  occurs  in  myelocythaemia  and  staphylococcal  infections, 
but  in  the  latter  only  slightly. 

Blood  Platelets. 

These  are  probably  derived  from  the  erythrocytes,  and  may 
possibly  not  be  present  in  normal  circulating  blood,  but  formed  in 
preparing  the  films.  Their  clinical  value  is  not  absolutely  certain. 
They  are  said  to  number  about  300,000  per  cubic  millimetre  in 
health.  They  are  colourless,  retractile,  discoidal  bodies,  some 
1-3  microns  in  diameter,  having  a  great  tendency  to  adhere  together 
and  having  an  affinity  for  basic  dyes. 

Hsemoconia. 

These  are  colourless  retractile  bodies,  0-5-4  microns  in  diameter, 
which  do  not  colour  with  ordinary  stains  and  are  of  unknown  origin 
and  function,  though  they  may  be  fat  particles,  as  shown  by 
Neumann. 

BLOOD  PUZZLES. 

Blood  puzzles  consist  of  bodies  which  from  the  first  have  been 
recognized  as  such  or  in  other  instances  have  been  thought  to  be 
parasites. 

It  is  difficult  to  give  a  systematic  account  of  these  bodies,  but, 
following  Balfour,  we  may  classify  them  as  follows: — 

A.  Heterogenetic:—  Not  in  the  blood. 

B.  Autogenetic: — Actually  in  the  blood. 

I.  Found  in  fresh  blood: — 

(a)  Erythrocytic. 

(b)  Leucocytic. 

II.  Found  in  stained  blood: — 

(a)  Erythrocytic. 

(b)  Leucocytic  or  lymphocytic. 


HETEROGENETIC—AUTOGENETIC  1901 

Heterogenetic. 

Tliese  are  external  or  adventitious,  and  may  be  divided  into: — 
I.  Those  belonging  to  the  glass  slide. 
II.  Those  belonging  to  cleaning  or  drying  materials. 

III.  Those  coming  via  the  air. 

IV.  Those  coming  from  the  skin. 

V.  Those  coming  from  the  intestines. 

The  Glass  Slide.- — Everyone  is  well  aware  of  the  peculiar  marks 
which  may  appear  on  old  glass  slides,  and  which  retain  the  stain, 
thus  giving  rise  to  pseudo-trypanosomes,  yeasts,  and  many  other 
forms. 

Perhaps  the  most  interesting  of  these  are  the  '  X  bodies ' 
(Horrocks  and  Howcl!)  which  appear  in  Romanowsky  films  as 
roundish  bodies,  with  a  small  blue  circular  centre  surrounded  by 
four  or  more  faint  concentrically  arranged  capsules,  and  which 
Chamberlain  and  Vedder  have  shown  to  be  artefacts  present  in  the 
glass  slide. 

Cleaning  and  Drying  Materials. — Cotton  fibres  may  be  introduced 
from  a  cloth  in  cleaning  slides.  Blotting-paper,  if  used  twice  for 
drying  blood  slides,  may  introduce  one  kind  of  blood  into  another 
or  bacteria  into  a  blood  film. 

The  Air. — Insect  scales,  plant  hairs,  animal  hairs,  yeasts,  and 
pollen  grains,  may  all  be  introduced  into  blood  films  from  the  air, 
and  especially  mult isept ate  fungal  spores. 

The  Skin. — Pieces  of  dirt,  epithelial  scales,  and  bacteria,  may  come 
from  the  skin. 

The  Intestine. — In  obtaining  films  during  a  post-mortem  or  from 
an  animal  which  has  been  shot  there  is  danger  of  contamination  of 
the  blood  with  spirochetes  and  other  organisms  from  the  intestine. 

Autogenetic. 

These  are  bodies  which  are  really  in  the  blood,  whether  natural 
products  or  artificial  productions. 

Fresh  Blood — Erythrocyte.— In  anaemic  blood  the  erythrocytes 
become  deformed,  forming  oval,  pear-shaped,  tailed,  or  irregular 
bodies  called  poikilocytes,  allied  to  which  are  the  peculiar  chain-like, 
droplet-like,  and  filament-like  bodies  figured  by  Nuttall  and  Balfour 
as  produced  when  taking  films  in  high  air  temperatures.  Some  of 
them  may  be  mistaken  for  parasites,  but  only  by  beginners. 

A  crcnation  seen  in  a  deformed  or  in  an  ordinary  corpuscle  may 
in  certain  focal  planes  look  like  a  malarial  parasite. 

Vacuoles  have  clear-cut  margins,  do  not  move,  do  not  possess 
pigment,  and  are  quite  clear,  yet  they  give  rise  to  trouble,  and  may 
b  ■  mistaken  for  piroplasma  or  for  malarial  parasites. 

rhe  glassy  body  mentioned  above,  when  easily  visible,  is  often 
mistaken  for  a  parasite,  and  is  probably  the  explanation  of  the 
'  maraglianos '  or  dehaemoglobinized  spots  which  have  been  de- 


lgo2  DISEASES  OF  THE  CIRCULATORY  SYSTEM 

scribed,  as  well  as  of  such  pseudo-parasites  as  those  mentioned  by 
Balfour  as  being  described  by  Foran  and  Breeze.  The  dark  ?pot 
mentioned  as  being  visible  in  the  maraglianos  may  be  the  centro- 
some. 

A  granule  from  a  leucocyte  or  a  blood  platelet  lying  on  an  erythro- 
cyte may  simulate  a  parasite. 

Leucocyte. — -The  leucocyte,  especially  the  eosinophile,  is 
responsible  for  the  free  granules,  and  worse  for  the  free  or  attached 
wavy  process,  which  is  apt  tobe  mistakenfor  a  spirochaete,  especially 
when  a  beginner  is  using  the  dark-ground  illumination. 

Stained  Blood — Erythrocyte.— When  the  glassy  body  swells  it 
gives  rise  to  pale  large  red  blood  cells  15-50  microns  in  diameter, 
which  are  the  half-moon-shaped  or  sickle-shaped  corpuscles  of 
Stephens  and  Christophers. 

The  hsemobyzed  stroma  is  the  cause  of  the  shadow  corpuscles,  and 
polychromatophilia  is  due  to  diffuse  colouring  of  the  reticulum, 
while  the  punctate  form  is  due  to  the  nodes  being  especially  tinted. 

Schuffner's  dots  are  caused  by  the  coloration  of  nodes  of  the  reti- 
culum in  older  cells,  while  pathological  karyolysis  of  the  nuclear 
plate  may  be  the  cause  of  the  Howell-Jolly  bodies  and  the  ring- 
shaped  bodies  of  Cabot,  and  perhaps  the  so-called  Paraplasma 
jiavigenum  is  due  to  the  same  cause. 

The  capsule  corpuscle  may  be  the  origin  of  Arnold's  nucleoids, 
Schmauch's  bodies,  Heinz's  corpuscles,  and  many  pseudo-parasites. 

A  blood  platelet  lying  on  an  erythrocyte  may  resemble  a  malarial 
parasite. 

Leucocyte. — The  puzzles  in  connection  with  the  leucocyte  or 
lymphocyte  may  be  divided  into: — 

1.  Extranuclear. 

2.  Intranuclear. 

Extranuclear. — Kurloff's  bodies  seen  in  the  large  lymphocytes, 
especially  in  guinea-pigs,  are  large  vacuoles  with  a  homogeneous 
structure,  and  may  be  a  secretion,  but  have  been  considered  to  be 
parasites.  They  take  a  purplish  or  reddish  colour  with  Giemsa's 
stain. 

Oval  or  round  rings  may  possibly  be  connected  in  some  way  with 
the  area  around  the  centrosome.  Ferrata's  plasmosomes  are  small 
metachromatic  bodies  which  are  thought  to  indicate  retrogressive 
changes:  they  may  be  derived  from  the  chromatin  of  the  nucleus. 

In  1912  Castellani  described  extranuclear  non-parasitic  bodies  in 
leucocytes.  They  take,  with  Giemsa's  stain,  a  blue  colour,  almost 
constantly  show  dots  of  chromatin,  and  measure  2-6  microns  in  diam- 
eter. They  also  occur  free  in  the  liquor  sanguinis,  and  are  by  him 
considered  to  be  degenerate  red  blood  cells  engulfed  by  the  leucocyt  c. 

Intranuclear. — The  nucleus  of  the  mononuclear  leucocyte  is  apt 
to  undergo  changes  and  to  show  bodies  with  a  blue  cytoplasm,  with 
or  without  chromatinic  spots,  which  look  very  like  parasites,  as  also 
described  by  Castellani  in  1913. 


BLOOD  PARASITES— LEU KMMI A  1903 

BLOOD  PARASITES. 

The  blood  may  contain  a  number  of  parasites — e.g.,  the  malarial 
parasites,  the  spirochetes,  the  trypanosomes,  the  kala-azar 
parasites — as  well  as  certain  worms — e.g.,  the  Microfilariae,  Schisto- 
soma hcematobium,  S.  japonicum,  and  S.  mansoni. 

ANEMIA  AND  ALLIED  CONDITIONS. 

Anaemia  is  common,  being  generally  associated  with  ankylo- 
stomiasis, malaria,  kala-azar,  chronic  dysentery,  or  in  women 
repeated  pregnancies  and  prolonged  lactation.  It  is  especially 
common  among  coolies  working  on  estates.  The  treatment  is  to 
remove  the  causal  agent,  and  then  to  administer  the  old  mixture  of 
sulphate  of  iron,  sulphate  of  magnesium,  and  nux  vomica  to  the 
poorer  classes,  while  intramuscular  injections  of  iron  alone  or  com- 
bined with  arsenic  or  sodium  glycerophosphate  are  more  scientific 
and  more  suitable  for  the  better  classes. 

Chlorosis  is  rare,  but  we  have  seen  cases  in  Europeans  and  in 
better-class  native  girls. 

Paransemia  Tropicalis. 

Everyone  residing  in  the  tropics  is  acquainted  with  the  pallor 
which  is  visible  in  the  faces  of  many  European  residents  who, 
apparently,  are  in  good  health.  An  examination  of  the  blood 
fails  toreveal  any  marked  diminution  in  the  red  cells  or  haemoglobin, 
or,  at  all  events,  no  such  reduction  as  would  be  compatible  with  the 
pallor.     We  have  used  the  term  paranaemia  to  indicate  the  condition. 

In  Chapter  III.,  section  Effects  on  the  Blood  (p.  75),  we  have 
shown  that  this  apparent  anaemia  has  been  carefully  studied  by 
W.  M.  Strong,  who  considers  that  this  pallor  is  really  caused  by  the 
deposition  of  pigment  in  the  epidermis.  This  pigment  renders  the 
skin  opaque  to  the  red  rays  contained  in  sunlight,  and  hence  the 
colour  reflected  therefrom  appears  to  the  eye  white. 

In  diagnosing  this  condition  care  must  be  taken  to  exclude  true 
anaemia  by  a  count  of  the  red  cells  in  the  blood  and  an  estimation 
of  the  haemoglobin. 

De  Langen  believes  there  are  real  differences  between  the  blood  of  Euro- 
peans in  the  Tropics  and  at  home:  a  shift  to  the  left  of  Arneth's  count,  dimi- 
nution of  cholesterin,  increase  in  blood  sugar.  He  attributes  to  the  hyper- 
glycemia the  low  fever  so  often  found  in  the  Tropics. 

LEUKAEMIA. 

Leucocythemia  cannot  be  said  to  be  very  rare,  at  all  events  in  our 
experience,  and  may  be  either  spleno-medullary  or  lymphatic  in 
type.  It  is  most  necessary  to  rem  mber  the  possibility  of  the 
occurrence  of  this  disease,  and  to  make  it  a  rule  to  examine  the  blood 
microscopically  before  performing  splenic  or  hepatic  puncture  in 
cases  of  splenomegaly. 

Pseudo-leukaemia  and  Banti's  disease  are  also  known. 


1904  DISEASES  OF  THE  CIRCULATORY  SYSTEM 


GENERAL  DROPSY. 

Cases  of  general  dropsy  not  due  to  heart  or  renal  disease  may  be 
caused  by  beri-beri  or  ankylostomiasis. 

THE  HEART. 

Heart  disease  has  not  been  carefully  studied  by  modern  methods 
in  the  tropics,  but  cases  of  heart-block  due  to  malaria  and  syphilis 
have  been  recorded  by  us. 

Pericarditis  and  endocarditis  are  not  as  common  as  in  other  regions, 
probably  because  rheumatism  is  rare,  and  therefore  they  are  due 
to  such  other  causes  as  gonococcal  infection,  etc.  Atrophies  of  the 
heart,  especially  brown  atrophy,  are  quite  common  as  the  result  of 
some  general  disease.  Heart-block  is  rare,  but  has  been  met  with. 
Rupture  of  a  perfectly  normal  myocardium,  the  pericardium  being 
intact,  is  recorded  by  Herzog  as  due  to  fracture  of  the  second, 
fourth,  and  fifth  ribs. 

Tropical  Heart. 

Under  this  heading  MacLeod  has  described  the  conditions  of 
palpitation  and  dyspnoea  on  going  up  hills  met  with  in  persons  who 
have  resided  long  in  the  tropics.  He  assigns  this  to  degeneration  of 
the  heart,  brought  on  by  the  heat  and  by  the  exceptional  work  which 
it  has  to  do  owing  to  the  changes  in  the  circulation  which  result 
from  the  high  temperature  of  the  tropics.  He  considers  this  to  be 
the  basis  of  the  syncopal  form  of  heat  exhaustion.  Ernest  Black 
believes  that  the  condition  is  associated  with  subnormal  blood 
coagulability,  and  recommends  the  administration  of  calcium  salts. 
The  salt  he  prefers  is  calcium  lactate,  which  he  gives  in  10-grain 
doses.  He  points  out  that  calcium  salts  are  essential  for  the  systole 
of  the  heart  as  well  as  for  the  normal  cogulability  of  the  blood,  and 
refers  their  beneficial  action  to  this  property.  He  considers  that 
citric  acid  or  its  salts  should  be  avoided  when  calcium  salts  are 
administered,  as  they  increase  the  calcium  excretion. 

THE  VESSELS. 

Atheromatous  degeneration  of  the  arteries  is  quite  common,  and 
aneurysm  is  found,  generally  affecting  the  thoracic  aorta,  while 
varicose  veins  and  varicocele  are  usual,  and,  associated  with 
hypertrophy  of  the  heart,  are  very  common  among  rickshaw  coolies. 

Thrombosis  is  often  met  with  as  the  result  of  typhoid  ftver  and 
other  diseases,  and  we  have  seen  thrombosis  of  a  coronary  artery 
with  myomalacia  cordis  or  aneurysm  of  the  heart. 

THE  SPLEEN. 

The  splei  n  is  affected  in  malaria,  kala-azar,  relapsing  fever,  etc., 
as  already  described.     Capsulitis  is  very  commonly   met  with  in 


REFERENCES  1905 

post-mortems,  but  splenic  abscess  is,  in  our  experience,  rare,  and 
may  be  of  entamcebic  origin.  Infarcts  and  tuberculosis  are,  how- 
ever, not  so  rare,  and  spleno-medullary  leukaemia,  as  has  been 
mentioned  above,  is  not  very  rare.  Rupture  of  the  enlarged  malarial 
spleen  has  already  been  mentioned,  and  may  cause  death  within  a 
few  minutes,  or  the  patient  may  live  for  several  hours. 

BONE-MARROW. 

The  importance  of  the  bone-marrow  is  often  overlooked  in  the 
tropics.  It  requires  especial  study  in  anaemias,  kala-azar,  and 
malaria. 


REFERENCES. 

Balfour  (ign).  Fourth  Report  of  the  Wellcome  Tropical  Research  Labora- 
tories, 109-126  (Blood  Puzzles  and  Fallacies).     London. 

Castellani  (191 2).  Journal  of  Tropical  Medicine  and  Hygiene  (Blood 
Puzzles).     London. 

Chalmers  and  Gibbon  (1918).  Journal  of  Tropical  Medicine  and  Hygiene 
(Heart-Block  in  a  Sudanese).     London. 

Chamberlain  and  Vedder  (1911).  Philippine  Journal  of  Science,  B,  vi. 
405  and  421  (Arneth  Count  and  X  Bodies).     Manila. 

Gulland  and  Goodall  (1914).  The  Blood.  (A  most  excellent  book.) 
Edinburgh. 

Strong,  W.  M.  (1916).  Transactions  of  the  Society  of  Tropical  Medicine, 
97-100.     London. 

Von  Schilling-Torgau  (1914).  Mense's  Handbuch  der  Tropenkrankheiten, 
2nd  edition,  ii.  1-149.     Leipzig. 


120 


CHAPTER  LXXXIII 
DISEASES  OF  THE  LIVER  AND  PANCREAS 

General  remarks— Tropical  liver — Amoebic  abscess  of  the  liver — 
Opisthorchiosis — Clonorcniosis — References. 

GENERAL  REMARKS. 

Diseases  of  the  liver  and  pancreas  are  of  common  occurrence  in 
the  tropics.  The  liver  may  be  affected  in  the  course  of  tropical 
fevers,  especially  in  malaria  and  kala-azar,  in  the  latter  of  which 
Rogers  has  described  a  special  form  of  cirrhosis.  The  disease 
called  '  infantile  biliary  cirrhosis  of  the  liver,'  described  by  Ghose 
and  Mackenzie  as  occurring  in  Calcutta  and  other  parts  of  India 
in  Hindu  and  Mohammedan  children,  appears  to  us  to  require 
reinvestigation,  with  a  view  to  deciding  whether  it  also  is  a  variety 
of  kala-azar.  It  is  said  to  attack  children  under  one  year  of  age, 
and  to  be  characterized  by  a  low  type  of  fever,  associated  with 
enlargement  of  the  liver  and  spleen,  jaundice,  pale  motions,  dark 
urine,  and  sometimes  vomiting  of  blood,  oedema,  and  ascites,  and 
ends  fatally  in  three  to  eight  months. 

Acute  yellow  atrophy  of  the  liver  is  not  as  uncommon  in  Ceylon 
as  in  Europe,  for,  on  an  average,  we  have  met  with  one  or  two  cases 
per  annum.  It  occurs  in  Ceylon  more  commonly  in  men  than  in 
women,  but  the  cause  appears  to  be  quite  obscure. 

An  extraordinary  case  of  acute  severe  hepatitis  and  gastritis, 
which  caused  a  considerable  haemorrhage  to  take  place,  filling  all 
the  small  biliary  ducts,  the  gall-bladder,  the  common  bile-duct, 
the  duodenum,  jejunum,  and  ileum  with  blood,  has  been  recorded 
by  one  of  us  in  Ceylon.  The  inflammation  occurred  in  a  stomach 
which  was  altered  by  chronic  atrophic  gastritis.  The  haemorrhage 
was  caused  by  the  blood  passing  from  the  damaged  hepatic  capil- 
laries into  the  minute  bile  channels,  and  was  due  to  the  destruction 
of  the  walls  of  these  capillaries  and  the  liver  cells.  No  definite 
cause  could  be  found  for  this  condit  ion,  which  is  decidedly  rare. 

Congestion  and  inflammation  of  the  liver,  together  with  abscess, 
are  common  in  the  tropics,  and  require  special  consideration  (p.  1910) . 

Atrophic  cirrhosis  of  the  liver  is  very  common  in  the  tropics,  and 
though  generally  there  is  a  history  of  alcohol,  still,  this  is  by  no 
means  always  so,  and  sometimes  the  cause  is  not  evident.  We 
believe  that  cirrhosis  of  the  liver  of  malarial  origin  is  much  less 

1906 


GENERAL  REMARKS  1907 

frequent  than  is  admitted  by^many  authors.     It  will  be  shown 
presently  that  various  parasites  cause  cirrhosis. 

Primary  cancer  of  the  liver  has  been  met  with,  but  is  very  rare. 
On  the  other  hand,  secondary  cancer  is  by  no  means  rare.  The 
only  non-malignant  growth  which  we  have  met  with  was  an  angioma. 
The  protozoal  parasites  which  occur  in  the  liver  are  Loeschia 
histolytica,  the  cause  of  liver  abscess;  Leishmania  donovani  and 
L.  infantum,  the  causes  of  kala-azar  and  the  infantile  kala-azar;  and 
the  malarial  parasites,  as  has  already  been  noted.  Coccidiosis  has 
been  found  in  the  tropics  in  man  several  times. 

With  regard  to  the  trematode  parasites-^  of  the  liver,  Fasciola 
hepatica  is  only  an  occasional  parasite  of  man.  Fasciohpsis  buski 
(rathouisi)  has  been  seen  in  a  Chinese  who  showed  obscure  liver 
symptoms,  and  no  doubt  microscopical  examination  of  the  faeces 
would  make  diagnosis  possible;  but  there  is  only  one  certain  case, 
and  the  information  regarding  the  symptoms  is  meagre.  Opisthor- 
chisfelineus and Amphimerus  noverca  arethc cause  of  opisthorchiosis, 
which  will  be  considered  later,  as  will  clonorchiosis,  caused  by 
Clonorchis  sinensis.  Dicroccelium  lanceatum  is  considered  to  be 
too  small  to  cause  any  serious  symptoms  while  living  in  the  bile- 
ducts.  Schistosoma  mansoni  and  S.  japonicum  may  both  affect  the 
liver  (pp.  1589-1867). 

With  regard  to  tape-worms ,  Taenia  echinococcus  is  not  common, 
but  we  have  met  with  one  case  of  echinococcus  in  Ceylon,  which 
was  brought  by  a  Boer  prisoner,  and  Begbie  has  recorded  another, 
not  in  the  liver,  but  associated  with  the  lung,  in  an  old  resident 
in  Ceylon.  One  of  us  has  recorded  an  invasion  of  the  liver  by 
Ascarides,  and  the  formation  of  abscesses  by  the  agency  of  these 
worms.  We  have  also  recorded  Porocephalus  armillatus  in  the 
liver. 

Disease  of  the  gall-bladder  is  common  in  the  tropics,  and  we  have 
met  with  acute  and  chronic  inflammations.  Gall-stones  are  often 
met  with,  probably  as  sequelae  to  typhoid  fever,  but  also  arising 
from  other  causes.  Suppuration  of  the  bile-ducts  we  have  only 
seen  once,  and  oedema  of  the  wall  of  the  gall-bladder  we  have  also 
only  found  once.  Obstructive  and  catarrhal  jaundice  are  met  with 
fairly  frequently  in  the  tropics. 

Rupture  of  the  liver  may  take  place  as  the  result  of  traumatisms, 
and  recently  Herzog  has  recorded  this  accident  in  a  Filipino  woman 
as  the  result  of  a  native  obstetrical  practice,  which  consists  of 
traction  on  a  cloth  wound  round  the  abdomen.  In  this  case  the 
rupture  had  been  caused  by  the  perforation  of  the  tip  of  the  eleventh 
rib  into  the  fatty  liver. 

The  pancreas,  in  our  experience,  is  not  infrequently  found 
diseased.  We  have  met  with  the  following  types  of  inflammation 
in  Ceylon: — 

1.  Acute  hemorrhagic  pancreatitis. 

2.  Acute  suppurative  catarrh  of  the  ducts. 


xgo8  DISEASES  OF  THE  LIVER  AND  PANCREAS 

3.  Subacute  pancreatitis. 

4.  Chronic  pancreatitis. 

(1)  Syphilitic  in  the  foetus. 

(2)  In  the  adult. 

(a)  Chronic  interlobular  pancreatitis. 

(b)  Chronic  interacinar  pancreatitis. 

(c)  Chronic  interlobular  and  interacinar  pancreatitis 

combined. 

It  should  be  remembered  that  the  subtertian  parasite  is  one  of 
the  causes  of  hemorrhagic  pancreatitis.  In  addition  we  have  seen 
cancer  of  the  pancreas  producing  a  blocking  of  the  duct  of  Wirsung, 
and  leading  to  a  ranula  which  contained  many  pancreatic  calculi. 
We  have  once  seen  an  ascaris  in  the  duct  of  Wirsung  associated 
with  a  hypergemic  condition  of  the  gland. 

After  this  brief  general  statement,  we  must  consider  congestion 
of  the  liver,  abscess  of  the  liver,  opisthorchiosis,  and  clonorchiosis. 

TROPICAL  LIVER. 

Synonyms. — Congestion  of  the  liver,  Hyperemia  of  the  liver, 
Indian  liver. 

Definition. — Congestion  of  the  liver  is  a  hyperaemia  brought 
about  by  many  conditions,  especially  gastro-intestinal  disorders. 

Remarks. — There  can  be  no  doubt  that  the  European  is  apt  to 
eat  and  drink  more  than  is  good  for  him  on  his  first  arrival  in  the 
tropics,  and  that  this  is  bound  to  lead  to  an  increase  of  blood  in 
the  liver,  which  physiological  condition  may  easily  become  a  con- 
gestion, with  later  blood  stasis  and  diminution  of  the  functional 
activity  of  the  organ. 

Climatology. — Congestion  of  the  liver  is  a  cosmopolitan  com- 
plaint, but  is  much  more  commonly  met  with  in  the  tropics  than 
in  the  Temperate  Zone. 

etiology. — Congestion  of  the  liver  is  brought  about  by  indiscre- 
tion in  diet,  such  as  too  much,  too  rich,  or  too  highly  spiced  foods, 
by  alcoholic  excess,  and  by  chills. 

Pathology. — Post  mortem  the  liver  is  found  to  be  swollen,  dark 
red  in  colour,  and  drips  with  blood  when  cut  into.  The  cells  are 
often  laden  with  fat,  and,  in  addition  to  the  changes  in  the  liver, 
there  will  be  added  the  pathological  changes  which  have  caused 
the  congestion,  and  which  are  generally  to  be  found  in  the  alimen- 
tary canal,  as  well  as  those  which  have  caused  the  death  of  the 
patient. 

Symptomatology.- — The  illness  begins  with  frontal  headache, 
malaise  and  loss  of  appetite,  with  nausea  or  sickness,  and  a  bitter 
taste  in  the  mouth  on  awakening  in  the  morning.  The  tongue  is 
coated,  and  there  are  the  usual  signs  of  dyspepsia,  associated  with 
constipation  and  the  passage  of  pale-coloured  motions.  The  liver 
is  enlarged  and  tender,  and  usually  there  is  a  sense  of  weight  in  the 
right  hypochondrium,  and  pain  below  the  right  scapula  or  in  the 


TROPICAL  LIVER  1909 

right  shoulder,  and  there  may  be  slight  signs  of  jaundice  in  the 
yellow  conjunctiva  and  sallow  skin.  The  urine  may  be  diminished 
in  quantity,  high-coloured,  and  with  high  specific  gravity,  and 
loaded  with  uric  acid  and  urates.  The  nervous  system  is  also 
affected,  and  the  patient  is  usually  very  cross  and  irritable.  The 
temperature  is  generally  normal,  but  sometimes  it  rises,  and  when 
above  ioo°  F.  it  is  usual  to  call  the  disease  hepatitis,  instead  of 
congestion  of  the  liver.  The  common  non-febrile  variety  lasts 
from  two  to  seven  days,  but  is  liable  to  recur. 

Varieties.- — Congestion  of  the  liver  may  be  acute  when  associated 
with  some  other  disease,  or  chronic  when  due  to  gastro-intestinal 
disturbance. 

Diagnosis. — -The  diagnosis  is  based  on  the  painful  enlargement  of 
the  liver,  which,  in  the  absence  of  other  disease,  is  usually  unaccom- 
panied with  marked  rise  of  temperature. 

Treatment. — In  the  acute  attack  it  is  as  well  to  keep  the  patient 
in  bed  and  begin  the  treatment  with  a  dose  of  calomel  (gr.  ii.  to 
gr.  v.),  followed  a  few  hours  later  by  a  saline  in  the  form  of  mag- 
nesium and  sodium  sulphates  or  Carlsbad  salts.  An  effervescing 
mixture  of  ammonium  carbonate  (gr.  iv.  to  gr.  v.)  and  sodium  bi- 
carbonate (gr.  xx.),  with  citric  acid  (gr.  xv.),  may  be  given  every 
three  hours,  or  a  mixture  containing  ammonium  chloride  in  seme 
combination.  At  the  same  time  hot  fomentations  or  a  thick  coat 
of  antiphlogistin  may  be  applied  to  the  region  of  the  liver.  The 
diet  should  consist  of  soups  and  milk,  diluted  with  Vichy  or  barley 
water,  and  no  alcohol  in  any  form  allowed. 

When  the  condition  has  become  chronic,  the  patient  must  be 
carefully  dieted  and  placed  upon  a  course  of  treatment  with  the 
above  effervescing  mixture  and  Vichy  (Grande  Grille),  and  when 
leave  in  Europe  is  available,  should  be  sent  to  Vichy,  Carlsbad, 
Harrogate,  or  Montecatini.  He  should  avoid  alcoholic  stimulants 
and  rich  food  of  every  description,  and  especially  tinned  :ood,  and 
should  restrict  his  diet  to  fowls,  clear  soups,  fish,  and  well-cooked 
vegetables  and  milk,  avoiding  meat  and  curries. 

Whenever  the  acute  attack  is  over,  the  patient  should  be  advised 
to  take  exercise  daily — walking,  riding,  golf,  or  tennis,  combined 
with  the  usual  so-called  liver  exercises. 

Prophylaxis. — Plain,  simple,  not  highly  spiced  food  should  be 
taken,  and  such  pernicious  drinks  as  the  heavy  forms  of  beer, 
sherry,  champagne,  etc.,  should  be  avoided.  If  any  form  of  alcohol 
is  to  be  taken  in  the  tropics,  this  should  be  Scotch  whisky,  well 
diluted,  or  light  clarets,  and  then  only  in  moderation.  Chills  must  be 
avoided  as  carefully  as  possible,  especially  when  there  is  a  land  wind, 
in  the  rains,  and  when  changing  from  a  warm  to  a  cooler  climate. 

With  regard  to  the  cold  bath,  there  is  no  doubt  that  the  majority 
of  people  are  unable  to  stand  this  in  the  tropics,  and  therefore  it 
is  better  to  use  water  with  the  chill  removed. 

Some  persons  are,  however,  distinctly  benefited  by  a  cold  bath, 
and  therefore  individual  peculiarities  must  be  considered. 


igio  DISEASES  OF  THE  LIVER  AND  PANCREAS 

The  most  dangerous  time  for  chills  is  in  the  night;  therefore  it  is 
as  well  to  sleep  with  some  light  blanket  placed  over  the  abdomen, 
and  in  flannel  night  attire.  In  the  daytime  a  woollen  undervest  or 
cholera-belt  may  be  worn.  The  clothes  must  be  carefully  changed 
whenever  they  become  damp. 

AMCEBIC  ABSCESS  OF  THE  LIVER. 

Synonyms. — Hepatic  abscess.  French:  Absces  du  Foie.  Italian: 
Epatite  Suppurativa.     German  :  Tropischer  Leberabszess. 

Definition.— Amoebic  abscess  of  the  liver  is  a  suppurative  hepa- 
titis, caused  by  Loeschia  histolytica — usuaUy  preceded  by  an  attack 
of  amoebic  dysentery. 

History. — Liver  abscess  was  known  to  the  ancients,  and  was 
operated  upon  as  far  back  as  the  days  of  Hippocrates,  while  Galen 
recognized  its  connection  with  dysentery,  and  Morgagni  studied  its 
morbid  anatomy.  During  the  nineteenth  century  the  disease  was 
carefully  studied  by  French  surgeons,  beginning  with  those  of  the 
army  of  occupation  in  Egypt,  and  also  by  the  French  colonial 
doctors  and  the  Indian  army  surgeons.  The  discovery  of  Amoeba  or 
Loeschia  emphasizedthe  connection  between  liver  abscess  and  dysen- 
tery. Kruse  and  Pasquale  were  the  fir st  t  o  regularly  find  amoebae  in 
the  liver  abscess,  and  to  state  that,  apart  from  the  amoebae,  the  pus 
was  sterile.  Later  researches  have  confirmed  this  discovery,  and 
have  demonstrated  that  the  pus  of  a  liver  abscess  does  not  contain 
bacteria  in  most  cases- — a  fact  which  agrees  with  our  experience — 
and  that  the  true  cause  of  the  malady  is  Loeschia  histolytica. 

Climatology. — Liver  abscess  is  essentially  a  disease  of  the  tropics 
and  subtropical  regions.  It  is  very  common  in  India  and  Indo- 
China,  rather  less  so  in  Ceylon,  Malaya,  Java.  Sumatra,  and  rare  in 
Southern  China.  In  Africa  it  is  common  in  Egypt  and  North  and 
West  Africa  (Gold  Coast).  In  America  it  appears  to  be  less  com- 
monly met  with,  being  rare  in  the  LTnited  States,  West  Indies,  and 
British  Guiana.  It  is  also  found,  though  rarely,  in  the  Temperate 
Zone,  in  Spain,  Italy,  France,  and  even  in  such  a  northern  country 
as  England.     There  is  no  seasonal  variation. 

/Etiology. — The  cause  of  the  suppuration  is  Loeschia  histolytica, 
and  perhaps  other  varieties  of  Loeschia.  It  is  more  common  in 
Europeans  than  in  natives,  and  more  so  in  males  than  females, 
and  is  usually  a  disease  of  adults.  The  most'impcrtant  predispos- 
ing cause  is  perhaps  alcohol. 

In  monkeys  one  of  us  has  recorded  the  occurrence  of  liver  abscess  due  to 
an  amoeba  (Loeschia  miitalli  Castellani,  1907). 

Pathology. — The  Loeschia  pass  from  the  bowel  via  the  portal 
vein  into  the  liver,  where  they  produce  coagulative  necrosis  of  the 
liver  cells,  which  become  formless  and  break  up  into  granular 
debris.  This  necrosis  is  thought  to  be  brought  about  by  means 
of  toxins  produced  by  the  Loeschia.  The  necrosed  area  undergoes 
liquefaction  and  form?  the  abscess,  the  contents  of  which  consist  ol 


AMOEBIC  ABSCESS  OF  THE  LIVER 


i.)  i  i 


debris,  endothelial  cells,  mononuclear  leucocytes  (rarely  pol^mci- 
phonuclears),  red  corpuscles,  haematoidin,  cholesterin,  and  rarely 
Charcot-Leyden  crystals.  The  pus  is  usually  sterile,  and  as  a  rule 
docs  not  contain  amoebae,  which  are  in  the  marginal  wall  of  the 
abscess,  and  may  extend  into  the  liver  tissue  for  some  distance 
from  the  focal  lesion.  After  the  abscess  has  been  opened,  amoeba; 
may  be  found  in  the  pus.  The  process  of  repair  has  not  been  fully 
worked  out,  but  it  appears  as  though  the  granulation  tissue  formed 
new  connective  tissue,  in  which  new  bloodvessels  and  proliferating 
bile-ducts  may  be  seen,  indicating  the  processes  which  may  lead 
1  o  repair. 

Usually  there  is  only  one 
abscess,  but  it  is  not  uncommon 
to  find  two,  and  there  may  be 
more.  The  abscess  is  generally 
found  in  the  posterior  part  of 
the  upper  portion  of  the  right 
lobe.  It  is  rounded  in  form, 
with  walls  composed  of  degene- 
rated liver  cells  and  granulation 
tissue.  Its  contents  may  be 
thick,  creamy  pus,  but  more 
usually  it  is  yellowish  or  brown 
coloured.  On  microscopical  ex- 
amination it  consists  largely  of 
detritus,  with  a  few  degenerated 
liver  and  pus  cells.  The  bacteria 
found  in  the  pus,  when  it  is  not 
sterile,  are  streptococci,  staphy- 
lococci, B.  coli  communis,  and 
B.  Pyocyaneus,  and  occasionally 
some  anaerobic  germs.  The 
abscess  varies  much  in  size,  from 
a  small  hollow  containing  only 
i  or  2  ounces  up  to  a  huge  cavity 
with  a  couple  of  pints  or  more 
of  pus,  while  even  larger  have  been  described.  The  size  of  the 
liver,  apart  from  the  abscess,  also  varies,  being  sometimes  increased 
and  sometimes  diminished.  Apart  from  the  liver  abscess,  there  are 
usually  signs  of  old  or  recent  dysentery  in  the  colon,  though  these 
may  be  absent.  There  may  be  abscesses  in  other  parts  of  the  body, 
the  spleen,  the  brain,  etc.,  but  these  are  rare. 

Symptomatology. — There  is  usually  a  history  of  a  previous  attack 
of  dysentery,  but  this  may  be  wanting.  The  disease  begins  in- 
sidiously with  signs  of  congestion  of  the  liver  and  fever.  This  fever 
is  important,  being  irregular,  sometimes  remittent,  sometimes 
intermittent,  sometimes  with  long  apyrexial  intervals. 

The  X  rays  may  show  that  the  movement  of  the  diaphragm  is 
diminished  on  the  right  side,  and  attention  has  also  been  called  to 


Fig.  775. — Amcebic  Abscess  of  the 
Liver. 


1912 


DISEASES  OF  THE  LIVER  AND  PANCREAS 


the  arched  '  cupola-like  '  curve  of  the  upper  aspect  of  the  liver,  as 
seen  by  radioscopy.  The  early  stage,  called  by  Rogers  the  '  presup- 
purative  stage,'  is  of  the  utmost  importance;  for  if  it  can  be  recog- 
nized and  appropriate  treatment  applied,  the  disease  may  be 
stopped  in  a  certain  number  of  cases.  If,  however,  this  is  not 
done,  rigors  may  take  place,  and  the  fever  usually  becomes  more 
severe,  and  a  typical  hectic  temperature  with  night-sweats  may 
ensue;  while  the  patient  complains  of  a  dragging  sensation  on  the 
right  side,  pain  under  the  right  shoulder-blade  and  in  the  right 
shoulder.  This  latter  is  a  referred  pain,  due  to  the  fact  that  the 
phrenic  nerve  arises  from  the  fourth  cervical  nerve-root,  the  fibres 
of  which  supply  the  skin  of  the  shoulder. 


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Fig.  776. — The  Temperature  Chart  of  a  Case  of  Abscess  of  the  Liver. 


A  patient  with  an  abscess  of  the  liver  often  possesses  a  most 
typical  f acies.  He  lies  on  his  back,  with  his  legs  drawn  up ;  his  face 
is  drawn,  and  of  a  pale  yellow  colour,  and  the  ocular  conjunctiva 
possesses  a  peculiar  bluey-whitish  colour.  It  is  said  that  sometimes 
the  right  pupil  is  dilated,  but  in  our  experience  this  is  not  a  constant 
symptom.  Generally  he  is  emaciated,  and  deep  inspiration  is  pain- 
ful; hence  the  breathing  is  costal  in  character,  and  often  there  is  a 
slight  cough.  The  hands  and  feet  are  often  cold  and  clammy  to 
the  touch. 

On  inspecting  the  abdomen  and  chest,  the  right  hypochondrium 
will  be  noticed  to  be  bulging,  while  the  liver  is  enlarged  and  tender. 
On  palpating  the  front  of  the  abdomen,  the  right  rectus  muscle  may 
be  felt  to  become  suddenly  rigid — a  most  characteristic  sign — while 
the  left  is  not  affected.  On  percussion  the  liver  is  found  to  be 
enlarged,  and  pain  may  be  produced  by  pressure  in  the  epigastrium 
or  over  an  intercostal  space.  These  painful  spots  are  of  importance 
in  localizing  the  site  of  the  abscess.     On  listening  over  the  lower 


SYMPTOMATOLOGY— DIAGNOSIS  1913 

part   of  the  chest,  fine  crepitations  or  friction  sounds  may  be 
heard. 

Usually  liver  abscess  is  accompanied  by  some  anaemia  and  some 
increase  in  the  number  of  the  total  leucocytes,  but  this  appears  to 
vary,  being  greater  if  the  abscess  is  small  and  deeply  seated,  and  less 
so  if  large  and  superficial.  According  to  Rogers,  the  ratio  of  white 
to  red  corpuscles  varies  from  1  :  517  to  1  :  126.  With  regard  to  the 
differential  count,  the  polymorphonuclear  leucocytes  are  but  slightly 
increased,  but  the  lymphocytes  are  usually  more  than  normal. 
Leger  gives  the  differential  count  as  being:  Polymorphonuclears, 
78-37  per  cent.;  lymphocytes,  17-44  per  cent.;  mononuclears,  3-15 
per  cent.;  and  eosinophils,  070  per  cent.,  which  closely  agrees 
with  Rogers'  figures,  which  are:  Polymorphonuclears,  74  to  87  per 
cent. ;  lymphocytes,  7  to  22  per  cent. ;  mononuclears,  3  to  7  per  cent. ; 
eosinophiles,  0  to  4  per  cent.  In  some  of  our  cases  there  was  no 
polymorphonuclear  leucocytosis,  while  on  several  occasions,  even  in 
non-malarial  subjects,  there  was  a  relatively  large  mononuclear  in- 
crease. The  number  of  sudanophile  leucocytes  tested  according  to 
the  Cesaris-Demel  method  is  often  increased. 

The  urine  is  usually  diminished,  and  its  excretion  is  said  to  be 
altered,  so  that  the  greatest  quantity  is  passed  between  12  midnight 
and  12  noon,  being  especially  increased  in  the  early  morning. 

If  the  abscess  is  allowed  to  continue  its  own  course,  it  may  burst 
into  the  lung,  causing  signs  of  pleurisy  and  pneumonia,  associated 
with  the  expectoration  of  characteristic  brown  or  reddish-brown 
gummy,  viscid,  purulent  matter;  or  into  the  stomach,  when  a 
similar  material  will  be  vOmited;  or  into  the  bowel,  when  it  will 
be  passed  per  anum.  It  may  also  burst  into  the  pericardium  or  the 
p  iitoneum,  or  into  the  vena  cava,  all  of  which  cases  are  bound  to 
end  fatally.     If  it  does  not  burst,  the  patient  may  die  of  exhaustion. 

The  duration  of  a  liver  abscess  is  very  variable,  being  from  a  few 
weeks  to  several  months,  and  even  years. 

Diagnosis. — The  diagnostic  points  in  abscess  of  the  liver  are:  A 
history  of  dysentery;  fever,  generally  of  a  serotinc  type,  with 
sweatings,  not  yielding  to  quinine;  painful  enlargement  of  the  liver; 
the  characteristic  pain  in  the  shoulder:  the  rigidity  of  the  right 
rectus;  the  loss  of  movement  in  the  right  side  of  the  diaphragm, 
and  the  frequent  cupola-shape  of  the  liver  on  radioscopy;  and, 
above  all,  the  discovery  of  the  pus  by  exploratory  puncture,  as 
described  below. 

The  differential  diagnosis  between  the  presuppurative  and  the 
suppurative  stages  is  often  impossible  without  a  puncture,  but 
sweating,  high  intermittent  temperature,  if  present  and  not  influ- 
enced by  the  emetine  treatment,  is  suspicious  that  suppurative 
changes  have  begun. 

Pleurisy  with  effusion  on  the  right  side  can  be  distinguished  from 
liver  abscess  by  the  presence  of  Grocco's  paravertebral  triangle  on 
the  left  side.  Moreover,  in  pleuritic  effusions  the  upper  limit  of 
the   dulness  is  horizontal,   while   in   liver   abscess  it    is  convex. 


1914  DISEASES  OF  THE  LIVER  AND  PANCREAS 

Another  diagnostic  point  to  which  Manson  has  drawn  attention  is 
that  the  enlarged  liver  gravitates  with  changes  of  position  much 
more  distinctly  than  pleural  effusions.  If  the  dulness  in  the  mid- 
axillary  line  diminishes  notably  when  the  patient  lies  on  his  left 
side,  the  case  is  probably  one  of  liver  abscess.  It  is  to  be  noted, 
however,  that  a  right  pleural  effusion  and  a  liver  abscess  may 
coexist.  Pneumonia  on  the  right  side  with  congestion  of  the  liver 
may  also  lead  to  difficulties,  which  must  be  met  by  careful  physical 
examination  and  the  microscopical  and  bacteriological  examination 
of  the  sputum.  Malarial  fever  can  be  diagnosed  from  the  fever  of 
hepatitis  by  examination  of  the  blood  and  the  presence  of  the 
enlarged  spleen.  In  those  cases  of  liver  abscess  in  which  fever  is 
the  only  symptom  the  diagnosis  may  be  extremely  difficult,  and 
may  require  all  modern  bacteriological  methods  to  exclude  Malta 
fever,  malaria,  septicaemia,  and  typhoid,  etc.  When  in  doubt,  an 
exploratory  puncture  should  always  be  made,  for  it  can  do  no  harm, 
and  may  relieve  the  congestion.  When  a  long  needle  is  introduced 
into  a  liver  abscess,  it  moves  regularly  with  respiration.  Purulent 
cholecystitis  in  most  cases  gives  no  trouble  on  diagnosis,  as  the 
enlarged  gall-bladder  can  be  easily  felt,  and  there  is  generally  a 
history  of  hepatic  colic. 

Syphilitic  gumma  of  the  liver  may  show  many  symptoms  in 
common  with  liver  abscess,  including  the  intermittent  fever,  as 
we  have  twice  noted.  The  positive  Wasserman  reaction  and  the 
action  of  potassium  iodide  in  full  doses  clears  the  diagnosis. 

Cases  of  leukaemia,  pseudo-leukaemia,  tropical  splenomegaly,  and 
kala-azar  have  been  mistaken  for  liver  abscess,  but  in  all  these  con- 
ditions the  spleen  is  also  greatly  enlarged. 

In  this  connection  we  may  emphasize  the  necessity  for  the  ex- 
amination of  the  blood  in  order  to  exclude  leukaemia,  otherwise  a 
fatal  haemorrhage  may  follow  such  a  simple  operation  as  puncture 
of  the  liver.  Liver  abscess  is  usually  easily  diagnosed  from  hydatid 
disease,  but  when  purulent  changes  have  taken  place  in  the  latter 
the  diagnosis  may  be  impossible,  except  by  the  history  and  the 
eosinophilia. 

Prognosis. — If  the  abscess  is  left  unoperated  for  a  long  time,  the 
prognosis  is  very  bad,  as  the  danger  of  exhaustion  and  septic  infec- 
tion is  great.  If  the  abscess  has  burst  into  the  lung,  the  prognosis 
is  also  bad.  but  better  than  if  it  had  burst  into  the  bowel.  Since 
operative  measures  have  come  into  more  common  use  the  mortality 
has  decreased,  according  to  Dujardin  Beaumetz,  from  82  per  cent, 
to  32  per  cent.  The  operation  wound  may  occasionally  become 
phagedenic. 

Treatment. — If  a  case  is  suspected  by  the  symptoms  and  blood- 
counts  to  be  in  the  '  presuppurative  stage,'  emetine  or  ipecacuanha 
should  be  administered,  and  should  be  given  with  the  precautions 
already  mentioned  under  Amoebic  Dysentery,  and  the  latter  must 
b  1  ontinued  for  several  weeks  after  every  sign  of  hepatitis  has 
'li-appeared. 


TREATMENT  191 5 

It,  however,  an  abscess  is  believed  to  have  formed,  there  should 
be  no  delay  in  making  an  exploratory  puncture. 

For  this  purpose  a  needle  3J  inches  in  length,  but  preferably  not 
longer,  because  of  the  danger  of  injuring  the  vena  cava,  should  be 
rendered  sterile  by  boiling  in  plain  water,  but  must  not  be  dipped 
into  an  antiseptic  lotion  nor  into  spirit.  This  needle  shoiild  be 
capable  of  being  fitted  on  to  a  glass  syringe  or  an  aspirator. 

The  patient  should  be  placed  under  chloroform,  and  all  arrange- 
ments should  be  made  so  that  an  operation  can  be  performed  at 
once  if  necessary. 

The  needle  should  be  driven  into  the  liver  in  the  region  of  any 
definite  swelling  or  pain,  or,  failing  these,  through  the  eighth  inter- 
costal space  in  the  anterior  axillary  line,  about  1  or  i|  inches  from 
the  costal  margin. 

The  direction  of  the  needle  should  be  inward,  slightly  upward 
and  backward,  because  the  usual  site  of  an  abscess  is  in  the  upper 
and  back  part  of  the  right  lobe. 

Aspiration  by  the  syringe  or  the  aspirator  may  reveal  pus,  or 
may  fail  to  do  so,  in  which  latter  event  the  needle  must  be  carefully 
and  slowly  withdrawn,  and  its  contents  ejected  on  to  a  clean  white 
dish,  to  see  if  it  is  composed  of  the  grumous  material  of  liver  abscess. 
The  needle  should  now  be  driven  into  the  liver  in  different  places 
and  directions  until  some  six  to  twelve  punctures  have  been  made. 
There  is  no  danger  in  this  procedure  if  performed  with  reasonable 
care,  and  it  may  even  benefit  the  patient  by  performing  what  has 
been  termed  '  hepatic  phlebotomy.'  When  the  abscess  has  been 
located,  the  needle  should  be  left  in  situ  as  a  guide,  and  one  of  two 
procedures  may  be  carried  out :  A.  Aspiration;  B.  Operation. 

The  operation  should,  however,  always  be  performed  if  the 
abscess  has  already  burst  into  the  lungs,  the  peritoneal  or  pleural 
cavities. 

A.  Aspiration. — 'This  is  preferable  if  the  abscess  is  small,  and 
consists  of  evacuating  its  contents,  and  the  injection  of  a  solution 
of  1  grain  of  emetine  hydrobromide  in  2  ounces  of  water,  or  the 
repeated  irrigation  of  the  cavity  with  a  solution  of  bi-hydrochloride 
of  quinine  (3  to  5  grains  to  the  ounce)  by  means  of  Rogers'  flexible 
sheathed  aspiration  cannula. 

B.  Operation. — An  operation  is  necessaryif  the  abscess  is  large, 
if  the  pus  is  not  sterile,  if  the  abscess  has  burst  into  the  lungs  or  a 
serous  cavity. 

The  site  of  the  operation  depends  upon  where  the  pus  has  been 
obtained.  Two  principal  places  may  be  mentioned:  (1)  through 
the  thoracic  wall;  (2)  through  the  abdominal  wall  below  the  ribs. 

Giordano  and  others  have  recommended  a  laparotomy  and  the 
localization  of  the  abscess  by  the  hand  prior  to  the  actual  operation 
f  1  »r  evacuation  of  the  pus.  This  may  be  useful  in  c  rtain  cases  when 
there  are  no  signs  indicating  the  position  of  the  abscess.. 

1.  Operation  through  the  Thoracic  Wall. — An  incision  should  be 
made  through  the  parietes,  including  the  site  of  the  puncture, 


igi6  DISEASES  OF  THE  LIVER  AND  PANCREAS 

through  which  pus  was  obtained.  After  the  skin  has  been  well 
retracted,  a  piece  of  a  rib  may  require  to  be  removed,  thus  ex- 
posing the  diaphragm  below  the  pleura,  which  must  be  incised  and 
stitched  to  the  margins  of  the  wound,  and  the  wound  well  packed 
with  gauze. 

The  liver  is  now  exposed,  and  two  methods  of  procedure  are  open 
to  the  operator — either  to  push  a  pair  of  dilating  forceps  along  the 
needle,  which  has  been  left  in  situ,  and  thus  to  open  up  the  cavity 
and  evacuate  the  pus,  and  then,  after  inserting  a  double  drainage- 
tube,  to  wash  out  the  cavity  with  the  quinine  solution  mentioned 
above,  close  up  the  wound,  fix  the  drainage-tube  in  position,  and 
dress  the  wound  aseptically,  or  to  adopt  Manson's  special  apparatus. 

Manson,  after  the  preliminary  incision,  thrusts  a  trocar  and 
cannula  into  the  abscess,  and,  after  withdrawing  the  trocar,  passes 
a  drainage-tube  stretched  on  a  probe  into  the  abscess  cavity,  and 
then,  withdrawing  first  the  trocar  and  then  the  probe,  the  drainage- 
tube  is  left  in  position  in  the  liver  abscess,  and,  being  firmly  gripped 
by  liver  tissue,  prevents  leakage  of  pus  into  the  abdominal  cavity. 

2.  Operationthrough  the  Abdominal  WalL — The  usual  method  is  to 
cut  down  upon  the  swelling  or  on  to  the  liver,  and  if  adhesions  are 
found,  to  evacuate  and  drain  the  abscess.  If  there  are  no  adhesions, 
the  liver  is  fixed  to  the  peritoneum  by  a  few  stitches  of  thick  catgut 
or  kangaroo  tendon,  but  preferably  not  silk,  and  the  wound  is  lined 
by  iodoform  gauze  and  left  for  two  days,  when,  adhesions  having 
formed,  the  abscess  can  safely  be  evacuated  as  described  above. 
Manson's  apparatus  can,  of  course,  be  used  in  this  position  as  well 
as  through  the  thoracic  wall. 

Post-Operative  Treatment. — The  dangers  of  the  operation  itself 
are  but  slight.  The  pleura  may  be  opened,  and  if  this  happens,  it 
should  be  carefully  closed  by  stitches. 

The  post-operative  complications  are  many,  and  include  haemor- 
rhage, pneumothorax,  pyothorax,  pyopneumothorax,  gangrene  of 
the  lung,  and  delayed  chloroform  poisoning,  while  a  second  abscess 
is  not  uncommonly  met  with,  and  must  be  relieved. 

After  the  operation  the  temperature  should  fall  to  normal,  and  if 
this  does  not  happen,  a  second  abscess  or  one  of  the  above  complica- 
tions may  be  suspected,  unless,  indeed,  it  is  due  to  imperfect 
drainage,  which  must  at  once  be  rectified. 

The  dressings  should  at  first  be  frequently  changed,  usually  twice 
a  day,  and  the  cavity  irrigated  with  quinine  lotion.  Good  drainage 
is  the  essential  of  the  post-operative  treatment,  and  care  must  be 
taken  that  the  drainage-tube  is  not  too  rapidly  shortened,  other- 
wise the  temperature  is  apt  to  rise. 

On  recovery,  the  patient  should,  if  possible,  be  given  a  holiday 
in  the  Temperate  Zone.  A  short  course  of  emetine  or  ipecacuanha 
after  the  operation  wound  has  quite  healed  is  distinctly  indicated 
in  order  to  prevent  the  formation  of  another  abscess. 


OPISTHORCHIOSIS—CLONORCHIO 


1917 


OPISTHORCHIOSIS. 

Definition.— Opisthorchiosis  is  an  invasion  of  the  bile-ducts  with 
Amphimerus  noverca  Braun,  1903  (p.  577),  and  0.  felineus  Rivolta, 
1885  (p.  576). 

Remarks. — A.  noverca  is  said  to  be  common  in  dogs  in  India, 
but  has  only  once  been  found  in  the  dilated  bile-ducts  of  an  Indian 
in  Calcutta,  who  died  with  dysenteric  symptoms. 

0.  fdineus  has  been  found  in  the  dilated  bile-      c  a 

ducts,  and  incidentally  also  in  the  intestine  of 
human  beings,  cats  and  dogs  in  Tomsk.  It 
caused  a  form  of  hepatic  cirrhosis. 

CLONORCHIOSIS. 

Definition. — Clonorchiosis  is  the  invasion  of 
the  bile-ducts  with  Clonorchis  sinensis  Cobbold. 

Climatology. — This  parasite  occurs  in  China, 
Indo-China,  and  Japan. 

Pathology. — These  parasites  occur  in  dogs  and 
cats,  but  the  method  of  infection  is  quite  un- 
known. In  man  they  live  in  the  bile-ducts,  in 
the  recesses  in  the  wall  of  the  dilated  gall- 
bladder or  of  the  bile-ducts,  and  in  the  duo- 
denum. They  may  also  be  found  in  abscesses 
apparently  unconnected  with  the  liver.  The 
ova  are  found  in  the  alimentary  canal  and  the 
faeces.  The  liver  becomes  enlarged,  and  may 
be  darker  in  colour,  while  it  is  atrophied  in  the 
neighbourhood  of  the  dilated  ducts.  The 
intestine  may  show  catarrhal  inflammation. 
Often  the  spleen  is  also  enlarged,  and  there  may 
be  ascites  or  oedema.  Ova  have  been  met  with 
in  the  abdominal  lymphatics,  while  the  flukes 
themselves  have  been  found  in  a  lumbar  abscess. 
The  blood  shows  an  eosinophilia. 

Symptomatology.— There  is  an  abnormal  appetite,  but  the  general 
health  remains  good  for  some  time,  though  the  liver  enlarges  and 
becomes  painful,  while  jaundice  may  be  present.  The  spleen  also 
enlarges.  The  disease  is  apparently  very  chronic,  but  towards  the 
end  emaciation,  ascites,  oedema  about  the  feet  and  legs,  and  diar- 
rhoea lead  to  death  from  exhaustion.     Abscesses  may  form. 

Diagnosis. — The  presence  of  the  worms  can  only  be  diagnosed  by 
finding  the  eggs  in  the  faeces  (see  p.  578). 

Prognosis. — The  prognosis  is  bad,  as  no  cure  is  known. 

Treatment. — An  attempt  may  be  made  to  kill  the  worms  by  thymol 
or  Filix  mas ;  otherwise  the  treatment  must  be  symptomatic. 

Prophylaxis. — Nothing  can  be  said  as  to  prophylactic  measures 
until  the  method  of  infection  is  known. 


Fig.  777.  - —  Opis- 
thorchis  felineus 
Rivolta. 

(After  Looss.) 


1 9i 8  DISEASES  OF  THE  LIVER  AND  PANCREAS 

REFERENCES. 

The  current  literature  is  found  in  the  Tropical  Diseases  Bulletin. 

Infantile  Biliary  Cirrhosis. 

Ghose  and  Mackenzie  (1895).     Lancet,  i.  321. 

Liver  in  Schistosomiasis. 

Phalen  and  Nichols  (1908).     Philippine  Journal  of  Science,  III.,  iii.  223. 

Pancreatitis  in  Ceylon. 

Chalmers   (1905).     Journal  of  the  Ceylon   Branch  of  the   British  Medical 
Association,  p.  1. 

Liver  Abscess. 

Armitage  (1919).     Jour,  of  Trop.  Med.,  April  15  (Amoebic  Abscess  of  Liver 

and   Brain) . 
Cantlie  (1907).     Journal  of  Tropical  Medicine  and  British  Medical  Journal 

(several  papers) . 
Castellani  (1908).     Rivista  Critica  di  Clinica  Medica. 
Castellani  (1908).     Jour,  of  Parasitology,  vol.  i.,  No.  2  (Abscess  of  the  Liver 

in  a  Monkey). 
Couteaud  (1908).     Bull.  Soc.  de  Path.  Exotique,  i.  7,  421. 
Giordano  (1899).     Annali  Med.  Navale. 
Helms  (1918).     Southern  Med.  Journal. 
Marchoux  (1908).     Annali  Med.  Navale,  i.  i,  38. 
Mathis  and  Leger  (191  i).     Recherches  de  Parasitologic  et  de  Pathologie 

au  Tonkin.     Paris. 
Mebane  (191 7).     Proc.  Med.  Assoc.  Isthm.  Can.  Zone. 
Pontano  (1918).     Policlinico.     Rome. 

Rho  (1908).     Mense's  Tropenkrankheiten  (Italian  edition). 
Rogers  (1908).     Fevers  in  the  Tropics,  p.  173. 

Opisthorchosis. 

Looss  (1905).     Mense's  Tropenkrankheiten,  i.  88. 

Clonorchiosis. 

Looss  (1907).     Annals  of  Tropical  Medicine  and  Hygiene,  vol.  ii. 
Scheube  (1903).     Diseases  of  Warm  Climates,  p.  361. 


CHAPTER  LXXXIV 

DISEASES   OF    DUCTLESS    GLANDS    AND 
METABOLISM 

General  remarks — The  thyroid  system — The  suprarenal  system — The  thymus 
system — Other  ductless  glands — Diabetes — Macies  perniciosa — References. 

GENERAL  REMARKS. 

Of  late  years  much  work  has  been  performed  with  regard  to  the 
ductless  glands,  their  functions,  and  their  part  in  the  production 
of  disease.  In  the  tropics  McCarrison  has  been  the  pioneer  with 
regard  to  the  thyroid  gland;  and  it  is  hoped  that  as  years  pass  the 
other  systems  will  be  equally  well  studied.  We  are  only  able  to  give 
these  important  subjects  a  passing  reference,  but  they  deserve  much 
fuller  attention,  and  for  this  purpose  we  offer  the  reader  references 
at  the  end  of  this  chapter. 

THE  THYROID  SYSTEM. 

The  thyroid  system  consists  of  the  thyroid  gland  and  the  para- 
thyroids, with  probably  the  addition  of  the  pars  intermedia  of  the 
pituitary  gland.  The  action  of  these  organs  has  been  the  object  of 
mucli  study  in  Europe  and  America,  as  can  be  noted  by  a  reference 
to  Biedl's  writings,  while  McCarrison  in  the  tropics  has  opened  up 
the  way  to  the  solution  of  many  diseases  in  an  excellent  manner. 

The  various  pathological  phenomena  associated  with  this  system 
may  be  divided  into  two  classes — viz.,  those  associated  with  hypo- 
thyroidism or  insufficiency  of  functional  activity,  and  those  connected 
with  hyperthyroidism,  or  excess  of  functional  activity,  and  each  of 
these,  again,  may  be  applied  to  the  thyroid  gland  or  to  the  para- 
thyroids. 

Thus  insufficient  activity  upon  the  part  of  the  gland  itself  may 
produce  benign  chronic  hypothyroidism  of  Hertoghe,  myxcedema, 
and  cretinism,  while  exalted  activity  is  believed  to  be  responsible  for 
goitre,  Graves'  disease,  and  psychic  exaltation.  The  parathyroid 
glands  when  working  insufficiently  may  cause  tetany,  myoclonia, 
myotonia,  myotonia  periodica,  and  paralysis  agitans,  but  when  in  a 
condition  of  hyper-  or  dysactivity  may  be  responsible  for  myas- 
thenia or  myotonia  periodica. 

With  regard  to  the  factors  which  produce  these  changes  in  the 

1919 


i92o  DISEASES  OF  THE  DUCTLESS  GLANDS 

thyroid  system  McCarrison  points  out  that  they  are  three  in  number 
— viz. : — 

A.  Nutritional. — Defective  and  improper  foods. 

B.  Infective. — Insanitary  surroundings,  bacterial  and  other 
toxins,  infectious  disease,  constipation,  intestinal  stasis,  and  their 
associated  toxaemias. 

C.  Psychical. — Fright,  grief,  worry,  consanguinity  in  marriage, 
and  heredity. 

He  shows  that  these  factors  can  produce  more  or  less  hyperplasia 
in  the  gland,  followed  by  fibrosis  and  atrophy,  and  that  during  this 
there  is  an  alteration  in  the  quantity  and  quality  of  the  secretion 
passed  into  the  blood. 

He  divides  the  hyperplasias  into  two  groups.  In  the  first  he 
places  those  of  endemic  areas  due  to  a  specific  infecting  agency,  such 
as  endemic  goitre,  slight  hypothyroidism,  and  he  shows  that  these 
conditions  in  the  parent  may  become  congenital  goitre,  hypothy- 
roidism, endemic  cretinism,  cretinous  idiocy,  with  deaf-mutism 
and  tetany  in  the  descendants. 

In  his  second  group  he  places  such  hyperplasias  as  are  due  to 
toxaemia  or  thyroiditis,  and  as  such  he  mentions  simple  toxaemia, 
goitre,  and  slight  hypothyroidism  as  one  section,  myxoedema  as  a 
second  section,  and  Graves'  disease  as  a  third  section;  and  these 
occurring  in  parents  may  produce  much  the  same  results  in  the 
descendants  as  in  the  first  class,  but  in  this  condition  it  will  be 
sporadic  and  not  endemic  cretinism. 

Diseases  of  the  thyroid  gland  are  quite  common  in  parts  of  the 
tropics  with  which  we  are  acquainted.  Myxoedema  has  been  seen 
by  us  in  Ceylon,  but  is  rarer  in  the  tropics  than  in  the  Temperate 
Zone;  goitres,  parenchymatous  and  adenomatous,  have  been  met 
with  by  ourselves  in  Ceylon  and  in  Africa,  and  by  Singer  in  Abyssinia. 
Exophthalmic  goitre  has  been  especially  noted  as  far  from  rare 
by  Singer  in  Abyssinia  and  Emile  in  East  and  Central  Africa,  but 
is  very  rare  in  India  and  Ceylon. 

ENDEMIC  GOITRE. 

Synonym. — Endemic  thyromegaly. 

Goitre  is  much  more  prevalent  in  the  tropics  than  has  been 
realized  hitherto,  and  we  have  met  with  it  frequently  in  Ceylon  and 
Africa. 

Climatology. — It  is  a  cosmopolitan  disease  which,  though  fre- 
quently met  with  in  hilly  districts,  is  also,  in  our  experience,  quite 
common  in  low-lying  lands.  It  does  not  appear  to  be  associated 
with  any  geographical  or  geological  condition. 

/Etiology .—The  general  tendency  of  the  present  time  is  to  con- 
sider that  goitre  is  a  parasitic  disease,  and  this  view  has  been 
strengthened  by  the  recent  important  experiments  of  McCarrison  on 
men  and  Bircher  on  rats,  which,  together  with  the  previous  ones  of 
Lustig,  Grassi,  and  many  others,  tend  to  show  that  the  causal  agent 


ENDEMIC  GOITRE  1921 

lives  in  earth  and  passes  via  potable  water  to  man,  in  whose  ali- 
mentary canal  it  passes  a  parasitic  existence.  The  nature  of  this 
contagium  vivum  is  unknown,  but  McCarrison  is  inclined  to  suspect 
an  amoeba.  Chagas  has  shown  that  goitre  is  a  part  of  the  syndrome 
in  chronic  American  trypanosomiasis. 

Symptomatology. — A  new-comer  to  an  endemic  district  may  notice 
after  a  few  weeks'  residence  that  the  neck  has  begun  to  swell,  and 
on  examination  this  is  found  to  be  due  to  an  incipient  goitre.  On 
removal  from  the  district,  or  after  almost  any  method  of  treatment, 


Fig.  778. — Goitre  in  a  Sinhalese  Woman. 

the  swelling  will  decrease.  If,  however,  the  person  continues  to 
reside  in  the  endemic  region,  the  swelling  will  either  continue  or 
return,  and  this  will  continue  to  occur  until  a  more  or  less  permanent 
hypertrophy  results.  Usually  the  swelling  affects  the  whole  gland 
uniformly,  but  often  one  lobe  may  be  more  hypertrophied  than  the 
other.  As  time  goes  on  the  gland  becomes  permanently  enlarged, 
and  may  undergo  cystic  or  adenomatous  changes. 

Treatment. — The  treatment  consists  in  removal  from  the  endemic 
area,  and  in  a  course  of  intestinal  antiseptics  eg.,  salol  and  thymol, 
10  grains  night   and  morning.     McCarrison  recommends  a  poly- 


1922  DISEASES  OF  THE  DUCTLESS  GLANDS 

valent  vaccine  made  from  the  bacilli  found  in  the  faeces  of  persons 
suffering  from  the  disease.  Iodine  therapy  is  strongly  recommended. 
The  syrup  of  the  iodide  of  iron  in  5-minim  dose^  combined  with 
5  grains  of  iodide  of  potash  is  advised  as  an  initial  dose,  and  this, 
may  be  gradually  increased  to  three  or  four  times  this  quantity, 
The  liquor  thyroidei  of  the  British  Pharmacopoeia  is  excellent, 
or  fresh  tabloids  in  doses  of  2-5  grains  combined  with  10  grains  of 
bicarbonate  of  soda  and  taken  at  night.  The  sour-milk  treatment 
has  also  been  recommended. 

Prophylaxis. — -The  most  important  prophylactic  measure  is  to 
filter  and  boil  the  drinking-water  when  compelled  to  visit  or  live 
in  an  endemic  region.  The  patient  must  also  lead  a  life  free  from 
emotion,  if  possible. 

Congenital  Goitre. 

McCarrison  has  pointed  out  that  this  is  extremely  common  in 
certain  Himalayan  villages.  Nearly  every  man  and  woman  in  these 
situations  is  goitrous,  and  congenital  goitre  may  be  present  in 
60  per  cent,  of  the  infants  at  the  breast.  The  mothers  of  these 
children  are  often  myxedematous.  The  condition  rarely  calls  for 
treatment,  as  the  victims  usually  die  at  or  shortly  after  birth  or 
1  ecover  spontaneously,  but  the  mother  and  child  may  be  given  the 
British  Pharmacopoeia  liquor  thyroidei,  of  which  1  to  2  minims 
may  be  given  to  the  child  at  night. 

Endemic  Cretinism. 

According  to  McCarrison,  the  cretinism  of  the  Himalayas,  which 
does  not  show  itself  until  about  six  months  after  birth,  may  be 
divided  into: — 

1.  The  myxedematous  type. 

2 .  The  nervous  type. 

Myxoedematous  Type.~Th.ere  is  failure  in  growth,  dwarfism, 
skeletal  deformities,  persistent  infantile  condition  of  the  sexual 
organs,  and  a  lack  of  intellect,  and  deafness  or  deaf-mutism,  as  well 
as  impai  ment  of  the  sensory  and  muscular  systems. 

Nervous  Type. — This  is  a  state  of  cretinous  idiocy  associated  with 
cerebral  diplegia  and  tetany. 

The  treatment  of  these  conditions  is  the  fresh  liquor  thyroidei 
(B.P.)  in  doses  of  1-2  minims  at  bedtime,  combined  with  grey 
powder  and  bicarbonate  of  soda  during  the  first  fortnight.  The 
dose  of  the  liquor  is  gradually  increased  until  5-10  minims  are  given 
in  a  day.  If  the  liquor  is  not  available,  the  dried  gland  in  powder 
may  be  given  in  \-\  grain  doses,  working  up  to  5-7  grains  per  diem. 

Endemic  Tetany. 

This  is  found  in  goitrous  districts  in  the  Himalayas,  where  it  is 
called  '  hatti  fallategen,'  or  turning  of  the  hands.  It  is  characterized 
by  bilateral,  intermittent,  and  usually  painful  spasms  of  the  hands 


THE  SUPRARENAL  SYSTEM  1923 

and  feet,  and  at  times  other  parts  of  the  body,  and  increased  ex- 
citability of  the  nervous  system. 

During  the  attack  calcium  salts  should  be  administered. 

The  curative  treatment  is  to  combat  the  intestinal  toxaemia  by 
calomel  and  intestinal  antiseptics,  followed  by  thyroid  therapy 
as  indicated  above.  Rickets  must  also  be  treated.  The  diet  should 
consist  of  milk,  and  meat  should  be  avoided. 

THE  SUPRARENAL  SYSTEM. 

In  1563  Bartholomeus  Eustachius  Sanctoseverinatus  recognized 
the  suprarenal  capsules  as  distinct  organs,  but  it  was  not  until  1855 
that  Addison's  researches  aroused  deep  interest  in  these  glands. 

No  case  has  been  as  yet  recorded  of  the  absence  of  these  capsules 
as  well  as  of  the  possible  accessory  suprarenals  in  man.  Acute 
suprarenal  suppression  is  caused  at  times  in  man  by  haemorrhage,  and 
we  quote  such  a  case  below.  The  syndrome  of  these  cases  is  fever, 
nervous  symptoms,  and  signs  of  peritonitis,  followed  by  death. 
Malaria  may  cause  these  signs. 

Chronic  suprarenal  suppression  may  be  caused  by  malaria,  and 
is  characterized  by  the  signs  of  Addison's  disease — viz.,  apathy, 
adynamia,  gastro-intestinal  and  nervous  disturbance,  associated 
with  bronzing  of  the  skin  and  mucous  membranes,  and  a  chronic 
cachexia,  with  frequently  attacks  of  diarrhoea  or  convulsions,  and 
ending  in  coma  and  death. 

In  the  tropics  we  have  met  with  Addison's  disease  once  in  a  Euro- 
pean, and  with  haemorrhage  into  both  the  suprarenal  capsules  twice 
— once  in  a  still-birth  after  a  breech  presentation  in  a  native  child, 
and  once  in  a  case  of  acute  suprarenal  haemorrhage  in  a  European 
lady.  This  last  showed  symptoms  so  remarkable  in  character 
that  a  brief  description  may  be  given. 

Acute  Suprarenal  Haemorrhage. 

After  a  year's  residence  in  Ceylon,  a  young  English  lady,  four  months 
pregnant,  was  suddenly  taken  ill  with  fever  associated  with  an  abnormally 
quick  pulse,  great  tenderness  above  the  umbilicus,  and  pain  in  the  small 
of  the  back  on  both  sides.  After  a  short  intermission  the  fever  returned, 
and  rose  to  1040  F.,  with  a  pulse  of  130,  and  quick  respirations;  the  abdomen 
became  much  distended  and  very  tender,  and  the  bowels  were  constipated. 
All  the  organs  were  normal,  as  was  the  urine.  Vomiting  did  not  begin  till 
near  the  end,  when  the  tongue  first  became  coated  and  then  dry.  Hiccough 
intervened  before  death  on  the  thirteenth  day.  Treatment  was  without 
success  in  any  way,  and  an  exploratory  laparotomy  revealed  no  abnormality 
beyond  bowels  distended  with  gas.  On  post-mortem  examination,  no 
pathological  phenomena  were  seen,  except  haemorrhages  into  both  suprarenal 
capsules,  and,  judging  by  the  histology,  this  may  have  been  a  case  of  localized 
malarial  infection  without  any  sign  in  the  blood. 

THE  THYMUS  SYSTEM. 

The  normal  weight  of  the  thymus  at  birth  is  13*26  grammes, 
and  it  should  increase  till  between  eleven  to  fifteen  years  of  age  it 


1924  DISEASES  OF  THE  DUCTLESS  GLANDS 

should  weigh  37-52  grammes  according  to  Hammar,  after  which  it 
decreases,  until  after  sixty-six  years  it  only  weighs  6«o  grammes, 
and  is  then  principally  composed  of  adipose  tissue.  In  1858 
Friedleben  published  the  only  monograph  on  this  gland  in  health 
and  disease.  The  gland  is  supposed  in  some  unknown  way  to  be 
associated  with  cert  aincases  of  sudden  death  (morsthymia),  especially 
when  there  is  the  so-called  status  thymicolymphaticus,  in  which  a 
much  enlarged  thymus  is  associated  with  hyperplasia  in  the  lymph 
glands  and  lymphoid  tissues  all  over  the  body. 

Only  once  have  we  encountered  a  persistent  thymus  gland  with 
seme  enlargement  of  the  lymphatic  glands,  and  this  was  in  a  case  of 
sudden  death. 

OTHER  DUCTLFSS  GLANDS. 

We  are  not  acquainted  with  observations  referring  to  the  ether 
internal  secretions  in  the  human  diseases  of  the  tropics. 

DIABETES. 

This  disease  is  extremely  common  in  the  tropics,  but  more 
e  pecially  in  Asia,  and  particularly  in  Ceylon,  though  we  have  met 
with  it  in  Africa. 

In  India,  according  to  Waters,  it  has  been  known  since  the  days 
of  the  Susruta  Samhita,  where  it  is  called  '  madhumeha.'  It  was 
said  to  be  unknown  among  the  Chinese  and  Japanese,  but  Reid  has 
collected  207  cases  in  China,  and  in  Korea  the  complaint  is  called 
'    weet  water  disease.' 

W(  st  says  that  it  is  rare  in  Hindu  women,  but  that  it  does  occur 
even  in  Hindu  widows,  and  in  general  it  may  be  said  to  be  much 
more  common  in  men  than  in  women,  and  is  most  frequently  met 
with  in  the  better  or  educated  classes. 

The  disease  is  the  same  as  in  the  Temperate  Zone,  and  will  not 
be  further  considered  here,  except  to  point  out  the  frequency  of 
boils  and  carbuncles  due  to  it,  and  also  the  occurrence  of  Kussmaul's 
coma,  which  may  be  induced  by  a  malarial  infection. 

Pentosuria. 

As  in  the  Temperate  Zone,  so  in  the  tropics,  pentosuria  may  occur, 
but  is  rare,  though  it  is  necessary  to  bear  in  mind  the  possibility 
of  its  occurrence  when  the  diagnosis  of  diabetes  is  made  on  the 
reduction  of  Fehling's  solution.  A  simple  method  of  diagnosis  is  by 
using  Castellani  and  Taylor's  mycological  method  of  examination 
of  the  urine  (see  Chapter  LXXXV.,  p.  1934). 

MACIES  PERNICIOSA. 

Dr.  Ernest  Black  gives  the  following  account  of  this  disease,  which  occurs 
among  the  aboriginal  natives  in  the  north  of  the  State  of  Western  Australia. 
It  has  also  been  reported  among  the  tribes  of  the  Northern  Territory  of  the 
Commonwealth,  where  it  is  called '  living  skeleton  '  disease. 


REFERENCES  1925 

Though,  the  white  settlers  regard  it  as  a  form  of  consumption,  it  is  not 
tubercular,  and  it  does  not  appear  to  be  associated  with  any  malignant 
growth.  It  does  not  correspond  clinically  with  any  known  tabetic  disease. 
In  one  case  seen  in  the  earlier  stages  the  pancreas  was  most  affected.  There 
is  a  progressive  enlargement  of  the  liver  and  spleen,  the  abdomen  becoming 
considerably  distended.  All  the  fat  disappears  and  the  muscles  atrophy, 
but  retain  the  power  of  movement.  The  appearance  is  quite  characteristic — 
extreme  emaciation  of  the  whole  body,  with  a  protruding  abdomen.  Ulti- 
mately, through  increasing  weakness,  walking  becomes  impossible,  a  serious 
matter  with  these  nomadic  people,  which  may  account  for  the  fact  that  the 
few  cases  of  long  duration  winch  were  observed  had  remained  near  white 
settlements.  The  course  of  the  disease  is  slow,  but,  so  far  as  could  be  ascer- 
tained, it  always  terminates  fatally.  Only  one  case  was  seen  in  a  child, 
who  died  within  a  year,  whereas  in  the  case  of  a  woman  who  appeared  to  be 
middle-aged  it  was  said  to  have  already  lasted  over  two  years. 

The  cause  of  the  disease  is  unknown.  No  parasite  has  been  found  in  the 
blood  of  patients  examined  in  the  endemic  areas. 

Further  investigation  is  necessary  to  see  whether  this  disease  is  a  type  of 
tropical  splenomegaly  {vide  p.  1303). 


REFERENCES. 

The  best  general  work  is  Biedl  (1913),  'The  Internal  Secretory  Organs,' 
London,  while  McCarrison  (1918),  '  The  Thyroid  Gland,'  is  of  very  considerable 
interest  to  the  tropical  practitioner. 

Castellani  and  Taylor  (191 7).  British  Medical  Journal,  December  29. 
Castellani  and  Taylor  (191 9).  British  Medical  Journal,  February  15. 
Castellani  and   Taylor    (1919).     Journal   of   Tropical   Medicine,    July    1. 

(Pentosuria  in  the  Tropics.) 
Emile  (1907).     Journal  of  Tropical  Medicine,  p.  21. 
Glogner  (1906).     Archiv  fur  Schiffs-  u.  Tropen-Hygiene,  x.  17.     (Rupture 

of  the  Spleen.) 
Herzog  (1908).     Philippine  Journal  of  Science,  ii.  1,  55.     (Rupture  of  the 

Heart  and  of  the  Spleen.) 
Macleod  (1898).     Journal  of  Tropical  Medicine,  i.  3.     (Tropical  Heart.) 
Maxwell  (1909).     Transactions  of  the  Society  of  Tropical  Medicine,  ii.  9. 

(Abscess  of  Spleen.) 
McCarrison  (1909).      Proceedings  of  the  Royal  Society,   B,  v.  81,  No.  B, 

545,  p.  31  (Goitre);  (1913)  The  /Etiology  of  Endemic  Goitre.     London. 
Singer  (1905).     Journal  of  Tropical  Medicine,  viii.  17.     (Goitre.) 
Waters  (1917).     Diabetes. 


CHAPTER  LXXXV 
DISEASES  OF  THE   URINARY  ORGANS 

General  remarks  — -  Bilharziosis  —  Urinary  amoebiasis  —  Oxaluria  — ■  Urinary 
myiasis  and  canthariasis — Chyluria- — Mycological  urinary  tests- — Test  for 
quinine  in  the  urine — References. 

GENERAL  REMARKS. 

Renal  disease  in  all  its  forms  is  frequently  met  with  in  the  tropics, 
where  nephrolithiasis,  pyonephrosis,  and  pyelitis,  with  all  their 
associated  phenomena,  are  by  no  means  rare.  Stone  in  the  bladder 
is  common  in  certain  regions,  as  is  prostatic  hypertrophy.  But 
the  only  disease  which  really  concerns  us  in  this  work  is  urinary 
bilharziosis,  caused  by  Schistosoma  hcBmatobiitm.  Tumours  of 
the  bladder  are  not  common  in  our  experience.  Prostatic  abscess 
is  met  with  at  times.  We  have  observed  various  mycoses  of  the 
genito- urinary  organs  due  to  fungi  of  the  genera  nocardia,  asper- 
gillus,  monilia,  cladosporium.  Native  children  in  some  parts  of 
Africa  (Sudan)  suffer  very  often  from  a  complaint  called  by  the 
Arabs  '  har  boul,'  characterized  by  severe  burning  on  passing  urine. 
This  condition  is  due  to  concentrated  acid  urine  and  the  presence  of 
gravel.     Cystinuria  is  rare,  but  we  have  met  with  a  case. 

In  the  present  war  a  form  of  nephritis  has  been  noticed  in  soldiers 
in  the  trenches  (trench  nephritis). 

BILHARZIOSIS. 

Synonyms. — Urinary  schistosomiasis,  Endemic  haematuria,  Bilharzia  disease. 

Definition.— Bilharziosis  is  infection  with  Schistosoma  hcema- 
tobium  Bilharz,  1852,  the  eggs  of  which  irritate  and  invade  the 
urinary  tract,  and  cause  haematuria  and  cystitis. 

History. — The  disease  has  been  endemic  in  Egypt  since  ancient 
times,  Ruffcr  having  demonstrated  calcified  eggs  of  S.  hcBmatobiitm 
in  mummies  of  the  twentieth  dynasty  (about  1250-ioooB.c).  Hae- 
maturia was  much  noticed  by  the  French  army  surgeons  in  1799 
to  1801;  but  it  was  not  till  1851  that  Bilharz  made  the  discovery 
that  the  disease  was  due  to  5.  hcBmatobiitm. 

Climatology.— Bilharziosis  is  prevalent  in  Africa,  especially  in 
Egypt  and  the  Cape,  but  it  is  also  met  with  in  Asia,  in  India,  Syria, 

1926 


DILHARZIOSIS 


1927 


and  Mesopotamia,  and  in  the  West  Indies.  In  Egypt,  according  to 
Sandwith,  infection  probably  takes  place  in  the  early  winter  months 
when  the  floods  have  subsided. 

/Etiology. — The  cause  of  the  disease  is  Schistosoma  hcematobium. 
The  life-history  is  described  in  Chapter  XXIV.,  p.  584.  The 
method  of  infection  is  by  the  cercariae  penetrating  the  skin  or 
mucous  membranes  and  developing  into  adults,  which  live  and 
copulate  in  the  portal  and  vesical  veins,  while  the  eggs  leave  the 
body  with  the  urine. 

It  occurs  in  any  race  and  at  any  age,  except  infancy,  but  is 
more  common  in  males  than  in  females,  due,  it  is  thought,  to  the 
men  washing  in  streams  and  working  in  the  fields  barefooted. 
According  to  Miss  Elgood's  investigations,  the  disease  is  common 
also  in  young  girls,  even  in  those  who 
do  not  bathe,  and  who  use  filtered 
water.  It  is  rare  in  Europeans,  being 
much  more  common  among  the  natives, 
in  whom  it  is  prevalent  among  the  working 
classes,  especially  the  field-labourers. 


Fig.  778A. — Miracidium 
of    Schistoso  na    Ha- 
inatobiun.  (  X  300  Di- 
ameters.) 
(Photomicrograph.) 


Fig.  778B. — -Photographs  of  Bulinus 
contortus. 

Pathology. — The  worms  live  in  the  porta 
vein,  but  proceed  to  the  venules  of  the 
bladder  to  lay  the  eggs.  The  irritation 
of  these  eggs  excites  a  round-celled  infiltra- 
tion, sometimes  of  a  very  extensive  nature, 
giving  rise  to  a  sort  of  bilharzial  granu- 
lation tissue — that  is,  a  tissue  composed  of 
round  cells  and  eggs.  Madden  divides 
the  pathological  changes  into  two  classes — the  hypertrophic  and  the 
atrophic.  In  the  former,  which  is  more  common  in  mucous  mem- 
branes, there  is  proliferation  of  the  epithelium,  with  the  formation 
of  flattened  projections  or  papillomata,  while  vesicles  may  also  form, 
and,  according  to  Madden,  by  bursting,  give  rise  to  the  ulcers  which 
at  times  are  seen. 

The  ova  may  escape  from  the  mucosa,  according  to  Looss,  without 
the  aid  of  ulceration,  by  working  their  way  between  the  epithelial 
cells  into  the  lumen  of  the  viscus.  Underneath  the  mucosas  the 
round-celled  infiltration  forms  the  typical  bilharzial  granulation 
tissue,  and  leads  to  much  thickening  of  the  wall  of  the  viscus,  and, 
proceeding   to   connective-tissue   formation,    may   cause   marked 


1928 


DISEASES  OF  THE   URINARY  ORGANS 


changes.     Lesions  may  also  be  found  from  the  pelvis  of  the  kidney 
to  the  meatus  urinarius,  but  are  most  common  in  the  bladder. 

Morbid  Anatomy. — The  earliest  changes  are  found  in  the  bladder 
in  the  formation  of  a  general  infiltration  and  thickening  of  the 
mucosa  with  bilharzial  tissue.  Over  this  thickened  mucosa  is  a 
layer  of  adherent  mucus,  which  is  apparently  protective.  In  this 
mucus  numerous  eggs  are  found.  Later  hyperaemic  patches  are 
found  associated  with  vesicles,  which  are  especially  marked  around 
the  trigone,  and  contain  a  whitish  fluid  in  which  there  are  eggs. 
The  hyperaemic  patches  increase  in  size  and  thickness,  and  the  whole 
bladder  becomes  much  thickened.     Papillomata  of  all  shapes  and 


Fig.  77SC. — Bladder  showing  Lesions  of  Bilharziosis. 


sizes  are  formed  principally  on  the  trigone  and  the  posterior  wall 
of  the  bladder.  These  papillomata  bleed  readily,  giving  rise  to  the 
haematuria. 

As  the  eggs  increase  in  amount,  connective  tissue  forms  round 
them,  and  they  die  and  become  calcined,  thus  giving  riseto  brownish- 
yellow,  sandy  patches,  not  protected  by  mucus,  and  leading  to  an 
atrophy  of  the  mucosa  of  the  viscus. 

The  urine  collects  in  the  hollows  between  the  papillomata,  and, 
decomposing,  gives  rise  to  phosphates,  which  produce  a  whitish 
incrustation  on  the  bladder  wall.  The  orifices  of  the  ureters  may 
become  obstructed,  giving  rise  to  backward  pressure,  causing  hyper- 
trophy of  the  ureters  and  hydronephrosis.  Septic  infection  is  very 
liable  to  spread  from  the  bladder  up  the  dilated  ureters  to  the 
kidney.  Bilharzial  tissue  may  also  form  in  the  ureters  and  the 
pelvis  of  the  kidney,  and  take  the  form  of  infiltrations  and  papil- 


5  YMPTOMA  TOLOG  Y  1929 

lomata.  Calculi  may  also  form  in  the  bladder,  and  interstitial 
nephritis  in  the  kidney. 

As  the  bladder  becomes  infiltrated  it  rises  in  the  abdomen,  and 
may  be  felt  above  the  pubes,  and  in  this  situation  infection  may 
spread  to  the  abdominal  wall.  In  this  case  the  typical  bilharzial 
tissue  forms  in  the  subcutaneous  tissue,  and,  working  its  way  to 
the  surface,  forms  a  sinus  lined  with  bilharzial  granulations  con- 
taining eggs  and  discharging  pus.  These  sinuses  may  spread,  and 
a  large  area  of  skin  become  involved. 

Bilharzial  tissue  may  also  form  in  the  prostate  and  urethra. 

Symptomatology. — The  incubation  is  not  known,  but,  according 
to  Sandwith,  it  varies  from  three  to  six  months.  At  first  no  symp- 
toms are  exhibited,  but  in  course  of  time  frequency  of  micturition, 
with  a  sensation  of  burning  in  the  perineum  or  along  the  urethra, 
may  be  noted,  while  there  is  some  straining  after  passing  urine.  In 
due  course  hematuria  appears,  beginning  with  a  few  drops  of  blood 
either  at  the  end  of  micturition  or  after  the  urine  has  been  passed. 
U.ually  there  are  no  symptoms  with  this  hematuria,  but  there  may 
be  scalding.  The  urine  is  clear  and  acid,  but  some  mucus  may  be 
passed,  which,  if  centrifugalized  or  allowed  to  settle,  shows  the 
typical  ova  and,  of  course,  red  cells,  leucocytes,  and  epithelial  cells. 
Usually  the  general  health  is  good,  but  pains  in  various  directions 
may  be  felt — e.g.,  in  the  back,  the  perineum,  the  gluteal  region,  or 
down  the  legs. 

Sooner  or  later  the  urine  begins  to  stagnate  in  the  hollows  in 
the  mucosa  formed  by  ulcers  and  by  papillomata.  When  this 
happens,  the  urine  becomes  alkaline  and  turbid,  containing  pus  and 
phosphates,  as  well  as  decomposing  blood  and  ova.  With  this 
decomposition  of  the  urine  cystitis  appears,  and  the  sufferings  of 
the  patient  begin  in  earnest,  with  at  first  increased,  and  later  almost 
constant  micturition,  scalding  pains  in  the  perineum  and  the 
scrotum,  together  with  tenesmus,  which  increase  until  he  can  rest 
neither  day  nor  night.  In  order  to  add,  if  possible,  to  his  miseries, 
the  prostate  may  enlarge  or  a  stone  may  form  in  the  bladder,  which 
may  be  composed  of  uric  acid  or  oxalates  covered  with  phosphates, 
or  simply  of  phosphates.  If  the  bladder  is  examined  in  this  stage 
it  will  be  found  to  be  thickened,  and  may  be  felt  above  the  pubes. 
Fistulse  may  form  in  the  abdominal  wall  above  the  pubes,  or  the 
urethra  may  be  attacked.  The  urethral  symptoms  begin  with 
localized  pain  and  the  formation  of  a  lump  which  develops  an 
abscess,  and  later  urinary  fistula'. 

The  patient  now  becomes  weak  and  anaemic,  and  begins  to  suffer 
from  pyonephrosis.  The  enlarged  kidneys,  and  at  times  even  the 
ureters,  may  be  felt  through  the  abdominal  wall.  In  course  of  time 
septicaemia  sets  in,  and  the  patient  dies.  On  the  other  hand,  cases 
which  have  left  the  endemic  area  may  slowly  recover,  the  ova  ceasing 
to  be  passed. 

Complications. — Retention  of  urine  from  blocking  of  the  urethral 
opening  by  papillomata  or  a  stone  may  occur.    Stone  in  the  bladder 


193° 


DISEASES  OF  THE  URINARY  ORGANS 


as  has  already  been  mentioned,  is  an  important  factor  in  increasing 
the  sufferings  of  the  patient,  but  its  symptoms  may  be  masked  by 
those  of  the  disease.  Urinary  fistulas  has  already  been  referred  to, 
and  cancer  may  also  occur  as  a  complication  of  the  disease,  but  is 
said  to  be  rare.  Ankylostomiasis  and  pellagra  and  other  diseases 
may  also  complicate  a  case. 

Diagnosis. — The  only  certain  diagnosis  is  by  the  discovery  of  the 
ova,  but  haematuria  in  the  endemic  area  must  always  be  regarded 
with  suspicion.  Centrifugalization  is  necessary  when  the  ova  are 
in  small  numbers. 

Fairley  recommends  a  complement  fixation-test  with  an  antigen  prepared 
from  livers  of  infected  snails. 

Prognosis. — The  prognosis  depends  largely  upon  the  possibilities 

of  infection,  and  is  therefore  better  if  removal  from  the  infected 

area  is  possible;  for,  according  to  Sandwith, 

'    /  j      '     -.-  most  cases  cease  to  pass  eggs  within  three 

years  of  leaving  that  area. 

Treatment.- — McDonagh  and  Christ opherson 
have  recommended  the  intravenous  injection 
of  tartar  emetic,  which  shouldbe  administered 
in  the  same  way  as  for  intestinal  schisto- 
somiasis (p.  1869).  Various  treatments,  such  as 
injections  of  sulphuretted  hydrogen  and  carbon 
dioxide  gases  into  the  bladder,  have  been 
suggested.  The  drug  commonly  used  in  the 
past  was  liquid  extract  of  male  fern,  in  5-minim 
doses,  three  times  a  day,  continued  for  a  long 
time.  It  is  said  to  reduce  the  haematuria  and 
lessen  the  discharge  of  eggs.  Emetine  has  been 
recommended  by  several  observers.  Madden 
recommends  the  washing  out  of  the  bladder 
with  injections  of  silver  nitrate,  beginning 
with  1  in  10,000,  and  increasing  the  strength 
gradually;  orquininein  a  4  per  cent,  solution; 
or  adrenalin  in  normal  saline  solution. 

In  addition,  boracic  acid,  in  5-grain  doses, 
three  times  a  day,  or  helmitol,  in  15-grain  doses,  three  times  a 
day,  urotropine,  salol,  benzoic  acid  may  be  given,  or  the  ordinary 
buchu  and  hyoscyamus  mixture  may  be  administered.  Large 
quantities  of  water  or  Vichy  water  should  be  drunk  to  wash  out  the 
urinary  passages. 

If  a  calculus  is  present,  it  must  be  removed  by  lithotrity  or  by 
perineal,  not  suprapubic,  cystotomy.  Cock's  operation  of  cys- 
totomy and  drainage  of  the  bladder  gives  relief  in  the  later  stages, 
but  Madden  says  that  this  only  lasts  for  a  few  days,  and  then  usually 
diarrhoea  and  septic  infection  set  in,  and  the  patient  dies  in  about 
two  weeks. 

With  regard  tofistulae,  they  ought  to  be  thoroughly  dissected  out 
and  this  may  mean  a  very  prolonged  operation  if  it  is  to  do  any  good. 


Fig.    778D. — Egg     oi- 
Schistosoma  hce- 

matobium  in  Urine. 

(Photomicrograph.) 


URINARY  AMCEBIAS1S  193 1 

McDonagh,  who  first  used  antimony  in  bilharziosis  in  1912,  prefers  colloidal 
antimony,  which  he  gives  intravenously  and  intramuscularly  in  doses  of 
0*5  c.c.  to  2  c.c.  of  a  0*2  per  cent,  emulsion. 

Salvarsan  has  been  used  by  several  observers,  with  doubtful  results. 

Prophylaxis. — As  the  method  of  infection  is  unknown,  it  can  only 
be  suggested  that  bathing  in  polluted  or  possibly  polluted  water  is 
dangerous,  and  drinking-water  must  be  carefully  boiled  and  filtered. 
The  urine  of  persons  suffering  from  the  disease  should  be  mixed 
with  some  disinfectant  before  being  disposed  of. 

URINARY  AMCEBIASIS. 

Definition. — Urinary  amoebiasis  is  the  infection  of  the  urinary 
tract  with  amoebae,  which  most  commonly  arc  Loeschia  liistolytica 
(Schaudinn,  1903). 


Fig.  779. — Precystic  Stage  of  Loeschia  histolytica  (Schaudinn,  1903, 
emandavit  Walker,  1911),  as  seen  in  Urine  in  a  Sudan  Case.  Fresh 
and  Unstained  Specimen.     (X  1,500  Diameters.) 

(Microphotograph.      This    illustration   may   be    examined    with    advantage 
by  means  of  a  reading  lens.) 

Historical. — In  considering  the  history  of  urinary  amoebiasis,  it  is 
convenient  to  divide  the  subject  into  infections  low  down  in  the 
urinary  tract,  into  those  which  are  situate  high  up,  and  into  those 
(jf  which  the  site  is  unknown. 

Low  Down  in  the  Urinary  Tract. — Amoebae  were  first  described  in 
urine  and  in  vagina]  scent  ion  by  Baelz  in  1883,  when  he  named  the 
particular  species  which  he  saw  Amoeba  urogenitalis  Baelz.  1883. 
This  amoeba  was  provided  with  a  synonym  by  K.  Blanchard  in  1885, 
when  lie  called  it  Amoeba  vaginalis  R.  Blanchard.  1885.  It  measured 
some  23-50  microns  in  diameter,  was  actively  motile,  extruded  short 
and  blunt  pseudopodia,  possessed  granular  cytoplasm  containing 


1932  DISEASES  OF  THE  URINARY  ORGANS 

a  vesicular  nucleus  and  phagocyted  red  blood-corpuscles,  while 
cystic  stages  of  the  same  organism  were  also  observed.  There  is, 
in  our  opinion,  no  reason  to  doubt  that  this  is  the  same  species  as  the 
organism  variously  known  at  the  present  time  as  Loeschia  histolytica 
(Schaudinn,  1903,  emendavit  Walker,  1911) ;  Entamoeba  histolytica 
Schaudinn,  1903;  Entamoeba  tetragena  Viereck,  1907;  Amxba 
dysenteries  Councilman  and  Lafleur,  1891;  and  Amoeba  coli  Loesch, 
1875 ;  and  by  various  other  names. 

The  unpleasant  point  is  that  if  the  rules  of  zoological  nomen- 
clature are  pressed  we  ought  to  call  the  amoeba  of  dysentery  by 
Loesch's  name. 

The  following  cases  are  known  to  us: — 

(1)  Baelz's patient  was  dying  from  pulmonary  tuberculosis,  and  it 
was  only  shortly  before  death  that  haematuria  associated  with  severe 
tenesmus  of  the  bladder  set  in,  and  Baelz  considered  that  the  bladder 
as  well  as  the  vagina  was  infected,  but  it  is  not  evident  from 
abstracts  of  his  paper  that  any  post-mortem  examination  was  made. 

(2)  In  Jiirgens'  1892  case  the  amoebae  were  found  by  post-mortem 
examination  to  come  from  mucous  cysts  in  the  bladder  of  an  old 
woman  who  had  suffered  from  cystitis,  and  in  whose  vagina  they 
were  also  found. 

(3)  In  1911  Craig  found  Loeschia  histolytica  Schaudinn,  1903, 
in  an  infection  of  the  bladder  in  which  the  autopsy  showed  a  minute 
fistula  between  the  ulcerated  intestine  and  the  bladder. 

(4)  Lynn's  1914  Costa  Rica  case  seems  to  have  been  probably 
caused  by  a  vesical  lesion,  as  the  patient  is  reported  to  have  felt '  a 
pain  in  the  trigonum  vesicas  at  the  end  of  micturition.'  He  responded 
very  well  to  emetine  treatment,  as  it  is  stated  '  in  the  course  of 
live  days  the  vesicle  tenesmus  was  relieved  and  the  urine  cleared  '; 
moreover,  there  was  no  return  of  the  symptoms  after  one  month. 

(5)  and  (6)  Scott  Macfie's  second  case  was  probably  a  bladder 
infection  associated  with  bilharziosis,  while  his  third  and  fully 
described  case  was  probably  an  infection  of  the  genito- urinary  tract 
in  the  neighbourhood  of  the  seminal  vesicles. 

High  up  in  the  Urinary  Tract. — In  these  cases  the  site  of  infection 
is  probably  in  the  pelvis  of  the  kidney. 

(7)  Posner's  1893  Berlin  case  began  with  a  rigor  and  the  passage 
of  urine  tinged  with  blood,  which,  when  examined,  showed  red  and 
white  blood-corpuscles,  hyaline  and  granular  casts,  and  large 
granular  bodies  50  by  28  microns,  which  slowly  altered  their  shape, 
and  which  contained,  among  other  things,  red  blood-corpuscles  and 
one  or  more  nuclei  and  some  vacuoles.  Posner,  probably  correctly, 
came  to  the  conclusion  that  the  pelvis  of  the  kidney  was  affected, 
but  seems  to  have  considered  that  this  infect  ion  began  in  the  bladder. 

(8)  A  similar  case  exhibiting  signs  of  pyelitis  without  any  vesical 
symptoms  has  been  recorded  by  Chalmers  and  O'Farrell  in  the 
Anglo-Egyptian  Sudan. 

Site  in  the  Urinary  Tract  Unknown. — (9)  We  have  been  unable 
to  refer  to  the  original  papers  written  by  Wijnhoff,  by  Jeffries,  and 


OXALURIA  1933 

by  Fisher,  and  are  therefore  unable  to  state  where  the  infection 
was  situate. 

(10)  The  very  brief  note  by  Ward,  Coles,  and  Friel  arouses  the 
doubt  as  to  whether  the  amoebae  really  came  from  the  patient, 
because  they  do  not  state  whether  these  bodies  were  merely  seen 
once,  or  whether  they  were  of  frequent  occurrence.  They  call  the 
organism  Amceba  urines  gramtlata,  but,  as  Fantham  has  pointed  out, 
in  no  case  can  this  name  stand. 

(n)  Scott  Macfie,  owing  to  the  non-return  of  the  patient  to  the 
hospital,  was  unable  to  define  the  site  of  the  infection  in  his  first  case. 

All  the  cases  which  we  have  met  with  have  been  associated  with 
symptoms  which  have  pointed  to  the  pelvis  of  the  kidney  as  the 
probable  source  of  infection. 

Climatology. — Cases  are  known  in  Europe,  Africa,  and  Asia. 

etiology. — It  is  possible  that  all  reported  cases  were  due  to 
Loesclu'a  histolytica. 

Symptomatology — Amoebic  Pyelitis. — With  or  without  the  history 
of  previous  amcebiasis  in  the  form  of  amoebic  dysentery  or  other 
amoebic  infection,  a  person  is  seized  with  an  attack  of  lumbar  pain 
associated  with  the  passage  of  turbid  urine,  with  or  without  blood, 
and  slight  fever,  the  temperature  rising  to  99°-ioo°  F. 

The  urine,  if  collected  and  examined  after  centrifuging,  will  be 
seen  to  contain  a  deposit  of  red  blood  cells,  leucocytes,  and  amoebae 
in  a  precystic  stage,  and  more  or  less  degenerate. 

The  blood,  when  examined,  has  been  found  to  show: — 

Polymorphonuclear  leucocytes             ..           ..           ..  6i-o 

Mononuclear  leucocytes             .  .           .  .           .  .           •  •  8-4 

Large  lymphocytes        . .           .  .           . .           .  .           •  •  22*4 

Small  lymphocytes         .  .           . .           .  .           . .           •  •  5*6 

Eo  Lnophile  leucocytes  ..          ..          ..          ..          ••  2-2 

Mastcells            .."        0-4 

Total loco 

Amoebic  Cystitis. — In  these  cases  there  is  pain  and  straining  at 
the  end  of  micturition.  On  examination  the  urine  shows  motile 
amoebae. 

Treatment. — The  treatment  is  to  give  urotropine  by  the  mouth  and 
emetine  intramuscularly. 

OXALURIA. 

Definition.— Oxaluria  is  the  deposit  in  abnormal  quantity  of 
oxalate  crystals  in  the  urine,  and  should  be  restricted  to  cases 
which  show  an  increase  in  the  quantity  excreted  in  the  day. 

Historical. — The  crystals  of  calcium  oxalate  were  discovered  by 
Donne  in  1838,  and  were  much  discussed  for  a  time,  being  made  the 
basis  of  the  oxalic  acid  diathesis  of  Prout,  Golding,  Bird,  and  Begbie ; 
but  as  a  result  of  Smoler  and  Bacon's  investigations,  this  theory 
fell  to  the  ground.  In  1896  Dunlop  attributed  them  to  the  oxalates 
in  the  food,  and  in  1900  Baldwin  conducted  a  series  of  experiments 


1934  DISEASES  OF  THE   URINARY  ORGANS 

upon  dogs,  and  showed  that  fermentative  intestinal  disturbances 
associated  with  the  absence  of  free  hydrochloric  acid  in  the  gastric 
juice  were  the  causal  agent. 

Climatology.- — It  may  occur  in  any  part  of  the  world,  but  is  very 
commonly  met  with  in  the  tropics,  in  Europeans  and  natives  alike. 
With  regard  to  its  presence  in  natives,  Burkitt's  observations  in 
Chandira  in  Eastern  Bengal  are  especially  interesting. 

^Etiology. — The  normal  quantity  of  calcium  oxalate  to  be  ex- 
creted in  the  urine  is  0-5  gramme  per  diem.  It  may  perhaps  come 
from  certain  vegetal  substances  in  the  diet,  but  it  is  more  likely  that 
it  is  in  some  way  associated  with  either  proteid  fermentation  in  the 
alimentary  canal  or  proteid  metabolism. 

Miss  Baldwin's  experiments  tend  to  show  that  if  the  carbohydrate 
food  of  a  dog  is  abnormally  increased  hypochlorhydria  may  result, 
and  with  it  oxaluria.  Burkitt's  observations  support  this,  as  he 
shows  that  the  Manipuris  (of  Mongolian  origin)  living  round 
Chandira  in  Eastern  Bengal,  and  consuming  nothing  but  vegetables 
and  fruit,  suffer  excessively  from  oxaluria.  Certainly  treatment  based 
upon  the  idea  of  too  little  acidity  in  the  stomach  is  most  successful. 

Symptomatology. — Dyspepsia,  pain  in  the  lumbar  region,  shoot- 
ing down  the  ureter,  burning  during  micturition,  and  even  haema- 
turia,  are  signs  of  oxaluria.  These  symptoms  may  or  may  not  be 
associated  with  signs  of  mild  neurasthenia.  If  unchecked,  oxaluria 
may  lead  to  the  formation  of  an  oxalate  calculus  in  the  kidney  or 
bladder,  accompanied  by  the  ordinary  signs  of  stone  in  the  kidney 
or  bladder. 

Treatment. — The  treatment  is  simple  and  certain.  A  few  minims 
of  the  dilute  pharmacopceial  preparation  of  nitrohydrochloric  acid 
combined  with  ^  drachm  of  the  compound  tincture  of  cinchona  bark 
and  1  ounce  of  the  compound  mixture  of  gentian,  given  three  times  a 
day  before  meals,  is  the  best  remedy. 

URINARY  MYIASIS  AND  CANTHARIASIS. 

See  Chapter  LXVIL,  pp.  1628  and  1640. 

CHYLURIA. 

This  is  generally  due  to  filariasis,  and  is  described  on  p.  1608. 
Cases  of  schistosomic  origin  occur,  and  Remlinger  has  placed  on 
record  two  cases  due  to  hydatids,  with  hydatid  membrane  in  the  urine. 
Quarelli,  in  1918,  drew  attention  to  a  malarial  chyluria  associated 
with  malarial  parasites  in  the  blood,  and  cured  by  quinine  therapy, 
occurring  in  a  person  who  had  never  left  Italy. 

URINARY  TESTS. 

Castellani  and  Taylor's  Mycological  Method  for  the  Detection  of  Glucose, 
Lactose,  Maltose,  and  Other  Carbohydrates  in  the  Urine. — The  tropical  prac- 
titioner generally  bases  the  diagnosis  of  diabetes  on  the  reduction  of  Fehling's 
solution  by  the  suspected  urine.     Fehling,  however,  may  be  reduced  by  a 


URINARY  TESTS 


1935 


number  of  other  substances  in  addition  to  glucose— for  instance,  by  lactose, 
galactose,  maltose — and  the  detection  of  such  substances  by  chemical  proce- 
dures is  long  and  requires  much  practice.  Castellani  and  Taylor's  mycological 
method  will  often  be  found  simpler  and  easier.  Castellani  and  Taylor  thought 
that,  just  as  various  carbohydrates  and  other  carbon  compounds  are  used  in 
the  identification  of  certain  bacteria  and  higher  fungi,  the  reverse  process 
might  also  be  carried  out — viz.,  bacteria  and  higher  fungi  might  be  used  for 
the  detection  and  identification  of  certain  chemical  substances.  For  many 
years  ordinary  baker's  yeast  (so-called  German  yeast)  has  been,  of  course,  used 
to  detect  glucose,  but  this  is  the  only  sugar  for  which  a  purely  mycological 
method  has  been  used  in  pathological  work,  and,  as  a  matter  of  fact,  it  is 
an  unscientific  method,  as  ordinary  baker's  yeast  very  often  ferments  galactose, 
maltose,  saccharose,  and  other  sugars,  in  addition  to  glucose.  If  a  urine,  there- 
fore, is  fermented  by  baker's  yeast,  this  does  not  mean  with  certainty  that  it 
contains  glucose,  as  stated  in  so  many  textbooks.  Castellani  and  Taylor 
determine  whether  a  substance  is  or  is  not  a  certain  carbohydrate  by  testing 
on  it  whenever  possible  the  action  of  two  germs  known  to  be  identical  in  all 
their  biochemical  reactions,  except  on  that  particular  carbohydrate.  For 
instance,  in  order  to  see  whether  a  certain  chemical  substance  reducing  Fehling 
is  maltose  or  not,  the  substance  is  tested  with  two  germs  which  are  known  to  be 
identical  in  all  their  biochemical  reactions,  except  on  maltose,  such  as  Monilia 
krusei  Castellani  and  Monilia  pinoyi  Castellani.  The  procedure  to  detect,  for 
instance,  maltose  in  the  urine  is  as  follows :  The  urine  is  collected  aseptically,  or, 
if  this  is  not  feasible,  is  distributed  in  sterile  tubes  (each  containing  a  small 
fermentation  tube)  as  soon  as  passed,  and  then  sterilized  in  Koch's  stove  for 
thirty  minutes  on  two  or  three  consecutive  days.  It  should  never  be  auto- 
claved,  as  autoclaving  may  alter  the  composition  of  the  sugars  and  other 
carbohydrates  present.  Two  tubes  of  the  aseptic  urine  to  which  one-third  or 
the  same  amount  of  sterile,  sugar-free,  peptone  water  has  been  added  (to 
facilitate  an  abundant  development  of  the  organisms)  are  inoculated — tube 
No.  i  with  Monilia  krusei  and  tube  No.  2  with  Monilia  pinoyi.  The  two  tubes 
are  incubated  at  350  C.  for  twenty-four  to  forty-eight  hours,  and  then  examined. 
If  No.  1  does  not  contain  gas,  while  No.  2  contains  gas,  the  urine,  according  to 
all  probability,  contains  maltose. 

To  understand  and  properly  carry  out  the  method  one  must  have,  of  course, 
an  exact  knowledge  of  the  biochemical  reactions  of  a  certain  number  of  bacteria 
and  higher  fungi,  which  can  be  found  at  pp.  944  and  1082.  The  working  and 
results  of  the  method  are  seen  at  a  glance  in  the  following  mycological 
formulas : — 

Urine  Fehling-reducing. 


Monilia 
Monilia 
Monilia 
Monilia 
Monilia 
Monilia 
Monilia 
Monilia 
Bacillus 
Bacillus 
Bacillus 
Bacillus 


balcanica  Castellani 
balcanica  Castellani 
krusei  Castellani     .  . 
krusei  Castellani     . . 
pinoyi  Castellani    .  . 
pinoyi  Castellani    .  . 
metalondinensis  Castellani 
metalondinensis  Castellani 
coli  sensii  stricto  Escherich 
paratyphosus  B  Shottmuller 
coli  Escherich 
paratyphosus  B  Shottmuller 


Gas    =glucose. 
Gas  }=1evulose. 

G°s)=maltose- 
Gas  }=galactose. 

°    ) 

Gas   >— pentoses. 

Gas  J 
'b    -=lactose. 


Urine  not  Fehling-reducing. 


Monilia  pinoyi  Castellani 

Monilia  rhoi  Castellani 

Bacillus  coli  Escherich 

Bacillus  pseudocoli  Castellani 

B.  paratyphosus  B  Shottmuller  var. 

B.  paratyphosus  A  Shottmiiller 


M. 


O 
Gas 

O 
Gas 
Gas 

O 


; saccharose. 
:  saccharose. 


H 


r=inosite. 


1936  DISEASES  OF  THE  URINARY  ORGANS 

URINARY  TEST  FOR  QUININE  ELIMINATION. 

At  times  it  is  necessary  for  the  physician  to  be  certain  that  quinine  is  being 
absorbed  by  the  patient,  and  at  others  that  the  patient  is  really  taking  the 
quinine  which  has  been  ordered.  Under  such  conditions  a  simple  easy 
urinary  test  which  will  indicate  the  presence  of  the  drug  in  the  urine  is  of  value. 
Such  a  test  can  be  performed  as  follows: — 

A.  To  2  cubic  centimetres  of  the  filtered  urine  contained  in  a  clean  test-tube 
add  £  cubic  centimetre  of  Tanret's  reagent.  This  reagent  is  a  mixture  of 
3  grammes  of  iodide  of  potash,  i  gramme  of  corrosive  sublimate,  and  20  cubic 
centimetres  of  glacial  acetic  acid,  in  such  a  quantity  of  distilled  water  as  will 
produce  in  all  60  cubic  centimetres. 

B.  If  the  patient  has  been  taking  quinine,  or  if  he  has  albumen  in  his  urine, 
the  operation  described  in  the  preceding  paragraph  will  give  rise  to  a  faint 
opalescence  or  a  white  cloud,  depending  upon  the  quantity  of  either  present. 

C.  Next  add  a  few  drops  of  absolute  alcohol,  when  the  precipitate  if  due  to 
quinine,  will  disappear,  while  that  caused  by  albumen  will  remain. 

This  reaction  appears  in  about  two  hours  after  taking  a  dose  of  quinin  , 
and  will  persist  for  twenty-four  hours  after  a  dose  of  5  grains,  and  lor  forty- 
eight  hours  after  that  of  20  grains  of  the  drug. 

REFERENCES. 
Bilharziosis. 

Anderson  (1905).     Wellcome  Research  Laboratories  Reports. 

Archibald  (1919).     Journal  of  Tropical  Medicine. 

Bandi  (191 3).     Journal  of  Tropical  Medicine. 

Castellani  (1903).     Annali  Med.  Navale. 

Christopherson  (1918).     Lancet,  ii.     London. 

Elgood  (1908).     British  Medical  Journal. 

Fairley  (1919).     Jour.  Royal  Aimy  Med.  Corps,  June. 

Flu  (191 2).     Centralblatt  fur  Bakteriologie. 

Leiper  (1918).     Researches  on  Egyptian  Bilharziosis.     London.     John  Bale, 

Sons  and  Danielsson. 
Looss    (1905).       Mense's   Tropenkrankheiten,   i.    (1911)    Journal  of   Tropical 

Medicine. 
Low  (1919).      journal  of  Tropical  Medicine. 
McDonagh  (1918).     Lancet,  September  14,  p.  371. 
Madden  (1907).     Bilharziosis.     London. 
Milton  (1902).     Journal  of  Tropical  Medicine. 
Ruffer  (1909).     British  Medical  Journal. 
Sandwith  (1904).     Practitioner,  October. 
Sandwith  (1905).     Medical  Diseases  of  Egypt,  p.  214. 
Sonsino    (1893).     Davidson's    Hygiene    and    Diseases    of    Warm    Climates, 

p.  905.     . 
Stock  (1906).     Lancet,  ii.  857. 
Taylor  (19119).     Lancet. 
Williamson  (1907).     Journal  of  Tropical  Medicnic,  p.  333. 

Urinary  Amoebiasis. 

Chalmers    and    O'Fakrell    (1917).     Journal    of    Tropical    Medicine    and 

Hygiene,  May  1,  97-100.     London. 
Craig  (191 1).     The  Pathogenic  Amoeba;  of  Man,  p.  455.     Philadelphia  and 

London. 
Fantham   (1916).     British  Medical   Journal,   vol.  i.,   April  15,   pp.  553-554- 

London. 
Fantham,  Stephens,  and  Theobald  (1916).     Parasites  of  Man.     London. 
Fischek   (1914).     Miinchener  Medizinische  Wochenschrift,  vol.  lxi.,  p.  473. 

M       hen. 


REFERENCES  1937 

Hartmann  (1913).     Handbuch  der  Pathogenen  Mikroorganismen,  vol.  vii., 

p.  641.     Jena. 
JUrgens  (1892).     Deutsche  Medizinische  Wochenschrift,  p.  454.     Leipzig. 
Kartulis    (1893).     Zeitschxift   fur    Hygiene    und    Infektionenskrankheiten, 

vol.  xiii.,  p.  2.     Leipzig. 
Lynn  (1914).     American  Journal  of  Tropical  Diseases,  vol.  ii.,  No.  3,  p.  205. 

New  Orleans. 
Posner  (1893).     Berliner  Klinische  Wochenschrift,  vol.  xxx..  No.  28,  p.  674. 

Berlin. 
Ward,  Coles,  and  Friel  (1916).     British  Medical  Journal,  vol.  i.,  April  8, 

p. 526.     London. 

Oxaluria. 

Baldwin  (1900).     Journal  of  Experimental  Medicine,  p.  27. 
Burkitt  (1909).     British  Medical  Journal,  vol.  i.,  p.  898. 

Urinary  Tests. 

Castellani  and  Taylor  (1917).  British  Medical  Journal  (The  Mycological 
Detection  and  Determination  of  Certain  Carbohydrates  and  other  Carbon 
Compounds  in  Pathological  Work),  December  29. 

Castellani  and  Taylor  (1919).  British  Medical  Journal.  (The  determina- 
tion of  Saccharosuria,  Inosituria,  and  Lactosuria  by  a  Mycological  Method) , 
February  15. 


CHAPTER  LXXXVI 
DISEASES  OF  THE  GENERATIVE   SYSTEM 

General  remarks — Male  generative  system — Endemic  funiculitis — Female 
generative  system — Tropical  puerperal  fever — Sutika — References — 
Addendum — Ante-  and  post-natal  pathology — Addendum  references. 

GENERAL  REMARKS. 

In  this  chapter  we  propose  to  include  a  few  general  remarks  upon 
the  male  and  female  generative  systems.  The  subjects  will  be 
merely  touched  upon,  as  space  forbids  anything  else. 

MALE  GENERATIVE  SYSTEM. 

In  Chapter  III.,  p.  JJ,  we  have  invited  attention  to  the  effects  of 
climate  upon  the  generative  organs,  and  have  noted  that  they  act 
more  vigorously  than  in  the  Temperate  Zone,  and  that  venereal 
excess  is  distinctly  more  deleterious  in  the  tropics  than  ir>  temperate 
climates.  We  have  also  noted  that  puberty  in  boys  appears  at  an 
earlier  age  in  the  tropics  than  in  other  climates. 

In  Chapter  V.,  p.  118,  we  have  touched  upon  the  subject  of 
Eugenics,  and  have  mentioned  the  ill-effects  of  alcoholism,  syphilis, 
gonorrhoea,  and  tuberculosis,  the  effects  of  which  are  much  the  same 
as  in  other  climates,  but  as  regards  the  first  we  have  set  forth 
its  evils  in  Chapter  X.,  p.  175.  In  reference  to  syphilis,  it  is  very 
common,  and  its  primary,  secondary,  tertiary,  and  inherited  effects 
can  be  abundantly  seen  among  natives,  as  may  be  judged  from 
Chapter  XCVII.  Gonorrhoea  is  very  common  among  all  classes  of  the 
population  and  all  races.  The  clinical  features  are  the  same  as 
observed  in  temperate  zones,  but  complications  are  much  more 
frequent,  owing  to  the  native  patients  consulting  a  doctor  only  when 
the  disease  is  of  long  standing.  We  have  seen  several  cases  of  gono- 
coccus  septicaemia  with  endocarditis  ending  fatally,  and  also  several 
cases  of  so-called  '  gonococcus  rheumatism.'  It  may  be  noted  that 
among  certain  natives  there  is  a  general  belief  that  the  disease  is  not 
of  sexual  origin.  African  porters  firmly  believe  that  it  is  due  to  pro- 
longed marching.  There  are  also  various  curious  superstitions  in 
connection  with  it.  In  Abyssinia,  according  to  Annaratone,  natives 
believe  it  is  contracted  by  passing  water  on  the  ground  illuminated 
by  moonshine,  or  by  passing  water  where  dogs  have  previously 
urinated.     Occasionally  true  cases  of  non-gonorrhceic  urethritis  are 

1938 


MALE  GENERATIVE  SYSTEM  1939 

met  with  (p.  1943);  in  a  few  of  these  cases  chlamydozoa-like  bodies 
have  been  described.  Rare  cases  of  urethritis,  with  black  discharge 
due  to  the  presence  of  Aspergillus  fumigatus,  and  cases  of  balanopos- 
thitis  due  to  monilias,  are  observed.  Neglected  strictures  are  by  no 
means  uncommon,  and,  as  we  have  already  stated,  one  of  these  ap- 
parently caused  intestinal  obstruction  and  death.  Extravasation  of 
urine  is  not  rare — at  all  events,  in  Africa — as  the  result  of  neglected 
stricture.  Elephantiasis  of  the  generative  organs  is  common  in  Africa, 
and  in  many  parts  of  tropical  Asia  and  America.  Hydroceles, 
chyloceles,  hematoceles,  orchitis,  and  epididymitis  are  all  common, 
and  bilharziosis  has  been  already  noted  by  us.  Epithelioma  of 
the  penis  is  associated  with  phimosis  and  the  accumulation  of 
irritating  secretions,  which  may  cause  balanitis.  In  these  circum- 
stances, if  no  treatment  is  carried  out,  epithelioma  may  result. 
Certainly  epithelioma  of  the  penis  is  rare  in  races  in  which  circum- 
cision is  performed. 

Castration  and  circumcision  are  still  performed  in  many  tropical 
countries.  As  regards  the  former,  it  may  be  restricted  to  the  simple 
removal  of  the  testes,  but  more  generally  the  penis  also  is  cut  away. 
This  operation  is  usually  performed  upon  small  boys.  Circumcision 
usually  takes  place  about  puberty,  but  in  some  races  it  is  performed 
at  an  early  age.  It  is  usually  associated  with  some  semi-religious 
rites  intended,  in  the  case  of  the  older  boys,  to  be  an  initiation  to 
sexual  life,  as  may  be  found  detailed  in  works  upon  anthropology. 
Christopherson  has  drawn  attention  to  the  mutilations  performed 
by  the  Abyssinians  upon  their  conquered  foes  in  times  of  war. 
This  consists  of  a  complete  castration — i.e.,  the  removal  of  the  penis 
and  testes — and,  as  may  be  imagined,  but  few  survive  such  a  muti- 
lation performed  on  the  field  of  battle.  The  result  of  these  opera- 
tions and  mutilations  is  the  formation  of  much  scar  tissue  surround- 
ing the  orifice  of  the  urethrae  and  the  pubes. 

With  regard  to  the  breast,  we  have  seen  extraordinary  hypertrophy 
of  the  male  breast. 

ENDEMIC  FUNICULITIS. 

Synonyms.— Suppurative  phlebitis  of  the  spermatic  cord,  Sup- 
purative corditis,  Cellulitis  of  the  spermatic  cord,  Cirsoitis  (Pfister). 

Definition. — Endemic  funiculitis  is  an  acute  specific  suppurative 
inflammation  of  the  spermatic  cord,  of  which  the  aetiology  is  not 
firmly  established. 

History. — -For  many  years  medical  men  practising  in  Ceylon  have 
noticed  the  occurrence  of  a  peculiar  form  of  acute  suppurative 
inflammation  of  the  spermatic  cord,  which  occasionally  takes  a 
true  epidemic  character,  numerous  cases  occurring  within  a  short 
period.  References  to  this  affection  may  be  found  in  almost  all 
the  medical  reports  for  the  colony  during  the  last  twenty  years. 
the  disease  being  variously  indicated  by  the  name  of  phlebitis  of  the 
cord  or  corditis.  It  was  considered  by  some  to  be  of  traumatic 
origin,  by  others  of  venereal  origin.     Some  practitioners  considered 


194° 


DISEASES  OF  THE  GENERATIVE  SYSTEM 


it  to  be  a  malarial  affection.  The  disease  was  investigated  by- 
Cast  ellani  first  in  1904,  and  more  completely  in  1907.  He  came  to 
the  conclusion  that  it  had  nothing  to  do  with  either  malaria  or 
gonorrhoea.  He  thought  the  malady  had  sufficiently  characteristic 
symptoms  to  be  ranked  as  a  separate  disease,  and  suggested  the 
name  '  endemic  funiculitis.'     The  affection  is  not  limited  to  Ceylon, 


■" 


Fig.     780. — Endemic   Funicu-     Fig.  781. — Transverse   Sections  of  the 

litis,  showing  Longitudinal  Cord  in  Endemic  Funiculitis. 

Section  of  the  Cord.  The    testes  and  epididymis  were  normal, 

The  testes  and  epididymis  are         but    the    tunica   vaginalis    held   a   small 

normal.  quantity  of  <j  fluid.     The   sections   of   the 

cord  are  arranged  in  an  arch  from  right 

to    left.     The  dilatedVveins,  which  were 

filled  with  pus,  are  clearly  visible. 

as  cases  occur  in  Southern  India,  and  an  identical  pathological 
condition  has  been  described  in  Egypt  by  Madden  in  1907  under 
the  name  of  cellulitis  of  the  spermatic  cord.  The  condition  described 
by  Wise  in  the  West  Indies  is  probably  the  same  pathological  entity . 
Of  great  importance  are  the  investigations  by  Coutts. 


ENDEMIC  FUNICULITIS  194 1 

/Etiology.— Among  Ceylon  practitioners  the  disease  was  con- 
sidered by  some  to  be  of  traumatic  origin;  others  believed  it  to  be 
of  venereal  origin,  and  yet  others  to  be  a  malarial  affection.  Castel- 
lani  found  in  all  the  cases  virulent  diplo-streptococci,  and  in  some 
cases,  one  in  1904  and  the  others  in  1909,  and  later,  a  microfilaria. 
This  microfilaria  is  morphologically  identical  with  Microfilaria  ban- 
crofti,  but  in  our  cases,  though  provided  with  a  sheath,  it  showed 
translation  movements.  The  cocci  are  practically  indistinguishable 
from  the  ordinary  streptococci  but  for  the  fact  that  some  decolourize 
by  Gram  in  sections  of  the  tissues  and  in  smears  from  the  pus, 
while  they  are  Gram-positive  in  cultures.  According  to  Coutts 
these  micrococci  are  often  found  in  the  urethra  of  natives.  He 
regards  the  suppurative  condition  of  the  cord  as  due  to  the  extension 
of  an  infection  from  the  urethra  by  way  of  the  vas  deferens.  Wise 
has  found  in  his  cases  F.  bancrofti  and  numerous  streptococci. 
Pfister  believes  the  disease  to  be  connected  with  bilharziosis.  We 
are  inclined  to  consider  the  malady  to  be  a  filarial  condition  with  a 
superadded  streptococcus  infection.  The 
filaria  probably  plays  the  more  impor- 
tant or  only  role  in  the  subacute  or 
chronic  cases,  while  the  streptococcus  is 
probably  the  causative  agent  of  the 
acute  symptoms  and  the  suppuration, 
and  of  the  symptoms  of  septicaemia. 

Predisposing  Causes. — A  certain  impor- 
tance must  be  given  to  a  sudden  chill 
or   to   some  form    of    traumatism.     In 
nearly  all  the  Ceylon  cases  the  disease 
begins  abruptly  after  taking  a  cold  bath     FlG     ?82   _  Transverse 
when  feeling  tired.     In  some  cases  the        Section  Inflamed  Cord. 
patient  gives  a  history  of  having  made        (Actual  Size.) 
an  effort,  such  as  in  lifting  a  weight,  etc. 

Pathology.— The  whole  of  the  spermatic  cord  is  highly  inflamed 
and  infiltrated.  The  circumference  of  the  cord  may  be  as  much  as 
3  to  3J  inches.  The  tunica  vaginalis  is  hyperaemic,  but  in  most 
cases  there  is  no  collection  of  fluid.  On  making  a  transverse 
section  of  the  cord,  yellow  creamy  pus  will  exude  from  the  opened 
veins  of  the  pampiniform  plexus,  as  well  as  from  the  vas  deferens. 
The  inflammation  is  not  localized  to  the  cord  only;  it  ordinarily 
extends  to  the  epididymis.  In  two  very  recent  cases  of  ours,  how- 
ever, the  epididymis  was  normal.  The  testicle  proper  remains 
generally  unaffected ;  there  is  occasionally  some  effusion  of  clear  fluid 
into  the  tunica  vaginalis.  The  histological  lesions  are,  briefly,  the 
following:  The  veins  of  the  pampiniform  plexus  are  much  dilated, 
and  present  a  cellular  infiltration  of  all  the  coats,  the  lumen  of  some 
veins  being  occupied  by  pus  cells  or  thrombi.  The  vas  deferens 
also  presents  a  well-marked  cellular  infiltration  of  its  mucous  mem- 
brane and  various  muscular  coats.  The  type  of  cellular  infiltration 
as  noted  by  Coutts  and  Castellani  is  mostly  mononuclear. 


1942 


DISEASES  OF  THE  GENERATIVE  SYSTEM 


Morbid  Anatomy.— At  the  post-mortem  examination  of  the  cases 
in  which  an  operation  has  not  teen  performed  in  time,  the  lesions 
found  are  those  of  a  septicemic  process.  The  skin  is  jaundiced,  and 
may  present  petechia?;  the  lungs  often  show  hypostatic  congestion; 
the  heart  is  flabby,  and  subpericardial  hemorrhages  are  often  seen. 
The  spleen  is  enlarged  and  soft.  The  liver  is  generally  enlarged,  and 
may  show  fatty  degeneration  or  cloudy  swelling.  The  kidneys  are 
often  congested. 

Symptomatology. — The  disease  begins  suddenly,  generally  after 
a  hard  day's  work  or  severe  exercise.  In  Ceylon  the  usual  history 
is  as  follows:  The  patient,  after  an  extra  hard  day's  work,  comes 
home  in  the  evening  very  tired,  but  not  feeling  unwell,  and  takes  a 

cold  bath  as  usual.  After  the 
bath  he  is  suddenly  seized 
with  a  shivering  fit,  the  tem- 
perature rising  very  high.  He 
feels  very  sick,  and  there  is  often 
actual  vomiting.  At  the  same 
time  he  complains  of  pain  along 
s  the  cord  and  the  epididymis. 
The  condition  becomes  rapidly 
worse,  and  the  patient  is  gener- 
ally taken  to  hospital  on  the 
second  or  third  day  of  the 
illness.  On  admission,  it  is 
usually  found  that  the  general 
condition  is  grave.  There  may 
be  continuous  vomiting,  and 
occasionally  hiccough;  the  tem- 
perature is  generally  above 
102°  F.,  and  the  pulse  small  and 
frequent.  At  the  physical  ex- 
amination it  will  be  seen  that 
the  inguinal  region  is  occupied 
by  a  large  cylindrical  swelling 
in  the  direction  of  the  cord. 
The  swelling  is  very  tender  on  pressure,  and  hard;  the  skin  is  not 
affected.  Generally  the  epididymis  is  somewhat  enlarged  and 
tender,  though  in  some  very  recent  cases  it  may  not  appear  to  be 
affected.  In  all  cases  the  testicle  proper  appears  to  be  normal; 
there  is,  as  a  rule,  no  effusion  in  the  tunica  vaginalis.  The  affection 
is  generally  localized  to  one  side  only,  but  occasionally  attacks  both 
sides.  On  examination  of  the  penis  and  scrotum  no  ulcers  will  be 
found,  no  signs  of  gonorrhoea,  and  no  signs  of  any  traumatic  lesions, 
though  in  several  cases  the  patient  gives  a  history  of  having  made 
an  effort  of  some  sort.  As  a  rule,  the  disease  has  no  tendency  to 
spontaneous  recovery.  If  an  operation  is  not  performed  in  time, 
signs  of  general  septicaemia  usually  set  in.  In  such  c;  ses  the  skin 
of  the  patient  often  becomes  jaundiced,  cutaneous  haemorrhages 


Fig.   783. — Endemic  Funiculitis 
in  a  Sinhalese  Man. 


NON-GONORRHCEAL  URETHRITIS  1943 

may  appear,  the  fever  is  of  an  intermittent  or  remittent  type,  the 
pulse  becomes  extremely  small,  there  is  often  hiccough,  and  the 
patient  dies  in  a  few  days. 

Varieties. — A  mild  form,  with  thrombosis  of  the  veins,  but  without 
suppuration,  is  at  times  met  with.  According  to  Coutts,  a  chronic 
form,  also  without  suppuration,  may  occur. 

Prognosis. — This  is  serious  in  the  ordinary  acute  form.  If  an 
operation  is  not  performed  in  time,  symptoms  of  general  septicaemia 
set  in,  and  the  case,  as  a  rule,  ends  fatally. 

Diagnosis.— The  disease  is  apt  to  be  confused  with  strangulated 
hernia  and  an  acute  elephantoid  condition  of  the  testicle  and  cord. 
From  the  former  endemic  funiculitis  may  be  differentiated  by  the 
history,  the  high  fever,  and  the  course,  which  is  somewhat  less  acute. 
In  some  cases,  especially  in  the  fulminating  forms,  operative  treat- 
ment alone  will  clear  the  diagnosis. 

From  an  acute  elephantoid  condition  it  may  be  differentiated  by 
the  absence  of  the  erysipelatous-like  redness  of  the  skin. 

Treatment. — Except  in  the  rare  mild  forms,  when  lead  lotion  and 
ichthyolointment.withor  without  ice  application,  maybe  sufficient, 
the  only  effective  treatment  is  surgical,  and  orchiotomy,  with 
section  of  the  inflamed  cord  as  high  up  as  possible,  is  imperative. 
Coutts  recommends  exposure  of  the  inflamed  cord  by  a  free  in- 
cision through  the  skin  and  external  oblique,  to  be  followed  by 
numerous  incisions  into  the  tumour.  The  wound  is  left  open,  and 
fomentations  applied  till  the  surface  is  clean.  The  wound  is  then 
left  to  heal  by  granulation.  Coutts  considers  that  in  this  way, 
though  the  testis  loses  its  generative  function  owing  to  the  oblitera- 
tion of  the  spermatic  duct  caused  by  the  inflammation,  its  internal 
secretion  is  unimpaired. 

When  the  disease  has  extended  beyond  the  internal  abdominal 
ring,  orchiotomy  must  be  performed  and  the  veins  left  unligatured 
while  fomentations  are  applied. 

NON-GONORRHGEAL  URETHRITIS. 

Urethral  muco-purulent  discharge  is  as  a  rule  of  gonorrhoeal  origin,  but 
Castellani  has  called  attention  to  a  number  of  forms  of  quite  different  aetiology, 
which  may  be  classified  as  follows : — ■ 

A.  Traumatic  Mucous  Urethritis. 

This  occasionally  arises  after  long  and  violent  continued  physical  exercise. 
One  is  rather  sceptical  in  admitting  such  a  type  of  urethritis,  and  practically 
all  the  cases  of  so-called  '  porter's  urethritis  '  we  have  seen  were  gonorrhoeal 
infections.  Still,  there  cannot  be  any  doubt  that  in  soldiers  and  native  porters 
doing  long  marches  day  after  day  a  slight  urethritis  with  scanty  mucous 
discharge  may  occasionally  develop,  even  in  individuals  who  have  never 
suffered  in  the  past  from  gonorrhoea.  The  secretion,  however,  in  our  ex- 
perience is  never  frankly  purulent. 

B.  Urethritis  of  Hyphomycetic  Origin. 

The  following  clinical  varieties  may  be  differentiated  : — 

1.  The  discharge  is  black,  greenish-black,  or  brownish-black,  generally  due 


1944  DISEASES  OF  THE  GENERATIVE  SYSTEM 

to  fungi  of  the  genus  Aspergillus  Micheli  and  Cladosporium  Link.     One  of  us 
has  described  some  of  these  cases  in  Ceylon. 

2.  Discharge  -whitish  or  yellowish.  Generally  fungi  of  the  genus  Monilia 
and  of  the  genus  Oidium  are  found. 

3.  Red  discharge.  Generally  due  to  a  red  pigment-producing  monilia  or 
cryptococcus,  or  to  a  non-pigmented  monilia,  and  associated  with  red  pigment- 
producing  bacilli  or  cocci. 

C.  Urethritis  associated  with  Animal  Parasites  :  I.  With  Protozoa ;  II.  With 
Animal  Parasites  Higher  than  Protozoa. 

I.  Urethritis  of  Protozoal  Origin. — The  following  varieties  may  be  dis- 
tinguished : — 

(1)  Urethritis  associated  with  Flagellates. — The  flagellates  found  belong  to 
the  genera  Trichomonas  Donn6,  Cercomonas  Dujardin,  Prowazekia  Hartmann 
and  Chagas.  In  one  of  our  cases  a  flagellate  with  four  flagelli  was  observed. 
It  is  doubtful,  however,  whether  the  flagellates  found  are  the  true  setiological 
agents  of  the  discharge. 

(2)  Urethritis  associated  with  Ciliales. — In  a  case  of  urethral  discharge  in  a 
native  man  we  observed  the  same  ciliate  we  have  fairly  often  noticed  in  Ceylon 
in  the  vaginal  secretion  of  native  women. 

(3)  Urethritis  associated  with  Amcebce. — We  have  seen  several  such  cases. 
The  amoebae  were  of  different  type;  in  one  case  it  closely  resembled  Loeschia 
histolytica. 

(4)  Spirochcetic  Urethritis. — This  type  of  urethritis  due  to  5.  urethralis 
Macfie  is  occasionally  met  with.  The  discharge  may  be  abundant  and  frankly 
purulent,  and  contains  an  enormous  number  of  spirochaetes.  It  must  be  noted, 
however,  that  spirochaetes  are  not  rarely  found  in  the  normal  urethra,  as 
shown  by  many  observers  and  in  the  tropics  by  Mendelson. 

(5)  Treponema  urethritis. — The  discharge  is  muco-purulent  and  contains  a 
large  number  of  treponemas  {Treponema  urethrale  Castellani) .  The  organism 
is  very  delicate,  stains  purplish  or  pinkish,  has  numerous  small  spirals,  all 
practically  of  the  same  size;  length  of  the  parasite  6  to  12  microns.  The  patient 
has  no  sign  of  syphilis,  and  Wassermann  is  negative.  Urethral  irrigation  of  a 
1  in  20,000  solution  of  hyd.  perchlor.  cures  the  condition. 

II.  Urethritis  associated  with  Animal  Parasites  Higher  than  Protozoa. 
— These  are  generally  due  to  larvae  of  flies  and  chance  parasites  setting  up  an 
inflammation  of  the  urethra. 

Balanoposthomycosis. — In  1881  Simon  of  Breslau  first  described  a  balano- 
posthitis  due  to  fungi,  and  occurring  in  persons  suffering  from  diabetes.  It 
is  probably  the  same  disease  as  that  referred  to  by  Rollo  in  1798,  by  Bardsley 
of  Manchester  in  1807,  by  Friedreich  in  Hanover  in  1864,  by  Hassal  in  1833, 
and  by  de  Beauvais  in  1874.  The  symptoms  consist  of  slight  itching  and 
burning  on  the  glans  penis  and  on  the  inner  aspect  of  the  prepuce,  and  is  asso- 
ciated with  erythema,  followed  by  superficial  ulceration  and  a  yellow  purulent 
discharge,  while  the  margin  of  the  prepuce  may  become  irritated  and  phimosis 
set  in.  On  examining  the  discharge  fungal  hyphae  of  a  moniliform  character 
may  be  seen.  Castellani  has  described  several  such  cases  due  to  fungi  of  the 
genus  Monilia. 

FEMALE  GENERATIVE  SYSTEM. 

Circumcision  is  exceedingly  common  among  native  races — e.g., 
among  the  semi-civilized  Arabs  and  the  Sudanese  of  Kordofan  and 
other  parts  of  the  Sudan  every  young  girl  when  aged  five  or  six 
years  undergoes  one  of  two  varieties  of  this  operation.  The  milder 
operation,  called  '  sunna  tahuret,'  or  circumcision  according  to 
religious  law,  consists  of  the  removal  of  the  clitcris  and  labia  minora, 
while  the  more  severe  cutting,  called  'Pharaoh's  tahuret,'  or  the  old 


FEMALE  GENERATIVE  SYSTEM  1945 

Egyptian  circumcision,  entails  in  addition  the  removal  of  the  upper 
two-thirds  of  the  labia  majora.  The  result  of  these  operations  is 
the  formation  of  scartissue,  and  hence  it  is  almost  always  necessary 
to  enlarge  the  vulvar  orifice  by  means  of  a  razor,  not  merely  at  the 
time  of  marriage,  but  again  at  the  birth  of  a  child,  when,  otherwise, 
it  would  be  difficult  for  the  head  to  emerge.  The  enlarged  orifice 
is  again  partially  closed  some  little  time  after  birth  of  the  child, 
and  therefore  incision  has  to  be  repeated  at  every  succeeding 
birth. 

In  1910  Wilson  studied  the  peculiar  elongation  of  the  nymphse 
found  in  Hottentot  women,  and  came  to  the  conclusion  that  it  was 
largely  produced  artificially. 

In  1917  Neve  drew  attention  to  the  fact  that  rickets  is  rare  in 
Kashmir,  but  that  osteomalacia  was  common  in  multiparous 
women,  in  whom  the  first  symptoms  appear  in  pregnancy  and  cause 
the  characteristic  deformity  of  the  pelvis. 

We  have  discussed  the  question  of  the  onset  of  puberty  and  the 
climacteric  in  Chapter  III.,  p.  77,  to  which  reference  may  be  made. 
Displacements,  inflammations,  and  tumours  of  the  female  generative 
organs  are  quite  common,  especially  uterine  fibromata  and  ovarian 
cysts.     Cancer  of  the  uterus  is  not  rare. 

VULVO-VAGINITIS. 

Every  type  of  vulvo-vaginitis  met  with  in  temperate  zones  is  also  found  in  the 
tropics,  and  gonorrhoeal  infections  are  very  common.  It  is  interesting  to 
note  that  we  have  found  in  the  vaginal  secretion  practically  all  the  organisms 
we  have  mentioned  under  the  heading  Pseudo-Gonorrhceal  Urethritis,  and 
that  there  are  forms  of  vulvo-vaginitis  associated  with  flagellates,  ciliates, 
amcebae,  spirochaetes,  treponemata,  and  fungi,  and  hence  it  is  quite  possible 
that  a  certain  number  of  cases  of  protozoal  and  hyphomycetic  urethritis  in 
man  are  contracted  in  reality  by  sexual  intercourse. 

Vulvo-vaginitis  associated  with  hyphomycetes  is  far  from  rare,  and  such 
cases  may  be  separated  into  two  principal  groups: — 

I.  Associated  with  fungi  of  the  genus  Aspergillus,  Sterigmatocystis,  Peni- 
cillium,  Cladosporium,  with  discharge,  which  may  be  dark-brownish  or  black. 

II.  Associated  with  fungi  of  the  genus  Monilia  and  the  genus  Oidium,  with 
white  or  yellow  discharge.  These  cases  may  present  two  different  clinical 
appearances :  some  are  characterized  by  the  presence  of  thrush-like  membranes 
on  the  vaginal  mucosa  {vaginal  thrush) ;  others  do  not  show  any  membrane  on 
the  mucosa,  but  the  discharge  is  purulent  and  very  thick.  In  the  tropics 
Castellani  has  found  fungi  principally  of  the  types  Monilia  pinoyi  Castellani, 
Monilia  tropicalis  Castellani.  In  temperate  zones  the  same  observer  with 
Taylor  have  found  Monilia  pinoyi  Castellani,  Monilia  londinensis  Castellani, 
Monilia  metalondinensis  Castellani,  and  other  species. 

VAGINAL  PROTOZOA. 

The  vagina  of  native  women  may  be  the  habitat  of  numerous  protozoa  apart 
from  Treponema  pallidum  and  spirochaetes.  We  record  the  presence  of  the 
following: — 

Sarcodina  : — 
Loeschia  histolytica  (Schaudinn,  1903). 
Loeschia  coli  Loesch,  1875. 


1946  DISEASES  OF  THE  GENERATIVE  SYSTEM 

Mastigophora  : — 

Oicomonas  vaginalis  Castellani  and  Chalmers,  1908. 
Prowazekia  vaginalis  Castellani  and  Chalmers,  191 8. 
Trichomonas  vaginalis  Donne,  1837. 
Tetratrichomonas  vagina  Castellani  and  Chalmers,  1918. 

Cilia  ta  : —  ' 

Balantidium  vaginale  Castellani  and  Chalmers,  191 8. 


TROPICAL  PUERPERAL  FEVER. 

Synonym. — Puerperal  septicaemia. 

Definition. — Tropical  puerperal  fever  is  an  infection  of  parturient 
or  puerperal  women  with  various  germs,  which  may  cause  a  local 
septic  condition  or  a  genera1  septicaemia. 

History.- — It  is  probable  that  puerperal  fever  has  been  prevalent 
throughout  the  world  in  all  ages  wherever  man  has  roamed,  but 
as  it  is  conveyed  from  infective  sources,  living  or  dead,  autcgenetic 
or  heterogenetic,  by  instruments  or  by  the  hands  of  the  attendants, 
to  the  uterus  of  the  parturient  woman,  it  is  obvious  that,  in  those 
primitive  tribes  in  which  little  or  no  aid  is  given  to  the  woman  in 
childbirth,  there  will  be  littlepuerperal  fever,  notwithstanding  that 
her  immediate  surroundings  may  be  insanitary. 

Usually  in  non-civilized  races  there  is  less  difficulty  with  child 
labour,  and  hence  less  damage  to  the  organs  of  generation,  and  con- 
sequently a  less  number  of  portals  of  septic  infection. 

The  reasons  for  this  easier  childbirth  are  not  well  known,  but  may 
■possibly  depend  upon  two  factors — i.e.,  the  mother  and  the  child. 
With  regard  to  the  mother,  the  fact  that  pregnancy  takes  place  at 
an  earlier  age  in  the  uncivilized  than  in  the  civilized,  and  the  fact 
that  the  woman  of  non-civilization,  from  spare  and  hard  living, 
is  oftenthinner  than  the  woman  of  civilization,  may  help,  even  if  her 
pelvic  measurements  are  relatively  smaller;  while  it  is  often  alleged 
t  hat  t  he  head  of  t  he  uncivilized  child  i  s  smaller  t han  t hat  of  a  civilized 
race,  and  it  has  even  been  asserted  by  Brooke  that  on  an  average 
the  child  weighs  1  pound  lighter  in  uncivilized  races.  If  these 
statements  are  correct,  they  will  help  to  explain  the  easy  child 
labours  and  the  less  amount  of  puerperal  fever  in  those  races. 

When  we  consider  old  native  civilizations  and  the  Caucasian  races, 
we  find  that  child  labour  is  difficult,  and  that  assistance  has  had 
often  to  be  rendered  to  the  parturient  woman  from  time 
immemorable,  and  that  puerperal  fever  in  isolated  cases  and  in 
epidemics  has  been  known  for  ages. 

Turning  to  one  of  the  old  civilizations  of  the  tropic  — viz.,  that 
seen  in  Ceylon — these  facts  are  well  borne  out  b}'  the  researches  of 
one  of  us  in  1907  into  the  vital  statistics  of  the  various  peoples 
inhabiting  that  island. 

These  inquiries  showed  that  the  deaths  of  women  in  childbirth 
were  higher  than  those  in  Europe,  and  that  the  principal  cause  was 
puerperal  fever. 


TROPICAL  PUERPERAL  FEVER  1947 

When  the  racial  incidence  was  investigated  it  was  found  that  the 
sociological  and  hygienic  factors  influencing  this  incidence  were 
marked,  as  the  percentage  of  the  total  annual  racial  deaths  attribut- 
able to  childbirth  and  principally  caused  by  puerperal  fever  was 
only  ot  per  cent,  for  Europeans,  while  it  was  1-2  per  cent,  for 
Sinhalese,  who  form  the  bulk  of  the  population,  o-8  per  cent,  for 
Tamils,  the  next  largest  native  community,  i-i  per  cent,  for  a 
mixed  native  and  European  race  known  as  burghers,  under  which 
heading  also  come  those  inhabitants  of  pure  Dutch  descent  from  the 
settlers  of  two  hundred  years  ago.  Many  of  these  burghers  are 
very  poor,  and  nearly  all  inhabit  towns  and  mostly  live  under  more 
insanitary  conditions  than  the  average  European.  The  Moham- 
medan communities  of  Arabs  and  Malays  have  a  mortality  of  1*2  per 
cent,  and  i-i  per  cent,  respectively. 

The  disease  is  known  to  have  been  not  uncommon  in  Bengal  since 
Twining  wrote  in  1833,  while  its  death-rate  in  Calcutta  for  1906-07 
was  i-2  per  cent,  of  the  total  deaths. 

With  regard  to  Egypt,  the  first  medical  accounts  of  the  fever  are 
contained  in  Pruner's  writings  published  in  1847,  where  it  is  stated 
t  hat  it  was  not  so  common  as  in  Europe,  but  an  epidemic,  extending 
from  Alexandria  to  Luxor,  is  mentioned  as  taking  place  in  1844. 

The  peoples  of  the  Anglo-Egyptian  Sudan  are  peculiarly  interest- 
ing from  the  point  of  view  of  our  present  study,  because  they  contain 
very  primitive  tribes,  semi-civilized  natives,  and  civilized  peoples. 

As  examples  of  the  primitive  tribes  we  may  consider  the  Nyam- 
Nyam,  who  live  in  the  southern  part  of  the Bahr-El-Ghazal  Province, 
and  the  Jur  or  Gour  tribe,  which  occupies  a  limited  area  of  that 
province  between  the  River  Gell  and  the  Rumbek-M'volo  road. 
In  these  tribes,  according  to  Anderson,  childbirth  is  usually  a  simple 
physiological  process  taking  place  for  the  first  time  when  the  woman 
is  in  her  teens,  and  managed  by  a  midwife,  who  is  simply  any  other 
woman  who  has  given  birth  to  a  child,  and  who  sees  that  everything 
connected  wit  h  the  part  urient  woman  is  strictly  clean,  and  placing  her 
on  a  bed  of  freshly  cut  leaves,  allows  Nature  to  do  the  rest,  with  the 
sole  exception  of  such  rare  cases  as  require  assistance,  when,  accord- 
ing to  the  same  authority,  she  calls  in  the  aid  of  some  small  boys. 
Under  these  primitive  conditions  puerperal  fever  must  be  rare.  The 
same  easy  childbirth  can  be  observed  among  the  Bedouins  of  Syria. 

Among  the  semi-civilized  Arabs  and  Sudanese  of  Kordofan  and 
other  parts  of  the  Sudan  every  young  girl  is  circumcised  as  described 
above.  This  procedure,  as  already  stated,  is  followed  by  the  forma- 
tion of  scar  tissue,  which  renders  it  almost  always  necessary  to  en- 
large the  vulvar  orifice  by  means  of  a  razor,  not  merely  at  the  time  of 
marriage,  but  again  at  the  birth  of  a  child,  when  otherwise  it  would 
be  difficult  for  the  head  to  emerge.  The  enlarged  orifice  is  again 
partially  closed  some  little  time  after  the  birth  of  the  child,  and 
therefore  the  incision  has  to  be  repeated  at  every  succeeding  birth. 

If  this  second  cutting  is  performed  carelessly  and  the  resulting 
wound  becomes  septic,  then  fever  ensues,  and  in  a  case  of  this  nature 


1948  DISEASES  OF  THE  GENERATIVE  SYSTEM 

we  have  found  streptococci  and  other  organisms.  These  people 
are  well  acquainted  with  puerperal  fever,  which  they  call  '  el 
jarat,'  or  sometimes  '  humma  nafas,'  or  when  slight  they  term  it 
milk  fever,  or  '  humma  laban,'  and  which  they  consider  to  be 
transmitted  from  one  case  to  another. 

The  civilized  peoples  of  Khartoum  and  Omdurman,  more  especially 
the  Greeks,  Syrians,  and  better-class  natives,  suffer  from febris  pnev- 
peralis  and  febris  in  puerperio,  but  no  statistics  are  available  to 
show  the  incidence  of  the  disease. 

As  regards  Zanzibar,  the  deaths  from  puerperal  fever  are  given 
as  eight  out  of  a  total  mortality  of  1,022,  of  which  572  are  female 
deaths  at  all  ages. 

In  none  of  the  above  statistics  is  it  possible  to  compare  the 
puerperal  deaths  with  the  number  of  births,  as  these  were  not 
accurately  known. 

In  the  West  Indies  and  in  Central  and  South  America  the  fever 
is  notuncommon,  andBrooke,  writing  in  1908,  with  his  experience  of 
the  West  Indies  and  Singapore,  says: — 

The  mortality  and  morbidity  from  puerperal  sepsis  and  the  infantile  death- 
rate  among  native  communities  are  enormous.' 

He  blames  the  village  midwife  or  handywoman,  who,  he  says, 
is  a  prejudicial,  ignorant,  and  dirty  person,  and  summarizes  his 
remarks  by  stating: — 

We  see  that,  for  the  native  woman  under  her  native  skies,  want  and  poverty 
may  play  havoc  with  the  child  that  is  to  be,  but  there  is  often  a  physical 
environment  of  ignorance  and  sepsis  during  labour  which  demands  the  attention 
of  public  opinion.' 

Our  experience  in  various  tropical  and  subtropical  regions 
supports  these  statements  made  by  Brooke. 

/Etiology. — Early  in  the  seventeenth  century  there  appeared  the 
idea  of  a  double  origin  for  the  fever — viz.,  the  autcgenetic  and  the 
heterogenetic — and  also  that  the  disease  was  microbic  in  origin 
(Kircher,  1671). 

In  1788  Denman  observed  that  the  disease  was  carried  from  cases 
of  puerperal  fever  to  healthy  lying-in  women  by  doctors  and  mid- 
wives,  which  view  was  strongly  supported  by  the  work  of  Alexander 
Gordon  in  Aberdeen  in  1795,  and  by  Oliver  Wendell  Holmes  in 
America  in  1843,  the  last-named  observer  asserting  that  not 
merely  could  it  be  conveyed  in  this  manner,  but  that  it  could  come 
in  a  similar  way  from  a  case  of  erysipelas  or  from  a  post-mortem, 
and  that  it  was  necessary  for  the  physician  to  disinfect  his  hands 
and  to  change  his  clothes  after  leaving  a  case  of  puerperal  fever. 
This  work  was  ably  supported  and  put  upon  a  sound  basis  by  Sem- 
melweiss,  whose  brilliant  researches  are  too  we  llknown  to  require 
recapitulation. 

With  these  investigations  the  heterogenetic  origin  of  the  disease 
was  firmly  established,  and  it  now  remained  for  the  bacteriologists 
to  show  the  nature  of  the  infective  material  which,  when  carried 
from  the  sick  to  the  healthy,  produced  the  disease. 


MTIOLOGY  1949 

In  1871  von  Recklinghausen  found  micrococci  in  the  bodies  of 
persons  dying  from  puerperal  fever.     The  next  important  step  was 
the  discovery  by  Pasteur  in  1878-79  of  his  '  microbe  en  chapelet 
iri  the  blood  of  puerperal  fever  patients. 

As  this  organism  belonged  to  the  genus  named  streptococcus  by 
Billroth,  in  1874,  Arloing  gave  it  the  name  Streptococcus  puerperalis, 
in  1884,  apparently  believing  that  it  was  distinct  from  the  organism 
named  S.  erysipelatos  Fehleisen,  1883,  which  is  more  popularly 
known  as  5.  pyogenes  Rosenbach,  1884.  Later  Furneaux-Jordan 
and  Mackay  have  revived  S.  puerperalis,  but  Arloing's  name  has 
priority  and  stands  for  a  synonym  of  S.  erysipelatos. 

A  new  phase  of  the  bacteriological  history  was  opened  in  1893  by 
Veillon  finding  an  obligatory  anaerobic  micrococcus  in  such  diseases 
as  Ludwig's  angina,  suppuration  of  Bartholin's  glands,  phlegmonous 
perinephritis,  etc.  This  organism,  which  he  called  Micrococcus 
fcetidus  Veillon,  1893,  though  usually  a  diplococcus,  can  exist  in 
short  chains,  and  therefore  may  well  be  a  streptococcus.  Halle,  in 
1898,  found  it  in  the  secretions  of  the  normal  vagina  as  well  as  in 
pus  from  Bartholin's  glands  and  in  the  exudate  of  retained  placentae. 
It  was  next  observed  by  Jeannin  in  1907  to  be  present  in  numerous 
cases  of  putrid  puerperal  infection,  and  is  thought  by  Veillon's 
pupils  to  be  the  same  organism  as  the  anaerobic  streptococcus  found 
in  vaginal  secretion  in  1897  by  Menge  and  Kroenig,  whose  work  had 
beenquestionedbyKoblankbut  supported  by  Nat vig,  Schottmuller, 
and  Hamm. 

In  1907  Gioelli  reported  the  presence  of  a  coccus,  thought  to  be  a 
staphylococcus,  which  he  found  in  a  peri-uterine  abscess  and  named 
Coccus  anaerobius  Gioelli,  1907,  while  in  1908  he  dealt  with  the 
question  of  the  bacteriology  of  puerperal  infections.  As  this  coccus 
produces  fcetid  gas  it  may  well  be  the  same  as  Veillon's  organism. 

In  1910  Schottmuller  increased  our  knowledge  as  to  the  strepto- 
cocci in  puerperal  fever  by  finding  a  new  obligatory  anaerobe,  which 
he  called  Streptococcus  putridus,  and  which  he  found  not  merely  in 
puerperal  fever,  but  also  in  otitis  media,  meningitis,  cysto-pyelitis, 
abscess  of  the  lung,  gangrene  of  the  lung,  and  empyema,  and  he 
followed  this  up  in  1911  by  two  papers  upon  the  aetiology  of  febris 
puerperalis  said  febris  in  puerperio. 

In  fifty  cases  of  febris  puerperalis  he  found  the  following  organisms 
to  be  present  thirty-three  times — i.e.,  in  66  per  cent.,  and  in  all 
severe  and  fatal  cases: — 

S.  erysipelatos  Fehleisen,  1883,  in  fifteen  cases  in  the  uterine  discharges  and 
in  two  of  these  also  in  the  peripheral  blood.  S.  putridus  Schottmuller,  1910, 
in  fifteen  cases  in  the  uterus,  including  five  blood  infections.  5.  erysipelatos 
with  S.  putridus  three  times  in  the  uterine  discharge,  with  both  together  in 
the  blood  once  and  separately  in  the  other  two  cases. 

He  also  met  with  Streptococcus  mitior  seu  viridans,  an  aerobic 
organism  first  described  by  himself  in  1903,  in  the  uterus  and  blood 
of  one  case. 

He  considers  that  there  are  two  distinct  methods  of  infection:  the 


1950  DISEASES  OF  THE  GENERATIVE  SYSTEM 

first  is  the  autogenous,  caused  by  organisms,  like  S.  putridus,  which 
lives  in  the  normal  vaginae  of  pregnant  and  puerperal  women,  and 
are  capable  of  being  carried  from  the  vagina  to  the  uterus  by  means 
of  instruments  or  by  the  hand.  This  form  he  considers  to  be  non- 
contagious. 

The  second  method  of  infection  is  the  heterogeneous,  caused  by 
5.  erysipelatos,  and  brought  from  an  external  source  of  infection 
to  the  puerperal  woman  as  just  described. 

Von  Lingelsheim,  in  1912,  considered  that  the  importance  of 
S.  putridus  must,  for  the  time  being,  remain  undecided,  as  it  lacked 
confirmation,  but  it  is  obvious  that  the  gas  production  alone  differen- 
tiates this  streptococcus  from  S.  erysipelatos  Fehleisen,  and  it 
appears  to  us  that  there  is  a  general  agreement  between  Schott- 
miiller's  organism  and  that  described  by  Veillon.  They  both 
produce  foetid  gas,  they  both  are  obligatory  anaerobes,  md  they  are 
both  found  in  the  vagina  and  also  in  association  w  ith  puerperal  f ever; 
and  they  have  both  been  found  in  severe  infections  in  other  parts  of 
the  body.  They  are  probably  the  same  organism  as  the  anaerobic 
vaginal  streptococcus  described  by  Menge  and  Kroenig,  and  also 
that  found  by  Gioelli  in  1907. 

All  these  organisms,  in  our  opinion,  should  be  classified  under 
the  name  of  S.  fcetidus  Veillon,  1893. 

In  1901  Lewkowicz  found  an  obligatory  anaerobic  streptococcus, 
which  he  named  S.  anaerobius  micros,  in  the  mouths  of  sucklings. 
In  1907  Jeannin  reported  that  it  was  present  fairly  frequemly  in 
puerperal  infections.  It  is  described  as  being  lanceolate  and  usually 
disposed  in  diplococcal  forms,  and  only  occurring  in  short  chains. 

In  1812  Furneaux-Jordan  published  an  important  lecture  upon 
'  Puerperal  Infection.'  He  and  Mackay  examined  the  uterine 
discharges  of  twenty-one  cases  of  puerperal  fever,  and  found  strepto- 
cocci in  seventeen  cases — i.e.,  80  per  cent.  This  streptococcus  was 
identical  in  all  cases,  and  was  said  to  be  quite  distinct  from  other 
streptococci,  and  so  the  name  Streptococcus  puerperalis  Furneaux- 
Jordan  and  Mackay,  1912,  was  given  to  it ;  but  we  have  noted  that 
Arloing  had  already  applied  this  name  in  1884  to  a  streptococcus 
which  he  obtained  from  cases  of  puerperal  fever,  and  which  he 
believed  to  be  distinct  from  S.  erysipelatos  and  S.  pyogenes,  the  only 
named  forms  at  that  time,  but  at  present  all  three  are  considered 
to  be  one  and  the  same  organism. 

In  1916  Chalmers  and  Atiyah  found  that  S.  salivarius,  S.  bovis 
(synonym,  S.  bovinus),  and  S.  versatilis,  were  causal  germs  in  the 
Anglo-Egyptian  Sudan,  and  traced  the  origin  of  these  germs  to 
human  saliva  (S.  salirarius),  zibla- — i.e.,  horse-dung  used  for  walls 
and  floors — bovine  fasces,  and  equine  faeces,  etc.  (S.  bovis  and  S. 
versatilis). 

The  known  puerperal  streptococci  are  therefore: — 

1.  5.  erysipelatos  Fehleisen,  1883. 

2.  S.  fcetidus  Veillon,  1893. 

3.  S.  anaerobius  Lewkowicz,  1901. 


/ETIOLOGY— METHODS  OF  INFECTION  1951 

4.  S.  mitior  Schottmiiller,  1903. 

5.  5.  pusrperalis  Furneaux- Jordan  and  Mackay,  19 12. 

6.  5.  salivarius  Andrewes  and  H order,  1906. 

7.  S.  bovinus  Broadhurst,  1915  (synonym,  S.  bovis  Chalmers  and 
Atiyah,  1916). 

8.  S.  versatilis  Broadhurst,  1915. 

Other  Organisms. — Streptococci  are,  however,  by  no  means  the  only  organ- 
isms found  in  puerperal  fever,  as  the  following  have  also  been  recorded: 
Aurococcus  aureus  (Rosenbach,  1884);  Albococcus  tetragenus  (Gaffky,  1884); 
Diplococcus  pneumonice  (Weichselbaum,  1887);  Diplococcus  gonorrhoea  (Bumm, 
1885);  Bacillus  coli  (Escherich,  1886);  but  Bacillus  typhosus  (Zopf,  1885) 
(Eberth's  bacillus)  only  rests  under  suspicion,  while  B.  pseudodiphtheriticus 
has  also  been  reported . 

Among  the  anaerobic  organisms  other  than  streptococci  the  following  have 
been  met  with  in  puerperal  infections :  Bacillus  emphysematosce  (Frankel,  1893) ; 
Bacillus  telani  (Fliigge,  1886);  and  a  vibrio  described  by  Curtis  in  1913,  and 
probably  by  Kroenigin  1895,  which,  though  deserving  of  a  definite  appellation, 
is  still  unnamed. 

Abortion. — A  very  interesting  point  is  the  question  whether  the  same  organ- 
isms are  found  post  abortum  as  post  partum.  This  was  investigated  by  Schott- 
miiller in  191 1,  more  particularly  in  criminal  abortions,  with  the  result  that 
he  found  the  following  organisms  arranged  in  order  of  frequency  to  be  present: 
5.  putvidus,  a  Staphylococcus,  B.  coli,  and  B.  emphysematosce ,  while  5.  erysipe- 
latos  was  relatively  rarely  met  with. 

Febris  in  Puerperio. — -Another  point  of  interest  is  the  organisms  causing 
febris  in  puerperio — i.e.,  the  slight  fever  known  by  Willis'  name  of  lacteal  or 
milk  fever,  which  is  frequently  met  with  post  partum.  This  has  also  been 
investigated  by  Schottmiiller  and  Heymann,  who  found  the  following  germs  to 
be  present:  5.  putridus,  a.  Staphylococcus,  B.  coli,  B.  erysipelatos,  B.  vagincs,  and 
B.  emphysematosa',  arranged  in  order  of  frequency. 

Thus  it  would  appear  that  the  same  organisms  occur  in  the  mild  and  in  i he- 
severe  infections,  a  fact  which  places  on  a  sound  basis  Willis'  observation  that 
the  mild  lacteal  may  become  the  severe  putrid  fever. 

Methods  of  Infection. — Adverting  to  the  methods  of  infection  of 
the  parturient  woman,  we  note  that  Geddes  in  his  '  Statistics  of 
Puerperal  Fevers,'  published  in  1912,  says  that  he  believes  99  per 
cent,  of  the  cases  are  due  to  those  conducting  the  labour.  A  state- 
ment of  this  nature  makes  it  imperative  to  possess  some  knowledge  as 
to  the  presence  or  absence  of  bacteria  in  the  normal  vulva,  vagina, 
and  uterus. 

This  has  been  investigated  by  many  workers  whose  researches  make  apparent 
that  the  vulva  at  birth  is  germ  free,  but  after  seven  to  eight  hours  it  contains 
micro-organisms  which  have  probably  been  acquired  from  the  secretion  of  the 
mother's  vagina,  the  air,  and  the  water  of  the  first  bath.  As  a  rule  the  follow- 
ing organisms  are  described  as  being  present  in  the  normal  vulvar  secretion : 
Obligatory  aerobes  :  Albococcus  tetragenus,  B.  coli,  and  B.  pseudodiphtheriticus. 
Aerobes  and  facultative  anaerobes  :  Albococcus  albus  and  B.  vagina.  Obligatory 
anaerobe  :  a  Streptococcus,  probably  S.fcetidus. 

With  regard  to  the  vagina  this  appears  to  be  free  from  micro-organisms  at 
birth,  at  which  time  its  secretion  is  acid,  which  is  said  to  be  due  to  carbonic  acid, 
and  is  also  bactericidal,  an  action  which  cannot  be  due  to  leucocytes,  which  are 
normally  absent. 

Some  twelve  hours  after  birth  the  first  bacteria  can  be  found  therein.  The 
secretion  remains  acid  during  life,  but  is  now  due  to  lactic  acid,  which  is  said 
to  be  present  in  a  strength  of  0*4  per  cent.,  and  appears  to  be  associated  with 
an  organism,  Bacillus  vagince  Doderlein,  1893. 


1952  DISEASES  OF  THE  GENERATIVE  SYSTEM 

The  normal  adult  secretion  has  a  bactericidal  action  when  tested  against 
staphylococci,  streptococci,  and  bacteria,  but  saprophytic  organisms  can  grow 
therein  and  may  be  obligatory  or  facultative  anaerobes,  but  are  generally  charac- 
terized by  having  acidophile  tendencies.  Anaerobic  organisms  are  common, 
but  obligatory  aerobes  are  not  frequently  met  with.  Pathogenic  organisms  are 
relatively  seldom  found  in  the  normal  secretion,  being  generally  Staphylococci, 
B.  coli,  and  B.  pseudodiphtheriticus. 

With  regard  to  the  normal  vaginal  secretion  during  the  puerperium,  its 
bactericidal  powers  are  markedly  increased  by  the  lochia,  and  they  do  not  return 
to  normal  until  several  days  after  the  birth  of  the  child.  Notwithstanding 
this  fact,  obligatory  and  facultative  anaerobic  streptococci,  staphylococci, 
and  bacteria  are  to  be  found,  as  has  already  been  indicated,  and  this  fact  appears 
to  us  to  be  of  the  greatest  importance  when  considering  the  method  of  infection 
of  puerperal  fever. 

The  secretion  of  the  normal  uterus  is,  by  a  consensus  of  opinion,  considered 
to  be  sterile. 

It  would  thus  appear  as  though  Geddes  was  correct  in  throwing 
the  responsibility  of  puerperal  infection  upon  the  attendants,  as 
both  autogenetic  and  heterogenetic  infections  are  probably  due  to 
them  in  some  way,  but  the  former  is  much  more  difficult  to  prevent 
than  the  latter. 

With  regard  to  the  latter,  the  researches  of  Chalmers  and  Atiyah 
have  thrown  suspicion  upon  cow  and  horse  dung  as  sources  of 
infection,  and  this  has  been  confirmed  by  the  work  of  Chalmers 
and  Marshall,  who  found  the  same  organisms  in  bovine  and  equine 
fseces. 

There  are  three  native  uses  of  cow  and  horse  dung,  and  they  are : — 

i .  Cow-dung  Poultice. — This  is  commonly  used  by  natives  throughout  the 
Sudan,  and  is  placed  on  any  painful  region  of  the  body,  and  is,  at  times,  applied 
to  the  lower  part  of  the  abdomen  and  even  to  the  external  genitalia  of  the  preg- 
nant woman,  and  in  this  way  may  bring  about  an  infection  of  the  vagina  with 
bovine  types  of  streptococci. 

2.  Cow-dung  Wash. — In  many  parts  of  the  tropics  it  is  not  uncommon  for 
the  natives  to  use  a  cow-dung  wash  for  the  floors  and  walls  of  dwelling-rooms 
for  the  purpose  of  keeping  away  biting  insects  and  also  white  ants,  and  although 
the  practice  does  occur  in  the  Anglo-Egyptian  Sudan  it  is  not  so  common  as 
in  other  parts  of  Africa  and  in  parts  of  Asia. 

Cow-dung,  however,  is  used  in  Khartoum  and  Omdurman  as  a  wash  for  the 
tops  of  ovens,  and  especially  of  those  used  for  baking  bread,  and  also  for  the 
walls  of  outhouses,  especially  those  used  for  storing  grains. 

3.  Zibla. — It  is  also  used  at  times  in  lieu  of  horse-dung  as  a  constituent  of 
a  mixture  called  zibla  which  is  applied  to  roofs  and  walls. 

As  this  wash  dries  it  must  form  dust,  which  must  pollute  the  air 
and  be  driven  hither  and  thither  by  the  strong  winds,  which  are 
often  present  in  certain  areas  of  the  Sudan,  and  as  the  researches 
of  Andrewes  and  Horder  have  demonstrated  that  streptococci  are 
resistant  to  desiccation,  it  is  possible  that  the  dust  derived  from  dried 
cows'  dung  may  contaminate  the  sterile  instruments  and  hands 
of  the  attendants  on  the  parturient  woman,  and  so  bring  about 
puerperal  infections,  which  would  belong  to  the  heterogenetic  type. 

Once  the  disease  has  been  started  it  is  always  possible  for  new 
cases  to  be  infected  from  previous  cases  by  the  agency  of  attendants, 
and  in  this  way  an  epidemic  may  arise  at  any  time,  or,  failing  this, 
the  infections  may  be  kept  up  indefinitely  by  the  same  means. 


PATHOLOGY  1953 

Pathology. — The  post-mortem  anatomy  shows  some  of  the  features 
well  known  in  Europe. 

Symptomatology. — There  seems  to  be  no  doubt  that  the  same 
organisms  can  cause  the  mild  '  febris  in  puerperio/  and  the  severe 
'  febris  p  ic.peralis.' 

Why  there  should  be  such  a  difference  is  not  clear,  and  must 
depend  in  some  way  or  another  upon  the  general  bodily  condition 
of  the  patient,  and  perhaps  upon  the  strength  of  the  streptococcal 
strain,  which,  as  is  well  known  from  laboratory  experiments,  varies 
considerably. 

Be  this  as  it  may,  there  can  be  no  doubt  that  one  and  the  same 
organism  infecting  the  uterus  can  cause  the  mild '  febris  in  puerperio ' 
or  '  milk  fever  '  and  the  more  severe  and  even  fatal  '  febris  puer- 
peralis,'  the  symptoms  of  which  vary  according  as  to  whether  there 
is  a  local,  more  or  less  extensive  infection,  or  a  septicaemia. 

Prognosis. — A  prognosis  may  be  arrived  at  by  observing  improve- 
ment or  the  reverse  in  the  clinical  symptoms,  but  more  accurate 
decisions  may  be  deduced  by  a  study  of  the  opsonic  indices  taken 
daily,  provided  that  the  causal  organism  is  known  and  is  available 
in  pure  culture,  the  index,  as  already  stated,  remaining  low  or 
sinking  in  serious  or  fatal  cases,  but  rising  as  improvement  sets  in. 

Diagnosis.— It  is  of  the  utmost  importance  that  any  fever  attack- 
ing a  puerperal  woman  in  the  tropics  should  be  assumed  to  be 
puerperal  fever  until  it  is  proved  to  be  something  else. 

The  presence  of  one  of  the  varieties  of  puerperal  fever  can  be 
confirmed: — 

i.  By  microscopical  examination  of  stained  smears  of  the  intra-uterine 
exudate  taken  aseptically  by  a  sterile  swab  passed  through  a  sterile  speculum 
inserted  into  a  previously  douched  vagina. 

2.  By  cultural  examinations  in  ascitic  broth  of  the  same  exudate  taken  in 
the  same  way,  and  incubated  aerobically  and  anaerobically  at  370  C.  and 
examined  at  the  end  of  twenty-four  and  forty-eight  hours. 

3.  By  a  low  opsonic  index  in  the  case  of  the  streptococcal  infections  as 
tested  against  the  causal  organism.  This  of  course  is  especially  applicable 
in  small  or  large  local  epidemics,  when  the  causal  organism  will  be  available  in 
pure  culture  in  the  local  bacteriological  institute. 

With  regard  to  the  differential  diagnosis,  the  most  important 
fever  whichrequires  attention  ismalaria  occurring  inthepuerperium, 
and  this  should  be  capable  of  easy  differentiation  by: — 

1.  An  examination  of  peripheral  blood  smears  for  the  parasites, 
or,  if  they  cannot  be  found,  by — 

2.  A  differencial  leucocytic  count,  with  the  discovery  of  a  distinct 
mononucleosis  which  cannot  be  explained  by  other  protozoal  infec- 
tions, such  as  amoebic  dysentery,  kala-azar,  etc. 

3.  Enlargement  of  the  spleen,  not  due  to  one  of  the  forms  of 
tropical  splenomegaly. 

If  these  three  tests  fail  to  decide  the  presence  or  absence  of 
malaria,  then  a  few  doses  of  quinine  should  be  administered,  and 
can  do  no  possible  harm,  and  may  even  benefit  the  patient  if  a  puer- 
peral infection  due  to  sfreptococci  or  bacteria  is  present.     In  our 

123 


1954  DISEASES  OF  THE  GENERATIVE  SYSTEM 

experience  this  quinine  is  best  administered  by  intramuscular 
injections,  with  or  without  oral  administration,  and  should,  in 
nervous  patients,  be  associated  with  a  dose  of  sodium  bromide.  If 
the  temperature  rapidly  declines  and  the  symptoms  improve  with 
the  quinine  therapy,  then  the  diagnosis  of  malarial  fever  may  be 
made,  but  if,  as  has  more  often  happened  in  our  experience,  the 
fever  continues,  then  the  disease  is  not  solely  caused  by  malarial 
parasites.  If  there  is  reason  to  suspect  that  the  puerperal  fever  is 
septicaemic  in  type,  or  if  early  enteric  fever  in  its  broades1  sense  is 
feared,  then  the  diagnosis  can  be  effected  by  removing  aseptically 
i  c.c.  of  peripheral  blood  from  a  vein  and  immediately  adding  this 
to  nutrient  broth  medium  contained  in  a  flask,  half  of  which  is  then 
incubated  aerobically  at  370  C,  while  the  other  half  is  incubated 
anaerobically  at  the  same  temperature,  and  both  are  examined  at 
the  end  of  twenty-four  and  forty-eight  hours. 

By  these  methods,  and  by  these  alone,  as  far  as  our  experience 
goes,  can  a  case  of  puerperal  fever  be  accurately  diagnosed. 

Treatment. — The  aim  of  the  rational  treatment  of  puerperal  fever 
must  be  to: — 

1.  Kill  the  causal  organisms. 

2.  Neutralize  their  toxic  effects. 

3.  Promote  the  normal  action  of  the  patient's  organs. 

In  order  to  kill  the  causal  organisms  they  must  be  attacked  in  the 
positions  in  which  they  are  living,  and  as  this  is  usually  the  wall  of 
the  uterus,  it  is  necessary  to  give  the  patient  an  anaesthetic  as  soon 
as  possible  and  to  thoroughly  investigate  the  walls  of  the  uterine 
cavity  in  order  to  discover  any  portions  of  placenta,  membranes, 
or  blood-clot,  and  at  the  same  time  to  observe  whether  there  is  any 
abscess  formation  in  the  vicinity  of  the  uterus  and  also  whether  there 
is  any  inflammation  of  the  tubes,  both  of  which  conditions  being 
treated  if  present. 

Usually  all  that  is  necessary  is  the  removal  of  offending  sub- 
stances from  the  uterus  by  means  of  a  mild  and  modified  form  of 
curettage,  followed  by  a  thorough  antiseptic  irrigation  of  its  cavity, 
which  is  then  drained. 

After  this  the  vagina  and  uterus  should  be  irrigated  twice  or  three 
times  a  day  with  an  antiseptic  solution  in  bad  cases,  and  less  fre- 
quently in  mild  cases. 

With  reference  to  the  second  heading — viz.,  the  toxic  effects  of 
the  organisms — if  these  are  at  all  marked  they  should  be  combated 
at  once  by  means  of  injections  of  antistreptococcal  serum  if  these 
ar ;  the  causal  organisms,  and  by  saline,  subcutaneous,  or  intravenous 
injections,  which  should  be  given  early  and  not  reserved  until  too 
late  for  beneficial  results  to  follow. 

The  third  point  is  a  matter  of  common  knowledge,  and  need  not 
delay  us  here. 


REFERENCES  1955 


SUTIKA. 


Synonym. — The  puerperal  diarrhoea  of  Bengal. 

Under  the  above  term  Dr.  Pearse,  the  Medical  Officer  of  Calcutta, 
gives  an  account  of  a  chronic  diarrhoea  associated  with  fever  which 
causes  a  death-rate  of  1-3  per  cent,  in  the  total  number  of  registered 
births  in  Hindu  and  Mohammedan  puerperal  women  of  all  ages  in 
that  city. 

The  disease  begins  with  diarrhoea  some  two  or  three  weeks  after 
delivery,  there  being  five  to  fifteen  watery,  frothy,  fermenting 
motions  per  diem  without  blood  or  mucus.  Along  with  the  diarrhoea 
there  may  be  loss  of  appetite  and  dyspeptic  symptoms,  rarely 
vomiting,  but  no  griping  pains  or  abdominal  tenderness.  The 
temperature  is  raised,  and  an  irregular  fever  lasts  throughout  the 
illness.  There  is  no  vaginal  discharge;  oedema  of  the  feet  is  noted 
as  a  late  symptom.  The  course  of  the  disease  varies.  Sometimes 
it  is  rapid,  and  kills  the  patient  in  a  few  months;  more  usually  it 
lasts  five  to  eight  months,  and  less  usually  it  continues  for  more 
than  twelve  months.  Towards  the  end  the  patient  becomes  weak 
and  emaciated,  and  dies  of  exhaustion.  The  case-mortality  is  not 
known. 

The  nature  of  this  disease  is  obviously  obscure,  and  requires 
investigation. 

REFERENCES. 

Endemic  Funiculitis. 

Castellani  (1904-14).     Ceylon  Medical  Reports. 

Castellani  (1908).     Lancet,  July. 

Castellani  (1908).     Annali  Med.  Navale,  April  and  May. 

Castellani  (1909).     British  Medical  Journal. 

Coutts  (1909).     Lancet. 

Goebel  (191 1).     Chirurgie  der  Heissen  Lander. 

Jones  (1909).     Lancet. 

Madden  (1907).     Lancet. 

Pfister  (1909).     Folia  Urologica. 

Wise  (1910).     Journal  of  Tropical  Medicine. 

Sutika. 

Pearse  (1908).     Journal  of  Tropical  Medicine,  November. 
Robertson    (1846).     Edinburgh   Medical  and   Surgical   Journal,   clxvii.   5b 
(Puberty  in  Indian  Women). 


I95& 


DISEASES  OF  THE  GENERATIVE  SYSTEM 


ADDENDUM. 
REMARKS  ON  ANTENATAL  AND  POSTNATAL  PATHOLOGY. 

General  remarks — Antenatal  pathology — Postnatal  pathology — References. 

General  Remarks. 

We  think  that  perhaps  a  few  remarks  concerning  antenatal  and 
postnatal  pathology  may  be  of  interest. 

Antenatal  Pathology. 

Much  useful  work  has  been  done  of  late  in  Calcutta  and  other 
tropical  towns  by  means  of  lady  health  visitors,  by  the  training 
and  provision  of  midwives,  as  well  as  by  the  training  of  school- 
teachers and  school-girls  in  matters  connected  with  hygiene.     The 


Fig.  784. — Polydactyi.ism. 

effect  of  skilled  attention  at  the  time  of  birth  has  been  indicated  by 
the  entire  absence  of  tetanus  neonatorum  amongst  babies  delivered 


Fig.  785. — Cyclops. 
(From  a  photograph  by  Sambon.) 

by  the  municipal  nrdwives  in  Calcutta,  and  by  the  extraordinarily 
low  death-rate  under  simUar  conditions  durinj  the  first  week  of 
life,  as  related  by  Miss  Lewis. 


ANTENATAL  PATHOLOGY 


1957 


There  can  be  no  doubt  that  this  is  the  right  step  to  cc-mbat  such 
diseases  as  puerperal  fever  and  infantile  mortality,  but  in  order 
to  insure  the  birth  of  a  healthy  child  the  mother  should  be  medically 
advised  in  the  early  days  of  pregnancy,  and  suitable  medicines 
given,  if  necessary,  as  so  many  monstrosities  and  abnormalities 
appear  in  the  tropics  that  some  care  is  required  to  diminish  their 
numbers. 


Fig.  786. — Ischiopagus  Tripus. 

Since  the  days  of  Licetus  many  attempts  have  been  made  to 
classify  monstrosities  by  such  authorities  as  Buff  on,  Blumenbach, 
Meckel,  Bischoff,  Foerster,  Fischer,  Ahlfield,  and  others,  while 
Ballantyne  has  written  a  most  interesting  book  on  the  subject. 

We  have  always  used  the  classification  introduced  by  Hirst  and 
Piersol  in  1892,  and  have  found  it  useful.     It  is  as  follows: — 

Hemiterata. — Anomalies  of  volume,  form,  colour,  structure,  disposition, 
number,  and  existence. 

Heterotaxis. — Splanchnic  inversion  and  general  inversion. 

Hermaphrodites. — True,  including  bilateral,  unilateral,  and  lateral,  and  false 
— i.e.,  with  double  sexual  external  genitalia,  but  unisexual  glands. 


1958  DISEASES  OF  THE  GENERATIVE  SYSTEM 

Monsters. — These  are  divided  into: — 

A.  Single  monsters  : — 

I.  Autositic: — ■  Ectromelus,       Symelus,      Exencephalus, 
Pseudencephalus,  Anencephalus,  Cyclocephalus,  and 
Otocephalus. 
II.  Omphalosite : — Paracephalus,      Acephalus,    Asomata, 
and  Anideus. 


Fig.  787. — Syncephalus  or  Janus. 
(This  form  of  monster  is  fairly  common  in  Ceylon.) 

B.  Composite  monsters  : — 

I.  Double  autositic  : — 

(a)  Terata  katadidyma  :— Diprosopus,    Dicephalus, 
Ischiopagus,  Pyopagus. 

(b)  Terata     anadidyma  : — Dipygus,     Syncephalus, 
Craniopagus. 

(c)  Terata    anakatadidyma  : — Prosopothoracopagus, 
Omphalopagus,  Rachipagus. 


POSTNATAL  PATHOLOGY  1059 

II.  Double  parasitic: — Heterotypic,     Hetet alius,    Poly- 
gnathus, Polymelus,  and  Endocyma. 
III.  Triple  monsters. 

Foetal  monstrosities  and  abnormalities  appear  to  be  much  commoner 
in  the  tropics  than  in  the  other  parts  of  the  world,  or  else  we  have 
been  singularly  fortunate  in  meeting  with  them.  This  is  hardly 
the  place  to  give  a  detailed  account  of  these  abnormalities,  but  we 
should  advise  the  tropical  practitioner  to  have  some  elementary 
ideas,  at  all  events,  on  the  subject,  and  therefore  we  indicate  in  the 
above  classification  the  varieties  known  and  in  the  references  the 
works  dealing  with  this  subject.  We  have  met  with  the  following : — 
Foetus  papyraceus,  cyclops,  agnathia:  several  double  monsters  of 
both  general  types,  including  a  specimen  of  symmetrical  janus; 
acephalic  monsters;  and  rachischisis,  meningocele,  non-development 
of  the  eye,  coloboma  iridis,  hare-lip,  cleft  palate,  branchial  fistula, 
non-development  of  the  thigh.  Microdactylism  has  been  reported 
from  the  Philippines,  and  pes  gigas  from  China. 

Further,  McCarrison  and  others  have  shown  that  endemic  cretin- 
ism is  brought  about  by  goitre  in  the  mother,  combined  with  psychic 
impressions  or  illnesses  during  the  pregnancy,  as  well  as  with  nutri- 
tional difficulties  and  difficult  labour;  and  it  should  be  the  duty  of  the 
Government  of  districts  in  which  goitre  is  endemic  to  take  steps  to 
combat  these  factors. 

Postnatal  Pathology. 

The  infantile  mortality  of  the  tropics  is  much  higher  than 
that  in  the  Temperate  Zone,  and  must  be  combated  by  '  Baby 
Welfare  Work, '  as  in  Europe,kwit  h  a '  Baby  Clinic  '  in  all  the  hospitals. 
In  Calcutta  daily  visits  are  paid  by  the  midwives  during  the  puer- 
peral period,  and  then  the  work  is  carried  on  by  the  lady  health 
visitor  by  weekly  visits  until  the  child  is  three  months  old.  Among 
other  matters,  the  feeding  of  the  mother  is  attended  to  by  organized 
private  charity.  A  pure  milk  supply  is  an  essential  in  every  com- 
munity, and  should  be  under  Government  control  and  at  a  cheap 
rate. 

Meningitis  is  rare  among  the  newborn,  and  seems,  according  to 
Barron,  to  be  mostly  associated  with  spina  bifida  and  to  be  caused 
by  Bacillus  coli,  staphylococci,  streptococci,  and  more  rarely  by  the 
pneumococcus,  the  meningococcus,  B.  lactis  aerogenes,  or  B.  pyo- 
cyaneus  ;  but  of  dl\,B.  coli  is  the  most  important  according  to  him. 
>  Breast-feeding  is  most  important,  and  it  may  be  that  it  helps 
to  raise  the  resistance  of  the  infant  against  disease. 

Weaning  is  a  difficult  and  dangerous  period  in  the  tropics,  and 
it  is  considered  that  if  possible  a  child  should  not  be  weaned  in  the 
very  hot  weather. 

In  calculating  out  the  dilutions  necessary  for  cow's  milk  it  will 
be  remembered  that  the  milk  of  the  Bos  indicus,  the  humpbacked 
cow,  is  very  rich  in  fat,  attaining  generally  about  5  per  cent,  thereof. 


i960  DISEASES  OF  THE  GENERATIVE  SYSTEM 

The  great  danger  of  this  period  is  diarrhoea  or  dysentery  from 
infections  with  amoebae  or  bacilli. 

All  the  diseases  which  attack  adults  in  the  tropics  may  affect  the 
child  after  birth,  and  the  special  features  which  they  show  have 
already  been  recorded,,  as  well  as  the  treatment,  in  the  chapters 
on  the  various  diseases,  and  need  not  be  repeated;  but  the  danger 
of  the  child  being  infected  with  tuberculosis  is  very  great,  especially 
in  the  slums  of  large  towns. 

Dosage  of  Drugs. — As  we  have  often  been  asked  for  the  dosage 
of  drugs  in  young  children,  we  give  the  following  rules: — Several 
drugs,  but  especially  opium,  require  to  be  given  with  caution,  as 
children  are  especially  susceptible  to  them;  but  excluding  these,  the 
best  method  so  far  published  for  the  determination  of  dosage  by 
age  is  Cowling's  rule  with  Brunton's  modification. 

In  brief,  it  is  to  take  the  full  adult  dose  and  divide  it  by  a  factor 
obtained  by  placing  the  child's  age  at  its  next  birthday  over  twenty- 
four  if  the  ordinary  British  weights  and  measures  are  used,  and 
over  twenty-five  if  the  metric  system  be  employed.  Fcr  example, 
suppose  that  the  full  adult  dose  is  6  grains  and  the  child's  age  next 
birthday  is  four  years,  then  the  factor  is  „V  (*.*.,  5)  and  the  dose 
is  1  grain. 

REFERENCES. 

Ballantyne  (1902  and  1904).     Manual  of  Antenatal  Pathology.     Edinburgh. 
Calcutta    Report    (1918).     Journal    of    Tropical    Medicine    and    Hygiene, 

September  2. 
Hirst  and  Piersol  (1892).     Human  Monstrosities.     Edinburgh 
McCarrison  (1918).     Goitre.     London. 


CHAPTER  LXXXVII 
DISEASES  OF  THE  LYMPHATIC  SYSTEM 

General  remarks — Climatic  bubo — Volvulosis — References. 

GENERAL  REMARKS. 

The  lymphatic  system  is  affected  in  many  general  diseases — as,  fcr 
example,  in  plague  and  trypanosomiasis — and  in  cosmopolitan  affec- 
tions like  septic  disease,  syphilis,  tuberculosis,  etc.  In  addition, 
there  is  the  enlargement  of  the  glands  in  the  inguinal  region  called 
'  climatic  bubo,'  and  the  various  pathological  phenomena  caused 
by  Filaria  bancrofti.  These  morbid  changes  are  varices  of  lymph- 
channels,  inflammations,  and  elephantiasis,  and  have  already  been 
discussed  in  the  chapter  on  Filariasis.  The  pathological  changes 
caused  by  Onchocerca  volvulus  must  be  mentioned  here. 

With  regard  to  the  serous  membranes,  pleurisy  and  empyema  are 
common,  while  peritonitis  from  the  perforation  of  a  typhoid  ulcer 
or  the  perforation  of  the  bowel  by  an  Ascaris,  as  has  been  recorded 
by  Ziemann  in  the  Cameroons,  or  from  the  extension  of  some  septic 
area — e.g.,  a  gonorrheal  salpingitis — are  all  met  with.  Chylous 
ascites  is  rare. 

CLIMATIC  BUBO. 

Synonym. — Glandula  idiopathica  (Brooke). 

Definition. — Climatic  bubo  is  the  enlargement  of  the  inguinal 
glands  associated  with  pain  and  fever,  the  cause  of  which  is  unknown. 

History. — The  history  of  this  disease  only  dates  back  to  1896, 
when  Rugc  reported  several  cases  suffering  from  inguinal  buboes, 
in  which  the  usual  causes  of  such  an  adenitis  were  all  absent,  and 
he  was  therefore  inclined  to  consider  the  disease  a  separate  entity 
dependent  probably  on  climatic  influences.  About  the  same  time 
Goding,  independently  of  Ruge,  published  a  series  of  observations 
apparently  of  the  same  nature,  while  more  recently  cases  have  been 
reported  by  many  observers. 

The  disease  has  been  recently  investigated  by  many  observers — 
e.g.,  Ruffer,  Luzzatti,  Vanzetti,  Rost,  Nattan-Larrier,  Letulle,  Ley, 
and  others. 

Climatology.— The  chief  geographical  distribution  of  climatic 
bubo  is  the  East  Coast  of  Africa,  the  West  Indies,  the  Straits 
Settlements,  and  China,  but  it  may  be  met  with  in  any  tropical 

1961 


i962  DISEASES  OF  THE  LYMPHATIC  SYSTEM 

and  subtropical  region.  Le  Dantec  quotes  cases  occurring  in 
Mauritius,  Tonkin,  and  Madagascar.  Low  and  Castellani  have 
described  a  case  in  Uganda,  while  Luzzatti  has  met  with  several 
cases  in  Chili.  We  have  observed  cases  in  Ceylon,  and  Skinner 
has  described  numerous  cases  in  Bengal.  Climatic  bubo  may  also 
occur  in  the  Temperate  Zone,  for  Scheube  has  come  across  several 
cases  in  Japan,  Gabbi  in  Sicily,  and  Rost  in  other  Mediterranean 
districts. 

/Etiology. — Though  various  micro-organisms  have  been  described, 
the  aetiology  of  the  disease  is  still  obscure. 

Ferraro,  from  one  of  his  cases,  isolated  an  organism  practically  identical 
with  Bacillus  pestis.  Hewlett  isolated  from  the  affected  gland  a  bacillus  not 
decolourized  by  Gram,  the  characters  of  which  were  somewhat  similar  to  those 
given  by  Kitasato  in  his  first  description  of  B.  pestis  ;  for  Kitasato  stated  at 
first  that  the  B.  pestis  was  not  decolourized  by  Gram.  Low  and  Castellani 
were  not  able  to  grow  any  organism  from  their  case.  Some  authors  have 
isolated  the  ordinary  pyogenic  cocci. 

Martin,  Suger,  Le  Sueur,  and  Fleurant  consider  climatic  bubo  to  be  a 
manifestation  of  malaria.  Schimm  believes  the  bubo  to  be  secondary  to  some 
intestinal  infection.  G.  Rost  believes  the  affection  to  be  of  sexual  origin, 
and  due  to  a  micro-organism  living  in  the  vaginal  mucosa  of  native  women. 

According  to  Cantlie,  climatic  bubo  is  a  form  of  attenuated  plague — Pestis 
minor — basing  this  opinion  on  the  fact  that  in  Hong  Kong  he  observed  several 
cases  of  so-called  climatic  bubo  to  precede  the  outbreak  of  an  epidemic  of 
true  plague.  He  has  been  confirmed  in  his  opinion  by  Hewlett's  discover 
mentioned  above.  Cantlie's  theory  is  supported  by  Luzzatti,  who  considers 
the  climatic  bubo  to  be  a  form  of  Parapestis.  Ernest  Black  suggests  that  the 
disease  may  be  due  to  an  insect  bite. 

Letulle  and  Nattan-Larrier  have  seen  in  the  cells  of  the  capillaries  minute 
bodies  which  they  believe  to  be  parasitic. 

In  our  opinion,  climatic  bubo  is  a  disease  per  se,  and  is  not 
related  to  plague. 

Predisposing  Causes. — The  condition  is  apparently  most  commonly 
met  with  in  sailors  and  stokers.  It  occurs  chiefly  in  young  adults, 
and  is  said  never  to  be  found  in  children. 

Pathology. — The  results  of  our  histological  researches  agree 
better  with  those  obtained  by  Vanzetti  in  Italy  on  the  material 
collected  in  South  America  by  Luzzatti  than  with  those  of  other 
authors. 

The  capsule  of  the  affected  gland  is  much  thickened,  and  the 
interstitial  tissue  is  very  abundant.  There  is  great  proliferation  of 
lymphocytes,  and  haemorrhagic  foci  are  noticeable  here  and  there. 
Very  characteristic  is  the  presence  of  numerous  typical  plasma  cells, 
while  the  so-called  retractile  Recklinghausen  cells  found  in  plague 
are  absent.  The  histological  structure  of  climatic  bubo  is,  therefore, 
totally  different  from  that  of  the  plague  bubo,  in  which,  as  was 
shown  by  the  classical  histological  investigation  of  Duerck,  plasma 
cells  are  absent  or  extremely  rare,  while  the  so-called  retractile 
Recklinghausen  cells  are  numerous. 

Symptomatology. — The  length  of  the  incubation  is  not  known, 
but  according  to  some  observers  it  may  be  prolonged.  Ley  and  Rost 
believe  that  it  can  extend  to  many  weeks.    The  onset  is  generally 


PATHOLOGY— DIAGNOSIS  1963 

gradual;  after  perhaps  two  or  three  days  of  vague  malaise  and  slight 
fever,  the  patient  complains  of  pain  in  one  or  both  of  the  inguinal 
regions,  which  increases  on  walking.  On  examining  the  parts, 
one  or  more  inguinal  glands,  or  occasionally  the  crural  glands  on 
both  sides,  or  more  frequently  one  side  only,  will  be  found  to  be 
enlarged,  very  painful  on  pressure,  and  hard.  The  swelling  may  be 
as  large  as  a  goose's  egg.  There  will  be  no  signs  of  lymphangitis 
present.  The  glands  may  become  greatly  enlarged,  reaching  the 
size  of  a  hen's  egg  or  larger,  but  in  most  cases  do  not  suppurate. 
Aspiration  by  means  of  a  syringe  will  draw  only  a  little  gland- 
juice,  occasionally  blood-stained,  but  no  pus.  The  liquid  will  be 
found  to  be  sterile. 

Fever  is  often  present  of  an  irregularly  remittent  or  inter- 
mittent type.  It  rarely  exceeds  1020  F. ;  and  is  higher  at  night 
than  in  the  morning.  The  duration  of  the  disease  is  variable,  from 
a  few  days  to  several  weeks,  and  rarely  months.  In  time  the  pain 
in  the  affected  region  gradually  disappears,  the  size  of  the  enlarged 
glands  decreasing.  As  a  rule,  the  affected  glands  remain  larger 
than  normal,  but  not  painful,  long  after  the  illness  is  over.  Occa- 
sionally a  relapse  occurs.  The  general  health  is  not  much  affected, 
though  the  patient  may  be  very  weak  and  unfit  for  work.  The 
spleen  is  not  enlarged.  The  examination  of  the  blood  may  reveal 
a  slight  leucocytosis;  Wassermann's reaction  is  negative;  the  urine  is 
normal.  Occasionally  a  trace  of  albumen  may  be  present.  Intes- 
tinal symptoms  are  generally  absent. 

Clinical  Varieties. — In  our  experience  an  acute,  a  subacute,  and 
a  chronic  type  of  climatic  bubo  may  be  distinguished.  The  acute 
type  is  always  accompanied  by  fever  and  severe  pains  in  the 
affected  glands.  All  the  symptoms  disappear  within  five  to  ten 
days.  In  the  subacute  and  chronic  type  lasting  from  a  few  weeks 
to  several  months  the  onset  may  be  insidious,  without  any  local 
pain  at  first,  and  fever  may  be  absent  altogether.  Moreover,  in 
some  cases  the  periglandular  tissues  become  inflamed,  suppuration 
may  take  place,  and  fistulous  tracks  may  develop. 

Diagnosis. — -The  absence  of  soft  chancre  on  the  genital  organs 
will  exclude  venereal  bubo  ;  the  absence  of  lymphangitis,  infected 
wounds,  insect-bites  on  the  legs  and  feet  will  exclude  the  ordinary 
symptomatic  bubo.  In  contrast  to  plague,  the  patient  does  not  look 
very  ill,  but  the  only  satisfactory  way  to  differentiate  acute  climatic 
bubo  from  a  mild  case  of  plague  is  the  puncture  of  the  affected  glands 
and  the  bacteriological  examination  of  the  gland-juice.  To  do  this 
the  skin  of  the  inguinal  regions  is  thoroughly  cleansed  with  spirit 
and  ether,  them  disinfected  with  a  perchloride  (1  in  1,000)  or  carbolic 
lotion  (5  per  cent.),  then  washed  again  with  ether  or  spirit,  or  more 
simply  the  skin  may  be  painted  with  tincture  of  iodine.  One  of  the 
enlarged  glands  is  then  aspirated  with  a  sterilized  syringe.  The 
gland- juice  which  is  drawn  off  is  then  examined  microscopically 
and  by  culture  method  in  the  ordinary  way  for  the  presence  of  the 
plague  bacillus. 


1964  DISEASES  OF  THE  LYMPHATIC  SYSTEM 

Climatic  bubo  is  generally  easily  distinguishable  from  attacks  of 
filarial  lymphadenitis,  which  is  generally  accompanied  by  very  high 
fever  and  severe  lymphangitis,  and  an  erysipelatous-like  condition 
of  the  leg.  During  and  after  various  intestinal  infections— as,  for 
instance,  typhoid  and  paratyphoid — occasionally  a  suppurative 
inflammation  of  some  lymphatic  glands — sometimes  the  inguinal 
glands — occurs.  In  such  cases  the  history  of  the  case — the  fact  that 
the  bubo  comes,  as  a  rule,  to  suppuration — and  the  bacteriological 
examination  of  the  gland-juice,  which  in  true  climatic  bubo  is 
sterile,  will  clear  the  diagnosis. 

Prognosis. — The  prognosis  is  favourable,  though  in  some  cases 
the  affection  may  last  for  several  months.  A  relapse  may  occa- 
sionally occur  shortly  after  the  first  attack  is  over,  sometimes 
on  the  side  previously  affected,  sometimes  on  the  other  side. 

Treatment. — The  treatment  is  merely  symptomatic,  consisting  cf 
complete  rest,  application  of  lead  lotion  on  the  affected  region,  or 
an  ichthyol  and  belladonna  ointment,  together  with  the  administra- 
tion of  a  mild  aperient,  and,  if  there  is  much  pain,  a  hot  fomenta- 
tion locally,  together  with  small  doses  of  opium  by  the  mouth.  In 
the  rare  cases,  where  signs  of  suppuration  are  noticeable,  incision 
of  the  glands  is  necessary,  using  the  ordinary  aseptic  precautions. 
In  protracted  cases  complete  surgical  removal  is  the  best  treatment. 
When  the  glands  remain  enlarged  after  the  acute  stage  has  passed 
off,  local  applications  of  tincture  of  iodine,  iodine  valsol,  or  an 
ointment  composed  of  30  grains  each  of  lead  iodide  and  potassium 
iodide  to  1  ounce  of  vaseline  may  be  of  benefit.  X-ray  treatment 
has  been  recommended  by  G.  Rost. 

VOLVULOSIS. 

Definition. — Volvulosis  is  a  disease  caused  by  Onchocerca  volvulus 
Leuckart,  1893,  and  characterized  by  the  formation  of  fibrous, 
cutaneous,  or  subcutaneous  tumours. 

History. — As  already  mentioned  on  p.  649,  these  tumours  were 
discovered  by  a  German  medical  missionary  to  contain  worms, 
which  were  described  by  Leuckart  in  1893,  and  subsequently  the 
disease  and  its  causative  worm  were  studied  by  Labadie-Lagrave 
and  Deguy  in  1899,  Prout  in  190 1,  Brumpt  in  1904,  Ziemann  and 
Vedy  in  1907,  and  Fiilleborn  in  1908,  the  last  paper  being  a  most 
valuable  contribution  to  our  knowledge  of  the  s-ubject. 

Climatology. — -The  disease  is  found  in  Africa,  at  Sierra  Leone, 
on  the  Gold  Coast,  and  in  Dahomey,  Cameroons,  and  the  north- 
east of  the  Congo,  where  it  is  variously  stated  to  affect  from  1  per 
cent,  to  10  per  cent,  of  the  population,  being  distributed  along  the 
banks  of  rivers.  Brumpt  found  it  along  the  Welle,  Cooke  in  Uganda, 
and  Parsons  in  Northern  Nigeria. 

/Etiology. — The  disease  is  caused  by  Onchocerca  volvulus  Leuckart, 
1893,  but  the  method  by  which  this  worm  is  introduced  into  the 
human  body  is  quite  unknown,   as  is  also  its  life-cycle  outside 


PA  THOLOGY— SYMPTOM  A  TOLOGY 


1965 


human  beings.  Brumpt  has,  however,  suggested  that  it  will 
probably  be  found  in  a  tsetse-fly,  because  of  its  riverine  distribution 
and  the  fact  that  microfilariae  have  been  found  in  the  peripheral 
circulation  by  Fiilleborn,  Rodenwalt,  and  others. 

Pathology. — The  adult  worms  lie  in  lymphatics,  the  anterior  end 
of  the  female  being  in  close  approximation  to  the  posterior  end 
of  the  male,  because  the  apertures  of  the  genital  apparatus  lie  in 
these  positions.  By  some  means — possibly  by  the  presence  of  the 
Mic  ofilarii,  or  possibly  by  toxic  waste-products— these  worms 
irritate  the  lymphatics^  causing  lymphangitis  and  perilymphangitis. 
These  inflammatory  processes  eventually  lead  to  the  formation  of  a 
fibrous  capsule  around  the  worms,  which  then  lie  in  a  portion  of  a 
vessel  cut  off  (?)  from  the  rest  of  the  lymphatic  system,  and  which 
forms  a  fibrous  subcutaneous  nodule  containing  male  and  female 
worms  and  Microfilaria. 


Fig.  7S8.- 


-Tumour  containing  Onchocerca  volvulus  Leuckart. 
(After  Fiilleborn.) 


On  opening  one  of  these  tumours  it  is  seen  to  consist  of  a  capsule 
of  fibrous  connective  tissue,  beneath  which  is  some  soft  caseous 
material  composed  of  endothelial  cells,  granular  debris,  and  Micro- 
filaria, and  to  enclose  a  central  space  containing  a  greenish,  semi- 
purulent  fluid.  The  worms,  which  are  usually  cut  across  in  several 
places  when  opening  the  tumour,  lie  partly  in  this  central  cavity 
and  partly  in  narrow  twisted  tunnels,  which  ramify  through  the 
walls  of  the  fibrous  capsule,  giving  it  a  network-like  appearance. 
Sometimes  the  central  cavity  is  not  obvious,  and  only  the  network 
of  tunn  'Is  is  seen  ramifying  through  the  connective  tissue. 

Symptomatology.— The  disease,  as  a  rule,  begins  insidiously  with 
malaise,  weakness,  vague  p  tins  in  various  regions  of  the  body,  and 
irregular  fever,  but  it  is  said  that  at  times  attacks  of  lymphangitis 


ig66  DISEASES  OF  THE  LYMPHATIC  SYSTEM 

may  be  noticed.  In  due  course  a  tumour  is  discovered  in  the  sub- 
occipital region,  the  elbow,  axilla,  side  of  the  chest,  iliac  region, 
gluteal  region,  or  popliteal  space.  These  tumours  vary  in  size  from 
a  pea  to  that  of  an  egg,  and  lie  in  the  skin  or  subcutaneous  tissue, 
in  which  they  are  freely  movable.  They  may  be  elastic  if  they 
contain  fluid,  or  firm  if  composed  mainly  of  fibrous  tissue.  They 
usually  remain  quiescent  for  years,  and  but  seldom  ulcerate. 

Bernard  and  Ouzilleau  believe  that  Onchocerca  volvulus  may  also  give  rise 
to  true  elephantiasis  in  certain  parts  of  Africa. 

Diagnosis. — The  presence  of  an  elastic  tumour  somewhat  re- 
sembling a  lipoma,  or  of  a  firm  fibrous  tumour  in  any  part  of  the 
body  of  a  person  who  has  resided  in  the  endemic  region,  should 
arouse  suspicions  as  to  the  presence  of  Onchocerca  volvulus. 

When  the  nodules  are  in  the  proximity  of  articulations  the  condi- 
tion may  closely  resemble  the  'juxt  a- articular  nodules '  (seep.  2260). 
The  microscopical  examination  of  the  contents  of  the  nodules 
obtained  by  tapping  with  a  syringe  or  by  excision  will  clear  the 
diagnosis. 

Prognosis. — These  little  tumour:  are  not  in  anyway  dangerous 
to  the  life  or  health  of  the  patient. 

Treatment. — Removal  by  incision  and  enucleation  is  quite  easy, 
and  devoid  of  danger. 

Prophylaxis. — As  the  life-cycle  of  the  parasite  is  unknown, 
nothing  can  be  said  as  to  prophylaxis. 


REFERENCES. 

Climatic  Bubo. 

Cantlie,  James  (1897).     Lancet,  January  2. 

Castellani  and  Low  (1903).     Journal  of  Tropical  Medicine,  December  15. 

Duerck  (1903).     Anatomischen  Veranderung  in  der  Bubonic  Pest.     Wien. 

Ferraro  (1903).     Ann.  Med.  Naval. 

Fleischner  (1909).     Archiv  fiir  Schiffs-  u.  Tropen-Hygiene. 

Gabbi  (1909).     Transactions  of  the  International  Medical  Congress,  Budapest. 

Goding  (1896-97).   British  Medical  Journal,  September  26,  1896;  and  June  12, 

1897- 
Luzzatti,  A.  (1906).     Ann.  Med.  Naval.,  p.  585. 
Manson  (191 8).     Tropical  Dieases.     London. 
Rost,  G.  (1912).     Archiv  fiir  Schiffs-  u.  Tropen-Hygiene. 
Ruge,  R.  (1896).     Archiv  fiir  Dermatol,  u.  Syph.,  No.  3. 
Sergent  and  Raynaud  (1918).     Bull.  Soc.  Path.  Exot.,  vol.  xi.,  No.  3. 
Skinner  (1897).     British  Medical  Journal,  January  9,  p.  78. 
Zur,  Werth  (1903).     Archiv  fiir  Schiffs-  u.  Tropen-Hygiene,  No,  1. 

Volvulosis. 

Brumpt  (1904).     Revue  de  Medecine  et  Hygiene  Trop. 

Fulleborn  (1908).     Beiheft  7,  Archiv  fiir  Schiffs-  u.  Tropen-Hygiene,  vol.  xii. 

Labadie-Legrave  et  Deguy  (1899).     Archiv.  de  Parasitologic,  p.  451. 

Manson  (1893).     Davidson's  Hygiene  and  Diseases  of  Warm  Climates,  p.  963. 

Prout  (1901).     British  Medical  Journal,  i.  209. 

Vf.dy  (1907).     Archiv  fur  Schiffs-  u.  Tropen-Hygiene,  p.  565. 


CHAPTER  LXXXVIII 

DISEASES    OF    CONNECTIVE    TISSUES, 
MUSCLES,  BONES  AND  JOINTS 

General  remarks — Somatic  taeniusis — Subcutaneous  filariases — Dracontiasis — 
Dermo-conjunctival  filariasis —  Loiasis  —  Calabar  swellings  —  Dubini's 
filariasis — Myositis  purulenta  tropica — Goundou — Boomerang  bones — 
Pes  gigas — Endemic  enlargement  of  the  os  calcis — References. 

GENERAL  REMARKS. 

The  diseases  of  the  connective  tissues  which  concern  us  are  mostly 
parasitic,  being  caused  by  the  cysticerci  of  tapeworms,  but  round 
worms  are  also  commonly  met  with,  especially  the  guinea-worm. 

With  regard  to  muscles,  a  disease  which  must  be  mentioned  is 
trichiniasis ,  which  is  said  to  be  far  from  rare  in  Northern  India. 
NecrosL,  caries,  and  tumours  of  bone  are  not  uncommon,  but 
rheumatoid  arthritis  is  rare,  and  tubercular  disease,  at  present,  is 
very  rare.  Gonorrheal  and  post-dysenteric  arthritis  are  met  with, 
and  filarial  synovitis  of  the  knee-joint  has  been  described  by 
Maitland.  Gout  is  rare,  but  we  have  seen  a  typical  case  in  a  native 
who  had  never  left  Ceylon. 

A  peculiar  condition  called  'trench  foot'  has  been  met  with  in  war  zones 
in  the  winter,  and  is  therefore  not  a  tropical  disease.  It  is  a  painful  con- 
gestion of  the  foot,  sometimes  leading  to  gangrene,  and  associated  with  the 
presence  of  spirochaetesand  other  organisms  in  the  bullae  (see  p.  2149). 

DISEASES   OF   CONNECTIVE  TISSUES. 

SOMATIC  T^ENIASIS. 

By  somatic  taeniasis  is  meant  the  invasion  of  the  body  by  the 
cysticercus  of  cestode  worms.  The  subject  is,  therefore,  divisible 
into — (a)  Cysticercosis,  or  infection  with  the  larvae  of  Tcenia  solium, 
which  occurs  now  and  again  in  the  connective  tissue  of  muscles, 
fasciae,  and  in  the  brain;  (b)  Echinococcosis,  which  is  the  infection 
of  the  body  with  the  hydatids  of  Echinococcus  granulosus,  and  of 
which  we  have  only  met  with  one  example  in  the  tropics,  and  even 
then  it  was  imported;  but,  judging  by  Begbie's  observations, 
it  would  appear  as  though  the  disease  was  endemic  in  Ceylon; 
(c)  Sparganosis,  which  is  the  invasion  of  the  body  by  Sparganum 
.m  inso.ii,  S.  baxteri,  or  S.  proffer,  all  of  which  have  been  sufficiently 
described  in  Chapter  XXV.,  p.  596. 

1967 


1 968  DISEASES  OF  CONNECTIVE  TISSUES 

THE  SUBCUTANEOUS  FILARIASES, 

Definition. — The  subcutaneous  filariases  are  infestations  of  the 
subcutaneous  tissue  by  the  adult  worms  of  species  belonging  to 
the  Filariidae  other  than  Filaria  bancrofti  Cobbold,  1877. 

Remarks. — The  form  of  filariasis  caused  by  F.  bancrofti  is  detailed 
in  Chapter  LXVL,  and  now  we  consider  those  in  which  the  adult 
worm  lives  in  the  subcutaneous  tissue.  The  varieties  of  this  form 
of  filariasis  are  dracontiasis,  or  guinea-worm  infection,  and  dermo- 
conjunctival  filariasis. 

DRACONTIASIS. 

Synonyms. — Dracunculosis,  Turkish  disease. 

Definition.- — Dracontiasis  is  the  infection  of  man  with  Dracunculus 
medinensis  (Linnaeus,  1758),  the  guinea-worm  (p.  651). 

History. — The  disease  has  been  knowr  from  very  remote  periods, 
and  it  is  probable  that  the  fiery  serpents  which  attacked  the 
Israelites  in  the  desert  were  guinea-worms,  and  that  the  serpent  on 
the  stick  was  an  illustration  of  the  method  of  extraction  advised. 

Plutarch  (a.d.  50-117)  gave  an  account  of  the  disease  as  seen  on 
the  shores  of  the  Red  Sea,  while  Galen  (a.d.  131-210),  who  never 
saw  a  case,  called  the  disease'  dracontiasis.'  Oribasius  also  mentions 
it  and  the  worm,  and  Aetius,  quoting  from  Leonides,  says  that  it 
occurs  in  the  legs  and  arms  of  people  in  Ethiopia  and  India.  Paul 
of  /Egina  stated  that  in  India  and  in  the  upper  part  of  Egypt  there 
was  a  class  of  worms  called  '  dracunculi,'  formed  in  the  muscular 
parts  of  the  body  such  as  the  arms,  thighs,  and  legs,  and  under  the 
skin  in  the  sides  of  children,  which  moved,  and  after  a  time  the  skin 
opened  and  the  head  came  out.  He  advises  that  this  be  fixed  with 
a  piece  of  lead,  the  part  placed  in  hot  water,  and  the  worm  gently 
pulled,  when  it  will  come  out  by  degrees;  but  if  during  this  process 
it  breaks,  there  will  be  much  pain.  Pollux  calls  it  a  corrupted 
nerve,  and  Actuarius  writes  about  its  presence  in  Egypt.  Avicenna 
calls  it  Vena  medina,  after  Medina,  where  it  was  common.  He  notes 
the  bleb  which  it  makes  in  the  skin,  and  its  protrusion  after  the 
bleb  bur^s.  He  recommends  ligatures  above  the  worm  and  baths 
to  make  it  come  out.  Huly  Abbas  says  that  it  occurs  in  India, 
Egyp+,  Ethiopia,  and  Libya,  while  Avenzoar  notes  that  it  is  most 
common  in  negroes.  Albucasis,  Rhases,  Bertapalia,  and  Guy  de 
Cauliac,  all  mentioned  the  disease,  and  the  last  named  calls  the 
worm  Vena  civilis  vel  medina,  while  Audry  considers  it  to  be  an 
animal.  Other  writers  on  this  subject  are  Joao  Rodrigues  de 
Castell  Branco  (1511-1568),  Linscholeri  (1599),  and  De  la  Motte 
Lambert  (1666).  In  1674  Velsch  wrote  a  book  on  the  subject  and 
siw  guinea-worms  everywhere. 

The  scientific  study  of  the  disease  and  its  parasite  dates  from  the 
work  of  Fedschenko  in  Central  Asia,  in  1870,  when  he  discovered  its 
development  in  the  cyclops,  the  integument  of  which  he  believed 
the  young  worms  pierced. 


DRACONTIASIS  1969 

Fedschenko's  observations  were  confirmed  by  Manson,  Blanchard, 
and  by  Wenyon  working  in  the  Sudan.  The  Cyclops  swallow  these 
embryo  worms  as  food,  and  Indian  observers  have  noted  that  the 
worms  are  at  first  coiled  up  in  the  stomach,  but  later  they  pierce 
the  wall  of  this  organ  and  escape  into  the  body  cavity,  and  may 
kill  the  cyclops.  In  the  body  cavity  they  shed  their  cuticle  about 
the  seventh  day  and  undergo  developmental  changes,  and  will 
remain  alive  in  this  cavity  for  some  fifty-three  days. 

In  1907  Leiper  proved  that  the  infection  of  man  was  per  os,  the 
cyclops  being  swallowed  in  water.  In  the  stomach  the  crustacean 
is  killed,  but  the  worm  escapes  through  the  digested  integument  of 
the  cyclops,  bores  it  sway  through  the  wall  of  the  vertebrate  stomach, 
and  in  about  eight  to  twelve  months  becomes  the  adult  female, 


Fig.  788X. — Guinea  Worm  somewhat  shrivelled  from  Action  of  Pre- 
serving Fluids.     (Half  Natural  Size.) 

measuring  some  30  inches,  but  during  this  process  she  moves  about 
and  finally  produces  the  blister,  where  water  can  be  touched,  and 
so  gets  her  young  into  water. 

In  1913  Turkhud  extended  our  knowledge  considerably,  and  has 
shown  that  a  man  who  drank  water  containing  infected  cyclops  on 
April  5,  1913,  showed  the  worm  on  March  18,  1914 — i.e.,  348  days 
later.  He  also  demonstrated  that  the  worm  would  not  develop  in 
Macacus  sinicus. 

Whether  there  is  more  than  one  kind  of  guinea-worm  is  not  known, 

but  Scheube  says  that  Cholokowski  has  described  an  unclassified 

filar ia,  several  inches  in  lengt  h,  which  causes  ulceration  of  t  he  fingers, 

and  even  gangrene,  in  Tiver,  in  Russia,  which  may  or  may  not  be  the 

same  worm. 

124 


197° 


DISEASES  OF  CONNECTIVE  TISSUES 


Climatology.— Dracontiasis  is  a  disease  of  the  tropics,  especially 
of  tropical  Africa,  and  particularly  of  the  West  Coast.  It  is  also 
known  in  Asia  Minor,  Persia,  and  India.  Although  coolies  infected 
with  the  worm  frequently  pass  from  India  to  Ceylon,  we  have  no 
evidence  that  the  latter  island  has  so  far  become  infected.  It  is 
also  known  in  the  Fiji  Islands.  It  was  introduced  into  America 
by  the  negro  slaves,  and  has  become  endemic  in  British  Guiana 
and  Brazil. 

./Etiology. — The  causation  of  the  disease  is  Dractmciihts  niedt- 
nensis  Linnseus,  1758,  taken  into  the  body  by  drinking  water 
containing  infected  cyclops,  which  are  most  abundant  during  the 
dry  season,  and  which  mostly  live 
near  the  bottom  of  wells  and 
collections  of  water. 


vijflfl 

1 

j 

k 

1  .-■" 

..J^    J& 

^jf* 

"  ~ 

sss 

--^Vr     J* 

n 

Fig.    789. — Guinea-Worm  under 
the  Skin. 

(From  a  photograph  by 
Christopherson.) 


Fig.  790. — Guinea-Worm  in  Process 
of  Extraction. 

(From  a  photograph   by 
Christopherson.) 


Pathology.- — On  entering  the  stomach  the  cyclops  is  killed  by  the 
action  of  the  acid  of  the  gastric  jiicc,  but  the  Dractincithis  is  stimu- 
lated, and,  dashing  about  energetically,  effects  its  escape  from  the 
cyclops,  and,  piercing  the  walls  of  the  stomach,  enters  the  con- 
nective tissue  of  the  mesentery  and  becomes  an  adult. 

After  a  time  the  fully-developed  female  begins  to  travel  in  search 
of  a  means  of  depositing  the  larvae  in  water,  and  therefore  usually 
wanders  into  the  leg,  and  forming  first  a  vesicle  and  then  an  ulcer 
in  the  skin,  discharges  the  larvae. 

Symptomatology. — The  worm  as  a   rule  produces  no  symptoms 


SYMPTOMATOLOGY  1971 

until  a  little  vesicle  appears  on  the  skin,  or  the  outline  of  the  worm 
is  noticed  under  the  skin,  but  urticarial  eruptions  have  been  ob- 
served by  several  authors  and  ourselves.  The  little  vesicle  bursts, 
leaving  a  round  hollow,  out  of  which  exudes  a  clear  fluid  full  of 
larvae,  and  at  the  bottom  of  which  lies  the  vaginal  orifice  of  the 
worm.  After  discharging  a  certain  amount  of  fluid,  the  anterior 
end  of  the  worm  extrudes  through  the  skin  opening,  and  is  either 
twisted  on  a  stick  or  fixed  in  position  by  a  piece  of  string  by  the 
native  patient.  It  is  not  advisable  to  pull  vigorously  on  the  pro- 
truded piece  of  worm,  as  it  is  liable  to  break,  and  if  this  happens 
a  serious  inflammation  of  the  affected  area  may  result.  The  wound 
usually  quickly  heals  after  the  worm  has  finally  been  extracted. 
The  usual  site  for  it  to  appear  is  about  the  feet  or  legs,  more  rarely 
the  hands  or  arms,  and  still  more  rarely  the  head  or  trunk. 

But  all  cases  are  not  so  simple,  and  aching  or  dragging  sensations, 
sometimes  accompanied  by  rigors  and  fever,  may  occur.  Rarely 
it  enters  a  knee-joint  and  causes  synovitis  or  arthritis.  Usually 
there  is  only  one  worm,  but  there  may  be  more. 

Blood.- — Dudgeon  and  Child  have  investigated  the  blocd  in  this 
disease,  and  find  a  marked  eosinophilia.  The  average  differential 
count  was  as  follows:  Polymorphonuclears,  63*6  per  cent.;  lympho- 
cytes, 18-4  per  cent.;  large  lymphocytes,  2-8  per  cent.;  mono- 
nuclears, 1-6  per  cent.;  eosinophiles,  13  per  cent. 

Diagnosis  and  Prognosis. — There  is  no  difficulty  in  the  diagnosis, 
and  the  prognosis  is  good. 

The  X  rays  are  useful  in  detecting  encysted  calcified  worms,  which  may 
cause  obscure  purulent  conditions. 

Treatment. — It  is  a  good  plan  to  massage  the  area  above  the 
vesicle,  and  try  with  a  little  patience  to  get  the  worm  out  whole, 
or,  if  it  is  visible  under  the  skin,  to  make  an  incision  and  remove 
it.  Natives  extract  the  worm  by  twisting  the  protruding  port  ion  on 
a  stick,  every  day  giving  a  turn  or  two.  A  better  plan  is  to  douche 
frequent ly  with  water  the  part  occupied  by  the  worm  until  she  gets 
emptied  of  all  the  embryos,  which  generally  takes  place  in  from 
two  to  three  weeks.  When  all  the  embryos  have  been  exudeel,  the 
worm  is  either  absorbed  or  tends  to  emerge,  and,  no  longer  resisting 
extraction,  can  be  easily  removed.  It  has  been  advised  (Emily) 
to  inject  a  r  per  1,000  solution  of  perchloridc  of  mercury  into  the 
swelling  caused  by  the  worm.  But  this  is  very  painful,  and  does 
not  appear  to  be  very  successful.  Some  authors  have  advised  the 
injection  of  10  to  15  minims  of  a  2  per  cent,  solution  of  cocaine  into 
the  protruding  portion  of  the  worm. 

Prophylaxis. — The  prophylaxis  is  very  simple — viz.,  the  drinking 
of  only  boiled  and  filtered  water.  Another  simple  method  suggested 
by  Leiper  is  to  pass  steam  into  the  wells. 

THE  DERMO-CONJIWCTIVAL  FILARIASES. 

Tiiesa  ate  Loiasis.  Calabar  swellings,  and  Dubini's  filariasis. 


1972  DISEASES  OF  CONNECTIVE  TISSUES 

LOIASIS. 

Definition. — Loiasis  is  a  subcutaneous  and  subconjunctival 
nlanasis  caused  by  Loa  loa  (Guiyot,  1778). 

Remarks.— Loa  loa,  which  is  carried  by  a  species  of  Chrysops,  af 
discovered  by  Leiper,  has  frequently  been  noticed  in  the  ocular  and 
palpebral  conjunctivae  crossing  the  bridge  of  the  nose,  in  the  skin 
over  the  sterno-mastoid  muscle,  or  that  of  the  scalp,  the  fingers,  the 
penis,  etc.,  and  much  more  rarely  in  the  anterior  chamber  of  the 
eye,  though  accounts  of  its  presence  in  the  vitreous  humour  require 
confirmation.     For  description  of  the  worm  see  p.  645. 

Climatology. — The  geographical  distribution  of  the  worm  is  con- 
fined to  the  West  Coast  of  Africa  from  Sierra  Leone  to  Benguela, 
but  is  most  particularly  Old  Calabar,  the  Cameroons,  and  the 
Ogome  River.  It  penetrates  some  six  hundred  miles  or  more  into 
the  interior  of  Africa. 

Symptomatology. — In  our  experience  it  usually  causes  but  little 
disturbance,  but  at  times,  when  in  the  conjunctiva,  it  'is  associated 
with  piercing  and  lancinating  pains,  uncertain  vision,  and  swelling 
of  the  eyelids.  It  is  probably  the  cause  of  the  Calabar  swellings 
mentioned  below. 

Treatment. — It  can  be  removed  by  an  incision  and  careful  traction. 
Hot  fomentations,  as  noted  by  Elliott,  cause  the  worm  to  come  to 
the  surface. 

CALABAR  SWELLINGS. 

Synonyms. — Kamerungeschwiilste,  Tropical  swellings,  Ndi-tot  = 
swelling  (Calabar). 

Definition. — Calabar  swellings  are  smooth,  temporary,  slightly 
raised  tumours  on  the  head,  arms,  hands,  ankles,  and  feet,  probably 
caused  by  the  presence  of  Loa  loa  (Guiyot,  1778),  and  possibly 
other  species  of  filaria  or  allied  genera  in  the  subcutaneous  tissue. 

History. — -For  many  years  it  has  been  known  that  peculiar  swellings 
occurred  in  the  people  living  in  Old  Calabar,  and  in  due  course  ac- 
counts appeared  in  works  of  travels  in  West  Africa,  but  it  was  not  till 
1895  that  Argyll  Robertson  described  them  as  a  distinct  disease,  using 
their  popular  nomenclature.  In  subsequent  years  he  published  several 
accounts  of  his  cases.  In  1898  Plehn  drew  attention  to  the  complaint, 
and  in  1899  Thompstone  published  an  account  of  a  case,  while 
Habershon  and  Kerr  in  1904,  Wurtz  and  Clerc  and  Stephens  in  1905, 
and  Ward  in  1906,  have  all  added  to  the  literature  of  the  subject. 

The  paper  by  Ward  is,  however,  of  especial  interest,  as  it  deals 
fully  with  the  history  of  the  disease. 

Climatology. — The  disease  is  only  known  on  the  West  Coast  of 
Africa,  particularly  in  the  regions  of  Southern  Nigeria  and  the 
Cameroons.  We  have  seen,  though  rarely,  a  similar  condition  in 
Ceylon,  where  the  existence  of  Loa  loa  has  not  been  reported. 

/Etiology  and  Pathology. — There  is  a  consensus  of  opinion  that  in 
some  way  these  swellings  are  caused  by  Loa  loa  Cobbold,  1864, 
but  this  has  never  been  definitely  proved. 


CALABAR  SWELLINGS 


1973 


The  way  in  which  the  worm  induces  these  peculiar  lumps  is  a 
matter  of  conjecture,  Argyll  Robertson  assigning  them  merely  to 
the  movements  of  the  parasite.  But  this  cannot  be  so,  otherwise 
the  swellings  would  occur  as  they  cross  the  bridge  of  the  nose, 
which  they  can  do  without  any  such  disturbance. 

The  next  theory  is  that  the  parasite  irritates  the  skin,  causing 
the  patient  to  rub  the  affected  area,  which  in  this  way  becomes 
mechanically  inflamed.  This  theory  was  originally  propounded 
by  Manson,  who  has  relinquished  it  in  favour  of  another  and  better 
explanation. 

Two  other  theories  suggest  that  the  parasite,  by  irritating  the 
nerve  endings,  either  directly  or  by  reflex  action,  causes  the  swell- 
ing; but  this  does  not  appear  likely,  as  they  ought  to  occur  wherever 
the  worm  travels.  Manson  in  1903  suggested  that  they  might 
be  brought  about  by  the  expulsion  of  the  microfilariae  from  the 
uterus  of  the  parent  worm,  and  this  appears  not  unlikely,  and  would 
explain  their  evanescent  character. 

Ward  is  not  satisfied  with  Manson's  theory,  and  suggests  that 
they  may  be  due  to  the  expulsion  of  waste  products  from  the  worm. 

Age,  sex,  and  employment  have  no  influenee  in  the  causation  of 
the  complaint. 

Symptomatology. — Sometimes  without  prodromal  symptoms,  or 
at  times  after  some  nausea  and  headache,  swellings  appear  on  the 
head,  face,  arms,  wrists,  hands,  fingers,  ankles,  or  toes,  lesscommonly 
on  other  parts  of  the  body.  The  reason  of  this  distribution,  accord- 
ing to  some  authors,  is  believed  to  be  the  small  amount  of  connective 
tissue  in  those  regions.  The  swellings  are  smooth,  firm,  slightly 
elevated  areas,  generally  about  the  size  of  half  a  goose's  egg  (5  to 
8  centimetres),  often  painless,  though  this  is  not  invariable.  There 
is  either  absence  of  or  only  very  slight  pruritus.  They  are  hot, 
and  do  not  pit  much  on  pressure.  They  appear  quickly,  last  for 
two  or  three  days,  and  disappear  gradually  or  rapidly,  and  are 
always  associated  with  an  intense  eosinophilia.  In  many  cases 
only  one  swelling  appears  at  a  time. 

Stephens  gives  the  differential  count  of  his  case  as — Polymorphonuclears, 
26  per  cent.;  lymphocytes,  23  per  cent.;  mononuclears,  1  per  cent.;  eosino- 
phils, 50  per  cent. 

Diagnosis. — There  is  no  difficulty  in  recognizing  these  fugitive 
swellings  in  persons  who  have  resided  in  the  endemic  region.  The 
presence  of  extremely  well-marked  eosinophilia  may  help  in  the 
diagnosis. 

Prognosis. — They  have  never  been  known  to  cause  serious  symp- 
toms, but  may  recur  for  many  years  after  the  patient  has  left  the 
tropics. 

Treatment. — This  is  unsatisfactory,  but  cool  applications  such  as 
diluted  liquor  plumbi  (5  per  cent.)  may  be  made  to  the  swellings, 
and  an  ichthyol  ointment  or  lotion  applied. 

Prophylaxis.— As  our  knowledge  of  the  life-cycle  of  Loa  loa  is  very 
incomplete  it  is  not  possible  to  lay  down  rules  for  the  prophylaxis. 


1974  DISEASES  OF  CONNECTIVE  TISSUES 


DUBINI'S  FILARIASIS. 

Definition. — Dubini's  filariasis  is  a  dermo-conjunctival  filariasis 
caused  by  Filaria  conjunctives  Addario,  1885. 

History. — The  immature  female  worm  was  originally  discovered 
by  Dubini  in  the  subconjunctival  tissue  of  a  man  in  Milan,  and  is 
possibly  the  same  as  that  described  as  Agamofilaria  oculi  humani 
von  Nordmann,  1832,  and  as  Agamofilaria  palpebralis  Pace,  1867, 
nee  Wilson,  1844.  I*1  I^8o  Babes  found  another  immature  female 
worm  in  a  calcined  nodule  in  the  gastro-splenic  omentum  of  a  woman 
in  Budapest.  He  named  it  Filaria  peritonei  hominis.  In  1885 
Addario  named  a  female  worm  extracted  by  Vadela  from  the  con- 
junctiva F.  conjunctiva.  Vadela's  case  was  a  woman  from  Catania 
in  Sicily.  In  1887  Grassi  gave  a  full  description  of  the  female 
worm,  calling  it  F.  inermis,  because  of  the  absence  of  papillae  on  the 
head.  In  1906  Alessandrini  found  it  in  an  abscess  in  subcutaneous 
tissue  of  the  arm;  and  in  1918  Graham  Forbes  met  with  two  cases  in 
the  subcutaneous  tissue  of  the  forearm  and  of  the  nose,  and  was 
the  first  to  describe  the  adult  male. 

It  is  the  same  as  the  worm  called  Filaria  papulosa  Rivolta,  found 
in  the  eye  of  an  ass  at  Pisa,  and  also  F.  apapillocephala  Condorelli- 
Francaviglia. 

Climatology. — The  worm  is  found  in  Italy,  Sicily,  Hungary, 
Macedonia,  and  Roumania.  It  is  a  parasite  of  the  horse  and  ass, 
and  but  rarely  of  man. 

/Etiology. — -It  has  been  suggested  that  the  worm  is  introduced 
by  the  bites  of  Chrysops  excutiens. 

Morbid  Anatomy. — The  nodule  containing  the  worm  consists  of 
fibrous  connective  tissue  with  round-celled  infiltration  and  traversed 
by  lymph  spaces. 

Pathology. — It  is  thought  that  the  worm  enters  a  lymphatic 
canal,  which  becomes  cut  off  and  is  surrounded  by  an  inflammatory 
reaction.  No  microfilariae  can  be  found  in  the  blood  or  in  the 
nodules. 

Symptomatology. — Marks  of  a  bite  have  been  seen  in  only  one 
case.  Usually  it  is  a  small  tumour  in  some  area  of  the  body  which 
is  the  first  sign  to  attract  attention. 

The  differential  blood  count  is  as  follows: — 


Polymorphonuclear  leucocytes 
Mononuclear  leucocytes 
Small  lymphocytes 
Eosinophile  leucocytes 
Basophile  leucocytes 


Per  Cent. 

47-0 
10-5 
38-0 

3'5 
1*0 


As  time  progresses  the  little  lump  may  beccme  hot  and  swollen, 
but  not  painful.  After  these  inflammatory  symptoms  have  lasted 
for  some  three  days  they  subside,  only,  however,  to  recur  again  in 
about  ten  to  fourteen  days,  and  this  cycle  recurs  and  recurs.    Some- 


DISEASES  OF  MUSCLES  1975 

times  an  abscess  forms  in  which  the  worm  or  its  remains  can  be 
found. 

Treatment. — The  correct  treatment  is  to  excise  the  nodule. 

Prophylaxis. — Nothing  can  be  said  under  this  heading,  as  the 
method  of  infection  is  unknown. 

DISEASES  OF  MUSCLES. 
MYOSITIS    PURULENT  A    TROPICA. 

Synonyms. — Muma  fever  (Samoa),  Bungpagga  (Northern  Gold 
Coast). 

History. — -This  condition  has  been  observed  in  various  parts  of 
the  tropics,  including  the  northern  territories  of  the  Gold  Coast,  by 
several  observers,  among  whom  Van  Polak,  Ziemann,  Kiilz,  may  be 
mentioned.  The  last-named  author  has  given  a  good  general 
account  of  the  malady. 

Climatology.  -The  disease  is  found  in  tropical  Africa  and  Sf.moa. 

/Etiology. — Some  authorities  suggest  that  it  is  due  to  a  Filaria. 

Symptomatology. — The  patient  ccmplains  of  rheumatoid  pains 
in  the  limbs  associated  with  fever  of  a  remittent  or  intermittent 
type.     Abscesses  form  in  the  muscles  in  various  parts  of  the  body. 

Treatment. — This  is  surgical,  the  abscesses  being  evacuated. 

DISEASES  OF   BONES. 

GOUNDOU. 

Synonyms. — Anakhre=big-nose ;  Henpuye=dog-nose. 

Definition. — Goundou  is  a  disease  of  unknown  causation,  charac- 
terized by  a  bony  swelling,  usually  bilaterally  symmetrical,  situated 
on  either  side  of  the  nose 

History. — -The  disease  was  first  described  by  Macalister  in  1882. 
under  the  term  of  '  the  horned  men  of  Africa.'  Lamprey  in  1887 
also  referred  to  the  disease  under  a  similar  term,  and  Strachan  drew 
attention  to  it  in  a  West  Indian  child  in  1894.  Maclaud  in  1895 
described  the  disease  which  he  saw  on  the  Niger  under  the  terms 
'  goundou  '  or  '  anakhre.'  In  1900  Chalmers  gave  an  account  of  the 
disease  as  seen  on  the  Gold  Coast,  and  Renner  as  seen  in  Sierra 
Leone.  Later  Braddon  recorded  a  case  in  Malaya,  and  others 
found  the  disease  in  Sumatra  and  in  China.  Friedrichsen  gave 
an  excellent  description  of  it  as  seen  in  East  Africa,  and  Nell  gave 
an  account  of  his  cases  on  the  Gold  Coast,  while  Cant  lie  records  a 
case  of  unilateral' goundou  in  a  European.  Lastly,  Roques  and 
Bouffard,  and  more  recently  Roubaud,  Blin,  Marchoux,  and 
Mesnil  and  Leger,  have  recorded  cases  in  monkeys— Papio  anubis, 
Cercopitlw.us  sp.  ?,  and  Callitrichci  is. 

The  first  three  observers  found  that  the  condition  affected  many 
bones  of  the  skeleton,  besides  the  nasal  bones.  Letulle  has  noticed 
a  somewhat  similar  condition  in  the  skull  of  an  ancient  Inca  found 
in  a  Peru  necropolis. 


1976 


DISEASES  OF  BONES 


Climatology. — The  disease  is  most  commonly  met  with  in  West 
Africa,  but  has  been  reported  from  East  Africa,  Malaya,  Sumatra, 
South  China,  and  the  West  Indies.  It  usually  affects  native  races, 
but  has  been  reported  in  one  Europ?an.  Usually  it  begins  in  the  first 
two  decades  of  life. 

/Etiology. — This  is  unknown,  though  the  association  with  yaws 
gave  rise  to  the  suspicion  that  this  was  the  aetiological  factor. 
Cantlie's  European,  however,  had  not  suffered  from  yaws,  and 
monkeys  do  not  suffer  spontaneously  from  yaws. 

Occasionally  in  yaws  patients  a  bilateral  or  unilateral  swelling 
of  the  nose  is  present  (pseudo-goundou  of  Brumpt),  but  it  quickly 
disappears  along  with  the  other  symptoms  of  yaws  under  treatment 
with  potassium  iodide  or  salvarsan,  which 
has  no  effect  on  true  goundou. 

Other  theories  have  been  that  it  was  a 
racial  trait,  or  that  it  was  due  to  a  larva  of 
a  fly,  but  these  are  certainly  not  correct. 
As  far  as  we  know,  it  is  never  congenital. 
Br  addon  thinks  that  it  is  a  disease  sui 
generis,  and  in  our  opinion  is  probably 
right. 

Pathology.— Whatever  the  cause  may  be, 
there  seems  no  reasonable  doubt  that  the 
infection  begins  in  the  nose;  for  although 
we  were  unable  to  find  any  abnormality  in 
the  nose  of  the  cases  we  have  seen,  still, 
there  was  always  a  history  of  some  obstruc- 
tion, pain  in  the  nose,  and  often  of  a 
bloody  discharge.  Moreover,  Friedrichsen 
describes  a  swollen  condition  of  nasal 
mucosa  with  almost  polypoid  excrescences. 
Leger  has  noted  microscopically  a  pro- 
liferation of  embryonal  cellular  elemenl  s 
derived  from  the  bone-marrow  infil- 
trating the  bone-tissues.  This  is  followed  later  by  a  true  process 
of  cicatrization. or  osteosclerosis.  If  this  is  correct,  it  is  quite  easy 
to  understand  that  the  vessels  passing  from  the  nose  through  the 
sutura  notha,  in  the  nasal  process  of  the  superior  maxilla,  can  can}' 
that  infection  to  the  periosteum,  which,  being  irritated,  proceeds 
to  an  excessive  formation  of  bone  in  the  area  of  that  suture.  This 
results  in  the  formation  of  a  ony  swelling,  composed  on  the  out- 
side of  a  thin  shell  of  compact  bone,  underneath  which  is  spongy, 
bony  substance  continuous  with  that  of  the  bone  from  which  it 
is  arising.  The  sutura  no/ha  is,  of  course,  found  in  all  human  skulls, 
and  is  not  peculiar  to  the  negro  race. 

The  bony  growths  are  attached  to  the  nasal  bone,  the  nasal 
process  of  the  superior  maxilla,  and  at  times  to  the  maxilla  itself. 
The  periosteum  strips  off  readily,  but  usually  shows  no  signs  of 
recent  inflammation. 


Fig.  791. — Goundou  in  a 
Native  of  the  Gold 
Coast. 


SYMPTOMATOLOGY—BOOMERANG  BONES  1977 

Symptomatology. — Generally  the  disease  begins  with  pain  in  the 
nose,  or  headache,  which  may  be  severe,  and  a  bloody  nasal  dis- 
charge, which  may  continue  for  some  six  to  eight  months.  When 
this  is  disappearing,  it  is  noticed  that  there  is  a  swelling,  usually 
symmetrically  placed  on  either  side  of  the  nose,  in  the  region  of 
the  nasal  bone  and  nasal  process  of  the  superior  maxilla.  Slowly 
and  steadily  these  lumps  increase  in  size,  interfering  with  vision 
(it  is  said  at  times  destroying  the  eyes),  and  giving  rise  to  a  hideous 
deformity  rather  like  a  Cynocephalus  monkey,  and  hence  called 
'  dog-nose.'  When  fairly  well  developed,  an  oval,  bony  swelling, 
with  its  long  axis  directed  downwards  and  outwards,  is  seen  sym- 
metrically placed  on  each  side  of  the  nose;  the  skin  over  the  tumour 
is  never  affected,  being  freely  movable;  and  usually,  when  ex- 
amined, the  nasal  mucosa  is  found  to  be  normal,  and  the  nasal  ducts 
are  patent,  but  there  may  be  swelling  and  even  polypoid-like  excres- 
cences. Occasionally  a  similar  growth  may  invade  the  nose, 
partially  blocking  the  nasal  cavity.  The  growth,  however,  may 
stop  at  any  stage  of  its  development,  and  proceed  no  farther. 
Some  authors  describe  a  curvature  of  the  tibiae  as  being  associated 
with  the  disease. 

Varieties. — Instead  of  being  bilaterally  symmetrical,  the  bony 
lump  may  develop  only  on  one  side  of  the  nose.  Orpen  has 
described,  in  addition  to  the  two  usual  tumours,  a  third  in  the 
malar  region. 

Diagnosis. — The  symmetrical  bony  swellings  at  the  root  of  the 
nose  are  characteristic,  but  must  be  distinguished  from  Brumpt's 
pseudo-goundou  of  frambcesial  origin  by  the  history  and  by  the 
inutility  of  salvarsan  and  potassium  iodide. 

Treatment. — Medical  treatment  is  useless,  and  removal  is  not 
merely  easy,  but  most  effective,  as  the  disease  is  known  not  to 
have  returned  some  six  or  seven  years  after  the  operation. 

Prophylaxis. — As  the  causation  is  doubtful,  nothing  can  be  said 
under  this  heading. 

BOOMERANG  BOXES. 

Synonym.— Boomerang  leg. 

Daflnition. — A  disease  of  the  long  bones  commencing  gradually, 
and  associated  with  pain,  tenderness,  and  longitudinal  bowing  of 
the  bones,  which  remain  permanently  deformed  after  the  acute 
symptoms  have  disappeared.  Several  conditions  are  apparently 
covered  by  this  term. 

History. — The  disease  was  first  described  in  the  second  edition 
(1913)  of  this  work  from  information  received  from  Ernest  Black. 
He  described  it  as  seen  in  the  aboriginal  natives  of  the  north  of 
Western  Australia  and  the  Torres  Straits  Islands.  In  1915  Brcinl 
and  Priestley  gave  an  account  of  the  disease  as  seen  in  Northern 
Queensland  and  Western  British  New  Guinea.  In  1918  Christopher- 
son  described  a  similar  condition  as  seen  in  the  Anglo-Egyptian 
Sudan. 


ig78 


DISEASES  OF  BONES 


Climatology. — The  disease  is  known  in  the  northern  portion  of 
Australia,  the  islands  of  the  Torres  Straits,  in  the  Sudan,  in 
British  New  Guinea. 

/Etiology. — This  is  unknown.  It  is  not  syphilitic,  tubercular, 
osteomalacic,  nor  due  to  rickets.  Black  considers  the  condition  to 
be  due  to  hypof unction  of  the  thymus  gland.  A  clinically  similar 
condition  is  undoubtedly  a  late  manifestation  of  yaws. 

Pathology. — The  disease  is  believed  to  begin  as  a  rarefying 
osteitis  which  causes  softening  and  permits  the  bending  of  the  bones. 
This  is  followed  by  a  condensing  osteitis  and  formation  of  periosteal 
bone  fixing  the  deformities. 

Morbid  Anatomy.— The  bending  in  the  tibia  takes  place  at  the 
junction  of  the  upper  with  the  middle  thirds.  The  bone  is  heavy, 
and  compact  in  the  centre  and  freer  at  the  ends.  The  narrow  cavity 
is  almost  filled  in  with  compact  bone. 


Fig.  792. — Boomerang  Disease. 
(From  a  photograph  by  Christopherson.) 

Symptomatology. — The  onset  is  gradual  in  young  natives  during 
the  period  of  growth.  There  are  pains  in  the  shins,  severe  enough 
to  prevent  walking,  and  the  skin  over  these  bones  is  tender.  The 
subcutaneous  tissues  become  inflamed,  and  there  is  some  febrile 
disturbance.  After  the  acute  symptoms  and  pain  have  subsided 
the  children  start  to  walk,  and  the  bones  bend  forward  gradually, 
thus  giving  rise  to  the  characteristic  deformity,  which  becomes 
permanently  fixed. 

Other  bones  may  become  similarly  affected. 

Treatment. — This  is  nil  at  present. 

Prophylaxis. — Unknown. 

PES  GIGAS. 

Synonym. — Congenital  partial  hypertrophy  of  the  foot. 

Definition. — Hypertrophy  and  fusion  of  the  inner  metatarsal 
bones,  with  club  formation  of  the  ends  of  the  toes. 

History. — Cousland,  in  the  Journal  of  Tropical  Medicine  for 
January,  1900,  gave  an  illustration  of  the  disease  as  seen  in  a  young 
Chinaman.  Raynaud  saw  the  disease  in  a  Kabyle  and  Legrand  in  a 
European. 

Symptomatology. — -The  condition  is  congenital,  and  may  be 
studied  by  the  X  rays,  when  it  will  be  seen  that  the  three  inner  meta- 


REFERENCES  1979 

tarsal  bones  are  hypertrophied,  and  the  second  and  third  united, 
while  the  terminations  of  the  toes  are  club-like.     In  Cousland's 
case  there  was  marked  hypertrophy  of  the  calf  muscles. 
Treatment. — It  has  not  been  treated  so  far  as  we  know. 

ENDEMIC  ENLARGEMENT  OF  THE  OS  CALCIS. 

Definition. — Endemic  enlargement  of  the  os  calcis  is  a  disease  of 
unknown  causation,  characterized  by  fever,  pain,  and  tenderness 
over,  and  subsequently  enlargement  of,  the  os  calcis. 

History  and  Climatology. — This  disease  was  first  described  by 
MacLean  in  1904  in  Fantis  and  Krooboys  in  the  Gold  Coast  Colony, 
and  subsequently  in  1905  by  Maxwell  in  natives  of  Formosa. 

/Etiology. — The  aetiology  and  pathology  are  obscure,  but  in 
some  way  it  is  connected  with  the  wet  season,  as  attacks  and 
recurrences  take  place  then. 

Symptomatology. — The  disee.se  begins  suddenly  with  fever, 
great  tenderness  over  the  os  calcis,  with  local  pains  so  severe  ar  to 
prevent  sleeping  and  walking.  In  three  to  seven  days  the  outer 
surface  of  the  bone  begins  to  increase  in  size,  and  continues  to  do 
so  for  some  two  weeks,  during  which  time  the  pain  lessens  and  the 
temperature  falls  to  normal. 

In  about  a  month  the  swelling  reaches  its  maximum  size,  at 
which  it  may  remain  for  about  one  to  two  months,  during  which 
time  the  pain  is  moderate  and  walking  is  possible.  After  this  the 
bone  diminishes  to  about  half  the  maximum  size,  but  sometimes 
considerable  enlargement  persists.-  Usually  the  disease  is  bilaterally 
symmetrical,  but  it  may  occur  on  one  side  only.  It  affects  the 
outer  surface  as  a  rule,  but  may  also  attack  the  posterior  third  of  the 
bone. 

Rarely  it  attacks  other  tarsal  bones,  but  has  never  bten  reported 
as  affecting  a  joint.  Yearly  recurrences  during  the  wet  season  are 
common. 

Treatment. — Medical  treatment  is  useless,  but  relief  is  given  by 
cutting  down  on  to  the  affected  area  and  trephining  a  hole  into  the 
bone. 

Prophylaxis. — Concerning  this  nothing  is  known. 

REFERENCES. 

Somatic  Taeniasis. 
Castellani  (1918).     Ann.  Med.  Navale. 
Chalmers  (1904).     Spolia  Zeylanica. 

Stiles  (1906).     Bull.  No.  25.  Hyg.  Lab.  U.S.  Pub.  Health  and  Mar.  Hosp . 
Service,  Washington,  1906. 

Dracontiasis. 

Dudgeon  and  Child  (1903).     Journal  of  Tropical  Medicine,  1903. 
Mackenzie  (1898).     Journal  of  Tropical  Medicine,  i.  113. 
Remlinger  (1904).     Comptes  Rendus  de  Soc.  de  Biolog.,  Ivii.  76.     Paris. 
Turkhud   (1914).     Report  of  the   Bombay   Bacteriological   Laboratory  for 
1913,  p.  15  (Turkhud's  experiments  on  man).     Bombay. 


1980  DISEASES  OF  CONNECTIVE  TISSUES 

Calabar  Swellings. 

Habershon  (1904).     Journal  of  Tropical  Medicine,  vii.  3. 
Kerr  (1904).     Journal  of  Tropical  Medicine,  vii.  195. 
Robertson  (1895).     Ophthalmic  Review,  xiv.  93;  1897,  Lancet,  i.  1744. 
Stephens  (1905).     Journal  of  Tropical  Medicine,  p.  107. 
Thompstone  (1899).     Journal  of  Tropical  Medicine,  p.  89. 
Ward  (1906).     Journal  of  Infectious  Diseases,  p.  37. 

Wurtz  et  Clerc  (1905).      Comptes  Rendus  de  la  Soc.  de  Biolog.,  lv.  1704. 
Paris.     Archiv.  Med.  Exper.,  xvii.  260. 

Dubini's  Filariasis. 

Forbes  (1918).     Transactions  of  the  Society  of  Tropical  Medicine,  October. 
London . 

Trench  Foot. 

Castellani  (191 7).     Journal  of  Tropical  Medicine  and  Hygiene.     London. 
Castellani    (1917).     Comptes   Rendus   Conference  Chirurgicale   Interalliee, 
p.  248 

Goundou. 

Bouffard  (1909).     Bulletin  Societe  de  Path.  Exotique. 

Brumpt  (1909).     Ibid. 

Chalmers  (1900).     Lancet,  vol.  i. 

Friedrichsen  (1906).     Journal  of  Tropical  Medicine,  p.  63. 

Leger  (1912).     Bulletin  de  la  Societe  Path.  Exotique. 

Marchoux  and  Mesnil  (1912).     Ibid. 

Orpen  (1904).     Annals  of  Tropical  Medicine  and  Parasitology,  ii.  4,  289. 

Roques  et  Bouffard  (1908).     Bull,  de  la  Societe  de  Path.  Exotique,  i.  295 

Weenberg  (1909).     Bulletin  Societe  de  Path.  Exotique. 

Boomerang  Bones. 

Black,  Ernest  (1913).     Private  communication. 

Breinl  and  Priestley  (1915).     Journal  of  Tropical  Medicine  and  Hygiene. 

Christopherson  (1918).     Proceedings  Royal  Society  of  Medicine. 

Enlargement  of  the  Os  Calcis. 

MacLean  (1904).     Journal  of  Tropical  Medicine,  p.  333. 
Maxwell  (1905).     Ibid.,  p.  82. 


CHAPTER  LXXXIX 
DISEASES   OF   THE   NERVOUS    SYSTEM 

General  remarks — Endemic  paralytic  vertigo — Latah — Banga — Schamanis- 
mus — Amok — Tropical  neurasthenia — Endemic  peripheral  neuritis — 
Erythromelalgia  tropica — Desert  hallucinations — Emotional  excitement 
— Delusions — Auto-suggestion — References. 

GENERAL  REMARKS. 

The  nerve  diseases  of  the  tropics  include  many  general  diseases 
already  dealt  with — e.g.,  pellagra,  leprosy,  beri-beri,  etc.  But 
apart  from  these  conditions,  meningitis,  cerebral  tumours,  cerebral 
hcemorrhages,  spastic  paralysis,  alcoholic  neuritis,  and,  more  rarely, 
arsenical  neuritis,  are  all  well  known.  Locomotor  ataxia  and  general 
paralysis — the  so-called  parasyphilitic  affections — -are  rare,  though 
syphilis  is  rampant.  The  cerebral  tumours  which  we  have  most 
commonly  met  with  are  endotheliomata  and  tubercular  or  syphilitic 
lesions.  Hysteria  is  common  among  the  better-class  natives, 
especially  among  the  young  women  educated  according  to  Western 
ideas. 

As  regards  insanity,  mania  and  melancholia  are  the  most  usual; 
but  dementia,  idiocy,  and  epileptic  insanity  are  not  uncommon. 
According  to  Spence,  the  burden  of  lunacy  in  Ceylon  is  light  as 
compared  with  England,  Scotland,  or  Ireland,  and  it  is  possible  that 
this  applies  not  merely  to  Ceylon,  but  to  other  countries.  But  apart 
from  these  diseases,  there  are  some  curious  nerve  or  nr'nd  affections 
which  must  be  considered  at  greater  length. 

Sexual  perversions  are  not  uncommonly  met  with  in  native  races. 

Homicidal  tendencies  are  generally  due  to  alcoholism,  or  to  long 
brooding  over  real  or  fancied  injuries.  Suicide  is  not  rare,  and  may 
be  approved  by  local  custom. 

Tropical '  kohler '  has  already  been  mentioned  (p.  76),  but  tropical 
neurasthenia,  endemic  vertigo,  and  other  conditions  must  Le  briefly 
touched  upon. 

War  Zone  Neuroses. — The  recent  war  has  greatly  improved  the 
general  knowledge  of  neurotic  conditions.  It  has  been  shown  that 
congenital  nervous  conditions,  concussion,  chronic  alcoholism,  and 
sexual  troubles  are  predisposing  causes;  while  exhaustion  due  to 
mental  or  physical  strain,  toxaemia,  insufficient  food,  pain,  excessive 
heat,  or  emotion  due  to  horrors  or  constant  pain,  traumatism,  particu- 
larly concussion,  are  the  exciting  causes.     The  neuroses  produced 

1981 


1982  DISEASES  OF  THE  NERVOUS  SYSTEM 

by  the  above-mentioned  causes,  according  to  Hurst,  are  neurasthenia, 
soldier's  heart,  stupor  and  amnesia,  psychasthenia,  hysteria, 
exaggerated  defensive  reflexes,  hyperthyroidism,  hyperadrenalism, 
and  shell  shock. 

The  pathology  of  some  of  these  conditions  has  been  carefully 
investigated  by  Mott.  Many  persons  suffering  from  shell  shock 
have  been  permitted  to  go  on  duty  to  the  tropics,  with  often  un- 
pleasant mental  results.  These  persons  are  especially  liable  to  be 
influenced  by  the  sun's  rays. 

ENDEMIC  PARALYTIC  VERTIGO. 

Synonyms. — Vertige  Paralysante,  Vertige  Ptosique,  Gerlier's 
disease,  Kubisagari,  Tourniquet. 

Definition. — Endemic  paralytic  vertigo  is  characterized  by  eye 
symptoms,  such  as  ptosis,  dimness  of  vision,  and  by  paralysis  of 
the  neck  and  extremities. 

History. — The  disease  was  first  described,  in  1884,  by  Gerlier  in 
Ferney,  in  Switzerland,  in  1886,  and  by  Miura,  in  1894,  in  Japan. 

Climatology.- — It  is  known  in  France,  Switzerland,  and  Japan, 
where  it  is  found  in  the  northern  provinces  and  in  the  island  of 
Shikoku.  It  begins  in  spring,  attains  its  greatest  numbers  in 
summer,  and  ends  in  autumn. 

/Etiology. — The  aetiology  is  entirely  unknown,  and  hence  there 
are  many  theories,  which  suggest  alcohol,  poisoned  bread  and 
lentils,  and  latent  malaria;  but  the  one  which  is  favoured  by  both 
Gerlier  and  Miura  is  the  association  of  the  disease  with  stables. 
Gerlier  says  that  in  the  valley  of  the  Lake  of  Geneva  it  is  not 
unusual  for  people  to  sleep  in  the  stables;  and  Miura  says  that  in 
the  regions  affected  in  Japan  it  is  usual  to  have  the  house  so  arranged 
that  a  part  is  used  as  a  stable,  while  the  remainder  is  occupied  by 
the  family. 

Futher,  it  is  associated  with  warm  weather.  Miura  gives  as 
exciting  causes  bodily  exertion  while  hungry  or  after  a  full  meal, 
writing,  reading,  steady  attention  to  anything,  uniform  movements, 
or  mixing  with  crowds;  while  the  attacks  are  diminished  by  rest 
and  change.  Couchoud  and  Shionoya  found  a  Gram- negative 
coccus  in  the  cerebro-spinal  fluid.  This  they  grew  artificially,  and 
stated  that  they  reproduced  the  disease  by  injecting  this  into  cats. 

Pathology. — This  is  quite  unknown. 

Symptomatology. — An  attack  begins  with  a  blurring  of  objects, 
everything  appearing  as  if  in  a  fog,  together  with  ptosis,  and,  less 
frequently,  a  diplopia  due  to  paralysis  of  the  internal  rectus,  with 
sometimes  photophobia,  disturbances  of  colour  vision,  and  hyper- 
emia of  the  optic  disc.  Then  follow  disturbances  of  speech  and  loss 
of  power  in  mastication,  and,  in  bad  cases,  of  deglutition.  At  the 
same  time  paralysis  of  the  muscles  of  the  back  of  the  neck,  the 
back,  and  th?  extremities  are  observed.  The  head  falls  forward, 
and  is  only  raised  with  difficulty;  hence  the  name  of  the  disease. 


ENDEMIC  PARALYTIC   VERTIGO  1983 

'  kubisagari,'  which  means  '  he  who  hangs  his  head.'  If  the  muscles 
of  the  back  are  paralyzed,  there  may  be  difficulty  in  raising  the 
body  from  a  stooping  posture.  Weakness  in  the  hands,  arms,  and 
legs  is  often  observed,  and  is  first  noticed  in  the  muscles  connected 
with  symmetrical  repeated  movements.  An  attack  lasts  from  ten 
to  fifteen  minutes,  and  varies  in  severity,  in  mild  cases  there  being 
only  pt osis  and  dimness  of  vision.  Between  the  attacks  the  patient 
is  perfectly  well  in  every  respect.  After  severe  attacks  there  may 
be  a  little  ptosis,  or  weakness  of  the  muscles  of  the  back,  neck,  hands, 
or  legs,  and  increased  reflexes. 

Diagnosis. — -The  characteristic  symptoms  are:  Ptosis  and  the 
falling  forward  of  the  head  and  neck.  These  symptoms  differentiate 
it  fora  the  other  forms  of  vertigo. 

Prognosis. — The  disease  is  never  fatal,  though  it  may  last  for 
many  years. 

Treatment. — The  first  requirement  is  removal  from  the  endemic 
area  and  from  living  in  close  proximity  to  stables.  Medicines  are 
not  of  much  use,  but  a  combination  of  potassium  iodide  and  arsenic 
is  recommended. 

LATAH. 

Synonyms. — Echomatism.  Mimicismus,  Sakitlatar,  Jumping,  Bah- 
tschi,  Myriakit,  Meriatschenje. 

Definition. — Latah  is  a  mental  condition  in  which  suggestion  is 
at  once  followed  by  uncontrollable  action  in  the  form  of  echolalia 
or  echokinesia,  of  which  the  mind  is  usually,  but  not  always, 
conscious. 

History. — The  convulsive  tics  have  been  carefully  studied  in 
Europe  by  Charcot,  Gilles  de  la  Tourette,  and  Guinon,  but  the 
allied  condition  '  la'ah  '  found  in  Malaysia,  as  well  as  similar  con- 
ditions found  in  other  parts  of  the  world,  have  as  yet  not  been  fully 
investigated.  Thanks  to  the  labours  of  O'Brien  in  1883,  Gilmour 
in  1892,  Van  Brero  in  1895,  Ellis  in  1897,  Gerrard  in  1904,  Manson 
in  1907,  Fletcher  in  1908,  Plan  in  191 1,  and  Abraham  in  1912, 
a  fair  amount  of  definite  information  with  regard  to  latah  is  avail- 
able. 

Climatology. — Latah  is  found  principally  in  the  Malay  Peninsula, 
Java,  Sumatra,  and  is  also  known  in  Siam.  in  Burma,  in  the 
Philippines,  Siberia,  and  among  the  Jumpers  of  North  America. 
Fletcher  has  rightly  drawn  attention  to  the  fact  that,  while  the 
disease  is  very  common  in  the  Malay  States,  it  is,  apparently,  rare 
in  the  Malays  who  have  emigrated.  Thus,  for  example,  it  does  not 
occur  among  the  large  colony  of  Malays  in  Ceylon,  which  may  be 
due  to  the  fact  that  they  originally  came  from  Batavia  in  Java, 
and  not  from  Malaya,  but  it  is  said  by  Fletcher  to  occur  in  Chinese, 
Tamils,  and  in  Europeans  living  in  Malaya.  The  Ikota  or  Samoyeds, 
and  the  Tigretier  of  Abyssinia,  are  said  to  suffer  from  similar  symp- 
toms.    In  children  the  disease  is  milder  than  in  adult  s. 

^Etiology. — The  exciting  cause  appears  to  be  any  sudden  start, 


1984  DISEASES  OF  THE  NERVOUS  SYSTEM 

producing  some  peculiar  movement,  after  which  any  unlooked-for 
action  may  be  imitated,  and  is  generally  accompanied  by  bad 
language.  The  mildest  form  of  the  disease  is  merely  an  exclamation 
or  a  scream  when  startled,  but  in  severe  cases  the  patient  will 
imitate  any  sudden  motion  or  obey  any  suggestion  made  to  him. 

Fletcher  relates  that  in  some  parts  of  the  Malay  States  it  is 
occasionally  impossible  for  a  judge  to  examine  the  witnesses,  as 
they  can  do  nothing  but  imitate  and  repeat  the  questions  put  to 
them. 

According  to  Abraham,  the  exciting  causes  are:  (1)  Auditory — 
e.g.,  an  unexpected  noise  behind  the  person;  (2)  visual — some  un- 
looked-for movement ;  (3)  tactile,  such  as  a  sudden  touch. 

The  predisposing  cause  would  appear  to  be  racial. 

Symptomatology. — -On  hearing  an  unexpected  noise,  seeing  or 
performing  a  sudden  movement,  or  being  surprised  by  a  touch,  the 
patient  repeals  either  the  action  seen  or  the  words  uttered,  and  at 
the  same  time  may  use  foul  language.  The  unfortunate  victim  is 
generally  conscious  of  his  words  and  actions,  of  which  he  may  be 
ashamed,  but  he  is  quite  unable  to  control  them.  The  most  graphic 
account  of  the  symptomatology  of  the  fully-developed  complaint 
is  that  given  by  Sir  Hugh  Clifford  in  his  '  Brown  Humanity,'  from 
which  we  are  kindly  permitted  to  give  an  extract.  The  disease  is 
best  seen  in  the  Malays,  and  as  no  white  man  knows  these  people  as 
Sir  Hugh  Clifford  knows  them,  the  following  is  of  peculiar  value: — 

'  The  most  typical  case  of  latah  within  my  experience  was  that  of  a  Selangor 
Malay  named  Sat,  who,  in  1887  and  1888,.  cooked  the  rice  for  me  and  for  ten, 
twenty,  or  thirty  Malays  who  were  then  living  in  my  house  at  Pekai.  He  was 
a  great  big,  heavy-featured,  large-boned,  clumsily-built  fellow,  very  solid, 
very  stupid,  very  phlegmatic — the  last  person  in  the  world  one  would  have 
thought  to  be  the  victim  of  any  nervous  disorder.  To  the  lay  mind  any 
abnormal  degree  of  sensitiveness  should  be  accompanied  by  a  somewhat 
ethereal  physique,  a  delicate  skin,  a  blue-veined  forehead,  tiny  hands  and 
feet,  and  a  highly-strung  organization.  To  none  of  these  things  could  poor 
Sat  lay  any  sort  of  claim ;  and  though,  no  doubt,  doctors  will  say  that  these 
are  by  no  means  invariable  accompaniments  of  a  highly  nervous  tempera- 
ment, I  must  own  that  Sat  looked  vastly  improbable  as  the  possessor  of 
anything  so  rarefied.  All  the  other  Malays  in  my  household  were  accustomed 
to  put  upon  Sat  most  unmercifully,  making  him  do  almost  the  whole  of  the 
work  that  should  rightly  have  been  shared  between  them  all.  Sat  never 
appeared  to  resent  this  arrangement,  and  he  never  made  any  complaint  to  me 
then,  or  at  any  later  time,  of  the  manner  in  which  his  fellows  treated  him. 

'  He  spent  almost  the  whole  of  his  day  in  the  great  ramshackle  room,  built 
out  over  the  river  on  supporting  piles  of  nibong,  in  which  the  large  wooden  box, 
filled  with  baked  clay,  which  served  as  our  simple  cooking-range,  occupied  the 
chief  place  in  the  centre  of  the  tala  floor. 

'  When  the  others  were  most  noisy,  Sat  was  still  silent.  When  some  of 
my  men  boasted  of  the  great  deeds  they  had  performed  in  the  old  days  in 
Selangor,  Sat  would  listen  obediently  to  the  thrice-told  tales,  stolidly,  but 
without  excitement.  Most  of  the  other  men  had  their  own  particular  chums, 
but  Sat  was  always  solitary,  and  he  never  appeared  to  have  any  ideas  in  that 
great  bullet-head  of  his  which  he  desired  to  exchange  with  his  neighbours. 

'  He  had  been  an  inmate  of  my  hut  for  nearly  a  year  before  anyone  dis- 
covered that  he  was  latah.  The  fact  came  to  light  quite  accidentally,  Sat 
being  startled  out  of  his  self-possession  by  the  sudden  capsizing  of  a  cooking- 


SYMPTOMATOLOGY  1985 

pot  over  which  he  was  watching.  A  boy  who  chanced  to  be  alone  in  the 
cook-room  with  Sat  made  an  instantaneous  grab  at  the  fallen  rice-pot,  and 
in  an  instant  Sat's  hand  was  in  the  fire,  grasping  the  burning  hot  metal.  He 
withdrew  his  Hayed  fingers  quickly,  as  the  pain  brought  to  him  consciousness 
of  what  he  had  done,  and  he  carried  them  at  once  to  his  head — that  queer, 
groping,  scratching  motion  which  is  an  invariable  accompaniment  of  latah — 
and  the  boy  at  his  side  needed  no  man  to  tell  him  that  Sat  was  a  victim  to  that 
extraordinary  affliction. 

'  With  the  wanton  cruelty  and  mischief  of  his  age,  the  boy  once  more  made 
a  feint  at  the  smoking  rice-pot,  and  again  Sat's  ringers  glued  themselves  for 
a  moment  to  the  scalding  metal,  and  returned  aimlessly  to  his  head. 

1  I  do  not  know  how  many  times  this  was  repeated,  but  Sat's  fingers  were 
in  a  terribly  lacerated  condition  when  at  last  someone  chanced  to  enter  the 
cook-room,  and  interfered  to  prevent  the  continuation  of  Sat's  torture. 

'  After  that,  though  I  did  all  I  could  to  protect  him  from  molestation,  Sat 
was  never,  I  fancy,  left  in  peace  for  long  by  the  other  men  of  my  household. 
Gradually,  in  the  course  of  a  couple  of  months  or  so,  this  man,  who  for  nearly 
a  year  had  shown  no  signs  of  being  the  victim  of  any  nervous  disorder,  was 
reduced  to  a. really  pitiable  condition.  The  occasional  latah  seizures,  which 
were  at  first  induced  by  the  persecutions  of  his  fellows,  ceased  to  be  abnormal 
phases,  and  became  the  chronic  condition  of  his  mind.  If  one  spoke  to  him, 
with  no  matter  how  much  gentleness,  he  would  repeat  the  words  addressed  to 
him  over  and  over  again,  aimlessly,  unintelligently,  without,  apparently, 
comprehending  their  meaning,  and  that  wandering,  groping  hand  of  his  would 
steal  to  his  head,  and  scratch  helplessly  at  his  close-cropped  hair. 

'  "  Sat,  listen,  Sat !"  I  would  say  to  him  as  quietly  and  as  reassuringly  as 
I  knew  how.  "  Listen  !  no  man  is  worrying  thee.  Try  to  listen  to  what  I 
say  to  thee."  Sat  would  make  answer,  and  then,  very  low,  in  a  whisper  under 
his  breath:  "  Listen,  listen,  listen,  listen,  listen  what  I  say  to  thee." 

'  I  instituted  a  fine  for  anyone  who  was  found  annoying  Sat,  but  it  was 
impossible  to  get  a  conviction,  for  the  unfortunate  victim  could  never  say 
who  the  man  was  who  had  teased  him  into  a  more  than  usually  severe  paroxysm 
of  latah. 

'  It  was  about  this  time  that  a  number  of  other  people  in  my  household  began 
to  develop  signs  of  the  affliction.  I  must  not  be  understood  as  suggesting  that 
they  became  infected  with  latah,  for,  on  inquiring,  I  found  that  they  had  one 
and  all  been  subject  to  occasional  seizures  when  anything  chanced  to  startle 
them  badly  long  before  they  joined  my  people;  but  the  presence  of  so  complete 
a  slave  to  the  affliction  as  poor  Sat  seemed  to  cause  them  to  lose  the  control 
which  they  had  hitherto  contrived  to  exercise  over  themselves.  One  of  the 
older  men  among  my  people — Pa'Cbim,  we  called  him — a  Malay  by  birth, 
and  of  some  standing  with  his  fellows,  came  to  me  and  begged  that  I  would 
see  that  no  one  did  anything  to  give  him  a  sudden  start,  since,  he  said,  only  a 
very  little  was  needed  to  make  him  latah  also.  Yet  this  man,  neither  then  nor 
later,  showed  any  signs  of  the  affliction.  He  probably  exercised  a  consider- 
able amount  of  self-control,  but  I  always  knew  that  in  a  moment  I  could  have 
broken  through  his  guard,  and  have  startled  him  into  as  complete  a  seizure 
of  latah  as  those  of  which  Sat  was  the  victim. 

'  One  day  a  curious  thing  happened,  which  I  will  relate  as  it  occurred, 
though  I  only  witnessed  the  end  of  the  incident. 

'  A  Trengganu  Malay,  who  had  a  cousin  among  my  people,  came  in  to  visit 
his  relative,  and  chanced  to  find  no  one  but  Sat  in  the  house.  The  latter 
invited  the  TrSngganu  man  to  partake  of  slrih,  and  they  squatted  down  on 
the  pentas,  or  raised  eating-platform,  in  the  centre  of  the  house,  with  the 
slrih-box  between  them.  The  villainous  small  boy  who  had  first  discovered 
Sat's  weakness  was  playing  about  in  the  room,  and  in  some  unholy  way  he 
had  learned  that  the  Trengganu  visitor  was  also  a  latah  subject.  He  seized 
a  long  rattan,  which,  I  think,  was  kept  in  the  room  by  one  of  the  older  men 
for  his  occasional  correction,  and  smote  the  slrih-box  as  it  lay  between  the 
two  betel-chewers,  making  the  wooden  covering  resound  with  the  smart  blow. 
The  sudden  and  unexpected  noise  at  once  deprived  both  men  of  all  power  of 

125 


1 986  DISEASES  OF  THE  NERVOUS  SYSTEM 

self-restraint.  Each  gave  a  sharp  cry  and  a  "  jump  " — to  use  the  colloquial 
expression — and,  since  there  was  nothing  to  distract  their  attention  from  one 
another,  they  fell  to  imitating  each  the  other's  gestures.  For  nearly  half  an 
hour,  so  far  as  I  could  judge  from  what  I  learned  later,  these  two  men  sat 
opposite  to  one  another,  gesticulating  wildly  and  aimlessly,  using  the  most 
filthy  language,  and  rocking  their  bodies  to  and  fro.  They  never  took  their 
eyes  off  one  another  for  sufficient  time  for  the  strange  influence  to  be  broken, 
and  at  length,  utterly  worn  out  and  exhausted,  first  Sat  and  then  the 
Trgngganu  man  fell  over  on  the  platform  in  fits,  foaming  horribly  at  the 
mouth  with  thin,  white  flakes  of  foam.  Men  came  running  to  me  for  help, 
many  having  witnessed  the  end  of  this  strange  scene,  and  when  I  had  doctored 
Sat  and  his  companion  back  to  consciousness,  I  tried  to  ascertain  from  them 
how  they  had  come  to  fall  victims  to  this  seizure.  They  could  tell  me  nothing, 
however,  for  they  only  remembered  that  before  their  trouble  came  upon 
them  they  had  been  chewing  betel-nut.  The  matter  was  sifted  out,  none  the 
less,  and  the  small  boy  who  had  been  the  cause  of  the  trouble  again  made 
the  acquaintance  of  the  piece  of  rattan,  and,  to  judge  by  his  cries,  found  the 
interview  an  unusually  painful  one.' 

From  the  above  account  it  will  be  seen  that  a  sudden  action 
will  inhibit  the  higher  centres  and  produce  reflex  movements  in 
imitation  of  those  performed  by  the  exciting  cause.  The  loss 
of  memory  of  what  has  taken  place  and  the  peculiar  movement  of 
the  hand  to  the  head  indicates  the  abrogation  of  the  higher  powers. 

Varieties.— There  are  two  varieties  of  the  complaint — the  im- 
pulsive and  the  mimetic.  The  former,  produced  by  a  sudden  shock, 
results  in  violent  action  or  bad  language,  of  which  the  patient  may 
be  very  ashamed.  The  mimetic  is  the  form  in  which  the  sufferer, 
no  matter  how  unwilling,  is  compelled  to  imitate. 

Allied  Complaints. — Latah  must  be  closely  related  to  those  curious, 
psychical  phenomena  seen  at  times  among  different  races,  the 
afflicted  people  being  variously  known  in  Europe  as  '  the  Jumpers,' 
'  the  Barkers,'  and  '  the  Jerks,'  and  must  also  be  allied  to  those 
states  of  excitement  into  which  people  pass  during  times  of  religious 
revivals.  In  our  experience  it  has  also  a  certain  resemblance  to 
some  cases  of  so-called  '  Maladie  de  Gilles  de  la  Tourette,'  the  main 
symptoms  of  which  are  echolalia  and  coprolalia. 

A  peculiar  psychical  outbreak  took  place  in  Madagascar  in  the 
years  1863-64  among  the  women  of  the  lowest  classes,  consequent 
on  the  profound  sensations  caused  by  the  violent  death  of  King 
Ramada  II.,  and  the  subsequent  changes  in  the  religion  and  laws. 
This  outbreak  is  said  to  have  been  identical  with  the  dancing  mania 
of  the  Middle  Ages.  It  is  interesting  to  remember  that  there  is  a 
strong  admixture  of  Malay  blood  in  the  natives  of  Madagascar, 
especially  in  the  ruling  classes. 

It  is  thus  seen  that  the  condition,  though  at  present  most  marked 
among  the  Malays,  is,  and  has  been,  world-wide  in  its  spread,  and 
is  really  due  to  the  possession  of  feeble  higher  centres  which  are 
easily  upset,  and  then  are  unable  to  control  the  lower  centres  in  the 
accustomed  manner. 

Diagnosis. — The  diagnosis  of  latah  is  based  upon  the  individual 
uncontrollably  performing  or  imitating  actions,  often  with  echolalia 
or  coprolalia. 


hANGA—SCHAMANISMUS  1987 

Prognosis. — Latah  is  said  never  to  end  in  insanity. 

Medico-Legal. — With  regard  to  the  medico-legal  aspect  of  latah, 
Fletcher  has  performed  an  experiment  with  a  severely  affected 
subject,  proving  that  suggestion  can  compel  a  latah  subject  to 
commit  a  crime  even  against  his  will.  He  concludes  that  in  latah 
crime  is  a  possibility  either  as — 

1.  An  act  resulting  from  an  imperfectly  controlled  inco-ordinate 
reaction  to  a  sudden  impulse;  or  as — 

2.  An  act  resulting  from  the  suppression  of  volition  in  the  severe 
forms,  the  determining  cause  of  which  is  a  criminal  suggestion  by  a 
second  person. 

In  evidence  of  the  first,  he  cites  two  Malays  going  through  a  forest 
'carrying  their  knives  for  cutting  wood.  A  twig  suddenly  snaps, 
■  and  the  first  man  falls  to  the  ground,  which  so  upsets  the  second 
one  that  he  also  falls  to  the  ground,  and  in  so  doing  accidentally 
wounds  the  first  man  with  the  knife  he  is  carrying.  In  evidence  of 
the  second,  he  places  a  dummy  in  a  bed  previously  occupied  by  a 
friend  of  a  latah  person  who  had  been  removed  without  the  latter's 
-knowledge.  Suddenly  the  latah  person  was  ordered  to  take  a 
knife  which  was  placed  in  a  handy  position,  and  stab  the  dummy  in 
the  bed.  The  latah  person  tried  not  to  do  this,  but  was  compelled 
to  obey  the  suggestion.  Thus,  it  would  appear  that  there  may  be 
a  near  connection  between  latah  and  crime. 

Treatment. — The  treatment  is  most  unsatisfactory,  but  auto- 
suggestion might  be  tried.  Abraham  states  that  some  patients 
have  cured  themselves  by  determination  not  to  succumb. 


BANGA. 

Definition. — -A  hysterical  condition,  chiefly  influencing  women 
above  the  age  of  puberty,  but  also  occurring  in  men  in  the  Welle 
District  of  the  Belgian  Congo. 

Symptomatology. — Fright  or  anger  may  induce  an  attack,  in 
which  the  body  is  shaken  by  convulsions,  followed  by  wild  cries  and 
rushes  out  into  the  open  country  or  forest  away  from  frequented 
paths.     Sometimes  it  is  accompanied  by  aphasia. 

Diagnosis. — It  is  said  to  be  separable  from  hysteria  by  the  absence 
1  of  the  stigmata  of  that  disease. 

Treatment. — Suggestion  appears  to  cure  these  cases. 


SCHAMANISMUS. 

Schamanismus  is  the  condition  of  excitement  into  which  certain 
'of  the  Dayaks  and  other  peoples  are  able  to  throw  themselves  for 
religious  purposes.  This  state  of  excitement  seems  to  be  attained 
by  leading  an  extremely  erotic  life,  and  appears,  by  its  singing, 
shrieking,  and  dancing  to  utter  weariness,  to  resemble  the  dancing 
mania  of  the  Middle  Ages,  and,  therefore,  to  be  related  to  latah. 


ig88  DISEASES  OF  THE  NERVOUS  SYSTEM 

AMOK. 

Definition. — Amok  is  a  psychical  disturbance,  which,  after  a 
period  of  depression,  suddenly  develops  into  a  violent  attempt  to 
kill  people,  of  which  no  memory  may  be  left,  and  after  which  a 
stuporous  condition  supervenes. 

Remarks. — Amok,  which  means  '  an  impulse  to  murder,'  is  a 
disease  frequently  found  among  the  Malays,  but  also  occasionally 
in  other  Oriental  races.  Abraham  thinks  that  there  may  be  some 
relationship  between  amok  and  latah. 

Climatology. — Amok  is  found  in  Malaysia  among  the  Bugis  of 
Celebes,  the  Malays  of  Indo-China,  Malacca,  and  the  Malay  States. 
It  is  also  said  to  occur  at  times  in  Trinidad  and  among  the  inhabi- 
tants of  India  and  Siberia. 

etiology. — The  exciting  cause  appears  to  be  a  strong  emotion  of 
anger,  sorrow,  or  fear,  after  which  a  pause  or  incubation  period  of 
depression  follows,  which  may  last  for  days  or  weeks,  during  which 
the  patient  broods  over  his  wrongs.  The  Dutch  believe  that  it  is 
induced  by  opium  smoking,  and  Miall  that  it  is  due  to  smoking 
haschisch  (Cannabis  indica) ;  but  these  causes  are  insufficient. 

Symptomatology. — The  attack  is  ushered  in  by  colour  sensations 
of  red  or  black,  with  or  without  vertigo,  and  the  patient  complains 
of  the  appearance  of  devils,  which  he  attempts  to  kill.  The 
amoker  usually  rushes  out  of  his  abode  and  attacks  friends  or  foes, 
young  or  old,  males  or  females,  with  his  kris,  or  flame-shaped  knife, 
or  by  firing  on  them  with  a  gun.  The  attack  usually  lasts  but  a 
short  time,  and  the  deeds  performed  during  that  period  are  not 
remembered.  After  the  attack  the  patient  passes  into  a  stuporous 
condition  or  deep  sleep,  which  may  last  for  a  long  time,  after  which 
he  remains  in  a  peculiar  excitable  condition  for  some  months. 

Allied  Complaints. — This  is  a  curious  pathological  entity,  and  may 
be  a  genuine  psychical  obliquity  closely  related  to  those  epileptoid 
seizures  investigated  in  Europe  by  Lombroso. 

Medico-Legal. — If  a  case  is  considered  genuine,  the  patient  must 
not  be  regarded  as  responsible  for  his  actions,  but  each  case  should 
be  judged  on  its  own  merits. 

Treatment. — -No  treatment  has  so  far  been  tried  in  the  prodromal 
stage,  as  far  as  we  know. 

TROPICAL  NEURASTHENIA. 

No  disease  among  Europeans  in  the  tropics  deserves  more  careful 
study  by  the  practitioner  than  neurasthenia,  because,  though  not 
in  itself  fatal,  still  it  leads  to  many  of  the  petty  worries  felt  and  bad 
tempers  exhibited,  and,  in  worse  cases,  may  seriously  hamper  good 
work  being  performed.  The  subject  has  been  ably  studied  by  Fales 
in  Americans  returning  from  the  Philippine  Islands. 

/Etiology. — Tropical  neurasthenia  is  apt  to  develop  in  white 
people  in  any  part  of  the  tropics, but  especially  in  those  which  are 


TROPICAL  NEURASTHENIA  1989 

subject  to  moist  heat,  and  in  some  cases  an  important  predisposing 
cause  is  the  sun's  rays,  the  effects  of  which  are  often  disregarded. 
Moreover,  the  white  man  is  generally  compelled  to  work  hard 
throughout  the  heat  of  the  day,  and  is  often  exposed  to  the  midday 
sun.  The  liability  to  the  disease  increases  with  the  length  of  resi- 
dence in  the  tropics.  Predisposing  causes  are  any  previous  illness, 
alcoholism,  and  overwork.  Fales  states  that  he  found  30  per  cent, 
of  the  men  and  50  per  cent,  of  the  women  who  had  resided  for  a 
year  or  longer  in  the  Philippine  Islands  the  subjects  of  such  severe 
neurasthenia  as  to  be  semi-invalids.  In  our  experience  the  disease 
is  extremely  common  all  over  the  tropics  in  Europeans  as  well  as 
in  the  natives  of  the  educated  class. 

Symptomatology. — In  addition  to  the  ordinary  signs  of  neuras- 
thenia, the  tropical  form  seems  to  markedly  affect  the  vascular 
system;  palpitation  is  very  common,  and  the  patients  suffer  from 
various  kinds  of  phobia,  especially  relating  to  diseases  of  the 
tropics. 

Treatment. — The  best  treatment  is  rest  and  change  of  climate 
and  mild  hydropathic  treatment.  If  this  is  not  possible,  hypo- 
dermic injections  of  sodium  glycero-phosphate — o-i  gramme  daily 
in  bad  cases — or  some  form  of  glycero-phosphate,  with  or  without 
polyformates,  by  the  mouth  in  mild  cases,  may  be  tried.  The 
patient  should  discontinue  cold  baths,  and  should  use  warm  baths, 
which  should  be  taken  at  night  if  there  is  sleeplessness.  Bromides 
are  occasionally  useful. 

Prophylaxis. — As  in  some  cases  the  disease  is  predisposed  by 
exposure  to  the  sun,  protection  is  required  against  thi  sun's  rays 
by  topees  lined  with  red,  and,  if  necessary,  by  red  underclothing 
or  clothes  made  from  the  '  solaro  '  fabric  already  mentioned,  and 
by  avoidance  of  the  midday  sun  as  much  as  possible,  and  the  total 
abstinence  from  alcohol. 

Persons  who  are  compelled  to  work  hard  under  unfavourable 
conditions  require  change  to  the  Temperate  Zone  at  relatively  short 
intervals — i.e.,  about  once  in  two  or  three  years. 

ENDEMIC  PERIPHERAL  NEURITIS. 

Synonym. — Akat  ama. 

Definition. — Endemic  peripheral  neuritis  is  a  disease  of  unknown 
origin,  characterized  by  numbness  and  intense  prickling  and 
burning  sensations  in  the  presence  of  cold  or  damp,  which  are 
temporarily  relieved  by  the  application  of  dry  heat. 

History.— The  disease  was  first  noticed  by  Wellman  in  Central 
Africa  in  1896,  and  described  by  him  in  1903.  It  affects  3  to  5  per 
cent,  of  the  Bantu  people,  who  are  by  profession  porters,  and  are 
much  impeded  in  their  work  by  this  complaint,  which  affects  young 
and  old,  male  and  female  alike.  Their  staple  food  is  maize,  which 
is  eaten  partially  cooked. 

Climatology. — The  disease  i>  found  in  that  plateau  of  Africa 


iggo  DISEASES  OF  THE  NERVOUS  SYSTEM 

which  is  5,000  to  6,000  feet  high,  and  is  situated  between  130  to 
140  south  latitude,  and  is  inhabited  by  the  Bihe,  Bailundo,  and 
Andulu  peoples,  all  of  whom  are  Bantus. 

./Etiology. — Wellman  was  unable  to  find  any  causative  organism 
in  the  blood  or  faeces.  Some  of  the  natives  also  suffered  from 
filariasis,  ankylostomiasis,  and  bilharziosis,  but  these  were  adven- 
titious. His  theories  are  that  it  may  be  caused  by  cold,  fermented 
maize,  or  nerve- star  vat  ion;  but  he  is  not  satisfied  with  any  of 
these  hypotheses. 

Morbid  Anatomy.- — In  bad  cases  there  is  some  swelling,  erythema, 
and  slight  oedema  of  the  affected  part;  still,  biopsies  of  the  skin 
revealed  nothing,  and  post  mortem  the  nerves  were  found  normal. 

Symptomatology. — The  disease  usually  begins  with  shooting, 
pricking,  or  crawling  pains  in  the  legs  and  forearms,  accompanied 
by  numbness,  together  with  an  erythematous  rash  and  swelling  of 
the  affected  area.  All  these  symptoms  are  increased  by  cold  and 
damp,  and  diminished  by  heat  and  dryness.  They  may  also  appear 
on  the  thighs  and  arms,  and  occasionally  on  any  part  of,  or  all  over, 
the  body.  The  gait  is  peculiar,  the  patient  appearing  to  walk  on 
the  toes  and  heels.  The  disease  may  last  for  years,  but  spon- 
taneous recovery  is  known. 

Diagnosis. — The  diagnosis  is  easy,  for  it  is  distinguished  from 
beri-beri  by  the  absence  of  pain  in  the  calves,  by  the  absence  of 
the  heart  symptoms,  and  of  the  paralysis;  from  elephantiasis  by  the 
swelling  being  transitory;  from  malaria  by  an  examination  of 
the  blood;  and  from  pellagra  by  the  symptoms  improving  during 
the  warm  season. 

Prognosis.- — This  is  good  as  to  life  and  general  health,  though  the 
course  of  the  malady  may  be  very  protracted. 

Treatment. — No  method  of  treatment  is  known  to  do  any  good. 


ERYTHROMELALGIA  TROPICA. 

Under  this  term  Gerrard  describes  a  nerve  condition  in  which 
natives  who  work  barefoot  on  roads  and  plantations  in  Malaya 
complain  of  a  feeling  of  pins  and  needles  in  the  soles  of  the  feet, 
followed  by  an  acute  burning  sensation,  which  prevents  walking  and 
sleeping.  Malaria  is  assigned  to  be  the  cause.  The  treatment 
recommended  is  to  place  the  feet  in  hot  salt-water,  which  is  said  to 
give  great  relief. 

DESERT  HALLUCINATIONS. 

Synonym.— Le  Ragle. 

D'Escayrac  de  Lauture  describes  hallucinations  of  the  senses  of 
sight,  hearing,  smell,  or  taste,  or  even  of  common  sensations,  which 
attack  persons  suffering  from  exhaustion  in  deserts.  The  causation 
is  probably  inanition.  Generally  the  attack  comes  on  at  night,  but 
it  may  occur  in  the  day-time,  when  it  is  considered  to  be  more 


REFERENCES  1991 

serious.  Usually  hallucinations  are  visual,  and  thus  stones  look 
like  buildings  or  large  rocks,  while  caravans  or  files  of  soldiers  may 
be  seen  which  do  not  exist.  It  has  nothing  to  do  with  true  mirage. 
Chalmers  has  met  with  a  case  which  occurred  in  the  Egyptian 
deserts,  in  which  the  attack  at  first  only  came  on  during  the  night, 
but  once  occurred  in  the  day.  Its  causation  appeared  to  be  due  to 
very  hard  work  and  mental  worry.  The  symptoms  quickly  dis- 
appear under  the  influence  of  rest,  better  food,  and  cessation  of  worry. 

EMOTIONAL  EXCITEMENT. 

Synonym.— Misala. 

Howard,  in  a  very  interesting  paper,  has  recorded  cases  of 
emotional  excitement  called  '  misala,'  which  vary  from  an  attack  of 
tropical  anger  to  a  condition  almost  bordering  on  mania,  which  can 
be  controlled  by  authoritative  commands,  or  which,  left  to  them- 
selves, pass  off  in  a  few  hours  or  days.  It  occurs  among  the  young 
adult  males  of  Nyassaland. 

DELUSIONS. 

Delusions  of  poisoning  and  of  bewitchment  are  common  in  Africa 
and  Asia,  and  probably  elsewhere,  and  are  common  explanations 
of  various  forms  of  disease  or  of  hysteria. 

AUTO-SUGGESTION. 

Every  practitioner  in  Africa  and  Asia  is  acquainted  with  the 
extraordinary  ease  with  which  a  native  can  die  if  he  makes  up  his 
mind  to  do  so.  The  actual  cause  of  death  is  often  exhaustion  due 
to  starvation.     It  should  be  treated  by  suggestion. 


REFERENCES. 

Abraham  (1912).     British  Medical  Journal.     London. 

Baker,    S.    (1896).     Journal   of   Nervous   and   Mental   Diseases,    vol.   xxiii. 

(Auto-Mimesis.)     New  York. 
Barry  (1910).     Indian  Medical  Gazette.     (Nervous  Breakdown  in  Burma.) 

Calcutta. 
Bennett,  A.  C.  (1889).     South  African  Medical  Journal.     (Jumpers.)     East 

London. 
Breitenstein,  H.  (1899).     Aerztliche  Centralblat-Anzeiger,  vol.  xi.     Wien. 

(Die  Latah-Krankheit.) 
Brero  (1905).     Mense's  Tropenkrankheiten,  i.  210. 
Catrou,   J.   (1890).     Etude  sur  la  Maladie  des  Tics  convulsifs.     (Jumping 

Latah,  Myriachit.)     Paris. 
Clifford.     Brown  Humanity.     London. 
CouchoudandShionoya  (1915).    Revue  deM6decine,  xxvi..  No.  5.    (Endemic 

Paralytic  Vertigo.) 
Ellis  (1897-98).     Journal  of  Medical  Science. 
Ellis,  W.  G.  (1897).     journal  of  Mental  Science.     (Latah.)     London. 


i992  DISEASES  OF  THE  NERVOUS  SYSTEM 

Fichera  (1914).     Riforma  Medica,  October.     (Endemic  Paralytic  Vertigo.) 
Fletcher  (1908).     Lancet,  vol.  ii. 

Gerrard  (1904).     Dublin  Journal  of  Medical  Science.    (Latah.)     Dublin. 
Gilmour,  A.  (1902).     Scottish  Medical  and  Surgical  Journal.     (Latah  among 

South  African  Natives.)     Edinburgh. 
Gimlette  (1897).     British  Medical  Journal. 
Fusco  (1918).     Malaria,  vol.  ix.,  Nos.  1,  2. 
Howard,  R.  (1910).     Transactions  of  the  Society  of  Tropical  Medicine  and 

Hygiene,    June.     (Emotional   Psychoses   among    Dark-Skinned   Races.) 

London. 
Hurst  (1918).     Medical  Diseases  of  the  War,  2nd  edition.     London. 
MacCurdy  (1918).     War  Neuroses.     Cambridge. 
Montel  (1916).     Bull.  Soc.  Med.-Chir.  Indochine,  vol.  vii.,  No.  8. 
Neal  (1884).     British  Medical  Journal.     London. 
O'Brien  (1883).     Journal  of  the  Royal  Asiatic  Society.     Singapore. 
Rodhain  (1915).     Bulletin  de  la  Societe  de  Pathologie  Exotique,  December, 

734-745.     (Banga.) 
Scheube  (1910).     Die  Krankheiten  der  Warmen  Lander.     Jena. 
Woods  (191S).     China  Med.  Jour.,  vol.  xxxii.,  No.  2. 


CHAPTER  XC 

DISEASES  OF   THE  ORGANS  OF  SPECIAL 

SENSE 

General  remarks — Diseases  of  the  eye — Diseases  of  the  ear — Diseases  of  the 

nose — References . 

GENERAL  REMARKS. 

It  is  not  usual  to  consider  the  diseases  of  the  organs  of  special  sense 
in  a  work  on  tropical  medicine,  but  all  the  diseases  of  the  tropics 
are  being  carefully  studied  at  the  present  time,  and  therefore  we 
are  of  the  opinion  that  a  few  cursory  remarks  on  the  above  subjects, 
from  the  point  of  view  of  the  general  practitioner,  may  be  of  some 
interest. 

DISEASES  OF  THE  EYE. 

The  history  of  the  study  of  eye  disease  in  the  tropics  has  still 
to  be  written,  but  anyone  interested  in  the  general  history  of  this 
branch  of  medical  science  is  referred  to  Hirsch,  '  Geschichte  der 
Augenheilkunde  '  (Leipzig,  1877),  which,  though  issued  as  a  separate 
little  volume,  was  originally  part  of  Graefe's  and  Saemich's  '  Hand- 
buch  der  Augenheilkunde,'  vol.  vii.  In  this  book  there  is  an 
account  of  the  ophthalmology  known  in  ancient  Egypt  and  India, 
as  well  as  the  history  before  and  during  the  Alexandrine  period  of 
medical  development.  It  will  suffice  to  say  that  eye  disease  is 
described  and  treated  in  the  Ebers  papyrus,  and  that  Susruta 
mentioned  76  diseases  of  the  eye,  of  which  9  were  of  the  joinings 
of  the  eye,  21  of  the  eyelids,  11  of  the  sclerotic,  4  of  the  black  part 
of  the  eye,  17  of  the  eye  in  general,  12  of  the  true  organ  of  vision, 
and  2  were  injuries.  In  recent  years  the  work  of  the  ophthalmic 
surgeons  of  India  and  Egypt  and  elsewhere  has  been  beneficial, 
not  merely  in  an  extension  of  knowledge,  but  more  importantly  in 
benefit  to  the  communities  of  the  lands  in  which  they  live.  Excel- 
lent work  has  been  done  by  the  travelling  ophthalmic  hospitals, 
such  as  those  provided  by  private  generosity  in  Egypt,  which  go 
from  district  to  district.  By  this  means,  natives  at  a  distance  from 
main  hospitals  are  enabled  to  obtain  expert  advice  and  treatment, 
which  can  be  carried  on  in  the  interval  between  a  visit  by  the  local 
hospital  and  dispensary. 

Another  excellent  institution  of  more  or  less  recent  origin  is 
the  Central  Ophthalmic  Hospital,  to  which  the  patient  can  be 

1993 


1994         DISEASES  OF  THE  ORGANS  OF  SPECIAL  SENSE 

sent  or  more  prolonged  expert  treatment.  A  model  hospital  of 
this  nature  can  be  found  in  the  Victoria  Eye  Memorial  in  Colombo, 
Ceylon.  The  prevalence  and  importance  of  eye  disease  in  the 
tropics  cannot  be  too  strongly  insisted  upon.  The  cases  of  oph- 
thalmia are  so  frequent  that  it  has  been  stated  that  in  no  region  of 
the  world  is  conjunctivitis  so  common,  which  may  be  due  to  the 
high  temperature  which  favours  the  growth  of  micro-organisms; 
to  the  overcrowded  and  filthy  native  dwellings,  which  favour  their 
dissemination;  to  the  dirty  habits  of  the  lower-class  natives;  and 
to  the  presence  of  large  numbers  of  flies  at  certain  seasons,  which 
also  materially  assist  in  the  spread  of  infection  from  the  diseased 
to  the  healthy.  Moreover,  these  factors  are  reinforced  by  the 
irritation  caused  by  the  glare  of  the  sun,  and  by  the  dust.  Blind- 
ness is  also  very  prevalent  in  the  tropics.  Denham,  in  his  report 
on  the  census  in  Ceylon  in  1911,  states  that,  in  a  population  of 
4,106,350  persons,  there  Were  3,957  blind  persons,  which  figures, 
when  analyzed,  showed  that  there  were  11  blind  men  and  8  blind 
women  in  every  10,000  men  and  women  in  Ceylon.  In  India,  in 
1901,  there  were  12  blind  men  and  12  blind  women  per  10,000  of  each 
sex;  while  in  England,  in  1901,  there  were  8  blind  men  and  7  blind 
women  per  10,000  of  each  sex. 

Dr.  Andreas  Nell,  in  his  statistics  of  the  Victoria  Eye  Memorial  Hospital  in 
Colombo,  Ceylon,  for  the  years  1906-1918,  shows  that  the  causes  of  blindness 
in  Ceylon  may  be  classified  as  follows : — 

Congenital  Causes. — These  included  malformations  of  the  eyeball,  and  syphilis 
acting  upon  the  optic  nerve,  retina,  and  choroid. 

Local  Eye  Diseases. — Ophthalmia  neonatorum,  Purulent  ophthalmia  in 
adults,  Catarrhal  ophthalmia,  Granular  ophthalmia,  Ulceration  of  the  cornea, 
Severe  paralysis  of  the  ocular  muscles,  and  Glaucoma. 

Traumatisms. — Injuries  from  sticks,  thorns,  and  edges  of  leaves  in  the  jungle, 
from  spikes  in  the  paddy  ear,  from  the  tips  of  the  blades  of  water-grasses. 
Some  of  these  injuries  are  at  first  trifling,  but  may  become  septic,  and  so  cause 
blindness. 

Constitutional  Diseases. — These  include  syphilis,  malignant  tumours,  leprosy, 
tuberculosis,  and  enteric  fever,  but  malarial  cachexia  was  not  met  with  as  a 
cause  of  blindness,  nor  was  ankylostomiasis. 

Drugs. — Alcohol  (most  common) ;  tobacco  (rare) ;  quinine  and  opium  (very 
rare) . 

There  can  be  no  doubt  that  blindness  arises  from  neglect  of  the 
trivial  cases  of  eye  disease,  and  from  septic  infection,  and  that, 
as  medical  aid  becomes  more  readily  available  and  hygiene  is  im- 
proved, this  serious  affliction  will  diminish  in  the  tropics. 

For  the  purposes  of  the  few  remarks  which  we  propose  to  make 
it  will  be  convenient  to  divide  the  subject  into:  A.  Eye  Diseases 
Proper;  and  B.  Eye  Complications  of  Tropical  Diseases. 

A.  EYE  DISEASES  PROPER. 

(Edema  of  the  Eyelids. 

Under  this  term  Chalmers  and  Marshall  mention  the  acute  swell- 
ing of  the  eyelids  in  Europeans  and  natives  in  Khartoum.     The 


EYE  DISEASES  PROPER  1995 

affected  area  shows  the  mark  of  a  bite,  and  may  perhaps  be  due  to 
an  ant,  perhaps  of  the  genus  Monomorium  Mayr,  1855. 

Congenital  Defects. 

These  are  by  no  means  uncommon  in  the  tropics,  and  our  experi- 
ence includes  cases  of  apparent  anophthalmia  or  microphthalmia, 
coloboma,  and  albinism. 

Colour  Blindness. 

This  is  of  importance,  and  natives  who  are  to  be  employed  as  pilots 
or  on  railways  should  be  examined  as  to  their  power  of  distinguishing 
colours;  and,  indeed,  if  this  has  been  neglected,  it  is  advisable  to 
examine  the  existing  employes,  as  the  results  of  such  examinations 
are  sometimes  surprising.  In  testing,  only  the  Eldridge-Green 
lamp  and  method  should  be  used. 

Errors  of  Refraction. 

A  subject  which  has  begun  to  attract  a  considerable  amount  of 
attention  is  the  condition  of  the  eyes  of  native  children  in  the  more 
modern  and  higher  class  native  schools,  as  regards  errors  of  refrac- 
tion; but  the  medical  inspection  of  native  schools  in  the  tropics  is 
at  present  neglected,  though  the  children  suffer  from  what  may  be 
termed  book  hunger,  and  so  strain  their  eyes  excessively. 

Foreign  Bodies. 

In  addition  to  the  usual  foreign  bodies  met  with  in  the  Temperate 
Zone,  small  flies  are  apt  to  get  into  the  eye  in  the  early  evening, 
and  some  of  these  are  very  irritating,  and  may  cause  congestion; 
or,  by  introducing  micro-organisms,  conjunctivitis.  Chalmers  and 
Marshall  record  the  finding  of  a  small  ant,  Monomorium  bicolor  var. 
nitidiventre,  firmly  fixed  by  its  jaws  on  to  the  ocular  conjunctiva  in 
a  person  in  Khartoum. 

Pterygium. 

In  this  disease  the  pinguecula,  being  irritated,  spreads  on  to  the 
cornea,  and  carries  the  conjunctiva  with  it,  thus  giving  rise  to 
triangular  folds  extending  from  the  ocular  conjunctiva  to  the  cornea 
on  the  inner  or  outer  aspects  of  the  eye.  It  is  very  common  in  the 
tropics,  especially  among  coolies  in  Indo-China. 

The  treatment  is  removal. 

Hyperemia  of  the  Conjunctiva. 

This  is  extremely  common,  being  caused  by  the  glare  of  the  sun 
or  by  the  dust,  especially  in  sandy  regions,  and  is  especially  apt 
to  occur  in  persons  who  have  some  slight,  and  perhaps  unnoticed, 
error  of  refraction.  It  is  also  more  liable  to  occur  in  persons  who 
have  some  congestion  of  the  naso-pharynx,  and  is  one  of  the  symp- 
toms of  rhinitis  spastica  vasomotoria.  Usually  the  symptoms  are 
but  slight,  but  the  eyes  are  inclined  to  water;  this  is  aggravated 


1996         DISEASES  OF  THE  ORGANS  OF  SPECIAL  SENSE 

by  exposure  to  light,  while  the  patient  may  complain  of  a  slight 
feeling  of  grit  in  the  eye  or  of  a  burning  sensation. 

On  examination,  a  portion  of  the  palpebral  and  of  the  ocular 
conjunctiva  is  seen  to  be  congested,  while  the  secretion  from  the 
Meibomian  glands  is  noticed  to  be  increased  in  amount  and  the 
eyes  to  be  watery.  Treatment  consists  in  bathing  with  warm 
2  per  cent,  solution  of  boric  acid,  in  giving  the  eye  rest,  and  in 
wearing  neutral-tinted  or  yellowish-tinted  glasses  (Xanthophylline), 
which  can  be  obtained  in  three  strengths — light,  medium,  or  strong. 

Conjunctivitis. 

This  is  extremely  common  in  the  tropics  among  natives  and 
Europeans,  and  may  be  clinically  subdivided  into — (i)  Conjunc- 
tivitis catarrhalis;  (2)  Conjunctivitis  gonorrhoea;  (3)  Ophthalmia 
neonatorum;  (4)  Conjunctivitis  trachomatosa;  (5)  Epitheliosis 
desquamativa;  (6)  Conjunctivitis  phlyctenulosa;  (7)  Conjunctivitis 
vernalis.  Diphtheria  is  not  common  in  the  tropics,  and  diphtheritic 
conjunctivitis  is  rare,  while  conjunctivitis  nodosa  is  extremely  rare, 
but  can  be  caused  by  caterpillar  hairs,  or  plant  hairs,  becoming 
embedded  in  the  conjunctiva. 

Conjunctivitis  Catarrhalis. 

This  may  be  subdivided  into  the  acute,  the  chronic,  and  the 
follicular  forms. 

The  Acute  Variety. — This  is  very  common  in  the  tropics,  where 
it  may  occur  in  epidemics.  The  most  common  cause  is  the  Koch- 
Weeks  bacillus,  which  may  induce  a  very  severe  form  of  inflam- 
mation; while  almost  as  frequently  the  Morax-Axenfeld  bacillus 
causes  a  milder  though  more  prolonged  attack,  often  called  angular 
conjunctivitis.  Rarer  causes  are  the  pneumococcus  and  staphy- 
lococcus. The  small  eye  fly  of  Ceylon  is  suspected  by  Castellani  and 
Perry  of  being  an  agent  in  the  spread  of  this  disease  in  Colombo. 

The  disease  begins  with  photophobia,  burning  and  itching  in  the 
eyes,  with  a  sensation  of  grit,  all  of  which  symptoms  are  more  pro- 
nounced in  the  morning  than  in  the  evening,  when  the  eyelids  are 
often  glued  together  by  the  dried  conjunctival  secretion. 

On  examination,  the  palpebral  and  ocular  conjunctivae  are  seen 
to  be  red  and  congested,  and  sometimes  to  be  marked  by  red  spots 
indicative  of  small  haemorrhages,  while  the  conjunctival  secretion 
is  increased  in  amount  and  may  have  particles  of  mucus  swimming 
in  it,  or  it  may  be  largely  composed  of  mucus,  or  in  severe  cases  it 
may  be  purulent.  Usually  both  eyes  are  attacked.  The  disease 
may  disappear  in  eight  to  fourteen  days  if  untreated,  but  more 
usually  it  becomes  chronic.  The  complications  most  commonly- 
observed  are  corneal  ulcer  and  iritis. 

The  best  treatment  in  severe  cases  is  to  evert  the  eyelids,  and  to 
lightly  mop  the  inflamed  conjunctiva  with  2  per  cent,  solution  of 
silver  nitrate,  followed  by  a  weak  solution  of  halt,  or  by  instilling  a 


EYE  DISEASES  PROPER 


1997 


10  per  cent,  solution  of  protargol,  or  10  to  25  per  cent,  of  argyrol. 
Ice  compresses  are  very  soothing.  For  the  inflammation  due  to 
the  diplobacillus  of  Morax  and  Axenfeld,  the  best  treatment  is  to 
instil  a  0-25  per  cent,  solution  of  zinc  sulphate  two  or  three  times 
a  day,  or  a  0-50  per  cent,  solution  once  a  day.  When  the  acute 
symptoms  have  subsided,  a  little  adrenalin  may  be  added  to  the 
zinc  sulphate  solution. 

In  order  to  prevent  the  sticking  together  of  the  eyelids,  a  2  per 
cent,  ointment  of  boric  acid,  or  a  \  per  cent,  strength  of  white  pre- 
cipitate ointment,  may  be  used. 

It  is  almost  unnecessary  to  state  that  no  bandage  should  be 
applied  to  the  eye,  or  that  the  disease  is  contagious,  and  that  it  is 
necessary  to  warn  the  patient's  friends  of  the  danger  of  the  attack. 

The  Chronic  Variety  may  be  the  sequela  to  an  acute  attack,  or  may 
be  in  the  form  of  the  angular  conjunctivitis  due  to  the  Morax- 
Axenfeld  bacillus,  or  due  to  eyestrain  or  local  injury  by  wind,  dust 
or  foreign  bodies,  or  the  use  of  alcoholic  liquors. 

The  symptoms  are  most  marked  at  night,  when  the  patient  feels 
as  though  a  foreign  body  was  in  the  eye  or  has  sensations  of  rainbow 
colours.  The  eyes  are  apt  to  burn  and  to  be  dazzled  by  light.  In 
the  morning  the  lids  are  stuck  together.  Sometimes  there  is 
excessive  secretion,  and  sometimes  there  is  lessened  secretion.  If 
neglected,  this  chronic  variety  may  last  for  years,  and  may  lead 
to  epiphora,  ectropion,  or  ulceration  of  the  cornea. 

The  treatment  is  the  same  as  for  the  acute  stage,  but  the  best 
therapy  is  the  zinc  sulphate  drops  in  the  form  of  a  ^per  cent,  solu- 
tion applied  night  and  morning. 

The  Follicular  Variety  may  occur  in  epidemics,  and  may  be  acute, 
when  it  is  usually  of  bacterial  origin;  or  chronic,  when  it  s  usually 
non-bacterial.  It  is  characterized  by  the  formation  of  small,  round, 
pale  granules  about  the  size  of  a  pin's  head,  and  is  easily  mistaken 
for  conjunctivitis  trachomatosa;  but  the  granules  are  usually  best 
marked  in  the  inferior  fornix,  while  those  of  trachoma  are  more 
marked  in  he  superior  '  ornix  and  tarsus,  which  must  be  most  care- 
fully examined  by  retroverting  the  lid  and  the  retrotarsal  fold  in 
order  to  be  certain  that  trachoma  is  absent.  In  the  acute  :  orm  the 
treatment  is  the  same  as  for  acute  catarrhal  conjunctivitis,  but 
when  chronic  it  is  usual  to  apply  copper  sulphate  treatment.  An 
ointment  of  1  in  1,000  copper  sulphate  or  1  in  100  copper  citrate  is 
recommended  by  some  authorities. 

Conjunctivitis  Gonorrhoica. 

This  is  so  well  known  that  no  special  reference  need  be  made 
to  it. 

Conjunctivitis  Neonatorum. 

This  is  usually  due  to  the  gonococcus,  but  may  be  caused  by  a 
streptococcus  or  probably  by  a  chlamydozoon. 


1998         DISEASES  OF  THE  ORGANS  OF  SPECIAL  SENSE 

Micrococci  and  Conjunctivitis. 

The  presence  of  Gram-negative  micrococci  may  be  due  to  infection  from 
the  generative  organs  by  the  gonococcus,  but  it  may  also  be  due  to  infection 
from  the  nasopharynx  via  the  lachrymal  ducts  by  the  meningococcus  and  the 
Micrococcus  catarrhalis,  which  is  merely  a  term  for  a  group  of  Gram-negative 
cocci.  The  Gram-negative  cocci  of  the  conjunctiva  may  be  roughly  separ- 
ated from  one  another  by  cultivation  in  sugar  media. 

Organism.  Glucose.  Maltose. 

Gonococcus  . .  . .  . .  . .  +  - 

Meningococcus  . .  . .  . .  J  J 

Micrococcus  catarrhalis      . .  . .  -  - 

Acid  only,  +  ;  acid  and  gas,  X  I  neither,  - . 

Conjunctivitis  Traehomatosa. 

Synonym. — Ophthalmia  iEgyptiaca. 

This  is  exceedingly  common  in  China,  where  70  per  cent,  of  the 
children  in  Hong  Kong  are  said  to  be  infected.  It  is  also  common 
in  many  other  parts  of  the  tropics,  especially  in  India,  Japan,  and 
South  America;  but  it  is  also  prevalent  in  North  Africa,  especially  in 
Egypt,  in  South  Africa,  in  Southern  Europe,  and  in  Porto  Rico. 
It  is  an  infectious  disease,  believed  by  many  authorities  to  be  due  to 
a  chlamydozoon  described  by  Halberstaedter  and  Prowazek.  A 
fungus — e.g.,  the  Microsporon  trachomatosum — has  been  described 
by  Noiszewski,  which  is  only  distinguishable  from  M alassezia  furfur 
by  the  smallness  of  its  conidia.  With  regard  to  the  chlamydozoon, 
it  occurs  in  the  cytoplasm  of  epithelial  cells  as  fine  granules,  which 
increase  in  size,  and  separate  so  as  to  enclose  a  cavity  at  first  free 
from  granules,  in  which  subsequently  very  minute  granules  appear. 

Probable  ^Etiology. — There  is  a  growing  suspicion  that  trachoma  is  essen- 
tially a  disease  arising  from  chronic  urethritis  in  men  and  chronic  vaginitis  in 
women,  because  cell-inclusions  of  a  chlamydozoan  nature  have  been  found  by 
several  observers  in  the  discharge  from  the  urethra  of  men  suffering  from 
gonorrhoea,  while  Castellani  has  found  similar  inclusions  in  a  man  in  Colombo 
who  is  believed  never  to  have  had  gonorrhoea.  Further,  similar  bodies  have 
been  found  in  the  vaginal  discharge  of  women  whose  children  have  suffered 
from  the  form  of  ophthalmia  neonatorum  in  which  no  gonococci  or  strepto- 
cocci can  be  found.  Further,  Castellani  has  found  similar  bodies  in  a  case 
which  may  have  been  one  of  the  rare  acute  inflammations  of  a  pure  trachoma 
without  granule  formation,  and  which  may  have  been  induced  in  the  acute 
form  because  the  woman  in  question  was  run  down  owing  to  the  acute  attack 
of  malaria  from  which  she  suffered.  This  case  emphasizes  the  fact  that  these 
bodies  should  be  looked  for  in  those  so-called  attacks  of  malarial  conjunctivitis 
which  are  found  associated  with  attacks  of  malarial  fever.  Finally,  Linder 
has  produced  a  chronic  conjunctivitis  by  transferring  the  secretion  of  vagina 
and  urethra  mentioned  above  to  monkeys.  This  experimental  conjunctivitis 
was  associated  with  the  formation  of  granules  clinically  and  anatomically 
resembling  the  conjunctivitis  traehomatosa  of  man. 

Method  of  Infection. — The  infection  is  carried  by  the  hands, 
towels,  handkerchiefs,  etc.,  from  the  sick  to  the  healthy.  There 
is  no  evidence  of  aerial  transmission.  The  agency  of  flies  in  the 
transmission  of  eye  disease  has  long  been  known — for  example, 
Budd,  in  1862,  considered  it  proven  that  they  transmitted  ophthal- 


EYE  DISEASES  PROPER  1999 

mia  aegyptiaca;  while  Laveran,  in  1880,  announced  that  the  same 
fact  applied  to  the  conjunctivitis  seen  in  Biskra;  and  Howe,  in  1888, 
stated  that  the  number  of  cases  of  conjunctivitis  in  Egypt  increased 
in  proportion  with  the  increase  of  flies,  and  were  more  prevalent  in 
the  Delta,  where  there  were  many  flies,  than  in  the  Desert,  where 
there  were  few.  Nuttall  and  Jephson  consider  the  spread  of 
ophthalmia  aegyptiaca  by  the  agency  of  flies  to  be  definitely  proved. 
The  '  pink  eye  '  of  school-children  in  Florida  is  believed  to  be  spread 
by  minute  flies  of  the  genus  Hippelates. 

That  some  other  actor,  in  addition  to  those  mentioned  above,  is 
necessary  to  explain  the  epidemiology  of  trachoma  is  evident  from 
the  fact  that  the  disease  does  not  often  spread  to  the  attendants 
or  to  inhabitants  of  the  same  house  as  the  infected  person.  This 
other  factor  may  be  some  local  derangement,  as,  for  example,  a 
slight  attack  of  conjunctivitis  ;  or  some  general  derangement,  as, 
for  example,  an  attack  of  fever. 

Pathology. — The  essential  feature  of  the  disease  is  a  round-celled  infiltration 
into  the  conjunctiva  associated  with  hypertrophy  of  the  papillae  of  that 
membrane. 

Morbid  Anatomy. — The  papillae  of  the  conjunctiva  are  hypertrophied  and 
the  trachoma  granules  are  formed  from  accumulations  of  round  cells  which  are 
peripherally  lymphocytes  and  centrally  mononuclear  leucocytes,  with  a  few 
macrophages.  These  cells  are  supported  by  a  delicate  connective  tissue 
which  contains  plasma  cells.  Pannus  is  a  layer  of  new-formed  connective 
tissue  which  is  rich  in  cells  and  bloodvessels. 

Symptomatology. — An  acute  attack  may  begin  with  acute  inflam- 
matory symptoms,  cedema  of  the  eyelids,  great  swelling  of  the  con- 
junctiva, and  profuse  purulent  secretion.  On  examination,  the 
conjunctiva  is  studded  with  the  typical  nodules,  but  these  may  not 
be  apparent,  and  may  even  at  first  be  absent.  These  acute  attacks 
may  be  complicated  with  corneal  ulcers. 

A  chronic  attack  often  begins  insidiously,  the  acute  phase  being 
absent,  very  mild,  or  unnoticed,  and  usually  the  patient  is  not  seen 
until  the  eyesight  is  dimmed  by  the  pannus  over  the  cornea.  In 
other  cases  the  disease  sets  in  with  photophobia,  pain,  and  watering 
of  the  eye;  the  lids  stick  together  in  the  morning,  and  there  is  dim- 
inution of  visual  acuity.  The  eye  is  not  fully  opened,  partly  because 
of  the  photophobia,  and  partly  because  the  upper  lid  is  swollen  and 
heavy.  On  everting  the  lids,  the  tarsal  and  transitional  conjunc- 
tivae are  found  to  be  swollen  and  red,  and  either  velvety  in  appear- 
ance, or  with  distinct  nodules  which  are  most  marked  on  the  upper 
lid.  These  nodules  or  granules  are  of  considerable  importance  in 
the  differentiation  between  trachoma  and  tollicular  conjunctivitis, 
and  it  is  to  be  specially  noted  that  those  of  trachoma  are  larger  in  the 
superior  fornix  than  in  the  inferior  fornix.  It  is  therefore  important 
to  examine  the  superior  retrotarsal  fold  very  carefully.  On  the 
tarsal  conjunctiva  the  granule  ■  are  not  so  prominent,  and  are  there- 
fore less  easily  seen.  A  trachoma  granule  is  typically  a  grey, 
roundish,  translucent  granule,  comparable  to  a  grain  of  boiled  sago 
in  appearance.     Harston's  sign  is  a  linear  groove  running  almost 


2000         DISEASES  OF  THE  ORGANS  OF  SPECIAL  SENSE 

horizontally  outwards  from  the  external  canthus.  The  hyper- 
trophy of  the  conjunctiva  increases  until  some  indefinite  limit  is 
reached,  when  it  ceases  and  cicatrization  sets  in;  but  if  the  hyper- 
trophy is  excessive,  it  may  last  for  years,  and  the  cicatrization  may 
develop  slowly  but  surely. 

The  cicatrization  shows  itself  at  first  as  whitish  striae  on  the  tarsal 
conjunctivae,  which,  becoming  more  numerous,  unite  into  a  net- 
work, the  meshes  of  which  are  occupied  by  the  hypertrophied  con- 
junctiva, which  gradually  diminish  as  cicatrization  proceeds,  until 
the  conjunctiva  becomes  pale  in  colour.  In  some  cases  this  cica- 
trization is  very  slight  and  hardly  noticeable,  while  in  others  it  may 
produce  serious  complications. 

The  loss  of  vision  is  due  to  pannus  and  ulceration  of  the  cornea, 
the  former  being  a  deposit  of  vesicular  gelatinous  tissue  on  the 
cornea,  which  becomes  uneven  and  raised  in  fine  projections;  while 
the  latter  may  occur  with  the  pannus  or  separately. 

The  sequelae  of  trachoma  may  be  classified  into: — 

(a)  Corneal  ulceration  and  pannus,  leading  to  opacities. 

(b)  Cicatrization,  leading  to  (i)  Trichiasis,  in  which  the  cilia  are 
turned  backwards  and  may  touch  the  cornea;  (2)  Entropion,  in 
which  the  border  of  the  lid  is  turned  backward;  (3)  Ectropion,  in 
which  the  lid  is  everted;  (4)  Symblephar on  poster ius,  in  which  the 
fornix  is  diminished  in  depth,  and  the  lid  is  tightly  fastened  to  the 
eyeball. 

(c)  Conjunctival  xerosis,  in  which  the  conjunctiva,  owing  to 
atrophy,  loses  its  secreting  powers,  and  becomes  dry  and  shrunken. 

Treatment. — The  acute  cases  are  to  be  treated  with  silver  prepara- 
tions, as  described  for  conjunctivitis. 

When  the  follicles  are  well  developed  it  is  usual  to  express  them 
by  means  of  a  flat  Grady's  forceps  or  by  the  roller  forceps  of  Knapp, 
but  this  must  be  performed  under  an  anaesthetic.  The  ruptured, 
surface  is  then  painted  with  a  solution  of  perchloride  of  mercury 
and  after  one  or  two  days'  interval  the  daily  application  of  solid 
copper  sulphate  is  commenced,  which  may  be  applied  pure  or  as  a 
Ginestou's  crayon,  which  consists  of  sulphate  of  copper,  i-o  gramme; 
orthoform,  0-5  gramme;  holocain  hydrochloride,  0*5  gramme;  gum 
tragacanth,  o-i  gramme;  and  water  as  may  be  required.  The 
above  are  the  quantities  required  to  make  a  pencil  5  centimetres 
in  length. 

Harston  strongly  recommends  treatment  by  carbon  dioxide  snow, 
which  has  produced  excellent  results  in  many  hands,  and  as  it  has 
only  to  be  applied  once  a  fortnight  is  useful  for  general  out-patient 
work.  It  is,  however,  very  painful,  and  this  pain  is  not  prevented 
by  cocaine,  which  therefore  need  not  be  used. 

Hegner  and  Baumm  have  advised  treatment  by  quartz  li^ht, 
while  other  methods  are  Galezowski's  excision  of  the  retrotarsal 
folds,  Kuhnt's  removal  of  the  tarsus,  while  treatment  by  Merk's 
extract  of  abrin,  Mayon's  X-ray  method,  and  Treacher  Collins's 
radium  treatment  may  be  mentioned. 


EYE  DISEASES  PROPER  2001 

Epitheliosis  Desquamativa. 

Synonym.- — Samoan  eye  disease. 

Under  this  term  Leber  and  von  Prowazek  have  described  a  form 
of  conjunctivitis  which  they  met  with  in  Samoa,  where  they  exam- 
in  d  and  treated  seventy-nine  fresh  infections.  They  consider  the 
causation  to  be  a  chlamydozoon — Lyozoon  atrophicans  Leber  and 
von  Prowazek,  1911 — which  is  found  in  the  milky  secretion  in  the 
form  of  trachoma-like  bodies,  which,  when  coloured  by  Giemsa,  show 
blue  poles  and  a  central  lacuna.  These  bodies  are  either  intra- 
cellular or  extracellular.  The  intracellular  bodies  form  what  is 
commonly  called  a  '  cell  inclusion  of  small  granules,'  which  take 
on  a  violet-r._d  colour  when  stained  by  Giemsa,  and  are  called  the 
'  el  incut  ary  bodies  '  and  lie  in  the  centre,  while  the  larger  initial 
bodies  he  at  the  periphery.  These  parasites  cause  a  hypertrophy 
of  the  cell  nucleus,  which  eventually  leads  to  an  atrophy  of  the  cell. 
The  disease  was  conveyed  to  guinea-pigs. 

The  symptoms  begin  with  pain,  photophobia,  and  livid  coloration 
of  the  upper  and  lower  lids,  while  a  milky  secretion  is  poured  out, 
which  is  composed  at  first  of  epithelial  cells  only,  but  may  become 
purulent.  Granules  similar  to  those  of  trachoma  do  not  develop, 
but  atrophy  of  the  conjunctiva  ensues.  The  treatment  recom- 
mended is  pyoktanin  in  the  proportion  of  1  in  1,000  to  1  in  100. 

Conjunctivitis  phlyctenulosa. 

This  is  not  very  frequently  met  with  in  the  tropics.  It  is  usually  found 
in  scrofulous  individuals,  and  is  characterized  by  the  presence  of  small 
vesicles   each  surrounded  by  a  reddened  zone. 

Conjunctivitis  Vernalis, 

Synonyms. — Conjunctivitis  .ZEstivalis,  Spring  catarrh. 

Definition. — A  chronic  form  of  conjunctivitis,  resembling  con- 
junctivitis trachomatosa,  but  occurring  in  the  spring  and  summer, 
and  disappearing  in  the  autumn  and  winter. 

Remarks. — -Spring  catarrh  is  apparently  not  so  rare  in  the  tropics 
as  in  the  Temperate  Zone,  as  Nell  informs  us  that  he  has  met  with 
thirty-eight  cases  in  Ceylon. 

/Etiology. — The  cause  is  unknown,  but  some  authorities  consider 
that  it  is  due  to  sunlight,  while  others  hold  that  it  is  an  infection 
from  the  skin. 

Symptomatology. — -On  the  approach  of  the  warm  weather  in 
spring  the  eyes  begin  to  itch  and  water.  The  conjunctiva  becomes 
red,  and  photophobia  is  experienced.  On  examination  the  con- 
junctiva is  seen  to  be  covered  with  broad,  flattened  papillae,  over 
which  a  bluish-white  film  is  seen.  The  affection  lasts  during  the 
summer,  wanes  in  the  autumn,  and  disappears  in  the  winter,  only 
to  recur  in  the  spring. 

Diagnosis. — The  diagnosis  must  be  made  by  the  history  and  by  the 
bluish-white  sheen  over  the  papillae.     It  resembles  trachoma,  but 

126 


2002  DISEASES  OF  THE  ORGANS  OF  SPECIAL  SENSE 

the  granules  are  broader,  harder,  and  paler,  while  the  history  is 
distinctive. 

Treatment. — Protective  glasses  must  be  worn,  and  zinc  sulphate 
lotion  (|  per  cent.)  dropped  into  the  eyes.  If  the  itching  is  very 
severe,  it  is  recommended  to  apply  a  few  drops  of  a  very  weak 
solution  of  acidium  aceticum  dilutum.     Iron  tonics  are  also  advised. 


Epithelial  Xerosis  of  the  Eye. 

This  condition  has  been  recorded  several  times  from  the  tropics. 
Archibald  has  recently  described  very  carefully  three  cases  in  the 
Sudan.  The  xerotic  patches  were  situated  on  the  conjunctiva 
external  and  close  to  the  corneal  margin  of  both  eyes  (Fig.  793). 
The  patches  were  greyish- white  in  colour  and  of  a  soft  viscid  con- 
sistency ;  the  superficial  layers  were  readily  removed  with  a  platinum 
loop;  the  deeper  layers,  however,  were  more  adherent  to  the  sub- 
jacent epithelium,  which  showed  a  brownish  pigmentation.     The 

bloodvessels  in  the  vicinity  of 
the  patches  were  congested. 
There  was  no  evidence  of  tra- 
choma or  inflammation  of  the 
eyelids.  The  whole  bulbar  con- 
junctiva was  moist,  and  could 
be  readily  moved  into  folds  by 
gentle  pressure  with  a  platinum 
loop.  There  was  an  absence  of 
pain  or  discomfort  associated 
Math  the  lesions,  which  appear 
to  have  had  a  duration  of 
several  years.  Vision  was  not 
impaired,  and  there  was  no 
evidence  of  night-blindness. 

/Etiology.  —  Scrapings  from 
the  xerotic  patches  showed  the 
presence  of  a  Gram-positive 
diphtheroid  organism  in  large 
numbers  which  was  obtained  in  pure  culture  from  the  cases.  This 
organism  (B.  xerosis  Neisser)  differed  from  the  true  Klebs-Loeffler 
bacillus  in  its  cultural  reactions,  and,  moreover,  was  non-pathogenic 
to  guinea-pigs. 

Treatment.— Attention  to  general  health  and  the  administration 
of  cod-liver  oil  internally  is  indicated.  The  affected  eyes  should  be 
protected  from  light  and  daily  douched  with  weak  boric  solution, 
followed  by  the  application  of  a  few  drops  of  a  1  per  cent,  solution 
of  protargol. 

Lachrymal  Sac. 

The  lachrymal  sac,  being  in  direct  connection  with  the  nose,  is 
very  liable  to  harbour  micro-organisms  and  fungi,  and  is  therefore 
a  possible  source  of  infection  for  the  conjunctiva  and  cornea. 


Fig.    793- 


-Epithelial 
the  Eye. 


Xerosis    of 


(From  a  photograph  by  Archibald.) 


EYE  DISEASES  PROPER  2003 

Cornea. 

Phlyctenular  keratitis  is  common  as  a  sequela  to  conjunctivitis 
phlyctenulosa,  both  of  which  act  as  common  predisposing  causes  to 
pterygium,  which,  according  to  Harston,  is  extremely  common 
among  the  Chinese. 

Ulcus  Serpens  Corneae. 

This  appears  as  a  greyish-white  ox  yellowish  slightly  depressed 
disc  near  the  centre  of  the  cornea,  the  rest  of  which  is  clouded.  It 
is  associated  with  iritis  and  turbidity  of  the  vitreous,  hypopyon, 
and  more  or  less  oedema  of  the  lids,  with  conjunctivitis,  cyclitis, 
photophobia,  and  pain,  except  in  the  so-called  '  torpid  '  cases.  The 
ulcers  increase  in  depth  and  extent;  perforation  occurs  into  the 
anterior  chamber,  which  contains  sterile  pus,  which  now  escapes,  and 
at  the  same  time  prolapse  of  the  iris  may  occur.  The  inflammation 
now  comes  to  an  end,  but  panophthalmia  may  occur.  The  most 
common  cause  in  the  tropics  is  the  pneumococcus,  which  may  often 
be  found  in  the  nose  of  the  same  patient.     The  prognosis  is  serious. 

Treatment. — -The  cauterization  of  the  ulcer  and  apparently  clear 
border  with  the  actual  cautery  is  an  imperative  immediate  treat- 
ment, followed  by  application  of  atropine,  iodoform,  or  orthoform 
powder,  or  1  per  cent,  xeroform  ointment,  or  callaryol  ointment 
3  per  cent. ,  and  moist  and  warm  compresses,  Harston  recommends 
douching  with  hydrogen  peroxide  as  an  adjuvant  to  the  usual 
treatment,  while  1  in  40  formalin  solution  is  also  recommended,  but 
must  be  preceded  by  cocaine,  as  it  is  very  painful.  Perforated  ulcers 
are  best  treated  by  iridectomy  on  each  side  of  the  synechia.  Har- 
ston operates  on  the  worst  eye  of  the  two  when  both  are  involved, 
as  operative  interference  is  apt  to  set  up  a  severe  irido-cyclitis  in 
the  poorly-nourished  Chinese  coolie,  with  eventual  loss  of  sight  in 
the  eye.     The  nasal  infection  must  also  be  treated  by  antiseptic 

douches. 

Ins. 

Diseases  of  the  iris  are  as  common  in  the  tropics  as  in  the  Tem- 
perate Zone.  Those  which  are  specially  connected  with  tropical 
disease  will  be  mentioned  below,  but  it  is  well  to  remember  that  in 
native  races  the  stroma  of  the  iris  is  laden  with  pigment,  which 
probably  accounts  for  its  slow  reaction  to  mydriatics. 

Cataract. 

This  disease  is  said  to  be  on  the  wane  in  the  Temperate  Zone,  but 
is  very  rife  in  the  tropics.  In  fact,  its  home  is  said  to  be  in  India, 
the  ophthalmic  surgeons  of  which  have  a  great  reputation.  Colonel 
Smith,  of  Jullundur,  has  perfected  a  complicated  but  most  successful 
operation  for  intracapsular  extraction. 

Sometimes  in  the  tropics  it  is  impossible  to  wait  until  the  cataract 
ripens,  and  operations  may  have  to  be  performed  on  immature 
cataracts.  To  meet  this  difficulty,  Nell  has  devised  a  modification 
of  the  usual  procedure,  which  consists  in  performing  a  zonulotomy 


2oo4         DISEASES  OF  THE  ORGANS  OF  SPECIAL  SENSE 

by  means  of  a  special  hook  introduced  through  the  corneal  wound 
made  for  a  cataract  extraction  and  under  the  iris.  After  this  pre- 
liminary proceeding  he  completes  the  operation  by  intracapsular 
extraction  of  the  lens. 

Glaucoma. 
Acute  glaucoma  is  rare  in  the  tropics,  while  chronic  glaucoma  is 
common;  but  the  signs,  symptoms,  and  treatment  are  the  same  as 
in  the  Temperate  Zone.     The  Elliot  operation  of  trephining,  with 
or  without  subsequent  iridectomy,  is  recommended. 

Fundus  Oculi. 

The  colour  of  the  fundus  oculi  depends  upon  the  amount  of  retinal 
pigment  present  and  to  a  less  degree  upon  the  amount  of  the 
choroidal  pigment  visible.  It  therefore  shows  variations  from  the 
European  standard  in  dark  and  yellow  races.  In  these  races  the 
amount  of  retinal  pigment  is  increased,  and  may  completely  conceal 
that  of  the  choroid,  and  so  produce  a  uniform  yellowish  colour,  as 
seen  in  the  Chinese;  or  a  dark  reddish,  or  even  an  almost  greyish- 
red  colour,  as  seen  in  the  various  negro  races. 

On  the  other  hand,  when  the  retinal  and  choroidal  pigments  are 
diminished,  as  in  albinism;  then  the  white  sclerotic  shows  through, 
and  the  fundus  becomes  of  a  lighter  red  colour  than  normal. 

Sunlight. 

The  effect  of  sunlight  on  the  eyes  has  been  studied  by  Sisson, 
who  considers  that  there  is  ample  proof  that  light  injures  the  eye, 
and  that  it  may  possibly  be  the  cause  of  some  diseases  of  the  eye, 
the  aetiology  of  which  is  but  little  understood.  Schmidt  considers 
that  nyctalopia  and  hemeralopia  may  be  caused  by  excessive  light. 
The  use  of  protective  xanthophylline  glasses  is  recommended. 

B.  EYE  COMPLICATIONS  OF  TROPICAL  DISEASES 

Malaria. 

Malaria  is  held  to  be  responsible  for  conjunctivitis,  serpiginous 
corneal  ulcers,  malarial  iritis,  and  retino-choroiditis,  as  well  as 
amaurosis. 

Until  a  few  years  ago,  the  majority  of  the  fevers  of  the  tropics, 
including  enteric  fever,  were  classified  as  malaria,  and  any  locil 
affection  of  an  unknown  nature  was  also  classified  in  the  same 
manner.  The  case  of  conjunctivitis  in  which  one  of  us  found  cell 
inclusions  would  a  few  3'ears  ago  have  been  named  malarial.  We 
are  therefore  of  the  opinion  that  the  existence  of  malarial  conjunc- 
tivitis has  not  been  proved. 

Keratitis  Dendritica—  This  keratitis  is  that  variety  of  herpes 
corneae  febrilis  (sometimes  called  'herpes  c<  rneae  zoster')  which 
gives  rise  to  those  ulcers  (formed  from  the  ruptured  herpetic 
vesicles)  which  extend  in  certain  directions  only  as  grey  forked 
stria'  with^lateral^branches,  which  break  down,   thus  forming  a 


EYE  COMPLICATIONS  OF  TROPICAL  DISEASES  2005 

branched  ulcer  with  grey  margins.  The  ulcer  then  becomes  clean, 
and  heals  after  one  to  three  months,  leaving  a  branched  opacity  of 
the  cornea.  This  is  one  form  of  corneal  ulcer  to  which  the  name 
'  serpiginous '  is  given,  but  it  equally  applies  to  ulcus  rodens  and 
keratitis  marginalis  superficialis,  which,  as  far  as  we  know,  have 
never  been  stated  to  be  of  malarial  origin.  Keratitis  dendritica 
was  first  described  by  Kipp  in  America,  who  stated  that  nine  out 
of  every  ten  cases  were  malarial. 

The  treatment  must  be  that  described  for  malaria,  as  well  as  con- 
stitutional, and  it  is  usual  to  recommend  that  the  ulcers  be  treated 
by  a  piece  of  blue  stone  whittled  to  a  fine  point,  and  carried  carefully 
along  the  furrow  made  by  the  ulcer,  or  by  careful  cauterization  by 
the  actual  cautery. 

Keratitis  Profunda— Synonyms. — Keratitis  parenchymal osa  cir- 
cumscripta, or  Central  parenchymatous  infiltration  of  the  cornea. 

This  is  said  by  Arlt,  among  other  causes,  to  be  brought  about  by 
chronic  malarial  cachexia.  It  begins  with  a  grey  opacity,  situate 
in  the  middle  and  deep  layers  of  the  centre  of  the  cornea,  and  over 
which  the  corneal  surface  is  grey  and  punctate.  Seen  with  a 
magnifying-glass,  the  opacity  resolves  into  dots  and  maculae,  or  grey 
interlacing  striae.  After  remaining  four  to  eight  weeks,  it  slowly 
abates  without  ulceration.  The  iris  may  be  hyperaemic,  and  there 
may  or  may  not  be  symptoms  of  inflammation  of  the  cornea,  which 
may  recover  completely,  or  with  some  opacity.  The  treatment 
would  be  the  same  as  for  malaria,  but  it  must  be  definitely  stated 
that  the  cause  is  unknown. 

Iritis. — Secondary  iritis  is  said  to  be  very  rarely  caused  by 
malaria,  but  even  this  is  open  to  doubt. 

Vitreous  Opacities. — Haemorrhage  and  serous  effusion  have  been 
described. 

Amaurosis. — -Malarial  amaurosis  is  described  in  Chapter  XL., 
p.  1181,  under  the  term  '  Amaurotic  Pernicious  Fever,'  but  may 
occur,  not  merely  during  an  attack  of  malaria,  but  as  a  sequel, 
and  as  such  was  described  by  Jacobi  in  1868,  and  later  byChiarini. 
It  is  due  to  atrophy  of  the  optic  nerve. 

Retino-choroiditis. — This  was  first  described  by  Poucet  as  occur- 
ring in  chronic  malaria,  but  it  is  also  found  in  the  acute  and  in  the 
chronic  forms.  In  the  acute  affection  the  vessels  of  the  retina  are 
filled  with  corpuscles,  many  of  which  contain  malarial  parasites. 
In  the  choroid  the  larger  vessels  contain  pigmented  leucocytes,  many 
of  which  contain  red  corpuscles  with  malarial  parasites.  The  retina 
is  hazy,  the  papilla  is  obscured,  and  there  are  retinal  haemorrhages. 
The  amblyopia  may  be  temporary  or  permanent.  In  the  chronic 
condition  there  is  atrophy  of  the  capillaries  of  the  choroid.  The 
macular  region  shows  small  whitish  dots,  in  the  centre  of  which 
ret  i  nal  pigment  can  be  seen.  These  changes  ext  end  1 6 1  he  periphery. 
Pathologically,  they  axe  coloid  masses  in  Bruch's  membrane. 

Suppurative  Uveitis.— Suppurative  choroiditis,  leading  to  destruc- 
tion of  the  eye,  has  only  been  described  by  Pemnoff. 


2006         DISEASES  OF  THE  ORGANS  OF  SPECIAL  SENSE 

Accommodation  Paralysis. — Accommodation  paralysis  and  spasm 
of  the  muscles  of  accommodation  have  been  described  bjr  Bull  and 
Slitting. 

Trypanosomiasis. 

Choroiditis,  cyclitis,  iritis,  and  optic  neuritis  of  a  temporary 
nature,  are  reported  as  occurring  in  sleeping  sickness,  as  well  as 
engorgement  of  the  iris  and  loss  of  the  light  reflex,  with  wide  dilata- 
tion of  the  pupil. 

Relapsing  Fevers. 

Iridocyclitis,  or  iritis,  is  a  frequent  complication  of  the  relapsing 
fevers,  and  though  it  ultimately  ends  in  a  cure,  it  is  usually  pro- 
tracted. 

Plague. 

Conjunctivitis  is  common  in  plague  as  an  initial  symptom;  later 
a  plastic  uveitis  with  hypopyon  and  keratitis  may  occur,  and  call 
for  special  treatment  by  administration  of  mercury,  local  installa- 
tion of  atropine,  and  blood  extraction  by  leeches. 

Leprosy. 

In  tubercular  leprosy  yellowish  translucent  nodules  of  a  non- 
vascular nature  may  develop  in  the  conjunctiva  near  the  cornea. 
Iritis  and  cyclitis,  with  or  without  the  formation  of  nodules,  may 
occur.  According  to  Wood,  more  than  half  the  anaesthetic  lepers 
of  South  Africa  suffer  from  eye  complications — e.g.,  paralysis  of  the 
orbicularis  palpebrarum,  ectropion  of  the  lower  lids,  epiphora, 
corneal  opacity,  and  ulcerations.  Of  the  tubercular  lepers  he  says 
90  per  cent,  are  affected  in  the  first  ten  years  of  the  disease,  and  if  they 
survive  they  become  blind.  They  suffer  from  invasion  of  the  lids, 
conjunctivae,  sclerotic,  cornea,  and  iris  by  the  disease,  and  in  addition 
may  suffer  from  paralysis  of  the  ciliary  muscle  and  irido-cyclitis. 
Heymans  finds  lagophthalmos  to  be  common.  Inic)i5  Stanziale  pub- 
lished experiments  on  the  eye  of  rabbits,  injecting  leprotic  material 
into  the  cornea. 

Cholera. 

Focal  necrosis  in  the  cornea  and  conjunctiva  has  been  reported  in 

convalescence  from  cholera,  while  a  form  of  cataract  depending 

upon  the  abstraction  of  water  takes  place  at  times  in  the  last  stage 

of  the  disease.  _ 

Dysentery. 

Conjunctivitis,  keratitis,  iritis,  and  irido-cyclitis  are  reported  in 
dysentery,  both  amoebic  and  bacterial. 

Hikan. 

Under  this  term  a  curious  disease  is  described  by  various  ob- 
servers, among  whom  Jeanselme  and  Risb.  The  main  symptoms 
appear  to  be  hemeralopia,  xerophthalmia,  dryness  of  the  skin,  and 
diarrhoea  occurring  in  young  children  in  Russia,  Brazil,  and  Japan. 
The  causation  is  unknown,  but  treatment  by  cod-liver  oil  is  said  to 
be  very  efficacious. 


EYE  COMPLICATIONS  OF  TROPICAL  DISEASES  2007 

Quinine. 

Amaurosis  associated  with  complete  deafness  may  set  in  after 
doses  of  less  than  1  gramme  of  quinine,  though  more  usually  after 
a  dose  of  3  grammes  and  upwards.  The  amaurosis  gradually  dis- 
appears, leaving  an  amblyopia  with  a  much  contracted  field  of  vision. 
This  result  is  due  to  a  destruction  of  the  ganglion  cells  of  the  retina 
by  the  quinine,  after  which  a  degeneration  of  the  optic  nerve  sets  in. 

The  symptoms  are  a  blanching  of  the  retina  and  disc,  due  to  spasm 
of  the  vessels,  and  loss  of  the  pupillary  light  reflex,  the  pupils  being 
widely  dilated.  It  should  be  differentiated  from  the  malarial 
amaurosis.  In  the  former  the  pupils  are  usually  widely  dilated, 
and  do  not  react  to  light,  while  in  the  latter  they  do  react  to  light. 

The  deleterious  effect  of  therapeutic  doses  of  quinine  has  often  been  ex- 
aggerated. Doses  of  10  to  15  grains  may  usually  be  given  three  times  daily 
for  long  periods  of  time  without  any  damage  to  the  eyes.  Jamieson  and 
Lindsay  have  noted  that  even  when  the  visual  field  is  found  to  be  contracted, 
the  prognosis  is  good  and  ultimate  expansion  of  the  field  may  be  expected. 

Atoxyl. 
Sudden  amaurosis  may  be  caused  by  atoxyl. 

Animal  Parasites. 

Ocular  Paragonimiasis. — Cysts  conta.mmgParagonimus  westermanni 
have  been  reported  as  occurring  on  the  eyelids  and  orbit,  and  so 
hindering  the  movements  of  the  eyeball  and  obstructing  the  vision. 

Ovular  Filariasis. — Loa  loa  has  been  noticed  in  the  ocular  and 
palpebral  conjunctiva  {vide  pp.  645  and  1972). 

In  addition  to  paragonimiasis  and  filariasis,  the  following  parasites 
occur  in  the  eye  or  its  adnexa:  Agamodistomum  ophthalmobium 
Diesing,  1850;  Monostomum  lentis  von  Nordmann.  1832  (both  of 
which  may  be  stages  of  Dicrocceliinn  lanceatum  Stiles  and  Hassell, 
1896);  Sparganum  mansoni  Cobbold,  1883;  Agamofilaria  oculi 
humani  von  Nordmann,  1832;  Agamofilaria  palpebralis  Pace,  1867, 
nee  Wilson,  1844;  Dermanyssus  gallincc  De  Geer,  1778  (which  may 
be  seen  as  a  dark  spot  embedded  in  the  cornea);  Demodex  follicii- 
lorum  Simon,  1842,  which  is  found  in  the  Meibomian  glands,  and 
may  cause  a  blepharitis.  The  larvae  of  Dermatobia  cyanivenlris 
Macquart,  1843,  has  been  found  by  Malgahaes under  the  palpebral 
conjunctiva  and  in  the  lachrymal  sacs  in  Brazil.  A  larva  of  Sarco- 
phaga  magnifica  Schincr,  1862,  has  been  found  in  the  anterior 
chamber  of  the  eye,  and  a  larva  of  a  species  of  Necrobia  in  a  sclerotic 
tumour ;  but  for  afuller  account  of  ocular  myiasis  see  Chapter  LXVII. 
Cysticercus  celhdosce  has  been  found  in  the  choroid,  which  it  may 
leave,  and,  passing  under  the  retina,  may  cause  detachment;  later 
it  may  perforate  the  retina  and  enter  the  vitreous,  or  it  may  enter 
the  retina  or  the  ciliary  region,  and  so  pass  directly  into  the  vitreous, 
where  it  appears  as  a  bluish-white  bladder,  with  or  without  a  pro- 
truded head.  The  eye  may  be  destroyed  by  irido-cyclitis.  Echino- 
coccal  invasion  is  very  rare. 


2008         DISEASES  OF  THE  ORGANS  OF  SPECIAL  SENSE 

Ophthalmomycoses. 

Definition. — Diseases  of  the  eye  and  its  adnexa  caused  by  various  fungi. 

History. — The  word  mycosis  was  introduced  by  Virchow  to  signify  a  disease 
caused  by  fungi,  being  first  used  for  aspergillosis  of  the  lungs.  The  interest 
in  fungi  as  causes  of  disease  was  first  aroused  by  Gruby,  who  in  1847  appears 
to  have  noticed  fungal  structures  in  lachrymal  concretions,  although  he  did 
not  publish  his  observations.  Helmbrecht  and  Robin  were  the  first  to  actually 
assign  a  disease  of  the  eyes  to  the  action  of  fungi.  They  observed  a  fungus, 
which  they  called  Leptomitus,  in  a  case  of  conjunctival  inflammation  asso- 
ciated with  epiphora.  In  1854  Graeffe  described  the  fungal  nature  of 
lachrymal  concretions,  and  in  1873  Cohn  showed  that  these  fungi  belonged  to 
the  genus  Streptothrix  (Nocardia).  In  1879  Leber  discovered  the  first  case  of 
keratomycosis  caused  by  Aspergillus  fumigatus.  From  this  date  until  com- 
paratively recently  fungi  went  out  of  fashion,  being  replaced  by  interest  in 
bacteria,  but  with  the  revival  of  interest  created  largely  by  Sabouraud  eye 
diseases  were  again  investigated,  and  in  1906  De  Beurmann  and  Gougerot  gave 
an  account  of  ocular  sporotrichosis,  and  in  1907  Danlos  and  Blanc  of  palpebral 
sporotrichosis,  and  Morax  described  a  form  of  keratomycosis  caused  by 
Glenospora  graphii,  and  Liegard  and  Landrieu  a  form  of  conjunctivitis  due 
to  Nocardia  dassonvillei,  while  in  19 12  Landrieu  reviewed  the  whole  subject 
of  ocular  mycoses  in  a  singularly  able  manner. 

Fungi. — The  following  fungi  have  been  recognized  in  various  diseases  of 
the  eye: — 

A.  Order  Ascomycetes. 

I.  Suborder  Gymnoacees. 

(a)  Family  Saccharomycetes. 

(1)  Genus  Cryptococcus. 

C.  dermatitidis  Gilchrist  and  Stokes,  1S9S. 

(2)  Genus  Saccharomyces,  several  species. 

(b)  Family  Gymnoasceas. 

(1)  Genus  Microsporon. 

AI.  lanosum  Sabouraud,  1907. 

(2)  Genus  Trichophyton. 

T.  tonsurans  Malmsten,  1S45,  and  other  speries  of  the 
same  genus. 

(3)  Genus  Achorion. 

A.  schocnleini  Lebert,  1845 

II.  Suborder  Carpoascees. 

Family  Perisporiaceae. 
Genus  Aspergillus. 

A .  fumigatus  Fresenius,  1775. 

B.  Order  Hyphomycetes. 

(1)  Genus  Nocardia. 

N.  bovis  Harz,  1877. 

N.  israeli  Kruse,  1896. 

N .  foersteri  Cohn,  1874. 

N.  dassonvillei  Brocq-Rousseau,  1907. 

(2)  Genus  Monilia. 

M.  albicans  Robin,  1853,  and  other  species  of  the  same  genus. 

(3)  Genus  Glenospora. 

G.  graphii  Siebenmann,  1889. 

(4)  Genus  Sporotrichum. 

S.  beurmanni  Matruchot  and  Ramond,  1905. 

Pathogenicity. — The  ocular  diseases  caused  by  the  above  fungi  may  be 
grouped  as  follows: — 


Ocular  Nocardiases. 


EYE  COMPLICATIONS  OF  TROPICAL  DISEASES  2009 

Fungus.  Disease. 

Cryptococcus  dermatitis  and  various  species  of  the 

genus  Saccharomyces  .  .  .  .  . .  .  .      Ocular  Blastomycosis. 

Mkrosporon  lanosum         j 

Trichophyton  tonsurans   J-       . .  . .  .  .  . .      Ocular  Tineas. 

Achorion  schoenleini 

Aspergillus  fumigatus    .  .  .  .  .  .  .  .      Ocular  Aspergillosis. 

Nocardia  bovis  "\ 

Nocardia  israeli 

Cohnistreptothrix  foersteri   j  '  ' 

Nocardia  dassonvillci  j 

Monilia  albicans  and  other  species  of  the  same  genus     Ocular  Moniliasis. 

Glenospora  graphii        . .  .  .  . .  . .  .  .      Ocular  Glenosporosis. 

Sporotrichum  beurmanni  .  .  .  .  .  .  .  .      Ocular  Sporotrichosis. 

Ocular  Blastomycosis. 

Ocular  blastomycosis  is  seen  in  the  form  of  Palpebral  Blastomycosis,  which 
begins  as  papules  which  increase  in  size  and  give  rise  to  pustules  covered  with 
crusts,  and,  later,  to  a  warty  condition,  which  may  become  red,  moist,  and 
granular.  In  other  cases  a  subdermal  nodule  is  formed,  which  may  ulcerate. 
The  causal  agent  is  Cryptococcus  dermatitis  Gilchrist  and  Stokes,  1898.  The 
diagnosis  is  made  by  culture  of  the  fungus. 

Ocular  Tineae. 

Tinea  palpebrarum  may  be  caused  by  Microsporon  lanosum  Sabouraud, 
1907,  by  various  species  of  Trichophyton,  of  which  that  most  commonly  found 
is  T.  tonsurans  Malmsten,  1845.  These  fungi  may  or  may  not  attack  the 
cilia.  If  they  do  so,  then  small  yellow  crusts  will  be  seeh  surrounding  a 
cilium.  On  the  removal  of  these  crusts,  small  pustules  will  be  seen.  When 
they  do  not  attack  the  cilia,  they  give  rise  to  herpetiform  lesions  on  the  eye- 
lids proper.  The  diagnosis  is  made  by  culture  of  the  fungus.  The  treatment 
consists  in  epilation,  warm  compresses,  and  tincture  of  iodine. 

Achorion  schoenleini  Lebert,  1S45,  the  fungus  of  favus,  may  also  attack  the 
eyelids. 

Ocular  Aspergillosis. 

About  two  days  after  a  slight  traumatism  to  the  eye,  irritation  is  felt,  fol- 
lowed by  pains,  and  the  formation  of  an  abscess,  and  later  an  ulcer.  The 
diagnosis  can  only  be  made  by  the  microscopical  or  cultural  examination  of 
scrapings  from  the  ulcer  or  of  the  pus  from  the  abscess.  The  treatment 
consists  in  curetting  and  applying  a  lotion  of  silver  nitrate  and  atropine  drops. 

Ocular  Nocardiases. 

Actinomycotic  conjunctivitis  was  first  described  by  Demicheri  in  1899, 
actinomycotic  corneal  ulcers  by  de  Bernardinis  and  de  Donna  in  1905,  and 
miliary  actinomycotic  metastases  in  the  choroid  by  Miiller  in  1903.  Con- 
junctivitis due  to  N.  dassonvillci  has  been  recorded  by  Liegard  and  Landrieu 
in  1911. 

Ever  since  the  days  of  C6soin  in  1 670  lachrymal  concretions  have  from  time 
to  time  been  recorded,  but  their  parasitic  nature  was  not  recognized  until 
Gruby  in  1848  found  that  they  were  really  fungal  in  origin.  This  fungus  is 
known  to  be  Cohnistreptothrix  foersteri.  The  concretions  occur  in  the  form  of 
minute  grains  in  the  lachrymal  sac,  from  which  they  can  easily  be  removed. 

Ocular  Moniliasis. 

Monilia  albicans  Robin,  1853,  one  of  the  organisms  of '  thrush,'  may  very 
rarely  attack  the  conjunctiva,  as  first  described  by  Piehler  in  1895.  Cases 
due  to  Monilia  tropicalis  Castellani  and  other  species  have  been  seen  by  us  in 
Ceylon. 


zoio         DISEASES  OF  THE  ORGANS  OF  SPECIAL  SENSE 

Ocular  Glenosporosis. 
So  far,  only  one  case  in  the  cornea  is  recorded.     It  was  found  in  1910  by 
Morax. 

Ocular  Sporotrichosis. 

Sporotrichal  infection  of  the  eyelids,  conjunctiva,  lachrymal  sac,  and  iris 
have  been  recorded,  but  are  as  yet  rare.  The  first  case  was  found  in  1905 
by  Danlos  and  Blanc,  the  second  case  in  1908,  the  third  in  1909.  Four  cases 
were  recorded  in  19 10,  and  three  in  191 1,  and  several  in  1912. 

DISEASES  OF  THE  EAR. 

The  diseases  of  the  ear  in  the  tropics  require  more  attention 
than  has  hitherto  been  bestowed  upon  them.  The  majority  are 
believed  to  resemble  those  found  in  the  Temperate  Zone.  A  few 
remarks  will  be  offered  with  regard  to  the  diseases  of  the  auricle, 
of  the  external  auditory  meatus,  and  with  regard  to  ear  complica- 
tions in  tropical  diseases. 

The  Auricle. 

Deformities  of  the  lobule  are  common  among  Indian  girls  and 
women,  who  drag  the  lobule  into  a  long,  pendulous  loop  by  means  of 
heavy  golden  ornaments,  or,  failing  these,  by  pieces  of  other  metals 
or  even  wood.  A  similar  condition  is  reported  by  Castellani, 
Bland-Sutton,  and  others,  as  occurring  among  the  Masai  and  the 
Kikuyu  people  of  East  Africa. 

Nepaul  Tumour.- — In  1833,  Campbell,  and  in  1835,  Bramley,  drew 
attention  to  a  peculiar  disease  of  the  skin  of  the  auricle  which  was 
endemic  in  the  village  of  Nilkantha,  situate  in  one  of  the  Nepaul 
valleys,  at  the  foot  of  the  Sheopuri  Hills.  The  disease  begins  as  a 
small  firm  swelling  of  the  skin  on  the  external  aspect  of  the  auricle, 
which  is  elastic  to  the  touch,  and  which  increases  until  it  reaches 
the  size  of  a  pigeon's  egg  in  four  to  eight  weeks.  It  is  adherent 
to  the  subcutaneous  tissues,  but  is  slightly  movable.  If  it  grows 
rapidly,  the  superjacent  skin  becomes  bluish,  and  a  painful  feeling  of 
tension  is  produced.  If  the  swelling  is  punctured,  a  thick  whitish 
fluid  exudes.  It  grows  until  it  reaches  the  size  of  an  orange  or  of  a 
child's  head,  and  it  may  attain  such  a  size  that  it  reaches  to  the 
patient's  shoulder.  After  a  time  its  contents  soften  and  become 
absorbed,  while  the  sac  of  the  tumour  shrinks,  leaving  the  ear 
much  thickened  and  shapeless.  Usually  both  ears  are  affected, 
and  sometimes  a  succession  of  tumours,  one  after  the  other,  may 
take  place.  The  causation  is  unknown.  It  is  more  common  in 
women  than  in  men.  Campbell  thinks  that  it  occurs  associated 
with  goitre,  which  would  suggest  a  parasitic  causation,  but  Bramley 
is  opposed  to  this  view. 

It  is  curious  that  there  is  so  little  literature  on  this  subject,  and 
that  neither  Scheube  nor  ourselves  are  acquainted  with  any  further 
papers  describing  this  disease. 

Lipoma. — Lipoma  of  the  lobule  of  the  ear,  often  on  both  ears,  is  reported  in 
Loango.  This  tumour  may  reach  the  size  of  a  walnut  or  a  child's  head,  and 
is  thought  to  be  due  to  the  fact  that  the  negroes  bore  their  ears  with  thorns 
or  with  pointed  strips  of  palm-leaves,  which  are  retained  in  the  lobe  of  the  ear 
lor  some  time. 


DISEASES  OF  THE  EAR  201 1 

Fibromata.  —  We  have  often  met  with  soft  small  fibromata 
attached  to  the  lobules  of  the  ears  of  the  negroes  on  the  Gold 
Coast,  which  can  readily  be  removed.  Perhaps  the  lipomata  of 
Loango  are  really  soft  fibromata. 

Keloid. — Keloid  is  met  with  on  the  auricle  in  West  African  natives, 
arising  after  insignificant  wounds,  such  as  ear-piercing,  etc.,  and  may 
form  large  tumours. 

External  Auditory  Meatus. 

Foreign  Bodies  are  commonly  met  with  in  the  tropics,  and  may 
consist  of  animate  objects,  such  as  beetles,  flies,  etc.;  or  inanimate 
objects,  such  as  pieces  of  wood,  etc.  Usually  their  presence  can 
easily  be  determined  by  inspection,  which  should  always  be  carried 
out  before  any  treatment  is  resorted  to.  The  first  treatment  should 
be  to  attempt  to  wash  the  body  out  of  the  meatus  by  means  of 
hot  boracic  lotion  and  an  ear  syringe,  unless  the  body  be  a  pea,  bean, 
or  grain  of  maize,  because  these  would  become  swollen  with  the 
water.  Under  these  circumstances,  it  is  better  to  instil  some 
glycerine  mixed  with  a  little  rectified  spirit  and  solution  of  cocaine, 
which  causes  them  to  contract,  when  a  camel's-hair  brush  dipped 
in  thick  collodion  may  be  carefully  applied  to  the  object.  After 
waiting  a  little  time  for  the  collodion  to  set,  traction  can  be  made 
and  the  object  removed.  Failing  these,  attempts  must  be  made 
to  remove  the  body  by  Guye's  fenestrated  forceps,  Politzer's  gouge 
forceps,  Troltsch's  aural  hook,  an  aural  curette,  or,  in  the  case  of 
impacted  steel  bodies,  the  electro-magnet.  If  there  is  much  swelling 
of  the  mucous  membrane  of  the  passage,  it  may  be  necessary  to 
apply  a  solution  of  cocaine  and  adrenaline,  after  which  extraction 
may  be  attempted.  It  is  often  advisable  to  administer  an  anaes- 
thetic if  a  body  is  impacted  in  a  child's  ear.  If  all  attempts  fail, 
an  operation  is  necessary, which  is  generally  performed  by  d  taching 
the  auricle  from  behind  and  exposing  the  bone  wall  of  the  external 
auditory  meatus,  a  portion  of  which  is  removed  if  necessary. 

Animal  Parasites. — Apart  from  foreign  bodies,  the  following 
animals  have  been  found  parasitic  in  the  external  auditory  meatus: 
CheyletidcB  :  C.  heyletus,  C.  eruditus  Schrank,  1781.  Tyroglyphid.ee  : 
Rhizoglyphus  parasiticus  Dalgetty,  190 1.  Demodicidce  :  Demodex 
Jolliculorum  Simon,  1842.  Larvae  belonging  to  the  Anthomyidae,  to 
Sarcophaga  camaria  Linnaeus,  1758,  to  Wohlfartia  magnifica  Schiner, 
1862,  and  to  Chrysomyia  macellaria  Fabricius,  1794. 

Otomycosis. — Otitis  externa  parasitica,  or  otomycosis,  is  fairly 
:ommon  in  the  tropics,  and  is  due  to  a  number  of  fungi,  among 
which  may  be  mentioned:  Mucor  pusillus  Lindt,  1886;  Licktheimia 
corymbifera  Cohn,  1884;  Lichtheimia  rcmosa  Lindt,  1886  (these  cause 
otomucormycosis);  Saccharomyces  ellipsoides  Rhees,  1870;  Moniha 
rhoi  Castellani,  1909;  Aspergillus  fumigahts  Frescnius,  1775;  Asper- 
gillus niger  von  Ticghem,  1867;  Aspergillus  flavus  De  Bary,  1870; 
Aspergillus  malignus  Lindt,  1889;  Aspergillus  r opens  De  Bary,  1870 
(these  cause  otomycosis  aspergillina). 


2012  DISEASES  OF  THE  ORGANS  OF  SPECIAL  SENSE 

These  fungi  cause  mild  inflammations  of  the  external  auditory 
meatus,  and  are  found  not  merely  in  natives,  but  also  in  Europeans. 

If  they  grow  superficially,  they  cause  no  symptoms;  but  if  they 
penetrate  into  the  mucous  membrane,  they  give  rise  to  itching,  and 
sometimes  to  pain.  If  they  grow  into  the  cerumen,  they  may  give 
rise  to  blocking  of  the  passage,  and  cause  tinnitus  aurium  and 
deafness. 

On  inspecting  the  ear,  it  will  be  seen  that  the  wall  of  the  audit 01-37 
meatus  is  covered  with  a  white  or  black  macerated  mucosa.  The 
diagnosis  can  be  made  by  microscopical  examination,  and,  if  neces- 
sary, by  cultivation.  The  treatment  is  to  syringe  with  a  watery 
solution  of  peroxide  of  hydrogen,  or  peroxide  solution  (2  parts)  and 
alcohol  (1  part)  once  or  twice  a  day,  followed  by  the  insufflation  of 
boracic  powder,  or,  if  there  is  eczema,  some  boracic  ointment. 
Damond  recommends  injecting  a  few  drops  of  a  dilute  solution  of 
sodium  iodide,  followed  by  the  injection  of  the  same  amount  of 
12  volumes  hydrogen  peroxide. 

Hypersecretion. — Excessive  secretion  of  the  products  of  the  ceru- 
minous  and  sebaceous  glands  of  the  external  auditory  meatus  is 
common  in  the  tropics,  and  is  probably  induced  by  some  hyperemia, 
perhaps  in  part  due  to  irritating  dust,  and  partly  to  the  hot,  damp 
air.  As  a  rule  both  ears  are  affected,  giving  rise  to  a  sensation  of 
fulness  and  heaviness  in  head,  diminution  in  hearing,  and  tinnitus 
aurium,  and  more  rarely  to  autophony,  while  pain  is  rare,  though 
neuralgia  may  occur,  and  reflex  coughing.  The  diagnosis  is  easily 
made  by  seeing  the  brownish-red  or  black  mass  filling  up  the 
meatus. 

If  the  plug  is  soft,  it  can  easily  be  removed  by  warm  syringing; 
if  hard,  it  requires  to  be  softened  by  a  warm  solution  of  bicarbonate 
of  soda  (20  grains  to  1  ounce  of  water)  or  glycerine  of  borax,  and 
then  to  be  removed  by  syringing.  If  deafness  persists  after  the 
cerumen  has  been  removed,  it  is  necessary  to  inflate  the  middle  ear 
by  a  Politzer's  bag,  which  must  be  used  with  care. 

Otitis  Externa  Circumscripta. —  Boils  due  to  the  entrance  of 
pyogenic  germs  into  a  sebaceous  gland  or  hair-follicle  are  not  rare. 
They  usually  cause  much  pain,  which  is  aggravated  by  moving  the 
jaw  or  touching  the  auricle,  and  may  cause  toothache,  salivation, 
and  vertigo. 

The  treatment  should  be  to  relieve  pain  by  cocaine,  and  the 
meatus  should  be  lightly  packed  with  gauze  soaked  in  weak  carbolic 
lotion.  Later  an  incision  may  be  made  into  the  boil  with  a  Dundas 
Grant's  furuncle  knife,  and  the  meatus  dressed  with  carbolized, 
glycerine  on  gauze.  To  relieve  the  irritable  condition  of  the  meatus, 
which  often  persists  after  the  boil  has  been  relieved,  a  little  cocaine 
or  boracic  ointment  combined  with  lanoline  may  be  applied,  and  a 
general  tonic  prescribed. 

Otitis  Externa  Ossificans. — Miiller  has  described  a  diffuse  inflammation  of 
the  mucosa  of  the  external  auditory  meatus  in  the  tropics  which  often  invades 
the  periosteum  and  leads  to  ossification,  and  may  cause  exostosis. 


EAR  COMPLICATIONS  OF  TROPICAL  DISEASES  2013 

Deaf  and  Dumb. 

The  number  of  deaf  and  dumb  people  is  relatively  high  in  certain 
parts  of  the  tropics — e.g.,  in  Ceylon  there  are  9  deaf  and  dumb 
males  and  7  females  out  of  10,000  persons  of  each  sex.  In  India 
there  are  6  males  and  4  females  our  of  10,000  persons  of  each  sex. 
There  is  a  deaf  and  dumb  school  in  Ceylon. 

Meniere's  Disease. 

This  disease,  which  is  characterized  by  severe  tinnitus,  and  vertigo 
is  often  met  with  in  the  tropics.  It  occurs  especially  in  planters,  who 
are  exposed  to  the  midday  sun.  The  patients  frequently  recover 
on  their  return  to  the  Temperate  Zone.  Large  doses  of  bromides 
are  useful. 

EAR  COMPLICATIONS  OF  TROPICAL  DISEASES. 

Leprosy. 

The  lobules  of  the  ear  are  especially  liable  to  be  attacked  in 
tubercular  leprosy,  and  are  usually  left  long  and  thickened  when 
the  disease  has  abated. 

Quinine. 

The  prolonged  or  considerable  use  of  quinine  may  cause  simple 
hyperemia  of  the  labyrinth,  and  may  be  associated  with  middle- 
ear  conge -tion,  as  described  by  Kirchner.  The  symptoms  are 
usually  tinnitus  aurium  and  deafness.  It  is  bilateral,  and  comes 
on  gradually.  The  quinine  should  be  stopped,  and  bromide  of 
ammonium  prescribed,  and  afterwards  cuquinine,  associated  with 
bromides,  may  be  administered. 

Arsenic. 

A  native  treatment  for  ear  disease  in  the  Dutch  East  Indies  is 
by  the  application  of  a  powder,  Warangangpulver,  containing  some 
90  to  96  per  cent,  of  arsenious  acid.  According  to  Benjamins,  this 
may  lead  to  destruction  of  the  auricle  and  obliteration  of  the 
external  auditory  meatus,  with  sometimes  necrosis  of  the  bone, 
and  even  fatal  haemorrhage  from  the  internal  carotid  artery. 

Malaria. 

Reports  of  suppurative  otitis  media  being  caused  by  malaria  cannot  be 
accepted  as  proven,  but  intermittent  otalgia,  intermittent  attacks  of  deafness, 
and  labyrinthine  vertigo  may  be  of  malarial  origin,  especially  if  relieved  by 
quinine. 

DISEASES  OF  THE  NOSE. 

Disease  of  the  nose  is  intimately  connected  with  disease  of  the 
ear,  and  to  a  less  degree  with  disease  of  the  conjunctiva.  The 
acute  catarrhal  rhinitis,  or  common  cold,  may  be  induced  by  pro- 
longed exposure  to  the  sun's  rays,  as  well  as  to  chills,  and  is  in  every 


2oi4  DISEASES  OF  THE  ORGANS  OF  SPECIAL  SENSE 

case  an  infection,  though  it  is  difficult  to  determine  the  actual 
micro-organism  causing  the  disease.  The  commonest  organism  is 
the  Micrococcus  catarrhalis.  The  tropical  affections,  are,  however, 
described  in  Chapter  LXXXI.,  p.  1875. 


REFERENCES. 

Eye  Diseases. 

Castellani  (191 2).     Journal  of  Tropical  Medicine,  November  1. 

Chalmers  and  Marshall  (191 8).     Journal  of  Tropical  Medicine  and  Hygiene, 

October  1,  p.  19b. 
Daniels  (1911).     Journal  of  Tropical  Medicine  and  Hygiene,  June.     London. 

(Keratitis  caused  by  Trypanosomes.) 
Denham,  E.  B.  (1912).     Census  of  Ceylon.     Colombo. 
Elliott  (1902-1916).     Numerous  papers  in  the  Indian  Med.  Gazette. 
Elliott  (1918).     Brit.  Med.  Jour.,  May  4  and  May  25. 
Faber   and   Starcke    (1908).      Nederlandsch  Tijdschrift  von  Geneeskunde, 

No.  14,  p.  1 106.      (Optic  Atrophy  in  Trypanosomes.) 
Fehr     (1907).     Deutsche     Medizinische     Vvochenschrift,     No.     49.     Berlin. 

(Atoxyl  and  the  Optic  Nerve.) 
Fuchs,    E.     (191 1).       Textbook    of    Ophthalmology.       Philadelphia.       (An 

English  translation  of  Professor  Fuch's  book,  which  is  one  of  the  most 

useful  of  the  larger  books  on  ophthalmologj.) 
Greef,  K.  (1909).     Klinisches,  Jahr.  xxi.  3,  606.     (Trachoma.) 
Harston,  G.  M.  (1912).     Transactions  of  the  Hong  Kong  Medical  Congress. 

Hong  Kong.     (A  most  excellent  paper  dealing  with  a  number  of  tropical 

eye  diseases.) 
Igersheimer     (1909).     Miinchener     Medizinische     Wochenschrift,     No.     24. 

(Atoxyl.) 
Jamieson  and  Lindsay  (1919).     Jour.  Royal  Amr}   Med.  Corps.  (Action  of 

Quinine  on  the  Visual  Apparatus). 
Landrieu  (1912).     These  de  Paris,  No.  396.    (Les  Mycoses  Oculaires.) 
Leber  and  v.  Prowazek  (191  i).     Archiv  fur  Schills-  und  Tropen-Hygiene. 

xiii.  409. 
Morax,  V.  (1906).     Annales  d'Oculistique,  cxxxvi.  394;  (1907)  ibid.,  cxxxvii. 

311;  (1910)  Bulletin  de  la  Societe  de  Pathologie  Exotique,  May.     (Ocular 

Manifestations  in  Trypanosomiasis.) 
Nattan-Larrier  and  Monthus  (1908).     Bulletin  de  la  Societe  de  Pathologie 

Exotique.     (Iritis  and  Trypanosomiasis.) 
Perry  and  Castellani  (1910).     Journal  of  Tropical  Medicine. 
Sergent,  E.  (1909).     Annales  de  l'lnstitut  Pasteur,  xxiii.  2,  3.     (Trachoma 

in  Algeria.) 
Sisson,  E.  O.  (1909).     Ophthalmology,  January. 
Talbot  (191 8).     Bull.  Soc.  Med.  Chir.  Indochina,  June. 
Ulbrick,    H.    (191  o).     Bulletin   de  la   Societe  de   Pathologie   Exotique,   iii. 

303-305. 
Wood  (191 3).     South  African  Medical  Record,  245-246.     (Eye  Affections  in 

Leprosy.) 
Yorke    (191 1).     Lancet,    clxxx.;    (1911)    Annals   of  Tropical   Medicine   and 

Parasitology,  No.  4,  p.  ^85.     (Cornea  in  Trypanosomiasis.) 

Diseases  of  the  Ear. 

Bramley  (1835).     Transactions  Calcutta  Medical  Society,  vii.  71. 
Campbell  (1833).     Transactions  Calcutta  Medical  Society,  vi.  428. 
Milligan   and    Wingrave    (1911).     Diseases    of   the    Ear.     London.     (An 

excellent  account  of  the  diseases  of  the  ear  and  associated  diseases  of  the 

nose  and  throat.) 
Sutton,  J.  B.  (1910).     Lancet,  June  11.     London.    (Deformities  in  Masai,  etc.) 


DIVISION  III.:  SKIN  DISEASES. 

Pyogenic  Infections. 

Dermatomycoses. 

Mycetoma  and  Paramycetoma. 

Dermatitis  Venenata. 

Ulcerations. 

Dermatozoiases. 

Dysidroses  and  Dystrophies. 

Miscellaneous  Diseases. 

Cosmopolitan  Diseases. 


CHAPTER  XCI 
PYOGENIC    DERMAL    INFECTIONS 

Preliminary  remarks — Pyogenic  infections:  The  pyoses — The  pyogenic  folli- 
culites— The  pyogenic  dermatites — References. 

PRELIMINARY  REMARKS. 

In  this  chapter  we  begin  a  brief  review  of  the  more  important  skin 
diseases  of  the  tropics.  As  this  Manual  is  not  a  work  on  skin  diseases, 
but  is  intended  for  the  tropical  practitioner,  we  have  arranged  these 
disorders  from  the  standpoint  of  the  practical  physician,  and  have 
avoided  a  scientific  classification.  The  chapters  include  pyogenic 
infections;  fungal  diseases,  with  the  mycetomas  considered 
separately;  the  dermatites  due  to  plants;  ulcers;  the  dermatites 
caused  by  animals;  disorders  of  sweating  and  of  nutrition;  and 
miscellaneous  and  cosmopolitan  diseases. 

PYOGENIC  INFECTIONS. 

The  skin  diseases  which  we  gather  together  under  this  heading 
are  all  caused  by  the  pyogenic  cocci,  and  may  be  distinguished  as 
follows : — 

A.  Skin  between  the  primary  lesions  not  inflamed : — 

I.  Non-follicular — The  Pyoses. 
II.  Follicular — The  Folliculites. 

B.  Skin  primarily  inflamed — The  Pyogenic  Dermatites. 

THE  PYOSES. 

Definition. — A  pyosis  is  a  non-follicular  dermal  infection  char- 
acterized by  the  appearance,  on  apparently  healthy  skin,  of 
vesicles  or  bullae,  the  contents  of  which  rapidly  become  purulent. 
It  is  not  associated  with  general  symptoms,  except  slight  fever 
in  the  early  stages  at  times,  and  is  due  to  the  action  of  pyogenic 
micrococci. 

Remarks. — The  type  of  this  variety  of  dermal  affections  is  'Pyosis 
mansoni,'  named  in  honour  of  Sir  Patrick  Manson,  G.C.M.G. 

Varieties.- — A  number  of  '  pyoses '  are  known  to  exist  in  the 

tropics,    and   these   may  be   differentiated   from  one  another   as 

follows: — 

2017  '27 


2018  PYOGENIC  DERMAL  INFECTIONS 

A.  Primary  lesions  usually  small  : — 

I.  Situate  typically  in  axillary  and  crural  regions,  with- 
out crusty  lesions — Pyosis  mansoni. 
II.  Situate  on  arms  and  legs,  with  thick  crusty  lesions — 

Pyosis  tropica. 
III.  Situate   on   palms;   rare;    no   crusty   lesions — Pyosis 
palmaris. 

B.  Primary  lesions  usually  large  : — 

I.  Typically  bullae  without  bright  yellow  crusts — Pyosis 

corletti. 
II.  Typically  large  vesicles  forming  circular  bright  yellow 
crusts — Pyosis  discoides. 

Pyosis  Mansoni. 

Synonym. — Pemphigus  contagiosus  (Manson). 
Definition. — Pyosis  mansoni  is  a  pyosis  with  primary^.lesions, 
usually  small,  but  mixed  with  bullae  and  affecting  the  axillary  and 


Fig.  794. — Pyosis  Mansoni. 


scroto-crural  regions.     It  is  very  common  in  the  damp  regions  of 
the  tropics. 

Historical  and  Geographical. — This  dermatosis  was  first  described 
by  Manson  under  the  term  pemphigus  contagiosus.      It    is   very 


PY0S1S  MAN  SON  I 


2019 


common  during  the  hot  season  in  China,  the  Malay  Peninsula, 
Ceylon,  and  Southern  India,  and  probably  in  many  other  parts 
of  the  tropics.  Castor  has  reported  it  from  Burma.  Very  often 
epidemics  occur  among  the  crews  of  men-of-war  stationed  in  the 
tropics,  as.,  .observed  by  Clayton,  or  in  offices,  as  observed  by 
ourselves. 

/Etiology. — Manson    found   a  diplococcus;  other  observers  have 
described  Leishmania-like  bodies;  in  Clayton's  and  our  experience 


Fig.  794A. — Pyosis  Mansoni. 
Same  case  as  Fig.  794,  but  more  magnified. 

the  examination  of  the  contents  of  the  vesicles  shows  the  presence 
of  cocci  generally  arranged  in  pairs,  and£having  often  a  gonococcus- 
like  shape.  They  are,  however,  Gram-positive,  and  in  cultures 
present  all  the  characters  of  the  Aurococcus  aureus  and  albits.  The 
disease  is  probably  spread  by  contact. 

Symptomatology. — The  affection  has  nothing  to  do  with  that 
group  of  diseases  to  which  writers  on  dermatology  apply  the  term 


2020  PYOGENIC  DERMAL  INFECTIONS 

'  pemphigus,'  for  it  is  much  more  closely  related  to  impetigo,  of 
which  we  consider  it  to  be  a  variety.  The  eruption  attacks  gener- 
ally the  axilla,  the  inguinal  and  crural  regions,  from  whence  it 
often  extends  to  the  abdomen  and  back  and  limbs,  rarely  affecting 
the  face.  It  is  extremely  contagious,  and  is  generally  more  severe 
in  individuals  who  perspire  profusely  and  suffer  from  prickly  heat. 
The  eruption  is  made  up  of  flattened,  roundish  vesicles,  which 
quickly  enlarge  to  the  size  of  a  small  pea.  Very  large,  flabby, 
pemphigoid  bullae  may  occur,  but  not  very  frequently.  The 
contents  are  at  first  transparent,  but  soon  become  turbid.  The 
vesicles  are  often  surrounded  by  a  pinkish  or  reddish  inflammatory 
halo.  On  being  pricked,  the  vesicle  collapses.  The  eruption 
does  not  usually  affect  the  general  health,  but  may  be  very  per- 
sistent, and  may  be  followed  by  crops  of  boils.  As  soon  as  the 
patient  goes  to  the  hills  or  to  a  cool  climate  it  disappears  spon- 
taneously. 

That  the  malady  is  merely  a  type  of  pyosis  or  impetigo  due  to  the  usual 
pyogenic  cocci  is  shown  by  some  cases  presenting  the  typical  bullae  on  the 
axillary  regions,  and  soon  after  or — though  rarely — at  the  same  time  boils 
on  the  arms  and  legs  and  impetiginoid  lesions  on  the  face. 

Diagnosis. — This  is  generally  easy,  the  only  difficulty  being  with 
chicken-pox.  The  absence  of  fever  and  the  situation  of  the  vesicles, 
which  in  pyosis  mansoni  usually  appear  in  the  crural  or  the  axillary 
regions,  however,  should  be  sufficient  to  exclude  this.  The  absence 
of  crusty  lesions  differentiates  the  disease  from  the  common  type 
of  impetigo  contagiosa. 

Prognosis. — The  eruption  is  very  persistent,  but  does  not  affect 
the  general  health,  except  when  complications  such  as  boils  develop. 

Treatment.— In  severe  cases  treatment  by  an  autogenous  vaccine 
may  be  tried.  Locally  the  affected  regions  should  be  disinfected 
regularly  twice  daily  with  a  solution  of  perchloride  of  mercury  (i  in 
2,000),  carbolic  acid  (2  per  cent.),  permanganate  of  potash  (1  in 
4,000),  hydrogen  peroxide  (10  percent.),  cyllin  (1  in  300),  lysol  or 
lysoform  (2  to  5  per  cent.).  After  this  the  vesicles  are  pricked,  and 
the  parts  again  washed  with  the  disinfectant,  an  antiseptic  powder 
being  then  thickly  applied,  such  as: — 


Xeroform    .  . 
Acidi  borici  (finely 
Talci  ven.    .  . 

powdered) 

■■  3i 
■■  3i 
••     Si 

Kurophen    .  . 
Talci  ven.    .  . 

••      3i 

Dermatol     .  . 
Talci  veD.    .  . 

••  3i 
••      Si 

In  some  patients  an  ointment  (europhen,  2  per  cent. ;  protargol, 
5  per  cent.)  answers  better;  the  protargol  ointment  should  never  be 
used  for  the  face  in  Europeans,  as  it  discolours  the  skin  after  a 
time.  It  may  be  noted  that  in  our  experience  the  white  precipitate 
ointment  (1  per  cent.),  which  is  so  efficacious  in  the  usual  impetigo 


PYOSTS  TROPICA 


of  the  Temperate  Zones,  has  very  little  or  no  effect  in  pyosis  man- 
soni.  After  the  eruption  has  disappeared,  it  is  advisable  to  use 
some  Condy's  fluid  or  other  disinfectant  in  the  bath  to  prevent 
relapses;  and,  if  the  skin  is  not  too  tender,  a  formalin  soap  may  be 
regularly  used.  The  underclothing  should  be  regularly  dusted  with 
one  of  the  above  powders. 

Pyosis  Tropica. 

Synonym. — Pyosis  Castellanii,  Kurunegala  ulcers,  Pyosis  Caffra. 

Definition. — Pyosis  tropica  is  characterized^ by  the) presence  of 
numerous  crusty  lesions  on  the  legs  and  arms,  caused  by  pyococci. 

Historical. — Under  the  name 
'  pyosis  tropica '  Castellani  de- 
scribed in  1909  a  skin  disease  very 
common  in  Ceylon  and  Southern 
India.  In  Ceylon  it  is  called  by  the 
natives  Kurunegala  sore,  as  it  is 
especially  common  in  that  district. 
Pyosis  tropica  has  been  reported 
from  other  tropical  countries.  It 
has  been  observed,  in  1912,  in 
Tripoli  by  Gabbi  and  Sabella;  in 
the  Anglo-Egyptian  Sudan  by 
Chalmers  and  O'Farrell,  in  1913;  in 
South  Africa  by  Ricono,  in  1916; 
and  by  Pip  er  in  1918. 

/Etiology. — The  disease  is  prob 
ably  due  to  the  usual  pyogenic 
cocci,  and  is  allied  to  the  ordinary 
impetiginous  and  ecthymatous 
conditions,  though  much  more 
severe.  Chalmers  and  O'Farrell 
grew  an  organism  from  their  case 
which,  differing  somewhat  from 
the  other  species  of  aurococcus, 
was  called  by  them  Aurococcus 
tropicus.  It  was  held  to  be  causal 
because  a  vaccine  made  from  it 
rapidly  cured  the  case,  but  had  no 
effect  on  a  case  of  Nile  boils;  but 
in  other  cases  other  varieties  of 
pyogenic  cocci  may  be  causal. 

Symptomatology. — The  patient,  generally  a  young  boy  or  girl, 
though  adults  may  also  suffer  from  it,  presents  on  the  legs,  arms,  and 
occasionally  all  over  the  body,  except  the  face,  numerous  crusty 
lesions,  occasionally  rupia-like,  of  a  dirty  blackish  or  yellowish 
colour.  If  the  thick  crust  is  removed,  a  shallow  ulcer  with  an 
irregular  margin  and  granulating  fundus  will  be  seen,  or  a  small, 
flattened,  or  hemispheric  nodule  the  size  of  a  pea,  with  a  pinkish, 


Fig.  795. — Pyosis  Tropica. 

The  white  patches  are  in  reality 
thick  yellow  crusts. 


2022  PYOGENIC  DERMAL  INFECTIONS 

smooth  surface.  Besides  these  large  lesions,  small  papulo-vesicles 
and  minute  pustules  are  often  present.  The  larger  lesions  are 
frequently  surrounded  by  a  halo  of  hyperpigmentation.  There  is 
severe  pruritus.  On  healing,  also,  the  ulcers  and  nodules  leave  a 
zone  of  hyperpigmentation  or,  more  rarely,  depigmentation.  In 
chronic  cases  plaques  of  hyperkeratosis  may  develop,  especially 
on  the  exterior  regions  of  the  arms  and  the  elbows. 

Diagnosis. — On  superficial  examination,  the  disease  might  be 
easily  mistaken  for  frambcesia.  In  contrast  to  frambcesia,  the 
ulcers  are  superficial,  and  the  nodules,  when  present,  are  generally 
smaller,  have  no  moriform  surface,  and  in  scrapings  from  the  lesions 
the  Treponema  pertenue  Castellani  is  absent.  From  scabies  it  is 
distinguished  by  the  absence  of  burrows  and  absence  of  the  Acarus. 
From  ecthyma,  to  which  it  is  closely  related,  the  condition  differs  by 
the  fact  tha+,  on  removing  the  crusts,  besides  the  ulcerative  lesions, 
rather  large,  smooth  hemispheric  nodules  may  be  seen. 

Prognosis. — The  disease  is  very  persistent,  but  the  general 
health  is  not  affected. 

Treatment. — If  the  disease  is  not  properly  treated,  it  has  a 
tendency  to  become  chronic.  In  some  cases  the  opsonic  treatment 
gives  satisfactory  results.  The  vaccine  should  be  prepared  with 
staphylococci  grown  from  the  lesions.  It  has  been  used  by 
Castellani  with  good  results  in  Ceylon  in  igio,  by  Chalmers  and 
O'Farrell  in  1913,  and  by  Pijper  in  1918.  Chalmers  and  O'Farrell 
gave  with  success  250  millions  of  an  autogenous  vaccine  to  an 
adult,  and  repeated  it  in  three  days;  Pijper  treated  children  with 
4  to  5  millions  of  an  autogenous  streptococcus  obtained  from  a 
case,  or  by  a  mixture  of  streptococci  and  staphylococci.  The  local 
treatment  consists  in  removing  the  crusts  by  soaking  them  with  a 
salicylic  oil  made  according  to  the  following  formula:- — ■ 

Acidi  salicylici    .  .  .  .  .  .  .  .  . .      gr.  xxx. 

Olei  ricini  .  .  .  .  .  .  .  .  q.s. 

Olei  olivae  .  .  .  .  .  .  . .  ad  giv. 

or  by  compresses  soaked  in  hot  boric  lotion. 

All  the  lesions  are  then  disinfected  with  a  solution  of  perchloride 
of  mercury  (1  in  1,000),  carbolic  acid  (2  per  cent.),  cyllin  (1  in  300), 
or  permanganate  of  potash  (1  in  4,000).  A  slightly  antiseptic 
ointment  is  then  applied,  such  as  europhen  (2  per  cent.),  iodoform 
(2  per  cent.),  protargol  (5  per  cent.),  calomel  (5  to  10  per  cent.). 
An  ointment  which  in  our  experience  is  often  efficacious  is  /3-naph- 
thol  gr.  ii.-v.,  acidi  carbolici  gr.  v.-x.,  vaselini  ad  gi. 

Pyosis  Palmaris. 

Definition. — Pyosis  palmaris  is  characterized  by  the  presence  of 
numerous,  discrete,  conical,  white  pustules,  which  do  not  form 
crusts  and  which  appear  on  the  palms  of  the  hands  of  native  children. 

Historical. — The  disease  was  described  some  ten  years  ago  by 
Castellani  in  native  children  in  Ceylon,  where  it  is  rare. 


PYOSIS  CORLETTI 


2023 


Climatology. — So  far  it  has  only  been  recorded  in  Ceylon. 

/Etiology. — Pyococci  are  present  in  the  lesions,  but  may  not  be 
the  true  cause. 

Symptomatology. — With  little  or  no  pruritus,  discrete,  conical, 
solitary  pustules  appear  on  the  palms  of  the  hands.  These  pustules 
do  not  coalesce  or  form  crusts,  and  are  not  surrounded  by  a  zone 
of  hyperaemia. 

Diagnosis.— It  is  distinguished  from  scabies  by  the  absence  of 
the  acarus,  from  ringworm  by  the  absence  of  a  fungus,  and  from 
syphilis  by  the  uselessness  of  the  specific  treatment. 

Treatment. — -Vaccines  may  be  tried. 

Pyosis  Corletti. 

Synonyms. — Impetigo  bullosa,  Impetigo  contagiosa  bullosa  of  Corlett. 

Definition. — Pyosis  corletti  is  an  acute,  contagious,  bullous  pyosis 
beginning  on  any  region  of  the  body,  and  characterized  by  the 
presence  of  medium-sized  and  large  bullae  arising  on  seemingly 
healthy  skin,  and  caused ]by }A urococcus*mollis  (Dyar,  1895). 


Fig.  796. — Pyosis  Corletti. 

Historical. — In  1899  Corlett  described  a  contagious  bullous  erup- 
tion as  being  endemic  in  Florida;  later  Singh  in  India  invited  atten- 
tion to  a  similar  disease.  In  1912  Reguzis  described  an  epidemic 
among  Europeans  in  Cairo.  In  19 15  Chalmers  and  O'Connor  gave 
a  description  of  an  epidemic  of  this  disease  as  seen  in  the  1st 
Battalion  of  the  Suffolk  Regiment  in  Khartoum. 

^Etiology . — The  causal  organism  so  far  found  is  Aurococcus  mollis 
(Dyar,  1895).  It  is  causal  because  (1)  it  is  the  only  organism 
present,  and  is  found  in  the  youngest  vesicles;  (2)  it  was  obtainable 


2024  PYOGENIC  DERMAL  INFECTIONS 

from  all  the  cases  of  the  Khartoum  epidemic,  and  a  similar  organism 
was  found  by  Corlett,  but  not  fully  defined;  (3)  a  vaccine  prepared 
from  it  cured  the  patients  quickly.  It  is,  of  course,  possible  that  the 
same  clinical  correlation  may  be  caused  by  various,  as  yet  unknown, 
allied  organisms. 

The  Khartoum  epidemic  was  traceable  to  a  case  of  '  Nile  boils,' 
caused  by  the  same  organism. 

Symptomatology. — The  incubation  period  is  unknown,  but  in 
some  cases  the  initial  lesion  is  a  small  papule  on  the  head  or  chest, 
which  is  so  quickly  followed  by  an  outbreak  of  bullae  that  the 
eruption  is  well  developed  in  two  days. 

The  essential  feature  of  the  eruption  is  a  bulla  arising  on 
apparently  healthy  skin,  and  measuring  about  2  cm.  in  diameter, 
but  associated  with  some  much  larger  blebs  measuring  about  twice 
this  size,  and  also  smaller  bullae  which  rapidly  increase  in  diameter. 

A  bulla  appears  to  start  as  a  small  vesicle  situate  in  the  epidermis, 
containing  a  clear,  watery  fluid.  This  vesicle  rapidly  increases  in 
size  until  it  forms  a  bulla,  the  walls  of  which  are  first  tense  and  the 
contents  watery,  but  later  they  become  flaccid  and  the  contents 
purulent. 

The  bulla  bursts,  the  contents  escape,  and  the  lesions  dry  up 
and  disappear,  usually  without  forming  a  scab,  but  in  the  case  of 
the  larger  lesions  it  leaves  behind  it  a  certain  amount  of  dark  dis- 
coloration of  the  skin,  indicating  the  affected  area. 

If  a  bulla  is  pricked  it  is  found  to  have  a  glazed,  parchment-like 
base.  The  edges  of  the  bulla  are  also  observed  to  be  undermined, 
and  it  is  apparent  that  the  increase  in  size  from  a  vesicle  or  small 
bulla  to  a  larger  one  is  by  the  spreading  outwards  of  the  edges.  If 
scratched,  excoriations  and  crusts  are  formed,  but  crusty  lesions 
are  rare  and,  when  present,  only  slightly  developed. 

The  bullae  are  situate  most  abundantly  on  the  thighs,  back,  and 
chest,  and  less  abundantly  on  the  neck,  arms,  and  legs,  and  more 
rarely  on  the  face  and  head.  The  axillary  and  scroto-crural  regions 
are  singularly  free  from  the  disease,  only  one  case  showing  a  slight 
amount  of  the  eruption  at  the  margins  of  the  axillae. 

There  are  no  constitutional  symptoms,  and  only  rarely  do  cases 
complain  of  a  slight  amount  of  itching,  which  is  probably  due  not 
so  much  to  the  eruption  itself  as  to  the  rubbing  of  the  clothing 
producing  slightly  raw  areas  where  bullae  have  burst.  When  this 
takes  place,  small  scabs  are  apt  to  form,  especially  if  the  patient 
scratches  the  area,  but  they  are  entirely  secondary  in  nature  and 
not  part  of  the  true  eruption. 

The  differential  leucocyte  count  based  on  1,000  cells  is: — 


Polymorphonuclear  leucocytes 
Mononuclear  leucocytes   . . 
Large  lymphocytes 
Small  lymphocytes 
Eosinophile  leucocytes 


86-7 

4*4 
3-2 

1-9 


Total      . .  . .  . .    ioo-o 


PYOSIS  CORLETTI  2025 

Diagnosis.— The  important  diagnostic  characters  of  the  eruption 
are  the  absence  of  constitutional  disturbance,  the  absence  of  severe 
itching,  the  presence  of  relatively  large  bullae  arising  from  apparently 
sound  skin  and  not  surrounded  by  inflamed  areolae,  the  absence  of 
marked  incidence  on  the  axillary  and  scroto-crural  regions,  the 
absence  of  crusts  and  of  streptococci,  the  presence  of  Aurococcus 
mollis,  and  finally  the  ready  reaction  to  treatment  by  a  vaccine 
prepared  from  this  organism. 

^Differential  Diagnosis.- — The  differential  diagnosis  must  be  made 
from  impetigo  contagiosa,  dermatitis  bullosa  plantaris,  pemphigus 
acutus,  and  pyosis  mansoni. 

It  can  readily  be  differentiated  from  impetigo  contagiosa  by 
the  absence  of  crusty  lesions  as  a  rule,  and  by  the  fact  that 
even  when  the  youngest  vesicle  is  examined  by  Sabouraud's 
methods  no  streptococcus  can  be  found  and  only  Anrococcus 
mollis  (Dyar). 

From  dermatitis  bullosa  plantaris  it  may  be  distinguished  by  not 
attacking  the  soles  of  the  feet  as  far  as  has  been  recorded,  by  not 
extending  between  the  toes,  and  by  the  absence  of  streptococci  and 
Epidermophyton  cruris  Castellani. 

From  pemphigus  acutus  it  can  be  recognized  by  the  absence  of  the 
severe  constitutional  disturbance. 

From  pyosis  mansoni  it  can  be  differentiated  by  the  fact  that  it 
does  not  begin  in  the  axillae  or  scroto-crural  regions,  and  that  it 
but  rarely,  and  then  lightly,  attacks  those  parts  which  are  the 
primary  seat  of  Manson's  pyosis. 

The  principal  feature  of  the  eruption  in  Manson's  disease  is 
flattened,  roundish  vesicles  which  enlarge  to  the  size  of  a  small  pea, 
while  large,  flabby,  pemphigoid  bullae  are  rare;  but  in  this  eruption 
large  pemphigoid  bullae  are  common.  In  Manson's  pyosis  the 
vesicles  are  often  surrounded  by  a  pinkish  or  reddish  inflammatory 
halo,  which  is  absent  in  the  present  eruption. 

Complication. — Eruptions  of  boils  may  occur. 

Sequela. — When  cases  are  not  treated  by  vaccine  therapy  there 
appears  to  be  a  liability  to  boils  as  a  sequela. 

Prognosis. — The  prognosis  is  excellent,  as  the  disease  is  rapidly 
cured  by  a  combination  of  vaccine  and  local  therapy. 

Treatment. — The  best  form  of  treatment  is  to  prepare  a  vaccine 
which  is  to  be  administered  in  200  and  450  million  doses,  with 
intervals  of  two  to  three  days  between  each  dose. 

In  order  to  expedite  the  cure  local  treatment  is  also  useful, 
and  this  consists  in  pricking  each  blister  and  catching  the  exuding 
fluid  on  swabs  dipped  in  1  in  1,000  lotio  hydrargyri  per- 
chloridi. 

After  pricking,  each  blister  should  be  thoroughly  disinfected  with 
the  same  lotion,  and  be  dusted  with  some  antiseptic  powder,  the 
cheapest,  but  not  the  best,  being  boric  acid,  while  the  same  with 
starch  should  be  used  for  dusting  the  clothing  in  order  to  attempt 
to  prevent  the  spread  of  the  infection. 


2026 


PYOGENIC  DERMAL  INFECTIONS 


A  vaccine  prepared  from  a  case  of  Pyosis  corletti  acts  also  generally  on  cases 
of  Nile  boils,  and  vice  versa.  This  is  easily  understood,  as  the  two  conditions 
are  due  to  the  same  organism — Aurococcus  mollis  (Dyar). 

Prophylaxis.- — The  important  points  in  the  prophylaxis  are  to 
realize  that  the  disease  may  originate  from  a  case  of  boils,  may  cause 
no  symptoms,  and  may  be  overlooked. 

Pyosis  Discoides. 

Definition. — Pyosis  discoides  begins  as  a  generalized  vesicular 
eruption  of  fairly  large  roundish  vesicles,  which  rapidly  become 
purulent  and  then  dry,  forming  circular,  discoidal,  bright  yellow 
crusts  surrounded  by  a  slightly  hypersemic  zone  and  associated  with 
pyogenic  cocci,  and  in  the  early  stages  often  accompanied  by  slight 
fever. 

Historical. — This  eruption  was  found  by  Castellani  in  ioi-j.h'n  a 
man  in  Ceylon,  and  again  in  the  Balkans. 


hie,    797. — Pyosis  Discoides. 
(From  a  rough  sketch  made  by  an  Austrian  prisoner  in  Macedonia.) 


^Etiology. — Streptococci  and  staphylococci  have  been  found  in  the 
lesions. 

Symptomatology. — The  symptoms  may  be  discussed  in  two 
stages: — 

Vesicular  Stage. — -There  is  a  profuse  generalized  eruption  of  fairly 
large  roundish  vesicles,  some  of  which  are  flaccid. 

Stage  of  Discoidal  Crusts. — The  contents  of  the  vesicles  arc  at 
first  clear,  but  soon  become  purulent,  and  then  dry  up,  forming 
circular,  discoidal,  bright   yellow  crusts,  firmlv  embedded  in  the 


THE  PYOGENIC  FOLLICULITES  2027 

deeper  layers  of  the  epidermis,  and  often  surrounded  by  a  hypera-mic 
halo.  When  these  firmly  fixed  crusts  are  removed,  shallow  circular 
ulcers  with  sharply  defined  edges  are  produced. 

General  Symptoms. — Constitutional  symptoms  are  of  the  slightest, 
but  during  the  first  few  days  of  the  eruption  there  may  be  slight 
fever. 

Diagnosis. — The  definition  indicates  the  principal  characters  of 
the  complaint.  As  regards  the  differential  diagnosis,  this  must 
be  made  from  chicken-pox,  in  which  the  bright  yellow,  discoidal, 
deeply  attached  crusts  are  absent. 

Treatment. — The  treatment  advised  is  1  per  cent,  white  precipitate 
ointment. 

THE  PYOGENIC  FOLLICULITES. 

These  are  pyogenic  affections  of  the  hair  follicles  caused  by  cocci. 
The  following  varieties  may  be  differentiated : — 

A.  Deep-seated  in  the  hair  follicle;  occur  anywhere — Tropical 

boils. 

B.  Superficially  situate  in  the  hair  follicle;  found  on  the  legs 

and  thighs — Purulent  folliculitis  of  the  legs. 

Tropical  Boils. 

Synonyms. — Tropical  furunculosis,  Nile  boils,  Mango  boils. 

Definition. — A  tropical  boil  is  a  deep-seated  purulent  inflammation 
of  a  hair  follicle  due  to  pyococci. 

Remarks. — -Furunculosis  is  very  common  in  the  tropics.  It 
does  not  differ  from  what  one  sees  in  Europe  except  that  it  is  often 
of  much  severer  type,  and  has  a  great  tendency  to  spread  all  over 
the  body.  The  individual  boils  are  frequently  of  very  large  dimen- 
sions and  extremely  painful.  There  may  be  fever.  The  condition 
is  very  common  in  people  who  perspire  much  and  suffer  from  prickly 
heat. 

etiology. — -It  is  due  to  staphylococci.  Carbuncle,  especially  of 
the  neck  and  gluteal  regions,  with  deep  infiltration  and  multiple 
openings,  is  not  rarely  associated  in  our  experience  with  ordinary 
boils.  The  so-called  '  Nile  boils  '  have  been  examined  bacteriologi- 
cally  by  Chalmers  and  Marshall  and  by  Archibald,  and  have  been 
shown  to  be  generally  caused  by  Aitrococcus  mollis  (Dyar,  1895). 

E.  Blackdescribesundertheterm'  furunculuscontagiosus  '  a  benign  multiple 
furunculosis  observed  by  him  in  Brazil. 

Treatment. — -The  quickest  and  most  reliable  method  of  cure  in 
cases  of  multiple  boils  is,  in  our  experience,  Wright's  vaccine 
treatment,  the  vaccine  being  prepared  from  staphylococci  isolated 
from  the  patient,  or  being  prepared  from  organisms  known  to  occur 
in  a  given  district.  When  this  treatment  cannot  be  carried  out, 
the  administration  of  fresh  yeast,  half  a  wine-glassful  twice  daily,  or 
of  yeast  preparations  internally,  will  be  found  to  be  useful  in  some 


2028  PYOGENIC  DERMAL  INFECTIONS 

cases — e.g.,  two  or  three  ceridin  pills  twice  daily.  Ichthyol  tablets 
(gr.  v.),  twice  daily,  may  also  be  given,  or  calcium  sulphide  (gr.  \) 
may  be  administered,  but  their  beneficial  effect  is  doubtful.  Diluted 
sulphuric  acid  (ni  xx.-xxx.),  well  diluted,  every  four  hours  may  be 
tried.  Occasionally  a  small  boil  may  be  aborted  by  applying  a 
droplet  of  pure  carbolic  acid  by  means  of  a  pointed  pencil  of  wood 
drilled  into  the  centre  of  the  papule,  or  four  or  five  drops  of  i  in  30 
solution  of  carbolic  acid  may  be  injected  beneath  the  boil,  or 
Unna's  carbolic  and  mercury  plaster  may  be  used,   or  spirit   of 


Fig.  798. — Purulent  Folliculitis  of  the  Legs  and  Thighs. 

camphor  may  be  applied  several  times  daily.  For  old  indurated 
boils  the  continuous  application  of  a  carbolic  lotion  (2  to  5  per  cent.) 
on  lint  occasionally  causes  them  to  become  absorbed.  Large  boils 
in  which  suppuration  has  taken  place  should  be  opened,  but  it  is 
a  mistake  to  open- them  too  soon.  As  a  preventive,  a  salicylic- 
alcoholic  lotion  (1  to  2  per  cent.),  used  after  the  daily  bath,  is 
advantageous,  and  it  is  also  advisable  to  use  a  little  Condy's  fluid 
or  cyllin  in  the  bath. 

Stanoxyl  by  the  mouth  only  is  not  satisfactory,  but  is  said  to  give  good 
results  when  administered  in  baths. 


THE  PYOGENIC  DERMATITES  2029 

Purulent  Folliculitis  of  the  Legs. 

Definition. — A  purulent  inflammation  attacking  many  hair 
follicles  of  the  legs  and  thighs. 

Historical  and  Geographical.— The  condition  is  extremely  common 
in  Ceylon  and  Southern  India,  in  the  former  especially  among  the 
moormen.  It  was  investigated  by  Castellani  some  years  ago.  A 
very  similar  or  identical  condition  has  been  noted  by  R.  Cranston 
Low  in  Scotland  in  miners  working  in  mines  flooded  with  water. 

/Etiology. — It  is  apparently  due  to  the  usual  pyogenic  cocci. 

Symptomatology. — The  patient  presents  on  his  legs— especially 
the  extensor  region — numerous  whitish  conical  pustules.  Each 
pustule  is  pierced  by  a  hair.  The  pustules  remain,  as  a  rule,  separate, 
do  not  increase  in  size  to  any  extent,  and  do  not  coalesce  nor  form 
crusty  lesions.  After  a  time  the  skin  of  the  legs  may  show  a 
peculiar  parchment-like  appearance.  The  examination  of  the  pus 
contained  in  the  pustules  shows  the  presence  of  the  ordinary 
staphylococci. 

Prognosis. — The  disease,  if  left  untreated,  runs  a  very  long  course. 

Treatment. — The  treatment  consists  in  depilation,  application  of 
antiseptic  dressings,  and,  later,  the  application  of  an  antiseptic 
ointment  or  paste.  In  obstinate  cases  the  opsonic  treatment, 
carried  out  with  a  vaccine  prepared  from  the  staphylococci  grown 
from  the  lesions,  gives  good  results.  The  following  ichthyol  appli- 
cation may  be  found  useful: — Ichthyol,  2  drachms;  glycerine, 
1  drachm;  distilled  water  to  1  ounce. 

THE  PYOGENIC  DERMATITES. 

Definition. — The  pyogenic  dermatites  are  inflammations  pre- 
dominantly of  the  surface  of  the  skin,  which  are  caused  by  the 
pyococci. 

Remarks.— The  old  term  eczema  was  introduced  by  iEtius  of 
Amida,  in  the  sixth  century  a.d.,  for  the  breaking  out  of  burning, 
itching,  non-ulcerating  vesicles,  and  was  used  by  Willan  for  an 
eruption  of  minute  vesicles,  non-contagious,  closely  crowded  together, 
formingthinflakes  and  crusts  when  the  fluid  they  contain  is  absorbed, 
and  due  to  irritation  whether  internally  or  externally  applied.  The 
causes  which  Willan  had  in  mind  were  mercury  applied  internally 
and  the  rays  of  the  sun  externally. 

After  years  of  confusion  the  modern  tendency  is  to  consider  that 
the  word  '  eczema  '  is  a  cloak  for  ignorance. 

In  lieu  of  it  the  word '  dermatitis  '  may  be  employed,  if  by  this  is 
meant  an  inflammation  predominantly  of  the  surface  of  the  skin. 
So  defined,  dermatitis  may  be  classified  into: — 

1.  Dermatitis  due  to  chemical  causes. 

2.  Dermatitis  due  to  physical  causes. 

3.  Dermatitis  due  to  parasites. 


2030  PYOGENIC  DERMAL  INFECTIONS 

The  term  eczema  should  only  be  used  when  the  practitioner  is 
unable  to  assign  its  proper  cause  to  a  dermatitis.  The  term  is  there- 
fore a  cloak  for  ignorance  of  the  causation  of  the  dermal  condition. 

In  the  present  section  we  are  considering  a  part  of  the  third  class 
of  dermatites — viz.,  those  due  to  parasites— and  in  particular  that 
subclass  which  is  brought  about  by  the  pyococci. 

We,  however,  propose  to  further  restrict  our  remarks  to  merely 
the  streptococcal  dermatites,  and  will  consider  them  under  two 
headings — -viz. : — 

Primary  Streptococcal  Dermatites. 
Secondary  Streptococcal  Dermatites. 

The  Primary  Streptococcal  Dermatites. 

(Definition. — A  primary  streptococcal  dermatitis  is  an  inflammation 
predominantly  of  the  surface  of  the  skin,  localized  or  generalized,  and 
caused  by  streptococci. 

Remarks. — Streptococci  appear  to  have  been  first  observed  in 
cutaneous  lesions  by  Crocker  in  1881,  and  to  have  been  later 
identified  by  Brockhart  as  Streptococcus  erysipelatosus  Fehleisen, 
1883.  Later  they  were  carefully  described  by  Whitfield,  Colcott 
Fox,  and  many  other  observers,  including  ourselves.  Colcott  Fox 
classified  streptococcal  skin  lesions  with  those  which  occur  in  the 
course  of  grave  systemic  affections,  those  which  are  lesions  of  the 
hypoderm,  those  which  are  primary,  and  those  which  are  secondary 
cutaneous  lesions. 

With  regard  to  the  primary  streptococcal  dermatites,  these  are 
sufficiently  numerous,  but  for  our  present  purpose  we  will  restrict 
our  attention  to  those  found  in  the  tropics,  which  are  dermatitis 
veldis,  dermatitis  pratensis,  and  dermatitis  ciipoliformis,  which  may 
be  distinguished  from  one  another  as  follows: — 

A.  Nodules  not  produced  : — 

I.  Begins  as  a  large  blister  or  bulla,  and  forms  a  super- 
ficial sore  with  ragged  edges,  and  a  fresh  clean  floor 
in  recent,  or  a  parchment -like  floor  in  old  cases — 
Dermatitis  veldis. 
II.  Begins  as  a  small  irritable  papule  or  papulo-vesicle, 
which  ulcerates,  glazes  over,  spreads,  and  finally 
gives  rise  to  an  area  defined  by  a  raised  margin,  inside 
which  are  deep  fissures  and  ulcerated  areas,  and  often 
in  later  stages  papillomatous  outgrowths — Dermatitis 
pratensis. 

B.  Nodules  produced — Dermatitis  cupolijormis. 

DermatitisJVeldis. 

Synonyms.—  Veld  sore,  Barcoo  rot,  Gift  zeer,  Brand  zeer. 
Definition. — A  primary  streptococcal  dermatitis  characterized  by 
the  formation  of  a   bulla,  followed   by   a   superficial   sore,  which 


DERMATITIS   VELDIS  2031 

becomes  very  chronic,  but  does  not  lead  to  papillary  acanthotic 
formations. 

History. — -For  long  the  Bushmen  of  the  region  known  as  Barcoo 
River,  North  Queensland,  have  suffered  from  sores  which  they  call 
Barcoo  rot.  In  the  Transvaal  the  inhabitants  are  afflicted  with  a 
sore  which  they  call  '  gift  zeer  '  or  poison  sore,  while  in  the  Free 
State  the  residents  are  attacked  by  a  similar  sore  which  they  call 
'  brand  zeer  '  or  burn  sore. 

In  1901  Ogston  and  in  1904  Harman  reported  upon  these  condi- 
tions under  the  name  '  veld  sore/  a  term  used  by  the  English  settlers 
in  South  Africa.  Harman  further  proved  that  it  was  the  same  as 
Barcoo  rot  by  the  evidence  of  Australian  Bushmen  who  had  suffered 
from  the  one  in  Australia,  and  from  the  other  in  South  Africa 
recognizing  them  as  the  same.  In  1913  Black  gave  us  his  personal 
experiences  of  Barcoo  rot.  In  1917  Martin  met  with  a  similar 
condition  in  the  Anzac  Mounted  Division  operating  in  the  desert 
east  of  the  Suez  Canal,  and  again  it  was  recognized  by  the  men  who 
had  seen  or  experienced  Barcoo  rot  to  be  the  same  complaint. 

Climatology. — The  disease  is  known  to  occur  in  Tropical  Australia, 
South  Africa,  Egypt,  and  Equatorial  Africa. 

/Etiology. — Harman  obtained  staphylococci  and  streptococci  from 
his  cases.  He  was  inclined  to  consider  his  yellow  staphylococcus 
as  the  causal  organism,  and  called  it  Micrococcus  vesicans,  but  it  is 
more  probable  that  the  causal  agent  is  the  streptococcus  which 
may  be  known  provisionally  as  Streptococcus  vesicans,  and  which  may 
be  only  a  synonym  for  some  more  fully  worked  out  species  such  as 
S.  versatilis  Broadhurst,  1915.  The  disease  can  be  reproduced  in 
man  by  inoculating  the  fluid  of  the  blisters  on  to  a  raw  place  in 
the  skin. 

Pathological  Histology. — The  fresh  unopened  blister  has  been 
studied  by  Harman,  who  found  that  it  occurred  in  the  layers  of  the 
epidermis.  The  stratum  corneum  is  raised,  forming  the  roof  of  the 
blister,  which  begins  as  a  cleft  in  the  stratum  lucidum.  The  epider- 
mis is  never  wholly  absent  from  the  floor,  which  is  composed  of 
swollen  cells  of  the  stratum  lucidum  and  stratum  granulosum.  The 
dermis  shows  a  moderate  degree  of  leucocytic  invasion  beneath 
the  floor  of  the  ulcer.  Cocci  in  the  form  of  diplococci  or  short  chains 
are  found  in  spaces  between  the  cells  of  the  epidermis. 

Symptomatology. — The  dermatitis  begins  by  the  patient  feeling  a 
pricking  or  burning  sensation  in  some  part  of  the  body.  On  ex- 
amining this,  he  finds  that  on  the  site  of  some  small  abrasion  there 
is  a  little  blister  surrounded  by  a  hyperaemic  zone.  The  blister 
quickly  increases  in  size  until  it  may  attain  that  of  a  shilling,  but 
more  usually  it  grows  slowly,  and  when  the  size  of  a  sixpenny-piece 
is  reached  it  usually  bursts,  setting  free  some  sero-purulent  fluid 
and  forming  a  superficial  ulcer  with  a  red  floor  and  roundish  or 
somewhat  festooned  margins. 

The  floor  of  the  ulcer  remains  dry  like  parchment.  The  ulcer  may 
be  painful,  but,  especially  at  the  beginning,  there  is  frequently 


2032  PYOGENIC  DERMAL  INFECTIONS 

more  itching  than  pain.  The  proximal  lymphatic  glands  may  be 
enlarged.  Several  such  sores  may  be  present  at  the  same  time. 
The  hands,  forearms,  feet,  and  legs  are  mostly  affected.  Harman 
has 'seen  as  many  as  twenty  such  sores  on  one  man.  The  duration 
of  the  affection  varies  between  one  and  three  months,  but  loccasion- 
ally  may  last  as  long  as  six  months.  J 

Treatments — The  correct  treatment  is  by  vaccines,  either  auto- 
genous or  from  a  locally  prepared  stock.  The  local  treatment  con- 
sists in  keeping  the  sores  dressed  with  antiseptic  lotions,  such  as 
perchloride  of  mercury  (i  in  4,000),  or  in  washing  the  sores  with  a 
disinfecting  lotion,  and  then  applying  an  antiseptic  powder,  paste, 
or  ointment,  such  as  europhen  (1  to  3  per  cent.),  iodoform  (1  to  3  per 
cent.),  protargol  (5  to  10  per  cent.),  or  calomel  (5  to  10  per  cent.). 

Barcoo  Rot. 

For  the  reasons  given  above  we  consider  Barcoo  rot  to  be  a 
condition  identical  with  dermatitis  veldis.  It  must,  however,  be 
admitted  that  the  descriptions  given  by  some  authors  may  include 
other  conditions.  For  example,  Black  described  it  as  forming  a 
crust  which  becomes  larger,  thicker,  and  harder  until  horny  in 
consistence  and  difficult  to  remove.  There  is  very  little  itching  or 
pain. 

Pain  states  that  the  term  '  Barcoo  rot  '  is  very  loosely  applied.  According 
to  him  the  original  '  Barcoo  rot  '  was  scurvy.  Owing  to  the  improved 
conditions  of  living  scurvy  disappeared,  and  the  younger  Bushmen  applied 
the  name  to  any  superficial  obstinate  sore.  Two  conditions  at  least  are 
now  covered  by  the  term:  a  seasonal  staphylococcal  infection,  occurring 
generally  in  the  autumn,  and  a  deep-seated  trichophytosis  of  the  hands. 

Dermatitis  Pratensis. 

Definition. — Dermatitis  pratensis  is  a  primary  streptococcal  der- 
matitis characterized  by  starting  as  a  papule  spreading  by  ulceration, 
and  forming  in  late  stages  acanthotic  papillary  formations. 

Historical. — The  disease  has  been  studied  by  Castellani  in  Equa- 
torial Africa  and  by  Chalmers  and  Archibald  in  the  Anglo-Egyptian 
Sudan.  We  give  it  the  name  dermatitis  pratensis  to  bring  it  into 
line  with  the  other  dermatites. 

^Etiology. — The  causative  organism  is  a  streptococcus  which  can 
be  found  in  the  polymorphonuclear  leucocytes,  in  the  lesions,  and 
can  easily  be  grown  in  pure  culture.  In  some  cases  in  the  Anglo- 
Egyptian  Sudan  the  organism  obtained  was  Streptococcus  versatilis 
Broadhurst,  1915,  which  is  a  normal  denizen  of  equine  faeces,  from 
which  the  infection  probably  comes.  Its  causal  relationship  depends 
upon  not  merely  its  presence  in  cases  of  the  disease,  but  upon  the 
fact  that  vaccines  prepared  from  it  will  quickly  cure  not  merely  the 
person  from  whom  the  growth  was  obtained,  but  other  patients  also. 

Pathological  Histology. — When  sections  are  made  along  a  papillo- 
matous projection  of  the  acanthotic  variety  it  will  be  seen  that  the 
outer  covering  is  epidermal  in  nature,  and  that,  superficially,  it  is 


DERMA  TITIS  PRA  TEN  SIS 


2033 


covered  by  masses  of  scales,  both  on  its  free  surface  and  on  the  sur- 
face looking  towards  another  process. 

This  epidermis  shows  the  defect  of  cornification  called  '  parakera- 
tosis '  by  Auspitz,  while  with  regard  to  the  rete  there  is  a  certain 
degree  of  acanthosis. 

The  corium  is  full  of  dilated  vessels,  and  is  also  slightly  cedematous 
and  fairly  cellular. 

The  cells  consist  of  forms  with  a -large,  well-stained  nucleus  and 
a  fringe  of  cytoplasm,  which  [are  supposed  to  be  derived  from  con- 
nective tissue  cells.  Plasma  cells  and  mast  cells  may^also  be  seen, 
as 'may  an  occasional  polymorphonuclear  leucocyte. 


Fig.  799. — Dermatitis  Pratensis. 


Turning  now  to  the  non-papillomatous  regions,  there  is  a  well- 
defined  epidermis  with  parakeratosis  and  acanthosis,  while  the 
cellular  infiltration  of  the  corium  is  denser.  It  is  somewhat 
oedematous. 

Raw  areas  show  parakeratoses,  which  are  distinguished  by  the 
extraordinary  development  of  the  acanthosis. 

In  the  region  where  the  epidermis  is  missing  all  trace  of  a  normal 
corium  is  lost  superficially,  and  it s  place'is  taken  by  a  fibrocellular 
exudate. 

Embedded  in  this  exudate  can  be  seen  the  remains  of  the  acan- 
thotic  prolongations  of  the  epidermal  cells. 

In  this  fibrocellular  mass  lie  numerous  bloodvessels  filled  with 
corpuscles,  while  patches  of  serous  exudation  can  also  be  observed. 

The  cells  of  the  mass  are  largely  composed  of  the  same  cells  as  in 
the  corium  of  other  pieces,  but  the  amount  of  polymorphonuclear 

r?8 


2034  PYOGENIC  DERMAL  INFECTIONS 

leucocytes  in  certain  regions,  and  more  especially  superficially,  is 
marked. 

In  the  deeper  part  of  the  section  isolated  pieces  of  the  ordinal y 
connective  tissue  of  the  corium  can  be  seen,  while  finally,  in  the 
depth  of  the  section,  well-defined  connective  tissue  is  seen  containing 
here  and  there  scattered  collections  of  cells  of  the  same  nature,  as 
already  described  for  other  portions  of  the  tissue. 

The  sweat  glands  are  much  damaged,  and  surrounded  by  cells 
of  the  usual  type  found  in  these  lesions. 

Still  deeper  one  meets  with  fatty  tissue,  between  the  cells  of 
which  lies  an  accumulation  of  the  typical  cells  of  the  lesion. 

Symptomatology. — The  eruption  begins  as  a  small  pruriginous 
papule  or  papulo-vesicle,  which  increases  in  size  and  ulcerat  es,  scabs 
over,  and  extends  at  its  margins.  When  fully  developed  it  is 
surrounded  by  a  raised  margin,  behind  which  small  papilla  may 
be  noted,  which  in  older  cases  give  rise  to  very  distinct  papillomatous 
outgrowths.  The  surface  of  the  sore  is  composed  of  deep  fissures 
and  a  few  ulcerated  areas,  which  exude  a  serous  fluid,  which  is  apt 
to  form  crusts.  These  ulcerated  areas  and  fissures  are  separated 
by  other  areas  coated  by  a  thin  epidermal  covering,  which  gives  rise 
to  a  false  pealing  appearance.  The  whole  condition  spreads  slowly 
from  the  margin. 

Diagnosis. — This  is  sufficiently  effected  by  the  table  given  on 
p.  2030. 

Prognosis. — -The  prognosis  is  good  provided  that  the  patient  is 
otherwise  healthy. 

Treatment. — The  best  treatment  is,  without  doubt,  an  auto- 
genous vaccine,  but  a  polyvalent  local  (i.e.,  made  from  local  strains) 
vaccine  acts  quite  well. 

We  generally  give  10  millions  to  commence  with,  then  50,  and, 
if  necessary,  100  millions. 

The  affected  part  in  chronic  cases  may  be  painted  with  iodine  and 
a  dry  dressing  applied. 

Dermatitis  Cupoliformis. 

Synonym. — Tropical  ecthyma  (Castellani). 

Definition. — Dermatitis  cupoliformis  is  characterized  by  com- 
mencing as  dusky  red  macules,  which  are  follicular  or  perifollicular, 
which  either  disappear  or  slowly  become  cupoliform  nodules,  which 
after  a  time  break  down  and  ulcerate. 

Historical. — This  disease  was  first  described  by  Castellani  in  1914 
as  seen  mostly  in  Europeans  in  Ceylon.  Subsequently  he  met 
with  the  disease  in  the  Balkans. 

Climatology. — So  far  it  is  only  reported  from  Ceylon  and  the 
Balkans. 

/Etiology. — It  is  caused  by  a  streptococcus  belonging  to  the  erysi- 
pelatous group  (vide  Chapter  XXXVI.,  p.  929),  which  is  named 
S.  tropicalis  Castellani,  1914. 


DERMATITIS  CUPOLIFORMIS 


z°35 


Symptomatology. — The  disease  begins  as  superficial,  dusky  red, 
follicular,  or  perifollicular  slightly  itching  macules  on  the  feet  and 
legs.  Some  of  these  spots  disappear,  while  others  become  slowly 
larger,  raised,  hard,  infiltrated,  and  cupoliform,  reaching  the  size  of 
a  pea  or  a  small  cherry.  After  a  time  the  centre  of  the  nodule 
breaks  down  and  forms  an  ulcer,  with  a  reddish  floor  and  undermined 
edges. 

These  ulcers  are  somewhat  painful  and  very  slow  to  heal,  and  when 
this  does  take  place  it  produces  patches  of  hyperpigmentation. 
The  course  of  the  disease  is  very  long,  lasting  at  times  more  than 
a  year. 

Diagnosis. — The  characteristic  features  of  the  eruption  are  the 
presence  of  raised,  hard,  rather  large  cupoliform  nodules,  some  of 
which  show  a  central  ulcer  with  undermined  edges. 


Fig.  Soo. — Dermatitis  Cupoliformis  of  the  Foot. 


The  differential  diagnosis  has  to  be  made  from  Oriental  sore  by 
the  absence  of  Leishman-Donovan  bodies. 

From  ecthyma  it  may  be  distinguished  by  the  absence  or  rarity  of 
the  pustular  lesions  with  a  brownish  crust.  In  ecthyma  the  initial 
lesions  are  always  pustular,  there  being  generally  discrete  flat 
pustules;  when  these  rupture  a  brownish  crust  is  formed  beneath 
which  suppuration  goes  on.  In  the  condition  known  as  '  ecthyma 
gangrenosum,'  occasionally  met  with  in  cachectic  children,  especially 
during  convalescence  from  varicella  and  other  exanthemata,  the 
initial  lesions  are  vesicular  or  pustular,  and  no  nodules  are  present. 

In  pyosis  tropica  the  ulcers  do  not  show  undermined  !edges,  and 
pustular  lesions  are  present. 


2036  PYOGENIC  DERMAL  INFECTIONS 

In  purulent  folliculitis  oj  the  legs  there  are  no  ulcers,  only  pustules 
pierced  by  hairs  being  present. 

Prognosis. — The  condition  runs  a  very  long  course  and  is  difficult 
to  cure,  unless  treated  by  an  autogenous  vaccine. 

Treatment. — An  autogenous  vaccine  is  the  correct  treatment,  and 
generally  produces  a  cure  in  two  to  three  /weeks.  Local  treatment 
by  antiseptic  lotions  is  also  recommended. 

The  Secondary  Streptococcal  Dermatites. 

Only  two  forms  of  this  affection  concern  us,  and  both  are  second- 
ary to  infections  with  Epidermophyton  cruris  Castellani.  They  are 
dermatitis  inter  digitalis  and  dermatitis  bullosa  plantaris. 

They  may  be  differing  phases  of  the  same  affection,  but  they  can 
be  differentiated  as  follows:— 

A.  Situate    primarily    between    the    toes.     Bulhe    absent — 

Dermatitis  inter  digitalis. 

B.  Situate  primarily  on  the  soles.     Bullae  present— Dermatitis 

bullosa  plantaris. 

Dermatitis  Interdigitalis. 

Synonyms. — Dermatitis  rimosa  of  the  toes,  Mango  toe  (Ceylon), 
Frieira  (Brazil). 

Definition. — Dermatitis  interdigitalis  is  a  streptococcal  dermatitis 
secondary  to  an  infection  of  the  parts  between  the  toes  caused  by 
Epidermophyton  cruris  Castellani. 

Historical. — This  affection,  which  is  popularly  known  in  Ceylon 
as '  Mango  toe,'  was  first  brought  into  prominence  by  Sabouraud's 
observation  that  the  primary  cause  was  an  infection  by  Epidermo- 
phyton cruris  Castellani.  In  1910  Castellani  found  that  very  often 
there  was  a  secondary  streptococcal  infection. 

A  somewhat  similar  affection  was  described  long  ago  by  Martin  Costa 
in  Brazil,  who  stated  that  the  condition  was  very  common  among  natives, 
who  called  it '  frieira.'  He  believed  it  to  be  caused  by  the  heavy  perspira- 
tion, and  accumulation  of  dust  and  dirt  between  the  toes. 

Geographical  Distribution. — It  is  extremely  common  in  Southern 
India,  Burma,  Ceylon,  and  many  other  tropical  countries,  being 
the  cause  of  great  discomfort  to  European  residents,  especially 
during  the  hot  season. 

/Etiology. — The  condition  seems  to  be  a  pyogenic  infection, 
starting  generally  on  slight  lesions  produced  by  a  localization  of 
Epidermophyton  cruris  Castellani  to  the  toes.  This  localization 
of  the  fungus  was  first  observed  by  Sabouraud.  The  fungus  per  se 
in  this  situation  gives  rise  to  very  slight  symptoms  very  often  only 
some  scaliness  and  pruritus. 

Symptomatology. — The  patient  first  complains  of  great  itching 
between  the  toes,  without  there  being  present  any  papular  or 
vesicular  lesion.     On  scratching  to  relieve  this  itching,  portions 


DERMATITIS  BULLOSA   PLANT ARIS 


2037 


of  the  epidermis  become  removed,  and  small,  superficial,  red,  irritable 
abrasions  are  seen.  These  become  severer,  and  deep,  extremely  pain- 
ful fissures  appear  between  the  toes  in  almost  all  the  cases.  This 
dermatitis  is  difficult  to  cure,  but  disappears  rapidly  on  the  patient 
going  to  the  hills  or  to  Europe.  It  may  remain  quiescent  for  long 
periods,  and  then  reappear  again.  During  the  periods  of  quiescence 
some  pruritus  may  occasionally  be  felt,  and  the  skin  between  the 
toes  may  easily  crack  or  be  slightly  scaly. 

Treatment. — This  consists  in  keeping  the  patient  at  rest  for  a  few 
days,  dressing  the  affected  parts  continuously  with  diluted  carbolic 
lotion  [\  per  cent.),  or  resorcin  lotion  (h  to  1  per  cent.),  and  later 
applying  a  zinc  oxide  paste,  hazeline  cream,  or  a  bismuth  boric 
ointment  (bismuth  subnitratis,  gr.  xxx. ;  acidi  borici,  gr.  xv. ; 
vaseline,  lanoline,  aa  3iv.).  The  stockings  should  be  white,  and 
should  be  changed  at  least  twice  daily,  and  should  be  boiled  before 
use.  If  a  fungus  is  found  in  the  lesions,  an  antimycotic  treatment 
should  be  carried  out  when  the  acute  stage  is  over,  or  during  the 
quiescent  periods,  by  means  of  silver  nitrate  (3  per  cent.),  or  a 
strong  solution  of  potassium  permanganate  (gr.  xxx.  to  5L), 
painted  on  once  or  twice  daily;  or  tincture  of  iodine  may  be  used 
if  the  lesions  are  dry  and  there  are  no  excoriations. 

Dermatitis  Bullosa  Plantaris. 

Synonym. — Foot -tetter  (Cantlie). 

Definition. — Dermatitis  bullosa  plantaris  is  a  streptococcal 
dermatitis,  often  secondary  to  an  infection  of  the  soles  of  the  feet, 
caused  by  Epidermophyton  cruris  Castellani. 

Historical  and  Geographical  Distribution. — This  affection  was 
first  described  by  Cantlie  in  China,  but  cases  are  met  with  in  all 
tropical  countries. 

Etiology. — The  disease  is  probably  a  streptococcus  infection, 
one  of  us  having  isolated  a  very  virulent  strain  of  the  germ  from 
the  blebs  of  a  number  of  cases.  In  several  of  our  cases  this  strepto- 
coccus infection  developed  on  some  superficial  lesions  due  to  a 
localization  of  Epidermophyton  cruris  Castellani  to  the  soles. 

Symptomatology. — -It  commences  with  blebs  on  the  sole  of  the 
foot.  The  blebs  ultimately  break,  and  by-and-by  bare  scaly  flakes 
of  skin  form,  and  extend  all  over  the  sole  and  between  the  toes. 
There  is  intense  itching.  Occasionally  the  condition  spreads  to  other 
parts  of  the  body.  It  usually  dies  away  in  the  cold  season,  but 
recommences  in  the  hot  season.  According  to  Cantlie,  patients 
who  have  returned  to  Europe  see  their  affection  reappearing  regu- 
larly every  summer  for  ten  or  twenty  years  after  leaving  the  tropics. 

Prognosis. — The  condition  is  of  difficult  cure,  and  relapses  occur. 

Treatment. — In  the  acute  stage  the  patient  must  stay  at  com- 
plete rest,  and  antiseptic  dressings,  such  as  mercury  perchloride 
(1  in  4,000)  or  carbolic  acid  (£  per  cent.),  applied  continuously. 
Later  a  lead  lotion  (liq.  plumbi,  3ii.,  aq.  destil.  ad  gx.),  and  still 


2038  PYOGENIC  DERMAL  INFECTIONS 

later  some  antiseptic  powder  (dermatol  or  zinc  oxide)  may  be 
used.  In  our  cases  ointments  were  always  badly  borne.  In 
mild  cases  we  advise  taking  a  foot-bath  twice  daily  in  warm  boric 
(i  per  cent.)  or  permanganate  (i  in  4,000)  solution,  besides  which 
the  blebs  should  be  pricked  with  a  sterile  needle  and  touched  with 
a  solution  of  permanganate  (gr.  xx.-xxx.  to  si.),  followed  by  dressing 
with  zinc  oxide,  dermatol,  or  some  similar  powder. 

If  the  eruption  develops  on  lesions  due  to  fungi,  when  the  acute 
stage  is  passed  off,  an  antimycotic  treatment  should  be  carried  out 
by  applying  with  care,  and  very  little  at  a  time,  a  silver  nitrate 
solution  (3  to  5  per  cent.)  if  there  are  moist  lesions,  or  tincture  of 
iodine  if  the  lesions  are  dry. 

Cantlie  recommends  the  application  of  pastes  and  plasters  as  palliatives. 
Alanson  advises  the  use  of  a  daily  foot-bath  of  a  2  per  cent,  solution  of  carbolic 
acid  for  half  an  hour. 

REFERENCES. 

Pyosis  Mansoni. 

Castellani    (1904-1914).     Ceylon    Medical    Reports    and    Journal    Ceylon 

Branch  British  Medical  Association. 
Castor  (1911).     Journal  of  Tropical  Medicine. 
Manson  (1909).     Tropical  Diseases. 

Pyosis  Tropica. 

Castellani  (1904- 191 4).     Ceylon  Medical  Reports. 

Castellani    (1910).      Journal   Ceylon  Branch   British   Medical   Association, 

January. 
Chalmers  and  O'Farrell  (1913) .     Journal  of  Tropical  Medicine  and  Hygiene, 

December  15. 
Gabbi  and  Sabella  (1912).     Malaria. 
Pi j  per  (191 8).     South  African  Medical  Record,  May  25. 

Pyosis  Corletti. 

Chalmers   and    O'Connor    (1915).     Journal   of   Tropical   Medicine,    73-78. 

London. 
Morris  and  Dore  (1917).     Diseasesof  the  Skin.     London. 

Pyosis  Discoides. 

Castellani  (191 7).     Journal  of  Tropical  Medicine. 
Castellani  (191 8).     Annali  di  Medicina  Navale. 

Dermatitis  Cupoliformis. 

Castellani  (1914).     Journal  Ceylon  Branch  British  Medical  Association,  June. 
Castellani  (1916).    Journal  of  Tropical  Medicine  and  Hygiene,  February  16. 

Pyosis  Palmaris. 
Castellani  (1904-1914).   Ceylon  Medical  Reports  and  Journal  Ceylon  Branch 
British  Medical  Association. 

Purulent  Folliculitis  of  the  Legs. 
Castellani  (1904-1914).     Ceylon  Medical  Reports  and  Journal  Ceylon  Branch 

British  Medical  Association. 
Castellani  (1907).     Arch.  f.  Schiffs-und  Tropcn-Hygiene,   Bd.  xi.  (Orsonic 

treatment). 
Cranston  Low  (1912).     Communication  by  letter. 


REFERENCES 


2039 


Dermatitis  Rimosa. 

Castei.lani  (1904-1912).     Ceylon  Medical  Reports  and  Journal  Ceylon  Branch 

British  Medical  Association. 
Castellani  (1918).     Ann.  Med.  Nav.,  vol.  i.,  Nos.  3,  4. 

Dermatitis  Bullosa  Plantaris. 
Cantlie  (1908).     Journal  of  Tropical  Medicine. 
Castellani  (1904-1914).     Ibid,  and  Journal  Ceylon  Branch  British  Medical 

Association. 
Harman  (1908).     British  Journal  of  Dermatology. 
Manson  (1908).     Journal  of  Tropical  Medicine. 
Morris  (1908).     British  Journal  of  Dermatology. 

Dermatitis  Pratensis. 

Castellani   (1904-1914).     Ceylon  Med.   Reports  and   Jour.   Ceylon   Branch 

British  Med.  Association. 
Chalmers    and    Archibald    (191S).       Journal    of    Tropical    Medicine    and 

Hygiene,  July  15. 
Harman  (1904).     Journal  of  Pathology  and  Bacteriology,  p.  1.     London. 

Barcoo. 

Black,  Ernest  (1913).     Communications  by  letters. 

Martin  (191 7).     British  Medical  Journal,  June  9. 

Morris  and  Dore  (191 3).     Journal  of  Dermatology,  xxv.  259-261.     London. 

Pain  (191 7).     British  Medical  Journal. 


CHAPTER  XCI1 
TROPICAL    DERMATOMYCOSES 


Tropical  dermatomycoses — Tinea  cruris — Tinea  alba — Tinea  albigena — Tinea 
sabouraudi  tropicalis — Tinea  nigro  circinata — Tinea  capitis  tropicalis — 
Tinea  barbae  tropicalis — Tinea  ciliorum — Tinea  unguium  tropicalis — Tinea 
imbricata — Tinea  intersecta — Tinea  flava — Tinea  nigra — Erythrasma — 
Blastomycosis — Sporotrichosis- — Cryptococcosis  epidermica — Intertrigo 
saccharomycetica  —  Aspergillosis  —  Pennicilliosis  —  Acladiosis  —  Crypto- 
coccosis epidermica — Pinta — Piedra — Trichomycosis — Rarer  nodular  and 
gummatous  affections  of  hyphomycetal  origin — References. 

Tropical  dermatomycoses — that  is  so  say,  tropical  skin  diseases 
caused  by  fungi  higher  than  bacteria- — may  be  classified  as  follows : — 

Tropical  Dermatomycoses. 

Ep.  cruris  Castellani,  1905,  common  variety  of 
Tinea  cruris  (dhobie  itch). 

Ep.  perneti  Castellani,  1907,  variety  of  Tinea 
cruris. 

Ep.  rubrum  Castellani,  19C9,  variety  of  Tinea 
cruris. 

T.  nodoformans  Castellani,    191 1,   variety  of 
Tinea  cruris. 

T.    macfadyeni    Castellani,    1905,    variety   of 
Tinea  alba. 

T.  albiscicans  Nieuwenhuis,  1907,  Tinea  albi- 
gena. 

T.  blanchardi  Castellani,   1905,  Tinea  sabou- 
raudi tropicalis. 

T.   ceylonense   Castellani,    1908,   Tinea  nigro- 
circinata. 

T.  soudanense  Joyeux,  19 12 

T.  violaceum  Bodin,  1902 

T.  violaceum  Bodin,  1902,  var.  decalvans 
Castellani,  191 1 

T.  currii     Chalmers     and      Marshall, 
1914 

T.  discoides  Sabouraud,  1909 

T.  violaceum  Bodin,   1902,    var.   khar- 
toumense  Chalmers  and  Macdonald , 

1915 
T.  polygonum  Uriburu,  1909 
T.  exsiccatum  Uriburu,  1909  J  > 

Microsporum  flavescens  P.  Horta,  1912,  variety 

of  Tinea  capitis  and  corporis. 
En.    tropicale    Castellani,     191 4.     Tinea    im- 
bricata. 
En.    indicum    Castellani,     191 1,    Tinea    im- 
bricata. 
En.  castellanii  Perry,  1907,  Tinea  intersecta. 
2040 


I.  Due  to  fungi  of  the 
genus  Epidermophyton 
Lang,  1879,  Tricho- 
phyton Malmsten,  1845, 
Microsporum  G  r  u  b  y, 
i843 


II.  Due  to  fungi  of  the 
genus  Endodermophy- 
ton  Castellani,  1909 


TROPICAL   DERMA  TOMYCOSES 


2041 


III.  Due     to     fungi    of     the  j 

genus  M  a  I  a  s  s  e  z  i  a\M.  tropica  Castellani,  1905,  Tinea  fiava. 
Baillon,  1889  J 

IV.  Due     to     fungi    of     the  )  C.  mansoni  Castellani,  1905,  Tinea  nigra. 

madagascariense    Verdun,    191 3,    peculiar 

nodular  affection. 


fungi     of     the"!  C 
genus        Cladosporium  -C 
Link,  1809 
Due     to     fungi     of     the"l 
genera    Saccharomyces 
Meyen,    1838,    Crypto- 
coccus  Kiitzing,  Cocci- 
dioides     Rixford     and 
Gilchrist,     1897,     Mo- 
nilia  Persoon,  1797 


Several 


of 


species,      some     oll-rT     •   ,•  „r 

■   F,        .'  ,    ,   ,       Varieties        of 

which       incompletely  }■.  1     .    „     „  •„ 

-.      ,     ,  r         J  I  blastomycosis, 

investigated  J 


VI. 


VII. 


Due     to     fungi    of     the 
genus   Nocardia   sensu 
lato,    Toni  and  Trevi-* 
san,   1889,  and  Cohni- 
streptothrix  Pinoy  1911 


Due  to  fungi  of  the 
genera  Sporotrichum 
Link,  1809,  Hemispora 
Yuillemin,  1906,  En- 
antiothamnus  Pinoy, 
1 9 1 1 ,  Scopnlariopsis 
Bainier,  1907,  Clado- 
sporium Link,  1809, 
Acremonium  Link, 
1809,  Acladium  Link, 
1809 


Varieties  of 

sporotri- 
chosis found 
in     the 
tropics. 


Various 

types  of 

gummatous 

affections. 


VIII 


IX. 


fN.  minutissima  Burchardt,  1859,  erythrasma. 
N.  carougeaui  Brumpt,   1910,  juxta-articular 

nodules. 
N.  rivierei  Verdun,  1912,  nodular  affection. 
C.    tenuis    Castellani,     1912,     trichomycosis 

axillarum. 
C.  thibiergei  Pinoy  and  Ravaut,  1909,  nodular 
V.         affection. 
Sporotrichum  beurmanni  Matru- 

chot  and  Ramond,  1905 
S.  schenki  Hektoen  and  Perkins, 

1900 
S.  asteroides  Splendore,  191 1 
S.  indicum  Castellani,  1908 
Hemispora    stellata     Vuillcmin,\ 

1906 
Enantiothamnus    braulti   Pinoy, 

1912 
Scopulariopsis  blochi  Matruchot, 

1911 
Cladosporium      madagascariense 

Verdun,  1913 
Acladium  castellanii  Pinoy,  19 16' 
Aspergillus  bouffardi  Brumpt,  1906 
1  Sterigmatocystis  nidulans  Eidam,  1883 
fungi    of    the  !  Madurella  mycetomi  Laveran,  1902 
Aspergillus  '  M.  bovoi  Brumpt,  1910 

M.  tozeuri  Nicolle  and  Pinoy,  1906 
Indiella  mansoni  Brumpt,  1906 
/.  reynieri  Brumpt,  1906 
/.  somaliensis  Brumpt,  1906 
Nocardia  madurce  Vincent,  1894 
N.  asteroides  Eppinger,  1890 
N.  pelletieri  Laveran,  1906 
N.  bovis  Harz,  1877 
C.  isracli  Kruse,  1896 
1 806,   Monospori  um    Sporotrichum  beurmanni  Matruchot  and 
Bonorden      and     Sac-  Ramond,  1905 

cardo,  1898,  Glenospora    Monosporium   apiospermum   Saccardo, 
Berkeley     and     Curtis  191 1 

1876  ;  Glenospora  khartoumensis  Chalmers  and 

Archibald,  1916 
G.semoni  Chalmers  and  Archibald,  I9X7 
Due    to    fungi    of    theM.    barbce    Castellani,    1907,    Aspergillosis   of 
genera  Aspergillus)  hairy  parts. 

Micheli,      1727,    Peni-  I  P.    barbcz    Castellani,     1907,     Penicilliosis    of 
cillium  Link,    1809         I  hairy  parts. 


Due    to 

genera 
Micheli,  1725,  Sterig- 
matocystis Cramer, 
1869,  Madurella 
Brumpt,  1905,  In- 
diella Brumpt,  1906, 
Nocardia  Toni  and 
Trevisan,  1889,  Cohni- 
streptothrix  Pinoy  191 1, 
Sporotrichum       Link, 


2042  TROPICAL  DERMATOMYCOSES 

( Aspergillus  Micheli,  1 725       \ 
X.  Due    to     fungi    of    the)  Pe-nicillium  Link,  1809  („. 

genera  j  Monilia  Persoon,  1791  I FlDta' 

\Montoyella  Castellani,  190 7] 
XI.  Due    to    fungi    of    the  [ T-  gigwtevtm  Behrend,  pitdra. 

genus       Trickosporuml  Species    as    yet  not    well  fTr°picCaJ  „  Vf  Ye~ 

ReVir^nrl    T«™                  I          a  *.  ■     j  -       ties  of  nodular 

i^enrena,  1690                             determined  .•  ,!,„„,    „„„;„ 

\.  ^      trichomycosis. 

XII.  Due    to     fungi    of    the"! 

genus       Pilyrosporum  \P^yrospovum  canthei  Castellani,  1907,  variety 
Sabouraud,  1903  J  of  tropical  seborrhcoa. 

From  the  above  table  it  will  be  seen  that  tropical  dermatomy- 
coses  sensu  stricto — viz.,  occurring  only  in  the  tropics — are  com- 
paratively few.  Most  of  them  are  endemic  also  in  temperate  zones, 
though  occurring  there  rarely,  or  at  any  rate  less  frequently  than 
in  the  tropics.  We  may  mention  as  examples  tinea  cruris  and 
Madura  foot.  The  same  remark,  however,  applies  to  every  other 
branch  of  tropical  medicine. 

The  frequency  of  dermatomycoses  in  the  tropics  is  probably  due 
to  the  hot,  damp  climate  being  very  favourable  to  the  growth  of 
vegetal  parasites. 

TINEA  CRURIS  (DHOBIE  ITCH). 

Synonyms. — Tinea  tropicalis,  Tinea  inguinalis,  Tinea  axillaris, 
Eczema  marginatum. 

Definition. — The  term  '  tinea  cruris  '  indicates  a  group  of  epider- 
mophytoses and  trichophytoses  which  are  clinically  characterized 
by  their  tendency  to  develop  on  the  scroto-crural  and  inguinal 
regions. 

Historical  and  Geographical. — Tinea  cruris  is  extremely  common 
all  over  the  tropics;  it  is  met  with  also  in  subtropical  regions,  and 
in  temperate  zones,  being  first  described  by  Hebra  in  Europe  under 
the  name  of  eczema  marginatum.  In  1905,  Castellani,  as  the 
result  of  the  investigation  of  numerous  cases,  came  to  the  conclusion 
that  it  should  be  separated  from  the  ordinary  forms  of  tinea  corporis, 
and  MacLeod  suggested  the  name  tinea  cruris  for  the  affection. 
For  the  fungus  most  frequently  found  in  such  cases,  characterized 
by  the  yellowish  cultures,  Castellani  used  the  name  Trichophyton 
cruris.  Pernet  found  and  described  a  fungus  for  which  Castellani 
suggested  later  the  name  Trichophyton  perncti.  In  1907  Sabouraud 
investigated  in  a  complete  manner  the  condition  in  France  which  he 
called  tinea  inguinalis.  There  can  be  no  doubt  that  tinea  inguinalis 
and  dhobie  itch,  or  tinea  cruris,  are  the  same  entity,  as  Sabouraud 
and  Pinoy,  having  compared  cultures  of  Epidermophyton  cruris 
isolated  in  Ceylon  with  those  found  in  France,  have  found  them 
identical. 

Castellani's  further  researches  have  shown  that  other  fungi 
besides  Ep.  cruris  may  give  rise  to  tinea  cruris,  each  species  giving 
rise  to  a  slightly  different  clinical  variety  of  the  eruption. 


TINEA   CRURIS  (DHOBIE  ITCH)  2043 

/Etiology. — According  to  Castellani's  researches,  at  least  three 
different  species  of  Epidermophytons  and  one  of  Trichophyton  may 
give  rise  to  the  eruption — Epidermophyton  cruris  Castellani,  Ep. 
perneti  Castellani,  Ep.  rubmm  Castellani,  and  Trichophyton  nodo- 
formans  Castellani — and  there  are  probably  several  other  not  yet 
described  species. 

The  description  of  these  fungi  is  given  in  Chapter  XXXVIII.  (see 
p.  10 14).  Attempts  at  experimental  reproduction  of  the  disease 
made  by  Sabouraud  and  one  of  us  in  human  beings  and  monkeys 
have  failed. 

Symptomatology. — The  term  '  dhobie  itch  '  is  used  very  loosely  in 
the  tropics  by  the  lay  public  to  denote  practically  any  pruriginous 
skin  affection.  The  term  is,  however,  specially  used  to  denote  a 
form  of  severe  pruriginous  affection  which  mostly  affects  the 
inner  surface  of  the  thighs,  occasionally  the  axilla,  and,  in  stout 
women,  the  regions  under  the  breasts.  It  is  in  this  stricter 
meaning  that  the  term  is  used  by  medical  men  practising  in  the 
tropics. 

The  clinical  features  of  the  affection  correspond  to  Hebra's 
'  eczema  marginatum.'  In  a  well-marked  case  the  perineum, 
scrotum,  and  the  inner  surface  of  the  thighs  present  large  festooned 
patches,  with  an  elevated  abrupt  margin;  the  whole  of  the  patches 
are  bright  red,  or,  in  a  later  period,  the  margin  only  is  red,  while 
the  rest  of  the  patch  is  of  a  fawnish  colour,  or  even  of  normal  colour. 
The  pruritus  is  unbearable.  Owing  to  scratching,  a  secondary 
pyogenic  infection  or  an  eczematous-like  dermatitis  may  develop. 
The  disease,  if  not  properly  treated,  is  extremely  chronic;  the 
condition  improves  during  the  cold  season,  but  gets  worse  again 
during  the  hot  months.  Patients  who  suffer  badly  from  dhobie 
itch  may  get  almost  well  in  a  few  days,  without  any  treatment, 
on  going  to  the  hills;  on  returning  to  the  plains  the  pruritus  and  all 
the  other  symptoms  reappear.  The  affection  has  been  known  to 
last  for  many  years.  It  is  to  be  noted  that  after  a  time  the  eruption 
may  spread  to  the  other  parts  of  the  body — the  abdomen,  the 
trunk,  legs,  etc.  In  such  situations  it  may  develop  in  rings,  or 
may  form  solid  elevated  dark  red  patches;  while  the  disease  may 
be  clinically  indistinguishable  from  ordinary  tinea  circinata.  In 
some  cases,  though  rarely,  the  eruption  starts  first  on  the  chest 
and  arms,  and  from  there  spreads  later  to  the  armpits  and  cruro- 
inguinal  regions. 

Clinical  Varieties. — The  above  description  mostly  applies  to  the 
disease  as  produced  by  Epidermophyton  cruris,  which  is  the  com- 
monest fungus  found,  and  by  Ep.  perneti.  In  the  cases  due  to  Ep. 
rubrum  the  affected  parts  often  present  from  the  very  beginning 
an  eczematoid  appearance.  The  edge  is  perhaps  not  so  raised  as 
in  other  types  of  tinea  cruris,  but  very  abrupt,  made  up  of  numerous 
rather  small,  close-set  papules,  covered  at  times  by  minute  bloody 
crusts  due  to  scratching.  The  eruption  may  also  be  present  in 
the  shape  of  large  complete  or  incomplete  gyrations  enclosing  normal 


2044 


TROPICAL  DERMATOMYCOSES 


skin,  or  solid  patches  may  be  seen.     The  variety  due  to  Ep.  rubrum 
has  great  tendency  to  spread  to  other  regions  of  the  body. 

In  the  (cases  caused  by  Trichophyton  nodojormans  the  eruption 
has  thick  elevated  margins,  and  along  the  edge  deep-seated  nodules 
resembling  '  blind  boils  '  are  present,  the  fungus  being  capable  of 
attacking  the  hair  follicles  and  having  [pyogenic  [properties.  The 
infection  [may  spread  from  the  inguinal  [regions  to  other  parts  of 
the  body.  We  have  seen  a  case  presenting  a  nodular  eruption  due 
to  this  fungus  in  the  [groins,  and  at  the  same  time  presenting  a 
typical  kerion  barbae  due  to  the  same  organism  on  the  right  cheek. 


Fig.  8oi. — Dhobie  Itch  of  the  Cruro-Inguinal  Regions:  Tinea  Cruris. 

From  the  same  case   (due  to  Epidermophylon  cruris  Castellani)  as  the 
coloured  plate. 


Regions  of  the  Body  affected. — The  eruption,  as  already  stated, 
is  "generally  localized  to  'the  cruro-inguinal  and  axillary  regions, 
hence  the  name  '  tinea  cruris  seu  inguinalis  ' ;  but  the  same  fungi 
may  spread  in  many  cases  from  those  regions  to  any  other  part  of 
the  body,  except  the  scalp.  In  some  few  cases  the  eruption  may 
first  appear  on  the  arms  or  chest,  etc.,  and  then  spread  to  the  groins 
and  armpits,  or  may  never  affect  these  regions.  Hence  the  terms 
'  tinea  cruris '  and  '  tinea  inguinalis '  are  not  altogether  appro- 
priate, and  the  term  '  tinea  tropicalis,'  or  the  native  term  '  dhobie 
itch,'  might  be  used  as  general  terms  to  cover  all  the  localizations. 

A  localization  of  great  importance  noted  by  Sabouraud,  and  later 


Ill 

< 


CO  MM  UNICA  BILI T  Y 


2°45 


by  Whitfield,  is  when  the  fungi  invade  the  skin  between  the  toes 
(tinea  interdigitalis).  In  this  situation  the  fungus — it  is  generally 
Ep.  cruris — -may  remain  for  years,  the  fungus  per  se  giving  rise  to 
practically  no  objective  symptom,  except  perhaps  a  little  scaliness, 
but  generally  induces  very  severe  pruritus,  especially  in  the  hot 
weather.  This  localization  of  the  fungus  is  often  the  starting-point 
of  secondary  bacterial  affections  causing  a  most  distressing  der- 
matitis, known  to  the  planters  by  the  name  of  '  mango  toe,'  and 
already  described  on  p.  2036. 

Communicability. — Tinea  cruris  is  known  in  the  East  as  dhobie 
itch,  from  the  popular  belief  that  it  is  contracted  from  linen  which 


Fig.  802. — Dhobie   Itch   of   the   Axillary    Regions:   Tinea  Axillaris. 
Case  due  to  Epidermophyton  cruris  Castellani. 


has  been  contaminated  while  being  washed  by  the  dhobie '(native 
laundryman).  As  to  how  far  this  belief  is  correct  we  are  not  in  a 
position  to  say.  We  have  never  succeeded  in  finding  the  fungus 
in  clothes  newly  received  from  the  dhobie,  either  microscopically 
or  by  inoculating  small  portions  of  the  linen  in  sugar  media.  We 
are,  however,  inclined  to  think  that  the  popular  belief  may  to  a  cer- 
tain extent  be  correct.  We  have  been  told  by  old  sufferers  from 
dhobie  itch,  who  used  to  be  frequently  reinfected,  that  on  their 
ceasing  to  give  their  clothes  to  the  dhobie,  and  having  them  washed 
in  the  house  instead,  the  disease  did  not  again  affect  them.  In 
Colombo  dhobies  are  in  the  habit  of  washing  the  clothes  in  a  lake, 


204b 


TROPICAL  DERM  ATOM  YCOSES 


or  in  small  pools  of  water  more  or  less  stagnant.  It  is  certain  that 
clothes  belonging  to  infected  persons  are  washed  together  with 
other  clothes.  Dhobie  itch  is  very  contagious;  true  epidemics 
occur  in  schools  and  among  soldiers  in  barracks. 

Prognosis. — If  the  affection  is  not  energetically  treated,  it  has  a 
tendency  to  become  very  chronic  and  last  for  years.     Occasionally 

the  eruption  spreads  to  the  whole 
body,  forming  rings  or  solid  patches; 
at  other  times  a  distressing  der- 
matitis develops  on  old  dhobie-itch 
patches,  due  to  scratching.  Tinea 
cruris  may  disappear  during  the 
cold  season,  or  when  the  patient 
goes  to  the  hills,  only  to  reappear 
as  soon  as  the  hot  season  com- 
mences. During  the  period  of  qui- 
escence the  skin  of  the  affected 
regions  often  shows  a  brownish  dis- 
coloration, furfuraceous,  somewhat 
similar  to  erythrasma. 

Diagnosis. — The  diagnosis  is  easy 
in  recent  cases,  the  festooned 
appearance  of  the  eruption,  limited 
by  a  sharp,  elevated,  bright  red 
edge,  being  quite  typical.  In  old 
cases,  especially  when  secondary 
lesions  due  to  scratching  are  present, 
the  diagnosis  may  be  very  difficult, 
the  affection  being  often  mistaken 
for  eczema. 

In  doubtful  cases  the  micro- 
scopical examination  will  be  of 
great  help.  It  must,  however,  be 
noted  that  in  old  cases  the  fungus 
may  be  extremely  scarce,  the  myce- 
lium being  practically  absent,  and 
only  a  few  spores  being  found ;  it  is 
well  to  take  the  scrapings  for  micro- 
scopical examination  from  the  edge 
of  the  eruption.  The  differential 
diagnosis  must  be  made  from  ery- 
thrasma, intertrigo,  and  eczema. 
,  ^In  erythrasma  the  patches  have  a  fawnish  or  dark  reddish  colour, 
and  present  often  a  fine  pityriasic  desquamation;  the  eruption  is  not 
limited  by  a  raised  red  edge;  the  fungus  Nocardia  minutissima 
Burchardt  is  quite  different  from  the  fungi  found  in  dhobie  itch. 

Intertrigo  is  very  common  in  the  tropics,  especially  in  corpulent 
persons.  The  lesions  are  very  superficial,  have  not  a  festooned 
contour,  and  the  margin  is  not  sensibly  elevated ;  no  Epidermophyton- 


Fig.     803. — Dhobie 
the      Axillary 
Tinea  Axillaris. 


Itch    of 
Regions: 


Case  due  to  Epidermophylon 
cruris  Castellani. 


TREA  TMENT  2047 

or  Trichophy  ton-like  fungi  are  found.  Saccharomycetic  intertrigo 
is  rare;  there  is  no  elevated  margin,  and  the  fungus  is  found  to  be  a 
Saccharomyces  (S.  samboni). 

Primary  eczema  of  the  scrotum,  and  of  the  skin  of  the  thighs  in 
contact  with  it,  is  as  frequent  in  the  tropics  as  it  is  in  temperate 
zones.  The  eczema  is  generally  of  the  moist  variety;  the  moist 
surface,  the  absence  of  the  festooned  elevated  margin,  distinguish 
it  from  tinea  cruris.  As  already  stated,  however,  an  eczematous- 
like  dermatitis  due  to  scratching  often  develops  after  a  time  on  old 
dhobie  itch  lesions. 

Diagnosis  of  the  Toes'  Localization. — The  complaining  of  severe 
itching  between  the  toes,  even  if  there  are  no  objective  symptoms 
whatever,  should  in  the  tropics  always  arouse  the  suspicion  of  a 
possible  local  fungus  infection,  especially  if  the  patient  suffers  at 
the  time,  or  has  been  suffering,  from  tinea  cruris,  and  scrapings 
should  be  made  and  examined  microscopically.  It  is  important 
to  make  the  diagnosis,  as  by  treating  the  condition  the  develop- 
ment of  that  distressing  dermatitis  known  as  mango  toe  (see  p.  2036) 
may  often  be  prevented. 

Treatment. — Our  usual  line  of  treatment  is  as  follows : — 

Mild  Cases. — A  resorcin  salicylic  ointment  applied  twice  daily: 
Resorcin,  3L ;  salicylic  acid,  gr.  x. ;  vaseline,  lanoline,  aa  3iv. 
Tincture  of  iodine  also  is  very  efficacious,  but  induces  a  certain 
amount  of  smarting,  and  must  be  applied  with  care  and  in  only 
very  recent  cases  with  no  eczematoid  lesions.  In  some  cases  we 
use  Vleminckx'  solution  or  lotio  calcii  sulphurati  (slaked  lime  4, 
sublimed  sulphur  4,  distilled  water  35;  boil  together,  evaporate,  and 
filter  to  produce  20  of  solution),  pure  or  diluted.  A  sodium  hypo- 
sulphite solution  (sodium  hyposulphite  3n->  aq.  §i.)  may  also 
be  used. 

Severe  Cases. — We  use  a  chrysarobin  ointment  (2  to  5  per  cent., 
a  good  formula  being  chrysarobin  gr.  x.-xxv.,  unguentum  zinci  §i.). 
The  result  is  generally  fairly  successful.  The  patient  should  be 
informed  that  the  medicine  stains  the  linen,  often  irritates  the  skin, 
which  may  become  cedematous  and  dusky  red,  and  that  occasionally 
unpleasant  evidences  of  absorption  may  take  place,  with  fever, 
diffuse  erythema,  and  haematuria.  Chrysarobin  should  never  be 
used  when  there  is  some  affection  of  the  kidneys.  The  irritation 
induced  by  the  chrysarobin  ointment  may  be  allayed  by  calamine 
lotion,  lead  lotion,  or  an  ichthyol  ointment  1  per  cent. 

Chrysarobin  is  obtained  from  araroba,  which  is  known  by  the  name  oi 
'  goa-powder  '  all  over  the  East.  The  crude  goa-powder,  partly  dissolved 
in  vinegar,  is  often  used,  but  frequently  induces  very  severe  inflammatory 
symptoms. 

In  obstinate  cases  we  use  local  applications  of  turpentine-oil  in  the 
morning,  and  at  night  a  resorcin  salicylic  ointment;  if  the  parts  are  much 
inflamed,  at  night  simply  a  boric  ointment.  This  treatment  gives  good 
results.  Turpentine  is  generally  well  borne,  but  patients  often  complain  of 
a  smarting  and  burning  sensation  a  quarter  of  an  hour  after  the  application. 
Exceptionally  one  meets  with  patients  who  cannot  stand  turpentine. 


204S  TROPICAL  DERMATOMYCOSES 

Cases  complicated  with  Eczematous  Dermatitis  and  Fissures. — In 
such  cases,  in  our  experience,  it  is  better  to  use  at  first  a  soothing 
treatment  by  lead  lotion,  or  a  solution  of  resorcin  (J  to  i  per  cent.), 
or  glycerin,  boracis  in  rose-water,  with  the  object  of  first  healing 
the  eczematous  lesions.  Later,  to  the  rhagades  which  so  often 
develop  in  the  inguinal  regions,  we  apply  a  solution  of  nitrate  of 
silver  (arg.  nitr.,  gr.  v.-xv. ;  sp.  seth.  nitr.,  §i.).  We  touch  with  this 
solution  the  rhagades  and  the  moist  parts;  this  application  is  some- 
what painful,  but  the  pain  soon  disappears,  and  the  fearful  itching 
is  relieved  almost  immediately;  moreover,  the  nitrate  of  silver 
destroys  the  fungus.  At  night  we  apply  a  mild  ichthyol  ointment 
(i  per  cent.)  or  hazeline  cream  all  over  the  eruption;  as  soon  as  the 
parts  have  become  less  moist,  we  begin  the  chrysarobin  treatment. 
A  precaution,  which  must  always  be  observed  during  and  after  the 
treatment,  to  prevent  reinfection  is  to  dust  all  the  undergarments 
with  antiseptic  powder — for  instance,  Manson's  powder  (ac.  bor., 
zinc,  ox.,  amyli,  aa.  p.  ?eq.) ;  salicylic  powder  (ac.  salicyl,  gr.  x.; 
talci  venet.,  §i.) ;  menthol  powder  (menthol,  gr.  v.;  alcohol,  q.s. ; 
talci  venet.,  gi.) ;  dermatol  powder  (dermatol,  gr.  xx. ;  talci,  gi.) 
It  is  advisable  to  wear  small  bathing-pants,  which  can  be  washed 
in  the  house. 

Treatment  of  Generalized  Dhobie  Itch.- — When  the  eruption  is 
diffused  all  over  the  body,  the  simplest  treatment  is  as  a  rule  the 
application  of  tr.  iodi  or  lin.  iodi,  treating  only  one  portion  at 
a  time.  A  chrysarobin  ointment  (2  to  5  per  cent.)  may  also  be  used. 
Treatment  of  Dhobie  Itch  localized  to  the  Toes.- — During  the  quies- 
cent periods,  or  when  there  is  only  pruritus  and  a  little  scaliness, 

tincture  of  iodine  may  be  used,  or  an 
«  alcoholic    solution   of    salicylic    acid 

>-  ^  f,  (2  per  cent.).     When  there  are  acute 

symptoms  of   dermatitis,   the  treat- 
ment must  be  at  first  a  soothing  one, 
Q j.  as  described  on  p.  2037. 

.^  TINEA  ALBA. 

■  ^\ 

Remarks. — Tinea  alba  is  in  reality 

^  <£  /^*=C^     only  a  form  of  generalized  dhobie  itch; 

^°  "^oav.  J?  *ne  term  is  applied  to  various  diffuse 

^  ^W^7  trichophytic  and  epidermophytic  con- 

ditions which  give  a  white  powdery 

I  IG.      804.— I'UNGUS    FOUND     IN  ,       5>,  ,    •  r   ,  ■,     r        ,  ■        J 

a  variety  of  Tinea  Alba:     appearance  to  the  skin  of  the  natives. 

Air.  macjadycni  Castellani.        Historical. — This     condition    was 

first  described  by  Castellani  in  1905  in 
Ceylon.  Cases  have  been  recently  reported  by  Pijper  in  South  Africa. 

/Etiology. — The  commonest  fungi  found  are  Epidermophyton 
rubrum  Castellani,  1909,  and  Atrichophyton  macfadyeni  Castellani, 
1905  [Trichophyton  macfadyeni) ,  the  description  of  which  is  given 
on  pp.  1009  and  1016. 


TINEA  ALU  A 


2049' 


Symptomatology. — The  arms,  legs,  chest,  and  occasionally  the 
whole  body,  present  a  diffuse  eruption  of  white  powdciy  appear- 
ance, this  being  due  to 
the  very  numerous  small 
white  pityriasic  squamae 
present.  The  margins 
of  the  eruption,  when 
the  causative  fungus  is 
Ep.  rubrum,  may  be  dis- 
tinctly raised  and  dotted 
with  minute,  close-set 
papules. 

Course  and  Prognosis. — 
The  course  is  very  chronic. 
Apparently  the  fungi  have 
a  disturbing  action  on  the 
production  of  pigment  in 
the  skin,  and  after  some 
years  white  leucodermic 
patches  may  develop, 
in  which  no  fungus  is 
found. 

Diagnosis. — This  is  based 

on     the     diffuse     eruption 

with     the     abundant     fine 

pityriasic       desquamation, 

and  with  well-marked  limits 

-and      the     microscopical      FlG-  8°5;r7™*\        r?^°JrP 
r  mophyton  nibvum  Castellani. 


w  '^•WB' 

*c 

M 

H 

wk 

'■   m  1 

-z^MMmb 

Fig.  806. — Tinea  Alba. 


examination.  It  is  quite  easily 
distinguished  from  tinea  im- 
bricata  by  the  squamae  being 
pityriasic,  very  small,  easily 
detached.  In  leucoderma  the 
surface  is  smooth,  no  squamae 
being  present  and  no  fungus 
found.  As  already  stated, 
however,  if  the  eruption  is 
left  untreated  for  a  long 
time,  leucodermic  patches  may 
develop. 

Treatment. — The  best  treat- 
ment is  by  a  chrysarobin 
ointment  (2  to  5  per  cent.), 
applied  with  the  precautions 
already  mentioned.  Tincture, 
of  iodine  and  liniment  of  iodine 
may  also  be  used. 

129 


TROPICAL  DERMA  TO  MY  COSES 


TINEA  ALBIGENA. 


This  trichophytosis  was  first  described  by  Nieuwenhuis  in  Java. 
Nieuwenhuis'  researches  have  been  confirmed  and  enlarged  by 
Jeanselme  in  Indo-China  and  in  Siam;  in  the  latter  country  the 
disease  is  known  as  khi.  The  disease  is  fairly  common  in  the  Malay 
Archipelago,  and  is  occasionally  met  with  in  Ceylon. 

/Etiology.- — The  affection  is  due  to  a  Trichophyton  first  described 
by  Nieuwenhuis- — T.  albiscicans  Nieuwenhuis,  1907. 

The  spores  in  fresh  preparations  from  scrapings  are  almost  always 
absent;  the  mycelium  tubes  are  straight,  occasionally  showing  a 
double  contour;  they  are  often  dichotomous.  Nieuwenhuis  has 
grown  the  fungus,  using  Sabouraud's  sugar  media;  the  growth  is 
very  slow;  the /colonies  are  whitish,  and  show  a  powdery  surface. 


[Fig.  S07. — Tinea  Albigena. 


Symptomatology.— The  eruption  generally  affects  the  palms  of 
the  hands  and  the  soles  of  the  feet,  but  may  extend  to  the  fore- 
arms and  legs,  and  may  affect  the  nails.  It  begins  with  the  appear- 
ance of  small  pruriginous  spots  on  the  palms  and  soles;  the 
epidermis  becomes  raised,  and  bulhe  develop,  containing  at  first 
clear  serum;  the  bullae  break,  and  the  skin  remains  dry  and  peels 
off;  the  parts  remain  tender,  and  there  is  desquamation  and  pruritus. 
A  process  of  diffuse  keratosis  develops,  the  palms  and  soles  becoming 
double  their  usual  thickness;  deep  fissures  may  be  formed  at  1he 


TINEA   SABOURAUDI  TROPICA  LIS  2051 

natural  folds.  Several  horny  semidetached  discs  can  often  be 
seen  at  the  dilated  orifices  of  the  sweat  glands.  The  affection  is 
very  chronic;  it  may  begin  in  youth  or  in  adult  life.  After  some 
time  a  process  of  apigmentation  of  the  skin  sets  in,  white  patches, 
leucoderma-like,  developing,  and  extending  often  to  the  legs  and 
arms. 

Treatment. — Tincture  of  iodine  and  chrysarobin  ointment  (1  to 
5  per  cent.)  answer  fairly  well,  but  the  apigmented  patches  are  not 
cured. 

TINEA  SABOURAUDI  TROPICALIS. 

This  trichophytosis  was  first  described  by  Sabouraud  in  patients 
returning  from  Indo-China,  Japan,  and  Tonkin.  We  have  seen  a 
few  cases  in  Ceylon. 

Etiology. — The  disease  is  caused  by  the  fungus  Trichophyton 
blanchardi  Castellani,  1905  (synonym,  T.  sabouraudi  Castellani, 
1905).  The  term  T.  sabouraudi  cannot  be  applied  to  this  Tricho- 
phyton, as  this  name  has  already  been  used  for  another  Tricho- 
phyton— T.  sabouraudi  R.  Blanchard,  1905.  This  fungus  cannot  be 
grown  on  Sabouraud' s  media  or  any  other  media  we  have  tried. 
Microscopically  the  mycelial  tubes  do  not  show  a  double  contour,  and 
are  not  very  straight;  they  are  often  banana-shaped.  The  seg- 
ments of  the  mycelium  are  all  separated;  the  mycelial  spores  are 
roundish,  and  are  shed  without  forming  a  filament  by  their  union. 
They  are  of  various  sizes. 

Symptomatology. — The  eruption  generally  commences  on  the 
uncovered  parts  of  the  body,  generally  on  the  legs;  the  patients 
often  state  that  they  think  the  disease  is  due  to  prolonged  immer- 
sion in  stagnant  water.  The  affection  begins  with  erythematous 
patches,  the  surfaces  of  which  are  covered  with  minute  pityriasic 
squamse.  After  reaching  the  diameter  of  about  1  or  i|  inches,  the 
patches  become  circinate.  The  circination,  however,  is  incom- 
plete; it  is  only  segmentary.  In  dependent  positions  large  poly- 
cylic  patches  may  be  seen,  but  only  one-half  or  one-third  of  the 
circles  are  clearly  seen,  the  rest  being  badly  defined.  The  base  of 
the  patches  at  this  stage  is  of  a  very  dark  bistre-brown  colour. 
The  border  shows  polymorphic  lesions,  fine  pityriasic  squama, 
minute  vesicles  and  papules.  The  pruritus  is  very  marked,  and 
excoriations,  due  to  scratching,  are  constantly  present.  In  chronic 
cases  a  thickening  of  the  skin,  with  lichenification,  takes  place, 
specially  at  the  circinate  borders. 

Treatment. — The  disease  is  difficult  of  cure  in  the  tropics,  though 
it  may  disappear  spontaneously  on  the  patient  proceeding  to 
Europe.  Chrysarobin  ointment  (1  to  4  per  cent.)  is  the  best 
treatment. 


2052  TROPICAL  DERMATOMYCOSES 

TINEA  NIGRO-CIRCINATA. 

This  trichophytosis  has  been  observed  by  one  of  us  among  Sin- 
halese natives. 

/Etiology. — The  eruption  is  due  to  a  Trichophyton- — T.  ceylonense 
Castellani,  1908.  The  spores  are  very  few  in  number,  roundish, 
rather  large  (4  ju),  and  showing  a  double  contour.  The  mycelial 
tubes  are  about  3 J  /u,  in  breadth,  generally  straight.  The  fungus 
does  not  grow  on  any  of  the  ordinary  or  Sabouraud's  media. 

Symptomatology. — The  eruption  is  found  most  frequently  on 
the  neck  and  scrotum,  and  consists  of  a  few  rings  with  thick,  elevated 
margins,  the  encircled  skin  being  black — much  darker  than  the 
healthy  skin — but  not  thickened  nor  presenting  papules,  vesicles, 
or  pustules.  The  edge  is  thick,  elevated,  of  a  dark  colour,  with 
the  upper  portion  pinkish  or  occasionally  covered  by  a  dark  crust. 
The  eruption  often  heals  spontaneously,  leaving  dark  roundish 
patches  at  the  previous  seat  of  the  lesions. 

Prognosis. — The  eruption  may  disappear  spontaneously,  and 
the  treatment  is  easy. 

Diagnosis. — The  only  dermatomycosis  to  which  it  has  a  slight 
resemblance  is  Tinea  sabourandi.  The  latter,  however,  is  very 
chronic,  and  invades  large  portions  of  the  body;  the  rings  are 
segmentary,  not  complete,  and  the  edge  is  not  so  thick  and  elevated. 

The  condition  may  have  also  to  be  distinguished  from  a  circinate 
frambceside  or  ringworm  yaws,  in  which  no  fungus  is  found,  while 
Treponema  pertenue  Castellani,  is  present. 

Treatment. — Tincture  of  iodine,  freely  applied,  answers  well. 

TINEA  CAPITIS  TROPICALIS. 

Definition. — Tinea  capitis  tropicalis  is  ringworm  of  the  head 
as  seen  in  the  tropics. 

History. — Celsus  in  the  second  chapter  of  the  sixth  book  of  his 
'  De  Medicina  '  gives  an  account  of  ringworm  of  the  head  under  the 
name  '  porrigo.'  His  words  are:  '  Porrigo  auten  est,  ubi  inter  pilos 
quaedam  quasi  squamulae  surgunt,  eaeque  a  cute  resolvuntur;  et 
interdum  madent,  multo  saepius  siccae  sunt.' 

Bishop  Fortunatus,  who  lived  in  the  sixth  century  A.D.,  uses  the 
name  '  tinea  '  in  the  following  passage:  '  Lavans  capita  egenorum, 
defricans  quicquid  erat,  crustam,  scabiem,  tineam  nee  tpurulentam 
fastidiens.' 

In  the  tenth  century  Ali  ben  Abbas  (often  written  Haly),  who 
lived  in  Persia,  described  the  complaint  under  the  terms  '  sahafati ' 
and  '  alvathim.' 

The  Anglo-Saxons  applied  the  word  '  teter  '  to  any  kind  of  skin 
disease  which  itched,  and  in  this  form  it  was  used  in  middle  English. 
In  the  fourteenth  century  Guy  de  Chauliac  wrote  a  work  on  surgery 
in  which  he  used  the  word  '  teigne,'  deriving  it  from  '  tenir.' 

With  the  advent  of  printing  it  was  called  '  tetters,'  in  England 


PLATE    IX. 


V,W> 


TINEA    NKJRO-CIRCINATA. 


n«o Waiwston *Sor«,L«d  Ediit. 


'■  ('  page  2052 


TINEA   CAPITIS  TROPICALIS  2053 

{vide  Langham's  '  Garden  of  Health,'  1633),  but  in  or  before  the 
sixteenth  century  the  word  '  ringworm  '  {vide  Levins  or  Levens, 
'  Manipulus  Vocabulorum,'  London,  1570)  had  appeared  for  the 
disease  tinea  circinata.  In  1695  Willis  in  his  '  London  Practice  of 
Physick '  devoted  a  chapter  to  the  subject  of  the  running  scab, 
tetter,  or  ringworm. 

With  a  history  such  as  this  it  is  not  astonishing  that  the  early 
English  writers  on  tropical  medicine  refer  to  the  same  disease  as 
seen  in  tropical  countries. 

Thus  in  1746,  in  his  work  on  the  diseases  of  Barbados,  Hillary 
says  that  it  was  noticed  by  the  first  voyagers  to  the  West  Indies, 
and  that  it  probably  is  the  same  disease  as  that  called  by  the  natives 
cowrap.'  He  gives  a  good  clinical  description  of  tinea  circinata  as 
he  saw  it  in  Barbados,  and  he  is  supported  by  Wright  ('  Essays  on 
the  Malignant  Fever  of  the  West  Indies '),  who  stated  that  it  was 
common  in  Jamaica. 

Winterbottom  in  1803,  under  the  term  '  herpes,'  describes  the 
disease  in  Sierra  Leone,  calling  it  serpigo,  ringworm,  or  tetters,  and 
distinguishing  it  from  kra-kra. 

So  far  it  would  appear  as  though  only  the  body  ringworm  or  tinea 
circinata  was  meant  by  the  terms  '  tetters  '  and  '  ringworm,'  but  in 
1817  Bateman,  the  pupil  of  Willan,  who  completed  his  master's  great 
work  on  skin  diseases,  published  an  atlas  on  the  same  subject,  in 
which  Plate  XXXIX.  induces Sabouraud  tobelieve  that  he  recognized 
the  identity  of  the  two  conditions.  In  1824  Plumbe  showed  that 
inoculation  of  ringworm  of  the  scalp  would  cause  ringworm  of  the 
body,  and  vice  versa. 

These  publications  appear  to  have  stirred  the  practitioners  of  the 
tropics  to  study  the  disease,  as  it  was  described  in  India  by  Young, 
in  1826,  and  in  the  Malay  Archipelago  by  Lesson,  in  1829. 

In  1832  Alibert  published  the  first  edition  of  his  celebrated 
'  Monographic  des  Dermatoses,'  which  stimulated  the  continental 
medical  mind  of  the  day,  as  is  reflected  by  Smith's  description  of 
the  disease  in  Peru,  in  1840,  and  Pruner's  in  Egypt,  in  1847. 

In  1839  Schonlein  discovered  the  fungus  causing  favus. 

In  1842  Gruby,  who  had  already  repeated  Schoenlein's  observa- 
tions on  the  parasite  of  favus,  discovered  a  new  cryptogam  in  tinea 
barbae,  which  was  an  ecto-endothrix. 

In  1843  he  found  Microsporum  audouini,  and  six  months  later,  on 
April  1,  1844,  he  described  an  endothrix  as  the  parasite  of  herpes 
tonsurans.  It  is,  however,  but  just  to  state  that,  without  Sabouraud's 
generous  treatment,  much  of  Gruby' s  work  might  have  been  per- 
manently overlooked. 

In  1845  Malmsten  gave  the  name  of  Trichophyton  to  the  parasite 
of  tinea  tonsurans. 

It  is  asked  that  the  reader  will  kindly  observe  the  spelling  of  the 
names  of  these  two  genera.  Gruby  called  the  one  Microsporum, 
not  Microsporon,  and  Malmsten  named  the  other  Trichophyton,  not 
Trichophytum. 


2o54  TROPICAL  DERMATOMYCOSES 

These  researches  naturally  aroused  much  interest,  and  in  1855 
Heymann  showed  that  the  disease  existed  in  the  East  Indies,  but 
it  is  noticeable  that  he  makes  no  mention  of  observing  a  parasite  in 
the  affection. 

In  1874  Blanc  described  the  occurrence  of  the  disease  in  Abyssinia, 
where  Merab  states  that  it  is  very  common,  and  where  it  is  treated 
by  the  juice  from  the  fruits  and  leaves  of  Bryonia  deoica  and  by 
tobacco  powder,  as  well  as  by  sulphur  ointment. 

In  1872  the  Army  Sanitation  Commission  induced  the  British 
Government  to  instruct  Tilbury  Fox  and  Farquhar  to  obtain  a 
better  knowledge  of  the  endemic  skin  diseases  of  India,  and  to  bring 
about  an  agreement  between  the  profession  in  India  and  England  as 
to  nomenclature,  typical  characters,  varieties,  and  probable  causes 
of  these  diseases.  Thanks  to  the  interest  of  Lord  Granville,  Lord 
Kimberley,  and  Sir  Alexander  Armstrong,  this  inquiry  was  extended 
to  China,  Japan,  Egypt,  Algeria,  the  West  Indies,  and  Honolulu, 
and  the  finished  report  was  published  in  1876. 

The  net  result  of  this  inquiry  as  far  as  ringworm  was  concerned 
was  unfortunate,  as  it  led  to  the  dogmatic  assertion  that  the  ring- 
worm of  the  body  in  the  tropics  was  the  same  as  that  of  temperate 
climes. 

In  1873  van  Leent  drew  attention  to  the  large  number  of  cases  of 
ringworm  of  the  head  in  Chinese  in  the  island  of  Banka,  in 
Malaysia. 

In  1878  Corre  gave  a  description  of  the  disease  and  its  parasite 
as  seen  in  Nossi-Be. 

From  1890  the  possibility  of  plurality  in  the  species  of  Tricho- 
phyton was  raised,  but  it  was  not  until  Sabouraud  in  1892  began 
those  brilliant  researches  which  he  has  carried  on  to  the  present  day 
that  this  was  definitely  established.  In  this  year  he  showed  that 
ringworm  of  the  scalp  could  be  divided  into  two  main  groups- — viz., 
those  with  small  spores  belonging  to  the  genus  Microsporum  Gruby, 
1843,  and  those  with  large  spores  belonging  to  the  genus  Tricho- 
phyton Malmsten,  1848.  The  large-spored  fungi  of  the  scalp  he 
divided  into  five  species,  which  were  afterwards  named  Trichophyton 
crateriforme  =  T.  tonsurans,  T.  acuminatum  —  T.  sabouraudi,  T.  gyp- 
seum,  T.  violaceum,  and  T.  rosaceum. 

In  1893  he  further  divided  the  Trichophytons  into  (wo  groups, 
which  he  named  Endothrix  and  Ecto-Endothrix  (Ectothrix),  and 
which  corresponded  with  Gruby's  two  divisions.  His  researches 
were  speedily  confirmed  by  many  observers,  among  whom  may  be 
mentioned  Adamson,  Colcott  Fox,  Malcolm  Morris,  White,  and 
Mibclli. 

In  1900  Matruchot  and  Dassonville  showed  that  the  Trichophytons 
were  closely  allied  to  the  Gymnoascaceae,  and  that  Ctenomyces 
serrata  Eidam,  1880,  when  injected  into  animals  produced  a  Tricho- 
phyton-like  mycelium  and  eruption. 

The  further  history  may  perhaps  be  better  discussed  according 
to  the  countries. 


TINEA  CAPITIS  TROPICALIS  2051 

Brazil. — The  history  of  ringworm  in  Brazil  appears  to  date  from 
the  appearance  of  Silva  Araujo's  '  Atlas  des  Maladies  de  la  Peau,' 
which  contained  an  account  of  favus  and  of  a  Trichophyton  causing 
sycosis,  both  supported  by  microscopical  observations. 

Later  Fernando  Terra  grew  Achorion  schoenleini  from  an  atypical 
case  of  favus,  and  some  form  of  fungus  from  a  case  of  tinea  capitis 
tropicalis,  which  was  traceable  to  infection  from  a  cat,  and  was  there- 
fore probably  T.  jelineum.  The  sixth  Brazilian  Congress  of  Medicine 
and  Surgery,  held  in  1907,  is  remarkable  for  the  appearance  of 
papers  on  ringworm  in  which  the  parasitic  fungi  were  studied 
according  to  Sabouraud's  classical  methods.  It  was  at  this  meeting 
that  Rabello  announced  that  he  had  found  T.  violaceum,  M.  audouini, 
and  M.  lanosum. 

In  1909  Lindenberg  reported  the  presence  of  T.  sabouraiidi.  Horta 
announced  that  M.  jelineum  has  been  found  in  a  considerable 
number  of  cases  at  Sao  Paulo,  and  also  isolated  T.  album  Sabouraud, 

I9°7'  .  ,      r        J 

In  1911  Horta  discovered  M.  flavescens,  and  in  1914  he  found 

a  new  Trichophyton,  which  was  subsequently  described  and  named 

T.  griseum  by  Vasconcellos. 

Argentina. — In  1907  Uriburu  discovered  M.fulvum,  and  in  1909 
T.  exsiccatum  and  T.  polygonum. 

Central  America. — In  1913  Brumpt  named  a  peculiar  parasite, 
discovered  by  Darier  in  a  dermatosis  resembling  pinta,  T.  carateum. 
This  disease  was  found  in  Central  America. 

Africa. — In  1896  Courmont  described  two  forms  of  tinea  capitis 
tropicalis  seen  in  Senegal. 

In  1902  Bodin  found  T.  violaceum  Bodin  in  North  Africa. 

In  1904  Jeanselme  announced  that  Courmont  had  found  M. 
audonin'i  among  the  negroes  of  Senegal,  and  that  Sabouraud  and 
himself  had  found  a  Trichophyton  (subsequently  named  T.  circon- 
volutum  by  Sabouraud  in  1909)  in  white  people  returning  from  the 
Western  Sudan. 

In  1912  Joyeux  discovered  T.  soudanense  in  the  Western  Sudan. 

Ceylon.- — In  1905  Castellani  discovered  T.  violaceum  var.  decalvans 
in  tinea  capitis  tropicalis,  T.  macjadyeni  Castellani,  in  tinea  corporis 
tropicalis,  and  T.  blanchardi  Castellani  in  tinea  sabouraudi  tropicalis.. 
a  term  also  used  for  the  disease  caused  by  T.  circonvolutum  Sabouraud. 

In  1908  he  observed  T.  ceylonense  Castellani,  in  cases  of  tinea 
nigro-circinata. 

In  1 912  he  found  T.  nodoformans  Castellani  in  tinea  barbae 
tropicalis  and  in  tinea  ciliorum. 

Tropical  Queensland. — In  1914  Priestley  discovered  M.  scorteum 
Priestley  in  tinea  corporis  tropicalis. 

In  the  Anglo-Egyptian  Sudan  Chalmers  and  Marshall  found 
Trichophyton  currii  Chalmers  and  Marshall,  1914,  to  be  the  cause  of  an 
epidemic,  and  later  Trichophyton  discoides  Sabouraud,  1900,  in 
one  case,  while  Chalmers  and  Macdonald  have  met  with  numbers 
of  cases  due  to  T.  violaceum  Bodin,  1902,  var.  khartoumense. 


2056 


TROPICAL  DERM ATOM YCOSES 


Geographical  Distribution. — Tinea  capitis  is  found  in  every  part 
of  the  tropics,  but  its  incidence  varies  from  country  to  country,  and 

is  far  less  common  than  epi- 
dermophytoses and  tricho- 
phytoses of  the  body. 

In  our  experience  tinea 
capitis  is  less  common  in  India, 
Ceylon,  and  tropical  Africa 
than  in  Europe  and  America. 
On  the  other  hand,  it  is  ex- 
tremely common  in  American 
negroes. 

/Etiology.  —  The  following 
fungi  have  been  found  in  cases 
of  tinea  capitis  tropicalis: — 

Genus  Microsporum  Gruby, 
1843. 

1.  M.  audouini  Gruby,  1843, 
in  Brazil,  Western  Sudan, 
Northern  Africa  and  Mada- 
gascar. 

2.  M.  fulvum  Uriburu,  1907, 
in  the  Argentine. 

3.  M.  scorteum  Priestley, 
1914,  in  Tropical  Queensland. 


! 

SHttl  ^ 

1  '  ■ 

Fig. 
[Tr. 


808. — Tinea    Capitis    due    to 
violaceum  Bodin  var.  decalvans. 


Genus  Trichophyton  jMalmsten,  1848. 

1.  T.  circonvohttum  Sabouraud,  1909,  in  Senegal  and  Dahomey. 

2.  T.  exsiccatum  Uriburu,  1909,  in  the  Argentine. 

3.  T.  polygonum  Uriburu,  1909,  in  the  Argentine. 

4.  T.  sabouraudi  R.  Blanchard,  1895,  in  Brazil. 

5.  T.  soudanense  Joyeux,  1912,  in  Western  Sudan. 

6.  T.  violaceum  Bodin,  1902,  in  North  Africa. 

7.  T.  violaceum  Bodin,  1902,  var.  decalvans  Castellani,  1905,  in 
Ceylon. 

8.  T.  violaceum  Bodin,   1902, 
Macdonald,  1915,  in  the  Sudan. 

9.  T.  currii  Chalmers  and  Marshall,  1914,  in  the  Sudan. 


var.   hhartoumense  Chalmers  and 


Genus  Ectotrichophyton  Castellani  and  Chalmers,  1918. 
E.  discoides  (Sabouraud,  1909)  in  the  Anglo-Egyptian  Sudan. 

Genus  Achorion  Remak,  1845. 

1.  A.  schoenleini  Leber!,  1845,  in  the  Anglo-Egyptian  Sudan 
Egypt,  Tunis,  Tripoli,  Algeria,  China,  causing  favus. 

2.  A.  quinckeanum ^Zopf,;  1890 ;  the  cause  of  mouse-favus,  rarely 
infects  man. 


TINEA  CAPITIS  TROPICA  LIS  2057 

3.  A.  gypsenm  Bodin,  1907;  very  rare. 

The  description  of  all  these  fungi  is  found  in  Chapter  XXXVIII., 
p.  988. 

Symptomatology. — It  may  be  said  in  a  general  way  that  the 
principal  clinical  signs  are  the  same  in  the  tropical  types  of  the 
affection  as  in  the  temperate  zones,  though  the  medical  man  who 
has  studied  the  subject  thoroughly  will  soon  be  able  to  detect  small 
clinical  differences,  and  will  soon  realize  that  as  a  general  rule 
each  species  of  fungus  gives  rise  to  a  slightly  different  type  of 
disease. 

Tinea  Capitis  Microsporica  (Microsporosis). — Tinea  capitis  due  to  fungi  of 
the  genus  microsporum,  usually  known  by  the  term  microsporons  in  derma- 
tological  literature,  is  rare  in  tropical  and  subtropical  countries.  The  affection 
attacks,  usually,  only  children.  The  affected  patches  are  studded  with  stumps 
of  broken  hair,  which  are  loosened  and  brittle,  have  lost  their  natural  gloss,  and 
show  a  whitened  appearance  caused  by  the  fungus  producing  a  greyish  sheath 
round  the  hair.  The  microscopical  examination  of  the  affected  hair  after 
treatment  with  liquor  potassae  will  show  presence  of  so-called  spores,  roundish 
or  ovoid,  2-4  fi  in  diameter,  irregularly  distributed,  while  those  of  the  tricho- 
phytons are  often  larger  (3-8  fi),  square  with  rounded  angles,  or  somewhat 
oblong,  and  arranged  in  definite  regular  chains. 

Tinea  Capitis  Trichophytica  [Trichophytosis). — This  is  common  in  the 
tropics  and  may  be  caused  by  a  number  of  trichophytons  which  have  been 
mentioned  in  the  ^Etiology.  In  Chapter  XXVIII.,  p.  995,  we  have  given  a 
botanical  classification  of  the  genus  Trichophyton,  creating  several  subgenera. 
In  most  dermatological  works,  however,  a  simpler  classification  is  followed. 
Two  groups  are  differentiated:  endothvix  and  endo-ectothrix,  the  latter  cor- 
responding to  the  original  Sabouraud's  ectothrix.  The  endo-ectothrix 
group  is  subdivided  into  two  types:  with  large  spores  (megaspores),  with 
small  spores  (microides).  Those  of  the  microides  type  produce  a  greyish 
sheath  round  the  hairs,  like  the  microsporons,  but  the  so-called  spores  are 
arranged  in  regular  chains,  a  feature  never  observed  in  the  microsporons. 
The  microides  trichophytons  are  pyogenic,  and  often  cause  kerion. 

As  we  have  already  stated,  each  species  of  trichophyton  gives  rise  to  a 
slightly  different  clinical  type  of  the  affection.  Among  the  many  types  we 
may  briefly  notice  "  Black-dot  tinea  tonsurans  "  and  "  Tinea  decalvans 
tropicalis." 

Black-dot  Tinea  Tonsurans. — -This  type  is  common  in  Europe,  but  is  at  times 
observed  also  in  subtropical  and  tropical  countries.  It  is  caused  by  Tricho- 
phyton sabouraudi  Blanchard,  usually  known  in  dermatological  literature 
by  the  name  of  Trichophyton  acuminatum.  The  scalp  presents  scurvy  patches 
with  minute  dark  dots,  best  seen  with  a  lens.  These  dots  are  pigmented, 
coiled  up  stumps. 

Tinea  Decalvans  Tropicalis. — This  variety,  described  by  Castellani,  is  common 
in  Ceylon.  It  generally  attacks  children,  especially  of  the  moormen  com- 
munity. The  scalp  presents  one  or  several  white  patches  covered  with  an 
enormous  number  of  heaped-up  white  pityriasic  scales.  The  scales  and  the 
broken  hairs,  examined  microscopically,  show  presence  of  an  endo-ectothrix 
fungus,  which,  when  cultivated,  shows  some  characters  of  T.  violaceum 
Bodin  (T.  violaceum  Bodin  var.  decalvans  Castellani).  A  very  serious  symptom 
is  that  the  patches  as  a  rule  remain  permanently  bald. 

Tinea  Capitis  Favica  (Favus). — This  affection,  common  in  Southern  and 
Eastern  Europe,  is  found  in  some  subtropical  countries,  such  as  certain  parts 
of  North  Africa  and  China,  but  is  rare  in  the  tropics.  The  condition  is  recog- 
nized by  the  sulphur-coloured  cup-shaped  scabs,  the  peculiar  mousy  odour 
and  presence  of  atrophic  scarring.  The  hair  is  lustreless  and  discoloured, 
but  does  not  break  off  as  in  rin-rworm. 


2058  TROPICAL  DERMATOMYCOSES 

Diagnosis.— This  is  based  on  the  clinical  characters  mentioned, 
and  on  the  microscopical  examination  of  the  hairs  and  squamae 
in  liquor  potassae.     Cultural  methods  should  also  be  used. 

Prognosis. — This  is  rather  bad  in  the  common  variety  found  in 
Ceylon,  due  to  T.  violaceum  var.  decalvans,  as  the  patches  in  most 
cases  remain  permanently  bald,  though  fortunately  they  are,  as 
a  rule,  of  small  dimensions.  The  treatment  of  every  type  of  tinea 
capitis  is  long  unless  X  rays  are  used. 

Treatment. — -The  Rontgen  rays  treatment,  using  Sabouraud's 
method,  is  by  far  the  best  and  quickest.  Details  on  the  technique 
will  be  found  in  any  up-to-date  book  on  dermatology.  In  many 
tropical  places  this  treatment  is  out  of  the  question,  and  epilation 
and  application  of  turpentine  oil,  tincture  of  iodine,  or — with  care— 
a  chrysarobin  ointment  (2  to  5  per  cent.)  must  be  resorted  to. 

Garrett  recommends  the  application  of  liquor  ferri  perchloridi  fort.  (B.P.) 
after  thorough  cleaning  of  the  patches  with  benzene.  Sabouraud  at  one 
time  recommended  the  internal  administration  of  tallium  acetate.  Cicero 
uses  a  5  per  cent,  solution,  giving  as  many  drops  as  is  represented  by  twice 
the  number  of  kilogrammes  of  the  child's  weight. 

TINEA  BARBAE  TROPICALIS. 

The  same  remarks  can  be  made  on  this  subject  as  on  tinea  capitis. 
Cases  are  found  in  the  tropics,  though  apparently  less  frequently 
than  in  temperate  zones,  and  the  fungi  have  so  far  been  very  little 
investigated.  In  Northern  Africa  a  fungus  commonly  found  is 
Trichophyton  violaceum  Bodin;  in  Ceylon  T.  nodoformans  Castellani 
is  often  found.  .] 

Symptomatology. — The  dry  variety,  with  scaly,  often  gyrated 
lesions,  and  the  pustular  variety,  with  purulent  folliculitis,  can  be 
distinguished. 

'•^We  have  seen  a  typical  case  of  kerion  barbae  due  to  T.  nodo- 
formans in  a  person  who  was  suffering  from  tinea  cruris  due  to  the 
same  fungus. 

Diagnosis. — The  diagnosis,  in  the  pustular  type,  is  based  on  the 
spreading  folliculitis  with  brawny  swelling  and  the  microscopical 
examination  of  the  hair;  in  the  scaly  type,  on  the  frequent  gyrate 
type  of  the  eruption  and  the  microscopical  examination  of  the 
scales  and  hair. 

Prognosis. — The  disease  takes  a  long  time  to  get  well,  even  under 
appropriate  treatment. 

Treatment. — This  consists  in  epilation  of  the  affected  region, 
each  day  clearing  a  square  inch  or  so,  followed  by  the  application 
of  some  antiseptic  ointment  such  as  Crocker's  ointment  of  sulphur, 
3ss.-3i.;  ac.  carbol.,  3SS-!  lanolin  c  oleo,  §i. ;  or  oleate  of  copper, 
3ss.  to  Si. 

Tinea  Ciliorum. 

We  have  seen  a  case  of  this  affection  in  a  man  suffering  from  generalized 
dhobie  itch,  due  to  T.  nodoformans.  The  lid  was  swollen  and  red,  many 
cilia  were  broken,  and  there  was  purulent  inflammation  of  the  hair  follicles. 


TINEA    UNGUIUM  TROPICALIS  2<> 50 


TINEA  UNGUIUM  TROPICALIS. 

Synonym. — Onychomycosis  tropicalis. 

Cases  of  tinea  unguium,  or  onychomycosis,  occur  in  the  tropics. 
and  are  generally  due  to  the  same  fungi  producing  dhobie  itch, 
both  Epidermophytons  and  Trichophytons.  The  nails  of  the  fingers 
as  well  as  of  the  toes  may  be  affected.  Tinea  unguium  may  be 
caused  also  by  fungi  of  the  genus  Endodcrmophyton,  the  nails  being 
often  affected  in  tinea  imbricata. 

Symptomatology. — The  affected  nails  have  often  a  peculiar 
yellowish  opaque  or  blackish  discoloration,  and  a  rough  surface; 
they  become  brittle,  and  splitting  and  chipping  of  the  free  border 
takes  place. 

The  diagnosis  is  principally  based  on  the  microscopical  ex- 
amination of  scrapings.  A  soaking  in  liq.  potassae  (40  per  cent.) 
for  twenty-four  hours  is  often  necessary  to  disintegrate  the  nail 
substance  and  to  find  the  fungi. 

Treatment. — -This  is  most  difficult.  The  affected  nails  must  be 
softened  by  rubbing  in  liquor  potassse,  and  then  wet  dressings  of 
hyposulphite  of  soda  (25  per  cent.),  or  a  solution  of  potassium  iodide 
grms.  x.,  iodine  grm.  i.,  water  1,000  c.c,  must  be  regularly  applied. 
In  the  onychomycosis  found  in  cases  suffering,  or  having  suffered, 
from  tinea  imbricata,  the  daily  application  of  resorcin  in  tincture  of 
benzoin  (3L  to  §i.)  is  useful. 


TINEA  IMBRICATA  (TOKELAU). 

Definition. — The  term  '  tinea  imbricata  '  is  used  to  denote  a 
tropical  dermatomycosis,  or,  more  correctly,  a  group  of  dermato- 
mycoses,  due  to  fungi  of  the  genus  Endodermophyton  Castellani,  and 
clinically  characterized  by  the  presence  of  extensive,  flaky,  scaly 
patches,  the  scales  being  large,  tissue-paper-like,  firmly  adherent 
by  their  bases,  and  arranged  in  concentric  rings  or  parallel  lines. 

Synonyms. — As  is  the  case  with  several  other  tropical  diseases, 
such  as  frambcesia  and  Oriental  sore,  there  is  a  very  large  number 
of  synonyms,  which  may  be  classified  as  follows  :— 

(a)  From  the  name  of  the  centres  where  the  disease  is  rife;  for 
instance,  the  term  '  Tokelau,'  generally  used  by  French  writers,  is  in 
reality  the  name  of  an  island,  Tokelau,  where  the  malady  is  very 
common.  Other  synonyms  are  'Tokelau  ringworm,'  used  by 
Tilbury  Fox,  '  Bowditch  ringworm,'  the  name  Bowditch  being  used 
by  some  writers  to  indicate  the  island  of  Tokelau,  '  South-west 
Gune,'  the  term  '  gune  '  meaning  skin. 

(b)  From  the  name  of  the  patient  who  first  introduced  the  disease 
in  certain  countries.  In  the  island  of  Tokelau,  for  instance,  the 
disease  used  to  be  known  as  '  Le  Pita,'  from  '  Peter,'  the  name  of 
the  native  of  Tamana,  one  of  the  Gilbert  Islands,  who,  according  1o 
Turner,  in  1850  introduced  the  disease  into  Tokelau. 


ao6o  TROPICAL  DERM ATOM Y  COSES 

(c)  From  certain  clinical  appearances : '  Tropical  ichthyosis,'  a  bad 
term,  as  in  the  tropics  true  ichthyosis  is  far  from  rare;  '  Dermato- 
mycosis  chronica  figurata  exfoliativa  '  (Tamson) ; '  Herpes  f arinosus  ' 
(Ritter) ;  'Herpes  desquamans '  (Turner);  'Tinea  imbricata,'  a 
term  introduced  by  Manson,  and  which  is  now  the  one  most  generally 
used. 

(d)  From  the  generic  name  given  to  the  fungus :  '  Aspergillosis '  of 
Wehmer;  'Lepidophytosis'  of  Tribondeau ;  'Endodermophytosis'  of 
Castellani. 

(e)  From  the  name  of  the  authors  who  have  more  completely 
studied  the  disease:  '  Manson's  herpes,'  '  Turner's  herpes,'  etc.,  the 
term '  herpes  '  being  used  by  Roux  and  others  in  the  obsolete  meaning 
of  epiphytic  skin  disease. 

(J)  Terms  apparently  of  unknown  origin,  such  as  '  Gugo,'  a 
denomination  much  used  in  the  Marshall  Islands;  '  Cascado,'  a  term 
used  in  the  Molucca  Islands;  '  Buckwar,'  etc. 

History. — The  first  recognizable  account  of  the  condition  is  to  be 
found  in  Dampier's  '  Voyage  Round  the  World,'  published  in  1789. 
Dampier  saw  the  disease  in  the  Philippine  Islands  in  Mindanoa,  in 
Guam,  and  in  the  Ladrone  Islands.  About  the  end  of  the  same 
century  Dentrescasteaux  described  cases  of  the  same  condition  in 
Tonga.  In  1811  Marsden  observed  it  among  the  natives  of  Polo 
Mas,  on  the  west  coast  of  Sumatra.  In  Alibert's  '  Atlas,'  published 
in  1832,  there  is  a  reference  to  the  disease.  In  1841  the  disease  was 
recognized  by  the  medical  officers  attached  to  the  United  States 
Exploratory  Expedition  led  by  Commodore  Wilkes,  and  Fox  in 
1844  described  it  under  the  name  of  '  gune,'  the  term  used  by  the 
Gilbert  Island  natives. 

In  the  reports  of  the  Samoa  Medical  Mission  for  the  year  1869 
there  is  a  good  description  of  the  malady  by  Geo.  Turner.  In  1874 
Tilbury  Fox  gave  a  description  of  the  complaint  under  the  term 
'  Tokelau  ringworm,'  and  noted  the  presence  of  a  fungus  in  the  scales 
sent  to  him  from  the  tropics.  He  considered  it  to  be  identical,  or 
very  similar  to,  the  fungus  of  European  ringworm.  From  the 
drawings  given  the  fungus  described  by  him  seems,  however,  not 
to  have  been  a  trichophyton-like  organism,  but  an  aspergillus-like 
contamination.  From  that  time  discussion  began,  which  went  on 
for  several  years,  on  the  subject  whether  the  disease  was  a  separate 
entity  or  merely  European  '  ringworm  '  modified  by  the  different 
climatic  conditions.  Apparently  the  great  majority  of  the  European 
authorities,  who,  however,  had  no  personal  experience  of  the 
condition,  were  against  considering  the  disease  a  separate  one,  while 
the  medical  men  practising  in  the  tropics  generally  believed  it  to  be 
a  different  disease  from  ringworm.  Valuable  researches  were  carried 
out  by  McGregor  in  1870  and  Koniger  in  1878.  Manson's  researches 
on  the  malady — in  China  from  1879  to  T^2 — are  by  far  the  most 
important.  He  gave  a  complete  clinical  description  of  the  malady, 
and  introduced  the  very  appropriate  name  of  tinea  imbricata; 
moreover,  he  very  correctly  described  the  microscopical  appearances 


TINEA  IMBRICATA   (TOKELAU) 


2061 


of  its  fungus,  though,  as  might  be  expected,  using  the  technique  of 
that  time,  attempts  at  growing  it  did  not  succeed.  More  recently 
the  condition  has  been  studied  by  Tr ibondeau,  Nieuwenhuis,  Wehmer , 
and  many  others.  Castellani  has  succeeded  in  growing  the  fungus 
artificially,  and  in  reproducing  the  disease  by  inoculating  pure 
cultures  of  it ;  he  has  shown  also  that  there  is  more  than  one  variety 
of  the  affection  and  more  than  one  species  of  the  fungus.      He  has 


Fig.  809. — Tinea  Imbricata. 


demonstrated  that  the  aspergillus-like  fungi  described  by  a  number 
of  authorities  are  merely  saprophytes,  and  that  the  true  aetiological 
agents  are  those  fungi  for  which  he  has  created  the  genus  Endo- 
dermophyton. 

Climatology. — The  home  of  tinea  imbricata  seems  to  have  been 
the  Malay  Peninsula,  from  whence  it  spread  towards  the  south  and 
the  east  to  many  islands  of  the  South  Pacific,  northwards  to  some 


2062 


TROPICAL  DERMATOMYCOSES 


Fig.  Sio. — Tinea  Imbricata. 


Fig.  8ii.  -Tinea  Imbricata. 


TINEA    TMBRICATA  {TOKELAU) 


2063 


parts  of  China,  as  far  as  Foochowjand  Formosa,  and  westwards  to 
Burma  and  Ceylon.  The  Gilbert  group  of  islands  seems  to  have 
become  heavily  in- 
fected since  the  begin- 
ning of  last  century. 
In  1859  it  ^  sa-id  that 
a  native  of  Tamana, 
an  island  of  the  Gilbert 
group,  affected  with  the 
malady,  landed  at 
Bowditch,  an  island 
called  also  Tokelau,  in 
1859.  From  that  year 
onwards  the  disease 
spread  rapidly  all  over 
the  Bowditch  or  Toke- 
lau Island.  The  Tamana 
man  who  brought  the 
disease  was  called 
Peter,  hence  the  disease 
becamejknown  in  Bow 


Fig. 812.— Fungus  in  the  Scali 
(From  a  stained  preparation  ) 


ditch  or  Tokelau  as  '  Le  Pita' — viz.,  '  The  Peter.'     From  Tokelau 
the  disease^ spread  to  Samoa,  according  to  Turner  and  Koniger,  in 


f 


Fig.  81^. — Tinea  Imbricata. 


1869,  and  to  many  other  islands,  where  it  became  known  as 
Tokelau.  At  the  present  time  the  disease  is  extremely  common 
in  the  Malay  Peninsula,  some  parts  of  Indo-China  and    Southern 


2064 


TR0P1 CA  L  DERMA  TOM  YCOSES 


China,  Borneo,  Samoa,  Java,  the  Solomon  Islands,  New  Guinea, 
Sumatra,  Fiji.     According  to  Daniels,  the  disease  was  first  intro- 
duced into  Fiji  by  some  Solomon  Islanders  in   1870,   and  within 
the  following  two  years  became  extremely  prevalent.     In  certain 
of  the   Pacific   Islands   one-third   to    one-half   the  population  is 
affected.    The  disease  is  common  in  some  districts  of  the  Philippine 
Islands,  the  Ladrones,  the  Loyalty  Islands,  New   Caledonia,  and 
some  districts  of  Burma.     Until  1904  the  disease  was  believed  to  be 
non-existent  in  Ceylon,  but  in  that  year  Castellani  recorded  the 
first  case.      During  the  last  few  years  the    disease   has   greatly 
spread  in  this  island,  and  it  is  now  fairly  common,  though ^not 
so  common  as  in  the  Malay  Peninsula  or  Fiji.     India  is  said  to  be 


Fig.  814. — Tinea  Imbricata. 


so  far  immune,  but  two  typical  cases  hailing  from  Southern  India 
have  been  seen  by  Castellani.  Cases  have  been  reported  from 
Brazil  and  other  parts  of  tropical  America,  but  some  doubt  has  been 
expressed  as  to  their  being  cases  of  true  tinea  imbricata.  The  cases 
so  far  reported  from  Africa  are  also  doubtful. 

The  climatic  conditions  favourable  to  the  rapid  development  and 
spread  of  the  disease  are  represented  by  a  warm,  damp,  equable 
climate,  with  a  temperature  of  8o°  to  900  F.,  the  same  climate,  as 
Manson  so  truly  remarks,  that  is  favourable  to  the  growth  of  cocoa- 
nuts;  in  fact,  the  geographical  distribution  of  tinea  imbricata 
corresponds  almost  exactly  to  the  districts  where  cocoanuts  thrive. 
In  those  countries  which,  though  at  certain  times  extremely  hot, 


TINEA   IMBRICATA  (TOKELAU) 


2065 


have  a  cold  and  cool  season — such  as  many  parts  of  India  and  China 
— the  disease  apparently  does  not  spread. 

/Etiology. — The  aetiology  of  this  dermatomycosis  has  been  the 
subject  of  numerous  controversies.  Manson  first,  in  1872,  de- 
scribed a  trichophyton-like  organism  in  the  squamae;  with  the 
laboratory  technique  of  that  time  attempts  at  cultivation  did  not 
succeed.  Blanchard  considered  it  non-cultivable,  and  called  it 
Trichophyton  concentricum '  ;  on  the  other  hand,  Nieuwenhuis 
stated  that  it  was  quite  easily  cultivated  direct  on  solid  media  from 
the  squamae,  and  was  characterized  by  the  colonies  being  craterif  orm. 
His  results  were  not  confirmed.  In  recent  years  the  general  opinion 
has  been  that  aspergillus-like  fungi  were  the  real  cause  of  the  disease. 
Tribondeau  described  fructifications  somewhat  similar  to  those  of  an 
aspergillus,   and  created  for  the  fungus  the   genus  Lepidophyton 


Fig.  815. — Tinea  Imbricata. 

(A€7rts=scale ;  </>u-rov=plant).  Wehmer  has  described  it  as  a  true 
aspergillus — Aspergillus  tokelau.  The  investigations  carried  out 
by  Castellani  have  demonstrated  that  the  aspergillus  and  aspergillus- 
like  fungi  have  nothing  to  do  with  the  disease.  When  they  are 
present  in  the  squamae,  they  are  merely  saprophytes  or  contamina- 
tions. By  using  a  special  technique  he  has  succeeded  in  growing 
the  true  fungi  causing  the  disease,  which  must  be  placed  in  the  genus 
Endodermo  phyton.  Castellani  recognized  at  first  two  species,  and 
later  four:  Endodermo  phyton  indicum,  Endodermo  phyton  tropicale, 
Endodermophyton  concentricum,  and  Endodermo  phyton  mansoni.  It 
is  probable  that  further  investigation  will  reveal  the  existence  of  some 
more  species.  The  description  of  these  fungi  will  be  found  in 
Chapter  XXXVIII.,  p.  1016. 

Predisposing  Causes. — As  regards  age,  many  authorities  state  that 
the  disease  is  more  common  in  children  than  in  adults.     In  Ceylon, 

130 


ao66 


TROPICAL  DERMATOMYCOSES 


however,  the  condition  is  rare  or  absent  in  infants  and  children, 
while  the  persons  affected  are  generally  young  adults,  but  it  may 
be  found  also  in  very  old  persons.  Women  are  attacked  less  fre- 
quently than  men.  Villagers  and  people  living  in  the  country  are 
much  more  liable  to  contract  the  malady  than  people  living  in 
large  towns.  It  is  doubtful  whether  there  is  any  racial  disposition. 
In  Fiji,  however,  it  has  been  observed  that  while  extremely  common 
in  the  indigenous  population,  it  is  comparatively  rare  among  the 
immigrant  Indian  coolies.  The  Tongans  also  are  said  to  contract 
the  disease  rarely,  and  this  relative  immunity,  according  to  them, 
is  due  to  the  habit  they  have  of  regularly  anointing  their  bodies — 


Fig.  816. — Tinea  Imbricata  of  the  Forearm  (Old  Case). 


a  habit  not  shared  by  the  Fijians.  A  hot,  moist,  equable  climate 
seems  to  be  the  most  suitable  for  the  development  of  the  fungus 
and  the  spreading  of  the  disease.  Manson  has  justly  remarked 
that  the  climate  which  is  suitable  for  the  growth  of  cocoanuts  is 
also  the  best  for  the  fungus  of  tinea  imbricata. 

Symptomatology. — The  eruption  begins  with  one  or  several  small, 
roundish  or  oval,  slightly  raised,  dark  brownish  patches,  very  itching. 
Soon  the  central  portion  of  each  patch  splits,  and  a  ring  of  flaky  large 
scales  attached  at  the  periphery  is  formed.  This  scaly  ring  extends 
peripherally,  and  in  the  meantime  another  brownish  patch  appears  in 
the  centre  at  the  site  of  the  first  brown  spot ;  the  new  brownish  patch 
breaks,  and  a  second  scaly  ring  is  formed,  which  extends  peri- 
pherically  inside  the  first  ring,  and  so  on  until  a  very  large  roundish 
patch  is  formed,  containing  several  concentric  scaly  rings.  Manson 
has  aptly  compared  this  formation  of  rings  to  concentric  ripples 


PLATE    X. 


TINEA    IMBRICATA. 


Ceo'V»ter«oiv  *  Sons  Ltd  Ediiv 


To  fate  page  2066 


TINEAVIMBRICA  TA    {TOKELA  U) 


2067 


produced  by  a  stone  thrown  into  a  pool  of  water,  and  when  the 
eruption  starts  from  many  points,  as  is  often  the  case  owing  to  auto- 
infection,  it  is  as  if  a  shower  of  stones  had  fallen  in  the  pond,  and 
many  systems  of  spreading  rings  are  produced  which  intersect  each 
other  in  various  directions,  and  give  rise  to  a  more  complex  pattern. 
The  patches  extend  at  the  rate  of  a  quarter  to  half  an  inch^a  week. 
In  a  well-marked,  advanced 
case  of  the  disease  the  skin 
of  practically  the  whole 
body  is  covered  with  round 
patches,  each  of  which 
presents  several  concentric, 
not  inflamed,  scaly  rings. 
The  scales  are  flaky,  re- 
sembling tissue  paper,  of 
large  size — up  to  half  an 
inch  in  length — dry,  of  a 
dirty  greyish  or  brownish 
colour,  and  slightly  curled. 
The  largest  scales  are 
generally  found  on  the 
back.  Each  scale  has  a 
free  border,  and  is  firmly 
attached  by  the  opposite 
side;  the  free  border  of 
each  scale  is  towards  the 
centre  of  the  circle,  while 
the  attached  border  is 
towards  the  periphery.  If 
the  scales  are  removed, 
rings  of  concentric  circular 
dark  lines  remain  visible, 
a  quarter  to  half  an  inch 
apart.  The  number  of 
rings  forming  the  patch 
varies;  as  many  as  eight 
and  ten  may  be  present 
in  the  same  patch.  The 
eruption  may  spread  to 
any  part  of  the  body  except  the  scalp.  Though  several  authors 
state  that  the  eruption  never  affects  the  face  or  axilla,  and  rarely 
the  palms  and  soles,  it  is  often  observed  in  such  situations.  The 
nails  may  be  affected  and  become  much  thickened,  with  rough 
surface  and  deep  cracks.  Scrapings  examined  in  liq.  potassae 
show  the  fungus.  The  fungus  never  invades  the  hair  follicles. 
The  general  health  is  not  much  affected,  but  the  patients  complain 
■of  the  disfigurement  and  of  the  unbearable  pruritus.  The  pru- 
ritus greatly  increases  apparently  if  the  patient  is  given  certain 
diets— for  instance,  dry-fish  diet.     In  the  hot  season  the  pruritus  is 


Fig.  817. — Tinea  Imbricata. 


2o68 


TROPICAL  DERMATOMYCOSES 


much  more  marked.  The  disease  is  very  chronic  and  very  difficult 
to  cure.  In  many  cases  the  blood  shows  a  certain  degree  of 
eosinophilia,  the  number  of  eosinophile  leucocytes  varying  between 
6  and  16  per  cent.  In  some  cases  the  eosinophilia  is  probably 
due  to  the  presence  of  intestinal  worms ;  the  eosinophilia  is,  however, 
observed  also  in  some  cases  in  which  the  microscopical  examination 
of  the  faeces  does  not  show  any  ova  of  worms.  In  very  old  cases 
the  eosinophilia  is  more  marked  than  in  recent  ones,  and  signs  of 
anaemia  may  be  present. 

Clinical  Varieties.- — The  eruption  may  after  a  time  or  from  the  very 
beginning  have  a  diffuse  appearance  instead  of  that  of  concentric 


Fig.  818. — Experimental    Tinea    Imbricata    obtained    by    inoculating 
C  ultures  of  Endodermophyton  tropicale. 


rings.  The  scales,  however,  are  typical  and  identical  to  those  found 
in  the  concentric  type — viz.,  they  are  large,  tissue-paper-like, 
partially  covering  each  other  like  tiles  on  a  roof,  and  most  of  them 
firmly  adherent  by  their  bases.  One  variety  of  the  disease  is 
characterized  by  the  facility  with  which  extensive  pieces  of  epi- 
dermis can  be  stripped  off — a  condition  almost  comparable  to 
moulting. 

The    same   fungus — viz.,   either    Endodermophyton   tropicale    or 
E.  indicum — may  give  rise  at  times  to  the  concentric  type,  at  other 


TINEA  IMBRICATA   (TOKELAU)  2069 

times  to  the  diffuse  type.  In  some  cases  the  lesions  caused  by 
E.  indicum  seem  to  be  slightly  different  from  those  given  by 
E.  tropicale,  the  lesions  caused  by  the  former  being  perhaps  a  little 
more  superficial  and  the  scales  not  situated  so  close  together.  Further 
researches  will  probably  show  that  there  are  several  other  species  of 
Endodermophytons,  each  of  which  will  probably  give  rise  to  a 
slightly  different  type  of  the  disease. 

Experimental  Reproduction  of  the  Disease. — The  disease  is  easily 
reproduced  in  human  beings  by  inoculating  scales,  as  was  done  by 
Manson,  or  pure  cultures  of  the  fungi,  as  done  by  Castellani.  The 
incubation  period  by  the  first  procedure  is  eight  to  ten  days. 
By  inoculating  cultures  of  the  fungi  the  incubation  period  is  generally 


Fig.  819.- — -Experimental  Tinea  Imbricata  obtained  by  inoculating 
Cultures  of  Endodermophyton  indicum. 

Compare  with  Fig.  818.     Note  the  different  clinical  appearance  from  experi- 
mental tinea  imbricata  induced  by  Endodermophyton  tropicale. 

somewhat  longer  (twelve  to  twenty  days),  but  the  eruption  develops 
typically.  It  is  of  interest  to  note  that  if  very  old  cultures  are  used 
instead  of  young  ones  the  inoculation  may  fail  completely,  or  merely 
an  evanescent,  superficial,  papuloid,  trichophytic-like  patch  may 
be  induced. 

Diagnosis. — This  is  easy,  the  presence  of  concentric  rings  fringed 
with  large  tissue-paper-like  scales  being  characteristic.  Even  when 
the  concentric  rings  are  not  present  and  the  eruption  is  diffuse  the 
diagnosis  is  not  difficult,  being  based  on  the  characteristic  large,  dry, 
tissue-paper-like  scales,  overlapping  each  other  like  tiles  on  a  roof, 
and  containing  under  microscopical  examination  an  enormous 
amount  of  interlacing  mycelial  tubes. 


2070  TROPICAL  DERMATOMYCOSES 

Differential  Diagnosis — Ringworm. — Tinea  imbricata  has  an  abso- 
lutely different  clinical  aspect  from  any  type  of  body  ringworm; 
inflammatory  signs  are  totally  absent,  and  the  scales  are  very  large, 
flaky,  firmly  attached  by  their  bases,  and  arranged  in  parallel  lines  or 
concentric  circles.  The  scales  contain  an  enormous  amount  of  the 
fungus. 

Ichthyosis. — The  medical  man  newly  arrived  in  the  tropics  often 
mistakes  the  disease — when  of  the  diffuse  type — for  ichthyosis,  so 
much  so  that  it  has  also  received  the  name  of  tropical  ichthyosis. 
The  microscopical  examination  of  the  scales  will  clear  the  diagnosis 
at  once. 

Pityriasis  rubra. — In  tinea  imbricata  there  is  not  the  intense 
hyperemia  of  the  skin,  and  the  scales  are  firmly  attached.  The 
microscopical  examination  will  clear  the  diagnosis  in  any  doubtful 
case. 

Tinea  intersecta. — Tinea  intersecta  begins  in  a  manner  somewhat 
similar  to  tinea  imbricata,  dark-brownish  patches  being  present  at 
first,  and  the  fungus  in  both  eruptions  growing  between  the  super- 
ficial and  deep  strata  of  the  epidermis.  In  contrast  to  tinea  imbri- 
cata, however,  the  eruption  never  develops  in  concentric  rings,  the 
scales  are  not  firmly  attached,  and  the  cure  is  easy. 

Prognosis. — The  disease  has  no  tendency  to  spontaneous  cure, 
and  the  treatment  is  difficult.  The  general  health  is  not  much 
affected,  but  the  patient  complains  of  the  disfigurement,  which  is 
very  great,  and  of  the  pruritus,  which  in  the  hot  season  may  be 
unbearable.  Europeans  complain  also  of  pain,  especially  if  the 
fungus  attacks  the  hands.  In  very  chronic  cases  signs  of  anaemia, 
general  weakness,  and  emaciation  may  appear.  Coolies  affected  with 
the  malady  in  an  advanced  stage  are  unable  to  work  owing  to 
the  extreme  pruritus;  hence  the  disease  is  of  great  economical 
importance,  as  it  may  greatly  decrease  the  supply  of  labour  on 
estates,  etc. 

Treatment. — Every  medical  man  practising  in  the  tropics  well 
knows  how  difficult  is  the  treatment  of  tinea  imbricata.  It  is  easy 
to  obtain  a  temporary  improvement,  and  even  a  disappearance  of 
the  eruption;  but  as  soon  as  the  treatment  is  discontinued  the 
eruption,  as  a  rule,  starts  afresh. 

Strong  iodine  liniment,  as  recommended  by  Manson,  or  resorcin 
dissolved  in  tincture  of  benzoin  (resorcin,  3ii. ;  tr.  benz.  co.,  §i.),  as 
recommended  by  Castellani,  or  chrysarobin  ointment  (5  per  cent.) 
give,  on  the  whole,  the  best  results. 

In  the  Colombo  Clinic  of  Tropical  Medicine  one  of  us  made  various 
experiments  to  test  the  efficacy  of  the  various  medicaments  by  applying 
simultaneously  different  liniments,  ointments,  etc.,  to  symmetrical  parts  of 
the  body,  and  comparing  the  result.     According  to  his  results: — 

Sulphur  has  practically  no  effect  whatever  on  the  fungus. 

Turpentine  generally  induces  a  slight  improvement,  some  scales  disappear- 
ing, and  the  skin  becoming  smoother;  the  improvement,  however,  is  not  per- 
manent, and  as  soon  as  the  turpentine  application  is  discontinued  the  typical 
scales  reappear. 


TINEA  IMBRICATA   {TOKELAU)  2071 

Calomel  and  other  ointments  of  mercurial  preparations  do  not  induce  any 
improvement  in  the  eruption. 

Thymol  and  Naphthol  ointments  may  cause  a  slight  improvement. 

Carbolic  A  rid  and  Epicarin  ointments  have  no  effect  whatever. 

Cyllin  ointment  (20  to  50  per  cent.)  may  induce  a  temporary  im- 
provement. 

Formalin  is  very  effective  for  localized  patches.  The  usual  40  per  cent, 
solution  is  applied  with  care,  treating  each  time  a  small  portion  of  the  erup- 
tion. Formalin  often  causes  severe  pain  and  a  certain  degree  of  inflammation, 
which  is  best  relieved  by  applications  of  iced  water.  Soon  after  the  applica- 
tion of  formalin  the  patches  become  dark  brownish,  which  colour  lasts  for  a 
few  days,  when  they  clear.  Care  must  be  taken  not  to  apply  the  formalin 
to  too  large  portions  of  the  skin,  and  not  to  repeat  the  application  too  often ; 
otherwise  a  peculiar  form  of  apigmentation,  similar  to  leucodermic  patches, 
may  appear  later  on,  to  which  disfigurement  coloured  patients  strongly 
object. 

Chrysarobin. — The  repeated  application  of  chrysarobin  ointment  (30  grains 
to  1  ounce  of  vaseline)  may  induce  a  strikingly  rapid  improvement  in  cases 
which  are  not  of  long  standing.  The  eruption,  however,  recommences  a 
few  days  or  weeks  after  its  apparent  disappearance.  Chrysarobin  is  a  very 
toxic  medicament;  the  patient  must  be  watched  and  the  urine  regularly 
examined.  In  one  of  our  cases  symptoms  of  absorption  appeared  after  a 
single  application. 

Salicylic  Acid  and  Methyl  Salicylate  have  very  little,  if  any,  action  on  the 
fungus. 

Tinctura  Iodi  and  Linimentum  Iodi. — Tinctura  iodi,  freely  applied,  in- 
duces a  very  marked  improvement,  which,  however,  is  not  permanent. 
Strong  iodine  liniment,  as  recommended  by  Manson,  is  most  effective;  it 
cannot  be  used  freely,  however,  on  patients  with  a  delicate  skin,  such  as 
women  and  children. 

Resorcin  and  Tincture  of  Benzoin. — Resorcin,  alone  or  mixed  with  salicylic 
acid  in  alcoholic  solution  and  in  ointments,  has  very  little  efficacy.  If, 
however,  resorcin  be  dissolved  in  tinctura  benzoini  composita  (60  to  120  grains 
of  resorcin  to  1  ounce  of  the  tincture  of  benzoin),  very  good  results  are 
obtained ;  it  is  now  the  routine  treatment  for  tinea  imbricata  in  the  Colombo 
Clinic.  It  is  to  be  noted  that  tincture  of  benzoin  without  resorcin  has  very 
little  action  on  the  eruption.  The  resorcin,  dissolved  in  tincture  of  benzoin, 
should  be  applied  freely  once  or  twice  daily  on  the  affected  regions.  If  the 
whole  body  be  affected,  one  day  one  half  is  painted,  and  the  other  days 
the  other  half,  alternately.  The  treatment  must  be  continued  for  several 
weeks.  Once  or  twice  a  week  the  patient  is  given  a  very  hot  bath,  and 
scrubbed  all  over  with  sand-soap.  Symptoms  of  absorption  are  rare;  it  is 
always  prudent,  however,  to  proceed  at  first  with  care,  as  it  is  well  known 
that  individuals  may  be  met  with,  though  rarely,  showing  idiosyncrasy  for 
resorcin. 

Prophylaxis. — -Some  authorities  recommend  isolation;  this  is  good 
wherever  possible,  but  in  regions  where  the  disease  is  or  has  become 
endemic  usually  the  great  number  of  people  suffering  from  the  affec- 
tion render  the  measure  hardly  practicable.  In  those  tropical 
countries,  however,  where  the  disease  has  not  yet  appeared,  the 
medical  officers  would  do  well  to  be  on  the  look-out  for  it,  and  if  a 
case  is  reported  the  patient  should  certainly  be  kept  isolated  and 
thoroughly  treated  before  being  allowed  to  mix  with  the  general 
population,  and  all  infected  clothing  should  be  boiled  or  burnt. 
We  have  seen  an  epidemic  of  tinea  imbricata  in  a  hospital  in  which 
a  patient  suffering  from  the  disease  was  admitted  and  allowed  to 
mix  with  the  other  patients.     There  is  a  general  native  belief  that 


20J2 


TROPICAL  DERMATOMYCOSES 


anointing  the  body  with  cocoanut  oil  or  other  oil  will  prevent 
infection;  there  may  be  some  truth  in  the  belief,  but  such  a  measure 
cannot  be  carried  out  in  Europeans.  Any  itchy,  scaly  spot  in  the 
slightest  way  suspicious  of  incipient  tinea  imbricata  should  be 
immediately  treated  with  lin.  iodi,  chrysarobin  ointment,  or  resorcin 
dissolved  in  tr.  benzoini.  While  the  treatment  of  tinea  imbricata 
in  an  advanced  stage  is  extremely  difficult,  it  is  easy  to  stop  the 
initial  patches  by  these  means. 


TINEA  INTERSECTA  (vide  Plate  XL). 

This  dermatomycosis  and  its  fungus  were  first  described  by  Cas- 
tellani  in  1907.     It  occurs  in  Ceylon  and  Southern  India. 

etiology. — If  a  por- 
tion of  one  of  the  brown 
patches  or  a  scale  be 
removed  and  treated 
with  liquor  potassae, 
the  fungus  is  easily 
detected.  The  fungus 
(Endodermophyton  cas- 
tellanii  Perry,  1907) 
grows  between  the 
superficial  and  the 
deep  strata  of  the  epi- 
dermis. It  is  present 
on  the  inner  surface 
of  the  scales,  but  not 
on  the  external  surface. 
A  very  remarkable 
fact  is  the  extreme 
rarity  of  free  spores; 
in  fact,  in  several  cases 
one  does  not  succeed 
in  finding  spores.  The 
mycelium  is  fairly 
abundant,  though  far  from  being  so  abundant  as  in  tinea  imbricata. 
It  is  composed  of  long,  straight  articulated  threads,  which  are 
sometimes  dichotomous,  the  breadth  being  between  3  and  3J  ju. 
Each  segment  presents  in  fresh  preparation  two  refractile  bodies, 
one  at  each  extremity.  No  aspergillar  fructifications  nor  clusters 
of  spores  are  seen.  Attempts  at  growing  the  fungus  have  succeeded 
only  in  one  case,  the  growth  being  somewhat  similar  to  that  of  Endo- 
dermophyton indicum  Castellani  (p.  1020) . 

Symptomatology. — The  eruption  begins  with  small  oval  or 
roundish,  very  slightly  elevated  itching  patches,  generally  situated 
on  the  arms,  legs,  chest,  and  back.  The  margins  of  these  dark 
spots  are  at  first  slightly  elevated,  and  dotted  often  with  minute 
dark  papules.      The  patches  are  dark  brown  in  colour,  much  darker 


Fig.  820. — Fungus  of  Tinea  Intersecta. 
(From  a  scale  in  liq.  potassae.) 


PLATE    XI. 


TINEA   INTERSECTA   (Forkakm) 


o.Waterstcr.kSons.Ltd  Edii 


To  fact  page  -">72 


TINEA   FLAVA 


2073 


than  the  surrounding  skin,  and  presents  a  smooth,  tense  surface  at 
first;  they  increase  in  size  slowly,  and  some  coalesce.  After  a 
certain  time  the  surface  of  the  patches  is  no  longer  tense;  it  becomes 
somewhat  shrivelled  and  dry;  superficial  cracks  appear  in  it,  so 
that  white  lines  are  visible  intersecting  the  brown  surface.  Later 
the  cracks  become  deeper,  the  epidermis  splits,  and  several  flaky, 
curled-up  scales,  whitish  inside  and  dark  on  the  outer  surface,  are 
seen;  the  scales  are  often  removed  by  friction,  and  whitish  roundish 
patches  only  remain.  The  eruption  never  develops  in  concentric 
rings  like  tinea  imbricata;  the  patches  remain  isolated  or  fuse  to- 
gether, forming  irregular  larger  patches.  Some  patches  may  disap- 
pear spontaneously  after  a  time.  The  general  health  of  the  patient 
does  not  seem  to  be  affected.  In  some  patients  there  is  a  slight 
degree  of  eosinophilia. 

Diagnosis. — When  the  eruption  is  in  the  very  first  stage  it  might 
be  mistaken  for  a  form  of  pityriasis  versicolor.  In  pityriasis  versi- 
color, however,  the  epidermis  does  not  split;  moreover,  in  tinea 
intersecta  the  fungus  is  not  found  on  the  surface:  it  grows  between 
the  superficial  and  deep  layers  of  the  epidermis.  Tinea  imbricata 
begins  in  a  manner  somewhat  similar  to  tinea  intersecta,  dark 
brownish  patches  being  present,  and  the  fungus  in  both  eruptions 
growing  between  the  superficial  and  deep  layers  of  the  epidermis. 
In  contrast  to  tinea 
imbricata,  however, 
the  eruption  of  tinea 
intersecta  never  de- 
velops in  concentric 
rings ;  is  far  less  severe, 
as  patches  may  heal 
spontaneously;  and  is 
cured  without  much 
difficulty. 

Treatment.  —  Tinc- 
ture of  iodine  and  the 
usual  antiseptic  oint- 
ments, such  as  chrysa- 
robin  (2  to  5  per  cent.) , 
answer  well. 


TINEA  FLAVA 

(vide  Plate  XII.). 


Fig.  821. — Fungus  of  Tinea  Flava  ^OldCase). 

(From  a  specimen  stained  by  the  Morris- 
Walker  method.) 


Synonyms.  —  Trop- 
ical Pityriasis  Ver- 
sicolor of  the  old 
authors,  Microsporosis  Flava  (Castellani),  Achromie  Parasitaire 
(Jeanselme),  Pityriasis  Versicolor  Flava  (Castellani),  Achromia 
Squamosa  (Crocker). 


°74 


TROPICAL  DERM  ATOMY  COSES 


This  dermatomycosis  is  extremely  common  in  all  tropical 
countries,  and  especially  so  in  Southern  India,  Ceylon,  Malaya. 
Java,  Indo-China,  and  China.  By  many  authors  it  has  been,  and 
is  still,  confused  with  the  ordinary  pityriasis  vesicolor  of  temperate 
zones;  the  investigations  of  Castellani  and  Jeanselme,  however, 
have  clearly  proved  that  it  is  a  different  affection. 

etiology. — The  affection  is  due  to  Malassezia  tropica  Castellani, 
1905.     The  mycelial  threads  are  generally  thick,  with  numerous 


Fig.  822.- — Tinea  Flava  on  the  Face  of  a  Sinhalese. 


swellings,  constrictions,  and  other  irregularities  in  their  shape. 
The  spores  are  roundish  or  oval  (3»50  to  4-50  fi),  and  have  a  double 
contour.  In  recent  cases  the  fungus  is  abundant,  with  plenty  of 
mycelium  and  spores  which  often  run  into  clusters.  In  old  chronic 
patches  the  fungus  becomes  very  scanty;  the  spores  are  not 
numerous,  and  generally  do  not  collect  in  clusters;  the  mycelium  is 
very  scanty,  and  is  even  more  irregular  in  shape  than  it  is  in  recent 
patches  (degeneration  forms  of  the  fungus).  For  full  description 
of  the  fungus  see  p.  1099. 


TINEA   FLA  VA 


2075 


Symptomatology.— The   affected  parts   are  yellowish,    of  much 
lighter  colour  than  the  surrounding  healthy  skin;  the  yellow  colour 


ft 


£■     Wmm.         BBBMBI1 


Fig.,  823. — Tinea  Flava  on  the  Back. 


Fig.  824. — 'Tinea  Flava  of  the  Arm. 

may  be  of  various  tinges,  from  dark,  deep  orange-yellow  in  some 
cases  to  very  light  canary-yellow  in  others.     The  patches  are  ot 


2076 


TROPICAL  DERMATOMYCOSES 


various  sizes,  generally  roundish,  smooth,  sharply  denned,  with 
margins  not  elevated,  or  only  slightly  so.  Sometimes  the  patches 
are  irregularly  festooned,  and  may  encircle  an  area  of  healthy  skin. 
Occasionally  the  encircled  healthy  skin  appears  to  be  intersected 
by  many  yellowish,  ribbon-like  lines  originating  from  the  surround- 
ing yellow  patch.  The  regions  more  frequently  affected  are,  in 
order  of  frequency,  the  face,  neck,  chest,  and  abdomen.  Large 
portions  of  the  body  may  be  involved.  There  is,  as  a  rule,  no 
pruritus.  The  patches  are  not  desquamating,  or  only  very  slightly 
so.  The  course  of  tinea  flava  is  very  chronic.  In  the  natives  of  the 
lower  classes  it  appears  in  childhood  in  the  shape  of  tiny  spots  on 
the  face  and  chest,  spreading  slowly  during  years;  thej^  may 
coalesce,   covering  practically  the  whole   of  the  face  and  chest. 


Fig.  825. — Tinea  Flava:  Variety  Guttata. 


One  is  occasionally  surprised  to  see  a  native  whose  face  and  chest 
are  quite  light  in  colour;  on  closer  examination,  it  may  be  found 
that  this  lighter  appearance  is  due  to  a  diffuse,  very  light-coloured 
form  of  tinea  flava,  covering  the  whole  of  the  face,  neck,  and  chest. 
In  Ceylonese  native  women,  when  the  patches  of  tinea  flava  are 
small,  light,  and  situated  on  the  face,  they  are  considered  to  be 
beauty-spots,  and  are  highly  appreciated  by  the  ladies  and  their 
admirers.  Such  patches  are  called  in  Sinhalese  '  alu-hama,'  which 
means  ashy  skin  (alu,  ash;  hama,  skin).  There  is  also  another  word 
used  by  native  poets  for  such  condition — -'gomera,'  which  means 
skin  dotted  with  beauty-spots.  The  disease,  which  is  extremely 
common,  attacks  mostly  natives,  but  occasionally  Europeans  also. 
In  Europeans  the  patches  are  yellowish-reddish  or  pinkish  (tinea 
rosea) ,  and  may  be  due  to  different  strains  of  M.  tropica. 


TINEA   FLAVA 


2077 


Prognosis. — The  disease  is  very  chronic  and  has  no  tendency  what- 
ever to  spontaneous  cure,  but  the  general  health  is  not  affected. 

Diagnosis.-— Pityriasis  versicolor  of  temperate  zones  is  not  of  so 
light  a  tinge  as  tinea  flava,  never  attacks  the  face,  and  is  curable 
with  the  greatest  facility;  while  tinea  flava  affects  the  face  more 
frequently  than  any  other  part  of  the  body,  and  is  curable  only 
with  difficulty. 

Tinea  Alba. — Occasionally  there  may  be  some  difficulty  in  dis- 
tinguishing tinea  flava  of  a  light  variety  from  tinea  alba.  In  con- 
trast to  tinea  flava,  the  patches  of  tinea  alba  are  not  smooth,  and 
the  fungi  belong  to  the  genera  Trichophyton  and  Epidermophyton. 


Fig.  826. — Tinea  Flava  on  the  Back  of  a  European. 


Tinea  Flava  and  Pinta  are  easily  distinguished  by  the  characters 
of  their  respective  fungi,  the  fungus  found  in  pinta  never  having 
the  characters  of  a  Malassezia. 

Lenco derma  patches  have  a  characteristic  dead-white  colour, 
are  often  surrounded  by  a  hyperpigmented  border,  and  no  fungus 
is  found. 

In  Circumscribed  Scleroderma  (Morphoea)  the  patches  may  present 
a  peculiar  yellowish  tinge,  which  in  coloured  patients  may  resemble 
tinea  flava.  In  tinea  flava,  however,  there  is  no  change  in  the 
texture  of  the  skin,  which  is  still  pliable,  and  does  not  exhibit  the 


2078  TROPICAL  DERMATOMYCOSES 

peculiar  parchment-like  feeling  of  scleroderma.  The  microscopical 
examination  will  clear  the  diagnosis  in  any  doubtful  case. 

In  Europeans,  tinea  flava,  taking  often  a  reddish  colour  (hence  the 
term  '  tinea  rosea  '),  especially  if  the  patient  has  been  exerting  him- 
self and  is  perspiring,  might,  on  superficial  examination,  be  mis- 
taken for  a  form  of  Seborrhea  corporis.  The  microscopical  examina- 
tion will  clear  the  diagnosis,  no  Malassezia  fungus  being  found  in 
seborrhcea  corporis. 

Treatment. — Tinea  flava  shows  no  tendency  to  spontaneous  cure, 
unless  the  patient  moves  to  a  cold  climate.  Even  then,  very  often 
the  cure  is  only  apparent,  as  the  condition  reappears  during  the 
hot  weather.  The  treatment  is  difficult.  Turpentine  applied  daily, 
followed  by  a  naphthol  or  epicarin  ointment  (2  to  5  per  cent.),  or 
a  salicylic-resorcin  ointment  (resorcin  31.,  acidi  salicyli  gr.  x., 
vaselini  §i.),  is  often  successful,  but  the  treatment  must  be  con- 
tinued for  months.  On  covered  parts  of  the  body  tincture  of  iodine 
may  be  used,  or  a  chrysarobin  ointment  (2  per  cent.). 

It  is  to  be  noted  that  in  several  cases  the  fungus  of  tinea  flava  has  apparently 
a  deep  permanent  disturbing  action  on  the  pigmentation  processes  of  the 
skin,  as,  even  when  the  fungus  has  been  destroyed,  the  patches  may  remain 
of  a  lighter  colour  than  the  surrounding  skin  for  a  long  time,  though  ultimately 
they  become  again  normally  pigmented. 


TINEA  NIGRA. 

Synonyms. — Pityriasis  Nigra  (Castellani),  Microsporosis  Nigra 
(Castellani). 

This  affection  is  fairly  common  in  India,  Ceylon,  Java,  Federated 
Malay  States,  and  China.  The  first  account  of  this,  or  a  very 
similar,  dermatomycosis  was  published  by  Manson  in  China  in 
1872.  Manson's  observations,  however,  were  forgotten,  as  they  were 
not  quoted  by  him  in  his  subsequent  works.  Castellani,  in  1905, 
redescribed  the  disease  in  Ceylon,  and  succeeded  in  growing  the 
fungus.  j 

/Etiology. — The  affection  is  caused  by  a  fungus  of  the  genus 
Cladosporium — C.  mansoni  CasteUani,  1905.  The  fungus  is  found 
very  abundantly  in  the  lesions;  the  mycelial  elements  are  rather 
short — 18  to  20  fj,  in  length,  and  2\  to  3J  jll  in  breadth.  Sometimes 
they  may  be  irregular  in  outline,  bent,  banana-shaped.  The  spores 
are  globular,  and  most  of  them  very  large — 5  to  8  fi.  They  are 
frequently  arranged  in  clusters. 

The  fungus  is  easily  cultivated  by  inoculating  scrapings  of  the  affected 
patches  on  maltose  agar.  After  two  to  four  days  roundish  hemispheric  colonies 
appear,  which  are  black,  but  at  first  have  usually  a  greenish  tinge,  and  may 
present  at  the  periphery  some  radiating,  delicate,  pale  greenish  hyphae. 
These  colonies  may  remain  separate  or  more  often  gradually  coalesce  into  a 
jet-black  knobby  mass,  deeply  rooted  into  the  medium. 

The  fungus  grows  well,  though  less  abundantly,  on  the  other  sugar  agars, 
and  also  on  ordinary  agar.     In  broth  and  peptone-water  the  growth  is  very 


PLATE    XII. 


TINEA   FLAVA  ON   THE   FACE   and 
TINEA   NIGRA   ON   THE   NECK. 


GeoWiterstoiv  1  Sons  Ltd  Edm 


To  fact  page  207  S 


TINEA  NIGRA 


2079 


slow,  and  takes  place  at  the  bottom  of  the  tubes,  with  formation  of  a  black 
or  greenish-black  sediment. 

The  optimum  temperature  for  the  growth  of  the  fungus  is  betwen  300  and 
320  C.;  above  350  C.  and  under  250  C.  the  growth  is  much  slower,  and  may  be 
nil  under  200  C.     Further  details  on  the  fungus  may  be  found  on  p.  1100. 

Symptomatology. — The  affected  parts  are  of  a  black,  dull,  lustre- 
less colour,  much  darker  than  the  surrounding  dark,  healthy  skin 
of  the  native.  The  patches  may  be  small,  roundish,  and  separated 
from  one  another,  or  may  coalesce;  the  patches  are  often  slightly 
elevated,  and  may  present  a  slight  desquamation.  Little,  if  any, 
pruritus  is  present.  The  face  is  not  usually  affected,  though  the 
eruption  may  be  found  on  practically  any  other  region  of  the  body. 
The  neck  and  upper  portion  of  the  chest  are  apparently  the  regions 
most  frequently  affected.  Tinea  nigra  usually  attacks  natives. 
We  have,  however, 
seen  it  also  in  one  of 
our  European  patients, 
who  went  for  a  pleasure 
trip  to  Burma,  where 
he  remained  about  a 
month.  On  coming 
back  to  Ceylon,  he 
noticed  a  small, 
roundish,  very  slightly 
elevated,  non-desqua- 
mating, black  patch 
on  the  palm  of  his  left 
hand.  There  was  no 
pruritus.  The  patch 
spread  slowly  for  two 
months,  reaching  the 
size  of  a  sixpenny- 
piece.  It  disappeared 
after  a  single  applica- 
tion of  formalin ;  three 
months  later  it  re- 
appeared in  the  same  place  as  a  tiny  black  dot,  which  slowly 
spread.  Another  application  of  formalin  caused  it  to  again  dis- 
appear. From  the  patch  a  fungus  was  grown  identical  with  the  one 
found  in  native  cases. 

Mixed  Infections. — A  mixed  infection  of  tinea  nigra  and  tinea 
flava  is  somewhat  frequently  met  with.  Several  of  our  patients 
had  on  the  neck  a  few  round  patches  of  tinea  nigra,  and  on  the 
face  some  smooth,  yellow,  roundish  patches  of  tinea  flava. 

Diagnosis. — The  characters  of  the  fungus,  and  the  fact  that  the 
disease  is  easily  curable,  readily  distinguish  tinea  nigra  from 
pinta.  Pityriasis  versicolor  is  generally  of  lighter  colour  than  tinea 
nigra,  and  the  fungus  (Malassezia  versicolor)  is  morphologically  very 
different,  and  cannot  be  grown.  In  chloasma  bronzinum  no  fungus 
is  found. 


Fig.  827. — Fungus  of  Tinea  Nigra. 


2o8o 


TROPICAL  DERMATOMYCOSES 


Treatment. — The  disease  is  easily  curable,  except  when  it  attacks 
the  palms  of  the  hands,  where  the  treatment  must  be  more  pro- 
longed. A  salicylic-alcoholic  lotion  (2  per  cent.),  foUowed  by  a 
resorcin  ointment  (resorcin,  3i-;  vaseline,  §i.),  answers  well.  When 
the  patches  are  small,  pure  formalin  may  be  used  with  care. 


ERYTHRASMA. 

This  affection  is  frequently  met  with  in  the  tropics,  and  is 
common  on  the  continent  of  Europe,  though  apparently  rare  in 
America. 

/Etiology. — It  is  caused  by  a  fungus  discovered  by  Burchardt 
in  1859 — Nocardia  minutissima  Burchardt.     This  hyphomycete  is 

very  delicate  and  slender,  less  than 
1  jul  in  breadth;  is  found  in  the 
superficial  horny  layer  of  the  affected 
parts.  Ducrey  and  Reale  claim  to 
have  succeeded  in  cultivating  it,  but 
their  results  have  not  been  confirmed. 
The  description  of  the  fungus  is  found 
on  p.  1061. 

Symptomatology. — The  eruption 
generally  affects  the  genito-crural  and 
axillary  regions,  but  may  occasionally 
spread  to  other  parts  of  the  body.  It 
is  characterized  by  the  presence  of 
brownish-reddish  patches,  rounded  or 
irregularly  shaped,  but  with  well-defined 
borders.  The  borders  are  not  elevated; 
the  surface  of  the  patches  appears 
slightly  furfuraceous,  and  has  often 
a  somewhat  greasy  feeling.  There  are 
no  subjective  symptoms,  except  occa- 
sionally slight  itching. 

Diagnosis.  — -  Erythrasma  is  easily 
distinguished  from  tinea  versicolor 
and  tinea  flava  by  the  reddish  tinge  generally  present;  by  the 
characteristic  difference  of  its  sites  of  development,  and  by  the  micro- 
scopical examination,  which  will  reveal  the  presence  of  Nocardia 
minutissima  Burchardt,  a  fungus  morphologically  very  different 
from  Malassezia  furfur  £  Robin  or  M.  tropica  Castellani.  The 
differential  diagnosis  from  tinea  cruris  has  been  discussed  in  this 
chapter  under  the  heading  Tinea  Cruris  (p.  2042). 

As  first  noticed  by  Manson,  after  tinea  cruris  has  been  cured,  the 
genito-crural  region  may  in  some  cases  present  for  years  a  peculiar 
brownish  discoloration,  and  be  slightly  furfuraceous — a  condition 
resembling  erythrasma;  in  such  cases  neither  Epidermophyton 
cruris  Castellani  nor  Nocardia  minutissima  Burchardt  will  be  found. 
Treatment. — Washing  the  parts  with  ordinary  soap  and  warm 


Fig.  828. — Erythrasma. 


BLASTOMYCOSIS 


2081 


water,  carbolic,  tar,  or  sand-soap,  and  then  regularly  applying  a 
resorcin-salicylic  ointment  (resorcin,  gr.  x.  to  xxx. ;  ac.  salicyl., 
gr.  x.  to  xx.;  vaseline,  §i.),  will  soon  cause  the  eruption  to  disap- 
pear. Instead  of  the  ointment,  a  hyposulphite  of  soda  (1  drachm 
to  1  ounce)  or  sulphurous  acid  lotion  may  be  used. 

BLASTOMYCOSIS. 

Synonyms. — Saccharomycosis  Hominis,  Oidiomycosis,  Dermatitis 
Blastomycetica,  Blastomycetic  Dermatitis,  Zymonematosis. 

Definition. — The  term  blastomycosis  covers  a  group  of  closely 
allied  pathological  conditions  due  to  fungi  of  the  genera  Saccharo- 
myces,  Cryptococcus,  Coccidi- 
oides,  Oidium,  and  Monilia, 
generally  characterized  by  the 
presence  of  warty  patches  and 
minute  epidermal  abscesses. 

Historical  and  Geographical. 
• — Wernike,  in  1890,  described 
in  Buenos  Ayres  two  cases  of 
papillomatous  eruption  in 
which  he  found  peculiar  bodies 
which  were  at  first  considered 
to  be  protozoa,  hence  the  disease 
was  called  '  protozoic  derma- 
titis.' Later  Gilchrist  and 
Ophiils  showed  them  to  be 
vegetal  parasites.  Gilchrist,  in 
1894,  described  yeast-like 
organisms  in  sections  taken 
from  a  scrofuloderma-like 
eruption.  In  the  same  year, 
independently,  Busse  and 
Buschke  published  a  case  of 
a  pyaemia-like  condition  due 
to  a  Cryptococcus.  The  disease 
has  been  investigated   chiefly 


Fig.  829.- 


-Blastomycosis  of  Leg. 

by  American  observers,  among  whom  Ricketts,  '(Ormsby,  Hyde, 
Montgomery,  and  Pusey  may  be  mentioned.  The  malady  occurs 
in  the  tropics,  and  one  of  us  has  reported  several  cases  from  Ceylon, 
while  Phalen  and  Nichols  have  described  numerous  cases  from  the 
Philippine  Islands,  Leger  two  cases  in  Tonkin,  and  Lutz,  Splendore, 
and  others,  cases  from  South  America. 

/Etiology. — The  fungi  found  belong  to  the  genera  Saccharomyccs, 
Cryptococcus,  Coccidioides,  Monilia,  including  in  the  last-mentioned 
genus  the  following  non-sufficient ly  defined  genera:  Zymonema, 
Parasaccharomyces,  Parendomyces.  The  description  of  these  fungi  is 
found  in  Chapter  XXXIX.,  p.  1035.  There  are  also  higher,  not  yet 
well-determined   fungi,    all   of   which   are   apparently   capable   of 

131 


2082 


TROPICA L  DERMA  TOMYCOSES 


inducing  identical  clinical  conditions.     In  the  tissues  all  the  organ- 
isms exist  as  yeast-like,  oval,  or  roundish  cells. 

Among  the  organisms  which  cause  the  disease,  Ricketts  distinguished  four 
types: — 

i.  Blastomycetoid  or  yeast-like  type:  reproduction  by  budding;  in  cultures 
only  oval  or  roundish  cells  are  seen,  while  mycelial  tubes  are  as  a  rule  absent. 

2.  Cryptococcus-like  type:  reproduction  by  endosporulation  within  the 
tissues. 

3.  Endomyces-liketype:  the  cultures  present  abundant  submerged  mycelium, 
which  breaks  up  into  chains  of  endoconidia;  proliferation  by  budding  is  rare. 

4.  Hyphomycetoid  type:  cultures  present  aerial  hyphae  and  submerged 
mycelium;  proliferation  by  gemmation  occasionally  seen.  There  are  many 
transition  forms  between  these  four  groups. 


Fig.  830. — Blastomycosis  of  the 
Upper  Lip:  Ulcerative  Stage. 


Fig.  831. — Blastomycosis  of 
the  Mouth. 


(From  a  case  in  the  Colombo  Clinic.)        (From  a  photograph  by  Splendore.) 


Histopathology. — There  is  marked  proliferation  of  the  epithelial 
layers,  with  elongated,  irregularly  shaped  down-growths  into  the 
corium,  and  epithelial  globi  are  seen.  The  cells  of  the  rete  are 
swollen,  and  there  is,  between  the  cells,  a  polymorphonuclear  leuco- 
cytic  infiltration.  Here  and  there  minute  miliary  abscesses  are 
present.  In  these,  numerous  polymorphonuclear  and  mononuclear 
leucocytes  are  found,  also  epithelioid  cells  and  giant  cells,  some 
containing  the  parasite.  It  is  in  the  miliary  abscesses  that  -the 
organism  is  mostly  found.  The  corium  presents  a  general  cellular 
infiltration  made  up  of  polymorphonuclear  leucocytes  and  young 
<  o  ri  jctive-tissue  cells.  The  vessels  are  dilated  and  their  walls 
thickened.     Sp'endore  has  noted  that  when  the  lymphatic    glands 


BLASTOMYCOSIS 


2083 


are  affected,  which  is  of  rare  occurrence,  they  may  present  histo- 
logically a  tubercular  appearance. 

Symptomatology.— The  disease,  as  seen  by  us  in  Ceylon,  is 
characterized  by  the  presence  of  elevated  warty  patches  showing, 
especially  at  their  margins, 
minute  epidermal  abscesses, 
and  often  small  ulcers 
covered  by  yellowish  crusts. 
The  eruption  may  be  gyrate. 
The  lesions  at  a  later  stage 
may  become  more  deeply 
ulcerated,  the  process  of 
ulceration  generally  begin- 
ning at  their  centre.  There 
is  very  little  or  no  pain, 
and  very  slight  or  no  pruritus. 
The  lesions  may  heal  spon- 
taneously, leaving,  as  a  rule, 
soft,  smooth  scars.  Occa- 
sionally the  affection  recom- 
mences afte~  a  time  in  the^scar.  The  lymphatic  glands  are  not 
often  involved.  In  some  cases  subcutaneous  abscesses  and  gumma- 


Fig.  832. — Blastomycotic  Ulcer. 
(From  a  photograph  by  Splendore.) 


Fig.  833. — Blastomycosis  Glutealis. 
(From  a  case  in  the  Colombo  Clinic.) 

like  swellings  may  be  formed.  All  regions  of  the  body  may  be 
affected.  The  course  is  very  chronic,  the  disease  lasting  often  for 
many  years. 


2o84  TROPICAL  DERMATOMYCOSES 

Clinical  Varieties. — Several  varieties  can  be  distinguished: — 

i.  The  common  cutaneous  type,    or  North  American  and 
Asiatic  type. 

2.  The  oro-pharyngeal  blastomycosis. 

3.  The  Coccidioides  blastomycosis. 

4.  The  gluteal  blastomycosis. 

1.  Common  Cutaneous  Type. — The  description  we  have  given 
of  the  disease  refers  to  this  type,  which  is  quite  common  in  Ceylon. 
Southern  India,  Philippine  Islands,  Indo-China,  Tonkin,  and  prob- 
ably in  many  other  parts  of  the  tropics.  A  very  frequent  localization 
in  Ceylon  is  the  upper  lip  (see  Fig.  830),  the  disease  extending 
later  occasionally  to  the  nasal  mucosa,  and  very  rarely  to  the 
oral  mucosa.  In  several  of  our  cases  a  monilia-like  fungus  was 
grown. 

2.  Oral  Blastomycosis. — This  variety  has  been  investigated  by 
Lutz  and  Splendore  in  South  America.  Splendore  considers  the 
fungus  to  be  a  Zymonema,  and  calls  the  disease  zymonematosis. 
As  most  authorities  do  not  accept  the  genus  Zymonema,  we  place  the 
fungus  in  the  genus  Monilia  (see  p.  1079).  The  skin  lesions 
are  identical  with  those  found  in  the  common  type  of  the  malady, 
but  the  infection  spreads  to  the  oral  mucosa,  lips,  gums,  soft  and 
hard  palate,  giving  rise  to  numerous  small,  verrucoid,  papillomatous, 
or  frambcesiform  patches,  which  later  may  undergo  deep  ulceration. 
The  disease  later  invades  the  pharynx,  nose,  larynx,  and  bronchi, 
and  often  terminates  fatally. 

3.  Blastomycosis  Coccidioides  (synonym,  Protozoic  disease)  was 
described  by  Wernike  of  Buenos  Ayres  in  1890,  and  later  by  Posadas ; 
it  was  further  investigated  by  Ophiils,  Mofht,  and  others.  It  was 
at  first  considered  to  be  of  protozoal  origin.  The  lesions  on  the 
skin  are  somewhat  similar  to  those  found  in  the  more  usual  type  of 
blastomycosis — viz.,  verrucose  patches  with  minute  epidermal 
abscesses— but  are  generally  of  larger  size,  and  visceral  complications 
are  the  rule,  the  malady  terminating  almost  always  fatally.  In  the 
affected  tissues  peculiar  large  structures  are  seen,  some  of  which 
may  contain  as  many  as  100  spore-like  bodies  (see  p.  985). 

4.  Gluteal  Blastomycosis— -This  condition  was  described  by  Kar- 
tulis  some  years  ago  in  Egypt.  We  have  often  observed  it  in 
Ceylon.  The  skin  of  the  gluteal  region — one  nate  or  both  nates — 
presents  a  diffuse  induration,  and  is  cribrated  with  the  opening 
of  sinuses,  from  which  a  thin  pus  exudes.  The  sinuses  may  be 
very  deep  and  connected  with  each  other,  but  in  our  cases  did 
not  communicate  with  the  intestine.  The  pus  does  not  contain 
grains,  as  is  the  case  with  actinomycosis.  The  patient  may  com- 
plain of  pain  and  discomfort  on  sitting  down.     The  disease  is  chronic. 

Maxwell  has  reported  from  Formosa  cases  of  a  fistulous  disease  of  the 
buttocks,  which  may  be  of  the  same  nature.  He  is  inclined,  however,  to 
consider  them  to  be  of  amoebic  origin. 


BLASTOMYCOSIS 


2085 


Diagnosis. — This  is  based,  in  the  usual  type  of  the  malady,  on 
the  presence  of  verrucose  patches  with  micro-abscesses,  in  which  the 
fungi  are  found.  The  disease  has  been  often  confused  with  tubercu- 
losis verrucosa,  with  a  syphilide,  with  an  epitheliomatous  lesion, 
and,  in  the  tropics,  with  atypical  frambcesia  and  even  ringworm. 
The  microscopical  examination  and  cultivation  of  scrapings,  or, 
better,  of  the  pus  of  the  miliary  abscesses  present  in  the  lesions,  will 
be  necessary  to  clear  the  diagnosis.  A  droplet  of  the  pus,  or  a 
minute  portion  of  teased  tissue,  is  placed  on  a  slide  with  a  drop 
of  a  30  per  cent,  solution  of  potassium  hydrate,  and  a  cover-glass 
is  placed  on  the  preparation;  after  about  half  an  hour  in  a  temperate 
climate,  and  generally  a  few  minutes  only  in  a  tropical  climate,  the 
tissue  and  pus  cells  are  disinte- 
grated by  the  potash  solution,  while 
the  organisms,  being  resistant,  can 
be  easily  seen.  Cultures  should 
also  be  made  from  the  pus.  It 
is   important  to   note  that   yeast- 


Fig.  834. — Fungus  found  in  Der- 
matosis Hyphomycetica  Indica. 
(Broth  Culture.) 


Fig.  835. — Dermatosis  Hypho- 
mycetica Indica  (see 
p.  2086). 


like  organisms  may  be  frequently  found  as  saprophytes  on  the 
surface  of  various  ulcerated  skin  lesions,  which  have  nothing  to  do 
with  true  blastomycosis. 

Oral  blastomycosis  may  occasionally  be  confused  with  espundia, 
from  which  it  is  differentiated  by  the  absence  of  Leishmania  and 
presence  of  fungi.  Blastomycosis  coccidioides  is  easily  diagnosed  by 
the  presence  of  bodies  containing  numerous — as  many  as  100 — 
endospores.  Gluteal  blastomycosis  is  distinguished  from  actino- 
mycotic and  mycetomatous  conditions  by  the  absence  of  the  grains 
and  the  characters  of  the  fungi;  from  a  syphilitic  condition  by 
the  inefficacy  of  a  mercurial  treatment;  from  tubercular  fistulous 


2086  TROPICAL  DERM ATOM Y COSES 

disease  by  the  massive  diffuse  induration,  and  absence  of  tuber- 
cular cutireaction. 

Prognosis. — The  disease  very  rarely  heals  spontaneously.  The 
general  health  in  the  common  type  of  the  malady  is  not  much 
affected,  but  the  patients  complain  of  the  disfigurement.  Occa- 
sionally the  organisms  from  the  skin  lesions  enter  the  general  cir- 
culation, and  a  condition  similar  to  pyaemia  develops.  Cases  of 
systemic  blastomycosis  terminating  fatally,  without  any  skin  lesion, 
have  also  been  described.  The  prognosis  of  blastomycosis  cocci- 
dioides  and  oral  blastomycosis  is  bad,  while  blastomycosis  glu- 
tealis  is  most  persistent,  though  the  general  health  is  not  much 
affected. 

Treatment. — Potassium  iodide,  given  in  large  doses  (gr.  xv.  to  xx. 
three  or  four  times  daily),  has  a  beneficial  effect,  though  it  is  not 
so  efficacious  as  in  sporotrichosis.  The  application  of  Rontgen  rays 
to  the  lesions  is  useful.  In  mild  cases  the  local  application  of  various 
disinfectants — e.g.,  perchloride  of  mercury  (i  in  1,000),  diluted 
tincture  of  iodine,  etc.,  may  bring  about  a  cure.  The  following 
ointment  is  useful,  especially  in  the  localization  to  the  upper  lip: 
Ichthyol,  gr.  xv. ;  ung.  belladonnas,  3ii. ;  vaselini,  ad  §i.  No 
treatment  is  apparently  of  much  use  in  blastomycosis  cocci- 
dioides,  in  oropharyngeal  blastomycosis,  or  in  blastomycosis 
glutealis. 

Dermatosis  Hyphomycetica  Indica. — This  term  has  been  used  by  Castellani 
to  indicate  a  peculiar  hyphomycetic  condition  he  has  once  seen  in  Ceylon. 
The  patient  had  a  number  of  gummatous  swellings  and  indurated  patches, 
but  no  warty  lesions  were  present  anywhere.  A  fungus  was  isolated  which 
in  various  sugar  broths  and  ordinary  broth  produced  very  long  filaments, 
but  owing  to  an  accident  could  not  be  further  studied. 


SPOROTRICHOSIS. 

Schenk,  in  1898,  described  a  case  of  multiple  chronic  abscesses  in 
the  pus  of  which  a  Sporotrichum  was  found.  Hektoen  and  Perkins 
reported  two  similar  cases  also  in  the  United  States  in  1900.  De 
Beurmann  published  in  1903  a  case  of  similar  nature  in  France. 
De  Beurmann  and  Gougerot,  from  1906  onwards,  have  published 
many  cases,  and  have  completely  investigated  the  subject  of  human 
sporotrichosis  bacteriologically  and  histologically,  as  well  as 
clinically.  Their  researches  have  been  confirmed  by  Gaucher 
and  Monier-Vinard,  Duval  and  Fago,  Vaquez,  Bonnot,  Lambry, 
Adamson,  Esmeni,  and  many  others.  Cases  have  been  reported 
from  the  tropics  by  Lutz  and  Splendore  in  Brazil,  and  by  us  in 
Ceylon.  Clair  has  observed  the  disease  in  Arab  stokers  on  board 
some  steamers  of  the  Messageries  Maritimes  Company. 

/Etiology. — The  fungi  causing  the  disease  belong  to  the  genus 
Sporotrichum  Link,  1809,  of  which  nine  species  have  been  so  far 
described  in  man: — 


SPOROTRICHOSIS 


2087 


(S.  schenki  Hektoen  and  Perkins,  190 1. 
5.  beurmanni  Matruchot  and  Ramond,  1905. 
S.  dori  de  Beurmann  and  Gougerot,  1906. 
S.  gougeroti  Matruchot,  1910. 
Sporotrichum  Link,  1809  \  S.  jeanselmei  Brumpt  and  Langeron,  1910. 
S.  indicum  Castellani,  1908. 
S.  asteroides  Splendore,  1909. 
S.  lesnei  Vuillemin,  19 10. 
S.  councilmani  Wolbach,  Sisson  and  Meier,  191 7. 

For  the  description  of  these  organisms,  see  chapters  on  Fungi 
(p.  1117). 

The  species  so  far  found  in  the  tropics  are — S.  beurmanni  Matru- 
chot and  Ramond  in  Brazil  and  Africa,  S .' asteroides  Splendore,  1909, 
in^Brazil,  and  S.  indicum  Castellani,  1908,  in  Ceylon.  These  fungi 
are  morphologically  very  similar.  In  the  human  lesions  the  fungus 
appears  morphologically  as  a  yeast,  and  is  very  scarce.  In  cultures 
mycelial  threads  and  numerous  spores  are  seen.  The  spores  are 
ovoid,  5  to  6  n  in  length  by  3  to  4  ^  in  breadth.  The  mycelial 
filaments  are  very  slender  (2  p)  in  S.  beurmanni  and  S.  schenki  ; 


Fig.  836. — Sporotrichic  Lymphangitis. 
(From  a  photograph  by  Splendore.) 


somewhat  broader  (21  to  3  /*)  in  S.  indicum.  S.  asteroides  is 
characterized  by  the  presence  of  peculiar  radiate  bodies  in  the 
affected  tissues.  These  fungi  grow  easily  on  the  ordinary  culture 
media,  best  of  all  on  Sabouraud's  peptone-glucose  agar.  Colonics 
develop  from  the  fourth  to  the  tenth  day  as  small  white  points, 
surrounded  by  a  delicately  rayed  aureola  of  whitish  colour.  They 
gradually  increase  in  size,  coalesce,  become  convoluted,  and  take 
a  dark  greyish,  brownish,  and  even  black  colour.  These  fungi, 
according  to  De  Beurmann,  may  perhaps  live  saprophytic  on  veget- 
ables (lettuce-leaves,  and  other  kinds  of  vegetables  used  as  salads) 
and  on  insects  (flies,  caterpillars,  larvae).  According  to  De  Beur- 
mann, infection  takes  place  by  contact  with  unclean  vegetables. 


2088  TROPICAL  DERMATOMYCOSES 

The  fungi  may  also,  apparently,  live  saprophytically  in  the  oral 
cavity  and  pharynx  of  certain  individuals,  who  then  become  carriers. 

The  rat,  mouse,  monkey,  cat,  and  very  young  guinea-pigs,  are  all 
more  or  less  susceptible,  and  may  be  infected  by  subcutaneous  or 
intraperitoneal  inoculation.  The  rat  is  the  most  susceptible 
animal.  In  it  Lutz  and  Splendore  have  described  a  spontaneous 
sporotrichosis  due  to  a  Sporotrichum  apparently  identical  with 
S.  beurmanni.  Moore  and  Davis  have  described  a  case  following 
the  bite  of  a  field-mouse.  The  patient's  blood  agglutinated  equally 
well  S.  schenki  and  5.  beurmanni.  The  affection  has  also  been 
observed  to  occur  spontaneously  in  the  dog  (Gougerot  and  Caravan) 
and  in  the  mule  (Fontoynont  and  Carougeau)  in  Madagascar. 

Histopathology. — The  histopathology  of  the  cases  due  to  S. 
beurmanni  has  been  investigated  by  De  Beurmann  and  Gougerot; 
that  of  the  cases  due  to  S.  asteroides  by  Splendore;  that  of  the 
cases  due  to  S.  indicum  by  ourselves.  Whatever  the  causative 
species  of  Sporotrichum,  the  histological  lesions  are  apparently 
the  same,  and  correspond  to  the  three  principal  types  described 
by  De  Beurmann  and  Gougerot — viz.,  (i)  An  epithelioid  type, 
with  presence  of  giant  cells — this  corresponds  to  the  tuberculoid 
type  of  De  Beurmann  and  Gougerot;  (2)  a  lympho-connective 
tissue  or  syphiloid  reaction;  (3)  a  polymorphonuclear  or  ecthy- 
matiform  type. 

Symptomatology. — In  a  well-marked  case,  several  gummatous- 
like  swellings,  situated  in  the  subcutaneous  tissue,  are  present  on 
various  parts  of  the  body — the  arms,  legs,  and  trunk.  The  size 
varies  from  that  of  a  small  pea  to  that  of  an  orange.  On  palpation, 
they  are  hard,  resistant  at  first ;  later  they  soften,  the  skin  becomes 
reddish  or  violaceous  and  after  a  time  perforates.  From  the 
fistulous  opening  a  yellowish  homogeneous  pus  is  slowly  evacuated. 
or  at  times  a  thin  serous  discharge.  In  some  cases  the  suppuration 
ceases,  granulation  sets  in,  and  a  coarse  cheloid-like  scar  remains. 
In  other  cases  the  fistulous  opening  enlarges  and  a  crateriform 
ulcer,  with  often  a  fungating  fundus,  develops.  The  lymphatic 
glands  may  occasionally  become  affected.  The  course  of  the  disease 
is  very  chronic.  In  some  cases  deep  gummata  develop  under  the 
periosteum  of  various  bones,  and  in  the  muscles.  Large  granulating 
ulcerations  may  form  in  the  buccopharynx  and  larynx  The  general 
health,  as  a  rule,  is  not  much  affected. 

Clinical  Varieties. — The  commonest  varieties  met  with  are: — 

1.  The  localized  type,  with  sporotrichic  chancre  and  ascending 
sporotrichic  lymphangitis. 

2.  The  disseminated  gummatous  type. 

3.  The  disseminated  ulcerative  type,  presenting  often  poly- 
morphic lesions — viz.,  syphilitic-like,  tubercular-like,  ecthymatous, 
rupial,  furuncular. 

4.  The  extracutaneous  type,  with  sporotrichic  lesions  of  the 
mucous  membranes,  the  muscles,  the  articulations,  the  bones,  the 
organs  of  special  sense,  the  internal  organs — lungs,  kidneys,  etc. 


ACLADIOSIS  2089 

De  Beurmann  has  put  on  record  a  case  of  mycetoma  of  sporotrichic  origin. 
Cases  of  systemic  sporotrichosis  have  been  described. 

Diagnosis. — The  principal  clinical  signs  on  which  to  base  a 
probable  diagnosis  of  sporotrichosis  are  the  presence  of  gumma-like 
lesions  while  the  patient  is  in  a  good  general  state  of  health;  the 
mixture  of  lesions  of  different  appearance;  partial  cup-shaped 
softening  of  the  nodes,  breaking  down  in  the  centre  and  ending  in 
ulceration,  with  violaceous  edges  generally  undermined;  presence 
of  viscous  pus  or  of  a  serous  lemon-yellow  discharge;  indolent 
evolution;  absence  in  most  cases  of  enlarged  glands.  The  definite 
diagnosis  can  only  be  made  by  bacteriological  methods.  The  simple 
microscopical  examination  of  the  pus  of  the  abscesses,  or  scrapings 
of  the  ulcers,  is  not  sufficient,  as  the  fungus  is  extremely  scarce. 
Cultivation  must  be  resorted  to.  A  few  glucose-agar  tubes  are 
inoculated,  and  kept  at  room-temperature  without  capping.  After 
four  to  ten  days  the  first  colonies  of  Sporotrichum  will  appear. 

Treatment.— Potassium  or  sodium  iodides  in  full  doses  (15.^0 
20  grains  three  to  four  times  daily),  well  diluted  in  water  or  milk, 
induce  a  rapid  disappearance  of  all  the  lesions.  In  persons  who 
cannot  take  potassium  iodide,  saiodin  in  the  same  dose  may  be 
given  in  cachets.  The  ulcerated  lesions  may  be  dressed  with  a 
lotion  of  potass,  iodide  10  parts,  iodine  1  part,  water  500  parts. 
Surgical  measures  should  be  avoided. 

Pinoy  has  noted  that  the  action  of  the  iodides  is  increased  by  a  salt -free  diet. 

Prophylaxis. — Any  small  wound  should  be  disinfected  with  tr.  iodi. 

ACLADIOSIS. 

Definition. — An  ulcerative  dermatomycosis  caused  by  Acladium 
castellanii  Pinoy. 

Historical  and  Geographical  Distribution.— The  condition  has  been 
observed  by  Castellani  since  1907  in  Ceylon,  but  he  did  not  fully 
describe  it  until  1916.  Cases  have  been  observed  in  Ceylon,  the 
Federated  Malay  States,  and  Macedonia. 

./Etiology. — The  condition  is  caused  by  a  fungus  which  Castellani 
isolated  in  Ceylon.  Cultures  were  sent  to  Professor  Pinoy,  of  the 
Pasteur  Institute,  who  investigated  it  botanically  and  classified  it, 
giving  it  the  name  of  Acladium  castellanii  Pinoy,  1916.  Professor 
Pinoy's  description  may  be  quoted: — 

'  The  growth  on  artificial  media  (such  as  carrot,  potato,  glucose  agar) 
consists  of  many  small  roundish  masses,  which  later  on  may  coalesce,  covered 
by  spiculated  formations,  giving  them  a  prickly  appearance,  and  consisting  of 
erect,  straight  filaments,  parallel  to  each  other,  or  at  times  interlacing.  These 
filaments  are  approximately  2  microns  in  diameter,  and  carry  laterally  pseudo- 
conidia  of  variable  shape,  cylindriform,  pyriform,  or  spherical,  attenuated  in 
size  at  their  points  of  insertion.  Most  of  these  pseudoconidia  are  4  microns 
in  length,  with  a  breadth  of  3  microns.  This  type  of  fructification  recalls 
the  type  Acladium  described  by  Bodin  in  certain  species  of  the  genus 
Trichophyton  (Malmsten,  1848). 

'  These  pseudoconidia  become  detached  and  then  develop  by  sprouting, 
and   mycelial   filaments   are   formed.     Certain    filaments   produce   spherical 


2ogo  TROPICAL  DERMATOMYCOSES 

chlamydospores  arranged  in  small  strings,  as  found  in  certain  fungi  oi  the 
genus  Fusarium.  These  small  chains  of  chlamydospores  are  very  frequently 
terminal,  the  dimensions  being  variable — 8-10  microns  '  (Fig.  595.  p.  1113)- 

In  cultures  on  carrot  and  potato  the  colonies  are  white,  on  glucose 
agar  often  amber  colour.  Very  old  cultures  may  show  a  certain 
amount  of  pigmentation  (see  p.  1112). 

Histopathology. — The  histopathological  investigation  of  the  con- 
dition is  far  from  completed.  From  the  preliminary  investigation  it 
would  seem  that  the  lesions  are  very  similar  to  those  one  sees  in 
sporotrichosis,  and  that  three  types  of  lesions  may  be  distinguished: 

(1)  An  epithelioid  or  tuberculoid  type,  with  presence  of  giant  cells; 

(2)  a  lympho-connective  tissue  type  (syphiloid) ;  (3)  polymorphonu- 
clear type  (ecthymatous). 

Clinical  Symptoms. — In  a  well-marked  case  ulcerative  lesions  are 
present  all  over  the  body,  though  they  are  in  smaller  number  or 
absent  altogether  on  the  face,  scalp,  palms,  and  soles.  Most  of  the 
ulcers  are  sharply  defined,  roundish  or  oval,  with  red  granulating 
fundus.  Their  appearance  is  well  shown  in  the  illustration,  a 
photograph  of  a  Ceylon  case.  In  many  cases  there  is  abundant 
purulent  secretion,  which  collects  and  dries  up  in  thick  yellow  crusts, 


Figs.  837  and  838. — Acladium  castellanii  Pinoy:  Hanging-Drop 

Culture. 

(a)  After  twenty-four  hours',   (b)  after  three  days'  growth. 

covering  the  ulcers.  Gummata-like  nodules  and  furuncle-like 
lesions  may  be  observed.  The  superficial  lymphatic  glands  may  be 
enlarged.  The  lesions  in  most  cases  give  very  little  pain,  or  none 
at  all ;  itching  is  often  completely  absent,  but  occasionally  the  patient 
complains  of  slight  pruritus.  The  general  condition  of  the  patient 
is  not  seriously  affected  for  a  long  time,  but  he  often  complains  of  a 
certain  degree  of  weakness  and  discomfort.  Not  infrequently  there 
is  serotine  fever.  The  blood  has  been  examined  in  two  cases  in  the 
tropics;  in  one  case  in  the  Balcanic  Zone:  Wassermann  reaction 
negative.  In  the  first  two  cases  red  blood-corpuscles  and  haemo- 
globin were  slightly  below  the  normal;  in  one  there  was  eosinophilia 
(5  per  cent.),  which  may  have  been  due  to  a  concomitant  Ascaris 
lumbricoides  infection.  In  the  Macedonian  case,  the  blood  of  which 
was  examined,  there  was  a  distinct  leucocytosis  (16,000  leucocytes) 


ACLADIOSIS  2091 

of  the  polymorphonuclear  type;  in  this  patient  there  was  abundant 
purulent  secretion  and  serotine  fever,  which  on  some  days  reached 
1020  and  1030  F. 

Diagnosis. — A  positive  diagnosis  can  be  made  with  certainty  only 
by  cultural  methods.  The  microscopical  examination  alone  is  of 
very  little  use,  hyphomycetic  elements  being  as  a  rule  absent  micro- 
scopically in  the  scrapings  from  the  ulcers  and  contents  of  nodules. 
The  material  should  be  inoculated  in  glucose  agar  tubes.  Four  to 
eight  days  after  inoculation  small,  yellowish,  amber-coloured  colonies 
appear;  they  enlarge  fairly  rapidly,  become  hemispheric,  and  often 
coalesce  in  a  knotty  mass.  At  times  the  colonies  may  not  fuse 
together ;  each  colony  then  remains  separate,  reaches  a  large  size,  and 
occasionally  presents  peculiar  radiating  furrows  as  seen  in  certain 
species  of  trichophytons.  In  many  cases  where  the  material  has 
been  collected  from  ulcerated  lesions,  the  fungus  grows  in  symbiosis 
with' a  coccus,  and  it' may  be  difficult  to  separate  the  two  organisms. 


Fig.  839. — Acladiosis  of  the  Arm. 

The  malady  is  often  taken  for  a  syphilitic  condition.  The  history, 
the  negative  examination  of  the  lesions  for  spirochetes,  the  failure 
of  mercury  and  salvarsantreatment,  will  exclude  it.  When  the  lesions 
are  covered  by  raised,  thick,  bright,  yellow  crusts  the  condition  must 
be  differentiated  from  yaws:  in  acladiosis,  on  removing  the  crusts, 
ulcers  are  found,  while  in  yaws,  the  typical  frambcesiform  nodules 
will  be  seen;  in  scrapings  from  yaws  lesions  the  treponema  will  be 
found.  Acladiosis  can  be  differentiated  from  sporotrichosis  and 
other  affections  of  hyphomycetic  origin  by  cultural  methods. 

Prognosis. — The  course  of  the  disease  may  be  very  long,  and 
there  is  very  little  or  no  tendency  to  spontaneous  cure;  but  if  a 
proper  treatment  is  carried  out  a  cure  can  be  obtained  fairly  rapidly 
in  the  majority  of  cases.  A  few  cases  respond  to  treatment  ex- 
tremely slowly. 

Treatment. — Potassium  iodide  given  in  full  doses  (20  gr.  ter  diem) 
acts  satisfactorily.  The  drug  appears  to  act  at  times  more  rapidly 
if  given  according  to  Professor  Pinoy's  method — viz.,  in  conjunction 


2o92  TROPICAL .DERM ATOMYCOSES 

with  a  salt-free  diet.  If  potassium  or  sodium  iodide  is  not  well 
borne,  sajodin  and  other  similar  preparations  may  be  tried,  but  the 
result  is  not  so  satisfactory.  Mercury  and  arsenic  have  no  effect  on  the 
course  of  the  malady.  As  regards  local  treatment,  it  is  sufficient  to 
keep  the  ulcers  clean  by  using  a  weak  mercury  per  chloride  lotion. 

CRYPTOCOCCOSIS  EPIDERMICA. 

Synonym.— Saccharomycosis  epidermica  (Castellani). 

Historical  and  Geographical. — This  condition  was  first  described 
by  Castellani  in  Ceylon.  We  have  recently  found  cases  in  the 
Sudan  and  in  the  Balcanic  Zone. 

etiology. — The  causal  organism  is  Cryptococcas  epidettnidis 
Castellani,  1914. 

Symptomatology.- — The  condition  is  fairly  frequent  in  Europeans 
who  have  resided  for  some  years  in  the  tropics,  but  is  also  found  in 
natives.  It  is  characterized  by  the  presence  on  the  arms,  and  more 
rarely  on  the  chest  and  neck,  of  small  roundish  patches  of  a  dirty 
yellow  or  brownish  colour,  which  can  generally  be  removed  by 
thorough  scraping.  These  patches  consist  of  large  numbers  of 
blastomyces-like  elements  of  various  size,  rounded  or  oval,  which 
so  far  have  not  been  cultivated. 

Treatment. — Thorough  scraping  with  sand-soap  and  hot  water  is 
generally  sufficient  to  remove  the  patches.  In  obstinate  cases  a 
salicylic  sulphur  ointment  is  useful. 

INTERTRIGO  SACCHAROMYCETICA. 

Synonym. — Intertrigo  Blast omycetica. 

Remarks. — Cases  of  this  affection  have  been  observed  by  Castel- 
lani in  Ceylon,  and  similar  ones  have  later  been  reported  by 
Whitfield  and  others  in  Europe.  The  affection  is  apparently  rare. 
It  generally  attacks  the  scroto-crural  and  axillary  regions.  The 
affected  skin  is  red,  and  there  may  be  slight  exudation.  The 
borders  of  the  eruption  are  fairly  well  marked,  but  never  elevated. 
In  most  cases  there  is  not  much  itching,  and  the  affection  may 
recover  spontaneously. 

^Etiology. — In  scrapings  a  Saccharomyces  (S.  samboni  Castellani, 
1907),  which  is  easily  cultivated  on  sugar  media,  is  found,  or  in  other 
cases  fungi  of  the  genus  Monilia. 

Treatment. — The  treatment  consists  in  washing  the  affected  parts 
with  potassium  permanganate  lotion,  1  in  4,000,  or  resorcin,  1  in  100; 
followed  by  the  application  of  powders  of  boric  acid  3L,  talci  §i. ;  or 
salicylic  acid  gr.  x.,  talci  §i. 

ASPERGILLOSIS  AND  PENICILLIOSIS  OF  HAIRY  PARTS. 

The  affected  hairs — generally  those  of  the  beard  and  moustache, 
occasionally  of  the  axilla — present  dirty  greyish  or  whitish  puncti- 
form  formations,  which  on  microscopical  examination  are  seen  to 
consist  of  penicillar  or  aspergillar  fungi  (Penicilliitm  barbce,  Asper- 


PI  NT  A 


2093 


gillus  barbcs).     Occasionally  both  types  of  fungi  are  found  on  the 

same  patient.     The  affection  is  very  chronic.     The  diagnosis  is 

easy,  the  characteristic  aspergillus  and  penicillium  fructifications 

distinguishing    this    condition  from   other 

parasitic  nodular  affections.    The  simplest 

method   of  treatment   is  by  shaving,  and 

afterwards   using   regularly    a    medicated 

soap,  such  as  carbolic  soap,  tar  soap,  or 

sulphur  soap.     If  the  patient  does  not  wish 

to   shave   his  beard,    turpentine    may    be 

tried. 

In  natives  who  do  not  bathe  frequently,  such 
as  old  persons  and  beggars,  the  skin  presents 
often  large  dark  patches  due  to  accumulated  dirt, 
in  which  aspergillar  and  penicillar  fungi  are 
often  present,  living  saprophytically.  This  con- 
dition has  nothing  to  do  with  pinta,  as  a  thorough 
scrubbing  with  soap  will  remove  the  dirt  and  the 
aspergillar  and  penicillar  fungi  which  may  be 
present. 


Fig.  840. — Penicillium 
fructification , 


PINTA. 


Synonyms. — Mai  de  los  Pintos,  Mai  del  Pinto,  Caraate,  Tina. 
Q uirica,  Pannus  Carateus  (Alibert),  Tache  Endemique  des  Cordil- 
lieres  (Alibert),  Lota,  Cativi,  Bulpiss  (Lerch). 

Definition. — The  term  '  pinta  '  does  not  indicate  a  single  disease, 
but  a  group  of  closely  allied  dermatomycoses  characterized  by  the 
presence  of  patches  of  various  colour,  due  to  different  species  of  fungi 
of  the  genera  Aspergillus ,  Penicillium,  Monilia,  and  Montoyclla. 

History. — The  disease  first  began  to  draw  the  attention  of  medical 
writers  in  the  eighteenth  century,  though  it  was  apparently  well 
known  to  the  inhabitants  of  the  affected  regions  since  remote  times, 
as  it  is  found  to  have  formed  the  subject  of  prayers  and  supplications 
used  by  the  Aztecs  centuries  before  the  Spanish  Conquest. 

A  short  description  of  the  malady  is  found  in  the  Encyclopaedia 
of  Polanko,  of  Mexico,  in  1760;  and  in  Juan  de  Velasco's  '  Historia,' 
in  1789,  in  Columbia.  Velasco  believed  the  malady  to  have  been 
imported  by  African  slaves.  A  fairly  complete  description  is  given 
by  Alibert,  in  1829,  under  the  name  of  '  tache  endemique  des  Cor- 
dillieres,'  or  'pannus  carateus.'  Among  the  modern  authors,  the 
clinical  and  pathological  investigation  of  Gomez,  Uribe,  Vribechyel, 
Iryz,  Ruiz  y  Sandoval,  Gastambide,  may  be  mentioned. 

More  recently  the  investigation  into  the  aetiology  of  pinta  by 
Montoya  has  been  of  the  greatest  importance. 

Climatology. — Pinta  is  practically  limited  to  tropical  America, 
where  it  is  found  in  Venezuela,  Peru,  Chili,  Central  American  States, 
Mexico.  Cases  have  been  reported  from  Brazil.  It  is  extremely 
common  in  Columbia,  where,  according  to  Montoya,  4  per  cent,  of 
the  total  population  is  affected.  There  the  patient  affected  with 
the  disease  is  called  '  caratejo.'     The  disease  is  not  equally  dis- 


2094  TROPICAL  DERMATOMYCOSES 

tributed;  in  each  country  there  are  localities  where  the  disease  is 
common,  while  other  districts  are  almost  unaffected.  In  Columbia 
it  is  the  northern  province  of  Santander  which  is  more  particularly 
affected;  in  Mexico  the  disease  is  most  frequently  found  in  the 
provinces  of  Tabaxo,  Chiaspas,  Valladolid,  Michoacan. 

A  few  cases  of  pinta  have  been  reported  from  Egypt  by  Madden, 
Goodman,  and  Sandwith,  and  previously  Legrain  described  some- 
what similar  cases  from  Tripoli  and  the  Sahara.  Legrain,  however, 
did  not  find  any  fungus.  A  few  isolated  cases  have  also  been 
reported  from  the  Gold  Coast,  and  others  from  the  Philippine  Islands 
by  P.  G.  Woolley.    In  Ceylon  and  India  only  imported  cases  are  seen. 

^Etiology. — Previously  to  Ruiz  y  Sandoval  and  Montoya's  in- 
vestigations the  disease  used  to  be  ascribed  to  many  different  causes. 
Some  authors  believed  it  to  be  due  to  the  mineral  salts  (sulphates) 
contained  in  the  waters  of  the  mines  and  other  localities  where  the 
malady  is  endemic;  others  considered  it  to  be  due  simply  to  insani- 
tary conditions,  insufficient  food,  and  a  hot  and  damp  climate; 
others,  again,  believed  the  affection  to  be  induced  by  the  action 
on  the  skin  of  volcanic  cinders;  while,  according  to  some  authorities, 
the  malady  was  an  hereditary  complaint. 

Ruiz  y  Sandoval,  in  Mexico,  first  detected  the  parasitic  nature 
of  pinta.  He  believed  there  was  only  one  species  of  fungus  to  be 
found  in  the  affection,  and  that  the  different  colours  of  the  patches 
were  due  to  the  different  depths  at  which  the  fungus  was  growing 
in  the  various  strata  of  the  epidermis.  Montoya's  classical  re- 
searches in  1898  clearly  showed  the  plurality  of  species  and  genera 
of  the  fungi  found  in  the  disease,  and  demonstrated  that  each  variety 
of  pinta  is  due  to  a  different  fungus.  More  than  twenty  different 
species  were  found  by  him. 

In  the  present  state  of  our  knowledge  of  pinta  it  is  impossible 
to  give  a  satisfactory  classification  of  these  fungi.  The  principal 
ones  may  be  collected  into  the  following  groups: — 

I.  Fungi    of    genus    Aspergillus  :    Aspergillus   pictor   Blanchard, 

1895,  and  several  other  species.  A.  pictor  is  found  in  the 
pure  violet  variety  of  pinta;  the  other  species  are  observed 
in  the  pure  blue  and  bluish  and  violet-black  varieties,  as 
well  as  in  a  form  of  the  red  variety.  Several  of  these  species 
are  not  in  reality  true  Aspergilli,  as  they  possess  organs  of 
fructification  intermediate  between  those  of  the  genus 
Aspergillus  and  those  of  the  genusPenicillium. 

II.  Fungi  of  genus  Pcnicillium :  Penicillium  montoyai  Castellani, 

1907,  and  several  other  species.  They  are  found  in  some 
greyish-violet  varieties  of  pinta. 

III.  Fungi  of  genus  Monilia  :  Monilia  montoyai  Castellani,  1907. 

Found  in  some  cases  of  white  pinta. 

IV.  Fungi  of  genus  Montoyella  :  Montoyella  nigra  Castellani,  1907. 

Found  in  one  variety  of  black  pinta.  M.  boxini  Castellani, 
1907.      Found  in  a  red  variety  of  pinta. 


PI  NT  A  2095 

The  term  Aspergillus  (Trichophyton)  pictor,  introduced  by  Blanchard  in 
1895,  when  the  plurality  of  species  of  the  fungi  found  in  pinta  had  not  yet 
been  demonstrated,  is  now  used  in  a  restricted  sense  to  indicate  the  Asper- 
gillus found  in  the  pure  variety  of  the  disease. 

Montoya  believes  that  the  fungi  found  in  Columbian  pinta,  or  caraate,  are 
different  species  from  those  found  in  Mexican  pinta. 

Appearance  oj  the  Fungi  in  Fresh  Preparations. — Scrapings  from 
the  patches  examined  in  liquor  potassas  show  in  most  cases  between 
the  epithelial  cells  long  dichotomous  mycelial  tlireads,  from  which 
shorter  and  thicker  branches  take  origin  at  various  points.  These 
thicker  branches  terminate  in  comparatively  large  fructifications. 
The  morphological  characters  of  these  fructifications  vary  according 
to  the  species  and  genus  of  the  fungus  present.  They  may  be  typical 
aspergillar  or  penicillium-like  fructifications,  or  they  may  show 
intermediate  characters  between  those  of  Aspergillus  and  Peni- 
cillium. In  many  cases  the  fructification  organ  is  represented  by 
a  pear-shaped  or  triangular  formation,  surmounted  by  five  to  six 
rods  (sterigmata),  each  of  which  supports  a  string  of  five  to  six 
spores.  The  number  of  these  spores,  however,  may  vary.  They 
are  globular,  have  a  smooth  surface,  show  a  double  contour,  and 
their  diameter  is  much  larger  than  that  of  the  mycelial  tubes. 

In  the  cases  where  the  fungus  present  is  a  Monilia  or  a  Monloyella, 
such  or  similar  fructifications  are  absent,  and  only  mycelial  tubes 
and  some  scattered  spores  are  seen. 

Cultures. — The  various  fungi  found  in  pinta  are  easily  cultivated, 
the  best  medium  being  Sabouraud's  maltose  agar.  The  optimum 
temperature  is  between  300  and  400  C. 

The  composition  of  Sabouraud's  medium  is: — 

Maltose        .  .           .  .  .  .  . .  •  •  4  grammes. 

Peptone  (Chassaing)  .  .  .  .  .  .  1  gramme. 

Agar             . .          . .  .  .  .  .  1  -5  grammes 

Distilled  water        . .  .  .  . .  .  .  100  c.c. 

Culturally,  the  fungi  may  be  divided  in  five  groups: — 

1.  Those  showing  in  cultures  aspergillar  fructifications. 

2.  Those  showing  penicillium  fructifications. 

3.  Those  showing  intermediate  fructifications  between  the  Asper- 
gillus and  the  Penicillium. 

4.  Those  showing  simpler  fructifications  characteristic  of  the 
genus  Monilia — viz.,  a  mycelial  thread  terminating  in  a  single 
string  or  small  bunch  of  roundish  spores. 

5.  Those  in  which  higher  organs  of  reproduction  are  absent,  and 
reproduction  takes  place  somewhat  similarly  to  what  is  observed  in 
the  genera  Microsporum  and  Trichophyton — by  conidia  and  terminal 
segmented  and  unsegmented  '  spindles.'  The  fungi  of  this  group, 
found  by  Montoya  in  a  variety  of  black  pinta,  by  Bodin,  and  later 
by  Castellani,  in  a  variety  of  red  pinta,  constitute  the  genus  Mon- 
toyella. 

Insulation  Experiments. — -Montoya  has  tried  to  infect  rabbits, 
using  various  cultures  of  the  fungi  found  in  the  disease.     On  several 


2096  TROPICAL  DERMATOMYCOSES 

occasions  a  desquamation  of  skin  and  loss  of  hair  was  observed, 
and  some  chromatic  patches  appeared.  Uribe  succeeded  in  inocu- 
lating several  mulattoes. 

According  to  Montoya,  the  fungi  of  pinta  live  saprophytically  in 
certain  waters,  especially  in  those  of  mines  and  localities  where  the 
temperature  is  constantly  high.  He  states  that  he  obtained  pure 
cultures  of  the  pinta  fungi  direct  from  such  waters.  He  has  also 
found  the  same  fungi  as  ectoparasites  on  the  bodies  of  mosquitoes 
of  the  genus  Culex,  on  sandflies  (Simulium),  and  on  the  body  of 
some  bugs  (Clinocoris) ,  which  are  very  common  in  the  mines.  He 
believes,  therefore,  that  mosquitoes  and  other  insects  play  a  role 
in  the  transmission  of  the  disease. 

In  some  old  chronic  cases  of  pinta  an  Acarus — somewhat  resem- 
bling Acarus  scabiei,  though  larger- — has  been  found  to  live  in  the 
epidermal  squamae,  and  some  writers  believe  that  this  Acarus  also 
plays  a  part  in  the  transmission  of  the  malady. 

Predisposing  Causes. — What  the  older  authors  believed  to  be 
the  true  causes  of  pinta — -viz.,  a  hot,  damp,  climate;  insanitary 
surroundings  and  poor  feeding;  the  mineral  salts  contained  in  the 
waters — are  only  predisposing  causes,  some  of  which,  however,  are 
of  great  importance.  The  hot,  damp  climate  favours  the  growth 
of  the  fungi;  the  water  of  the  mines,  which  contains  a  large  amount 
of  mineral  salts  (especially  sulphates),  produces  after  a  time  in 
those  who  use  it  for  washing,  etc.,  a  dermatitis  with  fissures  and 
other  eczematous-like  lesions  which  greatly  facilitate  the  infection. 
All  races  are  liable  to  be  attacked  by  the  disease,  but  mulattoes 
seem  to  be  particularly  prone  to  become  infected.  Albinos  are  said 
to  be  immune.  Both  sexes  are  equally  liable  to  become  infected, 
though  males,  on  account  of  their  occupations,  are  more  frequently 
affected.  The  malady  generally  appears  between  the  age  of  fifteen 
and  twenty-five,  but  it  may  appear  at  any  age,  and  has  been  seen  in 
children  three  or  four  years  old. 

It  has  been  observed  that  individuals  of  the  negro  race  are  more 
liable  to  contract  the  black  variety  than  any  other  kind  of  the 
disease,  while  whites  are  especially  liable  to  contract  the  red  variety. 
Miners  and  agricultural  labourers  are  affected  in  most  cases  by  the 
violet  variety. 

Symptomatology. — The  disease  begins  very  gradually.  After  an 
incubation  period  varying,  according  to  different  authors,  between 
a  few  weeks  and  some  months,  one  or  several  small  slightly  pruri- 
ginous  spots  appear  on  uncovered  parts  of  the  body.  The  spots 
increase  very  slowly  in  size,  and  some  may  fuse  together.  They  are 
roundish,  or  may  have  an  irregular  outline.  At  first  they  are 
hardly  raised  above  the  normal  skin.  The  surface  of  the  patches 
is  generally  dry  and  rough,  and  is  covered  with  fine  pityriasic 
squamae  in  recent  cases,  with  larger  and  thicker  scales  in  older 
ones.  Occasionally,  in  chronic  cases,  the  surface  of  the  patches, 
instead  of  being  dry,  may  be  moist  or  somewhat  greasy  or  glutinous. 
The  hairs  of  the  affected  regions  become  atrophied,  and  later  on 


PINTA  2097 

fall  out.  The  shedding  of  hair  is  not  due  to  the  fungi  invading 
directly  the  hair;  it  is  due  to  a  peculiar  fibrosis  of  the  hair  follicle, 
at  the  place  of  the  hair  a  hard  formation  remaining,  like  a  grain  of 
sand  (fibroid  folliculitis  of  Montoya). 

Pruritus  is  generally  well  marked,  especially  at  night-time.  There 
are  often  patches  of  hyperkeratosis  on  the  palms  and  soles,  and  the 
normal  lines  and  sulci  appear  much  deeper. 

Old  chronic  cases  occasionally  exhale  a  peculiar  musty  odour, 
which  has  been  compared  to  the  smell  of  cat's  urine,  or  to  the  bad 
smell  of  dirty  linen  kept  in  a  warm,  damp  place. 

The  affection  may  spread  to  the  whole  body,  except  the  palms 
of  the  hands  and  the  soles  of  the  feet.  The  nails  are  never  attacked. 
The  scalp  is  not  usually  affected. 

The  disease  has  no  tendency  to  spontaneous  cure.  Its  course  is 
very  chronic,  and  may  last  the  whole  of  the  patient's  life. 

Some  of  the  older  authors  state  that  the  patients  during  the  incubation 
period  suffer  from  fever,  vomiting,  and  diarrhoea.  Montoya  says  that  pinta 
patients  have  not  got  an  odour  sui  generis,  as  stated  by  most  observers.  In 
cleanly  patients  no  smell  whatever  is  noticeable,  apart  from  the  peculiar 
odour  of  the  negro  race. 

Clinical  Varieties. — -Clinically,  six  different  varieties  may  be  dis- 
tinguished, each  of  which  shows  several  subvarieties : — 

1.  The  Black  Variety. 

2.  The  Blue  Variety. 

3.  The  Violet  Variety. 

4.  The  Red  Variety. 

5.  The  Yellow  Variety. 

6.  The  White  Variety. 

Black  Variety. — The  patches  are  of  a  black  colour,  and  are  very 
often  found  on  the  face,  though  they  may  be  present  on  any  other 
part  of  the  body  except  the  palms  and  soles,  similarly  to  all  the 
other  varieties.  The  patches  are  hardly  raised,  and  their  surface 
is  slightly  desquamating.  Pruritus  is  generally  complained  of,  but 
is  not,  as  a  rule,  so  unbearable  as  in  the  other  varieties.  Black 
pinta  is  found  in  negroes  more  frequently  than  in  individuals  of 
Caucasian  race.  The  course  is  very  chronic.  The  treatment  is 
difficult,  though  not  so  difficult  as  in  the  other  varieties. 

Black  pinta  shows  two  subvarieties — one  is  characterized  by  the 
presence  of  patches  of  a  black-violet  colour;  the  other  by  patches 
of  jet-black,  indian-ink  black  colour.  The  fungus  found  in  the 
first  is  an  Aspergillus  (species  undetermined) ;  in  the  second  a  Mon- 
toyella  (M.  nigra). 

Blue  Variety. — This  is  much  less  frequent  than  black  pinta.  The 
patches  are  of  a  blue  colour.  They  generally  begin  to  appear  first 
on  the  dorsum  of  the  hands,  and  then  tend  to  spread  over  the 
whole  body — uncovered  as  well  as  covered  parts.  There  generally 
is  intense  pruritus. 

The  fungus  usually  found  in  blue  pinta  is  Aspergillus. 

132 


2og8  tropical  dermatomycoses 

Violet  Variety. — Apart  from  the  colour  of  the  patches,  which  is 
violet,  the  clinical  symptoms  and  course  of  this  variety  are  identical 
with  those  of  blue  pinta.  It  is  extremely  common  among  rural 
labourers  and  miners. 

There  are  numerous  subvarieties  of  violet  pinta.  In  some  cases 
the  patches  are  of  a  pure  violet  colour;  in  other  cases  the  colour 
may  be  violet-greyish,  violet-brownish,  violet-purplish.  There  are 
cases  in  which  the  patches  are  at  first  of  a  greenish  colour,  to 
become  violet-bluish  later  on.  The  fungus  found  in  the  pure  violet 
pinta  is  an  Aspergillus  (A.  pictor  Blanchard,  1895);  the  fungus 
found  in  the  violet-greyish  cases  is  a  Penicillium — P.  montoyai 
Castellani,  1907;  the  fungi  found  in  the  other  varieties  are  Aspergilli 
or  fungi  presenting  transition  characters  between  the  Aspergillus  and 
the  Penicillium. 

Red  Variety. — This  is  the  commonest  variety  found  in  white 
patients.  The  patches  first  develop,  as  a  rule,  on  the  dorsum  of  the 
hands  and  feet,  and  spread  to  large  portions  of  the  body.  The 
patches  are  red — often  brick-red — and  usually  show  a  rather 
abundant  desquamation.  Pruritus  is  very  distressing,  especially 
at  night-time.  Secondary  lesions  due  to  scratchings  and  inocula- 
tion of  pyogenic  micro-organisms  are  not  rare.  Ulcerative  lesions 
have  been  reported  by  several  observers  as  occasionally  occurring. 

In  some  cases  of  red  pinta  an  Aspergillus  (species  not  determined) 
is  found;  in  others  a  fungus  of  the  genus  Montoyella — M.  bodini 
Castellani,  1907,  found  by  Bodin  in  1903  in  a  patient  who  was  under 
the  treatment  of  Darier. 

Castellani,  in  1907,  found  the  same  or  a  very  similar  Montoyella  in  a  case 
of  red  pinta  observed  in  a  European  sailor  who  had  long  been  in  tropical 
America.  In  this  case  the  disease  had  not  yet  spread  much.  Besides  the 
red  patches,  there  was  on  the  right  forearm  a  small  greyish-violet  spot,  in 
which  a  fungus  was  found,  which  gave  Penicillium  fructifications  in  cultures 
(P.  montoyai) . 

Red  pinta  is  more  serious  than  any  other  variety,  as  it  affects 
not  only  the  superficial  strata  of  the  epidermis,  but  the  rete  Mal- 
pighii  as  well  as  the  corium. 

Yellow  Variety. — Very  common  among  half-castes.  It  generally 
begins  on  the  chest  or  arms.  The  patches  are  yellow,  and  at  first 
are  not  pruriginous  and  not  desquamating.  In  old  cases,  however, 
there  is  pruritus.  This  variety  is  very  frequently  mixed  with 
patches  of  white  pinta,  and  is  difficult  to  cure.  The  fungi  found 
belong  to  the  genera  Monilia  and  Aspergillus. 

White  Variety. — The  patches  are  of  a  dull  wliite  colour,  and  are 
generally  very  large.  The  surface  is  usually  rough  and  desquamat- 
ing, but  at  times  it  may  be  smooth.  In  some  cases  a  fungus  of  the 
genus  Monilia  is  present,  but,  according  to  Montoya,  in  other  cases 
no  fungus  whatever  is  to  be  found.  Montoya  considers  the  white 
variety  of  pinta  to  represent  in  many  cases  the  ultimate  retrogres- 
sive stage  of  all  the  other  varieties  except  the  red.  The  patches 
of  white  pinta  would  be  in  such  cases  in  reality  unpigmented 


PINTA  2099 

leucoderma-like  areas  due  to  the  disturbing  action  of  the  various 
fungi  on  the  pigmentation  processes  of  the  skin. 

Montoya's  belief  on  the  nature  of  white  pinta  in  some  cases  is  supported 
by  Castellani's  observations  on  tinea  flava  and  tinea  alba.  In  both  these 
dermatomycoses  white,  pseudo-leucodermic  patches  may  occasionally  be  seen 
long  after  the  fungus  has  died  out,  and  these  patches  may  remain  unpig- 
mented  for  months  and  years. 

Mixed  Variety. — Not  infrequently  the  same  patient  may  be 
affected  with  several  varieties  of  pinta,  presenting  a  grotesque 
tattooed  or  piebald  appearance. 

It  is  especially  white  pinta  which  is  found  associated  with  one 
or  more  of  the  other  varieties. 

Diagnosis. — This  does  not  present  any  difficulty  in  the  countries 
where  the  disease  is  endemic.  In  any  doubtful  case  the  micro- 
scopical examination,  supplemented  when  necessary  by  the  use  of 
cultural  methods,  will  clear  the  diagnosis. 

Differential  Diagnosis — Tinea  nigra. — In  contrast  to  the  black 
variety  of  pinta,  tinea  nigra  is  very  superficial,  does  not  extend  to 
large  portions  of  the  body,  may  attack  the  palms  of  the  hands,  is 
not  pruriginous,  is  easily  cured  except  when  affecting  the  palms. 
The  microscopical  examination  of  scrapings  from  patches  of  tinea 
nigra  will  show  mycelial  tubes  of  irregular  shape  and  large  globular 
spores  collected  in  bunches.  The  spores  are  grouped  together  in  a 
somewhat  similar  manner  to  what  one  sees  in  pityriasis  versicolor. 

Tinea  Flava. — In  contrast  to  yellow  pinta,  the  fungus  of  tinea 
flava  is  a  Malassezia,  has  the  same  morphological  characters  of  the 
fungus  found  in  pityriasis  versicolor,  and  cannot  be  grown  arti- 
ficially. 

Tinea  Albigena  and  Tinea  Alba. — These  are  generalized  tricho- 
phytic  and  epidermophytic  affections,  and  are  easily  distinguished 
by  the  characters  of  the  fungi. 

Leprosy  can  be  distinguished  from  white  pinta  lesions  by  the 
sensibility  not  being  impaired  in  pinta. 

Only  white  pinta  patches  with  no  fungus  might  be  mistaken  for 
leucoclerma  on  superficial  examination.  White  pinta  is  very  often 
associated  with  other  varieties  of  pinta,  which  are  easily  diagnosed. 
Leucodermic  patches  are  smooth,  non-pruriginous,  and  the  skin 
surrounding  them  is  often  hyperpigmented. 

Prognosis. — Pinta,  though  not  a  fatal  disease,  must  be  considered 
a  serious  affection,  as  its  cours>  is  chronic  and  the  treatment  very 
difficult.  In  most  cases  the  general  health  remains  satisfactory, 
but  the  disfigurement  is  very  distressing  to  the  patients,  who  often 
become  nervous  and  irritable.  The  pruritus,  which  is  generally 
more  marked  at  night,  is  also  a  caure  of  great  distress  and  sleep- 
lessness. 

Treatment. — The  popular  treatment  in  Columbia  is  citrine  oint- 
ment (mercury  nitrate  ointment).  Other  parasiticides  have  been 
tried,  with  a  varying  degree  of  success.  When  the  eruption  is  at 
the  very  beginning,  tincture  of  iodine  may  suffice.     The  best  results 


TROPICAL  DERMATOMYCOSES 


have  been  obtained  by  using  chrysarobin  (chrysarobin,  gr.  x.  to  xxx. ; 
ung.  zinci  ox.,  gi.).  This  must  be  applied  cautiously.  When  th ", 
malady  affects  large  tracts  of  the  body,  only  a  portion  should  be 
treated  at  a  time,  to  prevent  as  far  as  possible  symptoms  of  absorp- 
tion, The  urine  should  be  regularly  analyzed  during  the  treat- 
ment. The  chrysarobin  ointment  must  not  be  applied  to  the  face, 
lest  a  severe  conjunctivitis  should  develop.  For  the  face  a  resorcin, 
or  resorcin-sulphur,  or  resorcin-salicylic,  or  salicylic  acid  ointment 
(resorcini,  gr.  xxx.  to  3i. ;  ac.  salicylici,  gr.  xv. ;  vaseline,  gi.),  is 
advisable,  or  citrine  ointment  may  be  used. 

Montoya  recommends  chrysarobin  dissolved  in  chloroform  (chrysarobin 
10  parts,  chloroform  90  parts).  Apply  with  a  fine  brush.  When  dry,  apply 
gutta-percha  dissolved  in  chloroform  (gutta-percha  10  parts,  chloroform 
90  parts) . 

Chrysarobin  may  conveniently  be  applied  in  the  form  of  a  vernisol  varnish 
(5  to  10  per  cent.). 

PIEDRA. 

Synonym.- — Trichosporosis  Tropica. 

Definition. — Piedra  is  a  mycotic  disease  of  some  parts  of  South 
America  causing  very  hard,  small  nodosities  on  the  hair. 

Historical  and  Geographical. — The  condition  has  been  known 
locally  in   Columbia  since  remote  times,   but   the  first   scientific 

descriptions  are  due  to  Desenne 
,  i;i./_  (1878),  Morris  (1879),  Osario,  and 

Megalhaes.      More    recently   the 
^--.0<;-_          condition    has    been   studied   by 


Fig.  841. — Transverse  Section 
through  a  pledra  nodule. 


Fig.  842. — Piedra. 

Juhel  Renoy,  Pernet,  J.  M.  H. 
MacLeod,  Horta,  and  others. 
This  disease  of  the  hair  is  com- 
mon in  some  districts  of  Columbia, 
especially  the  valley  of  Canca; 
but  closely  allied  conditions  are 
observed  in  several  parts  of  the  tropics,  and  occasionally  in 
temperate  zones  {piedra  nostras). 

/Etiology. — If  an  affected  hair  is  washed  in  ether,  and  then 
treated  with  liquor  potassse,  and  examined  microscopically,  the 
nodules  will  be  seen  to  consist  of  large  polyhedric  refringent  bodies, 
held  together  by  an  amorphous  substance  acting  as  cement. 
These  bodies  are  the  spores  of  the  fungus  causing  the  disease 
{Trichosporitm  giganteiim  Behrend,  1890).  The  description  of  the 
fungus  is  given  on  p.  1101.  In  Columbia  it  is  generally  believed 
that  the  infection  takes  place  by  washing  the  hair  with  a  mucila- 
ginous oil,  much  used  by  the  women  of  the  country.     In  British 


PIEDRA  2ior 

Guiana  natives  consider  it  to  be  due  to  bathing  in  certain  white 
or  milky  waters,  while  it  does  not  occur  if  they  bathe  in  the  brown 
peat  bush  waters. 

Symptomatology. — The  hair  of  the  head  of  women,  and  less  fre- 
quently the  hair  of  the  head  and  beard  of  men,  is  affected.  The 
affected  hairs  present  strings  of  pin-head-sized  nodosities,  which 
are  better  felt  than  seen.  The  nodosities  may  be  very  numerous, 
and  are  found  on  the  surface  of  the  hair-shaft,  either  on  one  side  or 
surrounding  it  like  a  sheath.  They  are  black  and  hard,  though  not 
so  hard  as  the  name  piedra  (stone)  would  imply,  and  a  kind  of 
crepitation  is  produced  when  the  hair  is  combed.  There  is  often 
matting  and  knotting  of  the  hair.  The  disease  is  chronic,  and  the 
nodosities  do  not  disappear  spontaneously. 

Horta  has  described  a  variety  of  piedra  in  Brazil,  characterized  by  the 
nodules  containing  large  cyst-like  structures,  which  Pinoy  considers  to  be 
probably  asci  (see  p.  1 102) . 

Diagnosis. — The  microscopical  examination  of  the  nodosities 
renders  the  diagnosis  easy. 

Prognosis. — The  affection  is  of  long  duration,  and  has  no  tendency 
to  spontaneous  cure. 

Treatment. — This  is  difficult.  It  has  been  recommended  to  apply 
a  5. per  cent,  salicylic  alcoholic  solution  or  benzene  and  turpentine  to 
the  hair,  and  to  wash  the  head  regularly  with  a  perchloride  lotion 
(1  in  2,000).     In  obstinate  cases  it  is  necessary  to  shave  the  head. 

Trichosporosis  indica. 

In  India  and  Ceylon  a  condition  similar  to  piedra  is  occasionally  observed. 
It  is,  however,  much  less  severe,  a  few  minute  nodules  only  being  present 
on  the  hairs  of  the  beard  and  moustache,  and  the  hair  of  the  scalp  being 
rarely  affected.  The  fungus  seems  to  be  different  from  that  of  the  Columbian 
piedra. 

Trichosporosis  of  Temperate  Zones. 

Cases  of  trichosporosis  of  temperate  zones  or  piedra  nostras  (tinea  nodosa) 
have  been  described  by  Biegel  (1869),  Caro,  Behrend,  Unna,  Pick,  Vuillemin. 
The  nodosities  in  such  cases  have  been  found  on  the  hairs  of  the  moustache 
and  beard,  not  on  the  hairs  of  the  head.  The  fungi  are  slightly  different  from 
Trichosporum  giganteum.  Several  species  have  been  described- — Trichospcrrum 
beigeli  Rabenhorst,  1867,  T.  ovoides  Behrend,  1890,  T.  ovale  Unna,  1896. 

TRICHOMYCOSIS  FLAVA,  RUBRA,  NIGRA. 

Synonyms.— Trichomycosis  axillaris,  Trichonocardiasis,  Tropical 
lepothrix,  Castellani's  Trichomycosis,  Trichomycosis  chromatica, 
Chromotrichomycosis. 

Definition. — A  nodular  affection  of  the  hair,  usually  of  the  axillary 
regions,  caused  by  Cohnistreptothrix  tenuis  Castellani  (Nocardia  tenuis 
Castellani),  either  alone  or  in  symbiosis  with  chromogenic  cocci. 

Historical. — Nodular  affections  of  the  hair  have  been  described 
by  European  observers  under  various  names,  such  as  Lepothrix 
(E.  Wilson),  Trichomycosis  nodosa  (Patterson),  Trichomycosis 
palmellina  (Pick),  but  a  great  deal  of  confusion  has  existed  until 


2102  TROPICAL  DERMATOMYCOSES 

recently  on  the  subject,  very  different  clinical  descriptions  having 
been  given  and  the  condition  being  ascribed  to  widely  different 
germs. 

Paxton,  Wilson,  Pick,  and  later  Payne,  Patterson,  Crocker, 
Pusey,  etc.,  described  the  hairs  as  presenting  irregular ly  lobed 
masses  of  hard  consistency  in  which  were  often  embedded  some  of 
the  fibres  of  the  cortex. 

According  to  Crocker,  the  fibres  of  the  whole  shaft  may  be  split 
up  and  the  hair  may  break  off  with  a  brush-like  termination.  The 
researches  on  the  aetiology  by  various  authorities  gave  the  most 
widely  different  results,  various  bacilli  being  described  by  Payne  and 
Patterson,  a  diplococcus  by  Eisner  and  later  Sonnenberg,  and  a 
micrococcus  by  Colombini,  etc.  Babes,  Pick,  Balzer,  and  Bar- 
themly  considered  that  the  Bacillus  prodigiosus  played  a  role  in  the 
causation  of  the  affection. 

In  1911  Castellani  carried  out  an  investigation  in  the  tropics, 
describing  the  condition  as  seen  there  and  differentiating  three 
varieties — the  yellow  variety,  the  black  variety,  the  red  variety. 
He  demonstrated  that  the  yellow  variety  was  caused  by  a  nocardia 
(Nocardia  or  Cohnistreptothrix  tenuis  Castellani) ;  the  black  variety 
by  the  same  nocardia  plus  a  black  pigment  producing  coccus 
(Nigrococcus  nigrescens  Castellani)  living  in  symbiosis  with  it;  the 
red  variety  by  the  same  nocardia  plus  a  red  pigment  producing  coccus 
living  in  symbiosis  with  it,  and  which  was  later  on  called  Rhodococcus 
castellanii  by  Chalmers  and  O'Farrell.  Castellani's  work  was 
confirmed  and  amplified  inthe  Sudan  by  Chalmers  and  O'Farrell,  who 
suggested  for  the  affection  the  term  '  trichonocardiasis ' ;  in  West 
Africa  by  Macfie,  who  described  a  variet}'  of  the  red  type:  jusca  ; 
and  by  various  observers  in  several  other  countries.  In  1915-1918 
Castellani  observed  in  the  Balcanic-Adriatic  Zone  the  three  varieties 
he  had  described  in  the  tropics,  and  found  the  same  organisms. 

etiology. — The  researches  of  Castellani  have  demonstrated  that 
the  yellow  variety  is  due  to  a  very  thin,  bacillary-like  fungus,  for 
which  he  proposed  the  name  Nocardia  tenuis ,  later  changed  into 
Cohnistreptothrix  tenuis.  The  black  and  red  varieties  are  due  to  a 
symbiosis  of  this  fungus  with  chromogenic  cocci,  a  coccus  producing 
black  pigment  in  the  black  variety,  a  coccus  producing  a  red  pigment 
in  the  red  type. 

Nocardia  tenuis  Castellani,  1912  [Cohnistreptothrix  tenuis  Castellani,  1912).— 
The  microscopic  examination  of  the  nodules  reveals  the  presence  of  enormous 
numbers  of  bacillary-like  bodies,  which  are  Gram-positive,  but  not  acid-fast. 
If  the  nodules  are  kept  in  alcohol  or  formalin  for  several  months,  the  fungus 
apparently  loses  partially  or  totally  its  property  of  being  stainable  by  Gram's 
method.  They  vary  in  length.  4  to  10  fx  and  more;  the  average  breadth  is 
approximately  0-3  to  06  fx;  they  may  be  straight  or  variously  bent,  occasion- 
ally branching;  they  are  fairly  closely  packed  together,  and  are  embedded 
in  an  amorphous  cementing  substance.  In  regard  to  cultivation,  Chalmers 
and  O'Farrell  observed  some  slight  growth  in  hanging  drops  of  equal  parts 
of  human  serum  and  normal  saline.  Macfie  in  one  case  succeeded  in  cultivating 
the  fungus  on  ascitic  agar,  the  colonies  being  very  small  and  translucent. 


TRICHOMYCOSIS  AXILLARIS  FLAVA  2103 

Characters  of  the  Coccus-like  Organism  found  in  the  Black  Variety  {Micrococcus 
or  Nigrococcus  nigrescens  Castellani,  igi  1). — It  is  a  Gram-positive,  rather  large, 
non-motile  coccus,  which  in  certain  media  may  take  the  appearance  of  a 
cocco-bacillus.  Sugar  media  are  more  suitable  for  the  growth  of  the  organism 
than  the  ordinary  agar. 

Sabouraud  Agar. — Colonies  appear  twenty-four  to  forty-eight  hours  after 
inoculation.  They  are  roundish,  at  first  white,  but  after  a  couple  of  days 
the  centre  of  each  colony  turns  black,  and  this  pigmentation  slowly  spreads 
excentrically.     After  a  time  the  colonies  coalesce  into  a  jet-black  mass. 

Glucose. — Growth  similar  to  Sabouraud,  but  slightly  less  abundant.  The 
black  pigmentation  develops  from  the  centre  of  the  colonies  and  slowly 
spreads  towards  the  periphery. 

Ordinary  Laboratory  Agar. — Growth  much  less  abundant  than  on  most 
sugar  agars,  and  black  pigmentation  less  marked. 

Levulose  Agar. — Identical  to  glucose. 

Saccharine  Agar. — The  pigmentation  is  less  pronounced,  and  does  not 
spread  to  the  whole  of  the  growth. 

Raffinose  Agar. — Same  as  saccharine. 

Lactose  Agar. — Scanty  pigmentation. 

Alkaline  Maltose  Agar. — Black  pigmentation  well  marked,  though  in 
many  cases  it  does  not  extend  to  the  whole  of  the  growth. 

Acid  Maltose  Agar. — Growth  less  abundant  than  on  acid  maltose.  Black 
pigmentation  well  marked.  • 

Mannite  Agar. — As  alkaline  maltose. 

Inulin  Agar. — As  alkaline  maltose,  but  pigmentation  less  pronounced. 

Saccharose. — As  inulin. 

Glycerine  Agar. — Abundant  growth,  the  whole  of  which  after  a  time  becomes 
of  jet-black  colour. 

Galactose. — As  inulin. 

Adonite. — Like  acid  maltose. 

Serum. — Growth  fairly  abundant,  but  there  is  only  a  trace  of  pigmentation. 
The  medium  is  not  liquefied. 

Gelatine. — No  liquefaction.  The  growth  on  the  surface  shows  after  a 
time  some  dark  pigmentation,  but  the  colonies  along  the  stab  are  white. 

Milk. — No  change. 

Broth. — General  turbidity.  A  thin  pellicle  is  often  present.  The  micro- 
scopical examination  shows  cocci  arranged  in  pairs  or  irregularly.  They  are 
not  capsulated. 

Peptone  Water. — Some  growth  at  the  bottom,  while  the  rest  of  the  tube  is 
clear. 

Sugar  Broths. — No  formation  of  acid  or  gas. 

Indol. — Most  strains  produce  a  trace  of  indol. 

Characters  of  the  Coccus-like  Organism  found  in  the  Red  Variety  of  the 
Affection. — The  coccus  found  in  the  red  variety  is  more  difficult  to  isolate 
and  grow  than  the  coccus  observed  in  the  black  type  of  the  affection.  As 
a  rule  it  grows  better  and  shows  more  pigment  on  ordinary  agar  than  on 
sugar  media.     It  is  non-motile  and  Gram-positive. 

Agar. — The  growth  is  at  first  white,  then  a  red  or  red-yellowish  or  yellow 
spot  appears  in  the  centre.  The  pigmentation  very  slowly  progresses  towards 
the  periphery,  but  seldom,  if  ever,  spreads  to  the  whole  of  the  growth.  On 
maltose  and  glucose  agar  the  same  pigmentation  is  present,  but  on  most  of  the 
other  sugar  media  no  pigment  is  produced.  Gelatine  and  serum  are  not 
liquefied.  This  coccus,  as  already  stated,  is  Gram-positive  and  non-motile. 
The  coccus  has  been  recently  further  investigated  by  Chalmers  and  O'Farrell, 
who  have  observed  that  the  best  medium  for  showing  the  pigment  is  the  potato . 
They  have  called  the  coccus  Rhodococcus  castellanii. 

Symptomatology. — The  affected  hairs  of  the  axilla  present 
nodular  formations,  plainly  visible  to  the  naked  eye,  of  rather  soft 
consistency.     They  are  easily  removed  by  scraping  with  a  tri- 


2104 


TROPICAL  DERMATOMYCOSES 


angular  needle  or  any  similar  instrument.  The  formations  are 
either  yellow  or  black,  or,  less  frequently,  red.  They  may  be  very 
abundant,  and  form  a  yellow,  or  black,  or  red  sheath  round  the 
hair  (Figs.  843  and  844),  which  may  at  times  become  lustreless  and 
depigmented.  The  same  patient  may  have  two  varieties:  The  hairs 
of  one  armpit  may  show  the  yellow  variety,  while  the  hairs  of  the 
other  armpit  may  present  the  black  type.  Sometimes  the  same 
individual  hair  may  present  some  of  the  nodules  yellow  and  others 
black,  or,  rarely,  red.  We  have  Inot  yet  observed  all  the  three 
varieties  present  at  the  same  time  on  the  same  patient. 

The  microscopical  examination  with  a  low  power  shows  that  the 
affect ed^hair  is  covered  at  several  places  by  roundish  formations, 


jfc 

*^ah 

pps^^^P^JM 

's"rrf'~ 

Fig.  843. — Trichomycosis  Axillaris  Flava. 


Fig.  844. — Trichomycosis  Axillaris  Nigra. 


partially  or  totally  encircling  the  shaft.  Using  a  higher  power, 
these  formations  will  be  seen  to  consist,  in  the  yellow  variety,  of 
enormous  numbers  of  bacillary-like  bodies  embedded  into  an 
amorphous  cementing  substance.  In  the  red  and  black  varieties 
in  addition  to  these  masses  of  bacillary  bodies  which  are  the  my- 
celial segments  of  the  Nocardia  (Cohnistreptothrix) ,  large  groups  of 
cocci-like  bodies  are  observed.  The  affection  in  our  cases  was  never 
associated  with  chromidrosis.     It  may  attack  the  pubic  hair. 

Macfie  has  described  a  subvariety  of  the  red  type,  of  less  vivid  colour: 
fusca.  It  is  caused  by  Cohnistreptothrix  tenuis  plus  a  coccus  wluch  seems  to 
be  a  variety  of  M.  castellanii. 


TRICHOMYCOSIS  AXILLARIS  FLAVA  2105 

Diagnosis. — -This  is  based  on  the  presence  of  yellow,  black,  or 
red,  rather  soft,  nodules  on  the  hairs  of  the  axillary  regions,  which, 
on  microscopical  and  cultural  examination,  show  presence  of 
Nocardia  tenuis  (Cohnistreptothrix  tenuis)  alone,  or  with  Micrococcus 
(Nigrococcus)  nigrescens  or  Micrococcus  (RJwdococciis)  castellanii. 

Differential  Diagnosis. — The  condition  must  be  differentiated 
from  the  other  nodular  parasitic  conditions  of  the  hair,  viz. : — 

1.  Trichosporosis  tropica,  or  piedra. 

2.  Unna's  trichosporosis,  or  piedra  nostras. 

3.  Behrend's  trichosporosis,  or  '  nodular  trichomycosis.' 

4.  Beigel's  trichosporosis,  or  tinea  nodosa. 

5.  Du  Bois's  trichosporosis. 

1.  Trichosporosis  tropica,  or  piedra,  generally  affects  the  hair 
of  the  head.  The  nodules  are  extremely  hard,  hence  the  name 
'piedra.'  The  fungus  found  belongs  to  the  genus  Trichosporiim 
(Trichosporiim  giganteum  Behrend,  1890). 

2.  Unna's  trichosporosis,  or  piedra  nostras,  has  been  described 
by  Unna  in  the  hair  of  the  moustache  and  beard.  It  is  due  to 
Trichosporon  ovale  (Unna,  1896). 

3.  Behrend's  trichosporosis,  or  '  nodular  trichomycosis,'  described 
by  Behrend,  affecting  the  hair  of  the  beard.  It  is  due  to  Tricho- 
sporiim ovoides  (Behrend,  1890). 

4.  'Beigel's  trichosporosis,'  or  'tinea  nodosa,'  discovered  in 
London  by  Cheadle  and  Morris,  and  later  in  Breslau,  Nancy,  etc. 
It  attacks  the  hairs  of  the  head,  and  is  due  to  Trichosporiim  beigeli 
(Rabenhorst,  1867). 

5.  Du  Bois's  trichosporosis  of  the  hairs  of  the  pubic  region  due 
to  Trichosporiim  glycophiles  (Du  Bois,  1910). 

Trichomycosis  axillaris  flava,  rubra,  and  nigra  has  nothing  to  do 
with  piedra  or  with  any  other  form  of  trichosporosis,  as  no  Tricho- 
sporiim is  found,  the  fungus  being  a  Nocardia  or  more  correctly  a 
Cohnistreptothrix,  with  very  thin,  bacillary-like  mycelium.  The 
types  of  the  condition  we  have  seen  in  Europe  are  very  similar  or 
identical  with  those  we  have  seen  in  the  tropics,  except  that  in 
temperate  zones  we  have  never  observed  the  black  variety.  The 
nodules  were  not  very  hard  and  the  hairs  not  brittle,  though 
European  observers  describe  the  European  type  as  being  charac- 
terized by  the  presence  of  hard  nodules  and  the  hairs  becoming 
brittle. 

Course  and  Prognosis.- — The  course  is  chronic,  but  the  condition 
may  subside  or  disappear  on  the  patient  going  to  a  cold  climate. 
The  affection,  if  of  very  little  pathological  importance,  has  a  certain 
practical  interest,  being  much  objected  to  by  patients,  especially 
by  ladies. 

Treatment. — The  treatment  originally  used  by  Castellani  is  often 
efficacious.  It  consists  in  dabbing  the  hair  two  or  three  times  daily 
with  a  solution  of  formalin  in  spirit  (3i.-*vi.)  and  applying  at  night 
a  sulphur  ointment  (2  to  5  per  cent.).  Shaving,  Tr.  Iodi,  and  a 
salicylic  alcoholic  lotion,  have  been  recommended. 


2106  TROPICAL  DERMATOMYCOSES 

RARER  NODULAR  AND  GUMMATOUS  AFFECTIONS  OF 
HYPHOMYCETIC  ORIGIN. 

Hemisporosis. 

Historical  and  Geographical. — Gougerot  and  Craven  described 
a  case  of  osteoperiostitis  due  to  Hemispora  stellata  Vuillemin  some 
years  ago.  Later  Auvray  and  Bidot  found  the  same  fungus  in 
a  generalized  nodular  affection,  and  De  Beurmann,  Clair,  and 
Gougerot  found  it  in  a  gumma  situated  on  the  penis  of  a  negro. 

/Etiology. — The  condition  is  due  to  a  fungus,  Hemispora  stellata 
Vuillemin,  the  description  of  which  is  given  on  p.  1108. 

Histopathology. — The  histological  lesions  resemble  those  of 
tuberculosis  cutis,  as  noted  by  Auvray  and  Bidot. 

Symptomatology. — Gumma-like  swellings  are  present,  either  single 
or  multiple.  These  may  later  ulcerate.  A  chronic  osteoperiostitis, 
with  thickening  of  the  tibia  somewhat  resembling  the  type  due 
to  syphilis,  has  been  described.     Mercury,  however,  had  no  effect. 

Diagnosis. — This  is  based  on  isolating  the  fungus.  The  fungus 
microscopically  is  seldom  if  ever  seen  in  the  lesions,  and  cultures 
are  necessary.  These  are  carried  out  in  the  same  manner  as  for 
sporotrichosis. 

Treatments — Potassium  iodide  given  in  full  doses  (gr.  xv.-xx.) 
three  times  daily  is  very  efficacious. 

Acremoniosis. 

There  is  only  one  case  on  record  of  this  condition  by  Potron  and 
Noisette  in  France.  The  condition  is  due  to  a  fungus,  Acremonium 
potronii  Vuillemin,  1911,  which  has  been  described  on  p.  1121. 
The  patient  had  fever,  which  was  at  first  suspected  to  be  typhoid, 
and  several  gumma-like  swellings  developed,  which  slowly  ulcerated. 
They  were  not  painful.     The  proximal  glands  were  not  enlarged. 

Diagnosis.- — This  is  based  on  finding  the  fungus  by  cultural 
methods. 

Treatment. — In  the  only  case  known  an  intensive  potassium 
iodide  treatment  cured  the  condition. 

Enantiothamnosis. 

Definition. — A  nodular  condition  due  to  a  fungus,  Enantio- 
thamnus  bratilti  Pinoy,  191 1. 

Historical  and  Geographical. — This  condition  has  been  described 
by  Brault  in  Northern  Africa,  who  isolated  the  fungus,  the  com- 
plete botanical  description  of  which  we  owe  to  Pinoy. 

etiology. — The  causative  fungus  is  E.  braidti  Pinoy,  191 1  (see 
p.  1096). 

Symptomatology.- — The  condition  in  the  only  case  so  far  known 
tiaracterized  by  the  presence  of  nodules  on  the  gluteal  regions, 


RARER  NODULAR  AND  GUMMATOUS  AFFECTIONS      2107 

the  size  of  a  pea  to  a  small  egg.  The  nodules  had  a  central  crateri- 
form  opening,  from  which  some  pus  exuded. 

Diagnosis. — This  is  based  on  cultivating  the  fungus  from  the 
lesions. 

Treatment. — This  is  surgical,  but  first  potassium  iodide  might  be 
tried. 

Cladosporiosis. 

Definition. — A  nodular  condition  due  to  Cladosporium penicilloides 
Gueguen,  1911. 

Remarks. — There  is  another  tropical  condition  due  to  a  fungus 
of  the  genus  Cladosporium — viz.,  tinea  nigra — but  this  affection 
is  clinically  so  different  that  we  do  not  give  it  under  the  heading 
Cladosporiosis.  We  have  given  a  separate  description  of  it  (see 
p.  1101). 

Historical. — Fontoynont  isolated  the  fungus  from  a  case  in  Mada- 
gascar. Gueguen  placed  it  in  the  genus  Cladosporium  and  named  it 
C.  penicilloides  Gueguen,  1911,  and  Verdun  called  it  C.  madagas- 
cariense  Verdun,  1913  [vide  pp.  1100  and  1101). 

Symptomatology. — In  the  only  case  so  far  known,  that  of  Fon- 
toynont, gummatous  nodules  were  present  on  the  leg,  some  of  which 
slowly  ulcerated. 

Treatment. — Potassium  iodide  has  apparently  very  little  efficacy 
in  this  condition. 

Scopulariopsosis. 

This  condition  is  due  to  Scopulariopsis  blochi  Matruchot,  1 9 1 1 ,  and  5.  koningii 
Vuillemin,  1912.  Two  cases  have  been  reported  so  far  from  France.  The 
patients  presented  gumma ta  and  verrucose  patches  on  the  skin.  Lymphan- 
gitis was  noted  in  one  case.  The  diagnosis  is  based  on  finding  culturally 
the  fungi.     The  treatment  consists  in  giving  large  doses  of  iodides. 

It  is  to  be  noted  that  Pinoy  and  other  authorities  doubt  the  pathogenic 
role  attributed  to  S.  blochi. 


REFERENCES. 

Tropical  Dermatomycoses. 

Adamson  (1908-1912).     British  Journal  of  Dermatology. 

Boucher  (1918).     Bull.  Soc.  Path.  Exot.,  April. 

Brooke  (1908).     Manual  of  Tropical  Medicine. 

Castellani  (1905-1919).  Various  papers  in  British  Medical  Journal,  Journal 
of  Tropical  Medicine,  Transactions  of  the  Royal  Society  of  Medicine, 
Transactions  International  Congresses  of  Dermatology,  New  York  and 
Rome,  Ann.  Med.  Nivale,  Archiv.  f.  Dermatologie  u.  Syphilis. 

Chalmers  and  Marshall  (1914)  and  (1915),  and  Chalmers  and  Macdonald 
(191 6).     Journal  of  Tropical  Medicine  and  Hygiene. 

Crocker  (1905).     Skin  Diseases. 

Crocker  (1908).     The  Journal  of  Cutaneous  Diseases. 

De  Beurmann  and  Ramond  (1903).     Annales  de  Dermatologie. 

De  Beurmann  and  Gougerot  (1906).     Annales  de  Dermatologie. 

Dore  (1915).     British  Journal  of  Dermatology. 

Graham-Little  (1915).     British  Journal  of  Dermatology. 

Greig  and  Maitra  (1918).     Indian  Jour.  Med.  Res.,  January. 

Jeanselme  (1907).     Dermatologie  Exotique.     Paris. 


2io8  TROPICAL  DERMATOMYCOSES 

MacLeod  (1916).     British  Journal  of  Dermatology. 

Montpellier  (1918).     Bull.  Soc.  Path.  Exot.,  May. 

Morris  and  Dore  (191 7).     Diseases  of  the  Skin.     London. 

Nieuwenhuis  (1908).     Archiv  fur  Dermatologie  u.  Syphilis. 

Phalen  and  Nichols  (1908).     Philippine  Journal  of  Science. 

Rho  (1897).     Malattie  dei  Paesi  Caldi. 

Sabouraud  (1907).     Archives  de  Medecine  Experimentale;  (1918)  Presse  Med. 

Splendore  (1912).     Bulletin  Path.  Exotique. 

Wehmer  (1903).     Centralblatt  fiir  Bakteriologie. 

Whitfield  (1908).     British  Journal  of  Dermatology. 

Pint a. 

Blanchard  (1903).     Parasites  Vegetaux  in  Bouchard's  Traite  de  Pathologie 

Generate. 
Bodin  (1903).     Annales  de  Dermatologie. 
Castellani  (1906-09).     Ceylon  Medical  Reports. 
Crocker  (1905).     Diseases  of  the  Skin. 
Gastambide  (1881).     Presse  Med.  Belg. 
Jeanselme  (1904).     Dermatologie  Exotique.     Paris. 
Madden  and  Goodman  (1901).     Records  of  the  English  Government  Medical 

School. 
Manson  (1918).     Tropical  Diseases. 
Montoya  y  Florez  (1898).     These  de  Paris. 
Ruiz  y  Sandoval.     Quoted  by  Montoya. 
Sandwith  (1905).     British  Medical  Journal. 
Sheube  (1903).     The  Diseases  of  Warm  Countries.     London. 
Woolley.     Report  on  Pinto  (Pano  Blanco). 

Trichosporosis. 

Castellani    (1904-11).     Ceylon   Medical   Reports;   (1918)  Ann.  Med.  Nav., 

vol.  i.,  Nos.  3,4. 
Crocker  (1906).     Diseases  of  the  Skin. 
Desenne  (1878).     Lancet. 
Horta  (1912).     Memorias  Instituto  Cruz. 
MacLeod,  J.  M.  H.  (1912).     British  Journal  of  Dermatology. 
Manson  (191 8).     Tropical  Diseases. 
Morris  (1879).     Lancet. 

Perxet  (1900).     British  Journal  of  Dermatology,  vol.  xii.,  p.  141. 
Vuillemin  (1907).     Annales  de  Parasitologic 

Trichomycosis  axillaris  flava,  nigra,  and  rubra. 

Castellani   (191  i).     British  Journal  of  Dermatology;   (1912)   Transactions 

of  the  Royal  Society  of  Medicine. 
Chalmers   and   O'Farrell   (1913),   and   Chalmers   and   Stirling   (1913). 

Annals  of  Tropical  Medicine  and  Parasitology. 
Macfie  (1917).     Annals  of  Tropical  Medicine  and  Parasitology,  vol.  x.,  No.  3, 

p.  283. 

Tinea  imbricata. 
Alibert  (1832).     Atlas. 

Anderson  (1880).     Edinburgh  Medical  Journal. 
Blanchard  (1901).     Annales  de  Parasitologic 
Bonnafoy  (1893).     Le  Tokelau. 
Brumpt  (1910).     Parasitologie. 
Castellani  (1910-1914).     Journal  Ceylon   Branch   British  Med.  Assoc,  and 

Reports  Ad.  Comra.  on  Trop.  Diseases. 
Castellani   (1913).       British   Journal  of  Dermatology,   vol.   xxv.,   No.    12. 

(General  account.) 
Dampier  (1789).     Voyage  autour  du  Monde. 


REFERENCES  2109 

Fox,  T.  (1874).     Lancet. 

Koniger  (1878).     Virch.  Arch. 

MacGregor  (1870).     Glasgow  Medical  Journal. 

Manson  (1879).     China    Imp.   Mar.  Cust.    Med.    Reports;  Med.   Times  and 

Gazette.     (181 8).  Tropical  Diseases.    London. 
Meedervoort  (1859).     Med.Tydsch.  v.  Geneesk. 
Mialaret  (1891).     Ann.  Med.  Naval. 
Nieuwenhuis  (1898).     Arch.  f.  Derm.  u.  Syph. 
Phlen  (1905).     Mense's  Handbuch. 
Pijper  (1918).     Journ.  of  Trop.  Med. 
Roux  (1888).     Traite  des  maladies  des  pays  chauds. 
Tamson  (1898).     Geneesk.  Tijdsch.  v.  Ned.  Ind. 
Tribondeau  (1899).     Arch,  de  Med.  Nav. 
Turner  (1870).     Glasgow  Medical  Journal. 

Acladiosis. 
Castellani    (1916).     Notes   on  a   New  Ulcerative   Dermatomycosis.     With 
Report  on  the  Causative  Fungus  by  E.  Pinoy,  British  Medical  Journal, 
October   7,    p.    486.     (1918).     Proceedings  Royal  Society  of  Medicine, 
1917,  vol.  xi.  (Section  on  Dermatology),  pp.  12-18. 


CHAPTER  XCIII 
MYCETOMA   AND    PARAMYCETOMA 

General  remarks — The  mycetomas — The  maduromycoses — The  actinomycoses 
— The  paramycetomas — The  pseudomycetomas— Actinomycosis  of  the 
body — Nodular  actinomycosis — Trench  foot — References. 

GENERAL  REMARKS. 

The  subject  of  the  mycetomas  has  for  years  been  in  an  exceedingly 
confused  condition,  because  there  has  been  no  clear  conception  as  to 
the  exact  meaning  of  the  term,  and  no  scheme  whereby  the  fungi 
associated  with  the  disease  could  be  identified.  Further,  the  curious 
relationship  of  the  disease  to  malignant  growths  of  various  descrip- 
tions does  not  appear  to  have  been  realized  until  lately.  The  labours 
of  Pinoy,  of  Brumpt,  and  those  of  Chalmers  with  Archibald  and 
Christopherson,  systematically  continued  for  years,  have  enabled  a 
certain  amount  of  information  to  be  gathered  together  in  under- 
standable form. 

There  are  three  distinct  conditions  which  require  to  be  studied — 
viz.,  the  Mycetomas,  the  Paramycetomas,  and  the  Pseudomyce- 
tomas— and  detailed  references  to  the  fungi  associated  with  these 
forms  will  be  found  in  Chapter  XXXIX.  (p.  1035),  which  deals 
with  the  Fungi  Imperfecti;  in  addition,  a  few  remarks  are  necessary 
with  regard  to  actinomycosis  of  the  body. 

THE  MYCETOMAS. 

Synonyms. — Madura  foot,  the  Fungus  disease  of  India,  Godfrey  and  Eyre's 
Tubercular  disease,  Endemic  degeneration  of  the  bones  of  the  foot,  Morbus 
tuberculosis  Pedis,  Morbus  Pedis  Entophyticus,  Podelkoma,  La  Maladie  de 
Ballingall,  Slipada,  Hatty-ka-Pung,  Keerenagrah  (signifying  a  dwelling  of 
worms),  Kirudeo  (signifying  a  dwelling  of  worms),  GhootJoo  Mahdee  (signify- 
ing eggs  of  insects,  probably  so  called  from  the  small  bodies  found  in  the  dis- 
charge). 

Nomenclature. — In  1846,  Colebrook  of  Madura  said  that  the 
disease  was  commonly  known  in  some  parts  of  Southern  India  as 
'  Madura  foot.' 

In  i860,  Vandyke  Carter  applied  the  term  '  mycetoma,'  or  fungus 
tumour  (/*w"7S,  a  fungus,  and  oi&j/ta,  a  tumour),  to  that  variety  of 
Madura  foot  which  contained  black  granules,  and  one  year  later 
included  under  this  name  the  white  or  yellow  variety  of  the  same 
complaint  with  which  he  had  become  acquainted. 


MYCETOMA  21  n 

Definition. — The  term  '  mycetoma  '  includes  all  growths  and 
granulations  which  produce  enlargement,  deformity,  or  destruction 
in  any  portion  of  the  tissues  of  man  or  animals,  and  which  are 
caused  by  the  invasion  of  the  affected  area  by  fungi  belonging  to 
different  genera  and  species,  which  produce  bodies  of  varying 
dimensions,  colour,  and  shape,  composed  of  hyphse,  and  sometimes 
chlamydospores,  embedded  in  a  matrix.  These  bodies,  which  are 
capable  of  giving  rise  to  mycelial  filaments,  on  germination,  are 
termed  '  grains,'  and  are  found  either  embedded  in  the  pathological 
tissue  forming  these  growths  and  granulations,  or  escaping  freely  in 
the  discharge  therefrom.  In  addition,  eosinophile  bodies  can  usually 
be  seen. 

Early  History. — According  to  Waring,  as  quoted  by  Collas,  the 
Sanscrit  work  '  Vaweda,'  by  which  is  probably  meant,  '  At'harva- 
veda,'  describes  a  disease  of  the  foot  termed  '  padavalmicum, ' 
which  causes  swelling  and  the  formation  of  little  fleshy  tumours, 
which,  after  an  interval  of  a  year  from  the  commencement  of  the 
disease,  discharge  a  peculiar  fluid. 

This  disease  is  distinguished  from  another  malady  of  the  foot 
which  is  called  '  slipatham,'  or  elephant  foot. 

If  the  above  is  a  correct  quotation  from  the  '  At'harvaveda,'  then 
the  Ancient  Indian  surgeons  must  have  distinguished  elephantiasis 
of  the  foot  from  such  conditions  as  might  have  been  produced 
therein  by  mycetoma,  yaws,  etc. 

It  is,  however,  curious  that,  like  Collas,  we  have  been  unable  to 
find  any  account  of  such  a  disease  in  the  writings  of  Susruta. 

The  term  'perical,'  used  by  Kaempfer  in  1712,  is  applicable  to  an)' 
enlargement  of  the  foot,  whether  caused  by  elephantiasis,  mycetoma, 
or  yaws,  but  the  Pondichery  missionary  of  1714  appears  to  have 
seen  the  disease  mycetoma,  and  possibly  the  actinomycotic  variety, 
because  he  describes  under  the  term  '  fourmiliere  des  vers  '  an  in- 
curable disease  of  the  foot  in  which  numerous  small  ulcers  form, 
which  intercommunicate  by  means  of  canals  full  of  worms.  These 
canals  are  described  as  being  peculiar  in  that  if  one  closes  another 
opens. 

Heyne  probably  recognized  some  sort  of  a  mycetoma,  in  1806, 
in  the  foot  of  the  Rajah's  brother  at  Cuddapah,  and  Brett's '  adipose 
sarcoma,'  described  in  1840,  may  have  been  of  the  same  nature. 

Madura  Foot  Period. — With  the  closing  years  of  the  last  period 
it  will  be  noticed  that  it  began  to  dawn  upon  the  medical  men  of 
India  that  there  existed  in  that  country  a  peculiar  disease  of  the 
foot,  and  this  was  emphasized  by  Gill  of  Madura,  who,  in  1842, 
described  a  condition  of  that  member  which  was  characterized 
by  marked  deformity  and  fungoid  excrescences,  from  which  flowed 
an  offensive  ichorous  discharge,  while  internally  the  disease  pro- 
duced a  condition  resembling  fibro-cartilage,  and  destroyed  joints, 
cartilages,  and  ligaments. 

Four  years  later,  Colebrook,  Gill's  successor  at  the  Madura 
Dispensary,   confirmed  these  observations,   and   stated  that   the 


2i  12  MYCETOMA  AND  PARAMYCETOMA 

disease  was  commonly  known  in  some  parts  of  India  as  '  Madura 
foot.'  As  no  mention  is  made,  as  far  as  we  know,  by  these  authors 
of  any  black  pigment  being  present  in  their  cases,  we  conclude  that 
probably  they  saw  the  actinomycotic  variety  of  mycetoma. 

It  is  interesting  to  note  that  about  this  time  (1845)  von  Langen- 
beck,  in  Kiel,  made  illustrations  of  some  curious  bodies  which  he 
considered  to  be  fungal  in  nature,  and  which  he  found  in  the  pus 
from  a  case  of  spinal  caries.  Unfortunately  he  never  published 
this  observation,  which  was  made  known  by  Israel  one  year  after 
Bollinger's  discovery,  which  will  be  mentioned  below. 

In  1848,  Lebert  found  some  peculiar  spherical  yellowish  bodies, 
about  the  size  of  a  pin's  head,  in  some  thick  gelatinous  pus  which 
Louis  had  obtained  from  an  abscess  associated  with  much  swelling 
of  the  thoracic  wall  in  a  man,  aged  fifty  years,  in  Paris.  These 
bodies  were  carefully  examined, both  microscopically  and  chemically, 
and  drawings  were  made  which  were  subsequently  published  by 
Lebert  (1857). 

We  have  examined  copies  of  these  drawings,  and  they  represent 
in  a  typical  manner  the  fungus  of  an  actinomycosis.  Lebert, 
however,  failed  to  recognize  their  fungal  nature. 

In  1855,  Smith,  in  London,  made  some  drawings  for  Paget  of 
a  tumour  of  the  upper  jaw,  in  which  an  organism  resembling  a 
ray  fungus  is  portrayed.  These  drawings  were  published  by 
Kanthack  (1896). 

Also  in  1855,  Ballingall,  in  India,  described  a  disease  of  the 
foot,  in  the  discharge  from  which  he  found  bodies  composed  of  large 
cells  with  transparent  fringes  containing  irregular  spicules,  or 
simply  composed  of  radiating  spicules  without  cells.  In  1858, 
Rustomji  described  a  variety  of  Madura  foot  in  which  he  found  small, 
soft,  yellowish  granules,  and  which  he  distinguished  from  another 
variety  of  the  same  disease,  in  which  he  found  a  dark,  soft,  thick 
substance.  Rustomji's  first  variety  we  call  yellow  actinomycosis 
and  his  second  variety  black  maduromycosis. 

We  will  now  consider  the  subject  of  the  Maduromycoses. 

THE  MADUROMYCOSES. 

Definition. — The  Maduromycoses  are  those  forms  of  mycetoma 
which  possess  grains  composed  of  large  segment  ed  mycelial  filament  s, 
possessing  well-defined  walls  and  usually  chlamydospores. 

History. — Excluding  some  ancient  references  discovered  by 
Collas,  to  which  Corre  has  drawn  attention,  and  which  will  be  con- 
sidered when  we  discuss  that  author's  writings,  the  history  of  the 
black  maduromycoses  commences  in  1845  in  India,  where  Garrison- 
Surgeon  Godfrey,  in  his  Departmental  Report  of  the  Public  Dis- 
pensary at  Bellary,  described  the  occurrence  of  a  considerable 
black  deposit,  much  resembling  fragments  of  coal,  in  a  foot  which 
had  been  amputated  because  it  was  affected  by  a  disease  which  was 
commonly  known  as  '  ulcus  grave,'  because  the  ulcers  and  sinuses 


MADUROMYCOSES  21 13 

produced  such  a  serious  condition  that  amputation  became  necessary. 
This  disease  he  had  described  in  the  same  report  for  the  preceding 
year,  designating  it  '  morbus  tuberculosis  pedis,'  because,  though 
he  recognized  it  to  be  dissimilar  from  other  recorded  diseases,  he 
looked  upon  it  as  a  local  tubercular  affection,  and,  influenced  by 
this  view,  he  considered  the  black  particles  mentioned  above  to  be 
accidental,  and  not  essential  parts  of  the  disease.  He  also  mentions 
that  it  was  known  to  the  natives  as  '  ghootloo  mahdee,'  from  the 
tubercular  irregularities  being  supposed  to  resemble  eggs. 

This  first  case  of  black  maduromycosis  occurred  in  a  native  aged 
about  thirty  years,  and  had  existed  four  to  five  years  before  ampu- 
tation was  performed.  The  morbid  appearances  are  described  as 
being  similar  to  those  fully  set  forth  in  his  1844  report,  with  the 
addition  of  there  being  in  this  instance  one  cyst  (or  excavated 
tubercle)  containing  melanotic  matter  about  the  size  of  a  small 
walnut,  and  extending  from  the  plantar  to  the  dorsal  aspect  of  the 
foot,  between  the  metatarsal  bones  of  the  great  and  second  toes, 
which  were  in  part  absorbed.  The  integuments  were  not  involved 
in  this  mass,  which  when  recent  had  an  angular  and  brilliant  black 
appearance  much  resembling  a  fragment  of  coal,  and  was  considered 
to  be  an  accidental  product  in  this  peculiar  case. 

Carter  says  that  the  second  volume  of  the  '  Indian  Annals  ' 
(probably  dated  about  1849)  on  p.  706  contains  an  account  of 
dark  granular  or  black  gritty  particles  being  found  among  the  bones 
and  in  the  sinuses  of  a  diseased  foot,  but  we  have  been  unable  to 
refer  to  this  work,  and  are  ignorant  of  the  name  of  the  discoverer 
and  of  the  date  and  place  in  which  this  observation  was  made.  The 
particles  in  question  were  examined  microscopically,  and  were 
believed  to  consist  entirely  of  dried  blood,  a  belief  which  lasted  for 
many  years. 

It  may  perhaps  be  advisable  at  this  point  to  draw  attention  to  the  fact  that 
Ballingall's  celebrated  observations  do  not  refer  to  the  black,  but  to  the  yellow 
variety  of  mycetoma,  and  hence  do  not  enter  into  this  history. 

Sub-Assistant  Surgeon  Bazonji  Rustomji  (1858),  of  the  Bhoo's 
Dispensary,  in  the  Province  of  Kutch,  drew  attention  to  the  fact 
that  there  were  two  forms  of  the  disease — viz.,  one  in  which  there 
was  no  granular  deposit,  but  only  a  substance  dark  in  colour  and 
soft  and  thick  in  consistence;  while  the  other  showed  small,  soft, 
yellowish  granules.  This  is  the  first  occasion,  as  far  as  we  know, 
when  a  differentiation  was  made  between  the  melanoid  and  the 
ochroid  varieties  of  the  disease,  but  Rustomji  did  not  recognize  the 
fungal  nature  of  the  bodies  in  question. 

Eyre  (i860)  states  that  in  every  foot  examined  by  him  there  were 
numerous  minute  tubercles  resembling  fish  roe,  which  were  found 
lying  beneath  the  muscles  and  extending  from  the  bones  to  beneath 
the  skin,  with  nodules  of  the  same  appearance  and  often  black  in 
colour.  This  paper  deals  with  the  external  characters  of  the  disease, 
its  previous  history,natural  course,  morbid  anatomy,  cetiology  (which 
was  doubtfully  thought  to  be  somewhat  tubercular),  and  treatment. 

133 


21 1 4  MYCETOMA  AND  PARAMYCETOMA 

In  i860,  Vandyke  Carter  began  a  series  of  classical  observations 
upon  the  black  and  yellow  forms  of  Madura  foot,  which  he  continued 
until  1874,  and  during  which  he  firmly  established  the  fungal 
nature  of  the  disease. 

His  first  paper  (i860)  was  entitled  '  On  a  New  and  Striking  Form 
of  Fungus  Disease  affecting  the  Foot  and  Prevailing  Endemically  in 
Many  Parts  of  India.'  In  his  second  publication  (i860)  he  clearly 
differentiated  between  the  white  or  ochroid  division  of  the  Myce- 
tomas, which  to-day  we  call  '  actinomycosis,'  and  the  black  or 
melanoid  variety,  which  we  now  name  'black  maduromycosis.' 
He  demonstrated  that  the  black  grains  were  of  true  vegetal  nature, 
with  a  black  friable  rind  composed  of  clear,  orange-tinted,  ovoid 
or  angular  cells  and  beaded  fibres  closely  arranged  so  as  to  form  a 
compact  structure,  and  in  addition  larger  vesicular  bodies  (seemingly 
comparable  to  gemmules  or  sporangia) ,  which  he  thinks  may  arise  at 
the  extremities  of  the  compressed  beaded  fibres  by  gemmation  and 
expansion.  The  pale  reddish-brown  central  part  of  the  larger 
sclerotes  was  composed  of  slender,  pale,  flattened,  and  branching 
fibres  arranged  in  bundles  and  intermixed  with  numerous  granules 
and  a  few  large  beaded  fibres,  the  septa  of  which  were  sometimes 
absent. 

He  placed  some  black  particles,  taken  from  a  foot,  on  cotton  soil 
moistened  with  animal  juices  and  enclosed  in  a  stoppered  bottle, 
which  he  left  unopened  for  two  and  three-quarter  years,  when  he 
found  a  thin  reddish  film  had  appeared.  Other  black  particles  sown 
on  rice  paste  for  the  same  length  of  time  remained  unchanged,  but 
on  opening  the  bottle  a  red  mould  speedily  made  its  appearance. 

With  reference  to  this  mould,  he  says:  '  It  had  not,  however,  a 
clear  connection  with  the  fungus  particles,  but  seemed  to  spring  up 
independently  of  them  upon  the  rice  whenever  this  was  exposed  to 
the  air.' 

This  statement  is  of  importance,  as  he  grew  a  fungus  from  the 
white  variety  which  was  pink  in  colour,  and  produced  sporangia 
resembling  those  of  a  species  of  the  genus  Mucor  Micheli,  1729,  but 
differing  therefrom  in  the  absence  of  a  columella,  which  should  have 
brought  it  under  the  genus  Mortierella  Coemans,  1863;  but  Berkeley, 
who  examined  the  growths  from  a  botanical  point  of  view,  classified 
it  under  the  genus  Chionyphe  Thienmann,  1839,  calling  it  Chionyphe 
carteri  Berkeley,  1862,  and  defining  it  as: — '  Hyphasmate  ex  albo 
flavorubroque,  sporangiis  demum  coccineis,  sporis  breviter  fusi- 
formibus.' 

The  genus  Chionyphe,  however,  was  never  recognized  by  myco- 
ogists  generally,  as  its  species  came  under  the  genera  Mortierella 
or  Mucor,  while  Chionyphe  carteri  was  most  undoubtedly  a  contami- 
nation, as  its  connection  with  the  black  or  white  grains  was  never 
proved,  as  we  have  noted  above  with  regard  to  the  former. 

Thus  we  may  conclude  that  although  Carter  gave  the  first  proof 
of  the  parasitic  nature  of  the  grains,  he  was  unable  to  produce 
growths  by  cultivation  from  either  the  black  or  the  white  varieties. 


MADUROMYCOSES  21 15 

In  i860,  Minas  wrote  upon  '  keereenagoah  '  of  the  foot,  as  seen  in 
the  Punjab.  The  terra  used  is  a  vernacular  word  signifying  worm 
disease.  He  states  that  the  characteristic  symptom  of  the  complaint 
is  gradual  enlargement  of  the  foot,  usually  starting  with  a  swelling 
in  the  sole  associated  with  the  presence  and  constant  discharge  of 
small  particles,  either  soft  or  black  and  hard,  from  fistulous  openings. 

Collas  (1861)  described  black  maduromycosis  as  seen  in  Pondichery. 
He  recognized  the  little  bodies  of  blackish  or  reddish  brown  colour, 
which  in  their  clearer  parts  seemed  to  be  formed  of  small  transparent 
cells,  which  he  could  not  sufficiently  study.  He  called  the  disease 
'  degeneration  endemique  des  os  du  pied.' 

H.  J.  Carter  (1862)  came  to  the  conclusion  that  the  fungus  of 
black  maduromycosis  was  nearly  allied  to  Mucor  stolonifer  Ehren- 
berg,  1818,  the  spores  of  which  in  an  amoeboid  state  he  considered 
entered  the  body  through  the  sudorific  ducts.  Berkeley  (1862) 
mentioned  the  fungus  in  question;  he  gave  it  the  name  Chionyphe 
carteri,  a  nomenclature  which  he  subsequently  repeated  (1865). 

In  1867,  Moore  reported  an  important  early  case  in  which  he 
effected  a  cure  by  cutting  and  scraping  away  all  the  diseased  tissues, 
and  he  augmented  this  in  1873  by  recording  two  more  cases  of  a 
similar  nature,  treated  in  the  same  way  with  a  like  result. 

In  1870,  Holmsted,  of  Hyderabad,  Sind,  found  a  thorn  of  irregular 
shape  and  \  inch  long  in  a  case  of  black  mycetoma,  in  which  it 
had  been  embedded  for  two  years.  In  the  same  year,  Bristowe 
described  and  figured  the  fungus  seen  in  the  black  particles  of  a 
foot  from  a  case  of  black  maduromycosis  amputated  in  Cantoor, 
and  demonstrated  to  the  Pathological  Society  of  London  by  Tilbury 
Fox.  Bristowe's  descriptions  and  figures  are  excellent,  and  amply 
confirm  Vandyke  Carter's  work.  Thudichum  chemically  examined 
the  black  pigment  of  this  case,  and  showed  that  it  was  not  derived 
from  blood. 

Hogg  (1872)  described  a  black  maduromycosis  from  India,  in 
which  he  was  able  to  observe  the  fungal  threads  and  to  resolve  them 
into  jointed  dissepiment ed  cells,  some  branching  out  and  attaining 
a  considerable  length,  while  others  terminated  in  an  enlarged  ovoid 
head.  He,  however,  believed  that  the  fungus  was  a  secondary 
product,  which  might  greatly  aggravate  but  did  not  originate  the 
disease,  and  suggested  that  it  might  be  introduced  at  the  time  of 
the  first  accident  when  the  foot  was  struck  against  a  stone,  or  by  the 
poultices  used  as  treatment  in  a  later  stage. 

Vandyke  Carter  (1874)  published  his  monumental  and  classical 
work  '  On  Mycetoma,  or  the  Fungus  Disease  of  India,'  which  con- 
cluded his  long-continued  labours  at  this  complaint. 

Lewis  and  Cunningham  (1875)  admitted  the  fungal  nature  of 
the  black  particles,  but  not  of  the  yellow  granules.  They  showed 
that  Chionyphe  carteri  had  nothing  to  do  with  black  or  yellow  grains. 

In  1876,  Berkeley  came  to  the  conclusion  that  Chionyphe  carteri 
had  nothing  to  do  with  mycetoma,  a  point  which  can  be  easily 
judged  from  the  passages  quoted  above. 


2ii6  MYCETOMA  AND  PARAMYCETOMA 

Notwithstanding  all  these  researches,  a  great  deal  of  confusion 
still  existed  with  regard  to  the  disease,  which  can  be  judged  by  a 
study  of  Fox  and  Farquhar's  (1876)  report.  It  was  admitted  that 
the  black  granules  were  fungal  in  nature,  but  it  was  contended  that 
they  were  not  causal  in  effect,  because  all  the  essential  features  of 
mycetoma  were  found  to  be  present  without  any  black  fungal 
particles,  and  because  there  was  not  sufficient  evidence  forthcoming 
at  the  time  in  proof  of  the  vegetal  character  of  the  yellow  grains, 
which  were  believed  to  be  essentially  fatty  in  nature.  It  was, 
however,  admitted  that  Moore's  observation  showing  that  the  black 
variety  could  be  cured  by  excision  of  all  the  particles  at  an  early 
stage  of  the  disease  was  a  strong  argument  in  favour  of  the  parasitic 
nature  of  mycetoma. 

Though  Carter  had  found  black,  yellow  or  white,  and  red  grains, 
still  the  general  belief  was  that  these  were  one  and  the  same  process, 
and,  moreover,  observers  of  this  period  must  have  seen  the  pseudo- 
mycetomatous  conditions  mentioned  above,  because  competent 
workers  appear  to  have  met  with  cases  in  which  they  were  unable 
to  find  any  grains,  although  the  clinical  appearances  resembled 
mycetoma. 

Corre  (1883)  placed  in  order,  completed,  and  revised  the  notes 
of  researches  made  by  Collas  since  his  publication,  already  men- 
tioned, in  1861.  In  these  notes,  which  were  published  after  his 
death,  Collas  desired  his  previous  name  for  the  disorder  to  be  altered 
to  '  La  Maladie  de  Ballingall,'  and  states  that  the  earliest  references 
to  the  disease  with  which  he  is  acquainted  can  be  found  in  Waring's 
paper,  and  in  one  of  the  sacred  books  of  the  East  which  he  calls 
'  Vaweda  '  (Ushta  wunga  hrethayum),  which  appears  to  us  to  be  the 
'  Atharvaveda.'  In  this  latter  work,  '  slipatham,'  or  elephant  foot, 
is  distinguished  from  '  padavalmicum,'  which  refers  to  an  incurable 
malady  of  the  foot  associated  with  swelling  and  the  formation  of 
fleshy  tumours,  from  which,  about  a  year  after  the  appearance  of  the 
first  symptoms,  there  exudes  a  peculiar  fluid.  He  also  points  out 
that  the  words  '  perikal,'  '  anaikal '  (Tamil) — this  means  Cochin 
leg — '  slipada  '  (Bengalese),  '  hatty-ka-poung  '  (Deccan),  are  applic- 
able to  elephantiasis  as  well  as  to  Madura  foot,  and,  therefore,  should 
not  be  specially  applied  to  the  latter,  as  they  really  mean  the 
'  leg  of  an  elephant.'  In  Ballary,  he  says,  the  disease  was  called 
'  gootloo  mahdee,'  because  the  swellings  on  the  foot  were  thought 
to  be  like  eggs;  while  in  Raj  put  ana  it  was  called  '  kirinagras/  or 
the  dwelling-house  of  worms,  because  the  sinuses  were  considered 
to  be  like  the  cavities  often  occupied  by  the  larvae  of  flies.  He  also 
says  that  in  1714  a  missionary  described  under  the  name  of  '  four- 
miliere  des  vers'  a  disease  of  Pondichery  which  was  incurable,  and 
in  which  numerous  ulcers  intercommunicated  by  means  of  small 
canals  full  of  worms,  which  were  peculiar  in  that  if  one  closed 
another  opened.  This  information  Collas  obtained  from  vol.  ii., 
p.  167,  of  a  book  published  in  Paris  in  1812,  and  entitled  '  Memoires 
sur  les  mceurs  et  coutumes  de  l'lnde  par  un  missionaire.'     Collas 


MADUROMYCOSES  2117 

also  points  out  that  in  1806  Heyne  saw  the  brother  of  a  Rajah  at 
Cuddapah  in  Hyderabad  with  a  foot  in  a  leprotic  state,  but  which 
was  considered  to  be  distinct  from  leprosy,  although  it  was  not 
known  what  the  nature  of  the  disease  might  be.  Collas  thinks  that 
this  must  have  been  mycetoma,  and  draws  attention  to  Brett's 
'  sarcomes  adipeux,'  in  which  he  says  it  is  difficult  not  to  recognize 
Ballingall's  disease. 

With  reference  to  the  above  names,  it  will  be  noted  that  they 
apply  to  any  form  of  mycetoma,  and  not  especially  to  black  myce- 
toma. The  name  '  Ballingall's  disease,'  in  our  opinion,  is  not 
applicable  to  the  black  mycetomas,  because,  as  already  indicated, 
he  was  not  acquainted  with  the  disease. 

In  1886,  Carter  gave  up  his  pink  mould,  and  drew  attention  to 
the  similarity  between  the  fungus  of  actinomycosis  and  that  of 
mycetoma. 

Kanthack  (1893)  studied  both  the  yellow  and  black  mycetomas, 
and  came  to  the  conclusion  that  the  former  agreed  morphologically 
and  structurally  with  actinomycosis,  but  with  regard  to  the  black 
grains  his  position  was  curious,  for  although  he  found  them  to 
consist  of  an  olive-brown,  glassy,  or  finely  granular  material,  in 
which  hollow  filaments,  radially  arranged,  were  embedded,  still 
he  regarded  these  as  degeneration  changes,  and  sought  to  prove 
that  the  granules  were  an  organism  allied  to  the  actinomycosis  fungus 
which  he  had  found  in  the  yellow  variety.  Thus,  like  Vandyke 
Carter,  he  believed  both  varieties  to  be  fungal  in  nature  and  to  be 
caused  by  the  same  fungus,  but  he  attempted  to  show  that  the 
fungus  of  the  yellow  variety  existed  in  the  black,  while  the  former 
observer  believed  the  reverse  to  be  true.  He  named  the  fungus 
Oospora  indica  Kanthack,  1893,  and  distinguished  the  two  varieties 
as  0.  indica  var.  flava  and  0.  indica  var.  nigra.  Unna,  to  whom 
he  sent  specimens,  however,  did  not  make  this  error,  but  says: — 
'  A  whole  series  of  important  distinctions  separate  the  two  fungi, 
and  there  is  no  question  of  their  identity.' 

Boyce  and  Surveyor  (1894),  in  a  most  important  paper,  first 
definitely  proved  that  the  fungi  existing  in  the  black  and  yellow 
varieties  were  quite  different,  and  thus  definitely  established  the 
two  main  divisions  of  mycetoma,  which  to-day  we  call  maduro- 
mycosis  and  actinomycosis.  They  showed  that  the  black  grains 
were  composed  of  a  large,  septate,  branching  fungus  embedded  in  a 
brown  pigmented  ground  substance,  which  was  readily  bleached 
by  eau  de  Javelle.  They  did  not  observe  spore  formation,  nor  was 
cultivation  attempted. 

In  the  same  year  Boccaro  also  differentiated  between  the  white 
and  the  black  varieties  of  the  disease. 

Chatterjee  (191 1)  observed  that  grains  placed  in  agar  and  glucose 
agar  tubes  increased  in  size  some  seven  to  eight  times  in  four  days, 
and  were  surrounded  by  fine  hair-like  structures  which  were  composed 
of  delicate  branching  mycelial  threads,  which  were  seen  to  come  from 
the  thick  black  threads.  On  potato,  the  growth  was  dry  and  black.  In 


21 1 8  MYCETOMA  AND  PARAMYCETOMA 

broth,  small  white  colonies  composed  of  radiating  threads  were  found 
sticking  to  the  walls  of  the  tube.  No  diffuse  growth  was  seen,  nor  did 
any  scum  form  on  the  surface.     Animal  experiments  were  negative. 

Mackenzie,  in  the  same  year,  appeared  to  obtain  similar  cultures 
on  agar;  at  first  the  growth  was  white  and  translucent,  with  radia- 
tions from  the  centre,  later  it  became  greyish  yellow,  there  being  a 
central  granule  surrounded  by  a  clear  zone  and  an  indented  margin. 
After  a  week  the  colony  became  a  deep  mahogany,  and  under  the 
microscope  exhibited  mycelial  structures. 

Semon  (1915)  reported  a  case  of  black  maduromycosis  which 
occurred  in  a  native  Indian  soldier  serving  in  France.  He  left 
India  about  October,  1914,  and  in  January,  1915,  he  injured  one  of 
his  feet  by  the  fall  of  an  ammunition  box.  The  patient  attributed 
the  disease  to  this  cause,  but  Semon  considers,  probably  correctly, 
that  he  must  have  been  infected  before  leaving  India.  A  typical 
mycetoma  developed  in  about  six  months,  and  the  pus  contained 
black  particles  in  which  a  central  mass  of  mycelium  obscured  entirely 
by  black  pigment  could  be  made  out,  but  no  proper  demonstration 
of  the  fungus  in  situ  could  be  made.  The  foot  could  not  be  ampu- 
tated, but  sections  were  made  of  some  of  the  tissue,  which  showed 
marked  vascular  hypertrophy,  polymorphonuclear,  plasma,  and 
connective  tissue  cells,  but  no  endo-  or  periarteritis  and  no  giant 
cells.  Growths  were  obtained  at  350  C.  on  agar-agar,  maltose  agar, 
and  Raulin's  fluid.  The  fungus  formed  a  central  black  portion  with 
a  peripheral  zone  of  white  or  grey,  and  in  the  course  of  ten  days  or 
less  became  black. 

In  1916  Chalmers  and  Archibald  grew  a  fungus  allied  to  that 
described  by  Semon  from  a  case  of  black  maduromycosis  found  in 
the  Anglo-Egyptian  Sudan,  and  in  19 18  defined  and  classified  the 
Maduromycoses. 

Climatology.- — The  Maduromycoses  are  known  to  occur  in  Europe, 
Africa,  Asia,  and  America,  but  not  in  Oceania. 

The  climatology  has  been  most  thoroughly  studied  for  black 
maduromycosis,  which  occurs  in  the  Anglo-Egyptian  Sudan,  where 
the  disease  was  first  described  by  Balfour  in  1904,  and  the  northern 
part  of  which  is  hot  and  arid.  He  gives  the  native  name  for  myce- 
toma as  '  Napt  Hindi  Nabit,'  and  states  that  the  black  variety  is 
most  frequently  encountered,  and  that  the  foot  is  the  part  principally 
affected,  while  the  inguinal  glands  are  often  involved.  In  1908, 
Wenyon  noted  its  presence  at  Bor,  which  is  hot  but  not  arid,  while 
Balfour's  researches  in  191 1  have  already  been  noted  in  the  historical 
section.  According  to  our  inquiries,  the  word  most  commonly  used 
by  natives  in  the  Sudan  is  '  en-nabt,'  which  means  '  the  growth.' 

In  addition  to  the  Anglo-Egyptian  Sudan,  the  following  is  a 
list  of  African  places  from  which  cases  of  black  maduromycosis 
have  been  reported : — Algeria,  Tunisia,  Somaliland,  Madagascar, 
Transkei  (South  Africa),  Senegal,  and  the  French  Sudan. 

In  Asia  the  disease  is  recorded  from  the  Yemen,  various  parts  of 
India,  Ceylon,  and  possibly  from  North  Borneo. 


MADUROMYCOSES  2 119 

In  America  it  has  been  described  in  the  United  States  by  Wright, 
and  in  the  West  Indies  by  Scheult. 

In  Europe  it  has  so  far  only  been  found  in  Italy,  Macedonia,  and 
Southern  Germany. 

This  distribution,  according  to  political  geography,  has  but  little 
meaning  when  the  object  being  studied  is  a  fungus,  and  for  further 
details  we  turn  to  plant  geography.  According  to  Drude,  climatic 
and  local  conditions  permit  the  division  of  the  surface  of  the  world 
into  six  zones  of  vegetation,  viz. : — The  Northern  Glacial  Zone, 
the  Northern  Cold  Winter  Zone,  the  Northern  Hot  Summer  Zone, 
the  Tropical  Zone,  the  Southern  Hot  Summer  Zone,  and  the  Southern 
Cold  Zone. 

The  black  maduromycoses  occur  in  the  Northern  Hot  Summer 
Zone,  which  includes  Spain  and  Italy,  North  America,  the  Sahara, 
Indo-China,  Malay  Archipelago,  the  United  States  (roughly  south 
of  Utah),  and  Mexico.  The  general  characters  of  this  region  are: — 
Very  hot  summer  temperatures  with  cold  nights  and  no  real  winter, 
but  with  varying  rainfall.  It  contains  very  dry  climates;  it  also 
contains  wet  areas.  The  black  maduromycoses  are  most  commonly 
met  with  in  the  dry  parts  of  this  area. 

The  Tropical  Zone,  which  appears  to  be  the  real  home  of  these 
fungi,  is  generally  humid,  but  contains  arid  regions  bordering  upon 
the  preceding.  In  this  zone  comes  the  Anglo-Egyptian  Sudan,  in 
the  northern  or  more  arid  part  of  which  black  maduromycoses  are 
common,  and  the  same  remarks  apply  to  Somaliland,  while  West 
Africa  is  mostly  moist. 

It  also  includes  the  greater  part  of  India,  in  which  the  distribution 
of  mycetoma,  according  to  Boccaro,  is  interesting. 

This  observer  states  that  Major  Prain  divided  India  into  six 
floral  regions,  viz. : — India  Deserta,  India  Diluvia,  India  Aquosa, 
India  Vera,  India  Sub-Aquosa,  and  India  Littorea,  while  black 
maduromycosis  is  found  in  only  India  Deserta  and  India  Vera,  and 
is  practically  almost  absent  in  other  regions. 

India  Deserta  includes  the  Indus  Plain  Region — i.e.,  Sind, 
Rajputana,  and  the  Punjab;  while  India  Vera  includes  the  Deccan 
Region,  consisting  of  the  dry  but  not  desert  triangle  between  the 
Western  and  Eastern  Ghats,  with  its  apex  at  Tinnevelly  and  its  base 
at  the  borders  of  the  plain  of  the  Ganges. 

The  white  varieties  of  mycetoma  are  also  found  in  this  area,  but 
are  outnumbered  by  the  black  maduromycosis,  while  in  India 
Deserta  the  preponderance  of  the  black  maduromycoses  is  even 
more  marked  than  in  India  Vera. 

In  Madura  and  adjoining  districts  of  Tinnevelly,  Palmcotta,  and 
Coimbatore,  situate  in  India  Vera,  mycetoma  is  very  common,  and 
the  climate  is  hot  and  arid. 

The  Southern  Hot  Summer  Zone  includes  South  Africa,  where 
the  disease  has  been  recorded,  but  where  it  is  apparently  rare. 

This  is  as  far  as  the  present  state  of  our  knowledge  permits  us 
to  go  with  regard  to  geographical  distribution,  and  more  research 


2120  MYCETOMA  AND  PARAMYCETOMA 

on  this  part  of  the  subject  is  required,  but  from  the  above  it  is 
obvious  that  heat  and  aridity  are  favourable  conditions  for  the  fungi 
which  cause  black  maduromycosis. 

Botanical  and  Zoological  Distribution. — Unfortunately,  we  are 
in  complete  darkness  as  to  the  characters  which  the  fungi  causing 
black  maduromycosis  assume  when  not  living  in  animals  or  on 
artificial  culture  media. 

Even  with  regard  to  those  forms  of  black  maduromycosis  due  to 
an  aspergillus,  we  are  quite  ignorant  as  to  whether  this  particular 
fungus  lives  on  soil  or  on  plants. 

/Etiology. — The  outstanding  feature  of  microscopical  specimens 
prepared  from  a  case  of  maduromycosis  is  the  presence  of  coloured 
granules,  black  in  black  maduromycosis,  whitish  or  yellowish  in 
white  or  yellow  maduromycosis,  and  red  in  red  maduromycosis. 

These  coloured  granules  are  called  '  grains,'  a  term  which  has  been 
defined  by  Chalmers  and  Archibald  as  follows: — 

'The  term  "granum"  or  grain  has  been  given  to  differently 
coloured  bodies  of  varying  consistence,  size,  and  shape,  found  in 
mycetomas,  and  composed  of  hyphae,  with  sometimes  chlamydo- 
spores,  embedded  in  a  matrix  and  giving  rise  to  mycelial  filaments 
on  germination.' 

The  aetiological  importance  of  these  grains  and  their  contained 
fungus  rests  upon  the  fact  that  they  are  present  in  all  forms  of 
maduromycosis  and  are  co-extensive  with  the  disease,  while  their 
complete  removal  effects  a  rapid  and  complete  cure. 

Animal  inoculations  have  been  successful  in  some  varieties,  thus 
affording,  in  these  instances,  a  full  and  convincing  proof  of  the  aetio- 
logy of  the  fungus — e.g.,  Pinoy's  and  Pepere's  varieties. 

The  aetiological  features  of  the  various  forms  of  maduromycosis 
are  set  forth  below  in  a  list  which  shows  the  Maduromycoses  classified 
— -firstly,  by  the  colour  of  the  grain ;  secondly,  by  the  geographical 
distribution;  and  thirdly,  by  the  discoverer's  name  or  names. 

I.  The  black  maduromycoses,  with  black  grains. 

II.  The  white  or  yellow  maduromycoses,  with  white  or  yellowish 
grains. 

III.  The  red  maduromycoses,  with  red  grains. 

I.  THE  BLACK  MADUROMYCOSES. 
These  may  be  divided  into: — 

A.  The  European  black  maduromycoses. 

B.  The  African  black  maduromycoses. 

C.  The  Asian  black  maduromycosis. 

D.  The  American  black  maduromycoses. 

A.  The  European  Black  Maduromycoses. 
(i)  Bassini's,  Kbbner's,   and   Schmincke's   black   maduromycoses, 
cspectively  found  in  Padua,  Italy,  and  in  Kissingen,  and  of  which 
iture  of  the  etiological  fungus  is  unknown. 


THE  BLACK  MADUROMYCOSES  2 121 

(2)  Bovo's  black  maduromycosis ,  found  in  Genoa,  and  of  which  the 
causal  agent  is  called  Madurella  bovoi  Brumpt,  1910,  but  this 
identification  must  be  accepted  with  reserve,  as  the  fungus  has  never 
been  cultivated,  and  may  not  agree  with  the  definition  of  the  genus 
Madurella,  as  altered  by  Pinoy  in  1912  subsequent  to  the  cultivation 
of  M.  mycetomi  and  M.  tozeuri. 

(3)  Pepere's  black  maduromycosis,  found  at  Domusnovas  in  the 
Province  of  Cagliari  in  Sardinia,  and  caused  by  Scedosporium 
sclorotiale  Pepere,  1914. 

B.  The  African  Black  Maduromycoses. 

(t)  Brumpt's  black  maduromycosis,  caused  by  Madurella  mycetomi 
(Laveran,  1902). 

(2)  Nicolle  and  Pinoy' s  black  maduromycosis,  caused  by  Madurella 
tozeuri  (Nicolle  and  Pinoy,  1908). 

(3)  Bouffard's  black  maduromycosis,  caused  by  Aspergillus  bouf- 
fardi  Brumpt,  1905. 

(4)  Chalmers  and  Archibald' s  black  maduromycosis,  caused  by 
Glenospora  khartoumensis  Chalmers  and  Archibald,  1916,  which 
has  now  been  recovered  three  times  in  the  Anglo-Egyptian  Sudan. 

These  African  black  maduromycoses  may  be  differentiated  from 
one  another  as  follows: — 

A.  Microscopical  preparations  sbow  aspergillar  heads — Bouffard's  black 

maduromycosis. 

B.  Microscopical  preparations  do  not  show  aspergillar  heads;  on  culture 

the  following  types  of  spore  are  obtained : — 

1.  The  aleuriosporal  form  of  conidium — Chalmers  and  Archibald's 

black  maduromycosis. 

2.  The  arthrosporal  form  of  thallospore: — 

(a)  Mycelium  greyish-white,  when  old,  yellowish  and  darkening 

the  media  in  sugar  cultures.  Spores  varying  in  dimen- 
sion from  2  to  5  microns.  Grains  black  and  sterile,  with 
a  diameter  from  0-5  to  1  millimetre,  formed  in  the  depths 
of  the  medium  in  cultures.  Can  invade  the  skin,  bone, 
muscles,  and  connective  tissue  of  man,  giving  rise  to  black 
grains  which  are  small,  hard,  round,  and  more  or  less  warty, 
and  which  morphologically  resemble  the  grains  formed 
in  the  cultures.  TJp  to  the  present  the  inoculation  into 
animals  is  negative.  Very  widely  spread  in  Africa. 
Isolated  by  Brault  from  a  mycetoma  with  black  grains  in 
Algeria — Brumpt's  black  maduromycosis. 

(b)  Mycelium  white,  becoming  yellowish  with  age,  and  darkening 

the  medium  in  sugar  cultures.  Spores  generally  small, 
2  microns  or  sometimes  even  5  microns  in  diameter. 
Grains  are  only  rarely  produced,  and  then  thej  appear  on 
the  surface  of  the  medium.  Occasionally  it  gives  rise  to  a 
mycetoma  in  man,  in  which  it  forms  black  amorphous 
grains  which  are  often  made  up  of  mycelial  rings  enclosing 
some  degenerate  cellular  elements  which  are  impregnated 
with  the  pigment  of  the  fungus,  and  also  of  small  diffuse 
masses  formed  solely  by  the  filaments  of  the  fungus  which 
have  a  yellow  membrane.  Inoculation  into  pigeons 
positive.  Isolated  b}  Nicolle  from  a  mycetoma  at  Tozeur 
— Nicolle  and  Pinoy' s  black  maduromycosis. 


2122  MYCETOMA  AND  PARAMYCETOMA 

C.  The  Asian  Black  Maduromycosis. 

There  is  only  one  type  known  at  present — viz.,  Carter's  black 

maduromycosis,  caused  by  Glenosporasemoni  Chalmers  and  Archibald, 

1917,  which  can  be  readily  differentiated  from  Glenospora  khartou- 

mensis  Chalmers  and  Archibald,  1916,  by  the  following  characters: — 

([)  Grown  on  clear  maltose  agar  in  Khartoum  after  twelve  days  in  an  un- 
capped tube  at  300  C. : — 

G.  semoni  produces  a  cupola-shaped,  large,  central  black  mass 
with  an  outlying  fringe  of  white. 

G.  khartoumensis  produces  a  black  growth,  consisting  of  a  central 
crumpled  ridge  or  hillock  placed  on  a  grooved  black  plateau,  and 
with  hardly  any  white  fringe. 

(2)  and  (3)  Grown  on  glucose  agar  and  blood  serum;  there  are  marked 
differences  between  the  two  fungi. 

D.  The  American  Black  Maduromycoses. 

(1)  Wright's  black  maduromycosis,  which  was  found  in  the  United 
States  in  an  Italian  woman  who  had  left  Italy,  where  black  maduro- 
mycosis occurs,  an  indefinite  number  of  years  before  the  onset  of 
the  malady.     The  systemic  position  of  the  causal  fungus  is  unknown. 

(2)  Seheult's  black  maduromycosis,  which  was  found  in  the  West 
Indies  in  a  native  of  India,  who  had  left  that  country  twelve  years 
before  the  onset  of  the  malady.  The  nature  of  the  causal  organism 
is  unknown. 


II.  THE  WHITE  OR  YELLOW  MADUROMYCOSES. 
These  may  be  divided  into : — 

A.  The  European  white  maduromycoses. 

B.  The  African  white  maduromycosis. 

C.  The  Asian  white  maduromycosis. 

A.  The  European  White  Maduromycoses. 

(1)  Brumpt  and  Reynier's  white  maduromycosis,  caused  by  Indiella 
reynieri  Brumpt,  1906,  with  a  large  soft  grain,  found  in  Paris. 

(2)  Tarozzi  and  Radaeli's  white  maduromycosis,  caused  by  Scedo- 
sporium  apiospermum  (Saccardo,  191 1),  with  a  small,  rather  hard, 
and  yellowish  grain,  found  in  Sardinia  and  Italy. 

B.  The  African  White  Maduromycosis. 
Nicolle  andPinoy's  white  maduromycosis,  due  to  Sterigmatocystis 
nidulans  (Eidam,  1883),  with  grains  of  size  varying  from  those 
which  are  almost  microscopic  to  others  about  the  size  of  a  pea,  of 
rounded  or  polyhedral  form,  and  of  variable  colour,  being  dirty 
white  or  yellowish-white,  and  soft  in  consistence,  and  found  in 
Tunisia. 


THE  MADUROMYCOSES  2123 


C.  The  Asian  White  Maduromycosis. 

Brumpt's  white  maduromycosis,  due  to  Indiella  mansoni  Brumpt, 
1905,  with  very  small  and  very  hard  white  grains,  found  in  India. 

The  differentiation  of  the  white  maduromycoses  may  be  effected 
as  follows: — 

A.  Grains  soft : — 

1.  Sterigmatocystic  heads  found  in  grains  and  in  cultures.     Grains 

not  like  a  ribbon  rolled  on  itself — Nicolle  and  Pinoy's  white 
maduromycosis. 

2.  No  such  heads  to  be  found  in  the  grains,  which  are  like  a  ribbon 

rolled  upon  itself — Brumpt  and  Reynier's  white  maduromycosis. 

B.  Grains  hard  : —  . 

1.  Grains  small,  yellowish,  not  reniform;  spore  of  the  type  of  a  coni- 

dium — Tarozzi  and  Radaeli's  white  maduromycosis. 

2.  Grains  small,  whitish,  reniform;  spore  of  the  type  of  an  arthro- 

spore — Brumpt's  white  maduromycosis. 


III.  THE  RED  MADUROMYCOSIS. 

Only  one  form  is  known  Balfour  and  Archibald's  red  maduromycosis,  which 
was  possibly  due  to  an  aspergillus,  because  aspergillar-like  heads  were  found 
in  the  grains.     It  occurred  in  the  Anglo-Egyptian  Sudan. 

Pathology. — The  causal  fungus  is  introduced  into  some  part  of 
the  body  by  a  wound  produced  by  a  thorn,  a  splinter  of  bamboo  or 
other  wood,  by  a  sharp  stone,  knife,  etc.,  but  once  introduced  into 
the  subcutaneous  tissues,  it  commences  to  grow,  the  original  wound 
in  the  meantime  healing.  Usually  the  growth  is  slow;  but  if 
Kemper  and  Jamieson's  case  was  true  mycetoma,  it  may  be  rapid, 
and,  indeed,  this  is  supported  by  Musgrave  and  Clegg's  inoculation 
of  Nocardia  asteroides  into  a  monkey's  feet,  in  which  the  swelling 
developed  in  ten  to  sixteen  days,  and  was  quickly  followed  by  sup- 
purative lesions.  As  the  fungus  grows,  it  destroys  the  tissues  of  the 
foot,  and  meets  with  but  little  reaction  on  the  part  of  the  body, 
and  no  attempt  is  made  to  repair  its  ravages.  The  reaction  on  the 
part  of  the  body  confines  itself  to  alymphocytic  infiltration  around 
the  fungus,  and  later  the  formation  of  granulation  tissue,  with 
epithelioid  and  giant  cells  at  times;  while,  finally,  fibrous  tissue  is 
formed  around  the  fungus  and  its  surrounding  cells,  and  the  vessels 
become  blocked  by  an  endarteritis  and  periarteritis.  This  appears 
to  be  an  attempt  to  encapsule  and  prevent  thespreadof  theparasitc, 
as  well  as  to  damage  it  by  cutting  off  its  food-supply. 

At  the  same  time  the  cellular  exudate  becomes  a  thin,  oily,  occa- 
sionally stinking,  pus,  and  works  its  way  to  the  surface,  forming 
apertures,  and  carrying  the  parasite  with  it.  This  must  be  con- 
sidered to  be  an  attempt  to  rid  the  body  of  the  fungus. 

In  the  meanwhile  the  parasite,  if  of  certain  species,  forms  special 
club-shaped  hyphae  considered  to  be  chlamydospores,  which  at  first 
serve  for  extracting  nutrition  from  the  surrounding  leucocytes,  but 


2i24  MYCETOMA  AND  PARAMYCETOMA 

later,  breaking  free  from  the  main  mass,  form  means  of  asexually 
propagating  the  fungus  in  the  foot.  Some  of  these  separated  clubs 
are  attacked  and  engulfed  by  leucocytes,  and  though  it  is  possible 
that  in  this  way  many  may  be  destroyed,  still,  Brumpt's  researches 
show  that  the  leucocyte,  with  its  enclosed  club,  may  wander  away 
from  the  diseased  area  into  healthy  tissue,  and  may  be  killed  by  the 
club,  which,  being  set  free,  grows  into  a  new  mass  of  fungus.  In 
this  way  the  fungus  may  be  disseminated  by  means  of  the  phago- 
cytes. 

When  surrounded  by  pus,  the  fungus  gathers  itself  into  granules, 
the  so-called  sclerotia,  which  show  externally  radially  arranged 
fibres  or  clubs,  and  internally  a  mass  of  mycelium  with  crystals  and 
debris,  the  latter  being  most  marked  in  the  centre.  These  granules 
escape  to  the  exterior,  and  form  the  yellow,  black,  or  pink  granules 
in  the  discharge.  As  the  fungus  grows  in  the  foot  the  connective 
tissues  and  the  muscles  undergo  vitreous  degeneration,  and  break 
up  into  debris,  amongst  which  pieces  of  nerves  and  tendons  may  be 
found,  while  even  the  bone  in  some  cases  becomes  attacked  by  a 
form  of  degeneration  and  disappears.  The  result  is  that  the  foot 
appears  much  swollen  externally,  and  shows  the  openings  of  the 
sinuses,  through  which  the  pus  and  the  fungoid  granules  escape; 
while  internally  the  normal  structure  may  have  completely  dis- 
appeared, being  replaced  by  degenerated  tissue,  debris,  sinuses, 
and  fibrous  sacs  containing  the  fungus  and  the  pus. 

The  result  is,  however,  not  merely  destruction  of  the  foot,  but 
also  great  bodily  waste,  due  to  the  continuous  discharge,  so  that 
the  patient  becomes  emaciated,  and  may  finally  die  of  cachexia. 
Morbid  Anatomy. — The  pathological  anatomy  of  black  maduro- 
mycosis  has  been  the  subject  of  a  fair  amount  of  investigation. 
Kanthack  merely  drew  attention  to  the  fact  that  the  black  masses 
were  always  to  be  found  embedded  in  dense  fibrous  tissue,  while  a 
few  pus  and  granulation  cells  were  to  be  seen  in  most  cases.  In  the 
fibrous  wall  yellowish-brown  or  black  pigment  could  be  found, 
while  fuchsin  bodies  were  present  in  most  specimens.  Unna's 
example,  obtained  from  Kanthack,  only  showed  fibrous  and  some 
granulation  tissue.  Boyce  and  Surveyor  drew  attention  to  the 
presence  of  small  round  cells, macrocytes,  and  giant  cells  surrounding 
the  fungus  in  cases  of  black  maduromycosis.  Their  microphoto- 
graphs  are,  however,  mainly  devoted  to  the  fungus,  while  their 
Fig.  22  evidently  depicts  a  very  young  piece  of  fungus  surrounded 
by  giant  cells. 

Wright  (1898)  stated  that  the  nodules  consisted  of  more  or  less 
atypical  connective  tissue,  in  the  cavities  of  which  the  granules  lay 
surrounded  by  polymorphonuclear  leucocytes,  loose  epithelioid  cells, 
and  cellular  detritus.  The  cavities  were  lined  by  either  a  wall  of 
vascular  granulation  tissue  or  by  masses  of  epithelioid  and  multi- 
nucleated giant  cells,  while  these  cells  closely  invested  other  granules, 
and  outside  of  this  tissue  lay  lymphoid  and  plasma  cells.  He  gives 
in  his  original  paper  four  excellentAlow-power  photographs,  of  which 


THE  MADUROMYCOSES  2125 

Figs.  4,  5,  and  6,  though  older,  if  examined  with  a  lens,  will  be 
seen  to  agree  more  or  less  with  Boyce  and  Surveyor's  Fig.  22. 

Oppenheim's  description  in  1904  mainly  deals  with  the  fungus, 
but  Brumpt's  account  of  the  histological  changes  induced  by 
Aspergillus  bouffardi  covers  all  the  important  points— viz.,  the 
polymorphonuclear  leucocytes,  the  lymphocytes,  the  giant  and 
epithelioid  cells,  the  connective  tissue,  the  cells  containing  brown 
pigment,  and  the  endarteritis.  On  Plate  XIX.,  Fig.  7,  and  Plate  XX., 
Figs.  1  and  2,  he  shows  appearances  resembling  those  described  by 
Boyce,  Surveyor,  and  Wright  in  a  young  grain  in  which  the  giant 
cells  are  situate  close  to  the  fungus. 

Boccaro,  writing  in  1909  in  general  terms  for  the  encapsulated 
form  of  both  white  and  black  mycetomas,  says: — 

'  The  fungal  hyphae  are  surrounded  by  round  cells,  held  together  by  a  delicate 
network  of  fine  bloodvessels,  the  cells  being  located  in  the  meshes  of  a  fibrillar, 
transparent,  reticulated  substance.  On  the  inner  side  of  the  group  of  round 
cells,  between  them  and  the  central  hyphal  mass,  is  a  collection  of  finely 
granulated  dibris,  and  on  the  outer  side,  in  most  preparations,  may  be  seen 
large  nucleated  cells,  giant  cells,  and  phagocytes.' 

This  description,  which  unfortunately  is  not  illustrated,  agrees 
well  with  our  observations. 

Balfour,  in  1911,  published  photomicrographs  of  black  maduro- 
mycoses  believed  to  be  due  to  Madurella  mycetomi  and  to  Aspergillus 
bouffardi,  but  did  not  describe  them. 

Babes  (1913)  gave  a  well-illustrated  account  of  Indian  black 
maduromycosis,  in  which  he  observed  far  less  cells  than  we  have 
noticed  in  immediate  relationship  to  the  fungus,  from  which  the 
giant  cells  were  separated  by  fibrous  connective  tissue.  He  drew 
attention  to  violet  and  reddish  rounded  bodies  enclosed  in  cells. 

In  1916  Chalmers  and  Archibald  gave  an  account  of  the  histology 
of  a  case  of  black  maduromycosis,  and  this  is  followed  in  the 
description  given  below. 

Fig.  845  shows  the  general  appearance  of  black  maduromycosis 
very  slightly  magnified.  It  will  be  observed  to  be  largely  composed 
of  fibrous  tissue  containing  black  particles 
— the  grains — and  some  spaces,  which  are 
formed  by  the  falling  out  of  some  of  the 
black  granules  during  preparation.  The 
spaces  demonstrate   the   character   of    the  F      g 

lacunae  occupied   by  the   grains   and  their    Black  Maduromycosis. 
surrounding  cells. 

The  fungal  mass  lies  embedded  in  cellular  tissue,  as  is  shown  in 
Fig.  846.  The  spaces  are  artefacts  produced  in  making  the  section, 
which  otherwise  is  as  natural  as  possible — i.e.,  is  not  bleached  or 
softened  in  any  way.  The  cracks  in  the  black  mass  are  also  arte- 
facts. Around  the  fungus  lies  a  mass  of  small  cells,  and  on  the 
upper  and  left  side  of  the  grain  are  seen  some  giant  cells,  which 
also  occur  in  other  parts,  but  are  not  in  such  close  relationship  to  the 
fungus;  then  comes  some  fibrous  tissue  containing  a  number  of 


2126  MYCETOMA  AND  PARAMYCETOMA 

cells,  bloodvessels,  and  lymph  spaces,  the  last  mentioned  being 
situate  towards  the  top  of  the  photograph  and  being  markedly 
dilated.  At  the  very  top  of  the  figure,  and  only  partially  shown, 
comes  the  dense  fibrous  connective  tissue  which  is  continuous  with 

■   .■■■■;-   ::/■/-•. 


5.     C*-.f 


Fig.  846. — Black  Maduromycosis. 

the  dense  tissue,  depicted  in  Fig.  846,  which  permeates  and  surrounds 
the  growth.  Therefore  the  main  features  of  the  tumour  may  be 
summarized  as  follows: — 

1.  Fungus. 

2.  Small  cells. 

3.  Giant  cells  and  large  cells. 

4.  Small  cells,  connective  tissue,  bloodvessels,  and  lymph 

spaces. 

5.  Dense  connective  tissue. 

The  cells  are  separated  by  a  variable  amount  of  fine  connective 
tissue,  which  also  supports  large  lymph  spaces  and  bloodvessels. 
Debris  and  pigmentary  granules  can  also  be  seen.  A  special  rare 
feature  of  this  layer  is  the  presence  of  mononuclear  cells  containing 
one  or  more  eosinophile  rounded  bodies,  which  were  first  observed 
in  this  pathological  condition  by  Kanthack,  and  subsequently  by 
ne  irly  all  the  other  workers  on  the  morbid  histology  of  the  black 


THE  MADUROMYCOSES  212; 

maduromycoses,  to  which  they  are,  however,  not  confined.  Their 
exact  nature  is  unknown,  but  they  are  probably  in  some  way  due 
to  the  fungus. 

On  inspecting  the  upper  part  of  the  cellular  mass,  it  will  be 
observed  that  the  white  fibrous  tissue  increases  in  amount,  but  is 
still  loose  and  contains  many  cells  in  its  meshes,  while  more 
externally,  and  situate  at  the  top  of  the  photograph,  is  seen  the 
denser  and  less  cellular  connective  tissue,  which  is  continuous  with 
that  separating  one  fungal  mass  from  another  and  surrounding  the 
whole  tumour.  In  this  connective  tissue,  cells  containing  yellowish 
granules  are  frequently  observed. 

There  are  also  many  lymph  spaces  and  bloodvessels,  but  the 
latter  at  times  show  signs  of  endarteritis  or  periarteritis,  by  which 
means  the  lumen  of  the  vessel  may  be  considerably  diminished  or 
even  closed. 

Very  rarely  do  the  fungi  invade  the  body,  and  rise  to  a  general 
infection. 

The  peculiarity  of  the  pathology  is  the  slight  reaction  which  the 
body  makes  against  the  invasion  by  the  fungus,  and  the  entire 
absence  of  any  attempt  at  repair. 

The  black  varieties  of  mycetoma  owe  their  colour  to  a  dark 
substance  which  the  fungi  secrete.  The  nature  of  this  black  sub- 
stance is  not  known.  It  is  soluble  in  hot  sulphuric  acid,  forming  a 
yellowish-red  solution,  but  is  not  soluble  in  cold  sulphuric  acid  nor 
in  potash  solutions.  According  to  Thudichum,  it  does  not  contain 
haemoglobin  in  any  form,  though  a  small  quantity  of  iron  is  present. 

In  more  advanced  cases  the  swollen  foot  shows  nodules  and 
openings  externally,  the  latter  of  which  lead  into  the  sinuses.  In 
sectionizing  the  foot  it  will  be  noticed  that  the  sinuses  which  run  in 
various  directions  are  communicating,  and  end  in  small  cavities 
containing  pus  and  the  fungus,  and  that  these  cavities  are  embedded 
in  degenerated  tissue  and  debris. 

The  bone  may  or  may  not  be  affected,  but  if  it  is,  the  whole  foot 
can  be  easily  cut  by  a  knife. 

Microscopically  the  tissues  show  degeneration  and  debris,  with 
fibrous  tissue  formation,  endarteritis,  and  periarteritis,  and  at  times 
absorption  of  the  bone. 

The  microscopical  examination  of  sections  of  the  tissues  typically 
affected — viz.,  of  alveolar  appearance — and  containing  mycotic 
grains,  show  a  central  roundish  mass — the  mycotic  grain — a  clear 
circular  space,  and  the  surrounding  degenerated  tissues.  The  clear 
space  is  due  to  the  fact  that  the  thin  purulent  matter  in  which  the 
granule  is  embedded  contracts  during  fixation  with  alcohol.  The 
mycotic  granule  is  composed  at  the  centre  almost  exclusively  of 
mycelial  elements  with  a  few  leucocytes;  more  externally  there  are 
masses  of  amorphous  substance,  staining  lightly  purplish  with  eosin, 
in  which  a  few  mycelial  threads  may  be  seen.  The  periphery  shows  a 
polymorphonuclear  infiltration.  The  walls  of  the  alveolar  cavities 
containing  the  granules  are  formed  of  young  connective  tissue  with 


2128 


MYCETOMA   AND  PARAMYCETOMA 


numerous  plasma  cells  and  occasionally  giant  cells;  there  is  a 
marked  proliferation  of  bloodvessels. 

Symptomatology. — The  disease  usually  begins  in  the  foot,  more 
rarely  in  the  hand,  and  still  more  rarely  in  the  leg,  knee,  neck,  or 
trunk.  There  may  or  may  not  be  a  history  of  a.  cut  or  injury  some 
time  previously.  In  any  case,  this  primary  injury  will  have  healed 
long  before  the  disease  is  well  established. 

The  incubation  period  in  well-recorded^cases  would  appear  to 
be  short ;  thus,  in  Musgrave  and  Clegg's  case,  one  month  after  the 


Fig.  847. — Mycetoma. 


primary  injury  the  wound  reopened  and  discharged  pus,  and  in 
their  experiments  on  monkeys  it  appeared  to  vary  from  ten  to 
sixteen  days.  Further  researches  on  this  point  are,  however, 
required. 

The  earliest  signs  are  either  pain  or  swelling  in  the  region  of  the 
original  injury,  which  is  usually  on  the  sole  of  the  foot,  between  the 
toes,  or  on  the  instep.  The  swelling  becomes  a  hard  lump,  on  the 
surface  of  which  a  bleb  may  form,  which  bursts  and  reveals  a  small 
opening  discharging  an  oily,  rarely  sanious,  thin,  offensive  pus,  in 
which  the  granules  characteristic  of  the  fungus  may  be  found. 


PLATE    XIII. 


MYCETOMA. 


Geo.Wkier3ron*Sona,L:d  Edii. 


To  fuce  page  2128 


THE  MADUROMYCOSES  2129 

Some  new  indurations  and  nodosities  appear  in  various  parts  of 
the  foot,  and  new  openings  are  formed,  while  the  whole  foot  begins 
to  swell  in  a  very  characteristic  manner.  First  the  arch  of  the 
foot  fills  up  and  disappears,  the  whole  sole  becoming  so  swollen  and 
convex  that  the  toes  are  no  longer  able  to  touch  the  ground,  and 
may  be  pushed  apart,  but  are  usually  not  affected  by  the  disease. 
At  the  same  time  the  dorsum  of  the  foot  becomes  studded  with 
nodules  and  openings.  The  colour  of  the  integument  may  be 
normal,  but  is  usually  darker  than  in  the  healthy  skin.  It  is  rarely 
oedematous.  The  openings,  when  examined  by  a  probe,  are  found 
to  lead  into  sinuses,  which  penetrate  deeply  into  the  tissues,  and  at 
times  even  into  the  bones  of  the  foot.  The  quantity  of  the  dis- 
charge varies  from  time  to  time,  being  increased  by  motion.  On 
palpating  the  affected  area,  it  is  found  to  be  elastic,  and  the  sensi- 
bility to  be  normal.   The  inguinal  glands  are  often  enlarged  and  hard. 

As  the  disease  progresses,  pain,  which  at  first  was  slight,  becomes 
more  marked,  especially  in  cold  weather.  The  patient  ceases  to 
be  able  to  place  the  foot  to  the  ground,  and  is  compelled  either  to 
walk  on  the  heel  or  to  use  a  support.  The  leg  begins  to  waste, 
and  after  a  long  time  the  patient  becomes  weak  and  anaemic  from 
the  constant  drain  on  the  system  by  the  discharge,  and  possibly 
also  by  toxins  produced  by  the  fungi.  General  constitutional  dis- 
turbance of  a  febrile  nature  is  rare. 

The  disease  is  very  chronic,  and  has  no  tendency  to  heal,  and  if 
not  treated,  will  eventually  cause  the  death  of  the  victim,  from 
exhaustion  or  diarrhoea,  after  lasting  some  ten  or  twelve  years. 

Diagnosis. — The  peculiar  swelling  of  the  foot,  with  a  hTling-up  of 
the  arch,  and  the  formation  of  sinuses  from  which  a  discharge 
containing  the  typical  grains  is  escaping,  enables  the  disease 
to  be  diagnosed  with  certainty  from  elephantiasis  or  tubercular 
disease  of  the  foot. 

The  variety  of  the  fungus  may  be  determined  by  examining  the 
grams  or  the  scrapings  of  the  sinuses  microscopically,  culturally, 
and  by  inoculations  in  animals. 

It  is  to  be  noted  that  the  typical  grains  may  for  a  time  be  absent 
from  the  purulent  liquid  exuding  from  the  sinuses.  In  such  cases 
squeezing  of  the  nodules  may  make  the  grains  appear,  or  a  nodule 
which  has  not  yet  opened  may  be  incised  and  the  contents  examined. 

Prognosis. — If  the  growth  is  observed  when  young,  small,  and 
lying  subcutaneously,  so  that  it  can  be  completely  removed,  the 
prognosis  is  good,  as  the  wound  heals  readily  and  the  growth  does 
not  recur. 

If,  however,  the  growth  has  lasted  some  time,  and  has  involved 
the  bones,  the  prognosis  is  not  good,  and  is  worse  if  the  lymphatic 
glands  are  also  implicated. 

Treatment. — Remove  the  growths  at  an  early  stage  and  as  com- 
pletely as  possible.  In  later  stages  amputations  well  above  the 
seat  of  any  lesion,  together  with  the  removal  of  any  enlarged 
lymphatic  glands,  is  the  only  possible  Ireatment. 

134 


2130  MYCETOMA  AND  PARAMYCETOMA 

Potassium  iodide  may  be  tried,  but  as  a  rule  internal  medicines 
and  vaccines  are  useless  for  this  form  of  mycetoma. 

Prophylaxis. — The  wearing  of  boots  and  shoes  and  not  walking 
barefoot  are  apparently  good  and  sensible  methods  of  prophylaxis. 

THE  ACTINOMYCOSES. 

Definition. — The  Actinomycoses  are  those  forms  of  mycetoma 
with  grains  composed  of  very  fine  non-segmented  mycelial  filaments, 
in  which  usually  the  walls  are  not  clearly  defined  from  the  contents, 
and  in  which  chlamydospores  are  absent. 

History. — This  period  opens  with  Bollinger's  epoch-making  work 
in  1876  on  the  lumpy-jaw  of  cattle,  a  disease  which  had  been  re- 
cognized since  1785,  and  in  which  he  found  the  constant  presence 
of  a  branching  organism.  This  fungus  was  examined  by  Harz 
(1877-78),  who  gave  it  the  name  Actinomyces  bovis,  but,  most  un- 
fortunately, this  generic  name  cannot  stand,  because,  unbeknown 
to  Harz,  it  had  already  been  used  by  Meyen  (1827)  for  a  fungus 
which  he  called  Actinomyces  horkelii,  which  is  in  no  way  related 
to  the  group  of  fungi  which  we  are  considering.  This  mistake 
launched  the  generic  name  applicable  to  these  organisms  on  to  a 
sea  of  change,  and  led  to  much  confusion. 

1.  Nocardia  bovis. — The  correct  name  for  Bollinger's  organism  is 
Nocardia  bovis  (Harz,  1877).  The  fungus  appears  to  have  been  first 
seen  in  man  by  Israel  in  1878.  Corre  (1883)  was  the  first  to  draw 
attention  to  the  similarity  between  actinomycosis  and  the  ochroid 
variety  of  mycetoma,  while  Acland  (1886)  was  the  second  observer 
to  demonstrate  the  presence  of  actinomycosis  in  man;  and  as  Israel's 
name  is  associated  with  quite  a  different  human  actinomycosis,  we 
propose  to  name  this  variety  Acland' s  actinomycosis.  In  1886, 
Vandyke  Carter,  as  we  have  already  stated,  also  drew  attention 
to  the  likeness  between  actinomycosis  and  mycetoma.  Finally, 
in  1891,  Bostroem  grew  N.  bovis  from  eleven  cases  of  actinontycosis 
in  man,  and  since  that  time  it  has  often  been  cultivated  and  de- 
scribed. It  is  a  nocardia  with  radially  arranged  filaments,  which 
show  club-like  enlargements  of  their  extremities,  caused  by  a  pro- 
tective thickening  of  the  walls  in  animals  and  less  commonly  in 
man,  and  having  abundant  Gram-positive  but  not  acid-fast  hyphae, 
some  of  which  end  in  chains  of  arthrospores. 

It  grows  well  aerobically  at  220  C,  but  better  at  370  C.  Anaerobic 
growths  are,  as  a  rule,  but  poorly  developed. 

It  may  form  a  dry  pellicle  on  the  surface  of  broth,  but  more 
usually  it  gives  rise  to  cohering  colonies  at  the  bottom  of  the  tube, 
and  in  either  case  the  medium  remains  clear. 

It  grows  slowly  on  gelatine,  producing  a  yellowish-white  growth 
and  slow  liquefaction,  beginning  about  the  seventh  day.  The 
resulting  fluid  may  or  may  not  be  dark  coloured.  On  blood  serum 
it  produces  poor  growths,  and  no  liquefaction  or  pigmentation  of 
the  medium. 


THE  ACTINOMYCOSES  213 1 

On  agar  and  glycerine  agar  it  forms  hard,  spherical,  white  colonies, 
which  give  rise  to  an  undulating  crateriform  growth,  having  a 
yellowish  or  greyish  tint,  which  in  its  turn  becomes  a  lichenoid 
ashen  grey  or  yellowish  mass  with  a  powdery  efflorescence.  On 
maltose  agar  it  forms  discrete  fawn-coloured  colonies,  later 
becoming  yellow,  dark  brown,  or  even  black,  while  the  medium  may 
be  slightly  darkened. 

On  potato  it  forms  confluent,  hard,  raised,  variously  coloured 
masses,  at  first  white,  but  becoming  greenish-yellow,  brown,  greyish- 
black,  or  even  black,  with  more  or  less  erosion  and  pigmentation  of 
the  medium  to  which  the  growth  is  very  adherent.  No  diastatic 
action  has  been  observed. 

Litmus  milk  is  first  reddened,  but  later  it  becomes  a  clear  brown 
alkaline  liquid.  It  is  pathogenic  for  man,  ox,  horse,  pig,  and  other 
animals,  while  experimentally  rabbits  and  guinea-pigs  have  been 
infected  by  intraperitoneal  inoculation. 

2.  Nocardia  asteroides. — Nocardia  bovis  (Harz,  1877)  is  not  the 
only  organism  known  to  cause  actinomycosis  in  man,  for  in  1890 
Eppinger  obtained  an  organism  which  he  called  Cladothrix  asteroides, 
and  which  is  now  known  as  Nocardia  asteroides  (Eppinger,  1890), 
from  the  lesions  in  a  case  of  pseudo-tuberculosis  of  the  lungs  and 
pleura,  with  old  caseous  nodules  in  the  apices  and  calcareous  degener- 
ation of  the  bronchial  and  supraclavicular  glands,  together  with  a 
cerebral  abscess  which  had  ruptured  into  the  ventricles.  The 
fungus  was  Gram-positive  and  acid,  but  not  alcohol-fast,  and  grew 
aerobically  on  laboratory  media,  and  was  pathogenic  for  laboratory 
animals.  It  was  afterwards  recognized  by  Almquist,  in  1890;  by 
Sabrazes  and  Riviere,  in  1894;  by  Aoyama  and  Miyamoto,  in  1900, 
in  Tokio;  by  MacCallum,  in  1902,  in  America;  and  by  Schabad,  in 
1903,  in  Russia.  It  is  also  the  same  as  the  fungus  described  by 
Musgrave  and  Clegg  (1907),  in  a  case  of  mycetoma  in  the  Philippine 
Islands,  under  the  name  Streptothrix  freeri. 

In  1909,  Lindenberg,  in  Brazil,  isolated  a  fungus  from  a  case  of 
mycetoma  of  the  left  leg,  which  began  in  the  popliteal  space,  and 
to  this  organism  he  gave  the  name  Discomyces  brasiliensis. 

He  was  very  careful  to  separate  it  from  N.  bovis  and  from 
N.  madurcB  (N.  indica),  but  he  does  not  appear  to  have  done  so 
with  regard  to  N.  asteroides.  We  therefore  offer  a  comparison  be- 
tween the  two  organisms  in  the  table  on  p.  2132. 

The  inoculations  into  animals  are  not  comparable,  as  Lindenberg 
did  not  use  monkeys.  He  was  unsuccessful  with  a  guinea-pig,  but 
does  not  say  how  he  inoculated  it,  while  Musgrave  and  Clegg  were 
successful  by  means  of  intraperitoneal  inoculations. 

The  differences  as  set  forth  between  N.  brasiliensis  and  N. 
asteroides  appear  to  us  to  be  very  slight,  and  therefore  we  are  able 
to  agree  with  Pinoy  in  his  belief  that  they  are  one  and  the  same 
organism. 

Also  Cranwell,  Bachmann,  and  Del  Pont  (1909)  gave  an  excellent 
and  well-illustrated  description  of  a  yellow  mycetoma  in  Buenos 


2132 


MYCETOMA  AND  PARAMYCETOMA 


Aires.  Unfortunately,  they  did  not  grow  it  on  inspissated  blood 
serum,  but,  as  far  as  we  understand  their  account,  we  should  classify 
this  organism,  which  they  did  not  name,  as  Nocardia  asteroides. 


Nature  of  Test. 

N.  asteroides  from    ,       N.  brasiliensis 
Musgrave  and  Clegg.          Lindenberg. 

Result  of 
Comparison. 

Seat  of  disease 

Mycetoma  of  foot.      Mycetoma  of  leg.        Difference  un- 
important. 

Grains 

Consistency    dough-  Consistency       soft  ;  No  important 
like;    colour     yel-      colour    yellowish-      difference, 
lowish-white ;  size      white;  size  o-i-0'^\ 
o«25-0'5     mm.     in      mm.  in  diameter, 
diameter. 

Clubs 

1 
Usually  absent.           Absent.                         Agree. 

Bacillary   and   coccal 
forms 

Numerous    bacillary  Bacillary  and  coccal  Agree, 
and      coccus  -  like      forms  present, 
varieties. 

Optimum       tempera- 
ture 

Slower     growth     at 
300     C.     than     at 
37°  C 

Better      growth      at 
room  temperature 
than  at  370  C. 

Slight  dis- 
agreement . 

Anaerobic  cultivation 

Does  not  grow. 

Does  not  grow. 

Agree. 

Broth 

Floating     fiat     par- 
ticles  which   later 
fall  to  the  bottom. 

Medium  not  affected. 

Small    particles 
which  later  fall  to 
the  bottom  of  the 
tube. 

Medium  not  affected. 

Agree. 

Gelatine 

No  liquefaction. 

No  liquefaction. 

Agree. 

Sabouraud's     glucose 
agar  at  370  C. 

Centre  yellow,   peri- 
phery    pink    to 
pinkish-white. 

Colonies  rose  violet. 

Slight  dis- 
agreement. 

Potato 

At  first  delicate  pink 
and    later    yellow 
ochre  centre  with 
pinkish    or    white 
periphery;    the 
medium    becomes 
darkened. 

At  first  a  rose  colour, 
and  later  a  yellow- 
orange  colour ; the 
medium    becomes 
brown . 

Agree. 

Serum 

Growth  slower.             Grows  very  badly  ai 
Colonies    at    first      37°  C. 

white,  later  diffuse  Colonies  white. 

pink. 

Later  pink  not 
mentioned 
in  N.  bra- 
siliensis. 

.Milk 

Yellowish  mass.           Yellowis  h-orangt 
No  coagulation.               pellicle. 

No  coagulation. 

Agree. 

THE  ACTINOMYCOSES  2133 

Nocardia  asteroides  possesses  Gram-positive,  acid,  but  not  alcohol- 
fast  hyphae,  which  are  without  club-like  enlargements.  It  pro- 
duces restricted  growths  aerobically  and  usually  anaerobically  at 
22°  C.  and  370  C,  but  nothing  is  stated  in  the  literature  we  have 
consulted  with  regard  to  any  odour  arising  from  these  cultures.  It 
does  not  liquefy  gelatine  or  blood  serum,  nor  has  it  any  diastatic 
action.  It  reddens  litmus  milk,  which  later  becomes  alkaline,  but  is 
not  coagulated  or  cleared.  It  grows  on  the  agars  and  on  potato, 
producing  reddish  (often  brick  red)  growths.  It  is  pathogenic  for 
monkeys,  rabbits,  and  guinea-pigs. 

3.  Nocardia  liquefaciens. — This  fungus  was  obtained  by  Hesse  in 
1892  from  a  man  in  Germany  with  a  left  inguinal  abscess  which  com- 
municated with  the  rectum.  Subsequently  other  abscesses  formed 
on  either  side  of  the  dorsal  spine.  The  pus  from  these  abscesses 
discharged  soft  yellowish  grains  about  the  size  of  a  millet  seed,  which 
contained  a  Gram-positive  fungus  which  did  not  possess  clubs. 
On  cultivation  it  grew  readily,  and  was  found  to  be  strictly  aerobic. 
In  gelatine  stabs  it  formed  a  nail-shaped  growth,  which  at  room 
temperature  in  Europe  was  only  visible  on  the  third  day,  while 
liquefaction,  beginning  on  the  fourth  or  fifth  day,  was  complete  by 
the  end  of  the  week.  The  liquefied  gelatine  was  not  discoloured, 
and  if  the  growth  stuck  to  the  glass  it  was  yellowish,  with  a  whitish 
covering.  On  blood  serum  it  formed  small  cloudy  granules  of  the 
same  colour  as  the  medium,  in  twenty-four  to  forty-eight  hours. 
Liquefaction  begins  at  the  end  of  the  first  week  and  proceeds  slowly, 
the  liquid  remaining  quite  clear  and  colourless,  and  only  after  some 
six  months  turning  to  a  reddish-yellow  colour.  In  broth  it  forms 
delicate  flakes  which  fall  to  the  bottom  of  the  tube,  and  consist  of 
a  lower  surface  which  is  yellowish-white,  and  an  upper  surface  which 
is  snow  white.  The  medium  remains  quite  clear.  No  surface 
growth  is  mentioned. 

On  agar  the  colonies  at  first  form  separate  rosettes,  which  remain 
distinct  for  a  time.  These  colonies  appear  to  resemble  the  gelatine 
culture,  being  yellowish  below  and  having  a  white  envelope.  The 
growth  on  glycerine  agar  is  more  vigorous  than  on  ordinary 
agar. 

On  potato  it  forms  small  yellow  nodules  by  the  second  day, 
which  later  become  covered  with  a  snow-white  efflorescence,  which 
does  not  alter.  Apparently  it  was  not  grown  on  glucose  agar,  milk, 
or  eggs.  Intravenous,  intraperitoneal,  and  subcutaneous  injections 
into  rabbits,  guinea-pigs,  and  white  mice  were  negative. 

Hesse  gave  it  the  name  Cladothrix  liquefaciens,  which  now  becomes 
Nocardia  liquefaciens  (Hesse,  1892),  and  it  appears  to  be  the  same 
organism  as  that  named  Streptothrix  buccalis  by  Goadby  in  1903, 
and  found  by  him  in  1899  in  the  mouth  in  cases  of  pyorrhoea. 
Goadby's  form  showed  clubs,  or  club-like  swellings.  It  precipitated 
the  casein  in  milk,  which  became  clear. 

4.  Nocardia  indica. — Kanthack,  1893,  studying  specimens  of  black 
and  yellow  mycetoma  which  came  from  India,  concluded  that  the 


2134  MYCETOMA  AND  PARAMYCETOMA 

latter  variety  was  a  true  actinomycosis,  and  attempted  to  show 
that  the  former  was  the  same,  only  in  a  degenerated  condition. 

He  only  examined  the  specimens  microscopically,  as  no  cultures 
were  possible,  and  named  the  fungus  in  question  Oospora  indica 
Kanthack,  1893,  calling  his  two  varieties  0.  indica  var.  flava  and 
0.  indica  var.  nigra.  The  name  of  this  fungus,  translated  into 
more  modern  nomenclature,  becomes  Nocardia  indica  (Kanthack, 

i893)- 

Boyce  and  Surveyor  (1894)  clearly  proved  that  the  melanoid 
variety  was  due  to  quite  a  different  fungus  from  that  causing  the 
ochroid  variety,  which  latter  they  considered  in  some,  but  possibly 
not  in  all,  cases  to  be  an  actinomyces,  a  conclusion  in  which  they 
were  supported  by  Hewlett  and  by  Boccaro.  The  latter  analyzed 
one  hundred  cases  of  Madura  foot,  of  which  the  vast  majority  were 
black  mycetomas,  while  seventeen  had  evidence  of  pricks  with  an 
acacia  (Babul)  thorn,  in  several  of  which  it  was  found  present  on 
examination. 

Kanthack's  name  appears  to  have  been  overlooked,  but  it  cer- 
tainly has  priority  as  regards  the  fungus  of  an  actinomycotic 
nature  causing  the  ochroid  variety  of  mycetoma  as  seen  in  India, 
but  difficult  of  recognition  in  that  it  was  not  cultivated. 

In  1892,  Gemy  and  Vincent  described  a  parasitic  disease  of  the 
foot  in  Algeria,  which  they  considered  analogous  to,  if  not  identical 
with,  the  ochroid  variety  of  Vandyke  Carter's  mycetoma. 

In  1894,  Vincent,  still  working  in  Algeria,  met  with  a  streptothrix 
in  a  similar  case.  This  fungus,  which  was  first  known  as  Strepto- 
thrix madune  Vincent,  1894,  is  believed  to  be  identical  with  the 
fungus  found  by  Boyce  in  London  in  an  agar  tube  inoculated  in 
India  from  a  case  of  the  ochroid  variety  of  mycetoma. 

This  streptothrix  found  by  Boyce  is,  of  course,  an  entirely  different 
organism  from  the  mucor-like  fungus  called  Chionyphe  carteri 
mentioned  above,  which  therefore  cannot  be  placed  in  the  list  of 
synonyms  of  N.  madurce,  as  has  been  done  by  some  authors. 

Boyce's  culture  showed  a  fungus  without  club-shaped  extremities 
which  grew  very  slowly  on  agar,  glucose  agar,  and  glycerine  agar, 
at  a  temperature  varying  between  350  C.  and  370  C.  No  formation 
of  pigment  was  observed,  but  it  was  remarked  that  the  organism 
closely  resembled  that  of  actinomycosis. 

In  1904,  Cornwall  reported  the  cultivation  of  Vincent's  organism 
in  India.  He  washed  the  grains  in  six  changes  of  sterile  salt  solution, 
and  then  planted  them  on  agar  in  tubes.  After  an  interval  of  one 
or  two  months  a  growth  appeared,  which  in  some  cases  assumed 
a  pink  colour  and  in  others  remained  a  dull  white.  In  subcultures 
it  grew  more  freely,  preserving  its  characteristics,  one  of  which  was 
to  adhere  so  closely  to  the  medium  that  each  nodule  had  to  be  liter- 
ally dug  out  when  it  was  required  to  transfer  it  to  another  tube. 
Puff-balls  formed  in  broth  and  hay  infusions,  while  it  was  noted 
that  the  fungus  required  plenty  of  oxygen  for  its  growth  and  only 
occasionally  formed  the  pink  pigment. 


THE  ACTINOMYCOSES  2135 

This  description  by  Cornwall  leaves  no  doubt  in  our  minds  that 
he  met  with  Vincent's  organism  in  a  case  of  the  ochroid  variety  of 
mycetoma,  and  if  this  is  correct,  then  Kanthack's  name  assumes  its 
priority  and  Vincent's  becomes  a  synonym,  and  the  correct  name  of 
the  fungus  is  Nocardia  indica  (Kanthack,  1893),  and  this  is  supported 
by  Strong's  culture  of  the  same  fungus  from  an  Indian  mycetoma 
in  1908. 

With  regard  to  the  remaining  history  of  the  fungus,  it  should  be 
noted  that  in  1898  Legrain,  and  in  1899  Brault,  again  described  its 
presence  in  Algeria,  while  in  190 1  Albertini  and  Desvernine  reported 
its  presence  in  Cuba,  and  in  1902  Brumpt  discovered  that  it  existed 
in  Abyssinia,  while  Sommer  y  Greco  demonstrated  its  presence  in 
the  Argentine  in  1904,  and  Williamson  in  Cyprus  in  1905,  in  which 
year  Brumpt,  in  his  classic  on  Mycetomas,  stated  that  he  had 
obtained  it  from  India,  Somaliland,  and  Senegal. 

In  the  same  year,  Pelletier  described  a  case  of  mycetoma  with 
red  grains  which  he  saw  in  Saint  Louis,  in  Senegal.  The  grains 
were  very  small,  from  0-4  to  0-5  millimetre  in  diameter,  and  of 
a  beautiful  vermilion  red  colour.  In  the  same  year  Laveran 
published  a  paper  upon  Pelletier's  mycetoma,  in  which  he  says  that 
it  was  possible  on  making  sections  of  the  tumour  to  easily  discern 
therein  little  red  spots  of  variable  size  which  stood  out  from  the 
surrounding  neoplasm.  These  grains  contained  a  large  number  of 
Gram-positive  micrococcal-like  bodies  embedded  in  a  ground 
substance.  These  bodies,  which  measured  07  micron  in  diameter, 
were  never  found  isolated,  but  always  in  masses  or  short  chains. 
No  trace  of  a  mycelium  could  be  seen,  and  for  this  reason  he  gave 
it  the  name  of  Micrococcus  pelletieri  Laveran,  1906.  But  coccal-like 
forms  are  commonly  found  in  nocardial  infections,  and  in  1912 
Thiroux  and  Pelletier  reported  that  this  red  mycetoma  was  fairly 
common  in  Senegal,  where  one  of  them  had  met  with  eight  cases, 
from  one  of  which,  a  suppurating  tumour  of  the  right  side  of  the 
chest,  they  obtained  cultures  on  Sabouraud's  medium  which  very 
much  resembled  those  of  N.  madtim,  but  differed  therefrom  in  the 
following  particulars: — 

1.  The  growths  were  ruby  red  from  their  commencement. 

2.  It  had  only  so  far  been  grown  on  Sabouraud's  gelatine. 

3.  The  growths  did  not  penetrate  into  the  gelatine,  and  were 
easily  detached. 

4.  In  the  parasitic  stage  the  organism  takes  the  form  of  a  micro- 
coccus in  zooglea. 

They  renamed  the  parasite  Oospora  pelletieri.  In  the  discussion 
on  this  paper,  Laveran  agreed  with  Thiroux  and  Pelletier's  finding, 
and  Pinoy  pointed  out  that  the  only  real  differences  between  it  and 
N.  madurcB  were  the  greater  intensity  of  the  red  colour  and  the 
more  abundant  sporulation.  Further,  he  suggested  that  the  correct 
name  was  Nocardia  pelletieri.  Under  these  circumstances,  N. 
pelletieri  would  become  simply  a  synonym  of  A7,  indica.  of  which 
the  full  list  of  synonyms  has  been  given  on  p.  1058. 


2136  MYCETOMA  AND  PARAMYCETOMA 

Clegg  and  Hobdy  (1916)  described  N.  indica  in  a  native  woman 
in  Hawaii. 

Nocardia  indica,  with  yellow  or  red  grains,  possesses  Gram- 
positive  but  not  acid-fast  hyphge,  without  clubs.  It  forms  restricted 
growths  under  aerobic  surroundings  at  220  C.  and  37  °  C,  but  will 
not  grow  under  strict  anaerobic  conditions.  The  cultures  are  without 
any  distinct  odour.  It  is  usually  said  not  to  liquefy  gelatine  or 
blood  serum,  but  Koch  and  Stutzer  say  that  it  has  a  peptonizing 
effect  after  a  long  time.  Milk  is  not  coagulated,  but  after  some 
time  is  cleared.  Pinkish  colonies  are  produced  on  the  agars  and 
on  potato.     It  is  non-pathogenic  for  animals,  as  far  as  is  known. 

5.  N.  garteni. — Garten,  1895,  met  with  an  organism  in  cases  of 
actinomycosis  in  man  which  he  called  Cladothrix  liquefaciens  No.  2, 
in  order  to  distinguish  it  from  Hesse's  fungus,  which  he  called 
Cladothrix  liquefaciens  No.  1 ;  but  Brumpt,  in  1910,  altered  Garten's 
name  to  Discomyces  garteni,  which  now  becomes  Nocardia  garteni 
Brumpt  (1910). 

This  fungus  was  grown  in  1895  by  Garten  from  the  lesions  of  a 
case  of  necrosis  of  vertebrae  and  ribs,  which  was  associated  with 
abscesses,  sinus  formation,  and  empyema.  The  grains  were  com- 
posed of  a  tangle  of  ramified  filaments  without  club  formation. 

The  organism  was  an  aerobe  which  grew  easily  on  various  media, 
producing  on  gelatine  fine  greyish-white  points.  On  the  fourth  day 
liquefaction  commenced,  and  was  completed  by  the  eighth  day. 
Nothing  is  said  as  to  the  liquid  being  coloured  in  any  way,  and, 
therefore,  we  must  assume  that  it  was  not  tinted.  On  agar,  gly- 
cerine, and  glucose  agar  it  formed  a  greyish-white  growth,  which 
became  somewhat  wrinkled  on  the  surface  after  two  to  three  days. 
The  wrinkles  are  deep  folds  on  glycerine  agar. 

On  serum  it  forms  a  white  layer,  which  becomes  wrinkled  and 
folded  after  forty-eight  hours,  when  commencing  liquefaction  may 
be  noted.  On  the  third  day  the  liquid  has  increased  considerably, 
and  by  the  sixth  day  the  whole  serum  is  reduced  to  a  perfectly  clear 
fluid.  On  potato  it  gives  rise  to  white  colonies,  while  the  surround- 
ing medium  becomes  greenish  in  colour.  It  apparently  was  not 
grown  on  eggs,  milk,  broth,  or  peptone  solutions.  It  is  pathogenic 
for  rabbits  and  guinea-pigs. 

6.  N.  krausei. — In  1899,  Krause  found  an  organism  in  an  abscess 
of  the  lower  jaw,  in  a  man  in  Germany,  which  was  characterized 
by  having  long  and  short  rods  and  club-like  forms  resembling  the 
diphtheria  bacillus. 

It  did  not  grow  at  220  C.  nor  on  gelatine  or  potato,  but  it  was 
a  facultative  anaerobe  which  formed  slightly  yellowish  colonies  on 
glycerine  agar  and  was  not  pathogenic  for  rabbits,  guinea-pigs,  or  mice. 

This  fungus  was  named  Streptothrix  krausei  by  Chester,  1901. 
which  name  has  become  changed  to  Nocardia  krausei  (Chester,  1901), 

Allied  to,  or  identical  with,  this  species  are  the  fungi  causing 
the  conditions  described  by  Mosetig-Moorhof,  Dor,  and  Poncet,  and 
often  called  '  pseudo-actinomycosis  '  or  the  mycoses  with  yellow 


THE  ACTINOMYCOSES  2137 

grains,  which  are  larger  than  those  of  the  ordinary  actinomycosis, 
while  they  are  less  numerous  in  the  pus.  Microscopically  they  show 
a  tangle  of  filaments  longer  and  larger  than  those  of  ordinary 
nocardias,  between  which  lie  micrococcal-like  debris.  They  never 
show  clubs  at  the  periphery,  and  do  not  grow  on  solid  media  like 
gelatine.  They  grow  quickly  in  broth,  forming  a  skin  on  the 
surface.  Cultures  on  serum  give  clavate  forms  like  the  diphtheria 
bacilli. 

The  fungus  causing  the  above  conditions  was  named  Nocardia 
ponceti  by  Verdun  in  1913,  and  may  be  a  synonym  for  N.  krausei 
(Chester,  1901)  for  the  following  reasons: — 

A.  The  pseudomycetomatous  condition  of  Poncet  does  not 

differ  from  the  definition  of  actinomycosis  given  at  the 
commencement  of  this  paper. 

B.  N.  ponceti  only  differs  from  N.  krausei  in  the  following 

details: — 

1.  Broth   is  rendered   turbid   and   has   a   bad   odour,   but 

Foulerton  has  pointed  out  that  this  turbidity, 
together  with  the  odour  which  was  described  as 
being  associated  with  these  growths,  may  have  been 
due  to  the  pus  not  being  collected  aseptically,  and 
therefore  the  turbidity  and  odour  may  have  been 
due  to  contamination,  as  in  addition  to  these  char- 
acters N.  ponceti  forms  a  typical  puff-ball,  just  like 
N.  krausei,  in  which  the  turbidity  and  odour  are 
absent. 

2.  According  to   Verdun,  it  does  not  grow  on  agar.     It  is 

not  known  whether  N.  krausei  grows  on  plain  agar,  but 
it  can  grow  on  glycerine  agar  and  (according  to  some 
authors)  on  glucose  agar. 

C.  They  resemble  each  other  in : — 

1.  Morphology. 

2.  They  both  possess  clavate  forms  like  the  diphtheria 

bacilli. 

3.  Both  grow  on  serum. 

4.  Neither  grows  on  gelatine. 

Other  reactions  are  given  for  one,  but  not  for  both  organisms, 
and  are,  therefore,  useless  for  purposes  of  comparison. 

We  therefore,  at  present,  see  no  reason  why  N.  ponceti  should  be 
considered  as  a  species  distinct  from  the  older  N.  krausei,  of  which  its 
name  becomes  a  synonym. 

7.  Nocardia  somaliensis. — Bouffard  observed  two  cases  of  a  myce- 
toma at  Jibouti,  in  French  Somaliland,  which  appears  to  b'e  peculiar 
both  in  its  histological  appearances  and  in  its  cultural  characters. 
Brumpt,  in  1906,  classified  this  fungus  in  his  new  genus,  Indiella 
Brumpt,  1906,  calling  it  I.  somaliensis  and  pointing  out  that, 
judging  by  the  descriptions  given  by  older  writers  in  India  of  the 
macroscopical  appearances  of  some  of  the  ochroid  varieties  of 


2138  MYCETOMA   AND  PARAMYCETOMA 

mycetoma,  this  variety  might  be  found  to  be  more  common  than 
Vincent's  N.  madurce  (=N.  indica  of  Kanthack). 

Balfour  (1911)  reported  the  presence  of  the  same  causal  agent 
in  a  case  of  mycetoma  of  the  hand  in  the  Anglo-Egyptian  Sudan, 
and  gave  a  photomicrographic  illustration  of  the  growth;  and  in 
the  same  year  Fulleborn  described  and  gave  excellent  illustra- 
tions of  a  case  from  South-West  Africa,  which  occurred  in  a 
Herero  aged  twenty  years.  A  study  of  Fulleborn's  preparation 
induced  Brumpt  to  alter  his  generic  diagnosis  for  the  fungus  which, 
in  1913,  he  classified  as  Discomyces  somaliensis,  which,  converted 
into  our  present  nomenclature,  becomes  Nocardia  somaliensis 
(Brumpt,  1906),  but  he  is  inclined  to  think  that  it  ought  to  form  a 
separate  genus  or  subgenus,  for  which  he  proposes  the  name 
Indiellopsis  Brumpt,  1913,  because  it  secretes  around  itself  in  the 
grain  a  hard  sheath,  insoluble  in  potash  and  in  eau  de  Javelle, 
which  no  other  nocardia  is  known  to  do. 

In  1916  we  met  with  this  fungus  in  a  mycetoma  of  the  foot  in 
Khartoum. 

The  grains  are  hard,  1  millimetre  in  diameter,  and  being  of  a 
reddish-yellow  colour,  resemble  the  eggs  of  fish.  The  fungus  will 
not  grow  on  hay  or  on  dura  broth,  but  it  quickly  produces  a  white, 
lichen-like,  folded  growth,  becoming  yellow  on  the  fifth  to  sixth  day 
on  potato,  but  this  growth  never  becomes  red  like  that  of  AT.  indica. 

Genus  Cohnistreptothrix. — In  1891,  Wolff  and  Israel  published  a 
beautifully  illustrated  account  of  a  streptothrix,  which  they  had 
isolated  from  two  cases  of  actinomycosis  in  man — viz.,  from  the 
lungs  and  from  a  retromaxillary  growth.  This  organism  was  con- 
sidered to  differ  from  N.  bovis  in  that  it  grew  best  anaerobically,  that 
branching  was  absent,  and  that  its  injections  into  animals  were 
regularly  positive  in  their  result.  These  three  characteristics 
induced  Kruse,  in  1896,  to  make  a  new  species  for  it  under  the  name 
Streptothrix  israeli.  In  191 1,  for  reasons  presently  to  be  set  forth, 
Pinoy  founded  a  new  genus,  Cohnistreptothrix,  with  Israel's  organism 
as  the  type  species,  and  therefore  its  name  becomes  Cohnistrepto- 
thrix israeli  (Kruse,  1896). 

It  appears  to  us  to  be  of  importance  that  the  reader  should  clearly  under- 
stand the  nature  of  the  organisms  included  in  this  genus,  and,  therefore,  we 
digress  from  our  main  subject  in  order  to  give  a  brief  history. 

Lachrymal  concretions  have  been  known  since  Cesoin  described  them  in 
1670.  In  1848,  Gruby,  examining  one  of  these  objects,  found  it  to  be  composed 
of  a  fungus,  which  he  believed  to  be  the  same  as  that  causing  favus;  but  Conn, 
in  1875,  examining  another  such  concretion,  also  saw  a  fungus,  for  which  he 
created  a  new  genus,  Streptothrix,  calling  the  fungus  in  question  Streptothrix 
foersleri  Cohn,  1875,  which  may  be  the  same  organism  as  S.  aureus  Du  Bois  de 
Saint  Sev6rin,  1895,  and  must  be  closely  related  to  Nocardia  tenuis  Castellani, 
1911,  which  belongs  to  the  same  genus,  and  as  its  colonies  on  agar  are  '  cere- 
briform,'  it  may  possibly  be  the  same  or  related  to  Streptothrix  radialus  and 
5.  cerebriformis,  both  described  from  cases  of  keratitis  by  Namyslowski  in 
1909,  as  well  as  the  more  aerobic  hyphal  form  of  Silberschmidt's  organism. 

Unfortunately,  a  mistake  was  made,  for  Cohn  was  not  aware  that  the  same 
streptothrix  had  already  been  given  by  Corda,  in  1839,  for  another  and  quite 
different  fungus,  which  is  known  as  Streptothrix  fusca  Corda,  1839,  and  which 


THE  ACTINOMYCOSES  2139 

is  to  be  found  in  all  works  of  any  importance  on  systemic  mycology.  There- 
fore, as  streptothrix  is  not  available,  after  many  changes,  the  generic  name 
has  become  Cohnistreptothrix  Pinoy,  191 1,  and  to  this  genus  Israel's  human 
organism  belongs.  It  differs  from  Bollinger's  type  of  fungus  in  growing  best 
anaerobically,  in  being  difficult  to  cultivate,  and  in  not  producing  arthro- 
spores.  Other  allied  organisms  are  Cohnistreptothrix  thibiergei  (Ravaut  and 
Pinoy,  1909),  also  found  in  actinomycosis  in  man;  Streptothrix  spitzi  Lignieres, 
1903,  found  in  cattle,  and  probably  identical  with  C.  Israeli,  as  may  be  Doyen's 
streptothrix;  while  Nocardia  carougeaui  Gougerot,  1909,  in  juxta-articular 
nodules,  and  Streptothrix  cuniculi  Schmorl,  1891,  probably  also  belong  to  this 
genus,  as  well  as  the  streptothrix  recently  discovered  in  a  liver  abcess  in 
America  by  Bloomneld  and  Bayne-Jones  (1915),  as  we  have  consulted  the 
authors  upon  this  point,  with  which  they  are  in  agreement.  Perhaps  the 
bacillus  described  by  Sawtschenko,  in  1896,  as  the  causal  agent  of  a  pseudo- 
mycetomatous  condition  may  also  belong  to  this  genus,  and  it  is  also  possible 
that  the  Coccobacillus  psendo-actinomycosis  polymorphus  Berestneff,  1898,  may 
be  the  same  as  the  chromogenic  anaerobic  streptothrix  obtained  from  human 
pus  by  Neschezadimenko  in  1908,  and  carefully  described. 

8.  Cohnistreptothrix  israeli. — This  organism  appears  to  be  of 
increasing  importance  in  human  pathology,  for,  according  to  Pinoy, 
it  appears  to  affect  man  more  often  than  Nocardia  bovis.  It  was 
first  discovered  in  man,  as  mentioned  above,  by  Wolff  and  Israel 
in  Germany,  and  has  since  been  found  in  thirteen  cases  in  the 
United  States  by  Wright.  It  has  also  been  found  in  cattle  by 
Lignieres  and  Spitz  (1904)  in  the  Argentine,  and  by  Pinoy  (1913)  in 
France. 

It  is  composed  of  short  and  long  rods,  some  of  which  show  club- 
like swellings,  while  in  old  cultures  spores  which  resemble  cocci  in 
appearance  can  be  seen.  It  grows  but  poorly  in  the  presence  of  air, 
but  much  better  anaerobically  at  370  C.  on  agar,  on  which  it  forms 
dew-like  drops,  which  later  become  yellowish  and  generally  remain 
discrete.  In  broth  it  forms  a  deposit  of  small  scaly  particles.  It 
does  not  grow  on  gelatine  at  the  room  temperature  of  Europe,  but 
egg  cultures  show  typical  branched  filaments  with  club-like  ends, 
which  later  break  up  into  bacillary  and  coccal  forms,  but  true 
arthrospores  (i.e.,  resistant  spores)  are  not  produced.  It  forms 
granulation  tumours  when  inoculated  intraperitoneally  into  rabbits 
and  guinea-pigs,  after  an  interval  of  four  to  seven  weeks.  In  these 
tumours  typical  actinomycotic  grains  can  be  found,  containing 
branched  filaments  with  clavate  ends. 

9.  Cohnistreptothrix  thibiergei. — This  fungus  was  discovered  in 
1909  by  Ravaut  and  Pinoy  in  a  case  of  actinomycosis  which 
produced  generalized  subcutaneous  and  intramuscular  nodules  in 
a  man  in  France. 

The  nodules  opened  and  discharged  blood-tinged  pus,  in  which 
the  fungus  was  seen  sometimes  in  isolated  bacillary  form  and  some- 
times as  very  small  white  grains,  which  in  the  tissues  might  measure 
some  80  microns  and  be  composed  of  a  radiating  mycelium  with  or 
without  fine  club  forms.  It  grows  well  aerobically  and  anaerobi- 
cally, but  the  former  produces  more  bacillary  and  the  latter  more 
filamentous  forms.  The  optimum  temperature  is  about  370  to 
380  C.     It  does  not  appear  to  be  pathogenic  for  laboratory  animals. 


2140  MYCETOMA  AND  PARAMYCETOMA 

Climatology. — The  geographical  distribution  of  this  variety  of 
mycetoma  is  as  follows: — 

I.  Black  actinomycosis  :  Only  one  variety  of  this  is  known — 
viz. : — 
Babes    and    Mironescu's    black    actinomycosis,    found    in 
Roumania  and  caused  by  an  unknown  fungus. 

II.  Yellow  actinomycosis  :  This  form  is  well  known  in  North 

America,  and  Sutton,  of  Kansas  City,  in  1913,  in  addition 
to  drawing  attention  to  four  previously  described  cases, 
added  two  from  his  own  practice.  The  usual  microscopical 
appearances  shown  in  yellow  actinomycosis  are  depicted 
in  Fig.  848,  but  the  only  method,  known  to  us,  of  distin- 
guishing the  nine  forms  of  actinomycosis  classifiable 
under  this  heading  is  by  cultivation,  as  will  be  indicated 
below.     The  nine  varieties  known  to  us  are: — 

1.  Israel's  yellow   actinomycosis,    found    in    Europe    and 

America  (North  and  South),  and  caused  by  Cohni- 
streptothrix  israeli  (Kruse,  1896). 

2.  Ravaut    and  Pinoy's  yellow    actinomycosis,    found    in 

France,  and  caused  by  Cohnistreptothrix  thibiergei 
Ravaut  and  Pinoy,  1909. 

3.  Acland's  yellow  actinomycosis,  found  in  Europe,  but 

the  distribution  of  this  form  requires  further  investi- 
gation.    It  is  caused  by  Nocardia  bovis  (Harz,  1877). 

4.  Bouffard's  yellow  actinomycosis,  found  at  Djibouti,  in 

French  Somaliland,  in  the  Anglo-Egyptian  Sudan, 
and  in  South-West  Africa,  and  caused  by  Nocardia 
somaliensis  (Brumpt,  1906). 

5.  Krause's  yellow  actinomycosis,  found  in  Europe,  and 

caused  by  Nocardia  kransei  (Chester,  1901). 

6.  Garten's  yellow   actinomycosis,  found   in   Europe,  and 

caused  by  Nocardia  garteni  (Chester,  1901). 

7.  Hesse's  yellow   actinomycosis,   found   in   Europe,    and 

caused  by  Nocardia  liquefaciens  (Hesse,  1892). 

8.  Chalmers    and    Christopher  son's   yellow    actinomycosis, 

found  in  the  Anglo-Egyptian  Sudan,  where  it  appears 
to  be  not  uncommon,  and  caused  by  Nocardia  con- 
voluta  Chalmers  and  Christ opherson,  1916. 

9.  Eppinger's    yellow    actinomycosis,    found    in    Europe, 

America  (North  and  South),  Asia,  and  Africa,  and 
caused  by  Nocardia  asteroides  Eppinger,  1890. 

III.  Red  (sometimes  yellowish)  actinomycosis  :  Only  one  form 

of  which  is  known: — - 
Carter's  red  (sometimes  yellowish)  actinomycosis,  found  in, 
India,  Hawaii,  Argentina,  Cuba,  Senegal,  Algeria 
Cyprus,  and  Somaliland,  and  caused  by  Nocardia 
indica  (Kanthack,  1893),  synonym,  Streptothrix  madurce 
(Vincent,  1894). 


THE   ACTINOMYCOSES  2 141 

This  organism  has  red  or  yellowish  grains,  which  produce  pinkish 
colonies  on  the  agars  (Plate  VI.,  Fig.  8)  and  on  potato.  Kan- 
thack's  name  was  overlooked  until  recently. 

/Etiology. — The  fungi  causing  actinomycosis  belong  to  the  genera 
Cohnistreptothrix  and  Nocardia,  and  are  best  arranged  by  consider- 
ing the  different  varieties  of  the  disease,  classified,  like  the  Maduro- 
mycoses,  according  to  the  colour  of  the  grain  and  the  name  of  the 
discoverer. 

They  may  be  divided  into: — 

I.  The  black  actinomycosis,  with  black  grains. 
II.  The  white  or  yellow  actinomycoses,  with  white  or  yellow  grain? . 
III.  The  red  (sometimes yellowish)  actinomycosis,  with  red  (some- 
times yellowish)  grains. 

I.  THE  BLACK  ACTINOMYCOSIS. 

Only  one  variety,  found  in  Europe,  is  known — viz.,  Babes  and 
Mironescu's  black  actinomycosis,  of  which  the  fungus  has  never  been 
classified. 

II.  THE  WHITE  OR  YELLOW  ACTINOMYCOSES. 

These  may  be  differentiated  by  the  characters  of  causal  organisms 
into: — 

A.  Fungus  difficult  of  cultivation,  grows  best  anaerobically, 

arthrospores  absent — Genus  1,  Cohnistreptothrix. 

(a)  Yellow  grains: — 

1.  Israel's  yellow  actinomycosis,  caused  by  C.  israeli 

Kruse,  1896. 

(b)  Very  small  white  grains:— 

2.  Ravaut  and  P inoy  s  yellow  actinomycosis,  caused  by 

C.  thibiergei. 

B.  Fungus  grows  readily  aerobically  and  produces  arthrospores 

— Genus  2,  Nocardia. 

(a)  Clubs  present: — 

3.  Acland's  yellow  actinomycosis,  caused  by  N.  bovis 

Harz,  1817. 

(b)  Clubs  absent. 

(e)   Hard  sheath  around  grains:— 

4.  Bouffard's    yellow    actinomycosis,    caused    by    N. 

somaliensis  Brumpt,  1906. 
(/)    Hard  sheath  absent. 
(m)  No  growth  on  gelatine. 

5.  Krause's    yellow    actinomycosis,     caused    by    N. 

krausei  Chester,  1901. 
(n)  Growth  on  gelatine. 
(0)  Blood  serum  not  liquefied: — 

6.  Eppinger's  yellow    actinomycosis,    caused    by    N. 

asteroides  Eppinger,  1890. 


2i42  MYCETOMA  AND  PARAMYCETOMA 

(p)  Blood  serum  liquefied. 

(w)  Pathogenic  for  laboratory  animals: — 

7.  Garten's  yellow  actinomycosis,  caused  by  N.  garteni 

Brumpt,  1906. 
(x)  Non-pathogenic  for  laboratory  animals. 
(y)  Gelatine  liquefied: — 

8.  Hesse's  yellow  actinomycosis,  caused  by  N.  lique- 

faciens  Hesse,  1892. 
(z)    Gelatine  not  liquefied : — 

9.  Chalmers  and  Christopher  son's  yellow  actinomycosis, 

caused    by    Nocardia    convoluta    Chalmers    and 
Christopherson,  1916. 

III.  THE  RED  (SOMETIMES  YELLOWISH)  ACTINO- 
MYCOSIS. 

There  is  only  one  known  variety — viz.,  Carter's  red  (sometimes 
yellowish)  actinomycosis,  of  which  the  causal  organism  is  Nocardia 
indica  (Kanthack,  1893). 

The  reasons  for  believing  that  these  are  the  causal  organisms  of 
the  disease  are  the  same  as  for  maduromycosis,  and  need  not  be 
repeated. 

Pathology . — This  is  much  the  same  as  in  maduromycosis. 

Morbid  Anatomy. — A  young  growth  removed  in  toto  can  be  divided 
into  two  portions,  viz. : — 

1.  A  dense  matrix. 

2.  A  number  of  irregularly  shaped  darker  bodies,  '  the  fungal 
masses,'  embedded  in  the  matrix. 

The  Matrix. — When  the  matrix  is  studied  by  the  aid  of  higher 
magnifications,  it  will  be  seen  to  be  composed  of  white  fibrous 
connective  tissue  containing  a  large  number  of  connective-tissue 
corpuscles,  and  here  and  there  a  bloodvessel  or  a  small  group  of 
bloodvessels  which  may  or  may  not  be  associated  with  a  collection 
of  cells,  and,  in  addition,  lymph  spaces  and  small  collections  of  fat 
cells  mostly  associated  with  the  bloodvessels.  When  these  vessels 
are  studied  more  carefully,  some  will  be  observed  to  be  more  or  less 
normal,  while  others  show  signs  of  periarteritis  or  endarteritis  of 
varying  degree,  which  produce  diminution  and  even  occlusion  of  the 
lumen. 

Connected  with  many  of  these  vessels,  and  often  more  or  less 
surrounding  them,  lie  dense  masses  of  cells,  which  when  carefully 
studied  appear  to  be  all  mononuclear.  They  are  not  all  of  the  same 
category,  however,  for  some,  judging  by  their  nuclei,  appear  to  be 
derived  from  the  endothelial  cells  of  the  vessels.  Another  type 
of  cells  is  characterized  by  a  darker  staining  nucleus,  and  appearing 
when  cut  in  certain  directions  as  though  it  possessed  very  little 
cytoplasm,  but,  when  seen  more  correctly,  has  a  relatively  fair 
quantity  of  cytoplasm  in  proportion  to  the  size  of  the  nucleus. 
The  nucleus  being  placed  excentrically,  and  the  cytoplasm  being 


ACTINOMYCOSIS 


2143 


non-granular  and  not  eosinophile,  this  cell  agrees  with  Unna's 
description  of  a  healthy  plasma  cell  as  seen  in  actinomycosis. 

A  third  type  of  cell  shows  a  large  vesicular  nucleus  situate 
excentrically  in  a  relatively  large  quantity  of  cytoplasm,  which  is 
either  eosinophile  or  contains  eosinophile  granules,  and  corresponds 
exactly  with  Unna's  description  of  degenerating  plasma  cells  as  seen 
in  actinomycosis. 

Fungal  Masses. — The  darker  irregular  bodies  seen  embedded  in 
the  matrix,  if  examined  by  the  aid  of  higher  magnification,  can  be 
seen  to  consist  of  fibrous  tissue  and  cells  surrounding  a  portion 
of  the  fungus,  and  have,  therefore,  for  purposes  of  distinction,  been 
termed  '  fungal  masses.' 


Fig.  84S. — Actinomycosis. 


When  a  typical  fungal  mass  is  examined  by  means  of  a  moder- 
ately high  magnification,  it  can  be  seen  to  be  composed  of  several 
distinct  areas,  which,  working  from  the  fibrous  tissue  matrix 
towards  the  fungus,  lie  in  the  following  order : — 

1.  The  Fibrous  Sheath. — This  is  continuous  with  the  fibrous 
tissue  forming  the  matrix  of  the  whole  growth,  as  already  described. 

2.  The  Fibrocellular  Layers. — Directly  under  the  dense  fibrous 
tissue  there  lies  a  thicker  or  thinner  area  composed  of  loose  fibrous 
tissue,  containing  in  its  meshes  cells  and  thin-walled  vessels;  this 
area  may  be  termed  the  fibrocellular  layers. 

3.  The  Cellular  Sheath. — Internal  to  the  fibrocellular  layers  comes 
a  mass  of  cells  which  may  be  called  the  cellular  sheath. 


2i44  MYCETOMA   AND  PARAMYCETOMA 

4.  The  Grain. — Situate  in  the  cellular  sheath  there  lies  a  more 
or  less  distinctly  or  indistinctly  striated  body,  of  varying  shape, 
and  often  with  irregular  edges,  which  is  the  grain,  and  is  composed 
of  the  fungus  and  its  surrounding  matrix. 

Fibrous  Sheath . — When  the  fibrous  connective  tissue  forming 
the  matrix  is  examined,  in  the  vicinity  of  a  fungal  mass,  it  will  be 
observed  to  show  collections  of  cells  at  intervals. 

Fibrocellular  Layers. — These  layers  are  composed  of  loose 
fibrous  tissue,  holding  in  its  meshes  plasma  cells,  healthy  and  de- 
generating polymorphonuclear  cells,  giant  cells,  and  bloodvessels. 

With  regard  to  the  giant  cells,  they  may  be  seen  to  contain  fungal 
masses,  or  these  may  be  observed  escaping  therefrom,  or  the  giant 
cells  may  be  remarked  to  be  separated  from  the  fungal  mass  by  a 
little  distance  and  to  be  damaged,  while  polymorphonuclear  cells 
lie  near  the  fungus,  and  the  adjacent  layers  of  the  fibrocellular  tissue 
may  be  observed  to  be  arranging  themselves  circularly  so  as  to 
circumscribe  the  new  fungal  growth,  and  so  to  commence  the  forma- 
tion of  a  new  fungal  mass. 

When  two  fungal  masses  lie  in  close  approximation  to  one  another 
without  the  intervention  of  dense  fibrous  tissue,  it  will  be  observed 
that  small  areas  of  the  fibrocellular  layers  adjoining  the  two  masses 
show  signs  of  granular  degeneration. 

Another  interesting  feature,  but  by  no  means  confined  to  the 
fungal  masses,  is  the  presence  of  cells  containing  one  or  several, 
small  or  large,  rounded  eosinophile  globules.  These  were  called 
fuchsin  or  Russell  bodies  by  Kanthack,  and  botryomycotic  bodies 
by  Archibald  (1911),  who  published  some  excellent  illustrations 
thereof  in  Plates  XV.  and  XVI.  of  the  medical  volume  of  the  Fourth 
Report  of  the  Khartoum  Laboratories.  They  are  a  product  of 
the  fungus,  and  are  frequently  seen  in  nocardial  infections  lying 
in  cells  at  a  distance  from  the  fungus,  in  which  case  they  are  a  great 
aid  in  diagnosis,  as  indicating  the  probable  presence  of  a  fungus 
somewhere.  They  are  also  seen  in  masses  cut  longitudinally  and 
lying  in  lymph  spaces.  They  have  been  recorded  by  all  workers 
at  actinomycosis  and  maduromycosis  since  the  days  of  Kanthack, 
and  appear  to  us  to  be  probably  the  same  material  as  that  forming 
the  club-like  dilatation  of  the  extremities  of  the  hyphse  in  N.  bovis 
and  other  nocardias,  and  that  they  may  possibly  be  a  protective 
substance  excreted  by  the  fungus  which  only  under  certain  con- 
ditions consolidates  into  the  eosinophile  form  and  into  the  clubs 
of  certain  species  of  nocardia. 

The  Cellular  Sheath.— All  our  observations  tend  to  support 
Brumpt's  view  that  primarily  the  fungus  is  enclosed  in  a  cell  which 
in  the  younger  fungal  areas  near  the  older  area  is  always  multi- 
nuclear. 

Further,  in  the  present  specimen,  there  can  be  no  doubt  that  the 
fungus  is  not  destroyed  by  the  giant  cell,  but,  on  the  contrary,  grows 
and  escapes  therefrom  and  starts  life  as  a  little  fungal  mass  of  its 
own,   in  which   instance  the  polymorphonuclear  leucocytes  now 


THE  PARAMYCETOMAS  2145 

appear  upon  the  scene,  and  the  fibre-cellular  coat  begins  to  circum- 
scribe the  cells  and  the  fungus,  while  the  damaged  remains  of  the 
giant  cell  are  seen  retiring  towards  the  periphery. 

Later,  the  mononuclear  cells  mentioned  above  appear,  and  these 
various  cells,  together  with  detritus  from  the  destruction  of  similar 
cells  situate  in  a  granular  network,  form  the  cellular  sheath  of  the 
grain,  as  shown  in  our  specimens.  This  description,  although 
varying  in  detail,  does  not  differ  materially  from  a  composite 
picture  such  as  can  be  derived  by  a  study  of  the  writings  of  Carter, 
Acland,  Kanthack,  Boyce  and  Surveyor,  Unna,  Schlegel,  Foulerton, 
Brumpt,  and  other  authors  who  have  studied  the  reaction  of  the 
body  against  different  species  of  the  genus  Nocardia. 

In  more  advanced  cases  the  morbid  anatomy  is  like  that  described 
in  maduromycosis,  with,  of  course,  the  difference  in  the  grain. 

Symptomatology,  Diagnosis. — These  are  the  same  as  for  maduro- 
mycosis. 

Treatment. — Vaccines  have  not  given  good  results  in  our  hands. 
The  correct  treatment  is  removal  whenever  possible,  but,  failing  this, 
iodide  of  potash  in  large  doses  may  be  administered. 

Prophylaxis. — This  is  the  same  as  for  maduromycosis. 

THE  PARAMYCETOMAS. 

Definition. — A  paramycetoma  is  a  disease  which  includes  all 
growths  and  granulations  producing  enlargement,  deformity,  or 
destruction  in  any  part  of  the  tissues  of  man  which  are  caused  by 
fungi  of  any  nature  whatsoever,  but  in  which  grains  are  either  absent 
or  so  few  and  so  small  as  to  escape  observation  without  prolonged 
search. 

History. — In  1917,  Chalmers  and  Archibald  first  proposed  this 
differentiation,  and  followed  it  up  in  1918  by  a  further  communi- 
cation. 

Clinical  Remarks. — The  Paramycetomas,  as  already  stated, 
cannot  be  recognized  without  microscopical  assistance,  because 
they  present  a  varied  group  of  clinical  forms  comprising  chronic 
ulcers  which  may  seem  to  be  non-malignant,  doubtfully  malignant, 
or  malignant,  of  growths  which  appear  to  be  innocent  or  which  are 
capable  of  diagnosis  as  doubtful  carcinomata,  epitheliomata,  or 
sarcomata,  or  with  reference  to  which  no  doubt  is  entertained  in 
the  mind  of  the  surgeon  attending  them. 

If  removed  in  the  more  innocent  forms  or  in  the  early  stages 
they  probably  do  not  recur,  but  in  the  later  stages  of  the  malignant 
forms  they  do  recur,  but  probably  then  as  true  malignant 
growths. 

As  a  diagnosis  cannot  be  made  clinically,  it  behoves  us  to  inquire 
upon  what  it  is  to  be  based. 

Diagnosis. — The  recognition  of  a  paramycetoma  is  based  entirely 
upon  microscopical  examination,  and  consists  in  finding  one  or 
more  of  the  following  features: — 

135 


2I46  MYCETOMA  AND  PARAMYCETOMA 

(a)  Peculiar  eosinophile  bodies. 

(b)  Fungal  filaments. 

(c)  Minute  grains. 

(d)  Cultures  and  animal  experiments. 

(e)  Minor  points. 

(a)  Peculiar  Eosinophile  Bodies.— These  are  single  bodies 
enclosed  in  cells,  or  several  large  and  apparently  free  bodies. 

In  our  opinion  these  bodies  are  composed  of  a  chemical  substance, 
apparently  formed  in  human  tissues  by  several  different  kinds  of 
fungi,  but  more  particularly  by  the  nocardias.  The  substance  may 
be  noted  lying  in  a  lymphatic,  or  in  the  form  of  these  bodies  in  cells 
at  a  considerable  distance  from  the  site  of  the  fungus.  Hence 
their  importance  in  diagnosis  and  the  necessity  on  discovering  them 
for  further  search  in  the  tissues,  or  the  patient,  for  a  fungus. 

(b)  Fungus  Filaments. — The  most  common  filament  to  be 
found  in  a  paramycetoma  is  the  nocardial  hypha.  These  are  easy 
of  recognition  to  the  trained  eye,  but  are  apt  to  be  mistaken  by 
persons  not  acquainted  with  mycology  and  to  be  recognized  as 
bacilli,  while  their  spores,  if  present,  may  be  considered  to  be 
micrococci. 

Other  forms  of  fungi,  however,  may  cause  a  paramycetoma — 
e.g.,  fungi  of  the  type  of  a  leptothrix. 

It  will  thus  be  seen  that  just  as  we  divided  the  mycetomas  into 
the  actinomycoses  and  the  maduromycoses,  so  can  the  paramyce- 
tomas  be  divided  by  the  nature  of  the  hyphal  filaments  into  the 
paractinomycoses  and  paramaduromycoses. 

(c)  Minute  Grains. — These  grains  are  very  minute  in  size,  and 
very  few  in  number,  and,  in  our  experience,  are  most  difficult  to 
find,  and,  indeed,  are  perhaps  often  absent  when  the  case  may  be 
due  entirely  to  hyphal  filaments  not  collected  into  grains. 

(d)  Cultures  and  Animal  Experiments. — We  have  been  un- 
fortunate with  our  attempts  at  cultivation  and  in  our  animal  inocu- 
lations, but  the  success  attained  by  the  Leytons  indicates  that  these 
can  be  done  at  all  events  with  certain  species  of  fungi.  Our  climatic 
difficulties  must  be  remembered  in  connection  with  our  failures. 

(e)  Minor  Points. — Among  minor  points  which  are  worth  noting 
are  the  presence  of  many  plasma  cells  either  in  good  condition  or 
degenerated. 

The  condition  of  the  vessels,  which  often  show  endarteritis  or 
periarteritis,  just  as  in  mycetoma,  is  also  worthy  of  note. 

Another  minor  point  is  a  peculiar  glassy  or  vitreous  macroscopical 
appearance,  which  is  due  to  a  degeneration  of  the  tissues  of  a  glassy 
nature,  and  must  not  be  mistaken  for  hyaline  degeneration. 

For  certain  diagnosis  the  fungal  filament  should  be  found,  but, 
failing  this,  the  eosinophile  body  is  of  the  utmost  importance. 
These  bodies,  if  associated  with  many  plasma  cells,  degenerated 
plasma  cells,  and  changes  in  the  bloodvessels  and  glassy  degenera- 
tion, are  almost  pathognomonic  of  the  presence  somewhere  of  a 
parasitic  fungus. 


THE  PSEUDOMYCETOMAS  2147 

The  differentiation  from  mycetoma  is  not  difficult,  as  the  grain 
is  readily  found  in  this  growth,  which  it  certainly  is  not  in  a  para- 
mycetoma. 

The  differentiation  from  malignant  growth  is  at  the  same  time 
very  easy  and  very  difficult.  Very  easy  because  at  once  the  speci- 
men appears  somewhat  different  from  the  typical  malignant  growth 
simulated,  and  very  difficult  because  it  may  require  prolonged 
search  before  definite  evidence  of  the  presence  of  a  fungus  is  found. 

Prognosis.— This  depends  upon  the  site  and  age  of  the  tumour 
and  its  association  with  malignant  characters  or  not.  If  the  last 
feature  is  absent,  and  the  growth  is  small  and  can  be  completely 
removed,  the  prognosis  is  good,  otherwise  it  is  bad.  If  glandular 
excision  is  performed,  the  presence  or  absence  of  infection  is  of  the 
utmost  prognostic  value. 

Treatment. — The  only  known  satisfactory  treatment  is  the  early 
and  complete  removal  of  the  growth  associated  with  glandular 
excision. 

THE  PSEUDOMYCETOMAS. 

Definition. — A  pseudomycetoma  resembles  a  mycetoma  clinically 
in  the  presence  of  swelling,  ulceration,  and  discharge,  but  differs 
therefrom  in  the  absence  of  grains,  and  from  a  paramycetoma  in 
the  absence  of  eosinophile  bodies. 


Fig.  849. — Pseudomycetoma  of  Frambcesial  Origin. 

History. — The  name  pseudomycetoma  was  first  used  by  Castellani 
to  indicate  a  peculiar  tertiary  condition  of  yaws,  which  he  described 
as  clinically  somewhat  resembling  mycetoma.  The  term  was  adopted 
by  us  in  the  second  edition  of  this  work. 

Remarks. — This  condition  is  now  well-known  to  occur  in  the 
tertiary  stage^of  framboesia  tropica  (yaws),  and  is  not  unfrequently 
seen  in  Ceylori.     Breinl,  in  New  Guinea,  has  described  a  similar 


2148  MYCETOMA  AND  PARAMYCETOMA 

condition,  known  to  the  natives  by  the  names  'roaki,'  '  buno,'  or 

'  auma,'  which  he  considers  is  a  separate  clinical  entity  from  yaws. 

He  says  that  the  foot  closely  resembles  Madura  foot,  without  the 

presence  of  the  typical  grains  in  the  pus. 

A  similar  condition  is  known  to  occur  in  sporotrichosis.  The 
foot  in  this  case  is  swollen  and  painful,  and  shows  subcutaneous  and 
deep  gumma-like  swellings.  Fistuke  discharging  pus  are  also  present. 
A  similar  condition  has  been  described  by  Austregesilo  as  being 
due  to  an  angiokeratoma  in  the  foot  of  a  negro  in  Brazil.  The 
foot  was  much  enlarged,  with  several  nodules,  from  which  white 
material  exuded.  Microscopical  sections  enabled  a  correct  diagnosis 
to  be  made.  The  whole  condition,  however,  resembled  a  n^cetoma, 
but  neither  grains  nor  fungal  hyphae  could  be  found.  His  paper 
contains  an  excellent  illustration. 

ACTINOMYCOSIS  OF  THE  BODY. 

Remarks. — The  fungi  producing  Madura  foot  may  occasionally  invade  other 
parts  of  the  body  instead  of,  or  in  addition  to,  the  foot.  They  may  attack  the 
skin  and  deeper  tissues  of  the  hands,  trunk,  mammae  in  females,  and  also  the 
deep  organs,  lungs,  heart,  liver,  brain.  For  such  conditions  the  term  '  myce- 
tomiasis  '  may  be  used,  and  when  the  fungi  found  are  Nocardia  bovis  and 
Nocardia  Israeli,  the  term  '  actinomycosis  '  is  generally  employed.  These  two 
fungi,  in  fact,  seldom  attack  the  foot.  Some  authorities  used  the  term  '  pseudo- 
actinomycosis  '  to  indicate  the  condition  induced  by  Nocardia  ponceii  Verdun, 
1912,  N.  liquefaciens  Hesse,  1S92,  N.  garteni  Brumpt,  1910. 

Symptomatology. — The  lesions  resemble,  to  a  certain  extent,  those  found 
in  the  foot.  The  condition  generally  begins  with  indolent  nodules  in  the 
skin  or  subcutaneous  tissues;  the  skin  over  them  becomes  tense  and  glossy, 
and  finally  the  nodules  break  down,  with  formation  of  sinuses,  from  which  a 
purulent  liquid  exudes,  containing  the  characteristic  granules,  of  various 
sizes  and  colour,  as  described  in  Madura  foot.  Occasionally  the  ulcerated 
lesions  become  fungoid  and  large,  and  papillomatous  purplish  tumours  may 
develop.  The  location  of  the  lesions  varies.  The  type  caused  by  Nocardia 
israeli  Kruse  and  N.  bovis  Herz,  or  true  actinomycosis,  as  found  also  fairly 
frequently  in  temperate  zones,  is  in  most  vases  situated  on  the  lower  region 
of  the  face  and  neck,  especially  in  the  tissues  under  the  jaw.  In  cattle  it 
produces  the  well-known  condition  known  as  wooden  tongue.  It  is  charac- 
terized by  the  presence  of  sulphur-yellow  grains  in  the  pus.  Of  actinomycosis, 
besides  the  cervico-facial  situation,  which  is  the  commonest,  the  following 
types  have  been  described:  The  parietal,  attacking  the  walls  of  the  thorax  and 
abdomen;  the  broncho-pulmonary;  the  abdominal  (liver,  etc.);  the  cerebral 
(very  rare),  in  addition  to  the  rare  type  situated  on  the  foot  (actinomycotic 
mycetoma). 

Prognosis. — This  depends  greatly  on  the  species  of  fungus  causing  the 
malady.  The  types  due  to  Nocardia  bovis,  Nocardia  israeli,  or  true  actino- 
mycosis, answer  well  to  a  potassium  iodide  treatment. 

Diagnosis. — This  is  based  on  the  presence  of  indolent  or  nodular  masses, 
breaking  down  with  formation  of  pus,  in  which  grains  containing  the  fungi 
are  found. 

Treatment. —  Potassium  iodide  in  full  doses  (gr.  xx.)  three  or  four  times  a  day 
should  always  be  administered. 

Nodular  Actinomycosis  of  Pinoy  and  Ravaut. 
Historical  and  Geographical. — This  condition  and  its  fungus  were  studied 
by  Pinoy  and  Ravaut  in  France. 

/Etiology. — The  condition  is  caused  by  a  Cohnistreptothrix .    Only  one  case  is 


TRENCH  FOOT  2149 

known,  described  by  Pinoy  and  Ravaut,  and  due  to  C .  thibiergei  Pinoy  and 
Ravaut,  1909  (see  p.  1066). 

Symptomatology. — In  the  only  case  on  record  there  were  numerous  sub- 
cutaneous and  intramuscular  gummatous  nodules,  which  had  developed  very 
slowly;  they  slowly  softened,  some  ulcerating.  In  the  pus  the  fungus  was 
found. 

Treatment. — Potassium  iodide  is  to  be  recommended. 

Other  nodular  actinomycoses  of  nocardial  origin,  and  character- 
ized by  the  presence  of  abscesses,  or  gummata  in  which  fungi  of 
the  genus  Nocardia  are  found,  have  been  described  by  Riviere  and 
others,  and  very  ably  in  England  by  Foulerton. 

Nocardial  Abscesses. 

Species  of  the  genera  Nocardia  and  Cohnistrefttothrix  may,  at 
times,  give  rise  to  abscesses  in  various  parts  of  the  body.  One  such 
case  was  described  by  Brought  on  Alcock  as  being  due  to  Nocardia 
asteroides  Eppinger. 

TRENCH  FOOT. 

Remarks. — Trench  foot  is  not  a  tropical  disease,  but  as  it  has  been  con- 
sidered to  be  of  hyphomycetic  origin  and  aetiologically  related  to  Madura  foot 
by  Raymond  and  other  recent  observers,  we  propose  giving  a  short  account 
of  the  condition. 

/Etiology. — -There  can  be  little  doubt  that  damp  cold  plays  a  very  important 
role  in  the  aetiology  of  the  disease,  but  there  is  much  difference  of  opinion  on 
the  point  whether  a  low  temperature  is  the  real  aetiological  factor  or  merely  a 
predisposing  cause.  Many  authorities  hold  that  trench  foot  is  a  separate 
entity  from  ordinary  congelation  conditions.  Raymond  and  Parisot  believe 
that  the  true  aetiological  agents  of  the  malady  are  fungi,  principally  Scopu- 
lariopsis  koningii  Oudemans  and  Sterigmatocystis  versicolor. 

According  to  Castellani's  researches,  cocci,  bacilli,  and  various  fungi  of  the 
genera  Scopulariopsis  Baisnier,  Aspergillus  Micheli,  Sterigmatocystis  Cramer, 
Penicillium  Link,  Monilia  Gmelin,  are  often  found,  but  they  are  probably 
secondary  invaders.  Castellani  has  noted  in  several  cases  a  spirochaete. 
Certain  authorities  consider  the  affection  to  be  a  form  of  avitaminosis. 

Among  the  predisposing  causes  one  may  mention  the  race — black  troops 
in  the  trenches  being  much  more  prone  to  develop  the  condition  than  white 
troops — fatigue  and  mental  depression,  and  the  ivearing  of  putties. 

Symptomatology. — In  a  well-marked  case  the  whole  foot  is  oedematous, 
swollen,  often  of  a  dark  red  colour,  and  painful  on  pressure.  Bullae  may 
develop,  and  after  a  variable  period  of  time  a  gangrenous  process  may  set  in; 
but  this  is  far  from  being  a  constant  feature,  and  can  be  frequently  avoided 
if  a  proper  treatment  is  carried  out.  There  are,  however,  fulminating  gan- 
grenous cases.  A  feature  of  the  condition  which  has  apparently  escaped  the 
attention  of  most  observers  is  the  presence  in  many  cases  of  a  low  inter- 
mittent fever,  even  when  there  is  no  sign  whatever  of  gangrene. 

Prognosis. — This  should  be  always  guarded,  as  even  if  symptoms  ol 
gangrene  do  not  occur  the  affection  may  run  a  very  long  course. 

Treatment.— Raymond  and  Parisot  recommend  a  boracic  camphorated 
lotion,  and  in  mild  cases  camphorated  oil.  Castellani  has  used  as  routine 
treatment,  with  good  results,  the  following: — Calcium  lactate  in  5  or  10  gr. 
doses  is  given  three  times  a  day,  and  the  affected  parts  are  painted  once  or 
twice  daily  with  an  ichthyol  lotion  (ichthyol  1  dr.,  aq.  ad  1  oz.),  and  very  lightly 
wrapped  in  cotton-wool.  It  is  advisable  to  keep  the  affected  foot  slightly- 
raised  by  means  of  cushions.  In  severe  gangrenous  cases  a  surgical  treatment 
is  necessary. 


2i5o  MYCETOMA  AND  PARAMYCETOMA 

Prophylaxis. — Trenches  should  be  kept  clean,  dry,  and  sanitary  as  far  as 
conditions  permit.  Officers  and  soldiers  should  receive  instructions  to  keep 
the  feet  scrupulously  clean,  and  wear  rubber  boots  in  wet  weather  when 
possible.     In  our  opinion,  putties  should  never  be  worn. 


REFERENCES. 

Full  references  to  literature  can  be  found  in  Musgrave,  Clegg,  and  Polk 
(1908),  Philippine  Journal  of  Science,  B.  III.,  and  continued  in  Chalmers  and 
Archibald's  and  Chalmers  and  Christopherson's  publications. 

Adami  and  Kirkpatrick  (1895).  Transactions  of  the  Association  of  Ameri- 
can Physicians,  x.  92. 

Alcock  (191 3).     British  Medical  Journal,  August  9. 

Austregesilo  (1912).     Archiv  fur  Schiffs-  und  Tropen-Hygiene. 

Balfour  (191  i).  Fourth  Report  of  the  Wellcome  Tropical  Research  Labora- 
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Bassini  (1888).     Archiv  per  le  Sc.  Med.  Torino,  xii.  309. 

Bouffard  (1902).     Ann.  d'Hyg.  et  de  Med.  Coloniale,  p.  636. 

Boyce  and  Surveyor  (1894).     Phil.  Trans.  Roy.  Soc,  185  B.     London. 

Brumpt  (1906).     Archiv.  de  Parasit.,  x.  489  (A  most  important  paper). 

Carter  (1874).  Mycetoma.  (Full  account  of  the  history,  the  fungus,  and 
excellent  illustrations.)     London. 

Castellani  (1903-1914).  Ceylon  Medical  Reports  and  Journal  Ceylon 
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Castellani  and  Chalmers  (191 3).  Manual  of  Tropical  Medicine,  2nd 
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Castellani  (1918).  Comptes  Rendus  de  la  Conference  Chirurgicale  In- 
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Castellani  (191 7).     Journal  of  Tropical  Medicine. 

Chalmers  and  Archibald  (191 5).  Fungi  Imperfecti.  Journal  of  Tropical 
Medicine  and  Hygiene.  John  Bale,  Sons  and  Danielsson.  (Definitions 
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(19 1 6).  Annals  of  Tropical  Medicine  and  Parasitology,  vol.  x.,  No.  2, 
September,  pp.  170,  216  (the  Maduromycoses,  and  also  contains  illustra- 
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Tropical  Medicine,  June  (Mycetomas  and  Pseudomycetomatous  Forma- 
tions ;  it  includes  an  account  of  Paramycetoma) .  See  also  New  Orleans 
Medical  and  Surgical  Journal,  November,  1917,  vol.  lxx.,  No.  5.  (1918). 
Journal  of  Tropical  Medicine  and  Hygiene,  xxi.,  177  (Paramycetoma). 

Chalmers  and  Christopherson  (1916).  Annals  of  Tropical  Medicine  and 
Parasitology,  vol.  x.,  No.  2,  September,  pp.  223-276  (contains  an  account 
of  the  Actinomycoses  and  a  classification  of  the  Nocardias).     Liverpool. 

Foulerton  and  Jones  (1902).  Transactions  Pathological  Society,  iii.  56. 
London. 

Godfrey  (1846).     Lancet,  p.  593  (one  of  the  earliest  full  accounts). 

Kaempfer  (1912).  Amcenitatum  Exoticarum  Politico,  Physico,  Medico, 
v.  561.     (First  modern  account.) 

Monnier  (1918).     Bull.  Soc.  Path.  Exot.  May. 

Musgrave,  Clegg  and  Polk  (1908).     Philippine  Journal  of  Science,  B.  III. 

Navarro  (1918).     Jour.  Amer.  Med.  Assoc,  September  21. 

Pepere  (1914).     Sperimentale,  No.  5. 

Polverini  (1904).     Lo  Sperimentale. 

Radaeli  (191 1 -1 2).     Ibid. 

Reynier  and  Brumpt  (1906).    Bull,  et  Mem.  Soc.  de  Chir.  de  Par.,  xxxii.  618. 

Scheube  (1903).     Diseases  of  Warm  Countries,  p.  552. 

Taraknath  (191 8).     Indian  Med.  Gazette,  January. 

Wise  (1867).     History  of  Oriental  Medicine,  ii.  365. 

Woolrabe  (1918).     Jour.  Trop.  Med.,  July  15. 


CHAPTER  XCIV 
DERMATITIS    VENENATA 

Definition  —  Remarks  —  Historical  —  Climatology  —  ^Etiology  — Symptoma- 
tology —  Diagnosis  —  Treatment  —  Prophylaxis  —  Varieties  —  Rhus 
group  —  Euphorbia  group  —  Urtica  group  —  Tectona  group — Rue  group 
— Buffalo  bean  group — Little-known  group — Doubtful  group — Refer- 
ences. 

Definition. — The  term  'dermatitis  venenata'  includes  a  number 
of  inflammatory  skin  lesions  caused  by  the  irritative  action  of 
poisonous  principles  contained  in  certain  plants. 

Remarks. — By  the  above  definition  it  will  be  observed  that  the 
term  '  dermatitis  venenata  '  is  here  used  in  the  restricted  sense  of 
being  only  caused  by  plants,  leaving  the  dermatitis  caused  by 
animals  to  be  treated  in  the  chapter  dealing  with  the  Dermato- 
zoiases  (p.  2200).  Neither  does  the  definition  include  dermatitis 
medicamentosa,  which  is  due  to  drugs  administered  internally  or 
externally,  nor  does  it  include  dermatitis  factitia,  which  is  caused 
artificially — e.g.,  beggars  rubbing  in  Ranunculus  scleratus  Linnseus 
to  produce  sores  for  the  purpose  of  inducing  pity  and  the  money 
usually  associated  therewith  or  recruits  or  soldiers  utilizing  various 
plants  for  purposes  of  malingering. 

Historical.— From  very  ancient  times  it  has  been  known  that 
certain  plants  have  stinging  properties — e.g.,  many  species  of  the 
genus  Urtica,  of  which  U.  urens  Linnseus  and  U.  divica  Linnaeus 
are  well  known  in  Europe — but  the  effects  of  which  are  slight  in 
comparison  with  the  results  produced  by  the  species  found  in  the 
East  Indies — e.g.,  U.  urentissima  Comm,  U.  crenulata  Roxburgh, 
U.  stimulans  Linnaeus,  and  U.  ferox  Forster.  One  of  the  earliest 
remarks  on  the  subject  is  to  be  found  in  Kaempfer's  '  Amoenitatum 
exoticarum,'  which  was  published  in  17 12,  and  in  which  he  refers 
to  the  action  of  lacquer  varnish  on  the  skin. 

From  that  time  onwards  scattered  references  may  be  found  in 
books  on  travel,  on  botany,  materia  medica,  poisons,  as  well  as  in 
textbooks  on  skin  diseases.  Thus  in  1862  Van  Hasselt  made  some 
references  to  the  subject,  as  did  Bazin  in  the  same  year,  while 
Piff  ard  in  1881  made  many  references  to  plants  supposed  to  be  causal 
agents. 

In  1887  White  gathered  the  whole  subject  together  in  his  work 
on  '  Dermatitis  Venenata,'  and  following  this  there  was  a  leading 
article  in  the  Lancet  on  the  dermatitis  produced  by  Primula  obconica 

2151 


2 1 52  DERMATITIS   VENENATA 

Hance,  1880.  In  1898  Blanchard  made  an  excellent  contribution 
with  regard  to  Arundo  donax,  and  was  followed  by  Havard  in  1899, 
Reynault  in  1902,  who  detailed  facts  with  regard  to  the  disease  as 
seen  in  Indo-China,  and  by  Wellman  in  1907,  who  considered  the 
stinging  plants  of  Angola.  Then  came  publications  by  Balch  (1906), 
Sabouraud  (1908),  and  the  Imperial  Institute  (1909),  the  last-named 
discussing  satin-wood.  After  this  there  are  the  papers  by  Kamgies- 
ser  in  1911,  Fordyce  1912,  Santa  Maria  1913,  Whitfield  1914,  and 
Letcher's  book  with  the  account  of  the  buffalo  bean  of  Rhodesia. 
In  1914  Hornsey  gave  a  good  account  of  the  '  rungus  poisoning  '  as 
seen  in  British  North  Borneo. 

In  1916  Vadala  again  referred  to  Arundo  donax,  and  in  1917 
Chalmers  and  Pekkola  gave  an  account  of  a  Sudanese  dermatitis 
venenata  caused  by  a  member  of  the  Rutaceae. 

Climatology. — With  regard  to  geographical  distribution,  it  is  a 
cosmopolitan  complaint,  being  found  in  all  parts  of  the  world.  It, 
however,  requires  further  study  in  the  tropics,  and  it  is  for  this 
reason  that  we  have  specially  brought  it  forward  in  connection  with 
skin  diseases. 

/Etiology. — The  causation  of  dermatitis  venenata  depends  upon: — 

I.  The  plant. 
II.  Personal  idiosyncrasy. 

III.  Confirmatory  test. 

IV.  The  active  principle. 

I.  The  Plant. — The  following  list,  largely  compiled  from  White's 
book,  but  altered  so  as  to  agree  with  our  definition  of  dermatitis 
venenata  and  to  include  tropical  plants,  gives  those  known  to  us 
to  cause  the  complaint: — 

Anacardiaceae :  Rhus  venenata  De  Candolle. 

Rhus  toxicodendron  Linnaeus. 

Rhus  diver siloba  Engler. 

Rhus  vernicijera  De  Candolle. 

Semecarpus  anacardium  Linnaeus. 
Ampelidaceae:  Cissus  pruriens  Welwitsch. 
Apocynaceae:  Nerium  oleander  Linnaeus. 
Araceae:  Arisama  triphyllum  Schott. 
Symplocarpus  fcetidus  Nutt. 
Araliaceae:  Arabia  spinosa  Linnaeus. 

Artocarpaceae:  Ant  inn's  toxicaria  Leschenault  de  la  Tour. 
Aurantiaceae:  Citrus  vulgaris  Risso. 
Berberidaceae:  Podophyllum  pcltatum  Linnaeus. 
Bignoniaceae:  Catalpa  bignonioides  Walter. 
Borraginaceae :  Borago  officinalis  Linnaeus. 
Cactaceae:  Cactus  grandiflorxis  Linnaeus. 
Compositae:  Erigeron  canadense  Linnaeus. 

Lappa  officinalis=L.  majus  Gaertner. 
Leuc anthem um  vulgar e  Lambert. 
Solidago  odora  Hooker  and  Arnold. 


/ETIOLOGY  2153 

Conifer* :  Abies  excel sa  Link. 

Juniper  us  virginiana  Thunberg. 
Juniper  us  sabina  Linnaeus. 
Connaraceae:  Thuija  occidentalis  Linnaeus. 

Cnestis  corniculatus  Lam. 
Crassulaceae :  Sedum  acre  Linnaeus. 
Euphorbiaceae :  Euphorbia  corollata  Linnaeus. 
Hura  crepitans  Linnaeus. 
Hura  brasiliensis  Willdenow. 
Hippomane  mancinella  Linnaeus. 
Jatropha  urens  Linnaeus. 
Stillingia  sylvatica  Linnaeus. 
Leguminosae:  Andira  araroba  Aguiar. 
Leucanthcmum  vulgar e. 
Mucuna  pruriens  De  Candolle. 
Stizlobium  stans  Kuntze. 
Linaceae:  Linum  usitatissimum  Linnaeus. 
Loasaceae:  Mentzelia  oligospermia  Nuttall. 

Mentzelia  lindleyi  Torrey  and  Gray. 
Loganiaceae:  Gelsemium  sempervirens  Aiton. 
Malvaceae :  Mai  ache  hirsuta  Kuntze. 
Orchidaceae :  Cypripedium  pubescens  Willdenow . 

C.  pubescens  Salisbury. 
Papaveraceae :  Sanguinaria  canadensis  Linnaeus. 
Phytolaccaceae:  Phytolacca  decandra  Linnaeus. 
Polygonaceae :  Polygonum  hydropiper  Linnaeus. 

Polygonum  acre  Hooker  and  Bentha.ni. 
Ranunculaceae:  Aconitum  napellus  Linnaeus. 
Anemone  nemorosa  Linnaeus. 
Anemone  patens  Linnaeus. 
Clematis  virginica  Thunberg. 
Delphinium  consolidum  Linnaeus. 
Rubiaceae :  Cephcelis  ipecacuanha  Richard. 

Cinchona  bark  and  quinine. 
Rutaceae:  Ailanthus  glandulosa  Desfontaines. 

Haplophyllum  tuberculatum  (Forskal,  1775)- 
Pilocarpus  pennatijolius  Engler. 
Ruta  graveolens  Linnaeus. 
Scrophulariaceae:   Verbascum  thapsus  Linnaeus. 
Solanaceae :  Datura  stramonium  Linnaeus. 
Thymelaceae:  Daphna  mezereum  Linnaeus. 
Tropaeolaceae :  Tropaiolum  majus  Linnaeus. 
Urabellif eras :  Thapsia  garganica  Linnaeus. 

Laportea  canadensis  Gaudichaud-Beaupre. 
Urticaceae :  Many  species  of  Urtica. 

This  is  a  long  list,  but  all  its  members  are  not  natives  of  the 
tropics,  in  which  the  more  important  families  are  the  Ampelidaceae, 
the  Anacardiaceae,  the  Apocyanaceae,  the  Artocarpaceae,  the  Con- 


2i54  DERMATITIS  VENENATA 

naraceae,  the  Euphorbiaceae,  the  Leguminosae,  the  Malvaceae,  the 
Rubiaceae,  the  Rutaceae,  the  Tropaeolaceae,  and  the  Urticaceae,  the 
genera  and  species  of  which  are  indicated  above. 

II.  Personal  Idiosyncrasy. — When  the  poisonous  principle  is 
contained  in  the  juice  of  cultivated  plants,  the  poisoning  is  largely 
met  with  among  gardeners,  florists,  and  people  associated  with 
plants  in  some  way;  when,  however,  the  poisoning  is  due  to  a 
principle  contained  in  some  special  hairs  of  a  plant,  whether 
cultivated  or  not,  it  is  obvious  that  anyone  may  be  affected ;  and 
when  it  is  due  to  principles  contained  in  the  dust  from  dry 
wood,  it  is  also  obvious  that  carpenters  and  persons  who  cut  or 
saw  this  wood  will  be  most  liable  to  be  affected. 

With  regard  to  the  first  series  of  cases,  in  our  experience, 
there  can  be  no  doubt  that  some  people  are  more  liable  to  the 
affection  than  others,  and  it  would  appear  that  certain  people 
suffering  from  any  form  of  seborrhcea  or  allied  condition,  no 
matter  how  mild,  are  especially  liable  to  be  troubled  by  dermatitis 
venenata. 

As  stated  in  the  previous  editions  of  this  book,  we  should  not  be  surprised 
if,  in  the  future,  it  will  be  found  that  certain  forms  of  dermatitis  venenata 
are  due  in  reality  to  some  parasitic  micro-organisms  living  in  the  plants  or 
woods,  and  which  get  inoculated.  The  fact  that,  for  instance,  satin-wood 
dermatitis  appears  several  weeks  after  handling  the  satin-wood  sawdust  is 
rather  in  favour  of  there  being  some  contagium  vivum  which  requires  some 
time  to  develop  and  multiply  sufficiently  to  cause  symptoms  of  disease. 

III.  Confirmatory  Test. — The  crucial  aetiological  test  is  to  remove 
the  patient  from  the  district  in  which  the  plant  grows,  to  cure  his 
dermatitis,  and  then,  after  a  lapse  of  time,  to  test  him  experimentally 
with  the  suspected  plant,  which,  if  the  genuine  causal  factor,  should 
reproduce  the  eruption. 

IV.  Active  Principle. — Unfortunately  at  present  hardly  anything 
can  be  said  upon  this  subject.  We  know  that  drugs  like  quinine 
can  cause  eruptions,  and  therefore  we  conclude  that  quinine  is 
the  active  principle  causing  the  eruption  produced  by  boiling  cin- 
chona bark;  but  with  regard  to  the  majority  of  the  plants,  we  are 
entirely  or  almost  entirely  ignorant  of  the  Ichemical  nature  of  the 
active  principle. 

Symptomatology. — Sometimes  the  symptoms  consist  merely  of 
itching,  with  or  without  an  erythematous  blush.  At  other  times 
there  may  be  marked  erythema,  with  cedematous  swelling  in  the 
affected  part,  which  is  often  the  face  or  the  hands,  or  both.  In  more 
severe  cases  a  true  dermatitis  may  be  present  with  papules,  vesicles, 
or  pustules,  with  or  without  such  general  symptoms  as  fever  and 
enlargement  of  the  local  lymphatic  glands. 

The  onset  is  generally  sudden,  and  the  affected  person  may  pre- 
viously have  been  in  excellent  health.  The  termination  is  in  quick 
recovery,  especially  if  the  causal  agent  is  removed. 

Diagnosis. — The  case  presents  the  ordinary  appearance  of  an 
acute  dermatitis,  and  it  requires  patience  and  acumen  to  trace 
this  to  its  correct  cause. 


DIAGNOSIS  2155 

The  characteristics  of  the  disease  are: — 

r.  Acute  dermatitis  appearing  suddenly  and  often  without 
apparent  cause  in  a  previously  healthy  person. 

2.  The  history  of  the  association  with  some  plant  by  handling 
or  being  affected  by  the  odour,  or  even  of  being  in  the  neighbourhood 
thereof. 

3.  There  may  be  history  of  previous  similar  attacks  when  in  the 
vicinity  of  the  suspected  plant. 

4.  The  rapid  recovery  on  removal  from  the  causal  plant. 

5.  The  return  of  the  symptoms  when  again  exposed  to  the  plant. 
The  differential  diagnosis  has  to  be  made  from  other  forms  of 

dermatitis,  which  can  usually  be  done  by  the  history  and  by  finding 
the  causal  plant,  but  this  will  not  help  with  certain  forms  of  acarine 
dermatitis  when  the  mite  infests  the  plant. 

In  such  a  case  the  only  possible  method  of  diagnosis  is  to  examine 
the  plant  and  the  patient  carefully,  so  as  to  exclude  the  presence 
of  these  insects,  and  to  reproduce  the  disease  by  means  of  a  plant 
found  to  be  quite  free  from  mites. 

Treatment. — The  essential  feature  of  the  treatment  is  to  remove  the 
plant  from  the  patient  or  the  patient  from  the  plant,  whichever  maybe 
most  convenient.  The  next  point  is  to  remove  all  irritating  substances 
by  copious  bathing  of  the  whole  body  in  water,  and  in  some  cases  to 
recleanse  the  affected  area  with  alcoholic  solutions.  Lastly,  soothing 
lotions  such  as  calamine  lotion  should  be  applied  to  the  inflamed  area. 

Strickler  has  tried  in  certain  types  the  injection  of  minute  doses  of  the 
poisonous  principles  extracted  with  absolute  alcohol. 

Prophylaxis. — When  the  patient  knows  that  he  is  susceptible  to 
the  influence  of  a  given  plant,  care  should  be  taken  to  avoid  it. 

Varieties.- — Dermatitis  venenata  may  be  divided  into  several 
groups  as  follows : — 

I.    The  Rhus  Group. — Plants  in  which  the  poisonous  principle  is 

contained  in  a  clear  watery  fluid. 
II.  The  Euphorbia  Group. — -Plants  in  which  the  poisonous  principle 

is  contained  in  a  thick  milky  fluid. 
III.    The  Urtica  Group. — Plants  in  which  the  poisonous  principle  is 

contained  in  fluid  in  special  hairs. 
IV.  The  Tectona  Group. — Plants  and  dried  hard  woods,  the  dust 

of  which  contains  the  poisonous  principle. 
V.  The  Rue  Group. — Plants  in  which  the  poisonous  principle  is 
apparently  volatile,  but  acts  mainly  when  the  plants  are 
handled. 
VI.  Buffalo  Bean  Group. — Plants  in  which  the  causal  agent  is 

innumerable  minute  hairs  which  penetrate  into  the  skin. 
VII.  The  Little-Known  Group. — This  is  a  group  containing  plants 
which  apparently  cause  dermatitis  venenata,  but  about 
which  information  is  very  defective. 
VIII.  The  Doubtjul  Group. — This  contains  plants  jwhich  probably 
do  not  produce  dermatitis  venenata,  but  perhaps  harbour 
a  mite  which  may  be  the  causal  agent. 


2i56  DERMATITIS   VENENATA 


I.  THE  RHUS  GROUP. 

This  group  includes  all  those  plants  in  which  the  poisonous 
principle  is  contained  in  a  clear,  watery  juice. 

The  ivy  or  sumac  belongs  to  the  genus  Rhus  Linnaeus,  which  is 
classified  either  as  a  genus  belonging  to  the  superfamily  Anacardio- 
ideae  in  the  family  Terebinthaceae,  or  more  simply  as  belonging  to 
the  family  Anacardiaceae.  The  genus  Rhus  includes  about  120 
species,  growing  in  nearly  every  part  of  the  world;  but  fortunately 
only  a  few  are  poisonous  to  man,  and  they  may  be  distinguished, 
as  a  rule,  by  their  inconspicuous  flowers  being  in  loose,  slender 
clusters  or  panicles  in  the  axils  of  the  leaves,  and  by  their  greyish- 
white  or  yellowish  dry  fruit. 

They  may  be  arranged  in  two  sections,  according  to  the  structure 
oi  their  leaves: — 

1.  Leaves  trifoliate. 

Rhus  radicans  Linnaeus. 
Rhus  toxicodendron  Linnaeus. 
Rhus  diversiloba  Torrey  and  Gray. 

2.  Leaves  pinnate. 

Rhus  vernix  Linnaeus. 
Rhus  pumila  Meerburg. 
Rhus  vernicifera  De  Candolle. 
Rhus  succedanca  Linnaeus. 

Rhus  radicans  Linnaeus  is  by  many  authorities  considered  to  be 
merely  a  variety  of  R.  toxicodendron.  It  is  common  in  the  Northern 
United  States,  while  the  latter  is  more  common  in  the  Southern 
United  States.  It  has  ovate  or  lozenge-shaped  leaflets,  which  are 
either  entire  or  toothed  and  pointed,  while  R.  toxicodendron  has 
obtusely  crenated,  lobed  leaves. 

Rhus  diversiloba  is  the  Californian  poison  ivy  or  poison  oak, 
with  rounded,  obtuse  leaflets. 

Rhus  vernix  (synonym,  R.  venenata)  is  the  poison  elder  or  poison 
sumac  of  the  United  States,  and  is  a  large  shrub  or  small  tree. 
It  is  very  poisonous. 

Rhus  pumila  Meerburg  is  a  small  erect  shrub,  found  in  the 
Southern  United  States. 

Rhus  snccedanea  Linnaeus  is  the  Japanese  wau-tree,  and  is  well 
known  in  Tonkin  and  in  South  China. 

/Etiology. — The  poisonous  principle  is  an  oil  (Toxicodendron , 
which  occurs  in  all  parts  of  the  plant  and  at  all  seasons,  and  not 
toxicodendric  acid,  which  is  merely  a  synonym  of  acetic  acid,  as 
was  formerly  thought  to  be  the  case. 

Symptomatology. — After  an  incubation  of  one  to  nine  days, 
there  is  at  first  itching  in  the  affected  area,  which  gradually  increases 
in  intensity,  and  is  associated  with  all  the  signs  of  inflammation, 
producing  an  appearance  not  unlike  erysipelas,  and  sometimes 
going  on  to  vesiculation.    The  parts  most  commonly  affected  are 


THE  EUPHORBIA  GROUP  2157 

the  eyelids,  face,  and  neck,  but  it  may  also  occur  on  the  hands  and 
feet.  Left  to  itself,  the  eruption  remains  well  marked  for  some  four 
to  five  days,  and  then  gradually  subsides,  serum  discharges  from 
the  vesicles,  and  after  some  desquamation  the  affected  area  returns 
to  normal  after  some  ten  to  twenty  days. 

Treatment.— Wash  the  affected  parts  thoroughly  with  soap  and 
water,  and  then  clean  with  a  lotion  of  alcohol  and  ether,  and  finally 
apply  the  ordinary  lead  and  opium  lotion  or  a  solution  of  acetate 
of  aluminium.    In  mild  cases  calamine  lotion  is  very  efficacious. 

Prophylaxis. — Remove  the  poisonous  ivy.  This  can  only  be 
performed  by  digging  up  the  roots. 

The  Lacquer  Poison. — Rhus  vemicifera  De  Candolle  is  the 
lacquer  or  varnish-tree  of  Japan.  Lacquer  poisoning  has,  however, 
been  described  on  p.  191,  and  need  not  be  repeated  here. 

The  Parsnips. — In  the  same  group  with  the  poisonous  ivies 
come  the  parsnips,  of  which Pastinaca  saliva  Thomas,  the  common 
parsnip,  and  Heracleum  lanatum  Mich  (H.  giganteitm  Fischer), 
the  cow  parsnip,  cause  symptoms  analogous  to  those  described  above. 
The  treatment  is  similar. 


II.  THE  EUPHORBIA  GROUP. 

|The  Euphorbia  group  is  placed  in  the  non-volatile  division, 
because,  although  it  is  definitely  known  that  the  milky  juice  if  it 
touches  the  skin  causes  dermatitis,  it  is  not  so  evident  that  any 
volatile  principle  contained  therein  can  act  at  a  distance,  though 
it  is  possible  that  it  does  so.  The  subject  requires  further  investi- 
gation. 

In  this  group  the  poisonous  principle  is  contained  in  a  thick  milky 
juice,  the  latex,  which  is  contained  in  special  lactiferous  cells. 

Hippomane  mancinella  Linnaeus  (Euphorbiaceae),  which  is  the 
celebrated  manchineel-tree  of  the  Grenadine  Islands,  is  also  found 
in  Colombia,  South  America,  where  it  is  called  '  Pedro  Fernandes ' 
or  '  mansanillo.'  It  causes  very  severe  pruriginous  and  painful 
urticaria  in  people  who  rest  under  its  shade.  According  to  Martinez 
Santa-Maria,  this  eruption  usually  disappears  in  about  twenty-four 
hours,  but  occasionally  it  may  last  for  two  or  three  days,  or  even 
longer. 

The  Euphorbias. — All  euphorbias  possess  more  or  less  irritating 
juices,  which,  if  rubbed  into  the  skin,  cause  inflammation.  The 
thick  milky  latex  is  acid,  and  contains  a  dense  oil,  which  is  very 
irritating.  As  an  example  of  this  group  may  be  mentioned  E. 
pilulifera  Linnaeus  or  E.  resinijer  Bergmann.  The  former  is  common 
in  many  parts  of  the  tropics,  and  the  latter  occurs  in  North  Africa. 

Hura  crepitans  Linnaeus,  of  Central  America  and  the  West  Indies, 
and  H.  brasiliensis,  of  Brazil,  possess  a  milky  juice,  said  by  Piffard 
to  cause  severe  swelling  of  the  face,  while  the  latter  was  employed  in 
Brazil  as  a  treatment  for  leprosy. 


2i58  DERMATITIS  VENENATA 


III.  THE  URTICA  GROUP. 


Urtica  Subgroup. — This  is  characterized  by  containing  its 
poisonous  principle  in  hairs. 

This  group  includes  the  nettles  which  belong  to  the  genus  Urtica 
Linnaeus,  of  which  U.  urens  is  the  common  European  type,  while 
U.  ferox  Forster  is  found  in  New  Zealand,  and  U.  pilulifera  Linnaeus 
occurs  in  the  Mediterranean  littoral. 

Laportea  Gauducheau  is  an  allied  genus,  of  which  L.  crenulata 
Roxburg  in  Bengal,  L.  stimidans  Weddel  in  Java,  and  L.  gigas 
Weddel  in  New  Holland,  produce  severe  urticarial  eruptions, 
associated  with  pain  lasting  for  several  days. 

The  genus  Urera  Gauducheau  belongs  to  the  same  family,  being 
found  in  tropical  Africa  and  America,  while  the  genus  Girardinia 
Gauducheau  is  found  in  tropical  Africa  and  Asia,  and  both  contain 
species  with  markedly  urticarial  properties. 

In  all  these  the  poisonous  principle,  which  is  said  to  be  of  the 
nature  of  an  aldehyde,  is  contained  in  a  special  poison  apparatus, 
which  consists  of  secreting  cells  which  pour  their  secretion  into 
awl-shaped  filaments,  or  hairs  which  are  filled  with  an  acrid,  non- 
volatile, albuminoid,  acid  liquid.  These  hairs  penetrate  the  skin, 
and  the  tip,  being  broken  in  the  process,  discharges  the  poison  into 
the  dermis.  The  poison  quickly  produces  the  well-known  urticarial 
eruption  associated  with  itching,  tingling,  and  even  pain. 

Primula  Subgroup. — In  the  same  group  come  quite  a  different 
series  of  plants— viz.,  the  primulas,  primroses,  etc.- — which  belong 
to  the  family  Primulaceae.  In  the  tribe  Primuleae  there  is  a  section 
called  '  Sinesis,'  which  contains  Primula  obconica  Hance.P.  sinensis 
Sabine,  P.  sieboldii  E.  Moir,  and  P.  cortusoiides  Linnaeus,  which 
possess  poison  glands  associated  with  hard  poisonous  hairs,  contact 
with  which  produces  acute  dermatitis,  which  often  begins  as  an 
erythema  on  the  face  or  back  of  the  hands,  and  spreads  quickly  to 
other  regions.  Soon  the  erythema  becomes  cedematous  and  swollen, 
and  vesicles  may  at  times  appear.  The  general  aspect  of  the 
patient  with  the  red  and  swollen  eyelids,  red  and  swollen  face,  and 
the  similar  eruption  on  other  parts  of  the  body,  closely  resembles 
erysipelas,  and  is,  without  doubt,  one  of  the  forms  of  the  complaint 
often  called  '  the  rose  ' — i.e.,  a  non-contagious  erysipelas. 

It  must,  however,  be  admitted  that  some  of  the  recurrent  erup- 
tions described  on  the  hands  and  face  of  persons  believed  to  be 
suffering  from  this  or  ivy-poisoning  are  suggestive  of  pellagra 
(see  p.  1700).  The  erythema  of  pellagra  is,  however,  generally 
confined,  to  areas  exposed  to  the  light,  and  is  usually  associated 
with  some  intestinal  or  nervous  symptoms.  It  is,  however,  as  well 
to  bear  in  mind  the  possibility  of  pellagra  in  cases  of  dermatitis 
on  the  hands  and  face  recurring  in  the  spring  or  autumn. 

The  usual  treatment  is  to  apply  calamine   lotion,  to  which  a 
little  menthol  or  opium  is  added. 


THE  TECTONA   GROUP  2159 

Orchid  Subgroups. — Cypripedium  spectabile  Salisbury,  of  the 
Orchidaceae,  is  also  said  to  possess  venomous  hairs,  while  C. 
pubescens  Willdenow  is  also  known  to  cause  a  dermatitis. 

Jatropha  urens  Linnaeus,  var.  stimidosa  Pohl,  growing  from 
Virginia  southwards,  has  stinging  bristles  and  is  called  '  tread 
softly. ' 

Malache  hirstita  Kuntze  (Malvaceae),  called  by  the  natives  of 
Angola  '  utiete,'  which  name  it  shares  with  other  stinging  species 
of  the  Malvaceae  in  the  same  locality,  has  been  investigated  by 
Wellman,  who  finds  it  to  be  armed  with  hairs  containing  a  very 
irritating  substance.  Other  examples  in  the  same  locality  are 
species  of  the  genera  Sida  and  other  species  of  Malache. 

Cisus  pruriens  Welwitsch  (Ampelidaceae)  is  another  of  Well- 
man's  stinging  plants.  The  fruit  is  covered  with  stinging  hairs. 
It  also  has  an  irritating  juice  around  the  seeds,  which  burns  the 
throat  if  an  attempt  at  mastication  is  made. 

Cnestis  corniculatus  Lam.  (Connaraceae)  is  a  vine  common  in 
Angola  and  called  sakupolopolo.  Wellman  had  an  unpleasant 
experience  with  the  hairs  from  a  pod. 

Several  other  species  belonging  to  the  same  genus  and  to  Rourea 
have  stinging  bristles  on  the  fruit. 

Stizlobium  stans  Kuntze  and  S.  pruriens  De  Candolle — synonym, 
Mucuna  pruriens  (Leguminosae),  and  called  by  the  natives  of  Angola 
'  eyumbi ' — are  armed  with  stinging  pelose  hairs;  Mucuna  pruriens 
is  the  cowhage  of  the  East  and  West  Indies. 

IV.  THE  TECTONA  GROUP. 

This  group  includes  trees,  the  handsome  wood  of  which  is  used 
for  the  ornamentation  of  saloons,  and  also  for  making  furniture. 
The  dried  hard  wood  gives  off  dust,  which  is  extremely  irritating 
to  some  people,  while  others  appear  not  to  be  affected.  One  attack 
appears  to  render  the  sufferer  more  liable  to  the  complaint,  and 
although  certain  authorities  claim  that  immunity  may  be  acquired 
by  attacks,  there  appears  to  be  considerable  doubt  on  this  point, 
and,  in  fact,  the  evidence  points  to  quite  the  reverse  being  true. 
The  best  known  of  these  dermatites  was,  until  recently,  that  caused 
by  the  wood  of  Tectona  grandis  Linnaeus,  commonly  called  '  teak,' 
which  gives  off  a  dry  essential  oil  in  the  dust  created  by  sawing, 
and  this  produces  a  severe  form  of  dermatitis  in  carpenters  and 
joiners,  which  tends  to  become  generalized,  and  may  be  of  long 
duration,  lasting  sometimes  for  months. 

The  effect  of  the  dust  of  '  satin-wood  ' — i.e.,  the  wood  of  Chlorox- 
ylon  swietenia  De  Candolle  from  Ceylon  and  the  East  Indies,  or 
the  wood  of  F agar  a  flava  (synonym,  Zanthoxylam  flavum)  from  the 
West  Indies  is  to  produce  a  dermatitis.  These  woods  contain  a 
crystalline  alkaloid  ('  chloroxylonne,'  C22H2307N),  which  has  been 
carefully  studied  by  Cash,  who  finds  that  twenty-two  days  after 
application  for  the  first  time  it  causes  a  dermatitis  which,  beginning 


2160  DERMATITIS  VENENATA 

with  itching,  gi  /es  rise  to  papules,  vesicles,  and  oozing-points  on  the 
inoculated  limb,  which  in  due  course  becomes  brawny  and  pits  on 
pressure.  In  a  little  time  the  swelling  spreads  to  the  eyelids  and 
face,  ears,  lips,  and  nose,  and  great  discomfort  is  experienced.  In  a 
few  days  a  nasal  catarrh  and  a  laryngeal  cough  appear.  This  cough 
is  of  an  explosive  nature,  as  though  a  hair  had  become  lodged  in  the 
throat,  and  although  the  secretion  at  first  is  slight,  later  it  becomes 
more  abundant.  The  experimental  illness  lasted  about  forty  days. 
Another  application  of  the  active  principle  produced  a  relapse  in 
forty  minutes. 

In  the  ordinary  way  the  first  attack  is  of  slow  development,  the 
symptoms  appearing  some  six  weeks  after  the  first  handling  of  the 
wood,  but  a  relapse  is  of  rapid  development. 

The  illness  begins  with  the  development  of  an  acute  inflammation 
of  the  skin  of  the  hands,  wrists,  face,  and  neck,  producing  an  appear- 
ance somewhat  resembling  erysipelas,  but  without  fever  or  con- 
comitant sickness.  The  inflamed  surfaces  discharge,  dry,  and 
finally  desquamate.  The  most  suitable  treatment,  according  to 
Cash,  is  to  apply  the  unguentum  glycerinis  plumbi  subacetates 
of  the  British  Pharmacopoeia  every  four  hours,  to  administer 
bromides  to  allay  the  irritation,  and  opium  to  relieve  the  laryngeal 
cough. 

Other  woods  with  similar  properties  are  ebony  (Diospyrus 
ebenum  Kon),  found  in  Ceylon  and  India  originally,  and  rosewood 
(Dalbergia  latifolia  Roxburg),  found  in  India. 

Andira  araroba  Aguiar  (Leguminosae),  the  Goa  powder  tree  of 
Brazil,  produces  an  irritating  dust  when  the  wood  is  cut  or  sawn,  so 
that  workmen  have  to  protect  their  faces. 

V.  THE  RUE  GROUP. 

Haplophyllum  Dermatitis.- — This  has  been  described  by 
Chalmers  and  Pekkola  as  occurring  in  the  Anglo-Egyptian  Sudan. 
It  is  caused  by  a  rue  named  Haplophyllum  tuberculatum  (Forskal, 
1775),  synonym  Ruta  tuber culata  (Fig.  850),  which  was  proved  to  be 
the  causal  agent  by  producing  the  dermatitis  in  the  susceptible 
person  by  bringing  him  experimentally  into  contact  with  the  plant 
for  a  few  seconds  some  time  after  he  had  been  cured  of  the  original 
attack.  At  the  time  of  the  experiment  the  person  in  question  was 
staying  in  a  place  far  distant  from  the  area  where  the  plant  grew, 
from  which  it  had  to  be  fetched  for  purposes  of  the  experiment.  The 
experimental  eruption  (Fig.  851)  appeared  in  about  eighteen  hours 
after  rubbing  the  forearm  for  a  few  seconds  with  the  leaves  and 
flowers,  which  were  partially  dry  after  their  long  journey.  The 
plant  only  affects  susceptible  people. 

In  the  original  attack  the  incubation  period  was  thirty  hours,  and 
began  as  small  red  papules  on  the  hands,  feet,  and  legs,  which 
became  swollen,  red,  and  itching,  and  were  associated  with  headache 
and  pain  in  the  epigastric  region,  but  no  fever.    The  lips,  lobules 


THE  RUE  GROUP 


2161 


of  the  ears,  and  eyelids  became  red  and  swollen,  and  there  was  much 
itching.  Later  the  face  became  swollen,  the  lips  cracked  and  oozed, 
and  the  lymph  glands  under  the  jaw  and  in  the  groin  enlarged. 
All  the  symptoms  rapidly  disappeared  when  he  ceased  to  work  among 
these  plants. 


Fig.  850. — Haplophyllum  tuberculatum. 

The'treatment  adopted  was  to  wash  the  whole  body  after  removal 
from  the  endemic  area  and  to  .apply  calamine  lotion. 


Fig.  851. — Experimental  Eruption. 


Other  Rues. — According  to  Bentley  and  Trimen,  Ruta  graveolens 
causes  redness,  swelling,  and  even  vesication  of  the  skin  if  much 
handled,  while  'Le  Maout  and  Decaisne  state  that  R.  montana, 
found  in  Spain,  produces  erysipelatous-like  conditions  and  ulcerating 
pustules  on  the  hands  of  those  who  gather  it. 

136 


2 1 62  DERMATITIS  VENENATA 

VI.  THE  BUFFALO  BEAN  GROUP. 

Letcher  has  written  an  interesting  account  of  the  sufferings 
produced  by  the  minute  hairs  of  the  pods  of  the  Buffalo  bean. 
This  bush,  with  its  silky  green  pods,  lives  along  the  Luia  River  in 
Portuguese  South  Africa.  The  little  hairs  settle  on  the  skin  and 
set  up  violent  irritation  and  burning,  lasting  about  one  hour 
despite  remedies.  Natives  plaster  themselves  all  over  with  mud. 
This  laconic  description  by  no  means  expresses  the  views  of  sufferers, 
who  look  upon  the  tree  as  one  of  the  '  choicest  creations  of  the  devil.' 

VII.  THE  LITTLE-KNOWN  GROUP. 

This  group  includes  dermatitis  due  to: — 

i.  Cashew  nut.  4.  Oleander. 

2.  Cinchona  quinine.  5.  Rungus. 

3.  Nasturtium.  6.  Upas. 

Seniecarpus  anacardium  Linnaeus  (Anacardiaceae),  the  common 
cashew  nut  of  the  tropics,  a  native  of  Tropical  America  and  natural- 
ized in  Africa  and  Asia,  is  said  to  cause  fumes  when  roasted  which 
may  blister  the  face.    The  mere  handling  of  the  plant  does  no  harm. 

Cinchona  (Rubiaceae)  [Quinine].- — Although  the  cinchona  tree 
itself  is  harmless,  yet  workmen  preparing  quinine  by  boiling  the 
bark,  those  who  make  the  sulphate,  and  those  who  bottle  the  powder, 
are  apt  to  suffer  from  erythema,  vesicles,  and  pustules,  which  appear 
upon  the  hands,  forearms,  and  genitalia  in  susceptible  persons. 
It  is  believed  to  be  due  to  emanations  from  the  drug  acting  upon 
susceptible  persons,  who  should  not  be  longer  employed  at  this 
work.  The  rash  disappears  in  two  to  four  weeks  after  ceasing  to 
work  with  quinine. 

Nasturtium. — Tropcsolum  majus  Linnaeus  (Tropaeolaceae),  which 
is  a  native  of  Peru,  will  cause  a  dermatitis  in  susceptible  persons 
when  handled. 

Oleander. — Nerium  oleander  Linnaeus  (Apocyanaceae),  the 
oleander  of  Palestine  and  the  East,  may,  in  susceptible  people, 
cause  symptoms  like  those  produced  by  the  Rhus  group,  but  this 
requires  confirmation. 

Rungus. — This  is  a  curious  affection,  described  in  British  North 
Borneo  by  Hornsey,  and  is  caused  by  contact  with  any  part  of  the 
tree  called  rungus  or  ringus  by  the  natives,  and  said  to  be  capable 
of  being  spread  from  a  victim  to  uninfected  persons.  Within 
twenty-four  hours  of  handling  the  tree  itching  se'.s  in,  and  this  is 
followed  by  a  papular  rash  associated  with  fever  and  malaise.  The 
rash  appears  first  on  the  parts  which  have  been  in  contact  with  the 
tree.  The  papules  become  vesicles  and  then  bullae,  filled  with  a 
serous  fluid,  and  these  if  secondarily  infected  may  give  rise  to  foul 
ulcers.    Some  people  are  immune.    The  condition  heals  naturally. 

Upas  Tree. — Antiaris  toxicaria  Lesch  (Artocarpaceae),  according 


THE  DOUBTFUL  GROUP  2163 

to  Loudon,  causes  cutaneous  eruptions  when  wounded,  while 
Hasselt  says  that  it  affects  the  Javanese  after  the  manner  of  the 
Rhus  group  when  they  come  in  contact  with  it.  This  requires  con- 
firmation. ] 

VIII.  THE  DOUBTFUL  GROUP. 

The  irritant  poisoning  caused  by  kaju-rugas,  the  juice  of  which 
produces  painful  bullae,  by  kaju  buta-buta,  which  causes  violent 
dermatitis  and  conjunctivitis,  have  not  been  well  studied,  neither 
has  the  poisonous  properties  of  the  well-known  daffodil;  in  fact, 
the  whole  subject  requires  further  study. 

Cane  Dermatitis. — A  peculiar  dermatitis  is  found  in  people 
handling  and  cutting  reeds  (Arundo  donax  Linnaeus)  in  Provence, 
some  parts  of  Italy,  some  districts  of  Greece,  and  other  countries. 
The  dermatitis  was  studied  by  Blanchard  and  many  observers, 
among  whom  Thiebierge,  Berlese,  Brigi,  Aravandinos,  Sfameni, 
and  Vadala,  may  be  mentioned.  It  starts  with  severe  itching 
and  erysipelatoid  eruption,  associated  with  the  formation  of  blebs, 
generally  on  the  uncovered  parts  of  the  body,  but  also  on  the  genital 
organs,  which  may  become  greatly  oedematous,  and  febrile  symptoms 
with  signs  of  coryza  may  appear.  After  a  few  days  the  rash  dis- 
appears, and  is  followed  by  desquamation. 

The  /Etiology  is  doubtful.  Some  authorities  consider  it  to  be  due, 
to  the  plant  itself,  others  to  a  fungus  (Ustilago  hypodytes  Schlecht) 
and  still  others  to  a  mite  (Aclerda  berlesi). 

Treatment  consists  in  applying  calamine  and  lead  lotions. 

Vanilla  Dermatitis. — This  is  often  called  Vanillismus,  and  is 
due  to  Vanilla  planijolia,  which  is  a  native  of  Eastern  Mexico,  but 
which  also  grows  naturally  in  Tropical  America  and  is  cultivated 
in  many  parts  of  the  tropics.  Workmen  when  handling  the  beans 
suffer  from  itching  of  the  hands  and  face,  while  the  skin  becomes 
covered  with  a  pruriginous  eruption  and  reddens,  swells,  and 
desquamates.  It  would,  however,  appear  that  this  is  not  due  to 
the  plant,  but  to  some  mite  thereon,  as  it  does  not  occur  in  some 
works.  It  is  said  that  only  persons  with  dry  skins  should  work 
with  vanilla,  as  the  least  drop  of  perspiration  or  moistening  of  the 
beans  causes  their  destruction  by  fungal  growth.  The  whole 
matter  requires  further  investigation. 


REFERENCES. 

The  best  general  references  are  to  be  found  in  the  Index  Catalogue  of  the 
Library  of  the  Surgeon-General's  Office,  United  States  Army,  Second  Series, 
vol.  xiv.,  1909,  p.  572:  Rhus  Poisoning;  vol.  xiii.,  1908,  pp.  814  and  815: 
Primula  Poisoning.  A  very  excellent  general  paper  is  Havard,  v.  (1899), 
Proceedings  of  the  Association  of  Military  Surgeons,  vol.  viii.,  p.  203,  but  the 
most  complete  account  is  White  (1887),  '  Dermatitis  Venenata,'  Boston. 

Balch  (1906).     Journal  of  the  American  Medical  Association. 

Bazin  (1862).  Lecons  theoriques  et  cliniques  sur  les  affections  cutanees.  Paris. 

Blanchard  (1898).     Archives  de  Parasitologic,  vol.  i.     (Arundo  donax.) 


2i64  DERMATITIS  VENENATA 

Bulletin  Imperial  Institute  (1909),  vii.  93 ;  (1911),  ix.  351.     (Satin- Wood.) 
Cash  (191 1).     British  Medical  Journal,  October  7,  p.  784.     London. 
Chalmers    and    Pekkola    (1917).     Bulletin    de    la    Societe   de    Pathologie 

Exotique,  x.  512.     (A  Sudanese  Dermatitis  Venenata.)     Paris. 
Cleland  (1914).     Australian  Medical  Gazette,  June  20.     (Plants  with  Acrid 

Juices.)     Sydney. 
Fordyce,  J.  A.  (1912).     Journal  of  American  Medical  Association,  p.  2043. 
Hornsey    (1914).     British    Medical    Journal,    April    4,    p.    759.     (Rungus 

Poisoning.)     London. 
Kanngiesser,  F.  (191  i).     Correspond. -Bliitt  fur  Schw.  Aerzte  xli.,  1041-1044. 

(Primula.)     Basle. 
Lancet  (1890).     Leading  article  on  Primula  obconica  and  Dermatitis,  ii.  612. 
Letcher  (191  i).     Big  Game  in  North-Eastern  Rhodesia,  p.  54.     London. 
Martinez  Santa-Maria  (1913).     Journal  of  Tropical  Medicine. 
Morton  (1918).     Jour.  Roy.  Nav.  Med.  Serv.,  vol.  iv.,  No.  4. 
Piffard  (1881).     Treatise  on  the  Materia  Medica  and  Therapeutics  of  the 

Skin.     New  York. 
Reynault   (1902).     Medecine   et   Pharmacie   chez   les   Chinois   et   chez   les 

Annamites.     (Dermatitis  Venenata  in  Indo-China.)     Paris. 
Sabouraud,  R.     (1908).     Clinique,  iii.  246.     Paris. 
Sfameni  (1912).     Malaria. 
Strickler  (1918).     Jour.  Cutan.  Diseases,  vol.  xxxvi.,  No.  6.     (Treatment  by 

Vegetable  Toxins.) 
Vadala  (1916).     Malaria,  February  and  April.     (Arundo  donax.) 
Van  Hasselt  (1862).     Handbuch  der  Giftlehre.     Braunschweig. 
Walker    (1916).     Introduction   to   Dermatology,    6th   edition,    109.     (Very 

excellent  account.) 
Wellman  (1907).     Journal  of  Tropical  Medicine  and  Hygiene,  185.     (Sting- 
ing Plants  of  Angola.)     London. 
Whitfield  (1914).     Lancet,  February  28,  p.  607.     (Primula  and  Rhus  cases.) 

London. 


CHAPTER  XCV 
ULCERATIONS 

Cutaneous  leishmaniasis  (Oriental  sore)  —  Muco-cutaneous  leishmaniasis 
(Espundia) — Indian  oropharyngeal  leishmaniasis — Ulcus  tropicum — 
Ulcus  interdigitale — Ulcus  infantum — Remarks  on  ulcers  in  the  tropics — 
Granuloma  inguinale — Papilloma  inguinale — References. 

CUTANEOUS  LEISHMANIASIS  (ORIENTAL  SORE). 

Synonyms. — Delhi  boil;  Aleppo  boil;  Biskra  boil;  Bagdad  boil 
Ulcera  de  Bauru  (Brazil);  Bouton  d'Orient;  Ulcere  d'Orient; 
Chancre  du  Sahara;  Dermite  Ulcereuse  Circonscrite  (Corre) ;  Ende 
mische  Beulenkrankheit ;  Bottone  d'Oriente;  Godownik,  i.e., 
'  yearly  boil '  (Caucasus) ;  the  Tartar  name  is  '  Il-jarassy  '  ('  il  '= 
year,  '  jarassy '=boil) ;  Tschiban,  i.e.,  'yearly  sore';  Dous-el- 
Kourmati,  i.e.,  'date  disease'  (Turkish);  Ghisud  (Abyssinia); 
Habb-es-Sanawi,  i.e.,  '  yearly  boil ';  Habb-es-Sanah,  i.e., '  boil  of  the 
year';  Bess-el-Temiir,  i.e.,  'date  disease'  (Arabian);  Salek,  i.e., 
'annual'  (Persian);  Pascha-churdj ,  i.e.,  'fly-bite';  Afghan  Jara, 
i.e., '  Afghan  plague  ';  Jaman  Dyscharagan,  i.e.,  '  malignant  ulcer  '; 
Taschkent  Jarassi,  i.e.,  '  Tashkent  ulcer '  (Tashkent) ;  Mycosis 
Cutis  Chronica  (Carter) ;  Lupus  Endemicus  (Lewis  and  Cunningham)  ; 
Endemic  Boil  Disease  (Scheube) ;  Granuloma  Endemicum  (Brooke) ; 
Furunculus  Orientalis  (Crocker) ;  Pian-Bois  (Guiana) ;  Sudan  nodules ; 
Cutaneous  leishmaniasis;  Leishman  nodules;  Parasitic  granuloma 
(Ferguson  and  Richards). 

The  so-called  Nile  boil  has  been  demonstrated  by  Modder  and 
Archibald  to  have  nothing  to  do  with  Oriental  sore,  being  of  pyo- 
genic origin.  The  so-called  Bucharest  boil,  also,  has  apparently 
nothing  to  do  with  Oriental  sore. 

Definition. — A  specific  ulcerative  affection  of  the  skin  caused  by 
Leishmania  tropica  Wright  and  its  varieties. 

History. — The  earliest  account  of  the  disease  is  to  be  found  in 
Russell's  description  of  Aleppo  boil  in  1756,  in  which  he  states 
that  the  inhabitants  believed  that  it  was  caused  by  the  drinking- 
water.  The  disease  was  also  described  by  Hasselquist  in  1762, 
Holland  in  1780,  Volney  in  1787,  Alibert  in  1832,  and  Guillon  in  1835. 
Tholozan,  in  1866,  appears  to  have  been  the  first  to  doubt  the 
^etiological  value  of  the  drinking-water;  but  Virchow  is  said  by 
Hirsch  to  have  been  the  first  to  suggest  that  the  true  cause  might 
possibly  be  a  parasite. 

2165 


2166  ULCERATIONS 

Smith  in  1868  and  Fleming  in  1873  claimed  to  have  found  eggs 
of  a  species  of  Distoma  in  the  sections  of  specimens  of  the  tissues 
derived  from  cases  of  Delhi  boil.  Carter  in  1875  described  a 
mycelial  fungus  and  spores.  In  1880  Laveran  stated  that  the  virus 
of  Oriental  sore  was  probably  carried  by  flies.  Deperet  and  Boniet, 
Duclaux  and  Heydenreich  cultivated  various  cocci  in  1884.  In  1885 
Cunningham  described  some  peculiar  parasitic  organisms  of  various 
size  and  shape,  often  endocellular,  easily  brought  in  evidence  by 
staining  with  gentian  violet.  Cunningham  inclined  to  regard  these 
bodies  as  representing  various  stages  of  the  development  of  a 
mycetozoal  parasite,  probably  belonging  to  the  group  of  the 
Monadidse. 

Riehl  (1886)  isolated  a  capsulated  micrococcus.  Finkelstein 
and  Chantemesse  (1887)  also  cultivated  a  micrococcus  similar  to 
the  organism  described  by  Duclaux.  Poncet  in  the  same  year 
described  a  coccus  in  sections  and  a  very  delicate  bacillus.  Le 
Dantec  and  Auche  in  1894  found  in  a  case  of  Biskra  boil  a  strepto- 
coccus and  the  Staphylococcus  albus.  In  1897  Nicolle  and  Nourry 
Bey  found  a  streptococcus  which  they  believed  to  be  specific. 
The  organism  was  very  slightly  virulent.  Attempts  to  inoculate 
monkeys  with  the  disease  did  not  succeed.  In  the  same  year 
Brocq  and  Veillon  cultivated  a  streptothrix  from  a  case  of  Aleppo 
boil.  Crendiropuolo  isolated  in  numerous  cases  a  bacillus,  prob- 
ably belonging  to  the  Proteus  group.  Firth  in  1891  stated  that 
he  had  been  able  to  confirm  the  presence  of  the  Cunningham 
parasitic  bodies  in  numerous  cases  of  Delhi  boil.  He  proposed 
for  the  parasite  the  name  of  Sporozoon  Jtmmculosum.  In  1898 
Borowsky  constantly  observed  in  twenty  cases  of  Sarten  ulcer  some 
peculiar  organisms  which  he  thought  to  be  protozoa.  In  fresh 
preparations  the  bodies  were  very  actively  motile,  and  presented 
a  spherical  shape;  sometimes  they  were  spindle-shaped.  The 
maximum  diameter  varied  from  0-5  to  3  fi.  The  cell-body  stained 
very  faintly.  The  nucleus  was  placed  eccentrically.  No  chro- 
matin bodies  could  be  put  in  evidence.  Schulgin  in  1902  con- 
firmed Borowsky's  results,  and  suggested  that  the  disease  might 
be  conveyed  by  mosquitoes.  In  1903,  in  a  case  of  tropical  ulcer 
occurring  in  a  boy  from  Armenia,  Wright  described  bodies  very 
similar  to  those  found  in  cases  of  kala-azar.  These  bodies  may 
possibly  be  identical  with  those  seen  by  Cunningham  in  1885. 
Wright's  discovery  has  been  confirmed  by  Mesnil,  Nicolle,  James, 
Strong,  Plehn,  Nattan-Larrier,  Splendore,  Carini,  Cardamatis, 
Wenyon,  Gabbi,  Lacava,  Balfour,  Archibald,  and  others,  who  have 
greatly  extended  our  knowledge  of  the  disease.  -Marzinowsky  and 
Bogrow  state  that,  independently  from  Wright,  they  found  similar 
bodies  in  cases  of  Pendjeh  ulcer  from  Persia.  In  1908  C.  Nicolle 
and  A.  Sicre  succeeded  in  cultivating  the  organism.  In  the  same 
year  and  1910  C.  Nicolle  and  his  co-workers  reproduced  the  disease 
in  monkeys  and  dogs,  and  in  1913  to  1914  Gonder,  Row,  and 
Laveran    infected    mice    and    other    rodents.     In    1917    Laveran 


ORIENTAL  SORE  2167 

published  a  most  useful  and  complete  treatise  on  the  malady  and 
other  leishmaniases. 

Geographical  Distribution. — The  disease  is  endemic  in  many 
tropical  and  subtropical  regions.  It  is  found  also  in  temperate 
zones.  In  Africa  it  is  found  in  Morocco,  Tunis,  Tripoli,  Algeria, 
and  Sahara  (Biskra,  Gafsa),  Egypt,  Sudan,  Congo,  West  and  East 
Africa,  and  South  Africa;  in  Asia  it  is  common  in  Syria  and  Asia 
Minor,  in  Mesopotamia,  Arabia,  Persia,  the  Caucasus,  Turkestan 
(Tashkent),  in  the  Turkmene  district  (Pendhe).  It  is  very  common 
in  some  parts  of  India,  especially  along  the  Valley  of  the  Indus,  in 
the  Rajputana  States,  and  in  the  North-West  Provinces  (Delhi, 
Multan,  Lahore).  In  Europe  the  affection  occurs  in  the  Crimea, 
Cyprus,  Crete,  and  Greece.  Cases  have  been  reported  by  Gabbi, 
Lacava,  and  others  from  Italy.  It  is  known  also  in  Brazil  and 
other  countries  of  South  America,  and  in  French  and  British  Guiana, 
where  it  is  known  as  Pian-bois,  or  forest  yaws,  and  has  been 
observed  by  Darling  in  Panama,  so  that  the  name  '  Oriental  sore  ' 
is  somewhat  misleading, 

It  is  generally  much  more  common  in  large  towns  than  in  the 
country.  In  some  cities  it  is  so  prevalent  that  even  visitors  of  a 
few  days  only  may  not  escape  it.  Its  occurrence  appears  to  be 
influenced  by  the  seasons,  as,  according  to  Hirsch,  in  the  tropics 
it  is  most  prevalent  at  the  beginning  of  the  cool  season,  and  in 
more  temperate  climates  at  the  end  of  summer.  Laveran 
says  that  in  Biskra,  from  September  to  October  inclusive, 
the  slightest  wound  tends  to  become  transformed  into  the 
'  bout  on.'  In  some  years  it  has  been  found  to  be  more  prevalent 
than  in  others. 

A  peculiarity  of  the  geographical  distribution  of  the  disease 
is  that  in  the  countries  where  it  is  endemic  its  distribution  is  not 
general,  but  is  confined  to  certain  districts  only;  hence  the  numerous 
local  names  given  to  the  malady,  as  Aleppo  boil,  Bagdad 
boil,  etc. 

/Etiology. — The  disease  is  caused  by  Leishmania  tropica  Wright, 
1903.  In  the  first  edition  of  this  book  we  expressed  the  belief  that 
future  investigation  would  show  that  there  are  several  varieties  of 
L.  tropica,  each  giving  rise  to  a  slightly  different  clinical  type  of 
the  affection,  and  this  has  come  true,  several  species  and  varieties 
having  been  described,  though  not  yet  generally  accepted.  The 
description  of  L.  tropica  and  its  varieties  is  found  in  Chapter  XIX., 
p.  378 .  Nicolle  and  Manceaux,  Laveran  and  others  have  occasionally 
succeeded  in  producing  in  monkeys  and  dogs  Oriental  sore  by 
inoculation  of  cultures.  Row,  by  inoculating  cultures  of  L.  dono- 
vani,  has  produced  cutaneous  lesions  in  monkeys,Jbut  such  lesions 
differ  histologically  from  true  Oriental  sore. 

Mesnil,  Nicolle,  and  Remlinger  have  observed  the  parasites  to  be  present 
occasionally  in  true  polymorphonuclear  leucocytes,  besides  being  found  in 
the  mononuclear  leucocytes  as  usual.  Mesnil  has  observed  in  some  cases 
a  typical '  bacillary  '  form. 


2168  ULCERATIONS 

The  medium  used  by  Nicolle  for  the  cultivation  of  the  parasite  is  a  modifica- 
tion of  Novy-McNeal  medium,  and  is  composed  as  follows: — 

Agar 14  grammes. 

Salt 6 

Water  900  c.c. 

This  is  dissolved  in  a  large  flask  in  a  Koch's  stove,  and  then  distributed  in 
tubes.  After  sterilization,  to  each  tube  is  added  one-third  rabbit-blood, 
collected  with  all  aseptic  precautions.  The  tubes  are  kept  aslant  for  twelve 
hours,  then  kept  at  370  C.  for  five  days,  after  which  they  are  kept  at  the 
ordinary  temperature  for  some  days  before  using.  This  medium  is  often 
referred  to  as  the  N.N.N,  medium.  Row  has  introduced  a  simple  haemo- 
globinized  saline  culture  medium. 

Histopathology. — The  histopathology  of  the  disease  has  been 
studied  by  Unna,  Leloir,  Kumm,  Riehl,  Wright,  Strong,  Bettmann 
and  von  Vasielewski,  Balfour,  Archibald,  Darling,  and  others.  The 
histological  lesions  in  the  common  ulcerative  variety  consist  essen- 
tially in  the  atrophy  and  disappearance  of  the  epidermis  of  the  part, 
and  in  a  very  extensive  cellular  infiltration  of  the  corium  and  papillae 
by  various  kinds  of  lymphoid  cells,  plasma  cells,  and  numerous  large 
roundish  cells  containing  a  single  faintly  stained  vesicular  nucleus 
and  large  amount  of  cytoplasm.  These  large  roundish  cells,  which 
are  probably  proliferated  endothelial  cells,  contain  often  many 
Wright's  bodies  closely  packed  together,  occupying  most  of  the 
available  space  between  the  nucleus  and  the  cell  periphery.  Darling 
in  his  case  found  that  the  corium  and  papillae  were  infiltrated  by 
newly  formed  cells,  lymphoid,  endothelial,  epithelioid,  giant,  and 
plasma  cells.  There  were  no  necrotic  areas,  and  a  polymorphic 
leucocytic  infiltration  was  not  noted.  Many  interpapillary  down- 
growths  were  seen  in  the  rete.  The  squamous  epithelium  was  sur- 
rounded by  a  mass  of  desquamated  epithelium  forming  the  crust. 
Thelymphatic  and  bloodvessels  in  the  deeper  laj^ers  of  the  skin  were 
surrounded  by  collections  of  lymphoid  cells.  Balfour,  Thomson,  and 
Archibald,  noted  the  following  principal  histological  features  in  their 
cases: — presence  of  vertical  epithelial  columns  extending  deeply 
downward,  with  a  few  cell-nests  and  isolated  masses  of  cell  infiltra- 
tion. The  dermis  is  infiltrated  with  cells  of  the  large  round  type, 
polymorphonuclear  leucocytes,  and  large  numbers  of  eosinophiles. 
This  cellular  infiltration  may  extend  to  the  sebaceous  glands  and 
hair  follicles. 

Communicability. — The  disease  may  be  conveyed  by  direct 
infection  from  person  to  person,  by  absorption  of  the  virus  through 
some  pre-existing  abraided  surfaces,  or  small  wounds  or  ulcers  of 
other  nature  present  on  the  skin.  The  reservoir  of  the  virus  would 
be  in  the  affected  persons  and  in  dogs,  which,  as  noted  as  long  ago 
as  1854  by  Vuillemin,  may  suffer  from  a  very  similar  or  identical 
affection.  Certain  authors  have  suspected  geckoes  and  lizards  to  be 
the  reservoir,  but  this  can  hardly  be,  as  these  animals  cannot  be 
experimentally  infected.  Camels,  too,  have  been  suspected  to  be  a 
reservoir  of  the  virus.  Insects,  especially  flics,  probably  play  a 
certain  role  in  the  transmission  of  the  disease.     That  flies  convey 


ORIENTAL  SORE 


2169 


the  disease  was  first  claimed  by  Seriziat  (1875)  and  by  Tscherepkin 
(1876). 

Tscherepkin  states  that  by  the  people  of  Tashkent  the  disease 
is  called  '  pascha-churdj , '  meaning  '  fly-bite.'  Laveran  thinks  that 
flies  carry  the  virus  on  their  feet  and  proboscis,  and  thus  convey 
infection.  Schulgin  and  others  believe  the  disease  to  be  conveyed 
by  mosquitoes.  Ed.  Sergent  and  Pressat  have  suggested  that 
some  '  Phlebotomus '  may  play  a  role  in  the  transmission  of  the 
disease,  while  Balfour  and  Thomson  suggest  that  the  bed-bug  may 
carry  the  infection.     Fleas  and  lice  have  also  been  inculpated. 

The  disease  is  inoculable  from  man  to  man,  as  is  clearly  proved 
by  the  experiments  of  Marzinowsky  and  Wenyon.  It  is  also  auto- 
inoculable. 


Fig.  852. — Oriental  Sore. 


Marzinowsky  inoculated  himself  with  Oriental  sore  by  putting  inside  the 
bulla  caused  by  an  artificial  burn  on  his  hand  some  material  (scraping)  derived 
from  an  Oriental  sore.  After  ten  days  from  the  inoculation  he  began  to  feel 
unwell  and  feverish,  and  suffered  from  headache  and  general  debility.  The 
fever  lasted  two  weeks.  With  the  beginning  of  these  general  symptoms  a 
papule  appeared  at  the  seat  of  inoculation,  which  slowly  developed  into  a 
typical  Oriental  sore.  Scrapings  contained  many  parasites.  Wenyon  has 
also  inoculated  himself,  and  he,  too,  presented  fever  before  the  skin  lesion 
appeared.  The  Bagdad  Jews,  according  to  Colvilli,  inoculated  their  children 
with  the  disease,  as  they  thought  that  after  having  recovered  once,  there 
was  no  danger  of  getting  it  again. 

Symptomatology. — After  an  incubation  period  varying  from  a 
few  days  to  some  weeks  or  several  months,  during  which  attacks 
of  irregular  fever  often  occur,  one  or  several  small  pruriginous  spots 
appear  on  the  skin  of  uncovered  parts  of  the  body,  not  much  dis- 


2170 


ULCERATIONS 


similar  at  the  very  beginning  from  mosquito-bites,  for  which  they 
are  often  taken  by  the  patients.  The  spots,  however,  instead  of 
slowly  fading,  become  red  and  shotty,  with  an  inflamed  areola, 
which  later  becomes  markedly  indurated.  The  papules  slowly 
enlarge  to  the  size  of  a  pea  or  bean;  the  surface  gradually  loses  its 
smooth  and  shiny  appearance,  and  becomes  covered  with  small  thin 
scales.  After  a  period  of  time,  somewhat  variable  in  length,  but 
generally  not  exceeding  three  to  four  months,  the  ulceration  of  the 
nodule  begins.      At  first  the  ulceration  is  very  superficial,   and 


Fig.  853. — Oriental  Sore  in  a  Persian  Soldier. 
(From  a  photograph  of  Drs.  A.  Bussiere  and  Nattan-Larrier.) 

exudes  a  yellowish  secretion,  which  soon  dries  into  a  hard,  adherent, 
darkish  scab.  Underneath  the  scab  the  ulcerative  process  and 
disintegration  of  the  nodule  continues  slowly  to  spread.  The 
tissues  surrounding  the  ulcers  may  become  cedematous.  If  later 
the  darkish  scab  be  removed,  an  ulcer  is  seen,  about  an  inch  or 
more  in  diameter,  with  sharp-cut,  jagged  edges  and  irregular  fundus, 
with  reddish-yellow,  sometimes  fungating  granulations.  The  ulcer 
is  generally  indolent,  or  but  slightly  painful.  The  neighbouring 
lymphatic  glands  are  not,  as  a  rule,  sensibly  enlarged,  unless  there 


ORIENTAL  SORE 


217X 


is  a  secondary  pyogenic  infection.  The  examination  of  the  blood 
taken  from  the  finger  shows  often  a  distinct  mononucleosis,  and  the 
coagulability  is  generally  increased.  The  total  number  of  leucocytes 
may  be  normal,  or  there  may  be  leucopenia,  or  during  the  attacks 
of  fever  leucocytosis.  In  the  blood  taken  from  non-ulcerated 
lesions  the  mononucleosis  is  much  more  marked. 

Healing  generally  sets  in  after  six  to  twelve  months  by  granula- 
tion, which  begins  in  the  centre  of  the  ulcer,  the  unhealthy-looking, 
large,  yellowish  granulations  giving  place  to  healthy  ones.  A 
whitish  or  pinkish,  often  depressed  and  disfiguring,  scar  remains 
at  the  seat  of  the  ulceration.  Aft erfe cicatrization,  the  sore  may 
break  down  again. 

Oriental  sore  may  be  single  or  multiple.  Two  or  three  are  fre- 
quently found  on  the  same  patient,  but  occasionally  there  are  many 
more,  and  may  spread  to  the  mucous  membranes  of  the  mouth  and 
nose.    The  sores  are  auto-inoculable  by  scratching. 

The  seat  of  the  ulcers  is  generally  on  uncovered  parts — feet, 
legs,  hands,  arms,  face.  They  are  very  seldom  observed  on  the 
palms,  soles,  or  scalp.  The  affection  attacks  people  of  any  race, 
sex,  and  age,  if  they  expose  themselves  to  the  infection. 

Course. — The  length  of  the  incubation  period  is  not  known  with 
certainty.  It  is  generally  stated  that  it  varies  between  a  few  days 
and  six  weeks.  Manson,  however,  has  observed  that  it  may  be 
as  long  as  five  months,  and  Wenyon,  who  inoculated  himself,  ob- 
served that  the  first  skin  lesions  appeared  six  and  a  half  months 
after  inoculation.  Manson  in  one  case  made  the  interesting  observa- 
tion that  the  appearance  of  the  sore  was  preceded  several  months 
by  a  fever  of  an  irregular  remittent  type,  not  influenced  by  quinine, 
and  having  some  features  of  the  fever  of  Indian  kala-azar.  This 
fever  was  also  noted  by  Marzinowsky  and  Wenyon,  who  inoculated 
themselves  experimentally.  Attacks  of  irregular  fever  during  the 
incubation  and  the  course  have  been  recorded  by  several  other 
authors.  During  one  of  these  febrile  attacks  Neumann  observed 
Leishmania  tropica  free  in  the  liquor  sanguinis  of  the  patient. 

The  duration  of  the  eruption  varies  from  four  or  five  months 
to  twelve  months  and  more.  Relapses  may  occur,  but  true  rein- 
fections are  rare. 

Clinical  Varieties. — The  following  clinical  varieties  may  be  dis- 
tinguished:— 

1.  The  common  variety — Oriental  sore  sensu  stricto — to  which  the 
description  given  above  refers.  This  variety,  which  is  the  usual 
type  met  with  in  Asia,  Africa,  and  South  Europe,  while  compara- 
tively rare  in  America,  is  characterized  by  the  presence  of  one  or 
several  nodules,  which  slowly  ulcerate,  with  or  without  symptom? 
of  general  infection,  such  as  fever  and  enlargement  of  the  spleen. 
Very  rarely,  in  addition  to  the  cutaneous  nodules,  there  may  be 
ulcerative  lesions  on  the  mucosa  of  the  mouth  and  nose,  as  noted 
by  Cardamatis  in  Greece  and  Lacava  and  Gabbi  in  Italy. 

2.  The  verrucose  variety,  described  by  Ferguson  and  Richards, 


2172 


ULCERATIONS 


and  later  by  Archibald  in  Egypt  and  the  Sudan,  so  called  from  the 
peculiar  verrucose  appearance  of  the  lesions. 

3.  The  keloidform  variety.  This  is  a  non-ulcerative  type  described 
by  Cambillet,  Balfour,  and  Thomson,  characterized  by  the  presence 
of  pinkish  nodules,  somewhat  keloid-like,  which  never  ulcerate. 
For  this  variety  Balfour  suggested  the  name  '  Leishman's  nodules, ' 
and  Brumpt  created  a  new  species  for  the  leishmania  found  _in  them 
— L.  nilotica  Brumpt,  1913. 

4.  The  frambcesiform  variety.  This  is  characterized  by  the  pres- 
ence of  numerous  nodules  capped  with  crusts  and  resembling  yaws 
(see  Fig.  854).  It  is  fairly  common  in  the  West  Indies,  where  it  is 
known  by  the  name  of '  forest  yaws,' '  Bosch-Yaws,'  or  '  Bush-Yaws.' 

5.  The  papillomatous  variety.  This  is  found  in  South  America, 
but  very  similar  types  seem  to  have  been  met  with  in  North  India. 

It  is  characterized  by  the  presence 
of  papillomatous  masses,  which 
are  generally  found  on  the  lower 
limbs,  and  are  designated  by  the 
Amazon  natives  with  a  word 
which  means  sponge.  The  natives 
believe  that  the  same  affection 
attacks  horses,  mules,  and 
donkeys. 

This  variety  runs  a  much  longer 
course  than  the  common  type  of 
Oriental  sore,  lasting  ten  to  fifteen 
years,  and  with  very  little  or  no 
tendency  to  spontaneous  cure.  It 
is  probably  due  to  a  species  of 
leishmania  biologically  different 
from  L.  tropica,  and  most 
authorities  consider  it  to  be  due 
to  L.  tropica  var.  americana, 
the  variety  of  leishmania  which  is 
the  cause  of  espundia  (see  below) . 

6.  The  deep  ulcerative  variety.  This  is  found  in  South  America, 
and  is  characterized  in  most  cases  by  the  presence  on  various  parts 
of  the  body  of  deep  large  ulcers  running  a  very  long  course  and  with 
practically  no  tendency  to  spontaneous  cure.  In  some  cases  the 
condition  is  localized  to  the  ear,  which  may  become  perforated 
(oreya  de  los  chicleros).  One  such  case  has  recently  been  recorded 
by  Low.  This  condition  is  often  in  reality  the  first  stage  of  espundia, 
and  is  due  to  L.  tropica  var.  americana  (p.  380). 

Diagnosis. — The  diagnosis  of  all  types  of  cutaneous  leishmaniasis  is 
made  with  absolute  certainty  only  by  examining  microscopically  the 
suspected  lesions  and  finding  the  leishmanias.  In  numerous  cases  of 
the  most  common  variety — Oriental  sore  sensu  stricto — the  diagnosis 
can  often  be  made  clinically,  taking  into  account  the  following  data  I— 

1.  The  patient  comes  from  or  is  living  in  an  affected  area. 


Fig.  854  — Forest  Yaws. 
(From  a  photograph  by  Sambon.) 


ORIENTAL  SORE  2173 

2.  The  few  eruptive  elements — often  one  single  element — situated 
as  a  rule  on  uncovered  parts  of  the  body. 

3.  The  course:  a  small  papule  which  slowly  enlarges  into  an 
indurated  nodule,  indolent,  smooth,  or  slightly  scaly,  and  after 
several  months  ulcerates. 

4.  The  proximal  lymphatic  glands  usually  not  enlarged.  I 

The  history,  the  absence  usually  of  enlarged  lymphatic  glands  and 
other  symptoms  of  syphilis,  and  the  uselessness  of  the  mercurial 
treatment,  will  help  in  excluding  syphilis.  In  frambcesia  there  is  a 
primary  lesion,  which,  after  a  time,  is  followed  by  a  general  granu- 
lomatous eruption.  We  have,  however,  seen  cases  of  frambcesia 
patients  who,  after  the  general  eruption  has  disappeared,  have 
remained  for  months  with  a  single  or  a  few  sores  closely  resembling 
the  Oriental  sore.  In  fact,  we  believe  that  in  a  certain  number  of 
cases  it  is  very  difficult  to  make  the  differential  diagnosis  between 
Oriental  sore  and  ulcers  of  tubercular,  syphilitic,  or  frambcetic  origin ; 
also,  at  times,  from  cancroid  when  the  ulcer  is  single  and  situated 
on  the  face.  In  our  experience,  the  only  reliable  way  to  come  to  a 
definite  diagnosis  in  difficult  cases  is  the  microscopical  examination. 
To  do  this  the  scab  is  removed,  and  a  scraping  is  taken  from  the 
floor  and  edges  of  the  ulcer.  The  preparation  is  then  coloured  with 
Leishman's  or  Giemsa's  stain,  or  any  other  of  the  numerous  modifi- 
cations of  Romanowsky's  method,  and  examined  for  the  presence  of 
Leishmania  tropica.  The  search  must  be  prolonged  in  some  cases, 
as  the  parasites  may  be  very  rare. 

Prognosis. — In  the  common  type  the  prognosis  is  good,  quoad 
vitam.  Very  occasionally  the  disease  may  end  fatally,  owing  to  the 
ulcers  becoming  phagedenic,  and  to  secondary  septicemic  and 
pyemic  processes.  In  some  rare  cases,  as  observed  by  Cardamatis  in 
Greece  and  Lacava  and  Gabbi  in  Italy,  the  ulcerative  lesions  may 
spread  to  the  mucosa  of  the  mouth.  Sometimes  the  scars  remaining 
after  the  ulcers  have  healed  up  shrink  considerably,  and  if  they  are 
on  the  face,  may  give  rise  to  serious  disfigurement. 

Treatment. — Tartar  emetic  is  a  specific.  It  is  best  given  by 
intravenous  injection,  using  a  1  per  cent,  solution  in  saline  or  simple 
distilled  water.  The  solution  should  not  be  autoclaved;  it  should 
be  filtered  through  a  Berkefeld  candle,  or  may  be  sterilized  in  flowing 
steam  on  two  or  three  consecutive  days.  Five  to  ten  c.c.  of  the  solution 
are  given  daily  for  five  to  ten  days,  then  every  other  day  or  twice  a 
week  until  fifteen  to  thirty  injections  have  been  given.  In  children 
one-third  or  half  doses  are  used.  The  intravenous  injections  should 
be  given,  taking  all  ordinary  precautions  and  making  sure  that  the 
needle  is  actually  in  the  vein  and  that  none  of  the  liquid  escapes  into 
the  surrounding  tissues.  Soon  after  the  injection  patients  at  times 
complain  of  metallic  taste,  giddiness,  and  nausea,  but  as  a  rule 
tolerance  for  the  drug  is  easily  established.  Occasionally  a  prolonged 
treatment  induces  diarrhoea,  and  the  patient  may  complain  of 
great  debility  and  muscular  stiffness.  Tachycardia  has  been  noticed, 
exceptionally,  and  a  few  cases  of  sudden  death  have  been  ascribed 


2174  UL  CERA  TIONS 

to  the  action  of  the  drug,  which  may  produce  a  severe  fatty  degenera- 
tion of  the  heart,  liver  and  kidneys. 

Tartar  Emetic  Carbolic  Solution. — This  contains  i  per  cent,  tartar 
emetic  and  J  per  cent,  carbolic  acid,  and  does  not  need  to  be  sterilized  or 
passed  through  a  Berkefeld  filter. 

Solutions  for  Intramuscular  Injection. — Intramuscular  injections  are 
in  certain  cases  very  convenient,  especially  in  children,  in  whom  the  superficial 
veins  are  often  small.  Unfortunately  the  usual  solutions  of  tartar  emetic 
and  other  antimonial  salts  are  painful,  and  may  induce  the  formation  of  an 
abscess.     The  following  formulas  will  be  found  fairly  satisfactory: — 

Formula  No.  i  (Castcllani). — Tartar  emetic,  gr.  viii. ;  ac.  carbolici,  n\x.; 
glycerin.,  fiiii.;  aq.  dest.,  ad  §i.;  J  to  i  c.c.  (8  to  16  minims)  every  other  day 
in  the  gluteal  region.  At  the  time  of  the  injection  there  is  as  a  rule  no  pain 
whatever,  but  a  few  hours  later  in  most  cases  there  is  a  certain  amount  of  pain 
and  an  infiltrated  patch  often  develops,  as  after  an  intramuscular  injection 
of  quinine  or  of  mercury  perchloride.  Care  should  be  taken  to  give  the  injec- 
tions in  different  spots,  never  giving  a  second  one  in  the  infiltrated  part.  If 
the  pain  and  infiltration  should  be  severe,  hot  fomentations  will  be  found 
useful. 

The  solution  is  prepared  in  bulk  in  a  sterile  bottle,  and  tested  for  sterility 
forty-eight  hours  after  preparation;  it  may  then  be  put  up  in  small  i  c.c. 
ampoules,  which  it  is  advisable  to  keep  in  a  cool  dark  place.  The  presence  of 
carbolic  acid  decreases  the  pain  induced  by  tartar  emetic  and  makes  the 
solution  sterile. 

Formula  No.  2  (Castellani). — Tartar  emetic,  gr.  viii.;  ac.  carbolici,  ITjx.; 
glycerin.,  3^-1  sodii  bicarb.,  gr.  \;  aq.  dest.,  ad  §i.  This  solution  differs 
from  No.  1  in  being  slightly  alkaline.  The  results  seem  to  be  the  same,  and  the 
pain  induced  by  it  appears  to  be  about  the  same  as  with  formula  No.  1 . 

Formula  No.  3  (M artindale) . — Antimoniioxidi.gr.  ^;  glycerin.,  aq.  dest., 
aa  Tt[xv.  (for  one  ampoule).  This  preparation  is  good  and  is  practically  pain- 
less, but  our  impression  is  that  the  curative  action  of  antimonium  oxide  is 
inferior  to  that  of  tartar  emetic. 

Oral  Administration  of  Tartar  Emetic. — The  oral  administration 
of  the  drug  may  be  useful  in  conjunction  with  the  intravenous  or  intramuscular 
injections.     The  following  mixture  is  often  very  convenient: — 

Tartar  emetic,  gr.  v.; sodii  bicarb.,  gr.  xxx.;  glycerin.,  §i.;  aq.  chlorof.,  §ii.; 
aquae,  ad  §iii.,  ^i.  to  3U-  m  water,  three  times  daily,  in  children;  double 
dose  in  adults.  The  presence  of  bicarbonate  of  soda  and  chloroform  water 
decreases  the  emetic  action  of  the  drug. 

Local  Applications  of  Antimonial  Preparations. — G.  C.  Low  has 
used  with  satisfactory  results  a  1  per  cent,  antimonial  ointment.  A  1  per  cent. 
antimonial  lotion  has  been  used  by  several  authorities  as  a  local  application 
to  the  sores,  and  certain  observers  have  used  tartar  emetic  in  powder,  but 
this  is  extremely  painful,  and  we  do  not  recommend  it. 

Before  the  introduction  of  tartar  emetic  the  treatment  of  Oriental  sore  was 
very  unsatisfactory.  Nitrate  of  mercury  ointment,  alum  ointment,  boric  acid, 
and  various  antiseptics  were  recommended,  with  very  poor  results.  Formalin 
often  irritates  the  ulcer,  and  may  produce  a  dermatitis.  Rontgen  rays  have 
been  tried,  without  any  good  results.  An  expectant  treatment  was  generally 
advised.  The  scabs  should  be  removed  by  boracic  acid  fomentation,  and 
then  the  sores  must  be  thoroughly  disinfected  once  or  twice  daily  with  a 
1  in  1,000  solution  of  perchloride  of  mercury  or  2  per  cent,  carbolic  acid,  after 
which  one  of  the  ordinary  antiseptic  ointments  (/3-naphthol,  gr.  v. ;  vaseline, 
§i.;  iodoform  or  europhen,  gr.  v. ;  ung.  ac.  borici,  §i.;  balsam.  Peru.,  gr.  v.;  to 
vaseline,  gi.)  or  an  antiseptic  powder  (iodoform  or  xeroform  or  boric  acid)  is 
applied. 

Salvarsan  and  atoxyl  have  been  used  without  any  good  result. 

Marzinowsky,  after  removing  the  crust  and  cleansing  the  ulcer  with 
antiseptic  lotion,  applies  a  10  per  cent,  lotion  of  ferropyrin  to  stop  the  bleeding,. 


MUCO-CUTANEOUS  LEISHMANIASIS  (ESPUNDIA)        2175 

and  then  applies  thoroughly  a  50  per  cent,  lotion  of  chininum  bimuriaticum 
daily.     He  says  recovery  takes  place  in  between  seven  to  eleven  days. 

Schulgin  advises  the  freezing  of  the  boil  with  ether.  He  used  this  method 
in  300  cases  with  good  results. 

Several  French  writers  advise  the  use  of  permanganate  of  potassium,  at 
first  in  powder  form,  and  later  as  a  5  per  cent,  ointment. 

Duncan  advised  placing  a  thin  piece  of  lead  over  the  ulcer,  and  then  ban- 
daging up. 

Emily  recommended  the  repeated  applications  of  boric  acid. 

Oudiourminsky  has  applied  to  the  treatment  of  Oriental  sore  Bier's  stasis 
method,  apparently  with  good  results. 

Chulguine  recommended  soaking  the  sore  with  a  solution  of  methylene  blue 
(10  per  cent.). 

Bussiere  advised  dilute  tincture  of  iodine  (10  per  cent.). 

In  other  cases  Bussiere  and  Nattan-Larrier  advised  excision  of  the  sore. 
Several  physicians  praise  the  use  of  silver  nitrate. 

Castellani  had  some  fairly  good  results  in  two  cases  by  washing  the  sores 
with  a  5  per  cent,  solution  of  protargol,  followed  by  the  application  of  a 
20  per  cent,  protargol  ointment.  The  protargol  ointment  cannot  be  used 
on  Europeans  when  the  face  is  affected,  as  the  protargol,  after  some  time, 
induces  a  discoloration  of  the  skin. 

Lincoln  and  Aviss  have  obtained  good  results  by  painting  the  sores  with 
a  native  gummy  fluid,  sold  in  native  bazaars  under  the  name  of '  raurath.' 

Timpano  injects  1  c.c.  daily  round  the  sore  of  a  1  per  cent,  solution  of 
carbolic  acid . 

Prophylaxis. — The  disease  being  very  contagious,  and  being  also 
probably  spread  by  some  blood-sucking  insects,  the  slightest  wound 
and  any  insect-bite  should  be  thoroughly  disinfected  with  carbolic 
acid  5  per  cent.,  or  tincture  of  iodine. 

MUCO-CUTANEOUS  LEISHMANIASIS  (ESPUNDIA). 

Synonyms. — Naso-oral  Leishmaniasis,  Uta,  Chancre  Espundique 
d'Escomel  (Laveran  and  Nattan-Larrier),  Leishmaniasis  cancer osa 
(A.  da  Matta),  Bubas  Braziliana  (Breda),  Smith's  disease,  Breda's 
disease,  Bueno  de  Miranda  and  Splendore's  Leishmaniasis,  American 
Leishmaniasis  (Laveran  and  Nattan-Larrier). 

Definition. — A  chronic  ulcero-granulomatous  affection  of  the  skin 
and  mucosa  of  the  mouth  and  nose  due  to  Leishmania  tropica  Wright, 
1903,  var.  americana  Laveran  and  Nattan-Larrier,  1912. 

Historical. — Espundia  seems  to  have  been  present  in  South 
America  since  time  immemorial.  According  to  Tamayo  espundia 
lesions  are  depicted  on  certain  water  vases  of  the  ancient  Incas. 
The  malady  has  been  known  to  local  medical  men  for  many  years  in 
Peru  and  other  parts  of  South  America,  though  it  was  often  confused 
with  frambcesia  and  blastomycosis.  Fairly  good  descriptions  of  the 
malady  were  given  by  Smith  in  1840  andTschudiin  1846,  and  later  by 
several  other  observers.  In  1895-1896  Breda  described  in  a  series 
of  important  publications  the  affection  in  Italy,  in  emigrants  return- 
ing from  Brazil,  under  the  name  of  Bubas  Braziliana,  and  considered 
it  to  be  due  to  a  bacillus  the  presence  of  which  was  confirmed  by 
Fiocca,  who  claimed  to  have  reproduced  the  disease  in  the  lower 
animals  by  inoculating  pure  cultures  of  the  organism.  Breda's  work 
was  confirmed  by  Verrotti  and  De  Amicis.    The  term  '  boubas,' 


2176 


ULCERATIONS 


used  by  Breda,  was  a  rather  unfortunate  one,  as  it  led  to  much 
confusion,  this  term  being  generally  used  by  tropical  authors  as  a 
synonym  for  frambcesia,  while  the  natives,  as  noted  by  Splendore 
and  others,  use  it  indiscriminately  to  indicate  various  ulcerative 
lesions  of  widely  different  nature. 

Escomel  in  191 1  gave  a  very  good  description  of  espundia  as 
found  in  Peru.  Further  investigation  has  shown  that  the  condition 
found  in  Brazil  is  identical  with  that  found  in  Peru. 

Bueno  de  Miranda  and  Splendore  first  found  leishmania  bodies 
in  the  ulcerative  lesions,  Splendore  making  a  very  complete  patho- 
logical and  clinical  investigation  of  the  condition,  and  succeeding  in 
experimentally  inoculating  it  in  monkeys.  Splendore  called  atten- 
tion to  the  fact  that  incultures  the  nagellum  of  the  Leishmania  found 
was  generally  longer  than  in  L.  tropica  ;  he  observed  also  that  with 

Giemsa's  reagent  the  parasite  stained 
usually  deeper  than  L.  tropica.  Laveran 
and  Nattan-Larrier  have  made  an 
important  study  of  the  parasite  in  tissues 
sent  to  them  by  Escomel,  and  noting 
the  very  frequent  peculiarity  of  the 
nucleus  being  flattened,  have  created  a 
new  variety:  L.  tropica  Wright,  1903, 
var.  americana  Laveran  and  Nattan- 
Larrier,  1912.  Vianna  had  previously 
created  a  new  species,  L.  brasiliensis,  but 
this  species  has  not  been  generally 
accepted.  More  recent  important  re- 
searches have  been  carried  out  by  Horta, 
Carini,  Lindenberg,  Rabele,  Morales, 
Darling,  Velez,  Araujo,  Chagas,  Alfr.  da 
Matta,  Aragao,  Strong,  Tyzzer,  Brues, 
Sellards,  Gastiaburu,  Flu,  Migone, 
Torres,  Christ  opherson,  and  many 
others. 
Geographical  Distribution. — The  disease  has  been  reported  from 
Peru,  Brazil,  Paraguay,  Argentina,  Colombia,  and  other  parts  of 
South  America.  In  Brazil  it  is  especially  common  in  the  regions 
between  the  State  of  St.  Paulo  and  the  State  of  Matto  Grosso,  near 
the  River  Tiete;  in  Peru  it  is  found  in  the  regions  of  Caralaya  and 
Sandia,  and  close  to  the  River  Madre  de  Dios.  Cases  have  been 
reported  from  Panama  and  Mexico.  It  has  been  found  in  the 
Anglo-Egyptian  Sudan  by  Christ  opherson. 

/Etiology. — The  disease  is  due  to  Leishmania  tropica  Wright,  1903, 
var.  americana  Laveran  and  Nattan-Larrier,  1912,  which  Vianna  con- 
siders to  be  a  separate  species,  L.  brasiliensis  Vianna,  1911  (see 
PP-378-  379<  and  380). 

Marbid  Anatomy  and  Histopathology. — Escomel,  in  a  chronic  case 
which  died  of  cachexia,  found  the  body  extremely  emaciated,  and  the 
espundial  lesions  extending  from  the  oral  cavity  to  the  pharynx, 


Fig.  855. — Espundia. 
(After  Splendore.) 


M UCO-CUTA NEO US  LEISHMA NIA SIS  {ESP UNDIA )        2177 

larynx,    and   trachea.    The   oesophagus  was   also   affected.    The 
organs  presented  amyloid  degeneration. 

The  histopathology  of  the  disease  has  been  well  investigated  by 
Breda,  Escomel,  De  Amicis,  Verrotti,  Splendore,  Carini,  and  recently 
very  completely  by  Laveran  and  Nattan-Larrier.  The  lesions  do  not 
show  any  characteristic  histological  feature,  theepithelial  strata  have 
disappeared,  and  are  substituted  by  a  fibro-leucocytic  membrane; 
there  is  a  large  amount  of  granulation  tissue,  with  numerous  mono- 
nuclear leucocytes  and  plasma  cells;  a  few  macrophages  may  be  seen. 


Fig.  856. —  Espundia. 
(After  Splendore.) 


Splendore  has  occasionally  seen  giant  cells;  no  cell  nests  have 
been  observed.  The  stroma  consists  of  some  fibrils,  which  are 
stained  with  difficulty.     The  lesions  are  not  very  vascular. 

Communicability. — The  infection  may  be  conveyed  by  direct 
contact  from  person  to  person,  the  virus  being  absorbed  through 
some  abraded  surface,  fissure,  or  small  wound.  It  may  also  be 
transmitted  probably  by  some  blood-sucking  insect,  most  patients 
stating  that  the  first  lesion  appeared  at  the  place  where  they  had 
been  bitten  by  some  insect.  Mosquitoes,  sand-flies,  certain  ticks 
and  certain  flies  (especially  tabanid)  have  been  inculpated. 

As  regards  the  reservoir  of  the  virus,  certain  observers  suspect  c:ogs.  in  which 
occasionally  a  similar  or  identical  affection  to  the  htman  one  may  be  fourd. 
In  Paraguay  there  is  a  popular  belief  that  the  rattle-snakes  are  the  reservoir 
of  the  virus. 

Darling  and   Townsend   have  brought    forward    the  hypothesis  that  the 

r37 


2178 


ULCERATIONS 


leishmania  is  an  adaptation  to  man  of  insect  flagellates.  In  this  connection 
one  may  quote  the  interesting  observations  made  by  Fantham  and  Porter, 
Laveran  and  Franchini,  who  have  succeeded  in  infecting  mammalia  with 
certain  flagellates  found  in  fleas  and  mosquitoes  (see  p.  363). 

Symptomatology.— The  incubation  period  is  unknown.  The 
malady  generally  begins  with  a  nodule  on  some  uncovered  part  of  the 
body,  which  fairly  quickly  breaks  down,  and  an  ulcer  is  formed. 
This  first  lesion  is  called  by  Escomel  '  espundial  chancre.'  It  is 
mostly  found  on  the  forearms,  legs,  chest,  trunk,  or  more  rarely  on 
the  face.     The  ulcer  is  generally  atonic,  roundish;  there  is  very 

little  or  no  pain,  the  fundus  is 
granulating,  and  there  is 
abundant  purulent  secretion 
which  dries  up,  forming  thick 
crusts.  The  ulcer  after  some 
months,  or  even  one  or  two  years, 
heals  up,  leaving  a  thick  scar. 
While  this  primary  ulcer  is  still 
open,  but  oftener  after  it  has 
healed,  the  characteristic  lesions 
occur  on  the  mucosa  of  the 
mouth  and  nose,  with  or  without 
the  appearance  of  further 
ulcerative  lesions  on  the  skin  of 
various  regions  of  the  body. 
The  lesions  on  the  mucosa  of 
the  mouth  are  ulcero-granulo- 
matous,  often  frambcesiform, 
and  may  invade  the  hard  and 
soft  palate,  the  gums,  the  labial 
mucosa;  they  may  form  on  the 
palate  a  diffuse  granulomatous 
mass,  with  deep  furrows.  The 
mucosa  of  the  nose  is  very  often 
attacked,  and  destruction  of  the 
cartilages  may  take  place,  induc- 
ing a  marked  deformation  of 
the  nose.  Alfr.  da  Matta  has 
noted  that  the  bones  are  not 
destroyed;  the  skin  is  often  cedematous,  and  patches  of  hard 
Oedema  may  be  found  below  the  eyes.  The  pathological  process 
may  extend  to  the  pharynx  and  larynx.  In  some  cases  the 
patient  may  become  aphonous.  and  complains  of  great  pain  during 
deglutition;  his  breath  may  be  very  offensive.  There  may  be 
serotine  fever. 

The  course  is  chronic;  the  disease  may  last  for  twenty  to  thirty 
years,  death  being  generally  due  to  some  intercurrent  disease.  In 
a  few  cases  the  affection  may  attack  mucosae  other  than  the  naso- 
oral,  and  pharyngeal.     For  instance,  a  case  of  vaginal  leishmaniasis 


Fig.     857.- 


-Espundia. 
Case. 


A     Sudan 


(From  a  photograph  by 
Christopherson.) 


MUCO-CUTANEOUS  LEISHMANIASIS  (ESPUNDIA)         2179 

has  been  recorded  by  Alfr.  da  Matta.  In  the  last  stage  the  patient 
becomes  cachectic,  and  his  appearance  may  be  that  of  a  carcino- 
matous patient. 

Prognosis. — Beforethe  introduction  of  tartar  emetic  by  Vianna  the 
prognosis  used  to  be  very  bad,  though  occasionally  when  the  diag- 
nosis was  made  as  soon  as  the  primary  cutaneous  lesion  appeared, 
and  this  was  destroyed,  the  further  progress  of  the  disease  was 
prevented. 

Diagnosis.- — The  disease  is  distinguished  from  the  usual  type  of 
dermal  leishmaniasis  (Oriental  sore)  by  its  very  long  course.  More- 
over, the  latter  invades  the  oral  mucosa  only  exceptionally,  though 
cases  have  been  reported  by  Cardamatis  in  Greece,  and  Lacava  and 
Gabbi  in  Italy.  From  blastomycosis  it  is  distinguished  by  the 
presence  of  a  leishmania,  and  absence  of  yeast-like  or  monilia-like 
fungi.  From  syphilis  it  can  be  diagnosed  by  the  uselessness  of  the 
mercurial  and  salvarsan  treatment;  from  morva  by  the  absence  of 
B.  mallei  Loffler  and  Schiitz;  moreover,  morva  is  very  rare  or  absent 
in  those  regions  where  espundia  occurs.  The  condition  is  distin- 
guishable from  tuberculosis  by  the  different  histological  lesions; 
from  frambcesia  by  the  absence  of  the  frambcesiform  eruption  on 
the  body,  by  the  absence  of  the  Treponema  pertenue  Castellani,  and 
by  the  uselessness  of  the  salvarsan  treatment. 

Treatment. — Tartar  emetic,  first  used  in  the  disease  by  Vianna, 
is  a  specific.  The  usual  1  per  cent,  solution  in  saline  or  distilled 
water,  filtered  through  a  Berkefeld  candle,  or  sterilized  in  flowing 
steam,  is  given  by  intravenous  injection  (5  to  10  c.c.  per  injection) 
for  several  periods  of  five  days  each  until  twenty  or  thirty  injections 
have  been  given.  The  same  solution  may  be  used  as  a  iocal  applica- 
tion to  the  sores,  for  syringing  the  nose,  etc. 

Strong  solutions  or  tartar  emetic  in  powder  form  should  not  be 
used,  as  they  give  rise  to  severe  pain. 

Mild  antiseptic  mouth-washes  such  as  diluted  glycothymolin  and 
listerin  or  potassium  permanganate  (1  in  5,000)  should  be  freely  used. 

According  to  Escomel,  if  the  primary  lesion  be  excised  or  destroyed,  the 
further  course  of  the  disease  is  prevented. 

Prophylaxis. — Abrasions,  fissures,  and  any  ordinary  traumatic 
small  sores,  should  be  kept  well  disinfected  and  protected  with 
antiseptic  dressings,  to  prevent  infection  with  the  espundia  virus. 
Any  insect  bite  should  immediately  be  touched  with  tincture  of 
iodine. 

INDIAN  ORO-PHARYNGEAL  LEISHMANIASIS. 

Remarks. — It  may  be  of  interest  to  give  a  brief  account  of  an 
ulcerative  condition  of  the  throat  observed  by  one  of  us  in  two 
Europeans  who  had  long  been  living  in  India. 

/Etiology. — In  one  of  the  two  cases  observed,  scrapings  from  the 
ulcers  contained  typical  leishmania  bodies  very  similar  or  identical 
to  Leishmania  tropica  and  L.  donovani.     In  the  other — which  was 


2180  ULCERATIONS 

the  first  case  seen,  and  clinically  identical  to  the  second — no  leish- 
mania  was  found,  but  the  patient  had  to  go  back  to  India,  and  no 
repeated  examinations  could  be  carried  out.  We  are  inclined  to 
think  that  it  was  of  the  same  nature.  The  condition  may  have 
been  kala-azar,  with  ulcerations  on  the  throat,  though  this  mani- 
festation of  kala-azar  has  never  been  described;  moreover,  the 
general  health  was  not  so  affected  as  in  kala-azar  of  long  standing. 
It  was  not  Oriental  sore  with  complications  on  the  oral  mucosa,  as 
the  skin  had  never  been  affected;  moreover,  Oriental  sore  does  not 
run  such  a  long  course.  It  was  not  espundia,  as  there  were  no 
cutaneous  lesions  and  the  ulcers  were  not  frambcesiform. 

Symptomatology. — In  the  case  in  which  leishmania  bodies  were 
found  there  was  no  history  of  syphilis  or  of  any  ulcerative  lesion  on 
the  skin.  He  had  been  residing  for  a  long  time  in  India,  and  when 
he  consulted  one  of  us  at  Colombo,  was  going  on  a  long  holiday. 
He  was  a  tall,  rather  stout  man  (European)  of  thirty-eight  years 
of  age,  in  apparently  good  general  health,  but  he  complained  of 
intractable  ulcers  on  the  pharynx  and  soft  palate,  which,  according 
to  him,  had  been  present  for  the  last  nine  years,  and  which  gave 
a  certain  amount  of  discomfort,  though  they  were  not  very  painful. 
No  enlarged  lymphatic  glands  could  be  detected.  The  local  ex- 
amination showed  the  presence  of  several  ulcers  on  the  posterior 
wall  of  the  pharynx  and  on  the  soft  palate;  they  were  of  various 
sizes,  but  not  very  large,  mostly  £  to  £  centimetre  in  diameter; 
they  were  roundish,  and  some  of  them  not  very  deep.  Some  were 
covered  by  debris;  none  had  a  frambcesiform  appearance.  The 
patient  had  been  treated  in  various  ways,  including  a  very  energetic 
antisyphilitic  treatment,  without  any  effect.  The  microscopical  ex- 
amination of  scrapings  from  the  lesions  showed  leishmania  bodies, 
apparently  very  similar  or  identical  to  Leishmania  donovam. 
On  inquiry  the  fact  was  elicited  that  the  patient  had  been  occasion- 
ally suffering  from  attacks  of  fever,  believed  to  be  malaria,  for  the 
last  five  years.  The  physical  examination  of  the  patient  revealed 
nothing  abnormal,  but  the  spleen  on  percussion  appeared  to  be 
slightly  enlarged,  and  on  deep  inspiration  was  just  palpable. 

In  a  clinically  identical  condition  seen  in  a  previous  patient  no 
leishmania  was  found  in  the  ulcers,  but  no  repeated  examinations 
could  be  carried  out;  he  admitted  having  had  many  attacks  of 
what  he  called  '  malarial  fever.'  In  that  case  the  spleen  was  much 
enlarged,  though  the  examination  of  the  blood  revealed  absence  of 
malarial  parasites  and  pigment. 

Prognosis. — The  local  ulcers  were  most  intractable.  The  general 
health  did  not  seem,  however,  to  be  very  markedly  affected. 

Diagnosis. — This  is  based  on  the  microscopical  examination. 
Care  should  be  taken  to  make  a  deep  scraping  of  the  ulcer. 

Treatment. — This  should  be  the  same  as  for  espundia. 


ULCUS  TROPICUM  21 81 


ULCUS  TROPICUM. 


Synonyms. — Yemen  ulcer,  Aden  ulcer,  Annam  ulceration,  Cochin 
sore,  Mozambique  sore,  Sarnes  (Congo).  French  :  Ulcere  Phage- 
demique  des  Pays  Chauds.  Ulcere  Phagedenique  Endemique. 
Italian  :  Ulcera  Tropicale,  Phagedena  Tropica.  German :  Tropische 
Phagedenismus. 

Definition. — Ulcus  tropicum  is  a  tropical  chronic  sloughing  ulcer, 
which  may  take  a  phagedenic  character,  and  spread  down  to  the 
muscles  and  bones,  and  which,  left  to  itself,  shows  hardly  any  ten- 
dency to  heal. 

History. — Phagedenic  ulceration  is  mentioned  in  many  of  the 
early  works  on  tropical  medicine.  Thus,  Hunter  in  1792  refers  to 
it  in  Jamaica  in  the  following  terms: — 

'  Sores  .  .  .  spread  quickly,  and  form  large  ulcerated  surfaces.  .  .  . 
The  granulations  turn  flaccid,  and  even  mortify  in  parts.  The  por- 
tion skinned  over  ulcerates  afresh,  and  the  sore  becomes  larger 
than  ever.  Ulcers  of  some  standing  .  .  .  could  not  be  healed  in 
that  country.  .  .  .  Opportunity  was  taken  to  send  home  men  with 
ulcers.' 

After  this  date  there  are  numerous  references  to  the  complaint, 
which  is  generally  described  under  the  name  of  the  locality  in  which 
it  was  found,  which  accounts  for  many  of  the  above  synonyms. 
In  1862,  Rochard  took  a  broader  view  of  the  disease,  and  in  1864 
Le  Roy  de  Mericourt  introduced  the  term  '  Phagedenic  ulcer  of 
warm  countries.' 

In  1874,  Treille  suggested  that  the  disease  was  likely  to  prove 
to  be  of  a  parasitic  origin,  but  he  failed  to  demonstrate  any  parasite. 
Bacteria  have  since  been  described  by  many  observers,  and  more 
recently  spirochetes  have  been  considered  to  be  the  cause  of  the 
disease,  as  will  be  described  in  the  section  on  /Etiology. 

Climatology. — Ulcus  tropicum  is  found  in  all  tropical  and  sub- 
tropical regions  of  Africa,  Asia,  and  America.  There  are  localities, 
however,  such  as  the  hinterland  of  Aden,  the  low,  marshy  plains  of 
Cochin  China  and  Tonkin,  and  some  islands  of  the  Red  Sea,  where 
the  affection  is  particularly  common.  It  may  be  found  also, 
though  rarely,  in  temperate  zones,  cases  having  been  reported  from 
Greece,  Macedonia,  and  South  Italy. 

/Etiology. — Numerous  bacteria  have  been  described  by  Petit, 
Boniet,  Blaise,  Crendiropoulo,  as  being  the  cause  of  the  disease. 
Le  Dantec  described  in  the  lesions  the  fusiform  bacillus,  and  con- 
sidered it  to  be  the  cause  of  the  affection.  Vincent  found  in  addition 
to  the  fusiform  bacillus  numerous  spirochetes,  and  considered  that 
the  affection  was  due  to  the  association  of  the  two  germs. 
Vincent's  observations  have  been  confirmed  by  Smith  and  Peil  in 
Sierra  Leone,  Patton  in  Aden,  and  many  other  observers  in  various 
parts  of  the  tropics.  Prowazek  has  fully  described  the  spirochete 
which  he  named  Spiroclueta  schaudinni  Prowazek,  1907.  This 
term,   however,  is  a  synonym  for  S.  vincenti  Blanchard,   1906. 


2 1 82  ULCERATION 

The  important  researches  of  Keysselitz  and  Mayer,  and  the  more 
recent  ones  of  Wolbach  and  Todd,  confirm  Prowazek' s  work. 

Spiroschaudinnia  vincenti  Blanchard,  1906  (synonym,  Spiroschaudinnia 
schaudinni  Prowazek,  1907). — This  is  a  spiral-shaped  organism,  very  actively 
motile,  its  length  varying  between  10  [i  and  22  fi,  though  much  shorter  or 
longer  individuals  may  be  met  with.  The  coils  are  few  in  number,  and 
elongated.  The  organism  possesses  a  well-marked  undulating  membrane, 
which  is  best  brought  into  evidence  by  using  Lofner's  flagellar  stain.  A 
delicate,  rather  short  fiagellum  is  occasionally  seen  at  one  of  the  extremities. 
Forms  undergoing  longitudinal  division  are  frequently  observed.  Prowazek 
distinguishes,  also,  male  and  female  forms.  Variously  shaped  regressive 
and  rest  forms  may  be  seen.  According  to  Prowazek,  Spiroschaudinnia 
vincenti,  apart  from  being  more  slender,  has  the  greatest  resemblance  to  the 
spirochaste  which  Prowazek  himself  and  Hofman  have  described  in  a  form  of 
balanoposthitis. 

The  S.  vincenti  is  often  found  mixed  with  other  types  of  spirochsetes,  some 
slender,  some  thick. 

According  to  Le  Dantec,  Brault,  Vincent,  and  others,  ulcus  tropicum  is 
identical  with  the  so-called  '  hospital  phagedaena  '  which  used  to  rage  in  hos- 
pitals of  all  countries  before  the  antiseptic  era.  In  our  opinion  ulcus  tropicum 
is  a  separate  disease,  though  occasionally,  owing  to  secondary  infections,  it 
may  take  phagedsenic  characters  similar  to  those  found  in  hospital  gangrene. 

Inoculation  Experiments — Communicability. — Experiments  to  in- 
oculate the  disease  in  men  and  in  the  lower  animals  have  been  made 
by  several  authors.  Blaise  inoculated  himself  with  the  secretion 
of  a  case  of  ulcus  tropicum,  but  no  ulcer  was  produced — only  a 
slight  superficial,  purulent  lesion,  probably  due  to  pyogenic  cocci 
present  as  secondary  infectious  agents  in  the  secretion  which  had 
been  used  for  the  inoculation.  Blaise  tried  to  inoculate  the  disease, 
also,  in  guinea-pigs,  but  without  any  definite  result.  Similar  experi- 
ments on  the  lower  animals  by  Jourdeuil  and  Gayer  failed.  Hal- 
berstadter  tried  to  reproduce  the  affection  in  monkeys  (orang- 
outang and  Macacus  cynomolgus),  but  without  success. 

It  would  seem,  therefore,  that,  to  a  certain  extent,  the  disease 
is  not  directly  contagious.  It  is  probable  that  some  insects  or 
other  blood-sucking  vermin  may  play  an  important  role  in  the 
transmission  of  the  disease.  In  Ceylon,  patients  often  state  that 
the  ulcer  developed  at  the  site  of  a  leech-bite.  Leeches  are  ex- 
tremely common  in  Ceylon  and  other  tropical  countries.  Prowazek 
in  Java  has  examined  many  leeches,  but  he  never  found  any  spiro- 
chetes except  once.  The  spirochete  observed,  however,  was  quite 
different  from  Spiroschaudinnia  vincenti.  Prowazek  examined, 
also,  on  many  occasions  the  mud  of  rice-fields,  but  of  spirochetes  he 
found  only  S.  plicatilis,  and  once  a  very  thin,  short,  very  actively 
mobile  spirochete. 

P/eiisposing  Causes. — A  hot,  damp  climate  is  said  to  have  a  pre- 
disposing influence,  as  cases  of  ulcus  tropicum  occur  more  frequently 
in  the  hot  rainy  season  and  marshy  lowland  localities  rather  than 
in  dry  or  higher  regions.  It  may  be  that  it  is  in  hot,  marshy  places 
that  the  carriers  of  the  infection  thrive. 

The  disease  is  very  common  among  the  poorer  classes  of  the 
population,  who  go  barefooted  and  wear  but  scanty  clothes.     We 


ULCUS  TROPICUM 


2183 


have  observed  it  very  often  in  beggars  and  in  scabies  patients. 
The  disease  is  much  more  common  in  adults  than  in  children,  in 
men  than  in  women. 

Histopathology. — This  has  been  thoroughly  studied  by  Keysselitz 
and  Mayer,  and  by  Wolbach  and  Todd.  The  surface  of  the 
ulcer  is  covered  often  by  a  tenacious  membrane  composed 
almost  solely  of  coarse-meshed  hyaline  fibrin,  with  detritus 
and   masses  of  spirochetes   and  various    bacteria.     The  fundus 


Fig.  858. — Ulcus  Tropicum:  Typical. 

and  walls  consist  of  granulation  tissue,  which  does  not  present 
any  characteristic  feature.  The  deeper  tissues  and  corium 
surrounding  the  ulcer  present  a  heavy  lymphoid  and  plasma  cell 
infiltration,  and,  as  noted  by  Wolbach  and  Todd,  numerous  eosino- 
philes  are  found  in  the  vicinity  of  small  vessels.  On  microscopical 
examination  of  vertical  sections  of  the  ulcer,  it  will  be  seen  that 
the  superficial  layers  of  the  fundus  show  a  large  amount  of  granular 
detritus  and  numerous  foci   of  leucocytic  infiltration,  while  the 


2184 


ULCERA  TIONS 


deeper  layers  consist  of  fairly  dense  fibrous  tissue.  Hemorrhagic 
foci  are  to  be  seen  in  various  parts,  and,  as  observed  by  Keysselitz 
and  Mayer,  fusiform  bacilli  and  spirochaetes  are  found  in  the  super- 
ficial layers,  while  in  the  deeper  strata  only  spirochaetes  are  present. 

Symptomatology. — The  affection  is  generally  found  on  the  lower 
limbs,  especially  the  lower  third  of  the  leg,  the  ankle  and  dorsum 
of  the  foot.  Occasionally  it  may  develop  on  other  uncovered  parts 
of  the  body.  It  is  single  in  most  cases,  but  two  or  more  ulcers  may 
be  found  in  some  patients. 

Ulcus  tropicum  begins  with  the  appearance  of  a  small,  painful, 
occasionally  pruriginous  papule  or  papulo-pustule,  surrounded  by 
a  deeply  infiltrated  dusky  red  areola.  The  initial  lesion  soon 
undergoes  purulent  and  degenerative  changes,  which  rapidly  extend 
to  the  infiltrated  area.     A  sloughing  process  sets  in,  and  an  ulcer 


Fig.  859. — Ulcus  Tropicum:  Early  Stage. 


is  formed,  which  gradually  extends  in  depth  and  surface.  The 
mirgins  are  not  sensibly  raised,  nor  thickened,  unless  the  case  be 
very  old.  They  are  not  perpendicularly  cut,  nor  undermined,  as 
a  rule,  the  whole  ulceration  having  generally  a  roundish  or  oval 
outline,  and,  when  the  secretion  is  removed,  a  concave  fundus.  The 
parts  surrounding  the  ulcers  are  often  cedematous,  and  somewhat 
painful  on  pressure.  It  is  remarkable,  however,  how  comparatively 
little  pain  there  is  in  many  cases. 

When  the  patients  are  first  seen,  the  whole  ulcer  is  generally 
covered  with  a  thickish,  dirty  greyish  secretion,  exhaling  a  highly 
offensive  odour.  On  removing  the  secretion  the  fundus  will  be 
found  to  be  of  a  red  colour,  or  in  chronic  cases  pale  pinkish,  and 
feebly  granulating. 

The  fundus  is  often  somewhat  infundibular  in  its  central  area, 
and  not  rarely  may  present  a  circular  raised  ridge,  which  divides 


ULCUS  TROPICUM 


2185 


the  ulcer  into  two  portions — an  external  more  superficial  one,  and 
an  internal  infundibuliform  one. 

Occasionally,  if  left  untreated,  the  ulcer  may  take  a  real  phage- 
denic character,  involving  a  large  surface,  and  deepening  till  the 
deeper  structures — muscles,  tendons,  and  periosteum — are  affected. 

The  course  is  always  chronic,  lasting  for  months — in  fact,  the 
ulcer  has  hardly  any  tendency  to  spontaneous  healing  if  untreated. 
Healing  takes  place  by  a  very  slow  process  of  granulation,  and 
begins  from  the  periphery.  A  thick,  whitish,  often  disfiguring 
scar  is  left  at  the  place  of  the  ulcerations.  At  times,  however,  the 
cicatrix  is  at  first  very  delicate,  and  the  ulcer  may  break  out  again 
after  the  least  irritation  or  traumatism. 

The  microscopical  examination  of  the  greyish,  bad-smelling  secretion  shows 
leucocytes  undergoing  various  degenerations,  some  red-blood  cells,  threads 
of  connective  tissue,  and  very 
often  spirochetes  and  fusiform 
bacteria  of  various  types,  some- 
times accompanied  by  the  usual 
pyogenic  cocci.  In  old  untreated 
cases  larvae  of  flies  may  be  found, 
small  acarids,  and  ants. 

Diagnosis. — According  to 
Le  Dantec,  Vincent,  and 
several  other  observers,  ulcus 
tropicum  is  identical  with 
'  hospital  phagedena.'  The 
fact,  however,  that,  in  con- 
trast to  '  hospital  phage- 
dena,'  ulcus  tropicum  shows 
very  little  or  no  direct  con- 
tagiousness, and  in  most 
cases  is  self-limited,  clearly 
shows,  in  our  opinion,  that 
the  two  are  separate  diseases. 

Diff  arential  Diagnosis — Frambcesia. — The  lesions  in  frambcesia  are 
generally  multiple — either  granulomatous  or  ulcerative.  Scrapings 
from  frambcesia  lesions — after  the  superficial  strata  have  been  re- 
moved— will  often  reveal  the  Treponema  per tenue  Castellani,  which 
is  much  more  slender  than  any  of  the  spirochetes  found  in  ulcus 
tropicum.  Occasionally  an  ulcerative  frambcesia  lesion  may  become 
infected  with  the  virus  of  ulcus  tropicum.  In  our  experience, 
however,  the  reverse  is  much  more  common — viz.,  an  ulcus 
tropicum  becomes  infected  with  frambcesia  virus,  takes  a  papil- 
lomatous appearance,  and  is  followed  by  a  general  eruption  of 
frambcesia  granulomata. 

Syphilis. — Ulcus  tropicum  does  not  show  usually  the  clean-cut 
margins  and  the  punched-out  circular  or  reniform  appearance,  with 
the  frequent  wash-leather  slough  on  the  surface,  of  a  tertiary  ulcer. 
The  mercury  and  potassium  iodide  treatment  has  no  influence  on  it. 


Fig.  860. — Ulcus  Tropicum. 


2i86 


ULCERATIONS 


Oriental  Sore. — An  old-standing  Oriental  sore  ma}'  present  some 
characters  of  a  chronic  ulcus  tropicum,  though  generally  a  tropical 
ulcer  is  much  larger.  The  process  of  ulceration  and  breaking 
down  is  very  slow  in  Oriental  sore,  while  it  is  very  rapid  in  ulcus 
tropicum.  In  difficult  cases  the  search  for  Leishmania  tropica, 
which  is  present  in  Oriental  sore,  will  clear  the  diagnosis. 

Ulcus  Cruris  Varicosum. — There  are  often  varicose  veins  visible, 
the  parts  surrounding  the  ulcer  are  congested  and  frequently  ecze- 
matous,  the  ulcer  is  often  shallow  and  irregular. 

Ulcers  of  Tubercular  Origin. — They  are  rare  on  the  lower  ex- 
tremities, and  their  development  is  long  and  insidious.     In  ulcus 


Fig.  86i. — Ulcus  Tropicum. 


tropicum  the  tubercular  cuti  and  ophthalmic  reactions  are  negative 
unless  the  ulcer  develops  in  a  tubercular  patient. 

Blastomycosis — Sporotrichosis. — In  blastomycosis  there  are  gener- 
ally warty  patches  with  minute  abscesses;  while  the  lesions  of 
sporotrichosis  often  show  at  first  the  characters  of  gummata. 
The  bacteriological  examination  will  reveal  the  presence  of 
the  fungi. 

Acladiosis. — The  ulcerative  lesions  are  multiple  and  of  smaller 
dimensions.  The  bacteriological  examination  will  reveal  the  pres- 
ence of  Acladium  castellanii  Pinoy. 

Mvcosis  Fungoides. — Is  generally  preceded  by  a  general  pruri- 
ginous  dermatitis  of  various  character,  lichen-planus-like,  psoriasis- 


ULCUS   TROPICUM  2187 

like,  eczematous-like.  The  ulcerative  lesions  are  multiple,  and 
have  the  characters  of  granulomata. 

Prognosis. — If  untreated,  tropical  ulcer  has  very  little  or  no  ten- 
dency to  spontaneous  recovery,  and  in  some  cases  may  extend, 
damaging  the  deeper  structures,  tendons,  muscles,  nerves,  and 
vessels.  Occasionally  a  general  septicaemia  and  pysemia  may  super- 
vene. In  countries  where  frambcesia  is  endemic  the  ulcer  often 
gets  infected  with  its  virus,  and  the  patient  develops  a  general 
eruption  of  frambcesia. 

Traatmeit. — Salvarsan,  neosalvarsan,  and  their  substitutes  have 
been  adnvnistered  by  intravenous  or  intramuscular  injection  by 
Werner,   Hallenberger,  and  others,  with  success  in  certain  cases. 


]B*!?r«v. 

¥#&r*& 

■  1  i^w 

i 

V 

* 

$gr  t 

Fig.  862. — Ulcus  Tropicum,  with  Cornu  Cutaneum. 

The  details  of  the  treatment  are  found  in  the  chapter  on  Fram- 
boesia  (p.  1560).  Mercury  and  potassium  and  sodium  iodides  are 
useless,  but  calcium  iodide  (gr.  iii.),  well  diluted,  three  times  daily, 
seems  occasionally  to  be  of  some  slight  benefit.  As  regards  local 
treatment,  the  patient,  whenever  possible,  being  kept  at  rest,  the 
dirty  greyish,  foul-smelling  secretion  is  removed  by  using  a  disin- 
fecting solution,  such  as  mercury  perchloride,  1  in  1,000;  cyllin, 
1  in  300;  hydrogen  peroxide,  10  per  cent.;  permanganate  of 
potash,  1  in  2,000. 

For  the  first  few  days  it  is  better  not  to  apply  any  so-called 
disinfectant  ointments  or  powders:  simply  keep  the  ulcer  covered 
with  gauze,  moistened  as  often  as  possible  with  one  of  the  disin- 
fecting solutions   already  mentioned.      This   generally  stops  the 


2188  ULCERATIONS 

formation  of  the  greyish,  dirty  secretion.  The  ulcer  will  then 
appear  clean  and  of  a  pinkish  colour ;  but  whatever  be  the  further 
treatment  used,  whether  powders  (iodoform,  boracic  acid)  or 
disinfecting  ointments  (white,  red  precipitate,  or  iodoform  oint- 
ments), the  improvement  will  be  very  slow,  and  several  weeks,  and 
often  months,  will  elapse  before  a  firm  cicatrix  is  formed.  Much 
quicker  results  will  be  obtained  by  using  a  protargol  ointment. 
The  ulcer  is  cleaned  every  morning  with  a  perchloride  lotion  (i  in 
1,000) ;  then  a  protargol  ointment  (5  to  10  or  20  per  cent.)  is  thickly 
spread  on  a  piece  of  lint  or  gauze  and  applied  to  the  ulcer,  which 
is  then  fairly  firmly  bandaged. 

The  superiority  of  the  protargol  treatment  over  other  kinds  of  local  treatment 
is  patent  in  many  cases.  Castellani,  who  introduced  it  for  ulcus  tropicum, 
made  the  fo llowing  experiment:  in  a  patient  presenting  two  ulcers  of  little 
difference  in  size  and  deepness,  one  on  the  right  leg,  one  on  the  left,  he  treated 
the  one  on  the  right  leg,  which  was  slightly  larger  and  deeper,  with  protargol, 
and  the  one  on  the  left  leg  with  iodoform.  The  ulcer  treated  with  protargol 
healed  in  three  weeks,  the  one  treated  with  iodoform  in  two  months. 

A  silver  nitrate  ointment  (£  per  cent.),  or  a  silver  nitrate  (£  per  cent.), 
balsam  of  Peru  (2  per  cent.),  ointment  may  also  be  used. 

To  accelerate  cicatrization  allantoin  preparations  have  been  used,  and 
also  scharl  chroth  powder.  Salvarsan  has  been  used  locally  as  a  powder, 
but  this  method  is  not  advisable,  as  it  induces  a  very  severe,  painful  inflam- 
mation. Boigey  and  Vincent  recommend  a  powder  consisting  of  10  parts  of 
fresh  hypochlorite  of  soda  and  90  parts  of  boric  acid. 

ULCUS  INTERDIGITALE. 

This  affection  is  not  rare  among  natives.  It  was  described  in  1909 
by  Castellani,  whose  work  has  been  recently  confirmed  by  Breinl, 
Martinez  and  Lopez.  The  patient  complains  of  some  itching 
between  the  toes,  though  no  papules  or  vesicles  are  seen.  After  a 
few  days  a  fissure  appears,  which  rapidly  deepens,  and  enlarges  into 
a  large  oval  ulcer  with  a  dull,  dark  red  fundus  and  sodden-looking 
margins.  There  is  practically  no  discharge  whatever.  The  ulcer 
is  generally  very  painful.  The  skin  surrounding  the  ulcers  does 
not  show  signs  of  inflammation.  Under  proper  treatment  the 
ulcer  heals  in  a  few  days.  The  patient  must  remain  at  rest,  washing 
the  ulcer  twice  daily  with  a  1  per  cent,  carbolic  lotion,  followed  by 
dressing  with  a  bismuth-boric  iacid  'ointment  :— 

Bismuthi  subnitratis     . .  . .  . .  . .      gr.  xxx. 

Acidi  borici         . .  . .  . .  . .  gr.  xv. 

Vaseline  . .  . .  . .  . .  . .  . .     §i. 

ULCUS  INFANTUM. 

Historical  ani  Geographical.— Under  this  name  Castellani  de- 
scribed a  rather  rare  ulcerative  condition  of  the  legs  met  with  in 
Ceylon  among  children,  both  native  and  European.  His  researches 
have  been  confirmed  by  various  observers,  among  whom  Gabbi 
and  Sabella  in  Tripoli.  The  condition  is  found  in  Ceylon,  India, 
and  North  Africa. 


ULCUS  INFANTUM 


2189 


etiology. — This  is  unknown.  A  bacillus  which  cannot  be  grown 
is  the  only  germ  present  in  most  cases;  but  as  to  its  serological 
role  nothing  can  be  said  definitely. 

Symptomatology. — A  reddish  spot  appears  on  some  part  of  the 
leg.  The  spot  becomes  slightly  elevated,  and  shows  a  yellowish 
central  point.  The  yellowish  point  breaks  down,  and  a  small  ulcer 
appears,  generally  of  circular  shape,  and  with  a  red  fundus.  The 
ulcer  secretes  a  yellowish,  thickish  secretion,  which  dries  into  a 


Fig.  863. — Ulcus  Infantum. 

yellow  crust.  If  after  some  days  the  crust  is  removed,  the  ulcer 
will  be  found  much  larger  and  deeper— the  size  of  a  shilling  to  a 
half-crown  piece.  The  ulcer  is  generally  indolent,  except  on  pres- 
sure. There  may  be  a  little  pruritus.  The  ulcer  may  be  single 
or  multiple.  The  inguinal  lymphatic  glands  may  become  enlarged, 
and  occasionally  the  child  has  fever.  The  duration  is  between  four 
to  six  weeks  and  three  or  four  months.  On  healing,  a  permanent 
whitish  scar  is  left. 


2igo  ULCERATIONS 

Diagnosis.- — The  ulcus  infantum  is  differentiated  from  ulcus 
tropicum  by  the  less  severe  symptoms,  by  being  almost  always 
multiple,  by  the  smaller  dimensions  of  the  sore,  by  the  absence  of 
spirochaetes,  and  by  the  absence  of  any  tendency  to  phagedena. 
In  contrast  to  veldt  sore  the  ulcers  are  deep,  and  the  crust  very 
thick.    No  streptococcus  is  found. 

Treatments — -Touch  the  ulcers  with  pure  hydrogen  peroxide  once 
every  other  day,  and  dress  them  with  simple  boric  acid  lotion 
(2  per  cent.). 

REMARKS  ON  ULCERS. 

Ulcerative  conditions  of  the  skin  are  extremely  common  in  the 
tropics.    They  may  be  classified  as  follows: — 

1.  Cutaneous  leishmaniasis. 

2.  Ulcus  tropicum. 

3.  Ulcus  infantum. 

4.  Veldt  sore. 

5.  Ulcus  interdigitale. 

6.  Gangosa  ulcers. 

7.  Leprotic  ulcers. 

8.  Ulcers  of  frambcesial  origin. 

9.  Elephantoid  ulcers. 

10.  Blastomycetic,    sporotrichitic,  acladiotic,    and,    gener- 
ally, hyphomycetic  ulcers. 
11    Cancerous  and  sarcomatous  ulcers. 

12.  Tubercular  ulcers. 

13.  Syphilitic  ulcers. 

14.  Glanders  ulcerations. 

15.  Ulcers  of  pyogenic  origin  (pyosis  tropica). 

16.  Ulcers  due  to  varicose  veins. 

17.  Undetermined  chronic  or  subchronic  ulcerations. 

The  ulcerative  conditions  which  may  be  considered  as  strictly 
tropical  and  well  defined,  such  as  Oriental  sore,  ulcus  tropicum,  etc., 
have  already  been  described.  The  cosmopolitan  ulcerations,  such 
as  the  syphilitic  ones  and  those  due  to  varicose  veins,  show  the  same 
characters  in  the  tropics  as  in  temperate  zones,  except  that  very 
often,  owing  to  their  being  neglected  for  a  long  time,  they  may 
present  enormous  dimensions,  and  may  show  secondary  infections 
and  become  phagedenic.  Ulcers  due  to  varicose  veins  are  very 
common  among  rickshaw  coolies,  who  have  to  run  and  stand  for 
hours  at  a  time.  It  is  remarkable  how  quickly  they  heal  in  most 
cases  in  these  coolies,  if  the  patient  is  kept  at  rest  for  some  time; 
whereas  in  temperate  zones  the  healing  of  varicose  veins  ulcers  is 
of  very  long  duration. 


REMARKS  ON  ULCERS  2191 

Undetermined  Subchronic  and  Chronic  Ulcers. 

Knowledge  of  this  group  of  ulcers  is  scanty,  but  the  investiga- 
tions of  Strong,  Stitt,  Rho,  Wherry,  and  Clegg,  and  others  have 
thrown  some  light  on  this  subject.  Our  experience  tallies  with 
that  of  Stitt,  and  we  therefore  consider  that  such  ulcers  may  be 
roughly  divided  into  three  groups: — 

1.  Septic  Ulcers — Ulcerations  following  on  Neglected  Wounds. 

2.  Painless  Chronic  Ulcers. 

3.  Diphtheroid  Ulcers. 

Septic   Ulcers — Ulcerations   following   on  Neglected   Wounds. — 

These  are  of  pyogenic  origin  and  often  very  large  dimensions. 
They  are  generally  of  roundish  or  irregular  shape,  and  may  be  very 
deep.  The  secretion  is  abundant,  purulent,  and  contains  the  various 
staphylococci.  If  the  pus  is  removed,  and  a  scraping  taken  from 
the  fundus,  the  preparation  will  show  numerous  polymorphonuclear 
leucocytes  and  various  cocci.  These  ulcers  do  not  show  tendency 
to  spontaneous  cure,  but  heal  quickly  under  an  antiseptic  treatment. 
We  generally  treat  them  with  hydrargyrum  perchloride  (1  in  2,000). 
The  opsonic  treatment  also  gives  good  results. 

Nichols  has  called  attention  to  discharging  sores  in  the  Philippine  Islands, 
called  'puente,'  which  are  produced  by  the  natives  applying  some  lime  to  the 
skin,  and  afterwards  betel  powder,  with  the  object  of  counter-irritation. 

Painless  Chronic  Ulcers.— A  small  red  scaly,  slightly  itching  spot 
appears,  generally  on  the  legs,  and  gradually  enlarges  for  about 
four  to  eight  weeks,  when  the  affected  area  begins  to  exude  a  serum 
which  quickly  dries  into  crusts.  Under  the  crust  ulceration  slowly 
takes  place.  At  first  the  ulcers  are  shallow,  and  may  have  under- 
mined edges;  later  they  are  often  punched  out,  and  may  become 
indurated.  There  is  no  pain,  except  slight  pain  on  pressure,  and 
the  general  health  is  not  affected.  Healing  takes  place  under  the 
crust,  and  lasts  between  two  and  twelve  months.  A  pale  cicatrix, 
with  hyperpigmented  margins,  is  left. 

As  noted  by  Stitt,  scrapings  from  the  fungus  show  a  prevalence 
of  mononuclear  cells,  polymorphonuclears  being  practically  absent. 
No  pyogenic  organisms  are  found. 

Treatment. — The  treatment  is  difficult.  Cauterization  dors  Very 
little.  In  some  cases  the  application  of  bismuth  subnitrate,  xero- 
form,  novoform,  dermatol,  and  firm  bandaging  is  useful.  In  others 
a  protargol  ointment  (5  to  10  per  cent.),  or  a  nitrate  of  silver 
(£  per  cent.)  balsam  of  Peru  (1  per  cent.)  ointment  is  of  advantage. 
Allantoin  preparations  may  also  be  used.  When  the  ulcers  are 
very  large  and  atonic,  skin  transplantation  may  be  necessary. 

Diphtheroid  Ulcers. — An  angry  red.  painful  spot,  often  surrounded 
by  vesicles,  appears  on  the  legs.  Within  a  few  hours — twelve  to 
forty-eight — -the  affected  area  is  turned  into  a  dark  greyish  or 
blackish  membrane.     If  this  membrane  be  removed,  an  ulcer  will 


2i92  UL  CERA  TIONS 

be  found  covered  with  greenish  pus.  The  membrane  reforms 
rapidly,  and,  apart  from  the  dark  colour,  it  closely  resembles  a 
diphtheria  membrane.  These  ulcers  extend  rapidly,  but  do  not 
take,  as  a  rule,  a  true  phagedenic  character.  The  margins  after 
some  time  may  become  indurated,  but  do  not  show  a  punched-out 
appearance.  Scrapings  taken  from  the  fundus  show  numerous 
polymorphonuclears.  The  course  is  very  long.  These  ulcers  are 
with  difficulty  distinguishable  from  true  ulcus  tropicum  except  by 
the  absence  of  Spiroschaudinnia  vincenti  Blanchard. 

Treatment. — Excision  is  not  to  be  advised,  as  in  Stitt's  and  our 
own  experience,  when  this  has  been  done,  additional  lesions  have 
appeared.  Bier's  passive  congestion  method  is  painful,  and  does 
not  improve  the  condition.  On  the  whole,  the  best  treatment  is 
to  keep  the  ulcers  well  disinfected  with  a  perchloride  lotion  (i  in 
2,000),  occasionally  touching  them  with  pure  hydrogen  peroxide. 
Should  the  ulcers  become  phagedenic,  the  application  of  pure 
carbolic  is  advisable. 

GRANULOMA  INGUINALE. 

Synonyms. — Ulcerating  granuloma  of  the  pudenda,  Granuloma 
Venereum  (Brooke),  Esthiomene  de  la  vulve. 

Definition. — Granuloma  inguinale  is  a  chronic  granulomatous 
affection  of  probable  protozoal  origin  attacking  the  generative 
organs,  from  which  it  spreads  to  the  inguinal  regions  and  the  peri- 
neum. 

History. — In  1896  Conyers  and  Daniels  described  a  disease  of 
the  generative  organs  in  both  men  and  women  in  British  Guiana 
which  was  very  painful,  disfiguring,  and  contagious.  Daniels 
thinks  that  it  was  previously  described  by  Macleod  and  Maitland 
in  India.  Since  then  papers  have  appeared  on  the  subject  by 
Ozzard,  Galloway,  Wise,  Donovan,  Siebert,  Flu,  Martini,  Gabbi, 
Sabella,  Torres,  Rabello,  Pijper,  Mayer,  Newham  and  Low,  and 
many  others. 

Climatology. — It  occurs  in  British  Guiana,  the  West  Indian 
Islands,  West  Africa,  South  Africa,  India,  South  China,  and  Northern 
Australia;  but  is  rare  in  Ceylon,  Malaya,  Sudan,  and  Central  Africa. 
It  has  been  reported  from  Northern  Africa  (Tripoli)  by  Gabbi  and 
Sabella.  A  similar  or  identical  condition  has  rarely  been  met  with 
in  Europe  and  North  America. 

/Etiology. — It  appears  in  the  genitalia  of  both  sexes  after  puberty, 
but  is  rare  after  forty-five  years  of  age. 

Donovan,  in  1905,  described  certain  peculiar  rod-like  bodies 
2/ibyi/x,  lying  singly  or  in  groups  in  mononuclear  cells,  obtained 
by  scraping  the  sores.  Donovan  stated  that  the  bodies  looked  '  like 
gigantic  bacilli  with  rounded  ends,'  but  left  the  nature  of  them  un- 
decided Siebert,  in  1907,  carried  out  an  investigation  on  material 
originating  from  various  countries,  demonstrating  the  same  or 
similar  bodies  in  all  instances,  but  referring  to  them  as  diplococci. 


GRANULOMA   INGUINALE  2193 

Markham  Carter,  in  1910,  described  the  parasites  as  '  bean-shaped 
bodies  resembling  the  gregariniform  stage  of  a  herpetomonas  or  a 
crithidium,'  and  came  to  the  conclusion  that  the  affection  was  due 
to  either  a  herpetomonas  or  a  crithidium. 

Flu,  in  1911,  in  South  America  confirmed  Siebert's  work,  but 
considered  the  bodies  to  be  bacilli,  with  capsules,  and  not  cocci.  At 
the  same  time,  however,  he  called  attention  to  the  possibility  of 
the  bodies  being  a  stage  of  a  chlamydozoal  infection.  Martini,  in 
1913,  announced  that  he  had  succeeded  in  cultivating  the  germs 
described  by  Siebert  and  Flu  on  blood  agar.  He  described  them  as 
anaerobic,  capsulated,  Gram-negative  diplococci,  and  stated  that 
he  had  succeeded  in  producing  granulomata  in  mice  by  inoculation 
of  cultures,  though  he  failed  with  guinea-pigs  and  rabbits.  In  the 
same  year  Aragao  and  Vianna  also  stated  that  they  had  succeeded 
in  growing  the  bodies,  which  they  considered  to  be  of  bacterial 
nature,  using  the  term  '  calimmato-bacterium  granulomatis.'  Their 
work  was  confirmed  by  De  Souza  Araujo. 

It  is  very  doubtful  whether  the  cultures  obtained  by  all  these 
observers  are  in  reality  cultures  of  Donovan's  bodies.  The  inocula- 
tion of  vaccines  made  from  such  cultures  do  not  induce  any  im- 
provement. 

Wise,  in  1907,  found  in  the  eruption  spirochaetes  resembling  Treponema 
pallidum  and  Spiroschaudinnia  refringens,  together  with  small  bodies  con- 
sisting of  a  thin  capsule  surrounding  a  clear  unstained  space,  in  the  middle  of 
which  was  a  curved  chromatic  rod,  which  was  thinner  in  the  centre  and 
club-shaped  at  either  end.  He  found  from  two  to  twenty-five  of  these  in  the 
leucocytes.  Cleland  confirmed  Wise's  observations,  and  called  the  spirochaete 
5.  aboriginalis  Cleland,  1909. 

Bosanquet  confirmed  the  presence  of  spirochaetes  in  sections,  associated 
with  numerous  bacteria,  but  did  not  consider  the  spirochaetes  to  be  the  aetio- 
logical  agents  of  the  affection.  De  Souza  Araujo  observed  that  after  the 
injection  of  salvarsan  the  spirochaetes  disappeared,  but  the  condition  did  not 
get  better;  hence  he  came  to  the  conclusion  that  the  spirochaetes  had  nothing 
to  do  with  the  aetiology  of  the  disease. 

Cleland  and  Hickinbotham,  in  1909,  published  further  observations  on 
granuloma  inguinale,  and  stated  that  spirochaetes  were  present  only  in  a 
certain  number  of  cases,  while  they  constantly  found  large  numbers  of  diplo- 
bacillary  bodies.  Le  Dantec,  in  191 1,  was  still  of  opinion  that  the  malady 
was  of  tubercular  origin.  Torre  and  Rabello  believed  it  to  be  a  form  of  sporo- 
trichosis, and  Greco  a  blastomycosis.  Pijper,  in  a  recent  interesting  publica- 
tion, has  definitely  brought  forward  a  chlamydozoon  theory,  and  considers 
that  the  variously  shaped  bodies  described  by  so  many  observers  are  stages 
of  the  same  organism,  a  stage  of  which,  in  Pijper's  opinion,  closely  resembles 
the  initial  or  elementary  bodies  described  by  Prowazek  in  the  development  of 
the  Guarnieri  bodies. 

Communicability. — The  disease  is  generally  transmitted  by  sexual 
intercourse. 

Cleland  states  that  in  West  Australia  the  malady  is  especially  common 
among  '  gins  '  (native  women),  and  there  is  an  idea  prevalent  among  the 
white  settlers  that  the  girls  become  infected  by  connection  with  dogs,  in  which 
animals  a  condition  similar  or  identical  with  granuloma  venereum  is  said  to  be 
found.  Ernest  Black,  who  has  made  a  thorough  investigation,  states  that 
Cleland's  hypothesis  is  untenable. 

138 


£194 


ULCERATIONS 


Pathology. — According  to  Galloway,  the  microscopical  changes 
begin  some  distance  from  the  lesion,  and  consist  of  a  round-celled 
infiltration  into  the  upper  regions  of  the  corium.  This  induces 
the  papillae  to  increase  in  length,  thus  producing  the  typical  papule, 
and  at  the  same  time  causes  an  elongation  of  the  interpapillary 
processes  of  the  epidermis,  until  they  are  some  eight  or  ten  times  their 
original  length. 

The  connective  tissue  of  the  corium  swells  and  disappears,  and 
its  place  is  taken  by  a  round-celled  infiltration,  which  consists  of 
leucocytes,  Unna's  plasma  'cells,  mast  cells,  and  connective-tissue 
cells.  Giant  cells  are  not  found.  The  leucocytes  are  the  ordinary 
polymorphonuclear  leucocytes,  while  Unna's  cells  are  characterized 


■ 

**'m 

'f 

-  ■;: 

&f  1 

\ 

^®s 

*T''  ■'-'  .S^H 

Fig.  864. — Granuloma  Inguinale. 
(From  a  photograph  hy  Sambon.) 

by  possessing  a  rounded  nucleus,  with  a  certain  amount  of  sur- 
rounding protoplasm  containing  basophile  granules.  The  connec- 
tive-tissue cells  are  spindle-shaped.  The  cells  of  the  epidermis  are 
modified  over  the  papule  by  becoming  swollen,  hyaline,  and  show- 
ing mitosis.  The  stratum  granulosum  fails  to  develop  its  kerato- 
hyalin  granules,  and  eventually  disappears  halfway  up  the  papule, 
as  does  the  stratum  corneum,  so  that  on  the  summit  the  different 
layers  of  the  epidermis  cannot  be  differentiated. 

There  is  neither  caseation  nor  suppuration,  but  in  the  older  parts 
of  the  specimen  the  cells  of  the  infiltration  become  swollen  and 
disappear,  and  in  their  place  there  appears  cicatricial  connective 
tissue,  which  causes  the  papule  to  shrink  and  the  whole  area  to 
assume  a  scar-like  appearance. 


GRANULOMA   INGUINALE 


2195 


Symptomatology. — The  disease  in  the  male  begins  on  the  penis,  as 
a  rule,  as  a  papule  or  small  nodule,  which  extends  over  skin  and 
mucosa  by  peripheral  growth,  which  is  aided  by  the  formation  of  new 
papules  and  nodules  at  the  growing  margin  and  in  the  healthy  skin. 

It  grows  into  the  groins,  causing  the  hair  to  fall  out,  and  between 
the  scrotum  and  the  thighs,  and  from  thence  backwards  into  the 
perineum  and  around  the  anus,  into  which  it  may  pass. 

When  fully  developed,  it  appears  as  a  mass  of  nodules  or  papules, 
without  deep  ulceration  as  a  rule,  but  with1  a  thin,  offensive  dis- 
charge. In  the  older  regions  it  shows  some  attempt  at  healing  in  the 
formation  of  dense  scar  tissue.     There  is  very  little  pain  or  pruritus. 

In  the  female  the  process  begins  as  a  papule  on  the  labium  minus, 
and  then  extends  jinto  the  vagina,  along  the  perineum,  around  the 


Fig.  865. — Granuloma  Inguinale. 
(From  a  photograph  by  Sambon.) 


anus,  and  up  the  rectum,  and  into  the  groins.  The  growth  extends 
into  the  tissue  between  the  rectum  and  the  vagina,  and  may  give 
rise  to  rectovaginal  fistula?.  The  whole  growth  is  also  much  more 
liable  to  ulcerate  in  the  female  than  in  the  male. 

The  lesions  may  become  cedematous,  and  present  an  appearance 
analogous  to  elephantiasis. 

Bonne  and  Verhagen  have  described  a  case  in  which  the  disease  after  a 
time  attacked  the  upper  lip  and  ala?  nasi. 

Varieties. — -Daniels  lays  stress  upon  the  fact  that  the  disease 
varies  much  in  different  races.  In  negroes  it  is  more  granular,  and 
spreads  farther;  in  Indians  it  is  less  marked;  in  Fijians  it  is  softer, 
and  separate  areas  more  common. 

Diagnosis. — It  is  most  likely  to  be  confused  with  syphilis,  lupus, 
and  epithelioma.     From  syphilis  it  can  be  differentiated  by  the 


2ig6  ULCERATIONS 

absence  of  the  secondaxy  eruption  and  the  inefficacy  of  mercurial 
treatment.  Lupus  is  very  rare  in  such  situations,  and  in  epithelioma 
the  lymphatic  glands  would  be  early  infected.  In  doubtful  cases 
microscopical  examination  of  a  piece  of  the  diseased  tissue  will 
enable  the  diagnosis  to  be  made  from  lupus  as  well  as  from 
epithelioma. 

Prognosis. — The  disease  as  a  rule  does  not  affect  the  general 
health,  but  is  extremely  chronic,  lasting  for  years. 

Treatment. — Tartar  emetic,  though  not  efficacious  in  every  case, 
should  always  be  given  a  thorough  trial.  The  treatment  is  carried 
out  in  the  same  way  as  for  cutaneous  leishmaniasis  (see  p.  2173). 

Tartar  emetic  was  first  used  in  granuloma  inguinale  in  1913  by  Arago, 
Vianna,  and  De  Souza  Araujo.  Breinl  and  Priestley  confirmed  the  work  of 
these  observers  in  a  case  in  Australia,  and  very  shortly  after  Newham  ar,d 
Low  in  a  case  in  Europe.  Low,  however,  reported  later  on  a  complete  failure 
of  the  tartar  emetic  treatment  in  another  case. 

Greig  and  Curjel  consider  that  tartar  emetic  benefits  the  condition  only 
when  given  in  very  large  doses;  according  to  them  the  drug  acts,  not  as  a  true 
specific,  but  as  a  general  protoplasmic  poison. 

The  best  local  treatment  is  radiotherapy  with  X  rays,  which  has  been  found 
quite  successful  in  Madras.  If  these  are  not  available,  antiseptic  lotions  should 
be  applied,  and  then  portions  excised,  or  the  diseased  areas  may  be  scraped 
and  then  cauterized.  Conyers  and  Daniels  recommend  the  application  of 
an  ointment  of  salicylic  acid  (gr.  xxx.),  unguentum  creosoti  (§i.). 

Certain  observers  claim  to  have  had  good  results  with  salvarsan  and  neo- 
salvarsan.  The  technique  of  the  treatment  has  been  described  in  the  chapter 
on  Framboe  da  (p.  1 560).     Large  closes  of  potassium  iodide  are  said  to  be  useful. 

PAPILLOMA  INGUINALE  TROPICUM. 

Synonym. — Acanthoma  Inguinale  (Castellani). 

A  peculiar  papillomatous  affection  of  the  inguinal  regions  is  not 
rare  among  Tamils.  Further  experience  will  probably  show  that 
other  races  are  also  affected.  Women  are  apparently  more  liable 
to  the  disease  than  men,  inasmuch  as,  although  the  number  of  male 
patients  in  the  Colombo  Clinic  and  hospitals  is  much  larger  than 
the  number  of  female  patients,  not  a  single  case  has  been  detected 
among  men. 

Symptomatology. — One  or  both  inguinal  regions  are  occupied  by 
extremely  numerous  tall  filiform  vegetations  of  a  pinkish  or  darkish 
colour.  No  ulcerative  lesions  are  present.  There  is  neither  pain 
nor  pruritus.  The  general  health  does  not  seem  to  be  affected.  The 
affection  is  very  chronic,  and  is  probably  contagious,  but  nothing 
is  known  of  the  aetiology.  In  the  cases  so  far  observed  the  genital 
organs  of  the  patient  were  normal,  and  there  was  no  history  of 
gonorrhoea  or  any  other  venereal  disease. 

Treatment. — The  treatment  is  surgical — removal  of  the  vegeta- 
tion by  the  knife  and  cauterization.  The  patient,  as  a  rule,  how- 
ever, will  not  consent  to  the  operation. 


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Path.  Exot. 
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Hopkins  Hospital  Reports,  vol.  viii.,  October. 
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von  C.  Mense,  i.  52.    Leipzig. 
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f.  Chir.,  1920,  p.  1062). 
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Strong  (1906).     Philippine  Journal  of  Science,  p.  91. 
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Unna  (1896).     Histopathology  of  Diseases  of  the  Skin,  p.  475. 
Werner  (1912).     Arch.  f.  Sh.  v.  Trop. 
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Granuloma  Inguinale. 

Aragao  (1919).     Brazil  Medico. 

Aragao  and  Vianna  (1913).     Memor.  do  Inst.  Osw.  Cruz,  vol.  v.,  No.  2,  ref. 

(1914).  Trop.  Dis.  Bull.,  vol.  iv. 
Bonne  and  Verhangen   (1918).     Geneesk.   Tijdschr.  v.  Nederl-Indie,   vol. 

lviii.,  No.  2. 
Bosanquet  (1909).     Parasitology,  vol.  ii.,  No.  4. 

Breinl  and  Priestley  (1916).     Med.  J.  of  Australia,  vol.  i.,  March,  ref. 
Breinl  and  Priestley  (1918).     Jour.  Trop.  Med.,  February  21. 
Carter,  Markham  (1910).     Lancet,  vol.  ii. 

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CHAPTER  XCVI 
THE    DERMATOZOIASES 

Classification — Hexapode  dermatites — Creeping  eruption — Circinate  creeping 
eruption — Dermatitis  macrogyrata — Chilopode  dermatites — Acarine  der- 
matites— Copra  itch — Grain  itch — Scabies — Nematode  dermatites — 
Cestode  dermatites — References. 

CLASSIFICATION. 

The  term'  dermatozoiasis,'  in  the  widest  sense  of  the  word,  means 
any  skin  disease  of  animal  origin,  but  it  is  usually  restricted  to 
indicate  those  skin  lesions  which  are  caused  by  metazoan  parasites. 
Used  in  this  restricted  sense,  dermatozoiasis  includes: — 

I.  Hexapode  dermatites. 
II.  Chilopode  dermatites. 

III.  Acarine  dermatites. 

IV.  Nematode  dermatites. 
V.  Cestode  dermatites. 

I.  HEXAPODE  DERMATITES. 

The  Hexapode  Dermatites  include  the  lesions  of  the  skin  caused 
by  either  the  bites,  the  stings,  or  the  presence  of  the  larvae  or  the 
pregnant  female  of  various  species  of  the  Hexapoda. 

These  hexapode  dermatites  may  be  divided  into  four  classes: — 

i.  Dermatites  caused  by  bites  of  the  adult. 

2.  Dermatites  caused  by  blistering  fluids  excreted  by  the 

adult. 

3.  Dermatites  caused  by  stings  of  the  adult. 

4.  Dermatites  caused  by  the  presence  and  bites  of  the  larvae. 

5.  Dermatites  caused  by  the  presence  of  the  imago. 

||i.  Dermatites  caused  by  Bites  of  the  Adult. 

These  lesions  are  most  commonly  due  to  bites  of  species  of  the 
families  Pediculidae  (p.  753) ;  Clinocoridae  (p.  762) ;  Anthocoridae 
(p.  766) ;  Reduviidae  (p.  767) ;  Aradidae  (p.  770) ;  Culicidae  (p.  774) : 
Psychodidae  (p.  806);  Simuliidae  (p.  810),  Tabanidae  (p.  817): 
Muscidae  (p.  831),  and  by  species  of  the  orders  Siphonaptera  (p.  837) 
and  Hymenoptera  in  which  comes  the  family  Formicidae,  or  ants 
(p.  222). 


HEXAPODE  DERMATOSES  2201 

The  bites  of  these  insects  are  either  considered  in  pp.  223-226,  or 
in  the  references  given  above,  and  need  not  be  further  considered 
except  with  regard  to  the  Pediculidae.  which  cause  the  dermatosis 
called  Pediculosis. 

Pediculosis. 

Synonyms. — Phthiriasis,  Vagabond's  disease. 

Definition. — Pediculosis  is  a  term  applied  to  the  various  lesions, 
primary  and  secondary,  induced  by  the  bites  of  Pediculus  humanus 
Linnaeus,  1758,  Pedicidus  corporis  de  Geer,ji778,  and Phthirius  pubis 
Linnaeus,  1758  (pp.  755-757)- 

Remarks. — -Pediculosis  is  extremely  common  in  the  tropics, 
where  it  is  an  everyday  sight  to  see  the  lower-class  natives  busily 
employed  in  killing  the  lice  in  their  friends'  heads.  It  is  also 
commonly  present  in  all  armies  on  active  service,  and  as  lice  are 
carriers  of  such  diseases  as  typhus,  relapsing  fever,  and  trench 
fever,  etc.,  they  have  assumed  a  very  important  position  in  the 
recent  war. 

j*Etiology. — Pediculosis  is  due  to  the  irritation  caused  by  the 
venom  injected  during  the  bites  of  the  three  species  of  lice  mentioned 
in  the  definition. 

Pathology. — The  mouth  parts  of  a  louse  consist  of  two  tubes 
one  inside  the  other ;  the  outer  chitinous  tube,  called  the  proboscis, 
is  composed  of  the  fused  labrum  and  labium,  and  is  armed  with  a 
collar  of  minute  curved  hooklets,  while  the  inner  membranous  tube 
is  composed  of  the  maxilk-e  and  mandibles,  and  is  called  the  suctorial 
tube.  When  about  to  bite,  the  louse  inserts  its  hard  proboscis  into 
a  sweat  duct,  everts  its  small  hooklets,  and  thus  obtains  a  hold 
upon  the  skin.  It  then  protrudes  the  suctorial  tube,  which  it 
drives  deep  into  the  skin  of  the  host  until  it  reaches  the  blood.  It 
is  during  this  process  that  it  probably  injects  the  venom  from  its 
salivary  glands,  but  the  nature  of  this  poison  is  quite  unknown, 
although  its  presence  is  with  reason  suspected  owing  to  the  pruritus 
caused  by  the  bites  of  the  lice. 

Having  reached  the  blood,  it  proceeds  to  fill  itself  to  repletion, 
pumping  the  blood  into  its  alimentary  canal  by  means  of  the 
chitinous  pharyngeal  pump.  After  feeding,  it  withdraws  its  pro- 
boscis, and  the  blood  fills  up  the  orifice  and  coagulates,  forming  a 
minute  red  papule.  Considerable  pruritus  is  now  felt,  and  the 
victim  scratches  vigorously  to  relieve  this  sensation,  and  often 
produces  marked  excoriations,  which  may  become  secondarily 
infected  with  the  common  pyogenic  cocci,  causing  purulent  lesions. 
Repeated  biting,  associated  with  injection  of  the  venom,  and 
constant  scratching,  leads  to  pigmentation  of  the  skin,  causing 
the  so-called  pityriasis  nigra  of  Willan,  or  melanoderma  pediculis. 
If  this  process  is  continued,  the  skin  becomes  thickened  and  deeply 
pigmented,  and  forms  the  so-called  '  vagabond's  disease.'  The  pig- 
mentation is  naturally  not  observable  in  very  dark  skins,  and  may 


2202  THE  DERMATOZOIASES 

not  be  so  entirely  dependent  upon  the  scratching  as  is  usually 
stated,  but  may  be,  in  part  at  least,  caused  by  the  venom. 

Symptomatology.- — The  essential  symptom  is  pruritus,  which 
need  not  be  localized,  but  may  be  general,  accompanied  by  the 
presence  of  the  minute  papules  with  bright  red  centres,  but  this 
simple  picture  is  generally  complicated  by  the  erythema  or  ex- 
coriations set  up  by  the  scratching  induced  by  the  pruritus,  and 
this  again  may  be  complicated  by  the  appearance  of  pustules, 
due  to  secondary  pyogenic  infections,  which  dry  and  leave  scabs.  In 
these  cases  the  neighbouring  lymph  glands  are  usually  enlarged.  Very 
rarely  may  pediculosis  give  rise  to  general  symptoms,  such  as  fever. 

Varieties. — Three  clinical  varieties  of  pediculosis  are  described — 
Viz.,  pediculosis  capitis,  pediculosis  corporis,  and  pediculosis  pubis. 

Pediculosis  capitis  is  caused  by  Pediculus  humanus  Linnaeus, 
T758>  which,  though  usually  confined  to  the  hairy  regions  of  the 
head,  may  rarely  be  found  in  other  parts  of  the  body.  They  are 
grey  on  Europeans,  and  brownish  or  even  black  in  colour  upon  dark- 
skinned  natives,  and  are  said  to  be  yellow  on  Chinese,  and  orange- 
coloured  on  Hottentots.  They  often  infect  European  ladies,  prob- 
ably coming  from  the  native  ayahs,  and  thus  a  very  dark  pediculus 
may  be  found  on  a  fair  European.  They  cause  intense  irritation  of 
the  head,  and  may  give  rise  to  secondary  impetiginous  lesions  and 
enlargement  of  the  lymphatic  glands,  especially  those  of  the  back 
of  the  head,  and  in  very  dirty  people  with  long  hair  they  may  cause 
the  peculiar  condition  of  matted  hair  called  '  plica  polonica.' 

Pediculosis  corporis. — This  is  caused  by  Pediculus  corporis  de 
Geer,  1778.  These  pediculi  live  in  the  clothing,  especially  in  thick 
seams,  and  are  therefore  to  be  found  on  natives  in  the  region  of  the 
waist,  where  the  clothing  is  twisted  into  a  thickish  roll.  In  Euro- 
peans the  most  common  site  for  their  attacks  is  the  back  of  the 
shoulders,  where  the  small  papules  with  the  bright  red  centres  and 
the  linear  scratches  may  be  seen. 

Pediculosis  pubis. — Phthirius  pubis  lives  wherever  there  are 
large  thick  hairs — viz.,  on  the  hairs  of  the  pubis,  or  the  eyelids 
or  eyebrows,  and  of  the  beard  and  armpits.  Here  again  it  is  accom- 
panied by  the  characteristic  signs.  In  addition,  Morrison's  spots 
or  maculae  ceruleae  may  be  seen  in  the  form  of  small,  roundish  or 
oval  greyish-blue  maculae,  which  are  thought  by  some  authorities 
to  arise  from  the  pigment  on  the  thorax  of  the  louse  opposite  the 
anterior  pair  of  legs,  but  which  more  probably  arise  from  the  action 
of  the  venom.  The  reddish  deposits  seen  on  the  hairs  are  said  to 
be  the  faeces  of  the  parasite.  The  eggs  may  be  seen  as  small,  oval 
bodies  attached  to  the  hairs. 

Diagnosis. — The  diagnosis  depends  upon  the  history  of  pruritus 
of  a  more  or  less  severe  type,  usually  worse  in  some  given  region, 
and  by  the  appearance  of  scratches  associated  with  the  little  papules 
and  the  discovery  of  the  lice  on  the  body  or  in  the  clothing,  which 
must  be  that  usually  worn  by  the  patient.  The  rare  diffuse  pig- 
mented forms  of  pediculosis  may  be  mistaken  for  Addison's  disease 


HEXAPODE  DERMATOSES  2203 

or  the  suprarenal  form  of  malaria,  but  may  be  recognized  by  the 
rinding  of  the  lice,  the  non-diminution  of  the  muscular  power, 
and  by  the  presence  of  the  pruritus.  From  scabies  it  may  be  dis- 
tinguished by  the  lack  of  lesions  on  the  hands  and  wrists,  and  the 
absence  of  the  sarcoptes. 

Treatment. — Pediculosis  capitis  maybe  treated  by  soaking  the  hair 
with  petroleum  (care  being  taken  not  to  approach  a  light),  followed 
by  a  good  wash  with  soap  and  water,  the  whole  process  being  re- 
peated in  twenty-four  hours.  Another  method  is  to  sponge  the 
hair  little  by  little  with  carbolic  acid  (1  in  40),  or  soak  long  hair  in 
carbolic  lotion  (1  in  80)  followed  by  a  good  wash  with  soap  and  water, 
and  later  by  a  lotion  of  acetic  acid  (25  per  cent.),  used  to  loosen  the 
eggs,  which  are  then  removed  by  the  use  of  a  small-toothed  comb. 

Another  method  of  killing  the  parasites  is  by  dabbing  the  hair  with 
xylol,  remembering,  however,  the  danger  of  fire  with  this  inflam- 
mable substance. 

Impetigo  contagiosa  may  be  treated  by  an  ointment  composed 
of  ammoniated  mercury  (5  grains)  and  lard  (1  ounce),  and  in 
children  the  hair  may  be  cut  and  this  ointment  may  be  applied. 

Pediculosis  corporis. — The  clothing  and  the  bedding  must  be 
disinfected  by  steaming  or  boiling,  and  the  patient  must  have 
several  large  baths,  with  free  use  of  soap  and  water,  as  well  as  a 
soothing  calamine  lotion  (40  grains  calamine  to  1  ounce  of  water) 
for  application  to  the  irritated  skin.  Lice  destruction  is  more 
fully  detailed  on  pp.  1338,  1339. 

It  is  important  to  remember  that  the  eggs  of  P.  corporis  are  often 
attached  to  the  lanugo  hairs.  Merely  cleaning  the  clothing  is  often 
useless.  Rub  or  spray  the  whole  body  with  paraffin  and  take  a 
warm  bath. 

Martini  recommends  a  depilatory  consisting  of  strontium  sulphate  2  parts, 
zinc  oxide  1  part,  talc  1  part.  This  is  mixed  with  a  little  water  and  applied 
as  a  paste  for  ten  minutes,  when  it  is  removed  and  some  olive  oil  used  to 
soothe  the  irritation. 

Pediculosis  pubis. — A  white  precipitate  ointment  (5  to  10  per 
cent.)  or  an  ointment  of  oleate  of  mercury  (5  per  cent.,  6  drachms^) 
with  ether  (2  drachms)  will  kill  parasites  and  ova,  after  which  cala- 
mine lotion  may  be  applied  to  allay  the  irritation. 

Clinocorosis. 

Bugs  produce  wheals,  with  central  red  spots  surrounded  by  zones  of  hyper- 
aemia.  A  solution  of  menthol  (5  grains  in  1  ounce  of  rectified  spirits)  will 
relieve  the  irritation;  or,  if  the  area  has  been  scratched,  the  application  of 
a  lotion  of  carbolic  acid  (r  in  40)  is  preferable.     As  regards  prophylaxis,  see 

P-  765- 

Siphonapteriasis. 

Flea-bites  are  characterized  by  small  red  papules  with  dark  red  centres, 
and  are  to  be  distinguished  from  the  maculo-papules  of  enteric  fever,  which 
disappear  on  pressure.  The  linen  of  a  person  probably  suffering  from  flea- 
bites  should  be  inspected  for  the  brown  faecal  marks  made  by  the  fleas.  For 
further  details,  see  pp.  857  and  908.  To  keep  these  pests  away,  some  powdered 
camphor  may  be  used. 


2204  THE  DERMATOZOIASES 

Formiciasis. 

Ant-bites  usually  only  produce  local  pain,  inflammation,  and  swelling;  but 
the  larger  tropical  ants  may  cause  faintness,  shivering,  and  even  temporary 
paralysis  by  their  bites.  In  Ceylon  the  very  small  ants,  which  infest  the  beds, 
produce  urticarial  pomphi.  These  bites  are  best  treated  by  applying  a 
solution  of  carbolic  acid  (i  in  20),  and  as  a  preventative  against  ants  infecting 
beds  some  powdered  camphor  may  be  dusted  in  the  sheets  (see  p.  222). 

2.  Dermatites  caused  by  Blistering  Fluids  excreted  by  the  Adult. 

The  insects  which  act  in  this  manner  are  the  well-known  '  blister 
beetles  '  (vide  p.  226),  which  cause  the  eruption  called  '  Seasonal 
bullous  dermatitis'  (synonym,  Seasonal  vesicular  dermatitis),  which 
we  will  now  describe. 

Seasonal  Bullous  Dermatitis. 

Definition. — Seasonal  bullous  dermatitis  is  characterized  by  an 
epidemic  of  bullae  of  varying 'size  and  shape  in  healthy  people  at  a 
definite  season  of  the  year.  The  bullae  or  blisters  are  followed  by 
sensations  of  itching,  burning,  or  (pain,  and  are  caused  by  blister 
beetles. 

Historical. — Beetles  have  been  known  to  cause  blisters  and 
eschars  on  the  skin  since  the  days  of  Archigenes,  a  contemporary  of 
Celsus,  or,  according  to  other  authors,  since  the  time  of  Aretaeus 
the  Cappadocian.  Pliny  says  that  authorities  differ  as  to  the  origin 
of  the  blistering  [fluid,  some  thinking  that  it  comes  from  the  mouth 
and  others  from  the  feet.  Moffat,  in  1634,  wrote  a  long  chapter  on 
these  insects,  and  Linnaeus,  Fabricius,  and  Latreille  gathered  to- 
gether quite  an  amount  of  information  on  these  beetles  and  their 
varieties. 

In  1890  Beauregard  wrote  a  large  book  on  '  Les  Insectes  Vesi- 
cants,' but  notwithstanding  all  this  ancient  and  modern  knowledge 
works  on  tropical  medicine  were  singularly  silent  on  the  subject. 

In  1912  P.  Da  Silva  drew  attention  to  an  outbreak  of  this  eruption 
among  cultivators  on  the  banks  of  the  rivers  Sao  Francisco,  Itapi- 
curu,  and  Jacuricy,  in  the  interior  of  Bahia,  which  was  traced  to  a 
vesicant  beetle,  Pcederus  cohtmbinus.  In  1913  Adolf  Eysell  men- 
tioned P.  peregrinus  as  the  cause  of  the  same  eruption  in  the  island 
of  Sunda,  in  the  Malay  Archipelago.  In  1915  Rodhain  and  Houssiau 
saw  the  disease  in  Leopoldville,  in  the  Belgian  Congo,  and  Bequaret 
at  Boma.  In  1916  P.  A.  Ross  noted  it  at  Nairobi,  in  British  East 
Africa,  and  in  1917  Chalmers  and  King  gave  an  account  of  its  occur- 
rence in  Khartoum,  Anglo-Egyptian  Sudan. 

./Etiology. — The  blisters  are  caused  by  the  fluid  which  exudes  from 
the  joints  of  the  legs,  especially  the  so-called  knee-joint  of  certain 
species  of  insects  belonging  to  the  order  Coleoptera  Linnaeus,  1735, 
and  to  the  families  Staphylinidce  Leach,  1817,  and  Cantharidcs  Leach, 
1817.  The  following  is  a  list  of  those  known  to  cause  the  complaint, 
though  doubtless  many  more  insects  can  do  so  equally  well: — 


SEASONAL    BULLOUS  DERMATITIS  2205 

Staphylinidce  : — 

Pcederus  columbinus  de  Laporte,  1832. 
Padenis  peregrinus  Fabricius,  1801. 
Paderus  cerebripunctatus  Epp  (?).  \ 

CantharidcB  : — 

Epicanta  sapphirina  Macklin,  1845. 
Epicauta  tomentosa  Macklin,  1845. 

The  seasonal  occurrence  is]due  to  the  fact  that  the  adult  insects 
are  only  present  for  a  limited  period  in  the  year,  the  remainder  of 
which  is  occupied  by  the  long  and  complicated  development. 

Symptomatology. — So  long  as  the  insect  merely  walks  over  the 
skin,  and  is  not  irritated,  it  does  no  harm.  If,  however,  it  starts  to 
crawl  up  the  arm,  down  the  neck,  or  up  the  trousers,  it  is  soon 
annoyed  by  the  clothing  and  excretes  the  blistering  liquid. 

If  only  a  small  quantity  of  this  fluid  is  ejected,  then  only  a  single 
small  bulla  may  form,  but  if  the  insect  moves  a  series  of  these  may 
be  produced.  If,  however,  the  blistering  fluid  is  well  rubbed  into 
an  area,  then  an  eschar  forms,  with  considerable  surrounding  irri- 
tation. Occasionally,  instead  of  a  series  of  blisters,  one  long 
blister  may  extend  a  considerable  distance  along  the  forearm  or 
down  the  back. 

Usually  there  are  no  immediate  symptoms,  and  it  is  only  after  an 
interval  of  twelve  to  twenty-four  hours  that  an  itching  or  burning 
sensation,  or  even  severe  pain,  invites  attention  to  the  affected  area, 
when  the  blister  or  blisters,  varying  in  size  and  number,  as  already 
stated,  are  to  be  found  full  of  yellowish  serum  and  situated  on  an  ery- 
thematous areola. 

As  a  rule  the  victim  does  not  see  the  insect  and  may  not  remem- 
ber one  crawling  on  him,  and  he  may  be  entirely  at  a  loss  to  account 
for  the  blisters.  It  is  here  that  the  difficulty  of  diagnosis  arises  in 
that  the  practitioner  may  see  only  one  or  two  cases,  and  at  the 
moment  may  not  think  about  these  insects. 

If  pricked  and  carefully  treated,  they  quickly  vanish  and  cause 
no  further  trouble;  but  if  they  burst,  and  are  allowed  to  be  rubbed 
by  the  clothing,  they  become  raw,  very  tender,  and  painful — a  con- 
dition which  may  last  for  days. 

More  rarely  a  considerable  portion  of  the  blistering  liquid  ap- 
pears to  get  well  rubbed  into  one  spot,  and  then  a  small  white 
eschar  is  formed  which  may  be  surrounded  by  an  extensive  in- 
flammatory areola,  with  its  surface  raised  above  the  central  necro- 
tic area  and  covered  with  numerous  small  red  papules.  The  whole 
region  becomes  very  painful  and  tender,  and  some  couple  of  weeks 
elapse  before  healing  is  completed,  which  generally  takes  place 
without  any  cicatrization.  Secondary  septic  infections  are  rare. 
After  being  en  evidence  for  some  three  to  four  weeks,  the  beetles 
disappear  and  the  epidemic  ceases  for  the  year. 


2206  THE  DERMATOZOIASES 

Diagnosis. — The  characteristic  features  of  seasonrl  bullous 
dermatitis  are  as  follows : — 

i.  The  sudden  appearance  of  bullae,  varying  in  size  and  number, 
surrounded  by  a  certain  amount  of  inflammatory  redness. 

2.  The  persons  in  whom  the  bullae  are  found  are  usually  in 
good  health,  and  as  a  rule  they  are  unable  to  assign  a  cause  for 
the  eruption. 

3.  The  bulla?  are  single  or  grouped  together,  often  in  a  row. 

4.  There  is  no  tendency  to  bilateral  symmetry. 

5.  In  a  given  individual  usually  only  one  region  of  the  body  is 
affected. 

6.  A  number  of  healthy  people  living  in  the  same  place  may  be 
similarly  affected  at  the  same  time. 

7.  The  bullae  only  appear  during  a  certain  season  of  the  year. 
The  differential  diagnosis  requires  to  be  made  from  the  following 

accidents  and  diseases  causing  bullae:- — 

1.  Seasonal  bullous  dermatitis  may  be  readily  separated  from 
the  bullae  caused  by  burns  and  scalds,  and  by  chemicals,  by  the 
history  of  the  case. 

2.  It  has  also  to  be  differentiated  from  the  various  forms  of 
Hydroa  as  follows: — 

(a)  It  can  be  separated  from  the  milder  forms  of  dermatitis 
herpetiformis  by  the  absence  of  severe  itching  and  of  circinate  and 
papular  erythematous  lesions,  and  by  the  absence  of  the  tendency 
of  the  bullae  to  be  grouped  like  herpes. 

(b)  From  the  rare  form  of  dermatitis  herpetiformis  called  hydroa 
pruriginosa  it  can  be  diagnosed  by  the  larger  size  of  its  bullae, 
which  do  not  appear  in  successive  crops. 

(c)  From  dermatitis  recurrens  it  can  be  distinguished  from  the 
hiemal  variety  by  only  appearing  in  warm  weather,  and  from  the 
aestival  in  not  being  papulo-vesicular  in  character. 

3.  It  may  be  differentiated  from  herpes  zoster  by  the  absence 
of  severe  pain,  lasting  for  three  to  four  days  before  the  appearance  of 
the  eruption,  and  by  the  non-distribution  of  the  bullae  in  Head's  areas. 

4.  From  Acute  Pemphigus  it  is  easily  separated  by  the  absence 
of  the  severe  constitutional  symptoms. 

5.  It  can  be  recognized  as  distinct  from  dermatitis  venenata, 
due  to  plants,  by  the  absence  of  the  marked  oedema  and  erythema, 
which  generally  attack  the  face,  hands,  and  genitalia,  and  by  the 
presence  of  bullae. 

6.  It  is  easily  separable  from  Dermatitis  caused  by  mites,  as 
these  give  rise  to  small  wheals  and  vesicles,  and  not  to  bullae. 

7.  Ant  and  tick  bites,  stings  of  wasps,  bees,  scorpions,  centipedes, 
etc.,  are  at  once  differentiated  because  the  eruption  in  Ihe  present 
instance  is  bullous. 

As  the  eruptions  described  by  Rodhain  and  Houssiau  and  by  Ross 
are  stated  to  be  vesicular,  it  is  possible  that  these  may  be  differen- 
tiated clinically  from  this  bullous  type,  while  it  certainly  is  not 
so  severe  as  the  eruption  describe  d  by  P.  Da  Silva,  in  that  ulcera- 


HEXAPODE  DERMATOSES  2207 

tion  and  cicatrization  are  absent,  but  perhaps  these  may  be  only 
differences  in  details  and  not  in  essentials. 

Prognosis. — This  is  good.  Cases  recover  fairly  rapidly  and  as 
a  rule  without  cicatrization,  hence  the  outlook  as  regards  rapidity 
of  cure  and  the  absence  of  scarring  is  good. 

It  will,  however,  be  remembered  that  P.  Da  Silva  describes  a  much 
severer  form  of  dermatitis  than  that  mentioned  here,  and  that 
this  was  followed  by  cicatrization. 

Treatment. — The  best  treatment  is  to  prick  the  blister  and  apply 
a  dressing  of  1  in  So  carbolic  acid,  but  the  majority  of  the  victims 
just  let  the  lesions  alone,  and  they  heal  up  rather  more  slowly  than 
when  treated  and  are  more  painful.  If  they  become  rubbed,  they 
are  often  very  painful. 

3.  Dermatites  caused  by  Stings  of  Adults. 

Stings  are  mainly  caused  by  species  belonging  to  the  family 
Apidae  of  the  Hymenoptera,  which  includes  the  bees  and  wasps. 
A  description  of  these  stings  will  be  found  on  pp.  219-222. 

4.  Dermatites  caused  by  Larvae. 

The  larvae  of  various  species  of  the  (Estridae  and  Muscidae  are 
compelled  to  undergo  their  development  in  the  skin  of  some  warm- 
blooded animal,  and  as  these  are  plentiful,  as  a  rule  the  flies  do  not 
attack  man,  who  only  occasionally  suffers  from  their  effects,  and 
when  he  does  the  pathological  condition  is  usually  named  dermal 
myiasis  (p.  163 1).  Other  larvae — as,  for  example,  that  of  Auchmero- 
myia luteola  Fabricius,  1805 — are  blood-suckers. 

Blood-sucking  Dipterous  Larvae. 

Only  a  very  few  blood-sucking  dipterous  larvae  are  known,  and 
these  belong  to  two  genera,  which  may  be  distinguished  from  one 
another  as  follows: — 

A.  Abdomen  long  and  narrow,  with  unequal  segments  and 

distinctly  longer  than  the  thorax — Auchmeromyia  Schiner 
and  Bergenstamm,  1819. 

B.  Abdomen  short  and  broad,  with  equal  segments  and  but 

little  longer  than  thorax — Chceromyia  Roubaud,  191 1. 

There  are  two  species  belonging  to  the  last-named  genus — viz: — 

Chceromyia  cheer ophaga  Roubaud,  191 1. 
Cluzromyia  boneti  Roubaud,  191 1. 

Neither  arc  known  to  attack  man.  They  live  in  the  burrows  of 
the  wart-hog  and  the  ant-bear  in  the  Sudan.  There  are  also  two 
species  belonging  to  Auchmeromyia — viz: — 

Auchmeromyia  luteola  (Fabricius,  1805). 
Auchmeromyia  pragrandis  Austen,  1910. 

Both  these  may  attack  man. 


2208  THE  DERMATOZOIASES 

Auchmeromyia  luteola  (Fabricius,  1805)  lays  its  eggs  in  soil  con- 
taminated with  faecal  matter  or  urine  around  or  inside  native  huts 
in  the  Congo  (hence  its  name  Congo  floor  maggot),  Central  and 
Northern  Mozambique,  Eastern  Transvaal,  East  Africa,  Nyassaland, 
and  Kordofan.  The  larva,  escaping  from  the  egg,  seeks  the  cracks 
and  crevices  in  the  mud  floors  of  these  huts  or  pass  into  dirty  native 
mats.  When  hungry,  these  larvae  are  thermotoxically  drawn  to  a 
temperature  of  38°  C.,  and  hence  they  attack  man,  both  biting  and 
sucking  blood.  When  replete,  the  researches  of  Roubaud  show  that 
they  are  no  longer  thermophilus.  Under  favourable  conditions  the 
larvae  become  pupae  in  some  fifteen  days,  but  under  unfavourable 
circumstances  larval  existence  may  be  prolonged  for  seventy-six 
days.  Only  the  larvae  are  blood-suckeis,  and  they  may  be  killed 
by  sprinkling  the  floor  with  Jeyes'  fluid. 

Auchmeromyia  prcegrandis  Austen,  1910,  is  found  in  South  Africa. 

Irritating  Lepidopterous  Larvae. 

The  larvae  or  caterpillars  of  many  genera  of  Lepidoptera  are  well 
known  to  possess  tegumentary  glands,  which  secrete  an  irritating 
fluid,  which  passes  from  the  gland  to  hollow  hairs.  These  are  the 
instruments  by  which  the  caterpillar  injects  this  fluid  into  the  skin, 
causing  erythema  and  irritation. 

White  gives  long  lists  for  Europe  and  America,  while  Wellman  has 
studied  the  subject  in  Angola,  where  he  mentions  larvae  belonging 
to  the  Arctiidae,  Limacodidae,  and  Liparidae,  and  gives  details  con- 
cerning one — viz. : — 

Ochipia  is  a  native  name  signifying  '  that  which  burns,'  and  is 
applied  to  the  larvae  of  the  tiger-moth,  which  is  very  irritating. 

Irritating  Coleopterous  Larvae. 

Wellman  says  that  in  Angola  there  is  a  coleopterous  larva  called 
Ochisia  (Noli  me  tangere),  which  possesses  bristles  which  can  pene- 
trate into  the  sole  of  the  foot  and  cause  pain,  inflammation,  and 
sloughing.     It  is  related  to  the  genus  Drilus,  of  the  Malacodermata. 

Dermal  Myiasis. 

This  subject  has  been  discussed  in  Chapter  LXVIL,  p.  1631,  and 
need  not  be  further  mentioned,  except  to  invite  attention  to  Baier's 
work,  published  in  1740,  entitled  '  De  generatione  insect ortim  in 
corpore  humano,'  and  Clarke's  paper  in  1797  to  the  Linnaean  Society 
of  London,  establishing  the  relationship  between  the  larvae  and  the 
adult  insects  in  the  (Estridae.  Smith's  paper  at  the  1881  Inter- 
national Medical  Congress  is  also  of  interest. 

Creeping  Eruption. 

Synonyms. — Larva  migrans.  Bulgarian  :  NovaBolcst,  Pulziasta 
Bolest.  German  :  Hautmaulwarf.  Northern  Nigeria  :  Larbish  or 
CErbiss. 


CREEPING  ERUPTION 


220Q 


History. — This  disease  was  first  described  by  A.  Lee  in  1875. 
Later  on,  Procke,  Blanchard,  Topsent,  Fiilleborn,  Macfie  and  others 
have  recorded  several  cases.  It  is  not  rare  in  some  parts  of  Europe, 
Africa,  and  Asia,  and  in  South  America.  We  have  seen  numerous 
cases  injCeylon.     It  is  extreme!y,rare  in  North  America. 

/Etiology  and  Pathology.— Larvae  of  the  genera  Gastrophilus. 
G.    hcemorvoidalis   and  G.   nasalis,    (Estrotnya  satyrus,   Hypoderma 


Fig.  866. — Larva  Migrans. 


yom,  and  H.  lineata  have  been  found  in  several  cases.  In  others 
no  larva  whatever  wasjfound.  Looss  states  that  the  same  clinical 
picture  may  be  caused  occasionally  by  ancylostoma  and  strongy- 
loides  (Anguillula)  larvae,  or  even  by  an  inanimate  'object  like  ia 
piece  of  horsehair. 

Symptomatology. — The  eruption  is  characterized  by  the  presence 
of  a  narrow  raised  red  line,  £  to  1  inch  broad.  This  line  extends 
daily  one  or  several  inches,  and  is  generally  sinuous,  but  may  be 

139 


2210  THE  DERMATOZOIASES 

straight.  While  the  advancing  end  progresses,  the  opposite  end 
slowly  fades  away.  The  duration  of  the  malady  is  long — generally 
several  months,  but  occasionally  two  or  three  years.  There  is  much 
pruritus. 

Treatment. — Hypodermic  injections  of  various  disinfectants 
have  been  .ried  with  little  success.  Hutchins  recommends  a 
cocaine  injection,  followed  by  the  injection  of  I  or  2  drops  of 
chloroform. 

Circinate  Creeping  Disease. 

In  Ceylon  cases  are  met  with  of  a  peculiar  eruption,  which  is 
possibly  of  the  same  nature  as  the  creeping  disease  previously 
described,  though  larvae  were  not  found. 

The  condition  is  characterized  by  the  presence  on  the  back  of 
the  hands  of  a  ringed  eruption,  with  markedly  elevated,  thick, 
angry,  red  borders.  In  all  the  cases  the  eruption  started  suddenly 
after  the  patient  had  been  gardening  and  handling  turf.  There 
may  be  one  ring  or  several.  The  skin  inside  the  rings  is  normal. 
The  rings  expand  excentrically.  The  patients  complain  of  the 
extreme  irritation,  and  in  all  the  cases  stated  that  they  felt  some- 
thing creeping  along  the  red  circles,  as  though  a  worm  had  got 
inside  in  handling  the  turf.  The  duration  varies,  but  it  generally 
does  not  exceed  two  or  three  weeks. 

/Etiology. — -The  eruption  does  not  appear  to  be  a  form  of  derma- 
titis venenata,  due  to  touching  certain  plants  and  vegetables. 
Possibly  it  is  due  to  some  larva  entering  the  skin,  but  so  far  the 
search  for  larvae  has  been  fruitless.  No  trichophyton-like  fungus 
is  present.  | 

Treatment. — Liq.  plumbi  and  other  soothing  applications  are 
generally  useless.  The  best  results  are  obtained  by  continuously 
applying  on  lint  a  diluted  alcoholic  solution  of  resorcin: — 

Resorcin  . .  .  .  .  .  .  .  ..31. 

Sp.  rect.  .  .  .  .  .  .  .  .  .  .  .  .      gii. 

Aq.dest.  ad  Jxii 

Dermatitis  Macrogyrata. 

Dermatitis  macrogyrata  is  a  rare  condition  found  in  Ceylon  and 
South  India,  of  unknown  causation,  and  characterized  by  the 
presence  on  the  palms  of  the  hands  of  one  or  two  very  large  gyra- 
tions formed  by  scaly  and  crusty  lesions.  On  removing  the  crusts 
and  scales  a  broad  shallow  furrow  can  be  seen  situate  in  the  epi- 
dermis. The  eruption  is  associated  with  pain,  sometimes  severe, 
but  there  is  seldom  any  pruritus.  The  condition  is  most  persistent, 
and  in  our  cases  neither  fly  larvae  could  be  found  nor  fungi  isolated. 
In  none  of  our  cases  was  there  history  of  syphilis,  and  potassium 
iodide  and  mercury  had  no  effect.  The  treatment  is  most  unsatis- 
factory. Antimycotic  substances,  such  as  chrysarobin  and  tincture 
of  iodine,  have  no  effect.     The  application  of  a  lotion  of  liquor 


DERMATOMYIASIS  (JIGGER)  22 11 

plumbi  (3ii.)i  tincture  of  opium  (3i.)  diluted  with  8  ounces  of  water, 
or  of  dressing  soaked  in  o-5lper  Jcent.  oflresorcin,  may  cause  a  slight 
improvement . 


r% 

- 

$ ''■* 

***■ 

i 

v. 

J8 

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Ul 

BjBffcft 

Fig.  867. — Dermatitis  Macrogyrata. 

5.  Dermatites  caused  by  the  Presence  of  the  Imago. 

At  times  the  impregnated  |female  insect  burrows  into  the  skin 
while  the  eggs  mature. 
A  good  example  of  this  is  Dermatophilus  penetrans  Gnerin,  1838. 

D3rmatophiliasis  (Jigger). 

Synonyms. — Nigua  (Honduras),  Chique  (Salvador),  Chica  (Colum- 
bia), Bicho,  Tunga  (Brazil),  Pique  (Argentine),  Chique  (French 
Colonies) . 

Definition. — Dermatophiliasis  is  the  invasion  of  the  skin  and 
subcutaneous  tissue  by  the  pregnant  female  jigger  {Dermatophilus 
penetrans). 

Remarks. — The  home  of  the  jigger  is  in  tropical  America,  from 
230  N.  to  280  S.,  but  it  and  its  wanderings  over  the  world  have  been 
sufficiently  described  on  p.  862.  At  present  it  is  found  in  South 
America,  West  and  East  Africa,  Madagascar,  Uganda,  India,  and,  it 
is  said,  China. 

Pathology. — The  pregnant  female  jigger  pierces  the  skin  obliquely 
near  the  nails  and  between  the  toes,  but  it  may  occur  in  any  part 
of  the  foot,  and  even  on  the  arms,  scrotum,  and  face.  All  but  the 
last  two  segments  are  embedded  in  the  skin.  These  last  segments 
plug  the  orifice  and  discharge  the  egg5:. 


2212  THE  DERMATOZOIASES 

Symptomatology. — The  symptoms  begin  with  itching  and  irrita- 
tion, generally  in  some  part  of  the  foot,  especially  the  toes,  and 
often  under  the  toe-nail.  On  inspection,  a  small  dark  dot  (the  last 
two  abdominal  segments  of  the  parasite)  is  noticed  in  the  skin.  If 
left  alone,  painful  inflammation  and  suppuration  develops  around 
the  distended  abdomen  of  the  parasite,  giving  rise  to  a  swelling 
which  may  attain  the  size  of  a  small  pea,  in  the  centre  of  which  is 
seen  a  depression  containing  the  black  dot,  and,  finally,  ulceration 
takes  place,  and  the  body  of  the  parasite  is  thrown  off,  but  not 
until  all  the  eggs  are  laid. 


Fig.  868.— Dermatophiliasis.     (After  Newstead.) 

a,  Group  of  jiggers;  b,  isolated  jiggers;  c,  pits  left  by  jiggers; 
d,  lateral  view  of  jiggers  deep  in  the  skin. 

When  the  parasite  hasbeen  dislodged  by  treatment  or  suppuration, 
a  small  ulcer  is  left,  which  is  very  liable  to  septic  or  other  bacterial 
infections.  These  infections  may  lead  to  phagedena,  gangrene,  and 
tetanus.  When  the  feet  are  badly  affected,  walking  is  impossible, 
which  is  of  especial  importance  in  carriers  and  native  troops. 

Treatment. — The  treatment  is  t  he  careful  removal  of  t  he  little  insect 
with  a  clean  needle,  after  rubbing  weak  carbolic  ointment  (i  per  cent.) 
or  lotion  (i  to  2  per  cent.)  into  the  foot,  and  cleansing  and  dressing  the 
little  wound  antiscptically  with  a  lotion  of  perchloride  of  mercury. 


ACARINE  DERMATOSES  2213 

In  cases  of  heavy  infection,  Quir6s  recommends  the  use  of  petroleum,  or 
of  an  ointment  consisting  of  salicylic  acid  1  part,  ichthyol  4  parts,  vaselin  4 
parts. 

Prophylaxis. — Prophylaxis  consists  in  keeping  the  house  clean, 
and  pigs,  poultry,  and  cattle  kept  away  therefrom.  High  boots 
should  be  used,  and  especial  care  should  be  taken  not  to  go  to  a 
ground-floor  bathroom  with  bare  feet.  The  feet,  especially  the 
toes  and  under  the  nails,  should  be  carefully  examined  every  morn- 
ing to  see  if  any  black  dot  can  be  discovered,  when  the  jigger  should 
be  at  once  removed,  and  in  this  way  suppuration  will  be  prevented. 
It  is  advisable,  also,  to  sprinkle  the  floors  with  carbolic  lotion, 
Jeyes'  fluid,  or  with  pyrethrum  powder,  or  with  a  strong  infusion  of 
native  tobacco,  as  recommended  by  Low  and  Castellani. 

II.  CHILOPODE  DERMATITES. 

Centipedes,  when  they  bite,  cause  local  itching  followed  by  intense  pain, 
which  spreads  over  the  whole  limb  when  the  bite  is  on  an  extremity.  A  red 
spot  appears  at  the  site  of  the  bite,  and  this  enlarges  and  becomes  black,  and 
is  sometimes  associated  with  lymphangitis,  adenitis,  headache,  vomiting, 
dizziness,  irregular  pulse,  and  mental  anxiety. 

The  treatment  is  to  bathe  the  parts  with  a  solution  of  ammonia  (1  in  5 
or  1  in  10),  and  to  apply  a  dressing  of  the  same  solution,  and  if  there  is  much 
swelling  an  ice-bag,  while  if  the  pain  is  severe,  an  injection  of  morphia  may  be 
necessary;  while  later,  fomentations  are  required  for  the  local  inflammation 
(see  also  pp.  217-218). 

III.  ACARINE  DERMATITES. 

The  Acarine  Dermatoses  include  the  skin  lesions  caused  by  the  ticks 
andmites.  The  tick  bitesare  described  on  pp.215  and  217.  Themites 
(pp.  690-693  and  724-732)  which  most  commonly  attack  man  are: — 

Dermanyssiisle. 

Dermanyssus  gallince  de  Geer,  1778. 

Dermanyssushirudinis  Hermann,  1804. — These  mites  produce 

a  papular  eczematous  dermatitis  in  poultrymen. 
Holothyrus  coccinella  Gervais,  1842,  cause  a  swelling  in  the 

part  attacked. 

Trombidid^e. 

Microtrombidium  akamushi  Brumpt,  1910,  is  the   cause   of 
Tsutsugamushi  disease. 

Microtrombidium  holosericeum  Linnaeus,  1746,  has  a  larva 
(Leptus  autumnalis)  which  causes  irritation  in  England  in 
the  autumn,  and  is  called  the  harvest  mite.  As  a  fairly 
effective  preservative  for  this  pest  the  following  may  be 
used: — Oil  of  lavender  lllvhi.,  spirit  of  camphor  n\xxx., 
oil  of  eucalyptus  3i.,  soap  liniment  ad  §i. 

Trombidium  tlalsahuate  Lemaire,  1867,  is  the  tlalsahuate  of 
Mexico,  which,  with  the  allied  species  called  the  balata 
mite  of  the  Guianas,  are  well-known  plagues,  burrowing  into 
the  skin,  and  causing  intolerable  itching  and  painful  little 
blisters;  but  the  zoological  names  of  these,  as  well  as  of  the 


22i4  THE  DERMATOZOIASES 

'  pou  d'agonte'  of  Guiana,  the  '  niaibi '  of  New  Granada,  the 
'  Colorado  '  of  Cuba,  the  '  mouqui '  of  Para,  and  the  '  bete 
rouge  '  of  Martinique  and  Honduras,  are  not  known. 

Trombidium  wichmanni  Oudemans,  1905,  is  the  gonone  of 
Celebes,  whose  larvae  attack  man,  burrowing  into  the  skin 
as  just  described  above. 

Trombidium  vandersandei  Oudemans,  1905,  is  the  gonone  of 
New  Guinea,  which  acts  like  T.  wichmanni. 

The  Leptus  stage  of  an  unknown  Trombidium  is  reported 
in  North  Queensland. 
Tetranychid^e. 

Tetranychus  molestissimus  Weyenbergh,  1886,  causes  severe 
itching  in  the  Argentine  and  Uruguay  during  the  months 
December  to  February,  by  thrusting  its  hypostome  into 
the  skin,  and  thus  causes  '  Bicho-colorado  itch.' 

ElJPOPlD,E. 

Tydeus  molest  us  Moniez,  1889,  is  the  cause  of  '  Guano  itch.' 
Tarsonemid^e. 

Pediculoides  ventricosus  Neuport,  1850.  is  the  cause  of  'grain 
itch,'  and  being  a  parasite  of  the  pink  bollworm  of  cotton,  is 
found  in  cotton  infested  with  this  pest,  and  from  this 
source  has  attacked  persons  handling  the  infected  cotton  in 
Egypt  and  England. 
Tarsonemus  uncinates  and  T.  intcctus  are  also  known  to 
attack  man. 

TYROGLYPHID.E. 

Tyroglyphus  longior  Gervais  var.  cast  ell  anii  Hirst,  191 2,  is  the 

cause  of  '  copra  itch.' 
Tyroglyphus  siro   Linnaeus,  1758,  and  Aleurobis  jarince  de 

Geer  are  believed  to  be  the  cause  of 

vanillismus. 
Glyciphagus  prunorum  Hermann  is  the 

cause  of  '  grocer's  itch.' 
Rhizoglypiws  parasiticus  Dalgetty,  iqoi, 

is  the  cause  of  a  type    of    so-called 

'coolie  itch'  of  the  feet.     Bell  states 

that  it  causes  a  large  circular  super- 
ficial  sore   on  the  sole  of  the  foot. 

This  is  produced  by  numbers  of  the 

parasite  invading  the  skin. 
Sarcoptid^:. 

Sarcoptes  scabiei  var.  hominis  Linnaeus,     t,        0^        „, .     , 
_/o    •     ,1  f        i  •       •  Fig.    869. — Rhizoely- 

1758,  is  the  cause  <>l  scabies  m  man.  phus     parasiticus: 

In  addition   to   this   common   parasite,         Male. 

there    an-    several    varieties,    usually         (After  Dalgetty.) 

occurring    in    the    domestic   animals, 

which  may  at  times  attack  man — e.g.,  Sarcoptes  scabiei  var. 

canis,  found  in  the  dog;  S.  scabiei  var.  ovis  in  the  sheep; 


ACARINE  DERMATOSES  2215 

S.  scabiei  var.  equi  in  the  horse;  S.  scabiei  var.  suis  in  the 
pig;  S.  scabiei  var.  auchenice  in  the  lama;  S.  scabiei  var. 
cameli  in  the  camel. 
Notcedres  cati  var.  cafo'  Hering,  1838,  found  in  cats,  may  occur 
in  man. 

Demodicid^;. 

Demodex  folliculorum  Simon,  1842,  is  said  to  be  the  cause  of 
certain  inflammations  in  seborrhcea.  Some  authors  con- 
sider them  to  be  of  importance  in  the  carriage  of  certain 
diseases,  such  as  leprosy  and  cancer. 

Rarer  Acarince,  which  attack  man  occasionally,  are  Trombidium 
striaticeps  Heim  and  Oudemans,  1904,  on  fowls  and  dogs ;  T.  ameri- 
canum  Riley  and  T.  irritans ;  Metatrombidimn  poriceps  Heim  and 
Oudemans,  1904,  on  fowls  and  dogs;  Microtrombidiitm  meridionale 
and  M.  pusillum  Hermann. 

Copra  Itch. 

Definition.— A  very  pruriginous  dermatitis,  found  in  people 
handling  copra,  and  caused  by  Tyroglyphus  longior  Gervais  var. 
castellanii  Hirst  (p.  729). 

Historical  and  Geographical. — This  dermatitis  was  described  by 
Castellani  in  1911,  who  observed  it  in  Ceylon  in  people  handling 
copra,  and  considered  it  to  be  due  to  an  acarus-like  parasite,  swarm- 
ing in  many  samples  of  copra.  He  sent  the  specimens  of  the  para- 
site to  Hirst,  who  described  it  as  a  new  variety  of  Tyroglypluis — 
Tyroglyphus  longior  Gervais  var.  castellanii  Hirst. 

Castellani's  researches  have  been  recently  confirmed  by  Graham 
Little,  Whitfield  and  Ditlevsen. 

etiology.  —  The 
mite  is  present  in 
huge  numbers  in 
certain  samples  of 
copra,  and  may  occa- 
sionally be  found  on 
the  skin  of  the 
patients,  but  remains 
on  the  skin  only 
temporarily,  as  it  pIGi  g_0 — microphotograph  of  the  Tyrogly- 
does  not  bury   itself.  phus  of  Copra  Itch.    (X40.) 

It  apparently  induces 

the  dermatitis  in  the  same  manner  as  Pcdicidoides  ventricosus 
Neuport,  which  lives  in  diseased  cereals,  produces  an  eruption  in 
persons  handling  such  cereals. 

Experimental  Reproduction.-- When  copra  dust  containing  the 
mite  is  rubbed  into  the  skin,  itching  frequently  begins  very  shortly 
after,  and  twenty-four  to  forty-eight  hours  later  an  extremely 
pruriginous  urticarial  or  papuloid  eruption  often  develops.  The 
same  result  is  obtained  by  picking  the  mites  out  of  copra  dust  and 


22i6  THE  DERMATOZOIASES 

placing  them  (alone,  without  any  dust)  on  the  skin  under  a  covering, 
such  as  a  piece  of  lint  kept  in  place  by  a  bandage.  The  pustular 
stage  did  not  occur,  but  this  being  due  to  scratching  and  secondary 
pyogenic  infections,  there  was  no  time  for  it  to  develop,  all  the 
people  refusing  to  go  on  with  the  experiment  after  the  second  day. 
Some  individuals  seem  to  be  unaffected  by  the  presence  of  the 
mite  or  the  copra  dust  containing  it. 

Symptomatology. — The  hands,  arms,  legs,  and  'sometimes  the 
whole  body  except  the  face,  present  fairly  numerous,  very  prurigi- 
nous  papules,  often  covered  by  small,  bloody  crusts  due  to  scratch- 
ing; papulo-pustules  and  pustules  are  also  generally  present.  The 
eruption  has  no  tendency  to  spontaneous  cure  while  the  patient 
goes  on  working  in  the  infected  mills. 

Diagnosis. — On  superficial  examination  the  condition  may  be 
easily  mistaken  for  scabies,  but  burrows  are  not  present  and  the 
two  parasites  are  very  different. 

Treatment. — The  best  treatment  is  the  daily  application  of 
/3-naphthol  ointment  (5  to  10  per  cent.).  The  action  in  these  cases 
cannot  be  compared  to  what  takes  place  in  scabies,  because  in  copra 
itch  the  acarus-like  parasite  remains  for  only  a  short  time  on  the 
body,  and  in  most  cases  when  the  ointment  is  applied  at  night  the 
mites  are  no  longer,  there.  It  may  act  as  an  antipruritic  antiseptic, 
and  in  this  way  diminish  scratching  and  secondary  pyogenic  in- 
fections. It  is  probable  also  that  a  small  amount  of  the  ointment 
may  remain  on  the  skin  after  the  morning  bath  and  be  repellent  to 
the  mite,  in  this  way  preventing  the  daily  reinfection  which  other- 
wise takes  place. 

Grain  Itch. 

Synonyms. — Straw  itch,  Barley  itch,  Dermatitis  Schambergi,  TJrticarioid 
Dermatitis,  Dermatitis  Ditropenotus,  Aureoveridis,  Acara  Dermatitis  urti- 
carioides,  Schamberg's  disease,  Straw-mattress  disease,  Cotton-seed  Dermatitis. 

Definition. — Grain  itch  is  a  dermatosis  caused  by  Pediculoides 
ventricosus  Neuport,  1850  (vide  Figs.  343-345,  p.  728). 

History. — During  the  last  fifty  to  sixty  years  this  disease  has  been 
recognized  in  Europe,  but  only  since  1901  in  America,  when  Scham- 
berg  described  it.  In  1909,  Goldberger  and  Schamberg  found  that 
it  was  caused  by  the  same  mite  as  in  Europe.  Since  1914,  when 
Willcock  drew  attention  to  the  matter,  it  has  been  well  known  to  be 
present  in  cotton  seed  infested  with  the  pink  bollworm,  of  which  it  is  a 
parasite,  and  from  which  it  has  passed  to  man  to  Egypt  and  England. 

Climatology. — It  is  found  in  Algeria,  where  it  is  common,  and  in 
other  parts  of  Northern  Africa,  in  Italy,  and  it  is  said  to  occur  in 
India.  Cases  have  also  been  recorded  from  France,  England,  Austria, 
and  Germany.  In  France  there  was  an  epidemic  as  long  ago  as  1850 
in  Bordeaux.  In  1867  some  cases  wrere  found  in  the  department  of 
Indre  and  in  1872  in  the  Canton  of  Creon. 

/Etiology. — The  disease  is  caused  by  Pediculoides  ventricosus 
Xcuport,  which  usually  feeds  upon  the  wheat-straw  worm  (Isosoma 
grande  Riley),  the  joint  worm  (Issoma  tritici  Fitch),  the  Angou- 
mois  grain  moth  (Sitotropa  cerealeUa)  and  the  caterpillars  of  the 


SCABIES  2217 

cotton  moth  (Gelechia  gossypiella).  The  mite  attacks  people;  it 
attaches  itself  to  the  skin  by  its  sucking  discs  and  claws,  and  prob- 
ably injects  some  irritaing  substance  into  the  skin  while  attempting 
to  obtain  nourishment. 

Symptomatology. — The  mite  causes  an  urticarial  and  papuloid 
eruption  on  the  breast,  arms,  face,  neck,  and  shoulders  of  persons 
handling  corn  and  barley,  or  cotton  seed,  which  has  no  tendency  to 
spontaneous  cure  while  the  people  continue  to  handle  the  infected 
grain.  The  symptoms  begin  after  an  incubation  of  twelve  to  sixteen 
hours  with  itching  and  the  appearance  of  wheals  surmounted  by 
vesicles,  which  are  usually  about  the  size  of  a  pin's  head.  These 
vesicles  may  at  times  pustules  in  a  few  hours.  Severe  cases  show 
febrile  symptoms,  vomiting,  and  albuminuria. 

Diagnosis.— The  presence  of  an  eruption  somewhat  resembling 
lichen  urticatus  in  people  handling  grain  or  straw  or  cotton  seed, 
or  sleeping  on  new  straw  mattresses,  should  always  arouse  suspicion 
of  the  presence  of  this  mite,  and  search  for  it  should  be  made  in  the 
grain  or  straw  or  cotton  seed. 

Treatment. — The  treatment  consists  in  removal  of  the  cause — 
i.e.,  of  handling  the  infected  grain — -and  the  application  of  soothing 
lotions,  such  as  calamine  lotion,  or  a  dilute  carbolic  acid  or  acetic 
acid  lotion. 

Scabies. 

Synonyms. —  Scabrities,  Psora  (term  wrongly  applied),  Itch, 
Courap  (=itch  Bontius),  Scabies  indica  (Sauvages),  La  gale 
(French),  Kraetze  (German),  Sarna  (Madeira),  Scabbia  (Italian). 

Definition. — Scabies  is  an  infection  of  the  superficial  layers  of  the 
skin  by  the  female  of  Sarcoptes  scabiei  var.  hominis  (Linnaeus,  1758), 
which,  making  a  minute  opening  into  the  horny  layer,  forms  a 
burrow  more  or  less  parallel  to  the  surface,  and  in  so  doing  causing 
itching.  Secondary  lesions  are  vesicles  (of  which  the  most  typical 
is  at  the  far  end  of  the  burrow,  immediately  beyond  which  lies  the 
acarus),  scratches,  scabs,  pustules,  and  a  superficial  dermatitis. 

History. — Aristotle  appears  to  have  known  the  itch  insect,  but  if  this  is  true 
the  knowledge  was  lost,  and  certainly  Avenzoor  in  the  twelfth  century  deserves 
the  credit  for  discovering  or  rediscovering  it.  Scaliger,  in  1557,  described  it 
as  being  globular  in  form  and  so  minute  as  to  be  scarcely  perceptible.  He  says 
that  the  people  of  Turin  called  it  scirro,  while  in  Gascony  it  was  known  as 
brigant.  He  also  described  the  burrows,  and  in  '  Exercitatio  194,  de  Subti- 
libus,'  numero  7,  he  states  that  when  extracted  it  shows  a  certain  amount  of 
movement,  and  when  crushed  between  the  nails  causes  a  slight  noise  and 
emits  a  little  fluid.  After  this  it  was  described  by  Ingrassius  of  Naples,  by 
Gabucinus,  by  Tobertus,  by  Aldrovandus,  but  more  especially  by  Mouffet 
in  his'  Insectorum,'  completed  in  1589.  In  1654  Hauptmann,  who  called  the 
acari'  Reitleisen,'  published  the  first  figure  of  the  mite  in  1654  and  again  in 
1657.  He  was  followed  by  Haffenreffer  in  1660,  by  Heintke  in  1 675,  who  gave 
extraordinary  illustrations  of  the  arachnid,  and  by  Ettmuller  in  1682,  whose 
illustrations  are  recognizable.  In  1683  Bonomo  and  Cestoni  published  their 
letter  to  Redi  on  the  subject,  and  in  1702  this  communication  was  read  by 
Mead  before  the  Royal  Society.and  published  in  the  Philosophical  Transactions. 
Bonomo  described  and  figured  the  egg.  He  was  followed  by  Morgagni  in  his 
fittv-fifth  letter,  Book  IV.,  bv  Bonanni  in   1691;  by  Linnasus  in  1767,  who 


2218  THE  DERMATOZOIASES 

named  it  Acarus  in  his  '  Systema  Naturae,'  calling  it  Acarus  exulcerans,  but 
earlier  in  '  Entomologia  Faunas  Suecicae  '  he  termed  it  Acarus  humanus  suo- 
cutaneus,  and  in  the  thirteenth  edition  of  the  '  Systema,'  1788,  Acarus  siro  is 
separated  from  A  cams  scabiei.  It  was  described  by  Schaefier  in  1766,  by 
DeGeerin  1778,  by  Fabricius  in  1780,  by  O.  F.  Miillerin  1776,  and  by  Latreille 
as  Sarcoptes  hominis;  by  Baker  in  1744,  by  Casal  in  1762,  by  Wichman  in 
1786,  and  by  Adams  in  1905.  Adams  says  that  in  Madeira  there  is  a  disease 
due  to  ouco'es  which  is  not  itch,  being  associated  with  fever,  but  is  due  to  a 
small  animalcule.  Excluding  the  observations  (sic)  of  Gales  we  next  come  to 
Gras'  pamphlet  which  appeared  in  1834,  and  to  Raspail's  work  which  was  also 
published  in  the  same  year,  and  which  established  firmly  the  belief  in  the 
arachnid. 

In  1861  Fuerstenberg  wrote  a  monumental  work  on  the  subject 
entitled  '  De  Kratzmilben  der  Menschen  und  Thiere.'  Finally, 
in  1915,  Charles  Singer  wrote  an  interesting  history  of  the  small 
animalcule.  Notwithstanding  all  this  scientific  work,  the  derma- 
tologists were  for  long  sceptical  as  to  the  causal  action  of  the  small 
parasite — e.g.,  Bateman — but  Erasmus  Wilson,  in  1842,  was  quite 
clear  on  this  point. 

Climatology. — Scabies  is  known  all  over  the  world,  and  has  local 
names  in  all  localities.  It  is  very  common  in  the  tropics,  and  is  more 
frequently  met  with  in  the  low  country  than  in  the  hills. 

/Etiology.— The  causal  agent  is  the  mite  Sarcoptes  scabiei  var. 
hominis  (Linnaeus,  1758),  which  lives  on  the  surface  of  the  skin,  but 
after  impregnation  the  female  burrows  into  the  epidermis,  making 
a  little  orifice  marked  by  slight  fraying  of  the  horny  layer.  From 
this  orifice  it  slowly  works  its  way  more  or  less  parallel  to  the  skin, 
but  penetrating  deeper  and  deeper.  In  so  doing  it  deposits  faeces 
and  eggs  along  the  burrow,  while  the  mite  itself  lies  buried  in  the 
horny  layer  at  the  far  end  of  the  burrow  and  just  beyond  a  small 
vesicle,  which  often  marks  its  position.  It  may  be  obtained  by 
opening  the  burrow  by  means  of  a  fine  needle  until  it  reaches  the 
grey  speck  which  marks  the  mite,  which  can  then  be  extracted. 
The  female  finally  dies  in  the  burrow,  and  the  males  are  believed  to 
expire  after  copulation,  but  the  species  is  kept  in  existence  by  the 
eggs,  which  produce  six-legged  larvae  in  some  four  to  eight  days. 
These  moult  several  times,  and  then  become  the  eight-legged  nymph, 
without  fully  developed  sexual  organs,  which  finally  becomes  the 
sexually  mature  mite.  The  adult  female  is  330-450  microns  in 
length,  but  the  male  is  smaller. 

More  rarely  'scabies  '  may  be  caused  by  the  mite  belonging  to  an 
animal,  but  the  infection  in  this  instance  does  not  last  long. 

The  vesicles  and  the  irritation  are  thought  to  be  caused  by  ex- 
cretions from  the  mite. 

Infection  generally  takes  place  by  contact,  and  hence  is  more 
common  among  the  poor,  who  are  crowded  together,  whereas  in  the 
better  classes  it  usually  begins  about  the  generative  organs,  and  is 
usually  thought  to  be  spread  by  sexual  intercourse. 

Symptomatology. — The  primary  symptom  is  itching,  especially 
when  warm  and  when  in  bed,  while  the  first  clinical  sign  is  a  small 
line  on  the  surface  of  the  skin,  and  which  may  be  reddish.     If  this 


NEMATODE  DERMATOSES  2219 

line  is  carefully  examined  with  a  lens  the  orifice  of  entry  may  be 
found  as  well  as  a  minute  vesicle  at  the  farther  end,  but  this  may 
be  absent.  Just  beyond  the  end  of  the  burrow  a  small  body  of 
greyish  glittering  appearance  may  be  seen  in  the  depth  of  the  epi- 
dermis if  examined  by  means  of  a  lens.     This  body  is  the  mite. 

In  addition  to  these  primary  lesions  secondary  signs  may  be  visible 
in  the  form  of  scratches,  papules,  pustules,  and  even  eczematous 
patches. 

The  primary  sites  are  between  the  fingers.,  the  wrists,  the  ulnar 
side  of  the  hands,  the  elbows,  the  front  of  the  armpits,  the  nipples, 
the  umbilicus,  the  penis,  the  gluteal  regions,  and  between  the  toes. 
In  the  tropics  in  cleanly  people  it  is  often  confined  to  the  scrotum. 
Diagnosis. — The  characteristic  signs  are  the  burrows  and  the 
distribution  of  the  eruption,  while  the  basis  of  the  diagnosis  is  the 
discovery  of  the  mite. 

Treatment. — Order  the  patient  to  take  a  hot  bath  and  to  scrub 
himself  all  over  with  soap  and  water,  and  then  to  rub  ell  over  the 
body  sulphur  ointment  of  the  British  Pharmacopoeia  from  the 
margin  of  the  hairy  scalp  to  the  soles  of  the  feet.  Next  day  only 
the  face  is  washed,  and  that  night  more  ointment  is  rubbed  in,  and 
the  same  treatment  is  applied  another  night.  Then  on  the  fourth 
a  hot  bath  is  taken  and  all  the  clothing  and  bed  linen  changed, 
the  old  underclothing  and  bed  linen  being  disinfected  by  being  placed 
in  boiling  water. 

This  usually  cures  the  eruption,  but  a  recurrence  may  occur  in 
about  a  week  if  any  ova  have  survived,  and  may  require  a  repetition 
of  the  treatment. 

The  sulphur  ointment  may  cause  a  slight  dermatitis  with  itching, 
which  may  be  mistaken  for  a  recurrence  of  the  affection.  In  order 
to  cover  the  odour  cf  the  sulphur  a  few  drops  of  oil  of  lavender  may 
be  added. 

Prophylaxis. — Every  person  suffering  from  itch  should  be  care- 
fully and  promptly  treated  in  order  to  avoid  epidemics. 

The  horse,  sheep,  dog,  cat,  wolf,  fox,  pig,  poultry,  and  many  other  animals, 
suffer  from  scabietic  conditions  due  to  mites  more  or  less  closely  allied  to  the 
Sarcoptes  scabiei  of  man.  These  mites  may  occasionally  be  transferred  to 
man,  and  induce  a  dermatitis  which  clinically  may  resemble  scabies,  though 
as  a  rule  much  less  severe. 

IV.  NEMATODE  DERMATOSES. 

Several  species  of  the  Nematode  cause  dermatoses—  e.g.,  Rltab- 
ditis  niellyi  Blanchard,  1885  (p.  627),  Strongyloides  stercoralis  Bavay, 
1876  (p.  628),  Filaria  bancrofti  Cobbold,  1877  (p.  633).  Onchocerca 
volvulus  Leuckart,  1893  (p.  649),  Loa  loa  Guyot,  1778  (p.  645), 
A gamo filaria  gear giana  Stiles,  1906  (p.  642),  Ancylostoma  duodenalc 
Dubini,  1843  (p.  666^,  and  Necator  americanus  Stiles,  1902  (p.  673). 

The  most  important  of  these  is  the  dermatitis  caused  by  the  two 
hist-named  worms.  This  dermatosis  is  described  under  the  heading 
Ankylostomiasis  on  p.  1764. 


THE  DERMATOZOIASES 


V.  CESTODE  DERMATOSES. 


The  cestode  dermatoses  are  usually  due  to  Sparganum  prolifer 
Ijima,  1905  (p.  606),  which  produces  nodules  in  the  skin,  which  are 
associated  with  considerable  swelling,  thus  giving  rise  to  an  appear- 
ance not  unlike  elephantiasis.  In  addition,  there  may  be  an  acne-like 
eruption  all  over,  the  body,  which  is  very  irritable  and  causes 
pruritus.  On  scratching  the  papules  and  producing  excoriations 
the  worms  may  escape,  while  on  incising  a  nodule  a  cyst,  with  one 
or  two  worms  embedded  in  slimy  jelly,  or  a  watery  fluid,  may  be 
found. 

After  lasting  for  some  weeks  or  months  the  cyst  walls  become 
firm  and  thick,  and  so  encapsulate  the  worms.  The  condition  may 
last  for  years.     There  is  no  known  treatment. 


REFERENCES. 

Seasonal  Bullous  Dermatitis. 

Chalmers  and  King  (191 7).     New  Orleans  Medical  and  Surgical  Journal, 

November. 
Rodhain  and  Houssian  (191 5).     Bull.  Path.  Exot. 

Creeping  Eruption. 

Blanchard  (1901).     Arch,  de  Parasitologic 

Braun-Seifert  (1908).     Die  tierischen  Parasiten  des  Menschen. 

Crocker  (1906).     Diseases  of  the  Skin. 

Fulleborn  (1908).     Archiv  fur  Schiffs-  u.  Tro pen- Hygiene. 

Hutchins  (1908).     Journal  of  Cutaneous  Diseases. 

Macfie  (191 8).     Journ.  of  Trop.  Med.,  February  i. 

Walker  (1916).     Introduction  to  Dermatology.     Edinburgh. 

Circinate  Creeping  Disease. 

Castellani  (1905-12).     Ceylon  Medical  Reports.     Ceylon. 

Dermatophiliasis. 

Ewing  and  Hartzell  (1918).     Journ.  Econ.  Entom.,  April. 
Fulleborn  (1908).     Beihefte  Archiv  fur  Schiffs-  u.  Tro  pen- Hygiene.     Ham- 
burg. 

Acarine  Dermatoses. 

Castellani  (191 2).     Journal  of  Tropical  Medicine  and  Hygiene,  December  16. 

London.     (Copra  Itch.) 
Cleland    (1913).     Journal    of    Tropical    Medicine    and    Hygiene.     London. 

(Australian  Acarine  dermatoses.) 
Ditlevsen    (1916).     Arch.  f.  Schiffs-u.   Tropen-Hygiene,  vol.   xxii.,   No.   23. 

(Acrodermatitis  e  Copra.) 
Goldberger  (1910).     The  Straw  Itch.     Washington. 

Graham  Little  (1915).     Proc.  R.  Soc.  Med.  (Derm.  Sect.),  vol.  viii.,  No.  6. 
Hirst  (1912).     Journal  of  Tropical  Medicine,  December  16.     London. 
Nixon  (1915).     Proc.  R.  Soc.  Med.  (Dermat.  Sect.),  vol.  viii.,  No.  6. 
O'Conner  (1919).     Transactions  Soc.  of  Trop.  Med. 
Willcock  (1914).     Agricultural  Journal  of  Egypt,  June. 
Whitfield  (1915).     Proc.  R.  Soc.  of  Med.  (Derm.  Sect.),  vol.  viii  ,  No.  6. 


REFERENCES 


Noxious  Larvae. 

Wellman  (igoy).     Journal  of  Tropical  Medicine,  185.     London. 
White  (1887).     Dermatitis  Venenata.     Boston. 

Blood-sucking  Dipterous  Larvae. 

Dutton,  Todd,  and  Christy  (1904).     Liverpool  School  of  Tropical  Medicine 

xiii.  49-54.     Liverpool. 
Graham  Smith  (1914).     Non-Blood-Sucking    Flies   in    Relation  to  Disease. 

Cambridge. 
Lelean  (1904).     British  Medical  Journal,  i.  245-246.     London. 
Roubaud  (1911).     Comptes  Rendus  de  l'Academie  des  Sciences,  September, 

553-554-     Paris.     (1913).  Bulletin  de  la  Societe  Pathologie  Exotique,  vi. 

128-130,  and  Bulletin  Scientinque  de  la  France  ct  de  la  Belgique,  xlvii. 

105-202. 


CHAPTER  XCVII 
DYSIDROSES   AND    DYSTROPHIES 

Hyperidrosis — Bromidrosis — Chromidrosis,  etc. — Dysidroses:  Prickly  heat — 
Cheiropomphotyx — Dysidrosis  exfoliativa — Dystrophies  :  Leucoderma 
— -Albinism — -Melung — -Chloasma  bronzinum  —  Dermatosis  festonata 
frontalis — Dermatosis  nigro-circinata — Ochrodermatosis — Melanonychia 
■ — Xanthoderma  areatum — Mongolian  spots — Tattooing — Ainhum — Sym- 
metrical palmar  erythema — Acrodermatitis  vesiculosa — References. 

HYPERIDROSIS. 

Remarks. — -This  condition,  as  well  as  bromidrosis,  is  a  cosmopoli- 
tan one,  but  for  climatic  reasons  both  are  so  common  and  important 
in  the  tropics  that  a  short  account  of  them  is  given  in  this  chapter. 

|Synonyms, — Idiopathic  hyperidrosis,  Idrosis,  Polyidrosis,  Ephi- 
drosis  Sudatoria. 

(Symptomatology. — Excessive  perspiration  may  be  generalized  or 
localized.  In  the  latter  case  it  is  generally  symmetrical,  the  regions 
most  frequently  affected  being  the  axillary  regions,  hands,  feet, 
and  genital  regions.  Other  regions  may  be  affected.  In  one  of 
our  native  assistants  during  the  hot  season  there  is  an  extremely 
severe  localized  hyperidrosis  of  the  anterior  region  of  the  neck, 
the  sweat  falling  down  continually  in  large  drops. 

Symptomatic  Hyperidrosis.- — This  occurs  in  many  tropical  diseases, 
especially  in  malaria,  Malta  fever,  etc.  Localized  one-sided  hyper- 
idrosis has  been  observed  by  us  in  some  cases  of  frambcesia. 

Prognosis. — In  the  idiopathic  type  the  prognosis  is  good,  the 
condition  disappearing  when  the  hot  season  is  over,  but  it  is  often 
associated  with  prickly  heat. 

Treatment. — For  the  general  hyperidrosis  common  during  the 
hot  season  we  are  not  in  favour  of  any  drastic  internal  treatment 
such  as  the  administration  of  belladonna.  In  fact,  we  think  it 
may  be  dangerous  to  stop  suddenly  this  hyperidrosis,  which  is  in 
reality  merely  a  physiological  fact.  For  such  cases  we  simply  recom- 
mend using  some  potassium  permanganate,  or  cyllin,  or  a  little 
menthol  alcoholic  solution  in  the  daily  bath,  and  dusting  of  the 
body  with  any  simple  antiseptic  powder,  such  as  zinc  oxide,  starch, 
and  boric  acid  in  equal  parts  (sec  Prickly  Heat,  p.  2224). 

In  really  severe  cases  of  generalized  hyperidrosis,  belladonna  or 
atropin  may  be  administered;  but  they  stop  the  secretion  only 
for  a  time,  and  must  be  pushed  till  unpleasant  symptoms  appear. 
Sulphur  and  acid  drinks  have  little  effect,  but  they  are  harm- 


BROMIDROSIS  2223 

less.     Sulphur  is  occasionally  given  by  us  in  cachets  (3  grains) 
three  times  daily  after  meals. 

In  localized  hyperidrosis  the  treatment  varies  according  to  the 
parts  being  non-excoriated  or  excoriated.  In  patients  not  present- 
ing excoriations,  naphthol  or  salicylic  or  formalin-alcoholic  lotions 
(1  per  cent.),  followed  by  a  salicylic,  boric,  or  tannoform  powder, 
are  very  useful.  If  there  are  excoriations  or  inflammatory  signs, 
no  alcoholic  lotions  should  be  used,  but  merely  water  solutions  of 
boric  acid  (2  per  cent.),  carbolic  (1  per  cent.),  permanganate  of 
potassium  (1  in  4,000),  and  occasionally  hydrogen  perchloride 
(1  in  2,000  to  1  in  4,000),  after  which  a  salicylic  or  boric  powder 
is  applied.  It  should  be  always  remembered  to  sprinkle  with  the 
same  powder  the  socks,  shoes,  and  undergarments. 

BROMIDROSIS. 

This  term  is  used  to  denote  offensive  sweating. 

^Etiology. — The  bad  odour  seems  to  be  due  to  the  growth  of 
various  bacteria,  as  observed  by  Thin,  and  is  due  not  only  to  the 
sweat,  but  also,  and  probably  in  a  higher  degree,  to  the  sebaceous 
secretion.  The  condition  is  very  common  in  native  races — negroes, 
Indians,  and  Chinamen  ;  most  natives  seem  to  have  it  to  some 
extent,  in  fact.  On  the  other  hand,  however,  it  is  to  be  noted  that 
certain  natives  state  that  they  can  detect  in  almost  every  European 
a  special,  disagreeable  odour.  Certain  authorities  are  of  opinion 
that  each  race  has  a  recognizable  different  odour. 

Symptomatology. — As  a  rule,  when  the  sweat  has  an  offensive 
odour,  there  is  also  hyperidrosis,  but  in  certain  cases  the  quantity 
of  sweat  is  not  more  than  usual.  The  condition  is  usually  localized, 
occasionally  general.  The  situation  of  bromidrosis  is,  in  order  of 
frequency,  the  feet,  the  axillary  regions,  the  perineum,  and  genital 
organs.  When  the  condition  affects  the  feet — the  commonest 
localization — the  odour  is  most  offensive,  and  has  been  compared 
to  that  of  putrid  cheese.  When  it  affects  the  axillary  regions,  the 
odour  is  offensive,  but  as  a  rule  is  of  a  different  character. 

Symptomatic  bromidrosis  has  been  described  in  pinta,  in  certain  cases 
of  Madura  foot,  in  acanthosis  nigricans,  after  eating  certain  foods,  etc. 

In  contrast  to  bromidrosis,  cases  have  been  described  of  certain  individuals 
having  a  pleasing  smelling  sweat,  with  the  odour  of  violets  or  musk.  There 
is  a  tradition  that  certain  saints  exhaled  a  pleasant  odour. 

Prognosis. — Except  in  those  cases  when  the  bad  smell  is  due  to 
accumulated  dirt — when  a  thorough  washing  with  carbolic  soap 
will  cure  the  condition — bromidrosis  is  not  of  easy  cure,  but  the 
bad  smell  may  be  hidden  in  various  ways. 

Treatment. — This  is  the  same  as  for  hyperidrosis,  but  formalin 
lotions  (|  to  3  per  cent.),  alcoholic  or  watery,  are  especially  useful, 
Lysoform  (2  to  5  per  cent.)  is  efficacious.  Afterwards  a  powder 
such  as  ac.  salicyl.  gr.  x.,  talci  gi.,  or  ac.  borici  3i-.  talci  §i.,  should 
be  used,  and  some  boric  acid  should  be  sprinkled  in  the  socks  and 


2224  DYSIDROSES  AND  DYSTROPHIES 

also  in  the  boots.  If  there  are  excoriations,  formalin  should  not 
be  used,  but  instead  hydrogen  peroxide  (10  per  cent.)  or  potassium 
permanganate  (i  in  4,000),  followed  by  boric  powder  or  a  dermatol, 
xeroform,  or  tannoform  powder  (31.  of  any  of  these  drugs  io  gi.  of 
talci).  Internal  treatment  is  not  of  much  use,  but  sulphur  (gr.  hi.) 
three  times  daily  may  be  tried.  One  of  us  had  good  results  in  a 
case  by  the  administration  of  urotropin,  gr.  x.,  thrice  daily. 

Chromidrosis. 

The  term  is  applied  to  coloured  excretion  of  sweat  or  sebum.  The  condi- 
tion affects  in  most  cases  the  armpits,  but  cases  have  been  described  affecting 
the  face,  chest,  abdomen,  inguinal  regions,  hands,  and  feet.  The  colour  has 
been  described  as  black,  blue,  red,  green,  yellow,  and  violet.  We  have  per- 
sonally observed  only  two  cases  of  chromidrosis.  In  both  the  axillary  regions 
were  affected,  the  colour  was  brick-red,  and  the  sweat  stained  the  clothes  red. 
In  one  of  the  cases  it  was  due  to  B.  prodigiosus,  in  the  other  to  a  red  pigment- 
producing  coccus. 

Phosphoridrosis. 

Synonym. — Phosphorescent  sweat. 

This  condition  has  been  described  by  Kostor  and  others,  but  is  very  rare. 
In  one  case  it  was  stated  that  it  appeared  after  eating  phosphorescent  fish. 
According  to  Beyerink  the  phosphorescence  is  due  to  photo-bacteria. 

Uridrosis. 

Small  white  crystals,  forming  a  sort  of  hoar-frost,  are  present  on  the  skin, 
due  to  excretion  by  the  skin  of  urinary  constituents,  especially  urea  and 
chlorides.  Nash  records  several  cases  of  a  whitish  deposit  on  the  skin  in 
native  children  and  natives,  which,  according  to  some  authorities,  may  have 
been  the  same  condition. 

Haematidrosis. 

Several  cases  of  hyperidrosis  with  red  blood  cells  and  leucocytes  in  the 
sweat  have  been  placed  on  record. 

Anidrosis. 

Idiopathic  total  anidrosis,  or  absence  of  sweat,  is  exceedingly  rare,  but  a 
diminution  in  the  secretion  of  sweat  is  often  observed.  There  are  people  in 
whom  the  bringing  about  of  perspiration  by  hot-air  baths  and  drugs  is  very 
difficult. 

Symptomatic  anidrosis  is  present  in  leprotic  patches,  and  may  be  of  diag- 
nostic value.  It  is  seen  also  in  sclerodermia,  general  or  circumscribed 
(morphaea),  and  in  xerodermia.  The  secretion  of  sweat  may  be  much  de- 
creased in  diabetes  and  certain  nervous  conditions. 

DYSIDROSES. 

Prickly  Heat. 

Synonyms. — Lichen  Tropicus,  Sudamina  Papulosa,  Miliaria 
Rubra,  Miliaria  Papulosa,  Salpullido  (Cuba),  Calor  Picante  (Minorca), 
Humon  El-Nil  (Arabic). 

Definition. — Prickly  heat  is  a  papular  or  papulo-vesicular  erup- 
tion, with  marked  pruritus,  and  associated  with  profuse  sweating. 

Geographical  Distribution. — The  condition  is  found  all  over  the 
tropics  and  subtropics.  It  may  be  observed  also  in  temperate 
zones  during  the  hot  season,  especially  at  sea-bathing  places. 


DYSIDROSES 


2225 


History. — •Bontius  described  the  affection  in  his  work,  '  De 
Medicina  Indorum';  Clcghorn  in  his  book,  'Diseases  of  Minorca,' 
identifies  it  with  sudamina;  he  states  that  the  term  used  in  Minorca 
to  indicate  the  eruption  was  color  picante.  Willan,  Johnson  (1821) 
and  other  English  observers  described  it  in  India  and  other  tropical 
countries  with  the  term  Lichen  tropicus.  Armand  in  1854  describes 
it  in  his  book,  '  L'Algerie  Medicale,'  using  the  name  Lichen  miliar 
pruriginosits  ;  he  mentions  that  sea-bathing  often  increases  the 
severity  of  the  eruption.  Mestre,  in  Cuba  in  1862,  wrote  a  very 
complete  paper  on  the  condition;  he  uses  the  term  '  salpullido.' 
In  more  recent  times  the  eruption  has  been  studied  by  Robinson, 
Torok,  Durham,  and  many  others. 

/Etiology  and  Pathology. — Politzer  considers  the  disease  to  be  due 
to  the  obstruction  of  the  flow  of  sweat  brought  about  by  the  cells 
of  the  epidermis  swelling  by  imbibition  from  the  excessive  sweat. 
Pearse  considers  it  to  be  due  to  an  acute  distension  of  the  sebaceous 
glands  by  their  own  secretion.  Robinson  states  that  the  inflam- 
mation is  about  the  sweat-pore,  while,  according  to  Torok,  it  has 
nothing  to  do  with  it.  In  our  experience,  the  inflammation  is  not 
always  about  the  sweat-pore. 

Durham  believes  prickly  heat  to  be  an  infective  disease,  caused  by  a  minute 
actively  motile  amoeba ;  his  results,  however,  have  not  been  confirmed. 

Symptomatology. — This  affection  is  extremely  common  in  tropical 
countries,  especially  in  new  arrivals.  The  eruption  consists  of  small 
pin-head  papules,  which  may  enlarge  to  the  size  of  a  millet-seed,  and 
even  larger.  The  papules  are  generally  conical,  angry  red,  and  often 
occupy  the  orifices  of  the  sudoriferous  follicles;  they  are  occasion- 
ally topped  by  a  small  vesicle,  the  contents  of  which  may  later, 
occasionally,  become  purulent.  Besides  the  papules,  roseola-like 
spots  are  often  seen;  these  in  some  cases  may  coalesce  and  form 
large  erythematous  patches.  Occasionally  minute  glass-like  vesicles 
of  sudamina  crystallina  are  also  present.  The  eruption  is  found  on 
the  parts  of  the  body  where  the  patient  perspires  most.  It  is  very 
commonly  observed  round  the  waist,  the  back,  chest,  arms,  and 
forehead;  it  may  extend  to  the  whole  surface  of  the  body,  except,  it  is 
generally  stated,  the  palms  and  soles.  In  our  experience,  when  the 
eruption  is  general,  the  palms  and  soles  also  may  be  affected ;  in  such 
situations,  however,  no  papules  are  found,  but  only  roseola-like  spots. 
We  would  also  call  attention  to  another  feature  found  in  cases  of 
acute  severe  general  prickly  heat  eruption:  in  several  such  cases 
the  oral  mucosa  and  the  fauces  will  appear  acutely  congested.  The 
congestion  subsides  on  the  disappearance  of  the  cutaneous  lesions. 

Diagnosis. — This  is  generally  easy;  from  eczema  it  is  distin- 
guished by  the  greatly  increased  flow  of  perspiration,  and  by 
the  absence  of  any  moist  lesions  during  the  whole  course  of  the 
malady.  Our  experience  is,  however,  that  in  some  cases  true 
eczema — especially  of  the  papular  type — develops  on  prickly  heat 
lesions.      In   cases  of  generalized  prickly   heat,   with  roseola-like 

140 


2226  DYSIDROSES  AND  DYSTROPHIES 

spots  on  the  palms  and  soles,  acute  patchy  congestion  in  the  oral 
mucosa  and  pharynx,  a  syphilide  must  be  excluded,  for  several  of 
our  patients  believed  themselves  to  be  affected  with  syphilis;  but 
the  extreme  pruritus  is  generally  sufficient  to  exclude  it. 

Prognosis.- — As  a  rule,  the  prognosis  is  good,  the  eruption  disap- 
pearing quickly  under  proper  treatment.  Tne  patient,  however,  com- 
plains of  the  severe  itching,  which  often  keeps  him  awake  at  night.  In 
some  few  cases  no  treatment  is  of  any  avail,  and  the  patient  must  be 
sent  up  to  the  hills ;  in  others,  crops  of  boils  develop,  or  pyosis  mansoni 
or  impetigo  contagiosa  may  supervene,  especially  in  children. 

Treatment. — The  patient  must  be  kept  cool;  he  should  not  take 
much  to  drink,  and  should  abstain  from  drinking  hot  tea.  Too 
warm  clothing  should  be  avoided;  flannel  and  woollen  things  often 
make  prickly  heat  worse.  In  such  cases  silk  underclothing  may  be 
recommended,  but  not  in  people  liable  to  abdominal  chills.  All 
underclothing  must  be  changed  at  least  once  daily  and  after  taking 
any  violent  exercise.  Sea-bathing  is  injurious.  The  treatment 
which  in  our  experience  has  answered  best  is  the  free  use,  several 
times  daily,  of  a  salicylic  alcoholic  lotion  (ac.  salicyl.  3i.,  spir.  rect. 
5viii.),  followed  by  the  general  application  of  a  salicylic  or  boracic  or 
camphor  powder,  such  as  ac.  salicyl.  gr.  x.,  talci  3L,  or  ac.  borici  Ji., 
talci  ven.  gi.,  or  camphor  gr.  xxxv.,  zinci  ox.  amyli  aa  gss.  It  is 
better,  as  a  rule,  to  avoid  greasy  preparations. 

After  the  eruption  is  cured  the  patient  should  be  directed  to  use 
some  Condy's  fluid,  cyllin,  or  other  disinfectant  in  the  bath,  and 
afterwards  to  apply  one  of  the  powders  mentioned  above. 

The  so-called  '  Castellani's  lotion,'  much  used  in  the  East,  consists  of 
menthol  gr.  x.,  ac.  salicyl.  gr.  ii.,  zinci  ox.  3vi.,  calaminae  3hi.,  spirit,  rect.  gii., 
glycerin.  3L,  aq.  rosae  ad  §vi.  It  should  be  diluted  with  the  same  amount  of 
water  when  applied  to  the  face  or  when  used  for  children. 

Cheiropompholyx. 

Synonyms. — Dysidrosis,  Pompholyx. 

This  affection  is  seen  in  the  tropics,  and  is  also  met  with  in  tem- 
perate zones  during  the  hot  season.  To  Tilbury  Fox  and  J.  Hutchin- 
son belongs  the  merit  of  having  separated  this  affection  from  eczema. 

./Etiology  and  Histopathology. — Tilbury  Fox  believed  the  disease 
to  be  due  to  accumulation  of  sweat  induced  by  the  blocking  of  the 
pores  of  the  sudoriparous  glands.  The  more  recent  researches  of 
Unna,  Norman  Walker,  Williams,  and  others  show  that  the  lesions 
are  of  an  inflammatory  character;  the  vesicles  are  found  in  the 
prickly  layer,  and  often  press  to  one  side  of  the  sweat  channel. 

Unna  described  a  bacillus  as  the  cause  of  the  disease.  Some  authorities 
consider  the  condition  to  be  of  neurotic  origin. 

Symptomatology. — The  eruption  is  found  in  individuals  who 
suffer  from  hyperidrosis.  It  is  characterized  by  the  presence  of 
deeply  ,seated  translucent  or  opalescent,  sago-like  vesicles  between 
the  fingers  and  toes;  the  vesicles  are  not,  as  a  rule,  surrounded  by 


DY  SID  ROSES  2227 

an  inflammatory  halo;  they  very  rarely  coalesce,  and  usually  do  not 
break,  but  dry  up  gradually,  being  thrown  off  with  the  exfoliating 
epidermis.  The  vesicles  in  many  cases  are  few  in  number ;  in  others 
they  may  be  numerous,  and  the  eruption  may  extend  to  the  palms, 
backs  of  the  hands,  and  occasionally  the  arms.  There  is  unbearable 
pruritus,  and  in  some  cases,  owing  to  the  scratching,  an  eczematous 
dermatitis  may  develop,  especially  between  the  toes. 

Diagnosis. — Some  authorities  still  maintain  that  cheiropompholyx 
is  merely  eczema.  In  our  experience,  the  disease  must  be  separated 
from  eczema,  the  principal  characters  of  differentiation  being  the 
deep  situation  of  the  vesicles,  the  fact  that  they  very  rarely  rupture, 
and  that,  as  a  rule,  they  are  not  surrounded  by  an  inflammatory 
zone;  moreover,  the  parts  affected  are  generally  bathed  in  sweat. 

Prognosis. — The  disease  is  not  a  serious  one,  and,  under  proper 
treatment,  the  eruption  heals;  but  the  tendency  to  recur  is  great. 

Treatment.— When  the  vesicles  are  few  in  number,  pricking  them 
with  a  sterile  needle,  washing  them  with  a  perchloride  lotion  (1  in 
2,000),  followed  by  the  application  of  a  1  to  2  per  cent,  naphthol  oint- 
ment, gives  much  relief.  When  the  vesicles  are  numerous,  and  the 
eruption  has  spread  to  the  backs  of  the  hands  and  arms,  calamine 
lotion,  to  which  a  little  menthol  and  alcohol  has  been  added,  answers 
well,  or  a  salicylic  alcoholic  lotion  (ac.  salicyl.  &.,  alcohol  rect.  §iv., 
aq.  ad  gviii.)  may  be  used. 

Dysidrosis  exfoliativa. 

This  affection,  described  by  Castellani,  is  closely  related  to 
cheiropompholyx.  The  affected  parts — generally  the  palms  of  the 
hands — are  bathed  in  continuous  perspiration,  and  large  flakes  of 
epidermis  exfoliate.  In  most  cases  no  cheiropompholyx-like  vesicles 
are  found;  in  fact,  no  vesicles  of  any  type  can  be  detected.  The 
affection  becomes  cured  spontaneously  on  the  patient  going  to  the 
hills  or  during  the  cold  season,  but  it  is  apt  to  recur. 

Bathing  the  affected  parts  with  a  resorcin  lotion  (|  per  cent.)  at 
first,  and  later,  when  the  desquamation  has  ceased,  the  application 
of  calamine  lotion,  is  useful. 

Sweat  Desquamation. 

Schornberg  has  applied  the  term  '  sweat  desquamation  '  to  the  minute 
whitish  scales,  often  arranged  in  rings,  and  found  on  the  palms  of  persons 
who  perspire  profusely.  The  condition  may  occasionally  be  confused  with 
a  syphilide,  from  which  it  is  differentiated  by  the  absence  of  other  syphilitic 
signs,  such  as  enlargement  of  the  lymphatic  glands,  etc.,  and  by  the  fact 
that  it  disappears  on  the  patient  going  to  the  hills. 

DYSTROPHIES. 

Leucoderma. 

Synonyms. — Leucopathia,  Vitiligo,  Acquired  leucopathia,  Ac- 
quired leukasmus,  Acquired  achromia,  Acquired  piebald  skin,  Mala- 
die  de  depigmentation  (O'Zoux). 


DYSIDROSES  AND  DYSTROPHIES 


Leucoderma  is  much  more  common  in  tropical  countries  than  in 
temperate  zones.     The  natives  of  Ceylon  and  India  have  a  dread  of 

developing  leucoderma,  and 
look  upon  it  as  a  loathsome 
disease. 

etiology  and  Pathology. — 
The  aetiology  is  unknown. 
It  is  generally  considered  to 
be  a  trophoneurosis.  Occa- 
sionally there  is  evidence  of 
hereditary  influences,  several 
members  of  the  same  family 
being  affected.  The  malady 
may  start  without  any 
apparent  cause,  or  in  some 
cases  may  begin  after  an 
injury,  after  a  burn,  after 
too  strong  a  caustication. 
In  fact,  the  application  of 
strong  remedies  should  be 
used  with  care  in  natives. 
We  have  seen  leucoderma 
patches  appearing  after  the 
application  of  pure  formalin. 
Patches  of  leucoderma  may 
develop  also  in  chronic  epiphytic  skin  diseases,  the  fungi  apparently 
having  a  deeply  disturbing  effect  on  the  pigment  formation. 


Fig.  871. — Leucoderma  in  a  Sinhalese 
Woman. 


Fig.  872. — Leucoderma  of  the  Hands  and  Arms. 

Symptomatology. — Leucoderma  is  characterized  by  the  presence 
of  non-pigmented  areas,  white,  ivory-like,  or  pinkish.  The  patches 
are  roundish  or  oval,  with  a  smooth  surface;  they  slowly  enlarge 
and  coalesce,  giving  rise  to  large,  irregularly  outlined  areas.  Occa- 
sionally almost  the  whole  body  becomes  affected;  more  often  it  is 


DYSTROPHIES 


!22Q 


the  face  and  hands  which  are  affected,  and  there  may  be  a  certain 
symmetry.  The  initial  patches  are  often  surrounded  by  a  zone 
of  hyperpigmentation.  Occasionally  within  the  white  areas  small 
dot-like  zones  of  pigmentation  arc  left.  The  hairs  of  the  affected 
parts  frequently  become  white,  but  sometimes  remain  of  normal 
colour.  The  white  patches  do  not  show  any  marked  change  in 
sensation;  there  is  never  anaesthesia;  in  many  cases  there  is  hyper- 
esthesia to  heat  and  light  stimulation.  The  texture  of  the  skin  re- 
mains normal;  occasionally  slight  atrophic  processes  may  be  noted. 
It  is  usually  stated  that  the 
general  health  is  not  im- 
paired. In  our  experience, 
however,  when  the  patches 
are  large  and  situated  on 
uncovered  parts  of  the 
body,  especially  the  face, 
symptoms  of  severe  as- 
thenia have  been  noticed. 
Moreover,  the  patients 
complain  that  they  cannot 
do  any  work  in  the  sun, 
as  they  experience  a 
burning  sensation  in  the 
white  patches,  and  they 
suffer  from  giddiness. 

Clinical  Varieties  — 
Melung  {Beta). — This  type 
of  leucoderma  was  first 
described      by      Ziemann, 

fairly     common 

West        African 

It  is  found  also 
in  Ceylon,  India,  and 
Burma,  in  the  last-men- 
tioned country  having 
been  described  by  Castor. 
The  affection  is  always 
symmetric,  and  attacks 
only  the  palms  or  the  soles, 
or  both  palms  and  soles. 
Small    areas    of    the    skin 


and     is 
among 

negroes. 


Fig.  873. — Leucoderma  in  a  Sinhalese. 


undergo  a  slow  process  of  depigmentation,  becoming  whitish  or 
yellowish;  there  is  no  alteration  of  sensibility.  The  depigmented 
areas,  which  are  generally  of  various  shape,  are  intermixed  with 
patches  of  normally  pigmented  skin,  so  that  the  palms  and  soles 
present  a  marmoriform  appearance. 

The  disease  is  chronic  and  incurable.  It  often  develops  in  child- 
hood, and  several  members  of  the  same  family  may  be  affected. 

A  variety  of  leucoderma  in  the  shape  of  two  small,  often  triangular 


2230  DYSIDROSES  AND  DYSTROPHIES 

spots,  one  at  each  angle  of  the  mouth,  has  been  observed  by  Pusey 
in  a  Burmese  girl  and  by  one  of  us  in  Ceylon.  The  mucosa  of  the 
lips  may  also  show  leucodermic  patches. 

Diagnosis.— The  diagnosis  is  generally  easy.  The  patches,  in  con- 
trast to  leprosy,  do  not  show  anaesthesia;  from  morphcea  it  is  distin- 
guished by  the  absence  of  any  abnormality  in  the  texture  of  the 
skin;  from  tinea  flava,  tinea  alba,  and  pinta,  by  the  absence  of  any 
fungus. 

Prognosis. — The  disease  may  be  said  to  be  incurable.  When  large 
patches  are  present,  the  patient  complains  often  of  asthenia,  and 
may  become  unfit  for  work,  especially  work  in  the  open  air  and  sun. 
Treatment. — The  disease  is  generally  incurable,  but  the  spreading 
of  the  patches  may  be  prevented,  and  occasionally  a  slight  improve- 
ment may  be  brought  about,  in  our  experience,  by  an  energetic 
arsenical  treatment.  We  generally  give  arsenious  acid  in  a  pill 
(gr.  5^)  three  to  six  times  a  day,  or  atoxyl  injections  (5  grains  every 
other  day).  Gillmore  has  tried  soamin  with  fairly  good  results. 
We  have  seen  no  benefit  from  the  administration  of  suprarenal 
extract,  as  recommended  by  several  authors.  The  white  colour 
may  be  partially  hidden  by  applying  a  lotion  of  nitrate  of  silver 
or  potassium  permanganate,  or  by  tattooing. 

Heidingsfelt  has  devised  an  instrument  consisting  of  a  group  of  ten  needles, 
which  are  put  in  movement  by  electrical  power.  In  this  way  tattooing  may 
be  performed  much  more  rapidly  than  by  hand. 

Sommer  claims  to  have  cured  several  cases  of  leucoderma  by  injections  of 
adrenalin. 

Albinism. 

Synonyms.  —  Congenital  leucoderma,  Congenital  leukopathia, 
Congenital  achromia,  Congenital  leukasmus. 

The  affection  is  found  in  the  tropics  more  frequently  than  in 
temperate  zones.  It  is  characterized  by  congenital  absence  of 
pigment  in  the  skin,  hair,  iris,  and  choroid.  There  are  cases,  how- 
ever, of  partial  albinism  in  which  only  the  skin  is  affected.  The 
skin  has  a  milky-white  or  pinkish  appearance;  the  iris  is  rose- 
coloured,  and  the  pupil  red.  There  is  intolerance  to  light;  hence 
the  pupils  will  be  generally  found  to  be  contracted,  and  the  patient, 
to  avoid  the  strong  light  stimulus,  may  go  about  with  the  head 
downwards.  Nystagmus  is  observed  in  several  cases.  The  hair  is 
generally  white  or  yellowish-white,  fine  and  silky.  We  have  seen 
albinos  with  red  hair.  Albinos  are  generally  poorly  built,  weak  and 
feeble  individuals. 

/Etiology  and  Pathology. — The  aetiology  is  unknown.  The  affec- 
tion is  more  often  observed  among  coloured  races  than  in  the  white 
races.  It  shows  a  certain  family  tendency.  It  is  said  that  cases 
occur  more  frequently  in  the  offsprings  of  consanguineous  marriages. 
The  histological  examination  of  the  skin  shows  absence  of  pigment 
as  the  only  abnormality. 

Treatment. — The  affection  is  incurable. 


DYSTROPHIES  2231 

Erythema  Solare. 

The  effects  of  sunlight  on  the  skin,  including  the  histology  of  the 
lesions,  have  already  been  discussed  in  Chapter  HI.,  pp.  83-85. 
They  are  caused  by  the  active  effects  of  the  rays  at  the  violet  end 
of  the  spectrum.  The  skin  of  the  parts  exposed  becomes 
erythematous,  swollen,  and  vesicles  and  bullse  may  appear. 
Desquamation  follows,  and  the  skin  is  often  left  pigmented 
(sunburn) . 

The  treatment  consists  in  applying  calamine  lotion,  and  later  ;any 
bland  ointment  such  as  simple  cold  cream. 

Dermatitis  Solaris. 

After  repeated  attacks  of  erythema  solare — or  at  times  without 
any  history  of  such — the  skin  of  the  hands  and  exposed  parts 
in  planters  and  other  people  living  an  outdoor  life  in  the  tropics 
becomes  slowly  reddened,  and  may  be  slightly  rough  to  the  touch. 
Freckles  and  hyperpigmented  spots  are  generally  present,  and  not 
rarely  small  telangiectasia.  In  a  later  stage  warty  patches  often 
appear,  and  the  dermatitis,  as  noted  by  McLeod,  may  somewhat 
resemble  the  dermatitis  produced  by  X  rays.  Atrophic  changes 
may  also  develop.  The  condition,  which  is  also  known  by  the  term 
tropical  skin,  is  somewhat  similar  to  what  Unna  called  '  seaman's 
skin  '  and  to  senile  atrophodermia  or  biotripsis  (seep.  2282). 

Diagnosis. — The  diagnosis  from  pellagra  has  already  been  dis- 
cussed (see  p.  1730). 

Prognosis. — The  dermatitis  is  very  obstinate,  but  generally 
becomes  cured  spontaneously  in  a  cold  climate. 

Treatment.— A  change  to  a  temperate  climate  is  the  only  effica- 
cious treatment.  Exposure  to  the  sun  is  to  be  avoided  as  much  as 
possible. 

Chloasma. 

Chloasma,  which,  as  is  well  known,  is  characterized  by  the  presence 
of  dark  brownish  or  dirty  yellowish  patches,  situated  commonly 
on  the  face,  is  of  frequent  occurrence  in  the  tropics  in  Europeans 
as  well  as  natives.  The  patches  are  plainly  distinguishable  in  the 
skin  of  Indian  and  Sinhalese  natives,  though  in  African  negroes 
they  may  be  indistinguishable.  The  condition  may  be  due  to 
several  causes,  and  the  following  types  may  be  mentioned: — 

1.  Chloasma  solare  (melasma  solare),  due  to  exposure  to  the 
sun.  A  similar  condition  may  be  due  to  exposure  to  a  powerful 
light  or  glare  of  any  kind,  and  may  even  occasionally  develop  in 
people  who  pass  a  long  time  on  glaciers  and  fields  of  snow.  Chloasma 
solare  is  found  among  Europeans,  half-castes,  and  also  in  natives. 
In  natives  who  wear  clothes  it  is  easy  to  see  that  the  parts  exposed 
to  the  sun  are  darker.  The  condition  is  generally  found  on  the 
face,  and  it  may  be  diffuse,  or  one  or  two  small  patches  only  may 
be  present.     The  colour  varies  from  a  slight  yeUowish-brownish 


2232  DYSIDROSES  AND  DYSTROPHIES 

to  a  deep  black  bronzine  one  (see  Chloasma  Bronzinum).  On  close 
examination  it  will  be  found  that  often  patches  of  hyper  pigmenta- 
tion are  seen  side  by  side  or  alternate  with  patches  of  depigmentation 
of  various  degree,  but  generally  slight.  The  patches  of  chloasma 
solare  may  appear  quite  suddenly  without  being  preceded  by 
erythema  solare;  in  one  of  our  cases  they  appeared  on  the  fore- 
head twenty-four  hours  after  a  motor-car  drive  in  the  midday  sun 
without  the  hood  on;  in  another,  a  European  lady,  who  had  a 
very  delicate  skin  and  was  used  to  wearing  gloves,  very  dark 
hyperpigmented  patches  appeared  on  the  back  of  the  hands  and 
wrists  twelve  hours  after  exposing  her  hands  without  gloves  to  the 
midday  sun.  In  addition  to  hyperpigmented  spots,  depigmented 
patches  also  developed. 

2.  Chloasma  caloricum,  from  exposure  to  heat,  or  possibly  the 
glare  of  fires.     We  have  seen  it  several  times  in  stokers. 

3.  Chloasma  traumaticum,  from  mechanical  irritation  of  any 
kind,  scratching,  etc. 

4.  Chloasma  toxicum,  due  to  irritating  drugs,  as,  for  instance, 
after  a  blister. 

5.  Chloasma  symptomaticum,  as,  for  instance,  chloasma  uterinum, 
found  during  pregnancy  or  during  chronic  diseases  of  the  female 
genital  organs.  Chloasma  uterinum  is  quite  common  in  Sinhalese 
women,  and  is  plainly  distinguishable. 

6.  Chloasma  malaricum  and  kala-azar  chloasma,  an  important 
type  of  chloasma  symptomaticum,  is  found  inpatients  suffering  from 
chronic  malaria  and  kala-azar.  A  diffuse  type  of  hyperpigmenta- 
tion  observed  in  chronic  malaria  and  closely  resembling  Addison's 
disease  has  already  been  described  (see  p.  1180). 

Hyperpigmentation  may  occur  also  in  syphilis,  leprosy,  tuber- 
culosis, diabetes,  and  many  other  chronic  diseases. 

In  India  a  '  pigmentary  fever  '  has  been  described  of  short 
duration,  and  said  to  be  characterized  by  the  appearance  of  hyper- 
pigmented patches  on  the  face  (see  p.  1461). 

Chloasma  Symmetricum. 

'  This  condition,  which  has  been  described  Castellani,  is  often 
met  with  in  Sinhalese,  who  greatly  object  to  it.  It  is  characterized 
by  the  presence  of  two  dark  brownish  chloasma  patches  situated 
symmetrically  one  on  each  cheek,  generally  on  the  malar  region. 
In  some  cases,  in  addition  to  these  two  patches,  a  third  one  is  found 
on  the  nose.  The  colour  of  the  patches  is  generally  dark  brownish, 
very  rarely  bronzine.  The  causation  is  unknown;  it  does  not  seem 
to  be  congenital.     No  treatment  is  of  any  avail. 

Chloasma  Bronzinum. 

This  somewhat  rare  affection  is  met  with  among  natives  as  well 
as  Europeans  in  India,  Ceylon,  the  Malay  States,  China,  and  other 


PLATE    XIV. 


CHLOASMA  BRONZINUM. 


oWaierstoiv  4  Sone  Ltd  Edm 


To  face  page  2232 


DYSTROPHIES 


2233 


tropical  countries.  It  was  first  observed  by  Cantlie,  who  called  it 
'  tropical  mask,'  and  was  later  described  by  one  of  us. 

/Etiology. — This  is  unknown,  but  a  life  in  the  open  air  with  daily 
long  exposure  to  a  tropical  sun  is  apparently  an  important  pre- 
-disposing  cause.  All  our  patients  were  European  planters,  or  native 
overseers  or  coolies. 

Symptoms.— Part  of  the  face  or  the  neck,  or  occasionally  the  whole 
face,  neck,  and  chest,  presents  a  peculiar  pigmentation,  resembling 
a  black  bronzine  mask;  the  pigmented  areas  slowly  but  steadily 
increase.  The  disease  is  very  chronic  and  incurable  if  the  patient 
remains  in  the  tropics.  The  general  health  is  not  impaired.  The 
examination  of  the  various  organs  is  negative.  The  blood  and 
urine  are  normal. 


Fig.  874. — Chloasma  Symmetricum. 


Diagnosis.— This  is  easy,  even  in  very  dark-skinned  natives,  the 
affected  parts  being  completely  black,  and  having  a  characteristic 
bronzine  hue. 

From  ordinary  chloasma,  which  is  not  rare — especially  among 
women — the  affection  is  easily  distinguished  by  the  bronzine  tint. 
The  absence  of  asthenia,  loss  of  flesh,  and  diarrhoea,  will  suffice  to 
distinguish  chloasma  bromArmmirom  Addison's  disease ;  the  history 
and  the  examination  of  the  blood  will  differentiate  it  from  malarial 
pseudo- Addison's  disease  ;  the  examination  of  the  urine  will  dis- 
tinguish it  from  diabetes  bronzinum.  Argyria  will  be  excluded  by 
the  history  and  by  the  fact  that  in  chloasma  bronzinum  the  mucosa? 
are  not  affected.  In  ochronosis  the  cartilages,  ligaments,  and  fibrous 
structures  become  pigmented,  and  the  discoloration  is  best  seen 
about  the  knuckles  and  the  tendons  of  the  hands  and  feet;  more- 
over, the  urine  often  blackens  on  exposure  to  the  air  (alcaptonuria). 

Prognosis  and  Treatment. — The  disease  seems  to  be  incurable, 
but  a  long  stay  in  a  temperate  zone  generally  improves  it. 


2234 


DYSIDROSES  AND  DYSTROPHIES 


Dermatosis  Festonata  Frontalis. 

Historical  and  Geographical. — This  condition  has  been  described 
by  Castellani  in  Ceylon.  It  has  recently  been  found  also  in 
IVlacedonia. 

Etiology . — This  is  unknown,  but  probably  a  continuous  exposure 
to  the  sun  and  glare  plays  a  certain  role  in  the  causation  of  the 
malady. 

Symptomatology. — The  affection,  which  in  its  severe  type  is  rare, 
is  found  in  Europeans  who  have  resided  for  many  years  in  the  tropics, 
and  who  have  lived  an  open-air  life,  such  as  planters  and  overseers, 
exposing  themselves  to  the  sun  for  long  periods  of  time. 

In  a  well-marked  case  (see  Fig.  875)  there  is  a  festooned  margin, 
at  times  slightly  raised,  often  of  a  vivid  bright  red  or  coppery  red 
colour,  while  the  skin  which  it  encircles  has  a  peculiar  whitish, 
occasionally   leucoderma-like    appearance,    and    may   be    slightly 


Fig.  875. — Dermatosis  Festonata  Frontalis. 

atrophied;  at  times  small  patches  of  hyperpigmentation  may  be 
present.  There  is  very  little  or  no  pruritus,  and  sensation  to  the 
touch,  pain,  heat,  and  coldjis  not  impaired. 

The  course  is  extremely  long,  the  affection  slowly  expanding 
peripherally,  and  in  a  tropical  climate  has  no  tendency  to  spon- 
taneous cure. 

Diagnosis. — The  affection  is  not  rarely  taken  for  a  tricophytic 
condition,  but  the  microscopical  examination  for  fungi  is  always 
negative,  and  an  antimycotic  treatment  does  not  induce  any  im- 
provement. From  a  syphilide  it  is  differentiated  by  the  negative 
Wassermann  and  by  the  uselessness  of  salvarsan,  potassium  iodide, 
and  mercury;  from  leprosy  by  the  sensation  being  normal. 

Prognosis. — The  general  health  of  the  patient  is  not  affected,  but 
the  affection  runs  an  extremely  long  course,  and  has  no  tendency 
to  spontaneous  cure  in  the  tropics.  It  gets  much  better  if  the  patient 
goes  to  reside  in  a  cold  country. 


DYSTROPHIES  2235 

Treatment.— The  treatment  is  very  unsatisfactory.  The  patient 
must  be  advised  not  to  expose  himself  to  the  sun  and  glare,  though  it 
is  doubtful  whether  the  condition  is  directly  due  to  such  exposure. 
A  wide-brimmed  topee  or  sun-helmet  lined  with  red  cloth  may  be 
used. 

Of  the  many  drugs  tried  ichthyol  seems  to  be  the  only  one  which 
at  times  keeps  in  check  the  condition,  occasionally  inducing  a 
slight  improvement.  It  is  given  internally  in  5  grain  doses  three 
times  daily  before  meals,  and  an  ichthyol  ointment  or  lotion 
(5  per  cent.)  may  be  applied  to  the  affected  skin  at  night,  while 
during  the  day  a  calamine  lotion  may  be  used. 

Mercury,  potassium  iodide,  and  arsenical  preparations  are  useless. 

Dermatosis  Nigro-Anulata. 

Historical  and  Geographical. — This  condition  has  been  described 
by  Castellani  in  Ceylon  natives  and  in  a  very  dark-skinned  gipsy 
in  Macedonia. 

/Etiology  and  Pathology. — This  is  unknown.  It  is  not  a  frambce- 
side,  as  the  lesions  are  not  influenced  by  salvarsan  and  potassium 
iodide;  nor  a  syphilide,  as  they  are  not  influenced  by  the  same  drugs 
nor  by  mercury;  moreover,  Wassermann  is  negative. 

Symptomatology. — The  condition  is  characterized  by  the  presence 
of  black,  elevated,  fairly  hard,  ring-like  or  elliptical  multiple  lesions, 
encircling  apparently  normal  skin.  There  is  no  pruritus,  sensation 
normal,  Wassermann  negative.  The  course  is  extremely  long, 
lasting  for  years,  with  very  little  change  in  the  aspect  of  the  lesions. 


^ 

:■. 

• 

1 

HB 

Fig.  876. — Dermatosis  Nigro-Anulata. 

Diagnosis. — The  affection  has  to  be  distinguished  hom  tinea  mgro- 
circinata  by  the  absence  of  fungi,  and  by  the  failure  of  any  anti- 
mycotic  treatment ;  from  a  circinate  jrambceside  by  the  uselessness 
of  potassium  iodide  and  salvarsan;  from  a  syphilide  by  the  useless- 
ness of  the  same  drugs Jand  of  mercury;  from  porokeratosis  jbyj.he 
multiplicity  of  the  lesions. 

Prognosis. — The  general  health  is  not  affected,  but  the  condition 
is  "most  persistent. 

Treatment. — This  is  very  unsatisfactory.  An  exfoliative  treat- 
ment by  means  of  a  salicylic  acid  ointment  occasionally  induces 
a  temporary  improvement. 


2236  DYSIDROSES  AND  DYSTROPHIES 


Ochrodermatosis. 

Synonym. — The  yellow  disease  (Castellani). 

Historical  and  Geographical. — This  condition  has  been  described 
by  Castellani  in  Ceylon,  in  Europeans  living  in  the  low  country. 

/Etiology. — Unknown.  The  patients  were  not  taking  any  drug 
and  were  not  exposing  themselves  to  the  action  of  any  toxic  sub- 
stance. On  the  strength  that  the  condition  gets  much  better  or 
disappears  on  the  patient  going  to  the  hills,  a  search  for  a  possible 
causative  organism  was  carried  out,  but  with  negative  results. 

Symptomatology. — The  face,  arms,  hands,  and  at  times  the  whole 
body,  are  of  a  bright  yellow  or  saffron  colour,  quite  different  from 
the  yellowish-greenish  colour  of  jaundice.  The  sclerotica?  remain 
completely  white;  the  urine  is  of  normal  colour  and  composition; 
the  sweat  is  not  coloured;  the  stools  are  normally  pigmented; 
the  liver  and  spleen  are  not  enlarged;  and  the  general  health  is  in 
no  way  affected;  but  naturally  the  patients  greatly  object  to  the 
disfigurement.  The  condition  improves  or  disappears  on  the 
patient  going  to  the  hills  or  to  Europe. 

Diagnosis. — The  bright  yellow  or  saffron  colour  is  different  from 
the  yellow  colour  generally  seen  in  jaundice.  Moreover,  the 
sclerotica?  remain  white,  and  the  urine  and  stools  are  of  normal 
colour.  The  anamnesis  and  special  analysis  of  urine  for  picric 
acid,  etc.,  exclude  the  ordinary  toxic  pigmentations.  The  condition 
is  distinguished  from  certain  types  of  chromidrosis,  as  the  sweat  is 
not  coloured  and  the  clothes  do  not  become  stained. 

In  ochronosis,  which  is  generally  congenital,  there  is  alcaptonuria, 
and  the  ligaments  and  cartilages  become  blackened. 

In  xanthoderma  arcatum  the  yellow  patches  remain  localized  to  the 
legs,  and  are  permanent. 

Treatments — The  only  successful  measure  seems  to  be  to  send 
the  patients  up-country.  On  the  hypothesis  that  the  condition 
might  possibly  be  of  parasitic  origin,  a  formalin  spirit  lotion 
(i  per  cent.)  was  prescribed  is  several  cases,  but  the  improvement ,  il 
any,  was  very  slight,  though  certain  patients  stated  that  they 
thought  the  condition  was  affected  in  a  beneficial  manner  by  it. 

Melanonychia. 

Synonyms.— Black  pigmentation  of  nails,  Melanonychia  falci- 
formis. 

Castellani  has  described  in  two  European  ladies  a  peculiar  con- 
dition of  the  nails  characterized  by  a  band  of  black  pigmentation 
along  the  free  border  of  the  nail.  On  superficial  examination,  it 
has  the  same  appearance  as  though  some  dirt  had  accumulated 
beneath  the  free  border  of  the  nail,  but  on  scraping  this  pigmen- 
tation does  not  disappear,  and  this  shows  that  the  condition  is  due 
to  some  pigmentation  in  the  substance  of  the  nail.  The  sufferers 
were  in  general  good  health,  not  using  any  internal  or  external 


PLATE    XV. 


XANTHODERMA   AREATUM. 


Geo'Vaurston  &  Sons  Ltd  Edm. 


To  fact  page  2237 


DYSTROPHIES  2237 

medicine  which  could  account  for  the  pigmentation,  and  the  nails, 
apart  from  this  line  of  pigmentation,  appeared  perfectly  normal. 
We  have,  later,  come  across  a  case  in  a  European  gentleman  and 
another  case  in  Macedonia. 
The  condition  slowly  disappears  spontaneously. 

Xanthoderma  Areatum. 

This  affection,  which  has  been  described  by  Castellani,  is  not 
infrequently  met  with  among  Europeans;  it  generally  affects  the 
lower  parts  of  the  legs;  it  starts  very  insidiously,  with  a  yellowish 
or  reddish-yellow  spot,  which  is  not  elevated;  the  surface  is  smooth, 
not  furfuraceous;  there  is  no  infiltration,  and,  apart  from  the 
colour,  the  affected  skin  is  normal.  There  is  no  pruritus  and 
no  pain.  The  yellow  spot  slowly  increases,  and  one  or  more  other 
spots  may  appear  near  the  first  one  or  at  a  distance.  Some  of  the 
spots  may  coalesce  together,  forming  a  large  yellow-red  patch  of 
irregular  or  various  outline.  The  larger  patches  also,  apart  from 
the  colour,  are  normal,  being  of  normal  consistency  and  elasticity. 
The  disease  is  very  chronic.  The  general  health  is  not  impaired; 
the  lymphatic  glands  are  not  enlarged,  and  the  blood  does  not  show 
any  abnormality;  urine  normal.  In  all  our  cases  syphilis  could  be 
excluded;  in  none  was  there  any  history  of  traumatism. 

Diagnosis. — -From  chloasma,  xanthoderma  areatum  is  readily 
differentiated  by  the  lighter  yellow  or  yellowish-red,  and  by  the 
different  situation.  The  affection  can  be  easily  distinguished  from 
xanthoma,  as  the  texture  of  the  skin  is  normal,  and  the  patches 
are  not  elevated.  In  pseudo-xanthoma  elasticum  of  Balzer  there  is 
an  eruption  consisting  of  mesh-like  patches  of  buff-coloured  infiltra- 
tion, lumpy  in  some  places,  in  others  linear.  It  must  be  distin- 
guished also  from  Schamberg's  so-called  '  cayenne-pepper'  condi- 
tion, characterized  by  the  presence  of  brownish-yellowish  patches 
on  the  legs,  made  up  of  small  puncta,  giving  rise  to  a  cayenne-like 
appearance  of  the  skin,  found  at  times  on  people  suffering  from 
varicose  veins. 

Treatment. — This  is  difficult ;  in  some  cases  an  energetic  exfoli- 
ating treatment  by  resorcin  pastes  (resorcin,  3ii. ;  ac.  salic,  gr.  xx. ; 
Lassar's  paste,  3L)  improves  the  condition  after  the  inflammation 
induced  by  the  paste  subsides. 

Mongolian  Spots. 

Synonym.— Mongolian  macula?. 

Definition. — A  congenital  condition  characterized  by  the  presence 
of  dark  bluish  spots  on  the  lower  sacral  region,  not  disappearing  on 
pressure. 

History. — The  first  complete  description  has  been  given  by  Baelz, 
who  found  them  almost  constantly  in  Chinese,  Koreans,  Japanese, 
and  Malays.  Later  Adachi,  Ashmead,  Martinotti,  Consiglio,  and 
others  have  further  investigated  the  subject.    Castor  and  Fink 


2238  DYSIDROSES  AND  DYSTROPHIES 

have  made  a  very  complete  study  of  it  in  Burma,  where  it  is 
extremely  common. 

Geographical. — The  condition  was  at  one  time  considered  to  be 
limited  to  Mongolian  races,  but  further  investigations  show  that 
it  is  found  in  other  races,  including  Europeans.  Martinotti,  and 
later  Consiglio,  have  found  it  in  Italy.  The  condition  has  recently 
been  observed  also  in  North  and  South  America. 

^Etiology. — The  condition  is  of  unknown  origin;  it  is  probably 
congenital. 

Symptomatology. — '  Mongolian  spots  '  appear  as  blackish-bluish 
or  mulberry-coloured,  smooth,  non-elevated  areas.  The  colour 
does  not  disappear  on  pressure ;  it  is,  as  already  stated,  blackish-blue. 
Some  portions  of  the  same  spot  may  be  darker  than  others  The 
texture  of  the  skin  is  normal;  there  is  no  pain  and  no  pruritus. 
They  are  mostly  roundish,  but  they  may  be  oblong  or  almost  square; 
they  may  be  single,  but  are  often  multiple,  five  or  six  or  more,  each 
spot  varying  in  size  from  |  centimetre  to  12  centimetres  and 
even  more.  The  patch  may  be  sharply  limited  or  the  colour  may 
fade  gradually  into  that  of  the  healthy  skin.  The  commonest 
situation  is  on  the  lower  spine,  sacral  region,  and  buttocks,  but 
they  may  be  found  practically  on  any  other  part  of  the  body.  The 
patches  appear  at  birth,  and,  as  a  rule,  disappear  between  the 
third  and  fourth  year. 

In  Burmese,  Castor  has  found  that  Mongolian  spots  are  extremely  frequent, 
and  are  situated  in  order  of  frequency  on  the  sacral  region  and  buttocks, 
waist,  arms,  legs,  shoulders,  head,  face,  neck.  Castor  identifies  with  the 
Mongolian  spots  also  the  pigmented  patches  so  often  found  in  natives  on  the 
oral  mucosa,  tongue,  and  lips. 

Diagnosis. — The  condition  is  easily  recognized,  the  roundish  or 
variously  shaped  bluish  patches,  generally  on  the  sacral  region 
and  buttocks,  being  characteristic;  its  being  present  from  birth 
distinguishes  it  from  patches  of  pigmentation  of  other  origin. 
The  complete  smoothness  and  normal  texture  of  the  skin  differenti- 
ates the  condition  easily  from  pigmented  moles.  In  those  rare 
cases  in  which  confusion  with  some  mycotic  condition  might  arise 
the  microscopical  examination  will  clear  the  diagnosis,  no  fungi, 
of  course,  being  present  in  Mongolian  spots. 

Course  and  Prognosis. — The  patches  generally  fade  or  disappear 
completely  about  the  third  or  fourth  year. 

Treatment. — The  treatment  is  nil,  nor  is  it  generally  asked  for, 
the  patches  most  frequently  being  on  covered  parts  of  the  body. 

Tattooing. 
Nomenclature. — The  word  'tattoo'  is  derived  from  'tattow,' 
used  by  Cook  and  Banks  in  their  journals  in  1789.  Tattow  was 
derived  from  '  tau  '  or  '  tatu,'  a  word  which  meant  'marking.' 
The  Maori  word  is  'amoca '  or  'moko,'  which,  however,  refers  to 
the  furrowing  of  the  skin — a  more  formidable  operation  than 
tattooing. 


DYSTROPHIES 


2239 


Definition. — Tattooing  is  the  formation  of  more  or  less  indelible 
marks  in  the  skin  by  means  of  rubbing  pigments  or  irritating  sub- 
stances into  slight  wounds  made  for  the  purpose. 

General  Account. — It  appears  to  us  that  tattooing  was  originally 
preceded  by  face  and  body  painting,  which  in  the  form  of  '  war 
paint  '  is  well  known  to  have  been  used  in  many  savage  tribes 
when  about  to  enter  into  combat  with  their  enemies.  At  first  this 
painting  was  very  simple,  and  consisted  in  merely  smearing  the 
face  with  some  form  'of  pigment,  but  eventually  in  certain  peoples 
it  became  more  and  more  elaborate.  Painting,  however,  is  only  a 
temporary  method  of  adornment,  and  many  {peoples  have  adopted 
in  its  place  the  permanent  tattooing.     The  essential  reason  Ifor 


Fig.  877. — Tattooing. 

tattooing  is  the  ornamentation  of  the  person,  but  taking  its  origin 
in  the  custom  of  painting  the  face  before  going  to  war,  it  is  generally 
more  elaborate  in  men  than  in  women. 

In  Africa  the  marks  have  a  most  varied  significance.  Thus, 
according  to  Hobley,  the  Ja-Luo  girls  are  tattooed  because  it  is 
thought  that  unless  this  is  done  a  woman  will  not  bear  children. 
Among  the  Ketosh,  the  warrior,  after  killing  an  enemy  in  warfare, 
has  two  rows  of  marks  tattooed  on  his  right  chest  and  shoulder, 
to  prevent  the  spirit  of  his  dead  enemy  bewitching  him. 

In  its  simplest  form  it  is  seen  in  West  Africa,  where  short  straight 
skin-cuts  are  made  by  means  of  a  sharp  piece  of  iron,  after  which 
some  pigment  or  irritating  substance  is  rubbed  into  the  wound, 
the  idea  being  to  produce  a  keloid.  If  this  fails,  another  cut  is 
made  into  the  same  place,  and  more  pigment  is  rubbed  in  until  the 


2240  DYSTDROSES  AND  DYSTROPHIES 

desired  result  is  attained.  These  cuts,  and  hence  the  subsequent 
keloids,  are  arranged  in  some  primitive  form  of  pattern.  More 
elaborate  patterns,  however,  may  be  met  with,  being  generally  in 
the  forms  of  curved  lines  or  scrolls  of  keloids.  Various  types  of 
tribal  keloid  tattooing  have  been  recently  studied  by  Miss  Zabo- 
rowska. 

In  the  Naga  Hills  of  Assam  the  lines  of  the  tattoo  follow  the 
contours  of  the  face. 

The  most  elaborate  designs  are  found  among  the  Maoris  of  New 
Zealand  and  the  natives  of  the  Pacific  Islands.  The  Polynesians 
use  lines  and  curves,  but  not  spirals,  the  highest  art  being  found 
among  the  Marquesans.  The  Maoris  are,  however,  not  content 
with  mere  tattooing,  in  which  pigment  is  rubbed  into  slight  cuts, 
for  in  their  '  moko  '  they  make  deep  furrows,  which  remain  more  or 
less  permanently  during  life.  According  to  Ling  Roth,  the  Maoris 
use  seven  patterns:  the  first,  the  linear,  composed  of  lines  of  dots 
or  strokes;  the  second  is  the  mat  or  plait-work  pattern,  composed  of 
parallel  lines,  in  groups  of  three,  arranged  more  or  less  alternately; 
the  third  is  the  ladder  pattern,  in  which  the  lines  are  arranged  in 
horizontal  groups  separated  by  clear  spaces  ;  the  fourth  is  the 
chevron  pattern,  being  composed  of  coils  with  long  tails  or  handles, 
the  interspaces  between  which  are  filled  in  by  slanting  lines  ;  the 
fifth  pattern  is  the  circinate  coil ;  the  sixth,  the  anchor  ;  and  the 
seventh,  the  trilateral  scroll.  This  last  pattern  is  said  to  imitate 
a  flower — Clianthus  puniceus.  According  to  the  same  author,  the 
Papuans  are  much  addicted  to  the  use  of  the  spiral  in  tattooing. 
The  Polynesians  use  simple  pricking  instruments,  while  the  Maoris, 
in  order  to  produce  the  deep  furrows,  use  special  instruments, 
shaped  somewhat  like  a  miniature  garden-hoe,  the  cutting  edge 
of  which  is  toothed.  These  instruments  were  at  first  made  of 
bone  or  hard  wood,  but  later  iron  was  introduced.  They  are  made 
to  cut  the  skin  by  means  of  blows  from  a  hammer  or  a  stick.  As  a 
result  of  the  wound  the  blood  flows  freely,  and  is  wiped  away  by 
the  hand  or  a  piece  of  stick,  after  which  the  pigment  is  rubbed 
into  the  wound.  The  nature  of  this  pigment  appears  to  vary,  and 
may  consist  of  charcoal,  obtained  by  burning  various  animal  or 
vegetal  substances.  The  hair  of  the  beard  has  to  be  pulled  out 
by  the  roots,  as  it  would  spoil  the  effect  of  the  tattoo  or  moko. 

The  pain  of  the  operation  of  moko  is  naturally  very  great,  especi- 
ally when  performed  on  the  lips,  and  hence  but  little  tattooing  can 
be  done  at  a  time,  and  it  takes  years  for  an  extensive  moko  to  be 
produced.  Inflammation  often  sets  in,  and  it  may  be  weeks  before 
the  wounds  heal.  The  Maoris  perform  post-mortem  tattooing  and 
moko  at  times,  but  this  is  to  be  distinguished  from  tattooing  made 
during  life  by  the  appearance  of  the  cuts  and  the  absence  of  sub- 
cutaneous colour. 

In  modern  times  the  art  of  tattooing  has  been  much  developed 
by  the  Japanese,  into  whose  country  it  was  introduced  about 
300  years  ago.     The  Japanese  artists,  by  using  special  instruments 


DYSTROPHIES  2241 

composed  of  fine  and  coarse  needles,  and  by  rubbing  in  various 
coloured  pigments,  produce  the  well-known  designs  so  commonly 
seen  on  the  arms  and  bodies  of  Europeans  and  Asiatics. 

Varieties.— The  different  varieties  of  tattooing  described  above 
may  be  classified  as  follows: — 

I.  Simple  tattooing. 

(a)  Without  furrows — tattooing  of  Japan  and  elsewhere. 

(b)  With  furrows — -moko  of  New  Zealand. 
II.   Keloid  tattooing — tattooing  of  Africa. 

Tattooing  is  not  free  from  danger,  for  blood-poisoning,  and  even 
death,  may  result,  while  syphilis  and  tuberculosis  of  the  skin  may  be 
acquired  through  the  wounds. 

Treatment. — When  the  marks  are  small,  excision  may  be  resorted 
to,  but  in  general  any  attempt  at  removal  fails.  Nicurowsky  re- 
moves the  tattoo  marks  by  blistering  with  Finsen  light  applied  in 
the  same  way  as  for  lupus.  Carbide  snow  may  also  be  used,  but 
the  application  must  be  prolonged,  and  a  scar  results.  When  the 
tattooing  is  performed  with  gunpowder,  it  is  said  that  the  marks 
can  be  removed  by  painting  with  di-iodide  of  ammonium  in  solu- 
tion, and  afterwards  with  dilute  hydrochloric  acid. 

Ainhum. 
Synonyms. — Quigila  (Brazil),  Sukha  Pakla  (India),  Faddidite 
(Madagascar),  Gundurum,  Affovi-burunkue  (Geges  tribes),  Banko- 
kerende  (Sudan),  Excresis  Spontanea  (A.  Collas).  Dactylolysis  essen- 
tialis  (G.  Beauregard),  Silva  Lima's  disease  (Egas  Moniz  de  Aragao), 
Esola  or  Ombanja  (Benguelo,  West  Africa). 


Fig.  878. — Ainhum. 


'  Anyum,'  or  '  ainhum,'  is  derived  from  a  Yoruba  word  meaning 
to  saw  or  to  cut,  and  is  used  by  the  Nagos. 

Definition. — Ainhum  is  a  chronic  disease  of  the  fifth,  and  more 
rarely  of  the  fourth  and  other  toes  which  occurs  in  native  races, 
and  is  characterized  by  jthe  formation  of  a  furrow  at  the  digito- 


2242  DYSIDROSES  AND  DYSTROPHIES 

plantar  fold,  which  deepens  and  extends  until  it  encircles  the  toe, 
which  is  finally  severed  from  the  foot. 

History. — The  disease  was  first  described  by  Da  Silva  Lima  in  1852. 
Clarke,  in  i860,  in  his  description  of  the  Gold  Coast,  drew  attention 
to  a  dry  gangrene  of  the  little  toe  found  in  negroes  in  that  region, 
and  considered  it  to  be  a  manifestation  of  yaws.  In  1867  Da  Silva 
Lima  further  studied  the  disease,  and  with  Wucherer  described 
fifty  cases  of  it  in  Brazil,  and  introduced  the  term  '  ainhum  ' ;  in  the 
same  year  Collas  wrote  an  account  of  the  disease.  Da  Silva  Lima 
ventured  no  explanation  of  the  disease.  In  1873  Crombie  described 
the  disease  as  occurring  in  India;  in  1876  Pirovano  found  it  in 
Buenos  Ayres;  and  in  1877  Corre  mentions  it  in  Reunion. 

It  is  reported  in  the  West  Indies  by  Potoppidian  in  1879;  in 
North  Carolina  by  Hornaday  and  Pitman  in  1881;  in  Nossi-Be  by 
Deblenne  in  1883;  in  Western  Virginia  by  Duhring  in  1884.  This 
last  observer,  along  with  Wile,  studied  the  disease  microscopically, 
considering  the  essential  pathological  feature  to  be  an  inflammatory 
oedema  of  the  hypodermis.  In  1886  Eyles  wrote  an  excellent 
account  of  the  pathological  histology  of  the  disease  as  seen  in  the 
Gold  Coast,  concluding  that  irritation  caused  an  internal  prolifera- 
tion of  the  epithelium,  which,  extending  into  the  cutis,  damaged 
the  vasomotor  nerves,  leading  to  a  spasm  of  the  vessels,  endarteritis 
obliterans,  fibrosis  of  the  cutis,  and  rarefying  osteitis,  whereby  the 
digit  is  separated  from  the  foot.  After  this  date  there  are  a  number 
of  papers,  among  which  may  be  specially  mentioned  those  by 
Moriera,  Dalgetty,  and  Maxwell  in  1900,  Muir  in  1903,  Ashley- 
Emile  in  1905,  and  Egas  Moniz  de  Aragao  in  1910. 

Climatology. — The  disease  is  known  in  South  America,  espe- 
cially in  Brazil  and  the  Argentina,  and  also  in  British  Guiana;  in 
North  America,  especially  in  the  Southern  United  States,  but  also, 
though  rarely,  in  the  Northern,  and  in  Canada.  It  also  occurs  in 
the  West  Indies.  In  Africa  it  is  especially  well  known  on  the  West 
Coast,  and  particularly  in  the  Gold  Coast,  but  it  also  occurs  in 
Algeria,  Egypt,  Sudan,  East  Africa,  Madagascar,  and  the  Transvaal. 
In  Asia  it  is  known  in  India,  China  (?),  and  Ceylon.  It  also  occurs 
in  Polynesia.     We  have  seen  a  case  in  an  Italian  peasant. 

^Etiology. — The  causation  of  the  disease  is  not  known.  The 
theories  suggesting  that  the  disease  is  due  to  leprosy,  wearing  rings, 
or  other  tight  bands,  self-mutilation,  may  be  dismissed  at  once,  as 
there  is  nothing  to  support  them. 

According  to  some  authorities — Le  Dantec,  Da  Silva  Lima,  etc. 
— the  hereditary  factor  has  a  certain  importance.  Da  Silva  Lima 
quotes  the  example  of  a  negro  family  all  the  members  of  which 
presented  the  condition. 

The  racial  factor  has  also  been  given  much  prominence,  for  the 
condition  practically  occurs  only  among  natives  and  mulattoes. 

Zambacho  Pasha,  Eyles,  and  Moreira,  are,  in  our  opinion,  correct 
in  their  view  that  the  reason  why  the  native  races  are  attacked  is 
because  they  walk  barefoot,  and  that  irritation  or  injury  to  the 


DYSTROPHIES  2243 

skin  of  the  little  toe  is  more  likely  to  occur  in  negroes,  who  often 
are  flat-footed.  It  is  more  common  in  males  than  in  females,  in 
adults  than  in  children,  and,  though  it  can  apparently  be  found  at 
any  age,  is  most  common  between  thirty  to  thirty-five  years. 

We  are  inclined  to  believe  that  the  condition  is  of  parasitic  origin,  the 
infection  taking  place  probably  through  the  small  superficial  lesions  or 
wounds  which  may  be  found  in  people  going  barefooted. 

Pathology. — The  constant  irritation  causes  the  epithelium  to 
proliferate  internally  and  depress  the  skin,  and  cause  the  fibrous 
tissue  of  the  cutis  to  proliferate.  There  is  also  an  endarteritis,  by 
which  the  blood-supply  is  gradually  cut  off  the  distal  portion  of 
the  toe,  which  therefore  becomes  cedematous  and  fatty,  while  the 
bone  undergoes  rarefying  osteitis,  so  that  the  digit  is  gradually 
separated  from  the  foot,  a  process  which  takes  place  through  the 
bone  of  a  phalanx.  The  histological  examination  at  the  line  of  the 
furrow  shows  proliferation  of  the  epidermis,  which  projects  down- 
wards into  the  cutis,  in  which  the  connective  tissue  is  increased  in 
quantity.  The  vessels  show  endarteritis  and  periarteritis;  the 
sweat-glands  show  proliferation  and  fatty  degeneration  of  the  cells. 
The  bone  is  in  a  condition  of  rarefying  osteitis. 

Distally  to  the  furrow  the  joints  are  effaced;  the  tissues  show 
fatty  degeneration  and  cedematous  infiltration.  No  organisms  can 
be  found. 

Symptomatology. — The  disease  is  purely  local,  and  is  not,  in  our 
experience,  attended  by  any  general  symptoms.  It  begins,  as  a 
rule,  as  a  furrow  on  the  inner  side  of  the  digit o-plantar  furrow, 
which  slowly  deepens  and  extends  laterally  and  dorsally  until  the 
two  wings  meet  on  the  dorsum  of  the  toe.  While  this  is  proceeding 
the  distal  portion  of  the  toe  becomes  swollen,  and  may  appear  as  a 
small  globule  surrounded  posteriorly  by  a  deep  groove,  by  which  it 
is  separated  from  the  rest  of  the  foot.  Often  an  ulcer  forms  on  the 
inner  side  of  the  groove,  and  may  cause  much  pain. 

Left  to  itself,  the  disease  will  last  from  two  to  ten  years,  though 
cases  have  been  reported  of  fifteen  to  fifty  years'  duration;  but 
eventually  the  toe  drops  off,  or  is  knocked  off,  or  is  removed.  The 
process  may,  however,  begin  again  in  the  stump. 

Usually  the  fifth  toe  is  affected,  but  in  about  10  per  cent,  of  cases 
the  fourth  toe  may  be  affected,  and  much  more  rarely  the  second 
or  the  hallux.  There  are  reports  of  the  affection  occurring  also  in 
the  fingers. 

Diagnosis. — The  diagnosis  affords  no  difficulty,  the  presence  of 
the  constricting  furrow  being  typical.  It  is  easily  differentiated 
from  leprotic  lesions  of  the  toes  by  the  sensibility  being  normal 
and  by  the  absence  of  signs  of  leprosy  in  other  parts  of  the  body. 

The  history  makes  the  diagnosis  clear  between  true  ainhum  and  a 
peculiar  congenital  ring-like  constriction  of  the  toes  described  by 
some  authors.  This  condition  is  present  at  birth,  and  its  course 
is.not  progressive. 


2244 


DYSIDROSES  AND  DYSTROPHIES 


Prognosis. — There  is  no  danger  to  life  in  the  disease. 

Treatment. — The  disease  is  best  treated  by  making  a  longitudinal 
cut  into  the  groove,  when  its  progress  may  be  stopped. 

Prophylaxis. — The  essentials  of  the  prophylaxis  are  cleanliness, 
and  the  wearing  of  stockings  and  boots  to  protect  the  foot  from 
injury. 

Symmetrical  Palmar  Erythema. 

Chalmers,  in  1899,  drew  attention  to  a  symmetrical  non-prurigin- 
ous  palmar  erythema  found  in  Europeans  on  the  Gold  Coast,  and 
extending  along  the  ulnar  side  of  the  palms  of  the  hands.  The  affec- 
tion was  very  persistent.     We  have  seen  similar  cases  in  Ceylon. 

Acrodermatitis  Vesiculosa  Tropica. 

Historical  and  Geographical. — This  skin  disease  was  described  by 
Castellani  in  Ceylon.     It  is  of  rare  occurrence. 

/Etiology. — This  is  unknown,  but  the  affection  may  be  of  neuritic 
origin.  It  does  not  seem  to  be  connected  with  leprosy,  in  all  our 
cases  the  search  for  Hansen's  bacillus  being  negative,  and  anaesthesia 
and  other  signs  of  leprosy  being  [absent.  No  history  of  traumatism 
was  elicited  in  our  patients. 


Fig.  879. — Acrodermatitis  Vesiculosa  Tropica. 

Symptomatology. — In  a  well-marked  case  the  skin  of  both  hands, 
especially  the  fingers,  appears  glossy  and  tense,  the  fingers  assuming 
often  a  tapering  shape.  Translucid  vesicles  the  size  of  a  millet  seed 
or  little  more  are  seen  deeply  embedded  in  the  skin  of  the  fingers. 
They  have  clear  contents,   and  the  bacteriological  examination 


REFERENCES  2245 

reveals  absence  of  any  bacterium.  They  may  apparently  remain  un- 
changed for  a  long  time,  then  may  slowly  disappear ;  or  a  few  may 
break,  leaving  very  small  superficial  ulcers,  which  heal  spontaneously 
and  do  not  coalesce.  The  patient  generally  complains  of  very 
severe  pains  in  the  hands  and  fingers,  which  may  be  continuous,  or 
may  be  of  a  neuralgic  intermittent  type.  Pruritus  is  absent.  There 
is  often  diffuse  hyperesthesia ;  anaesthesia  is  never  present.  No 
thickenings  are  found  along  the  nerves  of  the  arm.  The  general 
health  is  not  affected. 

Course  and  Prognosis. — The  course  of  the  disease  extends  to 
several  months,  and  occasionally  to  two  or  three  years,  with  periods 
of  great  improvement.  Ultimately  the  condition  may  get  cured 
spontaneously.  The  general  health  is  not  affected,  but  the  patient 
is  unable  to  work  with  his  hands. 

Diagnosis. — This  is  based  on  the  patient  complaining  of  severe 
pains  in  the  hands  and  fingers,  on  the  presence  of  deep-seated 
cheiropompholyx-like  vesicles,  on  the  glossy  skin,  and  on  the  long 
course  of  the  complaint. 

The  condition  is  differentiated  from  cheiropompholyx  by  the 
severe  pains  and  absence  of  hyperidrosis ;  from  a  leprotic  condition 
by  the  absence  of  anaesthetic  patches,  and  absence  of  other  signs  of 
leprosy  on  other  parts  of  the  body.  Moreover,  though  the  course 
is  long,  the  disease  generally  becomes  cured  spontaneously.  From 
dermatitis  repens  of  Crocker  and  acrodermatitis  perstans  of  Hallo- 
peau  by  there  not  being  history  of  traumatism,  by  absence  of 
exfoliative  lesions,  b}?  the  less  severe  objective  signs,  and  by  the 
absence  of  the  large  foci  of  disease  with  marked  borders  and  fringed 
with  sodden  epidermis,  which  is  thrown  up  by  the  undermining 
exudate. 

Treatment.— The  regular  application  of  an  ichthyol  ointment 
(2  to  5  per  cent.)  to  the  hands  and  fingers,  and  the  administration 
of  the  same  drug  (gr.  iii.)  three  times  daily  by  the  mouth  is  beneficial. 


REFERENCES. 

Melung. 

Balfour  (1911).     Wellcome  Reports. 

Castellani  (1904-1912).     Ceylon  Medical  Reports. 

Castor  (1911).     Journal  of  Tropical  Medicine.     (Lcucoderma.) 

Ziemann  (1903).     Uber  '  Melung,'  Archiv  fur  Dermatologie  u.  Syphilis. 

Chloasma  Symmetricum—Chloasma  Bronzinum— Xanthoderma  Areatum 
Dermatosis  Festonata  Frontalis. 

Cantlie  (1908).     Journal  of  Tropical  Medicine. 

Castellani  (1904-1914).     Ceylon  Medical  Reports. 

Castellani  (1910).     Journ.  Ceylon  Branch  British  Med.  Assoc,  January. 

Castellani  (191 7).     Journal  of  Tropical  Diseases,  October. 


22  46  DY  SID  ROSES  ASTD  DYSTROPHIES 


Mongolian  Spots. 

Adachi  (1902).     Anatomischer  Anzeiger. 
Ashmead  (1905).     Journal  of  Cutaneous  Diseases. 
Castor  (1912).     Journal  of  Tropical  Medicine. 
Consiglio  (1912).     La  Pediatria. 
Martinotti  (1909).     Giorn.  Mai.  vener.  e  della  Pelle. 

Dysidrosis  Exfoliativa. 
Castellani  (1904-19 i  2).     Ceylon  Medical  Reports. 

Sweat  Desquamation. 

Schomberg  (1908).     Journal  of  American  Medical  Association. 

Prickly  Heat. 

Bontius  (1641).     De  Medicina  Indorum. 

Castellani  (191 7).     Journal  of  Tropical  Medicine,  October  1. 

Castellani  (1918).     Ana.  Med.  Nay.,  vol.  i..  No.  3. 

Cleghorn.     Quoted  bv  Mestre. 

Mestre  {1879).     Cronica  Medico-Quirurgica  de  la  Habana. 

Tattooing. 

Ling  Roth  (1901).     Journal  of  the  Anthropological  Institute,  xxxi.  29. 
Zaborowska  (191 7).     Revue  Anthropologique,  July. 

Ainhum. 

Aragao    (1910).     Dermatologie    Tropicale.     Paris.     (Contains   full   bibliog- 
raphy.) 
Barton  (1918).     Journ.  Ro.  Nav.  Med.  Serv.,  vol.  iv.,  Xo.  4. 
Castellani  (1918).     Ann.  Med.  Nav.,  vol.  i..  Xo.  3. 
Clarke  (i860).     Transactions  of  the  Epidemiological  Society,  i.  105. 
Collas  (1S67).     Archives  de  Medecine  Navale,  p.  357. 
Crombie  (1873).     Indian  Medical  Gazette,  viii.  200. 
Dalgetty  (1900).     Journal  of  Tropical  Medicine,  ii.  193. 
Da  Silva  Lima  (1852).     Gazeta  Medica  da  Bahai. 
Eyles  (1886).     Lancet,  ii.  576.     (A  most  important  paper.) 
Maxwell  (1900).     Journal  of  Tropical  Medicine,  ii.  no. 
Moreira  (1900).     Monatshefte  f.  Prak.  Dermatologie,  xxx.  361. 
Muir  (1903).     Journal  of  Tropical  Medicine,  vi.  75. 

Symmetrical  Palmar  Erythema. 

Chalmers  (1S99).     Lancet. 


CHAPTER  XCVIII 
MISCELLANEOUS    DISEASES 

Craw-craw — Dermatitis  nodosa  rubra — Lichen  convex — Symmetrical  ear 
nodules — Ear  lipomata — Porter's  lipomata — Subcutaneous  nodular  lipo- 
matosis—  Multiple  pruriginous  tumours  of  the  skin  —  Angiofibroma 
contagiosum  tropicum — Multiple  pruriginous  tumours — West  Indian 
nodules  —  Mossy  foot — Botryomycosis  —  The  hyperkeratoses  —  Juxta- 
articular  nodules — Murmekiasmosis — References. 

CRAW-CRAW. 

Synonym, — Nodular  dermatitis  (A.  Plehn). 

^Etiology . — The  cause  of  the  malady  is  unknown.  Pijper  has 
described  a  diphtheroid  bacillus. 

In  the  Ceylon  gaols,  where  the  disease  is  common,  the  prisoners  believe  it 
is  due  to  the  diet  and  to  the  manner  of  cooking  the  rice. 

O'Neil  described  in  his  case  a  Microfilaria  which  Manson  is  inclined  to 
believe  to  be  probably  Microfilaria  perstans.  Nielly  described,  under  the 
name  of  'dermatose  parasitaire  '  or  '  craw-craw,'  a  papulo-vesicular  eruption 
in  which  he  found  nematode  embrvos  in  the  papulo-vesicles  and  blood  of 
the  general  circulation.  The  conditions  described  by  these  authors  are  not 
the  dermatosis  we  call  craw-craw,  and  resemble  more  what  Daniels  and 
ourselves  call  cooly  itch. 

Symptomatology. — Under  the  term  'craw-craw  '  African  natives 
denote  practically  any  pruriginous  skin  disease.  Our  African  experi- 
ence has  taught  us  that  most  of  the  so-called  craw-craw  cases  are 
cases  of  neglected  scabies  or  of  tinea  corporis,  or  what  Daniels  and 
ourselves  call  cooly  itch.  We  apply  the  term  'craw-craw'  to  a 
dermatosis  met  with  in  Africa,  in  Ceylon,  and  in  various  parts  of 
the  tropics,  characterized  by  the  presence  of  numerous  hard,  almost 
horny  papules,  occasionally  slightly  exfoliating  at  the  top,  varying  in 
size  between  a  millet-seed  and  a  small  pea.  Some  of  the  papules 
may  be  follicular.  They  are  not  of  constant  shape;  some  may 
be  roundish  and  flattened,  and  others  acuminate.  When  disappear- 
ing, they  may  leave  zones  of  hyperpigmentation.  The  eruption 
generally  affects  the  legs  and  arms,  but  may  spread  to  the  whole 
body,  excepting,  as  a  rule,  the  face  and  scalp.  Suppurative  and 
ulcerative  lesions  are  absent,  except  as  secondary  lesions  due  to 
scratching.  The  proximal  lymphatic  glands  may  be  hard  and  en- 
larged. The  disease,  if  not  properly  treated,  may  last  many^months, 
and  even  several  years ;  some  cases,  however,  become  cured  spon- 
taneously. 

2247 


2248 


MISCELLANEOUS  DISEASES 


Diagnosis. — The  disease  with  which  craw-craw  presents  the 
greatest  resemblance  is  prurigo.  It  is  distinguished  from  prurigo 
by  the  eruption  appearing  at  any  time  of  life,  and  not  only  in  child- 
hood; by  most  of  the  papules  being  larger,  of  horny  consistency, 
and  not  covered  by  a  small  bloody  crust,  as  is  often  the  case  in 
prurigo ;  and  by  the  fact  that  it  may  be  cured  spontaneously. 

The  disease  may  be  distinguished  from  tinea  corporis  by  the 
absence  of  any  fungus,  and  from  scabies  by  absence  of  burrows,  and, 
of  course,  the  absence  of  the  Acarus. 

Treatment.— The  regular  application  of  a  salicylic  spirit  lotion 
(2  per  cent.),  followed  by  /3-naphthol  ointment  (5  to  10  per  cent.)  for 

long  periods  of  time,  often  induces 
a  marked  improvement,  and  in 
many  instances  a  cure.  Internal 
treatment  (arsenic,  ichthyol,  etc.) 
does  not  seem  to  influence  the 
disease. 


Dermatitis  Pruriginosa  Tropica 
(Cooly  Itch). 

The  term  '  cooly  itch '  is  often  applied 
to  dermatoses  of  various  nature,  in- 
cluding scabies.  We  use  it  to  denote 
an  extremely  pruriginous  dermatitis 
affecting  coolies  and  occasionally  Euro- 
peans in  certain  parts  of  the  tropics, 
especially  in  the  low  country.  No  acari 
or  similar  parasites  are  found. 

etiology. — -The  aetiology  is  unknown; 
neither  fungi  nor  animal  parasites  have 
been  found.  It  may  possibly  be  due 
to  some  parasitic  agent  which  remains 
on  the  body  only  for  a  short  time  in 
analogy  to  Copra  itch  (p.  2215). 

Symptomatology. — The  eruption  is 
generally  found  on  the  arms  and  legs, 
but  may  extend  all  over  the  body, 
even,  though  rarely,  to  the  face.  The 
patient  complains  of  unbearable  pruritus. 
The  eruption  is  made  up  of  small  papules 
often  covered  by  bloody  crusts;  vesicles, 
papulo-pustules,  and  pustules  may  be 
present,  and  the  patient,  on  superficial 

examination,    may    be    considered    to    be  suffering    from    scabies,    but   no 

cunicula  arc  found,  and  no  acarus  is  observed. 

Prognosis. — The  eruption  is  very  obstinate,  and  may  last  for  months. 
Diagnosis. — The  absence  of  cunicula  and  of  the  sarcoptes  differentiates  it 

from  scabies. 

Treatment.— Sulphur  (3  to  10  per  cent.)  and  naphthol  ointments  (3  to  10  per 

cent.)  are  very  useful,  though  their  action,  as  remarked  by  Daniels,  is  much 

slower  than  in  scabies. 


Fig.  880/ — Craw-Craw. 


PLATE    XV 


DERMATITIS   NODOSA   RUBRA. 
In  reality  the  Papules  are  of  a  Brighter  Angry-Red  Colour. 


f"»eGWater»TGi'.»Sons,Lto  Edin 


To  face  page  2249 


DERMATITIS  NODOSA   RUBRA 


2249 


DERMATITIS  NODOSA  RUBRA. 

Historical  and  Geographical. — This  condition  has  been  described 
by  Castellani  in  Ceylon. 

/Etiology.— This  is  unknown. 

Symptomatology.— The  first  impression  received  on  seeing  a 
patient  suffering  from  this  peculiar  disease  is  that  he  is  suffering 
from  smallpox  in  the  papular  stage  of  the  eruption,  but  the  absence 
of  fever  and  the  closer  inspection  of  the  eruption  will  exclude  small- 
pox at  once.  In  a  well-marked  case  the  patient  presents  on  his 
face,  arms,  chest,  back,  and  practically  on  the  whole  body,  numerous 
large  papules  and  nodules. 
The  colour  of  the  eruptive 
elements  is  an  angry  red; 
the  shape,  hemispherical  or 
roundish;  the  size,  from  a 
small  split-pea  to  a  large 
pea.  The  surface  of  the 
papules  and  nodules  is 
smooth,  does  not  show 
umbilication,  nor  scales; 
their  consistency  is  hard; 
most  of  the  papules  are  not 
follicular.  There  is  unbear- 
able pruritus,  but  the 
malady  has  no  urticarial 
element  whatever.  Several 
of  the  superficial  lymphatic 
glands  are  enlarged  and 
hard.  In  several  cases  a 
well-marked  enlargement  of 
the  parotid  gland  is  present. 
The  blood  shows  a  certain 
degree  of  eosinophilia.  The 
course  of  the  disease  is  long 
■ — six  months  to  a  year,  and 

sometimes  much  longer  ;  the  nodules  become  gradually  smaller, 
and  may  disappear  completely ;  they  leave  no  scar  or  zones  of  hyper- 
pigmentation,  but  occasionally  the  skin  may  take  a  slightly  scaly 
or  eczematoid  appearance.     Recurrences  may  be  observed. 

Diagnosis. — From  a  syphilid e  by  the  extreme  pruritus  and  the 
inefficacy  of  mercury  and  potassium  iodide. 

From  smallpox,  the  papular  stage  of  which  it  closely  rest  mbles,  by 
the  absence  of  fever,  by  the  chronic  course,  and  by  the  fact  that  the 
papules  never  undergo  a  purulent  change  nor  leave  scars  on  healing. 

From  lichen  planus  by  the  papules  being  very  large,  and  by  their 
not  being  flattened,  umbilicated,  nor  polyhedric. 

From  pityriasis  rubra  pilaris  by  the  papules  being  very  large,  and 
most  of  them  not  follicular,  and  by  the  absence  of  plugs  and  scaling. 


Fig.  881. — Dermatitis  Nodosa  Rubra. 


225° 


MISCELLANEOUS  DISEASES 


From  acnitis  by  the  unbearable  pruritus  and  by  the  eruption  not 
being  chiefly  limited  to  the  face,  as  well  as  by  the  absence  of  subse- 
quent necrosis. 

Fromjolliclis  by  the  condition  not  being  limited  to  the  extremities, 
and  by  the  absence  of  central  crusts. 


Fig.  882. — Dermatitis  Nodosa  Rubra. 


From  erythema  multiforme  by  the  eruptive  elements  being  well- 
defined,  persistent,  solid  papules  and  nodules. 

Prognosis- -In  most  cases  the  general  health  is  not  much  affected, 
but  the  patient  complains  of  the  disfigurement  and  the  severe 
pruritus,  and  the  course  of  the  disease  is  a  long  one.  Occasionally, 
after  many  recurrences,  death  ensues. 


LICHEN  CONVEX 


2251 


Treatment. — Arsenic,  potassium  iodide,  mercury,  doinot  influence 
the  disease.  To  allay  the  pruritus  salicylic  alcoholic  lotions  (2  per 
cent.)  and  ointments  may  be  used. 

LICHEN  CONVEX. 

Synonym. — Lichen  Pilaris  Convex:  (Castellani). 

Historical  and  Geographical. — This  affection — which  has  been 
described  by  Castellani — is  very  common  in  Ceylon,  especially 
among  natives. 

Symptomatology. — The  regions  of  the  body  mostly  affected  are 
the  thorax,  dorsum,  and  shoulders.  The  disease  is  characterized 
by  the  presence  of  numerous  firm  papules,  all  ofwhich  are  follicular. 


Fig.  883. — Lichen  Convex. 


The  surface  of  the  papules  is  smooth;  no  squamae  or  (plugs  are 
found;  they  have  always  a  convex  surface,  and  may  be  'almost 
hemispheric,  ^-  to  \  inch  in  diameter.  The  colour  of  the  papules 
has  a  pinkish  hue  in  natives,  and  red  in  Europeans;  they  have  no 
inflammatory  base,  they  are  not  surrounded  by  any  halo  of  in- 
flammation, nor  is  there  hyperpigmentation,  nor  do  they  leave 
pigmented  areas  on  healing.  The  eruption  is  very  pruriginous. 
The  regions  affected  may  show  hyperidrosis.  The  general  health 
is  not  affected;  the  lymphatic  glands  are  not  enlarged;  in  a  few 
cases  the  blood  may  show  a  slight  degree  of  eosinophilia. 

The  course  is  long,  the  eruption  lasting  about  three  to  nine 


2252  MISCELLANEOUS  DISEASES 

months,  and  often  recurring.  When  the  eruption  heals,  no  hyper- 
pigmentation  is  left.) 

Diagnosis. — From  pityriasis  rubra  pilaris  by  the  papules  never 
showing  plugs  and  by  the  absence  of  scaling;  from  lichen  planus  by 
the  papules  not  being  flattened,  nor  polyhedric,  nor  umbilicated; 
from  dermatitis  nodosa  rubra  by  the  papules  being  always  follicular 
and  not  so  large;  from  a  syphilide  by  the  intense  pruritus;  from 
papular  eczema  by  the  papules  being  always  follicular  and  larger 
and  dome-like,  with  absolutely  no  inflammatory  base,  and  by  the 
skin  not  presenting  a  diffuse  inflammation,  whatever  the  stage  of 
the  disease.  Moreover,  even  when  the  eruption  is  of  long  standing, 
the  appearance  of  the  skin  between  the  papular  elements  remains 
quite  normal,  and  there  is  no  sign  of  what  the  French  call  lichenifi- 
cation. 

Prognosis.— The  eruption  lasts  for  several  months,  but  generally 
heals  spontaneously;  recurrences  are  observed.  The  general  health 
is  not  affected. 

Treatment. — Potassium  iodide,  mercury,  and  arsenic  have  no 
effect.  Externally,  antipruriginous  lotions  and  ointments  may  be 
used — as,  for  instance,  a  salicylic  alcoholic  lotion  (2  per  cent.), 
followed  by  a  naphthol  ointment  (2  to  5  per  cent.).  Change  to  a 
cool  climate  is  very  beneficial.  One  of  our  cases  improved  on  a 
vegetarian  diet. 

SYMMETRICAL  EAR  NODULES. 

This  condition  has  been  described  by  one  of  us  in  Ceylon  in  1910, 
but  further  experience  will  probably  show  that  it  is  to  be  found  also 
in  other  tropical  countries.  In  the  deep  substance  of  the  lobule  of 
both  ears — generally  the  condition  is  symmetrical — on  palpation, 
a  spherical  nodule,  hardly  visible,  is  felt.  Now  and  then  the 
nodule  becomes  much  larger,  very  tense,  and  may  then  present  a 
somewhat  translucid  appearance ;  after  some  days  it  becomes 
smaller  again,  and  r  ,ay  be  hardly  visible.  There  is,  as  a  rule,  no 
subjective  symptom  during  the  periods  of  quiescence  ;  a  feeling  of 
tension  and  slight  pain  during  the  periods  of  increase  of  size  of  the 
nodules. 

The  condition  is  not  leprotic,  there  being  no  anaesthesia  or 
other  sign  of  leprosy;  it  may  possibly  be  of  parasitic  origin,  but 
nothing  definite  can  be  stated,  as  none  of  our  patients  would 
allow  the  removal  of  the  nodule.  Further  investigation  may  show 
that  it  is  allied  to  the  peculiar  condition  called  Nepaul  tumour 
(see  Chapter  XC,  p.  2010). 

EAR  LIPOMATA. 

Symmetrical  lipomata  of  the  lobules  are  not  rare  (see  Chapter  XC, 
p.  2010). 


PORTER'S  LIPOMATA,   ETC.  2253 

PORTER'S  LIPOMATA. 

Porters  and  hammock  carriers  often  show  one  large  lipomatous 
mass  on  one  or  both  shoulders,  where  they  carry  weights,  or  where 
the  pole  on  which  the  weight  is  carried  presses. 

SUBCUTANEOUS  NODULAR  LIPOMATOSIS. 

Synonym. — Polymicrolipomatosis. 

This  condition  seems  to  be  common  in  the  tropics  in  Europeans 
and  natives  alike.  It  is  characterized  by  the  presence  of  subcu- 
taneous nodules,  found  only  on  palpation,  roundish  or  oval,  painless, 
the  size  of  a  pea  to  a  nut.  These  are  generally  situated  in  the 
subcutaneous  tissue  of  the  arms,  legs,  and  abdomen,  and  in  our 
experience  are  not  rarely  mistaken  for  enlarged  lymphatic  glands. 
On  tapping  them  with  a  sterile  syringe  only  a  trace  of  fatty  material 
is  removed,  which,  when  placed  on  a  slide,  promptly  dissolves  when 
heated  or  treated  with  ether.  The  microscopical  examination  of 
one  of  these  nodules,  surgically  removed,  showed  it  to  be  composed 
of  fatty  tissue.  Occasionally  the  tumours  become  much  larger  and 
may  be  plainly  visible. 

ANGIOFIBROMA  CONTAGIOSUM  TROPICUM. 

This  disease  was  first  described  by  Unna  and  von  Bassowitz.  So  far, 
cases  have  been  reported  from  the  southern  regions  of  Brazil  only. 

Symptomatology. — The  incubation  period  varies  from  fifteen  to 
twenty-five  days.  There  are  no  prodromal  symptoms.  The 
eruption  consists  of  vivid  red  papules,  which  soon  enlarge  into 
nodules  the  size  of  a  large  pea  to  an  almond.  The  eruption  may 
affect  any  part  of  the  body,  but  more  frequently  the  face,  neck, 
axillae,  and  genital  organs.  It  is  rarely  found  on  the  legs.  It  very 
frequently  affects  the  various  mucosas — oral,  nasal,  rectal,  and 
urethral.  The  nodules  present  a  smooth  surface,  of  a  violaceous 
colour,  and  they  are  somewhat  of  soft  consistency;  they  bleed 
severely  after  the  slightest  traumatism.  They  may  disappear  spon- 
taneously without  leaving  any  scar,  or  in  other  cases  secondary  in- 
fections may  set  in,  and  large  ulcers  develop.  The  eruption  is  not 
pruriginous,  there  is  no  fever,  and  the  general  health  is  not  impaired. 

etiology. — This  is  unknown,  but  the  disease  is  considered  to  be 
infectious.  According  to  Bassowitz,  the  infection  takes  place 
during  sexual  intercourse,  or  by  the  habit  the  people  of  Brazil  have 
of  taking  their  mate  (national  beverage),  using  the  same  cannule. 

Histopathology.— According  to  Unna's  investigation,  the  histo- 
pathology  is  quite  different  from  what  is  observed  in  frambcesia 
and  syphilis.  The  nodules  consist  of  fibrous  tissue,  with  scanty 
cells  intersected  by  extremely  numerous  bloodvessels. 

Diagnosis. — The  disease  must  be  distinguished  from  verruga 
peruviana  and  frambcesia.  In  verruga  peruviana  there  are  severe 
constitutional  symptoms — fever,  and  often  enlargement  of  the  liver 
and  spleen.     The  condition,  however,  is  considered  to  be  identical 


2254  MISCELLANEOUS  DISEASES 

with  verruga  sensu  stricto  (p.  1576),  by  Strong,  Tyzzer,  Brues, 
Sellards  and  Gastiaburu.  In  framboesia  the  nodules  have  a  mori- 
form  surface,  and  do  not  bleed  so  easily. 

Treatment. — Mercury  and  potassium  iodide  are  useless.  Basso- 
witz  recommends  iron  and  arsenic  internally,  and  externally  the 
injection  into  the  base  of  the  nodules  of  a  few  drops  [of  formalin, 
or  their  excision,  using  the  galvano-cautery. 

MULTIPLE  PRURIGINOUS  TUMOURS  OF  THE  SKIN. 

Schamberg  and  Hirschler  reported  in  1905  two  cases  of  multiple 
tumours  of  the  skin  in  negroes,  associated  with  itching.  The 
tumours  were  sharply  circumscribed  nodules,  from  the  size  of  a 
small  pea  to  a  large  hazel-nut,  situated  on  the  extremities.  They 
were  of  a  blackish  colour — the  smaller  smooth,  the  larger  covered 
with  a  horny  epidermis.  These  tumours  showed,  on  histological 
examination,  dilated  vessels,  cellular  infiltration,  with  numerous 
mast  cells,  and  the  formation  of  new  collagenous  fibres.  The  same 
eruption  was  previously  described  in  1880  by  Hardway  in  a  white 
woman. 

WEST  INDIAN  NODULES. 

This  affection,  which  seems  to  be  very  similar  to  the  preceding 
one,  has  been  described  by  Numa  Rat  in  natives  of  the  West 
Indies,  who  often  confuse  it  with  Guinea-worm.  The  eruption 
may  attack  any  part  of  the  body,  and  consists  of  subcutaneous 
nodules  varying  from  the  size  of  a  pea  to  that  of  a  small  nut. 
There  is  extremely  severe  pruritus,  and  the  natives  destroy  the 
skin  covering  the  nodules  with  caustics,  and  extract  the  nodules, 
which  appear  yellowish-white  and  have  a  cartilaginous  consistency. 

Histologically,  according  to  Macleod,  they  consist  mainly  of 
hypertrophied  connective  tissue  made  up  of  thickened  collagen 
bundles.    The  aetiology  is  unknown. 

MOSSY  FOOT. 

Synonym. — Piemugoso. 

This  affection  is  fairly  common,  according  to  Thomas,  in  the 
region  of  the  Amazon. 

The  foot  is  covered  with  dense,  warty,  very  vascular,  painful 
masses,  as  much  as  a  half  to  three-quarters  of  an  inch  thick,  which 
may  spread  to  the  leg. 

The  disease  is  very  chronic,  and  probably  of  parasitic  origin. 

The  suggestion  has  been  made  by  Cranston  Low  that  it  may  be  a  type  of 
tuberculosis  cutis  verrucosa,  and  by  Da  Matta  that  it  may  be  a  form  of 
leishmaniasis. 

BOTRYOMYCOSIS. 

Synonyms. — Botryoniycosis  Hominis,  Granuloma  Pyogenicum. 
Definition. — A   granulomatous   condition   characterized   by   the 
presence  of  coccal  bodies  of  various  size  and  collected  in  clusters. 


BOTRYOMYCOSIS  2255 

Historical  and  Geographical  Distribution. —  The  condition  was 
first  studied  in  horses,  in  which  it  occurs  often  in  the  testicular 
cord  after  castration:  but  it  is  common  also  in  the  pig,  dog,  and 
cattle.  Later  it  was  found  in  man  by  Dor  and  Poncet  in  Europe. 
In  the  tropics  it  has  been  observed  in  Ceylon  by  one  of  us. 

/Etiology. — The  condition  is  believed  by  some  observers  to  be  due 
to  an  organism  (Botryococcus  ascojormans  Kitt,  Micrococcus  botryo- 
genes  Rabe),  the  botanical  position  of  which  is  not  defined.  The 
organism  appears  in  the  lesions  under  the  form  of  spherical  bodies 
of  very  different  size  (o«8  to  12 /a),  singly  or  collected  in  clumps, 
Gram-positive,  and  to  a  certain  extent  acid-fast.  They  seem  to 
reproduce  by  a  process  of  endosporulation.  The  cultures  obtained 
by  some  authors  have,  however,  all  the  characters  of  a  staphylo- 
coccus. 

Some  authorities,  in  fact,  consider  the  disease  to  be  merely  a 
type  of  pyosis  due  to  the  usual  staphylococci.  Magrou,  using  a 
special  technique,  has  succeeded  in  experimentally  reproducing  the 
disease  by  inoculating  a  strain  of  Staphylococcus  aureus  isolated 
from  an  ordinary  case  of  sepsis.  M.  Nicolle  and  Cesari  have  shown 
that  the  serum  derived  from  horses  affected  with  botryomycosis 
neutralizes  staphylococcal  toxins.  Letulle  considers  the  disease 
to  be  due  to  an  amoeba,  and  his  results  have  been  confirmed  by 
Bureau  and  Labbe,  but  not  by  others. 

Pathology. — The  condition,  as  seen  by  us  in  the  tropics,  has  all 
the  characters  of  a  granuloma.  The  microscopical  examination  of 
sections  shows  young  connective  tissue  with  large  numbers  of 
plasma  cells.  Peculiar  claviform  bodies  have  been  described  by 
Magrou,  who  believes  them  to  originate  from  the  staphylococci. 
The  lesions  are  very  vascular.  Later,  denser  fibrous  tissue  is 
observed. 

Symptomatology. — The  condition  generally  develops  on  some 
suppurating  wound,  but  may  occur  upon  the  site  of  any  abrasion 
or  wound.  It  appears  as  a  small,  generally  cherry-red,  granu- 
lomatous nodule  or  mass,  often  roundish,  of  various  size — from 
a  pea  to  a  nut  or  larger.  Occasionally  the  nodule  may  be  pedicu- 
lated.  At  first  it  is  of  rather  soft  elastic  consistency:  later  may 
become  fibrous  and  much  harder.  There  is  very  little  tendency  to 
spontaneous  cure.  A  very  mild  type  of  botryomycosis  occasion- 
ally develops  after  vaccination.     We  have  seen  several  such  cases. 

Prognosis. — The  general  health  is  not  much  affected,  but  the 
condition  has  little  or  no  tendency  to  spontaneous  cure. 

Treatment.— Excision,  followed  by  light  cauterization  with  pure 
carbolic  or  chloride  of  zinc,  is  the  only  method  of  treatment.  The 
pedunculated  form  may  be  cured  by  ligature.  The  disease  may 
occur  again  after  operation,  but  this  is  rare. 

Prophylaxis. — Care  should  be  taken  to  keep  suppurating  wounds 
thoroughly  disinfected. 


2256  MISCELLANEOUS  DISEASES 


THE  HYPERKERATOSES. 


Definition. — A  hyperkeratosis  is  any  cutaneous  condition  in 
which  the  cells  of  the  horny  layer  have  a  greater  coherence  than 
normal,  as  tested  with  pepsin  and  hydrochloric  acid,  and  thus  tend 
to  pile  themselves  up  in  the  form  of  horny  scales. 

Remarks. — As  defined  above,  a  hyperkeratosis  is  more  a  symptom 
than  a  disease,  and  most  of  the  so-called  primary  hyperkeratoses  are 
probably  induced  by  some  chemical  change  produced  by  an  altered 
metabolic  condition  brought  about  by  some  infection. 

Thus  syphilis  and  frambcesia  tropica  are  often  believed  to  be  the 
disturbing  element  which  lays  the  foundation  of  these  changes,  even 
though  no  sign  of  their  specific  germs  can  be  found  in  the  lesions, 
which  may  appear  long  after  the  disappearance  of  other  features  of 
the  disease,  while  the  specific  treatment  for  these  complaints  has 
little  or  no  influence  on  the  hyperkeratosis. 

Further,  syphilis  can  certainly  act  upon  the  foetus  in  utero  and 
lay  the  bases  of  changes  of  metabolism,  which  may  result  in  the 
so-called  congenital  hyperkeratosis,  and  the  same  remarks,  to  a 
certain  extent,  appear  to  apply  also  to  tuberculosis. 

Classification. — -With  the  above  provisos,  the  hyperkeratoses  may 
be  classified  into: — 

A.  Hyperkeratoses  obviously  associated  with  a  causal  disease  : — 

i.  N on- follicular  : — 

Found  in  leprosy,   arsenical    poisoning,   and  hyperi- 
drosis. 
2.  Follicular : — 

Found  in  various  tubercular  and  syphilitic  affections, 
and  some  forms  of  lichen  and  acne. 

B.  Hyperkeratoses   of   unknown   origin   or   remotely   associated 

with  syphilis,  yaws,  tuberculosis,  etc.: — 

[a)  Develops  during  intra-uterine  life  :■ — 

Hyperkeratosis  universalis  congenita. 

(b)  Develops  during  post-uterine  life  : — 

i.  Generalized  affections: — 

Of  these,  ichthyosis  and  pityriasis  rubra  pilaris 
are  met  with  in  the  tropics. 
2.  Localized  affections: — 
(i.)  Non-follicular : — 

(i)  Without  acanthosis  or  markedly  dilated 
papillary  vessels — Kcratodermia. 

(2)  Without   acanthosis,  but  with  markedly 

dilated  papillary  vessels — Angiokerato- 
dermia. 

(3)  With  acanthosis,  but  without  markedly 

dilated     papillary     vessels  —  Acantho- 
keratodermia. 
(ii.)  Follicular — Keratosis. 


KERATODERMIA    CRIB  RATA  2257 

In  the  tropics  we  have  met  with  leprotic  and  syphilitic  hyper- 
keratoses, as  well  as  with  those  connected  with  lichen  planus.  We 
have  also  seen  ichthyosis,  pityriasis  rubra  pilaris,  and  keratosis 
palmaris  et  plantaris,  and  several  other  forms ;  but  of  all  these, 
three  forms  must  receive  a  little  further  notice — viz. : — 

1.  Keratodermia  cribrata. 

2.  Acanthokcratodermia  prsecornufaciens. 

3.  Keratoma  plantare  sulcatum. 

KERATODERMIA  CRIBRATA. 

Synonym.— Keratodermia  punctata. 

Definition. — It  is  a  localized  non-follicular  hyperkeratosis  of  the 
hands  and  feet,  appearing  in  post-uterine  life,  in  which  the  hyper  - 
keratosic  area  is  riddled  with  little  pits  caused  by  the  shedding  of 
little  corn-like  projections. 

Remarks. — In  the  tropics  it  was  first  described  by  Castellani  and 
then  by  Chalmers. 

/Etiology. — It  seems  that  it  is  in  some  way  associated  with 
yaws  or  syphilis  (congenital  or  acquired),  probably  by  changes 
effected  in  the  metabolism,  and  not  by  the  action  of  their 
parasites. 

Pathological  Histology. — The  essential  points  are  a  mild  chronic 
inflammation  of  the  dermis  and  a  hyperkeratosis  of  the  sweat  orifices, 
leading  to  the  formation  of  corn-like  projections,  which  are  freed 
laterally  and  finally  all  round,  and  then  fall  out,  leaving  a 
depression. 

Symptomatology. — The  palms  of  the  hands  or  soles  of  the  feet 
may  show  hyperkeratosis  associated  with  slight  itching.  In  the 
hyperkeratosic  area  there  are  many  corn-like  bodies,  some  of  which 
have  fallen  out  and  left  depressions.  The  condition  is  very 
chronic. 

Diagnosis. — The  bilaterally  symmetrical  hyperkeratosis  of  the 
palms  or  soles,  with  the  pits  in  the  thickened  areas  and  the  corn- 
like bodies,  are  characteristic. 

Treatment.— Nothing  is  known  to  permanently  benefit  the 
condition. 

ACANTHOKERATODERMIA  PR/ECORNUFACIENS. 

This  is  an  acanthokeratodermia  characterized  by  the  formation 
of  thickened  patches  of  epidermis  in  the  palms  of  the  hands  and  soles 
of  the  feet,  which  may  (in  the  latter  situation)  become  cracked  and 
fissured  and  break  down,  forming  painful  sores,  which  prevent  the 
patient  from  walking.  Sometimes  they  are  associated  with  a 
thickening  of  the  horny  layer  of  the  nail-bed,  thus  giving  rise  to  a 
peculiar  elevation  of  the  nail  called  by  Unna  hyperkeratosis  subun- 
gualis. Most  patients  have  been  affected  with  syphilis,  but  the 
specific  organisms  cannot  be  found  in  the  lesions,  and  antisyphihtic 

142 


MISCELLA  NEOUS  DISEASES 


treatment  is  generally  useless.  Pathologically  the  condition  resem- 
bles that  in  the  first  stage  of  the  production  of  a  cutaneous  horn, 
which, indeed,  had  formed  in  one  casereported  by  Colcott  Fox. 


V-  j£ '  i, . 


FlG.    884. ACANTHOKERATODERMIA    Pr<ECORNUFACIENS. 


FlG.    8S5. ACANTHOKERATODERMIA    PR.ECORNUFACIENS. 


KERATOMA  PLANTARE  SULCATUM. 

Historical  and  Geographical.— This  disease  was  first  described  by 
Castellani  in  Ceylon.  It  is  found  also  in  India  and  tropical  Africa, 
and  a  case  has  been  recorded  in  Macedonia. 

./Etiology. — This  is  unknown,  though  in  certain  cases  yaws  may 
perhaps  play  a  role  in  its  causation.  The  affection  is  much  more 
frequent  during  the  rainy  season,  and  occurs  generally  in  natives 
who  do  not  wear  shoes  or  sandals;  but  we  have  seen  a  typical 


KERATOMA  PLANTARE  SULCATUM 


2259 


case  in  a  European  of  good  social  standing.  It  improves  or  dis- 
appears completely  during  the  dry  season. 

Symptomatology. — The  epidermis  of  the  soles — especially  the 
anterior  portion — and  the  heels  is  greatly  thickened,  and  is  generally 
of  a  dark  yellowish  colour,  and  presents  numerous  deep  segmentary 
furrows,  straight,  semicircular,  or  ellipsoid;  these  furrows  appear 
black,  but  if  the  dirt  andjdust  accumulated  in  them  is  removed,  the 
fundus  of  these  sulci  will  jbe  found  to  be  whitish  or  pinkish.  There 
is  no  sign  of  any  .local  inflammation,  though  the  patient 'generally 
complains  of  tenderness'of  jthe  feet'  after  much  walking. 

Diagnosis.— This  is  based  on  the  presence  of  the  characteristic 
deep  sulci  and  punched-out  holes |in  the  thickened  epidermis,  which 
are  absent  inTesions  jof  jthe  {soles  of  the  jfeet  of  syphilitic  'origin. 


Fig.  886.- — Keratoma  Plantare  Sulcatum. 


Moreover,  a  mercury  and  potassium  iodide  treatment  has  no  effect 
whatever  on  the  malady.  In  yaws  the  lesions  of  the  soles  of  the 
feet  are,  generally,  either  granulomatous,  with  large  frambcesiform 
nodules  piercing  through  the  thick  epidermis,  or  a  diffuse  scaly 
condition  with  thickened  epidermis  is  observed.  The  rare  pitted 
condition  of  the  soles  of  the  feet  (p.  1550)  found  in  yaws  is  distin- 
guished by  its  lack  of  seasonal  incidence  and  by  the  history.  In 
the  condition  known  as  '  symmetrical  keratodermia  of  the  ex- 
tremities '  no  deep  sulci  are  found.  The  so-called  '  mal  de  meleda,' 
which  is  very  common  in  the  Island  of  Meleda  in  the  Adriatic,  is, 
according  to  Neumann  and  others,  identical  with  symmetrical  kera- 
todermia, and  no  deep  sulci  are  present. 

Prognosis. — The  general  health  is  not  affected,  but  the  condition 


226o 


MISCELLANEOUS  DISEASES 


may  last  for  months,  and  if  the  patient  has  much  walking  to  do, 
may  become  very  painful. 

Treatment. — Potassium  iodide,  mercury,  and  salvarsan  are  useless. 
Rest  and  local  applications  of  salicylic  ointment  or  salicylic  collodion 
(ac.  salicyl.,  3i- ;  collodion,  5L),  or  salicylic  plasters  induce  a  marked 
improvement. 

JUXTA-ARTICULAR  NODULES. 

jSynonyms. — ''Enno,'  Naride,  Macgregor's  nodules,  Steiner's 
tumours,  Jeanselme's  nodules. 

Historical  and  Geographical. — This  affection  was^first  briefly 
described  by  Macgregor  in  190 1  in  New  Guinea,  whokalso  suggested 
a  possible  parasitic  origin  of  it.  It  .was  later  more  fully  studied  by 
Steiner  in  natives  of  Java  and  by  Jeanselme  in  natives  of  Siam,  where 
it  is  known  as  '  enno.'  Jeanselme  introduced  the  very  (appropriate 
term  of  '  juxta-articular  [nodules.'     Fontoynont  and  Carougeau  in 


Fig.  887. — Juxta-Articular  Nodules. 


Madagascar  considered  the  cause  of  the  affection  to  be  a  fungus, 
Nocardia  carougeaui  Brumpt,  1910.  Cases  have  been  observed  in 
Northern  Africa  by  Gros  and  in  Ceylon  by  us,  also  by  Chalmers  and 
Archibald  in  the  Sudan.  The  disease  will  probably  be  found  to 
occur  in  many  other  tropical  and  subtropical  countries. 

^Etiology. — Macgregor,  Sterner,  and  Jeanselme  considered  the 
nodules  to  be  of  parasitic  origin,  while  Fontoynont  and  Carougeau 
found  a  fungus  which  they  believed  to  be  the  ^etiological  agent  of 
the  condition.     The  description  of  this  fungus — Nocardia  carougeaui 


JUXTA-ARTICULAR  NODULES 


2261 


Brumpt,  1910 — is  given  in  the  chapters  on  fungi  (see  pp.  1065  and 
1066).     Recently  the  presence  in  the  nodules  and  etiological  role 


Fig. 


-Juxta-Articular  Nodules. 


by  many  authorities.     Several 
to   be   a   late    manifestation   of 


of  this  fungus  has  been  doubted 
observers  consider  the  condition 
frambcesia. 

Symptomatology.— In  the  legs 
and  arms,  especially  in  proximity 
to  the  articulations,  several  no- 
dules are  found,  some  of  them  the 
size  of  a  walnut  or  more,  of  rather 
hard  consistency,  and  covered 
by  healthy  skin.  According  to 
Macgregor,  these  tumours  occur 
most  frequently  about  the  elbows, 
or  the  parts  of  the  body  coming 
in  contact  with  the  ground  when 
the  native  is  sleeping.  These 
nodules  at  first  are  rather  soft, 
and  are  situated  in  the  subcuta- 
neous tissue,  and  the  skin  may  be 
moved  above  them.  Later  they 
may,  apparently,  fuse  together, 
forming  hard,  large  tumours,  and 
adhere  to  the  skin,  which  gener- 
ally does  not  present  any  alter- 
ation. The  course  is  very  chronic, 
but  occasionally  the  nodules  may 
disappear  spontaneously. 

Treatment. — The  nodules  may  be  excised.     In  the   very  first 
stage  of  the  disease  a  potassium  iodide  treatment  might  be  tried. 


Fig. 


889. — murmekiasmosis 
Amphilaphes. 


2262 


MISCELLANEOUS  DISEASES 


MURMEKIASMOSIS  AMPHILAPHES. 

Chalmers  and  Christopher  son  have  described  a  case  (Fig.  889) 
of  spreading  warts,  associated  with  Cryptucoccus  myrmecice,  which 
grew  on  the  skin  of  the  face  and  neck,  destroyed  an  eye,  and  entered 
the  mouth. 

LYMPHO-FIBROMATOSIS. 

This  is  a  condition  of  elephantoid  fibrosis  (Fig.  890)  met  by  us 
in  Ceylon  and  Africa.     It  is  sometimes  associated  with  a  secondary 


\\ 

r-*\™ 

'}*$M 

1 

Hg 

'■ 

Fig.  890. — Lympho-Fibromatosis. 


pyogenic  eruption.  Some  cases  may  be  associated  with  filariasis, 
but  others  are  not.  The  skin  is  elevated  into  large,  raised,  flattened 
patches  of  fibrous  consistency.     The  condition  is  chronic.  I 

SEBORRHEA  SPINULOSA. 

This  condition  has  been  seen  by  Cast  ellani  and  Chalmers  in  various 
parts  of  the  tropics  and  the  Balkans.  It  is  characterized  by  the 
presence  of  numerous  yellow  plugs,  some  of  which  are  acuminate 
and  hard.  These  plugs  project  from  the  orifices  of  the  sebaceous 
ducts,  and  are  often  situate  on  an  oily  skin.  Ordinary  black  come- 
dones are  absent.  The  term  '  seborrhcea  spinulosa  '  probably 
covers  several  varieties  of  seborrhcea. 


REFERENCES  2263 

REFERENCES. 
Craw-Craw  and  Allied  Conditions. 

Castellani  (1904-14).     Ceylon  Medical  Reports  and  Journal  of   the   Ceylon 

Branch  of  the  British  Medical  Association. 
Daniels  (1912).     Tropical  Medicine.     London. 
Manson  (1908).     Tropical  Diseases. 
O'Neil  (1875).     Lancet. 

Pijper  (1917).     Journal  of  Tropical  Medicine. 
Plehn,  A.  (1905).     Mense. 
Plehn,  F.     Quoted  by  A.  Plehn. 

Dermatitis  Nodosa  Rubra. 

Castellani  (1910).     Journal  of  the  Ceylon  Branch  of  the  British  Medical 
Association,  January. 

Lichen  Convex. 

Castellani  (1906-12).     Ceylon  Medical  Reports. 

Castellani.     Journal  of  the  Ceylon  Branch  of  the  British  Medical  Associa- 
tion, 1910,  January. 

Symmetrical  Ear  Nodules. 

Castellani  (1906-13).     Ceylon  Medical  Reports. 

Castellani.     Journal  of  the  Ceylon  Branch  of  the  British  Medical  Associa- 
tion, 1909. 

Keratoma  Plantare  Sulcatum. 

Castellani.     Journal  of  the  Ceylon  Branch  of  the  British  Medical  Associa- 
tion, 1910,  January. 
Castellani  (1917).     Journal  of  Tropical  Medicine,  October  1. 

Angiofibroma  Contagiosum. 

Bassowitz  (1906).     Archiv  fur  Schiffs-  u.  Tropen-Hygiene. 

Multiple  Pruriginous  Tumours. 

Hardway  (1880).     Archives  de  Dermatologie. 

Schamberg  and  Hirschler  (1906).     Journal  of  Cutaneous  Diseases. 

West  Indian  Nodules. 
Numa  Rat  (1909).     Transactions  of  the  Society  of  Tropical  Medicine. 

Mossy  Foot. 

Thomas  (1910).     Transactions  of  the  Society  of  Tropical  Medicine. 

Botryomycosis. 

Brumpt  (1906).     Arch,  de  Parasitologic,  vol.  x. 

Cesari  (1912).     Bull.  Soc.  Centrale  de  Med.  Vet.,  p.  400. 

Dor  (1G98).     Congres  de  Chirurgie;  (1903)  Lyon  Medical,  July. 

Galli-Valerio  (1902).     Cent.  f.  Bakt.,  vol.  xxxi. 

Legroux  (1904).     These  de  Paris. 

Magrou  (191 1).     C.  R.  Societe  de  Biologie,  February. 

Magrou  (191 9).     Annales  Inst.  Pasteur,  May. 

Poncet  and  Dor  (1900).     Arch.  Generates  de  Med.,  February  and  March 

Vallillo  (191 1).     Pathologica,  No.  57. 


CHAPTER  XCIX 
COSMOPOLITAN    SKIN    DISEASES 

General  remarks — Pyogenic  infections — The  erythemata — The  exanthemata 
—Urticaria — Dermatitis  venenata — Parasitic  diseases — Bullous  eruptions 
— Herpes — Eczema,  psoriasis,  seborrhcea,  and  dermatitis  exfoliativa — 
Acne — Hyperidrosis  and  bromidrosis — Lichen — Tumours — Tuberculosis 
— Syphilis — Ichthyosis — Kaposi's  disease — Chloasma — Diseases  of  the 
hair  and  nails — Some  cosmopolitan  diseases  of  mucous  membranes. 

GENERAL  REMARKS. 

In  our  experience,  all  the  skin  diseases  met  with  in  temperate  zones 
are  also  found  in  the  tropics,  except  those  due  to  intense  cold,  such 
as  erythema  pernio  and  frost-bite,  and  even  these  may  also  be 
found  in  the  high  mountainous  regions  of  the  tropics. 

The  diagnosis  of  some  of  the  cosmopolitan  dermatoses  may,  owing 
to  the  colour  of  the  skin  of  native  races,  be  very  difficult  to  the 
medical  man  newly  arrived  in  the  tropics.  This  is  probably  the 
cause  of  some  of  the  statements  that  such  common  diseases  as  lichen 
planus  and  psoriasis  are  absent.  There  is  no  doubt,  however,  that 
some  dermatoses  which  are  frequently  met  with  in  temperate  zones 
are  less  common  in  the  tropics. 

It  is  stated  by  some  authorities  that  coloured  races  are,  on  the 
whole,  less  liable  to  skin  diseases  than  the  white  races,  but  the 
reverse  is  more  in  accordance  with  our  experience. 

A  few  remarks  as  to  the  normal  skin  of  native  races  may  be 
useful  before  proceeding  to  review  the  various  cosmopolitan  diseases. 
In  the  African  races  and  American  negroes  who  descend  from 
African  negro  stock  (Guinea  negroes,  Yoloffs,  Caffres)  the  whole 
skin,  especially  the  derma,  is  thicker  than  in  the  white  races.  In 
Indian  races  the  skin  is  about  the  same  thickness  as  in  Europeans, 
except  in  the  Tamils,  whose  skin  is  somewhat  thicker.  As  noted  by 
Howard  Fox,  the  glandular  system — sweat  glands  and  sebaceous 
glands — is  much  more  highly  developed  in  the  native  races,  espe- 
cially the  African  negroes.  The  sebaceous  secretion  is  the  cause  of 
their  peculiar  odour  and  the  shining  appearance  of  the  skin,  and 
the  large  secretion  of  sweat,  which,  owing  to  the  high  temperature, 
quickly  evaporates,  is  the  probable  cause  of  the  skin  feeling  cooler 
when  touched.  In  native  races  the  hairy  system  is  less  developed, 
except  on  the  scalp;  in  the  African  races  the  hair  of  the  head  is 
generally  curly  or  woolly;  in  Indian  races  it  is  usually  smooth. 

2264 


THE  HYPERKERATOSES  2265 

The  slight  development  of  lanugo  hair  is  the  cause,  as  noted  by 
Fox,  of  the  peculiar  velvety  feeling  of  the  negro  skin. 

The  most  important  characteristic  of  the  skin  of  tropical  native 
races  is  the  dark  pigmentation.  It  is  said  that  this  pigmentation 
is  not  present  at  birth,  but  develops  within  a  few  hours  to  several 
days  after  birth.  In  our  experience,  it  cannot  be  doubted  that  at 
the  time  of  birth  in  many  cases  the  babies  present  a  much  lighter 
colour  than  the  adult  people.  The  skin,  however,  is  not  whitish, 
but  of  a  muddy  brownish  colour,  and  darkens  greatly  within  a  few 
days — in  some  cases  is  quite  dark  also  at  the  time  of  birth.  It  is 
said  that  the  pigmentation  increases  till  puberty,  and  then,  after 
remaining  stationary  during  adult  life,  slowly  decreases  during  old 
age.  The  maximum  pigmentation  is  found  on  the  loins,  posterior 
portion  of  the  trunk,  shoulders,  buttocks,  and  thighs;  the  least  pig- 
mentation is  found  on  the  prepuce,  vulva,  palms,  and  soles.  In 
some  races  the  oral  mucosa  is  not  pigmented;  in  others  there  is  a 
patchy  dark  pigmentation  which  extends  often  to  the  tongue.  The 
dark  patches  on  the  tongue  have  been  considered  by  several  writers 
to  be  a  pathological  condition,  and  a  sign  of  ankylostomiasis.  We 
have  observed  such  patches,  however,  in  numbers  of  normal  natives. 
The  hair  is  said  to  become  white  at  a  later  date  among  negro  races 
than  in  Europeans;  we  have  not  noted  any  distinct  difference, 
either  among  them  or  the  natives  of  Asia. 

It  is  said  by  some  writers  that  native  races,  and  especially  the 
negro  African  races,  are  less  susceptible  to  pain  than  the  white 
man.  In  our  experience  there  is  hardly  any  difference  in  the 
ordinary  dolorific  sensibility,  but  the  thermic  sensibility  is  probably 
less. 

PYOGENIC  INFECTIONS. 

These  are  very  common  in  tropical  countries.  Impetigo  and 
Ecthyma  lesions  are  frequently  met  with.  The  symptoms  and 
course  are  identical  with  what  one  finds  in  temperate  zones,  and 
the  treatment  is  the  same — -removal  of  the  crusts,  disinfection  with 
a  lotion,  such  as  a  perchloride  of  mercury  (1  in  2,000),  and  dressing 
with  a  white  precipitate  ointment  (1  per  cent.). 

Boils. — -This  is  a  common  affection  in  the  tropics,  very  stubborn, 
and  difficult  to  cure.  The  quickest  and  most  reliable  method  of 
cure  in  cases  of  multiple  boils  is,  in  our  experience,  Wright's  vaccine 
treatment,  the  vaccine  being  prepared  from  staphylococci  isolated 
from  the  patient.  When  this  treatment  cannot  be  carried  out,  the 
administration  of  yeast  preparations  internally  will  be  found  to  be 
useful  in  some  cases — e.g.,  ceridin  pills.  Occasionally  a  small  boil 
may  be  aborted  by  applying  a  droplet  of  pure  carbolic  acid  by 
means  of  a  pointed  pencil  of  wood  drilled  into  the  centre  of  the 
papule.  For  old  indurated  boils  the  continuous  application  of  a 
carbolic  lotion  (2  to  5  per  cent.)  on  lint  occasionally  causes  them  to 
become  absorbed. 


2266 


COSMOPOLITAN  SKIN  DISEASES 


As  a  preventive,  a  salicylic  alcoholic  lotion  (i  to  2  per  cent.) 
used  after  the  daily  bath  is  advantageous. 

Sycosis  coccogenica. — This  is  fairly  common  in  both  Europeans 
and  natives.  In  the  negroes  Fox  has  often  observed  the  formation 
of  tiny  cheloidal  tumours  after  this  affection.  Depilation  and  the 
use  of  a  vaccine  is  the  best  method  of  treatment.  We  have 
observed  a  case  of  Dermatitis  papillaris  capillitii  (Kaposi). 

Erysipelas.- — Ordinary  erysipelas  due  to  streptococci,  and  to  be 
distinguished  from  the  filarial  erysipelatoid  attacks  preceding  the 
development  of  elephantiasis,  is  not  rare.  Ichthyol  ointment  or 
lotion  (10  per  cent.)  answers  well. 


THE  ERYTHEMATA. 

Erythema  solare  is  common  in  Europeans  recently  arrived,  and  in 
those  who  live  an  open-air  life,  such  as  planters.  It  is  followed 
by  pigmentation  (sunburn,  see  pp.  82  and  2231).     The  application 

of  calamine  lotion,  followed  by  the 
use  of  boric  vaseline  or  rose-ointment, 
is  beneficial. 

Erythema  intertrigo  is  very  fre- 
quently observed  in  corpulent 
persons.  Washing  the  parts  with  a 
potassium  permanganate  solution 
(1  in  5,000),  followed  by  application 
of  boric-talc  or  salicylic-talc  powder 
(acid,  boric.  3i-,  talci  §i.,  or  ac.  salicyl. 
gr.  x.,  talci  §i.),  is  useful.  Persons 
suffering  from  intertrigo  are  very 
liable  to  become  infected  with  tinea 
cruris. 

Erythema  nodosum  —  Erythema 
multiforme. — These  affections  are 
occasionally  met  with,  but  much 
more  rarely  than  in  temperate  zones. 
We  have  seen  two  cases  of  the 
variety  of  erythema  multiforme 
known  as  herpes  iris. 

Erythema  annulatum  and  Erythe- 
ma gyratum,   in    persons    suffering 
from  fever,  and  coming  from  tropical  Africa,  should  always  arouse 
the  suspicion  of  trypanosomiasis. 

Diffuse  Erythema  scarlatiniforme  and  Erythema  morbilliforme 
may  be  seen  in  some  malarial  patients.  They  may  occasionally  be 
caused  by  quinine,  but  in  most  cases  are  of  malarial  origin.  The 
diagnosis  of  erythemata  in  dark  natives  is  difficult.  The  medical 
man  of  long  experience,  however,  will  be  able  to  detect  a  peculiar 
shiny  aspect  of  the  skin  with  a  distinct  pinkish  tinge. 


Fig.  891. — Herpes  Iris. 


THE  EXANTHEMATA  2267 

Purpura. — Schonlein's  purpura,  Henoch's  purpura,  and  Werlhof's 
purpura  are  not  common  in  the  tropics,  though  we  have  seen  cases. 
A  symptomatic  purpura  eruption  is  occasionally  seen  in  the  last 
stage  of  kala-azar,  in  malaria  and  other  maladies. 

THE  EXANTHEMATA. 

Smallpox,  chicken-pox,  and  measles  are  very  common  in  the 
tropics,  though  scarlet  fever  is  but  rarely  met  with. 

Smallpox,  of  which  we  have  already  given  a  description  (p.  i486), 
is  very  common,  and  often  spreads  in  extensive  epidemics,  and 
may  present  the  confluent  type  and  the  hemorrhagic  type,  which 
is  rare  in  Europe.  In  colonies  under  European  rule  vaccination 
is  extensively  practised.  The  vaccine  does  not  retain  its  im- 
munizing properties  for  more  than  a  few  weeks  in  the  tropics,  and 
hence  it  is  advisable  for  each  colony  to  be  provided  with  a  central 
vaccine  depot  where  the  lymph  can  be  prepared  under  careful 
supervision.  Owing  to  the  habits  of  the  lower  classes  and  to  many 
of  the  vaccinators  being  non-medical  men,  serious  infections  with 
other  diseases  may  occur. 

Measles  may  be  difficult  to  recognize,  as  the  eruption  in  dark- 
skinned  races  is  better  felt  than  seen,  but  the  coryza  and  other 
symptoms  are  generally  sufficient  to  enable  a  correct  diagnosis 
to  be  made. 

URTICARIA— LICHEN  URTICATUS— PRURIGO. 

Urticarial  eruptions  are  as  frequent  in  the  tropics  as  in  temperate 
zones,  though  to  the  new-comer  the  diagnosis  of  urticaria  in  dark- 
skinned  natives  is  far  from  easy.  Of  lichen  urticatus  we  have  seen 
several  cases  among  European  and  half-caste  children,  and  of 
urticaria  pigmentosa  we  have  seen  one  case— a  European  child. 
We  have  observed  true  prurigo  of  Hebra  in  two  native  girls. 

DERMATITIS  VENENATA. 

Several  tropical  plants  and  grasses  produce  substances  highly 
irritating  to  the  skin,  but  the  subject  has  already  been  treated  in 
Chapter  XCIV.,  p.  2151.  The  dermatitis  so  caused  may  be  urticarial, 
erythematous,  eczematous-like,  or  bullous,  and  may  extend  to  large 
portions  of  the  body.  The  forms  of  dermatitis  venenata  due  to 
animal  agents,  such  as  ants,  bugs,  caterpillars,  etc.,  have  been 
already  mentioned  in  Chapters  XIV.  and  XCVL,  p.  2200. 

PARASITIC  DISEASES. 

Trichophytoses. — In  tropical  countries,  in  addition  to  the  tricho- 
phytoses peculiar  to  the  tropical  climate,  several  other  forms  ui 
trichophytic  affections  occur  which  are  clinically  identical  with 
those  met  with  in  temperate  zones,  such  as  tinea   circinata,  tinea 


2268 


COSMOPOLITAN  SKIN  DISEASES 


capitis,  tinea  barbae.  The  fungi  are,  however,  in  most  eases 
different  species  (see  p.  2052).  In  our  experience,  tinea  capitis 
is  less  common  in  India,  Ceylon,  and  tropical  Africa,  than  in 
Europe  and  America.  On  the  other  hand,  it  is  extremely  common 
in  the  American  negroes.  The  fungi  found  in  the  tropics  are 
generally    large-spored    ones.     Microsporum    audouini  has   never 

been  found  by  us.  Favus 
is  rare  in  tropical  Africa 
and  Asia,  but  common  in 
China,  Egypt  and  in  the 
Sudan. 

Pityriasis  versicolor. — 
The  pityriasis  versicolor 
of  temperate  zones  may 
be  found  in  the  tropics. 
It  is  to  be  noted,  how- 
ever, that  several  writers 
on  tropical  medicine  con- 
fuse pityriasis  versicolor 
with  another  dermato- 
mycosis  which  is  ex- 
tremely common — tinea 
flava  (see  p.  2073). 

Pediculosis  and  Scabies. 
— Pediculosis  capitis  is 
extremely  common, 
although  natives  gener- 
ally take  great  care  to 
keep  their  hair  in  good 
condition  by  regularly 
combing,  washing,  and 
oiling  it.  According  to 
Fox,  Carmichael,  and 
Pendergast,  pediculosis 
capitis  in  the  Southern 
States  of  North  America 
is  much  less  frequent  in 
the  negroes  than  in  the 
whites,  as,  according  to 
them,  the  negroes  take 
greater  pains  in  the  care 
of  the  scalp  than  do  the 
lower-class  whiles.  Pediculosis  corporis  and  Pediculosis  pubis  are 
as  frequent  in  the  tropics  as  in  temperate  zones,  and  so  is  scabies. 
Pediculosis  pubis  may,  however,  be  very  rare  or  absent  in  races 
accustomed  to  regular  shaving  of  the  pubic  hair.  For  description 
of  the  parasites  seeip.  753.      Scabies  is  described  on  p.  2217. 


Fig.  892. — Septic  Pemphigus. 


BULLOUS  ERUPTIONS 


2269 


BULLOUS  ERUPTIONS. 

Epidermolysis  bullosa  is  occasionally  observed. 

Pemphigus  vulgaris  and  Septic  pemphigus  cases  are  not  rare  in 
the  tropics.  In  the  cases  of  septic  pemphigus  we  have  always 
found  virulent  streptococci.  The  eruption  is  similar  to  what  one 
sees  in  temperate  zones.  We  have  seen  a  case  of  Pemphigus 
vegetans,  and  we  have  observed  a  typical  case  of  Pemphigus  folia- 
ceus,  contracted  in  Ceylon,  and  another  in  Indo-China.  Dermatitis 
herpetiformis  is  not  rare. 

Of  Hydroa  vacciniformis  we  have  seen  two  cases  in  European 
children.) 

HERPES. 

Herpes  facialis  febrilis  is  common  during  attacks  of  malarial  fever 
and  other  fevers,  but  very  rare,  as  is  well  known,  in  enteric. 

We  have  seen  in  European  children  a  similar  condition  to  what 
some  French  writers  call  fievre  licrpetique.  The  condition,  as  seen 
by  us,  is  characterized  by  a  sharp  attack  of  fever  lasting  about 


Fig.  893. — Psoriasis. 

twenty-four  hours,  and  at  the  same  time  by  the  appearance  of  a 
few  herpetic  vesicles — in  our  cases  on  the  thighs  and  buttocks. 

Herpes  progenitalis  is  very  common,  especially  in  Europeans. 

Herpes  zoster  (zona,  shingles)  is  frequently  met  with  in  Europeans 
and  natives. 


22JO 


COSMOPOLITAN  SKIN  DISEASES 


ECZEMA— ACRODERMATITIS  PERSTANS— PSORIASIS— 
PARAPSORIASIS— SEBORRHEA— DERMATITIS  EXFOLIATIVA. 

Eczema  is  extremely  common,  and  all  varieties  of  it  are  found 
in  the  tropics,  as  in  temperate  zones,  both  in1  natives  and  [Europeans. 
The  treatment  |  is 'often  very  difficult.  In  our  [experience  greasy 
preparations,  and  evenj  pastes  are  as  ja  rule  badly  borne  except 
in  some  chronic  cases.     Generally  speaking,  it  is  best  to  use  lotions 


Fig.  894. — Psoriasis  in  a  Sinhalese. 


Fig.  895. — Dermatitis  Exfoliativa 
in  a  Sinhalese. 


such  as  resorcin  (|  to  1  per  cent.)  or  liq.  plumbi  (2  per  cent.).  Some 
cases  of  eczema  will  improve  only  on  the  patient  going  to  a  cooler 
climate.  Wilson's  Eczema  verrucosum,  characterized  by  great 
dryness  and  hardness  and  warty  appearance  of  the  affected  part, 
is  frequently  met  with  among  natives,  in  whom  it  mostly  attacks 
the  toes. 

Acrodermatitis  Perstans. — We  have  seen  two  cases  of  a  very 
obstinate  chronic  dermatitis,  with  exfoliation,  on  the  extremities 


ECZEMA 


2271 


of  Sinhalese  natives,  apparently  identical  with  acrodermatitis  per- 
stans  of  Hallopeau.  They  were  different  clinically  from  the 
acrodermatitis  vesiculosa  described  by  one  of  us. 

Psoriasis  is  considered  by  most  writers  to  be  extremely  rare  or 
absent  in  native  races  in  the  tropics.  Rutz  states  that  he  never 
saw  a  single  case  of  psoriasis  in  a  negro  during  his  many  years  of 
practice' in  Martinique.  Howard  Fox,  senior,  thinks  that  possibly 
the  savages  of  Africa  are  free  from  psoriasis  on  account  of  exposure 
of  the  skin  to  sunlight,  and  that  the  negroes" of. Norlh  America 
have  inherited  this  pecu- 
liarity. In  our  experi- 
ence, psoriasis  is  fre- 
quently met  with  in  the 
tropics  in  Europeans  and 
natives  of  every  race. 

Seborrhoeic  affections 
are  common  in  the 
tropics,  especially  in 
Europeans.  A  sebor- 
rhceide  of  the  chest  is 
frequently  met  with,  and 
often  confused  with  ring- 
worm. The  microscop- 
ical examination  will 
clear  the  diagnosis.  The 
use  of  a  sulphur  ointment 
(5  per  cent.)  is  the  best 
treatment. 

In  Ceylon  a  peculiar 
form  of  seborrhcea  cap- 
itis with  yellowish  scales 
is  occasionally  seen  in 
European  children  be- 
tween four  and  twelve 
years  of  age.  This  affec- 
tion is  probably  due  to 
Pityrosporum  cantliei 
Castellani,  1908,  and 
quickly  disappears  when 
the  child  goes  to  cooler 
climates. 

Dermatitis  exfoliativa  (pityriasis  rubra)  is  not  rarely  met  with, 
occasionally  following  on  psoriasis.  In  Ceylon  we  have  observed 
two  cases  in  Sinhalese  natives.  The  amount  of  desquamation  was 
enormous.  On  removing  the  scales,  which  were  white,  the  skin 
appeared  of  an  angry  red  colour.  At  times,  on  superficial  examina- 
tion, certain  cases  may  be  mistaken  for  diffuse  tinea  imbricata. 


Fig.  896. — Dermatitis  Exfoliativa  simu- 
lating Tinea  Imbricata. 


2272  COSMOPOLITAN  SKIN  DISEASES 

ACNE  VULGARIS— ACNE  ROSACEA— ACNE  VARIOLIFORMIS— 
ACNE  CHELOID. 

Acne  vulgaris  and  Comedos  are  extremely  common  in  all  races. 
Both  types  of  acne — Acne  indurata  and  Acne  papulosa  et  pustulosa— 
are  observed.  The  treatment,  which  is  as  difficult  in  the  tropics  as  in 
temperate  zones,  is  based  on  the  use  of  medicated  soaps  and  sulphur 
or  ichthyol  lotions  or  ointments.  The  vaccine  treatment  may 
occasionally  give  good  results. 

Acne  rosacea  is,  in  our  experience,  comparatively  rare  in  the 
tropics,  though  we  have  seen  cases  in  all  races.  True  rhinoplixma 
we  have  also  observed. 

Acne  Varioliformis. — This,  in  our  experience,  is  as  frequent  in 
the  tropics  as  in  temperate  zones,  and  may  be  found  in  all  races. 
The  regions  of  the  body  more  commonly  affected  are  the  fore- 
head, temples,  the  front  of  the  sternum,  and  the  interscapular 
region. 

Acne  cheloid  is  very  common,  especially  among  native  races. 
The  back  of  the  neck  is  generally  affected.  Cases  of  Acnihs  and 
Folliclis  are  occasionally  seen.     These  are  probably  tuberculides. 

HYPERIDROSIS  AND  BROMIDROSIS. 

These  conditions  are,  for  climatic  reasons,  very  common  in  the 
tropics,  and  have  already  been  considered  (see  p.  2222).  The 
treatment  may  be  very  difficult.  Naphthol  or  salicylic  alcoholic 
lotions  (1  per  cent.),  followed  by  a  salicylic,  boric,  or  tannoform 
powder,  are  useful.  If  there  is  much  inflammation  of  the  skin,  no 
alcoholic  lotions  should  be  used,  but  simply  water  solutions  of  boric 
acid  (2  per  cent.)  carbolic  acid  (|-  per  cent.),  permanganate  of  potas- 
sium (1  in  5,000),  and  occasionally  hydrargyrum  perchloride  (1  in 
2,000  or  4,000),  after  which  a  salicylic  or  boric  powder  is  applied. 
The  same  powder  should  be  sprinkled  on  the  socks  and  shoes  and 
undergarments.  Internal  treatment  by  sulphur,  acid  drinks, 
etc.,  is  not  of  much  use.  Belladonna  and  atropin  will  stop  the 
secretion  for  a  time,  but  they  must  be  pushed  till  unpleasant 
symptoms  occur.  We  have  seen  a  case  of  chromidrosis  of  the  axilla 
in  a  native  boy  due  to  the  presence  of  a  bacillus  closely  allied  to  the 
Bacillus  prodigiosus,  and  another  due  to  a  red-pigment-producing 
coccus. 

Granulosis  rubra  nasi  is  occasionally  seen  in  half-caste  and 
European  children. 

LICHEN  PLANUS— LICHEN  SPINULOSUS— PITYRIASIS  RUBRA 
PILARIS— PARAKERATOSIS  VARIEGAT A— POROKERATOSIS. 

Lichen  planus  is  common  in  the  tropics  among  Europeans  and 
natives  of  the  various  races.  In  very  dark-skinned  natives  the 
diagnosis  may  be  difficult  to  the  medical  man  used  to  seeing  skin 


TUMOURS 


2273 


diseases  in  Europeans  only.  Apart  from  the  colour,  however,  the 
skin  lesions  are  identical,  the  papules  having  an  angular  outline 
and  a  flat,  occasionally  umbilicated,  shiny  surface.  When  the 
eruption  disappears,  it  generally  leaves  behind  some  pigmentation, 
which  is  extremely  well  marked  in  natives.  Lichen  nitidus  has  been 
seen  by  us  on  the  penis  of  a  half-caste  and  several  Europeans. 

Lichen  spinulosus  is  occasionally  met  with  in  children. 

Of  Pityriasis  rubra  pilaris  we  have  seen  a  case  in  a  European. 

Parakeratosis  variegata  was  seen  by  us  in  a  half-caste  patient. 
We  have  come  across  two  cases  among  natives  of  Mibelli  and 
Resphighi's  Porokeratosis.  We  have  seen  a  case  of  Granuloma 
annulare  in  a  European  planter  and  one  in  a  native  clerk. 


TUMOURS  OF  THE  SKIN. 

The  tumours  met  with  in  temperate  zones  are  met  with  also  in 
the  tropics  in  Europeans  as  well  as  natives.  There  is  no  doubt, 
however,  that  native  races  are  more  subject  to  some  classes  of 
tumours  than  to  others.  We  would  call  attention  to  the  extreme 
frequency  among  the  natives  of  cheloid,  the  common  occurrence  of 
fibroma  molluscum,  and  the  comparative  rarity  of  epithelioma  of 
the  face. 

CONNECTIVE-TISSUE    TUMOURS. 

Benign  Connective-Tissue  Tumours. 

Simple  fibroma,  Fibroma  pendulum,  and  Fibroma  molluscum 

(ncuro-fibromatosis  of  Recklinghausen)  are  very  frequently  met 
with  in  natives.  Myomata  are  occasionally  observed — in  our  cases 
always  on  the  face. 

Angiomata  are  not  rare,  and  multiple  Telangiectases  are  fairly 
common,  and  Lymphangiomata  very  frequent. 

Xanthoma  planum  and  Xanthoma  tuberosum  are  frequently 
observed. 

Xanthoma  diabeticorum  is  very  common  in  India  and  dylon, 
where  the  better  classes  suffer  greatly  from  diabetes.     An  example 
of  Balzer's  Pseudo-Xanthoma 
or  Elastorrhexis  affecting  the 
abdomen  was  observed  by  us 
in  a  half-caste  woman. 

Cheloid . — This  is  extremely 
frequent  in  native  races. 
According  to  some  authors, 
negroes  suffer  from  it  sixteen 
to  eighteen  times  as  much  as 
whiles.  In  Indian  races  it  is 
not  so  frequent  as  in  African 
natives,  but  still,  much 
more      frequent      than      in 


Fig.  097. — Cheloids. 


143 


2274 


COSMOPOLITAN  SKIN  DISEASES 


Europeans.  The  smallest  wounds,  such  as  those  made  in  tattooing, 
may  be  followed  by  cheloid.  In  Chinamen  it  often  follows  hypo- 
dermic injections  of  morphia. 

Malignant  Connective-Tissue  Tumours. 

Multiple  sarcomatosis  of  the  skin  is  rare.  We  have  seen  two  cases, 
both  in  Sinhalese  girls. 

Mycosis  fungoides  has  been  observed  by  us  once  only  in  a  half- 
caste  man. 

EPITHELIAL    TUMOURS. 

Benign  Epithelial  Tumours. 

Epithelial  moles  are  frequently  observed. 
Molluscum  contagiosum  is  met  with  in  all  races. 


Fig. 


-Molluscum  Contagiosum. 


Verrucae  and  Warts  are  extremely  common.  In  two  instances  we 
have  seen  Sinhalese  boys  covered  all  over  the  body  with  hundreds  of 
warts.     Filijorm  warts  are  met  with,  and  warts  on  the  genital  organs 


EPITHELIAL   TUMOURS 


2275 


J 


Fig.  899. — Molluscum  Contagiosum:  Histological  Features. 


Fig    900. — Fibroma  Molluscum  in  a  Sinhalese. 


2276 


COSMOPOLITAN  SKIN  DISEASES 


Fig.  qoi. — Fibroma  Molluscum:  Larger  Variety. 


Fig.  902. — Fibroma  Molluscum:  Larger  Variety. 


are  very  common.  Verruca  senilis  and  Verruca  seborrheica  are 
frequent.  The  best  treatment  for  ordinary  warts  is  carbon  dioxide 
snow. 

Escomel  has  drawn  attention  to  a  peculiar  treatment  for  warts  in  vogue 
among  certain  races  in  South  America.    These  people  apply  the  crushed  body 


MIXED  TUMOURS 


2277 


of  a  beetle  belonging  to  the  genus  Meloe  to  the  wart,  the  horny  layer  of  which 
has  been  first  scraped  off.  The  wart  disappears,  leaving  a  slight  whitish  scar. 
The  active  principle  is  to  be  found  in  the  beetle's  blood. 

Hyperkeratosis  of  the  whole  sole  is  often  observed  in  natives  going 
barefoot.'  We  have  seen  several  cases  of  Comu  cutaneum  ;  the 
situation  was  generally  on  the  hands,  but  in  a  case  the  condition 
developed  at  the  edge  of  an  ulcus  tropicum  (see  Fig.  862,  p.  2187). 

Malignant  Epithelial  Tumours. 

Rodent  ulcer  is  comparatively  rare  among  natives,  but  we  have 
seen  one  case  in  a  Sinhalese  woman.  We  have  observed  a  case  of 
Melanotic  carcinoma  and  two  of  Paget's  disease  of  the  nipple  among 
half-castes. 

MIXED  TUMOURS. 

Adenoma  sebaceum  of  the  face  has  been  seen  but  rarely  by  us. 
We  have  never  observed  in  the  tropics  cases  of  true  Angiokeratoma 
on  the  hands,  but  we  have 
seen  a  somewhat  similar  tumour 
on  the  scrotum  of  a  European. 
A  diffuse  type  of  angiokeratoma 
of  the  foot  somewhat  resem- 
bling mycetoma  has  been  de- 
scribed in  South  America 
(see  p.  2147). 

RHINOSCLEROMA. 

A  case  of  rhinoscleroma  has 
been  observed  by  us  in  an 
Indian  coolie,  and  Gros  has 
reported  the  occurrence  of  the 
disease  in  Algiers. 

TUBERCULOSIS  AND 

TUBERCULIDES— LUPUS 

ERYTHEMATOSUS. 

Lupus  vulgaris  is  met  with  in 
the  tropics  in  all  races,  but, 
according  to  our  observation,  is 
far  from  being  so  common  as  in 
Europe.  FIG.  9o3. 

Tuberculosis  verrucosa  cutis  is 
very  rare,  and    Scrofulodermia 

much  less  common  than  in  temperate  zones.  All  the  so-called 
tuberculides — Lichen  scrofulosorum,  Acne  scrofulosorum,  Bazin's 
Erythema  induratum,  Folliclis,  and  Acnitis — are  observed  but 
rarely  in  the  tropics. 


-Lupus  Vulgaris  in  a 
Sinhalese. 


227S 


COSMOPOLITAN  SKIN  DISEASES 


Lupus  erythematosus,  as  regards  which  we  agree  with  those 
writers  who  do  not  consider  it  of  tubercular  origin,  is  very  rare 
in  the  tropics. 

While  tuberculosis  of  the  lungs  is  at  the  present  time  extremely 
common  in  many  parts  of  the  tropics,  skin  affections  of  tubercular 
origin  are,  comparatively  speaking,  infrequently  met  with. 

SYPHILIS— VENEREAL  SORES— BALANO-POSTHITIS. 

At  the  present  date  syphilis  is  rampant  all  over  the  tropics. 
In  the  past  there  is  reason  to  believe  that  it  was  unknown  in  many 
of  those  tropical  regions  which  were  unopened  to  the  cosmopolitan 


Fig.  904. — Papulosquamous  Syphilide. 

trade.  According  to  Lambkin,  in  some  parts  of  Uganda  syphilis 
affects  more  than  half  of  the  population,  and  this  enormous  diffusion 
of  the  malady  has  taken  place  during  recent  years  since  the  country 


SYPHILIS  22  70 

has  been  opened  up.  Syphilis  is  very  frequently  observed  now  also 
in  all  the  other  regions  of  Africa,  and  is  very  common  in  tropical 
Asia.  It  has  been  noted  by  Fox  that  in  America  it  is  much  more 
frequent  among  negroes  than  among  whites.  In  our  experience,  the 
virulence,  as  well  as  the  symptoms  of  the  disease,  are  not  much 
different  from  what  one  sees  in  Europe.  We  can,  however,  confirm 
Brault's  observation  on  the  frequency  of  the  primary  sore  on  the 
supra-pubic  region  of  natives,  who  regularly  shave  their  pubis. 
Perhaps  the  general  enlargement  of  the  lymphatic  glands  is  more 


Fig.  905. — Pustular  Svphilide 


marked  in  natives,  and  circinate  and  pustular  syphilides,  as  ob- 
served by  H.  Fox,  are  more  common.  The  tertiary  ulcerative 
lesions  are  apt  to  become  of  enormous  proportions,  owing  to  second- 
ary infections,  and  to  the  patient  not  seeking  proper  medical  advice 
for  a  long  time.  Of  great  interest  is  the  fact  that  in  uncivilized 
native  races  the  so-called  parasyphilitic  affections  (progressive 
paralysis  and  tabes  dorsalis)  are  extremely  rare. 

As  regards  the  treatment  of  syphilis  in  the  tropics,  inunctions  are 
very  unpleasant  in  a  hot  damp  climate.     We  generally  prefer  the 


2  2  So 


COSMOPOLITAN  SKIN  DISEASES 


ordinary  internal  treatment  by  hydrargyrum  cum  creta,  gr.  i.,  three 
times  daily,  and  give  also  in  most  cases  several  injections  of  salvarsan 
or  neosalvarsan.  The  technique  of  the  salvarsan  treatment  has 
been  given  in  the  chapter  on  Framhoesia,  p.  1560.  We  use  also 
injections  of  various  preparations  of  mercury.  A  mixed  mercury 
and  potassium  iodide  treatment  is  of  advantage  in  some  cases. 
Natives  are  said  by  some  authors  to  be  extremely  susceptible  to 
mercury,  but  in  our  experience  this  has  been  exaggerated.     We 


Fig.  906. — Ulcer:  Tertiary 
Syphilis. 


Fig.  907. — Ichthyosis  in  a 
Sinhalese  Girl. 


generally  give  them  the  same  doses  as  to  Europeans.  Native 
doctors  give  often  mercury  disguised  in  various  ways.  Decoctions 
of  various  herbs  are  also  administered.  In  Abyssinia  and  Erythrrea 
a  decoction  of  a  herb  related  to  sarsaparilla  and  called  '  usciva,' 
is  much  used,  according  to  Annaratone. 

Venereal  Sores. — These  are  common  in  all  races,  but  are  more 
apt  to  take  a  phagedenic  character  in  the  tropics. 

Balano-posthitis. — Every  type  of  balano-posthitis  is  met  with 
in  the  tropics. 


ICHTHYOSIS 


2281 


ICHTHYOSIS— SCLERODERMA— MORPHEA. 

Every  type  of  Ichthyosis  is  met  with  in  the  tropics,  from  simple 
Xerodermia  to  Ichthyosis  hystrix.    Diffuse  Sclerodermia  is  rare, 


Fig.  908. — Ichthyosis. 

but  circumscribed  sclerodermia  (morphea)  is  rather  frequent.     We 
have  seen  a  case  of  Sclerema  neonatorum  in  a  Sinhalese  baby. 

KAPOSI'S  DISEASE— ACANTHOSIS  NIGRICANS— DARIER'S 

DISEASE. 

We  have  seen  in  the  tropics  several  cases  of  Kaposi's  disease 
(xerodermia  pigmentosa)  among  European  and  half-caste  children. 
\\V  have  come  across  in  the  tropics  a  case  of  Acanthosis  nigricans. 
We  have  observed  in  Ceylon  a  typical  case  of  Darier's  disease  in  a 
Sinhalese  beggar. 


LENTIGO— CHLOASMA . 

Freckling  cannot  be  seen  in  very  dark-skinned  natives,  but  is 
easily  visible  in  half-castes.  It  is  very  common  among  Europeans, 
especially  those  who  live  an  open-air  life,  and  are  much  exposed  to 
the  sun. 

Chloasma  is  a  very  common  affection  in  the  tropics,  and  is  found 
among  Europeans  as  well  as  natives.  The  dark  brownish  or  dirty 
yellowish  patches  of  chloasma  are  plainly  distinguishable  in  the 
skin  of  Indian  and  Sinhalese  natives,  though  in  African  negroes 
they  may  be  indistinguishable.     (For  more  details  see  p.  2231.) 


2282 


COSMOPOLITAN  SKIN  DISEASES 


BIOTRIPSIS. 

Cheatle  has  described  under  the  name  '  biotripsis,'  or  '  life-wear,' 
the  trophic  changes  which  take  place  in  the  skin  of  old  people. 
In  Europeans  the  skin,  especially  of  the  hands,  may  become  at 
places  shiny,  smooth,  inelastic,  more  or  less  pigmented  than  normal, 
and  scar-like  lesions  may  be  present.  Castellani  has  described  a 
somewhat  similar  condition  in  old  Sinhalese  in  whom  the  skin  on  the 


Fig.  909. — Biotripsis  in  an  Old  Sinhalese  Man,  simulating  a  Mild  Type 

of  Ichthyosis. 

legs  may  present  a  peculiar  appearance,  becoming  atrophic,  and  the 
superficial  layers  cracking.  The  condition,  on  superficial  examina- 
tion, might  be  taken  for  a  mild  type  of  ichthyosis.  It  is,  however, 
probably  a  trophic  condition  due  to  old  age.  Chalmers  and  Drew 
have  given  an  account  of  this  condition  as  seen  in  the  Sudan. 


DISEASES  OF  THE  HAIR  AND  NAILS. 

The  diseases  of  parasitic  origin  are  common,  and  have  been 
described.  Cases  of  Hypertrichosis  in  man  and  woman  are  occa- 
sionally met  with.  The  so-called  '  fragilitas  crinium,'  as  well  as 
Trichorrhexis  nodosa,  are  rare  in  natives,  this  being  probably  due 
to  the  habit  they  have  of  frequently  oiling  and  greasing  the  hair. 
We  have  seen  cases  of  Moniliform  hair  (monilithrix)  in  Sinhalese  and 
Tamils.  In  several  Sinhalese  decrepit  old  men,  who  wear  their 
hair  long,  and  do  not  take  care  of  it,  we  have  seen  a  condition  of 
inextricable  matting  of  the  hair  somewhat  resembling  Plica. 


DISEASES  OF  THE  HAIR  AND  NAILS  2283 

Canities  is  said  to  take  place  at  a  later  age  in  negroes  than  in 
Europeans,  but  in  our  experience  neither  in  negroes  nor  in  Indian 
races  is  there  any  distinct  difference.  Alopecia  of  every  origin  is 
met  with  in  the  tropics.  Alopecia  seborrhceica  is  very  frequent 
among  Europeans  and  educated  natives.  It  is  rare  among  the  low 
classes  and  coolies.  Alopecia  senilis  is  less  frequent  in  natives  than 
in  Europeans.  Alopecia  areata  is  apparently  rare  among  natives, 
but  recently  we  have  come  across  several  cases;  it  is  fairly  frequent 
among  Europeans.  We  have  seen  a  case  of  pseudo-pelade  of  Brocq 
(folliculitis  decalvans)  in  a  Sinhalese  man. 

All  the  diseases  of  the  nails  met  with  in  temperate  zones  are 
found  also  in  the  tropics.  Brittle  nails  (onychorrhexis),  ridged  nails, 
transverse  furrowing,  and  thinning  of  the  nails,  eggshell  nails, 
shedding  of  the  nails,  are  conditions  occasionally  seen.  Leuco- 
nychia,  or  whitening  of  the  nails,  either  in  spots  (leuconychia 
punctata),  linear  (leuconychia  striata),  or  affecting  the  whole  nail 
(leuconychia  totalis),  is  observed.  We  have  described  at  p.  2236  a 
peculiar  black  pigmentation  of  the  nails.  Onychia,  or  inflammation 
of  the  nail  matrix,  is  not  rare.  Ingrowing  toenail  is  common. 
So-called  nail  pterygium,  or  outgrowth  of  the  posterior  nail  fold,  is 
occasionally  seen,  or  the  opposite  condition,  exposure  of  the  root 
of  the  nail  (ficus  unguium),  may  be  met  with. 

We  have  never  observed  a  case  of  congenital  atrophy,  but  we 
have  seen  one  case  of  supernumerary  nails.  We  have  noted  with 
comparative  frequency  a  form  of  onychogryphosis  affecting  several 
members  of  the  same  family,  and  apparently  hereditary  to  a  certain 
extent.  The  nails  are  enormously  thickened,  and  much  longer 
than  usual.  All  the  nails  may  be  affected,  both  those  of  the  fingers 
and  those  of  the  toes. 

Onychomycosis  of  various  origin  is  a  common  affection,  and  has 
already  been  considered  (p.  2059). 


SOME  COSMOPOLITAN  DISEASES  [OF  MUCOUS 
MEMBRANES. 

Patches  of  Leucoplakia  of  the  tongue  are  common  in  natives,  and 
may  be  of  various  origin — -syphilitic,  frambcetic,  or  due  to  irritation 
caused  by  smoking  or  chewing  various  substances.  Cases  of  the 
so-called  circinate  pityriasis  lingua?  or  annulus  migrans  are  not 
rare.  Lingua  nigra  is  occasionally  seen.  We  have  already  called 
attention  to  the  dark  patches  found  on  the  tongue  in  natives,  and 
which  by  some  writers  have  been  described  as  a  sign  of  ankylo- 
stomiasis. These  pigmented  patches  are  roundish  or  oval,  and 
may  be  found  also  on  the  gums,  the  mucosa  of  the  lips,  on  the  soft 
and  hard  palate,  and  are  apparently  congenital.  A  condition 
which  might  be  called  red  or  purple  tongue,  and  which  often  puzzles 
the  newly  arrived  medical  man,  who  does  not  know  its  origin,  is 
extremely  common  in  Ceylon  among  the  coolies  and  lower-class 


2284  COSMOPOLITAN  SKIN  DISEASES 

natives,  and  is  simply  due  to  chewing  betel.  The  pigmentation 
slowly  disappears  on  the  native  discontinuing  the  use  of  betel. 
Cases  of  furrowed  tongue  (scrotal  tongue)  are  not  rare.  We  have 
seen  a  case  of  Fordyce's  disease  (pseudo-colloid  of  the  lips)  in- a  half- 
caste.  A  case  of  chelitis  exfoliativa  in  a  European  lady  and  cases 
of  perleche  have  been  observed  by  us  among  European  children. 
Under  the  term  seasonal  recurrent  ulceration  of  the  lips,  Gros  has 
described  a  very  superficial  ulceration  on  the  lower  lips  in  Algerian 
natives  which  is  very  common  in  the  hot  season,  and  is  due,  accord- 
ing to  him,  to  a  diplobacillus. 


REFERENCES. 

Annaratone  (1912).     Condizioni  Igieniche  Colonia  Eritrea.     Roma. 

Brault  (1909).     Bulletin  de  la  Societe  de  Pathologie  Exotique. 

Castellani  (1904-14).  Ceylon  Medical  Reports  and  Journal  of  the  Ceylon 
Branch  of  the  British  Medical  Association. 

Castellani  (1917).     Journal  of  Tropical  Medicine. 

Castellani  (191 8).     Annali  Med.  Navale,  vol.  i.,  No.  3. 

Chalmers  and  Drew  (1915).  Journal  of  Tropical  Medicine  and  Hygiene, 
May  1. 

Cheatle,  G.  L.  (1909).     British  Medical  Journal,  June  12,  i.  1411.     London. 

Crocker  (1903).     Skin  Diseases.     London. 

Escomel  (1909),     Bulletin  de  la  Societe  de  Pathologei  Exotique. 

Fox,  H.  (1907).  Transactions  Dermatological  Congress,  New  York.  Obser- 
vations on  Skin  Diseases  in  the  Negro.      (This  is  an  important  paper.) 

Gros  (1909).     Bulletin  de  la  Societe  de  Pathologie  Exotique. 

Jeanselme  (1904).     Dermatologie  Exotique. 

Morris  and  Dore  (191 7).     Diseases  of  the  Skin.     London. 

Pusey  (1907).     Dermatology.     London. 

Seoueira  (1919).     Dermatology.     London. 


INDEX 


The  figures  in  heavy  type  denote  the  chief  references. 


AAA  Disease,  9,  666 

A  A  T  Disease,  9 

Abies  excelsa,  2153 

Abdominal  Organs,  Diseases  of,  131 

Typhus,  1362,  1363 
Abnormalities,  Foetal,   1957 
Abors,  the,  54 

Arrow-poisons  of,   185 
Abortifacient  Poisons,  163,   169 
Abortion,  77 
Ab-oukine,  1535 
Abrin,  190,  1862 
Abrus  precatorius,   189-90 
Absces  du  Foie,  1910 
Abscesses 

Amoebic,   18,   287,    317,   321,   1525, 
1828,   1832,   1836,  1875, 
1893,  1907,  1910 
of  Brain,   1058,  1062, 
in  Enteric,  1401,  1402 
Helminthic 

Ascaris-caused,  1907 
Filarial,   1601,   1602,   1604,    1606 
Fungal,     1058,     1062,    1063,     10-4, 

2139,  2149 
Liver   (Hepatic  Abscess),  122,  321, 
335.    io(J3.    1064,   1 1 86, 
1521,  1907,  1908,  2139 
Amoebic,  18,  287,  317,  1521,  1525, 
1828,  1834,  1836,   1875, 
1893,  1907,  1910 
Multiple  Septic,   1525 
Multiple,  1061 

ot  Myositis  Parulenta  Tropica,  1975 
of  Neck,  Aspergillar,  1028 
Nocardial,  2149 
of  Paragonimiasis,   1586,   1587 
Protozoal,  335 
Pulmonary,  335,  1949 
Splenic,  1905 
Streptococcal,  927 
Tonsillar,  1061,  1  717 
of  Vertebral  Column,  1072,  1075 
Absorption  Test,  1397 
Abyssinian  People,  47 
Acanthia  leclularius,  763 
Acanthiadcs,  762 
Acanthias,  762 


Acanthobdellida,  688 
Acanthocephala,  621,  679 
Acanthocephaliasis      with       Gordia- 

ceiasis,  1777 
Acanthocera,  820 

Acanthocheilonema,  623,  632,  642 
References,  681 
Species 

drancunculoides ,  643 
grassii,  643 

Persians,  623,  643,  707 
recondita,  643 
Acanthokeratodermia,  2256 

Precornufaciens,  2257 
Acanthoma  Inguinale,  2196 
Acanthophis,  246 

antarcticus,  247,  251 
Acanthopterygii,  232 
Acanthosis,  2033 
nigrans,  2223 
nigricans,  2281 
AcanthosporidcB,  471 
AcanthuridcB,  232 
Acaiithurus   luridus,    232,     233,    234, 

240 
Acara  Dermatitis  Urticarioides,  2216 
Acarina,  206,  215,  690 

References,  741 
Acarina  of  Domestic  Animals  some- 
times    attacking     Man, 
2214-15 
Acarine  Dermatites,  691,  1730,  2200, 
2206,  2213 
Dermatoses,  References,  2220 
Acaropsis,  728 

mericourti,  728 
Acarus,  693,  2022,  2023,  2096 
agyptus,  724 
batatus,  726 
dysenteries,  729 
exnlcerans,  2218 
folliculorum,  732 
fuscus,  862 
sallina,  693 

humanus  subcutaneus,   2218 
reduvius,  720 
reflexus,  703 
reticulatus,  716 
285 


2286 


INDEX 


A  earns,  continued 

ricinus,  720 

scabiei,  2096,  22  iS 

siro,  2218 

tritici,  72^ 
Acaslyptus.  -40 
Acastelepoii .  278 
Accadia,  Medicine  in,  4 
Accidental  Poisoning,  161,  172 
Acclimatization,  88,  91 
Acclimatizing  Fever,  1229 
Accommodation  Muscles  of  the  Eye, 
Paralysis  and  Spasm  of, 
2005 
Acephala,  470 
Acephalina,  471 
Acs  p>.  >io 

Acephalus,  1958,  1959 
Acherontia  atropos,  226 
Aehinese,  the,  55 

Achorion,  9S6,  989,  1011,  1014,  1101, 
2056,  205S 

akromegalicum ,  1013 

arloingi,  1012,  1014 

atacion,  1013 
«m,   1013 

demergens,  1013 

dikr.on,  1013 

euihythrix,  1013 

gallina,  1014 

gypseum,   1012,   1014,  2037 

moniliforme,  1013 

quinckeanum,   1012,    1014,  2050 

radians,  10 13 

ruber,  1047 

schoenleinii.  1002,  1003,  1011.  1012, 
1067.  107S.  1 105.  2008, 
2009,  2050 

torsi ''.  1  ■  .'     101  ; 
Achroin.iticKS.  359,  401.  402,  501 

gibsoni,  501 

oesperuginus,  501,  S54 
Achromia.  Acquired,  2227 

Congenital.   2230 

Squamosa,  2. 
Achromie  Parasitaire,  207; 
Acid-fast      Organisms     in      Sputum, 
Indications  from,  1521 
Acidosis.  96 
Acinetaria,  296 
Ackee  Poisoning.   17;.   1695 

References,  1099 
Acladiosis,  2089,  2186 

Reference,  2109 
Acl  idiotic  Ulcers.  2190 

;»um,    987,    1 1 1 1.    1112,    1113, 

1114. 1115 
Dermatomycoses  due  to,  2041 
Species 

castellanii,  1112,  2041,  2186 

conspersutn,   1112 


\cland's  Actinomycosis,  2130 
Aclerda  berlesi,  1033,  2163 
Acne,  2264,  2272 

Cheloid,  2272 

Indurata,  2272 

Papulosa  et  Pustulosa,  2272 

Rosacea,  2272 

Scrofulosorum,  2277 

Sebacea,  732 

Varoliformis,  2272 

Vulgaris,  2272 
Acnitis,  2250,  2272,  2277 
Acocanthera,  181,  182 

deflersii,  182 

oubaio,  182 

schimperi,   182 

venenata,  1S2 
Acocantherin,  182 
Aconite,  Poisoning  bv,  124,  16^,  169, 

184,  189 
Aconitum,  163-4,  181,  1S4,  1S5 

ferox,  181,  1 84,  185,  189 

heterophylloide,  1 S4 

napellu  ,  2153 
Acquired  Achromia,  2227 

Leucopathia,  2227 

Leukasmus,  2227 

Piebald  Skin,  2227 
Acremoniosis,  2106 
Acremonium,  1121 

Dermatomycoses  due  to,  2041 

Species 

alternatum,  1121 
niveian,  1122 
potronii,  1122,  2106 
Acrochor dines,  245 
Acrodermatitis  perstans,  2270 

Vesiculosa,  2271 

Tropica.  2222.  2244 
Acromegaly  of   the    Piltdown    Skul 

112 

Actinism 

Aciinobacillus.  1066 

lignieresi,   1054 
Actinocephalida,  471 
Actinomyces,  1041 

albosporea,   1047 

albus,   1046 

d/»;,  1046 

aster oides,  1053 

bicolor,  1057 

6ovis,  1051.  1057,  1058,  2130 
sulphurcus.  1051,  1057 

ccllulosee,   1046 

chromogenes,  1046 

cuniculi,   1064 

diastatica,  1046 

.-  v    1046 
rochromogenes,  1046 

farcinicus,  1046 

jlavochromogenes,  1046 


INDEX 


1%§7 


A  ctinomyces,  continued 

flav-us,  1046 

glaucus,   1047 

grisea,  1046 

griseoflavus,  1046 

gruberi,  1047 

hominis,  1051,   1053 

horketii,  2130 

lacertce,  1057 

melanocyclus,  1047 

melanosporea,  1047 

tnicroparva,   1047 

monosporus,  1047 

musculorum  suis,  1057 

myriccB,  1046 

nivea,  1046 

parva,  1047 

pseudotuberculosis,  1057 

roseus,  1046 

ruber,  1046 

rubidaureus,  1050 

rubra,  1047,  1051 

thermophilus,  1047 

verrucosus,  1057 

violaceus,  1046 

viridochromogenes,  1046 
Actinomycetes,  1040 
Actinomycetine,  969 
Actinomycoses,  21 10,  2130 
Actinomycosis,     1040,     1041,     1057, 
1060,  1063,   1066,  21 10, 
2111,  2114,  2117,  2130 

Acland's,  2130 

Black,  2112,  2140,  2141 

of  Body,  21 10,  2148 

Nodular,  21 10,  2148 

Red,  2141,  2142 

True,  2148 

White     or     Yellow,      21 12,     2140, 
2141 
Actinomycotic  Conjunctivitis,  2009 

Corneal  Ulcers,  2009 

Miliary  Metastases  in  the  Choroid, 
2009 

Mycetoma,   2148 
Actinomvxidia,   528,   529 
Acute   Conditions   and   Diseases,  se 
chiefly  under  Names 

Yellow    Atrophy   of   Liver,    1507, 
1508'  1906 
Acytosporea,  504 
Adders,  250,  251 
Venom  of,  243 

Death,  247 
Addison's  Disease,  1181,  1529,  1531, 

1923,  2203 
Adelea,  474 

ovata,  473 
Adeleidea,  477 
Aden  Ulcer,  2 181 
Adenitis,  Equine,  929 


Adenium,  181,  183 
bochmianum,  183 
somalense,  179,  183 
Adenolymphoceles,   1608 
Adenoma  Sebaceum,  Facial,  2277 
Adenomatous  Goitre,  1920 
Adcno-meningee,  1363 
Adipose  Sarcoma,  2111,  2117 
Adobe  Tick  of  Mexico  and   Arizona, 

704 
Adolia,  222 

Adulteration  of  Foods,  95 
Adynamic  Remittent  Fever,  1168 
/Edes     calopus    (see    also    Stegomyia 

calopus),  876 
/Edincs,  786,  790,  799,  1137 
Aeropneusta,  690 
Aeta  Race,  49,  53 
/Etobatis  narinari,   232,   240 
Afar  or  Danakil  race,  47 
Afebrile  Tropical  Splenomegaly,  1289 

Infantile,   1303 
Affovi-burunkue,  2241 
Afghan  Jara  (or  Plague),  2165 
Africa,  Yaws  in,  1537 
Tropical 

Diseases  of,  124-5 
Poisons  of,  125 
Primitive  Medicine  of,  125 
African  Arrow- Poisons,  181 
Fish-Poisons,  188 
Maduromycoses 
Black,  2120,  2121 
White,  2120,  2122 
Myiases*  1631 

Dermal,  163s,  1637 
Rhinal,  1623,  1625 
Rat -poisons,  191 

W<  I    psing   Fevers,    444,    445,    447, 
691,  700,  706,  719,  1318 
References,  1324-5 
Tick    Fever,     20,     691,     694,    700, 

706,  1261,  1318 
Trypanosomiases  {q.v.),   1259 
References,  1281-2 
Afridol,  26 

Afrikanische  Schlafkrankheit,  1260 
Agamodistomum  ophthalmobium,  2007 

Reference,  594 
Agamofilaria,  623,  632,  641 
Reference,  681 
Species 

conjunctives,  623,  641 
georgiana,  623,  641,  642,  2219 
labialis,  623,  641 
oculi  humani,  623,  641,  642, 1974, 

2007 
palpebralis,  641,  642,  1974,  2007 
Agamomermis,  653 

restiformis,  632,  653 
Agchylostomiasis,    1761 


2288 


INDEX 


Age  in  Relation  to  Diet 

Quality,  103 

Quantity,  98 
Age-Limit  for  Entrance  into  Tropical 
Service,  128 


ta,  471 
Aggregatidcs,  471 
Aglypha,  244,  245 
Agrostemma  githago,  197 
Ague,  1 1 29 

Ailanthus  glandulosa,  2153 
Ainhum,  2222,  2241 

References,  2246 
Ainu  Race,  55 

Arrow-Poison  of,  184 
Aipysarus,  249,  251 
Akamushi,  726 
Akanrushi  Disease,   1350 
Akatama,  1989 

Akee-Poisoning,  see  Ackee-Poisoning 
Aker  Lampong,  185 
Akkad  Race,  54 
Alasion,  806 

Alastrim,  1471,  1474,  1491 
Albinism,  123,  124,  2222,  2230 

Ocular,  1995,  2004 
Albizzia  anthelmintica,  1699,  1756 
Albococcus,  925 

tetragenus,  1951 
Albumen  in  Urine  in  Relation  to  Fit- 
ness for   Tropical  Life, 
127 
Albuminuria,  132 
Albumon  in  Snake-Venom,  260 
Alcaligenes,  934,  935,  936,  1362,  1405 

fcecalis,  935,  936,  1409 

metalkaligenes,  936 

vivax,  936 
Alcaptonuria,  2232,  2236 
Alcohol,  Avoidance  of,  91,  1989 

Calories  produced  by,  97 

and  Heat-Stroke,  91,  1453,  1456 

Personal  and  Racial  Poison,  118,  175 
Alcoholic  Coma,  1456 

Dermatitis,   1730 

Drinks,  Cheap,  Danger  of,  175 

Neuritis,  1981 
Alcoholism,  118,  128,  131,  140,  1938, 
1981,  1989,  1997 

in  relation  to 

Crime,  Native,  173,  1981 
Employment  in  the  Tropics,  128 
Life  Assurance,  132 
War  Neuroses,  1981 

Acute,  1524 

Chronic,  1516,  1981 
Alculhuaques,  the,  57 
Aldrichinella,  792 
A lectorobius ,  702,  709 

capensis,  709 

coniceps,  709 


Alectorobius,  continued 

talaje  (talafe),  700,  709 
Aleppo  Boil,  378,  2165,  2166,  2167 
Aleuriospore,  1037,  1039,  n ir 
Aleuriosporinece,  1111 
Aleurisma,  11 12 
Aleurismacecs,  1111 
AleurismecB,  1111 
Aleurobius farince,  729,  2214 
Alga,  923 

Algerian  Relapsing  Fever,  1314 
Algide  Type  of    Subtertian  Malaria. 

1 1 69,  1 1 70 

Alimentary  Canal,  Derangements  of, 

1519,  1520 

Dermapteriasis  of,  1641 

Diplopodiasis  of,   1641 

Diseases  of,  131,  1738  sqq. 

Myiasis  of,  848,  853,  1631 

Spirochsetes  of,  450 
Alkaligenes    Parenteric,    1405,    1408, 

1409 
Alligators,   Traumatisms  caused   by, 

153 
Allobosca,  855 
Aloes,  170 
Alopecia  areata,  2283 

Seborrhceica,  2283 

Senilis,  2283 
Alu-hama,  2076 
Alvathim,  2052 
Alytcs  obstetricans,  355 
Ama-apaka,  1842 
Amaas,  1491 
Amauroascus,  986 
Amaurosis,  Atoxyl-caused,  2007 

Malarial,  n 81,  2004,  2005,  2007 

Quinine-caused,  1181,  2007 
Amaurotic      Type       of       Subtertian 

Malaria,  1181 
Amblyomma,  710,  711,  720,  723 

antericanus,  7O0-1 

annulipes,  723 

cajennense,  723 

dissimile,  700 

hassalti,  723 

hebresutn,  723 
Amblyopia,  post-Amaurotic,  2007 

Quinine-induced,  1201 
Amboyna  pox  or  pimple,  1356 
Ambycera,  751 
Amenorrhcea,  129 
Amentacece,  172 
Amerellao,  1761 

America,  Arrow- Poisons  of,  1S6 
Primitive  Medicine  in,  6 
Vegetal  Poisons  of,  168 

South,  Fish-Poisons  of,  188 
Trypanosomiasis      of      (Chagas' 
Disease),   10,    123,  391, 
427,  430,  1283 


INDEX 


2289 


America,  continued 

Tropical,  Diseases  of,  123-4 
American  Bilharziosis,  1864 

Black  Maduromycosis,  2120,  2122 
Frambcesia,  1538 
Leishmaniasis,  2175 
.Myiases 

Dermal,  1633 
Rhinal,  1623 
Rats  ami  Mice,  915 
Relapsing  Fever,  918,  1323 
Amerind  Division  of  Man,  42,  44,  55, 

124 
Amerosporece,  987 
Amiba,  299 

divergens,  299 
Aniino-Acids  in  Diet,  no 
Amitosis,  291 
Ammannia  baccifera,  190 
Ammonia,  Useless  for  Snake-Bite,  277 
Amnesia,  Tropical,  88 

War  Zone,  1982 
Amccba{ce)      [Entamoeba)       (see      also 
Loeschia),  29,  115,  298, 
875.   1520,    1776,    1838, 
1910,  1931,  i960,  2225 
Binucleate,  299,  322,  323,  324 
Classification  of  Species,  301 
Diagnosis,   313 
in  Infants  and  Foetuses,  320 
Life-cycle,  300-1 
in  Lungs,  320 
Reference,  328 
Species 

buccalis,  317 
coli,  18,  1932 
dentalis,  317 
dysenteries,  115,  1932 
gingivalis,  317 
li))iax,  1833 
//));a^-type,  298,  1833 
lobospinosa,   322 
maxillaris,  317 
mira,  324 
princeps,  299 
proteus,  299,  300,  301 
pulmonalis,  302,  320 
rotatoria,  393 
terricolor,  300 

urina-  granulata,  302,  1933 
urogenitalis,  313,  1931 
vaginalis,  1931 
verrucosa,  300 
vespertilio,  300 
Amdbenruhr,  1825 
Amcebiasis  (Amoebic  Dysenterv),  18, 
30,  287,    873,  877,  905. 
908,    1187,   1587,    1714, 
1825,  1832 
.Etiology,  18,  877,  1827 
Animal  Carriers,  877 


Amcebiasis,  continued 

Blood  Conditions,   1900 

Causal  Organisms,  115,  303,  317, 

321,  875,  877 
Climatology,  122,  124,  1826 
Complications,  1832 
Cyst  Carriers,  1833 
Definition,  1826 
Diagnosis,  1520,  1832-4 

Differential,       1833-4,       1S52, 

1853.  1953 
History,  1826 
Morbid  Anatomy,   1828-30 
Pathology,  1827-8 
Prognosis,  1834 
Prophylaxis,  1836 
References,  1862 
Sequelae,  1832,  1836,  1910 
Sex-incidence,  1827 
Spread,  877 

Symptomatology,  1830  sqq. 
Synonyms,   1825 
Table     of     Parasitic    Infection, 

877 
Treatment,  28-9,  1834-6 
Emetine,  313 
Acute  Type,  1830 
Atypical,  1832 
Chronic  Type,  1 830-1 
Latent  Type,  1828,  1830,  1831 
Mixed  Types,  1830,  1831-2 
Urinary,   1926,  1931 
References,  1936-7 
Amoebic  Abscesses,  18,  287,  317,  321, 
1525,   1828,   1832,  1836, 
1875,  1893,  1907,  1910 
Colitis,  1825 
Cystitis,  1933 

Dysentery,     1S25,    and    see   Amce- 
biasis 
Enteritis,  1825 
Fever,  1832 
Hepatitis,  1832 

Treatment,  29,  1835 
Liver  Abscess,  18,  287,  317,   1521, 
1525,  1828,  1834,  1836, 
1875,  1893,  1907,   1910 
References,  191 8 
Pyelitis,  1933 
Tonsillitis,  1747 
Urethritis,  1944 
Amozbidce,  298 
Amcebina,  298 

Amoeboid  Forms,  change  of,  lo  Tri- 
chomonas,  354 
Amcebosporidium,  492 

polyphagum,  497 
Amok,  176,  1981,  1988 
A  momum  zingiber,  172 
Amorites,  the,  47 
Amorphophallus  campanulatus,  184 

144 


2290 


INDEX 


Ampelidacece,  2152,  2153,  2I59 
Amphibia,  Parasites  of,  353,  355,  395, 
39S,  400,  461,  478,  480, 
488,  546,  549,  500 
Venomous,  240 
References,  241 
Amphimerus,  576,  577 

noverca,  577,  1907,  191 7 
Amphimonadidce,  333 
Amphistomata,  561 
Amphistomes,  558 
Amphistomum  hominum,  563 

watsoni,  562 
AmphitvetidcB,  604 
Amulets,  4,  5 

Amyloidosis,   1146,   1156,   1659,  1663 
Ana-worm,  161 9 
Anacardiacetz,   171,   178,   2152,   215^, 

2156,  2162 
Anacardioidece,   2150 
Anacardium  occidentale,   171,   178 
Anaemia  and  Allied  Conditions,  1895, 
1903 
Climatology,  122,  123,  124 
Parasites     associated     with     or 
causing,  552,  563,  663, 

!753-  *758.  1759,  1761. 
1764,  1765 

Febrile  Splenic,  1299 
Infantile,  20,  1299 

Infantum  Leishmania,  1299 

Malarial,  1150,  1164,  12 14,  1219 

Pernicious,  1169,  1575 

Post-Malarial,  11 51-2.  n 84 

Severe,  Bovine,  515 

Splenic,  1302,1303 
Febrile,  1299 

Infantile,  20,  1299 

Tropical,  75,  666 

Tunnel-Worker's,  1761 
Anaemias,  Bone-Marrow  in,  1905 
Anaemic  Dropsy,  Acute,  1690 

Low  Fever,  1470 
Anaikal,  21 16 
Anakhre,   1975 
Anal  coshol,  828 
Anamirta  cocculus,  187,  188,  191 

panniculata,  187,  191 
Anctmista,    173 
Ananas,  170 

Anaphylactic  Drug  Eruptions,  151 3 
Anaphylaxis,   114 
Anaplasma,  490,  491,  492 

canis,   501 

»iav>inale,  501 
Anaplasmosis,  Canine,   501 
Anatolian  Turks,  55 
Anchilostomanemia,  1761 
Anchylostomiasi,   1761 
Ankylostomiasis,   1761 
Ancistrodon,  250 


Ancistrodon,  continued 
bilineatus,   251 

contortrix,  250,  251,   254,  255 
halys,  251 
himalayanus,   251 
hypnale,  251 

piscivorus,  250,  251,   253,  254,  273, 
487 
Ancylostoma,  476,  552,  553,  624,  659, 
665,  1776,  1777 
Larvfe,     Migrations     of,     Diseases 

due  to,  553 
References,  682 
Species 
americanum  [Necator  americanus], 

673 

braziiiense,  674 
caninum,  671,  672 
ceylaniciou,  024,  674 
duodenale,   122,   124,  205-6,  621, 
624,     663,     664,      666, 
1273,  1552,  1554,  1593, 
1669,  1672,  1679,  1680, 
1761,  1762,  1763,  1764, 
1777,  1838,  2219 
Dermatitis  due  to,  553,  2219 
malayanum,  674 
Ancylostoma  Fever,  1767 
Ancylostomes,  9,   1639 
Ancylostomiasis,   1761 
AncylostomidcB,  623,  624,  659,  665 
Ancylostomina;,  665 
Ancyromonas,  334 
Andamanese,  the,  49,  53 

Food  of,  94 
Andira  araoba,  2153,  2160 
Androctonns  funestus,  207 
Andrum,   1595 
Anemia  intertropicalis,  1761 
Anemie  des  Pays  Chauds,  1761 
Anemone  nemorosa  (plants),  2153 

patens,  2153 
Anemone  scultatus,  204 
Anemones,  stinging,  203,  204 
Anencephalus,   1958 
Anethum  graveolens,   170 
Aneurysm,   1904 

Frambcesial,  1555 
Angeiomata,   123 
Angina,  Ludwig's,  1949 
Streptococcal,    1520 
Vincent's,  448,  452,  959, 1520,  1745, 

1747 
Angiofibroma  cuti  contagiosum  tropi- 
cum,  of  Bassewitz,  1568, 
2247,   2253 
References,  2262 
Angiokeratodermia,  2256 
of  Feet,  2148,  2277 
of  Hands,  2277 
of  Scrotum,  2277 


INDEX 


2291 


Angioma  of  Liver,  1907 

Angiomata,  2273 

Angioneurotic  (Edema,  1729,  1731 

Angiosporea,  471 

Angiostomidce,  623,  626,  628 

Angoumois  Grain-Moth,   parasite  of, 

2216 
Anguillula,  623,  627,  1639,  2209 
Larvae,  2209 
References,  680 
Species 

aceti,  623,  627 
intestinalis,  628 
stercoralis,   1758 
A  nguilli formes,  232 
Anguillulidcs,  623,  627 
Anguillulina,  623,   627 
Species 

putrefaciens,  623,   627 
References,  680 
Anguillulosis,  Intestinal,  1758 
Angular  Conjunctivitis,  1996,  1997 
Anhalonium  lewinii,  176 
Anideus,  1958 
Anidrosis,  Idiopathic,  2224 

Symptomatic,  2224 
Animal  Carriers  of  Disease   (see  also 
Rats,      Mice,      Ground 
Squirrel,         Tarbagan, 
p.  867),  872 
History,   876 
Hosts 

Definitive,  872,  873,  875-6 
Intermediary,  872,  873 
Intermediate,   873 
Imperfect  Carriage,  921 
References,  921 
Reservoirs  for,  875 
Terms     employed      concerning, 
872-6 
Diseases,  etc.,  carried  by 
Bacterial  Diseases,  897 
Cestode  Infections,  895 
Diseases  of  Unknown  Causation, 

920 
Nematode  Infections,  896 
Plague,  908 

Protozoal  Diseases,  877 
Trematode  Infections,  894 
Animal  -  Caused     Dermatites,     2015, 
2017 
Traumatisms,  115,  147-55 
Animal  Food-Poisoning,  193 
Parasites,   115,  285 

Diseases  due  to,  872,  1533,  1825, 

1944 
in    External    Auditory    Meatus, 

201 1 
of  Eye,  2007 
of    Man,    Carriage    of,   by  some 

other  Animal,  872 


Animal  Parasites,  continued 
of  Man,  continued 

Role  of,   as   Carriers  of  Disease 

(q.v.  above),  872  sqq. 
Sexual  Generation  Stage  of,  872 
Terms  for,  921 
Poisons,  163,  1695 
Spirochetes,  453 
Spiroschaudinnia,  452 
Substances    used    as  Aphrodisiacs, 
171,   172 
Animals,  Bites  of ,  Fevers  due  to,  1356 
sqq. 
Diseases     of,     due     to     Filterable 
Viruses,  541 
Spread  by  A  carina,  691 
Peruvian  Wart  in,  1569 
Poisonous,  203 

References,  227-9 
Tiypanosomes  of,  19-20,  409  sqq. 
Trypanosomiases  of,  1262 
Aniseed,  Oil  of,  191 
Anistomata,   709 
Ankylostomasie,   1761 
Ankylostomen-Krankheit,   1761 
Ankylostomiasis,    1283,    1672,    1673, 

.Etiology,   1762-3 

Carriers,   1762 

Causal  Agents,  672,  674,  1762 

Climatology,  122, 124, 133,  343,  1762 

Complications,   1768 

Definition,  1761 

Diagnosis,  1531,  1768 

Differential,    1182,    1288,    1297, 
1688,  1760,  1768 

in  Earth-Eaters,  1749 

Fever  of,  Probable  cause,  553 

Morbid  Anatomy,  1764 

Nomenclature,   1761 

in  Parenteric,  141 2 

Pathology,   1763-4 

in  relation  to  Pellagra,  1706,  1709, 
1727,   1731 

Prognosis,  1768 

Prophylaxis,   1771  sqq. 

Race  Incidence,  1763 

References,   1778-9 

Symptomatology,  1746,  1763,  1764, 
1903,   1904,  2265 

Synonyms,  1761 

Treatment,   559,   563,    1753,    1760, 
1768 

Ulceration,  2 181 
Annamese,  the,  54,  55 
Annulata,  683 

Annulus  migrans  linguae,  1746,  2283 
Anomomeristica,  690 
Anopheles,  see  with  Anopheiina 
Anophelinat  (Anopheles),  23,  224,  749, 
774.  776,  786-  791,  792 


2292 


INDEX 


Anophelincz  (Anopheles),  continued 
Bite  Prevention,  1205,  1209 
Breeding-places,    1139 
fir  Elimination  of,  1208-9 
Classification,  752-3,  790,  791,  SS3 
Definition,  752 
Definitive  Hosts  of  Plasmodia    873 

883 
History,  752 
Hyperparasites  of,   510 
Identification,  505 
Larvae,  784  sqq. 

Destruction  of,  1207-9 

Parasites  of,  546 
Life-History,   749 
Malaria-carrying,  19,  116,  289,  294, 

505,  508.  747-  79i.  793- 
873,  876,  S83,  884,  888, 
1129,  1131,  1132,  1133, 
1137  sqq.,  1202,  1203 
.Morphology,   752 
Natural  Enemies,  1140 
Ova,  783-4 

Plasmodial  Infection  of,  512 
Prophylaxis  regarding,  1204,   1206 
Species 

aitkeni,   793 

algeriensis,  793,   884 

apri,  662 

barberi,  792,   793 

bifurcatus,  793,  884,   11 38 

canis,  501 

claviger,  5 1 1 

cohcssus,  888 

Constance,  888 

corethvoides,  793 

costalis,   115 

constant,  795 

formosus,   793 

franciscanus,   792 

gigas,   793 

immaculatus,   793 

jamesi,  S88 

jeporensis,   888 

kochi,  886,  888 

kumassii,  888 

lindscni,   793 

maculipennis,  225,  367,  369,  377, 
776,  792,  8S4,  11 38 

marginale,  501 
var.  centvale,  501 

marginata,  655 

manritianns,   888 

ni^ripes,   793,   11 38 

paludis,   888 

perplexus,  792 

pseudopnnctipennis,   792 

punctipennis ,  792 

smithi,  793 

Uncertain 

apicumacula,   792 


AnophelincB  (Anopheles),  continued 
Species,  continued 

ferruginiensis,   792 
martini,  792 
punctimacala,   792 
pursati,  792,   888 
slrigi  macula,   792 
vestipennis,   792 
vincenti,  792,  888 
wellcomei,  793 
Synonyms,  752 

Wings  and  "Wing-veinings,  779-80 
Anophthalmus,   1995 
Anoplura,  218,  748,  749,  750,  752 

References,  760 
Anosmia,  Post-Malarial,  11 84 
Antarctophthirius,   759 
Ant-Bite  Fever   (Formiciasis),   2000, 

2204,  2206 
Antelopes,  etc.,  as  local  Reservoirs  for 

Trypanosomes,   392 
Antenatal  Pathology,   1956 
Anthelmintics,   168 
A)itJiocoridcB,  762.   766,  2200 
Anthocoris,  766,   767 
congolensis,   767 
kingi,   767 
Anthomyia  canicularis,  882 

radicum,   900,   905 
Antkamyides,    825,    852,   1627,    1628, 

1629,  2011 
Anthrax,   22,   24,   876,   899,   908 
Antiarin,   185 
Antiaris    toxicaria,    184,    185,    2152, 

2162 
Antilles,  Vegetal  Poisons  of,  168 
Antiluetin,  28 
Antimonial    preparations,    Poisoning 

by,   162,   170 
Antimony,   25.   26,   1275  sqq.,   1291 

Trioxide,   28 
Antivenenes,  243,  244 
Ants,  Bites  and  Venom  of,  219,  222, 
908,    1556,   1995,   2200, 
2267 
Biting  Species,  222 
Red,  Arrow- Poison  from,  222 
Red  House-,  Enemy  of  Bed-bugs, 

765 
Anyum  (Ainhum),  224 
Apatolestes,  823 
Aphaniptera,   857 
Aphanoascus,   1024 
Aphasic  type  of  Subtertian  Malaria, 

1175,   1176 
Aphides,   761 
Aphiochceta,  1629 

ferruginea,  824,  900,  1630 
Aphramia,  762,   766 

barys,  766 

hcsmatosiplion,  762 


INDEX 


2293 


Aphrodisiacs 
Animal,  171-2 
Vegetal,  171,  172,  177 
■  Aphthce  albcs  infantum,  1741 
lactamen,   1741 
lactantium,  1741 
Tropical,   1780 
Aphthaphyte,   1742 
Aphthoides  Chronica,  1780 
Aphthous  Stomatitis,  1780 
Apides,  Stinging  Species,  219,  2207 

References,  229 
Apiosoma,  492 

bigeminum,  497 
Apis  melliftca,  219 
Apocampta,  823 

ApocynacecB,  163,  164,  165,  169,  178, 
181,    184,    2152,    2153, 
2162 
Apodes,  232 
Aponomma,  710,  711,  720,  722 

gervaisi,  722 
Apoplexy,  Differential  Diagnosis  from 

Heat  Stroke,   1456 
Appendicitis,   ^Etiology,    553,     1739, 
1758-1760 
Diagnosis,  1520 

Differential,  1395,  1396,  1739 
Fungal,  1061 
Gangrenous,   1526 
Helminthic,  due  to 
Ascariasis,  654,   1758 
Schistosoma,  1739 
Trichuriasis,  553,  1758 
Appendicostomy,  1835 
Appendicular  Trench  Fever,  1504 
Aptera,  748,  857 
Aquilostomiasis,    1761 
Arab  doctors,   12  sqq.,   1535 
Arabia,  Diseases  of,     20 
Arabian  Medicine,  12-14 
Arabs,  the,  46,  47 
Aracecs,   172-3,  2152 
Arachnida(dce),  395,  397,  398,  689,  690 
Incerte  sedis,  732 
References,  228,  690 
Stinging  varieties,  206 
Arachniotus,  986 
Arachnolysin,  213 
Arachnomorphae,   212 
Aradidce,  762,  770,  2200 
Aralia  spinosa,  2152 
Araliacece,  172,  2152 
Aranea,  206,  211,  690 
References,  228-9 
Venom,  213-15 
Arawaks,  the,  59,  60 
Archibaldi    Parenteric,     1405,     i|<-s 

1411 
Archida,  222 
Archoplasm,  290,  291,  292 


ArctiidcB,  2208 
Arctomys,  915 

bobcB  (bobak),  913,  1423,  1424 
Flea  of,  869 
Areca  oberacea,  177 
Argas,  702,  703,  706 

cequalis,  703,  704 

americamts{a),  445,  703,  708 

brumpti,  216,   703,   704 

canestrinii,  709 

chinche,  703 

cucumerinus,  703,  704 

erraticus,  708 

hermanni,  703,  704 

kochi,  704 

marginatus,   703 

mauritianus,  703 

megnini,  708 

miniatus,  703,  704 

moubata,  706 

papillipes,   708 

persicus,   216,   453,   454,    700,   703, 
919,  1322 

pulchella,   704 

reflexus,  216,   700,   703,   704 

sanchezi,  703 

savignyi,  705 

tholozani,   708 

transgariepinns,   703,   704 

tuvicata,   708 
Argasidce,    216,    445,    453,    454.    694, 
696,  700,  701,  702,  703, 

1557 
Argyna,  2233 
ArhynchidcB,  680 
Arhynchobdellida,  685 
Arilus,   767 
AriscBma,   172 

curvatum,   190 

triphyllum,  2152 
Arm,  Elephantiasis  of,  161 1,   1617 
Armadillo,  881,  882,  1283,  1284 
Arneth  Count,  75,  1898-9 

Reference,  1905 
Arnold's  Nucleoids,  1902 
Aroidece,   184 
Avpagostoma,  693 
AvYibalzagia,  792,  884,  885 

intermedins,  885 

pseiidoiiiaculipes,  885 
Arrow-Poisons,  167,  180,222,  1695 

References,   186 
Arsenic,  25,  162 

as  Abortifacient,  170 

History,  26 

Locust-poisoning  by  (Sudan),  191 

Pseudo-cholera  due  to,  182] 

Rat-poisoning  by,  190,   [91 

Sulphides  of,  Cattle-poisoning   by, 
189 

Useless  for  Snake- Bite,  278 


3294 


INDEX 


Arsenical  Neuritis,  1981 
Poisoning,  165,  1673,  2256 
Antidotes,  191 
Chronic,  1674 
Criminal,  162,  189 
Arsenious    Oxide,    as    Cattle-Poison, 

189 
Arsenobillon,  27 
Arsenophenylglycin,  26,  27 
Arsenophenylmethyl  glycine,  28 
Arteries,     Atheromatous     Degenera- 
tion, of,  1904 
Thrombosis  of,  1904 
Arthritis,  Climatology,  124 
Sporotrichiim  in,  1121 
Gonorrhceal,   1967 
Post-Dysenteric,  1967 
Rheumatoid,  112,  113,  1967 
Arthrodynie,  1244 
Arthropoda  (Arthropods),  689 
Infection  in  and  by,  875,  1128 
Parasites,    and    Pathogenicity   of, 

361,  372,  376-  397-  47°. 
873,  876,  882,  1128, 
1533  et  alibi 

Reference,  741 

Stinging  Varieties,  206 
Arthropodic  Dysenteries,   1825,  1841 

References,  1863 
Arthrospore,  1037 
Arthrosporei,  987 
Arthrosporinece,  986,  1069,  1121 
Artocarpacece,  2152,  2153,  2162 
Artyfechinostomum,  583 

sufrartyfex,  581,  582,  583,  1752 
Arum  dracunciilns,   173 

montanum,   189 
Arundo  donax,  2152,  2163 
Arvicola  natanedzunni,  920 
Aryan  races,  47 
Aryo-Dravidian  peoples,  49 
Ascariasis,  1412,  1772,  1775 

Pancreatic,  553,  1908 
Ascaridce{des),    205,   552-3,   623,  624, 

653,  1756,  1907 
Ascaris,    9,    12,    621,    623,    653,   654, 

1739.  1758,' 1765,    I776- 

1777,  1961 
alata,   656 
canis,  653 

et  martis,  675 
lumbvicoides,    553,    623,    625,     653, 

075.     896,     908,      1273, 

1552,  1554.  1593.    1775. 

1777,  1838 
References,  682 
texana,  623,  653,  655 

References,  682 
trichiura,  677,  1758 
vermicularis,  657 
visceralis  et  renalis,  675 


Aschiza,  774,  825,  901 
Asci,  971,  978 
Ascites,  1 60 1 

Chylous,  1601,  1608,  1610,  1961 
Lymphatic,  1608 
Asclepiadacece,    169,    170,    173,    190, 

191 
Asclepiades,  Medical  Schools  of,  10 
Ascococcus,  925 
Ascomycete-spheria,  967 
Ascomycetes,    971,    978,    987,     1069, 
1070,  mi,  2008 
References,  1033 
Ascospores,  971 
Ascus  fructifications,  971 
Ashanti  race,  51 

Asia,  Arrow-Poisons  of,  181,  184-5 
Distribution  of  Disease  in,  120-2 
Frambcesia  in,  1537-8 
Asia  Minor,  Diseases  of,  120 
Asian  or  Asiatic 
Maduromycoses 
Black,  2120,  2122 
White,  2122,  2123 
Myiases 

Dermal,  1633,  1639 
Rhinal,  1622,  1626 
Relapsing  Fevers,  436,  445,  1315 

References,  1324 
Schistosomiasis,  1589 
Asiaticus  Parentericus,  1408,  1411 
Asilidcs,  774,  824 
Asomata,  1958 
Asp  of  Cleopatra,  247 
Aspergillacece,  1024,  103 1 
Aspergillales,  985,  986 
Aspergillar  Abscess  of  Neck,  1028 
Mycoses,  1031-2 
Pinta,  1032 

Pneumomycosis,  103 1,  1891 
Pseudo-Tuberculosis,    103 1,    1058, 
1059,   1891 
Aspergillomycoses,  1028,  1031 
Aspergillosis,  1027,  2060 
Bronchial,  1891 
of  Ear,  1030,  1031 
of  Eye,  103 1,  2009 
of  Hairy  Parts,  2041,  2092 
of  Lungs,  1030,  1031,  2008 
of  Nose,  1029,  1031-2 
of  Skin,  1032 
of  Urethra,  1032 
of  Wounds  and  Ulcers,  1032 
Aspergillus,    967,    969,     1024,     1026, 
mi,  1123,  1712,  1713. 
1886,  1891,  1926,  1944, 
1945,  2008,  2041,  2092, 
2093,  2097,  2098,  2123, 
2149 
Fructifications,  1018 
References,  1033 


INDEX 


2295 


Aspergillus,  continued 
Species 

barbce,  1024,  1020,  2041,  2092 
bouffardi,  1024,  1030,  2041,  2121. 

2125 
bronchialis,   1024,   1027,   1028 
flavescens,  1028,  171 3 
flavus,  1024,  1027,  1028,  201 1 
fontoynonti,   1024,   1028 
fumigatus,     1024,     1027,     1031, 
1713,  1891,  1939,  2008, 
2009,  201 1 
glaucus,  1029,  103 1 
herbariorum,    1024,    1025,    1027, 

1029 
Intermediate,  2094,  2095 
malignus,  1024,  1027,  1028,  201 1 
mayidis,   1029 
Yiidularis,    1030 
niger,  1030,  201 1 
nigrescens,  1024,  1027,  1030 
nigricans,   1030 

pictor,  1024, 1629,2094,2095,2098 
repens,  1024,  1029,  2011 
tokelau,  1017,  1032,  2065 
varians,  171 3 
Aspidelaps,  246 

scutatus,  251 
Aspidobothrii,  560 
Aspidobranchia,  890 
Aspidocotylea,  560 
Aspongopus  viduatus,  372 
AsporocystidcB,  473 
Assyrians,  the,  47 
Asthma,  129,  1875,  1900 
A  stigmata,  692,  729 
Astrology  and  Medicine,  3,  4 
Asylum  Dysentery,  1842,  1844 

Pellagra,  1705 
Ataxic  Subtertian  Malaria,  1175,  1176 
Atelosaccharomyces  breweri,  1075 
busse-buschki,  1073 
harteri,   1075 
rudeli,  1073 
Athens,  250 

chlorechis,  251 
Atheromatous    Degeneration    of   the 

Arteries,   1904 
Atisar,  1824 

Atmospheric  Electricity,  effects  of,  146 
Reference,   146 
Pressure,  78 

Effects  on  Man,  79,  142-4 
References,  146 
Temperature  and  Humidity,  67 
Effects  on  Man,  67  sqq.,  137  5^., 
113S-9,  1203 
Atoxyl,  Amaurosis  due  to,  2007 
Compounds,   26-7 
Formula,  27 

Sleeping  Sickness,  26,  njjjsqq. 


Atoxylate  of  Mercury,  20 
Atraclaspis,  250 

congica,  251 
A  trichophyton,  988,  989,  IOCS 

albisicans,   1008 

blanchardi,   1008 

ceylonense,  1008,  1009 

macfadyeni,   1008,   1009,  204S 

viannai,   100S,    1009 
.1  trichopogon,   803 
A  triplex,  200 

angustissima  vel  serrata,  200 

littoralis,  200 
Atriplicismus,  195,  200 

References,  202 
Atrophic  Cirrhosis  of  Liver,  1906-7 

Gastritis,  Chronic,  1906 
Atrophies,  Cardiac,  1904 
Atrophodermia  senilis,   1 730-1,  2231, 

2282 
Atrophy,    Acute    Yellow,    of    Liver, 
1224,  1507,  1508,  1906 

Brown,  of  Heart,  1904 
Atropine,   179 
Atropos  divinatoria,  749 
Atylotus,  819 

fulvus,  819 

rusticus,  819 
AtypidcB  (Aranea),  212 
Auchmeromyia,  832,  850,  1637,  2207, 
2208 

luteola,  850,  2207,  2208 
References,  856 

prcegrandis,  852,  2007,  2008 
Augers,  bites  of,  227 
Aulastoma,  686 
Auma,   2148 

Aural  Diseases,  2010,  2247,  2252.    see 
also  Ear 

Myiasis,  1622,  1626 

Type  of  Subtertian  Malaria,  11 81 
A  urantiacecB ,   2152 
Aureoveridis,   2216 
Auricle,  Diseases  of,  2010 
Aurococcus,  925,  931 

albus,  2019 

aurantiacus,   931 

aureus,  931,   I951.  20I9 

mollis,  931,  2023,  2026,  20 2  - 

tropicus,  931,  2021 
Aussatz,   1644 
Australasia,  Arrow-Poisons  of,  186 

Diseases  of,  122-3,  1538 

Helminths  of,  124 
Australia,  Pituri  of.  176,  177 

Poison-Pea  of,  action  of,    t8g 

Venomous  Snakes  of,  243,  247 
Australian  Aborigines,  49 

Food  of,  94 
Antositic  Monsters,  1958 
I  >ouble,  1958 


2296 


INDEX 


Auto-Suggestion,  1891,  1991 
Autumn  Fevers,  1129,  1362,  1371 
Aves,  Parasites  of,  394,  395,  401,  402 

432,     434-     435.     454- 
489-90,513,516,518-19, 
525,  533 
Trypanosomes  of,  395,  401,  402 

Avian  Malaria,  1131 
Polyneuritis,   109,   1675 

Avicenna,  13,  24,  1535 

Aviculariidee,  212 

Axilla,  Temperature-taking  in,  70 

Axillary  Gland  Enlargement,  indica- 
tions from,  1523 

Axoplasts,  466 

Axostyle,  331,  353 

Aymara  race,  57 

Aztecs,  6,  56,  57,  60 

Babesia  (see  also  Piroplasma) ,  21,  454, 
492 
bigemina,  715,  722 
bovis,  497 
canis,   493,    722 
equi,   714 

ovis,     713,  719,  724 
parva,  498,  712,  713 
Babesiasis,  691 

Canine,  493,  495,  496 
Baby  Clinics,  1959 
Baby-Doping  in  India,  169 
Bab}-  Welfare  Work,  1959 
Babylonian  Medicine,  4,  10,  1619 
Baccelli's  Mixture  in  Malaria,  11 90 
Bacillary  Dysenteries,  1825,  1841 
Dysentery,    1843,    see    also    under 

Dysentery 
Jaundice,  1522 
Bacillea,   959 
Bacillenruhr,   1841 
Bacillicea,  924,  932,  959 
Bacillus(i),  932,  933,  959,  1843,  1680, 
i960,  2166,  2181 
Intestinal,  Table  of,  944-5  sqq. 
Microsiphonales  mistaken  for,  1040 
Species 

aerofetidus,  961 
aerogenes  capsulatus,  961 
aertrycke,  939,  944,  1405,  1820 
aertrycke-type ,  181 2 
albofaciens,  933,  1784 
amylobacter,  962 
anthracis,  22,  1519 

symptomatici,  961 
archibaldi,   1405 
asiaticus,  121-2,  1411,  1412 
Biffi's,  1567-8 
bottle,  of  Malassez,  1077 
botulinus,  961 
cadaveris  sporogenes,  961 
calcis,  in 


Bacillus  (i),  continued 

Species,  continued 

carbonis,   961 

ceylonensis  A.  and  B.,  1406 
chauvcsi,  961 
cholera,  22 

suis,  1230 
cloaca  group,  1411 
coagulans,  935 

coli  communis,   258,   898,    1301, 
1371,  1567,  1712,  1841, 
1911,  1951.   1959 

dysentericus,  1841,  1844 
columbensis,  1405,  14 10 
cuenoti,  917 
danysz,  939 
diphtheria,  965,  1040,  1087 

Klebs-Loeffier,  899,  1520,  1521 

vitulorum,  1064 
Diphtheroid,  2247 
dysenteries,  935,  1844 

Baerthlein's,  1843 

Eberth's,  933,  935 

El  Tor,  No.  1,  1843 

Flexner,  1842,  1843,  1845 

Flexner-Manila  group,   1843 

Harris's,  1843 

Hiss-Russell/ 1 842,  1843,  1845 

Shiga-Kruse,    22,    1069,    1821, 
1831-2,  1845 

Shiga-Kruse  type,  1843 

Strong  type,  1843,  1845 

Tokio,   1843 

Wollstein's,   1843 

Y,  1842,  1843 

Y-type,  1844 
emphysematosa,  1951 
entericus,  113,  935,  1406 
enteritidis,   939,  1405 

sporogenes,  961 
erysipelatos,  1951 
jcBcalis    alkaligenes,    935.     1405, 

1409 
fcBcaloides,   1405 
fallax,   961 
du  Farcin,  1051 
felisepticus,    1424 
feseri,  959,  960 
fragilis,  933 
fusiformis,  448,  1520,  1745,  1747, 

1882,   2181 
Gaertner's,  195 
histolyticus,  961 
icteroides,   1230 

influenza,  933,  1497,  1498,  1521 
kandiensis,   1405 
Kedrowsky's,  1647 
khartoumensis,  1406,  1412,  141 3 
Koch-Weeks,     900,     902,     1996, 

1997 
lactis  aerogenes,  1959 


INDEX 


2297 


Bacillus (i),  continued 
Species,  continued 

leprce,  22,  1040,  1644,  1645,  1647, 

1653 
m'didis,   171 3 
mallei,   1466 
meta-alkaligenes,   1405 
metadysentericus,  935,  1842,  1843 
Morax-Axenfeld,  1996,  1997 
Morgan's,  899 
necrophorus,  1064 
necroseos,  1064 
Necrosis,  of  Bang,  1064 
novyi,  959 
cedematiens,  961 
cedematis  maligni,  961 
para-alkaligenes,  1405 
paracolon  group,  1365 
paradysentericus,  1842,  1843 
paratyphosus ,  22 

A,  195.  935 

A  and  B,  899,  939,  1362,  1363, 
1365. 1366  sqq.,  1370,  1375 

B,  195,  1820 

C,  1367 
parentevicus,   1406 
pellagra,   1 7 1 3 
perfringcns,  61 

pestis  [Pasteurella  pestis,  q.v.), 
22,  115,  900,  909,  912, 
917,  943,  1416,  1419, 
1423.  1523.  1962 

phlegmonis    emphysematosa,    961 

of  Potatoes,  171 3 

pritnitzi,   1405 

prodigiosus,  898,  2102,  2224,  2272 

proteus  group,  1812,  2166 

pseitdo-coli,  181 2 

pseudo-diphtheriticus,  1951  . 

pseudo-dysentevicus,  1844 

psittacosis,   1405 

puirificus  coli,  961 

pyocyaneus,  1841,  191 1,  1959 

pyogenes  fcetidus,  935 

of  Rauschbrand  auctores  [feseri], 
961 

rodella  III.,  962 

saccharobutyricus  immobilis,  961 

solanacearum,   171 3 

sporogenes,  961 

subfilis,  933,  959 

SM&ta7is-like,  171 3 

suipeslifer,  939 

tertius,  962 

tetani,  22,  961,   1951 

Tetanus  group,  962 

Tizzoni's,    1713 

tuberculosis,  22,  112,  553,  899, 
1040,  1058,  1521,  1528, 
1647,   1889 

typhi-exanthematici,  1 328 


Bacillus  (i),  continued 
Species,  continued 

typhosus,  22,  258,  898,  899,  905, 
908,   1184,    1347,    1362 
«??-.  1375.  ^o,  x95! 
vagince,  1951 
vivax,   1405 

von  Hibler,  VII.  and  IX.,  962 
welchii,  961 
wesenberg,  935 
X.,  1230 

X19  O,  in  Typhus,  1336 
Y,  962 

zeylanicus,  451,  1069 
in  Urine,  tests  for,  1935 
Bacteria,  112,  113,  1042 
Affecting  Maize,  171 3 
Terms  for,  921 
Intestinal,  Table  of,  944"5 
Oral,  1740 
Uterine,   1951 
of  Vulva,   1 95 1 
Bacterial  Characters  of  Spirochetes, 

436,  437.  917 
Diseases 

Animal  Carriers,  897 

Insect  Vectors,  23-4 
Dysenteries,  1825,  1841 

^Etiological  Classification,  1845 

Dysentery,  Acute,  1848 
Fevers,  1128,  1362 
Bactericidal  Properties  of  Sun-Rays, 

83 
Bacteridiea,  933,  958 
Bacteridium,  933,  958 

ceruginosum,  958 

prodigiosum,  933,  958 

pyocyaneum,  958 
Bacteriological  Diagnosis  of  Bacillary 
Dysentery,   1853-4 

Flora  in  Frambcesia  Lesions,  459 
Bacteriology,  22-3 

References,  965-6 
Bacterium,  932,  1041,  1042 

actino-cladothrix,  1051,  1057 

coli  communis,  935 
BacteriodecB,  933,  957 
Bacteroides,  933,  959 

fragilis,  933,  959 

fusiformc,  959 

Table  of,  960 
Badiane,  174 
Bael  Fruit,  1858 
Bagdad  Button,   Boil,  or  Sore,   120, 

380,  2165 
Baguette  interne,  353 
Bahtschi,   1983 
Balaninus  nucum,  1641 
Balanitis,  454,  1939 
Balano-Posthitis,  1939,  227S,  2280 
Balanoposthomycosis,  1944 


22g8 


INDEX 


Balantidic  Dysentery,  1825, 1837, 1S53 
Balantidium,  547 

coli,  18,  546,  547,  1777,  1837 
References,  550 

giganteus,  549 

Halicum,  1837 

minutum,  546,  548,  1837 
References,  551 

minutum  var.  Halicum,  548 

vaginale,   1946 
Balata  Mite,  2213 
Baleri,  417,  427 

Balfour's  Infective  Granule,  483 
Balkanella,  935,  940,  1362,  1406 

carolinoides ,  940 

coagalans,  935 

ginmai,   940 
Balla  mal  (fish),  1540 
Ballingall,  Maladiede,  2110, 2116,  21 17 
Bamber-green  Oil,  1206 
Bamboo  Hairs,  Traumatism  induced 
by,   157 

Juice  and  Fruit  as  Echolics,  170 
Bambusa,  170 
Banal  Fly,  811 
Ban  Bach,  1468 
Banded  Krait,  247 
Banga,  1981,  1987 
Bankokerende,  2241 
Banti's  Disease,  1305,  1903 
Bantu  race,  47,  53,  55 
Barawa,  16 10 
Barbados  Leg,  1610 
Barbeiro,  768 
Barcoo  Rot,   123,   2030,  2031,   2032 

References,  2039 
Barkers,  the,  1986 
Barley  Itch,  2216 
Barotse  race,  53 
Barraconda,  193 
Barringtonia  acutangula,  188 

raratonga,  164 

speciosa,  164 
Barronsia,  474 
Bartholin's  Glands,   Suppuration  of, 

1949 
Bartonella,   492,   502 

bacilli formis,  502,  1527,  1568,  1570, 

1576 
Basidia,   1032 

Fructifications,  971 
Basidiomycetes,  971,  978,  1032,  1039 

References,   1033 
Basommatophora,  892 
Basophilia,  1900 
Basophile  Leucocyte,   1898 
Bassewitz's  Angiofibroma  cuti  conta- 
giosum  tropicum,  1568, 
2247,  2253 
References,  2262 
Bassia  latijolia,   178 


Bassia  longifolia,  178 
Bat  Mite,  Achromaticus  in,  360 
Batavia,  Fever  of,  11 29 
Bathmostomum ,  672 
Batrachidcs,  233,  236 
Batrachus  grunniens,  233,  236 

tau,   233,   236 
Bats,    Parasites    of,    360,    405,    407, 

701,  704,  722,  763 
Battak  Arrow- Poison,  184 
Bauru,  Ulcers  of,  165,  380 
Bazin's  Erythema  induratum,  2277 
B dellidce,  728 
Bdellolarynx,  832,  846, 

sanguinolentus,  846 
Beans,  95 

Toxicity  of,  201,  121 3 
Bears,  Traumatisms  due  to,  148 
Bed-bugs,  see  Bugs,  below 
Bedouin  Dietary,  98-9 
Bedsores,  1402 
Bee-Disease,  529 
Beef  Worm,  1633 
Bee-Moth,  226 

Bee-Stings    and     Venom,     12,    215, 
219-22,  2207 

References,  229 
Bees,  Anatomy  of,  219-20 

Mucorine  disease  of,  973 
Beetles,  871,  895,  908 

as  Arrow- Poison,  180 

Venomous,  226-7 
References,  229 

Vesicant,  226,  2204,  2205 

as  Wart  cure,  2277 
Behrend's  Trichosporosis,  2105 
Beigel's  Trichosporosis,  2105 
Beinwurm,  651 
Beja,  or  Bisharu  Race,  47 
Belascaris,  623,  653,  656 

cati,   656 

mystax,  623,   1775 
References,  682 
Belladonna  Poisoning,  167 
Bellilda,  1756 
Belyando  Spew,  453,  1749 
Benedenia,  474 
Bengal  Spider-bite,  215 
Bengali  race,  47 

Diet  of,  100 
Bengali  a  depressa,  852,  1633,  1637 

References,  856 
Benign  Tumours,  2273,  2274 
Beni-Mzab  race,  47 
Berber  race,  46-7 
Berbevidaceee,  2132 
Berbiers,   1671 

Beri-beri,  109,  198,  11 84,  1671,  1709, 
1718,  1981 
jEtiologv,  theories  on,  105,  109, 
1533. 1672, 1673,1675,1678 


INDEX 


2299 


Beri-beri,  continued 

Climatology,  120,  122,  1693 
Complications,  1687 
Diagnosis,  1688 

Differential,  1688,  1690,  1990 
Diet,  1689 

Economics,   1672,   1681 
Etymology,  1671 
Fungi  associated  with,  167,  1680 
History,  1671-3 
Incidence 
Age,  1 68 1 
Class,  1672,  1681 
Race,  1 680- 1 
Sex,  1681 
Malaria  simulating,   11 76 
Morbid  Anatomy,  168 1-4 
Pathology,  1681 
Predisposing  Causes,   1680 
Prognosis,  1688 
Prophylaxis,  1689-90 
References,  1693-4 
Sequelae,  1688 

Symptomatology,  1684,  1904 
Synonyms,  1671 
Three  Forms,  1685 

Acute  Pernicious,  1685,  1689 
Rudimentary,       1685,       1687, 

1689 
Typical,  1685 
Treatment,  1688-9 
Trypanosome  in,  1284 
Vitamine,  109,  1673,  1675 
Infantile,  1690 

References,  1693-4 
Ship,  109,  1680,  1690 
Berme,   1633 
Berne,  828,  830,  1633 
Berrugas,  1566 
Bertilia,  762,  766 
valdiviana,   766 
Bertramia,  534 
Bertramiidee,  534 
Bess-el-Temiir,  2165 
Bessina,  1756 
Beta,   2229 
Beta-Naphthol    in    Ankylostomiasis, 

1 770-1 
Bete  Rouge,  725,  2213 
Betel-Chewing,     effects,     177,     1746, 

2284 
Beulenkrankheit,  Endemischer,  2165 
Bewitchment,  Delusions  of,  1991 
Bezzia,  802,  803,  805 

ornata,  805 
Bhang,  176 
Bible,    the,    References    to    Tropical 

Diseases  in,  9-10 
Biblical  Leprosy,  10,   1535,  1844 
Bibo,   706 
Bicheiro,   1623 


Bicho,  El,  1 87 1 
Bicho-Colorado  Itch,  221 
Bichugue,  768 
Big  Bed-bug  of  Utah,  760 
BignoniacecB,  188,  2152 
Bihimbo  Disease,  1673 
BikcBcidcB,  333 

Bile-ducts,  Parasites  in,  iyo; 
Bilharzia,  584 
Bilharzia  Disease,  1926 
Hilharziosis,     30,     112,     1727      1126 
1939,  I941 
.ZEtiology,  1927 
Causal  Organism,  587    i-yi 
Climatology,  1926-7 
Complications,  1929-30 
Definition,  1926 
Diagnosis,  1930 
History,  1926 
and  Invaliding,  130 
Morbid  Anatomy,  1928- . 
Prognosis,  1930 
Prophylaxis,  1931 
References,  1936 
Symptomatology,  1929 
Synonyms,  1926 
Treatment,  1 930-1 
American,  1864 
Hepatic,  1864 
Intestinal,  1864 
Rectal,  1864 
Urinary,  1926 
Biliary   Cirrhosis   of   the    Liver,    In- 
fantile, 1906 
References,   191 7 
Bilio-gastric  Fever,  1363 
Bilious  Continued  Fever,  1363 
Fever  (s),  1363 

Canine  (Canine  Babesiasis),  493 
Malignant,  1216 
Haemoglobinuric,  1216 
Remittent,  121 6,  1229,  1230 
Icteric,  13 17 
Malarial,  1165,  1168 
Septic,  1469 
Typhoid,  1308 
Binary  Fission,  288,  291,  292,  385-6 
Binnenkorper,  290 
Binucleata,  332,  436,  480 
Binucleate  Amoeba,  322,  323,  324 
Biotripsis,  1730-1,  2231,  2282 
Bird-eating  Spiders,  212 
Bird  Lice,  750,  751 
Bird  Malaria,  11 31 
Bird-Poisoning,  191 
Birds,    Parasites   of,    394,    395,    401, 
402,  432,  434,  435,  454, 
489-90,    513,    516,    518, 

519.  525.  533 
Polyneuritis  of,  109,  1675 
Bironella,  791 


23°° 


INDEX 


Bisayas,  the,  55 
Bish,  or  Bikh,  163 
Biskra  Boil,  2165,  2166,  2167 
Bites  of 
Animals 

Fevers  due  to,  1356  sqq. 
Traumatisms  caused  by,  147 
Insects,  Rashes  due  to,  1514,  1516, 

1517 

Larval  Hexapoda,  Dermatites  due 
to,  2200,  2207 

Man,   147 

Snakes,  242  sqq. 

Various  Creatures,  12 
Biting  Flies   (see  also  under  Names), 

23,  814,  1703,  1716 
Bitis,  250 

arietans,   250,  251,   1698 
Venom  of,  256,  269 

atropos,  251 

candalis,  251 

cornuta,  251 

gabonica,  251 

inornata,  251 

nasicornis,  251 

paringueyi,  251 
Black  Actinomycosis,  2112,2140,  2141 

Bug  of  the  Pampas,  768 

Death,  the,  141 6 

Fever,  1341 

Maduromycoses,  2120,  2122 

Pigmentation,    see   also    Addison's 
Disease,  Pigmentation,  etc. 
in  Chronic  Fevers,  151 9 
of  Nails,  2236,  2283 

Pinta,  2094,  2095 

Spores  in  Mosquitoes,  510,  513 

Tongue,  1061,  1074 

Vomit,  1232,  1520 
Black-Dot  Tinea  tonsurans,  2057 
Black- Pitted  Tick,  713 
Blackwater  Fever,   12 13,   1216,  1290 

Etiological  Theories,  1 218-21 

Climatology,  121 7-18 

Clinical  Classification,  1217 

Complications,  1224 

Convalescence,  1224,  1227 

Definition,  121 6 

Diagnosis,  1224,  1517,  1519,  1522 
Differential,    1224,    1238,    1507, 
1508,  1522 

Diet,  1226,  1227 

History,  1216-17 

and  Invaliding,  130,   1227 

Morbid  Anatomy,  1222 

Parasites  present  in,  1221 

Pathology,   1221-2 

Pigmentation  in,  1517,  1519 

Predisposing  Causes,  1221 

Prognosis,  1225 
Prophylaxis,  1228 


Blackwater  Fever,  continued 
Race  incidence,  1221 
Rash  of,  1 51 7 
References,   1228 
Relapse  in,  1226 
Sequelae,  1224 
Spirochetes  in,  1221 
Symptomatology,  1223-4 
Synonyms,  12 16 
Treatment  during  and  after  Attack, 

1225 
Varieties,  1224 
Bladder,  Stone  in,  1926,  1929,  1930 
Blandfordia,  584,  590,  592,  891 
bensoni,  891 
japonica,  891,  894,  1591 
nosophora,  592,  593,  894 
pyrrhostona,  891 
striatula,  891 
viridescens,  891 
Blapidce,   1640 
Blaps  mortisaga,  1640 
Blastocystis  enter  ocola,  354 

hominis,  354,  1833 
Blastomyces  dermatitis,  1073 
hessleri,  1074 
tonkini,  1075 

vitrosimile  degenerans,  1074 
Blastomycetes,  981 
Blastomycetic  Dermatitis,  20 Si 

Ulcers,  2190 
Blastomycoses,  981,  985 
Blastomycosis,  24,  1072,  1073,  1075, 
2081,  2193 
/Etiology,  2081-2 
Carriers,  2088 
Climatology,  2081 
Diagnosis,  2085 

Differential,  2085,  2186 
Histopathology,  2082-3 
History,  20S1 
Prognosis,  2086 
Symptomatology,  2083 
Synonyms,  1536,  1559,  2081 
Treatment,  2086 
Varieties,  2041,  2084 
American,  1079 
Coccidioides,  2084,  2085 
Intestinalis,  1780,  1781 
Non-coccidial,  474 
Ocular,  2009 
Oral,  2084,  2085 
Oro-Pharyngeal,  2084 
Palpebral,  2009 
Systemic,  1075 
Blastospore,  1037 
B/astosporinea,  986,  1069 
Blastrotrichece,  irn 
Blastulidium,  534 
Blattern,  i486 
Blennijormes,  233 


INDEX 


2301 


Blennorrhcea,  Chlamydozoal,  539 

Gonococcal,  539 
Blepharitis,  2007 
Blepharoceridce,  773,  813 

References,  813 
111 '-pharoplast,  330,  382,  383 
Blighia  sapida,  173,  1695,  1696 
Blindness  in  the  Tropics 

Causation,  124,  11S1,  1994,  2006 
Incidence,  122,  124,   1994 
Blister  Beetles,  226,  2204,  2205 
Blistering  Fluids  excreted  by  Adult 
Hexapoda,     Dermatites 
due  to,  2200,  2204 
Blood,  the,  1895 

Action  on,  of  Light,  88 
Analyses  of 
European,  108 
Male  Bengali,  108 
References,  1905 
Blood-Counts,  1898-9 
Arneth's,  1898 
Table,  1899 
Differential,  1898 
Blood  Parasites,  1903 
Blood  Platelets,  1900 
Blood-Pressure,  Effect  on,  of  Tempera- 
ture and  Humidity,  75 
Blood  Puzzles,  1895,  1900 
Autogenetic,  1900,  1901 
Heterogenetic,  1900,  1901 
Reference,  1905 
Spirochaetes,  443  sqq.,  452 
Blood-Sucking  Dipterous  Larvae 
Dermatites  due  to,  2207-8 
References,  2221 
Flies,  365,  771,  774  sqq. 
How  to  Collect,  748 
Methods  of  Infection  by,  874-5 
Parasites  of,  365,  814 
References,  855 
Blood- Vessels,  the,  Diseases  of,  1895 

1904 
Bloody  Flux,  1824 
Blowflies  (Calliphora),  846,  908 

(Sarcophagidce) ,  830 
Blue-bottle  flies,  846,  908 
Blue  Disease,  1341 
Blue  Tick  of  South  Africa,  459,  715 
Boa-constrictors,  487 
Bodily  Temperature  of  Man 
Normal,  69-71 
Regulation  of 
Chemical,  69 
Physical,  69 
B(>do,  335,  336,  337,  342,  364,  1833 
lacertcB,  339 
lens,  335,  342 
muscce-domesticce,  359,  365 
stercorals ,  342  , 
Bodonidce,  ^^^,  334,  336,  380 


Body,  Actinomycosis  of,  21 10,  2148 
Body  Systems,  Derangement  of,  1 51 2, 

1519 
Bohnenkrankheit,  201 
Boil  Disease,  Endemic,  2165 
Boils,  226,  931,  2020 

Aleppo,  378,  2165,  2166,  2167 

Bagdad,  120,  3S0,  2165 

Biskra,  2165,  2166,  2167 

Bucharest,  2165 

Delhi,  378,  380,  2165,  2166 

Diabetic,  1924 

in  External  Auditory  Meatus,  2012 

Mango,  2027 

Multiple,  2265 

Nile,  931,  2021,  2024,  2027,  2165 

Tropical,  2027 
Bolbodimyia,  820 
Bolest,  Nova,  2208 

Pulziasta,  2208 
Bombus  hortorum,  219 

lapidarius,  219 
Bombycides,  222-3 
Bone-Marrow,  the,  1895,  1905 
Bones,  Boomerang,  1967,  1977 
References,  1980 

Caries  of,  1967 

Diseases  of,  1967,  1975 
References,   1980 

of  Foot,  Endemic  Degeneration  of, 
2110 

Fracture  of,  124 

Frambcesial  Lesions  of,  1552,  1978 

Necrosis  of,  1967 

Tubercular  Disease  of,   1361,   1967 

Tumours  of,   1967J 
Bont,  723 
Book  Louse,  749 

Scorpion,  897 
Boomerang  Bones,  1967,  1977 

References,  1980 
Boophilus,  711,  714 

annulatus,  492 

australis,  492 

bovis,  714 

decoloraHts,  492 
Borboridcs,  901,  903 
Borborus  equinus,  903,  905 
Borna  Disease,  1477 
Borneo,  Arrow-poison  of ,  t8i,  184, 185 
Bos  indicus,  Milk  of,  1959 
Bosch-yaws,  2172 
Botkriocephaloidea,  600 
Bothriocephalus,  596.  6o4 

balticus,  604 

cordatas,  605 

cristatas,  604 

latissimns,  604 

latus,  604 

liguloides,  606 

tropicus,  613 


2302 


INDEX 


Bothriuridce,  207 
Botryomyces  ascoformans,  2255 
Botryomycosis,  2247,  2254 

hominis,  2254 
Botryotrichum,  1 1 1 2 
Botrytidcs,  987 
Botrytis,  11 17 

bassiana,  22,  1033 
Bots,  1630 
Bottle  Bacillus  of  Makiisez,  1077 

Flies,  825 
Bottone  d'Oriente,  2165 
Boubas,  1536,  1558,  1559,  2175-6 
Boulengerina,  246 

stormsi,  251 
Bouton  d'Alep,  378,  2165 

des  Andes,  1566 

d'Orient,  2165 
Bovidae,  Traumatisms  caused  by,  151, 

152 
Bovines,  Parasites  of,  492,  497 
Bowditch  Ringworm,  2059 
Bowel-disorders  of  Bengalis,  105 
Bowel (s),  Cancer  of,  1739 

Large,  Ulceration  of,  18 

Perforating  of,  by  Ascaris,  1961 

Tuberculosis  of,  1739 
Brachwasserwurm,  65 
Brachyaspis,  246 

carta,  251,  256,  272 
Brackycera,  773,  814 

heterodactyla,  774,  814,  824 

homcedactyla,  773,  814 
Brachydonus,  672 
Brachypoeon,  802,  803,  805 

vitiosus,  805 
Brahui  race,  47 
Brain,  Abscess  of,  1058,  1062 
Branchial  Fistula,  1959 
Branchiobdellida,  688 
Brand  Zeer,  2030,  2031 
BraulidcB,  854 
Braunia,  601 

jassyensis,  601,  607 
Brayera  anthelmintica,   1753 
Brazil,  Arrow-Poison  of,  186 

Vegetal  Poisons  of,  164,  168 
Brazil's     Crotalus     horridns     Serum, 

273 

Breakbone  Fever,  1244 

Breakheart  Fever,  1244 

Breast,  Diseases  of,  124 

Elephantiasis  of,  1611,  1617 
Male,  Hypertrophy  of,  1939 

Breast-Feeding,  1959 

Breda's  Disease,  2175 

Breeze-Flies,  815 

Brevirostrata,  711 

Brigant,  2217 

Blight's  Disease,  Rash  in,  1516 

Briophyta,  923 


Brill's  Disease,  1326,  1327,  1396 
British  Colonies,  Laboratories  in,  29 

War  Ration,  99,  100,  102 
British  Guiana, Vegetal  Poisons  of,  164, 

166 
Brittle  Nails,  2283 
Broken  Wing  Fever,  1244 
Bromatoxismus,i93 
Bromidrosis,  2222,   2223,  2264,   2272 

Symptomatic,  2223 
Bromine  for  Snake-Bite,  278 
Bronchi,     Inflammatory    and     other 
Affections      of,      1875, 
1882 
Bronchial  Aspergillosis,  1891 
Mucormycosis,  1892 
Oidiomycosis,  1889 
Penicilliosis,  1892 
Spirochsetosis,  452,  1875,  1882 
Sporotrichosis,  1892 
Penicilliosis,  1892 
Symptoms,  Indications  from,  1521 
Bronchite  sanglante,  1882 
Bronchitis,  1592,  1875 
Diagnosis,  1521 
Castellani's,  450,  452,  1882 
Chronic,  1060 
Fungal,    1084,    1087,    1091,    1095, 

1096,  1743,  1892 
Haemorrhagic,  1882 
Broncho-alveolar  Aspergillosis,  1891 

Moniliasis,  1886 
Bronchoblastomycosis,  1886 
Broncho-endomycosis,  1889 
Bronchohemisporosis,  1890 
Bronchomoniliasis,  1886 
Primary,  1886 
Secondary,  1889 
Bronchomucormycosis,  973,  977 
Bronchomycoses,    1080,    1081,   1084, 
1743,  1744,  1748,  1886, 
1890 
Diagnosis,  1521 

Differential,  1875,  1885 
Monilia  in,   1080,    1081,   1084, 
1086,  1087 
Tropical,    1880 

References,   1894 
Undetermined,  1892 
Broncho-Pneumonia,       1087,      1528, 

1587,  1592,  1887 
Broncho-Pulmonary      Spirochsetosis, 
Castellani's,  1882,    1885 
Bronchospirochaetosis,  21,  1875,  1882 
iEtiology,  1883 
Climatology,  1883 
Complications,  1885 
Definition,  1882 
Diagnosis,  1521,  1885 

Differential,   1875,   1885,   1889 
Experimental  Reproduction,  1884 


1 NDEX 


2303 


Bronchospirochaetosis,  continued 
History,  1882-3 
Method  of  Infection,  1884 
Mixed  Infections,  1885 
Predisposing  Causes,  1883 
Prognosis,  1885 
References,  1893-4 
Symptomatology,  1884-5 
Synonyms,  1884 
Acute,  1884 
Chronic,  1884-5 
Subacute,  1884 
Brown  Atrophy  of  the  Heart,  1904 
Sewer  Rat,  917 
Tick,  712 
Bruce's  Septicaemia,  1437 
Brucia  antidysentcrica,  1836 

sumatrana,  1836 
Briilots,  810 
Bryonia  devica,  2054 
Bubas,  24,  1535 
Braziliana,  2175 
Tranjilor,  1700 
Bubo  Climatic,  25,  1523,  1961 
References,  1966 
Varieties,  1963 
Symptomatic,  1963 
Venereal,  1963 
Bubonic  Plague,  1428,  see  also  under 

Plague 
Bucharest  Boil,  2165 
Buckwar,  2060 
Buckwheat  Poisoning,  202 
Bucnemia  Tropica,  1610 
Budding  Fungi,  979 
Buddleya,  1756 
Buena,  1535 

Buffalo-Bean  Dermatitis,  2152 
Buffaloes,   Traumatisms     caused   by, 

152 
Bufo  vulgaris,  355 
Bufonin,  240 
Bufotalin,  240 
Bugis,  the,  55 

Bugs,  Diseases   and  Parasites  carried 
by,  20,  23,  364,  370-2, 
379,  43°.  443.  882,  912, 
1283-4,       1329,       1416, 
1423,  1691,  2267, 
Enemies  of,  765,  767 
Cone-Nosed,  Bite  of,  767-8 
Fevers  carried  by,  n  28,  1283 
Bulam  Fever,  1229 
Bulbar  type  of  Subtertian   Malaria, 

1175,  1176 
Bulinus,  hosts   of   Schistosoma,  584, 
587,   892,  893,  894 
alexandrina,  893 
contortus,  587,  893 
dybowskii,  587,  893 
innesi,  587,  893 


Bullous    Dermatitis,     Seasonal,    226, 
2204 
References,  2220 
Eruptions,  2264,  2269 
Diagnosis,  151 3,  1518 
'  Bunches,'  1763 
Bumble-bees,  Stings  of,  219 
Bungarus,  246 

Venom   of,    243,    260   sqq.,    271, 
272,  273 
Species 

candidus,    247,     251,     259,     264, 

266,  272,  273 
ceylonicus,    247,    248,    251,    264, 

266,  267 
fasciatus,  247,  251,  266,  267,  273 
Bungpagga,  1469,  1975 
Buno,  2148 

Bunostomince,  665,  672 
Bunoslomum,  672 
Burma,  Vegetal  Poisons  of,  165 
Burmese,  the,  55 
Burns,  Severe,  Haemoglobinuria  after, 

1213 
Burrowing  Insects,  Skin  Lesions  due 

to,  124, 2211 
Bursariidce,  547 
Bursarinidcs,  547 
Bursata,  623,   659 
Buryats,  the,  55 
Bushman  Race,  51 

Arrow-Poisons  of,  180,  182,  184 
Food  of,  94,  96 
ButhidcB,  207 
Buthus  afer,  207 
Venom,  209 
maurus,  207 
occitanus,  206,  207 
Venom,  209,  211 
quinquestriatus,  207 
Venom,  208,  209,  210 
Butterflies,  Poisonous  Caterpillars  of, 

222 
Buttocks,     Fistulous     Diseases      of, 

2084 
Button  Scurvy,  1536 
Butyric  Acid  Fermentation,  Bacillus- 
caused,  22 
Byzantine  Medicine,  12,  17 

Cabot's  Ring-shaped  Bodies,  1902 
Cachectic  Fever,  1289 
Cachexie  Africaine,  1761 
Cacodmus,  762,  766 

ignolus,  766 

indicus,  766 

villosus,  766 
Cacodyl,  26 

Cactacea,  164,  168,  176,  2152 
Cactus  grandiflorus,  2152 

opuntia,  1569 


23°4 


INDEX 


Cadicera,  820,  821 

biclausa,  822 

chrysophila,  S22 

chrysostigma,   822 

distanti,  822 

flavicoma,   822 

melanopyga,  821 

obscura,  822 

quinquemaculata,   822 

ritbramarginata,   822 

speciosa,  822 
Caisson  Disease,  142-3 
Calabar  Bean,  178-9 
Calabar   Swellings,    820,    1967,    1971, 
1972 

References,   1980 
Calchecaquis,  the,  60 
Calculi,  Salivary,  1 740-1 

Tonsillar,  1747,  1748 

Urinary,  1926,  1929,  1930 
Calenture,  24 
Callimastigidce,   333 
Callionytnidce,  233 
Callionymus,  233 

lyra,  233,  234,  237 
Calliphora,   307,   832,   846,  877,   900, 
1632 

anthropophaga,  847 

azurea,  846,  1629 

erythrocephala,  846,  900,  905,  908, 
1626,   1629 

infesta,  847 

limea,  846,   1626 

macellaria,   847 

vomitoria,  846,  900,  1629 
Calliphorince,   1633,   1637 
Callodictyon,  348,  349 
Callophis,  246,  251 
Callotropis,   169 

gigantea,  169,  173 

procera,  169,  170,  189 
Calmette's  Serum,  271-2,  276 
Calobata  cibaria,  1629 
Calor  del  Higado,  1700 
Calor  Picante,  2225 
Calore  del  Fegato,  1 700 
Calorie,  Definition  of,  97 
Calories  in  Diet,  97 
Calverlina,  791 
Calymmato-bacterium  granulomatis, 

2193 
Cambay  Sore,  378 
Cambosa  arotnatica,  172 
Camel-bite,  151-2 
Camel-flies,  874 
Camelidce,   Traumatisms   caused   by, 

151 

Camels,  Trypanosomes  of,  409,  414 
Cameras  de  Sangue,  25 
Camp  Jaundice,  451,  453,  15°!.  I5°7. 
1508,  1519 


Canaanites,  the,  47 
Cancacao,   1761 
Cancer,  ^Etiology,  177,  981 
Climatology,  122,  124 
Fungi     associated     with,     1072, 

1074 
Spread  by  Mites,  732,  2215 

of  Bowels,  1739 

of  Breast  in  Mice,  454 

of  Intestine,  1862 

of  Lips,  Cheeks,  and  Tongue,  1741 

of  Liver,  1907 

Nasal,  123 

of  Pancreas,  1908 

Rectal,  1852,  1853 

of  Stomach,  1749 

of  Tongue,  1741 
Cancerous  Ulcers,  2190 
Candidates     for     Tropical     Service, 
Examination  to  ascer- 
tain Fitness  of,  127  sqq. 
Cane  Dermatitis,  1466,  2163 
Cangoura,  189 
Canguary,  1283 

Canidae,  Traumatisms  caused  by,  151 
Canine     Kala-Azar    (Leishmaniasis), 
374-5,  377,  1299 

Piroplasmosis,  493,  496,  497 
Canities,  2283 
Cannabis  indica,  1988 

sativa,  170,  176 
Canthariasis,  1619,  1640 

Dermal,  1641 

Gastro-intestinal,  1640 

Rhinal,  1640 

Urinary,  1641,  1926,  1934 
Cantharidce,  226,  1641,  2204,  2205 
Cantharidin,  227 
Cantharidine,  172 
Cantharis  vesicatovia,  172 
Capitas,  the,   60 
Capceta  pyaiercula,   1881 
Capsicum  annum,  173 

frutescens,  173 
Capsulitis,  1904 
Capybara,    Trypanosome  Disease  of, 

414 
Caraate,  2093 
Carabidce,   K>^o 
Caratejo,  2093 
Carawalla,  247,  248 
Carbohydrates  in  Diet,  96,  y<> 

Kstimation  of,  101 
Carbon  Dioxide  Poisoning,  1673,  1674 
Carbuncles,  151 9,  2027 

Diabetic,  1924 
Carceag  in  Sheep,  21 
Carcinoma,  Melanotic,  2277 
Carcinomata,  Fungal,  1074 

Ulcerating,  449,  452 
Circoma,  Faecal,  1739 


INDEX 


23°5 


Cardiac  Diseases,  132,  1895,  1904 

Symptoms  in  Subtertian  Malaria, 
1 1 79 
Cardiospasmus,  Tropical,  1750 
Caribi,   1871 
Caribs,  the,  59,  60 
Carica  papaya,  170 
Caries,  113 

of  Bone,  1967 

Dental,  124 

Spinal,  21 12 
Caris,  702,  703,  704 

vespertilionis,   704 
Carnivora,   Traumatisms  caused  by, 

147.   151 
Trypanosome  of,  406 
Carols,  703 
Carpoascees,  2008 
Carpoglyphus,   731 

alienus,   731 
Carriers     of     Disease,     see    Animal, 
Insect,    Parasites,  etc., 
a-  under  Names 
Carrion's     Disease    or    Fever,     503, 
504,    1566,    1567,   1 571, 
1575 
Treatment,    1577 
Carrot  Seeds,  170 
Caryophylhis  aromaticus,  172 
Casal's  Necklace  in  Pellagra,  1701 
Cascuta  reflexa,  170 
Cashew  Nut  Dermatitis,  2162 
Cassava,   1 72 
Cassia  beareana,  in  Blackwater  Fever, 

1227 
Castellanella,  396,  401,  402,  407,  408, 
409,  419,  1260 
Human     Trypanosomes     included 

in,  419 
Species 

hrucei,  408,   410,  426,   127,    1265, 

1272 
castellanii,  396,  402,  408,  419,  421, 
426,   1280,    1261,   1262, 
1264,  1265,  1268,  1273, 
1274.  1275,  1279 
equiperdutn,  40S,  411,  1272 
evansi,  408,  409,  410,  413,  1280 

var.  mborii,  410 
gambiensis,  396,  408,  419,  1260, 

1261,  1264,  1265,  1273, 
1^74.  1275 

Uinfranchii,  431 

nigeriensis,  430,  1261.  1264,  1269 

rhodesiensis,     408,      425,     1260. 

1262,  1264,  1265,  1273, 
1274,  1275,  1278,  I28c 

Castellani  Type  of  Sleeping  Sickness, 

879 
Castellani's  Absorption  Test,  1397 
Bronchitis,  1882 
Dermatitis  (Copra  Itch),  2215 


Castellani's  Dilution  method,  1390 

Gas-Agglutination  Test,  i  592 

Lotion,  2226 

Mixture,  28,  1562 

Non-Parasitic  Bodies  in  Leucocytes, 
1902 

Polyserum  method,  1392 

Pyosis,  2021 

Spirochaetosis,  1535 

Symptom,  1255 

Treponemosis,  1535 
Ctstellani -Low's  Symptom,  1273 
C  istellani-Taylor's  Test,  1934 
Castor  Oil  Plant,  170,  174 

Tick,  720 
Castoridce,  913 
Castration,  1939 
Catalpa  bignonioides,  2152 
Cataract,  2003,  2006 
Catarrh,    Acute    Suppurative,  of   the 
Pancreatic  Ducts,  1907 

Intestinal,  Nematodal,  1758 

Nasal,  1 52 1 

Spring,  539,  2001 
Catarrhal  Jaundice,  1508,  1509,  1907 

Rhinitis,  Acute,  2013-14 
Cat-Bite  Disease  or  Fever,  122,   151, 

1360,  1515 
Caterpillars,   Venomous,    222-3,    2267 
Catfish,  488 
C?.t-Louse,  608 
Cativi,  2093 
Cats,  Parasites  of,  486 

Plague  in,  1424 
Cattivo  Male,  1700 
Cattle,    Diseases    and    Parasites    of, 
391,  407,  409,  413  sqq., 

430.  454-  497-  701,  712, 
719,  722,  724,  2130 
Freeing  of,  from  Ticks,  701 
Cattle-poisoning,  165,  189 

List  of  Plants  used  for,  190 
Caucasic  Division  of  Man,  42,  44,  45 
Caul,  belief  concerning,  4 
Causation      of       Disease      (see     a/so 
.Etiology      under      the 
various  Diseases),  17 
Chemical,  115,  161 
Physical,  137 
Ciuatics  useless  for  Snake-Bite,  278 
Cditsus,  250 

rhombeatus,  251 
Cave  Rats,  915 
Cavity  Myiases,  1622,  1623 
C  'venne-pepper  Condition  of  Sclu'in- 

berg,  2237 
Celastrus  particulates  Seeds,  170 
Cell-inclusions,  539 
Cellia,  792,  796,885,  887 
albimana,  796,  887,  1598 
argyrotarsis,  785,  796,  887 
bigotii,  796 

145 


INDEX 


Cellia,  continued 

braziliensis,  796 

kochi,  796 

pharcensis,  796,  687 

pulcJiei  liunt,  796 

punctitlata,  796 

squamosa,  796 

tarsimaculata,  887 
Cellules  ovoides  470 
Cellulitis,  149,  150 

of  Spermatic  Cord,  1939 
Celosia  erygina,  1756 
Ceisas,  1 1- 1 2 
Centipede-Bite,  12 

Dermatitis  due  to,   2213 
Centipedes,  124,  217-18,  908 
Central  America,  Relapsing  Fever  of, 

919,  1323.  1324 
Central  Parenchymatous  Infiltration 

of  Cornea,  2005 
Centrodesmose,  316,  330 
Centrosomes,  290,  291,  330,  381,  3S2 
Cepluslis  ipecacuanha,  2153 
Cephalina,  470,  471 
Cephalomyia  ovis,   1625,   1633 
Cephalonts,  470 
Cephalopoda,  890 
Cephalotheca  magnusia,   1024 
Cerastes.  250 

Venom  of,  243,  271 

cormttus,  250,  251,  253,  258 
Ceratixodes,  710,  711,  720,  722 

piitits,  722 

signatus,  722 
Ceratolophus,  802,  803,  805 

femoratus,  805 

fulcithorax,  805 
Ceratomyxia,   529 
Cer  atomy  xidee,  529 
Ceratophvllus,  857,  864,  866 

abantis,  866 

acuttts,  867,  912,  1423 

agilis,  866 

auisu.i.  8(C) 

bipunctatus.  803 

californicus,  866 

castansus,  804 

fasciatus,  403,  404,  406,  866,  867, 
870,  911,  1422 

gallincs,  866 

londiniensis,  866,  867 

lucifer,  866 

niger.  866 

penicilliger.  866,  867 

pinn, tins,  866 

pollionis,  866 

silvantieri,  867 

walkeri,  866,  867 
Ceratopogon,  8<>  2.  803,  804,  805 
'■opogonince,  8oi,  802 
.  Ceratopsyllides,  861,  870 
'opsyllns,  870 


Cerbera  lactaria,  164 

manghas,  165 

odollam,  162,  164,  165,  169 

thevetia,  164,  165,  169,  170,  189 
CercaricE,  567 

Classification,  558-9 
Cercocystis,  599 
CercomoyiadidcB,  m,  334,  343 

References,  357 
Cercomonads,  325 
Cercomonas,  319,334,348,349.364,1944 

detracta,   343 

hominis,  334,  335,  350.  354 

inlestinalis,   354 

longicauda,  343 

musca-domesticce,  365 

parva,  343,  345 
Cercomonata,  319 

Cercopithecus,  Trypanosomes  of,  405 
Cereal  Foods,  95,  104-5 

Vitamines  of,  109,  no 
Cerebellar  Abscess,  1062 

Type  of  Subtertian  Malaria,   1175, 
1176 
Cerebral  Haemorrhages,  1981 

Tumours,  1981 

Type  of  Subtertian  Malaria,  I175 
1176 
Cerebro-Spinal-Fever-like   Su  btertian 

Malaria,  1171,  1172 
Cerebro-Spinal  Fever,  1456 
Non- Infective,  1469 

Fluid  in  Frambcesia,  1554 
Cerebro-Spinal  Meningitis,    120,    123, 

124.    1337.    I5°4.    l696, 

1697 
Epidemic,  1474 

.Etiology,  926,  1482-3 
Carriers   and   Contacts,    1477, 

1478,   1482,   1483,   1485 
Causal  Organisms,   1474,  1476 

s??.,  1482-3 
Climatology,   1475-6 
Definition,  1474 
Diagnosis,    1485,    1514,    151 7, 

1524 

Differential,  1456,  1485 
History  of  the 

Disease,  1474  s^. 

Organism,  1476  i^. 
Incubation  Period,  1483 
Infection,  Method  of,  1482 
Kernig's  Sign  in,  1483,  1485 
Mimicry,  1484 
Morbid  Anatomy,  1483 
Onset,    Course   and   Termina- 
tion,  148 }-; 
Pathology,  1483' 
Prognosis,   1485 
Prophylaxis,   14S2,  1S45 
Rash,   1514,  1516,   1517 
References,   1409-1500 


INDEX 


2307 


Cerebro-Spinal  Meningitis,  continued 
Epidemic,  continued 
Relapses,  1485 
Sequelae,   1485 
Symptomatology,  1483-4 
Synonyms,  1474 
Treatment,  1482 
Varieties,  14S4 
Paralysis    of     Sheep    and    Goats, 

Plants  causing,  189 
Trench  Fever,  1504 
Cerevisice,  1072 

Cervical  Gland  Enlargement,  Indica- 
tions from,  1522- ; 
Cesspool  Fever,  1363 
Cestoda,  17,  555,  590,  600 

of  Man,  601,  603-4 
Cestode  Dermatitis,  2200,  2220 
Eggs  from  Human  Fasces,  603-4 
Infections,  Table  of,  895 
of  the  Intestines,  1753 
Cestodes  digeneses,  600 

polyzoa,  600 
Cestoidaria,  500,  596 
Cestoidea,  555,  596,  600 
References,  618-20 
Table  of  Genera,  602 
Ceylancylostoma,       suggested       sub- 
genus, 674 
Ceylon,  Abor tifacients  of,  170 

Alcoholism  as  cause  of  Crimein,  175 
Anaemia  of,  1  701 
Diseases  of,  122 
Fish-Poisons  of,  187 
Infant  Mortality  in,  122 
Native  medicine  in,  3-4 
Plants  poisonous  to  Cattle  in,  190 
Poisons  used  in 
Inorganic,  162 
Organir,  163 

Vegetal,  102,  164,  163,  170 
Ceylon  Sore  Mouth,  1780 
Cheer omyia,  851 
boueti.  851 
chcuvophaga,   851 
Chcetechelvne  vesuviana,  740,  1641 
ChcstocladiacecB,  972 
Chcetopelina  olivacea,  213,  215 
Chagas'  Disease  (American  Trypano- 
somiasis, q.v.  under  Try- 
panosomiases), 881 
Chagasia,  791 
ChaideB,  298 
Cha'dea,  298 

Chailletia  toxicaria,  173,  191 
Chailletiacece,  173 
Chalmers    and    Archibald's   Maduro- 

mycosis,  2 121 
Chalmers   and    Christopherson's   Ac- 
tinomycosis,  see  Acland's   Actino- 
mycosis, 2140 
Chamar,   the,   49 


Chameleon  pumilis,  363 

Chance-Parasitism,    287,     546,     920, 

1944 
Chance  Transmission  of  Disease,  920 
Chancre,  1523 

Chancre  Espundique  d'Escomel,  2175 
du  Sahara,  2165 
!    '  Chandeliers  favigues,'  1012,  1013 
CharacecB,   923 

Charaka-Samhita,  6-7,  11 30,  1824 
Charas,    176 
Charms,  3,  4,  5,  51 
Chaulmoogra  Oil  in  Leprosy,  1664 
Chavica  betle  leaves,  177 
:    Check    Examination  of    Officials    on 
Arrival  in   the  Tropics, 
129 
Cheeks,  Cancer  of,  1741 
j    C  heir  acanthus,  630 
robustum,  630 
siamensis,  630 
I   Cheironomus,  804 
Cheiropompholyx,  2222,  2226 
Chelitis  Exfoliativa,  1746,  2284 
Cheloid,  2273-4 

Acne,  2272 
Cheloidal     Tumours      after      Sycosis 

coccogenica,  2266 
Chelonia,  Haemogregarines  of,  486-7 
Chemical  Causes  of  Disease.  115,  161, 
1533,  see  also  Deficiency 
Composition    of    Body   and    Food 
Stuffs,     96-7,     see    also 
Vitamines,  109 
Regulation  of  Body  Heat,  69 
ChenopodiacecB,  200 
Chenopodium  Oil  in  Ankylostomiasis, 

1770 
Chermes  modosus,  897 
Cheyletidce,  725,  727,  201 1 
Cheyletus,  727 

eruditus,  jzj,  201 1 
heyletus,    201 1 
Chiastopsylla,  864,   866 

rossii,  866 
Chibcha,  the,  57,  60 
Chichimecs,  the,  60 
Chichismo,   1700,   1710 
Chichismos,  124 

Chicken-pox  (Varicella),    1470,    1471. 
1486,  2207 
Diagnosis,  i486,  1518 

Differential,  i486,  1489-90,  2020, 
2027,  2035 
Varioloid,  1491 
Epidemic,  1491 
Chicken-Tick  of  U.S.A.,  704 
Chick-peas,  poisonous,  196 
Chigoe    (Jigger),    24,    123,    124     282, 
285,     857,     862,     2211, 
see    also  Dermatophihts 
penetrans 


2308 


INDEX 


Child-birth,    Ceylonese    superstitions 
on,  4 
Mortality  from,  Ceylon,  122 
Racial  differences  in,  1946-7 
Children,     Difficulty    of    rearing    in 
India,  132 
Diseases  of,  124 
English,   Dietaries  of,  Qualities  of, 

104 
European,    Effect   on,  of   Tropical 

Climates,  77,  89 
Food-losses  of,  from  Entozoal  Para- 
sites, 553 
Haemorrhagic    Febrile    Gastro-En- 

teritis  of,  1472 
Malaria  in 

Prognosis,   11 87 
Quinine  Dosage  for,  1191 
Spleen-rate  in,  1141 
Symptoms:  Various  forms,  11 59, 
1163,  1175 
Native,   as  Reservoirs  of  Malaria, 

1 1 31,  1 1 40 
New-Born,    Bullous   Eruptions   of, 

1518 
Pellagra  in,  1724-6,  1729 
Pink  Eye  of,  1999 
Pyloric  Stenosis  in,  1749 
Standard  Diets  for,  98 
Young,  Dosage  of  Drugs  for,  i960 
Chiliferidce,  547 

Chills,  Nasal  affections  due  to,  2014 
Chilodon,  546 

dentatus,  546,  547 
References,  550 
uncinatus,  546,  547 
Chilognatha,  689 
Chilomasfix,  348,  349 
References,   356 
Species 
bUtencourti,  349,  350 
caprcB,  349,  350 
caulleryi,  349,   350 
cuniculi,  349,  350 
intestinalis,  350 
mesnili,  334,  335,  349.  350,  1796, 

1833,  1840 
moiellcB,  349,  350 
Chilopoda,  217,  689,  739,  740,  1639, 
1641,  1841,  1881 
References,  229 
Venom  of,  218 
Chilopode  Dermatitcs,  2200,  2213 
Chilopodiasis,  1619,  1641,  1778 

Rhinal,  1881 
Chimpanzees,  Trypanosomes  of,  405 
Chimus,  the,  60 
China,  Aphrodisiacs  in,  172 
Diseases  of,  1  22 
Medicine  in,  4-5 
Chinantecs,  the,  56 


Chinch  or  Wall-Louse,  763 

Chinch  (Tick),  709 

Chinche  (Argas  americanus,  q.v.),  445 

Chinese,  the,  54,  55 

Chins,  the,  54 

Chionphys,  21 14 

carteri,  2114,  2115,  2116,  2134 
Chiorchis,  561 
Chiracanthiim  nutrix,  212 
Chironomidce,  773,  801,  920 

References,  813 
Chironomii,  801 
Chironomines,  801 
Chironomus,  801 
plumosas,  369 
Chitons,  890 

ChlamydobacteriacecB,   924 
ChlamydodontidcB,  546 
Chlamydophrys,  326 
enchelys,  303,  326 
stercorea,  326 
Chlamydospores ,  969,  1037,  1039 
Chlamydotomus  beigelii,  1103 
Chlam'ydozoa(oon),    538,    1328,    1968, 
2001,  2193 
Strongyloplasmata,  540 
Vera,  540 
References,  543 
Chloasma,  2237,  2264,  2281 
Bronzinum,  2079,  2222,  2232 

References,  2245 
Caloricum,  2232 
of  Kala-Azar,  2232 
Malaricum,  11 81,  2232 
Solare,  2231 
Symmetricum,  2232 
References,  2245 
Symptomaticum,  2232 
Toxicum,  2232 
Traumaticum,   2232 
Uterinum,  2232 
Chloromyxidce,  529 
ChlorophycecB,  923 
Chlorops  lepra,  1650 
Chlorosis,    1903 
Egyptian,  1761 
Tropical,   1761 
Chlovoxylon  swietenia,  2159 
Chloroxylonne,  2159 
ChoanephoYacecB,   972 
Chocho,  the,  56 
Cholecystitis,  Purulent,  191 4 
Cholera,  12, 195,  1069,1170, 1404, 1801 
Ambulatory  cases,  1809 
Bacillus  of,  22 
Carriers  (Flies,  etc.),  24,  876,  908, 

1805,  1806,  1809 
Sausal     Organism,     908,      1S01, 
1803,   1804,   1805,   1S10 
Climatology,  120,  121,  122  1 801-6 
Complications,  1810,  2006 


INDEX 


2309 


Cholera,  continued 

Convalescence,  1809,  2006 

Definition,  1801 

Diagnosis,  1810 

Epidemiology,  1S01-6 

History,  1801-6 

Morbid  Anatomy,  1807-8 

Parasites    associated   with,    304, 

334.      45L     547.      548, 
1810 
Pathology,   1806-7 
Prognosis,   181 2 
Prophylaxis,  181 5 

Private,  1815-17,  1819 
Public,  1815,  1817-19 
Vaccine,  23,  29,  128,  1816-17 
References,   1823 
References,   182 1-3 
Sequelae,   1810 
Spread  [see  also  Carriers,  above), 

1804-G 
Stages  in,   1809 
Symptomatology,  1808-9 
Synonyms,  1801 
Treatment,  1804,  181 2 
Asiatica,  962,  1801 
Gravis,  1809 
Sicca,   1809-10 
Choleraic  Bacillary  Dysentery,  1848, 
1850 
Diarrhoea,  1809,  1820 
Choleras,  876,  899,  1801 
Cholera,  1801 
Paracholera,   1801 
Pseudocholera,  1801 
Cholerine,  1809 
Cholesterin,  1227,  1673,  1678 
Chopped   Hair,   Cattle-poisoning   bv, 

189 
Chordodes,  679 
Chorea  Saltatoria,  215 
Chorioptes  bovis,  731 
Choroid,       Miliary       Actinomycotic, 

Metastases  in,  2009 
Choroiditis,  2006 
Retinal,  2004,   2005 
Suppurative,   2005 
Chortegans,  the,  60 
Choulats,  the,  60 
Christya    792 

Chromatoid    Granules    in     Trypano- 
soma, 382 
Chromelsporium,  1 1 1 7 
Chromidiosomes,   290 
Chromidrosis,  2224,  2236 

Axillary,   2272 
Chronic    Affections,    Conditions   and 
Diseases,       see       under 
Names  of  States  mani- 
festing Chronicity 
Chrozophora  plica/a,  190 


Chrysomyia,  832,  847 
Reference,  856 
Species 

macellaria ,  847,  1620,  1623,  1626, 

1628,  1632,  2011 
polita,   1629 

viridula,  848,  1623,  1632 
Chrysops,  816,  820,  896,  1972 
bicolor,  821 
cana,   821 
centurionis,  821 
dimidiata,  821 
dispav,  821 
distinctipennis,   821 
exeutiens,   1974 
magnifica,  82 1 
silacea,  821 
Chrysozona,  817 
Chthonobdella,  687 
Chummeries  and  Sanitation,  1373 
Chylocele,  1601,1605,  1608,  1610,1939 
Chylous    Ascites,    1601,    1608,    1610, 
1961 
Diarrhoea,  1608,  1610 
Effusions  of  Filarial  origin,    1595, 
1599,  1601,  1603,  1605, 
1608,  1617 
Chyluria,  1601,  1608,  1926,  1934 
Cicadas,   761 
Cilia,  291,   296 
Ciliar  Dysenteries,  1825,  1837 

References,   1863 
Ciliata,  296,   544 
Vaginal,   1946 
Ciliate  Urethritis,  1944 
Cimcznomonas  hominis,  354 
Cimex,  762 

lectularius,  763 
macrocephalus,   763 
pipestrelli,  407 
rotundatus,  766,   912 
Cinchona  bark,  4,  11 30,  1199 

Dermatitis  from,  2153,  2162 
Cinchona  officinalis  {see  also  Quinine) 

25.  56 
Cinchonin  Salts,  1200 
Cinchonism,  1181 
Cinnamonum  zeylanicum  bark,  173 
Circinate  Creeping  Disease  or  Erup- 
tion,  2200,  2210 
References,  2220 
Frambceside,   2235 
Pityriasis  Lingux,  1746,  2283 
Sypbilides,  2279 
Circulation,  Effect  on,  of  Temperature 

and  Humidity,  74-5 
Circulatory    System,     Derangements 
and    Diseases    of,    124, 
1519,  1521.  1895 
References,  1905 
Circulionida,   1641 


2310 


IXDEX 


Circumcision 

Female,   1944,  1947 

Male,   1939 
Circumscribed  Scleroderma,  2077-8 
Cirrhosis  of  Liver,  11 84,  1578,  1906-7 
Infantile  Biliary,  1906 

References,   191 7 
Post-Malarial,  11 84 
Cirsoitis,  1939 

Cisus  pruriens,  2152,  2156,  2159 
Cite!  I  us,  914,  915 

beecheyi,  867,  912,  915 

citellus,  915 
Citrus  vulgaris,  2152 
Cladoccelium  hepaticum,  565 
Cladorchiincs,   561 
Cladorchis,   561 

watsoni,  562 
References,  594 
Cladosporiaceez,   1070,   1099 
Cladosporosis,   2107 
Cladosporiiim,  1099,  1100,  1926,  1944, 

1945 
Dermatomycoses  due  to,  2041 
Species 

herbarium,  1100,  1101 
madagascariense,  2078,  2107 
mnnsoni,  1100,  2041,  2078 
penicilloides,  1100,  1101,  2107 
Cladothrix,  1041,  1042,  1068 
actniomyces,  1051,  1057 
asteroides,  1053,  1058 
brauner,   1045 
canis,   1053 

dichotoma,  1042,  1045,  1068 
invulnerabilis,  1046 
liqitefaciens,  1050,  1060,  2133,  2136 

No.  2,  1060 
modore,   1050 
odorifera,   1045,   1051 
polychromes,   1050 
thermophilis,   1047 
Claviform  bodies,  1011 
Claws  of  Animals,  Traumatisms  due 

to,  14S 
Cleft  Palate,  1959 
Clematis  virginica,  2153 
Cletus  varius,  369,  372 
Clibadiiim  asperum,  188 
Climacteric,  the,  in  the  Tropics,    77. 

1945 

Climate  (s),  see  Dangerous,  Temperate 
Tropical ;  see  also  Tem- 
perature and  Humidity 
Definition,  62 
Effects  of,  on  Children,  89 
Climatic  Bubo,  25,  1523,  1961 
References,   1966 
Varieties,  1963 
Causation  of  Disease,  117 
Fevers,  1129,  1252 


Climatology,  24,  39-41,  62 

References,  91 
Clinical  Diagnosis,  16-17,  I532 
Examination.   151 1 
Medicine,   24-5 
ClinocoridcB,  762 
Bites  of,  219 

Dermatitis  due  to.  2200,  2203 
ClinocorincB,   762 
Clinocoris,  762 

Change  of  Habits  of,  765 
Fungi  on,  2096 

Schizotrypamim  cruzi  carriers,  430 
Species 

boueti,  430,   763 

ciliatus,  763,  766 

columbarius,  763 

dissimilis,   763 

fcedus,  763 

improviso,   763 

inodorns,   763 

lectuiarius,    430,    443,    763,   882, 

1329.  137°.  ^5° 
pelosellns,  763 
peristercB,  763 
pipistreUi,  763 

rotundahis,  124,  370-2,  379,  430, 
763,  766, 1423 
Clinocorosis,  2203 
Cloaca,  943,  958 
cloacce,  958 
levans,  958 
Clonorchiosis,  1906,  1907,  190S,  1917 

References,   191 8 
Clonorchis,  576,   578 
References,  594 
Species 

endemicus.  ij,  578,  579 
Feline  (possible),  580 
sinensis,  17,  578,  579,  894,  1907, 
1917 
Clothing,  Advice  on,  to    be    given  to 
Candidates       for       the 
Tropics,  128,  129 
Hints  on,  69,  86,  89-90,  140 
Protective,   1989 
Clou  de  Gafsa,  378,  3  So 
Clupea,  193-4 
longiceps,  194 
thrissa,  193 
Cnemidospora,  471 
Cnestis  comiculatus,  2153,  2159 
Coast  Fever,  11 29 

in  African  Cattle, 71 2,  713 
Cobb's  Pigmentary  Fever,  1461 
Cnbra-di-capello,  246 
Cobra-Poisoning,      Treatment,      244, 

271  sqq. 
Cobra-Venom,    209,    221,    243,    253, 
257.     259,     260,      261, 
264  sqq.,  271-4 


INDEX 


2311 


Cobras,  246-7,  278 
Cocaine-Chewing,  17.5-6 
Coccacece,  924,  1679 

Reference,  966 
Coccal  Infections,  Fly-spread,  900 
Coccidia  found  in  Man,  475,  476 
Cocci dien  leberpsorosperv.iien,  476 
Coccidiidca,  469,  471,  477,  480 
Coccidioides,  981,  983,  985,  1S86,  2081 

Blastomycosis  due  to,  2084,  2085 

Dermatomycoses  due  to,  2041 

Species 

immitis,  537,  985 
pyogenes,  535,  985 
Coccidiomorpha,  461),  471 
Coccidiosis,  473,  474,  883 

Faecal,  475 

Hepatic,  474 

Intestinal,  475 
Coccidium.  473,  1250 

bigeminum,  var.  hominis,  475 

cuniculi,  476 

Hepatic,  of  Man,  476 

hominis,  475 

lacazei,  473 

ovifonne,  474,  476,  477 

perforans,  474,  475 
var.  kjellberg,  475 

posades,'  537 

pyogenes,  537 

schnbergi,  471,  472 

seeberi,  533,  1578 
Coccobacillus,  925 

pseudo-acti nomycosis   polymorphus, 
1034,  2139 
Cocculus   185 

amazonum.  185 

indicus,  189 

toxiferus,  185 
Coccus (i),  1680,  1982,  2019 

in  Acla-liosis,  2091 

Chromogenic,  21 01 

Pyogenic,  2017,  2201,  2255 

Red-pigment  producing,  in  Sweat 
2224 

Species 

ancerobius,  1946 
cacti,   761 
Cochin-China  Diarrhoea,  1780 
Cochin  Chinese,  the,  54 
Cochin  Leg,  1610 

Sore,  2 1 81 
Cochineal  Insect,  761 
Cockroach,  765 
Coco,  1535 
Coconuts,  Falling,  Traumatisms  due 

to,  156 
Ccelenterata,  203,  338 

References,   2 28 
Cceliac  Disease,  17S0,  1799 
Ccelodiazesis.   792 


CcclospovidiidcE,   534 
<  cenogonimus,  570 
Cofiee-drinking,  Excessive,  178 
Cohnistreptotkrix,    1041,    1063,    1747, 
1886,  2139,  2141,  21  |<i 
Dermatomycoses  due  to,  2041 
Organisms  included  in,  History  of, 

2138-9 
Species 

americana.  1064,  10O5 
carougeaui,  1065,  1066 
cuniculi,  10O4,  1065 
foersteri,  1065,    1066,    1067,  2009 
Israeli,    1063,    1064,    1005,    1066, 
2138,   2139,  2140,   2141 
neschezadimenki,  1004,  1065 
silberschmidti,  1003,  1004,  1065 
tenuis,    932,    1065,    1066,    1067, 
2041,  2101,   2102,   2105 
thibiergei,  1063,  1064,  1065,  1066, 
2041,  2139-40,  2141 
Table  of  Species  possibly  belonging 
to,  1065 
Cold,  Common,  1521,  2013-14 
Cold-Blooded  Vertebrates,   Try; v no- 
somes  Infecting,  395, 3S8 
Coleoptera,  748,  857,  871 
Infestation  by,  1639,  1640 
References,   871 
Venomous.  218,  226 

References,  229 
Vesicant,  2204,  2205 
Coleopterous  Larvaj,  Irritating    2208 
Colic,  Trematodal,  1752 
Colitis,  Amoebic,  1825 
Dysenteric,  538,  1836 
Polyposa,  1847 
Collection    of    Blood-Sucking    Flies, 

How  to  make.  748 
Collytricha  faba,  572 
Colmoyote,  1633 
Coloboma,  1995 

Iridis,  1959 
Colombian  Relapsing  or  Tick  Fever, 

444,  445,  919.  1324 
Colorado  (mite),  725,  2213 
Colour-Blindness  in  Natives,  130. 1995 
Colour  of  Clothing,  89-90 

Protective,  85,  86,  87 
Colpo  di  Calore,   1449 

di  Sole,  1 44 > > 
Colpoda,  5  17 

cucullus,  546,  547,  1837 
( 'olponema,  337 
( 'oluber  corais,  487 
( 'olubra,  242 
( 'olubridcs,  2  |.| 

Venom  of,  163 
Colubrina,  245 

Colubrine  Venom,  163,  243,  244,  254. 
256,  262-3,  264-8 


2312 


INDEX 


Colubrine,  Anti-Sera  for,  272,  273 
Columbensis    Parenteric,   1405    1408, 

1410 
Columella,  972 

Coma,  Alcoholic,  or  Renal,  Differen- 
tial Diagnosis  from  Heat 
Stroke,  1456 

Kussmaul's,  1924 

Renal,  1456 
Comatose  type  of  Subtertian  Malaria 

1 1 73.  H74 
Combretum  grandifiora,  183 
Comedos,  2272 
Common  Cold,  1521,  2013-14 

Continued  Fever,  1362 
Comoro  Islands,  Fish-Poison  of,  18S 
Composites,   2152 
Com'psomyia,  415 

rubrifrons,  847 
Concussion,  1981 
Cone-Nose  Bug  of  America,  bite  of 

767-8 
Cone-Nosed  Bugs,  Fevers  carried  bv 

1128 
Cones,  Bites  of,  227 
Confluent  Smallpox,  14S8 
Congenital  Achromia,  2230 

Eye  Defects,  1995 

Goitre,  1920,  1922 

Hyperkeratosis,  225G 

Leucoderma,  2230 

Leucopathia,  2230 

Leukasmus,  2230 

Malaria,  1134,  1142 
Reference,  1211 
Congestine,   204 

Congestion  of  Liver,  1906,  1908 
Congo  Floor-Maggot,  850,  2208 
Congo  Region,  Vegetal  Aphrodisiacs, 

of,  172 
Conicera,   1630 
Couidia,   969 

Conidiophore,  1035,  1036,  1039 
Conidiosporales,  1039,  1110 
Conidium,  1035,  1037,  1038 
;»,    1039 
ferts,  2153 
Con  1  palpi,   710 
Conjugates,  923 
Conjugation,  288 
Conjunctiva,  Focal  Necrosis  in,  2006 

Hyperaemia  of,  1995-6 

Loa  loa  in,  645,  1971,  1972,  2007 
Conjunctiva  Sporotrichosis,  2010 
Conjunctivae,    Chyle-extrusion    from. 

Filarial,  1617 
Conjunctiva]  Xerosis,  2000 
Conjunctivitis,  902,  1904,  1995,  1996, 
1998,  2003,  2006 

V  tinomycotic,  2009 

Angular,  1006,  1997 


Conjunctivitis,  -continued 

Catarrhalis,  1996 

Diphtheritic,    1996 

^Estivalis,   2001 

Gonorrhoica,  1996,  1997 

Malarial,  2004 

Mycotic,  1059,  2008 

Neonatorum,  539,  1997 

Nocardial,  1059,  2009 

Nodosa,   1996 

Phlyctenulosa,  1996,  2002 

Purulent,  1060 

Trachomatosa,  1996,  1998 

Ulcerative,  1060 

Vernalis,  1996,  2001 
Connaracecs,  2152,  2153 
Connective  Tissue 

Derangements  of,  15 19,  1524 

Diseases  of,  1967 
References,    1979 

Tumours  of 
Benign,  2273 
Malignant,  2274 
Conorhinus,  19,  767 

geniculates,  12S3-4 

megistus,   768 

nigrovarius,  767,  768 

protracfits,  767,  768 

renggeri,  767,   768 

rubrofasciatus,  372,  398,  767,  768-9 

sanguisugus,   767 

variegatus,  767 
Conservancy,  554 

Constipation,  Indications  from,  1520 
Consumption  (see  also  Phthisis},  132 
Contagion,  15 
Contagium  vivum,  22 
Contaminativc       Transmission       of 

Disease,  921 
Continued  Fevers 

Bilious,  1363 

Common,  1362 

Double,   1463 
References,   1473 

Korean,   1355 

Simple,  25,  1254,  1372 
Convection,  69 
Convulsions,  Infantile,  122 
Convulsive  Tics,  1983 

Tvpe  of  Subtertian  Malaria,   117^, 
1175 
Coolies,  Estate,  Anaemia  in,   1903 

Rickshaw,    Blood-vessel    affections 
of,  1904 

Sore  Feet  of  (Ground- Itch),  1764 
Ccoly  Itch,  553,  730,  2247,  2248 

of  Feet,  2214 
Copepoda,   739 

Copper.  Salts  of,  Poisoningby,  162, 170 
Copper  Sulphate,  Poisoning  by,   170, 


INDEX 


2313 


Copper-Head  Snake,  250 
Copra  Dust,  1876 

Itch,  729,  730,  2200,  2214,  2215,2248 
Coprolalia,   1986 
Copromastix,  348,  349 

prowazeki,  348 
Coptapsylla,  865 
Coral  Snake,  248 
Corals,  Stinging,  203,  204 
Coras,  the,  60 
Cordiceps  sinensis,  172 
Corditis,  Suppurative,  1939 
Cordylobia,  830,  832,  849 

References,  856 

Species 

anthropophaga,    849,    852,    1621, 
1632,   1633,   1637,   1638 
grunbergi,  849,  1637 
prcegrandis,  1637 
rodhaini,  850,  1633,  1637,  1638 
Coreotrypanosis,   1283 
Corethra,   793,   801 
CorethridcB,  773,  789,  801 
CorethrincB,  789 
Corethropsis,   11 12 
Coriaria,  176 

myrtifolia,  176 

rusci folia,   176 
Corizoneura,  822 

hast  a,  823 

lineatithorax,  823 

penetrabilis,  823 
Cormollote,  828,  1633 
Corn-cockle,  197 

Cornea,  Central  Parenchymatous  In- 
filtration of,  2005 

Focal  Necrosis  in,  2006 

Glenosporosis  in,  2010 

Opacity  of,  2006 

Phlyctenular  Keratitis  of,  2002 

Sore  on,  in  Rabbit,  378 

Ulcers  of,   1031,   1997,  2000,  2003, 
2004,  2006,  2009,  2201 
Cornu  cutaneum,  2277 
Covonella  ausiriaca,  245 
Corps  oviformes,  476 
Corrosive  Sublimate,  170 
Corynanthe  yohimbi,  172 
Corynebacterium ,  965,  1040 
Coryza  Spasmodica,  1S75 
Cosmopolitan  Diseases,  115 

of  Mucous  Membranes,  2264,  2283 

Fevers,  1128,  1474 

Skin  Disease,  2015,  2017.  2264 

Ulcerations,  2190 
Cossala,  1753 
Costiopsis,  348 
Cottiace,  232,  234,  237 
Cotton,    Pink-bolhvorm   of,    Parasite 
of,  attacking  Man,  2214, 
2216 


Cotton-Handler's  Itch,  2214 
Cotton-Moth    Caterpillars,    Parasites 

of,  2216 
Cotton    Plants    (Uganda),    Herpeto- 

monad  of,  367 
Cotton-Seed  Dermatitis,  2216 
Coitus  bubalis,  234 
gobio,  234 

scorpius,  232,  233,  234 
Cotylogonimus,  570 
heterophyes,  570 
Coup  de  Chaleur,  1449 
Coup  de  Soleil,  1449 
Courap  or  Cowrap,  2053,  2217 
Courmont's  Parasites,  998 
Cow-dung  Poultice,  1952 

Wash,  1952 
Cowhage,  2159 
Cow-Parsnip,  2157 
Crab  Louse,  757 
Crabs,    Fresh-water,  hosts  of    Para- 

gominus,  575 
Craigia,  298,  299,  300,  324 
References,  329 
Species 

hominis,  325 
migrans,  325 
Crambas  pinguinalis,  1640 
Craniopagus,  1958 
Craspedomonadidce,  333 
CrassulacecB,  2153 
Craw-Craw,  1497,  2247 

References,  2263 
Creeping  Disease,  or  Eruption,   123, 
1633,  1639,  2200,  2208 
References,  2220 
Circinate,  2200,  2210 
Cretinism,  120,  123,  1919 
Endemic,  1920,  1922,  1959 
Sporadic,   1920 
Cretinous  Idiocy,  1920 
Cricetincs,  915 
Crime  due  to  Alcoholism,  175,  1981 

in  relation  to  Latah,  1987 
Criminal  Poisoning,   161,   162 
Cristispira,  439 

anodontcB,  437,  43S,  439 
balbianaii ,  437,  439 
Crithidia,   358,    359,    360,    361,   367, 
369.  372-  376,  397 
Species 

campanulata,  369 
cleti,   369 

ctenophthalmi,   376 
cunninghami,  378 
fasciculata,  369 
gerridis,  363,  366,  367-8 
grayi,  401 

hyalommce,  362-3,  369 
hystrichopsyllce,  3^9,  376 
melophagia,  363,  369,  386,  388 


2314 


INDEX 


Crithidia,  continued 
Species,  continued 

minuta,  369 

Porter's  and  Wenyon's,  376 

pulicis,  369,  376,  479 

tabani,  819 
Crithidial    forms    of    Trypanosomes, 

389,  390 
Crithidium,  2193 

Crocodiles,  Parasites  of,  401,  480,  486 
Traumatisms  due  to,  12,  153,  514 
Crotalince,  249,  250,  251 
Crotalus,  250,  251,  252, 

Venom,  243,  253,  257,  258,  260, 
261,  262,  263,  269-70 
Anti-Sera  for,  272,  273* 
Species 

adamanteus,  251 

atrox,  251 

cerastes,  250,  251 

confluentus,  250,  251,  253,  487 

durissus,  243,  250,  253,  254,  259, 

272,  273 
horridus,  250,  251,  256,  269-70,  273 
mitcheUi,   251 
oregonus,  251 
scutulatus,   250 
terrificus,  251 
Croton  tiglium,  168,  185,  190 
Crotonus,  720 
Crustacea,  689,   739 
Cryptobia,  337,  338 
Cryptocerata,  761 
Cryptococcaceee,  1070,  1071 
Cryptococcosis  Epidermica,  2092 
Cryptococcus,  9S1,  1037,  1069,  1070, 
1071,  1782,  1886,  1944. 
20u8,  2081 
Dermatomycoses  due  to,  2041 
Species 

breweri,  1072,  1075 
capsulatus,  1076,  1669 
cerevisics,  1072 
corselli,  1072,  1074 
degenerans,  1072,  1074 
dermatitis,  1073,  2008,  2009 
epidermidis,  1075,  2092 
farciminosus,  1072,  1076 
gilchristi,  1073,  1079 
glutinus,  1072 
granulomatogenes,  1076 
guillermondi,  1072,  1075 
guttulatus,  1072 
harteri,  1075 
hcssleri,  1072,   1074 
hominis,  1069,  1071,  1072,  1073 
hudelo,  1075 
lesieuri,  1072,  1075 
Ungues  piloses,   1061,   1073,   1074 
lithogenes,  1076 
membranogenes,  1075 


Cryptococcus,  continued 
Species,  continued 

myrmecice,  1073,  1077,  2262 
niger,  1076 
plimmen,  1072,  1074 
rogeri,  1073 
ruber,  1076 
salmoneus,  1072,  1075 
sulfur eus,  1072,  1075 
tokishigei,  1076, 
tonkini,  1072,  1075 
zn'm,  1072 
(.  ryptocystes,  528,  529 
Cryptocystis  trichodectis,  60S 
Cryptogenic  Septicaemias.   1429 
Cryptostigmata,  692 
Crystallospora,  473 
CrystotrypanecB,  396 
Ctenizidce,  212 
Ctenocephalus,  864 

canis,  363,  608,  866,  867 
/e/?s,  608,  866,  867 
inusculi,  867 
serraticeps,  376 
Ctenocoridcs,  761 
Ctenomyces,  986 

serratus,  987,  1101,  2054 
Ctenophthalmus,  865,  866 
cBgyrtes,  367,  866 
assimilis,  866 
serraticeps,   867 
Ctenopsylla,  865,  866 
aganijfies,  866 
ellobius,  866 
musculi,  866,  867 
pectuniceps,  866 
selenis,  866 
spectabilis,  866 
taschenbergi,  866 
Cucumis  trigonus,  170 
CucurbitacecB,  170 
Cuicatecs,  the,  56 
Culerebrince,  826 

C«/e#,    23,   546,    774,    776,    792,    796, 
799,873,  896,  1 137,  2096 
Species 

cBStuans,  799 
agilis,  799 
alpinus,  799 
calopus,  799 
ciliaris,  799 
communis,  791, 

fatigans,   23,  369,  513.  542,  637, 
638,     799,     1244     s?)?.  , 
1527.  1.596,  1598 
frater,   799 
nemorosus,  513 
pallipes,  799 
plivtophagus,  799 
pipiens,    ^63,    366,    398,    432-3, 
519,  774,  799 


INDEX 


2315 


Culex,  continued 
Species,  continued 

pungens,  799,  1650 

fit  (us,  799 

vulgaris,  799 
Vectors  of  Filariasis,  747 

Possibly,  of  Dengue,  747 
CulicidcB,    771,    773,    774,   781,    801, 
1630,  2200 
Bites  and  Venom  of,  223  sqq. 

Treatment,  226 
Classification,  789 
Eggs,   771 

References,  229,  813 
Species  Carrying  Malaria,  791,  792, 

793.  794-  795.  79^ 
Important,  in  Tropical  Medicine. 
790 
Wings,  772 
CulicimorphcB,   801 
CulicincB,  398,  786,  790,  796 
Culicites,  Soi 

Cul-ick-um-ek  Plant,  Poisoning  by,  124 
Culicoides,  802,  804 
bvucei,  743 
grahamii,   805 
habereri,  805 
pulicaris,   804 
varius.   805 
Cultripalpi,   710 
Culture  Zone,  44 
Cupping  for  Arrow-wounds,  181 
Carari  as  Arrow-poison,  185,  186 
Curative.  Poisoning,  171 
Curin,  186 
Curupira,  813 

torrentium,  813 
Cutaneous  Blastomycosis,  2085 
Diseases    [see    also    under  Names), 
1 501,  2015,  2017 
Differentiation  of,  from  Pellagra, 
1730-1 
Eruptions,  Diagnosis  of,  1513 
Leishmaniasis  (see also  under  Leish- 
maniasis), 908,  2165 
References,   2197 
Localization  of  Subtertian  Malaria, 
Symptoms,   11 75,    1181 
Myiasis,  1632,  1633,  1637 
Pigmentation,     75,    84    sqq  ,     145, 
1529,  1531.  2232,  2265, 
2266,  see  also  Diseases 
in    which    occurring 
Diagnosis,   1513,   1519 
Spirochaetes,  448-9,  452 
Spirochsetosis,   15^5 
Tuberculosis,  2264,  2277 
Tumours,  2264,  2273 
Ulcerations,  2015,  2017 
Cuierebra  hominis,  1633 
noxialis,  828,  1633 


Cyanea  aipillata,  204 
Cyanophees,  Oscillatory,  437 
Cyanophyceee,  436,  923 
<  'yathomastix,  349 

hominis,  350 
Cyclasterella  scarlatinalis,  537 
Cyclitis,  2003,  2006 
Cyclocephalus,  1958 
Cycloleppteron,  780,  791,  884,  885 
grabbami,   888 
inediopunctatiiiii,  885 
nototrichum,  885 
Cyclones,   82 

Cyclophyllidea,  600,  601,  607 
Cyclops,  651,  739,  %9*,,  896 
(  yclorrhapha,  773,  774,  825,  901 
C.yclospora,  473 
Cyniphes  molestus,  810 
(  vuipidcs,  908 
Cynomyia,  831 

mortuorum,   831,   1629 
Cynomys,  914 
Cynorhcsstea,  693 
Cynorhcestes,  720 
Cypania,   173 
Cyprini-siluriformes,  232 
C ' yprinodontidce,   789 
Cvpripedium  pubescens,  2153.  2159 

spectabile,   2159 
Cyprus  Fever,  1437 
Cyrtoneura  sfabulans.  1629 
Cystic  swellings  of  Tibia,  1072 
Cysiicerci,  596 
Cvsticercoid,   599 
Cvsticercosis,    1967 
Cvsticercus,  599,  603 
acanthotrias,  601,   613 
bovis,  614 

celluloses,  613,  2007 
fasciolaris,  600 
Cystocercous  Cercarice,  559 
Cystici.  596 
Cystinuria,  1926 
Cystitis,  Amoebic,  103:; 

Schistosome-caused,  1926 
Cystoflagellata,   332 
Cysto-pyelitis,  1949 
Cystotrypanees,  396,  397 
('v^toivvpanosoma,  396,  397 

inteslinalis,  396,  397 
t'vsts,  Ovarian,  1945 
Cytamceba,  504 
Cytisus  cadjan,  195 
Cytoleichus  hominis,  731 

sarcoptoides,   731 
Cytomorpha,  297 
Cytooihon  group,  541 
Cytoplasm,  290,  291, 
Cytopyge  in  Nyctothents,  544 
Cytoryctes,  535,  540,  i486 
variola,  535,  540,  1487 


2316 


INDEX 


Cytospermium  hominis,  475 

villorum  intestinalis  canis  etfelis,  473 
Cytosporon,  504 

Dacryocystitis  1064,  1066 
Dacryolithes  of  Desmarres,  1067 
Dactylitis,  Multiple,  in  Yaws,  1552 
Dactylolysis  Essentialis,  2241 
Dactylophoridcs,   471 
Dactylosoma,  488 
Dactylosphera,  298 
Dadane,   1260 
Da-fil,  1595,  1610 

Daffodil,  poisonous  qualities  of,  2163 
Dajaksch,  Dart-poison  of  Borneo,  184 
Dalbergia  latifolia,  2160 
Dallengeria,  345 
Dais  or  Dhals,  105 
Dambul  Fever,  11 29 
Dam  din  Fly,  811 
Dancing  Mania,  1986,  1987 
Dangerous  Climates,  131 
Danilewskya,  478 
Daphne  guidium,  188 

mezereum,  2153 
Darier's  Disease,  474,  2281 
Darmtyphus,  1363 
Darnel,   197 

Dart-Poison  of  Borneo,  184 
Dasybasis  820 
Dasypeltince,   245 
Dasypeltis  scabra,  245 
Dasyphora  pratorum,  367 
Dasypus  novemcinctus,  881,  882,  1283, 

1284 
Datura   Poison,    124,    170,    173,   17S, 
190,  2153 

Species  yielding 

fastuosa,   170,   171,   178,   190 
stramonium,  2153 
Daucus  carota,  170 
Dau-ool-nl.  1595,  1610 
Davainea,  601,  602,  611 

asiatica,  601,  604,  611,  612 

niadagascariensis,     601,     604.     611, 
1758 
References,  619 
Davaineiasis,  1758 
DavaineincB,  601,  607,  611 
Deaf-Mutism,  1920 
Deafness,  Aspergillar,  103 1 

Cinchonal,   1181 

Malarial,  1181 

Post-Malarial,  11 84 

Tropical,  2013 
Death  Adder,  2.47 
Death  at  Will,  [991 
Death-Fish  (Hawaii),  194 
Death's-head  Moth,  226 
Debab,  414,  415,  874-5 
Debaromyces,  979 


Defensive      Reflexes,      Exaggerated, 

1982 
Deficiency  Diseases  (see  also  Beri-beri 

and  Pellagra),  109,  1533, 

1671,  1675,  1690,  1691, 

1709 
Definitive  Hosts  of  Animal  Parasites, 

872,  873,  921 
Defoimities  of  Lobule  of  Ear,  2010 

in  Papua,  123 
Degeneration  Endemique  des  Os  du 

Pied,  21 15 
Deinoceratince,  790 
Delhi   Boil  or   Sore,  378,   380,    2165, 

2166 
Deli,    Sumatra,    Pseudo-Typhus    of, 

J354-5 
Delirious  type  of  Subtertian  Malaria, 

1173,  1175 
Delphinium  consoliduni,  2153 
Delusions,  1991 
Demaiiacea,  1036 
Dementia,  1524,  1981 
Demodex,  731 

bovis,  734 

folliculorirm,  732,  2007,  2011,  2215 

phyl/oides,   734 
DemodicidcB,  692,  731,  201 1,  2215 

Reference,  742 
Demonology  and  Medicine,  3  sqq. 
Dendraspis,  246 

viridis,  251 
Dendrodichum  microsporus,  1032 
Dendromyir.eB,  790 
Dengue,  25,  1233,  1244,  1429,  1461 

/Etiology,  1246-7 

Blood  in,  1246,  1248 
Bodies  in,  1245,  1246 

Climatology,  122,  1244  sqq. 

Complications,   1249 

Course,  1247 

Definition,  1244 

Diagnosis,  1250,  151 5,  1527 

Differential,  1186,  1238,  1250, 
1253,  1258,  1313,  1395. 
1497,  1498,  1505 

History,  1244-5 

Insects  carrying,  23,  542.  747,  799, 
920,  1128,  1244 

Morbid  Anatomy    1247 

Onset,  1527 

Pathology,   1247 

Prognosis.   1250 

Prophylaxis,  116,  1250  . 

Rash,  1248,  1249,  1515 

References,  1242,  1253 

Reinfections,  1250 

Relapses,   1249 

Sequelae,    1249 

Symptomatology,  1247 

Synonyms,  1244 


INDEX 


2317 


Dengue,  continued 

Treatment,  1250 

Varieties,   1249 

Virus  filterable,  541,  542 
Dengue-like  Fevers,  1252 

References,  1253 
Denisonia,  246 

superba,  251 
Dental  Bridges,  1520,  1531 

Caries,  124 
Denticulate  Bodies  in  Microsporum, 

990 
Dermacentor,  700,  710,  711,  715,  1341 

albicollis,  716 

albipictus,  716 

andersoni,     700,     716,     717,     920, 
1341,   1342,  1343,  1344, 

13-15,  1348,  1349 

andersoni  group,  716 

electus,  700 

ferrugineus,   716 

marginatus,  700-1 

maturatus,  1341,  1348 

molestus,  700,   1 341-2,   1345 

nigrolineaius,   716 

nitens,  716 

occidentalis,   716 

parumapertus,   716 

pordalinus,  716 

reticulatus,  700,   716,   1341 

reticulatus  group,  716 

salmoni,  716 

salmoni  group,  716 

variabilis,   701,  716 

venustus,  700,  716,  717,  920 
Dermal  Canthariasis,  1641 

Leishmaniasis      {see     also      under 
Leishmaniasis),        908, 
2165 
References,  2197 

Myiases    (see    also    Myiases),    831, 
1623,  1631,  2208 
Traumatic,  1623,  1632 

Pyogenic  Infections,  2015,  2017 
Dermanyssince,  693,  2213 
Dermanyssus,  693 

gattina,  693,  2007,  2213 

hirudinis,  693,  2213 
Dermaphyton,   1077 
Dermapteriasis,  1619,  1639,  1641 
Dermatites,  691,  1501,   1730 

Acarine,  2200,  2206,  2213 

Alcoholic,  17^0 

Cestode,  2200,  2220 

Chilopode,  2200,  2213 

Hexapode,  2200,  2207,  22 11 

Nematode,   523,   1 763.   1764,   1771, 
2200,  2219 

Plant-caused,  2015,  2017,  see  also 
Dermatitis  Venenata 

Pyogenic,  2017.  2029 


Dermatites,  continued 
Streptococcal 

Primary,  2030 

Secondary,  2030,  2036 
Urticarioid,  2216 
Dermatitis,  1098 

Blastomycetica,  2081 

Bullosa  plantaris,  2025,  2030,  2037 

References,  2039 
Cane-cutter's,  1466,  2163 
Castellanii  (Copra-Itch),  2215 
Caused  by  Acarina,  691 
Chronic,  1 730-1 
Cinchona  Bark,  2162 
Cotton-seed,  2216 
Cupoliformis,  929,  2030,  2034 
Ditropenotus,  2216 
Eczematous,  2048 
Erysipeloid,  1058 
Erythematous,  1033 
Exfoliativa,  2264,  ~-7°,  2271 
Factitia,   2 151 
Herpetiformis,  2206,  2269 
Interdigitalis,  2036 

References,   2039 
Intertriginous,  982 
Macrogyrata,  2200,  2210 
Medicamentosa,  21 51 
Nodosa  rubra,  2247,  2249,  2252 

References,  2263 
Nodular,  2247 
Papillaris  capillitii,  2266 
Pellagrous,   171 5 
due  to  Phihirius  pubis,  758 
Poultryman's,  693,  2213 
Pratensis,  2030,  2032 
P/otozoic,  20S1 
Pruriginosa  tropica,  2248 
Quinine-caused,  2153,  2162 
Recurrens,  2206 
Reed-cutter's,  2163 
Rimosa,  2036 
Scarlatiniformis,  151 3 
Schambergi,   2216 
Seasonal  Bullous   (Vesicular),   226, 

2204 
Ulcerative.  1091,  n  12 

Chronic,  J073 
Vanilla,  2163 
Veldis,  2030 

Venenata,    191,   2015,    2017,    2151, 
2264,  2267 

.Etiology,  2152-4 

Climatology,  2152 

Definition,   2 151 

Diagnosis,  2154-5 

Differential,   1730,   2155,   2206 

History,  2151-2 

Personal  Idiosyncrasy  and,  2154 

Plants  causing,  2151-2,  2162 
Groups  of,  2155 


23l8 


INDEX 


Dermatitis,  continued 

Plants  causing,  continued 
List  of,  2152-3 
Prophylaxis,  2155 
References,  2163-4 
Symptomatology,  2154 
Treatment.  2155 
Vesicular,  Seasonal,  2004 
Devmatohia,  820    828 
bovis,  82 7 
cyaniventris,    828,    S30,    896,    897, 

1627,  1632,  1633,  2007 
diana,  827 
hominis,  828,   1619-20,   1621,   1635 

Synonyms,  1633 
kenics,  830,  1633 
mexicana,  1633 
noxialis,  828 
References,   856 
Dermatobia  Myiasis,  897 
Dermatobiasis,  1633 
Dermatococcus.   1600 
Dermatology.    Fungi    of   importance 

in,  981 
Dermatomycoses,    10S0,    1081.    2015, 
2017,  2041 
Tropical 

Classification,  2040 
References,   2107-9 
1  k-rmatomycosis     chronica     ngurata 

exfoliativa.  2060 
Dermatophiliasis,   25,   2210 

References,   2220 
Dennatophilus,  861 
ccecata,   861,   866,   86  7 
penetrans,  285,  861,  862,  864    866, 
1 260,  1273.  2211 
Dcrmatose  Parasitaire,  2247 
Dermatoses,  539 
Acarine,  221.3 
Xematode,  2219 
Dermatosis,   1097 

Festonata  Frontalis,  2222,  2234 

References,  2244 
Hyphomycetica  Indica,  2086 
Xi'-jro-Circinata,  2222    2235 
Dermatozoiases,     226,     2015,     2017, 
21 51,   2200,  2207.   2267 
Dermatropismus.  53Q 
Dermestes  lardarius,  164(1 

murtnus,  16  |" 
Dermite  Ulcereuse  Circonscritc    2165 
Dermo-Conjunctival  Filariasis.  [967, 
r968,  1971 
References,   1980 
Dermoptera,  [639,  1641 
I  >ermotagra,  1  72'..  [  730 
Derrid,  188 
Devris  elliptica,  184.  188 

ulit&nosa,  187 
Deseil  Hallucinations,  iq8t,  1990 


Desquamation,  Sweat,  2227 
Desvoidea,  789 
Deuteroanopheles,  883,  885 
Deuteroconidium{ia),  1037,  1038.  tioS 
Deuteromycetacccs,  1035 
Deuteromycetes,   1035.   1036 
Deutovum  of  Acarina,  691 
Devescovina,  351 
Devil-dancing,  4 
Devitrification,  82 
d'hatti  fallategen,  1922 
Dhobi  Itch,  1007,  2040    2042 
Dhome  majara  harik,  200 
Diabetes  Mellitus,  7,  122,  1525,  1743, 
1919,  1924,  1934,  2226, 
2232,  2233 
Reference,   1925 
Diabetic  Boils,  1924 
Diachlorus,  820 
Diagnosis,  Indian,  early,  7 

Microscopical  and  Clinical,   16 
of  a  Tropical  Fever,  1511 
Diamphidia  simplex,  1S0 
Dianella  nemorosa,  191 
Diaphoretic-like  Subtertian  Malaria, 

1173,  1174 
Diarrhoea,  Incidence,  122,  123,  124 
Organisms  associated  -with,  325, 
354.  355,  451.  466-  468, 
546.  547.  548,  55°.  563. 
569.  572 
Alba,   1780 
Choleraic,  1809,  1820 
Chronic,  325,  872 
Chylous,  160S,  1610 
Cochin  China,  1780 
Dysenteric,  569,  1824 
'Bacillary,  1848,  1851 
Trematodal,  1752 
Endemic,  1780 
Epidemic,  or  Summer.   899,    1780, 

1847 
Famine,  1780,  1798 
Flagellate,  877,  1780,  1796 
References,  1S00 
Table  of  Animal  Carriers,  878 
Hill,  1780,  r788.  1795 

References,  1S00 
Infantile,  1 20, 1 22, 1 23, 908, 1 847, 1 960 

Bacillary,  1S4S,  1851 
Low-Country,  Morning,  1780,  1796 
Lymph,  1608.  1610 
in  Paragonimiasis,  1587 
Puerperal,  of  Bengal,  1955 
Serous,  1820 
Trematodal,  1752 
Trench, 1820 
Diarrhoeal  attacks  and  Pellagra.  173 
Diarrhoeas,  25 

.Etiology,  18.  I2.| 

Diseases  in  which  present,  1520 


INDEX 


2310 


Diatomence,  923 
Diatomineura,  822 

hasta,  823 

linealithorax,  823 

penetrabilis,  823 

swauz's,  82  ^ 
Dibothriocephalidee,  602,  603,   604 
DibothriocephalincE,  601,  604 
Dibothviocrplialus,  601,  602,  604 

braani,  601 

cordatus,  601,  604,  605,  175'' 
Reference,  618 

cristatus,   604 

grandis,  601 

talus,  205.  553,  598,  601,  603,  604, 

895.  1757 
References,  618 
parvus,  601,  604,   605,  1757 
Dibothrium,  604 
latus,  604 
man sinn.   606 
Dibothrius,  (104 
Dicephalus    1958 
Dicercomonas,   345 
Dichapetalacea,   191 
Dichapetalum  toxicarium,  188 
Dichelacera,  820 
Dicrania,  82  3 
Dicvoceeliidce,  564,  580 
Dicrocelium,  580 
dendriticuui,   580 
lanceatum,  580,  1907,  2007 
References,   595 
Didymophyutce,  471 
Didymorphleps,  802 
Dietnenia,   246 

psammopkis,   251 
Dieniamaba,  298,  299,  323 
fragilis,  324 
References,   329 
Dienycleitus  viridescens,  401 
Dietetics,  8,  96  s^. 
Ancient,  94-5 
Bedouin,  96 
Bengalese,  95-6 
Bushman    96 
History,  24 
Indian    98 
Diets,  Calculation  of,  106-7 
Food  Factors  in 

Estimation  of,  as  to 
Quality,  101 
Quantity,  97 
Low  Protein,   107.   119 
Seasonable,   106 
Standard,  98  s^. 
Difamus,  349 

tunensis,   350 
Diffenbachia  sequina,  172-3 
Diffuse    Chronic    Periostitis    in     late 
Frambcesia,  1555 


Diffuse  Leucoderma,  131 
Digenea,   560 
Digestibility  of  Foods 
Coefficients,  101-2 
Definition,  101-2 
Digestion,     Effect    on,      of     Climatic 

Conditions,  76 
Digestive  System  Localization,  Sub- 
tertian    Malaria     with, 
Types  of,  1175,  1177 
Digitalin,  179 
Digitalis,  167,  169 
Dimorphus,  466 
Dinoflagellata,   332 
Dioctopkyme,  623,  674,  675 

renale,   623,   675 
DioctophymincB,   674 
Dioscorea,   173 
hirsuta,   184 
Dioscoreac&a,  184 
Diospyrus  ebemim,  2160 

montana,   190 
Diphtheria,   1740,  1996 

Bacillus  of,    965,    1040,    see  a/so 

under  Bacillus 
Climatology,  120,  122 
Diagnosis,  1521 

Bacteriological,  1520 
Differential,  1748 
Form    of    Gangosa    resembling, 

1879 
Mixed  Mycotic  Infections,  1748 
Rash,  151  7 
Fowl,  Filterable  Virus  of,  541 
Diphtheritic  Conjunctivitis,   1996 
Diphtheroid  Bacillus,  2247 

Ulcers,  2191-2 
Diphyllidea,  600 
Diphyllobothrium,  604 
Diplacanthus,  609 

nanus,  610 
Diplobacillary  Bodies,  2193 
Diplobacillus,  1746 
Diplococcus(i),  925,   927,  1600,   2019, 
2192,  2193 
crassus,  1477,  1478,  1482,  1497 
flavus,  L,  II.,  &  III.,  1478 
gonorrhoea,   1951 

intracellulars,    meningitides,    1474. 
1475,   1476,   1477.   1407 
mucosus,   1478 
pneumonia,  927,  1477,  1951 
in  Trichomycosis,  2102 
DiplodiscincB,  561 
Diplogonoporoses,   1757 
Diplogonoporus,  601,  602,  604,  605 
References,   618 
Species 

balcenopterus,  605 
brauni,  605,  17.57 
grandis,  605,  1  757 


2320 


INDEX 


Diplomastix  dahlii,  338 
Diplopoda,  689,  1639,  1641,  1841 

References,   741 
Diplopodiasis,   1619,   1641,  1778 
Diplospora,  473 
Diplo-streptococci,  1941 
Diplozoa,  333,  464 
Diprosopus,   1958 
Dips,  Tick-Eradication    701,  1348 

Formula,  1349 
Dipsadomorp  nines,  245 
Diptera,  218,   747,   748,   771,  900 

Collection  of,  772 

Larvae  of,   771,   895,   1631  passim, 
2207-8 
References,  2221 

References,  813,  855 

Venomous  Species,  223-6 
References,  229 

Wings,   771-2 
Dipygus,  1958 
Dipylidiasis,   1757 
DipylidiincB,  601,  607 
Dipylidium,  601,  602,  608 

caninum,  601,  608,  85 7,  S95,  1757 
References,  619 

cucumerinum,  608 
Dirofilaria,  623,  632,  644 

immitis,  633,  645,  1598 

magalhcesi,  623,  644, 
References,  681 
Discomyces,  1041,  1042 

asteroides,  1053 

bovis,  1051,  1057 

brasiliensis,  1053,  2131 

buccalis,  1061 

carougeaui,  1066 

decussatus,  1059 

foersteri,  1067 

freeri,  1058 

garteni,  1050,  1060,  2136 

holmesi,  1057 

lingualis,  1061 

madurcB,   1051 

miniitissimus ,  1053,  1062 

somaliensis,  1051,  2138 

thibiergi,   1064 
Discomycetacees,  1041,  1042 
Discophora,  683 

Discovery,  the,  of  the  Tropics,  15-16 
Disease,  Endemicity  of ,  114 

Evolution  in  relation  to,  112,  114, 

394 
Symptoms  of,  113 
Diseases  affecting  Tropical  Life  Assur- 
ance, 131 
Causation    of    (see    also    ^Etiology 
under     each     Disease), 
17  sqq.,  88,  113 
Chemical,  115,  161,  1533 
Parasitic,  115-17,872,  1533,  1535 


Diseases,      affecting     Tropical     Lift 
Assurance,  continued  • 
Causation  of,  continued 

Physical,  115,  137,  1449,  1533 
References,  141,  146,  157.  1460 
Change  of  Character  of,  114 
of    Deficiency,     109,     1533,     1671, 
1675,  1090,   1691,   1709 
Mentioned  in  Early  Medicine 
Egyptian,  9.  17  ' 
Indian,  7-8 
Jewish,  9-10,  17 
Miscellaneous,  2247 
References,  2263 
New,  1 13-14,  394 
Nomenclature  of,  287 
Spread   of,    by    Geographical   Dis- 
covery. 114 
Tropical,  112,  120-5,  1127  sqq. 
of  Unknown  Causation,  920,  1533 
Disinsection,  9 
Dispnee  Tropicale,  1S73 
Disporea,  529 
Disporocy slides,  473 
Disseminated  Sclerotic  type  of  Sub'.er- 
tian  Malaria,  11 75,  1176 
Dissenteria  Amebica,  1825 

Bacterica,   1841 
Distemper,    Canine,    Disease    resem- 
bling, 493 
Distera,  249,  251 
cyanocincta,  268 
semperi,  249 
Distichodenta ,  686 
Distoma  conns,  576 
crotali,  738 
durissi,  738 
echinatum,  582 
hepatis 

endemicum  sive  perniciosiun.  579 
innocuum,  578,  579 
sinense,  578 
spathulatum,   578 
Unnamed,  in  Delhi  Boil,  2166 
Distomata,  564 
Distomatidcs,  464 
Distomatosis,  Pulmonary,   15S4 
Distomea,  557,  560 
Distome  Cercaria,  558,  559 
Distomum  acuttwt,  572 
buski,   568 
cerebrate,  573 
crassum,   568 
gastrophilus,  572 
hepaticam,   565.   573 
heterophyes,  570 
lanceolatum,  576,  580 
oculi  humani,  565,  567 
ophthalmicum,  567 
pulmonale.  573,  574.  1584 
pulmonis,  573 


INDEX 


2321 


Distonntm,  continued 

rathouisi,  568 

ringeri,  57$,  574,  1584 

sibiricum,   576 

tcnuicolle,  576 
Divers,  and  others,  142-3 

Medical  Examination  of,  143 
Divisions  of  Mankind,  44  sqq. 
Djudsam,  1644 
Dochmiasis,  1761 
Dochmiosis,  1761 
Dochniius,   665 

ancylostomum,  666 

duodenalis,  666,  673 
Doehle's  Bodies,  1328 
Doenca  de  Sonno,  1260 
Dog- Bites,  12,  151 
Dog-Fleas,  375,  376,  1299,  1303 
Dog-Louse,  608 
Dog- Mites,  733 

Dog-Ticks,  693,  713,  719,  722 
Dogs,    Parasites    of,    411,    414,    483, 

492,  493,  515 
Doldrums,  80 
Dolichandrone  falcata,  188 
DolichopodidcB,  824 
Dolichos  jilosa,  195,  196 
Dolichus  catj ana,  195 
Doliocy slides,  471 
Doliophis,  246,  251 
Donedia  sitffvutescens,  124 
Donovan's  Bodies,  2193 
Dorcalccmus,  823 
Dosage  of  Drugs  for  Young  Children, 

i960 
Dothidiales,  985 
Dothienenterite,  1363,  1364 
Double  Autositic  Monsters,  1958 

Continued  Fever,  1463 
References,   1473 

Quartan  Fever,  n 

Parasitic  Monsters,   1959 
Douenca,  1283 
Dourine,  19,  391,  411-12 
Dous-el-Kourmati,  2165 
Dracontiasis     (Guinea-worm),     9  [O, 
1  I,   12,   17,   25,  623,  632, 
651,652,739,1298,  1524. 

1967,  1968,  1990,  2254 
Dracunculidee,  623,  624,  651 
Dracunculosis,  1968 
Dracunculus,  11,  12,  623,  632,  651 
Extraction,  9,  10,  17,  651 
References,  682 
Species 
ha,  645 
medinensis,  9,  623,  632,  651,  739, 

896,  1968,  1970 
ocitli,  645 
persariim,  651 
veterum,  651 


Dragonneau,  651 

Drainage  and    Malaria-control,  1138 

Dravidians,  46,  47,  49 

Dietary  of,  96 
Dvepanidium,  478,  488 

ranarum,  488 
Drepanidoicenia,  609,  610  -n 
lanceolata,  601,  611 
References,  619 
Drilus,  2208 
Dromedaries,  Mbori  of,  410,  417,  816 

Trypanosomes  of,  416 
Dropsy,  Acute  Anaemic,  1690 
in  Beri-beri,  1687 
Cardiac,  1904 

Differential  Diagnosis,  1688 
Epidemic,    109,    1671,    1672,    1675, 
1688,  1690 
/Etiology,  1533,  1691 
Climatology,  1691 
Definition,  1690 
Diagnosis,  1692 

Differential,  1688,  1692 
History,  1 690-1 
Insect  Spreaders,  1691 
Morbid  Anatomy,   1691 
Prognosis,  1692 
Prophylaxis,  1692 
References,  1694 
Sequelae,  1692 
Symptomatology,  1691 
Synonym,  1690 
Treatment,   1692 
General,  122,  1895,  1904 
Sleeping,  1260 
Drosophila    ampelophila,     903,     c.04, 

137° 
confusa,  367 
fencstvarum,  900 
funebris,  1630 
nielanogastra,  900,  1630 
DrosophilidcB,  901,  902,  903,  1630 
Drugs,    Diseases    and    Rashes,    etc., 
dueto,  1513,  1516,  1517, 
1522,    see   also   Quinine 
Hemoglobinuria,  1214 
I  leisure <>f,  lor  Young  Children,  [960 
Popular,  not  to  be  neglected,  4 
Producing  Haemoglobinuria,  1213 
Dryophis  prasinus,  245 
Duba,  1801 

Dubini's  Filariasis,  1761,  1967,  1971, 
1974 
References,  19S0 
I  >ii   Bois's  Trichosporosis,  2105 
Duboisia  hopwoodi,  176-7 
Duckweed-growing,  Larvicidal,   1  209 
Ductless  Glands,  Diseases  of,  1919 
References,   1925 

Subtertian  Malaria  attacking,  11 75, 
1180 

146 


2322 


INDEX 


Dumas  (Framboesial  nodules),   1550 

Dumb  Rabies.  151 

Dumbness     and     Deafness     in     the 

Tropics,  2013 
Dum-Dum  Fever,  20,  1289 
Dung  in  relation  to  Puerperal  Fever, 

I952 
Duplicidentata,  914 
Dura,  99,  105 
Dutch  East  Indies,  Fish-Poisons,  188 

Vegetal  Poisons,  164,  167 
Duttonella,  401,  408,  412-13 

Human  Trypanosomes  included  in, 

'419 
Species 

capvce-,  409,  412 

lanfranchii,  431 

pecorum,  409,  413 

simicB,  409,  413 

Trypanosomes  probably  included 

under,  413 
uniformis,  409,  413 
vivax,  402,  409,  412,  430,   1280, 
1281 
var.  macfiensis,  419 
Duttons  Disease  (African  Tick  Fever), 
19,691,  694,700,706,  1261, 1318 
Dwarfism,  123 
Dyaks,  55 

Arrow-Poison  of,  184 
Dysenteric  Colitis,  538,   1836 

Diarrhoea,   569,    1824,    1S48,    1851, 
1752 
Infantile,  1848,  1851 
Treatment,  1857-8 
Enteritis,  10G9 
Pseudo-cholera,  1820-1 
Dysenteric-like  attacks  and  Pellagra, 

I731 
Dysenterie  a  Amibes,  1825 

Amibicnnc,  1825 

Bacillaire,  [841 
Dysenteries,  25,   1501,   1824 
References,  1862-3 

Arthropodic,  1825,  1841 
References.  1863 

Bacterial,  1825,  1841 

Caused  by  Animal  Parasites,  1825 

Choleraic,  1848.  1858 

Chronic,  1848,  1850 

Entamcebic,  1825 

Entoplasmic,  1825,  1840 

Laveranic,  1825,  1836 

Leishmanic,  1825,  1837 
References,  1863 

Loeschial,  287,  1825 

Xemathelminthic,   1825,  1840 

Platyhelminthic,  1825,  1840 

Protozoal,  1825 

Schistosomic,  1867-8 

Spirochaetal,  451,  1825,  1838 


Dysenteroides,  934,  935,  938 
metadysentericus,  935,  938, 
var.  A,  B,  C,  D,  938 
Dysentery,    7,    12,    25,    1069,    1593, 
1663,  1687,  1858-9 
Climatology,  120  sqq. 
Complications,  200b 
Diagnosis,  1852  sqq. 
Insect  Vectors,  23,  747 
Parasites  found  in,  538,  547 
Symptomatology,  189 
Synonyms,  1824 
Term,  and  use  of,  1824 
Acarine,  729 
Amoebic  [see  also  Amcebiasis),  877, 

1825 
Pacillary,  1782,  1825,  1841,  1843 
.Etiology,  22,  1843-5 
Carriers,  1844,  1845,  1859 
Climatology,  1842-3 
Complications,  1 85 1-2 
Definition,  1841 
Diagnosis,  1852-4 

Differential,  1852-3 
History,  1841 
Infection,  1844-5 
Morbid  Anatomy,  1846-8 
Pathology,  1845-6 
Prognosis,  1S54 
Prophylaxis,  1859 
References,  1863 
Sequelae,  1852 
Seven  types  of,  1848 
Symptomatology,  1848  sqq. 
Treatment  of 
Carriers,  1859 
Mild  Cases,  1852-3 
Severe  Cases,  1855-7 
Serological,  ib. 
Vaccination      and      Vaccines, 
1 860- 1 
Gangrenous,  1848.  1849 
Balantidic,  1825,  1837,  1853 
Chronic,     325,     356,     1848,     1858, 

17S8,  1903 
Cuiar,  1825,  1837 

References,  1863 
Entoplasmic,  1840 
Flagellate 

Animal  Carriers,  877 
Table,  87S 
Gangrenous,    1830,    1831,    1835, 

1848,  1849 
infantile,  iq6o 
Spirocructic',  1825,  1838 
Dysidroses,  2015,  2017,  2222,  2224 

References,  2245-6 
Dysidrosis,  2226 
Exfoliativa,  2222,  2227 
Reference,  2246 
Dysodius  Inn  a  (us,  770 


INDEX 


2323 


Dyspareunia,  129 
Dyspepsia,  1749 

Acid,  Vomit  of,  1025 
Dysphagie  Tropicaie,  1750 
Dystrophies,  2015,  2017,  2222,2227 

References,  2245-6 
Dyticus  marginalis,  1641 

Ear,  Aspergillosis  of,  1028,  1029,  1031 

Lipomata  of,  2010,  2247,  2252 

Mycosis  of,  974 

Myiases  of,  1622,  1626,  201 1 
Ear- Affections  due  to 

Quinine,  1181,  2013 

Subtertian  Malaria,  1181 
Ear-Complications        of        Tropical 

Diseases,  2013 
Ear-Diseases,  1993,  2010,  2013 

References,  2014 
Ear- Lobule,  Affections  of,  2010-n 

Nodules,  Symmetrical,  2247,  2252 
References,  2263 
Ear-Tick  of  Cattle  and  Man,  708 
Earth-Eating,  1749,  1761 

Reference,  1751 
East  African  Relapsing  Fever,  13 18, 

1322     k. 
East  Coast  Fever  of  Cattle,  498     ' 
Eastern    Epidemics,    imported    into 
Europe,    1 5th   century, 

14-15 
Ebers  papyrus,  1761 
Eberthece,  933,  934 

Ebcrthus,  933,  934,  935,  936, 1362,  1405 
kandiensis,  936 
priztnitzi,  936 
talavensis,  936 
typhosus,  933,  935,  936,  940 
Ebony,  Dermatitis-causing,  2F6o 
Echidin,  254 
Echidna,  242 
Echidnine,  243 
Echidnophaga,  861,  866 
gallinacea,  866,  867 
lispus,  866 
murina,  866 
myrinecobis,  866 
rhynchopsylla,  867 
Echinococcal  Invasion  of  Eye,  2007 
Echinococcifer  echinococcus,  616 
Echinococcosis,  1967 
Echinococcus,  205,  601,  603,  616,  890 
References,  620 
Species 
cysticus 
fertilis,  617 
sterilis,  617 
granulosus,  601,  616,  1967 
hydatidosus 

var.  exogenus,  617 
var.  endogenus,  617 


Echinococcus,  continued 

Species,  continued 

uiultilocularis,  601,  616,  617 
osteoklaster,  617 
Echinodevmata,  poisonous,  205 

References,  228 
Echinophthividce,   753 
Echinophlhirius,  759 
EchinophthiriudcB,   759 
Echinorhynchidce,  680,  737 
Echinorhynchus,  680,  737,  1642 

crotali,  738 

gigas,  287 

hominis,  680 

moniliformis,  680 
Echinostoma,  581,  582 

ilocanum,  582,  1752 
References,  594 

malayanum,  581,  583,  1752 

revolulum,   582 
Echinostomes,  559 
Echinostomidce ,  504,   582 
Echinostomince,  581 
Echis,  242,  250 

"Venom   of,    263,    268,    269,    272, 

273.  274 
carinata,   250,   251,   268,   269,   272, 

273 
Echitoxin,  254 
Echokinesia,  1983 
Echolah'a,  1983,  1986 
Echolics,  Supposed,  170 
Echomatism,  1983 
Echuja  Arrow-poison,  183 
Echujin,  183 
Ecthyma,  2022,  2035,  2265 

Gangraenosum,  2035 

Tropical,  929,  2034 
Ecto-endothrix,  2053,  2054,  2057 
Ecto-parasites,  286 
Ectoplasm,  290 

Ectotrichophyton,     988,     9S9,     1002, 
1004,  1006,  2056 

album,  1003,  1004 

denticulatnm ,  1004,  1005,  1006 

discoides,  1003,  1004,  2050 

equinum,  1007 

jarinulentimi,  1004,   1005 

felineum,  1004,  1005,  1006 

granulosum,  1004,  1005,  1006 

lacticolor,  1004,  1005.  1006 

luxurians,  1003,  1004 

megnini,  1007 

nodoformans,   1007 

ochraceuni,  1003,  1004 

persicolor,  1004,  1005 

radio/atum,  1004,  1005,  1006 

verrucosum,  1003 

vinosum,  1807 
J^ctothrix,  2054 
Ectromelus,  1958 


2324 


INDEX 


Ectropion,  1997,  2000,  2006 
Ecuador,  Circhona-bark  first  used  in,  4 

Diseases  of,  124 

Helminths  of,  124 
Eczema,  123,  1701,  2029,  2030,  2046, 
2225,  2227,  2204.  2270 

Chronic,  of  Lunatics,  1729 

Marginatum,  2042,  2043 

Papular,  2252 

Primary,  Scrotal,  2047 

Verrucosum,  2270 
Edentata,  406 
Edyuo,  1698 
Eels,  400 
Efa,  250 

Egg-eating  Snakes,  245,  246 
Eggshell  Nails,  2283 
Egypt,  Life  Assurance  in,  132-3 
Egyptian  Chlorosis,  1761 

Dietaries,  98-9,  100-3,  105 

Medicine 

Alexandrian,  11 
Early,  8-9,  15,  17,  1619 

Races,  47 

Relapsing  Fever,  447 
Eichhornchen-Bisskrankheit,  1361 
Eidamella,  986.  987 

spinosa,  987 
Eimeria,  473,  474,  475 

oxyspora,   475,  476 

stiedce,  474,  475,  470,  477,  1909 

wenyoni,  475 
Eimeridea,  471,  477 
Eimeriella,  473 

nova,  473 
Eimerioinea,  469 
Eirmocystis,  471 
Ekiri,   1 85 1 
Elachisiodontince,  246 
Elesdendron  glaucum,  190 
Elapechis,  246 

guentheri,  251 
Elapiwmaiycetcece ,  986 
Elapinca,  246-51 

Australian,  Venom  of,  267 
Elapognathus,  246 

minor,  251 
Elaps,  246,  251 

corallinus,   248 

fulvius,  267 
Elasmobranchii,  232,  240 
Elastorrhexis,  2273 
Electric   Fans,    Traumatisms    caused 

by,  156 

Electrical  Conditions,  82 
Electricity,  Atmospheric,   Effects  of, 
146 

Reference,   146 
Elementary  Bodies,  539 
Elephant  Foot,  211 1,  2116 

Leg,  1610 


Elephant-Poisoning  (India),  1S9 
Elephantiasis,  1595,  1599,  1600,  1603, 
1610,  1961,  1966,  2116, 
2195,  2220 
.Etiology,  552,  639 
Climatology,  123,  124,  1597-S 
Definition,  1610 
Differential  Diagnosis,  1090 
History,  1595 
and  Life  Assurance,  132 
Prodromal  Filarial  Erysipelatoid 

Attacks,  2260 
Synonyms,  1610 
of  Various  Regions 
Arm,  161 1,  1617 
Breast,  1611,  1617 
Foot,   2111 
Generative  Organs,  1939    1943 

Leg,  1595.  1597-  1611 

Scalp,  1617 

Scrotum,  1597,  1610,  161 1,  1615 

Treatment,  161 6-1 7 
Vulva,  1611,  1617 
Arabum,  1610 
Circumscribed,  161 7 
Graecorum  (see  also  Leprosy),  11 12, 

1644 
Indica,  1610 
Italica,  1700 

Tuberosa  et  Scrotalis,  1610 
Elephantoid    Fever,    639,     1604 

Fibrosis,  2262 
Elephants,  Traumatisms  caused   by, 

Llisha'sTreatmentof  Heat  Stroke,  13a 
Elleipsisoina,  360,  488,  491..   502 

thomsoni,  502 
Ellipopteva,  752 
El  Takasha,  810 
Embadomonaditue,  345 
Embadomonas,  333,  345,  343 

References,  357 

Species 
agilis,  346 
alexeieffl,  346 
intestinalis,  347 
Emdya  vittati,  487 
Emericella,  1024 
Emerods,   10 
Emetine,  28-9,  183^-6 
Emmenagogues,  Reputed,  170 
Emotion,  1981 

Emotional  Excitement,  1991 
Emphysema,  1S75 
Empidts,  774.  824,  901 
Empusa  musca,  908 
Empyema,  1949,  1961 
Enantiothamnace<B,  1070,  1096 
Enantiothamnosis,  2041  2106, 
Enantiothantnus,  1096,  2041 

brattlti,  1096,  2041,  2106 


INDEX 


2325 


hvcapsidatete,  933,  934 
Encapsulates,  933,  934 
acidilactici,  934 
lactisaerogenes,  934 
pneumonia,  933,  934 
Encephalitis  lethargica,   1268 
Enchylema,  290 
Encrum  Van  dee,  1801 
Encystment  of  Protozoa,  291 
Endamceba,  301 
Endarteritis      type      of      Subtertian 

Malaria,  n 79 
Endemic  Boil  Disease,  2165 
Cretinism,  1920,  1922,  1959 
Degeneration  of  the  Bones  of  the 

Boot,  21 10 
Diarrhoea,  1780 

Enlargement  of    Os    Calcis,    1524, 
1967,  1979 
References,  1980 
Bever,  1362 
Funiculitis,  1522,  1938,  1939 

References,    1955 
Glandular  Fever,  1465 
Goitre,  1920,  1959 

References,  1925 
Hsematuria,  1926 
Haemoptysis,  15S4,  1885,  1889 
Hyperplasias,  1920 
Infections  and  Invaliding,  13c 
Malaria,   Region   of,    Investigation 

of,  1 1 4 1 
Neuritis 

Multiplex,  1671 
Peripheral,  1981,  1989 
Paralytic  Vertigo,  1981,  1982 
Peripheral  Neuritis,  1891,  1989 
Polyneuritis,  1671 
Tetany,   1922 
Thyromegaly,  1920 
Eudemicity  of  Disease.  114 
Endemische  Beulenkrankheit,  2165 
Endemischer  Magenkatarrh,  1254 
Endocarditis,  1904 
Infective,  1521,  1528 
Ulcerative,  1395,  1307 
Endoconidia,  969 
Endocyma,  1959 

Endodermophyton,   989,    1016,    2059, 
2061,  2065 
Dermatomycoses  due  to,  2040 
References,  1033 
Spei  ies 

castellanii,  1017,  1022,2040,  2072 

concenlricum,  1023 

indicum,  1017,  1020,  2040,  2065, 

2069 
mansoni,   1023 

Iropicale,  1017,  1018,  1021,  2065, 
2069 
Endodermophytosis,  ao6o 


Endolimax,  322 

Endomyces,  983,  1070,  1742,  1743 

albicans,  984,  1085 

blanckardi,   1091 

bronchialis,  1087 

burgessi,  1090 

entericus,  1088 

jcecalis,  1089 

guillermondi,  1088 

insolitus,   1089 

iniestinalis,  1089 

krusei,  1088 

nitidus,  1088 

niveus,  1088 

paratropicalis,  1087 

pinoyi,  1088 

pseudo-tropicalis,  1087 

rhoi,  1089 

tropicalis,  1086 

vuiUemini,  984,  1086.  1743 

zeylanica,  1088 
Endomycetacece,  978,  983 
Bndoparasites,  286 
Endoplasm,  290 
Endospores,  969 
Endotheliomata,  Cerebral,  1981 
Endothrix,  999-1001,  2054,  2057 
Endotrypanum,    380,    381,    401,    402, 
403,  405 

schaudinni,  405 
Endoxome,  290 
Energy,   Warning  on,  of  Candidates 

for  the  Tropics,  128 
English  House-Blies,  900 
Enhydris,  249,  251 

CUYtllS,    25I 

valakadien,  249,  251 

Venom  of,  253,  264,  268,  271,272 
En  Nabt,  21 18 
Enno,  2260 
Enoplidee,  623 
Entalacao,  1750 

Reference,   1951 
Entamoeba     {see    also    Amoeba,    and 
Loeschia),  298,  300,  301 

africana,  310 

blatlcB,  300,  301,  306,  877 

buccalis,  317 

biitschlii,  320 

coli,  303 

histolytica,  18,  320,  1932 

minuta,  311,  319,  320 

minutissima,  320 

mortinataliteni,  320 

)>nti'is,  303 

nana,  320,  323 

nipponica,  303,  319 

ovis,  320 

phagocytoides,   319 

tenuis,  320 

tetragena,  310,  311,  312,  315,  1932 


2326 


INDEX 


Entamoeba,  confirmed 

iropicalis,  303 

undulans,  319 

williamsi,  303 
Entamoebiasis,  287,  1825 
Entamcebic  Dysentery,  1825 
Enteric  (Typhoid)  Fever,  107s,  1184, 
1187,  1249,  1326,  1362, 

H37.  1577 
.Etiology,  22,  1362,  1363,  1366 
Atypical,  1378 

Diagnosis,  1388 
BloodConditionsin,  1381,1384,1385 
Carriers,  Human,   1365,  1367  sqq., 

1400,  1403 
Causal  Organisms,  22,  1362  passim 
Climatology,    120,    122,    123,    124, 

132,  1365 
Complications   in,    and    by,    1377, 

1381,  1388,  1717,  1727-8 

1733,  1741 
Course,  1380  sqq. 
Definition,  1362,  1363,  1395 
Diagnosis,  1388,  1517,  1528 
Bacteriological,  1389 
Differential,  1250,  1257,   1296-7, 
1303,  1312,  1313,  1347, 
1395,  1429,  1485,  1731, 
1914,  2203 
in  Inoculated  Persons,  1393 
in  Mixed  Infections,  1388,  1394, 
1397-8 
Diagnostic  Methods,  1389  sqq. 
Diet  during,  1400 
Epidemicity,  1371 
Haemorrhage  in,    1384,   1386,    1399 

Treatment,  1401 
Herpes  Facialis  Yebrilisrarein,  2269 
History,  1363-6 
Hygiene  during,  1399 
Immunity,  1372,  1375 
Incidence 
Age,  1373 
Class,  1373 
Season,  13 71 
Sex,  1373 
Incubation,  1374,  1379 
Infection,  1369 

Insects  spreading  (flies),  22,  24,  899, 
904.905,908,1369,1370 
Jaundice  rare  in,  1519 
Mixed  Infections,  1388,1394,  1397-8 
Morbid  Anatomy,  1375  sqq. 
Nomenclature,  1363,  1364 
Nursing,  importance  of,  1399-1400 
Onset,   1379 

Atypical,  1379-80 
Parasites  present  in,  549,  17-11 
Pathology,  1374-5 
Perforation  in,    1385,   1386,   1399, 
1401 


Enteric,  continued 

Predisposing  Causes,  1372-4 
Prognosis,  1398 
Prophylaxis,  29,  114 

Carrier-Control  ami  Treatment, 

1400,  1403 
Hygiene,  1403 
Immunization,  114,  128 
Vaccination,  128,  1403-4,  1407 
Rash  in,    1381,    1382,    1385,    1517, 

1528 
References,   141 3-14 
Relapse  after,  1388 
Sequelae,    1377,    1388,    1402,    1403, 

1907 
Spread  by 

Defective        Sanitation,        1371. 

1373-4 
Drinking- Water,  1364 
Food  -  Pollution,      1369,      1370, 

1371.  1373 
Human  Carriers,  1365,  1367  sqq., 

1400,   1403 
Insects,    22,    24,    896,    899,    904, 

905,  908,  1369,  1370 
Meteorological  Conditions,  1374 
Shell  and  other  Fish,  1371 
Symptomatology,  1378  sqq. 

Special  Symptoms,  1401 
Synonyms,  1362-3 
Treatment  during 
Attack,  1399 

Simple  Case,  1 399-1401 
Special    Symptoms,     1309, 
1401-2 
Convalescence,  1399,  1402-3 
Acute  Carrier,  1403 
Sequelae,  1403 
Simple  Case,  1402-3 
Medical,  1 400-1 
Vaccines  for,  23,  1365,  1401,  1403 
sqq. 
References,  1414-15 
Varieties,   1387-8 
Enteric  Fevers,  1362 
Enteric  Jaundice,  1507-8,  1509-10 
Enterica,  1362 
Entente  Septicemique,  1363 
Enteritis,  1060,  1076,  1095 
Causal  organisms,  1405 
Amoebic,   1825 
Chronic,   1663 
I  'ysenteric,   1069 
Enterocolitis,  548,  659 
Enteroide  Fevers,  1362 
Enteroidea  Group  of  Tropical  Fevers, 
1362,  1461,   146S,  1474, 
1 718,   see  also  Enteric, 
and  Paratyphoid 
.Etiology,    1128,  1362,   1366 
Classification,  1362 


INDEX 


2327 


Enteroidea,  continued 

Diagnosis,  1388,  1523,  1524,  1526, 
1527,  1528,  1530 
Differential,  1337,  1395,  1505 

Glandular  Enlargement  in,  1523 

References,   141 3-1 5 

Symptoms,  1520 
Enteroides,  935,  941,  1406,  1412 

entericus,  935,  941 

khartoumensis,  941 

paraentericus,  941 

vekanda,  941 
Entero-Dysentery,  1848,  1850 
Enteromonas,  345,  346 

hominis,  346,  1796 

References,   357 
Entomology,  History,  23 

Insect     Carriers     in     relation     to 
Epidemicity,  117 
Entoplasma,  1840 

castellanii,  538 
Entoplasmic  Dysentery,   1825,  1840 
Entozoa,  286,  553 

References,  593 
Entropion,  2000 

Environment,  Adaptation  to,  113 
Enyaliopsis  durandi,  S71 

peter  si,  871 
Eosinophilia,  1900 
Epatite  Suppurativa,  1910 
Epectinata,  690 
Epeira  diadema,  212,  213,  215 
EpeiridcB,  212 
Ephidrosis  Sudatoria,  2222 
Epicauta,  226 

flavicornis,  226 

sapphirina,  226,  2205 

tomentosa,  226,  2205 
Epidemic  Cerebro-spinal  Meningitis, 

1474 
Diarrhoea,  Infantile,  1847 
Dropsy,      1690,      see     also     under 

Dropsy 
Gangrenous  Rectitis,  25,  125,  1871 

References,   1872 
Jaundice,   1505 

Spirocha;tal,  918 
Remittent  Fever,  n  39.  1308 
Summer  Diarrhoea,  899,  1788,  1847 
Varioloid  Varicella,  1491 
Epidemicity  of  Disease,  117 
Epidemics,  Spread  of,  14,  15 
Epidemiology,  Modern,  start  of,  15 
Epidemische  Genickstarre,  1474 
Epidermolysis  bullosa,  2269 
Epidermophyton,     989.     1014,     2043, 
2059,  2077 
Dermatomycoses  due  to,  2040 
References,   1033 
Species 

castellanii,  2072 


Epidermophyton,  continued 
Species,  continued 

cruris,   1014,   1015,   1023,   2025, 
2036,  2037,  2040,  2042, 
2045,  2080 
gallince,   1014 
indicum,  2072 
inguinalis,  1015 
pemeti,  1015,  1016,  2040,  2043 
rubrum,   1015,   1016,  2040,  2043, 

2048,  2049 
siinii,  1015,  1023 
Epididymitis,  1587,  1939 
Epilepsy,  124 

associated    with   Paragonimiasis, 

1587 
Differential  Diagnosis  from  Heat 
Stroke,  1456 
Jacksonian,  1592,  1.593 
Epileptic  Ensanity,  1981 
Epiinys,  915 

alexandrinus,  916 
norvegicus,  910,  915,  916,  1420  sqq. 
Fleas  of,  867,  869-870 
and  Rat-bite  Fever,  1356 
rattus,  910,  912,  915,  1420  sqq. 

Fleas  of,  867,  869,  870 
rufescens,  916,  1420 
Epiphora,  1997,  2006,  2008 
Epiphytic  Skin  Diseases,  2060 

Leucoderma  in,  2228 
Epithelial  Cells  in  relation  to  Melan- 
osis, 87 
Moles,  2274 
Tumours,  2274 
Benign,  2274 
Malignant,  2277 
Xerosis  of  the  Eye,  2002 
Epithelioma,  2085,  2195,  2196 
Contagiosum,  541 
Facial  (rare),  2273 
of  Penis,  1939 
Epitheliosis  desquamativa,  539,  I996, 
2001 
Samoa n,  541 
Epizoa,  286 
EproboscidcB,  854 
Epsom  Salts,  170 
Epuvi,  222 

Equatorial  Belt,  63-4 
Equine  Diseases 

Lymphangitis,  1072 
Nagana,  411 
Piroplasmosis,  500 
Group  of  Streptococci,  928 
Parasites 
Spirochete,  454 

Trypanosomes,  413,  415,  416,  417 
Eremascus,  983 
EremospermetB,  1071 
Erephopsis,  822,  823 


2328 


INDEX 


Erethizontidce,  914 

Ergot,   198 

Ergotism,  195,  198,  1688,  171S 

Erigeron  canadense,  2152 

Eriophyidcs,  692 

Eristalis  arbustorum,  1630 

dimidiatus,   1630 

tenax,  1630 
Errors  of  Refraction,  1995 
Eruptions,  Bullous,  2264,  2269 
Diagnosis,  1513,  1518 

Cutaneous,  Diagnosis  of,  1513 

Diagnosis  by,  1529 

Erythematous,  151 3 

Faviform  1030 

Occasionally  associated  with  Sub- 
tertian  Malaria,  11 81 

Purpuric  in 

Kala-Azar,  2267 
Malaria,  2267 

Pustular,   1513,  1518,  1529 

Urticarial,  151 3,  1516 

Vesicular,  Diagnosis  of,  1513,  1517 
Erysipelas,  25,  929,  1514,  1518,  1701 

Non-Contagious,  2158 

Streptococcal,  2266 
Ervsipelatos    group    of    Streptococci, 

928,  929 
Erythema  annulatum,  2266 

Dermal,  84-5 

Gyratum,  2266 

Induratum,  of  Bazin,  2277 

Intertrigo,  2266 

Morbilliforme,  2266 

Multiforme,  2250,  2266 

Nodosum,  2266 

Palmar,  Symmetrical,  2222,  2244 
References,   2246 

Pellagrous,  88 

Pernio,  2264 

Scarlatiniforme,  i486,  22G6 
Diagnosis,  151 3 

Solare,  1730,  2231,  2266 
Erythemata,  the,  2264,  2266 

Malarial,  11 81 
Erythematous  Eruptions 

Diagnosis  of,  151 3 
Generalized,  151 3-14 
Localized,  1514-15 
Erythrasma,  2041,  2046,  20S0 
Erythrism,  123 
Erythrocyte,  the,  1895 

I'.]-  ><h1-Puzz1cs  of,  in 
Fresh  Blood,  1901 
Stained  Blood,  1902 
Erythrolampus  csscnlapii,  245 
Erythromelalgia,  201 

Tropica,  1981,  1990 

Type  of  Subtertian  Malaria,  11 79 
Erythrophlceum  guineense,  183 
judicialc,   179,  183 


Erythrophlcem,  183 
Eryx  conicus,  487 
Escamadura  del  Higado,  1700 
Eschatocephalidcs,  710 
EschaiocephahiS}      710,       711,       720, 
722 

vespertilionis,  722 
Escherichia,  935,  941,  1362,  1406 

cavicida,  942 

coli,  935.  941.  942 
imttabilis,  942,  943 

coliformis,  942 

colitropicalis,  942 

coloidella,  942 

coloides,  962 

griinthali,  942 

metacoli,  942 

iiiefacoloides,   942 

neapolitanus,  942 

oxytocics,  942 

paragriinthali,  942 

pseitdocoli,  942 

pseudocoloidella,  942 

psendocoloides,  942 

pseudocoscoroba,  941,  942 

vesiculosus,  942 
Escorpion,  278 
Eskimo,  the,  56 
Esola,  2241 
Espinlas,  25 

Esplenomegalia,  Tropical,  1303 
Espundia     (Muco-Cutaneous     Leish- 
maniasis),    3S0,     1 741, 
2165,  2175 

References,   2199 

Treatment,  28,   1290,   2196 
Essenes,  the,  10 
Esthiomene  de  la  Vulve,  2192 
Etheogenesis,  295 
Ethiopic    Division   of    Man,    42,    47, 

49,  51-3 
Ethnological  Section,  42 
Euarthropoda,  689 
Euascomycetes,  978,  985 
Eitbacteriales,  924 

Eucalyptus     Oil      and     Chloroiorm 
in  Ankylostomiasis, 

1769-70 
EujlageUata,  332 
Eugenics.  117,  118,  122,  1938 
lutglenoidina,  332 
Eugregarinaria,  471 
Euhcematopinince ,  759 
Euhcematopinus ,  759 

abnormis,  759 
Eidyes,  767 
Eumonodontus ,  672 
Eumycetes,  923,  971,  1025 
Eumyidea,  825,  981 
Euparyphium,  583 

malayanum,  583,  1752 


INDEX 


2329 


Euphorbia,  Poisonous  Species 

arborescens,  184 

candelabrum,  1S3 

cereiformis,  184 

corollata,  2153 

heptagona,  184 

pilulifera,  366-7,  2157 

resinijer,   2157 

tirucalli,  187,  190 

virosa,  184 
Euphorbiacecz,    163,    164,    166,     168, 
I72<  173.  174.  181,  183, 
184,     187,     190,     1698, 

2153.  2154 
EupopidcB,   2214 
Eupopoidea,  692,  724,  728 
Eurachnida,  690 

Eurasians  and  Eugenics,  119-20 
Europeans   in  the   Tropics,   Life    of, 

in  relation   to   Enteric, 

•1373 
Eurhipicephalus,  710,  711 
appendiculatus,  700,  712 
bursa,  700,  712 
evertsi,  700,  714 
pulchellus,  713 

sanguineus,  485,  700,  712,  713 
sinius,  700,  713 
Varieties 

erlangeri,  713 
hilgerti,  713 
shipleyi,  713 
Species  spreading  Piroplasma,  700 
European  Maduromycoses 
Black,  2120 
White,  2120,  2122 
Myiases 

Dermal,  1633,  1639 
Rhinal,  1623,  1626 
Relapsing    Fever,    436,    443,    445, 
918,  1308 
References,   1324 
Eurotiopsis,  1024 
Eurotirtm  flavum,  1028 
malignum,  1028 
nigrum,  1030 
fepens,  1029 
Euscorpius  europceus,  207 

Venom  of,  206 
Eusiemulium,  812 
Euspora,   471 

EustrongylidcE,  623,  624,  67 v 
Eustrongylus  gigas,  675 

visceralis,  '175 
Eutamias,  914 
Eutheria,  913 
Euthyneura,  890,  892 
Eutrichomastix,   351 
Evaporation,  68,  69-70 

Cutaneous  and  Heat-Stroke,  146 
Evil  Eye,  the,  3 


Evolution  in  relation  to  Disease,  112, 

114.  394 
Examination      of      Candidates      for 
Service  in  the  Tropics, 
127  sqq. 
Examiner  of  Candidates  for  Tropical 
Service 
Duties  of,  128  sqq. 
Warnings   which  should   be   given 
by,  127-8 
Exanthemata,   the,    1485   sqq.,   2264, 

2267 
Exanthematischer  Typhus,  1326 
Ex.mthesis  Athrosia,  1244 
Exencephalus,  1958 
Exccecana  agallocha,  190 
Excresis  Spontanea,  2241 
Exhaustion,  1981 
Exophthalmic  Goitre,  1920 
Exospores,  969 
I    Exostosis,  2012 
Expectation     of     Life     in     Tropical 

Natives,  133 
External  Auditory  Meatus 

Animal  Parasites  in,  201 1 
Diseases  of,  2010,   201 1,  2012 
Foreign  Bodies  in,  201 1 
Hypersecretion  in,  2012 
Myiases,  1623,  1631 
i   Extremities,    Symmetrical     Kerato- 
dermia  of,  2259 
Eye-Complications  of  Tropical  Dis- 
eases, 1654,  1660,  2004, 
Eye-Defects,  Congenital,  1995 
Kve-Diseases  and  Affections  (see  also 
under      Names),      122, 
124,    1727,    1993,   I997- 
2001,  2002,  2005 
References,  2014 
Proper,  1994 
Eye(s),  Animal  Parasites  in,  2007 
Foreign  Bodies  in,  1995,   1997 
Gonococcal  Infections  of,  1997 
Haemorrhage  of,  200 
Lesions  of,  in  Leprosy,   1654  sqq., 

1662,  2006 
Non-Development  of,  1959 
Protection  of,  89-90 

Xanothophylline   Glasses   for, 
1996 
Sunlight  as  affecting,  2004 
Xerosis  of 

Conjunctival,  200 
Epithelial,  2002 
Kye-Kly  of  Ceylon,  899,  002,  1996 
Eye-Hospitals,  1993-4 
Eyelids,       Fungal       affections       of, 
2009 
(Edema  of,  1994 
Sporotrichosis  of,  2010 
Eyumbi,  2159 


233° 


INDEX 


Fabismus,  201 

Refei'ences,  202 
Face,  Adenoma  sebaceum  of,  2277 

Epithelioma  of,  2273 

Myiasis  of,  1625 

Myomata  of,  2273 
Facial  Pallor,  1903 
Facies  in  Liver  Abscess,  1912 
Faddidite,   2241 
Faecal  Carcoma,  1739 

Coccidiosis,  475 
Fcecalis   Group   of   Streptococci,    928, 

930 
Faeces,  Human,  Spirosckaudinnia,  in, 

453 
Fagara  flava,  2159 
Fagopyrismus,  202 
Fall  Fever,  1362 
Famine  Diarrhoea,  1780,  1798 
Fanapepea,  349 

intestinalis,  350 
Fannia,  307,  852,  877,  1629 
References,  856 
Species 

canicularis,   852,  900,   904,   905, 

1627,  1628,  1629 
desjardensii,  853,  1629 
incisurata,  854,  1627,  1629 
manicuta,  854,  1629 
saltatrix,  854,  1629 
scalaris,     854,     900,     905,     1627, 
1628 
Fanti  Race,  51 
Fasciola,  565 
angusta,  567 
gigantea,  567 
gigantica,  567 

References,  594 
hepatica,  565,  876,  894,  1746,  1752, 
1907 
References,  594 
humana,  565 
lanceolata,  580 
Fascioletta,  582 
ilocanum,  582 
Fasciolidcs,  564 
Fasciolincs,  564,   565 
Fascioloidea,  561,   564 
Fasciolopsince,    564,   568 
Fasciolopsis,  568 

buski,  568,  894,   1742,  1840,  1907 

References,  594 
fiilleborni,  569,  1752 

Reference,  594 
goddardi,  569,  570 
Kwan's  Fluke,  568,  569 
rathouisi{}),  568,  1752,  1907 
Fat    Content    of    Food,    Estimation 

of,  101 
Fats  in  Diet,  96,  97,  103 
Faunus,  891 


Favic  Tarsus,  ion,  1012 
Faviform  Eruption,  1030 
Favism,  201,  1213 
Favolrichophyton,  1002,  1003 
Favus,  1004,  2057,  2268 

Causal  agent,  1012,  1014,  1063, 
1067,  1078,  2009,  2053, 
2158 

Tarsi,   1011,  1012 

Yellow  Bodies,  1012 
Febbre  Amarilla,  1229 

Climatica,  1254 

Emoglobinurica,  1216 

Estiva,  1254 

Gastrica,   1254 

Gialla,  1229 

Intermittente,  1129 

Maltese,  1437 

Mediterranea,  1437 

Palustre,   n 29 

Remittente  Bilioso,  1229 

Ricurrente,  1308 

dei  Tre  Giorni,  1254 

Tifoide,  1363 
Febbri  d'Aria,  11 29 

Malariche,   1129 

di  Stagione,  1129 
Febre    Amarelle    dos    Acclimatados, 

1229 
Febricula,  1249,  1254,  1372 
Febrile  Gastro-Enteritis,  Hac-morrha- 
gic,  of  Children,  1472 

Splenic  Anaemia,  1299 
Infantile,  20 

Splenomegaly,  1525,  1529,  1531 
Toxoplasmatic,  1531 
Tropical,  1303 

Urticaria,  1516 
Helminthic,  1516 
Febris  Acuta  Stomachica,  1363 

Castrensis  Gravis,  1467 

Columbensis,  1410 

Enclemica  cum  Roseola,  1244 

Flava,  1229 

Gastrica,  1363 

Hetica,  1363 

Intestinalis,  1363 

Lenta,  1363 

Mesenterica  Maligna,  13G3 

Mucosa,   1363 

Non-Pestilens,  1363 

Palustris  Remittens,  1468 

Pituitosa,  1363 

in    Puerperio,     1948,    1949,    I951. 

1953 
Puerperalis,i948,  1949,  1953 
Putrida,  1363 
Ouintana,  1501 
Recurrens,  1308 

Semitertianae  seu  Composita,  1363 
Sudoralis,  1437 


INDEX 


2331 


Febris,  continued 
Undulans,   1437 
Verminosa,  1363 
Volhynica,  1501 
Feet,  Foot 

Angiokeratoma  of,  2148,  2277 
Bones  of,  Degeneration,   Endemic, 

of,  2110 
Coolie  Itch  of,  2214 
Dermatitis  of,  in  Ankylostomiasis, 

1764 
Elephant,  2111,  2116 
Fourmiliere  des  Vers  in,  21 11,  21 16 
Madura  Foot,  21 10 
Necrosis  of,  156 
Mossy-Foot,  2247,  2254 

Reference,  2263 
Mycosis  of,  1123 
Soles  of,  Lesions  of 

Frambcesial,  1551,  2259 
Keratodermal,  2259 
Syphilitic,  2259 

Sore.  355. 

of  Coolies,  1764 
Trench  Foot,  1967,  21 10,  2149 
Ulcers  of,  1063,  1068,  21 12 
Felida?,  Traumatisms  caused  by,  148 
Feltinella,  791 

Female  Circumcision,  1944,  1947 
Generative    System,   Diseases    of, 
1938,  1944 
Fer-de-lance  (snake),  250 
Fermentation,  22 

Gastric,    1749 
Ferrata's  Plasmosomes,   1902 
Fertility,     Effect     on,     of     Tropical 

Climates,   77,   89 
Fever,  4 

Fever  and  Ague,  1604 
Fever (s)  ascribed  to   Mosquito-bites 
in  early  India,  7 
Associated  with  Swelling  of  Nasal 

Mucosa,  1466 
Hippocrates'  knowledge  of,  10 
References,   1472-3 
Acclimatizing,  1229 
Acute,  Traumatisms  in,  1512,  151 3 
Anaemic,  Low,  1470 
of  Ankylostomiasis,  553 
Autumn,   1129,   1362 
Bacterial,  1128,  1362 
Ban  Bach,  1468 
of  Batavia,  1129 
Bilious 
Malignant,  1216 
Remittent,  see  beloiv 
Septic,  1469 
Black,  1 341 
Blackwater,  1216 
Broken  Wing,  1244 
Bungpagga,  1469 


Fever (s),  continued 
Carried  by 

Arthropods,  11 28 

Mammals,  1128,  1211,  1356 

Mosquitoes,  1128,  1129 
Carrion's,  1575 
Cerebro-Spinal,  1456  ,1459 

Epidemic,   1474 
Cesspool,  1363 
Chronic,  1530 

Black  Pigmentation  in,  1519 
Climatic,  1129,  1252 
Coast,  1 129 

in  African  Cattle,  712,  713 
Cobb's  Pigmentary,  1461 
Continued,  1362,  1529,  1530 

Double,  1463 
References,  1473 

Korean,  1355 

Simple,  25,  1254,  1372 
Cosmopolitan,  Unclassified,  and  of 

War  Zone,  1128,  1474 
Dambul,  1129 
Dengue,   1244 
Dum-dum,  20,  1289 
Elephantoid,  639,  1604 
Endemic,  1362 
Enteric,  1362 
Fall,  1362 

Filarial,  1603  sqq.  passin 
Five  Days',  1501 
Flood,  1350 
Forrest's,  1462 
Frambcesial,  1544,  1551 
Gaiter,   1501 
Gambia,  19,  419,  1259 
Gaol,  1326 
Gastric,  1362 
Gibraltar,  1437 
Giraffe,  1244 
Glandular 

Endemic,  1465 

Pfeiffer's,  1522 
Goat,  1437 

Hamiocystozoon,  1468-9 
Hsemoglobinuric,  497 

Bilious,  1216 

Malarial,  1216 

Tropical,  1128 
Hemorrhagic       Febrile       Gastro- 
Enteritis    of    Children, 
1472 

Malarial,  1216 
Hay,  Tropical,  1875 
Heat,  Low,  1460,  1530 

Robb's,  1469,  153° 
Helminthic,  Intestinal,  1520 
Hyperpyrexia!,  1462-3 
References,  1473 

in  Sub-Tertian  Malaria.  1170 
Icteric,  13 17 


2332 


INDEX 


Fever (s),  continued 
Im-Pyeng,  1253 
Inflammatory,  1229 
Intermittent 
Low,  1530 

Malarial,  etc.,  1129,  1137,  1349, 
1464-5,  1526,  1528,  1529 
Non-Malarial,  1530 
High,  1465 
Low,  1464 
Tick,  1344 
Intestinal,  1362 
Irregular  Low,  1363 
Japanese  River,  1350 
Jungle,   1 129 
Kamerun,  11 29 
Kurunegala,  1129 
Kyoto,   1467 
Lent,  1362 
Leprotic,  1515,  1654 
of  Less  than  Eight  Days'  Duration, 
Diagnosis  of,  1512 
With     some     Striking    Physical 

Sign,  1 512 
With  no  such  Sign,  151 2,  1526 
Little,   1363 

Low  (see  also  Anaemic,  Heat,  Inter- 
mittent, Irregular  above), 

1363 
Macular,  of  Tunis,  1467 
Magdalena,  1229 

Malarial,    12,    18-19,    22,    25,    873, 
1129,  1517,  1526 

Canine,  493 

Haemoglobinuric,   1216 
Malay  States,  1355 
Malignant,  502-3 
Marsh,  n  29 

Mediterranean,  932,  1437,  1530 
Melanuric,  1216 
Meuse,  1501 
Miliary,  1308 
Milk,  1948,  1 95 1 

of  Mofe  than   Eight   Days'   Dura- 
tion,  1528 

With    Marked     Physical    Signs, 
1528 

Without  Marked  Physical  Signs, 

1529 
Mosquito-borne,     11 28,     see      also 

Malaria 
Mossman,  1  105-6 
Muma,  1 1)75 
Nakra,  1466 
X.isha,    1466 
Nervous,  1362 
Night-Soil,  1363 
Oroya,  1566 
(  hoplasmosis,  1468 
Pappataci,  1254 
Papular,  1471-2,  1515 


Fever  (s),  continued 

Parenteric   or    Paratvphoid,    13^2 

1404 
Periodic  One-Day,  1501 
Pfeiffer's  Glandular,  1522 
of  Physical  or  Probably  Physical 

Origin,  na8,  1356 
References,  1460 
Pigmentary,   2232 
Polish,  1 50 1 
Prison,  1326 
Protozoal   or   Probably   Protozoal, 

1128,   1129 
Puerperal,  1522,  1946 

Tropical,  1938,  1946,  1957 
Pythogenic,  1362 
Quartan,  1157,  1528 

Irregular    Subcontinuous,    11 57, 

1160 
Quinine,    1201 
Quotidian,  18,  1526,  1528 
Rangoon,  1462 
Rat-Bite  and  Cat-Bite,  1356 
Reiter's  Disease,  1468 
Relapsing,  1308 
Remittent,   578,   1501,  1523,   1528, 

1529,  153° 

Bilious,     Malarial,     1129,     1165, 
1168 

of  Cattle,  575 

Epidemic,  11 29,  1308 

Icteric,  13 17 

Non-Malarial.  1289 
Rheumatic,  133,  1250 
Roble's,  1462 

Rocky  Mountain  Spotted,  1341 
Roman,  11 29 
Salonica,   1501 
Sandfly,  1254,  x524 
Sarcosporidial,  1582 
Scarlet,  1485-6,  1513 
Schistosomic,  1867,  1869 
Septic,  1520,  1529 

Bilious,  1469 
Septicemic,  11 86 
Seven-Days',  1250 

Another  form,  1308 
Shank,  1501 
Sierra,  11 29 
Skoplji  or  Uskub,  1254 
Slow,  1362,  1437 
Spirillum,  1308 

Spotted,      1326,      1474,     see      also 
Rocky  Mountain,  above 
Spring,  1 1 29 
Subtcrtian,    1129,    see    also    under 

Malaria 
Summer,  1254 

Summer  to   Autumn   or   Summer- 
Autumn,  1 129,  1 164 
Tacamoeho,  1467 


INDEX 


2333 


Fever  (s),  continued 

Tert  an,    11,    11.29.,  see  also  under 

.Malaria 
Texas,  in  Cattle,  497,  715 
Thermic,  139,  1449,  1527 
Three-Days',  541,  806,   1244,  1249, 

1254 
Tick,  1318,  and  see  Tick  Fever 

Intermittent,  1344 
T  entsin,  1466 
Trematodal,  1752 
Trench,  1501 
Tropical,   11 28 

Diagnosis  of,   151 1 
Enteroidea   Group,    1188,    136?, 
1461,   1468,   1474,   1526 
Hay  Fever,  1875 
Unclassified,  1461 
Trypanosome,   1259,   1280 
Typho-Malarial,  1366 
.    Typhus,  1326 

Unclassified,   121,   122,   1128,   146l 
Undulant,  932 
Urticarial,  1589,  1590,  1593 
Naegeli's,  1462 
References,   1473 
Van  der  Scheer's,  1252 
Vesicular,  1470-1,  1517 
Volhynia,   1501 
War  Zone,  11 28,  1501 
Whitmore's,  1466 
Woolley's,   1467 
Yellow,  1229 
Fibroid  Folliculitis  of  Montoya,  2097 
Fibroma  Molluscum,  2273 
Pendulum,  2273 
Simple,  2273 
Fibromata,  123 

of  Ear-Lobule,  201 1 
Uterine,  1945 
Fibrosis,  1592,  1601 
Elephantoid,  2262 
Fibrous  Osteitis,   1552 
Fieber  Periodische,  1501 
Fiebre  de  la  Oroya,  1566 
Field  Bug,  763 
Fiery  Serpents,  651,  1968 
Fievre(s),  Bilieuse  Grave,  11 u> 
Hcmaturique,  1216 
Hemoglobinurique,  12 16 
Melanurique,  1216 
Boutonneuse  de  Tunisie,  1467 
Capriense,  1437 
Caprine,  1437 
Continue,  1363 
Gastrique,   1363 
Herpetique,  2269 
Jaune,  1229 

des  Creoles,  12 16 
Malariques,   11 29 
des  Marais,  11 29 


Fidvre(s),  continued 

Meningogastrique,   1363 

Nerveuse,  1363 

Paludiennes,  1129 

Palustre,  11 29 

de  Pick,  1254 

de  Pym,  1254 

a  Rechute,  1308 

Rouge,  1244 

Telluriques,  n 29 

des  Trois  Jours,  1254 

des  Trenchees,  1501 

Typhoide,  1363,  1664 

a  Vomissements  Noirs  des  Enfants, 
1472 
Figites  anthomyiarum,  908 

scutellaris,  908 
jiji,  Diseases  of,  123 
Filaire,  632 

7ilaria  (see  also  Agamofilaria,  and 
Microfilaria),  23,  332, 
623,  631,  644,  678, 
1273,  1714,  1975 

cethiopica,  651 

apapillocephala,  641,  1974 

bancrofli,    17,    18,    623,    632,    633, 
641,  644,  873,  876,  896, 
1596,  1941.  1968 
Embryos,    Table   of   Differences 
between      these,       and 
those  of  Loa  loa,  648 
History,  1595-7 
Hosts"  of 

Definitive,  873 
Intermediate,  873 
Pathogenicity,  1595,  1961,  2219 

communis,  633 

conjunctives,  1794 

cystica,  632 

demarquayi,  632,  639 

dermatemica,  633 

iliitrna,  645 

Doubtful  forms,   to  be  eliminated 
from  the  genus,  632-3 

(Ltiauiculus,  651 

rqui,   649 

gigas,  632 

hominis  bronchialis,  649 

hominis  oris,  632,  053 

inermis,  623,  632,  640,  641,  649 

juncea,  639 

kilimarce,  632 

labiato  papulosa,  649 

labralis,  640 

It  litis.  642 

mar  Us,  631,  632 

niellyi,  632 

noctuvna,  633 

oculi,  6  15 

ot  uli  humani,  641,  642 

Oral,  1740 


2334 


INDEX 


Ft/aria,  continued 

ozzardi,  623,  632,  639,  643 
palpebralis,  640,  641 
papulosa,  649,   1974 
perforans,  631 
peritonei  hominis,  641,  1974 
perstans,  643,  801 
piscium,  633 
restiformis,  632,  653 
romanorum  orientalis,  632 
sanguinis  hominis,  633 
cegyptiaca,  633 
major,  645 
minor,  643 
nocturna,  633 
perstans,  643 
subconjunctivalis,  645 
taniguchi,  639 
wuchereri,  633 
.zefcra  (fictitia),  632 
Filaria  Krankheit,  1595 
Filariadea,  631 

Filarial  Abscess,  1601, 1602,  1604,  1606 
Chyluria,   1934 
Disease,   1595 
Erysipelatoid     attacks      preceding 

Elephantiasis,  2266 
Fevers,  1603  sqq.  passim 
Hydrocele,  1595,  1596,  1601,  1G03, 

1605 
Lymph  Extravasations,  1608 
Lymph  Scrotum,  1595,   1596,  1601, 

1605 
Lymphadenitis,  1964 

Diagnosis,  1523 
Lymphangiectasis,  1603,  1605 
Lymphangitis,    1523,    1595,    1604, 

1964 
Lymphatic  Varix,  1595,  1599  1603 

1605,  1607 
Orchitis,  1595,  1603,  1605 
Phlebectasis,  1603,  1607 
Synovitis,  1967 
Tumours,  161 7 
Varix,   1607 
Filariases,  The,  1595 

Clinical  Description,  1603 
References,   161 8 
Treatment,   1603 
Subcutaneous,  1967,  1968 
Filariasi,  1595 

Filariasis,    17,    25,    639,    1131.    1595, 
2262 
.Etiology,  1533,  1595,  1598 
Climatology,  122,  124,  1595 
Definition,   1595 
Diagnosis,  1529 
Insect  Vectors,  743,  747,  1598 
Parasites    of,    see    Filaria,    and 

Microfilaria 
Rash  of,  1  5 1 4 


Filariasis,  continued 
Synonyms,  1595 
Caused  by  Filaria  bancrofti,  1595 
.Etiology,  1598-90 
Climatology,  1597-8 
Diseases  enumerated,  1595 
Morbid  Anatomy,  1602-3 
Pathology,  1600-2 
Dermo-Conjunctival,    1967,     1968, 
1971 
References,   1980 
Dubini's,  1671,  1967,  1974 

References,   1980 
Ocular,  1972,  1974,  2007 
Filaridtz,  631 
Filar  idea,  631 
Filarides,  631 

Filariidce,  621,  623,  626,   631,  1-14, 
1968 
References,  681 
Filariince,  631 
Filariose,  1595 
File  Fishes,  194 
Fileraria,  632 
Filiform  Warts,  2274 
Filosa,  326 

Filix  mas,  1753,  1771,  1869 
Filterable  Viruses,  541 

References,  543 
Finns,  the,  55 
First-Class  Lives,   127 
Fish,  see  also  Pisces 
Larvicidal,  789,  1208-9 
Parasites  of,   19,    337-8,   395,   398, 

400,  488,  534,  579 
Poisonous,  193-4,  230 

References,  241 
Traumatisms  caused  by  147,  154-5 
Fish-Poisons,  167,  187 
Fistula,  Branchial,  1959 
Fistulous   Disease   of  the    Buttocks, 
2084 
Tubercular  Disease,  2085-6 
Fitness  for  Tropical  Life,  127 

References,  134 
Five  Days'  Fever,  1252,  130S,  1501 
Flagella,  291,  296,  297,  330 
Flagellar  Vacuole,  370 
Flagellate  Diarrhoea,  1780,  1796 
Animal  Carriers  of,  877 

Table,  878 
References,  1800 
Tonsillitis,  1747 
Urethritis,  1944 
Flagellates  of  Arthropods,  372,  376 
in  Blood,  289-90 
of  Insects,  in  relation  to  Espundia, 

2177-8 
Oral,  1740 
Flagellosis  in  Plants,  367 
Flagellum  of  Trypanosoma,  382,  383 


INDEX 


2335 


Flat-Worms,  555 

Flea-Bites,  877,  908,  1337,  1516,  2203 

Fleas,  see  also  under  Names,  23,  749, 

895.  897.  137° 
Destruction  of,  91,  1433-4 
Diseases  and  Parasites  carried  by, 
20,    23,    115,    117,    285, 
363-  364.  369,  375-  376, 
479,  857,  876,  1650 
Plague-Spreading  (Human  and 
Rat  Plague),   115,  117, 
285,    747-     857,     1416, 
1419,  1420,  1421 
Most  Important  Species 

A.  Rat  to  Rat,  867 

B.  Rat  to  Man,  867 
Dog,   Vectors  of,    Kala-Azar,   375, 

376,  1299,  1303 
Rat,  23,  865,  867,  869,  870 
Table  of,  866 
Fleckfieber,  1326 
Flema  Salada,  1700 
Fh'xnerella 

paradysentery,  937 
pseudo-dysenteries 
var.  A,  937 
var.  Di,  937 
var.  D2,  937 
tangallensis,  937 
Flies  (Fly),  Adult  and  Larval,  see  also 
under  Names 
Change  of  Habits  of,  895-6 
Diseases  and  Parasites  spread  by, 
see  also  Myiasis,   1619, 
23.  24.  3°6,  3°7.  316-17, 
356,  363.  364.  365,  435- 
468,  747,  771,  873,  876, 
883,     897,     908,     920, 
1556,  I557-  !564>  1650, 
1805,  1807,  1841,  1844, 
i860,  1944,  1994,  1995, 
1998,  1999,  2166  et  alibi 
in  the  Eye,  1995 

Diseases    due    to,    995,     1998, 
1999 
Biting  and  Blood-sucking,  23,  365, 
814,  1703,  1716 
Collection  of,  748 
Method  of  Infection,  874-5 
Parasites  of,  365,  814 
References,  855 
House,     Diseases     and     Parasites 
carried  by,  24,  306,  307, 
316,  359,  364.  747-  77L 
873,      897,       see      also 
Fannia,      and      Musca 
domestica 
Crusade  against,   i860 
English  and  Tropical,  List  of,  900 
Parasitic,  814 
True,  825 


Flint's  Parasite,  737,  738 
Flood  Fever,  1350 
Flour  of  Wheat,  grades  of,  104 
Flusso  Sanguigno,  1824 
Fly,  see  Flies,  above 
'  Fly-Bite  '  (Oriental  Sore),  2165 
Fly-Crusades,  i860 
Fly-Disease  (Nagana,  q.v.),  410 
Foehn,  the,  81-2 

Fcetal  Abnormalities  and  Monstrosi- 
ties, 1957 
Fcstidus  Group  of  Streptococci,  928 
Foetus  Agnathia,  1959 
Cyclops,  1959 
Papyraceus,  1959 
Foie,  Absces  du,  1910 
Folk-Medicine  for  Snake  Bite,  277 
Folliclis,  2272,  2277 
Follicular  Conjunctivitis  Catarrhalis, 
1996,  1997 
Hyperkeratoses,  2256 
Tonsillitis,  1747 
Folliculites,  2017 
Pyogenic,  2027 
Folliculitis,  2250 
Decalvans,  2283 
Fibroid,  of  Montoya,  2097 
Purulent,  of  Legs,  2027,  2029,  2036 
References,  2038 
Fonlainea  pancheri,  1 74 
Food(s),    Absorption    of,    by    Intes- 
tinal     Parasites,       553 
Adulteration  of,  95 
Animal,  94,  95 

Chemical  Composition  of,  96-7 
Digestibility    of,     Coefficients     of, 

101-2 
Essentials  of,  96 
Eugenic  aspect  of,  119 
Evolution  of,  94 

Frambcesia  spread   by,  1556,  1557 
Poisonous,  193 

References,  202 
Till  Properly  Prepared,  172 
Preparation  and  Flavouring  of,  104 
Quantity,  97 
Tropical,  94 

References,   no- 11 
Vegetal,  94-5 
Food-Deficiency,      in      relation      to 
Disease,    see    Beri-beri, 
Pellagra,  etc.,  109,11-17, 
1673,  1675,  1690,  1691, 
1709 
Food-Factors  in  Diet,  Estimation  of, 
as  to 
Quality,  101 
Quantity,  97 
Food-Materials,  Classification,  of,  97 
Tropical,  104  sqq. 
Vitamine-containing,   109,  no 


2336 


INDEX 


Food-Peculiarities,  Racial,  104 
Food-Poisoning 
Animal,  193 

and  Beri-beri,  1673,  1674 
Pseudo-Cholera  due  to,  1820 
References,  202 
Vegetal,  193,  195 
Food-Ration,  British  War,  90,   100, 

102 
Food-Taboos,  95 
Foot,  see  Feet,  above 
Foot  and  Mouth  Disease,  535,  541 
Foot-Binding,  Pathological  Effects 

of,  155-6 
Foot-Tetter,  2037 
Foraminifera,  298,  303,  327 
Forcipomyia,  803 
Fordyce's  Disease,  1746,  2284 
Foreign  Bodies  in 

External  Auditory  Meatus,  201 1 
Eye,  1995.  1997 
Forest  Yaws,  2167,  2172 
Forficula  auricular ia,  1641 
Formalin  Sprays,  1207 
Formiciasis,  2000,  2004,  2006,  2267 
Formicidce,  see  also  Ants 
Formosans,  the,  55 
Biting,  Venom  of,  222 
References,  229 
Forrest's  Fever,  1462 
Foundations  of  Medicine,  6  sqq. 
418  (Spirarsyl),  27 
Fourmiliere  des  Vers  (in  Foot),  21  n, 

2116 
Fowl  Diphtheria,  541 
Pest,  541,  542 
Spirochetosis,  454 
Fowls,  Diseases  of,  due  to  Spiroschau- 
dinnia  marchouxi,  453 
Enemies  to  Ticks,  701 
Parasites  of,  353,  704 
Foxia  mansoni,  1100 
Fra-Fra  Arrow-poison,  180,  181 
Fragilitas  crinium,  2282 
Frambcesia     Tropica     (Yaws),     251, 
1187,  1533,  1535,  1558, 
21 1 1,  2176,  2187 
.Etiology,  461,  1538 
Bacteriological     Flora     present, 

459, 1538 
Blood  Conditions,  1553-4 
Causal  Organism,  21,  24,  436,  449, 
1-52.   457  sqq..  460,    |i»i. 
1536.  1538,  1539.  154°. 
1557.   1558-9.   1568 
Cerebrospinal  Fluid  in,  1554 
Climatologv,      122,      123,       124, 

1537 
Complement-Fixation  Reactions, 

1554 
Definition,  1535 


Frambcesia  Tropica,  continued 
Diagnosis,  1557 

Differential,       1557-9,       1568, 
1576,  1664,  2082,  2091, 
2173,  2185,  2253  2254 
Duration,  1542 
Economics,  1560 
Eye-Conditions,  1553 
Frambcesides  in,  1548,  1550-1 
Genito-Urinary  System  in,   1553 
Helminthic  Infections  in,  1552 
Histopathology,  1 540-1 
History,  1535 

Hyperidrosis  in,  1553,  2222 
Hyperkeratoses  in,    1545,    2256, 

2257 
Infection  of  Parents  by  Children, 

1543,  1556.  1557 
Inoculation  Experiments  on 

Man,  1538-9 

Monkeys,  etc.,  1539-40 
in     relation    to    Juxta-articular 

Nodules,  2261 
Lesions  in,  of 

Bones  and  Joints,  1552,  1978 

Hair  and  Nails,  1551 

Mucosas,  1 551 

Soles,   1551,  2259 
Muscular  Contraction  in,  1552 
Neuritis  in,  1552-3 
Patients  with,   Non-Immune  to 

Syphilis,  459 
Predisposing  Causes,  1540 
Prognosis,  1559-60 
Prophylaxis,   1564 
Pseudo-Goundou  in,   1976,   1977 
Pseudo-Mycetomatous  condition 

in,  2147 
References,   1564-5 
Regions  attacked,  1550 
Sequelae,  1876,  1877 
Spread  of,  by 

Insects,  25,  876,  908,   1556-7, 

1564 

Other  Means,  1543,  1556,  1564 
Stages  in 

(a)  Primary,  1541,  1542 
Frambcesoma,  1542 

(b)  Secondary,  1542,  1544 
Granulomatous,   1544  sqq. 

(c)  Tertiary,   1542,   1544 
{d)   Fourth,  1556 

Symptomatology,  1541 
Constitutional,  1551 
Cutaneous,    15.(2 
Synonyms,   1535 
Treatment,  28 
Local,  1564 
Various  Means 

Castellani's      Mixture,     28, 
1562-3 


INDEX 


2337 


Frambcesia  Tropica,  continued 
Treatment,  continued. 

Native  Methods,  1565 
Salvarsan,  etc.,  1560-2,  2280 
Tartar  Emetic,  1562 
Atypical,  2085 
Circinate,  2052,  2235 
Granulomata,  2185 
Frambcesial  Aneurysm,  1555 

Ulcers,  452,  2190 
Frambcesides,  1548,  1550-1,  2235 
Frambcesiform  Nodules  in  Keratoma 
Plantare  Sulcatum, 2259 
Frambcesoma,  1542 
Frambeetic  Onychia,  1550 

Paronychia,  1550 
Framosi,  1535 
Freckling,  2281 

Frienite,  or  Frien  Disease,  1033 
Frieira,  2036 
Frogs,    Parasites   of,    353,    355,    363, 

398,  400,  461,  488 
Frontier  Sore,  378 
Frost-Bite,  2264 
Fruit-Fly,  903,  904,  1370 
Fruits,  Heavy,  Traumatisms  caused 

by  Fall  of,  156 
Fuegians,  the,  56,  60 
Fuguismus,  122,  194 

References,  194 
Fulah,  or  Fulani,  the,  47,  51,  53 
Fundatus  tceniopygus,  789 
Fundus  Oculi,  2004 
Ftinftagefieber,  1501 
Fungacece,  923,  967,  968 

References,   977 
Fungal  Affections  of  Eyelids,  2009 
Diseases  of  Skin,  2015,  2017 
Gummatous  Affections,  11 12,  11 18, 

1 1 22,  1 1 24,  2041 
Rarer  forms,  2106 
Fungi,  923,  967 

in,  of,  and  associated  with 
Beri-beri,  167,  1680 
Ear,  201 1 
Eye 

(a)  List,  2008 

(b)  Diseases  with  which  asso- 

ciated,  200.) 

Hair,  see  Tinea,  etc. 
Histoplasmosis,  1669 
Maize,  171 2-1 3 

Sputum,  1084  sqq.  passim,  1521 
Stools  of  Normal  Persons,  1782 
Imperfecti,  965,  968,  986,  987,  1035, 
mi,  1 741  sqq. 
Parastica  Section,  1050 
Brevis  Subsection,  1050 
Species 
List,  1054 
Table,  1056 


Fungi  Imperfecti,  continued 

Parasitica  Section,  continued 
Major  a  Subsection 
Species 

List,   1050  sqq. 
Table,  1052 
Minora  Subsection, 
Species 
List,  105 1 
Table,  1055 
Saprophytica  Section,  1045 
Majora  Subsection 
Species 

List,  1045  sqq. 
Table,  104S 
Minora  Subsection 
Species 
List,  1047 
Table,  1049 
References,   1 124-5 
Treatment,    1044 
Pathogenic,  see  Mycology,  21,  967 
of  Plants,  198,  200 
Poisonous,  and  Poisoning  by,  124, 

172,  173,  198,  200 
Transmission  by  Flies,  24 
Fungus-Cellulose,  968 
Fungus  Disease  of  India,  21 10 
Funiculitis,  Endemic,  1522,  1938,  1939 

References,   1955 
Furcocercous  Cerearice,  559 
Furina,  246 

calonota,  251 
Furunculus  Contagiosus,   2027 
Orientalis,  2165 
Tropical,  2027 
Furrowed  Tongue,  1746,  2284 
Furrowing    of    the    Skin,     artificial, 

2238,  2240,  2241 
Fury,  Tropical,  76,  1981 
Fusaria,  653 
mystax,  656 
vermicular  is,  657 
Fusarium,  1 113 
Fusiform  Organisms  of  Vincent,   1745 

Gad-Flies,   815 
Gaigeria,  672 
Gaiter  Fever,  1501 
Gale,  La,  2217 
Gale  de  Saint  Ignace,  1700 
Galen,  12 

Galis  Pateros  (Yaws),  1535 
Gall-Bladder,  Diseases  of,  1907 
in  relation  to  Enteric,  1367 
Galla  Race,  47 
Galle  Leg,  1610 
Gallenfieber,  1216 
Gallinippcrs,  774 
Gall-Producing  Insects,  908 
Gall-Sickness,  20,  407 

147 


233§ 


INDEX 


Gall-Stones,  1907 

Galls  on  Plants,  caused  by  Acarina,69i 

Galyl,  27,  28 

Galziecte,  20,  407 

GamasidcB,   693 

Gamasoidea,  692 

Gimbia  Fever,  19,  419,  1259 

Gambusea  molliensia,  789 

Game    as     Reservoirs     for    Sleeping 

Sickness,  879.  880 
Gametes,  292 

Gametocytes,  294,  295,  469 
Gamocystis,  471 
Gangosa,  1555,  1741,  1875,  1876 

Ulcers,  2190 
*"   Varieties,  1879 
Gangrene,  156 

Acute  Traumatic,  149 

Dry,  in  Subtertian  Malaria,  11 79 

Gas,  961 

References,  966 

Hospital,  959,  2182 

of  Lung,  1949 

Spreading  Traumatic,  150 
Gangrenosa,  123 
Gangrenous  Appendicitis,  1526 

Dysentery,  1830,  1831,  1835 
Bacillary,  184S,  1849 

Rectitis  Epidemic,  25,  125,  1871 
References,   1892 

Trench  Foot,  2149 

Vaccinia,  151 8 
Ganja,  176 
Gaol  Fever,  1326 
Garib-guez,  1704 
Gas  Gangrene,  961 

References,  966 
Gasogenous  Group  of  Streptococci,  928 
Gasterostomes,   558 
Gastric  Diseases,  1749 

Disturbance  due  to  Kwan's   Fluke, 

1752 
Fermentation,  1749 
Fever,  1362 
Myiasis,  852 
Spirochetosis,  1749 
Symptoms  due  to  Cestodc  Parasites, 

1753 
Ulcer,  454 
Gastrisches  richer,  iv\; 
Gastritis, Atrophic,  Chronic,  1906 
Gastritis-type  of  Subtertian  Malaria, 

1177,  1178 
Gastrocystis,  530 
GastvodiscidcB,  561,  563 
Gaslrodiscus,  563 
eegyptiacus,  563 
hominis,  563,  1  75-' 
References,  594 
minor,  563 
secundas,  563 


Gastro-Enteritis  Climatica,  1254 
Endemica,  1254 

Haemorrhagic  Febrile,  of  Children, 
1472 
Gastro-Intestinal  Canthariasis,  1640 
Myiasis,  1620,  1621,  1622,  1628 
Scolechiasis,  1640 
Tract,  Diseases  of,  1241,  1731 
Gastro-Obium,  Sheep-poison,  189 
Gastrophilus,  825,  826,  1639,  2209 
equi,   827,   1630 
hcBmorrhoidalis,  1639,  2209 
nasalis,  1639,  2209 
pecorum,  828 
veterinns,  1639 
Gastropoda,  890 
Gastrothylacidcs,  561 
Gastroxides,  823 
Gattoo,  1535 

Ga vials,  Traumatisms  caused  by,  153 
Geese,  Diseases  of,  453 
Geigera  wellmani,  1699 
Gelbfieber,  1229 
Gelechia  gossypiella,  2216 
Gelseniium  sempervirens,  2153 
Gemmation,  288,  291,  292 
General  Diseases,  1533,  1535 
Causation 

Animal  Parasites,  1533,  1535 
Chemical,  1533 
Unknown,   1533 
Vegetal  Parasites,  1533 
Disturbance  of  Health,  indications 

of,  1520 
Dropsy,  122,  1895,  1904 
Paralysis,  1981 
Generative  Functional  Changes  due 
to  Subtertian    Malaria, 
1180 
System,    Derangements    of,    1519, 
1522 
Diseases  of,  1938 
Female,  124,  1944 
Male,  1938 
References,  i960 
Effect  on,   of  Temperature  and 
Humidity,  77 
Gelbsucht  group  of  Chilamydozoa,  540 
Genickstarre,  Epidemische,  1475 
Genitalia,  Warts  on,  2274 
Gcnito-Urinary  Organs 
in  Frambcesia,  1553 
Mycoses  of,  1926 
Geobdella,  688 
Geographical  Discovery  in  relation  to 

Disease,  114 
Geomyidee,  914 
Geophagy,  1749,  1761 

References,  1751 

Geophagy,  1749,  1761 

References,  1751 


INDEX 


2339 


Geophilus  carpophagits,  740 

cephalic  us.  740.  1O41,  1S81 

electricus,  740,  1641,  1881 

longicornis,  venom  of,  218 

siniilis,  740,   1641,   1881 
Geotrupes  vernalis,  1640 
Gerlier's  Disease,  1982 
German  Measles,  1490,  1513,  151 6 
Germ  theory  of  Disease,  15 
Gerris fossarutn,  Parasites  of ,  367,  372 

pallidum,  Parasites  of,  363,  368 
Ghibli  (wind),  81 
Ghisud,  2165 
Ghootloo,  or  Gootloo,  Mahdce,  21 10 

2113,  2116 
Giardia,  464,  466 

intestinalis,     466,   877,    878,    1796, 

1833 
Gibraltar  Fever,  1437 
Gift  Zeer,  2030,  2031 
GigantorhynchidcB,  680 
Gigantorhyncus,  680 
gigas,  680 
moniliformis,  680 
Gila  monster,  the,  124,  279 
Ginger,  172 
Gingivitis,  1520,  1744 
References,   1751 
Ulcerative,  1744,  1745 
Giraffe  Fever,  1244 
Girardinus,  789 
formosus,  789 
pceciloides,  789 
versicolor,  789 
Glanders,  965,  1529 
Ulcerations,  2190 
Glandula  Idiopathica,  1961 
Glandular  Disease  of  Barbados,  1610 
Enlargements,  1522-3,  1526,  1529, 
1532,       1551-2,       1587. 
1961,      2253,     see     also 
Hodgkin's  Disease 
Fever,  Endemic,  1465 

of  Pfeiffer,  1522 
System  in  Native  Races,  2264 
Glass,    Powdered,    Traumatisms   due 

to,  156-7 
Glass  Slides,  marks  on,  1901 
Glaucoma,  2004 
Glenospora,  11 12,  1113,  2008 
Dermatomycoses  due  to,  2041 
Species 

cur  list,   1 113,  1 1 14 

graphii,  1113,  1114,  2008,  2009 

khartoumensis,  1114.  1115,  2041, 

2121,  2122 
microspora  11 14 
ramorum,  1113 
sacchari,  11 14 

semoni,  1114,  1116,  2041,  2122 
Gkmosporosis,  Ocular,  2009,  2010 


Glires,  913 

Globi,  in  Leprosy,  1652 

Globidium,  360,  491 

Globularia,  381 

Gloriosa  superba,  115,    164,   165,  166, 

169,  170 
Glossina,  19-20,  747,  771,  832,  837 
Bite,   1269 

Classification,  844,  845 
Larva;,   771 
Parasites  of,  454 
Pathogenicity,   838,  844 
References,  856 
Species 

austeni,  845 
brevipalpis,  846 
brevipalpis  group,  846 
caliginea,  845 
fusca,  845 
fusca  group,  845 
fuscipleuris,  845 
longipalpis,  415,  417,  838,  845 
longipennis,  846 
medicorum,  846 

morsitans,  19,  23,  388,  390,  410, 
413,  415,  426,  843,  844, 
845,     880,     881,     1260, 
1262,  1264,  1265,  1278, 
1279 
morsitans  group,  845 
nigrofusca,  845 
pallicera,  845 
pallidipes,  845 

palpalis,   19,   23,   388,   389,   390, 
39i,  392,  393,  413,  415, 
417,    421,    424-5,    838, 
842,  843,  845,  878,  879, 
1260,   1262,  1264,  1265, 
1278,  1279 
Bionomics,  845 
palpalis  group,  845 
tabaniformis,  845 
tachinoides,   415,   417,    845,    881, 

1264 
ziemanni  n.  sp.,  846 
Trypanosomes     carried     by,     390, 

39i,  397.  413.  415.  417. 
421,    424-5,    426,    838, 
844,   1260,   1262,   1263 
Development  of,  389,  390 
Glossinella,  837 
Glossiphonia,  685 

Trypanoscwne  development  in,  389 
Glossiphoniida,  685 
Glugea,  529 

anomala,  529 
Gluteal  Blastomycosis,  2084,  2085 
Glycannia,  76 
GlycipJiagus,   729 

prunorum,  729,  2214 
Glycosuria,  132 


234° 


INDEX 


Glyphodon,  246 

tristis,  251 
Gnathobdellidce,  685 
Gnathostoma,  623,  629,  630 

siamense,  630 

spinigerum,  623,  630 
References,  681 
GnathostomidcB ,  623,  624,  629 
Gnats,  774 

Goa  Powder  Tree,  2160 
Goat  Fever,  1437 
Goat-Poisons,  189 

Goats  and  Goats'  Milk  in  relation  to 
Undulant  Fever,  1438 
sqq. 

Heartwater  in,  713,  723 

Parasites   of,    320,    369,    412,    413, 

4l6-  454 
Trypanosome-Diseases  of,  391 

Trypanosomes  of,  413 
Gobi  at,  415 
Gobora,   1303 
Godfrey  and   Eyre's  Tubercular 

Disease,  21 10 
Godownik  (Oriental  Sore),  2165 
Gofar,  1700 

Goitre,  120,  124,  1288,  1919,  1959, 
References,   1925 

Adenomatous,  1920 

Congenital,  1920,  1922 

Endemic,  1920,  1959 
References,   1925 

Exophthalmic,  1920 

Parenchymatous,  1920 
Golgi,  Cycle  of,  in  Plasmodia,  506 
Gomera,  2076 
Goniopsyllus,  865 
Gondwanaland,  and  Primitive  Man, 

42 
Gongylonema  pulchrum,  1740 
Gonidangium,  972 
Gonidia,  969 
Gonidiophores,  1972 
Goniops,  823 
Gonoblennorrhcea,  539 
Gonococcus,  1479,  1998 

Eye  Infection,  1997 

Rheumatism,  1938 

Septicaemia,  1938 
Gonone  (Mite),  727 
Gonorrhoea,  118,  926,  1938 

Causation,  926 

Treatment,  176 

Native,  risks  of,  171 

Unfitting  for  Tropical  Life,  127 
Gonorrhoeal  Arthritis,  1967 

Conjunctivitis,  1996,  1997 

[nfection,  1523 

Salpingitis,   1961 
Gootloomahdec,  2110,  2113,  211G 
Goraharik,  200 


Gordiacea,  621,  678 

Gordiaceiasis  and  Acanthoaphaliasis, 

1777 
Gordiidce,  679 
Gordius,  679 

aquaticus,  632,  679 

chiliensis,  679 

equinus,  649 

medinensis,  651 

pulmonalis  apri,  662 
Goro,   177 
Goundou,  124,  1967,  1975 

References,   1980 
Gout,  1967 

Gracilis  group  of  Streptococci,  928 
Graciloidece,  932,  933,  958 
Graciloides,  933,  958 

albofaciens,  933,  958 

tardus,  958 
Grseci  Elephantiasim,  1700 
Grseco-Roman  Medicine,  1 1 
Graham's  Parasite  in  Dengue,  23 
Grain  Itch,  2200,  2216 
Grammocephalus,  672 
Granular  Nocardiasis,  Tonsillar,  1747 
Granules,  Infective,  in 

Relapsing  Fevers,  919 
Spirochsetes,  385 

Metachromic,  290 

Metaplastic,  290 

Volutine,  290 
Granuloma  Annulare,  2273 

Coccidoides,  474 

Endemicum,  2165 

Gangrenosum,  1876 

Inguinale,  2165,  2192 

yEtiology,  448,  449,  452,  2192-3 
References,  2198-9 
Treatment,  28,  2196 
Varieties,  Racial,  2195 

Parasitic,  2165 

Pyogenicum,  2254 

Trichophytic,  1000,  1002 

Ulcerative,  122 

Venereum,  2192 
Granulomata    in     Framboesia,     1535 

sqq.  passim. 
Granulosis  Rubra  Nasi,  2272 
Graphium  penicilioides,  11 14 
Grass  Sickness,  1749 
Graves'  Disease,  191 9,  1920 
Grecian  Medicine,  8,  10 
Gregarina,  471 
Gregarincs,  469 
Gregarinida,  469 
Gregarinidce,  471 
Gregarinidea,  469 
Gregarinosis  Pulmonum,   15S4 
Grewia  Asiatica,  188 
Grocer's  Itch,  729,  2214 
Gromiidce,  326 


INDEX 


2341 


Ground  Itch,  553,  OOy,  1763,  1771 
Ground  Squirrel,  Flea  of,  867,  870 

Plague  spread  by,  867,  912 
Grouse,     Red,      Leucocytozoon     of, 

435 
Growth,      Effect     on,      of      Tropical 
Climates,  77 
Vitamine  of,  109 
Guano  Itch,  2214 
Guarana  Bread,  168,  177 

Seeds,  ib. 
Guaranene,  177 
Guarani  Peoples,  5y 
Guarnieri  Bodies,  2193 
Guatteria    veneficum,     Arrow-Poison, 
185 

GugO,  20()0 

Guiana,  Fish-Poisons  of,  188 

Guinea-Pigs,  Parasites  of,  353,  355, 
406 

Guinea-Worm  (Dracontiasis),  9-10, 
11,  12,  17,  25,  623,  632, 
651,  652,  739,  1298, 
1524,  1967,  1968,  1970, 
2254 

Guinea-worm,  see  also    Dracunculus, 

651 
Gujaralu  race,  47 

Gummatous  Affections,  Fungal,  11 12, 
1118,   1122,   1124,  2041 
Rarer  forms,  2106 

Lymphangitis,   11 18,   11 24 
Gums,  Inflammation  of,  1744,  1745 

Shrinkage  of,  1520 
Gundurum,  2241 
Gune,  2060 

South-west,  2059 
Gttrleya,  529 
Gusano,  828 

Macaco,  1633 

de  Monte,  1033 

Moyocuil,  1634 

Peludo,  1633 

de  Zancudo,  1634 
Gymnamcebida,  298 
Gymnascales,   1070 
Gymnoascacece,  986,  1)87,  noi,  2054 
Gyynnoascecs,  986,  987,  2008 
Gymnoacees,  2008 
Gymnoascus,  986 
Gymnocepkalous  Cercaria,  55, 
Gvmnocerata,  761,   762 
GymnospermecB,   1071 
Gymnosporea,  471 
Gymnosporidia,  504 
Gymnosiomata,  546 
Gynecoptwrus,  58  \ 
Gynocardia,  i<>(>  \ 
Gyrocoryna,  547 
Gyropidce,   751 
Gyropus,  751 


Habbeciacco  seeds,  1753 
Habb-es-Sanah,  2103 
Habb-es-Sanawi,  2165 
Habit  Poisons,  174 
Habure  Disease,  503 
Hadrus,  817 
Hamadipsa,  683,  687 

fallax,  688 

japonica,  688 

javanica,  688 

morsitans,  688 

talagalla,  688 

umbata,  688 

vagans,  688 

zeylanica,  685,  088 
H&madipsinee,  685,  687 
Hcemalastor,   722 
Hcemamceba,  504 

immaculata,  517,  1137 

laverani,  517 

var.  quartana,  512 

malarice,  512,  517 
var.  magna,  510,  512 
var.  quartancB,  512 
var.  tertiana,  510 

pvcscox,  517,   1 137 

relict  a,  513 

vivax,   510 
HcemamcebidcB,  504 
Hcemanthus  toxicaria,  184 
Hcsmaphysalis  710,   711,   719 

concinna,   719 

flavii,  719 

leachii,  700,  719 

marmorata,  716 

punctata,   699,   700,    719 

rosea,   714 
Haematemesis,  1749 
Heematobia,  832,   846 

aids,  837 

rufipes,   846 

sanguisugeus,  846 

stimulans,  846 
Hcematobosca,  832,  846 

atripalpis,   846 

perturbans,  846 
Haematoceles,   1939 
Haematochyluria,    1596,    1599.    1  601, 

1608 
Hcsmatococcus,  492 

fcow's,  497 

ozn's,   497 
Haemato-lymphuria,  1608 
Hamatomonas,  381,  504 

Ci'dHSi,     4O9 

HcBmatomyzidce,  753,  759 
Hcematomyzus,  750 

elephantus,   730 
Htzmatophyllum,  504 

miliaria,    505 
UcBmatopinidcB,  753,  758 


2342 


INDEX 


HcematopinincB,  758 
Hcematopinoides,  759 

squamosus,  759 
Hcematopinus,  752 

stephensi,  485,  753 

vituli,   649 
Hcem&topota,  817 

beringeri,  819 

bullatifrons,  819 

crudelis,  819 

daveyi,  819 

decora,  818 

grahami,  819 

italica,  367 

obscura,  819 

pluvialis,  819 

rubens,  819 

taciturna,  819 

vittata,  819 
Hcematosiphon,  762,  766 

inodorum,  763,  766 
Hcematosiphonincs,  762 
Hcsmatozoa,  and  Beriberi,  1679 
Hcematozoon  falciparum,  517 
Hematuria,  Endemic,  1926 

Schist  osome-caused,  1927 
Hmmatustoridce,  710 
Heementaria,  685 

ghiilanii,  685 

officinalis,  685 
Haemiconia,  1900 
Haemocultures,  1390 
Hcsmocystidium,  504,  516 

mesnili,  516 

metschnikowi,  516 

wtf/'<2,  516 

simondi,  516 

roumei,  516 

testudinis,  516 
Hcsmocytozoa,  477 
Hcsmocystozoon,  360,  361 
Fever  due  to,  1468-9 

brasiliense,  1468-9 
Hcenwdipsus,  759 
Hcemoflagellata,  289 
Haemoglobin  in  Urine,  1522 
Hemoglobinuria,  ^Etiology,  11 36 
Diagnosis,  1522 

Malarial,    1168,    1180,    1213,    1217 
s<7<7.,  1522 

Quinine,    202,    1201,    1213,     1214, 
1217,  1218,  1219,  1220, 
1224,  1522 
Haemoglobinurias 
Paroxysmal,  1 2 1 3 
Specific,  tji  ; 
Symptomatic,  1213 
Toxic,  1213,  1522 
Tropical,  1128,  1168.  1213 
Haemoglobinuric  Fever,  497 
Bilious,  1216 


Haemoglobinuric  Fever,  continued 
in  Cattle,  497 
Malarial,  121 6 
Tropical,  1128 
Hamogogus,  801 

Hcemogregarina   [Hcemogregarmes), 
360,  478,  483 

anarrhichadis ,  488 

bagenesis,  4S0,  487 

balfouri,  485 

bigenuria,  488 

billeti,  487 

bovis,  485 

canis,  479,  483,  713 

cantlei,  487 

crocodilinorum,  486 

crotali,  4S7 

/e/is,  486 

funambuli,  486 

gerbilli,  479,  485,  753 

hankini,  486 

hominis,  483 

inexpectata,  1306 

jaculi,  478,  479,  485 

lacertarum,  487 

lanceolata,  601 

laverani,  487 

leptodactyii,  48S 

mansoni,  487 

mauretania,  487 

mesnili,  487 

minima,  480,   488 

mirabilis,  487 

mocassini,  487 

muris,      479,       480,       4S1,       483, 
693 

WO/<£,    487 

nicoricB,  486 
platesscB,  488 
pococki,  487 
pythonis,  487 
quadrigemina,  488 
ranarum,  488 
rara,  487 
rarefaciens,  487 
r«Wt,  486 
refringens,  487 
robertsoni,  401 
rovignensis,  488 
schattochi,  487 
schaudinni,  487 
seligmanni,  487 
simondi,  483,   488 
splendens,  488 
stepanovi,  480,   486 
stepanoviana,  487 
temi,  487 
thomsoni,  487 
1'nnamed,  of  Rats,  479 
vittata,  487 
zamenis,  487 


INDEX 


2343 


Hcemogvegarinda  of 

Amphibia,  478,  480,  488 
Leeches,  480 
Mammalia,  47S,  483 
Ophidia,  480,  487 
Pisces,  478,  488 
Reptilia,  437,  478,  4S0,  486 
Sauria,  487 
Tortoises,  480,  486-7 
References,  526 
Hceniogregarinidcs,  477,   478,  480 
Haemolytic  Toxin  (Malarial),  203 
Hcsmomonas  precox,   517 
Hcemonchus,  624,   663 

contortus,  624,  663 
Hcemophilce,  932,   933 
Hemophilus,  933 

influenza,  933,  1497,  1498 
Heemopis,  686 
lacustre,  686 
sanguisuga,  355,  686 
HcBinoproteidcB,   478,   518 
Hcemoproteus,  518,  1136 
columbcB,   519,   525 
mansoni,  526 

noctua,  289,  381,  382,  434,  519 
oryzivorce,   526 
Hcsmoprotozoa,   290 
Haemoptysis,  568 

Parasites   associated   with,    568, 

574 
Endemic,  1584,  1885,  1889 
Parasitic,  1584 
Haemorrhages,  Gerebral,   1981 
of  Enteric,  1384,  1386,  1401 
Optic,  2005 
Post-partum,  77 
Suprarenal,  Acute,  1923 
Haemorrhagic  Bronchitis,  1882 
Diseases,    Differential   Diagnosis 
from  Small-pox,   1491 
Febrile    Gastro-Enteritis    of    Chil- 
dren, 1472 
Subtertian  Malaria,  11 73 
Malarial  Fever,  12 16 
Non-Febrile    Type    of    Subtertian 

Malaria,  1169 
Pancreatic         Affections,         1907, 

1908 
Pancreatitis-type     of     Subtertian 

Malaria,  11 77,    1178 
Purpura,   122,   1698 
Septicaemic   Group,  Organisms    of, 

Genus   including,  943 
Smallpox,  1488-9,  2267 

Differential  Diagnosis,  1491 
Haemorrhagin,  261 
Haemosiderin,  1145,  1147 
Hcemosporea,  478 

H&mosporidia,    290,    469,    477,    478. 
524 


Heemosporidium,  504 

q  a  a  r  tunes,  512 
sedecimancB,  517 
tertianum,  510 
itndecimance,   517 
vigesimoter Hants,  517 
Haemozoin,  293,  505,  518,  1134,  1145, 

1147,  1148 
Hair,  Diseases  of,  994,  2052,  2058, 
2100  sqq.,  2142,  2208, 
2264,  2268,  2282,  2284, 
see  also  Pediculosis 
Capitis,  Ringworm, 

Tinea,  etc. 
Effect    on,    of    Tropical    Climates, 

and  Sun-rays,  77,  88 
Moniliform,  2282 
Hair  Follicles,  Pyogenic  Affections  of, 

2027 
Hair-Catching  in  Electric  Fan,  156 
Hair,   Chopped,  Cattle-Poisoning  by, 

189 
Hairy  Parts   Aspergillosis  and  Peni- 
cilliosis of,  2041,  2092 
System  of  Native  Races,   2264-5 
Haiza,  1801 
HalarachnincB,  693 
Half-Castes,   119 

Hallucinations  in  Deserts,   1981,  1990 
H alter idium,  518,   1136,   1143 

danilewskyi,  518 
Halysis  lanceolata,   611 

solium,  612 
Halzoun,  567,  1746 
Reference,   1751 
Hamadryad,  247 
Hamitic  Races,  46 
Hamster,  Trypanosome  of,  406 
Hanmlaria,  623,  632,  649 
equi,  623 

lymphatica,  640,  649 
Hands,  Angiokeratoma  of,  2277 
Entanglement  of,  in  Electric  Fan, 

156 
Palms  of,  Frambcesides  of,  1 550-1 
Hansenia,  979 
Haplaria,  987 
Haplochilus,  789 
bifasciatus,  789 
grahami,  789 
pumilus,   789 
Haplographiacea,   1070,   1096 
Hdplomi,  789 
Haplophyllum  tuberculatum,  2153 

Dermatites  due  to,  2160 
Haplosporidia,  528,  534 

References,  543 
Haplosporidia,  534 
Haplosporidiidea,  534 
Haplosporidium,   534 
Har  boul,   1926 


=  344 


INDEX 


Hare -Lip,   123,   1959 
Harita  Sarhhita,  1761 
Harlequin  Snake,  267 
Harmattan,  the,  81 
Harpactor,  767 
Harpulia  arborea,  188 
Hartmanclla,   323 

hyalima,   323 
Hartmannia,  298 
Harvest  Bug  of  England,  725 
Harvest-Mites,  725,  2213 
Haschisch,  132,  176,  198S 
Ha,tty-ka-Pung,  2110,  2116 
Hausa  Race,  51 
Hautkratzschorf,  1639 
Hautmaulwarf,  1639,  2208 
Ha-van  tatat  Plant,  124 
Hay  Fever,  Tropical,  1875 
Head,  Ringworm  of,  Tropical,  2052 
Headache,  88 
Head-Gear,  Tropical,  89 
Head-Louse,  756,   see  also  Pediculus 

Capitis 
Health,  General  Disturbance  of,  indi- 
cations of,  1520 
Heart,  see  also  Cardiac 

Diseases  of,  135,  1895,  1804 

Hypertrophy  of,  1904 
Heart-Block,  11 79,  1904 

Reference,   1905 
Heartwater  in  Sheep  and  Goats,  713, 

72  3 
Heat,  Body,  see  Temperature,  Bodily 
Effects  of,  Warning  en,  of  Candi- 
dates  for    the   Tropics, 
128 
Midday,  Avoidance  of,  91 
Racial  Susceptibility  to,  2265 
Heat-Exhaustion,   139 
Treatment,  138 
Syncopal  form,  1904 
Heat-Fever,  Low,  1460,  1530 

Robb's,  1469 
Heat-Stroke,    see  also  Sunstroke,  24, 
88,  14*9,  1875 
Etiology,  139,  140,  144,  145,    146, 

M52-3 
Climatology,  120,  1 451-2 
Clinical   Identity    with   Sunstroke, 

146 
Convalescence,  1456 
Course,   1456 
Definition,   1449 
Diagnosis,  1456,  1527 

Differential,  11 86,  1450 
History,   1 450-1 
Incidence;  Age,  Occupation,  Race, 

and  Sex,  1453 
Onset,   1455,   1456 
Pathology,    141,   1453-4 
Predisposing  Causes,  1453  j 


Heat-Stroke,  continued 
Prodromata,   1455-6 
Prognosis,  1456-7 
Prophylaxis,  140,  1458 
References,   1460 

Symptomatology,  137,  138,   1455-6 
Synonyms,   1449 
Termination,  1456 
Treatment,  138,  1457-8 
Heat-Syncope,  1449,  1450,  1459 
^Etiology,  13,  140,  141 
Diagnosis,  1521,  1527 
References,   1460 
Symptomatology,  137,  138 
Heavy   Fruit,    Falling,    Blow    from, 
Traumatism  caused  by, 
156 
Hebrews,  the,  see  also  Jews,  47 
Hcctopsylla,  861 
Heinz 's  Corpuscles,  1902 
Helcosoma,  369 

tropicum,   20,   378 
Heliconea  brasiliensis,  789 
Hcliozoa,   297 
Hellvelales,  985 
Helminthiasis,    Animal    Carriers    of, 

887 
Helminthic  Diseases,  Infections,  and 
Invasions,      122,      124, 
1514,  1532,  1533,  1552, 
1739,  1752,  1753,  1758, 
1759,  1761.  1764,  1765, 
see       also      Ankylosto- 
miasis, 1761 
References,   1778-9 
Febrile  Urticaria,  1516 
Intestinal  Fevers,  1520 
Septicaemias,  1520 
Toxaemias,   1520,   1527,   1530, 
Helminthology,     Early,      7,     9, 

17,  18 
Helminthoma  Elastica,  1608 
Helminths,  Parasites  of,  470 
Helobdella   algira,  Trypanosomas 

394.  398,  4°° 
Heloderma  horridwn,  278 

suspectum,  124,  277,  278,  279 
Helodermatidce,  278 
Venom  of,  278-9 
References,  281 
Helophilus  pendulinus,  1630 
Heltu,  9,  666 

Hemelytra  of  Hemiptera,  761 
Hemeralopia,  2004,  2006 
Hemi-asci,  1070 
Hetniascomycetes,  978,  1070 
Hcmibungarus,  246,  251 
Hemiclepis,  337,  685 

nuirginata,   389 
Hemispora,  1108,  1742,  1743,  1886 
Dermatomycoses  due  to,    2041 


1532 
12, 


of, 


INDEX 


2345 


Hemispora,  continued 
Species 

rugosa,   1108,   1109,    1742,    1743, 

1748 
slellata,  1108,  2041,  2100 
Tabic  of,  1 109 
Hemisporales,  1039,  1108 
Hemispore,   1037 

Hemisporomycosis,  Tonsillar,   1748 
Hemisporosis,  1108,  2106 
Hemiptera,  748,  761 
References,  770 
Biting  Species,   218,  219,  369 
Hemiplegic  Subtertian  Malaria,  11 75, 

1146 
Hemiterata,  1957 
Hemp,  Indian,  132,  176,  1988 
Henoch's  Purpura,  1698,  2267 
Henpuye,   1975 

Hepatic  Abscess,  all  forms,   18,   122, 
287,317,  321,  335,  1063, 
1064,  1186,  1521,   1525, 
1834,  1836,  1875,  1893, 
1907,  1908,    1910,  2139 
Bilharziosis,  1864 
Coccidiosis,  474 
Coccidium  of  Man,  476 
Enlargement,      Indications     from, 

1525 
Hepatitis,  1909,  1914 

Acute  Severe,  with  Gastritis,  1906 
Amoebic,  1382 

Treatment,  1835 
Monilia  in,  1091 
Hepatozoon,  483 
muris,  483 

pzmiciosum,  479,  483 
Heplaphlebomyincs,  790 
Heracleum  giganteum,  2157 

lanatum,   2157 
Hermaphrodites,  19.57 
Hermaphroditism,  558 
Hermasson  minutus,  810 
Hernia,  124 
Carnosa,  1610 

External  and  Internal,  1739 
Strangulated,  194^ 
Herpes,  2053,  2264,  2269 
Corneae 

Febrilis,  2004 
Zoster,  2004 
Desquamans,  2060 
Facialis  febrilis,  2269 
Farinosus,  2060 
Iris,  2266 

Vesiculosus,  1006 
Manson's,  2060 
Progenitalis,  2269 
Tonsurans,  2053 
Turner's,  2060 
Zoster,  2206,  2269 


Herpetic  type  of  Subtertian  Malaria, 
1181 
'  Herpetomonas,  358,  359,  360,  361, 
362,  363,  364,  369, 
376,  381.  395.  397.  814. 
2193 
Infection  by,  363,  364 

Hereditary,  362 
Species 

aspongopi,  372 
bombycis,  367 
butschlii,  359,  366 
ctenocephali,  363 
ctenophthalmi,  367,  376 
culicis,  363 
davidi,  366-7 
drosophila,   367 
gracilis,  367 
hospei,  372 

jaculum,  363,  366,  372 
lesnei,  367 
lewisi,  403 

lyg&i.  372 

muscce- domestical,  295,  364,  365 

369 

pedicuh,  363,   753 
pycnosoma?,  366 
pyrrhocori,   372 
sarcophaga,   367 
stvatiomyia,  363 
subulata,  367,  816 
vespa?,  367 
Herpetomoniasis,   363,  372 
Herpetomonida?,  358 

References,  462 
Herpetomonina,  358,  1289 
Herpobdellida?,  685 
Herxheimer's  Reaction,  1201 
Heteralius,  1959 
Heteroconta,  923 
Heterocotylea,  560 
Heterokaryota,  290,  296,  544 

References,  550 
Heterometrus  matirus,  207 

Venom,  210,  211 
Heteromita,  335,  336,  343 
dahlii  apstena,  338 
lens,  342 
zeylanica,  343 
Hcteromitida,  336 
Heteromyia,  806 
Heteromyida?,  914 
Heteronchyia  dolosa,  799 
Heterophyes,  570 
References,  595 
Species 

heterophyes,  570,  1752 
Heterophyiida?,  564,  570 
Heteropoda,  891 
Heteroptera,  761 
Heteropus  ventricosus,   725 


2346 


INDEX 


Heterotaxis,   1957 
Heterotricha,  544,  547 
Heterotypus,   1959 
Hexamastix,  351,  356 
Hexaminoarsenobenzenes,  Partly  me- 
thylated, 28 
Hexamita,  464 
Hexapoda,  689,  743,  771 
Classification,  748 

Orders   Important   to   Medicine, 
748 
Diseases  spread  by,  743,  2200 
Enemies,  747 
Habits,  747 

Internal  Anatomy,  745-7 
Larvae,  Parasitism  of,  747 
Life-History,  747 

Metamorphosis,  747 
Morphology,  743  sqq. 
Pathogenicity,  747-8 
Pupae:  three  forms,  747 
References,  748 

Recent  Literature,  748 
Trypanosomes  of,  395,  397,  398 
Venomous  Species,  216  sqq. 
Wingless,  745 
Hexapode  Dermatites,  2200,  2207 
Hexathyridium  venarum,  567 
Hexatoma,  820 

High  Atmospheric  Temperatures,  137 
Intermittent  Fevers,  1330 
Non-Malarial,  1465 
Hikan,  2006 
Hill  Diarrhoea,  1780,  1788,  1795 

References,   1800 
Himalayan   Tribes,  Arrow-poison   of, 

184 
Himantarium  gervaisi,  740,  1641 
Himasthlince,  581,  583 
Himyarites,  the,  47 
Hinchazon,  1671 
Hindu  Medicine,  6,  141 7 

Races,  47 
Hippelates,   902,   1557,   1999 
flavipes,  902 
plebejns,  902 
pusio,  902 
Hippobosca,  855 

Parasites  carried  by,  407,  415 
Species 

camelina,  855 
capensis,  855 
equina,  855 
maculata,  855 
rufipes,  407,  855 
Ilippoboscida,  415,  854,  855 
Hippocentrum,  817,   819 
murphyi,  819 
slrigipennis,  819 
tritnaculatum,   819 
versicolor,  819 


Hippocrates,  Writings  of,  10-11,  1824 
Hippomane     mancinella,     173,     174, 

2153,  2157 
Hippopotami,    Traumatisms    caused 

by,  152 
Hirudinaria,  686,  687 

javanica,  687 
Hirudinea,  683 

References,  688 

Trypanosomes  of,  395,  397,  398 
Hirudiniasis,  1880 

Reference,   1 894 
Hirudinincs,  685 
Hirudo,  686 

asiatica,  686 

hildebrandti,  686 

medianalis,  337,  338,  684,  686 

multi striata,  684,  686 

nipponica,  686 

quinquestriata,   686 

saigonensis,  686 

septemstriata,  686 

sinica,  686 

timorensis,  686 

troctina,  686 
Histiogaster,  731 

spermaticus,  731 
Histoplasma,  359,  1076 

capsulatum,   1073,   1076,   1669 
Histoplasmosis,  1669,  1875 

.-Etiology,  1533 

References,  1670 
Histriobdellida,  688 
His-Wernersche  Krankheit,  1501 
Hitzschlag,  1449 
Hive-Bee,  Sting  of,  219 
Hodgkin's  Disease,  1529,  1532 
Hodi-potsy  (dermatosis),  1097 
Holoceria,  820 

nobilis,  820 
Holophrya  coli,  547 
Holothuria  argus,  205 
Holothurians,  205 
Holothyridce,  693 
Holothyrus,  693 

coccinella,  200,  693,  2213 
Holotricha,  546 
Ho-louan,  1801 
Homa  el  Hugga,  13 14 
Homa  en  Naxy,  13 14 
Homalomyia  canicnlaris,  852 
corvina,  365 
scalaris,  365 
HomalopsincB,  246 
Homicidal  Poisons,  162,  163  sqq. 

Tendencies,  1981 
Homma  Typhiusa,  1326 
Homologaster,  563 
Homoptera,  761 
Hondziekte,  493 
Honey,  94 


INDEX 


2347 


Hong    Kong    Medical    School    (Uni- 
versity), 5 
Hookworm  Disease,   1761 
Hoplocephalus,  246 

Venom  of,  243,  256 
curtus,  256 
variegatus,  251 
Hoplopleiu-ii,   759 
Hoplopsyllus,  864,  866,  870 
anomalus,  866,  867,  870 
Hormodendrum.  1097 
fontoynonti,  1097 
olviaceum,  1097 
Hormones,   no 
Horned  Viper,  250,  251 
Hornets,  Stings  of,  219 
Horrocks'  and  Howells'  Bodies,  1901 
Horse-Flies,  815 
Horsehair  as  cause  of  Creeping  Erup-   ] 

tion,   2209 
Horsehairs,  678 

Horses,  see  also  Equine,  Diseases  of, 
due  to   Trypanosomes, 
19-20,  391 
Parasites  of,  414,  415,  492 
Rabies  in,  152 

Ticks  infesting,  714,   715,  719 
Hospital  Gangrene,  959,  2182 
Phagedena,  448,  2182,  2185 
Hosts  of 
Bacteria 

Infected,  921 
Propagative,  921 
Protective,  921 
Parasites 
Animal,  117 
Definitive,  873,  921 
Human,  115,  117, 
Intermediary,  115,  116,  873,  921 
Intermediate,  921 
Hottentot  Race,  51,  53 

Arrow-Poisons  of,  184 
House  Flies,  see  also Fannia,  852,  and 
Musca  domestica,  903 
Common,  871 

Crusades  against,  i860 
Diseases  and  Parasites  carried  by, 
24,    306,  307,   316,  359, 

364.  747.  77L  873.  897 
English,  900 
Little,  904 
Tropical,  900 
Houses,  Construction,  etc.  of,  90 
Hova,  race,  55 
Howell- Jolly  Bodies,  1902 
Huaxtecs,  the,  60 
Human  Spirochaetes,  443  sqq. 
Humidity,  Effect  of,  on  Temperature, 
67-8      sqq.,       see      also 
Temperature   and   Hu- 
midity, 137 


Humma  laban,  1948 

Nafas,  194S 
Hundskrankheit,  1254 
Hungarians,  the,  54,  55 
Hungerpeste,   1308 
Hunting- Poisons,  187,  189 

References,   192 
Hura,  1633 
Huva  brasiliensis,  2157 

crepitans,  164,  168,  2153,  2157 
Hurricanes,  82 
Husano,   1633 
Hycsnanche  globosa,  184 
Hyalococcus  beigelii,  1103 
Hyalodixus,  298 
Hyalomma,  710,  711,  720,  723 
eegyptium,  362,  700,  723,  724 
affine,  723 
crassiiarsus,   723 
hippopotamense,  723 
monstrosum,  723 
rhipicephaloides,  723 
syriacum,  723 
Hyalospora,  471 
Hydnocarpus  venenata,  187 

wightiana,  1664 
Hydatid  Disease,  616,  191 4 

Alveolar  form,  617-18 
Hydrelaps,  249,  251 
Hydroa,  2206 

Pruriginosa,  2206 
Vacciniforme,  2269 
Hydrocele,  132 

Filarial,    1595.    1596,    1601,    1603, 
1605 
Hydrocotyle  javenica,  188 
Hydrocyanic      Acid,      in      Cassava 

172 
Hydrometridce,  762,  769 
HydrophidcB,  266,  268 
Hydrophinee,  246,  249,  251 
Hydrophis,  249,  251 
Venom  of,  268 
cantoris,  260 
obscurus,  251 
Hydrophobia  in  Man,    151,   see  also 

Rabies 
Hydrophobia-like  Subtertian  Malaria, 

1173,  1174 
Hydropneusta,  690 
Hydrops  Asthmaticus,  1671 
llydrotea,  852,  854 

meteor ica,  854,  1629 
Hydrus,  249,  251 

platurus,  251 
Hygiene,  Mosaic,  10 
Prophylactic,  554 
Tropical,  89 
1 1  via  arborea,  355,  394 
II  vlemyia,  852 
I    Hymenolepiasis,  1757 


=348 


INDEX 


Hymenolepis,  601,  002,  003,  008,   609, 
1776 

References,  619 

Species 

diminuta,  601,  604,  609,  895,  1757 
lanceolata,  601,  604,   611 
murina,  600 

nana,  124,  601,  603,  610,  1757 
var.  fraterna,  610 
Hymenoptera,    218,    219,    748,    2200, 
2207 

References,  229 
Hymenostomata,  546,  547,  550 
Hyoscyamine,  177 
Hyoscyamus  falezlez,  164,  166 

mulicus,   178 
Hyperadrenalism,  1982 
Hyperaemia  of  Conjunctiva,  1995-6 

of  Labyrinth,  Quinine-caused,  2013 

of  Liver,  1908 
Hyperchlorhydria,  1029,  1749 
Hyperidrosis,  1553,  2222,  2256,  2264, 
2272 

Symptomatic,  2222 
Hyperkeratoses,  the,  2247,  2256 

Congenital,  2256 

Follicular,  2256 

Non-follicular,  2256 

of  Sole,  2277 

Subungualis,  2257 

Universalis  congenita,  2250 

in  Yaws,  1545,  2256,  2257 
Hyperparasitism,   116,  287,  649 
Hyperpigmentation,   2231 

Diseases   in   which    present,    1180, 
1181,  2232 
Hyperplasias,  1920 

Endemic,  1920 

of  Thyroid  system,  1920 

Toxaemic,  1920 
Hyperpyrexial  Fever,  1462-3 

References,   1473 

in  Subtertian  Malaria,  1 1 70 
Hypersarcosis,  1610 
Hypersecretion  in  External  Auditory 

Meatus,  2012 
Hyperthyroidism,  1288,  1919,  1982 
Hypertrichosis,  2282 
Hypertrophy,  Cardiac,  1904 

of  Male  Breast,  1939 

Prostatic,  1926 
Hypha,  968 
Hyphales,  1035,  1036 
Hyphomycetacea,  1036 
Hyphomycetece,  987 
Hyphomycetes,  1036,  2008 

Terminology,  1037 

Vuillemin's  Classification,  1037 
Hyphomycetic  Ulcers,  2190 

Urethritis,  1939,  1943 

Vulvo- Vaginitis,  1945 


Hypnotoxin,  204 
Hypoaemia  intertropicalis,  1761 
Hypocriales,  985 
Hypoderma,  826,  827,  1627 

bovis,  827,  1619,  1633,   1639,  2209 

diana,  827,  1633,  1639 

lineata,  1633,  1639,  2209 
Hypopyon,  2006 
Hypothyroidism,  191 9,  1920 

Benign  Chronic  of  Hertoghe,   191 9 
Hypotricha,  544,  546 
Hysteria,  1981,  1987,  1991 

War  Zone,  1982 
Hysteriales,  985 
Hystrichopsylla,  865,  866 

narbeli,  866 

talpes,  369,  376,  866 

tripectinata,  866,  867 
Hystrichopsyllince,  864,  865,  866 

Iatrobdella,  686 

Icteric  Fever,  13 17 

Icteric     or     Icteroid    Typhus,    1229, 

1308 
Icterus  Castrensis  Gravis,  1501,  1505, 
see  also  Weil's  Disease 

etiology,  1506 

Convalescence,  1507 

Definition,  1506 

Diagnosis,  1507,  1517,  1519,  1522 
Differential,  1507-8,  1509 

History,  1506 

Onset,    Course     and    Termination, 
1506-7 

Pathology,  1506 

Pigmentation,  1519 

Prognosis,  1508 

Prophylaxis,  1508 

Rash,  151 7 

Rats  in  relation  to,  1506,  1508 

Relapse,  1507 

Symptomatology,  1506-7 

Synonyms,  1505 

Treatment,  1508 
Icterus  Castrensis  Levis( Camp  Jaun- 
dice, q.v.  also),  451,  453, 
1501,  1507,  1508 

Climatology,  1509 

Definition,  1508 

Diagnosis,  1509,  1519,  1522 
Differential,  1507,  1509-10 

Onset  and  Course,  1509 

Pigmentation,  151 9 

Prognosis,  1510 

Prophylaxis,  1510 

Symptomatology,  1509 
Stages  in,  1508,  1509 

Synonym,  1508 

Treatment,  1510 
Icterus  Febrilis  seu  Infectiosus,  1505 
IchthyobdellidcB,  685 


INDEX 


2349 


Ichthyosis,    1731,    2060,    2070,    2256, 
2257,  2264,  2281,  2282 
Hystrix,  2281 
Tropical,  2060,  2070 
Ichthyosporidium,  534 
Ichthyothere  cunabi,  188 
Ichthyotoxismus,  1673,  1674 
Idiocy,  124,  1891 
Cretinous,  1920 
Idiopathic  Hyperidrosis,  2222 
Idrosis,  2222 
Ikan  Satan,  235 
Ileo-Typhus,  1363 
Ilex,  Mate-yielding  Species,  177-8 
gongonha,  178 
paraguayensis,  177-8 
thccezyns,  178 
Il-jarassy,  2165 
Illegitimacy,  119 
Illicium,  174 
anisatum,  174 
religiosum,  174 
Imago    of     Hexapoda,    Presence    of, 
Dermatites      due      to, 
2200,   2211 
Imbundi  Poison  in  Ordeal-trials,  178 
I mnianoplasma,  491 
Immunity,  113 
Impaludisme,  11 29 
Imperfect  Carriage  of  Parasites,  921 
Impetigo,  753,  756,  2020,  2265 
Bullosa,  2023 

Contagiosa,  2020,  2025,  2203 
Primarum  Viarum,  1780 
Im-Pyeng  Fever,  1253 
Incas,  the,  56,  57,  59,  60 
Inchacao,  1671 
Incinerators,  1773 
Inclusion-Blennorrhcea,  539 
India,  Arrow-Poisons  of ,  181,  184 
Cattle-Poisoning    in,    Drugs     and 

Plants  used,  189-90 
Death-Rates  of,  120-2 
Diseases  of,  120-2 
Europeans  in,  132 
Fish-Poisons,  188 
Hunting-Poisons,  189 
Life  Assurance  in,  132 
Nitrogen-Excretion  in,    per   Urine, 

100 
Snakes  of,  Venom  of,  243 
Vegetal  Poisons,  163,  164,  165,  166, 
168,  169,  170-1 
Indian  Bed-bug,  766 
Dietaries,  98 
Hemp,  132,  176,  1988 
Kala-Azar,  20,  28,  372,   373,   1289, 
1670 
References,  1307 
Medicine,    Early,    6,    8,    15,    2111, 
2116 


Indian,  continued 

Oro  -  Pharyngeal        Leishmaniasis, 

2165,  2179 
Relapsing  Fever,  918,    1308,    1315 
Varieties,  13 17 
Indiella,  1101,  1107,  2137 

Dermatomycoses  due  to,  2041 
Species' 

mansoni,  1107,  2041,  2123 
reynieri,  1107,  2122 
somaliensis,  105 1,  2137 
Indiellopsis,  2138 

somaliensis,  1051 
Indigestion,     Intestinal,     Indications 

from,  1532 
Indische  Spruw,  1780 
Indo-China,    Arrow-Poison    of,    181, 
184 
Diseases  of,  122 
Indo-Chinese  Races,  54 
Indonesian  Races,  49 
Infanticidal  Poisoning,  163,  169 
Infantile      Afebrile      Splenomegalies, 

i3°3 
Beri-beri,  1690 

References,  1693-4 
Biliary  Cirrhosis  of  the  Liver,  1906 

References,  191 7 
Convulsions,  122 

Diarrhoea,  120,  122,  123,  908,  1847, 
i960 
Dysenteric,  Bacillary,  1848,  1851 
Epidemic,  1847 
Dysentery,  i960 
Kala-Azar,  1299 

Mortality,  120,  122,  124,  1957,  i959 
Scurvy,  1675 
Infantilism  of  Malarial  origin,  11 82 
associated    with    South   American 
Trypanosomiasis,  1288 
Infection,  15 

Definition,  874,  921 
Forms  of,  874  sqq. 
Infections,  Endemic,  and  Invalid- 
ing, 13° 
Infectious  Jaundice,  see  also  Weil's 
Disease,  1505 
Infective  Endocarditis,  1521,  1528 
lnfcktionikterus,  1505 
[nfektioser  Fieberhafter  lktcrus,  1505 
lnfezione  Malarica,  1129 
Inflammation  of 

Liver  (Hepatitis),  1091,  1832,  1906, 

1909,  1914 
Lungs  or  Pleura,  1521 
Nail  Matrix.  2283 
Stomach,  Diffuse,  1749 
[nflammatory  Fever,  1229 

Laryngeal  affections,  1875  sqq. 
Nasal  affections,  1875  sqq. 
Pulmonary  affections,  1875,  1892 


235° 


INDEX 


Influenza,  1461,  1497 

Causal  Organism,  933,  1497,1498, 

1521 
Diagnosis,  1498,  1521,  1526 

Differential,  1186,  1230,  1252, 
1257-8,       1337,      1395, 
1396,  1485,  1490,  1498, 
1505,  1885 
Onset,  1526 
Prophylaxis,  1499 
References,  1500 
Streptococcal  Complications   of, 

1521 
Treatment,  1499 
Typical  attack,  1497-8 
Catarrhal  type,  1498 
Cerebral  type,  1498 
Inflaenza  Estiva,  1254 
Malarica,  1254 
Infusoria,  296 
Infusorien  Diarrhoea,  1796 
Ingrowing  Toe-nail,  2283 
Inguinal     Glands,    Enlargement     of, 

1523,  1961 
Injectio  antimonii  oxidi,  28 
Injury-Simulating  Poisons,  163,  171 
Inoculation    for   Smallpox    practised 

in  Indian  medicine,  8 
Inorganic  Poisons,  162,  170 
Insanity,   88,    122,    124,    1524,    1891, 
see  also  Lunatics,  1729 
Epileptic,  1981 
Indian    due    to    use    of    Cannabis 

sativa,  176 
Post-Malarial,  11 84 
Insect   Carriers  of  Disease,    117,  see 
also  under  Disease   and 
Names  of  Insects 
Hosts    of   Protozoa,    see   Glossina, 
Mosquitoes,  Ticks,  etc. 
Insecta,  743 

Insectivora,  Trypanosomes  of,  406 
Insects,  Bites  and  Stings  of,  Rashes 
due  to,  1516,  1517 
in  the  Eye,  1995 
as  Food,  94,  96 
Injurious,  117,  123,  124 
Parasites    of,    364,    see   also  tinder 
Names  of  both 
Inshup,  1700 

Insolation,  see  Heat  Stroke,  1449 
Insurance 

Rejections,  Causes  for,  132 
Risks,  132,  133 
Intermediary  Host  of  Animal  Para- 
site, 115,  116,  873,  921 
Intermediate  Host  of  Animal  Para- 
sites, 873,  921 
Intermittens,  1 129 

Intermittent    Claudication    type    of 
Subtertian  Malaria,  1 1 79 


Intermittent,  continued 

Fevers,  1137,  1464,  1526,  1538 
Chronic,  1530 
High  and  Low,  1530 
Malarial,   1129,   1526,   1529 
Non-Malarial,    High    and    Low, 

1464-6 
Septic,  1529 
Malarial  Otalgia,  2013 
Tick  Fevers  of  Wyoming,  1349 
Internal    or    Cavity    Myiases,    1622, 
1623 
Tumours,    Nematodal,    see   Nema- 
tode section,  passim 
Intertrigo,  2046 

Blastomycetica,  2092 
Saccharomycetica,  2047,  2092 
Intestinal  Anguillulosis,  1758 
Bilharziosis,  1864 
Coccidiosis,  475 
Fevers,  1362 
Helminthic  Fevers,  1520 
Invasions,  1752 

References,   1778-9 
Indigestion,       Indications       from, 

1532 
Infections  in  Enteroidea,  1523 
Myiasis,  831,  854,  900,  905,  1841, 
1863 
Oro-Gastro,     1222,     1620,    1621, 
1628 
Nematodiases,  1758 
Obstructions,  1739,  1753 
Oro-Gastro -Myiasis,     1222,      1620, 

1621,  1628 
Polyparasitism,  1776 

References,   1779 
Sand, 1739 
Schistosomiasis,  1864 
Septicaemias    or    Toxaemias,    Hel- 
minthic, 1520 
Symptoms  indicative  of  Derange- 
ments    of     Alimentary 
Canal,  1520 
Tseniases,  601,  1753 
Trematodiases,   1752 
Ulceration,  1076 

Worms,    Infections    due      to,     see 
Helminthic    Infections, 
Toxaemias,  etc. 
Intestines,  the,  Remarks  on,  1739-40 
Intoxicants,  see  Stimulative  Poison- 
ing, 174-8 
Intoxication?,    Tropical,    tee    Chemi- 
cal Causes  of    Disease, 
161 
Intranuclear  Ccntrosome,  381 
Intussusception,  1739 
Invaliding,   130,   1227 
Invertebrata,   Parasites  of,   470,   534 
Iodine  for  Snake-Bite,  278 


INDEX 


2351 


Ionization    for  Pyorrhoea    alveolaris, 

1740 
Ipecacuanha,  28,  1834-6 
Ipoh,   or    Ipuh,    Arrow-Poison,    181, 

184,  1S5 
Ipoh  aker  (Malacca),  185 
Iridaceee,  Poisons  from,  164,  167 
Irido-Cyclitis,  2006,  2007 
Iris,  Affections  of,  2003,  2006,  2010 
Iritis,  2003,  2006 

Malarial',  2004,  2005 

Secondary,  2005 
Iron,  Sulphate,  Cattle-Poisoning  by, 

189 
Irregular  Low  Fever,  1363 

Subcontinuous      Quartan     Fevers, 
1157,  1160 
Irritants,  Abortifacient,  170 
Irritating  Larvae 

Coleopterous,  2208 

Lepidopterous,  2208 
Ischiopagus,  1958 
Ischnocera,  751 
Island  Disease,  1350 
Isodynamic  Law  of  Rubner,  97 
Isopleura,  890 
Isosoma  grande,  2216 

tritici,  2216 
Isospoya,  473 

bigemina,  473,  475 

hominis,  475 
Isotherms,  39-41,  62 
Itch,  the,  2200,  2217,  see  also  Scabies 

Barley,  2216 

Bicho-Colorado,  2214 

Cooly,  553,  730,  2247,  2248 
of  Feet,  2214 

Copra,  729,  730,  2200,  2214,  2215, 
2248 

Cotton-Handler's,  2214 

Dhobie,  1007,  2040,  2042 

Grain,  2200,  2216 

Grocer's,  729,  2214 

Ground,  553,  669,  1763,  1771 

Guano,  2214 

Straw,  2216 

Vanilla,  191,  2214 
Itch  Mites,  691,  729,  731,  2217 
Ixodes,  693,  710 
Ixodea,  693 
Ixodei,  709 
Ixodes,  693,  710,  711,  720 

annulatus,  714 

autnmnalis,  722 

bovis,  714,  1557 

camelinus,  724 

erinacei,  722 

hexagonus,  700,  722 

leachi,  719 

marmorata,  716 

moubata,  706 


Ixodes,  continued 

poortmani,   723 

reduvius,  722 

reticulatus,  716 

ricinns,  217,  487,  492,  700,  720 

rufus,  713 

sanguineus,  713 

s'ixpunctatus,  722 
Ixodida,  6 

IxodidcB,  'j.lj,  694,  696,  709 
Ivodidea,  710 
Ixodiden,  'jog 
Ixodides,  693,  709 
Ixodince  (syn.),  709,  710 

Neumann's  Classification,  701 
Ixodini,  709 
Ixodoidea,  215-17,  691,  692,  693  sqq. 

Importance  of,  in  Tropical  Medi- 
cine, 693 

Parasitic  on  Man,  List,  700 

References,  229,   741 
Ixodioplasma,  492 

specifiaim  bovum,  497 

Jackal-bite,  151 

Jacquinia  armillaris,  188 

Jadari,  i486 

Jak-Fruit,  Falling,  Traumatisms  due 

to,  156 
Jamaica  Dog- wood,  188 
Jamaica,  Vomiting   Sickness  of,    173, 

1233.  1695 
Jaman  Dyscharagan,  2165 
Janthinosoma  lutzi,  896-7,  1635 
Janus  or  Syncephalus,  1958,  1959 
Japan,  Diets  of  Workers  in,  99-100 
Diseases  of,  122 
Medicine  in,  5,  6 
J  \panese  the,  55 
Japanese    River    Fever,    726,    1347, 

1350 
Jarat,  El,  1948, 
Jatropha,  164,  166,  173 
cuvcas,  164,  166 
manihot,  1 72 
itreus,  2153 

var.  stimiilosa,  2159 
Jaundice,  569,  1516 

Diseases  in  which  present 
Acute  Fevers,  151 9 
Blackwater    Fever,    121 6,    1222, 

1223 
Pneumonia,  1507,  1508 
Relapsing  Fever,  1313,  1317 
Woolley's  Fever,  1467 
Yellow  Fever,  1236,  1237 
Varieties 

Bacillary,  1522 

Camp,  451,  453.  i5°i.  I5°7. 
1508,  1509,  see  also 
Icterus  Castrensis  Levis 


2352 


INDEX 


Jaundice,  continued 
Varieties,  continued 

Catarrhal,  1508,  1509,  1907 
Enteric,  1507 
Epidemic,  1505 

Spirochetal,  918 
Infective    {see   also    Weil's    Dis- 
ease), 1505 
Malarial,  1507,  1508,  1510 
Malignant   (Canine    Babesiasis), 

493 

Non-Febrile,  151 7 
Obstructive,  1907 
Septic,  1507,  1508 
Java,  Fish-Poisons  cf,  188 
Javanese,  the,  ^~, 
Jeanselme's  Nodules,  2260 
Jejen,  805 

Jelly-Fish,  Stings  of,  203,  204 
Jerks,  the,  1986 

Jesuits  and  Chinese  Medicine,  5 
Jettatura  di  Sole,  1700 
Jeun-Chenn,  172 
Jewish  Medicine,  9-10,  13 
Jigger    (Chigoe),    24,    123,    124,   282, 

285,     857,     862,     2210, 

see    also  Dermatophilus 

penetrans 
Jinja,  410 
Johannseniella,  805 
Joint  Worm,  Parasite  of,  2216 
Joints,  Diseases  of,  1967 
Ju-ju,  West  African,  3 
Julidcs,  689 
Juliformia,  689 
Julus  londinensis,  1641 

terrestris,  1641 
Jumpers,  the,  1986 
Jumping  (Disease)  or  Latah,  1983 

Leech,  688 
Jungle  Fever,  11 29 
Juniperus  sabina,  2153 

virginiana,  2153 
Jupuiala,  1700 
Jura  Tree,  166 
J uxta- Articular    Nodules,   123,   1063, 

1065,   1966,  2041,  2I^i), 

2247,  2260 

Kabure,  1589,  1590 
Kabyles,  the,  46 
Kaffir  Milk-pox,  1491 
Kafirido,  1698 

Kaju  bita-buta  Poisoning,  2163 
Kaju-rugas  Poisoning.  2163 
Kakhyers,  the,  49 
Kakke,  1671,  1672 
K;iki-lem-but,  1671 
Kala-Azar,    287,    1141,    1189,    1289, 
2180 
Anemia  in,  1903 


Kala-Azar,  continued 

Bodies  in,  1520,  2160 
Bone-Marrow  in,  1905 
Carriers  and  Reservoirs,  363,  372, 

373,  682-3 
Chloasma  in,  2232 
Climatology,  121,  1291 
Diagnosis,  1520,  1525,  1529,  1531 
Differential,  11 82,  11 86,  1445, 
1688,  1767,  1914,  1953 
Insect  Vectors,  363,  766,  1128 
Infection,  Method  of,  363,  364 
Liver  Affections  in,  1906 
Parasites,    363,    372,    373,    1525, 

I529,  1531.  1903,  1907 
and  see  Leishmania 
Purpura  Eruptions  in,  2267 
Spleen  in,  1904 
Symptoms,  1837 
Canine,   374-5,    377,    1299,    1303 
Cutaneous    or    Dermal     (Oriental 
Sore),    378,    380,    2165, 
see   also  Leishmaniasis, 
Dermal 
References,  2197 
Indian,  20,  28,  372,  373,     1670 

References,  1307 
Infantile,     1299,     see    also     Medi- 
terranean,  below 
Mediterranean,  1289,  1299 
^Etiology,  1299 
Causal  Organism,  374,  883,  1289, 

1299,  1907 
Climatology,  1299 
Complications,  1302 
Course,  1300-2 
Definition,  1299 
Diagnosis,  1302 

Differential,  1302-3 
History,  1299 
Onset,  1300 
Pathology,  1 299-1 300 
Prognosis,  1303 
Prophylaxis,  1303 
References,   1307 
Reservoirs  and  Carriers,  883 
Symptomatology,  1300 
Synonyms,  1299 
Treatment,  28,  1299,  1303 
Tropical,  1289 
/Etiology,  1 2  91 -2 
Blood  in,  1293-4 
Causal    Agent.    363,    883,    1289, 
1290,  1291,  1297,  1299 
Climatology,  1291 
Complications,  1295-6 
Course,  1295 
Definition.  1289 
Diagnosis,  1296 

Differential,       1296-7,       1302, 
1305.  x3°7 


IXDICX 


2353 


Kala-Azar,  continued 
Tropical,  continued. 
Diet,  1298 
!  listory,  1289-yi 
Incubation,  1294 
Morbid  Anatomy,  1294 
Onset,  12^15 
Pathology,  1292-3 
Predisposing  Causes,  1292 
Prognosis,  1297 
Prophylaxis,   1298 
Reservoirs    and    Carriers,     363, 

883 
Spread,  363,  883,  1292 
Symptomatology,  1294-5 
Synonyms,  1289 
Treatment,   1291,  1297-8 
Kala-Azars,  the,    and    Pseudo-Kala- 

Azars,   1289,  1303 
Kala-Dukh,  1289 
Kala-Jwar,  1289 
Kalmucks,  the,  55 
Kaltes  Fieber,  1129 
Kamerun  Fever,  1129 
Kameruns,  Vegetal   Aphrodisiacs  of, 

1172 
Kamerungeschwlilste,  1972 
Kaninloma,  1876 
Kaodzera,  1260 
Kaposi's    Disease,    88,     1731,    2264, 

2266,   2281 
Karabin,  167 
Karang  gatal,  204 
Kara  kist,  Venomous  Spider,  213 
Karens,  the,  54 
Karyolysus,  478 
Karyosomc,  290,   291 
Kashmiri  Race,  47 
Katayama  Disease,  588,  593,  1589 
/Etiology,  1.553,  1591 
Animal  Reservoirs,   1591 
Causal  Agent,  592,  593,  1589,  1590, 

1591 
Climatology,  1 590-1 
Complications,  1593 
Definition,  1589 
Diagnosis,  1593 
Disease  resembling, 
History,  1589-90 
Morbid  Anatomy,  1  591 
Pathology,  1591 
Prognosis,  i593"4 
Prophylaxis,   1594 
References,  1 
Stages  in,  1592 
Symptomatology,  1 591-2 
Synonyms,  1589 
Treatment,  1594 
Varieties,  1592-3 
Katayama  nosophora,  592,  1590 
Katipo,  Venomous  Spider,  212 


Kaumpuli,  1416 

Kawa,  176 

Kawain,  176 

Kedani       Disease,      1350,      see     also 

Tsutsugamushi    Fever 
K(  dani  (mite),  726 

Kedrowsky's  (Leprosy)  Bacillus,  1647 
Keereenagoah,  21 15 
Keerenagrah,  21 10 
Keloid,  Auricular,  201 1 

Tattooing,  2239-40,  2241 
Kendal's  Disease,  1229 
Kenyans,  Arrow- Poison  of,  185 
Kerandel's  Symptom,  1273 
Keratitis,  1063,  2006,  2138 
Dendritica,  2004-5 
Marginalis  supernciahs,  2005 
Parenchymatosa         circumscripta, 

2005 
Phlyctenular,  2002 
Profunda,  2005 
Punctata  leprosa,  165G 
Keratodermia,  2256 
Cribrata,  2257 
Punctata,  2257 
Symmetrical,    of   the    Extremities, 

2259 
Plantare  Sulcatum,  2257,  2258 
Keratomycosis,  1113,  in 4,  2008 

Aspergillina,  103 1 
Keratosis,  2256 
Palmaris,  2257 
Pilaris,  123 
Plantaris,  2257 
Kerion,  1004,  1005,  1006,  2057 
Barbae,  1008,  2044,  2058 
Celsi,  1006 
Kernig's  Sign,  1483,  1  L85,  1514,  1524, 

E528 
hevte'szia,  792 
Kharsivan,  27 
Khartoumensis     Parentericus,     1406, 

1  |<ks,  1412 
Khas,  the,  54 
Kho-sam  Powder,  1836 
Kiggelia  afvicana,  188 
Ki-mo,  1535 
King-Cobra,  247 
Kinetonucleus,    290,     530,    331,    337, 

381,    $82 
Kinnup  Poisoning,  166-7 
Kirghizes,  the,  55 
Kirinagras,  21 16 
Kirudeo,  2110 
Kitajima's  Lachesis  jlavoviridisSerum, 

273 

Klimafieber,  1129 
Klinophilos,   762 
Klossia,   474 
K I  oss  id  la,   474 
Knokkclkoorts,  1244 

148 


2354 


INDEX 


Koch's  Bodies,  490 

Kohlbrugge's  (Hyphomycetic)  theory 

of  Sprue,  1 781 
Kohler,  Tropical,   76,   1981 
Kola  Nut,  177 
Kolamin,  177 
Kombi  Arrow-Poison,   182 
Komlah,  Venomous  Caterpillar,  222 
Konje  Marree,  1260 
Koormat,  235 
Kopts,  the,  47 

Korean  Continued  Fever,  1355 
Koreans,  the,  55 
Koris,  762 
Korsakoff  type  of  Subtertian  Malaria, 

ii75,  H76 
Kosharriddki,  1610 
Kota-wen,  141 6 

Kousso  Flowers  for  Tamiasis,  1753 
Kpwesi  Race,  51 
Krabbea,  605 

grandis,  605 
Kraetze,  2217 
Kraits,  247 
Kra-kra,  2053 
Kreechkrankheit,  1639 
Krempf's  Splenomegaly,  1303,  1306 
Kreotoxismus,  195 
Kru  Race,  51 
Kubisagari,  1982 
Kunteb  Fly,  811 
Kurloff's     Bodies,      432.     434,     457, 

1902 
Kurrakan  (cereal),  1540 
Kurunegala  Fever,  n  29 

Ulcers,  2021 
Kussmaul's  Coma,  1924 

Subtertian      Malaria      resembling, 
1173,  1174 
Kwan's  Fluke,  568,  569,  1752 

Reference,   594 
Kyass  Arrow-Poison,  184 
Kyoto  Fever,  1467 

Laa  La-negulo,  1260 

Laboratories  in  British  Colonies,  29 

Laboratory      work      in       Diagnosis, 

1511-12,  1532 
Laboulbeniales ,  985 
Labyrinth,    Quinine-caused     Hyper- 
emia of,  2013 
Lacerta  agilis,  355 
Lacericz,  Hscmogregarines  of,  437 
Lacertilia,  242,  278 

References,  281 
Lachesis  250 

Venom,  256,  260,  269,  290 
Serum  for,  273 
Species 

anamallensis,  250,  256,  259 
borneensis,  251 


259 


Lachesis,  continued 
Species,  continued 
flavoviridis,  251, 
gramineus 

Venom  of,  Antisera  Ineffective 
for,  272,  273 
lanceolatus,  250,  251,  253,  259 
mutus,  251,  487 
sumatranus,  251 
Lachrymal  Concretions,  2008,  2009 
Sac,    as   source    of    Eye-Infection, 
2002 
Sporotrichosis  of,  2010 
Lacquer-Poison,  191-2,  2157 
Lacquer  Varnish,  action  of,  on  Skin, 

2151 
Lactation,    Prolonged,    Anaemia    due 

to,  1903 
Lacteal  Fever,  1948,  1951,  1953 
Lady  Health  Visitors,  1956,  1959 
Lcslaps,  693 

echidninus,  480,  483,  693 
Lcemopsylla,  859,  869 
cheopis,  869 
cleopatrce,  376 
Lafte,  235 
La  Gale,  2217 
Lagenaria  vulgaris,  190 
Lagocheilascaris,  623,  653,  657 
References,  682 
Species 

minor,  623,  657 
Lagophthalmos,  2006 
Lahooh,  1700 
Lahore  Sore,  378 
Lalangola,  1260 
Lamblia,  466,  1833 
intestinalis,  18 
Lamb's     Anti-Snake 

272-3 
l.amcllibranchia,  890 
Lamus,  767,  768 
geniculatus,  881 
infestans,  882 
niegistus,   388,   390, 

881,  882, 
sordida,  882 
Land  Leeches,  683 

Wind,  the,  81 
Lanfranchi's     Laboratory    Trypano- 

some  Infection,  1259 
Langhan's  Cells  in  Leprosy,  1651 
Lankesterella,  478 
ranarum,  488 
tritonis,  488 
Lankesteria,  471 
Lankoides,  935,  938,  1362,  1406 
ceylonensis,  var.  A  and  B,  938 
gintottensis,  938 
madam pensis,  938 
pyogenes,  735,  938 


Venom     Sera. 


427,  429,   768, 
1283,  1288, 


INDEX 


2355 


Lanolated  Seed-Lymph  for  Vaccina- 
tion, 1493,  1494 
LanthanotidcB,  279 
Lanthanothis  borneensis,  279 
Laos,  the,  54 
Laportea,  2158 

canadensis,  2153 

crenulata,  2158 

stimiihins,  2158 
Lappa  majus,  2152 

officinalis,  2152 
Lapps,  the,  55 
Larrey-Weil  Disease,  1505 
Larva  Migrans,  1639,  2208 
Larva?,    Dipterous,     771,    895,     1631 
passim,  2207-8,  see  also 
Myiasis,  1619 
References,  2221 

in  Ear,  201 1 

in  Eye,  2007 

Herpetomonads  in,  365,  367 
Larvicidal  Fish,  789,  1208-9 
Larvicides,  1208-9 
Larvofilaria,  873,  896 
Laryngeal  Stridor,  Indicative  of  Diph- 
theria, 1 521 
Larynx,     Inflammatory    and    other 
Affections  of,  1875  sqq. 
Lasianthus  flavescens,  1 84 
Lasiosiphon  eriocephalits,  187,  190 

speciosus,  170 
Latah,  1981,  1983 

.Etiology,  1983-4 

Allied  Complaints,  1986 

Climatology,  1983 

Definition,  1983 

History,  1983 

Medico-Legal  Aspect,  1987 

Prognosis,  1987 

Symptomatology,  1984-6 

Synonyms,  1983 

Treatment,  1987 

Varieties,  1986 
Latent      Malaria,      1142,      sec      also 
Malaria 

Plague,  1 41 8,  see  also  Plague 
Lathyrin,  196,  197 
Lathyrismus,  195,  196,  1688 

References,  202 
Lathyrus  aphaca ,  [96 

cicera,  196 

clymenuni,  196 

stitiviis,  196,  198 

tuber  osus,  196 
Latin  synonyms  for  Enteric,  1363 
Latirismo,  196 

Latrines  for  Ankylostomiasis  Prophy- 
laxis,  1772 
Latrodectus,  212 

mactans,  212,  214 

scelio,  212,  214 


Laurer's  Canal,   537,   558,   560,   563, 

574.  575.  581,  582 
Laveran,  Pioneer-founder  of  Tropical 

Medicine,  16,  18 
Laverania,  504,  517,  1219,  1273 
danilewskyi,  513 

malaria,    16,    510,    512,    513,    517, 
889,    1129,    1130     sqq., 
1143,        1145,        1148, 
1152    sqq.,    1160,    1164, 
1165,  1167,  1 1 68,  1179, 
1182,  1201,  1202,  1213, 
1214,  1218,  1221,  1836 
Crescent    Bodies   in,  518,    11 30, 
1201-2 
ranarum,  488 
Laveranic  Dysentery,  1825,  1836 

References,  1863 
Lead- Poisoning,  170,  189 
Lebbre,  1644 

Leberabzess,  Tropischer,  1910 
Lecithin,  no 
Leech-Bite  in  relation  to  Ulcus  tro- 

picum,  etc.,  685,  2182 
Leeches,  683 

Parasites  carried   by,    337,    338, 
365,  388,  389,  394,  395, 
397-  398,  400,  401,  480, 
486,  488 
Jumping,  688 
Marine,  488 
Medicinal,  686 
Water,  683 

Invasion  by,  1880 
Leg(s),  Barbados,  1610 
Cochin,  1 610 
Elephant,  1610 

Elephantiasis  of,  1595,  1597,  1611 
Galle,  1 610 

Purulent  Folliculitis  of,  2027,  2029, 
2036 
References,  2038 
Ulcerating  Nodules  of,  1101 
Ulcerative  Disease  of,  123 
Leger's  Disease,  1309 
Legumes  in  Diet,  105 
LeguminoscB,         Dermatitis-causing, 

2153.  2154.  2159 
Poisons    derived    from,    163,    164, 
167,  172,  178,  181,  184, 
188,  189 
Lehedanpachanai,  1824 
Leishman  Nodules,  2 1 1  > 5 
Leishman-Donovan  Bodies,  1525,  see 

Leishmania 
Leishmania,  20,   358,   359,   360,   361, 
369,    406,     490,     1529, 
*53*.  2035,  2085,  2193 
Insects  Carrying,  23,  375,  376,  377, 

766 
Pathogenicity,  369 


2356 


INDEX 


Leishmania,  continued 
References,  462 
Species 

braziliensis,  2176 
donovani,  20,  21,  23,  269,  370,372, 
378-  379,  763.  766,  883, 
1289,  1290,  1291,  1297, 

1299,  I3°5.  1837.  I9°7. 

2167,  2180 
vax.archibaldi  (Sudan  species), 

369-70,  373 
furunculosa,  378 
infantum,  20,  23,  369,  373,  377-8, 

S83,  1299,  1967 
nilotica,  2172 
tropica,    369,    378,    2165,    2167, 

2171,  2173,  2176,  2186 
var.  americana,  369,  380,  1740, 

2172,  2175,  2176 
var.  braziliensis,  380,  2176 

Leishmania  Infantum  Anaemia,  1299 
Leishmania-like  Bodies,  2019 
Leishmaniases,    1289,  see   also  Kala- 
Azar 
Symptomatology,  2178-9 
Synonyms,  2175 
Treatment,  2179 
Leishmaniasis 

^Etiology,  see  Leishmania  above 
Carriers   and   Reservoirs,    882-3, 

2168 
Climatology,    123,     see    Various 

forms 
Definition,  2175 
Diagnosis,  2179 
References,  1307 
Symptomatology,  2178-9,  and  see 

each  form 
Synonyms,     1289,     1299,    1536, 

1559,  2175 
Treatment,  364,  2179 
American,   Muco-Cutaneous  Naso- 
Oral    (Espundia,    q.v.), 
363,    1741,   2165,   2175, 
2180,  2185 
References,  2199 
Treatment,  28,  1290,  2196 
Cancerosa,  2175 
Canine,  374-5,  377,  1290,  1303 
Dermal     or    Cutaneous     (Oriental 
Sore),  20,  120,  363,  377. 
379,  380,  882,  908,  2035, 
2165,      2167-8,      2171, 

2173,  2180,  2186,  2190 
References,  2197 
Transmission,  2166,  2169-70 
Treatment,  2173-5 
Varieties,  2171-3 

Indian  Oro-Pharyngeal,  2165.  2179 
Lcishmanic  Dysentery,  1825,  1837 
References,  1863 


Lemmings,  915 

Lemon -Juice      in       Bicho,      i  1 871, 

1872 
Lent  Fever,  1362 
Lentigo,  2281 
Lepidophthirius,  759 

macrorhini,  759 
Lepidophyton,  1017,  2065 
Lepidophytosis,  2060 
Lepidoptera,  748 

Infestation  by,  1639,  1640 
Venomous  Species,  218,  222-3 
Reference,  229 
Lepidopterous       Larvae,      Irritating, 
Dermatites      due      to, 
2208 
Lepidoselaga,  817 

lepidota,  817 
Le  Pita,  2059,  2063 
Leporidce,  914 
Lepothrix  (disease),  2101 

Tropical,  2101 
Lepra  Cells,  1651 
Lepra  Italica  Maidica,  1700 

Maculo-Anaesthetica,  1654,  1659 
Tuberculosa,  1654 
Lepre,  La,  1644 
Leproma,  1651 
Lepromata  in  Lungs,  1653 
Leproses,  1706 

Leprosy,  9,  n,  12,  905,  1644,  1701, 
1981,  2117 
iEtiology,  1533.  1647 
Blood  in,  1657 

Causal  Organism,  22,  965, 
1040,  1644,   1645,   1647, 

1653 

Climatology,  120,  122,  123,  124, 
1646 

Complications,  1663 
Ocular,  2006 

Definition,  1644 

Diagnosis,  1663-4 

Differential,  1595,  1664,  2099, 
2230,  2234,  2244,  2252 

History,  1644-6 

Hyperkeratosis,  Non  -  follicular, 
in,  2256 

Hyperpigmentation  in,  2232 

Infection-problems,  Insect  Vec- 
tors, etc.,  732,  813,  S76, 
908,  1356,  1644,  1648 
sqq.,  2215 

Keratoses  of,  2257 

Morbid  Anatomy,   1652-3 

Pathology,  1650-2 

Prognosis,  1664 

Prophylaxis,  1647,  1649,  1666 

References,  1667-8 

Symptomatology,  1653-4 

Synonyms,  1644 


INDEX 


2357 


Leprosy,  continued 
Treatment,  2157 

Chaulmoogra  Oil,  1664,  1665 

Nastin,  1666 

Sodium  Gynocardate,  1665 

Biblical,  10,  1335,  1644 

Maculo-  Anaesthetic,   1654.   1659 

Mixed,  1663 

Nerve,  1659 

Nodular,  1654 

Smooth,  1654,  1659 

Tubercular,  1654 

Ear    Complications    and    Affec- 
tions, 2013 
Eye-affections  in,  1654  sqq.,  2006 
Urine  in,  1659 
Leprotic  Fever,  1515,  1654 

Patches,  Anidrosis  in,  2224 

Ulcers,  2190 
Leptidcs,  773,  814,  823 
Leptis,  823 

scolopacea,  823 

strigosa,  823 
Leptocercous  CercaricB,  559 
Leptocimex,  766 

boneti,  766,  882 
Leptoconops,  802,  803 

bezzii,  803 

inter ruptus,  803 

irritans,  803 

kertiszi,  803 

laiwce,  803 

stygius,  803 

torrens,  803 
Leptocoris  trivittatus,  372 
Leptodera,  623,  627,  628 

annulata,  245 

intestinalis,  62S 

niellyi,  627 

pellio,  623,  628 
Reference,  681 
Leptomitus,  2008 
Leptomonas,  358,  361 

biitschlii,  359 

drosophilce,  359 

musca-domesticcB,  365 
Leptospira,  n.g.,  1 17-  !  5°6 

icterohesmorrhagica,    \  \j 
Lcptotheca,  529,  1506 
Leptothrix,   1068,   1748,    2101 

buccalis  maxima.   [068 

fili  for  mis,,  1068 

innominata,  1068 

maxima,  1068 

ocitlnrum,    1066 

placoides,  1068 

v.iccmosa,  1068 
Leptus  akamushi,  1352 

autwnnalis,  2213 
Leptus  stage  of  unknown  Trombidium 
in  N.  Queensland,  2214 


Lessertia  annularis,  189 
Letargia  dei  Negri,  1260 
Leucanthemum  vulgare,  2152,  2153 
Leucocytes,  1897,  1898 

Puzzles  connected  with,  1902 
Leucocythemia,  1307,  1903 
Leucocytosis,  1900 
Leucocytozoon,  358,  431 
Classification,  477 
Species 

berestneffi,  435 
canis,  483 
caulleryi,  435 
danilewskyi,  432 
funambuli,  486 
lebceufi,  435 
lovati,  431,  432,  435 
macleani,  435 
majoris,  435 
mansoni,  435 
marchouxi,  435 
martini,  435 
muris,  483 
neavi,  435 

piroplasmoides,  360,  1076 
sabrazesi,  435 
sakharoffi,  435 
sm  it  hi,  435 
toddi,  435 
ziemanni,  431,  43 2 
Leucoderma,  85,  2222,  2227 
^Etiology,  2228 
Climatology,  123,  124,  2229 
Differential    Diagnosis,    2077, 

2099,  2230 
Pathology,  2228, 
Prognosis,  2230 
Symptomatology,  2228-9 
Synonyms,  2227 
Treatment,  2230 
'  Varieties,  2229-30 
Congenital,  2230 

Diffuse,  in  relation  to  Natives  as 
Employees,  131 
Leucodermic  Patches,  1664 
Leuconychia,  2283 
Punctata,  2283 
Striata,  2283 
Totalis,  2283 
Leucopathia,  Acquired,  2227 

Congenital,  2230 
Leucopenia,  1899 
Leucophrys  coli,  547 

Lingual,  1746,  2283 
Leucoplakia,  1741 
Leukaemia,  151 6,  1895,  1900,  1903 
Differential      Diagnosis,      1305, 
1525, 1529, 1531 
Lymphatic,  1903 

Spleno-medullary,      1303,        1903. 
1905 


2358 


INDEX 


Leukasmus,  Acquired,  2227 

Congenital,  2230 
Lewisonella  {Trypanosoma),  401,  402, 
403 
lewisi,  402,  403 
Leydenia  gemmipara,  326,  327 
Lice   (Louse),  see  also  Hcematopinns, 
Pediculi,Phthirius,Poly- 
plax,  etc.,  542,  608,  751, 
752  sqq.,  895 
Bites,  218 

Destruction  of,  9,  1338  sqq.,  1503 

Diseases   and    Parasites    carried 

by,  30,  442,  443,  479, 

757.   897,   917,  920, 

1308,  1309,  1326,  1329, 

I33i.  1332,  1423.  1527. 
1650 

Biting  (Mallophaga,  q.v.),  749 

Crab,  757 

Dog,  608 

Plant-infesting,  761 

Pubic,  757 

Sucking  [Anoplura,  q.v.),  749 

Wall,  763 
Lichen,  2264,  2272 

Acuminatus,  1496 

Convex,  1497,  2247,  2251 
References,  2263 

Miliar  Pruriginosus,  2225 

Nitidis,  2273 

Pilaris  Convex,  2251 

Planus,  2249,  2257,  2264,  2272 

Scrofulosum,  2277 

Spinulosus,  2272,  2273 

Tropicus,  2225 

Urticatus,  2217,  2267 
Lichen  Vaccine,  1496,  1516 
Lichenification,  2252 
Lichtheimia,  974,  1886,  1891 

corymbifera,  974,  976,  201 1 

ramosa,  974,  201 1 
Life  Assurance,  131 
Life  of  Europeans  in  the  Tropics  in 
relation  to  Enteric,  1373 
Life-Expectation  in  Tropical  Natives, 

133 
Life,  Tropical,  Fitness  for,  127 

References,  134 
Ligation  for  Poisoned-Arrow  Wounds, 

181 
Light,  as  Causing  Disease,  88 

Eye-Injuries  from,  2004 

Tropical,  86 
Light-Reflex,    loss    of,    in    Sleeping 

Sickness,  2006 
Lightning-Stroke,  142,  146 
Ligula  mansoni,  606 
LigulincB,  601,  604 

Reference,  6ig 
Liliacea,  163,  164,  169,  191 


Liliwa,  1604 
Limacodidce,  2208,  2221 
Limatince,  790,  801 
Limatus,  801 
Limax,  322 

agrestis,  355 

amcebcB,  322 
Limncsa,  892,  894 

humilis,  892 

oithonensis,   892 

stagnalis,   892 

truncatula,  892 

viator,  892 
Limnceidce,  892 
Limnatis,  683,  686 
Limnobdella,  686,  687 

australis,  687 

grandis,  687 

mexicana,  687 
Limosina  punctipennis,  898,  900 
Linacece,  2153 

Linear  Whitening  of  Nails,  2283 
Lingua  Nigra,  1061,  1074 
Lingual  Affections,  1061,  1074,  1746, 

2883 
Linguatula,  733 

proboscidea,  733 

quadriunicinata,  738 

serrata,  733,  1881 

tcsniodes,  733 
Linguatule  monilijorme,  736 
Linguatuliasis,  1881 
Lingiiatulida,  690,  732 

References,  742 

Species 

armillata,  734 
constricta,  734 
Linognathincs,  759 
Linognathus,  759 
Linum  usitatissimum,  2153 
Lions    and    other    Felidce,    Trauma- 
tisms due  to,  148 
Liorhynchus,  630 
LiotheidcB,  751 
Liparidcs,  222,  2208 
Lipognatha,  752 
Lipoids,  96,  97,  107,  no 
Lipomata,  123 

of  Ear,  2010,  2247,  2252 

of  Porters,  2247,  2253 
Lipomatosis,     Subcutaneous,    Nodu- 
lar, 2247,  2253 
Lipoptena,  855 
Lips,  Affections  and  Diseases  of,  2284 

Cancer  of,  1741 
Pseudo-Colloid  of,   1746,  2284 

Seasonal  Recurrent  Ulceration   of, 
1746,   2284 
l.ipitvus  bacillus,  750 
Lithium  Antimonyl  Tartrate,  28 
Lithobiidce,  740 


INDEX 


2359 


Lithobius,  740 
fortificatus,  740,  1641,  1881 
melanops,  740,  1641,  1881 
Little  Fever,  1363 
Little  House-Fly,  904 
Liver,  see  also  Hepatic 

Acute    Yellow    Atrophy   of,    1224, 

1507.  I5°8,  1906 
Cirrhosis  of,  1587,  1906 
Biliary,  Infantile,  1906 

Reference,  191 7 
Malarial,  1906-7 
Post-Malarial,  11 84 
Coccidium  of,  in  Man,  476-7 
Congestion  of,  1906,  1908 
Diseases  of,  1906 
Climatology,  124 
References,   191 8 
Enlargement  of,  1526,  1659 
Malarial,  1153,  1155,  H5<» 
Growths  on,  Malignant,  etc.,  1907 
Hyperaemia  of,  1908 
Inflammation  of,  1091,  1832,  1906, 

1909,  1914 
Necrotic  Areas  on,  1076 
Protozoal  Parasites  in,  1907 
Rupture  of,  Traumatic,  1907 
in  Schistosomiasis,  590 

Reference,  191 8 
Syphilitic  Gumma  of,  191 4 
Tropical,  1525,  1906,  1908 
Liver    Abscess    Amoebic    and    other, 
18,   122,  287,  317,  321, 
335.   1063.    1064.    "86, 
1521,  1525,  1834,  1836, 
1875,  1893,  1907,  1908, 
1910,2139 
Liver  Fluke,  557,  565,  1752,   see  also 

Fasciola  hepatica 
Liverpool   School  of  Tropical   Medi- 
cine, 20,  29 
Living  Skeleton  Disease,  1924 
Lizard-Bite,  12 
Lizards  as  Fly-catchers,  908 

Parasites   of,    353,    355,    401,    480, 

485,  487-8,  516 
Venomous,  278-9 
Loa,  623,  645 
Loascece,  2153 

Loa  loa,  285,  623,  645,  816,  820,  821, 
896,  1972,  1973,  2007 
References,  681 
Loa  loa  Dermatitis,  2219 
Lobelia  nicotiancefolia ,  190 
Lobosa,  298 

Lobule  of  Ear,  Deformities  of,  2010 
Fibromata  of,  2011 
Lipoma  of,  2010 
in  Tubercular  Leprosy,  2013 
Local  Winds,  81 
Locomotor  Ataxy,  1088,  1981 


Locomotory  System  in  Framboesia, 

1552 
Locust-Excreta  in  Water,  1862 
Locust-Poisoning,  191 
Loempoe,  1671 

Loeschia  {see  also  Amoeba  and  Enta- 
moeba),  285,    298,    300, 
301,   307,    316-17,    355, 
883,   1273,   1777,   1827 
References,  328 
Species 

in  Animals,  List  of,  321 
Classified  by  Habitat,  301-3 
Doubtful,  318-20 
brasiliensis,  302,  320 
buccalis,  302 
biitschli,  302,  320 
cobaycB,   321 

coli,  288,  292,  301,  302,  303,  306, 
3°7.  310.  312,  3J8,  320, 
321,    323,    1826,    1832, 
1833,  1945 
dentalis,   302 
dysenteries  europece,  302 
enter ica,  321 
fecalis,  321 
galloparvcB,  321 

gingivalis,  302,  303,  317,  1740 
hartmanni,  302,  319 
hartulisi,  303 

histolytica,  287,  288,  302,  303, 
306,  307,  308,  323,  476, 
877,  1184,  1826,  1S27, 
1831,  1832,  1833,  1907, 
1910,  1931,  1932,  1933, 

1944.  *945 
Nomenclature,  308 
Recent  Work  on,  310  sqq. 

hominis,  303 

Nomenclature,  308 

intestinalis,  321 

maxillaris,  302 

minuta,  302,   303,  312,   316,  319 

minutissima,  302,  320 

miurai,   303 

mortinatalium,  302,  320 

muris,  304,  321 

nana,  302 

nipponica,  302,  319 

nuttalli,  308,  321,  1910 

phagocytoides,  319 

pultnonalis,  302 

ranarum,  313,  321 

tennis,  320 

tetragena,  302,   1826 

tropicalis,  302.  313 

undulans,  302,  319,  355 

urogenitals,   302 
iamsi,  302,  320 
LoeschicB,  1910 
Loeschial  Dysentery,  287,  1825 


2360 


INDEX 


Loeschiasis,  287,  1825 

Loganiaceez,   163,   164,   168,   178,   181, 

184,   186,  2153 
Loiasis,  1967,  1971,  1972 
Loliin,  198 
Loliismus,  195,  198 

References,  202 
Lolium  temulentum,  195,  197,  198 
Lombardische  Aussatz,  1700 
London  School  of  Tropical  Medicine, 

29 
Lophocelomyia,  792 
Lophocet caries,  558 
Lophophyton,  989,  1014 

gallince,  1014 
Loss   of    Blood   due  to   Leech-Bites, 
683  sqq. 

of  Taste,  Post-Malarial,  11 84 
Lota,  2093 

Louse,  see  Lice,  above 
Louse-Group    of    Relapsing    Fevers, 

918,   1308 
Lousing  as  Typhus  Prophylaxis,  1338 

sqq. 
Low-Castellani's  Symptom,  1273 
Low-Country      Morning      Diarrhoea, 

1780,  1796 
Low  Fever,  1363 
Anaemic,  1470 
Irregular,  .1363 

Heat  Fever,  1530 

Intermittent  Fever,  1530 
Non-Malarial,  1464-5 

Protein  Dietaries,  107,  119 
Loxaspis,  762,  766 

barboris,  766 

mirandus,  766 

seminiteus,  766 
Luargol,  28 
Lucilia,  307,  365,  832,  848,  1632 

argyrocephala,  1632 

ccesar,  848,  900,  1626,  1629 

hominivorax,  847,  1625 

macellaria,  847 

nobilis,  848,  1626 

vegina,  848,  1629 

serenissima,  397 

sericata,  848,  1639 
Ludwig's  Angina,  1949 
Ludyl,  27-8 
Lues,  1416 
Lumbricus  canis,  655 
Lumpy-jaw  of  Cattle,  2130 
Lunacy,  1081,  see  also  Insanity 
Lunatics,  Chronic  Eczema  of,  1729 

Pellagra  in,  1729 
Lund's  Larva,  850,  1637 
Lungs,    Affections   of,    see   also   Pul- 
monary 

Abscess  of,  335,  1949 

Amoebae  in,  320 


Lungs,  continued 

Aspergillosis  of,  1031,  2008 
Diseases  of,  1528 
Gangrene  of,  1949 
Inflammatory  and  other  Affections 

of,  1875,  1892 
Lepromata  in,  1653 
Mucormycosis  of,  975,  976-7 
Mycosis  of,  974 
Pseudo-Granulomata  of,  1076 
Symptoms   in,    indicative   of  Res- 
piratory Disorders,  1521 
Tcenia  echinococcus  in,  1907 
Luohai  Race,  54 
Lupani  tono,  1535 
Lupus,  Climatology,  123 

Differential  Diagnosis,  2195,  2196 
Endemicus,  2165 
Erythematosus,  2277,  2278 
Vulgaris,  2277 
Lycopsylla,  865 
Lycosa  singoriensis,  212 
Venom,  213 
tarantula,  213 
Venom,  213,  215 
Lycosides,  212 

Venom  of,  213 
Lyctocoris,  766,  767 
campestris,  763,  767 
hospes,  370 
militaris,  372 
Lymph,  Diarrhoea,  1608,  1610 
Extravasations,  Filarial,  1608 
Gland    Enlargement,    1523,    1529, 
1532,       1551-2,       1587. 
2253 
Scrotum,  639,  1596,  1601,  1605 
Filarial,  1595,  1596,  1601,  1605 
Lymphadenitis,  226 

Filarial,  1523,  1595,  1964 
Lymphangiectasis,      Filarial,      1603, 

1605 
Lymphangiomata,  2273 
Lymphangitis,  226,  552,  631 
Equine,  1072 
Filarial.  1595,  1604 
Gummatous,  11 18,  11 24 
Lymphatic  Ascites,  1608 

Gland,  Varicose,  of  Filarial  origin, 
1595.  1599.  1601,  1603, 
1608 
System,    Derangements    of.    isiO. 
1522 
Diseases  of,  1961 
References,  1966 
Varix,   Filarial,    1595,    1599,    160s, 
1605 
Lymphocele,  1608,  1610 
Lymphococcus ,  1600 
Lymphocytes,  1897 
Lymphocytosis,  1900 


INDEX 


2361 


Lymphocytozoon  cobaye,  434,  455 
Lympho-Fibromatosis,  2262 
Lyinphohesmatocytozoon  parvum,  498 
Lymphosporidium  eqiti,  1076 
Lymphuria,  1608 
Lynch  ia,  525,  855 

Lyozoon  atrophicans,  539,  541,  2001 
Lyperosia,  832,  837 

alcis,  837 

exigua,  837 

flavoherta,  837 

it  titans.  837 

longipalpis,  837 

minuta,  837 

pallidipes,  837 

potans,  837 

punctigera,  837 

ritfipalpis,  837 

schillingsi,  837 

tliironxi,  837 

tit  Mans,  837 
Lytta  vesicatoria,  172 

Mabinzu  (larva),  850 
Machoira,  235 

M.u  ics  Perniciosa,  1919,  1924 
McConnell's  Fluke,  577 
Macrobdella,  686,  687 

sestertia,  687 
jl/acro-,  awd  micro-conidia,  969 
Macrodactylism,  1959 
Macrogametocyte,  294 
Macrogasier  platypus,  732 
MacronemcB,  987 
Macronucleus,  290 
Macropsylla,  865,  866 

hercules,  866 
Macrostoma,   349 
caulleryi,  349 
mesnili,   356 
Maculae,  Mongolian,  2237 
Macular  Fever  of  Tunisia,  1467 
Mac  ulo-  Anaesthetic     Leprosv,     1654, 

1659 
Madhumeha,  1924 

Madura  Foot,  1062,  1123,  1595,  2110, 
2111,  2112,  2148,  2149, 
2223 
Madurella,  1101,  1104,  1105,  2041 
Dermatomycoses  due  to,  2041 
Species 

bovoi,  2041,  2 1 21 

mycetomi,      1104,      1105,      1106, 

2041,  2121,  2125 
tozeuri,    1105,   1106,  2041,   2121, 
Madurese,  the,  55 
Maduromycoses,  21 10,  2112,  21 17 
iEtiology,     1 104,    1 105,    passim, 

'2120 
Botanical  and  Zoological  Distri- 
bution, 2120 


Maduromycoses,  continued 

Climatology,  1104,  1105,  2118 
Definition,  21 12 
Diagnosis,  2129 
Grains  in,  2120 
History,  21 12  sqq. 
Pathology,  2123 
Prognosis,  2129 
Prophylaxis,  2130 
References,  2150 
Symptomatology,  2128 
Treatment,  2129 
Varieties,  2120 
Black 

.Etiology,    noi,    1 104,    1 106, 
1114,  1116,  1123,  2112, 
2113,  2120 
Morbid  Anatomy,  2124 
African,  1116,  2118,  2120,   2121 
American,  2120,  2122 
Asian,  2120,  2222 
European,  2120 
Red,  2114,  2120,  2123 
White  or  Yellow,  2114,  2119,  2120, 
2122 
.Etiology,  1101,  1122 
African,  2120,  2122 
Asian,  2120,  2123 
European,  2120,   2122 
Vlagab.ua,  the,  56 
Magberi,  173 

Magie,  in  Medicine,  3  sqq.,  51 
Magnesium  Sulphate,  170 
MagnoliacecB,   174 
Magyar  Race,  54,  55 
Mahamari,  141 6 
Ma'idismus,  1700 
Maize,  95,  105 

Fungi  affecting,  171 2-1 3 
Majun,  176 
Mai  d' Arouse,  1704 
d'Asturias,  1700 
de  Bocha,  1745 
de  Caderas,  20,  391,  414 
ilr  0  1  venue,  1610 
de  Chicot,  1536 
de  Coeur,  1761 
du  Coit,  411 
d'Engasgo,  1750 
del  Higado,    1700,    1704 
de  Meleda,  2259 

d'Estomac  (Ankylostomiasis),  1761 
d'Estomac  (Geophagy),  1749 
del  Padrone,  1700,  1701 
del  Pinto,  2093 
de  los  Pintos,  2093 
de  la  Rosa,  1700,  1701,  1703,  1704 
Rosso,  1700 

de  Saint  Amans,  1700,  1704 
de    Sainte    Rose,    or    Rosa,    1700, 
1704 


2362 


INDEX 


Mai  des  Saintes  Mains,  1700 

della  Secca,  1254 

del  Sole,  1700 

della  Spienza,  1700 

della  Vipera,   1700 
Malabar  Swellings,  11 81 
Malacca,      Arrow-Poisons      of,     184, 

185 
Rat-Poison  of,  191 
Malache,  2159 

hirsuta,  2153,  2159 
Malacobothrii,  560 
Malacodermata,  2208 
Malacophycece,   1071 
Malacotylea,  560 
Malacozoa,  889 
Maladie(s) 

de  Ballingall,  21 10 
de  Depigmentation,  2227 
Filariennes,  1595 
de  Gilles  de  la  Tourette,  1986 
des  Plongeurs,  204 
de  Siam,  1229 
du  Sommeil,  1260 
des  Sucreries,  1671 
de  la  Teste,  1700,  1705, 
de  Weil,  1505 
Malaria,  9,   25,   131,    1129,    1863,  see 
also     Malarial     Fevers, 
and  Each  Form  of  Ma- 
laria under  Name,  below 
.Etiology,  285,  876,  1129,   1130, 
1131,  1132,  1202-3 
Exciting  Causes,  1132  sqq. 
Predisposing  Causes, 1 1 32, 1142 
Air-Temperature    as   Factor    in, 

1138-9,  1203 

Amyloid  Changes  in,  1146,  1156 

Anaemia    in,    and    after,     1150, 

1151-2,      1156,      1164, 

1169,  1903 

Blood-Conditions  in,  1144,  1148, 

1899,  1900 
Bone-Marrow    in,     1153,     1154. 

1155.  "56,  1905 
in  Children 

Convulsive  type,  11 75 
Prognosis,  1187 
Quinine-Dosage  for,  11 91,  1192 
Chills  in,  1147,  1 148 
Climatology,  120,  122,   123,  124. 
884    sqq.,    1138,    1139, 
1143 
Complicating  other  Diseases,  149, 
1 169,  1388-9,  1687,  1836 
Complications,  1169,  1184,  1187, 
1718,  1727,  1836,  1890 
Aural,  2007,  2013 
Ocular,  1 181,  2004,  2005,  2007 
Convalescence,     Treatment     in, 


Malaria,  continued 

Diagnosis,  1165,  1185,  1531 
Differential, 

of  each  Form,  11 65 
Methods,  11 86 
Signs,  1 1 85-6 
from  other  Diseases,  202,  1186, 
1250,  1252,  1253,  1257, 
1288,  1302,  1303,   1307, 
1312,  1313,  1317,  1337, 

1395.  i429,  1445.  H65. 
1485,  1498,  1505,  1513, 
1516,  1524,  1575-6, 
1767,  1875,  1885,  1914, 

1953.  x99° 
Double  Infection  in,  11 54 
Economics  of,  1203 
Erythemas  associated  with,  2266 
Erythrocytes    in,     1144,     114S, 

1149 
Erythromelalgia  due  to,  1990 
Endemic  Index,  1141-2 
Fever  of,  1 133"7.  *593 
Forms,    1156   sqq,   see  also  Each 

Form 
Relative    Seasonal    Incidence, 

1138 
Haemoglobin,  in,  1151 
Hamiozoin-Production  in,  11 30, 

1134.  "45 
Heart-Block  due  to,  1904 
Herpes  Facialis  Febrilis  in,  2269 
History,  18-19 
Hyperidrosis  in,  2222 
Hyperparasitism  in  relation  to, 

.    287 
Immunity  in,  11 34,  1142 
Incidence,    see  also  Climatology 
above 
Age,  1131,  W40,  1142,  1187 
Locality,     n  30,     1131,     1142, 

1187 
Occupation,  1139,  11 42 
Race,  1134,  1140,  1142,  1187 
Season,    10,    1129,1138,    1142 
et  alibi 
Incubation  Periods,  1133 
Infection,  11 33 
Factors  of,  11 32 
Process,  506,  889,  1133 
Rate,  Estimation  of,  11 40 
Sources    11 31.    11 40,    see   also 
Insects,   Parasites,   and 
Reservoirs 
Insects     Spreading     (Anop'heles, 
Hexapoda,    Mosquitoes, 
etc.,  q.v.),  16-17,   18-19. 
23.  285,  505,  743,  747 
800,  873,  876,  883  sqq.. 
888,    1129,    1131,    1132, 
1137  sqq.  passim 


INDEX 


2363 


Malaria,  continued 

Jaundice  rare  in,  151 9 
Knowledge  on,  of  Celsus,  11 
Leucocytes  in,  11 50-1 
Leukaemia  in,  1169 
Liver  Cirrhosis  due  to,  1906-7 
Enlargement  in,    1153,    1155, 
1 1 56 
Meteorology      in      relation     to, 
1138-9,  1143,1144,  1203 
Morbid  Anatomy,  11 32  sqq. 
Onset,  1 135,  1527 
Mortality,  1 187 

Parasites  associated  with,  16,  18, 
1129,    1130,    1132    sqq., 
1148,    1156   sqq.,    1161, 
1 164,     1908,     see     also 
Cruz's,       1132,       1 13  7, 
Hcemamceba       immacu- 
lata,    1 1 37,    Hcsmamce- 
ba   prcscox,    1 1 37,    La- 
loir's,    1132,    Laverania 
malar  ice,      517,      1129, 
Plasmodium      malarice, 
1 1 29;    Plasmodium    vi- 
vax,  510,  512,  1129 
Definitive  Hosts,  289,  883 
Development  and  Multiplica- 
tion, 289 
Differences    between,    in    Ac- 
tion, etc.,  1134,  II35"7. 
"44.  "45 
Differential  Characters,  518 
Effect  on,  of  Quinine,  1201-2 
Incubation,  11 33 
Infection,  1133  , 
Insect    Vectors,     see    Insects 

Spreading,  above 
Lesions  due  to,  11 52  sqq. 
Life-Cycle,  115,  116 
Life-History,  in  relation  to  the 

Fever,  11 33  sqq. 
Toxins     produced     by,      295, 
1133,  1135,  1144,  1145, 
1146,  1147-8 
Typical  Plasmodidce  (q.v.),  505 
Pathology,  11 44 

Chemical,  n  46-8 
Pigmentation    in,     n  30,     11 34, 
1145,  1180,  1181,  1182, 

i53i 
in  Pregnancy 
Prognosis,  11 87 
Quinine  in,  1191,  1201 
Prognosis,  1187 

Prophylaxis.      1  M>.      1J3,      1138, 
1202,   [603,   1705 
References,  121 1 
Antimosquito,  1205  sqq. 
Educational,  1203-4 
Quinine,  1204-5 


Malaria,  contiuned 

Purpura  Eruption  in,  2267 
Rash  in,  1256,  1513,  1514 
Recurrences,  507 

Chill  as  provoking,  11 83 
Relapses,  507,  n 36,  1143,  n 46, 
1156,   1159,   1163,   1182 
Treatment,  n  90-1 
Reservoirs 

Man,  1131,  1132,  1140  sqq. 

Native  Children,  1131,  1140 
Mosquitoes,  n 39,  n 40 
Sequelae,  n  84 
Spleen- Rate,  1141-2 
Splenic     Puncture,     Diagnostic, 

1186 
Splenomegaly,  1141,   1 152,  n  53, 
IX55>  1 1 56,  1162,  1167, 
1169,  1182,  1185,  1525, 
1531,  1904 
Suprarenal    Affections    due    to, 

1923 
Symptoms,     1 1 32,     1 134,     1 1 47, 
1148,  1150,  1152,  1153, 
1156,  1158  sqq.,  1182 
in  Convalescence,  1147 
Prodromal,  1133 
and  Special  Conditions,  Treat- 
ment of,  1197-8 
Synonyms,  11 29 
Treatment,  All  forms,  11 88 
in  Acute  Attack,  n  88-9 
Baccelli's  Mixture  in,  11 90 
Climatic,  1143 
Dietetic,  n  97 
Drugs    other    than     Quinine, 

1202 
During     Course      of      Fever, 

1189-90 
During  Relapses,  11 90-1 
Essential,  n  88 
Quinine,      25-6,      506,      11 31, 

118S,  1192,  1196 
Specific,  by  Quinine,  n 88 
Symptomatic,    1196 
Tartar  Emetic,  1202 

References,   121 2 
Theoretical  Considerations  on, 
1199 
Wassennan  Reaction,  in  1152 
Acute,  1145,  1140,  1152 

Attacking  Suprarenals,   1526 

Diet  in,  11 97 

Differential    Diagnosis,    1296, 

[526 
Morbid  Anatomy,   1152 
Treatment,  During  and  After, 
Attacks,     1 1 88,      1189, 
1 190 
Sympi omatii  .  1196 
Tertian,  1161 


2364 


INDEX 


Malaria,  continued 

Avian,  Parasite  of,  513 
Chronic,  1129,  1130,  1182 

Advanced  Condition  of,  1146, 

1155-6,  1182 
etiology,  1 1 82 
in  relation  to  Blackwater  Fever, 

1219 
Blood-Changes,  .11 51 
Chloasma  in,   2232 
Diagnosis,  1182,  1525,  1531 

Differential,  11 82,  1305 
Exacerbation    of,     Splenome- 
galy in,  1525 
Lesions  in,  11 52,  1153  sqq. 
Leucopenia  in,  1151 
Morbid  Anatomy,   1152,  1155 
Pigmentation  in,    11 80,    11 82, 

2232 
Sequelae,  11 55 
Symptomatology,   11 82 
Treatment,  1196,  1199 
Quartan,  11 57 
Tertian,  1161 
Comatose   type,    other   than   Sub- 
tertian,  1 1 82 
Congenital,  11 34,  1142, 

Reference,   121 1 
Convulsive  Type,  in  Children,  n  75 
Endemic 

Areas  and  Regions,  30 
Investigation  of,   11 41 
Latent,     507,     1142,    11 46,     11 56, 
1183 
^Etiology,  1 1 42 
Activation  of,  1 148-9,  11 86 
Pathology  of,  11 33,  n 42 
References,  1211 
Malignant 

Canine  [Canine  Babesiasis],    493 
Human,  see  Subtertian,  below 
Masked,    11 68,    see    also      Latent, 

above 
Mixed  Infections,  1160,  1164,  1165, 

1168 
Pernicious,  1129,  1150,  1171,  1182 
.Etiology,  1 1 82 
Diagnosis,  1520,  1522 

Differential,  1456 
Prognosis,  11 87 
References,  1211 
Treatment,  n 89 

Precautions  advised,  1198 
by  Quinine,  11 89,  n  93 
Quartan,  10,   12,  1129,   1134,  1157 
/Etiology,  1 157 
Climatology,  124 
Diagnosis,  1185,  1528,  1530 
Incubation  Period,  n 33 

Insect  Carriers,  884,  886  sqq. 
Lesions,  11 52 


Malaria,  continued 
Quartan,  continued 

Parasites  of,   513,   1129,   1130, 

"37.  "45-  II49.  1152, 
see      also     Plasmodium 
malaria 
Prognosis,  11 87 
Relapses  in,  1183 
Treatment,  11 88,  1193 
Acute,  1 157 
Chronic,  11 57,  1160 
Double,  11,  1 157,  1160 
Irregular    Subcontinuous,    1137, 

1160 
Mixed  Infections,  1157,  1160 
Simple,  1 1 57 
Subintrant,  11 60 
Triple,  or  Quotidian,  11 57,  1160 
Quotidian,  10,  1137 
^Etiology,   1 183 
Diagnosis,  1528,  1530 
Parasite  of,  1132,  11 37 
Prognosis,   11 87 
Reinfection  in,  1183 
Remittent    or    Continuous,     11 60, 

1167 
Subtertian,  11,1129,1130, 1164,1468 
^Etiology,  1 1 64 
Blood  in,  n  45,  1149 
Climatology,   124 
Diagnosis,  11S5,  1528,  1530, 

Differential,  1238 
Erythrocytes  in,   1145,  1149 
Incubation  Period,  1133 
Insect  Carriers,  884  sqq. 
Morbid  Anatomy,  1152,  1155 
Parasite  of,   517,   11 29,    11 30, 
"33.  "37.  "45.  "46, 
1 164,    see    also    Laver- 
ania  malaria,  517 
Lesions  due  to,  11 53  s^.,1908 
Prognosis,  1187 
Symptomatology,   n 34,   1137. 

"53  saa-<   "66  sqq. 
Treatment,  11 88-91,  11 93 
Atypical,  11 65,  1168 

Neuralgias,  ovaritic,  of,  11  So, 

1 184 
in   relation  to   Pseudocholcra, 

1820 
Symptoms,  11 70 
Syndromes  with  Localisation, 
1168,  1175 
Circulatory    System,     1 1 75, 

1179 
Cutaneous,  n 75,  1181 
Digestive  System,  11 75, 1177 
Ductless  Glands,  1175.  1180 
Nervous  System,  1175 
Organs    of    Special    Sense, 
"75,  1181 


INDEX 


236; 


Malaria;  continued 
Subtertian,  continued 

Syndromes     with     Localisation, 
continued 
Respiratory   System,    1175, 

1178 
Urogenital     System,     11 75, 
1180 
Syndromes  without   Localisa- 
tion, 1 168,  1169 
With      .Marked      Fever     on 
First  Examination,  1170 
Hyperpyrexial  Fever, 

1170-1 
Syndromes     Not    Resem- 
bling   Specific    Fevers, 
1170,  1173-5 
Syndromes  Resembling  a 
Specific  Fever,  1190, 
1191-3 
Cerebro  -  Spinal  -  like, 

1  171.H72 
Malta-Fever-like,  1171 
Scarlet  Fever-like,  n  71 

1173 
Sleeping-  Sickness -like, 

1 1 72 
Typhoid-like,  11 71 
Typhus-like,  1171,  1172 
\V<  dPs  Disease-like,  1 1 71 , 

1172 
Yellow- Fever-like,  1 1 71 , 
1172 
Without    Marked  Fever   on 
First  Examination, 

1169- 70 
Algide  type,  11 69,  1170 
Anaemic  type,  1 1 69 
Haemorrhagic    Non-Fe- 
brile type,  1 1 69 
Mental  types,  II69-70 
Pseudo-Alcoholic    type, 

1169,   1170 
Yrello\v- Fever-like,  11  86 
Typical  Fevers,  1165 
Bilious  Remittent,  1165,  1168 
Double,  1165,  1167 
Irregul  ir,  n  65,  1167 
Mixed  [nfe(  tions,  1165,  1168 
Remittent,    1  [65,  1167 
Simple.   1165 
Suprarenal  form,    [296    2203 
Tertian 

Benign,  n,  12,  11  29,  ",i°.  H61 

.Etiology,    [l6l 
Blood  m    1 1 49 
Diagnosis,  1  [85,  1528,  1530 
Erythrocytes  in,  1145,  114Q 

In.  nil  itionl'erio.l,  1133,1161 
Insect  Carriers,  884  sqq. 
Morbid  \n/tomy,  1152, 115? 


Malaria,  continued 
Tertian,  continued 
Benign,  continued 

Parasite  of,  510,  11 29,  11 30, 
1137,     1145,     see     also 
Plasmodium  vivax 
Lesions  due  to,  1550 
Prognosis,  11 87 
Post-War  Cases,  in  England, 

1138 
Relapses  in,  11 83 
Treatment,  11 88 
Acute,  1 1 61 
Chronic,  1161,  1164 
Double   or     Quotidian,    u6r, 

1163 
Irregular  Subcontinuous,  1161, 

1164 
Mixed  Infections,  1161,  1164 
Simple,   1 161 
Malignant,  see  Subtertian,  above 
Tropical,  n  64 
Malarial      Amaurosis,      1181,      2004, 
2005,  2007 
Blood-Serum,  Toxic,  203 
Cachexia,   n  46,   1155,  11 56,   11 82, 
1297,  16S8 
Treatment,  n  99 
Chyluria,  1934 
Ear- Affections,  1181 
Erythemata,  11 81 
Eye- Affections,  11 81,  2205 
Fever  (syn.  for  Typhoid),  1366 
Fever(s),  12, 18-19,  22,25,  873.  1129, 
1153,    1211,  1517,  1526, 
2180,  see  also  Malaria 
.Etiology,  1 1 29 
Anaemia,  1214 

Blood  Parasites  of,  1129,  1132 
Case  Reduction,  1209,  1210 
Classification,  1156 
Complications,  1184 
Definition,  11 29 
i  M  i  gnosis,  1 51 7,  1526 

Differential,  19,  22,  1914 
Hisrtory,  11 30 
Immunity,   1 134 
Insect  Vectors,  see  Anopheles, 

etc.,  87  3 
\. uiifih  luture,   C129 
Parasites  of,  1129 
Pathology,  1 1  1  1 

References,  1  - 1  1 
Prophylaxis,   1138 
References,  1210-12 
Reservoirs,  1 131 
Synonyms,  1129 
Treatment,  25 
Acute,  1 1 45 
Atypical,  11  so 
Bilious  Remittent,  1165,  1168 


2366 


INDEX 


Malaria,  continued 
Fever(s),  continued 

Canine,  493 

Chronic,  11 30 

Hemorrhagic,  1216 

Pernicious,  11 82 

Quartan,   1528 

Quotidian,  1528 

Subtertian,  n 29 

Tertian,  11 29,  see  also  Malaria 
Hemoglobinuria,  1168,  1180,  1213, 
1216,  1217,  1218,  1219, 
1220,  1225 

Diagnosis,  1522 
Haemoglobinuric  Fever,  1216 
Infections,  Old,   Re-awakening  of, 

I5I3 

Intermittent  Otalgia,  2013 

Jaundice,  1507,  1508,  1510 

Mimicry,  1165,  1168 

Nephritis,  1926 

Neuritis,  11 80,  11 84 

(Edema,  Patchy,  11 81 

Polyneuritis,  11 84 

Pneumonia,  1184 

Pseudo-Addison's  Disease,  2233 

Pseudocholera,  1820,  1821 

Reinfections,  11 83 

Splenomegaly,  123,  1525 

Surveys,  1209 

Urticaria,  1181 

Vitreous  Opacities,  2005 
Malassezin,  1077,  1097,  2078,  2099 

Dermatomycosis  due  to,  2041 

Species 
furfur,  1097,  1099,  1998,  2080 
tropica,   1097,   1099,  2041,   2074, 

2076,  2080 
versicolor,  2079 
Malattia  della  Insolazione  di  Prima- 
vera,   1700 

da  Mensa,  1299 

della  Miseria,   1700 

del  Sonno,  1260 
Malay  Bug,  768 

Malaya,  Arrow-Poisons  of,  184-5 
Malay  Race,  54,  55 
Malay  States  Fever,  1355 
Male  Breast,  Hypertrophy  of,  1939 

Generati  ve  System,  Diseases  of ,  1 93  8 
Male  Fern,  1930,  see  also  Filix  mas 
Malignant  Bilious  Fever,  1216 

Fever,  Causal  Agent,  502-3 

Pustule,  1 519 

Tertian  Fever,    see   Malaria,   Sub- 
tertian,  1 1 64 

Tumours,  1074 

»f  Connective  Tissue,  2274 
Epithelial,  2277 

Ulcer  (Oriental  Sore),  2165 
Mallophaga,  748,  749,  750 

References,  760 


Malta   Fever,  1437,  see   also   Undu- 

lant  Fever 
Malta-Fever-like  Subtertian  Malaria, 

1 1 71 
Malta  Fieber,  1437 
Malvacece,  2153,  2154,  2I59 
Mammalia,  Bites  of,  Fevers  due  to, 

1128,  1356 
Carrying   Disease    {see   also   tinder 

Names  of  Species,  etc.), 

913 
Parasites   of,    478,    483,   546,    751, 
752   sqq. 
Trypanosomes  of,  395,   401,  for 
minutitB,  see  tinder  Try- 
panosomes 
Suspect  of  Poisoning,  279-80 
Venomous,  271 
Man,  Bites  of,  147,  155 
Primitive,  42 
Divisions,   44 
Mana  Kodra,  200 
Manbhum  Arrow- Poisons,   185 
Manchineel  Poisoning,  173,  174 
Manchineel-Tree,  2157 
Manchu  Race,  56 
Manchurian    Relapsing    Fever,    918, 

i3°8.  i3!5. 

Mandibulata,  750 

Mandingo  Race,  51 

Mango  Boils,  2027 

Mango  Fruit,  1  540 

Mango  Toe,  2036,  2045, 

Mangosteen  Rind,  1858 

Mangkassaras,  the,  55 

Mangrove-Flies,  815' 819 

Manguinhosia,  792 

Mania,  1524,  1981,  see  also  Amok, 
1988,  Kohler,  76,  1981, 
Latah,  1983,  Lunacy, 
1981,  Melancholia,  1524, 
and  Mental  Symptoms, 
130 

Manihot  utilissima,  172,  190 

Mansanillo,  2157 

Manson,  Sir  Patrick,  Pioneer  of 
Tropical  Medicine,  16, 
17,  18,  19 

Mansonia,  796 
ovata,  1857 
pseudotitillans,  1598 
uniformis,  1598 

Manson's  Herpes,  2060 

Mantati  Race,  53 

Manuch,  173 

Marasma,  1743 

Marda  tal  biccia,  1299 

Margaropus,  497,  710,  711,  714 
annulalus,  700,  734 
Varieties 

argentinus,  715 
australis,  497,  715,  1557 


Fever, 
1318 


2047 


INDEX 


2367 


Mar  gar  opus,  continued 

annulatus,  continued 
Varieties,  continued 
calcaratus,  715 
caudatus,  715 
dugesi,  715 
uiicrophilis,  715 

decolorants,  454,  698,  714,  715 

lounsburyi,  714 

winthemi,  714 
Marine  Leeches,  485 
Marmots,  914 

and  Plague,  913,  1  4 _:  j 
Marmotta,  914,  915 

bobak,  915 

mtirmota,  915 
Marschfieber,  1129 
Marsh  Fever,  n  29 
Marshall-Plehn's  Dots,  1149 
Masai  Race,  47 
Mask,  Tropical,  2233 
Masked  Bug,  767 

Malaria,  1168 
Masks,  use  of,  in  Plague,  1435 
Mastigocladium  blochi,   1124 
Mastigophora,  291,  296,  297,  330 

Doubtful  Genera,   360 

Morphology,  330-1 

References,   356-7 

Sub-Classes,  331-2 

Vaginal,  1946 
Mastigote,  331 
Mate,  177,  178 
Mattari,  1756 

Mauling  by  Wild  Beasts,  115,  147 
Maurer's  Dots,  517,  1147 
Mauvais  Dartre,  1700 
Mayfly  Larvae,  812 
Maya  Race,  56,  57,  60 
Mazamorra,  1763 
Mazatee,  the,  56 
M'betalala,  1326 

Mbori  of  Dromedaries,  410,  417,  816 
M'Boundon,    African  Ordeal-Poison, 

178 
Mbwa  Fly,  811 
Meal-Broth  Beetles,  895 
Measles,  114,  120,  1486,  2267 
Diagnosis,  151 3,  151 5 

Differential,  1250,  1253,   1490, 
1491 
Rash,  1513,  1515,  1517 
Virus,  Filterable,  541 

Fever  resembling,   1471 

Haemorrhagic,  1491 
Mecistocirrus  fordi,  663 
Mediaeval  Medicine,  14 
Medical  Methods,  Mosaic,  9-10 

Missionaries,  5 
Medicinal  Leeches,  686 

Plants,  4 


Medicine 

Foundations  of 

Ancient,  6  sqq.,  2111,  2116 
Mediaeval,  14 
Modern,  14 
Primitive,  3 
Tropical 
Early,   16 
Modern,  16  sqq. 
References,  30 
Mediterranean  Fever,  932,  1437,  1530 

Kala-Azar,    374,    883,   1289     1299 
1907 
References,   1307 
Meeta  bish,  169 
Megalotnorphce,  212 
M egarhinince ,  786,  790 
Megaspores,  2057 
Megastoma,  466 
Melancholia,  1524,  1981 
Melanconiales,  1036 
Melanesians,  the,  49,  53 
Melania,  17,  575,  891 

hastula,  891 

Hbertina,  891,  894 
Melaniidce,  891 
Melanin,  87 
Melanochroi,  45,  46-7 
Melanoderma  Pediculis,  2201 
Melanolestes,  767,  769 

abdominalis,  769 

morio,  769 
Melanonychia,  2222,  2236 

Falciformis,  2236 
Melanosis,  87 

Melanotic  Carcinoma,  2277 
Melanuric  Fever,  1216 
Melasma  Solare,  2231-2 
Melianthacce,  164,  166 
Melianthus,  164,  166 

major,  164 
Meliococca,  164 

Poisoning  by,  164,  166  sqq. 
Melitensis  Septicaemia,  1437 
Melitococcaemia,  1437 
Melitococcie,  1437 
Meloe,  2277 

proscarabcBiis,  1641 

visicatorius,  172 
Melolontha,  1640 
Melon  Seeds,  1756 
Melophagus,  855 

ovinus,  363,  369,  855 
\IHung,  2222,  2229 

References,  2245 
Melusina,  810 
Melusinidce,  810 
Membrano-UlcerativeGingivitis,  1 745 

Pharyngitis,  1745 

Stomatitis,  1745 

Tonsillitis,  1745 


2368 


INDEX 


Menabea  Venenata  in  Ordeals,  179 
Meniere's  Disease,  2013 

Type   of   Aural   Affection  in  Sub- 
tertian  Malaria,  1 181 
Meningite      Cerebro-Spinale      Ep>ide- 

mique,  1474 
Meningitic  type   of   Subtertian   Ma- 
laria, 1 1 75 
Meningitis,  1066,  1949 
Diagnosis,  1528 
Acute,  139 

Cerebro-Spinal,  epidemic,  1474 
.Etiology,  926,  1474,  1475 
Climatology,  120,  123,  124,  1475 
Diagnosis,  1485 

Differential,  1337,  1485 
Mimicry,  1484 
Morbid  Anatomy,  14S3 
Pathology,  1483 
Prognosis,  1485 
Prophylaxis,  1485 
Relapses,  1485 
Sequelae,  1485 
Symptomatology,  1483 
Varieties,  1484 
Neonatorum,  1959 
Meningocele,  123,  1959 
Meningococcus,  1477  SQQ>  I482,  1697, 
1959,   1998 
Present   State  of    Knowledge    on, 
1479-80 
Meningo-Encephalitis      of      Sleeping 

Sickness,  1259,  1260 
Mcningo-Myelitis    of    Sleeping    Sick- 
ness, 1259 
Menispermacece,  188 
Menorrhagia,  129 
Menosporidee,  471 
Menstruation,  77 

Mental    Symptoms    and    Invaliding, 
130 
Type  of  Subtertian  Malaria,  11 69 
Mentzelia  lindleyi,  2153 

oligosperma,  2153 
Mercurial  Poisoning,  1862 
Mercury  Compounds,  27 
Perchloride,  162,  170,  189 
in  Treatment  of  Sleeping  Sickness. 
27 
Menatschenje,   1983 
Mermis,  653 

Mcnn  it  hides,  623,  632,  653 
Merozoites,  293,  294,  469 
Mesagonimus  heterophyes,  570 
pulmonale,  573 
westermani,  573 
Mesobdella,  688 
gemmata,  688 
Mrsomitosis,  291 
Mesopotamia,  Diseases  of,  120 
Mesotheler,  212 


Metabolism,  Diseases  of,  191 9 

References,  1925 
Metachromic  Granules,  290 
Metadysentery,  ^Etiology,  1845 

Bacillus  of,  1842,  1843 
Metagonimus,  570,  571 

yokogawai,  571,  894,  1752 
Metallic  Salts,  2S 
Metamitosis,  291,  292 
Metaplastic  Granules,  290 
Metastigmata,  692 
Metastriata,  711 
Metastrongylidee,  623,  659,  662 
Metastrongy 'lines,  662 
Metastrongyhis,  624,  662 

apri,  624,  662 

holosericeum,  2213 
Metatrema,  563 
Metatrombidium,  727 

poriceps,  727,  2215 
Metazoa,  Definition,  552 
Metazoan  Parasites,  287,  552 
of  Man,  552,  554 

Skin  Lesions  due  to,  2200 
Meteorology,  62 

References,  91  sqq. 
Metorchiina,  575 
Methyl  Alcohol,  175 
Meurd  Djilben,  196 
Meuse  Fever,  1501 
Meve's  Plastokonten,  1896 
Mexican  Races,  56-7,  60 
Mexico,  Aztec  Medicine  of,  6 

Northern,  Diseases  of,  124 
M'Faug,  African  Ordeal- Poison,  178 
Miana   (Persia),  Relapsing   Fever   of, 
691,  919,  1322 

References,  1325 
Miainomyces,  1117 
Mice  and  Rats  (see  also  Rats),  916 

Fleas  of,  865,  867 
Table  of,  866 
Micvoascus,  1024 
Microbe  en  Chapelet  of  Pasteur,  1949 

du  Cholera  des  Poles,  933 
Micrococcees,  924,  931 
Micrococcus^),  924,  925,  1230,  1941, 
1998,    2166,    1437   sqq., 

1444.  1445.  1447.  1462, 

1465,  2102 
Anaerobic,  of  Veillon,  1949 
beigelii,  1103 
castellanii,  2103,  2105 
catarvhalis,  147S,  1521,  1998,  2014 
cinereus,  1478-9 
fcetidus,  1949 
melitensis,  925,  932.  1290 
nigyescens,  1067,  2102,  2103 
paramelitensis,    1437,    1439,    M4*i 

1447 
pelletieri,  1051,  1058,  2135 


INDEX 


2369 


Micrococcus^),  continued 
pemphigicontagiosi,  931 
pemphigineonatorium,  931 
of  Pneumonia,  933 
pseudomelitensis,  1437,  1439,  1441, 

H47 
vesicans,  2031 
Microfilaria,    337-9,    623,    632,    640, 
896,    967,    1596,    1599, 
1903,   1965 
Periodicity  k>,  554,  633,  636 
Reference,  681 
Species 
bancrofti,    633,    636,    641,    O47. 

1596,  1601-2,  1941 
diurna,  045,  047 
nocturna,  10,  634 
per  stuns,  2247 
pkilippinensis,  023,  640 
powelli,  023,  640 
Microgamete,  294,  295 
Microgametocyte,  294 
Microides,  2057 
Micromonas  mesnili,  542 
Micromyces  hoffmanni,  1047 
Microneurum,  902 

funicolum,  899,  902 
Micronucleus,  290 
Micropechis,  246 

elapoides,  251 
MicropezidcB,  1629 
Microphthalmias,  1995 
Microrchis,  561 

Microscopical  Diagnosis,  16,  17 
Microsiphonales,  1039,  1040 
Microspirouema  pallidum,  455 
Mnrosporidia,  295,  528 
Microsporidiosis  of  Bees,  529 
Murosporidium  polyedricum,  529 
Microsporoides    minutissimus,     1053, 

1062 
Microsporon,  1014,  1015,  2008,  2053, 
2057,  2095 
audouini,  2268 
var.  canis,  993 
var.  equinum,  993 
furfur,  1099 
gracile,  1053 
lanosum,  2008,  2009 
mawsowi,  1100 
mentagrophytes,  1005 
trachomatosum,  1998 
tropicum,  1099 
Microsporosis,  2057 

Capitis  (see  a/so  Tinea  Capitis),  991, 

992,  994 
Flava,  2073 
Nigra,  2078 
Microsporum,    986,    989,    990,    1101, 
2054,   2056,  2057,   2254 
Dermatomycoses  due  to,  2040 


Microsporum,  continued 
Species 

audouini,    990,    991,   994,    2053, 

2055,  2056 
depauperatum,  991,  994 
felineum,  991,  993 
flavescens,  991,  994,  2040,  2055 
fulvum,  991,  993,  995,  2056 
gracile,  1061 
iris,  i)i)i,  994 
lanosum,  991,  993,  2053 
minimum,  990,  991,  993 
minutissimum,  1053,  1060 
Parasitic  in  Man,  991 
pubescens,  991,  993 
scorteum,  991,  995,  2055,  2056 
tardum,  991,  993 
tomentosum,  991,  994 
umbonatum,  991,  992 
velveticum,  991,  992 
villosum,  991,  994 
Types 

Acladium,  990,  991 
Glabrous,  990,  991 
MicrotincB,   915 
Microtrichophyton,  1002,  1004 
mentagrophytes,  1004,   1005 
Microtrombidium,  725 

akamushi,  726,  727, 1350  s^.,  I5I0» 
2213 
Reference,  741 
iiulumnalis,  725-6 
brumpti,   726 
meridionale,  2215 
pusillum,  726,  2215 
vandersandei,  727 
wichmanni,  726,  727 
Microvelia,  367 
MidasidcB,  824 

Midday  Heat,  Avoidance  of,  91 
Middle-Ear      Congestion,       Quinine- 
caused,  2013 
Midges  [Chironomidts),  801 
Midges  (Psychodidee) ,  806 
Midwives,  1956,  1959 
Miliare  Cristalline  Febrile,  1468 
Miliary  Actinomycotic  Metastases  in 
the  Choroid,   2009 
Fever,  1308 

Tuberculosis,  Acute,  1396 
Milk  in  relation  to 

Enteric,  1364,  1371 
Infant  Mortality,   120 
Fungi  in,  1076 
Impurities  in,  95 
Vitamine  of,  Growth  in,  109 
Dilutions  for  Infant-feeding,  1959 
Milk  Fever,  1948,  1951 
Milk-Pox,  Kaffir,  1491 
Millepora,  204 
alcicomis,  204 

149 


23  7° 


INDEX 


Millepora,  continued 
complanata,  204 
verrucosa,  204 
Millet,  95,  105 
Millet  Blanchet,  1741 
Milletia  seriacea,  164,  16/ 
'  Millions,'     and      other     Larvicidal 

Fish,  1208,  1209 
Mimicismus,  1983 
Mimicry,  Malarial,  1165,  11 68 
Minahasans,  the,  55 
Minckinia,  474 
Mineral  Acids,  Poisoning  by,  162 

Substances  in  Diet,  96 
Miners'  Anaemia,  1761 
Miracidia,  558 
Mirunta,  1633 
Misala,  1991 

Miscellaneous  Diseases,  2247 
References,  2263 
Skin  Diseases,  2015,  2017 
Mishmi,  the,  54 

Arrow-Poison  of,  184 
Misteca-Zapoteca  family  of  Mexican 

races,  57 
Mite-Bites,     Dermatoses      due      to, 

2213 
Mites,     691,     908,     2163,     see     also 
Acarina 
Burrowing,  124 

Disease-Carrying,     1350,    see    also 
Microtrombidium,  725 
Mitosis,  291,  292 

Mitragyna  speciosa  Leaves,  as  Substi- 
tutes for  Opium,  178 
Mixe,  the,  56 
Mixed  Infections  with  Parasites,  548, 

549 
Leprosy,  1663 
Tumours,  2277 
Moccasin   Snake-Venom,  Serum   for, 

273 
Mochlonyx,  801 
Moderation,   Motto  for  Tropic  Life, 

128 
Modern   Medicine,    Foundations    of, 

14  sqq. 
Mccpysylla,  865 
Mcesa  indica,  187 

lanceolata,  1  756 
Mois,  the,  54 

Arrow-Poison  of,  1  s 4 
Moko,  2238,  2240,  2241 
Moles,  Epithelial,  2274 
Molestia,  1283 

do  Barbeiro,  1283 
Mollugoliro,  1753 
Mollusc  Hosts  of 

Paragonimus,  1585 

Schistosoma  japonicum,  1590,  1591 

Trematodes,  17,  889 


Mollusca,  889 
Venomous,  227 
Reference,  229 
Molluscum  Contagiosum,  Non-Cocci- 
dial,  474,  541,  542,  2274 
Momba,  1535 
Momordica  charanta,  170 

cymbalaria,  1 70 
MonadidcB,  2166 
Monas,  355 
lens,  335,  342 
prodigiosa,  933 
pyophita,  335 
rotatorium,  393 
Mongolian   Spots,   or  Maculae,   2222, 
2237 
References,  2246 
Mongolic  Division  of  Man,  42,  44,  54 
Mongolo-Dravidians,  49 
Mongota,  1260 

Monilia,  981,  983,  1070,  1078,  1079, 
1084,  1742-3,  1886, 
1888,  1889,  1891,  1926, 
1939.  1944.  1945-  2008, 
2041,  2081,  2084,  2093, 
2094,  2098,  2149 
Species 

Biochemical      and       Cultural 
Characters   of   Certain, 
Table,  1082-3 
alba,  1084,  1089 
albicans,  968,   1084,   1085,  1743, 

1781,  1782,  1889,  2008, 
2009 

aurea,  1028,  1079,  1080 

balcanica,  981,  1081,  1084,  1090 

bethaliensis,  1091,  1887 

blanchardi,  10S4,  1091 

bonordens,  1091 

bronchialis,  1084,  1087,  1743 

burgessi,  1090 

Candida,   969,   1086,   1091,  1742, 

1887 
caoi,  1092 

chalmersi,  1084,  1087 
cutanea,   1092 
decolorans,  1085,  1782 
digitata,  1025 
enterica,  1084,  1085,   1088,  1781, 

1782 
fcscalis,  1085,  1089,  1782 
guillermondi,  1084,  1088,  1887 
harteri,  1092 
insolita,  1084,  1085,  1086,  1089, 

1782,  1887 
intestinalis ,     1085,     1089,    1781, 

1782 
kochi,  1092 
koningii,  11 24 

krusei,  1081,  1084,  1088,  1887 
lactea,  1085,  1887 


INDEX 


'■37* 


Monilia,  continued 
Species,  continued 
lacticolor,  1085,  1887 
londinensis,  1084,  1743,  1945 
htstigi,  1084,  1090 
macedoniensis ,  1084,  1087 
metalondinensis,       1081,       1084, 

.1085,  1743,  1945 
nwtatropicalis,  1087 
montoyai,     1084,      1092,     2094, 

1085,  1743,  1945 
naiarroi,  1081,  1064,  1085,  1090 
negrii,  1084,  1887 
nitida,  1084,  1089,  1887 
nivea,  1084,  1088,  1887 
parabalcanica,  1084,  1085,  1090 
parachalmersi,   1084,  1087 
parakrusei,  1081,  1084,  1092 
parapinoyi,  1742,  1743 
paratropicalis,  1084,  1087,  1887 
perieri,  1092 
perryi,  1084,  1090 
pictor,  1092 
pinoyi,    1081,   1084,  1085,    1088, 

I742>  1743.  l887-  !945 
pseudoguillermondi,  1084,  1088 
pseudolondinensis ,  1084 
pseudometalondinensis,  1081 
pseudotropicalis,  1084,  1087, 1887 
psilosis,  1782 
pulla,  1030 

pulmonalis,  1084,  1090 
pulmonea,   1091 
Wtoi,  1089,  201 1 
rosea,  1084,  1091 
rugosa,  1084,  1748 
associated  with  Sprue,  1781 
subtilis,  1091 
tropicalis,  1084,  1085,  1086,  1742, 

1743,  1748,  1782,  1887, 

1945 
zeylanica,  1084,  1088,  1743 
Moniales,  1036 

Moniliases    (see    a/so    Blastomycosis, 
2081,  Sprue,  1780,  etfc), 
1081  sff<?.,  1782 
Broncho-alveolar,  1886 
Ocular,  2009 
Moniliform  Hair,  2282 
Moniliformis,  608 
Moniliomycoses,  1084,  1748 
M<  >niliomycosis,  Tonsillar,  1748 
Monilitkrix  of  the  Hair,  2282 
Monkeys,  Parasites  of,  353,  355,  404, 

413,  483,  493  et  alibi 
Monocercomonas,  349,  351 

hominis,  350,  354 
Monocereous  Cercarice,  559 
Monocystidea,  471 
Monocystis,  471 
agilis,  470 


Monogenea,  560 
Monomorium,  1995 

bicolov  var.  nitidiventre,  1995 
pharaonis,  765 
Monoplegic  Subtertian  Malaria,  11 75, 

1176 
Monospora,  979 
Monosporidia,  471 
Monosporium,  1121,  1123 

Dermatomycoses  due  to,  2041 
Species 

apiospermum,  1121,  2041 
sclerotiale,  1123 
Monosporogenea,  529 
Monostichodonta,  686 
Monostomes,  558 
Monostomum  lentis,  565,  567,  2007 

References,  595 
Monotosporacece,  11 11 
Monotremata,  279-80 
Monozoa,  333 
Monsoons,  64-6,  78,  79,  81 
Monsters 

Composite,  1958-9 
Single,  1958 
Monstrosities,  Fcetal,  1957 
Montoyella,  989, 1023,2093,  2094,2095 
bodini,  1023,  2094,  2098 
nigra,  1023,2094,  2097 
Moon,  the,  Rays  of,  Effects  of,  88 
Moon-Stroke,  142 
Mopans,  the,  60 
Moquinia,  688 
Morosa  collina,  164 
Morbus  Dormativus,  1260 
Elephas,  1610 
Pedis  Entophyticus,  21 10 
Tuberculosis     Pedis,     2110,     2113, 

2116        — 
Weilii,  1505 
M  or  delta,  1641 
M  or  dellidcs,  1641 
Mordvins,  the,  55 
Moringa  pterygosperma  Bark,  1 70 
Morphia,   Hypodermic  Injections  of, 

Cheloid  after,  2274 
Morphine  Injector's  Septicaemia,  1466 
Morphinism,  Chronic,  effects  of,  175 
Morphcea,  1664,  2224,  2230,  2281 
Mortality,  Infantile,    120,    122,    124, 

1957.  1959 
Mortierella,  21 14 
Movtierellaceez,  972 
Morrison's  Spots,  2202 
Morso-di-Topso,  1356 
Morsthymia,  1924 
Mosaic  Hygiene,  10 

Knowledge  of  Animal  Parasites,  596 
Quarantine,  10 
Treatment  of  Disease,  9,  10 
Moschni,  198 


2372 


INDEX 


Mosquito-Bite,    Pathogenicity  of,    7. 
16  sqq.,  23,   222-5,  285, 
see  also  Anopheles,   and 
Malaria 
Venom  of,  2224-5 
Effects,  226 
Treatment,  226 
Mosquito-Proofing  of  Bodies,  Houses, 

etc.,  1205-6 
Mosquito-Reduction  Methods,  1206-7, 

1209 
Mosquito-Worms,   896,   1634 
Mosquitoes,  see  also  Anopheles,  Culex 
Stegomia,    etc.,    17,    18, 

x9,  774 
Fungi  on,  2096 
House- Dwelling,  787 
Parasites  of,  17-18,  287,  397,  398, 

637-9,  640-1,  644 
Rash  due  to,  151 7 
Ship-Haunting,  796 
as    Spreaders    of    Disease,     16-17, 
18    sqq.,    23,    285,    503, 
800,  873,  876,  883  sqq., 
888,     1128    sqq.,     1131, 
1132,    1137   sqq.,    1229, 
1635,  1650,  2166 
Mossman  Fever,  1465-6 
Mossy  Foot,  2247,  2254 

Reference,  2263 
Mostaki,  198 
Moths,     Poisonous     Caterpillars     of, 

222-3 
Motuca-Fly,  817 
Mountain    Fever    (Undulant   Fever), 

1437 
Mountain  Sickness,   143-4 
Mouqui  (mite),  2213 
Mouth,  Diseases  of,  1739,  1740,  1745 
References,   1751 
Parasites  of,  461,  448  sqq.,  1740 
Temperature-Taking  in,  70,  71 
Mouth-Symptoms  indicative   of   Ali- 
mentary Derangements, 
1520 
Movements,    Energetic,    Useless     for 

Snake-Bite,  278 
Moyocuil,  1633 
Mozambique  Sore,  2181 
Muco-Cutaneous  Leishmaniasis    (Es- 
pundia),    17,    41,  2165, 
2175 
References,  2199 
Mucor,  967,  972,  973,  1886,  1892,  21 14 
References,  977 
Species 

corymbifer,  974 
crustaceus  albus,   1025 
herbariorum,  1029 
mucedo,  973,  1892 
pusillus,  974,  201 1 


Mucor,  continued 
Species,  continued 
racemosus,  171 2 
sphcsrocephalus,  973 
stolonifer,  21 15 
vulgaris,  973 
Mucoracecs,  972 
Mucorales,  972 

Mucormycoses,  967,  973,  976 
Bronchial,  1S92 
General,  974,  977 
of  Lungs,  975-7 
Nasal,  976 
Mucous     Membranes,    Cosmopolitan 
Diseases  of,  2264,  2283 
Muculo,  854,  1 65 1 
Mucuna  pruriens,  2153,  2159 
Mudar,   173 
Mu  ghetto,  1 741 
Muguet,  1 74 1 
Muki-muki,  194 
Multiceps,  612 
cosnurus,  612 
Multipara,  Osteomalacia  in,  1943 
Multiple  Pruriginous  Tumours  of  the 
Skin,  2247,  2254 
References,  2263 
Sarcomatosis,  of  the  Skin,  2274 
Septic  Liver  Abscesses,  1525 
Telangiectases,  2273 
Muma  Fever,  1975 
Mumps,  1526 

Munchi  Arrow-Poison,  183 
Mundas,  the,  Food  of,  96 
Mundulea  suberosa,  187 
Munhiyo,  1437,  1673 
Mureena  helena,  232,  233 

moringa,  232 
MurcsnideB,  232,  233 
Muridce,  914,  915 
Murines .  915 
Murmekiasmosis  Amphilaphes,  1073, 

1077,  2247,  2262 
Murrina,  415 
Mus  chrysophilus,  869 
decumanus,  693,  916 
musculus,  867 
rattus,  915 
Musca,  307,  832,  846,  877,  903 
corvina,  900,  1629 
domestica.     Habits     of,     Parasites 
carried  by,  and  Diseases 
spread    by,     307,     365, 
377.  379,  415.  747.  883, 
887,  900,  903,  908,  1626, 
1629,    see   also    House- 
fly, 
var.  determinata,  900 
hispaniola ,  1  72 
lepra,  1650 
lutcola,  850 


INDEX 


2.373 


Musca,  continued 
macellaria,  847 
nebula,  397,  900 
nigra,  1829 
pattoni,  899,  900 
putrida,  846,  1632 
vomitoria,  1626 
Muscardin,  1033 

MuscidcB,  814,  825,  831,  1626,  1628, 
1629,  1632,  1633,  1637, 
2200 
Eggs,  772 
Larvae,  771,  1620 

Dermatites  due  to,  2200,  2207 
Tribes 

acaly  pirates,  774 
calyptratce,  774 
Muscidifurax  raptor,  908 
Muscince,  832,  846,  903,  1626 
Muscles,  Diseases  of,  1967,  1975 
Muscoidea,  825 

acalyptratce,  825,  901 
calyptratcB,  825,  901 
Muscular  Rheumatism,  124 

System,    Derangements    of,    1519, 
1523 
Diseases  of,  1967,  1975 
Work,  and  Heat-Stroke,  141 
Mushrooms,  Chinese  use  of,  172 
Myase  Cutanee,  1632 
Furonculeuse,  1632 
Rampante  Sous  cutanee,  1632 
Myasis,  1632 

Cutanea,  1632 
Mycetoma,  1058,  1 104-5,  1106,  1107, 
1 714,  2015,  2017,  2041, 
2085,  2110,  2277 
References,  2150 
Actinomycotic,  1055,  2148 
Aspergillar,  1032 
ISLick,  1030,  1104,  21145^.,  2125 
Ochroid,  21 14 
White,  1107,  211^  sqq. 

Vincent's,  1058 
Yellow,  21 13  sqq. 
Mycetoma-like  Disease,  1 1 1 8 
Mycetomas,  The,  2085,  2110 

Two  Mai  n  Divisions  of,  2 1 1 7 
Mycetomiasis,  2148 
M ycobacteriacecB ,  924,  965,  1040 
Mycobacterium,  965,  1040 
diphtheria,  965 
lepra,  965,  1644 
malei,  965 
tuberculosis,  965 
Mycoderma,  1071,  1073,  1782 
cutaneum,  1092 
pulmoneum,  1091 
subtile,  1091 
vini,  1742 
Mycogone,  11 12 


Mycological  Urinary  Tests,  1934 
Mycology,  967 

Pathogenic,  History,  21 
MycophycecB,  1071 
Mycosis  (es),  2008 
Definition,  967 
Aspergillar,  103 1-2 
Black,  of  the  Tongue,  Fungi  in,  976 
Cutis  Chronica,  2165 
of  Foot,  1 123 
Fungoides,  2186-7,  2274 
of  Genito-Urinary  Organs,  1926 
Nasal,  974 
Ocular,  2008 
Pulmonary,  976 
Tonsillar,  1747 
Mycterotypus,  802,  803 
Myelitis,  1688 
Myelitic    Subtertian    Malaria,    11 75, 

1176 
Myeloblasts  of  Naegeli,  1898 
Myelocythaemia,  Blood-Conditions  in, 

1900 
Myelopathia  Tropica  Scorbutica,  1671 
Mygale,  212 

Myiases,  The,  and  Allied  Conditions, 
1619 
^Etiology,  771,  814,  825,  827,  830, 
831,    846,    848,    852-4, 
895,  1533,  1621 
Allied  Conditions,  1639 
Animal     Carriers,     Hosts,     and 

Reservoirs,  895-6 
Definition,  896,  1619 
Diagnosis,  1622 
History,  1 61 9-2 1 
Nomenclature,   161 9 
Pathology,  1622 
Prophylaxis,  1622 
References,  1641 
Symptomatology,  1622 
Treatment,  1622 
of    Alimentary   Canal,    848,    853, 

1631 
Aural,  1622,  1626,  201 1 
of  Cavities,  1622,  1623 
Dermal    or    External    (Subcutan- 
eous), 1623,  1631,  1632   . 
1633,  1637 
African,  1633,  1637 
American,  1633 
Asian,  1633,  1639 
European,  1633,  1639 
Facial,  1625 
Neotropical,   1633 
Traumatic,  1623,  1631,  1632 
Intestinal,   Gastric  or  Oro-Gastro- 
Intestinal,  824,  830,  831, 
848,  852,  854,  900,  905, 
1620,  1621,  1622,  1628, 
1841,   1863 


2374 


IX  HEX 


Myiases,  continued 

Ocular,  1622,  1625,  1627,  2007 

Oral,  1625 

Rhinal,  831,  846,  1620,  1622    1623, 

1625,   1626 
Subcutaneous,  see  Dermal,  above 
Urinary,    853,    1620,    1622,    1628, 

1926,   1934 
"Vaginal,  1622,  1628 
Mylabris  cichorii,  172 

nubica,  227 
MyliobatidcB,  232,  240 
Myliobatis  aquila,  232 
Myocardium,  Rupture  of,  1904 
Myoclonia,  191 9 
Myomalacia  Cordis,  1904 
Myomata,  Facial,  2273 
Myomycosis,  1060 
Myonemes,  330,  382,  470 
Myositis,  1582 

Purulenta     Tropica,     1469,     1523, 
1529,  1967,  1975 
Myotoma,  191 9 

Periodica,  191 9 
Myriakit,  1983 
Myriapoda,  549 
Myriase  do  Sero,  846 
Myristica  fragrans,  173 
Myrmica,  Venom  of,  222 
MyrtacecB,  164,  172 
Myxidiidce,  529 
Myxidium,  529 
Myxobacteriales,  924 
Myxobolidce,  529 
M yxococcidium  stegomyice,  1230 
Myxocystes,  529 
Myxoedema,  1919,  1920,  1922 
Myxomycetes,  923,  971 
Myxosporidia,  528 
Myxotrichum,  986 
Myzomyia,  791,  793,  885 
Malaria  Carriers,  793,  886 
Species 

aconita,  793,  886,  888 
albirostris,  794,  886 
azriki,  794 

culicifacies,  786,  794,  886 
d'thali,  793,  888 
formoscensis,  886,  888 
funesta,  793,  886,  888 
hispaniola,  794,  886 
indefinala,  793 
jehafi,  793 
kumassi,  886 
leptomeres,  794 
listoni,  794,  888 
longipalpis,  793 
ludlowi,  793 
lutzii.  793,  888 
mangy  ana,  793 
nil  1,  794 


Myzomyia,  continued 
Species,  continued 

pyretophoroides,  793 

rhodesiensis,  794 

rossi,  638,  786,  793,  888,  1598 

sinensis,  888 

iessellata,  793 

thorntoni,  794 

tnrkhudi,  794,  886 
Myzorhynchella,  791,  885 
Malaria  Carriers,  887 
Species 

arabiensis,  887 
Myzorhynchus,  792,  795,  884 
Malaria  Carriers,  795,  888 
Species 

albotcBniatus,  795 

bancrofti,  795 

barbirostris,  795,  888 

coustani,  795 

mauritianus,  795,  888 

minutus,  795,  1598 

nigerrimus,  795,  1598 

pahtdis,  795,  888 

pseiidobarbirostris ,  795 

pseudopictus,  795 

sinensis,  795 

strachani,  795 

umbrosus,  795 

vanus,  795 

Xaegeli's  Myeloblasts,  1898 
Urticarial  Fever,  1462 
References,   1473 
Naegleria,  298,  300 

punctata,  300 
Nagana,    Animals   affected   by,    391, 
411 
Causal  Agent  and   Insect  Vectors, 

19.  386>  39i>  4IQ.  -U4. 
838 
Climatology,  414 
Serum,     Trypanolytic    Action    of, 

392 
Treatment,  411,  1262 
Nagas,  the,  54,  55 
Nahuas,  the,  56,  57,  60 
Xail      Matrix,       Inflammation      of, 

2283 
X.iils,   Black  Pigmentation  of,   2236, 
2283 
Diseases  of,  909,  2257,  2264,  2282, 

2283 
Supernumerary,  2283 
Naja,  246 
anhieta,  251 
bitngarus,  246-7,  251 

Venom   of,    259,    260,  264,   266, 
272,  273 
flava,  251 

Venom  of,  268 


INDEX 


2375 


Naja,  continued 
goldii,  251 
haje,  247,  251 

Parasites,  516 

Venom,  243,  247,  253,  266,  271 
melanoleuca,  251 

Venom,  268 
nigricollis,  247,  251 

Parasites,  516 

Venom,  268 
regalis,  247 
samarensis,  251 
tripudians,  246,  251 

Parasite,  487 

Venom,    243,    254,    264-6,    268, 

273 
Nakhra  Jawhur,  1466 
Nakra  Fever,  1466 
Nambiavu,  502 
Nantundua,  871 
Nanukayami,  1510 
Napt  Hindi  Nabit,  21 18 
Narcotics,    see    Sedative    Poisoning, 

174  sqq. 
Naride,  2260 

Nasal    (see    also    Rhinal)     Affections 
and      Diseases,       1993, 
2013,  2173 
Aspergillosis,  1029,  103 1-2 
Cancer,  123 

Catarrh,  Common,  1521 
Goundou,  1975 
Inflammatory,  1875  sqq. 
Irritation  in  Oxyuriasis,  1776 
Mucormycosis,  976 
Mycosis,  974 
Myiasis,  846,  1620,    1622,    1623, 

1625,  1626 
Polypus,  1578 
Spirochetosis,  1882 
Tumours,  2277 
Ulceration,  123,  1882 
Mucosa,     Fevers    associated    with 
Swelling  of,  1466 
Proliferation  of,  in   Rhinospori- 
diosis,  534 
Symptoms  indicative   of   Respira- 
tory Derangement,  1 52 1 
Nasha  Fever,  1466 
Nasonia  brevicornis,  908 
Naso-Oral  Leishmaniasis,  1741,  2175 
Naso-Pharyngitis,  1882 
Nasturium  Dermatitis,  2162 
Native  Employees,  130 

Examination  of,  130-1 
Invaliding  of,  131 
Races,  Tropical,  Alcoholism  among, 
effects  of,  175 
Colour  of,  protective,  85,  and  see 

2264-5 
Expectation  of  Life  in,  133 


Native  Races,  continued 

Glandular  System  of,  2264 
Hairy  System  of,  2264-5 
Life  Asssurance  among 
Egyptian,  133 
Indian,  132 
Normal  Skin  of,  2264 

Dark  Pigmentation  of,    2265 
Sebaceous  Secretion,  2264 
Susceptibility  of,  to 
Heat,  2265 
Pain,  2265 
Naushah,  13 14 
Nauta,  893 
N'diank,  1819 
Ndi-tot,  1972 
N'dulu,  1260 

Nebenkorper,  Nucleus  de  reliquat,  or 
Rest    Body,    293,    299, 
334.  335-  47°.  5°6,  5°7. 
535 
Necator,  624,  659,  672 
africanus,  673 
americanus,    124,    624,    667,     673, 

1595.  I761-  r762.  J763. 

1777 
Dermatitis  due  to,  2219 
Neck  Abscess,  Aspergillar,  1028 
Necrobia,  1627,  2007 
Necrosis  of  Bone,  1967 

Focal,  in  Cornea,  etc.,  2006 
of  Foot,  156 
Necrotic  areas  in  Liver,  107C 
Neclurus,  258 
Neglected  Strictures,  1939 

Wounds,  Ulceration  following  on, 
2191 
Negri  Bodies,  20,  535 
Negritoes,  49,  51,  53 

Arrow- Poisons  of,  186 
Negro  Consumption,  1761 

Lethargy,   1260 
Neisseria,  925 
References,  966 
Species 
flava,  926 

gonorrhoea,  925,  926 
Heterogeneous  group,  926 
intracellularis,  926,  1474,  1482 
parameningitidis,  926 
pseudomeningitidis,  926 
sicca,  926 
Nelavare,  1260 
Nemathelminthes,  621 
References,  680-2 
Poisonous,  205 
References,  228 
Species  associated  with  Beri-beri, 
1679,  1680 
Nemathelminthic  Dysenteries,   1825, 
1840 


2376 


INDEX 


Nematocera,  773,  774 
Nematoda,  621,  622 

Bursata,  623,  624,  659 

Xon-Bursata,  623,  624-5,  627 

References,  680-2 
Nematode  Dermatites,  2200,  2219 

Embryos  in  Skin  affection,  2247 

Infections,  Table,  896 

Worms,  908,  1 71 3-1 4 
Nematodiases,  Intestinal,  1758 
Nematodirus,  624,  662 

References,  682 

Species 
filicollis,  663 
gibsoni,  624,  663 
Nematoideum  tracheale,  652 
Nematomyci,  1036 
Nematospora,  979 
Nemorhina,  837 

palpalis,  838 
Neoanopheles,  883 
Neocellia,  792 

stephensi,  887 
Neokharsivan,  27 
Neomyzomia,  791,  794 

elegans,  794 
Neopsylla,  865,  866 

bidentatiformis,  866,  867 

isacanthus,  866 

pentacanthus,  866 
Neora  lepida,  222 
Neorhynchidce,  680 
Xeosalvarsan,  1202 

Formula,  27 
Neosporidia,  293,  296,  297,  528 

References,  543 
Neotoma,  915 

fuscipes  372,  398 
Neotomince,  915 
Neotrichophyton,  988,  989,  1001 

flavum,  1002 

plicatile,  1002 
Neotropical  Dermal  Myiasis,  1633 
Nepa  cinerea,  363,  366,  372 
Nepaul      Tumour     of     Ear,      2010, 

2252 
Nephritic  type  of  Subtertian  Malaria, 

1 1 80,  1 1 84 
Nephritis,  1663 

Malarial,  1180,  n  84 

Trench,  1926 
Nephrolithiasis,  1926 
Nephrophages,  729 

sanguinarius,  729 
Neriodorin,  167-8 
Nerium  odorum,  164,  167-8,  169,  170 

oleander,  2152,  2162 
Nerve  Leprosy,  1659 
Nervenfieber,  1363 
Nervous  Fever,  1362 

Irritability,  88 


Nervous    System,  Derangements    of, 
1519,  1524,  1552 
Diseases  of,  124,  1981 

References,  1991 
Effects   on,  of  Temperature  and 

Humidity,  76,  89 
Symptoms,  in  Atypical  Subter- 
tian Malaria,  11 75 
Nesokia  bengalensis ,  870 
Neuralgias,  Malarial,  11 80,  11 84 

Post-Malarial,  11 84 
Neurasthenia,  88 
Tropical,  1981,  1988 
War  Zone,  1982 
Neuritis,  1587 
Alcoholic,  1 981 
Arsenical,  1981 
Malarial,  11 84 
Multiplex  Endemica,  1671 
Ocular,  2006 
Peripheral,  1680 

Endemic,  1981,  1989 
in  Yaws,  1552-3 
Neuroctena  anilis,  365 
Neuro-Fibromatosis,  2273 
Neurolepride,  1651 
Neuroptera,  748 

Neuroryctes  hydrophobic,  535,  540 
Neuroses  of  War  Zone,  1981-2 
Neurotoxins  of  Snake  Venom,  255-7 
Neurotropic      principles      of      Snake 

Venom,  244 
New-Born    Children,    Bullous   Erup- 
tions in,  1518 
New  Cacodyl,  26 

Diseases,    Evolution    of,    112,   114, 

394 
New   Hebrideans,  Arrow-Poisons  of, 

186 
Newt,  American,  Trypanosome  of ,  401 
Ngumba-Fly,  830 
Niaibi  (mite),  725,  2213 
Nicolaidi's    Radio-Active    Serum    for 

Pellagra,    1732 
Nicollia,  491,  492,  500 

quadrigemina,  500 
Nigerian  Arrow-Poisons,  1S4 
Night-Soil  Fever,  1363 
Nigrococcus,  925,  932 

cyaneus,  932 

fuscus,  932 

nigrescens,  932,  2102 
Nijrsine  africana,  1 756 
Nile  Boils,  931,  2021,  2024,  2027,  2165 
Nimetta-Fly,  811 
Nipple,  Paget's  Disease  of,  2277 
Niquirans,  the,  60 
Nirmus,  750 
Nissl's  Bodies,  11 55 
Nitrobacteria,  932,  933 
Nitrobacterium,  933 


INDEX 


2377 


Nitrobacterium  nilrobacter,  933 
Nitrogen,     Excretion    of,    in     Urine; 
India,  100,  101 
Metabolization     of,     by     Various 
Races,  100,  101 
Nkoulou,  1535 

Nocardia,  965,  1040,  1041, 1123,  1521, 
1747,  1886,  1892,  1926, 
2008,  2141,  2148,  2149 
Dermatomycoses  due  to,  2041 
Species 

actinomyces,  1057 

alba,  1046 

albida,  1046 

albosporea,  1047 

appendicis,  1050,  1054,  1061 

asteroides,  1053,  1058,  2123,  2131, 

2140,  2141,  2149 
Comparison  of,  with  N.  brasi- 

liensis,  Table,  2132 

aurantiaca,  1047 

aurea,  1060 

beta,  1046 

berestneffi,  new  name,  1054 

bovis,  969,  1040,  1041,  1051,  1054, 
1057,  1063,  1066,  1747, 
2008,  2009,  2130,  2131, 
2132,  2138,  2139,  2140, 

2141,  2148 
luteo-rosea,  1058 
sulphur  ea-alba,  1058 

brasiliensis,  1068 

Comparison  of,  with  N.  aster- 
oides, Table,  2132 

bruni,  1054 

buccalis,  1054,  1061,  1067 

Candida,  1051,  1060 

canis,  1053 

carnea,  1047,  1060 

carongeaui,  1063,  1066,  1966, 
2041,  2139,  2260 

chalcea,  1047 

chromogena,  1060 

cinereonigra,  1046 

citrea,  1046 

ccelicolor,  1047 

convoluta,  1053,  1062,  2140.  2142 

dassonvillei,  1054, 1059,2008,2009 

decussata,  1057,  1059 

dichotoma,  1045 

enteritidis,  1051,  1060 

equi,  1054 

erythrea,  1047 

farcinica,  1046,  1051 

foersteri,  1059,  2008 

foulertoni,  1054,  1892 

fusca,  1060,  2102 

garleni,   1050,   1060,  2136,   2142, 

2148 
gedanensis,  1053,  1892 
glauca,  1047 


133-4, 
2140, 


2009, 


2140, 


2133. 


2132, 
2138 


Nocardia,  continued 
Species,  continued 
graminarium,  1051 
hoffmanni,  1047 
hominis,  1053 
hominis  III.,  1061 
indica,  1051,  1058,  2131,  2 

2135,  2136,  2138, 

2142 
invulnerabilis,  1046 
israeli,    1041,  1053,    2008, 

2041,  2048 
krainskii,  1047 
krausei,  1054,  2136,  2137, 

2141 
lanfranchii,  1058 
lasserei,  1057,  1061 
leishmani,  1053,  1892 
lignieresi,  1054 
liguire,  1057 

lingualis,  1051,  1061,  1074 
liquefaciens,    1050,    1060, 

2140,  2142,  2148 
londinensis,  1054 
lutea,  1062 
luteola,  1050,  1060 
madurce,  1053,  1058,  2131, 

2133,  2134,  2135, 
melanocycla,  1047 
melanosporea,  1047 
microparva,  1047 
minutissima,    1053,    1061,   2041 

2080 
modorS,  1050 
monospora,  1047 
nigra,  1054,  1062,  1748 
odorifera,  105 1,  1060 
orangica,  1046 
parva,  1047 

pelletieri,  1053,  1058,  2041, 
pijperi,  1054.  1060 
pluricolor,  1047 
ponceti,  1054,  1060,  2137,  2 
pseudotuberculosa,  1892 
puhnonalis,  1054,  1059,  18c 
rivierei,  1053,  1061,  2041 
rosea,  1046 

rosenbachi,  1053,  1058 
rubea,  1046 
rubra,  1051 
saprophytica,  1045 
somaliensis ,   1053,   2137-8, 

2141 
tenuis,    1063,    1066,    1067, 

2102,  2105,  2138 
therntophila,  1047 
thibiergi,  1066,  2149 
urinaria,  1057 
valvules,  1054 
violacea,  1046 
Xncardiacecc,   1040 


2135 


2140, 
2IOI, 


237« 


INDEX 


:i49 


Nocardial  Abscesses 
Nocardiases 

Granular,  of  Tonsils,  1747 
Ocular,  2009 
Pulmonary,  1892 
Diagnosis,  1521 
References,  1894 
Nocardiomycosis,  Tonsillar,  1747 
Noctuidcs,  1640 

Nodular  Actinomycosis,  2 no,  2148 
Affections  of  Fungal  Origin,  2041, 
2042 
Rarer  Forms,  2106 
Dermatitis,  2247,  2249,  2252 

References,  2263 
Leprosy,  1654 
Lipomatosis,   Subcutaneous,   2247, 

2253 
Trichomycosis,    2101,    2105,    2042, 
2105 
Nodules  due  to  Cestodes,  2220 
Jeanselme's,  2260 
Juxta-Articular,  2260 
Sudan,  2165 
Symmetrical,  of  the  Ear,  2247,  2252 

References,  2263 
Ulcerated,  of  Leg,  1101 
West  Indian,  2247,  2254 
References,  2263 
Nodules  and  Muscle  Tenderness,  in- 
dications from,  1529 
Noguchi's  Ancistrodon  piscivorus  Se- 
rum, 273 
Pure  Crotalus  Serum,  273 
Nohu,  235 
Noma,  448 
Nomenclature  of 
Disease,  287 
Parasites,  rules  for,  287 
Nomomeristica,  690 
Non-Blood-Sucking    Flies,    Herpeto- 

monads  of,  365 
Non-Bursata,  623,  624-5,  627 
Non-Oontagious  Erysipelas,  2158 
Non-Development  of 
Eye,  1959 
Thigh,  1959 
Non-Febrile  Jaundice,  151 7 
Pustular 

Syphilides,  151 8 
Tuberculides,  151 8 
Pyoses,  Rashes  due  to,  151 7 
Non-Fermenting    Group    of    Strepto- 
cocci, 928 
Non-Follicular  Hyperkeratoses,  2256 
Non-Gonorrhceic      Urethritis,       539, 

1938-9,  1943 
Non-Malarial  Fevers 

Intermittent,     High    and     Low, 
1464-5 
Inferences,  1472 


Non-Malarial  Fevers,  continued 
Quartan,  1470 
Remittent,  1289 
Non-Pathogenic    Organisms,    Poten- 
tial    Pathogenicity    of, 
114 
Nona,  1268 
North  African  Relapsing  Fever,  1308, 

1 3 14 
North    American    Relapsing    Fever, 

1323 
Norwegian  Beri-beri,  1690 
Nose,  Affections  of,  see  Nasal,  above, 
see  also  Rhinal,  etc. 

Partial  Blocking  of,  indicative    of 
Diphtheria,  1521 
Nosema,  287,  510,  513,  529 

apis,  529 

bombycis,  529 
Nosoparasites,  1069 
Notechis,  246,  247 

pseudechis,  243,  247,  253 

scutatus,  247,  251,  253,  272,  273 
Notosdres,  731 

cati  var.  cati,  2215 
Notostigmata,  692 
Nova  Bolest,  1639,  2208 
Novarsenobenzol,  27 
Novarsenobillon,  27 
Novy's    Rat-Disease,    Virus  of,    Cul- 
tivable and   Filterable, 

54i 

Noxious  Larvae,  Dermatites  due  to, 
2200,  2207 
References,  2220 
N'tansi,  1260 
Nubians,  47 
Nuche,  828 
Nucleophaga,  298 

Nucleus  of  Protozoan  Parasites,  290 
Nucleus    de    reliquat,    293,     see    also 

NebenkSrper 
Nucleolus,  290 
Nutcherr  (cereal),  1540 
Nutmegs,  173 

Nutrition  of  Skin,  Disorders  of,  2105, 
2017,   see  also  Biotr  p- 
sis,  2282 
Nuttalia,  491,  492,  500 
Species 

decumani,  500 
equi,  500 
herpetedis,  500 
microti,  500 
muris,  500 
ninense,  500 
Nux  vomica,  189 
Nyctalopia,  2004 
Nyctcribida,  854 
Nvctotherus,  544 
References,  551 


INDEX 


2379 


Nyciotkerus,  continued 
Species 

africanus,  546,  549,  550,  1837 

faba,  546,  548,  549,  1837 

giganteus,  546,  549,  1837 

Known  in  Man,  549 
Nyssorhynchus,  792,  795,  S85 
Carriers  of  Malaria,  887 
Species 

atinulipes,  795,  887 

brunipes,  796 

fuliginosus,  795,  796,  887 

indiensis,  796 

jamesii,  796 

karwari,  796,  888 

maculatus,  796,  887 

maculipalpis,   796 
var.  indiensis,  887 

masteri,  795 

nivipes,  796 

phiUppinensis,  796 

pvetoriensis,  796 

stephensi,  795,  887 

theobaldi,  796,  887 

tibani,  796 

willmori,  796,  887 

Obermeyer's  Relapsing  Fever,  763, 

765 
Obstruction,  Intestinal,  1739,  1753 
Obstructive  Jaundice,  1907 
Oceania,  Diseases  of,  123 

Vegetal  Poisons,  164 
Oceanic  Races,  49,  55 
Ochindundu,  767 
Ochipia,  222,  2208 
Ochisia,  226,  2208 
Ochrodermatosis,  2222,  2236 
Ochroid  Maduromycoses,  21 13  sqq. 
Ochromyia  anthropophaga,  849,  1637 
Ochronosis,  2233 
OctomitidcB,  464 
Octomitus,  464,  465 

dujardini,  465 

hominis,  465 

intestinalis,  465 

muris,  465 
Octosporea  muscce-domesticcB ,  295 
Ocular  Albinism,  1995,  2004 

Aspergillosis,  103 1,  2009 

Blastomycosis,  2009 

Filariasis,  1972,  1974,  2007 

Glenosporosis,  2009,  2010 

Haemorrhage,  2005 

Moniliasis,  2009 

Mycoses,  2008 

Myiasis,  1622,  1625,  1627,  2007 

Neuritis,  2006 

Nocardiases,  2009 

Opacities,  2000,  2005,  2006 

Paragonimiasis,  2007 


Ocular  Albinism,  continued 
Refraction,  Errors  of,  1995 
Sporotrichosis,  2008,  2009,  2010 
Symptoms  in   Subtertian   Malaria, 
1181 
Odontopsyllus,  866 

charlottensis ,  866,  867 
telegoni,  866 
Odours,  Racial,  2223 
(Ecacta,  802,  805 
furens,  805 
hostilissima,  805 
(Eciacus,  762,  766 
hirudinis,  766 
vicarius,  766 
(Ecology,  116 

(Edema,  Indications  from,  1531 
Parasites  causing,  552 
Rashes  associated  with,  1 514-15 
Angioneurotic,  1729,  1731 
of  Eyelids,  1994 
Patchy,  Malarial,  11 81 
Quincke's,  11 81 
Tropical,  1693 
War  Zone,  1693 
(Enanthe  crocata,  188 
(Esophageal  Vein-Dilatation,  1749 
Q£sophagosfomum,  624,  659,  661 
References,  682 
Species 

apiostomum,  661 
brumpti,  624,  661,  1840 
dentatum,  661 
stephanostomum 
var.  dentigera,  661 
var.  thomasi,  624,  661,  1841 
subulatum,  661 
(EstridcB,  825,  1627,  1630,  1632,  1633, 
2208 
Larvae  of 

Dermatites  due  to,  2207 
Reference,  856 
GLstvincB,  825 

(Estromyia  satyrus,  1639,  2209 
(Estrus,  826 
guildingi,  1620,  1633 
hominis,  828,  1620,  1633 
humanus,  1633 
ovis,  827,  1625,  1627,  1633 
(Eufs  d'Helminthes,  476 
Officials,    Tropical,    see    also    Candi- 
dates 
Check  Examination  of,  on  Arrival, 
129 
Ogmodon,  246 

vitianus,  251 
Oicomonadidce,  333,  334 
Oicomonas,  334,  343.  1833 
References,   357 
Species 
anatis,  336 


2380 


INDEX 


Oicomonas,  continued 
Species,  continued 
canis,  336 
gallinarum,  336 
hominis,  335,  1796 
mutabilis,  335 
perryi,  336 
pyophila,  335 
vaginalis,  336,  1946 
Oicomonata,  1838 
Oidiomycosis,  1073,  2081 
Bronchial,  1889 
Oral,  1 741 
Tonsillar,  1748 
Oidiumiia),    981,    1070,    1073,    107S, 
1093,  1742,  1743,  1748, 
1886,  1890,  1891,  1944, 
1945,  2081 
Reference,  1124 
Species 

albicans,  1085,  1741,  1781 
asteroides,  1093,  1095,1743,  1782, 

1890 
aureum,  1079 
coccidioides  {Coccidioides  immitis), 

985 
cutaneum,  1092 
furfur,   1099 
immitis,  985 
lactis,  1093,  1742,  1890 

var.  A,  1095 
matalense,     1093,      1096,     1742, 

1890 
porriginis,  1012 
protozoides,  985 
pulmoneum,  1091 
roseum,  1091 
rotundatum,    1093,    1095,     1743, 

1748,  1782,  1890 
schoenleini,  1012 
in  Sprue,  1095,  1782 
subtile,  1099 
subtile  cutis,  ioqr 
tonsurans,  999 
tuckeri,  1  7  |  _: 
Table  of,  1094 
willia,   1 782 
Oil  of  Aniseed,  191 
of  Chenopodium,  1770 
Useless  for  Snake  Bite,  277 
Oiling  of  Water,  Larvicidal,  1208 
Old  World  Rats  and  Mice,  915 
Oleander  Dermatitis,  2162 
Oleanders,  Poisons  from,  165,  167 
Oleina,  983 
Olfersia,  855 
Oligosporogenea,  529 
Oligotricha,  547 
Ombanja,  2241 
Omphalopagus,   1958 
Omphalositic  Monsters,  1958 


Onchocerca,  623,  632,  649 
References,  681 
Species 
gibsoni,  649 
gutturosa,  649 

volvulus,    623,    649,    1961,    1964, 
1966 
Dermatitis  due  to,  2219 
OnchocercincB,  631,  649 
Onchophora,  689 
Onchosphere,  599 
Onions,  97 
Onyalai,  1698 

References,  1699 
Onychia,  2283 

Frambcetic,  1550 
Onychogryphosis,  2283 
Onychomycosis,   1026,   2283 

Tropicalis,  2059 
Onychorrhexis,  2283 
Ookinete,  295 
Ooniycetes,  972 
Oordh  dal,  196 

Oospora,  987,  1041,  1042,  1078,  1105, 
1117 
asteroides,  1053,  1058 
bovis,  1051,  1057 
buccalis,  1054,  1061 
canina,  1078 
dorice,  1046 
foesteri,  1066,  1067 
guignardi,  1046 
hominis,  1061 
indica,  1051 

var.  -flava,  2117,  2134 
var.  nigra,  2117,  2134 
lingualis,  1061 
metschnikovi,  1045 
minutissima,  1053,  1062 
pelletieri,  1053,  1058,  2135 
perieri,  1092 
porriginis  1012   . 
pulmonalis,  1054 
pulmonea,  1091 
tozeuri,  1105,  11 06 
OiisporacecB,  986,  1070,  1078 
Oosporangium,  971 
Oospores,  971 

Ootype  of  Watsonius  watsoni,  562 
Opacities,  Ocular,  of  Various  Causa- 
tion, 2000,  2005,  2006 
Opalines,  544,  545,  546 
Ophidia,     Parasites     of,      401,     480, 
487 
Venomous,  242 

References,  280-1 
Venoms  of,  History,  242-4 
Ophidismus,  242 
,   Ophiodes,  722 

Ophiotoxin,  254 
1   Ophryocystis,  471 


INDEX 


2381 


Ophthalmia,  120,  124,  899,  900,  902, 
908,  1994 

iEgyptiaca,  1998  u$ 

Neonatorum,  1996,  1997 

Nodosa,  1996 
Ophthalmomycoses,  2008 
OpilioacaridcB ,  692 
Opiliones,  690 
Opisthobranchiata,  892 
Opisthoglyplia,  245 
Opisthorcliiidce,  564,  575 
Opisthorchiincs,  575 
Opisthorchiosis,  1906,  1907,  1917 

References,  191 7 
Opisthorchis,  557,  576,  1776,  1908 

caninas,  577 

ft  Uncus.  576,  1907,  191 7 
References,  594 

novevca,  577 

References,  595 

pseudofelineus,  576 

viverrini,    577 
Opisthothelce,  212 
Opium,  169,  178 

Use  and  Abuse  of,  169,  175 
Opium  Poisoning,  169 

Differential  Diagnosis  from  Heat- 
stroke,   1456 
Oppilacao,  1283,  1761 
Oppilatio,   1 761 

Optic     Affections,    see    Eye,    Ocular, 
and  under  Names,  2005 
Oral  Blastomycosis,  2084,  2085 

Diseases  and  Infections,  263,  1740, 

1745 
Myiasis,  1625 
Oidiomycosis,  1741 
Spiroschaudinnia,  448,  450,  452 
Temperatures.  70,  71 
Treatment     in      Ankylostomiasis, 

1771 
Treponema,  461 
Orchid  Subgroup  of  Dermatitis-c  aus- 

ing  Plants,  2159 
Orchidacecs,  2153,  2159 
Orchitic  type  of  Subtertian  Malaria, 

1 1 80 
Orchitis,  1939 

Filarial,  1595,  1603,  1605 
Ordeal,  Trial  by,  Poisons  used  in,  178-9 
Organic   Preparations    as    Aphrodisi- 
acs, 172 
Poisons,  162  sqq. 
Organs,    Localized   Derangement   of, 

1512.  1524 
Organs  of  Special  Sense,  Diseases  of, 

1993 
References,  2014 

Subtertian  Malaria  attacking,  11 75, 
1181 
Oribatida,  692 


Oriental     Sore      (Cutaneous     Leish- 
maniasis, q.v.),  20,  2165 
p    References,  2197 
Ornithoctona,  855 
Ornithodoros,  702,  705,  919 
Species 

csqualis,  704 

americanus,  708 

canestrini,  705 

coriaceus,  708 

erraticus,  705 

furcosus,  705 

lahorensis,  708 

megnini,  700,  708,  13 19 

miliaris,  708 

moubata,  20,  216,  430,  440,  445, 

453.  691,  7°°-  702.  7°5. 
706,  767,  919,  1318 
pavimentosus,  768 
radis,  709 
savignyi,  696,  700,  705,  919 

var.  ccBca,  706 
talaje,  217,  919 
tholozani,  700,  705 
turicata,  216-17,  700,  708,  919, 
1319,  1324 
Parasitic  to  Man,  700 
Ornithoglossum  glaucum,  igo 
Ornithomyia,  855 
lagopodis,  526 
Ornithorhyncus  paradoxus,  279,  280 
Oro-Gastro-Intestinal  Myiasis,   1222, 

1620,  1621,  1628 
Oro  Poisoning,  164,  168 
Oro-Pharyngeal  Blastomycosis,   2084 

Leishmaniasis  Indian,  2165,  2179 
Oroya  Fever,  1566,  1567,  1575 

Causal  Agent,  502,   503,  504,   542, 

157°>  x576 
Diagnosis,  1527 

Differential,  1568,  1576 
Orpiment,  27 
Ortholfersia,  855 
Orthoptera,  748,  871 
Parasites  of,  546 
Orthorrhapha,  773,  814 
nematocera,  774,  801 
Os  Calcis,  Endemic  Enlargement  of, 
1524,   1967.   1979 
References,  1980 
Oscillaria,  504 
OscinidcB,  901,  902 

Reference,  856 
Osier's  Parasite,  737 
Osmanli  Turks,  55 
Osseous    System,    Derangements    of, 

1519,  1523,  1552 
Ostariophysi,  232 
Osteitis,  Fibrous,  1552 
Osteomalacia  in  Multipara,  1943 
Osteomata,  123 


2382 


INDEX 


Osteomyelitis,  113,  1523,  1529 
Osteoperiostitis,  2106 
Otalgia,  Intermittent,  Malarial,  2013 
Otitis,  1059 
Acute,  1023 

Externa  Circumscripta,  2012 
Ossificans,  2012 
Parasitica,  201 1 
Media,  1025,  1949 
Suppurative,  2013 
Otocephalus,  1958 
Otomi,  the,  56,  57 
Otomucormycosis,  974,  976 
Otomycosis,    967,     974,     975,     1029, 
1032,  1078,  1084,  1089, 
1113,  1114,  1117,  2011 
Aspergillina,  1031,  201 1 
Ouabain,  182 
Ouabaio,  182 
Oucoes,  2218 
Ourari  or  Curari,  185,  186 
Ova   in    Sputum,    indications    from, 

1521 
Ovaenya,  853,  1631 
Ova-Herero,  the,  53 
Ovambo  Arrow- Poison,  183 
Ovarian  Cysts,  1945 
Ovaritic  Neuralgias,   Malarial,    1180, 

1184 
Ovaritis  type  of  Subtertian  Malaria, 

1180 
Overwork,  1989 
Ovoplasma,  488,  491 

anucleatum,  491,  1468 
Ovoplasmosis,  1468 
Ovovitellin,  260 
Owl- Midge,  905 

Owl,     Little,     Development    in,    of 
Hesmoprotens       noctucB, 

519.  524 

Owls,    Leucocytozoon    danilewskyi   of, 

432  sqq. 
Oxalate  Poisoning,  1673,  1674 
Oxalis  anthelmintica,   1753 
Oxaluria,  1926,  1933 

References,  1937 
Oxygenacees,  986 
Oxyporus  subterraneus,  1640 
Oxyuriasis,   1776 
Oxyurides,  623,  626,  657 
Oxyuris,  623,  657,  1776,  1777 

vcrmicularis,    122,    124,    286,    623, 
632,  637,  1776,  1777 
References,  682 

P  ACHYCROPOIDKUS  dllbillS,    908 

Pachydermia,  1610 
Pachyrhizus  angulatus,  188 
Pachyrrhizid,  188 
Pacific  Islands,  Races  of,  49 
Vegetal  Poisons  of,  164 


Padavalmicum,  2111,  2116 
Pcederus,  226 

columbinus,  226,  2204,  2205 

cribipunctata,  226 

elongatus,  1640 

peregrintis,  226,  2204,  2205 
Paget's  Disease  of  the  Nipple,  2277 
Pain,  Racial  Susceptibility  to,  2265 
Painless  Chronic  Ulcers,  2 191 
Pakitsar,  1824 
Palate,  Cleft,  1959 
Paleolithic  Arrow- Poisoning,  180 
Paleopathology,  11 2-1 3 
Palicourea  marcgravii,  191 
Palisota  barteri,  183 
Palliata,  889 
Pallor,  86 

Facial,  1903 
Palmar      Erythema,       Symmetrical, 
2222,  2224 
References,  2246 
Palms  and  Soles,  Frambcesial  Erup- 
tions on,  1 550-1 
Palpebral  Blastomycosis,  2009 

Sporotrichosis,  2008 
Palpigrada,  690 
Palpomyia,  802,  803,  806 
Paludism,  11 29 
Paludisme,  1129 
Paludismo,   n  29 
Pampean  Races,  60 
Pamperos,  the,  81 
Panax  quinquefolium  Root,  172 
Pancreas,   Ascaris   Infection  of,  553, 
1908 

Cancer  of,  1908 

Diseases  of,  1906,  1907 
References,  191 8 

Symptoms    associated    with,    De- 
ductions    from,     1524, 

1525 
Pancreatic  Ducts,  Acute  Suppurative 

Catarrh  of,  1907 
Pancreatitis,  Reference,  191 8 
Various  Forms 
Acute,  1525 

Chronic,  1532,  1788,  1908 
Haemorrhagic  Acute,  1907 

Subtertian  Malaria  resembling, 
1177.  1178 
Subacute,  1908 
PandinidcB,  207 
'  Pandu  roga  ',  666 
Pangonia,  820,  822 
beckeri,  823 
comata,  823 
gulosa,  823 
rostrata,  823 
ri'tppellii,  823 
varicolor,  823 
Pangonincs.  817.  820 


INDEX 


2383 


Pani-ghao,  1764 
Pan-maa  (beetle),  172 
Panneuritis  Hndemica,  1671 
Pannus,  1999,  2000 

Carateus,  2093 
Panophthalmia,  2003 
Panoplites  africanus,  638,  644 
Pansporoblast,  292,  293 
Pantapoda,  690 
Papajos,  the,  60 
PapaveracecB,  2153 
Papilionidcs,  1640 
Papilloma  Inguinale,  2165,  2196 

References,   2199 
Papillomata,  Cutaneous,  123 
Pappataci  Fever,  1233,  1254 

.Etiology,  1255 

Castellani's  Sign  in,  1256,  1257 

Climatology,  1255 

Complications,  1258 

Course,  1257 

Definition,  1250 

Diagnosis,  1257,  1527 

Differential,  1250,   1257-8,   1337, 

1497.   M98,   1505,   1514 

History,  1254 

Immunity,  1256 

Incubation,  1256 

Insect  Carriers,  542,  547,  809,  810, 
920,  1.128,  1254,  1255 

Morbid  Anatomy,  1256 

Onset,  1256,  1527 

Pathology,  1255-6 

Prognosis,  1258 

Prophylaxis,  1258 

Rash,  1 51 4 

References,  1242,  1258 

Relapses,  1258 

Sequelae,  1258 

Symptomatology,  1256-7,  1429 

Synonyms,  1244,  1254 

Transmission,  920,  see  also   Insect 
Carriers  above 

Treatment,  1258 

Varieties,  1258 

Virus,  Filterable,  54J 
Papua,  Diseases  of,  123 
Papuans,  the,  49,  53 
Papular  Eczema,  2252 

Eruptions,     Diagnosis     of,      1513, 
1515 

Fever,  1471-2,  1515 
Papulo-Pustular    Eruption   in    Glan- 
ders, 1529 
Papulo-Vesicular    Vaccinia,     1496-7, 

1516 
Parabasal,  353 
Paracephalus,  1958 
Paracholera,  801,  1804,  1819 

.Etiology,  962,  964,  1819,  1820 

References,  966,  1823 


Parachordodes,  679 
alpestris,  679 
pustulosus,  679 
tolosanus.  679 
violaceus,  679 
Paradysentery,  1842,  1845 
Paraframbcesial  Affections,  1556 
Parafuchsin.  26 
Paragonimiasis,  1584 

.Etiology,  287,  575,  1533,  1584 
Complications,  1587 
Climatology,  1585 
Definition,  1584 
Diagnosis,  1521,  1587 

Differential,  1875 
History,  1584 
Pathology,  1586 
Prophylaxis,  1587 
References,   1588 
Symptomatology,  1587 
Synonyms,  1584 
Treatment,  1587 
Abdominal,  1587 
Cerebral,  1587 
Generalized,  1587 
Ocular,  2007 
Thoracic,  1587 
Paragonimus,  572,  1776 
compactus,  573 
kellicotti,  573,  574 
ringeri,    287,    552,    572,    573,    575, 
894,    1584,    1585,    1885. 
1889 
rudis,  573 

westermanni,  573,  1584,  2007 
Paragordius,  679 
cinctus,  679 
tricuspidatus,  679 
varius,  679 
Paraguay  Tea,  177-8 
Parakeratosis,  2033 

Variegata,  2272,  2273 
Paraleprosis,  1663 
Paralysis,  123,  1587 

Accommodation,    of    Eye-Muscles, 

2005 
Agitans,  1919 
General,  1981 

of  Orbicularis  palpebrarum,  2006 
Progressive,  2279 
Spastic,  1981 
Sudden,   173 
from  Tick-bite,  872 
Paralytic,    Vertigo,    Endemic,    1981, 

1982 
Paramosba,  298,  300,  324 
eilhardi,  324-5 
hominis,  325 
Paramoscioides  costatus,  393 
Paramcecium,  381,  393 
aurelia,  545-6 


2384 


INDEX 


Paramcecium,  continued 
coli,  547 
costatum,  393 
loricatum,  393 
Parameningococcus,  1478,  1479 
Paramphistomidcs,  561 

Reference,  594 
ParamphistomincB,  561 
Paramphistomoidea,  561 

References,  594 
Paramphistomum,  561 

watsoni,  562 
Paramycetoma,     1741,     2015,     2017, 

2110,  2145 
Paramycetomas,  21 10,  2145 

References,  2150 
Paranaemia  Tropicalis,  75,  1903 
Parangi,  1535,  1536 
Parapestis,  1962 
Paraplasm/*,  491 

flavigenum,   1231,   1233,   1902 
Paraplasmata,  1903 
Paraplegia  Mephitica,  1671 
Parapsyllus,  865 

Parasaccharomyces,  1080,  1092,  1742, 
2081 
harteri,  1080 
Parasites,  Definition  of,  285 
Endemicity  of,  115 
Evolution  of,  113 
Animal,  285 

Diseases     due     to,     285,     1533, 

1535 
Nomenclature,  287 

Rules  of,  287 
Reproduction,  286 
Intestinal,  122,  123 
Metazoan,  287,  552 
Periodical,     286,      554,     see     also 

Microplaria 
Protozoan,  287,  288 
Diseases  due  to,  1533,  1535 
References,  328-9 
Stationary,  285-6 
Temporary,  285 

Vegetal,   115,   285,  872,   922,  923, 
1533.1679 
Parasitic  Arthropods, Diseases  due  to, 
1 128,    see    also   Arthro- 
poda 
Diseases 

Endemic,  116 

Study  of,  1 1 6- 1 7 
Limitation  of,  by  Food   Supply 
of    Insect   Transmitter, 
691 
,of  the  Skin,  2264,  2267 
Unspecified,  122 
Flies,  814,  825 
Granuloma,  2165 
Haemoptysis,  1584 


Parasitic,  continued 
Infection 

Methods  of,  553,  554 
Prophylaxis,  554 
Monsters,  Double,  1959 
Worms 

Carried  by  Arthropods,  24,  873, 

876,  908 
Diseases   due  to,    1533,  see  also 
Helminthic      Diseases, 
1752 
Parasitism,   Chance,    287,    546,    554, 
920,   1944 
Effects  according  to 

Absorption  of  Food,  553 
Bacterial    Infection    introduced 

by  Parasite,  553 
Condition  of  Host,  553 
Migration  of  Parasite  in  Body, 

553 
Organ  affected,  552-3 
Species,  condition  and  numbers, 

552 
Hygiene    as    Prophylaxis    against, 

554 
Permanent,  286 

True,    554,    see    also    Hyperpara- 
sitism,   116,   and  Poly- 
parasitism,  1776 
Parasyphilis,  122,  1981,  2279 
Parathyroid  Glands,  Diseases  of,  191 9 
Paratyphoid     Fevers,      1362,      1363, 
1404,     1466,    1810,    see 
also    Parenteric,    1404, 
and  B.  paratyphosus,  in 
Bacillus  (i) 
Bacilli  of,  22,  1363 

Reference,  965 
Carriers,  1370 
Immunization  against,  114 
Prognosis,  1398-9 

Prophylactic  Vaccination,   23,   128 
Para-Undulant  Fever,  1441,  1447 
Parenchymatous  Goitre,  1920 
Parendomyces,  1080,  2081 

balzeri,  982 
Parenterica,  1362 

Definition,  1362,  1404 
Parenteric  Fevers,  1362,  1404 
^Etiology,  1362,  1405-6 
Classification,  1405-6 
Climatology,  1405 
Diagnosis,  1407 

Differential,  1395,  1397 
Frequency  of,  1406-7 
History,  1405 
Morbid  Anatomy,   1406 
Pathology,  1406 
Prognosis,  1398,  1407 
Prophylaxis,  1407 
References,  1414 


INDEX 


2385 


Parenteric  Fevers,  continued 

Symptomatology,  1406 

Synonyms,  1404 

Treatment,  1407 

Varieties,  1408 
Parhesmatopota,  820 

cognata,  820 
Pariodontis,  865 
Parleala,  1700 

Paronychia,  Framboetic,  1550 
.  Paropisthorchis,  577 

caninus,  577 
Parotid  Glands,  1524 

Swelling  of,  1526 
Paroxysmal   Hemoglobinuria,    121 2 
Parrots,    Epizootic  of,   Transmissible 

to  Man,  1408 
Parsnips,    Dermatitis-causing,    2157 
Pascha-churdj,  2165,  2169 
Parthenogenesis,  295,  337 
Pasteurella,  933,  943 

cholercegallinarum,  943 

coscoroba^  941,  943 

gallincs,  933 

pcstis    (B.   pestis,   q.v.),    943,    1416 
1419 
Pasteurellece,  933,  943 
Pastinaca  saliva   Dermatitis-causing, 

2157 
Patagiamyia,  884 

M  daria-carriers,  885 

pseudopunctipennis,  885 
Patagonians,  the,  56 
Patchy  Malarial  (Edema,  11 81 
Patek,  1535 
Paspalum    scrobiculatum,     190,     195, 

199,  200 
Paspalismus,  195,  199 

References,  202 
Passumaks,  the,  55 
Pathogenic     Potentiality     of     Non- 
pathogenic Organisms, 

"4.   394 
Patient  Carrying  on  Ordinary  Work 
Acute  Fevers  of,  without  Striking 
Physical  Sign,  1526 
Unable  to  Carry  on  Usual  Duties 
Acute  Fevers  of,  without  Strik- 
ing Physical  Sign,  1527 
Paul  of  .Egina,  12,  17 
Paullinia,  [64 
pinnata,  10 1.   [68,  186 
sorbilis,  168,  177 
Paulowilhelmia  speciosa,  188 
Pausinystalia  trilhesti,  172 
IV-brine  of  Silkworms,  52^ 
Pechadi,  200 
Pe  1  male  Bodies,  990 
Pectinibranchia,  890 
Pectinifera,  690 
Pectobothrii  560 


Pedicince,  754 
Pedicinus,  758 
eurygastes,  758 
longiceps,  758 
microps,  758 
piageti,  758 
Pediciilidce,  753,  2200 

Mouth-parts,  and  Mode  of  Blood- 
sucking, 752,  2201 
Pediculina,  752 
Pediculince,  754 
Pediculoides,  728 
tritici,  728 

ventricosus,  728,  2214,  2216 
Pediculosis,  2201,  2268 
Capitis,  2202,  2268 
Corporis,  2202,  2268 
Pigmented  forms,  2203 
Pubis,  2201,  2202,  2203,  2268 
Pediculus,  380,  755,  see  also  Lice 
Diseases  spread  by,  542,  1308  sqq., 

1501,  1650,  1679 
Nomenclature,  750 
Rash  due  to,  1516 
Species 
asini,  752 

capitis,  755,  756,  897,  1679 
cervicalis,  755 
columbcs,  750 
consobrinas,  755 

corporis,     363,    755,    757,    1308, 
i3°9.  I3M.  1315.  1326, 
1329.  I33i.  T-332.  2201, 
2202,  2203 
Spreader  of  Trench  Fever  (q.v.), 
1 501  sqq. 
huinanus,  755,  1308,  1309,  1329, 
1332,  2201,  2202 
var.  capitis,  755 
nigritarsum,  755 
pubis,  757 
punctatus,  755 
suis,  752 

vestimentorium,  542 
vititli,  752 
Pedipalpi,  690 

Pedro  Fernandas  (manchineel),  2157 
Peenash,  1621,  1626 
Pelandria,  1700 
Pelargonium  flabelliform,  1857 

tuber  osa,  1857 
Pelecorhy nchus,  823 
Peliosis,  1698 

Rheumatica,  1516 
Pellagra,  1700,  1788,  1981 

.Etiological  Theories,  105,  109,  124, 

920,  1533,  1708 
Climatology,  124,  133,  1706 
Complications,  151 4,  171 7,  1727-8, 

1733 
Definition,  1700 

150 


2  386 


INDEX 


Pellagra,  coyitinued 
Diagnosis,  1728-9 

Differential,  1688,  1 730-1,  1990, 
2231 

Diet.  !733 

Effect  in,  of  Sun-rays,  80 

Erythema  of,  2158 

Histopathology,   1 720-1 

History,   1700-6 

Incidence 

Age,  Condition  and  Sex,  171 7 
Seasonal,  1708,  1716,  1722 

Insect     Vector,    suspect,     812-13, 
1716,  1717,  1733 

Maize  in  relation  to,  105,  1073  sqq., 
passim 

Morbid  Anatomy,   171 9-21 

Pathology,  171 8 

Parasites  associated  with,  1713  sqq. 

Predisposing  Causes,  171 7 

Prognosis,  1731 

Prophylaxis,  1733-4 

References,  1734-5 

Relapses,  1731 

Symptomatology,  1721-7 

Synonyms,  1700 

Treatment,  1732-3 

Water  in  relation  to,   1707,   171 3, 
1715,  1717,  1725 
Pellarella,  1700,  1701 
Pellarina,  1700 
Pellodera  pellio,  628 
Pellote,  176 
Pelomyxa,  298,  323 
Pelor  filamentosum,  232,  238 

japonicum,  239-40 
Pelvic  Deformity  due  to  Osteomalacia, 

1945 
Examination  of  Women   going  to 
the  Tropics,  129 
Pemphigus,  2020 
Acutus,  2025,  2206 
Contagiosus,  2018 
in  Children,   124 
Foliaceus,  2269 
Neonatorum,  151 8 
Septic,  1518,  2269 
Vegetans,  2269 
Vulgaris,  2269 
Penicillidia  dufoitri,  S54 
Penicilliopsis,  1024 
Penicilliosis,  Bronchial.  1892 
of  Hairy  Parts,  2041,  2092 
Penicillium,   987,    1024,    1025,   mi, 
1123,  1836,  1891,   1892, 
1945,  2093,  2098,  2149 
Dermatomycoses  due  to,  2041 
Species 

barbcB,  1024,  1026,  2041,  2092 
brevicaule,    var.    hominis,     1024, 
1026 


Penicillium,  continued 
Species,  continued 

crustaceum,  1024,  1025 
crustatum,  1892 
expansum,  1025 
glaucum,  1025,  1712 
Intermediate,  2094,  2095 
minimum,  1024,  1025 
montoyai,  1024,  1025,  2094,  2098 
pictor,  1025 
pruriosum,  1024,  1026 
Penis,  Epithelioma  of,  1939 
Penjdeh  Ulcer,  2166 
Pentastoma,  Pentastomum,  73 J 
constrictum,  734 
denticulaium ,  733 
diesingi,  734 
euryzonum,  734 
leonis,  734 
moniliformis,  736 
polyzonum,  734 
protelis,  734 
subcylindvicum,  738 
tcsnoides,  733 
Pentatrichomonas,  352,  356 
ardindelteili,  356 
bengalensis,  356 
Pentosuria,  1924 
Pepper,  Black,  170 
Perciformes,  232 
Perforation  of  Bowel  by  Ascaris,  1961 

of  Typhoid  Ulcer,  1961 
Perical,  1595,  1610,  2111,  2116 
Pericarditis,  1904 
Pericoma,  806 
Peridinece,  923 
Perillopus,  367 
Perilymphangitis,  651 
Perinephritis,  Phlegmonous,  1949 
Periodic  One-day  Fever,  1501 
Periodical  Winds,  80,  81 
Periodische  Fieber,  1501 
Periostitis,  1075 

Chronic  Diffuse  in  late   Frambce- 

sia,  1535 
Digital,  Multiple,  in  Yaws,  1552 
Peripatus,  689 
Peripheral,  Neuritis,  Endemic,  1981, 

1989 
Peviplaneta,  765 
Periplast,  330,  331 
Pevisporiacece,  2008 
Perisporiales,  985 
Peritonitis,  1058,  1961 
Peritricha,  546 
Perleche,  1746,  2284 
Permanganate  of  Potash  as  Antidote 
to 
Arrow-Poison,  181,  182 
Snake-Bite,   243,   275,  277,   280, 
1804,  1812 


INDEX 


2387 


Permanent  Winds,  79 

Perneirus,  1671 

Pernicious  Anaemia,  1169,  1575 

.Malaria    (see   also   Malaria,    Perni- 
cious), 1129,  1182 
Persia,  Diseases  of,  120 
Persian  Relapsing  Fever,  919,  1322 
Pertussis,  120 
Peruvian  Disease,  Acarine,  691 

Wart,  1566 
Pes  Febricitans,  1610 

Gigas,  1959,  1967,  1978 
Pest  of  Havana,  1229 
Peste,  Die,  141 6 
Peste,  La,  1416 
Peste  Bubbonica,  1416 
Pestis,  1 410 

Americana,   i22<» 
Petite  Verole,  i486 
Peyote,  124 
Peyottl,  176 
Pezizales,  985 
Pfeifferia  princeps,  474 
Pfeiner's  Glandular  Fever,  1522 
Pfenderius,  561 

Phacelia  infundibuliformis,  124 
Phacidiales,  985 
Phcenocystes,  528 
Phcsophycece,  923 

Phagedsena,     Hospital,     428,     2182, 
2185 

Tropica,  2 181 
Phagedcnismus,  Tropische,  2 181 
Phagocytosis,  293 
Phalangomyia  debilis,  504 
Phanerogams,  923 
Pharaoh's  Tahuret,  1944 
Pharyngeal     Invasion     by    Fasciola 
hepatica  (Halzoun),i  74(1 
Pharyngitis,    Membrano-ulcerative, 

1745 
riitisinidce,  871 
Phauloixodes,  711 

rufus,  713 
Phialidalinets,  mi,  1123 
Phialide,  1037,  1039 
Philcsmatomyia,  832,  833 

gurnei,  833 

msignis,  833 

lineata,  833 
Philcsmon,  688 

grandicheri,  688 

pungens,  688 
Philippine     Islands,      Arrow-Poisons 
of,  1 86 

Diseases  of,  122 

Fish-poisons  of,  188 

Races  of,  55 

Vegetal  Poisons  of,  173 
Plulipowicz's  Sign,  in  Entari<  .  1  }8i 
PhilopteridtB,  751 


Phimosis,  1939 

Phlebectasis,  Filarial,  1603,  1607 

Phlebitis,  Suppurative,  of  Spermatic 

Cord,  1939 
Phlebotomince,  806 
Phlebotomus  Fever,  1254 
Phlebotomus  (fly),  802,  806,  1527 
Diseases  and  Parasites  carried  by, 
363.    379-8o,    542,    806, 
809,  810,  919,  920,  1568 
Species 

angustipennis,  809 
antennalus,  809 
argentipes,  809 
babu,  809 
cruciatus,  809 
duboscquii,  809 
himaiayensis,  809 
legeri,  809 
major,  809 
malabaricus,  809 
mascitii,  809 
minutus,  809 

var.  africana,  809 
nigerrimus,  809 
papatasii,  542,  809,  810,   1254, 

1255 
perniciosus,  809 
perturbans,  809 
rostrans,  809 
squamiplairis,  809 
verrucarum,  810,  919,  1568 
vexator,  809 
Phlegmasia  Malarica,  1610 
Phlegmonous    Inflammation   of    Sto- 
mach, 1520,  1749 
Perinephritis,  1949 
Phlyctenular  Keratitis,  2002 
Phcenicians,  the,  47 
Phonergates     blcoloripes,     219,     691, 

767 
Phopalosylla,  865 
Phora  femorata,  900,  904 
pallipes,  1630 
rufipes,  1630 
PhoridcB,  824,  900,  1630 
Phosphorescent  Sweat,  2224 
Phosphoridrosis,  2224 
Phosphorus  Deficiency,  and  Beriberi, 
1673,  1678 
Yellow,  Rat-Poisoning  by,  190-1 
Phrenitis,  1474 
Phryganea  grandis,   1640 
Phthiriasis,  2201,  2202,  2203,  2268 
Phthirius,  752.  754,  757 
pubis,  757,   2201,   2202 
Phthisis,    7,    122,    1659,    1663,    1875, 
1885,   1893 
Abdominalis,  1780 
Acute,  1526 
Phya  africanus,  894 


23S8 


INDEX 


Phycomycetes,  923,  971,972,    1070 
Phyllomonas,  334 
P/iysa,  894 

Physalia  pelagica,  204 
Physaloptera,  623,  630 
References,  681 
Species 

caucasica,  623,  631 
mordcns,  623,  631 
Physalopteridce,  623,  624,  630 
Physic-Nut,  166 

Physical  Causes  of  Disease,   24,   67, 
115,    137,    147,    156-7, 
1128,  1356,  1449 
References,  92,  141,  1460 
Regulation  of  Body  Heat,  69 
Physidce,  894 
Physoclisti,  232 
Physogaster  larvamm,  728 
Physopsis  africana,  894 
Physostigma   venenosum    in    Ordeals, 
178 
Antidote,  179 
Physostomi,  232 
Phytobdella,  688 
nieyeri,  688 
moluccensis,  688 
Phytolacca  decandra,  2153 
Phytolaccacece ,  2153 
Phytomonadina,  332 
Pian,     or     Pians,     24,     1535,     1536. 

1538 
Pian-Bois,  380,  2165 
Pichia,  979 
Picric  Acid,  26,  1202 
Piebald  Skin,  Acquired,  2227 
Piedra,  1101,  1102,  2100,  2105 

Nostras,  2105 
Pigeons,  Parasites  of,  353,  355 

Poisoning  of,  191 
Pigmentation,  Cutaneous,  75,  84  sqq., 
145,   1181,    1529,   1531, 
2203,  2232,  2236,  2265, 
2266,  see  also  Diseases 
in  which  present 
Diagnosis,  151 3,  1519 
Facial  Pallor  due  to,  1903 
Sources 

Cells  of  Epidermis,  87 
Haemoglobin,  87 
of  Nails,  2230,  2236,  2283 
of  Tongue,  1731,  1746,  2265,  2283 
Pigmentary  Fever,  2232 
Pigmeophorus,  908 
Pigs,  Parasites  of,  353,  355 

Wild,  Traumatisms  due  to,  153 
Pilobolus  crystallinus,  967 
Pilocarpus  pennatifolius,  2153 
Piltdown  Skull,  the,  112 
Pi  mas,  the,  60 
Pine- Apple,  Unripe,  170 


Pink  Bollworm  of  Cotton,  Parasite  of, 
affecting     Man,     2214, 
2216 
Pink  Eye,  1527,  1999 
Pinoyella,  1015,  1023 

simii,  1023 
Pinta,   124,   1025,   1029,   1032,   1084, 
2042,  2077,  2079,  2093, 
2230 
References,  2108 
Varieties        and       Subvarieties, 
2097-9 
Red,  2094,  2095 
White,  1092,  2094,  2095 
Piophila,  902 

casei,  900,  902,  1626,  1630 
Piper  methysticum  Root,  176 

nigrum,  170 
Piperacecs,  170,  176 
Pi  pi  Is,  the,  60 
PipiocladiacecB ,  972 
Piroplasma,   21,   215,   359,    360,    369, 
419,  492,  1328,  1341 
Classification  by  Hosts,  492-3 
Insect  Vectors,  21,  23,  700,  712 
Species 

annulatum,  497,  700 
aristotelis,  498 
avicularis,  493 
bigemina(um),  497,  499,  700 
bovis,  21,  492,  497 
caballi,  492 
canis,  21,  493,  700 
cervi,  498 
divergens,  492 
donovani,  20 
equi,  700 
gibsoni,  497 
minense,  498 
muris,  493,  498 
mutans,  499 
ovis,  492,  497,  700 
parva,  712 
pithed,  493,  498 
theileri,  498 
Piroplasmodidce,  477,  478,  488,  491 

References,  527 
Piroplasmosis,  Bovine,  497 
Canine,  493,  496,  497 
Equine,  500 
Hominis,  1341 
in  Various  Animals,  21,  498 
Pisces,  Parasites  of,  478,  488,  52S-9, 
see  also  Fish 
Venomous,  230 
References,  237 
Piscidia  erythrina,  186,  188 
Piscidin,  188 
Pisciola,  685 

geometra,  337,  338 
Pito  Bug,  Bite  of,  770 


INDEX 


:389 


Pittospovece,  188 
Pittosportim  densiflorum,  188 
Pituitary  Gland,  pars  intermedia  of, 

1919 
Pituri,   176-7 
Piturine,  177 
Pityocera,  823 
Nigra,  2078,  2201 
Rubra,  2070,  2271 

Pilaris,  2249,  2252,  2256,  2257 
Sicca,  1009 

Simplex  capitis,  1077,  1078 
Versicolor,  1099,  2073,  2268 
Flava,  2073 
of    Temperature     Zones,     2074, 

2077 
Tropical,  2073 
Pityrosporum,  107 1,  1077 
cantliei,  1077,  1078,  2271 
malassezi,  1077 
ovale,  1077 
Placobdella,  685 
Plagiostoma  coli,  547 
Plagiostominidcs ,  547 
Plague,  4,  149,  i363.  1*16,  1566 

.Etiology,  285,  909,  1 1 28,  1419 
Animal    Reservoirs    other    than 

Rats,  1423,  1424 
Bacillus  of,    22,    115,    900,    1416 
passim,  see  also  B.pestis 
(Pasteurella  pestis) ,  943 
Blood  Changes  in,  1427 
Climatology,  120,  121,  122,  1419 
Complications,  Ocular,  2006 
Course,  1426-7 
Definition,  1416 
Diagnosis,  1429,  1517,  1523 
Differential,  1395-6,  1963 
Endemicity,  141 9 
Epidemiology,  1416  sqq. 
Fleas  as  Spreaders  of,   23,    115, 
117,  285,  747,  857,  869, 
908,  1416,  1418,  1431 
Most    Important   with  regard 

to,  867 
Spreading  the  Disease  from 

A.  Rat  to  Rat,  867 

B.  Rat  to  Man,  867 
History,   1416  sqq. 
Incidence 

Seasonal,  1419,  1423 
Sex,  1423 
Incubation,  1426 
Insect  Vectors,  23,  115,  117,  285, 

747,  857,  900,  908,  1  1 1 1  > 

1418,  1431 
Mixed  Infection  with  Relapsing 

Fever,   14J0 
Morbid  Anatomy,  1425-6 
Mortality  from,  India,  121 
Pathology,  1424-5 


Plague,  continued 

Predisposing  Causes,  1423 

Prognosis,  1430 

Prophylaxis,  23,  128,  1431 

Rash,  1 51 7 

Rats  in  relation  to  '10,  867,  912, 

1432,  see  also  Rats 
References,   1436 
Rodents  spreading  867,  912-13 
Sequelae,  1428 
Sera  for,  1430-1 

Symptomatology,  1426-7,  2006 
Synonyms,  141 6 
Transmission,     see     also     Fleas, 
Insect    Vectors,     Rats, 
and  Rodents,  above 
Chart,  917 
Treatment,  1 430-1 
Vaccines  for,  23,  1434-5 
Ambulatory,  1427,  1428 

of  Athens,   15 
Biblical,  10 

Bubonic,    912,    1416,    1419,    I423- 
1427,  1428 
Climatology,  913 
Diagnosis,  1429 

Differential,  1338,  1354 
Spread  of,  912,  1423 

Principal  Insect  Vectors,  869 
Glandular,  12 
Latent,  141 8 

Pneumonic,  1418,  1419,  1427,  1428 
iEtiology,  1423 
Diagnosis,  1429 

Diff  rential,  1498,  1875 
Spread  of,  912,  1422-3 
Septicsemic,  Acute,  etc.,  1418,  1427, 
1428 
.'Etiology,  1423 
Diagnosis,  1429 

Differential,      1337,      i429-3°. 
1498 
Spread  of,  1423 
Plague-Rat  of  Bombay,  917 
Plague  in  Rats,  1416,  1420 

Seasonal  Incidence,  909-10,   1420 
Planobdella,  688 
molesta,  688 
quoyi,  688 
PlanorbidcB,  892 
Planorbis,  892,  893,  894 

Intermediate     Hosts     of     Schisto- 
soma, 584,  587,  589,  590 
Species 

boisseyi,  587,  589,  590,  893,  1865 
corneus,  893 
cultratus,  589 

i;i(,ulelupensis,  587,  589,  1865 
laurenti,  893 
olivacdiis,  587,  893 
Plant-Caused  Dermatites,  2015,  2017 


2390 


INDEX 


Plant-Lice,  761 

Plants  Causing  Dermatitis  Venenata, 
2151-2,  2162,  2267 
Groups  of,  2155 
List  of,  2152-3 

Buffalo     Bean    Group,     2155, 

2162 
Doubtful  Group,  2155,  2163 
Euphorbia  Group,  2155,  2157 
Little-known      Group,      2155, 

2162 
Rhus  Group,  2155,  2156 
Rue  Group,  2155,  2160 
Tectona  Group,  2155,  2159 
Urtica  Group,  2155,  2158 
Diseases  of,   Spread  or  Caused  by 

Acarina,  691 
Fungi  of,  198,  200 
Herpetomonince  of,  361,  366-7 
Medicinal,  4 

Poisonous,  4,  51,  117,  124,  162,  163 

sqq.,  187-8,  190,  193,  195 

Water-holding,   Removal  of,   1208 

Plasmodia,      Malaria-causing,      11 29, 

see  also  Lavsrania  ma- 

larice,    517,    and   under 

Names 

PlasmodidcB,  477,  478,  504 

References,  527 
Plasmodium,  504,  1273 
Abnormal  Forms,  510 
Animal  Hosts,  510 
in  Blood,  in  Beriberi,  1679 
Cultivation,  510 
Definition,  504 
Differentiation,  504 
Insect     Vectors,      505,     see      also 

Mosquitoes 
Life-History,  505  sqq. 
Malarial  Parasites,  typical,  505 
Nomenclature,  504-5 
Reproduction 

Schizogony,  504,  506 
Sporogony.  508 
Sexual  and  asexual  forms,  506  sqq. 
Species 
Found  in 

Birds,  513,  516 
Lizards,  516 
Mammals,  510,  515,  516 
List 

bovis,  515 
brasilianum,  516 
canis,  515 
caucasicam,  513 
cynomolgi,  515 
danilewskyi,  513 
diploglossi    516 
equi,  516 
falciparum,  517 
golgi,  512 


Plasmodium,  continued 
S^pecies,  continued 

immaculatum,  517 
inui,  515 
kellicotti,  574 
kochi,  515 
ma j oris,  516 

malaria,    510,    512,    873,    889, 
1129,  1130,  1133,  1134, 
1137,  1138,  1139,  1143, 
1145,  1152,  1156,  1157, 
1160,  1164,  1218 
quartanum,  512 
tertianum,  510 
var.  quartancB,  512 
var.  quotidiancB,  517 
var.  tertiancB,  510 
monosoma,  516 
murinum,  516 
pitheci,  515 
prcecox,  517 
relictum,  513 
tenue,  513,  1132,  1137 
tropiduri,  516 
vassali,  516 
vaughani,  516 

vivax,     295,     510,     518,     889, 
1129  sqq.,  passim.,  1137, 
"43.  H45.  1152,  1153, 
1155,  1156,  1160,  1161, 
1164,  1202,  1218 
Plasmodromata,  296,  297,  469  sqq. 
Plasmosomes  of  Ferrula,  1902 
Plasmotomy,  293 
Plastic  Uveitis,  2006 
Plastin,  290 

Plastokonten,  Meve's,  1896 
Platodes,  555 

Platterbsenkrankheit,  196 
Platybdella  solea,  488 
Platyhelmia,  555 
References,  593 
Poisonous,  205 
References,  228 
Platyhelminthes,  555 
Platyhelminthic     Dvsenteries,     1825, 
1840 
References,  1863 
Platymalakia,  892 
Platypoda,  891 
l'laturus,  249 
Pleistophora,  529 
Plerocercoid(s),  599,  602 
Pleurococcus  beigeli,  1103 

prolifer,  606 
Pleurisy,  1913,  1961 
Pleuropneumonia,  Bovine,  541 
Plica  polonica,  2202,  2282 
Plotosus  arab,  232,  233,  234,  235 
Plumbagin,  170 
I'lumbaginacecB,  170,  171 


INDEX 


2391 


Plumbago,  170-1 
rosea,  170-1 
zeylanica,  170,  190 
Pnenmococcus,  933,  1477,  1521,  1959, 

2003 
Pneumocystis  carini,  404 
Pneumomycosis,     Aspergillar,     10  31, 

1891 
Pneumonia,    Amcebae  in   Lungs  and 
Sputum  in,  320 
Causation,  923,  927 
Climatology,  124,  131 
Diagnosis,  1519,  1521 

Differential,  1337,  1395,  1396, 

I485.  i5°7.  i5°8,  1875, 
1 91 4 
.  Malarial,  11 84 
Pneumonic    Plague,    1428,    see    also 

under  Plague 
Pneumothorax,  1091 
Pocomans,  the,  60 
Podelkoma,  21 10 
Podocapsa,  983 
Podogona,  690 
Podophyllum  peltatum,  2152 
Poison  Elder  (U.S.A.),  2156 
Poison-Foot,  176 
Poison  Ivy  (U.S.A.),  2156 
Poison  Oak  (U.S.A.),  2156 
Poison-Pea  of  Australia,  189 
Poison  Sumac  (U.S.A.),  2156 
Poisoning,  Accidental,  172 
of  Cattle,  165,  189,  190 
Criminal,  162,  170 
References,  179 
Delusions  of,  1991 
by  Food,  1693,  1694 
Animal,  193 
Vegetal,  195 
Forms    of,    associated    with    Beri- 
beri, 1673,  1674 
Lacquer,  191-2,  2157 
in  Ordeal,  178-9 
Stimulative  and  Sedative,  174-8 
Tropical,  161,  1553,  1695 
Poisonous  Animals,  203 
References,  227-9 
Fish,  193-4,  230, 

References,  241 
Food,  193 

References,  202 
Fungi,  1  24,  172,  173,  198,  200 
Plants,  4,  51,  117,  124,  162,  163  sqq., 

187-8,  193,  195 
Substances,    used    as    Food    when 
properly  prepared,  1 72 
Poisons,  161 

Abortifacient,  163,  169 
Accidental,  161,  172 
Animal,  193 
Aphrodisiac,  171-2 


Poisons,  continued 

Arrow,  167,  180,  222,  1675 

References,  186 
in  Byzantine  Medicine,  12 
Classification,  161 
Curative,  171 
Definition,  161 
Diseases  due  to,  1533,  1695 
Food,  193,  195,  1693,  1694 
Homicidal,  162  sqq. 
Infanticidal,  163,  169 
Inorganic,  162,  170 
Injury- Simulating,  163,  171 
Organic,  162  sqq. 

Pseudocholera  due  to,  1820,  1821 
Racial,  118,  174,  175 
Rat,   173,   190 

References,  179,  186,  192,  202 
Suicidal,  163,  169,  194 
Stimulative  and  Sedative,  174-8 
Stupifacient,  to  facilitate  Robbery, 

163,  170 
Used  in 

Fishing,  Hunting,  and  Trade,  187 

sqq. 
Trial  by  Ordeal,  178-9 
War,    etc.,    see    Arrow-Poisons, 
above 
Vegetal,   162  sqq.,    172    sqq.,    191, 
193.  695,  729 
Polagarynuum,  534 
Poliomyelitis,  Virus  filterable,  541 

Acute  Anterior,  920 
Polish  Fever,  1501 
Polistachya,  1756 
Pollaplasiogonei,  600 
Pollenia,  852 

rubis,  365,  852,  900,  1629 
Polpolcans,  the,  56 
Polyarthritis  in  Dengue,  1249 
Polycystidea,  471 
PolydesmidcB,  690 

Polydesmus  complanatus,  690,  1641 
Polygnathus,  1959 
Polygonacece,  2153 
Polygonum  acre,  2153 

livdropiper,  2153 
Polyidrosis,  2222 
Polymastia,  351 

melolonthcB,   353 
Polymelus,  1959 
Polymicrolipomatosis,  2253 
Polymorphonuclear  Neutrophile  Leu- 
cocyte, 1898 
Polymyositis,  151 5 
Polyneuritis,  see  also  Beriberi,  1671 
Avian,  109,  1675 
Endemica,  1671 
Malarial,  1176,  1184 
Polyneuritic  type  of  Subtertian  Ma- 
laria, 1 1 75,  1176, 1 184 


=  39- 


INDEX 


Polypapilloma  tropicum,  1535 
Polyparasitism,  Intestinal,  1776 
References,  1779 

Rare  Infections,  1779-8 

Treatment,  1777 
Polypi,  Nasal  and  other,  1578  sqq. 
Polyplax,  759 

spinulosa,  404,  759 
Polysporea,  529 
Polysporocy  slides,  473,  474 
Polysporogenea,  529 
Poly  stoma  proboscideum,  738 

tcenoides,  733 
Polystomea,  557,  560 
Polytricha,  547 
Polyaric  type  of  Subtertian  Malaria, 

1 1 80 
Polyvalent  Vaccines,  23,  29,  see  also 
Vaccines 

Sera  against  Snake  Venoms,  273 
Pompholyx,  2226 
Porokeratosis,  2235 
Ponera,  222 
Ponos,   374,   1299 
Pont  la  brassica,  1640 
Pontobdella,  685 

muricata,  389,  398-400 
Poon,   184 

Populus  spinosa  Buds,  172 
Porocephaliasis  (Porocephalosis),  124, 

734.  737.  1533.  l642 
References,  1643 
Pulmonary,  1875 
Porocephalus,  733,  734 
Species 

aonycis,  736 

armillatus,   734,    736,    737,    738, 

1642,  1643,  1907 
crocidurce,  737,  1642 
crotali,  738,  1042 
humboldtii,  738    ■ 
Imperfectly  described,  in   Man, 
737  sqq. 
Flint's  Parasite,  737,  738 
naje,  737,  738,  1642 
O  iler's  I  '."■,' site,  737 
Welch's  Parasite,  737 
moniliforme,  738 
moniliformis,  73  |.  736,1642,  1643 
Porospora,  471 
gig  mtea,  471 
Porosporidee,  471 
Por.i^o,  2052 
Porter's  Lipomata,  2247,  2253 

Urethritis,  1943 
Porthesia  chrysorrhcra,  223 
Porto  Rii  an  Anaemia,  1  761 
Porto   Rico   Commissions  on    Anky- 
lostomiasis,       Prohpy 
lactic        Recommenda- 
tions of,   1774-5 


Portuguese  Man-of-War,  204 
Posadasia  esferiforme,  985 
Post-Dysenteric  Arthritis,  1967 
Post-Malarial     Affections     in     War 
Zone  Cases,  11 85 

Anaemia,  1151-2,  1184 

Insanity,  1184 

Loss  of  Taste,  11 84 

Neuralgias,  11 84 

Vertigo,  11 84 
Post  -  Mortem       Decomposition      of 
Food,    Poisoning  from, 

195 
Post-Natal  Pathology,  1956,  1959 
Post-Partum  Haemorrhage,  77 
Potatoes,  95 
Potter's  Disease,  1692 

References,  1694 
Potu  Flies,  810,  811 
Pou  d'Agoute,  2213 
Pou  d' Agouti,  725 
Poultryman's  Dermatitis,  2213 
Powdered    Glass,    Traumatisms   due 

to,  156-7 
Pre-Dravidian  tribes,  47,  49 
Pregnancy (ies),  Advice  on,  129 
Ceylonese  precautions  during,  4 
Frequent,  Anaemia  due  to,  1903 
Malaria,  Prognosis  in,  1187 
Quinine  Treatment,  1191 
and  Plague,  1427 
and  Relapsing  Fevers,  131 2,  1313 
and    Tropical    Febrile    Splenome- 
galy, 1305 
Premiums,  Insurance,  Adjustment  of, 

132 
Pre-Natal    Conditions    affecting    In- 
fantile Mortality,  122 
Pressure,  Atmospheric,  78 
Effects  on  Man,  79,  142-4 
References,  146 
and  Radiation,   142,  1446 
References,  146 
Prevention  of  Disease,  125 
Priapism  type  of  Subtertian  Malaria, 

1180 
Prickly  Heat,  2020,  2027,  2222,  2224 

References,  2246 
Primary    Streptococcal     Dermatites, 

2030 
Primitive  Man,  Migrations  and  Divi- 
sions of,  42 
Medicine,  3 
1'ii  inula     Subgroup     of     Dermatitis- 
causing  Plants,  2158 
cortusoiides,  2158 
obconica,  2 151,  2158 
sieboldii,  2158 
«t  sinensis,  2158 
PrimulucecB,  2158 
PrimulecB,  2158 


INDEX 


2393 


Primulex  sinesis  section,  215S 

Prionotus,  767 

Prionurus  amoureuni,  207 

citrinus,  207 
Prison  Fever,  1326 
Pristirrhynchomyia  lineata,  833 
Proboscida?,  Traumatisms  caused  by, 

*53 
Proctamasba,  298 
Proflagellata,  435 
Proglottides,  596  et  alibi 
Progressive  Paralysis,  2279 
Promitosis,  291,  292 
Pro nopes,  823 
Prophialidalinecs,    11 11 
Prophialide,   1037,  1039 
Prophylaxis,    see    also    Serotherapy, 
'  and       Vaccinotherapy, 
29,  125,  131 
Prorhipidoglossamorpha,  S90 
Prosimulium,   812 
Prosopothoracopagus,  1958 
Prostatic  Hypertrophy,  1926 
Prostigmata,  692,  724 
Prostomata,  560 
Prostriata,  711 
Protarthropoda,  689 
ProtecB,  933,  943 
Protective  Colouring  of  Natives,  85, 

and  see  2264-5 
Protein  Dietaries,  Low,  107,  119 
Proteins  in  Diet,  96,  97,  99 

Biological        value       of,        102, 

106 
Calculations  on,  106 
Estimation  of,  101 
Proteosoma,  504 

grassii,  513 
Proteroglypha,  240,  246 
Protetramitus,  348 
Proteus,  933,  943,  1069 
difflnens,  943 
in.  tadiffluens,  943 
paradiffluens,  943 
proteus,  943 

Small,  399,  see  also  Amoeba 
vulgaris,  933,  943 
Protists,  113,  288 
Protoanopheles,  883 
Proto-asci,  1070 
Protoascomyceles,  978 
Protoconidium,  1037,  1108 
Protodiscales,  985 
Protokaryon,  290 
Proto-Malays,  the,  49 
Protoiiio)i(i(/ina,  330,  332,  (.64 
Proto-Polynesian  Race,  49 
Protozoa,  18,  203,  287,  908 

Associated   with    Beri-beri,    1679, 

1680 
Definition,  288 


Protozoa,  continued 

Disease-causing,      18,      203,      287, 
see  a/so  Protozoal  Para- 
sites, below 
References,  328 
Toxin-yielding,  203 
Venomous,  203 
References,  227-9 
Protozoal,    Protozoan,   or    Protozoic 
Bodies  found  in  Dysen- 
tery, 538 
Characters  of  Spirochartes,  437 
Dermatitis,  2081 
Diseases,  877,  2084 

Animal  Carriers  of,  877 
Dysenteries,  1825 

References,  1862-3 
Fevers,  11 28,  1129 
Parasites,  287,  288 
Classification,  296-7 
Encystment,  291 
Hosts  of,  288,  295 

Insect,  18  sqq. 
Infecting  Embryo,  289 
in  Liver,  1907 
Morphology,  290-1 
Nomenclature,  Rules  of,  287 
of  Mouth,  1740 
Pathogenicity,  295  sqq. 
References,  328-9 
Remarks,  288 
Reproduction,     286,     288,     291, 

292,  293.  295 
Species  and  Varieties,  297 
IncertcB  sedis,  528,  530,  535 
cyrtasterella  scarlatinis,  537 
References,  543 
Vaginal,  List  of,  1945 
Toxins, '203 
Urethritis,  1944 
Protozoology,  History,   18 
Protrichomonas,  351 
Prowazekella,  n.g. 

lacertce,  339 
Prowazekia,  335,  337,  339,  360,  1833, 
1944 
References,  357 
Species 

asiatica,  339,  340 
cruzi.  339,  342 
javensis,  339,  342 
parva,   339,  342 
urinaria,  339,  340 
vaginalis,  339,  342,  1946 
weinbergi,  339,  342 
Pruriginous    Tumours,    Multiple,    of 
the  Skin,  2247,  2254 
References,   Z2(>} 
Prurigo,    Distinguished    from    Craw- 
craw.  2248 
True,  2267 


2394 


INDEX 


Pruritus   caused   by   Bite   of    Argas 
brumpti,  704 
in  Dermatites,   2248,   2249,   2250, 

2251,  2254 
in  Pediculosis,  2201,  2202,  2203 
in  Pinta,  2097,  2099 
in  Pyosis  tropica,  2022 
Vaginal,  1028 
Prussic  Acid,  169 
Pseudechis,  246 

Venom,  243,  244,  258,  261,  271 
porphyriacus,  251 
Pseudelaps,  246 
muelleri,  251 
Pseudencephalus,  1958 
Pseudo-Addison's  Disease,  2232 

Malarial,  1180,  1181,  2233 
Pseudo-Alcoholic  type  of  Subtertian 

Malaria,  1169,  1170 
Pseudo-Anginal   type    of    Subtertian 

Malaria,  11 79 
Pseudo-Appendicitis    type    of    Sub- 
tertian Malaria,  1177 
Pseudoaspis  carta,  487 
Pseudo-Banti's  Disease,  1306 
Pseudo-Bronchitic  type  of  Subtertian 

Malaria,  11 78 
Pseudocerastes,  250 

persicus,  251 
Pseudochirus  peregrinus,    Bodies   in, 
found  by  Sambon,  538 
Pseudo-Cholecystitis    type    of    Sub- 
tertian   Malaria,    1177, 
1178 
Pseudocholera,  1801 

Caused  by  Poisons,  18c  •.  1821 
Dysenteric,   1 820-1 
of  Food-Poisoning,  1820 
Malarial,  1177,  1820,  1821 
Pseudo-Cirrhosis  type  of  Subtertian 

Malaria,  n 77,  1178 
Pseudocladorchis,  561 
Pseudo-Colloid  of  Lips,  1746,  2284 
Pseudodisciis,  561 
Pseudodiphtheria  1087,  1740 
Pseudo-Dysenteries,  1825,  1861 
Pseudo-Dysentery,  1852-3 

Type  of  Subtertian  Malaria,  11 77 
Pseudo-Gonorrhceal  Urethritis,    1945 
Pseudo-Goundou      in     Yaws,     1976, 

1977 
Pseudogranulomata  of  Lungs,  1076 
Pseudo-Helmintbiasis,  746 
Pseudo-IntestinaJ  Sand,  1739" 
Pseudo-Kala-Azars,  the,   1128,    1289, 

1303,  1 53 1 
1 '  :eudo  Leukaemia,  1003,  [914 
Pseudolfersia,  855 
Pseudolimax,  322 

Pseudo-Liver  Abscess  type   of   Sub- 
tertian Malaria,  11 77 


Pseudo-Meningococcus,  1478 
Pseudomycetomas,  1064,  21 10,  2147, 

2277 
Pseudomycosis,  Aspergillar,  103 1 
Pseudomyzomyia,  885 

Carriers  of  Malaria,  886 

ludlowi,  886 
Pseudonavicellcs,  470 
Pseudo-Parasites,  287,  1901,  1902 
Pseudo-Pelade,  2283 
Pseudo-Pellagra,  1705,  1730 
Pseudophyllidea,  600 

carus,  604,  609 
Pseudo-Pleuritic  type  of  Subtertian 

Malaria,  11 78,  1179 
Pseudo-Pneumonic  type  of   Subter- 
tian Malaria,  1178,  1179 
Pseudopodia,  291,  296,  297 
Pseudorhabditis ,  628 

ster  cor  alls,  628 
Pseudorhynchota,  752 
Pseudoscorpions,  690,  908 
Pseudo-Smallpox,  1491 

Type  of  Subtertian  Malaria,  11 81 
Pseudospira,  439 
Pseudo-Sprue,  1780,  1783,  1794 

References,  1800 
Pseudosirongyles,  623,  674 
Pseudo-Tuberculosis,  Aspergillar, 

1031,  1058,  1059,  1897 
Pseudo-Typhus,  1350 

of  Deli,  Sumatra,  1354-5 
Pernio-Xanthoma,  2273 

Elasticum,  2237 
Psilosis  Linguae  et  Mucosa?  Intestini, 
1780 
Pigmentosa^,  1731 

Pigmentosa  of  Barbadoes,  1788 
Psittacosis,  1395,  1396 

Parenteric,  1425,  1408 
Psocida>,     relationship     of,     to     the 

Mallophaga,  749 
Psora,  2217 
Psorala,  172 

corytifolia,  172 

glandulosa,  172 
Psoriasis,  449,  2264,  2270,  2271 

Palmaris  and  Plantaris,  Syphilitic, 

Psoropermien,  475,  476 
Psorospermium  citniculi,  474 
Psoroptes  equi,  731 
Psy<  hasthenia,  1982 
Psychic  Exaltation,  191 9 
Psychoda,  806,  900 

phalcenoides,  905 
PsychodidcB,  773,  806,  2200 

References,  813 
Psychodina,  806 
Psychoneurosis  Maidica,  1700 
Psychophana,  802 


INDEX 


2395 


Psychoses,  76,  123,  1524,  1891,  1983 

Ptenophthalmits  cegyrtes,  376 

Pteridophyta,  923 

Pterois  antennata,  232,  238 

Pleromalidce,  908 

Pier  optus     vesperlilionis,      Achroma- 

ticits  in,  360 
Pterygium,  1995,  2002 

of  Nails,  2283 
Ptomaine-Poisoning,  195,  1810,  1820, 
1862 
Diagnosis,   151 4 
Rash,  1514,  1516 
Ptychobothriidce,  604 
Puberty,  77,  1945 
Pubic  Louse,  757 
Puccini  a  rosea,  11 17 
Pudenda,   Ulcerating  Granuloma  of. 

2192 
Puente,  2191 

Puerperal  Diarrhoea  of  Bengal,  1955 
Disease,  122 
Fevers,  927  sqq.,  1522 

Tropical,  1938,  1946,  1957 
Septicaemia,  1946 
Puff-Adder,  250,  251 
Pulex,  857,  859,  865,  866,  867 
brasiliensis,  869 
cheopis,  869 
gallina,  693 

irritans,    369,   396,   608,   857,   866, 
867,  868,  911,  1422 
ditgesi,  869 
minimus,  862 

cutem  penetrans,  862 
murinus,  869 
pallidus,  869 
penetrans,  862 
pliilippinensis,  869 
serraticeps,  375,  376 
PulicidcB,  857,  861,  864 

of  Rats  and  Mice,  Table  of,  866 
Pulicince,  864,  866 
Pulmonary  Abscess,  335,  1949 
Aspergillosis,  103 1,  2008 
Distomatosis,  1  58  1 
Inflammatory   Affections,    1875, 

1892 
Mucormycosis,  975  sqq. 
Mycosis,  974 
Nocardiasis,  1521,  1892 

References,  1894 
Streptothromycosis,  1 892 
Tuberculosis,  1889,  1893,  2278 
Pulmonala,  892 

Pulse-Rate,    Effe<  t    on,  of  Tempera- 
ture     and     Humidity, 

74-5 
Pulziasta  Bolest,  1639,  2208 
Punaise  de  Miana,  704 
Punjabi  Race,  47 


Pupipara,  749,  774,  854 

References,  856 
Purgatives,  Abortifacient,  170 
Purpura,  2267 

Haemorrhagica,  122,  1698 
Henoch's,  1698,  2267 
Schonlein's,  2267 
Variolosa,   1448-9 

Fulminans,  1489 
Werlhof's,  2267 
Purpuric  Eruptions,  1513,  1516, 1519, 

2267 
Puru,  1535 

Purulent   Folliculitis  of  Legs,    2027, 
2029,  2036 
References,  2038 
Myositis,  1469,  1523,  1529 
Pus,  1064,  1096 

Pustular  Eruptions,  1513,  1518 
Syphilides,  151 8,  2279 
Tuberculides,  151 8 
Pustule,  Malignant,  151 8 
Puttees  and  Trench  Foot,  2149,  2150 
Pyaemias,  1337,  1395,  1397 
Pyans,  1536 

Pycnosoma,  832,  848,  1626 
chloropyga,  900 
marginale,  848,  898,  900 
megacephala,  848 
piitorum,  365,  368,  848,  1626 
Pyelitis,  1530,  1926 

Amoebic,  1933 
Pvgiopsylla,  864,  866 
colossus,  866 
In  Hi,  866 
rainbowi,  866 
Pygmies,  African,  5,1,  53 
Arrow-Poisons  of,  183 
of  New  Guinea,  49 
Pyloric  Stenosis  in  Children,  1749 
Pyococci,    or    Pyogenic    Cocci,    2021, 

2023,  2027,  2255 
Pyogenic    Dermal   Affections,    2015, 
2017,  2029,  2264.  2265 
1  (ermatites,  2017,  2029 
Folliculites,  2027 
Granuloma,  2254 
( ttcers,  2190 
Vaccines,  23 
Pyonephrosis,  1926 
Pyopagus,   1958 
Pyorrhcea,  461,  1520,  i7<>} 

Alveolaris,  112,  113,  318,  1740,  1744 
Pyoses,  2017 
Non-Febrile,  Rashes  due  to,  1517 

Varieties,   2017.   2018 
Pyosis,   Jin  7 
Caffra,  2021 
Castellanii,  2021 
Corletti,  931,  151 7,  2018,  2023 
References,   20^8 


2396 


INDEX 


Pyosis,  continued 
Discoides,  2018,  2026 

References,  2038 
Mansoni,  931,  2017,  2018 

References,  2038 
Palmaris,  2018,  2022 

References,  2038 
Staphylococcal,  2255 
Tropica,  or  tropicalis,    931,    201 S, 
2021,  2035,  2 1  go 
References,  2038 
Pyrenomycetes,  985,  1032 
Pyrethrum  Sprays,  1207 
Pyretophorus,  791,  794,  885 
Malaria-carrying,  886 
Species 

ardensis,  795 

aureosquamiger,  794 

austeni,  794 

chaudoyei,  794,  888 

cinereus,  794 

costalis,  638,  794,  795,  886,  11 38, 

"39 

jeyporensis,  794 

marshalli,  795 

merus,  795 

minimus,  794 

migzomy fades,  794,  886 

nigrifasdatus,  794 

nursei,  794 

palestinensis,  794 

pitchfordi,  794 

pseudocostalis,  795 

sergenti,  794,  888 

superpictus,  794,  886 

thomtoni,  794 
Pyrexia  of  Unknown  Origin,  1501 
Pyrgula,  891 

Pyrheliometer  of  Angstrom,  the,  144 
Pyrosoma,  492 

bigeminum,  497 
Pyrrhocoris  aptera,  372 
Pythogenic  Fever,  1362 
Pythons,  244,  487 
Pyxima  frenzeli,  470 

Quarantine,  Mosaic,  10 

in  Tick-Prophylaxis,  701 
Quartan  Fever(s),  10,  1129 
Double,  11 
Non-Malarial,  1470 

Malaria  (q.v.),  1528 
Quartana.  duplex,  1157 

Simplex,  1157 

Triplex,  1 157 
Quarter-Evil,  961 

Sub-Group  of  Anaerobic  Bacilli,  959 
Quiche,  the,  60 
Quichuas,  the,  57,  60 
Quicklime,  170 
Quigila,  2241 


Quincke's  (Edema,  11 81 
Quinine  Amaurosis,   1181,  2007 
Amblyopia,  1201 
Aural    Symptoms    due    to,    11 81, 

2013 
Dermatitis,  2153,  2162 
Effects  of,  on 

Malarial  Parasites,   1 201-2 
Man,  1200 
Elimination,  Urinary  Test  for,  1926, 

1936 
Fever,  1201 
Forms  of,  1 199-1200 
Haemoglobinuria,   202,   1201,   1213, 
1214,      1217-20,      1224, 
1522 
History  of,  25-6 
Idiosyncrasy,  1187,  1216 
New  Salts  of,  1200 
Ocular    Symptoms    due    to,    11 81, 

2007 
Prophylaxis,  1202,  1204 
References,  121 1 
Therapy,  15-6,  1188 

Administration,  Methods  of,  11 93 
sqq. 
Time  of,  1 192-3 
Dosage,  11 92 
Duration    of    Treatment,     1192, 

1198 
Theoretical     Consideration     on, 
1199 
Quinine-Test   of  Candidates   for  the 

Tropics,  128,  129 
Quinsy,  1061,  1747 
Quintan  Fever,  1501 
Quirica,  2093 

Quisqualis  indica,  in  Ascariasis,  1775 
Quotidian  Fever,  10,  1526 

Malaria,  1528 
Qushuf,  1700 

Rabbits,  Corneal  Sore  in,  378 

Parasites  of,  406,  474,  490,  833 
Rabelaisia      philippinensis,      Arrow- 
Poison  from,   186 
Rabies,  Animals  affected  by,  151,  152 
Dumb  form,  151 

Parasites  present  in,  20,  151,  440, 
535.     539,     54i.     1569. 
157° 
Races,  Tropical,  39  sqq.,  42  sqq. 

References,  60-1 
Rachipagus,  1958 
Rachischisis,  1959 
Rachitis,  124,  1303,  1923,  1945 
Racial  Food  Peculiarities,  104 
Odours,  2223 
Poisons,  118,  174,  175 
Susceptibility  to    Heat   and    Pain, 
2265 


Index 


2397 


Radesyge,  1536 
Radiation,  69,  142,  144-6 

Solar,  144-6 

References,  146 
Radio-active  Serum  of  Nicolaidi  for 

Pellagra,  1732 
Radiolaria,  297 
Ragle,  Le,  1990 
Raii,  Venomous,  232 
Raillietiella,  733 
Railway      Prophylaxis       for      Heat 

Stroke,  1458 
Rana  esculenta,  355,  394 

speciosum,  394 

temporaria,  355,  394 

trinodis,  394 
Rana  Trunjilor,   1700 
Ranee,  Parasites  carried  by,  355,   394 
Randia  dumetorium,  170,  187 
Rangelia,  491,  492,  502 

vitalli,  502 
Rangoon  Fever,  1462 
RanunculacecB,  163-4,  !8i,  184,  2153 
Ranunculus  scleratus,  2151 
Rapau  de  Mer,  235 
Rarer     Nodular     and     Gummatous 
Affections    of    Hypho- 
mycetic  origin,  2106 
Rasahus,  767,  769 

biguttatus,  769 
Rashes,    sec    Eruptions,     1516,    1259 
et  alibi 

Vaccination,  1494 
References,  1500 
Rat    to    Man,    Fleas    which    spread 

Plague  from,  867 
Rat    to    Rat,    Fleas    which    spread 

Plague  from,  867 
Rat- Bite  Disease,  151 
Rat-Bite  Fever,  151,  1356 

etiology,  1357-8 

Causal  Organism,  447,  450,  1357-8 

Climatology,  122,  1357 

Complications,  1359 

Definition,  1356 

Diagnosis,  1360,  1515 

Differential,  1337,  r395.  1  396 

Incubation,  1358 

Morbid  Anatomy,  1358-"" 

Onset,  1359 

Pathology,  1358 

Prognosis,  1360 

Prophylaxis,  1360 

Rash,  1 51 5 

References,  1361 

Relapse,  1359 

Symptomatology,  1358-9 

Synonyms,  1356 

Treatment,  13 13,  1300 

Varieties,  1359 
Rat-Disease,  Novy's,  541 


Rat-Fleas,    403,    867,    869,    see    also 
Xenopsylla  cheopis,  869 
Plague-trans  mission  by,  23, 1 41  Osqq. 
Rat-Plague,  909-10,  1416,  1420 
Post-mortem  Appearances  in,  14.16 
Seasonal  incidence,  909-10,  1420 
Rat-Poison,  173,  1901-1 
Rat-Snakes,  244,  245 
Rattam  -  seedam  -  banthalaporado, 

1824 
Rats,  Diseases  spread  by,  878,   896, 
918,  1506,  1508 
Plague    so    spread,     10,     115, 
915,  917.  J4i6  sqq. 
Fly-catching  by,  908 
Leprosy-like  Disease  of,  1645 
Parasites  of,    19,    403,    404,    479 

sqq.,  483,  486,  918 
Species     specially     subject     to 
Plague,  917,  1420 
Field,  Parasites  of,  485 
Wood,  915 

Parasites  of,  398 
Rats  and  Mice,  915 
Fleas  of,  865,  867 
Table  of,  866 
Rattenbeetziekte,  1356 
Ratlenbisskrankheit,  1356 
Rdttenkonig  CercaricB,  559 
Rattlesnakes,  249,  250 
Distribution,  124,  251 
as  Reservoirs  of  Espundia,  363,  2177 
Venom  of,  243 
Rauwolfia  serpentina,  190 
Raynaud's  Disease,  201,  1213 
Rays,  Poisonous,  240 
Bishop,  240 
Eagle,  240 
Sting,  240 
Rectal  Bilharziosis,  1864 
Rectitis,    Epidemic   Gangrenous,    25, 
123,  1871 
References,  1892 
Rectum,  Temperature-taking  in,  71 
Red  Actinomycosis,   2142.     See  also 

under  Actinomycosis 
Red  Ants,  Arrow- Poison  of,  222 
House,  Enemies  of  Bugs,  765 
RedicB,  558,  567 
Red-Leg  Tick,  Spreader   of    Babesia 

equi,  714 
Red     Maduromycosis,     2123,      2125, 
for    details    see     under 
Maduromycosis 
Red  Pinta,  2094,  2095.  for  details  see 

under  Pinta 
Red  Tongue,  1746,  2283-4 
Redwater  Fever,  497,  501,  715 
ReduviidcB,  691,  762,  767,  1284,  2200 
Bites  of,  219 
References,  770 


2398 


INDEX 


Reduviolus,  767,  769 
subcoleoptratus,  769 
Reduvins,  767 

personatus,  767 
Reed-Cutters'  Dermatitis,  2163 

Disease,  1033 
Refraction,  Errors  of,  1995 
Regnum  Vegetabile,  923,  968 
Reighardia,  733 
Reiter's  Disease,  1468 
Rejangs,  the,  55 

Relapsing    Fevers,    10,    1308,    1363, 
1505,  1528,  1530 
Causal  Organisms  (all  forms),  436, 

444  sqq.,  452,  1322 
Climatology,    120,    122,    124,    133, 

and  see  each  form 
Complications,  Ocular,  2006 
Diagnosis,  1519,  1525.  1528,  1529, 
and  see  each  form 
Differential,     1238,     1253,    131 2, 
1313,  1337,  1395,  1429, 
1485,  1505,  1507,  1508 
Insect  Vectors,  actual  and  suspect 
(all    forms),    691,    748, 
754.  763.  765,  917.  9i8, 
919,   1128,  1308,   1322, 
see  also  Lice,  and  Ticks 
Louse  Group,  918,  1308 
Pigmentation  in,  1519 
Spleen  in,  1904 
Tick  Group,  919,  1308 
in  Relation  to  Typhus,  1326,  1330 
Varieties 

African,  919,  1318 

References,  1324-5 
East  African,  445,  919,   1318, 

1322 
North  African,  447,  918,  919, 
1308,  1314 
Egyptian,  447 
References,  1322 
West  African,  444,  445,  1318 
American,  446,  447,  918,  1323 
References,  1324 
Central  American,   919,  1323, 

1324 
North  American,  1323 
South  American,  1323,  1324 
Colombian,    444,    445,    919, 
1324 
Asiatic,  436,  445,  1315 
References,  1324 
Indian,  918,  1308,  1315 

Varieties,  131 7 
Mam  hurian,   918,   1308,    1^15. 

1318 
Persian  Miana,  691,  919-,  1322 
Dutton's   (African    Tick  Fever), 
19,  69] .   694,   700,  706, 
1261,   1318 


Relapsing  Fevers,  continued 
Varieties,  continued 

European,    436,    443,    445,    918, 
1308 
References,  1324 
Obermeyer's  form,  763,  765 
Relapsing  Type  of  Fevers,  1528,  1529 

Chronic,  1530 
Religion,  Food-regulation  by,  95 
Religious     Character     of     Primitive 
Medicine,     3     sqq.,     51, 

54-  55 
Remittent  Fever  (Malaria),  11 29 
Remittent  Fever  (Relapsing  Fever), 

1308 
Remittent    Fever    (Typhoid),     1362, 

1366,   1371,   1372 
Remittent  Fever, 
Bilious,  121 6 

of    Cattle    due    to    Plasmodium 

bovis,  515 
Diseases  associated  with,  1523 
Epidemic,  1308 
Non-Malarial,  1289 
Russian,  1501 
Remittent    or    Continuous    Type    of 

Fevers,  1528,  1529 
Renal    Coma,  Differential    Diagnosis 
from  Heat  Stroke,  1456 
Disease,  1926 
Dropsy  in,  1 904 
Reptilia,  Parasites  of,  478,  480,  486, 

5l6<  526 
Trypanosomas,  395,  398,  401 
Traumatisms  caused  by,  153-4 
Venomous,  242 
References,  280-1 
Research,  29 
Reservoirs  of  Animal  Parasites,  875, 

921 
Respiration,  Effects  on,  of  Tempera- 
ture and  Humidity,  73 
Respiration  Calorimeter,  the,  97 
Respiratory  Affections  due  to  Meta- 
strongylus  apri,  662 
Organs,  Diseases  of ,  1873,  1875 
Climatology,  121  sqq. 
Spirocha?tes  of,  449,  452 
System,    Derangements    of,    1519. 
1521,  1552 
Subtertian     Malaria     attacking, 
1175,  1178 
Rest  Body,  293,  see  also  Nebenkbrper 
Retinal  Detachment,  2007 
Krtino-Choroiditis,     Malarial,     2004, 

2005 
Rhabditis,  623,  627 
genitalis,  628 
niellyi,  623,  627 

Dermatitis  due  to,  2ji«i 
References,  681 


INDEX 


2399 


Rhabdonema,  628 
inlestinalis,  628 
Rheumatic  Fever,  133,  1250 
Rheumatism,  131 
Gonococcal,  1938 
Muscular,  124 
Rheumatoid  Arthritis,  112,  113,  [967 
Rhinal  Canthariasis,  1640 
Chilopodiasis,  188 1 
Myiasis,     831,     846,     1620,     1622, 
1623 
African,  1623,  1625 
American,  1623 
Asian,  1623,  1626 
European,  1623,  1626 
Scolechiasis,  1640 
Rhincoprion,  861 

penetrans,  857,  862,  863 
Rhinchopriontdes,     et     Hectopsyllidte, 

861 
Rhinitis,  Acute  Catarrhal,  2013-14 
Nervosa,  1875 

Spastica  Vasomotoria,  1875,  1995 
References,  1894 
Rhinocephalus,  246 
Rhinoceri,  Traumatisms   caused   by, 

*52 
Rhinocladium,  11 17 

asteroides,  11 20 

beurmanni,  1118,  1119 

gougeroti,  11 20 

lesnei;  11 21 
Rhinomyza,  823 

costata,  823 

denlicornis,  823 

edentula,  823 

fused,  823 

maculata,  823 
pusilla,  823 
umbraticola,  823 

Rhinopharyngitis,  450,  452 
Acute,   1 52 1 
Mutilans,  1876 
S]>irochaetica,  1521, 
Khinophyma,   2272 
Kliinoscleroma,  2277 
Rh inosporidiida,  530, 
Khinosporidiosis,  1578 

.Ktiology,   1533.   1579 

Climatology,  1578 

1 )(  liuition,  1578 

1  li^tory,  1578 

Diagnosis,  1581 

Morbid   Anatomy,    1 579-80 

Pathology,  1580 

Prognosis,  1581 

Prophylaxis,  1581 

References,  1583 

Symptomatology,  534.  l5&° 

Treatment,  1581 
Non-coccidial,  474 


1881 


533 


Rhinosporidium,  533 

References,  543 

Species 

kinealyi,  533,  1578 
seeberi,  533,  1578,  1579 
h'hipicentor,  710,   711,  715 

bicornis,  700,  715 

vicinus,   715 
Rliipicephalce,  710 
Rhipicephalince,  710 
Rhipicephalus,  711,  714 

bilenus,  712 

bursa,  492 

ellipticum,  719 

gladigev,  715 

prcetentatus,  713 

sanguineus,  39S,  430,  492 

senegalensis,  713 
Rhipidostoma  leach i,  719 
Rhipistoma  leachi,  719 
Rhipistomidce ,  710 
Rhipistomidea,  710 
Rhizoglyphus,  729 

parasiticus,  729,  201 1,  2214 
Rhizomastigina,  332 
Rhizomastix,  334 
Rhizomucor,  975,  1886,  1892 

parasiticus,  975,  976 

septatus,  975 
Rhizoplast,  290,  291,  330,  381 
Rhizopoda,  297 
Rhizopus,  975,  1892 

Mtger,  975,  1074 
Rhizostoma  cuvieri,  204 

put ini,  204 
Rhodesiense  Type  of   Sleeping   Sick- 
ness, 880,  881 
h'hodnius  prolixus,  430 
Rhodococcus,  925,  931 

castellanii,  931,932, 1067,  2102,  2103 

fulvus,  931,  932 

roseus,  931,  932 
Jiliododendron  arboreitni,  190 
Rhodomyces  exubescens,  1092 
Rhodophycece,  923 
Rhopalocercous  Cercaricc,  559 
Rhophoteira,  857 

Z?Ams,   Species   associated   with   Der- 
matites 

diversiloba,  2152,  2156 

putnila,  2156 

radicans,  2156 

succedanea,  2156 

toxicodendron,  2152,  21  v> 

venenata,  2152 

vernicifera,  191-2,  2152,  2150 
•  'U,  2156 
Rhycopus  nigricans,  ijiz 
Rhynchelaps,  246 

aus tralis,  251 
Rhyncobdellida,  G85 


2400 


INDEX 


Rhynchoidomonas,  360,  380,  381,  397 

lucilice,  397 
Rhynchoprium,  703 

columbce,  703 

pevsicum,  703 

spinosunt,  708 
Rhynchostomi,  690 
Rhyngota,  761 
Rice,  95,  99,  100,  104-5,  107 

and  Beriberi,  105,  109,  1674  sqq. 

Vitamines  in,  105,  109,  1676 
Ricin,  1862 
Ricinice,  693 
Ricinidce,  750 
Ricinus,  750 
Ricinus  communis,  Poisoning  by,  1 74, 

190 
Rickets,  Climatology,  124,  1923,  1945 

Splenomegaly  of,  1303 
Rickettsia    Bodies  in  Trench   Fever, 
&c,  1502-3,  1505 

pediculi,  1503 

prowazeki,  1328,  1330,   1332,    1345, 

1503 
Ridged  Nails,  2283 
Rihagan,  1761 
Rinderpest,  189 
Ringworm,  2085,  2271 

^Etiology,    21,    991    sqq.,    1078, 
1782,    2203,    2053.,    see 
also  Tinea  Capitis 
Climatology,  123,  2059,  2080 
Black-dotted,  999 
of  Body,  2070 
of  Hair,  994 
of  Head,  Tropical,  2052 
Ringworm  Yaws,  1545,  2052 
Risipola  Lombarda,  1700 
Roads,  Colour  of,  and  Shading,  of  90-1 
Roaki,  2148 
Robbery,    Stupefying    Poisons    used 

to  facilitate,  170-1 
Robb's  Heat  Fever,  1469,  1530 
Robles'  Fever,  1462 
Rocky     Mountain     Spotted     Fever, 
134 1,     for    details     see 
Spotted    Fever   of   the 
Rocky  Mountains 
Rodent  Ulcer,  2277 
Rodents,    see   also    Epimys,    Ground 
Squirrel,  Mice,  and  Rats 
Parasites  carried  by,  405,  406,  407, 

493 

Roman  Fever,  1129 

Roosbeen  von  Surinam,  1610 

Root -Fly,  905 

Rose,  the  (disease),  2158 

Rosewood,  Dermatitis-causing,  2160 

Ross,  Sir  Ronald, Discoverer  of  Spread 
of  Malaria  by  Mosqui- 
toes, 16,  18,  19,  896 


Rosette  Formation  in  Trypanosoma, 

386 
Rossiella,  491,  502 

rossi,  502 
Roundworms    (see    also    Xematahel- 

minthes),  1967 
Rourea,  2159 

oblongifolia,  189 
Rubiacece,  178,  184,  191,  2153,  ~I54- 

2162 
Rubner's  Isodynamic  Law,  97 
Rflckfallfieber,  1308 
Ruhr,  1824 
Rungus  Poisoning  (Dermatitis),  2152, 

2162 
'  Running         amok,'        176,       1981, 

1988 
Running  Scab,  2053 
Rupture  of  Liver,  1907 

of  Myocardium,  1904 
Russian  Remittent  Fever,  1501 
Ruta  graveolens,  2153,  21 61 

montana,  2 161 

tuber culata,  2160 
Rutacece,  2153,  2154 

Dermatitis  due  to,  2152 

Sablier  Crepitans,  168 
Sabouraudi  Tropicalis,  1009 
Saccharomyces,  979,  981,  1069,  1070, 
1073,  1712,  1742,  1782, 
1886,  2008,  2009,  2047, 
2081 

albicans,  1085,  1742 

angince,  982 

balzeri,  982 

blanchardi,  981 

cantliei,  1078 

capilliiii,  1077 

cerevisiecB,  1072 

ellipsoides,  982,  201 1 

granitlatus,  981 

granulomatogenes,  10  70 

hominis,  982 

krusei,   1088 

UgucB-piloscB,  1074 

lithogenes,  1076 

ovalis,  1077 

roseus,  982 

ruber,  1076 

samboni,  982,  2047,  2092 

sphcericus,  1077 

tumefaciens,  981 
Saccharomyceiacece,  978 
Saccharomycetales,  978 
Saccharomycetic      Dermatomyc<  ses, 
2041 

Intertrigo.  2047,  2092 

Stomatitis,  1741 
Saccharomycodes,  <>'<> 
Saccharomycopsis ,  979 


INDEX 


2401 


Saccharomycosis    Epiclermica,    1075, 
2092 
Hominis,   2081 
Saccobranchus  fossilis,  232,  235 
Safat,  1535 
Safraiiin,  26 
Sahafati,   1535 
Sahara,  Chancre  du,  2165 
Sahib's  Disease,  1289 
St.    Francis   of   Assisi   and   Pellagra, 

1700-1,  1711 
Sakai,  the,  49 

Arrow-Poison  of,  184 
Sakitlatar,  1983 
Sakupolopolo,  2159 
Salamandaridin,  240 
Salamandarin,  240 
Salamanders,  Parasites  of,  355 

Venom  of,  240 
Salamandra  maculosa,  355 
Salek,  2165 

Salivarius  group  (Streptococci),  938 
Salivary  Calculi,  1 740-1 
Salmonella,    935,    938,    1362,     1405, 
1408,  1411,  1853 
Groups  of 

Paratyphoid-Asiaticus,  939-40 
Morgan,  939 
Veboda,  939 
Species 

eertrycke,  939 
archibaldi,  940 
asiatica,  940 

var.  mobilis,  940 
Carolina,  940 
enteritidis,  939 
gaertneri,  940 

paratyphi,  935,  938,  939,  940 
paratyphosus     A     and    B,    939, 

940 
pseudo-asialica,  940 
psittacosis,  939 
suipestifer,  939 
typhimurium,  939 
veboda,  939 
willegoda,  939 
wolince,  939 
Salonica  Fever,  1501 
Salpingitis,  Gonorrhceal,  1961 
Salpullido,  2225 
Salso,  1700 

Salt  in  Food,  53,  94,  96,  97,  107 
Salvarsan,  27,  1202 
Sambon's      Theory       of       Pellagra- 
etiology,  1714 
Samoan  Eye  Disease,  2001 
Samoyed  Tribes,  4,  55 
Sanaga  Smallpox,  1491 
Sanbilang,  235 
Sand,  Intestinal,  1739 
Pseudo-intestinal,  1739 


Sandflies,  810,  1128,  1254,  1257,  1258, 
151 7,     2096,     see     also 
Phlebotomus  and  Sinui- 
UidcB 
Sandfly  Fever,  1254 
S;uuhvorm  Disease,  122-3 
S(tn«itinens  Group  of  Streptococci,  928 
Sanguisuga,  686 

San  Salvador,  Hunting-Poison  of,  189 
Sanitation,   Importance  of,   89,    119, 

124,    131 
Santonin  in  Ascariasis,  1775 
Saoria,   1756 

Sttpindacecs,  164,  166,  168,  188,  1696 
Sapindus  rarak,  188 
Sapium  insigne,  190 
StpotacecB,  178 
Sappinia,  323 
Saprophytica,  1045 
Saprospira,  439 
Saraat,  1535 

Sarcocele  d'Egypte,  1610 
SarcocystidcB,  290,  530 
Sarcocystin,  203 
Sarcocystis,  530,  1582,  1583 
References,  543 
Species 

ammodromi,  533 
aramidis,  533 
bertrami,  532 
blanchardi,  532 
hueti,  532 
kortei,  532 
leporum,  533 
lindemanni,  532,  1581 
mieschierana,  530,  532 
muris,  1581,  1582 
setophaga,  533 

tenella  or  tenellcs,  203,  531,  532 
var.  bicbali,  532,  1582 
San  ode,  334,  335 
Sarcodina,  296,  297 

Vaginal,  1945 
Sarcoma,  Adipose,  .211 1,  21 17 
Sarcomata,  123,  1072,  1074 
Sarcomatosis,  Multiple,  of  Skin    2274 
Sarcomatous  Ulcers,  2190 
Sarcomes  Adipeux,  21 17 
Sarconissus,  722 

Sarcophaga,  415,  830,  90°.  1621,  i<>2<>, 
1629 
affinis,  830,  1629 
aurifinis,  900 
carnaria,     830,     900,     1626,     1628, 

1629, 1632,  201 1 
carnosa,  1626 
chrysostoma,  831,  1632 
lucmatodes,  831,  1629 
hcemnyrhoidalis,  367,  830-1,  1629 
lambens,  831 
latifrons,  1629 

151 


2402 


INDEX 


Sarcophaga,  continued 

magnified,  1626,  1629,  1632,  2007 

meigeni,  1626,  1629 

nura,  1626 

plinthopegga,  1632 

plinthopya,  831 

regiilaris,  1626 

ruficornis,  831,  1632,  1639 

ntralis,  1626,  1629 

trivia/is,  904 

ivohlfarti,  1626,  1629 
Sarcophagidez,   825,   830,  1626,   1627, 

1629,  1632 
Sarcophagula,  900 
Sarcophila,  830,  831 

latifrons,  831 

meigeni,  831 

ntralis,  831 
Sarcopsylla,  861 
Sarcopsyllidce,  861 
Sarcopsyllintz,  866 
Sarcoptes,  731,  2248 

hotninis,  2218 

minor,  731 

scabiei,  1650,  2203 
var.  auchenia,  2214 
var.  canis,  2214 
var.  e<^«,  2214 
var.   hominis,    731,    2214,    2217, 

2218,  2219 
var.  01/is,  2214 
var.  swis,  2214 
Sarcoptides,  729,  731,  2214 

References,  742 
Sarcoptoidea,  692,  729 
Sarcosporidia,  528,  530 
Sarcosporidioses,  the,  1578,  1581 
Sarcosporidiosis.iEtiology,  1533, 1582 

Causal  organisms,  1581 

Climatology,  1582 

Definition,  1581 

Diagnosis,  1582 

Heat  in  relation  to,  1582,  1583 

History,  1581-2 

Morbid  Anatomy,  1582 

Prognosis,  1582 

Prophylaxis,  1583 

References,  1583 

Symptomatology,  1582 
Sarcosporidiotoxin,  295 
Sardinella  neohowii,  194 
Sardinia,  Fish-Poisons  of,  188 
Sarna,  2217 
Sarnes,  21  Si 
Sarten  Ulcer,  2166 
Satin-Wood  Dermatitis,  2152,2159-60 
Saturation  Test,  1397 
Sauria,  Hamogregarina  of,  4S7 
Savannah  Flower,  169 
Scab,  Running,  2053 
Scabbia,  2217 


Scabies,    691,    729,    731,    2022,   2023, 
2200,  2203,  2216,  2217, 
2218,  2248,  2268 
Indica,  2217 

Neglected,  and  Craw-craw,  2247 
Scabietic     Conditions     of     Domestic 
Animals,  affecting  Man, 
2219 
Scabnties,  2217 
Scalp,  Elephantiasis  of,  161 7 
Scaphopoda,  890 
I    ScarabceidcB ,  1640 
Scarlatina,  Virus  of,  Filterable,  54 
Scarlet  Fever,  120,  124,  131,  1485-6, 
2267 
Diagnosis,  151 3 

Differential,  1250,  1253,  1517 
Organisms  associated  with,  537, 

540,  541,  1075 
Rash  of,  1513,  1517 
Hemorrhagic,  1491 
Scarlet-Fever-like      Subtertian      Ma- 
laria, 1 1 71,  1173 
Scatophaga,  363,  365 
hoitentota,  363 
lutaria,  365 
stercoraria,  905 
Scedosporiiim,  11 21,  1122 
acremonioides,  11 22 
apiospermum,  1121,  1122,  2122 
sclerotiale,  1122,  1123,  2121 
ScenopinidcB,  824,  900 
Scenopinns  fenestralis,  824,  900 
Schamanismus,  1987    • 
Schamberg's  Disease,  2216 
Schenk's  Sporotrichosis,  11 19 
Schionniomyces,  979 
Schistosonia,  17,  558,  584,  859 
Christophers  and  Stephens',  593 
hcemaiobium,     17,    584,    588,    645, 
1596,  1864,  1902,  1926, 
1927 
Hosts,  893,  894 
Ova,  588,  645 
References,  595 
japonicum,    584,    589,    590,    1589, 
1590,  1776,  1840,  1903, 
1907 
Hosts,  590,  891,  894,  1590,  1591 
Ova,  590,  592 
References,  595 
mansoni,   17,  584,  587,  590,  1273, 
1777,  1840,  1869,  1903, 
1907 
Hosts,  587,  590,  893,  894,  1865 
Ova,  587  sqq.,  1864  sqq. 
References,  595 
New,  in  a  Hsematuria  patient,  593 
Schistosomiases,  Climatology  of,  124, 
133,  see  also  Bilharzio- 
sis 


INDEX 


2403 


Schistosomiasis,     Disqualification    of 
Natives  as   Employees, 

130 

Liver  in:  Reference,  1918 
Asiatic,  1589 
Intestinal,  590,  1864 
.Etiology,  1865 
Climatology,  1805 
Complications,  1869 
Definition,  1864 
Diagnosis,  1520,  1869 
History,   1864-5 
Pathology,  1865-7 
Prognosis,  1869 
Prophylaxis,  1869 
References,  1870 
Symptomatology,  1867-9 
Synonyms,  1864 
Treatment,  1869 
Varieties,  1867-9 
Japonica,  1589 

rrinary  (fJilharziosis,<7.D.),587, 1926 
Schistosomic  Dysentery,  1867-8 
Fever,  1867,  1869 
Hematuria,  1927 
Schistosomidce,  564,  584,  1752 
Schistosomum  cattoi,  590 
Schizocystina,  471 
Schizocystis,  471 
Schizogony,  288,  292,  293,  294 
Schizogregarince,  471 
Schizogregarinaria,  471 
Schizomycetacea,  924 
Schizomycetes,  922,  923,  1040 
Nomenclature  Rules,  922 
References,  965-6 
Schizonts,  293 
Schizophora,  774,  825,  901 
Schizopkyta,  436 

osaccharomyces,  979 
Schizotrypanum,  380,  381,  387,  401 
cruzi,  387,  391,  393.  4QI.  4J9.   *27< 
1268,  1283,  1284,  1288, 

Schizsoirypanose,  1283 
Schmauch's  Bodies,  1902 
Schonlein's  Disease,  1698 

Purpura,  2267 
Schools  of  Tropical  Medicine,  20,  29 
Schridde's  Granules,  1897 
Si  hfiffner's  Dots,  293,  1902 
Schwamchen,  1741 
Schwarzwasserfieber,  1216 
Scillitine  Poison,  166 
Si  i one,  823 
Scirro,  2217 
Sciurida,  914 
Sciurince,  914 
Sciuropterus,  914 
Sciurus,  914 
Sclerema  Neonatorum,  2281 


Sclerodermia,  2281 
Anidrosis  in,  2224 
Circumscribed,  2077,  2281 
Diffuse,  2281 
Scleroparei,  232 
Sclerostoma  duodenale,  666 
Sclerotic  Tumour,  2007 
Sclerotium  beigelianum,  1103 
Scolechiasis,  161 9 

Gastro-intestinal,  1640 
Rhinal,  1640 
Scolex,  596  sqq. 
Scolopendra  cingnlata,  218 
geophilus  longicornis,  218 
gigantea,  218 
heros,  218 

morsitans,  217,  218 
Scolopendridce,  2 1 7-1 8j 
Parasites  of,  740 
References,  229 
Venom  of,  218 
Scopulariopsis,  n  11,  1123,  2107,  2149 
Dermatomycoses  due  to,  2041 
Species 

blochi,  1123,  1124,  2041,  2107 
brevicaule,  11 23 
,  communis,  1123 
koningii,  1123,  1124,  2107,  2149 
repens,  n  23 
rubellus,  11 23 
rufulus,  1123,  1124 
Scorbuto  Alpino,  1700,  1702 

Montano,  1700 
Scovpcena,  232,  233 
Species 

diabolus,  232,  233 
grandicornis,  232,  233 
porcus,  232,  232 
scropha,  238-9 
Venom,  238-9 
Scorpcenidce,  232,  233,  238 
St  "ipionidea,  206 
References,  228 
Scorpions,  Bite  and  Venom  of ,  12,  124, 
206,  215,  690 
Venom  of,  as  Arrow- Poison,  180 
Book,  897 
Scottatura  di  Sole,  1700 
Scrofulodermia,  2277 
ScrophulariaceeB,  2153 
Scrotal  Eczema,  Primary,  2047 

Tongue,  1746,  2284 
Scrotum,  Angiokeratoma  of,  2277 
Elephantiasis  of,  1597.  1610,  161 1, 
1615 
Treatment,  1616-17 
Lymph,  639,  1596,  1601,  1605 
Scurvy,    25,    109,    122,    1516,    1675, 
1 701,  1718,  2032 
Button  form,  1536 
Infantile,  1675 


2404 


INDEX 


Scutigera  coleoptrata,  740 
Scutigeridcs,  740 
Scutula,  1011,  1012,  1014 
Scytho-Dravidian  Peoples,  49 
Sea  Urchin  of  the  Red  Sea,  205 
Seaman's  Skin,  2231 
Seasonal     Bullous    Dermatitis,    226, 
2204 
References,  2220 
Diets,  106 
Recurrent      Ulceration     of     Lips, 

2284 
Vesicular  Dermatitis,  2204 
Sebaceous  Secretion  of  Normal  Na- 
tive Skin,  2264 
Ssborrhcea,  2215,  2262,  2271 
Capitis,  1077,  1078,  2271 
Corporis,  2078 
Spinulosa,  2262 
Seborrhceic  Affections,  2271 
Seborrhoeide  of  Chest,  confused  with   ] 

Ringworm,  2271 
Secondary  Streptococcal  Dermatites, 

2030,  2036 
Sedative  and  Stimulative  Poisoning, 

174-8 
Sedum  acre,  2153 
Segestria  perfida,  213 
Seidelin's  Bodies,  1231,  1233 
Selachii,  Larger,  Traumatisms  caused 

by,  154-5 

Venomous,  232 
Selasoma,  820 
Selenomastix,  334' 
Selenomonas,  334 
Semangs,  the,  49,  53 
Semecarpus  anacardium,  2152,  2162 
SemiscolecincB,  685 
Semitic  Races,  46,  47 
Siin-iang-hoa  Buds,  172 
Senile  Atrophodermia,  1730-1,  2231, 

2282 
Sepedon,  246 

hcemachates ,  248,  251 
Venom  of,  267-8 
Sepedonium,  1112 
Sepsides,  901,  902,  1630 

Reference,  856 
Sepsis,  900 

punctwn,  900 

violacea,  902 
Septic  Disease,  Lymphatic  Affections 
in,  1961 

Fevers,  1520,  1529 
Bilious,  1469 

Infections,  1523 
.11    Absorption,  153 1 

Jaundice,  1507,  1508 

Multiple  Liver  Abscesses,  1525 

Pemphigus,  151 8,  2269 

Ulcers,  2191 


Septicaemia (s),  927,  929,   1337,   1516, 
1517,   1527,  1914 

Cryptogenic,  1429 

due  to  Deep  Suppuration,  1528 

Gonococcal,  1938 

Helminthic,  1520 

Melitensis,  1437 

of  Morphine  Injectors,   1466 

Puerperal,  1946 
Septicaemic  Fevers,  11 86 

Hemorrhagic  Group  of  Organisms, 
Genus  including,  943 

Plague,   1428 
Sergentella  hominis,  537,  1583 
Sergentelliasis,  1578,  1583 
Serjania,   188 

ichthyoctova,  188 

httalis,  188 

piscatoria,  188 
Serology    in    Bacterial    Dysenteries. 

1855-7 
Sero-Phthisis    Perniciosa    Endemica, 

1671 
Serotherapy,  History  of,  22 
Serous  Diarrhoea,  1820 
Serpiginous  Corneal  Ulcers,  2004 
Serpigo,  2053 
Serromyia,  806 
Serum     Injections,      Rash    due    to, 

1516 
Serut-Flies,  815,  819 
Setaria,  649 
equi,  649 
Seven  Days  Fever,  1186,  1244,  1249, 

1250,  1312 
Reference,  1253 
Seven    Days'    Fever    (not    Rogers'), 

1308 
Sewage  Disposal, -1859 
Sexual  Perversions,  1981 
Shaamba,  the,  47 
Shamanism,  4,  54,  55,  56 
Shank  Fever,  1501 
Shans,  the,  54,  55 
Sharks,     Traumatisms     caused     by, 

154-5 
Sharras,  the,  55 
Shashitsu,  746,  1350 
Shauia,  the,  46 
Shedding  of  Nails,  2283 
Sheep,  Heartwater  in,  713,  723 

Parasites  of,  21,  320,  369,  391,  412, 

416,    454,    492,    497-8. 

557.  565.  567,  723 
Liver    fluke    (Fasciola    hepatica, 

q-v.),  557 

Sheep-Disease  due  to  Piroplasma  ovis, 

497-8 
Sheep-Poisons,  189 
Sheep  Rot,  567 
Sheep-Ticks,  708,  723 


INDEX 


2405 


Shell-Shook  and  Effect  of  Sun-rays, 

1982 
Shigella,  934,  935,  936 

dysenteries,  935,  936 
Shima  Disease,  1350 
Shima  mushi  Disease,  1350 
Shimamushi  (mite),  726 
Shin,  Trench,  1501 
Shingles,  2269 

Ship  Beriberi,  109,  1680,  1690 
Ship  Rat,  917 
Shipada,  1610 
Shluh,  the,  46 
Shoshoneans,  the,  56,  57 
Siamese,  the,  54,  55 
Sibbens  or  Si  wens,  1536 
Siberia,  Shamanism  in,  4,  55 
Siberian  Races,  55 
Sick  Leave,  130 
Sida,  2159 
Sierra  Fever,  1129 

SierraLeone,  Vegetal  Poison  of,  1 64,168 
Siesta,  the,  88 
Siguatera,  193 
Silkworm  Disease,  529,  1032 
Siluridee,  232 
Silva  Lima's  Disease,  2241 
Silvanus  surinamensis,  226,  871 
Silvius,  820,  821 

decipiens,  821 

fallax,  821 
Simaruba  officinalis  Bark,  1836,  1858 
Simonea  folliculorum,   732 
SimpleContinued Fever,  25, 1254,1372 

Fibroma,  2273 

Toxaemia,  1920 

Xeroderma,  2281 
Simplicidentata,  913 
SimuliidcB,    773,    810,    812-13,    1650, 
1716-17,   1718,  2200 

References,  813 
Simulides,  810 
Simulincs,  810 
Simulites,  810 

Simulium  or  Melusina,  Sio 
Siiiiitliiini  Flies,  363,  920,  2096 

columbaczense,  811 

da»niosu»i,   811 
Icollis,  811 

hirtipes,  811 

indicum,  811 

reptaws,  810 

venastum,  811 
Sinhalese,  the,  47 
Siphona,  846 

Siphonaptera,    748,    749,    857,    2200, 
see  also  908,  2203 

References,  871 
Siphonapteriasis,  2200,  2203 
Siphonella  funicola,  902 
Siphonophora,  338 


Siphonopoda,  890 
Siphunculata,  752 
Siriasis,  12,  1449 
Sirkari  Disease,  1289 
Sirocco,  the,  81,  82 

di  Levante,  82 
Sistrurus,  250 
catenatus,  251 
miliar ius,  250,  251 
ravus,  250,  251 
Sitotoxismus,  195,  1673,  1674 
Sitotvopa  cerealella,  2216 
'606,'  see  Salvarsan,  27 
Skin,  Aspergillosis  of,  1032 

Effect  on,  of  Tropical  Climates,  77 
Furrowing    of,    Artificially,     2238, 

2240,  2241 
Normal,  of  Native  Races,  2264-5 
Pigmentation  of,  Natural,  and  due 
to  Disease,  or  to  Sun- 
rays,  82,   84,   89,   1 180, 
15I3,  1519,  1531.  2231, 
2264,  2266 
Seaman's,  2231 

Senile  Changes  in,  1730,  2231,  2282 
Spirochetes  of,  448,  452 
Sunlight  as  affecting,  83-5,  2231 
Tattooing  of,  2222.  2238 
Medical,  2230 
Ornamental,  2338 
Trench, 1501 
Tropical,  2231 
Tuberculosis  of,  2264,  2277 
Tumours  of,  2264,  2273 

Multiple    Pruriginous,    22,    47. 
2254 
References,  2263 
Skin  Affections  due  to 
Echinodermata,  205 
Millepora,  204 
Tr achy  medusa,  204 
Zoantharia,  204 
Pyogenic,  2264,  2265 
Skin    Diseases,    122,    123,    124,    927, 
1 501 ;    see   also  Derma- 
tites,  2213.  and  Derma- 
tozoiascs,  2200 
Cosmopolitan,  2015,  2017,  2264 
Differentiation  of,  from    Pellagra, 

1 730-1 
Epiphytic,  Leucodcrma  in,  2228 
Parasitic,  2264,  2267 
Skin    Eruptions,    in    Acute    Fevers, 

1512,  1513 
Skin-Irritation 
Acute,  83-4 
Chronic,  84-5 
Skm  Lesions,  due  to 

Metazoan  Parasites,   2200 
Poisonous    Plants,     2151-2,     2155, 
2162,  2167 


2406 


INDEX 


Skoplji  or  Uskub  Fever,  1254 
Slavic  Branch  of  Caucasic  Races,  46 
Sleeping  Dropsy,  1260 
Sleeping   Sickness     (African   Human 
Trypanosomiasis),   550, 

1259,  1260,  1476 
Animal    Carriers    and    Reservoirs, 

425,   878,   881,    1264-5, 

1279-80 
Blood  in,  1271-2 
Cerebral  Stage,  1269,  1270-1 
Cerebro-Spinal  Fluid  in,  386,  1266 
Characteristic  Features,  1259 
Climatology,  124 
Complications,  1273,  1961,  2006 
Course,  1269-70 
Definition,  1260 
Diagnosis,  1273,  1514,  1523,  1524, 

I532 
Methods,  1274-5 
Distribution,    26,    124,    419,    420, 

425,  1263 
Epidemiology,  1263-4 
Erythemas  associated  with,   1270, 

1514,   2260 
Febrile  or  Glandular  Stage,  1269-70 
Histopathology,   1266-9 
History,  1261 
Incubation,  1269 
Insect   Vectors,    19,   23,    747,    838, 

843,  844,  876,  881,  1128, 

1260,  1262,  1263,  1264, 
1265,  see  also  Glossina 

Morbid  Anatomy,  1266-9 
Occupation  in  relation  to,  1265 
Parasites    present   in,    other   than 

Trypanosomes,  1273 
Pathology,  1265-6 
Predisposing  Causes,  1265 
Prognosis,  1275 
Prophylaxis,  116 

Personal,  1280 

Public,  1278  sqq. 
References,  1 281-2 
Remarks,  12  60-1 
Symptomatology,  1269 
Synonyms,  1260 
Three  Types  of,  1264 
Treatment,  26,  28,  1262,  1275 

of  Natives,  12  78 

Symptomatic,  1278 
Trypanidcs  in,  1270,  1514,  2266 
Trypanosomes  Causing  and   Asso- 
ciated with,  19,  20,  391, 

419,    42O,    421,    425,   427, 

878,   1259  sqq.  passim., 
1273,  see  also  that  head 

Aflagellate  forms,  386 
Types  of 

Castellani,  879 

Stephens  and  Fantham,  880,  881 


Sleeping-Sickness,  continued 
Urine  in,  1272-3 
Varieties,  1273 
Sleeping  Sickness  Bureau,  1262 
Slipada,  2110,  2111 
Slipatham,  2 no,  21  n 
Sloths,  Trypanosome  of,  405 
Slow  Fever,  1362,  1437 
Smallpox  (Variola),  5,  25,  1470,  1471, 
1486,  1491,  1492,  1566 
/Etiology,  1487 

Chlamydozoa  of,  539,  540,  541,  542 
Climatology,    120,    121,    122,    124, 

'1487,  2267 
Cytoryctes  variola  in,  535,  540 
Definition,  i486 

Diagnosis,  1489,  1515,  1517,  1519 
Differential,    1250,    1337,    i486, 
1489-91,  1505,  2249 
Epidemics  of,  2267 
History,  1486-7 
Inoculation      for,      practised      in 

India,  8 
Infection,  route  of,  1487 
Parasite  of,  535,  540 
Prophylaxis 
Vaccination 

Hints  on,  2267 
Importance  of,  1491 
Rash,  1515,  1517,  1519,  2267 
Spread,  1487 
Symptomatology,  487 
Synonyms,  i486 
Varieties,  1488-9 

Confluent,  1488,  2267 
Haemorrhagic,  1488-9,  2267 

Pustulosa,  1488-9 
West  Indian  modified,  1491 
Virus     of,     Filterable,     539,    541, 

543 
Small  Proteus,  399,  see  also  Amccba 
Smithia,  491,  492,  501 
microti,  501 
talpcB,  501 
Smooth  Leprosy,  1654,  1659 
Snails,  Intermediate  Hosts  of  Scliis- 
toma,  893 
Parasites   of,    353,    355,   559,   567. 
57°.  584.  587.  59i,  876 
Venomous,  227 
Snake-Bite,  12,  122,  124,  1698 
Diagnosis,  273 
History,  24J-4 
Indian  Mortality  from,  242 
Prophylaxis,  278 
Prognosis,  274 
Rash,  1 51 6 

Treatment,     24^,     244,     271    sqq., 
280 
Oil  useless,  277 
Snake- Stones,  277 


INDEX 


2407 


Snake-Venoms,  24 

Active   Principles  of,    243,    244, 

255  sqq.,  262-3 
Anti-Sera  for,  244,  271,  276 
as  Arrow- Poison,  180 
as  Cattle-Poisons,  189 
Chemical  Analysis,  253-5,  271 
Collection  of,  252-3 
Effects,  264  sqq.,  271 
Entry  into  Body,  263 
Excretion,  271 
Immunity  to,  243,  271-3 
Minimum  Lethal  Dose,  203-4 
Physical  Characters,  253 
Preservation,  253 
Symptomatology,  189,  190 
Three  Kinds,  244 
Snakes,  Blood-Parasites  of,  353,  355, 
401,  51G,  736,  737,  738 
Venomous,  242 

Apparatus  and  Act  of  Striking, 
251-2 
Soamin,  26 

Social  Diseases,  see  Gonorrhoea,  926, 
Syphilis,  2278,  and  Tu- 
berculosis, q.v. 
Socotrine,  170 
Solanacece,     164,     166,     170-1,      173, 

176-7,  178,  2153 
Solano  (wind),  81,  82 
Solar  Radiation,  144-6 

References,  146 
Solaro  Fabric,  96,  1989 
Soldier's  Heart,  1982 
Solenoglypha,  249 
Solenopotes,  759 

Soles,     of    Feet,     Hyperkeratosis    of 
whole  of,  2277 
Parasites  of,  488 

in      Yaws,       Lesions      of,       1551, 
2259 
Solidago  odor  a,  2152 
Solifuga,  690 
Somal  Race,  47 
Somatic  Taeniases,  601 ,  1 967 
Sommerfieber,  1254 
Somomyia  montevidensis,  847 
Sonnenstich,  1449 
Sonsino's  Disea.se,  1864 
Sordes,  1384 
Sore  Feet,  553 

of  Coolies,  [764 
Sure-  Throat,  Streptococci  in,  930 
Sores,  Cambay,  378 
Cochin,  2 1 81 
Mozambique,  21  Si 
I  (riental,  2165 
Veldt,  2030,  2031,  2190 
Venereal,  2278,  2280 
Sorghum,  105 
Souma,  391,  412,  415,  417,  816 


South  African  Vegetal  Poisons,  164, 

166,  167,  189 
South  America,  see  Brazil,  eU 
South    American    Relapsing    Fevers, 
919,  1323,  1324 
Trypanosomiasis  (Chagas'  Disease), 
19,  1283,  see  also  under 
Trypanoscmiases 
South-west  Gune,  2059 
Spalangia  niger,  908 
Sparganosis,  1967 
Sparganum,  601,  602,  606 
References,  619 
Species 

baxteri,  601,  606,  607 
mansoni,  601,  606,  1967,  2007 
prolifer,  601,  606,  1967 
Dermatoses  due  to,  2220 
Spargosis  Fibroareolaris,  1610 
Sparrow-Poisoning,   191 
Spasm  of  Ocular  Accommodation 

Muscles,   2005 
Spastic  Paralysis,  1981 
Special  Sense,  Organs  of,  Diseases  of, 

1993 

References,  2014 

Subtertian  Malaria  attacking,  11 75, 
1181 
Specific     Blackwater     Fever,      121 3, 
1216 

Hemoglobinurias,  121 3 
Spedalskhed,  1644 
SpelceorhynchincB,  701 
Spermatic  Cord,  Cellulitis  of,  1939 
Suppurative  Phlebitis  of,    1939 
Spermophilus,  915 

citellus,  913,  1424 
Sphczriales,  985 
Sphcerocystis,  471 
Sphcerogyna  ventricosa,  728 
Sphceromyas,  806 
Sphczropsidales,  1036 
Spliarospora,  529 
Spheerotilus,  1071 

Sphagni  Group  of  Streptococci,  928 
Sphodrus  leucophthalanus,  [640 
Sphyrcena,  193 
Spider  as  Arrow-Poison,  180 
Spiders,  124,  211,  908 

Bite  (sting),  12,  124,  212,  214-15 

References,  228-9 

Venom,  213  sqq. 
Spigelia  anthelmia,  164,  168,  1872 
Spilogaster  divisa,  1630 
Spina  bifida,  1959 

Spinal     Caries,     Bodies    in    Pus    of, 
2112 

Cord,  used  as  Aphrodisiac,  172 
Spine-Protection,  89 
Spirarsyl,  27,  28 
Spiriliacees,  024,  962 


>4oS 


INDEX 


Spirillum,  962,  1838 
duttoni,  21,  444 
eurygyrata,  450 
hachaizce,  451 
zeylanicum,  1068 
Spirillum  Fever,  1308 
Spirits  in  relation   to  Disease,  early- 
ideas  on,  3  sqq. 
Spirobacillus  zeylanicus,  451,  1069 
SpirochcBta    (Spirochaetes),    215,    296, 
358,  434,  437,  454,  917, 
1903,     see    also    Spiro- 
schaudinnia,    below 
of  Animals,  453  sqq. 
in  Blackwater,  1221 
Characters  resembling 
Bacteria,  436,  437 
Protozoa,  437 
Diseases  with  which  associated, 

2°-u  443  sqq-.  44S,  541. 
920,  i22i,  1230,  1318, 
1350    sqq.,    1467,    1538, 

l7l5,  1745.  I746.  2°9i, 
2181 
Human,  443 

Differentiation  of,  452-} 
from  Pseudo-Spirochaetcs, 
45i 

of  Alimentary  Canal    450,  452 

of  Blood,  443,  452 

Cutaneous,  448,  452 

in  Faeces,  451,  453 

Respiratory,  449,  452 

Urinary.  451,  453 

Urethral,  451,  453 

in  Vomit,  453 
Infective  Granule  in.  385 
Insect  Vectors,  23  et  alibi 
in  Nose,  1521 

Placenta  traversed  by,   289 
in  Sputum,  1521 
Vaginal,  1945 
in  Yellow  Fever,  44S 
Species 

acuminata,  1538 

anodontcB,  439 

bronchialis,     1881,    18S2       1883, 

1884 
buccalis,  1883 
carteri,  436 

duttoni,  20,  436,  444,  452 
evansi,  409 

exanthematotyphi,   1330,   1332 
gallica,  1502 
gallinarum,  433 
ictcroluzmorrhagica,  447 
interrogans.  1231 
macaci.  453 
minuta,   1881 
morsusmuris,  447 
novyi,  \  56 


Spirochceta,  continued 
Species,  continued 
obermeyeri,  443 
obtusa,  1538 
pallida,  21,  455 
pallidula,  457 
pertenuis,  457 
plicatilis,  436,  437,  439 
recurrentis,  439,  443 
refringens,  1538 
schaudinni,  2 181 
urethralis,   1944 
Spirochcetacea,  358,  431,  435 

References,  462 
Spirochaetal   Dysenteries,   451,    1825, 
1838 
Jaundice,  1505 

Epidemic,   191 8 
Rhino-pharyngitis,    1521,   1881 
Urethritis,  451,  453,  1944 
Spirochaete-like   forms  in   the   Little 

Owl,  434 
Spirochaetes,   see    Spirochceta,    above, 
and     Spiroschaudinnia, 
below 
Spirochcetidce,  436 

Ticks  spreading,  700 
Spirochetose    Bronchopulmonaire   de 

Castellani,  1882 
Spirochaetoses,  691,  1308 
Spirochaetosis,  Avian,  454 
Bronchial,  452,  1875,  1882 
Bronchopulmonary,  in  Cats,  1885 
Castellani's,  1535 
Cutaneous,  1535 
Gastric,  1749 

Icterohaemorrhagica  (see  also  Weil's 
Disease),  1505 
Subtertian    Malaria    resembling, 
1171,  1172 
Mixed  Infections,  1885 
Nasal,  1882 

Rhino-Pharyngeal,  1521,  1881 
Spiroflagelldta,  435 
Spironema  pallidum,  455 
Spiroptera  hominis,  633 
Spiroschaudinnia,  439 

Insect    Carriers,    440-1,    442,    445, 

453,  691,  700 
Oral,  450,  452,  453 
References,  462 
Species 

aboriginalis,  448,  2193 
acuminata,  449,  452,  459 
anserina,  453 
balanitidis.  454 
berbera,  447,  452,  918,  13 14 
bronchialis,  449,  452 

References,  462 
buccal  is.  450,  453,   1740 
bufonis,  454 


INDEX 


2409 


Spiroschaudinnia,  continued 
Species,  continued 

carteri,  436,  445,  446,  452,  918, 
1315,  1316,  1323 
References,  462 
culicis,  454 

dentin  111,  450,  453,   1740 
duttoni,  201,  436,  440,  443,  444, 

452.  453-  7°°.  7°6.  7° 7. 
1315,  1318,  1319,  1323, 

i324 
Forms  like,  in  Relapsing  Fever, 

919 
References,  462 
equi,  454 

eurygyrata,  450,  1838 
glossing,  454 
gracilis,  454 
granulosa,  454 
hebdomadis,  448,  1510 
icterohesmorrhagica,    447,    451, 

452,  918,  1500 
lutrcB,  454 
macaci,  453,  13 16 
marchouxi,    440,    442,    453,    700, 

1322 
microgyrata,  454 
minuta,  450,  452 
>»//;'.?,  451,  453  . 
morsusmurus,     447,     452,     454, 

..  1356.  1358,  1360 
neveuxii,  454 
novyi,   436,   441,   442,   443,   445, 

446,     452,     918,     1315, 

1323. 1324 
obermeyeri,  1309 
obtusa,  449,  452,  459 
ovina,  454 

phagedenis,  449,  452 
pseudopallida,  449,  452 
recttrrentis,    20,    436,    437,     139, 
440,    441-2,    443,     11,. 
452.     765.     9i8,     1308, 
i3°9.  1315.  1323 
refringens,  456,  450.  2193 
ross?,  442.  445,  1319,  1322 
schaudinni,  448,  452,  2182 
subtil  is,  450 
thcileri,  454,  700,  715 
Unnamed,  in   I  'sori.isis.    |  pi 
urethra,  451,   153 
vespertilionis,  454 
vincenti,  448,452,  2181,2182,2192 
Spiroschaudinnides,  4  35 
Spirosotna,  962 

lingualis,  1051 
Spirulina  genus,  in  relation   to   the 

Spiroch32t.es,  437 
Spitting-Snakes,  267-8 
Spleen,  l  dseases  of,  1895,  1904 
References,  1925 


Spleen-Enlargement,    see    Splenome- 
galy, 6e/ow 
Spleen-Rupture,  1185 
Splenic  Abscess,  1905 
Anaemia,  1302,  1303 
Febrile,  1299 
Infantile,  20 
Splenomedullary    Leukaemia,     1303, 

1903,  1905 
Splenomegaly  (ies),  133,  483,  490,  1076 
Differential  Diagnosis,  1303 
Diseases    with    which    associated, 
1524-5,       1529,       I531- 
Il,59.      I9°3,     see     also 
Malaria 
Febrile,  123,  1303,  1525,  1529,  1531 
Krempf's,  1303,  1306 
Toxoplasmatic,  Febrile,  1531 
Tropical,  1531,  191 4,   1925 
References,  1307 
Afebrile,  1289,  1303,  1306 

Infantile,  1303 
Febrile,  1289,  1303 
Spleno-Typhoid    form     of     Enteric, 

1388 
Sporadic  Cretinism,  1920 
Sporangium,  969 
Sporisorium  maidis,  1703,  171 2 
Sporocephalum  roseum,  in 7 
Sporocyst  Stages  of  Trematoda,  558, 

507 
Sporogony,  288,  293,  294,  295 
Sporont,  294 
Sporophora,  969 
Sporophoralinecz,  1 1 1 1 
Sporophore,  1037,  1039 
SporophorinecB,  1121 
Sporoplasm,  470 
Sporotrichinece,  mi,  1117 
Sporotrichosis,  2086,  2193 
/Etiology,  2086-8 

List  of  Fungi,  2087 
Climatology,  2086 
Cuti-reaction  in,  969 
Diagnosis,  2089 

Differential,  2091,  2186,   2193 
Histopathology,  2088 
Prophylaxis,  2o8g 
Pseudomycetoma-likc  Condition 

in,   2148 
Symptomatology,  2088 
Treatment,  2089 
Varieties,  2041,  2088 
I  '.mnchial,  1892 
European,  tug 
Ocular,  2008,  200.1,  2010 
Palpebral,  2008 
Schenk's,  1119 
Tropical  Varieties,  20  1 1 
Sporotrichosis-like  Condition,  Monilia 
in,  1092 


2410 


INDEX 


Sporotrichum,  987,  1081,  1117,  1886, 
1892,  2008,  2086,   2089 
Dermatomycoses  due  to,  2041 
Species 

asteroides,  1117,  ni8,  1120,2041, 

2087,  2088 
beurmanni,     1117,     1118,     1119, 
2008,  2009,  2041,  2087, 
2088 
bronchiale,  1117,  1118 
councilmani,    1117,    1118,    1121, 

2087 
dermatodes,  1032 
dori,  1 117,  1 1 18,  1119,  2087 
furfur,  1099 

gougeroti,  11 17,  11 18,  1120,  2087 
indicum,  11 17,  11 18,  1120,  2041, 

2087,  2088 
inquinatum,  1117 
jeanselmi,  11 17,  11 18,  1120,  2089 
lesnei,  1117,  1118,  1121,  2087 
mentagrophytes,  1005 
minutissimum,  1053,  1061 
obducens,  1117 

schenki,  1117,  1118,  2041,  2087 
Sporotrichitic  Ulcers,  2190 
Sporozoa,  296 
Sporozoites,  294 
Sporozoon  furunculosum,  378,  2166 

rattengift,  1356 
Spotted  Fever,  1326,  1474 
of  Idaho,  1341 
of  Montana,  1341 
Spotted  Fever  of  the  Rocky  Moun- 
tains, 1329,  1341,  1350 
^Etiology,  1343 
Animal  Reservoir,  1341,  1345 
Climatology,  1342-3 
Complications,  1437 
Convalescence,  1347 
Course,  1346-7 
Definition,  1341 
Diagnosis,   151 4 

Differential,  1347-8,  1354 
Histopathology,  1346 
History,  1 341-2 
Incidence 
Age,  1345 
Season,   1343 
Sex,  1345 
Insects  Spreading,  21,  691,  700-1, 
716,  717,  718,  920,  1128, 
1341 
Morbid  Anatomy,  1345-6 
Onset,  1346 
Pathology,  1345 
Predisposing  Causes,  1345 
Prognosis,   1348 
Prophylaxis,   1348-9 
Rash,  1  514 
References,  1349 


Spotted  Fever,  continued 

Rickettsia  bodies  in,  1^45 

Symptomatology,  1346-7 

Synonyms,  1341 

Termination,  1347 

Treatment,  1348 

Virus  of,  1343-5 
Spotted  Whitening  of  Nails,  2283 
Spots,  Mongolian,  2222,  2237 
References,  2246 

Morrison's,  2202 
Spring  Catarrh,  Chlamydozoa  in,  539 

of  Eyes,  2001 
.    Fevers,  11 29 

Sprue,  1080,  1085,  1095,  1096,  1780, 
1851,  1852 

^Etiology,  1 781-3 

Climatology,  122,  1781 

Complications,  1787 

Definition,  1780 

Diagnosis,  1787-8 

Differential,  1731,  1788 

Histopathology,  1784-5 

History,  1780 

Inclusion-bodies  in,  539 

Morbid  Anatomy,  1785 

Prognosis,  1788 

References,   1799- 1800 

Symptomatology,  1785-7 

Synonyms,  1780 

Treatment,  1788 
Dietetic,  1789 
Medical,  1793 
Sputum,  Fungi  in,  1084,  1088,  1090, 
1091,  1092,  1521 

Parasites  and  Ova  in,  .320,  1521 
Squills,  166 

Squirrel-Bite  Disease,  1361 
Squirrels,  914 

Ground,  Plague  spread  by,  869,  870 
Tick  Infesting,  719 

Indian,  Trypanosome  of,  407 

Palm,  Parasite  of,  486 
Ssa'htso,  1756 
Stable-Fly,  834,  904 
Stables,     Vertigo-Disease    associated 

with,  1982 
Staph ylinidce,  226,  1640 

Vesicant,  2204,  2205 
Staphylinus  fuscipes,  1640 

politus,  1640 

punctulatus,  1640 

splendens,  1640 
Staphylococcal  Pyosis,  2255 
Staphylococcus^),    1951,    1959,    2026, 
2027,  2029,  2030,  2032 

albus,   2166 

pyogenes  aureus,  1602 
State,  the,  and  Tropical  Medicine,  29 
Status  Thymicolymphaticus,  1924 

Typhosus,  1386,  1387 


INDEX 


2411 


Steatozoon  folliculorum,  732 
Stegomyia,    747,    774.    789,   796,   873, 
876,     896,     920,     1 1 37, 

1527 

Species 

africana,  798 

albipes,  798 

albocephala,  798 

albolateralis,  798 

albomarginata,  799 

amesii,  799 

annulirostris,  797 

apicoargentea,  798 

argenteomaculata ,  798 

argenteopunctata,  798 

assamensis,  798 

auriostriata,  798 

calopus  (fasciala),  see  fascia  let 
below 

crussipes,  799 

ei tibia,  798  ^ 

fasciata  (calopus,  f rater),  Vector 
of  Dengue,  and  of  Yel- 
low Fever,  23,  379,  398, 
541,  644,  747,  796,  797, 
799,  876,  1229,  1232, 
1233,  1234,  1244  sqq. 

frater  (fasciata),  see  fasciata, 
above 

grantii,  798 

lilii,   797 

mediopunctata,  798 

minuta,  799 

Dtiitiitissima,  798 

nigeria,  797 

periskelqta,  797 

poweri,  798 

pseudonigeria,  798 

pseudonivea,  7<)8 

pseudoscutellaris,  637,  641,  1596, 
1598 

punctolateralis,  798 

sctttcllaris,  797 

sttnpsoni,  798 

terrens,  798 

thomsoni,  797 

tr {punctata,  799 

Uncertain 
desmotes,  799 
lamberti,  799 
leucomeres,  799 
striocrara,  799 

w-alba,  797 

wellmanii,  798 
Steiner's  Tumours,  2260 
Stemphylium   polymorphum,    11 14, 

1742 

Stenoglossa,  890 
Stenomahts  muscarum,  908 
Stenophora,  471 
Stenosis,  Pyloric,  1749 


Stentorinida,  547 

Stephanocircus,  866 
dasyuri,  866 
simpsoni,  866 
thomasi,  866 
Stephanolepsis  hispid  its,  194 
Stephanopharynginee,  561 
Stercobilin,  1147 
Sterciilia,  177 

Sterigmatocystis,     1024,     1030,    mi, 
1123,  1886,  1891,  1945, 
214') 
Dermatomycoses  due  to,  2041 
Species 

antacustica,  1024,  1030 
nidulans,  1024,   1030,  2041,  2122 
nigra,  1024,  1032,  1891 
versicolor,  2149 
Sternberg-Hearsey     Treatment     for 
Blackwater  Fever,  1225 
Stethomyia,  791,  883 

aitkeni,  888 
Slibasonia,  820 
Stick  Insects,  871 

Stigmatogaster  subterraneus,  740,  1641 
Stilbacece,  1037 
Stilbella,  1037 
StilbellacecB ,  1036 
Stilbum,  1037 
Stimulants,  Evolution  of,  95 

Useless  for  Snake-Bite,  278 
Stimulative  Action  of  Sun-Kays,  83 

and  Sedative  Poisoning,  174-8 
Stinging  Plants,  2 151,  2152 
Stings  or  Bites  of  Insects,  Dermatitcs 
due  to,  1514,  1516,  1517, 
2200,  2206,  2207 
Stizlobium  pruriens,  2159 

sfcms,  2153,  2159 
Stock-Poisoning,  190 

ich,  Cancer  of,  1749 
Diffuse  Inflammation  of,  1749 
Diseases  of,  1730,  1749 

References,  1751 
Phlegmonous      Inflammation      of, 

1520,  1749 
Symptoms,  indicative  of  Derange- 
ment    of     Alimentary 
Canal,  1520 
Ulcers  of,  1749 
Stomachida,  653 

Stomatitis,  123,  1061,  1075,  1788 
Aphthous,  1 780 
Saccharomycetic,  1741 
Ulcerative,  1745 
Stomoxy dines,  832,  833 
Stomoxys,  380,  771,  832,  833,  899,  cjoo 
References,  856 
Species 

bengalensis,  833 
bilineata,  834 


2412 


INDEX 


Stomoxys,  continued 

Species,  continued 
bouffardi,  834 
bouvieri  var.  clara,  834 
brunnipes,  833,  834 
calcitrans,  410,  S33,  834,904,  905. 
dacnusa,  833 
geniculates,  410 
glauca,  834 
griseiceps,  834 
indica,  833 
inornata,  834 
intermedia,  834 
korogwensis,  834 
lafonti,  834 
mg-ra,  833,  834,  835 
oblongopunctata ,  833-4 
ochrosoma,  834 
omega,  834 
plurinotata,  833 
pratti,  834 
pitlla,  834 
siliens,  834 
stellata,  834 
teniatus,  834 
triangularis,  834 
varipes,  834 
Stone   in    the    Bladder,    1926,    1929, 

193° 
Straits  Settlements,  Diseases  of,  122 

Infant  Mortality  in,  122 
Stramatinia,  formerly  Endoconidntiti, 

987 
Strangles,  929 
Strangulated  Hernia,  1943 
Straliomyia  chameleon,  363 
Sir atiomy idee,  814 
Straw  Itch,  2216 
Straw-Mattress  Disease,  2210 
Streblidce,  854 

Strcptobacillus  of  Tizzoni,  and  Pella- 
gra, 1 71 3 
Streptococcal  Angina,  1520 

Complications  of  Influenza,  1521 
Dermatitcs 
Primary,  2030 
Secondary,  2030,  2036 
Erysipelas,  2266 
Groups,  928 
Infections,  Oral,  1740 
Tonsillar,    1747 
Strcptococcece,  924,  925 
Streplococcus(i),  925,  027,   <)2!5.    13.57. 
1782-3,  1 891,  1948  M/</  , 
1  959,  20  50,  2032    .:  [66, 
2269 
Referem  es   966 
Species 

930 
anaerobius,  928 
micros,  1950 


Streptococcus(i),  continued 
Species,  continued 
anguinosus,  930 
Bonome's,  1476,  1477 
bovinus,  927,  930,  1950,  1951 
bovis,  1950 
capellettii,  928 

corj'^^  contagiosa  equorum,  929 
epidemicus,  929 
e<?t«,  929 
equinus,  929 
erysipelatos,  927,  929,  931,  1949, 

1950,  1951 
erysipelatosus,  2030 
fcBcalis,  930 

fcetidus,  928,  1950,  1 95 1 

hcemolyticus ,  931 

mitior,  929,  930,  931,  1951 

sew  viridans,  1949 
mitis,  929,  930 
mucosas,  931 

puerperalis,  929,  1945,  1950,  1951 
putridus,  1949,  1950,  1 951 
pyogenes,  929,  931,  1602, 
1891,  1948,  1950, 
salivarius,  927,  1950,  1951 
tropicalis,  929,  2034 
versatilis,    927,    930,    932, 

1951,  2031,  2032 
vesicans,  2031 
viridans,  931 

Sireptoneufti,  890 
Streptothrix,  1041,   1042,  2008, 
2139,  2166 

actinomyces,  1051,  1057 

a/6a,  1046 

alfiido-flava,  1046 

Almquist,  I.,  II.,  &  III 

alpha,  1046 

aquatilis,  1057 

aurea,  1063,  1066,  2138 

aurianlica,  1047 

of  Berestneff,  1054 

6eta,  1046 

Bonvicini's,  1057 

buccalis,  1050,  1054,  1067,  2133 

Candida,  1051 

caprce,  1053 

cornea,  1047 

cerebriformis,  1063,  1066,  2138 

chalcea,  1047 

chondri,  1057 

chromogena,  1045 

Chromogenic  Anaerobic,  of  Nes<  he- 
zadimenko,  2139 

(  mereonigra  aromatica,  1046 
'■/<>;-,    104  7 

funiculi,  1063,   1064,  2139 

I ''Mil's,  from  a  Horse,   1054 

Doyen's,  2139 

enter itidis,  1051 


1728, 
1 95 1 


195°. 


=  138. 


1046 


FN Dl  X 


2413 


Streptothrix,  contimu  d 

eppingeri,  1053,  1058 

erythrea,  1047 

farcinica,  1051 

[lava,  104O 

foersteri,   1041,    1046,    1059,    1063, 
1066,  1067,  2138 

freeri,  1053,  21 31 

fusca,  1042,  1063,  2138 

Gasperini's,  1054 

geda>ie>isis,  1051,  1053 

gelatinosa,  1057 

1  uni,  1051 

hominis,  1053,  1054,  1061 
I-.  1054 
II.,  1053,  1054 
111.  &  IV.,  1050,  1051,  1054 

/minified,  1045 

israeli,   1063,    1064,    1066,    2138 

krausei,  1054,  2136 

lathridii,  1051 

lehmann,  1057 

leproides,  1646,  1600 

leucea,  104!) 

saprophytica,  1045  • 

liquefaciens,  1050 

hiieola,  1050 

madurcB,  1051,  1058,  2134,  2140 

melanolica,  1045 

murisratti,  1056 

mycetomi,  1 104,  110O 

necrophora,  1064 

New  Arid-fast,    [O53 

» /<,';«,   1045,  1054 

nigrescens,  1045 

orangica,   1046 

pluricolor,  1047 

polychromogenes,  1057 

pseudotuberculosa,  1892 

pyogenes,  1046 

radiata,  1063,  1066,  2138 

rosenbachi,  1053,  105S 

rubra,  1047,  1051 

spitzi,  1057,  1063,  1064,  2139 

valvules  destruens,  1054 

violacea,  1046 
Streptothromycosis,  Pulmonary    [892 
Strictures,  Neglected,  1939 
Strombodes  jeuneri,  535 
Strongoplasma,  1  v->s 
Si ron gyles,  623,  659 
Strongylidee,  623,  624,  659 

\gyloides,    623,    626,    628,    [639 
1777,  2209 

stercoralis     (vel     intcstnnilis)      122 
623,    628,    1758,     1777 
1782 
I  >ermatites  due  to,   22 1  9 
References,  681 
Strongyloidosis,  1758 
Strongyloplasmata,  539 


Strongylus,  659 
bronchialis,  649 
colubriformis,  664 
contortus,  663 
duodenalis,  666 
elongatus,  662 
lilicollis,  663 

>*£'".  675 

instabilis,  664 

longevaginalis,  662 

paradoxus,  662* 

placci,  663 

proloburus,  664 

quadridentatus,  666 

renalis,  675 

sabtilis,  664 
*  sttis,  662 
Strop/huitluts,   181,   182-3,  x^4 

barika,  182' 

ciab&,   182 

glabris,  182 

Iiispidus,  182 

kambe,  182 

lanosus,  182 
Strychnine,      164,      167,      168,      185, 
191 

for  Snake-Bite,  277 
Strychnos,  168 

castelniceana,  186 

colubrina,  164,  168 

creuaw.#i,  186 

ico/a,  178,  183 

ignatii,  164,  168 

maingayi,  184,  185 

;n<;v  vomica,  164,  168,  187 

Jiiw^,  184,  185 

loxifcra,   186 

loallichiana,  184,  185 
Stupefying  Poisons  used  with  Intent 

to  Rob,  163,  1 70-1 
Stupor,  1982 
Stygeromyia,  832,  837 

maculosa,  837 

sanguinaria,  837 

woosnami,  837 
Stylommatophora,  892 
Stylorhynchida,  471 
Sul). u  uteBroncho-Spiroehaetosis,  1884 
Subcutaneous  Filariases,  1967,  1968 
Myiasis,  1623,  1632 
Nodular  Lipomatosis,  2247,   2253 
Subpangonia,  823 

Subtertian  Malarial    Fevers   (m<    <•!/»<> 
Malaria,       Subtertian), 
1129  * 
Subtropical,  Zone,  40,  41 
Sucking  Worms,  555,  557 
Sudan,    the,    Poison    used    in,    with 

intent  to  Cure,  171 
Sudan  Nodules,  2165 
Sufura,  1 761 


2414 


INDEX 


Sugar-Cane  Workers,  Diseases  of 
Dermatitis,  1466 
Mossman  Fever,  1465-6 

Suglacura,  1633 

Suicidal  Poisons,   163,   169,   194 

Suicide,  1981 

Suidae,  Traumatisms  caused  by,  15} 

Sukha  Pakla,  2241 

Sulphur  as  Anti-mosquito  Pro- 
phylactic, 1206 

Sumatra,  Arrow-Poison  of,  181,  184 
Fish-Poisons  of,  188 

Sumatran  Races,  55 

Sumerians,  the,  54 

Summer  to  Autumn  Fevers,  1129, 
1 1 64 

Summer-Autumnal  Fevers  (Sub* 
tertian  Malarial  Fevers) , 
1 1 64 

Summer  Diarrhoea,  Epidemic,  899,. 
1788,  1847 

Summer  Fever,   1254 

Sumpfneber,  1129 

Sunburn,  83,  84,  85,  1730,  2231,  2266 

Sundanese,  the,  55 

Sunlight,  Effect  of,  on 
Eye,  2004 
Skin,  83-5,  2231 

Sun-Rays,  Effects  of,  82,  115,  2014, 
see  also  Pigmentation, 
Sunburn,  Sunstroke, 
Tropical  Clothing,  etc. 

Surma  Tahuret,  1944 

Sunstroke,    88,    91,    132,    139,    1258, 

1449,  145°,  1451 
Clinical    Identity   of,   with    Heat- 
stroke (q.v.),  146 
Sun-Traumatism,  1449 
Supan's  Lines,  39,  62 
Superbine  Poisoning,  166,  167 
Supernumerary  Nails,  2283 
Superstitions,  Medical,  3  sqq. 
Suprarenal  Capsules,  Symptoms  asso- 
ciated with,  1524,  1526 
Haemorrhage,  Acute,  1923 

Subtertian    Malaria    resembling, 
1180 
System,  Diseases  of,  1919,  1923 
Suppression,   1923 
Suppuration   of   Bartholin's   Glands, 

1949 
Suppurative  Choroiditis,  2005 
Corditis,  1939 
Otitis  media,  2013 
Phlebitis  of  Spermatic  Cord,   1939 
Uveitis,  2005 
Surra,  391,  409,  1262 
Insect  Carriers,  410,  835 
Serum,  Trypanolytic  action,  392 
Trypanosomes  of,  19,  391,  409 
Surra-like  Disease  in  Cattle,  417 


Susruta,  7,  1824 
Susruta  Samhita,  7  ,1924 
Sutika,  1955 
Sweat,  Coloured,  2224 

of    Malaria    Patient,    Toxicity    of, 
1147 

Phosphorescent,  2224 

Pleasant-smelling,  2223 
Sweat  Desquamation,  2227 

Reference,  2246 
Sweat   Secretion   increased   in    Dia- 
betes, etc.,  2224 
Sweating,  Disorders  of,  2015,  2017 

Excessive,  2222-3 

Offensive,  2223 
Sweet-Water  Disease,  1924 
Swellings,  Tropical,  1972 
Swine,  Parasites  of,  539,  547 
Swine-Pest,  539 
Sycorax,  806 
Sycosis,  1002 

Coccogenica,  2266 

Trichophytic,  1005 
Symblepharon  posterius,  200  ) 
Symelus,  1958 
Symmetrical  Ear  Nodules,  2247,  2252 

Keratodermia  of  the  Extremities, 
2259 

Palmar  Erythema,  2222,  2244 
Symphoromyia,  823 
Symplocarpus  foetidus,  2152 
Symptomatic  Bubo,  1963 

Hemoglobinurias,  1213 

Hyperidrosis,  2222 
Symptoms 

Kerandel's,  1273 

Low-Castellani's,  1273 

Winterbottom's,  1273 
Synanchia  brachio,  232,  233,  234 

verrucosa,  232,  233,  234 
Syncephalus,  1958 
Synclonus  Beriberia,  1671 
Syngamus,  678 

kingi,  678 

trachealis,  678 
Synkaryon,  294 
Synochus  Biliosis,  1363 

Putrida,  1326 
Synovitis,  156 

Filarial,  1967 

of  Knee,  1596,  1617 
Syphilides,    2085,    2177,    2234,    2235, 
2249,     252 

Chronic,  1730 

Circinate,  2279 

Pustular,  1518,  2279 
Syphilis,  7,   15,   118,  455,   1187,   1535, 
1540,  1644,  1663,  1718, 
1938,2257 
Action  of,  on  Foetus  in  uiero,  2256 
Blood  Changes  in,  1553 


INDEX 


M'5 


Syphilis,  continued 

Causal   Organism,    21,    436,  455, 

457.  1570 
Climatology,  122,  123,  124,  132, 

Complement  Fixation  in,  1554 

Diagnosis,  1530 

Differential,  1382,  1557-8, 
1747,  2023.  2173,  2185, 
2195,  -J-".  2253 

in  relation  to  Framboesia,   459, 

£53&,  1539,  1556 

Inoculation  for,  439 
Treatment,  2279,  2280 

Native,  1  749,  2280 
Virus  of,  1 569,  1  570 

Congenital,  1556 

Eruption  indicative  of,  1518 
Syphilitic  Affections,  2085,  2091 
Hyperkeratosis  in,  2256,  2257 

Cerebral  Tumours,  1981 

Gumma  of  Liver,  191 4 

Heart-Block,  1904 

Hyperpigmentation,  2232 

Keratoses,  2257 

Infection,  Disqualifying  for  Trop- 
ical Life,  127 

Lymphatic  Affections,  19G1 

Splenomegaly,  1303 

Ulcers,  2185,  2190 
Syriac  Medicine,  1 1 
Syringospora,  1  -  \i 

albicans,  1742 

robini,  1085,  1742 
Syrphida,  825,  901,  1627,  1630 
Syr  pints,  1627 
Systems,  the,  Diseases  of,  1873 

TabanidcB  (Tabanid  Flics,  or  Taba- 
nids)  773,  814,  815,  823, 
874,  899,  2200 

Parasites  carried  by,  367,  369,  410, 
415,  816,  874-5 

References,  856 
Tabanincs,  817 
Tabanus,  817,  819,  821 

africanus,  819 

bovinus,  819 

ditceniatus,  816,  819 

fasciatus,  819 

glaucopis,  367,  816 

gratus,  819 

hilar ius,  819 

kingi,  pupa,  817 

lineola,  410 

memoralis,  816 

nigritus,  816 

taniola,  819 

fergestinus,  369 

tropicus,  410 
Tabardillo,  24 


Tabernamontana  malaccensis,  [84 

Tabes  Dorsalis,  2279 

Tacamocho  Fever,  1467 

Tache    Endemique    des    Cordillieres, 

2093 
Tachina  larvarum,  1629 
TachinidcB,  1629 
Tcenia,  596,  601,  602.  612,  1776 
References,  619,  620 
Species 

acutissima,  611 

cegyptiaca,  610 

africana,  601,  602,  603,  614,  1756 

anseris,  611 

anserum,  611 

artnata  hutnana,  612 

bremneri,  601,  602,  603,  615, 1750 

canina,  608 

confusa,  601,  602,  603,  615,  1756 

crassicollis,  600 

cncumerina,  608 

cucurbitina,  612,  613 

demerariensis,  611 

dentata,  604,  612,  613 

diminuta,  609 

echinococcus,  61 6,  1907 

elliptica,  608 

flavopunctata,  609 

Found  in  Man,  601 
Table  of,  602 

grisea,  604 

hominis,  601,  602,  603,  615,  1756 

hvdatigena,  616 

lanceolata,  611 

lata,  604,  613 

Icptocephala,  609 

madagascariensis,  61 1 

mediocanellata,  613 

membraneacea,  604 

mermis,  613 

minima,  619 

niurina,  610 

nana,  610,  616 

pellucida,  612 

philippina,   601,    602,    603,    615, 

.1756 
pisiformis,  601 
rhinaria,  733 

saginata,  122,  205,  6oi,  602,  60^, 
612,  613,895,  1753 
Food-absorption  by,  553 
solium,  122,  601,  602,  603,  612, 
63  j,  895,  1967 
var.  abietina,  6]  j 
ttsnitsformis,  601 
tenella,  604 
tropica,  613 
varesina,  609 
vulgaris,  604,  512 
zittavensis,  613 
Subgenera,  612 


2416 


INDEX 


Tceniarhynchus,  601,  602,  612 

a f vicuna,  614 

fuscopennatus,  644 

hominis,  615 

philippina,  615 

saginata,  614 
Taeniases  • 

Intestinal,  601 ,  1753 

Rare,  1756 

Somatic,  601,  1967 

Treatment,  559,  1753 
Native,  1753 
TczniidcE,  601,  602,  607 

Eggs:    Scheme    for     Recognizing, 
603-4 

Sub-families,  607  sqq. 
Tceniincs,  601,  607,  612 
T  cenioglossa ,  890 
Tagala  Race,  55 
Tahaga,  414 
Tahuret 

Pharaoh's,  1944 

Sunna,  1944 
Tai  Race,  54 
Tala-chini,  278 
Talipes  equino-varus,  123 
Tamias,  914 
Tampan,  706 

Tanghinia  venenifera,  in  Ordeals,  179 
Tanjore  Pill  for  Snake-Bite  (useless). 

278 
Tank- Worm,  651 
Tanqua,  629 
Tany  pints,  801 
Tanypus    Larvae,  Herpctomonad  of, 

367 
Taol  suba,  1690 
Taon,  1690 

Tapeworms,  9,  596,  602,    907,  sec  also 
Taenia 

Cysticerci  of,  600,  601,  857,  1967 
Tapioca,  172 
Tapura  guyanensis,  188 
Tapuya  Race,  60 
Tarantismus,  215 
Tarantula  Spider,  212 

Bite  of,  2«^»  -j^.  I  3 

Venom  of,  213 
Tarasco  Race,  37 
Tarbagans  and  Plague,  867,  913.  915, 

1423,  1424 
Tarbardillo,  El,   1320 
Tarbophis  savignyi,  Venom  of,  245 
TarsonemidtB,  728,  2214 
Tarsonemus  hominis,  728 

intectus,  2214 

monougniculosis,  728 

uncinates,  221  1 
Tartar  Emetic,  28,   170,   1202,   1275, 
1297,  1279,  2174 

References,  121 2 


Taschkent  Jarassi,  2165 

Tasiorchis,  561 

Tasmanian  Race,  9,  53 

Taste,  Loss  of,  Post-Malarial,  11 84 

Tatar  Race,  55 

Tattooing,  2222,  2238 

Medical,  2230 

Ornamental,  2238 

References,  2246 

Sequela;,  2274 
Tattow,  2238 
Tatu,  1283,  2238 
Tatusia  novemcincta,  1283 
Tau,  2238 
Tch'oungtis'ao,  172 
Tea-Drinking,  Excessive,  178 
Tea-Dust,  1876 

Monilia  in,  1084,  1089,  1090,  1091, 
1887,  1891 

Other  Fungi  in,  1891 
Tea-Factory  Cough,  1887,  1890 
Teak- Dust  Dermatitis,  2159 
Tebi,  1303 
Tecpanec  Race,  57 
Tectona  grandis,  2159 
Teeth,     Condition     of,     for     Candi- 
dates  for  the  Tropics, 
128 

Crowned,  Stopped  or  Bridged,  1520, 

i53i 
Tehuelche  Race,  56 
Teichomyza  fusca,  1629 
Teigne,  2052 

Telangiectases,  Multiple,  2273 
Teleosporidia,  293,  296,  297,  469 

References,  526 
Teleostei,  232,  240,  789 
Teleostomi,  233 

Temperate   Climates,    Return   to,   in 
relation  to  Life  Assur- 
ance, 132 
Essential  for 

White  People,  129-30 
Women,  130 
Temperature,   Atmospheric,  in  rela- 
tion to  Malarial  Fevers, 
1138-9,  1203 
Effect  of,  on  Parasites,  116 
High,    in     relation    to    Disease, 

137 
References,  141 
Axillary,  70 
of  Body,  Effect  on,  of 
Clothing,  69 

High    Atmospheric    Tempera- 
tures, 137 
and  Varying  Humidity,  71 
Investigation  methods,  70-1 
Normal,  69-71 
Oral,  70,  71 
Rectal,  71 


INDEX 


2417 


Temperature  and  Humidity,  67,  137 
Effects  of,  on 
Blood,  75-6 
Circulation,  74-5 
Digestion,  76 
Generative  Organs,  jj 
Growth,  77 

Man,  generally,  67,  137 
Nervous  System,  76 
Respiration,   73 
Skin,  77 

Urinary  System,   76-7 
Tenebrio  moletor,  1640,  1641 
Tenebrionidte,  1640 
Tenesme,  1824 
Tenesmus,  12 
Tentacularia,  649 

subcompressa,  649 
Tephrosia,  188 
piscatoria,  188 
toxicaria,  188 
vogelii,  188 
Terata  anadidyma,  1958 
anakatadidyma,  1958 
katadidyma,  1958 
Terebinthacetz,  2156 
Terebvidce,  Bites  of,  227 
Ternek  Arrow-Poison,  184 
Ternidens,  660 

deminutus,  660 
Tersesthes,  802,  803 
Tertian  Fever,  n 

Malarial     Fevers,    1129,     see    also 
Malaria,  Tertian,  1161 
Tertiana  Duplex,  11 61 

Simplex,  1161 
Test  Diets,  101 
Testacea,  326 
Testicles  of  Animals  as  Aphrodisiacs, 

172 
Tests 

Absorption  (Saturation),  1397 
Gas- Agglutination,  1392 
Urinary 

Mycological,  1926,  1934 
for  Quinine  Elimination,  1926, 
1936 
References,  1937 
Tetanic  type  of  Subtertian  Malaria, 

1173,  1175 
Tetanus,  22,  156 

Symptomatology,  189 
Infantile,  120 
Neonatorum,  1956 
Tetany,  1919,  1920 

Endemic,  1922 
Teter,  2052 
T,-tia,  1535 
Tetrachilomastix,  348 
Tetramitidee,  333,  334,  345,  348 
Tetramitidince,  345,  347,  349 


Tetramitus,  345,  348,  349 

bocis,  350 

mesnili,  350 
Teh any chides,  725,  727,  2214 
Tetranychus,  727 

molestissimus,  727,  2214 

tetarius  var.  russeolus,  727 
Tetraphora,  802 
Tetrapoda,  692 
Tetratrichomastix,  351 
Tetratrichomonas,  352,  353,  355 

gallinarum,   352 

prowazeki,  355 

vagina,  1946 

vaginalis,  356 
Tetraphyllidea,  600 
TetrasporocystidcB,  473 
Tetrodin,  194 
Tetrodon,  194 

chrysops,  194 

fluviatilis,  bite  of,  234 

hispidus,  194 

IcBvigatus,  194 

lunaris,  194 

pardalis,   194 

pennantii,  194 

poicelonotus,  194 

porphyreus,  194 

rivulatus,  194 

rubripes,  194 

stellatus,  194 

sticonotus,  194 

vermicularis,  194 
Tetrodonic  Acid,  194 
Tetters,   2052.   2053 
Teutonic    Branch    of    the    Caucasic 

Races,  46 
Texas  Fever  in  Oxen,  497,  715 
Thalassin,  204 
Thalassophis,  249,  251 
Thallassophryne,  233,  234,  236 

maculosa,  233,  236 

reticulata,  233,  236 
Thallophyta,  923,  968 
Thallosporales,  986,  1039,  1069 
Thallospore,  1037 
Thanotophidia,  244,  245, 

Indian,  243 
Thapsia  garganica,  2153 
Thaumastocera,  820 

akwa,  820 
Thecamcebida,  298,  326 
Thecosoma,  584 
Theicomyza  fusca,  365 
Theileria,  490,  491,  492,  498 

buffali,  500 

cellii,  500 

m  utans,  499 

parva,  490,  498,  504,  1568 
Thelavia  rostrella,  1024 
Thelohania,  529 

152 


2418 


INDEX 


Theobald's  Classification  of  Culicidce, 

790 
Therapliosa  avicularis,  212,  214-15 

blovidi,  212 

javanensis,  212,  215 
Tkeraphoscs,  venomous  Spiders,  214-5 
Thereva  nobilitata,  1630 
Therevidce,  824,  1630 
Theridiidcs,  212 

Tkeridium  lugubre,  Bite  of,  214 
Venom  of,  215 

tredecim  guttatum,  212 
Therioplecles,  819 

borealis,  819 

micans,  819 

montanus,  819 

tropicus,  819 
Thermic  Fever,  139,  1449,  1527 
Thermometrical  Pseudo-Fever,  1512 
Theurgic  Medicine,  3  sqq.,  51,  54,  55 
Thevetia  ahovai,  164,  168 
Thevetin-Poisoning,  165 
Thevetosin,  168 
Thiara,  891 

Thickening  of  Nails,  2283 
Thigh,  Non-development  of,  1959 
Thim'ni,  1625 
Thinning  of  Nails,  2283 
Thiobacteriales,  924 
Thorn-Wounds    in     relation    to    the 
Maduromycoses,    2123, 

2134 
Three   Days'  Fever  541,   806,    1244, 
1249,  1254 
Insect  Vector,  806 
Virus,  filterable,  541 
Throat,  Diseases  of,  1739 
References,  1751 
Inflammatory  and  other  Affections, 

of,  1875  sqq. 
Symptoms,  indicative  of  Aliment- 
ary Derangements,  1520 
Thrombosis,  1904 
Thrush,  1741 

Fungi  Associated  with,  and  Caus- 
ing,   984,    1061,     1080, 
1081,  1084,  1085,  1086, 
1087,  1091,  1092,  1741, 
1742,   1788 
References,  1751 
Vaginal,  1945 
ThymelacecB,  2153 
Thugs,  Datura-Poisoning  by,  171 
Thunderstorms,  82 
Thymol,  in  Ankylostomiasis,  1769 

History  of,  29 
Thymus  System,   Diseases  of,    191 9, 

1923 
Thyroid  Gland,  and  System,  Diseases 
of,  1 91 9 
References,  1925 


Thyroid  Type  of  Subtertian  Malaria, 

1 1 80 
Thyroiditis,  1920 
Thyromegaly,  Endemic,  1920 
Thysanoptera,  748 
Thuija  occidentalis,  2153 
Tibetans,  the,  55 
Tibeto-Chinese  Mongol  Races,  55 
Tibia,  Cystic  Swellings  of,  1072 
Tibu  People,  47  • 

Tick-Bite,      215,      216,      217,      693, 

767 
Tick-Bite  Dermatoses,  2213 
Tick-Eradication       Methods,       701, 

1348-9 
Tick   Fever,    African    (Dutton's    Re- 
lapsing Fever),  19,  691, 
694,     700,     706,     1 261, 
1318 
References,   1324-5 
Colombian,  444,  445,  1324 
of  Miana,  691,  700,  1322 

References,  1325 
of  Rocky  Mountains,    691,    692, 
694,  700,  1341 
References,   1349 
West  African,  444,  445 
of  Wyoming,  1349 
Tick  Group  of  Relapsing  Fevers,  919, 

1308,  1318 
Tick  Paralysis,  719,  872 
Ticks,     691,     692,     see     also     under 
Scientific  Names 
Diseases  and  Parasites  Spread  by, 

21,     23,     362,     363,     380, 
397,      446-I,     442,     444, 

445.  454.  479,  4^5.  4^7. 
492  sqq.,  691,  692,  694, 
700-1,  707,   1308,  1341, 
1 340,  1  (150  et  alibi 
Enemies  of,  701,  767 
Parasitic  on  Man,  List  of,  700 
Prophylactic  Measures  against,  701, 

1348-9 
References,  229 
Vernacular  Names 
Black-pitted,  713 
Blue,  715 
Bont,  723 
Brown,  712 
Castor-oil,  720 
Dog,  713,  719.  722 
Fowl,  704 
Red-leg,  714 
Variegated,  723 
Tic      polonga,     163,     249,     see     also 

Vipera  russelli 
Tics,  Convulsive,  1983 
Tidswell's     Noiechis     scatatus     Ptrs. 

Serum,  272,  273 
Tientsin  Fever,  146'. 


INDEX 


2419 


Tifo  Addominale,  136 
Esantematico,  1326 
Petecchiale,  1326 
Tiger-Mot h  Larvae,  Irritation  caused 

by,  222,  2208 
Tiger- Poisoning  (India),  189 
Tigers,  Traumatisms  due  to,  148,  149 
Tilletia  levis,  1032 
Timba,  188 
Timboin,  168 
Tina,   2093 

Tinea  Alba,  2040,  2048,  2077,  2099, 
2230 
Albigena,  1008,  2040,  2050,  2099' 
Axillaris,  2042 
Barbae,  993,  1007,  2053,  2268 

Tropicalis,  2058 
Capitis,  992,  993,  1000,  2052,  2056, 
2267-8 
Favica,  2057 
Microsporica,   2057 
Trichophytica,  2057 
Tropicalis,  1001,  2052 
Varieties   of,    Causal  organisms, 
2040 
Ciliorum,  2058 
Circinata,  999,  1007,  2053 
Corporis,  993,  1002,  1009 
Neglected,  2247 
Pustular,  1005,  1006 
Tropicalis,  1009 

Variety    of:     Causal    organism, 
2040 
Cruris,     1000,     1016,    2040,     2042, 
2058 
Regions  of  Body  Affected,  2043, 

2044 
Sequela?,  2080 
Treatment,  2047 
Varieties,  2043-4 
Decalvans  Tropicalis,  2057 
Flava,  123,  1097,  1099,  2041,  2073, 

2079,  2099,  2268 
Imbricata     (Tokelau),    123,     1017, 
1020,  1022,  1033,  2040, 
2059,  2060 
etiology,  2040,  2065 
Age,  Race,  and  Sex,   Incidence, 

2066 
Climatology,  2061-5 
Definition,  2059 
Diagnosis,  2069 

Differential,  2070 
Disease  mistaken  for,  2271 
Economics  of,  2070 
Experimental    Reproduction   of, 

2060 
Predisposing  Causes,  2066 
Prognosis,  2070 
Prophylaxis,  2071-2 
References,  2108-9 


Tinea  Imbricata,  continued 

Symptomatology,  2066-8 

Synonyms,  2059-60 

Treatment,  2070-1 

Varieties,  2068-9 
Inguinalis,  2042,  2044 
Interdigitalis,  2045 
Intersecta,  1017,  1023,  2040,  2070, 

2072 
Nigra,  1100,  1101,  2041,  2078J 
Nigro-circinata,    1009,  2040,   2052, 

2235 
Nodosa,  2105 
Palpebrarum,  2009 
Rosea,  2076,  2078 
Sabourandi  Tropicalis,  2040,  2051, 

2052 
Tonsurans,  2053 

Black-dot,   2057 
Tropicalis,  2042,  2044 
Unguium  Tropicalis,  2059 
Versicolor,  1097 
Tinea?,  Ocular,   2009 
Tinnitus  Aurium,    1192,    1201,    2012, 
2013 
.  Aspergillar,  1031 
Post-Malarial,  11 84 
Tinoso,  25 
Tipula      Larvae,     Embadomonas    in, 

347 
Tipularia  culiformis,  801 

latipennis,  810 
TipulidcB,  801,  1630 
Tireoidite  parasitaria,  1283 
Tlalsahuate  (mite),  2213 
T'neuta,  Sheep-Poison,  189 
Toads,  as  Ffy-catchers,  908 

Parasites  of,  488 

Venom  of,  240 
Toar,  195 
Tobacco,   175 

in  Arrow-Poison,  184 

as  Infanticidal  Poison,   itxj 
Tochu-bio,  1350 
Todas,  the,   Food  of,  96 
Toddia,  360 

Toe,  Mango,  2036,  2045,  2047 
Toe-nail,  Ingrowing,  2283 
Togoland,  Arrow- Poison  of,  180 
Tokelau,  Tokelau  Ringworm,  or  Tinea 
Imbricata,     123,     2059, 
2060 
Toltec  Race,  57 
Tom,  24,  sec  also  Jigger 
"  Tondante  peladoide  ",   999 
Tona,  1535 
Tonga,   1535 

Tongue,   Affections  and  Diseases  of, 
2283 

Black  Mycosis  of,  976 

Betel-staining  of,  1746,  2284 


2420 


INDEX 


Tongue,  continued 

Cancer  of,  1741 

Dark    Patches    on,    in    Ankylosto- 
miasis, 1746,  2283 

Furrowed,  1746,  2284 

Leucoplakia  of,  1746,  2283 

Pigmentation  of,  1731,  1746,  2265, 
2283 

Red,  or  Purple,  1746,  2283 

Scrotal,  1746,  2284 

Wooden,  in  Cattle,  2148 
Tonsillar  Abscesses,  1061,  1747 

Affections,  1745,  1747 

Hemisporomycosis,  1748 

Inflammations,  1740 

Moniliomycosis,   1748 

Mycoses,  1747 

Nocardiasis,  1747 

Nocardiomycosis,  1747 

Oidiomycosis,  1748 
Tonsillitis,  1250 

Fungi  in,  982,  1743 

Amoebic,  1747 

Flagellate,  1747 

Follicular,  1747 

Membrano-ulcerative,   1745 

Subacute,  1743 
Torahumera  Race,  60 
Torcel,  828,  1633 
Tormina,  1824 
Tornadoes,  82 

Torres  Straits  Islands,  Diseases  of  123, 
Tortoises,     Parasites    of,    401,    480, 

486-7 
Toruahebue,  1260 
Torula,  987,  1042,  1071,  11 17 

abbreviata,  987 

olivacea,  987 
Torulacei,  987 
Torulaspora,  979 
Tourniquet,  1982 
Toxaemias,   1920 

due  to  Deep  Suppuration,  1528 

Helminthic,  1520,  1522,  1527,  1530 
Intestinal,   1520 

Simple,  1920 
Toxaemic  Hyperplasia,  1920 
Toxalbumins  of  Snake-Venom,  243-4, 

254 
Toxascaris,  623,  653,  655,  656 
canis,  623,  655,  1775 

References,  682 
limbata,  655 
Toxic  Hemoglobinurias,  1213,  1522 
Toxicodendrol,  2156 
Toxicological  Laboratories,  Need  for, 

162 
Toxicology,  4,  8,  12 

History,  24 
Toxobodo,  342 
intestinalis,  342 


Toxoplasma,     359,     360,?  488,    1289, 

1525,  1529 

avium,  489 

canis,  489 

cavicB,  489 

cuniculi,  489,  490 

/ran  gee,  490 

gondii,  489,  490 

musculi,  489 

neophrontis,  489 

pyrogenes,    489,    490,    1304,    1305, 

1306 
ratti,  489 
sciuri,  489 
sporophilcB,  489 
talpcB,  489 
Unnamed  in 

Cryptoprocla  ferox,  489 

Mycetes  seniculus,  489 
Toxoplasmatic  Febrile  Splenomegaly, 

Toxoplasmidce,  478,  488 

References,  527 
Toxoplasmosis,     1303,     1305,     1525, 

1529 

Trachinidce,  233,  234,  236-7,  238-9 
Trachinus  araneus,  233,  234,  236 

draco,  233,  234,  238 

radiatus,  233,  234,  237 

vipera,  233,  234 
Trachoma,  1997,  1998 

Chlamydozoa  in,  539,  540,  541,  542, 
1998 

Fungus  in,  1998 

Opacities  due  to,  2000 
Trachoma  Bodies,  541 
Tr  achy  derma  horriditm,  278 
Trachymedusce,  204 
Trade-Poisoning,  191,  1695 

References,  192 
Trade-Wind  Belts,  63,  64 
Trade-Winds,  80 
Transmission,  Definition  of,  874,  921 

Ingestive,  874 

Penetrative,  874 
Transverse      Furrowing     of      Nails, 

2283 
Traumatic     Dermal    Myiasis,     1623, 
1632 

Mucous  Urethritis,  1943 

Rupture  of  Liver,  1907 

Spreading  Gangrene,  150 
Traumatisms 

in  Acute  Fevers,  1512,  1513 

Due  to 

Ferocious  Beasts,  115,  147 
Other  Physical  Causes,  155 

References,  157 
War,  1 981 
'  Tread  softly  '  Plant,  2159 
Tree-Snakes,  245 


INDEX 


2421 


Trematoda,  552,  555,  559,  560 

Mollusc  Hosts  of,    17,   558,   559 

889 
References,  593 
Digenetic,  Development  of,  558-9 
Trematode  Infections,  889 
Climatology,  122 
Diagnosis,  559 
Fevers,  1752 
Intestinal,  1752 
Mixed,  1777 
Prophylaxis,  559-60 
Table  of,  894 
Treatment,  559 
Parasites,  of  Liver,  1907 
Worms,  of  Human  Intestine,  List  of, 
1752 
Trematodiases,  Intestinal,  1752 
Tremors,  Malarial,  n  85 
Trench  Diarrhcea,  1820 

Choleraic,  1821 
Trench  Fever,  1501 
etiology,  1503 
Causal     Organism,    search      for, 

1502-3 
Climatology,  1503 
Definition,  1501-2 
Diagnosis,  1527 

Differential,  1505,  1527 
History,  1502-3 
Incubation-period,  1503-4 
Lice  as  Vectors,  754,  920,  1501 
Onset,     Course,      Intermissions, 
and  Termination,  1501, 

1504-5.  1527 

Prognosis,  1505 

Prophylaxis,  1505 

Rash,  1504,  1505 

Reference,  1510 

Rickettsia  bodies  in,  1345, 1502-3 

Symptomatology,  1501,  1503-4 

Synonyms,  1501 

Treatment,  1505 

Varieties,  1505 
Appendicular,  1504 
Cerebro-spinal,  1504 
Dengue-like,  1505 
Typhoidal,  1505 
Trench  Foot,  1967,  21 10,  2149 

Reference,  1980 
Nephritis,  1926 
Shin,  1 501 
Skin,  1 501 
Treponema,  454 
Oral,  461 
Spoi  :ies 

calligvruw ,    \6\ 

dcntium,  641 

intermedium,  461 

macrodentium,  1740 

microdentium,  461,  1740 


Treponema ,  continued 
Species,  continued 
minei,  4<>i 
minuium,  461 
mucosum,  461,  1740 
pallidum,  21,  434,  454,  455,  461 , 
1945.  2193 
References,  463 
parvum,  461 

pertenue,     21,     24,     457,     1535, 
1538,  1539,  1540.  1557. 
1558-9,      1568,      1576, 
1664,  2022,  2052,  2185 
References,  463 
refringens,  461 
stytopygce,  461 
terminii,  461 
triccale,  461 
Unnamed,  in  Frog,  461 
urethra,  461 
urethrale,  1944 
vivax,  461 
Treponema  Urethritis,  1944 
Treponemata,  289,  296,  436 
TreponemidcB,  436,  454 
Treponemosis,  Castellani's,  1535 
Trial    by    Ordeal,    Poisons    used   in, 

178-9 
Triatoma,  j6j 
diminuta,  430 
geniculata,  1283,  1284 
infestans,  1284 

megista,  414,  429,  881,   882,   1283, 
see  also  Lamus  megistus 
protracta,  398 
sordida,  430,  1284 
vitticeps,  430 
Tricercomonas,  348 

hominis,  349 
Trichiasis,  2000 
Trichina,  675 
contorta,  627 
cystica,  633 
spiralis,  676 
Trichinella,  623,  675,  1679,  1680 
spiralis,  285,  623,  676 

Wanderings   of,    Symptoms   due 
to,  553 
TrichinellidcB,  623,  675 
Trichinellincs,  675 
Trichiniasis  or  Trichinosis,  1967 
Causal  Agent,  553,  676 
Diagnosis,  1515,  1523 

Differential,  1395,  1396 
Rash,  1 51 5 
Trichocephaliasis,  1758 
Trichocephalus  dispar,  6jj 
hominis,  677 
trichiura,  1758 
Trichocercous  Cercaria,  559 
Trichocomacea,  986 


2422 


INDEX 


Trichocysts  in  Holotricha,  545 
Trichodectes,  751 
canis,  608 
subrostratus,  608 
Trichodectidce,  751 
Trichoderma  roseum,  11 17 
Trichomonadince,  345,  351 
Trichomonas,  331,  349,  352,  1944 
Change  of,  to  Amoeba,  354,  355 
Species 

batrachorum,  352,  353,  355 

cavice,  353,  355 

columbarum,  353,  355 

dysenteries,  353,  355 

evansi,  409 

Found  in  Man,  353-6 

hominis,     18,      319,      353,     354, 

1777 
nitestinalis,  350,  354,  549,  1273 
irregularis,  354 
lacertce,  353,  355 
lewisi,  403 

limacis,  352,  353,  355 
perronciti,  353,  355 
pulmonalis,  353,  355 
sm»s,  353,  355 

vaginalis,    352,    353,    354,    1273, 
1946 
Trichomonata,  319,  1838 
Trichomycetes,  1040 
Trichomycosis 
Forms  of, 

Axillaris,  2101 
Axillarum,  2041 
Flava,  2 1 01 

Axillary,  1067 
Fusca,  2102 
Nigra,  2101 
Nodosa,  2101 
Nodular,  2105,  2042 
Palmellina,  2101 
Rubra,  932,  2101 
References,  2108 
Trichonocardiasis,  2101,  2102 
Trichopalpus,  823 

obscurus,  823 
Trichophytic  Granuloma,  1000,  1002 
Trichophyton,     986,     987,     988,     989. 
995,    997.    hoi.    "13. 
2008,  2053,  2054,  2055, 
2056,  2057,  2059,  2077, 
2095 
Dermatomycoses  due  to,  2040 
Species 

acuminatum,  999,  2054,  2057 
albisicans,  1008,  2040,  2050 
album,   1004,  2055 
asteroides,  1005 
balcaneum,  1009 

Biological    Characters,     Table 
of,  1010 


Trichophyton,  continued 
Species,  continued 

blanch  ardi,     1008,     1009,     2040 

2051,  2055 
carateum,  2055 
castellanii,  1015 
cerebriforme,  1002 
ceylonense,  1009,  2040,  2052 
circonvolutum,   998,    1000,   2055, 

2056 
concentricum,  1017,  2065 
crateriforme,  999,  2054 
cruris,  1015,  2042 
currii,     995,     998,     1001,     2040, 

2055,  2056 
denticulatum,  1006 
discoides,  1003,  1004,  2040,  2055 
effractum,  998,  1001 
endothrix,  999 
equinum,  1007 
exsiccatum,     998,      1000,     2040, 

2055,  2056 
farinulentum,   1005 
felineum,  1006,  2055 
fumatum,  998,  1001 
glabrum,  998,  1000 
granulosum,  1006 
griseum,  2055 
gypseum,  1005,  1006,  2054 
lacticolor,  1006 
macfadyeni,     1009,    2040,     2048, 

2055 
megalosporum  endothrix,  999 
megnini,  1007 
mentagrophytes,  1005,  1006 
minimum,  993 
niveum,  1006 
nodoformans,    1007,    2040,    2043, 

2044,  2055,  2058 
ochraceum,  1004 
perneti,  2042 
persicolor,  1005 
pictor,  1029 
pilosum,  998,  999 
plicatile,  1000 
polygonum,     998,     1001,     2040, 

2055,  2056 
purpureum,  1016 
radians,  1006 
radiolatum,  1006 
regulare,  998,  1001 
rosaceum,  1007,  2054 
roseum,   1007 

sabouraudi,  996,  998,  999,  1008, 
2051,  2054.  2055,  2056, 
2057 
sudanense,  998,  1000,  2040,  2055. 

2056 
sulphureutn,  998.  1000 
tonsurans,   995,   998,    999,   1001, 
1002,   2008,   2009,   2054 


INDEX 


2423 


Trichophyton,  continued 
Species,  continued 

umbilicatum,  998,  1001 
verrucosum,  1003 
viannai,  1008,  1009 
vinosum,  1007 

violaceum,  998,  1000,  1004,  2054, 
2055,  2056,  2058 
var.  decalvans,  998,  1000,  2040, 

2055.  2056 
var.  khartoumensis,  998,  1000, 
1001,  2040,  2056,  2057, 
2058 
Trichophyton  Vaccines,  969 
Trichophytoses,  986,  988 
Trichophytoses,  2051,  2052 
Vaccines  for,  969 
Tropical,  2267 
Trichophytosis,  iooo,  2057 
Circinata  disidriformis,  1006 
Equine,   ioo<> 
of  the  Nails,  999 
Trichoprosoponina?,  790 
Trichopterous    Larvae,    Embadomonas 

in.  346 
Trichorrhexis  Nodosa,  2282 
TrichosomidcB.  623,  629,  675 
Trichcfspherium,  298 
Trichosporum     (Trichosporon),     1101, 
1117 
beigeli,  1101,  1102,  1103,  2101,  2105 
giganteum,  1101,  1102,  2100,  2101, 

2105 
glycophile,  1102,  1103,  2105 
ovale,  1102,  1103,  2101,  2105 
ovoides,     1101,     1102,     1103,     2101 
2105 
Trichosporium,  1101 
Trichosporosis,  1101 
Forms  of 

Behrend's,  2105 
BeigeTs,  2105 
D11  Bois's,  2105 
Indica,  2101 

of  Temperate  Zones,  2100,  2101 
Tropica,  2100,  2105 
Unna's,  2105 
References,  2108 
TrichostrongylidcB,     623,      624,     659, 

662 
Trichostrongylns,  624.  664 
References,  682 
Spe<  :ies 

colubriformis,  624,  664 
orientalis,  624.  664 
probolurus,  624,  664 

.  Usformis,  664 
sublilis,  664 
vitrinus,  624,  664,  665 
Trichothecium,  m^;,  1116 
roscinn.  1 1  Ti).  1117 


Trichuriasis,  1758 

^Etiology,  1759 

Chmatology,  1759 

Definition,  1758 

Diagnosis,  1 760 

History,  1758-9 

Morbid  Anatomy,  1760 

Nomenclature,  1758 

Pathology,  1759-60 

Prognosis,  1760 

Prophylaxis,  1760 

References,  1778 

Symptomatology,   1760 

Synonyms,   1758 

Treatment,  1760 

Varieties 

Appendicular,  1760 
Intestinal,  1760 
Trichiirince,  675,  676 
Trichuris,  623,  676,  1739,  1758.  I765. 

1776,  1777 
trichiura,  122,  553,  623,  677,  1273, 

1552,  1554.  1593.  l679, 
1680,  1758,  1759,  1760, 

1777.  l838 
Trigla  hirundo,  232,  233 
Triglidce,  232 
Trigliformes,  232 
Trilobius  gracilis,  366 
Trimastigamceba,  298,  300 

philippinensis,  300 
Trimastix,  345 
Trimorphodon   bisculatus,  Venom  -of, 

245 
Trinoton  luridum,  750 
Triodontophorus,  624,  659,  660 

deminutus,  624,  660 
Triodontus,  660 
Triple  Monsters,  1959 
Tritaaophya  Typhodes,  1363 
Triton  crista tus,  Parasite  of,  355 

Venom  of,  240 
Tritons,  Trichomonas  in,  355 
Troglotrema,  572 
Troglotremidee,  564,  572 
Trombididce,  725,  2213 

Dermatitis-causing,  2213 
Trombidium,  725 

americanus  (Leptus),  725,  2215 

irritans  (Leptus),   725,  2215 

musccs,  908 

muscarum,  908 

striaticeps,  2215 

tlalsahuate,  725.  2213 

vandersandei,  22  1  1 

wichmanni,  2214 
7  rombidoidea,  692,  72  |,  725 
TropceolacecB,  2153.  2154,  2162 
Tropceloliim  ma  jus,  2153.  2162 
Trophonucleus,    290,    331,    337,    381, 
382 


2424 


INDEX 


Trophozoites,  293,  304 
Tropical  Amnesia,  88 
Aphthae,  1780 
Boils,  2027 
Bronchomycoses,  1875,  1886 

References,  1894 
Cardiospasmus,  1750 
Chlorosis,  1761 
Climates,  39-40,  62 

Divisions  of,  39,  62  sqq. 
Clothing,  89,  90,  1989 
Countries,    Inhabitants    of,    Three 

Classes  of,  112 
Dermatomycoses 
Classification,  2040 
References,  2107-9 
Diseases,  112,  1 12 7  sqq. 
Complications  of 
Ear,  2013 
Eye,  2004 
Dissemination    of,   by  the  War, 

29-30 
Distribution,  120-5 
Endemicity,  114 
Epidemicity,  117 
Evolution,  112,   114,  394 
Geographical  Discovery  and,  114 
References,   125-6 
Tropical  Diseases  Bulletin,  29 
Tropical  Diseases  Bureau,  1262 
Tropical    Diseases    Research    Fund, 

29 
Tropical  Ecthyma,  929,  2034 
Fever,  Diagnosis  of  a,  151 1 
Fevers,  1128  sqq. 
Foods,  94 

Materials  of,  104 

Little-known,  no 
References,   no- n 
Furunculosis,  2027 
Fury,  76,  1981 

Haemoglobinurias,  1128,  1168,  1213 
Head-Gear,  89 
Heart,  1904 

Heat,  Exposure  to,  Warning  on,  of 
Candidates       for       the 
Tropics,  128 
Hygiene,  89 
Ichthyosis,  2060,  2070 
Kala-Azar,  883,  1289 
Kohler,  76,  1981 
Lepothrix,  2101 

Life,  Fitness  for,  Examination  for, 
127 
References,  134 
Life- Assurance,  131 
Light,  86 
Liver,  1525,  1906,  1908 

Varieties,  1909 
Malaria,    n  64,    see    also    Malaria, 
Subtertian 


Tropical,  continued 
Mask,  2233 
Medicine 

Early,  16 

History,  3,  17  sqq. 

Modern,  16 

References,  30  sqq. 

Schools  of 

Liverpool,  20,  29 
London,  29 

Treatment,  25-7 
Neurasthenia,  1981,  1988 
Qidema,  1693 
Phagedaena,  2 181 
Pityriasis  Versicolor,  2073 
Poisonings,  161,  1533,  1695 

References,  179,  186,  192,  202 
Polypapilloma,  1535 
Puerperal      Fever,      1938,       1946, 

1957 

Pyosis,  931,  2018,  2031 

Races,   39  sqq.,  42  sqq. 
References,  60-1 

Ringworm  of  the  Head,  2052 

Skin,  2231 

Splenomegalies,  1289,  1303,  1925 
References,  1307 

Swellings,  1972 

Ulcer,  2166,  see  also  Ulcus  tropicum 

Zone,  39 
Tropics,  the,  Classification,  39 

Discovery  of,    effect   on   Medicine, 
15-16 
Tropidechis,  246 

carinata,  251 
Tropidonotus,  244 

fasciatus,  245 

natrix,  245 

piscator,  244,  487 
Tropische  Phagedenismus,  2 181 
Tropischer  Leberabzess,  1910 
Trygon  pastinaca,  232,  240 

sephen,  240 

walga,  240 
Trygonidce,  232,  240 
Trypaflavin,  26 
Trypanomonas  lewisi,  403 

murium,  403 
Trypanomorpha,  518 
Trypanophis,  336,  337,  380 

grobbeni,   338 
Trypanoplasma,  336,  337,  380 

abramidis,  338 

barbi,  338 

borreli,  338,  388 

claries,  338 

cyprini,  338 

dendrocceli,  338 

guernei,  338 
gurneyorum,  338 

intestinalis,  338 


INDEX 


2425 


Trypanoplasma,  continued 
keysselitzi,  338 
truttee,  338 
varium,  338 
ventriculum,  338 
Trypanoplasmata,  337 
Trypanorhyncea,  600 
Trypanosoma   (see  also  Castellanella, 
CystotrypanecB,      Cysto- 
trypanosoma,  Duttonella, 
Endotrypanum,    Schizo- 
trypanum     cruzi,     Try- 
panosomecB,      Trypocas- 
tellanellece) ,   19-20,   380, 
381,396,  398,  518,  1260 
passim,      1523,      1524, 
1532,   1903 
in  Beri-beri,  1284 
Classification,  380-1,  394-5 

New,  395,  1260 
Crithidial  Stage,  389 
Diseases  caused  by,  1259 
Hcsmoproteidcz  as  Stages  of,  518-19 
Herpetomonincs  in  relation  to,  365 
Hosts  of  (see  also  Species  found  in, 
below),    395    sqq.,    685, 
816 
Vertebrate     and     Invertebrate, 

383,  391-3 
Definitive    and    Intermediate, 
396 
Infecting 

Invertebrates,  383,  387,  389-91, 

395,  396-8 
Vertebrates,  383,  384-5,  388,  391 
Cold-Blooded,  389, 395, 398-401 
Warm-Blooded,       395,       396, 
401-3 
Non-Pathogenic,  403 
Pathogenic,  403,  407 
Insects    Transmitting,     410,     753, 
763,  816,  835,  844,  855, 
857,  see  also  Glossina 
Involution  Forms,  392 
Method  of  Infection,  388,  391 
Piroplasma  in  relation  to,  360 
Polarity,  383 
sensu  lato,  397 

Groups    and     Species    included 
therein 

I-.  413-15 
II.,  416-17 

HI..  417 
Sexual  Forms,  So-called,  387 
Species 
Pound  in 
Amphibia,   353,  395,  398,  400, 
see  also  in  Frogs,  below 
Animals,  409  B^ 

Cold-Blooded,  398      1 
Warm-Blooded,  401 


Trypanosoma,  continued 

Species  Found  in,  continued 
Arachnida,  395,  397,  398 
Aves,     353.     381,     395.     401- 

402 
Bats,  405,  407 
Blood  -  sucking      Arthropoda, 

397 

CamellincB,  410,  414 

Carnivora,  406 

Cattle,  Horses,  Sheep,  and 
Goats,  391,  407,  409, 
412,  414  et  alibi 

Crocodiliu,  401 

Edentata,  406 

Fish,  381,  395,  398 

Frogs,  353,  381,  393,  398,  400. 
402,  480 

Hexapoda,  395,  397,  398 

Hirudinea,  395,  397,  398 

Insectivora,  406 

Lizards,  353,  401 

Mammalia,  353,  381,  395,  401, 
403 
Non-Pathogenic,  395,  403 
Pathogenic,    391,    395,    403, 
407 

Man,  353,  391,  417  sqq. 

New  Classification  and  No- 
menclature, 418,  419, 
1260 

Monkeys,   353,   405,  408,   409. 

413 
Ophidia,  353,  401 
Reptilia,  395,  398,  401 

Pigs,  353 

Rodents,  353,  381,  405,  406, 
407,  408,  409 

Tortoises,  401 

Ungulata,  405 
Incertse  Sedis,  431  sqq. 
List  of 

abramidis,  400 

accouchii,  405 

americanum,  407 

annamense,  414,  415 

arvicanthidis,  406 

avium,  402,  526 
minus,  402 

bandicotti,  405,  406 

barbcB,  400 

berberum,  414,  415 

blanchardi,  405,  406 

boueti,  401 

bovis,  417 

boylei,  398 

hrucei,  19.  381,  385,  389.  391, 
592,  393,  407,  418,  419, 
838,  876,  878,  880,  881 

caprcB,  409 

carcassii,  400 


2426 


INDEX 


Trypanosoma,  continued 
Species,  continued 
List  of,  continued 

castellanii,  19,  382,  384,  385 
386,  387,  388,  389,  390, 
39i,  392,  393-  396,  4°2, 
408,  418,  421,  838,  844, 
878,  879 
New  Name,  419,  1260,  1261 

cazalboui,  389,  391,  412,  413, 
414,  415 

cellii,  414,  415 

chagasi,  400 

Christopher  si,  398 

citelli,  405 

cobitis,  400 

confusum,  402,  415,  416 

congolense,  392,  413,  416,  417 

criccti,  405,  406 

cruzi  (Schiz.cruzi),  19,402,  41 8, 
419.  427,  768,  881,  882, 
1283,  1284.  1288 

culicis,  398 

cuniculi,  405,  406 

damonice,  401 

daniliewskyi,  400 

dimorphon,  391,  413,  416,  417 

dimorphon-type,  397 

dionisi,  407 

dovhni,  400 

duttoni,  405,  406 

elegans,  400 

elephantis,  417 

elmassiani,  414 

eothricis,  402 

«7»i,  410 

equinum,  20,  391,  392,  393,  414 

equiperdum,  19,  386,  391,  392, 

393.  4°7.  415 
erythrolampri,  401 
evansi,    19,   28,   387,   393,   407, 
414,  415.  4i8.  835 

var.  mborii,  410 
euflwst-type,  414,  415,  431 
evotomys,  405 
fordii,  419 
franki,  407 
frobeniusi,  417 

gambiense,  19,  391,  407,  418, 
419,  878 

var.  longum,  418,  419 
giganteum,  417 
grayi,  390,  39] 
£Tosi,  405 
hrndersoni,  400 
himalayanum,    \'<~ 
hippicum,    (.13,  415 
hominis,    \  1  'i 
ignotum,    (.13 
indicum,  j  <  >  5 .  407 
ingens,  1  ij 


Trypanosoma,  continued 
Species,  continued 
List  of,  continued 

inopinatum,  398,  4CP,  480 

intestinale,  396,  397 

lagonostictce,  402 

lanfranchii,  431 

laverani,  402 

legeri,  406 

leothricis,  402 

leporis  sylvatici,  405 

leschenaulti ,  401 

leucisi,  400 

lewisi,  19,  381,  386,  387,  388, 

402,  403,  404,  406,  407, 

418,  422,  753,  857 
/ez£>m-type,  402,  407 
limeatus,  405 
/wis,  455 

marocanum,  414,   415 
megaderma,  405 
microti,  405,  406 
minasense,  405 
mitktesauri,  407 
musculi,  405,  406 
myoxi,  405,  406 
nabiasi,  405 
najce,  401 

nanum,  391,  416,  417 
nelspruitense,  400 
nepveui,  419 
nicolleorum,  405,  407 
nigeriense,  418,419,420,430,878 
noctucs,   398,  524 
otospermophili,  405 
paddcB,  402 
pecaudi,  391,  417,  427 
pecorum,  408,  41(1 
Pellegrini,  400 
peromysci,  405 
perlenue,  401 
pestanai,  406 
petrodronii,  405 
phoxini,  400 
primeti,  401 
prowazeki,  405 
pythonis,  401 
rabinowitschi,  418 
rai«,  381 

ra;'«,  389,  398,  422 
ratforum,  403 
remaki,  398 
rhesii,  405 
rhodesiense,    19,   28,    384,    388, 

vi".    mi.  392,  .|<>7.    p... 

418,419,844,878,880  88] 
rotatorium,  393,  .i<><>.    |<>-.    |8o 
rotatorium-type,    102 
rougeti,  \  1  1 
roitlei,   i'"» 
ruiherfordi,  407 


INDEX 


2427 


Trypanosoma,  continued 
Species,  continued 
List  of,  continued 
saccobranchi,  400 
sanguinis,  381,  393,  403 
scardini,  400 
sericis,  406 
si  mice,  408 
somalense,  400 

soudanense,  409,  413,  414,  415 
spermophili,  405 
squalii,  400 
talpa,  406 

theileri,  20,  405,  407,  855 
tinces,  400 
togolense,  413,   414 
transvaalense,  407 
triatomce,  398 
lullochi,  398 
Uganda?,  410,  418 
ugandense,  421,  878 
undulans,  400 
undulina,  478 
uniforme,   408 
urublewskii,  407 
venezuelense,  409,  414,  415 
vespertilionis,  407,  763 
vickersce,  405 
vittata,  389 

?m;a#,  389,  391,  4°8.  412,  418, 
419,  430,  878,  881 
New  Name,  402 
znt;a#-like,  418 
jnwa*  sub-group,   408 
yakimoffi,   400 
ziemanni,  398,  433,  436 
Little-known,  401,  417 
Monomorphic,  408 
Morphologically  alike,   Biologic- 
ally distinct,  418 
Non-Pathogenic,  395,  403 
Pathogenic,    391,   407,   413,    414 

s^.,  1259 
Polymorphic,  383,  407 
Unnamed 

in  American  Newt,  401 
from  Chai-Chai,  413 
Edington's,  from  Zanzibar,  413 
from  Southern  Rhodesia,  415 
Unclassifiable,     401,     405     sqq., 
413  sqq. 
Verterbrate  Reservoirs,  392,425, 426 
Trypanosome  Fevers,  1259,1261,  1280 
References,  1281^2 
Synonyms,  19,  1259 
Infections,    see  also   Trypanosome 
Fevers,  and  Trypanoso- 
miases 
Methods   of  Infection,    388  sqq., 

391-2 
Symptoms,  391-2 


Trypanosomes,  396,  398 
Trypanosomen  Fieber,  1260 
Trypanosomes,      see      Trypanosoma, 

above 
Trypanosomiase  braziliera,  1283 
Trypanosomiases 

Animal,     19.     J24.     4T7.     454.    see 

also       under       Names, 

Insects  spreading,   19,  747,   878, 

see  also  Glossina 
Treatment,  1262 
Trypanosomes    of,     19-20,     391, 
392,  409  sqq.,  875 
Experimental,  1274 

Drugs  tested,  26,  28 
Human 

African,     124,     1259,     see     also 
Sleeping         Sicknesses, 
1260,  and  Trypanosome 
Fevers,  1259 
Form  not  specified,  1767 
South    American:    Chagas'    Dis- 
ease, 19,  881,  1283 
^Etiology,  1284 
Animal       Reservoirs,       881-2, 

1283,  1284 
Table,  882 

Blood  in,   1287-8 
Climatology,   19,  123,   1284 
Definition,  1283 
Diagnosis,    1288,    1523,    1525, 

I531 
Differential,  1288 
Histopathology,  1285 
History,  1283-4 
Insects     Spreading,    19,    427, 
768-9,  881,  1128,  1283, 

1284,  see    also    Lamus 
megista 

Morbid  Anatomy,  1285 
Pathology,  1284-5 
Prognosis,    1288 
Prophylaxis,  1288 
References,  1288 
Sequela?,  1288 
Symptomatology,  1286-8 
Synonyms,  1283 
Transmission,       see       Insects 

Spreading,  above 
Treatment,  1288 
Trypanosome  of,  19,  402,  418, 
419,  427,  768,  881,  882, 
1283,  1284,  1288 
Varieties,  1286 
Acute,  1286 
Chronic,  1284,  1286,  1287 

Goitre  in,  1  92  1 
Subacute,  1286-7 
Trvpanosomidce,  290,   331,    m,    534, 
358,  380 
References,  462-3 


2428 


INDEX 


Trypanosomincs,  358,   380 
Trypanosomonas,  381 
Typanotoxyl,  26 
Trypanozoon,  381 

lewisi,  403 
Trypocastellanellece,  396 

Divisions    and    Classification,    401 

Tsaraath,  1644 

Tsetse-Flies,  see  also  Glossina,  19, 
23.  838,  875,  876,  879, 
1128,  1263,  1264,  1265,' 

1965 
Diseases  Spread  by,  1259 
Tsutsugamushi  (mite),  726 
Tsutsugamushi     Disease     or     Fever 
(Japanese     or     Kedani 
River  Fever),  1342, 1350 
etiology,  1 35 1 
Allied  Fevers,  1350,  1354 
Causal  Insect,  691,  694,   726,  920, 
1128,   1350,   1351,  2213 
Class-Incidence,  1351,  1352 
Climatology,  122,  1350-1 
Complications,  1353 
Convalescence,  1353 
Course,  1352-3 
Definition,  1350 
Diagnosis,  1354,  1516,  1523 

Differential,  1347,  1348,  1354 
History,  1350 

Incubation  and  Onset,  1352 
Pathology,  1352 
Prognosis,  1354 
Prophylaxis,  1354 
Rash,  1 516 
References,  1355 
Seasonal  Incidence,  1351,  1352 
Symptomatology,  1352-3 
Synonyms,  1350 
Treatment,  1354 
Varieties,  1353 
Tuaregs,  the,  46-7,  51 

Poisoning  by,  166 
Tuberales,  985 
Tubercle  of  Bone,  1967 
Tubercular  Disease,  of  Godfrey  and 
Eyre,  21 10 
Fistulous  Disease,  2085-6 
Lepers,  Blindness  in,  2006 
Leprosy,   1654 

Ear  Complications  of,  2013 
Tumours,  Cerebral,  1981 
Ulcers,  2186,  2190 
Tuber  culariacecB,  1036 
Tuberculides,  2272,  2277,  2278 
Non-Febrile,  Pustular,  151 8 
Tuberculosis,  112,  1718 

Bacillus  of,  22,  119,  965 
Climatology,   119,  122,  123,   124, 
133 


Tuberculosis,  continued 

Complicating      other      Diseases, 
1687,  1731,  1743,  1885, 
1889 
Diagnosis,  1521,  1528,  1530 
Hyperkeratoses  in,  2256 
Hyperpigmentation  in,  2232 
Insect  Vectors,  24,  876,  908 
Lymphatic  Affections  in,  1961 
Mixed    Infections,     1687,     1731, 

1743,  1885,  1889 
Risks  from,  to  Babies,  i960 
Tuberculin  Reaction  in,  969 
Acute,  Diagnosis,  1526 
Bone,  in  Chinese  '  Lily  '  Feet,  156 
Bowel,  1739 
Cutaneous,  2264,  2277 
Miliary,  Acute,  1395,  1396 
Pulmonary,   1889,   1893,  2278 
Verrucosa  cutis,  2085,  2254,  2277 
Tula  Manugina,  1260 
Tulip,  Wild,  Poison  from,  167 
Tumbu  Disease,  1637 
Tumours,  Indications  from,  1531 
Aural,  2010,  2252 
of  Bone,  1967 
Cerebral,  Syphilitic,  1981 

Tubercular,  1981 
Cheloidal,  after  Sycosis  coccogenica, 

2266 
of  Connective  Tissue,  2273 
Benign,  2273 
Malignant,  2274 
Cutaneous,  2264,  2273 
Epithelial,  2274 
Benign,   2274 
Malignant,  2277 
Filarial,  161 7 
Fungi,  associated  with,  1072,  1074, 

1096 
Innocent,  1072 
Internal,    due   to   Nematodes,    see 

that  section,  passim 
Malignant,   1074,  2274,  2277 
Mixed,   2277 

Multiple  Pruriginous  of  the  Skin, 
2247,  2254 
References,  2263 
Nasal,  2777 
Nepaul,  2010,  2252 
Schistosomic,  1867,  1868 
Sclerotic,  2007 
Steiner's,  2260 

of  Verruga  Peruviana,  1566  sqq. 
in  Volvulosis,  1964  sqq. 
Tungus  Race,  55 
Tunisia,  Macular  Fever  of,  1467 
Tunnel-krankheit,   1761 
Tunnel-Workers'  Anscmiar  1761 
Tun-tun,  1761 
Tupi-Guaranian  Family,  59,  60 


INDEX 


2429 


Turbellaria,  555 
Turki  Peoples,   55 
Turkish  Disease,  1968 
Turkish  Race 

Anatolian,  55 

Osmanli,  55 
Turkoman  Race,  55 
Turner's  Herpes,  2060 
Tydeus  molestus,  728,  2214 
Tylenchus,  627 

putrefaciens,  627 
Tylophova  fasciculata,  190,  191 
Typhios,  1 
Typhloceras,  865,  866 

poppei,  866 
Typhlopsylla,  865,  866 

agyrtes,  867 

assimilis,  867 

prosuma,  866 

pseudogyrtes,  866 
Typlopsyllitue,  864,  865,  866 
Typhoid,  1075,  11S4,  1187,  1577,  1964 
Typhoid  Fever,  see  Enteric,  1362 
Vaccines  for,  1365,  1401 
Polyvalent,  23 

Bilious,  1308 
Typhoid-like      Subtertian      Malaria, 

1171 
Typhoid  Ulcers,  Perforation  of,  1961 
Typho-Lumbricosis,   1775 
Typho-Malaria,  1184,  1388-9 
Typho-Malarial  Fever,  1366 
Typho-Pellagra,     1514,     1727,     1731, 

1733 
Typhoon,  82 
Typhus  (Typhoid),  1363 

Abdominal,  1362,  1363 

Biliosus  nostras,  1505 

Exanthematischer,  1326 

Exanthematicus,  1326 

Exanthematique,  1326 
Typhus  Fever,  15,  1069,  125(5,  1326, 

1363 
.Etiology,  1332 

Bacilli  present  in,  1328,  1336-7 
Blood-Changes  in,  1334,  1336 
Bodies  in  Blood  in,  1327  sqq. 
Causal   Agent,    1326,    1327   sqq., 

I33L  1332 

Climatology,      120,      124,      133, 
1330-1 

Complications,  1327.  1333,  1336 

Convalescence,  1335 

Course,  1333  sqq. 

Definition,  1326 

Diagnosis,  1336 

Differential,  1250,  1258,  [312 
1313,  1317,  1327  -8, 
1347.  x395.  1396,  1429, 
1485,  1490,  1505.  1507. 
1508,  1516,  1529,  1530 


Typhus  Fever,  continued 

Epidemiology,  1327,  1331-2 

History,  1226-30 

Immunity,  1332 

Incubation,  1333 

Lice  as  Vectors,   542,   756,   920, 
1128,  1326,  1329 

Morbid  Anatomy,  1332-3 

Onset,  1333 

Pathology,  1332 

Prognosis,  1338 

Prophylaxis,  1330,  1338  sqq. 

Rash,  1334,  1510,  1529 

References,  1340 

Rickettsia    prowazeki    in,     1328, 
1332,  1345,  1503 

Seasonal  Incidence,  1331 

Sequela?,  1336 

Serology,  1330,  1338 

Symptomatology-,  1333-5 

Synonyms,  24,  1326 

Termination,  1335 

Treatment,  1338 

Varieties,  1335-6 

Virus,  Filterable,  541,  542 
Gangliaris  vel  Entericus,  1363 
Hepatique,  1505 
Hysterico-verminosus,  1363 
Icteroides,  1229,  1308 
Mitior,  1363 
Nervosus,  1363 
Petechialis,  1474 
Recurrens,  1308 
Tyroglyphidcs,  729,  201 1,  2214 

References,  741 
Tyroglyphus,  729,  908 
longior,  729 

var.  castellanii,  729,  2214,  :  2J5 
siro,  729 

U  H  A  disease,  9 
Uciunga  Arrow-Poison,  1 1 5 
Udenocera,  820 
Ugro-Finn  Peoples,  55 
Ulcera  de  Bauru,  2165 

Tropicale,  21 81 
Ulcerating  Carcinomata,  449,     52 

Granuloma,  28,  122,  2192 

Nodules,  1 1 00 
of  Leg,  noi 
Ulcerations,  2006,  2165 

of  Annam,  2 181 

Chronic     and    Subchronic,     2190, 
2191 
Painless,  2 191 

Cosmopolitan,  2190 

Corneal,    1031,    1997,    2000,    2003, 
2004,  2009,  2201 

Cutaneous,  2015,  2017 

in  Glanders,  2100 

of  Intestines,  18,  1076 


2  4  3° 


INDEX 


Ulcerations,  continued 

of    Lips,     and    of    Ear,    Seasonal 

Recurrent,  1746,  2284 
Nasal,  123,  1882 
following   on    Neglected    Wounds, 

2191 
References,  2197 
Ulcerative  Conjunctivitis,  1060 
Dermatitis,  1091.  1112 

Chronic,  1073 
Diseases,  see  also  Gangosa,   1876 

of  Legs,  etc.,  123 
Endocarditis,  1395,  1397 
Gingivitis,  1744,  1745 
Lesions  of  Tertiary  Syphilis,  2279 
Stomatitis,  1745 
Ulcere  d'Orient,  2165 

Phagedenique  Endemique,  2 181 

des  Pays  Chauds,  21 81 
Ulcers,  1523 

Classification  of,  2190 

Fly-Larvae  in,  830,  831,  848 

Indications  from,  1531 
Acladiotic,  2190 
of  Aden,  2 181 
Aspergillar,  1032 

Corneal,  103 1 
in  Bacillary  Dysentery,  1846,  1847 
of  Bauru,  380,  see  also  165 
Blastomycetic,  2190 
Cancerous,  2190 
Diphtheroid,  2 191 -2 
of  Foot,  1063,  1068,  21 12 
Frambcesial,  452,  1554,  2190 
in  Gangosa,  2190 
Gastric  (in  Fox),  454 
Hyphomycetic,  2190 
Intestinal,    in   Animal   Trypanoso- 
miasis, 454 
Jigger-caused,  2212 
Kurunegala,  2021 
due  to  Leech-bites,  685 
Leprotic,  2190 

Malignant  (Oriental Sore, q. v.),  2103 
Monilial,  1091 

of  Paragonimiasis,  1586,  1587 
in  Pellagra,  171 4 
Penjdeh,  2166 
Pyogenic,  2190 
Rodent,  2004,  2277 
Sarcomatous,  2190 
Sarten,  2166 
Septic,  2191 
Sporotrichitic,  2190 
Spreading,  122 
of  Stomach,  1749 
Syphilitic,  2185,  2190 
of  Taschkent,  2165 
Tropical,  see  Ulcus  Tropicum,  21 81 
Tubercular,  2186,  2190 
Typhoid,  Perforation  of,  1691 


Ulcers,  continued 

Undetermined;  References,  2199 
of  Varicose  Veins,  2186,  2190 
Yemen,  21 81 
Ulcus  Cruris  Varicosum,  2168,  2190 
Grave,  in  Foot,  21 12 
Infantum,  2165,  2188,  2190 

References,  2199 
Interdigitale,  2165,  2188,  2190 
Rodens,  2004,  2277 
Serpens  Cornea,  2003,  2004 
Tropicum,    448,    452,    2166,    2181, 
2277 
Differential      Diagnosis,      2190, 

2192 
Perforation  in,  1961 
References,  2199 
Uled-Nails,  the,  46 
Ultra-Microscopic  (Filterable)  Viruses , 

54i 
Ulvina,   1071 
Umbellifercs,  2153 
Umor  Salso,  1700 
Uncinaria,  665 

americana,  673 
Uncinariasis,  1761 

Unclassified  Fevers,    121,    122,    1128, 
1461 

References,  1472 
Undulant  Fever,  1254,  1437 

^Etiology,  1 128,  1439 

Blood-Changes,  1443 

Carriers    and    Reservoirs,    1438, 
1440,  1447 

Causal    Agent,     22,     932,     1437 
passim 

Class  Incidence,  1442 

Climatology,  1439,  1673 

Complications,  1444 

Course,  1442-3 

Definition,  1437 

Diagnosis,  1444-5,  1527.  153° 
Differential,    11 80,    1302-3, 
1445,  1767,  1914 

History,  1437-9 

Hyperidrosis  in,  2222 

Incubation,  1441 

Morbid  Anatomy,  1441 

Onset,  1441-2,  1527 

Pathology,  1441 

Prognosis,  1445 

Prophylaxis,  1446-7 

References,  1448 

Sequelae,  1444 

Spread,  Modes  of,  1438,  1 440-1, 

1447 
Symptomatology,  1441-3 
Synonyms,  22,  1437 
Treatment,  1445-6 
Varieties,  1443-4 
Ambulatory,  1440,  1443,  1444, 1447 


l\  DEX 


2431 


Undulant    -   Fever-like       Subtertian 

Malaria,  1 1 71 
Undulina,  381 
ranarum,  393 

Ungulata,    Traumatisms   caused    by, 
151  sqq 

Trypanosomes  of,  405,  407 
Unknown    Germs   spread    by   Ticks, 

700-1 
Unna's  Trichosporosis,  2105 
I 'p. is  Antiar,  185 

Dermatitis,  2162 

Tieute,  185 

Tree  Poison,   184,   185 
Ura,  828,  830 
Uraemia,  1337 
Uranoscopidce,  233 
Uranoscopus  scaber,  233 
UranotcanincB,  780,  790 
Uraons,  the.  Food  of,  96 
Urechites  suberecta,  164,  169 
Urechitin,  169 
Urechitoson,  169 
Urethra,  Aspergillosis  of,   1032 
Urethritis,  Hyphomycetic,  1939,  1943 

Non-Gonorrhceic,  539,  1938-9,  1943 

of  Porters,  1943 

Protozoal,  194  \ 

Spirochaetic,  452,  453,  1944 

Traumatic,  Mucous,  1943 
Uretritis  Cystica,  Bodies  of,  537 
Urhur,  195 
Uridrosis,  2224 

Urinary  Amcebiasis,  1920,  1931 
Referen<  es,    11)36-7 

Canthariasis,  1641,  1926,  [934 

Calculi,  1926,  1929,  1930 

Myiasis,  863, 1620, 1622,  1628,  1926, 

1934 
Organs,  Diseases  of,  1921) 

References,  1936-7 
Schistosomiasis  (Bilharziosis,  q.v.), 

587,  1926 
Spirochetes,   451 

System,    Derangements    of,    1519, 
1522 
Ktfects  on,  of  Temperature  and 
Humidity,   76-7 
Tests 

Mycological,  1926.,  1934 
for  Quinine  Elimination,  1936 
References,  1937 
Urine,  Albumen-free,  Essentia]  in  Men 
for  Tropical  Service,  127 
Constituents  in 
M  lie  Bengali  :,  108 
Male  Europe. ins,  108 
Examination  of,  in  Pregnancy,  129 
I  hemoglobin  in,  Diagnosis,   1522 
of  Natives,  Examination  of,  1 30 
Nitrogen-Excretion  in,  in  India,  100 


l  Tnbilin  in  Malaria,  1 1  17 
Urogenital  Organs,  Subtertian  Malaria 

affecting,  1175,  1 180 
/  tyonema,  550 

caitdatitm,  547,  550,  1740,  1837 

■marinum,  550 
Urosporidium,  534 

Ursidae,  Traumatisms  caused  by,  148 
Urtica,  21 51,  2153 

crenulata,  2 151 

divica,  2 151 

fei'ox,  2151,  2158 

pilutifera,  2158 

stimulans,  2151 

urens,  2151,  2158 

urentissinra,  2 151 
Urticacece,  2153,  2154 

Arrow- Poisons  from,   1S1,   1S4 
Urticaria,  2264,  2267 

Febrile  Helminthic,  1516 

Malarial,  n  81 

Pigmentosa,  2267 
Urticarial  Eruptions,   2267 
Diagnosis,  1513,  1516 

Fevers,  1589,  1590,  1593 
Naegeli's,  1462 
References,   1473 
Urticarioid  Dermatitis,  2216 
Usciva,  2280 
Ustilaginece,  1032 
Ustilago,  1033 

carbo,  1032 

hypodytes,  1032,  2163 
Uta  Bueno,  2175 
Utahs,  the,  56 
Uterine  Fibromata,  1945 
Uterus,  Action  on,  of  Quinine,   1201 

Bacteria  of,  1951 
Utiete,  2159 
Uveitis,  Plastic,  2006 

Suppurative,    2005 

Vaccination  for  Alastrim,  1491 

for  Candidates  for  Tropical  Service, 
128 

for  Variola,  1491 

Sa  fe  Methods,  1493 
Vaccination  Rashes,  1494 

References,  1500 
Vaccine,  Lichen,  1496,  1516 

Lymph,  Preparation,  1493-4 
Va<  1  ines,  22-3 

Polyvalent,  23,  29 

Tetravaccines,  etc.,  23 
Vao  uii.i.  540,  541,  543,  1494,  1495 
References,  1500 
Treatment,  1496 

Gangrenous,  151 8 

Generalized,  1494,  151 8 

Localized,  1494-5 

Papulo-Vesicular,  1496-7,  1516 


2432 


INDEX 


Vaccinotherapy,  History,  22-3 
Vacuoli,  290,  291,  382 
Vagabond's  Disease,  2201 
Vaginal  Bacteria,  1951 

Discharge,  Monilia  in,  1085,  1090 
Mastigophora,  1946 
Myiasis,  1622,  1628 
Protozoa,  List  of,  1945 
Pruritus,  1026 
Sarcodina,  1945 
Spirochetes,  1945 
Thrush,  1945 
Yahlkamfia,  298,  299,  321 
References,  328 
Species 
albida,  322 

binncleata,  322,  323,  324 
diploidea,  322,  323,  324 
froschi,  322 
guttula,  322 
lacertce,  322 
lacustris,  322 
lamellipoda,  322 
Umax,  321,  322,  323 
lobospinosa,  322 
nana,  323,  324,  1833 
pcsdophthora,  323 
polypodia,  322 
punctata,  321 
tachypodia,  322 
Vajuolo,  i486 

Van  der  Scheer's  Fever,  1252 
Vanilla  Dermatitis,  2163 

Itch,  191,  2214 
Vanilla  planifolia,  191,  2163 
Vanilla-Poisoning,  191 
Vanillismus,  191,  729.  2163,  2214 
VaranidcB,  278 
Variable  Winds,  81 
Varicella,  i486,  see  also  Chicken-pox 
Varioloid,  1489 
Epidemic,  19*9 
Varicocele,  ig°4 

Varicose   Lymphatic    Glands   of    Fi- 
larial origin,  1595.  1599, 
1601,  1603,  1608 
Veins,  1904 

Ulcers  due  to,  2186,  2190 
Variegated  Tick,  723 
Variola,  i486,  see  also  Smallpox 
Hemorrhagica,  1488-9 
Pustulosa,  1488,  1489 
Varioloid,  1489 
Varicella,  1491 
Epidemic,  191 9 
Varix,     Lymphatic,     Filarial,     1595, 

1603,  1605,  1607 
Varnish-Tree  of  Japan,  2157 
Vascular  Modifications  du-  to  Solar 

Rays,  84,  88 
Veddahs,  the,  Food  of,  94 


Vegetal  Aphrodisiacs,  172 
Food  Poisoning,  193,  195 
Parasites,  115,  285,  872,  922,  923, 

1533.  1679 
Poisons,    162,   163,   164,    191,   193, 
195,  729,  1695,  see  also 
Dermatitis  Venenata 
Veillon's  Anaerobic  Micrococcus,  1949 
Vein-Dilatation,  (Esophageal,  1749 
Vejovidce,  207 

Veldt  Sore,  2030,  2031,  2190 
Veliger,  889 
Vena  medinensis,  O51 
Venereal  Bubo,  1963 

Disease,  118-19,  124,  127-8 
Sores,  2278,  2280 
Venomous  Animals,  203 
African,  125 
Amphibia,  240 

References,  241 
Bites    or    Stings    of,    Rash    from, 

1514 

Mammalia,  271 
Pisces,  230 

References,  241 
Protozoa  to  Arthropoda,  203 

References,  227-9 
Reptilia,  242 

References,  280-1 
Vent  d'Espagne,  82 
Ver  de  Case,  850 
du  Cayor,  849 
Macaque,  828,  1620 
Moyoquil,  828 
Veratrine,  169 
Verbascum  thapsus,  2153 
Verderame,  of  Maize,  1703 
Verme,  1633 

Vermiformia,  680,  692,  731 
Verole,  Petite,  i486 
Verruca  Seborrhceica,  2276 
Senilis,  2276 
Vulgaris,  541 
Verrucae,  2274 
Verruga  of  the  Andes,  1566 
Andicola,  1566 
Blanda,  1566 
de  Castilla,  1566 
de  Crapaud,  1566 
Mular,  1566 
Verruga  Peruviana,  1566 
.Etiology,  1533.  I569 
Biffi's  Bacillus  in,  1567-S 
Bodies  seen  in  Blood  in,  1  ,70 
Climatology,  123,  1568-9 
Complications,  1575 
Critical  period,  1575 
Definition,  1566 
Diagnosis,  1575 

Differential,    1557,    1568. 
1575-6,  2253-4 


INDEX 


2433 


Verruga  Peruviana,  continued 
Histopathology,  1571-2 
History,  1566-8 
Incidence 

Locale,  1569 

Occupation,  1569 
Insect     Vector,    suspect,      542, 

810,  919,  1568 
Morbid  Anatomy,  1571 
Pathology,  1570-1 
Prognosis,  1576-7 
Prophylaxis,  1577 
References,  1577 
Sequelae,  1575 
Symptomatology,       1566      sqq., 

1573-5 
Synonyms,  1566 
Treatment,  1577 
Varieties,  1575 

Virus    of,    Filterable,    and   Dis- 
tinct    from     that      of 
Oroya  Fever,  542 
Acute  or  Severe,  1575 
Apyrexial,  1567,  1568,  1572,  1573 
Eruptive  or  Mild,  1572-5 
Forme  Miliare,  1573 
Forme  Mulaire,  1573 
Verruga  de  Sangre,  1566 

de  Zapo  6  de  Quinua,  1566 
Vertebral  Column,  Abscess  of,   1072, 

io75 
Vertebrates,  Acarine  Parasites  of,  693 
Cold-Blooded,    Trypanosomes    In- 
fecting, 398 
Loeschia  in,  List,  321 
Verticillium  graphii,  1 1 1 4 
Vertige  Paralysant,  1982 

Ptosique,  1982 
Vertigo,    Endemic    Paralytic,    1981, 
1982 
Post-Malarial,  11 84 
Vesicular  Dermatitis,  Seasonal,  226, 
2204 
References,  2220 
Eruptions,  Diagnosis  of,  1513,  1517 
Fever,  1470-1,  1517-18 
Vespa  crabro,  219,  367 
ger  mania  219 
orientalis,  219,  221 
vulgaris,  219 
VespcB,  Stings  of,  219,  221 
Vetches,  Poisonous,  196-7 
Red,  196 
Spanish,  196 
Vibrio,  962,  1838 
albensis,  963 

cholera,  96,  1801,  1803,  1804,  1805, 
1810,  1819 
El  Tor  variety,  963 
comma,  962 
of  Curtis,  1951 


Vibric,  continued 
drennani,  963 
freseris,  1820 

gindha,  962,  963,  964,  1820 
insolitus,  962,  964 
kegallensis,  962,  964,  1820 
lingualis,  105 1 
liquefaciens,  964 
metschnikovi,  963 
of  Orticoni,  1820 
paracholercB,  964 
sputigenus,  964 
striatus,  964 
subtilis,  933 
terrigenus,  963 
wolfii,  964 
wiesechensis,  964 
zeylanicus,  1068 
Vibrion  Septique,  959,  961 

Reference,  966 
Vibrios,  Groups  of 

Aerobic,  963 

Albensis,  963 

Cholera,  963 

Drennani,  963 

Funkier-Prior,   963 

Gindha,  963,  964 

Metschnikovi,  963 

Terrigenus,  963 
Vibriothrix,  1068,  1838,  1839 

zeylanica,  1839 
Vicia  faba,  201 
Vigna  catjang,  195 

filosa,  195 
Vincent's  Angina,  448,  552,  959,  1520, 

1745.  1777 
Vinegar  Eel,  627 
Vipera,  250 
ammodytes,  251 
berus,  250,  251 
Venom,  258 
lebetina,  251 
raddii,  251 
renardii,  251 
russellii,  250,  251 

Venom  of,  163,  243,  253,  259,  260, 
263,  264,  268-9 
Treatment,  244,  272,  273 
Viperidce,  244,  245,  249 
Viperince,  249,  250,  251 
Viperine  Venom,  163,  243,  244,  253, 
254,  256,  257,  262,  263, 
268-70,  271,  1520 
Anti-Sera  for,  273 
Vipers,  242,  244 

Venom  of,  163,  242 
Virgin  Islands,  Diseases  of,  124 
Viruelas,  i486 
Vitamines,  97,  109 

and  Beri-beri,  109,  1673,  1675 
Cooking  to  Conserve,  109 

153 


2434 


INDEX 


Vitamines,  continued 

Distribution,  109-10 

Lipoids  in  relation  to,  no 

Processes  destructive  of,  109,  no 

in  Rice,  109 

of  Scurvy,  109 

Specific,  of  Growth,  109 
Vitiligo,  2227 

Vitreous  Opacities, Malarial,  2005 
Vlekkoorts,  1326 
Voles,  915 

Volhynia  Fever,  1501 
Volutine,   386 

Granules,  290 
Volvox  chaos,  299,  301 
Volvulosis,  1 961,  1964 

References,  1966 
Volvulus,  Intestinal,  1939 
Vomit,  Human,  Spiroschaudinnia  in, 

453 
Vomiting,  Deductions  from,  1520 
Vomiting  Sickness  of  Jamaica,   173, 
1233,  1695 

References,  1699 
Vorticellce,  546 
Vuilleminella,  989 
Vulva,  Bacteria  of,  1951 

Elephantiasis  of,    161 1,    1617 
Vulvo-Vaginitis,  1945 

Waba  Arrow-Poison,  182 
W.ibain,  182 

Wabajo  Arrow-Poison,  182 
Wanomi  Arrow-Poisons,  183 
Wahuma  Race,  47 
Wall-Louse,  763 
Walsura  piscidia,  187 
Walterinnesia,  246 

cBgyptica,  251 
War,    The,    and    Tropical    Medicine, 
29-30 

and  Venereal  Disease,  119 
War  Ration,  British,  99,  100 
War-Zone  Fevers,  1128,  1501 
References,  1510 

Neuroses,  1981-2 

CEdema,  1693 

Post-Malarial  Affections,  n  85 
Warangangpulver,  2013 
Warble,  1636-7 
Warble-Flies,  825 
Warburg's  Tincture,  1194,  1200 
Ward's     System     for     Divisions     of 

Tropical  Climates,  62 
Wargla  Race,  46,  47 
Warm-Blooded   Vertebrates,    Trypa- 

nosomes  of,  395,  401 
Warra,  173 
Warts,  1073,  2274-6 
Treatment,  2276 
Native,  2276-7 


Warts,  continued 
Filiform,  2274} 
on  Genitalia,  2274 
in  Verruga  Peruviana,  1566  sqq. 
Washerwoman's  Fingers,  173  1 
Waskia,  347 

intestinalis,  348 
Wasp-Stings,   12,  219,  221 
Dermatites  due  to,  2207 
Wasps,  908 
Wassermann    Reaction    in    Malaria, 

1152 
Water,   Contaminated,  in  relation  to 
Amoebic  Dysentery,  1827 
in  Diet,  96 

Food  Value  of,  97 
in  relation  to  Enteric,  1364,   1371 
Oiling  of,  1 108 
Water-Bugs,  Crithidia  in,  367,  769 
Water  Leeches,  683,  1880 
Water  Moccasin,  250 
Water-Snakes,  246,  249,  250 
Water-Supply,  Defective,  as  cause  of 
Disease,  124 
Plentiful  Essential,  107 
Watsonius,  561,  562 
watsoni,  562,  1752 
Wau-Tree  (Japan),  2 156 
Wayatholechell,   1824. 
Weaning,  1959-60 

Weapons,  Poisons  used  on,  see  Arrow- 
Poisons,  180 
Weasel-Bite,  1356,  1361 
Wechselfieber,  n  29 
Werlhof's  Purpura,  2267 
Weil's  Disease,  Infective  Jaundice  or 
Icterus  Castrensis  Gra- 
vis (q.v.),  447,  448,  452, 
1224,  1313,  1397,  1467, 
1501,  1505,  1509,  1517 
Two  types  of,  1508 
Weil's-Disease-like     Subtertian    Mal- 
aria,  1171,   1172 
Weilschen  Krankheit,  1505 
Welch's  Parasite,  737 
Well-Screening,   1208  * 

Wenku,  1303 
Werlhof's  Purpura,  2267 
Wesenbergus,  935,  940,  1362,  1406 
fevmentosus,  940,  941 
giumai,  9  1 1 

wesenbergi,  935,  940,  041 
West  Africa,  180,  182 
Arrow-Poisons,  183 
Native  Medicine,  3 
West  African  Relapsing  Fever,  13 18 
Tick  Fever,  Causal  agent,  444,  445 
Vegetal  Poisons,  164,  168,  169,  172 
West  Indian  Fish-Poison,  188 
Modified  Smallpox,  1491 
Nodules,  2247,  2254 


INDEX 


5435 


Wheat,  95,  99,  104 

Wheat-Straw    Worm,     Parasite     of, 

2216 
Wheel  Bug,  767 
Whip-worm  Infection   (Trichuriasis), 

1758 
\\  hite  Pinta,  1092,  2094,  2095 
White  or  Yellow 

Actinomycoses,  2141 
Maduromycoses,  2120,  2122 
African,  2120,  2122 
Asian,  2122,  2123 
European,  2120,  2122 
Whitening  of  Nails,  2283 
Whit  mania,  686,  687 

ferox,  687 
Whitmore's  Fever,  1466 
Whooping-Cough,  120 
Willia,  979,  983,  1886 

anomala,  983 
Window-Fly,  824,  900 
Winds,  79 

Wing-Cells  of  Insects,  745 
Wings  of  Hemiptera,  761 

Hexapoda; 745 
Wirsung's  Duct,  Blocking  of,  1908 
Withania  somnifera,  190 
Withmorei,  322 
Wohlfartia,  830,  831 

magnifica,  831,  1627,  2011 
Wolf-Bite,  151 
Wolof  Race,  51 
Women 

Examination  of,  as  to  Fitness  for 
Tropical  Life,    129 
on      Return      to      Temperate 
Climate,  130 
Standard  Diets  for,  98 
Native,  Life  Assurance  of,  132-3 
Poisons  used  by,  169-70 
Wood- Bee,  Sting  of,  219 
Wood- Rats,  915 

Parasites  of,  398 
Wooden  Tongue  in  Cattle,  21  |S 
Woods,  Ornamental,  Dust  of,  causing 

Dermatites,  2159 
Woolley's       Fever      with      [aundice, 

1467 
Work,     Mechanical,     Diet-quantities 

for,  99-100 
Worms,  Intestinal,  Disease  production 
by,  285,  1533, 1752 
Parasites  of,  470 

Parasitic,   carried  by   Arthropods, 
873.  876 
in  Blood,  1903 
Diseases  due  to,  1533 
Transmission  by  Flies,  24,  908 
Wounds,  Aspergillosis  of,  1032 

Neglected,      Ulceration     following 
on,  2191 


Wurmkrankheit,  1761 
Wyoming,    Intermittent  Tick  Fever 
of,  1349 

X  Bodies  in  Blood  Films,  1901 

Reference,  1705 
Xanthochroi  Division  of  Mankind,  45, 

46 
Xanthoderma   Areatum,   2222,  2236, 
2237 

References,  2245 
Xanthoma  Diabeticorum,  2273 

Planum,  2273 

Tuberosum,  2273 
Xanthophylline  Glasses  for  the  Eyes, 

1996 
Xenodon  severus,  245 
Xenopsylla,  865,  866,  869,  870 

astia,  1422 

brasiliensis,  866 

cheopis,  23,  124,  860,  866,  867,  869, 
870,  911,  912,  1422 

cleopaircB,  376 
Xeroderma,  Anidrosis  in,  2224 

Pigmentosum,  88,  1731,  2281 

Simple,  2281 
Xerophthalmia,  2006 
Xerosis,  Conjunctival,  2000 

Epithelial,  of  the  Eye,  2002 
Xilocopa  violacea,  219 
Xiphidiocer  caries,  359 
Xylocrypta,  806 

Yakuts,  the,  55 
Yangonin,  176 

Yaws,    1535,    for   details,    see  Fram- 
bcesia 
Bosch-,  2172 
Forest-,  2167 
Yaws-Flies,  1632 
Yaws  Ringworm,  2052 
Yaya,  1536 
Yearly  Sore,  2165 
Yeast,  22 

Treatment   by,    of  Tropical    Boils, 
2027-8 
Yeasts,   Achromaticus  considered  as, 

360 
Yeki.   1  416 

Yellow  Actinomycosis.  2140.  see  also 
undo-  Actinomycosis 
Atrophy,     Acute,    of    Liver,    1507, 

1508,  1906 
Disease,  2236 
Yellow   Fever,    24,   876,    1207,    1229, 
1472 
/Etiology,  1233 
Blood  in,  1235 
Climatology,  1232-3 
Complications,  1238 
Course,  1236  sqq. 


2436 


INDEX 


Yellow  Fever,  continued 

Definition,  1229 

Diagnosis,  1238,  1519 

Differential,  1186,  1224,  1238, 
1250,  1312,  1313,  1317, 
1395.  1396,  1507,  1508, 
1517,  1522,  1697 

Diet,  1240 

Endemic,  25 

Faget's  Sign  in,  1237,  1238 

History,  1229-32 

Immunity,  1235 

Incubation,  1236 

Insect  Vector,  23,  541,  542,  747, 
796,  878,  919,  1128, 
1229,  1230,  1233,  1240, 
see  also  Stegomyia 
fasciata 

Morbid  Anatomy,   1236 

Pathology,  1235 

Pigmentation,  1519 

Prognosis,  1238 

Prophylaxis,        116,       123,       1231, 
1240-2 

Rash,  1 51 7 

References,  1242-3 

Sequelae,  1238 

Spirochsetes  in,  448,  1230 

Sternberg's  Mixture  in,  1239 

Symptomatology,  1236-8 

Synonyms,  1229 

Transmission,  see  Insect  Vectors, 
above 

Treatment,  1239-40 

Urine,  in,  1235 

Varieties,  1238 

Virus,  Filterable,  541,  542 

Vomit  in,  1234  sqq.,  1520 
Yellow-Fever-like  Subtertian  Malaria, 

1171,  1172,  1186 
Yemen  Ulcer,  21 81 


Yerba  mate,  177-8 
Yercumby,  173 
Ifoshubia,  726 
^ttimbehe  Bark,  172 
Yohimbine  Hydrochloride,  172 
Yokogawa,  571 

yokogawai,  571 
Yoruba  Race,  51 
Yumas,  the,  60 
Yumbehoa  Bark,  172 
Yuncas,  the,  59 

Zamenis  flagelliformis,  487 

hippocrepis,  487 

mucosas,  244,  245 
Zanthoxylum  flavtim,  2159 
Zapodides,  914 
Zea  mats,  1709 
Zeism,  1709 
Zibla,  1952 
Zingiber  aeccs,  172 
Zoantharia,  204 
Zona,  2269 
Zooparasites,  285 
Zoosporangium,  969 
Zoospores,  969 
Zootrophotoxismus,    193 
Zoque,  the,  56 
Zousfana,  414 
Zulu  Peoples,  53 
Zygocystis,  471 
Zygomycetes,  972 
ZgyophyllacecB,  ,164,  166 
Zygosaccharomyces,  979 
Zygosis,  294,  295 
Zygosoma,  471 
Zygospores,  971 
Zygote,  292,  874,  921 
Zymonema,  1079,  2081,  2084 

gilchristi,  1073,  1079 
Zymonematosis,  2081,  2084 


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